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{
"age": 44,
"case_id": "PMC11131420_01",
"case_text": "On average, a sample respondent is 44 years old and has 6.8 years of education (Table 1). About one third of respondents are male. The average household counts 6.6 members, with a dependency ratio of 0.53, indicating that about half of members are not in the active age group (15 to 60). The mean annual household income is 947 USD, corresponding to a local purchasing power of 1,894 USD in 2021, thus implying 5.2 USD PPP per day. Almost half of households own a radio, while only 13% owns a television. Most respondents agree that vaccines are important for children (95%), effective (87%), safe (85%) and compatible with their religious beliefs (74%). Consequently, general vaccine acceptance is very high (Figure 3, Panel A). Almost nine out of ten households indicate to have vaccinated their children against tuberculosis, diphtheria, polio, measles, and yellow fever, while 98% of households vaccinated their children against at least one of these diseases. In sharp contrast, only 22% of respondents indicated they would accept the COVID-19 vaccine if it was available to them. This is much lower than the mean stated COVID-19 acceptance rate of 80% found in a sample of 10 low- and middle-income countries in Asia, Africa and South America, but in line with other studies reporting lower COVID-19 vaccine acceptance and confidence in African countries and the DR Congo in particular.\nRespondents with a stated willingness to take the vaccine (N = 129) indicated they would do so to protect themselves (91%), their family and household (78%) and their community (63%). Respondents who did not accept the vaccine (N = 412) were asked to motivate their choice in an open question. After categorizing their open answers, six main answer categories emerged (Figure 3, Panel B). The largest group among them (31%) indicated a general lack of trust in the COVID-19 vaccine and its efficacy. About 27% expected that they might get COVID-19 from the vaccine or feared other, potentially mortal, side-effects. Illustrative answers included \"To avoid Corona contamination,\" \"This vaccine kills people\" and \"It's poison.\" More than 1 out of 10 (13%) suspected that they would not receive a real vaccine, mentioning, e.g., \"It's a fake vaccine,\" \"It's a bad vaccine. White people want to eliminate us,\" \"The vaccine sent to Africa is dubious.\" Others indicated that it is their personal choice not to take the vaccine (14%), that they doubted the existence of COVID-19 (10%), or they felt no need to take the vaccine as they believed they would not get sick (5%).\nWe find rather low levels of institutional trust, ranging between a low of 17% for the president with respect to his management of the COVID-19 crisis and a high of 46% for general trust in local authorities (Figure 4). Overall, we find that institutional trust is systematically lower within the COVID-19 context, and systematically lower for institutions higher up in the administration. In line with the opinion poll by the Congo Research Group, trust in the cardinal is considerably higher than trust in the president.\nFigure 5 presents the results of the survey experiment, relying on t-tests to assess differences in means between the control group and the treatment group.5 On average, the hypothetical vaccination of President Tshisekedi has no effect on vaccine acceptance (Panel A). However, we find trust in the president to be an important moderating variable. Among respondents who trust the president, exposure to his hypothetical vaccination raises vaccine acceptance with 24 percentage points, from 0.32 to 0.56, a sizeable difference that is significant at the 5%-level (Panel B). Among respondents who indicated not to trust the president, vaccine acceptance is seven percentage-points lower among those in the treatment group (0.13 compared to 0.20), but, with a p-value of 0.11, the result is just shy of being statistically significant at the 10%-level (Panel C).\nThe hypothetical vaccination of the cardinal in the survey experiment failed to boost vaccine acceptance, even among respondents who indicated to trust the cardinal (Panels D-F). Despite the higher perceived trustworthiness of the cardinal, these results suggest that the Cardinal's actions play no role in influencing respondents' vaccine acceptance. This aligns with the conclusion of Abu-Akel et al. that, in times of health crises, it is health experts and government officials - those in a position to manage the crisis and be held accountable for it - who are likely to exert the greatest influence on public opinion.\nThese findings are confirmed in a multivariable logistic regression that controls for the respondent- and household level covariates identified above (Table 2). The results in Column (1) relate to equation (1). We find that, on average, neither the president treatment nor the cardinal treatment in the survey experiment significantly affected vaccine acceptance. Our results do confirm the importance of institutional trust; respondents who trust the president when it comes to managing the COVID-19 crisis are twice more likely to indicate that they are willing to get a COVID-19 vaccine (p < 0.01). In contrast, trust in the cardinal is not associated with stated vaccine acceptance. In Column 2, we estimate equation (2) and include interaction terms to explore how trust in the president and the cardinal affect the survey experiment treatment effects. We find that public trust strongly reinforces the impact of the president treatment. Specifically, stated vaccine acceptance for respondents who trust the president and were exposed to the president treatment is 4.75 times higher (p < 0.01) than that of respondents in the base category (those who do not trust the president and were not exposed to president treatment).6 The results do not indicate a statistically significant interaction between the cardinal treatment and trust in the cardinal.\nFour out of five respondents (486 out of 600) were interviewed after the broadcasting of President Felix Tshisekedi's vaccination. However, media access is low in our study area, and the news may not have reached everyone. For instance, Figure 6 shows that the large majority of respondents did not watch television (91%) or listen to the radio (57%) in the week prior to the interview. Hence, it is no surprise that only 89 respondents reported being aware of the President's inoculation.7 The actual exposure to the president's vaccination is thus much smaller, covering just 18% of the sample interviewed after the president got vaccinated.\nIn Column 3 of Table 2 we add an indicator variable for respondents who were interviewed after President Tshisekedi got vaccinated on 13 September 2021. In Column 4, we further add a variable that captures whether a respondent was aware of the president's vaccination. In addition, we add variables capturing respondents' knowledge of politics and include measures to capture how often they listened to the radio or watched television in the week prior to the interview - thereby estimating equation (3). The results show that being interviewed after the president's vaccination does not by itself affect stated vaccine acceptance. We only find an impact for those who indicated being aware of the president's vaccination; these respondents are 197% more likely to indicate that they are willing to get a COVID-19 vaccine (p < 0.01).8\nBeing aware of the president's vaccination may be correlated with other characteristics that can influence vaccine acceptance. While we control for a large set of likely confounding covariates, it is possible that other, unobserved, characteristics are driving our findings. Relying on the procedures suggested by Altonji et al. and Oster we formally assess the threat of such omitted variable bias. We find that selection on unobservables would have to be 5.97 times larger than selection on the included variables to fully explain away our estimated effects on awareness of the president's vaccination. Appendix 4 discusses the methodology and results in detail. Taken together, the findings suggest that our qualitative conclusions are not sensitive to omitted variable bias.\nOur results demonstrate that the impact of the president's vaccine role modelling is moderated by trust and depends on media outreach and access. In Figure 7 we make our findings more concrete by presenting predictive margins based on the most inclusive regression specification presented in Table 2. Panel A presents predictive margins for the survey experiment, by trust in the president. Holding all other covariates at their mean values, we find that for Congolese who report trusting the president, the experiment strongly boosted vaccine acceptance from 27 to 52%, nearly a doubling. However, for those who mistrust the president, the survey experiment decreased acceptance from 17 to 11%. Panel B focuses on the president's public vaccination. The estimated predictive margins imply that being aware of the president's vaccination, while holding all other covariates at their mean values, increases vaccine acceptance from 15 to 35%.",
"gender": "Male"
}
] |
PMC11131420
|
[
{
"age": 21,
"case_id": "PMC10869667_01",
"case_text": "A 21-year-old male from Bidar, Karnataka, presented with complaints of nonproductive cough and grade III-IV shortness of breath for three days. History of fever and sore throat for five days. The patient is a known type II diabetic and is on medications. There was no history of nausea, vomiting, constipation, pain in the abdomen, diarrhea, or chest pain. Upon presentation to the hospital, the patient was oriented and cooperative with the following vital signs: blood pressure of 110/60 mmHg, pulse rate of 100 bpm, respiratory rate of 30/minute, and saturation of peripheral oxygen (Spo2) of 85%. On respiratory examination, bilateral air entry was present with normal breath sounds, and there was no lymphadenopathy. Routine blood investigations like CBP showed decreased hemoglobin (8.7mg/dl), RBC count (3.29 million/cu.mm), MCH (26.4 pg), MCHC (30.9 g/dl), RDW (14.1%), and platelet count (1.35 lakh/cu.mm). Serum potassium (2.8mg/dl) and magnesium (1.6mg/dl) levels were decreased. The patient was kept nil by mouth (NBM) started on 5 liters of oxygen, initial empirical antibiotic therapy with intravenous (IV) Doxycycline 100 mg, Metronidazole 500mg, and other supportive medications. A chest radiograph showed ill-defined homogenous opacities in bilateral lung fields. HRCT chest revealed multiple variable-sized nodules with central cavitations diffusely scattered in bilateral lungs (Figures 1A-1D). Based on these chest imaging findings, the initial differential diagnosis of pulmonary tuberculosis, pulmonary metastasis, and other infective etiologies was given. Diagnostic workups for pulmonary tuberculosis (bronchoalveolar lavage for AFB and GeneXpert MTB) and pulmonary metastasis (PET-CT) were negative. Samples were sent for blood culture and sensitivity, which revealed isolates of Burkholderia pseudomallei within three days, which established the diagnosis of thoracic melioidosis. Based on blood culture and sensitivity reports, the patient was started on specific intravenous antibiotics (Ceftazidime 2gm, Avibactem 0.5gm, Meropenem, and Sulbactum 1.5gm) and was continued for two weeks. Serum potassium and magnesium levels were corrected with intravenous KCl 80 meq in 500ml of normal saline (NS) over five hours (100ml/hr), intravenous magnesium 2gm in 500ml of NS stat, followed by 1gm in 100ml of NS, and monitoring the levels regularly. With the above management, the patient's oxygen saturation (SpO2) slowly improved, requiring no oxygen support; SOB, abdominal distension, guarding, and rigidity decreased; and normal serum potassium and magnesium levels were achieved. The patient was discharged on room air with oral antibiotics (Tablet Trimethoprim 160mg, Sulfamethoxazole 800 mg, and Tablet Doxycycline 100mg) for 12 weeks, and the patient showed symptomatic improvement on follow-up visits.",
"gender": "Male"
}
] |
PMC10869667
|
[
{
"age": 21,
"case_id": "PMC10499275_01",
"case_text": "A 21-year-old female patient reported to the Department of Oral and Maxillofacial Surgery, with a chief complaint of swelling over her right cheek region for 12 years causing significant facial deformity and asymmetry. Swelling was seen since the age of six years, was small initially and slowly progressed to attain a size of 6 cm x 5 cm. On clinical examination, there was an extra-oral swelling over the right side of the midface, involving infraorbital rim, zygoma, zygomatic arch, maxilla and lateral side of the nose around 6 cm x 5 cm, which was hard in consistency causing significant facial asymmetry [Figure 1]. Intra-orally, there was swelling palpable over the right maxillary alveolar ridge involving the vestibule, extending from teeth #14-18 region (till maxillary tuberosity), which was hard in consistency with loss of vestibular space [Figure 2]. Necessary investigations were advised and all were in normal range. After clinical examination, differential diagnoses included simple bone cyst, ossifying fibroma, FD, osteoid osteoma and low-grade intermedullary osteosarcoma. Further radiological investigations included orthopantomogram which revealed a 'ground-glass appearance' and cone-beam computed tomography (CBCT) of skull involvement of right side maxilla, zygoma, nasal bone, sphenoid bone and pterygoid plates [Figure 3]. Incisional biopsy was done intra-orally and was diagnosed as FD [Figure 4]. Since the patient did not have any functional deformity, we performed surgical recontouring and reshaping using modified Weber-Ferguson incision. A high-speed bur was used to shape the bones after sections of the lesions were removed using an osteotome for aesthetic purposes. We split the bone cortex and removed in 'piecemeal' manner [Figures 5 and 6]. A biopsy of the removed bone revealed FD, with areas of fibrosis and woven bone. The post-operative course was uneventful, and the patient was satisfied with the appearance [Figure 7].",
"gender": "Female"
}
] |
PMC10499275
|
[
{
"age": 84,
"case_id": "PMC11223887_01",
"case_text": "An 84-year-old Japanese woman presented to the emergency department with sudden onset of severe headache in the early morning. Her severe headache continued when she arrived at the hospital, but her consciousness was clear (E4V5M6 on the Glasgow Coma Scale), and there were no abnormal neurological findings. Head computed tomography (CT) showed diffuse subarachnoid hemorrhage (SAH) (Fig. 1A). The source image of CT angiography showed an aneurysm on the surface of the left cerebellum (Fig. 1B), and angiography showed a fusiform aneurysm at the distal segment of the left posterior inferior cerebellar artery (PICA) (Fig. 1C, D).\nShe had been diagnosed at another hospital with poorly differentiated carcinoma of the parotid gland with confirmed metastases in the liver, pancreas, and lung. Treatment with chemotherapy was being considered. Blood samples taken at the time of the visit showed no inflammatory findings or abnormalities of the coagulation system.\nShortly after arriving at the hospital, the patient's level of consciousness decreased to E1V1M4 on the Glasgow Coma Scale. There was no evidence of rebleeding, and it was determined that the patient's loss of consciousness was exacerbated by increased intracranial pressure in the posterior fossa. Although the cause of the aneurysm was unknown, the decision was made to perform an emergency aneurysmectomy and external decompression with placement of ventricular drainage. The operation was performed with the patient in the prone position through a median suboccipital craniotomy. The dura was incised, and a hard, black hematoma was found on the surface of the cerebellum, with presumably an aneurysm within it. The PICA proximal and distal to the aneurysm was cut, and the aneurysm was removed together with the hematoma (Fig. 2A).\nHematoxylin-eosin staining of the surgical specimen showed blood vessels within the hematoma, some of which were dilated and appeared to form an aneurysm (Fig. 2B). Tumor cells adhered to and formed a layer on the intima (Fig. 2C). The tumor cells were pale with vacuoles and rich in nuclear atypia (Fig. 2D), similar to tumor cells of known parotid carcinoma (Fig. 2E); thus, they were considered to be metastases of parotid carcinoma.\nElastica van Gieson staining showed that the internal elastic lamina, smooth muscle, and adventitia of the vessel wall were preserved in non-aneurysmal areas (Fig. 3A), whereas the internal elastic lamina disappeared in aneurysmal areas, and the smooth muscle layer and adventitia were very thin (Fig. 3B). The adjacent small branch was completely embolized by the tumor (Fig. 3B, arrowhead). Masson's trichrome staining showed partial disruption of adventitia continuity and spread of tumor cells into the hematoma outside the aneurysm (Fig. 3C). Cerebrospinal fluid cytology was negative, and dissemination was considered unlikely. Based on the above, it was thought that the tumor plug derived from the parotid carcinoma destroyed the normal structure of the vessel wall and the weakened vessel formed an aneurysm and ruptured.\nAfter surgery, the patient's consciousness improved and stabilized, and there was no obvious evidence of rebleeding, such as intracranial or trunk. Follow-up MRI on day 30 showed no obvious metastatic findings in the brain parenchyma; however, there was a punctate high-intensity signal on diffusion-weighted imaging in the left cerebral hemisphere, suggesting asymptomatic cerebral infarction due to tumor embolization (Fig. 4A). Furthermore, follow-up CT on day 30 showed a small SAH in the parietal region (Fig. 4B). However, CT angiography at that time did not include the parietal area and the aneurysm could not be detected (Fig. 4C). Three days later, the patient became comatose again, and head CT showed a cerebral hemorrhage in the right frontal lobe (Fig. 4D). Repeat CT angiography showed a fusiform aneurysm within the hematoma at the distal segment of the right middle cerebral artery (Fig. 4E). Since the primary disease was not under control, the family preferred conservative treatment, and respiratory failure due to impaired consciousness progressed, and the patient died 2 days after the hemorrhage.\nWritten informed consent for publication of the patient's information and images was obtained from her family.",
"gender": "Female"
}
] |
PMC11223887
|
[
{
"age": 40,
"case_id": "PMC11169871_01",
"case_text": "Patient 1 (a 40-year-old man) suffered from nausea, vomiting, visual disorders, and other signs of increased intracranial pressure. He underwent cerebral enhanced magnetic resonance imaging (MRI), which revealed that the tumor size was 5.2 x 4.1 x 3.8 cm (Figures 1A-C). The preoperative CT venography (CTV) indicated patency of venous sinuses (Figure 1D). Then, the operation was performed with the patient lying in a prone position, and an occipital and sub-occipital craniotomy was done to expose the confluence of sinuses, superior sagittal, and transverse sinus (Figure 1E). The dura was opened supratentorially to reduce the blood supply, and the gelatin sponge and cotton tape were used to stop the sinuum bleeding, but it is more difficult than ever to stop bleeding. Then, the major part of the meningioma was resected infratentorially to release the compression of the cerebellum. The transverse sinus was opened after the removal of the meningioma and reconstructed by the autologous fascia. Postoperative enhanced MRI showed complete resection of the meningioma, but the patency of the venous sinus in the confluence of sinues area was somewhat affected (Figures 1F-I) and the patient had postoperative headache and received corresponding treatment.",
"gender": "Male"
},
{
"age": 39,
"case_id": "PMC11169871_02",
"case_text": "Patient 2 (a 39-year-old woman) had chronic headache and underwent cerebral enhanced MRI, which revealed that the FM size was 2.9 x 2.4 x 2.1 cm, and the tumor was close to the cerebral vein of Galen (Figures 2A-D). She was operated by laying her in a prone position, and the occipital craniotomy was performed to expose the superior sagittal sinus as well as the confluence of sinuses. Based on previous experience, to avoid venous sinus bleeding, we designed a longitudinal \"skull bridge\" to provide the support for suspending the dura to compress and stop bleeding of the superior sagittal sinus (Figures 2E, F and Supplementary Video 1). After suspending and opening the dura supratentorially parallel to the superior sagittal sinus, local decompression was achieved by cerebrospinal fluid (CSF) release. There was no brain swelling or venous bleeding, allowing the complete removal of the meningioma without deep cerebral drainage vein injury. Postoperative head CT/CTV showed complete resection of the tumor, and the venous sinuses was unobstructed (Figures 2G, H).",
"gender": "Female"
},
{
"age": 56,
"case_id": "PMC11169871_03",
"case_text": "Patient 3 (a 56-year-old woman) also suffered from chronic headache and underwent a cerebral enhanced MRI, which revealed the tumor size of 2.6 x 3.3 x 4.0 cm (Figures 3A-C). The surgical method was identical to that of patient 1 and patient 2. A transverse skull bridge was left to suspend the dura after an occipital and suboccipital craniotomy for protecting the transverse sinus (Figure 3D and Supplementary Video 2). Then, the dura was opened infratentorially and supratentorial parallel to the transverse sinus and along the superior sagittal sinus, allowing a perfect overview and access to the tumor. The combination of the infratentorial and supratentorial approach facilitated complete resection of the meningioma without damaging any venous sinus. Complete tumor resection, as well as patency of the sinuses, was confirmed by preoperative and postoperative head CT/CTV imaging (Figures 3E, F).\nThe intraoperative bleeding volume of three patients was 4,500, 1,000, and 800 mL, respectively. The durations of surgery, intensive care unit (ICU), and hospital stay of the patients are shown in Table 1. The histopathological examinations of all three patients demonstrated meningiomas of meningothelial type, and they have been discharged on postoperative days 7 to 9.\nPostoperative follow-up of these patients was crucial in monitoring for any potential complications or recurrences following surgical intervention. Follow-up imaging at 1 year after resection showed no evidence of tumor recurrence. Neurological examinations of the patient's cognitive function, motor skills, and overall wellbeing at 1 year post-surgery were similar to the preoperative evaluation. Additionally, all three patients did not undergo any additional treatments such as radiation therapy. Overall, diligent postoperative follow-up care showed that these FM patients recovered well without any morbidity on follow-up at 1 year.",
"gender": "Unknown"
}
] |
PMC11169871
|
[
{
"age": 95,
"case_id": "PMC10557962_01",
"case_text": "A 95-year-old female presented to the ER with a desquamating rash with oral, optic, and genital involvement concerning for SJS, Figures 1 and 2. The patient's past medical history was significant for chronic kidney disease (CKD) stage IV, diastolic congestive heart failure, gout, hyperlipidemia, and hypertension. Upon reviewing the patient's home medication list by the ER clinical pharmacist and the ER physician, oral allopurinol 100 mg daily was identified as the newest drug which was started 10 days prior to developing this rash. While performing a medication history review, the patient reported having a similar reaction 5 years ago secondary to allopurinol which was discontinued and planned to be stopped indefinitely. Upon admission to the hospital, the patient was started on high-dose steroids with intravenous (IV) methylprednisolone for 3 days, followed by a prolonged steroid taper. Additionally, the patient had ocular complications and decreased vision secondary to sloughed mucosa on the lashes and around the eyelids, Figure 3. Ophthalmology consultation was obtained, and the patient was started on erythromycin 0.5% ointment, ciprofloxacin 0.3% eye drops, prednisolone acetate 1% eye drops, and cyclosporine 0.05% eye drops. On day 3, the patient's rash started improving and on day 4, the patient was able to open her eyes. During her hospital stay, the patient contracted superimposed cellulitis with Methicillin-resistant staphylococcus aureus bacteremia (MRSA) and was started on IV antibiotics. After 1 month of hospital stay, the patient's skin lesions were completely resolved. During her hospitalization, our patient also developed acute kidney injury (AKI) requiring hemodialysis.",
"gender": "Female"
}
] |
PMC10557962
|
[
{
"age": 43,
"case_id": "PMC10808894_01",
"case_text": "A 43-year-old man with no known traditional coronary artery disease risk factors and a previous history of pulmonary embolism in 2022 due to long-distance travel completed T. Rivaroxaban 15 mg BD for three months. He presented with acute shortness of breath with exertion, which worsened over three days. It was associated with palpitation. There were no other associated symptoms. Upon arrival at the emergency department, his blood pressure was 118/87 mmHg, and his pulse rate was 107 bpm with 100% saturation under room air. Other clinical examinations revealed no significant findings. Initial blood investigations showed total leucocytes 7.1x109/L, hemoglobin 17.2 g/dL, and platelets 372x109/L. His coagulation profile showed activated partial thromboplastin time (aPTT) of 34.30 secs, prothrombin time (PT) of 14.70 secs, and international normalized ratio (INR) of 1.08. His troponin T level was 26 (normal range <15pg/L). Other blood investigations were within the normal range. ECG showed sinus rhythm, right axis deviation, poor R wave progression, and deep symmetrical T inversion at V2-V4 (Figure 1). There was also the presence of minimal T inversion in leads II, III, and AVF as compared to the precordial lead.\nThe chest X-ray was grossly normal. His initial diagnosis was non-sT elevation myocardial infarction (NSTEMI), and he was admitted to the hospital by the general medical team. Dual antiplatelet and anticoagulant were initiated. Echocardiography was performed the next day and showed dilated right ventricle (RV), right ventricle fractional area changes (FAC) of 29%, McConnell's sign, and mobile thrombus at main pulmonary artery bifurcation (Videos 1-3). Computed tomography pulmonary angiography confirmed the presence of saddle pulmonary thrombus at the bifurcation of the pulmonary trunk extending to the left pulmonary artery until subsegmental branches (Figure 2 and Figure 3). His CT coronary angiography showed normal coronaries.\nHe subsequently received thrombolysis with intravenous streptokinase 250,000 units for 30 minutes, followed by 100,000 units over 24 hours after cardiology team consult. He was discharged well from the ward after one week of hospitalization with T. Rivaroxaban 15 mg BD for three months, and unfortunately, he did not turn up for follow-up at three months.",
"gender": "Male"
}
] |
PMC10808894
|
[
{
"age": 45,
"case_id": "PMC10656737_01",
"case_text": "A 45-year-old male patient diagnosed with a squamous cell carcinoma on his left cheek. The tumor demonstrated regression by radiation therapy (66 Gy) 7 months ago. However, the anterior part was ulcerated and gradually formed a penetrating defect after 1 month. Histopathological examination confirmed squamous cell carcinoma, staged clinically as T4N1M0. With the assistance of VSP and 3D printing technology, the reconstruction utilising both flaps was successfully performed (Figures 1, 2).",
"gender": "Male"
}
] |
PMC10656737
|
[
{
"age": 35,
"case_id": "PMC11022868_01",
"case_text": "On March 7, 2018, a 35-year-old Chinese female patient presented with a one-year history of persistent erythematous papules and infiltrative plaques on the nose without any obvious triggers. Initially, a hard nodule the size of rice grains appeared on the right alar part of the nose, which was painless and itchy. Over time, the skin lesions gradually increased in size, became thick, and diffused across the entire nose. Infiltrating plaques also developed on the upper jaw. Initially, the patient was diagnosed with rosacea. However, the discovery of infiltrating plaques in the upper jaw indicated a more complex condition that required closer attention.\nPast and family history revealed no similar diseases within the family. Since the onset of the illness, the patient's urine, stool, and weight remained normal. Skin examination revealed diffuse erythematous papules, infiltrations, and hypertrophic plaques on the entire nose and upper jaw, with a smooth surface (Figure 1A-C). Dermoscopy showed a bright red background with diffuse telangiectasia, but no obvious keratinized hair follicle structures (Figure 2A). Laboratory examinations, including antinuclear antibody, anti-dsDNA antibody, anti-Ro, anti-La, and Borrelia, as well as direct immunofluorescence serology, yielded negative results. Blood and urine routine tests, liver and kidney function tests, chest X-ray, and ECG all showed no obvious abnormalities. Maxillary CT plain scan with enhancement revealed several findings: (1) a soft tissue nodule in the right soft palate, with multiple enlarged lymph nodes in both necks, and thickening and enhancement of nasal soft tissue; (2) right frontal sinus and ethmoid sinusitis. Histopathological examination of the biopsy sample showed a normal epidermis and an inflammatory infiltrate consisting of dense perivascular lymphocytes, as well as lymphocytes surrounding hair follicles and sweat glands in the dermis. Immunohistochemistry demonstrated a predominance of CD4+ T cells compared to CD8+ T cells (Figure 2B and C). The immunohistochemical panel further revealed positive staining for CD3, CD4, CD8, CD20, CD43, CD68, CD1a, and Ki-67 (10%), while staining for CD123, CD56, GB, PAS, and acid-fast organisms was negative (Figure 3A-K). TCR gene rearrangement analysis did not show any clonal amplification peaks in the target fragment. Differential diagnosis included rosacea and lymphoma. Based on the clinical and histological characteristics observed, and the absence of evidence supporting cutaneous lymphoma in the immunohistochemical studies, the definitive diagnosis of JLIS was established. \nMinocycline, known for its anti-neutrophil differentiation and lymphocyte proliferation effects, is commonly used in clinical practice due to its minimal side effects. In this case, the patient was prescribed oral Minocycline at a dose of 100mg twice a day. After 4 weeks of treatment, a significant improvement was observed with an 80% regression of infiltrative erythema, prompting a reduction in Minocycline dosage. During the outpatient follow-up conducted 2 months later, complete clearance of the skin changes on the nose and upper jaw was observed, leading to the discontinuation of Minocycline treatment (Figure 4A-C). No adverse reactions were observed, and there was no recurrence during the 5-year observation period. The patient is currently still under follow-up.",
"gender": "Female"
}
] |
PMC11022868
|
[
{
"age": 45,
"case_id": "PMC10713245_01",
"case_text": "A 45-year-old male with a past medical history of T4-T5 spinal cord injury in 1994 and multiple hospitalizations for infections requiring extended courses of antibiotics was admitted for severe muscle spasms, abdominal pain, nausea, and vomiting. Labs on admission demonstrated neutrophilic leukocytosis and high anion gap metabolic acidosis secondary to lactic acidosis. A computed tomography (CT) scan of the abdomen and pelvis revealed a left hip joint fluid collection and appendiceal wall thickening concerning for appendicitis. Blood cultures were obtained, and empiric antibiotic therapy was initiated with intravenous (IV) cefepime and vancomycin. The patient was evaluated by the surgical team and felt to not have acute appendicitis. The patient then underwent left hip arthrocentesis with return of 3 mL of bloody, cloudy synovial fluid. Due to the small volume, fluid analysis was not performed and the sample was sent for Gram stain and culture which were negative. Blood cultures also revealed no growth. IV cefepime and IV vancomycin were continued for eight days until the patient was discharged, and upon discharge he was transitioned to IV cefepime and IV daptomycin through a PICC line (Bard, double lumen, 5 French catheter) for 4 weeks as an outpatient. Both according to our electronic medical records and outside medical records that we have received, there is no previous documentation of PICC insertion in this patient. Unfortunately, the patient did not show for his hospital follow-up in the infectious disease clinic.\nThree months later, the patient was readmitted due to concerns for another episode of septic arthritis in his left hip. Upon admission he was noted to still have his left upper extremity PICC from his previous hospitalization, indicating that the PICC was in place for approximately three months, about eight weeks longer than it was supposed to be in place. The PICC remained in place during this time because the patient was lost to follow-up after his previous discharge and did not show for his follow-up appointment in the infectious disease clinic and was therefore unable to have it removed. It is unclear if the patient's PICC was cared for during this time. Two sets of peripheral blood cultures were obtained, and the patient underwent left hip drain placement by interventional radiology from which cultures were negative. A superficial culture obtained from the patient's chronic left hip wound was reported as positive for normal flora consistent with the site. On hospital day 3, both sets of blood cultures became positive with reported growth of Gram-negative rods at which point the patient was started on IV piperacillin/tazobactam. A repeat pair of quantitative blood cultures was obtained which revealed growth of Gram-positive cocci in clusters 15 hours later. IV vancomycin was initiated, and the infectious disease service was consulted with the recommendation to continue current antibiotics, remove the PICC, and obtain repeat blood cultures. By this time, the Gram-negative rods had been identified as Trueperella bernardiae by matrix-assisted laser desorption/ionization time of flight (MALDI-TOF). It was suspected that the initial Gram stain had been over-decolorized resulting in the read of Gram-negative rods. T. bernardiae was not worked up further for antibiotic susceptibility, but a decision was made to continue piperacillin/tazobactam for antibiotic therapy based on review of the literature concerning T. bernardiae. The Gram-positive cocci from the repeat blood cultures were subsequently identified as methicillin-resistant Staphylococcus aureus (MRSA). Search for an alternative source of infection was negative, and the patient improved after removal of the PICC, so although no segmental cultures of the catheter body or definitive studies of the catheter were performed, the final diagnosis of central line-associated bloodstream infection from his PICC was made on a clinical basis. Repeat paired quantitative blood cultures obtained after PICC removal were both negative for growth at five days, after which the patient was discharged on IV piperacillin-tazobactam for two weeks for the T. bernardiae bacteremia and IV daptomycin for four weeks for his MRSA bacteremia, both through a tunneled PICC line. The tunneled PICC line was subsequently removed after completion of this regimen.",
"gender": "Male"
}
] |
PMC10713245
|
[
{
"age": 18,
"case_id": "PMC10467352_01",
"case_text": "An 18-year history of open reduction and internal fixation for a distal radius fracture was observed in a 63-year-old male patient's left wrist. He was recently involved in a car accident and was admitted to our emergency department. The patient had no comorbidities, no smoking and came from an urban environment.\nOn physical examination, the wrist showed noticeable deformation and exhibited signs of deep abrasion, with skin and muscle contusion. The patient was incapable of moving his wrist and experienced discomfort even during passive movements. No deficits in vascular or neurological function were observed. X-ray imaging indicated a peri-implant fracture located proximal to the plate in the radius, along with a fracture in the ulnar shaft. The plate remained affixed to the distal radius, and the radiocarpal joint exhibited a dorsal tilt. Furthermore, the patient had radiocarpal and radioulnar arthritis, along with a malunion of the distal radius (Figure 1). The patient underwent surgical treatment using a volar approach. A skin incision was made over the previous surgical scar, and the plate and screws were removed. Subsequently, the reduction was performed. With the radius reduction, the ulna was also reduced, obtaining a stable reduction. After that, internal fixation was performed using a dynamic compression plate (DCP) for the radius fracture and a Kirschner wire for the shaft ulnar fracture. Considering the skin injuries in the ulnar approach, we chose to treat it with a Kirschner wire. Postoperative images confirmed a successful reduction in fractures (Figure 2). After surgery, the forearm was immobilized with a splint for 30 days. After the removal of the splint and Kirschner wire, the patient began rehabilitation to restore the range of motion in his forearm and wrist. Unfortunately, the patient did not follow regular follow-up appointments, which hindered clinical and radiological evaluation.",
"gender": "Male"
}
] |
PMC10467352
|
[
{
"age": 28,
"case_id": "PMC10790793_01",
"case_text": "We report the case of a 28-year-old Caucasian woman, who came to the attention of the Plastic Surgery department due to the presence of left leg macrosomy with excess of cutaneous and subcutaneous soft tissues, resulting from venous-lymphatic malformation (Figure 1).\nAt the age of 7, she underwent a safenectomy of the right leg, at the age of 9-10, she had multiple varicectomies of the right leg. At the age of 13, she underwent an epiphysiodesis of the left leg to surgically correct the leg length discrepancy. A more recent varicectomy of the right leg was performed at the age of 27.\nA radiological work up of the patient was performed through chest x-ray and contrast-enhanced MRI. The former, by means of the antero-posterior project, reveled a slight spinal scoliosis. The latter specifically revealing fatty replacement of the anterior and medial compartment of the left thigh, at T1-weighted sequences (Figure 2). At T1-weighted enhanced sequences, diffused vascular malformations were identified in the left thigh.\nFollowing a multidisciplinary consultation, the patient was submitted to surgery.\nIn June 2021, we performed a suction-assisted lipectomy (approximately 2000 mL of lipoaspirate) of the internal and external thigh, trocanteric and subgluteal region of the left leg.\nThe left gluteal region was still notably afflicted by dermal and adipose excess, resulting in a significant functional constraint and a high degree of asymmetry with respect to the contralateral gluteal region.\nIn November 2021, the patient underwent another aspiration lipectomy (approximately 1600 mL of lipoaspirate from the anterior, lateral and medial left thigh) combined with resection of wide lozenge of skin and subcutaneous tissue from the left gluteal region.\nThe patient returned to our institution in June 2022 referring the persistence of functional limitations caused by the remaining presence of dermal and adipose excess in the left leg. Also, a hypertrophic erythematous scar was reported in the subgluteal fold, resulting from previous dermo-adipose resection.\nIn June 2022, she underwent a further resection of a wide lozenge of skin and subcutaneous tissue of the left medial thigh via surgical asportation combined with lipoaspiration of the anterior and medial left thigh and of the genial region (approximately 1000 mL of lipoaspirate). (Figure 3)\nAfter a thorough multidisciplinary consultation, the patient underwent a series of surgical procedures. These interventions were necessitated by the surplus adipose tissue, which created surgical complexities due to the need to consider the patient's vascular and skeletal anomalies, thereby heightening the risk of bleeding. Notably, there were no instances of recurrence in this patient. The successive surgeries were carefully planned to safeguard vascular integrity, significantly mitigating the risk of bleeding. This approach also contributed to enhancing the patient's functional outcomes.\nFollowing the last surgery, the patient was followed up every month for six months via outpatient care, reporting subjective amelioration of her thigh circumference. During the last checkup, she reported to be satisfied with the morpho-functional result obtained and expressed her willingness to undergo further surgical procedures, if deemed appropriate.",
"gender": "Female"
}
] |
PMC10790793
|
[
{
"age": 37,
"case_id": "PMC10893992_01",
"case_text": "A 37-year-old male presented at an orthopedic specialty hospital with right knee pain after a fall from a truck ramp. The patient heard a pop and had severe, sharp pain in his right knee. In the emergency room, X-rays and CT imaging demonstrated a comminuted bicondylar TPF with metaphyseal dissociation. The medial tibial plateau was depressed by 5 mm. The patient was placed in a knee immobilizer, made non-weight bearing, and scheduled for outpatient follow-up with a local orthopedic surgeon. The patient was lost to follow-up and referred to our clinic six months after the fall. His chief complaint was an inability to ambulate with severe pain and instability in the knee. X-rays demonstrated a malunion of the bicondylar tibial plateau and depressed medial plateau with possible increased condylar width and varus alignment (Figure 1A-1C). CT scans showed healed fractures, and an MRI was ordered to rule out osteochondral defects and meniscus tears. The patient was indicated for corrective osteotomy.\nThe surgical technique was a medial opening wedge proximal tibial osteotomy. The patient was placed in a prone position, and an incision was made centered over the medial aspect of the gastrocnemius. The medial soft tissue sleeve was elevated off the proximal tibia in a subperiosteal fashion while maintaining the medial collateral ligament (MCL) insertions (Figure 2A). Next, a sagittal saw was used to make a medial tibial osteotomy. The medial proximal tibia was elevated to create an opening wedge osteotomy to correct varus deformity. Afterwards, a fibula strut allograft with a plate/screw construct was placed (Figure 2B). Beta-tricalcium bone filler was used to fill the void (Figure 2C). Postoperatively, the patient was made non-weight bearing for three months. Range of the motion was encouraged as tolerated.\nAt the first month follow-up, the patient's pain was well controlled, and range of motion exercises were done regularly. No paresthesia, numbness, or wound dehiscence was noted. Repeat X-rays demonstrated intact hardware with evidence of healing fracture lines compared to immediate postoperative images (Figure 3A, 3B). Fragments and the knee were appropriately aligned. No significant soft tissue or joint effusion was appreciated on imaging.",
"gender": "Male"
}
] |
PMC10893992
|
[
{
"age": 93,
"case_id": "PMC10879725_01",
"case_text": "A 93-year-old female, with a history of hypertension, type II diabetes, coronary artery disease, and a distant history of a duodenal ulcer, presented to the emergency department with four days of right upper quadrant (RUQ) abdominal pain and associated nausea, jaundice, and dark colored urine. She did not report vomiting, diarrhea, or notable weight loss. Prior to the presentation, the patient was in good health and lived alone.\nUpon initial evaluation, the patient appeared jaundiced with scleral icterus and had RUQ abdominal tenderness with mild distension of the abdomen. No hepatosplenomegaly or abnormal bowel sounds were appreciated. A hepatic function panel was significant for a mixed pattern of liver injury with elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) (Table 1). Of note, mildly elevated titers of ALP measuring 107-117 U/L were appreciated on multiple laboratory studies dating back 16 months prior to her presentation. Her levels of ALT and AST, however, were normal prior to this admission. CA 19-9 was markedly elevated, and her total bilirubin was increased, which was consistent with an obstructive pattern of hyperbilirubinemia (Table 1). Liver synthetic function as assessed by prothrombin time was normal. There was no leukocytosis or anemia. Lipase was within normal limits. A urine study showed elevated urobilinogen and large amounts of bilirubin. A CT scan of the abdomen and pelvis revealed a soft-tissue density measuring 1.9 x 1.5 x 1.9 cm within the distal common bile duct with marked intra- and extrahepatic bile duct dilatation, and variable pancreatic duct dilatation (Figure 1). There were multiple poorly defined hepatic lesions of varying sizes. The patient was admitted for further evaluation of a possible malignancy.\nEndoscopic ultrasound was subsequently done, showing a predominantly hypoechoic mass in the distal common bile duct, which measured about 20 mm and caused significant biliary dilation (27 mm). Tissue cores of the mass were then collected via fine needle aspiration (FNA). This was quickly followed by endoscopic retrograde cholangiopancreatography where a protuberant, downward-facing papilla with stricture of the common bile duct was noted. Additional intraductal biopsies were taken with forceps, and the biliary stricture was palliated with a 10 mm x 6 cm fully covered metal biliary stent. The patient tolerated the procedures well and was discharged home in stable condition two days after the procedure while biopsy results were pending.\nThe biopsy results from the FNA demonstrated a well-differentiated neuroendocrine tumor: WHO, Grade 3 (Figure 2). On microscopic examination, there were singly scattered sheets and groups of cells with round to ovoid pleomorphic nuclei, salt and pepper chromatin, frequent mitotic figures, and inconspicuous nucleoli. Similarly, the forceps biopsy from the bile duct stricture showed sheets of neoplastic cells with oval nuclei, salt-and-pepper chromatin, and a small amount of cytoplasm (Figure 3). Immunohistochemical stains revealed the tumor cells to be positive for cytokeratin AE1/AE3, synaptophysin, chromogranin, and SSTR2A. P53 immunostain showed diffuse strong expression. MIB-1/CD45 immunostain demonstrated a Ki-67 proliferative index of 90%. The morphologic features and immunohistochemical profile from this sample were again consistent with well-differentiated neuroendocrine tumors (WHO, Grade 3).\nThe patient did well clinically after discharge from the hospital. Her primary complaints had been pain, fatigue, and reduced appetite although these were reportedly mild, and she had not required medication for symptom control after biliary stenting. At her follow up appointment with oncology a few weeks after discharge, she decided to forego any further testing and treatment for her condition. A periodic review of her records indicated that the patient was deceased two months after her initial presentation to the emergency department.",
"gender": "Female"
}
] |
PMC10879725
|
[
{
"age": 43,
"case_id": "PMC10800751_01",
"case_text": "A 43-year-old woman was admitted because of a palpable mass in her left flank, with accompanying symptoms of dysuria and worsening pain in the abdomen. A huge tumor occupying the left side of the abdomen was found on CT-Scan examination, therefore she was referred to our hospital for further treatment. Six years ago, she had experienced left abdominal pain. The pain was dull, and intermittent, with a visual analog scale (VAS) of 1-2, which was eventually left untreated. She also denied any weight loss. During admission, a physical examination showed remarkable bulging on the left flank. A painless, mobile hard tumor was found on palpation. Blood examinations showed mild anemia and hypoalbuminemia. By the pattern of the disease, the patient was initially diagnosed with liposarcoma (Fig. 1).\nSurgical exploration with excision of the retroperitoneal mass was decided as treatment modality in this case. Intraoperative findings showed a mass surrounding both the left renal artery and vein with persistent adherence. Preservation of renal vascular failed, therefore subsequent left nephrectomy was performed along with resection of the retroperitoneal tumor (Fig. 2). There were no other invasions or relations to any adjacent organs, including the rectum, sigmoid colon, or uterus. The patient had uneventful postoperative care and was discharged as planned.\nHistologically, the neoplasm appeared sarcomatoid, composed of a relatively solid and diffuse cell pattern with ovoid and stellate nuclei and spindle cells. The neoplasm had moderate nuclear anaplasia with minimal necrotic areas and mitotic figs. (0-2 mitoses per High Power Fields) (Fig. 3). This neoplasm was initially judged as a rhabdomyosarcoma. However, subsequent immunochemistry examination demonstrated positive staining for vimentin, desmin, and focal SMA, while myogenin, MyoD1, MDM2, and S-100 were negative. The Ki-67 index was expressed in 5-10 % of tumor cells with minimal proliferation showing the indolent characteristics of this neoplasm (Fig. 4). Based on these findings, the diagnosis was changed into a retroperitoneal solitary fibrous tumor.\nNo adjuvant treatment was given following the procedures, and the patient remained symptom-free. A post-operative CT-scan was performed 6 months later, with no detectable mass on the left renal fossa or any adjacent organs (Fig. 5).",
"gender": "Female"
}
] |
PMC10800751
|
[
{
"age": 58,
"case_id": "PMC11239392_01",
"case_text": "A 58-year-old female patient previously diagnosed with acute ileus was transferred to our hospital on July 16, 2021. She presented with abdominal pain and distension, vomiting, and cessation of flatulence and defecation for 2 days. The patient had no known history of health issues prior to admission.\nAbdominal physical examinations on admission were conducted as follows:\nInspection: protuberance of abdomen and intestinal patterns were observed.\nPalpation: abdominal tenderness without rebound tenderness or muscle tonus, no palpable liver and spleen below the costal margin, and no palpable abnormal mass in the abdomen.\nPercussion: percussion of whole abdomen showed tympanic resonance and negative shifting dullness.\nAuscultation: bowel sounds were audible at a rate of 8 times/min as well as the sound of gas passing through water, but no vascular murmur was detected.\nThe body mass index (BMI) of the patient was 19.29.\nLaboratory parameters were as follows: white blood cells 12.74x109/L (normal range, 3.5-9.5x109/L), neutrophils 85.7% (normal range, 40-75%), hemoglobin 102 g/L (normal range, 130-175 g/L), and procalcitonin 0.15 ng/mL (normal range, 0-0.05 ng/mL). Enhanced abdominal CT revealed a swirling distribution of the small intestine in the right middle and lower abdomen, thickening and narrowing of the local intestinal wall, significant dilation of the area above the lumen stenosis, presence of gas and fluids in the cavity, and multiple irregular lipoid-like density foci in the abdominal cavity that were not enhanced ( Figures 1A-C ).\nThe initial diagnosis was multiple masses in the small bowel with secondary volvulus, requiring emergency exploratory laparotomy. During surgery, abnormal dilation of the small bowel was observed between 80 and 220 cm from the ileocecal valve, with a maximum diameter of ~14 cm, and the diseased intestine was folded and twisted. Subsequently, complete resection of the affected intestine was performed, followed by primary anastomosis.\nSpecimen examination revealed that the inner wall of the diseased intestinal lumen was covered with over 100 lipomas of varying sizes, with the largest measuring around 8.0 cm in diameter, in addition to scattered necrotic bleeding points and abnormal mesentery fat distribution ( Figure 2 ). Postoperative pathological diagnosis indicated small intestinal lipomatosis with local hemorrhage ( Figures 3A, B ). The patient recovered successfully after surgery and was discharged on July 23, 2021. After 20 months of follow-up, no recurring symptoms of discomfort were reported. The BMI of the patient increased to 21.79 and abdominal enhanced CT imaging revealed no signs of recurrence ( Figures 4A, B ).",
"gender": "Female"
}
] |
PMC11239392
|
[
{
"age": 13,
"case_id": "PMC11127645_01",
"case_text": "We present the case of a 13-year-old female child who initially presented at the age of 3 years with complaints of easy fatigability, multiple joint pain, decreased appetite, and irritability lasting for one month. She was initially evaluated at a nearby health center and subsequently referred to Tikur Anbessa Specialized Hospital (TASH) for further investigation due to severe anemia of unknown etiology. The patient had received multiple transfusions of whole blood and packed red blood cells. She was then linked to the Haemato-oncology clinic but was lost to follow-up for approximately 10 years.\nAt the current age of 13 years, the patient returned to TASH with a complaint of easy fatigability, intermittent joint pain, decreased appetite, and lightheadedness persisting for the past 3 years. Her fatigue had progressively worsened, initially occurring with walking but later affecting even ordinary activities. Additionally, she reported a history of intermittent diarrhea and constipation, with periods of remission lasting for 2 years. The diarrhea episodes were described as yellowish to brownish in color and occasionally mixed with blood, occurring 3-4 times per day and alternating with episodes of constipation. The patient also experienced intermittent colicky abdominal pain, which worsened with changes in bowel habits. She had sought medical attention at various healthcare facilities and received unspecified oral medications as well as multiple blood transfusions. Subsequently, she was referred to the pediatric gastrointestinal clinic at TASH for further evaluation.\nPhysical examination at TASH revealed a pulse rate of 100 beats per minute, respiratory rate of 22 breaths per minute, and axillary temperature of 36.6 C. Anthropometric measurements indicated a weight of 22 kg, height of 125 cm, and a body mass index for age between -2 and -3 standard deviations (SD) on the Z-score, indicating moderate acute malnutrition. The patient exhibited pale conjunctivae and palmar pallor. Based on the clinical presentation and findings, a diagnosis of moderate acute malnutrition and anemia associated with chronic diarrhea secondary to inflammatory bowel disease (IBD) was made.\nThis case highlights the challenges encountered in the management of a patient with coexisting sickle cell disease and ulcerative colitis. The prolonged period of loss to follow-up underscores the importance of consistent medical care and regular monitoring for individuals with complex medical conditions. Further investigations and targeted treatment plans will be implemented to address the patient's specific needs and improve her overall health and quality of life.\nFollowing the investigations conducted, the case report provides the following findings and management:\nThe patient's white blood cell count was elevated at 14,500/mm3, with a differential count showing 36.5% neutrophils and 49.4% lymphocytes. The platelet count was 92,900/mm3, indicating thrombocytopenia. Hemoglobin level was 6.6 g/dL, hematocrit was 20.4%, and mean cell volume (MCV) was 91.5 femtoliters. Mean cell hemoglobin was 29.6%, indicating hypochromic red blood cells, and red cell distribution width was elevated at 28.4%.\nStool examination did not reveal any significant abnormalities. Renal and liver functions were normal, and serology for hepatitis B surface antigen, hepatitis C virus, and HIV were negative.\nLactate dehydrogenase (LDH) level was elevated at 273 mg/dL, indicating increased cell turnover. Peripheral morphology of red blood cells showed mild anisochromia (normochromic to hypochromic), mild anisopoikilocytosis with frequent polychromatophilic red blood cells, a few fragmented red blood cells (\"boat-shaped\"), and sickled red blood cells Figure 1.\nAbdominal ultrasound revealed diffused circumferential thickening of the cecum to sigmoid colon, indicating bowel wall inflammation. The spleen was not visible (absent), indicating functional asplenism.\nBased on the above findings, a diagnosis of moderate acute malnutrition, severe anemia, inflammatory bowel disease (ulcerative colitis), and asplenia secondary to sickle cell disease was made.\nThe patient received packed red blood cell transfusion to address the severe anemia. Hydroxyurea, a medication that can help reduce sickling of red blood cells, was initiated. However, despite treatment, the patient continued to experience bloody diarrhea.\nA colonoscopy was performed, revealing edematous and erythematous mucosae with continuous irregular rectal and sigmoid ulcers, as well as multiple erosions and ulcers throughout the colon. Biopsy of the colon showed expanded lamina propria with inflammatory infiltrates, basal plasmacytosis, lymphoid nodule formation, marked crypt dropout, minimal fibrosis, low-grade dysplasia areas, and polypoid changes. Separate ulcer surfaces and fibrinopurulent and granulation tissue fragments were also observed Figure 2.\nBased on the colonoscopy findings, the patient was diagnosed with ulcerative colitis. Treatment with prednisolone, a corticosteroid to reduce inflammation, and amoxicillin prophylaxis (likely to prevent infection) was initiated.\nOn subsequent follow-up assessments, the patient showed noticeable clinical improvement, suggesting a positive response to treatment.\nThe case report underscores the complexity of managing a patient with multiple coexisting conditions, including sickle cell disease, ulcerative colitis, severe anemia, and moderate acute malnutrition. The treatment approach involved addressing the specific conditions with appropriate interventions, including transfusion, hydroxyurea, prednisolone, and amoxicillin prophylaxis. Regular follow-up and monitoring will be crucial to ensure continued improvement and long-term management of the patient's conditions.",
"gender": "Female"
}
] |
PMC11127645
|
[
{
"age": 42,
"case_id": "PMC10619528_01",
"case_text": "A 42-year-old woman presented to our hospital with a complaint of severe headache and vomiting for 5 days. Her headache would increase by lifting her head or sitting up. Her present symptoms started 1 week after receiving a booster dose of mRNA COVID-19 vaccine (Pfizer-BioNTech). She had on and off headaches and neck pain in the past. She had no pertinent past medical history, trauma, lumbar puncture or oral contraception. She never underwent a nasal swab. A neurological examination revealed an orthostatic headache and absence of focal neurological deficit.\nThe patient was investigated with magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) of the brain (Fig. 1A and 1B). Drooping splenium of the corpus callosum was noted along with effaced perimesencephalic and prepontine cisterns. The pontomesencephalic angle and mammillopontine distance were grossly reduced, representing brain stem sagging, and cerebellar tonsils were reaching caudally 3 mm below McRae's line. A contrast-enhanced MRI was not performed. This constellation of findings represents intracranial hypotension. In addition, small haemorrhagic subdural collections were seen over the frontal convexities. There was no cerebral infarct or intraparenchymal haemorrhage.\nThe MRI also revealed a T1 and T2 hyperintense thrombus filling the superior sagittal, left transverse and sigmoid sinuses. On MRV, these sinuses did not exhibit flow-related enhancement (Fig. 1C and 1D). The right transverse, sigmoid and straight sinuses were patent with normal signal on the venogram.\nThe only significant abnormality on blood investigation was raised D-dimer (791 ng/ml). In particular, there was no thrombocytopenia. Two days after the MRI, a lumbar puncture was performed in the supine position; CSF opening pressure was very low and not detectable. A few drops of CSF were sent to the lab and the CSF analysis was unremarkable. A CT myelogram (Fig. 2) was performed, which showed epidural CSF leakage along the bilateral nerve roots from L1 to L5 vertebral levels.\nBased on the findings of CSF leakage on the CT myelogram, the patient was treated with an epidural blood patch for SIH. She was also started on anticoagulation for CVT. Follow-up MRI and MRV (Fig. 3) conducted after 6 months showed recanalisation of the superior sagittal, left transverse and sigmoid sinuses. There was resolution of subdural collections, and features of SIH were no longer seen. The patient has been on regular follow-up in our neurology clinic and her symptoms have been relieved significantly.",
"gender": "Female"
}
] |
PMC10619528
|
[
{
"age": 50,
"case_id": "PMC10800741_01",
"case_text": "We report the case of a 50 years old patient with no previous pathological history, who consulted for neck pain and bilateral cervicobrachial neuralgia evolving for 4 months, progressively worsening and becoming associated with an important functional disability. Symptomatic treatment as well as physiotherapy failed to release symptoms.\nClinical examination showed a slight paravertebral muscles contracture with neck stiffness. No motor or sensory deficit were observed.\nRadiographs showed a lytic image of the axis without basilar impression or signs of occipitocervical junction instability (Fig. 1).\nCT scan was performed showing a lytic image of the axis without signs of occipitocervical junction instability (Fig. 2); The scan-guided biopsy performed by the radiology team involved taking 3 samples containing soft tissue and bone for histological examination. Despite this, the anatomopathological result was inconclusive, and surgical biopsy curettage was deemed necessary to progress in the diagnostic and therapeutic management.\nMRI showed an infiltrating process of the whole vertebral body and odontoid process of the axis with invasion of its right sided posterior arch and soft tissue. (Fig. 3).\nConsidering that the bone lesion may potentially lead to occipitocervical instability, we opted for a curettage biopsy of the posterior arch of C2 with occipito-C4 instrumented fusion using posterior iliac crest graft. (Fig. 4).\nThe diagnosis of SBP was established based on the findings of histological examination and multiple myeloma was excluded based on the results of laboratory tests.\nPostoperatively, an adjuvant radiotherapy protocol was prescribed with a dose of 45 Gy as well as a chemotherapy. The evolution was favorable at 4 years fellow-up without progression to multiple myeloma. However, he complained from limitation of neck mobility and limited opening of the mouth.\nImaging assessment at the last follow up showed a solid arthrodesis without signs of local tumoral recurrence (Fig. 5).",
"gender": "Male"
}
] |
PMC10800741
|
[
{
"age": 82,
"case_id": "PMC10967536_01",
"case_text": "On March 8, 2023, an 82-year-old postmenopausal woman was admitted to our Department of Gynecology with abdominal distention. She had no other physical complaints.\nThe patient's symptoms started about 2 weeks before admission.\nThe patient's past medical history included tonsillectomy and minilaparotomy tubal ligation about 40 years before this presentation.\nThere was no relevant family history of the disease.\nGeneral examination of the patient revealed a body temperature of 36.1 C, pulse rate of 100 beats per minute, respiratory rate of 20 cycles per minute, and a blood pressure of 159/96 mmHg. Auscultation revealed slightly diminished breath sounds in both lungs, which were dull to percussion. The cervix was atrophic; neither the uterus nor the adnexae were palpable.\nThe patient's hematology, urinalysis, and biochemistry results were normal. The serum CA125 concentration was 1040 U/mL (normal, 0-35 U/mL); the results of carcinoembryonic antigen, alpha-fetoprotein, CA153, CA199, and HE4 were unremarkable. A drainage tube was placed in the left pelvic cavity, and a total of 3650 mL of ascites was withdrawn. The ascites was yellow and transparent, with no blood detected and a white blood cell count of 180 x 106/L (95% lymphocytes and 5% neutrophilic granulocytes). The biochemical analysis of the ascites revealed the following findings: total proteins 41.2 g/L, alkaline phosphatase 23.0 U/L, sialic acid 34.9 mg/dL, lactate dehydrogenase 95.0 U/L, adenosine deaminase 4.0 U/L, and amylase 35 U/L.\nCombined transvaginal and transabdominal ultrasonography showed massive pelvic ascites and a large irregular mass (13.1 cm x 8.2 cm) with hypoechoic features on the left side of the pelvic cavity (Figure 1A and B). Chest computed tomography (CT) confirmed the presence of bilateral pleural effusions (Figure 2). Abdominal CT revealed a pelvic soft tissue mass (10.9 x 8.2 x 14.3 cm) with clear boundaries, heterogeneous density, no obvious enhancement, and an artery originating from the left ovarian artery (Figure 3A and B).\nThe patient underwent pelvic mass fine-needle puncture and drainage of ascites guided by abdominal ultrasound; cytologic analysis of the fluid samples from these procedures found no tumor cells present in the ascites and identified the pelvic mass as a spindle-cell, sex-cord stromal tumor. Immunohistochemical analysis revealed that vimentin, alpha-Inhibin, CD56, CR, and WT-1 were all positive; SF-1, Melan-A, CK, S-100, CD34, P53, and SMA were all negative; and the positivity rate of Ki-67 was approximately 3%.\nA postmenopausal woman with a pelvic mass, ascites, pleural effusion, and a high level of CA125 could easily be misdiagnosed as having an ovarian malignancy. The differential diagnoses for our patient included ovarian cancer, ovarian fibroma, and ovarian thecoma. Clinicians should have a high index of suspicion of malignancy, but they should be fully aware of the range of differential diagnoses and assess adequately before operating. To further clarify the diagnosis, in view of a comprehensive preoperative evaluation, our patient's diagnosis had to be confirmed histopathologically. Furthermore, coronary angiography revealed multiple coronary artery lesions with varying degrees of stenosis, as well as mixed plaques in the proximal tube wall of the left anterior descending branch with moderate to severe luminal stenosis. So, we invited cardiologist to assist us in the preoperative evaluation. After the exclusion of absolute surgical contraindications, the patient was scheduled for an exploratory laparotomy.\nRegardless of whether the patient's pelvic mass is benign or malignant, surgical removal of the pelvic mass is the mainstay of treatment. Therefore, an exploratory laparotomy:including total abdominal hysterectomy, bilateral adnexectomy, and pelvic drainage:was performed under general anesthesia. The surgical findings were as follows: The volume of faint yellow ascites was approximately 200 mL; the left ovary was enlarged to approximately 13 cm x 11 cm with an irregular surface, hard texture, and complete capsule; the left fallopian tube, the right adnexa, and the uterus did have any obvious morphological abnormalities. There were no other obvious findings in the comprehensive surgical exploration. Histopathologic examination of the intraoperative frozen tissue section of the suspected left adnexal ovarian fibrothecoma later confirmed a final diagnosis of left ovarian fibrothecoma (Figure 4).\nThe patient recovered well postoperatively and was discharged on postoperative day 7. Outpatient follow-up evaluation 2 months after the surgery included chest CT revealing that the pleural effusion had resolved (Figure 5). The ascites had also resolved, the CA125 level returned to normal, and the full workup and physical examination detected no obvious abnormalities.",
