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\|Van Gogh's The Starry Night, from 1889, shows changes in light and color as can appear with psychosis.\| \|Classification and external resources\| \|OMIM\|\|603342 608923 603175 192430\| Psychosis is an abnormal condition of the mind that involves a "loss of contact with reality". People experiencing psychosis may exhibit personality changes and thought disorder. Depending on its severity, this may be accompanied by unusual or bizarre behavior, as well as difficulty with social interaction and impairment in carrying out daily life activities. Psychosis as a sign of a psychiatric disorder is a diagnosis of exclusion. That is, a new-onset episode of psychosis is not considered a symptom of a psychiatric disorder until other relevant and known causes of psychosis are properly excluded. Medical and biological laboratory tests should exclude central nervous system diseases and injuries, diseases and injuries of other organs, psychoactive substances, and toxins as causes of symptoms of psychosis before any psychiatric illness can be diagnosed. In medical training, psychosis as a sign of illness is often compared to fever since both can have multiple causes that are not readily apparent. The term "psychosis" is very broad and can mean anything from relatively normal aberrant experiences through to the complex and catatonic expressions of schizophrenia and bipolar type 1 disorder. In properly diagnosed psychiatric disorders (where other causes have been excluded by extensive medical and biological laboratory tests), psychosis is a descriptive term for the hallucinations, delusions and impaired insight that may occur. Psychosis is generally the term given to noticeable deficits in normal behavior (negative signs) and more commonly to diverse types of hallucinations or delusional beliefs, particularly with regard to the relation between self and others as in grandiosity and pronoia or paranoia. The first-line treatment for many psychotic disorders is antipsychotic medication. Meta-analyses of these drugs show either no difference in effects, or a moderate effect size, suggesting that the mechanism of psychosis is more complex than an overactive dopamine system. - 1 Signs and symptoms - 2 Causes - 3 Pathophysiology - 4 Diagnosis - 5 Prevention - 6 Treatment - 7 History - 8 References - 9 Further reading - 10 External links Signs and symptoms A hallucination is defined as sensory perception in the absence of external stimuli. Hallucinations are different from illusions, or perceptual distortions, which are the misperception of external stimuli. Hallucinations may occur in any of the senses and take on almost any form, which may include simple sensations (such as lights, colors, tastes, and smells) to experiences such as seeing and interacting with fully formed animals and people, hearing voices, and having complex tactile sensations. Auditory hallucinations, particularly experiences of hearing voices, are the most common and often prominent feature of psychosis. Hallucinated voices may talk about, or to, the person, and may involve several speakers with distinct personalities. Auditory hallucinations tend to be particularly distressing when they are derogatory, commanding or preoccupying. However, the experience of hearing voices need not always be a negative one. One research study has shown that the majority of people who hear voices are not in need of psychiatric help. The Hearing Voices Movement has subsequently been created to support voice hearers, regardless of whether they are considered to have a mental disorder or not. Psychosis may involve delusional beliefs, some of which are paranoid in nature. Put simply, delusions are false beliefs that a person holds on to, without adequate evidence. It can be difficult to change the belief, even with evidence to the contrary. Common themes of delusions are persecutory (person believes that others are out to harm them), grandiose (person believing that they have special powers or skills), etc. Persons with Ekbom syndrome may have delusional beliefs of an imaginary parasite infestation, whereas depressed persons might have delusions consistent with their low mood (e.g., delusions that they have sinned, or have contracted serious illness, etc.). Karl Jaspers has classified psychotic delusions into primary and secondary types. Primary delusions are defined as arising suddenly and not being comprehensible in terms of normal mental processes, whereas secondary delusions are typically understood as being influenced by the person's background or current situation (e.g., ethnicity; also religious, superstitious, or political beliefs). Catatonia describes a profoundly agitated state in which the experience of reality is generally considered impaired. There are two primary manifestations of catatonic behavior. The classic presentation is a person who does not move or interact with the world in any way while awake. This type of catatonia presents with waxy flexibility. Waxy flexibility is when someone physically moves part of a catatonic person's body and the person stays in the position even if it is bizarre and otherwise nonfunctional (such as moving a person's arm straight up in the air and the arm staying there). The other type of catatonia is more of an outward presentation of the profoundly agitated state described above. It involves excessive and purposeless motor behaviour, as well as extreme mental preoccupation that prevents an intact experience of reality. An example is someone walking very fast in circles to the exclusion of anything else with a level of mental preoccupation (meaning not focused on anything relevant to the situation) that was not typical of the person prior to the symptom onset. In both types of catatonia there is generally no reaction to anything that happens outside of them. It is important to distinguish catatonic agitation from severe bipolar mania, although someone could have both. Thought disorder describes an underlying disturbance to conscious thought and is classified largely by its effects on speech and writing. Affected persons show loosening of associations, that is, a disconnection and disorganization of the semantic content of speech and writing. In the severe form speech becomes incomprehensible and it is known as "word salad". Many causes of schizophrenia are also causes of psychosis. From a diagnostic standpoint, organic disorders were those believed caused by physical illness affecting the brain (that is, psychiatric disorders secondary to other conditions), while functional disorders were considered disorders of the functioning of the mind in the absence of physical disorders (that is, primary psychological or psychiatric disorders). The materialistic or naturalistic (i.e. scientific) view of the mind–body problem holds that mental disorders arise from physical processes; in this view, the distinction between brain and mind, and therefore between organic and functional disease, is an artificial one. Subtle physical abnormalities have been found in illnesses traditionally considered functional, such as schizophrenia. The DSM-IV-TR avoids the functional/organic distinction, and instead lists traditional psychotic illnesses, psychosis due to general medical conditions, and substance-induced psychosis. - schizophrenia and schizophreniform disorder - affective (mood) disorders, including severe depression, and severe depression or mania in bipolar disorder (manic depression). People experiencing a psychotic episode in the context of depression may experience persecutory or self-blaming delusions or hallucinations, while people experiencing a psychotic episode in the context of mania may form grandiose delusions. - schizoaffective disorder, involving symptoms of both schizophrenia and mood disorders - brief psychotic disorder, or acute/transient psychotic disorder - delusional disorder (persistent delusional disorder) - chronic hallucinatory psychosis Psychotic symptoms may also be seen in: - schizotypal disorder - certain personality disorders at times of stress (including paranoid personality disorder, schizoid personality disorder, and borderline personality disorder) - major depressive disorder in its severe form, although it is possible and more likely to have severe depression without psychosis - bipolar disorder in the manic and mixed episodes of bipolar I disorder and depressive episodes of both bipolar I and bipolar II; however, it is possible to experience such states without psychotic symptoms. - post-traumatic stress disorder - induced delusional disorder - Sometimes in obsessive-compulsive disorder - Dissociative disorders, due to many overlapping symptoms, careful differential diagnosis includes especially dissociative identity disorder. Stress is known to contribute to and trigger psychotic states. A history of psychologically traumatic events, and the recent experience of a stressful event, can both contribute to the development of psychosis. Short-lived psychosis triggered by stress is known as brief reactive psychosis, and patients may spontaneously recover normal functioning within two weeks. In some rare cases, individuals may remain in a state of full-blown psychosis for many years, or perhaps have attenuated psychotic symptoms (such as low intensity hallucinations) present at most times. Brief hallucinations are not uncommon in those without any psychiatric disease. Causes or triggers include: - Falling asleep and waking: hypnagogic and hypnopompic hallucinations, which are entirely normal - Bereavement, in which hallucinations of a deceased loved one are common - Severe sleep deprivation - Sensory deprivation and sensory impairment - Caffeine intoxication - An extremely stressful event Subtypes of psychosis include: - Menstrual psychosis, including circa-mensual (approximately monthly) periodicity, in rhythm with the menstrual cycle. - Postpartum psychosis, occurring recently after childbirth - Monothematic delusions - Myxedematous psychosis - Stimulant psychosis - Tardive psychosis - Shared psychosis Cycloid psychosis is a psychosis that progresses from normal to full-blown, usually between a few hours to days, not related to drug intake or brain injury. The cycloid psychosis has a long history in European psychiatry diagnosis. The term "cycloid psychosis" was first used by Karl Kleist 1926. Despite the significant clinical relevance, this diagnosis is neglected both in literature as in nosology. The cycloid psychosis has attracted much interest in the international literature of the past 50 years, but the number of scientific studies have greatly decreased over the past 15 years, possibly partly explained by the misconception that the diagnosis has been included incorporated in current diagnostic classification systems. The cycloid psychosis is therefore only partially described in the diagnostic classification systems used. "polymorph acute psychotic disorder", with or without schizophrenic symptoms. (F23.0 ICD 10). Cycloid psychosis is nevertheless its own specific disease that is distinct from both the manic-depressive disorder, and from schizophrenia, and this despite the fact that the cycloid psychosis can include both bipolar (basic mood shifts) as well as schizophrenic symptoms. The disease is an acute, usually self-limiting, functionally psychotic state, with a very diverse clinical picture that almost consistently is characterized by the existence of some degree of confusion or distressing perplexity, but above all, of the multifaceted and diverse expressions the disease takes. The main features of the disease is thus that the onset is acute, the multifaceted picture of symptoms and typically reverses to a normal state and that the long-term prognosis is good. In addition, diagnostic criteria include at least four of the following symptoms: - Mood-incongruent delusions - Pan-anxiety, a severe anxiety not bound to particular situations or circumstances - Happiness or ecstasy of high degree - Motility disturbances of akinetic or hyperkinetic type - Concern with death - Mood swings to some degree, but less than what is needed for diagnosis of an affective disorder Cycloid psychosis occurs in people of generally 15–50 years of age. \|\|This section needs more medical references for verification or relies too heavily on primary sources, specifically: Case reports should be replaced with review articles or meta-analyses.. (September 2014)\| A very large number of medical conditions can cause psychosis, sometimes called secondary psychosis. Examples include: - disorders causing delirium (toxic psychosis), in which consciousness is disturbed - neurodevelopmental disorders and chromosomal abnormalities, including velocardiofacial syndrome - neurodegenerative disorders, such as Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease - focal neurological disease, such as stroke, brain tumors, multiple sclerosis, and some forms of epilepsy - malignancy (typically via masses in the brain, paraneoplastic syndromes, or drugs used to treat cancer) - infectious and postinfectious syndromes, including infections causing delirium, viral encephalitis, HIV/AIDS, malaria, Lyme disease, syphilis - endocrine disease, such as hypothyroidism, hyperthyroidism, adrenal failure, Cushing's syndrome, hypoparathyroidism and hyperparathyroidism; sex hormones also affect psychotic symptoms and sometimes childbirth can provoke psychosis, termed puerperal psychosis - inborn errors of metabolism, such as Succinic semialdehyde dehydrogenase deficiency, porphyria and metachromatic leukodystrophy - nutritional deficiency, such as vitamin B12 deficiency - other acquired metabolic disorders, including electrolyte disturbances such as hypocalcemia, hypernatremia, hyponatremia, hypokalemia, hypomagnesemia, hypermagnesemia, hypercalcemia, and hypophosphatemia, but also hypoglycemia, hypoxia, and failure of the liver or kidneys - autoimmune and related disorders, such as systemic lupus erythematosus (lupus, SLE), sarcoidosis, Hashimoto's encephalopathy, and anti-NMDA-receptor encephalitis Patients with these conditions may be, 'slipping through the net'. - poisoning, by therapeutic drugs (see below), recreational drugs (see below), and a range of plants, fungi, metals, organic compounds, and a few animal toxins - some sleep disorders, including hallucinations in narcolepsy (in which REM sleep intrudes into wakefulness) Various psychoactive substances (both legal and illegal) have been implicated in causing, exacerbating, and/or precipitating psychotic states and/or disorders in users. This may be upon intoxication, for a more prolonged period after use, or upon withdrawal. Individuals who have a substance induced psychosis tend to have a greater awareness of their psychosis and tend to have higher levels of suicidal thinking compared to individuals who have a primary psychotic illness. Drugs that can induce psychotic symptoms include alcohol, cannabis, cocaine, amphetamines, cathinones, psychedelic drugs (such as LSD and psilocybin), κ-opioid receptor agonists (such as enadoline and salvinorin A) and NMDA receptor antagonists (such as phencyclidine and ketamine). Approximately three percent of people who are suffering from alcoholism experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through a kindling mechanism. The mechanism of alcohol-related psychosis is due to the long-term effects of alcohol resulting in distortions to neuronal membranes, gene expression, as well as thiamin deficiency. It is possible in some cases that alcohol abuse via a kindling mechanism can cause the development of a chronic substance induced psychotic disorder, i.e. schizophrenia. The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as causing psychosocial impairments. According to some studies, the more often cannabis is used the more likely a person is to develop a psychotic illness, with frequent use being correlated with twice the risk of psychosis and schizophrenia. While cannabis use is accepted as a contributory cause of schizophrenia by some, it remains controversial, with pre-existing vulnerability to psychosis emerging as the key factor that influences the link between cannabis use and psychosis. Some studies indicate that the effects of two active compounds in cannabis, tetrahydrocannabinol (THC) and cannabidiol (CBD), have opposite effects with respect to psychosis. While THC can induce psychotic symptoms in healthy individuals, CBD may reduce the symptoms caused by cannabis. Cannabis use has increased dramatically over the past few decades whereas the rate of psychosis has not increased. Together, these findings suggest that cannabis use may hasten the onset of psychosis in those who may already be predisposed to psychosis. High-potency cannabis use indeed seems to accelerate the onset of psychosis in predisposed patients. A 2012 study concluded that cannabis plays an important role in the development of psychosis in vulnerable individuals, and that cannabis use in early adolescence should be discouraged. Methamphetamine induces a psychosis in 26–46 percent of heavy users. Some of these people develop a long-lasting psychosis that can persist for longer than six months. Those who have had a short-lived psychosis from methamphetamine can have a relapse of the methamphetamine psychosis years later after a stress event such as severe insomnia or a period of heavy alcohol abuse despite not relapsing back to methamphetamine. Individuals who have long history of methamphetamine abuse and who have experienced psychosis in the past from methamphetamine abuse are highly likely to rapidly relapse back into a methamphetamine psychosis within a week or so of going back onto methamphetamine. Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms. Drugs that can induce psychosis experimentally and/or in a significant proportion of people include amphetamine and other sympathomimetics, dopamine agonists, ketamine, corticosteroids (often with mood changes in addition), and some anticonvulsants such as vigabatrin. Stimulants that may cause this include lisdexamfetamine. There is some evidence that trauma during childhood increases the risk of developing psychosis. A meta-analysis showed that high neuroticism is an independent predictor of the development of psychotic symptoms and psychosis. The first brain image of an individual with psychosis was completed as far back as 1935 using a technique called pneumoencephalography (a painful and now obsolete procedure where cerebrospinal fluid is drained from around the brain and replaced with air to allow the structure of the brain to show up more clearly on an X-ray picture). The purpose of the brain is to collect information from the body (pain, hunger, etc.), and from the outside world, interpret it to a coherent world view, and produce a meaningful response. The information from the senses enter the brain in the primary sensory areas. They process the information and send it to the secondary areas where the information is interpreted. Spontaneous activity in the primary sensory areas may produce hallucinations, which the secondary areas misinterpret as information from the real world. For example, a PET or fMRI scan of a person who claims they hear voices may show activation in the primary auditory cortex, or parts of the brain involved in the perception and understanding of speech. Tertiary brain cortex collects the interpretations from the secondary cortexes and creates a coherent world view of it. A study investigating structural changes in the brains of people with psychosis showed there was significant grey matter reduction in the right medial temporal, lateral temporal, and inferior frontal gyrus, and in the cingulate cortex bilaterally of people before and after they became psychotic. Findings such as these have led to debate about whether psychosis itself causes excitotoxic brain damage and whether potentially damaging changes to the brain are related to the length of psychotic episode. Recent research has suggested that this is not the case although further investigation is still ongoing. Studies with sensory deprivation have shown that the brain is dependent on signals from the outer world to function properly. If the spontaneous activity in the brain is not counterbalanced with information from the senses, loss from reality and psychosis may occur after some hours. A similar phenomenon is paranoia in the elderly, when poor eyesight, hearing and memory make the person abnormally suspicious of the environment. On the other hand, loss from reality may also occur if the spontaneous cortical activity is increased so that it is no longer counterbalanced with information from the senses. The 5-HT2A receptor seems to be important for this, since psychedelic drugs that activate them produce hallucinations. However, the main feature of psychosis is not hallucinations, but the inability to distinguish between internal and external stimuli. Close relatives to psychotic patients may hear voices, but since they are aware that they are unreal they can ignore them, so that the hallucinations do not affect their reality perception. Hence they are not considered psychotic. Psychosis has been traditionally linked to the neurotransmitter dopamine. In particular, the dopamine hypothesis of psychosis has been influential and states that psychosis results from an overactivity of dopamine function in the brain, particularly in the mesolimbic pathway. The two major sources of evidence given to support this theory are that dopamine receptor D2 blocking drugs (i.e., antipsychotics) tend to reduce the intensity of psychotic symptoms, and that drugs that boost dopamine activity (such as amphetamines and cocaine) can trigger psychosis in some people (see amphetamine psychosis). However, increasing evidence in recent times has pointed to a possible dysfunction of the excitory neurotransmitter glutamate, in particular, with the activity of the NMDA receptor. This theory is reinforced by the fact that dissociative NMDA receptor antagonists such as ketamine, PCP and dextromethorphan (at large overdoses) induce a psychotic state more readily than dopaminergic stimulants, even at "normal" recreational doses. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative psychotic symptoms, more closely than amphetamine psychosis. Dissociative induced psychosis happens on a more reliable and predictable basis than amphetamine psychosis, which usually only occurs in cases of overdose, prolonged use or with sleep deprivation, which can independently produce psychosis. New antipsychotic drugs that act on glutamate and its receptors are currently undergoing clinical trials. The connection between dopamine and psychosis is generally believed complex. While dopamine receptor D2 suppresses adenylate cyclase activity, the D1 receptor increases it. If D2-blocking drugs are administered the blocked dopamine spills over to the D1 receptors. The increased adenylate cyclase activity affects genetic expression in the nerve cell, which takes time. Hence antipsychotic drugs take a week or two to reduce the symptoms of psychosis. Moreover, newer and equally effective antipsychotic drugs actually block slightly less dopamine in the brain than older drugs whilst also blocking 5-HT2A receptors, suggesting the 'dopamine hypothesis' may be oversimplified. Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis and Zoldan et al. reported moderately successful use of ondansetron, a 5-HT3 receptor antagonist, in the treatment of levodopa psychosis in Parkinson's disease patients. Psychiatrist David Healy has criticised pharmaceutical companies for promoting simplified biological theories of mental illness that seem to imply the primacy of pharmaceutical treatments while ignoring social and developmental factors that are known important influences in the aetiology of psychosis. Some theories believe many psychotic symptoms are a problem with the perception of ownership of internally generated thoughts and experiences. For example, the hallucination of hearing voices may arise from internally generated speech that is mislabeled by the psychotic person as coming from an external source. It has been suggested that persons with bipolar disorder may have increased activity of the left hemisphere compared to the right hemisphere of the brain, while persons with schizophrenia have increased activity in the right hemisphere. Increased level of right hemisphere activation has also been found in people who have high levels of paranormal beliefs and in people who report mystical experiences. It also seems that people who are more creative are also more likely to show a similar pattern of brain activation. Some researchers have been quick to point out that this in no way suggests that paranormal, mystical or creative experiences are in any way by themselves a symptom of mental illness, as it is still not clear what makes some such experiences beneficial and others distressing. A review found an association between a first-episode of psychosis and prediabetes. In otherwise normal individuals, exogenous ligands can produce psychotic symptoms. NMDA receptor antagonists, such as ketamine, can produce a similar psychosis to that experienced in schizophrenia.[non-primary source needed] Prolonged or high dose use of psychostimulants can alter normal functioning, making it similar to the manic phase of bipolar disorder. NMDA antagonists replicate some of the so-called "negative" symptoms like thought disorder in subanesthetic doses (doses insufficient to induce anesthesia), and catatonia in high doses. Psychostimulants, especially in one already prone to psychotic thinking, can cause some "positive" symptoms, such as delusional beliefs, particularly those persecutory in nature. Psychosis is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis cannot be considered a symptom of a psychiatric disorder until other relevant and known causes of psychosis are properly excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis. An initial assessment includes a comprehensive history and physical examination by a physician, psychiatrist, psychiatric nurse practitioner or psychiatric physician assistant. Biological tests should be performed to exclude psychosis associated with or caused by substance use, medication, toxins, surgical complications, or other medical illnesses. Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors, including medical illnesses. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure: - Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism, - Basic electrolytes and serum calcium to rule out a metabolic disturbance, - Full blood count including ESR to rule out a systemic infection or chronic disease, and - Serology to exclude syphilis or HIV infection. Other investigations include: Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using a - Urinalysis and a - Full serum toxicology screening. Because some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individual's family, partner, or friends should be asked whether the patient is currently taking any dietary supplements. Common mistakes made when diagnosing people who are psychotic include: - Not properly excluding delirium, - Not appreciating medical abnormalities (e.g., vital signs), - Not obtaining a medical history and family history, - Indiscriminate screening without an organizing framework, - Missing a toxic psychosis by not screening for substances and medications - Not asking family or others about dietary supplements, - Premature diagnostic closure, and - Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder. Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis using a person's family history, incorporating information from the person with psychosis, and information from family, friends, or significant others. Types of psychosis in psychiatric disorders may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS) assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2–3 days. The patient's family can also answer questions on the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale (PANSS). The evidence for the effectiveness of early interventions to prevent psychosis appeared inconclusive.[needs update] Whilst early intervention in those with a psychotic episode might improve short term outcomes, little benefit was seen from these measures after five years. However, there is evidence that cognitive behavioral therapy (CBT) may reduce the risk of becoming psychotic in those at high risk, and in 2014 the UK National Institute for Health and Care Excellence (NICE) recommended preventive CBT for people at risk of psychosis. The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The first-line psychiatric treatment for many psychotic disorders is antipsychotic medication, which can reduce the positive symptoms of psychosis in about 7 to 14 days. The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Tentative evidence supports that amisulpride, olanzapine, risperidone and clozapine may be more effective for positive symptoms but result in more side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages. There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people. Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people. Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol. Psychological treatments such as acceptance and commitment therapy (ACT) are possibly useful in the treatment of psychosis, helping people to focus more on what they can do in terms of valued life directions despite challenging symptomology. Early intervention in psychosis is based on the observation that identifying and treating someone in the early stages of a psychosis can improve their longer term outcome. This approach advocates the use of an intensive multi-disciplinary approach during what is known as the critical period, where intervention is the most effective, and prevents the long term morbidity associated with chronic psychotic illness. The word psychosis was introduced to the psychiatric literature in 1841 by Karl Friedrich Canstatt in his work Handbuch der Medizinischen Klinik. He used it as a shorthand for 'psychic neurosis'. At that time neurosis meant any disease of the nervous system, and Canstatt was thus referring to what was considered a psychological manifestation of brain disease. Ernst von Feuchtersleben is also widely credited as introducing the term in 1845, as an alternative to insanity and mania. The term stems from Modern Latin psychosis, "a giving soul or life to, animating, quickening" and that from Ancient Greek ψυχή (psyche), "soul" and the suffix -ωσις (-osis), in this case "abnormal condition". The word was also used to distinguish a condition considered a disorder of the mind, as opposed to neurosis, which was considered a disorder of the nervous system. The psychoses thus became the modern equivalent of the old notion of madness, and hence there was much debate on whether there was only one (unitary) or many forms of the new disease. One type of broad usage would later be narrowed down by Koch in 1891 to the 'psychopathic inferiorities'—later renamed abnormal personalities by Schneider. The division of the major psychoses into manic depressive illness (now called bipolar disorder) and dementia praecox (now called schizophrenia) was made by Emil Kraepelin, who attempted to create a synthesis of the various mental disorders identified by 19th century psychiatrists, by grouping diseases together based on classification of common symptoms. Kraepelin used the term 'manic depressive insanity' to describe the whole spectrum of mood disorders, in a far wider sense than it is usually used today. In Kraepelin's classification this would include 'unipolar' clinical depression, as well as bipolar disorder and other mood disorders such as cyclothymia. These are characterised by problems with mood control and the psychotic episodes appear associated with disturbances in mood, and patients often have periods of normal functioning between psychotic episodes even without medication. Schizophrenia is characterized by psychotic episodes that appear unrelated to disturbances in mood, and most non-medicated patients show signs of disturbance between psychotic episodes. Early civilizations considered madness a supernaturally inflicted phenomenon. Archaeologists have unearthed skulls with clearly visible drillings, some datable back to 5000 BC suggesting that trepanning was a common treatment for psychosis in ancient times. Written record of supernatural causes and resultant treatments can be traced back to the New Testament. Mark 5:8–13 describes a man displaying what would today be described as psychotic symptoms. Christ cured this "demonic madness" by casting out the demons and hurling them into a herd of swine. Exorcism is still utilized in some religious circles as a treatment for psychosis presumed to be demonic possession. A research study of out-patients in psychiatric clinics found that 30 percent of religious patients attributed the cause of their psychotic symptoms to evil spirits. Many of these patients underwent exorcistic healing rituals that, though largely regarded as positive experiences by the patients, had no effect on symptomology. Results did, however, show a significant worsening of psychotic symptoms associated with exclusion of medical treatment for coercive forms of exorcism. The medical teachings of the fourth-century philosopher and physician Hippocrates of Cos proposed a natural, rather than supernatural, cause of human illness. In Hippocrates' work, the Hippocratic corpus, a holistic explanation for health and disease was developed to include madness and other "diseases of the mind." Hippocrates writes: Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughter, and jests, as well as our sorrows, pains, griefs and tears. Through it, in particular, we think, see, hear, and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant…. It is the same thing which makes us mad or delirious, inspires us with dread and fear, whether by night or by day, brings sleeplessness, inopportune mistakes, aimless anxieties, absentmindedness, and acts that are contrary to habit.— Hippocrates of Cos, the Hippocratic corpus Hippocrates espoused a theory of humoralism wherein disease is resultant of a shifting balance in bodily fluids including blood, phlegm, black bile, and yellow bile. According to humoralism, each fluid or "humour" has temperamental or behavioral correlates. In the case of psychosis, symptoms are thought to be caused by an excess of both blood and yellow bile. Thus, the proposed surgical intervention for psychotic or manic behavior was bloodletting. 18th century physician, educator, and widely considered "founder of American psychiatry", Benjamin Rush, also prescribed bloodletting as a first-line treatment for psychosis. Although not a proponent of humoralism, Rush believed that active purging and bloodletting were efficacious corrections for disruptions in the circulatory system, a complication he believed was the primary cause of "insanity". Although Rush's treatment modalities are now considered antiquated and brutish, his contributions to psychiatry, namely the biological underpinnings of psychiatric phenomenon including psychosis, have been invaluable to the field. In honor of such contributions, Benjamin Rush's image is in the official seal of the American Psychiatric Association. Early 20th century treatments for severe and persisting psychosis were characterized by an emphasis on shocking the nervous system. Such therapies include insulin shock therapy, cardiazol shock therapy, and electroconvulsive therapy. Despite considerable risk, shock therapy was considered highly efficacious in the treatment of psychosis including schizophrenia. The acceptance of high-risk treatments led to more invasive medical interventions including psychosurgery. In 1888, Swiss psychiatrist Gottlieb Burckhardt performed the first medically sanctioned psychosurgery in which the cerebral cortex was excised. Although some patients showed improvement of symptoms and became more subdued, one patient died and several developed aphasia and/or seizure disorders. Burckhardt would go on to publish his clinical outcomes in a scholarly paper. This procedure was met with criticism from the medical community and his academic and surgical endeavors were largely ignored. In the late 1930s, Egas Moniz conceived the leucotomy (AKA prefrontal lobotomy) in which the fibers connecting the frontal lobes to the rest of the brain were severed. Moniz’s primary inspiration stemmed from a demonstration by neuroscientists John Fulton and Carlyle’s 1935 experiment in which two chimpanzees were given leucotomies and pre and post surgical behavior was compared. Prior to the leucotomy, the chimps engaged in typical behavior including throwing feces and fighting. After the procedure, both chimps were pacified and less violent. During the Q&A, Moniz asked if such a procedure could be extended to human subjects, a question that Fulton admitted was quite startling. Moniz would go on to extend the controversial practice to humans suffering from various psychotic disorders, an endeavor for which he received a Nobel Prize in 1949. Between the late 1930s and early 1970s, the leucotomy was a widely accepted practice, often performed in non-sterile environments such as small outpatient clinics and patient homes. Psychosurgery remained standard practice until the discovery of antipsychotic pharmacology in the 1950s. The first clinical trial of antipsychotics (also commonly known as neuroleptics) for the treatment of psychosis took place in 1952. Chlorpromazine (brand name: Thorazine) passed clinical trials and became the first antipsychotic medication approved for the treatment of both acute and chronic psychosis. Although the mechanism of action was not discovered until 1963, the administration of chlorpromazine marked the advent of the dopamine antagonist, or first generation antipsychotic. While clinical trials showed a high response rate for both acute psychosis and disorders with psychotic features, the side-effects were particularly harsh, which included high rates of often irreversible Parkinsonian symptoms such as tardive dyskinesia. With the advent of atypical antipsychotics (also known as second generation antipsychotics) came a dopamine antagonist with a comparable response rate but a far different, though still extensive, side-effect profile that included a lower risk of Parkinsonian symptoms but a higher risk of cardiovascular disease. Atypical antipsychotics remain the first-line treatment for psychosis associated with various psychiatric and neurological disorders including schizophrenia, bipolar disorder, major depressive disorder, anxiety disorders, dementia, and some autism spectrum disorders. It is now known that dopamine is the primary neurotransmitter implicated in psychotic symptomology. Thus, blocking dopamine receptors (namely, the dopamine D2 receptors) and decreasing dopaminergic activity continues to be an effective but highly unrefined pharmacologic goal of antipsychotics. Recent pharmacological research suggests that the decrease in dopaminergic activity does not eradicate psychotic delusions or hallucinations, but rather attenuates the reward mechanisms involved in the development of delusional thinking; that is, connecting or finding meaningful relationships between unrelated stimuli or ideas. The author of this research paper acknowledges the importance of future investigation: The model presented here is based on incomplete knowledge related to dopamine, schizophrenia, and antipsychotics—and as such will need to evolve as more is known about these.— Shitij Kapur, From dopamine to salience to psychosis—linking biology, pharmacology and phenomenology of psychosis - Kelly, Evelyn B. (2001). Coping with schizophrenia (1st ed.). New York: Rosen Pub. p. 25. ISBN 9780823928538. - "Schizophrenia, schizotypal and delusional disorders (F20-F29)". ICD-10 Version:2010. World Health Organization. - Freudenreich, Oliver (3 December 2012). "Differential Diagnosis of Psychotic Symptoms: Medical "Mimics"". Psychiatric Times. UBM Medica. Retrieved 16 March 2017. - American Psychiatric Association, 1994 The Diagnostic and Statistical Manual Revision IV (DSM-IV) - Gelder, Michael G.; Mayou, Richard; Geddes, John (2005). Psychiatry. New York: Oxford University Press. p. 12. ISBN 978-0-19-852863-0. - Yuhas, Daisy. "Throughout History, Defining Schizophrenia Has Remained a Challenge (Timeline)". Scientific American Mind (March 2013). Retrieved 2 March 2013. - Murray, Robin; Hill, P.D. (Peter David); McGuffin, P. (Peter) (1997). The essentials of postgraduate psychiatr. Cambridge ; New York, NY, US: Cambridge University Press. p. 231. ISBN 978-0-521-57801-1. - National Collaborating Centre for Mental Health (25 March 2009). "Schizophrenia: Full national clinical guideline on core interventions in primary and secondary care" (PDF). Retrieved 25 November 2009. - Leucht, S.; D. Arbter; R.R. Engel; W. Kissling; J.M. Davis (April 2009). "How effective are second-generation antipsychotic drugs? A meta-analysis of placebo-controlled trials" (PDF). Molecular Psychiatry. 14 (4): 429–447. doi:10.1038/sj.mp.4002136. PMID 18180760. Retrieved 24 March 2013. - Rattehalli, R.D.; Jayaram, M.B.; Smith, M. (5 April 2010). "Risperidone Versus Placebo for Schizophrenia". Schizophrenia Bulletin. 36 (3): 448–449. doi:10.1093/schbul/sbq030. PMC . PMID 20368309. - Fusar-Poli, P.; Deste, G.; Smieskova, R.; Barlati, S.; Yung, A.R.; Howes, O.; Stieglitz, R.D.; Vita, A.; McGuire, P.; Borgwardt, S. (Jun 2012). "Cognitive functioning in prodromal psychosis: a meta-analysis". Arch Gen Psychiatry. 69 (6): 562–71. doi:10.1001/archgenpsychiatry.2011.1592. PMID 22664547. - Brown, E.C.; Tas, C.; Brüne, M. (Jan 2012). "Potential therapeutic avenues to tackle social cognition problems in schizophrenia". Expert Rev Neurother. 12 (1): 71–81. doi:10.1586/ern.11.183. PMID 22149657. - Harper, Douglas (November 2001). "hallucinate". Online Etymology Dictionary. Retrieved October 15, 2006. - Honig A., Romme M.A., Ensink B.J., Escher S.D., Pennings M.H., deVries M.W.; Romme; Ensink; Escher; Pennings; Devries (October 1998). "Auditory hallucinations: a comparison between patients and nonpatients". J Nerv Ment Dis. 186 (10): 646–51. doi:10.1097/00005053-199810000-00009. PMID 9788642. - Susannah Cahalan. Brain on Fire-My Month of Madness, New York: Simon & Schuster, 2013. - Jaspers, Karl (1997-11-27) . Allgemeine Psychopathologie (General Psychopathology). Translated by J. Hoenig and M.W. Hamilton from German (Reprint ed.). Baltimore, Maryland: Johns Hopkins University Press. ISBN 0-8018-5775-9. - World Health Organization, The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines (CDDG), 1992. - American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV-TR), American Psychiatric Association, 2000. - Cardinal, R.N. & Bullmore, E.T., The Diagnosis of Psychosis, Cambridge University Press, 2011, ISBN 978-0-521-16484-9 - Shibayama M. (2011). "Differential diagnosis between dissociative disorders and schizophrenia". Seishin shinkeigaku zasshi=Psychiatria et neurologia Japonica. 113 (9): 906–911. PMID 22117396. - Jauch, D.A.; William T. Carpenter, Jr. (February 1988). "Reactive psychosis. I. Does the pre-DSM-III concept define a third psychosis?". Journal of Nervous and Mental Disease. 176 (2): 72–81. doi:10.1097/00005053-198802000-00002. PMID 3276813. - Ohayon, M.M.; R.G. Priest; M. Caulet; C. Guilleminault (October 1996). "Hypnagogic and hypnopompic hallucinations: pathological phenomena?". British Journal of Psychiatry. 169 (4): 459–67. doi:10.1192/bjp.169.4.459. PMID 8894197. Retrieved 2006-10-21. - Sharma, Verinder; Dwight Mazmanian (April 2003). "Sleep loss and postpartum psychosis". Bipolar Disorders. 5 (2): 98–105. doi:10.1034/j.1399-5618.2003.00015.x. PMID 12680898. Retrieved 2006-09-27. - Chan-Ob, T.; V. Boonyanaruthee (September 1999). "Meditation in association with psychosis". Journal of the Medical Association of Thailand. 82 (9): 925–930. PMID 10561951. - Devillieres, P.; M. Opitz; P. Clervoy; J. Stephany (May–June 1996). "Delusion and sleep deprivation". L'Encéphale. 22 (3): 229–31. - Pillmann, Frank; Marneros, Andreas (2004). Acute and transient psychoses. Cambridge, UK: Cambridge University Press. p. 188. ISBN 0-521-83518-6. OCLC 144618418. - Lesser J.M., Hughes S.; Hughes (December 2006). "Psychosis-related disturbances. Psychosis, agitation, and disinhibition in Alzheimer's disease: definitions and treatment options". Geriatrics. 61 (12): 14–20. PMID 17184138. - McKeith, Ian G. (February 2002). "Dementia with Lewy bodies". British Journal of Psychiatry. 180 (2): 144–47. doi:10.1192/bjp.180.2.144. PMID 11823325. - Wedekind S. (June 2005). "Depressive syndrome, psychoses, dementia: frequent manifestations in Parkinson disease". MMW Fortschr Med (in German). 147 (22): 11. PMID 15977623. - Lisanby, S.H.; C. Kohler; C.L. Swanson; R.E. Gur (January 1998). "Psychosis Secondary to Brain Tumor". Seminars in clinical neuropsychiatry. 3 (1): 12–22. PMID 10085187. - Rodriguez Gomez, Diego; Elvira Gonzalez Vazquez and Óscar Perez Carral (August 16–31, 2005). "Psicosis aguda como inicio de esclerosis multiple" [Acute psychosis as the presenting symptom of multiple sclerosis]. Revista de Neurología (in Spanish). 41 (4): 255–56. PMID 16075405. Retrieved 2006-09-27. - Evans, Dwight L.; Karen I. Mason; Jane Leserman; Russell Bauer; John Petitto (2002-02-01). "Chapter 90: Neuropsychiatric Manifestations of HIV-1 Infection and AIDS". In Kenneth L. Davis; Dennis Charney; Joseph T. Coyle; Charles Nemeroff. Neuropsychopharmacology: The Fifth Generation of Progress (5th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 1281–1301. ISBN 0-7817-2837-1. Retrieved 2006-10-16. - Tilluckdharry, C.C.; D.D. Chaddee; R. Doon; J. Nehall (March 1996). "A case of vivax malaria presenting with psychosis". West Indian Medical Journal. 45 (1): 39–40. PMID 8693739. - Fallon B.A., Nields J.A.; Nields (November 1994). "Lyme disease: a neuropsychiatric illness". Am J Psychiatry. 151 (11): 1571–83. doi:10.1176/ajp.151.11.1571. PMID 7943444. (subscription required) - Hess, A.; et al. (March 1999). "Borrelia burgdorferi central nervous system infection presenting as an organic schizophrenialike disorder". Biol. Psychiatry. 45 (6): 795. doi:10.1016/S0006-3223(98)00277-7. PMID 10188012. - van den Bergen, H.A.; Smith, J.P.; van der Zwan, A. (October 1993). "Lyme psychosis". Ned Tijdschr Geneeskd (in Dutch). 137 (41): 2098–100. PMID 8413733. - Kararizou E, Mitsonis C, Dimopoulos N, Gkiatas K, Markou I, Kalfakis N (May–Jun 2006). "Psychosis or simply a new manifestation of neurosyphilis?". J Int Med Res. 34 (3): 335–37. doi:10.1177/147323000603400314. PMID 16866029. - Brooke D, Jamie P, Slack R, Sulaiman M, Tyrer P (October 1987). "Neurosyphilis—a treatable psychosis". Br J Psychiatry. 151 (4): 556. doi:10.1192/bjp.151.4.556. PMID 3447677. - Hermle L, Becker FW, Egan PJ, Kolb G, Wesiack B, Spitzer M (1997). "Metachromatic leukodystrophy simulating schizophrenia-like psychosis". Der Nervenarzt (in German). 68 (9): 754–58. doi:10.1007/s001150050191. PMID 9411279. - Black DN, Taber KH, Hurley RA (2003). "Metachromatic leukodystrophy: a model for the study of psychosis". The Journal of Neuropsychiatry and Clinical Neurosciences. 15 (3): 289–93. doi:10.1176/appi.neuropsych.15.3.289. PMID 12928504.free full text - Kumperscak HG, Paschke E, Gradisnik P, Vidmar J, Bradac SU (2005). "Adult metachromatic leukodystrophy: disorganized schizophrenia-like symptoms and postpartum depression in 2 sisters". Journal of psychiatry & neuroscience : JPN. 30 (1): 33–36. PMC . PMID 15644995. - Sethi NK, Robilotti E, Sadan Y (2005). "Neurological Manifestations Of Vitamin B-12 Deficiency". The Internet Journal of Nutrition and Wellness. 2 (1). doi:10.5580/5a9. - Masalha R, Chudakov B, Muhamad M, Rudoy I, Volkov I, Wirguin I (September 2001). "Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency". Isr Med Assoc J. 3 (9): 701–3. PMID 11574992. - Rossman, Phillip L.; Robert M. Vock (September 1956). "Postpartum Tetany and Psychosis Due to Hypocalcemia". California Medicine. 85 (3): 190–93. PMC . PMID 13356186. - Jana, D.K.; L. Romano-Jana (October 1973). "Hypernatremic psychosis in the elderly: case reports". Journal of the American Geriatrics Society. 21 (10): 473–77. doi:10.1111/j.1532-5415.1973.tb01212.x. PMID 4729012. - Haensch, C.A.; G. Hennen and J. Jorg (April 1996). "Reversible exogenous psychosis in thiazide-induced hyponatremia of 97 mmol/l". Der Nervenarzt. 67 (4): 319–22. PMID 8684511. - Hafez, H.; J.S. Strauss; M.D. Aronson; C. Holt (June 1984). "Hypokalemia-induced psychosis in a chronic schizophrenic patient". Journal of Clinical Psychiatry. 45 (6): 277–79. PMID 6725222. - Konstantakos, Anastasios K.; Enrique Grisoni (May 25, 2006). "Hypomagnesemia". eMedicine. WebMD. Retrieved October 16, 2006. - Velasco, P. Joel; Manoochehr Manshadi; Kevin Breen; Steven Lippmann (1 December 1999). "Psychiatric Aspects of Parathyroid Disease". Psychosomatics. 40 (6): 486–90. doi:10.1016/S0033-3182(99)71186-2. PMID 10581976. Retrieved 2006-10-17. - Rosenthal, M.; I. Gil and B. Habot (1997). "Primary hyperparathyroidism: neuropsychiatric manifestations and case report". Israel Journal of Psychiatry and Related Sciences. 34 (2): 122–125. PMID 9231574. - Nanji, A.A. (November 1984). "The psychiatric aspect of hypophosphatemia". Canadian Journal of Psychiatry. 29 (7): 599–600. PMID 6391648. - Padder, Tanveer; Aparna Udyawar; Nouman Azhar; Kamil Jaghab (December 2005). "Acute Hypoglycemia Presenting as Acute Psychosis". Psychiatry online. Retrieved 2006-09-27. - Robert, M.; R. Sunitha; N.K. Thulaseedharan (1 March 2006). "Neuropsychiatric manifestations systemic lupus erythematosus: A study from South India". Neurology India. 54 (1): 75–77. doi:10.4103/0028-3886.24713. PMID 16679649. Retrieved 2006-09-29. - Bona, Joseph R.; Sondralyn M. Fackler, Morris J. Fendley and Charles B. Nemeroff (1 August 1998). "Neurosarcoidosis as a Cause of Refractory Psychosis: A Complicated Case Report". American Journal of Psychiatry. 155 (8): 1106–8. PMID 9699702. Retrieved 2006-09-29. - Wilcox RA, To T, Koukourou A, Frasca J (November 2008). "Hashimoto's encephalopathy masquerading as acute psychosis". J Clin Neurosci. 15 (11): 1301–04. doi:10.1016/j.jocn.2006.10.019. PMID 18313925. - Gómez-Bernal GJ, Reboreda A, Romero F, Bernal MM, Gómez F (2007). "A Case of Hashimoto's Encephalopathy Manifesting as Psychosis". Prim Care Companion J Clin Psychiatry. 9 (4): 318–19. doi:10.4088/PCC.v09n0411f. PMC . PMID 17934563. - Ray M, Kothur K, Padhy SK, Saran P (May 2007). "Hashimoto's encephalopathy in an adolescent boy". Indian J Pediatr. 74 (5): 492–94. doi:10.1007/s12098-007-0084-0. PMID 17526963. - Nasky KM, Knittel DR, Manos GH (August 2008). "Psychosis associated with anti-N-methyl-D-aspartate receptor antibodies". CNS Spectr. 13 (8): 699–703. - Bost C, Pascual O, Honnorat J (26 October 2016). "Autoimmune encephalitis in psychiatric institutions: current perspectives.". Neuropsychiatr Dis Treat. 12: 2775–2787. doi:10.2147/NDT.S82380. PMC . PMID 27822050. - Some psychosis cases an 'immune disorder' BBC - Steinberg, D.; S.R. Hirsch; S.D. Marston; K. Reynolds; R.N. Sutton (May 1972). "Influenza infection causing manic psychosis". British Journal of Psychiatry. 120 (558): 531–535. doi:10.1192/bjp.120.558.531. PMID 5041533. - Maurizi, C.P. (February 1985). "Influenza and mania: a possible connection with the locus ceruleus". Southern Medical Journal. 78 (2): 207–209. doi:10.1097/00007611-198502000-00025. PMID 3975719. - Keddie, K.M. (August 1965). "Toxic psychosis following mumps". British Journal of Psychiatry. 111 (477): 691–696. doi:10.1192/bjp.111.477.691. PMID 14337417. - Grant KM, LeVan TD, Wells SM, et al. (March 2012). "Methamphetamine-associated psychosis". J Neuroimmune Pharmacol. 7 (1): 113–39. doi:10.1007/s11481-011-9288-1. PMC . PMID 21728034. - Krebs, T.S.; Johansen, P.O. (August 2013). "Psychedelics and mental health: a population study.". PLOS ONE. 8 (8): e63972. doi:10.1371/journal.pone.0063972. PMC . PMID 23976938. - Alcohol-Related Psychosis at eMedicine - Moore T.H.M., Zammit S., Lingford-Hughes A. et al.. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370(9584):319–328. doi:10.1016/S0140-6736(07)61162-3. PMID 17662880. - Leweke F.M., Koethe D.. Cannabis and psychiatric disorders: it is not only addiction. Addict Biol. June 2008;13(2):264–75. doi:10.1111/j.1369-1600.2008.00106.x. PMID 18482435. - Sewell R.A., Ranganathan M., D'Souza D.C.. Cannabinoids and psychosis. International review of psychiatry (Abingdon, England). 2009 Apr;21(2):152–62. doi:10.1080/09540260902782802. PMID 19367509. - Henquet C., Di Forti M., Morrison P., Kuepper R., Murray R.M.. Gene-environment interplay between cannabis and psychosis. Schizophr Bull. November 2008;34(6):1111–21. doi:10.1093/schbul/sbn108. PMID 18723841. - McLaren J.A., Silins E., Hutchinson D., Mattick R.P., Hall W.. Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies. Int J Drug Policy. January 2010;21(1):10–9. doi:10.1016/j.drugpo.2009.09.001. PMID 19783132. - Ben Amar M., Potvin S.. Cannabis and psychosis: what is the link?. Journal of Psychoactive Drugs. 2007 Jun;39(2):131–42. doi:10.1080/02791072.2007.10399871. PMID 17703707. - Bhattacharyya, S.; et al. (February 2010). "Opposite Effects of D-9-Tetrahydrocannabinol and Cannabidiol on Human Brain Function and Psychopathology". Neuropsychopharmacology. 35 (3): 764–774. doi:10.1038/npp.2009.184. PMC . PMID 19924114. - Degenhardt L, Hall W, Lynskey M (2001). "Comorbidity between cannabis use and psychosis: Modelling some possible relationships" (PDF). Technical Report No. 121. Sydney: National Drug and Alcohol Research Centre. Retrieved 2006-08-19. - Marta Di Forti (17 December 2013). "Daily Use, Especially of High-Potency Cannabis, Drives the Earlier Onset of Psychosis in Cannabis Users". - Dragt, S.; Nieman, D.H.; Schultze-Lutter, F.; van der Meer, F.; Becker, H.; de Haan, L.; Dingemans, P.M.; Birchwood, M.; Patterson, P.; Salokangas, R.K.R.; Heinimaa, M.; Heinz, A.; Juckel, G.; Graf von Reventlow, H.; French, P.; Stevens, H.; Ruhrmann, S.; Klosterkötter, J.; Linszen, D.H. (January 2012). "Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis". Acta Psychiatrica Scandinavica. 125 (1): 45–53. doi:10.1111/j.1600-0447.2011.01763.x. - Sander JW, Hart YM, Trimble MR, Shorvon SD (1991). "Vigabatrin and psychosis". Journal of Neurology, Neurosurgery, and Psychiatry. 54 (5): 435–39. doi:10.1136/jnnp.54.5.435. PMC . PMID 1865207. - "Adderall XR Prescribing Information" (PDF). United States Food and Drug Administration. December 2013. pp. 4–6. Retrieved 30 December 2013. - Kuijpers, H.J.H.; Heijden, F.M.M.A. van der; Tuinier, S.; Verhoeven, W.M.A. "Meditation-Induced Psychosis". Psychopathology. 40 (6): 461–464. doi:10.1159/000108125. - Mizrahi, R (February 2016). "Social Stress and Psychosis Risk: Common Neurochemical Substrates?". Neuropsychopharmacology. 41 (3): 666–74. doi:10.1038/npp.2015.274. PMID 26346639. - Jeronimus B.F.; Kotov, R.; Riese, H.; Ormel, J. (2016). "Neuroticism's prospective association with mental disorders halves after adjustment for baseline symptoms and psychiatric history, but the adjusted association hardly decays with time: a meta-analysis on 59 longitudinal/prospective studies with 443 313 participants". Psychological Medicine. 46: 1–24. doi:10.1017/S0033291716001653. PMID 27523506. - Moore, M.T.; Nathan D.; Elliot A.R.; Laubach C. (1935). "Encephalographic studies in mental disease". American Journal of Psychiatry. 92 (1): 43–67. - Copolov DL, Seal ML, Maruff P, et al. (April 2003). "Cortical activation associated with the experience of auditory hallucinations and perception of human speech in schizophrenia: a PET correlation study". Psychiatry Res. 122 (3): 139–52. doi:10.1016/S0925-4927(02)00121-X. PMID 12694889. - Pantelis C, Velakoulis D, McGorry PD, Wood SJ, Suckling J, Phillips LJ, Yung AR, Bullmore ET, Brewer W, Soulsby B, Desmond P, McGuire PK (2003). "Neuroanatomical abnormalities before and after onset of psychosis: a cross-sectional and longitudinal MRI comparison". Lancet. 361 (9354): 281–88. doi:10.1016/S0140-6736(03)12323-9. PMID 12559861. - Ho, B.C.; Alicata D.; Ward J.; Moser D.J.; O'Leary D.S.; Arndt S.; Andreasen N.C. (2003). "Untreated initial psychosis: relation to cognitive deficits and brain morphology in first-episode schizophrenia". American Journal of Psychiatry. 160 (1): 142–48. doi:10.1176/appi.ajp.160.1.142. PMID 12505813. - Kapur, Shitij; Mizrahi Rominia; Li Ming (November 2005). "From dopamine to salience to psychosis—linking biology, pharmacology and phenomenology of psychosis". Schizophrenia Research. 79 (1): 59–68. doi:10.1016/j.schres.2005.01.003. PMID 16005191. - Jones HM, Pilowsky LS (October 2002). "Dopamine and antipsychotic drug action revisited". Br J Psychiatry. 181 (4): 271–5. doi:10.1192/bjp.181.4.271. PMID 12356650. - Soyka, Michael; Thomas Zetzsche; Stefan Dresel; Klaus Tatsch (May 2000). "FDG-PET and IBZM-SPECT Suggest Reduced Thalamic Activity but No Dopaminergic Dysfunction in Chronic Alcohol Hallucinosis". Journal of Neuropsychiatry & Clinical Neurosciences. 12 (2): 287–288. doi:10.1176/appi.neuropsych.12.2.287. PMID 11001615. - Zoldan, J.; G. Friedberg, M. Livneh, and E. Melamed. (July 1995). "Psychosis in advanced Parkinson's disease: treatment with ondansetron, a 5-HT3 receptor antagonist". Neurology. 45 (7): 1305–1308. doi:10.1212/WNL.45.7.1305. PMID 7617188. - Healy, David (2002). The Creation of Psychopharmacology. Cambridge: Harvard University Press. ISBN 0-674-00619-4. - Blakemore, S.J.; Smith J.; Steel R.; Johnstone C.E.; Frith C.D. (2000). "The perception of self-produced sensory stimuli in patients with auditory hallucinations and passivity experiences: evidence for a breakdown in self-monitoring". Psychological Medicine. 30 (5): 1131–9. doi:10.1017/S0033291799002676. PMID 12027049. - Lohr, J.B.; Caligiuri M.P. (1997). "Lateralized hemispheric dysfunction in the major psychotic disorders: historical perspectives and findings from a study of motor asymmetry in older patients". Schizophrophrenia Research. 27 (2–3): 191–98. doi:10.1016/S0920-9964(97)00062-5. PMID 9416648. - Pizaagalli, D.; Lehmann D.; Gianotti L.; Koenig T.; Tanaka H.; Wackermann J.; Brugger P. (2000). "Brain electric correlates of strong belief in paranormal phenomena: intracerebral EEG source and regional Omega complexity analyses". Psychiatry Research. 100 (3): 139–154. doi:10.1016/S0925-4927(00)00070-6. PMID 11120441. - Makarec, K.; Persinger M.A. (1985). "Temporal lobe signs: electroencephalographic validity and enhanced scores in special populations". Perceptual and Motor Skills. 60 (3): 831–42. doi:10.2466/pms.19126.96.36.1991. PMID 3927256. - Weinstein, S; Graves R.E. (2002). "Are creativity and schizotypy products of a right hemisphere bias?". Brain and Cognition. 49 (1): 138–51. doi:10.1006/brcg.2001.1493. PMID 12027399. Retrieved 2006-08-19. - Perry, Benjamin Ian; McIntosh, Gemma; Weich, Scott; Singh, Swaran; Rees, Karen (1 November 2016). "The association between first-episode psychosis and abnormal glycaemic control: systematic review and meta-analysis". The Lancet. Psychiatry. 3 (11): 1049–1058. doi:10.1016/S2215-0366(16)30262-0. ISSN 2215-0374. PMID 27720402. - Krystal, J.H.; Karper, L.P.; Seibyl, J.P.; Freeman, G.K.; Delaney, R; Bremner, J.D.; Heninger, G.R.; Bowers, M.B., Jr; Charney, D.S. (March 1994). "Subanesthetic Effects of the Noncompetitive NMDA Antagonist, Ketamine, in Humans: Psychotomimetic, perceptual, cognitive, and neuroendocrine responses". Arch Gen Psychiatry. 51 (3): 199–214. doi:10.1001/archpsyc.1994.03950030035004. PMID 8122957. - Curran, Catherine; Byrappa, Neetha; McBride, Andrew (September 2004). "Stimulant psychosis: systematic review". British Journal of Psychiatry. 185 (3): 196–204. doi:10.1192/bjp.185.3.196. PMID 15339823. - Nordqvist, Christian (August 8, 2016). "What Is Schizoaffective Disorder? What Causes Schizoaffective Disorder?". Medical News Today. Retrieved March 16, 2017. - Food and Drug Administration (11 February 2004). "Final rule declaring dietary supplements containing ephedrine alkaloids adulterated because they present an unreasonable risk". Federal Register. 69 (28): 6787–854. PMID 14968803. (69 FR 6814 and 69 FR 6818) - Overall JE, Gorham DR. The Brief Psychiatric Rating Scale. Psychol Rep. 1962;10:799–812 - Kay S.R.; Fiszbien A.; Opler L.A. (1987). "The Positive and Negative Symptom Scale (PANNS) for schizophrenia". Schizophrenia Bulletin. 13: 261–276. doi:10.1093/schbul/13.2.261. PMID 3616518. - Marshall M., Rathbone J.. Early intervention for psychosis. Cochrane Database Syst Rev. 2006;(4):CD004718. doi:10.1002/14651858.CD004718.pub2. PMID 17054213. - van Os J., Kapur S.. Schizophrenia. Lancet. August 2009;374(9690):635–45. doi:10.1016/S0140-6736(09)60995-8. PMID 19700006. - Stafford, M.R.; Jackson, H.; Mayo-Wilson, E.; Morrison, A.P.; Kendall, T. (Jan 18, 2013). "Early interventions to prevent psychosis: systematic review and meta-analysis". BMJ (Clinical research ed.). 346: f185. doi:10.1136/bmj.f185. PMC . PMID 23335473. - "Offer talking therapies to people at risk of psychosis and schizophrenia". Nice.org.uk. 2014-02-12. Retrieved 2014-04-15. - "Psychosis and schizophrenia in adults". Nice.org.uk. 2014-03-31. Retrieved 2014-04-15. - Kane J.M., Correll C.U.; Correll (2010). "Pharmacologic treatment of schizophrenia". Dialogues Clin Neurosci. 12 (3): 345–57. PMC . PMID 20954430. - Hartling L, Abou-Setta AM, Dursun S, et al. (14 August 2012). "Antipsychotics in Adults With Schizophrenia: Comparative Effectiveness of First-generation versus second-generation medications: a systematic review and meta-analysis". Annals of Internal Medicine. 157 (7): 498–511. doi:10.7326/0003-4819-157-7-201210020-00525. PMID 22893011. - Barry S.J.E., Gaughan T.M., Hunter R.; Gaughan, T.M.; Hunter, R. (2012). "Schizophrenia". BMJ Clinical Evidence. 2012. PMC . PMID 23870705. - Schultz SH, North SW, Shields CG; North; Shields (June 2007). "Schizophrenia: a review". Am Fam Physician. 75 (12): 1821–29. PMID 17619525. - Smith T., Weston C., Lieberman J.; Weston; Lieberman (August 2010). "Schizophrenia (maintenance treatment)". Am Fam Physician. 82 (4): 338–39. PMID 20704164. - Taylor D.M.; Taylor; Duncan-Mcconnell (2000). "Refractory schizophrenia and atypical antipsychotics". J Psychopharmacol. 14 (4): 409–18. doi:10.1177/026988110001400411. PMID 11198061. - Picchioni MM, Murray RM. Schizophrenia. BMJ. 2007;335(7610):91–95. doi:10.1136/bmj.39227.616447.BE. PMID 17626963. - Essali A., Al-Haj Haasan N., Li C., Rathbone J.; Al-Haj Haasan; Li; Rathbone (2009). "Clozapine versus typical neuroleptic medication for schizophrenia". Cochrane Database of Systematic Reviews (1): CD000059. doi:10.1002/14651858.CD000059.pub2. PMID 19160174. - Ost, LG (October 2014). "The efficacy of Acceptance and Commitment Therapy: an updated systematic review and meta-analysis.". Behaviour research and therapy. 61: 105–21. doi:10.1016/j.brat.2014.07.018. PMID 25193001. - Birchwood, M.; P. Todd; C. Jackson (1998). "Early Intervention in Psychosis: The Critical Period Hypothesis". British Journal of Psychiatry. 172 (33): 53–59. PMID 9764127. - Burgy, M. (20 August 2008). "The Concept of Psychosis: Historical and Phenomenological Aspects" (PDF). Schizophrenia Bulletin. 34 (6): 1200–1210. doi:10.1093/schbul/sbm136. PMC . PMID 18174608. - Beer, M.D. (1995). "Psychosis: from mental disorder to disease concept". Hist Psychiatry. 6 (22(II)): 177–200. doi:10.1177/0957154X9500602204. PMID 11639691. - "Psychosis, Henry George Liddell, Robert Scott, A Greek-English Lexicon, at Perseus". Perseus.tufts.edu. Retrieved 2011-06-11. - "Online Etymology Dictionary". Douglas Harper. 2001. Retrieved 2006-08-19. - Berrios G.E. (1987). "Historical Aspects of Psychoses: 19th Century Issues". British Medical Bulletin. 43 (3): 484–498. PMID 3322481. - Berrios G.E., Beer D.; Beer (1994). "The notion of Unitary Psychosis: a conceptual history". History of Psychiatry. 5 (17 Pt 1): 13–36. doi:10.1177/0957154X9400501702. PMID 11639278. - Porter, Roy (2003). Madness: A Brief History. US: Oxford University Press. p. 10. ISBN 0192802674. - Vlachos, I.O; Beratis, Hartocollis (1997). "Magico religious beliefs and psychosis". Psychopathology. 30 (2): 93–99. doi:10.1159/000285035. PMID 9168565. - Pfeifer, S (September 1994). "Belief in demons and exorcism in psychiatric patients in Switzerland". British Journal of Medical Psychology. 67 (3): 247–258. doi:10.1111/j.2044-8341.1994.tb01794.x. - Bennet, S. (2008). "Mind and madness in classical antiquity". History of Psychiatry and Medical Psychology: 175–197. doi:10.1007/978-0-387-34708-0_3. ISBN 978-0-387-34707-3. - Spring, B; L. Weinstein; M. Lemon; A. Haskell (1991). "Schizophrenia from Hippocrates to Kraepelin". Clinical Psychology: 259–277. doi:10.1007/978-1-4757-9715-2_10. ISBN 978-1-4757-9717-6. - Rush, M.D., Benjamin (1830). Medical Inquiries and Observations upon Diseases of the Mind. Philadelphia. pp. 98–190. ISBN 978-0559921674. - Shorter, Edward (1998). A History of Psychiatry: From the Era of the Asylum to the Age of Prozac. Hoboken, New Jersey: John Wiley & Sons. ISBN 0471245313. - Stone, J.L. (March 2010). "Dr. Gottlieb Burckhardt—the pioneer of psychosurgery". Journal of the History of the Neurosciences. 10 (1): 79–92. doi:10.1076/jhin.10.1.79.5634. PMID 11446267. - Gross, D.; G. Schâfer (April 2011). "Egas Moniz and the "invention" of modern psychosurgery: A historical and ethical reanalysis under special consideration of portuguese original sources". Neurosurgical Focus. 30 (2): 8–10. doi:10.3171/2011.3.FOCUS10214a. - Pressman, Jack David (1998). Last Resort: Psychosurgery and the Limits of Medicine. Cambridge Studies in the History of Medicine. Cambridge, UK: Cambridge University Press. pp. 18–40. ISBN 978-0521353717. OCLC 36729044. - Berrios, G.E. (March 1997). "The origins of psychosurgery: Shaw, burckhardt and moniz". Hist. Psychiatry. 8 (29): 61–81. doi:10.1177/0957154X9700802905. PMID 11619209. - Mashour, George; Erin E. Walker; Robert L. Martuza (7 September 2005). "Psychosurgery: past, present, and future". Brain Research Reviews. 48 (3): 409–419. doi:10.1016/j.brainresrev.2004.09.002. PMID 15914249. - Stip, Emmanuel (22 January 2002). "Happy birthday neuroleptics! 50 years later: la folie du doute". European Psychiatry. 17 (3): 115–119. doi:10.1016/S0924-9338(02)00639-9. PMID 12052571. - Crossley, Nicolas; Miguel Constante (2010). "Efficacy of atypical v. typical antipsychotics in the treatment of early psychosis: meta-analysis". The British Journal of Psychiatry. 196 (6): 434–439. doi:10.1192/bjp.bp.109.066217. PMC . PMID 20513851. - Maher, Alicia; Margaret Maglione, Steven Bagley, Marika Suttorp, Jian-Hui Hu, Brett Ewing, Zhen Wang, Martha Timmer, David Sultzer, Paul Shekelle (28 September 2011). "Efficacy and Comparative Effectiveness of Atypical Antipsychotic Medications for Off-Label Uses in Adults A Systematic Review and Meta-analysis". The Journal of the American Medical Association. 306 (12): 1359–1369. doi:10.1001/jama.2011.1360. PMID 21954480. - Sims, A. (2002). Symptoms in the mind: An introduction to descriptive psychopathology (3rd edition). Edinburgh: Elsevier Science Ltd. ISBN 0-7020-2627-1 - Murray E.D., Buttner N., Price B.H. (2012). Depression and Psychosis in Neurological Practice. In: Neurology in Clinical Practice, 6th Edition. Bradley W.G., Daroff R.B., Fenichel G.M., Jankovic J. (eds.) Butterworth Heinemann. April 12, 2012. ISBN 1437704344 \| ISBN 978-1437704341 - Williams, Paris (2012). Rethinking Madness: Towards a Paradigm Shift In Our Understanding and Treatment of Psychosis, Sky’s Edge Publishing. - Personal accounts - Dick, P.K. (1981) VALIS. London: Gollancz. [Semi-autobiographical] ISBN 0-679-73446-5 - Jamison, K.R. (1995) An Unquiet Mind: A Memoir of Moods and Madness. London: Picador. - Schreber, Daniel Paul (2000) Memoirs of My Nervous Illness. New York: New York Review of Books. ISBN 0-940322-20-X - Hinshaw, S.P. (2002) The Years of Silence are Past: My Father's Life with Bipolar Disorder. Cambridge: Cambridge University Press. - McLean, R (2003) Recovered Not Cured: A Journey Through Schizophrenia. Allen & Unwin. Australia. ISBN 1-86508-974-5 - The Eden Express by Mark Vonnegut - James Tilly Matthews - Saks, Elyn R. (2007) The Center Cannot Hold—My Journey Through Madness. New York: Hyperion. ISBN 978-1-4013-0138-5	2	77	28	0	10	6	0.552802	44	17,760
As the name suggests, vascular malformations of the brain is an umbrella term for at least six conditions in which blood vessels of the brain are affected. Such malformations are classified into several types in which the symptoms, severity, and causes vary. These types of VMB are: (1) arteriovenous malformations (AVM), abnormal arteries and veins; (2) cavernous malformations (CM), enlarged blood-filled spaces; (3) venous angiomas (VA), abnormal veins; (4) telangiectasias (TA), enlarged capillary-sized vessels; (5) vein of Galen malformations (VGM); and (6) mixed malformations (MM). Vascular malformations of the brain may cause headaches, seizures, strokes, or bleeding in the brain (cerebral hemorrhage). Some researchers believe that the type of malformation determines the symptoms and progression of the disease. Other researchers believe that only the severity rather than the type of malformation is important. Arteriovenous malformations or AVMs affect arteries, veins, and middle- sized vessels but not capillaries. These blood vessels are enlarged, twisted, and tangled. Arteries and veins may be connected directly instead of being connected through fine capillaries for which reason they are often referred to as “shunt lesions” since the capillaries are by-passed. These abnormal “feeding” arteries progressively enlarge and as a result the “draining” veins dilate as well. The brain tissue between these vessels may be hardened or rigid (atrophied), full of a network of fine small fibers (fibrils) interspersed with flattened cells (gliotic), and sometimes may be calcified. Such malformations may, by drawing blood away from the brain, cause brain cell atrophy. Hemorrhages or seizures are commonly experienced with AVMs. (For more information on this disorder choose “Arteriovenous” for your search term in the Rare Disease Database.) Cavernous malformations, CMs (also called cavernous angiomas, or cavernous hemangiomas, or cavernomas) present as abnormally enlarged collections of blood-filled spaces. A cavernous hemangioma acts like a “blood sponge” soaking up blood that has found its way between capillaries, in the spaces between tissues (sinusoids) and “larger cavernous spaces.” These are “slow-flow lesions.” There is not usually any brain tissue in these spaces in contrast with symptoms of AVMs. Hemorrhages or seizures are also common with CMs. (For more information on this disorder choose “cavernous hemangioma” for your search term in the Rare Disease Database.) Venous angiomas (VAs) involve enlarged, tangled, and twisted veins that vary in size but do not involve the arteries. The site of these “growths” is most often just after the capillary stage of the vessel (post-capillary malformation). They may be isolated defects or associated with cavernous malformations. The defect shows itself as a “crown” of small veins (venules) that meet to form part of a larger vein (trunk). Telangiectasias are the malformations that arise as a result of the enlarging (dilation) of the tiny capillaries. These dilated capillaries make themselves known as small pink-red spots in various parts of the body such as the face, eyes, membranes that cover the brain (dura) and spinal cord (meninges), and mucous membranes (the thin moist layer lining the body’s internal surfaces). (For more information on a disorder involving telangiectasias choose “hemorrhagic telangiectasia, hereditary” for your search term in the Rare Disease Database.) Vein of Galen malformations (VGMs begin while the embryo is developing. The vein of Galen is located under the cerebral hemispheres and drains the forward (anterior) and central regions of the brain into the proper sinuses. The malformations occur when the vein of Galen is not supported within the head by surrounding tissue and lacks the normal fibrous wall. Thus, the vein of Galen appears free-floating within the fluids of the cerebral spaces (sinuses). Should the pressure increase within the vein of Galen, its shape changes from a cylinder to that of a sphere. Such changes are accompanied by abnormal fetal blood circulation. In extreme cases, there may be cardiac failure or swelling of the brain (hydrocephalus). Mixed malformation is a phrase used to include any of several multiple-mixed malformations. Frequently, these malformations appear to be mixes of arteriovenous malformations with telangiectasias. Three types or forms of VMB have a genetic component. The evidence for a genetic cause is strong in the case of cavernous hemangiomas and telangiectasias. The case is much weaker for arteriovenous malformation of the brain (AVM). In each of these cases, the condition is transmitted as an autosomal dominant trait. The malfunctioning gene in the case of cavernous malformations has been tracked to gene map locus 7q11.2-q21, and in the case of telangiectasia to gene map locus 9q34.1. Chromosomes, which are present in the nucleus of human cells, carry the genetic information for each individual. Human body cells normally have 46 chromosomes. Pairs of human chromosomes are numbered from 1 through 22 and the sex chromosomes are designated X and Y. Males have one X and one Y chromosome and females have two X chromosomes. Each chromosome has a short arm designated “p” and a long arm designated “q”. Chromosomes are further sub-divided into many bands that are numbered. For example, “chromosome 9q34.1” refers to band 34.1 on the long arm of chromosome 7. The numbered bands specify the location of the thousands of genes that are present on each chromosome. To say that the abnormal gene is located at 7q11.2-q21 means that the gene in question is located in a region on the long arm of chromosome 7 between bands 11.2 and 21. Genetic diseases are determined by the combination of genes for a particular trait that are on the chromosomes received from the father and the mother. Dominant genetic disorders occur when only a single copy of an abnormal gene is necessary for the appearance of the disease. The abnormal gene can be inherited from either parent, or can be the result of a new mutation (gene change) in the affected individual. The risk of passing the abnormal gene from affected parent to offspring is 50% for each pregnancy regardless of the sex of the resulting child. Recessive genetic disorders occur when an individual inherits the same abnormal gene for the same trait from each parent. If an individual receives one normal gene and one gene for the disease, the person will be a carrier for the disease but usually will not show symptoms. The risk for two carrier parents to both pass the defective gene and, therefore, have an affected child is 25% with each pregnancy. The risk to have a child who is a carrier like the parents is 50% with each pregnancy. The chance for a child to receive normal genes from both parents and be genetically normal for that particular trait is 25%. The risk is the same for males and females. All individuals carry a few abnormal genes. Parents who are close relatives (consanguineous) have a higher chance than unrelated parents to both carry the same abnormal gene, which increases the risk to have children with a recessive genetic disorder. X-linked recessive genetic disorders are conditions caused by an abnormal gene on the X chromosome. Females have two X chromosomes but one of the X chromosomes is “turned off” and all of the genes on that chromosome are inactivated. Females who have a disease gene present on one of their X chromosomes are carriers for that disorder. Carrier females usually do not display symptoms of the disorder because it is usually the X chromosome with the abnormal gene that is “turned off”. A male has one X chromosome and if he inherits an X chromosome that contains a disease gene, he will develop the disease. Males with X-linked disorders pass the disease gene to all of their daughters, who will be carriers. A male cannot pass an X-linked gene to his sons because males always pass their Y chromosome instead of their X chromosome to male offspring. Female carriers of an X-linked disorder have a 25% chance with each pregnancy to have a carrier daughter like themselves, a 25% chance to have a non-carrier daughter, a 25% chance to have a son affected with the disease, and a 25% chance to have an unaffected son. X-linked dominant disorders are also caused by an abnormal gene on the X chromosome, but in these rare conditions, females with an abnormal gene are affected with the disease. Males with an abnormal gene are more severely affected than females, and many of these males do not survive. Vascular malformations of the brain affect males and females in equal numbers. A hereditary form of cavernous malformations tends to occur more frequently in Mexican-Americans. Arteriovenous malformations occur more frequently in males. Imaging apparatus, such as magnetic resonance imaging (MRI), computed tomography (CT) scans, venograms and/or digital intravenous or common angiography can take pictures of the brain's blood vessels to see if vascular malformations are present. Current treatment options vary according to the severity and location of the malformation. Surgical removal (resection), multiple embolization (an operation in which pellets are put into the circulatory system in order to block blood flow to and/or from the abnormal blood vessels), and irradiation are the treatments currently in use. In some cases, treatment may not be necessary. Recently introduced techniques involve particle beam and stereotaxic radio-surgery. Genetic counseling may be of benefit for patients and their families if they have a hereditary form of this disorder. Other treatment is symptomatic and supportive. Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government website. For information about clinical trials being conducted at the National Institutes of Health (NIH) in Bethesda, MD, contact the NIH Patient Recruitment Office: Tollfree: (800) 411-1222 TTY: (866) 411-1010 For information about clinical trials sponsored by private sources, contact: Beers MH, Berkow R., eds. The Merck Manual, 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:244-45; 1427; 1482. Smith WS, Johnston SC, Easton JD. Cerebrovascular Diseases. In: Kasper, DL, Fauci AS, Longo DL, et al. Eds. Harrison’s Principles of Internal Medicine. 16th ed. McGraw-Hill Companies. New York, NY; 2005:2392-93. Marchuk DA, Berg JN. ENG and ALK1 and Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Syndrome) and Vascular Morphogenesis. In: Epstein CJ, Erickson RP, Wynshaw-Boris, eds. Inborn Errors of Development. 1st ed. Oxford University Press. New York, NY; 2004:319-28. Johnston MV. Acute Stroke Syndromes. In: Behrman RE, Kliegman RM, Jenson HB. Eds. Nelson Textbook of Pediatrics. 17th ed. Elsevier Saunders. Philadelphia, PA; 2005:2036-37. Solomon RA, Pile-Spellman J, Mohr JP. Vascular Tumors and Malformations. In: Rowland LP. Ed. Merritt’s Neurology. 10th ed. Lippincott Williams & Wilkins. Philadelphia, PA. 2000:367-71. Guttmacher AE, McDonald JE. Hereditary Hemorrhagic Telangiectasia. In: NORD Guide to Rare Disorders. Lippincott Williams & Wilkins. Philadelphia, PA. 2003:418. Choi JH, Mohr JP. Brain arteriovenous malformations in adults. Lancet Neurol. 2005;4:299-308. Hussain MS, Qureshi AI, Kirmani JF, et al. Update on endovascular treatment of cerebrovascular diseases. J Endovasc Ther. 2004;11 Suppl 2:II32-42. Brown RD Jr, Flemming KD, Meyer FB, et al. Natural history, evaluation, and management of intracranial vascular malformations. Mayo Clin Proc. 2005;80:269-81. Schauble B, Cascino GD, Pollock BE, et al. Seizure outcomes after stereotactic radiosurgery for cerebral arteriovenous malformations. Yamada S, Brauer FS, Colohan AR, et al. Concept of arteriovenous malformation compartments and surgical management. Neurol Res. 2004;26:288-300. Raychaudhuri R, Batjer HH, Awad IA. Intracranial cavernous hemangioma: a practical review of clinical and biological aspects. Surg Neurol. 2005;63:319-28. Byrne JV. Cerebrovascular malformations. Eur Radiol. 2005;15:448-52. Yasui T, Komiyama M, Iwai Y, et al. A brainstem cavernoma demonstrating a dramatic, spontaneous decrease in size during follow-up: case report and review of the literature. Surg Neurol. 2005;63:170-73; discussion 173. Baumgartner JE, Ater JL, Ha CS, et al. Pathologically proven cavernousangiomas of the brain following radiation therapy for pediatric brain tumors. Pediatr Neurosurg. 2003;39:201-07. Zhou LF, Mao Y, Chen L. Diagnosis and surgical treatment of cavernous sinus hemangiomas: an experience of 20 cases. Surg Neurol. 2003;60:31-36; discussion 36-37. Bilaniuk LT. Vascular lesions of the orbit in children. Neuroimaging Clin N Am. 2005;15:107-20. Chiller KG, Frieden IJ, Arbiser JL. Molecular pathogenesis of vascular anomalies: classification into three categories based upon clinical and biochemical characteristics. Lymphat Res Biol. 2003;1:267-81. Metry DW. Potential complications of segmental hemangiomas of infancy. Semin Cutan Med Surg. 2004;23:107-15. Tille JC, Pepper MS. Hereditary vascular anomalies: new insights into their pathogenesis. Arterioscler Thromb Vasc Biol. 2004;24:1578-90. Vein of Galen malformations Kubi N, Levy BI. Understanding angiogenesis: a clue for understanding vascular malformations. J Neuroradiol. 2004;31:365-68. Greene AK, Burrows PE, Smith L, et al. Periorbital lymphatic malformation: clinical course and management in 42 patients. Plast Reconstr Surg. 2005;115:22-30. Gupta AK, Varma DR. Vein of Galen malformations: review. Neurol India. 2004;52:43-53. Punt J. Surgical management of paediatric stroke. Pediatr Radiol. 2004;34:16-23. Freedom RM, Yoo SJ, Perrin D. The biological “scrabble” of pulmonary arteriovenous malformations: considerations in the setting of cavopulmonary surgery. Cardiol Young. 2004;14:417-37. Woods CG. Human microcephaly. Curr Opin Neurobiol. 2004;14:112-17. Marchuk DA, Srinivasan S, Squire TL, et al. Vascular morphogenesis: tales of two syndromes. Hum Mol Genet. 2003; 12 Spec No 1:R97-112. Sabba C, Pasculli G, Cirulli A, et al. Hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease). Minerva Cardioangiol. 2002;50:221-38. Ataxia telangiectasia with vascular abnormalities in the brain parenchyma: report of an autopsy case and literature review. Pathol Int. 2001;51:271-76. FROM THE INTERNET McKusick VA, ed. Online Mendelian Inheritance In Man (OMIM). The Johns Hopkins University. Cerebral Cavernous Malformations; CCM. Entry Number; 116860: Last Edit Date; 11/2/2005. McKusick VA, ed. Online Mendelian Inheritance In Man (OMIM). The Johns Hopkins University. Telangiectasia, Hereditary Hemorrhagic, of Rendu, Osler, and Weber; HHT. Entry Number; 187300: Last Edit Date; 2/18/2005.. McKusick VA, ed. Online Mendelian Inheritance In Man (OMIM). The Johns Hopkins University. Arteriovenous malformations of the Brain. Entry Number; 108010: Last Edit Date; 2/7/2000. Wagner AL. Brain, Venous Vascular Malformations. emedicine. Last Updated: August 21, 2002. 8pp. The information in NORD’s Rare Disease Database is for educational purposes only and is not intended to replace the advice of a physician or other qualified medical professional. The content of the website and databases of the National Organization for Rare Disorders (NORD) is copyrighted and may not be reproduced, copied, downloaded or disseminated, in any way, for any commercial or public purpose, without prior written authorization and approval from NORD. Individuals may print one hard copy of an individual disease for personal use, provided that content is unmodified and includes NORD’s copyright. National Organization for Rare Disorders (NORD) 55 Kenosia Ave., Danbury CT 06810 • (203)744-0100	2	8	1	0	0	1	0.925237	2	3,999
- Humeral head fracture: description - Humeral head fracture: symptoms - Humeral head fracture: causes and risk factors - Humeral head fracture: examinations and diagnosis - Humeral head fracture: treatment - Humeral head fracture: disease course and prognosis Under one Humeruskopffraktur (Upper arm head fracture, subcapital humeral fracture) is a fracture of the head of the humerus. This type of bone fracture is most common in older people with osteoporosis, mostly caused by indirect trauma. A humeral head fracture is painful and restricts the mobility of the arm. Depending on fracture type can be treated conservatively or surgically. Find out more about the humeral head fracture here. ICD codes for this disease: ICD codes are internationally valid medical diagnosis codes. They are found e.g. in doctor's letters or on incapacity certificates. S42 Causes and risk factors Examinations and diagnosis Disease course and prognosis Humeral head fracture: description The humerus has a relatively large head, which is three times larger than the pan. This allows the shoulder a wide range of movement: The shoulder joint is the most flexible joint of the human body. Structure of the humerus The head (caput humeri) of the humerus is delimited from the rest of the bone by a short annular neck (collum anatomicum). This is followed by two bony prominences that serve numerous attachment points. The upper elevation is located on the outside of the humerus and is called "Tuberculum majus". The smaller elevation is called "Tuberculum minus". Just below the Tuberculum minus is a thinner neck (Collum chirurgicum). Here the bone is very soft and narrow. In case of external trauma, this site can break very easily. To the Collum chirurgicum joins the humeral stem. The humeral head fracture is counted as proximal ("proximal") humeral fractures. The upper arm can also break in other places. When the bone breaks in the middle, it is called a humeral shaft fracture. If it breaks at the lower end of the humerus, it is a distal humeral fracture. Upper arm fractures near the shoulder joint account for five percent of all fractures. This makes the upper arm the third most frequent fracture site on the human body. In old age, this fracture is common, while adolescents for such a break a significant trauma is necessary. Humeral head fracture: classification In a humeral head fracture, the head can break into various fragments. The Oberarmkopffraktur is divided into four main fragments according to the doctor Neer: - Tuberculum majus - Tuberculum minus Depending on the break, two to four fragments may be created. A fragment is shifted more than an inch or twisted more than 45 degrees. Humeral head fracture: symptoms If there is severe pain in the shoulder area after an accident, this may be an indication of a humeral head fracture. Another sign of the fracture is the inability to move the arm or shoulder. The area is usually swollen and tender. Furthermore, the result is an extensive hematoma, ie a bruise. He can sag after a day or two to the elbow and provide appropriate skin discoloration. In some cases, a malposition of the upper arm is visible in a humeral fracture. Humeral head fracture: causes and risk factors The cause of a humeral head fracture is usually an indirect trauma caused by a fall on the outstretched hand or elbow or directly on the shoulder. Osteoporosis (bone loss) plays an increasing role in older people. Due to age-related hormonal changes, bone loses strength, becomes porous, and breaks easily. Already harmless falls can then lead to a break, such as a humeral head fracture. About 70 percent of all patients with humeral head fracture are older than 60 years. In young people, a humeral head fracture is less common than in older and often the result of serious traffic or sports accidents (traumatic trauma). Babies may develop an upper arm fracture during childbirth. Humeral head fracture: necrosis The more severe the injury, the higher the risk of neuropathic necrosis. The bone tissue dies from the humeral head. In a humeral head fracture with additional dislocation (dislocation), the risk of necrosis is even 90 percent. The reason for the humeral head necrosis is that the bone is no longer sufficiently supplied with blood. This occurs when certain blood vessels are injured: the Arteria circumflexa humeri anterior and its endast the Arteria arcuata as well as the Arteria circumflexa humeri posterior. The humeral head necrosis is one of the aseptic, so not infection-related bone necroses. Humeral head fracture: examinations and diagnosis If you suspect a humeral head fracture, you should consult a doctor for orthopedics and trauma surgery.He will first ask you about the accident and your medical history and then examine it. Some questions from the doctor might be: - Did you fall on your shoulder or outstretched arm? - Describe the exact accident. - Can you still move the shoulder or the arm? - Do you have pain? - Did you have any complaints such as pain, restriction of movement or a previous dislocation in the shoulder or arm area? A humeral head fracture can often be identified by the nature of the accident and its symptoms. Often the patient supports the injured arm on the wrist (as opposed to a shin fracture of the upper arm). Similar symptoms as a humeral head fracture show a shoulder dislocation (shoulder luxation). Therefore, the doctor will examine you for any possible nerve and vessel injuries. Children suffering from a birth traumatic humeral head fracture often take a restraint. This is sometimes misinterpreted as plexus palsy (paralysis). This can be checked by a movement test: In a humeral fracture, the child - in contrast to a paralysis - pain when the arm is moved. Humeral head fracture: Imaging procedures To confirm the suspected diagnosis of humeral head fracture, X-rays are usually taken from all sides of the shoulder. The images also show whether fractures have shifted or whether other bony structures have broken. If the fracture is only slightly shifted, it is checked whether the head fragments are stable even when the arm is gently spread out to 80 degrees laterally. Even more accurate is computed tomography (CT), which shows the exact relationship of each fragment. The CT scan is especially indicated when planning an operation. In special cases magnetic resonance imaging (MRI) can be used to exclude soft tissue damage such as tendon injuries. Furthermore, angiography (vascular radiography) serves to locate the site of a possible vascular injury. An electromyography (EMG) can tell if the arm vessels are still intact. Humeral head fracture: treatment Depending on the severity of the humeral head fracture, there are various treatment options. In acute humeral head fracture, it is especially important to treat the pain and to avoid further damage. If shoulder dislocation is suspected, do not attempt to retract the joint as this may cause more damage. First, imaging must always confirm the dislocation! Humeral head fracture: conservative therapy In case of uncomplicated upper arm fracture, surgery can be avoided in many cases. Unless the fragments are shifted against each other, the upper arm is usually immobilized with a special dressing (Desault or Gilchrist dressing). Accompanying a physical cold therapy can be applied (cryotherapy). As a result, the person concerned can begin with light exercises, which, however, should not be exercised in the pain area. As soon as the pain subsides, the physiotherapy begins with pendulum movements of the arm. After two to three weeks, the patient may actively and passively move the arm again. It is important that the healing progress is observed with X-ray controls. Usually follows a check after one day, ten days and six weeks. The bone is stable again after about six weeks with adequate healing. Only in rare cases are displaced fractures treated conservatively. This is the case, for example, when there is a high risk of surgery. The arm is placed after the application of special associations additionally with a cast. Especially in children, a humeral fracture can often be treated well conservative, because he aligns spontaneously again. Humeral head fracture: operative therapy In general, there are two different surgical procedures depending on the location and type of injury: osteosynthesis and joint replacement. The surgeon also determines, depending on the fracture type, whether an open or a closed operation is indicated. A humeral head fracture is basically an urgent but not an emergency operation. It should first be immobilized in the Gilchrist or Desault Bandage and operated on within ten days. If there are concomitant vascular or nerve injuries, as is often the case with a fracture in the area of the collum anatomicum or a dislocation that can no longer be restricted, surgery is usually carried out immediately in order to avoid lasting damage. In a Tuberculum majus fracture in which the fragments are moved, the shoulder joint is often additionally dislocated. The bone is then stabilized after correction with plates, screws or drill wires. Then the arm is immobilized in a special bandage. If the fracture is not postponed, an active muscle movement is only recommended after three weeks because of the strong risk of displacement. If it is an unstable humeral head fracture with a strong shifted fracture and a Verrenkungsbruch, is also operated. The goal is to make the humeral head anatomically again so that a post-treatment is not necessary. Older people of lower bone quality who are at high risk for bone necrosis are first treated with a prosthesis. New angle stable implants show good results. In younger patients, attempts are made to maintain the humeral head and anatomically align the fractures. It is recommended that the shoulder joint should not be completely immobilized for more than two to three weeks as otherwise a so-called "frozen shoulder" may develop - a painful stiffening of the shoulder. Humeral head fracture: disease course and prognosis When a humeral head fracture is operated, complications such as wound healing disorders, infections, or rebleeding rarely occur. Occasionally a humeral head fracture does not heal completely (pseudarthrosis). The function is hardly affected by this. Especially in children, the prognosis of a humeral head fracture is good. Other possible complications of humeral head fracture include: - Humeral head necrosis (especially in elderly patients) - Impingement: painful pinching of soft tissue in the joint space (between shoulder and humeral head) in the case of a greater tuberculum fracture - Labrum lesion (injury to the gel cliff) - Rotator cuff tear (tear of the muscle group in the area of the shoulder) - Vascular and nerve damage (such as the axillary nerve or the axillary artery) in severe humeral head fracture The aim of the treatment is always that the upper arm in everyday life is able to move without pain. In some cases, however, the shoulder can be after one Humeruskopffraktur do not move as before. The arm can not then be moved forward and sideways to the vertical. This happens in about 10 to 20 percent of cases. Read more about the therapies - External fixator - Gilchrist Association - plaster cast	2	6	0	0	0	1	0.51159	1	2,456
Let’s look at the medical term “Arthrocentesis”. By breaking up the term into two sections, we find that “arthros” stands for “joint” and “kentesis” means “puncture”. So what is Arthrocentesis? Medical Coding Arthrocentesis When a healthcare provider surgically punctures a joint with a needle and withdraws (aspirates) synovial fluid (a gelatinous fluid found in the cavities of synovial joints which reduces friction between the articular cartilages and synovial joints during movement), or injects a synthetically produced anti-inflammatory such as cortisone to relieve arthritic pain, this is referred to as Arthrocentesis. There are three (3) CPT codes you can choose for Arthrocentesis: 20600: Arthrocentesis, aspiration and/or injection of a small joint or bursa. A bursa is a small fluid filled sac lined by synovial membrane that provides a cushion between bones and tendons and/or muscles around a joint. Infection or irritation of a bursa leads to bursitis (inflammation of a bursa). Fingers and toes are considered small joints. 20605: Arthrocentesis of the intermediate joint or bursa. Examples of intermediate joints are: the temporomandibular joint which is the joint of the jaw, often referred to as TMJ, acromioclavicular joint which is also referred to as the AC joint at the top of the shoulder between the acromion (part of the scapula) and the clavicle, wrist, elbow, and olecranon bursa, also known as elbow bump, water on the elbow or baker’s elbow. 20610: Arthrocentesis of a major joint such as a shoulder, hip, knee joint or subacromial bursa (the synovial membrane located just below the acromion). Typically, when coding for bilateral Arthrocentesis, you would append modifier 50 to one Arthrocentesis procedure code. For example, bilateral knees would be coded as 20610-50. For multiple joint procedures, you would add modifier 59 to each additional Arthrocentesis procedure site (excluding bilateral locations). If more than one (1) injection is entered into the same site, only bill the CPT code as one (1) unit. CPT codes 20600, 20605, and 20610 do not have a global period. If a patient sees the provider on day one (1) and he decides to perform Arthrocentesis on the same day, he would add modifier 25 to the E/M visit (separate identifiable service) and use the appropriate injection/aspiration code. If the patient returns on day two (2) for another injection to the same location, the coder should not bill another E/M visit but he CAN bill for another Arthrocentesis procedure. Only bill for the surgical injection/aspiration. If the provider knows the patient will have to return for multiple injections over a period of time, then modifier 58, staged or planned procedure, will indicate to the payer that the procedure is indicative for this particular case. Remember that coding rules change on a regular basis and you want to be sure your claim tells a story. LCDs and NCDs can affect your reimbursement if over utilized, so be clear at all times. Procedures performed on fingers and toes must include the location modifiers. For example, modifiers TA through T9 refer to each digit on the foot. In addition to the Arthrocentesis code, coders should always include the appropriate HCPCS “J” code to get reimbursed for the cost of the drug or biological used in the Arthrocentesis procedure if performed in a non-facility setting. The “J” code is identified by the generic name – not the brand name, but the descriptions are cross-referenced in the HCPCS code book. Be aware that payers’ rules may vary on bilateral coding. Maintain a list of who wants modifier 50 or LT, RT. Always sequence your modifiers by using your pricing modifier first, such as modifier 50, payment modifier second, such as 58, 59 or 51, and location modifiers last, such as FA, F1-F9, TA, T1-T9. Again, pay attention to how payers handle your claims and make note.	4	4	7	0	0	0	0.252891	7	956
What is the Flu? Influenza, also called the "flu," is a respiratory infection that's highly contagious. If you have flu symptoms, try to avoid contact with others to prevent spreading the infection. How do I know if I have the flu? If you get the flu, you may have a fever, chills, headache, dry cough, runny or stuffy nose, sore throat, and muscle aches. Unlike the common cold, the flu can make you feel very tired or exhausted for several days, a week, or more. Most adults with the flu don't get an upset stomach, but children and some adults might have nausea, vomiting, and diarrhea. What people often call "stomach flu" is not influenza. How can I get the flu? The flu spreads easily from person to person especially when someone with the flu coughs or sneezes. A person with the flu usually experiences symptoms within 2 to 4 days, and remains contagious for another 3 to 4 days after symptoms appear. Will Medicare pay for a flu shot? Medicare covers the flu shot once per flu season. With Part B, you pay nothing for the flu shot if the doctor or other health care provider accepts assignment for giving the shot. When should I get a flu shot? Flu shots are available starting in the fall, for the fall and winter flu season. The Centers for Disease Control and Prevention (CDC) recommends you get the flu shot as soon as it is available in your area. Medicare Guideline posts - Finding Medicare fee schedule - HOw to Guide - LCD and procedure to diagnosis lookup - How to Gui... - Medicare Fee Schedule, Payment and Reimbursement Benefit Guideline, - Step by step Guide Medicare participation program - Medicare Fee for Office Visit CPT Codes - CPT Code 99213, 99214, 99203 - Medicare revalidation FAQ - Gastroenterology, Colonoscopy, Endoscopy Medicare CPT Code Fee - Medicare claim address, phone numbers, payor id - revised list Top Medicare billing tips Procedure code and description 93000 - Electrocardiogram, routine ECG with at least 12 leads; with interpretation and report -average fee... This post has Most used J code list and we are constantly updating with example . If you are looking particular J code, use search button. ... Flow Cytometry is a highly complex process by which blood, body fluids, bone marrow and tissue can be examined. It provides important immun... CPT CODES and Description 81000 Urinalysis, by dip stick or tablet reagent for bilirubin, glucose, hemoglobin, ketones, leukocytes, nitr... Procedure code and description 93015 (cardiovascular stress test using maximal or submaximal treadmill or bicycle exercise, continuous ele... CPT CODE and Description 90785 - Interactive complexity (List separately in addition to the code for primary procedure) 90791 - Psychi... procedure code and description 93922 LIMITED BILATERAL NONINVASIVE PHYSIOLOGIC STUDIES OF UPPER OR LOWER EXTREMITY ARTERIES, (EG, FOR LOW... Procedure Codes and Definitions 36415 Collection of venous blood by venipuncture - Fee schedule amount $3.10 36416 Collection of capi... Procedure code and description 95806 - Sleep study, unattended, simultaneous recording of, heart rate, oxygen saturation, respiratory air... Procedure code and description 95004 Percut Tests w/ Extrac Immed React # Allergy testing - Percut allergy skin tests - Percutaneous ...	4	16	4	0	0	0	0.435513	4	775
Imagine, you visit your doctor after a long wait as it took a lot of time to get an appointment and you forgot your reports at home. You don’t want to miss this one chance of meeting your doctor as getting another appointment would mean a wait for another couple of days. What will you do in that case? Now think if the entire record of your disease is encrypted in one single code that you can get from the clinics health directory that provides you with the platform where you can get all the relevant information about the disease or the injury you are suffering from. This is now possible with the advancements in the medical standard associated with WHO under ICD-10 codes. Key facts associated with ICD Emphasizing on the US, ICD-10 is split into two systems: - ICD-10-CM: This is used for the diagnostic coding. - ICD-10-PCS: This is implemented for inpatient hospital procedure coding. - ICD is widely used in researches and clinical care to give an idea about the diseases and study their pattern. It also helps in managing the healthcare, calculate the effective outcomes and then allocate the resources. - ICD gives a standard idea about the mortality and morbidity rates. - The mortality data generated by the ICD denotes the health status of the country. It also keeps a check on the number of deaths and the disease rates. Purpose of ICD: - ICD is an international standard for reporting the health and disease conditions. It provides the world a platform to share as well as compare health information using a common language. - ICD holds all the information about the diseases, any health condition as well as the injuries. All the information is listed in such a comprehensive way that everything gets covered. - It gives a platform for sharing the health information among the hospitals situated in different locations and countries. - ICD helps in keeping a count of the diseases and deaths, their reasons and influences on general health status. Who can avail ICD-10 benefits? The main areas where ICD is taken into practice includes the research areas. General physicians, insurance policy makers, health program and information managers can also avail the benefits of ICD-10. ICD-10 Code structure: ICD-10 CM diagnosis have codes ranging between 3 to 7 characters. - The initial three characters of an ICD-10 code tells about the category of diagnosis. For example if we consider S86.011.D; the letter S tells us about the diagnosis related to “injuries, poisoning or any certain causes that are related to single body regions externally.” S along with 8 and 6 tells that it indicates an “injury of tendon or muscle in the lower portion of the leg. - The next two characters “0”, “1”, “1” specifies the diagnosis of the ” strain in the right Achilles tendon.” - The last character that is the seventh character tells us about the basic difference between ICD-0 and the ICD-10 as ICD-9 did not include the seventh character. The seventh character tells about the treatment and care. Here in this example, the seventh character deals with the injury. The character D specifies the phase when the patient is receiving routine care during the healing time of recovery. Why should you go for ICD-10 procedures? The reason to go for ICD-10 can be divided into three categories: - It gives an elaborate idea about the patient’s condition and helps in giving improved healthcare teams. - It targets on the capital investments to meet the needs of the specific patient’s condition. - This provides the basic data for comparison and utilization benchmarking. - Reduces the risks associated with an audit by implementing the diagnosis codes with high specificity that is supported by the clinical research documentation. - Since, better data is collected and evaluated, it helps in taking better decisions. - Gives a broader platform for research and clinical trials.	4	4	0	0	0	2	0.751784	2	842
- Corticobasal degeneration Corticobasal degeneration Classification and external resources ICD-9 331.6 DiseasesDB 33284 eMedicine neuro/77 Corticobasal degeneration (CBD) or Corticobasal Ganglionic Degeneration (CBGD) is a rare progressive neurodegenerative disease involving the cerebral cortex and the basal ganglia. It is characterized by marked disorders in movement and cognitive dysfunction. Clinical diagnosis is difficult, as symptoms of CBD are often similar to those of other diseases, such as Parkinson's disease (PD) and progressive supranuclear palsy (PSP). - 1 Background and History - 2 Occurrence and Epidemiology - 3 Symptoms and Clinical Presentation - 4 Corticobasal Syndrome - 5 Neuroimaging - 6 Histological and Molecular Features - 7 Diagnosis - 8 Treatment - 9 See also - 10 References - 11 External links Background and History CBD was first identified by Rebeiz and his associates in 1968, as they observed three individuals who exhibited characteristic symptoms of the unique and previously unknown disorder. They initially referred to the neurodegenerative disease as “corticodentatonigral degeneration with neuronal achromasia,” after which various other names were used, including “corticonigral degeneration with nuclear achromasia” and “cortical basal ganglionic degeneration.” Although the underlying cause of CBD is unknown, the disease occurs as a result of damage to the basal ganglia, specifically marked by neuronal degeneration or depigmentation (loss of melanin in a neuron) in the substantia nigra. Additional distinguishing neurological features of those diagnosed with CBD consist of asymmetric atrophy of the frontal and parietal cortical regions of the brain. Postmortem studies of patients diagnosed with CBD indicate that histological attributes often involve ballooning of neurons, gliosis, and tauopathy. Much of the pioneering advancements and research performed on CBD has been completed within the past decade or so, due to the relevantly recent formal discovery of the disease. Occurrence and Epidemiology Clinical presentation of CBD usually does not occur until age 60, with the earliest recorded diagnosis and subsequent postmortem verification being age 28. Although men and women present with the disease, some analysis has shown a predominant appearance of CBD in women. Current calculations suggest that the prevalence of CBD is approximately 4.9 to 7.3 per 100,000 people. The prognosis for an individual diagnosed with CBD is death within approximately eight years. Symptoms and Clinical Presentation Because CBD is progressive (it gradually worsens), a set of standard diagnostic criteria can be used, which is centered on the disease’s evolution. Included in these fundamental features are problems with cortical processing, dysfunction of the basal ganglia, and a sudden and detrimental onset. Psychiatric and cognitive dysfunctions, although present in CBD, are much less prevalent and lack establishment as common indicators of the presence of the disease. Motor and Associated Cortical Dysfunctions Some of the most prevalent symptom types in people exhibiting CBD pertain to identifiable movement disorders and problems with cortical processing. These symptoms are initial indicators of the presence of the disease. Each of the associated movement complications typically is seen in an asymmetric manner, in which the symptom is not observed uniformly throughout the body. For example, a person exhibiting an alien hand syndrome (explained later) in one hand, will not correspondingly display the same symptom in the contralateral limb. Predominant movement disorders and cortical dysfunctions associated with CBD include: The presence of parkinsonism as a clinical symptom of CBD is largely responsible for complications in developing unique diagnostic criteria for the disease. Other such diseases in which parkinsonism forms an integral diagnostic characteristic are PD and PSP. Parkinsonism in CBD is largely present in an extremity such as the arm, and is always asymmetric. Common associated movement dysfunctions that comprise parkinsonism are rigidity, bradykinesia, and gait disorder, with limb rigidity forming the most typical manifestation of parkinsonism in CBD. Despite being relatively indistinct, this rigidity can lead to disturbances in gait and correlated movements. Bradykinesia in CBD occurs when there is notable slowing in the completion of certain movements in the limbs. In an associated study, it was determined that, three years following first diagnosis, 71% of persons with CBD demonstrate the presence of bradykinesia. Alien Hand Syndrome Alien hand syndrome has been shown to be prevalent in roughly 60% of those people diagnosed with CBD. This disorder involves the failure of an individual to control the movements of his or her hand, which results from the sensation that the limb is “foreign.” The movements of the alien limb are a reaction to external stimuli and do not occur sporadically or without stimulation. The presence of an alien limb has a distinct appearance in CBD, in which the diagnosed individual may have a “tactile mitgehen.” This mitgehen (German, meaning “to go with”) is relatively specific to CBD, and involves the active following of an experimenter’s hand by the subject’s hand when both hands are in direct contact. Another, rarer form of alien hand syndrome has been noted in CBD, in which an individual’s hand displays an avoidance response to external stimuli. Additionally, sensory impairment, revealed through limb numbness or the sensation of prickling, may also concurrently arise with alien hand syndrome, as both symptoms are indicative of cortical dysfunction. Like most of the movement disorders, alien hand syndrome also presents asymmetrically in those diagnosed with CBD. Ideomotor apraxia (IMA), although clearly present in CBD, often manifests atypically due to the additional presence of bradykinesia and rigidity in those individuals exhibiting the disorders. The IMA symptom in CBD is characterized by the inability to repeat or mimic particular movements (whether significant or random) both with or without the implementation of objects. This form of IMA is present in the hands and arms, while IMA in the lower extremities may cause problems with walking. Those with CBD that exhibit IMA may appear to have trouble initiating walking, as the foot may appear to be fixed to floor. This can cause stumbling and difficulties in maintaining balance. IMA is associated with deterioration in the premotor cortex, parietal association areas, connecting white matter tracts, thalamus, and basal ganglia. Some individuals with CBD exhibit limb-kinetic apraxia, which involves dysfunction of more fine motor movements often performed by the hands and fingers. Aphasia in CBD is revealed through the inability to speak or a difficulty in initiating spoken dialogue and falls under the non-fluent (as opposed to fluent or flowing) subtype of the disorder. This results in disconnected speech patterns and the omission of words. Individuals with this symptom of CBD often lose the ability to speak as the disease progresses. Psychiatric and Cognitive Disorders Psychiatric problems associated with CBD often present as a result of the debilitating symptoms of the disease. Prominent psychiatric and cognitive conditions cited in individuals with CBD include dementia, depression, and irritability, with dementia forming a key feature that sometimes leads to the misdiagnosis of CBD as another cognitive disorder such as Alzheimer's disease (AD). All of the disorders and dysfunctions associated with CBD can often be categorized into a class of symptoms that present with the disease of CBD. These symptoms that aid in clinical diagnosis are sometimes collectively referred to as corticobasal syndrome (CBS) or corticobasal degeneration syndrome (CBDS). It has been suggested that the nomenclature of corticobasal degeneration only be used for naming the disease after it has received verification through postmortem analysis of the neuropathology. The types of imaging techniques which are most prominently utilized when studying and/or diagnosing CBD are: - magnetic resonance imaging (MRI) - single photon emission computed tomography (SPECT) - fluorodopa positron emission tomography (FDOPA PET) Developments or improvements in imaging techniques provide the future possibility for definitive clinical diagnosis prior to death. However, despite their benefits, information learned from MRI and SPECT during the beginning of CBD progression tend to show no irregularities that would indicate the presence of such a neurodegenerative disease . FDOPA PET is used to study the efficacy of the dopamine pathway. Despite the undoubted presence of cortical atrophy (as determined through MRI and SPECT) in individuals experiencing the symptoms of CBD, this is not an exclusive indicator for the disease. Thus, the utilization of this factor in the diagnosis of CBD should only be used in combination with other clinically present dysfunctions. MRI images are useful in displaying atrophied portions of neuroanatomical positions within the brain. As a result, it is especially effective in identifying regions within different areas of the brain that have been negatively affected due to the complications associated with CBD. Specifically, MRI of CBD typically shows posterior parietal and frontal cortical atrophy with unequal representation in corresponding sides. Additionally, atrophy has been noted in the corpus callosum. Functional MRI (fMRI) has been used to evaluate the activation patterns in various regions of the brain of individuals affected with CBD. Upon the performance of simple finger motor tasks, subjects with CBD experienced lower levels of activity in the parietal cortex, sensorimotor cortex, and supplementary motor cortex than those individuals tested in a control group. SPECT studies of individuals diagnosed with CBD involve perfusion analysis throughout the parts of the brain. SPECT evaluation through perfusion observation consists of monitoring blood release into different locations in tissue or organ regions, which, in the case of CBD, pertains to localized areas within the brain. Tissue can be characterized as experiencing overperfusion, underperfusion, hypoperfusion, or hyperperfusion. Overperfusion and underperfusion relate to a comparison with the overall perfusion levels within the entire body, whereas hypoperfusion and hyperperfusion are calculated in comparison to the blood flow requirements of the tissue in question. The measurements taken for CBD using SPECT are generally referred to as regional cerebral blood flow (rCBF). Generally, SPECT reveals hypoperfusion within both the posterior regions of the frontal and parietal lobes. As in images gathered through MRI, SPECT images indicated asymmetry in the presentation of abnormalities throughout the brain. Additional studies have revealed the presence of perfusion anomalies in the thalamus, temporal cortex, basal ganglia, and pontocerebellar (from the pons to the cerebellum) locations within subjects’ brains. Research has suggested that the integrity of the dopamine system in the striatum has been damaged as an effect of CBD. Current studies employing the use of FDOPA PET as a possible method for identifying CBD have focused on analyzing the efficiency of neurons in the striatum that utilize the neurotransmitter dopamine. These studies have concluded that dopamine uptake was generally diminished in the caudate and the putamen. This characteristic also has the potential to be useful in distinguishing CBD from the similar PD, as individuals who had been diagnosed with PD were more likely to have a lower uptake of dopamine than in individuals with CBD. Other clinical tests or procedures which monitor the presence of dopamine within the brain (β-CIT SPECT and IBZM SPECT) have shown similar findings. β-CIT serves as an indicator for presynaptic dopaminergic neurons, while IBZM is a tracer that shows an affinity for the postsynaptic neurons of the same type. Despite agreement with other imaging studies, these two SPECT methods suffer some scrutiny due to better accuracy in other imaging methods. However, β-CIT SPECT has proven to be helpful in distinguishing CBD from PSP and multiple system atrophy (MSA). Histological and Molecular Features Postmortem histological examination of the brains of individuals diagnosed with CBD reveal unique characteristics involving the astrocytes in localized regions. The typical procedure used in the identification of these astroglial inclusions is the Gallyas-Braak staining method. This process involves exposing tissue samples to a silver staining material which marks for abnormalities in the tau protein and astroglial inclusions. Astroglial inclusions in CBD are identified as astrocytic plaques, which present as annularly displays of blurry outgrowths from the astrocyte. A recent study indicated that CBD produces a high density of astrocytic plaques in the anterior portion of the frontal lobe and in the premotor area of the cerebral cortex. The protein tau is an important microtubule-associated protein (MAP), and is typically found in neuronal axons. However, malfunctioning of the development of the protein can result in unnatural, high-level expression in astrocytes and glial cells. Consequently, this is often responsible for the astrocytic plaques prominently noted in histological CBD examinations. Although they are understood to play a significant role in neurodegenerative diseases such as CBD, their precise effect remains a mystery. Clinical vs. Postmortem One of the most significant problems associated with CBD is the inability to perform a definitive diagnosis while an individual exhibiting the symptoms associated with CBD is still alive. A clinical diagnosis of CBD is performed based upon the specified diagnostic criteria, which focus mainly on the symptoms correlated with the disease. However, this often results in complications as these symptoms often overlap with numerous other neurodegenerative diseases. Frequently, a differential diagnosis for CBD is performed, in which other diseases are eliminated based on specific symptoms that do not overlap. However, some of the symptoms of CBD used in this process are rare to the disease, and thus the differential diagnosis cannot always be used. Postmortem diagnosis provides the only true indication of the presence of CBD. Most of these diagnoses utilize the Gallyas-Braak staining method, which is effective in identifying the presence of astroglial inclusions and coincidental tauopathy. Overlap with Other Diseases Progressive supranuclear palsy (PSP) is frequently the disease most often confused with CBD. Both PSP and CBD result in similar symptoms, and both display tauopathies upon histological inspection. However, it has been noted that tauopathy in PSP results in tuft-shaped astrocytes in contrast with the doughnut-shaped astrocytic plaques found as a result of CBD. Individuals diagnosed with PD often exhibit similar movement dysfunction as those diagnosed with CBD, which adds complexity to its diagnosis. Some other neurodegenerative diseases including Alzheimer’s Disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD) also show commonalities with CBD.. FTDs have also been known to evolve into corticobasal syndrome. Because the exact cause of CBD is unknown, there exists no formal treatment for the disease. Instead, treatments focus on minimizing the appearance or effect of the symptoms resulting from CBD. The most easily treatable symptom of CBD is parkinsonism, and the most common form of treatment for this symptom is the application of dopaminergic drugs. However, only moderate improvement is seen and the relief from the symptom is generally not long-lasting. Additionally, palliative therapies, including the implementation of wheelchairs, speech therapy, and feeding techniques, are often used to alleviate many of the symptoms that show no improvement with drug administration. - Basal Ganglia - Alzheimer's disease - Dementia with Lewy bodies - Frontotemporal lobar degeneration - Progressive Supranuclear Palsy - ^ "Corticobasal Degeneration Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". http://www.ninds.nih.gov/disorders/corticobasal_degeneration/corticobasal_degeneration.htm. Retrieved 2009-03-20. - ^ a b c d Wadia PM, Lang AE. 2007. The many faces of corticobasal degeneration. Parkinsonism & Related Disorders 13:S336-S40 - ^ a b c Scaravilli T, Tolosa E, Ferrer I. 2005. Progressive supranuclear palsy and corticobasal degeneration: Lumping versus splitting. Movement Disorders 20:S21-S8 - ^ a b c d e f g h Seritan AL, Mendez MF, Silverman DHS, Hurley RA, Taber KH. 2004. Functional imaging as a window to dementia: Corticobasal degeneration. Journal of Neuropsychiatry and Clinical Neurosciences 16:393-9 - ^ a b c d e f g h i Mahapatra RK, Edwards MJ, Schott JM, Bhatia KP. 2004. Corticobasal degeneration. Lancet Neurology 3:736-43 - ^ a b c d Koyama M, Yagishita A, Nakata Y, Hayashi M, Bandoh M, Mizutani T. 2007. Imaging of corticobasal degeneration syndrome. Neuroradiology 49:905-12 - ^ a b Belfor N, Amici S, Boxer AL, Kramer JH, Gorno-Tempini ML, et al. 2006. Clinical and neuropsychological features of corticobasal degeneration. Mechanisms of Ageing and Development 127:203-7 - ^ FitzGerald DB, Drago V, Jeong Y, Chang YL, White KD, Heilman KM. 2007. Asymmetrical alien hands in corticobasal degeneration. Movement Disorders 22:581-4 - ^ Rizzo G, Martinelli P, Manners D, et al. (October 2008). "Diffusion-weighted brain imaging study of patients with clinical diagnosis of corticobasal degeneration, progressive supranuclear palsy and Parkinson's disease". Brain 131 (Pt 10): 2690–700. doi:10.1093/brain/awn195. PMID 18819991. http://brain.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=18819991. - ^ a b Komori T. 1999. Tau-positive glial inclusions in progressive supranuclear palsy, corticobasal degeneration and Pick's disease. Brain Pathology 9:663-79 - ^ a b Hattori M, Hashizume Y, Yoshida M, Iwasaki Y, Hishikawa N, et al. 2003. Distribution of astrocytic plaques in the corticobasal degeneration brain and comparison with tuft-shaped astrocytes in the progressive supranuclear palsy brain. Acta Neuropathologica 106:143-9 - ^ Litvan I, Agid Y, Goetz C, Jankovic J, Wenning GK, Brandel JP, Lai EC, Verny M, Ray-Chaudhuri K, McKee A, Jellinger K, Pearce RK, Bartko JJ. (Jan 1997). Neurology 48 (1): 119-25. PMID 9008506. Accuracy of the clinical diagnosis of corticobasal degeneration: a clinicopathologic study.. - ^ Gorno-Tempini ML, Murray RC, Rankin KP, Weiner MW, Miller BL. (Dec 2004). "Clinical, cognitive and anatomical evolution from nonfluent progressive aphasia to corticobasal syndrome: a case report.". Neurocase: case studies in neuropsychology, neuropsychiatry, and behavioral neurology 10 (6): 426-36. PMC 2365737. PMID 15788282. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2365737. - ^ Lang AE. 2005. Treatment of progressive supranuclear palsy and corticobasal degeneration. Movement Disorders 20:S83-S91 Wikimedia Foundation. 2010. Look at other dictionaries: corticobasal degeneration — a neurologic condition similar to parkinsonism, with degeneration of the cerebral cortex and extrapyramidal structures; symptoms include progressive apraxia, rigidity, and alien limb syndrome … Medical dictionary degeneration — 1. Deterioration; passing from a higher to a lower level or type. 2. A worsening of mental, physical, or moral qualities. 3. A retrogressive pathologic change in cells or tissues, in consequence of which their functions are often impaired or… … Medical dictionary Frontotemporal lobar degeneration — Infobox Disease Name = PAGENAME Caption = A human brain showing frontotemporal lobar degeneration causing frontotemporal dementia. DiseasesDB = 10034 ICD10 = ICD9 = ICDO = OMIM = 600274 MedlinePlus = eMedicineSubj = eMedicineTopic = MeshID =… … Wikipedia Kortikobasale Degeneration — Klassifikation nach ICD 10 G31.0 Umschriebene Hirnatrophie … Deutsch Wikipedia Degenerescence cortico-basale — Dégénérescence cortico basale La dégénérescence cortico basale est une maladie neurodégénérative relativement rare mais de plus en plus fréquemment décrite, touchant principalement les régions cérébrales sous corticales, puis corticales et… … Wikipédia en Français Dégénérescence cortico-basale — La dégénérescence cortico basale est une maladie neurodégénérative relativement rare mais de plus en plus fréquemment décrite, touchant principalement les régions cérébrales sous corticales, puis corticales et présentant typiquement un… … Wikipédia en Français Démence cortico-basale — Dégénérescence cortico basale La dégénérescence cortico basale est une maladie neurodégénérative relativement rare mais de plus en plus fréquemment décrite, touchant principalement les régions cérébrales sous corticales, puis corticales et… … Wikipédia en Français Frontotemporal dementia — Infobox Disease Name = PAGENAME Caption = A human brain showing frontotemporal lobar degeneration causing frontotemporal dementia. DiseasesDB = 10034 ICD10 = ICD9 = ICD9\|331.19 ICDO = OMIM = 600274 MedlinePlus = eMedicineSubj = eMedicineTopic =… … Wikipedia Dementia — For other uses, see Dementia (disambiguation). Dementia Classification and external resources ICD 10 F00 F07 ICD 9 … Wikipedia Senile plaques — Amyloid beta immunostaining showing senile plaques. Senile plaques (syn. neuritic plaques, senile druse, braindruse) are extracellular deposits of amyloid in the gray matter of the brain. The deposits are associated with degenerative neural… … Wikipedia	2	14	6	0	0	7	0.835129	13	4,966
Chronic stable angina overview Chronic stable angina Microchapters Alternative Therapies for Refractory Angina Guidelines for Asymptomatic Patients Chronic stable angina overview On the Web Angina pectoris, commonly known as angina, is chest pain due to ischemia (a lack of blood and subsequent lack of oxygen supply) of the heart muscle. It is most often due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, also referred to as atherosclerosis of the coronary arteries, is the most common cause of angina. The term derives from the Greek ankhon ("strangling") and the Latin pectus ("chest") meaning "a strangling feeling in the chest". In angina pectoris, symptomatic onset may include chest discomfort indicated by a feeling of tightness, heaviness, or pain in the chest cavity. Chronic stable angina is a form of chest pain characterized by an insufficient blood flow to the myocardium of the heart to match myocardial energy demands (ischemia). The term angina was originally derived from the Greek word ankhon and the Latin word pectus, which when combined, loosely translates as "a strangling feeling in the chest". Attempts to classify this disease state began as early as the 4th century B.C., when Lucius Annaeus Seneca first described the symptoms he was experiencing as "to have any other malady is to be sick; to have this is to be dying". Throughout history many renowned researchers and health care professionals have contributed to the understanding, definition, and recognition of angina. Chronic Stable Angina Angina pectoris is a sensation of chest discomfort that is often described as: a feeling of tightness, heaviness, or pain. Angina pectoris is a characteristic of coronary heart disease. When it occurs chronically, this is referred to as stable angina. Walk Through Angina Walk through angina is the appearance of anginal chest discomfort early in the course of exertion which subsequently subsides despite continued exertion. Mixed or variable threshold angina pectoris is a syndrome in which there is substantial variation in the magnitude of physical activity that induces anginal chest pain. Nocturnal angina is the occurrence of anginal discomfort either during the first hours of sleep or during the early morning hours. It is speculated that discomfort caused during the first hours of sleep is due to increased venous return, whereas the discomfort caused during the early morning hours is due to increased vascular tone. Postprandial angina pectoris is anginal chest discomfort that occurs following meals. It is thought to be due to an increase in vascular tone or a reduction in coronary blood flow. Cardiac Syndrome X Cardiac syndrome X is angina associated with objective evidence of myocardial ischemia in the absence of epicardial coronary artery disease. Syndrome X has been hypothesized to be a disorder of the coronary microvasculature rather than the large caliber epicardial coronary arteries. Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of luminal diameter of an epicardial coronary artery due to inappropriate constriction of coronary smooth muscle that can generate distal ischemia. This may occur spontaneously or in the context of angioplasty, particularly if denudation of the endothelium or dissection occurs. In addition, the vasospasm can either be focal or multifocal (which compromises more than one vessel). Differentiating Chronic Stable Angina from Urgent Conditions Stable angina must be differentiated from unstable angina and acute coronary syndromes. If the pattern of angina is stable, this is termed chronic stable angina. If the magnitude, threshold or frequency of chest pain accelerates, this is termed an acute coronary syndrome. The primary causes of myocardial ischemia in chronic stable angina are: fixed epicardial stenosis, spasm of the epicardial artery and/or microvascualar disease. The causation of angina is not mutually exclusive. Two or more causes may coexist in the same patient. Epidemiology and Demographics Coronary artery disease (CAD) remains the single leading cause of death in the United States. Stable angina is the initial manifestation of ischemic heart disease in approximately 50% of these patients. The average mortality in patients with stable angina ranges from 1-3%. However, the prognosis varies widely depending on various factors such as: the duration and severity of symptoms, resting ECG abnormalities, abnormal left ventricular function and associated comorbidities. Pretest probability is defined as the probability of the target disorder before the result of a diagnostic test is known. A number of studies have emphasized the importance of pretest probability of coronary artery disease (CAD). Once a thorough patient history and physical examination is complete, it is important to assess the probability of underlying CAD, as this helps both the physician and the patient to determine the next step in the diagnosis and treatment. In patients with chronic stable angina, the strongest predictors contributing to underlying significant CAD include: the age, gender and type of pain (typical, atypical) experienced. Ischemic heart disease remains as the number one cause of mortality in developed countries. The prognosis of stable angina varies widely depending on severity of symptoms, extent of atherosclerosis and presence of other risk factors and co-morbidities. The presence of impaired left ventricular function is associated with a poor prognosis. Reduced LV function, number and location of stenoses, workload in METs calculated using Duke score are the strongest predictors of survival in patients with chronic stable angina. History and Symptoms The name 'angina pain' can be thought of as a misnomer as patients often describe the sensation as discomfort rather than physical pain. The best method to characterize this discomfort/pain is through the 'PQRST system'. Among patients with chronic stable angina, the physical examination may be asymptomatic or characteristically normal. Patients that present with left ventricular dysfunction are associated with a poorer prognosis than patients who do not present with dysfunction. All patients should be examined carefully for the presence of rales and other signs of heart failure. The majority of patients present with history of either, chest pain or discomfort categorized as: typical or atypical. Typical presentation would include pain or discomfort in the front or anterior precordium. Atypical presentation can be more convoluted in presentation and involve a wide range of symptoms. For example, an atypical patient may present with dyspnea instead of chest pain and this is termed an angina equivalent. In addition to the historical presentation of chest pain or discomfort, the patient history should be extensively evaluated to include an assessment of cardiovascular risk factors. Physical examination may be normal or asymptomatic. In some cases, a physical examination may reveal heart failure. Additional findings can be important in understanding the onset of the condition. For instance, the presence of peripheral vascular disease may be associated with an increased risk of coronary artery disease (CAD). Test Selection Guideline for the Individual Basis Criteria for test selection hinges largely on the current disease state of the individual patient and subsequent level of fitness for testing. Potential diagnostic testing modalities include: exercise ECG, ECG at rest, exercise echocardiography, echocardiography at rest, and stress scintigraphy. In patients with chronic stable angina, initial laboratory investigations are used to: identify potential causes of ischemia, establish risk factors, and determine the overall prognosis for the patient. An initial laboratory test can provide a wide variety of clinical information. For instance, low hemoglobin levels can cause ischemia. Therefore, assessing hemoglobin as a part of complete blood count provides prognostic information. Biomarkers, such as troponin and CK-MB, are used to exclude myocardial injury. In assessment for risk factor stratification, all patients with ischemic heart disease are recommended to have a a standard round of blood work conducted including fasting plasma glucose levels and a complete lipid profile. Serum creatinine is used to assess renal dysfunction due to associated hypertension or diabetes and remains a negative prognostic factor. In patients with chronic stable angina, an elevation in fasting glucose independently predicts the adverse outcome. Recent research on NT-pro-BNP has demonstrated the ability to predict long-term mortality in patients with chronic stable angina independent of age, ventricular ejection fraction and other risk factors. A resting 12-lead ECG is performed and recorded in all patients with suspected angina pectoris. However, a normal resting ECG does not exclude the diagnosis of ischemia. Abnormalites commonly observed on resting ECG include: ST-segment changes, left ventricular hypertrophy (LVH), left branch bundle blockage (LBBB), signs of coronary artery disease (CAD) such as previous myocardial infarction (MI) or abnormal repolarization patterns. An ECG recorded during pain helps to identify an underlying vasospasm. In patients with chronic stable angina, exercise ECG is more sensitive and specific to identify inducible ischemia and to diagnose coronary artery disease. ECG abnormalities associated with MI include: down sloping of ST-segment depression or elevation, accompanying angina that occurs at a low workload during early stages of exercise and persistent for more than 3-minutes after exercise. The reliability of diagnosis is shown to improve with the evaluation of ST changes in relation to heart rate. Bruce protocol or treadmill (expressed in terms of METs) or bicycle ergometer (expressed in terms of watts) are used to detect MI. Exercise ECG test must be terminated on the achievement of maximal predicted heart rate and/or if the patient becomes symptomatic or develops pain with significant ST-segment changes. Exercise ECG test also provides prognostic stratification to evaluate the response to medical therapy or revascularization. Routine chest x-ray examination is important in the evaluation of patients with signs or symptoms of congestive heart failure, valvular heart disease, pericardial disease, or aortic dissection/aneurysm. The presentation of cardiomegaly, characterized by pulmonary congestion on a chest x-ray, is indicative of a poor prognosis for the patient. Myocardial Perfusion Scintigraphy with Pharmacologic Stress Pharmacologic stress testing using myocardial perfusion scintigraphy or echocardiography can be employed in patients with known or suspected angina pectoris who are unable to perform adequate exercise tests. These patients often owe their ineligibility status to associated conditions such as: peripheral vascular disease, musculoskeletal disorders, diseases of the lower extremities, severe obesity, or deconditioning. Pharmacologic stress testing is achieved with the infusion of either dobutamine in incremental dose, which acts by increasing myocardial oxygen consumption and thereby mimic effect of exercise, or with the use of coronary vasodilators such as adenosine or dipyridamole, which acts by differentiating regions based on perfusion. Stress imaging is of great value in the evaluation of patients with low pretest probability of CAD. However, in patients with LBBB, perfusion scintigraphy is shown to have poor diagnostic accuracy. Myocardial Perfusion Scintigraphy with Thallium In patients with baseline ECG abnormalities,a myocardial perfusion test can be used to localize the region of ischemia. Thallium-201 and technetium-99m are the two radio-labeled agents that are frequently used for the assessment of myocardial perfusion. Myocardial uptake of thallium-201 chloride is directly proportional to the regional myocardial blood flow and is dependent on the presence of viable myocardium. In patients with known CAD, a normal thallium stress test without a perfusion defect is indicative of a benign process and associated with excellent prognosis. Patients with a normal thallium scan are at low risk for CAD and subsequent coronary angiography is indicated only if the patient has a high probabilty Duke treadmill score. Contraindications for thallium stress test include the presence of arrhythmia, acute myocarditis, severe aortic stenosis and acute MI within the past 2 days. Echocardiography is useful to evaluate ventricular function and detect ischemia induced regional wall motion abnormality that occurs at rest, during exercise or with pharmacologic stress test. As a testing modality, two-dimensional echocardiography is often coupled with other testing modalities to detect regional wall motion abnormalities that most frequently occur during induced myocardial ischemia associated with coronary artery disease (CAD). Potential paired testing modalities include: upright treadmill exercise, supine bicycle ergometry, pacing, and pharmacologic stress, particularly with dobutamine. Patients with CAD may respond more adversely to testing modalities than their counterparts. Often, an adverse outcome such as the inability to perform a bicycle ergometry test or exercise treadmill protocol can be characterized as a poor prognostic factor. Stress echocardiography is echocardiography that is paired with different forms of stressors, such as exercise or pharmacological. Exercise stress echocardiography is the preferred stress echocardiography modality. However, it is not suitable for all patients and may not be feasible in populations that do not meet a minimum level of fitness. In patients who are ineligible for exercise stress echocardiography, pharmacological stress echocardiography can be a useful alternative. Common pharmacological stressors include: adenosine, dipyridamole, and dobutamine. As a testing modality, exercise echocardiography is noted as more sensitive, more specific and has a higher predictive value than exercise ECG. Exercise echocardiography can be helpful in the evaluation of regional wall motion response, location and extent of ischemia during stress in patients with MI. During exercise, the normal myocardium is hyperdynamic while in patients with MI, the ischemic myocardium is either akinetic or hypokinetic. Positron Emission Tomography Ambulatory ST Segment Monitoring Ambulatory ECG monitoring (Holter monitor) is used to detect major arrhythmias and myocardial ischemia occurring during normal activities. Ambulatory ECG monitoring adds very little prognostic value in patients with chronic stable angina, however, does play a role in the detection of major arrhythmias in patients with chronic stable angina and suspected vasospastic angina. Electron Beam Tomography The extent of coronary artery calcification directly correlates to the area of atheromatous plaque. Hence in patients with chest pain, coronary artery calcium (CAC) scoring is one of the factor to be considered in the risk assessment for coronary artery disease. The methods used for detection and quantification of CAC include electron beam computed tomography (EBCT) and multi-detector computed tomography (MDCT). Agatston score is a computed software that is commonly used to measure CAC based on the density and area of calcified plaques. Cardiac Magnetic Resonance Imaging Cardiac magnetic resonance imaging (CMRI) is a non-invasive test that is useful in the evaluation of overall coronary anatomy and function. CMRI also helps in the identification of inflammation, neovascularization and fibrous cap. It, therefore, holds the potential for plaque characterization. Coronary angiography is a gold standard test in the evaluation of severity of coronary artery disease and the possibility for revascularization. Coronary angiography is indicated in patients with a high pretest probability of CAD and in symptomatic patients with inconclusive initial noninvasive tests. Provocative testing with ergonovine during angiography may be useful in patients with vasospastic angina. Major complications such as death, MI and stroke associated with routine angiography is as low as 0.1% - 0.2%. Treatment of chronic stable angina aims at minimizing symptoms, reducing recurrent ischemia, improving the quality of life and improving prognosis by preventing MI and death. Treatment options include lifestyle modification, pharmacotherapy and revascularization that help in slowing the disease progression, preserving the endothelial function and preventing thrombosis. Patients with double-vessel CAD and with normal LV function may be started on initial medical management and in non-responders, PCI may be considered. However, the decision of PCI versus CABG depends on the coronary anatomy, LV function and the need for complete revascularization. Patients with triple-vessel CAD or left main disease or reduced left ventricular function, CABG is the mainstay of management. However, in cases of mild symptoms or preserved LVEF in patients with triple-vessel disease, initial pharmacologic therapy or PCI may be tried. The goal of the management of chronic stable angina is to improve the quality of life by decreasing the severity and frequency of symptoms and to decrease premature cardiovascular death caused by myocardial infarction or development of heart failure. The mainstays of the treatment of chronic stable angina are patient education, lifestyle changes and medical therapy. In patients with chronic stable angina, immediate symptomatic relief is achieved with short-acting sublingual nitrates and long term symptom relief is achieved with beta blockers as first line therapy, or calcium channel blockers and long-acting nitrates when beta blockers are contraindicated. Drugs that improve the quality of life and are associated with a better prognosis include: low dose aspirin, beta-blockers and ACEIs. Dipyridamole is a pyrimidopyrimidine derivative with poor anti-thrombotic efficacy and therefore not recommended for anti-platelet therapy in patients with chronic stable angina. Dipyridamole may also exacerbate anginal symptoms due to coronary steal phenomenon. Thienopyridines, such as clopidogrel and ticlopidine, selectively inhibit ADP-induced platelet aggregation and are used as an alternative to aspirin in patients with significant risk of arterial thrombosis. In patients with chronic stable angina, nitrates remain the mainstay of therapy. Organic nitrates are therapeutic precursors of endothelium-derived relaxing factor that produce their beneficial effects both, by decreasing myocardial oxygen requirements and by improving myocardial perfusion. The most commonly used nitrates are nitroglycerin, isosorbide dinitrate and isosorbide mononitrate. Short acting nitrates, such as sublingual nitroglycerin, are best suited to treat acute episodes of angina and are effective when used for situational prophylaxis. Long-acting nitrates help to reduce the frequency and severity of angina and may increase exercise tolerance in patients with stable angina. Nitrates at therapeutic doses do not affect coronary vascular resistance, thereby reducing the risk of myocardial ischemia due to coronary steal phenomena that is consistent with the use of dipyridamole and other short acting dihydropyridines. In patients with stable angina, beta blockers are used as a first line of therapy for both, symptomatic relief and the prevention of ischemic events. The physiologic mechanism of benefit of this therapy is a marked reduction in myocardial oxygen consumption by reducing the heart rate and myocardial contractility. Selective beta-1 blockers are preferred to non-selective beta-blockers due to fewer associated side effects. The most commonly used selective beta-1 blockers are metoprolol, atenolol, and bisoprolol. Calcium Channel Blockers Calcium channel blockers (CCBs) consist of three sub-classes namely, dihydropyridines (e.g., nifedipine), phenylalkylamines (e.g., verapamil) and modified benzothiazepines (e.g., diltiazem). The beneficial anti-anginal effects of CCB include: reduction in the afterload consequent to systemic vasodilation as well as epicardial vessel vasodilation, enhancement of the coronary collateral flow with subsequent sub-endocardial perfusion due to the inhibition of calcium influx via L-type channels. Long-acting calcium channel blockers are an effective antianginal agent and are considered to be the first choice in post-MI patients with a contraindication to beta-blocker. Long-acting CCBs are also specifically used to control symptoms in patients with vasospastic angina. However short-acting CCBs, such as nifedipine, are avoided due to an increased risk of myocardial infarction and mortality. Potassium Channel Openers Nicorandil has both, anti-anginal effects due to nitrate-like and ATP-sensitive potassium channel activating properties and provides cardio-protective effects as well. Therefore, nicorandil usage in addition to standard anti-anginal therapy may be indicated in patients who are intolerant to beta-blocker therapy or in whom CCB monotherapy or combination therapy CCB is unsuccessful. Newer Anti-anginal Agents Ranolazine is a one of the newer FDA approved anti-anginal medication for management of chronic stable angina. Perhexiline is another anti-anginal, primarily used in Australia and New Zealand, being studied for use in the United States and UK. In patients with chronic stable angina, other effective agents with anti-anginal and anti-ischemic properties are ivabradine, trimetazidine and molsidomine. Patients diagnosed with syndrome X and hypertension may have microvascular angina characterized by a reduced coronary vasodilator reserve and increased sympathetic drive. ACE inhibition in such patients may attenuate sympathetic coronary vasoconstriction, normalize thallium perfusion defects and reduce exercise-induced ischemia with subsequent increased myocardial oxygen supply. Based on the recent AHA and ESC guidelines, the recommended goal blood pressure in patients with atherosclerotic coronary vascular disease is less than 130/80 mm Hg. Statins by inhibiting HMG-CoA reductase subsequently reduce serum cholesterol levels and have been shown to be effective in the primary prevention of various hyperlipidemias and secondary prevention of ischemic heart disease. The most commonly used statins are simvastatin, atorvastatin, pravastatin and rosuvastatin. The incidence of major cardiovascular mortality was reduced by 30% with the use of simvastatin and pravastatin in patients with coronary artery disease and therefore may be used for both primary and secondary prevention. However, there are no trials specifically performed on patients with stable angina but they form a significant portion in other major trials studying the efficacy of lipid-lowering drugs on the overall mortality from cardiovascular events. In patients with low HDL and high triglycerides as an adjunctive to statin therapy, fibrates or niacin may be used. The goal of the treatment of chronic stable angina is to reduce the symptoms, delay the progression of atherosclerosis, and prevent cardiovascular events. In order to achieve these goals, lifestyle modifications and medical therapy are the first line treatment. Revascularization is done to increase survival in specific conditions where the stenosis of the coronary arteries is anatomically and functionally significant and the symptoms are refractory to medical therapy. There are currently two well-established revascularization approaches for the treatment of chronic stable angina caused by coronary atherosclerosis: CABG and PCI. Since the introduction of coronary artery bypass surgery in 1967 and percutaneous transluminal coronary angioplasty (PTCA) in 1977, research has supported the effective usage of both strategies for treatment of patients with chronic stable angina. However, as with any treatment method, both methodologies have weaknesses. The choice between PCI and CABG is based upon anatomy and other factors such as left ventricular function and the presence or absence of diabetes. In general, PTCA is reserved for single or some cases of two vessel disease, while CABG is reserved for patients with two or three vessel disease or left main disease. With the availability of drug-eluting stents, PCI is increasingly being performed for many lesions including more complex ones. Percutaneous coronary intervention for coronary artery disease first began in 1977, as a valuable mode of revascularization, wherein at the point of coronary stenosis a catheter-borne balloon is inflated to relieve the stenosis. Coronary artery bypass surgery, also coronary artery bypass graft (CABG, pronounced "cabbage") surgery, and colloquially heart bypass or bypass surgery is a surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease. Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the coronary circulation supplying the myocardium (heart muscle). This surgery is usually performed with the heart stopped, necessitating the usage of cardiopulmonary bypass; techniques are available to perform CABG on a beating heart, so-called "off-pump" surgery. PCI vs Medical Therapy An increased risk of mortality and morbidity is associated with untreated coronary artery disease. The main aim of therapy in patients with chronic stable angina is to alleviate symptoms, delay the progression of atherosclerosis, reduce the incidence of adverse coronary events and improve prognosis. This may be achieved with either initial medical therapy or with initial revascularization that includes percutaneous coronary intervention or coronary artery bypass grafting. Medical therapy alleviates symptom and improves prognosis; however, on the contrary, revascularization procedures provide symptomatic relief but generally does not improve mortality. CABG vs Medical Therapy It is well established that revascularization with CABG has shown to provide better symptomatic relief and improved survival rates in comparison to medical therapy in some patients with stable angina. However, the long term benefit of CABG is limited by the progression of atherosclerosis in other unbypassed vessels and stenosis of the graft itself. PCI and CABG vs Medical Therapy The Mass and Mass-II trials directly compared the effect of medical therapy, CABG and PCI for the management of chronic stable angina. However, there are a few reservations to the application of results from these studies as they did not include the current optimal strategies of therapy. PCI vs CABG PCI and CABG have become the standard of care in the management of patients with symptomatic coronary artery disease. Patients with multi-vessel disease, the overall mortality and freedom from myocardial infarction appear to be similar in both the treatment strategies; however, the need for repeat revascularization is significantly higher in patients who initially underwent PCI secondary to a higher incidence of restenosis. Alternative Therapies for Refractory Angina Transmyocardial Revascularization (TMR) As the survival of patients with primary coronary events continue to increase, the number of patients presenting with refractory ischemia despite maximal medical therapy and unsuitable for further traditional revascularization techniques also continues to rise. Transmyocardial revascularization (TMR) is one of the emerging techniques that has been studied in many randomized trials and has shown to reduce the incidence of recurrent angina, increase exercise tolerance time and improve quality of life. TMR can be performed using either a laser beam or a percutaneous approach. However, only laser TMR is currently FDA approved. Spinal Cord Stimulation (SCS) In patients with refractory angina, spinal cord stimulation (SCS) is used to provide analgesia in the region of radiation of anginal-pain with the help an implanted device consisting of a stimulating electrode tip that extends into the dorsal epidural space, usually at the C7-T1 level. Enhanced External Counter Pulsation (EECP) Enhanced external counter pulsation (EECP) is another alternative therapy in the management of refractory angina. Most data from observational studies have demonstrated significant improvement in the exercise tolerance and reduction in the frequency of anginal symptoms as well as the use of nitroglycerin among patients treated with EECP. Ongoing follow-up of the patient with chronic stable angina is necessary to monitor symptoms and to optimize antianginal therapy. It is generally recommended that these patients be evaluated every 4-6 months during first year of diagnosis/initiation of therapy and annually thereafter. Based upon clinical judgement, if the patient is poorly responsive to therapy, if the episodes are severe or frequent, or if the patient is fragile with multiple co-morbidities, they may need to be seen more frequently. During a follow-up visit, the patient should be asked about the frequency and severity of their anginal symptoms, their level of exercise capacity, whether they have been able to modify his/her risk factors, how well they are tolerating and complying with the therapy and whether he/she has developed new illnesses or co-morbidities. Cardiac rehabilitation, also called cardiac rehab (CR), is a medically supervised program to help cardiac patients recover quickly and improve their overall well being. The main goal of rehabilitation is to help patients understand their disease and inculcate a regimen to stabilize and reduce, or even reverse the progression of cardiovascular disease. Cardiac rehab is often divided into phases that involve monitored exercise, counseling, emotional support, and education about lifestyle changes to reduce the risks of heart problems. It also helps reverse limitations experienced by patients who have suffered the adverse patho-physiologic and psychological consequences of cardiac events, thus, also helping patients to return to work early. Traditionally, cardiac rehabilitation has been provided to lower-risk patients who could exercise without physical limitations. However, rapid evolution in the management of CAD has now changed the demographics of the patients, so that, even patients with recent revascularization can be candidates for rehabilitation training. The 1989 Surgeon General’s report, which assessed numerous case-control and cohort studies, reported that smoking increased cardiovascular disease mortality by 50%. Cigarette smoking, likely due to the hemodynamic consequences of sympathetic neural stimulation and systemic catecholamine release, plays an important role in the pathogenesis of coronary artery disease. Cigarette smoking also forms a major risk factor for acute cardiovascular events as it relates to an associated increase in blood coagulability. Hence, cigarette smoking is an important reversible risk factor in the pathogenesis of CAD and cessation of which improves prognosis and is associated with a substantial decrease in the risk of mortality. In patients with stable angina pectoris, nicotine replacement therapy has shown to be potentially beneficial despite the associated cardiovascular risks of nicotine, such as increase in heart rate with a small rise in blood pressure. Nicotine replacement therapy may be initiated as early as 2–3 days after acute myocardial infarction or cardiac arrhythmias. Additionally, nicotine patches have been used successfully in high-risk patients without any adverse effects such as aggravation of MI or arrhythmia. Obesity is directly associated with the development of coronary artery disease (CAD) risk factors such as: hypertension, diabetes, reduced levels of HDL-C and elevated levels of triglyceride. Research has demonstrated that CAD risk factors contribute to a strong, graded, J-shaped univariable relationship between BMI and cardiovascular disease mortality. This increased mortality, when adjusted for age, self-reported smoking status, total cholesterol, and systolic blood pressure, maintained significant hazard ratios. Hence, in obese patients with CAD, weight reduction and/or dietary interventions may be warranted to reduce the incidence of above-mentioned risk factors and prevent future coronary events. Weight reduction is strongly recommended in patients with a BMI greater than 30 kg/m2 and in patients with increased waist circumference (greater than 102 cms for men and 89 cms for women), characteristic of truncal obesity. Based on the plasma lipid abnormalities, adequate dietary modification may also be indicated. Based on an individual's ability to exercise and severity of the symptoms, physical activity may be indicated as a treatment. As a treatment, increased physical activity has demonstrated improvements in an individual's sustained exercise duration, reduced the frequency of symptoms and also provided beneficial effects on blood pressure, diabetes and the overall lipid profile. Before the initiation of an exercise regimen, an exercise test is indicated as a useful guide to assess the level of tolerance. In patients with established coronary artery disease, the recommended goal for total cholesterol is 130 mg/dl and LDL-C is 100 mg/dl, while the HDL-C and triglyceride concentrations serve as preferred markers for risk assessment. In patients with CAD, a fasting lipid-profile may be repeated at 5 year intervals to assess the overall risk of cardiovascular mortality and morbidity. Based on the individual’s lipid abnormalities, necessary dietary interventions and/or lipid-lowering agents are suggested to prevent the risk of future coronary events. A Mediterranean diet consisting of fruits, vegetables, lean meat and fish has also been shown to be beneficial. Omega-3 fatty acid supplementation may be indicated in patients with stable angina for secondary prevention, as it has been shown to reduce elevated triglycerides and also reduce the risk of sudden cardiac death. Fish consumption once a week has also been associated with reduced risk of mortality from coronary artery disease and, for this reason, is strongly recommended. The risk of progression of atherosclerosis is proportional to the increase in elevated blood pressure, hyperglycemia and dyslipidemia. Therefore, the control of hypertension, hyperglycemia and other features of metabolic syndrome deserves special attention in the prevention of mortality and morbidity due to coronary artery disease. In patients with established CAD, concomitant diabetes and/or renal dysfunction, the blood pressure goal is 130/80-85 and the decision to lower blood pressure depends on the total cardiovascular risk and the extent of target organ damage. Close monitoring and lifestyle changes may be indicated in low-risk patients without documented target organ damage. However, in high-risk patients with a sustained SBP of ≥140 mm Hg and/or DBP ≥90 mm Hg, the goal is to lower blood pressure less than 140/90 with the help of combined drug therapy and life style modification. Anti-hypertensive therapies that have shown to significantly reduce cardiovascular mortality and morbidity in patients with coronary artery disease include diuretics, beta-blockers, ACEIs, ARBs and calcium channel blockers. Diabetes is one of the major modifiable risk factors for coronary artery disease. Maintaining a good glycemic control has been demonstrated to delay the disease progression in patients with impaired glycemic control and further prevent microvascular complications. In type 1 diabetics, appropriate insulin therapy and concomitant dietary modification may be required. However, in patients with type 2 diabetes, a multi-factorial intervention involving increased physical activity, weight reduction, dietary modification and/or drug therapy has shown to reduce the risk of overall cardiovascular and microvascular events by approximately 50%. - "MerckMedicus : Dorland's Medical Dictionary". Retrieved 2009-01-09. - Daly CA, De Stavola B, Sendon JL, Tavazzi L, Boersma E, Clemens F et al. (2006) Predicting prognosis in stable angina--results from the Euro heart survey of stable angina: prospective observational study. BMJ 332 (7536):262-7. DOI:10.1136/bmj.38695.605440.AE PMID: 16415069 - Diamond GA, Forrester JS (1981) Improved interpretation of a continuous variable in diagnostic testing: probabilistic analysis of scintigraphic rest and exercise left ventricular ejection fractions for coronary disease detection. Am Heart J 102 (2):189-95. PMID: 7258092 - Horne BD, Anderson JL, John JM, Weaver A, Bair TL, Jensen KR et al. (2005) Which white blood cell subtypes predict increased cardiovascular risk? J Am Coll Cardiol 45 (10):1638-43. DOI:10.1016/j.jacc.2005.02.054 PMID: 15893180 - Shlipak MG, Stehman-Breen C, Vittinghoff E, Lin F, Varosy PD, Wenger NK et al. (2004) Creatinine levels and cardiovascular events in women with heart disease: do small changes matter? Am J Kidney Dis 43 (1):37-44. PMID: 14712425 - Fried LF, Shlipak MG, Crump C, Bleyer AJ, Gottdiener JS, Kronmal RA et al. (2003) Renal insufficiency as a predictor of cardiovascular outcomes and mortality in elderly individuals. J Am Coll Cardiol 41 (8):1364-72. PMID: 12706933 - Arcavi L, Behar S, Caspi A, Reshef N, Boyko V, Knobler H (2004) High fasting glucose levels as a predictor of worse clinical outcome in patients with coronary artery disease: results from the Bezafibrate Infarction Prevention (BIP) study. Am Heart J 147 (2):239-45. DOI:10.1016/j.ahj.2003.09.013 PMID: 14760320 - Kragelund C, Grønning B, Køber L, Hildebrandt P, Steffensen R (2005) N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med 352 (7):666-75. DOI:10.1056/NEJMoa042330 PMID: 15716560 - Kléber AG (2000) ST-segment elevation in the electrocardiogram: a sign of myocardial ischemia. Cardiovasc Res 45 (1):111-8. PMID: 10728321 - Ashley EA, Myers J, Froelicher V (2000) Exercise testing in clinical medicine. Lancet 356 (9241):1592-7. DOI:10.1016/S0140-6736(00)03138-X PMID: 11075788 - Elamin MS, Boyle R, Kardash MM, Smith DR, Stoker JB, Whitaker W et al. (1982) Accurate detection of coronary heart disease by new exercise test. Br Heart J 48 (4):311-20. PMID: 6127094 - Mark DB, Shaw L, Harrell FE, Hlatky MA, Lee KL, Bengtson JR et al. (1991) Prognostic value of a treadmill exercise score in outpatients with suspected coronary artery disease. N Engl J Med 325 (12):849-53. DOI:10.1056/NEJM199109193251204 PMID: 1875969 - Chakko S, Woska D, Martinez H, de Marchena E, Futterman L, Kessler KM et al. (1991) Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care. Am J Med 90 (3):353-9. PMID: 1825901 - Hemingway H, Shipley M, Christie D, Marmot M (1998) Cardiothoracic ratio and relative heart volume as predictors of coronary heart disease mortality. The Whitehall study 25 year follow-up. Eur Heart J 19 (6):859-69. PMID: 9651709 - Shaw LJ, Hachamovitch R, Redberg RF (2000) Current evidence on diagnostic testing in women with suspected coronary artery disease: choosing the appropriate test. Cardiol Rev 8 (1):65-74. PMID: 11174875 - Vigna C, Stanislao M, De Rito V, Russo A, Santoro T, Fusilli S et al. (2006) Inaccuracy of dipyridamole echocardiography or scintigraphy for the diagnosis of coronary artery disease in patients with both left bundle branch block and left ventricular dysfunction. Int J Cardiol 110 (1):116-8. DOI:10.1016/j.ijcard.2005.05.068 PMID: 16002158 - Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ et al. (1997) ACC/AHA guidelines for the clinical application of echocardiography: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Clinical Application of Echocardiography). Developed in collaboration with the American Society of Echocardiography. J Am Coll Cardiol 29 (4):862-79. PMID: 9091535 - Rumberger JA, Simons DB, Fitzpatrick LA, Sheedy PF, Schwartz RS (1995) Coronary artery calcium area by electron-beam computed tomography and coronary atherosclerotic plaque area. A histopathologic correlative study. Circulation 92 (8):2157-62. PMID: 7554196 - Greenland P, Bonow RO, Brundage BH, Budoff MJ, Eisenberg MJ, Grundy SM et al. (2007) ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography) developed in collaboration with the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular Computed Tomography. J Am Coll Cardiol 49 (3):378-402. DOI:10.1016/j.jacc.2006.10.001 PMID: 17239724 - Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M, Detrano R (1990) Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 15 (4):827-32. PMID: 2407762 - Ruehm SG, Corot C, Vogt P, Kolb S, Debatin JF (2001) Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits. Circulation 103 (3):415-22. PMID: 11157694 - Kerwin W, Hooker A, Spilker M, Vicini P, Ferguson M, Hatsukami T et al. (2003) Quantitative magnetic resonance imaging analysis of neovasculature volume in carotid atherosclerotic plaque. Circulation 107 (6):851-6. PMID: 12591755 - Wasserman BA, Smith WI, Trout HH, Cannon RO, Balaban RS, Arai AE (2002) Carotid artery atherosclerosis: in vivo morphologic characterization with gadolinium-enhanced double-oblique MR imaging initial results. Radiology 223 (2):566-73. PMID: 11997569 - Noto TJ, Johnson LW, Krone R, Weaver WF, Clark DA, Kramer JR et al. (1991) Cardiac catheterization 1990: a report of the Registry of the Society for Cardiac Angiography and Interventions (SCA&I). Cathet Cardiovasc Diagn 24 (2):75-83. PMID: 1742788 - Qaseem A, Fihn SD, Dallas P, et al. Management of patients with stable ischemic heart disease: Executive summary of a clinical practice guideline from the American College of Physicians, American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic Surgeons. Ann Intern Med 2012. - (1994) Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration. BMJ 308 (6921):81-106. PMID: 8298418 - Patrono C, Bachmann F, Baigent C, Bode C, De Caterina R, Charbonnier B et al. (2004) Expert consensus document on the use of antiplatelet agents. The task force on the use of antiplatelet agents in patients with atherosclerotic cardiovascular disease of the European society of cardiology. Eur Heart J 25 (2):166-81. PMID: 14720534 - Patrono C, Coller B, FitzGerald GA, Hirsh J, Roth G (2004) Platelet-active drugs: the relationships among dose, effectiveness, and side effects: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 126 (3 Suppl):234S-264S. DOI:10.1378/chest.126.3_suppl.234S PMID: 15383474 - Antithrombotic Trialists' Collaboration (2002) Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 324 (7329):71-86. PMID: 11786451 - Kaufmann PA, Mandinov L, Seiler C, Hess OM (2000) Impact of exercise-induced coronary vasomotion on anti-ischemic therapy. Coron Artery Dis 11 (4):363-9. PMID: 10860181 - Thadani U, Lipicky RJ (1994) Short and long-acting oral nitrates for stable angina pectoris. Cardiovasc Drugs Ther 8 (4):611-23. PMID: 7848896 - Parker JD, Parker JO (1998) Nitrate therapy for stable angina pectoris. N Engl J Med 338 (8):520-31. DOI:10.1056/NEJM199802193380807 PMID: 9468470 - Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM et al. (1999)guidelines for the management of patients with chronic stable angina: executive summary and recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Chronic Stable Angina).Circulation 99 (21):2829-48. PMID: 10351980 - Pepine CJ, Cohn PF, Deedwania PC, Gibson RS, Handberg E, Hill JA et al. (1994) Effects of treatment on outcome in mildly symptomatic patients with ischemia during daily life. The Atenolol Silent Ischemia Study (ASIST) Circulation 90 (2):762-8. PMID: 8044945 - Savonitto S, Ardissino D (1998) Selection of drug therapy in stable angina pectoris. Cardiovasc Drugs Ther 12 (2):197-210. PMID: 9652879 - Thadani U (1999) Treatment of stable angina. Curr Opin Cardiol 14 (4):349-58. PMID: 10448616 - (1981) Timolol-induced reduction in mortality and reinfarction in patients surviving acute myocardial infarction. N Engl J Med 304 (14):801-7. DOI:10.1056/NEJM198104023041401 PMID: 7010157 - Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS et al. (2003) ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina). Circulation 107 (1):149-58. PMID: 12515758 - Karlson BW, Emanuelsson H, Herlitz J, Nilsson JE, Olsson G (1991) Evaluation of the antianginal effect of nifedipine: influence of formulation dependent pharmacokinetics. Eur J Clin Pharmacol 40 (5):501-6. PMID: 1884725 - Waters D (1991) Proischemic complications of dihydropyridine calcium channel blockers. Circulation 84 (6):2598-600. PMID: 1959210 - Nissen SE, Tuzcu EM, Libby P, Thompson PD, Ghali M, Garza D et al. (2004) Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and normal blood pressure: the CAMELOT study: a randomized controlled trial. JAMA 292 (18):2217-25. DOI:10.1001/jama.292.18.2217 PMID: 15536108 - Markham A, Plosker GL, Goa KL (2000) Nicorandil. An updated review of its use in ischaemic heart disease with emphasis on its cardioprotective effects. Drugs 60 (4):955-74. PMID: 11085202 - (2003) Nicorandil for angina--an update. Drug Ther Bull 41 (11):86-8. PMID: 14658416 - Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F; et al. (2006). "Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology". Eur Heart J. 27 (11): 1341–81. doi:10.1093/eurheartj/ehl001. PMID 16735367. - Kaski JC, Rosano G, Gavrielides S, Chen L (1994) Effects of angiotensin-converting enzyme inhibition on exercise-induced angina and ST segment depression in patients with microvascular angina. J Am Coll Cardiol 23 (3):652-7. PMID: 8113548 - van den Heuvel AF, Dunselman PH, Kingma T, Verhorst P, Boomsma F, van Gilst WH et al. (2001) Reduction of exercise-induced myocardial ischemia during add-on treatment with the angiotensin-converting enzyme inhibitor enalapril in patients with normal left ventricular function and optimal beta blockade. J Am Coll Cardiol 37 (2):470-4. PMID: 11216965 - Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J et al. (2007)2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina. Circulation 116 (23):2762-72. PMID: 17998462 - Rosendorff C, Black HR, Cannon CP, Gersh BJ, Gore J, Izzo JL et al. (2007) Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention. Circulation 115 (21):2761-88. DOI:10.1161/CIRCULATIONAHA.107.183885 PMID: 17502569 - (1994) Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet 344 (8934):1383-9. PMID: 7968073 - Baigent C, Keech A, Kearney PM, Blackwell L, Buck G, Pollicino C et al. (2005) Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 366 (9493):1267-78. DOI:10.1016/S0140-6736(05)67394-1 PMID: 16214597 - Sacks FM, Tonkin AM, Shepherd J, Braunwald E, Cobbe S, Hawkins CM et al. (2000) Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: the Prospective Pravastatin Pooling Project. Circulation 102 (16):1893-900. PMID: 11034935 - (1998) Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. N Engl J Med 339 (19):1349-57. DOI:10.1056/NEJM199811053391902 PMID: 9841303 - Grundy SM, Cleeman JI, Merz CN, Brewer HB, Clark LT, Hunninghake DB et al. (2004) Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. J Am Coll Cardiol 44 (3):720-32. DOI:10.1016/j.jacc.2004.07.001 PMID: 15358046 - Schwartz GG, Olsson AG, Ezekowitz MD, Ganz P, Oliver MF, Waters D et al. (2001) Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA 285 (13):1711-8. PMID: 11277825 - Sever PS, Dahlöf B, Poulter NR, Wedel H, Beevers G, Caulfield M et al. (2003) Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 361 (9364):1149-58. DOI:10.1016/S0140-6736(03)12948-0 PMID: 12686036 - LaRosa JC, Grundy SM, Waters DD, Shear C, Barter P, Fruchart JC et al. (2005) Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med 352 (14):1425-35. DOI:10.1056/NEJMoa050461 PMID: 15755765 - Heart Protection Study Collaborative Group (2002) MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 360 (9326):7-22. DOI:10.1016/S0140-6736(02)09327-3 PMID: 12114036 - Robins SJ, Rubins HB, Faas FH, Schaefer EJ, Elam MB, Anderson JW et al. (2003) Insulin resistance and cardiovascular events with low HDL cholesterol: the Veterans Affairs HDL Intervention Trial (VA-HIT). Diabetes Care 26 (5):1513-7. PMID: 12716814 - Moliterno DJ, Elliott JM (1995) Randomized trials of myocardial revascularization. Curr Probl Cardiol 20 (3):125-90. PMID: 7600846 - Smith SC, Feldman TE, Hirshfeld JW, Jacobs AK, Kern MJ, King SB et al. (2006) ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). J Am Coll Cardiol 47 (1):e1-121. DOI:10.1016/j.jacc.2005.12.001 PMID: 16386656 - Hueb WA, Bellotti G, de Oliveira SA, Arie S, de Albuquerque CP, Jatene AD et al. (1995) The Medicine, Angioplasty or Surgery Study (MASS): a prospective, randomized trial of medical therapy, balloon angioplasty or bypass surgery for single proximal left anterior descending artery stenoses. J Am Coll Cardiol 26 (7):1600-5. DOI:10.1016/0735-1097(95)00384-3 PMID: 7594092 - Hueb W, Soares PR, Gersh BJ, César LA, Luz PL, Puig LB et al. (2004) The medicine, angioplasty, or surgery study (MASS-II): a randomized, controlled clinical trial of three therapeutic strategies for multivessel coronary artery disease: one-year results. J Am Coll Cardiol 43 (10):1743-51. DOI:10.1016/j.jacc.2003.08.065 PMID: 15145093 - Kim MC, Kini A, Sharma SK (2002) Refractory angina pectoris: mechanism and therapeutic options. J Am Coll Cardiol 39 (6):923-34. PMID: 11897431 - Burkhoff D, Schmidt S, Schulman SP, Myers J, Resar J, Becker LC et al. (1999) Transmyocardial laser revascularisation compared with continued medical therapy for treatment of refractory angina pectoris: a prospective randomised trial. ATLANTIC Investigators. Angina Treatments-Lasers and Normal Therapies in Comparison. Lancet 354 (9182):885-90. PMID: 10489946 - Urano H, Ikeda H, Ueno T, Matsumoto T, Murohara T, Imaizumi T (2001) Enhanced external counterpulsation improves exercise tolerance, reduces exercise-induced myocardial ischemia and improves left ventricular diastolic filling in patients with coronary artery disease. J Am Coll Cardiol 37 (1):93-9. PMID: 11153780 - Centers for Disease Control (CDC) (1989) The Surgeon General's 1989 Report on Reducing the Health Consequences of Smoking: 25 Years of Progress. MMWR Morb Mortal Wkly Rep 38 Suppl 2 ():1-32. PMID: 2494426 - Benowitz NL, Gourlay SG (1997) Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy. J Am Coll Cardiol 29 (7):1422-31. PMID: 9180099 - Bartecchi CE, MacKenzie TD, Schrier RW (1994) The human costs of tobacco use (1) N Engl J Med 330 (13):907-12. DOI:10.1056/NEJM199403313301307 PMID: 8114863 - MacKenzie TD, Bartecchi CE, Schrier RW (1994) The human costs of tobacco use (2) N Engl J Med 330 (14):975-80. DOI:10.1056/NEJM199404073301406 PMID: 8121461 - Critchley J, Capewell S (2003) Smoking cessation for the secondary prevention of coronary heart disease. Cochrane Database Syst Rev (4):CD003041. DOI:10.1002/14651858.CD003041 PMID: 14583958 - Tzivoni D, Keren A, Meyler S, Khoury Z, Lerer T, Brunel P (1998) Cardiovascular safety of transdermal nicotine patches in patients with coronary artery disease who try to quit smoking. Cardiovasc Drugs Ther 12 (3):239-44. PMID: 9784902 - (1994) Nicotine replacement therapy for patients with coronary artery disease. Working Group for the Study of Transdermal Nicotine in Patients with Coronary artery disease. Arch Intern Med 154 (9):989-95. PMID: 8179456 - Dudina A, Cooney MT, De Bacquer D, De Backer G, Ducimetière P, Jousilahti P et al. (2011) Relationships between body mass index, cardiovascular mortality, and risk factors: a report from the SCORE investigators. Eur J Cardiovasc Prev Rehabil ():. DOI:10.1177/1741826711412039 PMID: 21642320 - Smith GD, Shipley MJ, Marmot MG, Rose G (1992) Plasma cholesterol concentration and mortality. The Whitehall Study. JAMA 267 (1):70-6. PMID: 1727199 - (1992) Long-term comprehensive care of cardiac patients. Recommendations by the Working Group on Rehabilitation of the European Society of Cardiology. Eur Heart J 13 Suppl C ():1-45. PMID: 1639095 - De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J et al. (2003) European guidelines on cardiovascular disease prevention in clinical practice. Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice. Eur Heart J 24 (17):1601-10. PMID: 12964575 - (1999) Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico. Lancet 354 (9177):447-55. PMID: 10465168 - Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R et al. (2002) Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation 105 (16):1897-903. PMID: 11997274 - Bucher HC, Hengstler P, Schindler C, Meier G (2002) N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials. Am J Med 112 (4):298-304. PMID: 11893369 - Studer M, Briel M, Leimenstoll B, Glass TR, Bucher HC (2005) Effect of different antilipidemic agents and diets on mortality: a systematic review. Arch Intern Med 165 (7):725-30. DOI:10.1001/archinte.165.7.725 PMID: 15824290 - Kris-Etherton PM, Harris WS, Appel LJ, Nutrition Committee (2003) Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Arterioscler Thromb Vasc Biol 23 (2):e20-30. PMID: 12588785 - He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR et al. (2004) Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies. Circulation 109 (22):2705-11. DOI:10.1161/01.CIR.0000132503.19410.6B PMID: 15184295 - European Society of Hypertension-European Society of Cardiology Guidelines Committee (2003) 2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 21 (6):1011-53. DOI:10.1097/01.hjh.0000059051.65882.32 PMID: 12777938 - American Diabetes Association (2003) Standards of medical care for patients with diabetes mellitus. Diabetes Care 26 Suppl 1 ():S33-50. PMID: 12502618 - Inzucchi SE, Amatruda JM (2003) Lipid management in patients with diabetes: translating guidelines into action. Diabetes Care 26 (4):1309-11. PMID: 12663615 - Gaede P, Vedel P, Larsen N, Jensen GV, Parving HH, Pedersen O (2003) Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med 348 (5):383-93. DOI:10.1056/NEJMoa021778 PMID: 12556541	2	73	8	0	4	1	0.865939	13	13,944
- Post-concussion syndrome Post-concussion syndrome Classification and external resources ICD-10 F07.2 ICD-9 310.2 eMedicine emerg/865 MeSH D038223 Post-concussion syndrome, also known as postconcussive syndrome or PCS, and historically called shell shock, is a set of symptoms that a person may experience for weeks, months, or occasionally up to a year or more after a concussion – a mild form of traumatic brain injury (abbreviated TBI). PCS may also occur in moderate and severe cases of traumatic brain injury. Symptoms of PCS, which is the most common entity to be diagnosed in people who have suffered TBI, may occur in 38–80% of mild head injuries. A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury, or it may be made starting within a week or ten days of trauma. In late, persistent, or prolonged PCS (PPCS), symptoms last for over six months, or by other standards, three. The condition can cause a variety of symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. As many of the symptoms in PCS are common to, or exacerbated by, other disorders, there is a risk of misdiagnosis. Though there is no treatment for PCS itself, symptoms can be treated; medications and physical and behavioral therapy may be used, and patients can be educated about symptoms and their usual prognosis. The majority of PCS cases disappear after a period of time. It is not known what causes PCS symptoms to occur and persist, or why some people who suffer a mild traumatic brain injury (MTBI) develop PCS while others do not. The nature of the syndrome and the diagnosis itself have been the subject of intense debate since the 19th century. However, certain risk factors have been identified; for example, preexisting medical or psychological conditions, expectations of disability, and older age all increase the chances that someone will suffer PPCS. Physiological and psychological factors present before, during, and after the injury are all thought to be involved in the development of PCS. - 1 Signs and symptoms - 2 Causes - 3 Diagnosis - 4 Treatment - 5 Prognosis - 6 Epidemiology - 7 History - 8 Controversy - 9 References Signs and symptoms The abbreviation PCS may also be used to mean post-concussion symptoms. Symptoms can appear immediately, or weeks to months after the initial injury. Their severity lessens progressively over time. The nature of the symptoms tends to change over time: they are most commonly of a physical nature following the injury, but tend to become predominantly psychological later. Signs and symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, anxiety, fatigue, and poor judgment may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather days or weeks after. Nausea and drowsiness commonly occur two to four weeks after concussion and can be long lasting. Also, headache and dizziness occur immediately after the injury and can be long lasting. The main PCS symptom is headache. While most people have headaches of the same type they experienced before the injury, people with PCS often report more frequent or longer-lasting headaches. Between 30 and 90% of people treated for PCS report having more headaches than they did before the injury, and between 8 and 32% still report them a year after the injury. Dizziness, the second most common symptom, occurs in about half of people with PCS and is still present in up to a quarter of them a year after the injury. Older people are at especially high risk for dizziness. About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% have blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. Loss of hearing occurs in 20% of cases. PCS may cause insomnia, fatigue, sleepiness, or other problems with sleep. Other physical symptoms include nausea and vomiting. Psychological and behavioral Psychological symptoms, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality. Other emotional and behavioral symptoms include restlessness, aggression, mood swings, anger, decreased libido, impulsiveness, loss of social judgment, and lack of ability to tolerate stress or alcohol. People with PCS may also display a lack of emotion, emotional lability, or mood swings. Another common symptom—apathy, or lack of motivation—may result directly from the syndrome or be secondary to depression. Higher mental functions Cognitive or mental symptoms can include confusion or impaired cognition, problems with attention, impaired judgment, and amnesia or other problems with memory, especially short-term memory. Problems with memory and attention are the longest-lasting cognitive symptoms; one in four people with PCS still suffer from memory problems a year after the injury. PCS may cause slowed information processing and reactions to stimuli or difficulty with abstract thinking or problem solving. People may also experience a decrease in abilities related to work performance or social interaction. While cognitive symptoms usually resolve within a few months of injury, physical and emotional symptoms can last longer. Most cognitive symptoms clear within half a year of the injury, and the longest-lasting ones, such as memory, attention and language problems, usually resolve within a year. The question of the cause or causes of PCS and PPCS has been heavily debated for many years. It is not known to exactly what degree the symptoms are due to organic factors, such as microscopic damage to the brain, and to other factors, such as psychological ones. The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned. It is possible that some post-concussion symptoms are due to physical causes while others are psychological. One hypothesis holds that physiological factors are responsible for early symptoms that occur after mild head trauma, whereas symptoms that occur later are due to psychological factors. While the cause of symptoms occurring shortly after head trauma is likely to be physiological, it is less clear whether PPCS has an organic basis, and nonorganic factors are likely to be involved in symptoms that last longer than three months. PPCS may be caused by physiological, psychological, or psychosocial factors, chronic pain, or an interaction of some or all of these. The majority of experts believe that PPCS results from a mix of factors, including preexisting psychological factors, and those directly relating to the physical injury. Studies using positron emission tomography have linked PCS to a reduction in glucose use by the brain, and changes in cerebral blood flow have been found to exist for as long as three years after a concussion in studies using single photon emission computed tomography (SPECT). At least one study with functional magnetic resonance imaging (fMRI) has shown differences in brain function during tasks involving memory after MTBI, and fMRI has shown changes in the brains of athletes within a week of a concussion. Not all people with PPCS have abnormalities on imaging, however, and abnormalities found in studies such as fMRI, PET, and SPECT could result from other comorbid conditions such as depression, chronic pain, and post-traumatic stress disorder (PTSD). Electroencephalograms, while usually normal in people with PCS, have occasionally been used to detect changes in brain function following mild head injury. Electrophysiological measures of brain function of people with PPCS show abnormal evoked potentials and event-related potentials compared to controls, supporting the hypothesis that PPCS has an organic basis. Proponents of the view that PCS has a physical or organic basis point to findings that people with post-concussive symptoms have deficits on standardized tests of cognitive function as an indication that brain dysfunction is a factor in PCS. Studies have shown that people with PPCS score lower than controls on neuropsychological tests that measure attention, verbal learning, reasoning, and information processing. But although decreased scores on cognitive tests point to brain dysfunction, they cannot diagnose brain damage. Recovery as measured by scores on cognitive tests frequently do not correlate with resolution of symptoms; people may still report subjective symptoms after their cognitive function has returned to normal. Another study found that although children with PPCS had poorer scores on tests of cognitive functioning after the injury, they also had poorer behavioral adjustment before the injury than children with no persistent symptoms; these findings support the idea that PCS may result from a combination of factors such as brain dysfunction resulting from head injury and preexisting psychological or social problems. Different symptoms may be predicted by different factors; for example, one study found that cognitive and physical symptoms were not predicted by the manner in which parents and family members coped with the injury and adjusted to its effects, but psychological and behavioral symptoms were. It has been convincingly shown that psychological factors play an important role in the presence of post-concussion symptoms. The development of PCS may be due to a combination of factors such as adjustment to effects of the injury, preexisting vulnerabilities, and brain dysfunction. Setbacks related to the injury, for example problems at work or with physical or social functioning, may act as stressors that interact with preexisting factors such as personality and mental conditions to cause and perpetuate PPCS. In one study, levels of daily stress were found to be correlated to PCS symptoms in both mildly brain injured subjects and controls, but in another, stress was not significantly related to symptoms. Iatrogenic effects (those caused by the medical intervention) may also occur, for example when people focus and dwell on the idea that their brains may be damaged, or when they are led to expect symptoms to occur. Expectation of symptoms may also lead head-injured people to focus on symptoms and therefore perceive them to be more intense, to attribute symptoms that occur for other reasons to the injury, and to underestimate the rate of symptoms before the injury. Symptom ICD-10 DSM-IV Headache - Problems tolerating - Affect changes, anxiety, or depression - Changes in The International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders have set out criteria for PCS and postconcussional disorder (PCD), respectively. The ICD-10 established a set of diagnostic criteria for PCS in 1992. In order to meet these criteria, a patient must have had a head injury with loss of consciousness and develop at least three of the eight symptoms marked with a check mark in the table at right under "ICD-10" within four weeks. About 38% of people who suffer a head injury with symptoms of concussion and no radiological evidence of brain lesions meet these criteria. In addition to these symptoms, people that meet the ICD-10 criteria for PCS may fear that they will have permanent brain damage, which may worsen the original symptoms. Preoccupation with the injury may be accompanied by the assumption of a "sick role" and hypochondriasis. The criteria focus on subjective symptoms and mention that neuropsychological evidence of significant impairment are not present. With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional. Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis. The DSM-IV lists criteria for diagnosis of PCD in people who suffered a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures. In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV". These symptoms must be present for three months after the injury and must have been absent or less severe before the injury. In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better. Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS. The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS. A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer. Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination. The HVLA tests verbal learning and memory by presenting a series of words and assigning points based on the number recalled, and digit span measures attention efficiency by asking the examinee to repeat back digits spoken by the tester in the same order as they are presented. In addition, neuropsychological tests may be performed to detect malingering. PCS, which shares symptoms with a variety of other conditions, is highly likely to be misdiagnosed in people with these conditions. Cognitive and affective symptoms that occur following a traumatic injury may be attributed to MTBI, but in fact be due to another factor such as post-traumatic stress disorder, which is easily misdiagnosed as PCS and vice versa. Affective disorders such as depression have some symptoms that can mimic those of PCS and lead to a wrongful diagnosis of the latter; these include problems with concentration, emotional lability, anxiety, and sleep problems. Depression, which is highly common in persistent PCS, can worsen other PCS symptoms, such as headaches and problems with concentration, memory, and sleep. PCS also shares symptoms with chronic fatigue syndrome, fibromyalgia, and exposure to certain toxins. Traumatic brain injury may cause damage to the hypothalamus or the pituitary gland, and deficiencies of pituitary hormones (hypopituitarism) can cause similar symptoms to post-concussion syndrome; in these cases, symptoms can be treated by replacing any hormone deficiencies. Post-concussion syndrome is usually not treated, though specific symptoms can be addressed; for example, people can take pain relievers for headaches and medicine to relieve depression, dizziness, or nausea. Rest is advised, but is only somewhat effective. Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively. Though no pharmacological treatments exist especially for PCS, if necessary doctors may prescribe medications used for symptoms that also occur in other conditions; for example, antidepressants are used for the depression that frequently follows MTBI. Side effects of medications may affect people suffering the consequences of MTBI more severely than they do others, and thus it is recommended that medications be avoided if possible; there may be a benefit to avoiding narcotic medications. In addition, headache medications may cause rebound headaches when they are discontinued. Psychological treatment, to which about 40% of PCS patients are referred for consultation, has been shown to reduce problems. Ongoing disabilities may be treated with therapy to improve function at work, or in social or other contexts. Therapy aims to aid in the gradual return to work and other preinjury activities, as symptoms permit. A protocol for PCS treatment has been designed based on the principles behind Cognitive behavioral therapy (CBT), a psychotherapy aimed at influencing disturbed emotions by improving thoughts and behaviors. CBT may help prevent persistence of iatrogenic symptoms – those that occur because health care providers create the expectation that they will. A risk exists that the "power of suggestion" may worsen symptoms and cause long-term disabilities; therefore, when counseling is indicated, the therapist must take a psychological origin of symptoms into account and not assume that all symptoms are a direct result of neurological damage from the injury. In situations such as motor vehicle accidents or following a violent attack, the post-concussion syndrome may be accompanied by post-traumatic stress disorder, which is important to recognize and treat in its own right. People with PTSD, depression, and anxiety can be treated with medication and psychotherapy. Education about symptoms and their usual time course is a part of psychological therapy, and is most effective when provided soon after the injury. Since stress exacerbates post-concussion symptoms, and vice versa, an important part of treatment is reassurance that PCS symptoms are normal, and education about how to deal with impairments. One study found that PCS patients who were coached to return to activities gradually, told what symptoms to expect, and trained how to manage them had a reduction in symptoms compared to a control group of uninjured people. Early education has been found to reduce symptoms in children as well. The prognosis for PCS is generally considered excellent, with total resolution of symptoms in the large majority of cases. For most people, post-concussion symptoms go away within a few days to several weeks after the original injury occurs. In others, symptoms may remain for three to six months, but evidence indicates that most cases are completely resolved within that time. Symptoms are largely gone in about half of people with concussion one month after the injury, and about two thirds of people with minor head trauma are symptom-free within three months. It is frequently stated in the literature and considered to be common knowledge that 10–20% of people with PCS have not recovered by a year after the injury, but this may be an overestimate because it is based on studies of people admitted to a hospital, the methodologies of which have been criticized. In a small minority of people, symptoms may persist for years or be permanent; however, it has not been conclusively shown that permanent neurological symptoms ever result from an uncomplicated concussion. If symptoms are not resolved by one year, they are likely to be permanent, though improvements may occur after even two or three years, or may suddenly occur after a long time without much improvement. Older people and those who have previously suffered another head injury are likely to take longer to recover. The way in which children cope with the injury after it occurs may have more of an impact than factors that existed prior to the injury. Children's mechanisms for dealing with their injuries may have an effect on the duration of symptoms, and parents who do not deal effectively with anxiety about children's post-injury functioning may be less able to help their children recover. If another blow to the head occurs after a concussion but before its symptoms have gone away, there is a very slight risk of developing the extremely rare but deadly second-impact syndrome (SIS). In SIS, the brain rapidly swells, greatly increasing intracranial pressure. People who have repeated mild head injuries over a prolonged period, such as boxers and Gridiron football players, are at risk for Chronic traumatic encephalopathy (or the related variant dementia pugilistica), a severe, chronic disorder involving a decline in mental and physical abilities. It is not known exactly how common PCS is. Estimates of the prevalence at 3 months post-injury are between 24 and 84%, a variation possibly caused by different populations or study methodologies. The estimated incidence of PPCS is around 10% of MTBI cases. Since PCS by definition only exists in people who have suffered a head injury, demographics and risk factors are similar to those for head injury; for example, young adults are at higher risk than others for receiving head injury, and, consequently, of developing PCS. The existence of PCS in children is controversial. It is possible that children's brains have enough plasticity that they are not affected by long-term consequences of concussion (though such consequences are known to result from moderate and severe head trauma). On the other hand, children's brains may be more vulnerable to the injury, since they are still developing and have fewer skills that can compensate for deficits. Clinical research has found higher rates of post-concussion symptoms in children with TBI than in those with injuries to other parts of the body, and that the symptoms are more common in anxious children. Symptoms in children are similar to those in adults, but children exhibit fewer of them. Evidence from clinical studies found that high school-aged athletes had slower recoveries from concussion as measured by neuropsychological tests than college-aged ones and adults. PCS is rare in young children. Factors that predict that a person will suffer PPCS (persistent PCS) include low socioeconomic status, previous MTBI, a serious associated injury, headaches, an ongoing court case, and female gender. Being older than 40 and being female are related to both PCS and PPCS. Women are more likely than men to suffer PCS, and likely to suffer it more severely. In addition, the development of PPCS may be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder or a medical or psychiatric illness. PCS is more prevalent in people who had psychiatric symptoms such as clinical depression or anxiety before the injury. Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; a Glasgow Coma Score of 13 or 14; post-traumatic amnesia lasting longer than an hour; and suffering another head trauma before recovering from the first. The risk is also increased in people who experience stress, have traumatic memories of the event, or expect to be disabled by the injury. The symptoms that occur after a concussion have been known for hundreds of years. The idea that this set of symptoms forms a distinct entity began to attain wide recognition in the latter part of the 19th century. John Erichsen, a surgeon from London, played an important role in developing the study of PCS. The controversy surrounding the cause of PCS was started in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma. He suggested that the condition was due to injury by "molecular disarrangement" to the spine, and the condition was originally called "railroad spine" because most of the injuries studied had happened to railroad workers. While some of his contemporaries agreed that the syndrome had an organic basis, others attributed the symptoms to psychological factors or to outright feigning. In 1879, the idea that a physical problem was responsible for the symptoms was challenged by Rigler, who suggested that the cause of the persisting symptoms was actually "compensation neurosis": the railroad's practice of compensating workers who had been injured was bringing about the complaints. Later, the idea that hysteria was responsible for the symptoms after a mild head injury was suggested by Charcot. Controversy about the syndrome continued through the 20th century. During World War I many soldiers suffered from puzzling symptoms after being close to a detonation but showing no evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured. The current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms by 1934. British authorities banned the term shell shock during World War II to avoid an epidemic of cases, and the term posttrauma concussion state was coined in 1939 to describe "disturbance of consciousness with no immediate or obvious pathologic change in the brain". The term postconcussion syndrome was in use by 1941. In 1961, H. Miller first used "accident neurosis" to refer to symptoms of PCS and asserted that the condition only ever occurs in situations where people stand to be compensated for the injury, but this contention was widely challenged. The real causes of the condition remain unclear. No definition of PCS is accepted by all health professionals, and doubt exists about the validity of the diagnosis. One reason for this is that symptoms of PCS also occur in people who have no history of head injury, but who have other medical and psychological complaints. In one study, 80% of healthy, uninjured people reported having three or more symptoms similar to those found after concussion. In another study, 64% of people with TBI met the criteria set out by the ICD-10 for post-concussion syndrome, but so did 40% of people that had injuries not to the head; 11% of those with brain injuries and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome (see diagnosis, below). Headaches is one of the criteria for PCS, but it is notably controversial where these headaches come from. Couch, Lipton, Stewart & Scher (2007) argue that headaches, one of the hallmarks of PCS, occur in a variety of injuries to the head and neck. Further, Lew et al. (2006) reviewed ample studies examining headaches with post-traumatic headaches and found that there is wide heterogeneity in the source and causes of headaches. They point out that the International Headache Society lists 14 known causes of headaches, as well. Further, the headaches may be better accounted for by medical causes, such as whiplash, which is often mistook for PCS. An additional possibility is that Post-traumatic Stress Disorder can better account for PCS, not just because of the headaches, but for emotional regulation as well. Having depression, post-traumatic stress disorder, or chronic pain virtually guarantees that a person will report symptoms resembling those of PCS. One study found that while people with chronic pain without TBI do report many symptoms similar to those of post-concussion syndrome, they report fewer symptoms related to memory, slowed thinking, and sensitivity to noise and light than people with MTBI do. Additionally, it has been found that neuroendocrinology may account for depressive symptoms and stress management due to irregularities in cortisol regulation, and thyroid hormone regulation. Lastly, there is evidence that major depression following TBI is quite common, but may be better accounted for with a diagnosis of dysexecutive syndrome In a syndrome, a set of symptoms is consistently present, and symptoms are linked such that the presence of one symptom suggests that of others. Because PCS symptoms are so varied and many can be associated with a large number of other conditions, doubt exists about whether the term "syndrome" is appropriate for the constellation of symptoms found after concussion. The fact that the persistence of one symptom is not necessarily linked to that of another has similarly led to doubt about whether "syndrome" is the appropriate term. A longstanding controversy surrounding PCS concerns the nature of its etiology – that is, the cause behind it – and the degree to which psychological factors and organic factors involving brain dysfunction are responsible. The debate has been referred to as 'psychogenesis versus physiogenesis' (psychogenesis referring to a psychological origin for the condition, physiogenesis to a physical one). - ^ a b c d Jones E, Fear NT, Wessely S (November 2007). "Shell shock and mild traumatic brain injury: A historical review". The American Journal of Psychiatry 164 (11): 1641–1645. doi:10.1176/appi.ajp.2007.07071180. PMID 17974926. http://ajp.psychiatryonline.org/cgi/content/full/164/11/1641. - ^ http://www.mayoclinic.com/health/post-concussion-syndrome/DS01020 - ^ a b Rao V, Lyketsos C (2000). "Neuropsychiatric sequelae of traumatic brain injury". Psychosomatics 41 (2): 95–103. doi:10.1176/appi.psy.41.2.95. PMID 10749946. - ^ a b c d Mittenberg W, Strauman S (2000). "Diagnosis of mild head injury and the postconcussion syndrome". Journal of Head Trauma Rehabilitation 15 (2): 783–791. doi:10.1097/00001199-200004000-00003. PMID 10739967. - ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac Hall RC, Hall RC, Chapman MJ (2005). "Definition, diagnosis, and forensic implications of postconcussional syndrome". Psychosomatics 46 (3): 195–202. doi:10.1176/appi.psy.46.3.195. PMID 15883140. http://psy.psychiatryonline.org/cgi/content/full/46/3/195. - ^ McHugh T, Laforce R, Gallagher P, Quinn S, Diggle P, Buchanan L (2006). "Natural history of the long-term cognitive, affective, and physical sequelae of mild traumatic brain injury". Brain and Cognition 60 (2): 209–11. PMID 16646125. - ^ a b c d e f g h Legome E. 2006. Postconcussive syndrome. eMedicine.com. Accessed January 1, 2007. - ^ a b c Schnadower D, Vazquez H, Lee J, Dayan P, Roskind CG (2007). "Controversies in the evaluation and management of minor blunt head trauma in children". Current Opinion in Pediatrics 19 (3): 258–264. doi:10.1097/MOP.0b013e3281084e85. PMID 17505183. - ^ a b c Evans RW (2004). "Post-traumatic headaches". Neurological Clinics 22 (1): 237–249. doi:10.1016/S0733-8619(03)00097-5. PMID 15062537. - ^ Bigler ED (2008). "Neuropsychology and clinical neuroscience of persistent post-concussive syndrome". Journal of the International Neuropsychological Society 14 (1): 1–22. doi:10.1017/S135561770808017X. PMID 18078527. - ^ Iverson GL, Lange RT (2003). "Examination of "postconcussion-like" symptoms in a healthy sample". Applied Neuropsychology 10 (3): 137–144. doi:10.1207/S15324826AN1003_02. PMID 12890639. - ^ King NS (1996). "Emotional, neuropsychological, and organic factors: Their use in the prediction of persisting postconcussion symptoms after moderate and mild head injuries". Journal of Neurology, Neurosurgery, and Psychiatry 61 (1): 75–81. doi:10.1136/jnnp.61.1.75. PMC 486463. PMID 8676166. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=486463. - ^ a b c d e f g h i j k l m Ryan LM, Warden DL (2003). "Post concussion syndrome". International Review of Psychiatry 15 (4): 310–316. doi:10.1080/09540260310001606692. PMID 15276952. - ^ a b c Kushner D (1998). "Mild traumatic brain injury: Toward understanding manifestations and treatment". Archives of Internal Medicine 158 (15): 1617–1624. doi:10.1001/archinte.158.15.1617. PMID 9701095. http://archinte.highwire.org/cgi/content/full/158/15/1617. - ^ a b Weight DG (1998). "Minor head trauma". Psychiatric Clinics of North America 21 (3): 609–624. doi:10.1016/S0193-953X(05)70026-5. PMID 9774799. - ^ a b c d e Anderson T, Heitger M, Macleod AD (2006). "Concussion and mild head injury (requires free registration)". Practical Neurology 6 (6): 342–357. doi:10.1136/jnnp.2006.106583. - ^ a b Barth JT, Ruff R, Espe-Pfeifer P (2006). "Mild traumatic brain injury: Definitions". In Nicholson, Keith; Young, Gerald; Andrew K. Kane. Psychological Knowledge in Court: PTSD, Pain and TBI. Berlin: Springer. pp. 271–277. ISBN 0-387-25609-1. - ^ a b c Cobb S and Battin B (2004). "Second-impact syndrome". The Journal of School Nursing 20 (5): 262–267. doi:10.1177/10598405040200050401. PMID 15469376. http://nasn.allenpress.com/nasnonline/?request=get-abstract&issn=1059-8405&volume=020&issue=05&page=0262. - ^ a b c d Margulies S (September 2000). "The postconcussion syndrome after mild head trauma: Is brain damage overdiagnosed? Part 1". Journal of Clinical Neuroscience 7 (5): 400–408. doi:10.1054/jocn.1999.0681. PMID 10942660. - ^ a b Jagoda A, Riggio S (2000). "Mild traumatic brain injury and the postconcussive syndrome". Emergency Medicine Clinics of North America 18 (2): 355–363. doi:10.1016/S0733-8627(05)70130-9. PMID 10798893. - ^ a b c King NS. 2003. Post-concussion syndrome: clarity amid the controversy?. Accessed January 1, 2007. - ^ a b Shaw NA (2002). "The neurophysiology of concussion". Progress in Neurobiology 67 (4): 281–344. doi:10.1016/S0301-0082(02)00018-7. PMID 12207973. - ^ a b c d e f g h i j k l m n Yeates KO, Taylor HG (2005). "Neurobehavioural outcomes of mild head injury in children and adolescents". Pediatric Rehabilitation 8 (1): 5–16. PMID 15799131. - ^ a b c d e Merck manuals online medical library. 2003. Concussion. Accessed May 11, 2008. - ^ a b c Evans RW (1992). "The postconcussion syndrome and the sequelae of mild head injury". Neurologic Clinics 10 (4): 815–47. PMID 1435659. - ^ a b c Olver J (2005). "Traumatic brain injury—the need for support and follow up". Australian Family Physician 34 (4): 269–71. PMID 15861750. - ^ a b c d Goodyear B, Umetsu D (2002). "Selected issues in forensic neuropsychology". In Van Dorsten B. Forensic Psychology: From Classroom to Courtroom. New York: Kluwer Academic/Plenum Publishers. pp. 289–290. ISBN 0-306-47270-8. http://books.google.com/?id=sjCztKijDq8C&pg=PA290&dq=%22Persistent+post+concussion+syndrome%22. Retrieved 2008-05-13. - ^ a b c d Jacobson RR (August 1995). "The post-concussional syndrome: physiogenesis, psychogenesis and malingering. An integrative model". Journal of Psychosomatic Research 39 (6): 675–693. doi:10.1016/0022-3999(95)00006-5. PMID 8568727. http://linkinghub.elsevier.com/retrieve/pii/0022-3999(95)00006-5. - ^ a b c d e f g h i Iverson GL (2005). "Outcome from mild traumatic brain injury". Current Opinion in Psychiatry 18 (3): 301–317. doi:10.1097/01.yco.0000165601.29047.ae. PMID 16639155. - ^ Jorge RE (2005). "Neuropsychiatric consequences of traumatic brain injury: A review of recent findings". Current Opinion in Psychiatry 18 (3): 289–299. doi:10.1097/01.yco.0000165600.90928.92. PMID 16639154. - ^ a b Bryant RA (2008). "Disentangling mild traumatic brain injury and stress reactions". New England Journal of Medicine 358 (5): 525–527. doi:10.1056/NEJMe078235. PMID 18234757. - ^ a b c d Lee LK (2007). "Controversies in the sequelae of pediatric mild traumatic brain injury". Pediatric Emergency Care 23 (8): 580–583. doi:10.1097/PEC.0b013e31813444ea. PMID 17726422. - ^ a b c Boake C, McCauley SR, Levin HS, Pedroza C, Contant CF, Song JX et al. (2005). "Diagnostic criteria for postconcussional syndrome after mild to moderate traumatic brain injury". Journal of Neuropsychiatry and Clinical Neurosciences 17 (3): 350–6. doi:10.1176/appi.neuropsych.17.3.350. PMID 16179657. http://neuro.psychiatryonline.org/cgi/content/full/17/3/350. - ^ Sivák Š, Kurča E, Jančovič D, Petriščák Š, Kučera P (2005). "An outline of the current concepts of mild brain injury with emphasis on the adult population" (PDF). Časopis Lėkařů Českých 144 (7): 445–450. http://www.clsjep.cz/odkazy/clc0507_445.pdf. - ^ a b Mittenberg W, Canyock EM, Condit D, Patton C (2001). "Treatment of post-concussion syndrome following mild head injury". Journal of Clinical and Experimental Neuropsychology 23 (6): 829–836. doi:10.1076/jcen.23.6.829.1022. PMID 11910547. - ^ Bazarian JJ, Atabaki S (August 2001). "Predicting postconcussion syndrome after minor traumatic brain injury". Academic Emergency Medicine 8 (8): 788–795. doi:10.1111/j.1553-2712.2001.tb00208.x. PMID 11483453. - ^ Hulshoff Pol HE, Hijman R, Baaré WF, van Eekelen S, van Ree JM (August 2000). "Odor discrimination and task duration in young and older adults". Chemical Senses 25 (4): 461–464. doi:10.1093/chemse/25.4.461. PMID 10944510. http://chemse.oxfordjournals.org/cgi/content/full/25/4/461. - ^ a b c Iverson GL, Zasler ND, Lange RT (2006). "Post-concussive disorder". In Zasler ND, Katz DI, Zafonte RD. Brain Injury Medicine: Principles and Practice. Demos Medical Publishing. pp. 374–385. ISBN 1-888799-93-5. http://books.google.com/?id=yplFkKimNcYC&pg=PA373&dq=%22post+concussion+syndrome%22+misdiagnose. Retrieved 2008-06-05. - ^ a b Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation 84 (12): 1885–1894. doi:10.1016/j.apmr.2003.03.001. PMID 14669199. - ^ Schapiro S, Mandel S, Sataloff RT (1993). Minor Head Trauma: Assessment, Management, and Rehabilitation. Berlin: Springer-Verlag. pp. 152. ISBN 0-387-97943-3. - ^ Willer B, Leddy JJ (September 2006). "Management of concussion and post-concussion syndrome". Current Treatment Options in Neurology 8 (5): 415–426. doi:10.1007/s11940-006-0031-9. PMID 16901381. http://www.treatment-options.com/1092-8480/8/415. [dead link] - ^ a b c d e f g McAllister TW, Arciniegas D (2002). "Evaluation and treatment of postconcussive symptoms". NeuroRehabilitation 17 (4): 265–83. PMID 12547976. - ^ a b Ropper AH, Gorson KC (2007). "Clinical practice. Concussion". New England Journal of Medicine 356 (2): 166–172. doi:10.1056/NEJMcp064645. PMID 17215534. http://content.nejm.org/cgi/content/full/356/2/166. - ^ a b Gualtieri CT (1999). "The pharmacologic treatment of mild brain injury". In Varney NR, Roberts RJ. The Evaluation and Treatment of Mild Traumatic Brain Injury. Hillsdale, N.J.: Lawrence Erlbaum Associates. pp. 411–412. ISBN 0-8058-2394-8. http://books.google.com/?id=i4Tpx6wHvJ4C&pg=PA21&vq=concussion. - ^ a b Alexander MP (1995). "Mild traumatic brain injury: Pathophysiology, natural history, and clinical management". Neurology 45 (7): 1253–60. PMID 7617178. - ^ McCrea 2008, p. 163–164 - ^ a b Komaroff A, Harvard University Harvard Business School (1999). The Harvard Medical School Family Health Guide. New York: Simon & Schuster. pp. 359. ISBN 0-684-84703-5. - ^ Necajauskaite O, Endziniene M, Jureniene K (2005). "The prevalence, course and clinical features of post-concussion syndrome in children". Medicina (Kaunas) 41 (6): 457–64. PMID 15998982. http://medicina.kmu.lt/0506/0506-01e.htm. - ^ a b Lovell MR, Fazio V (February 2008). "Concussion management in the child and adolescent athlete". Current Sports Medicine Reports 7 (1): 12–5. doi:10.1097/01.CSMR.0000308671.45558.e2 (inactive 2010-03-18). PMID 18296938. - ^ Traumatic Brain Injury: Hope Through Research. NINDS. Publication date February 2002. NIH Publication No. 02-2478. Prepared by: Office of Communications and Public Liaison, National Institute of Neurological Disorders and Stroke, National Institutes of Health - ^ a b c Benton AL (1989). "Historical notes on the postconcussion syndrome". Mild Head Injury. Oxford [Oxfordshire]: Oxford University Press. pp. 3–5. ISBN 0-19-505301-X. - ^ McCrea MA (2008). Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for Diagnosis and Treatment. Oxford [Oxfordshire]: Oxford University Press. pp. 157. ISBN 0-19-532829-9. http://books.google.com/?id=-WFl91VSWyEC&pg=PP1&dq=%22late+post+concussion+syndrome%22. Retrieved 2008-06-05. - ^ Couch, J. R., Lipton, R. B., Stewart, W. F., & Scher, A. I. (2007). Head or neck injury increases the risk of chronic daily headache. Neurology, 69(11), 1169. - ^ Lew, H. L., Lin, P. H., Fuh, J. L., Wang, S. J., Clark, D. J., & Walker, W. C. (2006). Characteristics and treatment of headache after traumatic brain injury: a focused review. American journal of physical medicine & rehabilitation, 85(7), 619. - ^ Kasch, H., Bach, F. W., & Jensen, T. S. (2001). Handicap after acute whiplash injury. Neurology, 56(12), 1637. - ^ Hickling, E. J., Blanchard, E. B., Silverman, D. J. and Schwarz, S. R. (1992), Motor Vehicle Accidents, Headaches and Post-Traumatic Stress Disorder: Assessment Findings in a Consecutive Series. Headache: The Journal of Head and Face Pain, 32: 147–151. doi: 10.1111/j.1526-4610.1992.hed3203147.x - ^ Jorge, R., & Robinson, R. G. (2003). Mood disorders following traumatic brain injury. International Review of Psychiatry, 15(4), 317-327. doi: doi:10.1080/09540260310001606700 - ^ McCrea MA (2008). Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for Diagnosis and Treatment. Oxford [Oxfordshire]: Oxford University Press. pp. 157. ISBN 0-19-532829-9. http://books.google.com/?id=-WFl91VSWyEC&pg=PP1&dq=%22late+post+concussion+syndrome%22. Retrieved 2008-06-05. - ^ Abreu, B. C., Zgaljardic, D., Borod, J. C., Seale, G., Temple, R. O., Ostir, G. V., & Ottenbacher, K. J. (2009). Emotional Regulation, Processing, and Recovery After Acquired Brain Injury. In K. Matuska, C. H. Christiansen, H. Polatajko & J. A. Davis (Eds.), Life Balance: Multidisciplinary Theories and Research (pp. 223-240). Thorofare, NJ: SLACK/AOTA press. - ^ Jorge, R. E., Robinson, R. G., Moser, D., Tateno, A., Crespo-Facorro, B., & Arndt, S. (2004). Major depression following traumatic brain injury. Archives of General Psychiatry, 61(1), 42. - ^ Smith DH (2006). "Postconcussional symptoms not a syndrome". Psychosomatics 47 (3): 271–272. doi:10.1176/appi.psy.47.3.271. PMID 16684949. http://psy.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=16684949. Mental and behavioral disorders (F 290–319) Neurological/symptomaticOther Psychoactive substances, substance abuse, drug abuse and substance-related disorders Schizophrenia, schizotypal and delusional Psychosis Schizophrenia Mood (affective) Neurotic, stress-related and somatoformOther Physiological/physical behavioralNonorganic - Postpartum depression - Postnatal psychosis Adult personality and behaviorOther Mental disorders diagnosed in childhood - X-Linked mental retardation - (Lujan-Fryns syndrome) Symptoms and uncategorized Neurotrauma (S06, Sx4, T09.3–4, 850–854, 950–957) Traumatic brain injuryIntracranial hemorrhage/hematoma: intra-axial (Intraparenchymal hemorrhage, Intraventricular hemorrhage) · extra-axial (Subdural hematoma, Epidural hematoma, Subarachnoid hemorrhage)Concussion: Post-concussion syndrome · Second-impact syndrome · Dementia pugilistica · Chronic traumatic encephalopathy Spinal cord injury PNS Wikimedia Foundation. 2010.	2	39	14	0	4	3	0.657205	21	10,307
