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9. Harmful in NYHA class II-IV heart failure a. Thiazolidinediones b. Calcium channel blockers (CCB): The nondihydropyridine calcium channel blockers have negative inotropic properties and are considered harmful in patients with a low ejection fraction and therefore are not recommended. Amlodipine is the only CCB that may be considered in the management of hypertension or ischemic heart disease in patients with heart failure as it has neutral effects on morbidity and mortality (Yancy et al., 2013). c. Nonsteroidal anti-inflammatory drugs (NSAIDs) and COX-2 inhibitors Box 58-1 Medication Management for Systolic Heart F ailure with Low e jection Fraction ( e F) (Continued) Table 58-1 ACE Inhibitors Drug Initial Dose ACE Inhibitors Captopril 6. 25 mg three times daily Enalapril 2. 5 mg twice daily Fosinopril 5-10 mg daily Lisinopril 2. 5-5 mg daily Perindopril 2 mg daily Quinapril 5 mg twice daily Ramipril 1. 25-2. 5 mg daily Trandolapril 1 mg daily Angiotensin Receptor Blockers Candesartan 4-8 mg daily Losartan 25-50 mg daily Valsartan 20-40 mg twice daily Aldosterone antagonists Spironolactone 12. 5-25 mg daily Eplerenone 25 mg daily Beta-blockers Bisoprolol 1. 25 mg daily Carvedilol 3. 125 mg twice daily Carvedilol CR 10 mg daily Metoprolol succinate extended-release 12. 5-25 mg daily Hydralazine and isosorbide dinitrate Fixed-dose combination 37. 5 mg hydralazine/20 mg isosorbide dinitrate three times daily Hydralazine and isosorbide dinitrate Hydralazine 25-50 mg, three or four times daily and isosorbide dinitrate 20-30 mg three or four times daily Adapted from Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Drazner, M. H., et al. (2013). 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Journal of the American College of Cardiology, 62(16), e147-e239. 572 CHAPTER 58 | Heart Failure
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hypertension (see Chapter 60, Hypertension, for the related guidelines) and myocardial ischemia as well as symptom management with the judi-cious use of diuretics. k. IC D device therapy is recommended as primary prevention for patients with DCM or ischemic heart disease; with an EF < 35% and NYHA class II or higher heart failure or with an EF < 30% and NYHA class I heart failure; or who are on guideline-directed therapy and are at risk of sudden cardiac death (Mc Murray et al., 2012). CRT is recommended for patients with EF < 35% after 3 months of optimal medi-cal therapy, in sinus rhythm with a QRS duration of 150 ms or greater, or with left bundle branch (LBBB) morphology (Yancy et al., 2013). l. E nd-of-life and palliative care i. C onsider for patients who have advanced persistent symptoms at rest despite pharma-cologic therapy ii. R ecurrent heart failure hospitalizations iii. P oor quality of life, including little or no ability to conduct activities of daily livingiv. N eed for continuous intravenous inotropic support v. F urther advanced heart failure therapy is not clinically indicated or is unwanted vi. C onsider hospice referral vii. Adv anced directives and durable power of attorney should be in place m. A ppropriate follow-up for interventions imple-mented or anticipated implementation. n. C ollaborate with prescribing providers regarding the ongoing treatment plan as well as elimination of the medications or treatments that cause or exacerbate heart failure. C. Client education and support 1. The p atient must be able to adhere to the treatment plan and have adequate resources to comply effectively with the regimen. Instituting the plan may take time. The patient and patient's support must have an understanding of the treatment regimen, disease progression and potential complications, which will require ongoing education. Anticipate barriers to the treatment plan as this may prevent future complications. Table 58-2 Loop Diuretics Drug Initial Dose Loop diuretics Bumetanide 0. 5-1 mg once or twice daily Furosemide 20-40 mg once or twice daily Torsemide 10-20 mg daily Thiazide diuretics Chlorothiazide 250-500 mg once or twice daily Chlorthalidone 12. 5-25 mg daily Hydrochlorothiazide 25 mg once or twice daily Indapamide 2. 5 mg daily Metolazone 2. 5 mg daily Aldosterone antagonists (potassium-sparing diuretics)Amiloride 5 mg daily Spironolactone 12. 5-25 mg daily Triamterene 50-75 mg twice daily Sequential nephron blockade Metolazone 2. 5-10 mg daily + loop diuretic Hydrochlorothiazide 25-100 mg once or twice daily + loop diuretic Chlorothiazide (IV) 500-1,000 mg daily + loop diuretic Adapted from Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Drazner, M. H., et al. (2013). 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Journal of the American College of Cardiology, 62(16), e147-e239. 573 Plan
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2. M ended Hearts (www. mendedhearts. org/) is an organization for individuals with heart disease. Patients must pay to join. They have group meetings, hospital visiting programs, an annual convention, educational resources, and various events. Patients can join a local chapter. re Ference S Bennett, M. K., Gilotra, N. A., Harrington, C., Rao, S., Dunn, J. M., Freitag, T. B., et al. (2013). Evaluation of the role of endomyocardial biopsy in 851 patients with unexplained heart failure from 2000-2009. Circulation. Heart Failure, 6(4), 676-684. Criteria Committee of the American Heart Association. (1994). Nomenclature and criteria for diagnosis of diseases of the heart and great vessels (9th ed. ). Boston, MA: Little Brown. Go, A. S., Mozaffarian, D., Roger, V. L., Benjamin, E. J., Berry, J. D., Blaha, M. J., et al. (2014). Heart disease and stroke statistics—2014 update: A report from the American Heart Association. Circulation, 129(3), e28-e292. Mc Murray, J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Bohm, M., Dickstein, K., et al. (2012). ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The task force for the diagnosis and treatment of acute and chronic heart failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. European Heart Journal, 33(14), 1787-1847. Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., et al. (2015). Heart disease and stroke statistics—2015 update: A report from the American Heart Association. Circulation, 131(4), e29-e322. National Center for Chronic Disease Prevention and Health Promotion, Division for Heart Disease and Stroke Prevention. (2013). Heart failure fact sheet. Retrieved from www. cdc. gov/DHDSP/data_statistics/fact _sheets/fs_heart_failure. htm National Clinical Guideline Centre (UK). (2014). Acute heat failure: diagnosis and management. Retrieved at http://www. nice. org. uk /guidance/cg187 Patel, M. R., White, R. D., Abbara, S., Bluemke, D. A., Herfkens, R. J., Picard, M., et al. (2013). 2013 ACCF/ACR/ASE/ASNC/SCCT/SCMR appropriate utilization of cardiovascular imaging in heart failure: A joint report of the American College of Radiology appropri-ateness criteria committee and the American College of Cardiology Foundation appropriate use criteria task force. Journal of the American College of Cardiology, 61(21), 2207-2231. T ang, W. H. W., & Francis, G. S. (2010). The year in heart failure. Journal of the American College of Cardiology, 55(7), 688. Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Drazner, M. H., et al. (2013). 2013 ACCF/AHA guideline for the manage-ment of heart failure: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Journal of the American College of Cardiology, 62(16), e147-e239. 2. I t is also important to provide both verbal and written information to the patient and his or her support system. This information should include but is not limited to heart failure education, symptoms, prognosis, complications, and disease management. The patient should be referred to social services in order to ensure that a full spectrum of resources is available. Social services are useful in providing emotional support for both the patient and support system to improve coping skills and provide any additional financial resources. VI. Self-management r esources and tools A. Patient education 1. A merican Heart Association (www. heart. org /HEARTORG/Conditions/Heart Failure/Heart -Failure_UCM_002019_Sub Home Page. jsp). The Amer-ican Heart Association has print and online education materials and online videos. Websites are available in Spanish, Chinese, Vietnamese, and English. 2. C enters for Disease Control and Prevention (www. cdc. gov/heartdisease/materials_for_patients. htm). 3. M edline Plus from the National Library of Medicine and National Institutes of Health (www. nlm. nih. gov /medlineplus/heartfailure. html). Provides an inter-active tutorial in English and Spanish and extensive resources for aspects of the disease. 4. H eart Failure Matters (www. heartfailurematters . org/en_GB). This is an interactive, multilingual, educational website containing animations, videos, and tools for patients with heart failure. It is available in English, French, German, and Spanish. It has a family and caregiver section and links to a variety of other related websites. 5. H eart Failure. org (www. heartfailure. org/). Provides online education as well as additional links to other resources. 6. M ega Heart. com (http://megaheart. com/). Provides recipes and dietary support and recommendations. B. Community support groups 1. The A merican Heart Association offers a variety of community events and support groups for individuals with heart disease. 574 CHAPTER 58 | Heart Failure
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is increasing (Langenberg, Corey, Ashley, Leong, & Straus, 1999; Xu et al., 2006). A total of 20-25% of the adult population has serologic evidence of HSV-2 infection (Fleming et al., 1997). Subclinical viral shedding is common in the first few years after the primary HSV infection and then becomes less frequent—from 25% of days in the first year after infection to 4% of days in later years. The majority of genital infections are acquired during contact with persons unaware that they have the infection and who are asymptomatic when transmission occurs. In addition, individuals may not attribute symp-toms such as vulvar rashes, irritation, or fissures with genital herpes ulcers. Thus, subclinical viral shedding and unrecognized mild symptoms are key factors in both horizontal (to a partner) and vertical (mother to newborn) transmission (Schillinger et al., 2008). HSV-2 infection is an important risk factor for both HIV acquisition (T odd et al., 2006) and trans-mission. Persons with dual HIV and HSV infec-tions are more likely to shed both viruses from open herpes ulcers caused by HSV-2, offering an explana-tion for the increased risk of HIV transmission from individuals with HSV-2 infections (Schacker et al., 1998). Conversely, the likelihood of horizontal acqui-sition of HIV infection significantly increases from twofold to three-or fourfold in persons with HSV infection, as a result of open herpes lesions coming into contact with the bodily fluids of an HIV infected partner (Freeman et al., 2006). Neonatal infection with HSV is associated with high neonatal morbidity and mortality. The risk for transmission to the neonate from an infected mother is high (30-50%) among women who acquire genital herpes near the time of delivery and low (< 1%) among women with prenatal histories of recurrent herpes or who acquire genital HSV during the first half of pregnancy (CDC, 2015). Most pregnant women with a history of recurrent genital I. Intr oduction and general background Herpes simplex is a DNA virus belonging to the herpes virus group. The virus causes a recurring vesicular eruption to the skin or mucus membrane surfaces that have a prior contact exposure. Similar to other herpes viruses, after initial infection, a latent state is established that can be followed by reactivation of the virus and recurrent local disease. Herpes simplex virus (HSV) infection is lifelong. The course of disease, however, varies among individuals from asymptomatic to recurrent clinical presentations. Management of genital HSV should address the chronic nature of the disease rather than focusing solely on treatment of acute episodes of genital lesions (Centers for Disease Control and Prevention [CDC], 2015). A. Types of HSV 1. HS V-1 HSV-1 is responsible for most of the infections in the face and upper body. Oral and perioral lesions, often referred to by the public as “cold sores” or “fever blisters,” are common presentations. HSV-1 can infect mucus membranes or abraded skin at any site including the eye, the genitals, and nongenital skin. Serious manifestations of HSV disease, such as encephalitis and meningitis, are rare in the immu-nocompetent patient. HSV is a common infection worldwide. Each year in the United States, there are approximately 500,000 primary infections (Scott, Coulter, & Lamey, 1997). HSV-1 is commonly transmitted in childhood with 90% of individuals seropositive for HSV-1 by the fourth decade of life (Buddingh, Schrum, & Lanier, 1953; Corey, 1986). 2. HS V-2 HSV-2 is responsible for most genital skin infections. Most cases of recurrent genital herpes are caused by HSV-2, although seroprevalence trends show that the percentage of genital herpes caused by HSV-1 Hattie C. Grundland and Geraldine Collins-Bride Herpes s Implex Infe Ct Ions© Eliks/Shutterstock; © donatas1205/Shutterstock 575 59Chapt Er
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B. Clinical presentations: primary, nonprimary first-episode, and recurrent HSV 1. P rimary infection This is the first clinical episode of genital herpes in an individual without antibodies to HSV-1 or HSV-2. Primary infection can be severe with painful genital ulcers and systemic symptoms, such as fever, myal-gias, malaise, and tender inguinal lymphadenopathy. Lesions classically appear as vesicles or pustules that open in 12-24 hours to form shallow ulcers. Symptoms usually occur within a few weeks after infection and resolve within 2 weeks (Figure 59-1). Complications of HSV infection are more likely in primary infection and can include aseptic meningitis, sacral autonomic nervous system dysfunction, and disseminated lesions (Corey, Adams, Brown, & Holmes, 1983). 2. N onprimary first-episode infection This is the first clinical episode of herpes in an individual with serologic evidence of prior infection with either HSV-1 or HSV-2. The clinical presentation usually is less severe compared to primary infection with fewer local lesions, mild to no systemic symp-toms, and shorter duration of symptoms (Corey et al., 1983; Kimberlin & Rouse, 2004). 3. R ecurrent infection Recurrent clinical episodes of herpes typically are less severe than primary and nonprimary first herpes can deliver their infants vaginally with a risk of neonatal transmission of less than 1% (Prober et al., 1987). According to the 2015 CDC sexually transmitted disease treatment guidelines, women without known genital herpes should be counseled to abstain from vaginal intercourse during the third trimester with partners known or suspected of having genital herpes. In addition, pregnant women without known orolabial herpes should be advised to abstain from receptive oral sex during the third trimester with partners known or suspected to have orolabial herpes. In women with active genital lesions at the time of delivery, a cesarean section delivery is recommended. There is limited evidence that the use of routine serologic screening for HSV-2 or prophylactic antiviral therapy given in the third trimester in women with a history of recurrent HSV decreases neonatal herpes infection, and therefore neither intervention is recommended (CDC, 2015; U. S. Preventive Services T ask Force, 2014). However, suppressive acyclovir treatment late in pregnancy reduces the frequency of cesarean delivery among women who have recurrent genital herpes by diminishing the frequency of recur-rences at term (Scott et al., 2002; Sheffield, Hollier, Hill, Stuart, & Wendel, 2003). T reatment may not protect against transmission to neonates in all cases (Pinninti et al., 2012).-6-4-2 02 Sexual contact Lesions noted Physician contacted Duration viral shedding Vesicle pustule Symptoms Wet ulcer Healing ulcer-crust New lesion formation common Lesions start to heal Symptoms gone unless lesions irritated Lesions healed46 81 01 21 41 61 82 0Days Systemic sympto ms Local sympto ms Figure 59-1 Clinical Course of Primary Genital Herpes Simplex Virus Infection Reproduced from Corey, L., Adams, H. G., Brown, Z. A., & Holmes, K. K. (1983). Genital herpes simplex virus infections: Clinical manifestations, course, and complications. Annals of Internal Medicine, 98(6), 958-972. Reprinted with permission. 576 CHAPTER 59 | Herpes Simplex Infections
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3. S ymptomatology a. F ever, headache, malaise, myalgias, and tender lymph nodes b. B urning pain, tingling, hyperesthesia, or itching of involved skin and mucous membranes defines the prodromal symptoms of recurrent infection preceding outbreak of lesions by a few hours to up to 2 days. c. D epending on the site of infection i. Ge nital lesions: dysuria, urinary retention, sacral or genital paresthesias, rectal tenes-mus, and constipation ii. Or al lesions: facial paresthesias, mouth pain (gingivostomatitis), difficulty eating, and visual disturbances or pain d. N o symptoms B. Objective 1. V ital signs: fever infrequent, most common in primary infection or with secondary complications, such as aseptic meningitis 2. S kin: tender, single, or clustered vesicles, pustules, or ulcers on a clean erythematous base. Ulcers may appear crusted over in the period before resolution. Lesions most frequently occur in or around the mouth, on the vulva, on penile glans or shaft, or perianally. May occur on distal fingers (herpetic whitlow), especially of healthcare workers. 3. E ye: unilateral conjunctivitis, blepharitis with vesicles on the lid margin, keratitis with dendritic lesions, or with punctuate opacities on ophthalmic examination 4. M outh: small ulcers located on the soft palate, buccal mucosa, tongue, or floor of the mouth 5. L ymph: may have tender, nonfluctuant regional lymphadenopathy, especially in primary outbreaks. 6. Ge nitourinary: may see urethral, vaginal, or rectal discharge depending on severity of involvement. If rectal involvement, on anoscopy may see either ulcerations (not distinct lesions) and/or swollen inflamed mucosa. III. Assessment A. Determine the diagnosis 1. Pr imary 2. N onprimary first episode 3. R ecurrent 4. A symptomatic 5. Othe r conditions that may explain the patient's presentation:episodes. Systemic symptoms are uncommon. Time of healing of local ulcers and duration of viral shed-ding is shorter (Wald, Zeh, Selke, Ashley, & Corey, 1995). T riggers that may cause recurrent disease include acute illness, stress, sunlight, fatigue, men-strual periods, and unknown factors. Fifty percent of patients with recurrent episodes experience prodro-mal symptoms, such as sensitivity to touch (hyperes-thesia), local tingling or itching, and peripheral nerve pain (Kimberlin & Rouse, 2004). A smaller number of patients develop frequent recurrence of HSV out-breaks that can cause both physical and emotional distress. For individuals who experience six or more outbreaks yearly, suppressive antiviral therapy should be offered (CDC, 2015). Although the medical com-plications from recurrent infection are uncommon, the psychosocial and psychosexual impact can cause significant distress for patients. 4. A symptomatic infection In asymptomatic infections, an individual has serum antibodies yet there is no history of clinical outbreaks. Unrecognized mild symptoms of HSV-2 are com-mon, however, and may account for nearly two-thirds of individuals with what appears to be asymptomatic infections (CDC, 2015). II. Database A. Subjective 1. P ast medical history and situational factors (may include but are not limited to) a. H istory of similar ulcer eruption (i. e., location of lesion and duration of the outbreaks). Note results of culture if done previously. b. H istory of contact exposure to individual with known HSV infection c. H istory of stimulus known to trigger eruption: sunlight, menses, fever, other illnesses, stress, and increased sexual activity d. H istory of rash, eczema, and erythema multiforme e. H istory of immunocompromise: HIV/AIDS, leukemia, lymphoma, other malignancies, auto-immune diseases, and posttransplant patients f. H istory of sexual practices, including oral-genital contact g. C urrently pregnant 2. O ccupational history a. E xposure history b. T ype of profession (e. g., healthcare worker and dentist [herpetic whitlow]) c. C ontacts and personal protection577 Assessment
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a. I nfectious genital ulcer diseases: syphilis, chan-croid, lymphogranuloma venereum, or granu-loma inguinale b. N oninfectious genital ulcers: Behçet syndrome, Crohn's disease, or fixed drug eruption c. M ucopurulent cervical discharge: chlamydia, gonorrhea, or mycoplasmas d. V ulvar rashes: allergic contact dermatitis (especially poison oak or poison ivy vulvitis), impetigo, psoriasis e. Or olabial ulcers: aphthous stomatitis f. H erpes zoster g. Othe r etiologies of proctitis B. Severity Assess the severity of the infection including diagnosis of complications: 1. U rine retention resulting from bladder neck spasm 2. P roctitis, particularly in men who have sex with men (Klausner, Kohn, & Kent, 2003) 3. C onstipation 4. Di fficulty eating solid foods 5. S econdary bacterial infections caused by streptococci or staphylococci 6. E rythema multiforme 7. H erpes keratitis 8. Di sseminated herpes 9. A septic meningitis 10. N eonatal herpes 11. E motional stress and psychological morbidity especially seen with recurrent genital HSV IV. Goals of clinical management A. Choose a cost-effective approach for diagnosing HSV infection B. Select a treatment plan that addresses the patient's symptom severity, frequency of recurrence, transmission risk to uninfected partner, and cost C. Select an approach that maximizes patient adherence D. Provide an education plan that empowers patients to cope with a chronic, recurrent sexually transmitted disease through self-management resources V. p lan A. Screening The American Academy of Family Physicians and the U. S. Preventive Services T ask Force (USPSTF) recom-mend against routine serologic screening for the general population and for pregnant women to prevent neonatal HSV infections. Counseling around the risks and benefits of serologic screening should be discussed and offered to select groups of patients including patients who may have HSV-infected sex partners and HIV-positive patients (American Academy of Family Physicians, 2009; USPSTF, 2014). HSV serologic testing should be considered for persons presenting for evaluation of sexually transmitted infections (STIs), especially for those persons with mul-tiple sex partners; persons with HIV infection; and men who have sex with men (MSM) at increased risk for HIV acquisition (CDC, 2015). B. Diagnostic tests 1. HS V viral culture if active lesions are present. The gold standard for diagnosis of HSV if an active lesion is present. Viral culture is highly specific (> 99%) but sensitivity depends on the stage of the lesion. Sensitivity is highest (90%) when lesion vesicles are unroofed and the base of an ulcer can be sampled. As lesions start to heal, the culture sen-sitivity decreases rapidly (sensitivity at ulcer stage = 70% and crust stage = 30%) (Corey et al., 1983). Determination of the HSV-type of infection predicts recurrence risk (50% with HSV-2, 10% with HSV-1) but otherwise is not necessary or helpful. 2. HS V polymerase chain reaction (PCR). PCR is highly sensitive but at significantly increased cost. PCR is now approved by the Food and Drug Administration for testing of anogenital specimens but cost prohibits this method of testing in the major-ity of clinical settings. PCR should be used to detect HSV in spinal fluid in cases where central nervous system infection is suspected. 3. C ytology (Pap or Tzanck). Is no longer recommended due to low sensitivity and specificity. 4. T ype-specific herpes virus serology. Antibodies to HSV-1 and HSV-2 can be detected any-where from 3 weeks to 3 months after infection and remain indefinitely. T esting may be clinically useful in the following cases:a. T o rule out HSV diagnosis if the serology is negative at least 6 weeks after the onset of the outbreak578 CHAPTER 59 | Herpes Simplex Infections
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b. T o determine primary herpes infection if patient is seronegative during initial symptoms then converts to seropositive after 6 weeks from the onset of the outbreak c. I n asymptomatic patients who have a sex partner with genital herpes d. F or patients at increased risk for STIs (i. e., multi-ple sex partners, HIV infection, and among MSM at increased risk for HIV acquisition) who request comprehensive STI screening (CDC, 2015) 5. Di agnostic tests as necessary to rule out etiologies other than HSV infection include syphilis serology to rule out primary or secondary syphilis. 6. H IV screening should be offered to all patients. C. Management 1. P reventive a. A void contact with persons with a known or sus-pected active herpes lesion b. U se of condoms, gloves, or other barrier methods c. A void or decrease exposure to known recurrence triggers d. A ntiviral medications used to treat or suppress recurrent outbreaks or prophylactic therapy of an infected person to prevent horizontal trans-mission to an uninfected partner (T able 59-1) 2. S ymptomatic a. S itz bath or cool compresses b. T opical anesthetic or viscous lidocaine as needed Table 59-1 Drug T reatment of Herpes Simplex Infections Hs V tr eatment type Drug Dosage n otes Oral HSV primary Acyclovir* 200 mg orally five times daily or 400 mg orally three times daily for 7-10 days Begin treatment early in infection Oral HSVEpisodic treatment for recurrent symptoms Acyclovir 200 mg orally five times daily for 10 days Treatment for recurrent oral herpes offers mild benefit. Topical antiviral medications are not recommended due to limited clinical benefit (i. e., docosanol 10%, penciclovir 1%, acyclovir 5%). Genital HSV primary Acycloviror400 mg orally three times a day for 7-10 daysor200 mg orally five times a day for 7-10 days Extending treatment is an option if healing is incomplete after 10 days of therapy Famcicloviror250 mg orally three times a day for 7-10 days Valacyclovir 1 g orally twice a day for 7-10 days Genital HSVEpisodic therapy for recurrent symptoms Acycloviror400 mg orally three times a day for 5 days or800 mg orally twice a day for 5 daysor800 mg orally three times a day for 2 days Begin treatment at first sign of infection; an option for patients with mild or infrequent recurrent symptoms (< 6 outbreaks per year) Immuncocompromised patients can have longer duration and more severe symptoms. Consider increasing the doses of antiviral drugs to improve clinical healing in immunocompromised patients Famcicloviror125 mg orally twice daily for 5 daysor1,000 mg orally twice daily for 1 dayor500 mg once, followed by 250 mg twice daily for 2 days Valacyclovir 500 mg orally twice a day for 3 days or 1 g orally once a day for 5 days (continues)579 Plan
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(Continued) c. A nticonstipating diet or stool softeners as needed d. N onsteroidal anti-inflammatory medications to reduce pain e. A ntiviral medications for primary or recurrent outbreaks (T able 59-1) 3. C riteria for consultation or specialty referral a. Ge neralized involvement b. A ny complications present c. P regnancy 4. F ollow-up a. A s medically indicated for patients with primary herpes, depending on the severity of the infectionb. N ot medically necessary for follow-up with infrequent recurrent outbreaks, although some patients may require follow-up visits to focus on counseling and education c. P atients on suppressive therapy should be reeval-uated every 12 months D. Patient education 1. Go al: Educate on the clinical course of the disease, emphasizing risk factors for HSV transmission. Address concerns and feelings to help patients cope with herpes as a chronic disease. Recommended counseling topics listed in the 2015 CDC STD T reatment Guidelines can be found in Figure 59-2. Table 59-1 Drug T reatment of Herpes Simplex Infections Hs V tr eatment type Drug Dosage n otes Genital HSV Suppressive therapy Acycloviror400 mg orally twice a day An option for patients with more frequent or severe symptoms (> 6 outbreaks per year) Shown to decrease transmission in discordant couples with HSV-2 Patients and their partners should be counseled that suppressive therapy reduces but does not eradicate viral shedding. Famciclovir or250 mg orally twice a day Valacyclovir 500 mg orally once a day or1 g orally once a day (for episodes ≥ 10 per year) HSV treatment in patients with HIV For guidelines on HSV treatment in people with HIV, see Chapter 66, Primary Care of HIV-Infected Adults* *Intravenous acyclovir therapy should be provided for patients who have severe primary HSV disease or complications that necessitate hospitalization (e. g., disseminated infection, pneumonitis, or hepatitis) or central nervous system complications (e. g., meningitis or encephalitis). The r ecommended regimen is acyclovir, 5-10 mg/kg body weight intravenously every 8 hours for 2-7 days or until clinical improvement is observed, followed by oral antiviral therapy to complete at least 10 days of total therapy. Data from Centers for Disease Control and Prevention. (2015). 2015 sexually transmitted diseases: Treatment guidelines. Retrieved from http://www . cdc. gov/std/tg2015/herpes. htm. f IGure 59-2 Genital H s V Counseling topics The following topics should be discussed when counseling persons with genital HSV infection: the natural history of the disease, with emphasis on the potential for recurrent episodes, asymptomatic viral shedding, and the attendant risks of sexual transmission the ef fectiveness of suppressive therapy for persons experiencing a first episode of genital herpes in preventing symptomatic recurrent episodes use of episodic therapy to shorten the duration of recurrent episodes importance of informing current sex partners about genital herpes and informing future partners before initiating a sexual relationship580 CHAPTER 59 | Herpes Simplex Infections
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VI. s elf-management resources and tools A. Patient education 1. B asic fact sheet address frequently asked questions by patients about HSV infection can be printed from the Centers for Disease Control and Prevention: www. cdc. gov/std/herpes/stdfact-herpes. htm. 2. H erpes Resource Center American Sexual Health Association (1-800-230-6039; http://ashastd. org) 3. N ational Institute of Allergy and Infectious Disease (http://niaid. nih. gov) B. Community support groups 1. The Herpes Resource Center has an affiliated network of local support (HELP) group for people concerned about herpes simplex virus. The network of support groups can be accessed on the American Sexual Health Association website (http://ashastd. org). referen Ces American Academy of Family Physicians. (2009). Summary of AAFP recommendations for clinical preventive services. Retrieved from http:// www. aafp. org/online/en/home/clinical/clinicalrecs. html. Baeten, J. M., Donnell, D., Ndase, P., Mugo, N. R., Campbell, J. D., Wangisi, J., et al. (2012). Antiretroviral prophylaxis for HIV prevention in heterosexual men and women. New England Journal of Medicine, 367, 399-410. Buddingh, G. J., Schrum, D. I., & Lanier, J. C. (1953). Studies of the natural history of herpes simplex infections. Pediatrics, 11(6), 595-610. Centers for Disease Control and Prevention. (2015). 2015 sexually transmitted diseases: Treatment Guidelines. Retrieved from www. cdc. gov /std/tg2015/herpes. htm/. Corey, L. (1986). Genital herpes. In A. Nahmias & B. Roizman (Eds. ), The herpes viruses (pp. 1-35). New Y ork: Plenum Press. Corey, L., Adams, H. G., Brown, Z. A., & Holmes, K. K. (1983). Genital herpes simplex virus infections: Clinical manifestations, course and complications. Annals of Internal Medicine, 98(6), 958-972. potential for sexual transmission of HSV to occur during asymptomatic periods (asymptomatic viral shedding is more frequent in genital HSV-2 infection than genital HSV-1 infection and is most frequent during the first 12 months after acquiring HSV-2) importance of abstaining from sexual activity with uninfected partners when lesions or prodromal symptoms are present ef fectiveness of daily use of valacyclovir in reducing risk for transmission of HSV-2, and the lack of effectiveness of episodic or suppressive therapy in persons with HIV and HSV infection in reducing risk for transmission to partners who might be at risk for HSV-2 acquisition ef fectiveness of male latex condoms, which when used consistently and correctly can reduce (but not eliminate) the risk for genital herpes transmission (Martin et al.,2009) HSV infection in the absence of symptoms (type-specific serologic testing of the asymptomatic partners of persons with genital herpes is recommended to determine whether such partners are already HSV seropositive or whether risk for acquiring HSV exists) risk for neonatal HSV infection increased risk for HIV acquisition among HSV-2 seropositive persons who are exposed to HIV (suppressive antiviral therapy does not reduce the increased risk for HIV acquisition associated with HSV-2 infection) (Baeten et al., 2012) Asymptomatic persons who receive a diagnosis of HSV-2 infection by type-specific serologic testing should receive the same counseling messages as persons with symptomatic infection. In addition, such persons should be educated about the clinical manifestations of genital herpes. Pregnant women and women of childbearing age who have genital herpes should inform the providers who care for them during pregnancy and those who will care for their newborn infant about their infection. Reproduced from Centers for Disease Control and Prevention. (2015). 2015 sexually transmitted diseases: Treatment guidelines. Retrieved from http://www. cdc. gov/std/tg2015/herpes. htm. f IGure 59-2 Genital H s V Counseling topics (Continued)581 References
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Fleming, D. T., Mc Quillan, G. M., Johnson, R. E., Nahmias, A. J., Aral, S. O., Lee, F. K., et al. (1997). Herpes simplex virus type 2 in the United States, 1976 to 1994. New England Journal of Medicine, 337(16), 1105-1111. Freeman, E. E., Weiss, H. A., Glynn, J. R., Cross, P. L., Whitworth, J. A., & Hayes, R. J. (2006). Herpes simplex virus 2 increases HIV acquisition in men and women: A systematic review and meta-analysis of longitudinal studies. AIDS, 20, 73-83. Kimberlin, D. W., & Rouse, D. J. (2004). Clinical practice. Genital herpes. New England Journal of Medicine, 350(19), 1970-1977. Klausner, J. D., Kohn, R., & Kent, C. (2003). Etiology of clinical proctitis among men who have sex with men. Clinical Infectious Disease, 38(2), 300-302. Langenberg, A. G., Corey, L., Ashley, R. L., Leong, W. P., & Straus, S. E. (1999). A prospective study of new infections with herpes simplex virus type 1 and type 2. Chiron HSV Vaccine Study Group. New England Journal of Medicine, 341(19), 1432-1438. Martin, E. T., Krantz, E., Gottlieb, S. L., Magaret, A. S., Langenberg, A., Stanberry, L., et al. (2009). A pooled analysis of the effect of condoms in preventing HSV-2 acquisition. Archives of Internal Medicine, 169, 1233-1240. Pinninti, S. G., Angara, R., Feja, K. N., Kimberlin, D. W., Leach, C. T., Conrad, D. A., et al. (2012). Neonatal herpes disease following maternal antenatal antiviral suppressive therapy: a multicenter case series. Journal of Pediatrics, 161, 134-138. Prober, C. G., Sullender, W. M., Yasukawa, L. L., Au, D. S., Y eager, A. S., & Arvin, A. M. (1987). Low risk of herpes simplex virus infections in neonates exposed to the virus at the time of vaginal delivery to mothers with recurrent genital herpes simplex virus infections. New England Journal of Medicine, 316, 240-244. Schacker, T., Ryncarz, A. J., Goddard, J., Diem, K., Shaughnessy, M., & Corey, L. (1998). Frequent recovery of HIV-1 from genital herpes simplex virus lesions in HIV-1-infected men. JAMA, 280(1), 61-66. Schillinger, J. A., Mc Kinney, C. M., Garg, R., Gwynn, R. C., White, K., Lee, F., et al. (2008). Seroprevalence of herpes simplex virus type 2 and characteristics associated with undiagnosed infection. Sexually Transmitted Disease, 35(6), 599-606. Scott, D. A., Coulter, W. A., & Lamey, P. J. (1997). Oral shedding of herpes simplex virus type 1: A review. Journal of Oral Pathology Medicine, 26(10), 441-447. Scott, L. L., Hollier, L. M., Mc Intire, D., Sanchez, P. J., Jackson, G. L., & Wendel, G. D., Jr. (2002). Acyclovir suppression to prevent recurrent genital herpes at delivery. Infectious Diseases in Obstetrics and Gynecology, 10, 71-77. Sheffield, J. S., Hollier, L. M., Hill, J. B., Stuart, G. S., & Wendel, G. D. (2003). Acyclovir prophylaxis to prevent herpes simplex virus recurrence at delivery: A systematic review. Obstetrics & Gynecology, 102, 1396-1403. T odd, J., Grosskurth, H., Changalucha, J., Obasi, A., Mosha, F., & Balira, R. (2006). Risk factors influencing HIV infection incidence in a rural African population: A nested case-control study. Journal of Infectious Disease, 193(3), 458-466. U. S. Preventive Services T ask Force. (2014). Guide to clinical preventive services. Retrieved from http://www. ahrq. gov/clinic/pocketgd1011 /gcp10s1. htm. Wald, A., Zeh, J., Selke, S., Ashley, R. L., & Corey, L. (1995). Virologic characteristics of subclinical and symptomatic genital herpes infections. New England Journal of Medicine, 333(12), 770-775. Xu, F., Sternberg, M. R., Kottiri, B. J., Mc Quillan, G. M., Lee, F. K., & Nahmias, A. J. (2006). T rends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA, 296(8), 964-973. 582 CHAPTER 59 | Herpes Simplex Infections
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Hypertension is a continuous and independent risk factor for cardiovascular disease, and the presence of addi-tional risk factors (elevated total cholesterol, high-density lipoprotein cholesterol < 35, smoking, diabetes, and left ven-tricular hypertrophy as the most significant) compounds the risk from HTN. Elevated systolic BP (SBP) and diastolic BP (DBP) are each considered important risk factors. Diastolic HTN is a stronger cardiovascular risk factor and more common before the age of 50 than systolic HTN. However, systolic HTN is more common after the age of 50 than diastolic HTN. Diastolic BP may actually decrease whereas systolic blood pressure increases with aging. This is most likely due to the progressive stiffening of the arte-rial circulation that occurs with aging (Weber et al., 2014). C. Classification and Treatment Goal Recommendations In 2004, the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and T reatment of High Blood Pressure ( JNC 7) categorized BP as follows: (1) normal, (2) pre-HTN, (3) HTN stage 1, and (4) HTN stage 2 (T able 60-1). The designation of “pre-HTN” is meant to identify those individuals at high risk of developing frank HTN who may benefit from adapt-ing lifestyle modifications that either lower BP or slow the rate of progression ( JNC 7, 2004). This stage should not be viewed as a disease category, but rather as a warning and an incentive for care providers to strongly counsel these individuals regarding lifestyle modifications. These indi-viduals are not candidates for medication treatment unless they also have diabetes or kidney disease (U. S. Department of Health and Human Services [USDHHS], 2004). The eighth JNC report in 2014 specifically focused on evidence to support the need to initiate antihyper-tensive pharmacologic therapy at specific BP thresh-olds (see T able 60-1) and whether there is evidence to support adjusting pharmacologic treatment to specified BP goals ( James et al., 2014). The panel members also changed general recommendations on how aggressively to treat older adults (over age 60) based on their extensive I. Intr oduction and definition Hypertension is one of the most common conditions seen in primary care and is also considered one of the most significant preventable causes of disease and death, primarily because of its association with heart disease, stroke, and renal fail-ure ( James et al., 2014). Most patients with hypertension have additional risk factors, including dyslipidemias, glucose intolerance or diabetes, a family history of early cardiovascular events, obesity, and/or cigarette smoking (Weber et al., 2014). Unfortunately, successful treatment of hypertension has been poor overall, and in some communities, fewer than 50% of all hypertensive patients have adequately controlled blood pressure (Weber et al., 2014). A. Prevalence The National Health and Nutrition Examination Survey (NHANES) (Nwankwo, Y oon, Bury, & Gu, 2013) reported the prevalence of hypertension (HTN) in 2011-2012 among U. S. adults aged 18 and over was approximately 30% with similar distribution across races and sexes. The prevalence does increase with age and is highest among older adults and is highest among non-Hispanic black adults at 42%. The World Health Organization (WHO, 2013) considers HTN to be the main attributable risk factor for death worldwide. According to a 2013 WHO report, HTN is responsible for at least 45% of worldwide deaths due to heart disease and over 50% of deaths due to stroke. The number of adults with a diagnosis of HTN rose from 60 million in 1980 to over a billion in 2008. The prevalence of hypertension is greatest in middle-and low-income countries with larger populations and poorer access to health care (WHO, 2013). B. Definition Hypertension is an elevation in arterial blood pressure (BP) confirmed when the average of two or more (seated) readings done at two or more office visits is greater than 140 systolic or 90 diastolic. Judith Sweet and Steve Protzel Hy Perten SIon© Eliks/Shutterstock; © donatas1205/Shutterstock 58360Chapt Er
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review of the evidence accumulated since JNC 7 in 2004 ( James et al., 2014). However, there was disagreement among members of the JNC 8 and overall controversy among experts about the recommendations made for older adults, specifically from the American Society of Hypertension (ASH) and the International Society for Hypertension (ISH) (Ram, 2014). The following recommendations were made by JNC 8 panel members regarding when to initiate pharmacologic treatment ( James et al., 2014): 1. I n the general population ≥ age 60, initiate medication treatment at SBP ≥ 150 mm Hg or DBP ≥ 90 mm Hg and treat to a goal of SBP < 150 and DBP < 90. a. ( corollary to #1): If pharmacologic treatment for persons ≥ 60 years old lowers BP to less than 150/90 and the treatment is well tolerated without adverse effects, the treatment does not need to be adjusted. 2. I n the general population < 60, begin medication at DBP ≥ 90 and treat to a goal < 90. 3. I n the general population < 60, begin medication to lower BP at SBP ≥ 140 with a goal of SBP < 140. 4. I n the population ≥ 18 years old with diabetes, initiate medication at SBP ≥ 140 or DBP ≥ 90 and treat to a goal of SBP < 140 and/or DBP < 90. 5. I n the population > 18 with chronic kidney disease (CKD), begin pharmacologic therapy at SBP ≥ 140 or DBP ≥ 90 and treat to a goal of SBP < 140 and/or DBP < 90. 6. The ASH/ISH guidelines differ from these recom-mendations in recommending treating all adults 18-79 at a BP ≥ 140/90. For adults age ≥ 80 years old, the ASH/ISH guidelines recommend that treatment should start at BP of ≥ 150/90 or ≥ 140/90 if diabetic or with renal disease, respectively. II. Database (may include but is not limited to) A. Subjective 1. M ost patients are asymptomatic. a. A lthough most patients are asymptomatic, some may experience headaches, dizziness, blurred vision, tinnitus, chest pain, shortness of breath, nausea, vomiting, extremity swelling, or anxiety, which may be unrelated to actual elevated blood pressure or be caused by end-organ damage. 2. The fo llowing symptoms suggest secondary causes for HTN. a. M uscle cramps, polyuria, weakness, and exces-sive thirst: primary aldosteronism (rare) b. H eadache, pallor, palpitations, sweating, and flushing: pheochromocytoma (very rare) c. H irsutism, easy bruising, and symptoms of diabetes mellitus: Cushing's syndrome (rare) d. S evere chest pain radiating to back: aortic dissection or aneurysm (common)Table 60-1 A Comparison Between JNC-7 and JNC-8 Blood Pressure (BP) Definitions Jn C-7 defines by BP classification J n C-8 defines by BP treatment threshold BP Classification Systolic BP mm Hg Diastolic BP mm Hg Population Systolic BP mm Hg tr eatment t hreshold Diastolic BP mm Hg tr eatment t hreshold Normal < 120 and < 80 General population aged ≥ 60 years≥ 150 ≥ 90 Prehypertension 120-139 or 80-89 General population 18-60 years≥ 140 ≥ 90 Stage 1 hypertension140-159 or 90-99 In the population aged ≥18 years with chronic kidney disease≥ 140 ≥ 90 Stage 2 hypertension≥ 160 or ≥100 In the population aged ≥18 years with diabetes≥ 140 ≥ 90 Data from James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J., et al. (2014). 2014 evidence-based guidelines for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA, 311(5), 507-520. doi: 10. 1001/jama. 2013. 284427. 584 CHAPTER 60 | Hypertension