"gender": "Female"
}
] |
PMC10967536
|
[
{
"age": 30,
"case_id": "PMC10756947_01",
"case_text": "The patient was a 30-year-old woman with a chief complaint of protrusive lips, proclined. Maxillary incisors, anterior spacing, and recession on mandibular incisors. Extra-orally, she had a convex profile with an acute nasolabial angle, a strain on the circumoral muscles while closing her mouth, and a proclination of the upper incisors was observed when the patient smiled. No symptom of temporomandibular disorders was detected (Figure 1A,B).\nIntraorally, the patient was classified with a Class I molar relationship on both sides, a Class I canine relation on the right side, a Class II canine relationship on the left side, and peg-shaped lateral incisors. The patient only had three lower incisors present, with the lower right lateral incisor missing, diastemas in the maxillary and mandibular anterior teeth because of the tongue's position, and recession on the lower incisors. The upper and lower arch forms were typically developed, and a flat Curve of Spee was observed. The patient demonstrated Bolton's tooth size discrepancies because of the three lower incisors. The upper midline coincided with the facial midline. The lateral cephalometric analysis showed a skeletal Class I jaw relationship with proclined upper and lower incisors. Both the upper and lower lips were in front of the E-line (Figure 1C).\nThe treatment plan was multidisciplinary, involving fixed orthodontics, periodontics, and prosthodontic interventions in stages. 3D simulation was planned for the patient to analyze the size of the 3 lower incisors.\nIn the upper arch, the anterior segment was distalized using two mini screws, and in the lower arch, the retraction was carried out using a sliding technique with reverse curve 17 x 25 SS wire and power chains so as to control the tipping of the upper and lower incisors (Figure 2). Class III elastics were utilized to improve the anchorage on the lower arch. Before the class III elastics were started, the patient was advised to undergo removal of all the third molars in the upper and lower arches. The goal of orthodontics treatment was to reduce the proclination of the upper and lower anterior teeth, close the diastema on the upper, make the space on the lower smaller for prosthodontic intervention, and achieve good occlusion. After treatment, restorations were placed on the three mandibular incisors.\nAfter a 1-month waiting period post debonding of the braces, gingival grafting was carried out using the subepithelial CTG technique (Connective tissue grafting tunnel technique) in the mandibular anterior region (Figure 3). The connective tissue graft was acquired from the right maxillary quadrant in the area mesial to the premolars and the first maxillary molar. 2% Lignocaine hydrochloride with adrenaline was used for local anesthesia, and then the first incision was given parallel to the long axis of the palate. The thickness of the flap was kept sufficient to ensure no tearing of the tissues. Root planning was done on the lower incisors before placement of the graft.\nThe harvested graft was sutured over the exposed root surfaces. Pressure was applied over the graft for a few minutes, and a periodontal pack was placed for healing. The patient was recalled after 2 weeks, the sutures were removed, and the healing appeared normal (Figure 3B,C).\nAfter graft healing, restorations were placed in the mandibular arch from left to right lower canines. These were also intended to help close the diastema and provide good retention for the three lower incisors (Figure 4A,B,C).",
"gender": "Female"
}
] |
PMC10756947
|
[
{
"age": null,
"case_id": "PMC11081788_01",
"case_text": "A male patient in his early 30s with no medical history was initially admitted to the intensive care unit with acute hypoxic respiratory failure in the setting of COVID-19 infection. He received COVID-19 treatment per protocol as well as high-flow nasal cannula 60 % fraction of oxygen at 40 L per minute to keep oxygen saturation above 92 %. After 5 days, improvement in oxygenation was noted. However, fatigability was persistent, and a mild rising leukocytosis was observed. A chest x-ray (CXR) showed extensive bilateral opacities; some concerning for possible cavitation. However, a follow-up computed tomography (CT) of the chest showed bilateral infiltrates but negative for cavitary lesions (Fig. 1). Four days later, his course was complicated by a spontaneous right-sided pneumothorax (PNX) thought to be caused by persistent cough. A CT-guided chest tube was placed to treat the PNX. A routine follow-up CXR was concerning for a loculated pneumothorax and evolving multifocal infection (Fig. 2a). A new CT chest was notable for the known pneumothorax and pneumomediastinum now with development of several thin-walled cysts, the largest being 8.5 cm by 6.8 cm, without significant ground glass surrounding, and primarily consistent with pneumatocele formation (Fig. 2b). A surveillance CT chest was notable for increased size of the pneumatoceles with new air fluid levels. Even though the clinical status was unchanged, the presence of enlarging pneumatoceles with air-fluid levels (Fig. 2c-e) was concerning for a superimposed infection. After extensive negative infectious evaluation, including MRSA nasal swab, urine Streptococcus pneumoniae and Legionella Antigens, serum Aspergillus, serum Cryptococcus, urine Histoplasma, induced Sputum for Gram Stain, Aerobic, Fungal, and AFB Cultures, initial empiric antimicrobial regimen with piperacillin-tazobactam was discontinued. Subsequently, the patient's chest tube was removed and enhanced airway clearance measures were implemented. The patient clinically improved and was safely discharged home on room air.",
"gender": "Male"
},
{
"age": null,
"case_id": "PMC11081788_02",
"case_text": "At the 3-month follow-up, the patient reported an ability to perform all his normal activities without restriction. He denied any cough, chest pain or shortness of breath at rest or exertion. He had not yet tried any routine exercise as most of the facilities were closed due to the COVID-19 pandemic. It was decided that we would continue to monitor him clinically and radiographically with a CXR and clinic follow-up in 6-months Fig. 3a shows a CXR taken at the 3-month follow-up with improved, yet persistent pneumatoceles. At the 9-month follow-up, the patient remained asymptomatic. A month prior to this visit, he started running daily for approximately 30 minutes, without any cough, shortness of breath, or chest pain. He was looking forward to resuming strength training, now that his preferred gym was back in full operation. Fig. 3b shows a follow-up CXR at 9 months with resolution of pneumatoceles. Given resolved pneumatoceles without further complications, he was recommended to follow up as needed due to his excellent clinical status.",
"gender": "Male"
}
] |
PMC11081788
|
[
{
"age": 69,
"case_id": "PMC11439626_01",
"case_text": "In early August 2021, a 69-year-old woman who had been in menopause for 18 years was admitted to the hospital with irregular vaginal bleeding for 10 days. The patient underwent transcervical resection of endometrium and dilatation and curettage. Pathology in combination with abdominal and pelvic magnetic resonance imaging (MRI) examination confirmed that the tumor was an endometrial clear cell carcinoma (Type II EC) with a size of 1.5x0.9x0.3 cm3 ( Figure 1 ; Supplementary Table 1 ).\nHistopathological examination was performed and the IHC exhibited estrogen receptor (ER)-, progesterone receptor (PR)-, MSH2 (+), MSH6 (+), MLH1 (+), PMS2 (+), HER2 (2+), and Ki-67 proliferation marker (Ki-67) (30-40%) ( Supplementary Figure 1 ). Based on the 2018 endometrial clinical trial fluorescence in situ hybridization (FISH) evaluation criteria, tumors were assessed as HER2 FISH negative ( Supplementary Figure 2 ). Following the guidelines of the American Joint Committee on Cancer, 8th edition, the patient's tumor node metastasis (TNM) classification was determined as pT3aN0M0, indicating stage IIIA.\nIn late August 2021, the patient underwent laparoscopic total extrafascial hysterectomy, bilateral adnexectomy, pelvic lymph node dissection, and paraaortic lymph node resection. Following the surgical procedure, the patient received adjuvant chemotherapy, which involved the administration of four cycles of albumin paclitaxel plus carboplatin starting in September 2021 ( Supplementary Table 1 ). Throughout this treatment, the patient experienced severe bone marrow suppression (grade IV) and gastrointestinal reactions (grade III). In November 2021, postoperative adjuvant radiotherapy (External radiation therapy: Three dimensional adaptive intensity-modulated radiation therapy (IMRT) with PTV = 2Gy x 23F = 46Gy; Internal irradiation: Iridium-192 high-dose rate after close range treatment: 6Gy x 2F = 12Gy) was conducted for the patient ( Supplementary Table 1 ).\nIn September 2022, abdominopelvic MRI revealed the presence of abdominal and peritoneal metastases ( Figure 1 ). Due to the patient's prior history of severe adverse reactions following postoperative adjuvant chemotherapy, as well as the short interval between the completion of adjuvant radiotherapy and the recurrence, the patient does not meet the criteria for chemotherapy-palliative radiotherapy as outlined in the Chinese Guidelines for the Diagnosis and Treatment of Endometrial Cancer (v2022).\nIHC staining demonstrated low PD-L1 expression (tumor proportion score < 1%) for the primary tumor ( Supplementary Table 2 ). NGS data indicated low TMB (2.01 muts/Mb) and MSI score (4.70) for the primary tumor ( Supplementary Table 2 ). Moreover, blood samples obtained at metastases also indicated a low bTMB (1.0 muts/Mb) and bMSI score (5.72) ( Supplementary Table 2 ). Collectively, these results indicated that the patient was unlikely to benefit from immunotherapy. Additionally, due to the unavailability of tumor tissues from metastatic lesions, cells derived from abdominal fluid were collected and made into wax blocks for HER2 IHC, which detected a low level of HER2 expression (IHC 1+) ( Supplementary Figure 3 ). Since anti-HER2 ADCs have been reported to be effective in HER2-low expression cancers, the patient was recommended the cross-indication anti-HER2 ADC, RC48 (initially at a dosage of 60 mg, followed by 120 mg every two weeks). After 3 cycles of treatment, the computed tomography (CT) scan showed significantly reduced in the pelvic metastatic lesion by 65% ( Figure 1 ). There has been a notable decrease in carbohydrate antigen 125 (CA-125) level ( Supplementary Figure 4 ). After 10 cycles of treatment, CT examination unveiled the vanishing of multiple metastatic lesions ( Figure 1 ), while the CA-125 level returned to its normal range ( Supplementary Figure 4 ). The patient's response to treatment was assessed using the RECIST 1.1 guidelines, which determined CR. In June 2023, positron emission tomography-CT examination revealed a sustained stability without any signs of progression ( Figure 1 ). The CA-125 level remained within the normal range ( Supplementary Figure 4 ). The evaluation of efficacy continued to demonstrate a CR. The patient experienced grade II bone marrow suppression (manifested as leukopenia) during treatment. There were no serious adverse reactions during the application of RC48 treatment. Until August 2024, the patient had maintained an excellent response with no progression signs.",
"gender": "Female"
}
] |
PMC11439626
|
[
{
"age": 53,
"case_id": "PMC10878757_01",
"case_text": "A 53-year-old female patient was admitted to the hospital due to \"13 days of right eye swelling and pain, 10 days of vision loss, and 1 day of fever.\" This patient developed right eye swelling and pain 13 days before admission, with the right-sided headache and no discomforts such as fever, nausea, and vomiting. She visited a local hospital for head computed tomography (CT) and self-reported that the results were not significantly abnormal. Ten days before admission, she noticed decreased visual acuity in the right eye with a yellowish purulent discharge. Therefore, she visited an ophthalmic hospital. Intraocular pressure was 31 mmHg in the right eye and 14 mmHg in the left eye. Ocular ultrasound showed vitreous organic substances in the right eye and vitreous opacity in the left eye. Then, she visited the general hospital for an abdominal ultrasound, which revealed no obvious abnormalities and only multiple polyps in the gallbladder. After that, she visited the ophthalmic hospital again, and 202.90 mg/L C-reactive protein (CRP) was tested. CT results suggested multiple nodules in the right lung and a mass shadow in the right lobe of the liver. In addition, this patient underwent \"vitrectomy in the right eye, lens phacoemulsification, and silicone oil injection\" seven days before admission. During the surgery, large areas of retinal necrosis were observed in the right eye. After the surgery, the right eye swelling and pain of the patient were aggravated, accompanied by a foreign body sensation and increased yellowish purulent eye discharge. The culture of eye discharge showed Kp ++++ (detailed drug sensitivity test results are shown in Table 1). Postoperative blood routine examination exhibited 15.53 x 109/L leukocytes, 90% neutrophils, 122 g/L hemoglobin, 54.00 x 109/L platelets, and 98.47 mg/L CRP. One day before admission, the patient had a fever of up to 37.8 C with chills and vomited once (the vomitus was stomach contents). The routine urine examination during the fever demonstrated glucose 4 +, urinary ketone 1 +, urine occult blood +, and yeast-like fungi +. Later, the patient was admitted to our department for further diagnosis and treatment. This patient has had diabetes for 2 years, but her glycemic control is poor because she does not take \"metformin and glibenclamide\" regularly.. Over 20 days before admission, she developed gross hematuria without fever and painful, urgent, or frequent urination after four intermittent enemas in the beauty parlor, which were not diagnosed and treated. Hematuria disappeared after approximately 5 days. This patient denied a history of hypertension, coronary heart disease, and cerebrovascular disease.\nAfter admission, all immune markers were measured, which illustrated 1730.00 mg/dL immunoglobulin G and no abnormalities in other markers. In addition, no obvious abnormality was observed in antineutrophil cytoplasmic antibodies. Two blood cultures both showed no bacterial growth. Fecal culture results were as follows: Enterococcus faecalis, 25%; yeast-like fungi, 25%; and Escherichia coli, 50%. The results of other tests including routine biochemical test are presented in Table 2. Echocardiography showed no valve excrescences. On the 5th day after admission, the three-phase enhanced CT of the whole abdomen suggested liver abscess and embolus formation of the right hepatic vein (Figure 1). In abdominal color ultrasound, no abnormalities were observed in the liver, gallbladder, pancreas, and spleen. On the 16th day after admission, abdominal enhanced CT displayed that the size of the abscess in the right lobe of the liver was 3.4 cm, which was smaller than before (Figure 2). The magnetic resonance imaging (MRI) of the head displayed multiple mini-brain abscesses (Figure 3). Ocular MRI indicated inflammatory lesions around the right eye ring and changes consistent with postoperative changes in the right eye (Figure 3).\nBased on her medical history and laboratory test results, the patient was diagnosed with liver abscess, endophthalmitis (the right eye), and brain abscesses. After admission, the patient was successively intravenously injected with 1 g meropenem (q8 h) for 1 day and with 1 g meropenem (q8 h) combined with 50 mg tigecycline (q12 h; the initial dose was doubled; anti-infection therapy) for 2 days. Nevertheless, the temperature of the patient was poorly controlled; therefore, antibiotic treatment was adjusted. Specifically, she was given intravenous injection of 1 g imipenem/cilastatin (q8 h) combined with 50 mg tigecycline (q12 h) for 5 days and anti-infection treatment of 200 mg etimicin (qd8) combined with 2 g Moxalactam (q12 h) for 17 days, supplemented by symptomatic treatment such as blood sugar control, anticoagulation, and local antibiotics for the eye. After treatment, the temperature and inflammatory indicators, such as hemogram, CRP, and procalcitonin (PCT) of the patient decreased (Figures 4 and 5). The re-examination of the abdomen with enhanced CT revealed that the abscess was smaller than before. The patient was discharged with medicine after her condition improved. The patient had no fever and was generally well. After discharge, the right eyeball was removed in the ophthalmic hospital.",
"gender": "Female"
}
] |
PMC10878757
|
[
{
"age": 71,
"case_id": "PMC10945424_01",
"case_text": "A Chinese female, who is 71-year-old, came to our hospital, (The Affiliated Yantai Yuhuangding Hospital of Qingdao University) for treatment due to \"More than half a year after the discovery of the back rash\" in 14 November 2021.\nThe patient described no other discomfort prior to this visit and no history of multiple chest wall nodules.\nPhysical examination revealed multiple scattered red papules on the back, protruding from the surface of the skin with clear boundaries and no itching (Figures 1A-D). No abnormalities were found in the bilateral mammary glands, and no mass was palpated. There is no palpable mass in the abdomen, and there is no tenderness on palpation. There are no positive signs in other parts.\nA needle biopsy was performed in the dermatology outpatient department of our hospital. Histopathological studies showed mild keratinization in the epidermis of the skin tissue, chronic inflammatory cell infiltration around small vessels in the superficial dermis and subcutaneous adipose septum, moderate and mild heterotypic cells scattered among collagen fibers in the dermis, arranged in a nest-like pattern. Immunohistochemistry showed strong positive for estrogen receptors (ER) and progestogen receptors (PR), both ER and PR percentages are 80%, positive for CK7, GATA-3, GCDFP15 and KI67, as well as negative staining of CK20 and E-cadherin (Figure 2, The image shows only part of the results). Combined with the above results, breast cancer metastasis was considered.\nOn 19 November 2021, the patient then underwent a thorough examination. Tumor markers indicate that carbohydrate antigen 153 (CA153) is 126 U/mL (normal range 0-25 U/mL), and no abnormalities are found in the rest. Breast ultrasonography revealed a hypoechoic nodule in the left breast tomography, located 6 cm away from the nipple in the direction of 1-2o'clock, 0.7 x 0.6 cm in size, irregular in shape, aspect ratio<1, unclear boundaries, uneven internal echo, and attenuation of rear echo. There is no obvious blood flow signal within the nodule. Breast imaging reporting and data system (BI-RADS) category 6 (Figure 3A). Enlarged lymph nodes can be seen in the left axilla, the largest being 0.8 cm x 0.4 cm, with full shape, clear boundaries, thickened cortex, clear lymph nodes, and no obvious blood flow signal in lymph nodes (Figure 3B). The pathological findings of the left breast hypoechoic area and left axillary lymph node after biopsy showed that the immunohistochemistry of the left breast hypoechoic area was strong positive for ER (90%) and PR (80%), and negative for human epidermal growth factor receptor 2 (HER2) and E-cadherin, P120 was positive in the cytoplasm, and the positive rate of Ki67 was about 30% (Figure 4). Combined with the morphological and immunohistochemical results, it was consistent with invasive lobular carcinoma (ILC) of the breast.\nSubsequent staging tests, including abdominal and chest CT, brain magnetic resonance imaging and, bone scan, revealed synchronous metastases to stomach. The pathological results of left axillary lymph nodes were consistent with the pathological findings of the breast. Abdominal enhanced computed tomography (CT) (Figure 5A) showed poor gastric filling, thickening of gastric wall, and mild to moderate enhancement on enhanced scans. The local intestinal wall of the ascending colon is rough and slightly thick. Gastroscopy and colonoscopy were recommended. Chest CT, brain magnetic resonance imaging and bone scan showed no obvious abnormality. On 21 November 2021, The patient underwent gastroscopy, and under the microscope, congestion and roughness of the gastric antrum mucosa were observed, accompanied by scattered erosive lesions. Two gastric antrum biopsies were performed, with soft texture. Chronic superficial atrophic gastritis is considered (Figure 5B). Pathological examination showed that a small number of heterotypic cells were infiltrated in the lamina propria on the mucosal surface of the antrum. Immunohistochemistry showed strong positive for ER (90%) and PR (80%), positive for CK7, KI67, GCDFP15 and GATA3, and negative for CK20 and E-cadherin, which was consistent with invasive lobular breast carcinoma metastasis (Figure 6, The image shows only part of the results).\nSubsequently, endocrine therapy with fulvestrant (500 mg, the first two times are 2 weeks apart, and every 4 weeks after that) combined with exemestane [EXE ] (25 mg, once a day) was started on 14 December 2021. After 3 months of treatment, the patient's rash disappeared (Figure 1D), and the breast and stomach lesions were stable, and the patient is still receiving treatment.\nOn 21 October 2022, a follow-up gastroscopy revealed alternating red and white mucosa in the gastric antrum, mainly in red. Scattered congested and rough mucosa can be seen on the anterior and posterior walls of the gastric antrum. Three biopsies were taken at the lesion site of the gastric antrum, with soft texture (Figure 7A). Pathological findings suggest chronic inflammation of mucosal tissue with mild intestinal metaplasia of glandular epithelium (Figure 7B). On 19 August 2023, tumor markers indicated a decrease in CA153 to 46.6 U/mL. Breast ultrasound shows no obvious nodules or liquid dark areas in the left breast layer; Lymph nodes can be seen in the left armpit, with a size of approximately 2 cm x 0.6 cm. The last application of fluvastatin was from 16 September 2023, and EXE continued to be orally administered daily. Our last follow-up was on 16 September 2023. The entire diagnosis and treatment process of the patient is shown in Figure 8.",
"gender": "Female"
}
] |
PMC10945424
|
[
{
"age": 10,
"case_id": "PMC10876891_01",
"case_text": "A male infant, aged 10 months, was admitted to the Pediatric Intensive Care Unit (PICU) of West China Second Hospital in August 2022. He presented with chief complaints of recurrent fever, cough, and shortness of breath persisting for 6 days, and cyanosis observed for 1 day. The fever was characterized as moderate to high, and the cough, noted as severe and productive, was associated with aspiration during feeding. The child was born at full term and has been breastfed ever since. He had no history of congenital heart disease, COVID-19, influenza virus, respiratory syncytial virus, or HAdV infection. On admission, physical examination revealed a temperature of 38.3 C, heart rate of 184 beats/min, respiratory rate of 57 times/min, blood pressure of 105/73 mmHg, blood oxygen saturation of 90% (5l /min oxygen flow via a mask), cyanosis of the face and lips, nasal flaring, and a positive inspiratory triple concavity sign. Upon auscultation, numerous coarse, moist rales and expiratory wheezing sounds were audible in both lungs. The fontanel was neither depressed nor bulging. Physical examination of the cardiovascular, digestive, and nervous systems revealed no abnormalities. Arterial blood gas (ABG) analysis revealed a pH of 7.408, partial pressure of oxygen (paO2) at 36.2 mmHg, partial pressure of carbon dioxide (paCO2) at 36.2 mmHg, oxygen saturation (SaO2) at 59.4%, bicarbonate (HCO3-) at 22.8 mmol/L, and lactate levels measured at 3 mmol/L. Routine blood examination showed white blood cells (WBC) were 13.0 x 109/L, neutrophil percentage was 80.8%, blood platelet (PLT) was 434 x 109/L, hemoglobin (HGB) was 127 g/L. C-reactive protein (CRP) was 28.2 mg/L, and procalcitonin was 2.2 ng/ml. Myocardial injury markers, liver and kidney function, coagulation parameters, echocardiography, and electrocardiogram were all within normal limits. Chest computed tomography (CT) showed double pneumonia with partial consolidation of the lower lobe of the right lung (lung window, Figure 1A) and slight enlargement of bilateral hilar lymph nodes (mediastinal window, Figure 1B). The initial diagnosis for the patient indicated severe pneumonia accompanied by respiratory failure.\nUpon admission, he underwent bi-level positive airway pressure (BiPAP) ventilation for assisted breathing. Meanwhile, he was treated with meropenem (60 mg/kg/day, q8h, for 14 days) for empiricalanti-infective therapy, methylprednisolone (3 mg/kg/day, q8h, for 3 days) to fight inflammation, albuterol combined with budesonide aerosol inhalation, intravenous gamma globulin (1 g/kg) to boost immunity, and ambroxol hydrochloride for expectoration. These interventions can temporarily relieve shortness of breath. On the 2nd day of admission, his condition was worsened by a persistent high fever and increased viscous airway secretions. We added vancomycin (40 mg/kg/day, q6h, for 14 days) to empirically treat Methicillin-resistant Staphylococcus aureus (MRSA) infection. On the 3rd day of admission, the blood culture and the sputum culture were negative. The polymerase chain reaction (PCR) of the throat swab for multiple respiratory pathogens showed HAdV was positive and bordetella pertussis, mycoplasma pneumoniae, influenza virus, boca virus, respiratory syncytial virus, and COVID-19 were negative. The serum G [(1-3)-beta-d-glucan] test and galactomannan (GM) test were negative. The metagenomic next-generation sequencing (mNGS) of blood revealed the presence of HAdV with specific sequences identified as 74,376 reads, showing high confidence. On the 4th day of admission, the SaO2 dropped again (85%-90%), and a reexamination of chest x-ray revealed increased lung consolidation. The ventilation mode was promptly switched to invasive ventilator-assisted ventilation, and a large amount of yellowish-white viscous sputum was sucked out of the tracheal tube. Fiberoptic bronchoscopy and bronchoalveolar lavage were performed. The white jelly dendritic obstruction in the left upper and lower bronchial lumens was observed by fiberoptic bronchoscope. No bleeding or new organisms were observed. Immediately, a bronchoscopic clamp was performed to remove numerous white plasmapheresis plugs (Figure 2). The pathology of bronchoplastic sputum suppositories showed exudate fibrin and mucus-like material with more inflammatory cells and histiocytic infiltration (Figure 3). Laboratory results of bronchoalveolar lavage fluid (BALF) were as follows: nucleated cell count of 160 x 106/L, with neutrophilic lobulated nucleated granulocytes accounting for 29% and lymphocytes accounting for 16%. No abnormalities were observed in acid-fast staining, silver hexamine and PAS staining, or alveolar lavage fluid culture. On the 6th day of hospitalization, the mNGS of the BALF revealed the presence of HAdV with specific sequences identified as 223,049 reads and high confidence. On the 8th day of admission, due to the patient's lung inflammation still progressing, we organized a multi-disciplinary treatment (MDT) involving the department of Pediatric Infectious Diseases and the department of Clinical Pharmacology. Despite the administration of intensive treatments including glucocorticoids, intravenous gamma globulin, and fiberoptic bronchoscopy, the patient's pneumonia condition deteriorated. Concurrently, mNGS of the BALF and blood samples indicated high load HAdV infection in this case. To prevent adenovirus replication and further damage to the lungs, we administered intravenous ribavirin (7.5 mg/kg, q12h, for 7 days, each infusion time >20 min) combined with INFalpha1b atomization (4 ug/kg/day, q12h, for 7 days) for antiviral therapy. On the 10th day of admission, the temperature remained below 37.5 C. We gradually lowered the ventilator parameters, and the patient's oxygen saturation could still be maintained above 95%. On the 12th day of admission, the demand for oxygen further decreased, and we lowered the ventilator parameters again. On the 14th day of admission, chest x-ray showed a significant reduction in lung consolidation. We replaced meropenem and vancomycin with intravenous ceftriaxone for sequential anti-infection (100 mg/kg/day, q12h, for 14 days). On the 16th day of hospitalization, the PCR of HAdV turned negative and the ABG analysis were completely normal. Mechanical ventilation was withdrawn and replaced with nasal high-flow oxygen therapy (8 L/min oxygen flow). Meanwhile, ribavirin and INFalpha1b were discontinued. On the 28th day of hospitalization, a repeat fiberoptic bronchoscopy revealed a smooth endothelial lining of the bronchial tubes with a small amount of thin white secretion, and no bronchial sputum plugs or plasmapheresis were observed. The ventilation mode was changed to nasal catheter oxygen inhalation (0.5 L/min oxygen flow) and switched to oral cefaclor (30 mg/kg/day, for 7 days) instead of intravenous ceftriaxone. On the 30th day, his oxygen saturation remained above 95% without oxygen intake, and there were no signs of fever, shortness of breath, or mental deterioration. The physical examination found that the positive signs in the patient's lungs had disappeared. The reexamination of chest CT revealed only a small amount of lung inflammation and a few pulmonary interstitial changes (lung window, Figure 1C), while it did not show pulmonary lymph node enlargement (mediastinal window, Figure 1D). Consequently, the infant was discharged from the hospital successfully and continued to take oral cefaclor for an additional 3 days after discharge. During the entire hospitalization period, serial weekly assessments of liver function, renal function, myocardial injury markers, and hemoglobin levels consistently yielded normal results. Additionally, no instances of rash or convulsion were observed.\nDuring the 6-month follow-up in the outpatient clinic, there were no instances of HAdV infection recurrence. Symptoms of recurrent coughing and milk choking did not appear. ABG analysis, blood routine, liver function, renal function, markers of myocardial injury, and hemoglobin indexes were all within normal ranges. The pulmonary function test and hearing screening showed normal results. Two repeat chest CT scans during follow-up revealed no imaging signs of solid lung lesions, interstitial lung changes, pulmonary atelectasis, or bronchiectasis. The timeline of treatment and progression is summarized in Figure 4.",
"gender": "Male"
},
{
"age": null,
"case_id": "PMC10876891_02",
"case_text": "A thorough review of the literature from 1970 to 2023 was undertaken, utilizing databases such as PubMed, Web of Science, Embase, and Medline. This search employed keywords including \"adenovirus\", \"intravenous infusion\", \"ribavirin\", \"plastic bronchitis\", and \"children\". From the selected articles, pertinent information was extracted, encompassing the first author's name, publication year, country of study, patient age range, underlying conditions, identified risk factors, treatment modalities, duration of treatment, observed drug side effects, and treatment outcomes. In Table 1, we have compiled data from six published articles detailing the administration of intravenous ribavirin for treating HAdV infection in pediatric patients. Additionally, Table 2 presents a synthesis of six published articles focusing on pediatric cases of adenovirus pneumonia with concurrent PB.",
"gender": "Unknown"
}
] |
PMC10876891
|
[
{
"age": 77,
"case_id": "PMC10724209_01",
"case_text": "A 77-year-old male presented at the emergency department in August 2020 with complaints of haematuria since several hours. He had a medical history of chronic renal disease diagnosed in December 2019 that was preceded by an episode of macroscopic haematuria with urinary retention for which he was catheterized. The patient had not recently experienced any urinary tract infections nor used any anticoagulant medication. Upon presentation at the emergency department, the bladder was irrigated to clear urine and the patient was discharged upon further outpatient examinations.\nTwo weeks later CT Intravenous Pyelography (CT IVP) was performed which demonstrated a diffusely irregularly thickened wall of the bladder on the cranioventral side. Cystoscopy revealed no evident irregularities at that time. Transurethral resection of the suspected lesion of the bladder wall was performed and pathological analysis revealed a urothelial carcinoma reaching into the musculus detrusor layer. Additional CT imaging of the thoracic and abdominal regions did not demonstrate any further metastases; therefore, the tumour was classified as a pT2N0M0 high grade carcinoma.\nAlthough surgical treatment through radical cystectomy with Bricker ileal conduit was considered possible, the patient opted for chemoradiation therapy as advised during a multidisciplinary consultation meeting due to his impaired renal function. The patient received radiotherapy with an elective nodal dose of 50 Gy and 63.25 Gy aimed at the primary tumour divided over five fractions per week for the duration of five weeks. Concurrently, the patient started chemotherapy through a single treatment with mitomycin and daily dose of capecitabine during the same five weeks. At four months follow-up, CT thorax, abdomen and cystoscopy revealed complete response and no metastases.\nEight months after the primary diagnosis, the patient presented at the emergency department with neck pain radiating towards the left side of his head. He had vomited and required support during walking due to ataxia. The patient was admitted for further diagnostic work-up.\nA CT and MRI scan of the brain showed a solitary 29 mm in diameter cerebellar mass in the right hemisphere with some hypodensities indicating partial necrosis of the lesion. Furthermore, due to tumour oedema a slight midline shifting causing compression of the brain stem and fourth ventricle was observed (Fig. 1, Fig. 2). Repeated thoracic and abdominal CT imaging did not demonstrate any other primary malignancy nor metastatic lesions of the primary tumour.\nAfter neurosurgical consultation, the cerebellar mass was surgically removed through a lateral suboccipital craniotomy. During surgery, the cerebellum first appeared swollen due to the mass, however quickly relaxed after opening of the cystic cavity and cerebrospinal fluid drainage. The tumour could be completely resected, using an ultrasonic aspirator (CUSA) with a small margin around the tumour. The dura was primarily closed, and the bone flap returned. Navigation was used during surgery to control the extend of resection and one day postoperatively confirmed on MRI finding. Postoperatively, dexamethasone could be stopped completely, and the patient was discharged two days after surgery from the hospital.\nDuring surgery, the samples had a brown-grey appearance with a lamellar structure, partially haemorrhagic. Histological analysis revealed an epithelial tumour featuring irregularly enlarged and partially polymorphous nuclei and substantial cytoplasm. Immunohistochemistry revealed that the tumour cells were positive for keratin 5/6, keratin 7, keratin 20, keratin 34 beta E12 and GATA-3. All histological findings matched the report of the primary urothelial origin (Fig. 3a, Fig. 3b).\nAfter treatment, the patient fully recovered and regained full physical functionality. Follow-up MRI examination one day after surgery showed a complete resection. The patient started post-operative stereotactic radiotherapy one month after surgery. A single dose of 18 Gy was administered to the resection cavity and surrounding cerebellar tissue.\nRepeat cystoscopy 12 and 18 months after initial presentation demonstrated no signs of recurrence of UC in the bladder. Additionally, at 18 months follow-up the patient underwent CT examination of the thoracic and abdominal regions which demonstrated no metastatic activity in the body. However, seven months after the first surgery, the patient showed recurrent signs of ataxia and MRI examination of the brain revealed a contrast enhancement without increased perfusion. Since it is clinically and radiologically difficult to distinguish recurrence from necrosis after SRS, we opted for early repeat MRI in a wait-and-scan matter. Radiological follow-up six weeks later, showed growth of the lesion with oedema and compression of the fourth ventricle and radiological signs of supratentorial hydrocephalus. Because of the mass effect and growing suspect of progressive disease, surgical decompression was discussed with the patient, and was opted for second surgery. The patient underwent re-resection of the lesion two weeks later and histological analysis confirmed metastatic recurrence with partially vital and partially necrotic tumorous tissue. The patient was referred for a second session of post-operative stereotactic radiotherapy. The patient died 5.5 months after the re-operation.",
"gender": "Male"
}
] |
PMC10724209
|
[
{
"age": 42,
"case_id": "PMC10979807_01",
"case_text": "Patient information: the patient is a 42-year-old female with a history of uterine fibroid surgery in 2014. She presented with irritative lower urinary tract symptoms and left lumbago persisting for several years.\nClinical findings: on clinical examination, the patient appeared generally well, and apyretic, with urinalysis indicating bacterial presence and leukocytes. There was no lumbar sensitivity, and the external genital examination was unremarkable.\nTimeline of the current episode: the patient's symptoms had been evolving for several years, leading to the current presentation.\nDiagnostic assessment: initial renal ultrasound revealed a double pyelocaliceal system in the left kidney, with dilatation of the upper system (31 mm) causing thinning of the renal parenchyma and dilatation of the lower system (18 mm) with preserved cortico-sinusal differentiation of the renal parenchyma. A 16-slice spiral CT urogram with intravenous contrast showed an enlarged left kidney (169.5 mm) with a double system and a ureterocele and ureterohydronephrosis of the upper system with a renal pelvis measuring 41.8 mm in the anteroposterior diameter, a laminated aspect of the renal parenchyma and excretory delay. The lower system is not dilated, secreting and excreting within the physiological time frame of a normal ureteral outlet (Figure 1).\nDiagnosis: the patient was diagnosed with ureteral duplicity and a left ureterocele complicated by upper tract obstruction.\nTherapeutic interventions: under spinal anesthesia, the patient underwent endoscopic ureterocelotomy. A 30 rigid cystoscope was used to visualize the ureterocele on the left lateral bladder wall, crossing the midline (Figure 2). Ureterocelotomy was performed using puncture-electrocoagulation (Figure 3).\nFollow-up and outcome of interventions: postoperative follow-up included clinical examination, ultrasound, and renal diethylene triamine penta-acetic acid (DTPA) scintigraphy performed three months after ureterocele treatment, showing improvement in drainage and symptom resolution.\nPatient perspective: the patient was satisfied with symptom improvement and pleased with endoscopic surgery due to its non-scarring nature.\nInformed consent: the patient's consent was voluntary and informed.",
"gender": "Female"
}
] |
PMC10979807
|
[
{
"age": 17,
"case_id": "PMC10629335_01",
"case_text": "A 17-year-old male without a medical history presented progressive symptoms during the past month, consisting of headaches, decreased visual acuity, and visual field impairment with right temporal hemianopia. The clinical examination found a conscious patient, slightly feverish, pulse was 78/min, and his blood pressure was 120/76 mm Hg. The lung examination was clear on auscultation. The chest radiograph was normal. Magnetic resonance imaging (MRI) of the brain shows a sellar-suprasellar lesion, isointense to hypointense on T1, isointense to hyperintense on T2 [Figure 1], enhanced heterogeneously with gadolinium [Figures 2a and b], with other small lesions in the posterior cerebral fossa and the hypothalamus. On investigation, cerebrospinal fluid (CSF) fluid analysis revealed lymphocytic pleocytosis, low glucose, and a high protein level. Polymerase chain reaction (PCR) for M. tuberculosis was positive in the CSF, and the results of the Interferon-Gamma Release Assays and Mantoux test were positive. Evaluation of pituitary function, on the other hand, revealed normal hormonal levels. All other serological tests, including the HIV test, yielded negative results.\nBased on clinical features, neuroimaging, and investigations, a diagnosis of meningitis tuberculosis with cerebral and pituitary tuberculoma was made. Treatment for tuberculosis was initiated with a 2-month combination of isoniazid, rifampicin, pyrazinamide, and ethambutol, followed by 7 months of isoniazid and rifampicin, associated with corticosteroid therapy, and the evolution was marked by the clinical improvement of the patient, even on the radiological level, by the disappearance of the lesion [Figures 2c and d].",
"gender": "Male"
}
] |
PMC10629335
|
[
{
"age": 39,
"case_id": "PMC11144825_01",
"case_text": "A 39-year-old, ASA 1 female, presented with a tongue base mass that was biopsy-confirmed to be benign pseudo-epitheliomatous hyperplasia. She was scheduled for transoral robotic surgery due to a 5-month history of progressive dysphagia associated with globus sensation and change in voice. No dyspnea, wheezing, or episodes of decrease in sensorium were noted. On assessment, airway physical examination revealed Mallampati class 1, mouth opening of 4cm, a thyromental distance of 6.5cm, full neck range of motion, there was no visible mass upon mouth opening (Figure 1A). However, preoperative indirect laryngoscopy revealed a smooth mucosal vallecular mass, abutting the epiglottis (Figure 1B). Oral cavity CT scan with contrast enhancement showed isodense nodular focus seen at the posterior aspect of the tongue measuring 2.9 x 2.8 x 3.3 cm indenting the oropharynx (Figures 2A-C). Blood counts, coagulation study, and chemistries were unremarkable. A collaboration between the otolaryngology, anesthesiology, and general medicine was necessary to discuss the perioperative management of the patient and to ensure a safe and successful procedure. Given the potential risks to the patient for difficult airway management and perioperative bleeding, the focus of the discussion is on the prevention of adverse events.\nBefore surgery, the patient received paracetamol (15 mg/kg), dexamethasone (0.1 mg/kg), and antibiotic prophylaxis. The patient was placed in a 30-degree back up position upon transfer to the operating room bed. The following monitors were attached to the patient: a 5-lead electrocardiogram, two pulse oximeters, one on each index finger, two non-invasive blood pressure cuffs, one on each upper arm, a peripheral nerve stimulator, and a nasopharyngeal thermometer. The second set of pulse oximeter and non-invasive blood pressure cuff was attached to each arm as a contingency plan in case one monitor malfunctions during the procedure as there is no means to access the patient due to the docked robotic arms. Likewise, two large bore intravenous access were secured in case of massive bleeding. Two units packed red blood cells and two units fresh frozen plasma blood products were secured for possible perioperative use. Pre-induction, the anesthesiologist and anesthesia machine were situated at the head part of the operating table. Post-induction, the anesthesia machine and the anesthesiologist were positioned at the lower end of the operating table away from the patient's airway (Figure 3). As a result of the intraoperative operating room set-up, an extended breathing circuit was utilized.\nThe airway management plan was to perform awake nasal fiberoptic intubation under remifentanil TCI and topical anesthesia using a spray-as-you-go (SAYGO) technique with 3 ml of lidocaine 2%. Cotton pledgets soaked in lidocaine 2% + oxymetazoline were used to block the branches of the anterior ethmoidal nerve and the sphenopalatine ganglion and for nasal vasoconstriction simultaneously. Lidocaine 10% spray was applied to the tonsillar pillars, oropharynx, and base of tongue via atomizer. A total of 120 mg of lidocaine 10% was used. Remifentanil TCI was started at a predicted effect site concentration of 1 ng/ml. The fiberoptic endoscope was pre-loaded with a softened and lubricated, cuffed size 7.0 nasal RAE endotracheal tube.\nOnce the patient was calm and comfortable yet awake, the primary anesthesiologist proceeded with the fiberoptic navigation of the airway. Once the carina was visualized, the tracheal tube was advanced through the fiberoptic anterograde guide. The position of the tracheal tube was also confirmed by end-tidal capnography and clinical confirmation of bilateral equal air entry. Anesthesia was induced using intravenous propofol (2 mg/kg). Remifentanil TCI rate was then adjusted to achieve a maintenance level of analgesia (1-2 ng/ml), and general anesthesia was maintained using sevoflurane to maintain a MAC value of 0.7-1.0. Neuromuscular blockade using rocuronium infusion at 5 mcg/kg/min was initiated to achieve continuous muscle relaxation for optimal surgical operating conditions. Throughout the procedure, the anesthesia team continuously monitored the patient's oxygen saturation, end-tidal CO2, and other vital signs.\nThe surgical team utilized the da Vinci Surgical System to access and operate on the base of tongue mass. A Dingman retractor was used and the robotic arms were positioned to provide access to the oral cavity (Figures 4A-B). The surgeon controlled the robotic arms using a console (Figures 4C-D). The base of tongue mass was identified and resected with negative margins (Figures 4E-F). The surgery was unremarkable and lasted for 1 hour and 10 minutes. Neuromuscular blockade was then reversed with Sugammadex (4 mg/kg) and a 100% train-of-four value was achieved.\nPatient was monitored in the post-anesthesia care unit (PACU) after being extubated in the operating room fully awake. The patient was transferred to the ward after two hours and was discharged from the hospital on the second postoperative day.",
"gender": "Female"
}
] |
PMC11144825
|
[
{
"age": 6,
"case_id": "PMC11349687_01",
"case_text": "The patient, male, aged 6 months, was admitted to our hospital 2 months prior because of shortness of breath. A chest computed tomography (CT) scan showed an abnormal mass in the right chest cavity, which was suspected to be in the right kidney, with a suggested diagnosis of CDH (Figure 1A). Chest ultrasonography confirmed that the right kidney had herniated into the right chest cavity (Figure 1B). The patient was diagnosed with ITK associated with CDH and was admitted to the hospital for treatment. The patient had no history of pneumonia, cough, sputum production, chest pain, cyanosis of the lips, or breathing difficulties. After admission, a contrast enhanced chest CT scan showed local discontinuity in the right diaphragm, the rotation position of the right kidney was significantly shifted upwards above the diaphragm, and the morphology of the right renal artery and vein was visible without stenosis. A hernia sac shadow could be seen at the discontinuous diaphragm, with thickening and significant enhancement of the upper wall of the hernia sac. Small blood vessels from the renal artery branch were observed running inside, suggesting infradiaphragmatic pulmonary sequestration and ITK associated with CDH (Figures 1C-F).",
"gender": "Male"
},
{
"age": null,
"case_id": "PMC11349687_02",
"case_text": "The patients' blood pressure was 85/61 mmHg, there was no instance of hematuria or proteinuria, creatinine was 14 micromol/L, and urea nitrogen was 2.96 mmol/L, which were all within the normal range. A complete preoperative examination was performed prior to surgical treatment. The child laid on the left side with single-lumen tracheal intubation and single-lung ventilation (selective occlusion of the affected main bronchus with a bronchial occluder). A closed chest was established, and an artificial pneumothorax was maintained at a pressure of 4-6 mm Hg (1 mmHg = 0 133 kPa) at a flow rate of 2 L/min. Using the three-port method and 30 thoracoscopy, the observation port was located between the 5th intercostal line of the subscapular angle, and the two operating holes were located between the 7th intercostal line of the axillary midline and the 7th intercostal line between the erector spinae muscle and subscapular angle. Microscopic observations revealed that the right kidney had herniated into the chest cavity on the posterolateral side of the diaphragm. The right kidney was brought back into the abdominal cavity. The hernial sac was thin (Figure 2A). Upon incision of the hernia sac, a bright red lesion with clear boundaries and an abnormal blood vessel supply was observed (Figures 2B,C). After cutting off the abnormal blood vessels, LigaSure TM was used to remove the diseased tissue, and the renal fat sacs and renal tissue were visible (Figure 2D). Interrupted suturing of the hernia ring was performed to seal the diaphragmatic hernia. A retrieval bag was used to remove the diseased tissue, which was sent for examination. Upon confirming that there was no active bleeding or air leakage, and that the lungs were in good condition, a closed chest drainage tube was placed. The time of resecting the sac and reconstructing the diaphragm was 55 min.",
"gender": "Unknown"
},
{
"age": null,
"case_id": "PMC11349687_03",
"case_text": "Postoperative pathological examination revealed infradiaphragmatic pulmonary sequestration. The postoperative vital signs of the patient were stable. On postoperative day 3, the closed thoracic drainage tube was removed and the patient was discharged. Two months after surgery, chest CT showed that the right kidney had returned to the abdominal cavity and the right diaphragm was in a normal position, renal ultrasound showed that blood flow in the right renal artery and vein were smooth (Figure 3).",
"gender": "Unknown"
}
] |
PMC11349687
|
[
{
"age": 48,
"case_id": "PMC10869315_01",
"case_text": "A 48-year-old female with a past medical history of bilateral breast prosthetic implants was referred to the cardiology department for preoperative evaluation before undergoing cosmetic surgery for breast augmentation due to abnormal findings on her ECG: sinus rhythm with right bundle branch block (RBBB), left anterior fascicular block, and first-degree AV block (Figure 1). She denied any prior cardiac history, cardiac surgery, or symptoms such as chest pain, shortness of breath, orthopnea, dyspnea on exertion, exercise intolerance, palpitations, presyncope, lightheadedness, or syncope. She was physically active and exercised on a regular basis. Physical examinations were unremarkable. A transthoracic echocardiography (TTE) illustrated an ASD, and cardiac magnetic resonance imaging (MRI), which was performed to evaluate anatomy, confirmed the presence of an ostium primum ASD, along with mild dilation of the bilateral atria and the left ventricle, moderate dilation of the right ventricle and an elevated pulmonary to systemic shunt (Qp/Qs) ratio of 1.7:1. Diagnostic cardiac catheterization revealed normal coronary arteries, pulmonary artery pressure, right- and left-sided filling pressure, but an elevated Qp/Qs ratio at 1.7:1 (Table 1).\nSurgical repair of the primum ASD was recommended and she was taken to the operating room. The intraoperative transesophageal echocardiogram further confirmed the presence of the ostium primum ASD (Figure 2), as well as additional cardiac anomalies including a cleft in the anterior leaflet of the mitral valve and membranous ventricular septal defect (VSD) (Figure 3). The patient successfully underwent repair of the primum ASD and VSD using cardiopulmonary bypass, employing patch repair and valvuloplasty with a mitral valve ring. Following the procedure, the patient was transferred to the intensive care unit; her hospital course was uneventful and and she was discharged a few days later.",
"gender": "Female"
}
] |
PMC10869315
|
[
{
"age": 14,
"case_id": "PMC11109676_01",
"case_text": "158.[130] For an inflammation of the intestines. If it happens to a person that his intestines (JCX_0794) are inflamed or he vomits stool and it does not find a way to pass through and the stool comes up again and the person vomits it, this disease is called ileus by the doctors. The disease is fatal for some if there is an inflammation of the intestines. If this disease arises from a constipation of stool, it is salvageable. And if the patient is a child that is fourteen years old, do baths and cataplasms and fumigations. If the patient is a young man that is twenty two years old, let his blood. If the patient is at the hight of his life, that is forty two years old, also let his blood and they shall not drink wine (JCLP_099) and let it be hot.\n159.[131] If the kidneys are inflamed and there is pain and pressure on the place, where the inflammation of the kidneys is and these people have fever and vomit bile. Let the blood of these people. 2. Grind the kernels of fenugreek (JCLP_212) and of rue (JCLP_157) and the seed of dill (JCLP_073) and macerate with water (JCLM_036) and put it on the area of the kidneys. 3. Let him drink the crushed seed of a pumpkin (JCLP_153) mixed with honey (JCA_0024) and with wine (JCLP_099). On top of the kidneys put a hot poultice of good warm wine (JCLP_099) and good warm cloth (JCLP_151). 4. Apply the plaster that is called Of Gruel, by the doctors JCX_0854 plaster and spread on the cloth (JCLP_151) place it onto the kidneys, where the pain is. 5. Dissolve wax (JCA_0576) and add rose oil (JCLP_181) and yolk (JCX_0114) of an egg (JCA_0105) and macerate them and put on top of the kidneys with cloth (JCLP_151).\n160.[132] Diabetes is called, if he urinates as soon as he drinks, and he does this frequently and every hour. Let these drink the juice of polygonum (JCLP_164) or the so-called JCU_2493. Boil it with thick black wine (JCLP_099) and let him drink. 2. Boil dates (JCLP_222) and let him drink the juice. 3. Boil the leaves of myrtle (JCLP_134) with wine (JCLP_099) and let him drink. 4. On top of the kidneys put boiled barley flour (JCLP_100) with water (JCLM_022). Then once it has boiled also add vinegar (JCLP_142) and rose oil (JCLP_181) and boil it, then add pounded tendrils of vine (JCLP_016) and pounded leaves of vine (JCLP_016) and pounded JCLP_078 and put it on the kidneys.\n161.[133] Fissures are called by the doctors, if the testicles split or the anus. Useful for these are crushed pine resin (JCLP_177) macerated in rose oil (JCLP_181) and applied to the split areas, but roast the pine resin (JCLP_177) in the sun. Then crush yolk (JCX_0114) of an egg (JCA_0105) put it on top of the wounds or opium (JCLP_145) with JCX_0114. 2. Rub dry leaves of ivy (JCLP_087) onto the wound. 3. Mix ashes (JCX_0126) of the leaves of ivy (JCLP_087) with rose oil (JCLP_181) and put them into a of lead (JCLM_024) vessel and stir it and then apply. But first wipe the wounds. Wine (JCLP_144) instead of water (JCLM_022) but let the wine (JCLP_099) be warm. Then rub crushed dry roses (JCLP_181). 4. Rub crushed lead white (JCLM_042) and litharge (JCLM_018) onto the wounds. If the crotch is inflamed, pound the tender leaves of vine (JCLP_016) and mix them with lead white (JCLM_042) and put them on top on the inflammation. 5. Rinse the crotch first with cold water (JCLM_022) of the sea (JCX_0496). If there is none of the sea (JCX_0496), take salt (JCLM_002) and water (JCLM_022). Then pound JCLP_078 and mix it with lead white (JCLM_042) and yolk (JCX_0114) of an egg (JCA_0105) and put it on the inflammation of the crotch. Crotch is called what we are ashamed to show the others.\n162.[134] If someone swallows leeches by mistake, let him drink salt water (JCLM_004) with water (JCLM_022). 2. Mix ground nitron (JCLM_023) with water (JCLM_022) and let him keep it in his mouth. And let him move this water (JCLM_022) back and forth in his mouth. Let him also eat garlic (JCLP_197). 3. Grind JCU_0677 and mix them with acrid vinegar (JCLP_142) and let him drink them.\n163.[134] If someone eats a lot of green/fresh mushrooms and almost chokes. Force him to vomit like this, just let him drink olive oil (JCLP_053) and he will vomit. 2. Let him drink tendril (JCLP_090) ashes (JCX_0126) with a lot of vinegar (JCLP_142) and wine (JCLP_099) that is two parts of vinegar (JCLP_142) and one part of wine (JCLP_099). 3. Grind the so-called nitron (JCLM_023) and let him drink it as well as you gave to drink the ashes (JCX_0126) of a tendril (JCLP_090). 4. Boil eggs (JCA_0761) of a bird (JCA_2319) in vinegar (JCLP_142) and wine (JCLP_099) and let him drink boiled. 5. Boil wormwood (JCLP_028) with wine (JCLP_099) and let him drink. 6. Boil melissa (JCLP_129) and ground nitron (JCLM_023) with honey (JCA_0024) and add also a little water (JCLM_022) and let him drink. 7. Boil rue (JCLP_157) with olive oil (JCLP_053) add also wine (JCLP_099) and let him drink. 8. Boil oregano (JCLP_141) with wine (JCLP_099) and honey (JCA_0024) and let him drink. 9. As far as possible, let him vomit, so that he expels it and also bathe him frequently.\n164.[135] If the milk (JCX_0085) turns into cheese in the stomach of a person. Let him drink the dry leaves of JCLP_167 with water (JCLM_022) and pound the fresh ones and let him drink their juice. 2. Boil thyme (JCLP_066) with wine (JCLP_099) and let him drink. 3. Rennet (JCA_2401), whatever kind there is, let him drink with vinegar (JCLP_142) just well crushed.\n165. If all hair of the head falls out. Do this treatment. That is grind maidenhair (JCLP_004) and mix it with gum ladanum (JCLP_110) and make it like JCX_1263 and put it on top of the entire head. 2. Burn the root of asphodelus (JCLP_027) and macerate the ashes (JCX_0126) with table oil (JCLP_232) and apply to the head. 3. Grind the bark of fresh reed (JCLP_075) and make it smooth with vinegar (JCLP_142) and put it on the head. 4. Mix ground pepper (JCLP_154) with wine (JCLP_099) and vinegar (JCLP_142) and apply to the entire head. 5. Pound the leaves of a wild fig tree (JCLP_207) and of a domesticated fig tree (JCLP_207) and macerate them with honey (JCA_0024). And put them on the head. 6. Burn the skin of a hedgehog/sea urchin (JCA_1087) and mix its ashes (JCX_0126) with vinegar (JCLP_142) and table oil (JCLP_232) and apply to the head. 7. Burn a sea urchin (JCA_1832) just with its shell and mix its ashes (JCX_0126) with vinegar (JCLP_142) and table oil (JCLP_232) and apply to the head. 8. Grind the root of elm tree (JCLP_172) well and mix it with lard (JCA_0077) of a bear (JCA_0435) and apply to the head. 9. Crushed stavesacre (JCLP_003) and sulphur (JCLM_033) and split yellow orpiment (JCLM_006) and mix it with vinegar (JCLP_142) and apply. 10. Mix lead white (JCLM_042) and ground litharge (JCLM_018) with vinegar (JCLP_142) and olive oil (JCLP_053) and apply. 11. Wash lime (JCLM_007) with water (JCLM_022) and pour out the water (JCLM_022) and add old olive oil (JCLP_053) and apply to the head. 12. Shave his whole head well and take vinegar (JCLP_142) and dissolved lard (JCA_0077) of a goose (JCA_0246) and apply. 13. Dissolve lard (JCA_0077) of a goat (JCA_0966) and add cedar oil (JCLP_083) and vinegar (JCLP_142) and apply to the head very calmly. 14. Apply crushed JCX_1560 and mastic (JCLP_125) with vinegar (JCLP_142) to the head. 15. Shave his whole head well and add vinegar (JCLP_142) and dissolved lard (JCA_0077) of a goose (JCA_0246) and apply to the head. 16. Apply mercury (JCLM_037) and saliva (JCA_0904) of a person and spikenard oil (JCLP_136) to the head. 17. Mix dissolved lard (JCA_0077) of a fox (JCA_0624) with vinegar (JCLP_142) and wine (JCLP_099) and apply to the head. 18. Pound beetroot (JCLP_189) and mix their juice with vinegar (JCLP_142) and table oil (JCLP_232) and apply to the head. 19. Mix dry ground mouse (JCA_2443) dung with vinegar (JCLP_142) and table oil (JCLP_232) and apply to the head. 20. Grind the root of celery (JCLP_186) and mix it with vinegar (JCLP_142) and apply to the head. 21. Add rust (JCLM_028) of iron (JCLM_027) and vinegar (JCLP_142) and table oil (JCLP_232) and let it do for one night and one day and apply to the head. 22. The leaves of hyoscyamus (JCLP_217) applied as a cataplasm with vinegar (JCLP_142) but first pound them and crushed pine resin (JCLP_177) with lard (JCA_0077) of a crane (JCA_1646) and marrow (JCA_0307) of a deer (JCA_0366) and vinegar (JCLP_142) and mix everything well and apply. 23. Macerate gum ladanum (JCLP_110) with wine (JCLP_099) and with myrtle oil (JCLP_134) and apply to the head. 24. Pound the tender shoots of mastic (JCLP_209) and macerate them all with rose oil (JCLP_181) and wine (JCLP_099) and put them on the head.\n166. On pityriasis of the head. Grind the root of lily (JCLP_101) and apply to the head. 2. Grind the root of a mulberry tree (JCLP_208) and add vinegar (JCLP_142) and macerate and apply to the head. 3. There is a plant called quince (JCLP_203). Grind its root and mix it with vinegar (JCLP_142) and apply. 4. Macerate gum ladanum (JCLP_110) with vinegar (JCLP_142) and apply. 5. Grind the seeds or the leaves of wild cress (JCLP_077) and mix them with vinegar (JCLP_142) and apply. 6. Crush coriander (JCLP_091) and the seed of rue (JCLP_157) or its leaves. And also add vinegar (JCLP_142) and macerate and apply. 7. Pound the leaves of ivy (JCLP_087) and apply their juice to the head. 8. Grind the root of beetroot (JCLP_189) and apply its juice to the head. 9. Pound wild rue (JCLP_157) and also crush litharge (JCLM_018) and pound stavesacre (JCLP_003) and add vinegar (JCLP_142) and myrtle oil (JCLP_134) as much as required and unify these and apply to the head. 10. Mix ground sulphur (JCLM_033) with myrtle oil (JCLP_134) and apply. 11. Grind the root of beetroot (JCLP_189) and apply the juice to the head. 12. Mix crushed litharge (JCLM_018) and salt (JCLM_002) and wine (JCLP_144) and olive oil (JCLP_053) and apply to the head. 13. Add the root of wild cucumber (JCLP_001) and lupine (JCLP_118) and boil these with water (JCLM_022) and rinse with water (JCLM_022). 14. Boil fenugreek (JCLP_212) and also pound the leaves of beetroot (JCLP_189) and mix its juice with water (JCLM_022) of fenugreek (JCLP_212) and apply to the head. 15. Macerate the ashes (JCX_0126) of a tendril (JCLP_090) with water (JCLM_022) and apply.\n167.[136] Alphoi are called if the person develops something like the kernels of a lentil (JCLP_219) on his face. It is useful for lichen and leprosy. Pound rosemary (JCLP_050) and mix it with cedar oil (JCLP_083) and apply just also add table oil (JCLP_232). 2. Mix crushed sulphur (JCLM_033) and litharge (JCLM_018) and stavesacre (JCLP_003) and table oil (JCLP_232) and apply to the head. 3. Boil fat resinous wood (JCLP_046) with table oil (JCLP_232) and apply. Just also add litharge (JCLM_018) and vinegar (JCLP_142). Apply in the bath. 4. Mix very finely ground marble (JCLM_021) with white (JCX_0101) of an egg (JCA_0105) and apply. 5. Mix lead white (JCLM_042) and dry dung of a swallow (JCA_2853) and white (JCX_0101) of an egg (JCA_0105) and apply. 5. Grind the root of lily (JCLP_101) and mix it with vinegar (JCLP_142) and apply. 6. Grind the root of mulberry (JCLP_208) and macerate it with vinegar (JCLP_142) and apply. 8. Pound the leaves of a wild fig tree (JCLP_207) or also of a domesticated fig tree (JCLP_207) and macerate these with vinegar (JCLP_142) and put them on the location of the disease. 9. Mix crushed stavesacre (JCLP_003) and crushed sulphur (JCLM_033) with vinegar (JCLP_142) and apply. 10. Pound the leaves of JCLP_167 and also grind sulphur (JCLM_033) and add vinegar (JCLP_142) and macerate and apply. 11. Grind JCU_0278 and nitron (JCLM_023) and add vinegar (JCLP_142) and apply.\n168. Aphtha is if the mouth of a person has light membranes on the inside and also the gums. 1. Keep rose water (JCLP_181) in the mouth. 2. Boil JCLP_135 with wine (JCLP_144) and let him keep it in his mouth. 3. Let him chew black olives (JCLP_053) of an olive tree (JCLP_053) and let him keep it on his tongue. 4. Boil the peel of pomegranate (JCLP_182) with wine (JCLP_099) and keep in the mouth. 5. Boil stavesacre (JCLP_003) with vinegar (JCLP_142). 6......... let him keep in his mouth. 7. Mix JCLP_135 and rose water (JCLP_181) and honey (JCA_0024) and let him keep it in the mouth. 8. He shall chew the delicate leaves of a wild olive tree (JCLP_053) and he shall apply the juice of the leaves of an olive tree (JCLP_053). 9. Boil the leaves of a wild olive tree (JCLP_053) with vinegar (JCLP_142) and let him keep the juice in his mouth. 10. He shall chew the delicate leaves of bramble (JCLP_032). 11. Let the delicate leaves of bramble (JCLP_032) boil with vinegar (JCLP_142) and let him keep vinegar (JCLP_142) in his mouth. 12. There is JCLP_008 and it is called JCLP_214 and it produces quadrilateral round thorns. Boil the leaves of the thorny plant with rose water (JCLP_181) and apply to the gums.\n169. On amblyopia. Pound fresh rue (JCLP_157) and fennel (JCLP_123) and macerate their juice with honey (JCA_0024) and apply to the eyes on the outside. 2. Burn rosemary (JCLP_050) and mix the ashes (JCX_0126) with honey (JCA_0024) and apply to the eyes on the outside. 