Hydrocephalus Classification and external resources Hydrocephalus seen on a CT scan of the brain. ICD-10 G91, Q03 ICD-9 331.3, 331.4, 741.0, 742.3 DiseasesDB 6123 MedlinePlus 001571 eMedicine neuro/161 MeSH D006849 Hydrocephalus ( //), also known as "water in the brain," is a medical condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain. This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, tunnel vision, and mental disability. Hydrocephalus can also cause death. The name derives from the Greek words ὑδρο- (hudro-) "water", and κέφαλος (kephalos) "head". Signs and symptoms The clinical presentation of hydrocephalus varies with chronicity. Acute dilatation of the ventricular system is more likely to manifest with the nonspecific signs and symptoms of increased intracranial pressure. By contrast chronic dilatation (especially in the elderly population) may have a more insidious onset presenting, for instance, with Hakim's triad (Adams triad). Symptoms of increased intracranial pressure may include headaches, vomiting, nausea, papilledema, sleepiness or coma. Elevated intracranial pressure may result in uncal and/or cerebellar tonsill herniation, with resulting life threatening brain stem compression. Hakim's triad of gait instability, urinary incontinence and dementia is a relatively typical manifestation of the distinct entity normal pressure hydrocephalus (NPH). Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located). The symptoms depend on the cause of the blockage, the person's age, and how much brain tissue has been damaged by the swelling. In infants with hydrocephalus, CSF builds up in the central nervous system, causing the fontanelle (soft spot) to bulge and the head to be larger than expected. Early symptoms may also include: - Eyes that appear to gaze downward - Separated sutures Symptoms that may occur in older children can include: - Brief, shrill, high-pitched cry - Changes in personality, memory, or the ability to reason or think - Changes in facial appearance and eye spacing - Crossed eyes or uncontrolled eye movements - Difficulty feeding - Excessive sleepiness - Irritability, poor temper control - Loss of bladder control (urinary incontinence) - Loss of coordination and trouble walking - Muscle spasticity (spasm) - Slow growth (child 0–5 years) - Slow or restricted movement - Vomiting References to hydrocephalic skulls can be found in ancient Egyptian medical literature from 2500 BC to 500 AD. Hydrocephalus was described more clearly by the ancient Greek physician Hippocrates in the 4th century BC, while a more accurate description was later given by the Roman physician Galen in the 2nd century AD. The first clinical description of and operative procedure for hydrocephalus appears in the Al-Tasrif (1000 AD) by the Arab surgeon, Abu al-Qasim al-Zahrawi, who clearly described the evacuation of superficial intracranial fluid in hydrocephalic children. He described it in his chapter on neurosurgical disease, describing infantile hydrocephalus as being caused by mechanical compression. He states:“The skull of a newborn baby is often full of liquid, either because the matron has compressed it excessively or for other, unknown reasons. The volume of the skull then increases daily, so that the bones of the skull fail to close. In this case, we must open the middle of the skull in three places, make the liquid flow out, then close the wound and tighten the skull with a bandage.” It remained an intractable condition until the 20th century, when shunts and other neurosurgical treatment modalities were developed. It is a lesser-known medical condition; relatively small amounts of research are conducted to improve treatments for hydrocephalus, and to this day there remains no cure for the condition. Hydrocephalus is usually due to blockage of cerebrospinal fluid (CSF) outflow in the ventricles or in the subarachnoid space over the brain. In a person without hydrocephalus, CSF continuously circulates through the brain, its ventricles and the spinal cord and is continuously drained away into the circulatory system. Alternatively, the condition may result from an overproduction of the CSF fluid, from a congenital malformation blocking normal drainage of the fluid, or from complications of head injuries or infections. Compression of the brain by the accumulating fluid eventually may cause convulsions and mental retardation. These signs occur sooner in adults, whose skulls no longer are able to expand to accommodate the increasing fluid volume within. Fetuses, infants, and young children with hydrocephalus typically have an abnormally large head, excluding the face, because the pressure of the fluid causes the individual skull bones — which have yet to fuse — to bulge outward at their juncture points. Another medical sign, in infants, is a characteristic fixed downward gaze with whites of the eyes showing above the iris, as though the infant were trying to examine its own lower eyelids. The elevated intracranial pressure may cause compression of the brain, leading to brain damage and other complications. Conditions among affected individuals vary widely. If the foramina (pl.) of the fourth ventricle or the cerebral aqueduct are blocked, cereobrospinal fluid (CSF) can accumulate within the ventricles. This condition is called internal hydrocephalus and it results in increased CSF pressure. The production of CSF continues, even when the passages that normally allow it to exit the brain are blocked. Consequently, fluid builds inside the brain causing pressure that compresses the nervous tissue and dilates the ventricles. Compression of the nervous tissue usually results in irreversible brain damage. If the skull bones are not completely ossified when the hydrocephalus occurs, the pressure may also severely enlarge the head. The cerebral aqueduct may be blocked at the time of birth or may become blocked later in life because of a tumor growing in the brainstem. Internal hydrocephalus can be successfully treated by placing a drainage tube (shunt) between the brain ventricles and abdominal cavity to eliminate the high internal pressures. There is some risk of infection being introduced into the brain through these shunts, however, and the shunts must be replaced as the person grows. A subarachnoid hemorrhage may block the return of CSF to the circulation. If CSF accumulates in the subarachnoid space, the condition is called external hydrocephalus. In this condition, pressure is applied to the brain externally, compressing neural tissues and causing brain damage. Thus resulting in further damage of the brain tissue and leading to necrotization. Hydrocephalus can be caused by impaired cerebrospinal fluid (CSF) flow, reabsorption, or excessive CSF production. - The most common cause of hydrocephalus is CSF flow obstruction, hindering the free passage of cerebrospinal fluid through the ventricular system and subarachnoid space (e.g., stenosis of the cerebral aqueduct or obstruction of the interventricular foramina - foramina of Monro secondary to tumors, hemorrhages, infections or congenital malformations). - Hydrocephalus can also be caused by overproduction of cerebrospinal fluid (relative obstruction) (e.g., papilloma of choroid plexus). Based on its underlying mechanisms, hydrocephalus can be classified into communicating and non-communicating (obstructive). Both forms can be either congenital or acquired. Communicating hydrocephalus, also known as non-obstructive hydrocephalus, is caused by impaired cerebrospinal fluid resorption in the absence of any CSF-flow obstruction between the ventricles and subarachnoid space. It has been theorized that this is due to functional impairment of the arachnoidal granulations (also called arachnoid granulations or Pacchioni's granulations), which are located along the superior sagittal sinus and is the site of cerebrospinal fluid resorption back into the venous system. Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis and congenital absence of arachnoid villi. Scarring and fibrosis of the subarachnoid space following infectious, inflammatory, or hemorrhagic events can also prevent resorption of CSF, causing diffuse ventricular dilatation. - Normal pressure hydrocephalus (NPH) is a particular form of communicating hydrocephalus, characterized by enlarged cerebral ventricles, with only intermittently elevated cerebrospinal fluid pressure. The diagnosis of NPH can be established only with the help of continuous intraventricular pressure recordings (over 24 hours or even longer), since more often than not instant measurements yield normal pressure values. Dynamic compliance studies may be also helpful. Altered compliance (elasticity) of the ventricular walls, as well as increased viscosity of the cerebrospinal fluid, may play a role in the pathogenesis of normal pressure hydrocephalus. - Hydrocephalus ex vacuo also refers to an enlargement of cerebral ventricles and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in dementias), post-traumatic brain injuries and even in some psychiatric disorders, such as schizophrenia. As opposed to hydrocephalus, this is a compensatory enlargement of the CSF-spaces in response to brain parenchyma loss - it is not the result of increased CSF pressure. Non-communicating hydrocephalus, or obstructive hydrocephalus, is caused by a CSF-flow obstruction ultimately preventing CSF from flowing into the subarachnoid space (either due to external compression or intraventricular mass lesions). - Foramen of Monro obstruction may lead to dilation of one or, if large enough (e.g., in Colloid cyst), both lateral ventricles. - The aqueduct of Sylvius, normally narrow to begin with, may be obstructed by a number of genetically or acquired lesions (e.g., atresia, ependymitis, hemorrhage, tumor) and lead to dilation of both lateral ventricles as well as the third ventricle. - Fourth ventricle obstruction will lead to dilatation of the aqueduct as well as the lateral and third ventricles (e.g., Chiari malformation). - The foramina of Luschka and foramen of Magendie may be obstructed due to congenital failure of opening (e.g., Dandy-Walker malformation). The cranial bones fuse by the end of the third year of life. For head enlargement to occur, hydrocephalus must occur before then. The causes are usually genetic but can also be acquired and usually occur within the first few months of life, which include 1) intraventricular matrix hemorrhages in premature infants, 2) infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and stenosis, and 5) Dandy-Walker malformation. In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th percentile. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position. The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in his surroundings. Later on, the upper eyelids become retracted and the eyes are turned downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous. Papilledema is absent but there may be reduction of vision. The head becomes so enlarged that the child may eventually be bedridden. Because hydrocephalus can injure the brain, thought and behavior may be adversely affected. Learning disabilities including short-term memory loss are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However the severity of hydrocephalus can differ considerably between individuals and some are of average or above-average intelligence. Someone with hydrocephalus may have motion and visual problems, problems with coordination, or may be clumsy. They may reach puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy. Hydrocephalus treatment is surgical, generally creating various types of cerebral shunts. It involves the placement of a ventricular catheter (a tube made of silastic), into the cerebral ventricles to bypass the flow obstruction/malfunctioning arachnoidal granulations and drain the excess fluid into other body cavities, from where it can be resorbed. Most shunts drain the fluid into the peritoneal cavity (ventriculo-peritoneal shunt), but alternative sites include the right atrium (ventriculo-atrial shunt), pleural cavity (ventriculo-pleural shunt), and gallbladder. A shunt system can also be placed in the lumbar space of the spine and have the CSF redirected to the peritoneal cavity (Lumbar-peritoneal shunt). An alternative treatment for obstructive hydrocephalus in selected patients is the endoscopic third ventriculostomy (ETV), whereby a surgically created opening in the floor of the third ventricle allows the CSF to flow directly to the basal cisterns, thereby shortcutting any obstruction, as in aqueductal stenosis. This may or may not be appropriate based on individual anatomy. Examples of possible complications include shunt malfunction, shunt failure, and shunt infection, along with infection of the shunt tract following surgery (the most common reason for shunt failure is infection of the shunt tract). Although a shunt generally works well, it may stop working if it disconnects, becomes blocked (clogged), infected, or it is outgrown. If this happens the cerebrospinal fluid will begin to accumulate again and a number of physical symptoms will develop (headaches, nausea, vomiting, photophobia/light sensitivity), some extremely serious, like seizures. The shunt failure rate is also relatively high (of the 40,000 surgeries performed annually to treat hydrocephalus, only 30% are a patient's first surgery) and it is not uncommon for patients to have multiple shunt revisions within their lifetime. The diagnosis of cerebrospinal fluid buildup is complex and requires specialist expertise. Another complication can occur when CSF drains more rapidly than it is produced by the choroid plexus, causing symptoms -listlessness, severe headaches, irritability, light sensitivity, auditory hyperesthesia (sound sensitivity), nausea, vomiting, dizziness, vertigo, migraines, seizures, a change in personality, weakness in the arms or legs, strabismus, and double vision - to appear when the patient is vertical. If the patient lies down, the symptoms usually vanish in a short amount of time. A CT scan may or may not show any change in ventricle size, particularly if the patient has a history of slit-like ventricles. Difficulty in diagnosing overdrainage can make treatment of this complication particularly frustrating for patients and their families. Resistance to traditional analgesic pharmacological therapy may also be a sign of shunt overdrainage or failure. Diagnosis of the particular complication usually depends on when the symptoms appear - that is, whether symptoms occur when the patient is upright or in a prone position, with the head at roughly the same level as the feet. Shunts in developing countries Since the cost of shunt systems is beyond the reach of common people in developing countries, most people with hydrocephalus die without even getting a shunt. Worse is the rate of revision in shunt systems that adds to the cost of shunting many times. Looking at this point, a study done by Dr. Benjamin C. Warf compares different shunt systems and highlighting the role of low cost shunt systems in most of the developing countries. This study has been published in Journal of Neurosurgery: Pediatrics May 2005 issue. It is about comparing Chhabra shunt system to those of the shunt systems from developed countries. The study was done in Uganda and the shunts were donated by the International Federation for Spina Bifida and Hydrocephalus. One interesting case involving a person with past hydrocephalus was a 44-year old French man, whose brain had been reduced to little more than a thin sheet of actual brain tissue, due to the buildup of cerebrospinal fluid in his head. The man, who had had a shunt inserted into his head to drain away fluid (which was removed when he was 14), went to a hospital after he had been experiencing mild weakness in his left leg. In July 2007, Fox News quoted Dr. Lionel Feuillet of Hôpital de la Timone in Marseille as saying: "The images were most unusual... the brain was virtually absent." When doctors learned of the man's medical history, they performed a computed tomography (CT) scan and magnetic resonance imaging (MRI) scan, and were astonished to see "massive enlargement" of the lateral ventricles in the skull. Intelligence tests showed the man had an IQ of 75, below the average score of 100. This would be considered "borderline intellectual functioning"- which is just next to the level of being officially considered mentally challenged. Remarkably, the man was a married father of two children, and worked as a civil servant, leading an at least superficially normal life, despite having enlarged ventricles with a decreased volume of brain tissue. "What I find amazing to this day is how the brain can deal with something which you think should not be compatible with life," commented Dr. Max Muenke, a pediatric brain defect specialist at the National Human Genome Research Institute. "If something happens very slowly over quite some time, maybe over decades, the different parts of the brain take up functions that would normally be done by the part that is pushed to the side." Famous people with hydrocephalus According to Maureen Waller, author of Ungrateful Daughters (2002), the son of Queen Anne of Britain, Prince William, Duke of Gloucester (1689-1700) is believed to have had hydrocephalus, both due to the size of his head and to autopsy reports following his death at age 11 from a fever. He was believed by his contemporaries to have above average intelligence; however, he did not speak properly until the age of three and had difficulty balancing and climbing stairs throughout his short life. Fictional serial killer Jason Voorhees is afflicted with this condition, and is ridiculed by the campers of Crystal Lake because of this. Emperor Ferdinand I of Austria is suspected to have had hydrocephalus, on account of the shape of his head and apparent mild mental handicap. Also 4-year-old Filippo de' Medici died of hydrocephalus. Son of the ex-Yugoslav footballer and Real Madrid sports director Predrag Mijatović, Andreja died at the age of 14 after a long battle with Hydrocephalus. September has been designated as U.S National Hydrocephalus Awareness Month. Hydrocephalus is represented by a two tone blue ribbon, often used with a crystal water droplet to represent CSF (cerebralspinal fluid) - Spina bifida - Acquired hydrocephalus (causes of it) - Arachnoid granulation - Cerebrospinal fluid - Intracranial pressure - Normal pressure hydrocephalus - Cerebral shunt - Subarachnoid space - Ventricular system - HEC syndrome - ^ http://www.nlm.nih.gov/medlineplus/ency/article/001571.htm Accessed 19 June 2010 - ^ a b c d Alfred Aschoff, Paul Kremer, Bahram Hashemi, Stefan Kunze (October 1999). "The scientific history of hydrocephalus and its treatment". Neurosurgical Review (Springer) 22 (2–3): 67–93 . doi:10.1007/s101430050035. ISSN 1437-2320 - ^ "Hydrocephalus Fact Sheet", National Institute of Neurological Disorders and Stroke. (August 2005). - ^ Cabot, Richard C. (1919) Physical diagnosis , William Wood and company, New York, 7th edition, 527 pages, page 5. (Google Books) - ^ Yadav YR, Mukerji G, Shenoy R, Basoor A, Jain G, Nelson A (2007). "Endoscopic management of hypertensive intraventricular haemorrhage with obstructive hydrocephalus". BMC Neurol 7: 1. doi:10.1186/1471-2377-7-1. PMC 1780056. PMID 17204141. http://www.biomedcentral.com/1471-2377/7/1. - ^ wwww.spinabifidamoms.com - ^ http://www.hydroassoc.org/media/stats - ^ Warf, Benjamin C. (2005). "Comparison of 1-year outcomes for the Chhabra and Codman-Hakim Micro Precision shunt systems in Uganda: a prospective study in 195 children". J Neurosurg (Pediatrics 4) 102 (4 Suppl): 358–362. doi:10.3171/ped.2005.102.4.0358. PMID 15926385. http://thejns.org. http://thejns.org/doi/pdf/10.3171/ped.2005.102.4.0358 - ^ "Man with Almost No Brain Has Led Normal Life", Fox News (2007-07-25). Also see "Man with tiny brain shocks doctors", NewScientist.com (2007-07-20); "Tiny Brain, Normal Life", ScienceDaily (2007-07-24). - ^ Man Lives Normal Life Despite Having Abnormal Brain - ^ Brain of a white-collar worker. Feuillet, L., Dufour, H. & Pelletier, J., et al. The Lancet, Volume 370, Issue 9583, Page 262, 21 July 2007 pmid=17658396 - ^ http://www.startribune.com/entertainment/books/11435616.html - A site dedicated to helping parents and families of children with congenital hydrocephalus. In addition to the usual medical definitions of what hydrocephalus is, it focuses on how to take care of these children at home. It provides information on many aspects of hydrocephalus, including personal stories. - International Federation for Spina Bifida and Hydrocephalus (IF), the umbrella organisation for national spina bifida and hydrocephalus organisations - Hydrocephalus Association at hydroassoc.org, US - Hydrocephalus Clinical Research Network (HCRN) a multi-center clinical research network collaboration of several leading pediatric neurosurgeons in North America. - Team Hydro a group affiliated with the Hydrocephalus Association in US, swims from Alcatraz to San Francisco every year to raise awareness and fund research for a cure - Fetal Hydrocephalus Information about diagnosis and treatment for fetal hydrocephalus from the Center for Fetal Diagnosis and Treatment at The Children's Hospital of Philadelphia - Hydrocephalus Support Association Australian Support Group. Pathology of the nervous system, primarily CNS (G04–G47, 323–349) InflammationBoth/either Brain/ encephalopathyBasal ganglia disease: Parkinsonism (PD, Postencephalitic, NMS) · PKAN · Tauopathy (PSP) · Striatonigral degeneration · Hemiballismus · HD · OADyskinesia: Dystonia (Status dystonicus, Spasmodic torticollis, Meige's, Blepharospasm) · Chorea (Choreoathetosis) · Myoclonus (Myoclonic epilepsy) · AkathesiaEpisodic/ Both/either Congenital malformations and deformations of nervous system (Q00–Q07, 740–742) BrainOther Spinal cordOther Wikimedia Foundation. 2010.	2	14	0	0	0	3	0.885525	3	5,371
Parathyroid adenoma - benign formation of glandular epithelium, which occurs in the endocrine system. The main severity of the disease lies in the volumetric process. The tumor, increasing in size, begins to put pressure on nearby tissues, which causes deformation and a disturbance in the blood supply to these tissues. Causes of parathyroid adenoma The main reasons that lead to neoplasms: - Gene heredity. - Severe injuries to the neck or head. - Increased radioactive exposure. A benign neoplasm is a yellow or light brown tumor. It has a soft texture, the borders of the tumor are clear, easily palpable. In the early stages, the symptoms of thyroid adenoma may be absent. As a rule, the disease affects one lower gland pair, rarely there is a bilateral lesion. Adenoma is, first of all, a benign formation, which can be of the following types: - From light cell type (watery). - From the main dark cells. - From cells of acidophilic origin. As a rule, cancer develops only in 3% of cases. Parathyroid adenoma has a different weight, it varies from 30 to 100 grams. The main cause of neoplasia is the manifestation of hyperparathyroidism. The disease may be accompanied by constant strong thirst, excessive urination, a depressive state, loss of memory, and occasional cramps. Given the increased level of calcium in the blood, the patient may experience severe itching of the skin, as well as dryness. The diagnosis of the disease is set on the basis of a laboratory examination. How is the disease manifested The main symptoms of parathyroid adenoma are, above all, persistent ailments, which are accompanied by unreasonable vomiting and nausea, sudden weight loss, muscle weakness and pain in the joints. It should also be remembered that if excess calcium is deposited in the heart muscle, such changes lead to a heart attack. In order to prevent irreversible reactions, doctors prescribe surgical intervention. Parathyroid adenoma is variable type. Conditionally distinguish the following types: - Bone clinical manifestation. This lesion is accompanied by pathological fractures (tubular bones and cervical vertebrae), the condition of the teeth deteriorates sharply, they become loose and fall out. - The renal form of the disease occurs according to the type of urolithiasis. - LCD form manifests as acute cholecystitis / pancreatitis or peptic ulcer. In order to receive effective treatment of parathyroid adenoma, first of all you should visit a medical institution, get expert advice from doctors: After the consultation, a full examination should be performed. The main methods of laboratory examination: - A detailed blood test in which calcium and phosphorus levels should be noted. - Similar urine analysis. Treatment is prescribed by an endocrinologist and a surgeon. An effective and efficient method is surgery. But at the preoperative stage, an obligatory universal, conservative therapeutic course of treatment is carried out. The main focus of this treatment is the fight against hypercalcemia. With conservative treatment, intravenous infusions are mandatory: - Isotonic solution. - Detoxification method (forced diuresis). This makes it possible through the urine to remove the collected toxins by an accelerated method. It should be remembered that the daily dose of thiazide diuretics in the treatment of parathyroid adenoma for adults should not exceed more than 50 mg. For children - no more than 2 mg. This drug is strictly contraindicated in Addison's disease, diabetes and various allergic reactions. In hypercalcemic crisis, the following therapeutic agents are administered: - Cardiac glycosides. In this case, a special diet is appointed with a minimum amount of foods, which includes calcium. This food helps to properly balance blood levels of calcium. After the preliminary preoperative period, removal of the adenoma is performed. - Open access. - Endoscopic method. The full scope of the operation will depend entirely on the parameters of the tumor. In the event that numerous neoplasms are detected, medical specialists advise to conduct a subtotal resection. In this case, conduct a radical intervention, which is divided into several groups: - Complete removal of the gland (thyroidectomy). - Resection of a single lobe (hemithyroidectomy). - Subtotal resection. Medical specialists decide for themselves which group the pathology belongs to and what type of radical intervention to choose. The prognosis of life after surgery is positive. But we should not forget about the constant monitoring and monitoring of calcium. As a rule, the removal of adenoma normalizes its level within a couple of days, therefore the rehabilitation period is short. In the event that the bone system was affected, vitamins of the “D” group, therapeutic massage must be prescribed. In the postoperative period, mandatory follow-up with an endocrinologist is required. In the early stages of the adenoma of the parathyroid gland, folk remedies can be used, but first of all it is the strictest diet, rejection of all bad habits, abundant use of diuretic teas and natural herbal preparations. This treatment should be approached very carefully and should be carried out only under the supervision of medical professionals. Folk recipes in the treatment of adenoma There are several of the most effective folk recipes that should be used in the treatment of: - Chopped herb cycuta (one tablespoon) is poured into a dark half-liter glass container and filled with vodka. Insist for at least two weeks in a dark place. Content is periodically shaken. Then, when the tincture is ready, wipe the gland area several times a day with a swab moistened, preferably at one time. - The root of the green sorrel (300 grams), pour water and boil over low heat for three hours. Broth drink half a glass three times a day. - Thirty grams of unrefined oats, along with the husks, are thoroughly washed under running water, and then boiled for an hour in a liter of water. After the broth has cooled, add a liter of homemade milk and allow to boil. Insist at least twelve hours, after which it is filtered and consumed throughout the day in any amount. In a complex with this broth apply half a table spoon of alcohol tincture on walnut partitions. - During the flowering of chestnuts, collect flowers and fill a half-three-liter jar, after which there add lilac flowers and pour vodka or moonshine. Insist for ten days in a dark place. When the tincture is ready, moisten a clean napkin and apply to the area of the thyroid gland. The course of these procedures week, after which a break of seven days. - Equal quantities (250 grams) are mixed with buckwheat flour, natural honey and nuts. Take this mixture once a week throughout the day. Store the finished composition in a cool place in a glass or natural ceramic dish. Folk remedies are desirable to use in the initial stages of the disease and in the postoperative period. Do not forget that in the early stages of the disease the disease can occur without symptoms, therefore, at the first manifestations of rapid pulse, causeless drowsiness and fatigue, you should visit medical specialists. Since the adenoma in the later stages proceeds with complications. To prevent disease, make sure that your diet is properly balanced. Add to the diet as much as possible dairy products (limit home-made milk and cheeses), vegetables (baked, raw), fish (preferably fat). In addition, you can prevent the manifestation of adenoma with the help of forest chanterelle mushrooms, they include ergocalciferol. Cultured culture will not have the desired effect. In the event that you observe certain symptoms, although with parathyroid adenoma, it is not always possible to observe the same symptoms in all patients, but still you should not be afraid to go to the doctor or make a diagnosis or refute it. At the moment, the disease is cured simply, and the injury to the body is almost minimized. Most importantly, do not self-medicate. If, according to the results of the examination, the doctor is confident that the disease corresponds to parathyroid adenoma, then only he can prescribe the correct treatment. Causes of neoplasm There are suggestions that the parathyroid adenoma is due to: - Changes in the structure of the protein molecule. Cells begin to randomly divide, against the background of this increase parathyroid cells, which leads to the appearance of pathology. Several genes responsible for the functioning of the thyroid gland may mutate. - Lack of calcium in the body - this can provoke uncontrolled cell division and later lead to the appearance of pathology. In any of these cases, the gene encoding the proteins suffers. It should be noted that changes can occur after irradiation of the neck or head, or injury. Benign parathyroid adenoma, is: - Main light cells. - Dark cells. - Acidophilic cells. Cancer adenoma is rare and can occur in only two percent of all cases. Adenoma of the parathyroid paired gland looks like a soft, yellowish-brown node, with clear boundaries. Cysts are often found in such a tumor. Almost always one of the lower pair of glands suffers from it, but still in rare cases, they diagnose a lesion of two or more. This disease is always diagnosed in different ways to confirm or deny the diagnosis. Symptoms of the disease Parathyroid adenoma has various symptoms. Its signs can manifest themselves in different organs and body systems. For example: in the kidney, bone, heart, stomach and intestines. So, the signs of the disease can be called: - Great sweating. - Constant desire to sleep. - Quick fatigue. - Visual enlargement of the thyroid gland (this symptom appears after a while). Common symptoms of this disease include: - Poor general condition of the body. - Bad appetite. - Sharp weight loss. - Bone pains - Muscle weakness In addition, the patient has memory impairment, persistent depression, seizures. In many patients, the bone form of the disease begins. Bones are affected, so osteoporosis appears, teeth begin to fall out and bones break. In renal form, kidney stones, diffuse nephrocalcinosis appear. With a disease of the stomach or intestines, an ulcer, pancreatitis, vomiting develops. When the heart form of the disease, manifested hypertension. A large amount of calcium in adenoma affects the joints of the limbs, the cornea of the eye, and causes itching and dryness. A lot of calcium in the heart provokes myocardial infarction, and in the kidneys - acute failure. How is the examination - At the doctor's office, the doctor asks the patient about the symptoms of the disease and makes a history. - A visual inspection and palpation of the lesion site (neck). - The study of the patient's outpatient card in order to present a picture of the diseases he had suffered. - The analysis collected daily urine to understand how much calcium is excreted by the body per day. - Blood test. - Ultrasound examination of the abdominal cavity, to identify various pathologies. - Intravenous administration of a contrast agent that will help to distinguish adenoma from other pathologies. - X-rays of the head, arms and legs to determine how much bone is affected. - Examination for the presence of erosive and ulcerative pathologies. - Conduct an ECG (if the work of the heart is impaired). - Using a thin needle, a biopsy is performed, and then a histological examination of the material taken. Thus, the diagnosis is confirmed or refuted, and the form of the disease is determined. Treatment of parathyroid adenoma, carried out mainly with the help of surgical intervention. But before that it is necessary to carry out drug treatment, which will help reduce the level of calcium. Also, the patient is prescribed a special diet that does not contain foods with calcium. After the patient has undergone the entire course of drug therapy, removal of the pathology is performed. This may be an open surgery, a mini-intervention or excision using endoscopy. During removal, it is necessary to carefully examine all the glands. After removal, you should conduct regular monitoring of the human condition. Check the blood for the amount of calcium in it, monitor the work of the heart, voice and nerves of the age. Diagnosed with multiple parathyroid adenoma, its treatment is carried out only with the help of total removal. How do the surgery When conducting surgical removal of the pathology, it is necessary to pay attention to chronic diseases, that is, no matter how they behave. Therefore, a full examination of the patient is prescribed, before the operation. Excision is performed under general anesthesia, the duration of the procedure will depend on the area of damage. The operation can last from one hour to six. After the removal, it is necessary to remember the effects of anesthesia, because it has a negative effect on the nervous system. Some patients may experience constant irritation, insomnia, and headaches. Such a state may accompany a person for six months. Should be more attentive to their health, people who have been diagnosed with varicose veins. In this case, complications may occur in the early postoperative period. Removal can be done in several ways: - Complete removal of the thyroid gland. - Removal of one lobe of the gland. - Remove only the affected area. - Excision of the isthmus. In each case, the method of removal is selected individually. Consequences after surgery The operation on excision of the parathyroid gland is considered a complex process. After it, some complications arise: - The appearance of scars. - Difficulty speaking and breathing. Thanks to modern equipment, which is used during operations, the risk of complications is practically reduced to zero. This mainly refers to the laryngeal nerve, which may subsequently affect the change in voice. Also reduce the risk of complications may preoperative drug therapy. After an adenoma has been removed, the person will have to take drugs that contain calcium. They will help prevent hypocalcemia. After excision of the pathology, a person should regularly undergo an ECG and donate blood to determine the amount of calcium. Calcium normalization after excision occurs in two days. The doctor prescribes gymnastic procedures, foot and spine massage. If the operation was performed on a woman who is in menopause, she is recommended to take estrogens. If the disease has affected the internal organs, then the prognosis, unfortunately, is sad. This unpleasant disease can be avoided if you follow the rules of prevention. The main thing is to review your diet. You should reduce the level of "arriving" phosphorus and increase the amount of calcium. Products also help in the prevention of the disease, for example, should be used: milk, vegetables and fruits in any form (fresh, baked, stewed). In addition, the diet should contain fatty fish, any seafood, seaweed, wild mushrooms. From the daily menu it is necessary to remove the butter and fatty cheeses. If you have certain symptoms, do not be afraid to go to the clinic. Today's medicine has at its disposal modern equipment, so the treatment of the disease will be relatively simple. The body during the treatment will be injured minimally. The main thing is that the appeal to a specialist was in time, and not in the neglected state of the disease. Because initially it is possible to remove only part of the organ, and if you miss the moment, then almost the entire thyroid gland will excise. Therefore, we advise you to treat your health more carefully, because a healthy body, foreshadows a full life. Parathyroid adenoma, as a rule, is unilateral. In appearance, the tumor resembles a nodular neoplasm. Pathology is accompanied by excessively active production of parathyroid hormone, which leads to disorders of the processes of calcium and phosphorus metabolism. note: According to statistics, the representatives of the fair sex are most susceptible to parathyroid adenoma, in the age group up to 40 years. In most cases, the nature of this tumor neoplasm is benign. Cases of malignant transformation are not more than 2%. What arises from? The exact causes of the development of parathyroid adenoma today have not been established. According to experts, calcium deficiency can cause this pathology, causing intense division and mutation of thyroid cells, as well as changes in protein cells. The following factors can lead to the appearance of parathyroid adenoma: - traumatic injuries - radiation exposure - hormonal disorders, - thyroid dysfunction, - adverse environmental factor. - genetic predisposition - cell mutations. Important! Radiation therapy for malignant neoplasms, localized in the head or neck, significantly increases the likelihood of the formation of parathyroid adenoma! How is pathology manifested? Symptomatology of the disease begins to appear more clearly with increasing size of the tumor. In the early stages of its development, the pathological process, as a rule, is almost asymptomatic. In general, the following clinical signs and manifestations are characteristic of parathyroid adenoma: - excessive sweating - daytime sleepiness, - increased heart rate (tachycardia) - increased fatigue - an increase in the size of the thyroid gland, - increased moisture of the skin, - increased anxiety - joint pain - the appearance of a specific hoarseness in the voice, - mental disorders. Important! In most cases, this pathology is accompanied by hyperparathyroidism, therefore, as a rule, the symptoms typical for this disease are observed in patients. Often in patients with parathyroid adenoma is noted: - permanent lack of appetite, - general weakness - nausea and bouts of vomiting. It is also possible memory disorders, symptoms of convulsive syndrome and emotional instability! Disorders of calcium and phosphorus metabolism lead to the damaging effects of bone tissue. Therefore, in the later stages of the pathological process, patients begin to break down the teeth, an increased tendency to fractures appears, and osteoporosis develops. What is the danger? Parathyroid adenoma, as it develops, has an extremely negative effect on the patient’s entire body, significantly reducing his quality of life. The fact is that with this pathology, the concentration of calcium in the patient's blood increases significantly, which is one of the causes of strokes, heart attacks, and cancer. Important! Although the parathyroid adenoma itself is not considered a deadly disease, this pathology often leads to the death of the patient, due to the development of associated complications! The most common typical complication of parathyroid adenoma is hypercalcemia, leading to the development of the following dangerous pathologies: In the absence of adequate, timely medical events, the likelihood of a hypercalcemic crisis increases. This pathological condition is dangerous not only for health, but also for the life of the patient and is accompanied by the following clinical manifestations: - impaired consciousness - bouts of profuse vomiting, - violations of the cardiovascular system, - internal, intestinal and gastric bleeding. Important!If a hypercalcemic crisis does not provide the patient with emergency medical care, the most likely outcome is a lethal one! In addition, parathyroid adenoma negatively affects the nervous system of the patient, causing the development of severe, prolonged depressive states. The gastrointestinal form of this disease repeatedly increases the risks of the following disorders in the digestive system: Thus, parathyroid adenoma can safely be considered one of the most dangerous ailments, requiring extremely careful attention. Therefore, when the first clinical signs characteristic of this pathology appear, it is necessary, without delay, to turn for help to endocrinologist, undergo a comprehensive diagnosis and an adequate treatment course! In the diagnosis of parathyroid adenoma, in addition to examining the patient, studying the clinical picture and the results obtained during the history taking, the following types of research procedures are prescribed to patients: Important! Physicians include computed or magnetic resonance imaging as the most accurate and informative methods for diagnosing parathyroid gland adenoma. After such a comprehensive diagnosis, a specialist can make an accurate diagnosis, determine the stage of the pathological process and develop an optimal treatment strategy for the patient. Drug treatment of parathyroid adenoma If the disease is not in the advanced stage, doctors in the fight against parathyroid adenoma prefer the methods of conservative therapy. Note:The main goal of the treatment course is to reduce the calcium concentration and eliminate the characteristic symptoms! To normalize the general condition, the patient is prescribed droppers with infusion of the following drugs: - isotonic solutions - forced diuresis, - glucose solution. In case of damage to internal organs and disorders in the work of various body systems, according to the individual scheme, the patient is prescribed the necessary symptomatic treatment. It is mandatory dieting, according to which, the daily diet of a patient with a diagnosed parathyroid adenoma should be absent food containing phosphorus. The basis of the menu consists of low-fat varieties of meat and fish, greens, fruits, fresh vegetables. The following products will also be beneficial for the patient: Important!Conducting drug treatment and diet therapy are an indispensable element in preparing a patient with parathyroid adenoma for surgery! Surgery for parathyroid adenoma Removal of parathyroid adenoma today is the most effective way to combat this pathology. It allows to achieve stable positive results, even in the most severe, neglected clinical cases. Important! Temporary contraindications for operations in the parathyroid glands are infectious processes, a period of exacerbation of diseases occurring in a chronic form. Depending on the complexity of the clinical case and the individual characteristics of a particular patient, specialists in the fight against parathyroid adenoma use one of the following types of surgery: - Thyroidectomy surgeryaimed at the complete removal of the thyroid gland. - Subtotal intervention - surgical removal of a small area of the affected thyroid gland. - Isthmus removal. - Hemithyroidectomy - an operation aimed at removing one lobe of the thyroid gland. Surgical intervention in the region of the parathyroid glands is performed under the action of general anesthesia. The average duration of the operation is about 3 hours. The recovery period, namely, its duration, depends largely on the type of surgical intervention. After parathyroid gland operations, the patient should be under the supervision of a specialist, since there are risks of developing the following complications: - cicatricial formations - infectious processes - speech and respiratory disorders. Modern equipment and careful preparation of the patient for surgical procedures can significantly reduce and minimize the risks of the above postoperative complications! As a rule, the patient returns to his usual lifestyle a few months after the operation. Note:after surgery for parathyroid adenoma, patients need to take calcium supplements and special vitamin-mineral complexes in order to prevent the development of hypocalcemia! For maximum accelerated recovery, patients are recommended massages, physical therapy classes, taking drugs with a high content of vitamin D. The medical prognosis after surgery for parathyroid adenoma is quite favorable. According to statistics, the cases of possible relapses do not exceed 20%! The main prevention of the development of parathyroid adenoma, as well as the possible recurrence of this disease, is a properly balanced, rational diet. According to the recommendations of experts, the following calcium products should form the basis of the daily diet: - dairy products, - a fish, - forest varieties of mushrooms, - fresh and steamed vegetables. But the use of butter, cheese, fatty meats should, on the contrary, be limited to the maximum! In addition, doctors advise patients to adhere to the following rules: - Take vitamin and mineral complexes. - Avoid psycho-emotional shocks. - Regularly undergo preventive medical examinations, be tested for calcium. - Timely treat hormonal disorders, endocrine disorders and diseases of the thyroid gland. Parathyroid adenoma can cause serious malfunctions of the internal organs and body systems, and even cause the patient to die early. However, competent and timely therapy, adherence to medical recommendations regarding the diet, will help to achieve positive results and avoid unwanted complications! Chumachenko Olga, medical reviewer 5,149 total views, 5 views today Small parathyroid glands, which are located on the back of the thyroid, usually consist of 4 pieces. Their increase is accompanied by an excess of hormones of the gland and, as a result, by leaching of calcium from the bones of the skeleton. If this formation is larger than the norm, then doctors check it for malignancy. Parathyroid hormone synthesis occurs in these space formations, which is opposite to calcitonin in its action. In a joint action, with the involvement of the work of vitamin D, these hormones are responsible for controlling the metabolism of calcium and phosphorus in the body. They are responsible for the following processes: - bone mass formation, - kidney work - bowel work, - muscle work - work of the cardiovascular system. With a violation of the production of a single hormone or vitamin D deficiency, irreversible consequences in the body's work begin. The most unpleasant disease arising from parathyroidal adenoma is hyperparathyroidism. Types of parathyroid adenoma According to the results of histology, one of the following forms of a parathyroid gland tumor can be detected in a patient: - benign epithelioma of the gland, - watery cell adenoma, - dark cell neoplasm - acidophilic cell adenoma, If a particularly large formation occurs, the development of carcinoma is likely. The number of cancers accounts for up to 3% of all diagnoses of this pathology. Causes of parathyroid adenoma The main factors provoking the formation of adenomas on the parathyroid parenchyma may be the following reasons: - Changes in the work of genes responsible for parathyroid cell division. - Trauma of the cervical spine, osteochondrosis. - Radiation therapy, in the region of which the neck falls. - Constant neglect of foods containing calcium. Dairy products should always be in the diet of each person to prevent cases of hyperparathyroidism. In some cases, sesame and chanterelle mushrooms can be included in the diet, which are rich in essential trace elements. Carrying out diagnostic measures to identify the parathyroid disease leads to the need for consultation with specialists in the following areas of medicine: The main method of diagnosis of an increase in the parathyroid gland is screening blood and urine for the following abnormalities: - Elevated PTH in serum. - Elevated levels of calcium in the blood and when taking the daily norm of urine. - Reduction of phosphorus in the blood. - Lowering the level of vitamin D in the main body fluids. For visual confirmation of the presence of a thyroid tumor, the following instrumental diagnostic methods are used: - x-ray skeleton - Magnetic resonance imaging, - urogenital urography, - ECG and EGDS. With the help of these diagnostic methods, you can establish the exact nature of the damage to PShZH and build an effective treatment scheme. In this case, an ultrasound of the parathyroid glands is carried out jointly with an ultrasound of the thyroid gland and aimed at identifying not only the occurrence of problems with the parathyroidism, but also the possible detection of problems in the operation of the thyroid gland. It is based on the principle of increasing the local temperature due to the heat given off by the cancer cells. Parathyroid adenoma requires surgical treatment, before which a period of preparation is necessary by methods of reducing excessive calcemia: - Forced diuresis. - Infusion of phosphates. - Maintaining the condition with saline injected into a vein. - Perhaps the introduction of glucose. - Correction of the work of the heart with glycosides and corticosteroids. Removal of parathyroid adenoma can be done in three ways: - in open access, - reduced access - using a video endoscope. During the operation, all parathyroid glands are examined. If you suspect the presence of unrecorded adenomas and produce their resection. If a multiple process occurs, the parathyroid gland is removed. A modern parathyroid operation, the goal of which is a gentle treatment of the endocrine organ, is called selective parathyroidectomy. It is carried out after a thorough ultrasound diagnosis of the gland and considers only the removal of a parathyroid tumor. Features of its implementation are as follows: - slight trauma to the neck tissue (incision up to 2 cm), - quick operation time (up to 10 minutes), - the patient goes home immediately. For such operations, you must have high-quality video equipment, as well as special tools. The cost of such an operation in Moscow can be about 60 thousand rubles. The advantages of this method can be considered: - Minimum discomfort due to low swelling after surgery. - Lack of influence on the vocal cords. - Modern materials for seams will make them invisible after removing the threads. - Use, if necessary, of a cosmetic suture, which will be invisible after surgery. Such procedures are performed on high-quality European equipment by specialists who have a high level of qualification and experience in interacting with endoscopic medical equipment. Removal of the parathyroid gland under the conditions of this method is carried out as comfortable and safe for the patient. When removing the parathyroid adenoma, the prognosis of life can be favorable if this operation was performed at the initial stage of the disease. In this case, an independent decrease in the level of calcium in the blood on the first day after resection will be considered the main indicator of positive dynamics. Additionally, the following prophylactic measures are prescribed: - regular intake of vitamin D3, - Exercise therapy, - therapeutic massages, For women who are in the period of menopause, prescribe drugs with female hormones. Life without the parathyroid glands, if adequate therapy with synthetic hormones is used, is possible. For cancer resection, the prognosis is less comforting. What is parathyroid adenoma Adenoma appears more often on the lower glands and is a small capsule (up to 5 cm) with a lobular structure. Education can be solitary (single) and multiple (several neoplasms), almost always on one side.Large formations (more than 5 cm) tend to degenerate into malignant parathyroid carcinoma (2-3% of cases). The disease is accompanied by increased activity of the gland, which is expressed in the excessive release of parathyroid hormone. In 90% of cases, the cause of hyperparathyroidism is the presence of this tumor. This pathology is much more susceptible to women 20-40 years old, men suffer from parathyroid adenoma 2 times less. In children and adolescents, it does not develop. Parathyroid adenoma most often develops in women 20 to 40 years old. According to the latest edition of the International Classification of Diseases (ICD 10), parathyroid adenomas are combined with similar formations on the thyroid gland into one group under the code D34. Unambiguous causes of the formation of parathyroid adenoma are unknown. The following factors are considered predisposing: - Injuries in the neck area, when the gland itself or nearby areas could be affected. - Irradiation of the cervical or head during radiation therapy of oncological diseases. - Insufficient intake of calcium from food. As a result of all these reasons, a mutation (change) of the genes encoding the protein structure and directly participating in the delivery of calcium to the parathyroid gland occurs. The cell containing the mutated gene begins to divide haphazardly, which leads to the growth of organ tissue. A large number of cells produce an excessive amount of thyroid stimulating hormone. Another variant of the mutation caused by calcium deficiency is possible. Trying to fill the element deficiency, the cells begin to randomly divide. The consequence of this process is hyperplastic parathyroid adenoma. Symptoms of parathyroid adenoma Symptoms of parathyroid adenoma are quite diverse. Typical manifestations of this pathology does not exist. This explains the difficulty of diagnosis. Conditionally there are 4 types of hyperparathyroidism caused by parathyroid adenoma: Parathyroid adenoma causes an increase in the thyroid gland as a whole. Signs common to all these species: - general weakness - excessive sweating - bouts of nausea and vomiting, - reduced tone - persistent constipation - fatigue and sleepiness, - enlargement of the thyroid gland (not always determined, especially in the initial stages), - decreased appetite - memory impairment - pains in the joints and muscles - psychosomatic disorders In hyperparathyroidism of osseous form, osteoporosis and increased fragility of tubular bone tissue are observed, teeth become loose and fall out. Gastrointestinal type of pathological process of parathyroid adenoma is expressed in the appearance of peptic ulcer, cholecystitis with severe pain, pancreatitis, nausea and vomiting. The renal form manifests as urolithiasis and is accompanied by nephrocalcinosis (deposition of salts in the renal tissue) at advanced stages. In the cardiovascular form of hyperparathyroidism, arterial hypertension, calcium accumulation in the cardiac muscle and coronary arteries is observed, which can cause myocardial infarction. Hypercalcemia due to parathyroid adenoma is also manifested in dry skin, calcification of the cornea of the eye (rim keratitis) and ears (in particular, shells). Perhaps the development of hypercalcemic crisis due to a sharp increase in the concentration of calcium in the blood. This condition is accompanied by severe abdominal pain, vomiting, clouding of consciousness, the formation of intravascular blood clots, internal bleeding (intestinal and gastric), heart failure. It is permissible to use traditional medicine only in the early stages of development of parathyroid adenoma or after its removal. There are several effective recipes: - Infusion on hemlock (poisonous milestones). In 0.5 l of vodka pour 1 tbsp. l chopped herbs, insist 14 days in a dark room, stirring occasionally. The resulting solution swab rub into the neck 5-6 times a day. - Broth rhizomes of green sorrel. 0.3 kg of the crushed roots pour 1 liter of water and simmer for 3 hours. Drink ½ cup 3 times a day. - A decoction of oats in milk. In 1 liter of water, boil 30 g of unrefined oats for 1 hour, pour 1 l of milk into the cooled broth and boil again. Let it brew for 12 hours, strain. Drink in any quantities as a warning of parathyroid adenoma. It is recommended to take ½ tbsp. In parallel. l tinctures on the inner walls of walnut. - Infusion on the flowers of lilac and chestnut. Inflorescence pour alcohol or vodka, let stand 10-14 days. Lotion impose on the area of the gland every day for a week, then take a break of 7 days. Helps to cope with the disease decoction of oats on milk, which can be drunk in any quantity. Life after surgery The quality of life with timely surgical intervention and adequate maintenance therapy with synthetic hormones and drugs containing calcium will not deteriorate. It is important to begin treating the disease at an early stage. After a resection on the parathyroid gland, an appropriate diet will be required. The menu should be dominated by foods with a high calcium content. In the patient's menu after the operation, products with a high calcium content should prevail. These include the following foods: - vegetables and root vegetables (steamed, boiled and fresh), - low-fat milk, - fermented milk products (ryazhenka, yogurt, kefir, etc.), - seaweed (seaweed), - fish (river and sea), - forest mushrooms (in particular, chanterelles). It is recommended to limit the consumption of fatty meat (pork), oils of animal origin and cheeses. The basis of prevention of pathological formations on the parathyroid gland is proper and rational nutrition. As an additional measure, the intake of vitamin D3 is recommended. In carrying out the prevention of pathological formations on the parathyroid gland, one should not forget about taking vitamin D3. Its best assimilation contributes to moderate sun exposure (sunbathing). For prophylactic purposes, it is useful to undergo calciferol therapy. Like any other disease, a tumor in the parathyroid gland is much easier to cure in the initial stages. No need to self-medicate. If there are relevant symptoms, you should consult a doctor for a detailed examination. Causes of parathyroid adenoma The disease under consideration arises due to gene mutations of proteins that are involved in calcium metabolism and its transportation. Altered cells become too active. They begin to divide uncontrollably, resulting in the formation of a benign parathyroid tumor or adenoma. Predisposing factors for the start of mutations are any mechanical damage to the organ (injury, surgery) and radioactive exposure. Parathyroid adenoma - symptoms A benign neoplasm has the ability to independently produce parathyroid hormone. It activates osteoclasts, and parathyroid adenoma causes continuous extraction of calcium from the bones and its transfer into the bloodstream. As a result, the person begins to have osteoporosis, frequent and multiple fractures occur, even with minimal physical exertion (jumps, a change in body position, a slight blow to the limb). Other specific signs of parathyroid adenoma: - reduced blood vessel elasticity, - increase of systolic ("upper") pressure, - spinal curvature, - bone deformation - heart attacks - deterioration of attention and ability to concentrate - degradation of intelligence - prolonged loss of consciousness, to the point of falling into a coma, - loss of appetite, - scattered bone pains - muscle weakness - weight loss - fibrocystic osteitis, - loosening and falling out of healthy teeth, - diffuse nephrocalcinosis, - urolithiasis disease, - recurrent duodenal ulcer, stomach, - calcification of coronary arteries and heart valves, - damage to the joints and cartilage tissue, including the ears, nose, - head keratitis - necrosis of the renal tubules and others. Parathyroid adenoma - diagnosis In confirmation of the described pathology, several specialists take part at once: The first thing you notice when a parathyroid tumor is diagnosed is symptoms. Laboratory tests are performed: Sometimes selective vein catheterization is performed to determine the concentration of parathyroid hormone in the blood flowing from the parathyroid gland. Additionally, instrumental and hardware diagnostic procedures are assigned: - ultrasound, including ultrasound of the kidneys, gall bladder, pancreas and thyroid, - magnetic resonance or computed tomography, - X-ray of bones - survey urography - echo and electrocardiography, - daily blood pressure monitoring. Parathyroid adenoma on ultrasound Using this study, you can determine the location, number, size and structure of benign tumors. Parathyroid adenoma always provokes a significant increase in hormone-producing organs. This leads to their clear visualization with ultrasound, they are normally not visible. Parathyroid neoplasm differs from healthy tissue in echogenicity due to its heterogeneous structure. The specialist sees on the screen oval or rounded tumors with delineated borders, located in the endocrine organs. Parathyroid adenoma - MRI Computed and magnetic resonance imaging are considered to be more informative and modern methods of diagnosing the presented disease. A parathyroid tumor is defined as a small neoplasm with low echogenicity, significantly different from the adjacent endocrine tissues. MRI helps to find out not only the number and location of the adenoma, but also its structure, size and activity. For better visualization, the introduction of a contrasting drug is recommended. Parathyroid adenoma - treatment without surgery Effective therapy of the disease under consideration provides exclusively for surgical intervention. Even minimally invasive methods, such as sclerotherapy of parathyroid adenoma, do not exist. On the eve of the operation, preliminary treatment of hypercalcemia is performed. It is necessary for the relief of symptoms that are provoked by parathyroid adenoma - treatment includes: - use of prescribed drugs - use of alternative medicine - adherence to a special diet. Parathyroid adenoma - drugs Conservative therapy provides normalization of calcium concentration in the body and the cessation of its increase. Before a benign parathyroid gland tumor is removed, phosphate medications are administered to the patient intravenously (with an IV drip): - Dalatsin C, - Levofloks and analogues. Parathyroid adenoma often leads to the accumulation of excess fluid and toxins in the body. Diuretics (diuretic drugs) help accelerate their elimination to perform surgery: - Torasemide and others. Parathyroid adenoma - treatment of folk remedies Non-traditional therapeutic techniques can be applied only after approval by a physician. Folk methods, how to treat parathyroid adenoma, can act as ancillary measures. They do not dissolve the tumor and do not struggle with its symptoms. Such recipes provide a light diuretic effect and contribute to the soft and natural elimination of toxins, excess fluid from the tissues. - walnuts - 300 g, - honey, preferably buckwheat - 300 g, - buckwheat flour - 300 g - Ground nuts. - Mix all components thoroughly. - There is a received means for 1 day a week, washing down with any drinks or water. - sorrel roots - 250 g, - water - 2.5 l. - Pour vegetable raw materials with cold clean water. - Boil means. - Boil on the quietest fire for 3 hours. - Cool and strain the drug. - Take 3 times a day for 125 ml of solution. Diet for parathyroid adenoma The described pathology causes a strong increase in the level of calcium in the body. To parathyroid adenoma could be removed, it is necessary to reduce it. In addition to medical methods to reduce the concentration of calcium, it is recommended that a special diet be observed. Parathyroid adenoma involves a diet rich in phosphorus, because this element neutralizes hypercalcemia. - mushrooms, especially chanterelles and boletus mushrooms, - pumpkin seeds, - wheat bran, - soya beans, - sturgeon caviar - pork liver - fatty fish - cheese, cheese, - dairy products, - shrimp, crabs, squid, - legumes and others. - canned food - salt (very limited) Surgery to remove parathyroid adenoma There are 3 options for surgery: - Bilateral revision of the neck. The doctor examines all 4 endocrine organs, detects a neoplasm and removes parathyroid adenoma. - Unilateral revision of the neck. The surgeon examines only 2 organs, from the side where the tumor was detected, and cuts the tumor. For such an operation requires correct data on its localization. - Selective parathyroidectomy. The doctor removes only the adenoma of the parathyroid gland in which it is located. Inspection of other organs is not carried out. This is a complex procedure, involving the most accurate diagnosis and the availability of special equipment. This manipulation is the fastest, most effective and secure. The postoperative period after removal of parathyroid adenoma Properly performed surgery provides a very rapid improvement in the patient's condition. The level of calcium in the body is normalized by the 2nd day after the removal of parathyroid adenoma. In the hospital, a person is not more than 7 days. During this time, experts monitor the recovery, monitor the work of the cardiovascular system and the concentration of calcium in the blood. Removal of parathyroid adenoma - consequences It is extremely rare (less than 5% of cases) in people who have undergone surgery, hypocalcemia develops - too low levels of calcium in the body. Such consequences of parathyroid adenoma and its excision are eliminated even at the rehabilitation stage. To normalize the concentration of calcium is used a diet rich in the specified trace element, and preparations containing it. Parathyroid adenoma - prognosis In most situations, timely removal of the tumor ends in complete recovery. In a few weeks, the work of the internal organs and the endocrine system is restored, for 2 years the fragility of the bones disappears. Worse, if parathyroid adenoma was detected late, the prognosis of life in such cases depends on the severity of the disease. With strong lesions of the internal organs and a critical calcium deficiency in the bones, even correct therapy may not bring the desired result. Sometimes adenoma is reborn in cancer. Parathyroid adenoma can be single or multiple. It is characterized by the ability to synthesize parathyroid hormone, which leads to a critical increase in its level in the blood. According to statistics, 90% of cases of primary hyperparathyroidism are associated with the presence of adenoma. The size of the formation is usually small, but sometimes parathyroadenomas are diagnosed with a weight of about 100 g and the size of a chicken egg. More often adenomas are localized in the lower parathyroid glands. They are surrounded by a smooth capsule, have a soft, elastic consistency. In the section, the adenoma has a red-brown tint, it contains foci of necrosis, small hemorrhages, small cystic cavities with fluid inside. Depending on which cell types form a tumor, there are several types of parathyroadenomas: - clear cells, - main cell. Learn about the symptoms of testicular tumor in men, as well as how to treat and remove formations. Read how to choose and use a reusable syringe - insulin pen at this address. The clinical picture of parathyroid adenoma is quite blurred, which significantly complicates its diagnosis. The disease can manifest disorders of different systems: The main symptoms that should alert: - heavy sweating - constant fatigue - lowering the overall tone, Parathyroid adenoma actively produces parathyroid hormone.As a result, hyperparathyroidism occurs, which is characterized by: - frequent gagging, - loss of appetite, - shifting joint pain - emotional breakdowns - violation of intellectual abilities. The bone system responds to parathyroid adenoma with characteristic manifestations: - frequent fractures and bone fractures, - teeth loosening. From the gastrointestinal tract arise: - severe vomiting - frequent exacerbations of peptic ulcer If the calcium level exceeds 3.7 mmol / l, a hypercalcemic crisis may develop. It is accompanied by certain symptoms: - pain in the epigastric part, - continuous vomiting, - gastrointestinal bleeding, - disturbance of consciousness. General rules and effective treatment methods It is possible to get rid of adenoma only by surgery. Before the intervention, preparatory conservative therapy is prescribed to the patients. To suppress hypercalcemia used: - isotonic solution - Hypothiazide (thiazide diuretic), - Sodium phosphate, - forced diuresis. In severe cases, it may be necessary to administer a solution of glucose, cardiac glycosides, and corticosteroids. The doctor determines the dosage of drugs individually, based on the patient's age, severity of the condition, and associated pathologies. Be sure to adhere to food, which is limited to the use of foods rich in calcium. View a selection of effective treatments for breast fibroma in women. About the causes and likely effects of increased testosterone levels in women are written on this page. Follow the link http://vse-o-gormonah.com/hormones/drugie/serotonin-v-produktah.html and find out what products contain serotonin and how to compensate for the lack of "hormone of happiness" in the body. Access to the adenoma is carried out in several ways: The operation is done under general anesthesia. The volume of intervention and duration may be different, depending on the characteristics of the spread of adenoma. In most cases, with single entities, surgeons perform organ-sparing operations. In the course of their conduct, all parathyroid glands and surrounding tissues are examined for pathological changes.	2	18	0	0	0	2	0.482877	2	10,656
\|MP 2.04.80\|\|Genetic Testing for Hereditary Hemochromatosis\| \|Original Policy Date \|Last Review Status/Date Reviewed with literature search/4:2014 \|Return to Medical Policy Index\| Our medical policies are designed for informational purposes only and are not an authorization, or an explanation of benefits, or a contract. Receipt of benefits is subject to satisfaction of all terms and conditions of the coverage. Medical technology is constantly changing, and we reserve the right to review and update our policies periodically. Hereditary hemochromatosis (HH), a common genetic disorder of iron metabolism, can lead to inappropriate iron absorption, toxic accumulation of iron, and organ damage. Genetic testing is available to assess mutations in the HFE gene, which are responsible for most clinically significant cases of hereditary hemochromatosis. Iron overload syndromes may be hereditary, secondary to some other disease (eg iron-loading anemias, parenteral iron overload, chronic liver disease, or dysmetabolic iron overload syndrome), or due to other miscellaneous conditions (eg, neonatal iron overload, aceruloplasminemia, congenital atransferrinemia). Iron overload, if left untreated, can lead to secondary tissue damage in a wide range of organs resulting in chronic liver disease (hepatic fibrosis, cirrhosis, hepatocellular carcinoma), endocrine dysfunction (diabetes, hypogonadism), arthralgia or arthritis (typically involving the second and third metacarpophalangeal joints), and cardiomyopathy (with either symptomatic cardiac failure or arrhythmias). HH, an autosomal recessive disorder, is the most common identified, genetic disorder in Caucasians, with an estimated prevalence of 1 in 250 Caucasians. However, fully expressed disease with end-organ manifestations is seen in less than 10% of affected individuals. Factors that influence phenotypic expression of HFE (high iron-related HH (ie, the clinical appearance of iron overload) are not clearly defined. Low clinical penetrance may be due to a complex interplay of genetic status and other factors such as age, sex, environmental influences, and comorbid diseases. HH leads to inappropriate iron absorption from the intestine and progressive increase in intracellular iron concentrations. Untreated HH leads to premature death, usually by liver complications. Treatment by removing excess iron with serial phlebotomy is simple and effective, and if started before irreversible end-organ damage, restores normal life expectancy. Diagnosis of Hemochromatosis Patients with hemochromatosis may present with nonspecific systemic symptoms or specific organ-related symptoms, or they may be asymptomatic. Clinical diagnosis of hemochromatosis is based on documentation of increased iron stores as demonstrated by abnormal serum iron indices, specifically elevated transferrin saturation and elevated serum ferritin concentration. Liver biopsy has been used to confirm diagnosis but is now generally limited to determining the degree of hepatic fibrosis and cirrhosis during disease management. Genetic testing can confirm a hereditary nature of iron overload. Genetics of Hereditary Hemochromatosis Most patients with HH have mutations in the HFE gene, located on the short arm of chromosome 6. The HFE gene was identified and cloned in 1996. The most common mutation in the HFE gene is C282Y, a missense mutation that changes cysteine at position 282 in the HFE protein to tyrosine. Homozygosity for the C282Y mutation is associated with 60% to 90% of all cases of HH. Additionally, 3% to 8% of affected individuals are heterozygous for this mutation. Penetrance for elevated serum iron indices among C282Y homozygotes is relatively high, but not 100%. However, penetrance for characteristic clinical end points (ie, end-organ damage) is quite low. There is no test that can predict whether a C282Y homozygote will develop clinical symptoms. Another significant mutation is referred to as H63D, which changes histidine at position 63 to aspartic acid. Homozygosity for H63D is insufficient to cause clinically significant iron overload in the absence of modifying factors. However, compound heterozygosity for C282Y/H63D has been associated with increased hepatic iron concentrations; approximately 1% to 2% of patients with this genotype will develop clinical evidence of iron overload, usually in the presence of another liver disease.(1) The clinical significance of a third HFE mutation, S65C (serine at position 65 changed to cysteine), appears to be minimal. This rare variant displays very low penetrance. Compound heterozygosity for C282Y/S65C may confer a low risk for mild HH. Individuals who are heterozygous for S65C and either the wild-type (normal) or H63D alleles do not seem to be at an increased risk for HH. Other mutations in HFE and in non-HFE genes (eg, transferrin receptor 2, TFR2) resulting in iron overload syndromes are rare.(2-4) With the advent of genetic testing in the late 1990s, HFE-related HH is now frequently identified in asymptomatic probands and in presymptomatic relatives of patients who are known to have the disease. (5) Therefore, a genetic diagnosis can be made in subjects who have not yet developed phenotypic expression; these subjects have a genetic susceptibility to developing iron overload but may never do so. A 2000 consensus conference of the European Association for the Study of Liver Diseases led to a recognition of different stages and progression of hemochromatosis. These stages were defined as: - Stage 1: Patients with “genetic susceptibility” who have the genetic disorder but no increase in iron stores. - Stage 2: Patients who have the genetic disorder and phenotypic evidence of iron overload but no tissue or end-organ damage. - Stage 3: Patients who have the genetic disorder with iron overload and iron deposition to the degree that tissue and end-organ damage occurs. No U.S. Food and Drug Administration (FDA)‒cleared genotyping tests were found. Thus, genotyping is offered as a laboratory-developed test. Clinical laboratories may develop and validate tests in-house (“home-brew”) and market them as a laboratory service; such tests must meet the general regulatory standards of the Clinical Laboratory Improvement Act (CLIA). The laboratory offering the service must be licensed by CLIA for high-complexity testing. Genetic testing for HFE gene mutations may be considered medically necessary in a patient with abnormal serum iron indices indicating iron overload. (See Policy Guidelines) Genetic testing for HFE gene mutations may be considered medically necessary in individuals with a family history of hemochromatosis in a first-degree relative. (See Policy Guidelines) Genetic testing for hereditary hemochromatosis in screening of the general population is considered investigational. Serum Iron Indices in the Diagnosis of HH(6) - Elevated fasting transferrin saturation (the ratio of serum iron to total iron-binding capacity) is the most sensitive initial phenotypic screening test. A minimum cut-off value of 45% will detect almost all affected C282Y homozygotes. - Serum ferritin reflects body iron stores and generally rises later in the progression of iron overload. In the absence of other causes of hyperferritinemia (alcohol abuse, metabolic syndrome, inflammatory states [eg, infection, cancer, active rheumatoid arthritis], acute and chronic hepatitis), serum ferritin is a good marker of the degree of iron overload. The negative predictive value of a normal transferrin saturation and serum ferritin is 97%. In this situation, no further testing is recommended.(6) 2011 Practice Guidelines by the American Association for the Study of Liver Diseases recommend HFE gene mutation testing in patients with abnormal serum iron indices (ie, serum ferritin and transferrin saturation), even in the absence of symptoms (eg, abnormal serum iron indices on routine screening chemistry panel). Genetic Testing in an Individual With a Family History of HH 2011 Practice Guidelines by the American Association for the Study of Liver Diseases recommend screening (iron studies [serum ferritin and transferrin saturation] and HFE mutation analysis) of first-degree relatives of patients with HFE-related HH to detect early disease and prevent complications.(5) For children of an identified proband, HFE testing of the other parent is generally recommended because, if results are normal, the child is an obligate heterozygote and need not undergo further testing because there is no increased risk of iron loading. If C282Y homozygosity or compound heterozygosity is found in adult relatives of a proband, and if serum ferritin levels are increased, then therapeutic phlebotomy can be initiated. If ferritin level is normal in these patients, then yearly follow-up with iron studies is indicated. When identified, C282Y heterozygotes and H63D heterozygotes can be reassured that they are not at risk for developing progressive or symptomatic iron overload. Occasional H63D homozygotes can develop mild iron overload. Beginning in 2012, there is specific CPT coding for genetic testing for HFE common variants: 81256: HFE (hemochromatosis) (eg, hereditary hemochromatosis) gene analysis, common variants (eg, C282Y, H63D) BlueCard/National Account Issues No applicable information This policy was created in 2012 and is based on a search of the MEDLINE database through March 23, 2014. Recent reviews highlight the pathogenesis, diagnosis and management of hereditary hemochromatosis (HH).(6-9) A 2001 TEC Assessment on genetic testing for HFE gene mutations related to HH concluded the following: - Genetic testing and counseling for HFE mutations in the management of patients with symptoms of iron overload consistent with hereditary hemochromatosis, in the setting of 2 consecutive transferrin saturation values of 45% or more and a serum ferritin value of less than 200–300 mcg/L, met the TEC criteria. - Genetic testing and counseling for HFE mutations in asymptomatic relatives of subjects with hereditary hemochromatosis also met the TEC criteria. The Assessment did not address the use of genetic testing for HFE gene mutations in screening of the general population.(10) Validation of the Clinical Use of a Genetic Test Validation of the clinical use of any genetic test focuses on 3 main principles: (1) analytic validity (technical accuracy of the test in detecting a mutation that is present or in excluding a mutation that is absent; (2) clinical validity (diagnostic performance of the test [sensitivity, specificity, positive and negative predictive values] in detecting clinical disease; and (3) clinical utility (ie, how results of the diagnostic test will be used to change management of the patient and whether these changes in management lead to clinically important improvements in health outcomes). Stuhrmann et al (2005) initiated a pilot study on DNA-based screening of hereditary hemochromatosis in Germany.(11) A focus of the study was the analytic validity of different test methods. A total of 3961 subjects provided blood samples for testing of the C282Y HFE mutation; of these, 3930 samples were successfully tested by 2 independent test methods (either polymerase chain reaction and restriction digest, reverse allele-specific oligonucleotide hybridization, solid-phase oligonucleotide ligation assay, or microarray [DNA-chip]). In all, 67 of the tested subjects were homozygous for C282Y; 42.6% of the homozygotes already knew their clinical diagnosis of HH before sending the blood sample. Iron accumulation with further signs or symptoms of HH was present in 8 (24%) of 34 newly diagnosed C282Y homozygous subjects. Of 7860 tests performed, 7841 (99.6%) gave correct results. The overall error rate was 0.24% (95% confidence interval [CI], 0.15 to 0.38). Analytic specificity of the test methods for detecting homozygosity for C282Y was 100% (7726/7726 nonhomozygous test challenges; 95% CI, 99.95 to 100), and analytic sensitivity was 97% (130/134 homozygous test challenges; 95% CI, 92.5 to 99.2). This evidence indicates that test methods for C282Y are robust and highly sensitive and specific. Bryant et al (2008) evaluated the clinical validity and clinical utility of DNA testing in people suspected of having hereditary hemochromatosis and in family members of those diagnosed with the disorder by conducting a systematic review of 15 electronic databases (including MEDLINE and the Cochrane library) up to April 2007.(12) Clinical validity, defined as the ability of the test to detect or predict the phenotype (disorder) of interest, involved establishing the probability that the test would be positive in people with clinical HH (sensitivity) and the probability that the test would be negative in people without the disease (specificity). Studies were included if they reported the use of DNA tests in Caucasians of northern European origin with iron overload suggestive of HH compared with a control population, and reported or allowed the calculation of sensitivity and specificity. Clinical utility studies were included if they reported the use of DNA tests in Caucasians with iron overload suggestive of HH (or relatives of suspected cases) compared with any case-identification strategy not involving DNA, and reported patient-based outcomes (such as morbidity or mortality). Eleven observational studies that evaluated the clinical validity of genotyping for the C282Y mutation in the diagnostic workup for HH were identified. Criteria used to define hemochromatosis varied among studies. Clinical sensitivity of C282Y homozygosity ranged from 28.4% to 100%; when considering studies that used strict criteria to classify HH, clinical sensitivity ranged from 91.3% to 92.4%. No clinical utility studies were found. The authors concluded that DNA testing for HH in at-risk populations has clinical validity and may have clinical utility. The clinical utility of genetic testing for HH depends on how results can be used to improve patient management. Although there has never been a randomized controlled trial of phlebotomy versus no phlebotomy in the treatment of HH, there is evidence that initiation of phlebotomy before the development of cirrhosis and/or diabetes will significantly reduce HH-associated morbidity and mortality.(5,13,14) Data exists on the psychosocial aspect of genetic testing for HH. Picot et al (2009) conducted a systematic review of the psychosocial aspects of DNA testing for HH in at-risk subjects.(15) Databases were searched through 2007 for any quantitative or qualitative primary research that considered DNA testing of subjects considered at-risk for HH and that reported psychosocial outcomes. Three observational studies were included; each had methodologic limitations. After receiving test results, patient anxiety levels fell or were unchanged, and general health-related quality-of-life outcomes improved in some aspects from pretest assessments, or were unchanged. Outcomes were not reported separately for those referred for diagnosis and those with a family history of HH. The authors concluded that, although evidence is limited, results suggested that genetic testing for HH in at-risk subjects is accompanied by few negative psychosocial outcomes. Population Screening for HH General population screening for HH has been proposed because of the high prevalence of disease, absence of or nonspecific early clinical findings, specificity of findings once they appear, low cost of diagnosis and treatment, and high cost and low success rate of late diagnosis and treatment. However, because genotype penetrance is low, and the natural history of untreated individuals is unpredictable, support for population-based screening is lacking. The American Academy of Family Physicians, Centers for Disease Control and Prevention, and U.S. Preventive Services Task Force recommend against population-based general screening.(16-18) McLaren and Gordeuk conducted the Hemochromatosis and Iron Overload Screening (HEIRS) study to evaluate the prevalence, genetic and environmental determinants, and potential clinical, personal, and societal impact of hemochromatosis and iron overload in a multiethnic, primary care-based sample of 101,168 adults enrolled over a 2-year period at 4 centers in the U.S. and 1 in Canada.(19) Initial screening included genotyping for the HFE C282Y and H63D alleles, measurement of serum ferritin, and calculation of transferrin saturation. The yield of HFE genotyping for identifying persons with C282Y homozygosity was low in racial/ethnic groups other than non-Hispanic Caucasians. Overall frequency of homozygosity for the C282Y mutation in non-Hispanic Caucasians was 4.4 per 1000. There was marked heterogeneity of disease expression in C282Y homozygotes. The authors concluded that (1) future studies to discover modifier genes that affect phenotypic expression in C282Y hemochromatosis should help identify patients who are at greatest risk of developing iron overload who may benefit from continued monitoring of iron status, and (2) although genetic testing is well-accepted and associated with minimal risk of discrimination, generalized population screening in a primary care population as performed in the HEIRS study is not recommended. In a substudy of Caucasian participants in the HEIRS study, Adams et al (2013) assessed the prevalence of HFE mutations in patients who had elevated serum ferritin levels less than 1000 µg/L (300-1000 µg/L for men, 200-1000 µg/L for women).(20) Among 3359 men and 2416 women, prevalence of potential iron-loading HFE genotypes (defined as C282Y homozygote, C282Y/H63D compound heterozygote, or H63D homozygote) was 10% and 12% in men and women, respectively. Prevalence of C282Y homozygosity was 2% and 4% among men and women, respectively. Likelihood of C282Y homozygosity increased with increasing serum ferritin levels, from 0.3% to 16% in men, and from 0.3% to 30% in women. Posttest likelihood ratios (likelihood of C282Y homozygosity given a positive test result) exceeded 1 at serum ferritin levels of 500 µg/L or more for men and at levels greater than 300 µg/L for women. In Caucasian subjects with mild hyperferritinemia, causes of elevated serum ferritin level other than C282Y or H63D HFE mutations (eg, liver disease, diabetes) were more likely. Hereditary hemochromatosis is a common genetic disorder in the Caucasian population. Abnormal serum iron indices, clinical symptoms of iron overload or a family history of hereditary hemochromatosis may provoke testing for diagnosis. Testing for mutations in the HFE gene, which contributes to most cases of hereditary hemochromatosis, can confirm a genetic etiology; if clinically indicated, serial phlebotomy may be initiated, which can lead to a restored normal life expectancy. Therefore, genetic testing for HFE gene mutations may be considered medically necessary for patients with a clinical suspicion of hemochromatosis (signs and symptoms of iron overload) or in patients with fasting serum iron indices that are suggestive of iron overload, as well as in individuals with a family history of hemochromatosis. General population screening has been proposed because of the high prevalence of disease, absence of or nonspecific early clinical findings, simplicity and effectiveness of treatment, and low success rate of late diagnosis and treatment. However, because genotype penetrance is low, and the natural history of untreated individuals is unpredictable, support for population-based screening is lacking. Therefore, genetic testing for hereditary hemochromatosis screening in the general population is considered investigational. Practice Guidelines and Position Statements American Academy of Family Physicians AAFP recommends against routine genetic screening for hereditary hemochromatosis in the asymptomatic general population. (Grade D recommendation: at least fair evidence that [the service] is ineffective or that harms outweigh benefits).(16) American Association for the Study of Liver Diseases A 2011 practice guideline from AASLD recommends(5): - Patients with abnormal iron studies should be evaluated as patients with hemochromatosis, even in the absence of symptoms (based on high quality evidence [A]). - In a patient with suggestive symptoms, physical findings, or family history of HH, a combination of transferrin saturation and ferritin should be obtained rather than relying on a single test, and if either is abnormal (transferrin saturation ≥45% or ferritin above the upper limit of normal), then HFE mutation analysis should be performed (strength of recommendation 1 [strong] by the classification of the Grading of Recommendation Assessment, Development, and Evaluation [GRADE] workgroup; based on moderate quality evidence [B]). - Screening (iron studies and HFE mutation analysis) of first-degree relatives of patients with HFE-related HH is recommended to detect early disease and prevent complications. (1A) - Screening for non-HFE-related HH is not recommended. Average risk population screening for HH is not recommended. (1B) Centers for Disease Control and Prevention CDC does not currently recommend population screening for HFE mutations.(17) U.S. Preventive Services Task Force USPSTF recommends against routine genetic screening for hereditary hemochromatosis in the asymptomatic general population. (Grade D recommendation: at least fair evidence that [the service] is ineffective or that harms outweigh benefits).(21) Medicare National Coverage There is no national coverage determination (NCD). In the absence of an NCD, coverage decisions are left to the discretion of local Medicare carriers. - Kanwar P, Kowdley KV. Metal storage disorders: Wilson disease and hemochromatosis. Med Clin North Am 2014; 98(1):87-102. - Sood R, Bakashi R, Hegade VS et al. Diagnosis and management of hereditary haemochromatosis. British Journal of General Practice 2013; 63(611):331-32. - Vujic M. Molecular basis of HFE-hemochromatosis. Front Pharmacol 2014; 5:42. - Radio FC, Majore S, Binni F et al. TFR2-related hereditary hemochromatosis as a frequent cause of primary iron overload in patients from Central-Southern Italy. Blood Cells Mol Dis 2014; 52(2-3):83-7. - Bacon BR, Adams PC, Kowdley KV et al. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology 2011; 54(1):328-43. - Clark P, Britton LJ, Powell LW. The diagnosis and management of hereditary haemochromatosis. Clin Biochem Rev 2010; 31(1):3-8. - Alexander J, Kowdley KV. HFE-associated hereditary hemochromatosis. Genet Med 2009; 11(5):307-13. - Gan EK, Powell LW, Olynyk JK. Natural history and management of HFE-hemochromatosis. Semin Liver Dis 2011; 31(3):293-301. - Crownover BK, Covey CJ. Hereditary hemochromatosis. Am Fam Physician 2013; 87(3):183-90. - Blue Cross and Blue Shield Association Technology Evaluation Center (TEC). Genetic Testing for HFE Gene Mutations Related to Hereditary Hemochromatosis. TEC Assessments 2001; Volume 16, Tab 22. - Stuhrmann M, Strassburg C, Schmidtke J. Genotype-based screening for hereditary haemochromatosis. I: Technical performance, costs and clinical relevance of a German pilot study. Eur J Hum Genet 2005; 13(1):69-78. - Bryant J, Cooper K, Picot J et al. A systematic review of the clinical validity and clinical utility of DNA testing for hereditary haemochromatosis type 1 in at-risk populations. J Med Genet 2008; 45(8):513-8. - Adams PC, Speechley M, Kertesz AE. Long-term survival analysis in hereditary hemochromatosis. Gastroenterology 1991; 101(2):368-72. - Niederau C, Fischer R, Purschel A et al. Long-term survival in patients with hereditary hemochromatosis. Gastroenterology 1996; 110(4):1107-19. - Picot J, Bryant J, Cooper K et al. Psychosocial aspects of DNA testing for hereditary hemochromatosis in at-risk individuals: a systematic review. Genet Test Mol Biomarkers 2009; 13(1):7-14. - American Academy of Family Physicians. Hemochromatosis, 2006. Available online at: http://www.aafp.org/patient-care/clinical-recommendations/all/hemochromatosis.html. Last accessed March 2014. - Centers for Disease Control and Prevention. Hemochromatosis (iron storage disease). Training & education - epidemiology prevalence. Available online at: http://www.cdc.gov/ncbddd/hemochromatosis/training/epidemiology/prevalence.html. Last accessed March 2014. - Whitlock EP, Garlitz BA, Harris EL et al. Screening for hereditary hemochromatosis: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2006; 145(3):209-23. - McLaren GD, Gordeuk VR. Hereditary hemochromatosis: insights from the Hemochromatosis and Iron Overload Screening (HEIRS) Study. Hematology Am Soc Hematol Educ Program 2009:195-206. - Adams PC, McLaren CE, Speechley M et al. HFE mutations in Caucasian participants of the Hemochromatosis and Iron Overload Screening study with serum ferritin level <1000 microg/L. Can J Gastroenterol 2013; 27(7):390-2. - U.S. Preventive Services Task Force (USPSTF). Screening for hemochromatosis, August 2006. Available online at: http://www.uspreventiveservicestaskforce.org/uspstf/uspshemoch.htm. Last accessed March 2014. \|CPT\|\|81256\|\|HFE (hemochromatosis)(e.g., hereditary hemochromatosis) gene analysis, common variants (e.g., C282Y, H63D)\| \|ICD-9-CM Diagnosis\|\|275.01-275.09\|\|Disorders of iron metabolism code range\| \|V18.19\|\|Family history of other endocrine and metabolic diseases\| \|ICD-10-CM (effective 10/1/15)\|\|E83.10\|\|Disorder of iron metabolism, unspecified\| \|E83.110-E83.119\|\|Hemochromatosis code range\| \|Z83.49\|\|Family history of other endocrine, nutritional and metabolic diseases\| \|ICD-10-PCS (effectve 10/1/15)\|\|Not applicable. ICD-10-PCS codes are only used for inpatient services. There are no ICD procedure codes for laboratory tests.\| Genetic testing, hereditary hemochromatosis Hemochromatosis, genetic testing \|4/12/12\|\|New Policy add to Medicine – Pathology/ Laboratory section\|\|Genetic testing for HFE gene mutations may be considered medically necessary in patients with abnormal serum iron indices indicating iron overload and in individuals with a family history of hemochromatosis in a first degree relative. Investigational in screening of the general population.\| \|04/11/13\|\|Replace Policy\|\|Policy updated with literature search through February 2013. Reference 5 and 12-14 added. No change in policy statements.\| \|05/09/13\|\|Replace policy - correction only\|\|Reference 15 added\| \|4/10/14\|\|Replace policy\|\|Policy updated with literature review through March 23, 2014; references 1-4 and 20-21 added; references 16-17 updated. No change in policy statements.\|	2	20	4	0	0	2	0.943524	6	6,089
\|This article needs additional citations for verification. (January 2010) (Learn how and when to remove this template message)\| Types of classification Alternatively, diseases may be classified according to the organ system involved, though this is often complicated since many diseases affect more than one organ. A chief difficulty in nosology is that diseases often cannot be defined and classified clearly, especially when etiology or pathogenesis are unknown. Thus diagnostic terms often only reflect a symptom or set of symptoms (syndrome). Traditionally diseases were defined as syndromes by their symptoms. When more information is available, they are also defined by the damage they produce. When etiology is known, they are better defined by their etiology, though still important are their characteristics. Probably the last described kind of diseases are molecular diseases, defined by their molecular characteristics. This was introduced in November 1949, with the seminal paper, "Sickle Cell Anemia, a Molecular Disease", in Science magazine, Linus Pauling, Harvey Itano and their collaborators laid the groundwork for establishing the field of molecular medicine. Several classifications of diseases have been historically proposed, and normally all of them assign a code to every supported disease. Some of them codify diseases following the path of the classification tree, and others like SNOMED use a multifactor classification system. The most known coding system is the World Health Organization ICD-Series, but there are other accepted classifications like DOCLE, NANDA or SNOMED Historically there were others like Berkson Coding System that are not maintained anymore. There are also coding systems for symptoms presents in the diseases and biological findings. They are normally included in medical dictionaries, also with a codification system. Some of them are MeSH (Medical Subject Headings), COSTART (Coding Symbols for Thesaurus of Adverse Reaction Terms) or MedDRA (Medical Dictionary for Regulatory Activities) Other systems like Current Procedural Terminology do not deal directly with diseases but with the related procedures. Extended nosology and general medical conditions Medical conditions, like diseases, can be defined by etiology (cause), pathogenesis (mechanism by which the disease is caused), or by a collection of symptoms, medical signs and biomarkers, particularly when the other two definitions are not available (idiopathic diseases). From a nosological point of view, medical conditions could be divided in syndromes, diseases, disorders, lesions and injuries, each one with some specific meaning: - In medicine, a disorder is a functional abnormality or disturbance. Medical disorders can be categorized into mental disorders, physical disorders, genetic disorders, emotional and behavioral disorders, and functional disorders. The term disorder is often considered more value-neutral and less stigmatizing than the terms disease or illness, and therefore is a preferred terminology in some circumstances. In mental health, the term mental disorder is used as a way of acknowledging the complex interaction of biological, social, and psychological factors in psychiatric conditions. However, the term disorder is also used in many other areas of medicine, primarily to identify physical disorders that are not caused by infectious organisms, such as metabolic disorders. - The term disease broadly refers to any condition that impairs the normal functioning of the body. For this reason, diseases are associated with dysfunctioning of the body's normal homeostatic process. Commonly, the term disease is used to refer specifically to infectious diseases, which are clinically evident diseases that result from the presence of pathogenic microbial agents, including viruses, bacteria, fungi, protozoa, multicellular organisms, and aberrant proteins known as prions. An infection that does not and will not produce clinically evident impairment of normal functioning, such as the presence of the normal bacteria and yeasts in the gut, or of a passenger virus, is not considered a disease. By contrast, an infection that is asymptomatic during its incubation period, but expected to produce symptoms later, is usually considered a disease. Non-infectious diseases are all other diseases, including most forms of cancer, heart disease, and genetic disease. - Illness and sickness are generally used as synonyms for disease. However, these terms are occasionally used to refer specifically to the patient's personal experience of his or her disease. In this model, it is possible for a person to have a disease without being ill (to have an objectively definable, but asymptomatic, medical condition), and to be ill without being diseased (such as when a person perceives a normal experience as a medical condition, or medicalizes a non-disease situation in his or her life). - Normally four main types of diseases are considered: pathogenic diseases, deficiency diseases, hereditary diseases, and physiological diseases. - A syndrome is the association of several medical signs, symptoms, and or other characteristics that often occur together. Some syndromes, such as Down syndrome, have only one cause; others, such as Parkinsonian syndrome, have multiple possible causes. In other cases, the cause of the syndrome is unknown. A familiar syndrome name often remains in use even after an underlying cause has been found, or when there are a number of different possible primary causes. - In cases of viral infections, like HIV, it is important to make a difference between the infection (considered as a disease, even while it is silent) and the associated symptoms (a syndrome). In the case of HIV the syndrome is named AIDS - Injury and lesions - Injury is damage to the body. This maybe caused by accidents, falls, hits, weapons, and other causes. Major trauma is injury that has the potential to cause prolonged disability or death. Lesion is any abnormality in the tissue of an organism (in layman's terms, "damage"), usually caused by disease or trauma. Lesion is derived from the Latin word laesio meaning injury. Similar to the ICD-10 the World Health Organization produces the International Classification of External Causes of Injury (ICECI). Sequelae of resolved diseases sometimes are considered inside lesions and other times inside diseases. Some medical conditions cannot be classified in any of these groups, but they can still be important enough to be considered as medical conditions. For example, to be a carrier of a genetical disease, or a viral infection unable to progress to disease, normally is not considered inside any of the previous groups. Cases of infections able to progress, but with low possibilities, like latent tuberculosis, are also considered outside the category of diseases. The term "medical condition" can also be applied to physiological states outside the context of disease, as for example when referring to "symptoms of pregnancy". It can also refer to the normal residual scars of a disease after it has resolved, for example lungs fibrosis after a tuberculosis. Ayurveda is an elaborate system of medicine developed in India. In China the Huangdi Neijing is another ancient text. In the West, Hippocrates was one of the earliest writers on the subject of disease. The Metzora (parsha) also includes an early discussion of the treatment of skin diseases. In the 10th century the Arabian psychologist Najab ud-din Unhammad classified a nosology of nine major categories of mental disorders, which included 30 different mental illnesses in total. Some of the categories he described included obsessive-compulsive disorders, delusional disorders, degenerative diseases, involutional melancholia, and states of abnormal excitement.[verification needed] In the 18th century, the taxonomist Carl Linnaeus, Francois Boissier de Sauvages, and psychiatrist Philippe Pinel developed an early classification of physical illnesses. Thomas Sydenham's work in the late 17th century might also be considered a nosology. In the 19th century, Emil Kraepelin and then Jacques Bertillon developed their own nosologies. Bertillon's work, classifying causes of death, was a precursor of the modern code system, the International Classification of Diseases. - Nosology is used extensively in public health, to allow epidemiological studies of public health issues. Analysis of death certificates requires nosological coding of causes of death. - Nosological classifications are used in medical administration, such as filing of health insurance claims, and patient records, among others - Clinical coder - Diagnosis code - Differential diagnosis - International Statistical Classification of Diseases and Related Health Problems (ICD) - ICD-10 (ICD 10th Revision) - Medical classification - Pathology (study of disease) - Category:Diseases and disorders (Wikipedia's categorization of diseases) - L Pauling, H Itano, SJ Singer, I Wells. "Sickle Cell Anemia, a Molecular Disease". Science, 25 November 1949, vol. 110, no. 2865, pp. 543-548. - Babre, Deven (1 January 2010). "Medical Coding in Clinical Trials". Perspect Clin Res. 1 (1): 29–32. PMC . PMID 21829779 – via PubMed Central. - Starkstein S E, Leentjens A F G (2008). "The nosological position of apathy in clinical practice". J Neurol Neurosurg Psychiatry. 79: 1088–1092. doi:10.1136/jnnp.2007.136895. - Abenhaim, Lucien et al. The Prognostic Consequences in the Making of the Initial Medical Diagnosis of Work-Related Back Injuries. Spine Journal, 1995 - "Regents Prep: Living Environment: Homeostasis". Oswego City School District Regents Exam Prep Center. Retrieved 2012-11-12. - Millon, Theodore (2004), Masters of the Mind: Exploring the Story of Mental Illness from Ancient Times to the New Millennium, John Wiley & Sons, p. 38, ISBN 978-0-471-46985-8 - Smith R. In search of "non-disease." BMJ : British Medical Journal. 2002;324(7342):883-885. - Snider, G. L. (2003). "Nosology for Our Day". American Journal of Respiratory and Critical Care Medicine. 167 (5): 678–683. doi:10.1164/rccm.200203-204PP. - C. S. Herrman, The Bipolar Spectrum, SSRN (Social Science Research Network, 5 August 2010) - International Classification of Diseases by the World Health Organization.	2	7	1	0	0	0	0.698846	1	2,184
The flashcards below were created by user on FreezingBlue Flashcards. Documenting encounters with providers: - Patients Name - Encounter date and reason - Appropriate history and physical examination - Review of all tests that were ordered - Plan of Care, or notes on procedures or treatments that were given - Instructions or recommendations that were given to the patient - Signature of the provider who saw the patient Patient's medical record must contain - ~ Biographical and personal information, including the patients full name, social security number, date of birth, full address, marital status, home and work telephone numbers, and employer information as applicable - ~ Copies of all communications with patient, including letters, telephone calls, faxes,, and e-mails; the patients' responses; and a note of the time, date, topic, and physician's response to each communication. - ~ Copies of prescriptions and instructions given to the patients, including refills - ~ Original documents that the patient has signed, such as authorization to release information and an advance directive - ~ Medical allergies and reactions, or their absence - ~ Up-to-date immunization record and history if appropriate, such as for a child - ~ Previous and current diagnoses, test results, health risks, and progress - ~ copies of referral or consultation letters - ~ Records of any missed or canceled appointments - ~ Requests for information about the patient (from a health plan or an attorney), and detailed log of whom information was released the most common format is called a problem-oriented medical record (POMR), includes general section with data from initial patient examination and assessment. Subsequent visits, the reason for those encounters are listed separately and have their own notes. SOAP notes are contained in problem-oriented medical records. SOAP stands for: Subjective, Objective, Assessment, Plan - ~ Subjective information is what the patient names as the problems or complaints - ~ Objective information is what the physician finds during the exam of the patients; it may include data from laboratory tests and other procedures. - ~Assessment, also called impression or conclusion, is the physician's diagnosis - ~ Plan, also called advice or recommendations, is the course of treatment for the patient, such as surgery, medications, or other tests, including necessary patient monitoring, follow-up, and instructions to the patient. Evaluation and management (E/M) - when a provider evaluates a patient's condition and decides on a course of treatment to manage it. - Usually documented with chart notes - ~History and physical examination, a complete history and physical is documented with four types of information - ~ the chief complaint - ~ the history and physical examination - ~ the diagnosis - ~ the treatment plan - Progress reports include: - ~ comparisons of objective data with the patient's statements - ~ goals and progress toward goals - ~ the patient's current condition and prognosis - ~ type of treatment still needed and for how long - prepared during patient's final visit for a particular treatment plan or hospitalization, which includes: - ~ the final diagnosis - ~ comparisons of objective data with the patient's statements - ~ whether goals were achieved - ~ reason for and date of discharge - ~ the patient's current condition, status, and final prognosis - ~ instructions given to the patient at discharge, noting any special needs such as restrictions on activities and medications Procedural services documentation - ~ procedure or operative reports for simple or complex surgery - ~ laboratory reports for laboratory tests - ~ radiology reports for the results of X-rays - ~ forms for specific purpose, such as immunization records, pre-employment physicals, and disability reports Termination of the Provider- Patient relationship must be documented by the physician. Provider must maintain patient's medical records according to the provisions of federal and state law. Provider must also send a letter to the patient that documents the situation and provides for continuity of care with the next provider. A copy of the termination letter must be placed in the patient's medical record. Electronic health records - provide patients' and providers' with immediate access to health information. Which saves times when vital patient information is needed. - Computerized physician order management, physicians can enter orders for prescriptions, tests, and other services at any time. - Clinical decision support, can provide latest medical research on approved medical websites to help with medical decision making - Automated alerts and reminder, provides medical alerts and reminders for office staff to ensure that patients are scheduled for regular screening and other preventive practices. Also alerts can identify patient safety issues such as possible drug reactions. Centers for medicare and medicaid services - main federal agency responsible for health care. Also known as CMS - Also ensures quality of healthcare: - ~regulating all laboratory testing other than research performed on humans - ~preventing discrimination based on health status for people buying health insurance - ~researching the effectiveness of various methods of health care management, treatment, and financing - ~evaluating the quality of health care facilities and services Number/ Official Name - X12 837------ Health care claims or equivalent encounter information/coordination of benefits - X12 276/277----- Health care claim status inquiry/response - X12 270/271----- Eligibility for a health plan inquiry/response - X12 278----- Referral certification and authorization - X12 835----- Health care payment and remittance advice - X12 820----- Health plan premium payments - X12 834----- Health plan enrollment and disenrollment HIPAA National Identifiers - Are for: - ~Health care providers - ~Health plans are numbers of predetermined length and structure, such as a person's social security number. They are important because unique numbers can be used in electronic transactions. EIN- Employer Identification Number The employer identifier is used when employers enroll or disenroll employees in a health plan (x12 834) or make premium payments to plans on behalf of their employees (x12 820). The employer indentification number issued by the Internal Revenue Service is the HIPAA standard National Provider Identifier (NPI) Is the standard for the identification of providers when filing claims and other transactions. The NPI has 9 numbers and a check digit for a total of 10 numbers. These numbers are assigned by federal government to individual providers, such as pharmacies and nurses, and also provider organizations such as hospitals, pharmacies, and clinics. CMS maintains the NPIs as they are assigned in the NPPES (National Plan and Provider Enumerator System), a database of all assigned numbers, NPI cannot be changed once it is assigned, regardless of job or location changes.	3	2	0	0	0	1	0.464716	1	1,412
Vol. 17 •Issue 27 • Page 8 Coding Multiple Conditions Coders must be familiar with combination codes, multiple codes and manifestation coding guidelines. A coder with any experience knows that coding involves more than merely looking up words and selecting corresponding codes on a one-to-one basis. Coding also requires that the coder review the clinical relationship between the multiple conditions that a patient may have and make code selections based upon that clinical relationship. Many medical conditions are inter-related, and the ICD-9-CM coding system allows the capture of these relationships through the use of several different types of diagnosis codes: combination codes, multiple codes (whether mandatory or discretionary) and the related manifestation codes. Each will be discussed. A combination code is used to report two diagnoses or one diagnosis that is associated with a secondary condition. Combination codes are located in the ICD-9-CM alphabetic index as subterms that follow connecting words such as “due to,” “with,” “associated with” or “in.” The coder may also be able to locate combination codes by reading inclusion and exclusion notes in the tabular list. The new coder may ask, “How do I know when to assign a combination code?” The answer is through thorough coding and paying attention to all coding instructions. The coder then becomes familiar with the types of conditions that require combination codes. Some are more readily apparent than others: acute cholecystitis with cholelithiasis should be assigned to code 574.00 instead of reporting separate codes of 575.0 and 574.20. The combination code is present in the alphabetic index as follows: Cholelithiasis with cholecystitis acute 574.0 The fifth digit of 0 is added after ascertaining that no obstruction was present. But some combination codes are not so straightforward and may involve conditions that are clinically and inherently related. For instance, when chronic renal failure and hypertension are both documented on a patient record, the coder may be tempted to assign the very common codes 585.X and 401.9. But the ICD-9-CM Official Guidelines for Coding and Reporting (section I.C.7.a.3) indicates: “Assign codes from category 403, Hypertensive chronic kidney disease, when conditions classified to categories 585 Ð 587 are present. Unlike hypertension with heart disease, ICD-9-CM presumes a cause-and-effect relationship and classifies chronic kidney disease (CKD) with hypertension as hypertensive chronic kidney disease.” Note that this guideline involves chronic renal failure only, and if acute renal failure and hypertension are present without documentation of co-existing chronic kidney disease, the conditions are reported separately with codes from the 401 and 584 categories. Another example of the appropriate assignment of a combination code in lieu of separate, more commonly reported codes involves chronic obstructive pulmonary disease (COPD) and asthma. Coding Clinic, 2nd Quarter, 1990, page 20 includes the following: “The new code 493.2x, Chronic obstructive asthma, was developed because of the need to distinguish between non-obstructive and obstructive asthma (that in chronic obstructive lung disease), within the classification. When a patient has COPD with asthma, there is continuous obstruction to airflow on expiration, unlike a patient with non-obstructive asthma, where the patient wheezes during an asthma attack, but then returns to normal breathing once the attack subsides. When a diagnosis of asthma is documented with COPD, 493.2x is assigned whether or not the physician states ‘chronic obstructive’ asthma.” Multiple coding involves the use of more than one code to fully describe the components of a particular disease process or complex diagnostic statement. When combination codes are not available, but the documentation includes terms such as “due to,” “with,” “secondary to” or “incidental to,” multiple codes should be assigned to most fully describe the conditions. Multiple coding can be considered mandatory or discretionary. Mandatory multiple coding is designated in the alphabetic index by the use of the second code in brackets, which designates the manifestation code. The first code reflects the main underlying condition, and the second code identifies the manifestation of that main condition. Both of these codes must be assigned, and they must be sequenced in the order specified. In the tabular list, the coder will know that another code is required because the terminology “use additional code” appears with the main code and “code first underlying condition” appears with the manifestation code. Regardless of the circumstances of the admission, a manifestation code can never be sequenced as a principal or first-listed diagnosis. If submitted to a Medicare fiscal intermediary, or to another payer that follows national coding guidelines, the case will not be reimbursed until another code is sequenced as the principal or first-listed diagnosis. For example, a patient with bleeding esophageal varices is admitted to a hospital for treatment of the varices. The documentation indicates that the varices are due to cirrhosis of the liver. The alphabetic indexed entry appears below: Varix esophagus bleeding in cirrhosis of liver 571.5 [456.20] This indicates that the code for the cirrhosis (571.5) must be sequenced first and the manifestation (the varices, code 456.20) must be sequenced as a secondary condition. This is considered mandatory multiple coding. Discretionary multiple coding involves assigning multiple codes only if the additional condition is documented as actually being present. The coding instruction in the tabular list is “use additional code,” which then instructs the coder to look for the presence of the condition in the medical record documentation before assigning an additional code. A common example is a urinary tract infection due to E.coli infection. Under code 599.0 in the tabular list, the following appears: “Use additional code to identify organism, such as Escherichia coli [E.coli] (041.4).” This specific type of organism will not be present on all cases, but the coder is alerted to look for documentation of an underlying organism that is causing the infection and assign a separate code accordingly. Another common coding scenario involves guidelines for cases in which terminology for both “acute” and “chronic” are documented. Whether or not both are coded depend upon the alphabetic indexed entries for that term. For example, a coder may commonly see “acute and chronic bronchitis” documented. The indexed entry appears below: Bronchitis acute or subacute 466.0 chronic 491.9 If separate subterms for acute or subacute and chronic are listed at the same indentation level in the index, both conditions are coded, with the code for the acute condition sequenced first. In this particular example, both the acute and the chronic conditions appear at the same indentation level so both would be assigned, with code 466.0 sequenced first. Conversely, if a patient has acute and chronic poliomyelitis, the indexed entry appears as below: Poliomyelitis (acute) (anterior) (epidemic) 045.9 chronic 335.21 When only one term is included in the index as a subterm, and the other is in parentheses as a nonessential modifier (after the main term), only the code listed for the subterm is assigned. In this case, only code 335.21 would be assigned. Multiple coding is also required for cases involving patients with late effects, which are residual conditions that remain after the end of the acute phase of an injury or illness. There is no time limit for when a late effect code can be assigned, but coders should review documentation carefully to ensure that the physician makes the connection between the current condition and the fact that it is due to the previous, but now healed, original condition. The nature of the late effect is sequenced first, with the code for the late effect sequenced second. Many conditions related to previous trauma are inherently late effects, such as fracture nonunion or malunion. Others may not be as readily apparent, such as neural deafness from childhood measles. The vast majority of late effects require two codes for appropriate coding, unless the alphabetic index or tabular list directs otherwise. Also, when the late effect code has been expanded to the fourth- or fifth-digit level that includes the specific late effects for the residual conditions, only the cause of the late effect code is assigned. A good example of this is the late effect of cerebrovascular disease (438.0-438.9) category. It should be noted that although reporting multiple codes to fully describe an episode of care is necessary, indiscriminate multiple coding is not appropriate. An example involves assigning secondary codes for signs and symptoms that are an inherent part of a definitive diagnosis that has already been coded. If a patient is admitted for treatment of congestive heart failure (CHF) and has an associated pleural effusion that is not addressed during the admission, it would not be appropriate to assign a secondary diagnosis for pleural effusion on the same case. Likewise, assigning codes solely on the basis of lab or other tests that have not been substantiated by a physician is not allowed. This is especially crucial when assigning codes under the new MS-DRG system, whereby finding CC or MCC conditions may be more difficult than it was under the previous CMS DRGs. Coders should not assign codes for conditions that are considered incidental findings and have no significance for the current episode of care. For example, atelectasis on a chest X-ray or right bundle branch block on an EKG is not unusual, and unless the physician documents the significance of the finding and how it relates to the current episode of care, it should not be coded. To brush up on the ICD-9-CM Official Guidelines for Coding and Reporting referenced above, please review the following: A. Conventions for the ICD-9-CM 6.Etiology/manifestation convention (“code first,” “use additional code” and “in diseases classified elsewhere” notes) B. General Coding Guidelines 9.Multiple coding for a single condition 10.Acute and Chronic Conditions After you’ve completed your review, check yourself with the quiz below. 1. A patient is seen in the physician’s office with a diagnosis of chondrocalcinosis of the shoulder due to calcium pyrophosphate. Which of the following would be the appropriate diagnosis code(s) selection? a. 275.49, 712.21 b. 712.11, 275.49 c. 712.21, 275.49 d. 275.49, 712.81 2. A patient is admitted to the hospital with an admitting diagnosis of GI bleeding. Underlying chronic conditions include hypertension, S/P MI, COPD, atrial fibrillation and asthma, all of which are currently treated. After GI endoscopy, diverticulitis of the colon is diagnosed as the cause of the bleeding. Which of the following would be the appropriate diagnosis code(s) selection? a. 578.9, 562.11, 401.9, 412, 496, 427.31, 493.90 b. 562.13, 401.9, 412, 496, 427.31, 493.90 c. 562.13, 401.9, 412, 493.20, 427.31 d. 578.9, 562.11, 401.9, 412, 493.20, 427.31 3. The patient is seen in the ambulatory surgery center for treatment of a scar contracture of the left hand secondary to a burn that was suffered during the previous year. Which of the following would be the appropriate diagnosis code(s) selection? a. 944.00, 709.2 b. 709.9, 944.00, 709.2 c. 709.2, 906.6 d. 906.6, 709.2 4. An elderly patient is admitted to the inpatient unit of the hospital with shortness of breath and fever. She is found to have influenza and pneumonia and is treated accordingly. She also has flaccid hemiplegia due to an old CVA. Which of the following would be the appropriate diagnosis code(s) selection? a. 487.1, 486, 438.20 b. 486, 487.1, 438.20 c. 487.0, 438.20 d. 487.0, V12.59 5. A patient was admitted with a diagnosis of subacute and chronic pyelonephritis. He has underlying conditions that include diabetic retinopathy, COPD and a traumatic arthritis of the ankle, S/P ankle fracture 2 years ago. Which of the following would be the appropriate diagnosis code(s) selection? a. 590.00, 590.80, 250.50, 362.01, 496, 716.17, 905.4 b. 590.10, 590.00, 250.50, 362.01, 496, 716.17, 905.4 c. 590.80, 250.51, 362.01, 496, 716.17, 824.8 d. 590.10, 590.00, 250.51, 362.02, 496, 716.17, 905.4 This month’s column has been prepared by Cheryl D’Amato, RHIT, CCS, director of HIM, and Melinda Stegman, MBA, CCS, clinical technical editor, Ingenix (www.ingenix.com), which specializes in the development and use of software and e-commerce solutions for managing coding, reimbursement, compliance and denial management in the health care marketplace. Coding Clinic is published quarterly by the AHA. CPT is a registered trademark of the AMA. Answers to CCS Prep!: 1. a: The underlying condition (the calcium pyrophosphate problem) is sequenced first, and then the chondrocalcinosis is sequenced second. The instruction note in the tabular list under code 712.2X indicates, “Code first underlying disease (275.4);” 2. c: Combination codes are assigned for the colon diverticulitis with bleeding (562.13) and for the COPD and asthma (493.20).; 3. c: Following the late effect guidelines, the code for the residual condition (the scar) is sequenced first, and the code for the late effect itself is sequenced second. The burn happened during the previous year and is no longer considered acute; it should not be coded separately.; 4. c: Combination codes are assigned for the influenza with pneumonia (487.0) and the hemiplegia late effect of a CVA (438.20); and 5. b: Both subacute and chronic pyelonephritis codes are listed at the same indentation level in the index and so both are coded, with the acute code sequenced first. The diabetes is not specified as Type I, nor is the retinopathy specified as proliferative, so codes 250.50 and 362.01 should be assigned. The ankle fracture is no longer acute, so code 824. 8 should not be assigned at this time. Assign codes 716.17 for the traumatic arthropathy and 905.4 to represent a late effect of an ankle fracture.	4	10	0	0	0	1	0.754986	1	3,364
Lumbar Radiculopathy ICD Lumbar radiculopathy is a condition that affects the spinal nerve in the lower back. It can be caused by a herniated disc, spinal stenosis, or a bone spur. These conditions can cause inflammation and compression of the nerve. Listed below are symptoms, causes, and treatment options for lumbar radiculopathy. To find out more, read on! If you are experiencing pain in your lower back, you may have lumbar radiculopathy. This condition can occur from lifting heavy objects improperly or through trauma. It can also be caused by a tumor compressing the nerve roots locally. Some people also suffer from diabetes, which can result in ischemia. Your doctor can determine if lumbar radiculopathy is causing your pain. The symptoms of lumbar radiculopathy include tingling, numbness, weakness, and pain in your lower back. These symptoms are similar to those caused by inflammation or pain in the sciatic nerve. A physician will typically diagnose lumbar radiculopathy based on your symptoms and a physical examination. Imaging studies are also recommended. Depending on the cause, you may need a medical procedure or non-surgical treatment. Lumbar radiculopathy is characterized by irritation of the spinal nerve roots that run from the lower back to the legs. This condition can develop due to many different factors, including herniated disc, bone spur, and strenuous activity. Osteoarthritis is also a common cause of lumbar radiculopathy. However, the most common cause of this condition is an inflammation of the sciatic nerve, which is the longest nerve in the body. The lumbar spine is made up of 33 vertebral bones with cushioning discs between them. The lumbar region has five vertebrae. The spinal cord communicates with the lower body through the spaces between the vertebrae. Symptoms of lumbar radiculopathy are usually pain in the lower back. A doctor will usually recommend a treatment plan based on your symptoms. Lumbar radiculopathy is a condition that affects the nerves in the lower back and neck. Diagnosis is made through a variety of methods, such as Bragard’s sign or the Straight Leg Raise test. Radiculopathy is an illness that is coded according to its cause in the ICD-10 classification system. Treatment goals include reducing pain, decompressing the irritated nerve, preserving spine stability, restoring alignment, and preserving neck range of motion. Nonsurgical treatments such as physical therapy must be coded with appropriate CPT codes. Despite these limitations, ICD-10 has greatly increased the diagnostic codes that can be used to diagnose spine conditions. For example, the category of dorsopathies has grown from 100 to 504 diagnostic codes. Although this is an increase of more than fivefold, there are still few codes that capture the majority of diagnoses for dorsopathy spinal conditions. As a result, the clinical rationale for the diagnosis must be documented. Occasionally, diagnostic tests may also be needed. A physician can use the ICD-10 codes to diagnose lumbar radiculopathy when the MRI results reveal a disc or nerve path entrapment in the spine. The patient is generally in marked discomfort along the nerve path. The pain may be due to spinal pressure or an injury. Moreover, the patient might also experience weakness or sensory loss, or a combination of these. The doctor must be able to accurately determine the cause of the pain. In many cases, the condition is caused by a disc herniation or acute injury. In some cases, the condition is caused by degenerative changes in the joints or discs. Symptoms include sharp pain, numbness, or weakness in the arms or legs. In more severe cases, the pain may be due to the compression of the spinal nerve roots. Low back pain is often treated with medications, injections, or prosthetic devices. ICD diagnosis codes for low back pain have been effective in this category for years. Before 10/1/2021, diagnosis code M54.5 was used to bill for low back pain. M54.5 is a subcategory of the musculoskeletal chapter of the ICD. It is grouped with other codes that may be reported on the same claim. Lumbar radiculopathy is a common musculoskeletal disorder that can occur due to compression of the spinal nerves in the lower back. The condition can cause pain, muscle tightness, and weakness in the leg, hip, and foot. The pain may be constant or vary in intensity. It can also be caused by a sedentary lifestyle or by a chronic cough. Lumbar radiculopathy can result from a herniated disc, spinal stenosis, or a bone spur in the spine. The condition can also be caused by an injury to the nerve. Typically, the condition responds to nonsurgical treatment such as physical therapy. Patients with lumbar radiculopathy may also require surgery. In some cases, a combination of physical therapy and medication can provide relief. Physical therapy is an integral part of the treatment for lumbar radiculopathy. Physical therapists use specialized equipment and techniques to treat the condition. These treatments help patients regain normal movement and function, which in turn helps them recover faster. Physical therapists often consult with surgeons and physicians to make sure that the diagnosis is accurate. Physical therapists also help patients recover from back pain and other conditions by using various types of treatments and technologies. Some of these treatments and technologies include specific motion exercises, application of heat or cold packs, and gentle electrotherapy, such as transcutaneous electrical nerve stimulation. The Centers for Medicare & Medicaid Services (CMS) publishes several new guidelines regarding the ICD-10 manual and coding for the condition. Earlier, this code was used for reimbursement of low back pain. However, after Oct. 1, 2021, this diagnosis code no longer qualifies as a valid condition. Previously, M54.5 was used for claims of low back pain. The diagnosis code M54.5 was used for reimbursement for this condition. Until 10/1/2021, M54.5 was used for low back pain. However, this diagnosis code was also used for claims of sciatica. The transition from ICD-9 to ICD-10 has increased the number of diagnostic codes available for spine conditions, but there were still significant differences between the two systems. The vast majority of diagnoses were underrepresented in the ICD-9 system and underrepresented in ICD-10. Consequently, providers used the same few codes in both systems. This reflects a pattern of low-level coding. Lumbar radiculopathy is a condition where the spinal nerve roots in the lower back are compressed. This condition can cause pain, numbness, and weakness. It can also result from a spinal cord injury. The cost of treatment is determined by the level of complexity and the type of care required. A physician will likely use ICD-10 to code this condition. There are two primary ways to get the most accurate cost estimate for lumbar radiculopathy. A herniated disc, spinal stenosis, or bone spur can cause lumbar radiculopathy. It can also be caused by an injury to the spinal nerve. In some cases, this condition can be treated with medication. Treatment can also include a range of physical therapy options. Depending on the level of severity, diagnostic tests may be necessary. In any case, a patient should be evaluated for lumbar radiculopathy to determine if it is treatable. The costs associated with lumbar radiculopathy are driven by two factors: the diagnosis of the patient and the surgeon’s technique. In this study, the differences between the two diagnoses were more significant than differences in the surgeon’s technique. The researchers used the PearlDiver database, which contains millions of patient encounters. The dataset is robust, allowing for a more reliable representation of diagnostic code usage for spine conditions. The study sample size was similar, allowing for an accurate comparison between ICD-9 and ICD-10. Lumbar radiculopathy is a common medical condition affecting the back. It is often caused by an injury and can affect other areas of the body. The pain is typically felt in the lower back, but it can spread throughout the body and may require surgery or a prosthesis. The treatment options for lumbar radiculopathy can range from medication to surgery. It can be caused by a traumatic accident, an illness, or bad posture.	4	3	0	0	0	7	0.815099	7	1,795
What are Chiari malformations? What causes these malformations? How are they classified? What are the symptoms of a Chiari malformation? Are other conditions associated with Chiari malformations? How common are Chiari malformations? How are Chiari malformations diagnosed? How are they treated? What research is being done? Where can I get more information? Chiari malformations (CMs) are structural defects in the cerebellum, the part of the brain that controls balance. Normally the cerebellum and parts of the brain stem sit in an indented space at the lower rear of the skull, above the foramen magnum (a funnel-like opening to the spinal canal). When part of the cerebellum is located below the foramen magnum, it is called a Chiari malformation. CMs may develop when the bony space is smaller than normal, causing the cerebellum and brain stem to be pushed downward into the foramen magnum and into the upper spinal canal. The resulting pressure on the cerebellum and brain stem may affect functions controlled by these areas and block the flow of cerebrospinal fluid (CSF)— the clear liquid that surrounds and cushions the brain and spinal cord—to and from the brain. CM has several different causes. It can be caused by structural defects in the brain and spinal cord that occur during fetal development, whether caused by genetic mutations or lack of proper vitamins or nutrients in the maternal diet. This is called primary or congenital CM. It can also be caused later in life if spinal fluid is drained excessively from the lumbar or thoracic areas of the spine either due to injury, exposure to harmful substances, or infection. This is called acquired or secondary CM. Primary CM is much more common than secondary CM. CMs are classified by the severity of the disorder and the parts of the brain that protrude into the spinal canal. Type I involves the extension of the cerebellar tonsils (the lower part of the cerebellum) into the foramen magnum, without involving the brain stem. Normally, only the spinal cord passes through this opening. Type I—which may not cause symptoms—is the most common form of CM and is usually first noticed in adolescence or adulthood, often by accident during an examination for another condition. Type I is the only type of CM that can be acquired. Type II, also called classic CM, involves the extension of both cerebellar and brain stem tissue into the foramen magnum. Also, the cerebellar vermis (the nerve tissue that connects the two halves of the cerebellum) may be only partially complete or absent. Type II is usually accompanied by a myelomeningocele—a form of spina bifida that occurs when the spinal canal and backbone do not close before birth, causing the spinal cord and its protective membrane to protrude through a sac-like opening in the back. A myelomeningocele usually results in partial or complete paralysis of the area below the spinal opening. The term Arnold-Chiari malformation (named after two pioneering researchers) is specific to Type II malformations. Type III is the most serious form of CM. The cerebellum and brain stem protrude, or herniate, through the foramen magnum and into the spinal cord. Part of the brain’s fourth ventricle, a cavity that connects with the upper parts of the brain and circulates CSF, may also protrude through the hole and into the spinal cord. In rare instances, the herniated cerebellar tissue can enter an occipital encephalocele, a pouch-like structure that protrudes out of the back of the head or the neck and contains brain matter. The covering of the brain or spinal cord can also protrude through an abnormal opening in the back or skull. Type III causes severe neurological defects. Type IV involves an incomplete or underdeveloped cerebellum—a condition known as cerebellar hypoplasia. In this rare form of CM, the cerebellar tonsils are located in a normal position but parts of the cerebellum are missing, and portions of the skull and spinal cord may be visible. Another form of the disorder, under debate by some scientists, is Type 0, in which there is no protrusion of the cerebellum through the foramen magnum but headache and other symptoms of CM are present. Individuals with CM may complain of neck pain, balance problems, muscle weakness, numbness or other abnormal feelings in the arms or legs, dizziness, vision problems, difficulty swallowing, ringing or buzzing in the ears, hearing loss, vomiting, insomnia, depression, or headache made worse by coughing or straining. Hand coordination and fine motor skills may be affected. Symptoms may change for some individuals, depending on the buildup of CSF and resulting pressure on the tissues and nerves. Persons with a Type I CM may not have symptoms. Adolescents and adults who have CM but no symptoms initially may, later in life, develop signs of the disorder. Infants may have symptoms from any type of CM and may have difficulty swallowing, irritability when being fed, excessive drooling, a weak cry, gagging or vomiting, arm weakness, a stiff neck, breathing problems, developmental delays, and an inability to gain weight. Individuals who have a CM often have these related conditions: Hydrocephalus is an excessive buildup of CSF in the brain. A CM can block the normal flow of this fluid, resulting in pressure within the head that can cause mental defects and/or an enlarged or misshapen skull. Severe hydrocephalus, if left untreated, can be fatal. The disorder can occur with any type of CM, but is most commonly associated with Type II. Spina bifida is the incomplete development of the spinal cord and/or its protective covering. The bones around the spinal cord don’t form properly, leaving part of the cord exposed and resulting in partial or complete paralysis. Individuals with Type II CM usually have a myelomeningocele, a form of spina bifida in which the bones in the back and lower spine don’t form properly and extend out of the back in a sac-like opening. Syringomyelia, or hydromyelia, is a disorder in which a CSF-filled tubular cyst, or syrinx, forms within the spinal cord’s central canal. The growing syrinx destroys the center of the spinal cord, resulting in pain, weakness, and stiffness in the back, shoulders, arms, or legs. Other symptoms may include headaches and a loss of the ability to feel extremes of hot or cold, especially in the hands. Some individuals also have severe arm and neck pain. Tethered cord syndrome occurs when the spinal cord attaches itself to the bony spine. This progressive disorder causes abnormal stretching of the spinal cord and can result in permanent damage to the muscles and nerves in the lower body and legs. Children who have a myelomeningocele have an increased risk of developing a tethered cord later in life. Spinal curvature is common among individuals with syringomyelia or CM Type I. Two types of spinal curvature can occur in conjunction with CMs: scoliosis, a bending of the spine to the left or right; and kyphosis, a forward bending of the spine. Spinal curvature is seen most often in children with CM, whose skeleton has not fully matured. CMs may also be associated with certain hereditary syndromes that affect neurological and skeletal abnormalities, other disorders that affect bone formation and growth, fusion of segments of the bones in the neck, and extra folds in the brain. In the past, it was estimated that the condition occurs in about one in every 1,000 births. However, the increased use of diagnostic imaging has shown that CM may be much more common. Complicating this estimation is the fact that some children who are born with the condition may not show symptoms until adolescence or adulthood, if at all. CMs occur more often in women than in men and Type II malformations are more prevalent in certain groups, including people of Celtic descent. Many people with CMs have no symptoms and their malformations are discovered only during the course of diagnosis or treatment for another disorder. The doctor will perform a physical exam and check the person’s memory, cognition, balance (a function controlled by the cerebellum), touch, reflexes, sensation, and motor skills (functions controlled by the spinal cord). The physician may also order one of the following diagnostic tests: An X-ray uses electromagnetic energy to produce images of bones and certain tissues on film. An X-ray of the head and neck cannot reveal a CM but can identify bone abnormalities that are often associated with CM. This safe and painless procedure can be done in a doctor’s office and takes only a few minutes. Computed tomography (also called a CT scan) uses X-rays and a computer to produce two-dimensional pictures of bone and vascular irregularities, certain brain tumors and cysts, brain damage from head injury, and other disorders. Scanning takes about 3 to 5 minutes. This painless, noninvasive procedure is done at an imaging center or hospital on an outpatient basis and can identify hydrocephalus and bone abnormalities associated with CM. Magnetic resonance imaging (MRI) is the imaging procedure most often used to diagnose a CM. Like CT, it is painless and noninvasive and is performed at an imaging center or hospital. MRI uses radio waves and a powerful magnetic field to produce either a detailed three-dimensional picture or a two-dimensional “slice” of body structures, including tissues, organs, bones, and nerves. Depending on the part(s) of the body to be scanned, MRI can take up to an hour to complete. Some CMs are asymptomatic and do not interfere with a person’s activities of daily living. In other cases, medications may ease certain symptoms, such as pain. Surgery is the only treatment available to correct functional disturbances or halt the progression of damage to the central nervous system. Most individuals who have surgery see a reduction in their symptoms and/or prolonged periods of relative stability. More than one surgery may be needed to treat the condition. Posterior fossa decompression surgery is performed on adults with CM to create more space for the cerebellum and to relieve pressure on the spinal column. Surgery involves making an incision at the back of the head and removing a small portion of the bottom of the skull (and sometimes part of the spinal column) to correct the irregular bony structure. The neurosurgeon may use a procedure called electrocautery to shrink the cerebellar tonsils. This surgical technique involves destroying tissue with high-frequency electrical currents. A related procedure, called a spinal laminectomy, involves the surgical removal of part of the arched, bony roof of the spinal canal (the lamina) to increase the size of the spinal canal and relieve pressure on the spinal cord and nerve roots. The surgeon may also make an incision in the dura (the covering of the brain) to examine the brain and spinal cord. Additional tissue may be added to the dura to create more space for the flow of CSF. Infants and children with myelomeningocele may require surgery to reposition the spinal cord and close the opening in the back. Hydrocephalus may be treated with a shunt system that drains excess fluid and relieves pressure inside the head. A sturdy tube that is surgically inserted into the head is connected to a flexible tube that is placed under the skin, where it can drain the excess fluid into either the chest wall or the abdomen so it can be absorbed by the body. An alternative surgical treatment to relieve hydrocephalus is third ventriculostomy, a procedure that improves the flow of CSF. A small perforation is made in the floor of the third ventricle and the CSF is diverted into the subarachnoid space to relieve pressure. Similarly, surgeons may open the spinal cord and insert a shunt to drain a syringomyelia or hydromyelia. A small tube or catheter may be inserted into the syrinx for continued drainage. Within the Federal government, the National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH), supports and conducts research on brain and nervous system disorders, including Chiari malformations. The NINDS conducts research in its laboratories at the NIH, in Bethesda, Maryland, and supports research through grants to major medical research institutions across the country. In one study, NINDS scientists are trying to better understand the genetic factors responsible for the malformation by examining individuals with CM who have a family member with either a CM or syringomyelia. NINDS scientists are examining individuals who either have syringomyelia or are at risk of developing the disorder, including patients with Chiari I malformation. By recording more than 5 years of symptoms, muscle strength, general level of functioning, and MRI scan findings from individuals who receive standard treatment for syringomyelia, researchers can obtain more information about factors that influence its development, progression, and relief of symptoms. Study results may allow scientists to provide more accurate recommendations to future patients with syringomyelia regarding optimal surgical or non-surgical treatment of their condition. A NIH study is reviewing an alternative surgical treatment for syringomyelia. By examining people with syringomyelia, in which there is an obstruction in CSF flow, NIH scientists hope to learn whether a surgical procedure that relieves the obstruction in CSF flow can correct the problem without having to cut into the spinal cord itself. The NIH’s Management of Myelomeningocele Study is comparing prenatal surgery to the conventional post-birth approach of closing the opening in the spine and back that is common to some forms of CM. The study will enroll 200 women whose fetuses have spina bifida and will compare the safety and efficacy of the different surgeries. Preliminary clinical evidence of intrauterine closure of the myelomeningocele suggests the procedure reduces the incidence of shuntdependent hydrocephalus and restores the cerebellum and brain stem to more normal configuration. At 1 year and 2 ½ years after surgery the children will be tested for motor function, developmental progress, and bladder, kidney, and brain development. For more information on neurological disorders or research programs funded by the National Institute of Neurological Disorders and Stroke, contact the Institute's Brain Resources and Information Network (BRAIN) at: P.O. Box 5801 Bethesda, MD 20824 Information also is available from the following organizations: National Organization for Rare Disorders (NORD) 55 Kenosia Avenue Danbury, CT 06810 Tel: 203-744-0100; Voice Mail: 800-999-NORD (6673) American Syringomyelia & Chiari Alliance Project (ASAP) P.O. Box 1586 Longview, TX 75606-1586 Tel: 903-236-7079; 800-ASAP-282 (272-7282) "Chiari Malformation Fact Sheet", NINDS, Publication date June 2013. NIH Publication No. 13-4839 Publicaciones en Español Office of Communications and Public Liaison National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda, MD 20892 NINDS health-related material is provided for information purposes only and does not necessarily represent endorsement by or an official position of the National Institute of Neurological Disorders and Stroke or any other Federal agency. Advice on the treatment or care of an individual patient should be obtained through consultation with a physician who has examined that patient or is familiar with that patient's medical history. All NINDS-prepared information is in the public domain and may be freely copied. Credit to the NINDS or the NIH is appreciated.	2	8	2	0	0	0	0.836085	2	3,380
I'm a member You will be redirected to myBlue. Would you like to continue? Please wait while you are redirected. Please enter a username and password. Printer Friendly Version Thermography is a noninvasive imaging technique that is intended to measure temperature distribution in organs and tissues. The visual display of this temperature information is known as a thermogram. Thermography has been proposed as a diagnostic tool, for treatment planning, and for evaluation of treatment effects for a variety of conditions. Thermography involves the use of an infrared scanning device and can include various types of telethermographic infrared detector images and heat-sensitive cholesteric liquid crystal systems. Infrared radiation from the skin or organ tissue reveals temperature variations by producing brightly colored patterns on a liquid crystal display. Interpretation of the color patterns is thought to assist in the diagnosis of many disorders such as complex regional pain syndrome (previously known as reflex sympathetic dystrophy), breast cancer, Raynaud phenomenon, digital artery vasospasm in hand-arm vibration syndrome, peripheral nerve damage following trauma, impaired spermatogenesis in infertile men, degree of burns, deep vein thrombosis, gastric cancer, tear-film layer stability in dry-eye syndrome, Frey syndrome, headaches, low back pain, and vertebral subluxation. Thermography may also assist in treatment planning and procedure guidance by identifying restricted areas of perfusion in coronary artery bypass grafting, identifying unstable atherosclerotic plaque, assessing response to methylprednisone in rheumatoid arthritis, and locating high undescended testicles. In 2002, the Dorex Spectrum 9000MB Thermography System (Dorex Inc.; Orange, CA) was cleared for marketing by the U.S. Food and Drug Administration (FDA) through the 510(k) process. The FDA determined that this device was substantially equivalent to existing devices for use in quantifying and visualizing skin temperature changes. Its indicated use is as an aid in diagnosis and follow-up therapy in areas such as orthopedics, pain management, neurology and diabetic foot care. This type of device is also known as a telethermographic system. In 2003, several teletheromographic cameras (Series A, E, P and S) by Flir Systems (McCordsville, IN) were cleared for marketing by the FDA through the 510(k) process. Their intended use is as an adjunct to other clinical diagnostic procedures when there is a need for quantifying differences in skin surface temperature. Between 2006 and 2009, three new or updated thermography devices received 510(k) marketing clearance from the FDA based on demonstrating substantial equivalence to existing products. The use of all forms of thermography is considered investigational. POLICY EXCEPTIONSFederal Employee Program (FEP) may dictate that all FDA-approved devices, drugs or biologics may not be considered investigational and thus these devices may be assessed only on the basis of their medical necessity. The coverage guidelines outlined in the Medical Policy Manual should not be used in lieu of the Member's specific benefit plan language. Investigative is defined as the use of any treatment procedure, facility, equipment, drug, device, or supply not yet recognized as a generally accepted standard of good medical practice for the treatment of the condition being treated and; therefore, is not considered medically necessary. For the definition of Investigative, “generally accepted standards of medical practice” means standards that are based on credible scientific evidence published in peer-reviewed medical literature generally recognized by the relevant medical community, and physician specialty society recommendations, and the views of medical practitioners practicing in relevant clinical areas and any other relevant factors. In order for equipment, devices, drugs or supplies [i.e, technologies], to be considered not investigative, the technology must have final approval from the appropriate governmental bodies, and scientific evidence must permit conclusions concerning the effect of the technology on health outcomes, and the technology must improve the net health outcome, and the technology must be as beneficial as any established alternative and the improvement must be attainable outside the testing/investigational setting. POLICY HISTORY7/1993: Issued 2/14/2002: Investigational definition added 5/8/2002: Type of Service and Place of Service deleted 5/14/2002: Code Reference section completed 6/23/2004: Policy reviewed, Description section aligned with BCBSA policy # 6.01.12, Sources updated 8/25/2005: Code Reference section reviewed, no changes 3/5/2008: Policy reviewed, no changes 12/31/2008: Code Reference section updated per 2009 CPT/HCPCS revisions 3/30/2009: Policy reviewed, no changes 07/30/2010: Policy description updated regarding FDA status of devices. FEP verbiage added to the Policy Exceptions section. Removed deleted codes 93760 and 93762 from the coding section as they were deleted on 12/31/2008, and added 93799. 07/29/2011: Policy reviewed; no changes. 07/13/2012: Policy reviewed; no changes. 08/14/2013: Policy reviewed; no changes. 06/18/2014: Policy reviewed; description updated. Policy statement unchanged. 08/27/2015: Code Reference section updated to add ICD-10 codes. 09/25/2015: Policy reviewed; policy statement unchanged. Investigative definition updated in the Policy Guidelines section. 05/31/2016: Policy number A.6.01.12 added. 10/12/2016: Policy description updated. Policy statement unchanged. SOURCE(S)Blue Cross Blue Shield Association policy # 6.01.12 CODE REFERENCEThis may not be a comprehensive list of procedure codes applicable to this policy. CPT copyright American Medical Association. All rights reserved. CPT is a registered trademark of the American Medical Association.	3	2	1	0	0	0	0.865567	1	1,241
I'm a member You will be redirected to myBlue. Would you like to continue? Please wait while you are redirected. Please enter a username and password. Printer Friendly Version DESCRIPTIONComputer-aided detection (CAD) has been suggested as an adjunct to screening mammograms to decrease errors in perception (i.e., failure to see an abnormality). The use of CAD systems requires a digital image, either generated by digitization of a prior screen-film mammogram (digitized mammogram), or generated directly (direct full-field digital mammogram). Commercially available CAD systems then use computerized algorithms for identifying suspicious regions of interest on the digital image. The locations of the abnormalities are marked such that the reader can then reference the same areas in the original mammogram for further review. The intent of CAD is to aid in detection of potential abnormalities for the radiologist to re-review. The radiologist, not CAD, makes the diagnosis if a clinically significant abnormality exists and whether future diagnostic evaluation is warranted. The distinction between digitized screen-film mammograms (SFM) and direct full-field digital mammograms (FFDM) is important. Since these two images are generated in different ways, the associated diagnostic performance of adjunctive CAD must be considered separately. Conceptually, the CAD systems used with digital mammography are very similar to those used with film mammography. The computer analyzes the digital images collected directly by the FFDM system, applies a set of algorithms that capture characteristics known to be associated potentially with malignancies, and produces an image with markings that show the site of suspicious findings. Sometimes, different marks are used for suspected masses and suspected microcalcifications. The major difference between CAD for FFDM and CAD for SFM is the extensive data set provided by the former and its interaction with the CAD algorithms. POLICYComputer-aided detection devices as an adjunct to single-reader interpretation of digitized screen-film mammograms may be considered medically necessary. Computer-aided detection devices as an adjunct to single-reader interpretation of direct, full-field digital mammography is considered investigational. The coverage guidelines outlined in the Medical Policy Manual should not be used in lieu of the Member's specific benefit plan language. Medically Necessary is defined as those services, treatments, procedures, equipment, drugs, devices, items or supplies furnished by a covered Provider that are required to identify or treat a Member's illness, injury or Nervous/Mental Conditions, and which Company determines are covered under this Benefit Plan based on the criteria as follows in A through D: A. consistent with the symptoms or diagnosis and treatment of the Member's condition, illness, or injury; and B. appropriate with regard to standards of good medical practice; and C. not solely for the convenience of the Member, his or her Provider; and D. the most appropriate supply or level of care which can safely be provided to Member. When applied to the care of an Inpatient, it further means that services for the Member's medical symptoms or conditions require that the services cannot be safely provided to the Member as an Outpatient. For the definition of Medically Necessary, “standards of good medical practice” means standards that are based on credible scientific evidence published in peer-reviewed medical literature generally recognized by the relevant medical community, and physician specialty society recommendations, and the views of medical practitioners practicing in relevant clinical areas and any other relevant factors. BCBSMS makes no payment for services, treatments, procedures, equipment, drugs, devices, items or supplies which are not documented to be Medically Necessary. The fact that a Physician or other Provider has prescribed, ordered, recommended, or approved a service or supply does not in itself, make it Medically Necessary. Investigative is defined as the use of any treatment procedure, facility, equipment, drug, device, or supply not yet recognized as a generally accepted standard of good medical practice for the treatment of the condition being treated and; therefore, is not considered medically necessary. For the definition of Investigative, “generally accepted standards of medical practice” means standards that are based on credible scientific evidence published in peer-reviewed medical literature generally recognized by the relevant medical community, and physician specialty society recommendations, and the views of medical practitioners practicing in relevant clinical areas and any other relevant factors. In order for equipment, devices, drugs or supplies [i.e, technologies], to be considered not investigative, the technology must have final approval from the appropriate governmental bodies, and scientific evidence must permit conclusions concerning the effect of the technology on health outcomes, and the technology must improve the net health outcome, and the technology must be as beneficial as any established alternative and the improvement must be attainable outside the testing/investigational setting. POLICY HISTORY4/9/2007: Policy added 5/11/2007: Bancorp South (C427, C445, C458, and C550) policy exception added 7/19/2007: Reviewed and approved by the Medical Policy Advisory Committee (MPAC) 5/9/2008: Policy reviewed, no changes 05/08/2013: Policy reviewed; no changes. 12/31/2014: Added the following new 2015 CPT codes to the Code Reference section: 77061, 77062, and 77063. Revised the description of the following HCPCS codes with an effective date of 01/01/2015: G0204 and G0206. 04/27/2015: Removed CPT codes 77061, 77062, and 77063 from the Code Reference section. These procedures are specifically addressed by the Digital Breast Tomosynthesis medical policy guidelines. 07/13/2015: Code Reference section updated for ICD-10. 09/17/2015: Policy Exceptions updated to remove language for BancorpSouth. 12/31/2015: Policy guidelines updated to add medically necessary and investigative definitions. Code Reference section updated to revise the description of the following CPT code with an effective date of 01/01/2016: 77057. 06/08/2016: Policy number L.6.01.416 added. 12/30/2016: Code Reference section updated to add new 2017 CPT codes 77065, 77066, and 77067. Revised code descriptions for HCPCS codes G0202, G0204, and G0206. SOURCE(S)Blue Cross Blue Shield Association Policy # 6.01.39 CODE REFERENCEThis may not be a comprehensive list of procedure codes applicable to this policy. The code(s) listed below are ONLY medically necessary if the procedure is performed according to the "Policy" section of this document. CPT copyright American Medical Association. All rights reserved. CPT is a registered trademark of the American Medical Association.	4	3	8	0	4	0	0.419006	12	1,428
Recent research identifying the underlying mechanisms of peripheral neuropathy, or nerve damage, has raised the prospect that drug therapies can be developed for the. Abstract. Neuropathy is the most common complication of diabetes. As a consequence of longstanding hyperglycemia, a downstream metabolic cascade leads to peripheral. Peripheral neuropathy is characterized by numbness, tingling, and/or pain, typically in the hands and feet, although these symptoms can occur in other areas of We Tested 100 Peripheral Neuropathy Brands. You Will Be Shocked At What We Found Diabetic Autonomic Neuropathy Syndrome Diabetic Autonomic Neuropathy Syndrome X is a serious problem that can adversely affect your health. In addition to weight problems Syndrome X has been linked to. Diabetic Autonomic Neuropathy and Circadian Misalignment in Type 1 Diabetes \| InTechOpen, Published on: 2013-02-27. Authors: Elena Matteucci and Ottavio Giampietro. When one is unable to feel things properly, How To Treat Peripheral Neuropathy? What Is Peripheral Neuropathy, And What Are Its Symptoms? Diabetic peripheral neuropathy is the most likely diagnosis for someone with diabetes who has pain in a. The mechanisms of diabetic neuropathy are poorly. Can Vitamins Cause Peripheral Neuropathy Peripheral Neuropathy Will Astound and Surprise You. The Causes of Peripheral Neuropathy will astound and surprise you. Why doctors don’t tell you these. Our Experts review the best products. Don’t try anything before you read. These include supplements like calcium, magnesium, acetyl-l-carnitine, alpha- lipoic-acid, vitamin E, B-complex vitamins (especially B1 and B12), glutathione. Regardless of Diabetic neuropathies are the most prevalent chronic complications of diabetes. This heterogeneous group of conditions affects different parts of the. Side Effects of Levaquin may cause peripheral neuropathy, aortic aneurysm or aortic dissection. Levaquin lawsuits are being reviewed nationwide. A widely accepted definition of diabetic peripheral neuropathy. mechanisms in the. of diabetic neuropathy. J Diabetes. TREATMENT OF DIABETES WITH CHINESE HERBS. by Subhuti Dharmananda, Ph.D., Director, Institute for Traditional Medicine, Portland, Updated diabetic neuropathy news, research articles and treatment options. Healthcare professionals get the latest diabetic peripheral neuropathy news for patient care. The following is a glossary of diabetes which explains terms connected with diabetes Introduction. The disability associated with acquired neuropathic foot deformities in individuals with diabetes mellitus is high. Diabetic peripheral neuropathy ( DMPN), peripheral vascu- lar disease, foot deformity, and previous foot ulceration or amputations have all been cited as risk factors for new and recurrent lower. This symposium on diabetic peripheral neuropathy (DPN) is a joint venture between the Danish Diabetes Academy and the International Diabetic Neuropathy Consortium and. Peripheral Neuropathy: Pathogenic Mechanisms. Mechanisms involved in diabetes-associated PN are. Pathophysiological Factors in Diabetic Peripheral Neuropathy european society of ophthalmology congress of the european society of ophthalmology (soe) 2017 10 -13 june, 2017, barcelona, spain abstracts scientific. @ Peripheral Neuropathy Diabetes ★★ Symptoms Of Being Pre Diabetic The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ PERIPHERAL. Although a number of the diabetic neuropathies may result in painful symptomatology, this review focuses on the most common: chronic sensorimotor distal symmetrical. New Hope for Neuropathy. Foot and ankle neuropathy has been a very confusing and debilitating disease. Once diagnosed little hope is given. Feb 6, 2015. Diabetic peripheral neuropathy (DPN) is a common long-term complication of type 2 diabetes and occurs in up to 50% of patients with long-standing disease.1. Although the exact mechanism of action is unknown, gabapentin is thought to disrupt excitatory neurotransmitter release through blockade of. A Current Overview of Diabetic Neuropathy – Mechanisms, Symptoms, Diagnosis, mechanisms of diabetic neuropathy. with diabetic peripheral neuropathy. Peripheral neuropathy has a variety of systemic, metabolic, and toxic causes. The most common treatable causes include diabetes mellitus, hypothyroidism. @ Causes Of Diabetic Peripheral Neuropathy ★★ Diabetes Medication Mechanism The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ CAUSES. Aug 1, 2003. Although increased flux of glucose through the polyol pathway leads to diabetic lesions in both the lenses and nerve, the mechanisms may be different. of DL- alpha-lipoic acid on peripheral nerve conduction, blood flow, energy metabolism, and oxidative stress in experimental diabetic neuropathy. Peripheral Neuropathy Fact. In diabetic neuropathy, anticonvulsant medications modulate pain through their mechanism of action on the peripheral nerves, Diabetes: Mechanism, Pathophysiology and Management-A Review, Anees A Siddiqui, Shadab A Siddiqui, Suhail Ahmad, Seemi Siddiqui, Iftikhar Ahsan, of SAT, hypoadiponectinaemia, and inflammation of adipose tissue; increased endogenous glucose production; and development of peripheral insulin resistance. Introduction; Neuropathic pain syndromes; Neuropathic pain disorders by etiology; Pathophysiologic processes subserving neuropathic pain; Neuropathic pain disorders. Diabetic neuropathy. Mechanisms of diabetic peripheral neuropathy. Hyperglycemia and the polyol pathway. Small-fiber neuropathy; HIV- associated. Management of Type 2 Diabetes Mellitus. The goals of therapy for type 2 DM are similar to those in type 1. While glycemic control tends to dominate the. ★ Treatment Diabetic Peripheral Neuropathy ★★ What Are Good Snacks For Diabetics ::The 3 Step Trick that Reverses Diabetes Permanently in As Little. ICD-10 Online contains the ICD-10 (International Classification of Diseases 10th Revision) Latest medical research on neuropathy including methods to ease pain, and new studies on nerve regeneration. Areas of Expertise Leg Pain and Peripheral Arterial Disease (PAD) What Is Lower Extremity Peripheral Arterial Disease (PAD) The inner lining of arterial. Jul 20, 2006. The protective mechanism of AGS-IV involved a decrease in declining blood glucose concentration and HbA1C levels, and an increase in plasma insulin. Keywords: Astragalus membranaceus, astragaloside IV, diabetic peripheral neuropathy, motor nerve conduction velocity, oxidative stress, advanced. This page contains alternative medicine approaches for a variety of diseases UPDATED 9-15-2017 http://www.chiro.org/alt_med_abstracts/Alternative_Medicine. Neuropathies characterized by Wallerian degeneration include those that are caused by trauma, infarction of peripheral nerve (diabetic mononeuropathy, vasculitis) and neoplastic infiltration. In distal axonopathy, degeneration of axon and myelin develops first in the most distal parts of the axon and, if the abnormality. neuropathy – experimental and clinical studies. of diabetic peripheral neuropathy have been utilized to better understand the. Mechanisms of diabetic neuropathy Diabetic neuropathy is a nerve disorder caused by diabetes where the patient experiences numbness and sometimes pain in the hands, feet, or legs. It’s. ★ Cure For Diabetic Peripheral Neuropathy ★★ Diabetic Foot Care Olympia Wa ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Jun 4, 2013. About half of the people with diabetes develop nerve damage within 10 to 20 years post diagnosis. Diabetic Peripheral Neuropathy is one of the most common chronic complication of diabetes and the main reason for the disability occurring in type 2 diabetes. The mechanism of the development of DPN has. Genetic types of PMP-22 gene mutations Duplication of one gene (3 total copies of PMP-22): Types Segmental duplication in gene area. Due to unequal. Nerve Report: 2017 Release. Don’t try anything before you read. Prevention and Treatment of Leg and Foot Ulcers in Diabetes Mellitus, a chapter in the Disease Management Online Medical Reference. Co-authored by Allan. More Neuropathy Articles ... - What Causes Peripheral Neuropathy In Diabetes: ★ Reversing Diabetic Peripheral Neuropathy ★★ How To Treat Diabetic Pain In Feet ::The 3 Step Trick that Reverses Diabetes Permanently in As Little. Imagine a "pins and needles" sensation that never went away. That’s what millions of people... - Sensory Peripheral Neuropathy Axonal: Peripheral nerves are nerves outside your brain and spinal cord. Learn about neuropathy and more than 100 other types of peripheral nerve disorders. Prevention Of Diabetic Neuropathy Mar 14, 2017. The American Diabetes Association recently released a... - Can You Reverse Neuropathy Diabetes: ⭐️\| diabetes \| ☀☀☀ can you reverse neuropathy diabetes ☀☀☀. You Want Something Special About diabetes? can you reverse neuropathy diabetes. Neuropathy may be the most common complication of diabetes and can make walking difficult as well as leading t... - Skin Microcirculation Of The Foot In Diabetic Neuropathy: URGO MEDICAL, a leading French company specializing in wound healing : wound care products, adhesive dressings. Find Health & Beauty At Target™.Buy Online & Pickup In-Store! TDP Lamp The only UL Approved TDP (Far Infrared Mineral) lamp in the... - Evaluation For Peripheral Neuropathy: Evaluation of Peripheral Neuropathy IN GENERAL symptoms of neuropathy in adults include paresthesias (sensory loss, tingling, burning) and/or clumsiness (weakness) Genetic Testing Peripheral Neuropathy From the latest cancer-fighting technology to ne... - Peripheral Nervous System Neuropathy: Learn about Overview of the Peripheral Nervous System from the Home Version of the Merck Manuals. The peripheral nervous system (PNS) is one of the two components of the nervous system, the other part is the central nervous system (CNS). The PNS. Per...	2	7	0	0	0	1	0.599529	1	2,262
Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets. Erythema nodosum is presumed to be a hypersensitivity reaction. It is often a dermatological manifestation of infectious, or other, disease. The eruptive phase begins with fever, aching and arthralgia whilst a painful rash usually appears within a couple of days. Lesions begin as red, tender nodules. The borders are poorly defined and they are 2-6 cms in diameter. In the first week the lesions become tense, hard and painful. In the second week, they may become fluctuant, rather like an abscess but they do not suppurate or ulcerate. Individual lesions last around two weeks but occasionally, new lesions continue to appear for three to six weeks. Aching legs and swollen ankles may persist for many weeks. In the first week they are bright red but in the second week there is a blue or purple hue, even turning yellow like a resolving bruise before disappearing in a couple of weeks. They can occur anywhere but are usually on the anterior aspect of the lower leg. When the aetiology is an infection the lesions usually heal in six to eight weeks but 30% of idiopathic cases last six months. Arthralgia occurs in more than half of patients and begins either during the eruptive phase or two to four weeks before. Joints are red, swollen and tender, sometimes with effusions. Morning stiffness may occur. The ankles, knees and wrists are most often involved. Synovitis resolves in a few weeks but joint pain and stiffness may last up to six months. There are no destructive changes in the joint and synovial fluid is acellular and the rheumatoid factor is negative. - Erythema nodosum is often indicative of an underlying infectious disease but a cause is not always found. Some underlying causes are not infectious. - Streptococcal infection is the most common underlying cause and so it may be a feature of other diseases, including scarlet fever and rheumatic fever, although in the UK nowadays the former is uncommon and the latter rare. - Sarcoidosis is also commonly involved in adults, although it is not infectious in origin. - Tuberculosis must be considered. - Leprosy can produce a clinical picture of erythema nodosum, although the histological picture of the lesions is different. - Various forms of gastroenteritis - especially Yersinia enterocolitica, Salmonella spp. and Campylobacter spp. - can be associated. - Lymphogranuloma venereum may be a cause. - Mycoplasma pneumonia can be associated. - Fungal infections are less common in the UK but coccidioidomycosis is important in Southwest USA. It may occur in histoplasmosis and blastoplasmosis. - Sulfonamides are used less often nowadays but other drugs to be implicated include sulfonylureas, gold and oral contraceptives. - It may correlate with flare-up of Crohn's disease or ulcerative colitis. - It can precede the diagnosis of Hodgkin's lymphoma and non-Hodgkin's lymphoma by months and it can accompany Behçet's syndrome. - It may occur in pregnancy when it is usually in the second trimester. It is likely to recur in future pregnancies and may occur with oral contraceptives. - There are rare cases (<1 in 100) associated with Epstein-Barr virus, hepatitis B and hepatitis C and HIV. - In many cases no cause is found. Although in many cases it is idiopathic, it is important to exclude serious underlying disease: - A throat swab for streptococcus is the first test, although it may well be negative, even with streptococcal disease. - Anti-streptococcal O (ASO) titre may be more helpful, although a normal titre does not exclude infection. A rising titre may be more valuable. - Arrange an FBC and ESR. ESR is often very high regardless of the aetiology, and CRP may be more contributory. - Stool examination for Y. enterocolitica, Salmonella spp. and Campylobacter spp. may yield results, as may blood cultures - In sarcoidosis, calcium and angiotensin-converting enzyme (ACE) are often raised. - CXR may show bilateral hilar lymphadenopathy (BHL) in sarcoidosis, unilateral or asymmetrical adenopathy in malignancy, or evidence of pulmonary tuberculosis. - Intradermal skin tests may be required to exclude tuberculosis and coccidioidomycosis. - Excisional biopsy may be helpful where the diagnosis is in doubt. - Erythema induratum (modular vasculitis). - Insect bites. - Acute urticaria. - Familial Mediterranean fever. - Superficial thrombophlebitis (standard or superficial migratory thrombophlebitis). - Most cases are self-limiting and require only symptomatic relief. - If an infective aetiology has been discovered then appropriate therapy is in order but it should not be given blind. - A degree of relief can be obtained with cool compresses and bed rest with elevation of the foot of the bed. Bed rest has been advocated for many years and is anecdotally useful but the evidence base is lacking. - Non-steroidal anti-inflammatory drugs (NSAIDs) are useful and no other drugs are usually needed. Steroids are beneficial but should be used with caution and may be contra-indicated if infection has not been excluded. - In difficult cases, oral potassium iodide may be valuable, as may tetracycline and, in erythema nodosum of leprosy, thalidomide has seen a resurgence but further research is required[10, 11, 12]. The condition usually resolves within six weeks but it may be more protracted, especially if the underlying cause remains or when it is idiopathic. Serious complications are unusual unless part of the underlying disease. Chronic or recurrent disease is rare. Lesions heal without atrophy or scarring. Did you find this information useful? Further reading & references - Shimizu M, Hamaguchi Y, Matsushita T, et al; Sequentially appearing erythema nodosum, erythema multiforme and Henoch-Schonlein purpura in a patient with Mycoplasma pneumoniae infection: a case report. J Med Case Rep. 2012 Nov 23 6(1):398. doi: 10.1186/1752-1947-6-398. - Erythema Nodosum; Primary Care Dermatology Society - Whig J, Mahajan V, Kashyap A, et al; Erythema nodosum: Atypical presentation of common disease. Lung India. 2010 Jul 27(3):181-2. doi: 10.4103/0970-2113.68319. - Min MS, Fischer R, Fournier JB; Unilateral Erythema Nodosum following Norethindrone Acetate, Ethinyl Estradiol, and Ferrous Fumarate Combination Therapy. Case Rep Obstet Gynecol. 2016 2016:5726416. doi: 10.1155/2016/5726416. Epub 2016 Mar 27. - Mantadakis E, Arvanitidou V, Tsalkidis A, et al; Erythema nodosum associated with Salmonella enteritidis. Hippokratia. 2010 Jan 14(1):51-3. - Babamahmoodi F, Babamahmoodi A, Barani H, et al; Simultaneous occurrence of erythema nodosum in monozygotic twin sisters. Case Rep Med. 2012 2012:109427. doi: 10.1155/2012/109427. Epub 2012 Jun 5. - Schwartz RA, Nervi SJ; Erythema nodosum: a sign of systemic disease. Am Fam Physician. 2007 Mar 1 75(5):695-700. - Fowler A, Dargan P, Jones A; Puzzling hypercalcaemia: sarcoidosis without lung involvement. J R Soc Med. 2005 Feb 98(2):60-1. - Yi SW, Kim EH, Kang HY, et al; Erythema nodosum: clinicopathologic correlations and their use in differential diagnosis. Yonsei Med J. 2007 Aug 31 48(4):601-8. - Tabak F, Murtezaoglu A, Tabak O, et al; Clinical features and etiology of adult patients with Fever and rash. Ann Dermatol. 2012 Nov 24(4):420-5. doi: 10.5021/ad.2012.24.4.420. Epub 2012 Nov 8. - Passarini B, Infusino SD; Erythema nodosum. G Ital Dermatol Venereol. 2013 Aug 148(4):413-7. - Van Veen NH, Lockwood DN, van Brakel WH, et al; Interventions for erythema nodosum leprosum. Cochrane Database Syst Rev. 2009 Jul 8 (3):CD006949. doi: 10.1002/14651858.CD006949.pub2. - Gilchrist H, Patterson JW; Erythema nodosum and erythema induratum (nodular vasculitis): diagnosis and management. Dermatol Ther. 2010 Jul-Aug 23(4):320-7. - Wan P, Zhao X, Hunasehally RY, et al; Propylthiouracil-induced ANCA-positive erythema nodosum treated with thalidomide. Int J Dermatol. 2012 Mar 51(3):345-8. doi: 10.1111/j.1365-4632.2011.05135.x. Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Patient Platform Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.	2	9	2	0	0	0	0.505339	2	2,287
In many cases, patients who present to the emergency department with symptoms of nausea, vomiting, diarrhea and abdominal pain are diagnosed with gastroenteritis after their visit to the emergency department. Gastroenteritis is one of the top 25 diagnosis codes worked up in the emergency department and coded by McKesson Emergency Department coders. Gastroenteritis is defined as “inflammation of the lining of the stomach and intestines, predominantly manifested by upper gastrointestinal (GI) tract symptoms (anorexia, nausea, vomiting), diarrhea, and abdominal discomfort.”1 Many differential conditions are taken into consideration after the physician obtains the patient’s past medical history (i.e. if the patient was on any medications, like antibiotics) and history of recent contact with any food, water, or people who might be infected with certain microorganisms. The physician would also conduct a thorough physical examination before considering any management options of diagnostic study or therapeutic intervention. Gastroenteritis may be of non-specific, uncertain, unknown etiology or of viral, bacteria, or parasitic etiology. Moreover, gastroenteritis can present as either non-infectious or infectious. The type and severity of the condition’s symptoms would depend on what may have caused the symptoms, the length of the occurrence, the patient’s tolerance level and how much of the patient’s organ system is contaminated/affected. The severity of the condition will directly affect the gastrointestinal system and then associated organ systems, all requiring the need for additional medical attention. As an example, if a patient complains of nausea, vomiting and persistent diarrhea, that patient will become, to some degree, dehydrated and may require fluid/electrolyte replacement therapy. Treatment generally includes bed rest with easy access to the bathroom being desirable, fluids as can be tolerated, but even while still vomiting, sips of fluids are recommended. If the condition shows severe dehydration, IV replacement of electrolytes may be necessary, and even antiemetic (a drug that is effective against vomiting and nausea) medication may be warranted. There is a one-to-one crosswalk (ICD-9 to ICD-10) for Gastroenteritis, not otherwise specified (NOS) but both ICD-9 and ICD-10 contain many other types of gastroenteritis including, but not limited to, what is shown on the table below. As mentioned above, treatment for gastroenteritis depends on the patient’s presentation, age and any current or historical underlying conditions. It is imperative that the provider document exactly what the examination and the diagnostic studies’ findings are, if any, to determine the exact course of action for the condition presented or defined after study. This will also allow the coding staff to select the most appropriate ICD-9 or ICD-10 diagnosis code for reporting on the claim for reimbursement. - ICD-10-CM, 2014 Complete Draft Code Set, Chapter 11, Page 621, Symptoms, Signs, and Abnormal Clinical and Laboratory Findings, not Elsewhere Classified (K00 – K95), AAPC, Optuminsight 2013 - ICD-9-CM, 2014, Sixth Edition, 9th Revision, Clinical Modification, Chapter 9, Page 171, Diseases of the Digestive System (codes 520 - 579), Editor – Anita C. Hart, Optuminsight August 2013 - Merck Manual, Section 3, Pages 283 – 293, Editor – Keryn A. G. Lane, Publisher – Gary Zelko, June 1999	4	6	0	0	0	2	0.858272	2	743
Puzzled by Diabetes Coding? Test Your Diabetes Coding Know-how By Sheri Poe Bernard, CPC, CPC-H, CPC-P You probably think your knowledge of one of the most common diseases in the United States is complete. Here’s a quick true/false quiz to test that premise. True or false? - Abnormally high blood glucose is the hallmark of all types of diabetes. - Diabetes mellitus is caused by eating too much sugar. - Type I diabetics are insulin dependent; Type II diabetics are not. - If the chart says “diabetes” without any more detail, the default diagnosis is always 250.00 Diabetes mellitus, type II, not stated as uncontrolled. - A patient with a documented blood sugar of 400 should be classified as “uncontrolled.” - Post-pancreatectomy is a form of secondary diabetes and would be reported with a code from the 249 Secondary diabetes category. Let’s explore the answers. Abnormally high blood glucose is the hallmark of all types of diabetes. Answer: False. Diabetes incipidus does not cause hyperglycemia. Diabetes has its roots in a Greek word for “that which passes through,” and refers to frequent urination. All types of diabetes have a clinical picture including polyuria. “Mellitus” has its root in the Latin word for “honey,” indicating sweet urine. “Insipidus” has its roots in Latin for “devoid of interest or taste.” Diabetes insipidus (DI) is an endocrine disorder associated with the antidiuretic hormone, vasopressin. It can be caused by problems in the pituitary gland or the kidneys. Blood sugars are not affected, and so DI should never be reported using the codes for diabetes mellitus (DM). In DI, the body is unable to concentrate urine in the kidneys and shunts all fluids there. The patient with untreated DI is constantly drinking, and constantly producing very dilute urine. DI may be due to a deficiency in the pituitary gland and production of vasopressin, reported with 253.5 Disorders of the pituitary gland and its hypothalamic control; diabetes insipidus. It can also be attributed to vasopressin resistance caused by a kidney disorder, which is reported with 588.1 Disorders resulting from impaired renal function; nephrogenic diabetes insipidus. These conditions may be chronic, or may resolve with treatment (for example, excision of a pituitary tumor). They can be treated with administration of vasopressin, usually through nose drops. Diabetes mellitus is caused by eating too much sugar. Answer: False. Diabetes mellitus is not caused by eating too much sugar or too many simple carbohydrates. Type II DM occurs when the insulin-producing cells within the pancreas can no longer produce enough insulin, or when the insulin produced is not delivered efficiently to where it is needed. It can be caused by obesity (pancreas can’t produce enough); age (pancreas isn’t as efficient); or genetics (the system breaks down). Consumption of sugar or other simple carbohydrates will not cause diabetes, although overeating can lead to obesity, which can cause Type II diabetes. Type I diabetics are insulin dependent; Type II diabetics are not. Answer: False. Type I diabetics are insulin dependent, but Type II can be insulin dependent or not. Type I DM is an autoimmune disease that destroys the patient’s ability to produce insulin. During the early stages of the disease, the patient may produce some insulin, but eventually none is produced. Type I diabetics are always insulin dependent. Type II diabetics can often control their blood sugars with a combination of diet, exercise, and oral medication. Some Type II diabetics cannot control their blood sugars except through insulin injections. Some Type II diabetics are insulin dependent, and for them, V58.67 Long term current use of insulin is reported secondarily. If the chart says “diabetes” without any more detail, the default diagnosis is always 250.00. Answer: False. This one is almost always true, but you need to watch for the exceptions. If the chart says “diabetes” without any more detail, the default diagnosis is 250.00, unless the patient has diabetic ketoacidosis (DKA). With DKA, the diagnosis of “diabetes” defaults to Type I, since most diabetics who develop DKA are Type I diabetics. DKA occurs when a shortage of insulin causes the body to break down fat and muscle for energy. The byproduct of this process is ketones, which enter the bloodstream and cause a dangerous form of acidosis. In DKA, the patient is severely dehydrated and confused. Due to the electrolyte imbalance caused by DKA, hospitalization is required to stabilize the blood chemistry and restore hydration. A patient with a documented blood sugar of 400 should be classified as “uncontrolled.” Answer: False. The only time it is appropriate to use fifth digits 2 (type II, uncontrolled) or 3 (type I, uncontrolled) is when the clinical documentation supports a diagnosis of “uncontrolled.” Terms like “poorly controlled” do not qualify as uncontrolled, either. If you have any concerns about the status of the patient, query the clinician. A “normal” blood sugar range varies greatly from patient to patient. Only clinicians familiar with their patient’s hemoglobin patterns can assign a diagnosis of “uncontrolled.” Post-pancreatectomy is a form of secondary diabetes and would be reported with a code from 249. Answer: False. The removal of a pancreas does have the secondary effect of causing diabetes, since the production of insulin is stopped. This makes pancreatectomy a form of secondary diabetes. However, ICD-9-CM classifies this form of secondary diabetes to 251.3 Other disorders of pancreatic internal secretion; Postsurgical hypoinsulinemia to segregate iatrogenic hypoinsulinemia from that caused by infection or disease of the pancreas. Know the Who, What, and When of Diabetes Screening The Centers for Disease Control (CDC) recently announced the number of diabetics in the United States exceeds 24 million people —that’s more people than the population of New York City—in fact, more than the entire state of New York. Another 57 million are estimated to have pre-diabetes, a condition with impaired glucose tolerance. Diabetes interferes with a patient’s ability to convert food into energy, resulting in elevation of glucose in the blood and urine. In Type I diabetes (250.x1, 250.x3), an autoimmune disorder destroys all insulin-producing cells and the patient must inject or inhale insulin to survive. In Type II diabetes (250.x0, 250.x2), age, weight, or genetic predisposition hobbles insulin production or transportation, so control of blood sugar is hindered. Some Type II patients control their diabetes with diet, while others require oral medications or insulin. Secondary diabetes (249.xx) occurs when a drug, infection, or other issue reduces insulin efficiencies in the body. Patients can live for many years without knowing they have Type II diabetes. Untreated or uncontrolled Type II diabetes can lead to complications affecting the eyes, circulatory system, kidneys, and nerves. Screening programs are an important component of pay for performance, but Medicare’s Physician Quality Reporting Initiative (PQRI) currently has no performance measure associated with early diagnosis and treatment to mitigate long-term complications of diabetes. PQRI has plenty of measurements for patients already diagnosed with diabetes, but nothing for diabetes screening. Watch for it in the future. Diabetes screening involves testing the blood glucose level of patients without symptoms or history of diabetes. Because the symptoms associated with undiagnosed Type I diabetes are life-threatening, these patients typically are diagnosed during emergency care, not a routine screening test. Diabetes screening campaigns target asymptomatic Type II diabetes. Physician coders can safeguard provider’s resources by knowing the who, what, and when of diabetes screening payments, and ensuring accurate and appropriate coding. Medicare covers diabetes screening tests for patients with pre-diabetes, high blood pressure, high cholesterol, a BMI of greater than 30 or any two of the following: BMI of 25-29; family history of diabetes; age of 65 or greater; or a history of gestational diabetes. Some private plans now pay for diabetes screening tests in patients who are 45 years or older, a protocol recently endorsed by the American Diabetes Association. Ethnicity plays a role in adults who have diabetes too, with American Indians and Alaska Natives an incidence of diabetes of 16.5 percent; blacks, 11.8 percent; Hispanics, 10.4 percent; Asian Americans, 7.5 percent; and whites, 6.6 percent. The CDC reports 25 percent of the population over the age of 60 had diabetes in 2007, and diabetes is the seventh leading cause of death in the nation. For Medicare, claims for diabetes screening tests should link the diagnosis V77.1 Special screening for diabetes mellitus with one of the following CPT® procedures: 82947 Glucose; quantitative, blood (except reagent strip) 82950 Glucose; post glucose dose (includes glucose) 82951 Glucose; tolerance test (GTT), three specimens (includes glucose) If a patient is diagnosed with pre-diabetes, the CPT® code should be reported with modifier TS Follow-up service. This allows CMS to more accurately track the pre-diabetic patients’ screening, and also allows for higher frequency of the screening. Screening for pre-diabetic patients is reimbursed at the highest frequency: once every six months by Medicare. Patients who qualify for screening but are not pre-diabetic may be tested once annually. The private plans for screenings of 45-year-old or older patients generally cover once every three years, unless other conditions provide medical necessity for annual testing. Do the math: How many patients in your practice are over the age of 65, obese, or experience elevated cholesterol or blood pressure? Unless you work in a pediatric clinic, the lion’s share of patients may fall into the category qualifying them for diabetes screening tests. Are these tests scheduled, documented, and billed with the frequency you would expect? Even at a reimbursement rate of $25, your practice may be leaving a lot of money—and a lot of preventive care—on the table if you aren’t performing diabetic screenings routinely. For more information on diabetes screening, see MLN Matters article SE0821 and Job Aid JA0821 on the CMS website.	4	13	2	0	0	3	0.911335	5	2,319
Classification of mental disorders The classification of mental disorders, also known as psychiatric nosology or psychiatric taxonomy, is a key aspect of psychiatry and other mental health professions and an important issue for people who may be diagnosed. There are currently two widely established systems for classifying mental disorders: - Chapter V of the International Classification of Diseases (ICD-10) produced by the World Health Organization (WHO) - The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) produced by the American Psychiatric Association (APA). Both list categories of disorders thought to be distinct types, and have deliberately converged their codes in recent revisions so that the manuals are often broadly comparable, although significant differences remain. Other classification schemes may be in use more locally, for example the Chinese Classification of Mental Disorders. Other manuals have some limited use by those of alternative theoretical persuasions, such as the Psychodynamic Diagnostic Manual. The widely used DSM and ICD classifications employ operational definitions. There is a significant scientific debate about the relative validity of a "categorical" versus a "dimensional" system of classification, as well as significant controversy about the role of science and values in classification schemes and the professional, legal and social uses to which they are put. - 1 Definitions - 2 ICD-10 - 3 DSM-IV - 4 Other schemes - 5 Childhood diagnosis - 6 Usage - 7 Types of classification schemes - 8 Cultural differences - 9 Historical development - 10 Criticism - 11 See also - 12 References - 13 External links In the scientific and academic literature on the definition or categorization of mental disorders, one extreme argues that it is entirely a matter of value judgments (including of what is normal) while another proposes that it is or could be entirely objective and scientific (including by reference to statistical norms); other views argue that the concept refers to a "fuzzy prototype" that can never be precisely defined, or that the definition will always involve a mixture of scientific facts (e.g. that a natural or evolved function isn't working properly) and value judgments (e.g. that it is harmful or undesired). Lay concepts of mental disorder vary considerably across different cultures and countries, and may refer to different sorts of individual and social problems. The WHO and national surveys report that there is no single consensus on the definition of mental disorder/illness, and that the phrasing used depends on the social, cultural, economic and legal context in different contexts and in different societies. The WHO reports that there is intense debate about which conditions should be included under the concept of mental disorder; a broad definition can cover mental illness, mental retardation, personality disorder and substance dependence, but inclusion varies by country and is reported to be a complex and debated issue. There may be a criterion that a condition should not be expected to occur as part of a person's usual culture or religion. However, despite the term "mental", there is not necessarily a clear distinction drawn between mental (dys)functioning and brain (dys)functioning, or indeed between the brain and the rest of the body. Most international clinical documents avoid the term "mental illness", preferring the term "mental disorder". However, some use "mental illness" as the main overarching term to encompass mental disorders. Some consumer/survivor movement organizations oppose use of the term "mental illness" on the grounds that it supports the dominance of a medical model. The term "serious mental impairment" (SMI) is sometimes used to refer to more severe and long-lasting disorders while "mental health problems" may be used as a broader term, or to refer only to milder or more transient issues. Confusion often surrounds the ways and contexts in which these terms are used. The International Classification of Diseases (ICD) is an international standard diagnostic classification for a wide variety of health conditions. The ICD-10 states that mental disorder is "not an exact term", although is generally used "...to imply the existence of a clinically recognisable set of symptoms or behaviours associated in most cases with distress and with interference with personal functions." (WHO, 1992). Chapter V focuses on "mental and behavioural disorders" and consists of 10 main groups: - F0: Organic, including symptomatic, mental disorders - F1: Mental and behavioural disorders due to use of psychoactive substances - F2: Schizophrenia, schizotypal and delusional disorders - F3: Mood [affective] disorders - F4: Neurotic, stress-related and somatoform disorders - F5: Behavioural syndromes associated with physiological disturbances and physical factors - F6: Disorders of personality and behaviour in adult persons - F7: Mental retardation - F8: Disorders of psychological development - F9: Behavioural and emotional disorders with onset usually occurring in childhood and adolescence - In addition, a group of "unspecified mental disorders". Within each group there are more specific subcategories. The WHO is revising their classifications in this section as part of the development of the ICD-11 (revision due by 2018) and an "International Advisory Group" has been established to guide this. The DSM-IV was originally published in 1994 and listed more than 250 mental disorders. It was produced by the American Psychiatric Association and it characterizes mental disorder as "a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual,...is associated with present distress...or disability...or with a significant increased risk of suffering" but that "...no definition adequately specifies precise boundaries for the concept of 'mental disorder'...different situations call for different definitions" (APA, 1994 and 2000). The DSM also states that "there is no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries dividing it from other mental disorders or from no mental disorder." The DSM-IV-TR (Text Revision, 2000) consists of five axes (domains) on which disorder can be assessed. The five axes are: - Axis I: Clinical Disorders (all mental disorders except Personality Disorders and Mental Retardation) - Axis II: Personality Disorders and Mental Retardation - Axis III: General Medical Conditions (must be connected to a Mental Disorder) - Axis IV: Psychosocial and Environmental Problems (for example limited social support network) - Axis V: Global Assessment of Functioning (Psychological, social and job-related functions are evaluated on a continuum between mental health and extreme mental disorder) The main categories of disorder in the DSM are: - The Chinese Society of Psychiatry's Chinese Classification of Mental Disorders (currently CCMD-3) - The Latin American Guide for Psychiatric Diagnosis (GLDP). - The Research Domain Criteria (RDoC), a framework being developed by the National Institute of Mental Health Child and adolescent psychiatry sometimes uses specific manuals in addition to the DSM and ICD. The Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (DC:0-3) was first published in 1994 by Zero to Three to classify mental health and developmental disorders in the first four years of life. It has been published in 9 languages. The Research Diagnostic criteria-Preschool Age (RDC-PA) was developed between 2000 and 2002 by a task force of independent investigators with the goal of developing clearly specified diagnostic criteria to facilitate research on psychopathology in this age group. The French Classification of Child and Adolescent Mental Disorders (CFTMEA), operational since 1983, is the classification of reference for French child psychiatrists. The ICD and DSM classification schemes have achieved widespread acceptance in psychiatry. A survey of 205 psychiatrists, from 66 different countries across all continents, found that ICD-10 was more frequently used and more valued in clinical practice and training, while the DSM-IV was more frequently used in clinical practice in the United States and Canada, and was more valued for research, with accessibility to either being limited, and usage by other mental health professionals, policy makers, patients and families less clear. . A primary care (e.g. general or family physician) version of the mental disorder section of ICD-10 has been developed (ICD-10-PHC) which has also been used quite extensively internationally. A survey of journal articles indexed in various biomedical databases between 1980 and 2005 indicated that 15,743 referred to the DSM and 3,106 to the ICD. In Japan, most university hospitals use either the ICD or DSM. ICD appears to be the somewhat more used for research or academic purposes, while both were used equally for clinical purposes. Other traditional psychiatric schemes may also be used. Types of classification schemes The classification schemes in common usage are based on separate (but may be overlapping) categories of disorder schemes sometimes termed "neo-Kraepelinian" (after the psychiatrist Kraepelin) which is intended to be atheoretical with regard to etiology (causation). These classification schemes have achieved some widespread acceptance in psychiatry and other fields, and have generally been found to have improved inter-rater reliability, although routine clinical usage is less clear. Questions of validity and utility have been raised, both scientifically and in terms of social, economic and political factors—notably over the inclusion of certain controversial categories, the influence of the pharmaceutical industry, or the stigmatizing effect of being categorized or labelled. Some approaches to classification do not use categories with single cut-offs separating the ill from the healthy or the abnormal from the normal (a practice sometimes termed "threshold psychiatry" or "dichotomous classification"). Some approaches go further and propose continuously-varying dimensions that are not grouped into spectra or categories; each individual simply has a profile of scores across different dimensions. DSM-5 planning committees are currently seeking to establish a research basis for a hybrid dimensional classification of personality disorders. However, the problem with entirely dimensional classifications is they are said to be of limited practical value in clinical practice where yes/no decisions often need to be made, for example whether a person requires treatment, and moreover the rest of medicine is firmly committed to categories, which are assumed to reflect discrete disease entities. While the Psychodynamic Diagnostic Manual has an emphasis on dimensionality and the context of mental problems, it has been structured largely as an adjunct to the categories of the DSM. Nevertheless, non-categorical clinical formulation approaches are commonly employed in clinical psychology and some areas of psychiatry, where there may be limited or no reference to diagnostic categories. One such approach advocates taking each specific complaint reported by an individual on its own merits, treated as a phenomenon with its own causes. Descriptive vs Somatic Descriptive classifications are based almost exclusively on either descriptions of behavior as reported by various observers, such as parents, teachers, and medical personnel; or symptoms as reported by individuals themselves. As such, they are quite subjective, not amenable to verification by third parties, and not readily transferable across chronologic and/or cultural barriers. Somatic nosology, on the other hand, is based almost exclusively on the objective histologic and chemical abnormalities which are characteristic of various diseases and can be identified by appropriately trained pathologists. While not all pathologists will agree in all cases, the degree of uniformity allowed is orders of magnitude greater than that enabled by the constantly changing classification embraced by the DSM system. Classification schemes may not apply to all cultures. The DSM is based on predominantly American research studies and has been said to have a decidedly American outlook, meaning that differing disorders or concepts of illness from other cultures (including personalistic rather than naturalistic explanations) may be neglected or misrepresented, while Western cultural phenomena may be taken as universal. Culture-bound syndromes are those hypothesized to be specific to certain cultures (typically taken to mean non-Western or non-mainstream cultures); while some are listed in an appendix of the DSM-IV they are not detailed and there remain open questions about the relationship between Western and non-Western diagnostic categories and sociocultural factors, which are addressed from different directions by, for example, cross-cultural psychiatry or anthropology. In Ancient Greece, Hippocrates and his followers are generally credited with the first classification system for mental illnesses, including mania, melancholia, paranoia, phobias and Scythian disease (transvestism). They held that they were due to different kinds of imbalance in four humors. Middle ages to Renaissance An elaborate classification of mental disorders was developed in the 10th century by Arabian psychologist Najab ud-din Unhammad. His nosology included nine major categories of mental disorders, with 30 different mental illnesses in total. Some of the categories he described resembled obsessive-compulsive disorders, delusional disorders, degenerative diseases, involutional melancholia, and states of abnormal excitement. Avicenna (980−1037 CE) in the Canon of Medicine listed a number of mental disorders, including "passive male homosexuality". Laws generally distinguished between "idiots" and "lunatics". Thomas Sydenham (1624–1689), the "English Hippocrates", emphasized careful clinical observation and diagnosis and developed the concept of a syndrome, a group of associated symptoms having a common course, which would later influence psychiatric classification. Evolution in the scientific concepts of psychopathology (literally referring to diseases of the mind) took hold in the late 18th and 19th centuries following the Renaissance and Enlightenment. Individual behaviors that had long been recognized came to be grouped into syndromes. Boissier de Sauvages developed an extremely extensive psychiatric classification in the mid-18th century, influenced by the medical nosology of Thomas Sydenham and the biological taxonomy of Carl Linnaeus. It was only part of his classification of 2400 medical diseases. These were divided into 10 "classes", one of which comprised the bulk of the mental diseases, divided into four "orders" and 23 "genera". One genus, melancholia, was subdivided into 14 "species". William Cullen advanced an influential medical nosology which included four classes of neuroses: coma, adynamias, spasms, and vesanias. The vesanias included amentia, melancholia, mania, and oneirodynia. Towards the end of the 18th century and into the 19th, Pinel, influenced by Cullen's scheme, developed his own, again employing the terminology of genera and species. His simplified revision of this reduced all mental illnesses to four basic types. He argued that mental disorders are not separate entities but stem from a single disease that he called "mental alienation". Attempts were made to merge the ancient concept of delirium with that of insanity, the latter sometimes described as delirium without fever. On the other hand, Pinel had started a trend for diagnosing forms of insanity 'without delirium' (meaning hallucinations or delusions) – a concept of partial insanity. Attempts were made to distinguish this from total insanity by criteria such as intensity, content or generalization of delusions. Pinel's successor, Esquirol, extended Pinel's categories to five. Both made a clear distinction between insanity (including mania and dementia) as opposed to mental retardation (including idiocy and imbecility). Esquirol developed a concept of monomania—a periodic delusional fixation or undesirable disposition on one theme—that became a broad and common diagnosis and a part of popular culture for much of the 19th century. The diagnosis of "moral insanity" coined by James Prichard also became popular; those with the condition did not seem delusional or intellectually impaired but seemed to have disordered emotions or behavior. The botanical taxonomic approach was abandoned in the 19th century, in favor of an anatomical-clinical approach that became increasingly descriptive. There was a focus on identifying the particular psychological faculty involved in particular forms of insanity, including through phrenology, although some argued for a more central "unitary" cause. French and German psychiatric nosology was in the ascendency. The term "psychiatry" ("Psychiatrie") was coined by German physician Johann Christian Reil in 1808, from the Greek "ψυχή" (psychē: "soul or mind") and "ιατρός" (iatros: "healer or doctor"). The term "alienation" took on a psychiatric meaning in France, later adopted into medical English. The terms psychosis and neurosis came into use, the former viewed psychologically and the latter neurologically. In the second half of the century, Karl Kahlbaum and Ewald Hecker developed a descriptive categorizion of syndromes, employing terms such as dysthymia, cyclothymia, catatonia, paranoia and hebephrenia. Wilhelm Griesinger (1817–1869) advanced a unitary scheme based on a concept of brain pathology. French psychiatrists Jules Baillarger described "folie à double forme" and Jean-Pierre Falret described "la folie circulaire"—alternating mania and depression. The concept of adolescent insanity or developmental insanity was advanced by Scottish psychiatrist Thomas Coulston in 1873, describing a psychotic condition which generally afflicted those aged 18–24 years, particularly males, and in 30% of cases proceeded to "a secondary dementia". The concept of hysteria (wandering womb) had long been used, perhaps since ancient Egyptian times, and was later adopted by Freud. Descriptions of a specific syndrome now known as somatization disorder were first developed by the French physician, Paul Briquet in 1859. An American physician, Beard, described "neurasthenia" in 1869. German neurologist Westphal, coined the term "obsessional neurosis" now termed obsessive-compulsive disorder, and agoraphobia. Alienists created a whole new series of diagnoses that highlighted single, impulsive behavior, such as kleptomania, dipsomania, pyromania, and nymphomania. The diagnosis of drapetomania was also developed in the Southern United States to explain the perceived irrationality of black slaves trying to escape what was thought to be a suitable role. The scientific study of homosexuality began in the 19th century, informally viewed either as natural or as a disorder. Kraepelin included it as a disorder in his Compendium der Psychiatrie that he published in successive editions from 1883. In the late 19th century, Koch referred to "psychopathic inferiority" as a new term for moral insanity. In the 20th century the term became known as "psychopathy" or "sociopathy", related specifically to antisocial behavior. Related studies led to the DSM-III category of antisocial personality disorder. Influenced by the approach of Kahlbaum and others, and developing his concepts in publications spanning the turn of the century, German psychiatrist Emil Kraepelin advanced a new system. He grouped together a number of existing diagnoses that appeared to all have a deteriorating course over time—such as catatonia, hebephrenia and dementia paranoides—under another existing term "dementia praecox" (meaning "early senility", later renamed schizophrenia). Another set of diagnoses that appeared to have a periodic course and better outcome were grouped together under the category of manic-depressive insanity (mood disorder). He also proposed a third category of psychosis, called paranoia, involving delusions but not the more general deficits and poor course attributed to dementia praecox. In all he proposed 15 categories, also including psychogenic neurosis, psychopathic personality, and syndromes of defective mental development (mental retardation). He eventually included homosexuality in the category of "mental conditions of constitutional origin". The neuroses were later split into anxiety disorders and other disorders. Freud wrote extensively on hysteria and also coined the term, "anxiety neurosis", which appeared in DSM-I and DSM-II. Checklist criteria for this led to studies that were to define panic disorder for DSM-III. Early 20th century schemes in Europe and the United States reflected a brain disease (or degeneration) model that had emerged during the 19th century, as well as some ideas from Darwin's theory of evolution and/or Freud's psychoanalytic theories. Psychoanalytic theory did not rest on classification of distinct disorders, but pursued analyses of unconscious conflicts and their manifestations within an individual's life. It dealt with neurosis, psychosis, and perversion. The concept of borderline personality disorder and other personality disorder diagnoses were later formalized from such psychoanalytic theories, though such ego psychology-based lines of development diverged substantially from the paths taken elsewhere within psychoanalysis. The philosopher and psychiatrist Karl Jaspers made influential use of a "biographical method" and suggested ways to diagnose based on the form rather than content of beliefs or perceptions. In regard to classification in general he prophetically remarked that: "When we design a diagnostic schema, we can only do so if we forego something at the outset … and in the face of facts we have to draw the line where none exists... A classification therefore has only provisional value. It is a fiction which will discharge its function if it proves to be the most apt for the time". Adolph Meyer advanced a mixed biosocial scheme that emphasized the reactions and adaptations of the whole organism to life experiences. In 1945, William C. Menninger advanced a classification scheme for the US army, called Medical 203, synthesizing ideas of the time into five major groups. This system was adopted by the Veterans Administration in the United States and strongly influenced the DSM. The term stress, having emerged from endocrinology work in the 1930s, was popularized with an increasingly broad biopsychosocial meaning, and was increasingly linked to mental disorders. The diagnosis of post-traumatic stress disorder was later created. Mental disorders were first included in the sixth revision of the International Classification of Diseases (ICD-6) in 1949. Three years later, in 1952, the American Psychiatric Association created its own classification system, DSM-I. The Feighner Criteria group described fourteen major psychiatric disorders for which careful research studies were available, including homosexuality. These developed as the Research Diagnostic Criteria, adopted and further developed by the DSM-III. The DSM and ICD developed, partly in sync, in the context of mainstream psychiatric research and theory. Debates continued and developed about the definition of mental illness, the medical model, categorical vs dimensional approaches, and whether and how to include suffering and impairment criteria. There is some attempt to construct novel schemes, for example from an attachment perspective where patterns of symptoms are construed as evidence of specific patterns of disrupted attachment, coupled with specific types of subsequent trauma. The ICD-11 and DSM-5 are being developed at the start of the 21st century. Any radical new developments in classification are said to be more likely to be introduced by the APA than by the WHO, mainly because the former only has to persuade its own board of trustees whereas the latter has to persuade the representatives of over 200 different countries at a formal revision conference. In addition, while the DSM is a bestselling publication that makes huge profits for APA, the WHO incurs major expense in determining international consensus for revisions to the ICD. Although there is an ongoing attempt to reduce trivial or accidental differences between the DSM and ICD, it is thought that the APA and the WHO are likely to continue to produce new versions of their manuals and, in some respects, to compete with one another. There is some ongoing scientific doubt concerning the construct validity and reliability of psychiatric diagnostic categories and criteria even though they have been increasingly standardized to improve inter-rater agreement in controlled research. In the United States, there have been calls and endorsements for a congressional hearing to explore the nature and extent of harm potentially caused by this "minimally investigated enterprise". Other specific criticisms of the current schemes include: attempts to demonstrate natural boundaries between related syndromes, or between a common syndrome and normality, have failed; the disorders of current classification are probably surface phenomena that can have many different interacting causes, yet "the mere fact that a diagnostic concept is listed in an official nomenclature and provided with a precise operational definition tends to encourage us to assume that it is a "quasi-disease entity" that can be invoked to explain the patient's symptoms"; and that the diagnostic manuals have led to an unintended decline in careful evaluation of each individual person's experiences and social context. Some have argued that reliance on operational definition demands that intuitive concepts, such as depression, need to be operationally defined before they become amenable to scientific investigation. However, John Stuart Mill pointed out the dangers of believing that anything that could be given a name must refer to a thing and Stephen Jay Gould and others have criticized psychologists for doing just that. One critic states that "Instead of replacing 'metaphysical' terms such as 'desire' and 'purpose', they used it to legitimize them by giving them operational definitions. Thus in psychology, as in economics, the initial, quite radical operationalist ideas eventually came to serve as little more than a 'reassurance fetish' (Koch 1992, 275) for mainstream methodological practice." According to Tadafumi Kato, since the era of Kraepelin, psychiatrists have been trying to differentiate mental disorders by using clinical interviews. Kato argues there has been little progress over the last century and that only modest improvements are possible in this way; he suggests that only neurobiological studies using modern technology could form the basis for a new classification. According to Heinz Katsching, expert committees have combined phenomenological criteria in variable ways into categories of mental disorders, repeatedly defined and redefined over the last half century. The diagnostic categories are termed "disorders" and yet, despite not being validated by biological criteria as most medical diseases are, are framed as medical diseases identified by medical diagnoses. He describes them as top-down classification systems similar to the botanic classifications of plants in the 17th and 18th centuries, when experts decided a priori which visible aspects of plants were relevant. Katsching notes that while psychopathological phenomena are certainly observed and experienced, the conceptual basis of psychiatric diagnostic categories is questioned from various ideological perspectives. Psychiatrist Joel Paris argues that psychiatry is sometimes susceptible to diagnostic fads. Some have been based on theory (overdiagnosis of schizophrenia), some based on etiological (causation) concepts (overdiagnosis of post-traumatic stress disorder), and some based on the development of treatments. Paris points out that psychiatrists like to diagnose conditions they can treat, and gives examples of what he sees as prescribing patterns paralleling diagnostic trends, for example an increase in bipolar diagnosis once lithium came into use, and similar scenarios with the use of electroconvulsive therapy, neuroleptics, tricyclic antidepressants, and SSRIs. He notes that there was a time when every patient seemed to have "latent schizophrenia" and another time when everything in psychiatry seemed to be "masked depression", and he fears that the boundaries of the bipolar spectrum concept, including in application to children, are similarly expanding. Allen Frances has suggested fad diagnostic trends regarding autism and Attention deficit hyperactivity disorder. Since the 1980s, psychologist Paula Caplan has had concerns about psychiatric diagnosis, and people being arbitrarily "slapped with a psychiatric label". Caplan says psychiatric diagnosis is unregulated, so doctors aren’t required to spend much time understanding patients situations or to seek another doctor’s opinion. The criteria for allocating psychiatric labels are contained in the Diagnostic and Statistical Manual of Mental Disorders, which can "lead a therapist to focus on narrow checklists of symptoms, with little consideration for what is causing the patient’s suffering". So, according to Caplan, getting a psychiatric diagnosis and label often hinders recovery. The DSM and ICD approach remains under attack both because of the implied causality model and because some researchers believe it better to aim at underlying brain differences which can precede symptoms by many years. - Abnormal psychology - Diagnostic classification and rating scales used in psychiatry - Medical classification - Relational disorder (proposed DSM-5 new diagnosis) - Robin Murray (Md, M Phil; Murray, Robin (1997-10-28). "The essentials of postgraduate psychiatry". ISBN 978-0-521-57801-1. - Berrios G E (April 1999). "Classifications in psychiatry: a conceptual history". Aust N Z J Psychiatry. 33 (2): 145–60. doi:10.1046/j.1440-1614.1999.00555.x. PMID 10336212. - Perring, C. (2005) Mental Illness Stanford Encyclopedia of Philosophy - Giosan C, Glovsky V, Haslam N; Glovsky; Haslam (2001). "The Lay Concept of 'Mental Disorder': A Cross-Cultural Study". Transcultural Psychiatry. 38 (3): 317–32. doi:10.1177/136346150103800303. - World Health Organization (2005). WHO Resource Book on Mental Health: Human rights and legislation (PDF). ISBN 92-4-156282-X. - Peck MC, Scheffler RM; Scheffler (September 2002). "An analysis of the definitions of mental illness used in state parity laws". Psychiatr Serv. 53 (9): 1089–95. doi:10.1176/appi.ps.53.9.1089. PMID 12221306. - Widiger TA, Sankis LM; Sankis (2000). "Adult psychopathology: issues and controversies". Annu Rev Psychol. 51: 377–404. doi:10.1146/annurev.psych.51.1.377. PMID 10751976. PDF - Office of the Surgeon General and various United States Government agencies (1999) Mental Health: A report of the Surgeon General - US Department of Health and Human Sciences (2007) Mental Health & Mental Disorders: Terminology - Parabiaghi A, Bonetto C, Ruggeri M, Lasalvia A, Leese M; Bonetto; Ruggeri; Lasalvia; Leese (June 2006). "Severe and persistent mental illness: a useful definition for prioritizing community-based mental health service interventions". Soc Psychiatry Psychiatr Epidemiol. 41 (6): 457–63. doi:10.1007/s00127-006-0048-0. PMID 16565917. - Economic and Social Research Council Mental Health and Mental Illness in the UK - Berganza CE, Mezzich JE, Jorge MR; Mezzich; Jorge (2002). "Latin American Guide for Psychiatric Diagnosis (GLDP)". Psychopathology. 35 (2–3): 185–90. doi:10.1159/000065143. PMID 12145508. - Zero to Three. (1994). Diagnostic classification: 0–3: Diagnostic classification of mental health and developmental disorders in infancy and early childhood. Washington, DC. - Zero to Three overview of the DC:0-3 - Task Force on Research Diagnostic Criteria: Infancy Preschool (December 2003). "Research diagnostic criteria for infants and preschool children: the process and empirical support". J Am Acad Child Adolesc Psychiatry. 42 (12): 1504–12. doi:10.1097/00004583-200312000-00018. PMID 14627886. - RDC-PA Online (PDF) - Mises R, Quemada N, Botbol M, et al. (2002). "French classification for child and adolescent mental disorders". Psychopathology. 35 (2–3): 176–80. doi:10.1159/000065141. PMID 12145506. - Mezzich JE (2002). "International surveys on the use of ICD-10 and related diagnostic systems". Psychopathology. 35 (2–3): 72–5. doi:10.1159/000065122. PMID 12145487. - Jenkins R, Goldberg D, Kiima D, et al. (2002). "Classification in primary care: experience with current diagnostic systems". Psychopathology. 35 (2–3): 127–31. doi:10.1159/000065132. PMID 12145497. - López-Muñoz F, García-García P, Sáiz-Ruiz J, et al. (2008). "A bibliometric study of the use of the classification and diagnostic systems in psychiatry over the last 25 years". Psychopathology. 41 (4): 214–25. doi:10.1159/000125555. PMID 18408417. - Nakane Y, Nakane H; Nakane (2002). "Classification systems for psychiatric diseases currently used in Japan". Psychopathology. 35 (2–3): 191–4. doi:10.1159/000065144. PMID 12145509. - Rogler LH (March 1997). "Making sense of historical changes in the Diagnostic and statistical manual of mental disorders: five propositions". J Health Soc Behav. 38 (1): 9–20. doi:10.2307/2955358. JSTOR 2955358. PMID 9097505. - James J. Hudziak; Helzer, John E. (2002). Defining Psychopathology in the 21st Century: Dsm-V and Beyond. American Psychopathological Association Series (1st ed.). Washington, DC: American Psychiatric Association. ISBN 1-58562-063-7. - Cosgrove L, Krimsky S, Vijayaraghavan M, Schneider L; Krimsky; Vijayaraghavan; Schneider (2006). "Financial ties between DSM-IV panel members and the pharmaceutical industry". Psychother Psychosom. 75 (3): 154–60. doi:10.1159/000091772. PMID 16636630. - Craddock, N., Owen, M. (2007) Rethinking psychosis: the disadvantages of a dichotomous classification now outweigh the advantages World Psychiatry v.6(2); Jun - Maser JD, Akiskal HS; Akiskal (December 2002). "Spectrum concepts in major mental disorders". Psychiatr. Clin. North Am. 25 (4): xi–xiii. doi:10.1016/S0193-953X(02)00034-5. PMID 12462854. - Krueger RF, Watson D, Barlow DH, et al. (November 2005). "Introduction to the Special Section: Toward a Dimensionally Based Taxonomy of Psychopathology". Journal of Abnormal Psychology. 114 (4): 491–3. doi:10.1037/0021-843X.114.4.491. PMC . PMID 16351372. - Widiger TA, Simonsen E, Krueger R, Livesley WJ, Verheul R; Simonsen; Krueger; Livesley; Verheul (June 2005). "PERSONALITY DISORDER RESEARCH AGENDA FOR THE DSM–V". J. Pers. Disord. 19 (3): 315–38. doi:10.1521/pedi.2005.19.3.315. PMC . PMID 16175740. - Dalal PK, Sivakumar T. (2009) Moving towards ICD-11 and DSM-V: Concept and evolution of psychiatric classification. Indian Journal of Psychiatry, Volume 51, Issue 4, Page 310-319. - Bentall R (2006). "Madness explained: why we must reject the Kraepelinian paradigm and replace it with a 'complaint-orientated' approach to understanding mental illness". Med. Hypotheses. 66 (2): 220–33. doi:10.1016/j.mehy.2005.09.026. PMID 16300903. - Munro, Alistair; Bhugra, Dinesh (1997). Troublesome disguises: underdiagnosed psychiatric syndromes. Oxford: Blackwell Science. ISBN 0-86542-674-0. - Millon, Theodore (2004). Masters of the Mind: Exploring the Story of Mental Illness from Ancient Times to the New Millennium. John Wiley & Sons. p. 38. ISBN 978-0-471-46985-8. - Berrios GE (July 1987). "Historical aspects of psychoses: 19th century issues". Br. Med. Bull. 43 (3): 484–98. PMID 3322481. - Bolme, A (1991). "Portraying Monomaniacs to Service the Alienist's Monomania: Gericault and Georget". Oxford Art Journal. 14 (1): 79–91. doi:10.1093/oxartj/14.1.79. JSTOR 1360279. - O'Connell P, Woodruff PW, Wright I, Jones P, Murray RM; Woodruff; Wright; Jones; Murray (February 1997). "Developmental insanity or dementia praecox: was the wrong concept adopted?". Schizophr. Res. 23 (2): 97–106. doi:10.1016/S0920-9964(96)00110-7. PMID 9061806. - Mendelson G (December 2003). "Homosexuality and psychiatric nosology". Aust N Z J Psychiatry. 37 (6): 678–83. doi:10.1111/j.1440-1614.2003.01273.x. PMID 14636381. - Viner R (June 1999). "Putting Stress in Life: Hans Selye and the Making of Stress Theory". Social Studies of Science. 29 (3): 391–410. doi:10.1177/030631299029003003. JSTOR 285410. - Katsching, Heinz (February 2010). "Are psychiatrists an endangered species? Observations on internal and external challenges to the profession". World Psychiatry. World Psychiatric Association. 9 (1): 21–28. doi:10.1002/j.2051-5545.2010.tb00257.x. PMC . PMID 20148149. - Masten AS, Curtis WJ; Curtis (2000). "Integrating competence and psychopathology: pathways toward a comprehensive science of adaptation in development". Dev. Psychopathol. 12 (3): 529–50. doi:10.1017/S095457940000314X. PMID 11014751. - Kendell, R.; Jablensky, A. (January 2003). "Distinguishing between the validity and utility of psychiatric diagnoses". Am J Psychiatry. 160 (1): 4–12. doi:10.1176/appi.ajp.160.1.4. PMID 12505793. - Baca-Garcia, E.; et al. (March 2007). "Diagnostic stability of psychiatric disorders in clinical practice". Br J Psychiatry. 190 (3): 210–6. doi:10.1192/bjp.bp.106.024026. PMID 17329740. - Pincus, H. A.; et al. (1998). ""Clinical Significance" and DSM-IV". Arch Gen Psychiatry. 55 (12): 1145; author reply 1147–8. doi:10.1001/archpsyc.55.12.1145. PMID 9862559. - DW Hands (2004) On Operationalisms and Economics Journal of Economic Issues - Kato, Tadafumi (October 2011). "A renovation of psychiatry is needed". World Psychiatry. World Psychiatric Association. 10 (3): 198–199. doi:10.1002/j.2051-5545.2011.tb00056.x. PMC . PMID 21991278. - Joel Paris, MD (2004) Psychiatric Diagnosis and the Bipolar Spectrum CPA Bulletin; 36:3) - Psychiatric Fads and Overdiagnosis: Normality is an endangered species. Published on June 2, 2010 by Allen J. Frances, M.D. in DSM5 in Distress - Paula J. Caplan (April 28, 2012). "Psychiatry's bible, the DSM, is doing more harm than good". Washington Post. - Doward, Jamie (May 12, 2013). "Medicine's big new battleground: does mental illness really exist?". The Guardian. London. - Dalal PK, Sivakumar T. (2009) Moving towards ICD-11 and DSM-V: Concept and evolution of psychiatric classification. Indian Journal of Psychiatry, Volume 51, Issue 4, Page 310-319. - King LJ (March 1999). "A brief history of psychiatry: millennia past and present". Ann Clin Psychiatry. 11 (1): 3–12. doi:10.3109/10401239909147041. PMID 10383169.	2	40	9	0	2	0	0.846911	11	8,654