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e. C laudication: coarctation of aorta (rare to be found late in life) f. S noring and daytime fatigue: sleep apnea (common) g. P alpitations, insomnia, anxiety, and weight loss: hyperthyroidism (common) (see Chapter 66 on thyroid disorders for details) 3. S ymptoms suggestive of target organ damage a. E xertional chest pain, shortness of breath, orthopnea, peripheral edema, and paroxysmal nocturnal dyspnea: coronary artery disease or heart failure b. F atigue, pruritus, or peripheral edema: renal failure c. S yncopal episodes or dizziness, memory loss, motor weakness, speech difficulties, or other focal neurologic findings: cerebrovascular disease d. C laudication and sudden loss of vision: periph-eral arterial disease 4. P ast health history a. H istory and work-up of HTN (When was patient first told he or she has high BP?); course of treatment and complications including medi-cations tried and failed or with adverse effects. b. Di abetes, lipid abnormalities, gout, cardiovascular and cerebrovascular disease, and renal disease. c. U se of prescribed or over-the-counter drugs and street drugs that may influence BP or interfere with the effectiveness of an antihypertensive drug (e. g., hormonal contraceptives, steroids, nonste-roidal anti-inflammatory drugs, alcohol, cocaine, amphetamines, appetite suppressants or other “diet” supplements, tricyclic antidepressants, monoamine oxidase inhibitors, or decongestants [pseudoephedrine and phenylpropanolomines or analogues]) (T able 60-2). d. Die tary supplement use including products containing “herbal ecstasy,” ma huang/ephedra, ergot-containing products, and St. John's wort. e. I f overweight, note history of weight gain. 5. F amily history: history of HTN, stroke, sudden cardiac death, diabetes, heart failure, renal disease, or other cardiovascular disease. 6. P ersonal and social history: habits a. A lcohol use: chronic use and withdrawal elevates BP b. R ecreational or street drug use, especially cocaine, crack, and amphetamines; anabolic steroids; recent withdrawal from narcotics c. Die t: includes sodium intake, use of canned or prepared foods, vegetable and fruit intake, fat and cholesterol intaked. E xercise: type, frequency, and level of exercise e. T obacco use: not a cause of HTN but is an addi-tional risk factor for cardiovascular disease, and withdrawal may be associated with elevated BP f. E thnic or racial background g. M ay affect responsiveness to certain medications (see pharmacologic treatment section V. B. ) h. Othe r factors influencing BP control i. E motional stress including social support system (if any), family and living situation, employment and working situation and stress, ability to obtain and pay for healthcare services, and educational level and literacy (may affect understanding of treatment recommendations, and/or ability to read patient handouts) B. Objective 1. P hysical examination a. V ital signs including BP should be taken after the patient has been sitting quietly for at least 5 minutes with arm resting on a flat surface and feet on the floor. Additionally, the patient should not have used caffeine, tobacco, or alcohol and nor exercised for at least 30 minutes before the BP measurement. The initial evaluation should include a BP measurement in both arms. At least two measurements should be obtained with the average of the two recorded. Periodic standing BP measurements are recommended for those at risk for postural BP changes or with such symp-toms and when adding or changing medications. The preferred method of BP measurement is the auscultatory (not digital) method. A proper sized cuff is essential; the cuff bladder should encircle at least 80% of the arm to assure an accurate BP reading (USDHHS, 2004). b. C omplete a fundoscopic evaluation for arterio-venous nicking, arteriolar narrowing, papilloe-dema, hemorrhages, or exudates. c. A ssess neck for carotid bruits, distended veins, and enlarged thyroid. d. E valuate the heart for precordial heave, thrills, rate, murmurs, or other extra sounds, such as S3 and S4. e. Aus cultate the lungs for adventitious sounds (e. g., crackles and wheezing). f. E valuate the abdomen for bruits, enlarged kidneys, or striae. g. A ssess the extremities for diminished or absent peripheral arterial pulses, edema, or femoral artery bruits. h. N eurologic assessment as baseline and for evalu-ation of abnormal sensory, motor, and cognitive findings suggestive of target organ damage. 585 Database
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choice or suggest end-organ damage or secondary HTN), calcium (may be associated with renal disease and thyroid disease), thyroid-stimulating hormone (TSH) and free L-thyroxine (FT4) (for hyperthyroidism), and fasting lipid profile (as is associated risk factor) b. T welve-lead electrocardiogram (as baseline and/or for evidence of arrhythmias, conduction defects, ischemia and/or infarct, and/or left ventricular hypertrophy)2. Di agnostic tests a. L aboratory: urinalysis (for proteinuria or hema-turia suggesting end-organ damage or secondary HTN), fasting blood glucose or hemoglobin A1C (for hyperglycemia suggesting diabetes), hematocrit (for anemia suggesting other disease or polycythemia), serum potassium (may affect medication choice and/or suggest etiology or-organ damage), creatinine and estimated glo-merular filtration rate (may affect medication Table 60-2 Common Substances Associated with Hypertension in Humans Prescription Drugs Street Drugs and o ther “ n atural Products” Food Substances Chemical e lements and o ther Industrial Chemicals Cortisone and other steroids: (both corticosteroids and mineralosteroids), adrenocorticotropic hormone (ACTH)Cocaine and cocaine withdrawal Sodium chloride Lead Estrogens (usually just oral contraceptive agents with high estrogenic activity)Ma huang, “herbal ecstasy,” and other phenyl propanolamine analogues Ethanol Mercury Nonsteroidal anti-inflammatory drugs Nicotine and withdrawal Licorice Thallium and other heavy metals Phenylpropanolamines and analogues Anabolic steroids Tyramine-containing foods (with monoamine oxidase inhibitors)Lithium salts, especially the chloride Cyclosporine and tacrolimus Narcotic withdrawal Caffeine Erythropoietin Methylphenidate Sibutramine Phencyclidine Ketamine Ketamine Desflurane Ergotamine and other ergot-containing herbal preparations Carbamazepine St. John's wort Bromocriptine Metoclopramide Antidepressants (especially venlafaxine)Buspirone Clonidine (abrupt withdrawal) with or without the simultaneous initiation of beta-adrenergic blocking agents Pheochromocytoma: beta-adrenergic blocking agent without alpha-blocker first; glucagon Clozapine Weight loss drugs Modified from U. S. Department of Health and Human Services. (2004). Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) (NIH Publication no. 0405230) (p. 59). Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute, National High Blood Pressure Education Program, U. S. Department of Health and Human Services. Retrieved from http://www. nhlbi. nih. gov/guidelines/hypertension/jnc7full. htm. 586 CHAPTER 60 | Hypertension
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c. I f secondary HTN is suspected based on the patient's presentation, other tests should be included (T able 60-3) III. Assessment A. Determine the diagnosis (see Table 60-1) B. Severity 1. A ssess severity based on level of BP and presence or absence of other risk factors or other compelling diseases. a. H ypertensive emergencies are characterized by severe elevations in BP (> 180/120 mm Hg) and complicated by evidence of impending or progressive target organ dysfunction. They require immediate BP reduction (not necessarily to normal) to prevent or limit target organ damage (e. g., intracerebral hemorrhage or acute myocardial infarction). b. H ypertensive urgencies are those situations associated with severe elevations in BP without progressive target organ dysfunction (USDHHS, 2004). C. Significance and patient's motivation and ability Assess the significance of this diagnosis to the patient and to significant others. Additionally, assess patient's understanding of the disorder and willingness and abil-ity to follow a treatment plan, including lifestyle modifica-tions. This assessment should be made on an ongoing basis throughout follow-up visits. IV. Goals of clinical management A. Public health goal Reduce the cardiovascular and renal morbidity and mortality. B. Individual's goal related to self-management and patient adherence Choose a plan including medications, lifestyle modifica-tions, and follow-up that is tailored to the patient. C. BP goal (see section I, C for BP goals for different groups of affected individuals) V. Plan and management (see Figure 60-1 ) A. Lifestyle modification This is the first step in counseling and treating patients with pre-HTN and stage 1 HTN and is an essential component Table 60-3 Screening T ests for Identifiable Causes of Hypertension Diagnosis Diagnostic test Chronic kidney disease Estimated glomerular filtration rate Coarctation of the aorta Computerized tomography angiography Cushing's syndrome and other glucocorticoid excess states including chronic steroid therapy History; dexamethasone suppression test Drug induced or related History and drug screening Pheochromocytoma 24-Hour metanephrine and normetanephrine Primary aldosteronism and other mineralocorticoid excess states24-Hour urinary aldosterone level or specific measurements of other mineralocorticoids Renovascular hypertension Doppler flow study; magnetic resonance angiography Sleep apnea Sleep study with O 2 saturation Thyroid or parathyroid disease Thyroid-stimulating hormone, serum parathyroid hormone Reproduced from U. S. Department of Health and Human Services. (2004). Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) (NIH Publication no. 0405230). Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute, National High Blood Pressure Education Program, U. S. Department of Health and Human Services. Retrieved from http://www. nhlbi. nih. gov/guidelines/hypertension/jnc7full. htm. 587 Plan and management
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Adult aged ≥18 years with hypertensio n Select a drug treatment titration strategy A. Maximize first medication before adding second or B. Add second medication before reaching maximum dose of first medication or C. Start with 2 medication classes separately or as fixed-dose combination. Reinforce medication and lifestyle adherence. For strategies A and B, add and titrate thiazide-type diuretic or ACEI or ARB or CCB (use medication class not previously selected and avoid combined use of ACEI and ARB). For strategy C, titrate doses of initial medications to maximum. Reinforce medication and lifestyle adherence. Add and titrate thiazide-type diuretic or ACEI or ARB or CCB (use medication clas s not previously selected and avoid combined use of ACEI and ARB). Reinforce medication and lifestyle adherence. Add additional medication class (eg, β-block er, aldosterone antagonist, or others ) and/or refer to physician with expertise in hypertension management. Continue curren t treatment an d monitoring. b All races Black Nonblack Age ≥60 year s Blood pressure goal SBP <150 mm Hg DBP <90 mm Hg Blood pressure goal SBP <140 mm Hg DBP <90 mm Hg Age <60 year s Blood pressure goal SBP <140 mm Hg DBP <90 mm Hg All ages Diabetes presen t No CK D Blood pressure goal SBP <140 mm Hg DBP <90 mm Hg All ages CKD present withor without diabete s At goal blood pressure? No Yes At goal blood pressure? No Yes At goal blood pressure? No Yes Yes No Initiate thiazide-type diureti c or CCB, alon e or in combination. Initiate thiazide-type diuretic or ACEI or ARB or CCB,alone or in combination. a Initiate ACEI or ARB, alone or in combination withother drug class. a Set blood pressure goal and initiate blood pressure lowering-medicationbased on age, diabetes, and chronic kidney disease (CKD). Implement lifestyle interventions (continue throughout management). Diabetes or CKD present General population (no diabetes or CKD) At goal blood pressure? Figure 60-1 2014 Hypertension Guideline Management Algorithm Reproduced from James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J., et al. (2014). 2014 evidence-based guidelines for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA, 311(5), 516. doi: 10. 1001/jama. 2013. 284427. 588 CHAPTER 60 | Hypertension
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with HTN as an adjuvant therapy: (1) transcen-dental meditation and possibly other meditation techniques (the latter less studied) and (2) bio-feedback, device-guided breathing (such as the RESPe RATE, which is approved by the Food and Drug Administration as an over-the-counter product for stress reduction and adjunct to treating HTN; USDHHS, 2002). Other alternative approaches that have been used successfully but have not been adequately researched include acupuncture (including electroacupuncture), cognitive behavioral techniques for stress reduction, progressive muscle relaxation, and yoga (Eckel et al., 2013). B. Pharmacologic treatment (Table 60-4 ) Reducing elevated BP with medications has been shown in numerous studies to decrease the incidence of cardio-vascular mortality and morbidity. 1. F actors to be considered in the selection of therapy a. C ost of medication b. M etabolic and subjective side effects c. P otential drug-drug interactions d. C oncomitant diseases that may be beneficially or adversely affected by the antihypertensive agent chosen e. E thnicity and race: There is a great variance in HTN-related morbidity and mortality among various ethnic groups in the United States, because of many factors including physiologic differences in response to some drugs; socioeco-nomic conditions; access to healthcare services; attitudes and beliefs related to health informa-tion; and differences in lifestyle practices, such as diet (USDHHS, 2004). i. A frican Americans may respond to a low-sodium diet and diuretics with greater BP reductions than other demographic sub-groups ( James et al., 2014) Also, the JNC 8 panel recommends using a calcium channel blocker (CCB) rather than an angiotensin converting enzyme inhibitor (ACEI) initially in Blacks because of increased stroke risk in Blacks started initially on an ACEI in one large randomized control trial (The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group, 2002). ii. M exican Americans and Native Americans tend to have lower control rates of HTN than non-Hispanic whites and African Americans (USDHHS, 2004), which may mean closer attention to dietary sodium intake and/or greater need for use of medi-cations from two or more classes. of treatment for stage 2 HTN. In patients with prehyper-tension or mild stage 1 HTN, lifestyle modifications may be definitive therapy, and in others they may reduce the number and doses of antihypertensives required to reach goal BP and decrease risk of or delay progression to end-organ damage. 1. W eight a. W eight loss of as little as 10 lb (4. 5 kg) reduces BP or prevents HTN in many overweight individuals (USDHHS, 2004). 2. Die t a. The re is strong evidence that consuming a diet that emphasizes vegetables, fruits, whole grains, low-fat dairy, poultry, fish, legumes, nontropical vegetable oils, and nuts and limits intake of sweets, sugar-sweetened beverages, and red meats can benefit BP lowering (Eckel et al., 2013). The DASH (Dietary Approaches to Stop Hypertension) diet or the American Heart Association diet are diets consistent with these recommendations and generally recommended (American Heart Association [AHA], 2014; Heller, 2015). b. S trong evidence also exists for consuming no more than 2,400 mg of sodium daily, and reducing further to 1,500 mg/day is associated with greater BP reduction. Even reducing sodium intake by at least 100 mg a day, though not ideal, can lower BP (Eckel et al., 2013) 3. A lcohol Alcohol intake should be limited to 1 oz or less daily of ethanol (two drinks in men) and no more than 0. 5 oz (AHA, 2014). 4. E xercise Regular aerobic activity often lowers BP in adults. Three to four sessions a week of approximately 40 minutes each involving moderate to vigorous intensity exercise are recommended (Eckel et al., 2013). 5. T obacco abstinence For overall cardiovascular risk reduction, smoking cessation is essential and should be a major focus of counseling for providers. 6. Othe r lifestyle modifications or alternative treatments Numerous other modalities and lifestyle treatments have been tried and studied over the past several decades, but in general the research done on these strategies is less rigorous, or lacking in statistical power, to make strong recommendations (Eckel et al., 2013). However, several modalities have moderately good evidence to support recommending to patients with pre-HTN as a trial therapy and to any patient 589 Plan and management
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Table 60-4 Commonly Used Antihypertensive Medications* Class of Drug Drug n ame Usual Dose r ange (mg/day)Usual Daily Frequency Mechanism Comments Thiazide diuretics Chlorthalidone Chlorthiazide Hydrochlorathiazide Indapamide Polythiazide Metolazone (Zaroxolyn)12. 5-25 125-500 12. 5-50 1. 25-2. 5 2-4 2. 5-5. 01 1-2 1111Decreased plasma volume and extracellular fluid volume, decreased cardiac output initially, followed by decreased total peripheral resistance with normalization of cardiac output. Long-term effects include slight decreases in extracellular fluid volume. For thiazide and loop diuretics, lower doses and dietary counseling should be used to avoid metabolic changes (e. g., potassium, sodium losses). Check electrolytes 1-2 weeks after initiating these medications. Loop diuretics Bumetanide Ethacrynic acid Furosemide Torsemide0. 5-2 50-100 10-80 2. 5-102 1-2 21See thiazides. Higher doses may be needed for patients with renal impairment or congestive heart failure. Ethacrynic acid is the only alternative for patients with allergy to thiazide and sulfur-containing diuretics. β-Blockers Atenolol Betaxolol Bisoprolol Metoprolol Metoprolol extended release Nadolol Propranolol Propranolol long-acting25-100 5-20 2. 5-10 50-20025-10040-12040-16060-180 10-40111 1-2 11212Decreased cardiac output and increased total peripheral resistance; decreased plasma renin activity; atenolol, betaxolol, bisoprolol, and metroprolol are cardioselective. Selective agents also inhibit in higher doses (e. g., all may aggravate asthma). β-Blockers with intrinsic sympathomimetic activity Acebutolol Penbutolol Pindolol200-800 10-4010-40212See β-blockers Acebutolol is cardioselective. Use intrinsic sympathomimetic activity agents for those with bradycardia who must receive β-blockers. 590 CHAPTER 60 | Hypertension
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Angiotensin-converting enzyme inhibitors (ACEIs)Benzapril Captopril Enalapril Fosinopril Lisinopril Moexipril Perindopril Quinapril Ramipril Trandolapril10-40 25-100 5-20 10-4010-40 7. 5-30 4-8 10-80 2. 5-2. 0 1-412 1-2 1111111Block formation of angiotensin II by cleaving angiotensin I thereafter promoting vasodilation and reducing the circulation of aldosterone that results in decreased sodium and water retention. They also increase bradykinin and vasodilatory prostaglandins. Diuretic doses should be reduced or discontinued before starting angiotensin-converting enzyme inhibitors whenever possible to prevent excessive hypotension. May cause hyperkalemia in patients with renal impairment or in those receiving potassium-sparing agents. Can cause acute renal failure in patients with severe bilateral renal artery stenosis or severe stenosis in artery in a solitary kidney. Angiotensin II receptor blockers Candesartan Eprosartan Irbesartan Losartan Olmesartan Telmisartan Valsartan8-32 400-800150-300 25-100 20-4020-80 80-3201 1-2 1 1-2 11 1-2Blocks the angiotensin II receptor thus inhibiting the action of angiotensin II as noted previously. Bradykinin levels are not altered so there is lower incidence of an associated dry cough than with angiotensin-converting enzyme inhibitors. See angiotensin-converting enzyme inhibitors. Calcium channel blockers Amlodipine Diltiazem (Sutters, 2015)*Cardizem SR ® *Cardizem CD® *Dilacor XR® *Tiazac SA® Felodipine Isradipine Nicardipine Nicardipine SRNifedipine XLNisoldipine Verapamil (long acting and sustained release) (Sutters, 2015)2. 5-10 180-360 180-360180-480180-540 2. 5-2. 0 2. 5-5 20-4030-60 30-120 17-34 180-4801 1 111122221 1-2Block inward movement of calcium ion across cell membranes and cause smooth muscle relaxation. Dihydropyridines—more potent peripheral vasodilators than other calcium channel blockers and, as such, may cause more dizziness, headache, flushing, peripheral edema, and tachycardia. All can reduce sinus rate and produce heart block, especially in combination with other antihypertensives. *”In some patients treated once daily, the antihypertensive effect may diminish toward the end of the dosing interval (trough effect). Blood pressure (BP) should be measured just prior to dosing to determine if satisfactory BP control is obtained” (USDHHS, 2004, p. 11). Data from James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J., et al. (2014). 2014 evidence-based guidelines for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA, 311(5), 507-520. doi: 10. 1001/jama. 2013. 284427; Sutters, M. (2015). Chapter 11: Systemic hypertension. In M. A. Papadakis, S. Mc Phee, & M. W. Rabow (Eds. ), Current medical diagnosis and treatment (54th ed. ). New York: Mc Graw-Hill Education. 591 Plan and management
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C. Patient education It is essential that this be done in the language in which the patient is fluent (oral and written) and at a reading level appropriate to patient's education. When in doubt, aim at a sixth grade or lower level of reading. 1. P rovide oral and written information on cardiovascular risk factors associated with HTN and long-term prognosis of HTN if untreated. 2. El icit the patient's concerns regarding the diagnosis, including his or her acceptance of the diagnosis. 3. P rovide the patient with a written copy of his or her BP reading at each visit. If possible provide a wallet card that contains multiple readings. 4. C ome to a mutual agreement with the patient on BP goal. 5. P rovide specific, preferably written, information on lifestyle modifications that you are recommending for this patient. 6. Be sure to underscore the importance of the need to continue treatment, most likely for their lifetime. Emphasize “control does not mean cure” (USDHHS, 2004, p. 62) 7. E xplain that most individuals with HTN are usually asymptomatic, so the patient will not usually be able to tell if the BP is elevated or not based on his or her symptoms. 8. H ave the patient repeat his or her understanding of treatment regimen before the end of the visit. 9. I nclude in the patient education cautions regarding use of cold preparations and over-the-counter analgesics (e. g., pseudoephedrine, nonsteroidal anti-inflammatory drugs, respectively). 10. E ncourage the use of validated home BP-monitoring devices for interested and able patients, especially those with refractory HTN. D. Follow-up and monitoring 1. I f treating initially with lifestyle modifications alone, have the patient follow up in 3 months to assess both effectiveness on BP and the patient's ability to carry through lifestyle changes. 2. A fter initiating antihypertensive drug therapy, have the patient return in 1 month for a BP check and review of adverse or other effects of medications. 3. C ontinue follow-up visits at 1-to 3-month intervals until BP goal is achieved. 4. I f stage 2 HTN or with the presence of other comorbid conditions, such as diabetes or chronic kidney disease, more frequent visits may be warranted. iii. A frican Americans and Asians have a three to four times higher risk of developing angioedema and more cough associated with the use of angiotensin-converting enzyme inhibitors than whites (USDHHS7, 2004). 2. Ge neral treatment guidelines. a. C onsider first of all that most patients will require more than one drug to achieve good BP control (Weber et al., 2014). b. I n the general non-Black population, including those with diabetes, initial pharmacologic treat-ment should include a thiazide-type diuretic, CCB, ACEI, or angiotensin receptor blocker (ARB) ( James et al., 2014) c. I n the general Black population, including those with diabetes, initial pharmacologic antihyper-tensive treatment should include a thiazide-type diuretic or CCB ( James et al., 2014) d. I f goal BP is not reached within a month of treatment, add another agent from (a) or (b). Continue to assess BP regularly and adjust treatment regimen to desired BP goal. e. I f goal BP is not reached with two drugs, add a third from this list (CCB, ACEI, ARB, or thiazide diuretic). Note: Do not use an ACEI and ARB in same patient. f. I f goal BP is not reached with titration of drugs from this list due to a contraindication or the need to use more than three drugs, other antihy-pertensive medications (from other classes) may be used. g. C onsider referral to a hypertensive specialist if goal BP is not reached using four medications and after a careful review of patient's compliance with medication and lifestyle modifications. ( James et al., 2014) h. S implify the regimen to once daily dosing if possible for greater adherence. i. I n some patients on once-daily dosing, there may be a trough effect: waning of effectiveness of medications at the end of dosing interval. Therefore, it is best to measure the BP just before the next dose to determine the need for dosage adjustment (USDHHS, 2004). j. I n stage 2 HTN, consider starting therapy with two drugs, either as separate prescriptions or in fixed-dose combinations, because this increases the likelihood of reaching BP goal more promptly than with one agent (USDHHS, 2004). 592 CHAPTER 60 | Hypertension
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Heller, M. (2015). The DASH diet eating plan. Retrieved from http:// dashdiet. org/default. asp. James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J., et al. (2014). 2014 evidence-based guide-lines for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee ( JNC 8). JAMA, 311(5), 507-520. doi: 10. 1001/jama. 2013. 284427. Nwanko, T., Y oon, S. S., Bury, V., & Gu, Q. (2013) Hypertension among adults in the United States: National Health and Nutrition Examination Survey, 2011-2012 (NCHS data brief, no. 133). Hyattsville, MD: Centers for Disease Control and Prevention, National Center for Health Statistics. Retrieved from www. cdc. gov/nchs/data/databriefs/db133. htm. Ram, C. V. (2014). Hypertension guidelines in need of guidance. Journal of Clinical Hypertension, 16(4), 251-254. doi: 10. 1111/jch. 12306. Sutters, M. (2015). Chapter 11: Systemic hypertension. In M. A., Papadakis, S., Mc Phee, & M. W., Rabow (Eds. ), Current medical diagnosis and treatment (54th ed. ). New Y ork: Mc Graw-Hill Education. The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. (2002). Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering T reatment to Prevent Heart Attack T rial (ALLHAT). The Journal of the American Medical Association, 288 (23), 2981-2997. U. S. Department of Health and Human Services, U. S. Food and Drug Administration. (2002). Summary for The Intercure Ltd. RESPe RATE. Retrieved from http://www. accessdata. fda. gov/cdrh_docs/pdf2 /k020399. pdf. U. S. Department of Health and Human Services. (2004). Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) (NIH Publication no. 0405230). Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute, National High Blood Pressure Education Program, U. S. Department of Health and Human Services. Retrieved from http://www. nhlbi. nih. gov/guidelines/hypertension /jnc7full. htm. Weber, M. A., Schriffin, E. L., White, W. B., Mann, S., Lindholm, L. H., Kenerson, J. G., et al. (2014). Clinical practice guidelines for the management of hypertension in the community: A statement by the American Society of Hypertension and the International Society of Hypertension. Journal of Clinical Hypertension, 16(1), 14-26. doi: 10. 1111/jch. 12237 World Health Organization. (2013). A global brief on hypertension: Silent killer, global public health crisis (Document no. WHO/DCO/WHD/2013. 2). Retrieved from www. who. int/cardiovascular_diseases /publications/global_brief_hypertension/en/. 5. Onc e the BP is stable, schedule visits at 3-to 6-month intervals. 6. L aboratory follow-up a. C heck serum electrolytes 2-4 weeks after starting a diuretic. b. C heck serum potassium and creatinine 2-4 weeks after starting an angiotensin-converting enzyme inhibitor. c. C heck serum electrolytes and creatinine at least annually for all patients on antihypertensive medications. 7. H ave the patient bring in all medications to each follow-up visit. 8. F ailure to reach target BP goal a. C onsider nonadherence to medication or life-style recommendations, including excessive sodium intake or increased alcohol intake. b. C onsider use of over-the-counter medications or street drugs. c. E valuate for high levels of stress or psychiatric conditions that can affect BP, such as anxiety disorders and panic disorder. d. R econsider secondary causes for HTN. e. A lways maintain an attitude of empathetic concern and genuine interest in developing the best possible, workable plan for the patient, as a partner in treatment. re Feren Ce S American Heart Association (2014). The American Heart Association's diet and lifestyle recommendations. Retrieved from www. heart. org /HEARTORG/Getting Healthy/Nutrition Center/Healthy Eating/The -American-Heart-Associations-Diet-and-Lifestyle-Recommendations _UCM_305855_Article. jsp. Eckel, R. H., Jakicic, J. M., Ard, J. D., de Jesus, J. M., Houston Miller, N., Hubbard, V. S., et al. (2013). 2013 AHA/ACC guideline on lifestyle man-agement to reduce cardiovascular risk: A report of the American College of Cardiology/American Heart Association T ask Force on Practice Guidelines. Circulation, 129(25, Suppl. 2), S76-S99. doi:10. 1161/01 . cir. 0000437740. 48606. d1. 593 References
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denying a partner medical care or forcing alcohol or drugs upon him or her. 2. Se xual abuse is coercing or attempting to coerce any sexual contact or behavior without consent, marital rape, forcing sex after physical violence, treating one in a sexually demeaning manner, and birth-control sabotage. 3. E motional abuse involves undermining an individual's sense of self-worth, name calling, diminishing one's abilities, or damaging one's relationship with his/her children. 4. Eco nomic abuse is defined as making or attempting to make an individual financially dependent by controlling or withholding one's access to money or forbidding attendance at school or employment. 5. P sychological abuse is different from emotional abuse as it involves causing fear by intimidation through threats to harm self, partner, children, or other individuals/pets/property involved in the victim's life. It also involves forcing isolation from one's community or threatening the victim's immigration status or custody of his/her children. These categories of IPV are not mutually exclusive; they often present together as a complex ongoing pattern of abuse. Although all states have legislation that defines IPV, those definitions vary across states. IPV constitutes the willful intimidation, assault, battery, sexual assault, or other abusive behavior perpetrated by one family member, household member, or intimate partner against another (National Center for Victims of Crime, 2008a). In most state laws addressing IPV, the relationship necessary for a charge of domestic assault or abuse generally includes a spouse, former spouse, persons currently residing together or those that have within the previous year, or persons who share a common child. In addition, as of 2007, most states provide some level of statutory protection for victims of dating violence (National Center for Victims of Crime, 2008a). I. Intr oduction and general background Intimate partner violence (IPV) is a serious, preventable public health problem that affects millions of Americans (Centers for Disease Control and Prevention [CDC], 2015b). In the United States, IPV is also commonly referred to as domestic violence, and can occur among heterosexual or same sex partners, either current or former, and does not require sexual intimacy, legal ties, or even cohabitation (CDC, 2015b). The term IPV also encompasses dating violence, defined as violence committed by a person who is or has been in a social relationship of a romantic or intimate nature with the victim (U. S. Department of Health & Human Services, 2009). IPV involves a “pattern of abusive behavior” with the intention to intimidate, control, and instill fear in the victim (U. S. Department of Justice [USDOJ], 2015). Victims, survivors who withstand the violence, can be male or female, educated or illiterate, able bodied or disabled, wealthy or poor, and any age (National Center for Victims of Crime, 2008a). They can be of any racial, ethnic, or cultural background, of any sexual orientation, and of any immigra-tion/citizenship status; in fact, disclosure of IPV is often com-plicated for individuals who experience oppression or have fear of authority. According to the 2009 California Penal Code Handbook (Section 1M. 6, 137W, 242, 243, 273. 5), acts of partner abuse include those that intentionally or recklessly cause, or attempt to cause, bodily injury or that place another person in reason-able apprehension of imminent serious bodily injury. IPV is considered by many as a prelude to murder (Ferguson, 2007; Strack & Gwinn, 2011). For this reason, clinicians play an important role in identifying indications of abuse as well as risk factors that indicate that the abuse will reoccur or heighten. A. Definition and overview The U. S. Department of Justice (2015) defines IPV in terms of the following five categories: 1. Ph ysical abuse is defined as acts of hitting, slapping, shoving, grabbing, biting, etc. and also includes Rosalind De Lisser, Deborah Johnson, Jo Anne Saxe, and Cecily Reeves Int Im Ate P AR tne R V I o L en C e (Dome S t IC V I o L en C e)© Eliks/Shutterstock; © donatas1205/Shutterstock 594 61Chapt Er
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B. Prevalence and incidence In 2010 the Centers for Disease Control and Prevention's National Center for Injury Prevention and Control, in collaboration with the National Institutes of Justice and the Department of Defense, developed a telephone survey, the National Intimate Partner and Sexual Violence Survey (NISVS). The NISVS began collecting ongoing population-based surveillance data, generating accurate and reliable incidence and prevalence estimates for intimate partner violence, sexual violence, dating vio-lence, and stalking victimization (CDC, 2015a). The first report, released in 2014, stated that 20 people per minute are victims of physical violence by an intimate partner in the United States. The National Intimate Partner and Sexual Violence Survey data are summarized next. 1. S exual Violence by Any Perpetrator One in 5 women or 18. 3% of all women in the United States and 1 in 71 men or 1. 4% of all men in the United States have been raped at some time in their lives. This includes full and attempted forced penetra-tion and drug/alcohol facilitated violations. 2. S talking Victimization by Any Perpetrator One in 6 women or 16. 6% and 1 in 19 men or 5. 2% report stalking victimization in the United States. Table 61-1 National Intimate Partner and Sexual Violence Survey: Victimization by Race/Ethnicity Race/ ethnicity U. S. total Black n on- Hispanic White n on- Hispanic Hispanic American Indian or Alaska n ativem ultiracial n on-Hispanic Asian/ Pacific Islander Event % per total U. S. population Intimate Partner Violence (IPV), lifetime: WOMEN31. 5% 41. 2% 30. 5% 29. 7% 51. 7% 51. 3% 15. 3% IPV, lifetime: MEN 27. 5% 36. 3% 26. 6% 27. 1% 43. 0% 39. 3% 11. 5% IPV Rape Victimization during lifetime: WOMEN8. 8% 8. 8% 9. 6% 6. 2% * 11. 4% * IPV Rape Victimization during lifetime: MEN0. 5% * * * * * * IPV Sexual Violence other than rape: WOMEN15. 8% 17. 4% 17. 1% 9. 9% * 26. 8% * IPV Sexual Violence other than rape: MEN9. 5% 24. 4% 22. 2% 26. 6% 24. 5% 39. 5% 15. 8% IPV Stalking Victimization, lifetime: WOMEN** 9. 5% 9. 9% 6. 8% * 13. 3% * IPV Stalking Victimization, lifetime: MEN** * 1. 7% * * * * * No data as not statistically reliable due to small case count. ** Data not available. Data from Breiding, M. J., Smith, S. G., Basile, K. C., et al. (2014). Prevalence and Characteristics of Sexual Violence, Stalking, and Intimate Partner Violence Victimization—National Intimate Partner and Sexual Violence Survey, United States, 2011. MMWR, 63(SS08), 1-18. Retrieved from http://www. cdc. gov/mmwr/preview/mmwrhtml/ss6308a1. htm#Table1Stalking victimization results in victims feeling fearful that they or someone close to them will be harmed or killed by the stalker; 66% of female victims of stalking were stalked by a current or former partner, and 41% of male victims were stalked by a partner. 3. V iolence by an Intimate Partner One in 3 women (35. 6%) and 1 in 4 men (28. 5%) in the United States have experienced rape or violence and/or stalking by their intimate partner during their lifetime. Of those victims 1 in 4 women (24. 3%) and 1 in 7 men (13. 8%) have experienced severe violence, characterized by being hit by a fist or other object, beaten, or slammed against something hard. The survey also reports that half of all men and women have experienced psychological aggression. Of all victims of intimate partner violence, 69% of females and 53% of males experienced the first episode before the age of 25. 4. V iolence by an Intimate Partner Experienced by Race/Ethnicity (T able 61-1) C. Consequences Although the severity of IPV can vary, the type of IPV that is repetitive and prolonged has been most closely associated with negative health sequelae (Humphreys & 595 Introduction and general background
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Campbell, 2010). This violence results in nearly 2 million injuries and nearly 1,300 deaths. Of the IPV injuries, more than 555,000 require attention by a healthcare pro-vider, and more than 145,000 are serious enough to war-rant hospitalization for 1 or more nights. In 2008, nearly 45% of female homicide victims were killed by intimate partners (Bureau of Justice Statistics, 2009b). Of note, IPV is the leading cause of premature death from homi-cide and injury among African American women between the ages of 15 and 24 years (Rennison & Welchans, 2002). As noted in the NISVS, 24. 3% of women and 13. 8% of men in the United States have been a victim of severe physical violence and nearly 15% of women and 4% of men have been injured as a result (Breiding et al., 2014). Research suggests that the risk of suffering from six or more chronic physical symptoms increases with the number of forms of violence experienced, even when the last episode was over 30 years ago (Nicolaidis, Curry, Mc Farland, & Gerrity, 2004). IPV costs in the United States are estimated at $12. 6 billion on an annual basis, 0. 1% of the gross domestic product (Waters et al., 2004). IPV also results in more than 18. 5 million mental health-care visits each year and 13. 6 million days of lost produc-tivity from paid work and household chores among IPV survivors and the value of IPV murder victims' expected lifetime earnings (National Center for Injury Prevention and Control, 2003). In addition to the injuries inflicted during violent episodes, physical and psychological abuses are linked to a number of adverse health effects. These include arthri-tis; chronic neck or back pain; migraine or other types of headache; sexually transmitted infections (including HIV); chronic pelvic pain; peptic ulcers; irritable bowel syndrome; and frequent indigestion, diarrhea, or consti-pation (Coker, Smith, Bethea, King, & Mc Keown, 2000). Psychological consequences include posttraumatic stress disorder, depression, substance abuse, and suicidal behav-iors (Ellsberg, Jansen, Heise, Watts, & Garcia-Moreno, 2008). Six percent of all pregnant women are battered. Pregnancy complications, including low weight gain, anemia, infections, and first-and second-trimester bleeding, are significantly higher for abused women, as are maternal rates of depression, suicide attempts, and substance abuse (Parker, Mc Farlane, & Soeken, 1994). Health behaviors are also significantly affected by IPV and research demonstrates that the more severe the violence the more impaired the health behaviors become, including engaging in high-risk sexual behavior, using harmful substances, and unhealthy diet-related behaviors, all resulting in overuse of the health services (Heise & Garcia-Moreno, 2002). D. Risk factors Factors that should heighten the clinician's index of sus-picion regarding the possibility of IPV include medical records indicating repeated visits or previous injuries, a history of IPV or a history with inconsistent descriptions of injuries, and a past history of suicide attempts. Vague and nonspecific responses to questions with a history of anxiety, depression, sleeplessness, fatigue, or chronic somatic complaints may indicate intrafamilial crisis. Abuse is a frequent precipitant of suicide attempts, and those who attempt suicide are likely to have a history of IPV (Ellsberg et al., 2008). E. Special populations Special populations at increased risk of IPV include poor or homeless individuals; teenagers; pregnant or immigrant women; those with chronic illnesses (HIV) or disabili-ties; lesbian, gay, bisexual, and transgender individuals; and the elderly. Risks to note in these special populations and additional resources are highlighted in (T able 61-2). Clinicians should be aware of agencies or resources in the area that do focused work with these special populations. Clinicians should seek out additional information and culturally competent training to provide best practice care to these individuals. Table 61-2 Special IPV Risk Populations Risk Data Sources Chronic illness (HIV) The IPV risk for women with HIV may be as high as 67%, a rate three to four times greater than among HIV-negative women. HIV-positive women seem to experience IPV at rates comparable to HIV-negative women from the same underlying populations; however, their abuse seems to be more frequent and more severe. Brief, Vielhauer, & Keane, 2006; Cobb, 2008; Gielen et al., 2007 Individuals with disabilities Those with disabilities and deaf women have an increased risk of both typical and unique forms of violence. The greater the degree of cognitive impairment, the greater the risk for victimization and abuse. Barrett, O'Day, Roche, & Carlson, 2009; Curry, Powers, Oschwald, & Saxton, 2004596 CHAPTER 61 | Intimate Partner Violence (Domestic Violence)