3. Grind black ivy (JCLP_087) and put the juice into his nose. 4. Drip the juice of JCLP_035 into the inside of the eyes. 5. Apply the bile of geese (JCA_2858) to the eyes externally. 6. Mix crushed litharge (JCLM_018) with vinegar (JCLP_142) and table oil (JCLP_232) and apply to the eyes externally. 7. Mix ground Cappadocian salt (JCLM_002) with the juice of fennel (JCLP_123) and add unsmoked honey (JCA_0024) and mix it and apply it to the eyes externally. 8. Pound fennel (JCLP_123) and apply the juice to the eyes externally. 9. Grind the root of chelidonium (JCLP_231) and mix it with unsmoked honey (JCA_0024) and apply to the eyes externally.\n170.[137] It softens joint pain and hardening. Put gum ammoniacum (JCLP_015) one night and one day into acrid vinegar (JCLP_142) and once it gets soft, macerate it with honey (JCA_0024) and put it on top of the location of the joints. 2. Crush pyrethrum (JCLP_173) finely and pepper (JCLP_154) and add table oil (JCLP_232) and unify and apply the painful area. 3. Boil the fresh leaves of JCLP_167 with water (JCLM_022) and then pound these and put them onto the hardening and on the pain of the joints. 4. Mix cedar oil (JCLP_083) with table oil (JCLP_232) and apply onto the pain. 5. Burn the root of ivy (JCLP_087) and mix ashes (JCX_0126) with yolk (JCX_0114) of an egg (JCA_0105) and put it onto the pain. 6. Put crushed, very very fine pepper (JCLP_154) on top of the pain. And put JCU_2779 on top of the pepper (JCLP_154) and burn the area where the pain is. 7. Grind the seed of hyoscyamus (JCLP_217) and make it fine and also add very finely crushed nitron (JCLM_023) and drink it. 8. Apply lard (JCA_0077) of a deer (JCA_0649) or of a bird (JCA_0346) or of a bull (JCA_0466) or of a bear (JCA_0435) to the area where the pain of the joints is.\n171.[138] It dissolves and softens an apostema. Macerate pounded leaves of hyoscyamus (JCLP_217) with lard (JCA_0077) of a pig (JCA_0266) and put them on top onto the apostema. 2. Pound hypericum (JCLP_199) and put it on top of the area where the hardening is. 3. Pound the leaves of wild or domesticated monk's rhubarb (JCLP_111) and boil and put onto the area while warm. 4. Grind linseed (JCLP_116) and make it fine and boil with water (JCLM_022). Then add lard (JCA_0077) of a pig (JCA_0266) and macerate and put it on top onto the apostema. 5. Boil the leaves of mallow (JCLP_132) with water (JCLM_022) then pound them and put them on top of the area. 6. Boil the flour of darnel (JCLP_006) with sweet water (JCLM_022), then add lard (JCA_0077) of a pig (JCA_0266) and put it on top of the wound. 7. Boil barley (JCLP_100) flour and fine linseed (JCLP_116) with water (JCLM_022). Then add lard (JCA_0077) of a pig (JCA_0266), of a goose (JCA_0246) of a bird (JCA_0346), marrow (JCA_0307) of a deer (JCA_0366), lard (JCA_0077) of a bull (JCA_0466), of a panther (JCA_2364), of a bear (JCA_0990), of a male calf (JCA_0515), of a lion (JCA_0839), of a raven (JCA_1160), of a fox (JCA_0624), all dissolved, and add them and macerate and put it on top with a cloth (JCLP_151). 8. Take dung (JCA_0254) of a pigeon (JCA_0882) and vinegar (JCLP_142) and macerate and put it on top with a cloth (JCLP_151) onto the wound.\n172.[139] It softens aporyphas and ekbata. Mix finely ground JCU_0278 with propolis (JCA_0710) and put it on top. 2. Boil barley flour (JCLP_100) with the juice of beetroot (JCLP_189) and macerate well and apply them. 3. Pound the leaves of the plant mullein (JCLP_221) and put them on top. 4. Boil onion (JCLP_102) on coals (JCLM_015) and pound it and put it on top. 5. Pound onion (JCLP_102) and make it fine and apply as a cataplasm. 6. Grind the root of monk's rhubarb (JCLP_111) and macerate with lard (JCA_0077) of a goose (JCA_0246) and of a pig (JCA_0266) and put it on top. 7. Crush resin (JCLP_158) and sprinkle it on top.\n173.[140] If someone is bitten by a snake or a viper. Do this treatment. Pound the leaves of an apple tree (JCLP_131) and drink their juice with wine (JCLP_144). Also pound the leaves and put them onto the wound. 2. Pound the leaves of myrtle (JCLP_134) and put them on top of the wound. 3. Split a live JCA_1576 and put it onto the wound. 4. Pound mint (JCLP_063) and drink with warm water (JCLM_022). 5. Pound the leaves of JCLP_096 and put them onto the wound. 6. Crush all heal (JCLP_224) and mix it with table oil (JCLP_232) and apply to the area. 7. Grind the root of JCLP_051 and the leaves and mix them with lard (JCA_0753) of a deer (JCA_0649) and apply. 8. Apply dissolved lard (JCA_1490) of a bear (JCA_0435) onto the wound.\n174. If a person has indigestion. Let him drink dry crushed pennyroyal (JCLP_040) with wine (JCLP_099). 2. Grind crushed pepper (JCLP_154) and parsley (JCLP_120) seeds and crush it all together and let him drink it with fish (JCA_0526) sauce (JCA_0489) in the bath if it is coming along well. Make sure that he does not bathe if he evacuates the indigestion. 3. Let him drink crushed cinnamon (JCLP_086) and crushed rue (JCLP_157) seed together with warm water (JCLM_022). 4. Pound hyssop (JCLP_216) and let him drink it with water (JCLM_022).\n175. Therapy for cough. Grind the skin of carrot (JCLP_048) and let him drink it with wine (JCLP_144). 2. Grind gum of balsamodendrum (JCLP_034) and let him drink with wine (JCLP_144). 3. There is a plant called JCLP_051. Let him eat its root raw and boiled. 4. Let him eat the raw root of JCLP_051 with honey (JCA_0024). 5. Pound the leaves of rue (JCLP_157) and let him drink the juice. 6. Grind Pontic sumach (JCLP_175) and let him drink with water (JCLM_036). 7. There is a plant called polygonum (JCLP_164). Pound it and let him drink the juice. 8. Pound green wormwood (JCLP_028) and let him drink the juice. 9. Boil maidenhair (JCLP_004) with water (JCLM_022) and let him drink it with wine (JCLP_099). 10. Grind the root of white JCLP_008 and let him drink with water (JCLM_036). 11. Grind gum ammoniacum (JCLP_015) and make it fine and let him drink it with honey (JCA_0172) or with the juice of JCLP_045. 12. Boil purslane (JCLP_019) that is called purslane (JCLP_041) with vinegar (JCLP_142) and wine (JCLP_099) and let him eat it. 13. Put propolis (JCA_0710) on live coals (JCX_0499) and fumigate him. 14. Make green pine resin (JCLP_177) into kernels like chickpeas (JCLP_055) and let him swallow them with warm water (JCLM_022). 15. Fumigate him from below with lotus (JCLP_042). 16. Put yellow orpiment (JCLM_006) and all heal (JCLP_224) onto burning coals (JCX_0499) and fumigate him and let him swallow the smoke. 17. Put resin (JCLP_158) and frankincense (JCLP_114) and storax (JCLP_206) onto burning coals (JCX_0499) and fumigate. 18. Grind the fruit of JCLP_030 and make it fine and let him drink it with water (JCLM_036). 19. Let him eat the green shoots of cypress (JCLP_106) with vinegar (JCLP_142). 20. Boil rosemary (JCLP_050) with wine (JCLP_144) and let him drink it in the morning. 21. Boil the root of fennel (JCLP_123) with wine (JCLP_099) and let him drink. 22. Grind the seed of fennel (JCLP_123) and let him drink with wine (JCLP_144). 23. Boil the leaves of a pine (JCLP_156) and its tender twigs with wine (JCLP_144) and let him drink. 24. Grind the seed of hyoscyamus (JCLP_217) and let him drink it with water (JCLM_022). 25. Boil hyssop (JCLP_216) and rue (JCLP_157) with honey (JCA_0024) and wine (JCLP_099) and let him drink. 26. Boil the root of mullein (JCLP_221) with wine (JCLP_144) and let him drink. 27. Make fatty storax (JCLP_206) into kernels like of a chickpea (JCLP_055) and let him swallow it with wine (JCLP_099). 28. Make all heal (JCLP_224) into kernels and with white (JCX_0101) of an egg (JCA_0105) let him swallow these.\n176.[141] It brings down the milk of women and rushes down menstruation. Grind the seed of agnus castus (JCLP_115) and let her drink with wine (JCLP_144). 2. Boil the root of dill (JCLP_073) and let her drink. 3. Boil the seed of dill (JCLP_073) with water (JCLM_022) and let her drink the root of fennel (JCLP_123) and the leaves and the seed of ......... and let her drink. 4. Boil the shoot of dill (JCLP_073) or its seed with water (JCLM_022) let her drink. 5. Boil the seed, root and the leaves of fennel (JCLP_123) with wine (JCLP_144) and let her drink. 6. Grind nigella (JCLP_126) and let her drink with wine (JCLP_144). 7. Grind basil seed (JCLP_031) and let her drink it with water (JCLM_022). Next boil a cabbage (JCLP_098) and let her eat it. 8. Let her eat the boiled leaves of JCLP_174 and its tender shoots. 9. Rinse frequently with salt water (JCLM_004) of the sea (JCLM_011). 10. Pound JCLP_038 and apply its juice to the breasts of the woman and then sprinkle lead white (JCLM_042) on top. 11. Grind the leaves of hyoscyamus (JCLP_217) and apply their juice to the breasts. 12. Mix vinegar (JCLP_142) and water (JCLM_022) and salt (JCLM_002), then add lead white (JCLM_042) and ground litharge (JCLM_018) and mix it all and apply to the breasts.\n177.[142] If a woman can't give birth quickly. Take river crabs (JCA_0667) and put them on live coals (JCX_0499) and fumigate her and she will immediately give birth.\n178.[143] It softens roughness of the tongue. That is boil honey (JCA_0024) and keep fine cloth (JCLP_151) on top which has inside linseed (JCLP_116) and once the cloth (JCLP_151) starts to sweat from the vapour of the honey (JCA_0172) then rub it onto the tongue. 2. Pound fresh mint (JCLP_063) and make it fine and rub it onto the tongue. 3. Boil dried figs (JCLP_071) with water (JCLM_022) and the water (JCLM_022) of the dried figs (JCLP_071), let him keep it in his mouth. 4. Pound fresh mint (JCLP_063) and remove the juice and mix it with rose oil (JCLP_181) and chamomile (JCLP_227) and apply to the tongue. 5. Pound fresh mint (JCLP_063) and apply to the head. 6. Boil green mint (JCLP_063) with water (JCLM_022) and a little wine (JCLP_099) and keep this liquid in the mouth. 7. Chew the leaves of an olive tree (JCLP_053), keep it on the tongue.\n179. Therapy for dysuria. Boil wormwood (JCLP_028) with water (JCLM_022) and when it is boiling, mix it with wine (JCLP_099) and let him drink. 2. Boil asparagus (JCLP_026) with water (JCLM_022) and let him drink it. 3. Boil JCA_1310 with water (JCLM_022) and let him drink. 4. Grind JCU_0677 well and let him put them in front of the opening of the crotch. 5. Boil asparagus (JCLP_026) with water (JCLM_022) and let him drink it. 6. Grind the kernels of wild and domesticated grapes (JCLP_237) and drink with wine (JCLP_144). 7. Grind the seed of the plant clover (JCLP_215) and drink with wine (JCLP_144). 8. Boil JCLM_039 with wine (JCLP_144) and drink. The doctors call it pyrites (JCLM_026) stone (JCLM_019). 9. Pound a stone (JCLM_019) which is found in new sponges (JCA_2623) thoroughly and drink it with wine (JCLP_144). 10. Boil rosemary (JCLP_050) with wine (JCLP_144) and drink it. Take the root of chicory (JCLP_089), the bark of it, and the root of celery (JCLP_186) and the root of parsley (JCLP_120) and the root of fennel (JCLP_123) and the root of chicory (JCLP_068) and of dill (JCLP_073) and of wild and domesticated rue (JCLP_157) and let it boil with water (JCLM_022) and let him drink their juice. To these also add the root of a radish (JCLP_176) and of sowthistle (JCLP_062).\n180. On dysentery. Pound JCLP_078 let him drink the juice. 2. Crush myrrh (JCLP_133), the amount of a bean (JCLP_218), and let him drink it with wine (JCLP_144). 3. Boil the leaves of agnus castus (JCLP_115) with wine (JCLP_144) and let him drink. 4. Boil the leaves and shoots of bramble (JCLP_032) with wine (JCLP_099) and let him drink. 5. There is a plant called ground pine (JCLP_228). Boil it with wine (JCLP_144) and let him drink in the morning with wine (JCLP_099).\n181. If he has pain in the ear and does not hear. Do this treatment. That is grind nuts (JCLP_079) and their oil (JCLP_053) or that of sweet almonds (JCLP_017). Make it warm and drip it into the ear. 2. Drip JCLP_030 into the ear. 3. Drip the bile of a hare (JCA_0453) with milk (JCX_0085) of a woman (JCX_0118) into the ear. 4. Mix the bile of a raven (JCA_1160) with a good new honey (JCA_0024) and drip it into the ear. 5. Drip warm juice of an onion (JCLP_102) into the ear. Pound the root of asphodelus (JCLP_027) and drip the juice into the ear.\n182. If the menstruation of a woman is late. Do this treatment. That is let her drink the amount of six kernels of JCO_1382 in the morning with water (JCLM_022). 2. Boil maidenhair (JCLP_004) with water (JCLM_022) and let him drink in the morning. 3. Pound the leaves of stinging nettle (JCLP_211) and pound myrrh (JCLP_133) and mix it up and give it to another woman and let her put it into her womb of let her put it outside of her ........ 4. Pound hazelwort (JCLP_025) and let her drink it with honey (JCA_0024). 5. Pound the root of asphodelus (JCLP_027) and let her drink its juice with wine (JCLP_099).\n183.[184] If it happens to a pregnant woman that the child dies inside the womb. Do this treatment, so that it is expelled. Let her drink boiled wormwood (JCLP_028) with wine (JCLP_099). 2. Pound wormwood (JCLP_028) and macerate with honey (JCA_0024) and put it inside of her body. 3. Let her drink carrot (JCLP_048) grown somewhere without having sown its seed with wine (JCLP_144). 4. Grind the tear of a wild olive tree (JCLP_053) and let her drink it with wine (JCLP_144). 5. Grind the seed of JCLP_051 and let her drink it with honey (JCA_0024) and wine (JCLP_099) in the morning. 6. Boil the bark of capers (JCLP_076) or its root with wine (JCLP_144) and let her drink. 7. Let her drink fine cinnamon (JCLP_086) and fine myrrh (JCLP_133). 8. Boil the root of cyclamen (JCLP_104) with water (JCLM_022) and let her drink. 9. Grind the seed of parsley (JCLP_120) and let her drink it with water (JCLM_022). 10. There is a plant called clover (JCLP_215). Boil its leaves and the flowers and the seed with water (JCLM_022) and let her drink. 11. Boil oregano (JCLP_141) with water (JCLM_022) and let her drink. 12. Boil the root of elm tree (JCLP_172) with honey (JCA_0024) and wine (JCLP_099) and let her drink. 12. There is a plant called JCLP_241. Boil it with water (JCLM_022) and let her drink.\n184.[145] If someone is bitten by a snake or a viper. Grind the root of asphodelus (JCLP_027) and let him drink it boiled with wine (JCLP_099). 2. Grind the root of asphodelus (JCLP_027) well and put it on top onto the wound. 3. Let him drink crushed castor (JCA_0145) with wine (JCLP_144). 4. Grind the leaves of lily (JCLP_101) and put them on top of the wound. 5. Grind carob (JCLP_139) well and let him drink with wine (JCLP_144).\n185. It treats and expels what is called ermyngia by the common people, by the doctors worms. That is pound JCLP_078 and give its juice to drink with wine (JCLP_144). 2. Let him drink wormwood (JCLP_028) and the bile of a bull (JCA_1325), just boil the wormwood (JCLP_028) first with water (JCLM_022) then mix it and let him drink. 3. Grind bitter lupine (JCLP_118) and mix their flour with honey (JCA_0024) and let him eat. 4. Boil summer savory (JCLP_065) with water (JCLM_022) and let him drink. 5. Boil JCLP_098 with water (JCLM_022) and let him drink. 6. Grind the seed of cabbage (JCLP_098) and let him drink it with water (JCLM_022). 7. Boil the root of a mulberry tree (JCLP_208) with water (JCLM_022) and let him drink in the morning. 8. Boil the root of elm tree (JCLP_172) with honey (JCA_0024) and let him drink just add also wine (JCLP_099). 9. Soak the root of polypodium (JCLP_165) in syrup (JCO_0157) and eat it. 10. Boil hyssop (JCLP_216) with water (JCLM_022) and wine (JCLP_099) and let him drink it in the morning. 11. Grind the seed of a radish (JCLP_176) and let him drink them with water (JCLM_022). 12. Let him eat garlic (JCLP_197).\n186. If a person is suffering from the so-called sciatica. Let him drink crushed gum ammoniacum (JCLP_015). 2. Put gum ammoniacum (JCLP_015) into vinegar (JCLP_142) in the evening and let it boil. And once it is soft spread it into a cloth (JCLP_151) and put it on top of the location where it hurts. 3. Boil hazelwort (JCLP_025) with water (JCLM_022) and let him drink. 4. Boil hazelwort (JCLP_025) and honey (JCA_0024) and wine (JCLP_099) and let him drink it with water (JCLM_022). 5. Boil hyssop (JCLP_216) with honey (JCA_0024) and water (JCLM_022). Let him drink it in the morning. 6. Boil the root of asparagus (JCLP_026) with wine (JCLP_099) and let him drink. 7. Boil the seed of capers (JCLP_076) with wine (JCLP_099) and let him drink. 8. Boil the bark of the root of capers (JCLP_076) with wine (JCLP_099) and let him drink. 9. Boil centaury (JCLP_084) with wine (JCLP_099) and let it be given with a clyster. 10. Boil rue (JCLP_157) with olive oil (JCLP_053) ... and let him drink.\n187.[146] If his face gets yellow, which is called icterus by the doctors, by the locals chrysiasmos, do this treatment. Boil maidenhair (JCLP_004) with wine (JCLP_099) and let him drink. 2. Let him drink crushed aloe (JCLP_012) with water (JCLM_022). 3. Boil the root of asphodelus (JCLP_027) with wine (JCLP_099) and let him drink and he shall eat its shoots instead of vegetables. 4. Boil the tip of wormwood (JCLP_028) with water (JCLM_022) or with wine (JCLP_099) and let him drink. 5. Boil a centipede (JCA_2591) with water (JCLM_022) and let him drink. 6. Grind the seed of atriplex (JCLP_233) and let him drink it either with water (JCLM_022) or with yoghurt (JCA_2760). 7. Boil the root of monk's rhubarb (JCLP_111) with wine (JCLP_099) and let him drink. 8. Boil chamomile (JCLP_227) and let him drink the decoction. 9. Boil the root of chelidonium (JCLP_231) with wine (JCLP_144) and let him drink. 10. Boil the root of cyclamen (JCLP_104) with honey (JCA_0024) and water (JCLM_022) and let him drink.\n188. On headache. Grind the leaves of agnus castus (JCLP_115) and its seed and mix it with rose oil (JCLP_181) and apply to the head. 2. Pound JCLP_078 and mix its juice with rose oil (JCLP_181) and apply to the head. 3. Mix crushed aloe (JCLP_012) with rose oil (JCLP_181) and vinegar (JCLP_142) and apply to the forehead and the temples. 4. Grind bitter almonds (JCLP_017) well and mix them with vinegar (JCLP_142) and rose oil (JCLP_181) and apply to the forehead and the temples. 5. Grind bitter almonds (JCLP_017) and mix it with vinegar (JCLP_142) and rose oil (JCLP_181) and apply to the forehead and the temples. 6. Pound fresh leaves of vine (JCLP_016) and what is called by the common people tendrils, and by the doctors helikes of vine (JCLP_016). Pound these and mix also the leaves. And put it onto the part of the head where the pain is. 7. Pound fresh leaves of cabbage (JCLP_098) and put their juice into the nose, just warm. 8. Pound green mint (JCLP_063) and put it onto the forehead. 9. There is a plant called fleabane (JCLP_095). Pound its leaves and mix them with table oil (JCLP_232) and apply to the head. 10. Apply also its leaves. Grind fleawort (JCLP_235) and mix it with rose oil (JCLP_181) and vinegar (JCLP_142) and apply to the head. There is a plant called JCLP_038. By the doctors, it is called JCLP_204. Pound this and mix the juice with table oil (JCLP_232) and apply to the head. 12. Grind nigella (JCLP_126) and mix it with table oil (JCLP_232) and vinegar (JCLP_142) and apply to the head. 13. Grind mustard (JCLP_192) and macerate with honey (JCA_0024) and put it onto the forehead. 14. Boil domesticated rue (JCLP_157) with vinegar (JCLP_142) and rose oil (JCLP_181) and apply to the head and the forehead and the temples.\n189. [147] If his stomach runs. Do this treatment so that it stops. Take the root and the shoots of bramble (JCLP_032) and grind these and let him drink their juice. 2. Grind the root of an oak (JCLP_171) and boil it with wine (JCLP_099) and let him drink. 3. Boil the root and the leaves of JCLP_150 with wine (JCLP_099) and let him drink. 4. Boil the leaves of myrtle (JCLP_134) with wine (JCLP_099) and treat with a clyster. 5. Boil the seed of mastic (JCLP_209) with wine (JCLP_099) and treat with a clyster. 6. Boil the seed of mastic (JCLP_209) and its tender leaves with water (JCLM_022) and let him drink. 7. Boil gourd (JCLP_092) with wine (JCLP_099) and let him drink with wine (JCLP_099). 8. Boil the tender shoots of cypress (JCLP_106) with wine (JCLP_099) and let him drink. 9. Boil the leaves of JCLP_236 with wine (JCLP_099) and let him drink. 10. There is a plant called plantain (JCLP_023), grind its seed and let him drink it with water (JCLM_036).\n190.[148] For if someone is bitten by a dog. Do this treatment. That is pound melissa (JCLP_129) and let him drink with wine (JCLP_144). 2. Pound the leaves of JCLP_167 and mix them with ashes (JCX_0126) and put them on the wound. 3. Grind garlic (JCLP_197) and put it on top. 4. Grind garlic (JCLP_197) and let him drink it with water (JCLM_022). And let him also eat garlic (JCLP_197). 5. Pound rue (JCLP_157) and mix it with table oil (JCLP_232) and put it on the wound. 6. Pound tender leaves of a wild fig tree (JCLP_207) and macerate with honey (JCA_0024) and put it on top of the wound. 7. Pound polygonum (JCLP_164) and let him drink the juice with wine (JCLP_144).\n191. For a head cold. Do this treatment. Grind white dry dung (JCA_0254) of a dog (JCA_0920) and mix it with honey (JCA_0024) and put it onto the neck. 2. Put cedar oil (JCLP_083) onto the neck. 3. Warm up honey (JCA_0024) and water (JCLM_022) and let him keep it in his mouth. 4. Boil bran (JCLP_160) with water (JCLM_022) and syrup (JCO_0157) then sift it and let him keep the juice in the mouth and let him keep it a long time.\n192. Treat the so-called louxikan, called by the doctors hiccup, like this. Pound fresh mint (JCLP_063) and mix its juice with the juice of sour pomegranate (JCLP_182) and let him drink. 2. There is a plant called scolopendrium officinale (JCLP_196). Boil it with water (JCLM_022) and let him drink. 3. Pound aristolochia (JCLP_022) and let him drink with warm water (JCLM_036). 4. There is a plant called madwort (JCLP_013). Boil it with water (JCLM_022) and let him drink.\n193.[149] If someone is bitten by a rabid dog. Do this treatment. That is, there is a plant called gentian (JCLP_039). Boil its root with wine (JCLP_144) and let him drink. 2. Burn river crabs (JCA_0667) over burning coals (JCX_0499) and let him drink the ashes (JCX_0126) of the crabs (JCA_1919) with wine (JCLP_144). 3. Grate the so-called stone (JCLM_019) hematite (JCLM_001) on a whetstone and collect it. Let him drink it with wine (JCLP_144). 4. Gum of balsamodendrum (JCLP_034) drunk with wine (JCLP_144).\n194. The stones that are in the bladder and the kidneys. These expels the resin of vine (JCLP_016), let him drink this with wine (JCLP_144). 2. Boil the root of monk's rhubarb (JCLP_111) with wine (JCLP_144) and let him drink. 3. Let him drink the tear of an almond tree (JCLP_017) with vinegar (JCLP_142) and with broth. 4. Grind the root of asparagus (JCLP_026) and let him drink the juice. 5. Grind the root and leaves of scolopendrium officinale (JCLP_196) and let him drink. 6. Grind the bark of the root of capers (JCLP_076) and let him drink with wine (JCLP_144). 7. Grind liquorice (JCLP_043) and let him drink the juice with wine (JCLP_144). 8. Grind the root of quince (JCLP_203) and let him drink the juice with wine (JCLP_144). 9. Grind the root of periwinkle (JCLP_225) and let him drink the juice with wine (JCLP_144).\n195. Therapy for lichen and leprosy. There is a plant called JCLP_033. Pound its leaves and put them there. 2. Put the tear of a black of an olive tree (JCLP_053) in vinegar (JCLP_142) and let it soak one night and one day and then apply. 3. Burn the so-called mussel (JCA_2034) and mix the ashes (JCX_0126) with vinegar (JCLP_142) and apply. 4. Pound the leaves of damson (JCLP_047) and mix them with vinegar (JCLP_142) and apply. 5. Let the tear of damson (JCLP_047) soak in acrid vinegar (JCLP_142) and then apply. 6. Grind the root of JCLP_051 and mix it with vinegar (JCLP_142) and apply. 7. Grind JCU_0278 and the leaves of rosemary (JCLP_050) and add olive oil (JCLP_053) and liquid pitch (JCLP_244) and vinegar (JCLP_142) and mix and apply. 8. Boil cedar oil (JCLP_083) with vinegar (JCLP_142) and apply. 9. Grind nigella (JCLP_126) and mix it with vinegar (JCLP_142) and apply. 10. Grind the root of wild cress (JCLP_077) and apply with vinegar (JCLP_142). 11. Crush sulphur (JCLM_033) and pine resin (JCLP_177) and nitron (JCLM_023) and add vinegar (JCLP_142) and table oil (JCLP_232) and apply. This also helps for an itch of the genital parts.\n196. If the breasts of a woman or a man have hard areas. Pound the leaves of agnus castus (JCLP_115) and mix them with butter (JCA_0554) and put on top with cloth (JCLP_151). 2. Boil the root of asphodelus (JCLP_027) and the leaves and the flowers, boil and let him eat with vinegar (JCLP_142). 3. Pound the leaves of vine (JCLP_016) and mix them with butter (JCA_0554) and put them on top. 4. Grind the root of marsh mallow (JCLP_011) well and put it on top. 5. Pound fresh mint (JCLP_063) and put it on top.\n197. It inhibits the breasts of women and the testicles of children so that they do not get big. Pound the leaves of hyoscyamus (JCLP_217) and put them on top. 2. Pound the leaves of mandrake (JCLP_122) and put them on top. 3. Make litharge (JCLM_018) and lead white (JCLM_042) fine and mix with vinegar (JCLP_142) and apply. 4. Boil the leaves of beetroot (JCLP_189) with water (JCLM_022). And then pound them and put them on top. 5. Grind cumin (JCLP_105) finely and mix the flour with fine cereal (JCLP_194) and honey (JCA_0024) and macerate and apply as a cataplasm. 6. Grind rosemary (JCLP_050) and mix it with rose oil (JCLP_181) and put it on top. 7. Grind linseed (JCLP_116) and make it fine and fenugreek (JCLP_212) and mix it. Macerate with rose oil (JCLP_181) and put it on top. 8. Pound the leaves of mallow (JCLP_132) and monk's rhubarb (JCLP_111) and mix them with rose oil (JCLP_181) and apply as a cataplasm. 9. Mix of bean (JCLP_218) flour with honey (JCA_0024) and put it on top onto the breasts.\n198. [198] If someone is bitten by a bee or a wasp. Do this treatment. Pound the leaves of wild mallow (JCLP_132) and put them onto the bite. 2. Pound the leaves of domesticated mallow (JCLP_132) and put it there on the location. 3. Pound the tender leaves of laurel (JCLP_049) and put them on top. 4. Pound the leaves of melissa (JCLP_129) and put them on the wound. 5. Pound fresh rue (JCLP_157) and put it on the wound.\n199.[199] If his nose smells. Do this treatment. Pound the leaves of ivy (JCLP_087) and warm up the juice and drip it into the nose. 2. Pound the leaves of JCLP_167 and warm up the juice and drip it into the nose. 3. Pound fresh oregano (JCLP_141) and drip the juice into the nose. 4. Grind nigella (JCLP_126) and mix it with table oil (JCLP_232) and apply onto the outside of the nose and drip it into the inside. 5. Myrrh (JCLP_133), and mix it with milk (JCX_0085) of a woman (JCX_0118) and drip it into the nose.\n200.[152] If they beat each other and develop wounds. Do this treatment. That is pound the shoots of a plane tree (JCLP_161) and macerate with lard (JCA_0077) of a pig (JCA_0266) and apply to the wound. 2. Grind the socalled Lemnian earth (JCLM_017) and crush and macerate with water (JCLM_022) and apply. 3. Crush lump of earth (JCLM_009) and macerate with water (JCLM_022) and put it onto the wound. 4. Pound fresh mint (JCLP_063) and macerate with lard (JCA_0077) of a pig (JCA_0266) and apply. 5. Pound the tender leaves of mastic (JCLP_209) and put them on top. 6. Grind the tender leaves of bramble (JCLP_032) and put them on the wound.\n201. On infertility. Divide a JCU_1629 in half and take it with your left hand when there is neither sun nor moon and bind it into a linseed (JCLP_116) cloth (JCLP_151) and carry it and you will be astonished. 2. ...... the seed of hyoscyamus (JCLP_217) with milk (JCX_0638) of a horse (JCA_1908), put it into the skin of a deer (JCA_1761) and have it bound onto the arm and you will be astonished. 3. Put the plant ironwort (JCLP_191) into the skin of a deer (JCA_0793) and hand it over and let her carry it.\n202. If he vomits a lot even though he does not want to vomit. Do this treatment. Pound fresh mint (JCLP_063) and let him drink the juice with vinegar (JCLP_142) and wine (JCLP_099). 2. Pound a sour pomegranate (JCLP_182) and let him drink the juice. 3. Pound the tendrils of vine (JCLP_016) and let him drink the juice. 4. Roast lentils (JCLP_219) and let him eat it with honey (JCA_0024). 5. Let him eat roasted vetch (JCLP_146) with honey (JCA_0024).\n203.[153] For a cloud of the eyes. Do this treatment. Pound JCLP_051 and apply its juice to the eyes externally. 2. Crush cinnamon (JCLP_086) well and mix it with milk (JCX_0085) of a woman (JCX_0118) and apply to the outside of the eye. 3. Pound clover (JCLP_215) and mix its juice with honey (JCA_0024) and apply to the outside of the eye. 4. Crush gum ammoniacum (JCLP_015) and macerate with milk (JCX_0085) of a woman (JCX_0118) and apply to the outside of the eyes. 5. Crush myrrh (JCLP_133) and mix it with new honey (JCA_0024) and apply to the eyes. 6. Pound the leaves of fennel (JCLP_123) and put the juice into a bronze/copper (JCLM_040) vessel and let it be three days then take it out and apply to the eyes every hour and in the morning. 7. Pound the leaves of bramble (JCLP_032) and apply the juice to the eyes. 8. Macerate gum ammoniacum (JCLP_015) with milk (JCX_0085) of a woman (JCX_0118) and apply to the outside of the eyes.\n204. For pain of the eyes. Pound the leaves of a wild olive tree (JCLP_053) and apply the juice to the eyes. 2. Pound JCLP_078 and put it on top of the eyes. 3. Pound the leaves of purslane (JCLP_041) and mix them with bran (JCLP_160). Put it into the eyes. 4. Pound wormwood (JCLP_028) and make it smooth with honey (JCA_0024) and put it on top of the eyes. 5. Crush gum ammoniacum (JCLP_015) and unify with milk (JCX_0638) of a woman (JCA_1036) and apply to the eyes. 6. Pound the leaves of fennel (JCLP_123) and put the juice into a bronze/copper (JCLM_040) vessel and leave it for three days. Then take it out and apply to the eyes every hour and in the morning. 7. Pound the tender leaves of bramble (JCLP_032) and put them on top of the eyes. 8. Pound cyclamen (JCLP_104) and apply the juice with honey (JCA_0024) to the eyes. 9. Pound rosemary (JCLP_050) and macerate with honey (JCA_0024) and milk (JCX_0085) of a woman (JCX_0118) and apply to the eyes. 10. Pound mandrake (JCLP_122) and make the juice soft with bran (JCLP_160) or with barley flour (JCLP_100) and put it on the eyes. 11. Grate fresh gourd (JCLP_092) and pound the pieces and mix the juice with bran (JCLP_160). And macerate and put it on top onto the eyes. 12. Pound celery seed (JCLP_186) and mix its juice with bran (JCLP_160) and put it on the eyes. 13. Grind myrrh (JCLP_133) and mix it with honey (JCA_0024) and apply to the eyes. 14. Pound the leaves of hyoscyamus (JCLP_217) and mix them with bran (JCLP_160) and put them on the eyes. 15. Pound fresh roses (JCLP_181) and mix their juice with milk (JCX_0085) of a woman (JCX_0118) and apply. 16. Pound rue (JCLP_157) and mix its juice with bran (JCLP_160) and put it on the eyes. 17. Pound JCLP_078 and mix the juice with honey (JCA_0024) and apply to the eyes. 18. Pound mint (JCLP_063) and mix the juice with milk (JCX_0085) of a woman (JCX_0118) and apply. 19. Pound the tender leaves of bramble (JCLP_032) and mix the juice with with honey (JCA_0024) and milk (JCX_0085) of a woman (JCX_0118) and apply. 20. Grind fleawort (JCLP_235) and mix it with honey (JCA_0024) and milk (JCX_0085) of a woman (JCX_0118) and apply to the eyes. 21. Pound the tender leaves of an olive tree (JCLP_053) and mix them with honey (JCA_0024) and milk (JCX_0085) of a woman (JCA_1034) and apply to the eyes. 22. Pound the fresh leaves of reed (JCLP_075) and apply the juice to the eyes. Put the ground leaves on top.\n205.[154] For tooth ache. Do this treatment. Boil black JCU_0278 with vinegar (JCLP_142) and let him keep the vinegar (JCLP_142) where the pain is. 2. Boil the root of asparagus (JCLP_026) with vinegar (JCLP_142) and keep it in the mouth. 3. Grind the root of asphodelus (JCLP_027) and drip the juice into the nostril of the part that hurts. 4. Boil stavesacre (JCLP_003) with vinegar (JCLP_142) and honey (JCA_0172) and let him keep it in the mouth. 5. Boil the tender shoots of a plane tree (JCLP_161) with vinegar (JCLP_142) and keep it in the mouth. 6. Boil the leaves of bramble (JCLP_032) with vinegar (JCLP_142) and keep it in the mouth.\n206.[155] If the teeth are wobbly. Do this treatment. Let him bind the root of wild cress (JCLP_077) on his neck. 2. Boil hyssop (JCLP_216) with vinegar (JCLP_142) and let him keep it in his mouth. 3. Boil the bark of a mulberry tree (JCLP_208) with vinegar (JCLP_142) and keep it in the mouth. 4. Let him chew the root of henna (JCLP_149). 5. There is a tree called manna ash (JCLP_127), pound its leaves and let him keep them in the mouth. 6. Let the fruit of capers (JCLP_076) boil with vinegar (JCLP_142) and let him keep it in the mouth. 7. Let the bark of the root of capers (JCLP_076) boil with vinegar (JCLP_142) and let him keep it in the mouth. 8. Boil the leaves of pomegranate (JCLP_182) with vinegar (JCLP_142) and let him keep it in the mouth. 9. Boil the leaves of a wild olive tree (JCLP_053) with vinegar (JCLP_142) and keep it in the mouth.\n207.[156] If a person burns a part of the body. Pound plantain (JCLP_023) and put it on top of the burn. 2. Grind JCLP_078 put it on top. 3. Boil the leaves of a mulberry tree (JCLP_208) with olive oil (JCLP_053). Then chop the leaves into small pieces and put them on top.\n208.[157] For people with pain in the feet the root of JCLP_036 is useful. Grind it and put it where the pain is. 2. Grind the root of lily (JCLP_101) and put it where the pain is. 3. Grind the root of turnip (JCLP_044) and put it on top where the pain is. 4. Boil the seed of turnip (JCLP_044) with water (JCLM_022) and water (JCLM_022) rinse the feet with it. 5. Grind the root of a radish (JCLP_176) and apply it to the place. 6. Boil the seed of a radish (JCLP_176) with water (JCLM_022) and rinse the feet with this same water (JCLM_022). 7. Pound the leaves of cabbage (JCLP_098) and mix them with the flour of cereal (JCLP_194) and plaster over. 8. Grind the root of cyclamen (JCLP_104) and put it where the pain is. 9. Grind the root of the plant that is called bryony (JCLP_037) and put it on top of the pain.\n209.[158] If the joints of the feet or hands get stiff and like chalk stone. Do this treatment. Put gum ammoniacum (JCLP_015) into vinegar (JCLP_142) and let it do two days and nights and let it soak, then macerate with liquid pitch (JCLP_244), and put it on top of the pain, where the stiffening is. 2. Rinse the feet with sea (JCX_0496) water (JCLM_022) frequently. 3. Crush salt (JCLM_002) and the so-called nitron (JCLM_023) and mix it with table oil (JCLP_232) and apply frequently the pain of the joints.\n210.[159] Make it for someone to stop bleeding. Grind maidenhair (JCLP_004) and let him drink its juice with wine (JCLP_144). 2. Pound fresh mint (JCLP_063) and mix the juice with vinegar (JCLP_142) and wine (JCLP_099) and let him drink. 3. Let him drink the tear of almonds (JCLP_017) with wine (JCLP_144). 4. Pound the tender leaves of bramble (JCLP_032) and put them where the blood flows. 5. Pound fresh rue (JCLP_157) and macerate with table oil (JCLP_232) and put it where the blood flows. 6. Crush mint (JCLP_063) and put it into his nose. 7. Fresh leaves of JCLP_167 ground and applied to the nose, stops the flow of the blood. 8. Put sulphur (JCLM_012) without fire (JCLM_005) onto the nose.\n211.[160] If the stomach has an imbalance that is weakness and burns a lot from the inside, pound the leaves of polygonum (JCLP_164) and put them on the stomach. 2. Pontic sumach (JCLP_175) drunk with water (JCLM_036).\n212.[160] If the belly runs, this stops it. Make JCLP_135 also fine, let him drink it with wine (JCLP_144). 2. Pound the leaves of vine (JCLP_016) and the tendrils and let him drink the juice. 3. Grind the root of gentian (JCLP_039) and let him drink it with wine (JCLP_144).\n213.[160] If the stomach has heat inside. Pound the leaves of purslane (JCLP_041) and mix them with bran (JCLP_160) and put them on the stomach. 2. Boil wormwood (JCLP_028) with sesame oil (JCLP_190) and let him drink with wine (JCLP_144). 3. Eat unwashed lettuce (JCLP_119). 4. Grind the leaves of laurel (JCLP_049) and let him drink the juice. 5. Pound liquorice (JCLP_043) and let him drink the juice warm. 6. Grind the seed of parsley (JCLP_120) and let him drink them with wine (JCLP_099). 7. Let him eat domesticated or wild sowthistle (JCLP_062). 8. Boil this with water (JCLM_036) and let him drink. 9. Boil chamomile (JCLP_227) with water (JCLM_022) and let him drink. 10. Grind the root of aristolochia (JCLP_022) and put it on the stomach. 11. Boil asparagus (JCLP_026) and let him drink the juice.\n214. Therapy for those who are suffering from the spleen and are swollen. Grind the seed of agnus castus (JCLP_115) and let him drink them with wine (JCLP_099). 2. Grind the root and leaves of scolopendrium officinale (JCLP_196) and put them on the spleen. 3. Boil the root and also the leaves of scolopendrium officinale (JCLP_196) with water (JCLM_022) and let him drink. 4. Pound asparagus (JCLP_026) and let him drink the juice. 5. Boil JCLP_002 with water (JCLM_022) and let him drink the decoction. 6. Soak one ounce of gum ammoniacum (JCLP_015) in wine (JCLP_099) for three days and nights and let him drink this wine (JCLP_099). 7. Boil wormwood (JCLP_028) and figs (JCLP_207) and water (JCLM_022) and boil their juice and macerate darnel (JCLP_006) flour and make a cataplasm and put it onto the spleen. 8. Grind the bark of the root of capers (JCLP_076) with wine (JCLP_099) and let him drink. 9. Pound tender leaves of ivy (JCLP_087) and put them on the spleen. 10. Boil the tender leaves of ivy (JCLP_087) with wine (JCLP_144) and let him drink. 11. Pound wild cress (JCLP_077) and put it on the spleen for three hours. Boil the leaves of willow (JCLP_072) and the fruit and the bark of the root with water (JCLM_022) and let him drink.\n215.[161] If a person has colic. Do this treatment. Boil JCLP_002 with water (JCLM_022) and let him drink. 2. Let him drink the tip of dry dill (JCLP_073) and its seed with water (JCLM_022). 3. Boil rue (JCLP_157) with water (JCLM_022) and let him drink. 4. Pound marjoram (JCLP_184) and boil the juice with wine (JCLP_099) and let him drink. 5. Boil cumin (JCLP_105) with olive oil (JCLP_053) and administer this olive oil with a clyster. 6. Grind broad cumin (JCLP_162) and let him drink with water (JCLM_036). 7. Crush castor (JCA_0145) and let him drink it with wine (JCLP_099). 8. Grind the seed of JCLP_137 and let him drink it with wine (JCLP_099). 9. Rue (JCLP_157) and cumin (JCLP_105) and aniseed (JCLP_020); let him drink it with water (JCLM_022) and honey (JCA_0024).\n216.[162] If someone is bitten by a scorpion. Crush the fruit of asphodelus (JCLP_027) and let him drink with wine (JCLP_144). 2. Pound marjoram (JCLP_184) and mix it with vinegar (JCLP_142) and ground salt (JCLM_002) and macerate and put it on the wound. 3. Pound the root of henna (JCLP_149) and let him drink it with wine (JCLP_144). Pound melissa (JCLP_129) and let him drink it with wine (JCLP_144).\n217.[163] If it happens in a wound that worms are developing. Do this treatment in order to expel them. Pound the leaves of elm tree (JCLP_172) and put them on top. 2. Pound fresh wormwood (JCLP_028) and put it on top onto the wound. 3. Anoint with cedar oil (JCLP_083) and they will come out. 4. Do the same also if there are worms in the ear of a person.\n218.[164] If someone is bitten by a sea JCA_2750. Do this treatment. Boil sage (JCLP_054) with wine (JCLP_144) and let him drink. 2. Pound the leaves of sage (JCLP_054) and put it onto the wound. 3. Grind the seed of asphodelus (JCLP_027) and let him drink it with with wine (JCLP_144). 5. Pound the leaves of asphodelus (JCLP_027) and put them on the wound.\n219.[165] For those that are suffering from the spleen and from swelling. Boil marjoram (JCLP_184) with water (JCLM_022), then also add wine (JCLP_099) and let him drink. 2. Let him drink dry dung (JCA_0254) of cattle (JCA_1607) with wine (JCLP_144). 3. Boil the root of henna (JCLP_149) with water (JCLM_022). Then add wine (JCLP_099) and let him drink. 4. Grind the bark of capers (JCLP_076) and let him drink it with wine (JCLP_144). 5. Grind the root of hazelwort (JCLP_025) and let him drink it with wine (JCLP_144). 6. Grind the root of yellow flag (JCLP_009) and let him drink it with wine (JCLP_144). 7. Grind the root of a fig tree (JCLP_207) and mix it with barley (JCLP_100) flour and put it on top of the spleen just first boil the barley flour (JCLP_100) with water (JCLM_022). 8. Take the stone (JCLM_019) which is found inside the head of a frog and bind it onto the head of the swollen person. And it will be of great use.\n220.[165] Therapy for inflammation. Pound pennyroyal (JCLP_040) with bran (JCLP_160) and put it onto the spleen. Sift bitter lupine (JCLP_118), and macerate their flour with bran (JCLP_160) and water (JCLM_022) and put it on top. 3. Pound fresh leaves of laurel (JCLP_049) and mix them with crumbs of bread (JCLP_024) and put it on top. 4. Pound the leaves of cabbage (JCLP_098) and mix them with bran (JCLP_160) and macerate and put them on top. 5. Pound the leaves of fresh of a gourd (JCLP_092) and put them on top. 6. Pound the leaves of henna (JCLP_149) and put them on top. 7. Pound the tender leaves of a plane tree (JCLP_161) and boil them with wine (JCLP_144) and put them on top. 8. Pound the shavings of dried of a gourd (JCLP_092) and put them on top. 9. Boil the leaves of beetroot (JCLP_189) and pound them and put them on top of the inflammation. 10. Grind linseed (JCLP_116) and fenugreek (JCLP_212) seed and mix, add also water (JCLM_022) and let it boil and then add lard (JCA_0077) of a goose (JCA_0246), of a pig (JCA_0266), of a bird (JCA_2318), of a fox (JCA_0624), of a bear (JCA_0990), marrow (JCA_0307) of a deer (JCA_0649), lard (JCA_0077) of a bull (JCA_0466), lard (JCA_0077) of a male calf (JCA_0515). Dissolve it all and macerate and put it on top of the inflammation. Dissolve also lard (JCA_0077) of a lion (JCA_0839).\n221.[166] For loss of voice, cleansing. Let him eat raw and cooked garlic (JCLP_197). 2. Make all heal (JCLP_224) into an amount equal to the kernels of a chickpea (JCLP_055) and give him in the evening five and again five and let him swallow them and on top let him drink warm wine (JCLP_099) and he shall not eat anything.\n222. It gets rid of lice. Mix the tear of ivy (JCLP_087) with vinegar (JCLP_142) and apply to the head. 2. Boil rhododendron (JCLP_180) with water (JCLM_022) and wash the head with it while it is hot. 3. Pound stavesacre (JCLP_003) and mix it with table oil (JCLP_232) and apply it to the head.\n223.[167] For the so-called khoiradas. Pound plantain (JCLP_023) and put it on top. 2. Pound maidenhair (JCLP_004) and put it on top. 3. Mix the flour of lupine (JCLP_118) with vinegar (JCLP_142) and put them on top onto the wound. 4. Pound monk's rhubarb (JCLP_111) and mix it with vinegar (JCLP_142) and put it on top. 5. Grind linseed (JCLP_116) and put it on top. 6. Grind fleawort (JCLP_235) and put it on top with vinegar (JCLP_142). 7. Pound the so-called JCLP_038 and mix the juice with bran (JCLP_160) and put it on top. 8. Pound the root of cyclamen (JCLP_104) and put it on top. 9. Grind the root of JCLP_051 and put it on top. 10. Pound the root of JCLP_051 and let him drink the juice. 11. Let him drink also the juice of the root of it.\n224. Therapy for psora. Boil bitter lupine (JCLP_118) with water (JCLM_036) and water (JCLM_022) and rinse the psora warm with it. 2. Boil cedar oil (JCLP_083) with vinegar (JCLP_142) and apply in the bath. 3. Fry the heart of rhododendron (JCLP_180) and of myrtle (JCLP_134) with table oil (JCLP_232) and apply. 4. Pound the leaves of ivy (JCLP_087) and boil them with water (JCLM_022) and let him drink. 5. Boil rue (JCLP_157) with water (JCLM_036) and rinse in the bath. 6. Pound stavesacre (JCLP_003) also with olive oil (JCLP_053) and apply.\n225. It heals ear ache. Drip warm almond oil (JCLP_017) into the ear. 2. Drip oil (JCLP_053) of nuts (JCLP_079) into the ear. 3. Drip warm laurel oil (JCLP_049) into the ear. 4. Drip JCLP_030 into the ear. 5. Grind the seed of JCLP_051 and remove the juice and mix it with table oil (JCLP_232) and apply. 6. Pound mint (JCLP_063) and mix the juice with honey (JCA_0024) and drip it into the ear. 7. Pound the shavings of a fresh gourd (JCLP_092) and collect the juice and unify with rose oil (JCLP_181) and drip it into the ear. 8. Pound onion (JCLP_102) and drip the juice into the ear. 9. Boil fresh rue (JCLP_157) with olive oil (JCLP_053) and warm it up and drip it into the ear. 10. Drip radish oil (JCLP_176) into the ear. 11. Grind cumin (JCLP_105) and also add olive oil (JCLP_053) and boil. And warm it up and drip it into the ear. 12. Pound the root of asphodelus (JCLP_027) and mix the juice with crushed of myrrh (JCLP_133) and rosemary (JCLP_050) and drip into the ear.\n226.[168] If you want that someone is not thirsty. Do this treatment. Keep an olive (JCLP_053) JCO_2045 on your tongue. 2. Slurp an egg (JCA_0630) of a bird (JCA_0346) in the morning raw on empty stomach. 3. Boil the seed of lettuce (JCLP_119) and liquorice (JCLP_043) with water (JCLM_022) and let it cool down and give it to him and let him drink. 4. Boil dates (JCLP_222) and carob (JCLP_139) and liquorice (JCLP_043) and water (JCLM_022) and cool it down and let him drink.\n227. Alphoi is called if the person develops something like a black lentil (JCLP_219) on the face. Do this treatment. Crush white JCU_0278 and mix it with vinegar (JCLP_142) and apply. 2. Crush black JCU_0278 and mix it with olive oil (JCLP_053) and vinegar (JCLP_142) and apply either in the sun or near a fire. 3. Apply crushed sulphur (JCLM_033) and vinegar (JCLP_142). 4. Mix crushed litharge (JCLM_018) and sulphur (JCLM_033) and crushed stavesacre (JCLP_003) with vinegar (JCLP_142) and apply.\n228. If they develop something like a white lentil (JCLP_219) on the face, do this treatment. Crush dry myrrh (JCLP_133) and sulphur (JCLM_033) and mix it with vinegar (JCLP_142) and apply. 2. Mix the heart of ink-gall (JCLP_085) and liquid pitch (JCLP_244) and apply.\n229. Alopecia is if the hair of the head falls out. Do this treatment. Burn the leaves of reed (JCLP_075) and mix them with liquid pitch (JCLP_244) and lard (JCA_0077) of a sheep (JCA_0709) and shave the entire head and apply. 2. Mix crushed stavesacre (JCLP_003) and mastic (JCLP_125) and mercury (JCLM_037) and vinegar (JCLP_142) together and apply to the head. 3. Dissolve lard (JCA_0077) of a fox (JCA_0624) and of a goat (JCA_0478) add resin (JCLP_158) and vinegar (JCLP_142) and apply.\n230. Therapy for inflammation of the parotis. Mix lard (JCA_0077) of a male calf (JCA_0515) of cattle (JCA_0769) and lime (JCLM_007) and apply. 2. Grind fenugreek (JCLP_212) seed and cress seed (JCLP_077) and add also lime (JCLM_007) and apply.\n231. If someone urinates blood. Do this treatment. Boil carob (JCLP_139) and also crush yellow flag (JCLP_009) and mix it with the juice of carob (JCLP_139) and let him drink.\n232. For cough. Boil hyssop (JCLP_216) and pennyroyal (JCLP_040) and dried figs (JCLP_071) with water (JCLM_022) and let him drink. 2. Mix the crushed seed of rue (JCLP_157) and cumin (JCLP_105) and pepper (JCLP_154) with honey (JCA_0024) and let him drink. 3. Grind storax (JCLP_206) the same amount as a vetch (JCLP_146) and let him drink it with water (JCLM_022) for three days. 4. Let him drink crushed JCLP_140 and cumin (JCLP_105) and honey (JCA_0024). 5. Let him drink the seed of mustard (JCLP_192), ground a lot, with warm water (JCLM_022). 6. Grind the seed of cress (JCLP_077) smoothly and let him drink it with water (JCLM_022). 7. Pound the leaves of rue (JCLP_157) and mix the juice with butter (JCA_0330) and let him drink it and apply to the chest. 8. Pound JCLP_135 and mix its juice with honey (JCA_0024) and let him drink. 9. Boil pennyroyal (JCLP_040) with water (JCLM_022) and let him drink it with honey (JCA_0024). 10. Let him chew sesame (JCLP_190) frequently. 11. Crush pine resin (JCLP_177) and let him drink it with wine (JCLP_144). 12. Boil hyssop (JCLP_216) and pennyroyal (JCLP_040) and fenugreek (JCLP_212) with honey (JCA_0024) and wine (JCLP_099) and let him drink. 13. Boil dill (JCLP_073) and cumin (JCLP_105) and rue (JCLP_157) with wine (JCLP_099) and let him drink. 14. Boil pennyroyal (JCLP_040) and rue (JCLP_157) and butter (JCA_0330) with honey (JCA_0024) and water (JCLM_022) and let him drink in the bath. 15. Boil the leaves of celery (JCLP_186) with water (JCLM_022) and let him drink. 16. Apply butter (JCA_0330) to the chest. 17. Boil the leaves of rue (JCLP_157) and cumin (JCLP_105) and a little wine (JCLP_099) and apply to the chest. 18. Make crushed henna (JCLP_149) very fine and let him drink it with good wine (JCLP_144) in the bath.\n233.[169,170] If his mouth smells. Crush 15 kernels of pepper (JCLP_154) and burn carob (JCLP_139) and crush one hexagion of the peel of pomegranate (JCLP_182) and one ink-gall (JCLP_085) without a hole and mix it with honey (JCA_0172) and apply to the area that is rotten. 2. Apply good (JCX_1217). 3. Mix fine yellow orpiment (JCLM_006) with honey (JCA_0172) and apply hemp (JCLP_205) and put hemp (JCLP_205) with your finger into the mouth where the rot is. 4. Burn the bark of willow (JCLP_072) and sheet of paper (JCLP_230) and their ashes (JCX_0126), add also fine pepper (JCLP_154) and make it smooth with honey (JCA_0172) and put it on the rot. 5. Unify mercury (JCLM_035) and fine pepper (JCLP_154) and honey (JCA_0024) and apply to the area. 6. Mix the flour of lupine (JCLP_118) and the bile of a bear (JCA_0435) and apply it to the area.\n234.[171] For the bubonic plague that is aporufas. Macerate live lime (JCLM_007) and honey (JCA_0024) and JCX_2546 and put it on top.\n235.[172] For cramps. Boil the fine seed of a radish (JCLP_176) and ink-gall (JCLP_085) with wine (JCLP_099) and let him drink. 2. Fumigate the peel of pomegranate (JCLP_182) and dry resin (JCLP_158) from below. 3. Boil oregano (JCLP_141) with wine (JCLP_099) and let him drink.\n236. If someone swallows leeches. Let him drink boiled vinegar (JCLP_142). 2. Put JCU_0677 on top of coals (JCLM_015) and fumigate into the mouth. And let him swallow the smoke. 3. Leeches and snakes are expelled by drinking unripe olive oil (JCLP_053). 4. Mix butter (JCA_0330) and vinegar (JCLP_142). Then heat up iron (JCLM_027) well and put it inside and let it extinguish. Then let him drink the butter (JCA_0330) as well as the vinegar (JCLP_142).\n237. To bring down the milk (JCX_0085) of a woman (JCX_0362). Grind nigella (JCLP_126) and let her drink it with wine (JCLP_144) in the bath. 2. Grind the seed of fenugreek (JCLP_212) and put it on top of the breasts. 3. Let her eat onion (JCLP_102). 4. Let her eat lupine (JCLP_118) that are called lupines (JCLP_064). 5. Boil the root of fennel (JCLP_123) with wine (JCLP_099) and let her drink. 6. Boil the branches of stinging nettle (JCLP_211) with water (JCLM_022) and let her drink. 7. Pound mint (JCLP_063) and apply it warm to the breasts.\n238.[173] If the knees appear to be cold like ice. Mix fine lime (JCLM_007) and liquid pitch (JCLP_244) and macerate well and spread it on the cloth (JCLP_151) and put it on top. 2. Grind the kernels of laurel (JCLP_049) and sift and macerate with sea (JCX_1100) water (JCLM_022) and put them on a cloth (JCLP_151) and put it where the pain in the knees is just first sift the kernels of the laurel (JCLP_049).\n239. For problems urinating. Grind the root of lettuce (JCLP_119) and let him drink it in the morning with water (JCLM_022). 2. Grind the seed of cress (JCLP_077) and let him drink it with wine (JCLP_144). 3. Grind JCU_0677 and put it into the hole of the penis and he will immediately want to urinate. 4. Boil the root of celery (JCLP_186) and of a radish (JCLP_176) and leek (JCLP_169) with wine (JCLP_144) and let him drink it. 5. Boil the root of fennel (JCLP_123) and of celery (JCLP_186) with good old wine (JCLP_099) and let him drink it. 6. Let him eat crabs (JCA_1918) and let him also drink their juice. 7. Hazelwort (JCLP_025) pennyroyal (JCLP_040) and pepper (JCLP_154); let him drink with wine (JCLP_144) in the bath but let them boil first. 8. Crush the seed of celery (JCLP_186) and seven cloves of garlic (JCLP_197) together, boil with wine (JCLP_099) and let him drink. 9. Pound JCLP_035 and let him drink its juice. 10. Boil chamomile (JCLP_227) with water (JCLM_022) and let him drink. 11. Let him drink laurel oil (JCLP_049) with wine (JCLP_144) in the bath. 12. Boil the root of asparagus (JCLP_026) and willow (JCLP_072) with white wine (JCLP_099) and let him drink. 13. Boil plantain (JCLP_152) and maidenhair (JCLP_004) with water (JCLM_022) and let him drink. 14. Chop the feet and wings and head of a JCA_2158 and weigh them so that they come equal to four kernels and let him drink.\n240. On dysentery. The seed of fenugreek (JCLP_212) roasted in the sun and lentils (JCLP_219) and ink-gall (JCLP_085) and cumin (JCLP_105). Grind it all and let him drink with warm wine (JCLP_144) in the morning on empty stomach. 2. Let him drink the juice of JCLP_035 with wine (JCLP_144) and water (JCLM_022) warm in the morning.\n241. It brings down the menstruation of women and the urine (JCA_2332) and expels children from the womb and is useful for the spleen. Boil the plant called germander (JCLP_226) with wine (JCLP_144) and let her drink. 2. Fumigate all heal (JCLP_224) from below. 3. Crush all heal (JCLP_224) and put it outside on the hidden area of the woman. 2. Crush indigo (JCLP_117) and nigella (JCLP_126) and macerate with honey (JCA_0172) and make a cloth (JCLP_151) like a knot, put it inside and sew it together and give it to another woman and let her put it into her womb with her hand. Bind a thread to the knot and if you want to remove it pull the thread and you will take it out. This is called pessary by the doctors. 3. Make fresh all heal (JCLP_224) in a pessary.\n242.[174] For external and internal hemorrhoids. Boil the skin of a snake (JCA_2345) in table oil (JCLP_232) and put it on top of coals (JCX_0499) that are set on fire and fumigate, so that the smoke rises up to the affected area. 2. Boil the bark of the root of JCLP_150 with wine (JCLP_099) and let him drink inside the bath. And let him be fasting for four hours. 3. Sprinkle the flour of lupine (JCLP_118) on top once you have sieved it but first wipe them with wine (JCLP_099). 4. Grind the seed of the kernels of laurel (JCLP_049) and collect the juice and the heart of the kernels and make these fine and sprinkle it on top. 5. Burn the head of a tuna (JCA_1890) or a salted bonito (JCA_2359), the one that you have and sprinkle its ashes (JCX_0126) on top. 6. Crush dry equisetum (JCLP_069) that is called equisetum (JCLP_163) and let him drink with wine (JCLP_144). 7. Fry the root of equisetum (JCLP_163) in a pan with table oil (JCLP_232) and apply. 8. Crush lead white (JCLM_042) and mix it with milk (JCX_0085) of a woman (JCX_0118) and apply. 9. Grind the root of lily (JCLP_101) and mix it with barley flour (JCLP_100) and also add water (JCLM_022) and boil it and spread it on a cloth (JCLP_151) and put it on top. 10. Mix donkey (JCA_0619) milk (JCX_0085) and crushed JCX_0404 and apply. 11. Pound JCX_0114 and JCLM_031 and unify and apply. 12. Boil the seed of a mulberry tree (JCLP_208) and plantain (JCLP_152) with water (JCLM_036) and let him drink. First wipe the area with vinegar (JCLP_142), then take burnt leaves of reed (JCLP_075) and sprinkle them on top. Crushed dry soft dung (JCA_0254) of a dog (JCA_0920), rinse the area first with wine (JCLP_144) then sprinkle it on top. Burn yolk (JCX_0114) of an egg (JCA_0105) and sprinkle it on top.\n243.[175] For a person of whom the anus prolapses. Take crushed JCX_0404 and lead white (JCLM_042) and add wine (JCLP_099) and macerate and then apply. 2. Melilot (JCLP_128) and dry roses (JCLP_181) and crushed lead white (JCLM_042). Add also wine (JCLP_099) and boil it and then apply to the area. 3. Boil a mushroom (JCO_1450) with water (JCLM_036) and pound it and mix it with butter (JCA_0330) and macerate and apply to the area with your finger. 4. First apply wine (JCLP_099) to the area then take crushed fine sieved millet (JCLP_082) bran (JCLP_160) and sprinkle it on top like this and then put his colon back inside that has been anointed with bran (JCLP_160) of the millet (JCLP_082).\n244. If someone has flat worms. Do this treatment. Grind cress seed (JCLP_077) and crushed pepper (JCLP_154) and let him drink with water (JCLM_022) in the morning on empty stomach. 2. Grind nigella (JCLP_126) and let him drink it with unmixed wine (JCLP_099) or with fish (JCA_0526) sauce (JCA_0489). 3. Grind all heal (JCLP_224) and let him drink it with wine (JCLP_099). 4. Grind all heal (JCLP_224) and put it onto the navel of the person. 5. Grind the seed or the leaves of JCLP_096 and let him drink them with water (JCLM_022). 6. Let him eat garlic (JCLP_197) with old table oil (JCLP_232). 7. Pound fresh mint (JCLP_063) and let him drink the juice in the morning. 8. Mix crushed cumin (JCLP_105) with the bile of a bull (JCA_0466) and put it onto the belly button. 9. Macerate the flour of lupine (JCLP_118) with honey (JCA_0024) and put it on top. 10. Grind coriander (JCLP_091) finely and unify with table oil (JCLP_232) and put it onto the belly button. 11. Grind hemp seed (JCLP_238) and let him drink it with water (JCLM_022). 12. Boil tender stems of cabbage (JCLP_098) that is the tips with clean water (JCLM_022) then take one hexagion of the water (JCLM_022) and coarse salt (JCLM_002) one hexagion and he will expel the seed of the worms. 13. Grind the flour of lupine (JCLP_118) and wormwood (JCLP_028) and add laurel oil (JCLP_049) and macerate all together put it onto the navel.\n245.[176] For ekbata and aporyfas. Beetroot (JCLP_189) is useful and mix the juice with cereal (JCLP_194) flour and macerate them together and put it on top. 2. Macerate oak mistletoe (JCLP_067), crushed glass (JCLM_034) and JCX_2547 and table oil (JCLP_232) and put it on top. 3. Grind the green leaves of reed (JCLP_075) and mix the juice with very finely grated lead (JCLM_024) and macerate and put it on top. 4. Mix black crushed JCU_0278 with propolis (JCA_0710) and macerate and put it on top. 5. Crush dung (JCA_0254) of a wild pigeon (JCA_1393) and unify and macerate with honey (JCA_0024) and put it on top. 6. Crush dung (JCA_0254) of a goose (JCA_0543) and unify it and macerate with honey (JCA_0024) and put it on top. 7. Pound the root of monk's rhubarb (JCLP_111) and macerate with lard (JCA_0077) of a pig (JCA_0266) and put it on top.\n246. If someone urinates at night involuntarily. Do this treatment. That is boil JCLP_167 with wine (JCLP_099) and let him drink. 2. Crushed myrrh (JCLP_133) and the juice of JCLP_167 with wine (JCLP_099), let him drink it. 3. Let him drink the burnt hooves of a black pig (JCA_0952) with wine (JCLP_144). 4. Burn the bladder of a goat (JCA_0965) and let him drink it with vinegar (JCLP_142) and wine (JCLP_099). 5. Let him eat the tongue of a goose (JCA_0543). 6. Grind the kernels of laurel (JCLP_049) and the seed of rue (JCLP_157) and mix it and unify with rose oil (JCLP_181) and apply it to the crotch of the person. 7. Let him drink the testicles of a hare (JCA_0453) with good wine (JCLP_099). 8. Let him eat for three days the seed of wild rue (JCLP_157) that have been roasted in the sun. 9. Burn the throat of a crow (JCA_2385) and let him drink the ashes (JCX_0126) with wine (JCLP_144).\n247.[177] If someone is bitten by a viper. Pound rue (JCLP_157) and let him drink the juice. 2. Crush what is called by the doctors black cardamom (JCLP_018) and let him drink it with the juice of rue (JCLP_157). 3. Mix crushed mustard (JCLP_192) and cress seed (JCLP_077) with vinegar (JCLP_142) and apply.\n248.[179] For migraine. The entrails (JCX_0794) of the earth (JCX_0773) that is the large worms with which people catch the fishes (JCA_0594): roast these on the stove and mix in fifteen crushed kernels of pepper (JCLP_154) with vinegar (JCLP_142) and apply to the head. 2. Add ground dung of a wild pigeon (JCA_1392) to vinegar (JCLP_142) and apply. 3. Boil the seed of agnus castus (JCLP_115) with table oil (JCLP_232) and grind and apply to the forehead and the temples. 4. Macerate live lime (JCLM_007) with honey (JCA_0024) and apply. 5. Put the heart of rue (JCLP_157) into the ear and bind the head tightly and cover it well. 6. Grind bitter almonds (JCLP_017) and crushed mastic (JCLP_125) and mix it with vinegar (JCLP_142) and apply to the forehead. 7. Pound the tender shoots of ivy (JCLP_087) and mix the juice with rose oil (JCLP_181) and vinegar (JCLP_142) and apply. 8. Put dry leaves of rhododendron (JCLP_180) on burning coals (JCLM_015) and fumigate into the nose.\n249.[180] If someone is suffering from sciatica. Boil chickpeas (JCLP_055) with water (JCLM_022) and let him eat and let him drink the broth. 2. Boil the bark of the so-called wheat (JCLP_059) with water (JCLM_022) and let him drink. 3. Grind mustard (JCLP_192) and pepper (JCLP_154) and mix it with honey (JCA_0024) and apply. 4. Bind the root of cyclamen (JCLP_104) or laurel (JCLP_049) to the place. 5. Crush aloe (JCLP_012) and pine resin (JCLP_177) and pepper (JCLP_154) and put it on top on the area but first anoint the area with honey (JCA_0024). 6. Boil the leaves of cabbage (JCLP_098) and mix the ashes (JCX_0126) with lard (JCA_0077) of a pig (JCA_0266) and put it on top. 7. Boil table oil (JCLP_232) and fatty resinous wood (JCLP_046) and apply to the area. 8. Anoint the area where the pain is with the so-called JCU_1574. 9. Let him eat boiled garlic (JCLP_197) with table oil (JCLP_232), and fish (JCA_0526) sauce (JCA_0489). 10. Pound pennyroyal (JCLP_040) and pepper (JCLP_154) and macerate with water (JCLM_022) and put it on top. 11. Mix butter (JCA_0330) with dill oil (JCLP_073) and apply to the area. 12. Burn tendril (JCLP_090) and mix the ashes (JCX_0126) with liquid pitch (JCLP_244) and put it on top. 13. Pound the so-called JCLP_038 and mix its juice with bran (JCLP_160) and put it on top. 14. Pound the root of cyclamen (JCLP_104) and put it on top. 15. Hang the root of cyclamen (JCLP_104) around his neck. Pound the root of JCLP_051 and put it on top. Pound the root of JCLP_051 and let him drink the juice.\n250.[181] For those suffering from jaundice that is if their face gets yellow. Grind yellow orpiment (JCLM_006) and mix it with yolk (JCX_0114) of an egg (JCA_0105) and let him drink inside the bath. 2. Grind centaury (JCLP_084) and let him drink it with water (JCLM_022) in the bath. 3. Grind nigella (JCLP_126) and ginger (JCLP_060) and add vinegar (JCLP_142) and macerate and drip this vinegar (JCLP_142) into his nostrils. 4. Boil the root of cyclamen (JCLP_104) with wine (JCLP_099) and let him drink it warm. 5. Put the kernels of carob (JCLP_139) into wine (JCLP_099) and leave them for one day and one night, then let him drink the wine (JCLP_099). 6. Crush hare (JCA_0453) dung (JCA_0254) and let him drink with wine (JCLP_144). 7. Grind celery seed (JCLP_186) and let him drink with wine (JCLP_144) in the bath. 8. Let him drink boiled pennyroyal (JCLP_040) with wine (JCLP_099). 9. Boil fennel (JCLP_123) and dill (JCLP_073) and celery (JCLP_186) with water (JCLM_022) and let him drink. 10. Let him drink male calf (JCA_1215) and aquilaria agallocha (JCLP_138) and frankincense (JCLP_114) and castor (JCA_0145) and water (JCLM_036) of the holy Epiphany ceremony (JCO_1874) and gum ladanum (JCLP_110).\n251.[181] For leprosy. Grind the root of asphodelus (JCLP_027) and remove the juice. Grind also cress seed (JCLP_077) and the flour of darnel (JCLP_006) and unify these and macerate and add vinegar (JCLP_142) and apply to the leprous lesions. 2. Grind the root of asphodelus (JCLP_027) and collect the juice. Also crush sulphur (JCLM_033) and unify and apply to the leprous lesions.\n252.[182] For psora. Grind stavesacre (JCLP_003) and the seed of cress (JCLP_077) and add vinegar (JCLP_142) and macerate and apply it to the psora. 2. Grind the root of lily (JCLP_101) and mix it with honey (JCA_0024) and apply. 3. Grind sulphur (JCLM_033) and dung (JCA_0254) of a goat (JCA_1405) and add vinegar (JCLP_142) and apply it to the psora. 4. Boil the leaves of rhododendron (JCLP_180) with table oil (JCLP_232) then remove the leaves and add wax (JCA_0450) and crushed sulphur (JCLM_033) and apply to the psora in the sun. 5. Take rose oil (JCLP_181) and ground litharge (JCLM_018) and lead white (JCLM_042) and liquid pitch (JCLP_244) and vinegar (JCLP_142) and mix these and apply in the sun.\n253.[183] On lichen. Apply liquid pitch (JCLP_244) to the lichen. 2. Soak the tear of damson (JCLP_047) one day and one night in vinegar (JCLP_142) and apply. 3. Pound the leaves of agnus castus (JCLP_115) and put them on top or mix with vinegar (JCLP_142). 4. Crush the leaves of capers (JCLP_076) and mix them with vinegar (JCLP_142) and apply. 5. Grind frankincense (JCLP_114) and mix it with vinegar (JCLP_142) and apply. 6. Crush sulphur (JCLM_033) and mix it with vinegar (JCLP_142) and apply. This book comes to an end.",
"gender": "Female"
}
] |
PMC11109676
|
[
{
"age": 0,
"case_id": "PMC10838141_01",