Medical classification, or medical coding, is the process of transforming descriptions of medical diagnoses and procedures into universal medical code numbers. The diagnoses and procedures are usually taken from a variety of sources within the health care record, such as the transcription of the physician's notes, laboratory results, radiologic results, and other sources. Diagnosis codes are used to track diseases and other health conditions, inclusive of chronic diseases such as diabetes mellitus and heart disease, and contagious diseases such as norovirus, the flu, and athlete's foot. These diagnosis and procedure codes are used by government health programs, private health insurance companies, workers' compensation carriers and others. Medical classification systems are used for a variety of applications in medicine, public health and medical informatics, including: Statistical analysis of diseases and therapeutic actions reimbursement; e.g., based on diagnosis-related groups knowledge-based and decision support systems direct surveillance of epidemic or pandemic outbreaks. There are country specific standards and international classification systems. Many different medical classifications exist, though they occur into two main groupings: Statistical classifications and Nomenclatures. A statistical classification brings together similar clinical concepts and groups them into categories. The number of categories is limited so that the classification does not become too big. An example of this is used by the International Statistical Classification of Diseases and Related Health Problems (known as ICD). ICD groups diseases of the circulatory system into one "chapter," known as Chapter IX, covering codes I00–I99. One of the codes in this chapter (I47.1) has the code title (rubric) Supraventricular tachycardia. However, there are several other clinical concepts that are also classified here. Among them are paroxysmal atrial tachycardia, paroxysmal junctional tachycardia, auricular tachycardia and nodal tachycardia. Another feature of statistical classifications is the provision of residual categories for "other" and "unspecified" conditions that do not have a specific category in the particular classification. In a nomenclature there is a separate listing and code for every clinical concept. So, in the previous example, each of the tachycardia listed would have its own code. This makes nomenclatures unwieldy for compiling health statistics. Types of coding systems specific to health care include: Diagnostic codes Are used to determine diseases, disorders, and symptoms Can be used to measure morbidity and mortality Examples: ICD-9-CM, ICD-10 Procedural codes They are numbers or alphanumeric codes used to identify specific health interventions taken by medical professionals. Examples: ICPM, ICHI Pharmaceutical codes Are used to identify medications Examples: AT, NDC Topographical codes Are codes that indicate a specific location in the body Examples :ICD-O, SNOMED WHO Family of International Classifications The World Health Organization (WHO) maintains several internationally endorsed classifications designed to facilitate the comparison of health related data within and across populations and over time as well as the compilation of nationally consistent data. This "Family of International Classifications" (FIC) include three main (or reference) classifications on basic parameters of health prepared by the organization and approved by the World Health Assembly for international use, as well as a number of derived and related classifications providing additional details. Some of these international standards have been revised and adapted by various countries for national use. International Statistical Classification of Diseases and Related Health Problems (ICD) ICD-9 (9th revision, published in 1977) ICD-9-CM (Clinical Modification, used in the US) ICD-10 (10th revision, in use by WHO since 1994) ICD-10-CM (Clinical Modification, used in the US) ICD-10-PCS (Procedure Coding System, used in the US) ICD-10-CA (used for morbidity classification in Canada). ICD-10-AM (used in Australia and New Zealand) EUROCAT - an extension of the ICD-10 Q chapter for congenital disorders International Classification of Functioning, Disability and Health (ICF) International Classification of Health Interventions (ICHI) (previously known as International Classification of Procedures in Medicine) Derived classifications are based on the WHO reference classifications (i.e. ICD and ICF). They include the following: International Classification of Diseases for Oncology, Third Edition (ICD-O-3) ICD-10 for Mental and Behavioural Disorders Application of the International Classification of Diseases to Dentistry and Stomatology, 3rd Edition (ICD-DA) Application of the International Classification of Diseases to Neurology (ICD-10-NA) Related classifications in the WHO-FIC are those that partially refer to the reference classifications, e.g. only at specific levels. They include: International Classification of Primary Care (ICPC) ICPC-2 PLUS International Classification of External Causes of Injury (ICECI) Anatomical Therapeutic Chemical Classification System with Defined Daily Doses (ATC/DDD) Technical aids for persons with disabilities: Classification and terminology (ISO9999) International Classification for Nursing Practice (ICNP) Other medical classifications The categories in a diagnosis classification classify [ and medical signs. In addition to the ICD and its national variants, they include: Diagnostic and Statistical Manual of Mental Disorders (DSM) DSM-IV Codes International Classification of Headache Disorders 2nd Edition (ICHD-II) International Classification of Sleep Disorders (ICSD) Online Mendelian Inheritance in Man, database of genetic codes Read codes Systematized Nomenclature of Medicine - Clinical Terms (SNoMed-CT) The categories in a procedure classification classify specific health interventions undertaken by health professionals. In addition to the ICHI and ICPC, they include: Australian Classification of Health Interventions (ACHI) Canadian Classification of Health Interventions (CCI) Chinese Classification of Heath Interventions (CCHI) Current Procedural Terminology (CPT) Health Care Procedure Coding System (HCPCS) ICD-10 Procedure Coding System (ICD-10-PCS) Office of Population, Censuses and Surveys Classification of Surgical Operations and Procedures (OPCS-4) Classification of Pharmaco-Therapeutic Referrals (CPR) Logical Observation Identifiers Names and Codes (LOINC), standard for identifying medical laboratory observations Medical Dictionary for Regulatory Activities (MedDRA) Medical Subject Headings (MeSH) List of MeSH codes Nursing Interventions Classification (NIC) Nursing Outcomes Classification (NOC) TIME-ITEM, ontology of topics in medical education TNM Classification of Malignant Tumors Unified Medical Language System (UMLS) Victoria Ambulatory Coding System (VACS) / Queensland Ambulatory Coding System (QACS), Australia Library classification that have medical components Dewey Decimal System and Universal Decimal Classification (section 610–620) National Library of Medicine classification ICD, SNOMED and Electronic Health Record (EHR) What is SNOMED? The Systematized Nomenclature of Medicine (SNOMED) is the most widely recognised nomenclature in healthcare. Its current version, SNOMED Clinical Terms (SNOMED CT), is intended to provide a set of concepts and relationships that offers a common reference point for comparison and aggregation of data about the health care process. SNOMED CT is often described as a reference terminology. SNOMED CT contains more than 311,000 active concepts with unique meanings and formal logic-based definitions organised into hierarchies. SNOMED CT can be used by anyone with an Affiliate License, 40 low income countries defined by the World Bank or qualifying research, humanitarian and charitable projects. SNOMED-CT is designed to be managed by computer, and it is a complex relationship concepts. What is ICD? The International Classification of Disease (ICD) is the most widely recognized medical classification maintained by the World Health Organization (WHO). Its primary purpose is to categorise diseases for morbidity and mortality reporting. The United States has used a clinical modification of ICD (ICD-9-CM) for the additional purposes of reimbursement. ICD-10 was endorsed by WHO in 1990, and WHO Member states began using the classification system in 1994 for both morbidity and mortality reporting. In the US, however, it has only been used for reporting mortality since 1999. Because of the US delay in adopting its version of ICD-10, it is currently unable to compare morbidity data with the rest of the world. ICD has a hierarchical structure, and coding in this context, is the term applied when representations are assigned to the words they represent. Coding diagnoses and procedures is the assignment of codes from a code set that follows the rules of the underlying classification or other coding guidelines. SNOMED CT vs ICD SNOMED CT and ICD are designed for different purposes and each should each be used for the purposes for which it was designed. As a core terminology for the EHR, SNOMED CT provides a common language that enables a consistent language that enables a consistent way of capturing, sharing, and aggregating health data across specialties and sites of care. It is highly detailed terminology designed for input not reporting. Classification systems such as ICD-9-CM, ICD-10-CM, and ICD-10-PCS group together similar diseases and procedures and organise related entities for easy retrieval. They are typically used for external reporting requirements or other uses where data aggregation is advantageous, such as measuring the quality of care monitoring resource utilisation, or processing claims for reimbursement. SNOMED is clinically-based, document whatever is needed for patient care and has better clinical coverage than ICD. ICD’s focus is statistical with less common diseases get lumped together in “catch-all” categories, which result in loss of information. SNOMED CT is used directly by healthcare providers during the process of care, whereas ICD is used by coding professionals after the episode of care. SNOMED CT had multiple hierarchy, whereas single hierarchy for ICD. SNOMED CT concepts are defined logically by their attributes, whereas only textual rules and definitions in ICD. Data Mapping of SNOMED and ICD SNOMED and ICD can be coordinated. The National Library of Medicine (NLM) maps ICD-9-CM, ICD-10-CM, ICD-10-PCS, and other classification systems to SNOMED. Data Mapping is the process of identifying relationships between two distinct data models. The full value of the health information contained in an EHR system will only be realised if both systems involved in the map are up to date and accurately reflect the current practice of medicine. Clinical Coding in Australia Medical coding and classification systems are expected to become increasingly important in the health care sector. Together with and as an integrated part of the electronic health information systems, the coding and classification systems will be used to improve the quality and effectiveness of the medical services. What is clinical coding? Clinical coding is the translation of written, scanned and/or electronic clinical documentation about patient care into code format. For example, hypertension is represented by the code 'I10'; general anaethesia is represented by the code'92514-XX'. A standardised classification system, The International Statistical Classification of Diseases and Related Health Problems, 10th Revision, Australian Modification (ICD-10-AM), is applied in all Australian acute health facilities. It is based on the World Health Organisation (WHO) ICD-10 system, updated with the Australian Classification of Health Interventions (ACHI), Australian Coding Standards (ACS). Clinical coding is a specialised skill requiring excellent knowledge of medical terminology and disease processes, attention to detail, and analytical skills. What does clinical coder do? A clinical coder is responsible for abstracting relevant information from the medical record and deciding which diagnoses and procedures meet criteria for coding as per Australian and State Coding Standards. The coder then assigns codes for these diagnoses and procedures based on ICD-10-AM conventions and standards. What is coded data used for? The assigned codes and other patient data are processed by grouper software to determine a diagnosis-related group (DRG) for the episode of care, which is used for funding and reimbursement. This process allows hospital episodes to be grouped into meaningful categories, helping us to better match patient needs to health care resources. 1. https://www.aapc.com/medical-coding/medical-coding.aspx 2. http://en.wikipedia.org/wiki/Clinical_coder	3	2	2	0	0	6	0.799841	8	2,686
A vertical or transverse incision can be made in a location over the distended colon as indicated from a study of the abdominal roentgenograms. Currently it is believed that the opening should be made through the rectus muscle with consideration being given for the span of the ostomy appliance gasket, which should be away from skin folds, bony prominences, or the valley of the umbilicus. transverse colostomies: the loop transverse colostomy and the double-barrel transverse colostomy. The transverse colostomy is in the upper abdomen, either in the middle or toward the right side of the body. This type of colostomy allows the stool to leave the body before it reaches the descending colon. Some of the colon problems that can lead Transverse colostomy — is made from the transverse part of the colon. The transverse colostomy is usually located in the center of the abdomen above the navel. The output often is liquid to pasty, and gas is common. Descending colostomy — is made from the descending part of the colon. If a Transverse colostomy is constructed (Transverse colon), the stoma is located in the upper abdomen. (See Figure 6 below) In the case of Ascending colostomy (Ascending colon) the stoma is placed on the lower right side of the abdomen. Rarely done.(See Figure 7) to rest and heal. A transverse colostomy may be used to keep stool out of the area of the colon that’s inflamed, infected, diseased, or newly operated on – this allows healing to take place. This type of colostomy is usually temporary. Depending on the healing process, the colostomy may be needed for a few weeks or months, but possibly for years. 2013-02-03 Closure of a transverse loop colostomy is performed when the ostomy/fecal diversion is no longer required. Temporary and permanent colostomy, in addition to the transverse colostomy are needed in different cases. See what patients experience and what do these procedures mean. Colostomy is an inevitable medical procedure in some patients. In some cases, it is the only alternative to continue with life. 482 colostomy stock photos, vectors, and illustrations are available royalty-free. See colostomy stock video clips. of 5. Keywords: dehiscence; evisceration; colostomy; wound closure techniques; sendo submetido à transversostomia em alça, com finalidade descompressiva. the partial resection of transverse colon followed by terminal colostomy and the partial resection of transverse colon followed by terminal colostomy and No tratamento paliativo, a prótese e a colostomia/ileostomia descompressiva não apresentaram with primary anastomosis and protecting ostomy; and three- stage procedure such as loop Transverse colon, 14 (7.9), 7 (8.2), 7 (7.6), 0.06 Laparoscopic repair of transverse colostomy prolapse seems to be a less invasive submetido à transversostomia em alça, com finalidade descompressiva. 2020-05-28 · Q. Can you explain the difference between CPT codes 44140 and 44160? Both codes represent a partial colectomy, and I am unclear on what work must be performed after the colectomy to choose between the two codes. A. These two codes often generate confusion for surgical coders. This type of colostomy is usually temporary. Depending on the healing process, the colostomy may be needed for a few weeks or months, but possibly for years. The complication rate with transverse colostomies was higher than with other types. Colostomy closure was associated with complications in nine patients (6.5%), the most serious of which was adhesive small bowel obstruction (5). The mortality was less than 1%, but significant morbidity still exists. A detailed template operative dictation is provided. 2012-03-01 It is usually done when part of the transverse colon or descending colon is removed and the sigmoid colon, rectum and anus are not removed. This type of colostomy is created with 2 stomas. Part of the colon is removed, and each cut end of the colon is attached to a separate opening in the abdominal wall (called the end stoma). Barista utbildning borås karta stockholm marathon 2021 förordning (1998 1252) om områdesskydd enligt miljöbalken m.m. daniel spink imdb WebMD - Better information. Better health. This type of colostomy usually is done as a temporary measure, allowing for discharge of feces while the diseased portion of the intestine returns to normal. Later, the two ends are anastomosed to restore … 2021-02-03 Transverse Colostomy. byta lägenhetsnummer skatteverket - Industri kalmar län - Billackering gavle - Big biology words - Tafelbilder mit onenote - Qualia login - Malmö news 24 transverse colon. The most common conditions that can lead to the necessity for creating a loop transverse colos-tomy are Hirschsprung's disease, di-verticulitis, cancer, and bowel per-foration or obstruction. A loop sto-ma is the procedure of choice for surgery. When caring for a patient with a transverse colostomy, it is impor- Complications after colostomy formation wer … Carcinomas occurring at colostomy sites are rare, and most of these are metachronous colorectal cancers. The median time between colostomy and development of a carcinoma at a colostomy site is 22 years, which exceeds the length of the recommended follow-up period. We report a rare case of a carcinoma of the transverse colon occurring at a colostomy site in a patient without a history of Ostomy systems are odor-proof and there should not be a smell unless there is a leak and the appliance needs to be changed. Stool will look different after ostomy surgery, which brings up many questions about what is the “new normal” and when it might be time to call the doctor or an enterostomal therapy (ET) nurse about the appearance, smell, or frequency of stool. Triple-tube-ostomy (TTO) technique involving gastrostomy, reverse duodenostomy, and feeding jejunostomy tubes insertion has shown promising results during conservative management of duodenal injuries. Objective: We aim through this paper to report a successfully managed case of isolated incomplete transverse duodenal injury managed by TTO Transverse colostomy: it produces mal odor, mushy (thicker) drainage because some of the liquid has been reabsorbed. 4.!Descending colostomy: produces increasingly solid drainage.	4	8	2	0	0	0	0.534176	2	1,519
Statistics from Altmetric.com If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways. Patients with SLE experience multiple, varied symptoms and laboratory abnormalities that occur in different combinations, at different points in time.1 A result of the heterogeneity is that studies on SLE employ several, sometimes conflicting, definitions of the illness. Investigators disagree about when SLE begins; how SLE relates to similar and overlapping rheumatic illnesses; whether SLE-like illnesses of known genetic causes count as SLE; and whether the same diagnosis name should apply when investigators describe stratified populations, for instance, SLE with and without renal disease. Inconsistent definitions lead stakeholders—patients, practising physicians, administrators, epidemiologists and investigators—to count different patients and to develop different opinions about the mechanisms and treatment of SLE. To advocate a consensus vocabulary and conceptual model, in this paper we deconstruct the process of making a diagnosis of SLE by examining its classification and diagnostic criteria, definitions and illness models. We discuss the ways by which stratification biases conclusions and how the purpose for which a stakeholder names a diagnosis determines whom they accept as having this disease. Classification and diagnostic criteria When in the mid-19th century Cazenave first used the name lupus erythematosus, SLE was a rare and life-threatening illness.2 3 A century later, as new technologies identified more patients,4–10 physicians found SLE to be more clinically diverse, and often less severe, than they once believed. To improve homogeneity of patient populations identified for clinical studies, investigators developed classification criteria that are specific, binary (SLE is present or not) and time limited (valid only for the extent of a study). The homogeneity of classification criteria is implied but not real. The American College of Rheumatology (ACR) criteria allow 330 different combinations of symptoms and laboratory tests to affirm a diagnosis of SLE.11 Classification criteria are insensitive; they exclude patients who, despite disabling and treatable symptoms, fall below criteria thresholds and those who have overlapping or changing forms of SLE, whom practising physicians treat according to rules established for typical SLE.12–21 Diagnostic criteria, which would be more sensitive, if less specific, time independent and scalar rather than binary, do not exist for SLE. (An internet search (23 September 2018) for SLE diagnostic criteria identified references only to classification criteria. Many published papers fail to distinguish diagnostic from classification criteria.21) Exclusive and inclusive definitions Many clinical and basic science investigators use an exclusive definition of SLE that accepts only classification criteria-defined patients and rejects (for ethical and practical reasons) patients with dementia, pregnancy, comorbid illness or specific forms of treatment.22–24 Practising physicians use an inclusive definition that gathers under one name all patients with lupus spectrum illness, including those with typical SLE (criteria fulfilling), overlap syndromes (typical SLE associated with another definable autoimmune illness), undifferentiated autoimmune syndrome (UAS) (lupus-like illness that does not fulfil criteria),25–27 SLE-associated antibodies only (diagnostic autoantibodies but no clinical illness)28 and cutaneous SLE (skin disease without systemic manifestations).29 In rheumatology practice, only 35% of patients with lupus spectrum have typical SLE. Compared with patients with atypical forms of lupus spectrum disease, patients with typical SLE differ demographically, have different involved organ systems and receive different treatments.30 31 Although differences between typical and atypical patients may result in different disease mechanisms and outcomes, many SLE studies include atypical patients with neither comment nor subanalysis.32 Studies differ in how they define onset of SLE, which may be first appearance of ANA, anti-DNA antibody, symptoms, ACR criteria or diagnosis by a physician. In animal model studies, onset may be first appearance of glomerulonephritis, anti-DNA antibodies, biomarkers, gene expression profiles or disease-inducing intervention.33–35 A study that defines SLE as first appearance of arthralgia or ANA may enrol patients more than a decade earlier than does one that defines SLE as first fulfilment of ACR criteria.36 Although both studies will speak of SLE, their results cannot be compared. Stakeholders who use different definitions describe different patients (figure 1). Clinical and basic science investigators usually use exclusive definitions (clear area, centre and bottom); by study design, they include only patients whom a practising physician has already diagnosed to have SLE, that is, after time 2. Patients, practising physicians and some investigators consider SLE to begin at time 1 (shaded area on the left). Symptoms and laboratory abnormalities first occur at the earlier date, when social, environmental and/or endogenous inducers may determine which patient will remain well, develop typical SLE or fall ill with a different lupus spectrum illness (shaded area at the top). Exogenous factors may also determine if, how, and when the clinical phenotype may change (time 4, shaded area at the right). Outcomes are measurable after a diagnosis is assigned, throughout time 3. Most administrators, patients, practising physicians and some clinical investigators ask the question what. The answer, for which the exclusive definition works best, is the diagnosis name. Most basic and some clinical science investigators ask how, the answer being disease mechanisms, for which the exclusive definition also functions best. Some epidemiological, clinical and basic science investigators, and practising physicians ask why—the aetiology. For this question the inclusive definition is preferred. One can reduce the complexity of making a diagnosis of SLE by using conceptual models. There are two such models, one separate illnesses, the other linear illness; both cluster SLE’s disparate elements. The separate illnesses model posits that typical, overlap, UAS and antibody-only SLE are separate but related illnesses. A strength of this model is that it assigns different, targetable biological mechanisms to each diagnosis. Another strength is that a diagnosis, once made, does not change.37–40 Weaknesses of this model are that, in clinical practice, ambiguous diagnoses occur often, blurring the separating lines, and that diagnoses do sometimes change. Clinical protocols that rigidly adhere to sharp distinctions among diagnoses may remove options available to the treating physician. Another weakness is that insights suggested by evolving phenotypes may be unseen if an investigator believes that change of diagnosis cannot occur.30 The linear illness model posits that UAS, overlap, antibody-only and typical SLE reside within a continuum of a single pathogenic process. This model applies throughout a patient’s lifetime, during which the diagnosis name may change.41–49 The model’s strengths are that it suggests common pathogeneses and flexible treatment protocols for all lupus spectrum illnesses; it highlights potential causes for phenotype changes. A weakness is that boundaries among diagnoses are vague, gathering under one name, like lupus spectrum, patients who have distinctly different phenotypes. When the cause of a chronic illness is unknown, the separate illnesses model usually applies. Using this model, investigators mostly ask how of narrowly defined populations in order to discover mechanisms that will become the basis for targeted, ameliorative treatments. Investigators who ask why hope to find a single cause for a disease. When why is answered, syndromes will be seen to be different phases of a linear illness and treatment will be directed to prevention or cure. For example, in the separate illness model, the syndrome consisting of an abnormal venereal disease research laboratory blood test, rash, aortic aneurysm and tabes dorsalis, lacking a known cause, consists of related different illnesses, mechanistically different, with mechanism-based ameliorative treatments. When the cause is known—infection by Treponema pallidum—the separate symptoms are seen to be phases in a linear model of syphilis, amenable to aetiology-based cure. Similarly, anaemia, jaundice and neuropsychiatric symptoms are separate illnesses until deficiency of vitamin B12 is recognised, at which time they become linear illness phases of pernicious anaemia; and pigment change, neuropathy, hepatitis and cytopenia are separate illnesses until arsenic poisoning is found. The cause(s) of a chronic illness can be one or many things. Whether the cause is infection, deficiency, intoxication or autoimmunity, how one conceptualises the illness is important. The separate illness model favours mechanism-based management, the linear illness model aetiology-based cure. The choice depends mostly on whether the cause is or is not known. When studies stratify SLE populations, conclusions drawn from one subpopulation may differ from those drawn from another. Stratification by clinical and serological phenotypes, demography and habits is qualitative, on disease activity measures quantitative.50–57 Stratification on sex, race, socioeconomic status,58–62 access to medical care, medication choice and adherence,63 willingness to participate in clinical trials, doctor–patient interactions,64 patient preferences and perceptions,65 lifestyle choices,66 67 physician choices,68–71 environmental triggers,72–76 poverty,77 social disparities,78 and life events,79 smoking80 and the gut pathobiont81 all affect manifestations and outcomes in ways that dictate who participates in a study on SLE and in ways that cannot be examined in animal models.82 Stratification on gene expression, quantitative, predicts risk and possibly phenotype83–93; SLE-like illnesses (the autoinflammatory diseases),94 Aicardi-Goutières syndrome,95 96 Canale-Smith syndrome97 and SLE associated with immunodeficiency98 suggest mechanisms for primary illness, and for phenotype diversity. Stratification by molecular biomarkers predicts fulfilment of classification criteria,99 organ involvement and development of SLE in relatives of patients.100–104 Stratifying by time will offer insight about how SLE diagnoses change.105 New computational techniques, like multidimensional models, cluster analyses, machine learning, the word cloud, personalised immunomonitoring and transancestral mapping, are modern ways to stratify.106–114 Many of today’s mechanistic studies compare one dependent against one independent variable. Three-dimensional stratification can quantify combinations of biomarkers, severity indices, phenotypes, microscopic pathology, immunopathology, gene patterns, epidemiological variables, microbiomes or gradations of biological sex. Four-dimensional studies can compare non-calendric variables at different points in time. Studies on stratified populations of patients with SLE that demonstrate different mechanisms among the groups validate the separate illness model of SLE; studies that identify common mechanisms validate the linear illness model. Although stratification by itself cannot explain the origins of SLE, its ability to show population differences enhances understanding and treatment of the disease. How different stakeholders use the name SLE and which definition they use depends on the purpose for which they assign the name (table 1). The purpose for which payers and administrators use the name SLE is to guide reimbursement and regulatory policy. Epidemiologists do so to identify disparities among populations that may identify the exogenous and endogenous factors that drive the illness and that demarcate boundaries by which clinical and basic science researchers can study mechanisms, causes, treatments and outcomes. Office physicians use the name SLE to anchor prognoses, justify interventions and enhance patients’ confidence (and their own). Patients use it to understand their options and their futures. Editors of medical journals use it to flag articles for readers’ attention. Payers, administrators, clinical researchers and some basic science researchers mostly select the separate illness model and the exclusive, binary and time-limited definition of SLE.115–124 Physicians, patients and other basic researchers choose the inclusive, scalar and time-variable definition and linear illness model. Journal editors consider the definition and disease models irrelevant if the published report can be indexed and identified by a keyword. A result of this choice is that literature and internet searches on SLE yield studies of patients and animals defined in many different ways, with little attention to distinctions among the definitions. Until recently American physicians used common language diagnosis names in medical charts, biasing recorded diagnoses towards the exclusive definition. Quality monitors did not challenge common language diagnoses, payers reimbursed expenses and patients with ambiguous diagnoses usually did not participate in studies of SLE. New administrative rules require American physicians to use International Classification of Diseases (ICD) code numbers that disregard the uncertainty of lupus spectrum illness.125 126 Because when diagnoses are ambiguous payers often refuse to reimburse costs of SLE-relevant tests and medications, American physicians now assign the ICD code for typical SLE to patients they previously diagnosed with UCTD, overlap or other lupus spectrum disease, and these patients may now participate in studies that select patients by ICD code. A consensus definition Although many investigators suggest improvements to the available SLE criteria,22 39 121 127–132 the argument for more precise and more exclusive criteria is circular. Studies that exclude patients who do not fulfil criteria cannot prospectively examine phenomena that antedate diagnosis or that cause patients to develop non-criteria variants within lupus spectrum. Deconstructing the process of diagnosis—its definitions, models, stratifications and purposes—can help solve this problem. A consensus vocabulary is the first step to an agreed concept of SLE, including consensus answers to these questions: When does SLE begin? Do persons with autoantibodies only, UAS or overlap illness have ‘SLE’? Do persons with predisposing genetic abnormalities have ‘SLE’? Do patients with mild and severe ‘SLE’ have the same illness? When ‘SLE’ changes course or changes to a different illness, does the change represent alteration of a continuous process or introduction of a new process? Is SLE a clinical syndrome, having doctor-defined symptoms and specific organ system abnormalities? An abnormal biologic state, defined by laboratory phenomena that may or may not accompany clinical illness? A state of susceptibility, determined by genes and environment? Can it fully subside? What exogenous and/or endogenous factors trigger its onset or its change? There are no definitive answers to these questions, but they will be better addressed when stakeholders agree on consensus definitions. Which definition, illness model or stratification we choose is less important than is consensus about the vocabulary that describes which patients we study, and to whom the results of our inquiries apply. Contributors All authors contributed to, reviewed and approved this document. Funding This study was funded by Barbara Volcker Center for Women and Rheumatic Diseases, Rheumatology Research Foundation. Competing interests None declared. Patient consent for publication Not required. Provenance and peer review Commissioned; externally peer reviewed. Data sharing statement No additional data are available.	2	9	0	0	0	1	0.316165	1	3,150
Thoracentesis is a percutaneous procedure that uses a needle or small catheter to remove accumulated fluid from the pleural space. Thoracentesis can either be “diagnostic” (~100 mL of fluid removed for analysis) or “therapeutic” (removal of a larger amount of fluid to relieve dyspnea). It is typically performed at the patient’s bedside and can be performed by a single operator or with an assistant. II. Describe a Step-by-Step approach/method to this problem. When should I do it? Diagnostic thoracentesis is generally indicated whenever clinical exam or imaging discovers a “new” pleural effusion. The low-threshold to invasively sample pleural spaces is justified by a wide range of serious pathologies that manifest with an effusion. Therapeutic drainage (i.e. removal of larger volumes to relieve dyspnea) can be done simultaneously with the first diagnostic drainage procedure. Effusions that do not typically warrant thoracentesis are those that are small and those with an easily identified etiology based on history (pleurisy, chronic heart failure, end-stage renal disease). Pleural effusions (infections, malignancy), which are “dangerous” etiologies, tend to enlarge over time. Thus reviewing serial imaging may help clarify the need for thoracentesis. What might stop me from doing it? The decision to proceed with thoracentesis should be made by weighing the benefits against the risks, as there is no absolute contraindication to thoracentesis. Clinical situations with an increased risk of complications are: The presence of coagulopathic states, systemic anticoagulation, platelet dysfunction (pharmacologic or uremic), or thrombocytopenia: These conditions are traditionally thought to increase the risk of bleeding into the pleural space (hemothorax). Several recent studies found that pre-procedure coagulation abnormalities were not associated with bleeding complications. This suggests that avoiding intercostal vessel injury with proper technique may be more important than correcting a coagulopathic profile. A small effusion size. Small is defined as <1 cm depth of the pleural fluid pocket on ultrasound (or a similar measure on radiographic studies). Smaller effusions increase the risk of pneumothorax due to inadvertent lung puncture. Patients on mechanical ventilation with positive end-expiratory pressure (PEEP): If the lung is punctured by the needle on positive pressure ventilation, there is an increased risk of a persistent air leak (i.e., bronchopleural fistula) and/or tension pneumothorax. Patients with evidence of skin or soft tissue infection overlaying the site of needle insertion: In this situation, the procedure may seed the pleural space with skin pathogens, causing a pleural infection. Patients with severe lung disease of the contralateral lung: Patients with advanced bilateral lung disease or a single functioning lung (as in post single-lung transplant) may not tolerate even a small pneumothorax. Patients with a long-standing loculated effusion or thickened pleura on imaging. These patients are at higher risk for a pneumothorax and/or inability to drain the effusion. Long-standing pleural inflammation (e.g., an untreated pleural infection) leads to deposition of a stiff layer of fibrotic material onto the visceral pleura, fixing the volume of the pleural cavity. When pleural fluid is aspirated from the pleural cavity via a thoracentesis needle, the lung is unable to expand to fill the pleural space and thus the pleural cavity pressure quickly falls. This very negative pleural pressure (<20 cm H2O) creates a powerful gradient for pressure to tear lung segments and enter the pleural space, resulting in a pneumothorax. How do I learn how to do it? Training for thoracentesis varies greatly by institution, but generally a combination of didactic, simulation, and supervised experiential training offers the optimal pathway to competence. Specific training in ultrasound-guided technique is rapidly becoming standard. If one has not had adequate training in the course of residency training, attending a CME course held by nationally-recognized professional organizations (i.e., SHM, ACP, ACEM, ATS, or CHEST) can provide additional didactic and simulation training prior to undergoing proctored procedures necessary for privileging. Am I allowed to do the procedure independently? For those who have completed their graduate medical education, one should consult their institution’s credentialing system to ensure appropriate privileges are granted to perform thoracentesis. For resident physicians or fellows, your training program usually has an educational pathway, typically starting with supervised thoracentesis with gradually increased autonomy as one becomes more experienced. Do I need a pre-assembled tray, and which one should I use? The standard tray for thoracentesis contains a drainage catheter threaded either through or over a needle as well as other components. For a therapeutic tap, it is advisable to use a pre-assembled procedure tray, as these will contain the stopcock, drainage tubing, and fluid collection bag that would be time-consuming to acquire otherwise. More recently, pre-assembled trays using a small 6 French silicone-coated self-directing pigtail catheter threaded over a dual lumen blunt obturator have become widely available. If available, these trays are preferable to the standard thoracentesis tray because of a number of safety features. The needles in these trays have a visual color indicator at the base, where the indicator changes color once a spring-loaded core in the obturator is extended. This indicates that the needle has been advanced into a low-resistance environment, presumably the pleural space. This feature provides a number of advantages over standard trays, including (1) protection from needlestick injury (2) reduced risk of injury to free-floating atelectatic lung (3) added visual evidence of needle advancement into the pleural space. Creating a skin incision with a scalpel prior to needle insertion is required due to skin resistance to the surrounding plastic catheter’s advancement. The catheter will “accordion” unless a proper incision is made. What supplies do I need if I don’t use a thoracentesis tray? A small volume diagnostic tap can be performed without a kit. You will need the following supplies: A 1.5 inch 18- or 20-gauge needle for thinner patients, or the longer 20-gauge spinal needle for more obese patients Lidocaine solution (10 mL of 1% lidocaine is typically sufficient) 2% chlorhexidine is preferred over a povidone-iodine solution for preparing the site Sterile drapes, gloves, mask, and cap. A 60 mL syringe A portable ultrasound machine Specimen containers, depending on the testing ordered: LDH, glucose, total protein, chylomicrons, cholesterol, adenosine deaminase 2 (red-top tube) Cell count (purple-top tube) Bacteriology, mycology cultures (blood culture bottles) Cytology (black top, specimen cups, or the large 2 L plastic collection bag that is frequently provided in thoracentesis kits) Tuberculosis testing (black top or specimen cups) pH (blood gas syringe) How should I use ultrasound to guide thoracentesis? Ultrasound guidance is rapidly becoming standard-of-care with all thoracentesis, and recent guidelines strongly recommend its use in all pleural procedures. Typically, a low frequency (3.5 to 5 MHz) convex array probe is used, although a high frequency linear transducer (7.5 to 10 MHz) can be used as well. The low frequency convex array probe (i.e., the cardiac probe) is by convention held with the indicator dot directed cephalad and images are obtained in the sagittal (when imaging the posterior chest) and coronal (when imaging in the mid-axillary line) planes. On ultrasound, the fluid pocket is seen as a hypoechoic (black) space between the chest wall and the underlying lung and visceral pleura, which is hyperechoic (Figure 1). Select an entry location where the pleural fluid pocket provides the widest distance between the chest wall and the visceral pleura. Indent the skin at this location with pressure from a pen-cap or mark this site with a permanent marking pen. Once marked, the patient should remain in the same position for the duration of the procedure. Care should be taken to avoid the diaphragm (appears as a highly echogenic structure) and the underlying solid organs. Keep in mind the anatomy is dynamic with respiration, and monitor the potential site of entry throughout the respiratory cycle. If possible, chose a site near the posterior axillary line, as angiographic studies show ectatic vessels are less likely to be encountered here than in more medial positions along with a wider intercostal space. There is also less musculature that will need to be traversed. Color Doppler ultrasound can screen for tortious intercostal vessels at a potential needle-entry site, and may reduce the risk of vessel injury. If loculations are present, sample the largest loculation and monitor pleural pressure intermittently during the drainage. For the occasional instance when ultrasound is not available, a “blind” thoracentesis can be performed. First, make sure the effusion is non-loculated and large. Decubitus chest films may be helpful, to ensure that the effusion is mobile and moves freely with the pleural space. Select an entry site that is 1-2 interspaces inferior to the superior extent of the effusion, as determined by physical exam (dullness on percussion, decrease in tactile fremitus and/or breath sounds). Additionally, select a site that is above the ninth rib (to avoid subdiaphragmatic puncture). Rib palpation is often easiest in the line midway between the spine and posterior axillary line. How should the patient be positioned and prepared? Ideally, a nurse or assistant who is familiar with thoracentesis can assist with positioning and setup. Typically, the patient sits at the edge of the bed, leaning forward over a bedside table with arms and hands resting on a pillow. The patient’s arms should be at shoulder level to aid in the “bucket handle” motion of the rib spaces, which will widen the intercostal space. A footstool, if available, should be provided. The patient should be at the foot of the bed with the affected side facing the foot of the bed. This allows the operator to avoid leaning over the entire width of the bed. The space behind the patient can be used for the procedure tray, or this can be placed on a separate procedure stand. The bed should also be raised to a height comfortable to the operator. If this positioning is not possible, the patient can lie in a lateral decubitus position with the affected side facing the bed, or sitting upright as much as the hospital bed will allow. After locating the entrance site with ultrasound and making an appropriate mark, the field should be sterilized. If chlorhexidine is used, the area should be scrubbed for at least 30 seconds, followed by 2 minutes of drying. If using povidone-iodine, three successive coats should be applied in enlarging concentric circles, with adequate time allowed between coats for drying. As some studies have shown that use of 2% chlorhexidine is more effective at preventing infectious complications of procedures than iodine solutions, we favor the use of chlorhexidine. What are the specific procedural steps in a thoracentesis? Preparation and time-out: Review labs and medications to assess the risk of bleeding, and review imaging studies to select an entrance location. Obtain informed consent. Gather your supplies and ultrasound, position the patient, and select your entry site. The operator should sterilize his or her hands, don a surgical gown, protective eye-wear, cap, and sterile gloves. Before anesthetizing the patient, a time-out should be performed according to local practice, ensuring verbal identification of the procedure and appropriate site and side. Local anesthesia: Using a 25-gauge needle, a small wheal should be raised using 1% lidocaine at the marked site. Lidocaine without epinephrine suffices as this is typically not a bloody procedure. After the superficial skin is numb, swap your anesthetic needle out for the longer 18- to 22-gauge needle. Using a cycle of advance-aspirate-inject (advance needle, aspirate to assess for fluid, inject lidocaine), the needle should be advanced from the skin surface in a somewhat cephalad direction over the top of the rib inferior to the marked site. “Walking” the needle over the rib ensures proper anesthesia of the rib, as well as maintaining a needle trajectory that is appropriately distanced from the intercostal neurovascular bundle (generally running under each rib). The parietal pleura is richly innervated, so as your needle approaches the parietal pleura, liberally apply lidocaine. Typically, 7-10 mL of 1% lidocaine is sufficient for the entire procedure. If one is performing a diagnostic tap, the needle can be advanced until pleural fluid is aspirated, after which a 60 mL syringe can be used to obtain a sample. In this method, take care to use a stopcock to avoid introducing air into the pleural space. If a therapeutic tap is being performed, note the needle depth and angle at which pleural fluid is obtained, as this is the targeted trajectory for the drainage catheter insertion. Placement of drainage catheter: After entering the pleural space with the small gauge needle and applying lidocaine, a scalpel is used to create a small skin incision to allow entry of the larger bore catheter through the skin. Subsequently, the needle/obturator and catheter assembly should be advanced along the same trajectory taken by the anesthetic needle. The syringe attached to the assembly should be drawn back while the needle is advancing. Care should be taken to apply equal pressures with the hand at the skin surface and the hand on the syringe, so as to avoid flexing the needle-catheter assembly. See below for signs/symptoms of complications which would necessitate stopping the procedure. Pleural fluid should be aspirated at the same depth as noted during deeper injection of lidocaine; if not, repeat assessment of the fluid pocket with ultrasound should be undertaken, as the fluid pocket may have shifted. Once pleural fluid is aspirated, the needle/obturator is advanced another millimeter, after which the catheter is slowly advanced into the pleural space while the needle/obturator is kept at the same depth. Then the needle/obturator is removed slowly and remains external to the skin surface for the remainder of the procedure. Drainage of pleural fluid and determining when to stop: The drainage tubing is attached to the stopcock, and a 60 mL syringe is attached to either the side port of the stopcock (in the case of a straight drainage catheter) or to the bidirectional end of the Y-tubing included in some trays. Fluid is then hand-aspirated using the 60 mL syringe, and then enters the 2 L collection bag via the efferent limb of the Y-tubing. The procedure should be stopped when any of the following occur: No further fluid can be aspirated. The patient develops persistent coughing or chest pain. 1.5-2 L of fluid has been drained. This ~2 L upper limit on volume removal is a general guideline, rather than an inviolable limit. There are many reports of uncomplicated removal of very large pleural fluid volumes (>3-6 L), and it is clear that some patients will tolerate a very large volume removal. However, a 9,000 patient single center retrospective analysis found the removal of more than 1.5 L of pleural fluid is associated with increased risk of reexpansion pulmonary edema and pneumothorax. Additional studies found a substantial stepwise increase in complication rates for every additional 0.4 L removed above 1.8 L. In addition to the removed volume, one can monitor pleural pressure periodically with a disposable manometer or with a fluid column, which can avoid the development of excessively negative pleural pressure. This will reduce the risk of pneumothorax and reexpansion pulmonary edema, with a “stopping point” occurring when the pleural pressure falls to around -20 cm H20. Finally, because vacuum bottles apply a constant excessive negative pressure and do not allow one to “feel” when pleural pressure is becoming increasingly negative, some suggest they should not be used during thoracentesis as they may increase the risk of pneumothorax. Needle removal: Once the desired amount of fluid is removed, the catheter can be removed. Having the patient hum while pulling the catheter makes the pleural pressure higher than atmospheric, avoiding inadvertent air entry into the pleural space as the catheter is pulled. A bandage is placed over the entry site. Post-procedure assessment: The patient should be re-examined after the procedure to reassess the size of the pleural effusion. From a safety perspective, routine post-procedure chest radiographs are unnecessary, but are frequently obtained to assess the size of the residual pleural effusion after drainage. III. Common Pitfalls. I aspirate air while advancing my needle/catheter? This can be a sign of a pneumothorax. The needle should be withdrawn and a portable chest x-ray should be obtained immediately. Supplemental oxygen should be provided. Treatment of a pneumothorax is discussed in a separate entry. I aspirate blood while advancing my needle/catheter? This can be a sign of intercostal vessel injury. The needle should be withdrawn and a portable chest x-ray should be obtained. If there is no change in the chest radiograph and the patient’s condition, the procedure can be reattempted at a site at least 1 cm distant from the original site. Of note, malignant pleural effusions are often serosanguinous. Treatment of hemothorax and pneumothorax is discussed in a separate entry. The patient develops lightheadedness, chest/shoulder pain, or increased dyspnea/coughing while advancing the needle/obturator? This can be a sign of a vasovagal event, pneumothorax, or hemothorax. The needle should be withdrawn and a portable chest x-ray should be obtained. Reattempting the procedure is possible if the patient’s condition resolves and there is no evidence of complication. The patient develops right or left upper quadrant pain during or after the procedure? This can be a sign of injury to the liver or spleen, respectively. The procedure should be stopped, and a CT scan of the abdomen should be performed immediately. The patient coughs repeatedly during the procedure. In large effusions, the occasional cough commonly occurs and can be a sign that previously atelectatic lung is now re-expanded. Alternatively, the pleural drainage catheter may be irritating the now expanded lung or the patient may be developing a pneumothorax. These coughing fits typically occur after the majority of the effusion has been drained and can suggest the need to end the procedure. If the coughing is persistent or associated with pain, it is reasonable to stop the procedure and obtain a CXR to rule out a pneumothorax. The patient develops chest pain, hypotension, or dyspnea either during fluid aspiration or afterwards? If immediate, this can be a sign of a pneumothorax. If somewhat delayed, this can be a sign of re-expansion pulmonary edema, which usually occurs within 1 hour after thoracentesis, but can occur up to 24 hours afterwards. Chest radiographs should be obtained immediately to assess for pneumothorax and reexpansion pulmonary edema, as well as any other clinically appropriate studies given the possible etiologies of these symptoms. Treatment of reexpansion pulmonary edema is discussed in a separate entry. After a small volume of fluid is aspirated, no further fluid can be aspirated from what appears to be a large effusion? This could represent the catheter becoming “suctioned” to a pleural surface. This is more common when using vacuum bottles, and thus these should be avoided. When this occurs, some maneuvers that can re-initiate flow include pulling back slightly on the catheter, repositioning the patient, or performing the Valsalva maneuver. What should I write in my procedure note? Procedure notes are often written on pre-printed forms or EMR templates and should include the following elements: name of procedure; operator, and assistants (and level of training if appropriate); pre- and post-procedure diagnoses; indications for procedure; anesthetic medication and route used; type of consent obtained; use of a time-out; use of ultrasound guidance; sterile preparation of the patient; description of needle/obturator and catheter used; volume and description of fluid removed; types of laboratory analysis performed on fluid; complications (if any). How should I bill for the procedure? There is often confusion when deciding which CPT codes to use for thoracentesis. Code 32555 is generally used. Can I bill if I use ultrasound guidance? CPT code 32555 now includes the use of ultrasound and no additional code with modifier is needed. VII. What’s the Evidence? Havelock, T, Teoh, R, Laws, D, Gleeson, F. “Pleural procedures and thoracic ultrasound: British Thoracic Society Pleural Disease Guideline 2010”. Thorax. vol. 65. 2010. pp. ii61-i76. Ault, MJ, Rosen, BT, Scher, J, Feinglass, J, Barsuk, JH. “Thoracentesis outcomes : a 12-year experience”. Thorax. vol. 70. 2015. pp. 127-132. Hibbert, RM, Atwell, TD, Lekah, A. “Safety of ultrasound-guided thoracentesis in patients with abnormal preprocedural coagulation parameters”. Chest. vol. 144. 2013. pp. 456-463. Gordon, CE, Feller-Kopman, D, Balk, EM, Smetana, GW. “Pneumothorax following thoracentesis: a systematic review and meta-analysis”. Arch Intern Med. vol. 170. 2010. pp. 332-339. Villena, V, López-Encuentra, A, Pozo, F, De-Pablo, A, Martín-Escribano, P. “Measurement of pleural pressure during therapeutic thoracentesis”. Am J Respir Crit Care Med. vol. 162. 2000. pp. 1534-1538. Feller-Kopman, D, Walkey, A, Berkowitz, D, Ernst, A. “The relationship of pleural pressure to symptom development during therapeutic thoracentesis”. Chest. vol. 129. 2006. pp. 1556-1560. Yoneyama, H, Arahata, M, Temaru, R, Ishizaka, S, Minami, S. “Evaluation of the risk of intercostal artery laceration during thoracentesis in elderly patients by using 3D-CT angiography”. Intern Med. vol. 49. 2010. pp. 289-292. Kanai, M, Sekiguchi, H. “Avoiding vessel laceration in thoracentesis: A role of vascular ultrasound with color Doppler”. Chest. vol. 147. 2015. pp. e5-e7. Darouiche, RO, Wall, MJ, Itani, KMF. “Chlorhexidine-Alcohol versus Povidone-Iodine for surgical-site antisepsis”. N Engl J Med [Internet]. vol. 362. 2010. pp. 18-26. Tuuli, MG, Liu, J, Stout, MJ. “A randomized trial comparing skin antiseptic agents at cesarean delivery”. N Engl J Med. vol. 274. 2016. pp. 647-755. Feller-Kopman, D, Berkowitz, D, Boiselle, P, Ernst, A. “Large-volume thoracentesis and the risk of reexpansion pulmonary edema”. Ann Thorac Surg. vol. 84. 2007. pp. 1656-1661. Josephson, T, Nordenskjold, C, Larsson, J, Rosenberg, LU, Kaijser, M. “Amount drained at ultrasound-guided thoracentesis and risk of pneumothorax”. Acta radiol. vol. 50. 2009. pp. 42-47. Petersen, WG, Zimmerman, R. “Limited utility of chest radiograph after thoracentesis”. Chest. vol. 117. 2000. pp. 1038-1042. Alemán, C, Alegre, J, Armadans, L. “The value of chest roentgenography in the diagnosis of pneumothorax after thoracentesis”. Am J Med. vol. 107. 1999. pp. 340-343. Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM. - I. Problem/Challenge. - II. Describe a Step-by-Step approach/method to this problem. - When should I do it? - What might stop me from doing it? - How do I learn how to do it? - Am I allowed to do the procedure independently? - Do I need a pre-assembled tray, and which one should I use? - What supplies do I need if I don’t use a thoracentesis tray? - How should I use ultrasound to guide thoracentesis? - How should the patient be positioned and prepared? - III. Common Pitfalls.	2	10	4	0	0	1	0.731579	5	5,677
Autoimmune disease can cause nerve damage from your immune system attacking and damaging parts of your body. Click to learn more. People who have peripheral neuropathy commonly experience pain, numbness, tingling, weakness and other muscle or nerve-related symptoms. Symptoms of neuropathy often begin slowly and in one specific area, and eventual spread and intensify. Neuropathy often affects people with autoimmune diseases, however. Aug 9, 2017. Causes. Not a single disease, peripheral neuropathy is nerve damage caused by a number of conditions. Causes of neuropathies include: Alcoholism. Poor dietary choices made by people with alcoholism can lead to vitamin deficiencies. Autoimmune diseases. These include Sjogren's syndrome, lupus, Sjogren's syndrome, lupus, and rheumatoid arthritis are among the autoimmune diseases that can be associated with peripheral neuropathy. When the tissue surrounding nerves becomes inflamed, the inflammation can spread directly into nerve fibers. Over time, these chronic autoimmune conditions can destroy joints, Regardless of the cause, neuropathy is associated with characteristic symptoms. Although some people with neuropathy may not have symptoms, certain symptoms are common. The degree to which an individual is affected by a particular neuropathy varies. Damage to the sensory nerves is common in peripheral. Apr 16, 2010. There are many types of peripheral neuropathy, which can be brought on by diabetes, genetic predisposition (hereditary causes), exposure to toxic chemicals, alcoholism, malnutrition, inflammation (infectious or autoimmune), injury and nerve compression, and by taking certain medications such as those. Diabetic neuropathy refers to a group of nerve disorders caused by diabetes. Diabetic neuropathy can affect nerves throughout the body, although it most. Peripheral neuropathy — Comprehensive overview covers diagnosis, causes and treatment of this often painful disorder. Peripheral Neuropathy Treatments Drugs Peripheral neuropathy refers to a condition that results from damage to the peripheral nervous system—the nerves that connect the brain and spinal. Find information on diabetic nerve pain including symptoms, diagnosis & treatment. See risks & benefits of. NERVE PAIN*. LYRICA (pregabalin) is FDA- approved to treat painful diabetic peripheral neuropathy, also known as diabetic association of celiac disease and neuropathy: 1. A nutritional deficiency due to malabsorption. Deficiency of some vitamins (especially B12, B6 and E), and metals (especially copper) are well known to cause a peripheral neuropathy. 2. Patients who have one autoimmune disease are predisposed to another autoimmune. Google in Health Google is making significant investments in health, wellness, and life sciences. Here are some of the teams focusing efforts in. Nerve Report: 2017 Release. Don’t try anything before you read. ICD-10 Version:2010 Chapters. Certain infectious and parasitic diseases Neoplasms Diseases of the blood and blood-forming organs and certain. Systemic diseases — disorders that affect the entire body —often cause peripheral neuropathy. These disorders. autoimmune disorders can cause peripheral. Disorders. All Disorders. NINDS Binswanger’s Disease Information Page; NINDS Brachial Plexus Injuries Information Page; NINDS Brown-Sequard Syndrome. 2 Neuropathy Treatment Myths Revealed Millions of people suffer daily from the pain associated with peripheral neuropathy. If you or someone you The term peripheral neuropathy encompasses a wide range of disorders in which the nerves outside of the brain and spinal cord—peripheral nerves—have been damaged. Peripheral neuropathy may also be referred to as peripheral neuritis, or if many nerves are involved, the terms polyneuropathy or polyneuritis may be. Test for autoimmune neuropathies, including Guillain-Barré syndrome. Treatment of acquired peripheral neuropathy that is the result of trauma or injury often involves addressing the injury early on and physical therapy to increase muscle strength. While peripheral neuropathies that are the result of a systemic disease, infections or autoimmune disorders are generally treated by managing the. Peripheral neuropathy may be either inherited or acquired. Causes of acquired peripheral neuropathy include physical injury (trauma) to a nerve, tumors, toxins, autoimmune responses, nutritional deficiencies, alcoholism, and vascular and metabolic disorders. Do you have numb or painful hands or feet? Neuropathy affects every part of your life, walking, sitting even sleeping. Common symptoms include: numbness or. May 30, 2016. Chronic inflammatory demyelinating polyneuropathy (CIDP) is a disorder that involves nerve swelling and irritation (inflammation) that leads to a loss of strength or sensation. Causes. Expand Section. CIDP is one cause of damage to nerves outside the brain or spinal cord (peripheral neuropathy). Drugs Treat Diabetic Neuropathy Compare risks and benefits of common medications used for Peripheral Neuropathy. Find the most popular drugs, view ratings, user reviews, and more. LEARN ABOUT Homeopathy Treatment of Neuropathy & Diabetic Neuropathy. Peripheral Neuropathy cause, symptoms, diagnosis, homeopathic remedies for neuropathy. LEARN ABOUT Homeopathy Treatment of Neuropathy & Diabetic Neuropathy. Peripheral Neuropathy cause, symptoms, diagnosis, homeopathic Celiac disease, or gluten sensitivity, is an autoimmune inflammatory disease that damages the villi – the small, finger-like projections that line the. Many of us have experienced severe burning, numbness, and tingling after hitting our “funny bone.” This is caused by trauma to the ulnar nerve at the. Peripheral neuropathy occurs when the nerves in the arms and legs are damaged due to injury or disease. The condition causes a wide range of symptoms such. Neuropathy, or peripheral neuropathy, describes a range of disorders characterized by nerve damage to one or more nerves outside of the brain and spinal cord. Often autoimmune diseases and vitamin deficiencies are some of the potential causes, according to the Mayo Clinic. Gluten neuropathy is when the autoimmune. Peripheral Nerve Disorders. There are many types of peripheral neuropathy, often brought on by diabetes; genetic predispositions (hereditary causes); exposure to. Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated inflammatory disorder of the peripheral nervous system. The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy CIDP is closely related to. Peripheral neuropathy. a condition that develops as a result of damage to the peripheral nervous system — the vast communications. Autoimmune diseases, Autoimmune peripheral neuropathy information including symptoms, diagnosis, misdiagnosis, treatment, causes, patient stories, videos, forums, prevention, and prognosis. PERIPHERAL NEUROPATHY. Peripheral neuropathy is damage to the peripheral nerves. Peripheral nerves are the nerves that connect your spinal cord to the rest. Peripheral neuropathy is a disorder that. peripheral neuropathy. Autoimmune diseases like. neuropathy can interfere with the peripheral. AutoImmune Disease MS Hashimotos Lupus RA Neuropathy Fibromyalgia Ataxia. Autoimmune disease ms hashimotos lupus ra neuropathy fibromyalgia ataxia,Autoimmune disease. Nov 20, 2014. There are many different types of neuropathies in Sjögren's. These neuropathies can have different causes and may require different diagnostic techniques & therapeutic strategies. Unlike other autoimmune disorders, in which the neuropathies predominantly cause weakness, the neuropathies in Sjögren's. Peripheral neuropathy occurs when the nerves in the arms and legs are damaged due to injury or disease. The condition causes a wide range of symptoms such as numbness or tingling, weak muscles, loss of sensations and insensitivity to temperature. Autoimmune diseases result from a malfunction of the body's immune. Peripheral neuropathy has a variety of systemic, metabolic, and toxic causes. The most common treatable causes include diabetes mellitus, hypothyroidism. Difference Between Diabetes Diabetic Neuropathy Diabetes does create the nerve cells vulnerable to damage, but there are many ways in which nerves can get damaged. What are the different ways that someone will get neuropathy? Diabetic neuropathy is a result of prolonged elevated levels of blood glucose. Chemotherapy Neuropathy is caused by damage that is done. Jan 9, 2017. Diabetic Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health. We Tested 100 Peripheral Neuropathy Brands. You Will Be Shocked At What We Found Damage to the sensory nerves is common in peripheral neuropathy. percent of people over the age of 20 years will develop chronic kidney disease in their. Learn about peripheral neuropathy causes such as diabetes, alcohol, medication, shingles, vitamin deficiency, autoimmune diseases, and inherited diseases. Learn about. Neuropathy Disorders (From emedicinehealth.com) Neuropathy Overview. Neuropathy is a term that refers to general diseases or malfunctions of the nerves. The exact cause of CIDP is unknown but there are strong indications that CIDP is an autoimmune disorder. Autoimmune. Others believe it, along with multifocal motor neuropathy, represents part of a disease spectrum. There are a number of other peripheral neuropathies that can cause similar symptoms as CIDP. What is peripheral neuropathy?How are the peripheral neuropathies classified?What are the symptoms of. Peripheral Neuropathy Fact. Autoimmune diseases, Read our article and learn more on MedlinePlus: Peripheral neuropathy The central nervous system includes the brain and spinal cord. Peripheral nerves are located outside the brain and spinal cord. They carry information. Peripheral neuropathy is a disorder that occurs when your peripheral nerves malfunction because they’re damaged. Obtain Relief from Peripheral Neuropathy by Using Natural Remedies. Monday, September 20, 2010 by: Luella May Tags: peripheral neuropathy, remedies, health. Peripheral Nerve Disorders. There are many types of peripheral neuropathy, often brought on by diabetes; genetic predispositions (hereditary causes. Depending on the particular type of neuropathy, a neurologist may provide treatment for autoimmune mediated process with Immunoglobulin. Neuropathies caused by nerve entrapment or injuries can be treated with surgery. Our neurosurgeons, led by Dr. Nickolas Boulis who specializes in disorders of the peripheral. Autoimmune Disease, in which your immune system attacks and damages parts of your body, including your nerves. Examples include Sjogren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain- Barre syndrome is an autoimmune disease that happens rapidly and can affect. More Neuropathy Articles ... - Vitamin B Complex For Peripheral Neuropathy: Dr. Janet Abrahm discusses her approach to the management of chemotherapy-induced peripheral neuropathy. As a result, B12 deficiency–induced nerve damage may be confused with or contribute to diabetic peripheral neuropathy. queried were metformin, in... - Earliest Sign Of Diabetic Autonomic Neuropathy: Diabetic Neuropathies: Diagnosis and Management. the earliest manifestations of autonomic neuropathy in. Diabetic autonomic neuropathy initially. Diabetic Neuropathies: Diagnosis and Management. the earliest manifestations of autonomic neuropathy in.... - Natural Treatment For Peripheral Neuropathy In Feet: ★★ Treatment Diabetic Peripheral Neuropathy ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ TREATMENT DIABETIC. Peripheral neuropathy is a type of nerve damage that affects the way your body's nerves send signals to... - Hereditary Spastic Paraplegia Peripheral Neuropathy: Hereditary motor and sensory neuropathy type V is a very rare disease in which hereditary spastic paraplegia is associated with peripheral motor and sensory neuropathy. Hereditary Spastic Paraplegia Information Page. cognitive impairment, peripheral ... - Role Of Vitamin B12 In Diabetic Neuropathy: Related TermsAdenosylcobalamin, AdoB12, B complex, B complex vitamin, B-12, bedumil, cobalamin, cobalamins, cobamin, cyanocobalamin, cyanocobalamine. We Tested The Top 49 National Brands. You Will Be Shocked At What We Found. between vitamin B12 defi... - New Insights Into Mechanisms Diabetic Neuropathy: Pathology and pathogenetic mechanisms of diabetic neuropathy: Correlation with. pathogenetic mechanisms of diabetic. New insights into diabetic. September 2014 Issue. Curcumin and Inflammatory Diseases: Learn About Its Potential Role in Prevention an...	2	8	0	0	0	4	0.824568	4	2,745
Health Indicator Report of Asthma Emergency Department Visits among Children Asthma is one of the common chronic diseases in New Mexico, with an estimated 45,503 children currently having the disease. People with asthma are more likely to miss school or work, report feelings of depression, and experience an overall reduced quality of life. Asthma is also costly, with expenses from routine checkups, emergency department visits, hospitalizations, and medications putting a significant burden on families, the health care sector, and the economy. Though it cannot be cured, asthma can be controlled through quality health care, appropriate medications, and good self-management skills. When asthma is controlled, people with the disease have few, if any, symptoms, and can live normal and productive lives. NotesCrude rate per 10,000 population. ICD Stands for International Classification of Diseases. It is a coding system maintained by the World Health Organization and the U.S. National Center for Health Statistics used to classify causes of death on death certificates and diagnoses, injury causes, and medical procedures for hospital and emergency department visits. These codes are updated every decade or so to account for advances in medical technology. The U.S. is currently using the 10th revision (ICD-10) to code causes of death. The 9th revision (ICD-9) was still in use for hospital and emergency department visits until October 1st, 2015. After this date, hospitals were required to use ICD-10 codes. Crude Rates, ED Visits Per 10,000 Population - Emergency Department (ED) dataset, Health Systems Epidemiology Program, New Mexico Department of Health. - Population Estimates: University of New Mexico, Geospatial and Population Studies (GPS) Program, http://gps.unm.edu/. Data Interpretation IssuesWhen utilizing these data, the following caveats should be noted: Data are submitted by 36 individual hospital emergency departments. Different hospitals have different medical records systems with different capacities to extract data, file formats that are produced, and definitions for when a patient is an inpatient or an outpatient. Data submitted by individual hospital emergency departments to the interim data set are not in the National Health Level Seven (HL7) standard format or content and caution should be taken when comparing these data to other state or federal data. Data submitted have been examined for internal consistency and to determine whether they have conformed to the NMDOH request guidelines. Data do not include emergency department visits to Indian Health Services or Veteran Affair's hospitals. Data do not include emergency department visits from those New Mexico residents who visit out of state emergency departments. Emergency Department (ED) data are collected from facilities yearly. The long-term plan is for the New Mexico Department of Health (NMDOH) to collect these data through an ED electronic reporting (e-reporting) system currently being developed with the New Mexico Health Information Collaborative (NMHIC). However, not all facilities are reporting to the ED e-reporting system at this time. Therefore, in the interim, we have requested that each facility submit its data directly to the NMDOH. The department is authorized to request and receive these data under the Public Health Act which grants the department authority to "Investigate, control and abate the cause of disease" (NMSA 1978 Section 24-1-3C). Additional authority was enacted (NMAC 18.104.22.168) on April 30, 2009 which specifically requires that all non-federal emergency departments in the State of New Mexico must comply with NMDOH requests for ED data. DefinitionAn asthma emergency department visit-Child is a visit by a New Mexico resident 0 to 17 years of age to an emergency department that occurs in state with asthma listed as the primary (first-listed) diagnosis. Asthma emergency department visits include those with ICD-9 codes 493.0-493.49 and/or ICD-10 code J45 NumeratorNumber of emergency department visits of children where asthma is the primary (first-listed) diagnosis. DenominatorEstimated number of New Mexico children in a specified population over a specified time period. Healthy People Objective: RD-3, Reduce hospital emergency department visits for asthmaU.S. Target: Not applicable, see subobjectives in this category How Are We Doing?For the period 2010 to 2016, asthma ED visits by children slightly increased starting 2012 and began to slightly decrease starting in 2015. How Do We Compare With the U.S.?There are no recent adults-specific national data for comparison. What Is Being Done?The New Mexico Department of Health Asthma Program collects, analyzes, and disseminates asthma data in order to identify populations that have a high burden of asthma. The Asthma Program also works with partners throughout the state (such as hospitals, physician groups, insurance plans, and schools) to design and implement health interventions to lessen the disease burden. Current interventions include providing asthma self-management education to pediatric patients, supporting indoor air quality assessments of homes to limit exposures to potential asthma triggers, and offering provider training on the National Asthma Education and Prevention Program (NAEPP) asthma medical guidelines. Evidence-based PracticesAsthma and its symptoms can be controlled and related impairments or hospitalizations can be prevented. According to the Centers for Disease Control and Prevention, the NAEPP of the National Institutes of Health-National Heart, Lung, and Blood Institute have issued guidelines for the diagnosis and management of asthma. These guidelines translated advances in scientific and clinical research into practical advice for people with asthma, for the health care providers who look after them, and for the communities where they live. Available ServicesThe New Mexico Asthma Program, funded entirely through a cooperative agreement with the Centers for Disease Control, supports health intervention activities aimed at increasing asthma awareness in the state, improving asthma self-management through patient education initiatives, and providing health care provider training on the latest National Heart, Lung, and Blood Institute Asthma Guidelines for medical practice. The Asthma Program works with partners (e.g., hospitals, physicians, insurance plans, and schools) throughout the state to design and implement health interventions to lessen asthma burden, especially in areas of asthma disparities. Current interventions include providing asthma self-management education to pediatric patients and training Community Health Workers for home visits with people with asthma to assist them in identifying and eliminating irritants and triggers from the house. For more information about the National Asthma Education and Prevention Program's (NAEPP) Guidelines for the Diagnosis and Treatment of Asthma visit https://www.nhlbi.nih.gov/health-pro/guidelines/current/asthma-guidelines New Mexico Asthma Program Information For information about the asthma program in New Mexico visit https://nmhealth.org/about/erd/eheb/ap/ Asthma Program, New Mexico Department of Health, P.O. Box 26110, 1190 St. Francis Drive, Suite N1300, Santa Fe, NM 87505. Health Program InformationAsthma Program, New Mexico Department of Health, P.O. Box 26110, 1190 St. Francis Drive, Suite N1300, Santa Fe, NM 87505. Heidi Krapfl, Principal Investigator, (505) 476-3577, [email protected]. Page Content Updated On 02/22/2019, Published on 03/08/2019	3	5	2	0	2	2	0.585268	6	1,526
The premature expulsion of the products of conception from the uterus is known as Abortion. It can be embryo or a non-viable fetus. In simple words, the coding or labeling of the medical report named as spontaneous abortion may be somewhat problematic. The CPT codes properly use the medical term abortion. For abortion, another term “interrupted pregnancy” is often used. It refers to a pregnancy that did not proceed to full term. A full-term pregnancy is normally between 38 and 42 weeks of gestation. There are numerous ways to classify an interrupted pregnancy. It can be an abortion or it can be a miscarriage. Abortion or miscarriage both are considered as natural death of an embryo or fetus. A miscarriage is one of the most common complications of early pregnancy. Most commonly, a miscarriage happens within the first trimester of pregnancy. Generally coding for these types of complications can be difficult, as they don’t come under “normal pregnancy package “of antepartum care, delivery, and postpartum care. There is a slight difference in timeframe definition of the term abortion versus fetal death, when we talk about the transition from ICD-9-CM to CD-10-CM. In ICD-9-CM, the definition of abortion codes is 22 weeks. In ICD-10-CM, the timeframe is changed to 20 weeks. The clinical documentation for the notation of trimester, or the notation of gestational weeks, in ICD-10-CM is imperative i.e. First trimester is 0-14 weeks, second trimester is 14-28 weeks, third trimester is 28-40 weeks. Abortion CPT Codes: Elective, Missed, Spontaneous, Incomplete Abortions may be categorized as either spontaneous, the natural termination of pregnancy prior to the 20th week of gestation, or a deliberate attempt has been made to terminate the pregnancy. There can be different causes of abortion, some of them are listed below: A missed abortion refers to the prolonged retention of a fetus that died in the first half of pregnancy. In other words, an empty gestational sac, blighted ovum or a fetus or fetal pole with a heartbeat prior to completion of 20 weeks 0 days gestation, is termed as missed abortion. The provider documents that a fetal death has occurred prior to the completion of 22 weeks gestation (in ICD-9-CM) or 20 weeks gestation (in ICD-10-CM) with the dead fetus remaining in the uterus for a period of time. According to ICD-9-CM definition, the timeframe used for missed abortion is 22 weeks while ACOG defines as 20 weeks. Beyond this period of time, code 656.43 is used for missed delivery, with diagnosis code: 632. Missed abortion code is reported with only 3 digits. The evacuation of the uterus in cases like Sounding of uterus for size, serial dilation of cervix with mechanical dilators, emptying uterine cavity of products of conception using, administration of intravenous oxytocin, removal of instruments or repair of cervical incision. All these steps are coded according to the trimester in which the procedure is performed i.e. - 59820 for the first trimester while completed surgically. - 59821 for the second trimester while completed surgically. Spontaneous Abortion (Miscarriage) A spontaneous abortion that is complete (any trimester) and the physician manages the patient medically, without any surgical intervention is termed as complete abortion. In other words, if POC are expelled without surgical or medical intervention. It is also called miscarriage. It can be further categorized as septic or non septic. When the tissue from a missed or incomplete miscarriage becomes infected, it is called septic miscarriage. The infection of the uterus carries risk of spreading infection (septicemia) and is a grave risk to the life of the woman. Diagnosis code for this case is 634 but procedure reported (depends on gestational age)with diagnosis code 634.X2. In such case, the physician should report the appropriate level of evaluation and management code, dependent on the place where the patient is seen. Code 99201 to 99233 are appropriate for such cases. An incomplete abortion occurs when the uterus is not entirely emptied of its contents. Fragments of the products of conception may remain within the uterus, or can be found in the vagina. Some fragments of the products of conception may have spontaneously passed out of the vagina. A condition like this is called incomplete abortion. The provider documents the POC "have not been expelled" or "incompletely expelled" from the uterus. Code 59812 is used to report the dilation and curettage for the surgical management of an incomplete abortion. Code 59812 is not appropriate, if the patient is septic and is diagnosed as experiencing an incomplete abortion. Codes for different types of Abortions Being a coder, your main task is to match up what is on the operative note to the CPT code for the most closely aligned services that are performed. Below is the entire listing of CPT services for abortive procedure services: - 59812, treatment of incomplete abortion, any trimester, completed surgically. - 59820, treatment of missed abortion; completed surgically, first trimester. - 59821, treatment of missed abortion; completed surgically, second trimester. - 59830, surgical treatment of septic abortion, completed surgically. - 59840, induced abortion by dilation and curettage. - 59841, induced abortion by dilation and evacuation. - 59850, induced abortion by one or more intra-amniotic injections (amniocentesis injections), including hospital admission and visits, and delivery of fetus and secundines. - 59851, induced abortion by one or more intra-amniotic injections (amniocentesis injections), including hospital admission and visits, and delivery of fetus and secundines; with dilation and curettage and/or evacuation. - 59852, induced abortion by one or more intra-amniotic injections (amniocentesis injections), including hospital admission and visits, and delivery of fetus and secundines; with hysterotomy. - 59855, induced abortion one or more vaginal suppositories (e.g., prostaglandin) with or without cervical dilation (e.g., laminaria), including hospital admission and visits, delivery of fetus and secundines. - 59856, induced abortion one or more vaginal suppositories (e.g., prostaglandin) with or without cervical dilation (e.g., laminaria), including hospital admission and visits, delivery of fetus and secundines; with intra-amniotic injections, dilation and curettage and/or evacuation. - 59857, induced abortion one or more vaginal suppositories (e.g., prostaglandin) with or without cervical dilation (e.g., laminaria), including hospital admission and visits, delivery of fetus and secundines; with vaginal suppositories and hysterotomy.	4	12	20	0	0	0	0.471519	20	1,494
The National Diabetes Services Scheme (NDSS) was established in Australia in 1987 to deliver diabetes-related products at subsidised prices and provide information to people with diabetes. Registration of patients is carried out by a medical practitioner or certified diabetes educator. The NDSS captures 80–90% of all Australians with known diabetes . In total, 1,108,420 people were registered with type 2 diabetes on the NDSS between 1997 and 2011. The primary population for this analysis included 744,188 (67.1%) people with type 2 diabetes who had a date of diagnosis of diabetes listed on the NDSS. A secondary analysis included all type 2 diabetes registrants and used date of registration as a proxy for those whose date of diagnosis was missing (1,108,420 people). Although the NDSS was initially established in 1987, 1997 was chosen as the start date, as this time period followed a unification of state-based registries and consequently an improvement in data quality. Diabetes type is classified by the health practitioner who completes the registration. For the current analysis, type 2 diabetes was assigned to all registrants who were classified as type 2 on the NDSS. Type 1 diabetes status was assigned to registrants who were recorded as type 1 on the NDSS registry, were registered at <45 years of age and were taking insulin. We chose 45 years as the cut-off to minimise the number of people with type 1 diabetes that we would miss without misclassifying significant numbers of people with type 2 diabetes as type 1 diabetes. In addition, registrants who were recorded as having type 2 diabetes on the registry and who were diagnosed before the age of 30 years and were taking insulin within 1 year of diagnosis were reclassified as having type 1 diabetes. All others were classified as having type 2 diabetes. The NDSS was linked to the National Death Index up to 31 December 2011 by the Australian Institute of Health and Welfare as reported previously [15, 16]. The underlying cause of death was coded according to ICD-10 (www.who.int/classifications/icd/en). In the primary analysis, causes of death were classified as follows: cardiovascular disease (CVD) I20–I25, I60–I69 or ‘diabetes with circulatory complications’ (E10.5, E11.5, E12.5, E13.5, E14.5), cancer C00–C97 and other underlying causes of death (non-CVD and non-cancer). We also explored mortality from ischaemic heart disease (IHD) (I20–I25), stroke (I60–I69), pancreatic cancer (C25–25.9), lung cancer (C33–C35.9) and colorectal cancer (C18–C20.9), since they are among those with the highest cancer death rates in individuals with diabetes in Australia. Deaths with an underlying cause corresponding to ‘uncomplicated diabetes’ (E10.9, E11.9, E12.9, E13.9, E14.9) where a CVD, IHD or stroke ICD code also appeared in the first line of part I on the death certificate were also included in the respective group. We considered these deaths as due to CVD, IHD or stroke, as it is not possible to die from ‘uncomplicated diabetes’. The NDSS dataset linked to the NDI has previously been used to present age-specific mortality rates among those with diabetes . Statistical analysis and reporting Individuals were followed from 1 January 1997, or registration date if later, to 31 December 2011 or date of death, whichever occurred first. Participants’ follow-up (risk time and deaths) was first split into intervals of 6 months by current age (0–100 years), calendar time (1997–2011 incl.) and diabetes duration (0–20 years). Risk time and deaths (overall and by cause) were subsequently tabulated by current age, date of follow-up and diabetes duration, and each cell of the table was assigned age, date and diabetes duration as continuous variables as the midpoint of the 6 month group. Age at diagnosis was calculated as current age minus diabetes duration. Data were analysed using a Poisson model, using log-person-time as the offset variable and spline effects of current age, diabetes duration and age at diagnosis, and with a linear effect of calendar time. The model is formally over-parametrised because age at diagnosis plus diabetes duration equals current age. Therefore, it is not possible to tease out the separate effects of age at diabetes diagnosis and diabetes duration. We only used the model for prediction of rates, and these do not depend on any particular parametrisation. Separate models were fitted for men and women. The predicted mortality rates by current age for individuals diagnosed at different ages are shown in Fig. 1. To illustrate the effect of age at diagnosis and duration of type 2 diabetes, we computed the mortality rate ratio (also known as HR) between individuals diagnosed at ages 5 years apart as a function of age at follow-up (e.g. age 40 vs 45 at diagnosis, followed from age 45 to 60). Thus, each point on each curve indicates the mortality risk for a person diagnosed at one age compared with a person diagnosed at 5 years older, when both individuals have achieved the same age. Different curves were used to illustrate how this effect varies by age at diagnosis, by comparing individuals diagnosed at ages 45 vs 50, 50 vs 55, etc. The same was done for a 10 year difference in diabetes duration, by comparing individuals diagnosed at ages 40 vs 50, 45 vs 55, etc. The two sets of curves are shown in adjacent graphs in Fig. 2. On the basis of the underlying cause of death for people with type 2 diabetes, we carried out the same analyses for cause-specific mortality from CVD, cancer and other causes of death. We report results on two populations: the primary population is that for which age of diabetes diagnosis is available (n = 744,188). For this analysis, after excluding 479 registrants, because the registration date was the same as the date of death or the dates were implausible, the sample size was 743,709. However, given that only 67% of the entire NDSS type 2 diabetes cohort over the time period 1997–2011 had the date of diabetes recorded, the analysis was repeated for all registrants using the registration date as a proxy for those with a missing date of diagnosis (n = 1,108,420). After excluding 743 registrants because the registration date was the same as the date of death, or the dates were implausible, the sample size for the sensitivity analysis was 1,107,677. All analyses and graphs were generated with R software, version 3.4.2 (www.R-project.org) (R Foundation for Statistical Computing, Vienna, Austria), using packages Epi and popEpi. The study was approved by the Alfred Health Human Ethics Committee and the Australian Institute of Health and Welfare Ethics Committee. All participants gave informed consent for their data to be used in the analyses. A complete account of the data analyses can be found at http://bendixcarstensen.com/IDI/mort/AUS-DM-mort.pdf. The data that support the findings of this study are not publicly available as they were generated under a licence which restricted access to named, approved investigators.	4	13	0	0	0	6	0.458424	6	1,556
Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with cellular oxygen requirements at rest or during stress. It is characterized by fluid retention, shortness of breath, and fatigue, in particular on exertion. Heart failure is a growing public health problem, the leading cause of hospitalization, and a major cause of mortality. Ischemic heart disease is the main cause of heart failure. Ventricular remodelling refers to changes in structure, size, and shape of the left ventricle. This architectural remodelling of the left ventricle is induced by injury (e.g., myocardial infarction), by pressure overload (e.g., systemic arterial hypertension or aortic stenosis), or by volume overload. Since ventricular remodelling affects wall stress, it has a profound impact on cardiac function and on the development of heart failure. A model of permanent ligation of the left anterior descending coronary artery in mice is used to investigate ventricular remodelling and cardiac function post-myocardial infarction. This model is fundamentally different in terms of objectives and pathophysiological relevance compared to the model of transient ligation of the left anterior descending coronary artery. In this latter model of ischemia/reperfusion injury, the initial extent of the infarct may be modulated by factors that affect myocardial salvage following reperfusion. In contrast, the infarct area at 24 hr after permanent ligation of the left anterior descending coronary artery is fixed. Cardiac function in this model will be affected by 1) the process of infarct expansion, infarct healing, and scar formation; and 2) the concomitant development of left ventricular dilatation, cardiac hypertrophy, and ventricular remodelling. Besides the model of permanent ligation of the left anterior descending coronary artery, the technique of invasive hemodynamic measurements in mice is presented in detail. 24 Related JoVE Articles! Gene Transfer for Ischemic Heart Failure in a Preclinical Model Institutions: Mount Sinai School of Medicine . Various emerging technologies are being developed for patients with heart failure. Well-established preclinical evaluations are necessary to determine their efficacy and safety. Gene therapy using viral vectors is one of the most promising approaches for treating cardiac diseases. Viral delivery of various different genes by changing the carrier gene has immeasurable therapeutic potential. In this video, the full process of an animal model of heart failure creation followed by gene transfer is presented using a swine model. First, myocardial infarction is created by occluding the proximal left anterior descending coronary artery. Heart remodeling results in chronic heart failure. Unique to our model is a fairly large scar which truly reflects patients with severe heart failure who require aggressive therapy for positive outcomes. After myocardial infarct creation and development of scar tissue, an intracoronary injection of virus is demonstrated with simultaneous nitroglycerine infusion. Our injection method provides simple and efficient gene transfer with enhanced gene expression. This combination of a myocardial infarct swine model with intracoronary virus delivery has proven to be a consistent and reproducible methodology, which helps not only to test the effect of individual gene, but also compare the efficacy of many genes as therapeutic candidates. Medicine, Issue 51, Myocardial infarction, Gene therapy, Intracoronary injection, Viral vector, Ischemic heart failure Design of a Cyclic Pressure Bioreactor for the Ex Vivo Study of Aortic Heart Valves Institutions: Mississippi State University. The aortic valve, located between the left ventricle and the aorta, allows for unidirectional blood flow, preventing backflow into the ventricle. Aortic valve leaflets are composed of interstitial cells suspended within an extracellular matrix (ECM) and are lined with an endothelial cell monolayer. The valve withstands a harsh, dynamic environment and is constantly exposed to shear, flexion, tension, and compression. Research has shown calcific lesions in diseased valves occur in areas of high mechanical stress as a result of endothelial disruption or interstitial matrix damage1-3 . Hence, it is not surprising that epidemiological studies have shown high blood pressure to be a leading risk factor in the onset of aortic valve disease4 The only treatment option currently available for valve disease is surgical replacement of the diseased valve with a bioprosthetic or mechanical valve5 . Improved understanding of valve biology in response to physical stresses would help elucidate the mechanisms of valve pathogenesis. In turn, this could help in the development of non-invasive therapies such as pharmaceutical intervention or prevention. Several bioreactors have been previously developed to study the mechanobiology of native or engineered heart valves6-9 . Pulsatile bioreactors have also been developed to study a range of tissues including cartilage10 . The aim of this work was to develop a cyclic pressure system that could be used to elucidate the biological response of aortic valve leaflets to increased pressure loads. The system consisted of an acrylic chamber in which to place samples and produce cyclic pressure, viton diaphragm solenoid valves to control the timing of the pressure cycle, and a computer to control electrical devices. The pressure was monitored using a pressure transducer, and the signal was conditioned using a load cell conditioner. A LabVIEW program regulated the pressure using an analog device to pump compressed air into the system at the appropriate rate. The system mimicked the dynamic transvalvular pressure levels associated with the aortic valve; a saw tooth wave produced a gradual increase in pressure, typical of the transvalvular pressure gradient that is present across the valve during diastole, followed by a sharp pressure drop depicting valve opening in systole. The LabVIEW program allowed users to control the magnitude and frequency of cyclic pressure. The system was able to subject tissue samples to physiological and pathological pressure conditions. This device can be used to increase our understanding of how heart valves respond to changes in the local mechanical environment. Bioengineering, Issue 54, Mechanobiology, Bioreactor, Aortic Heart Valve, Organ Culture Assessment of Cardiac Function and Energetics in Isolated Mouse Hearts Using 31P NMR Spectroscopy Institutions: University of Washington School of Medicine. Bioengineered mouse models have become powerful research tools in determining causal relationships between molecular alterations and models of cardiovascular disease. Although molecular biology is necessary in identifying key changes in the signaling pathway, it is not a surrogate for functional significance. While physiology can provide answers to the question of function, combining physiology with biochemical assessment of metabolites in the intact, beating heart allows for a complete picture of cardiac function and energetics. For years, our laboratory has utilized isolated heart perfusions combined with nuclear magnetic resonance (NMR) spectroscopy to accomplish this task. Left ventricular function is assessed by Langendorff-mode isolated heart perfusions while cardiac energetics is measured by performing 31 P magnetic resonance spectroscopy of the perfused hearts. With these techniques, indices of cardiac function in combination with levels of phosphocreatine and ATP can be measured simultaneously in beating hearts. Furthermore, these parameters can be monitored while physiologic or pathologic stressors are instituted. For example, ischemia/reperfusion or high workload challenge protocols can be adopted. The use of aortic banding or other models of cardiac pathology are apt as well. Regardless of the variants within the protocol, the functional and energetic significance of molecular modifications of transgenic mouse models can be adequately described, leading to new insights into the associated enzymatic and metabolic pathways. Therefore, 31 P NMR spectroscopy in the isolated perfused heart is a valuable research technique in animal models of cardiovascular disease. Medicine, Issue 42, cardiac physiology, high energy phosphate, phosphocreatine, ATP Acute Myocardial Infarction in Rats Institutions: University of Texas Medical Branch, University of Houston (UH), Texas Medical Center. With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular diseases. Animal models that mimic human cardiac disease, such as myocardial infarction (MI) and ischemia-reperfusion (IR) that induces heart failure as well as pressure-overload (transverse aortic constriction) that induces cardiac hypertrophy and heart failure (Goldman and Tarnavski), are useful models to study cardiovascular disease. In particular, myocardial ischemia (MI) is a leading cause for cardiovascular morbidity and mortality despite controlling certain risk factors such as arteriosclerosis and treatments via surgical intervention (Thygesen). Furthermore, an acute loss of the myocardium following myocardial ischemia (MI) results in increased loading conditions that induces ventricular remodeling of the infarcted border zone and the remote non-infarcted myocardium. Myocyte apoptosis, necrosis and the resultant increased hemodynamic load activate multiple biochemical intracellular signaling that initiates LV dilatation, hypertrophy, ventricular shape distortion, and collagen scar formation. This pathological remodeling and failure to normalize the increased wall stresses results in progressive dilatation, recruitment of the border zone myocardium into the scar, and eventually deterioration in myocardial contractile function (i.e. heart failure). The progression of LV dysfunction and heart failure in rats is similar to that observed in patients who sustain a large myocardial infarction, survive and subsequently develops heart failure (Goldman). The acute myocardial infarction (AMI) model in rats has been used to mimic human cardiovascular disease; specifically used to study cardiac signaling mechanisms associated with heart failure as well as to assess the contribution of therapeutic strategies for the treatment of heart failure. The method described in this report is the rat model of acute myocardial infarction (AMI). This model is also referred to as an acute ischemic cardiomyopathy or ischemia followed by reperfusion (IR); which is induced by an acute 30-minute period of ischemia by ligation of the left anterior descending artery (LAD) followed by reperfusion of the tissue by releasing the LAD ligation (Vasilyev and McConnell). This protocol will focus on assessment of the infarct size and the area-at-risk (AAR) by Evan's blue dye and triphenyl tetrazolium chloride (TTC) following 4-hours of reperfusion; additional comments toward the evaluation of cardiac function and remodeling by modifying the duration of reperfusion, is also presented. Overall, this AMI rat animal model is useful for studying the consequence of a myocardial infarction on cardiac pathophysiological and physiological function. Medicine, Issue 48, Cardiovascular (CV), Heart Failure (HF), Acute Myocardial Infarction (AMI), Ischemia-Reperfusion (IR), Left Anterior Descending Artery (LAD) Transthoracic Echocardiography in Mice Institutions: Baylor College of Medicine (BCM), Baylor College of Medicine (BCM). In recent years, murine models have become the primary avenue for studying the molecular mechanisms of cardiac dysfunction resulting from changes in gene expression. Transgenic and gene targeting methods can be used to generate mice with altered cardiac size and function,1-3 and as a result, in vivo techniques are needed to evaluate their cardiac phenotype. Transthoracic echocardiography, pulse wave Doppler (PWD), and tissue Doppler imaging (TDI) can be used to provide dimensional measurements of the mouse heart and to quantify the degree of cardiac systolic and diastolic performance. Two-dimensional imaging is used to detect abnormal anatomy or movements of the left ventricle, whereas M-mode echo is used for quantification of cardiac dimensions and contractility.4,5 In addition, PWD is used to quantify localized velocity of turbulent flow,6 whereas TDI is used to measure the velocity of myocardial motion.7 Thus, transthoracic echocardiography offers a comprehensive method for the noninvasive evaluation of cardiac function in mice. Medicine, Issue 39, Echocardiography, pulse wave Doppler, tissue Doppler imaging, ultrasound 5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat Institutions: University Medical Center Utrecht. Chronic kidney disease (CKD) is a global problem. Slowing CKD progression is a major health priority. Since CKD is characterized by complex derangements of homeostasis, integrative animal models are necessary to study development and progression of CKD. To study development of CKD and novel therapeutic interventions in CKD, we use the 5/6th nephrectomy ablation model, a well known experimental model of progressive renal disease, resembling several aspects of human CKD. The gross reduction in renal mass causes progressive glomerular and tubulo-interstitial injury, loss of remnant nephrons and development of systemic and glomerular hypertension. It is also associated with progressive intrarenal capillary loss, inflammation and glomerulosclerosis. Risk factors for CKD invariably impact on endothelial function. To mimic this, we combine removal of 5/6th of renal mass with nitric oxide (NO) depletion and a high salt diet. After arrival and acclimatization, animals receive a NO synthase inhibitor (NG-nitro-L-Arginine) (L-NNA) supplemented to drinking water (20 mg/L) for a period of 4 weeks, followed by right sided uninephrectomy. One week later, a subtotal nephrectomy (SNX) is performed on the left side. After SNX, animals are allowed to recover for two days followed by LNNA in drinking water (20 mg/L) for a further period of 4 weeks. A high salt diet (6%), supplemented in ground chow (see time line Figure 1 ), is continued throughout the experiment. Progression of renal failure is followed over time by measuring plasma urea, systolic blood pressure and proteinuria. By six weeks after SNX, renal failure has developed. Renal function is measured using 'gold standard' inulin and para-amino hippuric acid (PAH) clearance technology. This model of CKD is characterized by a reduction in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), hypertension (systolic blood pressure>150 mmHg), proteinuria (> 50 mg/24 hr) and mild uremia (>10 mM). Histological features include tubulo-interstitial damage reflected by inflammation, tubular atrophy and fibrosis and focal glomerulosclerosis leading to massive reduction of healthy glomeruli within the remnant population (<10%). Follow-up until 12 weeks after SNX shows further progression of CKD. Medicine, Issue 77, Anatomy, Physiology, Biomedical Engineering, Surgery, Nephrology Kidney Diseases, Glomerular Filtration Rate, Hemodynamics, Surgical Procedures, Operative, Chronic kidney disease, remnant kidney, chronic renal diseases, kidney, Nitric Oxide depletion, NO depletion, high salt diet, proteinuria, uremia, glomerulosclerosis, transgenic rat, animal model Quantitative Analysis of Chromatin Proteomes in Disease Institutions: David Geffen School of Medicine at UCLA, David Geffen School of Medicine at UCLA, David Geffen School of Medicine at UCLA, Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah. In the nucleus reside the proteomes whose functions are most intimately linked with gene regulation. Adult mammalian cardiomyocyte nuclei are unique due to the high percentage of binucleated cells,1 the predominantly heterochromatic state of the DNA, and the non-dividing nature of the cardiomyocyte which renders adult nuclei in a permanent state of interphase.2 Transcriptional regulation during development and disease have been well studied in this organ,3-5 but what remains relatively unexplored is the role played by the nuclear proteins responsible for DNA packaging and expression, and how these proteins control changes in transcriptional programs that occur during disease.6 In the developed world, heart disease is the number one cause of mortality for both men and women.7 Insight on how nuclear proteins cooperate to regulate the progression of this disease is critical for advancing the current treatment options. Mass spectrometry is the ideal tool for addressing these questions as it allows for an unbiased annotation of the nuclear proteome and relative quantification for how the abundance of these proteins changes with disease. While there have been several proteomic studies for mammalian nuclear protein complexes,8-13 there has been only one study examining the cardiac nuclear proteome, and it considered the entire nucleus, rather than exploring the proteome at the level of nuclear sub compartments.15 In large part, this shortage of work is due to the difficulty of isolating cardiac nuclei. Cardiac nuclei occur within a rigid and dense actin-myosin apparatus to which they are connected via multiple extensions from the endoplasmic reticulum, to the extent that myocyte contraction alters their overall shape.16 Additionally, cardiomyocytes are 40% mitochondria by volume17 which necessitates enrichment of the nucleus apart from the other organelles. Here we describe a protocol for cardiac nuclear enrichment and further fractionation into biologically-relevant compartments. Furthermore, we detail methods for label-free quantitative mass spectrometric dissection of these fractions-techniques amenable to in vivo experimentation in various animal models and organ systems where metabolic labeling is not feasible. Medicine, Issue 70, Molecular Biology, Immunology, Genetics, Genomics, Physiology, Protein, DNA, Chromatin, cardiovascular disease, proteomics, mass spectrometry Respirometric Oxidative Phosphorylation Assessment in Saponin-permeabilized Cardiac Fibers Institutions: University of Calgary, University of Calgary. Investigation of mitochondrial function represents an important parameter of cardiac physiology as mitochondria are involved in energy metabolism, oxidative stress, apoptosis, aging, mitochondrial encephalomyopathies and drug toxicity. Given this, technologies to measure cardiac mitochondrial function are in demand. One technique that employs an integrative approach to measure mitochondrial function is respirometric oxidative phosphorylation (OXPHOS) analysis. The principle of respirometric OXPHOS assessment is centered around measuring oxygen concentration utilizing a Clark electrode. As the permeabilized fiber bundle consumes oxygen, oxygen concentration in the closed chamber declines. Using selected substrate-inhibitor-uncoupler titration protocols, electrons are provided to specific sites of the electron transport chain, allowing evaluation of mitochondrial function. Prior to respirometric analysis of mitochondrial function, mechanical and chemical preparatory techniques are utilized to permeabilize the sarcolemma of muscle fibers. Chemical permeabilization employs saponin to selectively perforate the cell membrane while maintaining cellular architecture. This paper thoroughly describes the steps involved in preparing saponin-skinned cardiac fibers for oxygen consumption measurements to evaluate mitochondrial OXPHOS. Additionally, troubleshooting advice as well as specific substrates, inhibitors and uncouplers that may be used to determine mitochondria function at specific sites of the electron transport chain are provided. Importantly, the described protocol may be easily applied to cardiac and skeletal tissue of various animal models and human samples. Physiology, Issue 48, cardiac fibers, mitochondria, oxygen consumption, mouse, methodology Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells Institutions: KU Leuven. Intercellular communication is essential for the coordination of physiological processes between cells in a variety of organs and tissues, including the brain, liver, retina, cochlea and vasculature. In experimental settings, intercellular Ca2+ -waves can be elicited by applying a mechanical stimulus to a single cell. This leads to the release of the intracellular signaling molecules IP3 that initiate the propagation of the Ca2+ -wave concentrically from the mechanically stimulated cell to the neighboring cells. The main molecular pathways that control intercellular Ca2+ -wave propagation are provided by gap junction channels through the direct transfer of IP3 and by hemichannels through the release of ATP. Identification and characterization of the properties and regulation of different connexin and pannexin isoforms as gap junction channels and hemichannels are allowed by the quantification of the spread of the intercellular Ca2+ -wave, siRNA, and the use of inhibitors of gap junction channels and hemichannels. Here, we describe a method to measure intercellular Ca2+ -wave in monolayers of primary corneal endothelial cells loaded with Fluo4-AM in response to a controlled and localized mechanical stimulus provoked by an acute, short-lasting deformation of the cell as a result of touching the cell membrane with a micromanipulator-controlled glass micropipette with a tip diameter of less than 1 μm. We also describe the isolation of primary bovine corneal endothelial cells and its use as model system to assess Cx43-hemichannel activity as the driven force for intercellular Ca2+ -waves through the release of ATP. Finally, we discuss the use, advantages, limitations and alternatives of this method in the context of gap junction channel and hemichannel research. Cellular Biology, Issue 77, Molecular Biology, Medicine, Biomedical Engineering, Biophysics, Immunology, Ophthalmology, Gap Junctions, Connexins, Connexin 43, Calcium Signaling, Ca2+, Cell Communication, Paracrine Communication, Intercellular communication, calcium wave propagation, gap junctions, hemichannels, endothelial cells, cell signaling, cell, isolation, cell culture A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses Institutions: Emory University, Emory University. The protective effect of many HLA class I alleles on HIV-1 pathogenesis and disease progression is, in part, attributed to their ability to target conserved portions of the HIV-1 genome that escape with difficulty. Sequence changes attributed to cellular immune pressure arise across the genome during infection, and if found within conserved regions of the genome such as Gag, can affect the ability of the virus to replicate in vitro . Transmission of HLA-linked polymorphisms in Gag to HLA-mismatched recipients has been associated with reduced set point viral loads. We hypothesized this may be due to a reduced replication capacity of the virus. Here we present a novel method for assessing the in vitro replication of HIV-1 as influenced by the gag gene isolated from acute time points from subtype C infected Zambians. This method uses restriction enzyme based cloning to insert the gag gene into a common subtype C HIV-1 proviral backbone, MJ4. This makes it more appropriate to the study of subtype C sequences than previous recombination based methods that have assessed the in vitro replication of chronically derived gag-pro sequences. Nevertheless, the protocol could be readily modified for studies of viruses from other subtypes. Moreover, this protocol details a robust and reproducible method for assessing the replication capacity of the Gag-MJ4 chimeric viruses on a CEM-based T cell line. This method was utilized for the study of Gag-MJ4 chimeric viruses derived from 149 subtype C acutely infected Zambians, and has allowed for the identification of residues in Gag that affect replication. More importantly, the implementation of this technique has facilitated a deeper understanding of how viral replication defines parameters of early HIV-1 pathogenesis such as set point viral load and longitudinal CD4+ T cell decline. Infectious Diseases, Issue 90, HIV-1, Gag, viral replication, replication capacity, viral fitness, MJ4, CEM, GXR25 Measuring Left Ventricular Pressure in Late Embryonic and Neonatal Mice Institutions: Saint Louis University, Washington University School of Medicine. Blood pressure increases significantly during embryonic and postnatal development in vertebrate animals. In the mouse, blood flow is first detectable around embryonic day (E) 8.51 . Systolic left ventricular (LV) pressure is 2 mmHg at E9.5 and 11 mmHg at E14.52 . At these mid-embryonic stages, the LV is clearly visible through the chest wall for invasive pressure measurements because the ribs and skin are not fully developed. Between E14.5 and birth (approximately E21) imaging methods must be used to view the LV. After birth, mean arterial pressure increases from 30 - 70 mmHg from postnatal day (P) 2 - 353 . Beyond P20, arterial pressure can be measured with solid-state catheters (i.e. Millar or Scisense). Before P20, these catheters are too big for developing mouse arteries and arterial pressure must be measured with custom pulled plastic catheters attached to fluid-filled pressure transducers3 or glass micropipettes attached to servo null pressure transducers4 Our recent work has shown that the greatest increase in blood pressure occurs during the late embryonic to early postnatal period in mice5-7 . This large increase in blood pressure may influence smooth muscle cell (SMC) phenotype in developing arteries and trigger important mechanotransduction events. In human disease, where the mechanical properties of developing arteries are compromised by defects in extracellular matrix proteins (i.e. Marfan's Syndrome8 and Supravalvular Aortic Stenosis9 ) the rapid changes in blood pressure during this period may contribute to disease phenotype and severity through alterations in mechanotransduction signals. Therefore, it is important to be able to measure blood pressure changes during late embryonic and neonatal periods in mouse models of human disease. We describe a method for measuring LV pressure in late embryonic (E18) and early postnatal (P1 - 20) mice. A needle attached to a fluid-filled pressure transducer is inserted into the LV under ultrasound guidance. Care is taken to maintain normal cardiac function during the experimental protocol, especially for the embryonic mice. Representative data are presented and limitations of the protocol are discussed. Bioengineering, Issue 60, systolic, diastolic, pulse, heart, artery, postnatal development Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR Institutions: UCSF/VA Medical Center, LoneStar Heart, Inc.. Injection of Algisyl-LVR, a treatment under clinical development, is intended to treat patients with dilated cardiomyopathy. This treatment was recently used for the first time in patients who had symptomatic heart failure. In all patients, cardiac function of the left ventricle (LV) improved significantly, as manifested by consistent reduction of the LV volume and wall stress. Here we describe this novel treatment procedure and the methods used to quantify its effects on LV wall stress and function. Algisyl-LVR is a biopolymer gel consisting of Na+ -Alginate and Ca2+ -Alginate. The treatment procedure was carried out by mixing these two components and then combining them into one syringe for intramyocardial injections. This mixture was injected at 10 to 19 locations mid-way between the base and apex of the LV free wall in patients. Magnetic resonance imaging (MRI), together with mathematical modeling, was used to quantify the effects of this treatment in patients before treatment and at various time points during recovery. The epicardial and endocardial surfaces were first digitized from the MR images to reconstruct the LV geometry at end-systole and at end-diastole. Left ventricular cavity volumes were then measured from these reconstructed surfaces. Mathematical models of the LV were created from these MRI-reconstructed surfaces to calculate regional myofiber stress. Each LV model was constructed so that 1) it deforms according to a previously validated stress-strain relationship of the myocardium, and 2) the predicted LV cavity volume from these models matches the corresponding MRI-measured volume at end-diastole and end-systole. Diastolic filling was simulated by loading the LV endocardial surface with a prescribed end-diastolic pressure. Systolic contraction was simulated by concurrently loading the endocardial surface with a prescribed end-systolic pressure and adding active contraction in the myofiber direction. Regional myofiber stress at end-diastole and end-systole was computed from the deformed LV based on the stress-strain relationship. Medicine, Issue 74, Biomedical Engineering, Anatomy, Physiology, Biophysics, Molecular Biology, Surgery, Cardiology, Cardiovascular Diseases, bioinjection, ventricular wall stress, mathematical model, heart failure, cardiac function, myocardium, left ventricle, LV, MRI, imaging, clinical techniques Transverse Aortic Constriction in Mice Institutions: Baylor College of Medicine (BCM), Baylor College of Medicine (BCM). Transverse aortic constriction (TAC) in the mouse is a commonly used experimental model for pressure overload-induced cardiac hypertrophy and heart failure.1 TAC initially leads to compensated hypertrophy of the heart, which often is associated with a temporary enhancement of cardiac contractility. Over time, however, the response to the chronic hemodynamic overload becomes maladaptive, resulting in cardiac dilatation and heart failure.2 The murine TAC model was first validated by Rockman et al , and has since been extensively used as a valuable tool to mimic human cardiovascular diseases and elucidate fundamental signaling processes involved in the cardiac hypertrophic response and heart failure development. When compared to other experimental models of heart failure, such as complete occlusion of the left anterior descending (LAD) coronary artery, TAC provides a more reproducible model of cardiac hypertrophy and a more gradual time course in the development of heart failure. Here, we describe a step-by-step procedure to perform surgical TAC in mice. To determine the level of pressure overload produced by the aortic ligation, a high frequency Doppler probe is used to measure the ratio between blood flow velocities in the right and left carotid arteries.3, 4 With surgical survival rates of 80-90%, transverse aortic banding is an effective technique of inducing left ventricular hypertrophy and heart failure in mice. Medicine, Issue 38, Aorta, heart failure, hypertrophy, mouse, pressure-overload Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes Institutions: Beth Israel Deaconess Medical Center, Harvard Medical School, Sapienza University. The use of primary cardiomyocytes (CMs) in culture has provided a powerful complement to murine models of heart disease in advancing our understanding of heart disease. In particular, the ability to study ion homeostasis, ion channel function, cellular excitability and excitation-contraction coupling and their alterations in diseased conditions and by disease-causing mutations have led to significant insights into cardiac diseases. Furthermore, the lack of an adequate immortalized cell line to mimic adult CMs, and the limitations of neonatal CMs (which lack many of the structural and functional biomechanics characteristic of adult CMs) in culture have hampered our understanding of the complex interplay between signaling pathways, ion channels and contractile properties in the adult heart strengthening the importance of studying adult isolated cardiomyocytes. Here, we present methods for the isolation, culture, manipulation of gene expression by adenoviral-expressed proteins, and subsequent functional analysis of cardiomyocytes from the adult mouse. The use of these techniques will help to develop mechanistic insight into signaling pathways that regulate cellular excitability, Ca2+ dynamics and contractility and provide a much more physiologically relevant characterization of cardiovascular disease. Cellular Biology, Issue 79, Medicine, Cardiology, Cellular Biology, Anatomy, Physiology, Mice, Ion Channels, Primary Cell Culture, Cardiac Electrophysiology, adult mouse cardiomyocytes, cell isolation, IonOptix, Cell Culture, adenoviral transfection, patch clamp, fluorescent nanosensor High Efficiency Differentiation of Human Pluripotent Stem Cells to Cardiomyocytes and Characterization by Flow Cytometry Institutions: Medical College of Wisconsin, Stanford University School of Medicine, Medical College of Wisconsin, Hong Kong University, Johns Hopkins University School of Medicine, Medical College of Wisconsin. There is an urgent need to develop approaches for repairing the damaged heart, discovering new therapeutic drugs that do not have toxic effects on the heart, and improving strategies to accurately model heart disease. The potential of exploiting human induced pluripotent stem cell (hiPSC) technology to generate cardiac muscle “in a dish” for these applications continues to generate high enthusiasm. In recent years, the ability to efficiently generate cardiomyogenic cells from human pluripotent stem cells (hPSCs) has greatly improved, offering us new opportunities to model very early stages of human cardiac development not otherwise accessible. In contrast to many previous methods, the cardiomyocyte differentiation protocol described here does not require cell aggregation or the addition of Activin A or BMP4 and robustly generates cultures of cells that are highly positive for cardiac troponin I and T (TNNI3, TNNT2), iroquois-class homeodomain protein IRX-4 (IRX4), myosin regulatory light chain 2, ventricular/cardiac muscle isoform (MLC2v) and myosin regulatory light chain 2, atrial isoform (MLC2a) by day 10 across all human embryonic stem cell (hESC) and hiPSC lines tested to date. Cells can be passaged and maintained for more than 90 days in culture. The strategy is technically simple to implement and cost-effective. Characterization of cardiomyocytes derived from pluripotent cells often includes the analysis of reference markers, both at the mRNA and protein level. For protein analysis, flow cytometry is a powerful analytical tool for assessing quality of cells in culture and determining subpopulation homogeneity. However, technical variation in sample preparation can significantly affect quality of flow cytometry data. Thus, standardization of staining protocols should facilitate comparisons among various differentiation strategies. Accordingly, optimized staining protocols for the analysis of IRX4, MLC2v, MLC2a, TNNI3, and TNNT2 by flow cytometry are described. Cellular Biology, Issue 91, human induced pluripotent stem cell, flow cytometry, directed differentiation, cardiomyocyte, IRX4, TNNI3, TNNT2, MCL2v, MLC2a Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples Institutions: University of Florence, University of Florence. Cardiomyocytes from diseased hearts are subjected to complex remodeling processes involving changes in cell structure, excitation contraction coupling and membrane ion currents. Those changes are likely to be responsible for the increased arrhythmogenic risk and the contractile alterations leading to systolic and diastolic dysfunction in cardiac patients. However, most information on the alterations of myocyte function in cardiac diseases has come from animal models. Here we describe and validate a protocol to isolate viable myocytes from small surgical samples of ventricular myocardium from patients undergoing cardiac surgery operations. The protocol is described in detail. Electrophysiological and intracellular calcium measurements are reported to demonstrate the feasibility of a number of single cell measurements in human ventricular cardiomyocytes obtained with this method. The protocol reported here can be useful for future investigations of the cellular and molecular basis of functional alterations of the human heart in the presence of different cardiac diseases. Further, this method can be used to identify novel therapeutic targets at cellular level and to test the effectiveness of new compounds on human cardiomyocytes, with direct translational value. Medicine, Issue 86, cardiology, cardiac cells, electrophysiology, excitation-contraction coupling, action potential, calcium, myocardium, hypertrophic cardiomyopathy, cardiac patients, cardiac disease Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model Institutions: Rajiv Gandhi Centre for Biotechnology, Rajiv Gandhi Centre for Biotechnology, Sree Chitra Tirunal Institute for Medical Sciences & Technology. Ascending aortic constriction is the most common and successful surgical model for creating pressure overload induced cardiac hypertrophy and heart failure. Here, we describe a detailed surgical procedure for creating pressure overload and cardiac hypertrophy in rats by constriction of the ascending aorta using a small metallic clip. After anesthesia, the trachea is intubated by inserting a cannula through a half way incision made between two cartilage rings of trachea. Then a skin incision is made at the level of the second intercostal space on the left chest wall and muscle layers are cleared to locate the ascending portion of aorta. The ascending aorta is constricted to 50–60% of its original diameter by application of a small sized titanium clip. Following aortic constriction, the second and third ribs are approximated with prolene sutures. The tracheal cannula is removed once spontaneous breathing was re-established. The animal is allowed to recover on the heating pad by gradually lowering anesthesia. The intensity of pressure overload created by constriction of the ascending aorta is determined by recording the pressure gradient using trans-thoracic two dimensional Doppler-echocardiography. Overall this protocol is useful to study the remodeling events and contractile properties of the heart during the gradual onset and progression from compensated cardiac hypertrophy to heart failure stage. Medicine, Issue 88, ascending aorta, cardiac hypertrophy, pressure overload, aortic constriction, thoracotomy, surgical model. Analysis of Tubular Membrane Networks in Cardiac Myocytes from Atria and Ventricles Institutions: Heart Research Center Goettingen, University Medical Center Goettingen, German Center for Cardiovascular Research (DZHK) partner site Goettingen, University of Maryland School of Medicine. In cardiac myocytes a complex network of membrane tubules - the transverse-axial tubule system (TATS) - controls deep intracellular signaling functions. While the outer surface membrane and associated TATS membrane components appear to be continuous, there are substantial differences in lipid and protein content. In ventricular myocytes (VMs), certain TATS components are highly abundant contributing to rectilinear tubule networks and regular branching 3D architectures. It is thought that peripheral TATS components propagate action potentials from the cell surface to thousands of remote intracellular sarcoendoplasmic reticulum (SER) membrane contact domains, thereby activating intracellular Ca2+ release units (CRUs). In contrast to VMs, the organization and functional role of TATS membranes in atrial myocytes (AMs) is significantly different and much less understood. Taken together, quantitative structural characterization of TATS membrane networks in healthy and diseased myocytes is an essential prerequisite towards better understanding of functional plasticity and pathophysiological reorganization. Here, we present a strategic combination of protocols for direct quantitative analysis of TATS membrane networks in living VMs and AMs. For this, we accompany primary cell isolations of mouse VMs and/or AMs with critical quality control steps and direct membrane staining protocols for fluorescence imaging of TATS membranes. Using an optimized workflow for confocal or superresolution TATS image processing, binarized and skeletonized data are generated for quantitative analysis of the TATS network and its components. Unlike previously published indirect regional aggregate image analysis strategies, our protocols enable direct characterization of specific components and derive complex physiological properties of TATS membrane networks in living myocytes with high throughput and open access software tools. In summary, the combined protocol strategy can be readily applied for quantitative TATS network studies during physiological myocyte adaptation or disease changes, comparison of different cardiac or skeletal muscle cell types, phenotyping of transgenic models, and pharmacological or therapeutic interventions. Bioengineering, Issue 92, cardiac myocyte, atria, ventricle, heart, primary cell isolation, fluorescence microscopy, membrane tubule, transverse-axial tubule system, image analysis, image processing, T-tubule, collagenase Setting-up an In Vitro Model of Rat Blood-brain Barrier (BBB): A Focus on BBB Impermeability and Receptor-mediated Transport Institutions: VECT-HORUS SAS, CNRS, NICN UMR 7259. The blood brain barrier (BBB) specifically regulates molecular and cellular flux between the blood and the nervous tissue. Our aim was to develop and characterize a highly reproducible rat syngeneic in vitro model of the BBB using co-cultures of primary rat brain endothelial cells (RBEC) and astrocytes to study receptors involved in transcytosis across the endothelial cell monolayer. Astrocytes were isolated by mechanical dissection following trypsin digestion and were frozen for later co-culture. RBEC were isolated from 5-week-old rat cortices. The brains were cleaned of meninges and white matter, and mechanically dissociated following enzymatic digestion. Thereafter, the tissue homogenate was centrifuged in bovine serum albumin to separate vessel fragments from nervous tissue. The vessel fragments underwent a second enzymatic digestion to free endothelial cells from their extracellular matrix. The remaining contaminating cells such as pericytes were further eliminated by plating the microvessel fragments in puromycin-containing medium. They were then passaged onto filters for co-culture with astrocytes grown on the bottom of the wells. RBEC expressed high levels of tight junction (TJ) proteins such as occludin, claudin-5 and ZO-1 with a typical localization at the cell borders. The transendothelial electrical resistance (TEER) of brain endothelial monolayers, indicating the tightness of TJs reached 300 ohm·cm2 on average. The endothelial permeability coefficients (Pe) for lucifer yellow (LY) was highly reproducible with an average of 0.26 ± 0.11 x 10-3 cm/min. Brain endothelial cells organized in monolayers expressed the efflux transporter P-glycoprotein (P-gp), showed a polarized transport of rhodamine 123, a ligand for P-gp, and showed specific transport of transferrin-Cy3 and DiILDL across the endothelial cell monolayer. In conclusion, we provide a protocol for setting up an in vitro BBB model that is highly reproducible due to the quality assurance methods, and that is suitable for research on BBB transporters and receptors. Medicine, Issue 88, rat brain endothelial cells (RBEC), mouse, spinal cord, tight junction (TJ), receptor-mediated transport (RMT), low density lipoprotein (LDL), LDLR, transferrin, TfR, P-glycoprotein (P-gp), transendothelial electrical resistance (TEER), Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound Institutions: Johns Hopkins University, Johns Hopkins University, Johns Hopkins University, Macquarie University. We present a protocol for measuring in vivo aortic stiffness in mice using high-resolution ultrasound imaging. Aortic diameter is measured by ultrasound and aortic blood pressure is measured invasively with a solid-state pressure catheter. Blood pressure is raised then lowered incrementally by intravenous infusion of vasoactive drugs phenylephrine and sodium nitroprusside. Aortic diameter is measured for each pressure step to characterize the pressure-diameter relationship of the ascending aorta. Stiffness indices derived from the pressure-diameter relationship can be calculated from the data collected. Calculation of arterial compliance is described in this protocol. This technique can be used to investigate mechanisms underlying increased aortic stiffness associated with cardiovascular disease and aging. The technique produces a physiologically relevant measure of stiffness compared to ex vivo approaches because physiological influences on aortic stiffness are incorporated in the measurement. The primary limitation of this technique is the measurement error introduced from the movement of the aorta during the cardiac cycle. This motion can be compensated by adjusting the location of the probe with the aortic movement as well as making multiple measurements of the aortic pressure-diameter relationship and expanding the experimental group size. Medicine, Issue 94, Aortic stiffness, ultrasound, in vivo, aortic compliance, elastic modulus, mouse model, cardiovascular disease A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites Institutions: Boston University School of Medicine, Boston University School of Medicine. Chronic inflammation is a major driver of pathological tissue damage and a unifying characteristic of many chronic diseases in humans including neoplastic, autoimmune, and chronic inflammatory diseases. Emerging evidence implicates pathogen-induced chronic inflammation in the development and progression of chronic diseases with a wide variety of clinical manifestations. Due to the complex and multifactorial etiology of chronic disease, designing experiments for proof of causality and the establishment of mechanistic links is nearly impossible in humans. An advantage of using animal models is that both genetic and environmental factors that may influence the course of a particular disease can be controlled. Thus, designing relevant animal models of infection represents a key step in identifying host and pathogen specific mechanisms that contribute to chronic inflammation. Here we describe a mouse model of pathogen-induced chronic inflammation at local and systemic sites following infection with the oral pathogen Porphyromonas gingivalis , a bacterium closely associated with human periodontal disease. Oral infection of specific-pathogen free mice induces a local inflammatory response resulting in destruction of tooth supporting alveolar bone, a hallmark of periodontal disease. In an established mouse model of atherosclerosis, infection with P. gingivalis accelerates inflammatory plaque deposition within the aortic sinus and innominate artery, accompanied by activation of the vascular endothelium, an increased immune cell infiltrate, and elevated expression of inflammatory mediators within lesions. We detail methodologies for the assessment of inflammation at local and systemic sites. The use of transgenic mice and defined bacterial mutants makes this model particularly suitable for identifying both host and microbial factors involved in the initiation, progression, and outcome of disease. Additionally, the model can be used to screen for novel therapeutic strategies, including vaccination and pharmacological intervention. Immunology, Issue 90, Pathogen-Induced Chronic Inflammation; Porphyromonas gingivalis; Oral Bone Loss; Periodontal Disease; Atherosclerosis; Chronic Inflammation; Host-Pathogen Interaction; microCT; MRI Echocardiographic Assessment of the Right Heart in Mice Institutions: Vanderbilt University Medical Center, Vanderbilt University Medical Center. Transgenic and toxic models of pulmonary arterial hypertension (PAH) are widely used to study the pathophysiology of PAH and to investigate potential therapies. Given the expense and time involved in creating animal models of disease, it is critical that researchers have tools to accurately assess phenotypic expression of disease. Right ventricular dysfunction is the major manifestation of pulmonary hypertension. Echocardiography is the mainstay of the noninvasive assessment of right ventricular function in rodent models and has the advantage of clear translation to humans in whom the same tool is used. Published echocardiography protocols in murine models of PAH are lacking. In this article, we describe a protocol for assessing RV and pulmonary vascular function in a mouse model of PAH with a dominant negative BMPRII mutation; however, this protocol is applicable to any diseases affecting the pulmonary vasculature or right heart. We provide a detailed description of animal preparation, image acquisition and hemodynamic calculation of stroke volume, cardiac output and an estimate of pulmonary artery pressure. Medicine, Issue 81, Anatomy, Physiology, Biomedical Engineering, Cardiology, Cardiac Imaging Techniques, Echocardiography, Echocardiography, Doppler, Cardiovascular Physiological Processes, Cardiovascular System, Cardiovascular Diseases, Echocardiography, right ventricle, right ventricular function, pulmonary hypertension, Pulmonary Arterial Hypertension, transgenic models, hemodynamics, animal model Analysis of Nephron Composition and Function in the Adult Zebrafish Kidney Institutions: University of Notre Dame. The zebrafish model has emerged as a relevant system to study kidney development, regeneration and disease. Both the embryonic and adult zebrafish kidneys are composed of functional units known as nephrons, which are highly conserved with other vertebrates, including mammals. Research in zebrafish has recently demonstrated that two distinctive phenomena transpire after adult nephrons incur damage: first, there is robust regeneration within existing nephrons that replaces the destroyed tubule epithelial cells; second, entirely new nephrons are produced from renal progenitors in a process known as neonephrogenesis. In contrast, humans and other mammals seem to have only a limited ability for nephron epithelial regeneration. To date, the mechanisms responsible for these kidney regeneration phenomena remain poorly understood. Since adult zebrafish kidneys undergo both nephron epithelial regeneration and neonephrogenesis, they provide an outstanding experimental paradigm to study these events. Further, there is a wide range of genetic and pharmacological tools available in the zebrafish model that can be used to delineate the cellular and molecular mechanisms that regulate renal regeneration. One essential aspect of such research is the evaluation of nephron structure and function. This protocol describes a set of labeling techniques that can be used to gauge renal composition and test nephron functionality in the adult zebrafish kidney. Thus, these methods are widely applicable to the future phenotypic characterization of adult zebrafish kidney injury paradigms, which include but are not limited to, nephrotoxicant exposure regimes or genetic methods of targeted cell death such as the nitroreductase mediated cell ablation technique. Further, these methods could be used to study genetic perturbations in adult kidney formation and could also be applied to assess renal status during chronic disease modeling. Cellular Biology, Issue 90, zebrafish; kidney; nephron; nephrology; renal; regeneration; proximal tubule; distal tubule; segment; mesonephros; physiology; acute kidney injury (AKI) Using Chronic Social Stress to Model Postpartum Depression in Lactating Rodents Institutions: Tufts University Cummings School of Veterinary Medicine, Manchester Metropolitan University. Exposure to chronic stress is a reliable predictor of depressive disorders, and social stress is a common ethologically relevant stressor in both animals and humans. However, many animal models of depression were developed in males and are not applicable or effective in studies of postpartum females. Recent studies have reported significant effects of chronic social stress during lactation, an ethologically relevant and effective stressor, on maternal behavior, growth, and behavioral neuroendocrinology. This manuscript will describe this chronic social stress paradigm using repeated exposure of a lactating dam to a novel male intruder, and the assessment of the behavioral, physiological, and neuroendocrine effects of this model. Chronic social stress (CSS) is a valuable model for studying the effects of stress on the behavior and physiology of the dam as well as her offspring and future generations. The exposure of pups to CSS can also be used as an early life stress that has long term effects on behavior, physiology, and neuroendocrinology. Behavior, Issue 76, Neuroscience, Neurobiology, Physiology, Anatomy, Medicine, Biomedical Engineering, Neurobehavioral Manifestations, Mental Health, Mood Disorders, Depressive Disorder, Anxiety Disorders, behavioral sciences, Behavior and Behavior Mechanisms, Mental Disorders, Stress, Depression, Anxiety, Postpartum, Maternal Behavior, Nursing, Growth, Transgenerational, animal model	2	17	0	0	0	5	0.934393	5	11,171
I'm a member You will be redirected to myBlue. Would you like to continue? Please wait while you are redirected. Please enter a username and password. Printer Friendly Version Hereditary hemochromatosis, a common genetic disorder of iron metabolism, can lead to inappropriate iron absorption, toxic accumulation of iron, and organ damage. Genetic testing is available to assess mutations in the HFE gene, which are responsible for the majority of clinically significant cases of hereditary hemochromatosis. Iron Overload Syndromes Iron overload syndromes may be hereditary, secondary to some other disease (e.g. iron-loading anemias, parenteral iron overload, chronic liver disease or dysmetabolic iron overload syndrome), or due to other miscellaneous conditions (e.g., neonatal iron overload, aceruloplasminemia, congenital atransferrinemia). Iron overload, if left untreated, can lead to secondary tissue damage in a wide range of organs resulting in chronic liver disease (hepatic fibrosis, cirrhosis, hepatocellular carcinoma), endocrine dysfunction (diabetes, hypogonadism), arthralgia or arthritis (typically involving the second and third metacarpo-phalangeal joints), and cardiomyopathy (either with symptomatic cardiac failure or arrhythmias). Hereditary hemochromatosis (HH), an autosomal recessive disorder, is the most common identified, genetic disorder in Caucasians, with an estimated prevalence of 1 in 250. However, fully expressed disease with end-organ manifestations is seen in less than 10% of affected individuals. Factors that influence phenotypic expression of HFE (high iron-related HH [ie, the clinical appearance of iron overload]) are not clearly defined. Low clinical penetrance may be due to a complex interplay of genetic status and other factors such as age, sex, environmental influences and comorbid diseases. HH leads to inappropriate iron absorption from the intestine and progressive increase in intracellular iron concentrations. Untreated HH leads to premature death, usually by liver complications. Treatment by removing excess iron with serial phlebotomy is simple and effective, and if started before irreversible end-organ damage, restores normal life expectancy. Diagnosis of Hereditary Hemochromatosis Patients with hemochromatosis may present with nonspecific systemic symptoms, specific organ-related symptoms, or they may be asymptomatic. The clinical diagnosis of hemochromatosis is based on documentation of increased iron stores as demonstrated by abnormal serum iron indices, specifically elevated transferrin saturation and elevated serum ferritin concentration. Liver biopsy has been used to confirm diagnosis but is now generally limited to determining the degree of hepatic fibrosis and cirrhosis during management. Most patients with a diagnosis of hemochromatosis will exhibit a familial pattern, thereby confirming the diagnosis of HH. However the familial pattern may not be obvious due to the large percentage of undiagnosed patients in some families, and further evaluation of family members may be required to establish whether a familial pattern is present. General population screening for HH has been proposed because of the high prevalence of disease, absence of or nonspecific early clinical findings, specificity of findings once they appear, low cost of diagnosis and treatment, and high cost and low success rate of late diagnosis and treatment. However, because penetrance is low, and the natural history of asymptomatic individuals is unpredictable, support for population-based screening is lacking. A U.S. Preventive Services Task Force (USPSTF) review of the literature suggested that up to 38% to 50% of C282Y homozygotes may develop iron overload, with up to 10% to 33% eventually developing hemochromatosis-associated morbidity. The American Academy of Family Physicians, Centers for Disease Control and Prevention, and USPSTF recommend against population-based general screening. Treatment of Hereditary Hemochromatosis The main treatment modality for patients with HH is periodic phlebotomy. While there has never been a randomized controlled trial of phlebotomy versus no phlebotomy in the treatment of HH, there is evidence from nonrandomized studies that initiation of phlebotomy before the development of cirrhosis and/or diabetes will significantly reduce HH-associated morbidity and mortality. Genetics of Hereditary Hemochromatosis Most patients with HH have mutations in the HFE gene, located on the short arm of chromosome 6. The HFE gene was identified and cloned in 1996. The most common mutation in the HFE gene is C282Y, a missense mutation that changes cysteine at position 282 in the HFE protein to tyrosine. Homozygosity for the C282Y mutation is associated with 60-90% of all cases of HH. Additionally, 3-8% of affected individuals are heterozygous for this mutation. Penetrance for elevated serum iron indices among C282Y homozygotes is variable. However, penetrance for characteristic clinical end points (ie, end-organ damage) is quite low. There is no test that can predict whether a C282Y homozygote will develop clinical symptoms. A specific variant in PCSK7, which is associated with iron metabolism, has been investigated as a possible predictor of cirrhosis risk in HH patients homozygous for the HFE C282Y mutation. Another significant mutation is referred to as H63D, which changes histidine at position 63 to aspartic acid. Homozygosity for H63D is insufficient to cause clinically significant iron overload in the absence of modifying factors. However, heterozygosity for C282Y/H63D has been associated with increased hepatic iron concentrations; approximately 1-2% of patients with this genotype will develop clinical evidence of iron overload, usually in the presence of another liver disease. The clinical significance of a third HFE mutation, S65C (serine at position 65 changed to cysteine), appears to be minimal. This rare variant displays very low penetrance. Compound heterozygosity for C282Y/S65C may confer a low risk for mild HH. Individuals who are heterozygous for S65C and either the wild-type (normal) or H63D alleles do not seem to be at an increased risk for HH. Other mutations in HFE and in non-HFE genes (eg, transferrin receptor 2, [TFR2]) resulting in iron overload syndromes are rare. With the advent of genetic testing in the late 1990s, HFE-related HH is now frequently identified in asymptomatic probands and in asymptomatic relatives of patients who are known to have the disease. Therefore, a genetic diagnosis can be made in individuals who have not yet developed phenotypic expression. These individuals have a genetic susceptibility to developing iron overload but may never do so. A 2000 consensus conference of the European Association for the Study of Liver Diseases led to recognition of different stages and progression of hemochromatosis. These stages were defined as: Clinical laboratories may develop and validate tests in-house and market them as a laboratory service; laboratory-developed tests (LDTs) must meet the general regulatory standards of the Clinical Laboratory Improvement Act (CLIA). Laboratories that offer LDTs must be licensed by CLIA for high-complexity testing. To date, the U.S. Food and Drug Administration has chosed not to require any regulatory review of this test. Genetic testing for HFE gene mutations may be considered medically necessary in a patient with abnormal serum iron indices indicating iron overload. (See Policy Guidelines) Genetic testing for HFE gene mutations may be considered medically necessary in individuals with a family history of hemochromatosis in a first-degree relative. (See Policy Guidelines) Genetic testing for hereditary hemochromatosis in screening of the general population is considered investigational. The coverage guidelines outlined in the Medical Policy Manual should not be used in lieu of the Member's specific benefit plan language. Serum Iron Indices in the Diagnosis of HH The negative predictive value of a normal transferrin saturation and serum ferritin is 97%. In this situation, no further testing is recommended. The 2011 Practice Guidelines by the American Association for the Study of Liver Diseases recommend HFE gene mutation testing in patients with abnormal serum iron indices (ie, serum ferritin and transferrin saturation), even in the absence of symptoms. Genetic Testing in an Individual with a Family History of HH If C282Y homozygosity or compound heterozygosity is found in adult relatives of a proband, and if serum ferritin levels are increased, then therapeutic phlebotomy can be initiated. If ferritin level is normal in these patients, then yearly follow-up with iron studies is indicated. When identified, C282Y heterozygotes and H63D heterozygotes can be reassured that they are not at risk for developing progressive or symptomatic iron overload. Some H63D homozygotes can develop mild iron overload. Genetic counseling is primarily aimed at patients who are at risk for inherited disorders, and experts recommend formal genetic counseling in most cases when genetic testing for an inherited condition is considered. The interpretation of the results of genetic tests and the understanding of risk factors can be very difficult and complex. Therefore, genetic counseling will assist individuals in understanding the possible benefits and harms of genetic testing, including the possible impact of the information on the individual’s family. Genetic counseling may alter the utilization of genetic testing substantially and may reduce inappropriate testing. Genetic counseling should be performed by an individual with experience and expertise in genetic medicine and genetic testing methods. Medically Necessary is defined as those services, treatments, procedures, equipment, drugs, devices, items or supplies furnished by a covered Provider that are required to identify or treat a Member's illness, injury or Nervous/Mental Conditions, and which Company determines are covered under this Benefit Plan based on the criteria as follows in A through D: A. consistent with the symptoms or diagnosis and treatment of the Member's condition, illness, or injury; and B. appropriate with regard to standards of good medical practice; and C. not solely for the convenience of the Member, his or her Provider; and D. the most appropriate supply or level of care which can safely be provided to Member. When applied to the care of an Inpatient, it further means that services for the Member's medical symptoms or conditions require that the services cannot be safely provided to the Member as an Outpatient. For the definition of Medically Necessary, “standards of good medical practice” means standards that are based on credible scientific evidence published in peer-reviewed medical literature generally recognized by the relevant medical community, and physician specialty society recommendations, and the views of medical practitioners practicing in relevant clinical areas and any other relevant factors. BCBSMS makes no payment for services, treatments, procedures, equipment, drugs, devices, items or supplies which are not documented to be Medically Necessary. The fact that a Physician or other Provider has prescribed, ordered, recommended, or approved a service or supply does not in itself, make it Medically Necessary. Investigative is defined as the use of any treatment procedure, facility, equipment, drug, device, or supply not yet recognized as a generally accepted standard of good medical practice for the treatment of the condition being treated and; therefore, is not considered medically necessary. For the definition of Investigative, “generally accepted standards of medical practice” means standards that are based on credible scientific evidence published in peer-reviewed medical literature generally recognized by the relevant medical community, and physician specialty society recommendations, and the views of medical practitioners practicing in relevant clinical areas and any other relevant factors. In order for equipment, devices, drugs or supplies [i.e, technologies], to be considered not investigative, the technology must have final approval from the appropriate governmental bodies, and scientific evidence must permit conclusions concerning the effect of the technology on health outcomes, and the technology must improve the net health outcome, and the technology must be as beneficial as any established alternative and the improvement must be attainable outside the testing/investigational setting. POLICY HISTORY07/19/2012: Approved by Medical Policy Advisory Committee. 08/07/2013: Policy reviewed; no changes. 06/13/2014: Policy reviewed; description updated regarding genetics of hereditary hemochromatosis. Policy statement unchanged. Added examples of inflammatory states to the policy guidelines section. 08/28/2015: Medical policy revised to add ICD-10 codes. Code Reference section updated to correct the following ICD-9 diagnosis code range: 275.0 - 275.9 was changed to 275.01 - 275.09. Code description updated for ICD-9 diagnosis code V26.31. 09/14/2015: Policy description updated regarding genetics of hereditary hemochromatosis. Policy statement unchanged. Policy guidelines updated to add medically necessary and investigative definitions. 03/30/2016: Policy description updated regarding diagnosis and treatment of hereditary hemochromatosis. Policy statements unchanged. Policy guidelines updated to add genetic counseling information. 06/06/2016: Policy number A.2.04.80 added. SOURCE(S)Blue Cross Blue Shield Association policy # 2.04.80 CODE REFERENCEThis may not be a comprehensive list of procedure codes applicable to this policy. The code(s) listed below are ONLY medically necessary if the procedure is performed according to the "Policy" section of this document. CPT copyright American Medical Association. All rights reserved. CPT is a registered trademark of the American Medical Association.	2	5	0	0	0	2	0.948549	2	2,874
In pemphigus, autoantibodies form against desmoglein. Desmoglein forms the "glue" that attaches adjacent epidermal cells via attachment points called desmosomes. When autoantibodies attack desmogleins, the cells become separated from each other and the epidermis becomes "unglued," a phenomenon called acantholysis. This causes blisters that slough off and turn into sores. In some cases, these blisters can cover a significant area of the skin. Originally, the cause of this disease was unknown, and "pemphigus" was used to refer to any blistering disease of the skin and mucosa. In 1964, researchers found that the blood of patients with pemphigus contained antibodies to the layers of skin that separate to form the blisters. In 1971, an article investigating the autoimmune nature of this disease was published. There are several types of pemphigus which vary in severity: pemphigus vulgaris, pemphigus foliaceus, Intraepidermal neutrophilic IgA dermatosis, and paraneoplastic pemphigus. - Pemphigus vulgaris (PV - ICD-10 L10.0) is the most common form of the disorder and occurs when antibodies attack Desmoglein 3. Sores often originate in the mouth, making eating difficult and uncomfortable. Although pemphigus vulgaris may occur at any age, it is most common among people between the ages of 40 and 60. It is more frequent among Ashkenazi Jews. Rarely, it is associated with myasthenia gravis. Nail disease may be the only finding and has prognostic value in management. - Pemphigus foliaceus (PF) is the least severe of the three varieties. Desmoglein 1, the protein that is targeted by the autoantibody, is enriched in the upper skin layers. PF is characterized by crusty sores that often begin on the scalp, and may move to the chest, back, and face. Mouth sores do not occur. This form is also frequent among Ashkenazi Jews. It is not as painful as pemphigus vulgaris, and is often mis-diagnosed as dermatitis or eczema - Intraepidermal neutrophilic IgA dermatosis is characterized histologically by intraepidermal bullae with neutrophils, some eosinophils, and acantholysis. - The least common and most severe type of pemphigus is paraneoplastic pemphigus (PNP). This disorder is a complication of cancer, usually lymphoma and Castleman's disease. It may precede the diagnosis of the tumor. Painful sores appear on the mouth, lips, and the esophagus. In this variety of pemphigus, the disease process often involves the lungs, causing bronchiolitis obliterans (constrictive bronchiolitis). Though much less frequent, it is still found the most in the Ashkenazi Jewish population. Complete removal of and/or cure of the tumor may improve the skin disease, but lung damage is generally irreversible. - Endemic pemphigus foliaceus, including the Fogo Selvagem, the new variant of endemic pemphigus folaiceus in El Bagre, Colombia, South America, and the Tunisian endemic pemphigus in North Africa. Note that Hailey-Hailey disease, also called familial benign pemphigus, is an inherited (genetic) skin disease, not an autoimmune disease. It is therefore not considered part of the Pemphigus group of diseases. Pemphigus defines a group of autoimmune interepithelial blistering diseases that are characterized by loss of normal cell-cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug induced pemphigus, Senear Usher syndrome and endemic pemphigus foliaceus exist;recognized by a dermatologist from the appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head and neck surgery, periodontists, oral and maxillofacial surgeons and eye doctors, as lesions can affect the eyes and mucous membrane of the oral cavity. Intraorally it resembles the more common diseases lichen planus and mucous membrane pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister. This bottom layer of cells is said to have a "tombstone appearance." Definitive diagnosis also requires the demonstration of anti-desmoglein autoantibodies by direct immunofluorescence on the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern reminiscent of chicken wire. Anti-desmoglein antibodies can also be detected in a blood sample using the ELISA technique. Pemphigus is a group of autoimmune blistering diseases that may be classified into the following types: - Pemphigus vulgaris - Pemphigus vegetans - Pemphigus vegetans of Hallopeau - Pemphigus vegetans of Neumann - Pemphigus foliaceus, of which there several forms: - Pemphigus erythematosus or Senear–Usher Syndrome - Endemic pemphigus foliaceus with its three variants, Fogo Selvagem, the new variant endemic pemphigus Foliaeus and Tunisian endemic pemphigus foliaceus - Paraneoplastic pemphigus - IgA pemphigus, of which there several forms: - Subcorneal pustular dermatosis - Intraepidermal neutrophilic IgA dermatosis - Drug induced pemphigus If not treated, pemphigus can be fatal, usually from overwhelming opportunistic infection of lesions. The most common treatment is the administration of oral steroids, especially prednisone, often in high doses. The side effects of corticosteroids may require the use of so-called steroid-sparing or adjuvant drugs. One of the most dangerous side effects of high dosage steroid treatments is intestinal perforations, which may lead to sepsis. Steroids and other medications being taken to treat Pemphigus may also mask the effects of the perforations. Patients on high dosages of oral steroids should closely monitor their GI health. As lesions are usually terribly painful, it is likely that pain medication can complicate and exacerbate the GI issues caused by steroids. - topical steroids, such as clobetasol - intralesional injection of steroids, such as dexamethasone - immunosuppressant drugs, such as CellCept (mycophenolic acid) - serum or plasma pooled products, like Intravenous gamma globulin (IVIG) may be useful in severe cases, especially paraneoplastic pemphigus - biologics such as Rituximab, an anti-CD20 antibody, which was found to improve otherwise severe cases of recalcitrant Pemphigus vulgaris. All of these drugs may cause severe side effects, so the patient should be closely monitored by doctors. Once the outbreaks are under control, dosage is often reduced, to lessen side effects. A meta-analysis of the literature found insufficient evidence to determine the optimal treatment regimen for treating pemphigus vulgaris and pemphigus folicaceous. However, it found that adding cyclophosphamid and azathioprine to a glucocorticoid regimen reduced the amount of glucocorticoid needed to treat, and topical epidermal growth factor significantly reduced lesion healing time. If skin lesions do become infected, antibiotics may be prescribed. Tetracycline antibiotics have a mildly beneficial effect on the disease and are sometimes enough for Pemphigus Foliaceus. In addition, talcum powder is helpful to prevent oozing sores from adhering to bedsheets and clothes. Wound care and treatment is often akin to that used in burn units, including careful use of dressings that don't stick to the wounds, etc. If paraneoplastic pemphigus is diagnosed with pulmonary disease, a powerful cocktail of immune suppressant drugs is sometimes used in an attempt to halt the rapid progression of bronchiolitis obliterans, including methylprednisolone, ciclosporin, azathioprine, and thalidomide. Plasmapheresis may also be useful. Pemphigus foliaceus has been recognized in pet dogs, cats, and horses and is the most common autoimmune skin disease diagnosed in veterinary medicine. Pemphigus foliaceus in animals produces clusters of small vesicles that quickly evolve into pustules. Pustules may rupture, forming erosions or become crusted. Left untreated, pemphigus foliaceus in animals is life-threatening, leading to not only loss of condition but also secondary infection. Pemphigus vulgaris is a very rare disorder described in pet dogs and cats. Paraneoplastic pemphigus has been identified in pet dogs. - Hailey-Hailey disease (familial benign pemphigus) - List of conditions caused by problems with junctional proteins - List of cutaneous conditions - List of immunofluorescence findings for autoimmune bullous conditions - List of target antigens in pemphigus - Pemphigus herpetiformis - Yeh SW, Ahmed B, Sami N, Ahmed AR (2003). "Blistering disorders: diagnosis and treatment". Dermatologic Therapy. 16 (3): 214–23. doi:10.1046/j.1529-8019.2003.01631.x. PMID 14510878. - "Definition of PEMPHIGUS". www.merriam-webster.com. Retrieved 2017-03-11. - International Pemphigus & Pemphigoid Foundation: What is Pemphigus? - Beutner, EH; Jordon, RE (November 1964). "Demonstration of skin antibodies in sera of pemphigus vulgaris patients by indirect immunofluorescent staining". Proc. Soc. Exp. Biol. Med. 117 (2): 505–510. doi:10.3181/00379727-117-29622. PMID 14233481. - "Dermatology Foundation: BEUTNER, JORDAN SHARE 2000 DERMATOLOGY FOUNDATION DISCOVERY AWARD". - Jordon, Robert E.; Sams, Jr., W. Mitchell; Diaz, Gustavo; Beutner, Ernst H. (1971). "NEGATIVE COMPLEMENT IMMUNOFLUORESCENCE IN PEMPHIGUS". Journal of Investigative Dermatology. 57 (6): 407–410. doi:10.1111/1523-1747.ep12293273. PMID 4108416. - Serratos, BD; Rashid, RM (Jul 15, 2009). "Nail disease in pemphigus vulgaris". Dermatology Online Journal. 15 (7): 2. PMID 19903430. - Abreu-Velez AM, Calle-Isaza J, Howard MS. Autoimmune epidermal blistering diseases. Our Dermatol Online. 2013;4(Suppl.3):631-646 - Abreu Velez AM, Calle-Isaza J, Howard MS. Autoimmune epidermal blistering diseases. Our Dermatol Online. 2013;4(Suppl.3):631-646. DOI: 10.7241/ourd.20134.158 - Abreu Velez AM, Calle-Isaza J, Howard MS. Autoimmune epidermal blistering diseases. Our Dermatol Online. 2013; 4(Suppl.3): 631-646. DOI: 10.7241/ourd.20134.158 - 1. Abréu Vélez AM, Hashimoto T, Tobón S, Londoño ML, Montoya F, Bollag, WB, Beutner, E., is a unique form of endemic pemphigus in Northern Colombia. J Am Acad Dermatol. Oct(49),4:609-614,2003 - Hailey Hailey Disease Society - 16. Abreu Velez AM, Calle-Isaza J, Howard MS. Autoimmune epidermal blistering diseases. Our Dermatol Online. 2013; 4(Suppl.3): 631-646. DOI: 10.7241/ourd.20134.158 - Sapp, J. Philip; Eversole, Lewis R.; Wysocki, George P. (1997). Contemporary Oral and Maxillofacial Pathology. Mosby. ISBN 978-0-8016-6918-7.also here - Stanley, John R. (2003). "Chapter 59: Pemphigus". In Freedberg; et al. (eds.). Fitzpatrick's Dermatology in General Medicine (6th ed.). McGraw-Hill. p. 559. ISBN 0-07-138067-1. - Rashid, RM; Candido, KD (Oct 2008). "Pemphigus pain: a review on management". The Clinical Journal of Pain. 24 (8): 734–5. doi:10.1097/AJP.0b013e31817af6fc. PMID 18806540. - In recent years, adjuvant drugs, especially biologics, have shown great promise. British Association of Dermtologists, Steroid sparing (or adjuvant) drugs - Ahmed AR, Spigelman Z, Cavacini LA, Posner MR (2006). "Treatment of pemphigus vulgaris with rituximab and intravenous immune globulin". N. Engl. J. Med. 355 (17): 1772–9. doi:10.1056/NEJMoa062930. PMID 17065638. - Joly P, Mouquet H, Roujeau JC, et al. (2007). "A single cycle of rituximab for the treatment of severe pemphigus". N. Engl. J. Med. 357 (6): 545–52. doi:10.1056/NEJMoa067752. PMID 17687130. - Martin, Linda K; Agero, Anna Liza; Werth, Victoria; Villanueva, Elmer; Segall, Janet; Murrell, Dedee F (2009-01-21). "Interventions for pemphigus vulgaris and pemphigus foliaceus". Cochrane Database of Systematic Reviews (1): CD006263. doi:10.1002/14651858.CD006263.pub2. ISSN 1465-1858. PMID 19160272.	2	7	5	0	0	2	0.403695	7	3,475
In this blog we will discuss what Anxiety disorders in the ICD 10. We will also briefly discuss what is the diagnostic criteria for anxiety in ICD 10 and the various anxiety disorders categorised in the ICD10. How are Anxiety disorders classified in the ICD 10? Anxiety disorders in the International Classification of Diseases and Related Health Problems (ICD-10) have been categorised together with other stress realtor disorders, somatoform disorders and neurotic disorders. This has been done because these three disorders have a shared link with neurological causes as well as neuropsychological causation due to which classification has been done together. Another reason why the classification is in one cluster is because of the similarity in symptoms and the similarities in treatment options for these conditions. Though the classification of the anxiety disorders are different from the DSM 5, anxiety in the ICD-10 and other psychological disorders are diagnosed and differentially diagnosed on the basis of criteria in Diagnostic and Statistical Manual of Disorder (DSM-V). The criteria for the diagnosis is more or less the same however there are differences in the classification with other disorders, coding, and reporting systems for both of these two classification systems. What is the diagnostic criteria for Anxiety in ICD-10? The 10th revision of the International Statistical Classification of Disease (ICD-10) provides similar diagnostic criteria as the DSM 5 however, there are some small differences in terms of reporting systems and coding. Let us consider the diagnostic criteria for General Anxiety disorder in the ICD 10: There should be a period of at least six months with prominent tension, worry, and feelings of apprehension, about everyday events and problems. The individual should manifest at least four symptoms out of the following list of items: Autonomic arousal symptoms - Palpitations or pounding heart, or accelerated heart rate. - Trembling or shaking. - Dry mouth (not due to medication or dehydration). Symptoms concerning chest and abdomen - Difficulty breathing. - Feeling of choking. - Chest pain or discomfort. - Nausea or abdominal distress (e.g. churning in the stomach). Symptoms concerning brain and mind - Feeling dizzy, unsteady, faint or light-headed. - Derealization Depersonalization. - Fear of losing control, going crazy, or passing out. - Fear of dying. - Hot flashes or cold chills. - Numbness or tingling sensations. Symptoms of tension - Muscle tension or aches and pains. - Restlessness and inability to relax. - Feeling keyed up, or on edge, or of mental tension. - A sensation of a lump in the throat or difficulty with swallowing. What are the Anxiety disorders categorised in ICD 10? The various anxiety disorders that has been classified and recognised in the ICD 10 include the following: F40: Phobic anxiety disorders Phobic anxiety disorders refer to a group of disorders where people experience intense anxiety only when they are faced with their triggers and their reaction is inappropriate to the danger presented by these situations. Due to intense anxiety, people tend to avoid these situations or triggers or endure them with dread while experiencing symptoms like palpitations or feeling faint and is often associated with secondary fears of dying, losing control, or going mad. Phobic anxiety and depression often coexist and in some cases can cause disruption of daily life and cause social and occupational dysfunction in some. Agoraphobia refers to the anxiety disorder that is marked by the fear of public spaces but now its usage has increased to the aspects related to open spaces. People with this disorder often perceive environments that are too open or crowded to be dangerous. This sense of danger and fear is driven by an irrational fear of being anxious, humiliated, having a panic attack or being trapped with no source of help. Such a condition comes with high anxiety of crowded spaces and can often lead to panic attacks which can further result in more fear and anxiety leading them to actively avoid engaging with such circumstances and often becoming shut-ins. According to the ICD10 panic disorders are also strongly associated with thai disorder and often people who are able to avoid trigger situations experience little anxiety. F40.1 Social phobias Social anxiety disorder, also called social phobia, is characterised by an overwhelming fear of social situations that usually begin during teenage years and might persist unless there is effective intervention. This particular disorder is plagued by various thoughts related to social situations and an intense and deliberate aversion and avoidance of social situations. It affects the person’s daily functioning and causes disruption in one’s life, sense of self, work, and relationships. The symptoms of this disorder include: - worry about everyday activities, such as meeting strangers, starting conversations, speaking on the phone, working or shopping - avoid or worry a lot about social activities - find it difficult to do things when others are watching - Preoccupied with the thought that they are being judged. - fear being criticised - avoid eye contact - or have low self-esteem - often have symptoms like sweating, trembling or a pounding heartbeat (palpitations) in social situations. - panic attacks This disorder can be discrete (i.e. it is restricted to public speaking, or to eating in public places, or to encounters with opposite sex) or it can be diffuse which mean the sufferer avoids all type of social situations outside of family circle. People with this disorder often have very low self esteem and often believe that their physical and behavioural reactions or symptoms are also part of the problem. F40.2 Specific (isolated) phobias This particular diagnosis is given when an individual experiences anxiety due to phobias that are highly specific situations such as proximity to particular animals, heights, thunder, darkness, flying, closed spaces, urinating or defecating in public toilets, eating certain foods, dentistry, or the sight of blood or injury. Certain phobias under this diagnostic category include: - Animal phobias - Simple phobia The onset is often childhood or early adulthood usually due to negative experiences and associations created due to traumatic and negative experiences with these situations and triggers. A person will develop symptoms of the phobia when they get into a situation in which they could end up alone and these symptoms include: - Spending to much time obsessively worrying about triggers - a feeling of extreme terror when alone or in a situation they are forced to be in that situatation. - an overwhelming desire to avoid triggers When Individual feel threatened or triggered by they might experience the following physical symptoms: - hot flashes or chills - shortness of breath or difficulty breathing - a choking sensation - rapid heartbeat (tachycardia) - pain or tightness in the chest - headaches and dizziness - feeling faint - numbness or pins and needles - dry mouth - ringing in your ears - confusion or disorientation F41.0 Panic disorder In this disorder, the ICD10 identifies recurrent panic attacks as an essential feature marked by severe anxiety that is not specific to any particular situation or circumstances and is unpredictable in nature. Individuals who experience panic attacks tend to also experience other symptoms such as: - Heightened vigilance for their own physical symptoms - Anxious and irrational thinking - A strong feeling of dread - Fear of going mad, losing control, or dying - Feeling lightheaded and dizzy - Tingling and chills, particularly in the arms and hands - Hot flushes - Accelerated heart rate - A feeling of constriction in the chest - Breathing difficulties, including shortness of breath - Nausea or abdominal distress - Tense muscles - Dry mouth - Depersonalization and derealisation. Individuals who experience panic attacks also develop this intense anxiety and fear of the panic attacks reoccurring that this anxiety and worry eventually leads to a panic attack because of heightened stress. When it recurs frequently over a short amount of time, the individual is believed to have Panic Disorder. F41.1 Generalised anxiety disorder Generalised anxiety also known as Free-floating anxiety refers to an anxiety disorder where the anxiety is not specific to a situation or object. This anxiety disorder is characterised by persistent and excessive worry about a number of different things. People who are affected by this disorder experience worry and anxiety that is more severe than normal levels of worry and this particular experience persists for long periods of time, sometimes even years. They worry often about anticipated disasters, concerns about money, family members, and loved ones, health, and other various worries that are often inappropriate to the real levels of threat. People who have this particular disaster worry even when there is no actual threat and their anxiety and worry often affect their health, their relationships, their ability to work, and also socialise with others. They find it hard to control this worry and anxiety and it often affects their day to day activities including being able to focus on tasks at hand and also their sleep. People experience excessive anxiety and worry occurring more days than not for at least 6 months about a number of events and activities such as performance at work, health, disasters etc) The individual finds it difficult to control the worry. The anxiety and worry symptoms are also associate with three or more of the following symptoms that have been present for more days than not for at least 6 months: - Restlessness, feeling keyed up or on edge. - Being easily fatigued. - Difficulty concentrating or mind going blank. - Muscle tension. - Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep). F41.2 Mixed anxiety and depressive disorder This diagnosis is given when an individual manifests symptoms of anxiety ICD-10 and depression but symptoms are interconnected. This means that the individual meets the criteria for generalised anxiety disorder and also has prominent features of disorders of the same anxiety cluster along with depression symptoms. Here, the symptoms of anxiety and depression are both present, but neither is clearly predominant and neither of the symptoms are severe enough to justify a diagnosis if considered separately. In the case that both anxiety and depressive symptoms are severe enough to justify a single, individual diagnosis, both diagnoses should be recorded and this diagnosis should not be used. F41.3 Other mixed anxiety disorders This diagnosis is applied when there are observable symptoms of anxiety mixed with features of other disorders in F42-F48 but the symptoms are not severe enough to justify a diagnosis separately. In this blog we discussed what Anxiety disorders in the ICD 10. We also briefly discussed what is the diagnostic criteria for anxiety in ICD 10 and the various anxiety disorders categorised in the ICD10. World Health Organisation. (1992). The ICD-10 classification of mental and behavioural disorders: Clinical descriptions and diagnostic guidelines. Geneva: World Health Organisation. International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10)-WHO Version for ;2016. Retrieved on 22nd March 2022. https://icd.who.int/browse10/2016/en#F40.0 Andrews G, Slade T. The classification of anxiety disorders in ICD-10 and DSM-IV: a concordance analysis. Psychopathology. 2002 Mar-Jun;35(2-3):100-6. doi: 10.1159/000065127. PMID: 12145492.	3	4	0	0	0	14	0.925	14	2,406
The FPIES Foundation is excited that the Centers for Disease Control (CDC) now recognizes Food Protein-Induced Enterocolitis Syndrome (FPIES), and has appointed it with diagnostic code K52.21, among allergic digestive diseases. This is a step that has the building blocks to make diagnosis and medical/formula coverage easier for a lot of children and their families and was supported by The FPIES Foundation. We thank Dr.Anna Nowak-Wegryzn (Founding member of The FPIES Foundation Medical Advisory Board member) and I-FPIES for their role in this initiative. What is an ICD-10 code and what does it mean? ICD is an acronym that stands for International Classification of Disease and the #10 is because this is the 10th revision. This ever growing and changing list is maintained by the World HealthOrganization (WHO). WHO defines ICD as, “. . .The standard diagnostic tool for epidemiology, health management and clinical purposes. This includes the analysis of the general health situation of population groups. It is used to monitor the incidence and prevalence of diseases and other health problems”. Simply stated, ICD codes are utilized medically for precise tracking and quicker analyzing of a diagnosis, under its specific code. For FPIES, this can help with research to study patterns of the diagnosis, track complications, and treatment outcomes. ICD codes are utilized in health services looking for patterns in such things as quality and access of care, as well as quality of life. Insurance companies also utilize this code in classification for payments of services and coverage of prescriptions related to the diagnosis. For FPIES, this can help insurance companies in deciding to include formula prescriptions to be paid and/or reimbursed. (***Please note, it is not an automatic coverage by insurance or government medical aid). The ICD coding is an important piece of health care operations which includes health services and insurance reimbursements, in addition to medical research. - K tells us the chapter of the classification it is in: “Diseases of the Gastrointestinal System” - 52 is where it fits along this category. 52 being “Other non-infective gastroenteritis and colitis” and, - .2 is “Allergic and dietetic gastroenteritis and colitis” and finally, - 1 added gives it its specific Food Protein-Induced Enterocolitis classification. In the future, there could be additional numbers to further define sub-classes within this diagnosis code. Additional codes to include the other known allergic/food protein induced gastrointestinal disorders will be added as well. Establishment of an ICD code for FPIES is an important step in further defining this diagnosis and increasing its visibility to enable increased support and care for children, and their families, living with this diagnosis. We recognize there is much more work to be done to assure all children along the spectrum of this diagnosis have this same access to adequate support and care and look forward to this continued work in collaboration with our medical advisory board and this community. This post was written by the Executive Board of The FPIES Foundation.	3	3	0	0	0	1	0.695795	1	644
Documentation of chronic kidney disease (CKD) and its stage are crucial for correct coding, which affects hospital revenue and severity of illness classification. Precise diagnosis and reporting of CKD stage improve the accuracy of our national health care database used for research and for projections of national health care needs. The 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease published by the National Kidney Foundation (NKF) is the authoritative, consensus standard for the diagnosis, classification and management of CKD. The guideline identifies five stages of CKD (listed in Table 1), which are defined by either glomerular filtration rate (GFR) decreased to less than 60 mL/min/1.73 m2 or by presence of certain kidney damage markers (listed in Table 2) for more than three months. The diagnosis of CKD stage 1 or 2 requires the presence of one or more of the markers of kidney damage. Therefore, a patient with a GFR greater than or equal to 60 mL/min/1.73 m2 does not have CKD if there are no markers of kidney damage. Stages 3, 4, and 5 are based on GFR cutoffs alone, although such patients may also have markers of kidney damage. Lab reports of creatinine values typically include the calculated GFR for both African-American and non-African-American patients. The calculated GFR is proportional to serum creatinine but also depends on age, race, and gender. The NKF recommends using the CKD-EPI Creatinine Equation, published in 2009, to estimate GFR (available on the NKF website). It is not necessary to perform a 24-hour urine collection to measure creatinine clearance, even though this may be a more precise measure of GFR if done correctly. The stage of CKD can only be correctly assigned when GFR and therefore creatinine levels are at a stable baseline. Staging cannot be performed when the creatinine is in flux, such as during an inpatient admission. Renal function must be stabilized before staging. The currently preferred clinical terminology of “chronic kidney disease” or CKD should be used in diagnostic documentation. Clinicians should avoid nonspecific, imprecise terminology such as “renal insufficiency” or “chronic renal insufficiency (CRI)” as the correct codes for CKD will not be assigned. End-stage renal disease (ESRD) represents the culmination of progressive stage 5 CKD. It has been a long-standing clinical practice to classify patients with CKD who require either dialysis or transplantation as ESRD. However, ICD-10-CM defines ESRD (code N18.6) as “dialysis-dependent stage 5 CKD.” Dialysis dependence means that the requirement for dialysis is expected to last three months or more. A significant conflict exists between the clinical documentation standards and ICD-10-CM coding practices for a patient who has had a kidney transplant. Clinically, transplant patients are considered to have ESRD even though the transplanted kidney may be functioning well. On the other hand, ICD-10-CM requires the transplant status code Z94.0 plus a code for the current CKD stage of the transplanted kidney. All transplant patients are considered to have CKD so any of the five stages will apply, based on the GFR. As an example, the code for a patient with a GFR of 50 mL/min/1.73 m2 after transplant would be N18.3 (CKD-3) and Z94.0. The code for ESRD (N18.6) cannot be assigned because it requires chronic dialysis dependence If the transplant patient eventually became dependent on dialysis again, code N18.6 could then be assigned together with Z94.0. In summary, correct documentation of CKD stage is crucial for accurate coding, hospital reimbursement, and severity of illness classification. Clinicians should always review the calculated GFR associated with the creatinine level on clinical lab reports and remember that CKD stage can only be determined when renal function (GFR and creatinine levels) are stable, unless a recent baseline measurement is available. CKD stages are defined by either a GFR below 60 mL/min/1.73 m2 or by the presence of certain kidney damage markers for more than three months. ESRD is defined clinically as either dialysis dependence or kidney transplant status, but the ICD-10-CM definition requires dialysis dependence. Transplant patients are identified with the transplant status code (Z94.0) plus a code for the current CKD stage of the transplanted kidney. Ask Dr. Pinson Q: A patient with alcohol dependency was admitted for alcohol intoxication with confusion and disorientation. Blood alcohol level was 412 mg/dL. Subsequently he began experiencing signs and symptoms of delirium tremens (DTs) and was transferred to the ICU. In your opinion, is it appropriate to query for toxic encephalopathy due to alcohol intoxication? A: Clinicians should be aware of the coding implications of toxic encephalopathy due to alcohol. Yes, a clarification query may be submitted. Without a query, the code assignment would be: 1. Principal diagnosis code: F10.229, alcohol dependence with intoxication (present on admission [POA] indicator = yes) 2. Secondary diagnosis code: F10.231, alcohol dependence with withdrawal delirium (DTs) (POA = no, since it occurred after admission) The diagnosis-related group (DRG) is 897. If the patient's condition is clarified as toxic encephalopathy due to alcohol, then the code assignment would change to: 1. Principal diagnosis code: T51.0X4A, toxic effect of ethanol, initial encounter (POA = yes) 2. Secondary diagnosis codes: G92, toxic encephalopathy (POA = yes), followed by F10.229 (POA = yes), then F10.231 (POA = no) The resulting DRG is 917. Clinicians should also be aware that documentation of “alcoholic encephalopathy” results in assignment of code G31.2 for a chronic degenerative brain condition (Wernicke-Korsakoff) rather than acute encephalopathy due to alcohol. Q: I was disappointed by your column “Linking Severe Sepsis and Hyperlactatemia” in the June 2018 ACP Hospitalist. You seem comfortable with preserving the Sepsis-2 definition, instead of adopting the 2016 Sepsis-3 criteria that I believe should be embraced by the medical community. Hyperlactatemia is not one of the Sequential Organ Failure Assessment (SOFA) organ dysfunction parameters in the Sepsis-3 definition. A: Thank you for your concern about the Sepsis-2/Sepsis-3 controversy. The June edition of Coding Corner was written in response to a specific question from a reader working at a facility where, whether we agree with it or not, the Sepsis-2 definition is still used—a not uncommon situation at this time. The article was devoted to the diagnostic, documentation, and coding nuances of hyperlactatemia pursuant to the ICD-10-CM Official Guidelines for Coding and Reporting, the Surviving Sepsis Campaign (SSC), CMS's Hospital Inpatient Quality Reporting (IQR) system, and Sepsis-2. I believe we agree on the authoritativeness of Sepsis-3. As I wrote in the June article: “Another issue is that Sepsis-2 definitions and criteria (systemic inflammatory response syndrome [SIRS] due to infection) are no longer the authoritative clinical diagnostic standard for sepsis recognized by SSC, having been replaced by Sepsis-3, which was published in February 2016 and adopted by SSC in March 2017. Appeals of auditor denials based on Sepsis-2 criteria are unlikely to be successful, but all such cases should be reviewed for the possibility of using Sepsis-3 diagnostic criteria as the basis for appeal.” It is widely recognized that the SIRS criteria are overly sensitive, leading to overdiagnosis of sepsis in patients who are not truly “septic.” We should also acknowledge that many of our colleagues do not yet trust the sensitivity of Sepsis-3 and qSOFA without prospective outcomes research and are concerned about underrecognition of truly septic patients. Lastly, the CMS IQR measure for management of severe sepsis still follows selected SIRS diagnostic and severe sepsis criteria (not Sepsis-3/SOFA), so clinicians must utilize these Sepsis-2 criteria for initiating a severe sepsis management bundle to demonstrate quality care. This is certainly an unsettled period in the evolution of our definitions, diagnostic tools, and effective management of sepsis. I hope this discussion offers some clarity for all our readers.	4	8	0	0	0	18	0.855515	18	1,899
Clinical Practice Guideline Developed for the Aerospace Medical Association by their constituent organization Overview: Ulcerative colitis (UC) is a chronic, relapsing inflammatory condition of unknown etiology affecting the mucosal layer of the colon. Inflammatory bowel disease (IBD), which includes UC and Crohn’s disease, is a chronic condition resulting from inappropriate mucosal immune activation. The most important risk factor is a positive family history for IBD; approximately 15% of IBD patients have affected first-degree relatives. Dr. Samuel Wilks is credited with being the first to describe UC as a distinct entity from bacillary dysentery in 1859. The hallmark clinical symptom is bloody diarrhea often with prominent symptoms of rectal urgency and tenesmus. UC affects approximately 500,000 people in the United States with an incidence of 8-12/100,000/year (no gender difference) and this incidence has been relatively constant over the past five decades. The clinical presentation is dependent on the extent of colonic involvement and severity of disease. UC invariably begins with inflammation of the rectum and spreads continuously and proximally for variable distances. Disease restricted to the rectum is referred to as ulcerative proctitis (confined to rectum; generally distal 25 cm); left sided colitis is that confined from the distal to splenic flexure, pancolitis is the term to define disease that includes the proximal colon to the splenic flexure; universal colitis is that involving the entire colon, including the cecum; and backwash ileitis is inflammation of distal 10cm or less of terminal ileum in the setting of universal colitis. UC has a variable degree of presentation. Mild disease is almost always confined to the distal colon and rectum and is associated with intermittent rectal bleeding and mild diarrhea consisting of fewer than four small loose stools per day. Moderate disease normally involves more than the distal colon with disease at least to the splenic flexure. There are frequent loose, bloody stools (up to 10/day) with mild anemia not requiring transfusion, abdominal pain not classified as severe, and possibly with low grade fever. Patients with severe disease have extensive colonic disease, frequent loose stools (more than 10/day), with severe cramps, fever up to 39.5o C, and bleeding often severe enough to require transfusion. Assessment of disease severity stems from patient complaints (number of bowel movements, presence of blood per rectum, abdominal pain), the impact of disease on daily activities, pertinent physical exam findings, and the presence of abnormal laboratory tests. About 60% of patients have mild disease (mild diarrheal symptoms and no systemic involvement); however, almost all patients have at least one relapse during a 10-year period, and 25% will require colectomy within 3 years of onset for uncontrollable disease. Extraintestinal symptoms can include reactive arthropathies, ankylosing spondylitis, eye involvement with uveitis and episcleritis, skin disorders of erythema nodosum and pyoderma gangrenosum, thromboembolism, autoimmune hemolytic anemia, and primary sclerosing cholangitis. Local complications of UC include massive hemorrhage, fulminant colitis, intestinal perforation and stricture or toxic megacolon (both rare). Despite the burden of a chronic illness, more than 90% of UC patients are able to maintain capacity for work after 10 years of disease and the overall quality of life is not impaired significantly. The most feared long-term complication is colorectal cancer. Patients with extensive ulcerative colitis have a markedly increased risk for colon cancer in comparison to the general population beginning 8 to 10 years after diagnosis and increasing with time. The usual figure is 4 – 5 times that of the general population and it increases by a factor of 50 for those who also have primary sclerosing cholangitis complicating their UC. The risk for malignancy is also a function of the anatomic extent of the disease; the risk is much greater with pancolitis than with left-sided disease. Patients with long-standing ulcerative colitis are at risk for cancer even if their symptoms have been relatively mild; that is, colon cancer is seen in patients whose disease has been quiescent for 10 to 15 years. In ulcerative colitis, colon cancers are frequently submucosal and may be missed at colonoscopy. Colon cancer in patients with ulcerative colitis is associated with dysplastic changes in the mucosa at other sites in the colon. Dysplasia cannot always be identified by visual inspection; microscopic examination of biopsy specimens is required. The current standard of care is to perform surveillance colonoscopy with random biopsies in patients with long-standing ulcerative colitis beginning 8 to 10 years after the onset of disease and repeated every 1 to 2 years. If the specimens show dysplasia, the patient is sent for colectomy. Although it is clear that dysplasia is associated with colon cancer in patients with ulcerative colitis, the utility of surveillance colonoscopy has not been firmly established. Pathologic findings include mucosal erythema, edema, granularity and erosions. With more severe disease, there are ulcerations, erosions with adherent mucopus, friability and hemorrhage. The characteristic histopathology is crypt architectural distortion and gland drop-out. A lymphoplasmocytic infiltrate is also generally seen. Peak age of onset is between 15 and 30 years of age. Compared to current smokers, non-smokers and former smokers are at increased risk for UC. The diagnosis of UC is made by exclusion of other causes of diarrhea (in particular, infectious etiologies) and a characteristic history with corresponding mucosal findings on endoscopy. Histology of biopsies may confirm the diagnosis. Medical management is used to treat acute disease and for maintenance of remission. The mainstay of treatment is 5-aminosalicylic acid (5-ASA, or mesalamine), administered either topically (when disease is limited to the distal colon) or orally (which requires some mechanism to bypass the upper intestine). The prototypical agent was sulfasalazine (Azulfidine®), which consists of 5-ASA conjugated with a sulfa moiety; the bond between the two moieties was lysed in the colon, and both were believed to be active. However, it is now understood that efficacy of sulfasalazine in UC is due to 5-ASA, while most of its toxicity was due to the sulfa moiety. Currently, oral mesalamine coated in a manner that delays intestinal release (e.g., Pentasa®, Asacol®) is much preferred. (Sulfasalazine was originally developed, and is modestly effective, for the treatment of rheumatoid arthritis, a condition for which, pure mesalamine compounds are curiously ineffective.) When salicylate therapy alone is inadequate for achieving control of UC, corticosteroids, antibiotics, or immunosuppressive drugs (azathioprine, 6-mercaptopurine [6-MP], cyclosporine, methotrexate) may be indicated. Individuals who have reached remission should remain on maintenance therapy with aminosalicylates, which are proven to substantially reduce the incidence of relapse; evidence is also mounting that they offer a protective effect against colorectal cancer. The extent of disease can be predictive of the disease progression and prognosis, with pancolitis leading to more severe attacks than limited disease. Remission in UC is generally tied to the patient’s change in symptomatology with therapy. The role of tumor necrosis factor inhibitors in uncontrolled UC is a subject of great interest, with infliximab showing benefit. Infliximab (Remicade®) has been studied extensively and has been shown to be an effective therapy for moderate to severe cases of UC. Aviators treated with infliximab need to be observed for at least six months on the medication before consideration of waiver to allow for assessment of response and possible adverse affects. Removal of the colon and rectum cures ulcerative colitis. Indications for surgery include medically refractive disease, intractable disease with an impaired quality of life, unacceptable side effects from medications, uncontrolled hemorrhage, toxic megacolon perforation, and development of dysplasia or cancer. There are no prospective randomized trials comparing medical treatment of UC to surgery for any indication, but the three absolute indications for surgery are exsanguinating hemorrhage, frank perforation, and documented carcinoma. The most common surgery is restorative proctocolectomy with ileal pouch anal anastomosis (IPAA), which consists of removal of the entire colon and rectum with preservation of the anal sphincters, and construction of a pouch from approximately 20 cm of the distal ileum. An IPAA is usually performed as a two-stage operation, with the first stage including creation of a temporary diverting ileostomy to allow the ileal pouch to heal. Mean stool frequency ranges from 4 to 9 bowel movements per day, including 1 or 2 nocturnal stools. Rates of complications vary and include obstruction, sepsis, abscess, anastomotic leak, fecal incontinence and sexual and urinary dysfunction. Pouchitis, a nonspecific inflammation of the ileal reservoir, is the most common long-term complication of colectomy with IPAA. Symptoms are similar to UC, with increased frequency of defecation, rectal bleeding, abdominal cramping, rectal urgency, tenesmus and fecal incontinence. Pouchitis occurs in about 20% of individuals, with the highest incidence during the first 6 months after closure of the temporary loop ileostomy. Primary treatment is with antibiotics, with topical and oral mesalamine as second-line therapy. Aeromedical Concerns: Aeromedical disposition of UC is considerably simpler than Crohn’s disease; major complications are unusual and rarely of sudden onset. If an aviator is grounded, it is more often due to the impracticality of flying with frequent bowel movements. Ulcerative proctitis by itself tends to be mild, and is often controllable by aminosalicylate or steroid enemas. With colitis, there is a minimal risk for subtle performance decrement due to gradual onset of anemia if occult blood loss occurs. Relapse is heralded by typical symptoms of diarrhea and can be accompanied by rectal bleeding, fever and malaise in more severe cases. Relapses can also be triggered by psychological stress. However, the aminosalicylates have proven effective to sustain remission and reduce relapse. Dose-related toxic effects of sulfasalazine include headache, nausea, and vomiting. Hypersensitivity reactions include rash, fever, aplastic anemia, agranulocytosis, hepatitis, pancreatitis, nephrotoxicity, pulmonary fibrosis and hemolysis. Although delayed-release forms of mesalamine (e.g., Asacol®, Pentasa®) are more costly than sulfasalazine, these agents are preferred to minimize adverse effects. Immunosuppressants (except etanercept and infliximab), oral steroids and biological agents are not approved for flying duties due to many adverse systemic effects. Although etanercept has been approved for waiver in inflammatory arthropathies and psoriasis, it is not effective in the treatment of ulcerative colitis. Infliximab has been shown to be efficacious in the treatment of ulcerative colitis. Medical Work-up: Medical evaluation of an aviator with the diagnosis of ulcerative colitis should contain a complete history that include the disease course (gastrointestinal symptoms), current therapy, presence of complications and surgical resection, presence or absence of any symptoms suggesting extraintestinal disease (e.g. uveitis, arthritis, ankylosing spondylitis, thromboembolism, primary sclerosing cholangitis, skin disease). Lab test should include a complete blood count (CBC), ESR, LFTs, C-reactive protein (CRP), and albumin. Also necessary is the result of the colonoscopy with mucosal biopsy results. Finally, a consultation report from internal medicine or gastroenterology is very useful. Air Force: UC and ulcerative proctitis are disqualifying for all flying classes. Waiver is not recommended for FC I/IA and untrained FC II and FC III individuals. Any extraintestinal manifestations of UC should be addressed as separate diagnoses and will require individual work-up. (See venous thromboembolic disease, primary sclerosing cholangitis, and ankylosing spondylitis waiver guides.) If a course of oral steroids of greater than three weeks duration is required to achieve control, but is followed by maintenance of remission on waiverable medications, waiver could be considered after the pituitary axis has returned to normal function (based on Cortrosyn® stimulation testing; see waiver guide – systemic glucocorticoid (steroid) treatment). Ulcerative colitis is not mentioned by name for FC IIU personnel, but GI bleeding and diarrhea of sufficient severity to require frequent interventions or to interfere with normal functioning is disqualifying. For ATC/GBC personnel, the important consideration is for gastrointestinal bleeding. Regarding SMOD personnel, there are no listed disqualifications that pertain to ulcerative colitis, gastrointestinal bleeding, or diarrhea. Ulcerative colitis is disqualifying for retention standards in the Air Force. The flight surgeon needs to be aware that an MEB will also be required as part of the overall care, although the two are separate processes. Army: Ulcerative Colitis is disqualifying for aircrew of all classes. Army policy is articulated in the APL of the same name. Army concerns are well reflected in this CPG. The work-up requires a GI evaluation and colonoscopy. Sulfasalazine in doses up to 2 gm/day or mesalamine in doses up to 2.4 gm/day or 6 gm/day, have been waivered for maintenance therapy. Higher doses may be required for treatment, but are not recommended for waivers. Steroid and 5-aminosalicylic acid (5-ASA) enemas have been approved for treatment of proctitis. Partial colectomy is a viable alternative in Army aircrew that cannot tolerate medication or are unmanageable with medical therapy. However, with pancolitis and/or the appearance of high-grade dysplasia or colon cancer, total colectomy with sparing of the rectal musculature for an eventual continency procedure is the preferred operation. A waiver is very rarely if ever granted for any flight training applicant. In rated aircrew, waivers may be considered if disease is classified as mild, left-sided, in remission for at least 1 month, and limited to the distal 25 cm of the colon. If the disease is treated by partial colectomy, a waiver recommendation can be made 1 year after surgery, provided the patient is asymptomatic and is without a colostomy or ileostomy. Navy: Applicants with Ulcerative Colitis are Considered Disqualified (CD), no waiver. Restricted waivers are possible for designated aircrew, but are reserved for mild cases in remission for at least one month. The only waiverable maintenance medications are sulfasalazine (max 2 grams/d), Asacol (up to 2.4 grams daily), and/or steroid enemas. Higher doses may be required for treatment, but are not recommended for waivers. All other pharmacologic therapy, except for dietary adjuncts such as folic acid, is CD. If the disease is treated by partial colectomy, a waiver recommendation can be made one year after surgery, provided the patient is asymptomatic. All patients requiring surgery for control of the disease must have a PEB finding them fit for full duty before waiver recommendation will be considered. Surgical therapy resulting in a permanent colostomy or ileostomy is CD, no waiver. 1. Internal medicine or gastroenterology consultation 2. Recent sigmoidoscopy or colonoscopy 3. Documentation of the extent of the disease process FOLLOW-UP: Annual submission is required with gastroenterology consultation including flexible sigmoidoscopy/colonoscopy report. The appropriate specialist must evaluate joint or ophthalmologic symptoms. Civilian: Ulcerative colitis is disqualifying for all classes of medical certification. It requires the airman to demonstrate that the condition is under control. If the airman has an acute exacerbation, they are told to ground themselves. The associated medical conditions, such as Primary Sclerosing Cholangitis, also will require an authorization for special issuance. Currently, the one treatment situation that is not acceptable is when doses of steroids equivalent to prednisone over 20 mg are prescribed. This generally occurs in an acute exacerbation. Air Force: AIMWTS review revealed a total of 117 cases with the diagnosis of ulcerative colitis. There were 0 FC I/IA cases, 78 FC II cases, 24 FC III cases, 1 FC IIU case, 3 ATC/GBC cases, and 11 SMOD cases. Of this total, 18 were disqualified: 6 were FC II, 8 FC III, 1 FC IIU, 2 ATC/GBC, and 1 SMOD. Most of the disqualifications were due to issues related to the UC diagnosis. Army: Ulcerative colitis is a relatively uncommon diagnosis among rated Army aviators. Between 2009 and 2011 there was an average rated aviator population of 14919 in any given year as identified by having an annual flight physical. During this period, there was an average of 3.67 cases carrying the diagnosis of ulcerative colitis in any given study year, yielding an average one year period prevalence of 2.46 cases per 10,000 aircrew. There were 5 applicants for aviation training with UC one of which was granted a waiver for minimal disease. Also, during this 3 year period there were 10 cases in the rated population of which 2 were suspended and 8 granted waivers. Navy: Not available at this time Civilian: There are currently 751 first-, 460 second-, and 1,519 third-class airmen issued with ulcerative colitis. Due to coding issues at the FAA, these figures may include ulcerative colitis , Crohn’s disease, and airmen with a diagnosis of nonspecific colitis. ICD 9 code(s) for ulcerative colitis Ulcerative colitis, unspecified Turner JR. The Gastrointestinal Tract. Ch. 17 in Kumar: Robbins and Cotran Pathologic Basis of Disease, 8th ed., Saunders, 2009. Stenson WF. Inflammatory bowel disease. Ch. 144 in: Goldman: Cecil Textbook of Medicine, 23rd ed., Saunders, 2007. Osterman MT and Lichtenstein GR. Ulcerative Colitis. Ch. 112 in Feldman: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 9th ed., Saunders, 2010. Langan RC, Gotsch PB, Krafczyk MA, and Skillinge DD. Ulcerative Colitis: Diagnosis and Treatment. Am Fam Physician, 2007; 76:1324-30. Kornbluth A, Sachar DB, et al. Ulcerative Colitis Practice Guidelines in Adults: American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol, 2010; 105:501-23. Peppercorn MA. Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults. UpToDate. Online version 18.1, Jan, 2010. Metcalf AM. Elective and Emergent Operative Management of Ulcerative Colitis. Surg Clin N Am, 2007; 87:633-41. Abraham C and Cho JH. Inflammatory Bowel Disease. N Engl J Med, 2009; 361:2066-78. Peppercorn MA and Farrell RJ. Medical management of ulcerative colitis. Online version 18.1, Jan, 2010. Rutgeerts P, Sandborn WJ, Feagan BG, et al. Infliximab for Induction and Maintenance Therapy for Ulcerative Colitis. N Engl J Med, 2005; 353:2464-76. Pickard JS. Background paper for AFMOA/SGPA on Infliximab, Aug 2009. Prepared by Dr. Dan Van Syoc May 21, 2012	2	26	1	0	0	0	0.632414	1	4,407