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(continues)Table 61-2 Special IPV Risk Populations Risk Data Sources Immigrant women More difficult for these women to seek or obtain help because of abusive partners using immigration status against her, threatening deportation. Language barriers, isolation, and a lack of familiarity with the United States social services system and legal rights. Fear that if she reports violence she will be treated with insensitivity, hostility, or discrimination by authorities. Low level of awareness about IPV among immigrants or refugees. Not seen as a problem in their community. May be recognized, but only as a family or private issue. Community members may condone IPV or do not consider various abusive or controlling acts to be IPV. Kulwicki & Miller, 1999; Moracco, Hilton, Hodges, & Frasier, 2005; Murdaugh, Hunt, Sowell, & Santana, 2004; Runner, Yoshihama, & Novick, 2009; Shiu-Thornton, Senturia, & Sullivan, 2005; Yoshihama, 2008 Lesbian, gay, bisexual, or transgender individuals Lifetime prevalence of IPV for women: Lesbian 43. 8%, bisexual 61. 1%, heterosexual 35. 0%. Lifetime prevalence of IPV for men: Gay 26. 0%, bisexual 37. 3%, heterosexual 29. 0%. Transgender: estimated 50% of transgender individuals report lifetime sexual violence Lesbian, gay, bisexual, or transgender individuals who are incarcerated are sexually assaulted at a rate 15 times higher than that of the general inmate population. FORGE, 2012; Walters, Chen, & Breiding, 2013 Poor or homeless IPV is the primary cause of family homelessness in 28% of cities surveyed across the United States, and 15% of homeless persons were victims of IPV. Between 25% and 50% of homeless families have lost their homes as a result of intimate partner abuse. Homelessness and poverty significantly increase a child's exposure to parental IPV. Women living in disadvantaged neighborhoods are more than twice as likely to be the victims of IPV as women in more affluent neighborhoods. U. S. Conference of Mayors, 2008; Institute for Children and Poverty, 2010 Pregnant women IPV in women of childbearing age may include reproductive coercion, sabotaged contraception, and forced pregnancy continuation or abortion, and may lead to gynecological disorders, pregnancy complications, unintended pregnancy, and sexually transmitted infections, including human immunodeficiency virus (HIV). Other adverse outcomes correlating with IPV include poor pregnancy weight gain, infection, anemia, tobacco use, stillbirth, pelvic fracture, placental abruption, fetal injury, preterm delivery, and low birth weight. The severity of violence may escalate during pregnancy or the postpartum period, and homicide has been reported as a leading cause of maternal mortality, with the majority perpetrated by a current or former intimate partner. Abused women were twice as likely to begin prenatal care during the third trimester and more likely to abuse substances before and during pregnancy. Bureau of Justice Statistics, 2009a; Cha & Masho, 2014; Chamberlain, &. Levenson, 2013; Cheng & Horon, 2010; Madkour, Xie, & Harville, 2014; Silverman et al., 2011; World Health Organization, 2013(Continued)597 Introduction and general background
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F. Screening The U. S. Preventive Services T ask Force (USPSTF) now recommends IPV screening and has found benefits of detection and early intervention to reduce violence and improve health outcomes in women of childbearing age (Moyer, 2013). The USPSTF, however, has deter-mined that current evidence is insufficient to assess the balance between the benefits and harms of screening for IPV in elderly or vulnerable adult populations (USPSTF, 2013). There are no current recommendations regarding screening men for IPV. II. t he focused IPV assessment and database (may include but is not limited to) A. Subjective Although many individuals may not bring up the subject of abuse on their own, many will discuss it in a private, confidential setting when asked simple, direct, non-judgmental questions. See T able 61-3 for approaches to phrasing questions. A variety of tools can be used to accurately measure victimization and offer the clinician specific scales in the areas of physical, sexual, psychological, and emotional victimization and stalking to guide their inquiries (Basile, Hertz, & Back, 2007; Thompson, Basile, Hertz, & Sitterle, 2006). 1. W hen IPV is identified: a. I t is important to determine the identity of the person allegedly inflicting the injuries and document the circumstances surrounding the event, any past history of abuse, the nature of the injuries, and use of any threats or weapons. Whenever possible, use the patient's exact words and quotation marks. b. Add itional history related to other health-risk behaviors (e. g., alcohol or drug use, tobacco) and chronic conditions, such as sleep problems, depression, and eating disorders, should be elicited. These conditions, along with currently being the victim of IPV, are predictors of the women's physical and psychological health (Svavarsdottir & Orlygsdottir, 2009). B. Objective Perform a complete head-to-toe examination or focused evaluation as indicated by history or report of injuries. Document the character and extent of all physical injuries, including areas of pain and tenderness, even if there is as yet no obvious bruising or injury. It is recommended to use photos or drawings whenever possible. Additional components of the physical examination are listed in T able 61-4. Table 61-2 Special IPV Risk Populations Risk Data Sources Teenagers The 2013 Youth Risk Behavior Surveillance reports a prevalence of physical dating violence between 13% (female) and 7. 4% (male) among youth in grades 9 through 12. The prevalence of youth reporting sexual dating violence was 14. 4% (female) and 6. 2% (male). Among adult victims of rape, physical violence, and/or stalking by an intimate partner, 22% of females and 15% of males report their first experience of partner violence occurred between 11 and 17 years of age. When youth responses were evaluated based on reported race, Hispanic females (13. 6/12. 9%) followed by white females (12. 9/14. 6%) and black males (8. 2/8. 9%) followed by Hispanic males (7. 0/6. 7%) reported the highest incidence of both physical and sexual dating violence, respectively. Numerous risk factors have been correlated with adolescent dating violence, ranging from individual (substance use, depression, anxiety, age/gender, race/ethnicity, personal violence history, acceptance of violent behavior) to relationship level (aversive family communication, harsh parenting, hostile friendships, low parental monitoring). Protective factors include high empathy, high grade point average, high verbal IQ, positive relationship with mother, and attachment to school. Detrimental consequences may include increased alcohol, cigarette, and marijuana use; increased internalizing; and decreased number of close friends. CDC, 2014b; Foshee, Reyes, Gottfredson, Chang, & Ennett, 2013; Keenan-Miller, Hammen, & Brennan, 2007; Miller et al., 2013; Silverman et al., 2011; Stöckl, March, Pallitto, & Garcia-Moreno, 2014; Vagi, Rothman, Latzman, Tharp Hall, & Breiding, 2013 (Continued)598 CHAPTER 61 | Intimate Partner Violence (Domestic Violence)
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Table 61-3 Screening History Questions USPSTF recommends use of a screening scale with women of reproductive age, elderly, and vulnerable. Those with the highest levels of sensitivity and specificity for identifying IPV are Hurt, Insult, Threaten, Scream (HITS; English and Spanish versions); Ongoing Abuse Screen/Ongoing Violence Assessment Tool (OAS/OVAT); Slapped, Threatened, and Throw (STa T); Humiliation, Afraid, Rape, Kick (HARK); Modified Childhood Trauma Questionnaire-Short Form (CTQ-SF); and Woman Abuse Screen Tool (WAST) (Rabin, Jennings, Campbell, & Bair-Merritt, 2009). HITS How often does your partner: (1) Physically hurt you? (2) Insult you or talk down to you? (3) Threaten you with harm? (4) Scream or curse at you? WAST (1) In general, how would you describe your relationship—a lot of tension, some tension, no tension? (2) Do you and your partner work out arguments with great difficulty, some difficulty, or no difficulty? (#3-#7 response options: often, sometimes, never) (3) Do arguments ever result in you feeling down or bad about yourself? (4) Do arguments ever result in hitting, kicking, or pushing? (5) Do you ever feel frightened by what your partner says or does? (6) Has your partner ever abused you physically? (7) Has your partner ever abused you emotionally? (8) Has your partner ever abused you sexually? For women of reproductive age, select a scale for physical/sexual, psychological-emotional, stalking screening based on evidence of sensitivity and specificity for identifying IPV as well as utility within the clinical setting. The clinician must remain alert to clinical clues of IPV, abuse, and neglect of all populations, inclusive of elderly and vulnerable adults, males, and prepubescent females and assess further when indicated on clinical grounds. Phrasing the Interview Questions 1. Begin with a framing statement such as “W e've started talking to all of our patients about safe and healthy relationships because it can have such a large impact on your health” (Chamberlain & Levenson, 2013). 2. Advise patient of the limits of confidentiality, based on state mandates. For example, “Before we get started, I want you to know that everything here is confidential, meaning that I won't discuss what is said unless you tell me that... (insert the laws in your state about what is necessary to disclose). ” 3. Sample questions: Phrasing Questions: The Use of One of the Victimization Scales for Physical-Sexual, Psychological-Emotional, Stalking. 1. “Are you in a relationship in which you have been physically hurt or threatened by your partner? Have you ever been in such a relationship?” 2. “Has your partner ever destroyed things that you cared about? Ever threatened or abused your children? Ever forced you to have sex when you didn' t want to?” 3. “What happens when you and your partner disagree or fight? Do you ever feel afraid of your partner?” 4. “Has your partner ever prevented you from leaving the house, seeking friends, getting a job, or continuing your education?” 5. “If your partner uses alcohol or drugs, is s/he ever physically or verbally abusive to you when using?” 6. “Do you have guns or other weapons in your home? If so, has your partner ever threatened to use them?” Table 61-4 Physical Examination Components of the Physical examination Assess general appearance: Level of distress Vital signs Other physical examination data: 1. Look carefully for multiple abrasions and contusions to dif ferent anatomic sites and multiple injuries in various stages of healing. 2. Most accidents involve the extremities, whereas IPV injuries often involve the face, neck, chest, breasts, abdomen, genitalia, or anus. Mental status examination: Evaluate mood, orientation, thought processes, and judgment. 599 The focused IPV assessment and database
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Table 61-5 Assessment Components of the Assessment Determine the diagnosis (not mutually exclusive). 1. History of prior IPV. 2. Recent IPV without observable injury. 3. Current history of IPV with observable injury. a. Report as required by state regulations. Determine the ICD (International Classification of Diseases) codes for IPV, which are divided into four categories (Rudman, 2000). 1. Adult maltreatment and abuse (995-81). 2. The primary diagnosis (underlying reason for admittance). 3. Modifier codes that provide details (E-codes). 4. History codes that provide information on previous incidents (V-codes). With ICD-10 implementation, code 995 will be replaced with T74 (confirmed) and T76 (suspected) and the coding will include: a. Suspected or Confirmed b. Encounter type (Initial encounter, Subsequent encounter, Sequela encounter) (Bryant, 2014) Assess for suicidal or homicidal ideation. Evaluate the safety of the patient and family members and children. Identify any immediate risk and need for emergency housing, legal, or social service consultations. Assess social support systems. Determine ongoing risk of IPV. Physical abuse ranking scale. More than five affirmatives indicate high danger (Wadman & Foral, 2007). 1. Throwing things, punching the wall—lower risk 2. Pushing, shoving, grabbing, throwing things 3. Slapping with an open hand 4. Kicking, biting 5. Hitting with closed fists 6. Attempted strangulation 7. Beating up, pinning to the wall or floor, repeated 8. Threatening with a weapon 9. Assault with a weapon—higher risk III. Assessment Evaluate the extent of any injuries and the need for imme-diate medical intervention. See T able 61-5 for additional components of the assessment. Assess the need for manda-tory reporting as cited in the respective state's penal codes (Durborow, Lizdas, O'Flaherty, & Marjavi, 2010). Legal requirement of health professionals to report suspected adult abuse to law enforcement is currently implemented in 16 states and remains a controversial issue. Victims report greater access to legal protection without the responsibility to report abuse themselves, a reduced sense of aloneness and guilt, teaching partners the seriousness of abuse, documenta-tion of the incident and potentially positive interaction with police. However, concerns such as the risk of retaliation, fear of lost custody of their children, anxiety induced by required interactions with a social worker or other government authorities, being victimized by the health system, financial responsibility for the intimate partner violence report, as well as loss of autonomy and confidentiality are reportedly more significant than the benefits (World Health Organization, 2013). Although mandatory reporting is thought by some 600 CHAPTER 61 | Intimate Partner Violence (Domestic Violence)
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Interventions designed to decrease health-risk behaviors, treat chronic health conditions or illnesses, and offer best practice first response to women who are victims of IPV can be offered to reduce the short-and long-term effects of violence on their physical and psychological health (Svavarsdottir & Orlygsdottir, 2009). Patient management includes treatment, consultation, referral, and follow-up care. In the event there is a history of recent sexual assault (within 72 hours), it is impor-tant to refer the patient to the sexual assault response team or emergency department. In most instances law enforcement involvement is necessary to authorize a forensic examination and a report is filed both via telecom-munications and in writing to the respective authorities. The clinician will follow the reporting guidelines as cited in the respective state's penal codes. C. Client/patient education Priority educational areas include the nature of IPV and the identification of emergency strategies. A per-sonalized safety plan for patients can be found at www. domesticviolence. org/personalized-safety-plan/ VI. Self-management r esources and tools A. Educational resources and support 1. The cl inician should be prepared to provide patient education brochures or frequently asked questions documents and to direct the patient to appropriate community agencies and support groups for victims of domestic violence (e. g., local shelters), statewide coalitions and helplines (e. g., Jane Doe in Massachusetts, APIADV in San Francisco, CA), and national resources, such as the National Domestic Violence Hotline (1-800 -799-SAFE, 1-800-799-7233, or www. thehotline. org), National Dating Abuse Helpline and Love Is Respect (1-866-331-9474, text 77054, or www. loveisrespect . org), or the National Sexual Assault Hotline (1-800 -656-HOPE or 1-800-656-4673). B. Resources for reducing stigma and increasing awareness of domestic violence 1. R esources for reducing stigma and increasing awareness of domestic violence can be found at www. nomore. org. Social media and campaign efforts may be appropriate for use within the clinic setting and to promote open disclosure with anticipatory guidance. C. Other services and resources 1. N ational Sexual Violence Resource Center (www . nsvrc. org)authorities to help the victim and perpetrator to receive treat-ment, many health professionals are concerned that victims may be discouraged from disclosing information based on compromised provider-patient confidentiality and individual autonomy. Other concerns include the expense in time and resources and the risk of retaliation or escalation in partner violence in the event of unsuccessful prosecutions (American College of Emergency Physicians, 2014; Feder, Wathen, & Mac Millan, 2013). Whether or not forensic requirements of the criminal justice system require mandated reporting, appropriate man-agement of the sexually assaulted patient is built upon thera-peutic communication and requires the clinician to address the medical and emotional needs of the patient within the context of patient-centered care. Providers must be informed of the laws governing mandated reporting in their regions. A summary of the Professions Mandated to Report can be found at www. ncsl. org/research/human-services/child-abuse-and-neglect-reporting-statutes. aspx#1 (Child Welfare Information Gateway, 2014). IV. Goals of clinical management The goals in managing victims of IPV include consistent screening through thoughtful inquiry in a safe and confiden-tial environment, identifying immediate injury and safety risks, appropriate reporting and referral, and the provision of information and support. Being aware of immigration concerns and cultural or ethnic differences is an important element in patient care. One of the earliest efforts to systemati-cally address IPV in the clinical environment was the develop-ment of RADAR, which remains commonly used in practice. RADAR summarizes action steps that the clinician can use to increase comfort and ability recognize and treat victims of IPV (Harwell et al., 1998) Remember to routinely inquire about partner violence Ask directly about violence (see questions in T able 61-3), always in a private area Document findings of suspected or reported partner violence in the patient's chart Assess patient safety (lethality or abuse scales) Respond, review patient options, and refer (Institute for Safe Families, 2002). V. Plan A. Diagnostic testing Obtain radiographs, computed tomography, or magnetic resonance imaging based on the extent of injury. B. Management (includes treatment, consultation, referral, and follow-up care)601 Self-management resources and tools
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A. Epidemiology 1. P revalence The prevalence of IBS is 1-2 in 10 or 10-20% of the population. Studies have also shown a preva-lence of 8-22 per 100 adults (Ringel et al., 2001). These numbers are difficult to assess because in many patients symptoms resolve and/or medical attention and treatment are not sought. Approximately 10-20% of patients with IBS actually seek care (Lehrer & Lichenstein, 2009). 2. I mpact The costs of healthcare use and absenteeism from work are substantial. It is estimated that approximately $8 billion is spent per year in the United States on the care of patients with IBS (Hauser, Pardi, & Poterucha, 2008). Annually, IBS accounts for 3. 5 million physician visits, 2. 2 million prescriptions, and 35,000 hospitalizations annually (Hauser, Oxentenko, & Sanchez, 2014). 3. R isk factors Female gender confers greater risk with a ratio of 2:1. These numbers may be somewhat inflated because females seek medical care more frequently than males; thus the number of men with IBS may not be accurately reported. The prevalence of IBS decreases with age; however, there have been rare cases of new-onset IBS in the elderly. There are no consistent racial or ethnic differences in individuals with and without IBS (Hauser et al., 2008). Although IBS seems to have a “familial component,” a confirmed genetic risk has not been clearly established. IBS has been associated with psychiatric illness and can also be exacerbated by stress, anxiety, and depression. Studies have shown that physical and sexual abuse may have a role in the development of IBS (Lehrer & Lichenstein, 2009). In some cases, the onset of symptoms can occur after acute I. Intr oduction and general background Irritable bowel syndrome (IBS) is a “functional bowel disorder,” a disorder of intestinal motility and visceral sensory perception. There are no structural or biochemical causes associated with IBS. Although often associated primarily with the lower intestinal tract, the signs and symptoms of IBS can be found along the entire gastrointestinal tract. The main symptoms of IBS are abdominal pain and discomfort associated with a change in the consistency or frequency of stool and relief of the pain with defecation (Ringel, Sperber, & Drossman, 2001). This constellation of symptoms led to the development of the Rome Criteria, which was done in conjunction with the World College of Gastroenterology in Rome, Italy, in 1998 (Rome I), again in 1999 (Rome II), and subsequently in 2006 (Rome III). The Rome criteria are used to aid in the diagnosis of IBS. The following is a list of the Rome III criteria for IBS diagnosis: recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months associated with two of the following features: Improvement with defecation, Onset associated with change in frequency of stool, and Onset associated with a change in the form of stools (Drossman, 2006). Other features that are included in the diagnosis are: Abnormal stool frequency (more than three bowel movements per day or less than three per week), Abnormal stool form, abnormal stool passage, passage of mucus, and abdominal bloating or distention (Drossman, Camilleri, Mayer, & Whitehead, 2002), and Exacerbation triggered by stressful life events. Diagnosis can be made if all other diagnoses, structural or metabolic, have been eliminated. One must keep in mind that symptom expression differs among patients and may be any combination of these factors. Karen C. Bagatelos, Geraldine Collins-Bride, and Fran Dreier Irr Ita Ble Bowel Syn Drome© Eliks/Shutterstock; © donatas1205/Shutterstock 60562Chapt Er
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inflammatory conditions of the gastrointestinal tract, such as postinfectious IBS. Food sensitivities and allergies may also have a role, although formal food allergy testing is generally not recommended. B. Pathophysiology The etiology of IBS is not completely understood. There are many possible mechanisms and causative factors. In some patients, IBS seems to be associated with visceral hyper-sensitivity as demonstrated by balloon distention studies (Yuan et al., 2003). These studies have shown that IBS patients have lower thresholds for pain. Balloon inflation in the sigmoid colon causes increased pain in IBS patients as opposed to normal controls (Horwitz & Fisher, 2001). Patients with IBS can have hypersensitivity throughout the entire digestive tract. IBS is also associated with altered bowel motility. Signals from the central nervous system are either exaggerated or diminished, which causes an increase or decrease in bowel motility (Horwitz & Fisher, 2001), thus explaining why some patients have diarrhea-predominant and others have constipation-predominant IBS. It has been postulated that serotonin or other neurotransmitters can play a role. There can be underexpression or overexpres-sion of some neurotransmitters or increased amounts of receptors in the central and enteric (intestinal) nervous system transmitting signals at abnormal rates. This etiology remains under investigation. The possible role of bacterial overgrowth and inflam-mation is also being investigated. Bacterial overgrowth may be the primary cause of IBS symptomatology in some patients as some individuals improve significantly with antibiotic treatment. In some patients, the flora of the digestive tract becomes imbalanced, with “bad” bacteria overcoming “good” bacteria. Psychosocial factors, such as stress and anxiety, and dietary factors can also play a role in the expression of this syndrome (Drossman et al., 2002). II. Database (may include but is not limited to) A. Subjective findings 1. P ast medical history a. M ultiple abdominal surgeries: can cause adhesions b. S urgery that has damaged the vagus nerve: any upper abdominal surgery, in particular gastric and esophageal surgeries, can cause diarrhea (Ukleja, Woodward, & Achem, 2002) c. P sychiatric illness, including trauma and abused. S ubstance abuse (including laxatives) e. Th yroid disease f. F ood sensitivities, especially lactose intolerance g. C arcinoid syndrome: causes profound diarrhea h. G astroesophageal reflux disease: frequently seen in patients with slow overall motility i. M edications prone to altering gastrointestinal motility, such as opiates, stimulants, or laxatives 2. F amily history: IBS, inflammatory bowel disease, colon cancer, diabetes, and thyroid disease 3. P sychosocial history a. H abits: alcohol, tobacco, or illicit drug use b. S ituational stressors, coping mechanisms, and social support systems c. E xercise and physical activity: sedentary lifestyle is commonly seen in patients with constipation and other bowel motility disorders d. Die t history: note typical diet, foods that trigger symptoms, amount of water and caffeine intake, use of artificial sweeteners (sorbitol, saccharin, or Nutra Sweet), chewing gum, and fiber intake 4. R eview of systems a. F ever, chills, weight gain or loss, and fatigue b. C hanges in skin, hair, nails, and other symptoms suggestive of thyroid disease c. L ower abdominal pain relieved with defecation, particularly in the left lower quadrant d. C onstipation, diarrhea, or alternating diarrhea and constipation e. B loating (upper and lower intestinal tract) and gas f. F requency of stools and presence of mucus or blood in the stool (patients with IBS typically do not have blood in the stool) g. A nxiety, depression, other psychiatric symptoms h. N ausea, vomiting, dyspepsia, and other upper gastrointestinal symptoms B. Objective findings 1. P hysical examination: a full physical examination is recommended with particular attention to: a. V ital signs (note any orthostatic changes), weight, and body mass index b. Th yroid examination c. A bdominal examination noting bowel sounds, any masses, and tenderness (especially in the left lower quadrant) d. P elvic examination noting any uterine or adnexal enlargement e. M ental status examination noting appearance, behavior, mood, affect, and thought content606 CHAPTER 62 | Irritable Bowel Syndrome
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III. a ssessment A. Determine the diagnosis IBS is a diagnosis of exclusion. That being said, many patients with IBS undergo expensive and unnecessary testing and continue to pursue diagnostic work-ups in search of the answer to “what is wrong with me?” The diagnostic and management approaches to patients with IBS rest with careful history and physical examination skills in additional to building a strong therapeutic alliance with the patient to help understand the underlying disorder and symptom-based treatment. The following diagnoses should be considered for all patients presenting with suspected IBS. 1. B acterial infections 2. C olon cancer 3. Div erticulosis and diverticulitis 4. Ea ting disorders 5. Ad hesions 6. F ecal incontinence 7. I n females: ovarian tumors, endometriosis, and adnexal cysts 8. I nflammatory bowel disease 9. A typical colitis, microscopic colitis, lymphocytic colitis, or eosinophilic gastroenteritis 10. Th yroid disease, diabetes, and other endocrine disorders 11. C eliac disease 12. D epression, anxiety, and other mental health disorders 13. P elvic floor dysfunction caused by pelvic floor damage 14. A rteriovenous malformations with bleeding 15. L arge polypoid mass (can cause constipation) or a malignant tumor 16. T rauma to the rectum 17. C arcinoid syndrome B. Severity Assess the severity of the disease. C. Significance Assess the significance of the symptoms and chronic nature of the disorder to the patient and significant others. IV. Goals of clinical management A. Assist the patient with medications, stress management, and psychosocial support. B. Prevent pain by performing adequate pain assessments and referring to pain management for assistance if needed. C. Assist the patient to achieve optimal level of functioning with daily activities and quality of life while living with a chronic, often relapsing disorder. V. Plan A. Screening There are no screening tests available for early detection or prevention of IBS. B. Diagnostic studies Based on symptoms and history 1. Die t diary. The diet diary is an essential initial diagnostic tool for IBS management. The diary helps both the patient and the clinician to make associations between symptoms and foods. It also engages the patient in a meaningful way as a partner in both the diagnostic and treatment processes. The diary should note time of meals and snacks, type and quantity of foods eaten, and associated gastrointestinal symptoms before or after food consumption, noting the time frame of symptom development. 2. F or recommended first-and second-line symptom-based diagnostic testing see T ables 62-1 and 62-2. 3. Al arm symptoms warranting a gastroenterology referral include: a. U nrelenting symptoms despite treatment b. R ectal bleeding, abnormal stool studies c. U nexplained anemia d. A norexia e. B lood in the stool f. S evere unrelenting diarrhea or constipation g. N octurnal symptoms h. On set in patients older than 50 years i. P alpable abdominal or rectal mass (Kolfenbach, 2007; World Gastroenterology Organization, 2009). These symptoms are particularly worri-some if the patient has a family history of inflam-matory bowel disease, celiac sprue, or colorectal cancer. C. Management The mainstay of any treatment regimen for patients with suspected or confirmed IBS is first and foremost to build a therapeutic alliance with the patient. The underpin-nings of this alliance include careful listening, valida-tion of symptoms, and compassion for the distress that 607 Plan
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Table 62-1 Initial Symptom-Based Diagnostic W ork-Up for Irritable Bowel Syndrome Diarrhea-Predominant Symptoms Constipation-Predominant Symptoms Upper Gastrointestinal- Predominant Symptoms Stool sample: culture and sensitivity, ova and parasites, and Clostridium difficile To rule out bacterial and parasitic infections Complete blood count with differential To look for evidence of anemia seen with malignancies, inflammatory bowel disease (IBD), and other systemic disease To look for leukocytosis seen with IBD and infections Upper gastrointestinal series with a small bowel follow-through To rule out structural abnormality or adhesions; also to evaluate transit time with constipation and diarrhea Stool sample for Giardia To rule out Giardia lamblia infection. Increased risk in individuals with immunocompromise and those with a recent travel history Thyroid-stimulating hormone To rule out hypothyroid disorders Abdominal sonogram To rule out gallstones Stool sample for fecal occult blood To rule out malignancy, IBD, and other systemic causes of intestinal bleeding Plain abdominal film (also called a “flat plate of the abdomen”) To look for a bowel obstruction or ileus, adhesions, and pseudo-obstruction Serum liver function tests To evaluate liver health and rule out hepatitis, cirrhosis, and other liver diseases Stool sample for fecal fat/pancreatic elastase Seen with malabsorption and pancreatic insufficiency Stool sample for fecal occult blood To rule out malignancy, IBD, and other systemic causes of intestinal bleeding Serum lipase and amylase To rule out pancreatitis Complete blood count with differential To look for evidence of anemia seen with malignancies, IBD, and other systemic disease To look for leukocytosis seen with IBD and infections Serum potassium and calcium To rule out hypokalemia and hypercalcemia, both associated with constipation Erythrocyte sedimentation rate Nonspecific marker of IBD and malignancy Fasting blood sugar To rule out diabetes mellitus, which can present with diarrhea because of diabetic gastroenteropathy Thyroid-stimulating hormone To rule out hyperthyroid disorders Electrolytes (depending on severity of symptoms) To look for electrolyte disturbances seen with severe diarrhea and malabsorption Data from American College of Gastroenterology Task Force on Irritable Bowel Syndrome. (2009); World Gastroenterology Organization Global Guideline. (2009). Irritable bowel syndrome: A global perspective, 1-20. 608 CHAPTER 62 | Irritable Bowel Syndrome
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corn syrup, and artificial sweeteners (sorbitol-containing products). It can be overwhelming to restrict all of these foods and substances at once. Often, selecting 1-2 food groups to eliminate and monitoring the effect is a reasonable approach to begin the dietary modification process. Referral to a nutri-tionist may also be helpful. b. Co ncentrated fiber to help form stools (i. e., 1/2-1 tablespoon daily working up to 1 heaping table-spoon of psyllium fiber or other similar fiber in 4 ounces of water one to three times per day, depending on symptoms and symptom response). Patients should try insoluble fiber, incorporated into their diet, such as whole grain foods, fresh fruits, fresh vegetables, wheat bran, and beans. Insoluble fiber absorbs water from the intestinal tract and helps to decrease diarrhea. c. L operamide, 4 mg orally two to four times daily, as needed to reduce stool frequency. d. E mpiric antibiotic trial (see options that follow) followed by a probiotic to treat bacterial over-growth and repopulate the intestines with ben-eficial flora. Probiotics have been found to be beneficial in some patients. A systematic review from the American College of Gastroenterology symptoms may cause for the patient. Such an alliance provides a platform for working with the patient through the symptom-based diagnostic and treatment process. There are few studies that offer convincing evidence of effectiveness in curing the IBS symptom complex (Akehurst & Kaltenthaler, 2001). Current treatment guidelines focus on symptom-based treatment manage-ment (World Gastroenterology Organization, 2009). 1. F or diarrhea-predominant symptoms: a. Die t All patients should try a low FODMAP diet. FODMAPs (fermentable oligo-, di-and mono-saccharides and polyols) are short-chain sugars that are poorly absorbed by the small intestine. Studies show that a low FODMAP diet may help reduce symptoms of gas, bloating, diar-rhea, and abdominal discomfort (Halmos, Power, Shepherd, Gibson, & Muir, 2014; Shepherd, Lomer, & Gibson, 2013). Limit the high FODMAP foods: gas-producing vegetables, such as onions, garlic, beans, broccoli, cabbage, Brussels sprouts, asparagus, and cauliflower. Other dietary restrictions include limiting dairy products, carbonated beverages, caffeine, alcohol, red meats, artifi-cial fats, sugars such as honey, high-fructose Table 62-2 Second-Line Symptom-Based Diagnostic W ork-Up for Irritable Bowel Syndrome Diarrhea-Predominant Symptoms Constipation-Predominant Symptoms Upper Gastrointestinal- Predominant Symptoms Celiac serologies (tissue transglutaminase Ig A most sensitive) To rule out celiac sprue disease Colonoscopy or flexible sigmoidoscopy with a barium enema To rule out mucosal (atypical colitis) or structural abnormalities Endoscopy To rule out celiac disease, gastric or duodenal ulcer, and gastroesophageal reflux disease with esophageal spasm Repeat stool sample for ova and parasites and Clostridium difficile To rule out a recurrent bacterial infection or C. difficile, commonly seen with recent history of antibiotic use Abdominal and pelvic computerized tomography scan To rule out cancer and other pathologic conditions Allergy testing (controversial) To look for food allergies Endoscopy To rule out celiac disease by taking small bowel biopsies looking for villous blunting with diarrhea, bloating, and pain Data from American College of Gastroenterology Task Force on Irritable Bowel Syndrome. (2009); World Gastroenterology Organization Global Guideline. (2009). Irritable bowel syndrome: A global perspective, 1-20. 609 Plan
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ii. L inaclotide (Linzess®), 290 mcg by mouth daily. Long-term safety profile is unknown. Consultation with gastrointestinal specialist is recommended. e. I ncrease oral fluids: water is best, followed by low-sugar-content fluids. f. P hysical activity: assist the patient in developing a regular daily exercise and activity plan. Physical activity has been shown to promote healthier bowel motility and overall better mental and physical health. 3. F or abdominal pain-predominant IBS: a. A ntispasmodic agents i. Dic yclomine (Bentyl®), 20 mg orally four times per day prn. Can titrate up to a maxi-mum of 160 mg per day. ii. H yoscyamine, 0. 125-0. 25 mg orally three-four times daily prn pain. T ake before food. Maximum dosage is 1. 5 mg in 24 hours. Because of anticholinergic properties, use these medications with caution in the geriatric population b. L ow-dose tricyclic antidepressants (help to reduce visceral sensation): amitriptyline 25 mg orally at bedtime, may titrate up to 100 mg at bedtime c. S erotonin reuptake inhibitor or other antide-pressant if depression is suspected. d. P ain management: suggest nonpharmacologic measures first, such as relaxation, acupuncture, and meditation. Avoid the use of narcotic analgesics because of their addiction potential. See Chapter 50 on chronic pain management for further suggestions. 4. F or alternating diarrhea and constipation: a. H igh-fiber diet (insoluble fiber) examples include whole grain foods; fresh fruits; fresh vegetables; wheat bran; beans; or a fiber supple-ment, such as psyllium husk, methylcellulose (Citrucel®), or Benefiber. The dose for constipa-tion is 1 tablespoon in 8 oz of fluid taken orally one to two times per day. The dose for diarrhea is 1 tablespoon in 4 oz of water taken orally one to three times per day. b. A ntidiarrheal medications during diarrhea phase (loperamide 4 mg orally two-three times daily) and laxative during constipation phase (poly-ethylene glycol, 18 g in 8 oz of liquid taken orally each day). c. E mpiric antibiotic followed by a probiotic. 5. F or abdominal bloating-predominant symptoms a. E mpiric antibiotic followed by a probiotic. T ask Force (2009) on the treatment of IBS concluded that Lactobacillus alone does not seem to be effective in single-organism studies and combinations of probiotic studies. However, Bifidobacterium does demonstrate some efficacy. Future studies are needed to determine the efficacy of specific strains of probiotics in the treatment of IBS (Aragon, Graham, Borum, & Doman, 2010). With further study, it may be possible to target symptoms with specific strains of bacteria that facilitate better targeting of treatment and enhanced efficacy (Spiller, 2008). At this time, it is not possible to make recommen-dations as to a specific brand or bacterial strain because no documented studies exist. There is also no standardization of these products. One of the following oral antibiotics regimens may be used:i. R ifaximin, 400 mg three times daily for 7 days ii. L evofloxacin, 500 mg daily for 7 days iii. C iprofloxacin, 500 mg twice daily for 7 days iv. M etronidazole, 500 mg three times daily for 7 days 2. F or constipation-predominant symptoms: a. H igh-fiber diet with the addition of dietary fiber, psyllium, or Benefiber® (i. e., 1 heaping table-spoon in 8 oz of fluids one to two times taken by mouth per day with plenty of water). Also, add insoluble fiber (see list mentioned previously). Insoluble fiber helps the stool absorb water to facilitate passage and prevent constipation. b. L axatives i. P olyethylene glycol (Miralax®), 18 g mixed in 8 oz of liquid one to two times per day, is very effective for constipation but patients may continue to experience bloating and abdominal pain ii. B isacodyl (Dulcolax®): 5-to 15-mg tablets as a single dose; may take up to 30 mg if com-plete bowel evacuation is needed; 10 mg suppository as a single daily dose prn iii. S enna or Cascara tablets should be avoided long term due to the increased risk of mela-nosis coli (dark pigment deposits in the lining of the large intestine), which can worsen constipation. c. E mpiric antibiotic treatment followed by a probiotic therapy as mentioned previously d. C hloride channel activator that acts to increase intestinal fluid secretion and intestinal motility:i. L ubiprostone (Amitiza®), 8 mcg orally twice daily, for women age 18 and older610 CHAPTER 62 | Irritable Bowel Syndrome
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d. U rinary 5-hydroxy indolacetic acid for carcinoid syndrome e. S mall bowel transit study for increased transit 3. P ain: evaluate small or large intestine for obstruction, intermediate obstruction, cancer, or adhesions. a. P lain abdominal radiograph for obstruction and intermediate obstruction b. C T scan of the abdomen for cancer and obstruction c. C T enterography for cancer, obstruction, and colitis d. U pper gastrointestinal series with a small bowel follow-through for adhesions; can also evaluate transit time E. Client education 1. A ssist the patient and family in verbalizing their concerns and coping strategies with respect to the disease process and management. 2. P rovide verbal and written information about the pathophysiology of IBS and treatment. 3. Di scuss what the patient can expect with diagnostic testing, preparation, and after-care. 4. E xplain the therapeutic benefits and side effects of any prescribed treatment. 5. R eassure the patient that assistance is available when needed. 6. E mphasize the importance of stress management and good mental health in coping with this disorderb. F ood diary to identify and eliminate any aggra-vating foods. c. Die t: avoid cruciferous vegetables (cauliflower, broccoli, cabbage, and so forth) and dairy products (T able 62-3). d. I ncorporate stress management strategies; if needed, refer for mental health treatment. In the event of refractory pain, a referral to gastroenter-ology is warranted. D. Follow-up Reevaluate the patient in 3-6 weeks after initial treatment program and evaluation are done. If symptoms persist, consider changing treatment regimen or obtaining further diagnostic testing as indicated based on predominant symptoms. The following are recommendations for further testing after the initial evaluation, which are often done by a gastroenterologist 1. R efractory constipation: evaluate colonic transit time, pelvic floor function, and adhesions by considering the following additional tests: a. C olonic transit test b. A norectal manometry c. R ectal sensation testing and emptying study 2. R efractory diarrhea: evaluate for bacterial over-growth, laxative abuse, atypical colitis, carcinoid syndrome, and increased colonic transit. a. S tool chemistry for surreptitious laxative abuse b. Duode nal aspirate for bacterial overgrowth c. C olonic biopsies for microscopic or collagenous colitis Table 62-3 Diet Strategies for the Management of Constipation and Diarrhea: A void the following Food S Constipation Diarrhea Prepared protein-laden foods: cooked, fried, baked, steamed, or canned Caffeine: found in coffee, tea, cola, and chocolate Wheat products: bread, pasta, cookies, pastries, and so forth Nicotine from cigarettes, chewing tobacco, and nicotine replacement products Supplementary iron Gas-producing foods, such as beans, broccoli, cabbage, and apples Dairy products: all dairy Dairy products that contain lactose Supplementary calcium High-sugar foods, such as juices, soda, candy, cookies, and other packaged sweets All processed foods Foods high in fat, such as bacon, sausage, butter, oils, and deep fried foods Sorbitol and xylitol, and other artificial sweeteners Data from American College of Gastroenterology Task Force on Irritable Bowel Syndrome. (2009); Halmos, E., Power, V., Shepherd, S., et al. (2014). A diet low in FODMAPs reduces symptoms of irritable bowel syndrome. Gastroenterology, 146-167. 611 Plan