"case_text": "A six-month-old male infant born post-term by cesarean section presented to our clinic with generalized blisters on the body. The blisters started to appear one month ago. The first lesion appeared on the left elbow area and later progressed to involve the other extremities, trunk, neck, and scalp. The most affected regions were the chest and back. The lesions were associated with severe itching, especially on the back, aggravated by rubbing and bathing. The parents denied any weight loss, vomiting, diarrhea, shortness of breath, or syncope. The infant was fed formula milk only. The parents did not relate any medication use as an exacerbating factor. The last vaccination was two months ago at the age of four months. The patient had no family history of any hematologic or dermatologic disease and did not have any significant developmental, medical, drug, surgical, or social history. Physical examination of the skin showed multiple tense vesicles and bullae mainly on the trunk. The underlying skin was diffusely thickened and erythematous, having an orange peel (peau d'orange) appearance (Figures 1A, 1B). Darier sign was not demonstrated; however, dermographism was demonstrated on the back and appeared positive (Figure 1C). Palms and soles were spared. Hair, nail, mucosae, and general physical and systemic examination revealed no abnormality.\nGiven the skin findings, our differential diagnosis included bullous mastocytosis, linear IgA bullous dermatosis, childhood bullous pemphigoid, and epidermolysis bullosa simplex, Dowling-Meara type. A complete blood cell count with differentials, C-reactive protein, liver, and renal function tests were within normal limits. Skin biopsies were obtained from three different skin lesions, including the bullous lesion, the infiltrative plaque, and the perilesional skin. Histological examination of the skin showed a subepidermal blister and a generalized infiltration of monomorphic granular cells concentrating within the papillary dermis with a few eosinophils (Figure 2). Giemsa stain was taken up by almost all infiltrating cells which confirmed the increased mast cells (Figure 3). Direct immunofluorescence was negative for IgG, IgA, and C3 which ruled out other immunobullous diseases and confirmed the diagnosis of bullous mastocytosis (Figure 4).\nThe parents were instructed to avoid all mast cell degranulation triggers such as shellfish, extremes of temperature, vigorous rubbing or friction, photo-exposure, drugs including sympathomimetics, non-steroidal anti-inflammatory drugs, narcotics, dextran, systemic anesthetics, and radiological contrast dyes. In addition, the patient was treated with cetirizine 2.5 mL syrup daily and mometasone 0.1% cream on the affected areas. A follow-up examination one week later revealed drastic improvement. The skin started to heal, the erythema reduced markedly, and no new vesicles developed (Figure 5).\nGiven the slightly increased risk of anaphylaxis in children with diffuse cutaneous mastocytosis, the patient was referred to pediatric hematology to prescribe an epinephrine auto-injector and exclude systemic mastocytosis. So far, the patient has been tested monthly for tryptase levels which were elevated, and the last test result was 82.2 mug/L. An abdominal ultrasound was also done which was normal.",
"gender": "Male"
}
] |
PMC10838141
|
[
{
"age": 2,
"case_id": "PMC10587696_01",
"case_text": "A thirty-two-year-old male from Bangladesh presented with a two-month history of intermittent fever. It was high-grade and used to subside with over-the-counter medications. He was a known patient of diabetic nephropathy for the last 3 years and initiated on maintenance hemodialysis for the last six months before presentation. He complained of right upper and lower limb weakness three days back which was progressive in nature with difficulty in standing and walking. There was no history of seizures, altered sensorium, vomiting, diplopia, and blurring of vision. There was no history of cough, shortness of breath, nasal blockage, sinus pain, or epistaxis.\nHe was evaluated and found to have normocytic normochromic anemia - 8.7 gm/dl. The total leukocyte count was 10,600 / cu mm. HIV status was negative. Brain MRI was performed to look for any space-occupying lesion in the brain as a part of right-sided hemiparesis evaluation. It showed an 18 x 20 mm, irregular, T2 hypointense lesion with central hyperintensity, diffusion restriction, and significant perilesional edema in the left cingulate region causing mass effect on the body of the corpus callosum and left lateral ventricle (Fig. 1). As the MRI suggested brain abscess immediate left frontoparietal craniotomy and excision were performed to drain the same. Abscess was seen at a depth of about 5 mm from the brain surface. The surrounding white matter was edematous. Intraoperatively the lesion seems to be yellowish, firm, friable, and avascular with surrounding edema. Total excision was performed and samples were sent for cultures and histopathology. Intra-operative pus grew filamentous septate fungi with pigmented walls on Saboraud's dextrose agar (Fig. 2). Speciation was done based on fungal morphology showing ellipsoidal to fusiform, dry conidia with pigmented hila arranged in branched chains and polymerase chain reaction detected it to be Cladophialophora bantiana. Bacterial culture and gene Xpert for mycobacterium tuberculosis were both negative. Antifungal susceptibility was performed in our inhouse microbiology laboratory and the MICs were as follows.\nHe was started on a combination anti-fungal regimen comprising injection liposomal amphotericin B at a dose of 5 mg/kg body weight and tablet voriconazole 400 mg twice a day for one day as a loading dose followed by 200 mg twice daily. He started to improve with defervescence and subsidence of headaches. Amphotericin B was given for initial 10 days and voriconazole was continued thereafter. Voriconazole trough level was measured and found to be adequate.\nHis sensorium was normal during discharge but hemiparesis was only partially improved. He was mobilized with active physiotherapy. Anti-fungal treatment was planned for a total of one year and he is under our close follow up as outpatient basis.",
"gender": "Male"
}
] |
PMC10587696
|
[
{
"age": 60,
"case_id": "PMC10834088_01",
"case_text": "A 60-year-old man originating from Sri Lanka presented to our emergency department with upper abdominal pain and diarrhea, sometimes accompanied by small amounts of fresh blood. Personal history included hypothyroidism under substitution with levothyroxine and asthma treated with formoterol/budesonide as needed. Travel and environmental history were unremarkable, family history for inflammatory bowel disease (IBD) was negative, no allergies were reported, and the patient denied the use of nicotine, alcohol, or illicit drugs. Clinical examination was unremarkable, and routine laboratory analysis showed no signs of inflammation. Abdominal computed tomography displayed discrete thickening of the intestinal wall due to possible colitis. The patient was treated symptomatically, and a follow-up endoscopic investigation was planned in an outpatient setting. A few days before the endoscopy, the patient presented again with acute deterioration, fever, abdominal pain, and persistent watery and bloody diarrhea.\nAt readmission, the patient presented in markedly reduced general condition, subfebrile (37.9 C), hypotensive, and bradycardic (92/57 mmHg, 48 bpm). Respiratory rate and oxygen saturation while breathing ambient air were within normal ranges. Physical examination revealed a distended abdomen with normal bowel sounds and diffuse tenderness on palpation with defense. Cardiac and pulmonary auscultation were unremarkable.\nLaboratory analysis now showed elevated leucocytes (10.7 x 109/microL) and C-reactive protein (225 mg/L), moderate normocytic normochromic anemia (hemoglobin 9.5 g/dL), elevated aminotransferases (ALAT 106U/L, ASAT 52U/L) and a mild hypokalemia. Serum lactate was normal. An abdominal CT scan showed progressive thickening of the intestinal wall. Additionally, splenic lesions, most likely of embolic origin, were found (Figures 1 and 2). Empiric antibiotic treatment with ceftriaxone and metronidazole was started, and a diagnostic test was performed.\nRecto-sigmoidoscopy revealed severe, left-sided erosive colitis. The biopsies showed moderate inflammation with neutrophilic crypt abscesses, indicating a diagnosis of ulcerative colitis. Oral and rectal mesalazine was added.\nTransthoracic and transesophageal echocardiography were normal, with no evidence of endocarditis, intracardiac thrombus, or persistent foramen ovale.\nBlood cultures showed no growth, and stool tests, including campylobacter, salmonella, shigella/EIEC, yersinia, clostridioides, parasites, and helminths, were negative. Serology for HIV, hepatitis A, B, C, EBV, CMV, and interferon-gamma tests were negative.\nIn the following days, the general condition progressively deteriorated with persistent fever and increasing inflammatory markers. Repeated endoscopy showed improvement of the colitis, and a CT scan showed enlarging splenic lesions. Skin examination revealed purulent bullae at various locations (Figures 3 and 4). Of note, abscesses developed within a few hours at explicit sites following puncture (pathergy effect). In addition, pain, redness, and swelling of several joints (i.e., right knee, left elbow, left metatarsal, right hand) were observed. Arthrocentesis of the left elbow drained 15 mL of putrid fluid, and differential cell analysis showed 76,000 cells/microL (95% neutrophils). A diagnostic puncture of the splenic lesions was performed and revealed a large amount of putrid fluid.\nEmpiric antibiotic therapy was escalated to piperacillin/tazobactam until negative microbiological test exams were received, including direct microscopy, culture, and eubacterial polymerase chain reaction. A timeline of inflammatory biomarkers, diagnostic investigations, and therapeutic regimens is provided in Figure 5. The patient remained hemodynamically stable.",
"gender": "Male"
}
] |
PMC10834088
|
[
{
"age": 15,
"case_id": "PMC10866739_01",
"case_text": "This case pertains to a 15-year-old male who presented with multiple congenital cardiac anomalies and received a diagnosis of BRWS at the age of seven. The patient exhibits phenotypic features consistent with BRWS, including hypertelorism, protruded tongue, wide nasal bridge, low-set ears, low posterior hairline with neck webbing and axillary pterygium. Additionally, the patient demonstrates an intellectual disability, evidenced by difficulty reading and limited verbal communication skills. At the age of six, Noonan syndrome was initially considered due to cardiac anomalies and suggestive dysmorphic features. However, Noonan syndrome was ruled out after the genetic testing for PTPN11, RAF1, SOS1, and SHOC2 yielded no pathogenic variants, and chromosomal analysis revealed a normal karyotype. Subsequently, the patient was diagnosed with BRWS based on clinical phenotype and the identification of a heterozygous pathogenic variant in the ACTG1 gene (c.50G>A; p.C17Y) through whole exome sequencing.\nSince birth, the patient has presented with multiple medical issues, including congenital bicuspid aortic valve with severe aortic valve insufficiency, myxomatous mitral valve with prolapse of anterior and posterior leaflets, and mild mitral regurgitation. Furthermore, the patient has experienced delayed developmental milestones, a horseshoe kidney, and a complete corpus callosum with thinning of its distal part. Given the complexity of the patient's condition, a multidisciplinary team consisting of a pediatrician, genetics specialist, urologist, and cardiologist has been involved in the patient's care.\nThe patient underwent regular follow-ups at the cardiology outpatient department and was well-controlled and asymptomatic while on lisinopril until the age of 13, when he began experiencing progressive shortness of breath and fatigue during exertion. This deterioration in his condition necessitated a surgical intervention, and he was scheduled for an elective Ross procedure in May 2022. Upon admission for the procedure, the patient reported experiencing exertional dyspnea classified as New York Heart Association (NYHA) class 2. A cardiovascular examination revealed a wide pulse pressure and a grade II-III diastolic murmur at the left sternal border. Prior to the procedure, the most recent chest X-ray images showed bilateral clear lung fields, with no signs of consolidation, pneumothorax, or pleural effusion (Figure 1). Additionally, echocardiogram views confirmed the presence of a dysplastic bicuspid aortic valve, severe aortic valve insufficiency with reversed flow at the abdominal aorta, myxomatous and significantly prolapsing mitral valve with both anterior and posterior leaflets exhibiting mild mitral valve insufficiency, and mild left ventricular dilation with normal left ventricular systolic function (Videos 1-3). This comprehensive assessment provided crucial information for planning the patient's upcoming elective Ross procedure. Based on the existing records, the patient underwent a Ross procedure through a median sternotomy incision. The procedure involved the transection of the aorta, excision of the aortic valve, mobilization of the coronary buttons, and extraction of the pulmonary autograft. Subsequently, the neo-aortic valve was implanted, and the coronary buttons were reattached. He had a smooth intra-operative course, and an intraoperative trans-esophageal echocardiography (TEE) revealed a severe aortic valve insufficiency (Figure 2), which was promptly repaired during the procedure, resulting in good myocardial function with no significant residual lesions.\nOn the second day post-procedure, seven intact midline sternotomy wires and an epicardial pacing wire, along with interval development of bilateral medial upper lobes and lower lung zone airspace opacities were noted (Figure 3). The patient was transferred to the Intensive Care Unit in a stable condition afterwards and was successfully extubated on the following day without any complications. However, on the seventh post-operative day, the patient experienced recurrent spikes of high-grade fever, prompting the initiation of empirical antibiotics and the involvement of infectious disease (ID) team. A work-up of urine culture, blood culture, Brucella abortus, Brucella melitensis, nasopharyngeal aspirate, and Q fever all yielded negative results. A chest computed tomography (CT) revealed a suprasternal collection with pre-sternal and retrosternal extension. In response, the ID team recommended a two-week course of vancomycin (10 mg/kg) and meropenem (20 mg/kg) and advised a repeat chest CT after this period. Subsequent CT scans indicated a moderate dehiscence of the sternotomy at the manubrium, potentially associated with the local infection. As a result, the antibiotic course was extended for an additional two weeks, and another chest CT was scheduled after this period, which showed a reduction in the size of the collection, necessitating an additional two weeks of antibiotics. Following consultation with the relevant cardiac surgery team, it was determined to discharge the patient and closely monitor their progress in the outpatient department. The ID team recommended a two-week course of oral ciprofloxacin and clindamycin upon discharge. A month later, the patient was discharged in a stable condition and prescribed angiotensin-converting enzyme inhibitors (ACEI) and aspirin. The last echocardiography before discharge revealed no obstruction in the left ventricular outflow tract (LVOT), trace neo-aortic valve regurgitation, unobstructed right ventricle-pulmonary artery (RV-PA) conduit, mild conduit valve regurgitation, mitral valve prolapse with mild regurgitation, mild tricuspid valve regurgitation, unobstructed PA branches, unobstructed aortic arch, no echo evidence of vegetations, mild reduction in left ventricular systolic function, and no pericardial effusion (Video 4).\nA year later, the patient was assessed in the outpatient clinic and was found to be clinically stable while taking a daily 81 mg aspirin tablet and a 2.5 mg ACEI tablet (lisinopril). The echocardiogram done then revealed normal aortic valve velocity, mild aortic valve insufficiency, normal pulmonary artery conduit gradient, mild pulmonary artery conduit insufficiency, no stenosis in the right or left pulmonary artery, thickened prolapsed mitral valve leaflets, moderate mitral valve insufficiency, dilated left ventricle, and preserved left ventricular function (Videos 5, 6).",
"gender": "Male"
}
] |
PMC10866739
|
[
{
"age": 32,
"case_id": "PMC11152519_01",
"case_text": "We present a 32-year-old male patient, a right-handed athlete, who presented with a bilateral (predominantly right upper limb) abduction paresis of 12 months duration, associated with progressive paresthesias and changes in the coloring of the upper limbs. As an important history before the consultation, he had been diagnosed with vascular Thoracic Outlet Syndrome in another institution for which he had undergone surgery. The right first rib had been resected in that procedure with an axillary approach on that side. After surgery, the patient developed persistence of previous vascular symptoms and loss of flexion strength in the right shoulder. On physical examination at our clinic, we observed a right-winged scapula together with an absence of commitment of the deltoid, triceps, supraspinatus, and infraspinatus muscles [Figure 1]. Magnetic resonance imaging of the right scapular region ruled out structural joint lesions at the level of the rotator cuff and the remaining ligament and muscle structures. The suspected diagnosis was traumatic injury of the long thoracic nerve, which was confirmed by electromyographic studies. The patient underwent physical therapy for 6 months without improvement. We, therefore, decided to perform surgical treatment 8 months after the onset of symptoms by means of a nerve transfer from the thoracodorsal nerve to the right long thoracic nerve. The reason for this indication was the absence of improvement in the paralysis observed up to that moment. The patient was positioned in dorsal decubitus, with the right upper limb in 90 abduction. A 15 cm skin incision was made on the right mid-axillary line, following the free border of the latissimus dorsi muscle. Dissection of the subcutaneous cellular tissue and aponeurosis of the latissimus dorsi muscle was continued until the right thoracodorsal nerve was identified by dissection and neurostimulation. Subsequently, the aponeurosis of the serratus anterior muscle was opened, which allowed the identification of the right long thoracic nerve, which had not responded to intraoperative motor stimulation [Video 1]. A donor branch of the right thoracodorsal nerve of similar size to that of the recipient was repaired to perform a nerve transfer in which the former would function as the axon donor and the latter as the recipient [Figure 2]. End-to-end neurorrhaphy was performed under microscopic magnification using a 9-0 nylon microsuture. Fibrin glue was used to coat the repair.\nA bandage was applied to immobilize the patient's shoulder in adduction and internal rotation for 2 weeks, after which physical therapy sessions were started with activation movements for the latissimus dorsi and pectoralis major muscles, 5 times a week for 90 min during the first 3 months, and then continued for the same duration, 3 times a week. During the sessions, the exercises described by Ray et al. were carried out, with evident and progressive results from the 4th month of physiotherapy.\nThe patient was monitored 6 months after surgery, with partial improvement of the winged scapula and good recovery of flexion and function of the right shoulder. At 12 months, there was complete resolution of the winged scapula, with full functional recovery and muscle strength of both the latissimus dorsi and pectoralis muscles. The patient reported that he was able to complete all his routine activities normally and also showed a decrease in preoperative pain with Visual Analog Scale, 5/10-2/10 [Figure 3].",
"gender": "Male"
}
] |
PMC11152519
|
[
{
"age": 66,
"case_id": "PMC11075582_01",
"case_text": "We report a rare case of a 66-year-old woman, who exhibited bilateral proptosis, diminished visual acuity, retrobulbar pressure, headaches, and orbital pain associated with swelling of the temporal region, over the course of recent months. The patient's condition prompted her visit to the emergency department due to worsening visual symptoms and excruciating headaches. A thorough physical and ophthalmological examination revealed stable hemodynamic and neurological status, alongside a noteworthy reduction in visual acuity and more pronounced right-sided exophthalmos.\nSubsequent cerebral MRI showed bilateral hyperostotic changes of greater wing sphenoid bone displaying hypo intensity on both T1 and T2 sequences (Figure 1) associated with bilateral thickening and enhancement of the dura in the anterior temporal area invading the cavernous sinus, the prechiasmatic portion of the optic nerve, and the lateral rectus muscle bilaterally more pronounced on the right side through the superior orbital fissure causing bilateral exophthalmos (Figure 2).\nA post-contrast sagittal MRI image showed thickening and enhancement of the free border tentorium cerebelli and the dura in the retroclival region (Figures 3 and 4).\nGiven the bone involvement, our initial differential diagnosis encompassed Paget's disease and fibrous dysplasia. Endoscopic transsphenoidal biopsy has been achieved to confirm the diagnosis immunohistologically. This confirmation is essential for determining the appropriate course of action depending on the nature of the lesion (benign or malignant). The pathological examination confirmed the infiltration of the bone by meningioma cells. Additional therapeutic interventions were deemed unnecessary. Following the definitive diagnosis, the patient was admitted to the neurosurgery department, where a subtotal but extensive removal combined with bony decompression of the cranial nerves at the superior orbital fissure and optic canal was achieved. Subsequently, our patient was referred to the radiotherapy department for further management, where a treatment protocol was established. The postponement of the cranioplasty to a later date was decided. Due to the increased likelihood of recurrence associated with the bilateral nature of the condition and the extent of infiltration of adjacent structures, the neurosurgery team opted for regular monitoring, with MRI scans every 3 months, over a period of approximately 2 years. If there are no signs of recurrence in the patient during this period, cranioplasty will be considered.\nAfter surgery and having completed all his radiotherapy sessions, follow-up MRI scans showed no obvious signs of recurrence over 1.5 years.",
"gender": "Female"
}
] |
PMC11075582
|
[
{
"age": 67,
"case_id": "PMC11440934_01",
"case_text": "A 67-year-old unemployed, Catholic, right-handed man with a 7-year history of primary hypothyroidism treated with levothyroxine 75 microg and intermediate-risk prostate adenocarcinoma (Gleason 4 + 3 = 7 and ISUP 3), with a low prostate-specific antigen (PSA) of 0.01 ng/dl, rising to 2 ng/dl, and last reported at 4.5 ng/dl with a doubling time of 3 months, was treated with radical prostatectomy and subsequent hormonal blockade (6-monthly application of leuprorelin). A clinical picture of 8 months of evolution is added with muscle weakness and fasciculations in the lower limbs that led to falls, 1 month after these symptoms he presented changes in the tone of voice and difficulty articulating words..\nIn addition, the patient initially presented dysphagia with liquids, which has progressed to solids. In the last month, he has experienced increased difficulty in breathing and in fasciculations. He has noticed weight loss, with a decrease in muscle mass very noticeable in his legs. In the neurological assessment, he was described as follows: alert; oriented in person, time, place, and circumstance; not fluent in the language, names, repetition, and understanding; flaccid dysarthria; judgment and abstraction without alliteration; and unaltered semantic and declarative memory. His gait was supported by a walker. In the evaluation of the cranial nerves, ocular movements with a limitation to supraversion, hypometric saccades, increased masseteric reflex, a central uvula, asymmetric elevation of the soft palate, decreased gag reflex, a tongue with hypotrophic edges, and fasciculations at rest were found. The strength in the upper extremities was preserved but the strength in the lower extremities was decreased by 3/5 proximal and 4/5 distal. He had an unaltered tone. Muscle tone without alterations. Hypotrophy in interosseous muscles and pelvic limbs. Biceps, triceps, styroradial, patellar, and bilateral Achilles reflexes were increased (+++/++++). There were fasciculations in all four extremities and in the tongue. Exteroceptive and proprioceptive sensation without alterations. Therefore, they integrated the following diagnoses 1. upper motor neuron syndrome and 2. lower motor neuron syndrome, probable ALS.\nThe neuropsychiatric assessment documented easy crying, sometimes feeling unmotivated, sometimes accompanied by laughter, and a greater deterioration of speech and memory (the patient writes on a cell phone to communicate). In addition to the probable picture of ALS, the probable coexistence of FTD was also considered.\nIt complements the diagnostic approach with EMG, which showed fibrillations and positive sharp waves, fasciculation potentials, increased amplitude and polyphasia. The MRI scan showed only data of generalized atrophy (Figure 1) and the 18F-FDG PET/CT scan of the brain (Figure 2) showed decreased metabolism in the cortex of the primary motor area and bilateral premotor, bilateral anterior cingulate, mild to moderate right temporal neocortex in its polar portion with extension to the entorhinal cortex, both caudates, and the posterior third of the putamen. Due to the antecedent of prostatic adenocarcinoma and suspicion of biochemical recurrence, an 18F-PSMA-1007 PET/CT scan was performed, which showed at least four bone-level uptake sites in the left seventh costal arch and sacrum without morphological translation (Figure 3).",
"gender": "Male"
}
] |
PMC11440934
|
[
{
"age": null,
"case_id": "PMC10513384_01",
"case_text": "In this case, the patient presented at 15 years of age with bone pain and splenomegaly. Routine laboratory values at the time showed a white blood cell (WBC) count of 28.8 x 103/mul and a hemoglobin level of 10 g/dl. Fluorescence in situ hybridization (FISH) was positive for BCR::ABL1. She was started on imatinib at this time. A high level of the BCR-ABL p210 transcript was detected at 58% IS at diagnosis and then detected at 103% IS. There was no p190 detected at diagnosis or during disease course.\nOn diagnosis, she was started on Imatinib 400 mg daily and achieved complete hematologic response (CHR) at 6 months and complete cytogenetic response (CCR) at 9 months. Records of her treatment response during this time are incomplete, and it is unclear whether she ever achieved a major molecular response MMR. Subsequently, she developed side effects of Imatinib including rash and periorbital edema leading to discontinuation in 2013. She was started on Nilotinib and had myalgias leading to discontinuation after 3 months. The degree of response that she achieved on nilotinib is unknown. She was initiated on Dasatinib in 2016 but this did not lead to improvement of side effects as she developed a rash and asthenia. This was again discontinued after 6 months. In June 2018, she was re-trialed on Dasatinib, but she discontinued it due to intolerable side effects. The degree of response she achieved on Dasatinib is unknown. In July 2019, she presented with hyperleukocytosis and a WBC of 32 x 103/mul and was treated with hydroxyurea. A bone marrow biopsy was performed, which was markedly hypocellular. She was restarted on Dasatinib 100 mg between July 2019 and March 2020. She was due for bone marrow transplant (BMT) but because of her intermittent adherence with TKIs, she was not a BMT candidate. While on Dasatinib, she developed persistent pancytopenia with platelet count as low as 11,000 despite dose reduction from 100 mg to 50 mg to 25 mg. She was given a course of steroids due to suspicion of immune thrombocytopenic purpura (ITP). She was transfusion dependent most of 2020. Dasatinib was discontinued due to pancytopenia. She was restarted on Nilotinib but again developed whole-body rash. Bone marrow biopsy in December 2020 showed CML with cellularity of 50% and hyper-lobulated megakaryocytes.\nIn March 2021, she transferred care to our center. She was initiated on Bosutinib 400 mg along with Eltrombopag in an effort to improve her transfusion-dependent thrombocytopenia. BCR-ABL1 PCR was 56% (IS) at the time. In May 2021, she underwent a bone marrow biopsy that was performed to evaluate her ongoing lack of molecular response and pancytopenia. This showed normal lymphocyte morphology and normal platelet morphology. Her granulocyte lineage showed a marked left shift; however, blasts were <1%, consistent with continued chronic phase. Next-generation sequencing (NGS) of the bone marrow aspirate showed the following mutations: ASXL1 p.Q976 alteration at 43% VAF, RUNX1 p.R201Q alteration at 27% VAF, and RUNX1 splice site alteration at 13% VAF. Given her lack of response to Bosutinib, she was switched to Ponatinib 30 mg. ABL sequencing was performed in April 2021 and May 2022 and both sequencing were negative for mutations.",
"gender": "Female"
},
{
"age": null,
"case_id": "PMC10513384_02",
"case_text": "Over the next year, she continued to have transfusion-dependent pancytopenia without evidence of molecular response to therapy ( Figure 1 ). She was once again evaluated for BMT; however, this process was repeatedly delayed due to social issues. In the spring of 2022, she was undergoing the final stages of workup for bone marrow transplantation, and required multiple admission for abdominal pain, nausea, vomiting, menorrhagia, and abdominal bleeding. Further workup at the time revealed a hemorrhagic cyst in the right ovary and hemoperitoneum. During this time, she continued to exhibit transfusion-dependent pancytopenia without obvious changes in kinetics. Hemoglobin remained stable before and after cyst rupture between 7.7 and 8.2. She was started on oral contraceptive (progesterone norethindrone) and an intrauterine device (IUD) was placed. Despite the aforementioned interventions, her symptoms persisted. She underwent diagnostic laparoscopy, which showed dense adhesions and firmness of the distal sigmoid colon and proximal rectum. Endoscopy and colonoscopy showed a tortuous colon, and mucosal petechiae in the stomach and colon. A biopsy of the colonic mucosa was unremarkable. Her pelvic pain continued, and she was found to have a ruptured ovarian cyst. A repeat bone marrow biopsy showed a hypercellular (>90%) marrow with 58% monocytes, and 13% marrow blasts/blast equivalents, consistent with progression to a CMML-like accelerated phase. In addition to blasts from bone marrow, the patient also had clonal evolution and splenomegaly while on therapy. Patient had leukocytosis greater than 10 x 109 (peak of 28.4). Basophils were not above 20%. NGS showed a new pathogenic IDH1 p.R132H mutation (27% VAF) and the previously detected RUNX1 splice site mutation (40% VAF), RUNX1 p.R201Q (1% VAF), and ASXL1 p.Q976 (39% VAF). During this hospitalization, she had symptoms of increased systemic inflammatory response including pleuritic chest pain and a large pericardial effusion with pericardial tamponade. Subsequent pericardiocentesis was performed with approximately 0.7 L of serous fluid initially removed and 4.22 L additionally drained. The etiology of pericardial tamponade was thought to be either pericarditis based on clinical presentation and electrocardiogram (ECG), or neoplastic, due to the abrupt onset of symptoms that coincided with progression to AP-CML. Pericardial fluid was sent for flow cytometric analysis and showed no evidence of lymphoma or acute leukemia with 37 monocytes seen on differential.\nShe underwent induction therapy with filgrastim, cladribine, cytarabine, and mitoxantrone (G-CLAM) for accelerated phase CML. Her bone marrow following G-CLAM treatment was hypocellular with no evidence of a myeloid neoplasm. NGS did not detect the previously identified IDH1, RUNX1, and ASXL1 variants, and quantitative PCR for the BCR::ABL1 transcript showed of 0.43% IS. As a bridge to BMT, she was started on ivosidenib, an IDH1 inhibitor.\nShe underwent stem cell transplantation from an unrelated donor. Currently, she is more than 100 days status post-transplant. Day +30 marrow studies showed a normocellular marrow with trilineage hematopoiesis and no increased blasts. Day +100 marrow studies showed hypocellular bone marrow with trilineage hematopoiesis, no increased blasts, and no definitive evidence of CML. Post-transplant, BCR::ABL1 remains undetectable by qPCR. NGS on day 30 and day 100 did not detect the previously identified IDH1, ASXL1, and RUNX1 variants. She achieved major molecular response (MMR) only after transplant. She did not achieve MMR while on TKIs.",
"gender": "Female"
}
] |
PMC10513384
|
[
{
"age": 63,
"case_id": "PMC11082382_01",
"case_text": "We report a rare case of warfarin resistance induced by ascorbic acid in a 63-year-old Chinese woman who underwent right modified radical mastectomy for breast cancer. She had a history of partial gastrectomy (reason unknown) more than 30 years ago and aortic valve replacement 16 years ago, and had been on warfarin anticoagulation since then. Her usual warfarin dose was 7.5 mg qd (once a day), and her INR was around 1.8. She also had thrombocytopenia (preoperative platelet count around 65*10^9^/L) and leukopenia since 2020. She presented with gingival bleeding 1 week before admission and subcutaneous ecchymosis on her left thigh on physical examination. She received interleukin-1 for thrombocytopenia. She was admitted on June 15 for breast cancer surgery and switched from warfarin to heparin sodium bridging (4000iu q12h, subcutaneous) based on the cardiothoracic surgery consultation, and discontinued it 1 day before surgery. She had the surgery on June 20 and resumed heparin sodium (4000iu q12h, subcutaneous) and warfarin anticoagulation (5 mg qd) on June 21, with an INR of 1.03. Heparin sodium was stopped on June 28. Warfarin anticoagulation was temporarily withheld due to incisional bleeding on June 24 (INR 1.13), and warfarin sensitivity gene testing was performed. Warfarin genetic testing primarily involves two genes: VKORC1 and CYP2C9. VKORC1 is the pharmacological target of warfarin, while CYP2C9 is the main enzyme responsible for its metabolism. Genetic variations in these genes can significantly influence an individual's response to warfarin, thus affecting the necessary dosage and overall efficacy of treatment. The gene test result showed CYP2C93(1075A>C) AA and VKORC1(1639G>A) GA genotypes, ruling out gene-related warfarin resistance. She was given ascorbic acid (0.2 g bid orally) and ferrous succinate tablets (0.2 g bid orally) to correct anemia due to hemoglobin 69 g/L on June 27. The reason for choosing ascorbic acid is based on the fact that following surgery, the patient exhibited symptoms of iron-deficiency anemia, a condition precipitated by sustained blood loss from the surgical incision. Moreover, it has been reported that, besides its antioxidant property, ascorbic acid can directly improve the sensitivity of the erythropoietin hormone and the uptake and recycling of iron. She restarted oral warfarin (6 mg qd) on June 29, but her INR did not return to the preoperative level (1.04-1.14) on July 1. The pharmacy department consultation suggested increasing warfarin to 10 mg qd on July 1, but the INR did not rise significantly after the dose adjustment. Upon comprehensive consideration of the patient's perioperative medication regimen, it is discerned that the short-term preoperative administration of IL-1 does not exert an influence on the anticoagulant efficacy of warfarin. Based on the previous literature, we suspected ascorbic acid-induced warfarin resistance and stopped ascorbic acid on July 4, and the INR increased to 1.21 and then gradually to around 1.5. On July 14, the dose of warfarin sodium was reduced to 7.5 mg, and the INR returned to target range afterwards. The patient was discharged because of her stable INR values (Figure 1). Figure 1 delineates the temporal progression of warfarin and ascorbic acid administration, in conjunction with low molecular weight heparin sodium bridging therapy, and the resultant International Normalized Ratio (INR) and Prothrombin Time (PT) values. Preoperatively, the patient was maintained on a warfarin regimen of 5mg, correlating with an INR of (2.06) and a PT of (24.1 s). Subsequent to warfarin cessation and initiation of low molecular weight heparin bridging, PT and INR values decreased to (10.6 s) and (0.92), respectively, permitting surgical intervention. Postoperative day two witnessed the reintroduction of warfarin at 5 mg daily, which precipitated a gradual elevation in PT. Despite the concomitant bidaily oral administration of ascorbic acid and an escalated warfarin dosage of 10mg, no appreciable augmentation in PT or INR was observed. Cessation of ascorbic acid led to a marked resurgence in both PT and INR values, and a subsequent reduction of warfarin to 7.5 mg daily facilitated a return to baseline preoperative metrics. The patient had good tolerance and no adverse events occurred. INR was stable and within normal range 1 month post-discharge during the follow-up.",
"gender": "Female"
}
] |
PMC11082382
|
[
{
"age": 28,
"case_id": "PMC11073592_01",
"case_text": "A 28-year-old female presented to the emergency department (ED) with frequent episodes of palpitations and 2 episodes of pre-syncope for the last 3 months which had not been investigated. She had no past medical or family history of cardiac disease or sudden cardiac arrest. She was not on any traditional supplements/medications. In the ED, she was symptom-free. Her vital signs were normal. The clinical examination was unremarkable except for an apical late systolic murmur. Her ECG showed sinus rhythm with an inverted T wave in lead III and AVF. While the patient was connected to a cardiac monitor, she suddenly collapsed, and the monitor showed wide complex tachycardia that degenerated into ventricular fibrillation (Fig. 1 and 2). The patient was successfully resuscitated and regained consciousness. ECG after resuscitation showed premature ventricular contraction with no new ischemic changes, no evidence of Brugada-type changes, prolonged QT, delta, or epsilon wave. Blood investigations indicated normal liver and renal function and ruled out infective and toxicological causes. Computed tomography coronary angiography showed normal origin of coronary arteries without stenosis. Transthoracic echocardiography declared bileaflet mitral valve prolapse (MVP) with moderate mitral regurgitation, mitral annulus disjunction (MAD) of 1 cm (Fig. 3), normal LV size, and function with an ejection fraction of 65%. The tissue Doppler imaging of the lateral mitral annulus showed a prominent mid-systolic spike of 21 cm/sec suggestive of the Pickelhaube sign (Fig. 4). The late gadolinium enhancement on cardiac MRI revealed inferior and inferolateral ventricular wall fibrosis with no evidence of inflammation or edema of the myocardium (Fig. 5). The investigation of this young patient who survived a cardiac arrest showed no evidence of ischemia, cardiac inflammation, or infiltrative disease in addition to the absence of a high-risk ECG pattern. However, she had evidence of bileaflet MVP associated with MAD and Pickelhaube sign on tissue Doppler of lateral mitral annulus in addition to the fibrosis of inferior and inferolateral LV wall which is highly suggestive of malignant MVP that is associated with ventricular arrhythmias and sudden cardiac death. As a secondary prevention, an implantable cardioverter defibrillator (ICD) was inserted. Follow-up after 6 months showed only multiple frequent premature ventricular contractions with no episodes of ventricular tachycardia.",
"gender": "Female"
}
] |
PMC11073592
|
[
{
"age": 61,
"case_id": "PMC10784751_01",
"case_text": "A 61-year-old male presented to our university outpatient clinic after referral. The patient was fitted with behind-the-ear hearing aids on both sides due to a sensorineural hearing loss existing for many years. Apart from that, there was no history of relevant ear pathology, ear surgery or new otogenic complaints. On clinical examination of the left ear, occlusive wax was removed and subsequently the external auditory canal was clear. The tympanic membrane was intact and clinically mobile when the Valsalva maneuver was performed. Examination of the right ear revealed equivalent findings. Weber's test was not lateralized and Rinne's test was positive on both sides. As an incidental, a black dot was found on the antero-inferior quadrant approximately symmetrically on both tympanic membranes (Figure 1). These dotts appeared static and could nether be manipulated nor removed, for example, by suction. In the supplementary medical history, it was excluded that the patient suffered from any coagulation disorders. In addition, the patient did not perform any welding work, or work with colorants.",
"gender": "Male"
}
] |
PMC10784751
|
[
{
"age": 21,
"case_id": "PMC10951757_01",
"case_text": "The first series of patients with hemispheric surgery to treat epilepsy was published in 1950 by Krynauw from South Africa. He reported on 12 patients, all of whom had a hemi-syndrome pre-operatively, and 10 suffered from different kinds of convulsions. The pre-surgical work-up was comprised of a surface EEG and a ventriculography in most cases. The oldest patient was 21 years old. Krynauw discussed the possible language transfer due to the early insult and the possible ipsilateral motor representation. He stated that \"disorders of behavior and personality are a marked feature of this group of cases, and the profound betterment in respect of mentality in all cases exceeds our best expectations.\".\nRasmussen summarized the Montreal experience of hemispheric surgery in the Penfield Lecture from 1982. A high rate of early and late hydrocephalus was described as related to anatomical hemispherectomy, in some cases with a delay of ten years or more. He and his team were the first who reduced the resective proportion of the procedure and disconnected larger parts of the hemisphere, leaving the tissue in place. Seizure outcome was still promising with the less invasive procedure. He concluded that \"preserving the frontal and occipital poles but disconnecting them from the rest of the brain, resulting in a functionally complete but anatomically subtotal hemispherectomy, retains the therapeutic effectiveness of a complete hemispherectomy while still protecting adequately against the serious late postoperative complication of superficial cerebral hemosiderosis and its associated neurological deterioration, hydrocephalus and sometimes death.\". This was the initial spark that pushed the evolution of modern disconnecting procedures, such as lateral transsylvian or the vertical hemispherotomies.\nIn general, the surgical tendency to minimize exposure and complications was a move from large resections, via smaller excisions towards an almost exclusively disconnective surgical procedure without any tissue resection. The basic prerequisite for this approach was the proven effectiveness in terms of seizure outcome. This tenet does not just apply to hemispherotomy but also to more circumscribed epilepsy surgery procedures such as the posterior disconnection.\nHemispheric disconnection procedures (HDPs) are typically applied in severe or catastrophic drug-resistant epilepsies in which most or all seizures are caused by a diffusely damaged single hemisphere, after sophisticated work-up has suggested a healthy contralateral hemisphere. Many patients considered for HDPs already present with hemiparesis, hemianopia and some degree of neuropsychological impairment. Severe drug-resistance is an important prerequisite for surgery.\nThe medical conditions for HDP can be summarized as a) acquired b) congenital and c) progressive pathologies.\nPerinatal infarction (Fig. 1), or intracerebral bleeding leading to large hemispheric defects with numerous cysts, causing drug resistant-epilepsy is one of the classical indications for any type of hemispheric disconnection procedures. Especially in this group with stroke-induced epilepsy, an alternative disconnection procedure has been described to avoid hemispherotomy. Most patients present with a neurological deficit, and depending on the time of infarction (intra-uterine or perinatal) neurological function may already (partly) be transferred to the healthy hemisphere, rendering them ideal candidates for HDP. Postoperative seizure outcomes in this group are among the most promising for HDP with seizure freedom rates of more than 90 %.\nMalformations of cortical development can be divided into two main groups: a) hemimegalencephaly (HME) and b) multi-lobar cortical malformations such as focal cortical dysplasia or polymicrogyria. Although these are two different entities, their clinical presentation and cardinal symptom is the same, namely drug resistant epilepsy (DRE). Hence, if MCDs are predominantly localized to one hemisphere, HDP can be considered as a treatment option.\nHME is a congenital developmental dysplastic malformation of the brain characterized by abnormal overgrowth of one hemisphere or some of its lobes, often resulting from a neuronal migration disorder.. The typical clinical presentation of HME includes severe DRE, contralateral motor deficit and cognitive impairment. Seizures typically begin in the early postnatal period and occur in more than 90 % of the patients. Drug resistance develops early and is typical for HME, which implies an early consideration for surgical treatment. Although hemispheric disconnection for HME shows a less seizure control compared to all other conditions treated by HDP, patients with HME can still achieve stable long-term seizure freedom in at least 60 % of cases and improvement of cognitive abilities in selected cases.\nSturge-Weber syndrome (SWS) is a rare, sporadic neurocutaneous disease (formerly: phakomatosis) with three variants. Types 1 and 2 are easily suspected due to presence of a typical port-wine stain facial angioma, whereas type 3 only has leptomeningeal angiomatosis, and is therefore less obvious, and presents with seizures in 75 %-90 % of the cases. Seizures are caused by vast pial angiomatosis, which can be localized within one lobe but often spreads over the entire hemisphere. Of note, it is presumed that the epileptogenic zone involves even larger areas of the cortex, going beyond the angiomatosis plaques. A very informative imaging modality to delineate the extension of the (calcified) pial angiomatosis is, next to the native bone-setting computed tomography (CT)-scan and the T1W MRI with contrast, the contrast-enhanced fluid-attenuated inversion recovery (FLAIR) sequence. Approximately 60 % of the patients with SWS will become drug-resistant making them excellent candidates for disconnecting procedures if the angiomatosis plaques are strictly localized to one hemisphere. Seizure outcome is favorable as long-term seizure freedom can be achieved in 80 % of the patients.\nRasmussen encephalitis (RE) is a very rare neurological disorder with estimated incidence rate of 2.4 cases in 1,000,000. It is characterized by inflammation of one hemisphere, progressive neurological deterioration, and cognitive decline as well as drug-resistant epilepsy. Recent findings suggest that the inflammation in RE is driven by a T-cell response. The typical course of RE includes a prodromal stage, acute stage (8-12 months) and a residual stage. The neurological deterioration and the occurrence of epilepsy typically mark the beginning of the acute stage. This stage is also accompanied by a progressive unilateral hemispheric atrophy usually starting in the insular lobe, which can be diagnosed by MRI (Fig. 2). RE usually affects only one hemisphere, despite its patho-immunological background. Progressive neurological deterioration ending with hemiplegia (as well as aphasia in the dominant hemisphere) and epilepsy are cardinal symptoms of the disease. Drug-resistance occurs in almost all cases, and about 50 % of the patients with RE will develop epilepsia partialis continua (EPC). HDP represents the only cure for seizures. Despite the unilateral nature of the disease and the early development of DRE, the decision and especially the timing of surgery is difficult since most patients initially present with only mild hemiparesis. Furthermore, immunosuppressive or immunomodulatory treatment has been shown to slow the disease and can be considered as suitable treatment prior to surgery especially in patients with slow disease progression and mild or no neurological symptoms. These treatment regimens seem to slow the disease but they are unable to cure RE and it is a matter of debate, whether they can improve long-term outcome. Even more importantly, immunosuppressive, or immunomodulatory treatments have little to no effect on epilepsy. Therefore, immune treatment modalities should not be a reason to postpone surgery, especially if RE develops rapidly. Thus, a functional HDP remains the only possible cure for seizures caused by RE, a decision, which must be weighed against the neurological impairment including hemiplegia and hemianopia. Of note, most of the patients achieve independent walking after rehabilitation, while fine movements of the fingers remains impaired, as generally occurs in HDP for other indications. The decision and timing of surgery on the language dominant side is even more challenging and therefore it is advisable, depending on the age of the patient, to proceed with a thorough investigation with fMRI or Wada tests to be able to estimate the risk for postoperative language impairment. Recent publications demonstrated that, although in pre- and young adolescent patients with RE, a functional HDP on the left (dominant) side, causes language function worsening in the acute postoperative phase, over the long-term these language functions can recover under intensive rehabilitation care.\nThe optimal timing of the procedures depends mostly on the severity of seizures and the underlying pathology. In young infants with very severe epilepsy caused by acquired pathologies, or malformations of cortical development, who present with already impaired neurological function, and who have a high incidence of sudden unexpected death in epilepsy (SUDEP), decision-making can be straight-forward. In very young children surgery can be performed in experienced epilepsy surgery centers despite the fact of low weight and blood volume, as reported by. Other experienced centers reported that HDP can be performed in infants from 4 months onward and may push the limit to 2.5 months. The earlier the surgery, the better the long-term outcome, since hemispherotomy represents a highly successful treatment option for seizure outcome, and seizures cessation will prevent the development of epileptogenic encephalopathy, which could negatively affect the healthy hemisphere as well. A recent multicenter and multinational study evaluated ultra-early epilepsy surgery before the age of 3 months. The study included 48 hemispheric surgeries. They found that ultra-early surgery was not associated with more permanent morbidity or mortality than surgery in older infants.\nThe timing of surgery in progressive pathologies like SWS and especially in RE is more challenging. Here, one should weigh the instant loss of neurological function due to the disconnecting procedure against the seizure burden and the risk for development of epileptogenic encephalopathy. This decision should be made on an individual basis. However, if the seizures are incapacitating one might be more prone to go for earlier surgery to at least preserve the possibility for transfer of neurological function to the healthy hemisphere before it has been damaged by ongoing seizures.\nTiming is also a challenge in children older than 5-7 years with underlying pathological conditions of the dominant hemisphere. Recent literature shows that language lateralization by resting state-fMRI is possible in children and can be helpful in the preoperative counseling. In general, experience shows that hemispheric disconnecting procedures are safe in terms of cognition at different ages regardless of the language dominance and that the postoperative outcome often resembles the preoperative condition.\nSince the first description in 1928 of an anatomic hemispherectomy for a right hemispherical tumor by Walter, the first description of this surgical procedure for epilepsy by McKenzie in 1938 and the publication of Krynauw in 1950 of a pediatric patient cohort after hemispherectomy, major changes in the technique have occurred, reflecting technological advancements and physiological - anatomical understanding. After several decades with a scarcity of publications, a new era started in the mid-1990s with several publications on the diversity of hemispherectomy and hemispherotomy techniques, and their respective outcomes and complications.\nIn the early days, this surgical procedure consisted of removal of an entire cerebral hemisphere sparing the basal ganglia for oncological or epileptological indications. Theodore Rasmussen (1910-2002), successor of Wilder Penfield as head of the Montreal Neurological Institute, and his group described the \"en bloc\" technique of resecting an entire hemisphere (French, 1955/). The previous technique was the piecemeal removal of the different lobes, as described by Dandy, Penfield and Krynauw respectively.\nDue to the necessarily large cerebral exposure, the wound and craniotomy are accordingly large. The craniotomy is planned in an anteroposterior (AP)-direction from the frontal towards the occipital pole and in a craniocaudal direction from almost the vertex towards the base of the middle cranial fossa. After this extensive hemicraniotomy, the dura is opened in different flap-directions almost up to the superior sagittal sinus. The middle and anterior cerebral arteries are divided and clipped, sparing the deep perforators of both as well as the large parasagittal bridging veins, since not all of them should be closed in the beginning because of the risk of brain swelling. The hemisphere can subsequently be retracted to visualize the corpus callosum. The callosotomy is performed, after which the frontal horn is entered. From the most anterior part of the ventricle a frontobasal disconnection is performed. Thereafter the ventricle is followed to the trigone, temporal horn and anterior hippocampus. Most frequently the hemispherectomy is performed in more than one \"en bloc\" step in which, after isolating the basal ganglia block, the frontal and temporal lobes are removed, followed by the parieto-occipital lobes. In most procedures the insular cortex is also removed. This \"classical\" anatomical hemispherectomy is nowadays still performed in a very minority of cases in some epilepsy surgery centers, especially in cases of recurring seizures or secondary to HME with a significantly distorted anatomy.\nDespite its effectiveness for seizure outcome, this technique is very time-consuming and appears to be associated with several complications, specified below.\nIn 1968 and 1983 some anatomically \"less-radical\" modifications were described by authors such as Ignelzi et al. and Adams et al., who respectively proposed the so-called hemidecortication in which \"only\" the epileptogenic cerebral cortex is removed, and the reduction of the volume of the resection cavity by plugging the foramen of Monro and suturing the convexity dura to the falx and tentorium, which reduced the rate of hydrocephalus complications.\nThese less invasive options had also several disadvantages which led most epilepsy surgery centers, from the mid-1990's, to adopt the non-anatomical, i.e., the functional hemispherectomy or hemispherotomy procedure. This procedure, first performed by Rasmussen in 1974, was an improvement to the anatomical hemispherectomy, and since then many surgical nuances have been described and will be explained below in a chronological order. All these less-invasive, less resective and more disconnective procedures have in common that, tracking/tracing along unilateral efferent and commissural anatomical structures, the following are progressively disconnected: corona radiata and internal capsule, frontobasal, and temporomesial structures as well as the insula and corpus callosum. To obtain seizure freedom it is critical to interrupt different unilateral, efferent, projective fiber tracts, e.g., the cortico-spinal tract, but also commissural fibers i.e., the corpus callosum or the hippocampal commissure have to be interrupted in order to prevent seizure spread to the other hemisphere. These more disconnective, less resective procedures are done to lessen complications, especially the development of hydrocephalus.\nVertical parasagittal hemispherotomy \nThe key principles of the Rasmussen approach were the resection of a large area between fronto-dorsal (F1/F2/F3) and anterior parts of the superior and inferior parietal lobules, a temporal lobectomy, a callosotomy and disconnection of the rest of the frontal/parietal and occipital lobes. After Rasmussen's description four other functional hemispherotomy techniques were described.\nPeriinsular hemispherotomy \nThis technique was first described by Delalande et al., in 1992. The patient is in a supine position, with the head fixated orthograde, in slight anteflexion. Neuronavigation is recommendable, especially in cases with a distorted anatomy, to perform a predominantly precentral localized craniotomy in order to have sufficient access for the anterior disconnection. With an average length of 5 cm and width of 3 cm, a frontal cortex resection is performed and through dissection of the white matter the lateral ventricle is entered. At the level of the roof of the lateral ventricle, the corpus callosum is encountered and the callosotomy is started with the corpus and splenium and completed with the genu and rostrum till the level of the anterior commissure. At the level of the trigone, the posterior fornix is cut to disconnect the hippocampus. The vertical disconnection line is performed lateral to the basal ganglia and thalamus, following the choroid plexus to the anterior part of the temporal horn where the amygdala is resected. The fronto-(basal) disconnection is performed by resection of the posterior gyrus rectus and frontobasal white matter until the anterior cerebral artery (ACA) and optic nerve can be visualized, after which an incision is performed to disrupt the fibers between anterior temporal horn and frontobasal cortex. Further technical variants have been proposed by Danielpour, Giordano and Baumgartner aiming to avoid or at least reduce the access to the ventricular system. In the vertical midline approach, a coronal incision of <10 cm is made above the coronal suture, followed by a 6 cm wide craniotomy that exposes the superior sagittal sinus. The first step is an interhemispheric approach allowing complete corpus callosum exposure. Callosotomy is then performed from the rostrum with the visualization of the pericallosal artery, to the splenium with visualization of the internal cerebral veins/vein of Galen confluence. Extraventricular dissection in the reflection line of the septum pellucidum avoids cerebrospinal fluid (CSF) leakage, and brain collapse at this time. Then the ventricle is opened, and lateral disconnection is performed from the temporal horn (behind the plane of the glomus of the choroid plexus) to the frontal horn, lateral to the choroid plexus that delineates the lateral limit of the thalamus, in a posterior to anterior direction until the anterior choroidal point. Anterior disconnection is then performed starting on the midline from the genual part of the cingulum, subpially following the ACA to the frontal base, and then moving laterally to the carotid bifurcation. This disconnection goes back to the level of the anterior commissure, which is a major difference to the lateral technique. The temporal disconnection is reached while following the vessels until the anterior choroidal point. The fimbria is disconnected posterolaterally to the splenium of the corpus callosum, in the medial wall of the ventricle atrium. At the end of the disconnection, the ventricular access is closed with fibrin glue, following irrigation of the ventricular cavities with saline after meticulous hemostasis, to avoid subdural collection (Fig. 3 and 4).\nThe patient is placed in a supine position with the head turned almost horizontally. This technique uses the transventricular approach for the mesial hemispheric disconnection in the same manner as the keyhole transsylvian approach (Fig. 3)(see below). The craniotomy is centered over the complete Sylvian fissure, exposing the suprasylvian circular sulcus as well as the frontal and temporal operculum. As the name says, two peri-insular windows for access to the frontal and the temporal ventricles are performed by resection of frontal and temporal operculum (T1) respectively. In the suprainsular window it is necessary to open the frontal horn in the entire AP direction (frontal horn - trigone) by resection of the fronto-parietal opercular cortex and thereby also transecting the corona radiata. From inside the ventricle, a complete callosotomy is performed with a disconnection at the splenial level of the fornix-fimbria hippocampi connection (psalterium-commissura hippocampalis) and an anterior frontal lobe disconnection from the rostrum in the direction of the sphenoid wing. In the infrainsular window, the superior temporal gyrus (T1) is resected from the uncus to the posterior part of the insula. Via the inferior circular sulcus, the temporal horn is entered, and a resection of uncus, lateral amygdala and anterior hippocampus is performed. Finally, the insular cortex is aspirated and the insula is disconnected at the level of the claustrum/external capsule.\nTranssylvian keyhole functional hemispherectomy \nAn alternative way to perform the peri-insular hemispherotomy is by entering the \"C\" shaped ventricle by a \"C\" shape corticectomy through F3, supramarginal gyrus, and T2 - then disconnecting the tissue from F3 to the Sylvian fissure at the level of the foramen Monro, and from T2 to the Sylvian fissure at the most anterior point of the temporal horn. At this stage, the insula is undermined at the level of the external or extreme capsule, the MCA is coagulated and transected at the level of the insular vallecula, and the entire peri-insular and insula are removed en bloc.\nThis is the third described technique and a surgical variation on the previous one. The technique was described in detail by Schramm in 1995, being supplemented by patient details and surgical outcome in 20 cases.\nJapanese modified periinsular hemispherotomy \nThe most essential surgical steps in this keyhole procedure are the following: 1. a curvilinear frontotemporal incision and a relatively small craniotomy centered over the entire Sylvian fissure and insula exposing the Sylvian fissure at the inferior part of the craniotomy. This technique is therefore especially suitable for cases with a certain amount of brain atrophy, such as patients with perinatal ischemic events, and RE cases. Craniotomy size (varying from 4 x 4 cm to 5 x 6 cm), preferably guided by neuronavigation, depends, among other things on the AP length of both corpus callosum (mostly 6.5 cm), insula (limen insulae)-basal ganglia block (pulvinar thalami) and the size of the ventricular system. 2. Then the Sylvian fissure is opened and both the inferior and superior circular sulci are visualized. Anatomically the frontal operculum can cover the superior circular sulcus for more than 3 cm whereas this is less so for the temporal operculum and the inferior sulcus (0.5-1.0 cm). The temporal horn is opened via the limen insulae (inferior sulcus) and an unco-amygala-hippocampectomy is performed. Subsequently the temporal horn is further opened following the circular sulcus to the frontal horn. 3. Via the tip of the frontal horn, a frontobasal disconnection is performed between the arachnoid covering the landmarks ACA basally in the midline and the MCA laterally. 4. Now, via the same route back from the frontal horn in the direction of the trigone, a complete intraventricular callosotomy is performed until the splenium is reached. To guide the callosotomy, in the first part, more anterior, the ACA branches are followed. When these arteries become too thin to follow, the falx can be used as a guide. In the splenial region, the falco-tentorial junction is followed down through the hippocampal tail to the temporal horn where the procedure started. All major arterial branches of MCA, ACA and posterior cerebral artery (PCA) are spared. Finally, the insular cortex is aspirated. One indication for not performing the keyhole procedure would be HME because of the enlarged hemisphere and atypical insular cistern. In these cases, the best solution is a temporal lobectomy or a frontoparietal operculum resection. With these resections, the surgery will be faster and the occurrence of brain swelling less problematic. Care should be taken to strictly avoid injury to the contralateral healthy hemisphere.\nThis surgical technique combines different aspects of the peri-insular technique and parts of the technique described by Delalande. The craniotomy is centered over the entire AP direction of the lateral ventricle. Resection of frontal operculum and corticectomy of the insular upper half is carried out. Via the white matter, a route is created to the lateral ventricle and from inside a complete callosotomy is performed. The procedure ends with a temporo-mesial disconnection by an amygdalo-hippocampectomy.\nAll these surgical disconnection techniques can be applied in patients with HME but specific attention should be paid to the more voluminous diseased hemisphere which sometimes preoperatively shows signs of midline displacement, displacement of the superior sagittal sinus to the opposite side and a much more complex anatomy because of dysplastic brain tissue, leading to a less demarcated gray-white matter transition zone. Therefore, in general, the recommendation is to perform a larger craniotomy and volume of tissue resection, e.g., a standard temporal lobectomy. Sometimes in a larger anatomical resection, the MCA or ACA can be clipped, which may decrease blood loss, but could increase postoperative ischemia and brain edema.\nAll patients should be transferred to a dedicated special care ward (medium or intensive care) for at least one night. Pediatric patients, and especially young infants, may need a blood transfusion. Almost all patients have a (slight) rise in body temperature, explained by \"aseptic meningitis\" and caused by CSF contamination with blood products. Routine external ventricular drainage (EVD) has been shown to reduce the rate of postoperative fever and hydrocephalus. In some centers a drain is left in situ for a couple of days till the CSF clears, but there is no recommendation based on clear evidence. Intraoperative extensive rinsing before closing might contribute to avoid postoperative hydrocephalus.\nIn the last 8 years some reports have described variations of the hemispherotomy technique. Kawai et al. described a variation for the vertical hemispherotomy, applied in 7 patients, with the main difference to Delalande's technique being that the authors used the interhemispheric, instead of transcortical, route. The second modification was the target for the anterior dissection plane, namely the anterior end of the foramen of Monro instead of the subcallosal area. They reported a good seizure outcome (International League Against Epilepsy (ILAE) Class 1 in 6 out of 7 patients) and less brain resection. An alternative variant for the hemispheric disconnection via an extraventricular route was described by. These authors developed this alternative procedure especially to reduce the chance of postoperative hydrocephalus.