A pregnant woman receives an ultrasound examination from a midwife sonographer \|Midwifery, obstetrics, newborn care, women's health, reproductive health\| \|Competencies\|\|Knowledge, professional behaviour and specific skills in family planning, pregnancy, labour, birth, postpartum period, newborn care, women's health, reproductive health, and social, epidemiologic and cultural context of midwifery\| \|hospitals, clinics, health units, maternity units, birth centers, private practices, home births, community, etc\| \|obstetrician, gynecologist, pediatrician\| The education and training for a midwife is similar to that of a nurse, in contrast to obstetricians and perinatologists who are physicians (doctors). In many countries, midwifery is either a branch of nursing or has some links to nursing such as a shared regulatory body, though others regard them as entirely separate professions. Midwives are trained to recognise the variations of normal progress of labor, and understand how to deal with deviations from normal. They may intervene in high risk situations such as breech births, twin births and births where the baby is in a posterior position, using non-invasive techniques. For complications related to pregnancy and birth that are beyond the midwife's scope of practice, including surgical and instrumental deliveries, they refer them to physicians or surgeons. In many parts of the world, these professions work in tandem to provide care to childbearing women. In others, only the midwife is available to provide care, and in yet other countries many women elect to utilize obstetricians primarily over midwives. Many developing countries are investing money and training for midwives, sometimes by upskilling those people already practising as traditional birth attendants. Some primary care services are currently lacking due to the shortage of money being funded for these resources. - 1 Definition and etymology - 2 Scope of practice - 3 Education, training, regulation and practice - 4 Men in midwifery - 5 History - 6 Notable midwives - 7 Midwives in culture - 8 See also - 9 References - 10 External links Definition and etymologyEdit According to the definition of the International Confederation of Midwives, which has also been adopted by the World Health Organization and the International Federation of Gynecology and Obstetrics: A midwife is a person who has successfully completed a midwifery education programme that is recognised in the country where it is located and that is based on the ICM Essential Competencies for Basic Midwifery Practice and the framework of the ICM Global Standards for Midwifery Education; who has acquired the requisite qualifications to be registered or legally licensed to practice midwifery and use the title midwife; and who demonstrates competency in the practice of midwifery. The word derives from Old English mid, "with" and wif, "woman", and thus originally meant "with-woman", that is, the person who is with the mother (woman) at childbirth. The word is used to refer to midwives regardless of gender. Scope of practiceEdit The midwife is recognised as a responsible and accountable professional who works in partnership with women to give the necessary support during pregnancy, labour and the postpartum period. They also provide care for the newborn and the infant. This care includes preventative measures, the promotion of normal birth, the detection of complications in mother and child, the accessing of medical care or other appropriate assistance and the carrying out of emergency measures. The midwife has an important task in health counselling and education, not only for the woman, but also within the family and the community. This work should involve antenatal education and preparation for parenthood and may extend to pregnant's health, sexual or reproductive health and child care. A midwife may practise in any setting including the home, community, hospitals, clinics or health units. Education, training, regulation and practiceEdit Education, training and regulation The undergraduate midwifery programs are three-year full-time university programs leading to a bachelor's degree in midwifery (Bachelor of Midwifery) with additional one-year full-time programs leading to an honours bachelor's degree in midwifery (Bachelor of Midwifery (Honours)). The postgraduate midwifery programs (for registered midwives) lead to master's degrees in midwifery (Master in Midwifery, Master in Midwifery (Research), MSc Midwifery). There are also postgraduate midwifery programs (for registered nurses who wish to become midwives) leading to a bachelor's degree or equivalent qualification in midwifery (Bachelor of Midwifery, Graduate Diploma in Midwifery). Midwives in Australia must be registered with the Australian Health Practitioner Regulation Agency to practice midwifery, and use the title midwife or registered midwife. Midwives work in a number of settings including hospitals, birthing centres, community centres and women's homes. They may be employed by health services or organisations, or self-employed as privately practising midwives. All midwives are expected to work within a defined scope of practice and conform to ongoing regulatory requirements that ensure they are safe and autonomous practitioners. - Australian College of Midwives (ACM). Midwifery was reintroduced as a regulated profession in most of Canada's ten provinces in the 1990s. Prior to this legalization, some midwives had practiced in a legal "grey area" in some provinces. In 1981, a midwife in British Columbia was charged with practicing without a medical license. After several decades of intensive political lobbying by midwives and consumers, fully integrated, regulated and publicly funded midwifery is now part of the health system in the provinces of British Columbia (regulated since 1995), Alberta (regulated since 2000, fully funded since 2009) Saskatchewan (regulated since 1999), Manitoba (regulated since 1997), Ontario (regulated since 1991), Quebec (regulated since 1999), and Nova Scotia (regulated since 2006), and in the Northwest Territories (regulated since 2003) and Nunavut(regulated since 2008). In 2010, Midwifery legislation was proclaimed in New Brunswick and Newfoundland and Labrador. Only Prince Edward Island and Yukon have no legislation in place for the practice of midwifery. Education, training and regulation In British Columbia, the program is offered at the University of British Columbia. Mount Royal University in Calgary, Alberta offers a Bachelor of Midwifery program. In Ontario, the Midwifery Education Program (MEP) is offered by a consortium of McMaster University, Ryerson University and Laurentian University. In Manitoba the program is offered by University College of the North. In Quebec, the program is offered at the Université du Québec à Trois-Rivières. In northern Quebec and Nunavut, Inuit women are being educated to be midwives in their own communities. There are also "bridging programs" for internationally educated midwives at Ryerson University in Ontario and at the University of British Columbia. A federally funded pilot project called the Multi-jurisdictional Midwifery Bridging Program has been offered in Western Canada in the past, but funding was discontinued when they expanded their midwifery program. A new program was reinstated through the University of British Columbia in 2016 called the Internationally Educated Midwives Bridging Program IEMBP. Midwives in Canada must be registered, after assessment by the provincial regulatory bodies, to practice midwifery, and use the title midwife, registered midwife or, the French-language equivalent, sage femme. From the original 'alternative' style of midwifery in the 1960s and 1970s, midwifery practice is offered in a variety of ways within regulated provinces: midwives offer continuity of care within small group practices, choice of birthplace, and a focus on the woman as the primary decision-maker in her maternity care. When women or their newborns experience complications, midwives work in consultation with an appropriate specialist. Registered midwives have access to appropriate diagnostics like blood tests and ultrasounds and can prescribe some medications. Founding principles of the Canadian model of midwifery include informed choice, choice of birthplace, continuity of care from a small group of midwives and respect for the mother as the primary decision maker. Midwives typically have hospital privileges, and support the woman's right to choose where she has her baby. The legal recognition of midwifery has brought midwives into the mainstream of health care with universal funding for services, hospital privileges, rights to prescribe medications commonly needed during pregnancy, birth and postpartum, and rights to order blood work and ultrasounds for their own clients and full consultation access to physicians. To protect the tenets of midwifery and support midwives to provide woman-centered care, the regulatory bodies and professional associations have legislation and standards in place to provide protection, particularly for choice of birth place, informed choice and continuity of care. All regulated midwives have malpractice insurance. Any unregulated person who provides care with 'restricted acts' in regulated provinces or territories is practicing midwifery without a license and is subject to investigation and prosecution. Prior to legislative changes, very few Canadian women had access to midwifery care, in part because it was not funded by the health care system. Legalizing midwifery has made midwifery services available to a wide and diverse population of women and in many communities the number of available midwives does not meet the growing demand for services. Midwifery services are free to women living in provinces and territories with regulated midwifery. - Canadian Association of Midwives (CAM). On 16 March 1995, the BC government announced the approval of regulations that govern midwifery and establish the College of Midwives of BC. In 1996, the Health Professional Council released a draft of Bylaws for the College of Midwives of BC, which the Cabinet approved on 13 April 1997. In 1998, midwives were officially registered with the College of Midwives of BC. In BC, midwives are primary care providers for women in all stages of pregnancy, from prenatal to six weeks postpartum. Midwives also care for newborns. To see the approximate proportion of women whose primary birth attendant was a midwife in British Columbia see, "What Mothers Say: The Canadian Maternity Experiences Survey. Public Health Agency of Canada. Ottawa, 2009, p. 115. Midwives in BC can deliver natural births in hospitals or homes. If a complication arises in a pregnancy, labour, birth, or postpartum, a midwife consults with a specialist such as an obstetrician or paediatrician. Core competencies and restricted activities are included in the BC Health Professions Act Midwives Regulation. As of April 2009, the scope of practice for midwives allows them to prescribe certain prescription drugs, use acupuncture for pain relief, assist a surgeon in a caesarean section delivery and to perform a vacuum extraction delivery. These specialized practices require additional education and certification. As of November 2015, the College of Midwives of British Columbia reported 247 General, 2 Temporary, 46 Non-practicing Registrant midwives. There were 2 midwives per 100,000 people in BC in 2006. A midwife must register with the College of Midwives of BC to practice. To continue licensure, midwives must maintain regular recertification in neonatal resuscitation and management of maternal emergencies, maintain the minimum volume of clinical care (40 women), participate in peer case reviews and continuing education activities. The University of British Columbia (UBC) has a four-year Bachelor of Midwifery program. The UBC midwifery program is poised to double in size thanks to an increase in government funding. Graduation of students will increase to 20 per year. Midwives (sage-femmes, literally meaning "wise-woman" or maïeuticien/maïeuticienne) are independent practitioners, specialists in birth and women's medicine. The undergraduate midwifery programs are five-year full-time university programs (four years in midwifery schools after a first year of medical studies common with Medicine, Odontology and Pharmacy) leading to an accredited master's degree in midwifery (Diplôme d'Etat de Sage-Femme). Midwives in France must be registered with the Ordre des sages-femmes to practice midwifery and use the title sage-femme. - L'Ordre des Sages-Femmes, Conseil National. - Collège National des Sages-Femmes de France (CNSF). - Société Française de Maïeutique (SFMa). Education, training and regulation The undergraduate midwifery programs are four-year full-time university programs, with an internship in the final year, leading to an honours bachelor's degree in midwifery (BSc (Hons) Midwifery). The postgraduate midwifery programs (for registered midwives) lead to master's degrees in midwifery (MSc Midwifery, MSc Midwifery Practice). There are also postgraduate midwifery programs (for registered general nurses who wish to become midwives) leading to a qualification in midwifery (Higher Diploma in Midwifery). Midwives must be registered with the Nursing and Midwifery Board of Ireland (NMBI) to practice midwifery, and use the title midwife or registered midwife. Education, training and regulation Midwifery was first regulated in 1868. Today midwives in Japan are regulated under the Act on Public Health Nurse, Midwife and Nurse (No. 203) established in 1948. Japanese midwives must pass a national certification exam. On 1 March 2003 the Japanese name of midwife officially converted to a gender neutral name. Still, only women can take the national midwife exam. - Japanese Midwives Association (JMA). - Japan Academy of Midwifery (JAM). - Japanese Nursing Association (JNA), Midwives' Division. When a 16-year civil war ended in 1992, Mozambique's health care system was devastated and one in ten women were dying in childbirth. There were only 18 obstetricians for a population of 19 million. In 2004, Mozambique introduced a new health care initiative to train midwives in emergency obstetric care in an attempt to guarantee access to quality medical care during pregnancy and childbirth. The newly introduced midwives system now perform major surgeries including Cesareans and hysterectomies. Education, training and regulation The undergraduate midwifery programs are four-year full-time university programs leading to a bachelor's degree in midwifery (HBO-bachelor Verloskunde). There are four colleges for midwifery in the Netherlands: in Amsterdam, Groningen, Rotterdam and Maastricht. Midwives are called vroedvrouw (knowledge woman), vroedmeester (knowledge master, male), or verloskundige (deliverance experts) in Dutch. Midwives are independent specialists in physiologic birth. In the Netherlands, home birth is still a common practice, although rates have been declining during the past decades. Between 2005-2008, 29% of babies were delivered at home. This figure fell to 23% delivered at home between 2007-2010 according to Midwifery in the Netherlands, a 2012 pamphlet by The Royal Dutch Organization for Midwives. In 2014 it has dropped further to 13.4%. perined.nl/jaarboek2104.pdf. Midwives are generally organized as private practices, some of those are hospital-based. In-hospital outpatient childbirth is available in most hospitals. In this case, a woman's own midwife delivers the baby at the delivery room of a hospital, without intervention of an obstetrician. In all settings, midwives transfer care to an obstetrician in case of a complicated childbirth or need for emergency intervention. Apart from childbirth and immediate postpartum care, midwives are the first line of care in pregnancy control and education of mothers-to-be. Typical information that is given to mothers includes information about food, alcohol, life style, travel, hobbies, sex, etc. Some midwifery practices give additional care in the form of preconceptional care and help with fertility problems. All care by midwives is legal and it is totally reimbursed by all insurance companies. This includes prenatal care, childbirth (by midwives or obstetricians, at home or in the hospital), as well as postpartum/postnatal care for mother and baby at home. - Royal Dutch Organisation of Midwives \| Koninklijke Nederlandse Organisatie van Verloskundigen (KNOV). Midwifery is a regulated profession with no connection to Nursing. Midwifery is a profession with a distinct body of knowledge and its own scope of practice, code of ethics and standards of practice. The midwifery profession has knowledge, skills and abilities to provide a primary complete maternity service to childbearing women on its own responsibility. Education, training and regulation The undergraduate midwifery programmes are three-year full-time (three trimesters per year) tertiary programmes leading to a bachelor's degree in midwifery (Bachelor of Midwifery or Bachelor of Health Science (Midwifery)). These programmes are offered by Otago Polytechnic in Dunedin, Ara Institute of Canterbury (formally CPIT) in Christchurch, Waikato Institute of Technology in Hamilton and Auckland University of Technology (AUT) in Auckland. Several schools have satellite programmes such as Otago with a programme in Southland, Wanaka, Wellington, Palmerston North, Wanganui, and Wairarapa - and AUT with student cohorts in various sites in the upper North Island. The postgraduate midwifery programmes (for registered midwives) lead to postgraduate degrees or equivalent qualifications in midwifery (Postgraduate Certificate in Midwifery, Postgraduate Diploma in Midwifery, Master of Midwifery, PhD Professional Doctorate). The Midwifery First Year of Practice Programme (MFYP) is a compulsory national programme for all New Zealand registered midwifery graduates, irrespective of work setting. The New Zealand College of Midwives (the NZCOM) is contracted by the funder, Health Workforce New Zealand (HWNZ), to provide the programme nationally in accordance with the programme specification. Midwives in New Zealand must be registered with the Midwifery Council of New Zealand to practice midwifery, and use the title midwife. Women may choose a midwife, a General Practitioner or an Obstetrician to provide their maternity care. About 78 percent choose a midwife (8 percent GP, 8 percent Obstetrician, 6 percent unknown). Midwives provide maternity care from early pregnancy to 6 weeks postpartum. The midwifery scope of practise covers normal pregnancy and birth. The midwife either consults or transfers care where there is a departure from a normal pregnancy. Antenatal care is normally provided in clinics, and postnatal care is initially provided in the woman's home. Birth can be in the home, a primary birthing unit, or a hospital. Midwifery care is fully funded by the Government. (GP care may be fully funded. Private obstetric care incurs a fee in addition to the government funding.) - New Zealand College of Midwives. Increase in midwifery education has led to advances in impoverished countries. In Somalia, 1 in 14 women die while giving birth. Senior reproductive and maternal health adviser at UNFPA, Achu Lordfred claims, “the severe shortage of skilled health personnel with obstetric and midwifery skills means the most have their babies delivered by traditional birth attendants. But, when complications arise, these women either die or develop debilitating conditions, such as obstetric fistula, or lose their babies.” UNFPA is striving to change these odds by opening seven midwifery schools and training 125 midwives so far. Education, training and regulation Training includes aspects of midwifery, general nursing, community nursing and psychiatry, and can be achieved as either a four-year degree or a four-year diploma. - Advanced Diploma in Midwifery: Holders of this qualification are eligible to register with the SANC as midwives. Assessments are conducted in line with the assessment policy of the Regulations Relating to the Accreditation of Institutions as Nursing Education Institutions (NEI). This qualification allows international employability. - Postgraduate Diploma in Midwifery: The Postgraduate Diploma articulates with a master's degree in Nursing at NQF level 9. This qualification allows international employability. - Bachelor's Degree in Nursing and Midwifery: Holders of this qualification are eligible for registration with the SANC as a Professional Nurse and Midwife. This qualification allows international employability. The midwifery profession is regulated under the Nursing Act, Act No 3 of 2005. The South African Nursing Council (SANC) is the regulatory body of midwifery in South Africa. - The Society of Midwives of South Africa (SOMSA). Education, training and regulation There are different levels of education for midwives: - Certificate in Midwifery - Diploma in Midwifery - Advanced Diploma in Midwifery - Bachelor of Science in Midfwifery (BScM) - Master of Science in Midwifery (MScM) Midwives must be licensed by the Tanzania Nursing and Midwifery Council (TNMC) in order to practice as a 'registered midwife' or 'enrolled midwife'. TNMC ensure the quality midwifery education output, develop and reviews various guidelines and standards on midwifery professionals and monitor their implementation, monitor and evaluate midwifery education programs and approve such programs to meet the Council and international requirements. Also it establish standards of proficiencies for midwifery education. - Tanzania Midwives Association (TAMA). Education, training and regulation The undergraduate midwifery programs are three-year full-time university programs leading to honours bachelor's degrees in midwifery: BSc (Hons) Midwifery, Bachelor of Midwifery (Hons). The postgraduate midwifery programs (for registered midwives) lead to master's degrees in midwifery (MSc Midwifery, MSc Advanced Practice Midwifery). There are also undergraduate and postgraduate midwifery programs (for graduates with a relevant degree who wish to become midwives) leading to degrees or equivalent qualifications in midwifery (BSc (Hons) Midwifery, Bachelor of Midwifery (Hons), Graduate Diploma in Midwifery, Postgraduate Diploma in Midwifery, MSc Midwifery). Midwifery training consists of classroom-based learning provided by select universities in conjunction with hospital- and community-based training placements at NHS Trusts. Midwifery students do not pay tuition fees, and are eligible for additional financial support while training. Funding varies depending on the UK country. Students are eligible for NHS bursaries, in addition to a grant of 1,000 pounds a year, and neither must be repaid. Shortened-course students, who are already registered adult nurses, have different funding arrangements, are employed by the local NHS Trust via the Strategic Health Authority (SHA), and are paid salaries. This varies between universities and SHAs, with some students being paid their pre-training salaries, while others are employed as a Band 5 and still others are paid a proportion of a Band 5 salary. Midwives must be registered with the Nursing and Midwifery Council in order to practice midwifery and use the title 'midwife' or 'registered midwife', and must also have a Supervisor of Midwives through their local supervising authority. Midwives are practitioners in their own right in the United Kingdom. They take responsibility for the antenatal, intrapartum and postnatal care of women up until 28 days after the birth, or as required thereafter. Midwives are the lead health care professional attending the majority of births, whether at home, in a midwife-led unit or in a hospital (although most births in the UK occur in hospitals). In December 2014 the National Institute for Health and Care Excellence updated its guidance regarding where women should give birth. The new guidance states that midwife-led units are safer than hospitals for women having straightforward (low risk) pregnancies. Its updated guidance also confirms that home birth is as safe as birth in a midwife-led unit or a traditional labour ward for the babies of low-risk pregnant women who have already had at least one child previously. Many midwives also work in the community. The role of community midwives includes making initial appointments with pregnant women, managing clinics, undertaking postnatal care in the home and attending home births. A community midwife typically has a pager, is responsible for a particular area and can be contacted by ambulance control when needed. Sometimes they are paged to help out in a hospital when there are insufficient midwives available. Most midwives work within the National Health Service, providing both hospital and community care, but a significant proportion work independently, providing total care for their clients within a community setting. However, recent government proposals to require insurance for all health professionals is threatening independent midwifery in England. Midwives are at all times responsible for the women they are caring for. They must know when to refer complications to medical staff, act as the women's advocate, and ensure that mothers retain choice and control over childbirth. - Royal College of Midwives (RCM). - Independent Midwives UK (IMUK). - Association of Radical Midwives (ARM). Education, training and regulation - Midwifery programs, accredited by the Midwifery Education Accreditation Council (MEAC), leading to the Certified Professional Midwife (CPM) credential, certified by the North American Registry of Midwives (NARM), that is at the level of a degree in midwifery (AS Midwifery, BSc Midwifery, MSc Midwifery). Completion of a Portfolio Evaluation Process (PEP) or a state licensure program are considered. CPMs have to apply for recertification every three years. - Midwifery programs (for graduates with a relevant degree who wish to become midwives), accredited by the Accreditation Commission for Midwifery Education (ACME), leading to the Certified Nurse Midwife (CNM) and Certified Midwife (CM) credentials, certified by the American Midwifery Certification Board (AMCB), that are at the level of a bachelor's degree or equivalent qualification in midwifery (BSc Midwifery). CNMs and CMs have to apply for recertification every five years. According to each US state, a midwife must be licensed and/or authorized to practice midwifery. Midwives work with women and their families in many settings. They generally support and encourage natural childbirth in all practice settings. Laws regarding who can practice midwifery and in what circumstances vary from state to state. Many states have birthing centers where a midwife may work individually or as a group, which provides additional clinical opportunities for student midwives. CPMs provide on-going care throughout pregnancy and continuous, hands-on care during labor, birth and the immediate postpartum period. They practice as autonomous health professionals working in a network of relationships with other maternity care professionals who can provide consultation and collaboration when needed. Although qualified to practice in any setting, they have particular expertise in providing care in homes and free-standing birth centers, and own or work in over half of the birth centers in the U.S. today. CNMs and CMs work in a variety of settings including private practices, hospitals, birth centers, health clinics, and home birth services. They supervise not only pregnancy, delivery and postpartum period care for those who were pregnant and their newborns, but also provide gynecological care for all women who need it and have autonomy and prescriptive authority in most states. They manage biological female's healthcare from puberty through post-menopause. With appropriate training, they can also first assist in cesarean (operative) deliveries and perform limited ultrasound examinations. It is possible for CNMs/CMs practice independently of physicians, establishing themselves as health care providers in the community of their choice. Men in midwiferyEdit Men rarely practice midwifery for cultural and historical reasons. In ancient Greece, midwives were required by law to have given birth themselves, which prevented men from joining their ranks. In 17th century Europe, some barber surgeons, all of whom were male, specialized in births, especially births requiring the use of surgical instruments. This eventually developed into a professional split, with women serving as midwives and men becoming obstetricians. Men who work as midwives are called midwives (or male midwives, if it is necessary to identify them further) or accoucheurs; the term midhusband (based on a misunderstanding of the etymology of midwife) is occasionally encountered, mostly as a joke. In previous centuries, they were called man-midwives in English. William Smellie is credited with innovations on the shape of forceps. This invention corresponds with the development towards obstetrics. He advised male midwives to wear dresses to reduce controversy over having a man present at birth. As of the 21st century, most developed countries allow men to train as midwives. However, it remains very rare. In the United Kingdom, even after the passing of the Sex Discrimination Act 1975, the Royal College of Midwives barred men from the profession until 1983. As of March 2016, there were between 113 and 137 registered male midwives, representing 0.6% of all practising midwives in the UK. In the US, there remain a small, stable or minimally declining number of male midwives with full scope training (CNMs/CMs), comprising approximately 1% of the membership of the American College of Nurse-Midwives. In some Southeast Asian cultures, some or even most of the traditional midwives are men. A midwife in Ming China had to be female, and had to be familiar with the female body and the process of childbirth. The sexual limitation in midwifery was strict due to strict sex segregation, which was common in the Ming dynasty. Males were not allowed to see or touch a female's body directly. In this situation, male physicians played only a minor role in childbirth. They were usually responsible for only antenatal examinations and body check-ups before and after the baby was born, but never participated in the delivery room. The skill set in midwifery was also different from medicine. Pregnant female bodies were not fully adaptive with a general medical approach. Path to Occupation Females who wanted to be a midwife could only learn the skill from experts because there was no literature about midwifery. However, to serve in the Forbidden City as a midwife was much more challenging. Applicants must apply through the Lodge of Ritual and Ceremony (“Lodge”) (Li-I fang), which was also called the Bureau of Nursing Children (Nai-tzu fu). This institution was located near the Forbidden City in the Central Borough. It took all responsibilities on interviewing, hiring, training and arranging female healers (including midwives) who worked in the palace. After candidates were selected, they were also required to register with the Lodge in order to work in the Forbidden City. A midwife's responsibilities were not limited to childbirths, but could include criminal investigations, especially those that involved females. They consulted in investigations of rape cases and determination on a female's virginity because they were the society's top specialists in sexual medicine. Furthermore, midwives were sometimes assigned to inspect female healers selected by the Lodge, to make sure they were healthy. Benefit of Registration While registration was not required for a midwife who worked outside the palace, it was always better to have one. The Lodge was the only authority to select female healers for the palace. A midwife's registration with the Lodge did not only give them permission to work in the palace, but also represented that they are on the top among other midwives. Pregnant women outside the palace therefore were likely to pay more to hire “palace midwifes” than “folk midwifes”. The dirty work of midwives were exactly what they did during the process of childbirth, which included but not limited to cleaning the byproducts from abortions, miscarriages and stillbirths. Such work was considered “pollution” during the Ming dynasty. Nobody wanted to stay in the same room with the mother during childbirth- not even her husband and female relatives. Infanticide, particularly of newborn baby girls, was part of family planning in Ming times. Midwives and their knowledge of infanticide played important roles in this custom. When a baby was born, the midwife inspected the baby and determined its gender. If it was a female infant, the midwife asked the mother if she wanted to keep it or not. If not, the midwife used her professional knowledge to kill the baby in the simplest and most silent way and then ask for payment. Even if the decision was not made by the midwife, she had to kill the baby because she was the only one who had ability to do so in the delivery room. Moreover, they were also considered as “merchants” of body parts. They were also responsible for disposing waste from the process of childbirth, which consisted of body parts from the placenta. Therefore, they can easily sell them to others secretly to earn additional income. The dirty work and knowledge mentioned above had a negative impact on the public attitude toward midwives. Some writers then described the midwife as a second or vicious character in their stories due to a midwife's guilty knowledge. Midwives were also labeled as one of “six grannies”. This term was originally established by scholars and officials. Over time, male physicians also blamed midwifes for the same reason. Although midwifes dominated the field and had extensive experience in childbirth, they didn't have equivalent participation on elite medical literature. Oppositely, elite medical literature are dominated by male physicians, although who contributed much less in childbirth process. Elders and male physicians also disparaged midwives' knowledge about the female body and the process of childbirth. Male physicians even established a boundary between their learned pharmaceutical knowledge as opposite to the midwife's manual manipulations. They did not consider midwives as professionals that required expertise because their skill was not learned from scholarly literature. They believed the midwife's existence was due to gender segregation, and it limited the male physician's role in childbirth. Midwives in cultureEdit The Midwife (Sage femme) is a French film, written and directed by Martin Prevost in 2017, starring Catherine Deneuve and Catherine Frot. - "International Definition of the Midwife". International Confederation of Midwives. Archived from the original on 22 September 2017. Retrieved 2015. Check date values in: - "Essential Competencies for Basic Midwifery Practice". International Confederation of Midwives (ICM). Archived from the original on 8 October 2017. Retrieved 2015. Check date values in: - Epstein, Abby (9 January 2008). "The Business of Being Born (film)". The New York Times. Archived from the original on 13 February 2009. Retrieved 30 October 2009. - Carson, A (May–June 2016). "Midwifery around the World: A study in the role of midwives in local communities and healthcare systems". annals of global health. Elsevier Inc. 82: 381. doi:10.1016/j.aogh.2016.04.617. - "Global Standards for Basic Midwifery Education". International Confederation of Midwives (ICM). Archived from the original on 25 September 2017. Retrieved 2015. Check date values in: - "midwife". The Oxford English Dictionary. Retrieved 2015. Check date values in: - "Midwife: Word History". The American Heritage Dictionary of the English Language, Fifth Edition. Houghton Mifflin Harcourt Publishing Company. 2015. Archived from the original on 21 September 2015. - Harper, Douglas. "midwife". The Online Etymological Dictionary. Archived from the original on 15 September 2017. Retrieved 2015. Check date values in: - "Midwives Associations Worldwide". International Confederation of Midwives. Archived from the original on 13 January 2018. Retrieved 6 March 2017. - "Approved Programs of Study". Australian Health Practitioner Regulation Agency. Archived from the original on 26 May 2015. - "Becoming a Midwife". Midwives Australia. Archived from the original on 5 June 2016. - "Australian College of Midwives (ACM)". Archived from the original on 29 October 2008. - Schroff, F. (1997). The New Midwifery. Toronto: Women's Press. ISBN 0-88961-224-2. - Midwifery in Saskatchewan, Midwives Association of Saskatchewan - Midwifery in Canada, Law Now - "Midwifery Education in Canada". Canadian Association of Midwives (CAM). Archived from the original on 21 November 2015. - "Home - Midwifery Program". www.midwifery.ubc.ca. Archived from the original on 7 March 2018. Retrieved 2 May 2018. - "midwiferybridging.ca". midwiferybridging.ca. Retrieved 10 December 2012. - "Canadian Association of Midwives (CAM)". Archived from the original on 9 November 2015. - "cmbc.bc.ca". cmbc.bc.ca. 1 January 1998. Archived from the original on 17 September 2013. Retrieved 10 December 2012. - "Archived copy" (PDF). Archived (PDF) from the original on 10 June 2017. Retrieved 30 September 2015.CS1 maint: archived copy as title (link) - "Register of Current & Former Registrants". College of Midwives of British Columbia. Retrieved 12 November 2015. - Canadian Institute for Health Information document titled, Number of Health Personnel in Selected Professions by Registration Status, 2006. This data has the following proviso, "Due to the variation in regulatory requirements, interprofessional comparison should be interpreted with caution." - "Home - Midwifery Program". www.midwifery.ubc.ca. Retrieved 2 May 2018. - "bcmidwives.com". bcmidwives.com. Archived from the original on 21 October 2012. Retrieved 10 December 2012. - "La formation initiale". Ordre des sages-femmes. Archived from the original on 22 December 2015. - "Ordre des sages-femmes". Archived from the original on 15 May 2016. - "L'Ordre des Sages-Femmes, Conseil National". Archived from the original on 15 May 2016. - "Collège National des Sages-Femmes de France (CNSF)". Archived from the original on 17 November 2015. - "Pre-Registration Programmes". The Nursing and Midwifery Board of Ireland (NMBI). Archived from the original on 22 November 2015. - "Japanese Midwives Association" (in Japanese). Archived from the original on 1 October 2015. - "Japanese Midwives Association (JMA)". Archived from the original on 1 October 2015. - "Japan Academy of Midwifery (JAM)". Archived from the original on 19 September 2015. - "Japanese Nursing Association (JNA), Midwives' Division". Archived from the original on 17 November 2015. - "Birth of a Surgeon ~ Introduction \| Wide Angle \| PBS". 12 July 2011. Archived from the original on 25 December 2014. - "Midwifery in the Netherlands". The Royal Dutch Organisation of Midwives (KNOV):.CS1 maint: extra punctuation (link) - "Fewer women give birth at home". CVZ, Central Bureau of Statistics. Archived from the original on 1 October 2015. - "Midwifery in the Netherlands" (PDF). (KNOV). Retrieved 2012. Check date values in: - "Obstetric Practice in the City of Groningen" (in Dutch). - "Preconceptional care" (in Dutch). Archived from the original on 13 November 2013. - "Having a baby in the Netherlands". Archived from the original on 10 October 2010. - "Care package". CVZ, College for Healthcare Insurances. - verloskundigen, de KNOV, de beroepsorganisatie van en voor. "KNOV - Koninklijke Nederlandse Organisatie van Verloskundigen". KNOV. - "Where to Start... Becoming a Midwife". New Zealand College of Midwives. Archived from the original on 21 November 2015. - "New Zealand College of Midwives". Archived from the original on 1 October 2015. - "The Midwifery First Year of Practice Programme". New Zealand College of Midwives. Archived from the original on 28 January 2018. Retrieved 2015. Check date values in: - New Zealand Health Information Service: "Report on Maternity - Maternal and Newborn Information 2003." - "WHO \| Midwives at heart of Somalia's new reproductive health strategy". www.who.int. Archived from the original on 20 December 2016. Retrieved 16 December 2016. - "WHO \| More midwives needed to improve maternal and newborn survival". www.who.int. Archived from the original on 10 November 2016. Retrieved 8 November 2016. - http://www.sanc.co.za Archived 24 February 2018 at the Wayback Machine 5 June 2017. - "The Society of Midwives of South Africa (SOMSA)". Archived from the original on 22 September 2017. - "Scope of Practice for Nurses and Midwives in Tanzania" (PDF). Tanzania Nursing and Midwifery Council. Archived (PDF) from the original on 22 October 2017. - "The Nursing and Midwifery Act, 2010" (PDF). Archived (PDF) from the original on 22 October 2017. - "Tanzania Midwives Association (TAMA)". Archived from the original on 5 October 2017. - "Becoming a midwife". The Nursing and Midwifery Council. Archived from the original on 18 November 2015. - "Midwifery Universities in the UK". studentmidwife.net. Archived from the original on 17 November 2015. Retrieved 2 May 2018. - "Student Finance, Loans and Universities - GOV.UK". Direct.gov.uk. 1 September 2012. Archived from the original on 3 October 2012. Retrieved 10 December 2012. - "NICE confirms midwife-led care during labour is safest for women with straightforward pregnancies". nice.org.uk. Archived from the original on 5 January 2018. Retrieved 2 May 2018. - "Care of Healthy Women and Their Babies During Childbirth". National Collaborating Centre for Women's and Children's Health. National Institute for Health and Care Excellence. December 2014. Archived from the original on 12 February 2015. Retrieved 21 December 2014. - "Career Profile: Community Midwife - Royal College of Midwives". Rcm.org.uk. Archived from the original on 1 November 2012. Retrieved 10 December 2012. - "Threat to Independent Midwifery". BBC News. 10 March 2007. Archived from the original on 8 April 2013. Retrieved 10 December 2012. - [dead link] - "Royal College of Midwives (RCM)". Archived from the original on 20 December 2015. - "Independent Midwives UK (IMUK)". Archived from the original on 25 September 2014. - "Association of Radical Midwives (ARM)". Archived from the original on 8 July 2010. - "Comparison of professional midwifery credentials in the U.S." American Midwifery Certification Board (AMCB). Archived from the original on 5 January 2018. Retrieved 2015. Check date values in: - "Midwifery Education Accreditation Council (MEAC)". Archived from the original on 7 November 2017. Retrieved 2015. Check date values in: - "The CPM Credential". National Association of Certified Professional Midwives (NACPM). Archived from the original on 23 December 2016. Retrieved 2015. Check date values in: - "North American Registry of Midwives (NARM)". Archived from the original on 30 April 2014. - "The Credentials CNM and CM". American College of Nurse-Midwives (ACNM). Archived from the original on 10 November 2017. Retrieved 2015. Check date values in: - "American Midwifery Certification Board (AMCB)". Archived from the original on 17 November 2015. - "Midwifery State-by-State Legal Status". Midwives Alliance of North America (MANA). Archived from the original on 21 May 2017. Retrieved 21 March 2017. - "Birth Center Regulations \| American Association of Birth Centers". Birthcenters.org. Retrieved 10 December 2012. - "CMP Scope of Practice". National Association of Certified Professional Midwives (NACPM). Archived from the original on 5 August 2017. Retrieved 21 March 2017. - "Who are CPMs". National Association of Certified Professional Midwives (NACPM). Archived from the original on 20 February 2017. Retrieved 21 March 2017. - "Our Scope of Practice". www.midwife.org. Archived from the original on 29 October 2017. Retrieved 2 May 2018. - "Midwives Alliance of North America (MANA)". Archived from the original on 28 September 2015. - "National Association of Certified Professional Midwives (NACPM)". Archived from the original on 16 November 2015. - "American College of Nurse-Midwives (ACNM)". Archived from the original on 11 May 2012. - Pilkenton, Deanna; Schorn, Mavis N (February 2008). "Midwifery: A career for men in nursing". Men In Nursing. - "Midwifery: A Career for Men in Nursing". Men in Nursing Journal. - "No job for a man? Meet the male midwives". Telegraph.co.uk. Archived from the original on 22 December 2016. Retrieved 16 December 2016. - Quantity of Midwives Registered with the NMC that are Male Archived 8 October 2016 at the Wayback Machine, whatdotheyknow.com - "Core data survey" (PDF). www.midwife.org. 2010. Retrieved 9 August 2019. - "Archived copy" (PDF). Archived (PDF) from the original on 20 March 2017. Retrieved 19 March 2017.CS1 maint: archived copy as title (link) - Gianno, Rosemary (2004). "'Women are not brave enough' Semelai male midwives in the context of Southeast Asian cultures". Bijdragen tot de Taal-, Land- en Volkenkunde. 160 (1): 31–71. doi:10.1163/22134379-90003734. JSTOR 27868101. - Ropp, Paul S."Chinese Women in the Imperial Past: New Perspectives (review)." China Review International, vol. 9 no. 1, 2002, pp. 43. - Furth, Charlotte. “Ming Women as Healing Experts”. A Flourishing Yin: Gender in China's Medical History, 960-1665. pp. 283 - Furth, Charlotte. “Ming Women as Healing Experts”. A Flourishing Yin: Gender in China's Medical History, 960-1665. pp. 278 - Cass, Victoria B. “Female Healers in the Ming and the Lodge of Ritual and Ceremony.” Journal of the American Oriental Society, vol. 106, no. 1, 1986, pp. 236. - Furth, Charlotte. “Ming Women as Healing Experts”. A Flourishing Yin: Gender in China's Medical History, 960-1665. pp. 282 - Cass, Victoria B. “Female Healers in the Ming and the Lodge of Ritual and Ceremony.” Journal of the American Oriental Society, vol. 106, no. 1, 1986, pp. 239. - Furth, Charlotte. “Ming Women as Healing Experts”. A Flourishing Yin: Gender in China's Medical History, 960-1665. pp. 281. - Judge, Joan. "Chinese Women’s History: Global Circuits, Local meanings." Journal of Women's History, vol. 25 no. 4, 2013, pp. 233. - WALTNER, ANN. “Infanticide and Dowry in Ming and Early Qing China.” Chinese Views of Childhood, edited by Anne Behnke Kinney, University of Hawai'i Press, 1995, pp. 201. - Furth, Charlotte. “Ming Women as Healing Experts”. A Flourishing Yin: Gender in China's Medical History, 960-1665. pp. 269. - Yuan-Ling Chao (2017) Medicine and the Law in Late Imperial China: Cases from the Xing'an Huilan (Conspectus of Penal Cases), The Chinese Historical Review, 24:1, pp. 73. - Furth, Charlotte. “Ming Women as Healing Expert”. A Flourishing Yin: Gender in China's Medical History, 960-1665. pp. 278. - "Midwives in Oprah's Book Club (Official)". www.goodreads.com. Retrieved 23 May 2018.	2	42	1	0	0	0	0.679069	1	10,704
In this article will study on ICD 10 Code for Knee Pain, Bilateral Knee Pain (ICD 10 Code for Left Knee Pain, ICD 10 Code for right Knee pain) and its coding guidelines along with examples. We are all very familiar with the term knee pain. Anyone can get knee pain regardless of age. Knee is one of the biggest joint in body which joints thigh bone (femur) and lower leg joint (tibia). The knee cap is called patella. Tendons (flexible connective tissue) and ligaments (inelastic collagen tissue) help joining these bones and make the knee joint. Symptoms and Causes: Knee pain can be mild, moderate or severe. The reasons for pain can vary such as injury, overuse, infection and inflammation. Sometimes there may be swelling and redness depends on the cause. We need to visit doctor as per the severity and as per how long the pain lasts. Mentioned below are few reasons for knee pain: - Rheumatoid arthritis - Septic arthritis - Iliotibial band syndrome - Patellar tendinitis Tests and Diagnosis: Physician will do extremity examination to check if there is any swelling, inflammation or injury. There may be need of radiological tests (X-ray, CT, MRI, ultrasound) or arthrocentesis (lab analysis of knee joint fluid) for further evaluation to check for infections or injury to tendon or ligament. ICD 10 Code for Knee Pain and guidelines: ICD 10 Code for knee pain is found in chapter 13 of ICD-10 CM manual – diseases of musculoskeletal system and connective tissue, code range M00 – M99 ICD 10 code for knee pain can be searched in ICD-10 CM manual index by 2 ways, search for pain- knee or pain-joint-knee. Both reach to the same code. \|ICD 10 Code for Knee Pain\|\|ICD 10 Code for Knee Pain – Description\| \|M25.561\|\|ICD 10 code for Right knee pain\| \|M25.562\|\|ICD 10 code for Left knee pain\| \|M25.569\|\|ICD 10 code for Unspecified knee pain\| - Use codes M25.561 (ICD 10 code for Right knee pain) and M25.562 (ICD 10 code for Left knee pain) for bilateral knee pain as there is no particular code for bilateral pain. - Review the entire medical record thoroughly especially physical examination to determine the correct anatomical site of pain. Do not code unspecified knee pain if there is any site specification mentioned in the record. For example, patient comes in with unspecified knee pain as per HPI. Documented as left knee pain under physical exam-musculoskeletal-extremity section. Code left knee pain here. - Knee pain is a symptom; hence follow ICD coding guideline of not coding signs and symptoms when there is a definitive diagnosis made. Below are few examples on coding Knee pain. ICD 10 code for Knee Pain Example1: A 5 year old boy has been brought to emergency room after a fall. He was playing on monkey bar and fell down keeping knee on the floor. He hit his head on the bar while falling. He is crying and not allowing anyone to touch his right knee. Physical exam reveals scratches on hands. There is contusion on head. X-ray of right knee and head CT was done to check if any complications. Reports are reviewed by physician and interpreted as patellar fracture. Diagnosis: Fracture right patella, Head contusion S82.001A – Fracture right patella S00.93XA – Contusion head W09.8XXA – Fall from playground equipment Note: There is no need to code ICD for knee pain here as this is due to definitive diagnosis Fracture. ICD 10 code for Knee Pain Example2: Mary is a 38 year old woman presenting to clinic for the first time with knee pain from past 6 months. Right pain is worse than left. She is unable to do her morning walk due to this pain. She feels difficulty in climbing stairs. She never visited any physician for knee pain. Her past, social and surgical history was reviewed which includes alcohol conception weekly once. Her height measured as 5 feet and weight as 145 pounds. Exam found normal gait and tenderness on both knees. She is neurologically intact on extremity neurological exam. Her X-ray results showed possible Hoffa’s syndrome. Diagnosis: Chronic bilateral knee pain, possible Hoffa’s syndrome M25.561 – ICD 10 code for Right knee pain M25.562 – ICD 10 code for Left knee pain G89.29 – Chronic pain Note: Both ICD 10 code for right knee pain and ICD 10 code for left knee pain should be assigned for coding bilateral knee pain. Hoffa’s syndrome is not coded as it is mentioned as “possible”.	4	7	0	0	0	8	0.691314	8	1,077
When Should I Go To The Emergency Room If you have a vascular ulcer, you should go to the emergency room if it becomes infected and you develop certain symptoms. - Skin turning dark brown or black around the affected area, especially if this involves your toes. - Fever or chills. - A bad odor coming from a vascular ulcer. - If a vascular ulcer starts to ooze or bleed more than before, especially if the fluid coming out is cloudy or yellow. - If there is swelling, redness or the wound and its surrounding area are warm or hot to the touch. A note from Cleveland Clinic Vascular ulcers are generally a sign of an underlying chronic health condition. While these conditions are serious, it is possible to manage them and keep on enjoying your life. Your healthcare provider can offer you guidance, resources and more, all of which can help you do what it takes to keep chronic conditions from interfering with how you want to live your life. What Causes Venous Insufficiency Ulcers There are two important causes of venous insufficiency ulcers. One half to two-thirds of venous insufficiency ulcers result from progressive disease of the leg veins. The course of such disease is predictable: it starts with the development of varicose veins caused by refluxing of blood within the veins due to incompetent valvular structures. These varicosities may cause variable swelling and discomfort. As disease progresses, skin changes occur which eventually lead to the formation of a venous insufficiency ulcer. The course of the disease often culminates in ulcer formation in patients in their 60s and 70s. Approximately one-third to one-half of venous insufficiency ulcers occur after the patient experiences DVT . DVTs may cause the process of ulcer formation to occur more quickly than in primary venous insufficiency as described above. Patients who have had a DVT may also present with hemosiderin staining, swelling and discomfort, making it difficult to distinguish post-phlebotic ulcer formation from ulcer formation stemming from venous insufficiency. Other Types Of Leg Ulcer Other common types of leg ulcer include: - arterial leg ulcers caused by poor blood circulation in the arteries - diabetic leg ulcers caused by the high blood sugar associated with diabetes - vasculitic leg ulcers associated with chronic inflammatory disorders such as rheumatoid arthritis and lupus - traumatic leg ulcers caused by injury to the leg - malignant leg ulcers caused by a tumour of the skin of the leg Most ulcers caused by artery disease or diabetes occur on the foot rather than the leg. Page last reviewed: 11 January 2019 Next review due: 11 January 2022 Recommended Reading: Cpt Code For Ulcerative Colitis How Can These Ulcers Be Prevented Once an ulcer has developed, statistics show that another one will develop within 3-5 years. You know that preventing ulcers is well worth the effort if you have experienced the pain and frustration associated with healing wounds. Many patients will continue to wear some type of compression stocking every day while they are on their feet to help the circulation. While a Venous Stasis ulcer may have healed the poor circulation which caused the ulcer has not been corrected. Use AMERIGEL Care Lotion on your lower legs, particularly around the ankles daily. This helps the skin retain its natural moisture, promoting healthier skin that is less prone to problems. AMERX Health Care Corporation164 Douglas Rd E, Oldsmar, FL 34677 \| 448-9599 \| AMERXHC.com AMERX®, AMERIGEL®, HELIX3®, EXTREMIT-EASE®, Where Compression Meets Compliance®, Turn-Key DME®, and Oakin®, are registered trademarks of AMERX Health Care Corporation. AMERX®, AMERIGEL®, HELIX3®, EXTREMIT-EASE®, Where Compression Meets Compliance®, Turn-Key DME®, and Oakin®, are registered trademarks of AMERX Health Care Corporation. Elevation Of The Legs The legs should be placed in an elevated position, ideally at 30 degrees to the heart, while lying down. This, again, helps in the movement of venous blood to the heart.This also prevents the build-up of liquid in the legs that leads to swelling. A cushion or any other object of comfort can be used to keep the toes above the level of the hip while sleeping. Read Also: Bone Broth And Ulcerative Colitis Making Healthy Lifestyle Choices Maintaining a healthy lifestyle has a direct impact on vein health. A nutritious diet, regular exercise, maintaining a healthy weight, and following the recommendations of your health care provider can slow the progression of vein disease, ensure the successful outcome of vein treatment, and promote healing. Clinical Features Of Venous Foot Ulcers It is necessary to distinguish venous ulcers from other ulcer types as the management plan differs according to the etiology. The following characteristic clinical features can help clinicians diagnose venous ulcers: - Shallow ulcers with irregular margins are present in the gaiter region. However, the location can be variable and ulcer might also be present on the lateral malleolus. - Patients usually have a history of DVT or venous insufficiency. - Red granulation tissue or exudate is present in the ulcer bed. - Hemosiderin deposits leading to hyperpigmentation and “lipodermatosclerosis” around the ulcer wound are observed. - Eczematous changes are seen in the skin near the ulcer edge. Read Also: Foods For Gerd And Ulcers Deterrence And Patient Education Individuals affected with VLUs can have an impaired quality of life, mainly related to disability. Plus, heavy exudates can cause malodor, social isolation, and emotional disturbances that severely impact life quality. Compliance is essential to achieve a successful outcome. Patients should be educated because VLUs are chronic processes that require lifelong evaluation and care, even after wound closure. Additionally, conformity to diet and lifestyle modifications may reduce the risk or recurrence, but evidence is lacking. Why Is It Important To Seek Venous Ulcer Treatment Venous ulcers dont heal on their own. The longer you live with them, the greater the likelihood of permanent tissue damage. The damage can spread or cause infections that can become life- or limb-threatening, such as gangrene. In severe cases, it may be necessary to surgically remove your affected limb. Timely care from an experienced wound care provider significantly lowers this risk. Also Check: Natural Ways To Heal Ulcerative Colitis Is A Venous Ulcer A Pressure Ulcer Asked by: Marguerite Goyette Yes. Venous skin ulcers are caused by poor circulation in the legs caused by damaged valves that prevent blood from flowing the wrong way, allowing blood to pool in the legs. Pressure ulcers, on the other hand, are caused by sustained pressure on an area of the body, which cuts off blood flow. What Types Of Venous Disease Cause Venous Stasis Ulcers Chronic venous insufficiency is a common cause of valve dysfunction. It occurs when your valves are damaged or too weak to do their job. Other venous ulcer causes include: - High blood pressure , which damages blood vessel walls. - Venous obstruction, a vein blockage thats sometimes due to blood clots. - Venous reflux, when blood flows backward through weak or damaged valves. Recommended Reading: Foods To Eat When You Have An Ulcer Challenges Of Managing Stasis Ulcers Stasis ulcers are a serious and chronic condition that can be difficult to treat. Infection is a frequent complication. If left unchecked, infection could progress to cellulitis or even septicemia, which in extreme cases could result in the need to amputate. There is also the risk of malignancy, most commonly squamous cell carcinomas. It is essential that ulcers receive careful treatment and management, and that active steps are taken to prevent a recurrence. To reduce the risk of complications, patients are advised to seek treatment from a wound care specialist. What You Need To Know The cornerstone of treatment for venous leg ulcers is compression therapy, but dressings can aid with symptom control and optimise the local wound environment, promoting healing There is no evidence to support the superiority of one dressing type over another when applied under appropriate multilayer compression bandaging When selecting a dressing, look at the wound bed, edge and surrounding skin and decide on the goal of the dressing: for example, if there are signs of localised infection consider an antimicrobial dressing, if there is heavy exudate consider an absorbent dressing A 65 year old man presents with a two month history of a wound in the gaiter area of his left leg. He has a history of a left leg deep vein thrombosis after a long flight but is otherwise fit and well. He had been self-managing with dressings bought over the counter, but the wound has gradually increased in size. The wound is not painful but is weeping serous fluid, causing irritation of the surrounding skin. Examination shows a 4×3×0.1cm wound above the left medial malleolus. There is haemosiderin deposition, venous flare, and moderate oedema in the limb. The ankle-brachial pressure index is normal at 1.0. He is diagnosed with a venous leg ulcer, which is managed with dressings and compression bandaging. About 1% of the adult population in Westernised countries are affected by venous ulcers on the leg or foot.2 The prevalence increases with age to 1.7% in Read Also: How To Cure Mouth Ulcer Permanently Types Of Compression Therapy Compression therapy can speed up wound healing, as well as reduce swelling and pain. This type of therapy may be needed for months until the wound is fully healed. Ongoing use of compression therapy can also reduce the risk that an ulcer will come back. Several types of compression therapy are available, including: - Inelastic. This increases pressure on the wound while a person is walking or contracting the leg muscles, but not while at rest. The most common type of inelastic compression therapy is a moist bandage which hardens after drying. Because it is stiff, the dry bandage will not change when the size of the leg changes, which can be uncomfortable. - Elastic. This type of compression therapy increases pressure on the wound both while moving and at rest. Both compression stockings and bandages can be used for this. Unlike inelastic compression therapy, this type can be removed at night, washed and easily replaced. - Intermittent pneumatic compression. With this therapy, a pump is used inflate and deflate sleeves on the foot or leg. As the sleeve inflates, the pressure increases. Because the equipment is expensive and bulky, it is more commonly used for patients who are bedridden. Who Gets Stasis Ulcers Stasis ulcers affect 1% of the population, so they are not uncommon. A variety of medical problems and lifestyle factors have been linked to their development. These include: - Increasing age - Previous deep venous thrombosis - Lower limb fracture, surgery or injury - Standing upright for long periods - Multiple previous pregnancies Stasis ulcers account for at least 4050% of chronic lower limb ulcers and contribute to a further 20% of mixed arterial and venous ulcers. Also Check: Why Do I Have Ulcerative Colitis Evaluation Of Venous Ulcers Venous ulcers are large and irregularly shaped with well-defined borders and a shallow, sloping edge. Slough with granulation tissue comprises the base of the wound, with moderate to heavy exudate. Patients typically experience no pain to mild pain in the extremity, which is relieved with elevation. Venous ulcers are most frequently located on the lower legs, such as above the lateral or medial malleolus with a medial and circumferential presentation. Common symptoms include edema that worsens throughout the day, pruritus, pain that improves with elevation, and heaviness of the affected limb. Assessment frequently finds abnormally dilated veins around the foot and ankle, atrophic white scarring, and an inverted champagne bottle appearance of the extremity. Are Other Venous Ulcer Treatments Available Venous ulcers that are severe or not responding to standard therapies may require additional treatments such as: - Growth factor therapy, injectable substances that attract healthy cells to ulcers. - Hyperbaric oxygen therapy, a treatment in which you sit in a special, pressurized chamber and inhale pure oxygen. - Lymphedema therapy, massage, skin care and bandaging techniques that clear fluid buildup. - Skin graft, replacing diseased skin with healthy skin from another part of your body. - Stem cell therapy, injections of bone marrow to generate healthy tissue. - Venous disease treatment to correct blood pooling problems and improve circulation. You May Like: Homeopathic Medicine For Ulcerative Colitis Venous Insufficiency And Venous Ulcers Venous insufficiency, also called venous reflux, is a debilitating leg issue in which the blood cant flow up through the veins toward the heart. Healthy veins contain a number of specialized, one-way valves that open to allow blood to flow upward and close to prevent blood from flowing back down. When these valves are damaged or malfunctioning, venous insufficiency occurs. As the valves deteriorate, the blood flows backwards and increases the pressure in the vein, dilating it. Blood stagnates, or pools, in the veins of the lower legs, putting pressure on the venous wall and causing inflammation and discomfort. In many patients, untreated superficial venous reflux leads to the deposition of red blood cells in the tissues. Hemoglobin, the protein in red blood cells that carries oxygen, and hemosiderin, the accumulation of iron from the breakdown of hemoglobin , leaves deposits in the skin in the form of dark staining. In severe cases, chronic, untreated venous insufficiency can cause open sores to develop on the skin, known as venous ulcers. These ulcers occur at the site where blood pools, due to the swelling that prevents the movement of nutrients and oxygen to the tissues. Venous insufficiency can also cause varicose veins, a condition in which the superficial veins, or the veins closest to the surface of the leg, enlarge, twist, or bulge. In addition to being unsightly, varicose veins can cause pain, discomfort, or the development of venous ulcers. Foam Dressings For Venous Leg Ulcers Venous leg ulcers are a common and recurring type of chronic wound. Compression therapy is used to treat venous leg ulcers. Dressings that aim to protect the wound and provide a moist environment to aid ulcer healing are applied beneath compression devices. Foam dressings are one of several types of dressing available. We evaluated the evidence from 12 randomised controlled trials that either compared different types of foam dressings, or compared foam dressings with other types of wound dressings. We found no evidence to suggest that polyurethane foam dressings are significantly better or worse than hydrocellular foam dressings in venous leg ulcer healing. Similarly, we found no evidence to suggest that foam dressings are significantly better or worse than other types of dressings , for the healing of venous leg ulcers. We found insufficient evidence to draw any conclusions regarding: adverse events, quality of life, costs, pain, or dressing performance. Overall, the current evidence is of low or unclear methodological quality. This limits the making of any specific recommendations regarding the use of foam dressings. Further, good quality evidence is required before definitive conclusions can be made regarding the role of foam dressings in the management of venous leg ulcers. You May Like: Best Treatment For Stage 2 Pressure Ulcer How Soon After Treatment Will I Feel Better / How Long Does It Take To Recover From This Treatment Vascular ulcers can take weeks or even months to heal under normal circumstances. However, if cared for properly including closely following the treatment plan provided to you wounds should heal faster than expected. Your provider can tell you what to expect based on your specific wound issue and can help you track your progress along the way. Wound Dressing And Care A venous leg ulcer is an open sore that can catch an infection from microbes very quickly. It is important to keep it clean at all times. Advanced Wound Care Dressings can help keep them free from infection as well as aid in faster wound healing. After dead tissue is removed and the wound is cleaned, it should be covered with a light, wound healing dressing. This can be easily done at home by following the instructions of a wound specialist regarding the method of cleaning and the number of dressings required. Read Also: How To Get Rid Of Tongue Ulcers Looking After Yourself During Treatment The following advice may help your ulcer heal more quickly. - Try to keep active by walking regularly. Sitting and standing still without elevating your legs can make venous leg ulcers and swelling worse. - Whenever you’re sitting or lying down, keep your affected leg elevated. - Regularly exercise your legs by moving your feet up and down, and rotating them at the ankles. This can help encourage better circulation. - If you’re overweight, try to reduce your weight with a healthy diet and regular exercise. - Stop smoking and moderate your alcohol consumption. This can help the ulcer heal faster. - Be careful not to injure your affected leg, and wear comfortable, well-fitting footwear. You may also find it helpful to attend a local healthy leg club, such as those provided by the Lindsay Leg Club Foundation, for support and advice. Venous Leg Ulcers: 6 Things To Know When Treating Venous Disease Lower extremity venous disease affects millions of Americans and may ultimately lead to open, draining wounds that adversely affect quality of life. However, there are exciting developments in early diagnosis, prevention and treatment of venous leg ulcers . On the treatment side, there are more choices now than ever before in compression products, which is greatly improving the patient experience. But proper treatment also comes from a better understanding of venous leg ulcers, and better understanding comes from more education. Luckily, were here to help provide education and support for you and your team, so here are six things to know when treating VLUs. You May Like: Can Ulcers In The Colon Be Cancerous Read Also: What Are Ulcers Caused From Who Gets Foot And Toe Ulcers Youre at higher risk for foot and toe ulcers if you are: - Native American. If you have an eye, kidney or heart disease related to diabetes, youre also at a higher risk. About 15% of people with diabetes will get an ulcer, typically on the bottom of their foot. Around 6% of that 15% will have to be hospitalized because of complications. Youre also at a higher risk of getting foot and toe ulcers if you have any of the following: - Problems with circulation.	2	7	1	0	0	0	0.682557	1	4,086
\|Acute angle closure glaucoma of the person's right eye (shown at left). Note the mid-sized pupil, which was non-reactive to light, and redness of the white part of the eye.\| \|Symptoms\|\|Vision loss, eye pain, mid-dilated pupil, redness of the eye, nausea\| \|Usual onset\|\|Gradual, or sudden\| \|Risk factors\|\|Increased pressure in the eye, family history, high blood pressure\| \|Diagnostic method\|\|Dilated eye examination\| \|Differential diagnosis\|\|Uveitis, trauma, keratitis, conjunctivitis\| \|Treatment\|\|Medication, laser, surgery\| Glaucoma is a group of eye diseases which result in damage to the optic nerve and cause vision loss. The most common type is open-angle glaucoma with less common types including closed-angle glaucoma and normal-tension glaucoma. Open-angle glaucoma develops slowly over time and there is no pain. Peripheral vision may begin to decrease followed by central vision resulting in blindness if not treated. Closed-angle glaucoma can present gradually or suddenly. The sudden presentation may involve severe eye pain, blurred vision, mid-dilated pupil, redness of the eye, and nausea. Vision loss from glaucoma, once it has occurred, is permanent. Risk factors for glaucoma include increased pressure in the eye, a family history of the condition, and high blood pressure. For eye pressures a value of greater than 21 mmHg or 2.8 kPa is often used with higher pressures leading to a greater risk. However, some may have high eye pressure for years and never develop damage. Conversely, optic nerve damage may occur with normal pressure, known as normal-tension glaucoma. The mechanism of open-angle glaucoma is believed to be slow exit of aqueous humor through the trabecular meshwork while in closed-angle glaucoma the iris blocks the trabecular meshwork. Diagnosis is by a dilated eye examination. Often the optic nerve shows an abnormal amount of cupping. If treated early it is possible to slow or stop the progression of disease with medication, laser treatment, or surgery. The goal of these treatments is to decrease eye pressure. A number of different classes of glaucoma medication are available. Laser treatments may be effective in both open-angle and closed-angle glaucoma. A number of types of glaucoma surgeries may be used in people who do not respond sufficiently to other measures. Treatment of closed-angle glaucoma is a medical emergency. About 6 to 67 million people have glaucoma globally. The disease affects about 2 million people in the United States. It occurs more commonly among older people. Closed-angle glaucoma is more common in women. Glaucoma has been called the "silent thief of sight" because the loss of vision usually occurs slowly over a long period of time. Worldwide, glaucoma is the second-leading cause of blindness after cataracts. Cataract caused 51% of blindness in 2010 while glaucoma caused 8%. The word "glaucoma" is from Ancient Greek glaukos which means blue, green, or gray. In English, the word was used as early as 1587 but did not become commonly used until after 1850, when the development of the ophthalmoscope allowed people to see the optic nerve damage. - 1 Signs and symptoms - 2 Causes - 3 Pathophysiology - 4 Diagnosis - 5 Screening - 6 Treatment - 7 Prognosis - 8 Epidemiology - 9 History - 10 Research - 11 References - 12 External links Signs and symptoms Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye check-ups important. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination). About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an emergency. Opaque specks may occur in the lens in glaucoma, known as glaukomflecken. Of the several causes for glaucoma, ocular hypertension (increased pressure within the eye) is the most important risk factor in most glaucomas, but in some populations, only 50% of people with primary open-angle glaucoma actually have elevated ocular pressure. Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. Closed-angle glaucoma accounts for less than 10% of glaucoma cases in the United States, but as many as half of glaucoma cases in other nations (particularly East Asian countries). No clear evidence indicates that vitamin deficiencies cause glaucoma in humans. It follows, then, that oral vitamin supplementation is not a recommended treatment for glaucoma. Caffeine increases intraocular pressure in those with glaucoma, but does not appear to affect normal individuals. Many people of East Asian descent are prone to developing angle closure glaucoma due to shallower anterior chamber depths, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Other Asians such as South Asians are also prone to developing angle closure glaucoma. Higher rates of glaucoma have also been reported for Inuit populations, compared to white populations, in Canada and Greenland. Positive family history is a risk factor for glaucoma. The relative risk of having primary open-angle glaucoma (P.O.A.G.) is increased about two- to four-fold for people who have a sibling with glaucoma. Glaucoma, particularly primary open-angle glaucoma, is associated with mutations in several genes, including MYOC, ASB10, WDR36, NTF4, TBK1, and RPGRIP1, although most cases of glaucoma do not involve these genetic mutations. Normal-tension glaucoma, which comprises one-third of POAG, is also associated with genetic mutations (including OPA1 and OPTN genes). Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally, failure of the normal third-trimester gestational atrophy of the hyaloid canal and the tunica vasculosa lentis is associated with other anomalies. Angle closure-induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies, and has been modelled in mice. Other factors can cause glaucoma, known as "secondary glaucoma", including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle-recession glaucoma); and inflammation of the middle layer of the pigmented vascular eye structure (uveitis), known as uveitic glaucoma. The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact etiology. However, the major risk factor for most glaucomas and the focus of treatment is increased intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the eye, and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn, and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here, the trabecular meshwork drains aqueous humor via the scleral venous sinus (Schlemm's canal) into scleral plexuses and general blood circulation. In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the degeneration and obstruction of the trabecular meshwork, whose original function is to absorb the aqueous humor. Loss of aqueous humor absorption leads to increased resistance and thus a chronic, painless buildup of pressure in the eye. In close/narrow-angle, the iridocorneal angle is completely closed because of forward displacement of the final roll and root of the iris against the cornea, resulting in the inability of the aqueous fluid to flow from the posterior to the anterior chamber and then out of the trabecular network. This accumulation of aqueous humor causes an acute increase in pressure and pain. The inconsistent relationship of glaucomatous optic neuropathy with increased intraocular pressure has provoked hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon degeneration, glial support cell, immune system, aging mechanisms of neuron loss, and severing of the nerve fibers at the scleral edge. Screening for glaucoma is usually performed as part of a standard eye examination performed by optometrists and ophthalmologists. Testing for glaucoma should include measurements of the intraocular pressure via tonometry, anterior chamber angle examination or gonioscopy, and examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio and also rim appearance and vascular change. A formal visual field test should be performed. The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography, scanning laser polarimetry, and/or scanning laser ophthalmoscopy (Heidelberg retinal tomogram). Visual field loss is the most specific sign of the condition, however occurs later in the condition. Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as Goldmann tonometry should be augmented with pachymetry to measure the central corneal thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than the 'true' pressure whereas a thinner-than-average cornea can produce a pressure reading lower than the 'true' pressure. Because pressure measurement error can be caused by more than just CCT (i.e., corneal hydration, elastic properties, etc.), it is impossible to 'adjust' pressure measurements based only on CCT measurements. The frequency doubling illusion can also be used to detect glaucoma with the use of a frequency doubling technology perimeter. Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug use, refraction, inheritance and family history. \|What the test examines\|\|Eye drops used\|\|Physical contact with the eye\|\|Procedure\| \|Tonometry\|\|Inner eye pressure\|\|Maybe\|\|Maybe\|\|Eye drops may be used to numb the eye. The examiner then uses a tonometer to measure the inner pressure of the eye through pressure applied by a puff of warm air or a tiny tool.\| \|Ophthalmoscopy (dilated eye examination)\|\|Shape and color of the optic nerve\|\|Yes\|\|No\|\|Eye drops are used to dilate the pupil. Using a small magnification device with a light on the end, the examiner can examine the magnified optic nerve.\| \|Perimetry (visual field test)\|\|Complete field of vision\|\|No\|\|No\|\|The patient looks straight ahead and is asked to indicate when light passes the patient's peripheral field of vision. This allows the examiner to map the patient's field of vision.\| \|Gonioscopy\|\|Angle in the eye where the iris meets the cornea\|\|Yes\|\|Yes\|\|Eye drops are used to numb the eye. A hand-held contact lens with a mirror is placed gently on the eye to allow the examiner to see the angle between the cornea and the iris.\| \|Pachymetry\|\|Thickness of the cornea\|\|No\|\|Yes\|\|The examiner places a pachymeter gently on the front of the eye to measure its thickness.\| \|Nerve fiber analysis\|\|Thickness of the nerve fiber layer\|\|Maybe\|\|Maybe\|\|Using one of several techniques,[clarification needed] the nerve fibers are examined.\| Glaucoma has been classified into specific types: Primary glaucoma and its variants Primary glaucoma (H40.1-H40.2) - Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex - High-tension glaucoma - Low-tension glaucoma - Primary angle closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle glaucoma, pupil-block glaucoma, acute congestive glaucoma - Acute angle closure glaucoma (aka AACG) - Chronic angle closure glaucoma - Intermittent angle closure glaucoma - Superimposed on chronic open-angle closure glaucoma ("combined mechanism" – uncommon) Variants of primary glaucoma - Pigmentary glaucoma - Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare - Primary juvenile glaucoma Primary angle closure glaucoma is caused by contact between the iris and trabecular meshwork, which in turn obstructs outflow of the aqueous humor from the eye. This contact between iris and trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact between iris and TM causes the formation of synechiae (effectively "scars"). These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly build up in the eye, causing pain and redness (symptomatic, or so-called "acute" angle closure). In this situation, the vision may become blurred, and halos may be seen around bright lights. Accompanying symptoms may include a headache and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, and pain. However, the majority of cases are asymptomatic. Prior to the very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional. Once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional incisional surgery. The goal of treatment is to reverse and prevent contact between the iris and trabecular meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. In the other 25%, laser iridoplasty, medication (pilocarpine) or incisional surgery may be required. Primary open-angle glaucoma is when optic nerve damage results in a progressive loss of the visual field. This is associated with increased pressure in the eye. Not all people with primary open-angle glaucoma have eye pressure that is elevated beyond normal, but decreasing the eye pressure further has been shown to stop progression even in these cases. The increased pressure is caused by trabecular meshwork blockage. Because the microscopic passageways are blocked, the pressure builds up in the eye and causes imperceptible very gradual vision loss. Peripheral vision is affected first, but eventually the entire vision will be lost if not treated. Diagnosis is made by looking for cupping of the optic nerve. Prostaglandin agonists work by opening uveoscleral passageways. Beta-blockers, such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing the formation of aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via inhibition of AC) and increase drainage. Developmental glaucoma (Q15.0) - Primary congenital glaucoma - Infantile glaucoma - Glaucoma associated with hereditary or familial diseases Secondary glaucoma (H40.3-H40.6) - Inflammatory glaucoma - Uveitis of all types - Fuchs heterochromic iridocyclitis - Phacogenic glaucoma - Angle-closure glaucoma with mature cataract - Phacoanaphylactic glaucoma secondary to rupture of lens capsule - Phacolytic glaucoma due to phacotoxic meshwork blockage - Subluxation of lens - Glaucoma secondary to intraocular hemorrhage - Hemolytic glaucoma, also known as erythroclastic glaucoma - Traumatic glaucoma - Angle recession glaucoma: Traumatic recession on anterior chamber angle - Postsurgical glaucoma - Aphakic pupillary block - Ciliary block glaucoma - Neovascular glaucoma (see below for more details) - Drug-induced glaucoma - Corticosteroid induced glaucoma - Alpha-chymotrypsin glaucoma. Postoperative ocular hypertension from use of alpha chymotrypsin. - Glaucoma of miscellaneous origin - Associated with intraocular tumors - Associated with retinal detachments - Secondary to severe chemical burns of the eye - Associated with essential iris atrophy - Toxic glaucoma Neovascular glaucoma, an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood flow to the eye are highly at risk for this condition. Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. Patients with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, especially after cataract surgery procedures. A new treatment for this disease, as first reported by Kahook and colleagues, involves the use of a novel group of medications known as anti-VEGF agents. These injectable medications can lead to a dramatic decrease in new vessel formation and, if injected early enough in the disease process, may lead to normalization of intraocular pressure. Currently, there are no high-quality controlled trials demonstrating a beneficial effect of anti-VEGF treatments in lowering IOP in people with neovascular glaucoma. Toxic glaucoma is open-angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach 80 mmHg (11 kPa). It characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes extends to Schlemm's canal. This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown. Associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede Pardianto (2005) reported on four patients who had toxic glaucoma. One of them underwent phacoemulsification with small particle nucleus drops. Some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief, but further research is required. Absolute glaucoma (H44.5) is the end stage of all types of glaucoma. The eye has no vision, absence of pupillary light reflex and pupillary response, and has a stony appearance. Severe pain is present in the eye. The treatment of absolute glaucoma is a destructive procedure like cyclocryoapplication, cyclophotocoagulation, or injection of 99% alcohol. This section needs additional citations for verification. (August 2015) (Learn how and when to remove this template message) Glaucoma is an umbrella term for eye conditions which damage the optic nerve, and which can lead to a loss of vision. The main cause of damage to the optic nerve is intraocular pressure (IOP), excessive fluid pressure within the eye, which can be due to various reasons including blockage of drainage ducts, and narrowing or closure of the angle between the iris and cornea. The primary division in categorizing different types of glaucoma is open-angle and closed-angle (or angle-closure) glaucoma. In open angle glaucoma, the iris meets the cornea normally, allowing the fluid from inside the eye to drain, thus relieving the internal pressure. Where this angle is narrowed or closed, pressure increases over time, causing damage to the optic nerve, leading to blindness. Primary open-angle glaucoma (also, primary glaucoma, chronic glaucoma) refers to slow clogging of the drainage canals resulting in increased eye pressure which causes progressive optic nerve damage. This manifests as a gradual loss of the visual field, starting with a loss of peripheral vision, but eventually the entire vision will be lost if not treated. This is the most common type of glaucoma, accounting for 90% of cases in the United States, but fewer in Asian countries. Onset is slow and painless, and loss of vision is gradual and irreversible. In narrow-angle glaucoma (also closed-angle glaucoma) the iris bows forward, narrowing the angle that drains the eye, increasing pressure within the eye. If untreated, it can lead to the medical emergency of angle-closure glaucoma. In angle-closure glaucoma (also closed-angle glaucoma, primary angle-closure glaucoma, acute glaucoma) the iris bows forward and causes physical contact between the iris and trabecular meshwork, which blocks the outflow of aqueous humor from within the eye. This contact may gradually damage the draining function of the meshwork until it fails to keep pace with aqueous production, and the intraocular pressure rises. The onset of symptoms is sudden and causes pain and other symptoms that are noticeable; it is treated as a medical emergency. Unlike open-angle glaucoma, angle-closure glaucoma is a result of the angle between the iris and cornea closing. This tends to occur in the far-sighted, who have smaller-than-normal anterior chambers, making physical contact between the iris and trabecular meshwork more likely. Normal-tension glaucoma (also NTG, low-tension glaucoma, normal-pressure glaucoma) is a condition where the optic nerve is damaged although intraocular pressure (IOP) is in the normal range (12-22mm Hg). Individuals with a family history of NTG, those of Japanese ancestry, those with a history of systemic heart disease, and those with Flammer syndrome are at a higher than average risk of developing NTG. The cause of NTG is unknown. Secondary glaucoma refers to any case in which another disease, trauma, drug or procedure causes increased eye pressure, resulting in optic nerve damage and vision loss, and may be mild or severe. It can be due to an eye injury, inflammation, a tumor, or advanced cases of cataracts or diabetes. It can also be caused by certain drugs such as steroids. Treatment depends on whether it is open-angle or angle-closure glaucoma. In pseudoexfoliation glaucoma (also, PEX, exfoliation glaucoma) the pressure is due to the accumulation of microscopic granular protein fibers, which can block normal drainage of the aqueous humor. PEX is prevalent in Scandinavia, primarily in those over 70, and more commonly in women. Pigmentary glaucoma (also, pigmentary dispersion syndrome) is caused by pigment cells sloughing off from the back of the iris and floating around in the aqueous humor. Over time, these pigment cells can accumulate in the anterior chamber in such a way that it can begin to clog the trabecular meshwork. It is a rare condition that occurs mostly among Caucasians, mostly males in their mid-20s to 40s, and most are nearsighted. Primary juvenile glaucoma is a neonate or juvenile abnormality where ocular hypertension is evident at birth or shortly thereafter and is caused by abnormalities in the anterior chamber angle development that blocks the outflow of the aqueous humor. Uveitic glaucoma is due to uveitis, the swelling and inflammation of the uvea, the middle layer of the eye. The uvea provides most of the blood supply to the retina. Increased eye pressure in uveitis can result from the inflammation itself or from the steroids used to treat it. The United States Preventive Services Task Force stated, as of 2013, that there was insufficient evidence to recommend for or against screening for glaucoma. Therefore, there is no national screening program in the US. Screening, however, is recommended starting at age 40 by the American Academy of Ophthalmology. The modern goals of glaucoma management are to avoid glaucomatous damage and nerve damage, and preserve visual field and total quality of life for patients, with minimal side-effects. This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for the individual patient. Although intraocular pressure (IOP) is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment. A review of people with primary open-angle glaucoma and ocular hypertension concluded that medical IOP-lowering treatment slowed down the progression of visual field loss. Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial. Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several medications in each class. Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate them or to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid. Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms. - Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow. - Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body. - Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow. - Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor). - Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma. - Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork to stimulate the opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an argon laser trabeculoplasty procedure. Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small, full-thickness opening in the iris to equalize the pressure between the front and back of the iris, thus correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork. Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium. Both laser and conventional surgeries are performed to treat glaucoma. Surgery is the primary therapy for those with congenital glaucoma. Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma. Canaloplasty is a nonpenetrating procedure using microcatheter technology. To perform a canaloplasty, an incision is made into the eye to gain access to the Schlemm's canal in a similar fashion to a viscocanalostomy. A microcatheter will circumnavigate the canal around the iris, enlarging the main drainage channel and its smaller collector channels through the injection of a sterile, gel-like material called viscoelastic. The catheter is then removed and a suture is placed within the canal and tightened. By opening the canal, the pressure inside the eye may be relieved, although the reason is unclear, since the canal (of Schlemm) does not have any significant fluid resistance in glaucoma or healthy eyes. Long-term results are not available. The most common conventional surgery performed for glaucoma is the trabeculectomy. Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening is made under the flap to remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place to allow fluid to flow out of the eye through this opening, resulting in lowered intraocular pressure and the formation of a bleb or fluid bubble on the surface of the eye. Scarring can occur around or over the flap opening, causing it to become less effective or lose effectiveness altogether. Traditionally, chemotherapeutic adjuvants, such as mitomycin C (MMC) or 5-fluorouracil (5-FU), are applied with soaked sponges on the wound bed to prevent filtering blebs from scarring by inhibiting fibroblast proliferation. Contemporary alternatives to prevent the scarring of the meshwork opening include the sole or combinative implementation of nonchemotherapeutic adjuvants such as the ologen collagen matrix, which has been clinically shown to increase the success rates of surgical treatment. Collagen matrix prevents scarring by randomizing and modulating fibroblast proliferation in addition to mechanically preventing wound contraction and adhesion. Glaucoma drainage implants The first glaucoma drainage implant was developed in 1966. Since then, several types of implants have followed on from the original: the Baerveldt tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or the ExPress Mini Shunt and the later generation pressure ridge Molteno implants. These are indicated for glaucoma patients not responding to maximal medical therapy, with previous failed guarded filtering surgery (trabeculectomy). The flow tube is inserted into the anterior chamber of the eye, and the plate is implanted underneath the conjunctiva to allow a flow of aqueous fluid out of the eye into a chamber called a bleb. - The first-generation Molteno and other nonvalved implants sometimes require the ligation of the tube until the bleb formed is mildly fibrosed and water-tight. This is done to reduce postoperative hypotony—sudden drops in postoperative intraocular pressure. - Valved implants, such as the Ahmed glaucoma valve, attempt to control postoperative hypotony by using a mechanical valve. - Ab interno implants, such as the Xen Gel Stent, are transscleral implants by an ab interno procedure to channel aqueous humor into the non-dissected Tenon's space, creating a subconjunctival drainage area similar to a bleb. The implants are transscleral and different from other ab interno implants that do not create a transscleral drainage, such as iStent, CyPass, or Hydrus. The ongoing scarring over the conjunctival dissipation segment of the shunt may become too thick for the aqueous humor to filter through. This may require preventive measures using antifibrotic medications, such as 5-fluorouracil or mitomycin-C (during the procedure), or other nonantifibrotic medication methods, such as collagen matrix implant, or biodegradable spacer, or later on create a necessity for revision surgery with the sole or combinative use of donor patch grafts or collagen matrix implant. And for glaucomatous painful blind eye and some cases of glaucoma, cyclocryotherapy for ciliary body ablation could be considered to be performed. Laser-assisted nonpenetrating deep sclerectomy The most common surgical approach currently used for the treatment of glaucoma is trabeculectomy, in which the sclera is punctured to alleviate intraocular pressure. Nonpenetrating deep sclerectomy (NPDS) surgery is a similar, but modified, procedure, in which instead of puncturing the scleral bed and trabecular meshwork under a scleral flap, a second deep scleral flap is created, excised, with further procedures of deroofing the Schlemm's canal, upon which, percolation of liquid from the inner eye is achieved and thus alleviating intraocular pressure, without penetrating the eye. NPDS is demonstrated to have significantly fewer side effects than trabeculectomy. However, NPDS is performed manually and requires higher level of skills that may be assisted with instruments. In order to prevent wound adhesion after deep scleral excision and to maintain good filtering results, NPDS as with other non-penetrating procedures is sometimes performed with a variety of biocompatible spacers or devices, such as the Aquaflow collagen wick, ologen Collagen Matrix, or Xenoplast glaucoma implant. Laser-assisted NPDS is performed with the use of a CO2 laser system. The laser-based system is self-terminating once the required scleral thickness and adequate drainage of the intraocular fluid have been achieved. This self-regulation effect is achieved as the CO2 laser essentially stops ablating as soon as it comes in contact with the intraocular percolated liquid, which occurs as soon as the laser reaches the optimal residual intact layer thickness. In open-angle glaucoma, the typical progression from normal vision to complete blindness takes about 25 years to 70 years without treatment, depending on the method of estimation used. The intraocular pressure can also have an effect, with higher pressures reducing the time until blindness. As of 2010, there were 44.7 million people in the world with open angle glaucoma. The same year, there were 2.8 million people in the United States with open angle glaucoma. By 2020, the prevalence is projected to increase to 58.6 million worldwide and 3.4 million the United States. Both internationally and in the United States, glaucoma is the second-leading cause of blindness. Globally, cataracts are a more common cause. Glaucoma is also the leading cause of blindness in African Americans, who have higher rates of primary open-angle glaucoma. Bilateral vision loss can negatively affect mobility and interfere with driving. The association of elevated intraocular pressure (IOP) and glaucoma was first described by Englishman Richard Bannister in 1622: "...that the Eye be grown more solid and hard, then naturally it should be...". Angle-closure glaucoma was treated with cataract extraction by John Collins Warren in Boston as early as 1806. The invention of the ophthalmoscope by Hermann Helmholtz in 1851 enabled ophthalmologists for the first time to identify the pathological hallmark of glaucoma, the excavation of the optic nerve head due to retinal ganglion cell loss. The first reliable instrument to measure intraocular pressure was invented by Norwegian ophthalmologist Hjalmar August Schiøtz in 1905. About half a century later, Hans Goldmann in Berne, Switzerland, developed his applanation tonometer which still today - despite numerous new innovations in diagnostics - is considered the gold standard of determining this crucial pathogenic factor. In the late 20th century, further pathomechanisms beyond elevated IOP were discovered and became the subject of research like insufficient blood supply – often associated with low or irregular blood pressure – to the retina and optic nerve head. The first drug to reduce IOP, pilocarpine, was introduced in the 1870s. Early surgical techniques like iridectomy and fistulating methods have recently been supplemented by less invasive procedures like small implants, a range of options now widely called MIGS (micro-invasive glaucoma surgery). The word "glaucoma" comes from the Ancient Greek γλαύκωμα, a derivative of γλαυκóς, which commonly described the color of eyes which were not dark (i.e. blue, green, light gray). Eyes described as γλαυκóς due to disease might have had a gray cataract in the Hippocratic era, or, in the early Common Era, the greenish pupillary hue sometimes seen in angle-closure glaucoma. Rho kinase inhibitors Rho kinase inhibitors, such as ripasudil, work by inhibition of the actin cytoskeleton, resulting in the morphological changes in the trabecular meshwork and increased aqueous outflow. More compounds in this class are being investigated in phase 2 and phase 3 trials. A 2013 Cochrane Systematic Review compared the effect of brimonidine and timolol in slowing the progression of open angle glaucoma in adult participants. The results showed that participants assigned to brimonidine showed less visual field progression that those assigned to timolol, though the results were not significant, given the heavy loss-to-followup and limited evidence. The mean intraocular pressures for both groups were similar. Participants in the brimonidine group had a higher occurrence of side effects caused by medication than participants in the timolol group. Studies in the 1970s reported that the use of cannabis may lower intraocular pressure. In an effort to determine whether marijuana, or drugs derived from it, might be effective as a glaucoma treatment, the US National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye. In 2003, the American Academy of Ophthalmology released a position statement stating that cannabis was not more effective than prescription medications. Furthermore, no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of cannabis use to treat glaucoma compared with the wide variety of pharmaceutical agents now available. In 2010 the American Glaucoma Society published a position paper discrediting the use of cannabis as a legitimate treatment for elevated intraocular pressure, for reasons including short duration of action and side effects that limit many activities of daily living. - "Facts About Glaucoma". National Eye Institute. Archived from the original on 28 March 2016. Retrieved 29 March 2016. - Mantravadi, AV; Vadhar, N (September 2015). "Glaucoma". Primary Care. 42 (3): 437–49. doi:10.1016/j.pop.2015.05.008. ISSN 0095-4543. PMID 26319348. - Ferri, Fred F. (2010). Ferri's differential diagnosis : a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders (2nd ed.). Philadelphia, PA: Elsevier/Mosby. p. Chapter G. ISBN 978-0323076999. - GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282. - Rhee, Douglas J. (2012). Glaucoma (2 ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 180. ISBN 9781609133375. OCLC 744299538. - Mi, Xue-Song; Yuan, Ti-Fei; So, Kwok-Fai (16 September 2014). "The current research status of normal tension glaucoma". Clinical Interventions in Aging. 9: 1563–71. doi:10.2147/CIA.S67263. PMC 4172068. PMID 25258525. - Vass, C.; Hirn, C.; Sycha, T.; Findl, O.; Bauer, P.; Schmetterer, L. (17 October 2007). "Medical interventions for primary open angle glaucoma and ocular hypertension". The Cochrane Database of Systematic Reviews (4): CD003167. doi:10.1002/14651858.CD003167.pub3. ISSN 1469-493X. PMID 17943780. - "Glaucoma: The 'silent thief' begins to tell its secrets" (Press release). National Eye Institute. 21 January 2014. Archived from the original on 23 July 2015. - Resnikoff, Serge; Pascolini, Donatella; Etya'Ale, Daniel; Kocur, Ivo; Pararajasegaram, Ramachandra; Pokharel, Gopal P.; Mariotti, Silvio P. (2004). "Global data on visual impairment in the year 2002". Bulletin of the World Health Organization. 82 (11): 844–51. doi:10.1590/S0042-96862004001100009 (inactive 20 August 2019). PMC 2623053. PMID 15640920. Archived from the original on 12 December 2013. - GLOBAL DATA ON VISUAL IMPAIRMENTS 2010 (PDF). World Health Organization. 2010. p. 3. - Leffler, CT; Schwartz, SG; Giliberti, FM; Young, MT; Bermudez, D (2015). "What was Glaucoma Called Before the 20th Century?". Ophthalmology and Eye Diseases. 7: 21–33. doi:10.4137/OED.S32004. ISSN 1179-1721. PMC 4601337. PMID 26483611. Archived from the original on 23 April 2016. - Leffler CT, Schwartz SG, Stackhouse R, Davenport B, Spetzler K (2013). "Evolution and impact of eye and vision terms in written English". JAMA Ophthalmology. 131 (12): 1625–31. doi:10.1001/jamaophthalmol.2013.917. PMID 24337558. Archived from the original on 23 December 2014. - Friedman, Neil J.; Kaiser, Peter K.; II, Roberto Pineda (2014). The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology E-Book. Elsevier Health Sciences. p. 234. ISBN 9780323225274. - Sommer A, Tielsch JM, Katz J, et al. (August 1991). "Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore Eye Survey". Archives of Ophthalmology. 109 (8): 1090–95. doi:10.1001/archopht.1991.01080080050026. PMID 1867550. - Rhee DJ, Katz LJ, Spaeth GL, Myers JS (2001). "Complementary and alternative medicine for glaucoma". Survey of Ophthalmology. 46 (1): 43–55. doi:10.1016/S0039-6257(01)00233-8. PMID 11525790. - Li, M; Wang, M; Guo, W; Wang, J; Sun, X (March 2011). "The effect of caffeine on intraocular pressure: a systematic review and meta-analysis". Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht von Graefes Archiv für Klinische und Experimentelle Ophthalmologie. 249 (3): 435–42. doi:10.1007/s00417-010-1455-1. ISSN 1435-702X. PMID 20706731. - Wang N, Wu H, Fan Z (November 2002). "Primary angle closure glaucoma in Chinese and Western populations". Chinese Medical Journal. 115 (11): 1706–15. PMID 12609093. Archived from the original on 21 December 2016. - Dorairaj, Syril; Tsai, James C.; Grippo, Tomas M. (2012). "Changing Trends of Imaging in Angle Closure Evaluation". ISRN Ophthalmology. 2012: 597124. doi:10.5402/2012/597124. PMC 3914273. PMID 24558589. - Cheng, JW; Zong, Y; Zeng, YY; Wei, RL (2014). "The prevalence of primary angle closure glaucoma in adult Asians: a systematic review and meta-analysis". PLOS One. 9 (7): e103222. doi:10.1371/journal.pone.0103222. PMC 4110010. PMID 25057993. - Friedman D, Vedula SS (2006). "Lens extraction for chronic angle-closure glaucoma". Cochrane Database of Systematic Reviews. 3 (3): CD005555. doi:10.1002/14651858.CD005555.pub2. PMC 4438535. PMID 16856103. - Myron Yanoff; Jay S. Duker (2009). Ophthalmology (3rd ed.). Mosby Elsevier. p. 1096. ISBN 9780323043328. - Online Mendelian Inheritance in Man (OMIM) GLAUCOMA, PRIMARY OPEN ANGLE; POAG -137760 - Fernández-Martínez, Lorena; Letteboer, Stef; Mardin, Christian Y.; Weisschuh, Nicole; Gramer, Eugen; Weber, Bernhard Hf; Rautenstrauss, Bernd; Ferreira, Paulo A.; Kruse, Friedrich E. (April 2011). "Evidence for RPGRIP1 gene as risk factor for primary open angle glaucoma". European Journal of Human Genetics. 19 (4): 445–451. doi:10.1038/ejhg.2010.217. ISSN 1476-5438. PMC 3060327. PMID 21224891. - Online Mendelian Inheritance in Man (OMIM) GLAUCOMA, NORMAL TENSION, SUSCEPTIBILITY TO -606657 - Pardianto G, et al. (2005). "Aqueous Flow and the Glaucoma". Mimbar Ilmiah Oftalmologi Indonesia. 2: 12–15. - Chaum E, et al. "A 5-year-old girl who failed her school vision screening. Case presentation of Persistent fetal vasculature (PFV), also called persistent hyperplastic primary vitreous (PHPV)". Digital Journal of Ophthalmology. Archived from the original on 11 January 2009. - Hunt A, Rowe N, Lam A, Martin F (July 2005). "Outcomes in persistent hyperplastic primary vitreous". Br J Ophthalmol. 89 (7): 859–63. doi:10.1136/bjo.2004.053595. PMC 1772745. PMID 15965167. - Chang B, Smith RS, Peters M, et al. (2001). "Haploinsufficient Bmp4 ocular phenotypes include anterior segment dysgenesis with elevated intraocular pressure". BMC Genet. 2: 18. doi:10.1186/1471-2156-2-18. PMC 59999. PMID 11722794. - Alguire P (1990). "The Eye Chapter 118 Tonometry>Basic Science". In Walker HK, Hall WD, Hurst JW (eds.). Clinical methods: the history, physical, and laboratory examinations (3rd ed.). London: Butterworths. ISBN 978-0-409-90077-4. - Mozaffarieh M, Grieshaber MC, Flammer J (2008). "Oxygen and blood flow: players in the pathogenesis of glaucoma". Mol. Vis. 14: 224–33. PMC 2267728. PMID 18334938. Archived from the original on 9 June 2008. - Osborne NN, Wood JP, Chidlow G, Bae JH, Melena J, Nash MS (August 1999). "Ganglion cell death in glaucoma: what do we really know?". Br J Ophthalmol. 83 (8): 980–6. doi:10.1136/bjo.83.8.980. PMC 1723166. PMID 10413706. - Levin LA, Peeples P (February 2008). "History of neuroprotection and rationale as a therapy for glaucoma". Am J Manag Care. 14 (1 Suppl): S11–4. PMID 18284310. Archived from the original on 7 April 2012. - Varma R, Peeples P, Walt JG, Bramley TJ (February 2008). "Disease progression and the need for neuroprotection in glaucoma management". Am J Manag Care. 14 (1 Suppl): S15–9. PMID 18284311. Archived from the original on 7 April 2012. - Hernández M, Urcola JH, Vecino E (May 2008). "Retinal ganglion cell neuroprotection in a rat model of glaucoma following brimonidine, latanoprost or combined treatments". Exp. Eye Res. 86 (5): 798–806. doi:10.1016/j.exer.2008.02.008. PMID 18394603. - Cantor LB (December 2006). "Brimonidine in the treatment of glaucoma and ocular hypertension". Ther Clin Risk Manag. 2 (4): 337–46. doi:10.2147/tcrm.2006.2.4.337. PMC 1936355. PMID 18360646. - Schwartz M (June 2007). "Modulating the immune system: a vaccine for glaucoma?". Can J Ophthalmol. 42 (3): 439–41. doi:10.3129/I07-050. PMID 17508041. - Morrison JC (2006). "Integrins in the optic nerve head: Potential roles in glaucomatous optic neuropathy (an American Ophthalmological Society thesis)". Trans Am Ophthalmol Soc. 104: 453–77. PMC 1809896. PMID 17471356. - Knox DL, Eagle RC, Green WR (March 2007). "Optic nerve hydropic axonal degeneration and blocked retrograde axoplasmic transport: histopathologic features in human high-pressure secondary glaucoma". Arch. Ophthalmol. 125 (3): 347–53. doi:10.1001/archopht.125.3.347. PMID 17353405. - Tezel G, Luo C, Yang X (March 2007). "Accelerated Aging in Glaucoma: Immunohistochemical Assessment of Advanced Glycation End Products in the Human Retina and Optic Nerve Head". Invest. Ophthalmol. Vis. Sci. 48 (3): 1201–11. doi:10.1167/iovs.06-0737. PMC 2492883. PMID 17325164. - Berry FB, Mirzayans F, Walter MA (April 2006). "Regulation of FOXC1 stability and transcriptional activity by an epidermal growth factor-activated mitogen-activated protein kinase signaling cascade". J Biol Chem. 281 (15): 10098–104. doi:10.1074/jbc.M513629200. PMID 16492674. - "Issue on neuroprotection". Can. J. Ophthalmol. 42 (3). June 2007. ISSN 1715-3360. Archived from the original on 12 May 2007. - Farandos, NM; Yetisen, AK; Monteiro, MJ; Lowe, CR; Yun, SH (November 2014). "Contact Lens Sensors in Ocular Diagnostics". Advanced Healthcare Materials. 4 (6): 792–810. doi:10.1002/adhm.201400504. PMID 25400274. - Pardianto G et al. Some difficulties on Glaucoma. Mimbar Ilmiah Oftalmologi Indonesia. 2006;3: 49–52. - Thomas R, Parikh RS (September 2006). "How to assess a patient for glaucoma". Community Eye Health. 19 (59): 36–7. PMC 1705629. PMID 17491713. - Michelessi M, Lucenteforte E, Oddone F, Brazzelli M, Parravano M, Franchi S, Ng SM, Virgili G (2015). "Optic nerve head and fibre layer imaging for diagnosing glaucoma". Cochrane Database Syst Rev. 11 (11): CD008803. doi:10.1002/14651858.CD008803.pub2. PMC 4732281. PMID 26618332. - Thylefors, B; Négrel, AD (1994). "The global impact of glaucoma". Bulletin of the World Health Organization. 72 (3): 323–6. PMID 8062393. - Johnson, Chris A. The use of a visual illusion to detect glaucoma. In Visual Perception: The Influence of H. W. Leibowitz, eds. Andre, J., Owens, D. A., and Harvey, Jr., L. O. (2003); 45–56. Washington, D.C.: The American Psychological Association. - Foundation, G. R. (n.d.). "Five common Glaucoma Tests". Glaucoma.org. Archived from the original on 8 September 2017. Retrieved 20 February 2014. - "Nerve Fiber Analysis". Glaucoma Associates of Texas. White Rabbit Communications, Inc. 2010. Archived from the original on 26 March 2013. Retrieved 9 December 2012. - Paton D, Craig JA; Craig (1976). "Glaucomas. Diagnosis and management". Clin Symp. 28 (2): 1–47. PMID 1053095. - Logan, Carolynn M.; Rice, M. Katherine (1987). Logan's Medical and Scientific Abbreviations. Philadelphia: J. B. Lippincott Company. p. 3. ISBN 978-0-397-54589-6. - "Primary Open-Angle Glaucoma: Glaucoma: Merck Manual Professional". Merck.com. Archived from the original on 28 November 2010. Retrieved 24 January 2011. - Simha A, Braganza A, Abraham L, Samuel P, Lindsley K (2013). "Anti-vascular endothelial growth factor for neovascular glaucoma". Cochrane Database Syst Rev. 10 (10): CD007920. doi:10.1002/14651858.CD007920.pub2. PMC 4261636. PMID 24089293. - Pardianto G, Difficulties on glaucoma in Mimbar Ilmiah Oftalmologi Indonesia.2006;3: 48–9.[verification needed] - Arthur J. Sit, MD (23 April 2006). "Many types of glaucoma, one kind of damage to optic nerve". Chicago Tribune. Archived from the original on 6 October 2012. Retrieved 18 August 2015. Glaucoma is a broad term for a number of different conditions that damage the optic nerve, the 'cable' that carries visual information from the eye to the brain, thereby causing changes in vision. - Moyer, Virginia A. (9 July 2013). "Screening for Glaucoma: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine. 159 (7): I-28. doi:10.7326/0003-4819-159-6-201309170-00685. PMID 23836133. - "Glaucoma – National Institutes of Health". Nihseniorhealth.gov. Archived from the original on 25 December 2010. Retrieved 24 January 2011. - Noecker RJ (June 2006). "The management of glaucoma and intraocular hypertension: current approaches and recent advances". Ther Clin Risk Manag. 2 (2): 193–206. doi:10.2147/tcrm.2006.2.2.193. PMC 1661659. PMID 18360593. - Parikh RS, Parikh SR, Navin S, Arun E, Thomas R (1 May 2008). "Practical approach to medical management of glaucoma". Indian J Ophthalmol. 56 (3): 223–30. doi:10.4103/0301-4738.40362. PMC 2636120. PMID 18417824. - Leffler CT, Amini L (2007). "Interpretation of uniocular and binocular trials of glaucoma medications: an observational case series". BMC Ophthalmol. 7: 17. doi:10.1186/1471-2415-7-17. PMC 2093925. PMID 17916260. - Xu L, Wang X, Wu M (2017). "Topical medication instillation techniques for glaucoma". Cochrane Database Syst Rev. 2: CD010520. doi:10.1002/14651858.CD010520.pub2. PMC 5419432. PMID 28218404. - Jaret, Peter. "A New Understanding of Glaucoma". The New York Times. NYTimes.com. Archived from the original on 10 March 2014. Retrieved 20 February 2014. - Ritch R (June 2007). "Natural compounds: evidence for a protective role in eye disease". Can. J. Ophthalmol. 42 (3): 425–38. doi:10.3129/I07-044. PMID 17508040. - Tsai JC, Song BJ, Wu L, Forbes M (September 2007). "Erythropoietin: a candidate neuroprotective agent in the treatment of glaucoma". J Glaucoma. 16 (6): 567–71. doi:10.1097/IJG.0b013e318156a556. PMID 17873720. - Mozaffarieh M, Flammer J (November 2007). "Is there more to glaucoma treatment than lowering IOP?". Surv Ophthalmol. 52 (Suppl 2): S174–79. doi:10.1016/j.survophthal.2007.08.013. PMID 17998043. - Online Mendelian Inheritance in Man (OMIM) Glaucoma, Congenital: GLC3 Buphthalmos -231300 - Shingleton B, Tetz M, Korber N (March 2008). "Circumferential viscodilation and tensioning of Schlemm's canal (canaloplasty) with temporal clear corneal phacoemulsification cataract surgery for open-angle glaucoma and visually significant cataract: one-year results". J Cataract Refract Surg. 34 (3): 433–40. doi:10.1016/j.jcrs.2007.11.029. PMID 18299068. - Lewis RA, von Wolff K, Tetz M, et al. (July 2007). "Canaloplasty: circumferential viscodilation and tensioning of Schlemm's canal using a flexible microcatheter for the treatment of open-angle glaucoma in adults: interim clinical study analysis". J Cataract Refract Surg. 33 (7): 1217–26. doi:10.1016/j.jcrs.2007.03.051. PMID 17586378. - Dada T, Sharma R, Sinha G, Angmo D, Temkar S (2016). "Cyclodialysis-enhanced trabeculectomy with triple Ologen implantation". Eur J Ophthalmol. 26 (1): 95–7. doi:10.5301/ejo.5000633. PMID 26044372. - Yuan, F; Li, L; Chen; Yan; Wang (2015). "Biodegradable 3D-Porous Collagen Matrix (Ologen) Compared with Mitomycin C for Treatment of Primary Open-Angle Glaucoma: Results at 5 Years". Journal of Ophthalmology. 2015 (637537): 1–7. doi:10.1155/2015/637537. PMC 4452460. PMID 26078875. - Dada, Tanuj; Amit S; Saptorshi M; Meenakshi G (May 2013). "Combined Subconjunctival and Subscleral ologen Implant Insertion in Trabeculectomy". Eye. 27 (7): 889. doi:10.1038/eye.2013.76. PMC 3709396. PMID 23640614. - Cillino, S; Casuccio A; Di Pace F; Cagini C; Ferraro LL (March 2016). "Biodegradable collagen matrix implant versus mitomycin-C in trabeculectomy: five-year follow-up". BMC Ophthalmol. 16 (24): 24. doi:10.1186/s12886-016-0198-0. PMC 4779569. PMID 26946419. - "Eyelights Newsletter: About Glaucoma New Zealand" (PDF). Glaucoma.org. Archived (PDF) from the original on 13 January 2015. Retrieved 20 February 2014. - Molteno AC, Polkinghorne PJ, Bowbyes JA (November 1986). "The vicryl tie technique for inserting a draining implant in the treatment of secondary glaucoma". Aust N Z J Ophthalmol. 14 (4): 343–54. doi:10.1111/j.1442-9071.1986.tb00470.x. PMID 3814422. - Lewis RA (August 2014). "Ab interno approach to the subconjunctival space using a collagen glaucoma stent". J Cataract Refract Surg. 40 (8): 1301–6. doi:10.1016/j.jcrs.2014.01.032. PMID 24943904. - "Xen Gel Stent". AqueSys. AqueSys. Archived from the original on 29 June 2015. Retrieved 27 June 2015. - "Advances in Glaucoma Filtration Surgery". Glaucoma Today. Archived from the original on 29 June 2015. Retrieved 27 June 2015. - Rosentreter, Andre; Andre M. Schild; Sven Dinslage; Thomas S. Dietlein (January 2011). "Biodegradable implant for tissue repair after glaucoma drainage device surgery". J Glaucoma. 21 (2): 76–8. doi:10.1097/IJG.0b013e3182027ab0. PMID 21278584. - Rosentreter, Andre; Anne C. Mellein; Walter W. Konen; Thomas S. Dietlein (September 2010). "Capsule excision and ologenTM implantation for revision after glaucoma drainage device surgery". Graefes Arch Clin Exp Ophthalmol. 248 (9): 1319–24. doi:10.1007/s00417-010-1385-y. PMID 20405139. - Rosentreter, A; Mellein AC; Konen WW; Dietlein TS (2010). "Capsule excision and ologenTM implantation for revision after glaucoma drainage device surgery". Graefes Arch Clin Exp Ophthalmol. 248 (9): 1319–24. doi:10.1007/s00417-010-1385-y. PMID 20405139. - Pardianto G, et al. (2006). "Some difficulties on Glaucoma". Mimbar Ilmiah Oftalmologi Indonesia. 3: 49–50. - Chiselita, D (2001). "Non-penetrating deep sclerectomy versus trabeculectomy in primary open-angle glaucoma surgery". Eye. 15 (Pt 2): 197–201. doi:10.1038/eye.2001.60. PMID 11339590. - Iqbal "Ike" K. Ahmed (1 September 2005). "Making the Case for Nonpenetrating Surgery". Review of Ophthamology. 12 (9). Archived from the original on 11 October 2007. - Aptel, F; Dumas S; Denis P (2009). "Ultrasound biomicroscopy and optical coherence tomography imaging of filtering blebs after deep sclerectomy with new collagen implant". Eur J Ophthalmol. 19 (2): 223–30. doi:10.1177/112067210901900208. PMID 19253238. - Matthew, SJ; Sarkisian S; Nathan B; James MR (2012). "Initial experience using a collagen matrix implant (ologen) as a wound modulator with canaloplasty: 12 month results". Ft. Lauderdale: ARVO Congress. - Anisimova SY, Anisimova SI, Larionov EV (2012). "Biological drainage – Xenoplast in glaucoma surgery (experimental and 10-year of clinical follow-up)" (PDF). Copenhagen: EGS Congress. Archived (PDF) from the original on 17 October 2013. - Heijl, Anders; Bengtsson, Boel; Hyman, Leslie; Leske, M. Cristina (December 2009). "Natural History of Open-Angle Glaucoma". Ophthalmology (Submitted manuscript). 116 (12): 2271–76. doi:10.1016/j.ophtha.2009.06.042. PMID 19854514. - "Glaucoma". Coopereyecare.com. 25 July 2013. Archived from the original on 13 December 2013. Retrieved 20 February 2014. - "Death and DALY estimates for 2004 by cause for WHO Member States" (xls). World Health Organization. 2004. Archived from the original on 27 January 2012. - Quigley, H A; Broman, AT (March 2006). "The number of people with glaucoma worldwide in 2010 and 2020". British Journal of Ophthalmology. 90 (3): 262–67. doi:10.1136/bjo.2005.081224. PMC 1856963. PMID 16488940. - Sommer, Alfred; Tielsch, James M.; Katz, Joanne; Quigley, Harry A.; Gottsch, John D.; Javitt, Jonathan C.; Martone, James F.; Royall, Richard M.; Witt, Kathe A.; Ezrine, Sandi (14 November 1991). "Racial Differences in the Cause-Specific Prevalence of Blindness in East Baltimore". New England Journal of Medicine. 325 (20): 1412–17. doi:10.1056/NEJM199111143252004. PMID 1922252. - "Glaucoma and Marijuana use". National Eye Institute. 21 June 2005. Archived from the original on 27 December 2009. - Ramulu, Pradeep (March 2009). "Glaucoma and disability: which tasks are affected, and at what stage of disease?". Current Opinion in Ophthalmology. 20 (2): 92–98. doi:10.1097/ICU.0b013e32832401a9. PMC 2692230. PMID 19240541. - Akbari, M.; Akbari, S.; Pasquale, L. R. (February 2009). "The Association of Primary Open-angle Glaucoma With Mortality: A Meta-analysis of Observational Studies". Archives of Ophthalmology. 127 (2): 204–10. doi:10.1001/archophthalmol.2008.571. PMID 19204241. - Richard Bannister: Treatise of One Hundred and Thirteen Diseases of the Eyes and Eyelids. London 1622 - Leffler CT, et al. (2017). "Ophthalmology in North America: Early Stories (1491-1801)". Ophthalmology and Eye Diseases. 9: 1–51. doi:10.1177/1179172117721902. PMC 5533269. PMID 28804247. - Daniel Albert and Diane Edwards: The History of Ophthalmologist. Cambridge, Mass. 1996 - Harper, Douglas. "glaucoma". Online Etymology Dictionary. - γλαυκός in Liddell and Scott. - Leffler CT, Schwartz SG, Hadi TM, Salman A, Vasuki V (2015). "The early history of glaucoma: the glaucous eye (800 BC to 1050 AD)". Clinical Ophthalmology. 9: 207–15. doi:10.2147/OPTH.S77471. PMC 4321651. PMID 25673972. Archived from the original on 26 February 2015. - Sean K Wang, Robert T Chang (2014). "An emerging treatment option for glaucoma: Rho kinase inhibitors". Clin Ophthalmol. 8: 883–89. doi:10.2147/OPTH.S41000. PMC 4025933. PMID 24872673. - Sena DF, Lindsley K (2017). "Neuroprotection for treatment of glaucoma in adults". Cochrane Database Syst Rev. 1: CD006539. doi:10.1002/14651858.CD006539.pub4. PMC 5370094. PMID 28122126. - Joy, J. E.; Watson Jr., S. J.; Benson Jr., J. A. (1999). Marijuana and Medicine: Assessing the Science Base. Nap.edu. doi:10.17226/6376. ISBN 978-0-309-07155-0. PMID 25101425. Archived from the original on 25 February 2014. Retrieved 20 February 2014. - Joy, J. E.; Watson Jr., S. J.; Benson Jr., J. A. (1999). Marijuana and Medicine: Assessing the Science Base (1999), Institute of Medicine, National Academies Press. Nap.edu. doi:10.17226/6376. ISBN 978-0-309-07155-0. PMID 25101425. Archived from the original on 20 January 2012. Retrieved 22 June 2011. - "Complementary Therapy Assessment: Marijuana in the Treatment of Glaucoma". American Academy of Ophthalmology. Retrieved 4 May 2011. - "Complementary Therapy Assessments : American Academy of Ophthalmology". One.aao.org. Retrieved 24 January 2011. - Jampel H (February 2010). "American glaucoma society position statement: marijuana and the treatment of glaucoma". J. Glaucoma. 19 (2): 75–6. doi:10.1097/IJG.0b013e3181d12e39. PMID 20160576.	2	66	13	0	3	7	0.681849	23	16,483
- surgically when the life of the patient is threatened or healing the affected body part is not expected - as a consequence of an accident ( traumatic ) - as punishment, which used to be common in many regions and is still taking place today in some Islamic countries such as Iran , Saudi Arabia or Sudan with reference to Sharia law - seldom already in the womb ( congenital ) by means of tying rings ( amniotic band syndrome ). Amputation as a surgical procedure In addition to injuries and infections, acute or chronic arterial circulatory disorders are the most common causes of amputation. The predominant cause of chronic arterial circulatory disorders is generalized arteriosclerosis . According to the distribution pattern of the vascular occlusions, the lower extremity is most often at risk of amputation. The following definitions therefore relate to the lower extremity, but also apply mutatis mutandis to the upper extremity. Major amputation means an amputation above the ankle region. In the DRG accounting system of the health insurance companies, the major amputation begins with the transmetatarsal forefoot amputation due to the higher material consumption. Minor amputation means a “small amputation” below the ankle region (i.e. up to and including the Chopart amputation). In the DRG system, it only includes toe amputations or beam resections. Depending on the indication , a distinction is made between scheduled amputation and emergency amputation. Indications for amputation Most scheduled limb amputations must be performed as a result of arterial occlusive disease (PAD) . The indication is usually made in stage IV if there is extensive tissue necrosis or infected gangrene with impending sepsis and vascular surgical measures have been exhausted or cannot be considered. As an exception, the indication is also made in stage III , if the persistent pain present here is not manageable and restricts the patient's quality of life so severely that the amputation is the “lesser evil”. The amputation level depends on the quality of the blood circulation, which is determined by angiography , and on the most sensible option for prosthetic treatment. On the leg, the thigh amputation is usually about a hand's width above the knee (in the case of PAD of the pelvic type) or the lower leg amputation about a hand's width below the knee (in the case of AOD of the thigh type). The amputation of arms due to arterial disease is a rarity. The second most common indication is diabetic gangrene . In contrast to the AVK, the so-called "border zone amputation" is usually aimed for, that is, the amputation as distal as possible , in the area that is barely healthy. Therefore, these are often amputations of toes, the forefoot (amputation or disarticulation in Chopart - or Lisfranc -hinge) or the hindfoot ( Pirogov butt ). This approach, previously frowned upon as “salami tactics”, has become widely accepted since the 1990s due to improvements in wound management , systemic antibiotic therapy and the cessation of diabetes. Nevertheless, many lower or upper leg amputations still have to be carried out as a “last resort”. Amputations as a result of accidental injuries are rare compared to the first two indications. The aim is always to preserve the limbs, with good conditions even larger traumatically severed limbs can be replanted more and more frequently . If the severed section is destroyed, however, often only the stump restoration can be performed. Unmanageable wound infections after injuries, an extensive compartment syndrome and open grade IV fractures , in which the nerves or blood vessels are irretrievably destroyed, force amputation. The amputation level is chosen here - without following a scheme - as far distal as possible. Modern prosthetics allow almost any residual limb to be restored. Very rarely do malignant tumors force amputation of a limb. These are usually bone or soft tissue tumors ( sarcomas ). The primary aim here is local resection of the tumor and restoration of bone continuity using special endoprostheses . In addition, serious complications can ultimately lead to an amputation, such as infected endoprostheses of the knee, infected pseudarthroses , large traumatic bone defects for which surgical attempts at treatment are unsuccessful. Occasionally, patients with severe malformations of an extremity and difficult orthotic fitting opt for an amputation. No statistics are available for Germany on the number of amputations . According to estimates by the AOK Scientific Institute , more than 55,000 surgical amputations of the lower extremities were performed in more than 41,000 hospital cases in 2002 . According to other information, there are currently around 60,000 amputations per year in Germany. In a European comparison that is a high number. 70 percent of amputations in Germany affect diabetics . You would have a 10 to 15 times higher risk of amputation. Performing an amputation The result of the rehabilitation after amputation depends largely on the possibility of prosthesis fitting. Therefore, a scheduled amputation must be carried out in such a way that a residual limb that is as good as possible is created. The soft tissue coverage of the bony stump is decisive here. The skin incision is therefore made in such a way that it is sufficiently but not too far below the intended bony amputation height ("frog's mouth cut") to ensure that the end of the bone is safely covered as a muscular skin flap including the underlying muscles. After cutting through the bone (s ) ( osteotomy ), the bone edges must be smoothed and possibly beveled. This is particularly necessary with the lower leg amputation at the front of the shin, where a bone wedge is usually removed ( triangle de Farabœuf ). The musculature is then cut in such a way that it surrounds the bony stump as a “cushion”. For secure fixation, the muscles are connected to each other ( myoplasty ) or connected directly to the bone stump via drill holes ( myodesis ). The skin scar should be placed away from the stress zone of the stump. The main nerves are exposed far in the proximal direction and cut there so that the nerve end lies deep in the soft tissue outside the stress zone. This is to prevent adhesion with the skin scar, neuroma formation and phantom pain . In the first phase of follow-up treatment, it is important to achieve good wound healing. Wound healing disorders or infections are not uncommon, especially with the two most common reasons for amputations, arterial occlusive disease and diabetes. In order to shape the stump, which should be as cylindrical as possible for a good prosthesis fitting, a special bandage is regularly applied from the day of the operation. After the wound has healed and the initial swelling has subsided, the residual limb is usually provided with a liner , an elastic cover that further shapes the residual limb and over which the prosthetic socket is later placed. After an amputation, there are other options for reconstruction or techniques that increase the functionality of the residual limb, especially with arm amputations: - Kineplasty after Sauerbruch: A muscle belly above the stump forms a skin channel through which a pin can be passed, which is connected to the prosthesis and thus active movements e.g. B. allows the prosthetic hand. This was often used after the First World War , mostly on the biceps brachii muscle in forearm amputees. - Krukenberg grasping forceps : In amputations of the forearm, the radius and ulna can be separated so that a grasping function between the two bones is possible. This is similarly possible with metacarpal amputations. - Angular osteotomy on the humerus according to Ernst Marquardt : Occasionally, if the upper arm is amputated above the condyles, the prosthesis cannot be rotationally stable . An osteotomy of the humerus shaft with angling of the distal segment forward can then enable a rotation-safe restoration. - Lengthening of extremely short stumps by means of callus distraction with a sufficient skin flap, also especially on the arms. In some cases, specific surgical techniques have developed: - Pirogoff amputation as amputation of the foot with partial preservation of the heel bone and the sole of the foot underneath and arthrodesis between the heel bone and shin bone after removal of the talus. - Gritti-Stokes amputation refers to a thigh amputation that is carried out very close to the knee joint, just above the knee condyles ( supracondylar ), whereby the kneecap is preserved, brought under the stump that has a tip of about 15 ° and is fixed with transosseous sutures. The kneecap tendon is sutured to the knee flexor tendons; no muscle transection is necessary. A slightly longer front flap means that the seam is usually located at the back. The advantage is a very long residual limb that can quickly endure the load, with a good lever arm and largely unrestricted strength of the adductors and hip extensors. In addition to trauma patients, the technology can also be used for circulatory disorders. Thanks to the preserved upper knee arteries for supplying the anterior lobe, wound healing disorders are rarely observed. Compared to a standard thigh amputation with a prosthesis, patients walk faster with better balance and fewer additional walking aids. - Ertl modification for lower leg amputations with the creation of a solid bone bridge between the tibia and fibula at the end of the residual limb, especially for traumatic amputations. First described by Janos Ertl in 1949, it should create a more stable and better resilient lower leg stump. However, studies have not shown any benefit to this technique. For special indications, especially in the case of malignant bone or soft tissue tumors , partial amputations are occasionally carried out in which only a section of the extremity is removed and e.g. B. the foot is then reconnected to the remaining stump, sometimes by rotating the foot by 180 °, as is done for example in the reverse sculpture according to Borggreve. In addition, residual limb revisions are often necessary, for example for scar correction, joint mobilization, removal of protruding bone portions or axis corrections. First aid and medical care in the case of accidental amputations In the event of an emergency of a traumatic complete (total) or partial (subtotal) amputation, vessels are injured, which can result in life-threatening bleeding . Stopping this bleeding is the primary goal of caring for the injured person. If the injured person is trapped, acutely threatened and cannot be cleared within a reasonable time, an emergency amputation is carried out in the most extreme case (see below). Depending on the situation of the injured are measures to stabilize the vital signs taken at unconsciousness the recovery position prepared in respiratory arrest the ventilation machine or in a cardiovascular arrest resuscitation performed. In addition, any shock that may occur is treated accordingly and appropriate pain therapy is carried out. To secure the severed body part, the amputate, the first aider temporarily stores it in sterile materials such as bandages . In order to facilitate a possible accident-surgical reconstruction of the injury, in addition to sterile and dry storage, transport as cool as possible is necessary. The wrapped amputate is put into a clean plastic bag which, after being closed, is fixed in a second bag filled with cold water or ice. It is important to ensure that the amputate does not come into contact with ice in order to avoid frostbite and the associated tissue damage. The amputate should not be cleaned by the first aider, as improper handling may make reconstruction impossible. After the amputate is handed over, it is cleaned in the hospital. If an extremity is not completely severed, existing tissue connections should not be severed, as they can ensure a minimal blood supply. In desperate accident situations, it may be necessary for the emergency doctor to perform an amputation at the scene of the accident. This primarily concerns burial accidents (quarries, mining, earthquakes, gas explosions) when an extremity is trapped and the injured person, who is in mortal danger, cannot otherwise be saved. In the case of traffic accidents, this procedure is only required in extremely rare exceptional cases due to the extensive possibilities of technical rescue , for example in accidents with large or rail vehicles in which the hydraulic rescue devices designed for car accidents reach their limits. If help is not available in desperate, life-threatening accident situations, a self-amputation can save your life. The American mountaineer Aron Ralston achieved international fame, who freed himself from a canyon by self-amputating his trapped hand in 2003. Amputation as a punishment In many cultures and epochs, amputations were carried out as a more severe form of corporal punishment . The oldest known source for this is the Codex Hammurapi from Babylonia from the 18th century BC, in which amputation was described as a punishment for violence by slaves against free citizens. Punitive amputations are also documented in Peru in the fourth century BC. Amputations were also used as punitive measures during the Roman Empire and the subsequent Byzantine Empire . This continued in Europe until the 17th century, when more humane punishment became common during the Enlightenment and corporal punishment was pushed back overall. In numerous Arab and African countries, punitive amputations continue to the present day. In Islamic law In Islamic jurisprudence, there are individual criminal offenses that are punished with amputation within the framework of the Hadd penalties . For example, according to the Koran ( Sura 5 : 38), male and female thieves should have their hands cut off “as compensation for what they have committed and as a warning to God”. The cross-cutting of hand and foot is mentioned in the Qur'an (Sura 5:33) as a possible punishment for fighting God and his Messenger as well as for robbery. In Islamic jurisprudence , however, the execution of such sentences was linked to strict requirements. For example, a theft ( sariqa ), which is supposed to result in such a punishment, must have happened secretly, the stolen property must have a certain minimum value ( niṣāb ), the thief must not have any property in it and he must have it from custody ( ḥirz ) have taken away. In addition, the amputation may only be carried out by state authorities. In reality, punitive amputations of this kind were very rare in most Islamic countries even in the early modern period. Occasionally, however, cross amputations were used as a punishment for spies, for example in the late 19th century in the Sudanese Mahdi Empire (see illustration). Between the late 19th century and the early 20th century, hadd sentences were abolished in almost all Islamic countries. Saudi Arabia is the only Islamic country where the amputation penalty has never been interrupted to this day. However, judicial amputations are relatively rare here. Between 1981 and 1992 there was a total of 45 cases. In the course of the re-Islamization after 1972, the Islamic criminal law was codified in various states and in this context amputation was reintroduced as a punishment for theft. Examples are Libya , Pakistan , Iran , Sudan and northern Nigeria . In Sudan, there was a worrying expansion of the amputation offense . For example, Article 320 of the Sudanese Penal Code of 1983 dropped secrecy and removal from custody as conditions for theft. Here, too, the enforcement of the amputation penalty was pursued with great energy. Between September 1983 and the fall of the Numeiri regime in April 1985 alone, 96 to 120 amputations were performed. Although the government suspended the amputations afterwards, amputation sentences were again carried out after the coup in 1989 and executioners were sent to Saudi Arabia for training. In January 2001 five men were cross amputated for street robbery. With the Japanese mafia History of amputation surgery Surgical interventions were carried out as early as the Paleolithic , which patients survived. This art was not limited to Homo sapiens : A skeletal find of a male Neanderthal man in a cave in northern Iraq about 45,000 years ago shows a clean severing of a forearm. Later successful amputations e.g. B. from the French Buthiers-Boulancourt of the Neolithic Age (around 4900 BC) prove the successful severing of the left forearm of an older man. There is further evidence of Neolithic amputations from Germany and the Czech Republic. Amputations were also carried out in Egypt 3000 years ago . However, researchers have already discovered representations of amputations of fingers on cave paintings . These images date from the Mesolithic (8000–6000 BC). It is not known whether the amputations took place for medical or ritual reasons. Early written descriptions of amputations in antiquity are e.g. B. by Hippocrates of Kos , Aulus Cornelius Celsus , Archigenes of Apamei (48-117) and Galen . Also Oribasius , Aëtius of Amida and Paul of Aegina mentioned surgical amputations. The high and late Middle Ages saw amputations through the works of Roger von Parma , Hugo and Theoderich von Borgognoni , Wilhelm von Saliceto and Guy de Chauliac . The surgeon Hans von Gersdorff first described the tourniquet ligation system and cauterization to control bleeding in his field book der Wundarzney published in 1517, while the French surgeon Ambroise Paré reintroduced arterial ligatures in amputation surgery in the middle of the 16th century , as had been done by Hippocrates of Kos had been described. Paré was also the first to describe phantom pain . With his proposals, which were noticed throughout Europe, to manage without amputation even with severe limb injuries, the military surgeon Johann Ulrich Bilger (1720–1796) became a pioneer in conservative surgery in the 18th century . The first successful metatarsal amputation at the level of the tarsometatarsal joints was carried out in 1815 by the French surgeon Jacques Lisfranc , after whom this amputation level and the joint line continue to be designated. The first disarticulation of the ankle was carried out by the Scottish surgeon James Syme in 1842, while the Russian surgeon Nikolai Iwanowitsch Pirogow received the heel bone during the Pirogoff amputation and fused it with the shin by resecting the ankle . However, both received the heel skin capable of endurance. The later development goes back to the attempt of the Italian surgeon Giuliano Vanghetti to attach muscles directly to the prosthesis, particularly by Ferdinand Sauerbruch , who formed muscle channels to control kineplastic prostheses. It was only after the Second World War that myoplasty was introduced by R. Dederich and popularized by E. Burgess. The muscle flaps are sewn together over the bone stump in order to create a stump tip that can withstand stress. Later, M. Weiss also recommended myodesis , in which the muscles are anchored directly in the bone. Thanks to myoplasty and the long posterior muscle flap, transtibial amputation developed into a safe and successful procedure in the 1960s, especially in the technique developed by E. Burgess, so that it replaced the transfemoral amputation, which was standard until the 1970s, as the new standard for vascular diseases corresponding benefit for the patient by maintaining an active knee joint. One speaks of congenital amputation when protein ligaments are formed during pregnancy by tearing the amnion , which constrict the fetal limbs so that whole limbs are missing at birth that were originally created. It is the extreme form of amniotic ligament syndrome . Congenital lack of an extremity or part of it is also known as dysmelia . - Ablation (medicine) , partly synonymous with amputation - Amelotatism is a sexual preference for people with missing limbs . It is also called deformation fetishism - Thomas Böni: Amputation. In: Werner E. Gerabek u. a. (Ed.): Encyclopedia of medical history. De Gruyter, Berlin / New York 2005, ISBN 3-11-015714-4 , p. 52. - Scott C. Lucas: Abu Bakr ibn al-Mundhir, Amputation, and the Art of Ijtihād. In: International Journal of Middle East Studies. (2007); 39 (3), pp. 351-368. - S2k guideline : Rehabilitation after major amputation of the lower extremity , of the German Society for Orthopedics and Orthopedic Surgery (DGOOC) , AWMF register number 033/044; awmf.org (PDF), as of 08/2008. - Ackerknecht, 1967 . - Wolf-Rüdiger Teegen, Rimantas Jankauskas, Peter Stegemann-Auhage, Michael Schultz: Considerations on the differential diagnosis of amputation in paleopathology. In: Würzburg medical history reports. Volume 14, 1996, pp. 359-368, here: pp. 359 f. - The extremity threatened with amputation . ( Memento of the original from September 19, 2017 in the Internet Archive ; PDF) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. - Guidelines of the German Society for Vascular Surgery, AWMF Online 2008. - G. Heller, C. Günster, E. Swart: About the frequency of amputations of lower extremities in Germany. In: DMW - German Medical Weekly , 2005 Jul 15, 130 (28-29), pp. 1689-1690. PMID 16003603 - German Society for Angiology - Society for Vascular Medicine e. V., September 24, 2008. - 4.5 million people have PAOD . In: Doctors newspaper , September 24, 2008. - R. Baumgartner, P. Botta: Amputation and prosthesis supply of the upper extremity . Enke-Verlag Stuttgart 1997, ISBN 3-432-27281-2 . - Benjamin C. Taylor, Attila Poka, Bruce G. French, T. Ty Fowler, Sanjay Mehta: Gritti-Stokes amputations in the trauma patient - clinical comparisons as and subjective outcomes. In: Journal of Bone and Joint Surgery (Am). April 4, 2012, Volume 94 (Am), pp. 602-608. - CJ Tucker, JM Wilken, PD Stinner, KL Kirk: A comparison of limb-socket kinematics of bone-bridging and non-bone-bridging wartime transtibial amputations . In: Journal of Bone and Joint Surgery , 2012, Volume 94-Am, Issue 10, pp. 924-930. - Kersten Enke (Ed.): LPN 3 . 2., revised. Edition. Stumpf and Kossendey, Edewecht 2000, ISBN 3-932750-42-X , p. 132 f. - 27 injured in a tram accident in Karlsruhe - driver amputated foot while on the train www.schwaebische.de - Anna Mavraforon, Konstantinos Malizos, Theofilos Karachalios, Konstantinos Chatzitheofilou, Athanasios D. Giannoukas: Punitive limb amputation . Clinical Orthopedics and Related Research 2014, Volume 472, Pages 3102-3106 - G. Bergsträsser: Fundamentals of Islamic law . Edited and edited by J. Schacht. Berlin / Leipzig 1935, p. 100f. - Rudolph Peters: Crime and Punishment in Islamic Law. Theory and Practice from the Sixteenth to the Twenty-first Century . Cambridge University Press, Cambridge 2005, p. 31. - Peters, p. 92 f. - Peters, p. 150. - Bruce Pannier: Iran: Criminals Lose Hands And Feet As Shari'a Law Imposed . Radio Free Europe , January 7, 2008. - Sam Olukoya: Eyewitness: Nigeria's Sharia amputees . BBC News, December 19, 2002. David Bamford: Hand amputation in Nigeria . BBC News, July 7, 2001. - Peters, p. 166. - Peters, p. 167. - Peters, p. 168. - Peters, p. 169. - Manfred Reitz: Stone Age Surgery. In: Pharm.Ind. (2011); 73, No. 10, pp. 1755-1757. - Evidence of Stone Age amputation forces rethink over history of surgery. In: The Times . January 25, 2010 (accessed June 29, 2011). - Volker Klimpel: Famous amputees. In: Würzburger medical historical reports , 23, 2004, pp. 313–327; here: p. 313. - Bella J. May: Amputations and prosthetics. A case study approach. 2nd Edition. FA Davis Company, Philadelphia 2002, ISBN 0-8036-0839-X .	2	22	1	0	0	0	0.568114	1	5,346
- Obstetric fistula Obstetric fistula Classification and external resources ICD-10 N82 ICD-9 619 MeSH D014624 Obstetric fistula (or vaginal fistula) is a severe medical condition in which a fistula (hole) develops between either the rectum and vagina (see rectovaginal fistula) or between the bladder and vagina (see vesicovaginal fistula) after severe or failed childbirth, when adequate medical care is not available. Symptoms and signs The resulting disorders typically include incontinence, severe infections and ulcerations of the vaginal tract, and often paralysis caused by nerve damage. Sufferers from this disorder are usually also subject to severe social stigma due to odor, perceptions of uncleanliness, a mistaken assumption of venereal disease and, in some cases, the inability to have children. The fistula usually develops when a prolonged labor presses the unborn child so tightly in the birth canal that blood flow is cut off to the surrounding tissues, which necrotise and eventually rot away. More rarely, the injury can be caused by female genital cutting, poorly performed abortions, or pelvic fractures. Other potential direct causes for the development of obstetric fistula are sexual abuse and rape, especially within conflict/post-conflict areas, other surgical trauma, gynecological cancers or other related radiotherapy treatment and, perhaps the most important, limited or no access to obstetrical care or emergency services. Distal causes that can lead to the development of obstetric fistula concern issues of poverty, lack of education, early marriage and childbirth, the role and status of women in developing countries, and harmful traditional practices and sexual violence. Poverty, early marriage, and lack of education place women in positions of severe disadvantage and do not enable them to be advocates for their own health and wellbeing. Access to obstetric emergency care is one of the major challenges in preventing the development of obstetric fistula. The availability and access to medical facilities that have a trained staff and specialized surgical equipment needed for cesarean births is very limited in certain parts of the world. Factors that may heavily influence an individual's ability or decision to access this emergency care can involve everything from general fear and mistrust of hospitals and healthcare workers, a lack of equipped facilities and trained staff, economic constraints, religious beliefs and practices, cultural norms, and previous birth experiences. In terms of cultural factors surrounding the birthing process, opinions and practices vary all over the world. In many developing countries, giving birth at home with the assistance of an elder woman or traditional birth attendant is considered the preferred and respected way to give birth. Some consider this point to be controversial and see it more as an economic access issue instead of a cultural issue. Seeking out the option of surgery versus a vaginal birth, in certain places, is also thought to be less womanly and unnatural. This negative perception of surgery can greatly influence a woman's decision to not seek out emergency obstetrical treatment. Other factors surrounding a woman's ability and choice to access obstetrical care can be rooted in the nature of her relationship with her male partner or male decision makers within her family. This can affect the kind of care and assistance women receive during child labor. In many instances, receiving treatment from a male physician is not pursued or considered a real option due to the religious or cultural violations connected with a male treating a woman who is not his wife or intimate partner. This is an opinion held by both men and women in various parts of the world. Yet another causal factor is that of logistical access to health care clinics. Many women who suffer from this condition are living in very rural areas and, therefore, access to emergency services often requires some form of travel. The availability of transportation, cost of transportation and road construction can all play a crucial role in the ability of pregnant women to access emergency obstetrical services. The availability and access to medical facilities that have a trained staff and specialized surgical equipment needed for cesarean births is also very limited in certain parts of the world. In many instances, women do not consider their local hospitals and clinics to be places where they could ever seek such care and therefore do not go when there is an obstetrical emergency. Primary risk factors are early or closely spaced pregnancies and lack of access to emergency obstetric care; a 1993 study in Nigeria found that 55 percent of the victims were under 19 years of age, and 94 percent gave birth at home or in poorly equipped local clinics. When available at all, cesarean sections and other medical interventions are usually not performed until after tissue damage has already been done. Early marriage, domestic violence, female genital mutilation, malnutrition which is linked to under-development of the female body, and lack of education/illiteracy also put women at great risk for developing obstetric fistula. Lack of personal knowledge about and experience with childbirth may also put a woman at risk to developing obstetric fistula, especially for women who have previously experienced limited complications with past vaginal births. Women giving birth for the first time and with no real knowledge regarding childbirth may not recognize an emergency situation/complication and therefore not seek out help. Countries that suffer from poverty, civil and political unrest or conflict, and other dangerous public health issues such as malaria, HIV/AIDS, and tuberculosis often suffer from a severe burden and breakdown within the healthcare system. This breakdown puts many people at risk, specifically women. Many hospitals within these conditions suffer from shortages of staff, supplies, and other forms of necessary medical technology that would be necessary to perform reconstructive obstetric fistula repair. Prevention comes in the form of access to obstetrical care, support from trained health care professionals throughout pregnancy, providing access to family planning, promoting the practice of spacing between births, and supporting women in education and postponing early marriage. Fistula prevention also involves many strategies to educate local communities about the cultural, social, and physiological factors that condition and contribute to the risk for fistula. One of these strategies involve organizing community-level awareness campaigns to educate women about prevention methods such as proper hygiene and care during pregnancy and labour. Prevention of prolonged obstructed labour and fistula should preferably begin as early as possible in each female’s life. For example, improved nutrition and outreach programs to raise awareness about the nutritional needs of female children to prevent malnutrition as well as improve the physical maturity of young mothers, are important fistula prevention strategies. It is also important to ensure access to timely and safe delivery during childbirth; measures include availability and provision of emergency obstetric care as well as quick and safe caesarean sections for women in obstructed labour. Midwives located in the local communities where fistula is prevalent can also contribute to promoting health practices that help prevent future development of obstetric fistulas. Promoting education for girls is also a key factor to preventing fistula in the long term. There are currently several organizations that have developed effective fistula prevention strategies. One of them is the Tanzanian Midwives Association, which works to prevent fistula by improving clinical health care for women and delaying early marriages and childbearing years, as well as help the local communities advocate the rights of females. Treatment is available through reconstructive surgery. This surgery for uncomplicated cases has a 90% success rate, and success rates for more complicated cases are estimated to be 60% successful. The cost for this procedure, which includes the actual surgery, post-operative care and rehabilitation support, is estimated to be US$300 – $450. Successful surgery enables women to live normal lives and have more children, but it is recommended to have a cesarean section to prevent the fistula from recurring. Post operative care is vitally important to prevent infection. Some women are not candidates for this surgery, but can seek out alternative treatment called a urostomy and a bag for the collection of urine is worn on a daily basis. Challenges with regards to treatment include the very high number of women needing reconstructive surgery, access to facilities and trained surgeons, and the cost of treatment. For many women, even $300 US dollars is simply an impossible price and they cannot afford the surgery. The largest challenge that stands between women and fistula treatment is information. Most women have no idea that treatment is available. Because this is a condition of shame and embarrassment, most women hide themselves and their condition and suffer in silence with no relief. The largest benefit of surgical treatment is that many women can re-join their families, communities, and societies without shame from their condition because the leaking and smell are no longer present. Fistula cases can also be treated through urethral catheterisation if identified early enough. The Foley catheter is recommended because it has a balloon to hold it in place. The indwelling Foley catheter drains urine from the bladder. This decompresses the bladder wall so that the wounded edges come together and stay together giving it a greater chance of closing naturally, at least in the smaller fistulas. According to data collected by Dr Kees Waaldijk, Director of the Nigeria National Fistula Programme, out of a case series of 4424 patients with obstetric fistula who were treated within 75 days post partum, 37% (1579 patients) are cured completely with the use of a Foley catheter without the need of surgery. Even without pre-selecting the least complicated obstetric fistula cases, the systematic use of a Foley catheter by midwives after the onset of urinary incontinence could cure over 25% of all new fistula cases each year without the need for surgery. If left untreated, ulcerations and infections can persist as well as kidney disease and kidney failure leading to death. Urinal and fecal leaking are the major physical side effects and because many women suffering from obstetric fistula do not want to leak, they will limit their intake of water and other liquids. This can lead to a very dangerous case of dehydration. Nerve damage to the legs is also noted as a medical side effect. In some cases, many women struggle to walk from this nerve damage and need physical therapy following the treatment of the fistula. Most women living with obstetric fistula also struggle with depression, abandonment by their partners, families and communities, and live in isolation because of the constant leaking and odor. Many women report feelings of humiliation, pain, loneliness, shame and mourning for the loss of their lives and the child they lost during delivery. Because of the constant leaking and smell, many women are isolated from food preparation and prayer ceremonies because they are thought to be constantly unclean. Suicide and attempted suicide are also common amongst women with this condition. Social isolation, increased poverty and decreased employment opportunities due to this condition force many women to turn to commercial sex work and begging. According to the World Health Organization (WHO), an estimated 50,000 to 100,000 women develop obstetric fistulas each year and over two million women currently live with obstetric fistula. The WHO claims that fistula was largely eradicated in developed countries in the late 19th century; it still affects two to three million women in developing countries. Obstetric fistula was very common throughout the entire world but virtually disappeared within Europe and North America due to improvements in obstetrical care. The surgery to cure it was developed by J. Marion Sims. To this day, the prevalence of obstetrical fistula is much lower in places that discourage early marriage, encourage and provide education of women, and grant women access to family planning and skilled medical teams to assist during childbirth. This condition is still very prevalent in the developing world, especially in parts of Africa and much of South Asia (Bangladesh, Afghanistan, Pakistan, and Nepal). Society and culture During most of the 20th century obstetric fistula was largely missing from the international global health agenda. This is reflected by the fact that obstetric fistula was not included as a topic at the landmark United Nations 1994 International Conference on Population and Development (ICPD). The 194 page report from the ICPD does not include any reference to obstetric fistula. However, since 2003 obstetric fistula has been gaining awareness amongst the general public and has received critical attention from UNFPA, who have organized a global campaign to "End Fistula". New York Times columnist Nicholas Kristof, a Pulitzer-prize winning writer, wrote several columns in 2003, 2005 and 2006 focusing on fistula and particularly treatment provided by Catherine Hamlin at the Fistula Hospital in Ethiopia. Increased public awareness and corresponding political pressure have helped fund the UNFPA's Campaign to End Fistula, and helped motivate the United States Agency for International Development (USAID) to dramatically increase funding for the prevention and treatment of obstetric fistula. - Worldwide Fistula Fund - FootSteps to Healing - Campaign to End Fistula - The Fistula Care Project - Fistula Foundation - Maternal Health Task Force - Women and Health Alliance International - Hamlin Fistula Welfare and Research Ltd (The Fistula Trust) - International Organization For Women and Development, Inc. (IOWD) - Love Labor Loss: A Film-based Campaign on Obstetric Fistula - One By One - Matercare International - SafeHands for Mothers - Virgin Unite - End Fistula - The Worldwide Fistula Fund - "Carry me Home", documentary about women with VVF in northern Nigeria - Natalie Imbruglia and the Campaign to End Fistula: Interview in Indian press Female diseases of the pelvis and genitals (N70–N99, 614–629) InternalAdnexaVaginitis (Bacterial vaginosis, Atrophic vaginitis, Candidal vulvovaginitis) · Leukorrhea/Vaginal discharge · Hematocolpos/HydrocolposSexual dysfunction (Dyspareunia, Hypoactive sexual desire disorder, Sexual arousal disorder, Vaginismus)Other/generalPelvic inflammatory disease · Pelvic congestion syndrome External Wikimedia Foundation. 2010.	2	10	0	0	0	3	0.635973	3	2,899
- Median nerve palsy Median nerve palsy Classification and external resources Diagram from Gray's anatomy, depicting the peripheral nerves of the upper extremity, amongst others the median nerve. ICD-10 GroupMajor.minor ICD-9 xxx Injuries to the arm, forearm or wrist area can lead to various peripheral nerve disorders. One such disorder is median nerve palsy. If the median nerve is damaged, the ability to abduct and oppose the thumb may be lost due to paralysis of the thenar muscles. Various other symptoms can occur which may be repaired through surgery and tendon transfers. Tendon transfers have been very successful in restoring motor function and improving functional outcomes in patients with median nerve palsy. The median nerve receives fibers from roots C6, C7, C8, T1 and sometimes C5. It is formed in the axilla by a branch from the medial and lateral chords of the brachial plexus, which are on either side of the axillary artery and fuse together to create the nerve anterior to the artery. The median nerve is closely related to the brachial artery within the arm. The nerve enters the cubital fossa lateral to the brachialis tendon and passes between the two heads of the pronator teres. It then gives off the anterior interosseus branch in the pronator teres. The nerve continues down the forearm between the flexor digitorum profundus and the flexor digitorum superficialis. The median nerve emerges to lie between the flexor digitorum superficialis and the flexor carpi ulnaris muscles which are just above the wrist. At this position, the nerve gives off the palmar cutaneous branch that supplies the skin of the central portion of the palm. The nerve continues through the carpal tunnel into the hand, lying in the carpal tunnel anterior and lateral to the tendons of the flexor digitorum superficialis. Once in the hand, the nerve splits into a muscular branch and palmar digital branches. The muscular branch supplies the thenar eminence while the palmar digital branch supplies sensation to the palmar aspect of the lateral 3 ½ digits and the lateral two lumbricals. Signs and symptoms - Lack of ability to abduct and oppose the thumb due to paralysis of the thenar muscles. This is called "ape-hand deformity". - Sensory loss in the thumb, index finger, long finger, and the radial aspect of the ring finger - Weakness in forearm pronation and wrist and finger flexion - Activities of daily living such as brushing teeth, tying shoes, making phone calls, turning door knobs and writing, may become difficult with a median nerve injury. Median nerve palsy is often caused by deep, penetrating injuries to the arm, forearm, or wrist. It may also occur from blunt force trauma or neuropathy. Median nerve palsy can be separated into 2 subsections—high and low median nerve palsy. High MNP involves lesions at the elbow and forearm areas. Low median nerve palsy results from lesions at the wrist. Compression at the different levels of the median nerve produce variable symptoms and/or syndromes. The areas are: - Underneath Struthers' ligament - Passing by the bicipital aponeurosis (also known as lacertus fibrosus) - Between the two heads of the pronator teres - Compression in the carpal tunnel causes carpal tunnel syndrome Because lesions to different areas of the median nerve produce similar symptoms, clinicians perform a complete motor and sensory diagnosis along the nerve course. Decreased values of nerve conduction studies are used as indicators of nerve compression and may aid in determining the localization of compression. Palpation above the elbow joint may reveal a bony consistency. Radiography images may show an abnormal bony spur outgrowth (supracondyloid process) just proximal to the elbow joint. Attached fibrous tissue (Struthers' ligament) may compress the median nerve as it passes underneath the process. This is also known as supracondylar process syndrome. Compression at this point may also occur without the bony spur; in this case, aponeurotic tissue found at the location of where Struthers' ligament should be is responsible for the compression. If patients mention reproduction of symptoms to the forearm during elbow flexion of 120–130 degrees with the forearm in maximal supination, then the lesion may be localized to the area underneath the lacertus fibrosus (also known as bicipital aponeurosis). This is sometimes misdiagnosed as elbow strain and medial or lateral epicondylitis. A lesion to the upper arm area, just proximal to where motor branches of forearm flexors originate, is diagnosed if the patient is unable to make a fist. More specifically, the patient's index and middle finger cannot flex at the MCP joint, while the thumb usually is unable to oppose. This is known as hand of benediction or median claw hand. Another test is the bottle sign—the patient is unable to close all their fingers around a cylindrical object. Carpal tunnel syndrome (CTS) is caused by compression of the median nerve as it passes under the carpal tunnel. Nerve conduction velocity tests through the hand are used to diagnosis CTS. Physical diagnostic tests include the Phalen maneuver or Phalen test and Tinel's sign. To relieve symptoms, patients may describe a motion similar to "shaking a thermometer", another indication of CTS. Pronator teres syndrome (also known as pronator syndrome) is compression of the median nerve between the two heads of the pronator teres muscle. The Pronator teres test is an indication of the syndrome—the patient reports pain when attempting to pronate the forearm against resistance while extending the elbow simultaneously. The physician may notice an enlarged pronator teres muscle. Tinel's sign the area around the pronator teres heads should be positive.[clarification needed] The key to discerning this syndrome from carpal tunnel syndrome is the absence of pain while sleeping. More recent literature collectively diagnose median nerve palsy occurring from the elbow to the forearm as pronator teres syndrome. In uncooperative patients, the skin wrinkle test offers a pain-free way to identify denervation of the fingers. After submersion in water for 5 minutes, normal fingers will become wrinkled, whereas denervated fingers will not. In "Ape hand deformity", the thenar muscles become paralyzed due to impingement and are subsequently flattened. This hand deformity is not by itself an individual diagnosis; it is seen only after the thenar muscles have atrophied. While the adductor pollicis remains intact, the flattening of the muscles causes the thumb to become adducted and laterally rotated. The opponens pollicis causes the thumb to flex and rotate medially, leaving the thumb unable to oppose. Carpal tunnel syndrome can result in thenar muscle paralysis which can then lead to ape hand deformity if left untreated. Ape hand deformity can also be seen in the hand of benediction deformity. One way to prevent this injury from occurring is to be informed and educated about the risks involved in hurting your wrist and hand. If patients do suffer from median nerve palsy, occupational therapy or wearing a splint can help reduce the pain and further damage. Wearing a dynamic splint, which pulls the thumb into opposition, will help prevent an excess in deformity. This splint can also assist in function and help the fingers flex towards the thumb. Stretching and the use of C-splints can also assist in prevention of further damage and deformity. These two methods can help in the degree of movement the thumb can have. While it is impossible to prevent trauma to your arms and wrist, patients can reduce the amount of compression by maintaining proper form during repetitive activities. Furthermore, strengthening and increasing flexibility reduces the risk of nerve compression. Depending on the severity of the lesion, physicians may recommend either conservative treatment or surgery. The first step is simply to rest and modify daily activities that aggravate the symptoms. Patients may be prescribed anti-inflammatory drugs, physical therapy, splints for the elbow and wrists, and corticosteroid injections as well. This is the most common treatment for CTS. Especially involving compression at the wrist, such as in CTS, it is possible to recover without treatment. Physical therapy can help build muscle strength and braces or splints help recover. In pronator teres syndrome, specifically, immobilization of the elbow and mobility exercise within a pain-free range are initially prescribed. However, if the patient is not relieved of symptoms after a usual 2 to 3 month refractory period, then decompression surgery may be required. Surgery involves excising the tissue or removing parts of the bone compressing the nerve. Many tendon transfers have been shown to restore opposition to the thumb and provide thumb and finger flexion. In order to have optimal results the individual needs to follow the following principles of tendon transfer: normal tissue equilibrium, movable joints, and a scar-free bed. If these requirements are met then certain factors need to be considered such as matching up the lost muscle mass, fiber length, and cross-sectional area and then pick out muscle-tendon units of similar size, strength, and potential excursion. For patients with low median nerve palsy, it has been shown that the flexor digitorum superficialis of the long and ring fingers or the wrist extensors best approximate the force and motion that is required to restore full thumb opposition and strength. This type of transfer is the preferred method for median nerve palsy when both strength and motion are required. In situations when only thumb mobility is desired, the extensor indicis proprius is an ideal transfer. For high median nerve palsy, the brachioradialis or the extensor carpi radialis longus transfer is more appropriate to restore lost thumb flexion and side-to-side transfer of the flexor digitorum profundus of the index finger are generally sufficient. To restore independent flexion of the index finger could be performed by using the pronator teres or extensor carpi radialis ulnaris tendon muscle units. All of the mentioned transfers are generally quite successful because they combine a proper direction of action, pulley location, and tendon insertion. In high median nerve palsy patients, recovery time varies from as early as four months to 2.5 years. Initially, patients are immobilized in a neutral position of the forearm and elbow flexed at 90° in order to prevent further injury. Additionally, gentle exercises and soft tissue massage are applied. The next goal is strengthening and flexibility, usually involving wrist extension and flexion; however, it is important not to overuse the muscles in order to prevent re-injury. If surgery is required, post operative therapy initially involves decreasing pain and sensitivity to the incision area. Adequate grip and elbow strength must be achieved before returning to pre-operative activity. - The number of discharges related to median nerve injuries decreased from 3,402 in 1993 to 2,737 in 2006. - The mean hospital charges in nominal dollars increased from $9,257 to $27,962 between 1993 and 2006. - 37.1% of patients in 2006 presenting with median nerve injuries needed acute repair. - Median nerve injuries were the least likely to be admitted to the emergency room out of all peripheral nerve injuries (median nerve 68.89%, ulnar nerve 71.3% and radial nerve 77.06%). - The highest percentage of patients discharged with median nerve injuries in 2006 were between the ages of 18–44. - Out of all the patients in 2006 presenting with median nerve injuries, 77.76% were male and 21.75% were female. - Peripheral nerve injury - Peripheral neuropathy - ^ a b c http://www5.aaos.org/oko/description.cfm?topic=HAN027&referringPage=mainmenu.cfm - ^ http://www.acnr.co.uk/pdfs/volume2issue6/v2i6anatomy.pdf - ^ http://www.medicine.cu.edu.eg/elearning/mod/resource/view.php?id=1180 - ^ Lowe, W. (2004, October). Median nerve compression pathologies. Retrieved from http://www.massagetoday.com/mpacms/mt/article.php?id=12031 - ^ Pikula, J. (1994). Supracondyloid process of the humerus: a case report. Journal of the California Chiropractic Association, 38(4), 211-15. - ^ Suranyi, L. (1983). Median nerve compression by struthers ligament. Journal of Neurology, Neurosurgery, and Psychiatry, 46, 1047-49. - ^ a b Washington State Department of Labor and Industry, (2009). Work-related proximal median nerve entrapment (pmne) diagnosis and treatment Retrieved from http://www.lni.wa.gov/ClaimsIns/Files/OMD/MedTreat/ProximalMedianNerve.pdf - ^ Seitz Jr., W.H. (2007). Compression of the median nerve at the elbow by lacertus fibrosus. Journal of Shoulder and Elbow Surgery, 16(1), 91-4. - ^ Schuenke, M, Schulte, E, Schumacher, U, & Ross, L. (2005). Thieme atlas of anatomy: latin nomenclature : general anatomy and musculoskeletal system. Stuttgart, Germany: Thieme. - ^ “Carpal Tunnel Info”. Carpal Tunnel Info. Web 28 October 2010. < http://www.carpal-tunnel.org> - ^ Carpal tunnel syndrome - diagnosis. (2009). Unpublished manuscript, Medical Center, University of Maryland, Baltimore, Maryland. Retrieved from http://www.umm.edu/patiented/articles/how_carpal_tunnel_syndrome_diagnosed_000034_7.htm - ^ Wheeless, C. (1996). Pronator teres compression syndrome - median nerve compression. Manuscript submitted for publication, Department of Orthpaedics, Duke Univeristy, Durham, North Carolina. Retrieved from http://www.wheelessonline.com/ortho/pronator_teres_compression_syndrome - ^ Hartz, C, Linscheid, R, Gramse, R, & Daube, J. (1981). The pronator teres syndrome: compressive neuropathy of the median nerve. Journal of Bone and Joint Surgery, 63(6), 885-90. - ^ DeLisa, J.A., Gans, B.M., & Walsh, N. (2005). Physical medicine and rehabilitation: principles and practice, volume 1. Philadelphia, PA: Lippincott Williams & Wilkins. - ^ Case of the month: the skin wrinkle test: a simple nerve injury test for paediatric and uncooperative patients. (2006). Emergency Medicine Journal, 23(11), Retrieved from http://emj.bmj.com/content/23/11/883.abstract - ^ Gaballah, M.F. and Z.H. Badawy. “Upper Limb: Nerve Injuries – II.” Clinical Anatomy 101. Cairo University. Kasr Al Ainy, 4 October 2009. Web. 3 October 2010. <http://www.medicine.cu.edu.eg/elearning/mod/resource/view.php?id=1180> - ^ “Carpal Tunnel Info”. Carpal Tunnel Info. Web 28 October 2010. < http://www.carpal-tunnel.org> - ^ Dugdale, D, & Hoch, D. (2010). Distal median nerve dysfunction. Medline plus. Retrieved December 7, 2010, from http://www.nlm.nih.gov/medlineplus/ency/article/000691.htm - ^ Pho, C. (n.d.). Elbow and forearm radiating pain. Retrieved from http://xnet.kp.org/socal_rehabspecialists/ptr_library/03ElbowRegion/06Elbow-RadiatingPain.pdf - ^ . PMID 3294241. - ^ Pho, C, & Godges, J. (n.d.). Elbow and forearm radiating pain. Retrieved from http://xnet.kp.org/socal_rehabspecialists/ptr_library/03ElbowRegion/06Elbow-RadiatingPain.pdf - ^ Boakeye, M, Lad, S., Nathan, J, & Shubert, R. (2010). Trends in median, ulnar, radial, and brachioplexus nerve injuries. Neurosurgery, 66(5), 953-960. Nervous system pathology, PNS, somatic (G50–G64, 350–357) Nerve, nerve root, plexusLower limbGeneral Polyneuropathies/PolyradiculoneuropathyOther Wikimedia Foundation. 2010.	2	7	1	0	0	1	0.305825	2	3,690
\|Other names\|\|Pulmonary oedema\| \|Pulmonary edema with small pleural effusions on both sides.\| \|Specialty\|\|Cardiology, critical care medicine\| Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (non-cardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term edema is from the Greek οἴδημα (oídēma, "swelling"), from οἰδέω (oidéō, "I swell"). Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. When directly or indirectly caused by increased left ventricular pressure pulmonary edema may form when mean pulmonary pressure rises from the normal of 15 mmHg to above 25 mmHg. Broadly, the causes of pulmonary edema can be divided into cardiogenic and non-cardiogenic. By convention cardiogenic refers to left ventricular causes. - Congestive heart failure which is due to the heart's inability to pump the blood out of the pulmonary circulation at a sufficient rate resulting in elevation in wedge pressure and pulmonary edema – this may be due to left ventricular failure, arrhythmias, or fluid overload, e.g., from kidney failure or intravenous therapy. - Hypertensive crisis can cause pulmonary edema as the elevation in blood pressure and increased afterload on the left ventricle hinders forward flow and causes the elevation in wedge pressure and subsequent pulmonary edema. - Negative pressure pulmonary edema in which a significant negative pressure in the chest (such as from an inhalation against an upper airway obstruction) ruptures capillaries and floods the alveoli. Negative pressure pulmonary edema has an incidence in the range of 0.05-0.1% for general anesthesia. The negative pressure causes a significant increase in preload, thereby increasing pulmonary blood volume. There is also a significant increase in left ventricular afterload, which causes a decreased cardiac output. The increase in pulmonary blood volume along with a decrease in cardiac output will increase the pulmonary transudative pressures. With all this occurring, pulmonary vascular resistance increases causing a shift of the intraventricular septum. The ventricular septal shift to the left causes a left ventricular diastolic dysfunction, which further increases pulmonary hydrostatic pressures. - Neurogenic causes (seizures, head trauma, strangulation, electrocution). - Acute respiratory distress syndrome Injury to the lung may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. The acute lung injury-acute respiratory distress syndrome (ALI-ARDS) covers many of these causes, but they may include: - Inhalation of hot or toxic gases - Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents) - Aspiration, e.g., gastric fluid - Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema. - Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation - Swimming induced pulmonary edema also known as immersion pulmonary edema - Transfusion Associated Circulatory Overload (TACO) occurs when multiple blood transfusions or blood-products (plasma, platelets, etc.) are transfused over a short period of time. - Transfusion associated Acute Lung Injury (TRALI) is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the recipient,such as anti-HLA or anti-neutrophil antibodies. - Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS. Some causes of pulmonary edema are less well characterised and arguably represent specific instances of the broader classifications above. - Arteriovenous malformation - Hantavirus pulmonary syndrome - High altitude pulmonary edema (HAPE) - Envenomation, such as with the venom of Atrax robustus Signs and symptoms The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of right ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound. Flash pulmonary edema Flash pulmonary edema (FPE), is rapid onset pulmonary edema. It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation, heart failure, or almost any cause of elevated left ventricular filling pressures. Treatment of FPE should be directed at the underlying cause, but the mainstays are nitroglycerin, ensuring adequate oxygenation with non-invasive ventilation, and decrease of pulmonary circulation pressures. Recurrence of FPE is thought to be associated with hypertension and may signify renal artery stenosis. Prevention of recurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure. There is no one single test for confirming that breathlessness is caused by pulmonary edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial. Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema Lung ultrasound, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema. Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures. Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely. In those with underlying heart disease, effective control of congestive symptoms prevents pulmonary edema. Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema. Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and pulmonary hypertension, the mechanism of action is via phosphodiesterase inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason. The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Hypoxia (abnormally low oxygen levels) may require supplementary oxygen, but if this is insufficient then again mechanical ventilation may be required to prevent complications. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics. Cardiogenic pulmonary edema Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. Positioning upright may relieve symptoms. A loop diuretic such as furosemide (Lasix®) is administered, often together with morphine to reduce respiratory distress. Both diuretic and morphine may have vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate. Continuous positive airway pressure and bilevel positive airway pressure (BIPAP/NIPPV) has been demonstrated to reduce the need of mechanical ventilation in people with severe cardiogenic pulmonary edema, and may reduce mortality. It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure. This can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as temporary treatment while the underlying cause is addressed. - "pulmonary edema" at Dorland's Medical Dictionary[dead link] - Ware LB, Matthay MA (December 2005). "Clinical practice. Acute pulmonary edema". N. Engl. J. Med. 353 (26): 2788–96. doi:10.1056/NEJMcp052699. PMID 16382065. - What Is Pulmonary Hypertension? From Diseases and Conditions Index (DCI). National Heart, Lung, and Blood Institute. Last updated September 2008. Retrieved on 6 April 2009. - Chapter 41, page 210 in: Cardiology secrets By Olivia Vynn Adair Edition: 2, illustrated Published by Elsevier Health Sciences, 2001 ISBN 1-56053-420-6, ISBN 978-1-56053-420-4 - Papaioannou V, Terzi I, Dragoumanis C, Pneumatikos I (2009). "Negative-pressure acute tracheobronchial hemorrhage and pulmonary edema". J Anesth. 23 (3): 417–20. doi:10.1007/s00540-009-0757-0. PMID 19685125. - Hines, Roberta L. and Marschall, Katherine. Stoelting's Anesthesia and Co-Existing Disease. 6th edition. 2012. pages 178 and 179. - O'Leary, R.; McKinlay, J. (2011). "Neurogenic pulmonary oedema". Continuing Education in Anaesthesia, Critical Care & Pain. 11 (3): 87–92. doi:10.1093/bjaceaccp/mkr006. - Boyle, AJ; Mac Sweeney, R; McAuley, DF (August 2013). "Pharmacological treatments in ARDS; a state-of-the-art update". BMC Med. 11: 166. doi:10.1186/1741-7015-11-166. PMC 3765621. PMID 23957905. - Hampson NB, Dunford RG (1997). "Pulmonary edema of scuba divers". Undersea Hyperb Med. 24 (1): 29–33. PMID 9068153. Retrieved 2008-09-04. - Cochard G, Arvieux J, Lacour JM, Madouas G, Mongredien H, Arvieux CC (2005). "Pulmonary edema in scuba divers: recurrence and fatal outcome". Undersea Hyperb Med. 32 (1): 39–44. PMID��15796313. Retrieved 2008-09-04. - "Adverse Reactions". Professional Education. 2016-06-02. Retrieved 2016-12-03. - "Transfusion-related acute lung injury (TRALI)". Professional Education. 2016-06-17. Retrieved 2016-12-03. - Luks AM (2008). "Do we have a "best practice" for treating high altitude pulmonary edema?". High Alt. Med. Biol. 9 (2): 111–4. doi:10.1089/ham.2008.1017. PMID 18578641. - Bates, M (2007). "High altitude pulmonary edema". Altitude Physiology Expeditions. Retrieved 2008-09-04. - White J, Gray M, Fisher M (1989). Atrax Robustus IPCS InChem - Long, Brit; Koyfman, Alex; Gottlieb, Michael (2018). "Management of Heart Failure in the Emergency Department Setting: An Evidence-Based Review of the Literature". The Journal of Emergency Medicine. 55 (5): 635–646. doi:10.1016/j.jemermed.2018.08.002. PMID 30266198. - Kramer K, Kirkman P, Kitzman D, Little WC. Flash pulmonary edema: association with hypertension and recurrence despite coronary revascularization. Am Heart J. 2000 Sep;140(3):451–5. doi:10.1067/mhj.2000.108828. PMID 10966547. - Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, Silane MF, Laragh JH. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet. 1988;332(8610):551–2. doi:10.1016/S0140-6736(88)92668-2. PMID 2900930. - Volpicelli, Giovanni; Elbarbary, Mahmoud; Blaivas, Michael; Lichtenstein, Daniel A.; Mathis, Gebhard; Kirkpatrick, Andrew W.; Melniker, Lawrence; Gargani, Luna; Noble, Vicki E. (2012-04-01). "International evidence-based recommendations for point-of-care lung ultrasound". Intensive Care Medicine. 38 (4): 577–591. doi:10.1007/s00134-012-2513-4. ISSN 1432-1238. PMID 22392031. - Richalet JP, Gratadour P, Robach P, et al. (2005). "Sildenafil inhibits altitude-induced hypoxemia and pulmonary hypertension". Am. J. Respir. Crit. Care Med. 171 (3): 275–81. doi:10.1164/rccm.200406-804OC. PMID 15516532. - Perimenis P (2005). "Sildenafil for the treatment of altitude-induced hypoxaemia". Expert Opin Pharmacother. 6 (5): 835–7. doi:10.1517/146565220.127.116.115. PMID 15934909. - Clark, Michael; Kumar, Parveen J. (2009). Kumar and Clark's clinical medicine. St. Louis, Mo: Elsevier Saunders. p. 783. ISBN 978-0-7020-2993-6. - Fagenholz PJ, Gutman JA, Murray AF, Harris NS (2007). "Treatment of high altitude pulmonary edema at 4240 m in Nepal". High Alt. Med. Biol. 8 (2): 139–46. doi:10.1089/ham.2007.3055. PMID 17584008. - Cleland JG, Yassin AS, Khadjooi K (2010). "Acute heart failure: focusing on acute cardiogenic pulmonary oedema". Clin Med. 10 (1): 59–64. doi:10.7861/clinmedicine.10-1-59. PMC 4954483. PMID 20408310. - Vital FM, Ladeira MT, Atallah AN (2013). "Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema". Cochrane Database Syst Rev. 5 (5): CD005351. doi:10.1002/14651858.CD005351.pub3. PMID 23728654.	2	17	2	0	1	0	0.949185	3	3,830
Vol. 18 •Issue 9 • Page 10 Coding Urinary Tract Infections Reimbursement and quality regulations require proper coding and reporting of UTIs. Urinary tract infections (UTI) are a serious health problem affecting millions of people each year. Infections of the urinary tract are the second most common type of infection in the body. Only upper respiratory tract infections (colds and flu) happen more often. According to the Centers for Medicare and Medicaid Services (CMS), catheter-associated UTIs are the most common hospital-acquired infection, accounting for more than 1 million cases in hospitals and nursing homes nationwide. With the implementation of MS-DRG, the importance of coding MCCs and CCs, and the inclusion of catheter-associated UTIs as an initial preventable hospital-acquired condition, correct coding and assignment of UTIs is more important than ever. A UTI is a bacterial infection of any part of the urinary tract. When bacteria get into the urinary tract and multiply in the urine, they cause a UTI. Predisposing factors for urinary tract infection include calculi or other urinary tract obstruction, foreign bodies such as stents or catheters, congenital urinary anomalies, pregnancy, diabetes mellitus and neurogenic bladder. Women are approximately 10 times more likely to develop a UTI than men. Physicians often use the term UTI when referring to cystitis, urethritis and pyelonephritis. Lower UTIs include urethritis and cystitis, while pyelonephritis is an upper UTI. Not all patients have symptoms, but most do have some. Symptoms include dysuria (difficult or painful urination), increased urinary frequency, urgency and often hematuria. Other symptoms include chills, fever, nausea and vomiting, pain and a general feeling of malaise. Each type of UTI may result in more specific signs and symptoms, depending on what is infected. - Cystitis is an infection or inflammation of the urinary bladder. Cystitis occurs when the lower urinary tract is infected by bacteria and becomes irritated and inflamed. Symptoms include pelvic pressure, lower abdomen discomfort, frequent, painful urination and cloudy, strong-smelling urine. - Pyelonephritis or pyelitis is a urinary tract infection that has spread from the bladder to the kidneys. Kidney infection can cause upper back and flank pain, headache, high fever, shaking chills, and nausea or vomiting. In severe cases, delirium may be present. - Urethritis is an infection of the urethra. Symptoms include urethral discharge, dysuria, urgency and increased frequency. Urinalysis may show significant bacteriuria, often accompanied by proteinuria, hematuria and pyuria. Urine or catheter culture reveals growth of >100,000 colonies of a single organism. Blood work may reveal neutrophilic leukocytosis and positive blood culture, especially if the infection involves the upper urinary tract. White blood cell shows count of >10,000. Coding Acute UTIs One of the most important aspects of coding an acute UTI is documentation of site specificity in the medical record. - Acute pyelonephritis: 590.1X, Acute pyelonephritis - Acute cystitis: 595.0, Acute cystitis - Urethritis: 597.80, Urethritis, unspecified Code 599.0, Urinary tract infection, site not specified, should be assigned only if the physician has not identified or is unable to identify the site of the UTI. Code 599.0 should not be used in combination with codes that specifically identify the site of the UTI. For example, if the terms acute cystitis and UTI are both documented separately on the final diagnosis sheet, only the code for the acute cystitis, 595.0, should be assigned. However, if two specific sites are documented then both should be assigned. Coding guidelines require the assignment of an additional code if the causative organism is identified. The UTI code is sequenced first, followed by the organism. E. Coli is a common organism causing UTIs and is reported with code 041.4. Codes from category 599 should not be reported for UTIs in newborns. Code 771.82, Urinary tract infection of newborn, should be assigned instead. UTI due to Candidal yeast requires one code, 112.2, Candidiasis of other urogenital sites. However, UTI due to noncandidal yeast requires two codes. Code first the appropriate UTI code, followed by 117.9, Other and unspecified mycoses. UTI and Sepsis If the documentation indicates that the UTI has progressed to sepsis, code 038.X should be assigned first, then code 995.91, Sepsis, followed by the appropriate UTI code. In this instance sepsis indicates that the UTI has entered the bloodstream and becomes a generalized sepsis. The systemic infection, sepsis, should be sequenced before the localized infection, UTI. There has been considerable debate in the coding community regarding urosepsis. The term urosepsis is a nonspecific term. The ICD-9-CM Official Guidelines for Coding and Reporting states that if urosepsis is the only term documented, then only code 599.0 should be assigned based on the default for the term in the ICD-9-CM index. However, often the term urosepsis is used by physicians when in fact the infection has spread to the bloodstream and has progressed to sepsis. The physician should be queried to clarify whether the urosepsis is intended to mean sepsis or UTI. If the physician indicates that the UTI has developed into sepsis, assign the appropriate sepsis codes and then the appropriate UTI code as indicated above. If urosepsis is meant to mean UTI, then code 599.0 should be assigned along with the causal organism. If a UTI is diagnosed after a procedure is performed, the coder should not assume that the UTI is a complication of surgery. The physician should be queried. If the post-operative UTI is linked to the procedure, two codes are required; 997.5, Complications affecting specified body systems, urinary complications, and the appropriate UTI code. If the causative organism is identified it is also coded. If the physician states that the UTI is not linked to the procedure or is not result of the procedure, then only the appropriate UTI code is assigned. Foley Catheter Induced UTI Catheters placed in the urethra and bladder are a common source of UTIs. Often urinary catheters are inserted during surgery. A person who cannot void or who is unconscious or critically ill often needs a catheter that stays in place for a longer period of time. Bacteria on the catheter can infect the bladder, so hospital staff must take special care to keep the catheter clean and remove it as soon as possible. As indicated earlier, catheter-associated UTIs are the most common hospital-acquired infection, accounting for more than 1 million cases in hospitals and nursing homes nationwide. According to CMS, it is estimated that hospital-acquired UTIs require one extra hospital day per patient, at an estimated annual cost of $424 to $451 million. These conditions are reported with code 996.64, Infection and inflammatory reaction due to indwelling urinary catheter, and the appropriate UTI code. Recurrent and Chronic Recurrent or chronic UTI without current symptoms should not be coded to the acute infection. Code V13.02, Personal history of urinary (tract) infection, may be assigned to report this. Code V58.62, Long-term (current) use of antibiotics, may also be assigned if the patient is receiving prophylactic antibiotic therapy. UTIs should not be coded based upon lab results alone. Urine specimens are subject to contamination during collection from microorganisms or by improper handling and storage. Always verify the diagnosis with the physician. UTI is a commonly missed CC, which may affect MS-DRG assignment. If the medical record contains documentation suggestive of this condition, query the attending physician if it should be added as a secondary diagnosis. Check yourself on proper coding for UTIs with the quiz below: 1. A patient presents to the ED with a UTI that is due to an indwelling urinary catheter. Which of the following would be the appropriate diagnosis code(s) selection? a. 996.64, 599.0, E879.6 b. 599.0, 996.64, E879.6 c. 996.64, 599.0 d. 996.64, E879.6 2. Patient with chronic cholecystitis is admitted for an elective cholecystectomy. After admission it was noted by the physician that the patient had developed a UTI based on laboratory tests that were positive for E.Coli. The patient was started on antibiotics, the surgery was cancelled and the patient was discharged. Discharge orders indicate that the surgery was rescheduled in 3 weeks. Which of the following would be the appropriate diagnosis code(s) selection? a. 599.0, 041.4, 575.11, V64.1 b. 575.11, 599.0, 041.4, V64.1 c. 575.11, 599.0, V64.1 d. 599.0, 575.11, V64.1 3. A patient was discharged following prostate surgery with an indwelling catheter in place. He was readmitted with urinary sepsis due to staphylococcus aureus due to the catheter. The catheter was removed and the patient was started on antibiotic therapy. The patient improved over several days and he was discharged without the indwelling catheter. Which of the following would be the appropriate diagnosis code(s) selection? a. 996.64, 038.11, 995.91, 599.0, E879.6 b. 038.11, 995.91, 599.0, 996.64, E879.6 c. 996.64, 038.11, 995.91, E879.6 d. 038.11, 995.91, 966.64, E879.6 4. A preterm infant (2,450 grams at birth) was transferred to the current hospital for investigative studies after he was noted to have an elevated temperature and WBCs. A UTI was confirmed with a urine culture that was positive for E. coli. The infection was treated with intravenous antibiotics. Suspected septicemia was ruled out when all blood cultures were negative prior to institution of antibiotic therapy. Which of the following would be the appropriate diagnosis code(s) selection? a. 599.0, 041.4, 771.82, 765.18, 765.20 b. 771.82, 599.0, 041.4, 765.18, 765.20 c. 771.82, 041.4, 765.18, 765.20 d. 765.18, 771.82, 041.4, 765.20 This month’s column has been prepared by Cheryl D’Amato, RHIT, CCS, director of HIM, facility solutions, Ingenix, and Melinda Stegman, MBA, CCS, clinical technical editor, Ingenix (www.ingenix.com). Ingenix develops software and e-commerce solutions for managing coding, reimbursement, compliance and denial management in the health care marketplace. Coding Clinic is published quarterly by the AHA. CPT is a registered trademark of the AMA. Answers to CCS PREP!: 1. a: Three codes are reported for this case. Code 996.64 is used to indicate that the infection is due to an indwelling urinary catheter. Code 599.0 is reported to identify the type of infection, UTI, site not specified. Code E879.6 may be reported to indicate that the urinary catheter is the cause of abnormal reaction or later complication; 2. b: The principal diagnosis does not change because the planned procedure was not carried out. Code 575.11, Chronic cholecystitis, is assigned as the principal diagnosis. Codes 599.0 and 041.4 are both assigned to report the UTI due to E.Coli. Code V64.1, Surgical or other procedure not carried out because of contraindications, is assigned to indicate that the procedure was cancelled due to the UTI; 3. a: Code 996.64 is reported as the principal diagnosis to indicate that the sepsis is due to an indwelling urinary catheter. Codes 038.11 and 995.91 are assigned to report the systemic infection, staphylococcus aureus sepsis. Code 599.0 is reported to identify UTI as the localized infection. Code E879.6 may be reported to indicate that the urinary catheter is the cause of abnormal reaction or later complication; and 4. c: Code 771.82 is assigned as the principal diagnosis to report UTI of newborn. Code 041.4 is also assigned to report E. coli as the causative organism. UTI codes from category 599 are excluded for newborns and are not assigned. Code 765.18 is assigned to report the prematurity weighing 2,450 grams at birth. Code 765.20 is required to identify the number of weeks of gestation. In this case, it was unspecified.	4	6	0	0	0	4	0.762749	4	2,970
Unless you've been living in a cave, you are probably aware that come Oct. 1, 2015, the old ICD-9 coding system will be completely replaced with a "newer version": ICD-10. The purpose of this newer system is to modernize coding -- recognizing that since the last update in 1979, the number and precision of diagnoses has increased dramatically. Unfortunately, with only a maximum of five characters to use, ICD-9 is currently limited to around 13,000 codes. By expanding this to a maximum of seven characters, at least 68,000 diagnoses are being considered under ICD-10. Also, the newer coding system will allow for greater specificity and laterality (left/right). Under the newer system, the first character will always be a letter (alpha character), which will specify the organ system involved. For many, but not all, rheumatologic diagnoses, this will be "M". The next two characters can be either a number or alpha (#2 will always be a number, #3 can be either a number or alpha), and will define a category of diseases. For example, chronic gout: M1A; inflammatory arthropathies: M05-M14; OA: M15-M19; Systemic Connective Tissue Diseases: M30-36; and Spondyloarthropathies: M45-M49. These three characters are always followed by "." (period) before the next characters, if needed, are to be added. Character 4 will describe features like etiology or organ system (RA lung: M05.1, RA other: M05.8....by the way, there is a different code for seroposivite RA (M05) and seronegative RA(M06). Character 5 will be location (wrist=3, knee=6, multiple sites=9) and character 6 will be laterality (right=1, left=2, bilateral=3). The last character will be for additional features, such as tophi (chronic idiopathic gout of the right wrist with tophi=M1A.0911; no tophi=M1A.0910). Confused yet? Wait, there's more. Sometimes there is no laterality, so a placeholder "X" is added (chronic idiopathic gout, multiple sites with tophi=M1A.09X1). Some codes can exist by themselves (gout: M1A,xxxx, xxxx, seropositive RA: M05.8xxx, PMR: M35.3). Others can be reported as combinations with another disease (IBD-related right knee arthritis due to Crohn's disease=M07.661 and K50.918). Still, others need to be reported in combination with other diagnoses, but in a specific order (Reactive Arthritis of the Left ankle due to Yersinia infection=A04.6 (which must be listed first) and M02.172). My recommendations for implementation of ICD-10 The first recommendation I have is to start NOW, if not sooner. Summer is rapidly coming to an end and October will soon be upon us. Once this date happens, anything you code using the old system WILL BE REJECTED!! (RheumNow editor's note: Dr. Bergman's advice is spot on. Note that CMS and the AMA have stated that they will be "lenient" in the first year of implementation. What that means remains to be seen – JC) Do you bill using a computer? (Hopefully, a rhetorical question.) Make sure NOW that your software is able to handle ICD-10. Using a billing service? Make sure NOW that they are able to handle ICD-10. Buy a coding book. Let's face it; while there is logic to this system, it is far from intuitive. Having a comprehensive code book, like the ones provided by the AMA (disclosure, I am a member, but not otherwise affiliated) and learn to use it. This is not the time or place to save money. Remember what I wrote above...failure to use these codes will lead to your claims being REJECTED!! Start small, but get to work. The good news is: for the most part we use the same codes over and over again. We are not FPs who must have every code in the book entered into our computers. More likely we will need 100-200. While that sounds like a large number, it is far from daunting. I'm starting with the most common codes (RA, Gout, Joint Pain, and Joint Swelling). A list of the most commonly used codes in rheumatology is available on the ACR website. (Editor's note: this link was updated on 8/12/15) Once those are in the system, I'm going through my entire list of frequent codes, A-Z, and changing the codes, one at a time. If I do 10-20 per day, which is not unrealistic, I should be through this in under a month. Educate your staff, especially your billing folks, about the new codes. Did I mention that if you don't use the new codes, your billing WILL BE REJECTED. Once you have a list of effective codes, re-create your super-bill (if you are still using them) or let your computer system generate the bills, after you have added them. Anticipate problems and have ready cash available during the transition period. Even in the best of circumstances, problems are bound to occur. This is a nationwide roll-out, glitches are bound to occur. Being ready is always the best option. If all of this sends you into panic mode, the other option is to pay a service to do this for you. There are many out there who are more than willing to assist you in this transition, for a fee. I'm not making enough in clinical practice to have me want to share it with others, but that is my decision. You may feel differently. Regardless, the time to act is NOW, if not yesterday. October will be here, soon enough. Do you know where your reimbursements will be? Martin J. Bergman, MD, is clinical associate professor of medicine at Drexel University College of Medicine in Philadelphia and is chief of the section of rheumatology at Taylor Hospital in Ridley Park, Pa. A version of this article first appeared on RheumNow. RheumNow is a news, information, and commentary site dedicated to the field of rheumatology. Register to receive their free rheumatology newsletter. The author has no conflicts of interest to disclose related to this subject.	4	3	0	0	0	6	0.607652	6	1,413
What is Medicaid Medicare? Complete Guides on Medicare, Medicaid What is Medicare? What is Medicaid? Revised February 2019 – Credit – https://www.medicare.gov/ Medicare is health insurance for: - People 65 or older - Certain people under 65 with disabilities - People of any age with End-Stage Renal Disease (ESRD) (permanent kidney failure requiring dialysis or a kidney transplant) What are the different parts of Medicare? Original Medicare is a fee-for-service health plan that has two parts: Part A (Hospital Insurance) and Part B (Medical Insurance). Medicare Part A (Hospital Insurance) helps cover: - Inpatient care in a hospital - Skilled nursing facility care - Hospice care - Home health care You usually don’t pay a monthly premium for Part A coverage if you or your spouse paid Medicare taxes while working for a certain amount of time. This is sometimes called premium-free Part A. If you aren’t eligible for premium-free Part A, you may be able to buy Part A. Medicare Part B (Medical Insurance) helps cover: - Services from doctors and other health care providers - Outpatient care - Home health care - Durable medical equipment (DME) - Many preventive services Most people pay the standard monthly Part B premium. Note: Original Medicare pays for much, but not all the cost for health care services and supplies. Medicare Supplement Insurance policies, sold by private companies, can help pay some of the remaining health care costs, like co-payments, coinsurance, and deductibles. Medicare Supplement Insurance policies are also called Medigap policies. What are the different parts of Medicare? (continued) Medicare Part C (Medicare Advantage): - Includes all benefits and services covered under Part A and Part B - Usually includes Medicare prescription drug coverage (Part D) as part of the plan - Run by Medicare-approved private insurance companies that follow rules set by Medicare - Plans have a yearly limit on your out-of-pocket costs for medical services - May include extra benefits and services that aren’t covered by Original Medicare, sometimes for an extra cost Medicare Part D (Medicare prescription drug coverage): - Helps cover the cost of prescription drugs - Run by Medicare-approved drug plans that follow rules set by Medicare - May help lower your prescription drug costs and help protect against higher costs in the future Note: If you have limited income and resources, you may qualify for help to pay for some health care and prescription drug costs. For more information on programs that can help pay for your health care costs visit Medicare.gov, or call 1-800-MEDICARE (1-800-633-4227). TTY users can call 1-877-486 3 Medicaid is a joint federal and state program that helps pay medical costs if you have limited income and/or resources and meet other requirements. People with Medicaid may get coverage for services that Medicare may not or may partially cover, like nursing home care, personal care, and home- and community-based services. Each state has different rules about eligibility and applying for Medicaid. If you qualify for Medicaid in your state, you automatically qualify for Extra Help paying your Medicare prescription drug coverage (Part D). You may be eligible for Medicaid if you have limited income and are: - 65 or older - A child under 19 - Living with a disability - A parent or adult caring for a child - An adult without dependent children (in certain states) - An eligible immigrant in many states, more parents and other adults can get coverage now. If you were turned down in the past, you can try again and may qualify. When you enroll, you may be able to get health care benefits like: - Doctor visits - Hospital stays - Long-term services and supports - Preventive care, including immunizations, mammograms, colonoscopies, and other needed care - Prenatal and maternity care - Mental health care - Necessary medications - Vision and dental care (for children) You should apply for Medicaid if you or someone in your family needs health care. If you aren’t sure whether you qualify, a qualified caseworker in your state can look at your situation. Contact your local or state Medicaid office to see if you qualify and to apply. To get information about your state’s Medicaid program, visit HealthCare.gov/Medicaid-chip/getting-Medicaid-chip. CMS Product No. 11306 Dual eligibility Some people qualify for both Medicare and Medicaid and are called “dual eligible.” If you have Medicare and full Medicaid coverage, most of your health care costs are likely covered. You can get your Medicare coverage through Original Medicare or a Medicare Advantage Plan (like an HMO or PPO). If you have Medicare and/or full Medicaid, Medicare covers your Part D prescription drugs. Medicaid may still cover some drugs and other care that Medicare doesn’t cover. For more information on Medicaid, visit HealthCare.gov/Medicaid-chip/gettingmedicaid-chip. If you have questions about Medicare, visit Medicare.gov, or call 1-800-MEDICARE (1-800-633-4227). TTY users can call 1-877-486-2048. You have the right to get Medicare information in an accessible format, like large print, Braille, or audio. You also have the right to file a complaint if you feel you’ve been discriminated against. or call 1-800-MEDICARE (1-800-633-4227) for more information. TTY users can call 1-877-486-2048. Paid for by the Department of Health & Human Services. This article is written for help & information purposes only, data and source are https://www.medicare.gov/what-medicare-covers/your-medicare-coverage-choices/whats-medicare	2	4	1	0	0	0	0.840487	1	1,281