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VI. Self-management e r esources A. The National Institutes of Health has multiple brochures for IBS patients (http://digestive. niddk. nih. gov/ddiseases/pubs/ibs/) B. Irritable Bowel Syndrome Association (www. ibsgroup. org/ibsassociation) C. IBS FODMAP Dieting Guide (www. ibsdiets. org/fodmap-diet/fodmap-food-list/) re Feren Ce S Akehurst, R., & Kaltenthaler, E. (2001). T reatment of irritable bowel syndrome: A review of randomized controlled trials. Gut, 48, 272-282. American College of Gastroenterology T ask Force on Irritable Bowel Syndrome. (2009). An evidence-based systematic review on the manage-ment of irritable bowel syndrome. American Journal of Gastroenterology, 104(Suppl. 1), S1-S35. Aragon, G., Graham, D. B., Borum, M., & Doman, D. B. (2010). Probiotic therapy for irritable bowel syndrome. Gastroenterology and Hepatology, 6(1), 39-44. Drossman, D. A. (2006). The functional GI disorders and the Rome III process. Gastroenterology, 130(5), 1377-1390. Drossman, D. A., Camilleri, M., Mayer, E. A., & Whitehead, W. E. (2002). AGA technical review on irritable bowel syndrome. Gastroenterology, 123(6), 2108-2131. Halmos, E., Power, V., Shepherd, S., Gibson, P. R., & Muir, J. G. (2014). A diet low in FODMAPs reduces symptoms of irritable bowel syndrome. Gastroenterology, 146(1), 67-75. Hauser, S. C., Pardi, D. S., & Poterucha, J. J. (2008). Mayo Clinic gastroen-terology and hepatology board review (3rd ed. ). Rochester, MN: Mayo Clinic Scientific Press. Hauser, S. C., Oxentenko, A. S., & Sanchez, W. (2014). Mayo Clinic gastro-enterology and hepatology board review (4th ed. ). Rochester, MN: Mayo Clinic Scientific Press. Horwitz, B. J., & Fisher, R. S. (2001). The irritable bowel syndrome. New England Journal of Medicine, 344, 1846-1850. Kolfenbach, L. (2007). The pathophysiology, diagnosis, and treatment of IBS. Journal of the American Academy of Physician Assistants, 20(1), 16-20. Lehrer, J. K., & Lichenstein, G. R. (2009). Irritable bowel syndrome. Retrieved from http://emedicine. medscape. com/article/180389-overview. Ringel, Y., Sperber, A. D., & Drossman, D. A. (2001). Irritable bowel syndrome. Annual Review of Medicine, 52, 319-338. Shepherd, S., Lomer, M., & Gibson, P. (2013). Short-chain carbohy-drates and functional gastrointestinal disorders. American Journal of Gastroenterology, 108(5), 707-717. Spiller, R. (2008). Review article: Probiotics and prebiotics in irritable bowel syndrome. Alimentary Pharmacologic Therapy, 28(4), 385-396. Ukleja, A., Woodward, T. A., & Achem, S. R. (2002). Vagus nerve injury with severe diarrhea after laparoscopic antireflux surgery. Digestive Diseases and Sciences, 47(7), 1590-1593. World Gastroenterology Organization. (2009). Irritable bowel syndrome: A global perspective. Milwaukee, WI: Author. Retrieved from www . worldgastroenterology. org/guidelines/global-guidelines /irritable-bowel-syndrome-ibs/irritable-bowel-syndrome-ibs-english. Yuan, Y. Z., T ao, R. J., Xu, B., Sun, J., Chen, K. M., Miao, F., et al. (2003). Functional brain imaging in irritable bowel syndrome with rectal balloon-distention by using f MRI. World Journal of Gastroenterology, 9(6), 1356-1360. 612 CHAPTER 62 | Irritable Bowel Syndrome
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B. Prevalence An estimated 43. 4% of Americans have total cholesterol levels ≥ 200 mg/d L and an estimated 31. 1% have LDL cholesterol levels ≥ 130 mg/d L (Centers for Disease Control and Prevention [CDC], 2011). Low-income adults and Mexican Americans are disproportionately affected by hyperlipidemia. C. Diagnostic classifications 1. I nherited disorders of LDL-metabolism a. D efinition and overview: Primary or genetic disorders of lipid metabolism are less common than other types of dyslipidemia, but they are often responsible for the most severe dyslipidemias. These disorders may be mono-genic or polygenic. They may result in elevated LDL-c with normal triglyceride levels or elevated triglycerides in isolation (see section C. 2., Hypertriglyceridemia). Most are rare outside of certain specific demographic groups. Primary disorders resulting in elevated LDL-c and normal triglycerides:i. F amilial hypercholesteremia ii. F amilial defective Apo B-100 iii. Aut osomal dominant hypercholesterolemia due to mutations in PCSK9 iv. Aut osomal recessive hypercholesterolemia v. S itosterolemia vi. P olygenic hypercholesterolemia vii. Ele vated plasma levels of lipoprotein(a) 2. H ypertriglyceridemia a. H ypertriglyceridemia is generally believed to be an independent risk factor for cardiovascular disease, but the amount of excess risk is small. Elevated levels of triglycerides are also associated with lower levels of HDL due to the physiology of metabolic pathways. b. M ay be primary, secondary, or multifactorial. I. Intr oduction and general background Cardiovascular disease (CVD) is the leading cause of death in the United States (Kochanek, Xu, Murphy, Miniño, & Kung, 2011). Many studies have demonstrated the relationship between serum cholesterol levels, particularly low-density lipoprotein (LDL-c) levels, with atherosclerosis and coronary vessel disease. For this reason, the identification and manage-ment of lipid disorders is of great significance in mitigating cardiovascular risk. Lipid metabolism involves several types of lipoproteins responsible for transporting cholesterol and triglycerides within endogenous and exogenous pathways for lipid synthesis and delivery, as well as reverse cholesterol transport. This phys-iology is not discussed in detail here; however, it is important to highlight that that different lipoproteins fulfill different roles. LDL's primary role is carrying cholesterol to extrahepatic cells, and its excess can result in atherogenesis. High-density lipoprotein (HDL) transports cholesterol from extrahepatic cells to the liver; it is antiatherogenic and higher levels of HDL are associated with lower cardiovascular risk. It is also important to remember that these pathways rely on normal functioning of the liver and the intestine, from where dietary cholesterol and triglycerides are absorbed. A. Definition and overview Lipid disorders are defined by elevations in serum lipids (cholesterol, phospholipids, or triglycerides). The phos-pholipids include LDL, HDL, very-low-density lipopro-teins (VLDL), intermediate-density lipoproteins (IDL), and chylomicrons. Lipid disorders fall into two main categories: (1) primary (genetic or inherited) disorders of lipid metabolism, and (2) lipid disorders that are secondary to other diseases (Durrington, 2003; Vodnala, Rubenfire, & Brook, 2012). For many patients, the causes of lipid disorders may be multifactorial with primary and secondary etiologies at play. Caitlin Garvey LIp Id d Isorders© Eliks/Shutterstock; © donatas1205/Shutterstock 61363Chapt Er
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c. P rimary lipid disorders causing elevated triglyc-erides and normal LDL i. F amilial chylomicronemia ii. A po A-V deficiency iii. GPI HBP1 deficiency iv. H epatic lipase deficiency v. F amilial dysbetalipoproteinemia vi. F amilial hypertriglyceridemia: autosomal dominant disorder and causes moderately elevated triglyceride levels vii. F amilial combined hyperlipidemia d. S econdary causes include obesity, type 2 diabetes with poor glycemic control, nephrotic syndrome, hypothyroidism, and pregnancy. Associated med-ications include tamoxifen, beta-blockers, immu-nosuppressives, HIV antiretrovirals, and retinoids. e. V ery high levels of triglycerides are associated with pancreatitis. In patients with hypertriglyc-eridemia, additional factors associated with pancreatitis include poorly controlled diabetes, excessive alcohol use, and drug-or diet-induced hypertriglyceridemia. 3. S econdary disorders of lipoprotein metabolism a. T ype 2 diabetes is one of the most important secondary causes of hyperlipidemia in primary care. b. Othe r secondary causes include: i. E xcessive alcohol use ii. H ypothyroidism iii. Obe sity iv. P regnancy v. C holestatic liver disease vi. N ephrotic syndrome vii. I mmunoglobulin excess viii. T obacco use (smoking) ix. M edications: oral estrogens, steroid hor-mones, protease inhibitors, and some atypical antipsychotics D. Treatment of hypercholesteremia for secondary prevention 1. Thi s includes treatment for patients with known coronary heart disease (CHD), cerebrovascular disease, or peripheral artery disease (PAD) E. Treatment of hypercholesteremia for primary prevention 1. Be cause the risk of cardiovascular disease (CVD) related events is smaller for those without known CVD, the absolute benefit of lipid-lowering therapy is smaller in primary prevention. II. d atabase A. Subjective 1. P ast health history a. C VD (coronary artery disease [CAD]/coronary heart disease [CHD], myocardial infarction [MI], angina, coronary revascularization, peripheral vascular disease, abdominal aortic aneurysm)i. P remature CAD should raise suspicion for primary lipid disorders b. H ypertension c. C erebrovascular disease d. E xcessive alcohol use e. H ypothyroidism f. Obe sity g. P regnancy h. C holestatic liver disease i. N ephrotic syndrome j. I mmunoglobulin excess k. P ancreatitis l. Di abetes mellitus 2. M edications a. M edications that can promote hyperlipidemia: oral estrogens, steroid hormones, protease inhibitors, and some atypical antipsychotics b. M edications that can promote hypertriglyceri-demia: tamoxifen, immunosuppressives, HIV antiretrovirals, and retinoids 3. F amily history a. F irst-degree relative(s) with dyslipidemia b. F irst-degree relative with premature CHD (e. g., before age 55 in men and 65 in women) 4. P ersonal-social history: health-related behaviors a. H igh dietary saturated fat and cholesterol intake (total cholesterol and LDL) b. E xcess total calorie intake c. S edentary lifestyle d. T obacco use (current and former) e. E xcess alcohol use B. Objective 1. P hysical exam a. M ost cases will lack physical exam findings, yet some findings may include:i. T endon xanthomas (may be seen in primary/ severe hyperlipidemias) ii. X anthelasmas (may be seen in primary/ severe hyperlipidemias)614 CHAPTER 63 | Lipid Disorders
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iii. P hysical exam may reveal evidence of secondary causes (e. g., findings consistent with diabetes mellitus) or pancreatitis b. Di agnostic tests i. L ipid panel reference ranges (adults) a. T otal cholesterol: 125-200 mg/d L b. LDL : < 130 mg/d L c. H DL: ≥ 40 mg/d L d. T riglycerides: ≤ 150 mg/d L e. V ery high triglycerides: ≥ 500 mg/d L ii. R isk calculators a. P ooled Cohort Equation (Stone et al., 2014) b. F ramingham (D' Agostino et al., 2008) III. Assessment A. Determining diagnosis 1. H yperlipidemia (pure, mixed, or unspecified) 2. H ypertriglyceridemia 3. S econdary causes of lipid disorders (e. g., type 2 diabetes with diabetic hyperlipidemia or hyperlipidemia due to steroid) B. Severity 1. A ssess severity of the disease with a need to treat based on history, physical, diagnostics, and calculated risk estimates using risk calculator C. Significance 1. A ssess significance to patient 2. C onsider significance to caregivers and family D. Motivation 1. A ssess patient's preferences and willingness to adhere to recommended treatment plan IV. Goals of clinical management A. Screening 1. U se cost-effective and evidence-based tools to identify patients at elevated risk for CVD events B. Treatment 1. R educe risk of CVD event C. Patient adherence 1. D evelop plan that fits patient preferences and ability to adhere to treatment V. p lan A. Screening 1. U. S. Preventive Services T ask Force (USPSTF) strongly recommends screening for lipid disorders in: a. M en ≥ 35 years old (Grade A) b. W omen ≥ 45 years old at elevated risk for coronary heart disease (CHD) (Grade A) c. M en 20-35 years old at elevated risk for CHD (Grade B) d. W omen 20-45 years old at elevated risk for CHD (Grade B) e. R isk factors for CHD: diabetes, previous history of CHD or noncoronary atherosclerosis, family history of cardiovascular disease before the age of 55 in first-degree male relatives or age 65 in first-degree female relatives, tobacco use, hyper-tension, and obesity. Grade d efinition A The USPSTF recommends the service. There is high certainty that the net benefit is substantial. B The USPSTF recommends the service. There is high certainty that the net benefit is moderate or there is moderate certainty that the net benefit is moderate to substantial. C The USPSTF recommends selectively offering or providing this service to individual patients based on professional judgment and patient preferences. There is at least moderate certainty that the net benefit is small. Modified from U. S. Preventive Services Task Force. (2008). Lipid disorders in adults (cholesterol, dyslipidemia): Screening. Retrieved from http://www. uspreventiveservicestaskforce. org/Page/Document/Update Summary Final/lipid-disorders-in-adults-cholesterol-dyslipidemia-screening. 2. U. S. Preventive Services T ask Force does not make recommendations for or against routine screening regarding screening for men 20-35 years old and women who are not at increased risk for CHD (Grade C). 3. N ote USPSTF Grade Definitions (U. S. Preventive Services T ask Force, 2008)615 Plan
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high-glycemic, and high-fructose foods. Particu-larly important for patients with very high tri-glycerides to avoid “refeeding” or binging, which can precipitate pancreatitis. b. P harmacologic management directed at lower-ing CVD risk: There are limited data to guide who is treated for hypertriglyceridemia and what medication to select. Cardiovascular risk reduc-tion can be achieved with statins and given this is the primary goal of all lipid-lowering therapy, they are considered first line even though they are not particularly effective in lowering serum triglyceride levels. c. P harmacologic management directed at lower-ing triglycerides: gemfibrozil, fenofibrate, nico-tinic acid, fish oil 5. T reatment of hypercholesteremia for secondary prevention a. Die t and lifestyle interventions are first line. b. A merican Heart Association diet (American Heart Association, 2014a) i. L ow saturated fat ii. Ae robic exercise iii. H ealthy weight c. P harmacologic management: American College of Cardiology (ACC) and American Heart Association (AHA) cholesterol treatment guide-lines (Stone et al., 2014)i. C ompared to previous guidelines, ACC/ AHA 2013 guidelines focus on statin therapy tailored for cardiovascular risk as assessed by their newly developed Pooled Cohort Equation. These guidelines deem-phasize previously relied upon LDL targets and nonstatin therapy. ii. S tatin therapy (see T able 63-1) a. C heck baseline liver enzymes and TSH prior to initiating statin therapy b. N onstatin therapy is not currently recommended as first-line pharmaco-logic management. Nonstatin agents may be used if statin therapy is contrain-dicated or not tolerated (see T able 63-2, Lipid-Lowering Agents). c. N onstatin agents do not add additional benefit when used in conjunction with statins iii. E ngage in evidence-based treatment of underlying disease contributing to disor-dered lipid metabolism, such as diabetes. B. Diagnostics 1. E valuate for primary causes a. H ypertriglyceridemia: suspect primary cause if fasting plasma triglycerides > 1,000 mg/d L b. Ele vated LDL-c: if levels greater than 95th percentile, suspect primary hyperlipidemia c. M olecular studies: rarely indicated given diagnosis is usually clinical and differentiation between specific types of primary hyperlipid-emias rarely informs management d. E valuate for secondary causes i. Di abetes: fasting glucose and/or glycohe-moglobin ii. E xcessive alcohol use: Alcohol Use Disorders Identification T est (AUDIT-c) (Bush, Kivlahan, Mc Donell, Fihn, & Bradley, 1998) iii. H ypothyroidism: thyroid-stimulating hor-mone (TSH) iv. N ephrotic syndrome and chronic renal insuf-ficiency: urine protein and serum creatinine v. H epatitis and cholestasis: liver function tests vi. Dr ugs: careful medication reconciliation e. P atient monitoring i. L ipid panels every 6-12 months to ensure adherence and efficacy of therapy C. Management 1. Befor e initiating therapy for any type of lipid disorder, evaluate and treat for hypothyroidism, nephrotic syndrome, and obstructive liver disease 2. E ven for patients with suspected or known primary hyperlipidemias, management should always involve evaluation and treatment of secondary causes 3. I nherited disorders of LDL-c metabolism a. S tatins and a second therapy (usually absorption inhibitor and/or bile acid sequestrant) are generally required at minimum. In some cases, particularly for patients with homozygous familial hypercholesterolemia, additional agents are required. b. A pheresis, a method for removing LDL from the blood, can also be used when pharmacologic therapy is not enough. 4. H ypertriglyceridemia a. L ifestyle: weight management with aerobic exercise and dietary portion control, low-fat diet with avoidance of high-carbohydrate, 616 CHAPTER 63 | Lipid Disorders
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Table 63-1 Summary of Statin Therapy statin Classification Indication Ther apy High Intensity Patients age ≤ 75 with clinical ASCVD* Patients with type 1 or 2 diabetes between 40 and 75 years of age and estimated 10-year risk ≥ 7. 5% †‡ Patients with LDL-c ≥ 190 mg/d L Expected to lower LDL-c ≥ 50% Atorvastatin 40-80 mg, Rosuvastatin 20-40 mg Moderate Intensity Patients age > 75 with clinical ASCVD Patients with type 1 or 2 diabetes between 40 and 75 years of age and estimated 10-year risk < 7. 5% Patients between 40 and 75 year of age with an LDL between 70 and 189 mg/d L and estimated 10-year risk ≥ 7. 5% Patients who are recommended, but cannot tolerate high-intensity statin therapy Expected to lower LDL-c 30-49% Atorvastatin 10-20 mg, Rosuvastatin 5-10 mg, Simvastatin 20-40 mg, Pravastatin 40-80 mg, Lovastatin 40 mg, Fluvastatin XL 80 mg, Fluvastatin 40 mg bid, Pitavastatin 2-4 mg Low Intensity Not recommended in AHA/ACC 2013 guidelines May be considered in patients who are recommended, but cannot tolerate, high-or moderate-intensity statin therapy Expected to lower LDL-c < 30% Simvastatin 10 mg, Pravastatin 10-20 mg, Lovastatin 20 mg, Fluvastatin 20-40 mg, Pitavastatin 1 mg *Clinical atherosclerotic cardiovascular disease (ASCVD) includes patients with history of acute coronary syndrome, myocardial infarction, angina, coronary revascularization, stroke, transient ischemic attack, or peripheral artery disease. †Pooled Cohort Equation can be used to estimate 10-year risk. This equation incorporates age, sex, race, total cholesterol, HDL cholesterol, systolic blood pressure, antihypertensive therapy, diabetes diagnosis, and tobacco use. ‡There is limited data for adults under age 40. If the adult under age 40 has diabetes and estimated 10-year risk ≥ 7. 5%, it is reasonable to consider statin therapy Adapted from Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Merz, C. N. B., Blum, C. B., Eckel, R. H., et al. (2014). 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Circulation, 129(25 Suppl. 2), S1-45. Table 63-2 Lipid-Lowering Agents Class Notes Statin (HMG-Co A reductase inhibitors)Block the enzyme required for a rate-limiting step in the synthesis of cholesterol. This is the only class of lipid-lowering medication shown to reduce mortality and is the only class advised by 2013 AHA/ACC guidelines. Statins lower LDL, lower triglycerides, and modestly raise HDL. Adverse effects include, but are not limited to, hepatotoxicity, myopathy, and increased risk for diabetes. Fibrates Includes gemfibrozil and fenofibrate. Works by inhibiting the secretion of VLDL (which transports endogenous triglycerides and cholesterol). Generally used to lower triglycerides, given limited efficacy in lowering LDL. Side effects include dyspepsia, gallstones, and myopathy. Absorption Inhibitors Includes ezetimibe. Works by blocking intestinal absorption of cholesterol. Effective in lowering LDL-c, particularly when used in combination with statin. Does not significantly affect triglycerides or HDL-c. Bile acid sequestrants Includes cholestyramine and colestipol. Works by reducing bile acid reabsorption from the intestine causing the liver to use available cholesterol for increased bile acid synthesis. Most common side effects are gastrointestinal related (bloating, constipation). Nicotinic acid (niacin) Reduces LDL-c and triglycerides. Can cause flushing and increased blood glucose levels. 617 Plan
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refere NCes American Heart Association. (2014a). The American Heart Association's diet and lifestyle recommendations. Retrieved from http://www. heart. org /HEARTORG/Getting Healthy/Nutrition Center/Healthy Eating/The -American-Heart-Associations-Diet-and-Lifestyle-Recommendations _UCM_305855_Article. jsp. American Heart Association. (2014b). Heart360. Retrieved from https:// www. heart360. org/Default. aspx?cid=9ea5cba5ffa4c87aab69dcac799a 03de. Bush, K., Kivlahan, D. R., Mc Donell, M. B., Fihn, S. D., & Bradley, K. A. (1998). The AUDIT alcohol consumption questions (AUDIT-C): An effective brief screening test for problem drinking. Ambulatory care quality improvement project (ACQUIP). Archives of Internal Medicine, 158(16), 1789-1795. Centers for Disease Control and Prevention. (2011). Vital signs: Prevalence, treatment, and control of high levels of low-density lipoprotein cholesterol. United States, 1999-2002 and 2005-2008. MMWR, 60(4), 109-114. D' Agostino, R. B., Sr., Vasan, R. S., Pencina, M. J., Wolf, P. A., Cobain, M., Massaro, J. M., et al. (2008). General cardiovascular risk profile for use in primary care: The Framingham heart study. Circulation, 117(6), 743-753. Durrington, P., (2003). Dyslipidaemia. Lancet, 362(9385), 717-731. doi: 10. 1016/S0140-6736(03)14234-1. Kochanek, K. D., Xu, J. Q., Murphy, S. L., Miniño, A. M., & Kung, H. C. (2011). Deaths: Final data for 2009. National Vital Statistics Reports, Vol. 60, No. 3. Hyattsville, MD: Centers for Disease Control and Prevention, National Center for Health Statistics. National Heart, Lung, and Blood Institute. (2014). Heart & vascular diseases. Retrieved from http://www. nhlbi. nih. gov/health/resources/heart. Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Merz, C. N. B., Blum, C. B., Eckel, R. H., et al. (2014). 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association T ask Force on Practice Guidelines. Circulation, 129(25, Suppl. 2), S1-S45. U. S. Preventive Services T ask Force. (2008). Lipid disorders in adults (cholesterol, dyslipidemia): Screening. Retrieved from http://www . uspreventiveservicestaskforce. org/Page/T opic/recommendation -summary/lipid-disorders-in-adults-cholesterol-dyslipidemia-screening. Vodnala, D., Rubenfire, M., & Brook, R., (2012). Secondary causes of dyslipidemia. American Journal of Cardiology, 110(6), 823-825. doi:10. 1016/j. amjcard. 2012. 04. 062. d. T reatment of hypercholesteremia for primary prevention i. Die t and lifestyle ii. I f treatment is pursued, consider moderate- or high-intensity statin iii. N onstatin lipid-lowering medication is not recommended in primary prevention 6. I nterprofessional team use and referral a. E ndocrine: Consider for refractory hyperlipid-emia or difficult to treat hyperlipidemias related to diabetes, obesity, or thyroid disease. b. N utrition: For overweight patients, weight loss through diet and physical activity c. T obacco cessation: The importance of tobacco cessation in reducing cardiovascular risk cannot be understated. For patients who use tobacco, motivational interviewing, nicotine replacement, pharmacologic therapy, and group support should be considered and offered as appropriate at each encounter. VI. s elf-management resources and tools A. Patient education 1. I nform the patient and/or caregiver that hyperlipidemia, especially elevated triglycerides, is associated with alcohol misuse and poor diet. Low HDL is associated with sedentary lifestyle, obesity, and smoking. B. Online resources 1. A merican Heart Association's Heart360 (American Heart Association, 2014b) 2. N ational Heart, Lung, and Blood Institute's heart and vascular disease patient information online publications (National Heart, Lung, and Blood Institute, 2014)618 CHAPTER 63 | Lipid Disorders
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(in order of frequency) ankylosing spondylitis, cord com-pression, a compression fracture, cancer, or cauda equine syndrome (see description in the following section) (Chou et al., 2007). These guidelines review the history and physical exam (PE) necessary to differentiate mechanical or degenerative LBP from more urgent causes. The treatment and patient education for causes of LBP that are appropriately managed by primary care providers are emphasized. For most patients, the history and physical exam is sufficient to exclude the “red flags” that suggest more serious disorders (T able 64-2) (Ehrlich, 2003). II. Database (may include but is not limited to) A. Subjective 1. H istory of present illness a. On set and duration (intermittent vs. constant) b. C ircumstances when first occurred (trauma? work related?) c. L ocation and radiation of pain: Atypical loca-tion such as midback is more common in cancer. Pain that is localized in the midbuttock may not be a spinal problem. The less frequently occur-ring piriformis syndrome (PS) is due to inflam-mation or spasm of the piriformis muscle that follows overuse or athletic injury. Because the muscle overlies the sciatic nerve, irritation of the piriformis muscle can cause the same sciatic nerve entrapment symptoms (see Section 7) as lumbosacral disorders. Thus, it is often difficult to differentiate. d. Qual ity and severity of pain: use specific descrip-tors and pain severity scale. e. P rogression of symptoms over time: Symptoms lasting > 3 months represent “chronic” LBP. I. Intr oduction/general background The lumbosacral spine is the fulcrum of the body. Its skeletal structure, muscles, and ligaments bear the stressors of bend-ing over, straightening up, lifting, carrying, and supporting the body's weight. So it is not surprising that up to 60% of the U. S. population will experience low back pain (LBP) at some time during their adult life (van Tulder, Koes, & Bombardier, 2002). After upper respiratory infections, back pain is the next most common reason to seek nonemergency care (Atlas & Deyo, 2001). The differential diagnosis for LBP is lengthy, and a precise diagnosis cannot be made in more than 80% of cases (Chou et al., 2007); yet 80% of episodes of LBP in a primary care setting will spontaneously improve in 1-2 weeks, and 90% resolve within 6 weeks. The diagnostic challenge is to identify those patients who require a more extensive or urgent evaluation at their initial presentation (Papadakis & Mc Phee, 2015). The differential diagnosis for LBP includes both muscular and focal spine disorders (i. e., disc herniation, spinal fracture, and stenosis of the spinal canal), regional nonspinal disorders (i. e., pelvic inflammatory disease, aortic aneurysm, and kidney stones), and systemic diseases (such as ankylosing spondylitis and metastatic cancer). Even if anatomic defects like narrowed disk space or the vertebral osteophytes of degenerative arthritis are found on x-rays, causality cannot be absolutely assumed, because these defects are also common in asymptomatic patients and increase in frequency with age (Ehrlich, 2003). In fact, more than one-third of asymptomatic individuals older than age 60 will have evidence of disc herniation or spinal stenosis on specialized imaging (Ehrlich, 2003). T able 64-1 lists the potential causes of LBP grouped by category. The most common causes are pain due to mechanical or degenerative processes. The most frequent sources of pain in these categories are lumbar-sacral strain and symp-tomatic herniated disc (Chou et al., 2007). The obligation for the clinician is to promptly identify those other patients whose pain may be due to urgent causes (“red flags”), such as H. Kate Lawlor Low Bac K Pa In© Eliks/Shutterstock; © donatas1205/Shutterstock 61964Chapt Er
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Table 64-1 Most Common Causes of Low Back Pain I. Mechanical (74%) A. Poor back or core abdominal muscle tone (may be secondary to obesity, pregnancy, or deconditioning) B. Chronic postural or lumbar-sacral strain II. Structural/Degenerative (17%) A. Degenerative joint disease (osteoarthritis, degenerative disc disease, facet process) (10%) B. Sacroiliitis C. Scoliosis, kyphosis D. Disc protrusion or herniation (4%) E. Spinal stenosis (narrowing of spinal canal) (3%) F. Osteoporosis G. Piriformis syndrome H. Cauda equina syndrome (characterized by lower extremity weakness and sensory loss, saddle anesthesia/fecal incontinence, urinary retention or incontinence) III. T rauma (6%) A. Fall B. W ork-related injury C. Compression fracture due to fall, osteoporosis, or chronic steroid use (4%) D. Subluxation of facet joint (spondylolisthesis) (2%) IV. Inflammatory Diseases (0. 3%) A. Ankylosing spondylitis (or other spondyloarthropathies) B. Rheumatoid arthritis V. Infection (0. 03%) A. Osteomyelitis B. Urinary tract infection (from indwelling catheter) C. T uberculosis D. IV drug abuse VI. Cancer (0. 7%) A. Multiple myeloma B. Metastatic cancer of prostate, breast, and lung C. Spinal cord tumors VII. Visceral Disease (2%) A. Dissecting abdominal aneurysm (usually history of hypertension) B. Renal disease C. Pelvic disease VIII. Psychogenic A. T ension/stress related B. Malingering (more often in setting of worker' s compensation claim) Data from Atlas, S., & Deyo, R. (2001). Evaluating and managing acute low back pain in the primary care setting. Journal of General Internal Medicine, 16, 120-131. 620 CHAPTER 64 | Low Back Pain
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Table 64-2 History and Physical Examination Findings Associated with Increased Likelihood of Serious Spine Condition (“red flags”) Disorder History Physical Exam/Studies for Diagnosis All Failure to improve > 6 weeks No relief with bed rest Cancer Age > 50 yrs Previous history of cancer (esp. multiple myeloma) Unexplained weight loss of > 10 lbs in 6 months Failure to improve after 1 month; worse at night No relief with bedrest Lymphadenopathy Plain lumbar-sacral (LS) spine films Magnetic resonance imagining (MRI) Elevated erythrocyte sedimentation rate (ESR) Fracture Age > 50 yrs; especially > 70 yrs Weight < 57 kg History of cancer (causes lytic metastases) History of smoking (increased risk of osteoporosis) History of significant trauma (fall from height, motor vehicle accident, or direct blow) History of osteoporosis Long-term steroid use (causes decreased bone density) Substance abuse (increased risk of falls; alcohol use) V ertebral point tenderness Plain LS spine film Bone Infection Fever, chills Pain increased at rest Recent skin or genital-urinary infection (history of indwelling catheter) Recreational injection drug use Immunosuppression Fever > 100ºF T enderness over a spinous process MRI Elevated ESR, positive C-reactive protein, elevated white blood count Ankylosing Spondylitis Male > female; < 45 years old Positive family history of irritable bowel disease (IBD), ankylosing spondylitis Pain > 3 mos; especially buttock pain Pain in latter part of night; morning stif fness Pain improved with exercise May be associated with IBD, psoriasis, uveitis, plantar fasciitis, or Achilles tendinitis May be decreased chest expansion Decreased spinal flexibility in sideways, frontal, and backward motions May be sacroiliac (SI) joint tenderness May be radiologic evidence of sacroiliitis on anteroposterior pelvic plain films Elevated ESR, positive C-reactive protein 90% + histocompatibility complex (HLA)-B27 Cauda Equina Syndrome Urinary retention or incontinence Bowel incontinence Progressive leg/foot weakness Sensory loss in lower extremity(ies) Saddle anesthesia Diminished anal sphincter tone Severe unilateral or bilateral leg/foot weakness Bladder distension MRI Data from Atlas, S., & Deyo, R. (2001). Evaluating and managing acute low back pain in the primary care setting. Journal of General Internal Medicine, 16, 120-131; Chou, R., Qaseem, A., Snow, V., Casey, D., Cross, J. T. Jr., Shekelle, P.,... American Pain Society Low Back Pain Guidelines Panel. (2007). Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Annals of Internal Medicine, 147(7), 478-491. 621 Database
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vi. Ac upuncture vii. H eat/cold application n. A ssociated signs and symptoms i. C onstitutional symptoms: fever, malaise, fatigue, weight loss (each suggests a more serious concern: osteomyelitis, abscess, or cancer) ii. O cular: painful, inflamed, or gritty eye (uveitis is associated with ankylosing spondylitis) iii. N eurologic a. S ciatica: burning pain that radiates down the posterior or lateral aspect of one or both legs past the knee—95% sensitive for nerve root irritation (Atlas & Deyo, 2001). Sciatica occurs with herniated disc, spinal stenosis, and piriformis syndrome. Other neu-rologic abnormalities and location of pain found in setting of sciatica help to identify which nerves are affected. See T able 64-3. b. S harp back pain when coughs or sneezes (indicative of disc compression) c. L eg pain with standing or walking (neurogenic claudication); relief with sitting (suggests spinal stenosis) d. L eg or foot weakness; gait disturbance; urinary retention or urinary incon-tinence; bowel incontinence (these f. A ggravating and alleviating factors g. W orse with bending, lifting, prolonged standing, or sitting (most common with mechanical back pain) h. W orse in AM: if pain less than 30 minutes after waking or shifting positions, suggests degenera-tive changes of vertebrae. i. R elief with activity; worse with rest (typical of ankylosing spondylitis) j. R elief with sitting or bending forward (sugges-tive of spinal stenosis) k. W orse with cough, bowel movement, or sneezing (suggests disc pathology) l. C omplaints of urinary retention or incontinence from loss of sphincter function, bilateral motor weakness of lower extremities, and decrease in sensation over buttocks or perineum (“saddle anesthesia”) suggest cauda equina syndrome—usually due to massive, centrally herniated disc causing compression of nerve roots of lower cord segments. m. I nterventions attempted to relieve pain and resultsi. M edications: (aspirin [ASA], nonsteroidal anti-inflammatory drugs [NSAIDS], acet-aminophen [Tylenol], and opioids) ii. H erbal products iii. C hiropractic care iv. P hysical therapy v. Ma ssage Table 64-3 Specific Nerve Root Impingements Associated with Particular Physical Examination Findings Strength Unilateral a ltered Sensation Reflex n erve Root Iliapsoas: have the patient seated with legs dangling over the edge of the examination table. Then stabilize the pelvis by placing your hand over the iliac crest while the patient actively raises the thigh from the table. Second, place your other hand over the distal femoral portion of the knee, and ask the patient to attempt to raise the thigh further from the table while you resist this motion. Compare resistance results testing on the other, uninvolved side (Hoppenfeld, 1976, p. 250). Anterior thigh/groin — L2 Quadriceps: squatting then rising, or strengthening a bent knee against resistance while seated Anterolateral thigh Patellar L3 Quadriceps; ankle dorsiflexion (heel walking) Medial ankle/foot Patellar L4 First toe dorsiflexion Dorsum of foot — L5 Ankle plantar flexion (toe walking) Lateral plantar foot Achilles S1 Note: Over 95% of herniated discs involve the L4-5 or L5-S1 interspaces (Chou et al., 2007). Data from Atlas, S., & Deyo, R. (2001). Evaluating and managing acute low back pain in the primary care setting. Journal of General Internal Medicine, 16, 120-131; Hoppenfeld, S. (1976). Physical exam of the spine and the extremities. East Norwalk, CT: Appleton-Century-Crofts/Prentice-Hall. 622 CHAPTER 64 | Low Back Pain
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f. C urrent worker's compensation claim or perma-nent disability g. J ob satisfaction 5. P ersonal/social (factors that may predict poorer or delayed resolution) a. Othe r pending litigation: occupational or trauma b. I mpact of pain on activities of daily living (ADLs) or current relationships c. H istory of depression d. Outs tanding disability claims e. P revious worker's comp claims f. H abits i. S moking (risk factor for osteoporosis) ii. I njectable drug use (risk factor for spinal infection) iii. A lcohol use (be alert to increased use for self-medicating pain) iv. R ecreational drug use B. Objective: physical exam Patient should be undressed. Exam should include but is not limited to: 1. H eight (loss of height suggests kyphosis, compression fracture) 2. W eight (unexplained weight loss may suggest cancer; low body weight is risk factor for osteoporosis; obesity is risk factor for osteoarthritis) 3. A ge (> 50 yrs at greater risk for cancer; > 75 yrs at greater risk for osteoporosis) 4. Ge nder (males at greater risk for ankylosing spondylitis; females > 30 yrs are largest population for PS). 5. V ital signs, including temperature (fever > 100°F suggests infection) 6. S pine (performed with patient unclothed in gown and underwear) In the absence of a history suggestive of a serious condition, systemic disease, and/or illness not local-ized to the back region (see T able 64-1), a focused spine and neurologic exam as described next should be an adequate screening exam to rule out serious or urgent causes of LBP, unless any red flags (see T able 64-2) are identified (Ehrlich, 2003). a. I nspection: look for changes in normal spine cur-vature that may occur if muscle spasm, scoliosis, hyperkyphosis, or ankylosing spondylitis b. S tanding: assess symmetry and posture c. P alpation: assess for bone tenderness versus muscle spasm. With patient forward flexed, assess for lateral curvature and rotation of the spine; may suggest scoliosis. Exclusively lateral symptoms in the aggregate suggest cauda equina syndrome resulting from cord compression, a surgical emergency) iv. A bdominal: pain or diarrhea (inflammatory bowel disease can be associated with anky-losing spondylitis) v. Ge nitourinary: dysuria, urinary frequency or urgency, recent indwelling catheter use (suggests urinary tract infection, pyelo-nephritis may present with flank pain and fever). Vaginal discharge, pelvic pain (sug-gests pelvic infection) vi. V ascular: chest pain or throbbing abdo min al pain (LBP with these symptoms may signal an abdominal aortic aneurysm) vii. S kin: history of psoriasis (associated with ankylosing spondylitis) or recent skin infection (may cause spinal infection) viii. P sychologic: recent sleep disturbances, depressed or anxious mood, diminished participation in social activities (may signal depression) o. P atient's concern/theory about of source of symptoms 2. P ast health history a. P rior spinal diagnoses, fractures or surgery, history of current or previous cancers b. P revious radiologic or imaging studies of spine. Prior bone density testing. c. M edications i. U sed for back pain (especially opiates: dosage and frequency) ii. P rescription (steroid use can be risk factor for osteoporosis and compression fractures) iii. O ver the counter iv. H erbal/alternative 3. F amily history a. D isc disease b. O steoporosis c. R heumatoid arthritis, ankylosing spondylitis d. V ascular disease e. S coliosis 4. Occ upational a. P hysical requirements of job b. H ow many hours worked per week c. N umber of hours spent in prolonged sitting (risk factor for piriformis syndrome and decon-ditioning) d. R ecent job injury e. P rior ergonomic assessments performed and results623 Database
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curve could signal hyperkyphosis. Palpate the area over the piriformis muscle at the sciatic notch if the patient complains of buttock pain. Eliciting tenderness with deep palpation suggests that the source of the patient's pain may be PS, not lumbar-sacral disorders. d. R ange of motion: assess flexibility as well as complaints of pain. Ask which movement causes the most pain. (Flexion causes increased pres-sure on the disc; extension narrows the diameter of the spinal canal [spinal stenosis]; lateral bend-ing causes increased pain if disc is herniated. ) e. G ait; check heel and toe walking separately (heel walk involves the anterior tibialis and L4 innervation; toe walk uses the gastrocnemius and S1 innervation) f. M easure leg length. (Difference of > 2 cm causes significant postural alteration that can result in LBP. ) 7. F ocused neurologic exam a. S traight leg raises (SLR): screen for nerve root irritation, most commonly due to a herniated disc in the L5 or S1 nerve roots. While patient is supine, the affected leg should be elevated by the clinician with the ankle dorsiflexed and the knee fully extended. A (+) response (“sciatica”) reproduces sharp or burning pain when the limb is raised to 30-70 degrees. This occurs in the setting of disc herniation or degenerative condi-tions causing neural foraminal stenosis, and less often, PS. The earlier the onset of pain during the test and the greater the severity, the more specific is the result. The SLR test is 64-98% sensitive, but less specific (11-61%) for lumbosacral disc herniation (Mc Gee, 2007). Additionally, sciatic symptoms that occur down the oppo-site leg during testing usually indicate a large disc herniation (Papadakis & Mc Phee, 2015). Sciatica due to spinal stenosis is more common in older patients, and pain is often bilateral (see T able 64-3 for exam findings associated with impingement of specific nerve roots). Pain that is limited to the back or the hip during the SLR is considered a (-) test. A (-) test argues against disc herniation of the L4-S1 area. If (+) SLR or a red flag is present, the clinician needs to pro-ceed with more detailed neurologic exam of the lower extremities as described in Section 8. Much less L4 and minimal L2 or L3 disc movement occurs during the SLR test, so that it is less useful in detecting disc herniation above L4. Flexing the knee with the patient in a prone position may reproduce the back and anterior thigh pain of upper lumbar disc hernia-tion (Goroll & Mulley, 2014). 8. E xpanded neurologic exam a. C omparative muscle strength testing of upper and lower extremities: knee, great toe, and ankle dorsiflexion b. D ermatomal sensation testing of lower extremi-ties and feet c. R eflex testing of patellae and Achilles tendon and Babinski d. M easure muscle mass of thighs and calves: difference of > 2 cm may indicate neurologic involvement of limb with smaller muscle mass. e. I f complaints and exam findings are consistent with cauda equine syndrome (severe unilateral or bilateral leg weakness, urinary retention/distended bladder, or fecal incontinence), check for saddle anesthesia and diminished anal sphincter tone. 9. S ystemic exam a. E ye exam: if c/o eye pain or irritation. Anterior uveitis can be associated with ankylosing spondylitis. b. P ulmonary exam (chest expansion decreased in ankylosing spondylitis) c. C ardiac exam : note evidence of aortic valve incompetence (can occur in ankylosing spondy-litis) including testing for aortic bruits to assess if aortic aneurysm is suspected as the source of LBP. d. U rinary exam: assess for distended bladder (saddle anesthesia and/or diminished anal sphincter tone with fecal incontinence and uri-nary retention suggests cauda equina syndrome, a surgical emergency) e. Ge nitourinary exam: note any pelvic tenderness or masses, or cervical motion tenderness or dis-charge (suggests pelvic inflammatory disease in females); urethral discharge or dysuria (can be associated with ankylosing spondylitis); prostate enlargement, tenderness, or masses (can signal infection or prostate cancer). f. A bdominal exam: pulsatile mass near umbilicus suggests an aortic aneurysm g. R ectal exam: check for saddle anesthesia of the perineum or diminished anal sphincter tone if suspicion of cauda equine syndrome C. Diagnostic tests (may include, but not limited to) 1. R adiographs: basic x-ray findings are poorly correlated with specific symptoms and are not sensitive for important abnormalities (Chou et al., 2007). In addition, in several studies of asymptomatic 624 CHAPTER 64 | Low Back Pain