\nIn 2018 reported on an endoscope-assisted functional hemispherotomy in two pediatric cases with chronic epilepsy due to perinatal strokes. Other reports on endoscope-assisted disconnective surgery have been published since. The main advantage is the smaller incision and craniotomy. Essentially, the surgery is identical to the vertical parasagittal approach. A linear paramedian incision, 2 cm anterior and 3cm posterior to the coronal suture is made, followed by a 4 cm long and 2 cm wide craniotomy. Following an interhemispheric complete callosotomy, the lateral ventricle is entered, and an anterior or frontobasal disconnection followed by the middle and posterior white matter disconnection between frontal and temporal horns up to the trigone. Finally, a hippocampal disconnection is performed (resecting the amygdala and disconnecting the posterior fornix). Due to long surgery duration with this procedure, a higher complication rate, like e.g., infections, could perhaps be associated compared to open surgery, but is in the scarce literature not clearly described.\nMRI guided laser interstitial thermal therapy (MRgLITT) enables real-time image-guided ablation of the predefined brain tissue region by applying laser energy via one or more stereotactically inserted laser probe(s). In 2012 first reported LITT therapy in 5 pediatric patients with different lesions. In the following years, different epileptogenic lesions like periventricular heterotopias, focal cortical dysplasia, tuberous sclerosis (Lewis) and hypothalamic hamartomas have been treated by LITT, but there are still very few studies report on (long-term) outcome. A recent systematic review on corpus callosotomy by this technique was published with the conclusion that all included studies on this topic only reach class IV evidence, so prospective trials are necessary to compare its effectiveness with that of standard open callosotomy. This, relatively new, \"minimally invasive\" treatment method with curative potential for chronic, drug-resistant, epilepsy was recently performed and described in a pediatric case whose multiple comorbidities consequently made it not suitable for open disconnective surgery. Crucial brain areas to be disconnected were established and disconnection could be performed by implantation of 5 laser catheters throughout the hemisphere. As this was the first case, no definitive conclusion or advise can be given at present. More recently, Chandra has applied a robotic thermocoagulation technique using radiofrequency (RF) ablation with the same technical concept of MRIgLITT.\nThorough knowledge of any procedure-associated complication cannot be overemphasized - this guides the surgeon to making an accurate and mature decision regarding surgery for the candidate, while allowing for early detection and proper management of any problems. Moreover, understanding of the underlying pathophysiological mechanism for each complication provides the opportunity for developing avoidance or mitigation strategies, improving the safety profile and overall outcome of a surgical procedure.\nAnatomical hemispherectomy constitutes the only therapeutic epilepsy surgery procedure that has been associated with mortality. Previous publications have reported mortality rates varying between 2 and 10 %. The extensive nature of hemispherectomy, the removal of multiple lobes, massive intraoperative blood loss, mainly due to sagittal sinus lacerations, and the sacrifice of multiple cortical veins leading to extensive, acute postoperative edema were a few of the causes of mortality. However, more recent clinical series have demonstrated that the mortality associated with various hemispherotomy techniques is minimal. Schramm et al. reported a mortality rate of 1.0 % in a large retrospective pediatric series while in the adult series of the same center the reported mortality rate was 0 %. Likewise, several recent pediatric series have reported 0 % mortality. The transformation of the procedure from an extensive resection to a minimal disconnection, the avoidance of cortical vessel coagulation of the pathological hemisphere, and the advances in neuroanesthesia during the last two decades may well explain the minimization of the associated mortality.\nMultifactorial morbidity has also been associated with the various hemispherectomy techniques, compromising their safety profile and limiting clinical use. The reported complications could be grouped into surgical, neurological, neuro-endocrinological and neurocognitive, mostly for analytic purposes. Superficial cerebral hemosiderosis, significant intraoperative blood loss requiring massive blood transfusions, the development of postoperative hydrocephalus necessitating shunt insertion, postoperative hematoma formation, persistent postoperative fever, and postoperative infection represent the most common reported surgical complications, especially following anatomical hemispherectomy. The existence of superficial cerebral hemosiderosis, a commonly reported complication in the original series, has been questioned by many authors. Indeed, all recently published series, either pediatric or adult, have reported no such cases, making the discussion about cerebral hemosiderosis of historical value only, probably due to the minimization of tissue destruction and blood loss. As a neuro-endocrinological complication due to hypothalamic injury during the frontal disconnection, SIADH or DI could occur and lead to severe life-threatening hypo- or hypernatremia and even to sinus thrombosis.\nA major concern regarding hemispherectomy has undoubtedly been the massive intraoperative blood loss and its serious metabolic sequences (induced tachycardia, circulatory instability, metabolic acidosis, hypothermia, severe electrolytic abnormalities etc.). The severity of intraoperative blood loss is reflected in the necessity for intraoperative blood transfusion. reported in an older series that all of their cases required blood transfusion. Similarly,, in a more recent series, reported that blood transfusion was necessary in all their cases. It has to be pointed out, however, that their series included solely pediatric patients aged under 6 months. Similarly, Roth et al. reported on children undergoing hemispheric surgeries before the age of 3 months, and all received blood transfusions. Since the era of hemispherotomy (minimization of brain tissue resection) instead of hemispherectomy (partial or complete hemispheric brain tissue resection) reported blood loss and the necessity for blood transfusion has decreased, especially with the lateral keyhole approaches and in the group operated via the vertical technique, probably because of smaller skin incisions and brain exposure.\nThe incidence of postoperative hydrocephalus comprises another worrisome complication associated with hemispherotomy. in their review article reported a 9-81 % hydrocephalus incidence in mixed populations (adult and pediatric), while the respective percentage in pediatric series was 23 %. Similarly, reported 2-26 % postoperative hydrocephalus in their systematic review. Recently published pediatric series reported lower hydrocephalus incidence around 13-14 %, while Lopez et al., in their review study found an overall 19 % hydrocephalus incidence. It has been postulated that certain pathological entities such as HME and multifocal cortical dysplasia are more frequently associated with the development of postoperative hydrocephalus, and the subsequent need for shunt insertion. The insertion of an EVD does not seem to reduce the incidence of definitive post-operative hydrocephalus, though other centers show a reduction of post-operative hydrocephalus.\nThe formation of a postoperative hematoma, infection (either a localized surgical wound infection or meningitis), and/or the occurrence of postoperative fever are frequently reported as cumulative surgical morbidity among many series, both in cases with hemispherotomy as well as hemispherectomy. Schramm et al. reported rates of 7.4 % in their adult series, and somewhat higher, 9.7 %, in their pediatric series. Likewise, reported hematoma/hygroma/infection rates of 10 %, while in the pediatric series the percentage was 14.8 %. Interestingly, Santos et al. reported 28.5 % surgical complications in their series. It has to be pointed out that they only included reoperations. Lopez et al., in their review study including 37 pediatric series, found that the hematoma formation rate varied between 10 and 36 %, and the incidence of postoperative infection ranged from 2 % to 7 %, while persistent postoperative fever was observed in up to 83 % of cases. The authors also found that certain pathological entities such as HME and SWS are more frequently associated with hematoma formation, while RE may predispose to the occurrence of postoperative fever. Kamath et al. have reported increased incidence of post-operative fever in patients with RE, while patients with underlying pathologies such as cortical dysplasia or polymicrogyria tended to have less severe fevers. The authors also found that the usage of an EVD may mitigate the possibility of post-operative fever. DiRocco et al. postulated that younger age may predispose to increased surgical complications.\nDespite the extent of disconnection and resection of cerebral tissue in hemispherotomy the incidence of unexpected neurological complications respectively sequelae are quite low. Permanent worsening of a pre-existing hemiparesis or de novo development of hemiparesis has been reported in the range of 8-21 %. More specifically, reported a worsening of hemiparesis in 8 % of their pediatric cases, found such worsening in 10 %, as well as. This percentage was higher in the adult series of, who reported a 21 % incidence. It has to be mentioned however, that even in cases with worsening of the preoperative hemiparesis, patients remained ambulatory after surgery. Postoperative worsening of language/speech was observed in 10 % of the adult cases. There are reports of temporary mutism, which spontaneously resolved. These symptoms occurred more frequently in dominant hemisphere involvement. Postoperative visual field and/or visual acuity worsening has been demonstrated in pediatric series. reported that 49 % of their pediatric cases developed de novo or had worsening of their preoperative strabismus. It is of interest, that the vast majority of these patients developed torticollis from compensating for their visual deficits. Similarly, reported in their pediatric series that 56 % of their cases had decreased visual acuity after surgery, 71 % experienced new visual field deficits while visual field impairment preexisted in others. In summary, a postoperative hemianopia is unavoidable in a complete hemispheric disconnection, yet in most cases it will not impair function, and various compensatory mechanisms have been described, so correction (such as treatment of the strabismus) may not be necessary. The degree of speech/language deterioration as well as loss of motor function on the contralateral side is much more difficult to predict in the preoperative counseling with the patient and family; however, especially in younger children, linguistic improvement is expected, even beyond the preoperative status.\nThe effect of hemispherotomy on neurocognitive status has not been adequately explored. The absence of such reports cannot however be considered as lack of such an impact. This issue remains to be more accurately studied in the future.\nThe role of the type of hemispherotomy technique in the development of certain complications is of great interest. The comparison between the existent series is extremely difficult due to different patient populations, underlying pathology, age of seizure onset, impact of various anti-seizure medication (ASM), and the utilization of various surgical techniques even in the same clinical series. in their pediatric series found no difference in the incidence of complications between the various surgical hemispherotomy techniques employed. On the other hand, reported that the peri-insular technique was associated with fewer complications. On the contrary Iwasaki et al. concluded in their pediatric series that the vertical hemispherotomy technique was safer, since it was associated with less frequent perioperative complications. It is apparent that the extraction of any statistically powerful conclusions from these series would not be very meaningful, given the limited number of participants, retrospective nature, and non-homogeneous character of these studies.\nOne important complication eventually leading to death could be an electrolyte imbalance, mainly caused by syndrome of inappropriate secretion of anti-diuretic hormone (SIADH), cerebral salt wasting, or diabetes insipidus due to hypothalamic ischemia when coagulating perforating arteries of the anterior communicating artery complex and the ACA when performing the frontobasal disconnection. Severe hypo- or hypernatremia and refractory brain edema may result in life threatening comatose state and death.\nIn the context of this manuscript, a survey with 12 to-the-point questions regarding the current practice of hemispheric disconnection procedures was composed and sent to different European centers performing epilepsy surgery. These centers were geographically well spread over Europe. The detailed survey answers are demonstrated in Table 1 and summarized below.\nIn most of the countries participating in this study, the practice of epilepsy surgery is centralized and, in most centers (N = 20/27, 74 %), only one neurosurgeon performs this type of complex surgery. Most centers started this surgery between 1980 and 2000 (N = 16/27 centers; 59 %), eight centers (37 %) between 2000 and 2010 and three centers (11 %) began performing this surgery after 2010. The two major techniques performed in all centers are the lateral transsylvian or the vertical parasagittal method with associated variants. Which of either technique is performed strongly depends on the center in which the epilepsy surgeon was trained. In 13 centers (n = 13/27; 48 %) only the lateral transsylvian technique was used, in eight centers (n = 8/27; 30 %) only the vertical parasagittal technique and six centers (22 %) used both techniques. Thirteen centers (48 %) treated only pediatric patients, thirteen centers (48 %) treated both pediatric and adult patients and one center (4 %) only adult patients. The \"classical\" causes for (catastrophic) drug-resistant epilepsy from one hemisphere were seen and treated in almost all centers (96 %). Finally, regarding the frequency of these complex surgeries per year, 15 centers (56 %) reported an increase, nine centers (33 %) no change and three centers (11 %) a decrease in these surgeries over the last 5-10 years.\nWe would like to emphasize that hemispheric surgery is an extremely complex intervention. It requires a highly experienced interdisciplinary team and specialized intraoperative and postoperative facilities to guarantee a favorable surgical outcome. Before performing hemispheric surgery, the epilepsy surgeon should undergo an elaborate exhaustive training by a colleague with profound experience in this sort of interventions/procedures. With hemispheric surgery, training in collaboration with other specialized centers is common practice.",
"gender": "Male"
}
] |
PMC10951757
|
[
{
"age": 71,
"case_id": "PMC10789897_01",
"case_text": "In May 2021, a 71-year-old female patient, never smoker, with negative familial history, presented with neck pain, radiating to the shoulder and left ear, associated to pharyngodynia and breakthrough pain lasting about a minute. At physical examination a mass of the tongue base occupying the left vallecula extended to the lingual face of the epiglottis and bilateral cervical lymphadenopathies were evident.\nContrast-enhanced computed tomography (CT) scan and 18F-fluoro-2-deoxy-D-glucose (FDG)-positron emission tomography (PET) confirmed the clinical findings and excluded distant metastases; an increased size of the nodular-looking thyroid gland suspected of primary thyroid cancer was further documented (Figure 1).\nA transoral biopsy of the laryngeal lesion turned positive for a poorly differentiated neuroendocrine tumor expressing synaptophysin, neuron-specific enolase (NSE), chromogranin A, pan-cytokeratin including cytokeratin AE1-AE2 and focally calcitonin. Circulating NSE was 13.4 microg/L (normal level <12.5 microg/L), and basal calcitonin serum level was 237 pg/mL (normal level <11.5 pg/mL).\nAt ultrasound examination, the thyroid presented increased size and bilateral nodulations, the largest in the right lobe (20 mm), classified as TIR2 by fine needle aspiration cytology, according to the Italian consensus for the classification and reporting of thyroid cytology.\nAfter multidisciplinary evaluation in April 2021, a supraglottic laryngectomy extended to the base of the tongue, bilateral selective neck dissection (level II-IV) and total thyroidectomy were performed.\nThe pathology report of the resected tumor demonstrated a SCUNC (Figure 2A), G3, with Ki-67 index 60-70% and expression of neuroendocrine markers: synaptophysin (Figure 2B), NSE (Figure 2C), chromogranin A (Figure 2D) and broad spectrum cytokeratins. The primary tumor was excised with clear surgical margins and was staged as pT4a pN3b for the evidence of metastases in 25 out of 57 removed cervical lymph nodes with extracapsular invasion (3/14 positive lymph nodes at the third right level, 9/10 positive at the second right level, 4/14 positive at the third left level, 2/11 and 7/8 at the left level B and A, respectively). Thyroid gland histology revealed hyperplastic thyroid without evidence of cancer.\nGenomic DNA from collected cancer tissue was extracted using a Qiagen DNA isolation kit (Qiagen Inc., Valencia, CA). Molecular analysis in Next Generation Sequencing with multigenic panel ONCOMINE and CUSTOM (Thermo Fisher Scientific, Bologna, Italy), revealed mutations in HRAS and MYC genes. Pyrosequencing analysis (Qiagen Inc., Valencia, CA, USA) showed a methylated MGMT gene.\nAfter 40 days from surgery, 18F-FDG PET and a CT scan showed the appearance of a subcutaneous nodulation measuring 8 mm on the right middle axillary line (SUVmax =2.6, Figure 3A). On clinical examination, the axillary nodulation was fixed and firm. Pathology confirmed the presence of a metastasis from poorly differentiated carcinoma with neuroendocrine differentiation, compatible with the primary resected. The serum calcitonin after surgery was not measured due to the high predictability of raised levels in the presence of extracapsular disease. From September 2021 to November 2021, the patient was treated with four cycles of chemotherapy with carboplatin AUC5 on 1 day and etoposide 100 mg/m2 on days 1-3, every 3 weeks, with granulocyte colony-stimulating factor (G-CSF) as primary prophylaxis for febrile neutropenia. The treatment was well tolerated except for G1 diarrhea.\nThe subsequent CT scan, performed in December 2021, showed stable disease (SD) with dimensional stability of the single metastasis (8 mm in diameter) on the right middle axillary, while the 18F-FDG PET revealed normalization of uptake (Figure 3B). The serum calcitonin level was 57.9 pg/mL.\nIn January 2022 the patient was evaluated for persistent cervicalgia and a phenytoin therapy was initiated in the suspect of a glossopharyngeal neuralgia. In March 2022, 18F-FDG PET showed a locoregional recurrence of disease, due to appearance of a pathological radiotracer uptake at the right lateral cervical area (II level, SUVmax =7) and at the right side of the parapharyngeal region (SUVmax =7). Interestingly, calcitonin levels raised up to 89.3 pg/mL (vs. 57.9 after 4 cycles of chemotherapy).\nFurthermore, the patient had persistence of neck pain, radiating to the shoulder blade and left ear, associated to pharyngodynia. After a new multidisciplinary evaluation, surgery was excluded for the extent of the disease and, considering the optimal metabolic response obtained with the previous treatment, the patient was started on a rechallenge with carboplatin and etoposide chemotherapy, which was well tolerated except for G1 nausea. After two cycles of treatment, a new 18F-FDG PET-CT showed disease progression as increased size and radiotracer uptake at the right submandibular space and homolateral parapharyngeal space.\nBecause of the lack of radiological response to first line treatment to which high-grade neuroendocrine tumors are usually sensitive, pathology revision was performed and confirmed a diagnosis of moderately differentiated NEN G2, with a Ki-67 index of 22.6%.\nThus, the case was also discussed at the Neuroendocrine Tumor Board and, in the light of histology and staging of disease, a second-line chemotherapy with capecitabine 500 mg twice daily on day 1 to 14 and temozolomide 200 mg daily on day 10 to 14 was administered to the patient for 3 cycles, with good tolerance.\nHowever, patient's general conditions declined in concurrence with pneumonia making her ineligible to an antiblastic treatment and was transitioned to best supportive care alone. The patient died in August 2022 because of pulmonary sepsis.\nDuring the entire clinical course, the patient was fully aware of her condition and actively asked to be informed for every treatment she received. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.",
"gender": "Female"
}
] |
PMC10789897
|
[
{
"age": 78,
"case_id": "PMC11416686_01",
"case_text": "A 78-year-old man with a past medical history of type 2 diabetes mellitus, hypertension, dyslipidemia, sick sinus syndrome (requiring pacemaker placement) and chronic kidney disease presented to our hospital with a one-day history of fevers and chills. Two years prior to admission, he was evaluated by the Hematology service for a new diagnosis of anemia (hemoglobin level: 8.0 g/dL). Laboratory workup suggested iron deficiency, and although a bone marrow biopsy was recommended, the patient declined and opted for medical management. Approximately three months prior to admission, he reported fever and dyspnea. Further investigation revealed his hemoglobin level had declined to 5.3 g/dL. An upper gastrointestinal endoscopy confirmed the diagnosis of advanced gastric cancer (cT3N3M0 Stage IIIb). The patient was scheduled for outpatient surgery, but before this could happen, he returned to the hospital with complaints of dyspnea and fever, leading to admission for concern of sepsis. On admission, his temperature was 38.5 C, and two sets of blood cultures grew Streptococcus dysgalactiae, subspecies equisimilis.\nInitially there was suspicion for infective endocarditis. However, the patient's examination did not reveal a new murmur or peripheral embolic phenomena, and transthoracic echocardiography showed no evidence of valvular vegetations. Additionally, rheumatoid factor was negative at 15 IU/mL, and his blood cultures cleared quickly. Therefore, he did not clinically meet criteria for endocarditis, prompting a workup for other potential causes of the bacteremia. Contrast-enhanced computed tomography (CT) of the chest, abdomen, and pelvis was negative for abscess or any findings suspicious for infection. The patient was treated with a 14-day continuous intravenous infusion of penicillin G (24 million units daily) for Streptococcus dysgalactiae bacteremia of unknown origin and responded well to the therapy. After completing treatment for bacteremia, he underwent distal gastrectomy, with resultant negative margins for malignancy. His postoperative course was uneventful, and he remained well for several weeks.\nOne month after discharge, the patient re-presented to the emergency department with a one-day history of fevers, chills, and malaise. He denied chest or abdominal pain and reported no new exposures or events since his last discharge, such as sick contacts, new sexual partners, substance use, or dental treatments. Upon admission, he was alert and oriented, with the following vital signs: Japanese Coma Scale I-1; body temperature, 38.8 C; pulse, 91 beats/min; blood pressure, 138/72 mmHg; respiratory rate, 26 breaths/min; and SpO2, 95 % on room air. Physical examination was significant only for petechial hemorrhages isolated to the toes. Laboratory tests indicated an elevated inflammatory response, with white blood cells at 7700/muL (normal range: 4000-11,000/ muL), with neutrophil predominance and an elevated CRP at 9.10 (normal range: < 0.5 mg/dL). Liver transaminases, albumin, electrolytes, and creatinine were normal. Contrast-enhanced CT revealed thickening of the upper thoracic esophageal wall and a solid lesion near the esophagus (Fig. 1). Given the patient's history, initial concerns were for gastric or esophageal cancer with lymph node metastasis.\nAs the patient met criteria for sepsis, intravenous ampicillin/sulbactam (3 g every 6 h) was started immediately upon admission. The following day, upper gastrointestinal endoscopy revealed grade M gastroesophageal reflux disease with edematous mucosa throughout the esophagus, and biopsies were negative for malignancy. Blood cultures obtained at admission again detected Streptococcus dysgalactiae subspecies equisimilis (minimum inhibitory concentration [MIC] to penicillin G <= 0.12 mcg/mL) and subsequent cultures after antibiotic administration remained negative.\nA repeat workup for infective endocarditis, including transthoracic and transesophageal echocardiography, showed no evidence of valvular vegetations. However, the case was still classified as confirmed infective endocarditis by the 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria. This classification was based on one major criterion - recurrent bacteremia with the same organism over a short period of time - along with four minor criteria: appearance of petechial hemorrhagic spots on the toes, elevated rheumatoid factor (22 IU/mL), fever (38.8 C), and the presence of a pre-existing cardiac condition or device (pacemaker). The antibiotic regimen was changed to a combination of penicillin G (24 million units per day) and gentamicin (3 mg/kg per day), with a tentative plan to continue penicillin G for 4 weeks and gentamicin for 2 weeks.\nAfter the initiation of antibiotics, the patient had an uneventful course until the 33rd day of hospitalization, when he suddenly vomited a large amount of blood, leading to immediate cardiopulmonary arrest. Despite resuscitation efforts, he could not be revived and passed away. A pathological autopsy was conducted to help elucidate the source of the recurrent Streptococcus dysgalactiae bacteremia and determine the cause of the massive bleeding. The autopsy revealed the presence of an aorto-esophageal fistula (Fig. 2) and an abscess (Fig. 3, Fig. 4) in the mediastinum, near the middle of the thoracic esophagus. The lumen was covered with fibrin (Fig. 5a), and relatively enlarged and reactive lymph nodes were scattered around it (Fig. 5b). An organized thrombus (Fig. 5c) was also noted, indicative of a chronically formed lesion. Gram stains of the tissue surrounding the abscess were negative for bacterial forms. The abscess was primarily situated from the muscularis propria to the submucosa of the esophagus (Fig. 4).\nClinically, the solid lesion seen on the initial CT (Fig. 1) was suspected to be an early sign of a mediastinal abscess, possibly seeded during the initial or recurrent bacteremia episodes. However, it could not be definitively concluded that the abscess had originated from the esophageal epithelium, and no other foci of infection were identified, making it challenging to determine the exact cause of the abscess based solely on the pathological findings. Additionally, the progression of tissue necrosis indicated that the source of the bleeding was an aorto-esophageal fistula, formed by the extension of the mediastinal abscess toward the aorta (Fig. 6). Pathologically, there were no signs of gastric cancer metastasis or recurrence, and no cardiac valvular abnormalities were identified.",
"gender": "Male"
}
] |
PMC11416686
|
[
{
"age": 12,
"case_id": "PMC10546250_01",
"case_text": "A 12-year-old girl, on treatment for autoimmune haemolytic anaemia, presented with a history of intermittent fever for 1-month, non-productive cough for 3 weeks and shortness of breath over the preceding 7 days. On examination, the patient was febrile with a heart rate (HR) of 156 beats/min and a high respiratory rate (RR) of 64/min. Chest radiography demonstrated ill-defined, bilateral air space opacities, with a few cystic lucencies in the right perihilar region (Figure 1). GeneXpert (sputum) detected mycobacterium tuberculosis (MTB) and the patient was started on antitubercular therapy (ATT). The respiratory failure necessitated ventilator support. Twenty days post-admission, the patient experienced sudden respiratory distress and a repeat CXR (Figure 2) demonstrated patchy opacities with an increased number of cystic lucencies in both lungs, along with the development of subcutaneous emphysema and pneumomediastinum. Contrast-enhanced CT (CECT) (Figure 2) revealed multiple thin-walled cysts, ground glass opacities (GGOs) and a few nodules bilaterally, along with pulmonary interstitial emphysema and pneumomediastinum. Multiple hypodense splenic granulomas and a few enlarged mediastinal and periportal lymph nodes were also seen. The patient responded well to treatment and was weaned off the ventilator within 10 days. A follow-up CXR (Figure 2) 5 months later appeared normal.",
"gender": "Female"
},
{
"age": 7,
"case_id": "PMC10546250_02",
"case_text": "A 7-year-old boy, previously diagnosed with disseminated TB, on ATT for 3 months and on home oxygen therapy, presented to the paediatric outpatient department with complaints of intermittent increased cough from before and was found to have decreased oxygen saturation on room air. He underwent a CXR (Figure 3) that revealed a left loculated pneumothorax. The patient was admitted for assessment of multidrug resistant (MDR) TB and air leak. Contrast-enhanced CT chest (Figure 3) confirmed the left pneumothorax and revealed a thick-walled cavity in the right middle lobe and multiple cysts in both lungs. A previous CECT chest 2 months prior (Figure 4) was reviewed and revealed GGOs, a few tiny cysts, multiple bilateral nodules, along with necrotic mediastinal and abdominal lymphadenopathy, and a few small hypodense lesions in the liver suggestive of non-calcified granulomas. There was an interval increase in the number and size of the lung cysts, with a decrease in the number of nodules. Sputum microscopy and culture were negative. Bronchoscopy indicated signs of chronic inflammation and destruction of the distal bronchial segments and provided abnormal early entry into numerous cavitary structures, unlike the non-diseased areas where the distal branches gradually became smaller in size and did not allow entry into the lung parenchyma. Bronchial washings sent for culture were positive for TB (rifampicin sensitive). The patient was continued on ATT and demonstrated subsequent improvement.",
"gender": "Male"
},
{
"age": 13,
"case_id": "PMC10546250_03",
"case_text": "A 13-year-old emaciated, underweight girl presented with a cough for 12 days and projectile vomiting, associated with altered sensorium, blurring of vision and double vision over the preceding 4 days. There was a history of low-grade fever for 1 month associated with decreased appetite, weight loss and night sweats. The patient also had a positive contact history for pulmonary TB from her grandmother. Non-contrast CT brain at another facility (not shown) revealed communicating hydrocephalus and a hypodense fluid collection in the prevertebral space at the C2-C3 vertebral level, suggestive of a prevertebral abscess. Clinical and cerebrospinal fluid (CSF) findings suggested the diagnosis of tuberculous meningitis and the child was started on ATT. During her hospital stay, she developed sudden respiratory distress. The CXR (Figure 5) revealed a left pneumothorax with a few infiltrates in the right mid zone. An intercostal drainage (ICD) tube was subsequently placed. Sputum GeneXpert detected MTB. A CT of the chest (Figure 5) demonstrated a left hydropneumothorax with underlying collapse, multiple centrilobular nodules and a TIB pattern in both lungs, a few tiny cysts in both upper lobes, patchy consolidation in the right lower lobe, mediastinal lymph nodes with calcification, and hepatosplenomegaly with multiple liver and splenic granulomas. The patient improved on ATT and follow-up CXR (Figure 5) after 5 months revealed resolution of the radiographic findings.",
"gender": "Female"
},
{
"age": 7,
"case_id": "PMC10546250_04",
"case_text": "A 7-year-old girl was admitted with complaints of fever over 3 weeks, tachypnoea and cough for 4 days. In view of the respiratory distress, the child was transferred to the paediatric intensive care unit on day 5 post-admission. Mycobacterium tuberculosis was detected on sputum GeneXpert evaluation, and ATT was initiated. On day 11, the child experienced a sudden exacerbation of her respiratory distress. The CXR (not shown) revealed a left pneumothorax, for which an ICD was inserted. Subsequent CECT chest (Figure 6) revealed extensive GGOs and confluent nodular opacities in both lungs with patchy consolidation in both lower lobes, along with small cysts and bronchiolar dilatation. Other CT findings were mediastinal lymphadenopathy, pulmonary interstitial emphysema in the left upper lobe, minimal left pneumothorax with a pleural effusion, hepatosplenomegaly and hypodense non-calcified granulomas in the liver and spleen. The spleen also demonstrated a few small wedge-shaped regions of non-enhancing parenchyma suggestive of old infarcts. The patient responded well to ATT and recovered.",
"gender": "Female"
},
{
"age": 0,
"case_id": "PMC10546250_05",
"case_text": "An 18-month-old male with disseminated MDR TB, on an MDR regimen for 5 months, with severe acute malnutrition and recurrent pneumothoraces was being followed up. The patient had a history of a recent admission with a right-sided pneumothorax (Figure 7) and pneumonia. He was managed with ICD tube drainage and IV antibiotics and subsequently discharged. A follow-up CXR (Figure 8) after 2 months showed multiple cystic lucencies and haziness in both lungs, predominantly in the upper zones. The CT chest (Figure 8) revealed resolving consolidation with associated architectural distortion and traction bronchiectasis in the perihilar regions along with multiple cysts of varying sizes in both lungs. The patient responded to ATT (MDR regimen) and subsequently recovered.",
"gender": "Male"
}
] |
PMC10546250
|
[
{
"age": 38,
"case_id": "PMC10630002_01",
"case_text": "A 38-year-old female patient was admitted to the hospital because a lung mass was found for 2 days. The lung examination revealed a space-occupying lesion in the middle lobe of the right lung. The patient had no clinical symptoms such as cough, sputum, and fever. The superficial lymph nodes were not palpable. The level of serum markers including CEA, NSE, and AFP showed normal.\nThe CT examination revealed a nodule in the inner segment in the middle lobe of the right lung. The nodule was about 13 mm x 12 mm x 13 mm in size. The blood vessel and bronchus ran naturally without any involvement (Figure 1(a)). There was a small cavity in the nodule, and the inner wall was smooth (Figure 1(b)). The nodule was slightly strengthened when enhanced by the scan (Figure 1(c)). There were shallow lobes and burrs on the edge (Figure 1(d)). No enlarged lymph nodes were found in the hilar and mediastinum. There is no pleural effusion on both sides of the chest. The radiologists considered the nodule as a lung cancer.\nThe operation of thoracoscopic lobectomy+regional lymph node dissection+closed thoracic drainage was performed. The operator found a grayish-white mucoid mass located in the medial segment of the right middle lobe. Its size was about 1.5 cm x 1.5 cm x 1.5 cm. The section was medium texture, with a small cyst in the middle of the mass. Group 11 lymph nodes of the right lung were swollen.\nA grayish-white lesion with a size of 1.2 cm x 1.0 cm x 1.0 cm was seen in the lung tissue section. Its boundary was not clear. The lesion was considered as benign lesion in intraoperative frozen pathology. A clear diagnosis needed to be determined after routine paraffin sections.\n (1) Histological Changes. There were two kinds of tumor cells in the lesion, namely, mucous cells and basal cells. Most of them were arranged in an adenoid structure, and a few were papillary structures. Some gland cavities expanded, and mucus was accumulated in the cavities (Figure 2(a)). The cavities were lined purely by mucinous luminal cells, and a continuous layer of basal cells was under the mucinous luminal cells (Figure 2(b)). The mucinous luminal cells did not show obvious atypia, and the nucleus was located at the base of the cells. There was abundant intracellular and extracellular mucus (Figure 2(c)). Under the base of the epithelium were round basal cells, most of which were arranged in a single layer. The basal cell size was relatively uniform, and no mitosis or necrosis was found (Figure 2(d)). Basal cells in some areas were not obvious (Figure 2(e)). The outer stroma of the basal layer was interstitial cells, with lymphocytes and plasma cells infiltrating. There were abundant interstitial cells in some sections (Figure 2(f)). No pleural invasion was found, and no metastasis was found in the lymph nodes of group 11 (0/10).\nP40, P63, CK5/6, and TTF-1 in continuous basal cells showed positivity (Figures 3(a) and 3(b)). SMA in interstitial cells showed positivity. CK7, Tyr1068 EGFR, and MUC1 in mucinous luminal cells all showed positivity, while NapsinA was focally positive (Figures 3(c) and 3(d)). Positive index of Ki-67 was about 2%.\nThe mucinous luminal cells and extracellular mucus were stained bluely by AB-PAS.\nNo tumor recurrence or metastasis was found in the patient's 2-year follow-up.\nThe pathological diagnosis was BA (distal type) (5th edition WHO, ICD-O code: 8140/0).",
"gender": "Female"
}
] |
PMC10630002
|
[
{
"age": 40,
"case_id": "PMC11340831_01",
"case_text": "A 40-year-old male patient had presented with the complaint of pain and swelling on the right side of the face for eight days. Progressively the swelling increased resulting in trismus and odynophagia. Swelling on the right side of the face extended from the right zygomatic arch to the inferior border of mandible (superoinferior extent) and from the right corner of mouth to the posterior border of ramus of mandible (anteroposterior extent). The swelling was firm, tender to palpation and very tense. Skin overlying the swelling was warm and erythematous. In addition, there was noticeable swelling below the inferior border of mandible on the right side. The interincisal opening was about 10 mm. There was progressive discolouration and necrosis of the skin over the right submandibular region [Figure 1a and b]. Even though interincisal opening was restricted, a carious mandibular second molar was seen on the right side, which was tender to palpation.\nA provisional diagnosis of right submandibular, submasseteric and buccal space infection along with necrosis of the overlying skin in the submandibular region was made. Radiological examination revealed periapical rarefaction associated with a carious mandibular right second molar [Figure 2].\nThe fascial space was drained extraorally via a submandibular incision. Parenteral medication and intravenous fluids were given to help improve the patient's general condition. Care was taken to maintain adequate hydration of the patient. After the abscess was drained and the swelling reduced, the interincisal opening improved. The odontogenic foci of infection were removed under local anaesthesia two days following the incision and drainage of the abscess. Both the procedures were not done simultaneously as the patient had trismus.\nAs the swelling on right side of the face and the pus discharge through the submandibular incision reduced, the wound was thoroughly debrided under local anaesthesia. Around 3-4 days following the incision and drainage of the abscess, when the necrotic tissue became defined, debridement was carried out and the wound was given periodic dressings to ensure formation of healthy granulation tissue. This allowed us to evaluate if further debridement was necessary. Following debridement, a defect of around 7 cm x 4 cm was evident in the submandibular region [Figure 3a].\nThe TPFF was planned to cover the defect. Under local anaesthesia, the flap was outlined and the pre-auricular incision was made to gain access to the temporoparietal fascia (TPF) [Figure 3b]. The superficial temporal artery (STA) was marked pre-operatively with a handheld Doppler, and the dissection was carried out within the subcutaneous plane from the inferior to superior direction for the ease of harvesting. Once the TPF was exposed, the STA was located and the TPF was elevated from the temporalis fascia. The plane of flap elevation was deep to the TPF. Due care was taken to prevent injury to the temporal branch of the facial nerve. Once the flap was raised, a soft tissue tunnel was created to deliver the flap to the recipient tissue bed where it was sutured with the help of vertical mattress sutures. The flap is tunnelled lateral to the zygomatic bone [Figure 3c]. The flap pivotal point was at the entry point of the vascular pedicle into the fascia, just above the zygomatic arch. The donor site was closed primarily in anatomic layers [Figure 3d and e].\nDuring subsequent follow-ups, it was observed that the donor site scar was well masked [Figure 3f]. There was no scar alopecia. Hair growth over the flap corresponded to the beard but was more than that of the beard, so the patient had to do regular trimming. The flap was well settled, adhered to the facial contours and there was reasonable facial symmetry on frontal as well as lateral profiles [Figures 4a-c]. The patient was satisfied with the aesthetic outcome and no functional deficits were reported.",
"gender": "Male"
}
] |
PMC11340831
|
[
{
"age": 76,
"case_id": "PMC10754631_01",
"case_text": "A 76-year-old woman, known to have cytomegalovirus (CMV) colitis diagnosed through a colonoscopy with colonic biopsy that tested positive for CMV, presented with ongoing diarrhea and rising CMV titers despite medical treatment with ganciclovir, foscarnet, and weekly IgG infusions. Over the course of four years, the patient had multiple hospital admissions. Ganciclovir resistance testing revealed a mutation, D843D/V, in the UL54 region, possibly causing resistance to ganciclovir, foscarnet, and cidofovir. Subsequently, she underwent various first-line, second-line, and investigational therapies, including interferon alpha, intravenous foscarnet, intravenous ganciclovir, valganciclovir, letermovir, leflunomide, and multiple cycles of interleukin-2 (aldesleukin) injections. Despite receiving multiple lines of treatment, her symptoms persisted, with worsening diarrhea and abdominal pain that required multiple emergency room visits. Her CMV titers remained elevated (Figure 1). Repeat CT scans of the abdomen and pelvis showed progression and worsening colon thickening, involving the entire colon and cecum compared to earlier scans that indicated involvement of only the ascending colon and cecum. A repeat colonoscopy (Figure 2) revealed pan colitis with ulceration, and the biopsy confirmed severe colitis with positive CMV inclusion bodies and immunohistochemistry from multiple sites of ulceration and inflammation (Figures 3(a) and 3(b)). The patient underwent a trial of fresh frozen plasma, which was unsuccessful. After exhausting all medical treatment options and due to the worsening of CMV colitis, a multidisciplinary decision was made to proceed with a pan colectomy, which was performed around mid-2021, as indicated by an arrow on Figure 1. Initial postoperative CMV titers remained elevated (Figure 1), but subsequent measurements ranged between 1000 and 2000 copies/ml, resulting in significant clinical improvement.",
"gender": "Female"
}
] |
PMC10754631
|
[
{
"age": 66,
"case_id": "PMC10876098_01",
"case_text": "The patient was a 66-year-old woman with a medical history of schizoaffective psychosis and chronic kidney disease stage 4 (G4A1) by Kidney Disease Improving Global Outcomes (KDIGO) criteria of unknown etiology. She was followed in a psychiatry outpatient clinic and, according to clinical records, was prescribed quetiapine and lorazepam; however, the ongoing therapy could not be confirmed upon admission. She was brought to the emergency department due to altered consciousness and language disturbances that had been progressing for a week. She denied any recent complications or cardiopulmonary, gastrointestinal, or genitourinary symptoms.\nOn physical examination, she appeared prostrate (scoring nine on the Glasgow Coma Scale, E3V2M4), pale, and dehydrated; afebrile, normotensive, and with a normal heart rate. She exhibited perioral fasciculations, dysarthria, flaccid tetraparesis, hyperreflexia, and bilateral clonus. Ocular motility was unremarkable without nystagmus. No muscular strength or sensory asymmetries were noted, with a flexor plantar reflex bilaterally.\nAmong the diagnostic tests conducted upon admission, acute kidney injury (KDIGO stage 2) was evident, with an estimated glomerular filtration rate (eGFR) of 11 mL/min/1.73 m2, hypernatremia with serum hyperosmolality, and hypothyroidism, as evidenced in Table 1.\nThe urinalysis revealed no significant alterations (Table 1). A 12-lead electrocardiogram (ECG) showed sinus rhythm with a heart rate of 82 beats/minute, peaked T-waves, and a prolonged QTc interval of 534 ms. Renal-bladder ultrasound ruled out obstructive pathology, and a cranial CT scan showed no acute vascular pathology or space-occupying lesions.\nShe was admitted to the internal medicine department for further evaluation and treatment, with psychotropic medications discontinued and intravenous fluid therapy initiated. During hospitalization, there was progressive improvement in renal function with fluid therapy; however, sustained polyuria with hypernatremia was observed. On the fourth day of admission, after contacting a day center assisting with the patient's medication management, it was discovered that she had been taking lithium carbonate, which should have been discontinued based on the assistant psychiatrist's recommendation over a year ago. A plasma lithium level was then measured, which was still close to therapeutic limits (lithium level of 0.6 mmol/L), even after five days of isotonic fluid therapy. The neurological, cardiological, and renal manifestations and fluid-electrolyte balance were consistent with chronic lithium intoxication.\nFrom a renal perspective, there was polyuria with intermediate urinary osmolality (518 mOsm/kg on admission), improvement in renal dysfunction, and sustained hypernatremia in a patient without preserved thirst reflex after intensive fluid therapy. A mixed mechanism is considered likely, involving osmotic diuresis (uremia) and partial nephrogenic diabetes insipidus.\nNeurological manifestations, characterized by encephalopathy with signs of both first and second neurons, are attributable to chronic lithium intoxication. Importantly, other acute neurological pathologies were ruled out, as the patient underwent cranial and cervical MRI and cerebrospinal fluid examination.\nAdditionally, the electrocardiographic changes and hypothyroidism were also attributable to this clinical picture.\nThe patient showed progressive clinical improvement, with a recovery of neurological status and significant improvement in functional performance with support from physical medicine and rehabilitation. Concurrently, there was normalization of renal function with intensified fluid therapy for positive fluid balance and discontinuation of the offending drug. It is worth noting that fluid therapy was halted on the twelfth day of admission, with no observed lithium rebound phenomenon, which can sometimes occur due to transcellular movement and slow drug diffusion.",
"gender": "Female"
}
] |
PMC10876098
|
[
{
"age": 34,
"case_id": "PMC10857918_01",
"case_text": "A 34-year-old, active-duty male orthopedic surgeon with a past medical history of allergic rhinoconjunctivitis was referred to the allergy clinic for evaluation and consideration of AIT. His symptoms consisted of rhinorrhea, sneezing, nasal congestion, and itchy, watery eyes. His symptoms had been present for several years occurring predominantly in the spring and fall but also perennially when exposed to animals such as cats, dogs, and horses. The patient was raised on a ranch where he was exposed to horses and cattle, but his current pet exposures only consisted of a dog.\nThe patient's exam was notable for injected conjunctiva, nasal mucosa edema, and a cobblestone throat. His symptoms were not alleviated with oral cetirizine and nasal fluticasone. He had previously been receiving AIT for 18 months, which had improved his symptoms but had not received AIT for six months due to a move to his current duty station.\nAn aeroallergen skin testing panel was performed with the addition of cattle and horsehair. Skin testing was positive for trees, weeds, molds, cats, dogs, dust mites, and horsehair; cattle hair was negative (Table 1). The risks and benefits of AIT were discussed with the patient who elected to proceed with restarting AIT. He was started on AIT for trees, weeds, molds, cats, dogs, dust mites, and horsehair in addition to counseling on aeroallergen avoidance. He responded well to AIT but, unfortunately, was not able to continue AIT because of a military deployment.",
"gender": "Male"
}
] |
PMC10857918
|
[
{
"age": 60,
"case_id": "PMC11377932_01",
"case_text": "A 60-year-old woman, who worked as a baker, presented with a complaint of a wound in her right ankle accompanied by pain (visual analog scale (VAS) 3/10) in the past three months. The complaint began with swelling in both lower limbs that got worse one year earlier. There was a change of skin color on both the patient's leg and foot which became darker over time. The patient had a history of hypertension. On physical examination of the medial side of the right ankle region, there was a solitary ulcer, sized 3x4 cm with irregular edges, erythema ulcer base accompanied by purulent discharge, dry distant tissue, edema (+), and hyperpigmentation on 1/3 mid of the lower leg until dorsal side of the foot ( Figure 1A). Plethysmography examination revealed her ankle and arm systolic pressure, then it was divided to get the ankle-brachial index (ABI) with a result of her left ABI was 1.25 and her right ABI was 1.06. There was severe reflux (duration >1000 ms) in above the knee (ATK) and below the knee (BTK) great saphenous vein (GSV) and moderate reflux (duration 500 ms - 1000 ms) in the common femoral vein and popliteal vein of both lower limbs from duplex ultrasound (DUS) examination of the lower extremity. No obstruction or thrombus was found in the deep vein. The flow of arteries in her both lower extremities was normal. The patient was diagnosed with CVI on both lower limbs with active VLU on medial side of the right ankle (C6sEpAsdPr). The venous clinical severity score (VCSS) was 15. The patient agreed to EVLA treatment on the right lower limb and received ceftriaxone antibiotics for five days. The procedure was done after the patient finished the antibiotics course.\nEVLA was performed under spinal anesthesia. Mapping was done on the right GSV. The diameter of the saphena-femoral junction (SFJ) was 11.0 mm, proximal ATK GSV 9.2 mm, medial ATK GSV 6.0 mm, distal ATK GSV ATK 6.1 mm, proximal GSV BTK GSV 5.2 mm, media BTK GSV 4.5 mm, and distal BTK GSV 3.0 mm. Double puncture was used on distal BTK and distal ATK GSV because of tortuosity and branching at distal ATK. Puncture and application of tumescent anesthesia were done by guided DUS. EVLA started 3 cm from SFJ with laser power of 6 W linear energy density (LEED) 50 J/cm at proximal until media ATK, 5 W LEED 40 J/cm at media ATK until proximal BTK, and 2W LEED 20 J/cm at proximal until distal BTK. The total ablated GSV length was 60 cm with a total of 850 mL tumescent. Lower extremity DUS on the next day showed perfectly obliterated ablated GSV, no thrombus found in the deep vein, and a patent epigastric vein. The patient was discharged one day after the procedure.\nThe patient's condition was assessed one week after EVLA, and she reported no more pain, significant rapid improvement of the ulcer, granulation tissue (+), and no more discharge ( Figure 1B). At follow-up until six months post-EVLA, the patient didn't have any complaints and had a healed ulcer. No recanalization of the treated segment was found by DUS examination. There was a 14-point improvement in VCSS score down to a score of 1.",
"gender": "Female"
},
{
"age": 50,
"case_id": "PMC11377932_02",
"case_text": "A 50-year-old male chef presented with complaints of wounds on his left ankle in the last two years accompanied by pain aggravated by walking (VAS 4/10). The patient had undergone EVLA on the left ATK GSV with phlebectomy eight months earlier, but there wasn't any improvement of the ulcer. The patient had wound care with a surgeon who suggested doing a lower extremity vessel evaluation. The patient had a history of hypertension, type 2 diabetes mellitus, and obesity with body mass index (BMI) of 39.45 kg/m 2. Physical examination of the left ankle region showed multiple ulcers sized 18x10 cm on the medial side, 8x5 cm, and 4x2 cm on the lateral side with irregular edges ( Figure 2A). The ulcer had an erythema base, purulent discharge, dry distant tissue, and edema (+). Hyperpigmentation of 1/3 mid of the left lower leg until dorsal side of the left foot. Plethysmography examination revealed his ankle and arm systolic pressure, then it was divided to get the ABI with a result of his left ABI was 1.14 and his right ABI was 1.10. Lower extremity DUS revealed perfectly obliterated proximal until distal ATK left GSV, severe reflux (duration >1000 ms) on BTK left GSV, common femoral vein, popliteal vein, and accessory veins of both lower limbs, and moderate reflux (duration 500 ms - 1000 ms) in right GSV ( Figure 3). No obstruction or thrombus was found in the deep vein. The flow of arteries in his both lower extremities was normal. The patient was diagnosed with CVI on both lower limbs and active VLU on medial and lateral side of the left ankle region (C6sEpAsdPr) with VCSS 23. The patient decided to undergo EVLA on the left lower limb. Previous results from culture of the ulcer base swab showed Pseudomonas aeruginosa (which is resistant to cefazoline). The patient received ceftriaxone and metronidazole for five days. The procedure was done after the patient finished the antibiotics course.",
"gender": "Male"
},
{
"age": 65,
"case_id": "PMC11377932_03",
"case_text": "A 65-year-old male farmer presented with complaints of ulcers with malodorous discharge at the right ankle accompanied by pain (VAS 4/10) in the past two years which became worse and enlarged in the past six months. Complaints begin with swelling of both lower limbs for 11 years. The patient had undergone various traditional treatments before such as the use of a flour mixture. The patient had a history of hypertension and diabetes mellitus, was an ex-smoker, and was obese with a BMI of 33.3 kg/m 2. Physical examination showed multiple ulcers sized 10x8 cm at lateral side of the right ankle and 8x3 cm at medial side of the right ankle with irregular edge, wet base with purulent discharge, erythema, edema (+), and hyperpigmentation from 1/3 proximal of the right lower leg until dorsal side of the lower foot ( Figure 4A). Plethysmography examination revealed his ankle and arm systolic pressure, then it was divided to get the ABI with a result of his left ABI was 1.22 and right ABI was 1.01. Lower extremity DUS showed severe reflux (duration >1000 ms) of bilateral GSV, small saphenous vein (SSV), common femoral vein, and popliteal vein. No obstruction or thrombus was found in the deep vein. The flow of arteries in his both lower extremities was normal. The patient was diagnosed with bilateral CVI with active VLU at medial and lateral side of right ankle region (C6sEpAsdPr), and VCSS was 22. The patient decided to undergo EVLA on the right lower limb first and received ceftriaxone and metronidazole five days before the procedure. The procedure was done after the patient finished the antibiotics course.\nEVLA was done under spinal anesthesia. Mapping was done along the right GSV and SSV. The diameter of SFJ was 12.0 mm, proximal ATK GSV was 7.5 mm, media ATK GSV was 7.0 mm, distal ATK GSV was 7.8 mm, proximal BTK GSV was 6.0 mm, media BTK GSV was 4.0 mm, and distal BTK GSV was 3.0 mm. The proximal SSV diameter was 7.0 mm, and the media SSV was 6.5 mm. Puncture by guided DUS was done at three locations for GSV: medial side of dorsalis pedis (distal from the ulcer), proximal BTK GSV with laser catheter introduced retrogradely, and proximal BTK GSV with laser catheter introduced until 3 cm passed SFJ. EVLA was done with laser power 6 W LEED 50 J/cm in proximal until media ATK GSV, 5 W LEED 40 J/cm in media ATK GSV until proximal BTK GSV, and 2 W LEED 20 J/cm in proximal until distal BTK. Puncture for SSV was done at media BTK, laser catheter was introduced until 5 cm passed Sapheno-poplitea Junction. EVLA at proximal until media SSV was done with laser power 4 W LEED 30 J/cm. The total ablated GSV length was 64 cm and the SSV length was 10 cm with a total of 850 mL of tumescent amount. Lower extremity DUS on the next day showed the ablated GSV and SSV were perfectly obliterated, no thrombus found, and a patent epigastric vein. Wound dressings of the ulcer and an elastic bandage were applied to the patient's right lower limb.\nThe patient was discharged two days after the procedure with optimal medical therapy to control his risk factor and the wound care was done by the nursing team that follows the TIME concept with modern wound dressing. At follow-up until six months, the patient did not have any complaints and the ulcer and skin condition had significantly improved. There was no ulcer left, hyperpigmentation was limited to 1/3 proximal of the right lower leg, and there was a scar (+) on the previously ulcerous region ( Figure 4B). No recanalization of the treated segment was found by DUS examination. There was a 17-point reduction of VCSS down to 5.",
"gender": "Male"
}
] |
PMC11377932
|
[
{
"age": 41,
"case_id": "PMC10589049_01",
"case_text": "A 41-year-old male with no significant past medical or family history, with occasional cigar and alcohol use, presented to the emergency room with a 2-week history of dyspnea, cough with clear phlegm, and fever. He endorsed having chronic joint pain and body aches. He had normoxemia and was hemodynamically stable with nonspecific T-wave abnormalities on his electrocardiogram. Splinter hemorrhage was noted with the rest of the clinical examination being normal. For the past eight months he had similar symptoms and was treated with oral and inhaled steroids, along with bronchodilators resulting in intermittent relief, followed by a recurrence when steroids were discontinued. He had an outpatient spirometry revealing moderate obstructive airway disease with a significant bronchodilator response. Outpatient computed tomography (CT) scan of thorax demonstrated bilateral ground glass opacities suspicious for infectious/inflammatory opacities. His early hospital workup was significant for leukocytosis with a white cell count of 18,000, absolute eosinophil count of 10.1, troponin of 64,000 and BNP of 4000 (Table 1).\nCT thorax showed bilateral upper lobe patchy opacities with an extensive respiratory and infectious disease workup was negative. He was treated for non-ST elevation myocardial infarction (NSTEMI) with dual antiplatelet therapy and therapeutic doses of low molecular weight heparin (LMWH). Troponin trended upwards to 84,000 but he had a normal transthoracic echocardiogram with no regional wall motion abnormalities. There was a strong clinical suspicion of viral myocarditis. Coronary catheterization study revealed coronary artery dissection of the mid right coronary artery (Fig. 1). There was significant stenosis in all three coronary arteries, nevertheless LMWH was discontinued due to the risk of expansion of intramural hematoma in the RCA. Aspirin and Ticagrelor were continued.\nDifferential diagnosis included occult systemic infectious disease, systemic connective disease, and hematological malignancy. Rheumatology serological work up and Infectious disease work up was negative. Serum protein electrophoresis ruled out the presence of monoclonal proteins. Peripheral smear showed marked eosinophilia with no increase in blast cells or morphologic dysplasia. CT head showed pansinusitis. After ruling out many of the aforementioned differential diagnosis, Eosinophilic granulomatous polyangiitis (EGPA) or neoplastic hypereosinophilic syndrome (HES) was considered likely.\nCardiac MRI revealed large, scattered areas of left ventricular subendocardial enhancing scars (late gadolinium enhancement) with myocardial hypoperfusion and smaller areas of necrosis. No large thrombus was identified. Diffuse edema of the myocardium was noted with Septal extracellular volume abnormally elevated at 32%. There was reduced systolic function with Left ventricular ejection fraction (LVEF) of 42% and borderline thickened left ventricular myocardium. The constellation of MRI findings was highly suggestive of eosinophilic myocarditis. Bone marrow biopsy demonstrated normocellular marrow (50% cellularity) with trilineage hematopoiesis, expanded eosinophils (41% of marrow cellularity) with no increase in blasts. The FISH panel for common diagnostic/prognostic chromosomal abnormalities associated with eosinophilia and chromosome karyotype was normal (negative for rearrangement of PDGFRA, PDGFRB, FGFR1 or BCR/ABL1). Bronchoscopy revealed normal endobronchial anatomy, endobronchial mucosa, and no evidence of diffuse alveolar hemorrhage (DAH) or eosinophilia.\nA diagnosis of Eosinophilic myocarditis secondary to EGPA satisfying American College of Rheumatology (ACR) criteria was made based on elevated eosinophilic count, asthma of 8 months duration, chronic sinusitis, nonspecific migratory pulmonary infiltrates on CT imaging, eosinophilic myocarditis type findings on cardiac MRI, and splinter hemorrhages on exam. The bone marrow biopsy/unremarkable FISH results made neoplastic hypereosinophilic syndrome unlikely. The presence of coronary artery dissection in the RCA, and myocarditis in our patient led to administration of pulse doses of Methylprednisone, and systemic Cyclophosphamide followed by tapering oral prednisone therapy. He was noted to be doing well about a year later in the outpatient when last seen.",
"gender": "Male"
}
] |
PMC10589049
|
[
{
"age": 27,
"case_id": "PMC11153700_01",
"case_text": "A 27-year-old female was referred by neurology to a precision medicine clinic for consideration of WES to look for an underlying genetic component to her intellectual disability and neurodevelopmental difficulties such as autism spectrum disorder (ASD), obsessive-compulsive disorder (OCD), tics, seizures, and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). PANDAS was suspected at age 22 after recurrent Streptococcal infections, when the patient developed encephalopathy. Other clinical presentations included photophobia, a small pituitary gland, polycystic ovarian syndrome (PCOS), amenorrhea, early menopause, and anosmia. The patient also had intermittent elevated iron labs associated with iron overload. See full pedigree (Figure 1).\nPrevious genetic testing had been performed around age 15 (Figure 2), including fragile X testing and evaluation of PTEN, neither of which yielded actionable results. In addition, a microarray was performed, which revealed a 10p15.1 (4,862,814-5,186,815) x1 deletion. However, this deletion was interpreted as not causal for the patient's presentation. Based on the iron overload, the HFE gene was evaluated for common variants associated with hereditary hemochromatosis (HH). The patient was found to have a heterozygous mutation in the HFE gene (p.Cys282Tyr) that is often associated with HH; however this causality is linked to homozygous presence of the p. Cys282Tyr allele. Individuals with heterozygous p. Cys282TyrY HFE variant do not usually develop iron overload. No other genetic findings were apparent with their previous genetic tests. Despite the multiple single gene and microarray tests, no explanation for the NDD, seizure history, and encephalopathy was identified (Figure 3A).\nUpon consultation with the precision medicine clinic, WES was performed, which revealed a missense mutation in the HNRNPU gene (c.2425-2A>G; rs1553281924), which was reported as pathogenic and is associated with HNRNPU-related neurodevelopmental disorder (HNRNPU-NDD) and developmental and epileptic encephalopathy-54 (DEE54). This variant is absent from Gnomad but has been reported in a patient with HNRNPU-NDD. OMIM reports of mutations in the HNUNPU gene with DEE54 (OMIM #: 617391) exhibit phenotypes that are consistent with the patient's ID/ASD, seizure history, and encephalopathy (Figures 2, 3B), and this variant was considered diagnostic by the referring neurologist. This HNRNPU gene mutation is predicted to disrupt a canonical splice acceptor site and interfere with splicing, though the consequence on protein structure is unknown. Given its occurrence in the splice site of the last exon, it remains uncertain what spliced product would be produced and whether the resulting protein would be in-frame or out-of-frame, hence making it challenging to predict its potential for nonsense-mediated decay.",
"gender": "Female"
},
{
"age": 0,
"case_id": "PMC11153700_02",