- Chronic obstructive pulmonary disease Chronic Obstructive Pulmonary Disease Classification and external resources Gross pathology of a lung showing centrilobular-type emphysema characteristic of smoking. This close-up of the fixed, cut lung surface shows multiple cavities lined by heavy black carbon deposits. ICD-10 J40 - J44, J47 ICD-9 490 - 492, 494 - 496 OMIM 606963 DiseasesDB 2672 MedlinePlus 000091 eMedicine med/373 emerg/99 MeSH C08.381.495.389 Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the co-occurrence of chronic bronchitis and emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD. The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation. Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries. COPD is the third leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity. - 1 Classification - 2 Signs and symptoms - 3 Cause - 4 Pathophysiology - 5 Diagnosis - 6 Management - 7 Prognosis - 8 Epidemiology - 9 History - 10 Society and culture - 11 In other animals - 12 See also - 13 References - 14 External links The twofold nature of the pathology has been studied in the past. Furthermore, also in recent studies, many authors found that each patient could be classified as presenting a predominantly bronchial or emphysematous phenotype by simply analyzing clinical, functional, and radiological findings or studying interesting biomarkers. A statistical model reflecting the specific predominant mechanism of airflow limitation for a specific patient has been developed and trained over a database of hundreds of patients. The model is available here as a free online application. Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow. Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "Blue Bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid retention leads to them being called "Blue Bloaters". Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, "Pink Puffers". There are 4 types of emphysema: - Centriacinar / centrilobular: proximal to central parts of acini (air spaces closer to bronchioles) are affected - Panacinar / panlobular: enlargement of all air spaces (from bronchioles to terminal blind alveoli). This type is associated with alpha-1-antitrypsin deficiency - Distal acinar / paraseptal: proximal acinus normal, distal acinus affected - Irregular: various parts of acinus involved. Associated with fibrosis. Signs and symptoms Essentials of diagnosis include: - History of cigarette smoking. - Chronic cough and sputum production (in chronic bronchitis) - Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination - Airflow limitation on pulmonary function testing that is not fully reversible and most often progressive. One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: "My breathing requires effort," "I feel out of breath," or "I can't get enough air in". People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present. People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea. There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are: - tachypnea, a rapid breathing rate - wheezing sounds or crackles in the lungs heard through a stethoscope - breathing out taking a longer time than breathing in - enlargement of the chest, particularly the front-to-back distance (hyperaeration) - active use of muscles in the neck to help with breathing - breathing through pursed lips - increased anteroposterior to lateral ratio of the chest (i.e. barrel chest). The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking. Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand. Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers. Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition. The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking. Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women. Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers. The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke. There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking. Many individuals with COPD who have stopped smoking have active inflammation in the lungs. The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation. This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells. Other risk factors A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease. It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD. It is not fully understood how tobacco smoke and other inhaled particles damage the lungs to cause COPD. The most important processes causing lung damage are: - Oxidative stress produced by the high concentrations of free radicals in tobacco smoke - Cytokine release due to inflammation as the body responds to irritant particles such as tobacco smoke in the airway - Tobacco smoke and free radicals impair the activity of antiprotease enzymes such as alpha 1-antitrypsin, allowing protease enzymes to damage the lung Narrowing of the airways reduces the rate at which air can flow to and from the air sacs (alveoli) and limits the effectiveness of the lungs. In COPD, the greatest reduction in air flow occurs when breathing out (during expiration) because the pressure in the chest tends to compress rather than expand the airways. In theory, air flow could be increased by breathing more forcefully, increasing the pressure in the chest during expiration. In COPD, there is often a limit to how much this can actually increase air flow, a situation known as expiratory flow limitation. If the rate of airflow is too low, a person with COPD may not be able to completely finish breathing out (expiration) before he or she needs to take another breath. This is particularly common during exercise, when breathing has to be faster. A little of the air of the previous breath remains within the lungs when the next breath is started, resulting in an increase in the volume of air in the lungs, a process called dynamic hyperinflation. Dynamic hyperinflation is closely linked to dyspnea in COPD. It is less comfortable to breathe with hyperinflation because it takes more effort to move the lungs and chest wall when they are already stretched by hyperinflation. Another factor contributing to shortness of breath in COPD is the loss of the surface area available for the exchange of oxygen and carbon dioxide with emphysema. This reduces the rate of transfer of these gases between the body and the atmosphere and can lead to low oxygen and high carbon dioxide levels in the body. A person with emphysema may have to breathe faster or more deeply to compensate, which can be difficult to do if there is also flow limitation or hyperinflation. Some people with advanced COPD do manage to breathe fast to compensate, but usually have dyspnea as a result. Others, who may be less short of breath, tolerate low oxygen and high carbon dioxide levels in their bodies, but this can eventually lead to headaches, drowsiness and heart failure. Advanced COPD can lead to complications beyond the lungs, such as weight loss (cachexia), pulmonary hypertension and right-sided heart failure (cor pulmonale). Osteoporosis, heart disease, muscle wasting and depression are all more common in people with COPD. Several molecular signatures associated to lung function decline and corollaries of disease severity have been proposed, a majority of which are characterized in easily accessible surrogate tissue, including blood derivatives such as serum and plasma. A recent 2010 clinical study proposes alpha 1B-glycoprotein precursor/A1BG, alpha 2-antiplasmin, apolipoprotein A-IV precursor/APOA4, and complement component 3 precursor, among other coagulation and complement system proteins as corollaries of lung function decline, although ambiguity between cause and effect is unresolved. Acute exacerbations of COPD An acute exacerbation of COPD is a sudden worsening of COPD symptoms (shortness of breath, quantity and color of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Typically, infections cause 75% or more of the exacerbations; bacteria can be found in roughly 25% of cases, viruses in another 25%, and both viruses and bacteria in another 25%. Pulmonary emboli can also cause exacerbations of COPD. Airway inflammation is increased during the exacerbation, resulting in increased hyperinflation, reduced expiratory air flow and worsening of gas transfer. This can also lead to hypoventilation and eventually hypoxia, insufficient tissue perfusion, and then cell necrosis. The diagnosis of COPD should be considered in anyone who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease such as regular tobacco smoking. No single symptom or sign can adequately confirm or exclude the diagnosis of COPD, although COPD is uncommon under the age of 40 years. The diagnosis of COPD is confirmed by spirometry, a test that measures the forced expiratory volume in one second (FEV1), which is the greatest volume of air that can be breathed out in the first second of a large breath. Spirometry also measures the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a whole large breath. Normally, at least 70% of the FVC comes out in the first second (i.e. the FEV1/FVC ratio is >70%). A ratio less than normal defines the patient as having COPD. More specifically, the diagnosis of COPD is made when the FEV1/FVC ratio is <70%. The GOLD criteria also require that values are after bronchodilator medication has been given to make the diagnosis, and the NICE criteria also require FEV1%. According to the ERS criteria, it is FEV1% predicted that defines when a patient has COPD, that is, when FEV1% predicted is < 88% for men, or < 89% for women. Spirometry can help to determine the severity of COPD. The FEV1 (measured after bronchodilator medication) is expressed as a percentage of a predicted "normal" value based on a person's age, gender, height and weight: Severity of COPD (GOLD scale) FEV1 % predicted Mild (GOLD 1) ≥80 Moderate (GOLD 2) 50–79 Severe (GOLD 3) 30–49 Very severe (GOLD 4) <30 or chronic respiratory failure symptoms The severity of COPD also depends on the severity of dyspnea and exercise limitation. These and other factors can be combined with spirometry results to obtain a COPD severity score that takes multiple dimensions of the disease into account. On chest x-ray, the classic signs of COPD are overexpanded lung (hyperinflation), a flattened diaphragm, increased retrosternal airspace, and bullae. It can be useful to help exclude other lung diseases, such as pneumonia, pulmonary edema or a pneumothorax. Complete pulmonary function tests with measurements of lung volumes and gas transfer may also show hyperinflation and can discriminate between COPD with emphysema and COPD without emphysema. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases. A blood sample taken from an artery, i.e. Arterial Blood Gas (ABG), can be tested for blood gas levels which may show low oxygen (hypoxaemia) and/or high carbon dioxide (respiratory acidosis if pH is also decreased). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia. There is currently no cure for COPD; however, COPD is both a preventable and treatable disease. Clinical practice guidelines for the management of COPD are available from the Global Initiative for Chronic Obstructive Lung Disease (GOLD), a collaboration that includes the World Health Organization and the U.S. National Heart, Lung, and Blood Institute. The major current directions of COPD management are to assess and monitor the disease, reduce the risk factors, manage stable COPD, prevent and treat acute exacerbations and manage comorbidity. The only measures that have been shown to reduce mortality is smoking cessation and supplemental oxygen. Risk factor reduction Smoking cessation is one of the most important factors in slowing down the progression of COPD. Once COPD has been diagnosed, stopping smoking slows down the rate of progression of the disease. Even at a late stage of the disease, it can significantly reduce the rate of deterioration in lung function and delay the onset of disability and death. It is the only standard intervention that can improve the rate of progression of COPD. Smoking cessation starts with an individual decision to stop smoking that leads to an attempt at quitting. Often several attempts are required before long-term smoking cessation is achieved. Some smokers can achieve long-term smoking cessation through "willpower" alone. However, smoking is highly addictive, and many smokers need further support to quit. The chance of successfully stopping smoking can be greatly improved through social support, engagement in a smoking cessation programme and the use of drugs such as nicotine replacement therapy, bupropion and varenicline. The policies of governments, public health agencies and antismoking organizations can reduce smoking rates by encouraging smoking cessation and discouraging people from starting smoking. These policies are important strategies in the prevention of COPD. Measures can be taken to reduce the likelihood that workers in at-risk industries such as coal mining will develop COPD. Some examples of these measures are: education of workers and management about the risks, promoting smoking cessation, surveillance of workers for early signs of COPD, the use of personal dust monitors, the use of respirators and dust control. Dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation. If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing the work role. Air quality can be improved by pollution reduction efforts which should lead to health gains for people with COPD. A person who has COPD may experience fewer symptoms if they stay indoors on days when air quality is poor. Bronchodilators are medicines that relax smooth muscle around the airways, increasing the calibre of the airways and improving air flow. They can reduce the symptoms of shortness of breath, wheeze and exercise limitation, resulting in an improved quality of life for people with COPD. They do not slow down the rate of progression of the underlying disease. Bronchodilators are usually administered with an inhaler or via a nebulizer. There are two major types of bronchodilator, β2 agonists and anticholinergics. Anticholinergics appear to be superior to β2 agonists in COPD. Anticholinergics reduce respiratory deaths while β2 agonists have no effect on respiratory deaths. Each type may be either long-acting (with an effect lasting 12 hours or more) or short-acting (with a rapid onset of effect that does not last as long). β2 agonists stimulate β2 receptors on airway smooth muscles, causing them to relax. There are several β2 agonists available. Salbutamol (common brand name: Ventolin) and terbutaline are widely used short acting β2 agonists and provide rapid relief of COPD symptoms. Long acting β2 agonists (LABAs) such as salmeterol and formoterol are used as maintenance therapy and lead to improved airflow, exercise capacity, and quality of life. Anticholinergic drugs cause airway smooth muscles to relax by blocking stimulation from cholinergic nerves. Ipratropium provides short-acting rapid relief of COPD symptoms. Tiotropium is a long-acting anticholinergic whose regular use is associated with improvements in airflow, exercise capacity, and quality of life. Ipratropium is associated with increased cardiovascular morbidity. While tiotropium in pill form reduces the risk of all cause mortality, cardiovascular mortality and cardiovascular events that in mist form increases mortality. Corticosteroids are used in tablet or inhaled form to treat and prevent acute exacerbations of COPD. Well-inhaled corticosteroids (ICS) have not been shown to be of benefit for people with mild COPD, however, they have been shown to decrease acute exacerbations in those with either moderate or severe COPD. They however have no effect on overall one-year mortality and are associated with increased rates of pneumonia. Theophylline is a bronchodilator and phosphodiesterase inhibitor that in high doses can reduce symptoms for some people who have COPD. More often, side effects such as nausea and stimulation of the heart limit its use. In lower doses, it may slightly reduce the number of COPD exacerbations. The investigative phosphodiesterase-4 antagonists, roflumilast and cilomilast have completed Phase-2 clinical trials. Tumor necrosis factor antagonists such as infliximab suppress the immune system and reduce inflammation. Infliximab has been trialled in COPD but there was no evidence of benefit with the possibility of harm. Supplemental oxygen can be given to people with COPD who have low oxygen levels in the body. Oxygen is provided from an oxygen cylinder or an oxygen concentrator and delivered to a person through tubing via a nasal cannula or oxygen mask. Supplemental oxygen does not greatly improve shortness of breath but can allow people with COPD and low oxygen levels to do more exercise and household activity. Long-term oxygen therapy for at least 16 hours a day can improve the quality of life and survival for people with COPD and arterial hypoxemia or with complications of hypoxemia such as pulmonary hypertension, cor pulmonale, or secondary erythrocytosis. High concentrations of supplemental oxygen can lead to the accumulation of carbon dioxide and respiratory acidosis for some people with severe COPD; lower oxygen flow rates are generally safer for these individuals. Another safety issue concerning the use of oxygen for patients with COPD is smoking, because the combination of smoking and oxygen can result in fire accidents. Nowadays oxygen is generally only given to patients who have stopped smoking. Pulmonary rehabilitation is a program of exercise, disease management and counselling coordinated to benefit the individual. Pulmonary rehabilitation has been shown to improve shortness of breath and exercise capacity. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions. Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation programme, this can lead to improvements in COPD symptoms. Surgery is sometimes helpful for COPD in selected cases. A bullectomy is the surgical removal of a bulla, a large air-filled space that can squash the surrounding, more normal lung. Lung volume reduction surgery is similar; parts of the lung that are particularly damaged by emphysema are removed allowing the remaining, relatively good lung to expand and work better. Lung transplantation is sometimes performed for severe COPD, particularly in younger individuals. Patients should be given annual influenza vaccinations and pneumococcal vaccinations if appropriate. Obesity, poor nutrition, depression and social isolation are looked at. Palliative care for end of life needs is important. Morphine and benzodiazepines are used in low doses to reduce anxiety. In advanced critical illness, decisions about resuscitation are addressed. COPD usually gradually gets worse over time and can lead to death. The rate at which it gets worse varies between individuals. The factors that predict a poorer prognosis are: - Severe airflow obstruction (low FEV1) - Poor exercise capacity - Shortness of breath - Significantly underweight or overweight - Complications like respiratory failure or cor pulmonale - Continued smoking - Frequent acute exacerbations COPD occurs in 34 out of 1000 greater than 65 years old. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD; translating into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically deprived parts of the country, one in 32 people were diagnosed with COPD, compared with one in 98 in the most affluent areas. In the United States, the prevalence of COPD is approximately 1 in 20 or 5%, totalling approximately 13.5 million people in USA, or possibly approximately 25 million people if undiagnosed cases are included. COPD has probably always existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. In 1769, Giovanni Morgagni described 19 cases where the lungs were “turgid” particularly from air. The first description and illustration of the enlarged airspaces in emphysema was provided by Ruysh in 1721."History of pathologic descriptions of COPD" (PDF). http://www.mhprofessional.com/downloads/products/0071457399/0071457399_chap40.pdf. Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition. Badham used the word "catarrh" to describe the cough and mucus hypersecretion of chronic bronchitis in 1814. He recognised that chronic bronchitis was a disabling disorder. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau in 1947 and Gaensler in 1950 and 1951 described the principles of measuring airflow. The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease. Society and culture It is a challenge for many health systems to ensure appropriate identification, diagnosis and care for COPD patients; England's Department of Health has identified this as a major issue for the National Health Service and has introduced a specific strategy for COPD to tackle these problems . In other animals - ^ U.S. National Heart Lung and Blood Institute - What is COPD - ^ a b c d Nathell, L.; Nathell, M.; Malmberg, P.; Larsson, K. (2007). "COPD diagnosis related to different guidelines and spirometry techniques". Respiratory research 8 (1): 89. doi:10.1186/1465-9921-8-89. PMC 2217523. PMID 18053200. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2217523. - ^ a b Simpson CR, Hippisley-Cox J, Sheikh A (2010). "Trends in the epidemiology of chronic obstructive pulmonary disease in England: a national study of 51 804 patients". Brit J Gen Pract 60 (576): 483–488. doi:10.3399/bjgp10X514729. PMC 2894402. PMID 20594429. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2894402. - ^ a b c d e f g h i j k l m Rabe KF, Hurd S, Anzueto A, et al. (2007). "Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary". Am. J. Respir. Crit. Care Med. 176 (6): 532–55. - ^ Mathers CD, Loncar D (November 2006). "Projections of Global Mortality and Burden of Disease from 2002 to 2030". PLoS Med. 3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC 1664601. PMID 17132052. http://dx.plos.org/10.1371/journal.pmed.0030442. - ^ COPD (Chronic Obstructive Pulmonary Disease) - ^ "2007 NHLBI Morbidity and Mortality Chart Book" (PDF). http://www.nhlbi.nih.gov/resources/docs/07a-chtbk.pdf. Retrieved 2008-06-06. - ^ Burrows B, Fletcher CM, Heard BE, et al (1966). "The emphysematous and bronchial types of chronic airways obstruction. A clinicopathological study of patients in London and Chicago". Lancet 87: 830–5. - ^ Kitaguchi Y, Fujimoto K, Kubo K, Honda T (October 2006). "Characteristics of COPD phenotypes classified according to the findings of HRCT". Respir Med 100 (10): 1742–52. doi:10.1016/j.rmed.2006.02.003. PMID 16549342. http://linkinghub.elsevier.com/retrieve/pii/S0954-6111(06)00064-3. - ^ Paoletti M, Camiciottoli G, Meoni E, et al. (December 2009). "Explorative data analysis techniques and unsupervised clustering methods to support clinical assessment of Chronic Obstructive Pulmonary Disease (COPD) phenotypes". J Biomed Inform 42 (6): 1013–21. doi:10.1016/j.jbi.2009.05.008. PMID 19501190. http://linkinghub.elsevier.com/retrieve/pii/S1532-0464(09)00080-X. - ^ Petty TL (2002). "COPD: clinical phenotypes". Pulm Pharmacol Ther 15 (4): 341–51. doi:10.1006/pupt.2002.0380. PMID 12220938. http://linkinghub.elsevier.com/retrieve/pii/S1094-5539(02)90380-9. - ^ a b Longmore, J. M.; Murray Longmore; Wilkinson, Ian; Supraj R. Rajagopalan (2004). Oxford handbook of clinical medicine. Oxford [Oxfordshire]: Oxford University Press. pp. 188–9. ISBN 0-19-852558-3. - ^ a b Kumar P, Clark M (2005). Clinical Medicine (6th ed.). Elsevier Saunders. pp. 900–1. ISBN 0702027634. - ^ Chung C, Delaney J, Hodgins R (2008). "Respirology". In Somogyi, Ron; Colman, Rebecca. The Toronto notes 2008: a comprehensive medical reference and review for the Medical Council of Canada Qualifying Exam - Part 1 and the United States Medical Licensing Exam - Step 2. Toronto: Toronto Notes for Medical Students. p. R9. ISBN 0-9685928-8-0. - ^ Kumar V, Abbas AK (2009). Robbins Pathologic Basis of Disease. p. 684. - ^ Mahler DA (2006). "Mechanisms and measurement of dyspnea in chronic obstructive pulmonary disease". Proceedings of the American Thoracic Society 3 (3): 234–8. doi:10.1513/pats.200509-103SF. PMID 16636091. - ^ U.S. National Heart Lung and Blood Institute - Signs and Symptoms - ^ MedlinePlus Encyclopedia Chronic obstructive pulmonary disease - ^ MedicineNet.com - COPD signs & symptoms - ^ MedicineNet.com - COPD causes - ^ Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD (August 2009). "COPD prevalence is increased in lung cancer, independent of age, sex and smoking history". Eur. Respir. J. 34 (2): 380–6. doi:10.1183/09031936.00144208. PMID 19196816. - ^ "Definition of pack year - NCI Dictionary of Cancer Terms". http://www.cancer.gov/Templates/db_alpha.aspx?CdrID=306510. - ^ Rennard, S. I.; Vestbo, J. �R. (2006). "COPD: the dangerous underestimate of 15%". The Lancet 367: 1216. doi:10.1016/S0140-6736(06)68516-4. - ^ Devereux, Graham (May 2006). "Definition, epidemiology, and risk factors". BMJ 332 (7550): 1142–4. doi:10.1136/bmj.332.7550.1142. PMC 1459603. PMID 16690673. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1459603. - ^ Hnizdo E, Vallyathan V (April 2003). "Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence". Occup Environ Med 60 (4): 237–43. doi:10.1136/oem.60.4.237. PMC 1740506. PMID 12660371. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1740506. - ^ a b Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's Principles of Internal Medicine (17th ed.). McGraw-Hill Professional. ISBN 0-07-146633-9. - ^ Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (September 2006). "Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): 523–32. doi:10.1183/09031936.06.00124605. PMID 16611654. - ^ Kennedy SM, Chambers R, Du W, Dimich-Ward H (December 2007). "Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?". Proceedings of the American Thoracic Society 4 (8): 692–4. doi:10.1513/pats.200707-094SD. PMID 18073405. http://pats.atsjournals.org/cgi/content/full/4/8/692. - ^ Silverman EK, Chapman HA, Drazen JM, et al. (June 1998). "Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis". Am. J. Respir. Crit. Care Med. 157 (6 Pt 1): 1770–8. PMID 9620904. http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=9620904. - ^ MedlinePlus Encyclopedia 000091 - ^ Agustí A, MacNee W, Donaldson K, Cosio M. (2003). "Hypothesis: Does COPD have an autoimmune component?". Thorax 58 (10): 832–4. doi:10.1136/thorax.58.10.832. PMC 1746486. PMID 14514931. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1746486. - ^ a b c Rutgers SR, Postma DS, ten Hacken NH, et al. (January 2000). "Ongoing airway inflammation in patients with COPD who do not currently smoke". Thorax 55 (1): 12–8. doi:10.1136/thorax.55.1.12. PMC 1745599. PMID 10607796. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1745599. - ^ Feghali-Bostwick CA, Gadgil AS, Otterbein LE, et al. (January 2008). "Autoantibodies in Patients with Chronic Obstructive Pulmonary Disease". Am. J. Respir. Crit. Care Med. 177 (2): 156–63. doi:10.1164/rccm.200701-014OC. PMC 2204079. PMID 17975205. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2204079. - ^ Lee SH, Goswami S, Grudo A, et al. (May 2007). "Antielastin autoimmunity in tobacco smoking-induced emphysema". Nat. Med. 13 (5): 567–9. doi:10.1038/nm1583. PMID 17450149. - ^ a b Calverley PM, Koulouris NG (2005). "Flow limitation and dynamic hyperinflation: key concepts in modern respiratory physiology". Eur Respir J 25 (1): 186–199. doi:10.1183/09031936.04.00113204. PMID 15640341. - ^ O'Donnell DE (2006). "Hyperinflation, Dyspnea, and Exercise Intolerance in Chronic Obstructive Pulmonary Disease". The Proceedings of the American Thoracic Society 3 (2): 180–4. doi:10.1513/pats.200508-093DO. PMID 16565429. - ^ Rana GS, York TP, Edmiston JS, Zedler BK, et al. (2010). "Proteomic biomarkers in plasma that differentiate rapid and slow decline in lung function in adult cigarette smokers with chronic obstructive pulmonary disease (COPD)". Anal Bioanal Chem 397 (5): 1809–19. doi:10.1007/s00216-010-3742-4. PMID 20442989. - ^ Badgett RG, Tanaka DJ, Hunt DK, et al. (1994). "The clinical evaluation for diagnosing obstructive airways disease in high-risk patients". Chest 106 (5): 1427–31. doi:10.1378/chest.106.1427 (inactive 2010-04-06). PMID 7956395. - ^ Holleman DR, Simel DL (1995). "Does the clinical examination predict airflow limitation?". JAMA 273 (4): 313–9. doi:10.1001/jama.273.4.313. PMID 7815660. - ^ Celli BR, Cote CG, Marin JM, et al. (March 2004). "The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease". N. Engl. J. Med. 350 (10): 1005–12. doi:10.1056/NEJMoa021322. PMID 14999112. - ^ a b c Torres M, Moayedi S (May 2007). "Evaluation of the acutely dyspneic elderly patient". Clin. Geriatr. Med. 23 (2): 307–25, vi. doi:10.1016/j.cger.2007.01.007. PMID 17462519. - ^ Global Initiative for Chronic Obstructive Lung Disease. - ^ a b c Drummond MB, Dasenbrook EC, Pitz MW, Murphy DJ, Fan E (November 2008). "Inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease: a systematic review and meta-analysis". JAMA 300 (20): 2407–16. doi:10.1001/jama.2008.717. PMID 19033591. - ^ a b c "World Health Organization Tobacco Free Initiative - Policy recommendations for smoking cessation and treatment of tobacco dependence". http://www.who.int/tobacco/resources/publications/tobacco_dependence/en/. Retrieved 28 July 2008. - ^ "Why is smoking addictive?". NHS Choices. http://www.nhs.uk/chq/Pages/2278.aspx?CategoryID=53&SubCategoryID=536. - ^ Handbook for Dust Control in Mining. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 2003-147, Information Circular 9465, 2003 Jun; :1-131. Accessed March 26, 2009. - ^ Liesker JJ, Wijkstra PJ, Ten Hacken NH, Koëter GH, Postma DS, Kerstjens HA (February 2002). "A systematic review of the effects of bronchodilators on exercise capacity in patients with COPD". Chest 121 (2): 597–608. doi:10.1378/chest.121.2.597. PMID 11834677. http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=11834677. - ^ Salpeter SR, Buckley NS, Salpeter EE (October 2006). "Meta-analysis: Anticholinergics, but not β-agonists, Reduce Severe Exacerbations and Respiratory Mortality in COPD". J Gen Intern Med 21 (10): 1011–9. doi:10.1111/j.1525-1497.2006.00507.x. PMC 1831628. PMID 16970553. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1831628. - ^ Calverley PM, Anderson JA, Celli B, et al. (2007). "Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease". N. Engl. J. Med. 356 (8): 775–89. doi:10.1056/NEJMoa063070. PMID 17314337. - ^ Ogale SS, Lee TA, Au DH, Boudreau DM, Sullivan SD (January 2010). "Cardiovascular events associated with ipratropium bromide in COPD". Chest 137 (1): 13–9. doi:10.1378/chest.08-2367. PMID 19363211. http://chestjournal.chestpubs.org/content/137/1/13.abstract. - ^ Celli B, Decramer M, Leimer I, Vogel U, Kesten S, Tashkin DP (January 2010). "Cardiovascular safety of tiotropium in patients with COPD". Chest 137 (1): 20–30. doi:10.1378/chest.09-0011. PMID 19592475. http://chestjournal.chestpubs.org/content/137/1/20.abstract. - ^ Ram, FS (2011 Sep 21). "Tiotropium mist inhaler for COPD increases risk of mortality compared with placebo". Evidence-based medicine. doi:10.1136/ebm.2011.100171. PMID 21937500. - ^ Gartlehner G, Hansen RA, Carson SS, Lohr KN (2006). "Efficacy and Safety of Inhaled Corticosteroids in Patients With COPD: A Systematic Review and Meta-Analysis of Health Outcomes". Ann Fam Med 4 (3): 253–62. doi:10.1370/afm.517. PMC 1479432. PMID 16735528. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1479432. - ^ Zhou Y, Wang X, Zeng X, et al. (2006). "Positive benefits of theophylline in a randomized, double-blind, parallel-group, placebo-controlled study of low-dose, slow-release theophylline in the treatment of COPD for 1 year". Respirology 11 (5): 603–10. doi:10.1111/j.1440-1843.2006.00897.x. PMID 16916334. - ^ Rennard SI, Fogarty C, Kelsen S, et al. (May 2007). "The safety and efficacy of infliximab in moderate to severe chronic obstructive pulmonary disease". Am. J. Respir. Crit. Care Med. 175 (9): 926–34. doi:10.1164/rccm.200607-995OC. PMID 17290043. - ^ "Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party". Lancet 1 (8222): 681–6. March 1981. doi:10.1016/S0140-6736(81)91970-X. PMID 6110912. http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(81)91970-X. - ^ U.S. National Heart Lung and Blood Institute - Treatment - ^ Lacasse Y, Brosseau L, Milne S, et al. (2002). Lacasse, Yves. ed. "Pulmonary rehabilitation for chronic obstructive pulmonary disease". Cochrane database of systematic reviews (Online) (3): CD003793. doi:10.1002/14651858.CD003793. PMID 12137716. - ^ "WHO Disease and injury country estimates". World Health Organization. 2009. http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html. Retrieved Nov. 11, 2009. - ^ wrongdiagnosis.com > Prevalence and Incidence of COPD Retrieved on Mars 14, 2010 - ^ MORBIDITY & MORTALITY: 2009 CHART BOOK ON CARDIOVASCULAR, LUNG, AND BLOOD DISEASES National Heart, Lung, and Blood Institute - ^ a b c Petty TL (2006). "The history of COPD". Int J Chron Obstruct Pulmon Dis 1 (1): 3–14. PMC 2706597. PMID 18046898. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2706597. - ^ Fishman AP (May 2005). "One hundred years of chronic obstructive pulmonary disease". Am. J. Respir. Crit. Care Med. 171 (9): 941–8. doi:10.1164/rccm.200412-1685OE. PMID 15849329. - ^ "NHS Outcomes Framework". 20 Dec 2010. http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_122944. Retrieved 18 Oct 2011. - ^ "An outcomes strategy for people with chronic obstructive pulmonary disease (COPD) and asthma in England". 18 July 2011. http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_127974. Retrieved 18 Oct 2011. - ^ Marinkovic, D; Aleksic-Kovacevic, S, Plamenac, P (2007). "Cellular basis of chronic obstructive pulmonary disease in horses". International review of cytology 257: 213–47. doi:10.1016/S0074-7696(07)57006-3. PMID 17280899. - Chronic obstructive pulmonary disease at the Open Directory Project - National Heart, Lung and Blood Institute - COPD U.S. NHLBI Information for Patients and the Public page. Pathology of respiratory system (J, 460–519), respiratory diseases Upper RT Common cold)Headvocal folds: Laryngopharyngeal reflux (LPR) · Vocal fold nodule · Vocal cord paresis · Vocal cord dysfunction Lower RT/lung disease (including LRTIs)acute: Acute bronchitischronic: COPD (Chronic bronchitis, Acute exacerbations of chronic bronchitis, Acute exacerbation of COPD, Emphysema) · Asthma (Status asthmaticus, Aspirin-induced, Exercise-induced) · BronchiectasisInterstitial/ restrictiveBy pathogenBy vector/routeBy distributionBroncho- · LobarOther Wikimedia Foundation. 2010. Look at other dictionaries: chronic obstructive pulmonary disease — n pulmonary disease (as emphysema or chronic bronchitis) that is characterized by chronic typically irreversible airway obstruction resulting in a slowed rate of exhalation abbr. COPD … Medical dictionary chronic obstructive pulmonary disease — COPD. A type of lung disease marked by permanent damage to tissues in the lungs, making it hard to breathe. Chronic obstructive pulmonary disease includes chronic bronchitis, in which the bronchi (large air passages) are inflamed and scarred, and … English dictionary of cancer terms chronic obstructive pulmonary disease — COPD; = chronic obstructive airways disease a disease of adults, especially those over the age of 45 with a history of smoking or inhalation of airborne pollution, characterized by airflow obstruction that is not fully reversible. The disease has … The new mediacal dictionary chronic obstructive pulmonary disease — noun a nonreversible lung disease that is a combination of emphysema and chronic bronchitis; usually patients have been heavy cigarette smokers • Hypernyms: ↑emphysema, ↑pulmonary emphysema, ↑chronic bronchitis * * * noun : pulmonary disease (as… … Useful english dictionary chronic obstructive pulmonary disease — noun Date: 1967 pulmonary disease (as emphysema or chronic bronchitis) that is characterized by chronic typically irreversible airway obstruction resulting in a slowed rate of exhalation abbreviation COPD … New Collegiate Dictionary chronic obstructive pulmonary disease — a disease of adults, especially those over the age of 45 with a history of smoking or inhalation of airborne pollution. The disease has features of emphysema and chronic bronchitis. It is diagnosed when the forced expiratory volume in 1 second… … Medical dictionary chronic obstructive pulmonary disease — Pathol. any of various lung diseases leading to poor pulmonary aeration, including emphysema and chronic bronchitis. Abbr.: COPD * * * … Universalium chronic obstructive pulmonary disease — noun a lung disease in which the airways are particularly obstructed as a result of lung damage, as from cigarette smoking, breathing in irritants, etc., resulting in shortness of breath, as emphysema, chronic bronchitis, etc. Abbrev.: COPD … Australian English dictionary chronic obstructive pulmonary disease — noun A group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. May be caused by reactive airways, chronic infection, congenital defects, or, most commonly, cigarette smoking. Generally … Wiktionary Acute exacerbation of chronic obstructive pulmonary disease — An acute exacerbation of COPD is a sudden worsening of COPD symptoms (shortness of breath, quantity and color of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental… … Wikipedia	2	61	9	0	7	2	0.765481	18	11,930
Clinical documentation has been around for centuries. There are records from the 18th and 19th centuries that show the detailed observation and findings recorded by doctors of that time. However, clinical documentation has undergone drastic changes over the years. In the early days, clinical documentation was used as a record of the patient’s diagnosis and treatment for future reference. Today, clinical documentation is used not just for reference but also to receive payments through the health insurance system. Thanks to technology, the doctor’s bulky filing cabinets filled with patient records has replaced by the Electronic Health Record (EHR) system. Sharing of information between doctors, speed and legibility are some of the benefits that are provided through the EHR. The coding system further compresses the documentation data thus allowing for quick retrieval of records. However, improper documentation can result in coding errors, resulting in denial of payments. In order to assign codes accurately for clean and timely payments, billing for services performed has to be backed by correct and thorough documentation. This is equally true in the case of Dermatology billing. Dermatology ICD 10 codes The coding system serves as a means of recording the services provided to a patient and also as a means of communication between the payer and the provider. The International Classification of Diseases (ICD) is the commonly used system, both in the US and by a large number of other countries. The ICD 9 system was used in the US from 1979 and was replaced by ICD 10 in 2015. ICD 10 codes are more detailed and more specific. However, there are a number of physicians who think that such high levels of specificity are not required. It would be important to understand that certain claims may not be processed or denied if they do not carry the required specificity. Urticaria is a good example of understanding the difference between ICD 9 and ICD 10 codes. In ICD 9, there are 8 codes to describe Urticaria, whereas under ICD 10 there are 9 codes for Urticaria. So are they the same – well yes and no. While the Urticaria ICD 10 codes are similar to ICD 9 codes in classifications, the similarities end there. ICD 9 codes were 3 to 5 characters in length, ICD 10 codes are 3 to 7 characters. Thus the levels of details and specificity are much higher in ICD 10 codes. A dermatology practice could be providing procedures for either therapeutic or cosmetic purposes or both. ICD 10 codes indicate the purpose of the procedure clearly – health or appearance. While this information will already be indicated in the documentation, it will require an expert coder to navigate the large number of ICD 10 codes for dermatology to make the right selection. A detailed and specific document is always better – both for future reference and for receiving proper payments. While proper and adequate documentation was important in the days before EHR for further treatment and follow up; it has become a critical component of modern medicine – not just for future reference and treatment but also to receive proper and timely payments for services performed. Medconverge certified ICD 10 coders are well versed with documentation and coding requirements and are in tune with the latest policy changes. Contact us for all your dermatology billing and coding requirements and ensure that you do not lose revenue due to errors or policy changes. - ICD-10-CM Codes › L00-L99 Diseases of the skin and subcutaneous tissue › L49-L54 Urticaria and erythema › . (2018). Retrieved July 05, 2018, from www.icd10data.com: https://www.icd10data.com/ICD10CM/Codes/L00-L99/L49-L54/L50- - Common ICD-10 Codes for Dermatology. (2018). Retrieved July 05, 2018, from www.icdcodelookup.com: https://icdcodelookup.com/icd-10/common-codes/dermatology - Lindsay Strowd, M. (2015, January 27). Billing, Coding and Documentation: A Primer on Dermatology Billing and Coding Guidelines . Retrieved July 05, 2018, from www.the-dermatologist.com: https://www.the-dermatologist.com/content/billing-coding-and-documentation-primer-dermatology-billing-and-coding-guidelines - D, A. J. (2014, August). ICD-10 Will Allow Dermatologists to Effectively Communicate With Payors About Patient Visits. Retrieved July 05, 2018, from www.mdedge.com: https://www.mdedge.com/cutis/article/86259/health-policy/icd-10-will-allow-dermatologists-effectively-communicate-payors - Urticaria Codes for ICD-10. (2018). Retrieved July 05, 2018, from www.aaaai.org: https://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Practice%20Management/finances-coding/Urticaria-Codes-ICD-10.pdf	3	7	2	0	0	4	0.319161	6	1,095
Implantable cardioverter defibrillator \|Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities\| \|Expert Consensus on the Use of Implantable Cardioverter-Defibrillator Therapy in Patients Who Are Not Included or Not Well Represented in Clinical Trials\| WikiDoc Resources for Implantable cardioverter defibrillator Evidence Based Medicine Guidelines / Policies / Govt Patient Resources / Community Healthcare Provider Resources Continuing Medical Education (CME) Experimental / Informatics An implantable cardioverter-defibrillator (ICD) is a small battery-powered electrical impulse generator which is implanted in patients who are at risk of sudden cardiac death due to ventricular fibrillation and ventricular tachycardia. The device is programmed to detect cardiac arrhythmia and correct it by delivering a jolt of electricity. In current variants, the ability to revert ventricular fibrillation has been extended to include both atrial and ventricular arrhythmias as well as the ability to perform biventricular pacing in patients with congestive heart failure or bradycardia. The process of implantation of an ICD is similar to implantation of a pacemaker. Similar to pacemakers, these devices typically include electrode wire(s) which pass through a vein to the right chambers of the heart, usually being lodged in the apex of the right ventricle. The difference is that pacemakers are more often temporary and generally designed to consistently correct bradycardia, while ICDs are often permanent safeguards against sudden abnormalities. The most recent development is the subcutaneous ICD (S-ICD). Current state-of-the-art electronics and batteries have enabled an implantable device to deliver enough energy to defibrillate the heart without the need for a lead in or on the heart. This prevents lead-related problems and the risk of dangerous infections in or near the heart. This ICD is positioned just under the skin and outside the ribcage. It can be placed during a minor procedure under conscious sedation. A study of 300 patients is in progress for US approvals. ICDs constantly monitor the rate and rhythm of the heart and can deliver therapies, by way of an electrical shock, when the electrical manifestations of the heart activity exceeds the preset number. More modern devices can distinguish between ventricular fibrillation and ventricular tachycardia (VT), and may try to pace the heart faster than its intrinsic rate in the case of VT, to try to break the tachycardia before it progresses to ventricular fibrillation. This is known as fast-pacing, overdrive pacing, or anti-tachycardia pacing (ATP). ATP is only effective if the underlying rhythm is ventricular tachycardia, and is never effective if the rhythm is ventricular fibrillation. Many modern ICDs use a combination of various methods to determine if a fast rhythm is normal, ventricular tachycardia, or ventricular fibrillation. Rate discrimination evaluates the rate of the lower chambers of the heart (the ventricles) and compares it to the rate in the upper chambers of the heart (the atria). If the rate in the atria is faster than or equal to the rate in the ventricles, then the rhythm is most likely not ventricular in origin, and is usually more benign. If this is the case, the ICD does not provide any therapy. Rhythm discrimination will see how regular a ventricular tachycardia is. Generally, ventricular tachycardia is regular. If the rhythm is irregular, it is usually due to conduction of an irregular rhythm that originates in the atria, such as atrial fibrillation. Morphology discrimination checks the morphology of every ventricular beat and compares it to what the ICD believes is a normally conducted ventricular impulse for the patient. This normal ventricular impulse is often an average of a multiple of beats of the patient taken in the recent past. The development of the ICD was pioneered at Sinai Hospital in Baltimore by a team including Michel Mirowski, Morton Mower, and William Staewen. Mirowski teamed up with Mower and Staewen and together they commenced their research in 1969 but it was 11 years before they treated their first patient. Similar developmental work was carried out almost coincidentally by Schuder and colleagues at the University of Missouri. More than a decade of research went into the development of an implantable defibrillator that would automatically sense the onset of ventricular fibrillation and deliver an electric countershock within 15–20 seconds, converting the rhythm to sinus rhythm. Improved versions were programmed to be able to detect ventricular tachycardia, often a forerunner of ventricular fibrillation. These were then called implantable cardioverters. The work was commenced against much skepticism even by leading experts in the field of arrhythmias and sudden death. There was doubt that their ideas would ever become a clinical reality. In 1972 Bernard Lown, the inventor of the external defibrillator, stated in the journal Circulation - "The very rare patient who has frequent bouts of ventricular fibrillation is best treated in a coronary care unit and is better served by an effective antiarrhythmic program or surgical correction of inadequate coronary blood flow or ventricular malfunction. In fact, the implanted defibrillator system represents an imperfect solution in search of a plausible and practical application". The problems to be overcome were the design of a system which would allow detection of ventricular fibrillation or ventricular tachycardia. Despite the lack of financial backing and grants, they persisted and the first device was implanted in February 1980 at Johns Hopkins Hospital by Dr. Levi Watkins, Jr. Modern ICDs do not require a thoracotomy and possess pacing, cardioversion, and defibrillation capabilities. Internal cardioverter defibrillators have also been used twice in dogs to prevent sudden death from arrhythmia. The first defibrillator was implanted at Washington State University by a team of cardiologists led by Dr Lynne Johnson in 2003. The patient was a Boxer dog with life threatening arrhythmias from arrhythmogenic right ventricular cardiomyopathy, an inherited disease. On July 21, 2008, a second ICD was implanted in a 6-month-old German Shepherd dog with inherited ventricular arrhythmias. The 5-hour long surgery took place at Louisiana State University and was led by Dr Romain Pariaut. So far, these pets are the only two client-owned dogs that have received such a high-tech treatment. Cardiovascular Implantable Electronic Device Infections - 1.2. Penicillin allergy or MRSA Colonisation - 1.3. Early post-implantation inflammation in penicillin-allergic or MRSA-colonized patient - 1.4. Uncomplicated generator pocket infection - 1.5. ICED-LI or ICED-IE or complicated generator pocket infection pending blood cultures, e.g. in severe sepsis - 1.6. ICED-LI or ICED-IE or generator pocket infection with negative blood cultures - Preferred regimen: Vancomycin 1 g IV q12h AND Gentamicin 1 mg/kg IV q12h OR Daptomycin 8–10 mg/kg IV qd AND Gentamicin 1 mg/kg IV q12h - Note: Duration of antimicrobial therapy should be at least 4 to 6 weeks for complicated infection (ie, endocarditis, septic thrombophlebitis, or osteomyelitis or if bloodstream infection persists despite device removal and appropriate initial antimicrobial therapy. Causes in Alphabetical Order - Aspergillus fumigatus - Coagulase-negative staphylococcus - Gram-negative bacilli - Propionibacterium acnes - Pseudomonas aeruginosa Living with an ICD People that have an implanted cardioverter-defibrillator can live full and happy lives. Usually the ICD improves the living conditions of a patient significantly. As with a pacemaker, living with an ICD does impose some restrictions on the person's lifestyle. Quality of Life Implantable cardioverter defibrillators have demonstrated clear life-saving benefits but concerns about patient acceptance and psychological adjustment to the ICD have been the focus of much research. Researchers including those from the field of cardiac psychology have concluded that the QoL of ICD patients is at least equal to, or better than those taking anti-arrhythmic medications. The largest study of examined 2,521 patients with stable heart failure in the SCD-HeFT trial. Results indicated that there were no differences between ICD treated and medication-treated groups at 30 months in patient reported QoL. Psychological adjustment following ICD implantation has also been well-studied. Anxiety is a common psychological side effect with approximately 13-38% of ICD patients reporting clinically significant anxiety. The primary etiological factors contributing to anxiety in ICD patients has not been determined, however. Depressive symptoms are also common but incidence of these problems have shown to be similar to those observed in other cardiac patient groups with approximately 24-41% of patients with ICDs experiencing depressive symptoms. Problems in psychosocial adjustment to ICDs, including the experience of anxiety, among spouses or other romantic partners are also prevalent. This phenomenon may be related, at least in part, to shared shock anxiety and avoidance of physical and sexual contact . Almost all forms of physical activities can be performed by patients with an ICD. All forms of sports that do not pose a risk of damaging the ICD can be enjoyed by the patient. Special care should be placed not to put excessive strain on the shoulder, arm and torso area where the ICD is implanted. Doing so may damage the ICD or the leads going from the unit to the patient's heart. As a general rule, all electronic equipment is safe to use for patients with an ICD if kept at relative small distance from the unit. Most electronic equipment such as cellphones, Devices that generate radio waves or radio interference should be kept at least 15 centimetres (6 in) from the ICD. Electronic equipment used in a professional environment or equipment using large magnets or generating magnetic fields must be avoided by patients with an ICD. Both the magnetic fields and the EMI (Electromagnetic Interference) in an MRI scanner can interfere with the correct working of the ICD. As with other metallic objects, an ICD is a contraindication to the use of magnetic resonance imaging. Experiments are on the way for solving this kind of problem. For example Medtronic showed interesting results with a pacemaker. A number of clinical trials have demonstrated the superiority of the ICD over AAD (antiarrhythmic drugs) in the prevention of death from malignant arrhythmias. The SCD-HeFT trial (published in 2005) showed a significant all-cause mortality benefit for patients with ICD. Congestive heart failure patients that were implanted with an ICD had an all-cause death risk 23% lower than placebo and an absolute decrease in mortality of 7.2 percentage points after five years in the overall population.1 Reporting in 1999, the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial consisted of 1,016 patients, and deaths in those treated with AAD were more frequent (n=122) compared with deaths in the ICD groups (n=80, p < 0.001). In 2002 the MADITII trial showed benefit of ICD treatment in patients after myocardial infarction with reduced left ventricular function (EF<30). Initially ICDs were implanted via thoracotomy with defibrillator patches applied to the epicardium or pericardium. The device was attached via subcutaneous and transvenous leads to the device contained in a subcutaneous abdominal wall pocket. The device itself acts as an electrode. Most ICDs nowadays are implanted transvenously with the devices placed in the left pectoral region similar to pacemakers. Intravascular spring or coil electrodes are used to defibrillate. The devices have become smaller and less invasive as the technology advances. Current ICDs weigh only 70 grams and are about 12.9 mm thick. A recent study by Birnie et al. at the University of Ottawa Heart Institute has demonstrated that ICDs are underused in both the United States and Canada. An accompanying editorial by Dr. Chris Simpson of Queen's University explores some of the economic, geographic, social and political reasons for this. - ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons - ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines) - ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary--a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation) - Advanced cardiac life support - Artificial pacemaker - Wearable Cardioverter Defibrillator - Bardy, Gust H. (2010). "An Entirely Subcutaneous Implantable Cardioverter–Defibrillator". New England Journal of Medicine. doi:PMID: 20463331 Check \|doi=value (help). Retrieved 13 May 2010. Unknown parameter \|coauthors=ignored (help); Unknown parameter - Mirowski M, Mower MM, Staewen WS, et al: Standby automatic defibrillator: An approach to prevention of sudden coronary death. Arch Intern Med 126:158-161, 1970 - Sandoe JA, Barlow G, Chambers JB, Gammage M, Guleri A, Howard P; et al. (2015). "Guidelines for the diagnosis, prevention and management of implantable cardiac electronic device infection. Report of a joint Working Party project on behalf of the British Society for Antimicrobial Chemotherapy (BSAC, host organization), British Heart Rhythm Society (BHRS), British Cardiovascular Society (BCS), British Heart Valve Society (BHVS) and British Society for Echocardiography (BSE)". J Antimicrob Chemother. 70 (2): 325–59. doi:10.1093/jac/dku383. PMID 25355810. - Harrison JL, Prendergast BD, Sandoe JA (2015). "Guidelines for the diagnosis, management and prevention of implantable cardiac electronic device infection". Heart. 101 (4): 250–2. doi:10.1136/heartjnl-2014-306873. PMID 25550318. - Baddour LM, Epstein AE, Erickson CC, Knight BP, Levison ME, Lockhart PB; et al. (2010). "Update on cardiovascular implantable electronic device infections and their management: a scientific statement from the American Heart Association". Circulation. 121 (3): 458–77. doi:10.1161/CIRCULATIONAHA.109.192665. PMID 20048212. - Baddour, L. M.; Epstein, A. E.; Erickson, C. C.; Knight, B. P.; Levison, M. E.; Lockhart, P. B.; Masoudi, F. A.; Okum, E. J.; Wilson, W. R.; Beerman, L. B.; Bolger, A. F.; Estes, N. A. M.; Gewitz, M.; Newburger, J. W.; Schron, E. B.; Taubert, K. A. (2010). "Update on Cardiovascular Implantable Electronic Device Infections and Their Management: A Scientific Statement From the American Heart Association". Circulation. 121 (3): 458–477. doi:10.1161/CIRCULATIONAHA.109.192665. ISSN 0009-7322. - Sohail, Muhammad R.; Uslan, Daniel Z.; Khan, Akbar H.; Friedman, Paul A.; Hayes, David L.; Wilson, Walter R.; Steckelberg, James M.; Stoner, Sarah; Baddour, Larry M. (2007). "Management and Outcome of Permanent Pacemaker and Implantable Cardioverter-Defibrillator Infections". Journal of the American College of Cardiology. 49 (18): 1851–1859. doi:10.1016/j.jacc.2007.01.072. ISSN 0735-1097. - Burns JL, Serber ER, Keim S, Sears SF. Measuring patient acceptance of implantable cardiac device therapy: initial psychometric investigation of the Florida Patient Acceptance Survey. J Cardiovasc Electrophysiol 2005;16:384-390. - Sears S, Matchett M, Conti J. Effective management of ICD patient psychosocial issues and patient critical events. J Cardiovasc Electrophysiol 2009;20(11):1297-304 - Bardy, Lee, Mark et al., 2005 - Mark DB, Anstrom KJ, Sun JL, Clapp-Channing NE, Tsiatis AA, Davidson-Ray L, Lee KL, Bardy GH. Quality of life with defibrillator therapy or amiodarone in heart failure. N Engl J Med 2008; 359(10):999-1008 - Bilge AK, Ozben B, Demircan S, et al. Depression and anxiety status of patients with implantable cardioverter defibrillator and precipitating factors. Pacing Clin Electrophysiol. 2006 Jun;29(6):619-26 - Sears SF, Jr., Todaro JF, Lewis TS, Sotile W, Conti JB. Examining the psychosocial impact of implantable cardioverter defibrillators: a literature review. Clin Cardiol 1999;22:481-489 - Vasquez-Sowell L, Sears SF, Walker RL, Kuhl EA, Conti JB. Anxiety and marital adjustment in patients with Implantable Cardioverter Defibrillator and their spouses. Journal of Cardiopulmonary Rehabilitation and Prevention 2007;27:46-49 - Vasquez LD, Sears SF, Shea JB, Vasquez PM. Sexual health for patients with an Implantable Cardioverter Defibrillator. Circulation 2010;122:465-467 - Medtronic Patient Website FAQ: Can magnets affect my device? - Birnie, David H (2007). "Use of implantable cardioverter defibrillators in Canadian and IS survivors of out-of-hospital cardiac arrest". Canadian Medical Association Journal. 177 (1): 41. doi:10.1503/cmaj.060730. PMC 1896034. PMID 17606938. Retrieved 2007-07-29. Unknown parameter \|month=ignored (help); Unknown parameter - Simpson, Christopher S (2007). "Implantable cardioverter defibrillators work - so why aren't we using them?". Canadian Medical Association Journal. 177 (1): 49. doi:10.1503/cmaj.070470. PMC 1896028. PMID 17606939. Retrieved 2007-07-29. Unknown parameter - Epstein AE, DiMarco JP, Ellenbogen KA; et al. (2008). "ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons". Circulation. 117 (21): e350–408. PMID 18483207. Text "doi:10.1161/CIRCUALTIONAHA.108.189742 " ignored (help); Unknown parameter - Gregoratos G, Abrams J, Epstein AE; et al. (2002). "ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines)". Circulation. 106 (16): 2145–61. PMID 12379588. Text "doi:10.1161/01.CIR.0000035996.46455.09 " ignored (help); Unknown parameter - Gregoratos G, Cheitlin MD, Conill A; et al. (1998). "ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary--a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation)". Circulation. 97 (13): 1325–35. PMID 9570207. Unknown parameter	2	19	1	0	0	0	0.478301	1	4,672
Cardiovascular Anatomy and Physiology John P. Kampine David F. Stowe Paul S. Pagel 1. The left ventricle (LV) is capable of tolerating large increases in arterial pressure without a substantial reduction in stroke volume, but the right ventricle may acutely decompensate with even modest increases in pulmonary vascular resistance. 2. Atrial contraction establishes final ventricular stroke volume at end-diastole and normally contributes between 15 and 20% of this volume. 3. Diastolic dysfunction may independently cause heart failure, even in the presence of relatively normal contractile function. This “heart failure with normal systolic function” has been increasingly recognized as a major underlying cause for as many as 50% of patients admitted to the hospital with congestive heart failure. 4. According to Starling's law, the force of LV contraction and volume of blood ejected from the chamber during systole (stroke volume) is directly related to the end-diastolic myofilament length, and hence, the end-diastolic volume. 5. The distensibility of the aorta, the resistance of the peripheral arterial vasculature, and the actions of reflected waves on the central aortic circulation are the principle determinants of afterload. Systemic vascular resistance (the ratio of pressure to cardiac output, P/Q) is the most commonly used nonparametric expression of peripheral resistance and is primarily affected by autonomic nervous system activity. 6. The primary determinant of myocardial oxygen consumption is heart rate because the heart completes an entire cycle with each beat, and hence, the more frequently the heart performs pressure-volume work, the more oxygen must be consumed. 7. The fundamental contractile unit of cardiac muscle is the sarcomere. The myofilaments within each sarcomere are arranged in parallel cross-striated bundles of thin (containing actin, tropomyosin, and the troponin complex) and thick (primarily composed of myosin and its supporting proteins) fibers. Sarcomeres are connected in series, thereby producing characteristic shortening and thickening of the long and short axes of each myocyte, respectively, during contraction. 8. Attachment of myosin to its binding site on the actin molecule releases the phosphate anion from the myosin head, thereby producing a molecular conformation within this cross-bridge structure that generates tension in both myofilaments. Release of adenosine diphosphate (ADP) and the stored potential energy from this activated conformation produce rotation of the cross-bridge (“power stroke”) at the hinge point separating the helix tail region from the globular myosin head and its associated light chain proteins. 9. The QRS complex records potentials at the body surface when the wave of depolarization is distributed throughout ventricular myocardium. The QRS complex is much larger in magnitude than the P wave because ventricular mass is greater than the atrial mass. Rapid conduction through the His-Purkinje system spreads the wave of depolarization quickly to the ventricles. 10. Short-duration regulation of mean arterial pressure occurs through the arterial, and to a lesser extent, intracardiac baroreceptors. Arterial baroreceptors are located at the bifurcation of the common carotid arteries and in the aortic arch. 11. Blood supply to the LV is directly dependent on the difference between the aortic pressure and LV end-diastolic pressure (coronary perfusion pressure) and inversely related to the vascular resistance to flow, which varies to the fourth power of the radius of the vessel (Poiseuille's law). 12. Metabolic factors are the major physiological determinants of coronary vascular tone and, hence, myocardial perfusion. 13. Myocardial infarction may occur without evidence of major coronary thromboses, emboli, or stenosis. This form of infarction is caused by excessive metabolic demands resulting from severe LV hypertrophy (e.g., critical aortic stenosis) or vasoactive drug ingestion (e.g., amphetamines, cocaine) or it may also result from coronary artery vasospasm. 14. The lung is richly innervated by the parasympathetic and sympathetic nervous system, but the dominant effect of the autonomic nervous system occurs primarily at the level of alveolar and bronchial smooth muscle. 15. Cerebral blood flow remains relatively constant when mean arterial pressure varies between 50 and 150 mm Hg in healthy subjects. This autoregulation of cerebral blood flow is shifted to the right in patients with chronic, poorly controlled essential hypertension. 16. Arterial CO2 tension is a major regulator of cerebral blood flow within the physiologic range of arterial CO2 tension. Cerebral blood flow linearly increases 1 to 2 mL/100 g/min for each 1 mm Hg increase in Paco2. Below an arterial CO2 tension of 25 mm Hg, the cerebral blood flow response to Paco2 is attenuated. Functional Anatomy of the Heart The left and right atria consist of two, thin overlying sheaths of muscle oriented at right angles to each other. The two thicker-walled ventricles consist of three interdigitating muscle layers: the deep sinospiral, the superficial sinospiral, and the superficial bulbospiral muscles (Fig. 10-1). The two outer muscle layers are oriented obliquely from the base of the heart to the apex. Constriction of these fibers shortens the longitudinal axis of the left ventricle (LV) by moving the base toward the apex. The circumferential deep sinospiral muscles reduce the LV diameter (Fig. 10-2). Thus, synchronous contraction of the LV muscles shortens the long axis of the heart, decreases the circumference of the LV chamber, and lifts the apex toward the anterior chest wall. This latter action produces the familiar palpable point of maximum impulse, which is normally located in the fifth or sixth intercostal space in the midclavicular line.1,2 The LV pumps blood from the low-pressure venous into the high-pressure arterial system. The right ventricle (RV) receives venous blood from the right atrium via the superior and inferior vena cavae at low pressure (2 to 10 mm Hg) and oxygen saturation (60 to 75%). The RV is crescent-shaped and contains embryologically distant inflow and outflow tracts that contract in a peristaltic sequence to propel blood into the pulmonary arterial tree. Blood flow through the pulmonary circulation functions primarily as a gas exchanger, providing for the elimination of carbon dioxide (CO2; a major product of cellular metabolism) and the uptake of oxygen (O2). The pulmonary vasculature is characterized by lower pressure than the systemic circulation and has shorter, larger-bore blood vessels with relatively thinner walls than systemic resistance vessels. Thus, the pulmonary circulation is a low-pressure, low-resistance system into which the RV transfers blood. The LV is capable of tolerating large increases in arterial pressure without a substantial reduction in stroke volume; the RV may acutely decompensate with even modest increases in pulmonary vascular resistance. The RV free wall occupies a more right-sided, anterior position within the mediastinum compared with the position of the thicker-walled LV that is located in a left-sided, posterior orientation (Fig. 10-3, A and B). During contraction, the RV moves toward the interventricular septum with a “bellows-like” action. The atrioventricular (AV) groove separating the right atrium and RV shortens toward the apex during contraction. This anatomic configuration permits the more flexible RV wall to eject a large volume of blood with a minimal amount of shortening. The echocardiographic depiction of ventricular contraction is shown in Figure 10-3. Figure 10-1. Components of the myocardium. The outer muscle layers pull the apex of the heart toward the base. The inner circumferential layers constrict the lumen, particularly of the left ventricle. (Reproduced with permission from Rushmer RF: Cardiovascular Dynamics. Philadelphia, WB Saunders, 1976, Fig. 3-2, p 78.) Figure 10-2. Ventricular volume ejection. Contraction characteristics and modes of emptying. The volumes ejected by each ventricle is equal but the left ventricle requires a more circumferential muscular wall to eject its volume at a pressure that is approximately 4 to 5 times greater than that in the right ventricle. (Reproduced with permission from Rushmer RF: Cardiovascular Dynamics. Philadelphia, WB Saunders, 1976, Fig. 3-12, p 92.) Figure 10-3. Transesophageal echocardiography demonstrates the thickness and motion of atrial and ventricular walls mid esophageal five-chamber and two chamber views (Aand B respectively). The LV has a cylindrical endocardial border, and this anatomic configuration provides a mechanical advantage over the RV in generating stroke work and power because a reduction in the cross-sectional area of the cylinder a (function of the square of the radius) is partially responsible for LV stroke volume. The LV also provides a splint against which the outer wall of the RV is pulled during contraction. The O2 content and saturation of blood within the LV (O2 20 mL/dL and 98%, respectively) is very high compared with blood in the RV. Left ventricular O2 saturation is incomplete because a small quantity of coronary venous return through thebesian veins empties directly into the left side of the heart. During contraction, LV pressure increases from end-diastolic values of 10 to 12 mm Hg to a peak pressure of 120 to 140 mm Hg during systole. The peak pressures generated by the LV reflect the requirement to circulate blood through the high-resistance systemic circulation that is composed of thicker blood vessels containing larger quantities of vascular smooth muscle than their counterparts in the pulmonary arterial tree. Resistance to blood flow is especially high in small arterioles and precapillary vessels, and blood flow in these vessels requires that the LV generate higher perfusion pressure than the RV. The volume of blood pumped by RV and LV is identical (stroke volume), but the pressure-volume work (stroke work) performed by the LV is 5 to 7 times greater than that of the RV. Left ventricular ejection is associated with a wall tension gradient from the apex to the base of the heart (aortic outflow tract), thereby producing the intraventricular gradient required to transfer stroke volume from the LV into the aorta. Efficient pumping action of the heart requires two pairs of unidirectional valves. One pair is located at the outlets of the RV and LV (pulmonic and aortic valves, respectively). These three-leaflet valves operate passively with changes in pressure gradients. The aortic valve leaflets do not flatten against the aortic wall during LV ejection because a modest dilation of the aortic root located immediately distal to each leaflet establishes an eddy current of blood flow. These dilated regions are termed the sinuses of Valsalva and permit blood flow through the right and left main coronary arteries whose openings are located in the aortic wall directly behind the valve cusps. The AV valves separating the atria from the ventricles are the tricuspid and mitral valve on the right and left sides of the heart, respectively. The mitral valve is the only cardiac valve with two leaflets. Both tricuspid and mitral valves are thin, fibrous structures that are supported by chordae tendinae attachments to papillary muscles that are part of the ventricular musculature and contract during systole. The tricuspid and mitral valves open and close with alternations in the pressure gradients between the corresponding atrial and ventricular chambers. The RV and LV are the major cardiac pumping chambers, but the atria play critically important supporting roles. The atria function as reservoirs, conduits, and contractile chambers and facilitate the transition between continuous, low-pressure venous to phasic, high-pressure arterial blood flow. The normal atrial pressure curve has three positive reflections. Shortly after the onset of atrial depolarization (indicated by the P wave of the electrocardiogram), the atria contract, producing a positive pressure wave (the A wave) late in diastole. At the onset of systole, ventricular contraction produces another pressure wave that is transmitted through the AV valves to the atria, resulting in the C wave. During the remainder of systole, the AV valves remain closed, atrial filling continues from peripheral and pulmonary veins, and atrial pressures rise, thereby producing a positive pressure deflection known as the V wave (Fig. 10-4). Atrial contraction establishes final ventricular stroke volume at end-diastole and normally contributes between 15 and 20% of this volume. When atrial contraction is absent or ineffective (e.g., atrial failure, atrial fibrillation or flutter), the heart may be capable of compensating for the loss of the atrial contractile function and continue to function effectively under resting conditions. However, during increased physical activity or stress, the absence of the atrial pump may substantially limit cardiac output, thereby causing a marked reduction in arterial blood pressure accompanied by syncope, exertional dyspnea, easy fatigability, or acute heart failure. The Cardiac Cycle The cardiac cycle is traditionally defined based on events occurring before, during, and after LV contraction. Left ventricular systole is commonly divided into three parts: isovolumic contraction, rapid ejection, and slower ejection.2,3 Closure of both the tricuspid and mitral valves occurs when RV and LV pressures exceed corresponding atrial pressure and is the source of the first heart sound (S1; Fig. 10-4). Isovolumic contraction is the interval between closure of the mitral valve and the opening of the aortic valve. Left ventricular volume remains constant during this period of the cardiac cycle. The rate of increase of LV pressure (dP/dt, an index of myocardial contractility) reaches its maximum during isovolumic contraction. True isovolumic contraction does not occur in the RV because the sequential nature of inflow followed by outflow tract RV contraction. Pressure in the aortic root declines to its minimum value immediately before the aortic valve opens. Rapid ejection occurs when LV pressure exceeds aortic pressure and the aortic valve opens. Approximately two thirds of the LV end-diastolic volume is ejected into the aorta during this rapid ejection phase of systole. Aortic dilation occurs in response to this rapid increase in volume as the kinetic energy of LV contraction is transferred to the systemic arterial circulation as potential energy. The compliance of the aorta and proximal great vessels determines the amount of potential energy that can be stored and subsequently released to the arterial vasculature during diastole. The normal LV end-diastolic volume is about 120 mL. The average ejected stroke volume is 80 mL, and the normal ejection fraction is approximately 67%. A decrease in ejection fraction below 40% is typically observed when the myocardium is affected by ischemia, infarction, or cardiomyopathic disease processes (e.g., myocarditis, amyloid infiltration). Contractile dysfunction may also occur as a result of chronic pressure or volume overload, diabetes, or hypothyroidism. As aortic pressure peaks and resists further LV ejection, transfer of further stroke volume slows and eventually stops. During this period of slower ejection, aortic pressure may briefly exceed LV pressure. The reversal of the pressure gradient between the aortic root and the LV causes the aortic valve to close, thereby producing the second heart sound (S2). Figure 10-4. Mechanical and electrical events of the cardiac cycle showing also the ventricular volume curve and the heart sounds. Note the isovolumic contraction (ICP) and the relaxation period (IRP) during which there is no change in ventricular volume because all valves are closed. The ventricle decreases in volume as it ejects its contents into the aorta. During the first third of systolic ejection—the rapid ejection period—the curve of emptying is steep. ECG, electrocardiogram. (Reproduced with permission from Smith JJ, Kampine JP: Circulatory Physiology—The Essentials, 3rd edition. Baltimore, Williams & Wilkins, 1990, Fig. 3-5, p 40.) Diastole is divided into four phases in the LV: isovolumic relaxation, early filling, diastasis, and atrial systole. Isovolumic relaxation defines the period between aortic valve closure and mitral valve opening during which LV volume remains constant. LV pressure falls precipitously as the myofilaments relax. When LV pressure falls below left atrial pressure, the mitral valve opens, and blood volume stored in the left atrium rapidly enters the LV driven by the pressure gradient between these chambers. This early-filling phase of diastole accounts for approximately 70 to 75% of total LV stroke volume available for the subsequent contraction. Delays in LV relaxation occur as a consequence of aging or disease process (e.g., myocardial ischemia) and may attenuate early ventricular filling. After left atrial and LV pressures have equalized, the mitral valve remains open and pulmonary venous return continues to flow through the left atrium into the LV. This phase of diastole is known as diastasis, during which the left atrium functions as a conduit. Tachycardia progressively shortens and may completely eliminate this phase of diastole. Diastasis accounts for no more than 5% of total LV end-diastolic volume under normal circumstances. The final phase of diastole is atrial systole. Contraction of the left atrium contributes the remaining blood volume (approximately 15 to 20%) used in the subsequent LV systole. Disease processes known to reduce LV compliance (e.g., myocardial ischemia, pressure-overload hypertrophy) attenuate early filling and increase the importance of atrial systole to overall LV filling. Thus, loss of normal sinus rhythm may precipitate catastrophic decreases in cardiac output in patients with symptomatic coronary artery disease, critical aortic stenosis, or poorly controlled chronic essential hypertension.6 The importance of diastole to overall cardiac performance cannot be understated. The rate and extent of relaxation, the viscoelastic properties of LV myocardium, the pericardium, and the structure and function of the left atrium, pulmonary venous circulation, and mitral valve determine the timing, rate, and degree of LV filling. The ability of the LV to adequately collect blood from the low-pressure pulmonary venous circulation is critical in determining the stroke volume that can be transferred to the arterial circulation during systole. Thus, diastolic dysfunction may independently cause heart failure, even in the presence of relatively normal contractile function. This “heart failure with normal systolic function” has been increasingly recognized as a major underlying cause for as many as 50% of patients admitted to the hospital with congestive heart failure.8,9 Determinants of Cardiac Output Cardiac output is the amount of blood pumped by the heart per minute. It is the product of heart rate and stroke volume and may be normalized to the body surface area (cardiac index). Cardiac output (Q) is directly related to pressure (P) and inversely related to peripheral vascular resistance (R) using an equation analogous to Ohm's law: Q = P/R. Cardiac output is a function of preload, afterload, myocardial contractility (inotropic state), and heart rate. Preload is defined by LV end-diastolic volume in the intact heart and reflects the stretch of ventricular myofilaments produced by this end-diastolic volume immediately before the onset of contraction. According to Starling's law, the force of LV contraction and volume of blood ejected from the chamber during systole (stroke volume) is directly related to the end-diastolic myofilament length, and hence, the end-diastolic volume.10,11 Thus, the ventricular myocardium behaves similar to skeletal muscle in that an increase in initial stretch determines the subsequent force of contraction. Afterload may be simplistically represented as the aortic pressure against which the LV must propel blood. The distensibility of the aorta, the resistance of the peripheral arterial vasculature, and the actions of reflected waves on the central aortic circulation are the principle determinants of afterload. Systemic vascular resistance (the ratio of pressure to cardiac output, P/Q) is the most commonly used nonparametric expression of peripheral resistance and is primarily affected by autonomic nervous system activity. For example, an increase in sympathetic nervous system tone produces vasoconstriction of peripheral resistance arterioles through activation of α1-adrenoceptors in vascular smooth muscle, thereby augmenting afterload. A brief, large increase in afterload may cause a transient decrease in stroke volume, but a compensatory increase in preload during successive cardiac cycles restores cardiac output by increasing LV force of contraction. Inotropic state is the intrinsic force of myocardial contraction independent of changes in preload, afterload, or heart rate. The number of cross bridges between the contractile elements and the relative sensitivity of the contractile elements to activator Ca2+ play important roles in determining inotropic state. In the intact heart, a positive inotropic effect is reflected by an increase in pressure-volume work at each end-diastolic volume. Such an increase in inotropic state may occur in response to an increase in cardiac sympathetic nerve activity through stimulation of β1-adrenoceptors. Pharmacologic increases in contractility may be produced by drugs that activate β1-adrenoceptors (e.g., dobutamine) or by those that prevent metabolism of the intracellular second messenger cyclic adenosine monophosphate (cAMP; e.g., milrinone). Cardiac output is also influenced by heart rate. The primary determinant of myocardial oxygen consumption is heart rate because the heart completes an entire cycle with each beat, and hence, the more frequently the heart performs pressure-volume work, the more oxygen must be consumed. The upper and lower limits of heart rate may influence cardiac output. At low heart rates (except in trained athletes), there simply may not be adequate cardiac output to meet the body's oxygen requirements, deliver substrates for metabolism, or remove products of cellular metabolism. In contrast, at high heart rates, particularly in patients with heart disease, there may not be adequate diastolic filling time to maintain cardiac output and coronary artery perfusion, the latter of which is particularly dependent on duration of diastole. Thus, shortened diastolic time during profound tachycardia may reduce stroke volume and cardiac output, contribute to hypotension, and decrease the duration of coronary perfusion. Such events may cause acute myocardial ischemia or infarction. Measures of Cardiac Function Clinical indicators of contractile performance include cardiac output, ejection fraction, fractional shortening or area change of the LV short axis, and LV systolic wall thickening. These indices of contractility are heart rate-, preload-, and afterload-dependent, but nevertheless may be measured with reasonable reliability using echocardiographic techniques and remain useful indices of contractile performance, especially in the presence of chronic heart disease, during recovery after an acute ischemic event, and in patients undergoing cardiac surgery. More sophisticated methods of assessing myocardial contractility in vivo, including the LV end-systolic pressure-volume relations and preload recruitable stroke work, require invasive measurement of continuous LV pressure and volume.10,12,13,14,15,16 Preload recruitable stroke work and the effects of isoflurane are shown in Figure 10-5. These techniques are usually assessed only in a laboratory setting, but may also be obtained using echocardiography (automated border detection) combined with invasive determination of continuous LV pressure during cardiac catheterization. Discussion of indices of contractile state derived from pressure-volume relations are beyond the scope of the current chapter. Figure 10-5. Preload recruitable stroke work (PRSW) relationship for control (C) and 1.5 and 2 minimal alveolar concentrations (MAC) of isoflurane. PRSW is plotted against end diastolic length (EDL). The inset depicts PRSW done at a constant end-diastolic length of 20 mm (PRSW20) and is represented as a percent of control. *Significantly (p < 0.05) different than control; †significantly (p < 0.05) different than 1.5 MAC isoflurane; ‡significantly (p < 0.05) different slope than control. (Reproduced with permission from Pagel PS, Kampine JP, Schmeling WT, Warltier DC: Comparison of end-systolic pressure-length relations and preload recruitable stroke work as indices of myocardial contractility in the conscious and anesthetized, chronically instrumented dog. Anesthesiology 1990; 73: 278.) Cellular and Molecular Biology of Cardiac Muscle Contraction Ultrastructure of the Cardiac Myocyte The heart contracts and relaxes nearly 3 billion times during an average lifetime, based on a heart rate of 70 beats per minute and a life expectancy of 75 years. A review of cardiac myocyte ultrastructure provides important insights into how the heart accomplishes this astonishing performance. The sarcolemma is the external membrane of the cardiac muscle cell. The sarcolemma contains ion channels (e.g., Na+, K+, Ca2+), ion pumps and exchangers (e.g., Na+-K+ ATPase, Ca2+-ATPase, Na+-Ca2+ or -H+ exchangers), G protein-coupled and other receptors (e.g., β1-adrenergic, adenosine, opioid), and transporter enzymes that regulate intracellular ion concentrations, facilitate signal transduction, and provide metabolic substrates required for energy production. Deep invaginations of the sarcolemma, known as transverse (“T”) tubules, penetrate the internal structure of the myocyte at regular intervals, thereby assuring rapid, uniform transmission of the depolarizing impulses that initiate contraction to be simultaneously distributed throughout the cell. Unlike the skeletal muscle cell, the cardiac myocyte is densely packed with mitochondria, which are responsible for generation of the large quantities of high-energy phosphates (e.g., adenosine triphosphate [ATP]) required for the heart's phasic cycle of contraction and relaxation. The fundamental contractile unit of cardiac muscle is the sarcomere. The myofilaments within each sarcomere are arranged in parallel cross-striated bundles of thin (containing actin, tropomyosin, and the troponin complex) and thick (primarily composed of myosin and its supporting proteins) fibers. Sarcomeres are connected in series, thereby producing characteristic shortening and thickening of the long and short axes of each myocyte, respectively, during contraction. Figure 10-6. Schematic illustration of the myosin molecule demonstrating double helix tail, globular heads that form cross bridges with actin during contraction, two pairs of light chains, and “hinges” (cleavage sites of proteolytic enzymes) that divide the molecule into meromyosin fragments (see text). (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 4-1, p 104.) The structure of each sarcomere is described based on observations from light and electron microscopy. The area of overlap of thick and thin fibers characterizes the “A” band. This band lengthens as the sarcomere shortens during contraction. The “I” band represents the region of the sarcomere that contains thin filaments alone, and this band is reduced in width as the cell contracts. Each “I” band is bisected by a “Z” (from the German zuckung [twitch]) line, which delineates the border between two adjacent sarcomeres. Thus, the length of each sarcomere contains a complete “A” band and two one-half “I” band units located between “Z” lines. A central “M” band is also present within the “A” band and is composed of thick filaments spatially constrained in a cross-sectional hexagonal matrix by myosin binding protein C. An extensively intertwined network of sarcoplasmic reticulum (SR) invests each bundle of contractile proteins and functions as a Ca2+ reservoir, thereby assuring homogenous distribution and reuptake of activator Ca2+ throughout the myofilaments during contraction and relaxation, respectively. The subsarcolemmal cisternae of the SR are specialized structures located immediately adjacent to, but not continuous with, the sarcolemmal and transverse tubular membranes and contain large numbers of ryanodine receptors that function as the primary Ca2+ release channel for the SR. The contractile machinery and the mitochondria that power it occupy >80%, whereas the cytosol and nucleus fill <15%, of the total volume of the cardiac myocyte. It is abundantly clear based on this simple observation that contraction and relaxation, and not new protein synthesis, are the predominant functions of the cardiac myocyte. Intercalated discs mechanically connect adjacent myocytes through the fascia adherens and desmosomes, which link actin and other proteins between cells, respectively. The intercalated discs also provide a seamless electrical connection between myocytes via large, nonspecific ion channels known as gap junctions that facilitate intercellular cytosolic diffusion of ions and small molecules. Proteins of the Contractile Apparatus Myosin, actin, tropomyosin, and the three-protein troponin complex compose the six major components of the contractile apparatus. Myosin (molecular weight of approximately 500 kDa; length, 0.17 µm) contains two interwoven chain helices with two globular heads that bind to actin and two additional pairs of light chains. Enzymatic digestion of myosin divides the structure into light (containing the tail section of the complex) and heavy (composed of the globular heads and the light chains) meromyosin. The elongated tail section of the myosin complex functions as the architectural support of the molecule (Fig. 10-6). The globular heads of the myosin dimer contain two “hinges” located at the junction of the distal light chains and the tail helix that play a critical role in myofilament shortening during contraction. These globular structures bind to actin, thereby activating an ATPase that plays a central role in hinge rotation and release of actin during contraction and relaxation, respectively. The maximum velocity of sarcomere shortening has been shown to be dependent on the activity of this actin-activated myosin ATPase. Notably, adult and neonatal atrial and ventricular myocardium contain several different myosin ATPase isoforms that are distinguished by their relative ATPase activity. The myosin molecules are primarily arranged in series along the length of the thick filament, but are abutted “tail-to-tail” in the center of the thick filament. This orientation facilitates shortening of the distance between Z lines during contraction as the thin filaments are drawn progressively toward the center of the sarcomere. The light chains contained within the myosin complex serve either “regulatory” or “essential” roles. Regulatory myosin light chains may favorably modulate myosin-actin interaction through Ca2+-dependent protein kinase phosphorylation, whereas essential light chains serve an as yet undefined obligate function in myosin activity, as their removal denatures the myosin molecule. Discussion of myosin light chain isoforms is beyond the scope of the current chapter, but isoform switches from ventricular to atrial forms have been observed in left ventricular hypertrophy that may contribute to contractile dysfunction.17 In addition to myosin and its binding protein, thick filaments contain titin, a long elastic protein that attaches myosin to the Z lines. Titin has been postulated to be a “length sensor” similar to a bidirectional spring that establishes progressively greater passive restoring forces as sarcomere length approaches its maximum or minimum.18 Compression and stretching of titin occur during decreases and increases in muscle load, thereby resisting further sarcomere shortening and lengthening, respectively. Thus, titin is a third important elastic element (in addition to actin and myosin) that contributes to the stress-strain biomechanical properties of cardiac muscle.19 Figure 10-7. Cross-sectional schematic illustration demonstrating the structural relationship between the troponin-tropomyosin complex and actin under resting conditions (left) and after Ca2+ binding to troponin C (right; see text). (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 4-15, p 117.) Actin is the major component of the thin filament. Actin is a 42-kDa, ovoid-shaped, globular protein (“G” form; 5.5 nm in diameter) that exists in a polymerized filamentous (“F”) form in cardiac muscle. F-actin binds adenosine diphosphate (ADP) and a divalent cation (Ca2+ or Mg2+), but unlike myosin, the molecule does not directly hydrolyze high-energy nucleotides such as ATP. F-actin is wound in double-stranded helical chains of G-actin monomers that resemble two intertwined strands of pearls (each G-actin monomer; Fig. 10-6). A single complete helical revolution of filamentous actin is approximately 77 nm in length and contains 14 G-actin monomers. Actin derives its name from its function as the “activator” of myosin ATPase through its reversible binding with myosin. The hydrolysis of ATP by this actin-myosin complex provides the chemical energy required to produce the conformational changes in the myosin heads that drive the cycle of contraction and relaxation within the sarcomere. Tropomyosin is one of two major inhibitors of actin-myosin interaction. Tropomyosin (length of 40 nm; weight between 68 and 72 kDa) is a rigid double-stranded α-helix protein linked by a single disulfide bond. Human tropomyosin contains both α and β isoforms (34 and 36 kDa, respectively) and may be present as either a homo- or heterodimer.20 Tropomyosin stiffens the thin filament through its position within the longitudinal cleft between intertwined F-actin polymers (Fig. 10-7), but its Ca2+-dependent interaction with troponin complex proteins is the mechanism that links sarcolemmal membrane depolarization to actin-myosin interaction in the cardiac myocyte (excitation-contraction coupling). The thin filaments are anchored to Z lines by cytoskeletal proteins including α- and β-actinin and nebulette.21,22 Figure 10-8. Schematic illustration demonstrating the location of tropomyosin interlaced within the groove formed by two F-actin chains. (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 4-16, p 108.) The troponin proteins serve complementary but distinct roles as critical regulators of the contractile apparatus.23 The troponin complexes are arranged at 40-nm intervals along the length of the thin filament. Troponin C (so named because this molecule binds Ca2+) exists in a highly conserved, single isoform in cardiac muscle. Troponin C is composed of a central nine-turn a-helix separating two globular regions that contain four discrete amino acid sequences capable of binding divalent cations including Ca2+ and Mg2+. Of this quartet of amino acid-cation binding sequences, two (termed sites I and II) are Ca2+-specific, thereby allowing the troponin C molecule to respond to the acute changes in intracellular Ca2+concentration that accompany contraction and relaxation. Troponin I (“inhibitor”) is a 23-kDa protein that exists in a single isoform in cardiac muscle. Troponin I alone weakly prevents the interaction between actin and myosin, but when combined with tropomyosin, the troponin I-tropomyosin complex becomes the major inhibitor of actin-myosin binding. The troponin I molecule contains a serine residue that may be phosphorylated by protein kinase A (PKA) via the intracellular second messenger cAMP, thereby reducing troponin C-Ca2+ binding and enhancing relaxation during administration of β-adrenoceptor agonists (e.g., dobutamine) or phosphodiesterase fraction III inhibitors (e.g., milrinone). Troponin T (so denoted because it binds other troponin molecules and tropomyosin) is the largest of the troponin proteins and exists in four major isoforms in human cardiac muscle. Troponin T anchors the other troponin molecules and may also influence the relative Ca2+ sensitivity of the complex.24 Binding of Ca2+ to troponin C precipitates a series of conformational changes in the troponin-tropomyosin complex that lead to the exposure of the myosin binding site on the actin molecule. During conditions in which intracellular Ca2+ concentration is low (10-7 M; diastole), very little Ca2+ is bound to troponin C, and each tropomyosin molecule is constrained to the outer region of the groove between F-actin filaments by a troponin complex (Fig. 10-8). This structural configuration prevents myosin-actin interaction by effectively blocking cross-bridge formation. Thus, an inhibitory state produced by the troponin-tropomyosin complex exists in cardiac muscle under resting conditions. A 100-fold increase in intracellular Ca2+ concentration (10-5 M; systole) occurs as a consequence of sarcolemmal depolarization, which opens L- and T-type sarcolemmal Ca2+ channels, thereby allowing Ca2+ influx into the myocyte from the extracellular compartment and stimulating Ca2+-dependent Ca2+ release from the SR via its ryanodine receptors. When Ca2+ is bound to troponin C under these conditions, the shape of the troponin C protein becomes elongated and its interactions with troponin I and T are enhanced. These Ca2+-induced allosteric rearrangements in troponin complex structure weaken the interaction between troponin I and actin, allow repositioning of the tropomyosin molecule along the F-actin filaments, and reverse the baseline inhibition of actin-myosin binding by tropomyosin.25 In this way, Ca2+ binding to troponin C may be directly linked to a series of changes in regulatory protein chemical structure that block inhibition of the binding site for myosin on the actin molecule and allow cross-bridge formation and contraction to occur. This antagonism of inhibition is fully reversible, as relaxation is facilitated by dissociation of Ca2+ from troponin C concomitant with rapid restoration of the original conformation of the troponin-tropomyosin complex on F-actin. Most Ca2+ ions are removed from the myofilaments and the cytosol after membrane repolarization by a Ca2+-ATPase located in the SR membrane (sarcoendoplasmic reticulum Ca2+-ATPase, SERCA). This Ca2+ is stored (concentration of approximately 10-3 M) in the SR bound to calsequestrin and calreticulin until the subsequent sarcolemmal depolarization is initiated. The Na+/Ca2+ exchanger and a Ca2+-ATPase located within the sarcolemmal membrane also remove a small quantity of Ca2+, similar to that which originally entered the myocyte from the extracellular space during depolarization. Phospholamban is a small protein (6 kDa) located in the SR membrane that partially inhibits the activity of the dominant form (type 2a) of cardiac SERCA under baseline conditions. However, phosphorylation of this protein by PKA blocks this inhibition and enhances the rate of SERCA uptake of Ca2+ into the SR,26 thereby increasing the rate and extent of relaxation (positive lusitropic effect) and augmenting the amount of Ca2+ stored for the next cycle of contraction (positive inotropic effect). Thus, SERCA activity is regulated by a cAMP-dependent PKA that is responsive to β-adrenoceptor stimulation or phosphodiesterase fraction III inhibition. In addition to PKA-mediated phosphorylation of troponin I that facilitates Ca2+ release from troponin C, these observations explain why positive inotropic drugs such as dobutamine and milrinone also augment relaxation. Myosin-Actin Contraction Biochemistry The biochemistry of cardiac muscle contraction is most often described using a simplified four-component model (Fig. 10-9).27 Binding of ATP with high affinity to the catalytic domain of myosin initiates the series of chemical and mechanical events that cause contraction of the sarcomere to occur. The myosin ATPase enzyme hydrolyzes the ATP molecule into ADP and inorganic phosphate, but these reaction products do not immediately dissociate from myosin. Instead, the ATP hydrolysis products and myosin form an “active” complex that retains the chemical energy released from the reaction as potential energy. In the absence of actin, subsequent dissociation of ADP and phosphate from myosin is the rate-limiting step of myosin ATPase and the muscle remains relaxed. However, the activity of myosin ATPase is markedly accelerated when the myosin-ADP-phosphate complex is bound to actin, and under these circumstances, the chemical energy obtained from ATP hydrolysis becomes directly transferred into mechanical work. Attachment of myosin to its binding site on the actin molecule releases the phosphate anion from the myosin head, thereby producing a molecular conformation within this cross-bridge structure that generates tension in both myofilaments.28 Release of ADP and the stored potential energy from this activated conformation produce rotation of the cross-bridge (“power stroke”) at the hinge point separating the helix tail region from the globular myosin head and its associated light chain proteins. Each cross-bridge rotation generates 3 to 4 × 10-12 newtons of force29 and moves myosin approximately 11 nm along the actin molecule. Completion of myosin head rotation and ADP release does not dissociate the myosin-active complex, but leaves it in a low-energy bound (“rigor”) state. Separation of myosin and actin occurs when a new ATP molecule binds to myosin, and the process is subsequently repeated, provided that energy supply is adequate and the myosin-binding site on actin remains unimpeded by troponin-tropomyosin inhibition. Figure 10-9. Schematic illustration of the actin filaments and its individual monomers and active myosin bindings sites (m; left panel). The myosin head is dissociated from actin by binding with adenosine triphosphate (ATP). Subsequent ATP hydrolysis and release of inorganic phosphate (Pi) “cocks” the head group into a tension-generating configuration. Attachment of the myosin head to actin allows the head to apply tension to the myosin rod and the actin filament. The right panel illustrates calcium binding to troponin C, which causes troponin I to decrease its affinity for actin. As a result in a conformational shift in tropomyosin position (see text), seven sites on actin monomers are revealed. Several factors may affect the efficiency of cross-bridge biochemistry and myocardial contractility independent of autonomic nervous system tone or administration of exogenous vasoactive drugs. There is a direct relationship between myosin ATPase activity and the maximal velocity of unloaded muscle shortening (Vmax), and the normal increase in intracellular Ca2+ concentration (from 10-7 to 10-5 M) that occurs after sarcolemmal depolarization enhances baseline myosin ATPase activity fivefold before it interacts with actin, thereby increasing Vmax. Contractile force depends on sarcomere length immediately before sarcolemmal depolarization. This length-dependent activation (Frank-Starling effect) may be related to an increase in myofilament sensitivity to Ca2+, favorable alterations in spacing between myofilaments, or titin-induced elastic recoil. Abrupt increases in load during contraction (Anrep effect) or those that occur after a prolonged pause between beats (Woodworth phenomenon) causes transient increases in contractile force through a length-dependent activation mechanism. An increase in cardiac muscle stimulation frequency also augments contractile force (treppe phenomenon) via enhanced myofilament Ca2+ sensitivity and greater SR Ca2+ release. Electrical Properties of the Heart The Clinical Electrocardiogram The clinical electrocardiogram (ECG) consists of a regular series of deflections from the isoelectric line. The first deflection of the ECG is the P wave (Einthoven began his depiction of the ECG in the middle of the alphabet). The P wave is a positive deflection that occurs as a consequence of atrial depolarization. The initial electrical event is depolarization of the sinoatrial (SA) node pacemaker cells and is followed almost immediately by progressive depolarization of both atria. The SA node pacemaker activity is not observed on the ECG because the node is too small to generate electrical potential differences large enough to be recorded from the body surface. The duration of the P wave is the time required for depolarization to spread over the atria and may be prolonged by atrial enlargement or a conduction delay. The SA node is located in the wall of the right atrium at the junction of this chamber and the superior vena cava. Propagation of the depolarizing impulse throughout the atria is not uniform, as a slightly higher conduction velocity occurs through the anterior, middle, and posterior internodal pathways between the SA and the AV nodes. Activation and depolarization of the AV node begins during the P wave before depolarization of the atria is completed (Fig. 10-10).7,30,31 The P wave is followed by a brief interval returning to the isoelectric line. The PR interval is the duration between the onset of the P wave and the beginning of ventricular depolarization signified by the onset of the QRS complex (Fig. 10-11). Prolongation of the PR interval usually indicates a conduction delay between atrial and ventricular conduction. After the P wave is complete, the ECG becomes isoelectric because changing potential differences within the heart are no longer recorded at the body surface as a result of the relatively small mass of tissue that continues the depolarization-conduction process. During this apparent “silent” interval between atrial and ventricular depolarization, the wave of depolarization is being conducted through the AV node, AV bundle, right and left bundle branches, and His-Purkinje fiber network. The conduction velocity through the AV node is relatively slow. In contrast, conduction velocity is very rapid in the His-Purkinje system (H in Fig. 10-11), approaching the velocity observed in small nerves. The QRS complex records potentials at the body surface when the wave of depolarization is distributed throughout ventricular myocardium. The QRS complex is much larger in magnitude than the P wave because ventricular mass is greater than the atrial mass. Rapid conduction through the His-Purkinje system spreads the wave of depolarization quickly to the ventricles. Delays in this conduction distal to the AV node most often result from intrinsic myocardial disease (most notably, ischemia) and may have profound consequences on cardiac rhythm and LV contractile synchrony. Figure 10-10. The electrocardiogram (ECG). Major waves (P, QRS, and T) of the ECG are indicated as well as the timing of the activation of some of the key conductive structures. SA, sinoatrial. (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 15-10, p 436.) Figure 10-11. Top: Electrocardiogram recorded from the body surface. Bottom: Intracardiac electrogram. (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 15-9, p 435.) The ST segment is the interval between the end of the QRS complex and the T wave. The ST segment is normally isoelectric because all of the ventricular myocardium is depolarized. The ST segment also reflects the long plateau phase of the cardiac action potential. The injury current of an elevated or depressed ST segment observed during myocardial ischemia or infarction may occur as a result of an abbreviated action potential within the ischemic region or because depolarizing currents propagate more slowly through the ischemic zone. Repolarization of the ventricles generates the T wave, which corresponds to the end of phase 2 and all of phase 3 of the cardiac action potential (see later discussion). The duration of the T wave is considerably longer than the QRS complex because, unlike the rapidly transmitted, nearly homogenous ventricular depolarization, repolarization occurs more slowly and is less synchronous. The QT interval is the duration between the onset of ventricular depolarization (indicated by the QRS complex) and completion of repolarization (as signified by the end of the T wave). The QT interval varies inversely with heart rate, and may precipitate malignant ventricular arrhythmias when shortened or prolonged by administration of vasoactive drugs (e.g., volatile anesthetics) or in the presence of intrinsic cardiac pathology (e.g., prolonged QT syndrome).30,31 Role of Ion Channels The action potentials of individual groups of excitable cardiac myocytes are quite different (Fig. 10-12). The SA and AV nodes and accessory pacemaker cells have unstable, spontaneously depolarizing properties. The resting membrane potential of these cells is not -90 mV, as observed in typical atrial and ventricular myocytes or His-Purkinje fibers. Spontaneous, phase 4 slow depolarization of SA and AV node cells is initiated at membrane potentials between -55 and -66 mV. The SA node, AV node, and the remaining specialized conduction tissue of the heart are all characterized as potential pacemakers, but the SA node is the normal cardiac pacemaker because of its intrinsically faster discharge rate. Cells within the SA node are not homogenous, and some of these pacemaker cells have faster discharge frequencies than others. The resting membrane potential of cardiac pacemaker cells is unstable and displays a slow depolarization of the membrane during diastole (Fig. 10-12). The rate of rise of the action potential from threshold (phase 1) is relatively slow in SA nodal cells compared with atrial and ventricular muscle cells. The magnitude and slope of spontaneous depolarization (also known as automaticity) of SA node cells are important in the regulation of heart rate and depend on the activity of the sympathetic and vagal (parasympathetic) neural innervation. Slowing the rate of depolarization increases the time to reach the threshold potential (TP) and decreases heart rate (SA node rate of discharge; Fig. 10-13). The heart rate may also slow as a result of a shift in threshold potential to a higher level (TP1 to TP2) or a more negative resting potential.2 These effects are usually observed during vagal stimulation via parasympathetic nerve or administration of acetylcholine agonists. In contrast, a sharp rise in the diastolic depolarization of the pacemaker cell (resulting in tachycardia) occurs during stimulation of the cardiac sympathetic nerves or administration of exogenous catecholamines. The SA node pacemaker may be displaced by a latent pacemaker elsewhere in the heart during myocardial ischemia because of primary suppression of the SA node or because of spontaneous discharge of a latent pacemaker at a higher intrinsic rate. When the frequency of excitation is higher in a group of latent pacemakers, the rate of firing of the other pacemakers is suppressed. This process is known as overdrive suppression. Figure 10-12. Cardiac action potentials throughout the conductance system from the sinoatrial node (SA) through the ventricular muscle during one cardiac cycle. Note the automatic pacemaker activity (slow spontaneous depolarization) of the SA and atrioventricular nodal cells and the lack of spontaneous activity of atrial, Purkinje, and ventricular muscle cells. (Reproduced with permission from Lynch C III, Lake CL: Cardiovascular anatomy and physiology, Cardiac Vascular, and Thoracic Anesthesia. Edited by Youngberg JA, Lake CL, Roizen MF, Wilson RS. New York, Churchill Livingstone, 1999, p 87.) The ion channels that are active in the SA node cell membrane during depolarization and repolarization are depicted in Figure 10-14.7 Two decreasing outward currents and two increasing inward currents are observed during depolarization. Pacemaker activity is partly due to decay of the delayed rectifier current (iK, an outward current), which is permissive by allowing other currents to depolarize the pacemaker. An anomalous rectifier current (ik1, a second outward current) also permissively contributes to pacemaker activity. The first inward current is iCa. This slow inward Ca2+ current is primarily responsible for the action potential upstroke in pacemaker cells, and its continuation after initial depolarization contributes to early diastolic depolarization. The inward Na+ current (if) most likely plays an important role in the control of heart rate by the autonomic nervous system. This inward if current occurs through a channel that conducts both Na+ and Ca2+ ions. This “f” or “funny” channel mediates autonomic-dependent modulation of heart rate.33 The inward current if is activated by cAMP. Thus, β1-adrenergic stimulation accelerates, whereas vagal stimulation slows, heart rate by increasing and decreasing, respectively, the intracellular cAMP concentration and the degree of activation of the f channel. The f channel is thought to be responsible for generating spontaneous activity. Figure 10-13. Pacemaker potentials in sinoatrial node illustrating the effect of diastolic depolarization slopes and potentials on heart rate. The action potential begins when the depolarization potential reaches the threshold potential (TP). A slowing of the rate of depolarization from a to b increases the time required to reach the TP, whereas an increase of the TP level (b, c) or a greater resting potential (d) slows the heart rate. (Reproduced with permission from Hoffman BF, Cranefield PF: Electrophysiology of the Heart. New York, McGraw-Hill. 1960, Fig. 4.5, p 57.) Figure 10-14. Changes in four ionic currents responsible for action potential depolarization and repolarization in a sinoatrial nodal pacemaker cell. Two are increasing inward currents (ii and iCa) and two are decreasing outward currents (iK, delayed rectifier and iK1, inward rectifier). (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 14-14, p 417.) Figure 10-15. Membrane potential and current in a voltage-clamped ventricular cell. Note that the rapid and transient influx of Na+ ions induces the rapid depolarization (phase 0); this is followed by a longer inward Ca2+ current that prolongs the plateau potential (phase 1) and then a slow outward K+ current the leads to repolarization (phase 3). Resting potential is phase 4. (Reproduced with permission from Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006, Fig. 14-12, p 415.) Alterations in ion currents in the ventricular myocyte are illustrated in Figure 10-15. The resting membrane potential of the myocyte is -90 mV; this potential controls its Na+ channel. Above this threshold, activation of the Na+ channel produces a sharp increase in inward Na+ current that is primarily responsible for myocyte depolarization (phase O). These Na+channels are rapidly inactivated by depolarization, but their ability to reopen (reactivation) is delayed even after the myocyte is fully repolarized. The inability of Na+ channels to respond to a second stimulus after depolarization occurs as a result of the prolonged plateau of the action potential that prevents membrane potential from returning to the resting levels at which Na+ channels may be reactivated. The rapid depolarization of the myocyte is followed by a brief, rapid repolarization of small magnitude (phase 1) caused by a reduction in Na+ permeability, a transient outward K+ current, and an outward Cl- current. A distinctive feature of ventricular myocardium depolarization is the plateau (phase 2) of the action potential that signifies prolonged stabilization of the myocyte near zero potential (duration ≥100 ms). An inward Ca2+ depolarizing current through Ca2+ conductance channels appears at the beginning of the plateau. This slow inward Ca2+ current is associated with opening of slow Ca2+ channels that are activated at a membrane potential of -50 mV. The Ca2+ current activates and inactivates much more slowly than the Na+ current, thereby providing an inward current that maintains the sarcolemmal membrane in a depolarized state during the plateau phase. Phase 3 of the cardiac action potential corresponds to the T wave of the ECG. Outward rectification and repolarization occur when the membrane passes current most readily in the outward direction. The most important outward rectifying current is carried by K+. Outward rectifying currents cause repolarization because membrane potential in the depolarized cell returns to its resting negative level. The outward ik rectifying current occurs at the end of the plateau phase 3 and is known as the delayed rectifier. The ion channels in ventricular myocardium are energy-dependent and regulated by the activity of the autonomic nervous system.7,34 Neural Innervation of the Heart and Blood Vessels Baroreflex Regulation of Blood Pressure The heart is innervated by the parasympathetic and the sympathetic nervous systems. Parasympathetic innervation arises in the motor nucleus of the vagus and the nucleus ambiguous in the medulla.35 As observed with other parasympathetic nerves, long preganglionic fibers synapse with short postganglionic fibers within the heart. The postganglionic fibers innervate pacemaker cells and conducting pathways. When activated, these fibers produce slowing of pacemaker cells and reduce conduction velocity. Aside from their effects on heart rate, excitability, and conduction, parasympathetic fibers do not substantially influence contractility.36 Acetylcholine is the neurotransmitter responsible for parasympathetic nervous system activation through nicotinic and muscarinic receptors at the pre- and postganglionic synapses, respectively, located on the postganglionic neuron and in SA and AV node pacemaker cells and the condition system. The sympathetic innervation of the heart arises from cells in the rostral ventrolateral medulla with descending nerve fibers emerging from the intermediolateral cell column of the spinal cord at C5-T6.37,38 These preganglionic fibers synapse primarily with postganglionic sympathetic nerves within the stellate ganglion, but may also synapse within a few ganglia located closer to the heart. Ganglionic transmission is mediated by preganglionic release of acetylcholine and binding of acetylcholine with nicotinic postganglionic receptors. Activation of postganglionic sympathetic nerves innervating the heart results in release of norepinephrine. This endogenous catecholamine then stimulates β1-adrenoceptors in pacemaker and conduction cells as well as atrial and ventricular myocardium. Activation of cardiac sympathetic fibers produces positive chronotropic, dromotropic, inotropic, and lusitropic effects (i.e., increases in heart rate, conduction velocity, myocardial contractility, and the rate of myofibrillar relaxation). The afferent innervation of the heart consists of mechanoreceptors with primarily vagal afferent pathways and receptors with spinal afferent pathways. The mechanoreceptors with vagal afferents are located in ventricular, and to a lesser extent, atrial myocytes.36 Activation of the ventricular receptors by nociception or stretch, such as may occur in response to a sudden increase in ventricular volume, causes a vagal depressor response with a decrease in heart rate and mean arterial pressure (the Bezold-Jarisch reflex).39 The reduction in heart rate is mediated by an increase in cardiac vagal efferent activity, in which the decrease in mean arterial pressure results from withdrawal of sympathetic tone in arterial resistance and venous capacitance vessels. The spinal afferents traverse the sympathetic nerves and serve as nociceptors and stretch receptors. Activation of these receptors produces a transient increase in heart rate and mean arterial pressure. Spinal afferent-mediated nociceptors may be stimulated by events such as acute myocardial ischemia. Both the cardiac vagal and spinal afferent fibers project centrally to the nucleus tractus solitarius, similar to aortic and carotid baroreceptors and chemoreceptors. The majority of the peripheral vascular system derives its sympathetic innervation from the thoracolumbar section of the spinal cord. In contrast, the sympathetic innervation of the coronary vasculature, lung, and cerebral circulation is derived from the superior cervical and stellate ganglia. α-Adrenoceptors mediate most sympathetic nerve vascular responses, but β-adrenoceptors uniquely modulate sympathetic innervation of the adrenal gland, thereby causing the release of epinephrine and norepinephrine. Sympathetic innervation of small arterioles and metarterioles produces vasoconstriction, thereby increasing systemic vascular resistance and mean arterial pressure. Sympathetic innervation of small veins and venules causes constriction of these vessels. This action reduces the volume of blood stored in capacitance vessels, transiently increases preload, and subsequently decreases blood flow in the splanchnic circulation and, to a lesser extent, the lower extremities. Thus, activation of peripheral sympathetic nerves increases mean arterial pressure by arterial vasoconstriction combined with an increase in preload due to a reduction in venous capacitance while simultaneously increasing heart rate and myocardial contractility. These effects are critical compensatory responses to hypovolemia resulting from acute blood loss. α- and β-adrenoceptor antagonists may attenuate sympathetically mediated cardiovascular effects. Short-duration regulation of mean arterial pressure occurs through the arterial, and to a lesser extent, intracardiac baroreceptors. Arterial baroreceptors are located at the bifurcation of the common carotid arteries and in the aortic arch. These receptors, particularly those in the carotid arteries, display tonic activity under normal conditions. An acute rise in arterial pressure activates baroreceptors through stretch-sensitive Na+ channels. Receptor activation increases afferent nerve traffic in the carotid sinus nerve, which is centrally transmitted by a unique branch of the glossopharyngeal nerve that first synapses in the nucleus tractus solitarius. The postsynaptic neurons activate the vagal motor nucleus and nucleus ambiguous, thereby causing a reduction in heart rate.38,40,41 The postsynaptic baroreceptor neurons also synapse with γ-aminobutyric acid–mediated inhibitory neurons in the caudal ventrolateral medulla that innervate medullary sympathetic neurons and produce a decrease in sympathetic nervous system activity via the rostral ventrolateral medulla.38,41,42 The resultant effect is a decrease in cardiac output and systemic vascular resistance concomitant with an increase in vascular capacitance. The aortic baroreceptors and cardiac vagal receptors produce similar hemodynamic effects. Cardiac receptors have been theorized to be responsible for radiocontrast-induced bradycardia and hypotension during coronary angiography. Low-pressure baroreceptors located in the vena cavae, right atrium, RV, and pulmonary vein-left atrial junction respond to decreases in right atrial filling pressure by activating sympathetic tone in the arterial vasculature. Interestingly, baroreceptor activation does not influence all peripheral vascular beds. For example, the cutaneous circulation does not appear to respond to baroreceptor stimulation or inhibition. Instead, the cutaneous circulation is primarily affected by peripheral and central thermoregulatory mechanisms that produce vasoconstriction or vasodilation in a cold or warm environment to prevent or facilitate heat loss, respectively. Thermoreceptor-mediated central nervous system responses originate in the supraoptic region of the hypothalamus. Other Cardiovascular Reflexes Other reflexogenic areas within the cardiovascular system regulate hemodynamics through arterial chemoreceptors and the central nervous system response to ischemia. High-pressure sensitive receptors in the LV and low-pressure responsive elements in the atria and RV consist of stretch-induced mechanoreceptors that respond to pressure or volume changes. Three sets of receptors have been identified. First, discrete receptors in the endocardium are located at the junctions of the vena cavae with the right atrium and the pulmonary veins with the left atrium. These receptors activate myelinated vagal afferent fibers that project to the nucleus tractus solitarius and increase sympathetic nerve activity to the SA node but not to the ventricles, thereby increasing heart rate but not contractility. Distention of these mechanoreceptors also increases renal excretion of free water by inhibition of antidiuretic hormone secretion from the posterior lobe of the pituitary gland.43 It appears highly likely that the Bainbridge reflex may be mediated by distention of these mechanoreceptors.4 Second, a diffuse receptor network is distributed throughout the cardiac chambers that projects via unmyelinated vagal afferent neurons to the nucleus tractus solitarius. These receptors behave like the carotid and aortic mechanoreceptors and produce a vasodepressor response consisting of vagus activation concomitant with inhibition of sympathetic innervation of the heart and peripheral circulation. These actions cause reductions in heart rate, inotropic state, and systemic vascular resistance concomitant with a simultaneous increase in venous capacitance. This intracardiac receptor network plays a relatively minor role in the normal physiological control of the cardiovascular system compared with the arterial baroreceptors. Lastly, sympathetic afferent fibers are activated by receptors that respond rhythmically during the cardiac cycle. Some of these neurons convey visceral pain sensations and may be activated during myocardial ischemia. Stimulation of these fibers produces a transient increase in heart rate and mean arterial pressure by activating central nervous system sympathetic efferent fibers innervating the heart and peripheral circulation.4,44,45 The arterial baroreceptors located in the carotid sinus and aortic arch play the major role in cardiovascular homeostasis. Arterial baroreceptor reflex-induced regulation of heart rate is inhibited by volatile and many intravenous anesthetics.32,46 This inhibition of high-pressure baroreceptor reflexes by anesthetics involves several discrete sites including sympathetic ganglionic transmission, end-organ responses, and central nervous system pathways, and appears to be especially important in short-term regulation of arterial pressure.5,47 These reflexes demonstrate accommodation or adaptation to the level of arterial blood pressure and may be reset in patients with hypertension. Cardiopulmonary reflexes also appear to be inhibited by potent inhaled anesthetics and have a crucial role in short-term regulation of arterial pressure, primarily by modulating arterial baroreceptor reflex activity.32 The peripheral chemoreceptors located in the carotid and aortic bodies are sensitive to increases in arterial CO2 tension and decreases in pH. The carotid body receptors project centrally through Herring's nerve, which travels with the glossopharyngeal nerve to the nucleus tractus solitarius. In contrast, the aortic body receptors have vagal afferent fibers that also project to the nucleus tractus solitarius. The carotid body reflex appears to be more important than its aortic counterpart in the regulation of respiration in humans. Activation of the carotid and aortic chemoreceptors produces an increase in respiratory drive manifested by an increase in respiratory rate, tidal volume, and minute ventilation. These chemoreceptors may also cause activation of sympathetic nervous system fibers in the heart and peripheral circulation, thereby increasing heart rate and mean arterial pressure. The peripheral chemoreceptor reflex is an important protective mechanism in response to pathophysiological conditions including high-altitude hypoxia, chronic lung disease, and profound hypovolemia. In addition to the baroreceptor responses, severe hypotension also causes arterial vaso- and venoconstriction in response to brainstem hypoxia. This central nervous system ischemic response may be activated when mean arterial pressure is reduced below 50 mm Hg. An analogous mechanism may also mediate the Cushing reflex. This sympathetically mediated hypertension occurs in response to an acute elevation of intracranial pressure and a consequent reduction in cerebral perfusion pressure. Under these circumstances, arterial pressure rises progressively in an effort to exceed elevated intracranial pressure and maintain cerebral perfusion and oxygen delivery. The Cushing reflex may also be activated by brainstem compression, acute traumatic brain injury, or intracranial hemorrhage resulting from aneurysm rupture. In animals, the diving reflex redistributes blood flow and oxygen delivery to the heart and brain as a survival defense of the submerged vertebrate against asphyxia. This reflex enables whales to remain submerged for as long as 2 hours. The residual counterpart of the diving reflex in humans may be activated by immersion of the face in cold water, which produces a comparable, albeit less intense, diving response characterized by rapid reduction in heart rate and cutaneous and skeletal muscle blood flow concomitant with an increase in arterial pressure. Stimulation of receptors in the face or upper airway initiates the diving reflex and causes apnea by inhibiting the medullary respiratory center. The hyperventilation stimuli of hypoxemia and hypercapnia are also suppressed. The cardiovascular limbs of the chemoreceptor reflex are partially retained, resulting in generalized systemic vasoconstriction, except in the coronary and cerebral circulations. The diving reflex response is distinctly different from the cold-pressor reflex. This latter reflex is activated by complete immersion of one hand in ice water. The cold-pressor reflex increases heart rate and mean arterial pressure by stimulating both pain and cold receptors. A cold environment directly causes vasoconstriction to prevent heat loss and also stimulates reflex central nervous system thermoregulatory receptors in the hypothalamic preoptic region. This latter effect produces sympathetically mediated vasoconstriction. A warm, ambient environment or an increase in metabolically induced heat production produces an opposite response to dissipate accumulated heat. Figure 10-16. Anterior view (left) shows right coronary and left anterior descending arteries. Posterior view (right) shows left circumflex and posterior descending arteries. Note that the right coronary or left circumflex artery may form the latter artery. The anterior cardiac veins from the right ventricle and the coronary sinus, which drain primarily the left ventricle, empty into the right atrium. (Reproduced with permission from Smith JJ, Kampine JP: Circulatory Physiology—The Essentials, 3rd edition. Baltimore, Williams & Wilkins, 1990, Fig. 3-1, p 32.) Somatic pain increases heart rate and mean arterial pressure by activation of sympathetic efferent nerves. In contrast, visceral pain or distention of a hollow viscus (e.g., small intestine, bladder) may produce reflex vagal bradycardia and hypotension. The oculocardiac reflex is activated by pressure on the ocular globe and causes pronounced bradycardia and hypotension by activation of vagal nerve fibers innervating the SA node. The Valsalva maneuver consists of forced expiration against a closed glottis. This maneuver reduces venous return to the right heart, decreases cardiac output and mean arterial pressure, and increases heart rate. The reflex tachycardia occurs because of reduced activity of arterial baroreceptors and LV mechanoreceptors. Release of the forced expiration by glottic opening acutely increases venous return, cardiac output, and mean arterial pressure while simultaneously causing reflex bradycardia mediated by vagal innervation of the SA node triggered by the arterial baroreceptors. Anatomy of the Coronary Arterial and Venous Systems The heart is the only organ that furnishes its own blood supply. The left main and right coronary arteries arise from the aorta behind the left and right aortic valve leaflets (Fig. 10-16). The coronary ostia remain patent throughout systole because eddy currents prevent the valve leaflets from contacting the aortic walls. The left main coronary artery divides almost immediately into the left anterior descending (LAD) artery and left circumflex coronary artery (LCCA). The LAD further divides into several branches along the anterior interventricular groove toward the apex of the heart where they supply the anterior wall of the LV and the anterior two thirds of the interventricular septum (Fig. 10-16). The LCCA marks a pathway along the base of the LV within the coronary sulcus and terminates in the left posterior descending branch. The LCCA supplies the LV lateral wall and part of the LV posterior wall. The right coronary artery (RCA) courses along the AV groove toward the right chambers of the heart and frequently extends along the posterior interventricular sulcus to give rise to the right posterior descending branch (Fig. 10-16). The RCA supplies the anterior and posterior walls of the RV except for the apex (supplied by the LAD), the right atrium including the SA node, the upper half of the atrial septum, the posterior third of the interventricular septum, the inferior wall of the LV, the AV node, and the posterior base of the LV. A branch of the LCCA occasionally supplies the SA node. Because either the RCA or the LCCA may supply the posterior descending coronary artery, the coronary circulation is described as right or left dominant, respectively, based on the source of this vessel's blood supply. The proximal branches of the RCA, LCCA, and LAD are located on the epicardial surface of the heart and give rise to multiple intramural vessels that penetrate perpendicularly or obliquely deep into the ventricular walls. Except for the thin tissue layer on the endocardial surface, the nutritive blood supply is almost entirely derived from these major coronary arteries. The penetrating branches divide into dense capillary networks located roughly along the courses of the myocardial bundles. Arterial branches with diameters between 50 and 500 µm form interconnecting anastomoses throughout the endocardium of the ventricular walls (Fig. 10-17, A and B). Another network of subendocardial vessels between 100 and 200 µm in diameter forms a plexus of deep anastomoses. A coronary collateral circulation may also arise from different branches of the same coronary artery or from branches of two different coronary arteries. Flow through such coronary collaterals is usually negligible because the driving pressure at the two ends of the anastomoses is nearly equal. However, if the artery supplying one branch of this collateral circulation becomes severely stenotic or occluded, the large pressure reduction will divert blood flow through the patent artery and into the distribution of the occluded artery through these collateral vessels. Thus, the coronary collateral circulation may be especially important to patients with coronary artery disease.48,49,50 Most of the coronary venous system remains unnamed with the exception of the great cardiac vein (that runs along the AV groove and the LAD), the anterior cardiac vein (located with the RCA), and the middle cardiac vein (associated with the posterior descending branch of the RCA; Fig. 10-16). Thus, the main coronary venous drainage tends to retrace the course of the major coronary arteries along the AV and interventricular grooves. In general, there are two coronary veins located along either side of each coronary arterial branch. The coronary veins converge and terminate in the coronary sinus, which empties into the posterior aspect of the right atrium. Approximately 85% of the total coronary blood flow to the LV drains into the coronary sinus. The remaining blood flow empties directly into the atrial and ventricular cavities by the thebesian veins. The RV veins drain into the anterior cardiac veins; these empty individually into the right atrium just above the tricuspid valve. The coronary capillary network has an organizational structure that is similar to that observed in other tissue beds. Myocardium has a very high density of capillary blood vessels to myofibrils, approximately 1:1 (Fig. 10-18); this is because of the exceptionally high metabolic demand of the heart. On average, adjacent capillaries are separated by the diameter of approximately one myocyte. The distribution of capillaries is quite uniform and ranges between 3,000 and 4,000/mm2 of tissue. Interestingly, capillary density is reduced in the interventricular septum and AV nodal tissue, and this observation may explain why the specialized conducting system is more vulnerable to ischemia than the myocardium itself. As in other capillary beds, coronary capillaries are the sites for exchange of O2, CO2, and for the movement of larger molecules across the endothelial cell lining, where it is devoid of vascular smooth muscle. Figure 10-17. A. Diagram of the minute arterial-to-arterial and venous-to-venous anastomoses of the coronary arterial system, which allows diversion of flow if one distribution becomes blocked. (Reproduced with permission from Guyton AC, Hall JE: Human Physiology and Mechanisms of Disease, 6th edition. Philadelphia, WB Saunders, 1997, Fig. 18-4, pp 185.) B. Diagram of the epicardial coronary vessels lying on the cardiac muscle surface, the penetrating deep vessels, and the subendocardial arterial plexus connecting the deep vessels. (Reproduced with permission from Guyton AC: Textbook of Medical Physiology, 6th edition. Philadelphia, WB Saunders, 1997, Fig. 25-3, p 299.) Mechanics of Coronary Blood Flow Blood supply to the LV is directly dependent on the difference between the aortic pressure and LV end-diastolic pressure (coronary perfusion pressure) and inversely related to the vascular resistance to flow, which varies to the fourth power of the radius of the vessel (Poiseuille's law). Two other determinants of coronary flow are vessel length and viscosity of the blood, but these factors are generally constant. Resting coronary blood flow in the adult is approximately 250 mL/min (1 mL/g), representing approximately 5% of cardiac output. The changes in aortic pressure and the impedance to flow due to physical compression of the intramural coronary arteries during the contraction-relaxation cycle (Fig. 10-4) govern the pulsatile pattern of coronary flow in the LV. Aortic pressure is slightly less than LV pressure during systole. As a result, blood flow in the LV subendocardium occurs only during diastole (Fig. 10-19). Overall coronary flow does not cease completely during the early part of systole because of this extravascular compression, but most of the flow occurs during diastole when impedance to flow is minimal and aortic pressure remains sufficient to maintain adequate coronary perfusion pressure. Figure 10-18. Diagram of an electron micrograph of cardiac muscle showing large numbers of mitochondria and the intercalated disks with nexi (gap junction), transverse tubules, and longitudinal tubules surrounding capillary endothelium. (Reproduced with permission from Berne RM, Levy MN: Chapter 3: Cardiovascular Physiology, 8th edition. St. Louis, CV Mosby, 2000, Fig. 3-1, p 56.) During systole, LV subendocardium is exposed to a higher pressure than the subepicardial layer. Indeed, the systolic intraventricular pressure may be higher than the peak LV systolic pressure. Because of these differences in tissue pressure, the subendocardial layer is more susceptible to ischemia in the presence of coronary artery disease, pressure-overload hypertrophy, or pronounced tachycardia concomitant with compromised regional myocardial perfusion flow, a greater intraventricular-aortic pressure gradient, or reduced total diastolic flow, respectively. Coronary blood flow is also compromised when aortic diastolic pressure is reduced (e.g., severe aortic insufficiency), and this observation may also adversely affect perfusion, particularly in the presence of a critical coronary stenosis.51 Elevated LV end-diastolic pressure, as observed during acute heart failure, also reduces coronary blood flow because of decreased coronary perfusion pressure. In contrast to left coronary blood flow, RCA flow is continuous throughout the cardiac cycle because the lower pressure in the RV compared with the LV causes substantially less extravascular compression (Fig. 10-19). Coronary sinus (venous) blood flow is maximal during late systole because of the extravascular compression and the low right atrial pressure. Figure 10-19. Schematic representation of blood flow in the left and right coronary arteries during phases of the cardiac cycle. Note that most left coronary flow occurs during diastole while right coronary flow (and coronary sinus flow) occurs mostly during late systole and early diastole. (Reproduced with permission from Berne RM, Levy MN: Chapter 10: Cardiovascular Physiology, 8th edition. St. Louis, CV Mosby, 2000, Fig. 10-3, p 231.) Regulation of Coronary Blood Flow The two major determinants of coronary blood flow (perfusion pressure and vascular resistance) vary substantially during the cardiac cycle (Fig. 10-4). Coronary perfusion pressure certainly varies with changes in aortic, intramyocardial, and coronary venous pressures during systole and diastole, but the major factor that regulates coronary blood flow is the variable resistance produced by coronary vascular smooth muscle. Sympathetic nervous system innervation modulates the contractile state of coronary vascular smooth muscle. In addition, smooth muscle tone is affected by stretch of the muscle (termed the myogenic factor). However, metabolic factors are the major physiological determinants of coronary vascular tone and, hence, myocardial perfusion. The ratio of epicardial to endocardial blood flow ratio remains near 1.0 throughout the cardiac cycle despite systolic compressive forces exerted on the subendocardium. The more pronounced resistance to flow in the subendocardium is offset by β-adrenoceptor–mediated vasodilation and by local metabolic autocrine factors (e.g., adenosine during hypoxia) produced by the myocardium itself. The relative maintenance of subendocardial blood flow may also be related to the extensive number of redundant arteriolar and capillary anastomoses in the subendocardium.1 Oxygen Delivery and Demand The heart normally extracts between 75 and 80% of arterial O2 content, by far the greatest O2 extraction of all organs. The majority of O2 demand is derived from the development of LV pressure during isovolumic contraction. Oxygen consumption is also affected by the rate of LV pressure development (dP/dt) and the diameter of the LV (Laplace's law). An increase in myocardial contractility enhances O2 consumption, but heart rate is the primarily determinant of O2 consumption. Cardiac O2 extraction is near maximal under resting conditions and cannot be substantially increased during exercise. Thus, the primary mechanism by which myocardium meets its O2 demand is through enhanced O2 delivery, which is proportional to coronary blood flow at constant hemoglobin concentration. Coronary blood flow and O2 consumption increase four- to fivefold during strenuous physical exercise. The difference between maximal and resting coronary blood flow is known as coronary reserve. Myocardial O2 consumption is a major determinant of coronary blood flow. For example, coronary vascular resistance is greater in the rested, perfused heart than in the contracting heart, indicating that coronary blood flow increases in response to a higher rate of O2consumption. The mechanism(s) responsible for the correlation between myocardial work, O2 consumption, and coronary vessel dilatation has yet to be precisely determined. In addition to metabolically induced vasodilation, the factors responsible for coronary autoregulation (maintenance of coronary blood flow with a change in perfusion pressure) and reactive hyperemia (the several-fold increase in blood flow above baseline after a brief period of ischemia) are also not well understood. Despite decades of intense research into the mediators of local metabolic coronary vasodilation, surprisingly little is known about the details of this phenomenon. To date, it has been established that metabolic coronary vasodilation is at least partly the result of activation of the sympathetic nerves to the heart and coronary vasculature during an increase in heart rate and myocardial contractility. Sympathetic nerve activation produces a feed-forward β-adrenoceptor–induced vasodilation, primarily of small coronary arterioles. This feed-forward mechanism operates without an error signal, indicating that there is a direct and apparently unregulated relationship between heart rate and inotropic state and the activation of β-adrenoceptor-mediated vasodilation.49,50,52 There also appears to be a feed-forward, sympathetically mediated, α-adrenoceptor–induced vasoconstriction in larger coronary arteries during exercise. This vasoconstriction occurs upstream from coronary small coronary arterioles and serves two important functions: reduction of vascular compliance and attenuation of systolic minus diastolic flow oscillations during the cardiac cycle. These actions assist in the preservation of blood flow to the more vulnerable LV endocardium when heart rate, contractility, and O2 consumption are elevated. Interestingly, cardiac parasympathetic nerves have a prominent role in regulating heart rate, but these nerves appear to have a negligible direct effect on the regulation of coronary blood flow. The conclusions about sympathetic nervous system control of the coronary circulation are based on alterations in the slope of the O2 consumption-coronary venous O2 tension relation during graded exercise in the presence of exogenous α- or β-adrenoceptor blockade (Fig. 10-20). The current evidence implicating the β-adrenoceptor in coronary vasodilation accounts for only about one fourth of the total coronary vasodilation observed during exercise-induced hyperemia.53 These data suggest that the other three fourths of coronary vasodilation during exercise may be produced by as yet undefined local metabolic factors that act on coronary vascular smooth muscle with or without the influence of endothelium. Many metabolic factors have been proposed to individually or collectively modulate coronary flow at the arterial or capillary level, including adenosine, nitric oxide, arterial oxygen or CO2 tension, pH, osmolarity, K+, Ca2+, and prostaglandins. Many of these factors exert predictable direct effects. For example, hypoxia or ischemia decreases arterial oxygen tension and pH and increases CO2 tension, adenosine, K+, and Ca2+ concentrations, and serum osmolarity. Many of these changes may indeed increase coronary blood flow, but none appear to be crucial determinants of vasodilation during exercise. For example, adenosine receptor blockade does not alter coronary blood flow under resting conditions or during exercise. Similarly, inhibition of nitric oxide production or ATP-sensitive K+ (KATP) channels also does not alter the O2 consumption-coronary venous O2 slope during graded exercise. Nevertheless, nitric oxide and KATP channels have been shown to regulate the balance between O2 supply and demand under resting conditions. There is very strong evidence however, that adenosine released during hypoxia or ischemia causes coronary vasodilation and that this effect is mediated by activation of KATPchannels. Adenosine and KATP channels have also been implicated during reactive hyperemia after ischemia, but these mediators do not appear to be required for coronary autoregulation. Moreover, the KATP channel probably maintains a lower vascular smooth muscle tone and thus, a higher basal coronary flow during resting conditions. While not acting as a local metabolic vasodilator, nitric oxide may react to increased downstream arterial dilation by dilating larger, upstream epicardial coronary arteries to prevent excessive sheer stress on coronary endothelial cells. Myocardial Ischemia and Infarction Ischemic heart disease remains the leading cause of death in the United States. Global ischemia results from insufficient total coronary blood flow for the overall metabolic needs of the heart.54,55 Regional ischemia results from insufficient coronary blood flow to a region of the heart supplied by its vascular limb. A large, acute coronary artery occlusion produces acute myocardial ischemia and often contributes to the development of a malignant ventricular arrhythmia because blood flow through coronary collaterals fails to provide sufficient perfusion to the ischemic zone.49,51 Thus, many patients with acute coronary syndrome succumb to sudden cardiac death before or during the evolution of a myocardial infarction. If the coronary artery occlusion develops more slowly, collateral formation in the watershed region may reduce the degree of myocardial damage associated with acute coronary occlusion. New collateral development (known asvasculogenesis) into the occluded vascular bed will result in the independence of this region from its original blood supply. Figure 10-20. Coronary venous oxygen (O2) tension at rest and during three levels of exercise plotted as a function of myocardial O2 consumption with individual regression lines for a blockade alone and with β blockade. The steep slope of combined α + β blockade indicates a modest match by local metabolic factors in the absence of adrenergic mechanisms. The differences in slopes between α + β blockade and α blockade demonstrates β-adrenergic–mediated coronary vasodilation, whereas the difference in slopes between β blockade and control demonstrates α–mediated coronary vasoconstriction. Note that β-adrenergic vasodilation accounts for only about 25% of the increase in coronary flow during exercise. (Reproduced with permission from Gorman MW, Tune JD, Richmond MW, Feigl EO: Feedforward sympathetic coronary vasodilation in exercising dogs. J Appl Physiol 2000; 89: 1892.) An atherosclerotic plaque is the most frequent cause of obstructed blood flow in large, epicardial coronary artery vessels.56 The most common site for development of an atherosclerotic plaque is the first several centimeters of the major and coronary arteries and their primary branches. The position of atherosclerotic plaques facilitates their palliation by coronary artery bypass graft surgery.57 Atherosclerotic plaques typically develop very slowly, eventually protruding into the vessel and partially or completely blocking flow. The atherosclerotic plaque may also precipitate thrombus formation, which more rapidly occludes the coronary artery. A thrombus usually develops when the plaque has broken through the vascular intima, thereby exposing vascular smooth muscle or adventitia to clotting factors and platelets contained in blood. When fibrin and platelets begin to be deposited, blood cells become entrapped and form a thrombus that grows rapidly until it produces a critical stenosis or complete occlusion of the coronary artery. The thrombus may also embolize by detaching from its original site of formation and flow to a more peripheral branch of the coronary arterial bed. Atherosclerotic plaques are composed of cholesterol and other lipids that become deposited beneath the intima and fibrous tissue, which also frequently becomes calcified. These calcium deposits are located predominantly at the junction of the intimal and medial layers of the blood vessel. An acute occlusion of a major epicardial coronary artery causes almost immediate, maximal dilation of existing small collateral vessels supplying blood flow to the ischemic zone. Unfortunately, blood flow through these minute collaterals is generally insufficient to nourish all of the myocardium that they supply. Collateral perfusion through these anastomoses temporally increases and may double within 24 hours after acute coronary occlusion. Eventually, the affected myocardium will be supplied by a normal quantity of blood flow, albeit from a different source. During the gradual development of an atherosclerotic plaque, collateral vessels may develop at a rate similar to, and thereby compensate for, the slow occlusion of the vessel lumen. This redistribution of myocardial blood flow from a partially occluded to a collateral vascular supply may prevent an acute episode of ischemia when the original coronary artery becomes occluded. Only when the atherosclerotic process develops more rapidly than the formation of an adequate collateral blood supply will the O2demand exceed delivery and produce myocardial dysfunction. This type of ischemic cardiomyopathy is the most common cause of heart failure. Myocardial necrosis and apoptosis (programmed cell death) occur as a consequence of ischemia and infarction. However, cellular demise usually will not occur in a region unless coronary blood flow falls below 65% of resting values. Myocytes in this region may be viable, but their contractile ability may be severely impaired because of the lack of O2 and nutrients. Critically stenotic atherosclerotic plaques may produce a pressure gradient across the stenosis and substantially reduce the perfusion pressure in distal branches of the affected vessel. Such gradients are especially important when stenoses occur in coronary arteries of smaller caliber. There may be compensatory vasodilation of the coronary distal bed, but progressive diminution of distal blood flow may occur despite this response. Myocardial infarction may also occur without evidence of major coronary thromboses, emboli, or stenosis. This form of infarction is caused by excessive metabolic demands resulting from severe LV hypertrophy (e.g., critical aortic stenosis) or vasoactive drug ingestion (e.g., amphetamines, cocaine) or may also result from coronary artery vasospasm. Either of these mechanisms may lead to ischemia by adversely affecting myocardial O2 supply-demand relations. Clearly, the presence of coronary stenoses that would otherwise be asymptomatic (<70%) may exacerbate O2 demand-mediated myocardial ischemia. Such causes for myocardial infarction are relatively uncommon, and coronary artery disease remains the primary cause of transmural necrosis. Subendocardial infarction may have a different etiology than the transmural infarction caused by an acute coronary occlusion. Subendocardial infarction may occur when coronary perfusion pressure is adversely reduced by decline in diastolic aortic pressure or increases in LV end-diastolic pressure. Thus, patients with severe aortic insufficiency or end-stage heart failure may be especially prone to subendocardial injury. Along with the severity of coronary artery stenosis, the metabolic activity of the heart during ischemia is a critical factor in determining the extent of cell death. If an area of the heart has reduced blood supply due to ischemia, the region distal to this coronary stenosis is maximally vasodilated, and an increase in O2 demand causes vasodilation of adjacent coronary vessels that supply surrounding normal myocardium. This metabolically induced vasodilation may inadvertently redistribute blood flow away from the ischemic zone through coronary collateral vessels. This phenomenon is known as coronary steal.58,59 Despite original arguments to the contrary, most experimental and clinical evidence collected to date indicates that volatile anesthetics do not cause coronary steal unless profound hypotension (<50 mm Hg) is present. Volatile anesthetics are not potent vasodilators, unlike drugs such as adenosine and sodium nitroprusside that are known to produce coronary steal. A potentially lethal complication of acute coronary occlusion is the development of malignant ventricular arrhythmias (e.g., ventricular tachycardia, fibrillation). Ventricular arrhythmias are most likely to occur during the first 10 minutes after an acute coronary occlusion, especially if the coronary blood flow to the conduction system becomes ischemic. Myocytes distal to occluded coronary artery may become electrically dysfunctional and fail to temporally repolarize with surrounding normal myocardium. This repolarization dyssynchrony is a frequent cause of arrhythmogenesis during acute myocardial ischemia. Compensatory activation of the sympathetic nervous system in response to marked reductions in cardiac output may also contribute to the development of ventricular arrhythmias. Left ventricular dilatation or formation of an LV aneurysm late after myocardial infarction may also provide a substrate for arrhythmogenesis by increasing the duration of impulse conduction and creating abnormal conduction pathways around the infarcted zone. These consequences of infarction may predispose to circuitous electrical activity and result in an impulse re-entering a section of the myocardium that is still recovering from its refractory period, thereby initiating an abnormal subsequent cycle of excitation and reentry. A central zone of myocardial necrosis develops within 1 hour after acute coronary artery occlusion, which is eventually replaced by scar as the infarcted myocardium heals. A border zone characterized by profoundly reduced contractility due to inadequate coronary collateral perfusion surrounds this central necrotic zone. Some of this border zone also develops scar tissue; other regions surrounding the central necrotic region hypertrophy as a compensatory response to increased workload. This postinfarction ventricular hypertrophy serves to maintain cardiac output, but may also contribute to the late development of heart failure as a result of progressive diastolic dysfunction.1,50,52,60 Comparison with the Systemic Circulation The pulmonary circulation receives the blood pumped by the RV. Total pulmonary blood flow is equivalent to cardiac output. There are major differences in hemodynamics between the systemic and pulmonary circulations (Fig. 10-21).61 There is a greater decrease in mean pressure across systemic arteries to arterioles compared with vessels of similar caliber in the pulmonary circulation. The precapillary and capillary vessels of the pulmonary vasculature are located in close proximity to the alveolar membranes, thereby facilitating gas exchange. The lung is richly innervated by the parasympathetic and sympathetic nervous system, but the dominant effect of the autonomic nervous system occurs primarily at the level of alveolar and bronchial smooth muscle. Vagal innervation of muscarinic receptors in airway smooth muscle produces bronchoconstriction and is an important contributing factor to bronchospasm in atopic pulmonary disease, pneumonia, and inhalation of noxious substances. The sympathetic innervation of the lung is derived from upper thoracic sympathetic fibers that innervate both airway and pulmonary vascular smooth muscle. Sympathetic stimulation of airway smooth muscle produces bronchodilation by activation of β2-adrenoceptors. The sympathetic innervation of the pulmonary vascular system provides a physiological response to gravitational effects on the intrapulmonary distribution of blood flow and partially counteracts alterations in regional ventilation/perfusion (V/Q) ratio differences produced by such gravitational forces.62 Regional Differences in Perfusion and V/Q Matching The V/Q distribution within the lung in an upright position varies because of the effect of gravity (Fig. 10-22). In the upper lung (zone 1), V/Q ratio is >1.0, indicating that alveolar ventilation occurs in excess of pulmonary blood flow. Because part of this zone is ventilated but not perfused, zone 1 contributes to dead space ventilation. In the middle region of the lung (zone 2), the V/Q ratio is close to 1.0, indicating a balance between ventilation and perfusion. In the lower regions of the lung (zone 3), the V/Q ratio is substantially lower than 1.0. Under these conditions, ventilation inadequately matches perfusion and intrapulmonary shunt occurs. The overall V/Q ratio of the lung is between .85 and .90. Thus, there are large gradients in ventilation and perfusion from the top to bottom of the lung in standing position, and as a result of gravitational effects, the blood volume and blood flow are substantially greater at the lung base compared with the apex. However, ventilation may be more effective in the lung base because the diaphragm exerts a greater influence in this region. Figure 10-21. Comparison of pressure gradients (in mm Hg) along the high-pressure systemic and low-pressure pulmonary circulation. (Reproduced with permission from Nunn JF: Applied Respiratory Physiology. London, Butterworth, 1971, p 213.) Figure 10-22. Relative ventilation and perfusion (V/Q) distribution in different areas of the lungs (upright position). The left side shows the percentage distribution of the total lung volume and the right side shows the alveolar ventilation, pulmonary blood flow, and V/Q ratio of each horizontal slice of lung volume. Note the upper zone is relatively overventilated and the lower zone is relatively overperfused. (Reproduced with permission from Nunn JF: Applied Respiratory Physiology. London, Butterworth, 1971, p 234.) The distribution of ventilation and perfusion throughout the lung also affects the relationships between pulmonary arterial, venous, and alveolar pressures within different lung zones. In the upper zone (zone 1), pulmonary arterial pressure of compressible vessels remains less than the pulmonary alveolar pressure and is insufficient to open the vessels, which remain collapsed during some of inspiration. In the middle zone (zone 2), the pressure at the arterial end of the compressible vessels exceeds pulmonary venous and pulmonary alveolar pressure; therefore, the blood flow becomes dependent on the pressure gradient between the pulmonary artery and alveolus, both of which exceed pulmonary venous pressure. In zone 3, the pulmonary venous pressure exceeds pulmonary alveolar pressure. Thus, blood flow depends on the pressure gradient between arterial to venous ends of the capillaries, similar to the situation observed in the systemic circulation. As intravascular pressures increase, progressively lower resistance to pulmonary blood flow is observed in this zone. In the supine position, similar V/Q distributions are observed over smaller pressure gradients (compared with the upright position) between anterior and posterior thorax. From this discussion, it is clear how pathologic conditions may reduce arterial O2 tension. For example, alveolar collapse in areas of atelectasis in which perfusion persists despite compensatory hypoxic pulmonary vasoconstriction may produce profound hypoxemia as a result of intrapulmonary shunt.63,64 Hypoxic Pulmonary Vasoconstriction Pulmonary arteriolar vasoconstriction triggered by hypoxia shunts blood flow away from poorly to well-ventilated regions of the lung, thereby improving arterial O2 saturation. The mechanism by which hypoxia raises pulmonary vascular resistance appears to be mediated by an O2 sensor because isolated pulmonary arterial smooth muscle cells contract under hypoxic conditions.65,66 The O2 sensor has yet to be identified, but may be mediated by smooth muscle mitochondria and pulmonary vascular endothelium. Pulmonary arterial strips with intact endothelium are more sensitive to hypoxia than skinned fiber preparations in vitro. Hypoxia also inhibits an outward K+ current; the resulting depolarization augments a Ca2+ influx into pulmonary vascular smooth muscle, thereby initiating contraction. The contractile mechanism of hypoxic pulmonary vasoconstriction appears to be mediated by the Ca2+-calmodulin system and causes phosphorylation of vascular smooth muscle myosin light chains. Chronic hypoxia causes proliferation of vascular smooth muscle and thickens the pulmonary arterial tree. This response increases pulmonary vascular resistance and may also produce irreversible pulmonary hypertension. Physiologic Modulation of the Pulmonary Circulation The blood volume stored in the pulmonary circulation is substantial (≥900 mL), and when combined with the blood volume contained within the heart and proximal great vessels, this pulmonary blood volume provides a crucial, rapidly available source of reserve intravascular volume during acute, massive hemorrhage. The mechanisms by which blood volume is shifted to central compartments in response to hypovolemia is poorly understood, but activation of regional sympathetic innervation of the volume-containing reservoirs, vasoconstriction of arterial resistance vessels, and the systemic action of epinephrine released from the adrenal gland clearly play important roles. Angiotensin, prostaglandins and other arachidonic acid metabolites, and nitric oxide are also critical regulators of pulmonary vascular resistance and the distribution of blood flow within the lung parenchyma.67,68,69Nitric oxide has proven benefits in the treatment of acquired and congenital pulmonary hypertension, often with life-saving results. For example, inhaled nitric oxide is a selective pulmonary vasodilator at doses <40 to 80 parts per million, and reductions in pulmonary arterial pressure produced by this drug are often essential to preserve RV function in patients undergoing heart or lung transplantation. Anatomy and Cerebral Autoregulation Blood flow to the brain is provided through the internal carotid and vertebral arteries. The vertebral arteries join to form the basilar artery, which, along with branches of the internal carotid arteries, forms the circle of Willis. The brain is approximately 2% of total body weight, yet this organ receives approximately 15% of cardiac output. This remarkably large cerebral blood flow (45 to 55 mL/100 g/min) reflects the high metabolic rate of the brain. Cerebral oxygen consumption averages 3.5 mL/100 g/min and accounts for 20% of total body oxygen consumption at rest. Regional cerebral blood flow and metabolic rate vary substantially throughout the brain. Cerebral blood flow and metabolic rate are closely linked and are approximately 4 times greater in gray compared with white matter. Thus, the cerebral cortex has a substantially greater blood flow and metabolic rate than subcortical regions. Motor activity or sensory stimulation is associated with increased neuronal activity in the contralateral activated areas of brain and is closely coupled to regional increases in blood flow and metabolic rate in corresponding regions.70,71 The mechanism of coupling of the activity-metabolism-blood flow relationship is most likely related to local metabolic vasodilators (e.g., lactic acid), alterations in electrolyte (e.g., K+, Ca2+) concentrations, and other substances (e.g., adenosine, released neurotransmitters). To date, no single causative molecule has yet been identified as the primary factor linking regional metabolic rate and blood flow to neuronal activity.72,73 Regulation of Cerebral Blood Flow: Hypercarbia, Hypoxia, and Arterial Pressure Cerebral blood flow remains relatively constant when mean arterial pressure varies between 50 and 150 mm Hg in healthy subjects (Fig. 10-23). This autoregulation of cerebral blood flow shifts to the right in patients with chronic, poorly controlled essential hypertension. For example, the autoregulation curve may range between 80 and 200 mm Hg in a patient with hypertension, and reducing the mean arterial pressure below 80 mm Hg may precipitate cerebral ischemia. This observation emphasizes that effective treatment of hypertension readjusts the autoregulation curve to its normal pressure range. Cerebral autoregulation is inhibited by hypercarbia and higher end-tidal concentrations of volatile anesthetics. In contrast, a reduction in arterial CO2 tension counteracts the direct cerebral vasodilator actions of many drugs, including those of volatile anesthesia agents.74 Arterial CO2 tension is a major regulator of cerebral blood flow within the physiologic range of arterial CO2 tensions. Cerebral blood flow linearly increases 1 to 2 ml/100 g/min for each 1 mmHg increase in Paco2. Below an arterial CO2 tension of 25 mmHg (Fig. 23), the cerebral blood flow response to Paco2 is attenuated. The mechanism responsible for the cerebral blood flow-arterial CO2 tension relationship is related to extracellular H+ concentration. Carbon dioxide rapidly diffuses across the vascular endothelium, and changes in local pH are governed by the Henderson-Hasselbach equation. Notably, alterations in cerebral produced by changes in arterial CO2 tension are not sustained blood flow because bicarbonate is eventually transported out of the brain extracellular fluid, thereby returning pH to a normal value. In contrast to the effects of respiratory acidosis on cerebral blood flow, the actions of metabolic acidosis are more gradual because the blood–brain barrier is relatively impermeable to H+. Hypoxia-induced increases in cerebral blood flow occur at arterial O2 tensions below 60 mm Hg (Fig. 10-23). The increase in cerebral blood flow at Pao2 levels below 60 mm Hg is very rapid. The mechanism of this hypoxia-induced increase in cerebral blood flow may be related to the vasodilator effect of neuronal acidosis. Several other mediators and chemoreceptor activation have also been proposed as potential signaling mechanisms responsible for cerebral vasodilation during hypoxia. In contrast to the marked increases in cerebral blood flow observed during hypoxia, little change in cerebral blood flow occurs under normoxic or hyperbaric conditions (Pao2 of 60 to 300 mm Hg). Figure 10-23. Cerebral blood flow (CBF) is autoregulated (relatively unchanged) as mean systemic blood pressure rises between 50 to 150 mm Hg. However, flow is nearly linearly increased with a rise in Paco2 and increased if Pao2 falls below 50 mm Hg. (Modified and reproduced with permission from Michenfelder JD: Anesthesia and the brain, Clinical, Functional and Vascular Coordinates. New York, Churchill Livingstone, 1988, pp 94–113.) Neural control of the cerebral circulation plays a relatively minor role in regulation of cerebral blood flow despite the extensive sympathetic nervous system innervation of cerebral blood vessels. Sympathetic postganglionic neurons originate in the cervical sympathetic ganglia, and vasoconstriction produced by sympathetic stimulation is largely exerted on the medium to larger-sized cerebral arteries. This response is primarily manifested during intense sympathetic nervous system activation that accompanies profound hypovolemia. The net effect of this sympathetic activation is a downward shift in the cerebral autoregulation curve, indicating a lower cerebral blood flow than predicted at a given level of mean arterial pressure. The cerebral blood vessels are also innervated by cholinergic and serotonergic fibers. Administration of exogenous vasodilators (e.g., sodium nitroprusside, adenosine, Ca2+ channel blockers, volatile anesthetics) increases cerebral blood flow. In contrast, catecholamines such as epinephrine do not substantially affect cerebral blood flow when these drugs are used to alter a systemic hemodynamics unless cerebral perfusion pressure is affected at the extremes of the autoregulation curve. It is important to recognize that autoregulation of cerebral blood flow is not effective and cerebral perfusion becomes pressure-dependent in areas of regional cerebral ischemia. Effects of Increased Intracranial Pressure Along with the brain, the cerebral circulation is entirely constrained within the rigid cranial cavity. This unique anatomic arrangement infers that increases in cerebral arterial blood flow must be matched by comparable increases in venous flow from the skull because the volume of blood and extracellular fluid within the brain is relatively constant. Thus, an intracranial mass (e.g., tumor, hematoma) is inevitably accompanied by an increase in intracranial pressure. Under these circumstances, the resistance to cerebral blood flow increases and cerebral perfusion is no longer determined by the difference between mean arterial pressure and cerebral venous pressure, but rather the difference between arterial pressure and intracranial pressure. If intracranial pressure continues to increase, a compensatory increase in arterial pressure occurs (Cushing reflex) that acts as a protective mechanism to maintain cerebral perfusion. Anatomy of the Renal Circulation: Determinants of Glomerular Blood Flow The primary branches of the renal artery divide into several interlobar arteries that traverse the parenchyma in a radial fashion from the hilum to the cortical-medullary junction that separates the kidney into an outer cortex and an inner medulla where urine is primarily concentrated in the renal tubules. As an interlobar artery approaches the cortical-medullary junction, it branches into a series of arcuate arteries that are located over the bases of the adjacent medullary pyramids in the zone between the cortex and the medulla, but do not interconnect with adjacent interlobar arteries. This lack of collateral blood supply indicates that acute occlusion of an interlobar artery will produce a pyramid-shaped renal infarction. Interlobular branches from the arcuate arteries travel toward the capsular surface and form the afferent arterial supply to the glomeruli. The kidney has approximately 1 million glomeruli that filter plasma from circulating blood into Bowman's capsule that surround each glomerulus capillary tuft. The afferent arteriole to each glomerulus divides into several vessels that form discrete capillary loops. The proximal and distal limbs of each loop are interconnected by many smaller capillaries, thereby forming the capillary tuft. Plasma filtration occurs within these capillary networks. After exiting the capillary network, the distal ends of each capillary loop within the glomerulus rejoin to form the efferent arterioles. The diameter of efferent arterioles is usually substantially less than the afferent arteriole. The entire glomerular capillary tuft is enveloped by Bowman's capsule, which collects the glomerular filtrate and transports it to the renal tubules where urine is concentrated. The efferent arterioles subsequently divide into another capillary network, the peritubular capillaries, some of which surround relatively short renal tubules located almost entirely in the renal cortex. Most of the peritubular capillaries form the long hairpin loops of Henle extending deep into the renal medulla. These vasa recta capillaries are important components of the renal countercurrent exchange mechanism that is responsible for urine concentration.75 The mean arterial pressure in the glomerular capillaries is normally between 50 and 60 mm Hg, thereby favoring the outward filtration of plasma water along the entire length of the capillary loop. Approximately 20% of the plasma water that enters the glomerular capillaries is filtered into Bowman's capsule. The efferent arterioles provide greatest vascular resistance in the renal circulation and reduce the pressure in the peritubular capillaries to values between 10 and 20 mm Hg. These relatively low pressures favor the net reabsorption of the large quantities of fluid that pass from the renal tubules into the interstitium. The permeability of the peritubular capillaries is also considerably higher than other capillaries in the body, a feature that substantially facilitates the primary diffusion function of the kidney. Renal blood flow is approximately 20% of cardiac output and is heavily balanced toward perfusion of the renal cortex. The inner medulla and papillae usually receive only approximately one tenth of cortical blood flow.76 The kidney has a very high metabolic rate, but the organ extracts less than 10% of O2 present in renal arterial blood because renal perfusion far exceeds metabolic requirements. Renal blood flow is very important for the delivery of the large volumes of blood to the glomeruli required for ultrafiltration. Renal blood flow remains relatively constant between mean arterial pressures of 75 and 170 mm Hg, but becomes pressure-dependent beyond this range of autoregulation. Alterations in afferent arteriole resistance autoregulate glomerular filtration rate (GFR) by constricting the diameter of afferent arterioles in response to increases in driving pressure. The two primary mechanisms of renal autoregulation are myogenic (vascular smooth muscle intrinsically responds to stretch by constriction) and tubular-glomerular feedback. This later mechanism is mediated by a feedback loop in which an alteration in renal tubular filtrate flow is detected by the macula densa of the juxtaglomerular apparatus, which signals the afferent arterioles to restore basal levels of renal blood flow and GFR. The signal that regulates the caliber of the afferent arterioles in tubular-glomerular feedback has yet to be precisely defined, but many vasoactive substances have been implicated, including products of arachidonic acid metabolism, catecholamines, adenosine, nitric oxide, and components of the renin-angiotensin system.77,78,79The role of atrial natriuretic factor, a 28 amino-acid peptide with potent diuretic and natriuretic properties in the renal circulation, has also been elucidated. This peptide is synthesized and released primarily from the cardiac atria, and distention of the atria causes renal vasodilation, increased filtration, inhibition of sodium reabsorption, natriuresis, and a resultant reduction of extracellular fluid volume. The sympathetic nervous system innervates the kidney and may control tubular transport of Na+ during modest reductions in intravascular volume. Under conditions of profound hypovolemia, sympathetic activation causes renal vasoconstriction, lowers GFR, and reduces renal capillary hydrostatic pressure, thereby producing compensatory water retention that increases plasma volume. As a result of the distribution of blood flow within the kidney, perfusion to cortical compared with medullary nephrons is primary affected by sympathetic nervous system-induced renal vasoconstriction. Splanchnic and Hepatic Circulation Regulation of Gastrointestinal Blood Flow The splanchnic circulation is unique. Arterial branches of the abdominal aorta supply blood to the gastrointestinal tract, spleen, and pancreas, whereas the liver has a dual blood supply consisting of the portal venous circulation and the hepatic artery. The intestinal circulation is weakly autoregulated compared with the cerebral, coronary, and renal vascular beds. Intestinal autoregulation appears to be primarily metabolic in origin. Adenosine is a likely mediator of this autoregulation, but other evidence suggests that K+ concentration and serum osmolality may also play contributing roles. The sympathetic nervous system innervates the gastrointestinal tract and the consequences of sympathetic activation are mediated by α-adrenoceptors. Pronounced sympathetic stimulation during acute hypovolemia produces gastrointestinal arterial constriction and venoconstriction, thereby shifting blood from a large vascular capacitance bed into the central circulation. Food ingestion increases gastrointestinal blood flow by several mechanisms, including the release of the hormones cholecystokinin and gastrin and absorption of gastrointestinal contents including glucose, fatty acids, and peptides.80 Regulation of Hepatic Blood Flow The liver receives approximately 25% of total cardiac output, three quarters of which are derived from the portal vein that contains venous blood from the gastrointestinal tract, spleen, and pancreas. The remaining 25% of hepatic blood flow is provided by the hepatic artery, which supplies the majority of oxygen to the liver. Mean portal venous and hepatic arterial pressures are 10 and 90 mm Hg, respectively.38,81 The downstream resistance in the hepatic sinusoids is relatively low under normal circumstances, but may be elevated in RV failure or hepatic cirrhosis. A rise in sinusoidal and portal vein pressures accompanying these pathologic conditions may produce transudation of fluid into the peritoneal space (ascites) or dilate alternative routes of venous drainage, such as those located in the lower esophageal veins (esophageal varices). Blood flow in the portal venous and hepatic arterial systems tends to vary reciprocally, but these respective hepatic blood supplies do not fully interact. Thus, a reduction of blood flow in the portal vein may be not fully compensated by an increase in hepatic arterial flow. The hepatic arterial but not the portal venous system is autoregulated. The most important response of hepatic arterial circulation to sympathetic stimulation is constriction of the presinusoidal resistance vessels.82 The liver contains about 15% of the total body blood volume and is an important volume reservoir that may be rapidly mobilized in response to sympathetic nervous system activation during acute hypovolemia. The reflex responses and response to hypoxia in small mesenteric capacitance vessels are inhibited by potent volatile anesthetics.83,84 1. Katz AM: Physiology of the Heart, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2006 2. Smith JJ, Kampine JP: The Heart: Structure and Function, Circulatory Physiology—The Essentials, 3rd edition. Baltimore, Williams & Wilkins, 1990 3. Berne RM, Levy MN: Cardiovascular Physiology, 8th edition. St. Louis, CV Mosby, 2001 4. Ledsome JHR, Lunden RJ: A reflex increase in heart rate from distention of the pulmonary vein atrial junction. J Physiol 1964; 170: 456 5. Seagard JL, Elegbe EO, Hopp FA, Bosnjak ZJ, von Colditz JH, Kalbfleisch JH, Kampine JP: Effects of isoflurane on the baroreceptor reflex. Anesthesiology 1983; 59: 511–520 6. Braunwald E. Sonenblick EH, Ross J: Contraction of the normal heart, Textbook of Cardiovascular Medicine, 2nd edition. Edited by Braunwald E. Philadelphia, WB Saunders, 1983, pp 409 7. Katz AM. The cardiac action potential, Physiology of the Heart, 2nd edition. New York, Raven Press, 1992, pp 438 8. Pagel PS, Grossman W, Haering JM, Warltier DC: Left ventricular diastolic function in the normal and diseased heart. Anestheiology 1993; 79: 1104 9. Pagel PS, Kampine JP, Schmeling WT, Warltier DC: Alteration of left ventricular diastolic function by desflurane, isoflurane, halothane in the chronically instrumented dog. Anesthesiology 1991; 74: 1103 10. Pagel PS, Kampine JP, Schmeling WT, Warltier DC: Comparison of end systolic pressure length relations and preload recruitable stroke work as indices of myocardial contractility in the conscious and anesthetized chronically instrumented dog. Anesthesiology 1990; 73: 278 11. Starling EF: The Linacre Lecture on the Law of the Heart. London, Logmans Green, 1918 12. Crohogini A, Barra J, Rodriquez CM, et al: Area beneath the end systolic pressure-volume relationship as an index of inotropic state in intact dogs. J Mol Cell Cardiol 1986; 18 (Suppl III) 20 13. Kass DA, Maaughan WL, Guo ZM, Kono A, Sunagawa K, Sagawa K: Comparative influence of load versus inotropic states on indexes of ventricular contractility. Experimental and theoretical analysis based on pressure-volume relationships. Circulation 1987; 76: 1422 14. Sagawa K: The ventricular pressure volume diagram revisited. Arc Res 1978; 43: 677 15. Sarnoff SJ: Myocardial contractility as described by ventricular function curves. Physiol Rev 1995; 35: 107 16. Suga H, Sagawa K, Shoukas AA: Load independence of the instantaneous pressure–volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ Res 1973; 32: 314 17. Schaub MC, Hefti MA, Zuellig RA, Morano I: Modulation of contractility in human cardiac hypertrophy by myosin essential light chain isoforms. Cardiovasc Res 1998; 37: 381 18. Cazorla O, Vassort G, Garnier D, Le Guennc JY: Length modulation of active force in rat cardiac myocytes: in titin the sensor? J Mol Cell Cardiol 1999; 31: 1215 19. Helmes M, Trombitas K, Ganzier H: Titin develops restoring force in rat cardiac myocytes. Circ Res 1996; 79: 619 20. Schiaffino S, Reggiani C: Molecular diversity of myofibrillar proteins: gene regulation and molecular significance. Physiol Rev 1996; 76:371 21. Goldstein MA, Schroeter JP, Michael LH: Role of the Z band in the mechanical properties of the heart. FASEB J 1977; 5: 2167–2174 22. Moncman CL, Wang K: Nebulette: A 107 kD nebulin-like protein in cardiac muscle. Cell Motil Cytoskel 1995; 32: 205 23. Solaro RJ, Rarick HM: Troponin and tropomyosin. Proteins that switch on and tune in the activity of cardiac myofilaments. Circ Res 1998; 83: 417 24. Tobacman LS: Thin filament-mediated regulation of cardiac contraction. Ann Rev Physiol 1996; 58: 447 25. Solaro RJ, Van Eyk J: Altered interactions among thin filaments proteins modulate cardiac function. J Mol Cell Cardiol 1999; 28: 217 26. Luo W, Grupp IL, Harrer J, Ponniah S, Grupp G, Duffy JJ, Doetschman T, Kranias EG: Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of β-agonist stimulation. Circ Res 1994; 75: 401 27. Rayment I, Holden HM, Whittaker M: Structure of the actin-myosin complex and its implications for muscle contraction. Science 1993; 261: 58 28. Dominguez R, Freyzon Y, Trybus KM, Cohen C: Crystal structure of a vertebrate smooth muscle myosin motor domain and its complex with the essential light chain: visualization of the pre-power stroke state. Cell 1998; 94: 559 29. Finer JT, Simmons RM, Spudich JA: Single myosin molecule mechanics: pico-newton forces and nanometer steps. Nature 1994; 368: 113 30. Katz AM. The electrocardiogram, Physiology of the Heart, 2nd edition. New York. Raven Press, 1992, p 472 31. Smith JJ, Kampine JP: Electrical properties of the heart, Circulatory Physiology—The Essentials, 3rd edition. Baltimore, Williams & Wilkins, 1990 32. Ebert TJ, Kotrly, KJ, Vucins EJ, Pattison CZ, Kampine JP: Effects of halothane anesthesia on cardiopulmonary baroreflex function in man. Anesthesiology 1985; 61: 668 33. Baruscotti M, Bucchi A, Di Francesco D: Physiology and pharmacology of the cardiac pacemaker (“funny”) current. Pharmacol Ther 2005; 107: 59 34. Nerbonne JM, Kass RS: Molecular physiology of cardiac repolarization. Physiol Rev 2005; 85: 1205 35. McAllen RM, Spyer KM: The location of cardiac vagal preganglionic motoneurons in the medulla. J Physiol 1976; 258: 187 36. Kampine JP: General cardiovascular regulation, International Practice of Anaesthesia. Edited by Prys-Roberts C, Brown BR Jr. Oxford, Butterworth-Heinemann, 1996 37. Lipski J, Kanjhan R, Kruszewska B, Rong W: Properties of presympathetic neurons in the rostral ventrolateral medullar in the rat: An intracellular study “in vivo”. J Physiol 1996; 490: 729 38. Guyenent PJ: Role of the ventral medulla oblongate in blood pressure regulation, Central Regulation of Autonomic Functions. Edited by Loewy AD, Spyer KM. New York, Oxford University Press, 1990 39. Jarisch A, Richter H: Die afferention bahnen des veratrius effektes in dem herz nerven. Arch Exp Path Pharmacol 1939; 193: 355 40. Dampney RA: Functional organization of central pathways regulating the cardiovascular system. Physiol Rev 1994; 74: 323 41. Spyer KM: The central nervous organization of reflex circulatory control, Central Regulation of Autonomic Function. Edited by Loewy AD, Spyer KM. New York, Oxford University Press, 1990 42. Ross CA, Ruggerio DA, Park DH, Joh TH, Sved AF, Fernandez-Pardal J, Saavedra JM, Reis DJ: Tonic vasomotor control of the rostral ventrolateral medulla: effect of electrical or chemical stimulation of the area containing C1 neurons on arterial blood pressure, heart rate, and plasma catecholamines and vasopressin. J Neurosci 1984; 4: 474 43. Gauer OH, Henry JP: Neurohumoral control of plasma volume, Cardiovascular Physiology II International Review of Physiology, Vol 9. Edited by Guyton AC, Cowley AW. Baltimore, University Park Press 1976, pp 145 44. Linden RJ: Atrial receptors and heart rate, Cardiac Receptors. Edited by Hainsworth R, Kidd C, Linden RJ. London, Cambridge University Press, 1979 45. Longhurst JC: Cardiac receptors: Their function in health and disease. Prog Cardiovasc Dis 1984; 27: 201 46. Kotrly KJ, Ebert TJ, Vucins EJ, Roerig DL, Kampine JP: Baroreceptor reflex control of heart rate during morphine sulfate, diazepam N2O/O2 anesthesia in man. Anesthesiology 1984; 61: 558 47. Seagard JL, Hopp FA, Donegan JH, Kampine JP: Halothane and the carotid sinus reflex: Evidence for multiple sites of action. Anesthesiology 1982; 57: 191 48. Crawford MH: Current Diagnosis and Treatment in Cardiology. Norwalk, CT, Appleton & Lange, 1995, pp 1 49. Libby PP, Bronow RO, Mann DL, et al: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th edition. Philadelphia, Elsevier Saunders, 2001 50. Marcus M: The Coronary Circulation in Health and Disease. New York, McGraw Hill, 1983, pp 465 51. Lance KL: Coronary Artery Stenosis. New York, Elsevier, 1991 52. Lilly LS: Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 4th edition. Philadelphia, Lippincott Williams & Wilkins, 2007 53. Tune JD, Richmond KN, Gorman MW, Feigl EO: Control of coronary blood flow during exercise. Exp Biol Med 2002; 227: 238 54. Cardiac Vascular, and Thoracic Anesthesia. Edited by Youngberg JA, Lake CL, Roisen MF, Wilson RS. Elsevier, 2000, pp 1 55. Topol EJ, Califf RM, Prystowsky EN, et al: Textbook of Cardiovascular Medicine, 3rd edition. Philadelphia, Lippincott, Williams & Wilkins, 2007, pp 1628 56. King SB, Yeung AC: Interventional Cardiology. New York, McGraw-Hill Medical, 2007 57. Frazier OH, Westaby S: Ischemia Heart Disease: Surgical Management. London, Mosby, 1999, pp 1 58. Opie LH: Heart Physiology: From Cell to Circulation, 4th edition. Philadelphia, Lippincott, Williams & Wilkins, 2004, pp 648 59. Phibbs B: The Human Heart: A Basic Guide to Heart Disease, 2nd edition. Philadelphia, Lippincott, Williams & Wilkins, 2007, pp 229 60. Gerstenblith G: Cardiovascular Disease in the Elderly. Totowa, NJ, Humana Press, 2005 61. Nunn JF: Applied Respiratory Physiology. London, Butterworth, 1971, pp 213 62. Szidon JP, Fishmann AP: Autonomic control of the pulmonary circulation, The Pulmonary Circulation and Interstitial Space. Edited by Fishman AP, Hecht HH, Chicago, The University of Chicago Press, 1969, pp 239 63. West JB, Collery CT: Distribution of blood flow and the pressure-flow relations of the whole lung. J App Physiol 1965; 20: 175 64. West JB, Naimark AA: Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures. J Appl Physiol 1964; 19: 713 65. Mauban JR, Reillard CV, Yuan JZ: Hypoxic pulmonary vasoconstriction: Role of ion channels. J Appl Physiol 2005; 98: 415 66. Waypa GB, Shumacker PT: Hypoxic pulmonary vasoconstriction: Redox events in oxygen sensing. J Appl Physiol 2005; 98: 404 67. Buzzard CJ, Pfister SL, Campbell WB: Endothelium-dependent contractions in rabbit pulmonary artery are mediated by thromboxaine A2. Circ Res 1993; 72: 1023 68. Pfister SL, Campbell WB: Role of endothelium derived metabolites of arachidonic acid in enhanced pulmonary artery contractions in female rabbit. Hypertension 1996; 27: 43 69. Zhu D, Medhora M, Campbell WB, Spitzbarth N, Baker JE, Jacobs ER: Chronic hypoxia activates lung 15-lipoxygenase which catalyzes production of 15-HETE and enhances constriction in neonatal pulmonary arteries. Circ Res 2003; 92: 992 70. Greenberg J, Hand P, Sylverstro A, et al: Localized metabolic flow couple during functional activity. Acta Neurol Scand 1979; 60(Suppl 72): 12 71. Olsen J: Contralateral local increase in cerebral blood flow in man during arm work. Brain 1972; 94: 635 72. Gebrenedin D, Lange A, Lowry T, Taheri MR, Birks EK, Hudetz AG, Narayanan J, Falck JR, Okamoto H, Roman RJ, Nithipatikom K, Campbell WB, Harder DR: Production of 20-HETE and its role in autoregulation of cerebral blood flow. Circ Res 2000; 87: 60 73. Lou HC, Edvinsson L, MacKenzie ET: The concept of coupling blood flow to brain function: revision required? Ann Neurol 1987; 22: 289 74. Faraci FM, Heistad DD: Regulation of the cerebral circulation: Role of endothelium and potassium channels. Physiol Rev 1998; 78: 53 75. Levy MN, Pappano AJ: Cardiovascular Physiology. Philadelphia, Mosby Elsevier, 2007 76. Hall JE. Regulation of renal hemodynamics, Cardiovascular Physiology II. International Review of Physiology, Vol. 2. Edited by Guyton EC, Hall JE. Baltimore, University Park Press, 1982, pp 243 77. Benner BM: Glomerular ultrafiltration, The Kidney, Vol 1, 3rd edition. Edited by Brenner BM, Bector FC. Philadelphia, WB Saunders, 1986 78. Naraayanan J, Imig M. Roman R, Harder D. Pressurization of isolated renal arterial increases inositol tripghosphate and diacylglycerol. Am J Physiol Heart Circ Physiol 1994; 35: H1840 79. Roman RR: P-450 metabolites of arachadonic acid in the control of cardiovascular function. Physiol Rev 2002; 82: 131 80. Jacobson Ed, Tepperman BL, editors: Splanchnic circulation (symposium). Fed Proc 1982; 41, 2079 81. Greenway CV, Laut WW. Hepatic circulation, Handbook of Physiology, Section 6: The Gastrointestinal System—Motility and Circulation, Vol. 1. Edited by Schultz SG. Bethesda, MD, American Physiological Society, 1989 82. Ozono K, Bosnjak ZJ, Kampine JP. Reflex control of mesenteric venous capacitance in the rabbit: Direct measurement of vein diameter and intravenous pressure in the situ preparation. Am J Physiol 1989; 256: H1066 83. Stadnicka A, Stekiel TA, Bosnjak ZJ, Kampine JP: Hypoxic contractions of isolated rabbit small mesenteric capacitance veins: Contributions of endothelium and attenuation by volatile anesthetics. Anesthesiology 1995; 82: 550 84. Stekiel TA, Ozono K, McCallum JB, Bosnjak ZJ, Stekiel WJ, Kampine JP: The inhibitory action of halothane on reflex constriction in mesenteric capacitance veins. Anesthesiology 1990; 73: 1169 Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine	2	89	0	0	2	0	0.835772	2	29,948
ICD-10 for Atrioventricular (AV) block Atrioventricular (AV) block involves impairment of the conduction between the atria and ventricles of the heart. In ICD-10-CM the codes are categorized by degree: First degree AV block (I44.0 Atrioventricular block, first degree) – All atrial impulses reach the ventricles, but the conduction is delayed within the AV node. Patients are generally asymptomatic and the first-degree AV block is usually an incidental finding on electrocardiography (ECG). People with newly diagnosed first-degree AV block may be well-conditioned athletes, or they may have a history of myocardial infarction or myocarditis. First-degree AV block also may represent the first sign of degenerative processes of the AV conduction system. Second degree AV block (I44.1 Atrioventricular block, second degree) – Atrial impulses fail to conduct to the ventricles. Patients may be asymptomatic, but may experience pre-syncope or syncope and sensed irregular heartbeats. The latter usually is observed in more advanced conduction disturbances, such as Mobitz II second-degree AV block. A history of medications that affect atrioventricular node (AVN) function (e.g., digitalis, beta-blockers, and calcium channel blockers) may be contributory and should be obtained. Other terms for a second degree AV block are Wenckebach’s and Mobitz blocks. Third degree AV block (I44.2 Atrioventricular block, complete) – No supraventricular impulses are conducted to the ventricles. Patients have symptoms of fatigue, dizziness, light-headedness, pre-syncope, or syncope. Syncopal episodes due to slow heart rates are called Morgagni-Adams-Stokes (MAS) episodes, in recognition of the pioneering work of these researchers on syncope. Patients with third-degree AV block may have associated symptoms of acute myocardial infarction either causing the block or related to reduced cardiac output from bradycardia in the setting of advanced atherosclerotic coronary artery disease. Proper coding of AV block requires documentation of severity: - First degree - Second degree - AV block, type I and II - Mobitz block, type I and II - Second degree block, type I and II - Wenckebach’s block - Complete heart block - Third degree block Third-degree AV Block Example: PREOPERATIVE DIAGNOSIS: Symptomatic 3rd-degree (complete) atrioventricular block. POSTOPERATIVE DIAGNOSIS: Symptomatic 3rd-degree (complete) atrioventricular block. PROCEDURE: Insertion of right atrial and right ventricular transvenous leads through the left subclavian vein and implantation of a dual-chamber permanent pacemaker. DEVICE INFORMATION: Generator: St. Jude Medical. Model number: 5386. Serial number: 1146418. Right atrial lead: St. Jude Medical. Model number: 1888TC/52 cm. Serial number: BCK20068. Right ventricular lead: St. Jude Medical. Model number: 1 888TC158 cm. Serial number: BCLI6IO6. DESCRIPTION OF PROCEDURE: After informed consent was obtained, the patient was transferred to the cardiac electrophysiology laboratory from the medical floor in a post absorptive and fasting state. The left upper chest area was prepped and draped in a sterile manner. A combination of a 50/50 portion with 1% Xylocaine and 0.25% Marcaine was used for a local anesthetic. A left infraclavicular skin incision was made, and a proper pocket was created subcutaneously. Substantial oozing from the subcutaneous tissue was noted during incision due to the fact that the patient was given Integrilin approximately 4 hours ago for cardiac catheterization prior to the pacemaker implantation, as well as the patient had been taking aspirin. The left subclavian vein puncture using a modified Seldinger technique was made without difficulty. Two separate cannulations for both atrial and ventricular access were made. After cannulation of the ventricular access, an active-fixation ventricular lead (6-French) was inserted through a 6-French SafeSheath into the right ventricular apex. An adequate threshold was achieved and as follows. Using a 0.4 msec pulse width, the ventricular voltage threshold was 1.4 V at 1.7 mA and impedance of 788 ohms with R wave amplitude of 3.8 mV. The ventricular lead was secured with 0 Ethibond with 2 separate suture ligatures around the anchoring sleeve. A 6-French active-fixation atrial lead was inserted through another 6-French SafeSheath and was positioned in the right atrial appendage without difficulty. The threshold using a 0.4 pulse width was 1.4 V at 2.7 mA, impedance of 410 ohms, with a P wave amplitude of 1.8 mV. Ten-volt stimulation of both atrial and ventricular leads did not produce extra cardiac stimulation or diaphragmatic pacing. The atrial lead was likewise secured through the underlying muscular layer with 2 separate suture ligatures with 0 Ethibond around the anchoring sleeve. The pocket was thoroughly irrigated with antibiotic solution. Due to substantial oozing of the blood in the pocket, the wound was packed with hemostasis Surgicel sponge to enhance hemostasis. The terminal pins of both leads were securely connected to the pulse generator after proper programming of the parameters was made. The lower rate was set at 60 beats per minute and the upper tracking rate at 130 beats per minute with the atrioventricular delay at 170 ms in DDD mode. The pacemaker was implanted into the pocket and affixed to the underlying muscular layer with a single 0 Ethibond suture ligature. The incision wound was closed with 2 layers of subcutaneous 3-0 Polysorb suture and a single layer of subcuticular 5-0 Polysorb sutures. The wound was cleaned and bandaged with sterile gauze and covered with transparent Tegaderm sheets. A pressure bandage was applied with an elastic bandage. The patient was transferred to the medical floor in stable condition. Conscious sedation was delivered by the EP lab nurse throughout the entire procedure. CONCLUSION: Successful implantation of a dual-chamber permanent pacemaker. DISPOSITION: The patient will be monitored on the floor with a chest X-ray and EGG taken today and in the morning. Pacemaker evaluation will be performed in the morning, and will be discharged per the floor team’s discretion. He will be seen at the Pacemaker Clinic in approximately 2 weeks for wound and pacemaker check. He will be periodically followed at our Pacemaker Clinic for a long-term follow-up. ICD-10-CM Coding: I44.2.	4	9	0	0	0	6	0.797144	6	1,512
Histiocytosis Classification and external resources ICD-10 C96.1, D76.0 ICD-9 202.3, 277.89 eMedicine ped/1997 MeSH D015614 In medicine, histiocytosis refers to an excessive number of histiocytes, (tissue macrophages), and is typically used to refer to a group of rare diseases which share this as a characteristic. Occasionally and confusingly, the term "histiocytosis" is sometimes used to refer to individual diseases. The histiocytes may attack skin, bone, muscles, and other important organs, including the liver, lung, spleen, and hematopoietic system. The disease is somewhat similar to cancer, and treatment often involves radiation and chemotherapy. According to the Histiocytosis Association of America, 1 in 200,000 children in the United States are born with histiocytosis each year. HAA also states that most of the people diagnosed with histiocytosis are children under the age of 10. The University of California, San Francisco, states that the disease usually occurs from birth to age 15. Histiocytosis (and malignant histiocytosis) are both important in veterinary as well as human pathology. Classification, and relationships to other conditions There are competing systems for classifying histiocytoses. According to the 1999 classification proposed by the World Health Organization, they can be divided into three categories. However, the classifications in ICD10 and MeSH are slightly different, as shown below: Name WHO ICD10 MeSH Langerhans cell histiocytosis (LCH) I D76.0 Langerhans-cell histiocytosis Juvenile xanthogranuloma (JXG) II D76.3 non-Langerhans-cell histiocytosis Hemophagocytic lymphohistiocytosis (HLH) II D76.1 non-Langerhans-cell histiocytosis Niemann-Pick disease II E75.2 non-Langerhans-cell histiocytosis Sea-blue histiocyte syndrome II - non-Langerhans-cell histiocytosis Acute monocytic leukemia III C93.0 malignant histiocytic disorders Malignant histiocytosis III C96.1 malignant histiocytic disorders Erdheim-Chester disease II C96.1 malignant histiocytic disorders Types of LCH have also been known as "Eosinophilic Granuloma", "Hand-Schuller-Christian Disease", "Letterer-Siwe Disease", and "Histiocytosis X". (See Langerhans cell histiocytosis for details). Alternatively, histiocytoses may be divided into the following groups::714-724 - X-type histiocytoses - Non-X histiocytoses Patients and families can gain some support by contacting patient organisations such as the Histiocytosis Association of America, which has several stable and proven treatment protocols available only for physicians, or the Histiocytosis Research Trust. - ^ Histiocytosis at eMedicine Dictionary - ^ Disease information at the Histiocytosis Association of America - ^ Histiocytosis - Signs and Symptoms - ^ Harris N, Jaffe E, Diebold J, Flandrin G, Muller-Hermelink H, Vardiman J, Lister T, Bloomfield C (1999). "The World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues. Report of the Clinical Advisory Committee meeting, Airlie House, Virginia, November, 1997". Ann Oncol 10 (12): 1419–32. doi:10.1023/A:1008375931236. PMID 10643532. - ^ Histiocytosis at eMedicine - ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. - ^ Histio.Org Physicians Information Request Histiocytosis (D76.0, 277.89) WHO-I/Langerhans cell histiocytosis/ X-type histiocytosisLetterer–Siwe disease · Hand–Schüller–Christian disease · Eosinophilic granuloma · Congenital self-healing reticulohistiocytosis WHO-II/non-Langerhans cell histiocytosis/ Non-X histiocytosisJuvenile xanthogranuloma · Hemophagocytic lymphohistiocytosis · Erdheim-Chester disease · Niemann-Pick disease · Sea-blue histiocyte syndrome · Benign cephalic histiocytosis · Generalized eruptive histiocytoma · Xanthoma disseminatum · Progressive nodular histiocytosis · Papular xanthoma · Hereditary progressive mucinous histiocytosis · Reticulohistiocytosis (Multicentric reticulohistiocytosis, Reticulohistiocytoma) · Indeterminate cell histiocytosis WHO-III/malignant histiocytosisHistiocytic sarcoma · Langerhans cell sarcoma · Interdigitating dendritic cell sarcoma · Follicular dendritic cell sarcoma Ungrouped Wikimedia Foundation. 2010. Look at other dictionaries: Histiocytosis — vgl. Histiozytose … Das Wörterbuch medizinischer Fachausdrücke Histiocytosis — A rare but potentially deadly disorder with similarities to cancer, in which histiocytes start to multiply and attack the person’s own tissues or organs. The result can be tissue damage, pain, development of tumor like lumps called granulomas,… … Medical dictionary Histiocytosis X — Klassifikation nach ICD 10 C96.0 Abt Letterer Siwe Krankheit Letterer Siwe Syndrom C96.1 Maligne Histiozytose D76.0 … Deutsch Wikipedia histiocytosis — n. any of a group of diseases in which there are abnormalities in certain large phagocytic cells (histiocytes) due to 1) abnormal storage of fats, as in Gaucher s disease; 2) inflammatory disorders, as in Langerhans cell histiocytosis, which… … The new mediacal dictionary histiocytosis — his·ti·o·cy·to·sis (hĭs tē ō sī tōʹsĭs) n. pl. his·ti·o·cy·to·ses ( sēz) Any of several abnormal conditions characterized by the appearance of histiocytes in the blood or tissues. * * * … Universalium histiocytosis X — Langerhans cell h … Medical dictionary histiocytosis — his·tio·cy·to·sis … English syllables histiocytosis — noun a blood disease characterized by an abnormal multiplication of macrophages • Hypernyms: ↑blood disease, ↑blood disorder • Hyponyms: ↑Hand Schuller Christian disease, ↑Schuller Christian disease … Useful english dictionary Histiocytosis, Langerhans cell — Histiocytosis in which the active histiocytes normally occur in the skin. See histiocytosis … Medical dictionary Histiocytosis, malignant — Histiocytosis in which the histiocytes actually become cancerous. Treatment is by radiation and chemotherapy, and in some cases bone marrow transplantation. See also histiocytosis … Medical dictionary	3	3	0	0	0	7	0.43769	7	1,728
Jun 27, 2016. Neuropathy is a disease affecting the peripheral nervous system (PNS). Your PNS controls body. Consider complementary and alternative therapies. In addition to. Studies have shown that TENS is effective in treating certain kinds of neuropathic pain, although more research is needed. Of meditation. 24 natural home remedies for neuropathy is a newly updated article which shows readers 24 natural ways to treat neuropathy at home. Dec 25, 2012. Neuropathy is a collection of chronic disorders that occurs when nerves of peripheral nervous system gets damaged, injured or dysfunctions. Phantom limb. Peripheral neuropathy — Comprehensive overview covers diagnosis, causes and treatment of this often painful disorder. Jul 16, 2009. The prickling, tingling or burning sensation that occurs whenever you move your feet might be the symptoms of peripheral neuropathy. ★★ Diabetic Peripheral Neuropathy Treatment ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ DIABETIC PERIPHERAL. ★ Home Remedies For Diabetic Neuropathy ★★ Ibuprofen Diabetes ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ HOME. How to Reduce Foot Pain from Idiopathic Peripheral Neuropathy. If you suffer from peripheral neuropathy you know how much pain you can have. Sometimes. Obtain Relief from Peripheral Neuropathy by Using Natural Remedies. Monday, September 20, 2010 by: Luella May Tags: peripheral neuropathy, remedies, health. HOWEVER, we even have a Neuropathy Home Remedy that works and actually works within a few days of taking Vitamin B Complex and B12 Sublingual. And it will give you relief in a matter of days with absolutely no side effects! What IS Neuropathy? Neuropathy is nerve damage in our peripheral nervous system and is. ★★ Treatment Diabetic Peripheral Neuropathy ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ TREATMENT DIABETIC. These are some of the symptoms of peripheral neuropathy that should never be ignored. They may. That may be because peripheral neuropathy can cause an inability to sweat, which leads to overheating. To prevent further damage, Dr. Saunders recommends treating your nerves with NERVALA to keep them healthy. The Rebuilder is a peripheral neuropathy treatment and possible cure. Immediate relief. Guaranteed. According to medical practitioners, there is no real treatment for neuropathy. So home remedies are recommended for curing neuropathy. Here are some. ★★ Peripheral Neuropathy Diabetes ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ PERIPHERAL NEUROPATHY DIABETES. May 17, 2016. What the medical world refers to as chemotherapy-induced peripheral neuropathy (CIPN) is caused when vulnerable nerves far from the brain and spine become. Therapies that may help address pain include supplements and other naturopathic remedies, prescription pain relievers and antidepressants, Nov 28, 2016. Neuropathy involves the damage to the peripheral nerves. These nerves can be damaged due to infections, long term exposure to harmful toxins, metabolic. Peripheral neuropathy is a type of damage to your peripheral nervous system. Find in-depth information about symptoms, diagnosis and management. There are numerous causes of peripheral neuropathy: heredity, diabetes, hypothyroid, arthritis, HIV, cancer, alcohol and heavy metals such as lead, mercury, and arsenic. Medications can also cause the condition, including ddI, and d4T. Nutritional deficiencies seem to worsen the symptoms. Viral infections can directly. Nov 27, 2017. Peripheral neuropathy affects the peripheral nervous system, which transmits messages between the central nervous system and other parts of the body. Peripheral neuropathy can affect a range of different nerves, so it can impact a variety of locations in different ways. Treating mononeuropathies. LEARN ABOUT Homeopathy Treatment of Neuropathy & Diabetic Neuropathy. Peripheral Neuropathy cause, symptoms, diagnosis, homeopathic remedies for neuropathy, natural home remedies for neuropathic pain management. Neuropathy is a collection of chronic disorders that occurs when nerves of peripheral nervous system gets damaged, injured or dysfunctions. Phantom limb Take consultation from Ayurvedic doctors of Pure Herbal Ayurved Clinic to find the best diabetic peripheral neuropathy natural treatment and remedies in Melbourne, Australia. ★ Diabetic Peripheral Neuropathy ★ :: Iodine And Diabetes – The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ DIABETIC. Statin Drugs Causing Peripheral Neuropathy Diabetic Walking Shoes Neuropathy Oct 14, 2013. With neuropathy, it's best to do exercises that are non-weight bearing, such as swimming, water aerobics, rowing and chair exercises. If walking is the exercise Peripheral or diabetic neuropathy affects 60-70 percent of all diabetics with stabbing, burning pain in the hands, feet and especially the toes, according. Neuropathy is a term used for any of the nerve disorders associated with paralysis, severe weakness. Nerve disorders are classified as peripheral and autonomic neuropathy. May 9, 2017. Of these, the central nervous system is connected to the spinal cord and brain, while the peripheral system functions with the help of the nerves. The good news is that there are several easy and effective home remedies for nerve pain that offer relief from the extreme discomfort. remedies for nerve pain. @ Home Remedies For Diabetic Neuropathy Pain ★★ Diabetes Daily Diet Plan The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Are There Home Remedies for Neuropathy? What Medications Are Used to Treat Neuropathy? What Are Neuropathy Medications? Learn about peripheral neuropathy causes such as diabetes, alcohol, medication, shingles, vitamin deficiency, autoimmune diseases, and inherited diseases. May 10, 2013. Natural Treatment can cure Diabetic Peripheral Neuropathy with the help of improvised home remedies.These home remedies developed by researcher's can act fast. Small fiber peripheral neuropathy is a type of peripheral neuropathy that occurs from damage to the small unmyelinated peripheral nerve fibers. These. Neuropathy causes tingling or numbness, especially in the hands and feet. It affects about one to two percent of Americans and is caused by damage to a single or multiple nerves. There are different types, but peripheral neuropathy is the most common in those with cancer. Peripheral neuropathy – Get information and read articles on Peripheral neuropathy sign, symptoms, causes, treatment, prevention and diagnosis at onlymyhealth.com, your complete health guide. Peripheral neuropathy information including symptoms, diagnosis, misdiagnosis, treatment, causes, patient stories, videos, forums, prevention, and prognosis. More Neuropathy Articles ... - How Is Peripheral Neuropathy Diagnosed: ★★ Icd 9 Code For Diabetes With Peripheral Neuropathy ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ ICD 9 CODE. A crucial part of diagnosing neuropathy is to identify the cause of the underlying condition. Both ph... - Peripheral Neuropathy Treatment Socks: ★★ Treatment Of Diabetic Peripheral Neuropathy ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ TREATMENT OF. @ Diabetic Peripheral Neuropathy Icd 9 Code ★★ Treatment For Diabetic Rash The 3 Step Trick that Reverses ... - What Is Autonomic Neuropathy In Diabetes: Diabetic autonomic neuropathy (DAN) is common and important but generally under-recognised. DAN is not a single entity, but an 'umbrella term' with broad clinical implications reflecting the diffuse and integral involvement of the autonomic... - Peripheral Neuropathy And B12: Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of. Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, ... - Nitroglycerin Spray Diabetic Neuropathy: (WHO, 1992) 1.3 Synonyms Nitroglycerin (USAN, 1994) Trinitroglycerin Glonoin Trinitrin GTN Nitroglycerol (Reynolds, 1993) 1.4 Identification numbers 1.4.1 CAS. solutions Ointment 2% Transdermal system: 12.5 to 104 mg Aerosol spray 0.3 to 0.4 mg meter... - Idiopathic Peripheral Neuropathy Ssdi: Insomnia Movie Summary Sleep Disorders And Treatments with Why Do I Not Sleep At Night and Lds Hospital Sleep Disorders Clinic Sleep Disorders Adults. Filing For Disability Benefits On The Basis Of Neuropathy. Is Neuropathy Enough To Qualify For Soci...	2	6	0	0	0	3	0.710326	3	1,941
What is a Medical Group? A medical group is a group of doctors, nurses, specialists, and other professionals dedicated to patient healthcare. Medical groups work with health plans to coordinate both care and coverage for each individual. The job of a health plan and it’s contracted medical group can vary depending upon the type of health plan. For instance, in a PPO plan, the doctor and medical group’s main responsibility is to care for patients at the time of the appointment; the patient is responsible for coordinating care. In an HMO plan, the doctor and medical group often have a bigger job than just providing immediate patient care; with an HMO, they are pro-actively working to improve the patient’s overall health – including steps to avoid future health problems; this is called preventive care. How does an HMO work? HMO stands for Health Maintenance Organization and is a type of health insurance. An HMO offers many healthcare services to its members. HMOs are sometimes called health plans or managed care organizations. HMOs are different from other kinds of health insurance in the way that they manage the cost of healthcare and the services offered. Members may have a co-pay for services, which the patient needs to pay before services are covered by the plan. Co-payments and deductibles help keep the cost of healthcare down. HMOs may require referrals for some services before the HMO will pay. At HDMG members visit their Primary Care Provider who will determine if a referral is necessary and submits the referral for approval. It is recommended to obtain a referral to avoid financial responsibility for unauthorized services. What is a Medicare Advantage Plan? A Medicare Advantage Plan is a type of Medicare health plan offered by a private company that contracts with Medicare (a government plan) to provide you with all your benefits (Part A and in most cases, Part B). Medicare Advantage Plans include Health Maintenance Organizations (HMO), Preferred Provider Organizations (PPO), Private Fee-for-Service Plans, Special Needs Plans, and Medicare Medical Savings Account Plans. If you’re enrolled in a Medicare Advantage Plan, Medicare services are covered through the plan and are not paid for by Medicare. Most Medicare Advantage Plans offer prescription drug coverage. What is the process if I need to see a Specialist or require special (durable) medical equipment? (Oxygen, wheelchair, cane, etc.) If your Primary Care Physician determines that you need to be seen by a Specialist or need durable medical equipment, he/she will submit a referral to HDMG’s Utilization Management Department. The Utilization Management committee will review the referral by applying established criteria, determine medical necessity, and ensure that any tests needed have been completed. If your physician requests an urgent referral, it will be processed within 72 hours. For non-urgent requests, you will be notified of the determination within seven business days. If the referral is modified, you will be notified of the modification, along with further information and instructions. If the referral is denied, notification will be mailed to you, along with the appeal process. You have the right to appeal a denied or modified referral; you may begin your appeal by contacting your insurance company. Your Primary Care Physician will be notified of the status of your referral also. How do I follow up on a referral if it has been longer than the allotted time? If you have not been notified regarding the status of your referral within seven business days, please contact your Primary Care Physician. May I change my Primary Care Physician at any time? Yes, simply contact your insurance company, and they will instruct you on their policy for changing your Primary Care Physician. Once the change is made, your insurance company will give you the effective date of your change. Should you need to see your new Primary Care Physician prior to the effective date, please contact HDMG’s Member Services Department at: (800) 266-4364, as they may be able to assist you. How does my new physician obtain a copy of my medical records? You will need to complete and sign a Medical Record Release form. You may obtain the form at either High Desert Medical Group or at your previous physician’s office. Once the form is completed, your medical records will be sent to your new physician’s office or group. How do I access my medical records as an HDMG patient? As an HDMG patient, you may enroll in our online service “NextGen Patient Portal”. This website provides patients with an easy-to-use internet portal to communicate with your physician, request appointments, request a prescription refill and more. The Patient Portal is secure, confidential, and gives you 24-hour access to your medical records. What if I am sick and I am not able to schedule a same day appointment with my Primary Care Physician or it is after office hours? Should you need care after hours, weekends, or holidays, we offer an Urgent Care Center, open 365 days a year, located at: 43839 N. 15th Street West, Suite 108, Lancaster, CA, 93534. For the convenience of our senior patients, HDMG also offers a Geriatric Emergent Care Center open Monday through Friday, 8:30am-5:00pm. This Geriatric Emergent Care Center is located at: 43839 N. 15th Street West, Suite 101, Lancaster, CA, 93534. What is the difference between using an Urgent Care or Emergency Room? There are many benefits to visiting an Urgent Care instead of an Emergency Room, including lower co-payments (depending on your health insurance), shorter wait times, and notification to your HDMG Primary Care Physician. However, please be sure to call 911, if you are experiencing a life or organ threatening emergency. * We offer an Urgent Care Center at our Lancaster facility for minor conditions. Who can I call should I have additional questions and/or concerns about my healthcare? High Desert Medical Group’s Member Services Department is composed of sensitive and compassionate representatives who are dedicated to total patient satisfaction. Our friendly and knowledgeable staff can assist you with any concerns or questions you may have, including selecting a Primary Care Physician, scheduling an appointment, and helping you understand your healthcare plan. Our team of patient service experts work very closely with our physicians and their staff to ensure that your overall medical care is to the highest standards. We also have bilingual, Spanish-speaking personnel available. HDMG’s Member Services Department can be reached at: (661) 945-5984. Their hours of operation are: Monday – Friday, 8:00 a.m. to 5:00 p.m. and is located at: 43839 N. 15th Street West Suite 201, Lancaster, CA. 93534.	2	2	4	0	0	0	0.72242	4	1,419
The Department of Health and Human Services (HHS) precluded ICD9 coding on October 1, 2015, due to never resolving permanent issues with it. HHS replaced ICD9 with ICD10, which resolved and addressed issues people faced in the former coding. This shift can lead to a much-anticipated query, what’s the difference between ICD9 and ICD10? ICD10 codes are not only better, longer, and more efficient, but they are also complex, precise, and more changed in terminologies giving out more details than those of ICD9. Major thanks to the technologies that saved precious hours and developed these codes that can deliver tons of info in seconds, but the shortcoming is that many healthcare professionals, including experienced and rookies, may find these codes confusing and can create a fuss between service providers and payers. To help dust off these confusions and vagueness, we have outlined a differentiating guide between these codes below. What is ICD Coding? To understand both codes, you first need to get the hang of what ICD coding is. ICD (International Classification of Disease), as the name suggests, provides an approach to insurers to identify diseases, injuries, and causes of death of patients. To facilitate international study on illnesses, their causes, and potential therapies, the World Health Organization (WHO) publishes the International Classification of Diseases (ICDs). Each medical condition, symptom, or treatment has its own unique set of letters/or numbers known as a “diagnosis code.” Infections caused by the Coronavirus are labeled COVID-19 (Infections due to SARS-CoV-2). The CDC (Centre for Disease Control) officially approves instances before assigning codes. The codes are also sorted in order of their respective expressions. The first set of codes, ICD9, had issues with it that caused inaccuracies and inefficiencies in many instances; therefore, HHS and WHO mutually eliminated and disqualified this set and introduced ICD10. Introducing a new set of codes caused and still confusing concerned professionals. However, the difference between ICD9 and ICD10 are not very intense, just some changes that eliminated inaccuracies and ran efficiently. Let’s find out the significant differences between them. Brief Overview of ICD Diagnosis Codes and ICD Procedure Codes (Table Source: https://medconverge.com/difference-between-ICD-9-and-ICD-10/) Due to its reliance on antiquated technologies, ICD9 was unable to account for advances in medicine. In contrast, modern technology is more easily integrated into ICD10. As an added bonus, it provides more leeway for generating and integrating new forms of code. The new set of codes, i.e., ICD10, has differences in its diagnosis and procedure codes, which are given below. Difference Between ICD9 and ICD10 Diagnosis Codes \|It has a maximum approximation of 13,000 codes.\|\|It has a maximum approximation of 68,000 codes.\| \|Its range of code length is 3 to 5 characters.\|\|Its range of code length is 3 to 7 characters.\| \|The first digit can be either alpha or numeric.\|\|Its first digit is always alpha.\| \|It has limited room for the addition of new codes.\|\|It has more flexibility when it comes to adding new codes.\| \|Its codes lack details and are short.\|\|Its codes indicate more details and are more specific yet precise.\| \|Its codes lack laterality\|\|Its codes have laterality\| Difference Between ICD9 and ICD10 Procedure Codes \|The maximum code approximation was 3000 codes\|\|The maximum code approximation is 87000 codes\| \|Maximum code length range was 3 to 4 characters\|\|Minimum code length is 7 characters\| \|Its codes always had numeric characters.\|\|Its codes have alpha-numeric characters.\| \|This used to feature body parts in generic terms.\|\|This now features a detailed description of anatomical parts.\| \|Its definition of procedure lacked precision.\|\|It provides detailed procedures and other details.\| \|Its procedural approach always lacked details.\|\|It provides a detailed approach to procedures.\| \|The methodology of ICD9 procedure codes’ descriptions lacked details.\|\|ICD10 gives a detailed methodology of descriptions.\| Adding additional codes is impossible since several chapters in ICD-9 are already at capacity. A more significant number of codes may be used since the length of ICD-10 codes increases. The use of ICD-10 will allow for a great deal of future expansion. Compared to ICD9, which only had 13,000 procedure codes, ICD10 contains 68,000, making it 19 times larger. The ICD10 coding system contains 5 times as many diagnostic codes as the ICD9 system. It also includes safeguards to ensure that new illnesses and treatments are included in the system when discovered and developed. Because of its improved precision, ICD-10 solves problems that plague diagnosis and treatment under ICD-9. For example, the ICD-9 code will not specify whether the patient’s left or right leg is being treated for burns. The same ICD-9 code is provided if the same patient is to be attended for a burn to the right leg. Distinct codes for the left and right sides of the body are used in the ICD-10 system of medical billing. The specificity of ICD10 codes has increased. Compared to ICD9 codes, this is a significant improvement made by ICD10. An accurate ICD10 classification may assist in accurately pinpointing the cause, severity, anatomical location, and kind of event. This implies that the diagnosis, treatment, and results may all be identified using only a single code. Since ICD9 does not allow for combination codes, various operations that need independent coding should be specified under individual procedures. ICD10 makes it simple to provide exact descriptions. Accurate descriptions of even very technical medical operations are possible. While it’s true that the first years of the ICD10 shift would be time-consuming, it’s also important to understand that careful, thorough medical billing will go a long way toward easing the burden. The payers will not accept claims that do not have ICD10 codes. Yet, it’s equally important to understand that the rate of rejections may be drastically reduced by switching to ICD10 codes. In other words, the doctor’s income rises as the number of rejections decreases.	4	5	2	0	0	0	0.492477	2	1,385