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individuals, disc degeneration was a common finding that increased with age (Atlas & Deyo, 2001). Therefore, plain x-rays of the spine have a very low sensitivity and specificity in the majority of cases, and should not be obtained for patients with nonspecific low back pain unless pain has persisted for > 6 weeks. a. Only c onsider plain radiograph of the lumbosa-cral spine when: i. The re are red flags in the patient's history or physical exam (see T able 64-2). ii. I f back pain is primarily in the high lumbar or thoracic regions (pain here is suggestive of a compression fracture or metastatic tumor) iii. I f the patient has not improved after a 6-week course of conservative therapy. b. C onsider pelvic radiograph to look for sacroiliitis if suspicion of ankylosing spondylitis based on patient's history or exam (Chou et al., 2007). c. C onsider chest x-ray if findings suggestive of abdominal aortic aneurysm. d. Adv anced radiographic studies (computerized tomography [CT], magnetic resonance imaging [MRI]) are appropriate to consider in the situa-tions below:i. I f severe or progressive neurologic deficits ii. I f suspicion of infection, tumor, or cauda equina syndrome, urgent study is warranted iii. I f sciatic symptoms suggest disc herniation or spinal stenosisa. T reat with course of conservative care first (see Plan, Section IV A), which may be sufficient (Atlas & Deyo, 2001). b. I f surgery is likely to be needed for unimproved symptoms of disc hernia-tion or spinal stenosis, consider referral to orthopedic or neurosurgical specialist before advanced studies are ordered, as they may have a particular preferred test. e. D espite frequent patient requests for imaging, its utility is largely limited to situations in which an interventional procedure is likely. Again, to emphasize this important point: in 22-26% of asymptomatic adults, disc herniations are seen on MRI. Asymptomatic patients over age 60 have up to 21% incidence of spinal stenosis ( Jarvik, 2002; Weinstein et al., 2006). Patient education is important to explain the risk of unnecessary radiation and to underscore the frequency of false-positive results. 2. R outine blood and urine testing is unnecessary. Select tests may be helpful if particular pathology is suspected:a. E rythrocyte sedimentation rate (ESR): if ques-tion of malignancy, ankylosing spondylitis, or consideration of infection b. C omplete blood count (CBC): may be used as screening test for neoplasms, infections, or inflammatory processes c. P rostate-specific antigen (PSA): if suspicion of metastatic prostate cancer d. U rinalysis: if question of urinary tract disease e. C-reactive protein: as screen for vertebral infec-tion or ankylosing spondylitis f. H LA-B27: as screen for ankylosing spondylitis (rate of reliability as a screen differs markedly among ethnic populations; strongest associa-tion with ankylosing spondylitis is in caucasians) (Khan, 2002). g. S erum calcium and vitamin D level if concern of osteoporosis h. A lkaline phosphatase 3. Ele ctromyography and nerve conduction studies should be reserved for use by specialists in recalcitrant or complex cases. III. a ssessment More than 85% of cases of acute LBP presenting to a primary provider cannot reliably be attributed to a specific disease or spinal abnormality (Chou et al., 2007) but will recover within 6 weeks of conservative therapy as described in the Plan, section IV (Papadakis & Mc Phee, 2015). A. Determine if evidence of nerve impingement due to disc herniation or spinal stenosis (Tables 64-2 and 64-3). B. Determine if presence of red flags suggests more serious pathology (cancer, infection, inflammatory condition, fracture; see Table 64-2). C. If no “red flags” are present, even if there is evidence of simple nerve impingement (i. e., sciatica but no evidence of cauda equina), treat as mechanical musculoskeletal back pain or PS, if presentation suggests it, and follow Plan outlined in section IV. D. Determine if medical-legal issues concerning possible worker's compensation or disability claim are present. If medical-legal issues, refer to a specialist. 625 Assessment
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b. Ac etaminophen at dosages up to 4 g/day produced relief equivalent to NSAIDS for patients who could not tolerate NSAIDS. c. The re was insufficient evidence to judge the independent benefit of ASA. d. O pioid analgesics offered moderate benefits in relieving pain not controlled by NSAIDS or acetaminophen. Their use should be limited to < 1 week and reserved for patients whose pain cannot be controlled by agents like NSAIDs or acetaminophen or who should not take these medications for other medical reasons. e. M uscle relaxants (e. g., diazepam, tizanidine, cyclobenzaprine, baclofen): use for < 2 weeks; reserved for patients whose pain cannot be controlled alone by NSAIDs or acetamino-phen because of true muscle spasm. Most effective when combined with NSAID or acetaminophen. f. The decision to prescribe antidepressants, anti-epileptic drugs, or epidural steroid injections for patients with sciatica should be left to a specialist. However, they were not shown to offer any independent, sustained pain relief. 3. F or Return to Work Guidelines, see the AHRQ Official Disability Guidelines at http://www. guideline. gov /content. aspx?id=47586. Modify as directed if sciatic symptoms still present. 4. F ile a “Physician's First Report of Injury” if symptoms are due to a work-related injury. B. Subacute low back pain (1-3 months) 1. P hysical measures (Chou & Huffman, 2007a) a. I ntermittent bed rest (of no more than 48 hours at a time) only if radicular symptoms persist b. M odify activity as needed to control symptoms c. L ow-stress aerobic exercise (walking, swimming) as tolerated; avoid heavy lifting, prolonged sitting and standing d. R efer workers with LBP beyond 6 weeks to a comprehensive return-to-work rehabilitation program. Effective programs are multidisci-plinary and involve case management, education about keeping active, behavioral treatment, and participation in an exercise program. e. E xercise training by PT or DO for improvements in posture, core stability training, physical con-ditioning, and activity modification to decrease physical strain are keys for ongoing manage-ment (Papadakis & Mc Phee, 2015). Current guidelines contraindicate spinal manipulation in people with severe or progressive neurologic deficits. IV. Plan A. Acute low back pain (acute: < 2-6 weeks; may include sciatica, but no red flags) 1. P hysical measures: in a synthesis of 17 randomized controlled trials of nonpharmacologic therapies for LBP (Chou & Huffman, 2007b), only the following interventions showed evidence of efficacy: a. Be d rest (BR) only if sciatic or muscle symptoms make walking/sitting difficult. Limit use of BR for only severe pain; bed rest for > 48 hours is not only of no value, it contributes to counterpro-ductive deconditioning (Ehrlich, 2003). b. P atient contact should be made at 1 week, 2-4 weeks, and 6 weeks to assess expected improvement in pain. Any worsening of pain or new/worsening of neurologic losses should be evaluated promptly. c. A void prolonged sitting or standing; get up at regular intervals (every 30 minutes) to walk and stretch the paraspinal muscles. d. Act ivity modification as warranted by pain level/ location. Avoid heavy lifting, extreme spinal flexion. e. L ocal application of moist heat or cold may offer relief. f. I f suspicion of PS, referral to physical therapist for training in stretching and strengthening of hip abductors, external rotators, and extensors. g. S pinal manipulation and gentle massage by physical therapist (PT) or osteopathic doctor (DO) may be helpful in producing short-term improvements in pain. Patients should not undergo spinal manipulation if they have radicu-lar symptoms or do back exercises not specifically designed for them as symptoms may be aggravated. h. Othe r nonpharmacologic therapies like acu-puncture, back schools, low-level laser, lumbar supports, traction, transcutaneous electrical nerve stimulation (TENS) units, and ultraso-nography lack reliable evidence of effectiveness in managing acute LBP. There have been no studies that evaluate the effect of different mat-tresses or pillows on pain intensity. 2. M edications. In a review of 51 randomized, controlled trials for the treatment of LBP from the Cochrane Central Registry of Controlled T rials (Chou & Huffman, 2007a): a. N SAIDS were superior to placebo for global improvement of back pain with or without sciatica. No one agent was found to be superior to any other drug in the same class. 626 CHAPTER 64 | Low Back Pain
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b. R efer for surgical evaluation if patient with sciatica has not improved after 4-12 weeks of conservative therapy, and/or imaging with CT or MRI shows lesion in an area that corresponds to symptoms. c. R efer for diagnostic/specialty evaluation if new red flag symptoms appear while patient is being treated with conservative therapy. d. R efer for evaluation by specialist if symptoms caused by a workplace injury or the patient plans to file a disability claim. 5. F or Return to Work Guidelines see the AHRQ Official Disability Guidelines at http://www. guideline. gov /content. aspx?id=47586. Modify as directed if sciatic symptoms still present. 6. P atient education (see sample patient education handout in Figure 64-1). a. P rovide written information that includes all the teaching points detailed in requirements described in management of acute episode of LBP 7. C areer counseling: consider referral for vocational evaluation if patient's work repeatedly produces back pain despite conditioning, and patient is not amenable to surgical correction. f. The re is insufficient evidence to recommend for or against any specific type of exercise program or its frequency. g. L ocal heat/cold if provides relief h. The re is insufficient evidence to recommend for or against acupuncture, massage therapy, herbal medicine, yoga, laser therapy, and diathermy. i. L umbar corsets (“back belts”), traction, TENS unit use, systemic steroids, and ultrasonography have failed to demonstrate benefit in numerous controlled trials. 2. M edications (Chou & Huffman, 2007b) a. N onnarcotic analgesics only (e. g., acetamino-phen, NSAIDs) unless contraindicated. Again, no single NSAID is superior to any other in controlling pain and symptoms. b. S hort-term use of benzodiazepines may offer some benefit if skeletal muscle spasm persists; other skeletal muscle relaxants did not dem-onstrate benefits in controlled trials (Chou & Huffman, 2007b). c. O pioids should be avoided because of risk of dependency or abuse, unless brief course (1-2 weeks) needed for severe pain d. C onsider course of tricyclic antidepressants (e. g., amitriptyline) if radicular pain is present. (When used for nerve pain, start at 10 mg at bedtime, then increase to 25 mg after 1 week, then up to 50 mg as maintenance dose). This is a subtherapeutic dose for depression. Caution with use in patients with history of bipolar affec-tive disorder, mood swings, glaucoma, or history of palpitations. 3. C onditioning (after initial pain has subsided) a. B iofeedback b. “B ack school” c. C onditioning training by PT, DO, or other health professional to improve core muscle strength. More rigorous conditioning regimens are associated with the best outcomes (Chou et al., 2007). d. E rgonomic evaluation of the workplace if symp-toms suggest aggravation by work activities. 4. R eferral for specialty evaluation (Atlas & Deyo, 2001) a. R efer to a specialist for consideration of epidural steroid injections if sciatic pain (suggesting disc herniation) remains incapacitating during the latter 6 weeks of conservative therapy. Typically, two injections will be given 3-4 weeks apart. Pain relief will be short term (averaging 3-6 weeks) but may help patient to manage during period between “end” of conservative therapy and point of surgical decision making. Cauda equina (spinal nerve roots)Disk Hern iated disk Compressednerve Sciatic ner ve (pain mayradiate downthe ner ve the entire lengthof the leg)Sciatic region Vertebra Annulus fibrosis Nucleus pulposus Painfulcompressednerve Cauda equina ofspinal cord Normal ner ve Herniated disk Figure 64-1 Sample Patient Education (T o accompany the patient education material noted on pages 628-631. )627 Plan
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What Is Back Pain? Fast Facts: An Easy-to-Read Series of Publications for the Public Back pain can range from a dull, constant ache to a sudden, sharp pain that makes it hard to move. It can start quickly if you fall or lift something too heavy, or it can get worse slowly. Who Gets Back Pain? Anyone can have back pain, but some things that increase your risk are: Getting older. Back pain is more common the older you get. You may first have back pain when you are 30 to 40 years old. Poor physical fitness. Back pain is more common in people who are not fit. Being overweight. A diet high in calories and fat can make you gain weight. T oo much weight can stress the back and cause pain. Heredity. Some causes of back pain, such as ankylosing spondylitis, a form of arthritis that affects the spine, can have a genetic component. Other diseases. Some types of arthritis and cancer can cause back pain. Y our job. If you have to lift, push, or pull while twisting your spine, you may get back pain. If you work at a desk all day and do not sit up straight, you may also get back pain. Smoking. Y our body may not be able to get enough nutrients to the disks in your back if you smoke. Smoker's cough may also cause back pain. People who smoke are slow to heal, so back pain may last longer. Another factor is race. For example, black women are two to three times more likely than white women to have part of the lower spine slip out of place. What Are the Causes of Back Pain? There are many causes of back pain. Mechanical problems with the back itself can cause pain. Examples are: Disk breakdown Spasms Tense muscles Ruptured disks Injuries from sprains, fractures, accidents, and falls can result in back pain. Back pain can also occur with some conditions and diseases, such as: Scoliosis Spondylolisthesis Arthritis Spinal stenosis Pregnancy Kidney stones Infections Endometriosis Fibromyalgia Other possible causes of back pain are infections, tumors, or stress. Can Back Pain Be Prevented? The best things you can do to prevent back pain are: Exercise often and keep your back muscles strong. Maintain a healthy weight or lose weight if you weigh too much. To have strong bones, you need to get enough calcium and vitamin D every day. 628 CHAPTER 64 | Low Back Pain FIg URE 64-1 Sample P atient Education (Continued)
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T ry to stand up straight and avoid heavy lifting when you can. If you do lift something heavy, bend your legs and keep your back straight. When Should I See a Healthcare Provider for Pain? You should see a healthcare provider if you have: Numbness or tingling Severe pain that does not improve with rest Pain after a fall or an injury Pain plus any of these problems: Trouble urinating Weakness Numbness in your legs Fever Weight loss when not on a diet. How Is Back Pain Diagnosed?To diagnose back pain, your healthcare provider will take your medical history and do a physical exam. Your healthcare provider may order other tests, such as: X-rays Magnetic resonance imaging (MRI) Computerized tomography (CT) scan Blood tests Medical tests may not show the cause of your back pain. Many times, the cause of back pain is never known. Back pain can get better even if you do not know the cause. What Is the Difference Between Acute and Chronic Pain? Acute pain starts quickly and lasts less than 6 weeks. It is the most common type of back pain. Acute pain may be caused by things like falling, being tackled in football, or lifting something heavy. Chronic pain lasts for more than 3 months and is much less common than acute pain. How Is Back Pain Treated? Treatment for back pain depends on what kind of pain you have. Acute back pain usually gets better without any treatment, but you may want to take acetaminophen, aspirin, or ibuprofen to help ease the pain. Exercise and surgery are not usually used to treat acute back pain. Following are some types of treatments for chronic back pain. Hot or Cold Packs (or Both) Hot or cold packs can soothe sore, stiff backs. Heat reduces muscle spasms and pain. Cold helps reduce swelling and numbs deep pain. Using hot or cold packs may relieve pain, but this treatment does not fix the cause of chronic back pain. Exercise Proper exercise can help ease chronic pain but should not be used for acute back pain. Your healthcare provider or physical therapist can tell you the best types of exercise to do. Medications The following are the main types of medications used for back pain: Analgesic medications are over-the-counter drugs such as acetaminophen and aspirin or prescription pain medications. (continues)629 Plan FIg URE 64-1 Sample P atient Education (Continued)
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Topical analgesics are creams, ointments, and salves rubbed onto the skin over the site of pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are drugs that reduce both pain and swelling. NSAIDs include over-the-counter drugs such as ibuprofen, ketoprofen, and naproxen sodium. Your healthcare provider may prescribe stronger NSAIDs. Muscle relaxants and some antidepressants may be prescribed for some types of chronic back pain, but these do not work for every type of back pain. Behavior Changes Y ou can learn to lift, push, and pull with less stress on your back. Changing how you exercise, relax, and sleep can help lessen back pain. Eating a healthy diet and not smoking also help. Injections Your healthcare provider may suggest steroid or numbing shots to lessen your pain. Complementary and Alternative Medical Treatments When back pain becomes chronic or when other treatments do not relieve it, some people try complementary and alternative treatments. The most common of these treatments are: Manipulation. Professionals use their hands to adjust or massage the spine or nearby tissues. T ranscutaneous electrical nerve stimulation (TENS). A small box over the painful area sends mild electrical pulses to nerves. Studies have shown that TENS treatments are not always effective for reducing pain. Acupuncture. This Chinese practice uses thin needles to relieve pain and restore health. Acupuncture may be ef fective when used as a part of a comprehensive treatment plan for low back pain. Acupressure. A therapist applies pressure to certain places in the body to relieve pain. Acupressure has not been well studied for back pain. Surgery Most people with chronic back pain do not need surgery. It is usually used for chronic back pain if other treatments do not work. You may need surgery if you have: Herniated disk. When one or more of the disks that cushion the bones of the spine are damaged, the jelly-like center of the disk leaks, causing pain. Spinal stenosis. This condition causes the spinal canal to become narrow. Spondylolisthesis. This occurs when one or more bones of the spine slip out of place. V ertebral fractures. A fracture can be caused by a blow to the spine or by crumbling of the bone due to osteoporosis. Degenerative disk disease. As people age, some have disks that break down and cause severe pain. Rarely, when back pain is caused by a tumor, an infection, or a nerve root problem called cauda equina syndrome, surgery is needed right away to ease the pain and prevent more problems. What Kind of Research Is Being Done? Highlights of recent research include: Cost and effectiveness comparisons of surgical versus nonsurgical treatments for various types of back pain Factors that go into patients' decisions about whether or not to have surgery for herniated disks National statistics on back pain costs Socioeconomic factors that relate to back pain costs and treatment. Goals of current research are to: Understand the many factors that can cause back pain Identify ways to prevent back pain Improve surgical and nonsurgical treatments for back pain Prevent disability in people who suffer from back pain. 630 CHAPTER 64 | Low Back Pain FIg URE 64-1 Sample P atient Education (Continued)
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For More Information About Back Pain and Other Related Conditions: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)Information Clearinghouse National Institutes of Health Website: http://www. niams. nih. gov The information in this publication was summarized in easy-to-read format from information in a more detailed NIAMS publication. To order Back Pain: Handout on Health full-text version, please contact NIAMS using the contact information above. To view the complete text or to order online, visit http://www. niams. nih. gov. Reproduced from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). (2015). Handout on Health: Back Pain. (NIH Publication No. 15-5282). Retrieved from http://www. niams. nih. gov/Health_Info/Back_Pain/default. asp#Fig1. C. Recurrent or chronic low back pain (> 3 months) 1. A ppropriate to do radiologic and/or imaging studies, and/or blood tests if not resolved yet, especially if pain arose from work setting 2. R efer to specialist for further evaluation/management if neurologic losses remain present despite compliance with conservative therapy, especially if pain is work-related or disability claim filed 3. P hysical measures (Chou et al., 2007) a. M odify activity to control symptoms; avoid heavy lifting, prolonged sitting/standing b. L ow-stress aerobic exercise c. Ma ssage d. Y oga as long as no radicular (sciatic) symptoms e. M anipulation by PT or DO may be helpful as long as no sciatic symptoms present f. Ac upuncture may offer additive short-term pain relief g. P atient-specific exercises and activities per PT or DO to improve core muscle strength and posture may reduce the likelihood of recurrence. h. E xercising in warm water can be effective anal-gesic. Do not do any exercises that increase the pain. i. E ncourage return to work and ADLs as tolerated j. A regular program of daily walking and low-stress aerobic activities once pain has resolved helps develop core muscle support 4. M edications (Chou & Huffman, 2007b) a. N onnarcotic analgesics only (acetaminophen or NSAIDs)b. C onsider a course of low-dose tricyclic antide-pressant if it has not been tried for back pain [see details under Subacute LBP: Section B2(b)]. 5. R efer to pain management specialist or physiatrist who specializes in the spine if insufficient relief with above measures and no evidence of structural disorder or discogenic cause of pain on imaging. 6. The re is strong evidence that several psychosocial factors correlate with the development of chronic back pain. Because strategies aimed at addressing these risk factors have not been individually evaluated, it is reasonable to refer the patient to a mental health professional trained in cognitive behavioral therapy. 7. C onditioning: can use if not previously attempted, or if had good relief with prior use a. B iofeedback b. “B ack school”: interdisciplinary rehabilitation most effective when presented at patient's worksite if involves a work-related injury (Chou & Huffman, 2007a) c. C onditioning training by PT or DO d. E rgonomic evaluation of workplace if symptoms suggest aggravation by work activities and evaluation not already conducted 8. P atient education (see sample in Figure 64-1) D. Follow-up care to prevent recurrence after symptoms have improved Because relapses in back pain are common—approach-ing 75% (Goroll & Mulley, 2014)—and the societal bur-den of chronic pain is large, strategies to prevent acute back pain from becoming chronic have been investigated. 631 Plan FIg URE 64-1 Sample P atient Education (Continued)
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clinically warranted and cost-effective in these types of cases? In a widely referenced study that followed 2,427 patients for 4 years (2000-2005), the cost effective-ness of surgery vs. nonoperative care was evaluated for the diagnoses of either disc herniation, degenerative spondylolisthesis, or spinal stenosis (Spine Patient Outcomes Research T rial; T osteson et al., 2011). For each diagnosis, cost per quality-adjusted life-year (QALY) was calculated to determine whether surgery or nonsurgical care was more cost effective as measured by patient-reported actual financial cost of medical care as well as satisfaction with quality of life for each image-confirmed diagnosis. After 4 years of a projected 9-year data collection, it appears that the cost of the surgery at the outset of the study was significantly eclipsed by the continuing costs sus-tained by the nonoperative patient population, pre-dominantly due to their productivity losses. Although total costs after 4 years remained higher for the sur-gically treated group, this difference was most mini-mal in patients with disc herniation ($6,994). This patient group noted a large improvement in their sciatic symptoms and an improved quality of life following surgery. The cost difference was highest for those with degenerative spondylolisthesis ($22,127). In patients with spinal stenosis, the higher cost in surgical patients compared with nonoperable care after 4 years was $13,127. These data support an argument that surgery is a cost-effective option for those patients who have a positive impression of the benefit of undergoing surgery for relief of protracted disc herniation symptoms after a prolonged period of continuing symptoms despite compliance with con-servative therapy and do not have red flags. However, it is important to note that patients who were reluctant to have surgery also recovered with nonoperative conservative treatment as long as they considered the pain as “tolerable,” and they did not have evidence of neurologic defects. Importantly, delaying or avoiding surgery did not cause additional neurologic injury or damage. 9. P atient education (see sample in Figure 64-1) a. P rovide written information that reinforces the clinician's information and includes:i. M ost common cause of symptoms ii. Di fference in symptoms caused by mus-culoskeletal strain vs. nerve root impinge-ment iii. R eassurance that testing rarely helpful ini-tially, and spontaneous resolution is most common iv. P hysical recommendations The U. S. Preventive Services T ask Force (USPSTF, 2007) and Agency for Healthcare Research and Quality (AHRQ, 2001) have synthesized the evidence on prevention: 1. Both r eports emphasized the importance of clinician education and support in explaining the usually benign course of LBP, even though symptoms may persist for more than 1 month. Written materials reinforcing the clinician's message are useful to provide as a supplement (see Resources at end of chapter). 2. A lthough both analyses determined that it is important to resume physical activity quickly after the acute pain has resolved, both concluded that there is insufficient evidence to recommend for or against the routine use of specific exercise interventions to prevent back pain. 3. C onsider encouraging the patient to attend a community-based exercise program or gym program to support performance of exercises and obtain benefit of peer support in strengthening core musculature, reducing likelihood of recurrence. 4. Othe r nonpharmacologic interventions listed in Plan section IV A 1 (h) were not found to offer additional benefit or relief. 5. I t has not been verified that a reduction in risk factors (i. e., obesity and smoking) will prevent the recurrence of back pain, although it intuitively seems a reasonable expectation. 6. The p hysical measures listed in C3 earlier in the Plan for Chronic LBP have not been validated as either preventing or not preventing recurring episodes of LBP. 7. The e arlier agents that have been recommended to avoid, still apply in preventing recurrences of LBP. 8. C onsult or refer for evaluation by an orthopedic spine surgeon or neurosurgeon if: a. S ymptoms consistent with cauda equina syndrome b. L ower limb weakness or sensory losses c. P rogressive neurologic deficit d. P resence of red flags (symptoms suggestive of cancer, bone infection, or ankylosing spondylitis require referral to other appropriate specialists) e. S evere spinal deformity f. A bnormal findings on CT or MRI g. F ailure to secure relief of symptoms, or worsen-ing of symptoms after 6 weeks of conservative measures described previously. Because the vast majority of cases of uncompli-cated LBP resolve within 6 weeks, even if there is evidence of nerve root irritation, a major question exists: when are the risk and cost of spinal surgery 632 CHAPTER 64 | Low Back Pain
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REFERE nc ES Atlas, S., & Deyo, R. (2001). Evaluating and managing acute low back pain in the primary care setting. Journal of General Internal Medicine, 16, 120-131. Agency for Healthcare Research and Quality. (2001). Guideline for the evidence-informed primary care management of low back pain. Retrieved from http://www. guideline. gov/content. aspx?id=37954. Chou, R., & Huffman, L. (2007a). Medications for acute and chronic low back pain: A review of the evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline. Annals of Internal Medicine, 147(7), 505-514. Chou, R., & Huffman, L. (2007b). Nonpharmacologic therapies for acute and chronic low back pain: A review of the evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline. Annals of Internal Medicine, 147(7), 492-504. Chou, R., Quaseem, A., Snow, V., Casey, D., Cross, J. T., Jr., Shekelle, P., et al. (2007). Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Annals of Internal Medicine, 147(7), 478-491. Ehrlich, G. (2003). Back pain. Journal of Rheumatology, 30(67), 26-31. Goroll, A. H., & Mulley, A. (2014). Primary care medicine (7th ed. ). Philadelphia: Wolters Kluwer Health. Hoppenfeld, S. (1976). Physical exam of the spine and the extremities. East Norwalk, CT: Appleton-Century-Crofts/Prentice-Hall. Jarvik, J. G., & Deyo, R. (2002). Diagnostic evaluation of low back pain with emphasis on imaging. Annals of Internal Medicine, 137, 586-597. Khan, M. A. (2002). Update on spondyloarthropathies. Annals of Internal Medicine, 136(12), 896-907. Mc Gee, S. (2007). The leg. In Evidence based physical diagnosis (2nd ed. ). St. Louis, MO: Saunders Elsevier. Papadakis, M., & Mc Phee, S. (Eds. ). (2015). Low back pain. In Current medical diagnosis and treatment (54th ed. ). New Y ork: Mc Graw-Hill Education. T osteson, A., T osteson, T., Lurie, J., Abdu, W., Herkowitz, H., Andersson, G., et al. (2011). Comparative effectiveness evidence from the spine patient outcomes research trial. Spine, 16(24), 2061-2068. van Tulder, M., Koes, B., & Bombardier, C. (2002). Low back pain. Best Practice and Research. Clinical Rheumatology, 16, 761-765. Weinstein, J., Lurie, J. D., T osteson, T. D., Skinner, J. S., Hanscom, B., et al. (2006). Surgical vs. non-operative treatment for lumbar disk herniation. JAMA, 296(20), 2441-2450. v. A nalgesic recommendations vi. E xercise/activity precautions vii. C all/see provider if a. N o improvement after 2 weeks of sciatic symptoms b. N o improvement after 6 weeks of nonspecific LBP c. S ymptoms progress in severity d. R ed flags occur viii. C onditioning/prevention recommendations once acute phase subsides V. Self-management r esources and tools See T able 64-4 for additional resources. Table 64-4 W eb-Based Patient Education Materials The Internet has volumes of information available on the causes, evaluation, and treatment of low back pain. The following are suggested because the vocabulary is appropriate for a lay audience, they do not focus exclusively on surgical remedies, and they are not overly long. This list is not exclusive; other websites may be found to be valuable as well. American Academy of Rheumatology. (2008). Back pain. Retrieved from http://www. rheumatology. org/I-Am-A/Patient-Caregiver/Diseases-Conditions /Living-Well-with-Rheumatic-Disease/Back-Pain. American Association of Neurological Surgeons. (2005). Cauda equina syndrome. Retrieved from http://www. aans. org/Patient%20Information/Conditions%20and%20Treatments/Cauda%20Equina%20Syndrome. aspx. Annals of Internal Medicine. (2009). Low back pain. Retrieved from http://www. medicinenet. com/low_back _pain/page4. htm. Family Doctor. (2009). An overview of low back pain. Retrieved from http://familydoctor. org/familydoctor/en /diseases-conditions/low-back-pain. html. National Institutes of Health. (2009). Low back pain fact sheet. Retrieved from http://www. ninds. nih. gov/disorders /backpain/detail_backpain. National Institute of Neurologic Disorders and Stroke (NIH). (2003). Low back pain fact sheet. Retrieved from http://www. ninds. nih. gov/disorders/backpain/detail _backpain. Web MD. (2008). Overview of low back pain. Retrieved from http://www. webmd. com/back-pain/tc /low-back-pain-treatment-overview. 633 References
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A. Healthy People 2020, summarized (U. S. Department of Health and Human Services, 2009) 1. Obj ectives retained from 2010 a. I ncrease the proportion of adults who are at a healthy weight. b. R educe the proportion of adults who are obese. 2. Obj ective retained but modified a. R educe the number of children and adolescents who are obese. b. F or individuals age 2 and older: increase the consumption of fruits, vegetables, whole grains, and calcium. Reduce the consumption of satu-rated fat and sodium. c. I ncrease the number of healthcare visits that include counseling or education for weight management. d. El iminate very low food security among children in U. S. households. 3. Obj ectives new to Healthy People 2020 a. P revent inappropriate weight gain in youth and adults. b. I ncrease the number of primary care providers who regularly calculate the BMI of their patients. c. R educe the consumption of calories from solid fats and sugars, increase the number of states with food standards for children, and increase the percentage of schools that offer nutritious food and beverages outside of school meals. d. C hanges in state-level policies for food outlets. 4. M easuring overweight and obesity: BMI provides a reasonable indicator for body adiposity and weight categories that may lead to significant health problems. BMI categories as defined by the National Institutes of Health include: a. 18. 5-24. 9 kg/m2 (normal) b. 25-29. 9 kg/m2 (overweight) c. 30-34. 9 kg/m2 (Class I obesity)I. Intr oduction and general background Obesity is a major public health concern in the United States. According to the 2011-2012 National Health and Nutrition Examination Survey (NHANES), obesity prevalence in adults has remained relatively constant at an overall rate of 35. 7% with 33. 1% of adults in the overweight category. There was an increase in obesity noted in older adults (particularly women) age 60 and older (Ogden, Carroll, Kit, & Flegal, 2014). Obesity trends are more prevalent in minority groups, lower socioeconomic groups, and less educated individuals and contribute to a number of significant chronic healthcare issues. In addition, an overweight and obese population contributes to substantial economic costs, estimated at $190. 2 billion annually (Institute of Medicine [IOM], 2012). Clinically, overweight is defined as a body mass index (BMI) of 25-29. 9 kg/m 2 and obesity as greater than or equal to 30 kg/m2. Overweight and obesity for those 18 years and older substantially increase the risks of morbidity for hyper-tension (HTN), dyslipidemia, type 2 diabetes, coronary artery disease, stroke, gallbladder disease, osteoarthritis, sleep apnea, and respiratory problems. Additional health risks include higher rates of endometrial, breast, prostate, and colon cancer. Overweight individuals also endure social stigmatization and discrimination (Centers for Disease Control and Prevention [CDC], 2009a, 2009c; IOM, 2012). The goal of Healthy People 2010 was to promote health and reduce chronic disease associated with diet and weight by reducing the number of adults 20 years or older with a BMI over 30 to 15% of the population. The Healthy People 2020 objectives, discussed next, have been expanded and modified to include changes in state policies, expectations for primary care visits, and nutrition and weight management counseling for individuals older than age 2. Although the goals are ambi-tious, weight-related diseases are a major preventable cause of death, pose an important public health challenge, and should not be overlooked (IOM, 2012; U. S. Department of Health and Human Services, 2000). Sherri Borden, David Besio, and Geraldine Collins-Bride OBe SIty© Eliks/Shutterstock; © donatas1205/Shutterstock 634 65Chapt Er
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b. A sian: men ≥ 90 cm, women ≥ 80 cm c. M iddle East, Mediterranean: men ≥ 94 cm, women ≥ 80 cm d. S ub-Saharan African: men ≥ 94 cm, women ≥ 80 cm e. C entral and South American: men ≥ 90 cm, women ≥ 80 cm ii. H igh-density lipoprotein (HDL): men < 40, women < 50 or niacin or fibrate use iii. T riglycerides: ≥ 150 mg/d L, or niacin or fibrate use iv. B lood pressure ≥ 130/85 or taking blood pressure medications v. F asting glucose ≥ 100 mg/d L or using diabetes medications C. Obesity in children and adolescents Child and adolescent obesity continues to have a high prevalence in the United States. Obesity is a serious health issue for children and adolescents for numerous reasons including risk of obesity in adolescence and adulthood; increased risk for cardiovascular disease (CVD), such as high blood pressure, high cholesterol, and type 2 diabetes (Whitaker, Wright, Pepe, Seidel, & Dietz, 1997); and alterations in body image with subsequent social stigmatization. In a meta-analysis of the association between BMI and health-related quality of life (HRQo L) among children and adolescents, Ul-Haq, Mackay, Fenwick, & Pell (2013) found that as BMI increased, HRQo L decreased from normal weight through overweight and obesity. In addition, obese children and adolescents have decreased HRQo L. For more discussion, see Chapter 16 on childhood obesity. D. Obesity in individuals with mental illness As in other populations, individuals with mental illness who are overweight or obese are at increased risk for developing chronic diseases, such as CVD and type 2 diabetes. Excessive weight gain is not always addressed by clinicians such as psychiatrists, primary care physicians, and advanced practice nurses, who feel poorly equipped to deal with this problem and fear patient treatment noncompliance or psychiatric symptom decompensation. There are no clear interventions to prevent and treat overweight and obesity in this population. Individuals with mental illness who gain more than 11 lbs in adult-hood have approximately twice the rate of type 2 diabetes (Boyd, 2002). Excessive weight gain and obesity is two to three times more prevalent than in the general popula-tion (Aquila, 2002). This increased occurrence has been strongly associated with several important factors includ-ing diet, exercise, environmental factors, and psychotropic medications. Individuals with mental illness tend to eat a diet higher in saturated fat and calories; consume greater d. 35-39. 9 kg/m2 (Class II obesity) e. Gr eater than or equal to 40 kg/m2 (Class III obesity) B. Causes of obesity in adults 1. The mos t common causes of obesity are the result of energy imbalances with excessive caloric intake from food, beverages, or alcohol and insufficient physical activity and/or sedentary lifestyle. Both genetic influences (in particular genes that affect the leptin receptor) and environmental influences are thought to play a significant role (Baron, 2015). 2. The fo llowing medical problems may also contribute to the etiology of obesity: a. H ypothyroidism b. C ushing syndrome c. H ypogonadism d. H ypothalamic injuries e. P olycystic ovary (Stein-Leventhal syndrome) f. P seudo-hypoparathyroidism g. I nsulinoma h. M edications may also contribute to overweight and obesity: corticosteroids; progesterone; anti-convulsants and psychotropic medications, in particular atypical antipsychotics, such as clozaril and olanzapine; insulin; and select oral hypogly-cemic agents 3. C onsequences of obesity: as weight increases to the categories of overweight and obesity, risks for chronic health problems increase. These health problems include: a. C oronary artery disease b. T ype 2 diabetes c. C ancers (endometrial, breast, and colon) d. HTN e. D yslipidemia f. S troke g. L iver and gallbladder disease h. S leep apnea and respiratory problems i. O steoarthritis j. G ynecological problems (abnormal menses and fertility problems) k. M etabolic syndrome (Kanaya, 2010). Also known as syndrome X, insulin resistance syn-drome, and the dysmetabolic syndrome, meta-bolic syndrome is a group of risk factors that confers higher risk for stroke, coronary artery disease, and type 2 diabetes. The syndrome includes three or more of the following criteria:i. W aist circumference according to population-specific criteria :a. W hite, European: men ≥ 102 cm, women ≥ 88 cm635 Introduction and general background