"case_text": "Another HNUNPU mutation has been reported that lies in a nearby genetic region to the variant described in this case report. This variant (HNRNPU c.2425-3C>A) has been linked to DEE54 and shares similarities with the patient in our study, such as seizure age of onset and seizure triggers, albeit with much more severe symptoms. Our patient exhibits mild dysmorphic features, such as widely spaced eyes and high arched eyebrows. Her first febrile seizure occurred at 10 months old, with subsequent seizures often triggered by fever spikes. Developmentally, this individual displayed only minor delays; sitting commenced at 9 months, walking at around 17 months, with no notable delays in speech or behavior. However, following the PANDAS diagnosis in 2015, behavioral difficulties escalated, characterized by increased agitation, aggression, and expressive language challenges during episodes. Symptoms of OCD and ASD also intensified post-PANDAS diagnosis. These observed phenotypes align with previous reports of HNRNPU gene mutations and DEE54. Most patients with HNRNPU mutations experience seizures, with 91% occurring before the child turns 2 years old. Furthermore, half of the patients evaluated in this study had ASD and/or significant autistic features. Obsessive-compulsive features have also been documented in several other reports.\nAlthough there is one other reported instance of this pathogenic mutation in ClinVar, the physical characteristics of individuals carrying this mutation have not been previously documented or reported. This novel variant represents a significant advancement in our medical understanding, contributing new insights to the field. In addition, three variants of uncertain significance (VUSs) were found in two genes (MFN2 and HSD17B4), classified as possibly relating to the observed phenotype. While there was no change in treatment plan based on the genetic testing, these results finally provided answers to the patient and their family as to the underlying cause of their symptoms.\nOver a year after WES was completed and based on the patient's borderline hemochromatosis presentation, a physician from the Benign Hematology and Transfusion Medicine department (associated with the Vascular Medicine Institute) contacted the precision medicine clinic to reanalyze the WES data for either: 1) compound heterozygotes for other HFE mutations along with p. Cys282Tyr, such as point mutations that created a premature stop codon (p.Tyr52Ter; p. Glu168Ter; p. Leu270Ter; p. Ala271Ter; p. His341Ter); 2) other mutations affecting the protein sequence (p.Asp141Tyr; Lys166Asn); or 3) the presence of genetic modifiers of the HFE genes such as: BMP2, BMP6, GNPAT, PCSK7 or variants in the genes for hepcidin (HAMP) or hemojuvelin (HJV). Reanalysis was completed on the data and no additional variants were found (Figures 2, 3B), thus the patient's intermittent elevated serum iron concentration remains unexplained. Because the WES data were easily accessible to the precision medicine team, these results could be gathered within 1-2 days and required no additional samples or testing, decreasing diagnostic costs and increasing the utility of the initial WES testing.\nSubsequently, the patient's maternal aunt was clinically diagnosed with hereditary hemorrhagic telangiectasia (HHT), without genetic testing. Familial diagnosis of HHT is important as it presents an opportunity for cascade screening of close family members. The patient's endocrinologist contacted the precision medicine clinic for WES reanalysis in light of this new family diagnosis. The main causal HHT genes were evaluated (ACVRL1, ENG, and SMAD4), which revealed no pathogenic variations (Figures 2, 3B). Though there are a few reported instances where large multi-exon deletions have been identified in HHT, the WES that was performed can detect deletions at least 1 kb in size. However, there remains a residual risk of missed small deletions and complex variants when the specific family genetic variant is unidentified. Nevertheless, the readily available ES results allowed for a swift reevaluation, minimizing, though not entirely ruling out, the need for individual assessment of the HHT genes. This efficient process underscores the utility of WES data, especially when organized systems allow for quick reanalysis as needed.",
"gender": "Female"
}
] |
PMC11153700
|
[
{
"age": null,
"case_id": "PMC10861315_01",
"case_text": "In 2020, a rheumatologist referred a male patient in his 50s to our thoracic department for a first right pneumothorax caused by a rheumatoid nodule rupture ( Fig. 1 ). He was being administered methotrexate and steroids to manage rheumatoid arthritis that started 10 years earlier. No other preexisting conditions were noted. The patient presented with pneumothorax in addition to rheumatoid arthritis symptoms and exhaustion.",
"gender": "Male"
},
{
"age": null,
"case_id": "PMC10861315_02",
"case_text": "The pneumothorax cavity gradually enlarged over 2 months, and the patient underwent thoracic drainage. Repeated pleurodesis was performed because of the presence of leaks; however, it was ineffective. The patient expressed a preference for the treatment to be completed in one operation as much as possible.\nSpigot filling is generally used when pleurodesis fails. However, in this case, the nodules were widely contiguous, and the feasibility of Spigot filling was uncertain; therefore, it was not performed.",
"gender": "Unknown"
},
{
"age": null,
"case_id": "PMC10861315_03",
"case_text": "The patient underwent surgery 3 months after the referral to our department under general anesthesia. Although a pleural defect was identified ( Fig. 2 ), the surrounding area was fragile, and direct suturing was not performed because it was judged to increase the wound size. Due to the expectation of widespread adhesion, we performed parietal pleural covering. A TachoSil covering was placed over the fistula ( Fig. 2 ), and the parietal pleura was dropped over the TachoSil. The patient remained in good condition for approximately 2 weeks, after which the pneumothorax recurred. \nA Clagett window and an Eloesser flap were not selected for the next course of action because of the requirement for long-term dressing changes. Similarly, conventional thoracoplasty was not selected because of its impact on appearance.\n Although no obvious intrathoracic infection was observed at this stage, we performed pedicled omentum filling. This choice was driven by several factors, including the expectation of strong adhesion, the patient's immunosuppressed state, concerns regarding future infection, and the rheumatologist's intention to use more potent antirheumatic drugs (Janus kinase inhibitors) in the future.",
"gender": "Unknown"
},
{
"age": null,
"case_id": "PMC10861315_04",
"case_text": "A second surgery was performed approximately 1 month after the initial surgery. The pedicled omentum was harvested in a stemlike manner through a median incision in the upper abdomen and guided into the thoracic cavity via a hole created in the diaphragm ( Fig. 3 ). The patient was discharged without major adverse events postoperatively on postoperative day 15 after pain control and rehabilitation. Regular follow-up was conducted every month, and approximately 2 years have passed since the treatment. During the postoperative period, the rheumatoid nodule increased and decreased repeatedly; however, we believe that due to its firm adhesion, the pneumothorax did not recur ( Fig. 4 ).",
"gender": "Unknown"
}
] |
PMC10861315
|
[
{
"age": 21,
"case_id": "PMC10906048_01",
"case_text": "A 21-year-old man with no smoking history and no significant past medical history presented with a persistent cough. Subsequent imaging revealed a lobular heterogeneous enhancing mass arising in the right lower. The physical exam was unremarkable. Computed tomography of the thorax as part of the preoperative evaluation showed the absence of other localization.\nThe mass was surgically removed. A lobectomy was performed for diagnostic and therapeutic purposes.\nGrossly, the tumor was multinodular, firm, and surrounded by a thin, and fibrous pseudo-capsule. It measured up to 6 cm in greatest dimension, endobronchial with an extension into the underlying lung parenchyma and no attachment to the visceral pleura. The cut surface had a whorled white tan appearance with focal myxoid and hemorrhage changes (Figure 1). The surgical margin was free of tumors.\nMicroscopically, the tumor was well-circumscribed and low to moderately cellular. It was composed of bland spindle cells arranged in crisscrossing fascicles within hyaline to myxoid stroma that tends to vary in different areas of the tumor (Figure 2). Tumor cells had scant wispy cytoplasm, uniform elongated nuclei with finely clumped chromatin and small inconspicuous nucleoli. The cells showed little mitotic activity. Epithelioid cells were present focally. There was a network of branching capillary-sized blood vessels. In some areas, the cellularity was increased, in a fibrous background. The transition between fibrous and myxoid areas was often abrupt. The pleura was free of tumors. Five pedicular lymph nodes were removed and they were reactive. Immunohistochemically, the neoplastic cells showed immunoreactivity for CD99 and MUC4 with a strong and diffuse expression of this antigen (Figure 3). They were negative for CK, SMA, EMA, H-caldesmon, Desmin, STAT6, MDM2, CD34, hormonal receptors, ALK (5A4, P80), and PS100. Cytogenetic and Molecular Genetic study was performed in France and showed the absence of SS18/SYT gene rearrangement.\nPathological diagnosis was made as \"low-grade fibromyxoid sarcoma\". Her postoperative course was uncomplicated and chemotherapy or radiotherapy wasn't given. She has remained well with no evidence of disease 6 months later.",
"gender": "Male"
}
] |
PMC10906048
|
[
{
"age": 38,
"case_id": "PMC11238649_01",
"case_text": "A 38-year-old male patient, with no significant medical history, suffered an electric shock from a street wire with a voltage of 13,800 volts. The electric shock involved a left hand entry point and a right retroauricular region exit point. This incident occurred while the patient was cleaning the roof of his house. The patient was reportedly in contact with an exposed electrical source, which resulted in the shock. Upon initial assessment, he exhibited symptoms consistent with electrical injury but no immediate life-threatening conditions.\nUpon admission to the emergency department, the patient was evaluated with a Glasgow Coma Scale score of 15, indicating full consciousness. His vital signs showed normotensive and tachycardic, with an oxygen saturation of 98% on room air (ambient FiO2). The physical examination revealed that he had sustained both superficial and deep second-degree burns on his face, the right retroauricular region, and thorax. Additionally, he had more severe third-degree burns on the left upper limb. These burns collectively covered approximately 25% of his total body surface area (TBSA). Upon arrival to the emergency room, there were no signs of inhalation injury such as soot in the mouth or trachea, ignited clothing, or burnt facial hair. In the intubation note from the anesthesiologist, who performed the orotracheal intubation under direct vision, the finding is referred to as airway edema, airway burn, carbonaceous sputum, and describes a bloody lesion on the affected vocal cord. Due to lack of equipment, initial video laryngoscopy could not be performed upon arrival to the emergency room.\nA notable clinical finding was the presence of stridor, a sign of potential airway compromise, which prompted the healthcare team to perform assisted mechanical intubation. This intervention was crucial for maintaining the patient's airway and ensuring adequate ventilation. Furthermore, the patient exhibited signs of compartment syndrome in his left forearm, a serious condition resulting from increased pressure within the muscle compartments. Consequently, a fasciotomy was performed as an emergency procedure to relieve this pressure and prevent further tissue damage (as depicted in Figure 1). During his hospitalization, the patient underwent a series of significant medical interventions. Notably, amputation of the left upper limb was necessitated due to severe vascular compromise (Figure 2). This drastic measure highlights the extent of the damage caused by the electrical injury. Additionally, an autologous skin transplant was performed, aiding significantly in his recovery process.\nThis positive development led the medical team to initiate the process of weaning him off assisted mechanical ventilation. Successfully transitioning from mechanical support is a crucial step in the recovery from severe injuries and respiratory compromise. Subsequent to the extubation, a control bronchoscopy was conducted to assess the airways. This examination revealed a lesion on the right vocal cord, which was identified as a secondary complication of the path of the electrical burn (Figure 3).\nThe patient's postoperative course involved continued conservative medical treatment, which proved to be effective. Remarkably, he remained asymptomatic throughout this period, exhibiting no signs of airway compromise, dysphagia (difficulty swallowing), or dysphonia (voice disorder). This absence of complications is noteworthy, considering the severity and extent of the initial injuries, including the lesion on the vocal cord. The patient was intubated for 10 days in intensive care. Although the literature states that prolonged intubation (greater than 14 days) increases the risk of vocal cord injury, the complications described as a result of this are generally complications in both vocal cords, most of the time. We do not know with certainty if the injury was caused by the intubation or if it was aggravated by it, but the findings in the anesthesiologist's intubation note give us a high index of suspicion that the injury was caused by the electric burn\nAfter a 34-day hospital stay, which included comprehensive care and monitoring, the patient's condition improved significantly. The successful management of his complex injuries and the absence of any major postoperative complications allowed for his eventual discharge. At the time of discharge, the patient's overall health had significantly improved, allowing him to leave the hospital, as depicted in Figure 4. However, it's important to note that some degree of dysphonia persisted. Due to financial constraints, the patient was only able to attend one follow-up consultation, during which persistent dysphonia was noted. Unfortunately, we were unable to conduct a comprehensive ENT examination to fully assess the patient's vocal cord function and determine the extent of recovery from the initial injury. The patient was subsequently lost to follow-up, limiting our ability to document long-term outcomes. Informed consent was obtained from the patient for the publication of this case report, ensuring adherence to ethical standards while maintaining confidentiality and anonymity.",
"gender": "Male"
}
] |
PMC11238649
|
[
{
"age": 14,
"case_id": "PMC10901254_01",
"case_text": "The patient is a 14-year-old boy with no significant past medical history who presented to the orthopedic department of a children's hospital for evaluation of a right hip pain. The patient reported that he fell down two months prior to the visit while playing football and heard a popping sound followed by pain in the posterior aspect of his right hip. The patient did not seek medical care at the time of injury and continued participating in physical activities like water skiing. As the pain did not resolve, he was then referred to orthopedics. Upon presentation to the orthopedic department, the patient described ongoing pain localized to the right ischial tuberosity and was associated with tingling down the posterior leg to the level of the mid-thigh. It was exacerbated by activity and improved with rest. There were no associated symptoms and no accompanying bruising. The severity of pain at the time of evaluation was as high as 4/10. The physical exam was significant only for decreased strength (3/5) with resisted knee flexion. The patient had not received imaging or treatment prior to the visit. Frontal and frog-leg radiographs (Figure 1A, 1B) of the pelvis were ordered for assessment.\nRadiographs revealed components of a healing right-sided ischial tuberosity avulsion fracture and a 5.8cm cluster of well-corticated, ovoid and crescent-shaped calcifications in the soft tissues near the ischial tuberosity and adjacent to the avulsed bone fragment. The affected ischial tuberosity displayed lucency and irregular margins. The unusual appearance of clustered, irregular calcific densities in the soft tissues in conjunction with the clinical context of persistent pain two months after injury raised concern for underlying calcified soft tissue mass. Evaluation with Magnetic Resonance Imaging (MRI) was warranted for further characterization (Figure 2A, 2B).\nMRI demonstrated a dark signal on both T1 and T2 weighted images suggesting calcifications. The appearance on MRI confirmed the diagnosis of ischial tuberosity avulsion fracture, and the area of concern in the adjacent soft tissues was due to the accumulation of callous adjacent to the originally avulsed bone fragment.\nThe patient was expected to make a full recovery with conservative management including rest, physical therapy, and progressive return to activity. The patient's right ischial tuberosity avulsion fracture improved clinically over several months and he was able to make a gradual return to his usual activities and sports.",
"gender": "Male"
}
] |
PMC10901254
|
[
{
"age": 65,
"case_id": "PMC11430215_01",
"case_text": "In July 2023, a 65-year-old female patient was referred to the Department of Stomatology in the Faculty Hospital in Pilsen due to an unhealed lesion with the formation of a fistula in the past 3 months after the extraction of tooth 46 in March 2023. This procedure was performed without any preventive measures, including antibiotic prophylaxis, primary wound closure, and/or using mouthwashes before and after surgery, etc. Since the tooth extraction, the patient has suffered from pain and an unpleasant feeling at the extraction site with pus discharged.\nThe patient's medical history includes severe psoriasis vulgaris including significant nails involvement of the upper and lower extremities and psoriatic arthritis of the distal interphalangeal joints. Additional conditions involved seropositive rheumatoid arthritis of 4th stage (immunoglobulins M (IgM) - and immunoglobulins A (IgA) - rheumatoid factors positivity, cyclic citrullinated peptide (aCCP) positivity) with the radiocarpal, carpometacarpal, metacarpophalangeal and proximal interphalangeal joints involvement, hypertension, subclinical hypothyroidism, and dyslipidemia. The patient has undergone several surgeries in the past, including a hysterectomy for a benign diagnosis, laparoscopic cholecystectomy for lithiasis, appendectomy, and total endoprosthesis of the right shoulder, left knee, and right hip because of osteoarthritis. Her pharmacological history includes Levothyroxine 25 mcg, Leflunomide 20 mg, Amlodipine 5 mg, Ramipril 2.5 mg, Rosuvastatin 20 mg, calcium 500 mg and vitamin D3 1000 IU. All medicaments are received once daily, and Ibuprofen 600 mg as needed. Rheumatoid arthritis was treated with methotrexate, which had to be discontinued in 2011 due to liver function alterations and lower intestinal dyspepsia. Since November 2020, the patient has been treated for psoriasis with anti-interleukin 17-A medication, secukinumab, currently at 300 mg once a month, which has led to significant improvement in both joint and skin conditions. Additionally, the patient received topical therapy with betamethasone dipropionate and salicylic acid for psoriasis. The patient had no allergies, and her history regarding substance abuse was negative.\nThe patient was diagnosed with MRONJ stage II (characterized by symptoms of infection) (Figure 1A), according to the staging system developed by American Association of Oral and Maxillofacial Surgeons (AAOMS). The patient's chief complaint was occasional pain at the site of extracted tooth 46. Clinically, a fistula with pus discharge in the oral vestibule of same area was noted. Teeth 44 and 45 were firm without looseness, painless on percussion. No swelling in the alveoli was present. The innervation of both, the inferior alveolar and the mental nerve, was undamaged and intact. Radiographic findings revealed significant osteolytic bone destruction and localized sequestration in the areas of teeth 45 and 46 of size 20x15x10 mm (Figure 1B-D). Teeth 45 and 44 were endodontically treated with definitive root fillings, with the apex of tooth 45 extending into the osteolytic defect. The tooth 44 has a small periapical lesion not associated with this defect. To address the current situation and prevent further complications, the patient underwent sequestrectomy and debridement of necrotic bone, as well as extraction of teeth 44 and 45 under local anesthesia. This procedure included a mucoperiosteal flap elevating in the range of teeth 44-47 (Figure 1E), smoothening of sharp bony edges and carefully dissecting and preserving of mental nerve (Figure 1G). The specimen of necrotic bone (Figure 1F) was sent for the histopathological examination (Figure 2A and B), and after local antisepsis the wound was closed primarily, with absorbable sutures (Figure 1H). Perioperative antibiotics were prescribed, specifically phenoxymethylpenicillin 1.5 MIU every eight hours orally for ten days. The patient was also advised to improve oral hygiene and chlorhexidine-containing mouthwash rinses. \nThe patient has been followed up regularly, with oral examinations showing signs of lesion healing. No signs of exudation or dehiscence have been detected. Similarly, imaging studies have revealed evidence of bone healing 7 months after surgery (Figure 1I-L).",
"gender": "Female"
}
] |
PMC11430215
|
[
{
"age": 59,
"case_id": "PMC10687791_01",
"case_text": "The patient was a 59-year-old incarcerated man with a past medical history of hypertension, insulin-dependent diabetes mellitus, ethanol use disorder, and schizophrenia. He was brought to the hospital after being found down and unresponsive in his jail cell. Initial clinical evaluation was remarkable for right-sided hemiplegia, aphasia, and right facial droop. Head computed tomography angiography revealed occlusion of the M2 (Sylvian) segment of the left MCA. Mechanical thrombectomy was performed with complete reperfusion of the affected brain parenchyma. The patient also incidentally tested positive for SARS-CoV-2 nucleic acid by nasal swab.\nFour days later, the patient developed a new right hemispheric disease and was found to have a new large acute infarct of the right posterior cerebral artery territory (Figure 1). Bilateral deep white matter ischemic changes were also identified with a beaded, \"rosary-like\" pattern tracking along the internal watershed zone of the right corona radiata in extension from the adjacent PCA infarct (Figure 1). Despite medical intervention, the patient died approximately a month following admission.\nExternal examination of the brain and attached vessels revealed multifocal moderate to severe atherosclerosis, including severe disease in the communicating segment of the right internal carotid artery with approximately 90% stenosis. Serial coronal sections revealed multiple lesions scattered throughout the cerebral hemispheres concerning acute/subacute to chronic infarcts. The largest involved the caudal right hemispheric deep grey matter and medial temporal lobe, extended to the right occipital pole, including the calcarine sulcus and visual cortex and corresponded to the PCA territory infarct identified on antemortem imaging. Adjacent to, but not contiguous with the large PCA infarct, was a separate, well-demarcated wedge/\"cigar-shaped\" lesion involving the right deep white matter, extending from the frontal pole to the parieto-occipital lobe (Figure 2). Hematoxylin and eosin-stained tissue sections from this second lesion revealed a subacute infarct with central necrotic debris, neuronal loss, rarefaction, macrophage infiltration, neovascularization, axonal spheroids, and gliosis (Figure 3).",
"gender": "Male"
}
] |
PMC10687791
|
[
{
"age": 12,
"case_id": "PMC10755869_01",
"case_text": "A 12-year-old girl presented with chronic, widespread, non-specific musculoskeletal pain. The girl had been adopted from an unkempt orphanage in Eastern Europe, where she had been placed by her birth mother. The girl's adoptive mother presented with anxiety regarding her daughter's adoption, and I believed that this anxious tension was translating to her adopted daughter, precipitating musculoskeletal pain. The adoptive mother was diagnosed as having an EMI of her daughter as an infant, resulting in PAIN. As the adoptive mother spoke, both the mother and the daughter sat with their eyes transfixed on the spot within the peripersonal space between them. The mother was encouraged to look through the image of the past and to see her daughter with today's eyes. This action simultaneously cleared the EMI and the Family Rule of compliance; without the EMI, no rule is necessary. Clearing the adoptive mother's EMI reduced all pain from the girl within 30 minutes of treatment. The client was given an appointment for an online follow-up call 1 month later, at which the child reported no recurrence of symptoms; this was maintained at the 2-month, 6-month, and 12-month follow-ups. It is as though the child's pain was acting as a cry for help on behalf of both the mother and child, who were trapped in PAIN.",
"gender": "Female"
},
{
"age": 15,
"case_id": "PMC10755869_02",
"case_text": "A 15-year-old girl with myalgic encephalomyelitis and chronic widespread non-specific musculoskeletal pain presented to the clinic with her mother. The girl had physically matured early, which her mother reported to be of great concern to her father. The mother reported that the father was lavishing extra attention on the girl to ensure his daughter did not start dating, destabilising the family system. It was suggested to the mother that this may be precipitating her daughter's symptoms while the daughter listened indignantly. It was fascinating to note the mother's eyes were averted, while her daughter's eyes were fixated. Both aversion and fixation are signs of fear. The mother was listening, avoiding looking at her daughter, and her daughter was glaring when the Family Rule was brought to their conscious awareness. This is against the rules! The EMI in this situation is held in place by the Family Rule \"Though must obey!\"; both are induced, and the EMI oppresses them. The action of naming the source frees all from the rule, including the father, and restabilises the family system. The client was given an appointment for an online follow-up call in 1-month. The mother reported that she had discussed our session with her husband, and the couple had begun spending more time on their relationship. Thus, the father had reduced the overwhelming attention given to his daughter. The daughter's pain and fatigue had diminished greatly. At the 6- and 12-month follow-ups, the daughter reported that she was without pain or fatigue.",
"gender": "Female"
},
{
"age": 48,
"case_id": "PMC10755869_03",
"case_text": "A 48-year-old woman presented with finger joint pain associated with rheumatoid arthritis that had persisted for the past 3 years. When talking about her past experiences, the client's eyes looked to her left; this was interpreted as an experiential timeline from left (her past) to the right (her future). Interestingly, when the client spoke of her arthritis, her eyes fixated upward and to the right. This was interpreted as indicative of an EMI that was generalizing over time. I described my observations and deductions to the client, who appeared astonished and began to recall a conversation with her mother approximately 35 years earlier. The client explained that her mother had early-onset rheumatoid arthritis at age 45 and had been told that if she had a daughter, the daughter would suffer the same fate. This EMI, created from the conversation with her mother, remained dormant until the client reached 45 years of age. As the client spoke, she displayed a PAIN; her eyes were wide as she appeared detached from the present and fully associated with her EMI of the past. By bringing the EMI to the client's awareness and explaining how her mother's adversity had transferred to her, the EMI cleared, and the client was fully associated with the present once more. At the 1-month follow-up appointment, pain and swelling had diminished, and flexibility had returned to the client's fingers. At the 6- and 12-month follow-ups, there was no recurrence of any pain.\nThe case vignettes demonstrate that bodily pain may be driven by PAIN. Attention to PAIN within a framework of Split-Second Unlearning may rapidly resolve bodily pain by clearing an EMI, allowing the HPA axis to return to a prestress state. The vignettes are examples of psychotherapeutic intervention; however, practitioners must appreciate that these clients did not require \"talking therapy.\" Often, clients are unaware that they are traumatised, either with a capital T or a lowercase t, although they are aware of bodily pain and require help from a practitioner. In vignettes 1 and 2, the parent and child must be present for the Family Rule to be broken or cleared. By gaining new insight into the psychological aspect of pathology, no blame is apportioned to the caregiver, and the EMI is cleared. We concur with Ecker and Vaz that the process of erasure clears any psychophysiological attachment to this emotional learning. In all cases, the Family Rule is the elephant in the room, which will continue to create misery and pain if the practitioner is unable or unwilling to address it.",
"gender": "Female"
}
] |
PMC10755869
|
[
{
"age": 72,
"case_id": "PMC10714361_01",
"case_text": "A 72-year-old female was referred to our hospital due to the presence of bilateral pulmonary masses. The masses were detected using chest radiography (Fig. 1A), which was performed prior to surgical treatment for hysteroptosis. The patient was an ex-smoker (0.5 pack daily from 20 to 50 years of age) and had worked at a factory producing automobile parts. She had suffered from hyperthyroidism in her 30s, hysteroptosis at the age of 66 years, and a parotid gland tumor at the age of 67 years. On examination, the body temperature of the patient was 36.5 C, blood pressure was 114/68 mmHg, and percutaneous oxygen saturation on room air was 98 % with a pulse of 107/min. Contrast-enhanced computed tomography revealed a mass (diameter: 40 mm) with a cavity at the right lung apex (Fig. 1B) and a nodule (diameter: 20 mm) with cavity in the left S8 (Fig. 1C). The levels of C-reactive protein were not elevated (0.1 mg/dL), and the white blood cell count was 7300/muL. The concentrations of all examined serum tumor markers, including carcinoembryonic antigen, cytokeratin 19 fragment (CYFRA21-1), pro-gastrin-releasing peptide, and soluble interleukin-2 receptor (sIL-2R), were within the normal range (Table). Sputum smear and culture for bacteria or acid-fast bacteria, as well as an interferon-gamma (IFNgamma) release assay yielded negative findings. Further examination through fluorodeoxyglucose-positron emission tomography-computed tomography showed hypermetabolic focuses in the right pulmonary mass, left pulmonary nodule, and uterus cervix. Transbronchial biopsy was performed on the mass in the right S1 thrice and the nodule in the left S8. The pathological findings showed granulomas and necrotic tissues with aggregation of inflammatory cells, including neutrophils and plasma cells, without any fungal organisms and acid-fast bacteria. However, a definitive diagnosis was not reached. Amoxicillin and clavulanate were administered for 1 month; however, the bilateral nodules progressed. Eight months after the first visit to our department, right upper pulmonary lobectomy was performed through VATS.\nPathological examination of the mass in the right S1 revealed necrotizing granulomas, which were partly characterized by palisading histiocytes (Fig. 2A and B). Furthermore, pulmonary vessels were involved in the granuloma. Although GPA was primarily considered, the possibility of necrotizing sarcoid granulomatosis, tuberculosis, or other granulomatous infections could not be ruled out. Ziehl-Neelsen and Grocott staining did not reveal the presence of any bacteria. Furthermore, polymerase chain reaction and culture did not detect tuberculosis or nontuberculous mycobacterium. Pseudomonas was cultured from the resected mass. The pathological findings suggested GPA; nevertheless, the patient was negative for PR3-and MPO-ANCA and had normal renal function. In addition, occult blood was not detected in the urine, and we did not observe any otolaryngologic abnormalities.\nFour months after the right upper lobectomy, the pulmonary nodule in the left lower lobe had progressed. Since the possibility of lung cancer could not be denied at that time, segmentectomy of the left S8 and S9 was performed by VATS. The pathological findings were similar to those recorded for the right pulmonary mass (Fig. 2C and D). Total hysterectomy was performed 9 months after segmentectomy of the left lung. Magnetic resonance imaging before undergoing total hysterectomy showed a high signal on T1-weighted contrast-enhanced images at the utero-vaginal border region (Fig. 3). Moreover, a necrotizing granuloma similar to the lung mass was observed in the vaginal fornix (Fig. 4A and B). Based on these pathological findings, we diagnosed this patient with GPA involving pulmonary and female genital lesions.\nAt 3 years and 4 months after resection of bilateral pulmonary nodules, a new nodule was detected in the right upper lobe of the lung, which remained asymptomatic. During observation, we noted an increase in the size of the nodules, accompanied by cavity formation (Fig. 5). The pathological findings obtained through transbronchial biopsy of these lesions were not specific. Nevertheless, recurrence of GPA was suspected, leading to treatment with oral prednisolone (30 mg daily). The treatment resulted in the immediate disappearance of the nodules; consequently, the dose of prednisolone was tapered and maintained at 5 mg daily.",
"gender": "Female"
}
] |
PMC10714361
|
[
{
"age": 58,
"case_id": "PMC10748668_01",
"case_text": "A 58-year-old lady with no significant past medical history presents for elective resection of large right pelvic sidewall mass. Pre-operative eGFR was >90. The patient underwent prophylactic ureteric stenting by the urology team with 6Fr multi-length ureteric stents. It was noted intra-operatively that the patient had a complete left sided duplex system requiring two left sided ureteric stents. All three ureteric stents were left on their strings and attached to a Foley's catheter for ease of removal post-operatively. There were no immediate stent-related complications.\nThe right pelvic sidewall mass was approached through a lower midline laparotomy. The mass was easily dissected off the pelvic side with the right ureter having been identified and protected throughout the case. The procedure was completed in approximately 2 hours with no significant blood loss. The patient received 1500 mL of crystalloid fluid intravenously during the procedure and produced 250 mL of clear urine. At the end of the case, the Foley's catheter and ureteric stents were removed without complication. A new 14Fr indwelling Foleys catheter was re-inserted for bladder management and assessment of post-operative fluid balance. In the 24 hours post-operatively the patient was noted to be oligo-anuric, producing roughly 5-10 mL of urine per hour with a reduction in eGFR from >90 to 37. Despite appropriate fluid resuscitation, the patient developed anuric renal failure. A bladder scan revealed 15 mL, which likely reflected the contents of the catheter balloon. Her renal function continued to decline to an eGFR of 18 at 48 hours post-operatively. A subsequent non-contrast Computer Tomography (CT) scan revealed bilateral hydronephrosis/hydroureter down to the level of the pelvic inlet without an obvious cause for obstruction (Figure 1).\nThe patient returned to theater for rigid cystoscopy, bilateral retrograde ureteropyelograms, and ureteric stent insertion. Retrograde studies showed large, bilateral mobile filling defects and gross hydroureteronephrosis (Figures 2 and 3). Distal ureteroscopy showed a white sloughy soft tissue mass partially obstructing the left vesicoureteric junction (VUJ) (Figure 4). Upon ureteric stent insertion there was rapid drainage of contrast/urine and sloughy material bilaterally. The patient's urine output and renal function subsequently returned to normal within 48 hours after ureteric stent insertion. The patient's ureteric stents were removed using a flexible cystoscope at 4 weeks post-operatively without complication. The patient's renal function remains at pre-operative baseline with an eGFR >90.",
"gender": "Female"
},
{
"age": 44,
"case_id": "PMC10748668_02",
"case_text": "A 44-year-old male with biopsy proven large retroperitoneal paraganglioma presented for elective resection. He was otherwise fit and well with no medical co-morbidities and a normal pre-operative hemoglobin count of 150 renal function with eGFR >90. Prophylactic pre-operative ureteric stenting was performed due to the anticipated complexity of the operation and proximity of the left ureter to the mass. Bilateral 6Fr multi-length stents were placed by the urology team, with some left sided upstream hydronephrosis noted intra-operatively likely secondary to extrinsic ureteric compression from the retroperitoneal mass. The ureteric stents were inserted without strings with the plan for outpatient removal after the patient's recovery from surgery. An indwelling Foley's catheter was inserted to monitor urine output.\nThe large left sided retroperitoneal mass was approached via a midline laparotomy. The tumor was noted to be densely adherent to the infra-renal aorta, Inferior Vena Cava (IVC), left kidney, and ureter. The patient was placed on ECMO before the tumor and involved structures were resected en-bloc, including left nephrectomy and low ureteric ligation (including removal of the left ureteric stent). A complex vascular reconstruction of the infra-renal aorta and IVC was performed by the vascular team. The procedure took 12 hours to complete with an estimated blood loss of 4,000 mL. Intra-operatively the patient received 10 units of packed red blood cells and 3,500 mL of crystalloid fluids to maintain mean arterial pressure >65 mmHg. Post-operatively on Day 0, the patient's haemoglobin was 105 and eGFR had reduced to 58. The patient remained intubated and was transferred to the ICU for supportive care.\nOn morning review, it was noted that only 10 mL of urine had drained since the patients return from theater despite appropriate intravenous fluid therapy. A bladder scan revealed an empty bladder. The patient was sent for an urgent CT abdomen/pelvis to further investigate. The right kidney showed normal enhancement with an appropriately positioned ureteric stent without evidence of hydronephrosis (Figures 5 and 6). A collapsed urinary bladder was also noted. The patient received further intravenous hydration despite appearing clinically euvolaemic. The patient's urine output remained at 0 mL by midday with a concurrent worsening of his AKI with eGFR declining to 19.\nThe patient was returned to theater for rigid cystoscopy, right retrograde pyelogram, and ureteric stent exchange. Immediately after the old ureteric stent was removed cystoscopically and copious ureteric slough/debris was seen exiting the right ureteric orifice. Subsequent retrograde ureteropyelogram showed moderate hydroureter/hydronephrosis (Figure 7). An 8Fr ureteric stent was re-inserted to further aid the decompression of the right kidney. A new 16Fr indwelling Foley's catheter was inserted to monitor urine output. The patients urine output immediately increased to 50 mL/hr with concordant improvement in eGFR to 60 within 3 days.\nIn case one, bilateral hydroureteronephrosis to the level of the VUJ without a clear obstructive cause on CT KUB could be explained by either mechanism. As the patient's three ureteric stents were removed at the conclusion of the case, VUJ edema, obstruction from sloughed papillae or a combination of both factors could be causative. During cystoscopy and retrograde pyelogram on the following day, large mobile filling defects were seen (Figures 2 and 3). On distal ureteroscopy these soft tissue masses were directly visualized (Figure 4). Re-insertion of ureteric stents resulted in prompt excretion of urine, contrast, and debris. Although the patient in case one did not have any additional risk factors for RPN and had a stable MAP throughout the case, modest reductions in blood pressure or normotensive ischemic renal injury may still be responsible for sloughed papillae.\nSimilarly, in case two, mild upstream hydronephrosis in the context of an appropriately positioned ureteric stent may support stent obstruction from VUJ edema or stent occlusion from slough papillae. However, due to the significant blood loss encountered in case two (4,000 mL) and fluctuant MAPs, renal ischemia and subsequent sloughing appears more likely. Additionally, prompt excretion of sloughy debris and urine was seen after replacement of the ureteric stent.",
"gender": "Male"
}
] |
PMC10748668
|
[
{
"age": 18,
"case_id": "PMC10903925_01",
"case_text": "An 18-year-old female patient reported to the Department of Orthodontics 18 months back with a chief complaint of upper front teeth being forwardly placed.\nExtraoral examination revealed a symmetrical mesoprosopic face form. The patient had a convex profile and a retrusive chin on profile examination. Lips were competent, the nasolabial angle was acute, and the mentolabial sulcus was deep (Figure 1).\nIntraoral examination revealed all permanent teeth erupted except the third molars. Extraction of upper premolars had been done along with strap-up of the upper arch in a private clinic. The lower arch was crowded and the upper anterior teeth were proclined. The anterior deep bite was seen with complete overlapping of the incisors. The upper and lower arches were U-shaped with Class II molar and canine relationships on both the right and left sides (Figure 2).\nPretreatment orthopantomogram (OPG) revealed all teeth present in all four quadrants including all third molars (Figure 3).\nCephalometric analysis revealed that the patient was in cervical vertebrae maturation index stage IV (completion) and had Class II skeletal bases, horizontal growth pattern, and proclined upper incisors depicted by 1 to NA angle of 26 degrees (Figure 4).\nModel analysis revealed proclination of the maxillary arch by 4 mm and the mandibular arch by 2 mm. Linder Harth index revealed a narrow maxillary arch, and Bolton's ratio for the anterior region and overall were 66% and 85%, respectively. Space discrepancy in the maxillary arch was 8 mm and for the mandibular arch was 2.5 mm.\nTreatment objectives were to align upper and lower arches with correction of lower crowding and anterior deep bite, reduce proclination of the upper anterior teeth (1 to NA angle being 26 degrees), achieve normal overjet and overbite, improve the profile, maintain Class II molar relationship, and achieve Class I canine relationship on both sides.\nOrthodontic phase\nAs the upper first premolars were already extracted prior in an outside clinic with strap-up using an MBT 0.022 slot of the upper arch, treatment was started by strap-up of the lower arch using the same MBT prescription. Initial leveling and alignment of the arches were started with round wires followed by rectangular wire until 0.019 x 0.025 stainless steel wire. At the extraction sites, there were closed 7 mm x 2 mm U-loops on a continuous 0.019\" x 0.025\" TMA archwire without any curve of Spee (Figure 5). The loops were activated extraorally, and when the archwire was placed in the molar tubes, the archwire rested gingivally in the vestibule. This wire was pulled and ligated in the bracket slots.\nAfter relieving the crowding in the lower arch and leveling and alignment of the upper arch, retraction of the upper arch was started using the K-SIR loop to achieve intrusion and retraction at the same time.\nResults\nAfter 18 months of fixed orthodontic treatment with the K-SIR loop, retraction of the anterior teeth was achieved along with a significant amount of intrusion causing correction of deep bite and proclination. Crowding in the lower arch was relieved. The patient profile improved extraorally (Figure 6).\nSpace closure in the upper arch and crowding were relieved in the lower arch while maintaining Class II molar relation intraorally (Figure 7).\nPost-treatment OPG was taken just before debonding to ensure root parallelism and the radiograph revealed parallel roots of all teeth (Figure 8).\nCephalometric analysis of the post-treatment lateral cephalogram revealed a significant reduction in 1 to NA angle from 26 degrees to 22 degrees which indicated a reduction in the proclination of the upper anterior teeth (Figure 9).",
"gender": "Female"
}
] |
PMC10903925
|
[
{
"age": 50,
"case_id": "PMC10746917_01",
"case_text": "A 50-year-old female patient presented with an enlarged mass on the volar aspect of the proximal interphalangeal (PIP) joint of her right middle finger. She noticed the mass a year before presentation and experienced painful triggering during finger extension over the last several months. Initially, she visited the family clinic due to the increasing frequency of triggering and catching, and a tentative diagnosis of a ganglion development was made in the absence of imaging examination. The symptoms worsened and, consequently, she was referred to our department, following which skin tethering on the volar and lateral sides of the proximal phalange was also observed.\nOn her physical examination, finger triggering, catching, and locking were observed during extension. A round, hard, 2-mm-wide non-tender mass was palpable on the volar side of the PIP joint of the middle finger. Skin findings showed a V-shaped skin depression on the PIP crease during finger locking (Figure 1a, b, Video 1) and linear skin depressions bilaterally on the sides of the proximal phalange (Figure 1c, d) during finger locking. Radiography revealed a bone tumor protruding from the volar side of the base of the middle phalanx (Figure 2a). Computed tomography showed that the cortex and medulla of the tumor were in continuity with the underlying bone (Figure 2b-d). Magnetic resonance imaging findings did not show a defined cartilage cap due to the small size of the tumor.\nThe patient was diagnosed with trigger finger caused by an osteochondroma, and a surgical resection was planned. A Bruner incision was made around the PIP crease of the middle finger, and intraoperative findings revealed that the C1 pulley was torn and the apex of the tumor was exposed beneath the skin (Figure 3a). The apex of the tumor interfered with the A3 pulley during finger extension (Figure 3b). Interestingly, linear skin depressions on the sides of the proximal phalange were found even after a skin incision that prevented direct contact between the tumor and overlying skin. The bone tumor compressed the flexor digitorum profundus (FDP) tendon to the ulnar side and penetrated the radial insertion of the flexor digitorum superficialis (FDS) tendon. The tendon was dissected from the base of the tumor, and the tumor was ultimately resected (Figure 3c). The FDS tendon and A3 pulley were repaired using a 5-0 nylon suture. The tumor was pathologically diagnosed as an osteochondroma. The triggering and locking phenomena disappeared after surgery, and the osteochondroma did not recur for a year.",
"gender": "Female"
}
] |
PMC10746917
|
[
{
"age": 12,
"case_id": "PMC10796608_01",
"case_text": "A male patient was referred for surgery for a traumatic dislocation of the left knee joint. The patient was 12 years old with a history of Pitt-Hopkins syndrome (identification of TCF4 gene mutation). He had underlying ASD and severe intellectual disability (Intelligence Quotient: 31). The patient was treated with aripiprazole (2 mg/day) and as-needed risperidone for irritability associated with ASD. His family consisted of his father, mother, and a 14 years-old brother. He was in the sixth grade at a school for special needs education and had been in a welfare facility for disabled children since the first grade of elementary school. He spent weekdays in the welfare facility and weekends at home. At the age of seven, he fell from a height and was diagnosed with traumatic dislocation of the left knee joint, which was treated conservatively with a brace, considering the difficulty in perioperative management. However, his gait gradually deteriorated, and he experienced frequent falls. Therefore, his family strongly desired surgical intervention, and he was referred to our hospital.\nBefore admission, we obtained information about the children's autistic symptoms from his parents and teachers. We obtained information directly from his parents as an outpatient first, and then obtained information from his teachers through online meetings and patient referral documents. The collected information was summarized according to a previously reported protocol (Table 1). In addition, his teachers explained about the picture cards that they typically used (Figure 1). Based on this information, we made the following decisions: (i) the patient was to be admitted in principle with his mother, (ii) when his mother had to go out for some reason, the medical staff would take care of the patient based on the information gathered before hospitalization as summarized in Table 1.\nAfter admission, surgery was performed the following day as scheduled. For analgesic management, continuous intravenous fentanyl injection was administered until the second postoperative day, after which the line was removed and followed by regular oral administration of acetaminophen and diclofenac suppository insertion as needed. Under this analgesic management protocol, the patient was kept calm except on the first day when he cried for pain. He was also emotionally stable with only environmental adjustments based on prehospital information, and he never needed risperidone. The postoperative course was uneventful, and the patient was transferred to a rehabilitation hospital as scheduled. We explained our management methods to the hospital.",
"gender": "Male"
}
] |
PMC10796608
|
[
{
"age": 70,
"case_id": "PMC10746375_01",
"case_text": "On March 2022, a 70-year-old female patient was referred to the Dental Unit of the San Giovanni di Dio and Ruggi d'Aragona University Hospital of Salerno for intraoral necrotic bone exposures of the anterior mandible, associated with submandibular swelling, pus discharge, and pain underneath the lower right and left central incisors since 6 months prior to the visit.\nThe patient's medical history included smoking habit (10 cigarettes per day for 46 years); thrombophlebitis of the right lower limb treated with rivaroxaban (20 mg orally, once a day); chronic autoimmune rheumatoid arthritis treated with intramuscular injection of methotrexate (10 mg, once a week) that was started since March 2009; subcutaneous administration of adalimumab (40 mg, once every 2 weeks) since January 2017; folic acid (5 mg orally, once a day) for her iron deficiency anemia; and atorvastatin (40 mg orally, once a day) for her hypercholesterolemia (Table 1).\nClinical examination of the oral cavity revealed the presence of 3 implant-supported prosthesis extended from 16 to 13, 34 to 36, and 44 to 45 and 2 fixed tooth-supported prosthesis extended from 12 to 23 and from 32 to 43. A 1.5 cm bone exposure area with pus discharge was noticed in the parasymphyseal zone, from 31 to 41 (Figure 1). An atrophic area on the dorsum of the tongue was also detected.\nOrthopantomography (OPT) and cone-beam computed tomography (CBCT) showed the presence of bone sequestration area extended from the lower left lateral incisor (32) to the lower right lateral incisor (42) and a periapical radiolucency around the apex of the lower central incisor (31 and 41), site of an underfilled root canal therapy (Figure 2).\nBased on these clinical and radiological findings, a provisional diagnosis of MRONJ was formulated, and the lesion was classified as stage 2 according to the American Association of Oral and Maxillofacial Surgeons staging system (Table 2).\nImmediately, adalimumab treatment was suspended after consulting her rheumatologist, and the patient started an antibiotic therapy course with amoxicillin and clavulanic acid (1 g orally, three times a day) assumed for 6 days. Patient was advised to use chlorhexidine digluconate 0.20% mouthwash two times a day for 10 days. On the follow-up, scheduled at the end of the prescribed drug therapy, the patient showed an evidence of clinical improvement, i.e., the swelling and pus discharge had resolved, and the MRONJ reversed from stage 2 to stage 1. The local therapy with chlorhexidine digluconate 0.20% mouthwash (twice a day) and ozonized mouthwash (twice a day) was prescribed as maintenance drug therapy for another 2 months. The patient was reviewed every 3 weeks.\nDuring an examination in June 2022, the mobilization of the exposed bone and the stabilization of MRONJ stage 1 were detected; considering this novel finding, the resection of the area of bone sequestration and extraction of the mandibular anterior teeth (32, 31, 41, 42, and 43) were performed under local anesthetic infiltration and antibiotic therapy (1 g orally, two times a day) assumed for 6 days from three days before surgical treatment. Furthermore, autologous platelet concentrates as hemostatic agents can improve healing in this case. The surgical specimen was fixed in neutral-buffered formalin, and its histopathological analysis showed areas of bone necrosis and fibrinoleukocyte tissue. Following the surgical treatment, local therapy with chlorhexidine digluconate 0.20% mouthwash (twice a day) for 2 weeks was prescribed and preventive oral hygiene care was given to the patient. The patient enters in a follow-up program every 3 months.\nOn October 2022, the patient showed intraoral wound healed without complications and without recurrence confirmed by radiographic control examination (Figure 3). Moreover, at the last follow-up examination in March 2023, the absence of clinical signs of ONJ and complete healing of the oral soft tissues were confirmed (Figures 4 and 5).\nAfter complete healing, the edentulous space will be replaced by placement of 2 implants in area 3.2 and 4.3 supporting a 5-unit splinted dental fixed dental prosthesis.",
"gender": "Female"
}
] |
PMC10746375
|
[
{
"age": 48,
"case_id": "PMC10545156_01",
"case_text": "A 48-year-old female with a 10-year history of pSS was seen in the out-patient clinic of Modern Medical Hospital, Damascus, Syria, in January 2021, complaining of an intense and disabling headache one week previously. The headache was characterised by a dull persistent pressing intensity and not responding to paracetamol, NSAIDs or codeine. On a visual analogue scale 0-10, she rated the intensity as 10; she was on 10 mg/week methotrexate. The diagnosis was based on the American College of Rheumatology, and the European Alliance of Associations for Rheumatism (ACR/EULAR) criteria. She had no previous history of headache, nor family history of cluster headache or migraine. Physical examination revealed bilateral glands enlargement (Fig. 1,2). The remain examination, including the neurological examination, was within normal limits. No signs were found concerning Raynaud phenomenon. Laboratory tests showed: haemoglobin 10.1 mg/dl (11.7-15.3), IgG 12.3 g/L (5.4-18.2), ESR 83 mm/hr and CRP 11.2 mg/dl (<6). The viral serology including HIV and hepatitis B and C virus, human parvovirus B19 IgM, Epstein-Barr virus IgM, Mycoplasma DNA, rapid influenza antigen and VDRL were also negative. Anti-streptolysin O antibody and anti-streptokinase antibody were negative. Borrelia IgG and IgM, and Treponema pallidum haemagglutination tests were negative. Immune profile tests showed anti-La 11.3 units/ml (n;<7 units/ml), and anti-Ro 17.1 units/ml (n;<7 units/ml).\nCerebral spinal fluid analysis was normal. Cerebral MRI and intracranial arterial and venous MRI angiography were normal.\nThe patient was treated with topical treatment for dry eye and dry mouth, and different doses of Predlone, ranging from 5-60 mg/day, according to the disease activity.\nShe had received three pulses of methylprednisolone 1000 mg and was started on azathioprine 150 mg (2 mg/kg/day) with a mild response to the headaches. Because of persistent disease activity, she received two initial IV doses of rituximab 375 mg/m2 every 2 weeks, with a clinical response, as her fatigue and headache were decreased. The ESR and CRP return to normal. At 6 months, disease activity decreased and the headaches also decreased, still persist but low intensity, and for that methotrexate was added at dose of 10 mg/week. Two years later on 10 mg/week methotrexate, she was in remission and had no headache.",
"gender": "Female"
}
] |
PMC10545156
|
[
{
"age": 72,
"case_id": "PMC11324273_01",
"case_text": "A 72-year-old Asian man with mild obesity and type 2 diabetes underwent cystectomy and ileal conduit reconstruction for muscle invasive bladder carcinoma 18 months before entering the hospital for the episode of this report. Before undergoing cystectomy, he had been first diagnosed with bladder urothelial carcinoma, high grade, pT1 by transurethral resection and followed by Bacillus Calmette-Guerin intravesical therapy. During the Bacillus Calmette-Guerin therapy, the bladder tumor had reemerged, and another transurethral resection revealed the tumor was muscle invasive urothelial carcinoma, pT2. Computed tomography showed no metastasis then and cystectomy and ileal conduit reconstruction were performed following 4 courses of gemcitabine and cisplatin chemotherapy. The pathology was urothelial carcinoma, pT3a with lymphovascular invasion. Five months after the cystectomy, metastatic urothelial carcinoma recurred in the lumbar vertebra, and pembrolizumab together with radiation therapy was started. The metastatic site remained the same size during nine courses of pembrolizumab treatment. Corporal metastasis and lumbar vertebrae metastasis had appeared after nine courses of pembrolizumab and the patient's treatment was changed to EV 1.25 mg/kg on days 1, 8, and 15 for a 28-day cycle was started. The patient's oncology treatment timeline is shown in Figure 1. He had received medical therapy of anagliptin 200 mg/day for diabetes mellitus when treated with EV. His fasting blood glucose was around 100-120 mg/dL during the treatment of days 1 and 8 of EV. It had risen to 226 mg/dL before day 15. The laboratory status just before day 15 of EV, which was his entrance to our hospital in this report, is presented in Table 1. The blood glucose control had been difficult regarding the hemoglobin A1c of 8.8% (Table 1). To control the high blood glucose, he was started on intensified oral treatment and insulin therapy. He then developed FN and was transferred to the intensive care unit (ICU). Despite intensified insulin therapy, his blood glucose remained high, and continuous intravenous insulin infusion (CVII) was started. The total insulin dose was stopped at a maximum of 316 units/day because of the caution for hypoglycemia which is anticipated after the reduction of the effect of EV. His blood gas showed acidosis, but anion gap (AG) did not increase, and urinary ketones were negative, which indicates that the patient did not develop DKA. The patient developed pyelonephritis and FN at the same period and he became septic 3 days after diagnosis. Under septic condition, noradrenaline was administrated for the circulatory instability due to hypovolemia and systemic inflammation. This hypovolemic and inflammatory condition also induced acute renal injury (AKI). Continuous hemodialysis filtration (CHDF) was adopted for hemodialysis with minimal circulatory fluctuation and there was also an additional intent of reducing the blood glucose levels in a sustained manner during blood purification. CHDF was performed at a blood flow rate of 100 mL/h, filtration pump flow rate of 800 mL/h, dialysate pump rate of 500 mL/h, and replacement fluid pump flow rate of 300 mL/h. Replacement fluid pump flow rates were modified accordingly. For the dialysis treatment, the membrane CH-1.8w (Toray Ind., Tokyo, Japan; polymethylmethacrylate: PMMA) was employed, which is known for polymethylmethacrylate hemofilter with an effective surface area of 1.8 m2. The treatment timeline for FN is presented in Figure 2. The blood glucose level gradually fell and the total insulin dose was reduced to 30-60 units/day after CHDF treatment. The clinical course is shown in Figure 2. Nutritional management and insulin dosage adjustments were then conducted to prevent the patient from developing DKA. Eventually, the patient's blood glucose levels stabilized with 3 units/day of insulin glargine and 5 mg/day of linagliptin, an inhibitor of dipeptidyl peptidase-4, and he was released from ICU. The patient had spent for total of 2 months in our hospital and was finally discharged. His blood glucose level stabilized after discharge from the hospital with only 5 mg/day of linagliptin without insulin and the fasting blood was around 100-150 mg/dL.",
"gender": "Male"
}
] |
PMC11324273
|
[
{
"age": 65,
"case_id": "PMC10482433_01",
"case_text": "A 65-year-old man was admitted to our hospital with recurrent intermittent stomachache in June 2022. He denied the symptoms of vomiting and nausea, fever, and loss of body weight. The physical examination (PE) did not show positive signs as well. Laboratory tests showed elevated levels of carcinoembryonic antigen (CEA, 271 ng/ml) and carbohydrate antigen 125 (CA125, 93.3 ng/ml). According to the symptom and the laboratory test results, malignancy was suspected. Therefore, he underwent a chest and abdomen computed tomography (CT) scan revealing an unevenly strengthened wall of the stomach body and multiple diffuse tumor metastases in the liver ( Figure 1A ). Further gastroscopy revealed an ulcerative neoplasm in the stomach body and the pathology examination demonstrated that it was adenocarcinoma ( Figure 1B ). Based on the above information, the patient was finally diagnosed with advanced gastric adenocarcinoma metastasizing to multiple abdominal lymph nodes and liver.\nBecause of the late stage of this patient, surgery was not recommended. Subsequently, the following therapy-related targets were detected: MLH1, MSH2, MSH6, and PMS2 were positive; CPS of PD-L1 (clone number 22C3) staining was 1; and HER2 staining was negative ( Figures 1C-I ). The standard first-line regimen was chemotherapy including CAPOX (oxaliplatin and capecitabine), SOX (oxaliplatin and S-1), or FLOT (oxaliplatin, fluorouracil and docetaxel). Because this patient and his family have expressed a desire to participate in clinical trials, he was screened and then included in a clinical trial titled \"Phase I/II Clinical Study of the Safety, Tolerability, Pharmacokinetics and Antitumor Activity of ASKB589 Injection in Patients with Locally Advanced or Metastatic Solid Tumors\" (NCT04632108) and received the CAPOX chemotherapy and ASKB589 combination therapy subsequently. ASKB589 is a monoclonal antibody drug targeting Claudin18.2 to induce ADCC and CDC to remove the tumor provided by ASK-Pharm Ltd. (China). The expression of Claudin18.2 in this patient was moderately positive, as detected by immunohistochemistry (IHC) staining. The regimen was as follows: ASKB589 (6 mg/kg) and oxaliplatin (130 mg/m2) were intravenously dripped on day 1, capecitabine (1,000 mg/m2) was orally infused twice a day from day 1 to day 14, and the above therapeutics were repeated every 3 weeks.\nHe received six courses of ASKB589 and chemotherapy in total from July 2022 to November 2022 ( Figure 2 ). CT scan revealed a satisfactory response (PR, almost cCR) with the liver masses almost disappearing and CEA decreased to the normal level ( Figures 3A, B ). However, he developed peritoneal effusion and hypoalbuminemia after 5 weeks of the treatment ( Figures 3A, C ). Meanwhile, prior to the start of therapy, he was found with proteinuria (1+), but blood creatinine and glomerular filtration rate (GFR) remained normal. As treatment continued, the patient developed a much larger volume of ascites and CA125 grew significantly, while there was no significant change in albumin and urine protein ( Figure 3 ). He was then treated supportively with paracentesis, human albumin, and diuretic drugs. Pathologic biopsy of the extracted ascites revealed no evidence of tumor cells but mainly lymphocytes. The laboratory examination showed a serum-ascites albumin gradient (SAAG) >11 g/L, total protein 6.4 g/L, lactate dehydrogenase (LDH) 56 IU/L, and adenosine amino hydrolase (ADA) 1.8 IU/L in the ascites. However, the ascites was not relieved significantly after the supportive treatment above. Therefore, he had to stop the anti-tumor therapy in December 2022 and did not receive other anti-tumor treatments like radiotherapy, chemotherapy, or immunotherapy anymore. Surprisingly, the ascites almost disappeared after the discontinuation and the CT images revealed a sustained reduction of masses in the liver even in April 2023 (more than 4 months after stopping the drug). This is a case where a patient developed large-volume recurrent ascites with concurrent regression of liver metastasis.",
"gender": "Male"
}
] |
PMC10482433
|
[
{
"age": 26,
"case_id": "PMC11265773_01",
"case_text": "A 26-year-old gravida 3, para 2, with a history of lower section cesarean section due to prolonged 2nd stage of labor in her second pregnancy. The patient had repeated visits to the emergency department for nausea and vomiting; she was treated with oral antiemetics and discharged home. In her 10th week of gestation, she was taken to the hospital by ambulance as she had intractable vomiting; her laboratory investigations showed hypokalemia (serum potassium = 3.1 mmol/L), ketonuria (+4), and she was dehydrated. The patient was admitted to the ward and started on intravenous (IV) fluids (Ringer lactate 100 mL/hour), promethazine 25 mg every 6 h and deep venous thromboprophylaxis with deltaparin 5,000 IU subcutaneously once daily. Otherwise, she remained hemodynamically stable.\nOn day 3 of admission, she complained of chest pain with breathing difficulty, palpitation, and hemoptysis. She was tachycardic (110 to 120 beats/min), tachypneic (28 to 30/min) feeling dizzy, and still vomiting. Details of the patient's vital signs and laboratory parameters are described in Table 1. Immediate computerized tomographic pulmonary angiography (CTPA) showed bilateral pulmonary embolism (Figure 1). In Figure 1, bilateral pulmonary embolism is marked by circles. She was transferred to the High Dependency Unit, started on a therapeutic dose of enoxaparin (1 mg/kg) and required non-invasive ventilation. Her echocardiogram showed PE with mild straining on the right ventricle. Along with supportive care, we added fentanyl and paracetamol for analgesia to the therapy. Both of her lower limb's ultrasound doppler scans were normal. With continued resuscitation and above-average therapy for the next 4 days, she progressively improved. Her tachycardia and tachypnea settled, and oxygen saturation was maintained on room air (96%-97%). She was transferred to the ward on day 6, then discharged home by day 10, on a therapeutic dose of enoxaparin (1mg/kg). The patient is followed in outpatient clinic at 3, 6 months and is doing well without any complications or complaints.",