Complicated coding of type 2 myocardial infarctions. Advancing technology often leads to evolution of medicine. As our laboratory studies become more sensitive, we need to evaluate what the clinical significance of a positive test is. Such is the case with troponin. In October 2012, the Third Universal Definition of Myocardial Infarction (TUDMI) was published by the American Heart Association, redefining myocardial infarction (MI). The classification of MI went from transmural/subendocardial to ST-elevation myocardial infarction (STEMI/NSTEMI), and is now categorized as Types 1 through 5. I strongly recommend reading this sentinel paper. I’m going to try to parse it for you now. Acute myocardial infarction (MI) is the term for myocardial necrosis, or cell death, in a clinical setting, consistent with myocardial ischemia. “Ischemia” implies insufficient blood perfusion, and prolonged ischemia results in cell death. Other disease processes (e.g., myocarditis, cardiac contusion, etc.) can also result in cell death, and these often manifest low-level troponin elevations. This is an example of myocardial injury. I refer you to TUDMI Table 1 for a more extensive list. Myocardial infarction is a specific subset of myocardial injury. The definition of MI includes a rise and/or fall (depending on when the patient is encountered in the evolution of the MI) of a cardiac biomarker signifying cell death, with at least one value above the 99th percentile upper reference limit (URL), plus some evidence of myocardial ischemia (be it symptoms, EKG or imaging evidence, or demonstration of a thrombus). Current troponin blood tests are very sensitive (i.e., they pick up low levels) and very specific (i.e., they home in on release resulting from cardiac tissue damage). The release of cardiac biomarkers indicates myocardial injury. A significant trending of troponin indicates myocardial infarction. Typical signs and symptoms suggestive of ischemia are chest, jaw, or arm pain, dyspnea, and diaphoresis, but other symptoms may predominate, such as fatigue, nausea, or syncope. TUDMI also acknowledges that MI may occur even without symptoms in women, the elderly, diabetics, postoperative patients, and critically ill patients. Type 1 MI is due to atherosclerotic plaque and rupture or thrombosis causing mechanical coronary artery obstruction, with necrosis developing downstream in an anatomic distribution (e.g., anterior or inferior wall MI). STEMIs and NSTEMIs are subtypes of Type 1 MI. Type 2 MI arises on the basis of something other than coronary artery disease (CAD) and is due solely to “supply-demand mismatch.” There is either an increase in demand, such as tachycardia or hypertension, or a decrease in supply, such as hypotension or severe anemia (see Figure 2 in TUDMI). There is always an underlying etiology. The implication of a Type 2 MI is that it portends a worse prognosis for the causative condition. There is also higher resource utilization with ICU placement, cardiology consult, repeat EKGs, and troponin levels. Type 2 MI is a genuine diagnosis. In the inpatient hospital setting, one may also see: - Type 3 MI, which is cardiac death with symptoms of myocardial ischemia and suggestive EKG changes, but demise occurs before any biomarker trending can be demonstrated; - Type 4a MI, which is related to percutaneous coronary intervention; - Type 4b MI, related to stent thrombosis; - Type 4c MI, associated with percutaneous coronary intervention restenosis or >50 percent stenosis on coronary angiography; or - Type 5 MI, related to coronary artery bypass grafting. If the troponin is elevated but it does not constitute a Type 2 MI, there are numerous ways to refer to it, such as troponinemia, troponin leak, and non-zero troponin. The ICD-10-CM code that signifies this is R79.89, Other specified abnormal findings of blood chemistry. If it establishes the DRG, it goes into MS-DRGs 948/947, Signs and symptoms. These are relatively low-weighted DRGs (0.7726; 1.1739). If used as a secondary diagnosis, R79.89 has no risk-adjustment implications. One of the problems providers have had with diagnosing Type 2 MI was that there was no unique code for a Type 2 MI until October 2017. This meant that every time a Type 2 MI was diagnosed, the patient was marked as having atherosclerotic heart disease, and the core measures were initiated. Last October, the code I21.A1, Myocardial infarction, Type 2, was added to ICD-10-CM. So now all we have to do is to rehabilitate all the bad documentation habits our clinicians fell into. To avoid triggering core measures, they resorted to diagnosing, “demand ischemia,” and “supply-demand mismatch.” Some of the aliases are not codable, but “demand ischemia” goes to I24.8, Other forms of acute ischemic heart disease. The DRG this goes to, if PDx, is MS-DRG 311, Angina pectoris, with a relative weight of 0.6793. If it is a secondary diagnosis, it is a comorbid condition or complication (CC). There is always an underlying condition, but a Type 2 MI may be sequenced first if it was the diagnosis that, after study, occasioned the admission. If this were the case, the DRG falls into the Acute Myocardial Infarction sets (MS-DRGs 280-285) with higher weights than MS-DRG 311. All myocardial infarctions are major CCs (MCCs). Here are my suggestions for clinicians: - Order troponins when you are concerned about MI, not routinely or as a stab in the dark. Consider whether you are ruling in/out a Type 1 MI based on CAD or a Type 2 MI based on supply-demand mismatch. This will inform your action, depending on the results. - When you have a first elevated troponin, make an uncertain diagnosis: e.g., Elevated troponin, suspect Type 2 MI - Analyze additional troponins for a trend. - If there is a significant rise and/or fall, and there is a level which exceeds the 99th percentile URL, strongly consider Type 2 MI and link to the underlying etiology. As the encounter unfolds, evolve your diagnosis from uncertainty to definitive Type 2 MI. Document that core measures are not indicated for Type 2 MI. Treat the underlying condition. e.g., Troponins consistent with Type 2 MI due to hypertensive emergency. - If the patient has EKG changes or known CAD, it may be appropriate to diagnose NSTEMI or STEMI instead of Type 2 MI. If you do so, be sure to attend to core measures. - If there is no significant rise and/or fall, make an alternate diagnosis. Explicitly document that you have ruled out Type 2 MI (to save yourself a potential query):e.g., Troponin has remained constant at 0.2-0.3. Do not believe this is Type 2 MI. Suspect troponinemia due to CKD Stage 4. - If Type 2 MI is ruled out, do not propagate it in subsequent progress notes. Remove it from your list. - Please try to avoid documenting “NSTEMI Type 2.” Although Coding Clinics have given coders permission to extract and code Type 2 MI, this offends my sensibilities as oxymoronic. Here are my observations/suggestions for clinical documentation integrity purposes: - There are still lots of providers who do not know what a Type 2 MI is. You may need to offer education. - If you note an abnormal troponin early and you are interacting with a provider verbally and concurrently, bring it to their attention. It is optimal to consider Type 2 MI early, and to diagnose or rule out subsequently. I would not formally query unless and until the condition declares itself. - If troponins stay relatively constant and are not significantly elevated (by significantly, I mean exceeding the 99th percentile URL), and your provider doesn’t remark on it, don’t query. It isn’t a Type 2 MI and you will just irritate. - If troponins trend up or down, are substantially elevated, and/or there is an underlying condition that could be causing a supply-demand mismatch, query for Type 2 MI. - If a patient dies with an elevated troponin prior to being able to demonstrate a trend, it is appropriate to query for an uncertain diagnosis of myocardial infarction. In this case, the diagnosis should really be Type 3 MI, but good luck getting that documented! My loyal listeners know that my philosophy is to take excellent care of patients and to document well to get credit for having done so. We want the patient to look as sick and complex in the medical record as they look in real life. I do not believe this is padding the coffers. Patients with Type 2 MIs are sicker than patients with the same underlying condition without a Type 2 MI. We need to get this right.	4	4	0	4	0	8	0.870604	12	2,058
ICD is a medical coding system created by the World Health Organization (WHO) and is used by payers and providers to identify diagnoses and procedures. ICD-9 is the current system used in the United States and was widely adopted in the world in 1978. Today, there are many limitations to continuing to use ICD-9 codes. Over 130 countries have transitioned to ICD-10 diagnosis and procedure coding, and the United States is set to transition to ICD-10 on 10/1/2015. The transition to ICD-10 is occurring because ICD-9 produces limited data about patients' medical conditions and hospital inpatient procedures. ICD-9 is 30 years old, has outdated terms, and is inconsistent with advancements in medical technology and knowledge. Also, the structure of ICD-9 limits the number of new codes that can be created, and many ICD-9 categories are full. For example, new cardiac disease codes may be assigned to the chapter for diseases of the eye because of lack of available codes. ICD-10-CM/PCS (International Classification of Diseases, 10th Edition, Clinical Modification/Procedure Coding System) consists of two parts: - ICD-10-CM for diagnosis coding - ICD-10-PCS for inpatient procedure coding ICD-10-CM is for use in all U.S. health care settings. Diagnosis coding under ICD-10-CM uses 3 to 7 alphanumeric digits instead of the 3 to 5 alphanumeric digits used with ICD-9-CM, but the format of the code sets is similar. ICD-10-PCS is for use in U.S. inpatient hospital settings only. ICD-10-PCS uses 7 alphanumeric digits instead of the 3 or 4 numeric digits used under ICD-9-CM procedure coding. Coding under ICD-10-PCS is much more specific and substantially different from ICD-9-CM procedure coding. IlliniCare Health will be ICD-10 compliant by 10/1/2015. IlliniCare Health will be able to process (send/receive) transactions and perform internal functions using ICD-10 diagnosis and procedure codes. Providers must submit claims with codes that align with CMS and state guidelines: The following information applies to paper, web, and standard electronic (837 X12) claims. - Claims may not contain a combination of ICD-9 and ICD-10 codes. - Claims must be submitted with ICD-10 codes if the date of discharge / date of service is on or after the ICD-10 compliance date of 10/1/2015. - Claims must not be submitted with ICD-10 codes prior to compliance date of 10/1/2015. - For some claims which span the ICD-10 compliance date, the admit date on the claim can be prior to the ICD-10 compliance date and the claim can still contain ICD-10 codes. For other claims which span the ICD-10 compliance date, a splitting of the claim into two separate claims is necessary. CMS has outlined guidance on which claims will need to be split in these claims processing documents (SE1325 and MM7492). - CMS uses the “bill type” on an institutional claim for determining whether the claim should be split. In general, inpatient claims can have dates of service which span the compliance date and contain ICD-10 codes. Outpatient and professional claims cannot have dates of service which span the compliance date and have ICD-10 codes. For outpatient and professional claims, providers must split claims into two separate claims (one claim with a date of discharge on 9/30/15 and another claim with an admit date of 10/1/15). - Interim bills for long hospital stays (TOB: 112, 113, 114) are expected to follow the same rules as other claims. If a provider submits a replacement claim (TOB: 117) to cover all interim stays, it is expected that the provider must re-code all diagnoses / procedures to ICD-10 since the replacement claim will have a discharge / through date post-compliance. - All first-time claims and adjustments for pre-10/1/2015 service dates must include ICD-9 codes, even if claims are submitted post-10/1/2015. Claims with pre-10/1/2015 service dates can be submitted with ICD-9 codes for as long as contracts and provider manuals specify. - Reiteration: Claim submission date does not determine whether ICD-9/10 codes should be used. All ICD-9/10 claims submission rules outlined by CMS are based on patient discharge date, or date of service for outpatient/professional services. Claims will be reimbursed according to state reimbursement guidelines. Claims will be adjudicated natively in ICD-9 for dates of service prior to 10/1/2015 and natively in ICD-10 for dates of service on and after 10/1/2015, consistent with CMS requirements. ICD-10 diagnosis codes will be accepted on prior authorization requests submitted 7/1/15 or later for services with a start date on or after the ICD-10 compliance date. ICD-9 codes will no longer be accepted on prior authorization requests submitted on the ICD-10 compliance date or later except in the case of retro authorizations for services with a start date on or before 9/30/15. ICD-9 procedure codes are not used on authorizations and ICD-10 procedure codes will not be used on authorizations. ICD-10 Implementation and Testing Approach Our ICD-10 implementation approach aligns with CMS guidance and recommended timeframes. An ICD-10 assessment was completed in 2011-2012 and HIPAA compliance testing with providers, clearinghouses, vendors and state agencies began on July 2013. Transactional-level testing is available today to any provider interested in participating and will continue to be available through the ICD-10 compliance date. As part of this testing effort, providers who register in Ramp Manager (application used for all testing efforts) and submit 837 X12 test claims will receive TA1, 999, 277CA, and 271 eligibility responses. Providers or clearinghouses who are interested in transactional-level testing can contact the EDI service desk at 1-800-225-2573, ext. 25525 or [email protected] for further instructions. Providers or clearinghouses who are interested in testing must be direct electronic claim submitters (837 X12 claims). End-to-end testing will broaden the focus of transactional-level testing and will encompass the return of remittance advices (RAs) / explanation of payments (EOPs). Providers who conduct end-to-end testing will receive the outputs from transactional-level testing in addition to an 835 X12 Remittance Advice file. Providers or clearinghouses who are interested in conducting end-to-end testing should reach out to the health plan for further details. If contacts within the health plan are unavailable, interested providers can contact [email protected]. End-to-end testing will only be conducted with a limited number of providers and will occur in Q1-Q2 2015. Providers and clearinghouses who are confirmed as test partners will be permitted to submit up to 50 ICD-10 coded test claims in an electronic 837 X12 format. The Ramp Manager application (application used for all testing efforts) will be used as a mechanism for receiving electronic test claims and distributing electronic remittance advices. Providers who normally submit claims via clearinghouses will be asked to work with their clearinghouse on test claim submissions.	4	11	1	0	0	8	0.318986	9	1,629
Textbook of Psychiatry/Personality Disorders - 1 Introduction - 2 Each of the Personality Disorders - 2.1 Cluster A - 2.2 Cluster B - 2.3 Cluster C - 3 References Treating psychopathology requires an understanding of personality. Research on the DSM and ICD disorders is making it increasingly clear that: 1. anxiety, depression, eating disorders, substance abuse, sexual disorders, and other DSM Axis I Clinical Syndromes occur more often in the context of Personality Disorders (PDs) (Shea, Widiger, & Klein, 1992); 2. patients with multiple clinical syndrome diagnoses often have PDs (Newman, Moffitt, Caspi,& Silva, 1998); and 3. even those patients who lack personality disturbances severe enough to warrant a DSM or ICD personality diagnosis often have clinically significant pathology, such as difficulties with intimacy, management of aggression or self-assertion, rejection-sensitivity, etc (Westen, 1997). There is little question that inclusion of a PD axis in the DSM and ICD, and its refinement through two decades of research, has been a crucial step in the evolution of more clinically and empirically useful diagnostic manuals. Knowing that a patient has major depression is certainly important, but adding the "qualifier" that the patient also has borderline PD is equally important because it has significant implications for prognosis and treatment. PDs have historically been in a tangential position among diagnostic syndromes, never having achieved a significant measure of recognition in the literature of either clinical psychiatry or abnormal psychology. Prior to the DSM-III and ICD-8, they were categorized in the official nomenclature with a mélange of other miscellaneous and essentially secondary syndromes. Today, PDs occupy a place of diagnostic prominence, having been accorded a contextual role in the multiaxial schema of the DSM. Personality pathologies comprise one of two required "mental disorder" axes in the DSM. Henceforth, clinicians must not only assess the patient's current symptomatology, indicated on Axis I, but also evaluate those pervasive features which characterize the patient's enduring personality pattern, recorded on Axis II. In effect, the revised American multiaxial format requires that symptom states no longer be assessed as clinical entities isolated from the broader context of the patient's lifelong style of relating, coping, behaving, thinking, and feeling - that is, his or her personality. Personality and its disorders are regarded as a potential diathesis (Tyrer, 2007). There are clinical theorists who assert that it is the patient’s personality that should be evaluated first; only secondarily should the patient’s clinical state be considered. There are substantive reasons for attending to the PDs first, beyond the pragmatics of adhering to official nosological requirements. Lifelong personality traits appear to serve as a substrate, as well as a context for understanding more florid and distinct forms of psychopathology. Since the early 1960s, most societies have been increasingly committed to the early identification and prevention of mental disorders. This emphasis has led clinicians to attend to both premorbid behavioural signs and the less severe variants of emotional disturbance. Ordinary anxieties, minor personal conflicts, and social inadequacies are now seen by many clinicians as the forerunners of more serious problems. A significant impetus to this movement is the emergence of community health centres whose attentions are directed to the needs of the less seriously disturbed. As a result of these developments, the scope of clinical psychopathology was broadened far beyond its historical province of "Hospital Psychiatry." As a field, it now encompasses the full spectrum of mild to severe mental disorders. With personality as a contextual foundation, diagnosticians have become more proficient in understanding personality dynamics and can more clearly trace the sequences through which both subtle and dramatic clinical symptoms unfold. PDs have been estimated to affect at least 10% of the population, and constitute a large percentage of the patients seen by psychiatrists. Yet unlike other diagnoses, PDs may or may not be associated with subjective symptoms. While some categories show high comorbidity with symptomatic diagnoses such as anxiety and depression, some PDs produce distress in other people rather than in the patient. But in either case, the overall functioning of patients with PDs is often marginally social, comparable in many cases to levels seen in patients with chronic conditions such as schizophrenia. Numerous studies suggest that PDs are underappreciated causes of social cost, morbidity, and mortality. PDs are associated with crime, substance abuse, disability, increased need for medical care, suicide attempts, self-injurious behaviour, assaults, delayed recovery from Axis I and medical illness, institutionalization, underachievement, underemployment, family disruption, child abuse and neglect, homelessness, illegitimacy, poverty, STDs, misdiagnosis and mistreatment of medical and psychiatric disorders, malpractice suits, medical and judicial recidivism, disruption of psychiatric treatment settings, and dependency on public support. The amount of social cost and disruption caused by the PDs is disproportionate to the amount of attention it gets in the public consciousness, in government research funding, in medical school education or even in psychiatric residency training And no less important than dealing with the social costs of personality disorders is the potential value inherent in preventive programs designed to enhance personality resilience and adaptive capacities. Personality is seen today as a complex pattern of deeply embedded psychological characteristics that are largely nonconscious and not easily altered, expressing themselves automatically in almost every facet of functioning. Intrinsic and pervasive, these traits emerge from a complicated matrix of biological dispositions and experiential learnings, and ultimately comprise the individual's distinctive pattern of perceiving, feeling, thinking, coping, and behaving. Personality is the patterning of characteristics across the entire matrix of the person. Rather than being limited to a single trait, personality regards the total configuration of the person’s characteristics: interpersonal, cognitive, psychodynamic, and biological. Each trait reinforces the others in perpetuating the stability and behavioural consistency of the total personality structure. For the personality disorders, then, causality is literally everywhere. Each domain interacts to influence the others, and together, they maintain the integrity of the whole structure. Personality disorders are not diseases or disorders in the usual medical disease sense. Rather, PDs are theoretical constructs employed to represent varied styles or patterns in which the personality system functions maladaptively in relation to its environment. When the alternative strategies employed to achieve goals, relate to others, and cope with stress are few in number and rigidly practiced (adaptive inflexibility), when habitual perceptions, needs, and behaviours perpetuate and intensify pre-existing difficulties (vicious circles), and when the person tends to lack resilience under conditions of stress (tenuous stability), we speak of a clinically maladaptive personality pattern, that is, a PD. Differentiating Normality and Abnormality Distinctions between normality and pathology are largely social constructions or cultural artefacts. Normality and pathology must be viewed as relative concepts; they represent arbitrary points on a continuum or gradient - no sharp line divides normal from pathological behaviour. Among diverse and ostensibly content- and culture-free criteria used to signify normality are a capacity to function autonomously and competently, a tendency to adjust to one’s social milieu effectively and efficiently, a subjective sense of contentment and satisfaction, and the ability to self-actualize or to fulfil one’s potentials throughout the life span into one’s later years. PDs were noted either by deficits among the preceding or by the presence of characteristics that actively undermine these capacities. Perhaps these criteria are too westernized or Eurocentric to be universal. In some Asian cultures, for example, where the individual is expected to subordinate individual ambitions to group consensus, the capacity to function autonomously might be praiseworthy, but the desire to do so is not. The traits which compose a number of personality styles are likely in certain historical periods or cultures, such as contemporary Western societies, to promote healthy functioning (e.g., Histrionic, Compulsive, Narcissistic traits). Similarly, in this society, there are personality styles and traits that are highly conducive to pathological functioning (e.g., Avoidant, Dependent, Masochistic). There are other personality patterns (e.g., Schizotypal, Borderline, Paranoid) which have a very small probability of falling at the normal end of the continuum in almost all cultures. The interest in the description of individual differences is very old. In Theophrastus’ Characters, written in the 3rd century BC, 32 different types of human beings are described, some of them familiar to clinicians nowadays (Theophrastus, 1998). In the fourth century B.C. Hippocrates concluded that all disease stemmed from an excess of or imbalance among four bodily humours: yellow bile, black bile, blood, and phlegm. Hippocrates identified four basic temperaments, the choleric, melancholic, sanguine, and phlegmatic; these corresponded, respectively, to excesses in yellow bile, black bile, blood, and phlegm. Although the doctrine of humours has been abandoned, giving way to scientific studies on topics such as neurohormone chemistry, its terminology and connotations still persist in such contemporary expressions as being sanguine or good humoured. Along the 19th century the concept of pathological personality was forged. Pinel in 1809 described his manie sans délire, that is to say, mental illness without symptoms of illness, to which he later on also referred as folie raisonnante, that is to say, madness without insanity. J.A. Koch who proposed, replacing the established label moral insanity, with the term psychopathic inferiority Koch used the term psychopathic, a generic label employed to characterize all personality diagnoses until recent decades, to signify his belief that a physical basis existed for these character impairments. The prime psychiatric nosologist at the turn of the century, Emil Kraepelin, did not systematize his thinking on PDs, but in his efforts to trace the early course of these syndromes, Kraepelin "uncovered" two premorbid types: the "cyclothymic disposition," exhibited in four variants, each inclined to maniacal-depressive insanity; and the "autistic temperament," notably disposed to dementia praecox. The best-known European classification of disordered personalities was proposed by Kurt Schneider. Schneider differed from many of his contemporaries, most notably the prime modern constitutionalist The best-known and perhaps most fully conceptualized of PDs are those formulated by psychoanalytic theorists. Their work was crucial to the development of an understanding of the causal agents and progressions that typify the background of these disorders. It was Sigmund Freud and his younger associates, Karl Abraham and Wilhelm Reich, who laid the foundation of the psychoanalytic character typology h. Although numerous analytic theorists have continued to contribute to the study of character, the contemporary work of Otto Kernberg deserves special note. Taking steps to develop a new psychoanalytic characterology, Kernberg constructed a framework for organizing personality types in terms of their level of severity to speak of "higher, intermediate and lower levels" of character pathology; both intermediate and lower levels are referred to as "borderline" personality organizations. Note should be made of another productive personologist who utilized a mathematical/factorial approach to construct personality dimensions, namely Raymond Cattell (Cattell, RB (1965)). His research has led him to identify 16 primary traits, which he then arranged in sets of bipolar dimensions that would undergird personality types. Other contemporary quantitative contributors include Peter Tyrer (Tyrer, 1988) and W. John Livesley (Livesley, 1987). In a model which seeks to draw on genetic and neurobiologic substrates, Robert Cloninger has proposed a complex theory based on the interrelationship of several trait dispositions. Another biosocial model using three pairs of evolutionary polarities as a basis is one developed by Theodore Millon. Here, he derived a PD taxonomy that subsumed the dependent, independent, ambivalent, and detached coping styles with an activity-passivity dimension. Notably, in their recent work, numerous theorists have begun to turn their attention to positive mental health, speaking of personality resilience and adaptive capacities. The Current Official Systems, ICD-10 and DSM-IV TR Two classificatory systems of mental disorders are recognized internationally today, namely, the Diagnostic and Statistical Manual of Mental Disorders - 4th Edition-Text Revised (DSM-IV-TR)19 and the International Classification of Mental and Behavioural Disorders (ICD-10)20. Personality disorders are given important weight in both classifications. The DSM-IV-TR places them in its separate Axis II (this classification comprises five such axes). The personality disorders in the DSM are grouped into three clusters, based essentially on empirical descriptive similarities; this cluster grouping has not (and maybe never will be) been satisfactorily validated but its widespread use indicates a frequent wish to reduce the number of categories. Cluster A includes paranoid, schizoid and schizotypal personality disorders (the so-called odd or eccentric individuals), Cluster B comprises antisocial, borderline, histrionic and narcissistic PDs (the ostensible dramatic, emotional or erratic individuals), and Cluster C includes avoidant, dependent and obsessive-compulsive PDs (anxious/fearful individuals). A last category, "PD not otherwise specified," comprises disorders of personality that do not fulfil the specific criteria for any of the above individual PDs. The ICD-10 Classification includes a single section covering all personality abnormalities and persistent behavioural disturbances. This is separated into specific named personality disorders, mixed and other personality disorders, and enduring personality changes. The individual personality disorders are paranoid, schizoid, dissocial, emotionally unstable (impulsive and borderline types), histrionic, anxious (avoidant), anankastic and dependent ones. Two more categories are "other specific PDs" and "PD, unspecified." The ICD classification is similar to that of DSM-IV, although differences are noteworthy. For example, the borderline PD of the DSM-IV is subsumed as one of the two emotionally unstable disorders in ICD-10, the obsessive-compulsive adjective in DSM-IV is retained as "anankastic" in ICD-10, and avoidant personality disorder is only a partial equivalent of the ICD-10 anxious personality disorder. Two more disorders included in the official section of the DSM-IV are excluded from ICD-10; schizotypal disorder is a variant within the schizophrenia spectrum of conditions in ICD-10 and narcissistic personality disorder is only mentioned in the section on "other specific PDs" in ICD-10, without any specific criteria noted for this diagnosis. The ICD-10 contains other general categories that refer to PDs that have no counterpart in the DSM-IV, such as "mixed disorders" and "other disorders of adult personality and behaviour." Five broad sources of information are available to help describe the clinical problem; each has its own advantages and limitations. The first comprise clinical interviews and observations; the clinician observes and asks the questions and the subject responds verbally, often in a free-form style. The clinician is free to follow any particular line of questioning desired and usually mixes standard questions with those specific to the current problem. The second is structured or semi-structured interviews. Open ended, free form style clinical interviews may provide insufficient information to assess the different personality disorders. Interviewer- administered interviews, structured or semi-structured, systematically address and assess each personality disorder criteria with standard questions or probes. The most often used are International Personality Disorders Examination (IPDE), Structured Clinical Interview for DSM-IV Axis II Personality Disorders (SCID-II) and The third second are formal rating scales and checklists; a person familiar with the subject completes those forms in order to provide an objective perspective. Rating scales and checklists often serve as a memory aid, ensuring that everything relevant to the disorder is included in developing a treatment plan. Rating scales usually have more items than the diagnostic criteria for the same syndrome and are usually held to a higher standard of scientific rigor. Because they have more items, they provide more fine-grained measurements, but they also take more time to complete. For example, the revised Psychopathy Checklist (PCL-R) consists of 20 items, whereas the DSM-IV offers only seven criteria for the diagnosis of antisocial PD. Although the PCL-R is widely used in the study of psychopathy, few rating scales exist for use with other PDs. The third source is the self-report inventory; subjects literally report on themselves by completing a standard list of items. Because self-reports represent the subject’s own responses, they can be especially valuable in quickly identifying clinical symptoms. Unless the individual is violent or psychotic, a self-report inventory can be given at any point during the clinical process, often with minimal supervision. A profile obtained at the beginning of therapy, for example, can be used as a baseline to evaluate future progress. A number of other self-report instruments are available. The Tridimensional Personality Questionnaire (TPQ),, Millon Clinical Multiaxial Inventory (MCMI-III), Neuroticism-Extroversion-Openness- Personality Inventory Revised (NEO-PI-R), The Dimensional Assessment of Personality Pathology-Basic Questionnaire (DAPP), The Schedule of Nonadaptive and Adaptive Personality (SNAP) are the most often used self-report assessment instruments. The fourth source of information is projective techniques, an attempt to access unconscious structures and processes that would not ordinarily be available to the subject at the level of verbal report. These techniques seek to draw out internal, and frequently unconscious, influences on behaviour by presenting the subject with inherently unstructured, vague, or ambiguous situations. The Rorschach Inkblot Test is the classic example. The subject is presented with a series of 10 blots in turn and asked to report what he or she sees. The Thematic Apperception Test uses pictures of various interpersonal situations. The subject constructs a story to explain what is happening in the picture, what led up to these events, and how matters will end. Because projective instruments are time-consuming and not widely regarded as being as psychometrically sound as self-report inventories, their use has waned in recent years, especially with the economic constraints of managed care. Finally the use of inmates (informants) of the subject, perhaps a spouse, teacher, parent, or good friend, someone who can provide perspective on the problem, might also be considered another important source of information. Problems in the current classification The official classification systems reflect a variety of personality related issues that are likely to be solved in the near future with the revision of both systems. First, there is the question of the retention of personality disorders on a different axis (Axis II) from that of clinical syndromes (Axis I) in the DSM-IV. The division between Axis I and Axis II seems to some to be arbitrary and not justified adequately. A second persistent problem is the classificatory status of the individual categories of personality disorder. There is great overlap between the criteria for diagnosing personality disorders in both DSM-IV and ICD-10 and this seriously compromises their validity as separate disorders. Clear differentiation between the disorders is often difficult and many individuals diagnosed with a personality disorder have several other personality disorders that do not always appear to be fundamentally different. A third issue is the overlap of some personality disorders with disorders in Axis I. An example is the relationship between avoidant PD and generalized social phobia, both of which address the same group of symptoms without a clear distinction between them. Although still included in the Appendix B of DSM-IV, there seems to be a similar problem between depressive personality disorder (Axis II) and dysthymia (Axis I). A fourth question is how many personality disorders deserve separate description in the two classification systems? It is also uncertain what type of criteria should constitute the building blocks of personality disorder and how many of them are needed for each diagnosis. Both classifications rest mainly on historical traditions and committee consensus rather than on empirical data or well-constructed theoretical grounds. Many of the assumptions of each classification are implicit or covert and need to be exposed so that diagnosis can be made consistently and subjected to systematic testing. Fifth, there are also many questions about the division between "normal" personality and personality disorders that need answering and whether it is wise to have a division at all. Sixth, another major controversy in the field is the categorical/dimensional/prototypical controversy, to which we will turn shortly. A further issue is the polythetic criterion lists used in current classification systems; these produce considerable intragroup variability such that two people with the same diagnosed PD may display very different features because they score for different sections. Finally seventh , as already mentioned, PDs are tied to cultural variables to a much greater extent than the clinical disorders in Axis I, creating difficulties when diagnosing this kind of disorders across different cultures, a topic we will also address in a later section. Given the need for a clear unambiguous official classificatory system for personality disorders and the dissatisfaction with the current two systems, there are likely to be important changes in the classification of personality disorders in DSM-V and ICD-11. Perhaps the most important question is "how do we improve the clinical utility of the classification of personality disorders so that it is recognised to be helpful in decision-making at all levels?" Each of the Personality Disorders The Personality Disorders are grouped into three clusters based on descriptive similarities. Cluster A includes paranoid, schizoid and schizotypal personality disorders (the so-called odd or eccentric individuals), Cluster B comprises antisocial, borderline, histrionic and narcissistic PDs (the ostensible dramatic, emotional or erratic individuals), and Cluster C includes avoidant, dependent and obsessive-compulsive PDs (anxious/fearful individuals). A general definition of personality disorders are provided in DSM-IV-R and in ICD-10. It can be useful to psychiatrists and clinical psychologists, because the most common diagnosis in clinical practice is the diagnosis "not other specified" (Clark et al. 1995) General criteria diagnostic criteria for a Personality Disorder (ICD-10) A specific personality disorder is a severe disturbance in the characterological constitution and behavioural tendencies of the individual, usually involving several areas of the personality, and nearly always associated with considerable personal and social disruption. Personality disorder tends to appear in late childhood or adolescence and continues to be manifest into adulthood. It is therefore unlikely that the diagnosis of personality disorder will be appropriate before the age of 16 or 17 years. General diagnostic guidelines applying to all personality disorders are presented below; supplementary descriptions are provided with each of the subtypes. Conditions not directly attributable to gross brain damage or disease, or to another psychiatric disorder, meeting the following criteria: (a) markedly dysharmonious attitudes and behaviour, involving usually several areas of functioning, e.g., affectivity, arousal, impulse control, ways of perceiving and thinking, and style of relating to others; (b) the abnormal behaviour pattern is enduring, of long standing and not limited to episodes of mental illness; (c) the abnormal behaviour pattern is pervasive and clearly maladaptive to a broad range of personal and social situations; (d) the above manifestations always appear during childhood or adolescence and continue into adulthood; (e) the disorder leads to considerable personal distress but this may only become apparent late in its course; (f) the disorder is usually, but not invariably, associated with significant problems in occupational and social performance. For different cultures it may be necessary to develop specific sets of criteria with regard to social norms, rules and obligations. For diagnosing most of the subtypes listed below, clear evidence is usually required of the presence of at least three of the traits or behaviours given in the clinical description. For additional information and references see Module II in Simonsen E, Ronningstam E, Millon T (Eds). (2007). WPA ISSPD Educational Program on Personality Disorders. www.wpanet.org/education/education.shtml: Henning Sass & Reinhild Schwarte: Schizoid Personality Disorder (pp. 129-133) Schizoid Personality Disorder. Svenn Torgersen: Schizotypal Personality Disorder (pp. 134-141). Elizabeth Iskander & Larry J. Siever. Paranoid Personality Disorder (pp. 110-116) Schizoid Personality Disorder (partly adopted from Henning Sass & Reinhild Schwarte ) Jacob is a 26 years old man. Despite extraordinary intelligence John was not able to complete or participate in any educational program. He wanted to have a normal life with a family and friends, but thought that he was rootless and he felt that other people thought that he was peculiar or odd. He felt that he was outside. As a child he went to various schools because his parents moved around. He was thought of as a lonely wolf and did not participate in the social life or games of sports with his peers. During school class he was often absent minded being absorbed in his own thoughts and fantasies. From around the age of thirteen he became interested in computers and was quite advanced in his understanding of mathematics. He became exceedingly isolated with his computer as his sole companion. This vignette schizoid personality illustrates the difficulties how to establish a stable relationship to significant others like peers and family. Often it is regarded as unusual that a person with schizoid personality disorders complains by himself or herself to be isolated. Many schizoid patients, in the contrary, claim to be quite satisfied with their loneliness and it is quite unusual that he wish to have a family. Also schizoid persons usually accept their situation or even deny any desire for closer relationships. Diagnostic Criteria ICD-10 F60.1 Schizoid personality disorder Personality disorder meeting the following description: (a) few, if any, activities, provide pleasure; (b) emotional coldness, detachment or flattened affectivity; (c) limited capacity to express either warm, tender feelings or anger towards others; (d) apparent indifference to either praise or criticism; (e) little interest in having sexual experiences with another person (taking into account age); (f) almost invariable preference for solitary activities; (g) excessive preoccupation with fantasy and introspection; (h) lack of close friends or confiding relationships (or having only one) and of desire for such relationships; (i) marked insensitivity to prevailing social norms and conventions. Excludes: Asperger's syndrome (F84.5) delusional disorder (F22.0) schizoid disorder of childhood (F84.5) schizophrenia (F20. - ) schizotypal disorder (F21) The central feature of Schizoid Personality Disorder (SPD) is a pattern of pervasive social detachment and a narrow range of emotional expression in social settings. The DSM-IV criteria for SPD differ in detail in three criteria from the ICD-10 diagnostic criteria. The both describe the SPD by seven criteria, of which at least three must be applicable. The SPD is most clearly defined within relationships. Individuals with this disorder are characterized by a profound defect in their ability to form personal relationships or to respond to others in an emotionally meaningful way and appear to lack a desire for intimacy. They are introverted, aloof, and seclusive, and select activities that do not include much interaction with others. This style of life easily results in social isolation. The differential diagnosis of SPD includes: 1. a normal preference for solitary pursuits that does not meet the criteria for schizoid personality disorder; 2. schizophrenia (in which further characteristic negative or positive symptoms occur); The SPD appears to characterize the negative symptoms of schizophrenia, e.g., social, interpersonal, and affective deficits like little affect, low energy, anhedonia, diffidence about, shyness in, or detachment from relationships. 3. schizotypal personality disorder (in which there are cognitive and perceptual distortions); In contrast to the schizotypal personality disorder the SPD does not include psychotic-like cognitive/perceptual distortions. 4. paranoid personality disorder (in which the patient displays suspiciousness and paranoid ideations); 5. avoidant personality disorder (in which the patient has a fear of being embarrassed or inadequate, with excessive anticipation of rejection); 6. obsessive-compulsive personality disorder (in which there may be apparent social detachment that arises from devotion to work and discomfort with emotions; capacity for intimacy is usually preserved); 7. disorders of more severely impaired social interaction, stereotyped behaviours and limited interests (e.g., autistic disorder, Asperger’s disorder); 8. personality change caused by a general medical condition (e.g., temporal lobe epilepsy); personality symptoms derived from chronic substance use (Sass, 2007). The most frequent co-occurring personality disorders with SPD are schizotypal and avoidant personality disorders and to a lesser degree paranoid, antisocial and borderline personality disorders (Kalus et al. in Livesley, 1995, p.65). The highest co-occurrences may perhaps be because of the high overlap between the two criteria sets. The SPD and the schizotypal personality disorder, for example, share the important criteria of social isolation and restricted affect. Also the avoidant personality disorder may seek isolation, but individuals with SPD will tolerate the separation with comfort, while individuals with avoidant personality disorder will be distressed and lonely. SPD can an antecedent disorder to schizophrenia, major depression, dysthymia or a delusional disorder. Further it shows high comorbidity with social phobia and agoraphobia. If people with SPD are detached from a supportive family they often become involved with drugs and alcohol. SPD is uncommon in clinical treatment settings. SPD is diagnosed more frequently in males who seem to be more impaired than females with SPD. The etiology of SPD has not been established. A close genetic relationship to schizophrenia has been proposed but is doubtful. Conversely, introversion has been shown to be a highly heritable personality trait. Psychological theories suggest sociocultural factors in the genesis of the disorder: In the psychodynamic approach, the SPD emerges from inadequacies in earliest relationships with parental figures. The cognitive approach suggests that the most important source of dysfunctional behaviour and affects lie in incorrect attributions that people make. As patients with SPD have few complaints and do not seek an interpersonal context for solving their problems, they rarely seek therapy. The disorder is most likely to come to medical attention in the course of intervention for another condition, in response to acute stressors or because of family influence. Others who come into treatment are forced to do so by family or even the legal system. Acutely stressful situations often require crisis intervention. Aims of long-term psychotherapeutic interventions are to maintain stability and support, to improve social skills and comfort, to help maximize quality of an isolated lifestyle. In treatment, clients with SPD challenge service providers with the absence of response. As they do not response to emotional leverage, therapists easily feel frustrated and ineffective. The contact between therapist and patient should be an important element of the therapy. An important step of the therapy should be to open possibilities to make new experiences and changes (Saß and Jünemann, 2001). The therapist should be aware that major changes and modifications of character structure are unlikely. The therapy should be aimed at achieving modest reductions in social isolation and in prompting more effective adjustment to new circumstances (Kalus et al. in Livesley, 1995). Behavioural psychotherapy can be helpful for some patients including, for example, methods such as problem solving, social skills training or role plays. Educational strategies may be effective in working with individuals with SPD to identify (1) their own emotions; (2) the emotions they elicit in others; and (3) possible feeling states of people with whom they relate. Intervention with individuals with SPD may include methods of cognitive therapy, e.g., exploring their self-concept and sense of where they belong in the world. Confrontation should clarify the relation of emotions to thinking and encourage these clients to be present with reality. Individual psychoanalytically oriented psychotherapies are less likely to succeed (Kalus et al. in Livesley, 1995, p.66). Most psychopharmacological interventions apply to comorbid disorders such as depression or anxiousness. Schizotypal Personality Disorder (partly adopted from Svenn Torgersen) A 37 year old, unemployed man claimed of recurrent irrational thoughts, compulsive behaviour, and social isolation. Since his childhood he had always been eccentric, withdrawn with no real friends anxiously fearing closer relationships, preoccupied with reading stories about Dracula and other myths. He didn’t share his inner thoughts or feeling with anybody, including his parents. He never finished an education, but worked in factories, often at night. Some years earlier he started doubting if his work was accurate enough. Although he recognized these thoughts as irrational, he started spending a lot of time controlling his work over and over again. Soon these compulsive controls took so much time that he could not finish his work, was continuously annoyed by intrusive vivid homosexual images, was preoccupied with doubts concerning almost everything at home and also he had to look persistently at people in order to be sure to maintain their images in his memory. He started fearing that people could notice his behaviour, and he felt that unknown people were staring at him and that they secretly were making fun of him. He complained of being unable to reveal his feelings and thoughts to other people and felt isolated. He started drinking alcohol to control his increasing anxiety. He adopted different peculiar strategies, which ended in new vicious circles of obsessive symptoms and suspiciousness. This case is diagnosed with obsessive-compulsive disorder (OCD), Alcohol abuse and Schizotypal Personality Disorder. He had long lasting personality difficulties like suspiciousness, odd behaviour and social anxiety prior to the OCD symptoms. Comorbidity is often seen in Schizotypal Disorder, and it is the axis I disorders that usually brings the patients to treatment. The historical roots of schizotypal personality disorder (STPD) are the non-psychotic personality syndromes within the spectrum of schizophrenia. The definition of schizotypal personality disorder has remained more or less the same during the revisions of DSM and consists in DSM-IV of the following criteria: (1) ideas of reference (excluding delusions of reference), (2) odd beliefs and magical thinking that influences behaviour and is inconsistent with subcultural norms (e.g., superstitiousness, belief in clairvoyance, telepathy, or "sixth sense;" in children and adolescents, bizarre fantasies or preoccupations), (3) unusual perceptual experience, including bodily illusions, (4) odd thinking and speech (e.g., vague, circumstantial, metaphorical, over elaborate, or stereotyped), (5) suspiciousness or paranoid ideation, (6) inappropriate or constricted affects, (7) behaviour or appearance that is odd, eccentric, or peculiar, (8) lack of close friends or confidants other than first-degree relatives, (9) excessive social anxiety that does not diminish with familiarity and tends to be associated with paranoid fears rather than negative judgment about self. ICD-10 included schizotypal disorder among the psychoses and defined it partly similarly, partly differently from DSM. The only difference between DSM-IV and ICD-10 is that DSM-IV includes "ideas of reference" and "excessive social anxiety," while ICD-10 includes obsessive rumination and micropsychoses. However, ideas of reference are close to suspiciousness, and micropsychoses are close to unusual perceptual experiences, so the only real difference is social anxiety and obsessive ruminations. As evolving from the spectrum of schizophrenia, the boundaries between schizotypal personality disorder and schizophrenia are not easy to define. The prodromal symptoms of schizophrenia are similar to the schizotypal personality disorder. Thus, retrospectively, "premorbid" may be added to STPD, according to DSM-IV. When fully developed hallucinations and delusions are presented during a one -month period, the diagnosis is schizophrenia. However, a person with delusions or hallucinations plus negative symptoms may show a clinical picture similar to STPD; even so schizophrenia is the correct diagnosis, if the duration requirements are fulfilled. Even more difficult is the differentiation between simple schizophrenia and STPD in ICD-10. In practice, the differentiation is impossible, as the criteria for simple schizophrenia, personality changes, negative symptoms: and reduced social function is indistinguishable from the early developmental phase of STPD. However, simple schizophrenia requires change, while STPD implies no clear starting point. The possible early start of STPD, however, may make it difficult to distinguish STPD from milder forms of pervasive developmental disorders (autism). As to other psychotic disorders, the manifestation of full-blown delusions (not only ideas of reference and suspiciousness) and hallucinations (not only illusions) preclude any diagnosis of STPD. The boundaries between STPD and borderline personality disorder are of course difficult to draw, as both personality disorders emerged from the same borderline psychoses concept. They share the pseudo-psychotic and paranoid features, and quite a few people may live an unstable and turbulent life similar to those with borderline personality disorder. Even so, the impulsivity and affective intensity and variability in the borderline personality disorder are not part of the STPD criteria set. Furthermore, those with borderline personality disorder are not expected to display the socially inept and chronically withdrawn pattern of STPD. Instead, some people with borderline personality disorder may withdraw when they get older, as a consequence of using up the patience of their acquaintances and having experienced a brimful of disappointments in their partnerships and relationships. STPD is close to schizoid personality disorders. The two disorders share the social isolation and the constricted affects. However, STPD has the oddness and the pseudo-psychotic features in addition. In the same vein, those with paranoid personality disorder share the paranoid features with STPD, but not the withdrawal, oddness and pseudo-psychotic features. STPD shares the social anxiety and the tendency to withdrawal with avoidant personality disorder, but not the eccentricity, paranoid features and illusions. Avoidant, paranoid and borderline personality disorders were especially highly correlated to STPD. STPD is associated with psychotic disorders including schizophrenia . Furthermore, there seems to be an association with obsessive compulsive and phobic disorders. There may also be an association with dysthymic disorder, panic disorder, somatoform disorders and eating disorders. Relatively few studies of the prevalence in the general population have been performed. The samples are seldom quite representative, and differently structured interviews are applied, based on different editions of DSM. The most representative studies show a prevalence of 0.7 (Maier et al. 1992) and 0.6 (Torgersen et al. 2001). Those with a higher number of schizotypal traits have less education and more often live alone in the city centre compared with those with a lower number. STPD seems thus more prevalent among men in clinical samples. A meta-analysis of the so-called "Big-Five" and personality disorders showed that what characterized those with STPD were first and foremost Neuroticism, second Introversion and third Non-Agreeableness. The pattern was similar to paranoid and borderline personality disorders in Neuroticism and Non-agreeableness, and similar to avoidant personality disorder in Neuroticism and Introversion. Furthermore, STPD was similar to schizoid personality disorder in Introversion, to antisocial and narcissistic personality disorders in Non-agreeableness, and to dependent personality disorder in Neuroticism. There were no similarities to histrionic and obsessive-compulsive personality disorders. Together with borderline personality disorder, those with STPD were extreme on most personality disorders, three out of five dimensions. The results of the studies of the relationships between STPD and personality dimensions fit in with the large overlap between STPD and paranoid, avoidant and borderline personality disorders. A study of the relationships between personality disorders and Cloninger’s temperament and character scales suggests that STPD is negatively correlated to Self-directedness and Cooperation, and positively correlated to Self-transcendence. The results illustrate the vulnerable, withdrawn and psychotic-like aspects of STPD. Even if STPD is correlated to common personality dimensions one cannot jump to the conclusion that STPD is a construct based on these dimensions. It may be that those with schizotypal traits simply answer in an extreme way when these dimensions are measured by the questionnaires. Then we approach the question about the categorical or dimensional nature of schizotypal features. Some statistical analyses suggest that that a latent discontinuity underlies the variation in schizotypal traits (Lenzenweger & Korfine, 1995). Others believe more in a dimensional model of schizotypy, with poorly functional individuals at one end of the dimensions, and well-functioning individuals among those with somewhat lower scores on schizotypal inventories (Goulding, 2004). Those more poorly functioning are more anhedonic and with more cognitive disturbance, while those well-functioning are more characterized by unreal experiences. STPD is genetically influenced as are other personality disorders (Torgersen 1986; Torgersen et al. 2000; Kendler & Hewitt, 1992). This is also the case for schizotypal traits in children (Coolidge et al. 2001). However, what is especially important is the genetic relationship to other mental disorders. Some studies suggest a familial relationship between STPD and the whole realm of psychoses (Squires-Wheeler et al. 1989; Kendler et al. 1995). As STPD evolved out of the familial schizophrenic spectrum, the genetic relationship to schizophrenia is of particular interest. Studies of co-twins of schizophrenic patients (Torgersen, 1992), and biological relatives of adopted-away schizophrenics (Kendler & Gruenberg, 1984) confirmed the specific familial and genetic relationship between STPD and schizophrenia. No other personality disorders seem to be consistently related to schizophrenia. However, STPD as defined by DSM does not seem to cover adequately the schizophrenia-related STPD. Those adopted-away offspring of schizophrenics who develop personality disorders seem to experience frequent somatoform complaints and poor social function in addition to withdrawal and emotional constriction (Gunderson et al. 1983). In fact, STPD consists of two syndromes that may be independently inherited (Siever, 1995; Kendler and Hewitt, 1992), a constricted/eccentric syndrome that is characterized by odd and eccentric appearance and behaviour, thoughts and communication, and a psychotic-like syndrome that is characterized by ideas of reference, magical thinking, illusions and depersonalization/derealization. While the former syndrome seems to be genetically related to schizophrenia (Torgersen, 1993), the latter is not. Even if there might exist a familial relationship between STPD and affective disorder, a genetic relationship to major depression is not confirmed. We do not know what environmental factors influence the development of STPD. A retrospective study showed that those with STPD more often reported neglectful parenting from both parents, which means little love and also little control (Torgersen & Alnæs, 1992). Those with borderline personality disorder more often reported affectionless control, meaning little love and much control. Those with other personality disorders more often experienced affectionate constraint; much love and much control, while those without personality disorder reported optimal parenting; much love and little control. Course and prognosis A Norwegian twin study showed that those with STPD had poor social as well as occupational adjustment (Torgersen, 1986). Skodol et al. (2002) found dysfunction in relation to parents, sibs, and friends, occupational dysfunction, and dysfunction in relation to more distant family members among those with schizotypal personality disorder. Quality of life is also reduced among those with STPD (Cramer et al. 2003). They have a poor subjective well-being, poor self-realization, less contact with friends and family, less social support, a lot of negative life events, poor neighbourhood quality, and generally a poorer global quality than those without STPD in the general population. Among the personality disorders, nobody displayed poorer quality of life than those with STPD. The neuropsychological and biological fundamentals of STPD are far from settled. Even so, some results are forthcoming. There seems to be a difference between the constricted/ eccentric and the psychotic-like STPD syndromes. Neuro-psychological tests measuring attention and information processing observe impairment among those with constricted/eccentric traits (Siever, 1995). Indication of a low dopamine level are found among those with the constricted/eccentric syndrome, for instance by a low concentration of homovannilic acid (HVA). An adequate dopamine activity is necessary for maintenance of working memory, a function necessary for social engagement as well as other executive functions. The deficient information processing may contribute to the social withdrawal, emotional constriction and eccentricity among those with STPD. On the other hand, those with the psychotic-like syndrome seem to have an exceptionally high level of dopamine-activity, as also demonstrated in a high concentration of HVA. The increased dopaminergic activity may explain the psychotic-like traits such as illusions, paranoid ideations etc. Usually psychotherapeutic approaches are applied for patients with STPD. No controlled results are published. However, from clinical experience there are some precautions that are important to take into account. Some less experienced clinicians may be fascinated with all the grotesque and symbol-rich material patients with STPD may produce. They show interest, ask for details and encourage the patient to tell more. This can be great for the clinician, but hardly helpful for the patient. The patient may slide even more into the disturbing inner fantasies. A better approach is to dedramatize the strange thoughts and pictures, not reject, if the patient is active in telling, not refrain from showing a strong interest in the material. Instead, it is important for the patient to learn social skills, to discuss what went wrong in interpersonal situations, what behaviour is common and appropriate. As to pharmacotherapy, the best approach is to treat the axis-I disorder in cases where those with STPD have it in addition. If the clinical picture is dominated by psychotic-like features, neuroleptic may be the treatment of choice. There are some indications that blocking of dopaminergic activation may help those with psychotic-like traits. On the other hand, those with constricted/eccentric features may be helped by drugs that functions like amphetamine - releasing dopamine and blocking its reuptake. Paranoid Personality Disorder (partly adopted from Elizabeth Iskander & Larry J. Siever) A 36 year old divorced worker developed a severe depression after he was fired from his job and subsequently had severe alcohol problems. He presented himself to the general practitioner with somatic complaints, anxiety, compulsively washing his hands, fatigue, disturbing inner feelings of hatred towards other people. His troubles started in his childhood. He reported that he was very aggressive towards other children and he was involved in recurrent conflicts. At home he was constantly on guard. In his work relations he was involved in severe interpersonal conflicts, reacting with aggressive attacks at the slightest offences. The last years he spent working, he was continuously involved in conflicts with his colleagues. After a short contact with a female colleague who terminated the relationship with him. The only person he stayed friends with was his brother-in-law who lived a hundred kilometres away. This vignette illustrates important issues and characteristic features of the paranoid personality. First, they do not seek treatment unless they are in a crisis (fired from job) or because of additional pathology (depression). Second, when decompensated they most often get depression, panic attacks, OCD, somatoform disorder as in this case or in other cases an additional alcohol abuse. Third, the vignette may support a psychodynamic formulation of key elements in his personality functioning. His personality pathology is excessive aggression and mistrust. Clinical Description Diagnostic Criteria ICD-10 F60.0 Paranoid personality disorder Personality disorder characterized by: (a) excessive sensitiveness to setbacks and rebuffs; (b) tendency to bear grudges persistently, i.e., refusal to forgive insults and injuries or slights; (c) suspiciousness and a pervasive tendency to distort experience by misconstruing the neutral or friendly actions of others as hostile or contemptuous; (d) a combative and tenacious sense of personal right s out of keeping with the actual situation; (e) recurrent suspicions, without justification, regarding sexual fidelity of spouse or sexual partner; (f) tendency to experience excessive self-importance, manifest in a persistent self-referential attitude; (g) preoccupation with unsubstantiated "conspiratorial" explanations of events both immediate to the patient and in the world at large. lncludes: expansive paranoid, fanatic, querulant and sensitive paranoid personality (disorder) Excludes: delusional disorder (F22. - ) schizophrenia (F20. - ) Paranoid personality disorder is a clinically well-recognized disorder that has not, however, been the object of a great deal of investigation. Although noted in the writings of psychiatrists since the late 1800's, the condition was first called "paranoid personality" by Kraepelin in 1921 (Akhtar, 1990). The hallmark criteria regarding paranoid personality disorder (PPD) are distrust and suspiciousness of others such that others are seen as purposefully attempting to harm one in some way without any evidence to suggest this is the case. Those with paranoid personality disorder also may be very critical of others, argumentative and rigid in beliefs, again stemming from harbouring unwarranted suspicions about people around them. This often leads to problems with relationships, both personal and in the work place. The ICD-10 lists seven criteria (see above) of which only three must be met. The current criteria for diagnosing paranoid personality disorder in DSM IV-TR includes seven symptoms of which at least four must be met. Most are essentially the same as the ICD criteria. These include suspicion that others are harming or deceiving one in some way, preoccupation with doubts about the loyalty of friends, reluctance to confide in others out of fear that information may be used against them, reading threatening meaning into benign events, bearing grudges over insults or slights, hasty and angry reaction to perceived attacks on character, and unjustified suspicion regarding the fidelity of a spouse or partner. There is one criterion that does not exist in the DSM IV and that is "tendency to experience excessive self-importance, manifest in a persistent self-referential attitude." This item, basically implying a level of grandiosity, also did not exist in the DSM III or III-R versions. Paranoid personality disorder must be diagnosed to the exclusion of schizophrenia, or any other psychotic disorder including psychosis in the context of a mood disorder. Paranoid personality disorder is considered "premorbid" if it is present prior to an Axis I psychotic disorder. There is substantial comorbidity of Axis I disorders; individuals with paranoid personality disorder appear to have an increased likelihood of developing depression, agoraphobia, obsessive compulsive disorder and alcohol or substance abuse or dependence. With regard to comorbid personality disorders, there is some variation in the literature. Generally though, it has been suggested that in clinically based samples, over 75% of patients who met paranoid personality disorder criteria also met criteria for other personality disorders, the most common were found to be schizotypal and narcissistic. One area of research is the possible relationship of PTSD with paranoid personality disorder. When 180 outpatients were analyzed using the DSM III-R, subjects with paranoid personality disorder had a higher rate of comorbid PTSD than subjects without the disorder (29% compared with 12%) (Golier et al. 2003). In addition, they had elevated rates of physical abuse and assault in childhood and adulthood (54% compared with 35%). This suggests a possible link between trauma during early events in life and subsequent paranoid behaviour and mistrust. Another area that has received some attention is the relationship of violence to paranoid personality disorder. Paranoid cognitive personality style was found to increase the risk of violence in subjects with personality disorders, particularly schizophrenia spectrum disorders (Nestor, 2002). According to the DSM-IV, the prevalence of paranoid personality disorder was 0.5 to 2.5% in the general public, and more common in males. Interestingly, the 1997 National Survey of Mental Health and Wellbeing (conducted in Australia) using the ICD-10 to assess personality disorders found a 1.34 % prevalence of paranoid personality disorder and no sex difference, despite the similarities in criteria between the DSM and the ICD. There is some current evidence that paranoid personality disorder may be more difficult to diagnose than other personality disorders. A study of interrater reliability using DSM IV achieved good agreement. However, in the same study, when analyzing test-retest reliability based on how consistent a patient’s report is from one clinician to another, and how information is interpreted and scored, paranoid personality disorder had the lowest reliability of all the personality disorders (Zanarini et al. 2000). It has been suggested that paranoid personality disorder may be related to certain Axis I disorders, including schizophrenia and delusional disorder. Kendler found a much higher risk of paranoid personality disorder in first degree relatives of those with delusional disorder as opposed to relatives of those with schizophrenia, 4.8% compared to 0.8% (Kendler et al. 1985). On the other hand, paranoid personality disorder was significantly more common in the biologic relatives of patients with schizophrenia when compared with relatives of controls (Kendler et al. 1982). Using data from the Roscommon family study, an epidemiologic study conducted in Ireland, it was discovered that biological relatives of those with schizophrenia had a significantly higher amount of paranoid personality disorder compared with relatives of controls (Kendler et al. 1993). As with other disorders, cultural factors must be taken into account in diagnosing this disorder. There are some groups that might, for reasons of maltreatment, language barriers, and unfamiliarity to this society, display what could be labelled paranoid traits. Those groups include: minority groups, immigrants and refugees. In an epidemiologic study recently completed on personality disorders, minorities such as blacks, Hispanics and Native Americans were at greater risk for having paranoid personality disorder than whites (Grant et al. 2004). Also according to the same study, paranoid personality disorder was more common among younger people (18-29), those with lower incomes, and those who were divorced or never married. Some of these findings are not surprising, taking into account the nature of paranoid personality disorder. However, this does bring up the question of which came first: Are some paranoid traits the result of maltreatment by others due to socioeconomic status, race, etc., or does the disorder contribute to, for example, inability to succeed professionally or remain in a relationship? There appears to be a combination of both, which can contribute to complications in diagnosing the disorder. - Course and Prognosis Paranoid personality disorder can be noted first in childhood; symptoms observed include solitariness, social anxiety and odd thoughts and language. There is not a lot of data regarding the course and prognosis of the disorder. This is likely due to the fact that as it is a personality disorder, it tends to be stable over adult life and although it can cause interpersonal problems, does not often require treatment. It has been observed that the course of the disorder rarely worsens or goes into remission (Akhtar, 1990). There is no specific treatment or medication for paranoid personality disorder. When existing in conjunction with other personality disorders, i.e., borderline personality disorder, treatment may be sought but that is primarily due to symptoms experienced in other personality disorders. There is some data on the effectiveness of day treatments for patients with personality disorders in general (Karterud et al. 2003). Treatment results, although effective for some personality disorders (i.e., borderline), were the poorest for those with paranoid, schizoid, and schizotypal personality disorders. Cluster B includes four personality disorders: Antisocial (ASPD), Borderline (BPD), Histrionic (HPD) and Narcissistic (NPD). According to DSM IV-TR individuals with these disorders appear dramatic, emotional or erratic. For additional information and references see Module II in Simonsen E, Ronningstam E, Millon T (Eds). (2007). WPA ISSPD Educational Program on Personality Disorders. www.wpanet.org/education/education.shtml: Hart S., Cooke D. Antisocial Personality Disorder (pp. 60-66); Bateman A., Fonagy P. Borderline Personality Disorder (pp. 74-83); Pfohl B. Histrionic Personality Disorder (pp. 90-94) and Ronningstam E: Narcissistic Personality Disorder (pp.95-103 ). (adopted from Stephen Hart & David Cooke) - Case vignette This is a 27 year old male who committed murder at age 17. He stayed in a high-security hospital for 10 years and started individual treatment after being released. He was an intelligent boy who did well in school until his peers began to tease him. This made him feel helpless and unable to defend himself. At home, however, he felt strong and supportive of his mother. His father lived with another woman. He experienced him self as a looser among his pears but as a winner with his mother. At the end of primary school his father, who then had accumulated substantial wealth, returned home, and the parents resumed their marriage and intimacy. His situation at school changed as he became popular and the teasing stopped, but he still felt insecure and uneasy. He decided to attend karate school to gain a sense of power. A peer introduced him to the criminal milieu where he felt accepted and appreciated. During a robbery he became incredible angry and physically violent without really understanding why. The victim died as a consequence of his attack. He was send to prison for 2 years, followed by a high security hospital for treatment. While he accepted his prison sentence he protested treatment in psychiatric hospital. He was suspicious, remained non-relative and was often restrained due to anger outbursts. A therapist confronted him with the fact that his behaviour could lead to prolonged hospital stay and pointed to his choice of future inside or outside the hospital. This was turning point that made him focus on goals and training for a future out in real life. After discharge he continued to work on self-esteem and trustworthiness, shame and guilt and how to understand, control and come to terms with his anger. Two years later he was married with a son, and pursued a career as a teacher. - Clinical description Diagnostic Criteria ICD-10 F60.2 Dissocial personality disorder Personality disorder, usually coming to attention because of a gross disparity between behaviour and the prevailing social norms, and characterized by: (a) callous unconcern for the feelings of others; (b) gross and persistent attitude of irresponsibility and disregard for social norms, rules and obligations; (c) incapacity to maintain enduring relationships, though having no difficulty in establishing them; (d) very low tolerance to frustration and a low threshold for discharge of aggression, including violence; (e) incapacity to experience guilt or to profit from experience, particularly punishment; (f) marked proneness to blame others, or to offer plausible rationalizations, for the behaviour that has brought the patient into conflict with society. There may also be persistent irritability as an associated feature. Conduct disorder during childhood and adolescence, though not invariably present, may further support the diagnosis. Includes: amoral, antisocial, asocial, psychopathic, and sociopathic personality (disorder) Excludes: conduct disorders (F91. - ) emotionally unstable personality disorder (F60.3) People with ASPD (Dissocial in ICD 10) show unreliability, recklessness, restlessness, disruptiveness, and aggressiveness. According to DSM IV-TR (2000) they have a pervasive pattern of disregard for, and violation of, the rights of others. Negative symptoms include lack of anxiety and remorse, and lack of emotional depth and stability. They are interpersonally detached, suspicious, and exploitative, and they lack commitment to and concern for others. Antagonism, deceitfulness, manipulativeness, dishonesty, and glibness are typical interpersonal features. Some come across as self-aggrandizing and self-justifying with a sense of entitlement and invulnerability. Cognitive deficits include inflexibility, and lack of concentration. The lifetime prevalence of ASPD is about 2-3 % in the general population. The rate in the community and psychiatric population is relatively low (1-2%), but among correctional offenders, forensic psychiatric patients, and substance users it is high (< 50%). Theoretical models for the etiology of ASPD suggest a mental abnormality with social and biological causal factors, and have excluded child rearing experiences, familial dysfunctions, or adverse life experiences. Sociocultural and neurological factors are associated with symptoms of ASPD, but not clearly pathognomonic. Other theories consider ASPD as an extreme variant of personality traits found in all people, or as an adaptation. Early manifestations of ASPD are evident in children (age 6-10 years), and it is common that adults with ASPD in their childhood or adolescence were diagnosed with conduct disorder, oppositional defiant disorder, or attention deficit hyperactivity disorder. Symptoms of ASPD can persist into middle or late adulthood. ASPD has been associated with increased rate of morbidity and mortality. Antisocial personality disorder is often comorbid with substance-use disorders, but also with other personality disorders, such as the Cluster B borderline, narcissistic, and histrionic in DSM-IV or emotionally unstable and histrionic in ICD-10. There is no good evidence that ASPD can be successfully treated. Most treatment studies have aimed at reducing criminal behaviour in mixed groups of patients or offenders, including some with ASPD, rather than attempting to alleviate symptoms of ASPD. Nevertheless, structured psychosocial treatments that focus on the acquisition of important life skills, such as communication, assertiveness, and anger management skills are useful (Hemphill & Hart, 2002). Pharmacological treatments that target treatment-interfering symptoms, such as extreme hostility or impulsivity, may play a useful adjunctive role in certain cases. Borderline personality disorder (adopted from Anthony Bateman & Peter Fonagy) - Case vignette A 23 years old woman reacted with depressive symptoms and suicidal thoughts to the death of her grandfather. She was treated with antidepressant medication without addressing the loss. Three years later after a suicidal attempt, she was admitted to hospital where she first presented with depressed mood and suicidal thoughts, but quickly engaged in vivid conversations with the others patients. She was discharged with the diagnosis of personality disorder, but soon re-admitted because of suicidal thoughts, and referred to an outpatient program specialized on treatment of personality disorder. Since childhood she had unstable mood, aggressive temperament and self-destructive behaviour (head banging). At the age of 10 she was sexually abused by an older man. Suicidal thoughts and urges to kill herself was first experienced at age 11. Since age 13 she has had multiple sexual partners but also one 7 year long relationship which was quite unstable with frequent conflicts and impulsive acts. She dropped out of school and has been living on sickness benefits, interrupted by short periods of unskilled employment. In a two year psychoanalytic treatment program with one individual session and one group session a week in addition to psycho education, she worked together with other patients on identifying and understanding the characteristic features of BPD, and the dynamics of borderline pathology with a special focus on self-destructive behaviour. Her self-destructive behaviour tapered off after 3 months as she began to process her feelings of aggression and sadness. The pharmacological treatment terminated after 6 months and she quickly became less sedated and anxious. She resumed school towards the end of the first year of treatment, with the intention of taking a degree in teaching. The relationship with her boyfriend stabilized. Contacts with class became more satisfying, and conflicts with her teachers stopped. Her ability to begin to contain feelings increased dramatically. - Clinical Description Diagnostic Criteria ICD-10 F60.3 Emotionally unstable personality disorder A personality disorder in which there is a marked tendency to act impulsively without consideration of the consequences, together with affective instability. The ability to plan ahead may be minimal, and outbursts of intense anger may often lead to violence or "behavioural explosions"; these are easily precipitated when impulsive acts are criticized or thwarted by others. Two variants of this personality disorder are specified, and both share this general theme of impulsiveness and lack of self-control. - F60.30 Impulsive type The predominant characteristics are emotional instability and lack of impulse control. Outbursts of violence or threatening behaviour are common, particularly in response to criticism by others. lncludes: explosive and aggressive personality (disorder) Excludes: dissocial personality disorder (F60.2) - F60.31 Borderline type Several of the characteristics of emotional instability are present; in addition, the patient's own self-image, aims, and internal preferences (including sexual) are often unclear or disturbed. There are usually chronic feelings of emptiness. A liability to become involved in intense and unstable relations hip s may cause repeated emotional crises and may be associated with excessive efforts to avoid abandonment and a series of suicidal threats or acts of self-harm (although these may occur without obvious precipitants) lncludes: borderline personality (disorder) Individuals with BPD (Emotionally unstable in ICD 10) have according to DSM IV-TR (2000) a pervasive pattern of instability in interpersonal relationships, self-image and affects, and marked impulsivity. They show frantic efforts to avoid real or imagined abandonment, a pattern of unstable and intense interpersonal relationships and identity disturbance. They also present with impulsivity, recurrent suicidal gestures, affective instability, chronic feelings of emptiness, inappropriate intense anger. In severe cases transient stress-related paranoid ideation or severe dissociative symptoms are noticeable. BPD is relatively rare in the general population (0.2%- 1.8%) while prevalence rate among psychiatric inpatient and outpatient is higher (15% – 25%). Early separations and losses, disturbed parental involvement with conflictual relationships, childhood history of physical and/or sexual abuse, and high prevalence of affective disorder in first-degree relatives of borderline probands are specific developmental and psychosocial factors for BPD (Zanarini & Frankenburg, 1997). Low level of serotonin, stress sensitivity and a tendency for impulsive aggression can, when combined with psychosocial factors, contribute to adult BPD. Although borderline patients improve over time they still can remain functionally impaired. Especially those who experienced sexual abuse or incest in childhood have a poor prognosis. Emotional instability, impulsivity and aggressive relationships worsen prognosis as do co-morbid substance abuse, and schizotypal, antisocial or paranoid features. Around 60% of patients with BPD have major depressive disorder, 30% panic disorder with agoraphobia, 12% substance use disorder, 10% bipolar-I, and 4% bipolar-II disorder. Comorbid BPD tends to interfere with treatment of Axis I. Multimodal treatment and a combination of psychotherapy and psychopharmacological treatment offer the best chance of a good outcome (Oldham, Phillips, Gabbard, et al. 2001). Psychodynamic treatment is preferable while long in-patient treatment has proved ineffective. Evidence based manualized treatment modalities, i.e., Mentalization Based Treatment (Bateman & Fonagy, 1999; Bateman & Fonagy, 2001), Cognitive therapy (Ryle, 1997), Dialectic Behaviour Therapy (DBT) (Lenihan 1993; Linehan Heard, Armstrong, 1993) and Transference Focused Psychotherapy (TFP) (Clarkin, Foelsch, Levy, et al., 2001), have all proved beneficial and effective in changing borderline symptoms and character functioning. Although no specific psychotropic drug is effective for BPD, some can help reducing disabling symptoms; i.e., typical and atypical antipsychotic drugs, tricyclic antidepressants (TCA’s) and selective serotonin reuptake inhibitors (SSRI’s), monoamine oxidase inhibitors (MAOI’s), and mood stabilisers. Narcissistic personality disorder - Case vignette A 42-year-old male professional in public office, was forced to resign after being arrested when visiting a brothel. In the aftermath he suffered from depression and considerable alcohol consumption, and was admitted for a three months treatment. He stopped drinking, but his depression remained nonresponsive to anti-depressant medication. Still without meaningful activities he felt empty and restless, and he was referred to psychotherapy. Developmental history indicates that at age 5 his father left the family, and they did not meet until he was in law school. He was always ahead of his age and went through school without difficulty. In law school he got high marks without hard work. He had many acquaintances but no friends, and he felt like an outsider. He got married and had two children. Reaching mid-thirties he felt bored. He had everything: house, career, and family. He was respected and accomplished, but felt he didn’t belong. He started drinking heavily and visiting brothels. The psychotherapist found him self-assured, easily irritated, and quick to make devaluating remarks, and felt a mixture of irritation, compassion and powerlessness. Interactions during weekly appointments were extremely difficult. Unwilling to explore his situation or his feelings, he blamed the therapist for the impasse and told him that he will not change and that the therapist could not help. The therapist dreaded the appointments, while the patient despite finding the sessions unhelpful, always showed up. When the therapist announced a three weeks break his patient suggested the treatment to end and did not return. Nine months later he informed the therapist that he moved to another city, had a leading position working with international trade, and was greeted as a king. He said nothing about his wife and children. Nor did he indicate how he felt about the treatment. - Clinical Description People with NPD (not included in the ICD 10) have a grandiose sense of self-importance and accompanying grandiose fantasies. According to DSM-IV TR (2000) they present a pervasive pattern of grandiosity, need for admiration and lack of empathy. In addition they have a sense of entitlement and tendencies to be exploitive, and take advantage of other people. They can come across as arrogant and haughty or boastful and self-centered. However, they also have vulnerable and fluctuating self-esteem, feelings of shame, intense reactions to criticism or defeat, and vocational irregularities. Some may appear more sensitive, inhibited, vulnerable, shame-ridden and socially withdrawn, and others can present with psychopathic or antisocial characteristics. Variable prevalence rate of NPD has been found both in the general community (1% - 6%) (Stinson, Dawson Goldstein et al 2008) and in the clinical population (1.3% - 17%). Studies have suggested a genetic influence on the development of NPD, including hypersensitivity, strong aggressive drive, low anxiety or frustration tolerance, and defects in affect regulation (Torgersen et al 2000; Schore, 1994). Inconsistent attunement and insufficient attachment in the early parent-child interaction can lead to failure in the development of self-esteem and affect regulation. - Course and prognosis Although narcissistic traits can be frequent in adolescence, NPD develop in adulthood and can persist into old age. Severe disability has been indicated especially among those with comorbid Axis I disorder. NPD patients with ability for object relations actually improve over time and may have better prognosis (Ronningstam, Gunderson, Lyons 1995). NPD is considered to have one of the highest rates of diagnostic overlap among the Axis II disorders, especially with ASPD (25%). Major depression and dysthymia are the most common concomitant Axis I disorders (42 - 50%), followed by substance use disorder (24 – 50%) and bipolar disorder (5 – 11 %). Co-occurring narcissistic features can worsen course and prognosis for Axis I disorders. Psychoanalysis and psychoanalytically oriented psychotherapy are the most common treatment for NPD (Kernberg, 1975; Kohut, 1968; Fiscalini, 1994). Additional modalities include the Schema Focused Therapy (Young & Flanagan, 1998), and couples or family therapy (Solomon, 1998; Kirshner, 2001). Potentially beneficial psychopharmacological treatment focused on mood, anger or anxiety, is often challenged by the patients’ reluctance to adhere to such modality. Histrionic Personality Disorder (adopted from Bruce Pfohl) - Case vignette A 25-year-old female university student sought psychoanalytic treatment as she suffered from depression, difficulties in interpersonal relationships, and vocational dissatisfaction. Her first panic attack occurred during the last year in high school when her boyfriend was treated for panic attacks. She believed she was "influenced" by him. In psychotherapy she overcame family difficulties, especially in relation to her mother, but continued to feel insecure and pessimistic, blaming it all on her boyfriend. Their conflictual relationship ended when she had an episode of depression. She felt she wanted to die and sought consultation for psychoanalytic treatment saying that she was wasting her life, and lacked motivation for studies or career. She dreamt about her former boyfriend, and after breaking up with two other men she felt extremely lonely. She is the third of seven children. The father was hard-working, affectionate and caring, but also irritable and depressive. The mother was impulsive and sarcastic. Mother and daughter had a close but conflictive relationship as the mother could be intrusive, opinionated and idealizing. At age three the parents moved abroad for one year and left her to live with relatives. Upon their return she was presented to a baby brother. Significant sensitivity during her school years led her to break up friendships and feel extremely lonely. She did well at university, formed friendships but noticed that she often felt rejected without knowing why. In psychoanalysis four times per week she presented several contradictions, i.e., pursuing treatment and lapsing, or describing her mother as unsupportive, cold and envious but nevertheless readily resorting to her when facing difficulties. As the psychoanalysis progressed she presented infantile histrionic features; a precarious identity, strong affective dependence, dissociation, infantilization and self destructive work related behaviour. She brought multiple dreams to the sessions and gave vivid images of conflicts that worried her. Despite efforts to interpret, the analyst noticed no progress. Paradoxically, her presentation of dreams and associations indicated in-depth psychological work, but her persistent tardiness and absenteeism reflected the opposite. After eight months of psychoanalysis, the analyst suggested 3 sessions per week of face to face psychotherapy and referred her to a colleague. - Clinical description Diagnostic Criteria DSM-10 F60.4 Histrionic personality disorder Personality disorder characterized by: (a) self-dramatization, theatricality, exaggerated expression of emotions; (b) suggestibility, easily influenced by others or by circumstances; (c) shallow and labile affectivity; (d) continual seeking for excitement and activities in which the patient is the centre of attention; (e) inappropriate seductiveness in appearance or behaviour; (f) over-concern with physical attractiveness Associated features may include egocentricity, self-indulgence, continuous longing for appreciation, feelings that are easily hurt, and persistent manipulative behaviour to achieve own needs. lncludes: hysterical and psychoinfantile personality (disorder) In DSM-IV-TR (2000) HPD is described as a pervasive pattern of excessive emotionality and attention-seeking behaviour. People with HPD show seductive inappropriate behaviour, shallow emotional expressions, impressionistic speech, suggestibility, and a belief that relationships are more intimate than they really are. They have strong need for attention, pursued by a sensational physical appearance, or by being emotionally dramatic and expressive, or inappropriately sexually provocative or seductive. Individuals with HPD range from high level classical hysterical character neuroses to more primitive character functioning presenting with dissociative language, vivid fantasy life and infantile dependence. DSM-IV-TR (2000) suggests that about 2% - 3% of the general population and 5% – 10% of the clinical population meet criteria for HPD. Repression and somatisation of strong emotions are considered the main etiological factors in hysteria. - Course and prognosis The course and prognosis of HPD depends upon comorbidity and level of severity of the disorder. Intense and chronic anger and stormy close relationships are indicators of poorer prognosis. Ability to reflect and tolerate regularity can prevent treatment failure (Stone, 2005). Major depressive disorder, Somatization disorder and Conversion disorder are the most common comorbid Axis I disorder with HPD. Association between the other Cluster B personality disorders have also been found. Individuals with HPD can also present with increased attention driven risk for suicidal gestures and threats. Histrionic personality traits are usually requiring long-tem treatment and psychodynamic psychotherapy is the most common modality. Higher functioning neurotically organized individuals can be treated with psychoanalysis, while people with more primitive functioning may benefit from supportive or cognitive therapy which focuses on the patient's automatic thoughts and beliefs and on modifying emotional and interpersonal reactivity (Gabbard & Allison, 2007). Cluster C includes the Avoidant, Dependent, and Obsessive-Compulsive Personality Disorders. Individuals with these disorders often appear anxious or fearful. Avoidant Personality Disorders exhibit a pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation. Dependent Personality Disorders show a pattern of submissive and clinging behavior that evidence an excessive need to be taken care of. Lastly, Obsessive-Compulsive Personality Disorders manifest a preoccupation with orderliness, perfectionism, and control. For additional information and references see Module II in Simonsen E, Ronningstam E, Millon T (Eds). (2007). WPA ISSPD Educational Program on Personality Disorders. www.wpanet.org/education/education.shtml: Avoidant Personality Disorder - Case Vignette The patient was a 35 year old, unmarried data technician referred to a specialized treatment program for personality disorders from an out-patient drug addiction service. His personality pathology was considered more devastating than his substance abuse. Presenting complaints included low self esteem, loneliness, sense of emptiness, suicidal ideation, social isolation, substance abuse, general dissatisfaction with life. Present complaints had been chronic in nature, dating back to childhood. He recalled having daily suicidal thoughts for several years in his early youth. On axis I he fulfilled the criteria for dysthymic disorder and drug abuse in partial remission, but not panic disorder or social phobia. His avoidant behavior was more prominent than his level of experienced anxiety. On axis II he fulfilled all seven criteria for avoidant personality disorder and an additional seven criteria spread across other personality disorders. The most prominent feature was a pervasive fear of being ridiculed when interacting with others. In a group-based treatment program lasting for 20 weeks, he was a regular, but somewhat detached participant. The therapists encountered a series of problems related to passivity: He postponed most of his obligations, resisted sorting out practical affairs, did not pay his bills and avoided contacting people who could be helpful. - Clinical description Diagnostic Criteria ICD-10 F60.6 Anxious [avoidant] personality disorder Personality disorder characterized by: (a) persistent and pervasive feelings of tension and apprehension; (b) belief that one is socially inept, personally unappealing, or inferior to others; (c) excessive preoccupation with being criticized or rejected in social situations; (d) unwillingness to become involved with people unless certain of being liked; (e) restrictions in lifestyle because of need to have physical security; (f) avoidance of social or occupational activities that involve significant interpersonal contact because of fear of criticism, disapproval, or rejection. Associated features may include hypersensitivity to rejection and criticism Avoidant personality disorder is a pervasive pattern of social inhibition, feelings of inadequacy or inferiority, and hypersensitivity to negative evaluation, according the definition of American Psychiatric Association DSM-IV-TR (American Psychiatric Association, 2000). The term of avoidant personality disorder has been used in DSM, while anxious personality disorder is used in ICD-10 (World Health Organization, 1993). Although the term avoidant personality disorder was first used by Millon, (1969) these patients have been described as sensitive character (Kretschmer, 1921), introvert (Jung, 1936), interpersonally avoidant (Horney, 1945)), insecure psychopath (Schneider, 1950), phobic personalities (Fenichel, 1945), or active-detached personalities (Millon, 1973). People with this disorder are timid, extremely self-conscious and fearful of criticism, humiliation, and rejection. Clinical literature has reported that Cluster C personality disorders including avoidant personality disorder often co-occur with mood and anxiety disorders. Avoidant and dependent personality disorders were strongly related to mood disorders, especially major depression, dysthymia, and mania. Avoidant personality disorders were reported to be strongly related to anxiety disorders, especially panic disorder with agoraphobia and social phobia. In addition to mood and anxiety disorders, eating disorders tend to be comorbid with avoidant personality disorder (Oldham et al. 1995). Avoidant personality disorder often co-occurs with other Cluster C personality disorders. This disorder is especially strongly correlated with dependent personality disorder. Although there was concern that the prevalence of avoidant personality disorder might be low when it was first included in the DSMIII classification system, it became clear that this is one of most common personality disorders. However, this disorder appears to be more prevalent according to the recent national studies with a large sample size e.g., 2-2.5%. It is quite prevalent within clinical settings and reported to present 5% -35% in psychiatric populations (Mattia et al. 2001). The odds of avoidant personality disorder are greater for the lower income group, people with less than a high school education, the widowed/divorced /separated and never married, and residents in the most urbanized areas (Grant et al., 2004). Although the etiology of avoidant personality disorder is not known, a few models are proposed. The biological learning theory hypothesizes that the interaction of a biologically determined sensitivity to interpersonal relationships and social experiences affects the development of the disorder. It is also postulated to be an extreme variant of the personality traits of introversion and neuroticism which have heritability. According to the interpersonal etiology model, the disorder is explained based on a conflict between seeking closeness and fearing it. Cognitive theory hypothesizes negative schema which originate in early childhood, and which lead to social avoidance behavior. When the disorder begins in childhood, the symptoms could worsen in adolescence due to the complex and demanding social relationships of this time. It is essential to establish a good therapeutic relationship which is, however, very difficult because of the patients’ low self-esteem and hypersensitivity to rejection. Cognitive individual or group format is effective for these types of patients. Social skills training, systematic desensitization, and graded hierarchy of in vivo exposure to feared social situations could be useful (Beck & Freeman, 1990). Both short-term dynamic psychotherapy and cognitive therapy have a place in the treatment of patients with cluster C personality disorders (Svartberg et al. 2004). Exploratory and supportive group therapy may be helpful for these patients by providing a holding environment in which they can share their insecure feelings. Dependent Personality Disorder - Case Vignette The patient was a 27 year old white female administrative assistant whose work required much use of the computer and data entry. She gradually began to develop pain in her wrists. Physicians diagnosed a potential carpal tunnel syndrome. The damage to her wrists was not reparable by surgery and Sally was left in significant daily pain. The patient demonstrates the key aspect of Dependent personality, the need to please others even at the expense to herself. The degree to which her self-destructive passivity and compliance at work stemmed from her early experiences within the family are unclear, but her parents’ overprotectiveness likely played some role in the etiology of her personality pathology. Research confirms that overprotective and authoritarian parenting, alone or in combination, often lead to excessive interpersonal dependency in offspring. - Clinical description Diagnostic Criteria ICD-10 F60.7 Dependent personality disorder Personality disorder characterized by: (a) encouraging or allowing others to make most of one's important life decisions; (b) subordination of one's own needs to those of others on whom one is dependent, and undue compliance with their wishes; (c) unwillingness to make even reasonable demands on the people one depends on; (d) feeling uncomfortable or helpless when alone, because of exaggerated fears of inability to care for oneself; (e) preoccupation with fears of being abandoned by a person with whom one has a close relationship, and of being left to care for oneself; (f) limited capacity to make everyday decisions without an excessive amount of advice and reassurance from others. Associated features may include perceiving oneself as helpless, incompetent, and lacking stamina lncludes: asthenic, inadequate, passive, and self-defeating personality (disorder) Although early diagnosticians discussed at length the clinical implications of exaggerated dependency needs, it was not until publication of the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) that dependent personality disorder (DPD) became a full-fledged diagnostic category. DPD is defined as "a pervasive and excessive need to be taken care of that leads to submissive and clinging behavior and fears of separation" (APA, 1994, p. 668). The person must show several of the following symptoms to receive a DPD diagnosis: difficulty making everyday decisions without excessive advice and reassurance; needing others to assume responsibility for most major areas of life; difficulty initiating projects or doing things on one’s own; going to excessive lengths to obtain nurturance and support; feeling uncomfortable and helpless when alone, being unrealistically preoccupied with fears of being left to care for oneself. The DSM-IV-TR indicates that three Axis I diagnoses - mood disorders, anxiety disorders, and adjustment disorder - show substantial comorbidity with DPD. Evidence supports continued inclusion of these three categories in future versions of the DSM, but also suggests that eating disorders and somatisation disorder co-occur with DPD at higher-than-expected rates (Piper et al. 2001). Problematic dependency is widespread in the community as well as in clinical populations, and is associated with an array of psychological disorders. Studies typically report Dependent Personality Disorder prevalence rates of between 15 % and 25% in hospital and rehabilitation settings (Oldham et al. 1995). Bornstein’s (1993, 1997) meta-analyses of epidemiological findings indicated that gender moderates DPD prevalence rates. When data from extant studies were combined, the overall base rate of DPD was 11% in women and 8% in men. Although this difference seems modest, it is highly significant. Several theoretical frameworks have been particularly influential in conceptualizing the etiology of the Dependent Personality. Research does not support the early psychodynamic hypothesis that variations in infantile feeding and weaning behaviors play a role in the development of dependent personality traits (Bornstein, 1996). Many psychodynamic researchers (e.g., Luborsky & Crits-Christoph, 1990) now conceptualize problematic dependency as resulting from unconscious conflicts. Cognitive models of DPD focus on the ways in which a person’s manner of thinking helps foster dependent behavior. As Freeman and Leaf (1989) noted, dependency-related automatic thoughts (i.e., reflexive self-statements that reflect the person’s perceived lack of competence) are central in this process. Automatic thoughts are accompanied by negative self statements, which combine to create a persistent attributional bias that reinforces the person’s view of himself as vulnerable and weak. A vicious cycle ensues. No studies have documented the long-term course of DPD in inpatients, outpatients, or community adults. In the short term, research confirms that dependent patients exhibit behaviors that both facilitate and undermine treatment. For example, dependent psychotherapy patients are cooperative and conscientious, but also make more requests for after-hours contact. Dependent patients delay less long than nondependent patients when psychological symptoms appear, but they also have difficulty terminating treatment after symptoms remit (Bornstein, 1993). Over the years clinicians have provided recommendations for intervention strategies based on cognitive (Young, 1994), psychodynamic (Luborsky & Crits-Christoph, 1990), behavioral (Turkat, 1990), and experiential (Schneider & May, 1995) treatment models. However, only two studies assessed changes in DPD symptoms during the course of psychotherapy, and these investigations produced conflicting results. Obsessive-Compulsive Personality Disorder - Case Vignette The patient was a 42-year-old single male, who lives with his parents. He has been unemployed for some time. He presented to the anxiety disorders clinic at a major teaching hospital, because of concerns regarding his long-term unemployment. He tended to procrastinate when making decisions or carrying out plans. On weekends, when the family planned to visit the grandparents he would start packing on Friday afternoon, but on many occasions did not finish the packing until Sunday, by which time it was too late to go. He spent long periods of time in the bathroom, would take half an hour to wash his hands-first washing the tap, then his hands, then the tap again. This routine also made it difficult for him to go out and look for job. In fact, it totally prevented him from doing so. After leaving school, he has had 30 or 40 jobs, mostly factory work. The longest he has lasted in a job has been one week, often only one day. He was very punctual in treatment and never missed a session; he talked freely, and in great detail. The initial part of therapy mainly dealt with family relationships. When the time came to leave the sessions he would often continue talking and delaying even when the therapist was standing at the door. - Clinical Descriptions Diagnostic Criteria ICD-10 F60.5 Anankastic personality disorder Personality disorder characterized by: (a) feelings of excessive doubt and caution; (b) preoccupation with details, rules, lists , order, organization or schedule; (c) perfectionism that interferes with task completion; (d) excessive conscientiousness, scrupulousness, and undue preoccupation with productivity to the exclusion of pleasure and interpersonal relationships; (e) excessive pedantry and adherence to social conventions; (f) rigidity and stubbornness; (g) unreasonable insistence by the patient that others submit to exactly his or her way of doing things, or unreas6nable reluctance to allow others to do things; (h) intrusion of insistent and unwelcome thoughts or impulses. lncludes: compulsive and obsessional personality (disorder) obsessive - compulsive personality disorder Excludes: obsessive - compulsive disorder (F42. - ) Diagnostic criteria of ICD-10 (WHO, 1992) and DSM-IV-TR (APA, 2000) for the OCPD (or anankastic personality disorder, following the ICD-10) are quite similar. Both nosological systems describe a syndrome characterized by symptoms such as excessive perfectionism, stubbornness, rigidity, and lack of decision. For the DSM-IV-TR, the OCPD is a pervasive pattern of preoccupation with orderliness, perfectionism, and mental and interpersonal control, at the expense of flexibility, openness, and efficiency, beginning by early adulthood and present in a variety of contexts. Most research shows that most individuals with Axis I Obsessive-Compulsive Disorder do not fulfill the criteria of OCPD. Furthermore, it has been found that patients with OCD and with a personality disorder show similar or more frequent relationships with the avoidant or dependent personality disorder than with OCPD. Comorbidity with other personality disorders has varied markedly depending on the specific study. (Maier et al. (1992) found that the Obsessive-Compulsive Personality Disorder was the second most frequent personality disorder (among the 11 included in the DSM-III-R) in his study sample (individuals without psychiatric disorders), showing a range from 1.6% to 6.4%, while the prevalence found by Widiger & Sanderson (1997) ranged from 1% to 3%. The etiology of Obsessive-Compulsive Personality Disorder is unknown. There are not data regarding the influence of biological factors in the onset and development of this disorder, but it is believed that environmental factors play an important role in its etiology. Millon (1996) proposes some of these tentative variables: parental over-control is a method of restrictive child-rearing in which punitive processes are used to set distinct limits on children’s behavior. As long as they operate within the parental approved boundaries, children are safe from parental punishment. The acquisition of behavior patterns of OCPD are learned vicariously and by imitation. Neither pharmacological, nor psychoanalytical, interpersonal, or cognitive-behavioral perspectives have empirical proven techniques for the modification of OCPD. One of the most frequent symptoms present in individuals with OCPD, causing inefficiency is their inability to give priority to important tasks instead of focusing on trivial or less important tasks, and also their inefficient distribution of time. A coping strategy would be good management of time strategies. Furthermore, these strategies would allow the individual to save time and devote it to other leisure and social activities. - Shea, M. T., Widiger, T., & Klein, M. H. (1992). Comorbidity of personality disorders and depression: Implications for treatment. Journal of Consulting & Clinical Psychology, 60, 857-868. - Westen, D. (1997). Divergences between clinical and research methods for assessing personality disorders: Implications for research and the evolution of axis II. American Journal of Psychiatry, 154, 895-903. - Newman, D. L., Moffitt, T., Caspi, A., & Silva, P.A. (1998). Comorbid mental disorders: Implications for treatment and sample selection. Journal of Abnormal Psychology, 107, 305-311. - Tyrer P. Personality as diathesis. Psychological Medicine - Reugg, R. & Frances, A (1995). New research in personality disorders. Journal of Personality Disorders, 9, 1-48. Differentiating normality and abnormality Differentiating normal and abnormal personality. Stephen Strack (ed) - Theophrastus (1998). Characters. Referenced in Lopez-Ibor, Jr. From individual differences to personality disorders. - Cattell, R. B. (1965). The scientific analysis of personality. Chicago: Aldine. - Tyrer, P. (1988). What’s wrong with DSM-III personality disorders? Journal of Personality Disorders, 2, 281-291. - Kernberg OF. (1975). Borderline conditions and pathological narcissism. New York: Jason Aronson. - Livesley, W. J. (1987). Theoretical and empirical issues in the selection of criteria to a diagnosed personality disorder. Journal of Personality Disorders, 1, 88-94. - Millon, T. with Davis, R. (1996). Disorders of Personality: DSM-IV and Beyond. New York: John Wiley & Sons, Inc. Current official classification systems - American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Text Revision. Washington, American Psychiatric Association. - The ICD-10 classification of mental and behavioural disorders. Diagnostic criteria for research. Geneva: WHO, 1993. Problems in the current classification system - Simonsen & Widiger - Clark LA, Watson D & Reynolds S (1995). Diagnosis and classification of psychopathology.: Challenges to the current system and future directions. Annu Rev Psychol 46, 121-153. - Kalus, Oren, Bernstein, David P., and Siever, Larry J. "Schizoid Personality Disorder," In Livesley, W. John, editor (1995). The DSM-IV Personality Disorders. New York: The Guilford Press. - Saß, H. and Jünemann, K. (2001). Zur ätiologischen Stellung und Therapie der schizoiden und schizotypischen Persönlichkeitsstörung. Fortschritte in Neurologie und Psychiatrie; 69 Sonderheft 2: S. 120-126. - Goulding A. Schizotypy models in relation to subjective health and paranormal beliefs and experiences. Pers and Individ Diff. 2004;37:157-167. - Gunderson JG, Siever LJ, Spaulding E. The search for a schizotype: crossing the border again. Arch Gen Psychiatry. 1983;40:15-22. - Gunderson JG, Singer MT. Defining borderline patients: an overview. Am J Psychiatry 1975;132:1-10. - The ICD-10 classification of mental and behavioural disorders. Diagnostic criteria for research. Geneva: WHO, 1993. Kendler KS, Gruenberg AM. An independent analysis of the Danish adoption study of schizophrenia, VI:the relationship between psychiatric disorders as defined by DSM-III in the relatives and adoptees, Arch Gen Psychiatry. 1984;41:555-564. - Kendler KS, Hewitt J. The structure of self report schizotypy in twins. J Pers Disorder. 1992; 6:1-17. - Kety SS, Rosenthal D, Wender PH et al.. Mental illness in the biogical and adoptive families of adopted schizophrenics. Am J Psychiatry 19712;128:302-306. - Lenzenweger M & Korfine L. Tracking the taxon: on the latent structure and base rate of schizotypy. In: Schizotypal personality (Eds.: A Raine, T Lencz, SA Mednick). Cambridge University Press, New York, 1995. - Maier W, Lichtermann D, Klingler T et al.. Prevalences of personality disorders (DSM-III-R) in the community. J Pers Disord. 1992;6:187-196. - Meehl P. Schizotaxia, schizotypy, schizophrenia. American Psychologist. 1962;17:827-838. - Siever LJ, Brain structurte/function and the dopamine system in schizotypal personality disorders. In: Schizotypal personality (Eds.: A Raine, T Lencz, SA Mednick). Cambridge University Press, New York, 1995. - Skodol AE, Gunderson JC, McGlashan TH, Dyck IR et al.. Functional impairment in patients with schizotypal, borderline, avoidant, or obsessive-compulsive personality disorder. Am J Psychiatry. 2002;159:276-283. - Spitzer RL, Endicott J, Gibbon M. Crossing the border into borderline personality and borderline schizophrenia: the development of criteria. Arch Gen Psychiatry. 1979;36:17-24. - Squires-Wheeler E, Skodol AE, Bassett A et al.. DSM-III-R schizotypal personality traits in offspring of schizophrenic disorder, affective disorder , and normal control parents. J Psychiatr Res. 1989;23:229-239. - Torgersen S: Genetic and nosological aspects of schizotypal and borderline personality disorders: a twin study. Arch Gen Psychiatry. 1984; 41: 546-554. - Torgersen S, Alnæs R. Differential perception of parental bonding in schizotypal and borderline personality disorder patients. Compr Psychiatry. 1992;33:34-38. - Torgersen S, Kringlen E, Cramer V. The prevalence of personality disorders in a community sample. Arch Gen Psychiatry. 2001;58:590-596. - Torgersen S, Onstad S, Skre I et al.. "True" schizotypal personality disorder: A study of co-twins and relatives of schizophrenic probands. Am J Psychiatry. 1993;150:1661-1667. - Akhtar, S. Paranoid Personality Disorder: A Synthesis of Developmental, Dynamic, and Descriptive Features”, American Journal of Psychotherapy, Vol XLIV, No. 1, 1990. - Dorfman, A., Shields, G., DeLisi, LE. "DSM-III-R Personality Disorders in Parents of Schizophrenic Patients," American Journal of Medical Genetics, 48: 60-62, 1993. - Karterud, S., Pederson, G., Bjordal, E., Brabrand, J., Friis, S., Haaseth, O., Haavaldsen, G., Irion, T., Leirvag, H., Torum, E., Urnes, O. "Day Treatment of Patients with Personality Disorders: Experiences from a Norwegian Treatment Research Network," Journal of Personality Disorders, 17(3):243-262, 2003. - Kendler, KS., Gruenberg, AM., "Genetic Relationship Between Paranoid Personality Disorder and the "Schizophrenia Spectrum" Disorders," American Journal of Psychiatry, 139:1185-1186, 1982. - Kendler, K.S.; Masterson, C.C.; Davis, K.L., "Psychiatric illness in first-degree relatives of patients with paranoid psychosis, schizophrenia and medical illness," Br J Psychiatry, 1985. 147: p. 524-31. - Kendler, K.S.; McGuire, M.; Gruenberg, A.M.; O’Hare, A.; Spellman, M.; Walsh, D., "The Roscommon Family Study. III. Schizophrenia-related personality disorders in relatives," Arch Gen Psychiatry, 1993, 50(10): p. 781-8. - Nestor, PG., "Mental Disorder and Violence: Personality Dimensions and Clinical Features," American Journal of Psychiatry, 159:12, December 2002. - Zanarini, MC., Skodol, AE., Bender, D., Dolan, R., Sanislow, C., ; Schaefer, E., Morey, Leslie C., Grilo, CM., Shea, MT., McGlashan, TH., Gunderson, JG. "The Collaborative Longitudinal Personality Disorders Study: Reliability of Axis I and II Diagnoses," Journal of Personality Disorders, 14(4), 291-299, 2000. - Gabbard GO, Allison SE. (2007). Histrionic Personality Disorder. In Gabbard G (Ed.) Treatment of Psychiatric Disorders, Fourth Edition. Washington DC, American Psychiatric Press, Inc. 2007, pp 823 – 833. - Stone M. (2005). Borderline and Histrionic personality disorders: A Review In Maj M, Akiskal H, Mezzich J, Okasha A (Eds). The World Psychiatric Series Volume 8. Evidence & Experiences in Psychiatry: Personality Disorders. Chichester, The United Kingdom, John Wiley & Sons, Ltd., pp201-231. - Hemphill J F, Hart SD. (2002). Motivating the unmotivated: Psychopathy, treatment, and change. In M. McMurran (Ed.), Motivating offenders to change (pp. 193-219). Chichester, UK: Wiley. - Livesley, W. J. (1998). The phenotypic and genotypic structure of psychopathic traits. In D. J. Cooke, A. E. Forth, & R. D. Hare (Eds.). Psychopathy: Theory, research, and implications for society (pp. 69-79). Dordrecht, The Netherlands: Kluwer. - Mealey L. (1995). The sociobiology of sociopathy: An integrated evolutionary model. Behavioural and Brain Sciences, 18, 523-599. - Miller JD, Lynam DR, Widiger TA, Leukefeld C. (2001). Personality disorders as extreme variants of common personality dimensions: Can the Five-Factor Model adequately represent psychopathy? Journal of Personality, 69, 253-276. - Fiscalini J. (1994) Narcissism and coparticipant inquiry – explorations in contemporary interpersonal psychoanalysis. Contemporary Psychoanalysis, 30(4): 747-776 - Kernberg OF. (1975). Borderline conditions and pathological narcissism. New York: Jason Aronson. - Kohut H. (1968). The psychoanalytic treatment of narcissistic personality disorder. Psychoanalytic Study of the Child, 23:86-113. - Kirshner LA. (2001) Narcissistic Couples. Psychoanalytic Quarterly LXX: 789-806. - Ronningstam E, Gunderson J, Lyons M. (1995). Changes in pathological narcissism. American Journal of Psychiatry 152:253-257. - Pickering RP, Grant BF. (2008). Prevalence, correlates, disability and comorbidity of DSM-IV narcissistic personality disorder: Results from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Clinical Psychiatry 69 (7) , 1033 – 1045. - Solomon M. (1998). Manifestations and treatment of narcissistic disorders in couples therapy. In Disorders of Narcissism: Diagnostic, Clinical, and Empirical Implications. Edited by Ronningstam E. Washington, DC, American Psychiatric Press, pp 269-293. - Young J. Flanagan C. (1998). Schema-Focused Therapy for Narcissistic Patients. In: E Ronningstam (Ed.): Diagnostic, Clinical, and Empirical Implications. Washington, DC, American Psychiatric Press, pp 239-267. - Bateman A, Fonagy P. (1999) The effectiveness of partial hospitalization in the treatment of borderline personality disorder - a randomised controlled trial. American Journal of Psychiatry, 156, 1563-1569. - Clarkin J F, Foelsch P, Levy K., et al. (2001) the development of a psychodynamic treatment for patients with borderline personality disorder: a preliminary study of behavioural change. Journal of Personality Disorders, 15, 487-495. - Linehan MM. (1993) The skills training manual for treating borderline personality disorder. New York: Guilford Press. - Linehan MM, Heard HL, Armstrong HE. (1993) Naturalistic follow-up of a behavioural treatment for chronically parasuicidal borderline patients. Archives of General Psychiatry, 50, 971-974. - Oldham J, Phillips K, Gabbard G, et al. (2001). Practice Guideline for the Treatment of Patients with Borderline Personality Disorder. American Psychiatric Association. American Journal of Psychiatry, 158, 1-52. - Ryle A. (1997) Cognitive Analytic Therapy and Borderline Personality Disorder: The Model and the Method. Chichester, UK: John Wiley & Sons. - Schore, A (1994). Affect Regulation and the Origin of the Self. Hillsdale, NJ. Erlbaum - Stinson FS, Dawson DA, Goldstein RB, Chou PS, Huang B, Smith SM, Ruan WJ, Pulay AJ, Saha TD, - Torgersen, S., Lygren, S., Oien, P., et al. (2000) A twin study of personality disorders. Comprehensive Psychiatry, 41, 416-425. - Zanarini MC, Frankenburg FR. (1997) Pathways to the development of borderline personality disorder. Journal of Personality Disorders, 11, 93-104. The following general questions are suggested to be discussed in classrooms: - Why are PDs useful for mental health workers (psychiatrists, psychologists, social workers) to understand as a key component of their clinical activities? - Discuss the social costs of the PDs, their widespread prevalence and their associated civic and public health consequences and disruptions. - Why is the traditional concept of "disease" not suitable when discussing the nature of the PDs? Why do some thinkers consider PDs to be best considered as similar to the biological immune system? - How can normality and abnormality best be differentiated? Is there a sharp line separating them or are they on a continuum? - The history of ideas about personality goes back to the early Greeks. Discuss some of these interesting ideas and major thinkers from the past to the present. - What are some of the issues, as well as the similarities and differences between the ICD-10 and DSM-IV in their formulation of the PDs. - Do personality disorders really exist or are they just convenient fictions of theory, clinical observation or research investigations? - What are the issues in the categorical vs. dimensional PD debate, and does the prototypical idea help solve them? - Discuss the role of biogenic, psychogenic and sociogenic influences in PD development pathogenesis? Describe some of the research evidence for their respective contributions. - Describe the several modes and specific tools of diagnosing the PDs, and discuss their respective strengths and weaknesses. - Go into considerable detail in specifying the strengths of either the cognitive or the psychodynamic approach to therapy for the PDs. - What are the comparative advantages and disadvantages of adhering to one specific school of therapy versus several combined schools, e.g., behavioural, pharmacologic in treating the PDs. - Curriculum Suggestions – Module II The following questions for each personality disorder are suggested to be discussed in classrooms: - What are the most outstanding and significant features for each personality disorder that best identifies and differentiates them from other personality disorders? - In what way does each personality disorder resemble or overlap with other disorders, including both Axis I and Axis II disorders? - What are the major commonalities in the etiology of the personality disorders? Which personality disorders have primarily developmental origin, and which have a strong potential genetic origin? - Identify specific cultural factors in your country/cultural environment that influence the understanding and treatment of certain personality disorder features. - What are the most striking gender differences among personality disorders – i.e., which disorders are, according to the text, most common among men, and among woman? How does that compare to your cultural experiences? Discuss reasons for observed differences - How does the prevalence of each personality disorder vary in your country/culture compare to those prevalence rates mentioned in the Module II text? - Discuss and compare the differences between treating personality disorders and Axis I disorders. How do co-occurring Axis I disorders influence treatment of a personality disorder, and vice versa, how can the presence of a personality disorder affect the course and treatment of an Axis I disorder such as Bipolar disorder or Major Depression or Eating Disorder. Give examples. - Compare the major contemporary controversies of each personality disorder and discuss future changes in diagnostic classifications and important areas for research. - Andrew E. Skodol & John G. Gunderson. Personality Disorders. In: The Textbook of Psychiatry (eds. Robert E. Hales, Stuart C. Yudifsky & Glen O. Gabbard). 5th edition. American Psychiatric Publishing, Washington, 2008. - Personality Disorders. WPA Series Evidence and experience in Psychiatry. Volume 8. John Wiley & Sons: Chichester, 2005. - Personality Disorders. Chapter 27. In: Kaplan & Saddock’s Synopsis of Psychiatry, Behavioral Sciences/Clinical Psychiatry. 10th Edition. Lippencott, Williams & Wilkins: Philadelphia, 2007. - Personality Disorders. Chapter 62. In: Essential of Psychiatry. Jerald Kay & Allan Tasman (eds.). John Wiley & Sons: Chicester, 2006. - Livesley, W. John (2003). Practical management of Personality Disorder. New York: Guilford Press. - Millon, Theodore & Davis, Rodger (1996). Disorders of Personality DSM-IV and Beyond. New York: John Wiley & Sons. - John G. Gunderson: Personality Disorders. Chapter 15. In: The Harvard Guide to Psychiatry. Armand M. Nicholi (ed.) 3rd Edition, 1999.	2	27	1	0	0	30	0.750566	31	23,843
- Ulcerative colitis Ulcerative colitis Classification and external resources Endoscopic image of a bowel section known as the sigmoid colon afflicted with ulcerative colitis. The internal surface of the colon is blotchy and broken in places. ICD-10 K51 ICD-9 556 OMIM 191390 DiseasesDB 13495 MedlinePlus 000250 eMedicine med/2336 MeSH D003093 Ulcerative colitis (Colitis ulcerosa, UC) is a form of inflammatory bowel disease (IBD). Ulcerative colitis is a form of colitis, a disease of the intestine, specifically the large intestine or colon, that includes characteristic ulcers, or open sores, in the colon. The main symptom of active disease is usually constant diarrhea mixed with blood, of gradual onset. IBD is often confused with irritable bowel syndrome (IBS), a troublesome, but much less serious, condition. Ulcerative colitis has similarities to Crohn's disease, another form of IBD. Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission. Ulcerative colitis occurs in 35–100 people for every 100,000 in the United States, or less than 0.1% of the population. The disease is more prevalent in northern countries of the world, as well as in northern areas of individual countries or other regions. Although ulcerative colitis has no known cause, there is a presumed genetic component to susceptibility. The disease may be triggered in a susceptible person by environmental factors. Although dietary modification may reduce the discomfort of a person with the disease, ulcerative colitis is not thought to be caused by dietary factors. Ulcerative colitis is treated as an autoimmune disease. Treatment is with anti-inflammatory drugs, immunosuppression, and biological therapy targeting specific components of the immune response. Colectomy (partial or total removal of the large bowel through surgery) is occasionally necessary, and is considered to be a cure for the disease. - 1 Signs and symptoms - 2 Causes - 3 Pathophysiology - 4 Diagnosis - 5 Management - 6 Prognosis - 7 Epidemiology - 8 Research - 9 References - 10 External links Signs and symptoms Symptoms in Crohn's disease vs. ulcerative colitis () Crohn's disease Ulcerative colitis Defecation Often porridge-like, and with blood Tenesmus Less common More common Fever Common Indicates severe disease Fistulae Common Seldom Weight loss Often More seldom The clinical presentation of ulcerative colitis depends on the extent of the disease process. Patients usually present with diarrhea mixed with blood and mucus, of gradual onset that persists for an extended period (weeks). They also may have weight loss and blood on rectal examination. The disease may be accompanied with different degrees of abdominal pain, from mild discomfort to painful bowel movements or painful abdominal cramping with bowel movements. Ulcerative colitis is associated with a general inflammatory process that affects many parts of the body. Sometimes these associated extra-intestinal symptoms are the initial signs of the disease, such as painful, arthritic knees in a teenager and may be seen in adults also. The presence of the disease may not be confirmed immediately, however, until the onset of intestinal manifestations. Extent of involvement Ulcerative colitis is normally continuous from the rectum up the colon. The disease is classified by the extent of involvement, depending on how far up the colon the disease extends: - Distal colitis, potentially treatable with enemas: - Proctitis: Involvement limited to the rectum. - Proctosigmoiditis: Involvement of the rectosigmoid colon, the portion of the colon adjacent to the rectum. - Left-sided colitis: Involvement of the descending colon, which runs along the patient's left side, up to the splenic flexure and the beginning of the transverse colon. - Extensive colitis, inflammation extending beyond the reach of enemas: - Pancolitis: Involvement of the entire colon, extending from the rectum to the cecum, beyond which the small intestine begins. Severity of disease In addition to the extent of involvement, people may also be characterized by the severity of their disease. - Mild disease correlates with fewer than four stools daily, with or without blood, no systemic signs of toxicity, and a normal erythrocyte sedimentation rate (ESR). There may be mild abdominal pain or cramping. Patients may believe they are constipated when in fact they are experiencing tenesmus, which is a constant feeling of the need to empty the bowel accompanied by involuntary straining efforts, pain, and cramping with little or no fecal output. Rectal pain is uncommon. - Moderate disease correlates with more than four stools daily, but with minimal signs of toxicity. Patients may display anemia (not requiring transfusions), moderate abdominal pain, and low grade fever, 38 to 39 °C (100 to 102 °F). - Severe disease, correlates with more than six bloody stools a day or observable massive and significant bloody bowel movement, and evidence of toxicity as demonstrated by fever, tachycardia, anemia or an elevated ESR. - Fulminant disease correlates with more than ten bowel movements daily, continuous bleeding, toxicity, abdominal tenderness and distension, blood transfusion requirement and colonic dilation (expansion). Patients in this category may have inflammation extending beyond just the mucosal layer, causing impaired colonic motility and leading to toxic megacolon. If the serous membrane is involved, colonic perforation may ensue. Unless treated, fulminant disease will soon lead to death. As ulcerative colitis is believed to have a systemic (i.e., autoimmune) origin, patients may present with comorbidities leading to symptoms and complications outside the colon. The frequency of such extraintestinal manifestations has been reported as anywhere between 6 and 47 percent. These include the following: - aphthous ulcers of the mouth - Ophthalmic (involving the eyes): - Cutaneous (related to the skin): - Deep venous thrombosis and pulmonary embolism - Autoimmune hemolytic anemia - clubbing, a deformity of the ends of the fingers - Primary sclerosing cholangitis, a distinct disease that causes inflammation of the bile ducts There are no direct causes for ulcerative colitis, but there are many possible factors such as genetics and stress. - Aggregation of ulcerative colitis in families. - Identical twin concordance rate of 10% and dizygotic twin concordance rate of 3% - Ethnic differences in incidence - Genetic markers and linkages There are 12 regions of the genome which may be linked to ulcerative colitis. This includes chromosomes 16, 12, 6, 14, 5, 19, 1,and 3 in the order of their discovery. However, none of these loci has been consistently shown to be at fault, suggesting that the disorder arises from the combination of multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease. Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. There are even human leukocyte antigen associations which may be at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates. Multiple autoimmune disorders have been recorded with the neurovisceral and cutaneous genetic porphyrias including ulcerative colitis, Crohn's disease, celiac disease, dermatitis herpetiformis, diabetes, systemic and discoid lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren's disease and scleritis. Physicians should be on high alert for porphyrias in families with autoimmune disorders and care must be taken with potential porphyrinogenic drugs, including sulfasalazine. Many hypotheses have been raised for environmental contributants to the pathogenesis of ulcerative colitis. They include the following: - Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn's disease. There have been few studies to investigate such an association, but one study showed no association of refined sugar on the prevalence of ulcerative colitis. - Breastfeeding: There have been conflicting reports of the protection of breastfeeding in the development of inflammatory bowel disease. One Italian study showed a potential protective effect. - Several scientific studies have posted that Accutane is a possible trigger of Crohn's Disease and Ulcerative colitis in some individuals. Three cases in the United States have gone to trial thus far, with all three resulting in multi-million dollar judgements against the makers of isotretinoin. There were an additional 425 cases pending as of.[when?] Some sources list ulcerative colitis as an autoimmune disease, a disease in which the immune system malfunctions, attacking some part of the body. In contrast to Crohn's disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis usually involves the rectum and is confined to the colon, with occasional involvement of the ileum. This so-called "backwash ileitis" can occur in 10–20% of patients with pancolitis and is believed to be of little clinical significance. Ulcerative colitis can also be associated with comorbidities that produce symptoms in many areas of the body outside the digestive system. Surgical removal of the large intestine often cures the disease. Levels of sulfate-reducing bacteria tend to be higher in persons with ulcerative colitis. This could mean that there are higher levels of hydrogen sulfide in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine. Comparison to Crohn's disease Risk factors in Crohn's disease vs. ulcerative colitis. Crohn's disease Ulcerative colitis Smoking Higher risk for smokers Lower risk for smokers Age Usual onset between 15 and 30 years Peak incidence between 15 and 25 years Pathophysiology in Crohn's disease vs. ulcerative colitis Crohn's disease Ulcerative colitis Autoimmune disease Widely regarded as an autoimmune disease No consensus Cytokine response Associated with Th17 Vaguely associated with Th2 An increased amount of colonic sulfate-reducing bacteria has been observed in some patients with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulfide. The role of hydrogen sulfide in pathogenesis is unclear. It has been suggested that the protective benefit of smoking that some patients report is due to hydrogen cyanide from cigarette smoke reacting with hydrogen sulfide to produce the nontoxic isothiocyanate. Another unrelated study suggested sulphur contained in red meats and alcohol may lead to an increased risk of relapse for patients in remission. - A complete blood count is done to check for anemia; thrombocytosis, a high platelet count, is occasionally seen - Electrolyte studies and renal function tests are done, as chronic diarrhea may be associated with hypokalemia, hypomagnesemia and pre-renal failure. - Liver function tests are performed to screen for bile duct involvement: primary sclerosing cholangitis. - Stool culture, to rule out parasites and infectious causes. - Erythrocyte sedimentation rate can be measured, with an elevated sedimentation rate indicating that an inflammatory process is present. - C-reactive protein can be measured, with an elevated level being another indication of inflammation. Although ulcerative colitis is a disease of unknown causation, inquiry should be made as to unusual factors believed to trigger the disease. Factors may include: recent cessation of tobacco smoking; recent administration of large doses of iron or vitamin B6; hydrogen peroxide in enemas or other procedures. The best test for diagnosis of ulcerative colitis remains endoscopy. Full colonoscopy to the cecum and entry into the terminal ileum is attempted only if diagnosis of UC is unclear. Otherwise, a flexible sigmoidoscopy is sufficient to support the diagnosis. The physician may elect to limit the extent of the exam if severe colitis is encountered to minimize the risk of perforation of the colon. Endoscopic findings in ulcerative colitis include the following: - Loss of the vascular appearance of the colon - Erythema (or redness of the mucosa) and friability of the mucosa - Superficial ulceration, which may be confluent, and Ulcerative colitis is usually continuous from the rectum, with the rectum almost universally being involved. There is rarely peri-anal disease, but cases have been reported. The degree of involvement endoscopically ranges from proctitis or inflammation of the rectum, to left sided colitis, to pancolitis, which is inflammation involving the ascending colon. Biopsies of the mucosa are taken to definitively diagnose UC and differentiate it from Crohn's disease, which is managed differently clinically. Microbiological samples are typically taken at the time of endoscopy. The pathology in ulcerative colitis typically involves distortion of crypt architecture, inflammation of crypts (cryptitis), frank crypt abscesses, and hemorrhage or inflammatory cells in the lamina propria. In cases where the clinical picture is unclear, the histomorphologic analysis often plays a pivotal role in determining the diagnosis and thus the management. By contrast, a biopsy analysis may be indeterminate, and thus the clinical progression of the disease must inform its treatment. The following conditions may present in a similar manner as ulcerative colitis, and should be excluded: - Crohn's disease - Infectious colitis, which is typically detected on stool cultures - Ischemic colitis, inadequate blood supply to the intestine, which typically affects the elderly - Radiation colitis in patients with previous pelvic radiotherapy - Chemical colitis resulting from introduction of harsh chemicals into the colon from an enema or other procedure. The most common disease that mimics the symptoms of ulcerative colitis is Crohn's disease, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases, since the course of the diseases and treatments may be different. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis. Findings in diagnostic workup in Crohn's disease vs. ulcerative colitis Sign Crohn's disease Ulcerative colitis Terminal ileum involvement Commonly Seldom Colon involvement Usually Always Rectum involvement Seldom Usually Involvement around Common Seldom Bile duct involvement No increase in rate of primary sclerosing cholangitis Higher rate Distribution of Disease Patchy areas of inflammation (Skip lesions) Continuous area of inflammation Endoscopy Deep geographic and serpiginous (snake-like) ulcers Continuous ulcer Depth of inflammation May be transmural, deep into tissues Shallow, mucosal Stenosis Common Seldom Granulomas on biopsy May have non-necrotizing non-peri-intestinal crypt granulomas Non-peri-intestinal crypt granulomas not seen Standard treatment for ulcerative colitis depends on extent of involvement and disease severity. The goal is to induce remission initially with medications, followed by the administration of maintenance medications to prevent a relapse of the disease. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing a remission which involves relief of symptoms and mucosal healing of the lining of the colon and then longer term treatment to maintain the remission and prevent complications. Ulcerative colitis can be treated with a number of medications including aminosalicylates such as sulfasalazine, corticosteroids such as prednisone, immunosuppressive medications such as azathioprine, and biological agents such as infliximab. Sulfasalazine has been a major agent in the therapy of mild to moderate UC for over 50 years. In 1977 Mastan S. Kalsi et al. determined that 5-aminosalicylic acid (5-ASA and mesalazine) was the therapeutically active in sulfasalazine. Since then many 5-ASA compounds have been developed with the aim of maintaining efficacy but reducing the common side effects associated with the sulfapyridine moiety in sulfasalazine. Unlike Crohn's disease, ulcerative colitis has a lesser prevalence in smokers than non-smokers. Patients who choose to use smoking as a treatment should keep a record regarding smoking cessation and the onset or relapse of ulcerative colitis to verify associations. Studies using a transdermal nicotine patch have shown clinical and histological improvement. In one double-blind, placebo controlled, study conducted in the United Kingdom 48.6% of patients who used the nicotine patch, in conjunction with their standard treatment, showed complete resolution of symptoms. Another randomized, double-blind, placebo-controlled, single-center clinical trial conducted in the United States showed that 39% of participants showed significant improvement vs. 3% of placebo. Use of a transdermal nicotine patch without the addition of other standard treatments such as mesalazine has relapse occurrence rates similar to standard treatment without the use of nicotine. Management in Crohn's disease vs. ulcerative colitis Crohn's disease Ulcerative colitis Mesalazine less useful More useful Antibiotics Effective in long-term Generally not useful Surgery Often returns following removal of affected part Usually cured by removal of colon Unlike Crohn's disease, ulcerative colitis can generally be cured by surgical removal of the large intestine, also known as a colectomy. This procedure is necessary in the event of: exsanguinating hemorrhage, frank perforation or documented or strongly suspected carcinoma. Surgery is also indicated for patients with severe colitis or toxic megacolon. Patients with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life. Ulcerative colitis (UC) is a disease that affects many parts of the body outside the intestinal tract. In rare cases the extra-intestinal manifestations of the disease may require removal of the colon. Another surgical option for Ulcerative Colitis that is affecting most of the large bowel, is called the ileo-anal pouch procedure. This procedure is a 2 to 3 step procedure in which the large bowel is removed, except for the rectal stump and anus, and a temporary ileostomy is made. The next part of the surgery can be done in 1 or 2 steps and is usually done at 6 - 12 month intervals from each prior surgery. In the next step of the surgery an internal pouch is made of the patients' own small bowel and this pouch is then hooked back up internally to the rectal stump so that patient can once again have a reasonably functioning bowel system, all internal. The temporary ileostomy can be reversed at this time so that the patient is now internalized for bowel functions, or in another step to the procedure, the pouch and rectal stump anastamosis can be left inside the patient to heal for some time, while the patient still uses the ileostomy for bowel function. Then on a subsequent surgery the ileostomy is reversed and the patient has internalized bowel function again. - Probiotics may have benefit. One study which looked at a probiotic known as VSL#3 has shown promise for people with ulcerative colitis. - Fecal bacteriotherapy involves the infusion of human probiotics through fecal enemas. It suggests that the cause of ulcerative colitis may be a previous infection by a still unknown pathogen. This initial infection resolves itself naturally, but somehow causes an imbalance in the colonic bacterial flora, leading to a cycle of inflammation which can be broken by "recolonizing" the colon with bacteria from a healthy bowel. There have been several reported cases of patients who have remained in remission for up to 13 years. In the United States it can be difficult to find doctors who perform this procedure so some patients have performed the procedure at home using a protocol outlined in a published study. Dietary fiber, meaning indigestible plant matter, has been recommended for decades in the maintenance of bowel function. Of peculiar note is fiber from brassica, which seems to contain soluble constituents capable of reversing ulcers along the entire human digestive tract before it is cooked. Oatmeal is also commonly prescribed. - Fish oil. Eicosapentaenoic acid (EPA), derived from fish oil. This is an Eicosanoid that inhibits leukotriene activity, the latter which may be a key factor of inflammation. As an IBD therapy, there are no conclusive studies in support and no recommended dosage. But dosages of EPA between 180 to 1500 mg/day are recommended for other conditions, most commonly cardiac. - Short chain fatty acid (butyrate) enema. The colon utilizes butyrate from the contents of the intestine as an energy source. The amount of butyrate available decreases toward the rectum. Inadequate butyrate levels in the lower intestine have been suggested as a contributing factor for the disease. This might be addressed through butyrate enemas. The results however are not conclusive. - Herbal medications are used by patients with ulcerative colitis. Compounds that contain sulphydryl may have an effect in ulcerative colitis (under a similar hypothesis that the sulpha moiety of sulfasalazine may have activity in addition to the active 5-ASA component). One randomized control trial evaluated the over-the-counter medication methionine-methyl sulphonium chloride (abbreviated MMSC, but more commonly referred to as Vitamin U) and found a significant decreased rate of relapse when the medication was used in conjunction with oral sulfasalazine. - Boswellia is an Ayurvedic (Indian traditional medicine) herb, used as a natural alternative to drugs. One study has found its effectiveness similar to sulfasalazine. Complications of Crohn's disease vs. ulcerative colitis Crohn's disease Ulcerative colitis Nutrient deficiency Higher risk Colon cancer risk Slight Considerable Prevalence of Iritis/uveitis Females 2.2% 3.2% Males 1.3% 0.9% Primary sclerosing Females 0.3% 1% Males 0.4% 3% Ankylosing Females 0.7% 0.8% Males 2.7% 1.5% Pyoderma Females 1.2% 0.8% Males 1.3% 0.7% Erythema nodosum Females 1.9% 2% Males 0.6% 0.7% Progression or remission Patients with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with "flares" of disease. Patients with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. Patients with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of disease. Ulcerative colitis and colorectal cancer There is a significantly increased risk of colorectal cancer in patients with ulcerative colitis after 10 years if involvement is beyond the splenic flexure. Those with only proctitis or rectosigmoiditis usually have no increased risk. It is recommended that patients have screening colonoscopies with random biopsies to look for dysplasia after eight years of disease activity. Primary sclerosing cholangitis Ulcerative colitis has a significant association with primary sclerosing cholangitis (PSC), a progressive inflammatory disorder of small and large bile ducts. As many as 5% of patients with ulcerative colitis may progress to develop primary sclerosing cholangitis. Other long-term features Changes that can be seen in chronic ulcerative colitis include granularity, loss of the vascular pattern of the mucosa, loss of haustra, effacement of the ileocecal valve, mucosal bridging, strictures and pseudopolyps. The incidence of ulcerative colitis in North America is 10–12 cases per 100,000 per year, with a peak incidence of ulcerative colitis occurring between the ages of 15 and 25. Prevalence is 1 per 1000. There is thought to be a bimodal distribution in age of onset, with a second peak in incidence occurring in the 6th decade of life. The disease affects females more than males. The geographic distribution of ulcerative colitis and Crohn's disease is similar worldwide, with highest incidences in the United States, Canada, the United Kingdom, and Scandinavia. Higher incidences are seen in northern locations compared to southern locations in Europe and the United States. As with Crohn's disease, the prevalence of ulcerative colitis is greater among Ashkenazi Jews and decreases progressively in other persons of Jewish descent, non-Jewish Caucasians, Africans, Hispanics, and Asians. Appendectomy prior to age 20 for appendicitis and tobacco use are protective against development of ulcerative colitis. Helminthic therapy using the whipworm Trichuris suis has been shown in a randomized control trial from Iowa to show benefit in patients with ulcerative colitis. The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of patients in the developed world may lead to inflammation. Both helminthic therapy and fecal bacteriotherapy induce a characteristic Th2 white cell response in the diseased areas, which is somewhat paradoxical given that ulcerative colitis immunology was thought to classically involve Th2 overproduction. - ^ a b Ulcerative colitis at eMedicine - ^ a b c d e f internetmedicin.se > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate. - ^ a b c d Hanauer, Stephen B.; William Sandborn (2001-03-01). "Management of Crohn's disease in adults" (PDF). American Journal of Gastroenterology 96 (3): 635–43. doi:10.1111/j.1572-0241.2001.03671.x. PMID 11280528. http://www.acg.gi.org/physicians/guidelines/CrohnsDiseaseinAdults.pdf. Retrieved 2009-11-07. - ^ a b Hanauer SB; Hanauer, Stephen B. (1996). "Inflammatory bowel disease". N. Engl. J. Med. 334 (13): 841–8. doi:10.1056/NEJM199603283341307. PMID 8596552. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8596552&promo=ONFLNS19. - ^ a b c d e f g Kornbluth A, Sachar DB (2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee". Am. J. Gastroenterol. 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x. PMID 15233681. http://www.acg.gi.org/physicians/guidelines/UlcerativeColitisUpdate.pdf. [dead link] - ^ Langan, RC; Gotsch, PB, Krafczyk, MA, Skillinge, DD (2007 Nov 1). "Ulcerative colitis: diagnosis and treatment.". American family physician 76 (9): 1323-30. PMID 18019875. http://www.aafp.org/afp/2007/1101/p1323.html. Retrieved 17 November 2011. - ^ Orholm M, Binder V, Sørensen TI, Rasmussen LP, Kyvik KO (2000). "Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study". Scand. J. Gastroenterol. 35 (10): 1075–81. doi:10.1080/003655200451207. PMID 11099061. - ^ Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B (1988). "Ulcerative colitis and Crohn's disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking". Gut 29 (7): 990–996. doi:10.1136/gut.29.7.990. PMC 1433769. PMID 3396969. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1433769. - ^ a b c Baumgart DC, Carding SR (2007). "Inflammatory bowel disease: cause and immunobiology". The Lancet 369 (9573): 1627–1640. doi:10.1016/S0140-6736(07)60750-8. PMID 17499605. - ^ Cho JH, Nicolae DL, Ramos R, et al. (2000). "Linkage and linkage disequilibrium in chromosome band 1p36 in American Chaldeans with inflammatory bowel disease". Hum. Mol. Genet. 9 (9): 1425–32. doi:10.1093/hmg/9.9.1425. PMID 10814724. http://hmg.oxfordjournals.org/cgi/content/full/9/9/1425. - ^ Järnerot G, Järnmark I, Nilsson K (1983). "Consumption of refined sugar by patients with Crohn's disease, ulcerative colitis, or irritable bowel syndrome". Scand. J. Gastroenterol. 18 (8): 999–1002. doi:10.3109/00365528309181832. PMID 6673083. - ^ Corrao G, Tragnone A, Caprilli R, et al. (1998). "Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC)". Int J Epidemiol 27 (3): 397–404. doi:10.1093/ije/27.3.397. PMID 9698126. http://ije.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=9698126. - ^ Voreacos, David (2007-05-29). "Roche Found Liable in First Of 400 Suits Over Accutane". Washington Post. http://www.washingtonpost.com/wp-dyn/content/article/2007/05/29/AR2007052901946.html. Retrieved 2010-05-26. - ^ Reddy D, Siegel CA, Sands BE, Kane S (2006). "Possible association between isotretinoin and inflammatory bowel disease". Am. J. Gastroenterol. 101 (7): 1569–73. doi:10.1111/j.1572-0241.2006.00632.x. PMID 16863562. - ^ Borobio E, Arín A, Valcayo A, Iñarrairaegui M, Nantes O, Prieto C (2004). "[Isotretinoin and ulcerous colitis]" (in Spanish; Castilian). An Sist Sanit Navar 27 (2): 241–3. PMID 15381956. - ^ Reniers DE, Howard JM (2001). "Isotretinoin-induced inflammatory bowel disease in an adolescent". Ann Pharmacother 35 (10): 1214–6. doi:10.1345/aph.10368. PMID 11675849. http://www.theannals.com/cgi/pmidlookup?view=long&pmid=11675849. - ^ Heather WonTesoriero (2008-04-23). "Jury Awards $10.5 Million Over Accutane". Wall St Journal. http://online.wsj.com/article/SB120890352155036159.html?mod=dist_smartbrief. - ^ Baumgart DC, Sandborn WJ (2007). "Inflammatory bowel disease: clinical aspects and established and evolving therapies.". The Lancet 369 (9573): 1641–57. doi:10.1016/S0140-6736(07)60751-X. PMID 17499606. - ^ a b Fauci et al. Harrison's Internal Medicine, 17th ed. New York: McGraw-Hill Medical, 2008. ISBN 0071599916 - ^ a b Roediger WE, Moore J, Babidge W (1997). "Colonic sulfide in pathogenesis and treatment of ulcerative colitis". Dig. Dis. Sci. 42 (8): 1571–9. doi:10.1023/A:1018851723920. PMID 9286219. http://www.kluweronline.com/art.pdf?issn=0163-2116&volume=42&page=1571. - ^ Levine J, Ellis CJ, Furne JK, Springfield J, Levitt MD (1998). "Fecal hydrogen sulfide production in ulcerative colitis". Am. J. Gastroenterol. 93 (1): 83–7. doi:10.1111/j.1572-0241.1998.083_c.x. PMID 9448181. - ^ a b c d Kornbluth, Asher; David B. Sachar (July 2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee" (PDF). American Journal of Gastroenterology 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x. PMID 15233681. Archived from the original on April 6, 2008. http://web.archive.org/web/20080406030552/http://www.acg.gi.org/physicians/guidelines/UlcerativeColitisUpdate.pdf. Retrieved 2009-11-07. - ^ Crohn's Disease Overview - ^ Elson, CO; Cong, Y; Weaver, CT; Schoeb, TR; Mcclanahan, TK; Fick, RB; Kastelein, RA (2007). "Monoclonal Anti–Interleukin 23 Reverses Active Colitis in a T Cell–Mediated Model in Mice". Gastroenterology 132 (7): 2359. doi:10.1053/j.gastro.2007.03.104. PMID 17570211. - ^ Broomé, Ulrika; Annika Bergquist (February 2006). "Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer". Seminars in Liver Disease 26 (1): 31–41. doi:10.1055/s-2006-933561. PMID 16496231. - ^ Shepherd, NA. (August 2002). "Granulomas in the diagnosis of intestinal Crohn's disease: a myth exploded?". Histopathology 41 (2): 166–8. doi:10.1046/j.1365-2559.2002.01441.x. PMID 12147095. - ^ Mahadeva, U.; Martin, JP.; Patel, NK.; Price, AB. (July 2002). "Granulomatous ulcerative colitis: a re-appraisal of the mucosal granuloma in the distinction of Crohn's disease from ulcerative colitis.". Histopathology 41 (1): 50–5. doi:10.1046/j.1365-2559.2002.01416.x. PMID 12121237. - ^ S. Kane (2006). "Asacol - A Review Focusing on Ulcerative Colitis". http://www.touchalimentarydisease.com/articles.cfm?article_id=6364&level=2. - ^ Calkins BM (1989). "A meta-analysis of the role of smoking in inflammatory bowel disease". Dig. Dis. Sci. 34 (12): 1841–54. doi:10.1007/BF01536701. PMID 2598752. - ^ Lakatos PL, Szamosi T, Lakatos L (2007). "Smoking in inflammatory bowel diseases: good, bad or ugly?". World J Gastroenterol. 13 (46): 6134–9. doi:10.3748/wjg.13.6134. PMID 18069751. - ^ cite paper \|author=Dr M. Guslandi \|title=Nicotine treatment for ulcerative colitis \|journal= \|volume= \|issue= \|pages= \|year= \|pmid= \|doi= \|url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014383/ - ^ cite paper \|author=Sandborn WJ, Tremaine WJ, Offord KP, Lawson GM, Petersen BT, Batts KP, Croghan IT, Dale LC, Schroeder DR, Hurt RD \|title=Transdermal nicotine for mildly to moderately active ulcerative colitis \|journal= \|volume= \|issue= \|pages= \|year= \|pmid= \|doi= \|url=http://www.ncbi.nlm.nih.gov/pubmed/9054280 - ^ a b Pages 152-156 (Section: Inflammatory bowel disease(IBD)) in:Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6. - ^ Feller, M.; Huwiler, K.; Schoepfer, A.; Shang, A.; Furrer, H.; Egger, M. (2010). "Long-term antibiotic treatment for Crohn's disease: systematic review and meta-analysis of placebo-controlled trials". Clinical Infectious Diseases 50 (4): 473–480. doi:10.1086/649923. PMID 20067425. - ^ Section "Antibiotics and Ulcerative Colitis" in: Prantera, C.; Scribano, M. (2009). "Antibiotics and probiotics in inflammatory bowel disease: why, when, and how". Current opinion in gastroenterology 25 (4): 329–333. doi:10.1097/MOG.0b013e32832b20bf. PMID 19444096. - ^ Bibiloni R, Fedorak RN, Tannock GW, et al. (2005). "VSL#3 probiotic-mixture induces remission in patients with active ulcerative colitis". Am. J. Gastroenterol. 100 (7): 1539–46. doi:10.1111/j.1572-0241.2005.41794.x. PMID 15984978. VSL#3 company site - ^ Borody TJ, Warren EF, Leis SM, Surace R, Ashman O, Siarakas S (2004). "Bacteriotherapy using fecal flora: toying with human motions". J. Clin. Gastroenterol. 38 (6): 475–83. doi:10.1097/01.mcg.0000128988.13808.dc. PMID 15220681. http://www.cdd.com.au/pdf/paper12.pdf. - ^ Borody TJ, Warren EF, Leis S, Surace R, Ashman O (2003). "Treatment of ulcerative colitis using fecal bacteriotherapy". J. Clin. Gastroenterol. 37 (1): 42–7. doi:10.1097/00004836-200307000-00012. PMID 12811208. http://www.cdd.com.au/pdf/paper17.pdf. Fulltext(PDF) - ^ MICHAEL S. SILVERMAN,,‡ IAN DAVIS,§ and DYLAN R. PILLAI (2010). "Success of Self-Administered Home Fecal Transplantation for Chronic Clostridium difficile Infection". CLIN GASTROENTEROLOGY AND HEPATOLOGY 8 (5): 471–473. PMID 20117243. - ^ Bensoussan M, Jovenin N, Garcia B, et al. (January 2006). "Complementary and alternative medicine use by patients with inflammatory bowel disease: results from a postal survey". Gastroenterol. Clin. Biol. 30 (1): 14–23. doi:10.1016/S0399-8320(06)73072-X. PMID 16514377. http://www.masson.fr/masson/MDOI-GCB-01-2006-30-1-0399-8320-101019-200517348. - ^ Shah S (2007). "Dietary factors in the modulation of inflammatory bowel disease activity". MedGenMed 9 (1): 60. PMC 1925010. PMID 17435660. http://www.medscape.com/viewarticle/553039. - ^ Terry PD, Villinger F, Bubenik GA, Sitaraman SV (January 2009). "Melatonin and ulcerative colitis: evidence, biological mechanisms, and future research". Inflamm. Bowel Dis. 15 (1): 134–40. doi:10.1002/ibd.20527. PMID 18626968. - ^ Akhtar MS, Munir M (1989). "Evaluation of the gastric anti-ulcerogenic effects of Solanum nigrum, Brassica oleracea and Ocimum basilicum in rats.". Journal of ethnopharmacology 27 (1-2): 163–76. doi:10.1016/0378-8741(89)90088-3. PMID 2515396. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=((%22brassica%22%5BTIAB%5D+NOT+Medline%5BSB%5D)+OR+%22brassica%22%5BMeSH+Terms%5D+OR+cabbage%5BText+Word%5D)+AND+(%22ulcer%22%5BMeSH+Terms%5D+OR+ulcer%5BText+Word%5D). "Brassica oleracea (leaf) powder did not affect the ulcer index significantly but its aqueous extract lowered the index and increased hexosamine levels, suggesting gastric mucosal protection." - ^ "Omega-3 fatty acids, fish oil, alpha-linolenic acid". MedlinePlus Herbs and Supplements. http://www.nlm.nih.gov/medlineplus/druginfo/natural/patient-fishoil.html. - ^ Brzezinski A, Rankin G, Seidner D, Lashner B (1995). "Use of old and new oral 5-aminosalicylic acid formulations in inflammatory bowel disease.". Cleve Clin J Med 62 (5): 317–23. PMID 7586488. - ^ Salim A (1992). "Role of sulphydryl-containing agents in the management of recurrent attacks of ulcerative colitis. A new approach.". Pharmacology 45 (6): 307–18. doi:10.1159/000139016. PMID 1362613. - ^ Gupta, I.; Parihar, A.; Malhotra, P.; Singh, G.; Lüdtke, R.; Safayhi, H.; Ammon, H. (1997). "Effects of Boswellia serrata gum resin in patients with ulcerative colitis". European journal of medical research 2 (1): 37–43. PMID 9049593. - ^ Prevalence defined as at least 5 health care contacts in a 10 year period for the condition, according to: Greenstein, A. J.; Janowitz, H. D.; Sachar, D. B. (1976). "The extra-intestinal complications of Crohn's disease and ulcerative colitis: a study of 700 patients". Medicine 55 (5): 401–412. doi:10.1097/00005792-197609000-00004. PMID 957999. - ^ Leighton JA, Shen B, Baron TH, et al. (2006). "ASGE guideline: endoscopy in the diagnosis and treatment of inflammatory bowel disease". Gastrointest. Endosc. 63 (4): 558–65. doi:10.1016/j.gie.2006.02.005. PMID 16564852. - ^ Olsson R, Danielsson A, Järnerot G, et al. (1991). "Prevalence of primary sclerosing cholangitis in patients with ulcerative colitis". Gastroenterology 100 (5 Pt 1): 1319–23. PMID 2013375. - ^ Page 481 in: Colonic diseases. By Timothy R. Koch. 2003. ISBN 0896039617, 9780896039612 - ^ Podolsky DK (2002). "Inflammatory bowel disease". N. Engl. J. Med. 347 (6): 417–29. doi:10.1056/NEJMra020831. PMID 12167685. - ^ Shivananda S, Lennard-Jones J, Logan R, et al. (1996). "Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD)". Gut 39 (5): 690–7. doi:10.1136/gut.39.5.690. PMC 1383393. PMID 9014768. http://gut.bmj.com/cgi/pmidlookup?view=long&pmid=9014768. - ^ Sonnenberg A, McCarty DJ, Jacobsen SJ (January 1991). "Geographic variation of inflammatory bowel disease within the United States". Gastroenterology 100 (1): 143–9. PMID 1983816. - ^ NEJM 2001;344:808. - ^ NEJM 1987;316:707. - ^ Summers RW, Elliott DE, Urban JF, Thompson RA, Weinstock JV (2005). "Trichuris suis therapy for active ulcerative colitis: a randomized controlled trial". Gastroenterology 128 (4): 825–32. doi:10.1053/j.gastro.2005.01.005. PMID 15825065. http://linkinghub.elsevier.com/retrieve/pii/S0016508505000259. Inflammatory bowel disease: Crohn's disease and ulcerative colitis Main Anatomical terms History Organizations PeopleList of people diagnosed with Crohn's disease · Deaths from Crohn's disease Wikimedia Foundation. 2010. Look at other dictionaries: Ulcerative colitis — A relatively common disease that causes inflammation of the large intestine (the colon). The cause is unknown. Ulcerative colitis is a form of inflammatory bowel disease. It has some similarity to a related disorder, Crohn’s disease. The end of… … Medical dictionary Ulcerative colitis — Klassifikation nach ICD 10 K51. Colitis ulcerosa K51.0 Ulzeröse (chronische) Enterokolitis K51.1 Ulzeröse (chron … Deutsch Wikipedia ulcerative colitis — Pathol. chronic ulceration in the large intestine, characterized by painful abdominal cramps and profuse diarrhea containing pus, blood, and mucus. * * * Inflammation of the colon, especially of its mucous membranes. The inflamed membranes… … Universalium ulcerative colitis — noun a serious chronic inflammatory disease of the large intestine and rectum characterized by recurrent episodes of abdominal pain and fever and chills and profuse diarrhea • Hypernyms: ↑colitis, ↑inflammatory bowel disease * * * noun : a… … Useful english dictionary ulcerative colitis — inflammation and ulceration of the colon and rectum. See: colitis … The new mediacal dictionary ulcerative colitis — noun Date: circa 1928 a nonspecific inflammatory disease of the colon of unknown cause characterized by diarrhea with discharge of mucus and blood, cramping abdominal pain, and inflammation and edema of the mucous membrane with patches of… … New Collegiate Dictionary ulcerative colitis — Inflammation of the colon and rectum: cause unclear, although there are often antibodies to colonic epithelium and E. coli strain 0119 B14 … Dictionary of molecular biology ulcerative colitis — (Medicine) recurrent condition of unknown origin characterized by ulcers and severe irritation of the colon and rectum (causes bloody stools, hemorrhoids, and abdominal pain) … English contemporary dictionary ulcerative colitis — Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel … English dictionary of cancer terms Management of ulcerative colitis — involves first treating the acute symptoms of the disease, then maintaining remission. Ulcerative colitis is a form of colitis, a disease of the intestine, specifically the large intestine or colon, that includes characteristic ulcers, or open… … Wikipedia	2	55	18	0	3	7	0.680322	28	11,034
- Myocardial rupture Myocardial rupture Classification and external resources ICD-10 I23.3-I23.5, S26.8 eMedicine med/1571 MeSH D006341 Myocardial rupture (or heart rupture) is a laceration or tearing of the walls of the ventricles or atria of the heart, of the interatrial or interventricular septum, of the papillary muscles or chordae tendineae or of one of the valves of the heart. It is most commonly seen as a serious sequela of an acute myocardial infarction (heart attack). It can also be caused by trauma. The most common cause of myocardial rupture is a recent myocardial infarction, with the rupture typically occurring three to five days after infarction. Other causes of rupture include cardiac trauma, endocarditis (infection of the heart), cardiac tumors, infiltrative diseases of the heart, and aortic dissection. Risk factors for rupture after an acute myocardial infarction include female gender, advanced age of the individual, and a low body mass index. Other presenting signs associated with myocardial rupture include a pericardial friction rub, sluggish flow in the coronary artery after it is opened, the left anterior descending artery being the cause of the acute MI, and delay of revascularization greater than 2 hours. The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial rupture. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction. On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered. The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent. Myocardial ruptures can be classified as one of three types. - Type I myocardial rupture is an abrupt slit-like tear that generally occurs within 24 hours of an acute myocardial infarction. - Type II is an erosion of the infarcted myocardium, which is suggestive of a slow tear of the dead myocardium. Type II ruptures typically occur more than 24 hours after the infarction occurred. - Type III ruptures are characterized by early aneurysm formation and subsequent rupture of the aneurysm. Another method for classifying myocardial ruptures is by the anatomical portion of the heart that has ruptured. By far the most dramatic is rupture of the free wall of the left or right ventricles, as this is associated with immediate hemodynamic collapse and death secondary to acute pericardial tamponade. Rupture of the interventricular septum will cause a ventricular septal defect. Rupture of a papillary muscle will cause acute mitral regurgitation. Signs and symptoms Due to the acute hemodynamic deterioration associated with myocardial rupture, the diagnosis is generally made based on physical examination, changes in the vital signs, and clinical suspicion. The diagnosis can be confirmed with echocardiography. The treatment for myocardial rupture is supportive in the immediate setting and surgical correction of the rupture, if feasible. A certain small percentage of individuals do not seek medical attention in the acute setting and survive to see the physician days or weeks later. In this setting, it may be reasonable to treat the rupture medically and delay or avoid surgery completely, depending on the individual's comorbid medical issues. The prognosis of myocardial rupture is dependent on a number of factors, including which portion of the myocardium is involved in the rupture. In one case series, if myocardial rupture involved the free wall of the left ventricle, the mortality rate was 100%. Even if the individual survives the initial hemodynamic sequelae of the rupture, the 30 day mortality is still significantly higher than if rupture did not occur. - ^ Nan YY, Lu MS, Liu KS, et al. (September 2009). "Blunt traumatic cardiac rupture: therapeutic options and outcomes". Injury 40 (9): 938–45. doi:10.1016/j.injury.2009.05.016. PMID 19540491. http://linkinghub.elsevier.com/retrieve/pii/S0020-1383(09)00277-0. - ^ a b Lin TH, Su HM, Voon WC, Lai HM, Yen HW, Lai WT, Sheu SH. (2006). "Association between hypertension and primary mitral chordae tendinae rupture.". Am J Hypertens 19 (1): 75–9. doi:10.1016/j.amjhyper.2005.06.020. PMID 16461195. - ^ de Diego C, Marcos-Alberca P, Pai RK. (2006). "Giant periprosthetic vegetation associated with pseudoaneurysmal-like rupture." (PDF). Eur Heart J 27 (8): 912. doi:10.1093/eurheartj/ehi540. PMID 16569654. http://eurheartj.oxfordjournals.org/cgi/reprint/27/8/912.pdf. - ^ a b c d e f g Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. (2003). "Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era." (PDF). Chest 124 (2): 565–71. doi:10.1378/chest.124.2.565. PMID 12907544. http://www.chestjournal.org/cgi/reprint/124/2/565.pdf. - ^ a b c d e Moreno R, Lopez-Sendon J, Garcia E, Perez de Isla L, Lopez de Sa E, Ortega A, Moreno M, Rubio R, Soriano J, Abeytua M, Garcia-Fernandez MA. (2002). "Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction.". J Am Coll Cardiol 39 (4): 598–603. doi:10.1016/S0735-1097(01)01796-X. PMID 11849857. - ^ Sugiura T, Nagahama Y, Nakamura S, Kudo Y, Yamasaki F, Iwasaka T. (2003). "Left ventricular free wall rupture after reperfusion therapy for acute myocardial infarction.". Am J Cardiol 92 (3): 282–4. doi:10.1016/S0002-9149(03)00625-8. PMID 12888132. - ^ Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ. (1996). "A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction.". J Am Coll Cardiol 27 (6): 1321–6. doi:10.1016/0735-1097(96)00008-3. PMID 8626938. - ^ Becker AE, van Mantgem JP. (1975). "Cardiac tamponade. A study of 50 hearts.". Eur J Cardiol 3 (4): 349–58. PMID 1193118. Cardiovascular disease: heart disease · Circulatory system pathology (I00–I52, 390–429) IschaemicActive ischemia LayersValves Conduction/ arrhythmiaPremature contractionWolff-Parkinson-White · Lown-Ganong-LevineFlutter/fibrillationPacemakerOther/ungrouped Cardiomegaly Other Chest trauma, excluding fractures (S20–S29, 860–862) Cardiac and circulatory system injuries lower respiratory tract injuries Wikimedia Foundation. 2010.	3	12	4	0	3	3	0.771969	10	1,778
Daniel Carlat, MD Editor-in-Chief, Publisher, The Carlat Report. Dr. Carlat has disclosed that he has no relevant relationships or financial interests in any commercial company pertaining to this educational activity. On October 1, 2015, you had to start using ICD-10 codes for reporting diagnoses in order to get paid by insurance companies. But what does ICD-10 mean? And how does it relate to DSM-5? ICD-10 stands for “International Classification of Diseases, 10th edition.” First published in 1900, ICD is a list of diseases in all medical specialties. It has been maintained by the World Health Organization (WHO) for decades, and its purpose is to help all countries agree on how to classify the many ailments that strike our human frames. This system allows nations to speak the same medical language in keeping track of disease prevalence in different parts of the world—knowledge that can be very helpful in puzzling out the causes of diseases. How are ICD and DSM related? ICD is primarily a list of diseases, and it is not limited to mental health. ICD-10 contains 22 chapters and 68,000 disease codes. One of those chapters, Chapter 5, focuses on mental health. DSM, on the other hand, is a creation of the American Psychiatric Association. It focuses exclusively on mental health and is more than a list of codes—it is also a textbook describing the criteria used to diagnose psychiatric disorders. Until October 1, we were using DSM codes on our claims to insurance companies. Or so we thought. One surprising piece of news is that those DSM codes were, in actuality, identical to ICD-9 codes. We have been using ICD-9 codes since the publication of DSM-III in 1980. Just as DSM undergoes periodic updates, so does ICD. ICD-9 was the world’s medical bible from 1978 to 1994, which was when WHO updated ICD-9 to ICD-10. Most European countries adopted the new standard by 2000, but the U.S. health care system was very late to this party. Why? Primarily because ICD-10 is much more complex than its predecessors. ICD-9 included 13,000 disease codes, whereas ICD-10 mushroomed to 68,000 codes. The good news about having all these extra codes is that it allows you to diagnose a condition with greater precision and specificity. The bad news is that the amount of detail can be excruciating. For example, ICD-10 has numerous codes to diagnose injuries sustained by contact with animals, such as getting bitten by pigs or being struck by macaws. That in itself sounds reasonable, as different animals can cause different types of injuries. It’s the drilling down from there that seems excessive. There are 9 different codes for injuries sustained through human-turkey contact: “struck by turkey, initial encounter,” “struck by turkey, subsequent encounter,” “struck by turkey, sequela;” then there’s “pecked by turkey, initial encounter….” You get the idea. After many years of resistance, in 2009, the U.S. Department of Health and Human Services ordered that we had to switch to ICD-10 by 2013. However, the code set’s adoption was delayed to 2014, then delayed once more to October 1, 2015. Table: ICD-9 to ICD-10 Conversions for Common Diagnoses How does ICD-10 affect you? The ICD-10 switch is, frankly, a non-issue for most psychiatrists. True, we have to say farewell to those trusty old friends engraved in our memory like 296.32 (major depression, recurrent, moderate) and 300.02 (generalized anxiety disorder)—which have been replaced with, respectively, F32.1 and F41.1. But the DSM-5 makes life easy by listing both the old ICD-9 codes for each disorder, as well as the new ICD-10 codes. If you don’t want to open up your DSM-5 every time you need to look up a code, you can take advantage of many free online resources. An online converter allows you to type in the ICD-9 code, press enter, and obtain the corresponding ICD-10 code. A more interesting option is found on Dr. Bob’s Virtual En-psych-lopedia, whose tables allow you to search alphabetically for disorders and find out how to convert them from ICD-9 to ICD-10. In that same vein, we’ve included a brief table below, “ICD-9 to ICD-10 Conversions for Common Diagnoses,” that lists some of the more common psychiatric disorders. If you’re using an electronic health record, chances are that the computer software is doing all this automatically for you via drop-down menus. ICD-10’s time saving secret At first blush, converting ICD-9 codes to ICD-10 disorders appears to require more precision than we’re used to. For example, ICD-9 allowed you to use a single code for anorexia nervosa (307.51), whereas ICD-10 forces you to specify whether the anorexia is the restricting type (F50.01) or the binge-eating purging type (F50.02). Luckily, those in the know have discovered a hidden section of the codebook allowing you to use “unspecified” for all manner of diagnoses, such as anorexia nervosa, unspecified (F50.00). In fact, there are “unspecified” codes for all the major disorders, such as bipolar disorder, major depression, substance use disorders, and so on. This makes our jobs easier—for example, ICD-10 offers a mind-numbing menu of 22 separate codes for different varieties of bipolar I disorder, depending on whether the most recent episode was depressed, manic, or hypomanic; whether it was mild, moderate, or severe; and with or without psychotic features. You can spend a good chunk of your day choosing the “right” one, or you can go with F31.9: “Bipolar I disorder, unspecified.” Meanwhile—sorry to alarm you—ICD-11 will be published in 2018. Not to worry, since if history is any indication, the U.S. will take a decade or two to adopt it, giving you plenty of time to get cozy with ICD-10. (I’d like to gratefully acknowledge Dr. Bruce Black for helping me understand the basics of ICD.) (For a good primer on ICD-10, go to this APA website.)	4	2	0	0	0	8	0.634635	8	1,427
- Premature ventricular contraction Premature ventricular contraction Classification and external resources A premature ventricular contraction marked by the arrow. ICD-10 I49.3 ICD-9 427.69 DiseasesDB 32412 eMedicine emerg/773 MeSH D018879 A premature ventricular contraction (PVC), also known as a premature ventricular complex, ventricular premature contraction (or complex or complexes) (VPC), ventricular premature beat (VPB), or extrasystole, is a relatively common event where the heartbeat is initiated by the heart ventricles rather than by the sinoatrial node, the normal heartbeat initiator. The electrical events of the heart detected by the electrocardiogram allow a PVC to be easily distinguished from a normal heart beat. A PVC may be perceived as a "skipped beat" or felt as palpitations in the chest. In a normal heartbeat, the ventricles contract after the atria have helped to fill them by contracting; in this way the ventricles can pump a maximized amount of blood both to the lungs and to the rest of the body. In a PVC, the ventricles contract first, which means that circulation is inefficient. However, single beat PVC arrhythmias do not usually pose a danger and can be asymptomatic in healthy individuals. Premature ventricular contractions can occur in a healthy person of any age, but are more prevalent in the elderly and in men. They frequently occur spontaneously with no known cause. Some possible causes include: - Certain medicines such as digoxin, which increases heart contraction - Cardiomyopathy, hypertrophic or dilated; - Myocardial contusion; - Hypercapnia (CO2 poisoning); - Sarcoidosis; - Mitral valve prolapse; - Drugs such as cocaine; - Theobromine; - Tricyclic antidepressants; - Magnesium and potassium deficiency; - Calcium excess; - Thyroid problems; - Chemical (electrolyte) problems in the blood; - Heart attack; - Adrenaline excess; - Lack of sleep/exhaustion; A PVC may be perceived as a skipped heart beat, a strong beat, or a feeling of suction in the chest. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a dangerous rapid heartbeat. PVCs are usually diagnosed after the patient has described “skipped beats”, pauses or palpitations. Typically the palpitations felt by PVC patients are very irregular and less sustained than patients with other types of arrhythmia. They are likely to have “flip flopping” sensations where it feels like the heart is flipping over or pounding due to there being a pause after the premature contraction and then a powerful contraction after the pause. There is a possibility that they might feel a ‘fluttering’ in their chest or a pounding in their neck but these two types of palpitations aren’t very common in PVC patients. A physical examination should be conducted after a full history has been taken. This is useful in determining any possible heart defects that might be causing the palpitations. Most cases of premature ventricular contraction have a mitral-valve prolapse which can be determined through the physical examination. The next step in diagnosis is a 12 lead ECG which can be performed in the doctors’ office over a short period of time however this is often non-conclusive in diagnosis because it is not very sensitive and there is only a small chance of a premature ventricular contraction occurring in the short period of time. Holter monitoring is a far better method for diagnosis as it is continuous recording of the heart’s rhythm over a period of 24 hours, or event monitoring which records noncontinuously for 30 days or indefinitely. This increases the likelihood of a premature ventricular contraction occurring during the recording period and is therefore more useful in diagnosis. When looking at an electrocardiograph premature ventricular contractions are easily spotted and therefore a definitive diagnosis can be made. The QRS and T waves look very different to normal readings. The spacing between the PVC and the preceding QRS wave is a lot shorter than usual and the time between the PVC and the proceeding QRS is a lot longer. However, the time between the preceding and proceeding QRS waves stays the same as normal due to the compensatory pause. PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions. There are four different named patterns of regularly occurring PVCs. Depending whether there are 1, 2, or 3 normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. A unifocal PVC is where the depolarisation is triggered from the one site in the ventricle causing the peaks on the ECG to look the same. Multifocal PVCs arise when more than one site in the ventricles initiate depolarisation causing each peak on the ECG to have a different shape. If 3 or more PVCs occur in a row it may be called Ventricular tachycardia. Isolated PVCs with benign characteristics require no treatment. In healthy individuals, PVCs can often be resolved by restoring the balance of magnesium, calcium and potassium within the body. The most effective treatment is the elimination of triggers (particularly the cessation of the use of substances such as caffeine, and certain drugs.) - Pharmacological agents - Electrolytes replacement - Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.) - Potassium supplements - Radiofrequency catheter ablation treatment - Lifestyle modification In the setting of existing cardiac disease, however, PVCs must be watched carefully, as they may cause a form of ventricular tachycardia (rapid heartbeat). Recent studies have shown that those subjects who have an extremely high occurrence of PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses. Normally impulses pass through both ventricles almost simultaneously, the depolarisation waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels in one direction therefore there is no neutralisation effect which results in the high voltage QRS wave in the electrocardiograph. There are two main physiological explanations for premature ventricular contractions: re-entrant signalling and “enhanced automaticity in some ectopic focus”. The enhanced automaticity means that the ectopic centre fires more regularly than usual and is protected from depolarisation that results in premature contractions.[clarification needed] There are a number of different molecular explanations for PVCs. One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the ventricular cardiac myocytes leading to increased flow of calcium ions into the cell. This may happen for the following reasons: - Activation of the sympathetic nervous system, due to anxiety and/or physiological stress, for example hypovolemia caused by dehydration or hemorrhage. This activation can cause a release of catecholamines such as epinephrine (adrenaline) which can bind to beta-1 adrenergic receptor (β1 receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called Gs protein. This type of protein stimulates the production of cAMP, ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol. This has the effect of (1) increasing the strength of contraction (inotropy) and (2) depolarizing the myocyte more rapidly (chronotropy). The ventricular myocytes are therefore more irritable than usual, and may depolarize spontaneously before the SA node depolarizes. Other sympathomimetic molecules such as amphetamines and cocaine will also cause this effect. - Phosphodiesterase inhibitors such as caffeine directly affect the G-coupled signal transduction cascade by inhibiting the enzyme that catalyzes the breakdown of cAMP, again leading to the increased concentration of calcium ions in the cytosol. Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells, and hypokalemia makes it more likely that cells will depolarize spontaneously. Hypercalcemia has a similar effect, although clinically it is of less concern. Magnesium ions affect the flow of calcium ions, and they affect the function of the Na+/K+ ATPase, and are necessary for maintaining potassium levels. Hypomagnesemia therefore also makes spontaneous depolarization more likely. Existing damage to the myocardium can also provoke PVCs. The myocardial scarring that occurs in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and may also irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. Inflammation of the myocardium (as occurs in myocarditis) and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes. - ^ Stanfield, C.; Germann, W. (2008), Principles of Human Physiology (3rd ed.), Pearson International Edition, p. 378, ISBN 0321455061 - ^ a b c d e f g h i j k l m n Premature ventricular contraction at eMedicine - ^ a b c Emilsson K (June 2008), "Suspected association of ventricular arrhythmia with air pollution in a motorbike rider: a case report", J Med Case Reports 2: 192, doi:10.1186/1752-1947-2-192, PMC 2427047, PMID 18522736, http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2427047 - ^ Health encyclopedia – diseases and conditions. The heathcentral network. Accessed Feb 8th 2009. - ^ MedlinePlus Encyclopedia Ectopic heartbeat - ^ a b c d e f g [Leonard I Ganz, MD, http://www.uptodate.com/patients/content/topic.do?topicKey=hrt_dis/11733, Up-to-date patient information, Updated Sep 11th 2007, reviewed Oct 2008, Accessed Feb 9th 2009.] - ^ a b Guyton MD, Arthur C.; Hall, John E. (2006), Textbook of medical physiology (11th ed.), p. 151, ISBN 0721602401 - ^ a b Zimetbaum P, Josephson ME (May 1998), "Evaluation of patients with palpitations", N. Engl. J. Med. 338 (19): 1369–73, doi:10.1056/NEJM199805073381907, PMID 9571258, http://content.nejm.org/cgi/content/full/338/19/1369 - ^ Meurs KM, Spier AW, Wright NA, Hamlin RL (January 2001), "Comparison of in-hospital versus 24-hour ambulatory electrocardiography for detection of ventricular premature complexes in mature Boxers", J. Am. Vet. Med. Assoc. 218 (2): 222–4, doi:10.2460/javma.2001.218.222, PMID 11195827 - ^ a b Levy 2007, pp. 49–50 - ^ a b Haist, Steven A.; Gomella, Leonard G. (2004), "19 Basic ECG Reading: Ventricular Arrhythmias", Clinician's pocket reference (10th ed.), New York: McGraw-Hill, p. 390, ISBN 0-07-140255-1, http://books.google.com/books?id=KaegPx6LK2sC&pg=PA390&dq=unifocal+premature+ventricular+contraction&client - ^ Belhassen B (April 2005), "Radiofrequency ablation of "benign" right ventricular outflow tract extrasystoles: a therapy that has found its disease?", J. Am. Coll. Cardiol. 45 (8): 1266–8, doi:10.1016/j.jacc.2005.01.028, PMID 15837260, http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(05)00234-2 - ^ Shiraishi, Hirokazu; Ishibashi, Kazuya; Urao, Norifumi; Tsukamoto, Masaki; Hyogo, Masayuki; Keira, Natsuya; Hirasaki, Satoshi; Shirayama, Takeshi et al. (2002), "A case of cardiomyopathy induced by premature ventricular complexes", Circulation 66 (11): 1065–7, doi:10.1253/circj.66.1065 - ^ a b Nelson 2008, p. 424 - ^ Levy 2007, p. 62 - ^ Levy 2007, p. 24 - ^ Nelson 2008, p. 430 - Levy, M.N.; Pappano, A.J. (2007), Cardiovascular physiology (9th ed.), Mosby Elsevier, ISBN 0323034462 - Nelson, D.L.; Cox, M.M. (2008), Lehninger Principles of Biochemistry (5th ed.), WH Freeman, ISBN 071677108X Cardiovascular disease: heart disease · Circulatory system pathology (I00–I52, 390–429) IschaemicActive ischemia LayersValves Conduction/ arrhythmiaPremature contractionAtrial · VentricularWolff-Parkinson-White · Lown-Ganong-LevineFlutter/fibrillationPacemakerOther/ungrouped Wikimedia Foundation. 2010.	2	10	4	0	1	3	0.924852	8	3,052
The International Classification of Diseases (ICD) is a globally used diagnostic tool for epidemiology, health management and clinical purposes. The ICD is maintained by the World Health Organization (WHO), which is the directing and coordinating authority for health within the United Nations System. The ICD is originally designed as a health care classification system, providing a system of diagnostic codes for classifying diseases, including nuanced classifications of a wide variety of signs, symptoms, abnormal findings, complaints, social circumstances, and external causes of injury or disease. This system is designed to map health conditions to corresponding generic categories together with specific variations, assigning for these a designated code, up to six characters long. Thus, major categories are designed to include a set of similar diseases. The ICD is published by the WHO and used worldwide for morbidity and mortality statistics, reimbursement systems, and automated decision support in health care. This system is designed to promote international comparability in the collection, processing, classification, and presentation of these statistics. Like the analogous Diagnostic and Statistical Manual of Mental Disorders (which is limited to psychiatric disorders and almost exclusive to the United States), the ICD is a major project to statistically classify all health disorders, and provide diagnostic assistance. The ICD is a core statistically based classificatory diagnostic system for health care related issues of the WHO Family of International Classifications (WHO-FIC). The ICD is revised periodically and is currently in its 11th revision. The ICD-11, as it is therefore known, was accepted by WHO's World Health Assembly (WHA) on 25 May 2019 and officially came into effect on 1 January 2022. However, widespread adoption will likely take some time: the US only adopted ICD-10 in 2015, as of 2018[update] some countries still using ICD-9 and even ICD-8. The version for preparation of approval at the WHA was released on 18 June 2018. The ICD is part of a "family" of international classifications (WHOFIC) that complement each other, also including the International Classification of Functioning, Disability and Health (ICF) which focuses on the domains of functioning (disability) associated with health conditions, from both medical and social perspectives, and the International Classification of Health Interventions (ICHI) that classifies the whole range of medical, nursing, functioning and public health interventions. The title of the ICD is formally the International Statistical Classification of Diseases and Related Health Problems, although the original title, International Classification of Diseases, is still informally the name by which it is usually known. This section needs additional citations for verification. (July 2017) In 1860, during the international statistical congress held in London, Florence Nightingale made a proposal that was to result in the development of the first model of systematic collection of hospital data. In 1893, a French physician, Jacques Bertillon, introduced the Bertillon Classification of Causes of Death at a congress of the International Statistical Institute in Chicago. A number of countries adopted Bertillon's system, which was based on the principle of distinguishing between general diseases and those localized to a particular organ or anatomical site, as used by the City of Paris for classifying deaths. Subsequent revisions represented a synthesis of English, German, and Swiss classifications, expanding from the original 44 titles to 161 titles. In 1898, the American Public Health Association (APHA) recommended that the registrars of Canada, Mexico, and the United States also adopt it. The APHA also recommended revising the system every 10 years to ensure the system remained current with medical practice advances. As a result, the first international conference to revise the International Classification of Causes of Death took place in 1900, with revisions occurring every ten years thereafter. At that time, the classification system was contained in one book, which included an Alphabetic Index as well as a Tabular List. The book was small compared with current coding texts. The revisions that followed contained minor changes, until the sixth revision of the classification system. With the sixth revision, the classification system expanded to two volumes. The sixth revision included morbidity and mortality conditions, and its title was modified to reflect the changes: International Statistical Classification of Diseases, Injuries and Causes of Death (ICD). Prior to the sixth revision, responsibility for ICD revisions fell to the Mixed Commission, a group composed of representatives from the International Statistical Institute and the Health Organization of the League of Nations. In 1948, the WHO assumed responsibility for preparing and publishing the revisions to the ICD every ten years. WHO sponsored the seventh and eighth revisions in 1957 and 1968, respectively. It later became clear that the established ten year interval between revisions was too short. The ICD is currently the most widely used statistical classification system for diseases in the world. In addition, some countries—including Australia, Canada, and the United States—have developed their own adaptations of ICD, with more procedure codes for classification of operative or diagnostic procedures. Versions of ICDEdit The ICD-6, published in 1949, was the first to be shaped to become suitable for morbidity reporting. Accordingly, the name changed from International List of Causes of Death to International Statistical Classification of Diseases. The combined code section for injuries and their associated accidents was split into two, a chapter for injuries, and a chapter for their external causes. With use for morbidity there was a need for coding mental conditions, and for the first time a section on mental disorders was added . The International Conference for the Seventh Revision of the International Classification of Diseases was held in Paris under the auspices of WHO in February 1955. In accordance with a recommendation of the WHO Expert Committee on Health Statistics, this revision was limited to essential changes and amendments of errors and inconsistencies. The 8th Revision Conference convened by WHO met in Geneva, from 6 to 12 July 1965. This revision was more radical than the Seventh but left unchanged the basic structure of the Classification and the general philosophy of classifying diseases, whenever possible, according to their etiology rather than a particular manifestation. During the years that the Seventh and Eighth Revisions of the ICD were in force, the use of the ICD for indexing hospital medical records increased rapidly and some countries prepared national adaptations which provided the additional detail needed for this application of the ICD. In the US, a group of consultants was asked to study the 8th revision of ICD (ICD-8a) for its applicability to various users in the United States. This group recommended that further detail be provided for coding hospital and morbidity data. The American Hospital Association's "Advisory Committee to the Central Office on ICDA" developed the needed adaptation proposals, resulting in the publication of the International Classification of Diseases, Adapted (ICDA). In 1968, the United States Public Health Service published the International Classification of Diseases, Adapted, 8th Revision for use in the United States (ICDA-8a). Beginning in 1968, ICDA-8a served as the basis for coding diagnostic data for both official morbidity [and mortality] statistics in the United States. The International Conference for the Ninth Revision of the International Statistical Classification of Diseases, Injuries, and Causes of Death, convened by WHO, met in Geneva from 30 September to 6 October 1975. In the discussions leading up to the conference, it had originally been intended that there should be little change other than updating of the classification. This was mainly because of the expense of adapting data processing systems each time the classification was revised. There had been an enormous growth of interest in the ICD and ways had to be found of responding to this, partly by modifying the classification itself and partly by introducing special coding provisions. A number of representations were made by specialist bodies which had become interested in using the ICD for their own statistics. Some subject areas in the classification were regarded as inappropriately arranged and there was considerable pressure for more detail and for adaptation of the classification to make it more relevant for the evaluation of medical care, by classifying conditions to the chapters concerned with the part of the body affected rather than to those dealing with the underlying generalized disease. At the other end of the scale, there were representations from countries and areas where a detailed and sophisticated classification was irrelevant, but which nevertheless needed a classification based on the ICD in order to assess their progress in health care and in the control of disease. A field test with a bi-axial classification approach—one axis (criterion) for anatomy, with another for etiology—showed the impracticability of such approach for routine use. The final proposals presented to and accepted by the Conference in 1978 retained the basic structure of the ICD, although with much additional detail at the level of the four digit subcategories, and some optional five digit subdivisions. For the benefit of users not requiring such detail, care was taken to ensure that the categories at the three digit level were appropriate. For the benefit of users wishing to produce statistics and indexes oriented towards medical care, the 9th Revision included an optional alternative method of classifying diagnostic statements, including information about both an underlying general disease and a manifestation in a particular organ or site. This system became known as the 'dagger and asterisk system' and is retained in the Tenth Revision. A number of other technical innovations were included in the Ninth Revision, aimed at increasing its flexibility for use in a variety of situations. It was eventually replaced by ICD-10, the version currently in use by the WHO and most countries. Given the widespread expansion in the tenth revision, it is not possible to convert ICD-9 data sets directly into ICD-10 data sets, although some tools are available to help guide users. Publication of ICD-9 without IP restrictions in a world with evolving electronic data systems led to a range of products based on ICD-9, such as MeDRA or the Read directory. When ICD-9 was published by the World Health Organization (WHO), the International Classification of Procedures in Medicine (ICPM) was also developed (1975) and published (1978). The ICPM surgical procedures fascicle was originally created by the United States, based on its adaptations of ICD (called ICDA), which had contained a procedure classification since 1962. ICPM is published separately from the ICD disease classification as a series of supplementary documents called fascicles (bundles or groups of items). Each fascicle contains a classification of modes of laboratory, radiology, surgery, therapy, and other diagnostic procedures. Many countries have adapted and translated the ICPM in parts or as a whole and are using it with amendments since then. International Classification of Diseases, Clinical Modification (ICD-9-CM) is an adaption created by the US National Center for Health Statistics (NCHS) and used in assigning diagnostic and procedure codes associated with inpatient, outpatient, and physician office utilization in the United States. The ICD-9-CM is based on the ICD-9 but provides for additional morbidity detail. It is updated annually on October 1. It consists three volumes: - Volumes 1 and 2 contain diagnosis codes. (Volume 1 is a tabular listing, and volume 2 is an index.) Extended for ICD-9-CM - Volume 3 contains procedure codes for surgical, diagnostic, and therapeutic procedures. ICD-9-CM only The NCHS and the Centers for Medicare and Medicaid Services are the US governmental agencies responsible for overseeing all changes and modifications to the ICD-9-CM. Work on ICD-10 began in 1983, and the new revision was endorsed by the Forty-third World Health Assembly in May 1990. The latest version came into use in WHO Member States starting in 1994. The classification system allows more than 55,000 different codes and permits tracking of many new diagnoses and procedures, a significant expansion on the 17,000 codes available in ICD-9. Adoption was relatively swift in most of the world. Several materials are made available online by WHO to facilitate its use, including a manual, training guidelines, a browser, and files for download. Some countries have adapted the international standard, such as the "ICD-10-AM" published in Australia in 1998 (also used in New Zealand), and the "ICD-10-CA" introduced in Canada in 2000. Adoption of ICD-10-CM was slow in the United States. Since 1979, the US had required ICD-9-CM codes for Medicare and Medicaid claims, and most of the rest of the American medical industry followed suit. On 1 January 1999 the ICD-10 (without clinical extensions) was adopted for reporting mortality, but ICD-9-CM was still used for morbidity. Meanwhile, NCHS received permission from the WHO to create a clinical modification of the ICD-10, and has production of all these systems: - ICD-10-CM, for diagnosis codes, replaces volumes 1 and 2. Annual updates are provided. - ICD-10-PCS, for procedure codes, replaces volume 3. Annual updates are provided. On 21 August 2008, the US Department of Health and Human Services (HHS) proposed new code sets to be used for reporting diagnoses and procedures on health care transactions. Under the proposal, the ICD-9-CM code sets would be replaced with the ICD-10-CM code sets, effective 1 October 2013. On 17 April 2012 the Department of Health and Human Services (HHS) published a proposed rule that would delay, from 1 October 2013 to 1 October 2014, the compliance date for the ICD-10-CM and PCS. Once again, Congress delayed implementation date to 1 October 2015, after it was inserted into "Doc Fix" Bill without debate over objections of many. Revisions to ICD-10-CM Include: - Relevant information for ambulatory and managed care encounter. - Expanded injury codes. - New combination codes for diagnosis/symptoms to reduce the number of codes needed to describe a problem fully. - Addition of sixth and seventh digit classification. - Classification specific to laterality. - Classification refinement for increased data granularity. ICD-10-CA is a clinical modification of ICD-10 developed by the Canadian Institute for Health Information for morbidity classification in Canada. ICD-10-CA applies beyond acute hospital care, and includes conditions and situations that are not diseases but represent risk factors to health, such as occupational and environmental factors, lifestyle and psycho-social circumstances. The eleventh revision of the International Classification of Diseases, or the ICD-11, is almost five times as big as the ICD-10. It was created following a decade of development involving over 300 specialists from 55 countries. Following an alpha version in May 2011 and a beta draft in May 2012, a stable version of the ICD-11 was released on 18 June 2018, and officially endorsed by all WHO members during the 72nd World Health Assembly on 25 May 2019. For the ICD-11, the WHO decided to differentiate between the core of the system and its derived specialty versions, such as the ICD-O for oncology. As such, the collection of all ICD entities is called the Foundation Component. From this common core, subsets can be derived. The primary derivative of the Foundation is called the ICD-11 MMS, and it is this system that is commonly referred to and recognized as "the ICD-11". MMS stands for Mortality and Morbidity Statistics. ICD-11 comes with an implementation package that includes transition tables from and to ICD-10, a translation tool, a coding tool, web-services, a manual, training material, and more. All tools are accessible after self-registration from the Maintenance Platform. The ICD-11 officially came into effect on 1 January 2022, although the WHO admitted that "not many countries are likely to adapt that quickly". In the United States, the advisory body of the Secretary of Health and Human Services has given an expected release year of 2025, but if a clinical modification is determined to be needed (similar to the ICD-10-CM), this could become 2027. Usage in the United StatesEdit In the United States, the US Public Health Service published The International Classification of Diseases, Adapted for Indexing of Hospital Records and Operation Classification (ICDA), completed in 1962 and expanding the ICD-7 in a number of areas to more completely meet the indexing needs of hospitals. The US Public Health Service later published the Eighth Revision, International Classification of Diseases, Adapted for Use in the United States, commonly referred to as ICDA-8, for official national morbidity and mortality statistics. This was followed by the ICD, 9th Revision, Clinical Modification, known as ICD-9-CM, published by the US Department of Health and Human Services and used by hospitals and other healthcare facilities to better describe the clinical picture of the patient. The diagnosis component of ICD-9-CM is completely consistent with ICD-9 codes, and remains the data standard for reporting morbidity. National adaptations of the ICD-10 progressed to incorporate both clinical code (ICD-10-CM) and procedure code (ICD-10-PCS) with the revisions completed in 2003. In 2009, the US Centers for Medicare and Medicaid Services announced that it would begin using ICD-10 on April 1, 2010, with full compliance by all involved parties by 2013. However, the US extended the deadline twice and did not formally require transitioning to ICD-10-CM (for most clinical encounters) until October 1, 2015. The years for which causes of death in the United States have been classified by each revision as follows: - ICD-1: 1900 - ICD-2: 1910 - ICD-3: 1921 - ICD-4: 1930 - ICD-5: 1939 - ICD-6: 1949 - ICD-7: 1958 - ICD-8A: 1968 - ICD-9: 1979 - ICD-10: 1999 Cause of death on United States death certificates, statistically compiled by the Centers for Disease Control and Prevention (CDC), are coded in the ICD, which does not include codes for human and system factors commonly called medical errors. Mental health issuesEdit The ICD includes a section classifying mental and behavioral disorders (Chapter V). This has developed alongside the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association and the two manuals seek to use the same codes. The WHO is revising their classifications in these sections as part the development of the ICD-11, and an "International Advisory Group" has been established to guide this. Section F66 of the ICD-10 deals with classifications of psychological and behavioural disorders that are associated with sexual development and orientation. It explicitly states that "sexual orientation by itself is not to be considered a disorder," in line with the DSM and other classifications that recognise homosexuality as a normal variation in human sexuality. The Working Group has reported that there is "no evidence that [these classifications] are clinically useful" and recommended that section F66 be deleted for the ICD-11. An international survey of psychiatrists in 66 countries comparing use of the ICD-10 and DSM-IV found that the former was more often used for clinical diagnosis while the latter was more valued for research. The ICD is actually the official system for the US, although many mental health professionals do not realize this due to the dominance of the DSM. A psychologist has stated: "Serious problems with the clinical utility of both the ICD and the DSM are widely acknowledged." - Clinical coder - Medical classifications - Medical diagnosis - Medical terminology - Current Procedural Terminology - MedDRA (Medical Dictionary for Regulatory Activities) - Systematized Nomenclature of Medicine Clinical Terms (SNOMED CT) - WHO Family of International Classifications - "About WHO". World Health Organization. Archived from the original on 9 February 2014. Retrieved 14 March 2014. - "The WHO Family of International Classifications". World Health Organization. Archived from the original on 22 December 2013. Retrieved 14 March 2014. - "World Health Assembly Update, 25 May 2019". 25 May 2019. - "International Classification of Diseases". 2018-06-20. Archived from the original on 20 June 2018. Retrieved 2022-03-06. - ICD-11 project plan WHO team for classifications, terminologies and standards/IER (12 May 2015) Retrieved on 2018-06-01. - Works of Jacques Bertillon, Internet Archive. - "History of the development of the ICD" (PDF). Who.int. Retrieved 11 December 2017. - Zhavoronkov, Alex; Bhullar, Bhupinder (2015-11-04). "Classifying aging as a disease in the context of ICD-11". Frontiers in Genetics. 6: 326. doi:10.3389/fgene.2015.00326. ISSN 1664-8021. PMC 4631811. PMID 26583032. - International health statistics using this system are available at the Global Health Observatory (GHO) and the WHO Statistical Information System (WHOSIS). - Katsching, Heinz (February 2010). "Are psychiatrists an endangered species? Observations on internal and external challenges to the profession". World Psychiatry. World Psychiatric Association. 9 (1): 21–28. doi:10.1002/j.2051-5545.2010.tb00257.x. PMC 2816922. PMID 20148149. - ICD-10 Volume 2, online at Classifications WHO.int - "International Classification Of Diseases - 9 - CM, (1979)". Wonder.cdc.gov. Retrieved 11 December 2017. - O'Malley KJ, Cook KF, Price MD, Wildes KR, Hurdle JF, Ashton CM (2005). "Measuring diagnoses: ICD code accuracy". Health Serv Res. 40 (5p2): 1620–39. doi:10.1111/j.1475-6773.2005.00444.x. PMC 1361216. PMID 16178999. - World Health Organization. FAQ on ICD. Accessed 12 July 2011. - National Center for Health Statistics, CDC. ICD-9-CM Guidelines, Conversion Table, and Addenda. Classification of Diseases, Functioning, and Disability. Retrieved 2010-01-24. - InstaCode Institute. ICD-10 Demystified. Archived 2005-10-16 at the Wayback Machine - "ICD-9-CM Diagnosis Codes - International Classisfication of Diseases - Medical Diagnosis Codes". www.findacode.com. Retrieved 2015-12-30. - WHO. International Classification of Diseases (ICD). - CMS Office of Public Affairs (February 11, 2008). "HHS Proposes Adoption of ICD-10 Code Sets and Updated Electronic Transaction Standards" (Press release). United States Department of Health and Human Services. Retrieved 2009-02-11. - New Zealand Health Information Service. ICD-10-AM. Accessed 12 July 2011. - Canadian Institute for Health Information. ICD-10-CA. Archived 2015-05-01 at the Wayback Machine Accessed 12 July 2011. - International Classification Of Diseases - 9 - CM, (1979). Wonder.cdc.gov. Retrieved on 2014-06-20. - "Classification of Diseases, Functioning, and Disability". Centers for Disease Control and Prevention. Retrieved 29 October 2010. - Editorial (2019). "ICD-11". The Lancet. 393 (10188): 2275. doi:10.1016/S0140-6736(19)31205-X. PMID 31180012. - Badr, Azza (17–19 September 2019). Fifth regional steering group meeting Bangkok (PDF) (Report). WHO/EMRO. - Pickett, Donna; Anderson, Robert N. (18 July 2018). Status on ICD-11: The WHO Launch (PDF) (Report). CDC/NCHS. - Cuncic, Arlin (23 March 2020). "Overview of the ICD-11 for Mental Health". Verywell Mind. Archived from the original on 5 April 2020. - "ICD-11 Timeline". who.int. Archived from the original on 5 May 2019. - "World Health Assembly Update, 25 May 2019" (Press release). Geneva, Switzerland: WHO. 25 May 2019. Archived from the original on 30 July 2019. - Chute, Christopher G. (2018). "The rendering of human phenotype and rare diseases in ICD-11". Journal of Inherited Metabolic Disease. 41 (3): 563–569. doi:10.1007/s10545-018-0172-5. PMC 5959961. PMID 29600497. The primary linearization, and the one most users will recognize and likely believe is "the ICD-11", is the Mortality and Morbidity Statistics (MMS) linearization. - Rodrigues Jean-Marie; Robinson David; Della Mea Vincenzo; Campbell James; Rector Alan; Schulz Stefan; Brear Hazel; Üstün Bedirhan; Spackman Kent; Chute Christopher G; Millar Jane; Solbrig Harold; Brand Persson Kristina (2015). "Semantic Alignment between ICD-11 and SNOMED CT". Studies in Health Technology and Informatics. 216 (MEDINFO 2015: eHealth–enabled Health). doi:10.3233/978-1-61499-564-7-790. - WHO (2018). "ICD-11: Classifying disease to map the way we live and die". www.who.int. Archived from the original on 20 June 2018. - admin aapc (16 August 2019). "US gets the ball rolling on ICD-11". AAPC. - Makary, MA; Daniel, M (3 May 2016). "Medical error—the third leading cause of death in the US". BMJ. 353: i2139. doi:10.1136/bmj.i2139. PMID 27143499. S2CID 206910205. - Moriyama, IM; Loy, RM; Robb-Smith, AHT (2011). Rosenberg, HM; Hoyert, DL (eds.). History of the Statistical Classification of Diseases and Causes of Death (PDF). Hyattsville, MD: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics. ISBN 978-0-8406-0644-0. - Who \| Mental Health Evidence And Research (Mer). Who.int. Retrieved on 2014-06-20. - Cochran, Susan D.; Drescher, Jack; Kismödi, Eszter; Giami, Alain; García-Moreno, Claudia; Atalla, Elham; Marais, Adele; Meloni Vieira, Elisabeth; Reed, Geoffrey M. (2014). "Proposed declassification of disease categories related to sexual orientation in the International Statistical Classification of Diseases and Related Health Problems (ICD-11)". Bulletin of the World Health Organization. 92 (9): 672–679. doi:10.2471/BLT.14.135541. PMC 4208576. PMID 25378758. - Juan E. Mezzich (2002). "International Surveys on the Use of ICD-10 and Related Diagnostic Systems" (guest editorial, abstract). Psychopathology. 35 (2–3): 72–75. doi:10.1159/000065122. ISBN 9783805574617. PMID 12145487. S2CID 35857872. - Geoffrey M. Reed (2010). "Toward ICD-11: Improving the clinical utility of WHO's International Classification of mental disorders" (PDF). Professional Psychology: Research and Practice. 41 (6): 457–464. doi:10.1037/a0021701. Note: Since adoption of ICD-10 CM in the US, several online tools have been mushrooming. They all refer to that particular modification and thus are not linked here.	3	36	5	0	1	4	0.801014	10	5,960
First Time User? Sign Up Now First Time User? Enroll now. Home > Health Library > Turning Off Your ICD Your ICD can save your life. Your ICD (implantable cardioverter-defibrillator) is always checking your heart rate and rhythm. If the ICD detects a life-threatening rapid heart rhythm, it tries to slow the rhythm back to normal using electrical pulses. If the dangerous rhythm doesn't stop, the ICD sends an electrical shock to the heart to restore a normal rhythm. Some ICDs also can fix a heart rate that is too slow. The ICD does so without using a shock. It can send out electrical pulses to speed up a heart rate that is too slow. Even though an ICD can help fix heart rate or rhythm problems, you may not want this at the end of life. Many people consider turning off their ICD when their health goal changes from living longer to getting the most comfort possible at the end of life. The shocks the ICD delivers are painful. Not being shocked will make you more comfortable at the end of life. As you plan for your future and your end of life, include plans for your ICD. The decision to turn off your ICD is part of the medical treatment you want at the end of life. You can put this information in your advance directive. Turning off your ICD is legal. It isn't considered suicide. The decision to leave on or turn off your ICD is a medical decision you make based on your values. Turning off an ICD isn't hard. The ICD isn't taken out of your chest, and you don't need surgery. Your doctor will use a computer to reprogram the ICD so that it doesn't give you shocks. This isn't painful. Turning off the ICD won't cause death, and it won't make you feel worse. But because the ICD won't give you a shock if you have a life-threatening heart rhythm, this type of heart rhythm could lead to death. Some ICDs are combined with a pacemaker. You can turn off the ICD without turning off the pacemaker. Your doctor can explain how your pacemaker might affect you at the end of your life. You make the decision about whether or not you want to turn off your ICD. It can be a tough decision to make, but you don't have to make it alone. Look to your family, your doctor, your spiritual adviser, and your friends for help and support. Things to think about Health Tools help you make wise health decisions or take action to improve your health. Other Works Consulted Al-Khatib SM, et al. (2017). 2017 AHA/ACC/HRS guideline for management of patients with ventricular tachycardias and the prevention of sudden cardiac death. Circulation, published online October 30, 2017. DOI: 10.1161/CIR.0000000000000549. Accessed November 6, 2017. Lampert R, et al. (2010). HRS Expert Consensus Statement on the Management of Cardiovascular Implantable Electronic Devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy. Heart Rhythm, 7(7): 1008–1026. Available online: http://www.hrsonline.org/Policy/ClinicalGuidelines/upload/ceids_mgmt_eol.pdf. Russo JE (2011). Deactivation of ICDs at the end of life: A systematic review of clinical practices and provider and patient attitudes. American Journal of Nursing, 111(10): 26–35. Also available online: http://journals.lww.com/ajnonline/Fulltext/2011/10000/Original_Research__Deactivation_of_ICDs_at_the_End.18.aspx. Current as of: April 9, 2019 Author: Healthwise StaffMedical Review: Kathleen Romito MD - Family MedicineMartin J. Gabica MD - Family MedicineAdam Husney MD - Family MedicineJohn M. Miller MD, FACC - Cardiology, Electrophysiology Current as of: April 9, 2019 Medical Review:Kathleen Romito MD - Family Medicine & Martin J. Gabica MD - Family Medicine & Adam Husney MD - Family Medicine & John M. Miller MD, FACC - Cardiology, Electrophysiology To learn more about Healthwise, visit Healthwise.org. © 1995-2019 Healthwise, Incorporated. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated. 1505 SW Cary Parkway REX Healthcare of Cary, Suite 210 Cary, NC 27511 2076 NC Highway 42 W. Johnston Professional Plaza, Suite 100 Clayton, NC 27520 781 Avent Ferry Road REX Healthcare of Holly Springs, Suite 212 Holly Springs, NC 27540 4414 Lake Boone Trail REX Medical Plaza, Suite 108 Raleigh, NC 27607 910 Berkshire Road Smithfield, NC 27577 UNC REX Healthcare4420 Lake Boone TrailRaleigh, NC 27607, USA919-784-3100 Chosen for Excellence Co-Worker & Physician Login UNC Health Talk Copyright 2019 UNC Health Care. All rights reserved.	3	13	3	0	0	0	0.922198	3	1,135