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II. Database A. Subjective 1. D evelopmental patterns and past medical history a. I nfant and childhood obesity: no correlation found in infancy; however, there seem to be links to intrauterine imprinting (Bray & Champagne, 2005). Obesity beginning at age range of 5-6 years has a documented correlation to adult obesity secondary to genetic and envi-ronmental factors, such as overfeeding, poor food choices, and sedentary lifestyle. b. Ado lescent obesity: adolescents with obesity are at an increased risk of CVD, type 2 diabetes, and respiratory and sleep problems. According to the American Academy of Child and Adolescent Psychiatry (2006), adolescent obesity is also associated with lower self-esteem, depression, anxiety, and obsessive-compulsive disorder. c. Obe sity of early adulthood (postpartum) d. M iddle-age obesity: decrease in metabolic rate, decrease in activity level, increase in body weight increases the risk of developing CVD and type 2 diabetes. e. P ast medical history of obesity-related medical problems: arthritis, gallbladder disease, HTN, CVD, diabetes, depression, and obstructive sleep apnea. 2. F amily history: note history of obesity; CVD; HTN; genetic syndromes; and thyroid, diabetes, and other endocrine disorders 3. Die tary history a. 24-hour recall of current usual intake: type and quantity of food, meal times, and variability of intake b. I ntake of high caloric foods: sugar, fats, and beverages (alcohol, soda, and fruit juices) c. M eal preparation: cooking techniques and use of fats and oils d. E motional and behavioral cues to eating i. I nternal and emotional reaction to self or others, and sabotaging thoughts, such as “I deserve a treat” ii. E xternal sight or smell of food; associations of food with time, place, or activity; and celebration or parties e. A vailability: cost and quality of food, cooking facilities, and food insecurity f. C ultural orientation to food and weight 4. E xercise and activity: note type and amount of daily activity, including assets and barriers to amounts of high-carbohydrate beverages; and eat a diet lower in fiber, fresh fruits, and vegetables. They also tend to exercise less, living a more sedentary lifestyle as a result of institutionalization and other factors (Greenberg, Chan, & Blackburn, 1999). Weight gain has also been reported during treatment with many medications, such as conventional antipsy-chotic agents, phenothiazines, and thioxanthenes, and was reported in novel antipsychotic agents, such as clozapine, risperidone, and olanzapine (Basson et al., 2001). Although novel antipsychotic medications improve psy-chiatric outcomes, estimates for associated weight gain range from virtually zero weight gain, as seen in zipra-sidone, to an average gain of 4-4. 5 kg after 10 weeks of treatment with both olanzapine and clozapine, to nearly 12 kg at 1 year with olanzapine (Allison et al., 1999; Fontaine et al., 2001). The variability of novel antipsychotic weight gain experienced by patients suggests that several factors are involved. Weight gain is often rapid in the first few weeks of treatment and then reaches a plateau. Weight gain with novel antipsychotic treatment has been correlated with an excessive appetite, thought to be directly related to the atypical antipsychotics affinity for histamine H1 receptors of blockade of the hypotha-lamic sites regulating satiety (Rummel-Kluge et al., 2010). Although lifestyle intervention is an important com-ponent in preventing and managing weight gain related to the second-generation antipsychotics (SGA), some studies have examined the off-label use of metformin in the management of SGA-induced weight gain. Metformin, an antidiabetic agent used mostly in type 2 diabetes, has also been used in patients with poly-cystic ovarian syndrome to induce ovulation. Because metformin is associated with some weight reduction in diabetic patients and is relatively well tolerated, several studies have aimed to determine the effect of metformin treatment on SGA-induced weight gain. In a system-atic review and meta-analysis by Bjorkhem-Bergman, Asplund, & Lindh (2010), the authors found that those on metformin had significant weight reduction, especially those who had gained weight on antipsychotic agents. Although there are still no current recommendations for the routine use of metformin in those prescribed SGA, a more recent systematic review conducted by Newall et al. (2012) concluded that if weight gain occurs despite lifestyle intervention, metformin should be considered as an adjunct therapy. Although the authors reported limi-tations in the primary research available, they concluded that metformin may be more useful in younger people and those with shorter SGA treatment duration. They recommend starting metformin in those who have gained greater than 10% of their body weight despite lifestyle interventions (Newall et al., 2012). 636 CHAPTER 65 | Obesity
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The examination should focus in particular on the thyroid, cardiovascular, pulmonary, mus-culoskeletal, and neurologic examination in all patients. b. M easuring abdominal circumference helps assess distribution of fat. Waist circumference provides a clinically acceptable measurement of abdominal fat before and during weight loss. Waist circumference in men should be less than 102 cm (40 in) and in women less than 88 cm (35 in). Cutoffs can be used to identify increased relative risk for the development of obesity-associated risk factors in most adults with a BMI from 25-34. 9. Waist circumference is measured by placing the measuring tape at the most superior point of the hip bone, keeping it horizontal, and taking the reading at the point of exhalation. c. The fo llowing complexes of physical signs may provide clues to underlying endocrine disorders:i. C ool, dry skin; hoarse voice and facial edema; thick tongue; delayed or absent deep tendon reflexes: consider hypothyroidism. ii. R ound, “moon face”; hirsutism; truncal obesity; purple striae; ecchymosis: consider Cushing syndrome. iii. S mall stature, lack of secondary sex charac-teristics, poor muscular development: con-sider hypogonadism. iv. S hort, stocky stature; round face; intel-lectual disability; joint deformities; cataracts; papilledema: consider pseudo- hypoparathyroidism 2. Di agnostic testing: depends on the severity of obesity, potential for secondary cause, and evaluation of obesity-related health risks. Consider the following tests: a. *Ele ctrolytes, fasting glucose, blood urea nitro-gen, and creatinine b. *Th yroid-stimulating hormone (T4 if on thyroid medication) c. *F asting low-density lipoprotein (LDL) and HDL cholesterol and serum triglycerides d. P ulmonary function tests and arterial blood gas e. S teroid studies: cortisol level and dexametha-sone suppression test f. H emoglobin A1C g. Gr owth hormones h. T estosterone i. F ollicle-stimulating hormone, luteinizing hormone, and prolactin levels*Most commonly ordered as initial screening testsexercise (affordability, access, level of priority, and seasonality) 5. S elf-image, self-esteem, and self-confidence: effect on relationships, jobs, and daily life 6. M otivation and interest in weight control 7. W eight loss and dieting history, including use of over-the-counter (OTC) medications, supplements, and herbal treatments; diuretics and laxatives; diet pills; and prescription drugs. Note history of binge and purge behavior or self-starvation 8. R eview of systems: in general, the mild to moderately obese individual is asymptomatic. In cases of class III obesity (BMI ≥ 40), the following symptoms can be manifestations of mechanical difficulties or medical consequences: a. Eas y fatigability and dyspnea on exertion b. S omnolence c. M alaise and weakness d. A bdominal bloating and dyspepsia e. A nkle swelling f. J oint pains, especially weight-bearing joints: low back, hips, knees, and ankles g. S kin rashes: acne and chronic candidiasis in skin folds h. M enstrual irregularities i. S ymptoms of depression j. T o rule out endocrine disorders, consider the following history i. L ethargy, ankle swelling, somnolence, heat or cold intolerance, hair loss, dry skin, constipation and menstrual irregularities: consider hypothyroidism. ii. Acne, increase in hair growth, change in facial appearance, easy bruising, and skin rashes: consider Cushing syndrome. iii. D elayed puberty, decreased or absent libido: consider hypogonadism. iv. A menorrhea or menstrual irregularities and hirsutism: consider polycystic ovary syndrome. v. A rthralgias, muscle cramps, weakness, numb-ness or tingling, seizures, and emotional lability: consider pseudo-hypoparathyroidism. B. Objective 1. P hysical examination a. M ost individuals who are obese require gen-eral observation; height, weight, and BMI mea-surement; and a complete set of vital signs. However, a complete physical examination is generally preferred to rule out secondary causes and evidence of obesity-related health risks. 637 Database
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IV. Goals of clinical management A. Risk reduction Being overweight or obese clearly increases morbidity and mortality, and strong evidence suggests that weight loss reduces risk factors for CVD and diabetes. Weight loss reduces blood pressure in both overweight hyper-tensive and nonhypertensive individuals, lowers serum triglycerides, increases HDL cholesterol, and generally produces reductions in LDL and total serum cholesterol. Additionally, modest weight loss of 5-10% reduces blood glucose levels and Hb A 1C in some patients with type 2 diabetes (National Heart, Lung, and Blood Institute [NHLBI], 1998). B. Prevention of obesity Although the physical consequences of obesity are a significant problem, the impact on self-esteem and body image is also an important factor to consider. Physical health is closely linked to mental health and physical problems may negatively affect a patient's body image. Clinicians can play an integral role in helping a patient understand the health risks associated with obesity. Therefore, one of the primary goals should be to initi-ate healthcare maintenance measures early to prevent or intervene in weight gain. It is important to take into account a variety of factors when choosing treatment plans to provide comprehensive holistic care includ-ing the patient's personal, cultural, and family history; knowledge of the development of chronic health condi-tions; and impact of overweight and obesity on body image. According to the IOM 2012 report, Accelerating Progress in Obesity Prevention, the following goals were recommended: Make physical activity an integral part of life Create food and beverage environments that ensure healthy food and beverage options are the routine, easy choice T ransform messages about physical activity and nutrition Expand the roles of healthcare providers, insurers, and employers Make schools a national focal point T o date, there is an explosion of healthy nutrition and regular physical activity messages in the media, along with farmers' markets, food labeling, and more “healthier food choices” even in the fast food industry. One of the biggest challenges facing providers and patients is the cost and access to healthier foods and physical activities for those patients with limited means. III. Assessment A. Determine the diagnosis Distinguish between secondary and primary obesity. Rule out endocrine disorders as described previously. B. Severity Assess the severity of obesity, including current and future health risks. C. Significance Assess the significance of obesity to the patient and sig-nificant others including impact on daily functioning, work, relationships, and self-esteem. D. Motivation and ability: 1. A ssess the motivation of the patient, including reasons for weight reduction, previous history of weight loss, understanding of the causes of obesity, ability to engage in action plan, and financial considerations. 2. A ssess stage of change (Prochaska & Di Clemente, 1982) to help identify possible interventions and develop patient-specific process goals and cognitive and behavioral therapy strategies (Fabricatore, 2007). a. P recontemplation: provide weight and health education and explain health benefits of exercise. b. C ontemplation i. I dentify and list advantages and disadvan-tages of weight loss (Brownell, 2000) ii. M ake a list of potential exercises and activities c. P reparation i. P ositive goal setting (specific, measurable, attainable, reasonable, and time limited) ii. E nvironmental control: stocking the refrig-erator with fresh vegetables and fruits, removing easy access to sweets and treats, eating slowly without distractions, using smaller plates and bowls, shopping from a list, menu planning, buying prepackaged healthy calorie-controlled meals to eat as “Plan B,” identifying possible alternative exercises, and monitoring such as checking weekly or biweekly weights at home, keeping a food record and exercise log iii. I dentify potential diet intervention (Figures 65-1 and 65-2) d. Act ion: implement goals of dietary and lifestyle change; reevaluate goals regularly to encourage additional progress. e. M aintenance: develop coping strategies for diet and exercise lapses. f. R elapse: encourage patient regarding positive accomplishments, reevaluate advantages and dis-advantages, and reinitiate preparation strategies. 638 CHAPTER 65 | Obesity
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FIGure 65-1 One-W eek Food r ecord Day 1 Calories Day 2 Calories Day 3 Calories Day 4 Calories Br eakfast Time Place Hunger level*Lunch Time Place Hunger level*Dinner Time Place Hunger level*Snack (please note all snacks) Exercise (continues)639 Goals of clinical management
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Day 5 Calories Day 6 Calories Day 7 Calories T o Document Intake: Breakfast Record everything you eat or drink during the day (as soon as possible after intake). List the food and amount eaten and calories to the best of your ability. For example:2 slices w/w Light bread 120 8 oz nonfat milk 90 1 hard-boiled egg 80 T otal 335 Goal 1: Goal 2: Feelings/Comments/Concerns Time Place Hunger level Lunch Time Place Hunger level Dinner Time Place Hunger level Snack (please note all snacks) Exercise * Hunger Level:1 = Starving 10 = Stuffed Produced by UCSF Nutrition and Food Services. Used with permission by UCSF Medical Center. FIGure 65-1 One-W eek Food r ecord (Continued)640 CHAPTER 65 | Obesity
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FIGure 65-2 W ellness Agreement A goal should be realistic and measurable based on baseline patterns Current diet recall indicates that patient has vegetables 3 times/week Unrealistic goal: I will eat lots of vegetables every day More realistic goal: I will eat a serving of vegetables at dinner 6 nights this week Work towards bigger goals over time Reward yourself for accomplishing your goal. Examples: take a bubble bath, rent a favorite movie, get a massage, sleep in late, or just pat yourself on the back! q Create no more than 3 goals per week q Check in with a supportive friend, family member, or health professional to help keep you on track. A check-in can be by phone, text or e-mail—taking advantage of current technologies Goal Rewar d Food Exercise Stress Management I will focus on these wellness goals for the week. Signature Date Produced by UCSF Nutrition and Food Services. Used with permission by UCSF Medical Center. 641 Goals of clinical management
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1 year, and seems to enhance weight loss modestly when used with diet and lifestyle changes. It also may help promote weight control. However, in 2010, the U. S. Food and Drug Administration (FDA) removed sibutramine from the market because of clinical trial data indicating an increased risk of cardiovascular adverse events, including heart attack and stroke, in the studied pop-ulation (Food and Drug Administration, 2010a). ii. Orl istat: a gastric lipase inhibitor, which reduces fat absorption by approximately 30%, is also approved for longer term use, up to 1 year, and results in modest addi-tional weight loss with diet and lifestyle change (Fabricatore & Wadden, 2003). The recommended dose is 120 mg three times daily. It is currently sold in lower doses (60 mg) OTC as Alli®. Typical side effects from Orlistat are primarily gastrointestinal including flatus, abdominal cramping, fecal incontinence, and oily fecal staining. Absorption of fat soluble vitamins may be reduced with Orlistat use. Patients with a history of kidney stones should not be pre-scribed this medication. There have been rare reports of severe liver injury, including liver failure in patients taking Orlistat (FDA, 2010b). Clinicians should educate all patients taking Orlistat about the signs and symptoms of liver disease (FDA, 2010b). iii. P hentermine: the most commonly pre-scribed appetite suppressant because of low cost, phentermine is approved for only short-term use (≤ 12 weeks) due to poten-tial for abuse. Side effects include increased blood pressure (Millen et al., 2014; Sacks et al., 2005). iv. P hentermine/topiramate (Qsymia®): appro-v ed for use in 2012, the drug increases metabolism and satiety for patients with BMIs over 30 kg/m 2 or greater and 27 kg/m2 with at least one weight-related medical comorbidity. As with other weight loss drugs, it is to be used in conjunction with low-calorie diets and increased activity and can result in weight loss on average of approximately 10%. Significant side effects include birth defects if taken during pregnancy, increased heart rate, vision problems, and potential suicidal thoughts or actions. V. Plan A. Management T reatment requires a fundamental change in lifestyle. Weight loss depends on adherence to an agreement outlining lifestyle changes that factor in individual motiva-tion, support systems, and underlying medical or psycho-logical conditions. The management plan should consist of the following considerations: 1. T reat the underlying cause, if secondary obesity. 2. Es tablish a patient agreement: determine short-and long-range goals and outcomes, using healthy body weight range based on BMI, patient's desired weight, and practitioner's assessment of desired weight. 3. M eal plans: although in the short-term lower carbohy-drate meal plans seem to result in weight loss without adverse health consequences (Baron, 2015; Gardner et al., 2007), using a variety of dietary interventions (including low-calorie meal replacements) is reason-able because there does not seem to be an advantage of one macronutrient distribution versus another (Sacks et al., 2009; Vesely & De Mattia, 2014). Induce a 500-to 1,000-calorie deficit to promote 1-to 2-lb weight loss per week resulting in approximately an 8-10% total weight loss outcome. Refer to a weight manage-ment group with comprehensive lifestyle interven-tions focusing on meal plans, lifestyle, and behavior therapy provided by team of professionals, which may include nutritionist, behaviorist, exercise special-ists, and trained practitioners (Millen, Wolongevicz, Nonas, & Lichtenstein, 2014) (Figure 65-3). 4. P hysical activity: discuss the health benefits of physical activity, even if weight loss is not accomplished. Assist the individual in developing an activity regimen, setting reasonable short-term goals to increase to a long-term goal of six times per week for 60 minutes per session. According to the National Weight Control Registry only 9% of participants in the registry reported keeping weight off without engaging in some physical activity. Walking seemed to be the most popular form of physical activity. Half of the participants also combined walking with another form of planned exercise, such as aerobics, bicycling, or swimming (Hill & Wing, 2003). 5. M edications: OTC appetite suppressants are not helpful with long-term management of obesity. Although they do reduce appetite, tolerance and dependence are potentially dangerous side effects. a. P harmacologic therapy i. S ibutramine: an appetite suppressant that has been used for long-term use, up to 642 CHAPTER 65 | Obesity
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FIGure 65-3 Instructions for u se of the Plate Method STEP 1: Fill Half (1/2) of Your Plate with Nonstarchy Vegetables. q Nonstarchy vegetables are low in calories, low in carbohydrate, and high in fiber. This means nonstarchy vegetables can help you feel full and more satisfied with your meal but not lead to weight gain and high blood sugar. q Aim for 1 to 2 cups of any vegetable (EXCEPT starchy vegetables listed in Step 3). q V egetables can be raw or cooked. STEP 2: Limit Protein to a Quarter (1/4) of Your Plate. q Choose lean meat, poultry, or fish. Your portion should not be bigger than the palm of your hand. Try 1 to 2 whole eggs or just the egg whites for lower cholesterol. q Choose tofu, nuts, or seeds. Aim for about 2 tablespoons of nuts and seeds or 1/2 cup of tofu. STEP 3: Limit Starch to a Quarter (1/4) of Y our Plate. q Starch is a source of carbohydrate. Carbohydrate turns into an important fuel, called glucose, and limiting the portion size of starch helps control body weight and blood sugar. q Choose a bun, tortilla, bread, bagel, rice, grains, cereal, pasta, or a starchy vegetable. If you choose bread, limit to 2 slices or 1/2 bagel. If you choose a hamburger/hotdog bun, limit to 1 bun. If you choose a tortilla, limit to 2 small tortillas or 1 large tortilla. If you choose rice, grains, pasta, cereal, or a starchy vegetable, limit the portion to no more than 1 cup— this is about the size of a woman's fist. Starchy vegetables include beans, potatoes, corn, yams, peas, and winter squash. q Choose most of your starches from whole grains, such as whole wheat bread or tortillas, brown rice, whole wheat pasta, whole grain and bran cereals, or beans. STEP 4: If Desired, Add 1 Portion of Fruit or Milk to Y our Meal. q Fruit, milk, and yogurt are also sources of carbohydrate. T o best control body weight and blood sugar, limit yourself to either fruit or milk at your meal. You may choose to save the fruit or milk as a snack. q Because high carbohydrate liquids can quickly raise blood sugar, avoid drinking fruit juice. q Examples of fruit portion sizes are: 1 small apple, orange, peach, pear, banana, or nectarine (or half of a larger fruit) 3/4 cup fresh pineapple chunks, blueberries, or blackberries 17 grapes 1 and 1/4 cups strawberries or watermelon 1 cup cantaloupe, honeydew, or papaya q Choose low fat or nonfat dairy products for heart health and weight control. q Examples of milk and yogurt portion sizes are: 1 cup (8 ounces) of nonfat, 1%, or soy milk 2/3 to 1 cup plain nonfat or aspartame-sweetened fruit yogurt STEP 5: Limit Added Fats. q A void adding fats to your foods like butter, margarine, shortening, mayonnaise, gravies, cream sauces, salad dressing, and sour cream. Instead, season foods with herbs and spices. q Cook using low fat methods such as baking, steaming, broiling, or grilling. A void frying foods. (continues)643 Plan
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for chronic weight management of adults who are overweight or obese and have at least one comorbidity such as hyperten-sion, diabetes, or dyslipidemia. Saxenda®, administered as a once daily subcutane-ous injection, has the same active ingredi-ent as Victoza® (liraglutide), a medication used to treat type 2 diabetes, but in different doses—1. 8 mg (Victoza®) versus 3 mg (Saxenda®). Three clinical trials were con-ducted for the safety and effectiveness of Saxenda® with 4,800 obese and overweight patients plus diet and exercise. In one study 62% of patients lost 5% or more of their baseline body weight versus 34% of placebo. In a second study that included patients with v. L orcaserin (Belviq®): selective serotonin 2C receptor agonist. Approved for use for weight loss in 2012, the drug binds to receptors that regulate appetite. Weight loss results are slightly less than phentermine/topiramate when used in conjunction with diet and lifestyle modifications but with fewer side effects (Verpeut & Bello, 2014). Most common adverse events include headache, nausea, and dizziness (Fidler et al., 2011). Other side effects may include hallucinations, valvulopathy, and changes in attention and memory. vi. L iraglutide (Saxenda®): a glucagon-like peptide-1 (GLP-1) receptor agonist, approved by the FDA in December 2014 Plate method For healthy meal planning Artichokes Asparagus Green beans Beets Broccoli Brussels sprouts Cabbage Carrots Cauliflower Cucumber Eggplant Greens Kohlrabi Leeks Lettuce Mushrooms Okra Onions Peppers Spinach Summer squash Tomato Tomato sauce Turnips Zucchini Lean meat Poultry Fish Tofu Eggs Nuts Seeds Lowfat cheese Bread Tortilla Bun Bagel Rice Pasta Cereal Grains Potatoes Corn Yams Peas Winter Squash Beans Fruit 1 portion fruit, if desired Milk 1 portion milk or yogurt, if desired ORStarch Protei n Non-starch y vegetables Figure 65-3 Instructions for Use of the Plate Method (Continued) Produced by UCSF Nutrition and Food Services. Used with permission by UCSF Medical Center. 644 CHAPTER 65 | Obesity
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1. R einforcement of successes and review of difficulties and barriers to change 2. R eevaluation of motivation and degree of adherence 3. R eevaluation of the individual agreement or contract C. Bariatric surgery This type of treatment is known to be the most effective and intensive treatment for morbid obesity, with improve-ment in medical comorbidities, such as HTN, diabetes mellitus, dyslipidemia, sleep apnea, and gastroesophageal reflux disease (in Roux-en-Y gastric bypass [RYGBP]). It is recommended for those who meet the surgical criteria and who have not been able to lose weight despite repeated attempts or maintain weight loss with diet and exercise (Sacks et al., 2005). Surgery may be appropriate for those who meet the medical screening criteria: BMI of greater than or equal to 40 or a BMI of 35-39. 9 with serious health-related problems, such as diabetes or high blood pressure. For patients considering weight loss surgery, the practi-tioner should perform a complete physical and thorough examination of the thyroid as part of the pretreatment evaluation. During this assessment, practitioners should focus on assessing the causes and complications of obesity, including family history of polycystic ovarian disease, hypothyroidism, and medications. The practitioner should screen for existing complications, such as type 2 diabetes, HTN, hyperlipidemia, atherosclerotic CVD, gallbladder disease, gout, cancers, osteoarthritis of the lower extremi-ties, and sleep apnea. Baseline and diagnostic assessments should include electrolytes, liver function tests, complete blood count, total cholesterol, HDL and LDL cholesterol, triglycerides, thyroid function tests, and an electrocardio-gram if a recent one is not available (NHLBI, 1998). 1. Othe r considerations a. M edical conditions that are contraindicated for bariatric surgery include end-stage lung disease, unstable CVD, multiorgan failure, and gastric varices. b. P sychiatric conditions with contraindications for weight loss surgery include current substance use, current heavy alcohol intake, active schizo-phrenia, severe intellectual disability, lack of knowledge regarding surgeries, and medical nonadherence (Bauchowitz et al., 2005). 2. T ypes of bariatric surgeries a. R oux-en-Y gastric bypass is the most popu-lar procedure in the United States (Baron, 2015). Performed both open and laparoscopi-cally, RYGBP is restrictive and malabsorptive in nature. It provides changes in physiology that seem to affect and reset energy equilibrium. type 2 diabetes, 49% lost 5% or more of their baseline body weight verses 16% of placebo. The most common side effects of Saxenda® include nausea, vomiting, diarrhea, head-ache, and constipation. The medication should be discontinued if an individual does not lose 4% of their baseline body weight in the first 16 weeks, as the medication is unlikely to be effective. It carries a black box warning for thyroid C-cell tumor risk. As a condition of FDA approval, additional postmarketing studies must include evalu-ation for safety, effectiveness, and dosing in pediatric patients, assessment of growth, sexual maturation, and central nervous system development in mice, as well as medullary thyroid carcinoma case registry of at least 15 years and evaluation of potential increases in breast cancer (FDA, 2014). b. P sychotropic medications, such as bupropion, fluoxetine, and sertraline, also have a short-term anorexic effect and can be helpful in treatment of individuals with coexisting depression. However, these medications are not approved for weight loss by the U. S. Food and Drug Administration (Sacks et al., 2005). c. I nvestigational products (Nkansah, 2010) i. B upropion/zonisamide (Empatic®): increases metabolism and suppresses appetite. ii. B upropion/naltrexone (Contrave®): increases metabolism and counteracts body “starvation effect. ” Bupropion is a norepinephrine/dopamine reuptake inhibitor used to treat depression and smoking cessation and naltrexone is an opioid antagonist used in the treatment of opioid and alcohol dependency. In trials, it appears to have greater weight loss associated with its use than Orlistat or lorcarserin, although less than phentermine/topiramate but with less severe side effects (Verpeut & Bello, 2014). 6. S upport groups, including family, friends, work-site support, and structured programs. 7. C ognitive-behavioral therapy for lifestyle modifi-cation can be a beneficial addition to a weight loss program. B. Follow-up Follow-up is a critical aspect of success in a weight manage-me nt program, either individual or group based, with frequent visits in the beginning, then negotiated with the patient and their support system. Follow-up should include the following: 645 Plan
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as RYGB. Studies indicate that RYGB is more effective at improving insulin sensitivity and beta-cell function than is sleeve gastrectomy (Kashyap et al., 2013). 3. P reoperative and postoperative care a. Die t and lifestyle modifications need to be reinforced. b. M edications must be evaluated at the time of surgery. With rapid weight loss, diabetes and antihypertensive medications need to be reduced or eliminated as needed (Pi-Sunyer & Nonas, 2004). c. A ll time-released medications (for RYGBP) and nonsteroidal anti-inflammatory drugs need to be evaluated for appropriateness. Ursodiol® is typically used to prevent bile sludge and stones, so patients who have an intact gallbladder are started on Ursodiol®. d. Di scussion with the surgeon should include medication evaluation for change in delivery (e. g., crushed, liquid, or quartered). e. R eferral should be made to a registered dietitian experienced with bariatric surgical patients for evaluation of diet and multivitamin and mineral requirement needs. f. I n addition to surgical complications, multiple early complications need to be monitored for including dehydration, dumping syndrome, nausea and vomiting, and lactose intolerance. Late complications, depending on the type of surgery, may include a variety of vitamin and mineral deficiencies (thiamine, folate, vitamin D, vitamin B 12, calcium, and iron and other fat-soluble vitamins for biliopancreatic diversion with duodenal switch); gallstones; weight regain; and other surgical complications. D. Patient and family education Patient education and instruction should revolve around the following issues and topics: 1. M ultifactorial etiology of obesity and associated health risks 2. M eal plan and nutrition counseling with provision of specific caloric and portion information, including sample menus 3. I mportance of exercise and physical activity scheduled into daily routine 4. F amily involvement and participation and support 5. P atient expectation geared to slow weight loss over months There is strong evidence to suggest that secretion of gastrointestinal hormones, such as grehlin, peptide tyrosine-tyrosine (PYY), and glucagon-like peptide-1, are altered by RYGBP helping to promote weight loss (Beckman, Beckman, & Earthman, 2010). Additionally, other factors such as increased bile acid concentration and altered gut microbiota may contribute to the effects on weight loss from RYGBP (Lutz & Bueter, 2014). Excess body weight loss is anticipated to be approximately 60-70%. b. Ad justable gastric banding is primarily restric-tive in nature. Placement of a foreign body-band around the upper portion of the stomach creates a small stomach pouch. Based on weight loss and tolerance, this is then adjusted with “fills” to decrease the flow rate of food into the larger portion of stomach to provide a longer feeling of fullness. Anticipated excess body weight loss is approximately 50%. Recent long-term studies in Europe, however, have shown that complications (such as band erosion and hiatal hernia) and lack of maintained weight loss have led to large numbers of patients having the band removed or converted to RYGBP; one study performed in a Dutch center found that after ~ 14 years over half the patients fell into this category (Aarts et al., 2014). c. The b iliopancreatic diversion with duodenal switch is primarily malabsorptive. Although expected excess body weight loss is anticipated at approximately 70%, the higher rates of severe side effects, such as diarrhea and nutritional deficiencies, make this surgery less frequently performed (Buchwald, 2005). d. V ertical sleeve gastrectomy is restrictive with the amount of weight loss similar to RYGBP. It is usually performed laparoscopically and limits the volume of food in the stomach by creating a small pouch slightly larger than that created by the lap band procedure. The procedure keeps the pylorus intact and removes the remainder of the stomach. One specific problem, which is unique to sleeve gastrectomy, is an increase in gastroesophageal reflux disease (GERD) symptoms after surgery leading to increased treatment and use of proton pump inhibi-tors (Sheppard, Sadowski, de Gara, Karmali, & Birch, 2014). Although weight loss appears to be similar among RYGB and sleeve gastrec-tomy, sleeve gastrectomy does not appear to be effective in resolving diabetes mellitus as well 646 CHAPTER 65 | Obesity
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Bauchowitz, A. U., Gonder-Frederick, L. A., Olbrisch, M. E., Azarbad, L., Ryee, M. Y., Woodson, M., et al. (2005). Psychosocial evaluation of bariatric surgery candidates: A survey of present practices. Psychosomatic Medicine, 67(5), 825-832. Beckman, L. M., Beckman, T. R., & Earthman, C. P. (2010). Changes in gastrointestinal hormones and leptin after Roux-en-Y gastric bypass procedure: A review. Journal of the American Dietetic Association, 110, 571-584. Bjorkhem-Bergman, L., Asplund, A. B, & Lindh, J. D. (2010). Metformin for weight reduction in non-diabetic patients on antipsychotic drugs: A systemic review and meta-analysis. Journal of Psychopharmacology, 25(3), 299-305. Boyd, M. A. (2002). Atypical antipsychotics: Impact on overall health and quality of life. Journal of the American Psychiatric Nurses Association, 8(4), 9-17. Bray, G. A., & Champagne, C. M. (2005). Beyond energy balance: There is more to obesity than kilocalories. Journal of the American Dietetic Association, 105, S17-S23. Brownell, K. D. (2000). The LEARN Program for weight management 2000. Dallas, TX: American Health Publishing Company. Buchwald, H. (2005). Consensus conference statement bariatric surgery for morbid obesity: Health implication for patients, health professionals and third-party payers. Journal of American College Surgery, 200, 593-604. Centers for Disease Control and Prevention. (2009a). Defining overweight and obesity. Retrieved from http://www. cdc. gov/obesity/defining. html. Centers for Disease Control and Prevention. (2009b). Obesity prevalence among low-income preschool-aged children—United States, 1998-2008. Morbidity and Mortality Weekly Review, 58(28), 769-773. Retrieved from www. cdc. gov/mmwr/preview/mmwrhtml/mm5828a1. htm. Centers for Disease Control and Prevention. (2009c). Overweight and obesity: Health consequences. Retrieved from www. cdc. gov/obesity /causes/health. html. Centers for Disease Control and Prevention. (2013). Obesity—United States, 1999-2010. Retrieved from www. cdc. gov/mmwr/preview /mmwrhtml/su6203a20. htm. Fabricatore, A. N. (2007). Behavior therapy and cognitive-behavioral therapy of obesity: Is there a difference? Journal of the American Dietetic Association, 107, 92-99. Fabricatore, A. N., & Wadden, T. A. (2003). T reatment of obesity: An overview. Clinical Diabetes, 21(2), 67-72. Fidler, M. C., Sanchez, M., Raether, B., Weissman, N. J., Smith, S. R., Shanahan, W., et al. (2011). A one-year randomized trial of lorcaserin for weight loss in obese and overweight adults: The BLOSSOM trial. Journal of Clinical Endocrinology Metabolism, 10, 3067-3077. Fontaine, K. R., Heo, M., Harrigan, E. P., Shear, C. L., Lakshminarayanon, M., Casey, D. E., et al. (2001). Estimating the consequences of anti-psychotic induced weight gain on health and mortality rates. Psychiatry Research, 101, 277-288. Food and Drug Administration. (2010a). FDA drug safety communication: FDA recommends against the continued use of Meridia (sibutramine). Retrieved from www. fda. gov/Drugs/Drug Safety/ucm228746. Food and Drug Administration. (2010b). Postmarket drug safety information for patients and providers. Retrieved from www. fda. gov/drugs /drugsafety/postmarketdrugsafetyinformationforpatientsandproviders /default. htm. VI. Self-management r esources A. For online and smart phone food record keeping to increase patients' awareness of their eating 1. w ww. fitday. com 2. w ww. myfitnesspal. com B. For healthy nutrition and weight loss diets 1. A merican Heart Association, www. heart. org, for healthy recipes, heart healthy tips, and risk calculators for heart disease 2. U. S. Department of Agriculture: www. choosemyplate . gov. This site has resources on the plate method, weight management and calorie counting, physical activity, healthy eating tips, and other nutrition information including printable materials for education. C. For physical activity and exercise resources 1. L et's Move!: www. letsmove. gov/ 2. A merican College of Sports Medicine: www. acsm. org 3. A merican Heart Association: www. heart. org/ 4. Act ive at Any Size: http://win. niddk. nih. gov/publications/active . htm#activeat 5. The re are also smart phone apps for measuring activity including step counting and GPS devices that appear be helpful in increasing awareness of activity (Morrison et al., 2014). re Feren Ce S Aarts, E. O., Dogan, K., Koehestanie, P., Aufenacker, T. J., Janssen, I. M., & Berends, F. J. (2014). Long-term results after laparoscopic adjustable gastric banding: A mean fourteen year follow-up study. Surgery for Obesity Related Diseases, 10(4), 633-640. Allison, D. B., Mentor, J. L., Heo, M., Chandler, L. P., Cappelleri, J. C., Infante, M. C., et al. (1999). Antipsychotic-induced weight gain: A comprehensive research synthesis. American Journal of Psychiatry, 156(11), 1686-1696. American Academy of Child and Adolescent Psychiatry. (2006). Facts for families: Obesity in children and teens. No. 79, updated May 2008. Retrieved from http://www. aacap. org/AACAP/Families_and_Y outh /Facts_for_Families/FFF-Guide/Obesity-In-Children-And-T eens -079. aspx. Aquila, R. (2002). Management of weight gain in patients with schizophrenia. Journal of Clinical Psychiatry, 63(Suppl. 4), 33-36. Baron, R. (2015). Nutritional disorders. In M. Papadakis & S. Mc Phee (Eds. ), 2015 current medical diagnosis & treatment (pp. 1246-1249). New Y ork: Mc Graw-Hill. Basson, B. R., Kinon, B. J., T aylor, C. C., Szymanski, K. A., Gilmore, J. A., & T ollefson, G. D. (2001). Factors influencing acute weight change in patients with schizophrenia treated with olanzapine, haloperidol, or risperidone. Journal of Clinical Psychiatry, 62, 231-238. 647 References
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Nkansah, N. (2010, February 26). Medications for obesity: Why no magic bullets? Presented at the Obesity Summit 2010, University of California, San Francisco, California. Ogden, C. L., Carroll, M. D., Kit, B. K., & Flegal, K. M. (2014). Prevalence of childhood and adult obesity in the United States 2011-2012. JAMA, 311(8), 806-814. Pi-Sunyer, F., & Nonas, C. (2004). Clinical monitoring. In G. D. Foster & C. A. Nonas (Eds. ), Managing obesity: A clinical guide (Chapter 3, pp. 43-64). Chicago, IL: American Dietetic Association. Prochaska, J., & Di Clemente, C. C. (1982). T ranstheoretical approach: T oward a more integrative model of change. Psychotherapy: Theory, Research and Practice, 20, 161. Rummel-Kluge, C., Komossa, K., Schwarz, S., Hunger, H., Schmid, F., Lobos, C. A., et al. (2010). Head-to-head comparisons of metabolic side effects of second generation antipsychotics in the treatment of schizo-phrenia: A systematic review and meta-analysis. Schizophrenia Research, 123, 225-233. Sacks, F. M., Bray, G. A., Carey, V. J., Smith, S. R., Ryan, D. H., Anton, S. D, et al. & Clinical Efficacy Assessment Subcommittee of the American College of Physicians. (2005). Pharmacologic and surgical manage-ment of obesity in primary care: A clinical practice guideline from the American College of Physicians. Annals of Internal Medicine, 142(7), 525-531. Sheppard C. E., Sadowski, D. C., de Gara, C. J., Karmali, S., & Birch, D. W. (2014, November 20). Rates of reflux before and after laparo-scopic sleeve gastrectomy for severe obesity. Abstract. Obesity Surgery. doi: 10. 1007/s11695-014-1480-y. Ul-Haq, Z., Mackay, D. F., Fenwick, E., & Pell, J. P. (2013). Meta-analysis of the association between body mass index and health-related quality of life among children and adolescents. Assessed using the pediatric quality of life inventory index. Journal of Pediatrics, 162, 280-286. U. S. Department of Health and Human Services. (2000). Healthy People 2010. Objectives. Retrieved from www. healthypeople. gov /2010/?visit=1. U. S. Department of Health and Human Services. (2009). Healthy People 2020 proposed objectives. Retrieved from www. healthypeople. gov/2020 /topics-objectives/topic/nutrition-and-weight-status Verpeut, J. L., & Bello, N. T. (2014). Drug safety evaluation of naltrexone/ buproprion for the treatment of obesity. Expert Opinion Drug Safety, 13(6), 831-841. Vesely, J. M., & De Mattia, L. G. (2014). Obesity: Dietary and lifestyle management. FP Essentials, 425, 11-15. Whitaker, R. C., Wright, J. A., Pepe, M. S., Seidel, K. D., & Dietz, W. H. (1997). Predicting obesity in young adulthood from childhood and parental obesity. New England Journal of Medicine, 337, 869-873. Food and Drug Administration. (2014). FDA approves weight-management drug Saxenda. Retrieved from www. fda. gov/News Events/Newsroom /Press Announcements/ucm427913. htm. Gardner, C. D., Kiazand, A., Alhassan, S., Kim, S., Stafford, R. S., Balise, R. R., et al. (2007). Comparison of the Atkins, Zone, Ornish and LEARN diets for change in weight and related risk factors among overweight premenopausal women. The A to Z Weight Loss Study: A randomized trial. JAMA, 297, 969-977. Greenberg, I., Chan, S., & Blackburn, G. L. (1999). Nonpharmacologic and pharmacologic management of weight gain. Journal of Clinical Psychiatry, 60(Suppl. 21), 31-36. Hill, J., & Wing, R. (2003). The National Weight Control Registry. The Permanente Journal, 7(3), 34-37. Institute of Medicine. (2012). Accelerating progress in obesity prevention: Solving the weight of the nation Washington, DC: National Academies Press. http://iom. edu/reports/2012/accelerating-progress-in-obesity-prevention. aspx. Kanaya, A. (2010, February 26). Obesity, metabolic syndrome, and diabetes: Making the connections. Presented at the Obesity Summit 2010, University of California, San Francisco, California. Kashyap, S., Bhatt, D., Wolski, K., Wtanabe, R., Abdul-Ghani, M., Abood, B., et al. (2013). Metabolic effects of bariatric surgery in patients with moderate obesity and type 2 diabetes: Analyses of a randomized control trial comparing surgery with intensive medical treatment. Diabetes Care, 36(8), 2175-2182. Lutz, T., & Bueter, M. (2014). The physiology underlying Roux-en-Y gastric bypass—A status report. Abstract. American Journal of Physiology, Regulatory, Integrative and Comparative Physiology, 307(11), R1275-R1291. Millen, B., Wolongevicz, D., Nonas, C., & Lichtenstein, A. (2014). American Heart Association/American College of Cardiology/The Obesity Society Guidelines for the Management of Overweight and Obesity in Adults: Implications and new opportunities for registered dietitian nutritionists. Journal of the Academy of Nutrition and Dietetics, 114 (11), 1730-1735. Morrison, L. G., Hargood, C., Lin, S. X., Dennison, L., Joseph, J., Hughes, S., et al. (2014). Understanding usage of a hybrid website and smartphone app for weight management: A mixed-methods study. Abstract. Journal of Medical Internet Research, 16(10). National Heart, Lung and Blood Institute. (1998). The clinical guidelines on the identification, evaluations, and treatment of overweight and obesity in adult: The Evidence Report. Retrieved from www. nhlbi. nih. gov/files /docs/guidelines/ob_gdlns. pdf. Newall, H., Myles, N., Ward, P. B., Samaras, K., Shiers, D., & Curtis, J. (2012). Efficacy of metformin for prevention of weight gain in psychiatric popu-lations: A review. International Clinical Psychopharmacology, 27, 69-75. 648 CHAPTER 65 | Obesity