"gender": "Female"
}
] |
PMC11265773
|
[
{
"age": 45,
"case_id": "PMC11325324_01",
"case_text": "A 45-year-old male, while working at a construction site, sustained severe injuries after falling approximately 4 m from a wooden structure and subsequently being struck by a cement mixer weighing around 10 tons. The patient suffered a complete fracture of the left femur in its lower third and a complex, open, comminuted fracture of the right tibia and fibula. Additionally, there was a rupture of the right calf tendon, extensive soft tissue contusion and critical perineal injury.Following the accident, the patient was promptly transported to the local hospital, the patient was taken to a local hospital, where upon arrival his heart rate was 140-150 beats/min, his blood pressure was 80/50 mmHg, his respiratory rate increased to 35 beats/min.It is very noteworthy urgent hemoglobin test revealed a critically low level of 41 g/L. After infusion of 1200 suspended red blood cells and 800 mL fresh frozen plasma, the trauma surgeon and orthopedic surgeon decided to treat the patient surgically.The multifaceted surgical procedure included the repair of a completely severed left thigh, the exploration and repair of a ruptured left femoral vein, and the debridement and suturing of the right calf. Additionally, the medical team conducted a nerve exploration and an anastomosis of the right anterior tibial artery. The right tibia-fibula fracture was addressed with a reduction and fixation using a Kerr needle, followed by external fixation.\nIntraoperatively, the team discovered a complete severance of the middle part of the patient's left femur, characterized by a narrow skin bridge of approximately 1 cm and active hemorrhage at the fracture site. Other significant findings included pronounced swelling of the proximal left thigh, scrotal edema and multiple irregular wounds on the right calf. Post-operatively, the patient was transferred to the intensive care unit for further monitoring and treatment. The blood was maintained at a rate of 90/60 mmHg at 2 u/h of hypophysin and 2.0 ug/kg.min norepinephrine, and the heart rate was 120-130 beats/min.Blood lactic acid levels were recorded at 11.0 mmol/L Meanwhile, the patient received substantial transfusions, comprising 2000 mL of suspended red blood cells, 2800 mL of fresh frozen plasma and 26 units of cryoprecipitate.The patient's blood pressure was maintained by continuous transfusions of blood products, while hemoglobin fluctuated in the range of 58 and 65 g/L . Given the patient's critical condition of hemorrhagic shock, an additional transfusion was administered, including 4000 mL of suspended red blood cells, 3200 mL of fresh frozen plasma and 20 units of cryoprecipitate.\nOn the morning of the second day post-injury, at 9 am, the patient's hemoglobin levels showed improvement, reaching 66 g/L. Consequently, the norepinephrine dosage was reduced to 0.5 ug/kg.min to maintain blood pressure of about 100/60 mmHg and heart rate of about 110 beats/min, and administration of pituitrin was ceased. Blood lactic acid levels were recorded at 4.0 mmol/L. Later, at 11 pm, the patient,was transferred from a local hospital to our emergency department, a process that spanned approximately 4 hours. During the transfer, the patient experienced repeated episodes of ventricular tachycardia, necessitating the intravenous administration of lidocaine 100 mg, followed by continued maintenance of 50 ug/kg.min.\nUpon arrival at our facility, the patient immediately exhibited ventricular fibrillation, leading to cardiac arrest within 10 seconds. Cardiopulmonary resuscitation (CPR) was promptly initiated. The resuscitation protocol included the administration of adrenaline to augment cardiac function and the reintroduction of norepinephrine at a rate of 2.0 ug/kg.min to sustain blood pressure. After 40 minutes of intensive resuscitative efforts, the patient's spontaneous cardiac rhythm was restored. Clinical observation noted bilateral pupils dilated to 3 mm with reactive light reflexes,stinging limb abnormal flexion, so the GCS score was 4T. Following resuscitation, an additional 2 units of suspended red blood cells were transfused.\nApproximately 30 minutes after stabilization, the patient's blood pressure showed slight improvement. Subsequently, an emergency whole-body CT scan was conducted in the radiology department, after which the patient was immediately transferred to the intensive care unit. Upon admission, a repeat blood gas analysis revealed critical findings: hemoglobin was undetectable, and significant acidosis was present. The patient's heart rate was elevated at 123 beats/min, body temperature was low at 34.5C, and blood pressure was measured at 72/40 mmHg despite the administration of norepinephrine at 2.0 ug/kg.min. These clinical indicators suggested the onset of the 'triad of death', characterized by hypothermia, acidosis and coagulopathy.\nIn response, the patient received aggressive resuscitative measures, including the continuous infusion of 4 units of suspended red blood cells, 800 mL of fresh frozen plasma, 1 unit of platelets, 20 units of cryoprecipitate and 3 g of human fibrinogen. These interventions successfully elevated the patient's hemoglobin to 65 g/L. Concurrently, in light of the patient's history of acute cerebral ischemia and hypoxia, body temperature was maintained around 36C, with continuous cooling of the head using an ice cap.\nThe patient's Injury Severity Score (ISS) was 28, and the Acute Physiology and Chronic Health Evaluation II (APACHE II) score was 30, indicating a high mortality risk coefficient of 89.56%. Urgent consultations with the Departments of Trauma Surgery and Vascular Surgery led to the diagnosis of injuries to the left femoral arteriovenous vein, left external iliac vein and internal iliac vein. Emergency embolization of the left femoral artery was performed by the vascular surgery team (Figure 1). The trauma surgery team recommended delayed debridement and vascular ligation once the patient's overall condition stabilized (Figure 1A-D).Meanwhile,the pelvis and the left lower limb stump should be fully pressurized and bandaged (Figure 2E). Postoperatively, the patient was administered 1 g of imipenem and cisteratin every 6 hours, the first 3 doses of teicoplanin every 12 hours, followed by a maintenance dose of 0.4 g daily. The patient also received continuous blood transfusion, hemostasis treatment, close monitoring of blood routine and coagulation (Table 1). The patient's liver function was mildly abnormal, but creatinine continued to rise, urine volume was only 20-30 mL/h, and systemic edema was obvious. Therefore, we gave the patient continuous renal replacement therapy (CRRT) with CVVHD mode and no anticoagulant. When the blood pressure gradually stabilized, the patient began to slowly ultrafiltration 100-200 mL/h.\nOn the second day post-admission, a comprehensive multidisciplinary team (MDT) consultation was conducted hospital-wide. Given the clinical finding of an impalpable right lower extremity dorsal foot artery and the indistinct boundary of necrosis, the trauma surgery team recommended initial debridement (Figure 2). Subsequently, the patient underwent debridement of the necrotic skin and subcutaneous tissue of both lower limbs, including the removal of hematomas at the stump of the left lower limb, and ligation of the left femoral artery and vein.\nBy the third day, the urology department engaged in a scrotal incision and exploration procedure to evacuate additional blood clots. Notably, there were no discernible abnormalities in the testis, epididymis and spermatic cord (Figure 2F).\nOn the fifth day of hospitalization, there was a notable stabilization in the patient's hemochrome and coagulation profiles.The patient's urine volume gradually recovered and CRRT treatment was discontinued. The boundary of necrosis on the patient's right lower limb, below the knee joint, became clearly demarcated. Consequently, the trauma surgery department proceeded with the debridement of the left lower limb and amputation of the right lower leg.\nSeven days following admission, with the reduction of sedation and analgesia, the patient regained clear consciousness and was able to comply with verbal instructions. This progress allowed for the initiation of continuous off-line rehabilitation training.\nOn the eighth day, significant advancement in the patient's recovery was marked by successful extubation and transition to oral tube intubation(Figure 2G-H).",
"gender": "Male"
}
] |
PMC11325324
|
[
{
"age": 52,
"case_id": "PMC10733929_01",
"case_text": "A 52-year-old male who underwent a robot-assisted laparoscopic radical prostatectomy in April 2019 in another hospital. After removal of the Foley catheter 15 days after surgery, he developed a rectal fistula and was treated with a colostomy and bladder catheter in May 2019. In November 2019, a perineal repair of the fistula was attempted without success. In January 2020, an abdominal approach was used without success and the patient was sent to us for repair. Flexible cystoscopy demonstrated the presence of a RUF located at the bladder neck that allowed the passage of the cystoscope into the rectum. The ureteric orifices were located about 2 cm away from the fistula. In September 2020, the patient was treated with a trans-perineal approach using the MPSF technique.",
"gender": "Male"
},
{
"age": 59,
"case_id": "PMC10733929_02",
"case_text": "A 59-year-old male diagnosed of prostatic adenocarcinoma pT3pN1Gleason4+3 who was treated 4 years earlier with open radical prostatectomy and adjuvant radiotherapy in another hospital. Two years later, he developed a vesicourethral anastomosis contracture, and he was treated with an endoscopic incision. A further vesicourethral anastomosis contracture associated with incrustation led to a transurethral resection of the bladder neck. The patient developed chronic pelvic pain and an intervening cavity with incrustation. Thus, he was treated with endoscopic lithotripsy. After, he developed a cavitating fistula between the bladder neck and the rectum and was sent to us for surgical treatment. The patient was treated with a trans-perineal approach using the MPSF technique.",
"gender": "Male"
},
{
"age": 72,
"case_id": "PMC10733929_03",
"case_text": "A 72-year-old male treated for prostatic adenocarcinoma with external beam radiotherapy in 2002 in another hospital. Due to biochemical recurrence, he was treated with cryotherapy in 2006 and developed a urethral stricture that was managed with dilatations. During one dilatation, a rectal perforation accidently occurred. The patient was treated with chronic indwelling bladder catheter. Urinary output through the rectum was negligible, and 1 year later he received an inflatable penile prosthesis. The patient had multiple urinary tract infections during the following years and developed a left renal staghorn stone. Thus, the patient underwent a left nephrectomy in 2019. Urinary output through the rectum increased, pneumaturia appeared and the patient was referred to us in February 2021. Urethroscopy revealed the presence of a stricture of the membranous urethra that could only be surpassed with a rigid ureteroscope. A 1.5 cm stone located in the left prostatic apex impacted in the recto-prostatic fistula. In November 2021, the patient was treated with a trans-perineal approach using the MPSF technique.\nWith the patient on the lithotomy position a cystourethroscopy was performed, the ureteric orifices localized, and its position related to the fistula assessed. If the ureteric orifices were located near to the fistula, they were stented with regular ureteric catheters to avoid inadvertent damage during surgery. In all cases, RUF was stented leaving a ureteric catheter inserted through the urethra and exteriorized through the anus.\nAn inverted trapezoidal incision centered over the mid-raphe is made in the perineum with the proximal aspect of the lateral incisions starting at the level of the ischial tuberosities. The distal aspect of the trapezoidal flap reaches up to the mid-portion of the scrotum (Fig. 1).\nA MPSF was harvested incorporating all the subcutaneous tissue between the skin and the bulbar urethra following the surgical technique described by Gil Vernet et al. for the elevation of scrotal skin flaps for urethroplasty. During this maneuver, the testicles, surrounded by the tunica vaginalis, were completely freed and positioned temporarily over the lower abdomen. The newly formed flap had a wide trapezoidal perineal base and a wide rectangular shape along the scrotal raphe and includes dartos, subcutaneous tissue, and scrotal septum. The flap was elevated following the ventral aspect of the urethra starting at the penoscrotal angle and dissecting up to the central tendon of the perineum (Fig. 2a-e).\nThe complete bulbar urethra was visible at this stage of the surgical technique and allows a complete dissection of its proximal aspect and the exposure of the surgical plane between the rectum and the posterior aspect of the prostate (Fig. 3). Fistula can be identified by the previous insertion of the ureteric catheter through the fistula (Fig. 4).\nThe fistulous tract was resected, the borders of the rectal orifice refreshed and closed with a single or double layer of absorbable stitches. Although two-layer closure is always advisable, the flexibility and mobility of the tissues often allow only a one-layer closure. In cases when the fistula is not associated with a urethral stricture, a simple transverse closure of the urethral orifice after being refreshed is enough. In case that a urethral stricture was associated with the fistula, an anastomotic urethroplasty was performed, either bulbo-prostatic or urethro-vesical in case that the patient had previously undergone a radical prostatectomy. Stepwise maneuvers of the elaborated perineal posterior urethroplasty may be used as necessary to achieve a tension-free bulbo-prostatic anastomosis (Fig. 5a, b).\nTo avoid recurrence of the fistula, the distal aspect of the MPSF is de-epithelialized and used as interposition flap (Fig. 6a-d). De-epithelialization can be done with scalpel or scissors and care should be taken to avoid damage of the subcutaneous vascularization.\nThe distal aspect of the de-epithelialized MPSF was fixed with 3 or 4 stitches to the anterior rectal wall, proximally to the location of the fistula to provide complete coverage of the rectal suture (Fig. 7a-c). The elasticity of the fat tissue allowed the flap to adapt well and efficiently to the space created between the rectum and the prostate. In our experience, it adapted better than the bulky gracilis flap.\nA drain was left, the testicles are repositioned to its original position and the skin is closed. The remnant scrotal skin has enough elasticity to allow a tension-free closure of the scrotal skin (Fig. 8a, b).\nThe mean duration of surgery was 315 min (300-360 min), mean days with drainage was 4 days, and mean hospital stay 5.7 days. Patients were instructed to get out of bed 48 h after surgery. The patients were kept on full dose of antibiotics for 7 days and with low dose of prophylactic nitrofurantoin until Foley catheter was removed.",
"gender": "Male"
}
] |
PMC10733929
|
[
{
"age": 8,
"case_id": "PMC10601876_01",
"case_text": "In March of 2021, an 8-year-old girl was referred to our retinal ward with a diagnosis of TMH. In the patient's medical records, it was noted that her both eyes were injured by several shotgun projectiles at the age of two. A blunt trauma to the right eye was documented, but she underwent intraocular foreign body removal and primary repair surgery for the left eye at a local hospital.\nAt the time of the visit to our clinic, the right eye had a best corrected visual acuity (BCVA) of 4/10, while the left eye was at the light perception level. The left eye had multiple corneal scarring resulting from prior injury, as shown in Figure 1 and funduscopic examination of the left eye was impossible due to corneal scars. In the examination of the right eye, no pathologies were evident in anterior segment, and intraocular pressure was 14 mm Hg. In the funduscopic examination, there was evidence of a TMH and perifoveal and peripapillary retinal scars, as shown in Figure 2. Optical coherence tomography confirmed the presence of a MH with minimum basal diameter of 418 microns in the right eye. Considering the patient's one-eye status, her parents' reluctance to undergo surgery, and the possibility of spontaneous closure of TMHs, it was determined to observe the patient and evaluate her visual acuity and MH condition.\nFour months later, in July 2021, there was an increase in the size of the MH (633 mum), but to our surprise, the patient's BCVA had reached approximately 6/10. The decision was made to continue the conservative follow-up every 4 months. The patient's BCVA improved to 8/10 at the final visit in March 2023, despite the size of the MH not changing substantially, as shown in Figure 3. Each measurement of the patient's BCVA was performed by two separate optometrists to further confirm vision improvement.\nSince the patient's BCVA was not compatible with MH, we suspected eccentric fixation which was confirmed with vvisuoscopy using direct ophthalmoscope, and the fixation point was inferior and temporal to the true fovea shown in Figure 2b. To the best of our knowledge, this is the first documented case of large MH with following development of eccentric fixation and good visual acuity.",
"gender": "Female"
}
] |
PMC10601876
|
[
{
"age": 45,
"case_id": "PMC10775730_01",
"case_text": "A 45-year-old woman was admitted to the Department of Endocrinology of our hospital in May 2022 for the treatment of a pituitary macroadenoma. She had a history of type 2 diabetes, hypertension, coronary artery disease, and euthyroid multinodular goiter, but no family history of autoimmune disease. Three years previously, she had presented with headache, visual impairment, and amenorrhea-galactorrhea syndrome. Initial investigations revealed mild hyperprolactinemia (72.55 ng/mL). Pituitary magnetic resonance imaging (MRI) examination revealed a pituitary macroadenoma of 15.5-mm diameter, a thin pituitary stalk that was displaced to the right, and the absence of the spontaneous hypersignal of the posterior pituitary lobe. The patient was treated with cabergoline 0.5 mg weekly but was lost to follow-up until May 2022, when she was referred to the Department of Endocrinology because of a recurrence of the same symptoms. On physical examination, she was found to have a body mass of 76 kg and a height of 167 cm, corresponding to a body mass index of 27.2 kg/m2, a blood pressure of 130/80 mmHg, a heart rate of 69 beats/minute, and a multinodular goiter. However, the physical examination was otherwise unremarkable. Further investigations revealed corticotropin, thyrotropin, and gonadotropin deficiencies (Table 1). An ocular examination revealed low visual acuity (4/10 for the right eye), an altered visual field, and right eye predominance. There was no papillary edema. Pituitary MRI examination revealed an intra and suprasellar mass measuring 13 x 11 x 16 mm that included hemorrhagic necrosis and had a discrete mass effect on her optic chiasm and pituitary stalk (Figure 1). These findings suggested a diagnosis of pituitary macroadenoma associated with apoplexy. The patient was treated with hydrocortisone and levothyroxine, and then transferred to the Neurosurgery department for total transsphenoidal resection of the mass. The surgeons described the mass as either a craniopharyngioma or a remodeled Rathke's pouch cyst (RPC). Histological examination revealed necrotic debris containing lanceolate cholesterol crystals with a polymorphic granuloma in contact with the necrotic tissue. It was composed of lymphocytes, plasma cells, and multinucleated macrophagic giant cells, as well as foamy histiocytes with clear cytoplasm (Figures 2 and 3). Postoperatively, the patient's symptoms improved, but her hypopituitarism persisted and she developed diabetes insipidus. Therefore, she was treated with hydrocortisone, levothyroxine, and desmopressin.\nTuberculosis was suspected as the etiology of the condition, but this was ruled out after a series of negative test results (chest X-ray, tuberculosis skin test, and sputum and urinary culture for Koch's bacillus). Furthermore, the patients did not have adenomegaly, fever, respiratory symptoms, knotty erythema, or uveitis; and her angiotensin converting enzyme activity was normal, at 43 IU/L (normal range, 35 to 70 IU/L). Computed tomography and bone scintigraphy examinations did not reveal any lesions. A salivary gland biopsy was histologically normal. Therefore, a diagnosis of XGH of a remodeled RPC was made through the exclusion of granulomatous diseases as possible diagnoses.\nThe reporting of this case conforms to the CARE guidelines. Written informed consent was obtained from the patient for her treatment and for the publication of this case report. Ethics approval for this case report was not required because of the retrospective nature of the study.",
"gender": "Female"
}
] |
PMC10775730
|
[
{
"age": 54,
"case_id": "PMC11286367_01",
"case_text": "A 54-year-old woman presented with a complaint of positive fecal occult blood test. Her past medical history included three years of treatment for hypertension. There was no family history of cancers including colorectum. Colonoscopy revealed a type 0-Is lesion in the lower rectum near the dentate line (Figure 1a), and biopsy showed tubular adenocarcinoma. Enhanced CT showed no lymph node nor distant metastasis. She was diagnosed with rectal cancer, and abdomino-perineal resection by open laparotomy method was performed. Pathology of the resected specimen revealed tubular adenocarcinoma (23x30 mm), T1b (SM 8000 mum), Ly0, V1a, PM0, DM0, pRM0, pN0, and pStageI (Figure 1b). No adjuvant chemotherapy was provided. Two years after rectal surgery, an elevated tumor marker CA19-9 (90 U/mL, normal range: <37 U/mL) was documented. The change of serum CA19-9 value during the perioperative period is presented in Figure 2. CEA value was within normal during the same period. Enhanced CT showed a round-shape nodule 2 cm in size on the left side of pelvic wall (Figure 3a). LLN recurrence was suspected, and she was referred to our hospital for further evaluation and treatment. PET-CT showed a high accumulation of 18 F-fluorodeoxyglucose (FDG) in the same lesion (Figure 3b). No other site of recurrence was detected. Contrast-enhanced MRI of the pelvis depicted a mass displaying a low signal on T2 (Figure 3c) and a slightly low signal on T1 (Figure 3d), leading to a diagnosis of isolated LLN recurrence. Uterine leiomyoma with malignant potential was also detected.\nBecause the enlarged LLN was isolated (No.263) and no other site of recurrence was detected, surgical resection of the lymph node by open laparotomy was performed. Concurrent total hysterectomy for uterine leiomyoma was also performed by gynecologists. Total blood loss during surgery was 610 g and duration was 341 minutes. Post-operative course was uneventful.\nMacroscopic finding of the resected lymph node revealed a light yellowish solid mass measuring 31x27x18 mm (Figure 4a). Microscopic findings were consistent with a metastatic lymph node originating from the recent rectal cancer (Figure 4b). No malignancy was observed in the uterus.\nAfter six months of adjuvant chemotherapy with Capecitabine + Oxaliplatin (CapeOX), and the patient remains free of recurrent disease 7 months since LLN resection.",
"gender": "Female"
}
] |
PMC11286367
|
[
{
"age": 29,
"case_id": "PMC10861033_01",
"case_text": "Motor vehicle accidents are one of the leading causes of mortality worldwide, and the leading cause of death for young adults 18-29 years old. In the United States, mortality from motor vehicle accidents is the 3rd leading nationwide cause of unintentional injury death, resulting in over 900,000 years of life lost annually as of 2020. Motor vehicle fatalities rank in the top 3 causes of death for individuals under the age of 34.\nThe National Highway Traffic Safety Administration (NHTSA) maintains the Fatality Analysis Reporting System (FARS), which tracks all traffic crashes in the USA since 1975 that involve at least one fatality. FARS data are used to inform safety decisions at the local, state, and national levels, and provide key insights into the efficacy of changing vehicle and roadway safety standards. To be included in FARS, a crash must occur on a public road and must result in at least one death within 30 days of the crash. Road fatalities in the US continue to decrease as better advanced safety technologies emerge and become standard features across the board. Occupant fatalities involving vehicles manufactured in the last five or ten years have decreased steadily, down significantly since 1975 (Fig 1A). Despite improvements, when compared to 15 peer nations, the United States ranks last in reducing the rate of annual vehicle fatalities, and fatalities in 2021 were the highest since 2005.\nOverall, evolving crash testing and vehicle standards are estimated to have prevented ~60% of all potential vehicle fatalities in the USA. However, the bulk of the fatality reduction is in males (Fig 1B). Qualitatively, female fatality rates have been relatively stable when compared to the overall trend. While historically males have driven more miles per licensed driver than females, that gap is steadily closing, with decreasing differences in licensure rates and driving exposure. Driving exposure for females has increased, and female drivers have been reported to display similar behavioral risk profiles to males when behind the wheel.\nGiven these trends, it is important to note that no vehicle crashworthiness test in the US involves an anthropomorphic test device (ATD) representative of the average adult female, despite clear evidence of the increase of female drivers over the last 20 years. The current US regulations only require crash testing with the 50th percentile adult male and 5th percentile adult female ATD. Prior research has shown that female drivers and vehicle occupants are more likely than males to suffer severe or fatal injuries when involved in a crash severe enough to result in fatality for an occupant involved in the crash. Female vehicle occupants are at higher risk of Abbreviated Injury Scale (AIS) 2+ (moderate) and 3+ (serious) injuries compared to males when controlling for a variety of factors, particularly to the lower extremities. This disparity between men and women in automobile crashes is a major public health issue with implications for automobile design, personnel protection, and governmental regulation. The goal of this paper is to utilize fatal crash data to assess the extent to which a difference in fatality risk exists for male and female occupants under matched crash conditions.",
"gender": "Female"
}
] |
PMC10861033
|
[
{
"age": 4,
"case_id": "PMC10635901_01",
"case_text": "A previously healthy four-year-old girl presented to her local hospital with persistent headaches and vomiting. She had a family history of breast and uterine cancer. Head computed tomography (CT) and magnetic resonance imaging (MRI) of the head revealed a well-demarcated tumor in the left temporal lobe homogenously enhanced with a gadolinium (Gd) contrast agent (Fig. 1-a, b). She underwent initial surgical resection at her local hospital, resulting in subtotal resection (Fig. 1-c). A second surgical resection was performed at our tertiary care center two months after the initial surgery due to the residual tumor progression, and gross total resection was achieved at the second surgery (Fig. 1-d).\nHistopathological findings of two nearly identical specimens taken from the patient's first and second surgical resections were consistent with pediatric diffuse HGA (isocitrate dehydrogenase-1 [IDH-1] wild-type) (Fig. 2-a). The findings revealed dense atypical cell aggregation in a partly myxomatous background, with several vessels showing marked microvascular proliferation (Fig. 2-a). Some atypical cells presented with a halo around the nuclei, showing an oligodendroglioma-like area (Fig. 2-b).\nOn immunohistochemistry (IHC), the atypical cells were positive for GFAP (glial fibrillary acidic protein; focal) (Fig. 2-c), nestin (focal), synaptophysin (focal), S-100 beta (focal), Olig2 (oligodendrocyte transcription factor 2), ATRX (alpha thalassemia X-linked mental retardation; wild-type), INI1 (wild-type), and H3K27 me3 (wild-type) and negative for epithelial membrane antigen, L1CAM (L1 cell adhesion molecule), IDH-1-R132H, p53, and H3K27M. MIB-1 labeling index was estimated at 70%-80% (Fig. 2-d). The status of 1p/19q was checked in the specimen from the second surgical resection, revealing a gain of 1q and 19q.) Tumor tissue collected from the intracranial region during the second surgery was analyzed using a FoundationONE assay (Foundation Medicine, Cambridge, MA, USA) (Table 1).\nThe patient then underwent extended focal radiotherapy at a dose of 54 Gray, concomitant with temozolomide (TMZ) at 75 mg/m2.) Routine MRI check-ups were conducted every two to three months after the second surgery. There had been no sign of recurrence until several months after the second surgery when she and her parents recognized a palpable bulge under the skin near the incision site. The lesion was tiny and elastic, without pain, rash, or tenderness in the skin. No evidence of recurrence within the intracranial region was observed. However, the lesion grew drastically over the next several weeks, eventually causing a rash and skin tenderness (Fig. 3-a). MRI demonstrated high intensity on diffusion-weighted imaging with ring enhancement using a Gd contrast agent, which we suspected to indicate inflammation or infected atheroma (Fig. 3-b, c). Simultaneously, her parents recognized a palpable node around her neck (Fig. 3-e).\nShe underwent surgical resection and curettage of the subcutaneous lesion. Pathological findings revealed metastasis of pediatric diffuse HGA (Fig. 2-e). The subcutaneous lesion was soft and grayish in color, encapsulated by a thick membrane, and located between the galea and the periosteum.\nFluorodeoxyglucose positron emission tomography (FDG-PET) performed soon after the resection of the subcutaneous lesion for systemic evaluation revealed pathological accumulation at the cervical lymph node (Fig. 3-f). Subsequently, the patient underwent lymph node dissection and the insertion of an implanted central venous catheter (Fig. 3-g). As with the subcutaneous lesion, the pathology of the examined lymph nodes confirmed the presence of metastasis from pediatric diffuse HGA (Fig. 2-f). No histopathologic differences were evident between the intra- and extracranial lesions.\nMRI conducted seven months after the second resection surgery showed dissemination in the intracranial region and spine (Figs. 1-e and 3-d). We prescribed additional spinal irradiation and intravenous TMZ injections at 150 mg/m2 for five days, followed by 23 days of rest. Despite this treatment being highly effective in managing the intracranial disseminated lesions, there was regrowth of subcutaneous lesions metastasized, and new palpable lymph nodes emerged (Fig. 1-f, g). She underwent two additional surgical resections for subcutaneous lesions with marginal skin tissue involvement. These extracranial lesions comprise grayish soft tumor tissue, with some areas showing yellowish and slightly elastic characteristics rather than soft tissue within the lesions (Fig. 3-h). However, controlling the intracranial disseminated, subcutaneous metastatic, and lymph node lesions became increasingly difficult (Fig. 1-h). Finally, at the age of five years (15 months after her initial diagnosis), the patient succumbed to the primary disease. Written informed consent was obtained from the patient's family to publish her anonymized medical findings and accompanying images.",
"gender": "Female"
}
] |
PMC10635901
|
[
{
"age": 30,
"case_id": "PMC11325451_01",
"case_text": "A 30-year-old male presented with a large right renal mass, discovered on renal ultrasound (US) performed due to a recent rise in creatinine levels from 2.0 mg/dL to 2.56 mg/dL with an estimated glomerular filtration rate (GFR) of 34. The renal ultrasound revealed a solid and heterogenous renal mass appearing 11.3 x 7.5 x 12.6 cm right side. He denied urinary complaints but noted vague abdominal discomfort. His past medical history included Jeune syndrome (asphyxiating thoracic dystrophy), chronic kidney disease (CKD), hypertension, hypercholesterolemia, retinitis pigmentosa, asthma, attention deficit hyperactivity disorder (ADHD), scoliosis, and obstruction of posterior urethral valves as well as a right uretero pelvic junction, both of which were repaired during childhood. His brother also had a past medical history of Jeune syndrome with renal failure, which required a kidney transplant. The family history was notable for appendiceal adenocarcinoma in his mother and prostate cancer in his father. The patient underwent a left renal biopsy as a toddler because of renal insufficiency, which revealed no gross abnormalities, and another renal biopsy at 29 years of age, revealing mesangial hyperplasia with focal glomerulosclerosis consistent with C1q nephropathy. Following the renal ultrasound, further work up with chest X-ray showed no evidence of metastases; however, magnetic resonance imaging (MRI) of the abdomen and pelvis without intravenous (IV) contrast revealed an 11.6- x 8.3- x 12.7-cm right lower pole mass with little normal kidney remaining (Figure 1).\nAn open right radical nephrectomy was performed. Pathology revealed a 13.8-cm epithelial predominant WT with favorable histology, pT3aN0 (Figure 2). The tumor had invaded into the segmental branches of the renal vein. Margins were negative. One hilar lymph node was excised and was negative for malignancy, confirming the classification of a stage II WT. Brain MRI was performed and revealed an empty sella turcica, but no evidence of the disease. DNA sequencing revealed a nearly genome-wide copy-neutral loss of heterozygosity for chromosomes 1p, 11p15, 16q, and 17p13.1. Mismatch repair was intact and nuclear expressions of MLH1, MSH1, MSH6, PMS2, and programmed death-ligand 1 (PD-L1) were normal.\nTypical adjuvant chemotherapy options for stage II WT, including vincristine, dactinomycin, and doxorubin, were discussed. Although these medications are not typically nephrotoxic, both patient and care team were concerned about organ damage, given the history of CKD with a post-operative GFR of 20 and his underlying genetic disorder.\nUltimately, the patient and family opted for close follow-up and surveillance imaging every 3 months for the first 3 years, then every 6 months for the following 2 years. It was decided to start by alternating an MRI of the abdomen/pelvis and chest computed tomography (CT) with an abdominal ultrasound and chest X-ray. After 2 years, the surveillance transitioned to abdominal ultrasound and chest X-rays alone. Positron emission tomography (PET) scans and contrast imaging were avoided due to the patient's history of CKD.\nThe first set of screening tests included a chest X-ray and abdominal ultrasound, which was normal, except for the chest X-ray noting scoliosis and the abdominal ultrasound revealing cysts in the liver and left kidney and sludge in the gallbladder. The most recent follow-up appointment was 14 months post-surgery and revealed no evidence of the disease. Informed consent was obtained for the publication of this case report, and Institutional Review Board (IRB) approval was waived.",
"gender": "Male"
}
] |
PMC11325451
|
[
{
"age": 19,
"case_id": "PMC11249992_01",
"case_text": "A 19-year-old nulligravid patient complained of abdominal pain and dyspepsia for about four months. There was no specificity in his medical, family, or psycho-social history. In the abdominal ultrasonography and MRI, a 9 cm diameter mass through solid/cystic components in the right adnexal area, interpreted as a dermoid cyst, was observed in the foreground (Fig. 1). Tumor markers were detected as CEA: 0.975 ng/mL, CA 19-9: 15.9 U/mL, and CA 125: 33.7 U/mL. The patient underwent laparoscopic right ovarian cystectomy with the preliminary diagnosis of mature cystic teratoma.\nMacroscopically, the tumor was 11x8x4 cm in size and contained hair, sebaceous material, and cartilage tissue. Microscopically, multilocular cyst, keratinized squamous epithelium, mucinous epithelium, skin appendages, hair shafts, adipose tissue, mature glial foci, chondroid and osteoid structures were observed. An insular focus was observed, consisting of monomorphic cells with a 0.9 cm diameter salt-and-pepper chromatin structure, round nuclei, eosinophilic cytoplasm, and monomorphic cells (Figs. 2, 3). Immunohistochemically, S100 (focal+), Synaptophysin (+), Chromogranin (+), CD56 (+) staining were observed. Ki 67 proliferation index was 6-7%, and mitosis was 3/2 mm2. Necrosis was not observed. All findings were evaluated as 'Atypical Carcinoid Tumor (WHO Grade 2). Non-invasive papillary structures with multifocal mild-moderate nuclear atypia lined with focal stratified cuboidal epithelium, some with fibrovascular cores, were observed around this focus (Figs. 4, 5). Necrosis was not observed. Immunohistochemically, S100 (+), GFAP (focal+), CK7 (focal+), PR (focal, weak+), p16 (focal+), p53 (-), CK20 (-), AMACR (-), Calretinin (-), and WT1 (-) immunoreactivity were detected. Mitosis was 2-3 /10 BBA. Ki 67 proliferation index was 1-2%. The present findings were interpreted as 'Atypical CPP (WHO Grade 2)'.\nSince the case was interpreted as 'Atypical Carcinoid Tumor, Atypical CPP Followed,' the patient was informed, and laparoscopic right salpingo-oophorectomy was performed as a complementary surgery. No abnormal cells were detected in the salpingo-oophorectomy material. Ga-68 Dotatate Positron Emission Tomography showed no evidence of malignancy holes containing any somatostatin deposits at the sixth postoperative month. The patient continues to be followed at 6-month intervals.",
"gender": "Male"
}
] |
PMC11249992
|
[
{
"age": 77,
"case_id": "PMC10864480_01",
"case_text": "A 77-year-old male with no family history of cancer suffered from upper abdominal pain for more than half a month in August 2020. An enhanced CT examination revealed suspicious malignant tumors in the left lung, left pleura, multiple lymph nodes (mediastinal, bilateral hilar, left clavicular area, hepatoduodenal ligament area, and retroperitoneum), as well as at the junction of the left and right lobes of the liver near the diaphragm apex and the right adrenal gland ( Figure 1A ). Additionally, the level of the serum tumor biomarkers CYFRA211, CEA, and CA724 were elevated above normal levels ( Figure 1B ). A liver biopsy performed on September 22, 2020, showed significant heterogeneity in tumor cells, indicating possible metastatic squamous cell carcinoma. Genetic testing of the liver metastasis tissue revealed EGFR p.G719C (mutation frequency 10.81%, number of supported reads 138; Figure 1C ) and PIK3CA mutation. Immunohistochemical staining of the liver metastasis lesion showed high infiltration of CD8 + and PD-L1 in both the tumor area and stroma, with CD68 + macrophages including M1-type macrophages (CD68 + CD163 -) and M2-type macrophages (CD68 + CD163 +) having good infiltration in the tumor area. Additionally, a minimal number of exhausted T cells (CD8 + PD1 +) were observed in the tumor ( Figures 2A-C ). Based on the above data, the patient was diagnosed with the rare EGFR-mutated LUSC at stage cT3N3M1c with high PD-L1 expression (TPS [tumor proportion score] = 90%) and high tumor mutational burden (TMB, 13.63 mutations/mb). According to the National Comprehensive Cancer Network (NCCN) guidelines, the second-generation EGFR-TKI was administered as a once-daily oral dose of 40 mg on September 25, 2020.\nHowever, the CT scan conducted in November 2020 revealed an enlargement of the lung and liver lesions in comparison to the previous scan, leading to disease progression (PD) as per the Response Evaluation Criteria in Solid Tumors (RECIST) scoring criteria ( Figure 1A ). Additionally, the levels of tumor markers CYFRA211, CEA, and CA724 experienced further elevation ( Figure 1B ).\nUpon developing resistance to Afatinib, a second mediastinal lymph node biopsy was performed, which revealed lung metastatic squamous cell carcinoma. We compared the results of genetic testing of liver metastatic tissue at the time of diagnosis and mediastinal lymph node metastatic tissue at the time of progression on afatinib therapy ( Table 1 ). NGS sequencing of the mediastinal lymph node tissue identified three pathogenic/likely pathogenic mutations: EGFR p.G719C (14.62%), PIK3CA p.E545K (12.16%), and TP53 p.Q331* (23.08%). Immunogenomic analysis indicated a high tumor mutation burden (17.52/Mb) and 99% expression of PD-L1 in tumor cells. Given the patient's age, physical condition, and in accordance with the NCCN guidelines, a combination of immunotherapy and chemotherapy was administered on November 17, 2020, for a total of four cycles. The treatment regimen included albumin-bound paclitaxel (200mg/m2, d1) + cisplatin (75mg/m2, d1) in combination with sintilimab (200mg, d0), with each cycle repeated every three weeks.\nBy February 2021, the CT examination showed significant reduction in the size of the lesions in the left lung, liver, and adrenal gland, accompanied by a decrease in size in the mediastinal lymph nodes compared to the previous examination ( Figure 1A ). As per the RECIST scoring criteria, the assessment result indicated a partial response (PR). The levels of tumor marker levels also significantly decreased ( Figure 1B ).\nThe patient continued to receive maintenance therapy with sintilimab for one year. In February 2022, a follow-up CT scan indicated tumor stabilization ( Figures 1A, B ). Blood plasma circulating tumor DNA (ctDNA)-NGS tests were performed simultaneously in November 2020 and September 2022, revealing a substantial decrease in the number and frequency of gene mutations (Fishplot) ( Figure 3A ). Moreover, quantitative analysis of ctDNA levels demonstrated a significant reduction (17.72 vs. 10353.37 HGE/ml), consistent with the radiological evaluation results ( Figure 3B ).",
"gender": "Male"
}
] |
PMC10864480
|
[
{
"age": 55,
"case_id": "PMC10927835_01",
"case_text": "The patient, a 55-year-old male, presented with head and neck pain, fever, and left limb weakness persisting for 5 days, accompanied by a peak temperature of 39.4 C. Subsequently, he developed progressive difficulties in rolling over and lower back pain. Additionally, the patient had a history of tuberculosis 10 years ago.\nUpon admission, the patient presented with basic vital signs including a blood pressure of 105/75 mmHg, a pulse rate of 100 beats per minute, a respiration rate of 15 breaths per minute, and an average body temperature of 38.2 C. Physical examination revealed an alert and cooperative mental state, neck percussion tenderness, forced head positioning, partial left-sided neck involvement, grade 3 muscle strength in the left upper limb and grade 5- muscle strength in the left lower limb along with mild abnormal gait. The patient exhibited hypoalgesia below the knee on the left lower limb, tendon hyperreflexia, and positive pathological signs. Muscle strength and sensation in the right limb were within normal limits.\nThe initial laboratory findings of the patient were as follows: the white blood cell (WBC) count was 9.32 x 109/L, with a neutrophil percentage of 80.2%. Cerebrospinal fluid (CSF) analysis revealed a WBC count of 495.60 x 106/L. In terms of CSF biochemistry, the total protein level measured at 616 mg/L and glucose level at 2.3 mmol/L. Revised: The patient's initial laboratory results showed a white blood cell (WBC) count of 9.32 x 109/L, with a neutrophil percentage of 80.2%. Analysis of cerebrospinal fluid (CSF) indicated a WBC count of 495.60 x 106/L, while CSF biochemistry revealed levels of total protein measuring at 616 mg/L and glucose measuring at 2.3 mmol/L. Results from cerebrospinal fluid culture, tuberculosis bacillus smear, general bacterial smear, special stain, and tuberculosis antibody tests all yielded negative results; similarly, no positive results were obtained from blood culture either. MRI of the spinal cord showed long nodules with low-signal T1-weighted and high-signal T2-weighted MRI in the level between cervical vertebrae 2 to thoracic vertebrae 1 with edge intensification observed on contrast-enhanced T1-weighted MRI images. Similarly lesion in left frontal lobe with circular intensification and edema observed in the surrounding brain tissue on contrast-enhanced T1-weighted MRI images. Chest CT scan revealed the presence of emphysema, chronic infection in both lungs, and evidence of prior tuberculosis infection (Figure 1). Abdominal examination did not identify any significant intraperitoneal lesions.\nAfter admission, the patient received initial treatment with ceftriaxone and meropenem for anti-infection purposes. In consideration of the potential presence of active tuberculosis, a comprehensive oral anti-tuberculosis regimen comprising isoniazid, rifampicin, and pyrazinamide was administered for several days. Subsequently, there was a sudden exacerbation of left limb hemiplegia (left upper limb muscle strength grade 0; left lower limb muscle strength grade 3; decreased sensation in the left knee joint). However, normal movement and sensation were observed in the right limb. Further sputum culture revealed Klebsiella pneumoniae as the causative agent while metagenomic next-generation sequencing (mNGS) analysis of cerebrospinal fluid confirmed Klebsiella pneumoniae as the pathogenic bacteria responsible for infection. Due to concerns regarding rapid disease progression potentially involving high cervical spinal cord and even medulla oblongata regions that could impact respiratory and circulatory function, an approved surgical intervention plan was implemented involving multi-point incision and drainage to eliminate cervical and thoracic intramedullary abscesses.\nDuring the surgical procedure, a purulent cavity measuring approximately 10 cm in length extended from the second cervical vertebra to the first thoracic vertebra. The pus cavity appeared yellow and white, with no discernible separation. Post-operative pus culture revealed an infection caused by Klebsiella pneumoniae, which exhibited sensitivity to most antibiotics tested (Figure 2). Anti-inflammatory treatment was administered using meropenem and linezolid, while anti-tuberculosis treatment was discontinued due to insufficient evidence. Following spinal cord surgery, muscle strength in the left upper limb improved to grade 3, muscle strength in the left lower limb improved to grade 4, and muscle strength in the right limb remained normal.\nThree weeks after spinal cord surgery, the patient experienced an abrupt onset of muscle weakness in the right upper limb (muscle strength: right upper limb, grade 3; right lower limb, grade 5). The head MRI revealed an enlargement of the lesion located at the left frontal lobe, accompanied by aggravated surrounding edema. The surgical indication was evident, and a complete removal of the abscess without rupture of its wall was achieved during excision. Dissection of the abscess exhibited a thickened wall and yellowish pus within the cavity, resembling that found in the spinal cord, and pus culture yielded negative results (Figure 3). Following brain surgery, administration of antibiotic drugs (meropenem and linezolid) continued for ten days, with a total antibiotic course duration lasting approximately 5 weeks. After the second operation, the muscle strength of the right upper limb briefly decreased to grade 0. Prior to discharge, there was recovery observed in right upper limb muscle strength to grade 4.",
"gender": "Male"
}
] |
PMC10927835
|
[
{
"age": 51,
"case_id": "PMC11385607_01",
"case_text": "A 51-year-old female patient was diagnosed with chronic kidney disease (stage 5) which was caused by polycystic kidney disease. This patient had a history of hypertension and no other complications, such as diabetes or coronary heart disease. Furthermore, she had no history of smoking or drinking wine. Her body mass index was 18.47. This patient had received hemodialysis since 2014. On 10 November 2015, an autologous AVF in the right wrist was created in our hospital which was occluded 1 month later. Then, we reconstructed an AVF in the right forearm during open surgery on 30 December 2015. This AVF was used for hemodialysis for approximately half a year and was occluded again. An ultrasound-guided PTA was performed to clear the occlusion on 29 June 2016, with a balloon of 5 mm x 40 mm. Shortly thereafter, this patient underwent replete angioplasty because of repleted stenosis in right forearm AVF on 11 October 2016, and 7 February 2017, with a balloon of 6 mm x 40 mm.\nOn 23 May 2017, this patient was hospitalized again because of decreased flow volume in the right forearm AVF. Preoperative ultrasonoscopy indicated a significant juxta anastomotic stenosis, with a diameter of 1.0 mm and a length of 1.5 cm (Figure 1A). No thrombosis or calcification was found. Because of the short duration of patency maintenance after each repeated PTA, after a discussion, the team decided to perform another PTA with RES placement in the right forearm AVF. Informed consent was obtained before the procedure.\nAfter the brachial plexus block, a 5F-R vascular sheath (Terumo, Tokyo, Japan) was inserted into the cephalic vein. A guide wire (Abbott Vascular, Santa Clara, California, USA) of 0.014 in. was advanced along the vein slightly across the stenotic lesion. A balloon of 5 mm x 20 mm was advanced along the guide wire and across the stenotic lesion to the anastomotic site, followed by balloon angioplasty of the stenotic lesion, the outflow vein, and the anastomotic site using 20-24 atm, repeated three times. The balloon was subsequently removed. Then the RES (NOYA, Beijing, China), a balloon-expandable stent with a diameter of 4.5 mm and length of 22 mm, was placed in the stenotic lesion with the guidance of ultrasonography (Figures 1B,C). The RES was fully expanded by a balloon angioplasty using 16 atm.\nAfter PTA and RES placement, the ultrasound images showed that the diameter of the brachial artery was 5.9 mm, with a flow volume of 521 ml/min. In the segment of the cephalic vein near an anastomosis, a 22 cm stent was observed. The stent was closely fitted to the vascular wall, and a color Doppler ultrasound showed filled blood flow through the stent, with a peak velocity of 210 cm/s (Figure 1D). The diameter of the middle segment of the forearm cephalic vein was 3.8 mm, with an intimal medial thickness of 1.4 mm and a peak velocity of 256 cm/s.\nThe right forearm AVF was patent for hemodialysis until the stent collapsed on 27 July 2018, with a primary patent duration of 14 months. No other postoperative complications occurred before the stent collapsed, such as thrombosis, heart failure, pseudoaneurysm, infection, or hemodialysis access-induced distal ischemia syndrome. Though the flow volume was acceptable, we still decided to expand the stent using PTA (Figure 2). On 30 July 2019, another restenosis occurred in the proximal part of the outflow vein of the right forearm AVF and was treated using ultrasound-guided PTA. On 26 December 2019, a thrombosis related to the restenosis in the proximal part was found by ultrasonography. Hence, the right forearm AVF was discarded. Instead, an arteriovenous graft (AVG) in the left forearm was constructed for maintenance hemodialysis since then, with one PTA procedure annually on average up to now.",
"gender": "Female"
}
] |
PMC11385607
|
[
{
"age": 51,
"case_id": "PMC10601816_01",
"case_text": "A 51-year-old female never-smoker patient presented with progressive shortness of breath and new left-sided pleural effusion in September 2022 (shown in Fig. 1). Cytological examination of the pleural effusion showed TTF-1-positive adenocarcinoma cells; however, no pulmonary primary tumor or other distant metastases could be identified by computed tomography scan and MRI of the brain (clinical staging cT0, cN0, cM1a). Next-generation sequencing of the tumor cells (TSO500 DNA and RNA) revealed a SQSTM1(exon 4)-NTRK2(exon 16) in-frame fusion (NM 003900, NM 006180). No additional targetable alterations were identified (shown in Table 1) and immunohistochemical staining of tumor cells for PD-L1 was 15%.\nA talc pleurodesis was performed and pleural drainage was set. In October 2022, first-line therapy with larotrectinib 200 mg daily orally was initiated. After 9 weeks of therapy, computed tomography scan showed CR with no evidence of the pleural effusion or any other tumor manifestation. After 10 weeks of treatment, the pleural drain could be removed due to minimal flow rate (1 mL per week). From week 9 to week 18, therapy had to be interrupted due to a grade 3 elevation of transaminases (ALT > AST). The serum bilirubin level and a coagulation test were normal. Hepatopathy screening revealed no evidence of viral or autoimmune etiology with signs of mild hepatic steatosis on ultrasound and normal FibroScan. After a 2-month treatment break, recovery to grade 1 hepatitis was observed. Re-exposure to larotrectinib at 50% dosage at week 18 resulted in a recurrence of grade 3 hepatitis within 9 days. As a result, the therapy had to be interrupted again (shown in Fig. 2) and even after renewed start with 20% of dose, a consecutive ALT increase occurred; therefore, treatment was permanently discontinued and a trial of treatment with entrectinib was instead initiated. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000533572).",
"gender": "Female"
}
] |
PMC10601816
|
[
{
"age": 70,
"case_id": "PMC10618109_01",
"case_text": "A 70-year-old male with a medical history of diabetes mellitus (DM), hypertension, and multiple myeloma (in remission phase) presented to the accident and emergency (A&E) department with respiratory symptoms of cough, shortness of breath, and fever. Nasopharyngeal swab polymerase chain reaction (PCR) was positive for COVID-19. His condition deteriorated, requiring ventilatory support and medical intensive care unit (MICU) admission. Two days after the admission, the patient was intubated. He was treated in line with the COVID-19 local protocol (hydroxychloroquine, dexamethasone, and antibiotics). He was tracheostomized after 14 days due to difficulty weaning off ventilation. Despite sedation cessation, his level of consciousness did not improve, warranting further neuroimaging. MRI of the head showed extensive brain parenchyma periventricular diffuse white matter with increased T2-signal intensity. Susceptibility-weighted images (SWI) showed subcortical microbleeds of the brainstem and the basal ganglia (Figure 1A D). A lumbar puncture showed no pleocytosis, with negative viral panel and cultures. COVID-19-related encephalopathy was suspected. He was treated with two doses of tocilizumab followed by convalescent plasma therapy; however, the patient did not improve. Laboratory investigations showed severe hyperkalemia requiring dialysis due to the failure of the initial medical measures. He spent 74 days in the MICU, which was complicated by refractory hyperkalemia despite dialysis; this culminated in cardiac arrest and death (see Table 2).",
"gender": "Male"
},
{
"age": 48,
"case_id": "PMC10618109_02",
"case_text": "A 48-year-old female with a past medical history of longstanding DM and hypertension presented to the A&E department with a 10-day history of fever, sore throat, and myalgia. COVID-19 PCR from a nasopharyngeal swab was positive. The chest X-ray showed bilateral infiltrates. MICU admission was necessary due to increased respiratory effort and oxygen demand; the patient required intubation and mechanical ventilation for 15 days. She was successfully extubated on day 15. On day 17, her level of consciousness deteriorated, warranting further medical investigations. No other metabolic derangement was uncovered.\nThe MRI of the head (Figure 2) showed faint bright signal intensity on the diffusion-weighted imaging (DWI), with a corresponding iso-signal on the apparent diffusion coefficient (ADC) and bright signal intensity on the T2/FLAIR sequence involving the precentral subcortical white matter; features were suggestive of encephalitis. Microbleeds were noted on the SWI sequence and were of variable size, involving the splenium of the corpus callosum. The clinical and radiological findings suggested possible COVID-19 encephalitis/critical illness-related microbleeds. The patient received two doses of tocilizumab (400 mg and 600 mg). Her level of consciousness gradually improved, and she continued to recover with intensive rehabilitation, addressing cognitive and critical illness neuromyopathy. The overall condition improved, and she was discharged with minimal assistance in walking with regular outpatient follow-up appointments (see Table 2).",
"gender": "Female"
},
{
"age": 57,
"case_id": "PMC10618109_03",
"case_text": "A 57-year-old male with no known medical history presented to the A&E department with respiratory symptoms and fever; subsequently, COVID-19 PCR from the nasopharyngeal swab was positive. The patient developed respiratory distress, warranting MICU admission and intubation. Due to the failure of weaning off ventilation, he was tracheostomized, totaling 56 days of intensive care stay. Glasgow Coma Scale (GCS) was 2T despite cessation of sedation, raising the suspicion of COVID-19-related encephalopathy, mainly because no other metabolic derangement was uncovered.\nAn MRI of the head (Figure 3) showed microbleeds predominately in the splenium of the corpus callosum. He received convalescent plasma. Unfortunately, the MICU course was complicated with septic shock and disseminated intravascular coagulation (DIC) with multi-organ failure. Despite maximum vasopressor support, the patient developed pulseless electrical activity and passed away on day 63 of his MICU stay (see Table 2).",
"gender": "Male"
},
{
"age": 74,
"case_id": "PMC10618109_04",
"case_text": "A 74-year-old male presented to the A&E department with respiratory symptoms of cough, shortness of breath, and fever. COVID-19 infection was confirmed via a nasopharyngeal swab. The next day, his condition deteriorated, requiring ventilatory support. Due to his impaired level of consciousness despite cessation of sedation, he was not weaned off ventilation and was eventually tracheostomized. Further clinical investigations revealed an MRI of the head with multiple acute lacunar infarcts in the right deep frontal region with diffusion restriction. SWI sequence showed numerous microbleeds with corpus callosum and deep gray matter consistent with possible overlapping findings of COVID-19 encephalopathy with critical illness cerebral microbleeds (Figure 4A D). The patient received one dose of convalescent plasma. The MICU course spanned over 95 days and was complicated by fungemia, and refractory septic shock with multi-organ failure, culminating in cardiac arrest (asystole) and death (see Table 2).",
"gender": "Male"
},
{
"age": 64,
"case_id": "PMC10618109_05",
"case_text": "A 64-year-old male with no significant past medical history presented to the A&E department with respiratory failure due to COVID-19 pneumonia, warranting MICU admission. The patient was intubated and subsequently tracheostomized on day 15. Laboratory studies showed a low platelet count (with a nadir of 31,000 per microliter) and positive heparin-induced thrombocytopenia studies. Throughout his MICU course, his level of consciousness failed to improve. The MRI of the head showed features suggestive of COVID-19-encephalopathy with microbleeds involving the corpus callosum, the subcortical and deep white matter, and the gray matter structures (Figure 5). No immunotherapy was utilized. His course was complicated by bilateral pneumothorax, acute kidney injury requiring renal replacement therapy, and secondary infection with resistant bacteremia. The patient's condition ultimately deteriorated; brainstem reflexes were absent, and he was declared brainstem dead after the 15th day of admission (see Table 2).",
"gender": "Male"
},
{
"age": 66,
"case_id": "PMC10618109_06",
"case_text": "A 66-year-old male with a medical history of DM, coronary artery disease, hypertension, and chronic kidney disease (CKD) presented to the A&E department with progressive respiratory symptoms. He was found to have a positive COVID-19-PCR nasopharyngeal swab. He was initially admitted to the inpatient unit for two days and then transferred to MICU by the Rapid Response Team (RRT) due to a deterioration in consciousness level requiring intubation. On day 21 of MICU admission, an MRI of the head showed bilateral symmetrical frontoparietal subcortical and deep white matter changes suggestive of COVID-19-related leukoencephalopathy; no microbleeds were present on the SWI sequence (Figure 6).\nHe received two doses of convalescent plasma. His hospital stay was further complicated by an acute kidney injury requiring renal replacement therapy and secondary infection with extensively drug-resistant organisms. Despite gradual improvement in consciousness, he was tracheostomized due to weaning failure after approximately one month of his MICU stay. He was transferred to a long-term care facility for further pulmonary and physical rehabilitation for severe critical illness myopathy (see Table 2).",
"gender": "Male"
},
{
"age": 67,
"case_id": "PMC10618109_07",
"case_text": "A 67-year-old male with a distant past medical history of Hodgkin's lymphoma in remission, hypertension, DM, CKD, and coronary artery disease presented to the A&E department with fever and severe shortness of breath and was diagnosed with COVID-19 pneumonia. He was admitted to the MICU and intubated ten days later due to increased oxygen requirement.\nDuring the hospital course, he developed septic shock with multi-organ failures and DIC requiring inotropes and renal replacement therapy (RRT). The patient was referred to nephrology for acute CKD following a significant elevation in creatinine levels from a baseline of around 150. The creatinine measurements showed a fluctuating upward trend: 187, 168, 152, 137, 148, 157, 298, 344, and 513 mumol/L. On November 11, 2020, the patient experienced a deterioration of health condition, marked by tachycardia, hypotension (blood pressure 75/50 mmHg), and fever. At that time, the patient was on 3 mug of phenylephrine. Laboratory tests revealed line-related Gram-negative bacteremia caused by Klebsiella pneumonia on the same day, following which the patient was put on intravenous antibiotics. The deterioration of renal function commenced on the same day, likely due to acute tubular necrosis (ATN) secondary to septic shock. The first hemodialysis session was initiated two days later in response to the worsening renal condition.\nA head MRI was performed nearly 30 days after admission to the MICU. It revealed multifocal parenchymal hemorrhagic foci on the SWI sequence, displaying findings that overlapped with those typically associated with critical illness and COVID-19 microbleeds (Figure 7). The patient's condition deteriorated, leading to his demise 35 days post-MICU admission (Table 2).",
"gender": "Male"
}
] |
PMC10618109
|
[
{
"age": 21,
"case_id": "PMC10800138_01",
"case_text": "We genetically analyzed an Iranian family with a consanguineous marriage with a 21-year-old boy with HHL. The family pedigree is depicted in Figure 1. The blood specimens were obtained from all family members. All available medical history was collected. The otolaryngologist evaluated all family members. \nIt was determined that the subject had sensorineural HL (SNHL) based on pure tone audiometry (PTA). There were no clinical manifestations in favor of the syndromic phenotype. DNA extraction was conducted using the salting out method. We solely performed whole-exome sequencing (WES) for the proband. DNA sequencing was carried out by SureSelect Human All Exon Kit V6 (Agilent Technologies Inc., USA) and Illumina HiSeq 4000 machine (San Diego, USA) in accordance with the manufacturer's instructions. Genetic sequence analysis detected a novel, homozygous substitution at c.9908A>C (NM_016239.4) in exon 61 of the MYO15A gene. Bioinformatic tools, including SIFT, PolyPhen-2, and MutationTaster, predicted that this mutation is probably pathogenic (Table 1).\nThe detected mutation in the proband was verified using Sanger direct sequencing (ABI 3130 Genetic Analyzer, California, USA). The sequences of used primers were as follows (forward primer: AAGCTGTGTCCCAGAAC AGG and the reverse primer ACAGGGCCT GAATCATGA AC). Figure 2 shows that the patient and his parents had the MYO15A mutation in the homozygous and heterozygous states, respectively. This missense mutation substitutes Lysine with Threonine (AAG>ACG) at the 3303-position of the MYO15A protein (Figure 2D). These observations suggest that NM_016239.4 (MYO15A): c.9908A>C; p. Lys3303Thr mutation could be the cause of the progress of NSHL. The detected mutation information is shown in Table 2 based on the Human Gene Mutation Database.",
"gender": "Male"
}
] |
PMC10800138
|
[
{
"age": 22,
"case_id": "PMC10860705_01",