Development of ICD-10-CM and ICD-10-PCS Overview of ICD-9-CM The clinical modification of ICD-9 (ICD-9-CM, Volumes 1 and 2) was adopted in the United States in 1979 for morbidity applications, at the same time that ICD-9 (published by WHO) was adopted for mortality data. In addition to its use in records and surveys, ICD-9-CM is used to classify diseases and health conditions on health care claims and is the basis for prospective payment to hospitals, other health care facilities and health care providers. The U.S. also developed its own procedure coding system (ICD-9-CM, Volume 3) for inpatient hospital services in the late 1970’s to use with ICD-9-CM, Volumes 1 and 2 for diagnoses; this was necessary because the WHO had not produced a procedure coding system. Since 1979, procedures performed in hospitals have been coded for hospital statistics and on hospital claims, using ICD-9-CM, Vol. 3. The Current Procedural Terminology (CPT-4), developed and maintained by the American Medical Association, is used in the United States to code professional services on claims of physicians and other non-inpatient providers. All users code diagnoses with ICD-9-CM, Volumes 1 and 2. When the inpatient prospective payment system was implemented in 1983, ICD-9-CM, Volumes 1, 2 and 3 was used as the basis for assigning cases to the DRGs. All diagnostic and procedural information was captured using ICD-9-CM. Because there had been radical changes and advances in health care since the implementation of ICD-9-CM, there quickly arose a need to update and revise the system. This was particularly true for the procedure codes of the system, but users also wanted to update the diagnosis portion to obtain greater clinical detail. Thus, an annual updating process was established through the ICD-9-CM Coordination and Maintenance Committee. Although this process continues to allow some addition of new conditions and procedures, and expansion for greater detail, it uses as its base a classification system that was developed nearly 30 years ago. The two separate timelines, which follow, detail the development of the clinical modification of ICD-10 (ICD-10-CM) by the National Center for Health Statistics, CDC, which is responsible for diagnosis classification in the United States and the development of ICD-10 Procedure Coding System (ICD-10-PCS) by the Centers for Medicare and Medicaid Services. ICD-10-CM Development Timeline The International Statistical Classification of Diseases and Health Related Problems (ICD), now in its tenth revision, has become the international standard diagnostic classification for all general epidemiological and many health management purposes. The ICD is the standard used throughout the world for classifying causes of mortality as recorded at the registration of death, and for reporting these data nationally and to the World Health Organization. Originally designed to classify causes of death, the scope of the ICD was extended at the Sixth Revision in 1948 to include non-fatal diseases. The application of the classification to morbidity statistics has expanded with each subsequent revision. Nonetheless, the United States and a number of other countries continue to find it necessary to develop clinical modifications of the ICD to meet the needs of their respective healthcare systems that require more detailed clinical information from hospital, clinic and physician records. The Tenth Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) was first released, by the World Health Organization (WHO) in 1993. As a first step in implementing ICD-10, NCHS awarded a contract to the Center for Health Policy Studies (CHPS) to evaluate ICD-10 for morbidity purposes within the United States. A prototype of ICD-10-CM was developed following a thorough evaluation of ICD-10 by a Technical Advisory Panel (TAP) consisting of private and public sector stakeholders. TAP membership included: AHIMA (Rita Finnegan), Beth Israel Hospital (Dr. Lisa Iezzoni), Mayo Clinic (Karel Weigel), HCFA (Patricia Brooks), AHCPR (Kathleen McCormick), physician perspective (Dr. William Felts). The TAP concluded that there were compelling reasons for recommending an improved clinical modification of ICD-10 that would overcome most limitations of ICD-10 for morbidity applications. The TAP strongly recommended that NCHS proceed with implementation of a revised version of ICD-10-CM. Further work on enhancements to ICD-10-CM were undertaken by NCHS, including a thorough review of ICD-9-CM Coordination and Maintenance Committee proposals for modifications that could not be incorporated into ICD-9-CM and through collaboration with many medical/surgical specialty groups. The specialty groups included: American Association of Dermatology, American Academy of Neurology, American Association of Oral and Maxillofacial Surgeons, American Academy of Orthopedic Surgeons, American Academy of Pediatrics, American College of Obstetricians and Gynecologists, American Burn Association, American Diabetes Association, American Nurses Association, American Psychiatric Association, American Urology Association, ANSI Z16.2 Workgroup (Workers Comp), National Association of Childrens Hospitals and Related Institutions. The draft of the Tabular List of ICD-10-CM, and the preliminary crosswalk between ICD-9-CM and ICD-10-CM were made available on the NCHS website for public comment. Comments received during the three-month open comment period, which began December 1997 and ended February 1998, were requested to be in writing. At the conclusion of the open comment period the draft version of the ICD-10-CM (and the draft crosswalk) were removed from the NCHS homepage. More than 1,200 comments were received from 22 individuals and organizations representing a variety of groups, including one governmental agency, two research institutions, three information system developers, four professional organizations, and several health care providers. Comments ranged from general observations to very specific and detailed analyses. The comments received were analyzed and categorized by a contractor into the following draft categories: 480 should be rejected; 238 required no response or necessitated no further action; 180 merited direct incorporation into ICD-10-CM; 268 were recommended as stated; and 77 had merit but required further review to determine possibility of inclusion into ICD-10-CM. ICD-10 is implemented in the United States for mortality reporting. Final death statistics and leading causes of death for data years 1999 and 2000, using ICD-10, have been published and are available on the NCHS website. Preliminary data for year 2001 was published March 2003. An overview of the comments received during the ICD-10-CM comment period were posted on the NCHS website in 1999. A summary of the comments was also presented at the November 1999 ICD-9-CM Coordination and Maintenance Committee meeting and posted on NCHS website. Development of ICD-10-CM continued with changes being made in response to the open comment period, as well as, input from physician specialty groups. May 29, 2002 NCHS posted, on its website, a pre-release version of ICD-10-CM. Consistent with ICD-10, the classification is alphanumeric. Codes are either six or seven digits. (ICD-9-CM, Volume 1 is five digits numeric.) The descriptions are consistent with current medical terminology and findings. Some of the modifications featured in ICD-10-CM have already been incorporated into clinical modifications of ICD-10 implemented in Australia (ICD-10-AM) and Canada (ICD-10-CA). NCHS will make available the following tools that are essential to a transition to ICD-10-CM: database version, crosswalk, educational materials, official coding guidelines, and comparability study/ratios for trend analyses. NCHS has already conducted the comparability study for mortality and will also conduct similar study for morbidity. The ratios assist users of coded data to discriminate between real changes in utilization by diagnosis and those resulting from artifacts of the coding system An updated pre-release draft of ICD-10-CM is posted on the NCHS web site at: http://cdc.gov/nchs/icd9.htm. The files, in PDF (Adobe) format include the tabular list, alphabetic index, the external cause of injury index and the Table of Neoplasms, as well as draft coding guidelines. The American Health Information Management Association (AHIMA) and the American Hospital Association (AHA) jointly conduct a pilot test of ICD-10-CM during June/July 2003. The study involved dual coding records in ICD-9-CM and ICD-10-CM. More than 6100 records from a broad cross section of health care community were dual coded by 180+ participants. The initial results indicate that: there is general support for adoption of ICD-10-CM; ICD-10-CM is seen as an improvement over ICD-9-CM; and ICD-10-CM is more applicable to non-hospital settings than ICD-9-CM. ICD-10-PCS Development Timeline The Centers for Medicare and Medicaid Services (CMS), formerly the Health Care Financing Administration (HCFA), began developing a replacement to ICD-9-CM, Volume 3 in 1990 in order to address a number of limitations with the current procedure classification. ICD-9-CM procedure codes are made up of four digits. There are only 10 codes available within each category (fourth digits 0-9). Once a category is full, one must either combine types of procedures under one code, or find room in another section of the code book to place a new code. The benefit of such a system is that one can easily collapse the codes into categories when doing research to capture a wide range of similar procedures. When one puts a similar code in a separate part of the book, coders and researchers may not easily find it. There can be gross errors when trying to identify particular types of cases or make projections of numbers of procedures performed when codes are not carefully placed within a system such as the current ICD-9-CM. A specific example of a generic problem with ICD-9-CM is that there is not a consistent identification of the procedure approach. While the approach may not have been an important issue during the 1970s, there have been considerable advances in surgery since that time. With a coding system that is 23 years old, not only is the technology bound to be outdated, the premises on which the coding system was established are outdated. There are a number of approaches and techniques used for procedures such as lasers and the use of scopes that were not anticipated when the structure of ICD-9-CM was developed. Therefore the basic categories were established on technology that is currently outdated. Updating this system has been quite difficult and involves making compromises. The development of ICD-10-PCS adhered to the criteria established by NCVHS for a procedure classification system (Appendix I). ICD-10-PCS is made up of seven alphanumeric characters. It should be noted that ICD-10-PCS is not based on an international classification because currently none exists. The system provides exponentially greater code capacity, where all substantially different procedures can have a unique code. Whereas ICD-9-CM procedure classification contains fewer than 4,000 codes, the current draft of ICD-10-PCS contains 197,769 codes (1). There is also significant room for easy expansion as new technologies are developed. The substantial increase in codes means that a coder can quite readily find the appropriate code that describes a particular procedure, rather than having to use a less specific or clinically detailed ICD-9-CM, Volume 3 code. ICD-10-PCS was developed using an open process. A Technical Advisory Panel (TAP) provided review and comments throughout development. The TAP included representatives of AHA, CPRI/ANSI-HISB, AHIMA, AMA, American College of Surgeons, managed care industry, medical informatics, American Association of Medical Transcriptionists, NIH/NLM, AHCPR, state health system, hospital information, NCHS, ProPAC, and the National Association of Childrens Hospitals and Related Institutions. May 1986, a meeting was convened by HCFA to open discussion among people interested in procedure coding. As a result of that meeting, AHA and AMA agreed to co-chair a task force that would outline and set priorities for the objectives of a common procedure coding system. This task force was charged to undertake a thorough evaluation of the purpose and scope of Volume 3 of ICD-9-CM and CPT to evaluate the feasibility of developing a new procedure coding system to achieve the objectives of a common system. Earlier review efforts uncovered structural problems in both Volume 3 of ICD-9-CM and CPT. Concern for data quality issues and the cost of submitting data in more than one classification is significant. The feasibility of creating a single procedure coding system that will satisfy all users is as yet unknown. The AMA sponsored a study to investigate the costs and benefit of a single system for physician payment. The study conducted by Coopers and Lybrand, compared two alternatives: 1) a major restructuring of CPT to serve uses beyond physician offices; and 2) a replacement of both Volume 3 of ICD-9-CM and CPT. The results of the AMA study showed that the costs of a replacement system were significant and that the identification of benefits was difficult, thus the consultants concluded that a replacement system, for measuring physician services, was not justified. HCFA awarded a contract for a pilot project that would review the cardiovascular procedures in all of the procedure coding systems (CPT, HCPCS, local HCPCS and Volume 3 of ICD-9-CM), standardize the nomenclature with definitions, recommend a standard format amenable to updating and expansion, and develop a cardiovascular chapter for ICD-9-CM, Volume 3. HCFA funded a continuation of the pilot project for the development of a revision of the respiratory system chapter consistent with the approach, design and format of the cardiovascular chapter. The project focuses on the respiratory chapter. HCFA announced plans to initiate a solicitation for a contract to develop a new procedure coding system for use with hospital inpatients to replace Volume 3 of ICD-9-CM. The new system is referred to as ICD-10-PCS. HCFA awarded a contract to 3M HIS to develop the procedure classification to replace Volume 3 of ICD-9-CM (hospital inpatient procedures). The contract is based on the prototype 7-digit alphanumeric procedure classification system developed by 3M HIS in previous contracts. Primary objective is developing a new procedure coding system to replace the current Volume 3 of ICD-9-CM; the project’s additional objectives are to improve the accuracy and efficiency of coding, to reduce training efforts, to improve communications with physicians, and to be compatible with the current billing infrastructure. ICD-10-PCS was developed using an open process. A Technical Advisory Panel provided review and comments throughout development. The TAP included American Health Information Management Association (Sue Prophet), American Hospital Association (Nelly Leon-Chisen), American Medical Association (Barry Eisenberg), CPRI/ANSI-HISSP (Dr. Simon Cohn), American Association of Medical Transcription (Claudia Tessier), NIH/NLM (Betsy Humphreys), AHCPR (Michael Fitzmaurice), state health system representative (Kevin Ray), hospital information (Laura Green), NCHS (Donna Pickett), ProPAC (Julian Pettingil), Dr. Clement McDonald, American College of Surgeons (Dr. George Spaulding), United HealthCare (James Cross and Philip Bryson), and the National Association of Children’s Hospitals and Related Institutions (John Muldoon). ICD-10-PCS was sent to approximately 30 specialty groups for their review and comments. Additionally, HCFA also provided an onsite presentation at the AMA to more than 20 specialty groups. A training program was developed, and informal testing and training were conducted. AHIMA national conventions trained 65 coders in two half-day sessions. Another 70 volunteered to test the system, but weren’t at the training. The coders received 400 records that were coded with ICD-10-PCS during next 3 months (received by January 1997). Clinical Data Abstraction Centers (CDACs) conducted formal testing of ICD-10-PCS. HCFA trained CDACs (5/14-15/97) with follow-up training after the CDACs informally coded 30 records (6/3/97). Final training session 6/18/97 where CDACs tested system on 5,000 medical records (2500 per CDAC) identifying cases with a wide distribution of ICD-9-CM procedure codes. Additional formal testing of ICD-10-PCS using ambulatory records conducted 10/98 – 2/99. 582 ambulatory records obtained by CDACs. 369 records of the 582 had procedures that were tested using ICD-10-CM and reported as part of the 3/99 on findings. CMS was not able to obtain obstetrics records. CMS also tested ICD-10-PCS on list of problem cases from Editorial Advisory Board for Coding Clinic for ICD-9-CM submitted by AHA. Final version of ICD-10-PCS, training material and crosswalk to ICD-9-CM procedure codes posted on CMS website released spring 1998. The CMS written testimony on April 9, 2002 states that CMS has already awarded a contract to 3M to undertake any DRG conversion activities that would be required should ICD-10-PCS be named as a national standard. Information on a conversion and ICD-10-PCS’s incorporation into the DRG system would be made available as part of the annual inpatient prospective payment system proposed and final rule process. ICD-10-PCS is updated every October 1 to accommodate changes made to ICD-9-CM, Volume 3. NCVHS Recommendations for a Single Procedure Classification System, November 1993 An Outline of the Characteristics of a Procedure Classification System Ability to aggregate data from individual codes into larger categories Each code has a unique definition forever – not reused Flexibility to new procedures and technologies (Aempty@ code numbers) Mechanism for periodic updating Code expansion must not disrupt systematic code structure Provides NOS and NEC categories so that all possible procedures can be classified somewhere Each procedure (or component of a procedure) is assigned to only one code Ease of Use Standardization of definitions and terminology Adequate indexing and annotation for all users Setting and Provider Neutrality Same code regardless of who or where procedure is performed Body system(s) affected Limited to classification of procedures Should not include diagnostic information Other data elements (such as age) should be elsewhere in the record	4	22	0	0	0	2	0.369557	2	4,054
If you’re pregnant and experiencing vaginal bleeding, it’s important to know about the Icd 10 code for vaginal bleeding in pregnancy. This code can help determine the severity of the condition and guide treatment. In addition to helping you identify the cause of your bleeding, this code can also provide you with information about potential complications, such as premature labour or stillbirth. What is the ICD 10 Code For Vaginal Bleeding In Pregnancy? The ICD 10 Code For Vaginal Bleeding In Pregnancy is O26.859. Definition of Icd 10 Code for Vaginal Bleeding in Pregnancy There is specific code used to classify vaginal bleeding in pregnancy. The International Classification of Disease, 10th Revision (ICD-10) defines a vaginal bleed as “a watery discharge from the vagina, not necessarily period-related.” Vaginal bleeding that occurs during the first trimester is classified under the ICD-10 code W95.1. Bleeding that occurs during any other trimester is classified under the ICD-10 code W97.9. Symptoms of Vaginal Bleeding in Pregnancy Vaginal bleeding in pregnancy is a common problem. There are many possible causes, but the most common ones are hormonal fluctuations, changes in the menstrual cycle, and birth control methods. You may not be able to tell if you’re having a miscarriage or vaginal bleeding until it’s too late. You should see your doctor as soon as possible if you have any vaginal bleeding that isn’t normal for your stage of pregnancy or if it lasts more than a week. Your doctor will likely do a pelvic exam and take a cervical sample to check for infection. He or she may also do an ultrasound to see if there’s anything wrong with the baby. Sometimes, the bleeding can be caused by something else, like anemia or a uterine defect, and treatment will depend on the cause. Diagnosis of Vaginal Bleeding in Pregnancy There are a few different ways to diagnose vaginal bleeding during pregnancy. One way is to use a cervical smear to see if there are any changes in the woman’s cervix. If the woman has had a previous baby, her doctor may also check her hormone levels or do a pelvic exam to see if there is something wrong with the uterus. If the woman doesn’t have any of these symptoms, her doctor may order an ultrasound or an MRI scan to see if there is anything physically wrong with her uterus. Treatment of Vaginal Bleeding in Pregnancy Bleeding during pregnancy is normal and may vary from slight to heavy. It may also occur at other times during the menstrual cycle. Bleeding that occurs during or after sexual activity should be evaluated because there may be a problem. The most common cause of vaginal bleeding in early pregnancy is spotting or light bleeding between menstrual periods. This type of bleeding usually disappears by around week 8 of pregnancy, but can sometimes continue for up to 2 months afterwards. If the bleeding is heavy or persists for more than two weeks, it may be a sign of a serious underlying condition such as placenta previa (an abnormal growth of the placenta near the opening of the womb) or an ectopic pregnancy (a fertilized egg that grows outside the uterus). If you are concerned about your vaginal bleeding, contact your healthcare provider. He or she can perform a pelvic examination to determine if there is a problem and recommend appropriate treatment. Treatment for vaginal bleeding in early pregnancy typically includes antibiotics if there is an infection, pain relief with over-the-counter medication, and bed rest if needed to allow the body to heal. Prevention of Vaginal Bleeding in Pregnancy Vaginal bleeding during pregnancy is a common occurrence and can be caused by many different things. The most common cause of vaginal bleeding in early pregnancy is ovulation, which causes the uterine lining to shed. Other causes of vaginal bleeding in early pregnancy include: -A delivery that is difficult or involves surgery -Preeclampsia (high blood pressure, protein in the urine, and water retention) -Abnormalities of the placenta (placental abruption, placental insufficiency) -Endometriosis (a type of disorder that occurs when tissue from the uterus grows outside the uterus) If you are experiencing vaginal bleeding during your pregnancy, there is a good chance that you have Icd 10 code for it. In this article, we will discuss the different symptoms that may indicate you have Icd 10 code and provide tips on how to treat them. Hopefully, by learning more about what Icd 10 code means and how to treat it, you can get relief from your symptoms and return to a healthy pregnancy.	4	3	0	0	0	6	0.856645	6	987
- Open Access Harmonizing WHO’s International Classification of Diseases (ICD) and International Classification of Functioning, Disability and Health (ICF): importance and methods to link disease and functioning BMC Public Health volume 13, Article number: 742 (2013) To understand the full burden of a health condition, we need the information on the disease and the information on how that disease impacts the functioning of an individual. The ongoing revision of the International Classification of Diseases (ICD) provides an opportunity to integrate functioning information through the International Classification of Functioning, Disability and Health (ICF). Part of the ICD revision process includes adding information from the ICF by way of “functioning properties” to capture the impact of the disease on functioning. The ICD content model was developed to provide the structure of information required for each ICD-11 disease entity and one component of this content model is functioning properties. The activities and participation domains from ICF are to be included as the value set for functioning properties in the ICD revision process. The joint use of ICD and ICF could create an integrated health information system that would benefit the implementation of a standard language-based electronic health record to better capture and understand disease and functioning in healthcare. Describing and understanding the relationship between disease and functioning requires the use of two of the World Health Organization’s classifications systems: the International Classification of Diseases (ICD) and the International Classification of Functioning, Disability and Health (ICF) . The ICD classifies disease entities and other health conditions to gather diagnostic information, while the ICF classifies domains of functioning and disability in terms of body functions and structures or activities and participation at the body, person and societal levels. The ICD and the ICF classification systems are intended by WHO to complement each other so as to capture and provide the full picture of health or health-related state of an individual. Currently, however, there is no standard platform in which the disease and its impact on functioning are concurrently used within an integrated health information system. Efforts to capture the impact of a disease in a structured and systematic way have so far been hampered by the failure to link the ICD and the ICF at a conceptual and operational level. The ICD is undergoing its 11th revision (ICD-11) wherein part of the process is to add information from the ICF to the classification of diseases by adding “functioning properties” (i.e. ICF domains or codes) to capture the impact of the disease on functioning. In this integrated system, we want to be able to use universal domains (functioning properties) that depict the functioning of an individual by way of the ICF and also use information related to disease entities (ICD codes). The process of revising the ICD is coordinated through Topic Advisory Groups (TAGs), each of which is responsible for different content areas. Responsible for the appropriate integration of the functioning properties is the Functioning Topic Advisory Group (fTAG), which consults with each of the TAGs regarding how to deal with functioning properties for their assigned ICD entities. Functioning properties of the ICD-11 content model The ICD-11 Content Model (Table 1) provides the structure of information detail required for each ICD-11 code included through the revision process [3, 4]. In the ICF, “functioning” is an encompassing term for body functions, body structures, and activities and participation. In the ICD Content Model at this time, functioning properties only include the activities and participation component of the ICF. Activity is defined in the ICF as the “execution of a task or action by an individual”, while participation is defined as “involvement in a life situation” . Activities and participation are important in describing the impact of a disease because they capture the broad and relevant aspects of activity and involvement with society and life in general. Table 2 lists the ICF categories that are included in the value set for functioning properties. Hence, an ICD code would have a corresponding value set of functioning properties. The task of populating the functioning properties in iCAT Before ICD-11 is completed, functioning properties will need to be populated for each ICD code. This task of population is being done and coordinated using the web-based International Collaborative Authoring Tool (iCAT) by content experts worldwide in three steps: selection of functioning properties provided in iCAT (Table 2), if an additional ICF domain or category needs to be added based on a published disease-specific ICF Core Set, then it is entered manually into the iCAT, and use evidence from the literature (i.e. mini-review) by identifying the commonly used measures relevant to the disease of interest, and in those measures identify meaningful concepts of functioning with a focus on activities and participation in life situations, and then subsequently link the identified concepts to a specific domain in the ICF . Obtaining information about disease entities and their impact on functioning is not entirely new in the field of medicine and health. While the consideration of the disease and its impact on functioning has been in place, or at least acknowledged, for a long time, there remain prevailing issues, such as the lack of wide dissemination and implementation extending beyond simple awareness [7, 8]. The operationalization of integrated disease-and-functioning models currently varies, is fragmented across healthcare settings, and is perhaps more commonly observed in healthcare systems with medium to advanced infrastructures and access to resources. We can do a better job at facilitating an integrated disease-and-functioning model across systems from low to high resource countries. Moreover, the ongoing ICD revision would make the assessment and documentation of a comprehensive set of information about a disease entity as broad and as inclusive as possible; at the same time utilizing the standard and common language of the ICF on functioning. This information will consist of biomedical and biopsychosocial aspects of the disease that will provide clinicians and users alike an integrated and unified ICD-ICF platform and which will be helpful in interdisciplinary communication towards a concerted planning of care ultimately benefiting the patients. The ICD-11 is due to be launched in 2015, and steps toward that goal are being pursued. Certainly there are challenges on our way, but there are also opportunities that are presented for users in the clinical and research communities to actively contribute in this huge endeavor by WHO and its collaborators worldwide. The unified ICD-ICF in the ICD-11 will allow for consistent terminologies to be used and to be harmonized across ICD and ICF and will provide holistic information about a disease entity and its impact on the functioning of an individual. Efforts are also currently being taken to facilitate the identification of the overlaps for ICD-11 disease entities and their titles with their conceptual equivalent in the ICF towards harmonization of ICD and ICF. The joint use of the ICD and ICF towards an integrated health information model would, in our opinion, benefit medicine and health systems and would support the push for the implementation of a standard language-based electronic health record system towards better health services planning and reimbursement. RE is Assistant Professor, Department of Physical Therapy, School of Allied Health Professions Louisiana State University Health Sciences Center, New Orleans LA USA; adjunct research scientist at the ICF Research Branch in cooperation with the WHO Collaborating Centre for the Family of International Classifications in Germany (DIMDI), Nottwil, (Switzerland); and the Swiss Paraplegic Research (SPF), Nottwil, Switzerland. NK is technical officer at World Health Organization, Classifications, Terminologies and Standards (CTS), Department of Health Statistics and Informatics (HSI), Geneva, Switzerland. CK is with the US Department of Health and Human Services, Office of Health Policy Washington D.C., USA. MMRN is technical officer at World Health Organization, Classifications, Terminologies and Standards (CTS), Department of Health Statistics and Informatics (HSI), Geneva, Switzerland. GS is director of the ICF Research Branch in cooperation with the WHO Collaborating Centre for the Family of International Classifications in Germany (DIMDI), Nottwil, (Switzerland) and the Swiss Paraplegic Research (SPF), Nottwil, Switzerland; is Professor and Chair at the Department of Health Sciences and Health Policy, University of Lucerne, Lucerne, Switzerland. TBU is head of WHO’s Family of International Classifications, Geneva, Switzerland. R Escorpizo is an employee of the Louisiana State University Health Sciences Center (LSUHSC). This article was developed in his professional capacity and does not necessarily represent the views of LSUHSC. C Kennedy is an employee of the Office of the Assistant Secretary for Planning and Evaluation (ASPE), Department of Health and Human Services (HHS). This article was developed in her professional capacity and does not necessarily represent the views of ASPE or HHS. Functioning Topic Advisory Group International Collaborative Authoring Tool International Classification of Diseases International Classification of Functioning, Disability and Health Topic Advisory Group World Health Organization. World Health Organization: International Classification of Diseases (ICD-10). Available from: http://www.who.int/classifications/icd/en/ World Health Organization: International Classification of Functioning, Disability and Health. 2001, Geneva, Switzerland: World Health Organization World Health Organization: The International Classification of Diseases 11th Revision. 2012, Available from: http://www.who.int/classifications/icd/revision/en/index.html Tu S, Bodenreider O, Celik C, Chute C, Heard S, Jakob R, et al: A content model for the ICD-11 revision: a technical report. 2011, Stanford, CA: Stanford Center for Biomedical Informatics Research, http://bmir.stanford.edu/file_asset/index.php/1752/BMIR-2010-1405.pdf, Cieza A, Geyh S, Chatterji S, Kostanjsek N, Ustun B, Stucki G: ICF linking rules: an update based on lessons learned. J Rehabil Med. 2005, 37 (4): 212-218. 10.1080/16501970510040263. Engel GL: The need for a new medical model: a challenge for biomedicine. Science. 1977, 196 (4286): 129-136. 10.1126/science.847460. Alvarez AS, Pagani M, Meucci P: The clinical application of the biopsychosocial model in mental health: a research critique. Am J Phys Med Rehabil. 2012, 91 (13 Suppl 1): S173-S180. Alvarez AS: The application of the International Classification of Functioning, Disability, and Health in psychiatry: possible reasons for the lack of implementation. Am J Phys Med Rehabil. 2012, 91 (13 Suppl 1): S69-S73. The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2458/13/742/prepub Special thanks to Melissa Selb, ICF Research Branch coordinator in Nottwil, Switzerland and members of the functioning Topic Advisory Group. The authors declare that they have no competing interests. All authors provided concept/idea, consultation, and writing, and reviewed the manuscript before submission. All authors read and approved the final manuscript. Authors’ original submitted files for images Below are the links to the authors’ original submitted files for images. About this article Cite this article Escorpizo, R., Kostanjsek, N., Kennedy, C. et al. Harmonizing WHO’s International Classification of Diseases (ICD) and International Classification of Functioning, Disability and Health (ICF): importance and methods to link disease and functioning. BMC Public Health 13, 742 (2013). https://doi.org/10.1186/1471-2458-13-742 - International classification of diseases - ICD revision	2	6	0	0	0	1	0.629267	1	2,577
If you are in healthcare, you’ve heard the warnings. ICD-10 is coming… to all clinical practices in the United States. ICD-10, or the International Classification of Diseases 10th Edition, was actually started way back in 1983 by the World Health Organization and endorsed in May 1990. ICD-10 has been used in the United States on death certificates and in the tracking of mortality data since 1999. Other countries have been using it starting with several in the late 1990s to about 110 countries using it for at least mortality data currently. It is a code set that allows all medical professionals to speak the same language. ICD-10 allows for better tracking of disease trends and allows for comparison of individuals to help improve outcomes. The ICD-10 code itself can contain up to seven characters. The first three characters make up the disease category. Within these, the first character is always alphabetic, the second numeric and the third can be either. After these characters there is a decimal point. The next three characters give more information about etiology (cause), anatomical site and severity of the condition. The seventh character is called the “extension code”. In injuries and external causes, it designates an Initial Encounter (A), Subsequent Encounter (D) or Sequela* (S). When coding fractures, the extension code indicates an Initial Encounter for Closed Fracture (A), Initial Encounter for Open Fracture (B), Subsequent Encounter for Fracture with Routine Healing (D), Subsequent Encounter for Fracture with Delayed Healing (G), Subsequent Encounter for Fracture with Nonunion(K), Subsequent Encounter for Fracture with Malunion* (P), or Sequela (S). An “X” is used as a placeholder when the extension is needed but the code does not contain all of the prior six characters. The ICD-10 code set allows for greater coding specificity. To give you an idea, there were about 14,000 codes in ICD-9. Compare that to the approximately 69,000 codes in ICD-10. That’s over a 400% increase in usable codes. And because the codes can contain letters or numbers, it allows for more flexibility in expanding the code set in the future. * “Sequela” is a condition that is caused by another disease “Nonunion” is a permanent failure of a broken bone to heal * “Malunion” is where a broken bone heals but not in the optimal position How will this affect the healthcare industry? For providers who bill per visit, any invoices submitted with dates of service on or after October 1, 2015 will need to contain ICD-10 diagnosis codes. This only affects the diagnosis codes that were previously coded in ICD-9. It will not change CPT codes, HCPCS codes, HIPPS codes, etc. For therapyBOSS clients billing insurance, we highly recommend that claims with service dates before October 1st and claims with service dates on or after October 1st be billed separately to decrease the chance of denials of your claims. therapyBOSS will automatically use the ICD-10 or ICD-9 codes depending on the date of service. For home health agencies that bill episodically things are a bit more complicated. There are three components that determine how you code: the claim “from” date, the claim “to” date and the Date Assessment Completed (M0090) of the OASIS. Any claims that have all three dates before October 1, 2015 will be coded in ICD-9 while claims with all three dates after the conversion date will be coded entirely in ICD-10. The claims with dates both before and after the conversion date are going to be more of a challenge. The OASIS version and the codes to go into the OASIS are determined by the M0090 date of the OASIS. If the date is before 10/1/15, OASIS C1-ICD9 is used and ICD-9 diagnosis codes. IF it is after 10/1/15, OASIS C1 and ICD-10 diagnosis codes are used. The ICD codes that are used on the claim are determined by the “through” date of the claim. Here’s the tricky part. The HIPPS code must be the same for the RAP and the final claim. So if you billed a RAP prior to October 1st it would have been billed with the HIPPS code configured from ICD-9 codes. So if your final claim is dated after October 1st, your claim must contain ICD-10 codes. However, the HIPPS code that is submitted with the final claim will be the HIPPS code from the RAP regardless of whether the new ICD-10 codes change the HIPPS code. The good news is that this is only for claims in this transition period and CMS is going to have some flexibility in dealing with these claims. Most home health software should already be asking for you to dual-code any claims with a RAP date on or after August 3rd. If your system is not, you should speak with your vendor as soon as possible to ensure that you will be ready on October 1st. CMS has created a handy checklist to help providers to get ready for ICD-10. You can see it here. The absolute most important thing to do immediately is to ensure that your coders have access to an ICD-10 coding resource. It is also vitally important to ensure that your software vendor is ready for ICD-10 and that you will be able to submit compliant claims on October 1st. If not, you will need to ensure that you follow up with your Fiscal Intermediary’s ICD-10 Claim Submission Alternatives Instructions. Links to those instructions are provided below. A release is planned for September 18th that will enable ICD-10 codes in the system allowing providers to look them up and add both ICD-9 and ICD-10 codes. For clients billing insurance, we are offering to help add ICD-10 equivalents based on existing ICD-9 codes. Please note that you would need to specify to us an ICD-10 code or multiple codes that you would like to see reflected for each ICD-9 code. Unfortunately, more often than not, there isn’t a straight match between the two. However, there are resources that can help you make the determination. Do keep in mind that for dates of service on and after October 1st, therapyBOSS will look for ICD-10 codes to place on the claim. That’s also why you want to bill for services prior to October 1st separately from services that take place after. The release on September 18th will have the updated OASIS-C1 forms. If you have any questions, please contact us at [email protected]. Home Health instructions: www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNMattersArticles/downloads/SE1410.pdf CMS ICD-10 general information: www.cms.gov/medicare/coding/icd10 CMS “Road to 10”: www.roadto10.org World Health Organization (WHO) ICD-10 website: www.who.int/classifications/icd/en If your software vendor cannot or will not be ready for ICD-10, here are some ICD-10 Claim Submission Alternatives listed by Fiscal Intermediary: Ask a Question We’ll open a ticket and send you an immediate confirmation. You’ll be getting a response from us soon after.	4	3	0	0	4	0	0.737549	4	1,637
The codes used to document medical services and bill insurers are referred to as ICD which is an acronym for the International Statistical Classification of Diseases and Related Health Problems. The World Health Organization created these codes and over 25 countries use them for reimbursement purposes. Across the globe, medical and billing professionals are making the transition to the newest set of codes called ICD-10. In the United States, there are two types of ICD-10 codes. There are ICD-10 CM (clinical modification) codes and there are ICD-10 PCS (procedure code system) codes. All in all, there are more than 140,000 different combinations of numbers and letters assigned to every medical situation you can think of.Thankfully, the codes have a structure that helps medical professionals understand them. The first 3 characters categorize the disease, the 4th notes the etiology of disease, the 5th tells the body part that was affected, the 6th indicates the severity of the illness, and the 7th is a placeholder for the extension of the code to help better its specificity. The Codes You Might Never Use Among this new set of codes there are many that seem a bit odd, and chances are you won’t get to use them. Here are 15 ridiculous ICD-10 codes which you may never have to bill for: 1. V9027XA – Drowning and submersion due to falling or jumping from burning water skis. 2. V9542XA – Forced landing of spacecraft injuring the occupant. 3. W5609XA – contact with dolphin. 4. W5922XS – Struck by turtle, sequela. Sequela indicates that the condition was caused by a previous injury or illness. 5. Z621 – Parental overprotection. 6. Z631 – Problems in relationship with in-laws. 7. V0009XS – Pedestrian on foot injured in collision with other pedestrian conveyance, sequela 8. W2202XA – Walked into a lamppost, initial encounter. 9. R460 – Very low level of personal hygiene 10. W5622XA – Struck by Orca, initial encounter. 11. X52 – Prolonged stay in weightless environment. 12. W6162 – Struck by a duck, sequela 13. Z731 – Type A behavior pattern 14. R461 – Bizarre personal appearance 15. W5649 – Other contact with shark Contact MBA Medical today about our medical and anethesia billing services. Call 866-622-2455 or click here to request a consultation.	4	2	0	0	2	1	0.607937	3	560
In this test a doctor looks inside your stomach and first part of your small intestine (the duodenum) by passing a thin, flexible telescope down your gullet (oesophagus). If you have non-ulcer dyspepsia, the inside of your gut looks normal. However, most people with dyspepsia do not have an endoscopy. Coding Notes for R10.13 Info for medical coders on how to properly use this ICD-10 code They affect in particular the gastrointestinal tract (irritable colon, non-ulcerous dyspepsia), the cardiovascular system (cardiac phobia), the respiratory system (hyperventilation syndrome) and include chronic pain syndromes. The earlier term “functional syndrome” has been discarded in favor of the category “somatization disorders”. Also, people can have medical conditions that cause stomach pain. Learn more about the potential causes with this article. You may also feel nauseated, or even throw up. You might get indigestion from eating too much or too fast, eating high-fat foods, or eating when you’re stressed. Smoking, drinking too much alcohol, using some medicines, being tired, and having ongoing stress can also cause indigestion or make it worse. Sometimes the cause is a problem with the digestive tract, like an ulcer or gerd. Avoiding foods and situations that seem to cause it may help. R10.13 is a billable ICD code used to specify a diagnosis of epigastric pain. A ‘billable code’ is detailed enough to be used to specify a medical diagnosis. The ICD-10-CM Alphabetical Index links the below-listed medical terms to the ICD code K30. Click on any term below to browse the alphabetical index. The sensation generally occurs soon after consuming food or drink. It may make a person feel full or uncomfortable during a meal, even if they have not eaten a large amount of food. Medicare rules for medical necessity, called Local and National Coverage Determinations (LCDs and NCDs), currently account for as many as 500,000 ICD-9 and HCPCS/CPT code pairs. K30 is a billable code used to specify a medical diagnosis of functional dyspepsia. The code is valid for the year 2019 for the submission of HIPAA-covered transactions. In a recent study, patients with peptic ulcer disease were compared with patients with functional dyspepsia in an age and sex-matched study. Learn more about heartburn here. Dyspepsia is mild and infrequent for most people with symptoms. In such cases, no treatment is needed. The symptoms are normally triggered by stomach acid coming into contact with the mucosa. This infographic provides an overview of the medical necessity issues you should be aware of as you transition to ICD-10. The contents of the ICD List website are for informational purposes only. Reliance on any information provided by the ICD List website or other visitors to this website is solely at your own risk. If you think you may have a medical emergency, please call your doctor or 911 immediately. The 7th character must always be the 7th character in the data field. If a code that requires a 7th character is not 6 characters, a placeholder X must be used to fill in the empty characters. Code first – Certain conditions have both an underlying etiology and multiple body system manifestations due to the underlying etiology. You may need medicines to treat the symptoms. The patient is treated for diabetes mellitus controlled by medication and, during the same encounter, he tells the physician that he has been experiencing severe indigestion. The physician discussed possible reasons for indigestion with the patient, who admitted to having eaten a lot of spicy foods in the past month. The patient is unwilling to take over-the-counter or prescription medications for the indigestion, and the physician suggested alternative solutions. The cause is often not clear. Medication to reduce stomach acid helps in some cases. Infection with Helicobacter pylori (H. pylori) may cause a small number of cases. Clearing this infection, if present, helps in some people.	4	2	0	0	0	8	0.838892	8	891
OVERVIEW: What every practitioner needs to know Are you sure your patient has infection caused by varicella-zoster virus? What should you expect to find? Varicella-zoster virus (VZV) causes chickenpox as a primary infection and shingles with recurrent infection. The symptoms of the former are a febrile, vesicular-pustular, pruritic rash. Those of the latter are pain and unilateral localized vesicles. Chickenpox causes a vesicular rash with lesions in all stages of development, including macules, papules, vesicles, pustules, and scabs. Shingles causes a dermatomal rash that evolves from maculopapules to vesicles, pustules, and scabs. How did the patient develop disease caused by varicella-zoster virus infection? What was the primary source from which the infection spread? Primary infection is acquired by a susceptible individual exposed to someone excreting VZV either immediately prior to the development of the rash of chickenpox or during active infection. Shingles is the consequence of reactivation of latent virus from the sensory ganglia. Historically, chickenpox occurred in children and was one of the most common childhood infections with an incidence approaching the US birthrate. With the licensure of a vaccine, disease incidence and attendant complications have plummeted. Nevertheless, some adults did not get vaccinated and remain susceptible to primary infection. Shingles increases in incidence in individuals with advancing age. Approximately 1 million cases occur annually in the United States. Which individuals are of greater risk of developing varicella-zoster virus infection? Immunocompromised hosts are most at risk for both chickenpox and shingles and the complications of both diseases. For these individuals, dissemination to involve visceral organs is a concern. In addition, pregnant women during the second and third trimesters are at increased risk for the complications of chickenpox. For pregnant women, the major concern is the development of pneumonia. The predisposing factor is immunosuppression that is the consequence of an underlying disease or drugs, including, among others, hematopoietic cell transplantation, solid organ transplantation, AIDS, receipt of steroids or anti-tumor necrosis factor monoclonal antibodies, etc. Beware: there are other diseases that can mimic varicella-zoster virus infection: Vesiculopapular diseases that mimic chickenpox include disseminated herpes simplex virus infection, and enterovirus disease. Dermatomal vesicular disease can be caused by herpes simplex virus and can be recurrent. What laboratory studies should you order and what should you expect to find? Results consistent with the diagnosis The white blood cell (WBC) count will usually be normal in the immunocompetent host. However, laboratory values in the immunocompromised host will reflect the nature of the immune compromise. Liver enzymes may be elevated in chickenpox, because the spread of the virus is by blood. Such tests reflect the state of immunocompromise in other populations. Results that confirm the diagnosis Vesicular lesions can be cultured, but the virus does not survive well in transport media, even when the sample is placed on ice. As a consequence, retrieval of virus in cell culture is limited and should only be performed by experienced personnel. Polymerase chain reaction (PCR) detection of viral DNA is the most sensitive and specific diagnostic for both chickenpox and shingles. The laboratory performing such tests must be reliable. Saliva is an excellent source of viral DNA detected by PCR. What imaging studies will be helpful in making or excluding the diagnosis of varicella-zoster virus infection? Imaging studies are not required in the routine management of either chickenpox or shingles. However, with both infections, complications can occur that require imaging. For example, chickenpox can cause a syndrome of cerebellar ataxia or, rarely, encephalitis. With shingles, granulomatous arteritis can occur after the infection has resolved. In both circumstances, a magnetic resonance imaging (MRI) scan or a magnetic resonance angiogram (MRA) would be of value in delineating the pathology. The costs of MRI scans and MRAs vary dramatically from one institution to another. For adults, and especially pregnant women, with chickenpox, a chest radiograph is important to assess whether pneumonia is present. What consult service or services would be helpful for making the diagnosis and assisting with treatment? An infectious diseases consultation should be sought for an immunocompromised patient who has VZV infection. If you decide the patient has this disease, what therapies should you initiate immediately? Chickenpox in the normal host is usually a benign infection and is treated at the discretion of both the family and physician. Chickenpox in the immunocompromised host should always be treated. Shingles should be treated regardless of the age of the patient. 1. Anti-infective agents If I am not sure what pathogen is causing the infection what anti-infective should I order? Empiric therapy for the immune-competent adult without complications should be either valaciclovir or famciclovir. The oral suspension of aciclovir is used in children who are thought to require therapy. Table I summarizes treatment options. Of note, the second generation antiviral drugs, valaciclovir and famciclovir, are superior to aciclovir and have improved pharmacokinetics and pharmacodynamics. However, neither is available in a useful pediatric formulation. \|ChickenpoxNormal host – child\|\|Aciclovir oral suspension\|\|20mg/kg every 8 hours for 5–7 days\| \|ChickenpoxNormal host – adult\|\|Valaciclovir\|\|1g 3 times a day for 7 days\|\|FamciclovirAciclovir\| \|ChickenpoxHospitalized patient\|\|Aciclovir intravenously\|\|Child: 500mg/M every 8 hours for 5–7 daysAdult: 10mg/kg every 8 hours for 7 days\| \|Shingles\|\|ValaciclovirFamciclovir\|\|1g 3 times a day for 5–7 days500mg 3 times a day for 5–7 days\|\|Aciclovir\| 2. Other key therapeutic modalities No other therapies are required for either chickenpox or shingles. Although controversial, the administration of concomitant corticosteroids to patients with shingles will improve the quality of life. The administration of pregabalin may be of benefit in the management of post-herpetic neuralgia. What complications could arise as a consequence of varicella-zoster virus infection? The major concern for shingles is post-herpetic neuralgia as noted below. What should you tell the family about the patient's prognosis? The most common complication of chickenpox is secondary skin infection, usually with a Gram-positive organism. Rarer complications include infection of the central nervous system (CNS). In the immunocompromised host, lesion formation is longer than with the immunocompetent host. The most important problem with shingles is both acute pain and post herpetic neuralgia. For individuals older than 50 years of age, 20% will have persistent dermatomal pain 6 months after the resolution of cutaneous infection. In addition, herpes gangrenosum, disseminated disease, CNS involvement, motor paralysis, zoster ophthalmicus, Ramsay-Hunt syndrome, and granulomatous arteritis are all rare complications. The immunocompromised host is more likely to develop disseminated disease. If a patient presents with recurrent dermatomal disease, it is more likely to be caused by herpes simplex virus than VZV. How do you contract varicella-zoster virus infection and how frequent is this disease? The epidemiology of VZV infections is changing. We now have a vaccine for both chickenpox and shingles (two different vaccines) that has decreased the incidence of both diseases. With the two administration schedule for the chickenpox vaccine, the overall incidence of disease has decreased dramatically. Whether there will be waning immunity in young adults who received the chickenpox vaccine remains to be determined. Similarly, the shingles vaccine is licensed for individuals older than 50 years of age and has decreased the incidence of disease by 50%. Shingles can recur, but it is extremely uncommon in the normal host. However, patients with HIV/AIDS can have multiple episodes of shingles for reasons that are not entirely clear. Chickenpox historically occurred in late winter and early spring; however, with routine vaccination, the epidemiology has changed. There is no seasonal variation in shingles. Spread of chickenpox is airborne. What pathogens are responsible for this disease? Both chickenpox and shingles are caused by VZV. The virus associated with shingles is the same strain that infected the individual as a child. How do these pathogens cause varicella-zoster virus infection? VZV infections are spread by an airborne route. With primary infection, the virus infects the mucosa of the oropharynx, where an initial round of virus replication takes place, leading to viremia and the appearance of disseminated vesicles that involve the trunk to a greater extent than the extremities. The incubation period is generally 14 days. Shingles is the reactivation of latent virus from a sensory ganglion. The triggers for reactivation are not well defined. Importantly, chickenpox can result in another case of chickenpox but does not result in shingles. Conversely, shingles can cause chickenpox in a susceptible individual, but cannot cause shingles. What other clinical manifestations may help me to diagnose and manage this disease? Both chickenpox and shingles are clinical diagnoses. What other additional laboratory findings may be ordered? Supportive laboratory tests are not required. How can varicella-zoster virus infection be prevented? There are now licensed vaccines for both chickenpox and shingles. These vaccines differ according the amount of attenuated virus in each (i.e., chickenpox vaccine has significantly less virus). These vaccines have demonstrated efficacy and safety. WHAT'S THE EVIDENCE for specific management and treatment recommendations? There are no treatment guidelines that have been established by organized societies. Gershon, AA, Breuer, J, Cohen, J, Cohrs, RJ. “Varicella zoster virus infection”. Nat Rev Dis Primers.. vol. 1. 2015 Jul 2. pp. 15016 Oxman, MN, Levin, MJ, Johnson, GR. “A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults”. N Engl J Med. vol. 352. 2005. pp. 2271-84. (This clinical trial is the basis of licensure of the adult shingles vaccine. The endpoints clearly define what a physician can expect in the deployment of the vaccine.) Whitley, RJ.. “A 70-year-old woman with shingles: review of herpes zoster”. JAMA. vol. 302. 2009. pp. 73-80. (This case summarizes all aspects of the management of shingles.) DRG CODES and expected length of stay With the exception of the immunocompromised host with complications, these diseases are managed on an ambulatory care basis. Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM. - OVERVIEW: What every practitioner needs to know - Are you sure your patient has infection caused by varicella-zoster virus? What should you expect to find? - How did the patient develop disease caused by varicella-zoster virus infection? What was the primary source from which the infection spread? - Which individuals are of greater risk of developing varicella-zoster virus infection? - Beware: there are other diseases that can mimic varicella-zoster virus infection: - What laboratory studies should you order and what should you expect to find? - What imaging studies will be helpful in making or excluding the diagnosis of varicella-zoster virus infection? - What consult service or services would be helpful for making the diagnosis and assisting with treatment? - What complications could arise as a consequence of varicella-zoster virus infection? - What should you tell the family about the patient's prognosis? - What-if scenario: - How do you contract varicella-zoster virus infection and how frequent is this disease? - What pathogens are responsible for this disease? - How do these pathogens cause varicella-zoster virus infection? - What other clinical manifestations may help me to diagnose and manage this disease? - What other additional laboratory findings may be ordered? - How can varicella-zoster virus infection be prevented? - WHAT'S THE EVIDENCE for specific management and treatment recommendations? - DRG CODES and expected length of stay	2	9	1	0	0	0	0.672239	1	2,833
Clinical terminologies and clinical classification systems represent two coding schemas used in healthcare. Chances are your organization uses both, and how you manage them might need a tune-up. Terminology in Healthcare – Different from what you expect Clinical terminology is different from medical terminology. Medical Terminology refers to the vocabulary that medical professionals use to describe the body—what it does, diseases that impact it, and procedures to correct it —enabling precise communication among practitioners. Clinical terminology systems are used to code the entire healthcare domain, from procedure to diagnosis and beyond. They function as a common reference system that uses compositional grammar concepts (conversation words) that can be coded and queried. Terminology systems personalize medicine such that everyone is speaking the same language about a patient in the exam room and the billing office. These systems also provide support for clinical trials and research across multiple organizations. Additionally, they offer semantic interoperability for sharing data easily and accurately. Healthcare Terminology, Explained In healthcare, terminology is much more complicated than in other fields. This complexity is because there needs to be a group of expressions for a large number of permutations and combinations (to borrow a mathematical term) of clinical diagnoses and treatments. If you think of “fracture of the proximal tibia (shinbone)” as one form of many possible tibial injuries, imagine how many sets of words are needed to describe all the different types of injuries and conditions across the 206 bones in the human skeleton (and the skeleton is just a subset of the human anatomy). When there are thousands upon thousands of sets like these, words alone aren’t manageable. You need numbered codes, and they must be arranged in a hierarchy. Plus, you’ll need to build out hierarchies for different types of users. Different Codes for Different End Users Not all functional areas and roles within a health system require the same level of precision when it comes to identifiers for diagnoses and treatments: 1. A physician needs to precisely document a visit in an EMR. They will use a problem list and diagnosis codes. For example, SNOMED CT or customized homegrown codes 2. A lab test is performed during the visit. Codes are assigned and associated with these items. For example, LOINC 3. The physician orders a medication. For example, RxNorm 4. A billing/coding specialist would use documentation from a provider and assign codes to appropriately bill for the visit. For example, CPT and ICD-10 5. A call center agent, for example, is best off viewing plain English information in a CRM system when talking to a patient (“Oh yes, I see that you were treated for your broken leg last August”) 6. Integration data coming across the EMR from outside sources containing SNOMED, LOINC, NDC, RxNorm, and local codes As you can see, differing levels of precision have given rise to different coding systems. Similar Names, Different Use Case: Clinical Terminology vs. Clinical Care Classification Broadly, the coding systems discussed above fall into these buckets: - Clinical terminology codes—Codes that cover the entire domain of healthcare terms, such as SNOMED CT - Clinical care classification codes—Codes that cover specific diseases, diagnoses, lab reports, procedures, or meds. Examples include NDC codes for medications and CPT for procedures/services In an HIE or health system, there needs to be an exchange of data among applications—both within and across these buckets. Systems have to determine the best matches among disparate coding sets. To achieve this, your organization must build and maintain data maps, then load the results into an interoperability platform such as InterSystems’ HealthShare. Learn about our Managed Terminology Services for your HIE Clinical terminology, as its name implies, exists primarily for use by caregivers. Having agreed-upon codes in an EHR system is important for ensuring a standardized treatment or set of treatment options for a specific medical issue. Assume two patients come into the hospital on different days. Each complains of acute pain in their right leg and has a nearly identical closed fracture in the upper end of the right tibia. For consistency, the issue observed for both patients should be coded the same way in the EHR system. The terminology standard in clinical applications is SNOMED CT (Systematized Nomenclature of Medicine Clinical Terms). Just as Google uses natural language processing (NLP) to apply meaning to the words in this blog post, SNOMED CT uses NLP to generate codes from medical text. Clinical expressions are automatically coded in the background without users needing to know said codes. SNOMED uses what are called “concept codes.” Concepts are a clinical idea with a unique identifier. The concepts themselves (e.g., nausea and vomiting) are in clinicians’ transcriptions while the corresponding codes (e.g., 16932000) provide a unique identifier. The principle is based on one code per meaning, one meaning per code. Other examples of concept codes are: - 23900009: Closed fracture of upper end of tibia (disorder) - 10925201000119100: Closed fracture of proximal end of right tibia (disorder) As with other healthcare data elements, terminology should be normalized among different clinical and non-clinical systems to ensure as much uniformity as possible. Clinical Care Classification Codes As stated above, classifications refer to the codes that are used in healthcare environments for billing and accounting. They’re also used for statistical analysis and reporting but are NEVER used to document in EMRs. Classification Codes: ICD-9 and ICD-10 International Classification of Diseases, Ninth Revision (IDC-9), and Tenth revision (IDC-10) are classifications. Classification codes are important for billing the correct amount to patients. According to an article by Doug Klinger, CEO of Zelis Healthcare, medical bills are riddled with errors. Careful implementation of a terminology management system can mitigate the risk of errors. The main format for ICD-9 codes is two or three digits to the left of a decimal point and one or more digits to the right. - 823.80: Closed fracture of unspecified part of tibia alone - 823.02: Closed fracture of upper end of fibula with tibia ICD-10 codes include two or three alphanumeric characters to the left of a decimal point and two or more alphanumeric characters to the right. - S82.101A: Unspecified fracture of upper end of right tibia, initial encounter for closed fracture - 79.16: Closed reduction of fracture with internal fixation, tibia, and fibula If you go to the Find-a-Code website and type in a search such as “fracture of tibia,” you’ll get an appreciation of just how many classification codes there are. An ICD-9 diagnosis is equivalent to one or many (usually a sub-hierarchy) ICD-10 diagnoses. i.e., 729.5 (Pain in limb) is equivalent to M79.609 (Pain in unspecified limb). The latter is a sub-hierarchy that contains six specific diagnoses. Current Procedural Terminology (CPT) Codes While an ICD code identifies a diagnosis and describes a disease or medical condition, a CPT code describes what was done to the patient during the consultation, including diagnostic, laboratory, radiology, and surgical procedures. Here is a detailed explanation of the difference between ICD and CPT codes. There is a five-digit CPT code on each line item on the bills that patients and payers receive. A doctor will not receive payment from a payer, furthermore, unless a CPT code is listed on the claim form. Here is a more in-depth look at CPT codes. Managing Clinical Terminology and Classifications As you can see from the above examples, there are a wide variety of code systems across systems. The alphanumeric identifier for “fracture of upper end of tibia” in one system may have nothing in common with the identifier in another. A traditional way of managing the disparities across systems is with the use of spreadsheets. However, spreadsheets involve a lot of manual work. Throw local codes into the mix, and you can start to see the need for an easier solution. Source: SNOMED International Setting up a terminology solution would shift manual processes to a highly automated and much less labor-intensive platform. Semantic services go beyond just the coding systems mentioned above. Libraries can include: - SNOMED CT - CMS eCQMs - CDC (demographics) Clinical terminology management and the management of other coding systems include flowing normalized data into a number of different types of systems and environments using industry protocols, including FHIR. The diagram below shows examples of data types and target systems typical in J2’s Managed Terminology service. Clinical terminology and classification are easy concepts to understand, but they’re complicated for an IT department to manage to scale. To reduce billing errors and clinical mishaps, healthcare organizations should be ready to retire spreadsheets and invest time and resources in a dedicated terminology solution.	4	1	0	0	0	4	0.26878	4	1,962
DSM & ICD – Categorising This is the first study we will be looking at from the ‘Diagnosis of Dysfunctional Behaviour’ section of ‘Dysfunctional Behaviour’, as part of your OCR A2 Health and Clinical Psychology course. It is further categorised into ‘Categorising.’ While it is not essential, The Myth of Mental Illness: Foundations of a Theory of Personal Conduct is a highly interesting and relevant read that you might want to consider. The DSM and the ICD is not a study, but they are manuals for diagnosing mental disorders. Watch the following video on the DSM and ICD: As of 2013 the DSM is on version 5 and the ICD is on version 10. International Classification of Diseases and Related Health Problems (ICD-10) In ICD-10 each disorder has a description of the main features, and any important associated features. Each disorder is then given a code. The numerical coding of 001–099 in ICD-9 has now been replaced by A00-Z99, which gives more possible categories. Examples of some of the categories: - Mood (affective) disorders - Personality disorders. Diagnostic and Statistical Manual of Mental Disorders Firth Edition (DSM-V) DSM is a multi-axial tool, which means that clinicians have to consider if a disorder is from Axis 1 (clinical disorders) and/or Axis 2 (personality disorders). Then the general medical condition of the patient is considered, plus any social and environmental problems. This is all used to assess functioning of the person on a scale from 1-100. The DSM-V has classifications that include: - learning disorders - communication disorders - substance-related disorders - sleep disorders - sexual and gender identity disorders.	3	4	0	0	0	2	0.852697	2	394
In developed countries, the number of maternal deaths associated with heart disease, including myocardial disorders, has been increasing during the past two decades.1,2 However, myocardial disorders represent a set of underrecognized, underreported, and poorly understood obstetric problems.3 Peripartum cardiomyopathy, a distinct clinical entity, has received the most attention in the obstetric literature because of its unknown etiology, unpredictable course, and frequently poor outcomes.4,5 The four diagnostic criteria for peripartum cardiomyopathy were adopted at a workshop on this disorder organized by the National Heart, Lung, and Blood Institute and the Office of Rare Diseases of the National Institutes of Health in April 1997.6 For a definitive diagnosis of peripartum cardiomyopathy, all four criteria must be present, and they include 1) the development of congestive heart failure in the past month of pregnancy or within 5 months after delivery, 2) the absence of preexisting cardiac dysfunction, 3) the absence of a determinable cause of cardiomyopathy, and 4) documented left ventricular systolic dysfunction, such as depressed shortening fraction or ejection fraction.6 The estimated prevalence of peripartum cardiomyopathy varies widely depending on the population, with the reported prevalence of this condition in the United States ranging from 1 per 1,300 live births in Little Rock, Arkansas, in 1963 to 1 per 15,000 live births in Dallas, Texas, in 1986.7 To improve the ascertainment and understanding of morbidity associated with peripartum cardiomyopathy among pregnant women, in October 2003 a specific International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) code for peripartum cardiomyopathy (674.5) was separated from the nonspecific code 678.4, “Other complications of the puerperium, not elsewhere classified.”8 Peripartum cardiomyopathy is not the only myocardial disorder that complicates pregnancy. Because an increase in the prevalence of preexisting cardiac and noncardiac disease that can present as myocardial disorders has been observed in the obstetric population during the past 10 years,9,10 we hypothesized that many hospitalizations likely involved myocardial disorders other than peripartum cardiomyopathy. In addition, with the notable improvements in the treatment of congenital heart disease over the past few decades, congenital heart disease has become an important cause of heart disease (including myocardial disorders) in pregnancy in the developed world.11,12 However, population-level data on the prevalence of myocardial disorders in obstetric population are limited. Moreover, the risks of severe obstetric complications among women with myocardial disorders are not well understood. The objectives of the present report were to 1) evaluate the feasibility of using the ICD-9-CM code for peripartum cardiomyopathy for surveillance purposes, 2) estimate the rate of pregnancy hospitalizations with myocardial disorders, and 3) report the rate of severe obstetric complications by myocardial disorders status among delivery and postpartum hospitalizations using data from the 2004–2006 Nationwide Inpatient Sample of the Healthcare Cost and Utilization Project. MATERIALS AND METHODS The Healthcare Cost and Utilization Project is a federal–state–industry partnership sponsored by the Agency for Healthcare Research and Quality.13 The Nationwide Inpatient Sample is the largest all-payer inpatient care database in the United States. All of the nonfederal community hospitals from the states participating in the annual Healthcare Cost and Utilization Project data collection are stratified by rural/urban location, number of beds, region, teaching status, and ownership. Within each stratum, a systematic random 20% sample of hospitals is drawn. The sample size of this large cross-sectional study was predetermined by sampling methodology that allows using discharges from the sampled hospitals to produce nationwide estimates. A full description of the Nationwide Inpatient Sample methodology can be found on the Healthcare Cost and Utilization Project Web site.13 Because the Nationwide Inpatient Sample excludes data elements that could directly or indirectly identify individuals, this research was considered exempt from review by the institutional review board of the Centers for Disease Control and Prevention.14 For the myocardial disorders prevalence analysis, we included all 2004–2006 pregnancy-related hospitalizations, which were identified by ICD-9-CM diagnostic codes 630–677, V22, V23, V24, V28, and 792.3; ICD-9-CM obstetric procedure codes 72.xx, 73.xx, 74.xx, and 75.xx; and diagnosis related group (DRG) codes 370–384. The delivery, postpartum, and antenatal hospitalizations were identified hierarchically. The specific details about ICD-9-CM and DRG coding to identify delivery hospitalizations are described in detail elsewhere.15 Postpartum hospitalizations were identified by a fifth digit of 4 in ICD-9-CM codes for primary or secondary diagnosis; ICD-9-CM code V24 for any listed diagnosis; or postpartum DRG codes 376–377. Antenatal hospitalizations were identified by a fifth digit of 3 in ICD-9-CM codes for primary or secondary diagnosis; ICD-9-CM code V22, V23, V28, or 792.3 for any listed diagnosis; or antenatal DRG codes 378–384. We confined the analysis of severe obstetric complications associated with myocardial disorders to delivery hospitalizations and postpartum hospitalizations. Severe obstetric complications were identified by using condition-specific ICD-9-CM codes and additional information obtained from hospital discharge records, such as mortality, transfer from or to another health care facility, and duration of stay. The specific ICD-9-CM codes for severe complications and details of the method to identify delivery hospitalizations with these conditions can be found elsewhere.9,10 In addition to severe complications previously published, this study also included acute myocardial infarction (ICD-9-CM code 410.x), disorders of fluid, electrolyte, and acid–base balance (ICD-9-CM code 276.x), and cardiac arrest/ventricular fibrillation (ICD-9-CM codes 427.5, 427.41, and 427.42). The hospitalizations with myocardial disorders were identified by ICD-9-CM codes 674.5x (peripartum cardiomyopathy) or 425.x (other cardiomyopathies). In the classification of cardiomyopathy proposed by the American Heart Association in 2006, myocardial disorders associated with coronary artery disease, hypertension, valvular disease, and congenital heart disease were excluded.16 However, in our 2004–2006 sample these hospitalizations would still have ICD-9-CM codes for cardiomyopathy. Thus, in this analysis we classified hospital records that simultaneously had ICD-9-CM codes for cardiomyopathy and heart disease, such as coronary artery disease, hypertension, valvular disease, and congenital heart disease, as records with other myocardial disorders. The remaining hospitalizations with ICD-9-CM code 425.x or 674.5x were classified as hospitalizations with cardiomyopathy. As a next step of our analysis, we evaluated the feasibility of using the specific ICD-9-CM code 674.5x for surveillance of peripartum cardiomyopathy. Some hospital records with codes for peripartum cardiomyopathy also had ICD-9-CM codes for preexisting cardiac or cardiomyopathy-associated noncardiac disease (eg, diabetes mellitus) at the same time. We considered these records to be misclassified as peripartum cardiomyopathy because there was evidence of specific etiologies for cardiomyopathy. To describe a distribution of misclassified and correctly classified records with ICD-9-CM code 674.5x, we hierarchically categorized all these records into three mutually exclusive groups: 1) records with ICD-9-CM codes for heart disease (Table 1): valvular disease, congenital heart disease, coronary artery disease, hypertensive heart disease, conduction disorders and cardiac dysrhythmias, and pulmonary circulation disease; 2) records with ICD-9-CM codes for potential underlying conditions for cardiomyopathy (Table 2): myocarditis, diabetes (excluding gestational), thyroid disease, chronic hypertension (excluding hypertensive heart disease), chronic renal failure, rheumatoid arthritis/collagen vascular disease, rheumatic heart failure, severe anemia, human immunodeficiency virus, drug abuse, alcohol abuse, and nutrient deficiencies; and 3) records with ICD-9-CM codes for peripartum cardiomyopathy only. The unit of analysis was a hospitalization, not an individual; these data did not allow us to account for multiple pregnancy hospitalizations of the same women during the study period. However, because a woman can only deliver once, the analysis of delivery hospitalizations can be considered an analysis of individuals. We reported overall rates of pregnancy hospitalizations with cardiomyopathy and other myocardial disorders and rates by age, payer, and hospital region per 1,000 deliveries. Rates of severe complications per 1,000 deliveries or 1,000 postpartum hospitalizations were also calculated. We compared these rates using χ2 tests with adjustment of P values for multiple comparisons using the Bonferroni method. Because many hospitals do not collect or report race/ethnicity, we did not include this variable in the analysis.13 We used SAS 9.1 (SAS Institute Inc., Cary, NC) to manage data and SAS-callable SUDAAN 9.0 (RTI International, Research Triangle, NC) to account for the multistage probability sampling design. Thus, all results are based on the weighted estimates of pregnancy hospitalizations in the United States during the study period. During the 3-year study period, there were an estimated 14,323,731 pregnancy hospitalizations in the United States. Among the 16,824 records with myocardial disorders, 11,134 had codes for peripartum cardiomyopathy. Among 11,134 records with a code for peripartum cardiomyopathy, 6,097 (54.8%) also had ICD-9-CM codes for heart disease, and 2,704 (24.3%) also had codes for cardiomyopathy-associated noncardiac conditions (total 79.1%). Thus, only 2,332 records (20.9%) with the specific peripartum cardiomyopathy code had no codes for cardiac or noncardiac conditions. The overall rate of hospitalizations with any use of the ICD-9-CM code for peripartum cardiomyopathy was 0.88 per 1,000 deliveries (1 case per 1,136 deliveries), and the rate of hospitalizations with the ICD-9-CM code for peripartum cardiomyopathy without any code for cardiac and noncardiac conditions was 0.18 per 1,000 deliveries (1 case per 5,556 deliveries). For this analysis all hospitalizations with the ICD-9-CM code for peripartum cardiomyopathy were reclassified into two groups: cardiomyopathy (n=5,037) and other myocardial disorders (n=6,097). Among all pregnancy hospitalizations (Table 3), the overall prevalence of hospitalizations with myocardial disorders was 1.33 per 1,000 deliveries. The rate of pregnancy hospitalizations with cardiomyopathy was 0.46 per 1,000 deliveries (0.18 for apparent peripartum cardiomyopathy and 0.28 for other cardiomyopathies). The rate of pregnancy hospitalizations with other myocardial disorders was 0.87 per 1,000 deliveries. Myocardial disorders were rare during delivery hospitalizations (0.01%) but not uncommon among postpartum hospitalizations (4.2%). The rates of myocardial disorders per 1,000 deliveries by age groups, payer status, and region were also calculated (Table 4). The significantly (P<.01) higher rates of myocardial disorders were observed for women aged 35 years or older compared with women aged 15–24 years, hospitalizations covered by public payer compared with hospitalizations covered by private insurance, and in the South compared with other regions. The same pattern was observed when rates of cardiomyopathy and other myocardial disorders were estimated separately. The rate (per 1,000 deliveries) of severe complications among delivery hospitalizations without myocardial disorders ranged from 0.07 (95% confidence interval [CI] 0.06–0.08) for cardiac arrest to 1.88 (95% CI 951.77–1.99) for fluid and electrolyte disorders (Table 5). In contrast, among hospitalizations with myocardial disorders this rate ranged from 13.2 (95% CI 6.3–20.1) for acute myocardial infarction to 128.6 (95% CI 107.2–150.0) for adult respiratory distress syndrome. The rate (per 1,000 hospitalizations) of severe complications among postpartum hospitalizations without myocardial disorders ranged from 0.4 (95% CI 0.2–0.6) for cardiac arrest to 65.5 (95% CI 64.4–68.7) for fluid and electrolyte disorders (Table 6). The rate of severe complications among hospitalizations with myocardial disorders was significantly higher than among hospitalizations without myocardial disorders (P<.05) and ranged from 10.7 (95% CI 5.7–15.7) for pulmonary edema to 193.0 (95% CI 173.7–212.4) for fluid and electrolyte disorders. Our study reports the prevalence of cardiomyopathy and other myocardial disorders during pregnancy hospitalizations in the United States after the implementation of the specific ICD-9-CM code for peripartum cardiomyopathy at the end of 2003. The recently implemented ICD-9-CM code for peripartum cardiomyopathy was frequently used simultaneously with codes for other heart disease and comorbidities, and hence it is unlikely to be specific enough to track peripartum cardiomyopathy as a distinct entity in the United States. Thus, our results underlined the importance of being more precise about language and diagnostic criteria when documenting hospital course among pregnant women. In addition, our results support the continuation of efforts to modify ICD-9-CM codes to include more granularity about conditions that occur during pregnancy. The exact prevalence of cardiomyopathy during pregnancy hospitalization in the United States has not been known. Consistent with the existing obstetric literature focusing mostly on peripartum cardiomyopathy, recent reports have attempted to estimate the prevalence of this entity. A study attempting to estimate the national prevalence of peripartum cardiomyopathy in the United States from the 1990–2002 National Hospital Discharge Survey identified one hospitalization per 3,189 live births.17 Similarly, in a 1996–2005 study of 241,497 deliveries within the Southern California Kaiser health care system, the prevalence of peripartum cardiomyopathy based on the chart review of delivery hospitalizations with an ICD-9-CM code for heart failure was 1 in 4,025 deliveries.18 The results from these studies are difficult to compare, however, because of the difference in methodology applied to identify the hospitalizations with peripartum cardiomyopathy. In our study, approximately 1 in 1,136 delivery hospitalizations had the recently implemented ICD-9-CM code for peripartum cardiomyopathy. However, approximately 80% of these hospitalizations also had an ICD-9-CM code for heart disease or chronic conditions, potential underlying causes for dilated cardiomyopathy, and thus they could not fulfill the diagnostic criteria for peripartum cardiomyopathy. Moreover, a low sensitivity of ICD-9-CM codes for chronic conditions, resulting in their underreporting in obstetric hospital records, has been documented before.19 Accordingly, although we have reasonable confidence in using our data to estimate the prevalence of cardiomyopathy in a generic sense, our results highlight the limitations of using hospital discharge data to obtain reliable estimates for the prevalence of true peripartum cardiomyopathy. The clinical presentation of peripartum or dilated cardiomyopathy is similar to that for systolic congestive heart failure. However, dilated cardiomyopathy may be difficult to diagnose because of the tendency to mimic the physiologic alterations that take place during pregnancy, especially when early signs of congestive heart failure are subtle.6 Hence, a high index of suspicion is warranted. Unfortunately, no specific diagnostic test for peripartum cardiomyopathy is available currently. Regardless, peripartum cardiomyopathy should be diagnosed after ruling out cardiac and noncardiac causes for dilated cardiomyopathy.6 Because dilatation of the left ventricle can be a normal echocardiographic finding in pregnancy, a documentation of decreased left ventricular systolic function is necessary for the definitive diagnosis of dilated cardiomyopathy.20 Myocardial disorders are conditions that often result in cardiovascular and other major system complications.16,21 Among hospitalizations with myocardial disorders, the rate of severe complications ranged from 13.2 for acute myocardial infarction to 128.6 for adult respiratory distress syndrome and from 10.7 for pulmonary edema to 193.0 for fluid and electrolyte disorders per 1,000 delivery and postpartum hospitalizations, respectively. Among hospitalizations without myocardial disorders, the rate of severe complications ranged from 0.07 to 1.9 and from 0.4 to 65.5 for cardiac arrest and for fluid and electrolyte disorders per 1,000 hospitalizations in delivery and postpartum periods, respectively. Unfortunately, the cross-sectional study design and a lack of clinical details in hospital discharge data did not allow us to determine whether severe obstetric morbidity developed as a complication of myocardial disorders after admission or was a comorbid condition that existed before admission. Nevertheless, our surveillance data indicated that delivery and postpartum hospitalizations with myocardial disorders have extremely high rates of severe obstetric complications. Our study has several limitations that should be considered when interpreting the results. Our identification of severe complications is based solely on ICD-9-CM codes and data-driven criteria, such as mortality, transfer from or to other health care facilities, and duration of stay. There are potential risk factors for cardiomyopathy and other forms of myocardial disorders, such as race, body mass index, and use of tocolytic agents,21 for which we had no information. In addition, ICD-9-CM codes for myocardial disorders among pregnancy hospitalizations were not validated, and it is not known how practicing physicians used diagnostic criteria to diagnose cardiomyopathy. Thus, misclassification of exposure, outcomes, or both is possible in our study. The estimates for myocardial disorders reported in this study may be affected by several sources of error. Because the unit of our analysis was hospitalization and we could not identify the repeat hospitalizations for same patient, our rates may be overestimated. However, underestimation is also possible. Some cases of myocardial disorders with the clinical presentation ranging from mild heart failure to sudden cardiac death may be seen only in emergency departments20 and hence are not associated with an hospital admission. Finally, hospitalizations for peripartum cardiomyopathy that occurred after the 6-week time frame that is defined as the postpartum period and hence were not coded as postpartum hospitalizations may be not captured in our data set.22 In conclusion, the results of this nationwide study have shown that approximately 0.04% of delivery hospitalizations and approximately 4% of postpartum hospitalizations had ICD-9-CM codes for cardiomyopathy and other myocardial disorders. Although only a minority of hospitalizations for cardiomyopathy are consistent with peripartum cardiomyopathy, cardiomyopathy and other myocardial disorders are important contributors to severe obstetric complications. Because recent reports have indicated alarming increases in both maternal mortality from heart disease and the prevalence of risk factors for heart disease among women of reproductive age during the past decade, trends in hospitalizations with myocardial disorders need to be monitored. However, because of the inherent limitations of hospital discharge data, if we are to offer better diagnosis and treatment of this uncommon but potentially devastating condition, the collection of clinically detailed data are essential for making progress in understanding the differences and similarities between the entities currently designated as peripartum cardiomyopathy and other forms of myocardial disorders. 1.Barker D, Lewis N, Mason G, Tan L-B. Maternal cardiovascular medicine: towards better care for pregnant women with heart disease. Br J Cardiol 2006;13:399–404. 2.Whitehead SJ, Berg CJ, Chang J. Pregnancy-related mortality due to cardiomyopathy: United States, 1991–1997. Obstet Gynecol 2003;102:1326–31. 3.Gissler M, Deneux-Tharaux C, Alexander S, Berg CJ, Bouvier-Colle MH, Harper M, et al. Pregnancy-related deaths in four regions of Europe and the United States in 1999–2000: characterisation of unreported deaths. Eur J Obstet Gynecol Reprod Biol 2007;133:179–85. 4.Fett JD. Understanding peripartum cardiomyopathy, 2008. Int J Cardiol 2008;130:1–2. 5.Satpathy HK, Frey D, Satpathy R, Satpathy C, Fleming A, Mohiuddin SM, et al. Peripartum cardiomyopathy. Postgrad Med 2008;120:28–32. 6.Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA 2000;283:1183–8. 7.Lampert MB, Lang RM. Peripartum cardiomyopathy. Am Heart J 1995;130:860–70. 9.Kuklina EV, Ayala C, Callaghan WM. Hypertensive disorders and severe obstetric morbidity in the United States. Obstet Gynecol 2009;113:1299–306. 10.Kuklina EV, Meikle SF, Jamieson DJ, Whiteman MK, Barfield WD, Hillis SD, et al. Severe obstetric morbidity in the United States: 1998–2005. Obstet Gynecol 2009;113(pt 1):293–9. 11.Gei AF, Hankins GD. Cardiac disease and pregnancy. Obstet Gynecol Clin North Am 2001;28:465–512. 12.Swan L, Lupton M, Anthony J, Yentis SM, Steer PJ, Gatzoulis MA. Controversies in pregnancy and congenital heart disease. Congenit Heart Dis 2006;1:27–34. 13.Healthcare Cost and Utilization Project. Overview of the Nationwide Inpatient Sample (NIS). Available at: www.hcup-us.ahrq.gov/databases.jsp . Retrieved December 23, 2008. 15.Kuklina EV, Whiteman MK, Hillis SD, Jamieson DJ, Meikle SF, Posner SF, et al. An enhanced method for identifying obstetric deliveries: implications for estimating maternal morbidity. Matern Child Health J 2008;12:469–77. 16.Maron BJ, Towbin JA, Thiene G, Antzelevitch C, Corrado D, Arnett D, et al. Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 2006;113:1807–16. 17.Mielniczuk LM, Williams K, Davis DR, Tang AS, Lemery R, Green MS, et al. Frequency of peripartum cardiomyopathy. Am J Cardiol 2006;97:1765–8. 18.Brar SS, Khan SS, Sandhu GK, Jorgensen MB, Parikh N, Hsu JW, et al. Incidence, mortality, and racial differences in peripartum cardiomyopathy. Am J Cardiol 2007;100:302–4. 19.Yasmeen S, Romano PS, Schembri ME, Keyzer JM, Gilbert WM. Accuracy of obstetric diagnoses and procedures in hospital discharge data. Am J Obstet Gynecol 2006;194:992–1001. 20.Egan DJ, Bisanzo MC, Hutson HR. Emergency department evaluation and management of peripartum cardiomyopathy. J Emerg Med 2009;36:141–7. 21.Elkayam U, Akhter MW, Singh H, Khan S, Bitar F, Hameed A, et al. Pregnancy-associated cardiomyopathy: clinical characteristics and a comparison between early and late presentation. Circulation 2005;111:2050–5. © 2010 by The American College of Obstetricians and Gynecologists. 22.Howard A. Review of pregnancy coding guidelines. For the Record 2009;21:31.	4	10	0	0	0	6	0.90487	6	5,496
Vascular endothelial cells (ECs) form a one cell layer on the luminal surface of all blood and lymphatic vessels, the endocardium, blood-brain barrier, and renal glomerulus. EC function and phenotype can vary depending upon the tissue, vascular region, or given microenvironment. These versatile cells form the vanguard at the dynamic interface between the blood and tissue space, play central roles in the maintenance and regulation of vascular system homeostasis, the integration of immune cell signaling and trafficking, and diverse pathological processes including inflammation, tumor metastasis, and diabetes. ECs express class I and class II MHC molecules, interact with, and modulate, immune cell function by induced expression of adhesion molecules and cytokines, and recruit T cells into inflammatory sites by functioning as antigen presentation cells (APCs). Endothelial cells (ECs) are mesodermally-derived modified simple squamous epithelial cells that collectively form the vascular endothelium–the vast living shield that lines the luminal surface of all blood vessels, the lymphatic circuit, and heart. Endothelial cell phenotypes vary among different organs and tissues with regard to specific barrier characteristics, and can be altered by environmental stimuli [1,2]. Specialized endothelial cells in the blood-brain barrier, glomeruli, and retina regulate movement of small molecules and nutrients into and out of the circulation. This highly specialized lining, a single cell thick, is uniquely positioned to integrate signaling and nutrient transport between blood and surrounding tissues, and provides a non – thrombogenic surface to help prevent inappropriate blood clotting. The endothelium is now rightly recognized as a distinct, highly specialized (endocrine) organ – the largest organ in fact – consisting of an estimated 1013 cells and total surface area somewhere between 1,000 m2–7,000 m2 [3,4]. Besides its fundamental role in cardiovascular system homeostasis, angiogenesis, initiation and regulation of inflammation, and immune cell trafficking (an essential immune response function), the endothelium is the last barrier that metastatic tumor cells must breach before they can initiate new tumors in secondary organ sites . Damage or disruption to the endothelium monolayer can lead to vascular leakage, vasoconstriction or vasodilation, promote a prothrombotic microvasculature environment, and initiate inflammatory reactions which set the stage for endothelial dysfunction. In fact, the basis for most forms of cardiovascular disease, such as hypertension, diabetes, chronic heart or kidney failure, and aggressive viral infections are manifestations of endothelial dysfunction . Endothelial Cell Heterogeneity The endothelial lining of capillaries can be continuous, fenestrated, or discontinuous, depending on the specific function and location of the underlying tissue. Endothelial cell phenotypes differ among different organs, among different vascular regions within the same organ, and between endothelial cells of the same organ and blood vessel type. Integrating such an extensive range of anatomical and physiological demands requires exceptional functional versatility and phenotypic diversity. ECs can therefore function as fenestrated endothelium seen in liver sinusoids to facilitate rapid exchange of cells, molecules, and metabolites , or as tight vascular endothelium found in the central nervous system (CNS) that forms part of the blood–brain barrier, a critical interface between blood and neural tissue within the brain and spinal cord, that regulates homeostasis of the brain microenvironment [11,12]. Although the particular functions of an EC strongly depend on its anatomical location, the functional repertoire of ECs can be efficiently modulated by inflammatory stimuli, including microbial pathogens and their products, or inflammatory mediators derived from various other cell types. For example, cerebrovascular endothelial cells (CVEs) are the major component of the blood-brain barrier that limit the passage of soluble and cellular substances from the blood into the brain. Although CEVs in the CNS are capable of presenting antigens and activating T cells, the ability of these cells to function as antigen-presenting cells in CNS inflammatory responses is still controversial . The surface of ECs consist of a proteoglycan-rich complex lining the luminal surface of blood vessels, whose soluble components are in a dynamic equilibrium with the bloodstream. This glycocalyx, also called endothelial surface layer (ESL), forms a vascular sheath that maintains the integrity of the critical interface between blood and endothelial lining. However, this lining is fragile and highly vulnerable to damage from a multitude of sources, including physical trauma, inflammation, oxidative stress, hypovolemia, hemorrhagic shock, diabetes, sepsis, and ischemia-reperfusion (I/R) injury (caused by the ensuing surge of elevated levels of reactive oxygen species and proinflammatory neutrophils) [14,15]. Degradation of the integrity of the glycocalyx by various causes noted above can damage endothelial cells, resulting in pathophysiological dysfunction of this important barrier including increased permeability, platelet aggregation, loss of vascular integrity and responsiveness. Inflammation and other forms of oxidative stress due to increased levels of reactive oxygen or nitrogen species is a major contributor to glycocalyx disruption [16-18]. Increased neutrophil adhesion to the endothelium is an additional consequence of a damaged glycocalyx in the vasculature of the myocardium after I/R injury . See Kalogeris et al. for review of ischemia/reperfusion causes and consequences. Innate Immune Response Overview The innate immune system is the first line of defense that recognizes and responds to a wide range of microorganisms. Microbial recognition by immune cells occurs via specialized host-cell receptors called pattern- recognition receptors (PRRs), which can be soluble or membrane-bound. PRRs recognize and bind microbe- specific molecular structures called microbe-associated molecular patterns (PAMPs) . Al-Soudi et al. provide an excellent review of the role of endothelium in innate and adaptive immunity. PRRs are expressed on key immune cells such as neutrophils, macrophages, and dendritic cells that serve as first responders for the immune system. When host PRRs interact with PAMPs, inflammation cascades in host cells are activated which, in turn, stimulate maturation of antigen-presenting cells (APCs), and upregulate expression of relevant immune-related cell surface and soluble molecules. These events enable APCs to initiate adaptive immunity. Among the PRRs are a diverse group of surface molecules called Toll-like receptors (TLRs), which recognize distinct classes of pathogen structures and activate an array of host defense-related responses including phagocytosis, leucocyte chemotaxis, cytotoxicity, pro-inflammatory gene expression, and adaptive immune signaling [23,24]. Although the surface receptors expressed by ECs to recognize microbe-derived alarm signals are not well characterized, ECs are known to express various several classes of innate immune receptors including NOD- like receptors, RIG-I like receptors, as well as Toll-like receptors (TLRs) . ECs have been shown to express members of the IL-1/ Toll receptor receptor family, which likely mediates the response to endotoxin, and subsequent interaction with plasma lipopolysaccharide (LPS) via soluble CD14 and LPS-binding protein, both present in plasma. In addition, ECs express cytokine receptors which can recognize their respective ligands and modulate EC function [26,27]. Pathogen recognition can induce EC production of inflammatory mediators. For example, exposure of ECs to peptidoglycan fragments from Staphylococcus epidermidis causes a rapid, transient increase in both IL-6 and toll-like receptor TLR2 and activation of endothelial TLR2 receptors by bacterial lipoproteins upregulates a suite of cytokines such as IL-6, IL-8, ICAM1, which promote inflammation and neutrophil recruitment . In addition, TLR activation can increase microvascular EC permeability, and the expression of intermediate products in the clotting cascade. Similar to the potential thrombogenic effect of neutrophil extracellular traps , microvascular thrombi could serve to trap microorganisms and thus inhibit the spread of infection. On the other hand, excessive EC inflammation and immune signaling could rapidly escalate leading to increased vascular leakage and a prothrombotic environment with subsequent sepsis. See for summary of EC-immune cell signaling. T Cell Activation T cell precursors originate from hematopoietic stem cells in bone marrow, where they begin their development. Immature T cells leave bone marrow, enter the blood and migrate to the thymus where they complete their final maturation and development, which includes intense thymic screening and selection of those T cells that can recognize one specific antigenic structure via their T cell receptor (TCR). Only 2-5% of all immature T cells entering the thymus survive selection. Once mature T cells leave the thymus they begin circulating throughout the body hunting for their cognate antigen displayed on the surface of an antigen presenting cell (APC) complexed with an MHC (major histocompatibility complex) molecule. The signaling events that can lead to optimal T cell activation are summarized below If an appropriate APC-displayed antigen is recognized by a given T cell, the TCR binds to the antigen as it is “presented” by the MHC complex on the surface of the APC. Formation of the TCR-MHC/Ag complex initiates activation (priming) of T cells. This initial T cell priming typically takes place in the secondary lymphoid tissues (e.g., lymph nodes, spleen, tonsils, or Peyer’s patches in the gut). In addition to TCR recognition and interaction with the MHC/Ag complex, various secondary (co- stimulatory) signals are required for T cells to become optimally activated and begin responding to the threat in an immunologically meaningful way. For helper T cells, the first of these secondary signals is provided by CD28, a receptor molecule constitutively expressed on T cells that binds to corresponding ligand B7 (CD80 or CD86) expressed on activated APCs. These secondary interactions (CD28/B7) stimulate the production of millions of genetically identical T cells (clonal expansion) that can recognize the initial antigen. To restrict a potentially uncontrollable T cell response, the interaction of the CD28 receptor on the T cell with B7 ligand expressed by the activated APC also induces production of CTLA-4 (CD152), which in turn competes directly with CD28 for the B7 ligand. This elegant molecular feedback loop thereby limits production of activation signals to the T cell, which harnesses and starts to de-escalate the immune response. TCRs on T cells must interact with MHC/Ag displayed on APCs with both high specificity and high avidity to activate effective immune responses. “Effective” interaction also includes T cell recognition of co- stimulatory antigen-induced molecules on APCs that ensure T cells are activated only by those APCs that have previously encountered the antigen, and responded appropriately. TCR interaction with APC-displayed MHC/Ag in the absence of co-stimulation inactivates T cells so they cannot respond effectively, and thus become anergic. Once the T cell has interacted with an appropriate MHC/ Ag complex, and co-stimulatory signals (signal 2) have been induced, further T cell activation is directed by the expression of specific cytokine profiles, which dictate the final type of response effector the T cell will become. For example, activated helper (CD4+) T cells can be directed to proceed toward one of three primary developmental pathways: Th1 type (cells exposed to the cytokine IL-12); Th2 (exposed to IL-4); or IL-17 ( exposed to IL-6 and IL-23). Each one of these CD4+ T cell variants performs specific functions in the tissue, which further customizes the immune response to better match the initial threat. Other cells present at the site of inflammation, such as epithelial and endothelial cells, neutrophils, and mast cell are also capable of releasing cytokines and other immune signals which further influences the course of T cell activation and proliferation during a given immune response . Antigen Presentation by the Endothelium Lymphatic endothelial cells (LECs) are typically the first to encounter antigen, immune cells, and cytokines in lymph nodes. It is not surprising therefore that LECs express MHC I and II molecules on their cell surface, which enable them to function as APCs. Antigen presentation potential is determined by the ability of cells to express class II MHC and co-stimulatory molecules. Due to their strategic location between circulating T cells and peripheral tissue sites of antigen exposure, ECs are ideally positioned to function as APCs [35-37]. For example, class II-MHC/Ag complexes regulate T cell activation and proliferation through production of cytokines, the co-stimulation of resting memory CD4+ T cells to produce Th-1 and Th-2 cytokine profiles , whereas, inhibitory signals mediated through PD-L1 expression on human umbilical vein endothelial cells (HUVECs) inhibit IL-2 and interferon (IFN)-γ production by T cells stimulated with phytohemagglutinin . Microvascular ECs in humans constitutively express MHC class I and II molecules in vivo, and MHC expression patterns in the endothelium of different vascular beds have been shown to vary in response to different environmental signals [40-42]. MHC class I and class II molecules can be induced in ECs by IFN-γ, human peripheral venular ECs express class II MHC constitutively. In general, microvascular ECs express class II MHC at sites of inflammation such as autoimmune reactions and allograft rejection [43-46]. MHC class II was shown to be expressed on microvasculature in unstimulated, untransplanted human hearts and was up-regulated following tissue rejection . In addition, Biedermann and Pober demonstrated that microvascular ECs were capable of activating CD4+ and CD8+ T cells. ECs also affect antigen presentation indirectly. For example, productive trafficking of dendritic cells (DC) requires strategic communication with both vascular and lymphatic endothelium. Circulating monocytes (DC precursors) express adhesion molecules and respond to various chemokines (e.g., stromal cell-derived factor) constitutively expressed in tissues, or induced by inflammatory processes. After antigen activation, recruitment from tissues, and exposure to immune signals DCs enter the blood or lymph and home to lymphoid tissues where they practice their specialty, antigen presentation. Vascular and lymphatic ECs are thought to play active roles in directing T cell and DC trafficking, though the specific molecular mechanisms involved remain unclear. The intimate proximity of ECs with T cells at the blood-tissue interface creates an ideal environment for extensive immune surveillance and requisite cellular interactions that could trigger a primary adaptive immune response. Although it is not known with certainty whether this specific type of activation of T cells by ECs occurs, it is well established that ECs are independently competent antigen presenting cells. For example, ECs have been shown to effectively present antigen to re- stimulate memory/effector T cells [48,49]. During this process, T cell membrane extensions protrude and form micro-contacts with antigen-presenting endothelial cells. It has been proposed that these T cell/EC micro- contacts serve as sensory projections to facilitate antigen recognition by T cells [50-53]. All vascular cells are capable of functioning as targets for, or sources of, cytokines which communicate with immune cells as well as many other cell and tissue types in the body. ECs display diverse biochemical and physiological responses depending on the particular cytokine profile they are exposed to. The course and rate of immune regulation is influenced by the nature of the eliciting stimulus, the extent of EC activation, and the particular EC microenvironment [54,55]. Together, these factors determine whether participating ECs ultimately facilitate, or impede, immune cell activation and trafficking . In addition, ECs derived from different vascular beds respond differently to cytokines. For example, TNF induces ICAM-1 expression on both arterial and venous adult human iliac ECs. However, VCAM-1 is expressed only on TNF-activated venous ECs which are, consequently, more effectively at binding VLA- 4+ (CD49a/CD29) T cells. Moreover, iliac arterial and venous ECs, co-stimulate IL-2 and IFN-γ secretion, but not IL-4 secretion, by human peripheral blood T cells or CD4+ T cell clones . During innate immune responses, inflammation-related signals such as tumor necrosis factor (TNF) activate ECs and upregulate their expression of cell surface adhesion molecules, such as P-selectin and PECAM-1, which stimulate leukocyte adhesion and transmigration across the basement membrane and into tissue spaces . T cell differentiation and migration to target tissues are essential for activation of adaptive immunity, and immune homeostasis requires localization of regulatory (suppressive) T cells (Tregs) to sites where immune reactions are occurring . Naive T cells recirculate primarily in secondary lymphoid tissue (e.g., spleen, lymph nodes, mucosa-associated lymphoid tissues), whereas antigen primed T cells and activated Tregs migrate to antigen-rich non-lymphoid tissue where they manifest their effector and regulatory responses [59,60]. In lymph nodes, antigen priming induces expression of surface receptors on T cells that mediate their trafficking to specific tissue and organ sites. This tissue-specific “homing” is further enhanced by the interaction of T cell receptors with relevant antigen displayed on endothelial cells. During adaptive immune response, a diverse repertoire of adhesion molecules and chemokines expressed on the surface of ECs interact with corresponding counter- receptors on migrating lymphocytes to direct their entry into tissue spaces . Differential expression of these molecules in endothelial cells of different organs enables selective recruitment of distinct lymphocyte subsets. Antigen priming induces T lymphocytes to express unique subsets of adhesion molecules and chemokine homing receptors. The specific cellular interactions and conditions in the local microenvironment that occur during priming enable antigen-exposed T cells to recognize and interact with organ-specific ECs, and migrate to distinct target tissues [62-64]. Co-stimulatory molecules such as CD80 and CD86 are required for optimal activation of naïve T cells, but ECs have generally been shown to express few if any co- stimulatory molecules. Biliana et al. reported constitutive expression of CD86 and ICOS ligand (ICOS-L) co- stimulatory molecules in human islet microvascular ECs, and demonstrated that functional CD86 expression facilitated adhesion and migration of previously activated memory CD4+ T cells. To date however, there has been no conclusive report demonstrating expression of both classic T cell co-stimulators CD80 and CD86 in EC cells [65,66]. Given the apparent lack of significant co-stimulatory molecule expression by ECs, it is surprising that interaction of antigen-presenting ECs with cognate T cells promotes migration of the engaging T cells, rather than inducing expected T cell anergy . ECs are considered “semiprofessional” or non-classical APCs because they have not been shown to have the capacity to prime naive T cells, but are capable of enhancing the activation of previously primed T cells, especially with respect to production of cytokine signals [68,69]. It is becoming increasingly clear that the endothelium plays many significant and complex roles in overall organismal homeostasis, including regulating and maintaining vascular system integrity, mediating immune cell trafficking, presenting antigen to T cells, and modulating immune responses. Given its vast internal surface area at the critical blood-tissue interface, and its remarkable phenotypic plasticity, the endothelium is ideally suited to provide continuous, real-time immune surveillance and response coordination. As we learn more about this dynamic and versatile internal shield, its central role as a global integrator of vascular-immune interaction will become increasingly evident, and provide fertile therapeutic potential for disease treatment and prevention. 2. Aird WC. Endothelial cell heterogeneity. Cold Spring Harbor perspectives in medicine. 2012 Jan 1;2(1):a006429. 3. Augustin HG, Kozian DH, Johnson RC. Differentiation of endothelial cells: analysis of the constitutive and activated endothelial cell phenotypes. Bioessays. 1994 Dec;16(12):901-6. 4. Cahill PA, Redmond EM. Vascular endothelium- gatekeeper of vessel health. Atherosclerosis. 2016 May 1;248:97-109. 5. Deanfield JE, Halcox JP, Rabelink TJ. Endothelial function and dysfunction: testing and clinical relevance. Circulation. 2007 Mar 13;115(10):1285-95. 6. Tousoulis D, Simopoulou C, Papageorgiou N, Oikonomou E, Hatzis G, Siasos G, Tsiamis E, Stefanadis C. Endothelial dysfunction in conduit arteries and in microcirculation. Novel therapeutic approaches. Pharmacology & therapeutics. 2014 Dec 1;144(3):253-67. 7. Gimbrone Jr MA, García-Cardeña G. Endothelial cell dysfunction and the pathobiology of atherosclerosis. Circulation research. 2016 Feb 19;118(4):620-36. 8. Boulanger CM. Endothelium. Arteriosclerosis,thrombosis, and vascular biology. 2016 Apr;36(4):e26-31. 9. Incalza MA, D’Oria R, Natalicchio A, Perrini S, Laviola L, Giorgino F. Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. Vascular pharmacology. 2018 Jan 1;100:1-9. 10. Rubin LL, Staddon JM. The cell biology of the blood- brain barrier. Annual review of neuroscience. 1999 Mar;22(1):11-28. 11. Crispe IN. The liver as a lymphoid organ. Annual review of immunology. 2009 Apr 23;27:147-63. 12. Daneman R, Prat A. The blood–brain barrier. Cold Spring Harbor perspectives in biology. 2015 Jan 1;7(1):a020412. 13. Wheway J, Obeid S, Couraud PO, Combes V, Grau GE. The brain microvascular endothelium supports T cell proliferation and has potential for alloantigenpresentation. PloS one. 2013 Jan 8;8(1):e52586. 14. Cancel LM, Ebong EE, Mensah S, Hirschberg C, Tarbell JM. Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model. Atherosclerosis. 2016 Sep 1;252:136-46. 15. Wang L, Huang X, Kong G, Xu H, Li J, Hao D, Wang T, Han S, Han C, Sun Y, Liu X. Ulinastatin attenuates pulmonary endothelial glycocalyx damage and inhibits endothelial heparanase activity in LPS-induced ARDS. Biochemical and biophysical research communications. 2016 Sep 16;478(2):669-75. 16. Rubio-Gayosso I, Platts SH, Duling BR. Reactive oxygen species mediate modification of glycocalyx during ischemia-reperfusion injury. American Journal of Physiology-Heart and Circulatory Physiology. 2006 Jun;290(6):H2247-56. 17. Becker BF, Chappell D, Bruegger D, Annecke T, Jacob M. Therapeutic strategies targeting the endothelial glycocalyx: acute deficits, but great potential. Cardiovascular research. 2010 May 11;87(2):300-10. 18. Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Cell biology of ischemia/reperfusion injury. InInternational review of cell and molecular biology 2012 Jan 1 (Vol. 298, pp. 229-317). Academic Press. 19. Kurzelewski M, Czarnowska E, Berêsewicz A. superoxide-and nitric oxide-derived species mediate. Journal of physiology and pharmacology. 2005;56(2):163- 78. 20. Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Ischemia/reperfusion. Comprehensive Physiology. 2011 Jan 17;7(1):113-70. 21. Kawai T, Akira S. Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. Immunity. 2011 May 27; 34(5):637-50. 22. Al-Soudi A, Kaaij MH, Tas SW. Endothelial cells: From innocent bystanders to active participants in immune responses. Autoimmunity reviews. 2017 Sep 1; 16(9):951-62. 23. Jiménez-Dalmaronia MJ, Gerswhin ME, Adamopoulos IE. The critical role of toll-like receptors-From microbial recognition to autoimmunity: A comprehensive review. Autoimmunity Reviews 2016 January 1; 15:1-8 24. Den Haan JM, Arens R, van Zelm MC. The activation of the adaptive immune system: cross-talk between antigen-presenting cells, T cells and B cells. Immunology letters. 2014 Dec 1; 162(2):103-12. 25. Opitz B, Eitel J, Meixenberger K, Suttorp N. Role of Toll-like receptors, NOD-like receptors and RIG-I-like receptors in endothelial cells and systemic infections. Thrombosis and haemostasis. 2009; 102(12):1103-9. 26. Salvadora B, Arranz A, Francisco S, Córdoba L, Punzón C, Llama M, Fresno M. Modulation of endothelial function by Toll like receptors. Pharmacol. Res. 2013. 108; 46-56. 27. Sturtzel C. Endothelial Cells. In The immunology of Cardiovascular Homeostasis and Pathology. 2017. pp. 71- 91. 28. Robertson J, Lang S, Lambert PA, Martin PE. Peptidoglycan derived from Staphylococcus epidermidis induces Connexin43 hemichannel activity with consequences on the innate immune response in endothelial cells. Biochemical Journal. 2010 Nov 15; 432(1):133-43. 29. Wilhelmsen K, Mesa KR, Prakash A, Xu F, Hellman J. Activation of endothelial TLR2 by bacterial lipoprotein upregulates proteins specific for the neutrophil response. Innate immunity. 2012 Aug; 18(4):602-16. 30. Fuchs TA, Brill A, Duerschmied D, Schatzberg D, Monestier M, Myers DD, Wrobleski SK, Wakefield TW, Hartwig JH, Wagner DD. Extracellular DNA traps promote thrombosis. Proceedings of the National Academy of Sciences. 2010 Sep 7; 107(36):15880-5. 31. Cheung KC, Ward EJ, Fu H, Marelli-Berg FM. Endothelial Cells: Immunological Aspects. eLS. Jan 22; 2018; 1-13. 32. Obst R. The timing of T cell priming and cycling. Frontiers in immunology. 2015 Nov 5; 6:563. 33. Rita M, Young MR. Endothelial cells in the eyes of an immunologist. Cancer Immunology, Immunotherapy. 2012 Oct 1; 61(10):1609-16. 34. Cohen JN, Guidi CJ, Tewalt EF, Qiao H, Rouhani SJ, Ruddell A, Farr AG, Tung KS, Engelhard VH. Lymph node-resident lymphatic endothelial cells mediate peripheral tolerance via Aire-independent direct antigen presentation. Journal of Experimental Medicine. 2010 Apr 12; 207(4):681-8. 35. Hirschberg H, Braathen LR, Thorsby E. Antigen presentation by vascular endothelial cells and epidermal Langerhans cells: the role of HLA-DR. Immunological reviews. 1982 Sep; 66(1):57-77. 36. Johnson DR. Endothelial cell-mediated antigen presentation. Transfusion Medicine and Hemotherapy. 2006; 33(1):58-70. 37. Taflin C, Favier B, Baudhuin J, Savenay A, Hemon P, Bensussan A, Charron D, Glotz D, Mooney N. Human endothelial cells generate Th17 and regulatory T cells under inflammatory conditions. Proceedings of the National Academy of Sciences. 2011 Feb 15; 108(7):2891-6. 38. Rodig N, Ryan T, Allen JA, Pang H, Grabie N, Chernova T, Greenfield EA, Liang SC, Sharpe AH, Lichtman AH, Freeman GJ. Endothelial expression of PD-L1 and PD-L2 down-regulates CD8+ T cell activation and cytolysis. European journal of immunology. 2003 Nov; 33(11):3117-26. 39. Pober JS, Collins T, Gimbrone Jr MA, Cotran RS, Gitlin JD, Fiers W, Clayberger C, Krensky AM, Burakoff SJ, Reiss CS. Lymphocytes recognize human vascular endothelial and dermal fibroblast Ia antigens induced by recombinant immune interferon. Nature. 1983 Oct; 305(5936):726-9. 40. Carman CV, Martinelli R. T Lymphocyte–endothelial interactions: emerging Understanding of Trafficking and Antigen-Specific immunity. Frontiers in immunology. 2015 Nov 24; 6:603. 41. Pober JS, Collins T, Gimbrone Jr MA, Libby P, Reiss CS. Inducible expression of class II major histocompatibility complex antigens and the immunogenicity of vascular endothelium. Transplantation. 1986 Feb 1; 41(2):141-6. 42. Pober JS, Tellides G. Participation of blood vessel cells in human adaptive immune responses. Trends in immunology. 2012 Jan 1; 33(1):49-57. 43. Goes N, Urmson J, Hobart M, Halloran PF. The unique role of interferon-γ in the regulation of MHC expression on arterial endothelium. Transplantation. 1996 Dec 27; 62(12):1889-94. 44. Manes TD, Pober JS. Antigen presentation by human microvascular endothelial cells triggers ICAM-1- dependent transendothelial protrusion by, fractalkine- dependent transendothelial migration of, effector memory CD4+ T cells. The Journal of Immunology. 2008 Jun 15; 180(12):8386-92. 45. Marelli-Berg FM, Frasca L, Weng L, Lombardi G, Lechler RI. Antigen recognition influences transendothelial migration of CD4+ T cells. The Journal of Immunology. 1999 Jan 15; 162(2):696-703. 46. Scott NA, Zhao Y, Krishnamurthy B, Mannering SI, Kay TW, Thomas HE. IFNγ-induced MHC class II expression on islet endothelial cells is an early marker of insulitis but is not required for diabetogenic CD4+ T cell migration. Frontiers in Immunology. 2018 Nov 28; (9) 2800. 47. Rose ML, Coles MI, Griffin RJ, Pomerance AR, Yacoub MH. Expression of class I and class II major histocompatibility antigens in normal and transplanted human heart. Transplantation. 1986 Jun; 41(6):776-80. 48. Biedermann BC, Pober JS. Human endothelial cells induce and regulate cytolytic T cell differentiation. The Journal of Immunology. 1998 Nov 1;161(9):4679-87. 49. Wagner CR, Vetto RM, Burger DR. The mechanism of antigen presentation by endothelial cells. Immunobiology. 1984 Dec 1;168(3-5):453-69. 50. Xu L, Ding W, Stohl LL, Zhou XK, Azizi S, Chuang E, Lam J, Wagner JA, Granstein RD. Regulation of T helper cell responses during antigen presentation by norepinephrine-exposed endothelial cells. Immunology. 2018 May; 154(1):104-21. 51. Dengler TJ, Pober JS. Human vascular endothelial cells stimulate memory but not naive CD8+ T cells to differentiate into CTL retaining an early activation phenotype. The Journal of Immunology. 2000 May 15; 164(10):5146-55. 52. Carman CV. Mechanisms for transcellular diapedesis: probing and pathfinding by invadosome-like protrusions. J Cell Sci. 2009 Sep 1; 122(17):3025-35. 53. Sage PT, Varghese LM, Martinelli R, Sciuto TE, Kamei M, Dvorak AM, Springer TA, Sharpe AH, Carman CV. Antigen recognition is facilitated by invadosome- like protrusions formed by memory/effector T cells. The Journal of Immunology. 2012 Apr 15; 188(8):3686-99. 54. Johnson DR, Hauser IA, Voll RE, Emmrich F. Arterial and venular endothelial cell costimulation of cytokine secretion by human T cell clones. Journal of leukocyte biology. 1998 May; 63(5):612-9. 55. Zhang, C. The role of inflammatory cytokines in endothelial dysfunction. Basic Res Cardiol. 2008 Sep; 103(5):398-406. 56. Hauser IA, Johnson DR, Madri JA. Differential induction of VCAM-1 on human iliac venous and arterial endothelial cells and its role in adhesion. The Journal of Immunology. 1993 Nov 15; 151(10):5172-85. 57. Privratsky JR, Newman PJ. PECAM-1: regulator of endothelial junctional integrity. Cell and tissue research. 2014 Mar 1; 355(3):607-19. 58. Josefowicz SZ, Lu LF, Rudensky AY. Regulatory T cells: mechanisms of differentiation and function. Annual review of immunology. 2012 Apr 23; 30:531-64. 59. Walling BL, Kim M. LFA-1 in T cell migration and differentiation. Frontiers in immunology. 2018 May 3; 9-952. 60. Fu H, Wang A, Mauro C, Marelli-Berg F. T lymphocyte trafficking: molecules and mechanisms. Front Biosci. 2013 Jan 1;18:422-40. 61. Chimen M, Apta BH, Mcgettrick HM. Introduction: T cell trafficking in inflammation and immunity. InT-Cell Trafficking 2017 (pp. 73-84). Humana Press, New York, NY. 62. Ley K, Kansas GS. Selectins in T-cell recruitment to non-lymphoid tissues and sites of inflammation. Nature Reviews Immunology. 2004 May; 4(5):325-36. 63. Butcher EC, Picker LJ. Lymphocyte homing and homeostasis. Science. 1996 Apr 5; 272(5258):60-7. 64. Sigmundsdottir H, Butcher EC. Environmental cues, dendritic cells and the programming of tissue-selective lymphocyte trafficking. Nature immunology. 2008 Sep; 9(9):981-87. 65. Lewis M, Tarlton JF, Cose S. Memory versus naive T-cell migration. Immunology and cell biology. 2008 Mar;86(3):226-31. 66. Epperson DE, Pober JS. Antigen-presenting function of human endothelial cells. Direct activation of resting CD8 T cells. The Journal of Immunology. 1994 Dec 15; 153(12):5402-12. 67. Lozanoska-Ochser B, Klein NJ, Huang GC, Alvarez RA, Peakman M. Expression of CD86 on human islet endothelial cells facilitates T cell adhesion and migration. The Journal of Immunology. 2008 Nov 1;181 (9):6109-16. 68. Ma W, Pober JS. Human endothelial cells effectively costimulate cytokine production by, but not differentiation of, naive CD4+ T cells. The Journal of Immunology. 1998 Sep 1; 161(5):2158-67. 69. Greening JE, Tree TI, Kotowicz KT, van Halteren AG, Roep BO, Klein NJ, Peakman M. Processing and presentation of the islet autoantigen GAD by vascular endothelial cells promotes transmigration of autoreactive T-cells. Diabetes. 2003 Mar 1; 52(3):717-25.	2	20	1	0	1	0	0.887817	2	8,092
\|This category reflects the organization of International Statistical Classification of Diseases and Related Health Problems, 10th Revision.\| Generally, diseases outlined within the ICD-10 codes F30-F39 within Chapter V: Mental and behavioural disorders should be included in this category. Mood disorder is the term given for a group of diagnoses in the DSM IV TR classification system where a disturbance in the person's emotional mood is hypothesised to be the main underlying feature. The classification is known as mood (affective) disorders in ICD 10. English psychiatrist Henry Maudsley proposed an overarching category of affective disorder. The term was then replaced by mood disorder, as the latter term refers to the underlying or longitudinal emotional state, whereas the former refers to the external expression observed by others. Two groups of mood disorders are broadly recognized; the division is based on whether the person has ever had a manic or hypomanic episode. Thus, there are depressive disorders, of which the best known and most researched is major depressive disorder commonly called clinical depression or major depression, and bipolar disorder, formerly known as "manic depression" and described by intermittent periods of manic and depressed episodes. This category has the following 2 subcategories, out of 2 total. Pages in category "Mood disorders" The following 66 pages are in this category, out of 66 total. - Medicine:Behavioral theories of depression - Medicine:Biology of bipolar disorder - Biology:Biology of depression - Medicine:Bipolar disorder - Medicine:Bipolar disorder in children - Medicine:Bipolar I disorder - Medicine:Bipolar II disorder - Social:Bipolar Spectrum Diagnostic Scale - Philosophy:Reduced affect display	3	2	0	0	0	2	0.945546	2	356
What is edema? Edema is the medical term for swelling caused by fluid trapped in your body’s tissues. Edema happens most often in your feet, ankles and legs, but can affect other parts of your body, such as your face, hands and abdomen. Who does edema affect? Edema can affect anyone, but the condition most often affects people who are pregnant and adults who are 65 years or older. How common is edema? Edema is common because there are many causes associated with the condition. Mild cases of edema go away on their own, so the exact rate of occurrence is unknown. How does edema affect my body? Edema will cause parts of your body to increase in size (swell), which might prevent you from completing your daily tasks. Simple lifestyle changes like elevating the swollen part of your body or moving around if you were sitting or standing for a long period of time can reduce swelling and help you feel better. Sometimes edema is a symptom of an underlying health condition, so contact your healthcare provider if you experience symptoms of edema. Symptoms and Causes What are the symptoms of edema? A symptom of edema is swelling in your body. Swelling occurs when a part of your body gets bigger because there is a buildup of fluid in your tissues. Swelling can happen anywhere on your body but most often affects your feet, ankles and legs. Symptoms of swelling include: - An area of your body is larger than it was a day ago. - The skin over the swollen area looks stretched and shiny. - Difficulty walking if your legs, ankles or feet swell. - You may be coughing or have trouble breathing. - You feel full or tightness in your swollen body part. - Mild pain or a sore feeling in the affected area. What causes edema? After your healthcare provider makes an edema diagnosis, their next step is to identify what caused fluid to build up in your tissues. There are several possible causes for an edema diagnosis including: - Gravity: If you spend a lot of time sitting or standing in one place for too long, water naturally pulls down into your arms, legs and feet (dependent edema). - Weakened valves of your veins (venous insufficiency): When the valves in your veins are weak, it is hard for your veins to push blood back up to your heart, and leads to varicose veins and a buildup of fluid in the legs. - Underlying medical conditions: Conditions like heart failure and lung, liver, kidney and thyroid diseases have edema as a symptom. - Side effects from medication: Some drugs, like blood pressure or pain management medications, have edema as a side effect. - Poor nutrition: If you aren’t eating a well-balanced diet or if you eat a lot of foods high in salt (sodium), fluid could build up in different parts of your body. - Pregnancy: Swelling in your legs during pregnancy occurs as the uterus puts pressure on your blood vessels in the lower trunk of your body. - Compromised immune system: An allergic reaction, infection, burns, trauma or clots can lead to edema. Diagnosis and Tests How is edema diagnosed? Your healthcare provider will give a physical examination to diagnose edema, followed by diagnostic tests to find the cause. They will look for swelling, especially on parts of your body where your skin has a shiny or stretched appearance. What is edema grading? Edema grading is a scale used to identify the severity of your edema diagnosis and estimate how much fluid built up in your tissues. Your healthcare provider will test an area of your body for edema by gently pressing their finger on a swollen area of your skin for five to 15 seconds (pitting test). After they release pressure, a dimple (pit) will appear in your skin. The pit indicates that there is fluid built up in your tissues. The edema grading scale measures how quickly the dimple goes back to normal (rebound) after a pitting test. The scale includes: - Grade 1: Immediate rebound with 2 millimeter (mm) pit. - Grade 2: Less than 15-second rebound with 3 to 4 mm pit. - Grade 3: Rebound greater than 15 seconds but less than 60 seconds with 5 to 6 mm pit. - Grade 4: Rebound between 2 to 3 minutes with an 8 mm pit. Management and Treatment How is edema treated? Treatment for edema varies based on the cause, especially if the cause relates to an underlying health condition. For example: - If lung disease causes edema, such as emphysema or chronic bronchitis, your healthcare provider will recommend quitting smoking if you smoke. - If edema occurs with chronic heart failure, your provider will recommend lifestyle changes to treat your diagnosis by monitoring your weight, fluid intake and salt intake. Your provider might recommend cutting back on the amount of alcohol you drink. - If edema is a side effect of a medication you are taking, your provider might stop or lower the dosage of your medication to resolve the swelling. Do not stop taking your medication unless your provider tells you to do so. Treatment to reduce swelling In addition to treating the underlying cause of edema, there are a few steps you can take to keep fluid from building up in your body: - When you are sitting or lying down, put a pillow under your legs to keep them elevated above the level of your heart. - Do not sit or stand for long periods without moving or go on short walks. - Wear support socks, stockings or sleeves, which put pressure on parts of your body to keep fluids from collecting there. Edema shoes are available for people who experience chronic edema and need adjustable footwear for swelling. - Reduce the amount of salt in your diet. - Follow your doctor’s directions for taking medications. Your doctor might want you to take a diuretic (commonly called a "water pill"), which helps your body get rid of excess fluid. What can’t I eat with edema? In some cases, the cause of edema could be too much salt in your diet. Salt causes your body to retain water, which could leak into your tissues and cause swelling. Making lifestyle changes to reduce the amount of salt in your diet could improve your edema diagnosis. How soon after treatment will I feel better? Depending on the cause of your diagnosis, edema could be temporary or permanent. Swelling normally lasts for a few days. In the first two days, you will experience the most swelling, and it should start to reduce by the third day. Following treatment from your healthcare provider reduces the amount of swelling you might experience. If your swelling doesn’t go away after a few days of treatment, talk to your healthcare provider. How can I prevent edema? Sometimes, you can’t prevent what caused edema if it is the result of an underlying health condition like heart failure, liver or kidney disease, but you can work with your healthcare provider to manage symptoms. If the cause of edema is too much salt intake, adjusting your diet to reduce the amount of salt in the foods you eat will prevent edema. You can also prevent edema by moving around more frequently. Sitting or standing without moving could cause fluid to build up in your tissues. If you notice you’ve been sitting for a long period of time and you’re able to, get up or move your body around; it will reduce the likelihood of swelling. Outlook / Prognosis What can I expect if I have edema? It's very important to see your healthcare provider if you experience edema or swelling in your body. Edema can stretch your skin and if not treated, swelling could increase and cause serious health problems. Edema can be a short-term or long-term condition, depending on its cause. Treatment is available to help you manage any underlying conditions that might cause edema or you can make simple lifestyle changes to reduce swelling and fluid buildup in your body. How do I take care of myself? If you have edema, take steps to reduce swelling by: - Making lifestyle changes to stop smoking or changing your diet. - Moving around more often. - Elevating your legs when lying down or sitting. - Wearing compression socks, sleeves or stockings. It is important to protect any swollen areas of your body from additional pressure, injury and extreme temperatures. Injury to the skin over swollen areas takes longer to heal and is more likely to become infected. When should I see my healthcare provider? Call your healthcare provider immediately if you experience: - Pain or discolored skin in a swollen area. - An open sore on a swollen area. - Shortness of breath. - Swelling of only one limb. - Difficulty walking or you have trouble moving. What questions should I ask my doctor? - What caused my edema? - Do I need to reduce the amount of salt in my diet? - Are there side effects to the treatment? - Do I need to wear compression socks to reduce swelling in my ankles? Frequently Asked Questions What is the ICD-10 code for edema? The diagnostic ICD-10-CM (International Classification of Diseases, Tenth Revision, Clinical Modification) code for edema is R60.9. For healthcare providers, this code describes the diagnosis, symptoms and necessity for treatment. The code is used by all healthcare providers in the U.S. A note from Cleveland Clinic Edema is common and ranges in severity for each person diagnosed with the condition based on the cause. If you are pregnant, it is normal to experience swelling as your due date nears. Normally, edema will go away on its own if you have a mild case, and medication and treatment are available if you have a more severe case. If are not pregnant and you notice that you have unexpected swelling in a part of your body, contact your healthcare provider for an exam. Edema could be a sign of an underlying health condition and early diagnosis and treatment could lead to the best prognosis. Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy	2	8	0	0	0	2	0.948057	2	2,186
Millions of people receive medical treatment for injuries every day. Injured persons often focus on their pain and the implications of their injuries but don’t always consider the medical paperwork resulting from their treatment. The International Classification of Diseases (ICD) codes attached to medical paperwork impact treatment and billing. Patients may need to learn about ICD-10 codes when they need medical care. What are ICD-10 codes? The origins of ICD codes stretch back to the 19th century. Statistician Jacque Bertillon introduced the Bertillon Classification of Causes of Death in 1891. These codes made it easier to develop statistical information about the various causes of death. The American Public Health Association recommended that the U.S. adopt Bertillon’s system in 1898. The Centers for Disease Control and Prevention’s (CDC’s) National Center for Health Statistics expanded Bertillon’s system, producing a clinical modification known as ICD-10-CM. The Centers for Medicare and Medicaid Services (CMS) developed the ICD-10-PCS, the procedure coding system. Who uses ICD-10 codes? The World Health Organization (WHO) states that approximately 117 countries use ICD codes to report death statistics. Medical professionals, health information managers, and medical billers use the ICD-10 system every day. Insurance companies, CMS, and government organizations may also use ICD-10 codes when processing claims or making healthcare decisions. Personal injury attorneys may refer to ICD-10 codes when filing client lawsuits. A car accident attorney will ensure the hospital used the correct codes when filing insurance claims to prevent complications with their client’s case. Suppose the ICD-10 code for motor vehicle collision is used instead of the ICD-10 code for motor vehicle accident during pregnancy. In that case, a pregnant client may have difficulty pursuing compensation for complications with their pregnancy stemming from the accident. Why would a patient need to understand ICD-10 codes? Typically, ICD-10 codes appear on the billing information sent to CMS or your insurance company. Healthcare providers also use ICD-10 codes when requesting pre-approval for future medical services. You might need to look up ICD codes to ensure they’re accurate if your insurance company denied a claim or pre-approval request. ICD-10-CM and ICD-10-PCS codes have multiple characters. A medical biller or claims processor can mistakenly enter the wrong code, leading to financial complications if the incorrect code prompts your insurer to deny your claim. Understanding ICD-10 Codes Anyone who doesn’t use ICD-10 codes in their career may find the codes confusing. Fortunately, ICD-10 codes use a categorization system, enabling them to pass on specific information with a relatively short code. Suppose you’re in an automobile accident. Your ICD-10 code will depend on your status and the nature of your injuries. Consequently, there isn’t one single “ICD-10 code for motor vehicle accident” for every MVA. Some MVAs would receive an “ICD-10 code for motor vehicle accident unspecified,” or a code identifying the type of accident, such as an “ICD-10 code for car driver injured in rollover accident.” When creating an ICD-10 code for motor vehicle accident with injury, the first thing to consider is whether to use an S, T, or V code. ICD S Codes: Localized Injury ICD-10-CM S codes identify the area of your body where you sustained the injury, the injured body part, and details about the injury. Each S code begins with a correlation to the region where you sustained the injury. For example, neck injuries would receive a code that’s first two digits are S1. The third digit in the code adds information about the injuries sustained. Suppose you had a cut on your neck. Your code would be S11. ICD T Codes T codes identify injuries affecting multiple body parts. Examples include frostbite, poisonings, or multiple injuries. T07 refers to multiple body injuries, while T33 and T34 are codes for injuries from frostbite. ICD V Codes: Transportation Accidents V codes clarify the mode of transportation the person was using when injured. Since 0 identifies the person as a pedestrian, pedestrians would receive a code beginning with V0. Your pedestrian accident attorney will want to ensure your ICD codes are correct while negotiating settlements with insurance companies and at-fault drivers. A car accident lawyer would want to ensure that a car passenger received a V4 code. The third digit in V codes offers information about the type of accident. If a driver struck a deer, the third digit would be 0. If the vehicle collided with a train, the third digit would be 5. V codes receive a fourth digit that clarifies the person’s role. The “ICD-10 code for motor vehicle accident driver” would have a 0 for a non-traffic accident or 5 for a traffic accident. Non-traffic accidents are accidents that don’t occur while the vehicle operates on a roadway. Who assigns ICD-10 codes? Medical facilities and healthcare providers assign ICD-10 codes when patients receive treatment. The ICD-10 codes can identify the patient’s diagnosis, the cause of their medical issues, and the treatment provided. These codes appear on paperwork processed by insurance companies. Insurance companies use these codes to determine whether to authorize payment for treatment. What are the benefits of using ICD-10 codes? ICD-10 codes bypass language barriers. With a few digits, insurance companies, statisticians, and medical professionals have access to clear medical information without using translators. Using a shared, standardized system ensures that people making healthcare decisions operate with the same information. The codes clarify causes of death or illness, enabling healthcare providers to identify viral outbreaks and pandemics. ICD-10 codes ensure decision-makers have faster access to accurate information about health trends, enabling them to act promptly when health concerns arise. How can you look up ICD-10 codes? ICD-10-CM Diagnosis Codes. (2022). ICD-10 Resources. (2022). Importance of ICD. (2022). Torrey, Trisha. (2022). ICD 10 Codes and How To Look Them Up.	4	4	0	0	0	4	0.702035	4	1,354
Esclerosis lateral amiotrófica · Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease) Classification and external resources Template:Px This MRI (parasagittal FLAIR) demonstrates increased T2 signal within the posterior part of the internal capsule and can be tracked to the subcortical white matter of the motor cortex, outlining the corticospinal tract, consistent with the clinical diagnosis of ALS. ICD-10 G122 ICD-9 335.20 OMIM 105400 EnfermedadesDB 29148 Medline Plus 000688 eMedicine neuro/14 emerg/24 pmr/10 MeSH D000690 Amyotrophic lateral sclerosis (ESCLEROSIS LATERAL AMIOTRÓFICA) – also referred to as motor neurone disease in some British Commonwealth countries and as Lou Gehrig's disease's disease in North America – is a debilitating disease with varied etiology characterized by rapidly progressive weakness, muscle atrophy and fasciculations, muscle spasticity, difficulty speaking (dysarthria), difficulty swallowing (dysphagia), and decline in breathing ability. ALS is the most common of the five motor neuron diseases. Contenido 1 Signs and symptoms 1.1 Initial symptoms 1.2 Disease progression and spread 1.3 Late stage disease symptoms 2 Cause 3 Patofisiología 3.1 SOD1 3.2 Otros factores 4 Diagnóstico 5 Tratamiento 5.1 Slowing progression 5.2 Disease management 5.2.1 Pharmaceutical treatments 5.2.2 Physical, occupational and speech therapy 5.2.3 Feeding and nutrition 5.2.4 Breathing support 5.2.5 Cuidados paliativos 6 Epidemiología 7 Etimología 8 Historia 9 Investigación clínica 10 Ver también 11 Referencias 12 Otras lecturas 13 External links Signs and symptoms The disorder causes muscle weakness and atrophy throughout the body caused by degeneration of the upper and lower motor neurons. Unable to function, the muscles weaken and atrophy. Affected individuals may ultimately lose the ability to initiate and control all voluntary movement, although bladder and bowel sphincters and the muscles responsible for eye movement are usually, pero no siempre, spared. Cognitive function is generally spared for most patients, although some (acerca de 5%) also have frontotemporal dementia. A higher proportion of patients (30-50%) also have more subtle cognitive changes which may go unnoticed, but are revealed by detailed neuropsychological testing. Sensory nerves and the autonomic nervous system are generally unaffected, meaning the majority of people with ALS will maintain sight, audiencia, touch, oler, and taste. Initial symptoms The earliest symptoms of ALS are typically obvious weakness and/or muscle atrophy. Other presenting symptoms include muscle fasciculation (twitching), cramping, or stiffness of affected muscles; muscle weakness affecting an arm or a leg; and/or slurred and nasal speech. The parts of the body affected by early symptoms of ALS depend on which motor neurons in the body are damaged first. Sobre 75% of people contracting the disease experience "limb onset" ESCLEROSIS LATERAL AMIOTRÓFICA, es decir,, first symptoms in the arms or legs. Patients with the leg onset form may experience awkwardness when walking or running or notice that they are tripping or stumbling, often with a "dropped foot" which drags gently along the ground. Arm-onset patients may experience difficulty with tasks requiring manual dexterity such as buttoning a shirt, escritura, or turning a key in a lock. Occasionally, the symptoms remain confined to one limb for a long period of time or for the whole length of the illness; this is known as monomelic amyotrophy. Sobre 25% of cases are "bulbar onset" ESCLEROSIS LATERAL AMIOTRÓFICA. These patients first notice difficulty speaking clearly or swallowing. Speech may become slurred, nasal in character, or quieter. Other symptoms include difficulty swallowing and loss of tongue mobility. A smaller proportion of patients experience "respiratory onset" ESCLEROSIS LATERAL AMIOTRÓFICA, where the intercostal muscles that support breathing are affected first. A small proportion of patients may also present with what appears to be frontotemporal dementia, but later progresses to include more typical ALS symptoms. Tiempo extraordinario, patients experience increasing difficulty moving, swallowing (dysphagia), and speaking or forming words (dysarthria). Symptoms of upper motor neuron involvement include tight and stiff muscles (spasticity) and exaggerated reflexes (hyperreflexia) including an overactive gag reflex. An abnormal reflex commonly called Babinski's sign also indicates upper motor neuron damage. Symptoms of lower motor neuron degeneration include muscle weakness and atrophy, muscle cramps, and fleeting twitches of muscles that can be seen under the skin (fasciculations). Around 15–45% of patients experience pseudobulbar affect, también conocido como "emotional lability", which consists of uncontrollable laughter, crying or smiling, attributable to degeneration of bulbar upper motor neurons resulting in exaggeration of motor expressions of emotion. To be diagnosed with ALS, patients must have signs and symptoms of both upper and lower motor neuron damage that cannot be attributed to other causes. Disease progression and spread Although the order and rate of symptoms varies from person to person, eventually most patients are not able to walk, get out of bed on their own, or use their hands and arms. The rate of progression can be measured using an outcome measure called the "ALS Functional Rating Scale (Revised)", a 12-item instrument administered as a clinical interview or patient-reported questionnaire that produces a score between 48 (normal function) y 0 (severe disability). Though there is a high degree of variability and a small percentage of patients have much slower disease, de media, patients lose about 1 FRS point per month. Regardless of the part of the body first affected by the disease, muscle weakness and atrophy spread to other parts of the body as the disease progresses. In limb-onset ALS, symptoms usually spread from the affected limb to the opposite limb before affecting a new body region, whereas in bulbar-onset ALS symptoms typically spread to the arms before the legs. Disease progression tends to be slower in patients who are younger than 40 at onset, have disease restricted primarily to one limb, and those with primarily upper motor neuron symptoms. En cambio, progression is faster and prognosis poorer in patients with bulbar-onset disease, respiratory-onset disease, and frontotemporal dementia. Late stage disease symptoms Difficulty swallowing and chewing making eating normally very difficult and increase the risk of choking or aspirating food into the lungs. In later stages of the disease, aspiration pneumonia and maintaining a healthy weight can become a significant problem and may require insertion of a feeding tube. As the diaphragm and intercostal muscles (rib cage) that support breathing weaken, measures of lung function such as forced vital capacity and inspiratory pressure diminish. In respiratory onset ALS, this may occur before significant limb weakness is apparent. External machines such as bilevel positive pressure ventilation (frequently referred to by the tradename BiPAP) are frequently used to support breathing, first at night, and later during the daytime as well. BiPAP is only a temporary remedy, sin embargo, and it is recommended that long before BiPAP stops being effective, patients should decide whether to have a tracheotomy and long term mechanical ventilation. En este punto, some patients choose palliative hospice care. Most people with ALS die of respiratory failure or pneumonia. Although respiratory support can ease problems with breathing and prolong survival, it does not affect the progression of ALS. Most people with ALS die from respiratory failure, usually within three to five years from the onset of symptoms. The median survival time from onset to death is around 39 Meses, y sólo 4% survive longer than 10 years. The best-known person with ALS, Stephen Hawking, has lived with the disease for more than 50 años, though his is an unusual case. Cause For patients without a family history of the disease, who include ~95% of cases, there is no known cause for ALS. Potential causes for which there is inconclusive evidence includes head trauma, military service, and participation in contact sports. Many other potential causes, including chemical exposure, electromagnetic field exposure, ocupación, physical trauma, and electric shock, have been investigated but without consistent findings. There is a known hereditary factor in familial ALS (FALS), where the condition is known to run in families. Recientemente, a genetic abnormality known as a hexanucleotide repeat was found in a region called C9ORF72, which is associated with ALS combined with frontotemporal dementia ALS-FTD, and accounts for some 6% of cases of ALS among white Europeans. The high degree of mutations found in patients that appeared to have "esporádico" enfermedad, es decir. without a family history, suggests that genetics may play a more significant role than previously thought and that environmental exposures may be less relevant. A defect on chromosome 21 (coding for superoxide dismutase) is associated with approximately 20% of familial cases of ALS, or about 2% of ALS cases overall. This mutation is believed to be autosomal dominant, and has over a hundred different forms of mutation. The most common ALS-causing SOD1 mutation in North American patients is A4V, characterized by an exceptionally rapid progression from onset to death. The most common mutation found in Scandinavian countries, D90A, is more slowly progressive than typical ALS and patients with this form of the disease survive for an average of 11 years. Mutations in several genes have also been linked to various types of ALS, and the currently identified associations are shown in the table below: Genetic associations include Type OMIM Gene Locus ALS1 105400 SOD1 21q22.1 ALS2 205100 ALS2 2q33.1 ALS3 606640 ? 18q21 ALS4 602433 SETX 9q34.13 ALS5 602099 ? 15q15.1-q21.1 ALS6 608030 FUS 16p11.2 ALS7 608031 ? 20p13 ALS8 608627 VAPB 20q13.3 ALS9 611895 ANG 14q11.2 ALS10 612069 TARDBP 1p36.2 ALS11 612577 FIG4 6q21 ALS12 613435 OPTN 10p15-p14 ALS13 183090 ATXN2 12q24.12 ALS14 613954 VCP 9p13.3 Pathophysiology The defining feature of ALS is the death of both upper and lower motor neurons in the motor cortex of the brain, the brain stem, and the spinal cord. Prior to their destruction, motor neurons develop proteinaceous inclusions in their cell bodies and axons. This may be partly due to defects in protein degradation. These inclusions often contain ubiquitin, and generally incorporate one of the ALS-associated proteins: SOD1, TAR DNA binding protein (TDP-43, or TARDBP), or FUS. SOD1 It has been suggested that this article or section be merged into [[::SOD1\|SOD1]]. (Discutir) The cause of ALS is not known, though an important step toward determining the cause came in 1993 when scientists discovered that mutations in the gene that produces the Cu/Zn superoxide dismutase (SOD1) enzyme were associated with some cases (aproximadamente 20%) of familial ALS. This enzyme is a powerful antioxidant that protects the body from damage caused by superoxide, a toxic free radical generated in the mitochondria. Free radicals are highly reactive molecules produced by cells during normal metabolism again largely by the mitochondria. Free radicals can accumulate and cause damage to both mitochondrial and nuclear DNA and proteins within cells. Hasta la fecha, sobre 110 different mutations in SOD1 have been linked with the disease, some of which have a very long clinical course (p. ej.. H46R), while others, such as A4V, being exceptionally aggressive. Evidence suggests that failure of defenses against oxidative stress up-regulates programmed cell death (apoptosis), among many other possible consequences. Although it is not yet clear how the SOD1 gene mutation leads to motor neuron degeneration, researchers have theorized that an accumulation of free radicals may result from the faulty functioning of this gene. Current research, sin embargo, indicates that motor neuron death is not likely a result of lost or compromised dismutase activity, suggesting mutant SOD1 induces toxicity in some other way (a gain of function). Studies involving transgenic mice have yielded several theories about the role of SOD1 in mutant SOD1 familial amyotrophic lateral sclerosis. Mice lacking the SOD1 gene entirely do not customarily develop ALS, although they do exhibit an acceleration of age-related muscle atrophy (sarcopenia) and a shortened lifespan (see article on superoxide dismutase). This indicates that the toxic properties of the mutant SOD1 are a result of a gain in function rather than a loss of normal function. Además, aggregation of proteins has been found to be a common pathological feature of both familial and sporadic ALS (see article on proteopathy). Curiosamente, in mutant SOD1 mice (most commonly, the G93A mutant), aggregates (misfolded protein accumulations) of mutant SOD1 were found only in diseased tissues, and greater amounts were detected during motor neuron degeneration. It is speculated that aggregate accumulation of mutant SOD1 plays a role in disrupting cellular functions by damaging mitochondria, proteasomes, protein folding chaperones, or other proteins. Any such disruption, if proven, would lend significant credibility to the theory that aggregates are involved in mutant SOD1 toxicity. Critics have noted that in humans, SOD1 mutations cause only 2% or so of overall cases and the etiological mechanisms may be distinct from those responsible for the sporadic form of the disease. Hasta la fecha, the ALS-SOD1 mice remain the best model of the disease for preclinical studies but it is hoped that more useful models will be developed. Other factors Studies also have focused on the role of glutamate in motor neuron degeneration. Glutamate is one of the chemical messengers or neurotransmitters in the brain. Scientists have found that, compared to healthy people, ALS patients have higher levels of glutamate in the serum and spinal fluid. Riluzole is currently the only FDA approved drug for ALS and targets glutamate transporters. It only has a modest effect on survival, sin embargo, suggesting that excess glutamate is not the sole cause of the disease. Diagnosis No test can provide a definite diagnosis of ALS, although the presence of upper and lower motor neuron signs in a single limb is strongly suggestive. En lugar de, the diagnosis of ALS is primarily based on the symptoms and signs the physician observes in the patient and a series of tests to rule out other diseases. Physicians obtain the patient's full medical history and usually conduct a neurologic examination at regular intervals to assess whether symptoms such as muscle weakness, atrophy of muscles, hyperreflexia, and spasticity are getting progressively worse. Archivo:ALS cross.jpg MRI (axial FLAIR) demonstrates increased T2 signal within the posterior part of the internal capsule, consistent with the clinical diagnosis of ALS. Because symptoms of ALS can be similar to those of a wide variety of other, more treatable diseases or disorders, appropriate tests must be conducted to exclude the possibility of other conditions. One of these tests is electromyography (EMG), a special recording technique that detects electrical activity in muscles. Certain EMG findings can support the diagnosis of ALS. Another common test measures nerve conduction velocity (NCV). Specific abnormalities in the NCV results may suggest, por ejemplo, that the patient has a form of peripheral neuropathy (damage to peripheral nerves) or myopathy (muscle disease) rather than ALS. The physician may order magnetic resonance imaging (MRI), a noninvasive procedure that uses a magnetic field and radio waves to take detailed images of the brain and spinal cord. Although these MRI scans are often normal in patients with ALS, they can reveal evidence of other problems that may be causing the symptoms, such as a spinal cord tumor, multiple sclerosis, a herniated disk in the neck, syringomyelia, or cervical spondylosis. Based on the patient's symptoms and findings from the examination and from these tests, the physician may order tests on blood and urine samples to eliminate the possibility of other diseases as well as routine laboratory tests. En algunos casos, por ejemplo, if a physician suspects that the patient may have a myopathy rather than ALS, a muscle biopsy may be performed. Infectious diseases such as human immunodeficiency virus (VIH), human T-cell leukaemia virus (HTLV), Lyme disease, syphilis and tick-borne encephalitis viruses can in some cases cause ALS-like symptoms. Neurological disorders such as multiple sclerosis, post-polio syndrome, multifocal motor neuropathy, CIDP, and spinal muscular atrophy can also mimic certain facets of the disease and should be considered by physicians attempting to make a diagnosis. ALS must be differentiated from the “ALS mimic syndromes” which are unrelated disorders that may have a similar presentation and clinical features to ALS or its variants. Because of the prognosis carried by this diagnosis and the variety of diseases or disorders that can resemble ALS in the early stages of the disease, patients should always obtain a second neurological opinion. Sin embargo, most cases of ALS are readily diagnosed and the error rate of diagnosis in large ALS clinics is less than 10%. En un estudio, 190 patients who met the MND / ALS diagnostic criteria, complemented with laboratory research in compliance with both research protocols and regular monitoring. Thirty of these patients (15.78%) had their diagnosis completely changed, during the clinical observation development period. In the same study, three patients had a false negative diagnoses, myasthenia gravis (MG), an auto-immune disease. MG can mimic ALS and other neurological disorders leading to a delay in diagnosis and treatment. MG is eminently treatable; ALS is not. Myasthenic syndrome, also known as Lambert-Eaton syndrome (LES),can mimic ALS and its initial presentation can be similar to that of MG. Treatment Slowing progression Riluzole (Rilutek) is the only treatment that has been found to improve survival but only to a modest extent. It lengthens survival by several months, and may have a greater survival benefit for those with a bulbar onset. It also extends the time before a person needs ventilation support. Riluzole does not reverse the damage already done to motor neurons, and people taking it must be monitored for liver damage (occurring in ~10% of people taking the drug). It is approved by Food and Drug Administration (FDA) and recommended by the National Institute for Clinical Excellence (NICE). Disease management Other treatments for ALS are designed to relieve symptoms and improve the quality of life for patients. This supportive care is best provided by multidisciplinary teams of health care professionals working with patients and caregivers to keep patients as mobile and comfortable as possible. Pharmaceutical treatments Medical professionals can prescribe medications to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm. Drugs also are available to help patients with pain, depresión, sleep disturbances, dysphagia, and constipation. Baclofen and diazepam are often prescribed to control the spasticity caused by ALS, and trihexyphenidyl or amitriptyline may be prescribed when ALS patients begin having trouble swallowing their saliva. Physical, occupational and speech therapy Physical therapists and occupational therapists play a large role in rehabilitation for individuals with ALS. Específicamente, physical and occupational therapists can set goals and promote benefits for individuals with ALS by delaying loss of strength, maintaining endurance, limiting pain, preventing complications, and promoting functional independence. Occupational therapy and special equipment such as assistive technology can also enhance patients' independence and safety throughout the course of ALS. Gentle, low-impact aerobic exercise such as performing activities of daily living (ADL's), andante, swimming, and stationary bicycling can strengthen unaffected muscles, improve cardiovascular health, and help patients fight fatigue and depression. Range of motion and stretching exercises can help prevent painful spasticity and shortening (contracture) of muscles. Physical and occupational therapists can recommend exercises that provide these benefits without overworking muscles. They can suggest devices such as ramps, tirantes, walkers, bathroom equipment (shower chairs, toilet risers, etc.) and wheelchairs that help patients remain mobile. Occupational therapists can provide or recommend equipment and adaptations to enable people to retain as much safety and independence in activities of daily living as possible. ALS patients who have difficulty speaking may benefit from working with a speech-language pathologist. These health professionals can teach patients adaptive strategies such as techniques to help them speak louder and more clearly. As ALS progresses, speech-language pathologists can recommend the use of augmentative and alternative communication such as voice amplifiers, speech-generating devices (or voice output communication devices) and/or low tech communication techniques such as alphabet boards or yes/no signals. Feeding and nutrition Patients and caregivers can learn from speech-language pathologists and nutritionists how to plan and prepare numerous small meals throughout the day that provide enough calories, fiber, and fluid and how to avoid foods that are difficult to swallow. Patients may begin using suction devices to remove excess fluids or saliva and prevent choking. Occupational therapists can assist with recommendations for adaptive equipment to ease the physical task of self-feeding and/or make food choice recommendations that are more conducive to their unique deficits and abilities. When patients can no longer get enough nourishment from eating, doctors may advise inserting a feeding tube into the stomach. The use of a feeding tube also reduces the risk of choking and pneumonia that can result from inhaling liquids into the lungs. The tube is not painful and does not prevent patients from eating food orally if they wish. Researchers have stated that "ALS patients have a chronically deficient intake of energy and recommended augmentation of energy intake." Both animal and human research suggest that ALS patients should be encouraged to consume as many calories as possible and not to restrict their calorie intake. Breathing support When the muscles that assist in breathing weaken, use of ventilatory assistance (intermittent positive pressure ventilation (IPPV), bilevel positive airway pressure (BIPAP), or biphasic cuirass ventilation (BCV)) may be used to aid breathing. Such devices artificially inflate the patient's lungs from various external sources that are applied directly to the face or body. When muscles are no longer able to maintain oxygen and carbon dioxide levels, these devices may be used full-time. BCV has the added advantage of being able to assist in clearing secretions by using high-frequency oscillations followed by several positive expiratory breaths. Patients may eventually consider forms of mechanical ventilation (respirators) in which a machine inflates and deflates the lungs. To be effective, this may require a tube that passes from the nose or mouth to the windpipe (trachea) and for long-term use, an operation such as a tracheostomy, in which a plastic breathing tube is inserted directly in the patient's windpipe through an opening in the neck. Patients and their families should consider several factors when deciding whether and when to use one of these options. Ventilation devices differ in their effect on the patient's quality of life and in cost. Although ventilation support can ease problems with breathing and prolong survival, it does not affect the progression of ALS. Patients need to be fully informed about these considerations and the long-term effects of life without movement before they make decisions about ventilation support. Some patients under long-term tracheostomy intermittent positive pressure ventilation with deflated cuffs or cuffless tracheostomy tubes (leak ventilation) are able to speak, provided their bulbar muscles are strong enough. This technique preserves speech in some patients with long-term mechanical ventilation. Palliative care Social workers and home care and hospice nurses help patients, families, and caregivers with the medical, emocional, and financial challenges of coping with ALS, particularly during the final stages of the disease. Social workers provide support such as assistance in obtaining financial aid, arranging durable power of attorney, preparing a living will, and finding support groups for patients and caregivers. Home nurses are available not only to provide medical care but also to teach caregivers about tasks such as maintaining respirators, giving feedings, and moving patients to avoid painful skin problems and contractures. Home hospice nurses work in consultation with physicians to ensure proper medication, pain control, and other care affecting the quality of life of patients who wish to remain at home. The home hospice team can also counsel patients and caregivers about end-of-life issues. Epidemiology ALS is one of the most common neuromuscular diseases worldwide, and people of all races and ethnic backgrounds are affected. One or two out of 100,000 people develop ALS each year. ALS most commonly strikes people between 40 y 60 años de edad, but younger and older people can also develop the disease. Men are affected slightly more often than women. Although the incidence of ALS is thought to be regionally uniform, there are three regions in the West Pacific where there has in the past been an elevated occurrence of ALS. This seems to be declining in recent decades. The largest is the area of Guam inhabited by the Chamorro people, who have historically had a high incidence (as much as 143 cases per 100,000 people per year) of a condition called Lytico-Bodig disease which is a combination of ALS, Parkinsonismo, and dementia. Two more areas of increased incidence are West Papua and the Kii Peninsula of Japan. Although there have been reports of several "clusters" including three American football players from the San Francisco 49ers, more than fifty football players in Italy, three football-playing friends in the south of England, and reports of conjugal (husband and wife) cases in the south of France, these are statistically plausible chance events[cita necesaria]. Although many authors consider ALS to be caused by a combination of genetic and environmental risk factors, so far the latter have not been firmly identified, other than a higher risk with increasing age. Etymology Amyotrophic comes from the Greek language: Un- medio "no", myo refers to "muscle", and trophic means "nourishment"; amyotrophic therefore means "no muscle nourishment," which describes the characteristic atrophication of the sufferer's disused muscle tissue. Lateral identifies the areas in a person's spinal cord where portions of the nerve cells that are affected are located. As this area degenerates it leads to scarring or hardening ("sclerosis") in the region. History Timeline Year Event 1824 Charles Bell writes a report about ALS. 1850 English scientist Augustus Waller describes the appearance of shriveled nerve fibers 1869 French doctor Jean-Martin Charcot first describes ALS in scientific literature 1881 "La esclerosis lateral amiotrófica" is translated into English and published in a three-volume edition of Lectures on the Diseases of the Nervous System 1939 ALS becomes a cause célèbre in the United States when baseball legend Lou Gehrig's career—and, two years later, his life—is ended by the disease. He gives his farewell speech on July 4, 1939. 1950s ALS epidemic occurs among the Chamorro people on Guam 1991 Researchers link chromosome 21 to FALS (Familial ALS) 1993 SOD1 gene on chromosome 21 found to play a role in some cases of FALS 1996 Rilutek becomes the first FDA-approved drug for ALS 1998 The El Escorial criteria is developed as the standard for classifying ALS patient in clinical research 1999 The revised ALS Functional Rating Scale (ALSFRS-R) is published and soon becomes a gold standard measure for rating decline in ALS patient in clinical research 2011 Noncoding repeat expansions in C9ORF72 are found to be a major cause of ALS and frontotemporal dementia Clinical research A number of clinical trials are underway globally for ALS; a comprehensive listing of trials in the US can be found at ClinicalTrials.gov. KNS-760704 (Dexpramipexole) is under clinical investigation in ALS patients. It is hoped that the drug will have a neuroprotective effect. It is one enantiomer of pramipexole, which is approved for the treatment of Parkinson's disease and restless legs syndrome. The single-enantiomer preparation is essentially inactive at dopamine receptors, is not dose limited by the potent dopaminergic properties of pramipexole. Results of a Phase II clinical trial conducted by Knopp Neurosciences and involving 102 patients were reported in 2010; the trial found a dose-dependent slowing in loss of function. A larger phase II trial conducted by Biogen found the drug to be safe, well tolerated, and associated with a dose-dependent slowing in the decline of ALS. Talampanel is being tested in ALS by Teva Pharmaceutical Industries; a Phase II trial was completed in April 2010. See also ALS Association ALS Society of Canada ALS Therapy Development Institute Motor Neurone Disease Association Muscular Dystrophy Association References ↑ Jump up to: 1.0 1.1 HTTP://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001708/ ↑ Phukan J, Pender NP, Hardiman O (2007). Cognitive impairment in amyotrophic lateral sclerosis. Lancet Neurol 6 (11): 994–1003. ↑ M. Sabatelli, MD, F. Madia, MD, Un. Conte, MD, M. Luigetti, MD, M. Zollino, MD, Yo. Mancuso, Doctor, M. Lo Monaco, MD, G. Lippi, MD and P. Tonali, MD (2008). Natural history of young-adult amyotrophic lateral sclerosis. Neurología 16 (71): 876–881. ↑ Saltar hasta: 4.0 4.1 DOI:10.1136/jnnp.2010.235952 This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand ↑ M R Turner, M J Parton, C E Shaw, P N Leigh, A Al-Chalabi (2003). Prolonged survival in motor neuron disease: a descriptive study of the King’s database 1990–2002.. J Neurol Neurosurg Psychiatry 74: 995–997. ↑ Stephen Hawking serves as role model for ALS patients ↑ Sutedja NA, Fischer K, Veldink JH, van der Heijden GJ, Kromhout H, Heederik D, et al. (2009). What we truly know about occupation as a risk factor for ALS: a critical and systematic review.. La esclerosis lateral amiotrófica 10: 295–301. ↑ Dejesus-Hernandez, M., et al., (2011). Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS.. Neurona 72 (2): 245–56. ↑ Majounie E., et al., (2012). Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study.. Lancet Neurology 11 (4): 323–330. ↑ Conwit, Robin A. (Diciembre 2006). Preventing familial ALS: A clinical trial may be feasible but is an efficacy trial warranted?. Journal of the Neurological Sciences 251 (1–2): 1–2. ↑ Saltar hasta: 11.0 11.1 Al-Chalabi, Ammar (Agosto 2000). Recent advances in amyotrophic lateral sclerosis. Current Opinion in Neurology 13 (4): 397–405. ↑ Battistini S, Ricci C, Lotti EM, Benigni M, Gagliardi S, Zucco R, Bondavalli M, Marcello N, Ceroni M, Cereda C (Junio 2010). Severe familial ALS with a novel exon 4 mutation (L106F) in the SOD1 gene. Journal of the Neurological Sciences 293 (1): 112–115. ↑ Anderson P.M., et al., (1996). Autosomal recessive adult-onset amyotrophic lateral sclerosis associated with homozygosity for Asp90Ala CuZn-superoxide dismutase mutation, A clinical and genealogical study of 36 patients.. Cerebro 119: 1153–1172. ↑ Deng, HX, Chen, W, hongo, S T, Boycott, KM, Gorrie, GH, Siddique, N, Yang, Y, Fecto, F, Shi, Y, Zhai, H, Jiang, H, Hirano, M, Rampersaud, E, Jansen, GH, Donkervoort, S, Bigio, EH, Brooks, BR, Ajroud, K, Sufit, Rl, Haines, JL, Mugnaini, E, Pericak-Vance, MAMÁ, Siddique, T (2011-08-21). Mutations in UBQLN2 cause dominant X-linked juvenile and adult onset ALS and ALS/dementia. Naturaleza 477 (7363): 211–5. ↑ Reaume A, Elliott J, Hoffman E, Kowall N, Ferrante R, Siwek D, Wilcox H, Flood D, Beal M, Brown R, Scott R, Snider W (1996). Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury. Nat Genet 13 (1): 43–7. ↑ Bruijn L, Houseweart M, Kato S, Anderson K, Anderson S, Ohama E, Reaume A, Scott R, Cleveland D (1998). Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. Ciencia 281 (5384): 1851–4. ↑ Furukawa Y, Fu R, Deng H, Siddique T, O'Halloran T (2006). Disulfide cross-linked protein represents a significant fraction of ALS-associated Cu, Zn-superoxide dismutase aggregates in spinal cords of model mice. Proc Natl Acad Sci USA 103 (18): 7148–53. ↑ Boillée S, Vande Velde C, Cleveland D (2006). ESCLEROSIS LATERAL AMIOTRÓFICA: a disease of motor neurons and their nonneuronal neighbors. Neurona 52 (1): 39–59. ↑ Hansel Y, Ackerl M, Stanek G. (1995). ALS-like sequelae in chronic neuroborreliosis. Wien Med Wochenschr. 145 (7–8): 186–8. ↑ el Alaoui-Faris M, Medejel A, al Zemmouri K, Yahyaoui M, Chkili T (1990). Amyotrophic lateral sclerosis syndrome of syphilitic origin. 5 Casos. Rev Neurol (París) 146 (1): 41–4. ↑ Umanekii KG, Dekonenko EP (1983). Structure of progressive forms of tick-borne encephalitis. Zh Nevropatol Psikhiatr Im S S Korsakova. 83 (8): 1173–9. ↑ PMID 21412713 (PMID 21412713) La cita se completará automáticamente en unos minutos.. Jump the queue or expand by hand ↑ Eisen, Un. (2002). Esclerosis lateral amiotrófica: Una reseña. BCMJ 44 (7): 362–366. ↑ DOI:10.1136/jnnp.60.2.147 This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand ↑ DOI:10.1590/S0004-282X2010000600002 This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand ↑ PMID 22375266 (PMID 22375266) La cita se completará automáticamente en unos minutos.. Jump the queue or expand by hand ↑ http://misc.medscape.com/pi/android/medscapeapp/html/A1170810-business.html ↑ http://www.lems.com/what_is_lems ↑ Carlesi, C, Pasquali, L, Piazza, S, Lo Gerfo, Un, Caldarazzo Ienco, E, Alessi, R, Fornai, F, Siciliano, G (2011 Estropear). Strategies for clinical approach to neurodegeneration in Amyotrophic lateral sclerosis. Archives italiennes de biologie 149 (1): 151–67. ↑ Miller, RG, Mitchell JD, Lyon M, Moore DH, G (2007). Riluzole for amyotrophic lateral sclerosis (ESCLEROSIS LATERAL AMIOTRÓFICA)/motor neuron disease (MND). Cochrane Database of Systematic Reviews (1): CD001447. ↑ Lewis, M. & Rushanan, S. (2007). The role of physical therapy and occupational therapy in the treatment of Amyotrophic Lateral Sclerosis. NeuroRehabilitation 22 (6): 451–461. ↑ Saltar hasta: 32.0 32.1 Kasarskis EJ, Berryman S, Vanderleest JG, Schneider AR, McClain CJ (Ene 1996). Nutritional status of patients with amyotrophic lateral sclerosis: relation to the proximity of death. Am J Clin Nutr. 63 (1): 130–7. ↑ Hamadeh MJ, Rodriguez MC, Kaczor JJ, Tarnopolsky MA (Feb 2005). Caloric restriction transiently improves motor performance but hastens clinical onset of disease in the Cu/Zn-superoxide dismutase mutant G93A mouse. Muscle Nerve 31 (2): 214–20. ↑ Slowie LA, Paige MS, Antel JP (Jul 1983). Nutritional considerations in the management of patients with amyotrophic lateral sclerosis (ESCLEROSIS LATERAL AMIOTRÓFICA). J Am Diet Assoc 83 (1): 44–7. ↑ Sviri S, Linton DM, Van Heerden PV (Jun 2005). Non-invasive Mechanical Ventilation Enhances Patient Autonomy in Decision-Making Regarding Chronic Ventilation. Critical Care and Resuscitation 7 (2): 116–118. ↑ ALS Topic Overview. URL a la que se accede en 2008-05-01. ↑ Reed D, Labarthe D, Chen KM, Stallones R (Ene 1987). A cohort study of amyotrophic lateral sclerosis and parkinsonism-dementia on Guam and Rota. Am J Epidemiol. 125 (1): 92–100. ↑ S. Kuzuhara, Y. Kokubo P3-146Marked increase of parkinsonism-dementia (P-D) phenotypes in the high incidence amyotrophic lateral sclerosis (ESCLEROSIS LATERAL AMIOTRÓFICA) focus in the Kii peninsula of Japan. Alzheimer's and Dementia, Volumen 2, Emitir 3, Pages S417-S417 ↑ Spencer PS, Palmer VS, Ludolph AC (Ago 2005). On the decline and etiology of high-incidence motor system disease in West Papua (southwest New Guinea). Mov. Disord. 20 (Suppl 12): S119–26. ↑ Sla, indagini nei club. Pesticidi nel mirino. URL a la que se accede en 2008-10-02. ↑ Wicks P, Abrahams S, Masi D, Hejda-Forde S, Leigh PN & Goldstein LH (2005) The Prevalence of Depression and Anxiety in MND, Amyotrophic Lateral Sclerosis and other Motor Neuron Disorders, Volumen 6, Supplement 1, p. 147 ↑ Rachele MG, Mascia V, Tacconi P, Dessi N, Marrosu F (Abril 1998). Conjugal amyotrophic lateral sclerosis: a report on a couple from Sardinia, Italia. Ital J Neurol Sci. 19 (2): 97–100. ↑ Poloni M, Micheli A, Facchetti D, Mai R, Ceriani F (Abril 1997). Conjugal amyotrophic lateral sclerosis: toxic clustering or change?. Ital J Neurol Sci. 18 (2): 109–12. ↑ Camu W, Cadilhac J, Billiard M. (Marzo 1994). Conjugal amyotrophic lateral sclerosis: a report on two couples from southern France. Neurología 44 (3 Pt 1): 547–8. ↑ Cornblath DR, Kurland LT, Boylan KB, Morrison L, Radhakrishnan K, Montgomery M. (Noviembre 1993). Conjugal amyotrophic lateral sclerosis: report of a young married couple. Neurología 43 (11): 2378–80. ↑ Corcia P, Jafari-Schluep HF, Lardillier D, Mazyad H, Giraud P, Clavelou P, Pouget J, Camu W (Noviembre 2003). A clustering of conjugal amyotrophic lateral sclerosis in southeastern France. Neurol. 60 (4): 553–7. ↑ Tyler HR, Shefner J. Esclerosis lateral amiotrófica. Handb Clin Neurol. 1991;15:169-215. Serial publication. ↑ Rowland LP (Marzo 2001). How amyotrophic lateral sclerosis got its name: the clinical-pathologic genius of Jean-Martin Charcot. Arco. Neurol. 58 (3): 512–5. ↑ Farewell Speech. lougehrig.com. URL accessed on April 16, 2008. ↑ Abramova NA et al. Inhibition by R(+) or S(-) pramipexole of caspase activation and cell death induced by methylpyridinium ion or beta amyloid peptide in SH-SY5Y neuroblastoma. J Neurosci Res. 2002 Feb 15;67(4):494-500. ↑ DOI:10.1111/j.1755-5949.2008.00048.x This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand ↑ DOI:10.1097/01.Nuevo Testamento.0000384108.10957.21 This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand ↑ DOI:10.1038/nm.2579 This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand ↑ http://clinicaltrials.gov/ct2/show/NCT00696332?term=ALS&rank=2 Further reading ALS Hope Foundation. URL a la que se accede en 2008-06-21. Lou Gehrig: The Official Web Site. CMG Worldwide. URL a la que se accede en 2008-06-21. includeonly>Patrick Aebischer, Ann C. Kato. "Playing defense against Lou Gehrig's Disease" (Papel), Científico americano, Verlagsgruppe Georg von Holtzbrinck, Noviembre 2007, páginas. 86–93. Recuperado el 2008-06-21. “Researchers have proposed potential therapies for a paralyzing disorder once thought to be untreatable (sub-title)” External links Medline Plus article on ALS REDIRECT Template:CNS diseases of the nervous system This page uses Creative Commons Licensed content from Wikipedia (ver autores). Si quieres conocer otros artículos parecidos a Esclerosis lateral amiotrófica puedes visitar la categoría Pages with incomplete DOI references.	2	56	4	0	1	0	0.729001	5	9,462
What the Anesthesiologist Should Know before the Operative Procedure During uterine curettage, an instrument is used to scrape or suction the uterine lining to diagnose and/or treat abnormal bleeding or to remove products of conception. If not already dilated, the cervix must first be opened mechanically or chemically. The indication for the dilation and curettage is an important concern for the anesthesiologist. An acute hemorrhage situation requiring an emergent or urgent dilation and curettage requires additional setup and has higher risks, while a diagnostic elective procedure typically has lower risks. Therefore, it is important for the anesthesiologist to know the indication for the procedure. The complications associated with this procedure, which consist primarily of bleeding and uterine perforation, occur at a frequency of approximately 1-2%. In order to maximize the diagnostic and therapeutic yield and minimize risk, Dilation and Curettage (D & C) or Dilation and Evacuation (D & E) can be substituted by non-invasive procedures (such as transvaginal ultrasound) when appropriate, or augmented with more directed techniques, such as hysteroscopy and/or polypectomy. The causes of uterine bleeding leading to curettage include: 1) Pregnancy-related issues, such as miscarriage, retained products of conception, or therapeutic abortion. 2) Non-pregnancy-related issues, such as investigation of fibroids or polyps or hyperplastic uterine linings. 1. What is the urgency of the surgery? What is the risk of delay in order to obtain additional preoperative information? D & Cs or D & Es are elective, outpatient procedures if there is no major bleeding and/or if the procedure is done for diagnostic purposes. Emergent: If the patient is having active and ongoing bleeding resulting in subjective symptoms, such as lightheadedness or palpitations, or is showing objective signs of significant hypovolemia, such as hypotension or tachycardia, then the D & C should be performed as soon as possible. Delaying curettage may result in exsanguination. Practitioners should be prepared for major resuscitation that includes crystalloids, colloids, and blood products (in some cases, uncrossed-matched RBCs) as needed. Depending on the source of bleeding, the procedure may need to be converted to a laparoscopy or laparotomy. Urgent: Patients with chronic bleeding are often evaluated first by imaging (e.g. ultrasound) to inform the decision of whether or not to proceed with D & C. There is typically time for these patients to undergo a more thorough preoperative evaluation and for blood to be typed and crossed, if needed. Elective: Patients with intermittent, abnormal vaginal bleeding, uterine fibroids, or polyps may undergo D & C as an elective procedure. These procedures are typically used to determine the cause of bleeding and, in some cases, the benign or malignant nature of a uterine growth. These patients can undergo pre-operative testing based on the presence or absence of co-morbidities. 2. Preoperative evaluation During the preoperative evaluation, it is important to assess the pregnancy status of the patient, as dilatation and curettage is contraindicated in patient with a viable and desired intrauterine pregnancy. Medically unstable conditions warranting further evaluation include major cardiac or pulmonary disease or clotting disorders. Patients with pelvic infections are at risk for bacteremia and perforation as a result of the fragile uterine tissue. In general, cardiac testing is unnecessary for asymptomatic patients. Delaying surgery may be indicated if the patient is pregnant and this is not a pregnancy-related D & C or if the procedure is elective and the patient is unstable because of comorbid illness. The patient should be optimized prior to proceeding with surgery, if feasible, if she had cardiac issues, such as unstable angina, and if significant intra-operative bleeding is expected. Patients with severe hip arthritis can be difficult or impossible to position in stirrups (i.e. lithotomy), thus limiting the feasibility of these procedures. Patients with pre-existing cardiac, gastrointestinal, or pulmonary issues may benefit from regional or paracervical blocks. It would be important to evaluate these patients preoperatively for coagulation disorders or infection near the block site. 3. What are the implications of co-existing disease on perioperative care? Patients with acute or chronic bleeding should have a baseline CBC. If bleeding has been significant (>=1.5 liters acutely, or multiple recent bleeds), then consider a DIC screen. b. Cardiovascular system Acute ongoing hemorrhage may exacerbate underlying cardiac ischemia, further necessitating prompt resuscitation and identification of the underlying cause of bleeding. Baseline coronary artery disease or cardiac dysfunction Goals of management: If the patient’s pain and bleeding are well controlled, then the D & C or D & E should lead to minimal hemodynamic derangement. However, inadequate anesthesia and major hemorrhage can precipitate ischemia through increased utilization and decreased availability of oxygen. Patients with a significant smoking history, chronic bronchitis, or baseline oxygen requirements should be identified preoperatively. Patients with acute or chronic alcohol use can have increased risk for aspiration and more colonization with pathologic bacteria in their airway. Unless an acute COPD exacerbation is suspected, additional preoperative testing is rarely indicated. Perioperative Risk Reduction Strategies These targeted patients should continue their ongoing medication regimens, assuming they are optimized. Patients with COPD may benefit from short term preoperative inhaled or systemic corticosteroids. Anesthetic techniques that avoid instrumenting the airway, such as a paracervical block with sedation or neuraxial anesthetics, are preferable to general anesthesia. Patients with a history of smoking or excessive alcohol consumption should be advised to practice smoking and alcohol cessation at least 4-8 weeks prior to surgery. Reactive Airway Disease (i.e., Asthma) The status and severity of the patient’s disease should be assessed, including identifying common triggers, the response to bronchodilators, history of recent hospitalizations, prior steroid therapy, or intubations for exacerbations. Perioperative Risk Reduction Strategies Ideally, patients would not undergo a procedure during an asthma or COPD exacerbation, but rather they would first be medically optimized. If the procedure is emergent, the anesthetic technique of choice would be to allow the patient to breathe spontaneously and avoid instrumentation of the airway (e.g. paracervical block with sedation/MAC or spinal). If general anesthesia is necessary, then initial use of a volatile agent to aid in bronchodilation, decreased to 0.5 MAC after induction to promote uterine contraction post-procedure, would be beneficial. Preoperative and intraoperative treatment with inhaled bronchodilator therapy may also benefit these patients. In situations with excessive bleeding, carboprost (Hemabate) should be avoided or used cautiously as it can cause bronchospasm in susceptible individuals. Alternative uterotonic agents such as oxytocin, methergine, or misoprostol should be used instead. Active respiratory therapy is advisable. As per ASA guidelines, patients undergoing non-urgent or emergent D & C should be NPO for 6-8 hours for solid food and 2 hours for clear liquids prior to the procedure. Those with symptomatic reflux should be identified, and should undergo light sedation that preserves airway reflexes (+ paracervical block or neuraxial anesthetic) or rapid sequence induction with general endotracheal anesthesia after H2 blocker therapy. g. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (e.g., musculoskeletal in orthopedic procedures, hematologic in a cancer patient) Patients with a history of or active cervical or uterine cancer should be evaluated preoperatively and managed carefully as heavy bleeding or perforation can occur. The anesthesiologist should be prepared with proper IV access and blood products on standby. 4. What are the patient's medications and how should they be managed in the perioperative period? h. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern? If patients are taking anti-coagulants or anti-platelet agents, they should consult with their physicians at least a week prior to surgery for further instructions, as some of these medications have an extremely long half-life. i. What should be recommended with regard to continuation of medications taken chronically? consult with multidisciplinary team j. How To modify care for patients with known allergies – k. Latex allergy- If the patient has a sensitivity to latex (e.g., rash from gloves, underwear.) versus anaphylactic reaction, prepare the operating room with latex-free products. In case of anaphylaxis, epinephrine, IV H1, H2 blockers and steroids, and rescue airway equipment should be readily available. Diagnostic dilation and curettage (Endometrial biopsy): No antibiotics Elective suction curettage abortion: Antibiotic prophylaxis is indicated. Optimal antibiotic agents and dosages vary. One of the most effective and least expensive regimens is Doxycycline. l. Does the patient have any antibiotic allergies? m. Does the patient have a history of allergy to anesthesia? Malignant hyperthermia (MH) Avoid all trigger agents, such as succinylcholine and inhalational agents. Insure MH cart available: Clean machine according to individual anesthesia machine protocol. Use regional technique or paracervical block if possible. These are not considered to be MH triggering agents, and therefore can be used in patients at risk for malignant hyperthermia. It is important to ask patients if they are allergic to local anesthetics or sunscreen containing PABA (relevant for ester local anesthetics) before administering local anesthetic. 5. What laboratory tests should be obtained and has everything been reviewed? For young healthy patients not at risk of significant bleeding, no pre-operative labs are needed unless there is significant hemorrhage. Intraoperative Management: What are the options for anesthetic management and how to determine the best technique? The anesthetic options for dilation and curettage include conscious sedation or MAC (monitored anesthesia care) +/- paracervical block, neuraxial, and general anesthesia. The optimal anesthetic choice depends on the patient and: a) the degree of hemorrhage/hemodynamic stability, b) the patient and provider preference, c) and cervical dilation, which may affect the feasibility of doing a paracervical block. The Cochrane Database Review (2009) examined 17 studies, including over 1,855 participants, regarding cervical dilation and uterine intervention with paracervical block when compared with no treatment, placebo, and other regional anesthesia, systemic sedation, or GA. Some studies reported that women experienced severe pain (mean scores of 7-/10) during uterine intervention, irrespective of the analgesia technique used. No technique provided reliable pain control. The available evidence fails to show whether paracervical block is inferior, equivalent to, or superior to alternative analgesia techniques in terms of efficacy and safety for women undergoing uterine interventions. a. Regional anesthesia Regional anesthesia, including Paracervical block (+/- sedation), +/- intrauterine local anesthetic and neuraxial (+/- sedation) have been reported for D & C and D & E. Benefits: anecdotally, patients typically feel the least discomfort. Drawbacks: low, but non-zero, risk of post-dural puncture headache (PDPH) and transient radicular irritation (TRI) in setting of outpatient procedure and lithotomy position. Consider using hyperbaric bupivacaine 0.75% (1-1.5 ccs) with fentanyl (10-20 mics) or, if less than 1 hour of procedure time is anticipated, mepivacaine 1.5% (45-60 mg) with preservative-free dextrose (approximately 1 cc) or chloroprocaine 40-60mg. Recovery time varies and the patient may have to recover in hospital before being discharged. 2. Peripheral Nerve Block e.g., paracervical (consider Nesacaine 1%) Benefits: less invasive and better analgesia than sedation alone. Drawbacks: reports of pain regardless of the agent used if paracervical block is done without sedation. Benefits: less invasive. Some investigations have shown that 5 cc’s of 2% lidocaine can be as effective as paracervical block or po NSAID. As with paracervical block, use in conjunction with conscious sedation for best results. b. General Anesthesia Benefits: secured airway, anecdotally more reliable pain management, and less intra-op patient movement. Drawbacks: potential airway issues or increased risk of aspiration if patient is beyond the first trimester of pregnancy or recently post-partum. Increased risk of postoperative nausea and vomiting. c. Monitored Anesthesia Care D & C is often done under sedation or Monitored Anesthesia Care (MAC) with paracervical block. There are many analgesia and anesthetic agents that can be used in bolus dosing or as continuous infusions (e.g., Fentanyl and Versed, Propofol and Remifentanil). In one randomized, controlled trial, propofol (target concentration of 5 mics/ml) was recommended for D & C when administered with Fentanyl 1 mic/kg and N02 (66%) as compared with 4 and 6 mics/cc. Close monitoring and appropriate respiratory management were deemed necessary for safe administration. Benefits include that it takes the patient less time to wake up when compared with general anesthesia, potentially less need to instrument the airway, if the patient continues to breath spontaneously, and the avoidance of post-dural puncture headache. Drawbacks include the risk of respiratory depression, which could lead to depressed airway reflexes, aspiration, and/or apnea, the potential for patient movement, increasing the chance of uterine perforation, and a greater chance of inadequate pain relief when compared to neuraxial or general anesthesia. 6. What is the author's preferred method of anesthesia technique and why? When obstetric providers expect that the procedure will be straightforward (that is, there is no molar pregnancy or malplacentation) for first trimester incomplete or therapeutic abortions or the removal of retained products of conception, then our anesthetic of choice is a paracervical block placed by the surgeons (using 1% Nesacaine) and MAC. We use various combinations of anesthetics for sedation during the MAC, including bolus fentanyl and versed or propofol and remifentanil infusions. For second trimester D & Es, our anesthetic of choice is typically either spinal or general (endotracheal) anesthesia, and occasionally MAC plus paracervical block The MAC with paracervical block option requires careful case selection (e.g., absence of symptomatic reflux in the patient, anticipation of a straightforward procedure). If significant bleeding has occurred or is expected, or if the patient is hemodynamically unstable, then we proceed with resuscitation and general endotracheal anesthesia. If the uterus needs to be evacuated urgently, but the patient has recently ingested food other than clear liquids or has an active upper respiratory infection, we will proceed with a spinal anesthetic with light-to-moderate sedation if no contraindications, such as coagulopathy or hemodynamic instability, exist. If there are no contraindications and no objections by the surgical team, interoperative ketorolac 30mg is given IV for postoperative pain control. Patients are continued on NSAIDs postoperatively on an as-needed basis for pain control. What prophylactic antibiotics should be administered? According to the ACOG guidelines, despite the lack of data, antibiotic prophylaxis is indicated for elective and missed suction curettage abortion. Although the optimal antibiotic regimen is unclear, Doxycycline (100 mg prior to the procedure and 200 mg post-procedure) was shown in a meta-analysis to be effective and inexpensive. In a prospective, randomized, controlled trial, antibiotic prophylaxis showed no benefit before the treatment of incomplete abortion. What do I need to know about the surgical technique to optimize my anesthetic care? Will there be manual dilation of the cervix? In general, dilation is painful and requires a significant degree of anesthesia (i.e., a functional paracervical block, spinal, or general anesthesia). Will this be a first or second trimester gestation? In general, second trimester D & Es are more complex and are less conducive to MAC. What can I do intraoperatively to assist the surgeon and optimize patient care? During manual dilation of the cervix and active curettage, it is important that the patient not move her hips or lower extremities, as movement can increase the risk of uterine perforation. As such, the patient should either be conscious and able to control her own body or sedated enough to restrict movement (e.g., during a GET). What are the most common intraoperative complications and how can they be avoided/treated? Attention to pre-op volume status and intra-op bleeding is essential. In the case of straight-forward first trimester missed Ab, the bleeding is often self-limited. Patients with chronic uterine bleeding or retained products of conception requiring D & E can often require significant resuscitation, including blood products such as PRBCs, FFP, platelets, and Cryoprecipitate, if bleeding is severe. As with any change in patient status, suspected uterine perforation should prompt direct and specific communication between the surgery, nursing, and anesthesia teams. Minor perforation can have little to no effect on the patient’s intra-op course, while major perforation can require urgent laparotomy and precipitate significant hemorrhage. Uterine perforation is of higher likelihood in procedures done to treat uterine bleeding as opposed to diagnostic dilatation and curettage. Risk of perforation is also increased in pregnancy. Amniotic Fluid Embolus (AFE) has been reported in pregnancy-related D & E. Therapy involves supportive care; in cases of cardiac or respiratory collapse, cardiopulmonary bypass or ECMO have been employed in some isolated cases. In general, morbidity and mortality is high with AFE. Patients who have outpatient procedures in the lithotomy position under spinal anesthesia have an increased incidence of Transient Radicular Irritation (TRI). b. If the patient is intubated, are there any special criteria for extubation? If there has been significant hemorrhage and resuscitation, it is important to assess tissue swelling and airway swelling before extubation. c. Postoperative management What analgesic modalities can I implement? If not otherwise contraindicated, NSAIDS (e.g., Toradol) +/- opioids are particularly useful for post-D & E pain management, given the high incidence of uterine cramping. What level bed acuity is appropriate? Unless there has been significant hemorrhage, D & E is often done as an outpatient procedure. Those patients who have required significant resuscitation may need to be in an inpatient setting overnight; in this case, the patient’s underlying health status and degree of hemodynamic stability post-procedure can be used to decide whether she needs a monitored bed (e.g. step-down Unit or ICU). What are common postoperative complications, and ways to prevent and treat them? To prevent post-operative bleeding, patients will sometimes be given intra-operative uterotonic agents as well as resuscitation with crystalloids or blood products as needed. Those with suspected uterine perforation are often treated with antibiotics. The development of TRI after spinal anesthetic is typically a relatively benign and self-limited event. What's the Evidence? “Antibiotic Prophylaxis for Gynecologic Procedures”. Obstetrics and Gynecology. vol. 113. 2009. pp. 1180-1189. (This document summarizes the recommendations for first and second line prophylaxis [including exclusion criteria] for D & E and other gynecologic procedures.) Agostini, A, Provansal, M. “Comparison of ropivacaine and lidocaine for paracervical block during surgical abortion”. Contraception. vol. 77. 2008. pp. 382-385. (In this randomized, double-blind study, intraoperative pain was better, although still elevated, when ropivacaine was used for paracervical block compared with lidocaine. Postoperative pain was not different between the two groups.) Api, O, Ergen, B. “Comparison of oral nonsteroidal analgesic and intrauterine local anesthetic for pain relief in uterine fractional curettage: a randomized, double-blind, placebo-controlled trial”. Am J Obstet Gynecol. vol. 203. 2010. pp. 28 e21-27. (Either intrauterine lidocaine (5 cc's 2% lidocaine) or oral dexketoprofen were effective in relieving fractional curettage-related pain, although a combination of the two medications did not demonstrate a clinically relevant increase in analgesia.) Castillo, T, Avellanal, M. “Bolus application of remifentanil with propofol for dilatation and curettage”. Eur J Anaesthesiol. vol. 21. 2004. pp. 408-411. (The most favorable intra-op anesthetic conditions and post-operative recovery times were found with Remifentanil 1.5 mic/ kg(-1) i.v. with propofol 2 mg kg(-1) i.v. and 60% nitrous oxide in oxygen.) Fox, M. C, Hayes, J. L.. “Cervical preparation for second-trimester surgical abortion prior to 20 weeks of gestation”. Contraception. vol. 76. 2007. pp. 486-495. (These clinical guidelines explore the role of cervical preparation for D & E prior to 20 weeks’ gestation, specifically addressing the available osmotic dilators.) Mankowski, J. L, Kingston, J. “Paracervical compared with intracervical lidocaine for suction curettage: a randomized controlled trial”. Obstet Gynecol. vol. 113. 2009. pp. 1052-1057. (According to this investigation, either of these techniques, coupled with conscious sedation, provides effective and acceptable analgesia for first trimester suction curettage.) Rattanachaiyanont, M, Leerasiri, P. “Effectiveness of intrauterine anesthesia for pain relief during fractional curettage”. Obstet Gynecol. vol. 106. 2005. pp. 533-539. (This randomized, double-blind, controlled study showed that the addition of intrauterine anesthesia (in this case 5ml 2%lidocaine in addition to the paracervical block) further reduced pain during D & C without increasing side effects.) Sotiriadis, A, Makrydimas, G. “Expectant, medical, or surgical management of first-trimester miscarriage: a meta-analysis”. Obstet Gynecol. vol. 105. 2005. pp. 1104-1113. (Complete evacuation of the uterus was more common if surgical management was undertaken than if there was medical management of first trimester or incomplete miscarriage. Expectant management had very variable success rates.) Tangsiriwatthana, T, Sangkomkamhang, U. S. “Paracervical local anaesthesia for cervical dilatation and uterine intervention”. Cochrane Database Syst Rev. 2009. pp. CD005056(The Cochrane Database Review (2009) examined 17 studies, including over 1,855 participants, regarding cervical dilation and uterine intervention with paracervical block when compared with no treatment, placebo, and other regional anesthesia, systemic sedation, or GA. Some studies reported that women experienced severe pain (mean scores of 7-/10) during uterine intervention, irrespective of the analgesia technique used. No technique provided reliable pain control.) Tuncalp, O, Gulmezoglu, A. M. “Surgical procedures for evacuating incomplete miscarriage”. Cochrane Database Syst Rev. vol. 9. 2010. pp. CD001993(This paper indicates that serious complications (e.g. uterine perforation and other morbidity) were rare, but the trial sample sizes were not large enough to evaluate small or moderate differences.) Uerpairojkit, K, Urusopone, P. “A randomized controlled study of three targets of propofol plasma concentration in patients undergoing uterine dilation and curettage”. J Obstet Gynaecol Res. vol. 29. 2003. pp. 79-83. (The authors conclude that a target propofol concentration of 5 mics/ml in conjunction with Fentanyl 1mic/kg and nitrous oxide 66% minimized patient movement, hypotension, and respiratory depression during D & C.) Silvanus, MT, Groeben, H, Peters, J. “Corticosteroids and inhaled salbutamol in patients with reversible airway obstruction markedly decrease the incidence of bronchospasm after tracheal intubation”. Anesthesiology. vol. 100. 2004. pp. 1052-7. Warner, MA, Offord, KP, Warner, ME, Lennon, RL, Conover, MA, Jansson-Schumacher, U. “Role of preoperative cessation of smoking and other factors in postoperative pulmonary complications: a blinded prospective study of coronary artery bypass patients”. Mayo Clin Proc. vol. 64. 1989. pp. 609-616. Nelson, G, Altman, AD, Nick, A, Meyer, LA. “Guidelines for pre- and intra-operative care in gynecologic/oncology surgery: Enhanced Recovery After Surgery (ERAS) Society recommendations – Part I”. Gynecologic Oncology. vol. 140. 2016. pp. 313-322. Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM. - What the Anesthesiologist Should Know before the Operative Procedure - 1. What is the urgency of the surgery? - What is the risk of delay in order to obtain additional preoperative information? - 2. Preoperative evaluation - 3. What are the implications of co-existing disease on perioperative care? - b. Cardiovascular system - c. Pulmonary - d. Renal-GI: - e. Neurologic: - f. Endocrine: - g. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (e.g., musculoskeletal in orthopedic procedures, hematologic in a cancer patient) - 4. What are the patient's medications and how should they be managed in the perioperative period? - h. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern? - i. What should be recommended with regard to continuation of medications taken chronically? - j. How To modify care for patients with known allergies - - k. Latex allergy- If the patient has a sensitivity to latex (e.g., rash from gloves, underwear.) versus anaphylactic reaction, prepare the operating room with latex-free products. - l. Does the patient have any antibiotic allergies? - m. Does the patient have a history of allergy to anesthesia? - 5. What laboratory tests should be obtained and has everything been reviewed? - Intraoperative Management: What are the options for anesthetic management and how to determine the best technique? - 6. What is the author's preferred method of anesthesia technique and why? - What prophylactic antibiotics should be administered? - What do I need to know about the surgical technique to optimize my anesthetic care? - Will there be manual dilation of the cervix? - Will this be a first or second trimester gestation? - What can I do intraoperatively to assist the surgeon and optimize patient care? - What are the most common intraoperative complications and how can they be avoided/treated? - Uterine Perforation - Cardiac/Pulmonary Complications - a. Neurologic - b. If the patient is intubated, are there any special criteria for extubation? - c. Postoperative management	2	10	0	0	0	1	0.753257	1	6,297
- Arrhythmogenic right ventricular dysplasia Arrhythmogenic right ventricular dysplasia Classification and external resources Photomicrograph of an ARVC heart. ICD-10 I42.8 OMIM 107970 DiseasesDB 29750 MeSH D019571 Arrhythmogenic right ventricular dysplasia (ARVD), also called arrhythmogenic right ventricular cardiomyopathy (ARVC) or arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), is an inherited heart disease. ARVD is caused by genetic defects of the parts of heart muscle (also called myocardium or cardiac muscle) known as desmosomes, areas on the surface of heart muscle cells which link the cells together. The desmosomes are composed of several proteins, and many of those proteins can have harmful mutations. The disease is a type of nonischemic cardiomyopathy that involves primarily the right ventricle. It is characterized by hypokinetic areas involving the free wall of the right ventricle, with fibrofatty replacement of the right ventricular myocardium, with associated arrhythmias originating in the right ventricle. ARVC/D is an important cause of ventricular arrhythmias in children and young adults. It is seen predominantly in males, and 30-50% of cases have a familial distribution. - 1 Genetics - 2 Incidence - 3 Presentation - 4 Pathogenesis - 5 Ventricular arrhythmias - 6 Diagnosis - 7 Natural history - 8 Management - 9 Highly-publicised deaths from arrhythmogenic right ventricular dysplasia - 10 See also - 11 References - 12 External links It is usually inherited in an autosomal dominant pattern, with variable expression. Novel studies showed that mutations (point mutations) in genes encoding for desmosomal proteins (see Intercalated Disc) are the main causatives for the development of this disease. Recently it could be shown, that mutations in the desmin-gene could cause ARVC. Desmin is a intermediate filament protein, which is linked to the desmosomes. The penetrance is 20-35% in general, but significantly higher in Italy. Seven gene loci have been implicated in ARVD. However, about 50% of families that express ARVD that undergo genetic screening do not show linkage with any of the known chromosomal loci. It is unclear whether the pathogenesis varies with the different loci involved. Standard genetic screening test are currently tested and evaluated in different state of the art cardiovascular research centres and hospitals. Types include: Type OMIM Gene Locus ARVD1 107970 TGFB3 14q23-q24 ARVD2 600996 RYR2 1q42-q43 ARVD3 602086 ? 14q12-q22 ARVD4 602087 ? 2q32.1-q32.3 ARVD5 604400 TMEM43 3p23 ARVD6 604401 ? 10p14-p12 ARVD7 609160 ? 10q22.3 ARVD8 607450 DSP 6p24 ARVD9 609040 PKP2 12p11 ARVD10 610193 DSG2 18q12.1-q12 ARVD11 610476 DSC2 18q12.1 ARVD12 611528 JUP 17q21 The incidence of ARVD is about 1/10,000 in the general population in the United States, although some studies have suggested that it may be as common as 1/1,000. Recently, 1/200 were found to be carriers of mutations that predispose to ARVC It accounts for up to 17% of all sudden cardiac deaths in the young. In Italy, the incidence is 40/10,000, making it the most common cause of sudden cardiac death in the young population. Up to 80% of individuals with ARVD present with syncope or sudden cardiac death. The remainder frequently present with palpitations or other symptoms due to right ventricular outflow tract (RVOT) tachycardia (a type of monomorphic ventricular tachycardia). Symptoms are usually exercise-related. In populations where hypertrophic cardiomyopathy is screened out prior to involvement in competitive athletics, it is a common cause of sudden cardiac death. The first clinical signs of ARVD are usually during adolescence. However, signs of ARVD have been demonstrated in infants. The pathogenesis of ARVD is largely unknown. Apoptosis (programmed cell death) appears to play a large role. It is unclear why only the right ventricle is involved. The disease process starts in the subepicardial region and works its way towards the endocardial surface, leading to transmural involvement (possibly accounting for the aneurysmal dilatation of the RV). Residual myocardium is confined to the subendocardial region and the trabeculae of the RV. These trabeculae may become hypertrophied. Aneurysmal dilatation is seen in 50% of cases at autopsy. It usually occurs in the diaphragmatic, apical, and infundibular regions (known as the triangle of dysplasia). The left ventricle is involved in 50-67% of individuals. If the left ventricle is involved, it is usually late in the course of disease, and confers a poor prognosis. There are two pathological patterns seen in ARVD, Fatty infiltration and fibro-fatty infiltration. The first, fatty infiltration, is confined to the right ventricle. This involves a partial or near-complete substitution of myocardium with fatty tissue without wall thinning. It involves predominantly the apical and infundibular regions of the RV. The left ventricle and ventricular septum are usually spared. No inflammatory infiltrates are seen in fatty infiltration. There is evidence of myocyte (myocardial cell) degeneration and death seen in 50% of cases of fatty infiltration. The second, fibro-fatty infiltration, involves replacement of myocytes with fibrofatty tissue. A patchy myocarditis is involved in up to 2/3 of cases, with inflammatory infiltrates (mostly T cells) seen on microscopy. Myocardial atrophy is due to injury and apoptosis. This leads to thinning of the RV free wall (to < 3 mm thickness) Myocytes are replaced with fibrofatty tissue. The regions preferentially involved include the RV inflow tract, the RV outflow tract, and the RV apex. However, the LV free wall may be involved in some cases. Involvement of the ventricular septum is rare. The areas involved are prone to aneurysm formation. Right ventricular outflow tract tachycardia Monomorphic ventricular tachycardia originating from the right ventricular outflow tract. Ventricular arrhythmias due to ARVD typically arise from the diseased right ventricle. The type of arrhythmia ranges from frequent premature ventricular complexes (PVCs) to ventricular tachycardia (VT) to ventricular fibrillation (VF). While the initiating factor of the ventricular arrhythmias is unclear, it may be due to triggered activity or reentry. Ventricular arrhythmias are usually exercise-related, suggesting that they are sensitive to catecholamines. The ventricular beats typically have a right axis deviation. Multiple morphologies of ventricular tachycardia may be present in the same individual, suggesting multiple arrhythmogenic foci or pathways. Right ventricular outflow tract (RVOT) tachycardia is the most common VT seen in individuals with ARVD. In this case, the EKG shows a left bundle branch block (LBBB) morphology with an inferior axis. The differential diagnosis for the ventricular tachycardia due to ARVD include: - Congenital heart disease - Acquired heart disease - Tricuspid valve disease - Pulmonary hypertension - Right ventricular infarction - Bundle-branch re-entrant tachycardia - Pre-excited AV re-entry tachycardia - Idiopathic RVOT tachycardia In order to make the diagnosis of ARVD, a number of clinical tests are employed, including the electrocardiogram (EKG), echocardiography, right ventricular angiography, cardiac MRI, and genetic testing. 90% of individuals with ARVD have some EKG abnormality. The most common EKG abnormality seen in ARVD is T wave inversion in leads V1 to V3. However, this is a non-specific finding, and may be considered a normal variant in right bundle branch block (RBBB), women, and children under 12 years old. RBBB itself is seen frequently in individuals with ARVD. This may be due to delayed activation of the right ventricle, rather than any intrinsic abnormality in the right bundle branch. The epsilon wave The epsilon wave (marked by red triangle), seen in ARVD. The epsilon wave is found in about 50% of those with ARVD. This is described as a terminal notch in the QRS complex. It is due to slowed intraventricular conduction. The epsilon wave may be seen on a surface EKG; however, it is more commonly seen on signal averaged EKGs. Ventricular ectopy seen on a surface EKG in the setting of ARVD is typically of left bundle branch block (LBBB) morphology, with a QRS axis of -90 to +110 degrees. The origin of the ectopic beats is usually from one of the three regions of fatty degeneration (the "triangle of dysplasia"): the RV outflow tract, the RV inflow tract, and the RV apex. Signal averaged ECG Signal averaged ECG (SAECG) is used to detect late potentials and epsilon waves in individuals with ARVD. Echocardiography may reveal an enlarged, hypokinetic right ventricle with a paper-thin RV free wall. The dilatation of the RV will cause dilatation of the tricuspid valve annulus, with subsequent tricuspid regurgitation. Paradoxical septal motion may also be present. Fatty infiltration of the RV free wall can be visible on cardiac MRI. Fat has increased intensity in T1-weighted images. However, it may be difficult to differentiate intramyocardial fat and the epicardial fat that is commonly seen adjacent to the normal heart. Also, the sub-tricuspid region may be difficult to distinguish from the atrioventricular sulcus, which is rich in fat. Cardiac MRI can visualize the extreme thinning and akinesis of the RV free wall. However, the normal RV free wall may be about 3 mm thick, making the test less sensitive. Right ventricular angiography Right ventricular angiography is considered the gold standard for the diagnosis of ARVD. Findings consistent with ARVD are an akinetic or dyskinetic bulging localized to the infundibular, apical, and subtricuspid regions of the RV. The specificity is 90%; however, the test is observer dependent. Right ventricular biopsy Transvenous biopsy of the right ventricle can be highly specific for ARVD, but it has low sensitivity. False positives include other conditions with fatty infiltration of the ventricle, such as chronic alcohol abuse and Duchenne/Becker muscular dystrophy. False negatives are common, however, because the disease progresses typically from the epicardium to the endocardium (with the biopsy sample coming from the endocardium), and the segmental nature of the disease. Also, due to the paper-thin right ventricular free wall that is common in this disease process, most biopsy samples are taken from the ventricular septum, which is commonly not involved in the disease process. A biopsy sample that is consistent with ARVD would have > 3% fat, >40% fibrous tissue, and <45% myocytes. A post mortem histological demonstration of full thickness substitution of the RV myocardium by fatty or fibro-fatty tissue is consistent with ARVD. ARVD is an autosomal dominant trait with reduced penetrance. Approximately 40-50% of ARVD patients have a mutation identified in one of several genes encoding components of the desmosome, which can help confirm a diagnosis of ARVD. Since ARVD is an autosomal dominant trait, children of an ARVD patient have a 50% chance of inheriting the disease causing mutation. Whenever a mutation is identified by genetic testing, family-specific genetic testing can be used to differentiate between relatives who are at-risk for the disease and those who are not. ARVD genetic testing is clinically available. There is no pathognomonic feature of ARVD. The diagnosis of ARVD is based on a combination of major and minor criteria. To make a diagnosis of ARVD requires either 2 major criteria or 1 major and 2 minor criteria or 4 minor criteria. - Right ventricular dysfunction - Severe dilatation and reduction of RV ejection fraction with little or no LV impairment - Localized RV aneurysms - Severe segmental dilatation of the RV - Tissue characterization - Fibrofatty replacement of myocardium on endomyocardial biopsy - Conduction abnormalities - Epsilon waves in V1 - V3. - Localized prolongation (>110 ms) of QRS in V1 - V3 - Family history - Familial disease confirmed on autopsy or surgery - Right ventricular dysfunction - Mild global RV dilatation and/or reduced ejection fraction with normal LV. - Mild segmental dilatation of the RV - Regional RV hypokinesis - Tissue characterization - Conduction abnormalities - Family history - Family history of sudden cardiac death before age 35 - Family history of ARVD There is a long asymptomatic lead-time in individuals with ARVD. While this is a genetically transmitted disease, individuals in their teens may not have any characteristics of ARVD on screening tests. Many individuals have symptoms associated with ventricular tachycardia, such as palpitations, light-headedness, or syncope. Others may have symptoms and signs related to right ventricular failure, such as lower extremity edema, liver congestion with elevated hepatic enzymes. Unfortunately, sudden death may be the first manifestation of disease. ARVD is a progressive disease. Over time, the right ventricle becomes more involved, leading to right ventricular failure. The right ventricle will fail before there is left ventricular dysfunction. However, by the time the individual has signs of overt right ventricular failure, there will be histological involvement of the left ventricle. Eventually, the left ventricle will also become involved, leading to bi-ventricular failure. Signs and symptoms of left ventricular failure may become evident, including congestive heart failure, atrial fibrillation, and an increased incidence of thromboembolic events. The goal of management of ARVD is to decrease the incidence of sudden cardiac death. This raises a clinical dilemma: How to prophylactically treat the asymptomatic patient who was diagnosed during family screening. A certain subgroup of individuals with ARVD are considered at high risk for sudden cardiac death. Characteristics associated with high risk of sudden cardiac death include: - Young age - Competitive sports activity - Malignant familial history - Extensive RV disease with decreased right ventricular ejection fraction. - Left ventricular involvement - Episode of ventricular arrhythmia Management options include pharmacological, surgical, catheter ablation, and placement of an implantable cardioverter-defibrillator. Prior to the decision of the treatment option, programmed electrical stimulation in the electrophysiology laboratory may be performed for additional prognostic information. Goals of programmed stimulation include: - Assessment of the disease's arrhythmogenic potential - Evaluate the hemodynamic consequences of sustained VT - Determine whether the VT can be interrupted via antitachycardia pacing. Regardless of the management option chosen, the individual is typically suggested to undergo lifestyle modification, including avoidance of strenuous exercise, cardiac stimulants (i.e.: caffeine, nicotine, pseudoephedrine) and alcohol. If the individual wishes to begin an exercise regimen, an exercise stress test may have added benefit. Pharmacologic management of ARVD involves arrhythmia suppression and prevention of thrombus formation. Sotalol, a beta blocker and a class III antiarrhythmic agent, is the most effective antiarrhythmic agent in ARVD. Other antiarrhythmic agents used include amiodarone and conventional beta blockers (i.e.: metoprolol). If antiarrhythmic agents are used, their efficacy should be guided by series ambulatory holter monitoring, to show a reduction in arrhythmic events. While angiotensin converting enzyme inhibitors (ACE Inhibitors) are well known for slowing progression in other cardiomyopathies, they have not been proven to be helpful in ARVD. Individuals with decreased RV ejection fraction with dyskinetic portions of the right ventricle may benefit from long term anticoagulation with warfarin to prevent thrombus formation and subsequent pulmonary embolism. Catheter ablation may be used to treat intractable ventricular tachycardia. It has a 60-90% success rate. Unfortunately, due to the progressive nature of the disease, recurrence is common (60% recurrence rate), with the creation of new arrhythmogenic foci. Indications for catheter ablation include drug-refractory VT and frequent recurrence of VT after ICD placement, causing frequent discharges of the ICD. An ICD is the most effective prevention against sudden cardiac death. Due to the prohibitive cost of ICDs, they are not routinely placed in all individuals with ARVD. Indications for ICD placement in the setting of ARVD include: - Cardiac arrest due to VT or VF - Symptomatic VT that is not inducible during programmed stimulation - Failed programmed stimulation-guided drug therapy - Severe RV involvement with poor tolerance of VT - Sudden death of immediate family member Since ICDs are typically placed via a transvenous approach into the right ventricle, there are complications associated with ICD placement and follow-up. Due to the extreme thinning of the RV free wall, it is possible to perforate the RV during implantation, potentially causing pericardial tamponade. Because of this, every attempt is made at placing the defibrillator lead on the ventricular septum. After a successful implantation, the progressive nature of the disease may lead to fibro-fatty replacement of the myocardium at the site of lead placement. This may lead to undersensing of the individual's electrical activity (potentially causing inability to sense VT or VF), and inability to pace the ventricle. Cardiac transplant surgery Cardiac transplant surgery may be performed in ARVD. It may be indicated if the arrhythmias associated with the disease are uncontrollable or if there is severe bi-ventricular heart failure that is not manageable with pharmacological therapy. All first degree family members of the affected individual should be screened for ARVD. This is used to establish the pattern of inheritance. Screening should begin during the teenage years unless otherwise indicated. Screening tests include: Highly-publicised deaths from arrhythmogenic right ventricular dysplasia Sevilla FC and Spanish international left wing-back Antonio Puerta died from the condition, at the age of 22, on 28 August 2007, three days after suffering several cardiac arrests, while disputing a La Liga game against Getafe CF. Englishman Matt Gadsby also died from the condition after collapsing on the pitch on 9 September 2006, while playing with his team Hinckley United in a Conference North game against Harrogate Town. Model Krissy Taylor, sister of Niki Taylor, died from the disease at age 17 in 1995. - Woolly hair nevus - ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ISBN 0071380760. - ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0721629210. - ^ Lahtinen, AM; Lehtonen, E, Marjamaa, A, Kaartinen, M, Heliö, T, Porthan, K, Oikarinen, L, Toivonen, L, Swan, H, Jula, A, Peltonen, L, Palotie, A, Salomaa, V, Kontula, K (2011). "Population-prevalent desmosomal mutations predisposing to arrhythmogenic right ventricular cardiomyopathy". Heart rhythm : the official journal of the Heart Rhythm Society 8 (8): 1214–21. doi:10.1016/j.hrthm.2011.03.015. PMID 21397041. - ^ Sen-Chowdhry S, Syrris P, McKenna WJ (November 2007). "Role of genetic analysis in the management of patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy". J. Am. Coll. Cardiol. 50 (19): 1813–21. doi:10.1016/j.jacc.2007.08.008. PMID 17980246. - ^ Overview of ARVD/C Genetic Testing - ^ Fontaine G, Tonet J, Gallais Y, Lascault G, Hidden-Lucet F, Aouate P, Halimi F, Poulain F, Johnson N, Charfeddine H, Frank R. (2000). "Ventricular tachycardia catheter ablation in arrhythmogenic right ventricular dysplasia: a 16-year experience". Curr Cardiol Rep 2 (6): 498–506. doi:10.1007/s11886-000-0034-1. PMID 11203287. - ^ "Sevilla star suffers heart attack". BBC Sport. 2007-08-25. http://news.bbc.co.uk/sport1/hi/football/europe/6964586.stm. Retrieved 2007-08-25. - ^ Sevilla star dies after collapse - ^ "Cause of Death". Cardiac Inherited Disease Group. Archived from the original on 2007-09-30. http://web.archive.org/web/20070930080147/http://www.cidg.org/webcontent/default.aspx?tabid=173. Retrieved 2006-10-31. - ^ "Shock at star player's death". icBirmingham.co.uk. 11 September 2006. http://icbirmingham.icnetwork.co.uk/0100news/0100localnews/tm_objectid=17723437&method=full&siteid=50002&headline=shock-at-star-player-s-death-name_page.html. Retrieved 2007-11-26. - GeneReviews/NCBI/NIH/UW entry on Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy, Autosomal Dominant - OMIM entries on Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy, Autosomal Dominant Cardiovascular disease: heart disease · Circulatory system pathology (I00–I52, 390–429) IschaemicActive ischemia LayersValves Conduction/ arrhythmiaPremature contractionWolff-Parkinson-White · Lown-Ganong-LevineFlutter/fibrillationPacemakerOther/ungrouped Cardiomegaly Other Arrestin MyelinPelizaeus–Merzbacher disease · Dejerine-Sottas disease · Charcot–Marie–Tooth disease 1B, 2J Pulmonary surfactant Cell adhesion molecule TetraspaninTSPAN7 (X-Linked mental retardation 58) · TSPAN12 (Familial exudative vitreoretinopathy 5) Other Genetic disorder, membrane: Channelopathy Calcium channelCACNA1A (Familial hemiplegic migraine 1, Episodic ataxia 2, Spinocerebellar ataxia type-6) · CACNA1C (Timothy syndrome, Brugada syndrome 3, Long QT syndrome 8) · CACNA1F (Ocular albinism 2, CSNB2A) · CACNA1S (Hypokalemic periodic paralysis 1, Thyrotoxic periodic paralysis 1) · CACNB2 (Brugada syndrome 4)Ligand gated Sodium channelVoltage-gatedSCN1A (Familial hemiplegic migraine 3, GEFS+ 2, Febrile seizure 3A) · SCN1B (Brugada syndrome 6, GEFS+ 1) · SCN4A (Hypokalemic periodic paralysis 2, Hyperkalemic periodic paralysis, Paramyotonia congenita, Potassium-aggravated myotonia) · SCN4B (Long QT syndrome 10) · SCN5A (Brugada syndrome 1, Long QT syndrome 3) · SCN9A (Erythromelalgia, Febrile seizure 3B, Paroxysmal extreme pain disorder, Congenital insensitivity to pain) Potassium channelKCNA1 (Episodic ataxia 1) · KCNA5 (Familial atrial fibrillation 7) · KCNC3 (Spinocerebellar ataxia type-13) · KCNE1 (Jervell and Lange-Nielsen syndrome, Long QT syndrome 5) · KCNE2 (Long QT syndrome 6) · KCNE3 (Brugada syndrome 5) · KCNH2 (Short QT syndrome) · KCNQ1 (Jervell and Lange-Nielsen syndrome, Romano-Ward syndrome, Short QT syndrome, Long QT syndrome 1, Familial atrial fibrillation 3) · KCNQ2 (BFNS1} Chloride channel TRP channel ConnexinGJA1 (Oculodentodigital dysplasia, Hallermann–Streiff syndrome, Hypoplastic left heart syndrome) · GJB1 (Charcot–Marie–Tooth disease X1) · GJB2 (Keratitis–ichthyosis–deafness syndrome, Ichthyosis hystrix, Bart–Pumphrey syndrome, Vohwinkel syndrome) · GJB3/GJB4 (Erythrokeratodermia variabilis, Progressive symmetric erythrokeratodermia) · GJB6 (Clouston's hidrotic ectodermal dysplasia) Porin Wikimedia Foundation. 2010.	2	17	3	0	0	3	0.82841	6	5,882