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vaginal secretions, blood, and breast milk. T ransmission occurs when an infected fluid enters the body of an HIV-uninfected person via a mucous membrane (particu-larly the rectal or vaginal mucosa) or the bloodstream. Vertical transmission, now rare in the United States, can occur during pregnancy, labor, delivery, or breastfeeding. Nonvertical HIV exposures that carry the highest risk for transmission are parenteral (blood transfusion, needle sharing during injection drug use, and percutaneous such as needle stick) and sexual (specifically anal and penile-vaginal sex) (Patel et al., 2014). Oral sex carries low risk of HIV transmission, and exposures through biting, spitting, throwing bodily fluids, and sharing sex toys have negligible risk (Centers for Disease Control and Prevention, 2014b; Patel et al., 2014; Pretty, Anderson, & Sweet, 1999). AIDS represents the advanced stages of HIV infection and is characterized by the progressive depletion of CD4 T lymphocytes, resulting in life-threatening HIV-related opportunistic infections (OI) and certain malignancies. For the purpose of disease surveillance, the Centers for Disease Control and Prevention (CDC) developed a case definition for AIDS that has been revised several times to reflect advances in testing, diagnosis, and treatment of HIV. The current case definition of AIDS includes all HIV-infected people with CD4 counts ≤ 200 cells/mm 3 or diagnosis of certain AIDS-defining illnesses (T able 66-1) (CDC, 2014d). The CDC has been tracking AIDS since 1981, when the first cases of a fatal pneumonia called Pneumocystis carinii (later renamed P. jiroveci) appeared in young, oth-erwise healthy gay men. Based on these data, there was an estimated cumulative total of over 1. 1 million cases of AIDS in the United States at the end of 2012 (CDC, 2014a). By 2011, there was an estimated cumulative total of 648,459 deaths from AIDS in the United States (CDC, 2014a). In addition to surveillance of AIDS cases, the CDC has fully established an HIV incidence surveillance system to effectively track trends in new HIV infections. As of 2008, confidential names-based reporting systems have been I. Intr oduction and general background Since the first cases of acquired immunodeficiency syndrome (AIDS) were diagnosed in 1981, there have been significant scientific advances in the understanding of the biology, natural history, and clinical management of human immunodeficien-cy virus (HIV) infection. Far from the bleak years of the early epidemic, HIV infection is now a manageable chronic condi-tion. Both the U. S. Department of Health and Human Services (USDHHS; 2015a) and the Infectious Diseases Society of America (IDSA) publish evidence-based guidelines identify-ing best practices in the clinical management of HIV/AIDS (Aberg et al., 2013). This chapter reviews and summarizes current DHHS and IDSA guidelines for those advanced practice nurses who do not have expertise in HIV/AIDS but who may be providing primary care for people living with HIV/AIDS (PLWH). The chapter also includes information on HIV screening and test-ing, because diagnosing new HIV infections is the first step in the HIV/AIDS care continuum, a model for evaluating the U. S. epidemic that has emerged in recent years (USDHHS, 2013). In addition to HIV screening and testing, clinicians who are generalists can provide primary care to PLWH, offer HIV-specific healthcare maintenance and disease prevention, and initiate or follow antiretroviral therapy (ART) in consulta-tion with HIV experts. A. Epidemiology HIV is the virus that causes AIDS. There are two types of HIV: HIV-1 and HIV-2. HIV-1 is the most prevalent glob-ally and, without treatment, typically progresses to death within 8-10 years. HIV-2 occurs mostly in West Africa and has a slower clinical progression (Maartens, Celum, & Lewin, 2014). This chapter focuses exclusively on HIV-1, and use of the term HIV should be understood as referring to HIV-1. HIV is transmitted through certain bodily fluids: semen, preseminal fluids (or preejaculate), rectal secretions, Suzan Stringari-Murray and Christopher Berryhill Fox Pr IMary Care o F HIV-In F e C ted a dult S© Eliks/Shutterstock; © donatas1205/Shutterstock 64966Chapt Er
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implemented in all 50 states, the District of Columbia, and six U. S. dependent areas (American Samoa, Guam, the Northern Mariana Islands, Puerto Rico, the Republic of Palau, and the U. S. Virgin Islands) (CDC, 2014a). The CDC (2014d) estimates that as of 2011 (the last year for which data are available), there were 1. 2 million PLWH age 13 years or older in the United States. In 2012, there was an estimated incidence of 47,989 new HIV infec-tions, with an incidence rate of 15. 3 per 100,000 (CDC, 2014a). HIV disproportionately affects gay, bisexual, and other men who have sex with men (MSM) in the United States. Although less than 4% of the male population is MSM, this group accounted for 57% of all diagnosed HIV/AIDS cases in 2011 (CDC, 2015c; Purcell et al., 2012). In 2011, women represented one-quarter of all diag-nosed HIV infections in the United States. Heterosexual activity accounted for 84% of new transmissions in this group (CDC, 2014a). Table 66-1 AIDS-Defining Illnesses in Adolescents and Adults Candidiasis of bronchi, trachea, or lungs Candidiasis of esophagus Cervical cancer, invasive Coccidioidomycosis, disseminated or extrapulmonary Cryptococcosis, extrapulmonary Cryptosporidiosis, chronic intestinal (> 1 month's duration)Cytomegalovirus disease (other than liver, spleen, or nodes), onset at age > 1 month Cytomegalovirus retinitis (with loss of vision)Encephalopathy attributed to HIVHerpes simplex: chronic ulcers (> 1 month's duration) or bronchitis, pneumonitis, or esophagitis Histoplasmosis, disseminated or extrapulmonary Isosporiasis, chronic intestinal (> 1 month's duration)Kaposi sarcoma Lymphoma, Burkitt (or equivalent term)Lymphoma, immunoblastic (or equivalent term)Lymphoma, primary, of brain Mycobacterium avium complex or Mycobacterium kansasii, disseminated or extrapulmonary Mycobacterium tuberculosis of any site, pulmonary, disseminated, or extrapulmonary Mycobacterium, other species or unidentified species, disseminated or extrapulmonary Pneumocystis jirovecii (previously known as Pneumocystis carinii) pneumonia Pneumonia, recurrent Progressive multifocal leukoencephalopathy Salmonella septicemia, recurrent Toxoplasmosis of brain Wasting syndrome attributed to HIV Modified from Centers for Disease Control and Prevention. (2014). Revised surveillance case definition for HIV infection—United States, 2014. MMWR, 63(3), 1-10. Retrieved from http://www. cdc. gov/mmwr/pdf/rr/rr6303. pdf. In recent years, new attention has been directed toward older adults living with HIV/AIDS in the United States., with 15% of PLWH now age 55 or older (CDC, 2013a). The graying of the HIV/AIDS epidemic in the United States is attributed to increased survival from ART, as well as infection with HIV later in life. Older adults may be unaware of their HIV risk or never offered testing by a healthcare provider. Compared to their younger counter-parts, older adults are more likely to discover their new HIV infections late in disease progression (CDC, 2013a). Although there are few data describing transgender populations, current evidence suggests that this group is at high risk for HIV, especially among male to female or transgender women (CDC, 2013b). In particular, trans-gender women who are sex workers, both in the United States and globally, have a high prevalence of HIV infec-tion. Data describing HIV incidence, prevalence, or risk among female-to-male or transgender men are severely lacking. 650 CHAPTER 66 | Primary Care of HIV-Infected Adults
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There are significant racial and ethnic disparities in HIV/AIDS incidence, prevalence, and survival in the United States, particularly among African Americans, who are the group most affected by HIV/AIDS (CDC, 2015b). African Americans comprise 12% of the U. S. population but accounted for 47% of all new HIV diagnoses in 2012 (CDC, 2015b). New HIV infections are increasing fastest in young African American MSM (ages 13-24), who had nearly twice the new infections as young white or Hispanic MSM in 2010 (CDC, 2015b). African American women have the highest incidence of non-MSM new HIV infec-tions in the United States, with an incidence rate 20 times that of white women and 5 times that of Hispanic women (CDC, 2015b). African Americans also had the highest HIV death rate in 2010 at 11. 6 per 100,000—a dramatic contrast from the death rates of whites (1. 1 per 100,000) and Hispanics (2. 8 per 100,000) (National Center for Health Statistics, 2014). Historically, most PLWH have been clustered in major metropolitan areas in three states: California, New Y ork, and Florida. Now urban and rural areas in the South, as well as the District of Columbia, have emerged as a locus of HIV/AIDS. The District of Columbia has the highest estimated prevalence rate of HIV in the United States and dependent areas at 2,721. 6 per 100,000 compared to 342. 1 per 100,000 overall (CDC, 2014a). Globally, there have been 78 million people infected with HIV since the start of the epidemic, resulting in 39 million deaths (United Nations Joint Programme on HIV/AIDS [UNAIDS], 2014). As of 2013, UNAIDS esti-mates that there were a total of 35 million PLWH globally, with the majority (70%) of cases in Sub-Saharan Africa. Heterosexual sex is the main mode of transmission in this region. Among countries, South Africa continues to carry the greatest HIV/AIDS burden, with 18% of global infec-tions (UNAIDS, 2014). Deaths from AIDS-related causes peaked globally in 2005 and have now fallen 35% with advances in prevention and treatment, as well as increased access to ART. Even so, in 2013, only 37% of PLWH globally had access to ART (UNAIDS, 2014). New HIV infections around the globe have decreased 38% since 2001 (UNAIDS, 2014). In 2013, there were 2. 1 million new HIV infections, compared to 3. 4 million in 2001. Despite this downward trend, certain groups remain highly vulnerable to new HIV infections, including ado-lescent and young women, MSM, transgender people, sex workers, intravenous drug users (IVDUs), and incarcer-ated individuals (UNAIDS, 2014). B. Pathogenesis and natural history of HIV infection T ransmission of HIV is followed within days to weeks by a nonspecific viral syndrome or seroconversion illness characterized by fever, generalized maculopapular rash, lymphadenopathy, and pharyngitis. Approximately 40-90% of patients acutely infected with HIV will experience this nonspecific and self-limiting viral syn-drome (Panel on Antiretroviral Guidelines for Adults and Adolescents [PAGAA], 2015a). The period of acute HIV infection is characterized by an initial burst of vire-mia. Recent infection is the phase up to six months after infection when HIV-specific antibodies are detectable. Individuals with acute HIV have high levels of replicat-ing virus, and transmission of HIV to an uninfected partner(s) is more likely during this phase of infection. Following transmission, HIV disseminates throughout the body infecting CD4 T-helper lymphocytes, a main tar-get of the virus. HIV enters the host cell by attaching and binding to coreceptors on the surface of the cell (CCR5 and CXCR4). Once in the cell cytoplasm, viral enzymes reverse transcribe viral RNA into viral DNA. Viral DNA enters the cell nucleus and integrates into the host cell genome. Once integrated into the host cell genome, HIV persists as a latent reservoir of virus despite fully suppres-sive ART (Hare, 2009). Research on the immunopathogenesis of HIV has resulted in an improved understanding of how HIV causes AIDS. An active site of HIV replication is the lamina propria of the gut wall, which is rich in lymphoid tissue and contains large numbers of CCR5 express-ing CD4 T-helper lymphocytes. During acute HIV, gut-associated lymphoid tissue (GALT) is rapidly infected and destroyed, leading to local inflammation and increased gut permeability. It is hypothesized that leak-age of microbes or “microbial translocation” from the gut results in a state of chronic immune system activation and inflammation (Douek, Picker, & Koup, 2003). Chronic immune system activation helps to sustain HIV replica-tion through the continuous production of HIV-infected activated CD4 cells, which produce HIV and perpetu-ate a continuous cycle of viral replication. High levels of virus in the blood (viral load) are associated with more rapid destruction of CD4 lymphocytes and more rapid clinical progression. If HIV infection goes unrecognized, over a period of months to years (on average, 8-10 years) progressive depletion of CD4 lymphocytes leads to immune system failure and death from HIV, usually as a result of AIDS-related illnesses (Figure 66-1). Once HIV infection is established, chronic inflammation and immune activation persist even in patients on ART who have undetectable viral loads. Currently recommended ART regimens are potent and effective in suppressing HIV replication but cannot eradi-cate HIV in host cells. Effective HIV treatment requires lifelong therapy and adherence to ART. Incomplete or intermittent adherence to ART can result in the failure to 651 Introduction and general background
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C. HIV primary care and the HIV care continuum HIV is now considered a chronic primary care disease. The HIV Care Continuum identifies a series of steps to fully engage and retain patients in primary care. Current esti-mates of HIV/AIDS care in the United States indicate that of those individuals who know they are HIV infected, only 37% are on ART, and of those individuals who are on ART, only 30% are virally suppressed (Figure 66-2). Nurse Practitioners (NPs) play an essential role in improving health outcomes of PLWH along all steps of the HIV Care Continuum (CDC, 2014e). The most significant impact for reducing HIV infections is achieved by providing HIV testing as a routine part of care in all medical settings and immediately linking patients diagnosed with HIV to medi-cal care. Once patients are engaged in care, rapid initiation of ART and viral load suppression improves individual health outcomes and prevents further transmission of HIV. T reatment with ART has significantly reduced deaths due to AIDS-defining illnesses (T able 66-1). Chronic conditions such as cardiovascular disease (CVD), fully suppress HIV replication and lead to the develop-ment of HIV-drug resistant virus. Significant improvements have occurred in the potency, tolerability, and frequency of dosing for ART regimens. Recommended regimens for initial treatment of HIV con-sist of a combination of three or more drugs. Several of these combinations are now available as daily single tab-let regimens (STR), which simplify therapy and support adherence by reducing pill burden (PAGAA, 2015a). Historically, the initiation of ART has been guided by CD4 T lymphocyte counts. Current evidence-based guidelines recommend ART for all regardless of the pre-treatment CD4 T lymphocyte count (T able 66-2). This recommendation is based on evidence from randomized controlled trials and observational studies that show a reduction in mortality for both AIDS-defining illnesses and non-AIDS-defining illnesses (e. g., cardiovascular, liver, or kidney disease) in individuals who are started on ART at higher pretreatment CD4 cell counts (PAGAA, 2015a). Figure 66-1 T ypical Course of HIV Infection During the period following primary infection, HIV disseminates widely in the body; an abrupt decrease in CD4+ T cells in the peripheral circulation is often seen. An immune response to HIV ensues, with a decrease in detectable viremia. A period of clinical latency follows, during which CD4+ T cell counts continue to decrease, until they fall to a critical level below which there is a substantial risk of opportunistic infections. (Adapted from Pantaleo et al., 1993. ) Reproduced from National Institute of Allergy and Infectious Diseases. (2010). The relationship between the human immunodeficiency virus and the acquired immunodeficiency syndrome. Retrieved from http://www. niaid. nih. gov /topics/hivaids/understanding/howhivcausesaids/pages/relationshiphivaids. aspx Culturable plasma viremia HIV RNACD4+ count1,200 ± Acute HIV syndrome Wide dissemination of virus Seeding of lymphoid organs1,100 1,000 900800700600500400300200100 0 Weeks CD4+ count (cells per mm3) Years03 6912 12 34 65 7891 011Clinical latency Death Opportunistic diseases107 106 105 104 103 1021/5121/2561/1281/64Culturable plasma viremia (dilutional titer)HIV RNA (copies per m L plasma) 1/321/161/81/41/20Constitutional symptoms Primary infection652 CHAPTER 66 | Primary Care of HIV-Infected Adults
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initiating and managing ART. Improved survival for PLWH has increased the prevalence of older adults (age > 50 years) living with HIV who have multiple chronic conditions complicated by HIV and HIV treatment. Improvements in life expectancy of PLWH beyond those that can be achieved with the use of ART will depend on optimal management of their multiple comorbidities. Most evidence-based guidelines for chronic diseases do not address the impact of HIV in the management of chronic diseases. T o address this gap in recommenda-tions the HIV Medicine Association (AAHIVM) of the Infectious Disease Society of America (IDSA) has devel-oped guidelines for managing comorbid conditions com-monly seen in PLWH (see Resources). The following is a summary of some of these recommendations. 1. H IV, CVD, and dyslipidemias: Despite effective ART, PLWH have an increased risk of CVD and myocardial infarction (MI) when compared to the general population. In a retrospective study of an HIV-infected urban population, sudden cardiac death occurred at a rate four time higher in HIV-infected compared to non-HIV-infected subjects (T seng et al., 2012). Underlying mechanisms proposed for this observed increased risk of MI include chronic immune activation and inflammation, ART-related side effects, and a greater prevalence of cardiovascular risk factors. Observational cohort studies of PLWH have documented past or current smoking in > 50% of study subjects as well as high rates of dyslipidemias (Friis-Møller et al., 2003). Nationally representative surveys of adults with HIV have shown that smoking prevalence is two times higher than in the general U. S. population (Mdodo et al., 2015). Strategies to address increased risk for CVD have included changing ART regimens associated non-AIDS-defining malignancies, diabetes, chronic obstructive pulmonary disease, osteoporosis, thromboem-bolic disease, liver disease, renal disease, and neurocogni-tive dysfunction are increasingly the most common causes of morbidity and mortality in PLWH (Antiretroviral Therapy Cohort Collaborative, 2008; Strategies for Management of Antiretroviral Therapy [SMART] Study Group et al., 2006). HIV care now consists of more than Table 66-2 Initiating Antiretroviral Therapy in T reatment-Naïve Adults and Adolescents Antiretroviral therapy (ART) is recommended for all HIV-infected individuals to reduce the risk of disease progression. ART is recommended for all (CD4) cell counts: CD4 count < 350 cells/mm3 (AI); CD4 count 350 to 500 cells/mm3 (AII); CD4 count > 500 cells/mm3 (BIII). ART is also recommended for HIV-infected individuals to prevent transmission of HIV. The strength of and evidence for this recommendation vary by transmission risks: perinatal transmission (AI); heterosexual transmission (AI); other transmission risk groups (AIII). Patients starting ART should be willing and able to commit to treatment and understand the benefits and risks of therapy and the importance of adherence (AIII). Patients may choose to postpone therapy, and providers, on a case-by-case basis, may elect to defer therapy on the basis of clinical and/or psychosocial factors. Rating of Recommendations: A = Strong; B = Moderate; C = Optional Rating of Evidence: I = Data from randomized controlled trials; II = Data from well-designed nonrandomized trials or observational cohort studies with long-term clinical outcomes; III = Expert opinion Data from U. S. Department of Health and Human Services, Panel on Antiretroviral Guidelines for Adults and Adolescents. (May 1, 2014). Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents, p. E-1. Retrieved from https://aidsinfo. nih. gov/guidelines. Figure 66-2 HIV/AIDS Care Continuum in the United States, 2011 Modified from Centers for Disease Control and Prevention. (2014). Vital signs: HIV diagnosis, care, and treatment among persons living with HIV—United States, 2011. Morbidity and Mortality Weekly Report, 63(47), 1113-1117. Retrieved from http://www. cdc. gov/mmwr /preview/mmwrhtml/mm6347a5. htm. 100% 86% 66% 37% 30% 0%20%40%60%80%100%120% HIV Infected (N=1. 2 million)Diagnosed Engaged in Medical Care Prescribed Antiretroviral Therapy (ART)Virally Suppressed653 Introduction and general background
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with dyslipidemias and body fat redistribution syn-dromes and an increased emphasis on managing traditional risk factors such as smoking, abnormal lipids, and hypertension. Abacavir, a component of some ART regimens, has been associated with an increased risk of CVD. Studies supporting this asso-ciation are conflicting and consensus on avoidance of abacavir in individuals at risk for MI has not been reached. Current ART treatment recommendations provide clinicians with guidance regarding regimen characteristics and consideration of specific clinical scenarios for the selection of initial ART regimens (PAGAA, 2015a). Lipid management guidelines published in 2013 by the American Cardiology Association/American Heart Association (ACA/AHA) have been shown to underestimate the need for statin therapy in PLWH who have CT evidence of coronary plaque, suggesting that population-based guidelines may be inadequate for PLWH (Zanni et al., 2014). Despite evidence suggesting that CV disease risk is underestimated, current recommendations for lipid management in the general population apply to PLWH. Use of lovas-tatin and simvastatin are contraindicated in patients on protease inhibitor containing ART regimens due to significant drug-drug interactions. Medications should be reviewed for known or potential interac-tions between ART and commonly prescribed statins, antihypertensives, anticoagulants, and antiplatelet medications (PAGAA, 2015a). 2. H IV and diabetes mellitus (DM): The prevalence of DM in PLWH has been noted to range between 4-14% (Brown et al., 2005; Friis-Møller et al., 2003). First-generation protease inhibitors (indinavir) have been shown to impair glucose metabolism, and older NRTIs (stavudine) are associated with lipoatrophy and lead to development of DM. PLWH also have a higher prevalence of conditions associated with DM such as chronic HCV and ART-related fat redistribution syndromes. Important clinical management differences for PLWH who are diagnosed with DM include drug-drug interactions between metformin and dolutegravir (PAGAA, 2015a) and Hb A1c discordance with fasting plasma glucose (FPG) levels. Some experts recommend use of FPG to screen for DM and suggest that lower target goals for Hb A1c may be needed (Monroe, Gelsby, & Brown, 2015). At this time, treatment goals, lifestyle modification, and clinical management of DM are the same as for the general population. 3. H IV and malignancies: There are three AIDS-defining cancers: Kaposi sarcoma (KS) caused by human herpes virus-8, Non-Hodgkin's lymphoma, and cervical cancer (T able 66-1). In addition to AIDS-defining cancers PLWH also have an increased risk of non-AIDS-defining cancers that are virally mediated or related to specific health behaviors: lung cancer (tobacco), liver cancer (HBV, HCV, and alcohol abuse), and anal cancer (HPV). Cervical cancer screening in women with HIV differs from the current U. S. Preventive Services T ask Force (USPSTF) recommendations for initiation of screening, frequency of screening, and management of abnormal Pap smears (T able 66-3). The incidence of breast, colon, and prostate can-cer is similar to the general population. Significant declines in the incidence and prevalence of KS and primary CNS lymphoma have occurred in with wide-spread use of ART. The incidence of cervical cancer has not changed with the introduction of ART, how-ever, the incidence of anal cancer has increased in both men and women. National multicenter studies are ongoing to determine cancer rates in PLWH to guide future policy on the impact of HIV infection on cancer risk and cancer related morbidity and mor-tality (U. S. National Institutes of Health, National Cancer Institute, n. d. ). Cancer is a disease of aging. As PLWH grow older and reach their normal life expec-tancy, providers will likely see more cancer diagnoses in HIV-treated populations. 4. H IV and renal disease: HIV infection is a risk factor for chronic kidney disease (CKD). Comprehensive clinical practice guidelines for management of CKD in PLWH have been published (Lucas et al., 2014). The spectrum of renal disease in HIV includes acute kidney injury and glomerular diseases (HIV-associated nephropathy) as well as CKD. Risks for kidney disease in PLWH include African American race, family history, CD4 count < 200 cells/mm 3, HIV viral load > 4,000 copies/m L, past use of neph-rotoxic drugs, family history, and comorbidities of hypertension, diabetes, and chronic HCV. An impor-tant source of kidney disease is HIV medication-associated kidney injury, with tenofovir disoproxil fumarate (TDF) of most concern. Kidney injury with tenofovir can be acute, presenting as proximal tubular dysfunction, or chronic with declines in GFR related to cumulative exposure to tenofovir. T enofovir alaf-enamide, (TAF) an oral prodrug of tenofovir, is now approved as a component of a fixed-dose combina-tion tablet for initial treatment of HIV. The poten-tial for adverse kidney and bone effects is less with TAF than with TDF. Cobicistat, a pharmacokinetic booster found in some ART regimens, is approved for use in patients with a creatinine clearance (Cr Cl) of > 70 m L/min. Recommendations for dosing of 654 CHAPTER 66 | Primary Care of HIV-Infected Adults
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Table 66-3 Healthcare Maintenance and Disease Screening test Fr equency Comments Mycobacterium tuberculosis (MTB) skin test (TST) and interferon-γ release assay (IGRA)Screen at entry into care and annually regardless of CD4 count PLWH who have latent tuberculosis infection (LTBI) have a 3-16% annual risk of active MTB Routine use of both TST and IGRA is not recommended. TST: Criteria for a positive skin test ≥ 5 mm induration at 48-72 hours. IGRA: Has advantages over TST for TB screening in adults with HIV, including single patient visit to conduct test; results available in 24 hours; does not cross-react in patients who have been previously vaccinated with BCG; and has higher specificity (92-97%) compared to TST. Disadvantages include cost and limited data on PLWH. Rescreen if CD4 increases to 200/mm 3 and previous TB screening was negative. Cytomegalovirus-CMV Ig GAt entry into care Screen in patients where likelihood of cytomegalovirus seropositivity is low (higher CMV seropositive prevalence in MSM and IDU). Herpes simplex virus (HSV-2)At entry into care Prevention of acquisition of HSV is recommended. Disclosure of HSV-2 in heterosexual HSV-2-discordant couples has been associated with reduced risk of transmission of HSV-2. PLWH who are seronegative for HSV-2 should ask their sexual partners to be screened for HSV-2 (BII). Neisseria gonorrhoeae (GC) and Chlamydia trachomatis (CT) Trichomonas vaginalis At entry into care regardless of symptoms and when clinically indicated (multiple partners, reported high-risk behaviors, recurrent STDs) Women < age 25 and/or high-risk men and women who test positive for GC, CT, and trichomoniasis Nucleic acid amplification tests (NAAT) are sensitive and preferred for both genital and extragenital sampling. Sexually active MSM, particularly ≤ 25 yrs, have a high burden of disease for CT and GC. NAATs are not approved by the Food and Drug Administration for testing rectal and oropharyngeal sites yet are sensitive and specific compared to culture. Check local health departments for guidance in using these tests. Sexual partners should be referred for evaluation, testing, and presumptive treatment if they had sexual contact with the partner during the 60 days preceding the patient's onset of symptoms or chlamydia diagnosis (Centers for Disease Control and Prevention, 2015d) Increased risk of HIV transmission and pelvic inflammatory disease in untreated trichomoniasis Reinfection rates of STDs are high and repeat of all positive tests at 3 months following treatment is recommended655 Introduction and general background (continues)
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Table 66-3 Healthcare Maintenance and Disease Screening test Fr equency Comments Syphilis-Venereal Disease Research Laboratory (VDRL) or Rapid plasma reagin (RPR)At entry into care and annually. More frequent screening (q 3-6 months) for those with multiple partners, sex without condoms, and partner recently treated for STDs Nontreponemal tests are sensitive and specific in PLWH. Some labs may use enzyme immunoassays (EIA) in syphilis testing algorithms followed by a reflex-quantitative, nontreponemal test if the EIA is positive. Screening for other STDs (GC and CT) at anatomic sites of exposure should be done when screening or treating syphilis Dilated retinal examination CD4 < 100 annually and when clinically indicated Screen for HIV-related retinopathy and asymptomatic cytomegalovirus retinitis. Chest radiograph Baseline If positive TB screening test and history and exam suggestive of preexisting lung disease Serum testosterone level Men Morning specimen In males with fatigue, weight loss, and erectile dysfunction Anal cancer screening Men and women. At entry and annually based on risk Incidence of anal cancer is increasing in PLWH due to improved length of survival and reduced rates of HPV clearance in PLWH despite ART. Although there are no national guidelines for anal cancer screening, some experts recommend screening (CIII). If resources for referral of abnormal anal cytology are not available, screening is optional (CIII). Cervical cancer screening≤ 30 yrs old: Screen at time of initial diagnosis. If normal, repeat in 12 months (BII). If 3 consecutive normal pap smears, repeat every 3 years. ≥ 30 years old:Pap testing only: At baseline, and every 12 months (BII). If results of the 3 consecutive Pap tests are normal, recommend follow-up Pap tests every 3 years (BII) See Chapter 20, Screening for Intraepithelial Neoplasia and Cancer of the Lower Genital Tract, for details. Women with HIV have a higher prevalence of HPV infection and increased incidence of cervical cancer compared to women who are not HIV infected. Begin screening at onset of sexual activity regardless of mode of transmission (e. g., sexual, perinatal exposure) but no later then 21 yrs old. Co-testing with HPV is not recommended for HIV-infected women < 30 yrs old. See Chapter 20, Screening for Intraepithelial Neoplasia and Cancer of the Lower Genital Tract, for additional details. Breast, prostate, colon, and lung Cancer screening guidelines for general population apply to PLWH Bone mineral density screen Perform baseline exam in postmenopausal women and men age > 50 yrs. PLWH have increased prevalence of osteopenia and osteoporosis and increased risk of fragility fractures compared to general population Rating of Recommendations: A = Strong; B = Moderate; C = Optional Rating of Evidence: I = Data from randomized controlled trials; II = Data from well-designed nonrandomized trials or observational cohort studies with long-term clinical outcomes; III = Expert opinion” as noted in table 66-2 Data from Centers for Disease Control and Prevention. (2010, June 25). Updated guidelines for using interferon gamma release assays to detect Mycobacterium tuberculosis infection in the United States, 2010. MMWR Recommendations and Reports, 59(RR05), 1-25. Retrieved from www. cdc. gov/mmwr/preview/mmwrhtml/rr5905a1. htm?s_cid=rr5905a1_e; Centers for Disease Control and Prevention. (2015). Sexually transmitted disease treatment guidelines, 2015. MMWR Recommendations and Reports, 64(RR3), 1-137. Retrieved from www. cdc. gov/mmwr/preview/mmwrhtml /rr6403a1. htm; Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. (2013). Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. Retrieved from http://aidsinfo. nih. gov /contentfiles/lvguidelines/adult_oi. pdf. (Continued)656 CHAPTER 66 | Primary Care of HIV-Infected Adults
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ART regimens in patients with renal and/or hepatic disease can be found in the treatment guidelines (PAGAA, 2015a). 5. H IV and bone disease: Low bone mineral density (BMD) is highly prevalent in PLWH (~15%), with a 3. 7-fold increase compared with age-matched controls, and rates of bone fracture for PLWH are higher than the general population (Y oung et al., 2011). The causes of low BMD are multifactorial and include traditional risks as well as HIV-specific risk factors such as chronic inflammation, ART-associated bone loss, and HIV/HCV confection. Following the initiation of ART, a 2-6% decrease in BMD occurs over the first 2 years of therapy (Mc Comsey et al., 2010). All ART regimens have been implicated in bone loss with tenofovir having the strongest association with an acute decrease in BMD compared to other NRTIs (Rothman & Bessesen, 2012). 6. H IV and chronic HBV and HCV: Chronic viral hepatitis is more prevalent in PLWH due to similar routes of transmission (sexual transmission and IDU). Coinfection with chronic HBV or HCV results in a more rapid progression to fibrosis and cirrhosis and an increased risk of hepatocellular carcinoma (HCC). Both HBV and HCV may complicate the treatment of HIV due to hepatotoxicity associated with ART. HIV/HBV coinfected patients have higher levels of HBV viremia and a lower likelihood of clearing their infection following acute HBV infection. All HIV-infected patients without evidence of immu-nity to HBV should be vaccinated with HBV vaccine (T able 66-4). There are three antiretroviral drugs from the NRTI class with activity against HBV: lamivudine, emtric-itabine, and tenofovir. Some are available alone or in a fixed-dose combination. HBV and HIV must be treat-ed concurrently with ART that is active against both infections. For example, the fixed-dose combination of abacavir/lamivudine is a recommended regimen for treating HIV when combined with dolutegra-vir, but is inadequate for effectively treating HBV (PAGAA, 2015a). T reating HBV with tenofovir only in an HIV-infected patient would be inadequate treat-ment for HIV and lead to HIV drug resistance. Return to immune competence with increases in CD4 lym-phocyte counts occurs after initiation of ART and can lead to reactivation of HBV-related liver disease. Liver transaminases must be followed more closely when initiating ART in HIV/HBV coinfected patients (Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents, 2013). HIV/HCV: The management of HCV is rapidly evolving, and several newer oral agents have been approved for treatment. Studies of HCV direct-acting antiviral agents (DAA) have shown that these drugs are safe and effective in HIV/HCV coinfection. PLWH who have chronic HCV have been catego-rized as high priority patients for treatment with these agents. (See Chapter 51, Chronic Viral Hepatitis. ) Recommendations for concomitant use of HCV DAAs and drug interactions with ART are provided in current guidelines (PAGAA, 2015b). II. HIV scr eening and testing A. Rationale Fourteen percent of Americans with HIV do not know that they are infected (CDC, 2014a), which has led the USDHHS (2014) to identify increasing awareness of HIV serostatus as a Leading Health Indicator in Healthy People 2020. Increased HIV serostatus awareness is also a goal of the National HIV/AIDS Strategy (White House Office of National AIDS Policy, 2010). Early detection of HIV infection benefits patients by creating an opportunity to initiate ART, thereby prevent-ing further immune destruction with its resulting morbid-ity and mortality. Knowledge of HIV serostatus also has major public health implications: Individuals with HIV who do not know their serostatus are the source of approx-imately 54% of new HIV transmissions (Marks, Crepaz, & Janssen, 2006). A person with unsuppressed virus is significantly more likely to transmit virus to a sexual or needle-sharing partner. Individuals with acute HIV infec-tion may have very high levels of HIV. Individuals may also unknowingly facilitate viral transmission by participating in high-risk behaviors that would otherwise avoid if they were aware of their HIV serostatus. In a nationwide survey of Americans, the top reasons that individuals gave for never receiving an HIV test were lack of perceived risk (#1) and testing had never been recommended by a doctor (#2) (Henry J. Kaiser Family Foundation, 2009). Therefore, it is incumbent upon clini-cians to discuss HIV risk with patients and offer routine testing. B. Guidelines 1. N ational recommendations a. The C DC (2006) recommends screening all patients ages 13-64 years, except in settings of low undiagnosed HIV prevalence (defined as < 0. 1%, or less than 1 in every 1,000 HIV tests is positive). 657 HIV screening and testing
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Table 66-4 Immunizations for HIV-Infected Adults All PLWH should be immunized according to CDC vaccine schedules for adults and adolescents. In general, the immune response to vaccines in PLWH is not as robust compared to HIV noninfected populations. Some clinicians may defer vaccines if an increase in CD4 T lymphocyte count to ≥ 200 mm 3 is anticipated as a result of initiating ART. Some vaccines should not be deferred regardless of CD4 cell count. Vaccines that are contraindicated in PLWH. Live attenuated intranasal influenza (LAIV-Flumist) Oral polio virus (OPV) Smallpox Typhoid oral vaccine (Ty21a) Bacillus Calmette-Guerin (BCG) *Close contacts of persons with HIV should receive all age-appropriate vaccines, with the exception of live OPV and smallpox vaccine Live vaccines that can be administered when CD4 counts are > 200 mm3. Measles/Mumps/Rubella (MMR): Vaccine schedule and dosing are the same as for the general population. Persons with HIV infection are at increased risk for severe complications if infected with measles. Newly diagnosed adults without acceptable evidence of measles immunity should receive mumps-measles-rubella vaccine unless they have evidence of severe immunosuppression (CD4 ≤ 200 mm 3). If necessary separate components of vaccine can be given. Varicella: Vaccine schedule and dosing are the same as for the general population People born before 1980 do not need to receive this vaccine. No studies have evaluated the vaccine in HIV-infected adolescents or adults. Varicella vaccination may be considered in HIV-seropositive/VZV seronegative persons ≥ 8 years old with CD4 counts ≥ 200 cells/mm 3. Do not administer during pregnancy. Varicella Zoster (VZV): Vaccine schedule and dosing are the same as for the general population Safety and efficacy in PLWH is unknown. Consider in patients 60 years of age with a CD4 > 200 mm 3. Serologic testing of prior exposure not required. If susceptible to VZV avoid exposure to individuals with varicella. Household contacts should be vaccinated to prevent transmission of varicella to PLWH. If a known or suspected VZV exposure occurs post exposure prophylaxis is recommended with Varicella Zoster Immune Globulin (VZIG). Yellow fever: Vaccine schedule and dosing are the same as for the general population Safe in patients without severe immunosuppression (CD4 > 200) Less immunogenic in PLWH Use with caution in persons on ART regimens containing CCR5 Inhibitors due to hypothetical concern regarding increased severity of vaccine-associated adverse events (Roukens, Visser, & Kroon, 2009). Vaccines that can be administered at any CD4 cell count. Inactivated, recombinant, subunit, polysaccharide, and conjugate vaccines and toxoids are safe and can be administered to all HIV-infected patients. Inactivated Influenza A & B virus infection-Inactivated Influenza: Vaccine schedule and dosing are the same as for the general population Indicated for all adolescent and adult PLWH regardless of age or comorbid conditions Hepatitis A: Vaccine schedule and dosing are the same as for the general population Immunize all nonimmune men who have sex with men (MSM) and those with increased risk of acquiring hepatitis A virus or at risk of experiencing severe illness if acutely infected with hepatitis A virus (HAV): chronic hepatitis B virus (HBV) or hepatitis C virus (HCV), injection drug use (IDU), hemophiliacs, and travel to high-risk areas. 658 CHAPTER 66 | Primary Care of HIV-Infected Adults
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Table 66-4 Immunizations for HIV-Infected Adults Hepatitis B: Vaccination schedule and dosing differ from general population. Engerix-B® 20 mcg/m Lor Recombivax HB® 10 mcg/m L at 0, 1, and 6 months (AII), Or Engerix-B® 40 mcg/m L or Recombivax HB® 20 mcg/m L) at 0,1,2 and 6 months (BI) or Combined HAV and HBV vaccine (Twinrix®) as a 3-dose series at 0, 1, and 6 months or as a 4-dose series at 0, 7, 21 to 30, and 12 months) (AII) Alternative Vaccine Dose for Non-Responders: HBV vaccine IM (Engerix-B® 40 mcg/m L or Recombivax HB® 20 mcg/m L) at 0,1,2 and 6 months (BI), Prevaccination screening includes anti-HBs, HBs Ag, and anti-HBc Presence of anti-HBs > 10 international units/m L (IU/m L) indicates immunity. Vaccinate all patients without immunity to HBV. Vaccinate patients with isolated anti-HBc (no detected anti-HBs or HBs Ag) Early vaccination is recommended before CD4 count falls below 350 cells/mm 3. However, in a patient with low baseline CD4 cell count, vaccination should not be deferred until CD4 reaches > 350 cells/mm3. Anti-HBs should be obtained 1 month after completion of the vaccine series. Anti-HBs < 10 IU/m L at 1month is considered a nonresponder. (BIII) For vaccine nonresponders revaccinate with second vaccine series (BIII) or for patients with low CD4 at time of first series, defer repeating series while awaiting a rise in CD4 count to ≥ 350 cells/mm 3. (C-III) Hemophilus influenzae type B (Hib) No longer indicated due to low risk of disease in HIV infected Human papillomavirus (HPV): Vaccine schedule and dosing are the same as for the general population. Cervical and anal intraepithelial neoplasia rates are significantly higher in HIV infected than general population. HPV vaccine is safe and immunogenic in HIV infected and the potential benefit is high. Catch-up immunizations are recommended for girls age 13-26 yrs. (do not administer during pregnancy) and for males age 13-26 yrs. Meningococcal: Vaccine schedule and dosing are the same as for the general population. Recommended only if some other risk factor present (e. g., medical, occupational, lifestyle, travel to endemic area). Streptococcus pneumoniae infection Vaccination schedule and dosing differ from general population: No past immunization for streptococcus pneumonia: If CD4 count ≥ 200: PCV-13 0. 5 m L IM × 1. PPV23 0. 5 m L IM or SQ at least 8 weeks after the PCV13 vaccine (AII). If CD4 count ≤ 200: PCV-13 0. 5 m L IM × 1. PPV23 can be offered at least 8 weeks after receiving PCV13 (CIII) or can wait until CD4 count increased to ≥ 200 cells/μL (BIII). For individuals who have previously received PPV23: One dose of PCV13 should be given at least 1 year after the last receipt of PPV23. (AII) PLWH have an increased risk of invasive pneumococcal disease compared to age matched controls. Both PCV-13 and PPSV-23 are recommended based on past immunizations for streptococcus pneumonia and CD4 counts. Revaccinate with PPV23 if: Age 19-64 years and ≥ 5 years since the first PPV23 dose Age ≥ 65 years, and if ≥ 5 years since the previous PPV23 dose(Continued) (continues)659 HIV screening and testing