"case_text": "A 22-year-old woman complained of extreme pain in her left upper arm and numbness in her fingers after carrying heavy acrylic plates. There was no family history of nervous system or musculoskeletal disease. Initially, she was unaware of the severity of the condition. She chose to stay at home and take a rest. However, her pain and weakness showed no signs of recovery, with obvious flexion weakness of her thumb and index finger within 2 weeks. Half a month after the onset of the disease, ultrasound examination at a local hospital revealed edema of the median nerve accompanied by constrictions. One month following the onset, she came to our outpatient clinic. The patient presented with a forced left elbow flexion position due to severe pain. Physical examination showed a severe paresis of the left flexor pollicis longus and index flexor digitorum profundus muscles (strength 2 on the Medical Research Council (MRC) scale), a moderate paresis for the middle flexor digitorum profundus (MRC 3), biceps brachii, flexor carpi radialis, and abductor pollicis brevis muscles (MRC 3-4), with mild hypesthesia first three fingers and the radial half of the ring finger (Figure 1). The rest of muscle strength, tendon reflexes, Tinel's sign and neck examination were unremarkable.\nAt first, we adopted conservative treatment for the patient including 2 weeks of steroid pulse therapy (1 mg/kg), etoricoxib and oral mecobalamin. However, the patient still complained of extreme pain described as shooting and drilling at night. Therefore, electromyography (EMG) and ultrasound examination were performed when she came to the clinic again.\nThe EMG results showed that the abductor pollicis brevis, flexor pollicis longus, flexor carpi radialis, and biceps brachii exhibited fibrillation potentials and positive sharp waves, indicating AIN and musculocutaneous nerve both involvement. The conduction velocity of Median nerve was 53 m/s and the compound muscle action potential (cMAP) of the biceps muscle, as shown in EMG, was 10.5 mV (Table 1).\nUltrasound examination of the median nerve showed nerve bundle swelling and multiple HLCs of left upper arm (Figure 2). Magnetic resonance imaging was not performed.\nThe Median nerve was exposed through 2 incisions in front of the elbow joint. Inspection of the median nerve revealed that nerve fascicles (mainly AIN) were partially swollen and hardened due to inflammatory thickening of the epineurium proximal to the medial epicondyle.\nAfter the thickened epineurium had been opened, multiple HLCs lesions along with AIN bundle were exposed. One of the fascicles showed 4 HLCs and other fascicles showed 3 HLCs (Figure 3).\nDuring surgery, a total of 7 HLCs were found at 10.5, 9.5, 9.0, 6.0, 2.0, 1.5 and 0 cm proximal to the medial epicondyle (Figure 3) in her AIN bundle and without any visible source of external compression. During surgical intervention, nerve epineurium and part of the interfascicular nerve were released and electrical stimulation was performed on the median nerve. A total of 1 mL Compound Betamethasone was injected underneath the affected AIN epineurium.\nAfter surgery, the left elbow was immobilized at 135 position with splint for 2 weeks. The next day, the patient's pain was almost relieved. One month after surgery, she was able to bend her thumb and index fingers actively, although still weak (MRC 2). 4 months after the surgery, she was able to bend her thumb and index finger (MRC 3). At the same time, her fingers were less numbed.",
"gender": "Female"
}
] |
PMC10860705
|
[
{
"age": 42,
"case_id": "PMC11182160_01",
"case_text": "A 42-year-old black female patient with a history of POAG presented for further evaluation. She had no other significant past medical history or past surgical history. She had no known drug allergies. Her medications included latanoprost [right eye (OD) once a day (QD)] for elevated eye pressure. Her visual acuity was 20/20 [both eyes (OU)]. The patient's refraction value was +0.50 -2.25 x 177 in the OD, and 0.00 -4.25 x 177 in the left eye (OS). Their IOP was 17 in the OD and 16 in the OS. The dark-room gonioscopy revealed that the Shaffer grade II angles were open, but occludable, with the pigmentation being heavier inferiorly than it was superiorly due to the iridolenticular rubbing of the iris against the lens. There was no peripheral anterior synechia detected. The patient's cup-to-disc ratio (CDR) was 0.65/0.65 in the OD and 0.6/0.6 in the OS. An inferior notch was noted in the OS. Optical coherence tomography of the optic nerve head (OCT-ONH) revealed an average retinal nerve fiber layer (RNFL) thickness of 79 um in the OD and 86 um in the OS. The Humphrey visual field (HVF) analysis findings revealed a visual field index (VFI) of 91%, with a mean deviation (MD) of -7.14 in the OD and a VFI of 87% with an MD of -8.73 in the OS. The central corneal thickness was 530 um in the OD and 540 um in the OS. The target IOP for this patient was 10 mmHg-14 mmHg for both eyes.\nAfter discussing options for treatment, the patient decided to undergo glaucoma surgery consisting of clear lens extraction and IOL placement, OMNI viscocanaloplasty, and a HYDRUS stent with an adjacent goniotomy in the OS. The patient agreed to the risks and benefits and underwent the surgery without experiencing any complications. After the surgery, the patient was prescribed prednisolone acetate (QID), ketorolac (TID), and ofloxacin (QID) for the left eye while discontinuing latanoprost, also in the left eye. The patient was instructed to keep their head elevated above waist level for the first week, including when sleeping at night. On the first day post operation, the patient's IOP was 23 mmHg in the OD and 9 mmHg in the OS. The patient was then instructed to take latanoprost in the right eye. The patient returned 3 weeks post operation, and their IOP was found to be 19 mmHg in the OD and 17 mmHg in the OS. The patient continued latanoprost in the right eye, and their dosing of prednisolone acetate and ketorolac were tapered down. The patient then returned 5 months post operation, at which point their visual acuity was found to be 20/20 in the OD and 20/20 in the OS. Their postoperative refraction value was 0.00 -2.50 x 006 in the OS, resulting in an improvement in refractive error, with a decrease of 1.75 D in astigmatism. The patient's IOP was stable, at 16 mmHg in the OD and 15 mmHg in the OS. The HVF analysis revealed improved visual fields, with a VFI of 95% and an MD of -5.26 dB in the OD and a VFI of 88% and an MD of -5.96 dB in the OS.",
"gender": "Female"
},
{
"age": 41,
"case_id": "PMC11182160_02",
"case_text": "A 41-year-old black female patient with a past medical history of anxiety and lupus and a past ocular history of glaucoma presented for further evaluation. The patient had no known allergies. The patient's glaucoma medications were dorzolamide-timolol [twice a day (BID) OU] and latanoprost [one time in the evening (QHS) OU]. The patient's visual acuity with glasses was 20/20 in the OD and 20/20 in the OS. Their refraction value was -3.50 -1.50 x 068 in the OD and -3.50 -2.00 x 095 in the OS. The IOP for this patient was 19 mmHg in the OD and 18 mmHg in the OS. The gonioscopy showed Shaffer grade III angles, with increased pigmentation inferiorly vs. superiorly in both eyes. The patient's CDR was 0.8/0.8 in the OD and 0.8/0.8 in the OS, with glaucomatous cupping and thinning of the neuroretinal rim (OU). The OCT-ONH revealed an average RNFL thickness of 62 microm and a CD of 0.81 in the OD, and an average RNFL thickness of 72 microm and CD of 0.76 in the OS. The HVF of the OD revealed a supranasal defect, with a VFI of 92% and an MD of -5.07 dB. The HVF of the OS revealed a central nasal defect, a VFI of 95%, and an MD of -2.80 dB.\nAfter discussing treatment options with the patient, they decided to undergo glaucoma surgery entailing clear lens extraction and IOL placement with OMNI viscocanaloplasty and a HYDRUS stent with an adjacent goniotomy in the OD. After the surgery, the patient was placed on prednisolone acetate (QID), ketorolac (TID), and ofloxacin (QID) in the right eye. The patient continued the use of latanoprost (QHS) and dorzolamide-timolol (BID OS). One month post operation, the patient's intraocular pressure was 19 mmHg in the OD and 15 mmHg in the OS. At this point, we began to taper the patient off prednisolone acetate and ketorolac. Their visual acuity 6 weeks post operation was 20/20 in the OD and 20/25 in the OS. The patient's intraocular pressure during this visit was stable, at 11 mmHg in the OD and 14 mmHg in the OS. Four months after undergoing glaucoma surgery, their intraocular pressure was 17 mmHg in the OD and 26 mmHg in the OS. At this point, the patient decided to undergo the same glaucoma surgery in her left eye due to the increase in the IOP. One day post operation, the patient's distance visual acuity was 20/25 in the OD and 20/25 in the OS. The intraocular pressure was noted to be 13 mmHg in the OD and 14 mmHg in the OS. Three weeks post operation, the patient's visual acuity was 20/25 in the OD, 20/25 in the OS, and 20/20 in OU. The intraocular pressure was found to be 14 mmHg in the OD and 14 mmHg in the OS. Four months post operation, her IOP was 12 mmHg in the OD and 10 mmHg in the OS and she was taking no medications. The HVF of the OD revealed a VFI of 91% and an MD of -4.93 dB, while the HVF of the OS revealed a VFI of 96% and an MD of -4.07 dB. The visual acuity was 20/20 in the OD and 20/20 in the OS. The refraction value was 0.00 -1.50 x 069 in the OD and +0.25 -1.00 x 093 in the OS. This represented a 3-diopter improvement in spherical equivalence.",
"gender": "Female"
},
{
"age": 49,
"case_id": "PMC11182160_03",
"case_text": "A 49-year-old black female patient with suspected glaucoma, in addition to diabetes and hypercholesterolemia, presented for further evaluation. The visual acuities for distance were 20/20 in the OD and 20/20 in the OS. The refraction for this patient was +2.25 SPH in the OD and +2.25 -0.50 x 084 in the OS. The IOP for this patient was 15 mmHg in the OD and 15 mmHg in the OS. The gonioscopy showed Shaffer grade III angles, with greater pigmentation observed inferiorly than superiorly. The CDR was 0.55/0.55 in the OD and 0.55/0.55 in the OS, with thinning of the inferior neuroretinal rim also observed. The HVF of the OD showed a VFI of 90% and an MD of -4.07, and that of the OS showed a VFI of 87% and an MD of -4.77. The OCT-ONH test revealed an average RNFL thickness of 89 microm in the OD and 79 microm in the OS. The corneal pachymetry showed a central corneal thickness of 497 microm in the OD and 492 microm in the OS. The patient was diagnosed with mild POAG. The patient was placed on latanoprost (QHS OU).\nTo reduce the need to take eye drops for the rest of their life, the patient provided informed consent and agreed to undergo glaucoma surgery entailing clear lens extraction and IOL placement with OMNI viscocanaloplasty and a HYDRUS stent with an adjacent goniotomy in the left eye. Following surgery, the patient was placed on prednisolone acetate (QID), ketorolac (TID), and ofloxacin (QID) in the left eye, while discontinuing latanoprost in the left eye. One day post operation, the patient's unaided visual acuity for distance was 20/60 in the OD and 20/20 in the OS. The measured intraocular pressure was 14 mmHg in the OD and 8 mmHg in the OS. The patient continued taking the postoperative medications for 3 weeks and then returned for follow-up. At the 3-week follow-up, the patient's best corrected visual acuity was 20/20 in both the OD and the OS. The patient's IOP was 14 mmHg in the OD and 14 mmHg in the OS. The refraction value was -0.50 -0.50 x 053 OS. This represented a 2-diopter improvement in the spherical equivalence. Ofloxacin was discontinued, and prednisolone acetate and ketorolac were tapered at this point. The patient was to continue taking latanoprost (QHS OD). The patient returned for follow-up at 6 months, at which point it was found that their IOP was stable, at 14 mmHg in the OD and 14 mmHg in the OS.",
"gender": "Female"
},
{
"age": 47,
"case_id": "PMC11182160_04",
"case_text": "A 47-year-old black male patient presented with a history of glaucoma. The patient was taking latanoprost (QHS OU), dorzolamide (BID OU), and brimonidine (TID OS). The patient's visual acuity was 20/20 in the OD and 20/20 in the OS with spectacle correction. The IOP was 17 mmHg in the OD and 17 mmHg in the OS. The refraction value was +0.50 -1.25 x 003 in the OD and +0.25 -1.75 x 003 in the OS. The dark-room gonioscopy showed grade II Shaffer angles that were narrowly occludable. The fundus exam revealed glaucomatous cupping in both eyes and an inferior notch in the OS. The CDR was 0.85/0.85 in the OD and 0.85/0.85 in the OS. The pachymetry test for this patient revealed a corneal thickness of 504 microm in the OD and 499 microm in the OS. The OCT-ONH showed an average RNFL thickness of 80 microm in the OD and 76 microm in the OS. The visual field testing for this patient revealed a VFI of 91% and an MD of -3.58 dB in the OD, and a VFI of 93% with an MD of -4.57 dB in the OS.\nThe patient provided informed consent and agreed to undergo surgery entailing a clear lens extraction and IOL placement, a HYDRUS stent, and OMNI canaloplasty in the right eye. After the surgery, the patient was placed on prednisolone acetate (QID), ketorolac (TID), and ofloxacin (QID) in the right eye. Five months post operation, the patient's best corrected visual acuity was 20/20 in the OD and 20/20 in the OS. The patient's IOP measurement was 14 mmHg in the OD and 14 mmHg in the OS. The visual field test for this patient revealed a VFI of 94% with an MD of -4 dB in the OD and a VFI of 89% with an MD of -8 dB in the OS.\nThe patient decided to undergo glaucoma surgery in the left eye, which entailed clear lens extraction and IOL placement with OMNI viscocanaloplasty and a HYDRUS stent with adjacent goniotomy. After surgery, the patient was placed on prednisolone acetate (QID), ketorolac (TID), and ofloxacin (QID) in the left eye. On the first day post operation, the patient's visual acuity was 20/20 in the OD and 20/50 in the OS. The IOP for this patient was 9 mmHg in the OD and 8 mmHg in the OS. Three weeks post operation, the patient's visual acuity was stable, at 20/20 in the OD and 20/20 in the OS. The final refraction value was -1.00 -1.00 x 173 in the OD and -0.50 -1.50 x 010 in the OS. The patient's IOP was stable, at 12 mmHg in the OD and 13 mmHg in the OS. At this point, the patient was tapered off prednisolone acetate and ketorolac.\nAt the 6-month follow-up, the patient's visual acuity was 20/20 in both eyes. While on latanoprost (QHS OU), their IOP was stable, at 12 mmHg in the OD and 13 mmHg in the OS. This resulted in a decrease of glaucoma medications needed, from two to one in the right eye, and from three to one in the left eye. The HVF revealed a VFI of 96% with an MD of -5.73 dB in the OD, and a VFI of 93% with an MD of -6.88 dB in the OS. The fundus photos taken revealed stable CDRs.",
"gender": "Male"
}
] |
PMC11182160
|
[
{
"age": 0,
"case_id": "PMC10667052_01",
"case_text": "A 5-month-old female infant presented with horizontal and rotational nystagmus of pendular characteristics, occasionally rebounding, which disappeared with fixation on near objects. Nystagmus was noted to be more intense on the hyperopic left eye. Fundoscopic examination was normal bilaterally at the time. Electroencephalography was characterized by sharp theta waves, nystagmus episodes, and slow delta waves during head movements originating from the parietal and occipital lobes. Imaging of the brain with computed tomography (CT) and magnetic resonance (MRI) was normal.\nLater in life, the patient was diagnosed with T2DM and obesity as well. Within a 5-year period (2016 to 2021), her metabolic profile, including vitamin B12, glucose profile (HbA1c, glucose tolerance tests), liver function tests, and complete blood count were normal except for vitamin D insufficiency (low levels of vitamin D3) at various time points. Abdominal ultrasound did not reveal abnormalities in the liver, common bile duct, portal vein, gallbladder, pancreas, spleen, or kidneys. Visual acuity was light perception in both eyes and had different diagnoses from different hospitals (Leber's hereditary optic neuropathy and retinitis pigmentosa).",
"gender": "Female"
},
{
"age": 17,
"case_id": "PMC10667052_02",
"case_text": "The patient presented in our department in 2021. She was 17 years old at the time. Best corrected visual acuity (BCVA) was light perception in both eyes. BCVA was light perception in both eyes reportedly since the age of 13. OCT scans of the macular region displayed significant photoreceptor layer disruption in both eyes with minimal preservation of this layer around the central fovea (Figure 1). Fluorescein angiography (FA) revealed vessel attenuation and hyperfluorescent areas in the posterior pole (window defects, Figure 2). Autofluorescence (FAF) revealed extended disruption of the retinal pigment epithelium (RPE) metabolic activity in the posterior pole and periphery OU (Figure 3). The findings on the electroretinogram (ERG, scotopic negative, photopic negative, and bright flash testing) and visual evoked potentials (VEP) were abnormal, with the recordings noted not surpassing electrical noise (Figure 4). Based on these findings, the diagnosis of early onset retinal dystrophy was established, with a recessive inheritance pattern. The presumed diagnosis at the time was Leber's hereditary optic neuropathy.\nFollowing the initial diagnosis, genetic DNA testing established the diagnosis of the Alstrom syndrome. DNA was isolated from whole peripheral blood, and simultaneous molecular control of the complete coding sequence of 125 genes of known function involved in hereditary retinopathies by the Next Generation Sequencing method (Ophthalmic Genetic Unit, Athens) was performed.\nClinical diagnosis was potential congenital malformation according to Leber's hereditary optic neuropathy. Molecular analysis was positive for pathogenic mutations. The heterozygous genetic variants c.4156dup, p.(Thr1386Asnfs*15) and c.(9542+1_9543-1)_(9784+1_9785-1) del involving exons 8 and 11, respectively, of the ALMS1 gene (Alstrom's syndrome) were detected (MIM 606844). Mutations in the ALMS1 gene are responsible for the Alstrom syndrome (MIM 203800).\nThe mutations identified in the genetic material of our patient are predicted to be pathogenic as they cause the premature termination of ALMS1 protein synthesis (protein truncating mutations). One of them, c.4156dup, p.(Thr1386Asnfs*15) has previously been reported in the international literature but with a different second mutation, while the second mutation reported here, which is recommended for the loss of exon 11 of the gene, has not been previously reported in similar published papers. Consequently, the combination of the two mutations has not been previously reported in the relevant literature.\nThe presence of the detected mutations c.4156dup, p.(Thr1386Asnfs*15) and c.(9542+1_9543-1)_(9784+1_9785-1) del of the ALMS1 gene in the genetic material of our patient is most likely the cause of her condition which according to her genetic diagnosis is the Alstrom syndrome, which belongs to the group of ciliopathies and is inherited with an autosomal recessive type of inheritance. It should be noted that the phenotypic manifestations of the Alstrom syndrome can appear at various times in a patient's life. They may also vary greatly both between families and between members of the same family.\nAll the children of our patient must necessarily be heterozygous carriers of one of the two detected ALMS1 gene mutations. As carriers of an autosomal recessive hereditary disease mutation, these children will be asymptomatic, provided the father is not also a carrier of a pathogenic mutation of the same gene.\nOur patient is additionally heterozygous for the genetic variant c.367>T, p.(Arg123Cys) of unclear clinical significance (VUS) in the RP1 gene (RP1 axonemal microtubule associated, MIM 603937). This genetic variant is registered in the international database of clinical genetic data ClinVar with the code 1025517 in the context of clinical control without clarification while it has not been reported in relation to the diseases associated with the RP1 gene in the international literature. Mutations in the RP1 gene are responsible for autosomal recessive and dominant retinitis pigmentosa 1 (retinitis pigmentosa 1, MIM 180100, AD, AR). The detected mutation is located in exon 2, and based on the available data, it would be associated with the recessive form of the condition for which the presence of two mutations is required. No second or potential pathogen was identified pathogenic mutation in the RP1 gene in our patient. Moreover, there are 2 heterozygotes in the gnomAD international control population genetic databases (with more than 120,000 exomes and 15,000 genomes) which means that this genetic deletion cannot cause severe disease at least in childhood. Consequently, it is not considered possible that this genetic variant is associated with the clinical status of the patient, especially in the light of the identification of the two pathogenic mutations in the ALMS1 gene.",
"gender": "Female"
}
] |
PMC10667052
|
[
{
"age": 58,
"case_id": "PMC10589413_01",
"case_text": "Patient information: a 58-year-old nulligravid female patient was admitted to our department with a four-week history of dyspnea New York Heart Association (NYHA) class III dyspnea and cyanosis. Her past medical history included only a cardiac murmur noted in childhood. On further questioning, the patient reported related that she had been diagnosed with TOF since the age of 22. Surgical correction had been suggested, but the patient repeatedly refused treatment.\nClinical findings: the physical examination was remarkable for an underdeveloped adult female with oxygen saturation of only 80% on room air. She was 1.56 m tall and weighed 46 kg with a body mass index of 19 kg/m2. Her pulse rate was 78 beats/min and her blood pressure was 107/68mmHg. Her lips and oral mucosa were cyanotic. Fingers and toes were clubbed and cyanotic with intact pulses (Figure 1). On cardiac examination, a grade five out of six holosystolic murmur was auscultated over the precordium with a palpable thrill at the apex. Jugular venous pressure was elevated. Pulmonary auscultation revealed clear lung fields. Additionally, hepatomegaly and mild peripheral edema were noted.\nDiagnostic assessment: the electrocardiogram displayed a regular sinus rhythm of 75 beats per minute, with right axis deviation, voltage criteria consistent with right atrial enlargement and right ventricular hypertrophy (RVH). Chest radiography revealed a right aortic arch (RAA) (Figure 2). Laboratory data included a hemoglobin level of 16.1 g/dl, a hematocrit of 42%, and thrombocytosis, other laboratory data were normal. A two-dimensional echocardiogram revealed moderate right atrial enlargement, right ventricular enlargement and hypertrophy with impaired systolic function, large perimembranous outlet ventricular septal defect (VSD) of 21 mm and an overriding aorta (Figure 3). Doppler examination revealed an infundibular obstruction with a right ventricular outflow tract (RVOT) gradient of 75 mmHg (Figure 4). The main pulmonary artery (MPA) and the right pulmonary artery were mildly hypoplastic compared with the left pulmonary artery. Contrast-enhanced computed tomography (CT) scan confirmed the finding of mild pulmonary artery hypoplasia. The MPA measured 10 mm, the right pulmonary artery measured 9 mm, and the left pulmonary artery measured 20 mm. It also showed RAA, VSD with overriding aorta, RVOT narrowing with RVH and aortopulmonary collateral channels (Figure 5, Figure 6).\nTherapeutic interventions: after careful consideration of the patient's wishes against corrective surgery and the increased surgical risk associated with the presence of RV dysfunction, the decision was made to manage medically.\nFollow-up and outcome: the patient was discharged one week later on diuretics and beta-blocker. During a 6-month follow-up, after discharge, she remained in NYHA class II.\nPatient perspective: the patient was satisfied with the medical management of her condition.\nInformed consent: written informed consent was granted by patients.",
"gender": "Female"
}
] |
PMC10589413
|
[
{
"age": 43,
"case_id": "PMC10957539_01",
"case_text": "A 43-year-old man with HF secondary to dyspnea was admitted to our hospital. The patient's height was 160 cm, body weight was 109 kg, and body mass index was 42.5 kg/m2. Past medical history included diabetes mellitus and sleep apnea. Upon admission, the patient experienced orthopnea and whole-body edema. Laboratory data indicated a creatinine of 1.3 mg/dl, an estimated glomerular filtration rate of 49 ml/min/1.73 m2 and an N-terminal pro-brain natriuretic peptide level of 4,177 pg/ml. Electrocardiography revealed sinus tachycardia and a left ventricular ejection fraction of 20% with diffuse left ventricular hypokinesis. Plain chest radiography revealed a cardiothoracic ratio of 66% and a costophrenic obtuse angle. The patient was diagnosed with AHF and was treated with intravenous furosemide and oxygen inhalation. However, the patient developed respiratory failure and low-output syndrome on the 7th hospital day. The patient was transferred to the cardiac care unit (CCU), and treatment with noradrenaline, dobutamine, and noninvasive positive pressure ventilation was initiated. On the 19th hospital day, right heart catheterization indicated Forrester subset IV (pulmonary artery wedge pressure, 27 mmHg; cardiac index: 1.6 L/min/m2), and coronary angiography revealed no significant stenosis. Based on the clinical course and endomyocardial biopsy of the right ventricular septum, the patient was diagnosed with idiopathic dilated cardiomyopathy on the 23rd hospital day. Because the patient was young and had developed catecholamine-dependent HF, heart transplantation was considered. However, severe obesity was an obstacle to registration. We started B-SES (G-TES; Homer Ion Laboratory, Tokyo, Japan) in parallel with normal cardiac rehabilitation and performed gradual withdrawal of catecholamines and titration of bisoprolol. On the 48th day of hospitalization, the patient was withdrawn from noradrenaline. The patient was transferred from the CCU to the general ward on the 92nd day. The patient's symptoms improved to NYHA II with titration of bisoprolol, ivabradine, valsartan, spironolactone, dapagliflozin and furosemide, along with cardiac rehabilitation. In addition, we provided life modification program to the patient because eating habits and sedentary life style had contributed to his obesity. The patient was discharged with a body weight of 75.6 kg on the 113th hospital day. This case report has anonymized patient information, and photographs including parts of the body (including the face) have been processed to ensure that the individual cannot be identified. We obtained written informed consent from the patient for publication.\nThe clinical course and contents of the rehabilitation program are shown in Figure 1. Range of motion and active assistive movement were performed from the 2nd to the 15th day due to unstable circulatory dynamics. Although sitting exercises were initiated on the 16th day, orthostatic hypotension and subjective fatigue were still observed. Standing exercises were initiated on the 30th day; however, the patient was unable to stand up because of orthostatic hypotension and leg fatigue. On the 43rd day, gait training in the room was initiated using a walker, and physical activity was interrupted due to orthostatic hypotension and subsequent fatigue.\nWeight loss has been identified as a major issue in improving mobility and registration for heart transplantation. In addition to normal cardiac rehabilitation, B-SES was started on the 48th day. The B-SES was placed around the lower trunk, thigh, and ankle (Figure 2). All muscles were simultaneously contracted for 20 min by an exponential growth wave of 250 ms pulses at a frequency of 4 Hz. At first, based on supplier recommendation and previous research, we have adopted low intensity protocol with a frequency of 4 Hz. The stimulus intensities were set to could cause visible contractions and increased to the maximum intensity tolerated by the patient within 3 days. The patient demonstrated good tolerance to B-SES, allowing for active participation, and B-SES was performed daily for 6 weeks. Heart rate (HR), blood pressure, double product (DP), and Borg scale scores were evaluated at 5, 10, 15, and 20 min, respectively, after the sessions started. At first, B-SES was performed in the supine position; however, systolic blood pressure (SBP) and DP increased. We changed the position to head-up at 10 , which improved treatment tolerability. In addition, we assessed the creatine kinase and glomerular filtration rate as the marker of overload, and no excessive elevation of creatine kinase and no decrease in glomerular filtration rate were observed during the B-SES period.\nWe evaluated the patient's muscle strength, quality, and physical performance (Table 1). Body composition was measured by using a bioelectrical impedance device (Body Composition Analyzer, InBody S10; InBody Japan Co., Ltd., Tokyo, Japan). Leg muscle mass, thigh circumference, and lower leg circumference were obtained as the averages of the left and right sides. Transverse images of the rectus femoris (RF) of the right thigh were obtained using real-time B-mode ultrasonography (Vivid S6; GE Healthcare, Tokyo, Japan). Ultrasonography was performed to examine muscle thickness (MT) and subcutaneous fat thickness (FT). In addition, muscle quality of the lower limbs was assessed using echo intensity (EI) images obtained from ultrasonography. Images of FT, MT of the RF (RFMT), and EI of the RF (RFEI) were obtained halfway between the anterior superior iliac spine and the proximal end of the patella. Physical function was evaluated every 2 weeks, and the treatment of B-SES were consequently modified. In this case, ultrasonography in the 2nd week revealed a decrease in FT, but no improvement was observed in RFMT and RFEI. Consequently, the settings of the B-SES were upregulated to a stimulus of 20 min at a frequency of 20 Hz, in the daytime, and a stimulus of 30 min in the evening at a frequency of 4 Hz. For high intensity protocol, we have adopted a frequency of 20 Hz, as per the effective frequency proposed in the past report.\nIn addition to using B-SES, nutrition therapy was planned with an energy requirement of 1,408-1,689 kcal and an amount of protein of 1.2-1.5 g/kg/day. Two medimeals Leucine plus and one protein jelly were added as nutritional supplementary food, and one medimeal Leucine plus was taken before starting B-SES to reduce fatigue during exercise and suppress muscle proteolysis. On the 50th day, gait training in the corridor was initiated with a walker. According to the up-regulation of the settings of B-SES and the contents of the trainings, nutritional therapy was changed to an energy requirement of 1,400-1,800 kcal. In addition, betahydroxy-betamethylbutyrate was ingested before and after B-SES. On the 75th day, aerobic exercise was initiated with Strength Ergo (Strength Ergo5 BK-ERG-051; Mitsubishi Mitsui Engineering Corporation, Aichi, Japan) in the rehabilitation room. Both daytime and evening B-SES settings were changed to a frequency of 20 Hz and stimulation time of 20 min on the 77th day. On the 92nd day, B-SES used ended due to discharge from the CCU, and gait training in the ward was included as a voluntary exercise. On the 113th day, the patient was discharged from the hospital.\nThe results of the physical function assessments are summarized in Table 1. Muscle strength and physical performance improved gradually. Body composition analysis revealed that body weight and fat mass had decreased, whereas muscle mass had increased. Muscle ultrasonography demonstrated that the FT had gradually decreased. The RFMT and the RFEI improved after up-regulation of the settings of the B-SES at the 2nd week. No adverse events were observed using B-SES. HR, SBP, and DP continued to increase after starting B-SES but decreased after 15 min (Figure 3).\nWe performed an expiratory gas analysis to estimate the exercise load and calorie expenditure during B-SES. Volume of oxygen (VO2) uptake was measured using an expired gas analyzer (Aeromonitor AE-310S; Minato Medical Science, Osaka, Japan) in the resting position and during B-SES. The B-SES settings included a frequency of 20 Hz and a stimulus of 20 min. Gas samples were collected for 5 min or more, and the average VO2 after breathing stabilization was analyzed. Calorie expenditure during B-SES was calculated using the formula: kcal/min = 3.5 x METs x body weight (kg)/200. This expiratory gas analysis revealed that VO2 in the resting lying position was 293.1 +- 34.9 ml and VO2 during B-SES was 455.9 +- 15.6 ml. Calorie expenditure during B-SES was 65.5 kcal.",
"gender": "Male"
}
] |
PMC10957539
|
[
{
"age": 36,
"case_id": "PMC11195724_01",
"case_text": "A 36-year-old male patient presented with dyspnoea, fatigue, and pre-syncope episodes during moderate exertion. Relevant history included surgery for a subvalvular mitral aneurysm (SMA) performed 14 years earlier. Although surgery was done suspecting a type A aortic aneurysm, the diagnosis was not confirmed intraoperatively. Detailed surgical notes were not available. Physical examination revealed a systolic-bar murmur in the third left intercostal space. 2D-transthoracic echocardiography and Doppler study displayed a large structure linked to the left ventricle through a narrow neck (Panel A, arrow), showing a turbulent jet filling a pseudoaneurysm (Panel B) with a high gradient between the ventricle and the pseudoaneurysm (Panel C). An operated SMA aneurysm was also observed (Panel D).\nA 64-slice gated CT (Panels E, F, and G, Supplementary data online, Movies S1, S2, and S3) with volume rendering (Panel H) confirmed the presence of SMA (Panel G) and also showed a massive pseudoaneurysm from the left ventricular outflow tract (LVOT), impacting the right atrioventricular groove and the ascending aorta, compressing the right ventricle (Panels G and H).\nBoth the LVOT pseudoaneurysm and SMA shape the atrioventricular groove without evident coronary artery compression (Panels I, J, and K). This image spotlight exemplifies the case of a patient with a long-standing LVOT pseudoaneurysm. LVOT pseudoaneurysms are rare, often post-infective endocarditis or cardiac surgery. Surgical repair is generally advised, but percutaneous closure (PC), when feasible, may be preferred in high-risk cases. However, due to PC unavailability and high surgical risk, the patient was managed conservatively with furosemide 40 mg twice a day; losartan 25 mg once a day, spironolactone 25 mg once a day, carvedilol 6.25 mg twice a day. He is currently in NYHA Class II.\nAo, aorta; Cx, circumflex artery; LA, left atrium; LAD, left anterior descending artery; LV, left ventricle; PAn, pseudoaneurysm; RCA, right coronary artery; RA, right atrium; RV, right ventricle.",
"gender": "Male"
}
] |
PMC11195724
|
[
{
"age": 10,
"case_id": "PMC10540602_01",
"case_text": "We present a case of a 10-year-old boy with GSD Ib. Due to the recurrent severe hypoglycemia and neutropenia at 1 month of life, GSD Ib was suspected and confirmed through genetic testing (the variants c.1042_1043del in homozygosity was found on the SLC37A4 gene). Since then, dietary management with small and frequent feedings was started. At 1 year of age, cornstarch was introduced, reaching a maximum dosage of 6.8 g/kg with a fasting period of up to 4 h. Due to the presence of neutropenia since the diagnosis, at 1 month of life, G-CSF (starting dose 2 gamma/kg/die) and antibiotic prophylaxis were initiated (evening single dose).\nSince the age of 7 years, the patient developed recurrent severe oral aphtosis and frequent infections, which were treated with increasing doses of G-CSF (up to a maximum dose of 9 gamma/kg/die during infections without interruptions). As a side effect, he developed severe splenomegaly and hypersplenism. The growth pattern was regular on the sixth percentile for weight and height on the WHO growth chart with a body mass index (BMI) of 15 kg/m2. No diarrhea nor abdominal pain was reported. At the age of 8 years, a gastroenterological consultation was performed: laboratory test showed a persistent mild increase in erythrocyte sedimentation rate (ERS) and negative C-reactive protein (CRP), fecal calprotectin was high (500 microg/g; normal value 50), ASCA IgA was found. Based on the clinical and laboratory assessment, a diagnosis of Crohn's-like disease was hypothesized.\nMagnetic resonance enterography (MRE) showed segmental thickening of the ascending colon wall at the ileocecal valve levels. The known splenomegaly was described with a bipolar diameter of 20 cm. The endoscopic evaluation displayed mucosal hyperemia of the cecum with edema, ulcerative lesion, and substenosis of the ileocecal valve. No other findings on the colon, sigma, and rectum were found. Chronic inflammation was reported at the histologic evaluation. Thalidomide was started in combination with G-CSF based on our previous experience in treating Crohn's disease children, its efficacy in treating oral aphtosis, and its immunomodulatory effect. Quick resolution of oral aphtosis was obtained with concomitant weight gain. However, after 9 months of treatment, no improvement at MRE and endoscopy evaluation was observed.\nAt the age of 9 years, we decided to add a new treatment with empagliflozin to the ongoing therapy, based on the recently reported efficacy of this drug in a few cases with GSD Ib and Crohn's-like disease in the literature.\nInformed written consent was obtained from the patient's parents, according to the International and Italian Metabolic Board (MetabERN), after discussing the potential benefits and adverse effects of the treatment.\nThe patient was admitted to the pediatric ward for clinical monitoring during the introduction of the new therapy. The starting dose was 0.1 mg/kg per day for the first 2 days, then increased to 0.2 mg/kg in two doses from day + 3 of treatment as planned by the Board of Italian and European experts coordinated by MetabERN. During admission, the patient's vital parameters, glycemia, and urine dipstick were monitored. Mild glycosuria was expectedly observed due to the drug's mechanism of action. Only one asymptomatic episode of hypoglycemia (58 mg/mL) was detected in the first days. No other adverse effects were observed. The patient continued the treatment at home, with weekly increases in dosage. Considering the good tolerance to the treatment, the dosage was increased to the target dose of 0.5 mg/kg per day indicated by previous studies after 30 days. Despite the glycosuria, no major urogenital tract infections occurred.\nClinically we observed that, despite the suspension of thalidomide after 45 days of empagliflozin treatment, no episodes of oral aphtosis were reported, and stools were solid. IBD remained clinically silent with a Pediatric Crohn's Disease Activity Index score equal to 0 at 3, 12, 18, and 24 months.\nAfter the beginning of the new treatment, the patient's weight and height significantly improved, with a gain of 17 kg in the following 2 years (going from the 33rd centile to the 70th percentile on the WHO growth chart). The height gain on the WHO growth chart went from the 7th to the 26th percentiles and the BMI improved from 19 to 24 kg/m2 (see Figure 1).\nAfter 4 months of empagliflozin therapy, laboratory results showed a normalization of erythrocyte sedimentation rate (ESR) with CRP always negative (Table 1). Calprotectin was used as an indicator of bowel inflammation and was persistently below 300 microg/g, a cutoff that identifies children with mucosal healing (see Table 1). The blood and bowel inflammatory index remained persistently negative during the 2 years of therapy (see Table 1). White blood cells and neutrophils improve over time (see Figure 2). The improvement in the number of neutrophils allowed for a progressive decrease in the G-CSF dosage with an absolute neutrophil count always above 1000/mmc even during the tapering phase of G-CSF (minimal dose 1 gamma/kg/die), until suspension after 18 months of empagliflozin treatment. Then white cell count remains above 4000/mmc and the absolute neutrophils count above 1500/mmc (see Figure 2). The tapering and the suspension of G-CSF led to a consequent gradual reduction of hypersplenism and splenomegaly observed at physical examination and the MRE imaging. Furthermore, while on empagliflozin, as expected from the drug action, we observed an increase in specific neutrophil subtypes (mature neutrophils) and a reduction in the immature subsets, no neutrophil function assay was performed. In addition, contrary to the mechanism of action of empagliflozin, based on our clinical experience, initiating this new treatment allowed our dietician to extend the fasting period up to 5 h without any changes in cornstarch dosage.\nA complete restaging of IBD was performed at 3 and 12 months after achieving the target dose of empagliflozin.\nAfter 3 months of empagliflozin therapy, MRE confirmed the thickening of the last ileal loop (maximum thickness 7 mm, longitudinal extension 4 cm), but found less edematous imbibition of the adjacent mesenteric adipose tissue and less thickening of the walls of the cecum next to the ileocecal valve. The G-CSF-induced splenomegaly with glycogen nodules was reduced with a bipolar diameter of 17 versus 20 cm. The ileocolonoscopy demonstrated the macroscopic resolution of ileal and cecal inflammation, with persistent ileocecal substenosis. The histological evaluation revealed minimal and nonspecific chronic inflammation with initial fibrotic aspects on the ileocecal mucosa.\nAt 12 months of therapy, MRE demonstrated complete resolution of the concentric thickening of the cecal walls, a reduction in the concentric thickening of the terminal ileal loop (maximum thickness 5 versus 7 mm and longitudinal extension of 2 versus 4 cm). The G-CSF-induced splenomegaly with glycogen nodules was unchanged with a bipolar diameter of 16.5 cm (normal median spleen long axis at 8-10 years is reported to be 9.2 cm). Colonoscopy showed an open ileocecal valve passed with only a light pressure, the stenosis previously described was no longer appreciable, and normal appearance of the terminal ileum and colon. Histology confirmed a complete inflammatory quiescence with reparative aspects in the right colon.",
"gender": "Male"
}
] |
PMC10540602
|
[
{
"age": 75,
"case_id": "PMC10962458_01",
"case_text": "In May 2023, a 75-year-old woman with a history of hypertension and no past SARS-CoV-2 infection was admitted to our hospital for chills, pyrexia (maximum temperature, 38 C), cough, headache, asthenia, myalgia, and lumbago. The patient had received two doses of Sinopharm/BIBP COVID-19 vaccine. Inquiring about her exposure to birds revealed that she had worked in a slaughterhouse and slaughtered chickens before the disease onset.\nThe patient was not tested for SARS-CoV-2 on admission to the hospital. Chest computed tomography (CT) on day 1 after admission revealed massive consolidation in the left lower lung and a left-sided pleural effusion (Figure 1), leading to a diagnosis of pneumonia. The laboratory test results revealed elevated white blood cell (WBC) and neutrophil counts, an elevated neutrophil percentage, and elevated levels of C-reactive protein (CRP), aspartate aminotransferase, fibrinogen, and D-dimer (Table 1). \nIntravenous piperacillin-tazobactam (4 g/0.5 g) was administered every 8 hours to treat pneumonia. However, 3 days after admission, the patient developed recrudescent pyrexia (maximum temperature, 39.2 C). Fiberoptic bronchoscopy revealed tracheitis and bronchitis with bronchial mucosal hyperemia in the left lower lobe and various subsegments.\nThe patient underwent bronchoalveolar lavage of the left lower lobe, and bronchoalveolar lavage fluid (BALF), blood, and nasopharyngeal swab (NPS) samples were tested using mNGS to identify the pathogen. Clinical samples were collected according to the standard protocol of our hospital. DNA was extracted from BALF, blood, and other clinical samples using a TIANamp Micro DNA Kit (DP316, Tiangen Biotech Co., Beijing, China), followed by DNA/RNA library construction, high-quality sequencing, and classification analysis, as described previously. The mNGS analysis detected C. psittaci in the BALF (sequence number: 874), peripheral blood (sequence number: 2), and NPS (sequence number: 4) samples, as well as SARS-CoV-2 Omicron XBB.1 in the BALF (sequence number: 1,847,027) and NPS (sequence number: 224,671) samples (Figure 2). \nThe mNGS results were confirmed using qPCR tests for C. psittaci and SARS-CoV-2. The primer sets targeted the OmpA and ORF/N genes of C. psittaci and SARS-CoV-2, respectively (Table 2). The qPCR detected C. psittaci nucleic acid in the BALF only (Ct: 24.59) and SARS-CoV-2 nucleic acid in both the BALF and NPS specimens (Ct: 38.57 and 31.07, respectively; Table 3). \nSerum samples were tested for SARS-CoV-2 immunoglobulin (Ig)M/IgG using chemiluminescence immunoassays, performed according to the instructions of Guangzhou Huayin Health Medical Group Co., Ltd. The patient tested negative for SARS-CoV-2 IgM (cutoff index, 0.87) and positive for SARS-CoV-2 IgG (cutoff index, 64.58).\nBased on these findings, the patient was diagnosed with psittacosis and SARS-CoV-2 coinfection. The antibiotic therapy was switched to intravenous moxifloxacin (MFX) (400 mg daily), and 2 days later, the fever resolved (Figure 3). The patient did not require specific treatment for SARS-CoV-2 infection. Repeat chest CT 1 week after starting MFX showed a reduction in the size of the lung lesions (Figure 1). As she was clinically stable, she was discharged with a prescription for oral MFX (400 mg daily). At a follow-up visit 1 week after discharge, she had almost fully recovered clinically. Follow-up chest CT showed a marked reduction in the size of the lung lesions (Figure 1), and SARS-CoV-2 nucleic acid testing of an NPS was negative.",
"gender": "Female"
}
] |
PMC10962458
|
[
{
"age": 69,
"case_id": "PMC11220517_01",
"case_text": "A 69-year-old woman, who was scheduled to undergo laparoscopic surgery for appendicitis, was found to have interstitial pneumonia (IP) shadows on a chest CT scan. She was referred to the respiratory department in July 2015. The chest CT examination revealed clustered cystic structures predominantly in the bilateral lower lobes and peripheral regions, along with thickening of the interlobular septa and features of traction bronchiectasis, resulting in a ground-glass-like shadow. In September 2015, a bronchoscopy was performed. Bronchoalveolar lavage fluid showed a predominance of lymphocytes, and in transbronchial lung biopsies performed in the upper, middle, and lower lobes of the right lung, a predominance of lymphocytes was observed, along with evidence of obstructive, somewhat older fibrosis with lymphocytic infiltration in the alveolar spaces, as well as active organizing fibrosis. These findings led to the diagnosis of Chronic Active Fibrosing Alveolitis. No findings suggesting collagen vascular diseases were observed in the blood tests (Table .1).\nBased on the above results and considering the results of examinations by dermatologists and rheumatologists, we clinically diagnosed IIP (cannot rule out FOP but NSIP).\nFrom September 2015, treatment was initiated with prednisolone at 30mg, which was subsequently tapered. However, the disease progression could not be controlled, and from March 2016, intravenous cyclophosphamide (IVCY) was administered in a total of 10 doses. (Table .2, Fig. 1).\nGradual progression of IP lesions on imaging, a decline in lung function, worsening respiratory condition, severe coughing, and increased breathlessness were observed. In July 2020, long-term oxygen therapy (LTOT) was introduced (a flow rate of 2 L per minute throughout the day and 3 L per minute during bathing). Furthermore, based on the progressive fibrosis observed on imaging (Fig. 1) and the ongoing decline in lung function over time (Table .2), a diagnosis of progressive pulmonary fibrosis (PPF) in interstitial lung disease (ILD) was made. In November 2020, Nintedanib therapy was initiated. However, despite efforts, the disease progression could not be controlled. The symptoms of breathlessness were so severe that even conducting a respiratory function test was not possible.\nIn an attempt to identify the cause of worsening symptoms, a right heart catheterization (RHC) was conducted in November 2021. The results showed mild pulmonary hypertension (mPAP23 mmHg), along with an exercise-induced elevation of PAP reaching mPAP35 mmHg during light handgrip exercises. Despite the patient's pulmonary hypertension being very mild, there was concern that even a slight increase in PAP could contribute to a significant decline in activities of daily living (ADL), equivalent to WHO functional class IV. Therefore, oral macitentan was initiated at a dose of 10 mg per day, with the hope of achieving some improvement in respiratory symptoms. The intention is to discontinue macitentan treatment at any time if its effectiveness is limited.\nJust four weeks after starting Macitentan therapy, the cough symptoms vanished. Imaging revealed improvement in the ground-glass-like shadow and infiltration in the alveoli, as well as thickening of the alveolar septa. There was an enhancement in activities of daily living (ADL), a reduction in KL-6 levels, and by May 2023, lung function demonstrated improvement. The required oxygen flow rate decreased, and at rest, breathing transitioned to room air without the need for oxygen inhalation. (Table .2)(Figs. 1 and 2, Fig. 3).",
"gender": "Female"
}
] |
PMC11220517
|
[
{
"age": 45,
"case_id": "PMC10734362_01",
"case_text": "A 45-year-old male with newly detected HIV and Hepatitis C, presented to us after being referred with a diagnosis of pneumonia with severe sepsis concomitant acute kidney injury. Upon arrival, the patient presented with tachycardia, with a heart rate of 110 beats per minute, and was hypoxic, as indicated by a blood oxygen saturation level (SpO2) of 88% while breathing room air. Other vitals were stable with a Glasgow Coma Scale score of 15/15 (Eye-opening E4. Verbal V5, and Motor M6). The patient was oxygenated with a nasal cannula at 2 liters per minute. SpO2 rose to 96%, and subsequently, the patient reported a notable increase in overall comfort and well-being. All the relevant investigations were sent. The patient's treatment regimen during admission included the following intravenous medications: (i) Piperacillin and Tazobactam (2.25 gm IV TDS), (ii) Acetaminophen, (iii) pantoprazole, (iv) fentanyl (25 microg single dose), and (v) Ringer lactate. The patient had no known comorbid conditions such as hypertension, coronary artery disease, or psychiatric illnesses. However, the patient did consume alcohol, cigarettes, and marijuana occasionally. There was no history of intravenous drug abuse or blood transfusion. Antivirals were not started because confirmatory tests were due. Arterial blood gas (ABG) analysis, chest X-ray, blood investigations, culture, and procalcitonin were normal. Toxicology screening results were negative. The patient's serum electrolyte levels were also normal, with potassium 4 mmol/L, magnesium 1.9 mg/dL, and calcium 9 mg/dL. Liver enzymes showed ALT 50 U/L, AST 35 U/L, ALP 134 U/L, total serum albumin 3.6 g/dl and total bilirubin 0.8 mg/dl. HIV viral load was 52,000 copies/ml, and CD4 level was 350 cells/mm3. The baseline electrocardiogram (ECG) (Image 1) obtained from the referring hospital was normal (HR: 78 bpm, QTc interval: 413 ms). No structural abnormalities were noted on echocardiography.\nThe patient was clinically and hemodynamically stable on the first and second day of ICU admission with normal lab values. On the third day of admission, he suddenly presented with abnormal behaviour, which involved pulling his intravenous cannula out and shouting violently. He had normal vitals and normal ABG. The serum electrolytes measured potassium at 4.8 mmol/L, magnesium at 1.8 mg/dl, and calcium at 8.5 mg/dl. Then, after injection, Haloperidol 2.5 mg was given intravenously. The patient stopped exhibiting abnormal behaviour and became calm. Ten minutes later, he suddenly developed TdP (QTc 650: ms), as shown in (Image 2).\nCardiopulmonary resuscitation (CPR) was started as per Advanced Cardiovascular Life Support (ACLS) guidelines. Unsynchronized shock was given three times at 200 Joules, and adrenaline 1 mg was given two times. The patient was intubated and kept on the ventilator after the return of spontaneous circulation. ECG obtained after CPR is shown in (Image 3) (HR: 83 bpm, QTc: 438 ms).\nMagnesium 2 gm was given slowly via IV push. The reversible causes for the cardiac arrest, including hypovolemia, hypoxia, hypothermia, hypo/hyperkalemia, cardiac tamponade, exposure to toxins, tension pneumothorax, and thrombosis, were diligently assessed and managed. ABG was done, which showed elevated lactate levels, and metabolic acidosis, and the patient was treated accordingly. Magnesium infusion was started at 2 gm/h. Nor adrenaline was started via continuous intravenous infusion for hypotension. Central venous catheterization and an arterial line were kept. Serial electrolyte monitoring was done with ABG. The cardiology department was informed regarding the case. Eight hours later, the patient went into asystole again, and the patient could not be revived despite resuscitation. The postmortem evaluation was not performed due to lack of consent. A timeline showing major clinical events in different time frames is shown in Figure 1.",
"gender": "Male"
}
] |
PMC10734362
|
[
{
"age": 9,
"case_id": "PMC11322092_01",
"case_text": "A 9-year-old, castrated male, domestic short-haired cat weighing 5.94 kg presented with hyporexia for a week. Ascites was detected during the initial examination. The cat had a history of a diet change five days prior to presentation, which was accompanied by symptoms including soft stools and vomiting. Approximately 500 mL of peritoneal fluid was removed via abdominocentesis on the day of presentation, after which there was no further vomiting and an improvement in the fecal consistency was noted. However, a decline in vitality and appetite occurred three days later, prompting second abdominocentesis to remove 420 mL of peritoneal fluid.\nBlood analysis, radiography, ultrasonography, fluid analysis, and ascitic fluid bacterial culture were performed at a referring hospital. Blood analysis revealed no remarkable findings except for an elevated serum albumin-to-globulin ratio (0.8). The serum feline pancreatic lipase level was mildly elevated (5.7 ng/mL; reference interval [RI] = < 3.5 ng/mL). Abdominal ultrasonography revealed edematous changes in the omentum and multiple hypoechoic nodules, each measuring <1 cm, in the peritoneum. Because both aerobic and anaerobic bacterial cultures of peritoneal fluid yielded negative results, the likelihood of the ascites being attributed to infection was excluded. Additionally, the serum concentration of N-terminal pro-brain natriuretic peptide was within the normal range, excluding heart disease as a potential cause of ascites. Despite thorough examination, the cause of the clinical signs and recurrent ascites was not found.\nThe first computed tomography (CT) scan was performed at the referring hospital to determine the cause of ascites. A mass demonstrating connectivity with the left leg of the pancreas was identified (Figure 1). The pattern was observed to be ill-defined and amorphous with irregular margins. It was approximately 1.18 x 1.16 x 1.12 cm (width x height x length) in size, and the ventral margin of the lesion was vague. No significant internal contrast enhancement was noted in any phase after imaging, and the lesion appeared homogenously hypodense compared with the normal pancreatic parenchyma. Lymph nodes, including the splenic, hepatic, pancreaticoduodenal, and jejunal lymph nodes, receiving lymphatic drainage from the mass lesion and pancreas, were mildly enlarged. Severe fat-stranding was observed around the mass, involving the surrounding peritoneum with nodules in a diffusely aggregated pattern, presumably due to fat necrosis (Figure 2). Additionally, a substantial amount of free fluid was noted in the abdominal cavity, but not in the pleural cavity, where the retro-abdominal cavity appeared intact with normal fat density. The abdominal wall exhibited irregularities with mixed nodular patterns, and peritoneal and mesenteric thickening was observed.\nThe cat was referred 4 days after CT. Physical examination revealed mild dehydration (5-6%). In complete blood cell counts (ProCyte Dx, IDEXX Laboratories, Westbrook, ME, USA), low lymphocyte (0.74 x 103/muL, RI = 0.92-6.88 x 103/muL) and high reticulocyte (82.4 x 103/muL, RI = 3.0-50.0 x 103/muL) counts were detected. The serum biochemistry profile (Hitachi XYZ, Hitachi Ltd., Tokyo, Japan) showed elevated serum creatinine (2.0 x 10 mg/dL, RI = 0.7-1.8 x 10 mg/dL), glucose (240 mg/dL, RI = 75-199 mg/dL), and lactate (5.28 mmol/L, RI = 0.50-2.50 mmol/L). In addition, serum symmetric dimethylarginine (15 microg/dL, RI = 0-14 microg/dL; IDEXX Laboratories, Westbrook, ME, USA) and amyloid A concentration (52.86 mg/L, RI = 0-10 mg/L; Bionote, Gyeoggi-do, South Korea) were increased. In the serum electrolyte profile (Roche Cobas c 9,180, Roche Diagnostics, Basel, Switzerland), a low sodium concentration (143 mmol/L, RI = 145-158 mmol/L) and a normal total calcium concentration (9.0 mg/dL, RI = 8.2-10.8 mg/dL) were detected. Abdominal ultrasonography revealed a large amount of ascites between the liver lobes, around the kidneys, and in the anterior bladder. The mesentery and fat tissue were hyperechoic and edematous (Supplementary Figure S1). The left leg of the pancreas was not clearly visualized; ascites was observed around the left end and the pancreatico-duodenal lymph nodes were enlarged. Approximately 320 mL of peritoneal fluid was drained via ultrasound-guided abdominocentesis. The peritoneal fluid appeared reddish and cloudy upon macroscopic examination (Supplementary Figure S2A). Cytological examination of the peritoneal fluid revealed modified transudate, predominantly composed of neutrophils and macrophages, with visible lymphoid cells (total nucleated cell count, 2,680 cells/muL; total protein: 3.4 mg/dL) (Supplementary Figure S2B). The albumin-to-globulin ratio of the peritoneal fluid was 0.9, and the Rivalta test result was negative, suggesting that feline infectious peritonitis was unlikely. Abdominal fat fine-needle aspiration (FNA) was performed under ultrasonographic guidance. Adipocytes and fat-phagocytizing macrophages were identified, and inflammation and macrophage infiltration were observed in the fat tissue. The specific feline pancreatic lipase value (IDEXX Laboratories, Westbrook, ME, USA) in the serum was within the normal range (<1.00 ng/mL, RI = < 3.5 ng/mL), but in the peritoneal fluid, it was elevated beyond the normal range observed in blood (3.78 ng/mL, RI in blood = < 3.5 ng/mL). Peritoneal fluid FPL values were obtained using the same methodology as that used for serum analysis. The pancreatic lipase level ratio of abdominal fluid level to serum level was >3.78. Considering the local FNA results and elevated serum amyloid A concentration, it was suggested that the observed intra-abdominal inflammation was associated with pansteatitis. Prompt prednisolone 0.5 mg/kg q24h (Solondo , Yuhan, Seoul, South Korea) and vitamin E 15 U/kg q24h (Grandpherol , Yuhan, Seoul, South Korea) were administered for anti-inflammatory and antioxidant purposes, as the possibility of secondary feline pansteatitis due to vitamin E deficiency could not be ruled out.\nDespite the anti-inflammatory treatment, there was no improvement in the clinical signs and ascites. An additional CT scan was performed on the 11th day after referral. No obvious differences were observed between it and the original CT scan. A mass showing connectivity with the left leg of the pancreas appeared on the pre-contrast images to be indistinctly delineated, as on previous imaging. However, the internal aspect of the mass after contrast administration was homogeneously hypoattenuated compared with the pancreatic parenchyma, and moderate peripheral rim enhancement was observed in the surrounding area. Severe fat stranding in the peritoneum and massive ascites were still evident. Additionally, a filling-defect-like lesion of approximately 3.48 x 2.92 x 3.52 mm (length x width x height) was observed in the blood vessel where the splenic vein flowed into the portal vein, noted in the cranio-lateral region of the mass. Possible compression of the splenic vein by the mass was considered (Supplementary Figure S3).\nBased on the findings of the second CT, a pancreatic tumor or chronic peritonitis secondary to pancreatic lipase leakage was considered the cause of recurrent ascites. Exploratory laparotomy was performed to determine the cause of the ascites, and the resected mass was presumed to be a pancreatic tumor. The falciform ligament was sclerosing and thickened (Supplementary Figure S4). In addition, fibrinous adhesion of the thickened abdominal wall with adjacent organs (Supplementary Figure S4B) and a substantial amount of ascites were observed. Nodular mass lesions and adhesions were identified in the abdominal organs, including the spleen, pancreas, intestine, and peritoneum. Due to these chronic inflammatory lesions, it was impossible to distinguish between the inflammation and the tumor on macroscopic examination. Furthermore, difficulty accessing the mass prevented its accurate sampling and removal. Nodular masses in the pancreas and surrounding inflammatory fat tissue were found to be severely diffuse, with chronic interstitial pancreatitis and peripancreatic steatitis with fibrosis. The second aerobic and anaerobic bacterial cultures from the peritoneal fluid were negative. Based on these results, the cat was diagnosed with SEP.\nAfter surgery, peripheral parenteral nutrition was initiated because of persistent anorexia in the cat. Ampibactam 22 mg/kg q12h (Sulbacin , Donggwang, Seoul, South Korea) IV was administered to prevent secondary infection, and a Fentanyl patch 12.5 microg/kg (Durogesic D-trans Patch , Janssen Korea, Seoul, South Korea) was used for pain management. Based on the dose of tamoxifen administered to dogs with SEP, tamoxifen 1 mg/kg q24h (Nolvadex , AstraZeneca Korea, Seoul, South Korea) PO was added to ameliorate peritoneal fibrosis. However, on the third day of tamoxifen administration, the patient exhibited worsening hypoalbuminemia and an elevated serum amyloid A concentration. The cat developed dyspnea due to pleural effusion and subsequently died.\nNecropsy findings showed that a multi-lobulated pancreatic tumor measuring 10 cm x 10 cm was tightly attached to the internal organs, including the stomach and intestines. The small and large intestines, along with the mesentery, exhibited adhesion and sclerosis, with disseminated multifocal seeding nodules of various sizes on the serosal surface (Supplementary Figure S5A). The abdominal wall was severely thickened and covered with strands of fibrinous materials and numerous disseminated nodules of various sizes (ranging from 1-5 mm in diameter). Transverse sections showed tight fibrosis and steatosis between the intestines, which compressed the intestinal lumen (Supplementary Figure S5B).\nHistopathologically, the pancreatic mass was composed of extensive adipose tissue, locally extensive infiltrates of phagocytizing macrophages, fibrous connective tissue, and small invasive proliferative glands (Figure 3A). The mass showed a typical histomorphology of pancreatic ductal adenocarcinoma with well-defined, small, irregular glands composed of single-layer ductal epithelial-like cells surrounded by abundant desmoplastic stroma (Figures 3B,C). Neoplastic cells were round to oval in shape with less eosinophilic cytoplasm and no zymogen granules, and the nuclei showed chromatin clusters and prominent nucleoli. Moderate anisocytosis and anisokaryosis were present with low mitotic figures. There was no evidence of cystic formation, accumulation of mucin, and lymphatic invasion. Immunohistochemistry (IHC) was performed to further confirm the origin of the tumor cells using anti-pancytokeratin antibodies. Normal pancreatic ducts were positive for pancytokeratin, and the neoplastic glands were consistently positive for pancytokeratin (Figure 3D), further suggesting the tumor to be of the pancreatic ductal origin. In addition, lymphocytic inflammatory cells infiltration, increased collagen, fibrin, and neovascularization, and denuded mesothelium were observed in visceral peritoneum, indicating the presence of SEP (Figures 3E-G). Extensive implantation of neoplastic nodules with desmoplasia was observed in the liver, stomach, peritoneum, mesentery, mesenteric lymph nodes, and urinary bladder (Figures 4A,B). Tumor emboli were also observed in the pulmonary blood vessels (Figure 4C). Based on these results, the cat was diagnosed with SEP secondary to presumed PDAC with extensive metastasis to other organs.",
"gender": "Male"
}
] |
PMC11322092
|
[
{
"age": 28,
"case_id": "PMC10864160_01",
"case_text": "A 28-year-old female presented to a hospital with a history of abdominal pain and amenorrhea for 7 weeks, prompting a suspicion of ectopic pregnancy. She underwent a dilation and curettage procedure, accompanied by methotrexate treatment, and subsequently followed by laparoscopic bilateral salpingectomy. Despite these interventions, no ectopic gestational sac was identified through any of the tests or surgeries performed. Her beta-human chorionic gonadotropin (b-hCG) levels continued to increase, and she was referred to our hospital for further treatment. Her vital signs remained stable; however, laboratory investigations revealed a hemoglobin level of 9.7 g/dL, indicating mild anemia. The urine pregnancy test yielded positive results, with a b-hCG level elevated at 33996 mIU/mL.\nAbdominopelvic CT was performed to accurately locate the ectopic pregnancy, revealing a 3.3 cm cystic mass in the precaval area beneath the third segment of the duodenum, characterized by thick and intense peripheral enhancement (Fig. 1A, B). The mass was identified an ectopic gestational sac, and no other focal lesion suspected of being a gestational sac was observed in the pelvic cavity (including the uterus and adnexa). A small amount of ascites with fat infiltration in the pelvic cavity, indicative of normal postoperative changes, was noted. Based on these findings, we established a diagnosis of retroperitoneal ectopic pregnancy.\nThe patient underwent laparoscopic removal of the ectopic gestational sac. Upon accessing the abdominopelvic cavity, the site at which bilateral salpingectomy was performed became apparent, and a gestational sac was evident in the precaval area covered by the peritoneum (Fig. 1C). Subsequent pathological examination confirmed that the cystic mass consisted of chorionic villi (Fig. 1D). After the surgery, the patient's b-hCG level gradually decreased, and she was discharged without post-surgical complications. Her symptoms improved within a month, and her b-hCG level dropped to 6.7 mIU/mL.\nThe Institutional Review Board of Hanyang University Hospital approved this case report and the requirement for informed consent was waived due to its retrospective nature (IRB No. HYUH 2023-06-004).",
"gender": "Female"
}
] |
PMC10864160
|
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