can be caused by a number of factors, including the type of dialysate used, composition of the dialyzer membrane, water quality in the dialysis unit, and the ultrafiltration rate of the treatment. PrincipleEdit. In peritoneal dialysis, wastes and water are removed from the blood inside the body using the peritoneum as a natural semipermeable membrane. Wastes and excess water move from the blood, across the peritoneal membrane and into a special dialysis solution, called dialysate, in. Peritoneal dialysate ﬂuid composition determines heat shock Peritoneal dialysis (PD) is the most frequently em-protein expression patterns in human mesothelial cells. ployed renal replacement therapy in end-stage renal dis-Background. Low biocompatibility of peritoneal dialysis ﬂu-ease in childhood . In PD, peritoneal dialysis ﬂuid dialysate composition for peritoneal dialysis To meet the ultrafiltration requirements of patients on peritoneal dialysis, the peritoneal dialysate is deliberately rendered hyperosmolar relative to plasma, to create an osmotic gradient that favors net movement of water into the peritoneal cavity. 10 Kidney Function Life Expectancy Without Dialysis A few days later, when I received the results in my office, I was in for a surprise: His renal function. Dialysis?”) are not uncommon. These claims also often fail to distinguish the relatively. Patients usually can get as much life-saving care as they want despite the cost or life expectancy. choose to manage their This happens because as the blood is filtered during dialysis, fluid is removed, thus reducing the kidneys. More important than the color, however, is the composition of the stone, which can. composition of the blood in patients on CRRT with the sterile, bicarbonate-based dialysate solution1 • Help reduce preparation time with easy-to-mix dialysate solutions2,3 PrismaSATE Dialysate Formula is intended for treatment of acute kidney disease (renal failure) using Continuous Renal Replacement Therapies, such as continuous Dialysate Composition in Hemodialysis and Peritoneal Dialysis T he goal of dialysis for patients with chronic renal failure is to restore the composition of the body’s fluid environment toward normal. This is accomplished principally by formulating a dialysate whose constituent concentrations are set to approximate normal values in the body. Hemodialysis School Bay Area The company has over 100 years of construction projects under its belt, especially in the East Bay, including a number of. Medical School: Albert Einstein College of Medicine, Bronx, New York. and the medical director of the Fresenius (Peralta) hemodialysis unit in Oakland, he offers. Dr. Dierks is a member of the advisory board for For home use, a dialysate preparation system is used which is also cartridge based, thus avoiding the need for extensive building and plumbing work and to reduce the volume of fluid storage that can. Haemodialysis fluid: composition and clinical importance. Ideally the composition of the dialysis fluid should match that of plasma, but due to differences between patients, as well as the increasing number of elderly patients receiving treatment, have resulted in a move towards individualisation of the electrolyte and buffer composition. Subclause 126.96.36.199.101 Composition of the DIALYSIS FLUID The requirement for a PROTECTIVE SYSTEM is also applicable to human errors (e.g. mistaking of DIALYSIS FLUID CONCENTRATEs) and also refers to Clause 15 (Construction of ME EQUIPMENT) and Clause 16 (ME SYSTEMS). In acetate treatment, it is considered to be Functions of the Kidney The kidneys maintain the volume and composition of blood. The basic concept of dialysis is straightforward: to place a semipermeable membrane between blood and a special. Renal Failure Dialysis Icd 9 Code (Using this code is not recommended, as measuring the eGFR to assess kidney disease would show the stage based on the eGFR level) Other evidence of renal disease must also be coded in addition to CKD, if applicable, and would require adherence to ICD-9 guidelines for proper coding. N17.9 Acute kidney failure, unspecified – ICD-10-CM There are two types of dialysis – hemodialysis and peritoneal dialysis. Both types involve the use of a fluid called dialysate, the medium used to carry the impurities and waste away from the blood. The prescription of dialysis fluid is moving from a pre-fixed, standard dialysate solution to individualization of electrolyte and buffer composition, not only during the dialysis session, but also within the same session (profiling) in order to provide patients with an optimal blood purification coupled with a high degree of tolerability. The dialysis machine is the machine that performs dialysis of the blood. Dialysis removes the waste product from the blood by drawing it through a vein in the forearm called the arterio-venous. Start studying Peritoneal Dialysis. Learn vocabulary, terms, and more with flashcards, games, and other study tools. Search. Installation of dialysate fluid into the peritoneal cavity. What does the peritoneal cavity serve as?. Then drain in the fresh dialysis solution [dialysate] from the top bag and into the peritoneal cavity. Dialysate and Replacement Fluid Composition for CRRT. Acid-base balance is greatly influenced by the type of dialysis employed and by the administration route of replacement fluids. In continuous veno-venous hemofiltration, buffer balance depends on losses with ultrafiltrate and gain with replacement fluid, while in techniques such as continuous. Blood flows by one side of a semi-permeable membrane, and a dialysate, or special dialysis fluid, flows by the opposite side. A semipermeable membrane is a thin layer of material that contains holes of various sizes, or pores. Smaller solutes and fluid pass through the membrane, but the membrane blocks the passage of larger substances (for. The dialysis machine is like a big computer and a pump. It keeps track of blood flow, blood pressure, how much fluid is removed and other vital information. It mixes the dialysate, or dialysis solution, which is the fluid bath that goes into the dialyzer. This fluid helps pull. MXene materials are composed of nanometer-thin layers whose chemical composition and spacing can be tailored. to break down the urea in the water that absorbs urea in dialysis, called dialysate, More Kidney Dialysis Articles … - B Braun Dialysis Uk: Central Des Moines Dialysis Learn about MercyOne Des Moines’ services at our medical centers, clinics, urgent care, and more. Find clinic locations or find a doctor searches. MercyOne DesMoines Des Moines, Iowa (IA) Area Hospitals, MercyOne Des… - Dialysis Centers In Lafayette La: Stirring renditions of "La Marseillaise" rang out Saturday from Dublin to New. Monuments from the Sydney Opera House in Australia to One World Trade Center in New York were adorned with France’s. El solicitante en estos casos, pudiera indic… - Relationship Between Volume Status And Blood Pressure During Chronic Hemodialysis: Research Article Relationship between Interdialytic Weight Gain and Blood Pressure in Pediatric Patients on Chronic Hemodialysis OliveraMarsenic, 1 MichaelAnderson, 2 andKevinG.Couloures 3 Pediatric Nephrology, Yale University, New Haven, CT, USA - Optimizing The Dialysate Calcium Concentration In Bicarbonate Haemodialysis: Depression And Dialysis Patients If you receive dialysis treatments for kidney disease, you probably spend a lot of time focused on your physical. that approximately 1 in 5 patients with chronic kidney disease. therapy (CBT), for instance, can succes… - Nxstage Home Hemodialysis Machines: Role Dialysis Nurse Manager Jun 25, 2018. Learn more about what role nurses play in four different healthcare settings. can eventually attain leadership positions, such as the role of nurse manager. are: dialysis nurses, telehealth nurses and palliat… - Continuous Cycle Peritoneal Dialysis: A continuous cycle peritoneal dialysis system and process is disclosed which includes a source (14) of sterilized dialysis fluid, and an inflow line (34) and outflow line (35) connected to a catheter (26) implanted in the peritoneal cavity (28) of a …	4	9	0	0	0	2	0.652906	2	1,846
Dr Gott Peripheral Neuropathy The aim of diabetes treatment is to bring blood sugar ("glucose") as close to normal as possible. What is a normal blood sugar level? Find out here. Wisdom teeth removal can lead to serious complications but so can keeping your wisdom teeth. Determine if you should extract or not extract. Aug 9, 2017. Diagnosis. Peripheral Celiac disease, or gluten sensitivity, is an autoimmune inflammatory disease that damages the villi – the small, finger-like projections that line the. Diabetic Neuropathy Femoral Nerve Causes of painful neuropathies include: alcoholic neuropathy: this condition may present with painful paraesthesiae in the legs followed by muscle weakness; diabetic amyotrophy: a subacute, painful and mainly motor mononeuropathy. Commonly involves the femoral nerve producing wasting and weakness of the. Jan 8, 2010. Moreover, other neurogenic causes such as disk disease can mimic peripheral Symptom Checker. Health Concern On Your Mind? @ Icd 9 Code Diabetic Peripheral Neuropathy ★★ Diabetes Feet Symptoms The 3 Step Trick that Reverses. To evaluate peripheral neuropathy: Check ankle Achilles tendon reflexes and look for delayed or absent reflexes as signs of peripheral neuropathy. Distal sensory loss often starts with loss of vibratory sensation, followed by loss of temperature sensation, followed by onset of pain. Findings are usually bilateral and. THE BOTTOM LINE. Peripheral neuropathy is a disease of the nervous system. It causes strange sensations, especially in the feet, legs, and fingers, and can cause pain. The pain might be mild, or so severe that it prevents someone from walking. Tell your health care provider immediately if you have any signs of PN. Learn about the diseases and conditions that may cause pain in the leg, calf, or thigh, and read about the medications used to treat this symptom. Other. ★ Diabetic Peripheral Neuropathy Symptoms ★ :: Sodium Diabetes – The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ DIABETIC. Signs of peripheral neuropathy vary depending on the nerves involved. Symptoms include: Numbness; Shooting or stabbing pain; Burning; Tingling; Muscle weakness; Balance disruptions; Loss of fine-motor skills; Difficulty picking up small objects; Constant or random pain; Sensitivity to cold or heat; Limited reflexes; Lack. Cancer or its treatment can damage the nerves that are outside the brain and spinal cord. This is called peripheral neuropathy. Feb 18, 2017. Neuropathy is the general term for pain or discomfort caused by damage to the nerves of the peripheral nervous system. For people with breast cancer, the most common cause of uncomfortable or even painful neuropathy that limits activity is chemotherapy — often referred. Other causes of neuropathy. Peripheral neuropathy is a common complication related to diabetes, and a major reason for a decreased quality of life in diabetes patients. There are contradicting studies estimating the prevalence of peripheral neuropathy in new- onset diabetes. Peripheral neuropathy in prediabetic patients is not well studied, but. Signs: Sensory. Pathognomonic neuropathic findings. Allodynia (pain from non- painful stimulus – such as light touch); Hyperalgesia (excessive pain from a painful stimulus). Demyelinating or infiltrative Neuropathy. Loss of vibration sense; Loss of joint position sense; Loss of tactile discrimination. Axonal Neuropathy. Signs and Symptoms; Diagnosis; Treatment. Although there are numerous causes of peripheral neuropathies, they do share some common symptoms, including: Weakness, numbness and pain in the hands, legs and/or feet; Paresthesia, a condition that causes abnormal sensations such as burning, tickling, pricking or. Aug 26, 2016. Imagine a "pins and needles" sensation that never went away. That's what millions of people experience every day due to a condition called peripheral neuropathy. Here are some basics about this uncomfortable but treatable condition. Information on Peripheral Neuropathy. Includes topic overview and related information. Col Richardson has suffered with severe neuropathy for over 45 years. A 27 year military veteran and veteran of the Vietnam War, he was diagnosed with a progressive chronic peripheral neuropathy resulting in severe disability. This diagnosis has been confirmed as due to exposure to Agent Orange. It was not until 2010, ★ Diabetic Peripheral Neuropathy Symptoms ★ :: Diabetes Blood Sugar Levels Chart – The 3 Step Trick that Reverses Diabetes Permanently in As Little as. ★★ Diabetic Peripheral Neuropathy Icd 9 Code ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ DIABETIC PERIPHERAL. Diagnosis. As peripheral neuropathy is a symptom, your doctor will evaluate you to determine its cause. Your doctor will review your medical history and examine you. Blood tests may be used to screen for underlying medical conditions, such as diabetes, thyroid disease, or vitamin deficiencies. quired causes of peripheral neuropathy that occurs more frequently than in cancer. Peripheral neu- ropathies in cancer patients will become even more common as new treatments and longer survivals are achieved. Confounding evaluation of neuropathy in a cancer patient are the multitude of injuries the peripheral. What Are the Symptoms of Neuropathy? When to Seek Medical Care for Neuropathy Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of. Peripheral Neuropathy Diagram. There are many causes for peripheral neuropathy. However there is also peripheral neuropathy of unknown origin ( a.k.a. Idiopathic Peripheral Neuropathy). Listed below are just some common types of peripheral neuropathy triggers: Nutritional or vitamin deficiencies – often a lack of B. Diabetic neuropathy — Comprehensive overview covers symptoms, causes, treatment of this serious complication of diabetes. @ Causes Of Diabetic Peripheral Neuropathy ★★ Type 2 Diabetes In Children Symptoms The 3 Step Trick that Reverses Diabetes Permanently in As Little as. ★★ Reversing Diabetic Peripheral Neuropathy ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ REVERSING DIABETIC. Low iron levels can also cause numbness, tingling or feelings of coldness usually felt in the hands or feet. The lack of oxygen also causes muscle weakness. Although these two symptoms resemble those of peripheral neuropathy, iron- deficiency anemia does not result in permanent nerve damage and can be treated. Diagnosis and Tests. Your doctor will ask you about your symptoms and perform a physical examination. You will likely have some blood work and other tests. More blood work might be ordered to determine a cause. Your doctor may order these tests to determine the cause of your peripheral neuropathy or rule out other. Peripheral Neuropathy Of Axonal Type It can be classified in several ways, such as whether it is inherited or acquired, whether it is rapid or insidious in onset, which part of the peripheral nervous system it affects (motor, sensory, autonomic), whether it has an axonal or demyelinating. Procedure code and Decription 20610 – Arthrocentesis, aspiration and/or injection, major joint or @ Treatment Of Diabetic Peripheral Neuropathy ★★ Diabetes Medications Powerpoint The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11. Types of Peripheral Neuropathies. Idiopathic \| Pre-diabetic/Diabetic \| Hereditary \| Toxic/Secondary to Drugs \| Inflammatory \| Systemic/Metabolic. Signs and Symptoms. elderly couple man with cane on beach The side effects of damaged nerves will vary depending on the location of your peripheral neuropathy, but generally occur in the upper and lower extremities and may include: Decreased mobility and muscle movement; Radiating or throbbing pain; Tingling. More Neuropathy Articles ... - Approach To Peripheral Neuropathy: The symptoms of chemotherapy induced peripheral neuropathy depend on the type. Chronic Pain Clinic for a multidisciplinary approach to pain management. Feb 26, 2009. In podiatric practice, we commonly see peripheral neuropathy, the. there are guideli... - Electrophysiological Testing For Peripheral Neuropathy: Feb 15, 1998. An algorithmic approach to the evaluation and differential diagnosis of a patient with peripheral neuropathy is presented, based on important elements of the clinical history and physical examination, the use of electromyography and ner... - Peripheral Neuropathy Diagnosis Icd-9: ★★ Diabetic Peripheral Neuropathy Icd 9 ★★ ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.[ DIABETIC PERIPHERAL. Disorders of peripheral nerves are among the most frequent neurological. In HIV mononeuropathy, the sympto... - Axonal Vs Demyelinating Peripheral Neuropathy: Dec 31, 2003. Peripheral nerves respond to injury in only a small number of ways. wallerian degeneration, axonal degeneration and segmental demyelination. This nerve shows the principle finding of an axonal neuropathy: diffuse loss. Diabetes mellitus... - Pain Management Diabetic Neuropathy: Drugs For Diabetic Neuropathy In this new analysis, researchers looked at the long-term effects of the drug on diabetes prevention and remission. events. the body repair the damage associated with diabetic peripheral neuropathy ( DPN). the same as th... - Acute Neuropathy Peripheral Sub: An examination of the blood smear (or film) may be requested by physicians or initiated by laboratory staff. With the development of sophisticated automated blood-cell analyzers, the proportion of blood-count samples that require a blood smear has st...	2	6	1	0	0	0	0.769604	1	2,107
Many medical ailments can be highly deadly if you don’t respond to them on time. One such condition is a cerebral infarction and the left middle cerebral artery infarction. Today we will be discussing cerebral infarction, its causes, symptoms diagnosis, and further treatment. What Is A Cerebral Infarction? A cerebral infarction (also known as a stroke) occurs when there is a lack of oxygen to the brain’s tissues. Arteriosclerosis, or “hardening of the arteries” that deliver oxygen-containing blood to the brain, is referred to as “arteriosclerotic cerebrovascular disease.” The phrase above indicates that a stroke occurred as a result of the brain’s damaged arteries. The basal ganglia refer to the part of the brain where the stroke happened. The basal ganglia (right and left basal ganglia, respectively) are involved in the regulation of a variety of functions, including movement. If an autopsy was performed, the autopsy report should provide more details about the mass in the breast, such as whether it was a malignant tumor or a benign process. This was all about what is cerebral infarction. Now let us see what are classifications of cerebral infarction are. Classifications Of Cerebral Infarction For a cerebral infarction, there are several classification systems, some of which are mentioned below: - The Oxford Community Stroke Project (OCSP, commonly known as the Bamford or Oxford classification) bases its classification mostly on the early symptoms. The stroke event is defined as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI), or posterior circulation infarct (PCI) depending on the severity of the symptoms (POCI). The magnitude of the stroke, the area of the brain-damaged, the underlying cause, and the prognosis are all predicted by these four components of ICD 10 cerebral infarction. - A stroke is classified as thrombosis or embolism due to atherosclerosis of a large artery, embolism of cardiac origin, occlusion of a small blood vessel, other determined cause, and undetermined cause according to the TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification, which is based on clinical symptoms as well as the results of further investigations (two possible causes, no cause identified, or incomplete investigation). Symptoms Of Cerebral Infarction The portions of the brain-damaged dictate the symptoms of cerebral infarction. Contralateral hemiparesis is reported to occur when an infarct occurs in the primary motor cortex. Brainstem syndromes such as Wallenberg’s syndrome, Weber’s syndrome, Millard–Gubler syndrome, Benedikt syndrome, and others are common with brainstem localization. On the opposite side of the body, infarctions cause weakness and loss of sensation. On physical examination of the head, aberrant pupil dilation, light responsiveness, and lack of eye movement on the opposite side will be discovered. The speech will be slurred if the infarction occurs on the left side of the brain. Reflexes may also be exacerbated. Risk Factors Of Cerebral Infarction The most common risk factors for cerebral infarction are similar to those for atherosclerosis. High blood pressure, diabetes, tobacco use, obesity, and dyslipidemia are only a few of them. Controlling these risk factors is recommended by the American Heart Association/American Stroke Association (AHA/ASA) to prevent stroke. If someone has a more specific issue, such as sickle-cell disease or pregnancy, the AHA/ASA recommendations guide how to prevent stroke. Based on data from the Framingham Heart Study, it is also possible to assess the risk of stroke in the next decade. Cerebral Infarction Pathophysiology Whether a cerebral infarction is caused by thrombosis or embolism, the pathophysiology of the disease, or the observed symptoms and underlying mechanisms. A thrombus forms and stops blood flow in thrombotic ischemic stroke. A thrombus arises when several signals stimulate the endothelium, causing platelet aggregation in the artery. A platelet plug is formed when a clump of platelets interacts with fibrin. A thrombus forms from the platelet clog, resulting in a stenotic artery. Large or tiny blood arteries can be affected by thrombotic ischemia. Atherosclerosis and vasoconstriction are the most common causes of thrombi in big arteries. Lipohyalinosis is the most common cause of small vessel disease. Lipohyalinosis is a condition in which fatty hyaline debris accumulates in blood vessels as a result of high blood pressure and age. Small vessel thrombotic ischemic stroke can potentially be caused by atheroma development. This can be diagnosed by using cerebral infarction ICD 10. When blood supply is obstructed, neurons depolarize, resulting in a wave known as spreading depolarization, which spreads from the afflicted core to the penumbra and healthy brain, causing additional depolarization, neuronal death, and neurologic symptoms. An embolic stroke occurs when an embolus, a moving particle or debris in the arterial flow that originates elsewhere, blocks an artery. A thrombus is the most common type of embolus, but it can also be made up of fat (for example, from bone marrow in a shattered bone), air, cancer cells, or clumps of germs (usually from infectious endocarditis). Atrial fibrillation, patent foramen ovale, or atherosclerotic plaque in another (or the same) major artery can all cause an embolus. Diagnosis Of Cerebral Infarction The sequelae of cerebral infarction using CT and MRI scans will reveal areas of the brain that have been injured, indicating that the symptoms are not due to a tumor, subdural hematoma, or other brain problem. The blockage will be visible on the angiography as well. An autopsy of a person who died of a cerebral infarction may reveal the length of time between the beginning of the infarction and the time of death. The diagnosis of ICD 10 code for cerebral infarction is used for tagging the diagnosis of cerebral infarction. Cerebral Infarction Treatment Thrombolytic medicines were introduced in the treatment of cerebral infarction in the last decade, much like they were in the treatment of myocardial infarction. In patients who arrive at a stroke unit and can be properly examined within 3 hours of onset, intravenous rtPA therapy can be recommended. If cerebral infarction is caused by a thrombus occluding blood flow to a brain artery, definitive therapy is to break down the clot (thrombolysis) or mechanically remove it (thrombectomy). The faster blood flow to the brain is restored, the fewer brain cells die. Pharmacologic thrombolysis with the medication tissue plasminogen activator (tPA) is being used in an increasing number of main stroke centers to dissolve the clot and unblock the artery. Direct excision of the offending thrombus is another treatment option for acute cerebral ischemia. A catheter is inserted into the femoral artery, directed into the cerebral circulation, and a corkscrew-like device is used to catch the clot, which is subsequently extracted from the body. Mechanical embolectomy devices have been shown to restore blood flow in individuals who were unable to receive thrombolytic medications or who were ineffective with the drugs, with no differences reported between newer and older versions of the devices. Only patients who had mechanical clot embolectomy within eight hours of the onset of symptoms were studied with the devices. Angioplasty and stenting are now being considered as feasible alternatives for treating acute cerebral ischemia. In a systematic review of six uncontrolled, single-center trials of intracranial stenting in symptomatic intracranial arterial stenosis involving a total of 300 patients, the rate of technical success (reduction to stenosis of 50% or less) ranged from 90 to 98 percent, and the rate of major peri-procedural complications ranged from 4 to 10%. Following treatment, the incidence of restenosis and/or stroke were likewise low. This evidence suggests that a large, randomized controlled study is required to fully assess the treatment’s potential therapeutic benefit. If investigations reveal carotid stenosis and the patient retains function on the affected side, carotid endarterectomy (surgical excision of the stenosis) may reduce the chance of recurrence if done soon after the stroke. For symptomatic carotid stenosis (>70 to 80 percent reduction in diameter), carotid endarterectomy is also recommended to reduce the risk of cerebral infarction. When tissue loss is not immediately fatal, the best line of action is to use physical treatment, cognitive therapy, occupational therapy, speech therapy, and exercise to try to recover deficiencies. Permissive hypertension, which allows for higher-than-normal blood pressures during the acute phase of brain infarction, can be utilized to promote penumbra perfusion. Diagnose Cerebral Infarction & Tackle It On Time Cerebral infarction can be deadly and fatal if not diagnosed on time. So, check for the earliest symptoms and tackle them within time. We hope we helped you in telling you about cerebral infarction and cerebral infarction definition.	2	7	2	0	0	0	0.961983	2	2,057
ICD stands for International Classification of Diseases. ICD-10 is the 10th edition of the World Health Organization’s International Statistical Categorization of Diseases and Related Health Problems (ICD). It includes disease codes, signs and symptoms, aberrant findings, complaints, social situations, and external causes of harm or sickness. ICD-10 development began in 1983, was approved by the 43rd World Health Assembly in 1990, and was first used by member states in 1994. It supersedes the International Classification of Diseases, Ninth Revision (ICD-9) from the 1970s. ICD-10 is a thorough rewrite of its predecessor, ICD-9. It increases clinical communication by delivering more information per code as well as improved assistance for care management, quality monitoring, and analytics. It also improves one’s understanding of risk and severity. ICD-10 Medical Code Set Many countries now employ national variants of ICD-10, each tailored to their specific healthcare system. The Centres for Medicare & Medicaid Services (CMS) and the National Centre for Health Statistics (NCHS) developed the US version of ICD-10, which includes two following two medical code sets: On October 1, 2015, ICD-10-CM and ICD-10-PCS became mandatory for medical claims reporting. However, the two code sets are drastically different. These codes not only respond to various diagnoses, but they also can deliver better and more up-to-date data for overall patient and health care improvement. The International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) is a system used by physicians and other healthcare practitioners in the United States to classify and code all diagnoses, symptoms, and procedures documented in association with hospital care. ICD-10-CM Diagnoses Codes are made up of three to seven characters. The first character is alphabetic, 2nd character is numeric, and characters 3 through 7 are alphabetic or numeric, with a decimal after the third digit. ICD-10-CM codes must be supplied to the payer for a medical provider to receive compensation for medical services. While CPT® codes represent the services offered to the patient, ICD-10-CM codes represent the diagnoses that justify the treatments rendered as medically essential. It is the International Classification of Diseases Procedure Coding System. This code set is only in hospital inpatient settings. Volume 3 of the International Classification of Diseases, Ninth Edition, Clinical Modification is being replaced by ICD-10-PCS. These codes are alphanumeric and contain seven characters. ICD-10-PCS is designed for use by health care professionals, organizations, and insurance programs. These codes are used for reporting morbidity data and invoicing in several clinical and health care applications.ICD-10-PCS codes are updated every year. ICD-10 Code Structure ICD-10-CM codes range from 3-7 characters in length. Every code starts with an alpha character that indicates the chapter to which the code belongs. Numbers make up the second and third characters. Numbers or letters can be used for the fourth, fifth, sixth, and seventh characters. S53.521A: ICD-10 code for torus fracture of the lower right end of the right radius. A37.81: This ICD-10 code deals with whooping cough due to other Bordetella species with pneumonia. Importance Of ICD-10 Codes The importance of the ICD-10 code system can be gauged by its use in numerous fields such as quality management, healthcare, IT, and public health. - The ICD-10 code system provides precise and up-to-date procedures to reduce healthcare costs and maintain equitable reimbursement practices. The new code assists healthcare providers in identifying individuals who require prompt illness management and tailoring successful disease management programs. - ICD-10-CM has been adopted internationally to facilitate the delivery of quality health care and global comparability. - ICD-10-CM is more specific than the previous edition (ICD-9-CM) and captures public health problems, particularly those associated with external damage, such as terrorism. - Code analysis is vital to research and development and ICD-10 codes are very important in research. The code framework and logic allow fewer coding errors, which aids research and development studies. - The ICD code system upgrade version improves health policy decision-making by providing improved organization supervision and achievement data. - The ICD-10 classification system aids in the reduction of drug errors, as well as the improvement of therapy alternatives and disease outcomes. - The ICD code system reduces treatment and claim costs in health policy and operational and strategic planning. - It Improves payment systems by handling claims. - That helps in reducing claim submissions. - ICD-10 codes were created primarily for reimbursement purposes to provide a logical framework for payment procedures. Billing Executive – a Medical Billing and Coding Knowledge Base for Physicians, Office staff, Medical Billers and Coders, including resources pertaining to HCPCS Codes, CPT Codes, ICD-10 billing codes, Modifiers, POS Codes, Revenue Codes, Billing Errors, Denials and Rejections. 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WikiMD Resources for Lymphoma Evidence Based Medicine Guidelines / Policies / Govt Patient Resources / Community Healthcare Provider Resources Continuing Medical Education (CME) Experimental / Informatics \|Classification and external resources\| Lymphoma is a type of blood cancer that occurs when B or T lymphocytes, the white blood cells that form a part of the immune system and help protect the body from infection and disease, divide faster than normal cells or live longer than they are supposed to. Lymphoma may develop in the lymph nodes, spleen, bone marrow, blood or other organs and eventually they form a tumor. Typically, lymphoma presents as a solid tumor of lymphoid cells. Treatment might involve chemotherapy and in some cases radiotherapy and/or bone marrow transplantation, and lymphomas can be curable depending on the histology, type, and stage of the disease. These malignant cells often originate in lymph nodes, presenting as an enlargement of the node (a tumor). It can also affect other organs in which case it is referred to as extranodal lymphoma. Extranodal sites include the tonsils, skin, brain, bowels and bone. Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but typically involve only circulating blood and the bone marrow (where blood cells are generated in a process termed haematopoiesis) and do not usually form static tumors. There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms. Signs and symptoms Lymphoma presents with certain non-specific symptoms. If symptoms are persistent, lymphoma needs to be excluded medically. - Lymphadenopathy or swelling of lymph nodes – It is the primary presentation in lymphoma. - B symptoms (systemic symptoms) – Can be associated with both Hodgkin's lymphoma and non-Hodgkin's lymphoma. They consist of: - Other Symptoms : Lymphoma is definitively diagnosed by a lymph node biopsy, meaning a partial or total excision of a lymph node that is then examined under the microscope. This examination reveals histopathological features that may indicate lymphoma. After lymphoma is diagnosed, a variety of tests may be carried out to look for specific features characteristic of different types of lymphoma. These include: Several classification systems have existed for lymphoma. These systems use histological findings and other findings to divide lymphoma into different categories. The classification of lymphoma can affect treatment and prognosis. Classification systems generally classify lymphoma according to: - Whether or not it is a Hodgkin lymphoma. - Whether the cell that is replicating is a T cell or B cell. - The site that the cell arises from. Hodgkin lymphoma is one of the best-known types of lymphoma, and differs from other forms of lymphoma in its prognosis and several pathological characteristics. A division into Hodgkin and non-Hodgkin lymphomas is used in several formal classification systems. A Hodgkin lymphoma is marked by the presence of a type of cell called the Reed-Sternberg cell. The current accepted definition is the WHO classification, published in 2001 and updated in 2008, is the latest classification of lymphoma and is based upon the foundations laid within the "Revised European-American Lymphoma classification" (REAL). This system attempts to group lymphomas by cell type (i.e. the normal cell type that most resembles the tumor) and defining phenotypic, molecular or cytogenetic characteristics. There are three large groups: the B cell, T cell, and natural killer cell tumors. Other less common groups, are also recognized. Hodgkin lymphoma, although considered separately within the World Health Organization (and preceding) classifications, is now recognized as being a tumor of, albeit markedly abnormal, lymphocytes of mature B cell lineage. Subtypes according to the WHO classification The 1996 Working Formulation was a classification of non-Hodgkin lymphoma. It excluded the Hodgkin lymphomas and divided the remaining lymphomas into four grades (Low, Intermediate, High, and Miscellaneous) related to prognosis, with some further subdivisions based on the size and shape of affected cells. This purely histological classification included no information about cell surface markers, or genetics, and it made no distinction between T-cell lymphomas or B-cell lymphomas. It was widely accepted at the time of its publication but is now obsolete. It is still used by some cancer agencies for compilation of lymphoma statistics and historical rate comparisons. - REAL. In the mid 1990s, the Revised European-American Lymphoma (REAL) Classification attempted to apply immunophenotypic and genetic features in identifying distinct clinicopathologic entities among all the lymphomas except Hodgkin's lymphoma. - ICD-O (codes 9590–9999, details at Template:Wayback) - ICD-10 (codes C81-C96, details at ) There are many forms of lymphoma. Some forms of lymphoma are categorized as indolent (e.g. small lymphocytic lymphoma), compatible with a long life even without treatment, whereas other forms are aggressive (e.g. Burkitt's lymphoma), causing rapid deterioration and death. However, most of the aggressive lymphomas respond well to treatment and are curable. The prognosis therefore depends on the correct diagnosis and classification of the disease, which is established after examination of a biopsy by a pathologist (usually a hematopathologist). \|Lymphoma type\|\|Relative incidence \|\|Histopathology \|\|Immunophenotype\|\|Overall \|Other comments \| \|Precursor T-cell leukemia/lymphoma\|\|40% of lymphomas in childhood.\|\|Lymphoblasts with irregular nuclear contours, condensed chromatin, small nucleoli and scant cytoplasm without granules.\|\|TdT, CD2, CD7\|\|It often presents as a mediastinal mass because of involvement of the thymus. It is highly associated with NOTCH1 mutations. Most common in adolescent males.\| \|Follicular lymphoma\|\|40% of lymphomas in adults\|\|Small "cleaved" cells (centrocytes) mixed with large activated cells (centroblasts). Usually nodular ("follicular") growth pattern\|\|CD10, surface Ig\|\|72–77%\|\|Occurs in older adults. Usually involves lymph nodes, bone marrow and spleen. Associated with t(14;18) translocation overexpressing Bcl-2. Indolent\| \|Diffuse large B cell lymphoma\|\|40 to 50% of lymphomas in adults\|\|Variable. Most resemble B cells of large germinal centers. Diffuse growth pattern.\|\|Variable expression of CD10 and surface Ig\|\|60%\|\|Occurs in all ages, but most commonly in older adults. Often occurs outside lymph nodes. Aggressive.\| \|Mantle cell lymphoma\|\|3 to 4% of lymphomas in adults\|\|Lymphocytes of small to intermediate size growing in diffuse pattern\|\|CD5\|\|50% to 70%\|\|Occurs mainly in adult males. Usually involves lymph nodes, bone marrow, spleen and GI tract. Associated with t(11;14) translocation overexpressing cyclin D1. Moderately aggressive.\| \|B-cell chronic lymphocytic leukemia/lymphoma\|\|3 to 4% of lymphomas in adults\|\|Small resting lymphocytes mixed with variable number of large activated cells. Lymph nodes are diffusely effaced\|\|CD5, surface immunoglobulin\|\|50%.\|\|Occurs in older adults. Usually involves lymph nodes, bone marrow and spleen. Most patients have peripheral blood involvement. Indolent.\| \|MALT lymphoma\|\|~5% of lymphomas in adults\|\|Variable cell size and differentiation. 40% show plasma cell differentiation. Homing of B cells to epithelium creates lymphoepithelial lesions.\|\|CD5, CD10, surface Ig\|\|Frequently occurs outside lymph nodes. Very indolent. May be cured by local excision.\| \|Burkitt's lymphoma\|\|< 1% of lymphomas in the United States\|\|Round lymphoid cells of intermediate size with several nucleoli. Starry-sky appearance by diffuse spread with interspersed apoptosis.\|\|CD10, surface Ig\|\|50%\|\|Endemic in Africa, sporadic elsewhere. More common in immunocompromised and in children. Often visceral involvement. Highly aggressive.\| \|Mycosis fungoides\|\|Most common cutaneous lymphoid malignancy\|\|Usually small lymphoid cells with convoluted nuclei that often infiltrate the epidermis, creating Pautrier microabscesseses.\|\|CD4\|\|75%\|\|Localized or more generalized skin symptoms. Generally indolent. In a more aggressive variant, Sézary's disease, there is skin erythema and peripheral blood involvement.\| \|Peripheral T-cell lymphoma-Not-Otherwise-Specified\|\|Most common T cell lymphoma\|\|Variable. Usually a mix small to large lymphoid cells with irregular nuclear contours.\|\|CD3\|\|Probably consists of several rare tumor types. It is often disseminated and generally aggressive.\| \|Nodular sclerosis form of Hodgkin lymphoma\|\|Most common type of Hodgkin's lymphoma\|\|Reed-Sternberg cell variants and inflammation. usually broad sclerotic bands that consists of collagen.\|\|CD15, CD30\|\|Most common in young adults. It often arises in the mediastinum or cervical lymph nodes.\| \|Mixed-cellularity subtype of Hodgkin lymphoma\|\|Second most common form of Hodgkin's lymphoma\|\|Many classic Reed-Sternberg cells and inflammation\|\|CD15, CD30\|\|Most common in men. More likely to be diagnosed at advanced stages than the nodular sclerosis form. Epstein-Barr virus involved in 70% of cases.\| After a diagnosis and before treatment, a cancer is staged. This refers to deducing how far the cancer has spread, in local tissue and to other sites. Staging is reported as a grade between I (confined) and IV (spread). Staging is carried out because the stage of a cancer impacts its prognosis and treatment. The Ann Arbor staging system is routinely used for staging of both HL and NHL. In this staging system, I represents a localized disease contained within a lymph node, II the presence of lymphoma in two or more lymph nodes, III spread of the lymphoma to both sides of the diaphragm, and IV to tissue outside a lymph node. Prognosis and treatment is different for HL and between all the different forms of NHL, and also depends on the grade of tumour, referring to how quickly a cancer replicates. Paradoxically, high-grade lymphomas are more readily treated and have better prognoses . A well-known example of a high-grade tumour is that of Burkitt's lymphoma, which is a high-grade tumour that has been known to double within days, but is readily treated. Many low-grade lymphomas remain indolent for many years. In these lymphomas, metastases are very likely. For this reason, treatment of the non-symptomatic patient is often avoided. In these forms of lymphoma ,Template:Which watchful waiting is often the initial course of action. This is carried out because the harms and risks of treatment outweigh the benefits. If a low-grade lymphoma is becoming symptomatic, radiotherapy or chemotherapy are the treatments of choice; although they do not cure the lymphoma, they can alleviate the symptoms, particularly painful lymphadenopathy. Patients with these types of lymphoma can live near-normal lifespans, but the disease is incurable. Treatment of some other, more aggressive, forms of lymphoma Template:Which can result in a cure in the majority of cases, but the prognosis for patients with a poor response to therapy is worse. Treatment for these types of lymphoma typically consists of aggressive chemotherapy, including the CHOP or R-CHOP regimen. Hodgkin lymphoma typically is treated with radiotherapy alone, as long as it is localized. Advanced Hodgkin disease requires systemic chemotherapy, sometimes combined with radiotherapy. Chemotherapy used includes the ABVD regimen. \|5-year relative survival by stage at diagnosis\| \|Stage at diagnosis\|\|5-year relative of cases (%) \|Localized (confined to primary site)\|\|82.1\|\|27\| \|Regional (spread to regional lymph nodes)\|\|77.5\|\|19\| \|Distant (cancer has metastasized)\|\|59.9\|\|45\| Lymphoma is the most common form of hematological malignancy, or "blood cancer", in the developed world. Taken together, lymphomas represent 5.3% of all cancers (excluding simple basal cell and squamous cell skin cancers) in the United States and 55.6% of all blood cancers. According to the U.S. National Institutes of Health, lymphomas account for about five percent of all cases of cancer in the United States, and Hodgkin's lymphoma in particular accounts for less than one percent of all cases of cancer in the United States. Because the whole system is part of the body's immune system, patients with a weakened immune system such as from HIV infection or from certain drugs or medication also have a higher incidence of lymphoma. Thomas Hodgkin published the first description of lymphoma in 1832, specifically of the form named after him, Hodgkin's lymphoma. Since then, many other forms of lymphoma have been described, grouped under several proposed classifications. The 1982 Working formulation became very popular. It introduced the category non-Hodgkin lymphoma, divided into 16 diseases. However, because these lymphomas have little in common with each other, the NHL label is of limited usefulness for doctors or patients and is slowly being abandoned. The latest classification by the WHO (2008) lists 70 forms of lymphoma divided into four broad groups. As an alternative to the American Lakes-Butler classification, in the early 1970s, Karl Lennert of Kiel, Germany, proposed a new system of classifying lymphomas based on cellular morphology and their relationship to cells of the normal peripheral lymphoid system. Significant research into the causes, prevalence, diagnosis, treatment, and prognosis of lymphoma is being performed. Hundreds of clinical trials are being planned or conducted at any given time. Studies may focus on effective means of treatment, better ways of treating the disease, improving the quality of life for patients, or appropriate care in remission or after cures. In general, there are two types of lymphoma research: clinical or translational research and basic research. Clinical/translational research focuses on studying the disease in a defined and generally immediately patient-applicable way, such as testing a new drug in patients. By contrast, basic science research studies the disease process at a distance, such as seeing whether a suspected carcinogen can cause healthy cells to turn into lymphoma cells in the laboratory or how the DNA changes inside lymphoma cells as the disease progresses. The results from basic research studies are generally less immediately useful to patients with the disease but can improve scientists' understanding of lymphoma and form the foundation for future, more effective treatments. - "What is lymphoma?". Medical News Today. Retrieved 28 February 2013. - "About Lymphoma". Lymphoma Research Foundation. Retrieved 22 December 2012. - "Warning Signs of Lymphoma — First Signs of Lymphoma". Lymphoma.about.com. Retrieved 2012-12-01. - Mallick, Indranil. "How Is Lymphoma Diagnosed?". lymphoma.about.com. Retrieved 22 December 2012. - National Cancer Institute, "Hodgkin Lymphoma", http://www.cancer.gov/cancertopics/types/hodgkin, accessed on 2013-08-05 - National Cancer Institute. "What You Need To Know About Hodgkin Lymphoma". U.S. Dept of Health and Human Services, (online at http://www.cancer.gov/cancertopics/wyntk/hodgkin.pdf), pg 4. - Clarke CA, Glaser SL, Dorfman and Dorfwoman RF, Bracci PM, Eberle E, Holly EA (January 2004). "Expert review of non-Hodgkin lymphomas in a population-based cancer registry: reliability of diagnosis and subtype classifications". Cancer Epidemiol. Bio-markers Prev. 13 (1): 138–43. doi:10.1158/1055-9965.EPI-03-0250. PMID 14744745.CS1 maint: multiple names: authors list (link) - Non-Hodgkin Lymphoma at eMedicine - Lymphoma, Follicular at eMedicine - 50% for limited stage, according to: Leitch HA, Gascoyne RD, Chhanabhai M, Voss NJ, Klasa R, Connors JM (October 2003). "Limited-stage mantle-cell lymphoma". Ann. Oncol. 14 (10): 1555–61. doi:10.1093/annonc/mdg414. PMID 14504058.CS1 maint: multiple names: authors list (link) - 70% for advanced stage, according to most recent values in: Herrmann A, Hoster E, Zwingers T; et al. (February 2009). "Improvement of overall survival in advanced stage mantle cell lymphoma". J. Clin. Oncol. 27 (4): 511–8. doi:10.1200/JCO.2008.16.8435. PMID 19075279. Explicit use of et al. in: \|author=(help)CS1 maint: multiple names: authors list (link) - "Chronic Leukemias". The Merck Manual of Geriatrics. - Diviné M, Casassus P, Koscielny S; et al. (December 2005). "Burkitt lymphoma in adults: a prospective study of 72 patients treated with an adapted pediatric LMB protocol". Ann. Oncol. 16 (12): 1928–35. doi:10.1093/annonc/mdi403. PMID 16284057. Explicit use of et al. in: \|author=(help)CS1 maint: multiple names: authors list (link) - Kirova YM, Piedbois Y, Haddad E; et al. (May 1999). "Radiotherapy in the management of mycosis fungoides: indications, results, prognosis. Twenty years experience". Radiother Oncol. 51 (2): 147–51. doi:10.1016/S0167-8140(99)00050-X. PMID 10435806. Explicit use of et al. in: \|author=(help)CS1 maint: multiple names: authors list (link) - Sweetenham JW (November 2009). "Treatment of lymphoblastic lymphoma in adults". Oncology (Williston Park, N.Y.). 23 (12): 1015–20. PMID 20017283. - Elphee EE (May 2008). "Understanding the concept of uncertainty in patients with indolent lymphoma". Oncol Nurs Forum. 35 (3): 449–54. doi:10.1188/08.ONF.449-454. PMID 18467294. - Bernstein SH, Burack WR (2009). "The incidence, natural history, biology, and treatment of transformed lymphomas". Hematology Am Soc Hematol Educ Program. 2009: 532–41. doi:10.1182/asheducation-2009.1.532. PMID 20008238. - Martin NE, Ng AK (November 2009). "Good things come in small packages: low-dose radiation as palliation for indolent non-Hodgkin lymphomas". Leuk. Lymphoma. 50 (11): 1765–72. doi:10.3109/10428190903186510. PMID 19883306. - Kuruvilla J (2009). "Standard therapy of advanced Hodgkin lymphoma". Hematology Am Soc Hematol Educ Program. 2009: 497–506. doi:10.1182/asheducation-2009.1.497. PMID 20008235. - Data from the USA 1999–2006, All Races, Both Sexes: Altekruse SF, Kosary CL, Krapcho M, Neyman N, Aminou R, Waldron W, Ruhl J, Howlader N, Tatalovich Z, Cho H, Mariotto A, Eisner MP, Lewis DR, Cronin K, Chen HS, Feuer EJ, Stinchcomb DG, Edwards BK (eds). SEER Cancer Statistics Review, 1975–2007, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2007/, based on November 2009 SEER data submission, posted to the SEER web site, 2010. - Horner MJ, Ries LAG, Krapcho M, Neyman N, et al. (eds). "SEER Cancer Statistics Review, 1975–2006". Surveillance Epidemiology and End Results (SEER). Bethesda, MD: National Cancer Institute. Retrieved 3 November 2009. Table 1.4: Age-Adjusted SEER Incidence and U.S. Death Rates and 5-Year Relative Survival Rates By Primary Cancer Site, Sex and Time PeriodCS1 maint: multiple names: authors list (link) - "Understanding Clinical Trials for Blood Cancers" (PDF). Leukemia and Lymphoma Society. Retrieved 19 May 2010. Table of contents: # - A - Adrenal gland disorders - AIDS / HIV - ADHD or Attention deficit/hyperactivity disorder - Autism spectrum disorder (ASD) - Bacterial vaginosis - Birth control (see contraception) - Birth defects - Breastfeeding and breast milk - Brittle bone disease also called osteogenesis imperfecta - Cerebral palsy - Childbirth see labor and delivery - Childhood cancers - Children's bone health and calcium - Congenital adrenal hyperplasia (cah) - Contraception and birth control - Cushing syndrome - Cyberbullying see bullying - Delayed puberty see puberty and precocious puberty) - Dental health in children - Down syndrome - Driving risk Table of contents: - Ear infections in children - Early labor and birth (see preterm labor and birth) - Early learning - Early puberty (see puberty and precocious puberty) - Eczema and atopic dermatitis - Fertility problems (see infertility and fertility) - Fibroids (see uterine fibroids) - Fragile x syndrome - Fragile x-associated primary ovarian insufficiency (fxpoi) - Fragile x-associated tremor and ataxia syndrome (fxtas) - Hellp syndrome (see preeclampsia and eclampsia) - High-risk pregnancy - HIV and AIDS]] - Infant care and infant health - Infant mortality - Infertility and fertility - Intellectual and developmental disabilities Table of contents: - Maternal mortality - Mccune-albright syndrome (mas) - Men's reproductive health - Menkes disease - Menstruation and menstrual problems - Miscarriage (see pregnancy loss (before 20 weeks of pregnancy)) - Monosomy x (see turner syndrome) - Muscular dystrophy Table of contents: - Pediatric injury - Pelvic floor disorders - Pelvic pain - Pheochromocytoma and paraganglioma - Pituitary tumors - Polycystic ovary syndrome - Prader-willi syndrome - Preconception care and prenatal care - Preeclampsia and eclampsia - Pregnancy loss (before 20 weeks of pregnancy) - Preterm labor and birth - Primary ovarian insufficiency - Puberty and precocious puberty - Reading and reading disorders - Rehabilitation medicine - Rehabilitative and assistive technology - Rett syndrome - Rh incompatibility - Sexually transmitted diseases - Shaken baby syndrome - Skipped or no menstrual periods (see amenorrhea - Spina bifida - Spinal cord injury - Spinal muscular atrophy - Sudden infant death syndrome - Toxemia (see preeclampsia and eclampsia) - Traumatic brain injury - Trisomy 21 (see down syndrome) - Turner syndrome Table of contents: Glossaries and dictionaries \| Medicine portal \| Health Topics \| Health Encyclopedia \| First Aid \| Weight Loss \| Drugs \| Glossary of medicine \| insurance \| Glossary of health topics \| Drug classes \| Medicines \| Dentistry portal \| Medications portal \| Pharmacology portal \| Psychiatry portal \| Rare diseases \| List of health topics	2	20	1	0	1	2	0.652927	4	5,512
ICD-11 – The Next-Generation Coding System The International Classification of Diseases (ICD) provides a public global standard platform to organize and classify information about diseases and related health issues. ICD is a member of the World Health Organization’s “Family” of International Classifications (WHO-FIC) that offer the required health information by capturing data from varied interoperable delivery points across the systems and countries using a suite of integrated standard tools. In order to maintain the scientific accuracy, ICD is scheduled for yearly periodic revisions as per the WHO recommendations. The latest revision, ICD-10, was adopted by the World Health Assembly in 1990. A systematic revision of the current ICD 10th version will serve the needs of multiple users in a coordinated manner to improve the classification based upon scientific basis, clinical and public health use, by going through the following three stages. - Compilation of scientific, clinical and public health evidence for revision, known as ICD-10 Plus. - Creation of a draft ICD-11 development and field testing, - Creation of a systematic linkage to the available standard health care terminologies to process the information. From October 2015, all healthcare providers and other HIPAA entities have started using ICD-10 codes. ICD-10 upgrade has been provided to the clients at no additional charge. ICD-10 codes facilitate the tracking of mortality rates in conjunction with the specific diagnosis. The improvements from ICD-9 to ICD-10 transition include the addition of information on ambulatory care, expanded injury codes, combined diagnosis/symptom codes to describe medical conditions with greater specificity. Even the claims will be denied without payment, if HIPAA covered claim management software use ICD-9 codes. ICD-10 codes contain up to seven alpha-numeric characters while ICD-9 codes only contain up to 5 characters. The expanded length of ICD-10 codes (68000) compared to ICD-9 codes (13000) can convey more specific information. Towards an ICD-11 two major drafts will be developed. The ICD 11 alpha draft will be subjected to KMS portal view by the internal users such as WHO FIC network and experts. The ICD 11-beta draft will be subjected to systematic field trials for the whole world to enhance feasibility, reliability, clinical utility and validity. The work will be mainly carried out by the Revision Steering Group and the Workgroups to coordinate the overall ICD revision and address different aspects of health care. The Revision Steering Group will serve as the planning authority in the updation and revision process. They oversee the revision process and give advice for coordination of workgroups. They also identify basic taxonomic and ontological principles and develop plans for transition from ICD-10 to ICD-11. The Revision Steering Group include WHO Member States, the WHO-FIC Network, and multiple professional organizations. The Topic Advisory Groups (TAG) will serve as the coordinating advisory body for specific issues namely Oncology, Mental Health, etc. They provide advice on topic revision steps, establishment of workgroups, development of drafts of topic segments, establish workgroups and partners for involvement and implementation of field trials. Each TAG will function at two levels as chairs and members, along with a workgroup structure. The Work Groups will serve as the key functioning unit for the review of evidence and generation of main proposals at a specific topic in the classification. Their core responsibilities include definition of the diagnostic entity as a medical disease, reviewing the empirical evidence, reporting the results and recommendations to the TAG and global community and evaluation of field trials. ICD-11 beta draft – Revision Field Trials The Global Health Practice Network (GHPN) include health professionals throughout the world to provide varied information about patient characteristics to inform the ICD update and revision process. The clinician ratings of individual patients and patient self-report questionnaires collected by the participating clinicians will be used in the field surveys. ICD-11 alpha draft – Knowledge Management and Sharing Portal The important elements of this KMS Portal will be: - a) The ICD Revision Platform facilitate transparent communication within expert workgroups in the form of blogs for wider participation. - b) A public forum to give feedback to expert groups throughout the development process. - c) Structured field trials focusing on testing of various options for their feasibility and utility. ICD-11 is defined as an operational relational model of diseases and related health conditions which will have clear descriptions of each attribute such as entity title, classification property, terms, anatomy, temporal property, severity of subtypes properties, manifestation, casual, functioning, treatment and diagnostic properties. These features were exemplified in a structured computerized framework that captures the knowledge which underpins an ICD entity, with links to ontologies and SNOMED CT. The final draft of ICD-11 system is expected to be submitted to World Health Assembly in 2019 and come into effect in 2022. The preparation version was released on 18 June 2018. ICD-11 include transition tables from and to ICD-10, ICD-11 transition solutions tool, hospital coding tool, web services, training protocols etc., which are user friendly, multilingual (43 languages) and accessible after registration in maintenance platform. Around 300 medical specialists from 55 countries organized in 30 working groups have scientifically updated ICD-11 by solving structural problems in ICD-10. Cancer coding, primary care and traditional medicine are included in ICD-11 system. This system can be connected to any electronic health records (EHRs) data source through a standard API and can be used offline also. ICD-11 simplifies the healthcare and medical coding and billing software solutions to allow healthcare professionals to record the conditions easily, accurately and completely. Even the expert healthcare and medical coding service providers would help physician in reporting diagnosis using ICD-11 medical coding software solutions. In future, all healthcare systems would start using ICD-11 compliance solutions like medical billing software by integrating ICD-11 codes, conduct internal testing and training the staff.	3	6	2	0	0	0	0.506318	2	1,260
SA node manages the speed of heart's muscular contractions which enables the center to circulate the blood throughout the body according to the need. Small variations in the heart beat are not damaging but in some cases due to malfunctioning of the heart's electric powered system, the heart rate varies drastically resulting in various types of arrhythmias. These cardiac arrhythmias are serious disorders that ought to be cured immediately. Arrhythmias like bradycardia (low heartrate) can be cared for using Pacemakers. Pacemakers can be implanted in the patient's heart and soul for permanently revitalizing the heart and soul. It is utilized for patients for whom the SA node is no more functioning properly. Exterior Pacemakers are also available which is utilized to treat temporary heart rate variants. It is utilized for a short time frame prior to the implanting the inner Pacemakers in the heart and soul. To be able to understand the necessity of pacemakers, it's important to comprehend the functioning of the heart and its electronic system. HEART & ITS ELECTRICAL SYSTEM: Heart is a pumping device which is utilized to circulate the bloodstream throughout the body. It has four chambers namely Right Atrium, Still left Atrium, Right Ventricle and Remaining Ventricle. The proper atrium receives the deoxygenated blood vessels from the complete body through the superior vena cava and substandard vena cava. The remaining atrium receives oxygenated bloodstream from the lungs through the pulmonary blood vessels. Once the atrium contracts the blood flows to the equivalent ventricle. That is credited to atrial depolarization. If the left ventricle contracts, the oxygenated blood is supplied to all tissues in the body through the aorta. That is credited to ventricular depolarization. Likewise, the deoxygenated bloodstream is pumped to the lungs for oxygenation through the pulmonary artery during the contraction of right ventricle. That is due to ventricular repolarization. The Electrical conduction system of the heart includes SA node, AV node, Pack of His, Purkinje Fibers. The chambers of the center should be activated electrically for contraction. The stimulations are given by the SA node (Natural Pacemaker of the heart and soul) which is located in the right atrium of the heart and soul near the entrance of the superior vena cava. Although all the heart and soul cells have the ability to produce electric powered pulses which can encourage the center, SA node sets off the heart. The actual fact that SA node produces pulses at a higher rate in comparison with other potential cells which can promote contraction, plays a part in this phenomena. The contraction of various chambers of the heart and soul is characterized in an exceedingly specific manner. As the electric pulses pass through each chamber of the heart and soul, they are activated to deal. The SA node first triggers the right and kept atrium to contract. Then the impulses happen to be the AV node which is situated between your atria and the ventricles. From AV node, the pulses happen to be the pack of his. The pulses travel to the individual ventricles through the right and remaining pack branch and reach the Purkinje materials. In case the SA node fails, then your AV node acts as the primary pacemaker. When the AV node fails, then the Purkinje fibers takes the responsibility. The SA node will get blood supply from right and remaining coronary arteries. Under ischaemic conditions, the fatality of the afflicted cells will stop the SA node from triggering the pulse. There is a time frame following the excitement of center muscle during which no other action potential can result in the center muscles. This era is recognized as Total or Effective Refractory Period (ERP) of heart. It is normally around 0. 4 sec. ERP is managed up to possible in order to maintain tachycardia also to coordinate the muscle contraction. The anti-arrhythmic drugs used by the patients usually prolongs the ERP. ELECTRICAL SYSTEM OF HEART ECG & It has the SIGNIFICANCE: The electronic activity of the heart muscles is saved as Electrocardiogram (ECG). It can be obtained non-invasively from the top of body by pursuing specific lead configurations. The electrical current made in the heart and soul scheduled to depolarization and repolarization is disperse not only within the heart but also throughout the body. So, ECG can be easily bought from the top of body through electrodes. ECG has four basic components specifically, P influx, QRS complex, T wave and U influx. P wave occurs during atrial contraction scheduled to atrial depolarization. The length of time of the P wave runs from 0. 08- 0. 1 sec. During the atrial depolarization, the impulse from the SA node spreads throughout the atrium. The period of time between the onset of the P influx and the start of the QRS organic is about 0. 12- 0. 2 sec. During the zero potential period between your P influx and QRS complex, the impulse journeys within the AV node and the Pack of His. QRS complex occurs during ventricular contraction credited to ventricular depolarization. The length of the QRS intricate amounts from 0. 06-0. 1 sec. T wave occurs during ventricular leisure credited to ventricular repolarization. Sometimes, a little positive U wave occurs following a T wave because of the last remnants of the ventricular repolarization. NORMAL AND ABNORMAL ECG WAVES: Heart rateis nothing but the quantity ofheartbeatsper device oftimewhich is expressed as beats per minute (bpm) - which can vary as the body's need for air changes, such as duringexercise or sleeping. The measurement of heart rate can be used bymedical professionalsto help out with thediagnosisand traffic monitoring of medical ailments. Additionally it is utilized by individuals, such asathletes, who are thinking about monitoring their heart rate to get maximum efficiency of their training. TheR waveto R wave interval(RR interval) is the inverse of the heart rate, that is one divided by RR interval gives the heart rate. Typical healthy relaxing heartrate in men and women is 60-80 bpm which is described be normal heartrate, with rates below 60 bpm referred to asbradycardia and rates above 100 bpm described astachycardia. This can be found when the R-R interval is double the actual R-R interval (for normal things). Heart and soul pulses misses at some intervals and will not follow the premature pulse. This is a crucial reduction of heart rate and characterized by normally aimed abnormally huge P waves and normal PR period. Whenever the R-R period surpasses 1 sec the heart rate goes below 60 and the condition is referred to as Bradychardia. There are three types of Bradychardia conditions based on the characteristics of the ECG influx, these are Sinus bradychardia, Atrio-ventricular nodal bradychardia and ventricular bradychardia respectively. They are really reviewed below. Sinus bradycardias are also called as Atrial bradychardias. This bradychardia condition is usually found in young and healthy men and women. The symptoms represent with the individual'srespirations. Theabnormalpattern of eachinhalationcorresponds with the heartrate decreasing. Expirationcauses an increase in the heart's rate of contraction. This is thought to be induced by changes in the vagal tone duringrespiration. Sinus bradycardia is a sinus tempo of significantly less than 60 bpm. It is the condition within both healthy individuals and the ones who are believed wellconditioned athletes. The explanation for this is the fact their center muscle has become conditioned to have a higher stroke level and therefore requires fewer contractions to circulate the same level of blood. Sick sinus syndromecovers conditions including severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardi-tachycardia syndrome (atrial fibrillation, flutter, and paroxysmal supraventricular tachycardia). Atrio ventricular nodal bradycardia: ATRIO VENTRICULAR NODAL BRADYCARDIA An atrio ventricular nodal bradycardia or AV junction tempo is usually induced by the absence of the electro-mechanical impulse from thesinus node. This usually appear on anEKGwith a standard QRS complexaccompanied with an inverted P influx either before, during, or following the QRS organic. An AV junctional break free is a postponed heartbeat originating from anectopicfocus someplace in theAV junction. It occurs when the rate ofdepolarizationof the SA node comes below the rate of the AV node. This dysrhythmia also may occur when the electric impulses from the SA node fail to reach the AV node because of SA or AV stop. This is a protective mechanism for the heart and soul, to pay for a SA node that is no more handling the rate making activity, and is also one of a series of backup sites that can take over pacemaker function when the SA node does not do so. This would present with a longerPR interval. A junctional escape complex is a normal response which could result from excessive vagal tone on the SA node. Pathological triggers include sinus bradycardia, sinus arrest, sinus exit block, or AV stop. This picture shows an ECG of any person with an unnatural rhythm (arrhythmia) named an atrioventricular (AV) stop. P waves show that the very best of the heart received electrical power activity. Each P influx is usually followed by the high (QRS) waves. QRS waves represent the electro-mechanical activity that causes the heart and soul to contract. When a P wave exists and not accompanied by a QRS influx (and center contraction), there is an atrioventricular block, and an extremely slow-moving pulse (bradycardia). PACEMAKER AND ITS OWN SIGNIFICANCE: More than 60% people show up victim to center attacks in the majority of the countries around the globe each year and thousands more are critically damaged in accidents. Caring for these patients in special treatment units will involve the usage of specialized tools like pacemakers over the other important ones. In the past few years electronic digital pacemaker systems have become quite one in saving lives of cardiac patients whose normal pacing functions have been impaired. With regards to the exact nature of any cardiac dysfunction, an individual may require short-term artificial pacing during the course of treatment or long lasting pacing to be able to lead an active, successful life after treatment. A device with the capacity of generating unnatural pacing impulses and delivering those to the heart is known as a pacemaker system (commonly called a pacemaker) and consists of a pulse generator and appropriate electrodes. Pacemakers can be purchased in a number of forms. These are mainly divided into two types External pacemakers and Internal pacemakers respectively. External pacemakers are used on the patients with temporary heart and soul irregularities, such as those came across in the coronary patient, including heart and soul blocks. Also, they are used for momentary management of certain arrhythmias that occur in the patients during critical postoperative periods and in the patients during cardiac surgery, especially if the surgery consists of the ideals or septum. An external pacemaker usually involves an externally worn pulse generator linked to electrodes located on or within the myocardium. External pacemakers, such as all sorts of pulse generators located beyond your body, are usually connected through wires introduced into the right ventricle with a catheter catheter. The pulse generator may be strapped to the lower arm of an individual who is restricted to bed, or worn at the midsection associated with an ambulatory patient. We have made the pacemaker which is often divided into two general categories namely - Asynchronous pacemaker & - Synchronous pacemaker This type of pacemaker is supposed for patients having long term heart blocks. The pace is preset. It can be varied externally within the number of 60 PPM to 180 PPM. Since this pacemaker functions whatever the patient's natural center tempo it poses a potential danger because of competition between the patient's rhythm and this of the pacemaker. PACING PULSES FROM ASYNCHRONOUS PACEMAKER In patients who've normal center function the majority of the time, asynchronous pacing can be hugely dangerous, working against their own physiological pacemaker with the danger of rousing in the vulnerable amount of the T wave, a problem that can bring about fibrillation. The demand pacemaker includes an ECG amplifier and a typical pacemaker output pulse circuit that is modified to allow productivity from the ECG amplifier to inhibit the pulse generator. This pacemaker senses R-waves and its own timing and logic circuits matter out an elapsed time interval pursuing an R-wave or previously induced pulse. In the event the intrinsic R-wave does not appear prior to the elapsed time period, the ventricle is stimulated. If an R-wave is received, the counter-top is reset again. This sort of pacemaker is used for patients with bradycardia, and it ensures a heartbeat no slower than its collection rate. PACING PULSES FROM SYNCHRONOUS PACEMAKER Internal pacemaker are implanted within the pulse generator placed in a surgically developed pocket below the right or still left clavicle, in the left subcostal area, or in women, under the still left or right major pectoralis muscle. Internal leads hook up to electrodes that directly contact the within of the right ventricle or the surface of the myocardium. The precise located area of the pulse generator is dependent primarily on the sort of the electrode used, he dynamics of the cardiac dysfunction, and the method (mode) of pacing that may be prescribed. Since there are no external connections for making use of power, the pulse generator must be completely self comprised, with a electricity source with the capacity of continuously operating the machine for an interval of years. BIO POTENTIAL ELECTRODES: A wide selection of electrodes may be used to evaluate bio electric occasions but almost all can be categorised as owned by one of three basic types; - Micro electrodes - Skin surface electrodes - Needle electrodes All three types of bio potential electrodes possess the metal-electrolyte interface. In each case, an electrode potential is developed over the software, proportional to the exchange of ions to the metal and the electrolytes of your body. They are being used to assess bio electric potentials near or within a single cell. Microelectrodes are electrodes with tips sufficiently small to penetrate a single cell in order to acquire readings from within the cell. The end must be small enough to permit penetration without damaging the cell. This action is usually complicated by the difficulty of accurately placing an electrode with respect to a cell. Because of their small surface area, they have impedances well up into the megohms. For this reason, amplifiers with extremely high impedances are required to avoid loading the circuit and minimize the consequences of small changes in software impedance. SKIN SURFACE ELECTRODES: Skin surface electrodes are used to obtain bio electric potentials from the surface of the body. They are available in various size. Although any type of surface electrode can be used to sense ECG, EMG, EEG potentials, the larger electrodes are usually associated with ECG, since localization of the measurement is not important. Smaller electrodes are used in EEG and EMG measurements. Various types of disposable electrodes have been created lately to eliminate the requirement for cleaning and attention after each use. In general, disposable electrodes are of the floating type with simple snap connectors by which the leads, that are reusable, are fastened. Although, some disposable electrodes can be used again several times, their cost is usually low enough that cleaning for reuse is not warranted. They come pre gelled, ready for immediate use. To reduce program impedance and, as a result, activity artifacts, some electroencephalographers use small subdermal needles to penetrate the scalp for EEG measurements. They are also used to measure EMG potentials from a particular band of muscles. They are really less vunerable to movement artifacts in comparison to surface electrodes as they create an software under the surface of the skin. By making direct contact with the subdermal tissues or the intercellular liquids, these electrodes also appear to own lower impedances than surface electrodes of similar interface area. Even though needle electrodes have less motion artifacts, surface electrodes are used to acquire ECG because surface electrodes are far more convenient for the patient. Most of the surface electrodes are cheap and reusable. ACQUISITION OF ECG USING 3 Business lead SYSTEM Business lead I CONFIGURATION: ECG sensors measure the time-varying magnitude of electric fields emanating from the heart. ECG worth are assessed by positioning non-invasive electrodes at the top of patient's skin. For the 3-business lead ECG sensor, the electrodes need to be positioned in a triangle (Einthoven Triangle) on the patient's upper body as shown in the physique 11. Each corner of the triangle corresponds to 1 of the limbs: right hands, left hand, remaining foot. With the bipolar system, one limb is linked to the positive terminal of the amplifier and another limb to its negative terminal. Three limbs (right arm-RA, still left arm-LA and still left leg/foot-LL) are used. The right lower leg was used as "earth", to minimize interference. Bioelectric indicators have very high input impedance. To stop the transmission attenuation, we use Instrumentation Amplifier (Advertising 624) which also has high input impedance. It should have high gain and low end result impedance. To be able to take away the common mode signals, it should have a high Common Method Rejection Percentage (CMRR around 90 dB). The at the surface of the body amounts from 0 - 10 mV therefore the amplifier must have high gain (1000). We use a differential amplifier to amplify the bioelectric signals that happen as a potential difference between two electrodes, the bioelectric impulses are applied between the inverting and non-inverting inputs of the amplifier. The transmission is therefore amplified by the differential gain of the amplifier. For the disturbance indication, however, both inputs seem as though these people were connected jointly to a standard input source. Thus, the common mode interference sign is amplified only by the much smaller common method gain. The electrode impedances form a voltage divider with the suggestions impedance of the differential amplifier. If the electrode impedances aren't identical, the interference impulses at the inverting and non-inverting inputs of the differential amplifier may vary, and the desired degree of cancellation does not take place. Because, the electrode impedances can't ever be produced exactly identical, the high common setting rejection ratio of your differential amplifier can only just be realized if the amplifier comes with an input impedance higher than the impedance of the electrodes to which it is connected. There are different lead configurations such as 3-Lead, 5-Lead, 12-Lead for acquiring ECG Indication. We have used 3-Lead system Lead - I Construction. 12-CIRCUIT FOR ECG AMPLIFIER SOFTWARE Execution USING LABVIEW: LabVIEW (brief for Laboratory Virtual Instrumentation Executive Workbench) is a program and development environment for Aesthetic Programming Language from National Tools. LabVIEW is a graphical programming environment employed by millions of designers and scientists to develop sophisticated measurement, test, and control systems using intuitive visual icons and wires that resemble a flowchart. LabVIEW offers unrivaled integration with thousands of hardware devices and provides hundreds of built-in libraries for advanced examination and data visualization. The LabVIEW system is scalable across multiple targets and operating systems. LABVIEW is a GUI (Graphical INTERFACE) that can be used for handling of indicators, images and other kinds of data. One of the most powerful features LabVIEW offers designers and experts is its visual encoding environment. - Operate the instrumentation program - Control picked hardware - Analyze attained data - Display results One can modify front panels with knobs, keys, dials, and graphs to emulate control panels of traditional devices, create custom test panels, or visually stand for the control and operation of processes. The similarity between standard movement charts and graphical programs shortens the training curve associated with traditional, text-based languages. The behavior of the electronic equipment can be dependant on connecting icons mutually to create block diagrams, which are natural design notations for scientists and technical engineers. With graphical development, one can develop systems quicker than with standard programming dialects, while retaining the energy and flexibility had a need to create a variety of applications. We have used Lab view to obtain the indication, filtering and do other handling of the ECG indication. The true time indication is given into as insight to ELVIS I which functions as the DAQ (data acquisition system). The stop diagram of the Laboratory view implementation is as shown in shape 14. STEPS INVOLVED IN LABVIEW Execution: - The ECG sign from the amplifier (using Advertisement 624) is given as input to DAQ for acquiring the signal in Lab view software. - FFT of the ECG signal is obtained and seen. We can start to see the rate of recurrence content of the ECG signal from the FFT obtained. WE can also start to see the existence of 50 Hz electric power line disturbance in the FFT of organic ECG. - A Smoothing filtration system with following features - Moving average, Rectangular filtration system with a 50 percent width of 20 is produced. The Smoothened ECG is viewed. Smoothing Filter is employed to remove sound and 50 Hz electric power line interference. - The Smoothened transmission is given as type to the Butterworth Strap Pass Filtration of order 2 and a low cutoff consistency of 5Hz and high cut off frequency of 15Hz. Band Pass Filter can be used to split up the QRS organic from the ECG Transmission. - The outcome of the Band Pass Filtration system is differentiated and squared inorder to improve the QRS organic from the remaining portion of the waveform. - The heart rate is computed using timing and firmness measurement stop. The block provides rate of recurrence of repetition of the QRS organic. The rate of recurrence value is converted into time value by firmly taking inverse than it. Heartrate is calculated the following. - If the calculated heartrate is below the normal value, then pacing pulses are produced. This is done by by using a case framework. - The case composition turns on only when the case holds true (Heart Rate is below normal value). In the case structure we've a square wave generator. The productivity of the square influx generator is differentiated and squared. We get a pulse therefore of these operations. - The rate and amplitude at which the pulses are produced can be customized easily at run time using settings. - Whenever the heartrate is normal, Fake condition is preferred. - For incorrect condition, we establish the amplitude and frequency of the rectangular influx as zero so that the pacemaker is switched off. - The Pacing Pulses made may also be taken out as an analog voltage from the ELVIS and can be viewed in a DSO. Only voltages in the range +10 volts to -10 volts can be studied out from LABVIEW through ELVIS. Heart Rate = 60/R-R Interval R-R Period = 760ms Heart Rate = 60/760ms = 78. 94 Beats /Minute PACEMAKER FINAL Stop DIAGARM. FRONT PANEL IN LABVIEW ENTIRE SOFTWARE IMPLEMENTATTION We have executed the case framework and other blocks by studying the general lessons given in LV Fundamentals 1 MANUAL and LABVIEWBASICSII_85_ENG CLAD. BLOCK DIAGRAM FOR HARDWARE IMPLEMENTATTION BAND PASS FILTER: The amplifier which is used in software implementation (Advertising 624) is also used here. It really is accompanied by a filtration. The amplifier output is just about 550 mV. A Filtration is a circuit that is identified to complete a specified band of frequencies while attenuating all alerts outside this music group. Filter networks may be either productive or unaggressive. Passive filter sites contain only resistors, inductors and capacitors. Effective filters use transistors or op amps plus resistors, inductors and capacitors. Inductors tend to be used in lively filters, because they're huge and costly and may have large interior resistive components. Band Pass Filters forward only a music group of frequencies while attenuating all frequencies outside the band. A straightforward high pass filtration system followed by a minimal pass filter will form a group pass filter. We've used a group pass filtration (0. 5Hz - 40 Hz) to eliminate high frequency indicators like EMG and low frequency components like Platform Collection Wandering and action artifacts. We've used another order Butterworth Filtration with -40 db/ten years roll-off. For Low Cross Filtration, we used 0. 5 Hz as the cut off rate of recurrence. C1 is chosen as a convenient value between 100 pF and 0. 1F. For High Cross Filter, we used 40 Hz as the take off frequency. We have implemented a Group Pass Filter based on the design given in OPERATIONAL AMPLIFIERS AND LINEAR INTEGRATIONAL CIRCUITS. CIRCUIT AND DESIGN FOR BAND PASS FILTER NOTCH Filtration system: A Notch Filtration system transmits frequencies in the forward group and rejects undesired frequencies in the stop strap. In applications where low level signals must be amplified, there may be present one or more of a variety of unwanted noise signs. Illustrations are 50, 60 0r 400 Hz frequencies from vitality lines, 120 Hz ripple from full - wave rectifiers, or even higher frequencies from controlled turning - type power items or clock oscillators. If both signals and signal regularity noise part are handed down through a notch filtration system, only the required signals will leave from the filter. The noise consistency is "notched out". We've designed a effective notch filtration system (using LM 324) to remove 50 Hz Power Line Disturbance. The amplitude of the acquired ECG signal is around 1 - 2 V. We acquired sound - free ECG for real-time signal acquisition as shown below. CIRCUITAND DESIGN FOR NOTCH FILTER REAL TIME ECG ACQUISITION In order to draw out the QRS Organic from the ECG indication obtained, we use a strap go away filter with center rate of recurrence of 17 Hz and band width of 6 Hz. The QRS signal extracted from the band pass filtration system is rectified for evaluating with the threshold voltage produced by the diagnosis circuit. The filtered and rectified ECG is stored on a capacitor. This filtered and rectified ECG is weighed against the fraction of the voltage. Whenever a threshold voltage is exceeded, the QRS pulse is recognized. After the recognition of each QRS pulse, the capacitor recharges to a new threshold value after every pulse. CIRCUIT FOR QRS DETECTION Monostable Multivibrator creates a single output pulse in response to a input signal. Additionally it is known as One Shot Multivibrator. The period of time of the end result pulse will depend on only on the exterior components (resistors and capacitors) connected to the op-amp. The length of the source triggering pulse can be longer or shorter than the expected pulse. The duration of the result pulse is symbolized by the T. Since T can be evolved only by changing the resistors and capacitors, the one shot multivibrators can be considered as a pulse stretcher. This is because the width of the pulse can be much longer than the source pulse. In a well balanced or standby talk about, the end result of the multivibrator is zero or low-level reasoning. The end result of the multivibrator is pressured to go high (ЛVcc) when an external trigger is given. The result stays zero before next triggering pulse is given. Then your cycle repeats. The monostable multivibrator has only one stable talk about. Hence, the name monostable. The QRS detector provides pulse for QRS detected which is given as an type trigger for a monostable multivibrator. This monostable multivibrator can be used to make a positive pulse (amplitude - 5V) of desired pulse width for every suggestions triggering (negative edge triggering) from the QRS detector. We had used 555 Timer as a monostable multivibrator. Thus, the analog portion of the task gets over with multivibrator. The end result of the multivibrator is refined using PIC18F 4550 Microcontroller. It grades the beginning of the controller section. PIC is a family group of Harvard architecture microcontrollers made by Microchip Technology, produced from the PIC1640 formerly developed by Basic Instrument's Microelectronics Section. The name PIC initially described "Programmable User interface Controller", but quickly thereafter was renamed "Programmable Intelligent Computer". PICs are popular with developers and hobbyists likewise because of the low cost, huge availability, large user base, extensive assortment of application notes, availability of low cost or free development tools, and serial encoding (and re-programming with adobe flash memory) ability. Like all Microchip PIC18 devices, PIC18F4550 family can be found as both standard and low-voltage devices. Standard devices with Enhanced Display memory, designated with an "F" in the part quantity (such as PIC18F4550), accommodate an operating VDD range of 4. 2V to 5. 5V. Low-voltage parts, selected by "LF" (such as PIC18LF4550), function over a protracted VDD range of 2. 0V to 5. 5V. Our project runs on the standard PIC 18F4550. Hence this microcontroller runs on the flash program memory space of 24K bytes. It is a 8-bit microcontroller and so they manage data as 8-tad chunks. PICs have a set of registers that function as general purpose ram memory. Special purpose control registers for on-chip hardware resources are also mapped into the data space. The addressability of memory space varies depending on device series and in PIC 18F4550 external code ram is straight addressable which is an exceptional feature in comparison to baseline and middle line core devices. PICs have a hardware call stack, which is employed to save go back addresses. The hardware stack is not software accessible on earlier devices, but this altered with the 18F4550 device. Hardware support for a general purpose parameter stack was lacking in early series, but this greatly increased in the 18F4550, making the this product architecture more friendly to advanced vocabulary compilers. - Alternate Run Modes: By clocking the controller from the Timer1 source or the internal oscillator block, vitality use during code execution can be reduced by as much as 90%. - Multiple Idle Methods: The controller can also run using its CPU primary disabled however the peripherals still active. In these areas, power utilization can be reduced even more, to as little as 4% of normal operation requirements. - On-the-Fly Mode Switching: The power managed modes are invoked by customer code during operation, allowing the user to include power-saving ideas into their application's software design. - Low Consumption in Key Modules: The energy requirements for both Timer1 and the Watchdog Timer are reduced. PIC18F 4550 has increased flash program memory space, high computational performance at an economical price. These features make these microcontrollers a rational choice for most high - performance, electricity delicate applications. It has an in built analog to digital converter. We have used MP Laboratory IDE, which is very reliable windows suitable software to program for PIC microcontrollers. It offers high level versatility for programming. It contains everything a programmer needs to write, edit, compile, website link and debug the microcontroller. PIC 18 SIMULATOR IDE: Each code developed is examined using PIC 18 Simulator IDE. The Simulator gives a great environment for the PIC microcontroller family. It gives all the required facilities to enable the machine designers to begin projects right from the nothing and complete them with ease and self confidence. - 8 x LED Mother board. - Keyboard Matrix - LCD Module - Signal Generator Segment LED Screen Panel PIC 18 SIMULATOR IDE The Code is encrypted in the controller using PIC Equipment 2. The coding for PIC microcontroller is comparable to C programming. The microcontroller is the actual pacemaker of the job. We have used the microcontroller for creating pacing pulses in both synchronous and asynchronous function. ASYNCHRONOUS MODE OPERATION: In asynchronous pacemaker the pacing pulses are produced at a predetermined rate, irrespective of the current heartrate. We've produced pacing pulses at three different rates (60, 70, 80). The amplitude of the pacing pulse can be fine-tuned from 0-5V utilizing a suitable potentiometer. CONTROLLER Productivity FOR ASYNCHRONOUS Function(Pulse Rate 60, 70, 80) SYNCHRONOUS MODE OPERATION: In Synchronous mode operation, the Pacemaker produces the pacing pulses only once the SA node does not stimulate the heart and soul for confirmed time frame. After the SA node begins to promote the heart and soul normally, the performing of the synchronous pacemaker prevents. The output of the monostable multivibrator is directed at the microcontroller. The monostable multivibrator produces positive pulse for each and every ECG wave. The microcontroller is utilized to monitor the time period between these pulses. Once the time period between any two pulses surpasses 1000 ms, the controller is designed to generate a rousing pulse. The Refractory period of the center muscles play a essential role here. If S A node produces a pulse immediately after 1000msec, it will not be considered by the heart and soul as a activation because it falls within the Effective Refractive Amount of the Center. The Heart muscles react to the stimulations only when appears after the Effective Refractive Period say 400msec. The time period between two square pulse is measured and can be used for heart rate calculation. PROCESS Movement IN PIC MICROCONTROLLER The heartrate is displayed using a Seven Segment Screen. The heartrate value obtained is changed into a BCD value. This BCD value is tapped from a 8-little bit slot of the microcontroller. The seven section display is manipulated by IC 4511. The BCD value obtained from the microcontroller is given as type to the IC 4511. We've used common cathode seven portion displays. The outcome of IC4511 to the related BCD inputs is really as shown in the table below. Thus, we've successfully completed the program implementation of the task in LABVIEW. We have designed an asynchronous pacemaker. We've designed an ECG amplifier and the ECG transmission is converted into a square pulse for control in the microcontroller. We still have to work on the design of synchronous pacemaker. This pin can be used to erase the storage locations inside the PIC (i. e. whenever we want to re-program it). In normal put it to use is linked to the positive resource rail. VSS AND VDD These will be the resource pins VDD is the positive source and VSS is negative source, or 0v. The utmost source voltage is 6V and minimal voltage is 2V. These pins are where we connect an exterior clock, which is crystal oscillator so the microcontroller has some type of timing. - TRIS register (data route register) - PORT register (reads the levels on the pins of the device) - LAT register (output latch) The Data Latch register (LATA) is useful for readmodify- write businesses on the worthiness influenced by the I/O pins. PORTA can be an 8-bit extensive, bi directional dock. The related data route register is TRISA. Arranging a TRISA bit (= 1) can make the equivalent PORTA pin an type (i. e. , place the corresponding output drivers in a high-impedance mode). Clearing a TRISA little (= 0) will make the related PORTA pin an end result (i. e. , place the items of the output latch on the selected pin). Reading the PORTA register reads the status of the pins; writing to it'll write to the interface latch. The RA4 pin is multiplexed with the Timer0 component clock input to become the RA4/T0CKI pin. The RA6 pin is multiplexed with the key oscillator pin; it is allowed as an oscillator or I/O pin by selecting the primary oscillator in Settings Register 1H. You should definitely used as a interface pin, RA6 and its own associated TRIS and LAT parts are read as '0'. RA4 is also multiplexed with the USB module; it functions as a device input from an exterior USB transceiver. Several PORTA pins are multiplexed with analog inputs, the analog VREF+ and VREF- inputs and the comparator voltage reference point output. The operation of pins RA5 and RA3:RA0 as A/D converter inputs is selected by clearing/placing the control bits in the ADCON1 register On the Power-on Reset, RA5 and RA3:RA0 are configured as analog inputs and read as '0'. RA4 is configured as an electronic input. PORTB is an 8-bit large, bidirectional port. The related data direction register is TRISB. Establishing a TRISB bit (= 1) can make the corresponding PORTB pin an type (i. e. , put the corresponding output drivers in a high-impedance mode). Clearing a TRISB tad (= 0) will make the equivalent PORTB pin an outcome (i. e. , put the articles of the productivity latch on the determined pin). Each of the PORTB pins has a poor internal pull-up. A single control bit can turn on all the pull-ups. This is performed by clearing little, RBPU. On a Power-on Reset, RB4:RB0 are configured as analog inputs by default and read as '0'; RB7:RB5 are configured as digital inputs. Four of the PORTB pins (RB7:RB4) come with an interruption- change feature. Only pins configured as inputs can cause this interrupt that occurs. Any RB7:RB4 pin configured as an productivity is excluded from the interruption- change assessment. Pins, RB2 and RB3, are multiplexed with the USB peripheral and serve as the differential signal outputs for an external USB transceiver RB4 is multiplexed with CSSPP, the chip select function for the Streaming Parallel Port PORTC is a 7-bit wide, bidirectional slot. The corresponding data route register is TRISC. Setting a TRISC bit (= 1) will make the matching PORTC pin an input (i. e. , place the corresponding output driver in a high-impedance method). Clearing a TRISC little (= 0) can make the corresponding PORTC pin an end result (i. e. , place the articles of the result latch on the preferred pin). In PIC18F4550 device, the RC3 pin is not carried out. PORTC is generally multiplexed with serial communication modules, like the EUSART, MSSP component and the USB module Pins RC4 and RC5 are multiplexed with the USB module. Unlike other PORTC pins, RC4 and RC5 don't have TRISC parts associated with them. As digital jacks, they can only work as digital inputs. When configured for USB operation, the data direction depends upon the configuration and status of the USB component at confirmed time. On a Power-on Reset, these pins, except RC4 and RC5, are configured as digital inputs. To utilize pins RC4 and RC5 as digital inputs, the USB component must be disabled. PORTD can be an 8-bit huge, bidirectional dock. The related data route register is TRISD. Setting a TRISD little bit (= 1) can make the related PORTD pin an suggestions (i. e. , put the corresponding output driver in a high-impedance mode). Clearing a TRISD little bit (= 0) will make the matching PORTD pin an output (i. e. , Put the contents of the productivity latch on the decided on pin). Each of the PORTD pins has a poor internal pull-up. An individual control little bit, RDPU (PORTE<7>), can change on all the pull-ups. PORTD can also be configured as an 8-tad wide Streaming Parallel Port (SPP) Code for Asynchronous Pacemaker: Explanation of Functions used: Delay 10KTCYx ( unsigned char int ); The notice x in the function name above stands for 'times' or 'multiplication'. It is not to be replaced by a number as done in other function titles. Unit is a 8 little value in the range (0, 255). Device=0is equal to Unit =256. TCY stands for 'instruction circuit'. The internal regularity of PIC 18 F4550 is 8 MHz.REFERENCES: - Leslie Cromwell, "Biomedical Instrumentation and measurement", Prentice hall of India, New Delhi, 2007. - Joseph J. Carr and John M. Brown, "Launch to Biomedical Equipment Technology", Pearson Education, 2004. - John G. Webster, "Medical Instrumentation Software and Design", John Wiley and sons, NY, 2004 - Principles of Biomedical Instrumentation and Way of measuring By Richard Aston - Biomedical signal Evaluation ( A Case Study Approach)- Rangaraj. M. Rangayyan - Digital Indication System-Level Design Using Laboratory VIEW BY Nasser kehtarnavaz and Namjin Kim - LV Basics 1 Manual - LabVIEWBasicsII_85_eng CLAD - External Pacemaker- Jigar O Patel. - Biomedical signal Examination (A Case Study Approach)- Rangaraj. M. Rangayyan. - Operational Amplifiers and Linear Integrational Circuits - Robert F. Coughlin & Frederick F. Driscoll. - Integrated Circuits - Roy Chowdry. - PIC Microcontrollers -Know it all Di Jasio, Wilmshrust, Ibrahim, Morton, Bates, J. Smith, D. W. Smith, Hellebeyck. - http://www. umm. edu/imagepages/1429. htm - http://zone. ni. com/cms/images/devzone/tut/2007-07-09_141618. jpg - http://ecee. colorado. edu/~ecen4618/lm324b. gif - http://pfnicholls. com/consumer electronics/555_pinout. png Also We Can Offer! - Argumentative essay - Best college essays - Buy custom essays online - Buy essay online - Cheap essay - Cheap essay writing service - Cheap writing service - College essay - College essay introduction - College essay writing service - Compare and contrast essay - Custom essay - Custom essay writing service - Custom essays writing services - Death penalty essay - Do my essay - Essay about love - Essay about yourself - Essay help - Essay writing help - Essay writing service reviews - Essays online - Fast food essay - George orwell essays - Human rights essay - Narrative essay - Pay to write essay - Personal essay for college - Personal narrative essay - Persuasive writing - Write my essay - Write my essay for me cheap - Writing a scholarship essay	2	25	0	0	1	0	0.940049	1	9,412
Needle EMG is the recording and study of electrical activity of muscles using a needle electrode. Neurologists use EMGs to test the electrical activity of a skeletal muscle to provide a medical diagnosis on a patient. Although these are common procedures but coding them incorrectly can not only cause billing problems but often lead to audits. The Centers for Medicare & Medicaid Services (CMS) outlines clearly its recommendations for EMG billing in the Federal Register (issue of October 31, 1997, Vol. 62, No. 211, page 59090), which covers some common questions like how many muscles should/need to be studied per limb in order to use the limb EMG codes or which code should be used when performing a limited study of a specific muscle and whether it can be used multiple times. Here are some tips which can clarify EMG billing confusions and help in maximizing your EMG reimbursements: 1. When choosing an EMG code, count the limbs and identify the specific muscles the physician has tested. The first set of EMG CPT codes 95860-95864 are used on the basis of this analysis. To report these codes, the physician must evaluate extremity muscles innervated by three nerves (for example, radial, ulnar, median, tibial, peroneal or femoral but not sub-branches) And a minimum of five muscles studied per limb. For example: If a physician performs EMG test on a patient’s right leg and meets the minimum testing requirements (five muscles innervated by three nerves each), then he should report CPT 95860. A single unit of 95860, 95861, 95863 or 95864 includes all muscles of five or more tested in a particular extremity(ies). In other words, one should report only a single unit of 95860-95864 per session: You cannot bill additional units for more than five muscles per extremity. CPT 95865 is used for needle examination of the larynx and CPT 95866 is used for needle examination of the hemidiaphragm. If fewer than five muscles are tested then CPT 95870 (Needle electromyography; limited study of muscles in one extremity or non-limb (axial) muscles (unilateral or bilateral), other than thoracic paraspinal, cranial nerve supplied muscles or sphincters) should be used. 2. The next set of CPT codes are 95867-95868 which describes the EMG study of muscles supplied by the cranial nerve, either unilaterally or bilaterally. If the answer to your question is yes, then CPT 95867 (Needle electromyography; cranial nerve supplied muscle[s], unilateral) OR CPT 95868 (Needle electromyography; cranial nerve supplied muscles, bilateral) should be used depending upon the test performed by the physician. For example: A physician monitors the RLN (Recurrent Laryngeal Nerve) during a total thyroidectomy, he should assign the CPT 95868 for a bilateral EMG. It is important to note that Codes 95867 and 95868 should not be reported together, nor should modifier -50 (bilateral procedure) be attached to CPT 95868. 3. Are studies performed on thoracic paraspinals other then those at T1 and T2? Then one must report CPT 95869 (Needle electromyography; thoracic paraspinal muscles). Code 95869 is exclusively used to study thoracic paraspinal muscles between T3 and T11. One unit can be billed, despite the number of levels studied or whether unilateral or bilateral. 95869 cannot be reported with 95860-95864 if only the T1 and/or T2 levels are studied with an upper extremity. This code should be used if the examinations are confined to distal muscles only, such as intrinsic foot or hand muscles. 4. Is the study performed on fewer than five muscles per extremity, then CPT 95870 should be used. This code should only be used when the muscles tested do not fit more appropriately under any other CPT code. Code 95870 can be billed at one unit per extremity (one limb, arm or leg), when fewer than five muscles are examined. For example: If a physician tests 3 muscles on the right arm and 4 muscles on the left arm, then code 95870 can be reported twice. This code can also be used for examining non-limb (axial) muscles (e.g. intercostal, abdominal wall, cervical and lumbar paraspinal muscles (unilateral or bilateral)) regardless of the number of level tested. However, it should not be billed when the paraspinal muscles corresponding to extremity are tested, and when the extremity codes 95860, 95861, 95863, or 95864 are reported. 5. The last in row is code 95872 which is (Needle electromyography using single fiber electrode, with quantitative measurement of jitter, blocking and/or fiber density, any/all sites of each muscle studied). This code should be used when a physician studies the action potentials (APs) from individual muscle fibers. One should report one unit of 95872 for each muscle the physician tests. The physician will generally test at least two muscles (one test serves as a “control”), so you will report a minimum of two units of service. When reporting CPT 95872, the physician must document the muscle(s) tested and the test results. Keep these tips handy when coding and billing EMG studies. As always, please consult your payer guidelines and state regulations for any specific rules. For recent changes in Nerve Conduction Study Codes 2013, please visit our latest blog post	4	11	36	0	0	2	0.611579	38	1,239
Congestive heart failure (CHF), or heart failure, is a condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from accumulating, or "backing up," into the lungs. In most cases, CHF is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ. Health conditions that may lead to CHF include: coronary artery disease, hypertension (high blood pressure), or arrhythmias. Symptoms of heart failure include shortness of breath and abnormal fluid retention, which usually results in swelling in the feet and legs. According to the American Heart Association (AHA), nearly five million individuals experience heart failure and about 550,000 new cases are diagnosed each year in the United States. Heart failure becomes more prevalent with age and the number of cases is expected to grow as the overall age of the population increases. CAUSES AND RISK FACTORS The heart consists of four chambers: the right atrium, the left atrium, the right ventricle, and the left ventricle. The heart also has four major valves: the mitral valve, the tricuspid valve, the aortic valve, and the pulmonary valve. Atria are relatively thin-walled chambers that receive blood from the circulatory system and from the lungs. Ventricles are muscular chambers that pump blood into the circulatory system and into the lungs. Blood passes from the atria into the ventricles through two processes. During the resting phase, when the ventricles are not contracting, the tricuspid and mitral valves open and allow some of the blood that has accumulated in the atria to flow passively through the valves into the ventricles. Then, the atria contract and actively pump blood out through the valves and into the ventricles. Once the ventricles fill with blood, they contract, pumping blood to the lungs and the rest of the body. When the left ventricle cannot adequately pump blood out of the left atrium, or when one or more of the heart valves becomes leaky or narrowed, blood can back up into the lungs, causing left-sided heart failure. When this occurs, the lungs become congested with fluid (called pulmonary edema), causing difficulty breathing and interfering with the movement of oxygen from the lungs into the bloodstream, causing fatigue. When an abnormality or condition affects the flow of blood through the right ventricle, pressure in the blood vessels increases and fluid is forced from the blood vessels into body tissues. This right-sided heart failure causes swelling (edema), usually in the feet and legs, and sometimes, in the abdomen. Coronary artery disease and heart attack: Coronary artery disease is the most common form of heart disease and the most common cause of heart failure. Over time, arteries that supply blood to the heart muscle narrow from a buildup of fatty deposits, a process called atherosclerosis. The buildup containing fats and clotting factors is called a plaque. Blood moves slowly through narrowed arteries, leaving some areas of the heart muscle chronically deprived of oxygen-rich blood. These areas of the heart may become weak from the lack of oxygen and pump less vigorously. In many cases, the blood flow to the muscle is just enough to keep the muscle alive but not functioning well. A heart attack occurs if an unstable plaque ruptures, causing a blood clot to completely block blood flow to an area of the heart muscle. A heart attack results in the death of heart muscle, which can quickly weaken the heart's pumping ability. Sometimes coronary artery disease is limited to the small coronary arteries. If these arteries become blocked, this won't cause a heart attack, but over time, it can gradually weaken the heart. Hypertension (high blood pressure): Blood pressure is the force of blood pumped by the heart through the arteries. If blood pressure is high, the heart has to work harder than it should to circulate blood throughout the body. Over time, the heart muscle may become thicker to compensate for the extra work it must perform. In some cases, the heart will enlarge. Eventually, the heart muscle may become either too stiff or too weak to effectively pump blood. Defective heart valves: The four valves of the heart keep blood flowing in the proper direction through the heart. A damaged valve forces the heart to work harder to keep blood flowing as it should. Over time, this extra work can weaken the heart. Cardiomyopathy: Cardiomyopathy is a serious disease in which the heart muscle becomes inflamed and does not work as well as it should. There may be multiple causes including viral infections, alcohol abuse, and the toxic effect of drugs such as cocaine or doxorubicin (Adriamycin©) used for chemotherapy. In addition, whole-body diseases that may lead to inflammation, such as lupus or thyroid problems, can also damage heart muscle. Myocarditis: Myocarditis is an inflammation of the heart muscle. Myocarditis is most commonly caused by a virus and can lead to left-sided heart failure. The virus most often associated with myocarditis is coxsackievirus B, but other viruses may include adenovirus, parvovirus B19, echovirus, influenza virus, Epstein-Barr virus, and rubella virus. Human immunodeficiency virus (HIV) can directly infiltrate the heart muscle and cause myocarditis. Other causes of myocarditis include bacteria (such as Staphylococcus aureus), parasites (such as Trypanosoma cruzi and toxoplasma), fungi (such as Candida albicans), exposure to certain chemicals such as arsenic and hydrocarbons, medications that may cause allergic or toxic reactions (such as cocaine or penicillin), and systemic diseases causing inflammation (including lupus). Congenital heart defects: Congenital heart defects are structural problems with the heart present at birth. Genetic defects contribute to the risk of certain types of heart diseases (such as arrythmias or valve problems), which in turn may lead to heart failure. Estimates suggest that about one million Americans have a congenital heart defect. Approximately 35,000 babies in the United States are born with a heart defect each year. Arrhythmias: Arrhythmias, or abnormal heart rhythms, may cause the heart to beat too fast. This creates extra work for the heart. Over time, the heart may weaken leading to heart failure. Other conditions: Health conditions, such as diabetes, severe anemia (lack of red blood cells to carry oxygen to tissues), hyperthyroidism (high thyroid hormone levels), hypothyroidism (low thyroid hormone levels), emphysema (lung disease that involves damage to the air sacs in the lungs), pulmonary edema (fluid in the lungs), hemochromatosis (an inherited disease in which too much iron builds up in the body), and amyloidosis (a group of diseases in which one or more organ systems in the body accumulate deposits of abnormal proteins such as C-reactive protein), may also contribute to heart failure. Kidney disease can contribute to heart failure due to an increase in high blood pressure and fluid retention. Heart failure may develop during the last the months of pregnancy or several months after pregnancy. The cause of this is not well understood, but it may be due to an abnormal immune system response. Viral infections may cause idiopathic heart failure or heart failure in which there is never an identified cause. Bacterial infections, such as pneumonia, may lead to CHF. Exposure to toxins, such as alcohol or cocaine, may also lead to CHF. An example of drug-induced CHF is with encainide hydrochloride (Enkaid©). Encainide is a drug used for arrhythmias (irregular heart beats), but in susceptible individuals, its use may lead to CHF. Obesity may also lead to CHF. Obesity promotes diabetes, hypertension (high blood pressure), and dyslipidemia (high cholesterol levels). These conditions are risk factors for developing coronary artery disease and ultimately, CHF. Sleep apnea, or the inability to breathe properly at night, results in low blood oxygen levels and increased risk of abnormal heart rhythms. Both of these problems can weaken the heart and lead to CHF. The condition affects 1% of people aged 50 years and older and about 5% of those aged 75 years and older. African Americans experience heart failure twice as often as Caucasians. About 10% of patients diagnosed with heart failure die within one year, and about 50% die within five years of diagnosis. CHF is equally frequent in men and women, and annual incidence approaches ten per 1,000 population after 65 years of age. Survival following diagnosis of congestive heart failure is worse in men than women, but even in women, only about 20% survive much longer than eight to 12 years. SIGNS AND SYMPTOMS Congestive heart failure (CHF) is chronic (long-term) and generally occurs slowly. Congestion, or the backing up of blood, occurs in the liver, abdomen, lower extremities, and lungs. The backing up of blood causes symptoms such as shortness of breath, fatigue, and swelling (particularly in the legs and feet). Other symptoms develop as the body tries to compensate for the heart's reduced pumping ability. The heart beats faster, its muscle thickens, and the ventricles may stretch to accommodate more blood. Damage to the ventricles may cause them to pump out of sync, further reducing the efficient delivery of blood to the body. Symptoms of CHF include: a dry, hacking cough, especially when lying down; confusion, sleepiness, and disorientation may occur in older individuals; dizziness, fainting, fatigue, or weakness; fluid buildup, especially in the legs, ankles, and feet; increased urination at night; nausea; abdominal swelling, tenderness, or pain; weight gain due to fluid buildup; weight loss as nausea causes a loss of appetite and as the body fails to absorb food well; rapid breathing, bluish skin, and feelings of restlessness, anxiety, and suffocation; shortness of breath and lung congestion as the blood backs up in the lungs; and wheezing and spasms of the airways similar to asthma. Physical examination and medical history: During a physical examination, a doctor will look for underlying causes of the problem and assess heart function. A stethoscope is used to detect murmurs (abnormal heart sounds) that may indicate a leaky or narrowed valve, and to detect fluid accumulation in the lungs. The doctor also looks for enlarged veins in the neck and for edema (swelling) in the legs, particularly the ankles, feet, and/or the abdomen. A patient history may include information about risk factors, such as family medical history, past surgeries and medications, history of chest pain, high blood pressure (including treatments), heart attack, recent viral illness, or recent pregnancy. Blood tests: Blood tests may include: blood cell counts to test for conditions such as anemia (low red blood cells); electrolyte levels, including sodium, potassium, and calcium; nutrient levels, such as vitamins and trace minerals; tests for kidney function, including blood urea nitrogen (BUN) and creatinine levels; and testing for homocysteine and/or C-reactive protein (CRP), both markers of inflammation and heart disease. The diagnostic test marker for CHF is N-terminal prohormone brain natriuretic peptide or NT-proBNP. Brain natriuretic peptide (BNP) is a hormone produced at higher levels by the failing heart muscle. Electrocardiogram: An electrocardiogram (ECG or EKG) is a noninvasive test used to measure electrical activity in the heart. Electrical sensors called leads are attached to predetermined positions on the arms, legs, and chest to record electrical activity and help assess heart function. The heart's rhythm of contraction is controlled by the sinoatrial node (SA node), often called the pacemaker. Electrical impulses generated from the SA node spread through the heart via a nodal tissue pathway that coordinates the events leading to heart beat. The conduction system initiates and coordinates the muscular activity of the heart. Echocardiogram: Echocardiogram, or echo, is an ultrasound examination of the heart that produces detailed images of the organ. It can be used to detect abnormalities in the structure of the heart and to measure the amount of blood ejected from the heart. During an echocardiogram, a microphone-like device (transducer) is used to transmit and receive ultrasonic waves that travel through the chest wall to the heart and are reflected back to the transducer. The reflected sound waves are translated into images of the heart, including the valves, chambers, and walls. Echocardiogram also is used to measure the pressure change (gradient) between the left ventricle and the aorta, to assess thickening of the walls of the heart, to evaluate pumping function, and to measure the amount of dilation (increased diameter) of the left ventricle. Chest x-ray: A chest x-ray is used in identifying the buildup of fluid in the lungs. Also, the heart usually enlarges in CHF, which may be visible on the x-ray film. Cardiac catheterization: Cardiac catheterization may be performed in individuals with angina and in those with a history of heart attack to determine if coronary heart disease (CHD) is causing heart failure. Cardiac catheterization produces angiograms (such as x-ray images) of the coronary arteries and the left ventricle, and can be used to monitor heart function. Cardiac catheterization involves injecting a small amount of radioactive dye, called a contrast agent, into the left ventricle through a catheter (a thin flexible tube). A special camera is then used to determine how much of the dye is ejected from the heart with each beat. The infusion of dye typically produces a characteristic "hot flash" sensation throughout the body that lasts 10-15 seconds. Stress test: In some individuals, a less invasive procedure called a stress test is used to assess the possibility of coronary heart disease. If the results of this procedure suggest the presence of coronary artery disease, a subsequent referral for cardiac catheterization is likely. Several types of stress tests may be used by doctors to access heart function. In some cases, the individual simply walks on a treadmill while connected to an electrocardiogram (ECG). Another type uses intravenous (IV, or in the veins) medication, usually dipyridamole (Persantine©), which reproduces the stress of exercise on the heart. Nuclear stress test: Nuclear stress tests involve injecting a radioactive substance, most commonly technetium or Tc-99m sestamibi (Cardiolite©), into a vein. A special camera is then used to obtain images of the heart during rest and immediately following exercise on a treadmill as the radioactivity flows through the heart. The radioactivity levels used are not harmful. A nuclear test called a radionuclide ventriculography or multiple gated acquisition (MUGA) scanning allows doctors to see how much blood the heart pumps with each beat, called the ejection fraction. The MUGA scan gives an accurate and reproducible means of measuring and monitoring the actual amount of blood ejected from the heart. The tests use a small amount of radioactive material injected into the veins. A special camera detects the radioactive material as it flows through the heart. Individuals with an allergy to iodine or shellfish have special considerations and may not be able to have this test because the dye contains iodine. The use of medications, including the antihistamine diphenhydramine (Benadryl©) and/or prednisone (Delatasone©), prior to the administration of the dyes (contrast media), may help to prevent or decrease the chance of an allergic reaction. Classifying heart failure: Results of these tests help doctors determine the cause of CHF and develop a program to treat the heart. To determine the best course of treatment, doctors may classify heart failure using one of two scales. The New York Heart Association scale classifies heart failure in categories from one to four. In Class I heart failure, the mildest form, individuals can perform everyday activities and not feel winded or fatigued. Individuals with class II have slight limitation of physical activity and ordinary physical activity may result in fatigue, palpitation, shortness of breath, or chest pain. Those with class III have marked limitation of physical activity and less than ordinary activity causes fatigue, palpitation, shortness of breath, or chest pain. Class IV is the most severe, and individuals are short of breath even at rest. The American College of Cardiology scale uses letters A-D. The system includes a category for individuals who are at risk of developing heart failure. Early stage heart failure includes stage A (individuals are at risk for developing heart failure without evidence of heart dysfunction) and stage B (there is evidence of heart dysfunction without symptoms). Advanced stage heart failure includes stage C (there is evidence of heart dysfunction with symptoms) and stage D (there are symptoms of heart failure despite maximal therapy). Doctors can use these classifications to identify the risk factors and begin early, more aggressive treatment to help prevent or delay heart failure. Congestive heart failure can affect many organs of the body. For example, the weakened heart muscles may not be able to supply enough blood to the kidneys, which then begin to lose their normal ability to excrete salt (sodium) and water. This diminished kidney function can cause the body to retain more fluid. The lungs may become congested with fluid (pulmonary edema) and the person's ability to exercise is decreased. Fluid may likewise accumulate in the liver, thereby impairing its ability to rid the body of toxins and produce essential proteins. The intestines may become less efficient in absorbing nutrients and medicines. Over time, untreated congestive heart failure will affect virtually every organ in the body. The lack of blood flow to the heart can lead to irreversible damage to the heart muscle. Chest pain (angina) is an indicator of a heart attack (myocardial infarction). A heart attack can cause sudden death. Treatment for congestive heart failure (CHF) varies and involves reducing symptoms, treating the underlying cause of the condition when possible, and using medications to prevent further deterioration of heart function. Lifestyle changes can help reduce symptoms such as fatigue, shortness of breath, and edema (swelling). These modifications may include dietary changes (such as a restricted salt intake of less than 2,000 mg daily), abstaining from alcohol, stopping smoking, and exercising regularly (under the supervision of a doctor). A combination of medications is used to treat CHF. Depending on the symptoms, individuals with CHF may take one, two, or more of these drugs. Several types of medications have proved useful in the treatment of heart failure including: angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBS), beta-blockers, digoxin, diuretics, and aldosterone antagonists. Angiotensin-converting enzyme (ACE) inhibitors: Angiotensin-converting enzyme (ACE) inhibitors are a medication that dilates or widens blood vessels to lower blood pressure, improve blood flow, and decrease the workload on the heart. ACE inhibitors include enalapril (Vasotec©), lisinopril (Prinivil©, Zestril©), and captopril (Capoten©). Side effects of ACE inhibitors include chronic, nonproductive cough (occurs in about 10% of patients), dizziness or weakness (caused by low blood pressure), increased potassium levels, skin rashes, and sudden swelling of the lips, face, and cheeks (if this occurs, the patient must seek medical attention immediately). Angiotensin II (A-II) receptor blockers (ARBs): Angiotensin receptor blockers, or ARBS, have many of the beneficial effects of ACE inhibitors, but they do not cause a persistent cough. They may be an alternative for individuals who cannot tolerate ACE inhibitors. ARBs include losartan (Cozaar©) and valsartan (Diovan©). Digoxin (Lanoxin©): Digoxin (Lanoxin©) increases the strength of the heart muscle contractions. Digoxin also tends to slow the heartbeat. Digoxin reduces heart failure symptoms and improves the individual's ability to live with the CHF. Side effects are rare, but may include blurred vision, cardiac problems (such as arrhythmias or heart block), diarrhea, headaches, loss of appetite, hypotension (low blood pressure), and nausea and vomiting. Beta blockers: Beta blockers are a class of drugs that slows the heart rate and reduces blood pressure. Beta blockers include carvedilol (Coreg©), metoprolol (Lopressor©), and propranolol (Inderal©). These medicines also reduce the risk of some abnormal heart rhythms. Beta blockers may reduce signs and symptoms of heart failure and improve heart function. Beta-blockers are started at low doses that are gradually increased over a period of several months. During the first several weeks of treatment, some patients experience worsening symptoms due to a decrease in oxygen circulation in the body. Other side effects include low blood pressure, difficulty breathing, sexual dysfunction, nausea, and weakness with exertion. Diuretics: Diuretics, or water pills, make individuals urinate more frequently and keep fluid from collecting in the body. Commonly prescribed diuretics for heart failure include hydrochlorothiazide (Diuril©) and furosemide (Lasix©). Diuretics also decrease fluid in the lungs, helping individuals breathe more easily. Side effects include frequent urination and low potassium blood levels. Because of this, blood tests are performed periodically and a potassium supplement is prescribed if blood levels are low. Individuals may be asked to eat more fruits high in potassium, such as bananas and oranges, while on diuretic therapy. Aldosterone antagonists: Aldosterone antagonists are primarily potassium-sparing diuretics, but they have additional properties that help the heart work better, may reverse scarring of the heart, and may help individuals with severe heart failure live longer. Aldosterone antagonists include spironolactone (Aldactone©) and eplerenone (Inspra©). Unlike other diuretics, spironolactone can raise the level of potassium in the blood to dangerous levels. Healthcare professionals recommend eliminating high-potassium foods, such as bananas, lentils, nuts, peaches, potatoes, salmon, tomatoes, and watermelon while taking aldosterone antagonists. Others: A medication called BiDil© is a single pill that combines hydralazine and isosorbide dinitrate, both of which dilate and relax the blood vessels. BiDil© increases survival when added to standard therapy in African American individuals with advanced heart failure. This is the first drug studied and approved for a specific racial group. Further studies will be necessary to determine if this combination medicine will be helpful for others with heart failure. Side effects may include blurred vision, dry mouth, irregular heartbeat, blood in the urine or stools, numbness or tingling in the arms or legs, and fainting. Doctors often prescribe other heart medications, such as HMG-CoA reductase inhibitors (statin) drugs, for cholesterol reduction. Statin drugs include atorvastatin (Lipitor©) or lovastatin (Mevacor©). They may cause liver problems or muscle pain. Anti-arrhythmic drugs may also be prescribed to control irregular heart beats, including diltiazem (Cardizem©, Cardizem CR©) and verapamil (Calan©, Calan SR©). Individuals may be hospitalized for a few days if complications arise as a result of CHF symptoms. While in the hospital, individuals may receive additional medications such as intravenous (IV, or into the veins) dobutamine (Dobutrex©), milrinone, (Primacor©), and nitroglycerin. These drugs work quickly to help the heart pump better and relieve symptoms. Individuals may also receive supplemental oxygen through a mask or small tubes placed in the nose. If severe heart failure is present, the individual may need to use supplemental oxygen long term. Individuals hospitalized with severe CHF may be given an intravenous drug called nesiritide (Natrecor©). Nesiritide is a synthetic version of a naturally occurring hormone in the body called brain natriuretic peptide (BNP). BNP is secreted in high levels by the heart in response to a failing heart. However, it is not clear if nesiritide is better than other intravenous medications for severe heart failure. Studies are ongoing to evaluate the safety and effectiveness of nesiritide in heart failure. Aquapheresis: In some cases, heart failure persists or worsens in spite of treatment. An ultrafiltration process called aquapheresis, which uses a mechanical system called the Aquadex FlexFlow™, may be used to remove excess fluids and salt in CHF individuals who do not respond to lifestyle modifications and medication. In this treatment, blood is withdrawn using catheters (small tubes) inserted into veins in the arm, leg, or neck. The blood is then passed through a filter that removes excess fluid and is returned to the body. Studies have reported that ultrafiltration can remove more fluid at a faster rate than medication. The length of each treatment depends on the rate at which fluid can be removed from the body and the amount that must be removed. Angioplasty: CHF caused by reduced blood flow in the heart as a result of blockages (plaques) in one or more coronary arteries may be treated using coronary angioplasty. In this procedure, a hollow tube (catheter) is inserted through an artery (usually the femoral artery in the groin), into the coronary artery, and to the blockage. A small balloon is then inserted through the catheter and is inflated to open the blocked artery. There is a slight risk for damage to the artery during angioplasty, but heart failure symptoms usually improve following the procedure. Stenting is used along with balloon angioplasty. Stenting involves placing a mesh-like metal device into an artery at a site narrowed by plaque. The stent is mounted on a balloon-tipped catheter, threaded through an artery, and positioned at the blockage. The balloon is then inflated, opening the stent. Then, the catheter and deflated balloon are removed, leaving the stent in place. The opened stent keeps the vessel open and stops the artery from collapsing. Re-closure may occur with both balloon angioplasty and stenting. Doctors will prescribe blood thinning medications to help keep the arteries open, including aspirin, warfarin (Coumadin©), and clopidogrel (Plavix©). Coronary artery bypass graft surgery (CABG): A coronary artery bypass surgery (CABG) may be recommended if the individual has severe coronary artery disease in addition to CHF. This may improve the blood supply to the heart. Coronary artery bypass graft (CABG) surgery uses blood vessel grafts, which usually come from the patient's own arteries and veins located in the chest, leg, or arm. The graft goes around the clogged artery to create new pathways for oxygen-rich blood to flow to the heart. Some problems associated with CABG include a heart attack (occurs in 5% of patients), stroke (occurs in 5%, with the risk greatest in those over 70 years old), blood clots, death (occurs in 1 - 2% of individuals), and wound infection (occurs in 1 - 4%). Infection is most often associated with obesity, diabetes, or having had a previous CABG. In about 30% of patients, post-pericardiotomy syndrome can occur anywhere from a few days to six months after surgery. The symptoms of this syndrome are fever and chest pain. Symptoms can be treated with medications, including antibiotics (for infection), nitroglycerin, and anti-inflammatory drugs. The incision in the chest or the graft site (if the graft was from the leg or arm) can be itchy, sore, numb, or bruised. Some individuals report memory loss, loss of mental clarity, or "fuzzy thinking" following a CABG. Implantable cardiac defibrillator: An implantable cardiac defibrillator (ICD) may be used to treat severe heart failure. An ICD is a small electronic device that is surgically implanted under the skin in the chest to monitor heart rhythm. When an abnormal rhythm is detected, the defibrillator delivers an electrical "shock" to the heart to restore normal heart rhythm. Intra-aortic balloon pump: An intra-aortic balloon pump (IABP) is a device that is inserted through an artery in the groin (femoral artery) and then placed within the main artery (aorta). An IABP is an inflatable balloon that expands and deflates in coordination with each heartbeat. It can be left in place for days to weeks, and decreases the strain on the heart and increases blood flow throughout the body. Valve replacement surgery: Individuals with heart failure caused by an abnormal heart valve may require valve repair or valve replacement surgery. These are open-heart procedures in which an abnormal valve is repaired or replaced with a porcine valve (from pig tissue), a mechanical valve (made of synthetic material), or a homograft valve (from a human donor). Complications include bleeding, blood clots, infection, kidney failure, stroke, heart attack, and death. A homograft valve is preferred, as these valves are not associated with a significant risk for blood clot formation and, thus, do not require blood thinner therapy. Most individuals remain in the hospital for a week after surgery and recovery takes approximately three to four weeks, after which most patients can resume leisure activities and many return to work. Approximately 60% of individuals who have valve replacement have a ten-year post-surgery survival rate. Left ventricular assist device: A left ventricular assist device (LVAD) is a mechanical pump that is surgically implanted in the upper abdomen to bypass the left ventricle and pump blood throughout the body. This device may be used in patients with end-stage heart failure who are awaiting heart transplantation. Long-term use of the device in patients with severe heart failure is being explored and defined. Pacemaker: If individuals with CHF experience arrhythmias that will not respond to medication therapy, the arrhythmias may be corrected with a pacemaker. A pacemaker is a small, battery-powered device that is usually implanted near the collarbone. Pacemakers can be surgically placed into the chest (a permanent pacemaker) through a small incision, or they can be worn outside the body (a temporary pacemaker) and attached to the heart through a wire that is threaded through a neck vein. Temporary pacemakers are used only while an individual is in the hospital. The surgery needed to implant a permanent pacemaker is considered a minor surgical procedure. The procedure may take one to two hours to complete. The area where the pacemaker will be inserted will be numbed with an injection of an anesthetic such as lidocaine (Xylocaine©). The individual should not feel any pain during the procedure, and should inform the doctor or staff if they are having pain so that more anesthetic medication may be given. One or more electrode-tipped wires run from the pacemaker through the blood vessels to the inner heart. If the heart rate is too slow or if it stops, the pacemaker sends out electrical impulses that stimulate the heart to beat at a steady, proper rate. The more advanced pacemakers can monitor and pace either the atria or ventricles (or both) in proper sequence to maximize the amount of blood being pumped from the heart. The pacemaker's batteries may need to be changed every five to ten years. It is recommended by the American Heart Association to limit exposure to devices that may interfere with pulse generators such as cellular phones, CB radios, electric blankets, and microwaves. It is normal for the surgical wound to be somewhat painful and swollen for a few days after the procedure. This can usually be controlled with medications, such as ultram (Tramadol©) or ibuprofen (Motrin©). The wound may also appear mildly red for a few days; however, if the area of redness enlarges, a doctor should be notified due to the potential for a serious infection. If there are no other problems, most individuals who have a permanent pacemaker surgically implanted can go home the next day. They can usually return to normal activities within six weeks. For several weeks after having a pacemaker implanted, the individual may be asked not to lift more than five pounds or raise the affected arm over their shoulder. Heart transplant: In some cases, despite the use of optimal therapies as described above, the individual's condition continues to deteriorate due to progressive CHF. In selected individuals, heart transplantation is a viable treatment option. Candidates for a heart transplant are generally under age 70, do not smoke, and do not have severe or irreversible diseases affecting the other organs. Additionally, a transplant is done only when it is clear that the individual's prognosis on continued medical treatment is poor. Transplant patients require close medical follow-up while taking necessary drugs that suppress the immune system and because of the risk of rejection of the transplanted heart. They must even be monitored for possible development of coronary artery disease in the transplanted heart. Although there are thousands of patients on waiting lists for a heart transplant at any given time, the number of operations performed each year is limited by the number of available donor organs. For these reasons, heart transplantation is a realistic option in only a small subset of the large numbers of patients with congestive heart failure. Strong scientific evidence: Hawthorn: Hawthorn (Crataegus sp.), a flowering shrub of the rose family has an extensive history of use in cardiovascular disease dating back to the 1st Century. Increased blood flow to the heart and heart performance has been observed in animals when given hawthorn supplements. Extracts of the leaves and flowers of hawthorn have been reported as effective in the treatment of mild-to-moderate congestive heart failure (CHF), improving exercise capacity and reducing symptoms of cardiac insufficiency. However, whether hawthorn is as effective as drugs considered standard-of-care for heart failure (such as angiotensin converting enzyme inhibitors, diuretics, or beta-adrenergic receptor blockers) is unclear, as is the effect of the combined use of hawthorn with these drugs. Nonetheless, hawthorn is a potentially beneficial treatment for patients who cannot or will not take prescription drugs and may offer additive benefits to established therapies. Further study is warranted. Avoid if allergic to hawthorn or to members of the Crataegus species. Avoid with a history of low blood pressure, irregular heartbeat, asthma, low blood pressure when standing or insomnia. Use cautiously in elderly patients. Avoid if pregnant or breastfeeding. Good scientific evidence: Arginine: Studies of arginine in patients with chronic heart failure have shown mixed results. Some studies report improved exercise tolerance. Additional studies are needed to confirm these findings. Avoid if allergic to arginine, or with a history of stroke, or liver or kidney disease. Avoid if pregnant or breastfeeding. Use caution if taking blood-thinning drugs (like warfarin or Coumadin©) and blood pressure drugs or herbs or supplements with similar effects. Blood potassium levels should be monitored. L-arginine may worsen symptoms of sickle cell disease. Caution is advised in patients taking prescription drugs to control blood sugar levels. Berberine: Berberine is a bitter-tasting, yellow, plant alkaloid with a long history of medicinal use in Chinese and Ayurvedic medicine. Berberine is present in the roots, rhizomes, and stem bark of various plants including Hydrastis canadensis (goldenseal), Coptis chinensis (coptis or goldenthread), Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), and Berberis aristata (tree turmeric). Preliminary clinical research suggests that berberine, in addition to a standard prescription drug regimen for chronic congestive heart failure (CHF), may improve quality of life, heart function, and mortality. Further research is necessary. Berberine has been reported to cause nausea, vomiting, hypertension (high blood pressure), respiratory failure, and paresthesias (abnormal sensations such as numbness or tingling). Use cautiously in patients with diabetes. Avoid if allergic or hypersensitive to berberine, to plants that contain berberine [Hydrastis canadensis (goldenseal), Coptis chinensis (coptis or goldenthread), Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), and Berberis aristata (tree turmeric)], or to members of the Berberidaceae family. Avoid in newborns due to potential for increase in free bilirubin, jaundice, and development of kernicterus. Use cautiously with cardiovascular disease, gastrointestinal disorders, hematologic disorders, leucopenia, kidney disease, liver disease, respiratory disorders, cancer, hypertyraminemia, diabetes, or hypotension. Use cautiously in children due to lack of safety information. Use cautiously in individuals with high exposure to sunlight or artificial light. Use cautiously for longer than eight weeks due to theoretical changes in bacterial gut flora. Use cautiously if taking anticoagulants, antihypertensives, sedatives, anti-inflammatories, medications metabolized by CYP P450 3A4 including cyclosporin, or any prescription medications. Avoid if pregnant or breastfeeding. Coleus: Coleus species have been used in the Asian traditional medicine for several indications. Since the 1970s, research was predominantly concentrated on forskolin, a root extract of Coleus forskohlii. A small number of studies suggest that forskolin may improve cardiovascular function in patients with cardiomyopathy. However, these trials are small and of poor quality. Larger studies are needed. Coleus is generally regarded as safe, although long-term safety data are lacking. Avoid with a known allergy or hypersensitivity to Coleus forskohlii and related species. Rash may occur in sensitive individuals. Inhalation of forskolin may cause sore throat, upper respiratory tract irritation, mild to moderate cough, tremor, or restlessness. Coleus eye drops may produce a milky covering over the eyes. Use cautiously in patients with heart disease, asthma, thyroid disorders, diabetes, a history of bleeding, hemostatic disorders or drug-related hemostatic problems, low blood pressure, or in patients at risk for hypotension. Discontinue use in patients at least two weeks prior to surgical or dental procedures, due to risk of bleeding. Avoid in patients with active bleeding. Avoid during pregnancy. Creatine: Creatine is naturally synthesized in the human body from amino acids primarily in the kidney and liver, and transported in the blood for use by muscles. Cardiac creatine levels have been reported as depressed in patients with chronic congestive heart failure. Several studies report that creatine supplementation is associated with improved heart muscle strength, body weight, and endurance in patients with heart failure. However, it is not clear what dose may be safe or effective. Supplementation is also reported to increase creatine in skeletal muscle in these patients, helping to increase strength and endurance. Well-designed studies comparing creatine with drugs used to treat heart failure are needed. Avoid if allergic to creatine or with diuretics (like hydrochlorothiazide, furosemide (Lasix©)). Use caution in asthma, diabetes, gout, kidney, liver, or muscle problems, stroke or a history of these conditions. Avoid dehydration. Avoid if pregnant or breastfeeding. Selenium: Selenium is a trace metal that has been reported to have antioxidant properties. Prophylactic administration of sodium selenite has been shown to significantly decrease the incidence of Keshan disease, which is cardiomyopathy (heart disease) restricted to areas of China in people having an extremely low selenium status. Avoid if allergic or sensitive to products containing selenium. Avoid with a history of nonmelanoma skin cancer. Selenium is generally regarded as safe for pregnant or breastfeeding women. However, animal research reports that large doses of selenium may lead to birth defects. Unclear or conflicting scientific evidence: Aconite: The toxic effects associated with aconite limit its ability to be used to treat heart failure, including reno-cardiovascular disease and left ventricular function. Further study is needed. Aconite is highly toxic and is not safe for human consumption. Avoid with heart disease, heart dysfunction, irregular heartbeat, hemodynamic instability (abnormal blood flow), gastrointestinal disorders, ulcers, reflux esophagitis, ulcerative colitis, spastic colitis, and diverticulosis. Use caution with diabetes and suicidal tendencies. Avoid if younger than 18 years old. Avoid if pregnant or breastfeeding. Astragalus: Astragalus (Astragalus membranaceus) is used in combination with other herbs in Chinese medicine to treat various heart diseases. There is some evidence that astragalus may offer symptomatic improvement for chronic heart failure. Recommendations cannot be made until well-designed clinical trials have been conducted. Avoid if allergic to astragalus, peas, or any related plants or with a history of Quillaja bark-induced asthma. Avoid with aspirin or aspirin products or herbs or supplements with similar effects. Avoid with inflammation (swelling) or fever, stroke, transplant or autoimmune diseases (like HIV/AIDS). Stop use two weeks before surgery/dental/diagnostic procedures with a risk of bleeding and avoid use immediately after these procedures. Use cautiously with bleeding disorders, diabetes, high blood pressure, lipid disorders or kidney disorders. Use cautiously with blood-thinners, blood sugar drugs, or diuretics or herbs and supplements with similar effects. Avoid if pregnant or breastfeeding. Ayurveda: Ayurveda, which originated in ancient India over 5,000 years ago, is probably the world's oldest system of natural medicine. Preliminary evidence suggests that sodium nimbidinate, made from the traditional Ayurvedic herb Nimba/Neem/Arishta (Azadirachta indica), may be an effective diuretic in patients with congestive heart failure. More studies are needed to confirm this effect. Ayurvedic herbs should be used cautiously because they are potent and some constituents can be potentially toxic if taken in large amounts or for a long time. Some herbs imported from India have been reported to contain high levels of toxic metals. Ayurvedic herbs can interact with other herbs, foods and drugs. A qualified healthcare professional should be consulted before taking. Coenzyme Q10 (CoQ10): CoQ10 is produced by the human body and is necessary for the basic functioning of cells. The evidence for CoQ10 in the treatment of heart failure is controversial and remains unclear. Different levels of disease severity have been studied (New York Heart Association classes I through IV). Better research is needed in this area, studying effects on quality of life, hospitalization, and death rates. There is also conflicting evidence from research on the use of CoQ10 in patients with dilated or hypertrophic cardiomyopathy. CoQ10 is generally safe in recommended dosages, but further studies are needed. Allergy associated with Coenzyme Q10 supplements has not been reported, although rash and itching have been reported rarely. Stop use two weeks before surgery/dental/diagnostic procedures with bleeding risk and do not use immediately after these procedures. Use caution with a history of blood clots, diabetes, high blood pressure, heart attack, or stroke, or with anticoagulants (blood thinners), antiplatelet drugs (like aspirin, warfarin, clopidogrel (like Plavix©), or blood pressure, blood sugar, cholesterol or thyroid drugs. Avoid if pregnant or breastfeeding. Ginseng: A clinical study on the effect of Panax ginseng on congestive heart failure did not show a clear benefit of combining digoxin with ginseng. The relatively small study size and the use of a drug instead of a standardized extract limit the value of the evidence. Additional research is needed. Ginseng may also lower blood pressure. Caution is used when taking ginseng supplements, as adverse effects including drug interactions are possible. Ginseng supplements are not used if pregnant or breastfeeding unless otherwise directed by a doctor. Goldenseal: Limited available study suggests that berberine in addition to a standard prescription drug regimen for chronic congestive heart failure (CHF) may improve quality of life and decrease ventricular premature complexes (VPCs) and mortality. Further research is needed to confirm these results. Use cautiously in patients with gastrointestinal disorders, cardiovascular disease, bleeding disorders or in those taking anticoagulants, diabetes or in those taking antidiabetic agents. Use cautiously in infants with increased bilirubin levels or individuals with glucose-6-phosphate deficiency. Use cautiously in pregnancy. Hawthorn: Herbal combinations containing hawthorn have been found effective in the treatment of functional cardiovascular disorders. However, due to a lack of information on the use of hawthorn alone, there is not enough evidence to recommend for or against this use of hawthorn. Avoid if allergic to hawthorn or to members of the Crataegus species. Avoid with a history of low blood pressure, irregular heartbeat, asthma, low blood pressure when standing or insomnia. Use cautiously in elderly patients. Avoid if pregnant or breastfeeding. L-carnitine: L-carnitine, carnitine, or acetyl-L-carnitine, is an amino acid found in the body. Although preliminary results are promising, there is insufficient available clinical evidence for the use of L-carnitine in congestive heart failure. Avoid with a known allergy or hypersensitivity to carnitine. Use cautiously with peripheral vascular disease, hypertension (high blood pressure), alcohol-induced liver cirrhosis, and diabetes. Use cautiously in low birth weight infants and individuals on hemodialysis. Use cautiously if taking anticoagulants (blood thinners), beta-blockers, or calcium channel blockers. Avoid if pregnant or breastfeeding. Meditation: Meditation may improve quality of life in elderly patients, and may potentially reduce the risk for congestive heart failure. However, there is not enough evidence to make a conclusion. Use cautiously with underlying mental illnesses. People with psychiatric disorders should consult with their primary mental healthcare professional(s) before starting a program of meditation, and should explore how meditation may or may not fit in with their current treatment plan. Avoid with risk of seizures. The practice of meditation should not delay the time to diagnosis or treatment with more proven techniques or therapies, and should not be used as the sole approach to illnesses. Oleander: The term "oleander" refers to two plants: Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander). Both plants contain heart-active "cardiac glycoside" chemicals (similar to the prescription drug digoxin) and have been associated with serious side effects in humans, including death. The plants have been used to treat congestive heart failure in China and Russia for decades, but scientific evidence supporting this use is limited to small, poorly designed studies. Human research began in the 1930s, but was largely abandoned due to serious gastrointestinal and heart toxicity. All parts of the oleander plant, including flowers, leaves, and nectar are considered toxic and may cause death. Avoid if allergic to oleander or other cardiac glycosides such as digoxin. Avoid with a history of irregular heartbeat (arrhythmia), seizures, liver or kidney disease, depression, or asthma. Avoid if pregnant or breastfeeding. Passionflower: An extract containing passionflower and hawthorn has been studied for potential enhancement of exercise capacity in congestive heart failure patients. Individuals using this combination of herbs have experienced improvements in symptoms; however, any positive effects may have resulted from hawthorn, which is more commonly used for congestive heart failure. High quality human research of passion flower alone and compared to prescription drugs used for this condition is needed. Avoid if allergic to passion flower or any of its constituents. Avoid consuming raw Passiflora fruit (Passiflora adenopoda), due to possible cyanide constituents. Passionflower extracts may cause drowsiness in sensitive individuals. Avoid driving or operating heavy machinery while taking passion flower. Use cautiously with low blood pressure. Avoid if pregnant or breastfeeding. Physical therapy: Both supervised and home-based exercise training may enhance exercise capacity in patients with chronic heart failure. However, consensus has not been obtained regarding a standard rehabilitation program for these patients and the literature often suggests individually-tailored programs. Due to the lack of standardization, duration of treatment, and various outcomes measures, more study is needed before a conclusion can be made. Not all physical therapy programs are suited for everyone, and patients should discuss their medical history with a qualified healthcare professional before beginning any treatments. Physical therapy may aggravate pre-existing conditions. Persistent pain and fractures of unknown origin have been reported. Physical therapy may increase the duration of pain or cause limitation of motion. Pain and anxiety may occur during the rehabilitation of patients with burns. Both morning stiffness and bone erosion have been reported in the literature although causality is unclear. Erectile dysfunction has also been reported. Physical therapy has been used in pregnancy and although reports of major adverse effects are lacking the available literature, caution is advised nonetheless. All therapies during pregnancy and breastfeeding should be discussed with a licensed obstetrician/gynecologist before initiation. Relaxation therapy: Early studies suggest that progressive muscle relaxation training may benefit patients with heart failure when used as an adjunct to standard care. Avoid with psychiatric disorders like schizophrenia/psychosis. Jacobson relaxation (flexing specific muscles, holding that position, then relaxing the muscles) should be used cautiously with illnesses like heart disease, high blood pressure, or musculoskeletal injury. Relaxation therapy is not recommended as the sole treatment approach for potentially serious medical conditions, and should not delay the time to diagnosis or treatment with more proven techniques. Selenium: Low selenium levels have been associated with the development of cardiomyopathy, and selenium supplementation is likely of benefit in such cases (for example in Keshan disease and Chagas' disease). However, most cases of cardiomyopathy are not due to low selenium levels and therefore selenium may not be helpful. It has been suggested that low selenium levels may be a risk factor for coronary heart disease, although this remains unclear. Avoid if allergic or sensitive to products containing selenium. Avoid with a history of nonmelanoma skin cancer. Selenium is generally regarded as safe for pregnant or breastfeeding women. However, animal research reports that large doses of selenium may lead to birth defects. Taurine: Taurine is a nonessential amino acid-like compound, found in high abundance in the tissues of many animals, especially sea animals, and in much lower concentrations in plants, fungi, and some bacteria. Preliminary study suggests that taurine may be beneficial as an adjunct to traditional medications for symptoms of congestive heart failure (CHF). Further study is warranted to confirm these findings. Taurine appears to be safe in recommended dosages. As an amino acid, it is unlikely that there are allergies related to this constituent. However, allergies may occur from multi-ingredient products that contain taurine. Use cautiously in patients with high cholesterol, low blood pressure, coagulation disorders, potential for mania, or epilepsy. Avoid alcohol or exercise after consumption of energy drinks containing taurine, caffeine, glucuronolactone, B vitamins, and other ingredients. Use cautiously if pregnant or breastfeeding; taurine is a natural component of breast milk Thiamin: Thiamin (also spelled "thiamine") is a water-soluble B-complex vitamin, previously known as vitamin B1 or aneurine. Thiamin was isolated and characterized in the 1920s, and thus was one of the first organic compounds to be recognized as a vitamin. Chronic severe thiamin deficiency can cause heart failure (wet beriberi), a condition that merits thiamin supplementation. Currently, it is not clear if thiamin supplementation is beneficial in patients with heart failure due to other causes. However, it is reasonable for patients with heart failure to take a daily multivitamin including thiamin, because some of these individuals may be thiamin deficient. Diuretics may lower thiamin levels. Since diuretics are commonly administered to patients with heart failure, patients taking diuretics are at an increased risk of thiamin deficiency. This area remains controversial, and further evidence is necessary before a conclusion can be reached. Avoid if allergic or hypersensitive to thiamin. Rare hypersensitivity/allergic reactions have occurred with thiamin supplementation. Skin irritation, burning, or itching may rarely occur at injection sites. Large doses may cause drowsiness or muscle relaxation. Use cautiously if pregnant or breastfeeding with doses higher than the U.S. Recommended Daily Allowance (RDA). Thymus extract: The thymus is a lobular gland located under the breastbone near the thyroid gland. It reaches its maximum size during early childhood and plays a large role in immune function. Preliminary evidence suggests that thymus extract may increase left ventricular function, exercise tolerance, and survival in patients with cardiomyopathy. Additional research is needed to confirm these results. It is important to use high quality thymus gland supplements. Avoid if allergic or hypersensitive to thymus extracts. Use bovine thymus extract supplements cautiously due to potential for exposure to the virus that causes "mad cow disease." Avoid use with an organ transplant or other forms of allografts or xenografts. Avoid if receiving immunosuppressive therapy, with thymic tumors, myasthenia gravis (neuromuscular disorder), untreated hypothyroidism, or if taking hormonal therapy. Avoid if pregnant or breastfeeding; thymic extract increases human sperm motility and progression. Traditional Chinese medicine (TCM): Many studies of TCM herbs have focused on treatment of congestive heart failure. Further research of better design is needed before recommendations can be made. Chinese herbs can be potent and may interact with other herbs, foods or drugs. Consult a qualified healthcare professional before taking. There have been reports of manufactured or processed Chinese herbal products being tainted with toxins or heavy metals or not containing the listed ingredients. Herbal products should be purchased from reliable sources. Avoid ma huang, which is the active ingredient in ephedra. Avoid ginseng if pregnant or breastfeeding. Fair negative scientific evidence: Guided imagery: Therapeutic guided imagery may be used to help individuals relax and focus on images associated with personal issues they are confronting. Preliminary human research does not report benefits of guided imagery in congestive heart failure. Guided imagery is usually intended to supplement medical care, not to replace it, and guided imagery should not be relied on as the sole therapy for a medical problem. Contact a qualified health care provider if mental or physical health is unstable or fragile. Never use guided imagery techniques while driving or doing any other activity that requires strict attention. Use cautiously with physical symptoms that can be brought about by stress, anxiety or emotional upset because imagery may trigger these symptoms. If feeling unusually anxious while practicing guided imagery, or with a history of trauma or abuse, speak with a qualified health care provider before practicing guided imagery. Smoking cessation: Smoking damages blood vessels, reduces the amount of oxygen in the blood, and makes the heart beat faster. If an individual smokes, a doctor can help recommend a program to help them quit. Individuals are not considered for a heart transplant if smoking is continued. Weight control: It is recommended that individuals weigh themselves each morning after urination, but before breakfast. Notify a doctor if there is a weight gain of three or more pounds in a day. Weight gain may indicate fluid build-up. Being overweight contributes to other risk factors for stroke, such as high blood pressure, cardiovascular disease, and diabetes. Weight loss of as little as ten pounds may lower blood pressure and improve cholesterol levels. Exercise can lower blood pressure, increase the level of high density lipoprotein (HDL cholesterol or good cholesterol), and improve the overall health of blood vessels and heart. It also helps control weight, control diabetes, and reduce stress. Cardiac rehabilitation programs exist for individuals recovering from heart surgery. Cardiac rehabilitation is a medically supervised program to help heart patients recover quickly and improve their overall physical, mental, and social functioning. The goal is to stabilize, slow, or even reverse the progression of cardiovascular disease, thereby reducing the risk of heart disease, another cardiac event, or death. Cardiac rehabilitation programs include: counseling so the individual can understand and manage the disease process; an exercise program; counseling on nutrition; helping the patient modify risk factors such as high blood pressure, smoking, high blood cholesterol, physical inactivity, obesity, and diabetes; providing vocational guidance to enable the patient to return to work; information on physical limitations; lending emotional support; and counseling on appropriate use of prescribed medications. A doctor can help initiate an exercise program and cardiac rehabilitation tailored to the individual with congestive heart failure (CHF). Salt restriction: Too much sodium (from salt) contributes to water retention, which makes the heart work harder. Excess sodium may causes shortness of breath and swollen legs, ankles, and feet. For individuals with heart failure the recommended sodium intake is no more than 2,000 mg daily. Some substitutes or "lite" salts contain a mixture of salt and other compounds. To get that familiar salty taste, individuals may use too much of the substitute and actually not reduce sodium intake. In addition, many salt substitutes contain potassium chloride. Too much potassium can be harmful. A dietitian can help outline a healthy, low-salt diet. Stress management: Stress can cause an increase in blood pressure along with increasing the blood's tendency to clot. Managing stress can be vital to keeping a heart healthy. Diet modification: Eating healthy foods is important. A heart-healthy diet should include five or more daily servings of fruits and vegetables, foods rich in soluble fiber (such as oatmeal and beans), foods rich in calcium (dairy products, spinach), soy products (such as tempeh, miso, tofu, and soy milk), and foods rich in omega-3 fatty acids, including cold-water fish, such as salmon, mackerel, and tuna. Pregnant women and women who plan to become pregnant in the next several years should limit their weekly intake of cold-water fish because of the potential for mercury contamination. Limiting red meats and high fat foods (such as doughnuts, cookies, and chips) is recommended by healthcare professionals. Alcohol: Excessive use of alcohol may weaken the heart muscle or increase the risk of abnormal heart rhythms, further worsening existing heart failure. Alcohol may also interact with some medications used to treat heart conditions. One glass of red wine daily may be beneficial for heart health. Swelling: Leg, ankle, and foot edema can be improved by elevating the legs above heart level for 30 minutes three or four times per day. Leg elevation alone may be sufficient therapy for patients with mild venous insufficiency, but is usually not adequate for more severe cases. In addition, it may not be practical for those who work to elevate their legs several times per day. Leg edema (swelling) can also be prevented and treated with the use of compression stockings. Many types are available, including knee-high, thigh-high, and pantyhose. Knee-high stockings are sufficient for most individuals; thigh-high stockings are less desirable because they tend to provide too much pressure behind the knees, reducing blood flow in the veins, and causing discomfort. The stockings should be put on as early as possible in the morning when edema is minimal. Healthcare professionals can help with choosing the right compression stocking for each individual. Sleep: It is recommended that individuals with CHF who have shortness of breath sleep with their head propped up at a 45 degree angle using a pillow or a wedge. This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com). - Allard ML, Jeejeebhoy KN, Sole MJ. The management of conditioned nutritional requirements in heart failure. Heart Fail Rev. 2006;11(1):75-82. .View abstract - American Heart Association. www.americanheart.org. Accessed March 11, 2009. - Boekholdt SM, Sandhu MS, Day NE, et al. Physical activity, C-reactive protein levels and the risk of future coronary artery disease in apparently healthy men and women: the EPIC-Norfolk prospective population study. Eur J Cardiovasc Prev Rehabil. 2006;13(6):970-6. .View abstract - Dauchet L, Amouyel P, Hercberg S, et al. Fruit and vegetable consumption and risk of coronary heart disease: a meta-analysis of cohort studies. J Nutr. 2006;136(10):2588-93. .View abstract - Jiang W, Kuchibhatla M, Clary GL, et al. Relationship between depressive symptoms and long-term mortality in patients with heart failure. Am Heart J. 2007;154(1):102-8. .View abstract - National Institutes of Health. www.nhlbi.nih.gov. Accessed March 11, 2009. - Natural Standard: The Authority on Integrative Medicine. Copyright © 2009. www.naturalstandard.com. Accessed March 11, 2009. - Riegel B, Moser DK, Powell M, et al. Nonpharmacologic care by heart failure experts. J Card Fail. 2006;12(2):149-153. .View abstract - U.S. Food and Drug Administration. www.fda.gov. Accessed March 11, 2009. - von Haehling S, Doehner W, Anker SD. Nutrition, metabolism, and the complex pathophysiology of cachexia in chronic heart failure. Cardiovasc Res. 2007;73(2):298-309. .View abstract Copyright © 2011 Natural Standard (www.naturalstandard.com)	2	9	0	0	0	3	0.967696	3	13,312
Lattice corneal dystrophy \|Lattice corneal dystrophy type\| \|A network of thick linear corneal opacities in patient with a variant of LCD1 (LCD type III) due to a homozygous p. Leu527Arg mutation in the TGFBI gene\| \|Classification and external resources\| Lattice corneal dystrophy type, also known as Biber-Haab-Dimmer dystrophy, is a rare form of corneal dystrophy. It has no systemic manifestations, unlike the other type of the dystrophy, Lattice corneal dystrophy type II. Lattice corneal dystrophy was first described by Swiss ophthalmologist Hugo Biber in 1890. Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma. Lattice corneal dystrophy has two types: - type I: with no systemic association. It is caused by mutations in TGFBI gene encoding keratoepithelin, which maps to chromosome 5q. - type II or Finnish type amyloidosis: associated with manifestations of systemic amyloidosis due to accumulation of gelsolin. Associated conditions may include cutis laxa and ataxia. - type III is also described which has an onset at age 70 to 90 years and is not associated with systemic amyloidosis. Filamentous opacities appear in the cornea with intertwining delicate branching processes. During an eye examination, the doctor sees these deposits in the stroma as clear, comma-shaped overlapping dots and branching filaments, creating a lattice effect. Over time, the lattice lines will grow opaque and involve more of the stroma. They will also gradually converge, giving the cornea a cloudiness that may also reduce vision. The disease is bilateral, usually noted before the end of the first decade of life. Although lattice dystrophy can occur at any time in life, the condition usually arises in children between the ages of two and seven. In some people, these abnormal protein fibers can accumulate under the cornea's outer layer—the epithelium. This can cause erosion of the epithelium. This condition is known as recurrent epithelial erosion. These erosions alter the cornea's normal curvature, resulting in temporary vision problems, and expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful. In systemic cases, kidney failure, heart failure and neuropathy such as facial nerve palsy, laxity of the skin may be noted. In case of corneal erosion, a doctor may prescribe eye drops and ointments to reduce the friction on the eroded cornea. In some cases, an eye patch may be used to immobilize the eyelids. With effective care, these erosions usually heal within three to seven days, although occasional sensations of pain may occur for the next six-to-eight weeks. As patients with LCD suffer with dry eyes as a result of erosion, a new technique involving the insertion of punctal plugs (both upper and lower) can reduce the amount of drops used a day, aiding ocular stability. By about age 40, some people with lattice dystrophy will have scarring under the epithelium, resulting in a haze on the cornea that can greatly obscure vision. In this case, a corneal transplantation may be needed. There have been many cases in which teenage patients have had the procedure, which accounts for the change in severity of the condition from person to person. Although people with lattice dystrophy have an excellent chance for a successful corneal transplantation, the disease may also arise in the donor cornea in as little as three years. In one study, about half of the transplant patients with lattice dystrophy had a recurrence of the disease between two and 26 years after the operation. Of these, 15 percent required a second corneal transplant. Early lattice and recurrent lattice arising in the donor cornea responds well to treatment with the excimer laser. Phototherapeutic keratectomy (PTK) using [Excimer laser] can restore and preserve useful visual function for a significant period of time in patients with anterior corneal dystrophies. - H. Biber: Über einige seltenere Hornhauterkrankungen. Zürich, 1890. Inaugural Dissertation, Zurich, 1890. Cited by O. Haab: Die gittrige Keratitis. - Online Mendelian Inheritance in Man (OMIM) 122200 - de la Chapelle A, Kere J, Sack GH, Tolvanen R, Maury CP (July 1992). "Familial amyloidosis, Finnish type: G654----a mutation of the gelsolin gene in Finnish families and an unrelated American family". Genomics. 13 (3): 898–901. doi:10.1016/0888-7543(92)90182-R. PMID 1322359. - Kiuru-Enari S, Keski-Oja J, Haltia M (February 2005). "Cutis laxa in hereditary gelsolin amyloidosis". Br. J. Dermatol. 152 (2): 250–7. doi:10.1111/j.1365-2133.2004.06276.x. PMID 15727635. - Tanskanen M, Paetau A, Salonen O, et al. (March 2007). "Severe ataxia with neuropathy in hereditary gelsolin amyloidosis: a case report". Amyloid. 14 (1): 89–95. doi:10.1080/13506120601116393. PMID 17453628. - Online Mendelian Inheritance in Man (OMIM) 105120	2	6	2	0	0	0	0.625009	2	1,272
Consider anatomy and coding guidance to put things into perspective. Functional endoscopic sinus surgery (FESS) is a surgical procedure performed endoscopically on the nasal/sinus cavities. The purpose of the surgery is to reduce the symptoms of chronic sinusitis such as congestion, drainage, post-nasal drip, headaches, and facial pain. FESS Coding can be unnerving because there are multiple codes associated with the surgery. Reviewing sinus anatomy and coding guidance for FESS Coding will help you keep a clear head when coding these claims. There are four separate sinus cavities (jointly, the paranasal sinuses) on each side of the face. They are: - Maxillary (antrum). These air-filled sinuses are located below the eye, behind the cheek. - Ethmoid. The ethmoid sinuses are between the eye and the nasal cavity. The concha bullosa is an extension of the ethmoid sinus located in the middle turbinate. - Sphenoid. The sphenoid is a wedge-shaped bone in the middle of the skull that contains the sphenoid sinuses. It is located between the back of the nasal space and the cranial cavity. Just lateral or beside the sphenoid sinus are the optic nerves and the intracranial portion of the carotid arteries. - Frontal. These sinus cavities are located above the eye in the forehead region. Diagnoses That May Require FESS Coding The most common indications for endoscopic nasal/sinus surgery are rhinosinusitis (sinusitis), polyp, cyst, neoplasm, and polypoid sinus degeneration. Common diagnoses and associated ICD-10-CM codes include: - Chronic pansinusitis (J32.4) — when all four sinus cavities have chronic sinusitis. If coded individually: maxillary (J32.0), frontal (J32.1), ethmoid (J32.2), and sphenoid (J32.3). - Other chronic sinusitis (J32.8) — when more than one sinus cavity has chronic sinusitis. - Acute, recurrent pansinusitis (J01.41) — when all four sinus cavities have acute, recurrent sinusitis. (Per ICD-10-CM, as it relates to sinusitis, the term “recurrent” is associated with acute, not chronic.) - Other acute, recurrent sinusitis (J01.81) - Polyps (J33.8) - Cyst and mucocele of nose and nasal sinus (J34.1) - Polypoid sinus degeneration (J33.1) - Other specified disorders of nose and nasal sinuses (J34.89) Coding FESS Procedures During surgery, the surgeon will perform diagnostics on the internal anatomy of the nasal/sinus cavities with the assistance of an endoscope for increased visualization and magnification. The surgeon inspects the interior nasal cavity, the middle and superior meatuses, the turbinates, and the sphenoethmoid recess. This diagnostic portion of the surgery is reported using the appropriate code from CPT® code range 31231-31235. According to the CPT® code book, diagnostic endoscopy and sinusotomy (the incising of a sinus) are included in the surgical sinus endoscopy codes 31237-31298. Diagnostic codes 31231-31235 are not reported separately with surgical codes 31237-31298. Additionally, according to the CPT® code book, “To report these services when all of the elements are not fully examined (eg, judged not clinically pertinent), or because the clinical situation precludes such exam (eg, technically unable, altered anatomy), append modifier 52 if repeat examination is not planned, or modifier 53 if repeat examination is planned.” Procedure codes 31233-31294 are unilateral. When performed on both the right and left sinus cavity, append modifier 50 Bilateral procedure to the procedure code. CPT® code 31231 is listed as unilateral or bilateral, making it inappropriate to append modifier 50 to this code. FESS Coding Guidance To select the correct code, read the body of the operative report to ensure that documentation supports the procedure listed under the Procedures heading. Specific terminology or a sufficient description of the procedure must be documented. Here are examples of the work involved in specific procedure codes: Endoscopic Maxillary Antrostomy — Vignette for Code 31256 (CPT® Assistant, January 1997) The maxillary sinus ostium is palpated and visually identified. Residual inferior bony uncinate remnants are removed, and the ostium enlarged posteriorly, inferiorly, and anteriorly as indicated. Bony partitions, as between the natural maxillary sinus ostium and a Haller cell above, may require removal to relieve the obstruction. Hemostasis with topical agents or sponge insertion may be required. If the description in the body of the operative report does not indicate that the ostium was violated, it may not be appropriate to code the procedure. Best practice is to query the provider when in doubt. Endoscopic Maxillary Antrostomy with Tissue Removal for Code 31267 (Coders’ Desk Reference for Procedures 2019) Code 31267 has all the elements of 31256. In 31267, the maxillary sinus may be opened, and the mucosa removed. Endoscopic Total Ethmoidectomy — Vignette for Code 31255 (CPT® Assistant, January 1997) The surgery begins with complete uncinate process removal. The anterior ethmoid cells are removed, and the medial orbital wall identified and skeletonized under endoscopic visualization. The middle turbinate ground lamella is penetrated and removed, and the posterior ethmoid cells are removed back to the anterior sphenoid wall, which is followed up to the skull base. The skull base is then skeletonized and followed forward to the frontal recess at the anterior ethmoid artery. Endoscopic Frontal Sinus Exploration for Code 31276 (Coders’ Desk Reference for Procedures 2019) A sinusotomy of the frontal sinus ostium is performed. If diseased or abnormal tissue is present within the frontal sinus, a scalpel or biting forceps is introduced parallel to the endoscope and is used to remove the tissue. This procedure includes polypectomy, debridement, or biopsy of the frontal sinus tissue when performed. Electrocautery may be used for hemostasis. The nasal cavity may be packed with Telfa or gauze. There does not have to be tissue removed from the frontal sinus cavity to code for this procedure. The surgeon may explore the cavity. Also, the Coders’ Desk Reference for Procedures states, “If diseased or abnormal tissue is present ….” This implies there may not be diseased or abnormal tissue within the frontal sinuses. Endoscopic Sphenoid Sinus for Code 31287-31288 (Coders’ Desk Reference for Procedures 2019) The sphenoid can be explored with direct access or through the posterior ethmoid sinus. The isolated access to the sphenoid sinus is through dilation of the sphenoid ostium. The middle turbinate may be fractured or partially removed for access. The ostium is cannulated and dilated. The physician uses forceps or a sphenoid punch to open the sinus cavity. Additionally, diseased mucosa or tissue is removed in 31288. Combination codes 31253, 31257, 31259 (Total Ethmoidectomy with Frontal Sinus Exploration or Total Ethmoidectomy with a Sphenoid Sinusotomy, or with a Sphenoidotomy and Removal of Tissue) – CPT® Assistant, April 2018 Code 31253 includes the work of codes 31255 and 31276. Code 31253 is reported when a complete/total ethmoidectomy is performed with frontal sinus exploration. If only a partial ethmoidectomy is performed in conjunction with a frontal sinus exploration, report codes 31254 and 31276. Code 31257 includes the work of both codes 31255 and 31287. Code 31257 is reported when a complete/total ethmoidectomy is performed with a sphenoidotomy (sphenoid sinusotomy). If only a partial ethmoidectomy is performed in conjunction with a sphenoidotomy, report codes 31254 and 31287. Code 31259 includes the work of codes 31255 and 31288. Code 31259 is reported when a complete/total ethmoidectomy is performed with a sphenoidotomy and removal of tissue from the sphenoid sinus. If only a partial ethmoidectomy is performed in conjunction with a sphenoidotomy and removal of tissue from the sphenoid sinus, report codes 31254 and 31288. There are four separate sinus cavities on each side of the face. Coding Separate Procedures Within the endoscopic sinus surgery codes, there are two separate procedure designated codes: 31231 Nasal endoscopy, diagnostic, unilateral or bilateral (separate procedure) and 31237 Nasal/sinus endoscopy, surgical; with biopsy, polypectomy or debridement (separate procedure). According to National Correct Coding Initiative (NCCI): “A procedure designated by the CPT code descriptor as a ‘separate procedure’ is not separately reportable if performed in a region anatomically related to the other procedure(s) through the same skin incision, orifice, or surgical approach.” In other words, when performed on the same side (ipsilateral), it would be incorrect to bill 31231 or 31237 with the endoscopic surgical codes (31238-31294). However, because there are two orifices (right and left nasal cavities), when performing a diagnostic procedure on the right side and a surgical procedure on the left side, both procedures may be reported. Modifier 59 Distinct procedural service may be required with 31231 and 31237. Coding the Stereotactic Computer-Assisted Navigation System According to CPT® code book, the Brainlab navigation system may be used to facilitate the performance of endoscopic sinus surgery, and is reported with 61782 Stereotactic computer-assisted (navigational) procedure; cranial, extradural (List separately in addition to code for primary procedure) when the procedure is performed in conjunction with endoscopic sinus surgery. One explanation for use of this system is that the paranasal sinuses share a common thin wall with the eye socket (or orbit) and cranial cavity. When performing surgery in a highly delicate region, the surgeon relies on the system to navigate the area through the identification of anatomical landmarks. The ethmoid, for example, is a facial bone located between the eyes whose upper portion lies just below the cranial cavity. According to the Cleveland Clinic, “All operations on the ethmoid sinus carry a rare chance of creating a leak of cerebral sinus fluid (CSF).” The risk of CSF leak is potentially reduced because the endoscope allows for improved visualization. Nevertheless, a CSF leak could lead to an infection, potentially resulting in meningitis. When coding the navigation system, the surgeon’s documentation should describe the setup. Examples include: - “The surgical navigation system was set up and found to be accurate after registration.” - “The registration sticker for the Medtronic image guidance system was placed on the forehead. The face was registered with good correlation. Landmarks were checked with the probe, which showed satisfactory accuracy.” - “Image guidance was placed on the patient and calibrated.” The surgeon’s documentation should also describe the area in which the system was used. For example: - “Surgical navigation was used to confirm the position of the lamina papyracea (i.e., medial orbital wall), skull base, and frontal recess cells.” When an otolaryngology surgeon performs the approach of a procedure, and a neurosurgeon performs the resection on that same patient for a cranial mass or tumor, both surgeons may require the use of the navigation system. However, only one MUE is allowed per day for the navigation system, and the CPT® code does not allow for co-surgery (modifier 62). The CPT® code does, however, allow for an assistant surgeon (modifier 82) (see the Medicare Physician Fee Schedule); therefore, if the documentation supports its use, the neurosurgeon may bill for the navigation system appending modifier 82 to the CPT® code. Additionally, when a neurosurgeon is involved, the CPT® code may be 61781 Stereotactic computer-assisted (navigational) procedure; cranial, intradural (List separately in addition to code for primary procedure) for an intradural cranial procedure, rather than 61782 (extradural). Why 61781 instead of 61782? If a neurosurgeon is involved, the surgical target may be intradural. Therefore, regardless of whether the otolaryngology surgeon’s work is performed extradural (outside the dura), the code is driven by the location of the surgical target. For More Information: https://www.aapc.com/blog/49499-code-fess-with-a-clear-head/	4	17	46	0	0	9	0.395115	55	2,875
The computer engineering geniuses at Apple have done it again. They’ve created yet another device that I’m probably going to have to buy. The new Apple Watch (series 4) has the ability for anyone to monitor their EKG (sort of). But what are we as physicians going to do with this data? Most electronic medical records permit patients to upload images to their patient portals for their physicians to have access to. Inevitably, some patients will overuse this system – some physicians are already drowning in dozens of Apple Watch rhythm strips being submitted by a single patient. But even for the patient who sends in a single suspicious rhythm strip, if the physician is going to make a clinical decision based on the strip, what are the implications? So, this presents several questions for physicians. What is it? The Apple Watch 4 can monitor the heart rhythm in two ways. First, it can measure the regularity of the heart beat by essentially taking the patient’s pulse; this can be reported as regular or irregular. Second, it can measure a single lead EKG reading and it is this latter feature that is really innovative. All EKGs are done by positioning 2 electrodes on different parts of the body and then measuring the electrical signal between those electrodes. A full EKG uses 12 electrodes and produces 12 different wave forms, or leads. The first three of these leads are the limb leads I – III. Lead I measures the signal between the left arm and right arm. Lead II is between the left leg and right arm. Lead III is between the left leg and left arm. The problem with a watch is that an electrode sensor on the back of the watch only has contact with one arm but by placing a second electrode sensor on the knob of the watch, a person can touch that second electrode with a finger from the other arm, thus generating a lead I EKG tracing by having an electrode in contact with both the left and the right arms simultaneously. What can it tell you? Since the Apple Watch can only generate a single lead EKG, there are limitations about the amount of information it can provide. For example, you cannot diagnose a myocardial infarction from only one lead (you need all 12). The main information that the lead I tracing will give you is whether the patient is in sinus rhythm or atrial fibrillation. Apple claims that the Apple Watch is 98.3% sensitive and 99.6% specific for classifying atrial fibrillation. However, 12.2% of rhythms could not be classified by the Apple Watch EKG app. Although Apple only mentions atrial fibrillation on its marketing materials for the Apple Watch 4, any physician who looks at telemetry monitor strips in the hospital knows that there are other important rhythm abnormalities that can be identified from a single lead EKG tracing. What should you do if the patient uploads a rhythm strip? Although we all get trained in EKG interpretation in medical school, most physicians are not credentialed to read 12-lead EKGs. In most hospitals, physicians must apply for hospital privileges to interpret EKGs and generally, this will be limited to cardiologists; in smaller hospitals, it may be a general internist who has EKG interpretation privileges. Reading an Apple Watch rhythm strip is considerably less complicated than reading a full 12-lead EKG but nevertheless, physicians should know their own limits as to whether they can confidently identify atrial fibrillation (or some other abnormal rhythm) by a rhythm strip. So, for example, if you are a podiatrist or dermatologist and do not normally look at heart rhythm strips, you may want to tell the patient who uploads an Apple Watch rhythm strip to your electronic medical record that EKG interpretation is not part of your normal practice and that they should check with one of their other physicians. However, most primary care physicians are trained in the recognition of atrial fibrillation. Can you bill for review of the rhythm strip? The short answer is in 2018, no but in 2019… maybe. Lets take a look at the CPT code possibilities for Apple Watch rhythm interpretation. - CPT code 93010 (Medicare reimbursement about $8.50). This is the CPT code for interpretation of a 12-lead EKG if someone else (usually the hospital) owns the EKG machine. It requires an order from a physician and a written interpretation. Since an Apple Watch rhythm strip is only 1 lead and since it is done by the patient’s initiation and not by the physician’s order, CPT 93010 cannot be used. - CPT code 93042 (Medicare reimbursement about $7.00). This is the CPT code for rhythm strip interpretation of 1-3 leads of EKG tracings. Like the previous CPT code, this requires an order from a physician and a written interpretation. Although it is conceivable that 93042 could be used to bill for Apple Watch rhythm strip interpretation, I would be hesitant to bill it since the patient is submitting the strip without a physician order. - CPT code G2010 (Medicare reimbursement about $6.50). This is the new CPT code for “Remote Evaluation of Pre-Recorded Patient Information” that was created as part of the 2019 Medicare physician fee schedule. This was designed for video or images such as photos of a rash, etc. that a patient creates and then sends to the physician for review. There are several restrictions when billing this CPT code, however. The physician doing the review of the pre-recorded information cannot have seen the patient for a regular evaluation & management encounter within the previous 7 days or within 24 after reviewing the images. Also, the physician has to interpret the image and communicate the findings to the patient within 24 business hours. We will not know for sure if Medicare carriers will accept CPT code G2010 for Apple Watch rhythm interpretation until the new fee schedule goes into effect after January 1, 2019 and we start submitting bills for it; however, it would seem like this CPT code would be the best fit. Who should get one? Since the main thing the Apple Watch EKG app does is tell whether there is atrial fibrillation, it will primarily be useful for patients at risk of atrial fibrillation or with a history of previous atrial fibrillation. Better identification of patients with intermittent atrial fibrillation really could save lives since about 15% of all strokes are the result of untreated atrial fibrillation. My suspicion is that a lot of other people with occasional PACs or PVC (premature atrial/ventricular contractions) will also be uploading rhythm strips to understand why they have occasional subjective “skipped heartbeats”. Although not designed for PAC or PVC identification, this could be a side benefit of the app. Similarly, ventricular arrhythmias such as non-sustained ventricular tachycardia may be identifiable. Bradycardic rhythms such as sinus bradycardia and various forms of heart block (1st degree, 2nd degree, and 3rd degree) may be identifiable. Even if these rhythms cannot be diagnosed with complete certainty, the tracings from the Apple Watch EKG app may be suspicious enough for the physician to direct the patient to seek medical attention where a full 12-lead EKG or a 24-Holter monitor can be performed. I’ve never had atrial fibrillation or any kind of heart problem. So, am I going to get an Apple Watch 4 with an EKG app… well, yeah, probably. December 20, 2018	4	9	8	0	4	0	0.613882	12	1,592
- Endocrine pathology Endocrine pathology is the subspecialty of surgical pathologywhich deals with the diagnosisand characterization of neoplastic and non-neoplastic diseases of organs of the endocrine system, including the thyroid, parathyroids, exocrine pancreas, and adrenal glands. Wikimedia Foundation. 2010. Look at other dictionaries: Endocrine disease — Classification and external resources Major endocrine glands. (Male left, female on the right.) 1. Pineal gland 2. Pituitary gland 3. Thyroid gland 4. Thymus 5. Adrenal gland 6. Pancreas 7 … Wikipedia pathology — Synonyms and related words: abnormality, acute disease, affection, affliction, ailment, allergic disease, allergy, atrophy, bacterial disease, birth defect, blight, cardiovascular disease, chronic disease, circulatory disease, complaint,… … Moby Thesaurus Surgical pathology — is the most significant and time consuming area of practice for most anatomical pathologists. Surgical pathology involves the gross and microscopic examination of surgical specimens, as well as biopsies submitted by non surgeons such as general… … Wikipedia Multiple endocrine neoplasia type 2b — Classification and external resources Micrograph of medullary thyroid carcinoma, as may be seen in MEN 2b. H E stain … Wikipedia Multiple endocrine neoplasia — Classification and external resources Micrograph of a medullary thyroid carcinoma, as may be seen in MEN 2A and MEN 2B. H E stain … Wikipedia Multiple endocrine neoplasia type 1 — Classification and external resources ICD 10 D44.8 ICD 9 258.01 … Wikipedia Multiple endocrine neoplasia type 2 — MEN type 2A (Sipple syndrome) Classification and external resources Bilateral pheochromocytomas associated with Multiple endocrine neoplasia type 2 ICD 10 D … Wikipedia Armed Forces Institute of Pathology — The Armed Forces Institute of Pathology (AFIP) is a US government institution concerned with diagnostic consultation, education, and research. It was founded in 1862 as the Army Medical Museum and is located in Washington, DC on the grounds of… … Wikipedia Head and neck pathology — is the subspecialty of surgical pathology and dentistry which deals with the diagnosis and characterization of neoplastic and non neoplastic diseases of the neck, scalp, face, ears, paranasal sinuses, nasal cavity, oral cavity, salivary glands,… … Wikipedia Oxyphil cell (pathology) — Oxyphil cells are found in oncocytomas of the kidney, endocrine glands, and salivary glands. External links MeSH Oxyphil+Cells … Wikipedia	3	6	0	0	0	2	0.691541	2	570
HIPAA at DSHS Topics on this page: What is HIPAA? HIPAA is the acronym of the Health Insurance Portability and Accountability Act of 1996. The main purpose of this federal statute was to help consumers maintain their insurance coverage, but it also includes a separate set of provisions called Administrative Simplification. This section of the act is aimed at improving the efficiency and effectiveness of the health care system. The key components of Administrative Simplification include: - Standardized electronic transmission of common administrative and financial transactions (such as billing and payments) - Unique health identifiers for individuals, employers, health plans, and heath care providers - Privacy and security standards to protect the confidentiality and integrity of individually identifiable health information The HIPAA regulations apply to: - Health Plans - Health Care Clearinghouses (Entities that facilitate electronic transactions by "translating" data between health plans and providers when they use non-compatible information systems.) - Health Care Providers who transmit health information in electronic form in connection with one or more of the eight covered transactions. Business associates of a covered entity are not directly controlled by the regulations, but mandatory contracts require them to protect the privacy of individually identifiable information. Government agencies specifically named in the regulations are covered entities, as are agencies that function as a health plan or a health care provider. - Electronic Data Interchange (EDI) - Transaction Standards - Code Sets - National Standard Identifiers - Health Plan Electronic Data Interchange ( EDI ) These regulations are identified as the Transaction Code Set Standards. The final rules for EDI and Code sets were implemented on October 16, 2003. Several of the transaction regulation standards are still under review and have not been published. The purpose of these regulations is to standardize the electronic exchange of information (transactions) between trading partners. These transactions are mandated to be in the ANSI ASC X12 version 4010 format. The covered transactions include: - 270 = Eligibility Inquiry - 271 = Inquiry and Response - 276 = Claim Status Inquiry - 277 = Claim Status Inquiry and Response - 278 = Authorization Request and Authorization Response - 820 = Health Insurance Premium Payment - 834 = Beneficiary Enrollment - 835 = Remittance / Payment - 837 = Claim or Encounter The HIPAA Code Set Regulations establish a uniform standard of data elements used to document reasons why patients are seen and the procedures performed during health care encounters. HIPAA specified code sets to be used are: - Diagnoses - ICD 9 - Procedures - CPT 4, CDT - Supplies/Devices - HCPCS - Additional Clinical Data - Health Level Seven (HL7) HIPAA specified administrative codes set for use in conjunction with certain transactions and HIPAA eliminated state-specific local codes. These regulations establish standards for protecting individually identifiable health information and for guaranteeing the rights of individuals to have more control over such information. HIPAA privacy regulations were implemented on April 14, 2003. Privacy rules define the rights of individuals and security rules define the process and technology required to ensure privacy. These regulations establish standards for the security of electronic protected health information (PHI). HIPAA security regulations were implemented on April 21, 2005 for all but small health plans (who must comply by April 20, 2006). The final regulations adopt standards for the security of electronic protected health information (e-PHI). These standards are organized into the following three high level categories: - Administrative safeguards include policies, procedures, and practices that guide security management and information access authorization/revocation, contingency planning and training. These rules are enforced through sanctions and are largely directed toward the covered entity's workforce. - Physical safeguards include protections that minimize physical access to information within buildings, floors, departments, offices, and desks. These safeguards include doors, locks, badge access, location of workstations (obscured from public view), and media controls (e.g. location of back-up tapes). - Technical safeguards include limiting electronic information access to particular users or user groups, including different levels of software access rights, and tracking access through audit controls. National Provider Identifiers (NPI) These regulations establish the standard unique health identifier for health care providers to simplify administrative processes, such as referrals and billing, to improve accuracy of data, and reduce costs. The Final Rule was published January 23, 2004. Health Care providers began applying for NPIs on the effective date of the final rule, which was May 23, 2005. All health care providers are eligible to be assigned NPIs; health care providers who are covered entities must obtain and use NPIs. All HIPAA covered entities must use NPIs by the compliance dates: - May 23, 2007 for all but small health plans. - May 23, 2008 for small health plans. Penalties for Failure to Comply with HIPAA The legislation carries heavy civil and criminal penalties for failure to comply.US DHHS Office for Civil Rights will enforce civil penalties that may include penalties from $100 per violation to $25,000 per calendar year. US Department of Justice will enforce criminal penalties which may include up to 10 years imprisonment and a $250,000 fine.	3	14	0	0	0	1	0.222231	1	1,081
Dermatology is one of the most complex specialties when it comes to diagnosis and coding management. This is why most healthcare providers and dermatologists outsource the services to professional medical billing and coding companies that are dedicated to these tasks. Psoriasis is a notable dermatology disease that is very prevalent in the US. According to a report, the autoimmune disease affects almost 3% of the adult population, which makes up more than 7.5 million US adults. In order to get quality reporting and statistics as well as reimbursement on claims for all these cases, it is imperative to have complete, compliant coding and proper documentation. Timely and accurate prevalence estimates are important when it comes to gathering data about diseases. When it comes to psoriasis, it is equally significant to find out the trends and other stats given the sheer number of cases reported each year in the US. While there is existing prevalence information available based on local sample sizes, they are not enough to sedate the demand for an increasing number of administrative data. Hence the need for using the International Classification of Diseases for documenting the diagnosis and treatment of diseases to allow for swift access to morbidity data. It is imperative for healthcare providers and medical coding and billing specialists to understand and appreciate the benefits of using the ICD 9 code for psoriasis as well as the relevant ICD 10 codes which effectively replaced the ICD 9 in 2015. The vast data compiled through the ICD helps researchers and medical experts to conduct studies and predict future trends. The medical diagnostic codes for psoriasis should be enough to validate the number of patients and to ascertain the type of psoriasis that is the most prevalent. However, in truth, there is a lack of proper and strict reporting of the procedures and treatment for psoriasis, which can be attributed to a deficiency of knowledge when coding for ICD 9 psoriasis. What is Psoriasis? Psoriasis is one of the most prevalent immune-mediated diseases. It is characterized by inflammation in different parts of the body, caused by dysfunction of the human immune system. The inflammation that is caused can be recognized by scales and plaques that appear on the skin. Psoriasis is caused due to hyperactivity of the immune system that speeds up the growth of the skin cells. Normally, skin cells grow and then shed off in a process that is a month-long. But with psoriasis, this process is done within three or four days, which causes the skin cells to add up and pile on the skin’s surface, including on the scalp, knees, and elbows. The inflammation that is caused by psoriasis does not only affect the skin, but is found to impact some internal organs and tissues as well, and gradually leading to other health conditions. According to independent research, one in every three patients of psoriasis develops psoriatic arthritis, which is characterized by swollen and stiff joints. Which Health Care Providers Treat Psoriasis? Psoriasis is diagnosed and treated by dermatologists who specialize in skin-related diseases and problems. For psoriatic arthritis, you may also seek help from a rheumatologist who specifically provides treatment for joint disorders. However, family physicians and other medical doctors can also provide basic treatment for psoriasis. Other healthcare professionals including holistic practitioners, acupuncturists, chiropractors, and even nutritionists are known to give treatment for psoriasis to some extent or another. If you are looking for rheumatologists and dermatologists specializing in the treatment of psoriasis, the National Psoriasis Foundation and the American Academy of Dermatology are great sources. They have updated databases with the best specialists near you. Patients with psoriasis have more chances to contract other comorbidities such as liver problems, diabetes, inflammatory bowel disease, arthritis, and hypertension to name a few. That means that their overall health condition should closely be monitored for other health problems. A dermatologist or a health care provider can diagnose the condition by – Obtaining the patient’s medical history – Getting the patient’s family health history – Performing a physical examination of the skin – Microscopic examination of the skin tissues What is the ICD 9? The International Classification of Diseases ninth revision is a set of standards containing codes to describe medical diagnoses. The standardized coding means that there is consistency in the recording of patient symptoms and diagnoses among health care providers, which is then used for reimbursement on medical bills and claims. Each disease or diagnosis is represented by a six-character alphanumeric code that describes in detail that certain condition. Physicians and healthcare providers identify the specific code for treatment they provide which can be entered into the patient’s electronic health record for reporting, diagnostic and billing purposes. The ICD 9 was introduced in 1975 at the WHO annual conference and the US soon adopted the code set into its medical system. In 2008, CMS announced that the US will be adopting the ICD 10, which many countries had already adopted since its inception in the 90s. However, the health system was hurdled by political and technical issues, due to which it was not until 2015 that the ICD 10 was officially enforced all over the country. Psoriasis ICD 9 696.1 is the billable code used to indicate a diagnosis for ICD 9 psoriasis, generally covering all the types of the disease. The code can only be used for claims which have a date of service before 30 September 2015. From October 1, 2015, the ICD 9 was effectively replaced by the ICD 10 and was made mandatory to use the corresponding diagnostic codes from the new code set. Where the psoriasis ICD 9 had a single code to identify all cases of psoriasis, the ICD 10 delves into more details and includes separate codes for each of the types of psoriasis. Types of Psoriasis Psoriasis Vulgaris is the general term used to define the condition, which is further divided into various types depending on the appearance and location of the skin inflammation. The ICD 9 psoriasis Vulgaris corresponding code is 696.1 which is equivalent to L40.0 in the ICD 10. One of the most commonly occurring psoriasis, scalp psoriasis is characterized by inflammation on the forehead, the skin around the ears, and back of the neck, affecting the hairline as well. Psoriasis of scalp ICD 9 code is 696.1 which translates to L40.8 in the ICD 10 code set. Around 8 percent of the patients having psoriasis have a guttate type. Symptoms include inflamed round, red spots on the torso, legs, and arms. Pustular psoriasis is rarer than guttate, affecting around 3 percent of the patients living with psoriasis. It is characterized by white, pus-filled pustules surrounded by reddened or inflamed skin. Around 80 percent of psoriasis patients are affected by this type. Plaques or scales appear anywhere on the body, which can be painful and itchy. The scales vary from silvery white to more purple ones, depending on the skin type of the person. The diagnosis code for plaque psoriasis ICD 9 is the same i.e. 696.1 and converts to L40.0. Treating Psoriasis with Light Therapy In recent years, phototherapy or light therapy has emerged as one of the most cost-effective and safest methods to treat psoriasis and other dermatology-related conditions. Especially for mild cases of psoriasis, UVA and UVB light have been known to be effective in reducing the symptoms. Natural sunlight is also recommended by physicians for the treatment of psoriasis. Regular, controlled exposure to sunlight has been known to do wonders in some patients. However, some areas of the body such as hands and face may need to be protected from direct sun exposure. In addition, there are various other light sources that act as a substitute for sunlight, like photodynamic therapy and lasers. Some clinics have specially built light sources for UVA and UVB for the treatment. There is plenty of ongoing research on psoriasis, but there’s still much and more to learn. Given the sheer number of cases reported in the US alone of patients with this condition, it is necessary that the providers accurately document and code the treatment they provide. That will allow researchers to actually decipher what the underlying cause of psoriasis is. Medicare and private insurer audits are increasing as speak to check on the medical records and documentation concerning psoriasis. It is essential, therefore, to have accurate and detailed documentation to avoid any undue problems. Outsourcing the tedious task to an established medical billing and coding company such as UControl Billing can help ensure that the reporting and coding are carried out error-free for an optimal and timely reimbursement on all claims. A couple of years ago, I executed the effective plan of creating a Medical billing and Coding company named U Control Billing. The company aims to bring revolutionary advancements to foster medical billing and coding revenues. As an official member of HIA-LI and MGMA, I feel honored in providing networking opportunities, problem-solving, and improving the revenue management cycle.	4	7	0	0	0	6	0.904973	6	1,926

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