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Table 66-4 Immunizations for HIV-Infected Adults Tetanus, diphtheria, and acellular pertussis (Td/Tdap): Vaccine schedule and dosing are the same as for the general population. Boost every 10 years Rating of Recommendations: A = Strong; B = Moderate; C = Optional Rating of Evidence: I = Data from randomized controlled trials; II = Data from well-designed nonrandomized trials or observational cohort studies with long-term clinical outcomes; III = Expert opinion Data from Centers for Disease Control and Prevention. (2015a). ACIP vaccine. Retrieved from www. cdc. gov/vaccines/hcp/acip-recs/index. html; Centers for Disease Control and Prevention. (2015e). Vaccines that might be indicated for adults based on medical and other indications. Retrieved from www. cdc. gov/vaccines/schedules/hcp/imz/adult-conditions. html; Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. (2013). Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: Recommendations from the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America (pp. Q-10, Q-11, U-2, V-1). Retrieved from https://aidsinfo. nih. gov/contentfiles/lvguidelines/Adult_OI. pdf. b. The U. S. Preventive Services T ask Force (2013) recommends screening all patients ages 15-65 years (Grade A recommendation), with screening of younger adolescents or older adults based upon HIV risk. 2. C onsent process for HIV testing: Historically, HIV testing involved separate written informed consent and extensive counseling. This process was found to be a barrier to testing and is no longer recommended (CDC, 2006). Both the CDC (2006) and the USPSTF (2013) recommend opt-out consent: a patient must specifically decline testing. Opt-out testing has been codified in the laws of many states; however, clinicians should refer to specific laws regarding consent requirements in their state of practice. A summary of these laws is available at the Clinicians Consultation Center (see Resources section). 3. R epeat screening: The CDC (2006) recommends repeat screening at least yearly for patients at high risk for HIV infection. The USPSTF (2013) states that there is insufficient evidence to make a recommendation, but it is reasonable to screen high-risk patients more frequently. Patients at high risk include: a. P eople who inject drugs and their sex partners b. P eople who exchange money or drugs for sex c. A nyone with an HIV-infected partner d. P eople with more than one sex partner e. P eople who have a sex partner who has multiple partners 4. S pecific recommendations for MSM: Due to the high burden of HIV/AIDS in this population, the CDC (2011) recommends screening sexually active MSM every 3-6 months. 5. H IV screening in pregnancy: The CDC (2006) and the USPSTF (2013) have published specific recommendations for HIV screening in pregnancy, which are available online (see Resources). C. Laboratory tests 1. H IV screening tests: HIV testing technology is divided into “generations,” with third-or fourth-generation assays preferred for screening today. Third-generation assays detect HIV Ig M antibodies, which appear about 20-23 days after infection. Fourth-generation assays (referred to as “combination,” “combo,” or “HIV Ab/Ag”) differentiate between HIV-1 and HIV-2, as well as detect both HIV Ig M antibodies and the HIV p24 antigen, which appears about 14-20 days after infection (Branson et al., 2014). These newer generations of assays are now widely available; however, clinicians may need to verify the generation of assay used at their specific clinical sites. 2. R apid testing: Rapid testing offers the advantage of a result within 20 minutes or less. As of 2014, there are six rapid HIV antibody tests and one rapid HIV antibody/antigen combination test available in the United States (Branson et al., 2014). A rapid HIV Ab/Ag combination test is preferred, because rapid HIV antibody-only tests rely on second-generation assays that may not detect HIV for weeks to months after infection (Branson et al., 2014). 3. H IV RNA viral load testing: HIV RNA is detectable by current assays approximately 10 days after infection (Branson et al., 2014). Because of the variability of HIV viremia, RNA viral load testing is not approved by the Food and Drug Administration (Continued)660 CHAPTER 66 | Primary Care of HIV-Infected Adults
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for diagnosis of HIV. However, viral load testing is appropriate to identify HIV in any patient with recent HIV risk and presentation of signs and symptoms consistent with acute retroviral syndrome. During this phase of infection, when plasma HIV RNA viral loads are reliably high, viral load testing may detect evidence of HIV before antibody or antigen tests become reactive. D. Linkage to care and partner services Once diagnosed with HIV, immediate linkage of the patient to medical care is essential. Clinicians should also initiate conversations about partner disclosure as soon as possible. Partners of individuals with new HIV diagnoses are at particular risk for infection, and if not already infect-ed, are prime candidates for HIV prevention services such as preexposure prophylaxis (Pr EP) and postexposure pro-phylaxis (PEP), which are discussed in Chapters 41 and 40, respectively. Patients may opt for self-disclosure to partners, dual disclosure (patient discloses to partners with a clinician or counselor available in the room to provide support and information), or third-party anonymous notifica-tion, in which a trained public health worker notifies partners of exposure and offers testing services with-out identifying the original patient. Clinicians should contact local public health authorities to check for availability of this service. III. d atabase A. Subjective 1. M edical history a. Obt ain documentation of positive HIV anti-body test. If HIV infection cannot be confirmed, repeat the HIV antibody test. b. Ac ute retroviral syndrome (ARS): review for past symptoms consistent with acute retro-viral syndrome, which may help to identify approximate date of HIV infection (USDHHS, PAAGAA, 2015a) c. Obt ain past CD4 counts (absolute and percent-age), CD4 nadir, and HIV-1 viral loads. d. A IDS defining illnesses and HIV-related con-ditions: opportunistic infections (OIs), malig-nancies, thrush, hairy leukoplakia, herpes simplex (HSV-2), varicella zoster virus (VZV), anemia, thrombocytopenia, anal and cervical cancer. e. A RT (in previously treated patients)i. P rescribed regimens: list all past regimens and antiretroviral (ARV) components of regimens, side effects, and adverse events. ii. D ocument start and stop dates for each regimen or component and changes in HIV viral load. iii. D ocument results of HIV resistance assays: genotype, phenotype, and tropism assays. Obtain past medical records to confirm information. iv. R eview past adherence issues with ART, untreated depression or other mental ill-ness, low health literacy, inadequate social support, active substance use, homeless-ness, nondisclosure of HIV status (PAGAA, 2015a). f. Othe r medications and allergies: complete a medication reconciliation of all prescribed and over-the-counter medications and complemen-tary therapies. g. T ransfusion of blood, platelets, or serum prod-ucts between 1975 and 1985; artificial insemina-tion from anonymous donor. h. C omorbid conditions: risk factors for cardio-vascular disease, past history of DM, coronary artery disease, emphysema, renal insufficiency, CKD, chronic HBV or HCV, dyslipidemias, and osteoporosis. i. P sychiatric/behavioral: major depression or other depressive disorders, suicidal ideation or past suicide attempts, anxiety and panic disor-ders, posttraumatic stress disorder. j. S exually transmitted diseases: history of past infections, treatment and treatment outcomes: herpes simplex-2, gonorrhea, chlamydia, chan-croid, syphilis, trichomoniasis, HBV, HCV, HPV. k. M ycobacterium tuberculosis (MTB) and latent Mycobacterium tuberculosis infection (LTBI). Results of tuberculin skin tests (TST) or inter-feron gamma release assay (IGRA). If patient has a history of LTBI record date, treatment, and CXR results. l. I mmunization status: see T able 66-4. m. W omen: last menstrual period (LMP), previous abnormal Pap smears, genital condyloma, recur-rent vaginal yeast infections, pelvic inflammatory disease (PID), gravid and para status, mammo-grams, bone mineral density screening. n. M en: genital or anal condyloma, abnormal anal Pap smear results and treatment, bone mineral density screening. 661 Database
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o. F oreign travel or residence in areas endemic for specific organisms (e. g., southwestern United States, coccidioidomycosis; Ohio and Indiana, histoplasmosis). Cat ownership and consump-tion of uncooked beef are risks for toxoplasmosis. p. P sychiatric: mental health issues or past psychi-atric care. 2. P ersonal and social a. A ge, gender, gender identity, race, ethnicity. b. S exual activity i. N umber and gender(s) of partners. ii. S exual practices: anal, penile-vaginal, oral. iii. U se of condoms or other barrier methods. c. S ubstance use: alcohol and illicit drug use. i. T ype and mode of ingestion. ii. I f injection drug use: injection practices and use of needle exchange programs. iii. I dentify substance use patterns (e. g., use of drugs or alcohol with sexual activity). d. C igarette smoking: i. A ge at onset, packs per day, number of pack years. ii. I f currently smoking, review past attempts to quit smoking and interest in smoking cessation. e. S ocial support, relationships, and housing: i. P atient's response to diagnosis ii. Di sclosure of HIV status to partner(s). Partner's HIV status. iii. H omeless or marginally housed and with-out stable housing. iv. R eferral to HIV/AIDS service organiza-tions and support groups. f. I ntimate partner violence (IPV) or sexual assault g. P ast incarceration 3. F amily history a. M alignancies, neurologic diseases, osteoporo-sis, atherosclerotic disease, and history of early coronary heart disease (i. e., MI in first-degree-relative before age 55 in males and before age 65 in females) 4. R eview of systems a. Ge neral: usual body weight, fever or drenching sweats, unintentional weight loss of more than 10%, and persistent fatigue or anorexia. b. D ermatologic: persistent skin rashes, recurrent outbreaks of HSV, easy bruising or bleeding, red-to violet-colored papular or macular lesions, pruritic papules. c. L ymph nodes: rapid or asymmetrical lymph node swelling or a change in the size of a node or tender lymph nodes. d. Ea r, nose, and throat: oral lesions or sores, peri-odontal disease, caries; painful or sensitive teeth. e. E yes: decreased visual acuity or vision loss. f. P ulmonary: cough, dyspnea, and hemoptysis. g. C ardiac: chest pain, murmurs, palpitations. h. G astrointestinal: diarrhea, nausea, emesis, bloat-ing, rectal pain, rectal lesions or discharge, bright red blood per rectum. i. Ge nitourinary and gynecologic: genital lesions or sores, dysuria, vaginal discharge, pelvic pain, contraception, and use of barrier methods dur-ing sexual activity. Men: penile discharge, testic-ular pain or lumps. j. A norectal: rectal pain or discharge. k. M usculoskeletal: weakness, arthralgia, myalgia, and risks for osteoporosis. l. N eurologic: persistent or severe headaches, changes in cognition, memory loss, confusion or forgetfulness, seizures, weakness, pain or numb-ness in hands or feet. m. P sychiatric: depression, anxiety, and insomnia. 5. F amily history: CVD, diabetes, renal disease, alcoholism, malignancies, substance use, HIV, depression, and emotional or physical abuse. B. Objective 1. Ge neral appearance and body habitus: wasting or unintentional weight loss, obesity, fat redistribution syndromes (dorsocervical fat pad, gynecomastia, or visceral fat accumulation), lipoatrophy (loss of subcutaneous fat in face and extremities), frailty. 2. H eight, weight, blood pressure, body mass index, waist circumference, and baseline Sp O2 resting and with exercise. 3. S kin: tinea, onychomycosis, folliculitis, seborrheic dermatitis, bruising or petechiae, herpes, molluscum contagiosum, condyloma, Kaposi sarcoma lesions (purplish macular, papular, or nodular lesions; discrete and well circumscribed; do not blanch with compression) 4. L ymph nodes: completed examination for presence of lymphadenopathy defined as > 1 cm in two or more noncontiguous extrainguinal sites, one of which may be cervical. Assess for asymmetry and consistency of node. 5. E yes: visual acuity and visual field testing. Examine for lesions on lids or sclera, funduscopic exam for hemorrhage, exudate, or cotton wool spots662 CHAPTER 66 | Primary Care of HIV-Infected Adults
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6. Or opharynx: ulcerations on tongue or mucous membranes. White coating on tongue or oropharynx (oral candidiasis), fringed lesions on lateral border or dorsum of tongue (hairy leukoplakia), inflammation or receding of gingiva (periodontal disease). 7. C ardiovascular: heart exam, pulses, and presence of lower extremity edema 8. C hest: lung exam 9. B reast: nodules or nipple discharge 10. A bdomen: enlargement of spleen or liver, masses, or tenderness. 11. G ynecologic/genitourinary: external lesions, condyloma, HSV. Speculum exam: Pap smear of cervix. Men: ulcers, condyloma, testicular masses. 12. A norectal: ulcers, fissures, digital rectal exam, anoscopy, and anal Pap smear. 13. N eurologic: screening exam, including mental status examination. Standard Mini Mental State Examination is not sensitive for detecting HIV-associated neurocognitive disorders. Montreal Cognitive Assessment (Mo CA) is recommended for baseline assessments (Chartier et al., 2014). IV. a ssessment A. Determine the diagnosis 1. H IV antibody testing 2. P lasma HIV RNA (viral load) B. Staging of disease and HIV drug-resistance testing 1. C D4 lymphocyte count2. Ge notypic resistance assays on all ARV-naïve patients at entry into care, regardless of whether ART will be initiated immediately. C. Motivation and ability HIV is associated with significant stigma and dispari-ties in healthcare outcomes. Common barriers to engag-ing and retaining patients in care include untreated mental illness, active substance use, nondisclosure of HIV status, transportation, childcare issues, homelessness or unstable housing, joblessness, health insurance, food insecurity, and lack of social support. During initial visits allow time to establish a therapeutic relationship, identify the patient's priorities and preferences for care, and address actual and potential barriers to care. V. Goals of clinical management A. Treatment Goals (USDHHS, PAAGA, 2015a) 1. D ecrease HIV-associated morbidity and mortality 2. P rolong survival and increase duration and quality of life 3. R estore and preserve immunologic function 4. Dur ably and maximally suppress plasma HIV viral load 5. P revent transmission of HIV B. Healthcare maintenance C. Support adherence to ART and retention in care D. Prevention of new infections VI. Plan A. Initial laboratory and diagnostic tests 1. Or der initial laboratory and diagnostic studies (T able 66-5). B. Management 1. I nitiate HIV-specific and routine healthcare mainte-nance for age and gender (T ables 66-3 and 66-4). 2. I nitiate ART: Initial recommended regimens for HIV change frequently based on data from clinical trials, cohort studies, and the experience of clinicians and community members actively engaged in HIV patient care. Clinicians should review the most current treatment recommendations (https://aidsinfo. nih . gov/guidelines) and consult with an HIV expert prior to initiating an ART regimen (http://nccc. ucsf. edu). Recommended initial regimens are those regi-mens studied in randomized controlled trials and shown to be optimally effective, tolerable, and easy to use. Additional regimens are listed as “alternative” or “other” based on reduced efficacy, tolerability, and/or limited data supporting use compared to “recom-mended” regimens. In some cases an alternative or other regimen may be the best regimen for the patient. Current treatment recommendations include guidance on selection of initial ART based on regimen character-istics and specific clinical scenarios (PAGAA, 2015a). 3. I nitiate antimicrobial prophylaxis to prevent first episode of HIV-related opportunistic infections indicated (T able 66-6). 663 Plan
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Table 66-5 Initial Laboratory and Diagnostic Studies laboratory test Fr equency and Comments HIV-1 antibody test HIV infection should be confirmed in all patients entering care, either through documentation or laboratory testing (see HIV screening and testing). Repeat an HIV antibody test if HIV diagnosis has not been confirmed. CD4 T-cell count, absolute and percentage At entry into care and every 3-6 months prior to initiation of ART. Every 3-6 months after initiation of ART or if CD4 cell count < 300 cells/mm 3 Every 6-12 months after 2 years on ART with consistently suppressed viral load (VL). Some experts recommend annual CD4 cell count if viral load durably suppressed > 2 years. Routine monitoring of lymphocyte subsets (e. g., CD8) other than CD4 absolute and percentage not recommended. HIV-1 RNA viral load (VL) Most important indicator of initial and sustained response to ART Viral load suppression is defined as a viral load persistently below the lower limits of detection for the assay used (HIV RNA < 20 to 75 copies/m L). Measured at entry into care, at initiation of therapy, and on a regular basis thereafter. Repeating viral load while not on therapy is optional (C-III). HIV resistance testing At entry into care and regardless of decision to initiate ART. HIV drug resistance has been demonstrated in 6-16% of transmitted HIV-1 infection commonly to nonnucleoside reverse transcriptase inhibitors (NNRTI) and nucleoside reverse transcriptase inhibitors (NRTI). Genotypic testing is preferred initial resistance assay to guide therapy in antiretroviral-naïve patients. HLA-B 5701 At entry into care or prior to starting an ART regimen containing abacavir to reduce risk of hypersensitivity reaction. An abacavir hypersensitivity reaction (ABC HSR) is a multiorgan clinical syndrome occurring in the first few weeks of abacavir initiation in 5-8% of patients positive for haplotype HLA-B5701. Re-challenge with abacavir following this clinical syndrome can cause a life-threatening hypersensitivity reaction. Patients who test HLA-B 5701 positive should not be prescribed ABC and their positive HLA-B 5701 results should be recorded as an abacavir allergy in the medical record. (USDHHS,) Coreceptor tropism assays Perform if a CCR5 antagonist is being considered as part of an ART regimen (AI). Tropism assay screens for HIV resistance to either CCR5 and/or CXCR4 virus. Requires HIV-1 plasma RNA of > 1,000 copies/m L. Consult with HIV specialist prior to ordering to determine need for assay and interpretation of results. HBV serology At entry into care and as clinically indicated. Screen for anti-HBs, anti-HBc, and HBs Ag. If chronically infected with HBV (see Chapter 51 on chronic viral hepatitis), order HBe Ag, anti-HBe, and HBV DNA. If isolated anti-HBc is detected, perform an HBV DNA. HCV serology At entry into care. Screen for HCV antibody and HCV RNA. Perform HCV genotype if HCV RNA detected (see Chapter 51 on chronic viral hepatitis). 664 CHAPTER 66 | Primary Care of HIV-Infected Adults
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Table 66-5 Initial Laboratory and Diagnostic Studies laboratory test Fr equency and Comments Complete blood count with white blood count differential At entry into care and every 3-6 months once ART initiated and when clinically indicated. Anemia of chronic disease, leukopenia, and thrombocytopenia are manifestations of untreated advanced HIV. Zidovudine (ZVD) causes anemia. Follow up q 2-8 weeks after initiation of ZVD. Basic chemistry panel At entry into care, every 3-6 months prior to initiation of ART, ART initiated, then every 3-6 months or as clinically indicated. Some experts suggest monitoring the phosphorus levels of patients on tenofovir. AST, ALT, total bilirubin At entry into care, q 6-12 months prior to initiation of ART, and with any ART modification. Once on ART, every 3-6 months and as clinically indicated. Fasting plasma glucose (FPG) or hemoglobin A1c At entry into care and annually if normal At time of initiation of ART or modification of ART Fasting lipid profile At entry into care, prior to initiation of ART, and as clinically indicated. Consider q 4-5 weeks after starting new ART regimen that affects lipids. Glucose-6-phosphate dehydrogenase (G6PD) Screen once at entry to care or before starting oxidant drugs. G6PD is a genetic variation that predisposes to hemolytic anemia if oxidative drugs are prescribed. Patients should be tested for G6PD before administration of dapsone or primaquine. An alternative agent should be used in patients found to have G6PD deficiency. Pregnancy test Prior to starting ART Toxoplasma gondii Toxo Ig G At entry into care for exposure to Toxoplasma gondii. If seronegative, counsel on prevention of new Toxoplasma infections. Avoid eating raw or undercooked meat. If the patient owns a cat that goes outdoors, recommend frequent litter change and thorough handwashing after changing litter box. Retest for Toxo Ig G if CD4 falls to < 100/mm 3 to determine need for primary prophylaxis for toxoplasmosis. Urinalysis, calculated creatinine clearance (Cr Cl), and estimated glomerular filtration rate (e GFR) At entry into care Prior to initiating or modifying ART Cr Cl of ≥ 70 m L/min required for initiation of drugs containing pharmacokinetic booster cobicistat. Some ART components require dose reduction in patients with renal insufficiency Once ART is initiated, monitor Cr Cl using the Cockcroft-Gault equation and e GFR using the MDRD equation q 6 months and more frequently in patients with additional risks for renal disease. Pregnancy Test Prior to initiation of ART Data from Aberg, J. A., Gallant, J. E., Ghanem, K. G., Emmanuel, P., Zingman, B. S., & Horberg, M. A. (2014). Primary care guidelines for the management of persons infected with HIV: 2013 update by the HIV Medicine Association of the Infectious Diseases Society of America. Clinical Infectious Diseases 58(1): e1-34. doi:10. 1093/cid/cit665; Department of Health and Human Services, Panel on Antiretroviral Guidelines for Adults and Adolescents. (2015). Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Retrieved from http://aidsinfo. nih. gov. (Continued)665 Plan
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Table 66-6 Prophylaxis to Prevent First Episode of Opportunistic Infections in HIV-1-Infected Adults and Adolescents Pathogen Indication Preferred t herapies a lternative t herapies Pneumocystis pneumonia (PCP)CD4 count ≤ 200 cells/mm3 Oropharyngeal candidiasis CD4+ ≤ 14% AIDS-defining illness CD4 > 200 but < 250 cells/mm 3 if unable to monitor CD4 q 3 months Trimethoprim/ sulfamethoxazole (TMP-SMX) 1 double strength (DS) PO daily or TMP-SMX 1 single strength (SS) daily TMP-SMX 1 DS three times weekly or Dapsone, 100 mg PO daily or Dapsone 50 mg PO BID or Atovaquone 1,500 mg PO daily Toxoplasma gondii encephalitis Toxoplasma Ig G positive with CD4 ≤ 100/mm 3 Regimens effective against toxoplasmosis also effective for PCPTMP-SMX 1 DS PO daily TMP-SMX three times weekly or TMP-SMX 1 SS daily or Dapsone 50 mg daily plus pyrimethamine 50 mg plus leucovorin 25 mg weekly Disseminated Mycobacterium avium (MAC)CD4 ≤ 50 cells/mm 3 No evidence of active disseminated MAC disease based on clinical assessment and blood culture Azithromycin 1,200 mg once weekly or Clarithromycin 500 mg BID or Azithromycin 600 mg PO twice weekly Rifabutin 300 mg daily Rule out active TB before starting rifabutin Latent Mycobacterium tuberculosis infection (LTBI)Positive screening test No evidence of active TB infection No prior history of treatment for active or latent TB Close contact with person with infectious TB, regardless of screening test result for LTBIIsoniazid (INH) 300 mg PO daily for plus pyridoxine 25 mg daily for 9 months Rifabutin (dose adjusted based on concomitant ART) × 4 months *Dose adjustment required for ART drug interactions for some MTB regimens Coccidioidomycosis A new positive Ig M or Ig G serologic test in patients who live in a disease-endemic area and with CD4 count < 250 cells/mm 3Fluconozole 400 mg PO daily Histoplasmosis capsulatum infection CD4 count ≤ 150 cells/μL and at high risk because of occupational exposure or live in a community with a hyperendemic rate of histoplasmosis (> 10 cases/100 patient-years)Itraconazole 200 mg PO daily As of June 2015, pyrimethamine is no longer available in retail pharmacies in the United States. If there is a delay in obtaining pyrimethamine for a patient who needs this drug, refer to the specific pathogen section in the opportunistic infections guidelines for alternative drug regimens. TMP-SMX DS once daily also confers protection against toxoplasmosis and many respiratory bacterial infections; lower dose also likely confers protection. Patients should be tested for glucose-6-phosphate dehydrogenase (G6PD) before administration of dapsone or primaquine. Alternative agents should be used in patients found to have G6PD deficiency. Modified from Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. (2013). Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. Retrieved from http://aidsinfo. nih. gov. 666 CHAPTER 66 | Primary Care of HIV-Infected Adults
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4. P rovide screening and counseling for prevention of HIV transmission. 5. I dentify and manage chronic comorbid conditions. 6. R efer patients with illnesses of unclear etiology or evidence of HIV drug resistance to HIV specialist. 7. R efer to social worker or AIDS service organization (ASO) for case management services: housing, mental health and substance abuse treatment, health insurance, eligibility for federally funded AIDS programs, transportation to clinic appointments, childcare, and parenting needs. C. Management issues specific to HIV-infected women 1. R eproductive counseling and contraception: Preconception counseling and referral to an HIV specialist should be provided for all women of childbearing age and their partners who desire pregnancy. The landmark AIDS Clinical T rials Group (ACTG 076) study demonstrated the safety and efficacy of ART in pregnant women for prevention of mother-to-child transmission of HIV (Connor et al., 1994). Pregnant women with HIV should be treated with ART regardless of stage of disease or CD4 cell count. Avoidance of breastfeeding in addition to the use of ART has virtually eliminated perinatal transmission of HIV in countries where access to HIV care is available. If a woman does not desire to become pregnant, provide preconception counseling and initiate discussions regarding contraception. Several protease inhibitors (PI) and nonnucleoside reverse transcriptase inhibitors (NNRTI) have drug interactions with oral contraceptives, causing changes in blood levels of ethinyl estradiol or norethindrone. Women on combined oral contraceptives (COC) and ART should use an alternative method of contraception. Progestin-only contraceptive methods seem to be effective and have no drug-drug interactions when used with currently approved ART regimens (Panel on T reatment of HIV-Infected Pregnant Women and Prevention of Perinatal T ransmission, 2014). Intrauterine devices are safe to use in women with HIV and provide a reliable long-term method of contraception (World Health Organization, 2009). 2. A RT regimen considerations in women: The goals of treatment for women are the same as for adults and adolescents. When constructing ART regimens for pregnant women, current recommended regimens are appropriate with some exceptions. Efavirenz should be avoided in women who are planning to become pregnant or are sexually active and not using an effective form of contraception (PAGAA, 2015a). If a woman becomes pregnant on efavirenz and has passed the first 5-6 weeks of the pregnancy, some experts recommend continuing an efavirenz-based regimen if the regimen is effective and well tolerated. Nevirapine is not recommended in treatment-naïve women with CD4 ≥ 250 cells/mm 3 unless risk outweighs benefits. Severe lactic acidosis is seen more commonly in women on ART and risks for lactic acidosis includes female gender, obesity, and pregnancy. Postmenopausal HIV-infected women have an increased risk of osteopenia and osteoporosis at an earlier age and an increased risk of fragility fractures. Clinicians may want to consider avoiding ART regimens that are associated with greater decrease in bone mineral density in postmenopausal women at increased risk of osteoporosis and fracture (PAGAA, 2015a). D. Management issues specific to transgender PLWH 1. T ransgender refers to individuals whose gender identity (basic sense of self as man, woman, both, or neither) or presentation is not congruent with the person's biological sex assigned at birth. Some transgender individuals may pursue surgery or use hormones to enhance feminine or masculine physical characteristics—though some may not. 2. S tigma and discrimination toward transgender individuals increases the likelihood of depression, suicide, intimate partner violence, substance use, and sexually transmitted infections other than HIV. T o combat stigma, healthcare settings should affirm transgender patients through appropriate staff training, gender-inclusive registration materials and restroom facilities, and use of the patient's preferred gender when addressing or referring to the patient. Clinicians caring for transgender PLWH should make use of community agencies providing support services for transgender individuals, and refer patients to those agencies. Clinicians without experience providing hormone therapy to transgender individuals should consult with providers who have clinical expertise in this area (see Resources). 3. H ealthcare maintenance for transgender PLWH is based on health risks and birth sex. In transgender women, digital rectal examinations and prostate cancer screening may be indicated based on age, other risk factors, and shared decision making by the provider and patient. In transgender men, pelvic examination, Pap smear, and mammography based on recommended guidelines should be provided. 667 Plan
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E. Prevention of new infections PLWH have a central role in the prevention of HIV transmission at the individual and population levels. Recognizing this role, a consortium of U. S. governmen-tal and nonprofit HIV/AIDS service organizations has produced recommendations for HIV prevention in clini-cal care settings with PLWH (CDC et al., 2014). These recommendations encourage providers to consider con-textual issues—individual, structural, social, ethical, and legal—when working with PLWH. In conversations with patients about HIV prevention, providers should be sen-sitive, respectful, culturally appropriate, and empower patients to engage in HIV prevention without blaming or shaming. Providers must acknowledge that patients have the right and responsibility to make HIV-prevention deci-sions for themselves. Above all, providers must support patients in treat-ment adherence and engagement in care in order to achieve viral suppression, reducing infectiousness. Support includes linking patients to care; providing refer-rals for services such as food assistance, housing, trans-portation to medical visits, and medication adherence counseling; and development of healthcare systems such as the medical home model that provide patients with wraparound care. Providers should discuss HIV risk behaviors with patients at every visit. Through education, coun-seling, and shared decision making, providers can support PLWH in setting realistic goals for HIV pre-vention using evidence-based risk reduction strategies. Providers should offer specific healthcare services that reduce the risk of HIV transmission such as condom distribution, referrals to syringe exchanges, screening for sexually transmitted infections, family planning care, and referral to treatment for substance use or psychiatric illness. Patients often have questions and fears regarding the legal ramifications of their HIV serostatus. Laws regard-ing HIV serostatus disclosure vary by state. Clinicians can become familiar with these laws at the website of the Center for HIV Law and Policy (see Resources). F. Patient education HIV education should be conducted over several visits to provide basic information on HIV treatment, prevention of secondary transmission, and indications for ART. It is important to emphasize that HIV is a chronic manageable disease and that improved quality of life can be expected if individuals are engaged in care and motivated to take ART. There are several excellent websites that can provide resources and guidance in HIV/AIDS patient and provid-er education (see Resources). VII. r esources A. General information 1. A IDS. gov: Gateway for HIV/AIDS information and resources from the U. S. Federal government, aimed at both clinicians and patients. www. aids. gov 2. C enters for Disease Control and Prevention's HIV/ AIDS Website: Basic information, statistical data, prevention tools, and clinician resources. www. cdc. gov/hiv/ 3. H enry J. Kaiser Family Foundation's HIV/AIDS Website: Policy analysis, global and national HIV/AIDS data, and links to patient resources, including Spanish-language patient information. http://kff . org/hivaids/ B. Clinical management 1. A IDS info: Portal for HIV/AIDS clinical guidelines, education materials, and research information from the DHHS. http://aidsinfo. nih. gov/ 2. A IDS Education and T raining Centers (AETC): National network of HIV experts that provide guidelines, training materials, webinars, clinical consultation, and technical assistance for healthcare providers caring for PLWH. Administered by the Ryan White HIV/AIDS Program of the Human Resources and Services Administration. http://aidsetc. org/ 3. U. S. Department of Health and Human Services. (2014). HIV/AIDS Bureau Guide for HIV/AIDS Clinical Care. http://hab. hrsa. gov/deliverhivaidscare /2014guide. pdf 4. C linician Consultation Center (CCC): Rapid phone and online consultation on HIV/AIDS management, PEP, Pr EP, perinatal HIV/AIDS, and HIV testing from HIV-expert clinicians at the University of California, San Francisco. Consultation services available nationwide. http://nccc. ucsf. edu/ 5. H IV In Site: Information on HIV biology, clinical management, policy, and research, developed by the Center for HIV Information at the University of California, San Francisco. Includes HIV In Site Knowledge Base, a complete online textbook. http://hivinsite. ucsf. edu 6. C enter of Excellence for T ransgender Health: Resources and guidelines for transgender patient care from the University of California, San Francisco. http://transhealth. ucsf. edu/668 CHAPTER 66 | Primary Care of HIV-Infected Adults
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7. H IVE (formerly the Bay Area Perinatal AIDS Center): Preconception and perinatal HIV/AIDS resources for patients, their partners, and healthcare providers. www. hiveonline. org/services/ 8. H IV Web Study: Case-based study modules on prevention and management from the University of Washington. http://depts. washington. edu/hivaids C. HIV medications 1. H IV In Site Database of Antiretroviral Drug Interactions: Searchable database of HIV drug interactions, provided by the University of California, San Francisco. http://arv. ucsf. edu/ 2. U niversity of Liverpool HIV Drug Interactions Portal: Searchable database of HIV drug interactions, as well as a link to a hepatitis C drug interactions database. www. hiv-druginteractions. org/ 3. S tanford University HIV Drug Resistance Database: Resource for analyzing HIV drug resistance. http://hivdb. stanford. edu/ D. Patient education and advocacy 1. P roject Inform: Education resources and advocacy for people living with HIV and hepatitis C. www. projectinform. org/ 2. A VERT. org: Large online compendium of HIV/ AIDS education materials, produced by AVERT, an international HIV/AIDS charity based in the United Kingdom. www. avert. org/ 3. H IV Health Reform Website: Patient and clinician education on the Affordable Care Act and HIV/AIDS care, produced by the AIDS Foundation of Chicago and Project Inform. www. hivhealthreform. org/ 4. H IV Nightline: Free, confidential emotional support and information on HIV/AIDS. Open nightly from 5 P. M. to 5 A. M. Pacific Standard Time. Nationwide toll free: 1-800-628-9240. 5. C enter for HIV Law and Policy: Comprehensive resource for legal and policy issues related to HIV. www. hivlawandpolicy. org/ E. Professional organizations 1. A ssociation of Nurses in AIDS Care (ANAC): National organization of nurses, including advanced practice nurses, dedicated to HIV/AIDS advocacy and patient care. Offers HIV specialty credentialing, presents an annual national conference, and publishes the journal JANAC. www. nursesinaidscare . org/2. A merican Academy of HIV Medicine (AAHIVM): National organization for HIV care providers, offering membership and HIV specialty credentialing to advanced practice nurses. www. aahivm. org/ re Feren Ce S Aberg, J. A., Gallant, J. E., Ghanem, K. G., Emmanuel, P., Zingman, B. S., Horberg, M. A., & Infectious Diseases Society of America. (2013). Primary care guidelines for the management of persons infected with human immunodeficiency virus: 2013 update by the HIV Medicine Association of the Infectious Diseases Society of America. Clinical Infectious Diseases, 58(1), e1-e34. doi: 10. 1093/cid/cit665 Antiretroviral Therapy Cohort Collaborative. (2008). Life expectancy of individuals on combination antiretroviral therapy in high-income countries: A collaborative analysis of 14 cohort studies. Lancet, 372(9635), 293-299. Branson, B. M., Owen, S. M., Wesolowski, L. G., Bennett, B., Werner, B. G., Wroblewski, K. E., et al. (2014). Laboratory testing for the diagnosis of HIV infection: Updated recommendations. Atlanta, GA: Centers for Disease Control and Prevention and Silver Spring, MD: Association of Public Health Laboratories. Retrieved from www. cdc. gov/hiv/pdf/HIVtesting Algorithm Recommendation-Final. pdf. Brown, T. T., Cole, S. R., Kingsley, L. A., Palella, F. J., Visscher, B. R., Margolick, J. B., et al. (2005). Antiretroviral therapy and the prevalence and incidence of diabetes mellitus in the multicenter AIDS cohort study. Archives of Internal Medicine, 165(10), 1179-1184. Centers for Disease Control and Prevention. (2006). Revised recommen-dations for HIV testing of adults, adolescents, and pregnant women in health-care settings. MMWR, 55(R14), 1-17. Retrieved from www. cdc . gov/mmwr/preview/mmwrhtml/rr5514a1. htm. Centers for Disease Control and Prevention. (2010, June 25). Updated guidelines for using interferon gamma release assays to detect Mycobacterium tuberculosis infection in the United States, 2010. MMWR Recommendations and Reports, 59(RR05), 1-25. Retrieved from www. cdc. gov/mmwr/preview/mmwrhtml/rr5905a1. htm?s_cid =rr5905a1_e. Centers for Disease Control and Prevention. (2011). HIV testing among men who have sex with men—21 cities, United States, 2008. MMWR, 60(21), 694-699. Retrieved from www. cdc. gov/mmwr/preview /mmwrhtml/mm6021a3. htm. Centers for Disease Control and Prevention. (2013a). HIV among older Americans [Fact sheet]. Retrieved from www. cdc. gov/hiv/pdf/library _factsheet_HIV_%20Among Older Americans. pdf. Centers for Disease Control and Prevention. (2013b). HIV among transgender people in the United States [Fact sheet]. Retrieved from www. cdc. gov/hiv /pdf/risk_transgender. pdf. Centers for Disease Control and Prevention. (2014a). Diagnoses of HIV infection in the United States and dependent areas, 2012. 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Centers for Disease Control and Prevention. (2014c). Monitoring selected national HIV prevention and care objectives by using HIV surveillance data—United States and 6 dependent areas—2012. HIV Surveillance Supplemental Report, 19(3). Retrieved from www. cdc. gov/hiv/pdf /surveillance_report_vol_19_no_3. pdf. Centers for Disease Control and Prevention. (2014 d). Revised surveillance case definition for HIV infection—United States, 2014. MMWR, 63(3), 1-10. Retrieved from www. cdc. gov/mmwr/pdf/rr/rr6303. pdf. Centers for Disease Control and Prevention. (2014e). Vital signs: HIV diagnosis, care, and treatment among persons living with HIV—United States, 2011. MMWR, 63(47), 1113-1117. Retrieved from www. cdc . gov/mmwr/pdf/wk/mm6347. pdf. Centers for Disease Control and Prevention. (2015a). ACIP vaccine. Retrieved from www. cdc. gov/vaccines/hcp/acip-recs/index. html. Centers for Disease Control and Prevention. (2015b). HIV among African Americans [Fact sheet]. 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Rothman, M. S., & Bessesen, M. T. (2012). HIV infection and osteoporosis: Pathophysiology, diagnosis, and treatment options. Current Osteoporosis Report, 10(4) 270-277. Roukens, A. H., Visser, L. G., Leo, G., & Frank, P. (2009). A note of caution on yellow fever vaccination during maraviroc treatment: A hypothesis on a potential dangerous interaction. AIDS, 23(4), 542-543. Strategies for Management of Antiretroviral Therapy (SMART) Study Group. (2006). CD4+ count-guided interruption of antiretroviral treatment. New England Journal of Medicine, 355(22), 2283-2296. T seng, A. H., Secemsky, E. A., Dowdy, D., Vittinghoff, E., Moyers, B., Wong, J. K., et al. (2012). Sudden cardiac death in patients with human immunodeficiency virus infection. Journal of the American College of Cardiology, 59(21), 1891-1896. United Nations Joint Programme on HIV/AIDS. (2014). The gap report. Retrieved from www. unaids. org/sites/default/files/media_asset /UNAIDS_Gap_report_en. pdf. U. S. Department of Health and Human Services. (2013). HIV/AIDS care continuum. Retrieved from https://www. aids. gov/federal-resources /policies/care-continuum/. U. S. Department of Health and Human Services. (2014). Healthy People 2020: HIV. Retrieved from https://www. healthypeople. gov/2020 /topics-objectives/topic/hiv/. U. S. National Institutes of Health, National Cancer Institute. (n. d. ). HIV/AIDS cancer match study. Retrieved from www. hivmatch. cancer. gov/index. html. U. S. Preventive Services T ask Force. (2013). Final recommendation statement: Human immunodeficiency virus (HIV) infection: Screening. Retrieved from www . uspreventiveservicestaskforce. org/Page/Document/Recommendation Statement Final/human-immunodeficiency-virus-hiv-infection-screening. Y oung, B., Dao, C., Buchacz, K., Baker, R., Brooks, J. T., & HIV Outpatient Study (HOPS) Investigators. (2011). Increased rates of bone fracture among HIV-infected persons in the HIV Outpatient Study (HOPS) compared with the US general population, 2000-2006. Clinical Infectious Diseases, 52(8), 1061-1068. Zanni, M. V., Fitch, K. V., Feldpausch, M., Han, A., Lee, H., Lu, M. T., et al. (2014). 2013 American College of Cardiology/American Heart Association and 2004 Adult T reatment Panel III cholesterol guidelines applied to HIV-infected patients with/without subclinical high-risk coronary plaque. AIDS, 10(28), 2061-2070. 671 References
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