An interesting case of pulmonary hypertension in nephrotic syndrome due to amphetamine use for attention-deficit hyperactivity disorder.

Pulmonary arterial hypertension (PAH) was first associated with stimulants use in the 1960s during an outbreak of amphetamine-like appetite suppressants (anorexigens). To date, various drugs and toxins have been correlated with PAH. Diagnosing PAH in nephrotic syndrome has always remained a challenge due to the overlap of signs and symptoms in clinical presentation between the two entities. Case presentation: In this report, the authors present an interesting case of a 43-year-old male, diagnosed with nephrotic syndrome secondary to minimal change disease, as well as currently presenting with PAH secondary to amphetamine. Clinical discussion and conclusion: Patients with nephrotic syndrome and end-stage renal disease should be regularly followed up and evaluated for comorbidities, complications, as well as adverse events from pharmacological intervention. In patients with end-stage renal disease hypertension control is key, stimulant use can precipitate poor blood pressure control especially in pulmonary arteries resulting in PAH. PAH can result in right ventricular dysfunction and heart failure that can further exacerbate renal dysfunction and vice-versa in a vicious cycle, deteriorating patient condition and quality of life.

Testicular Seminoma Presenting with Bilateral Blindness: Looking Beyond the Eye.

Cancer-associated retinopathy (CAR) is a rare cause of vision loss that was first reported in 1976. It is reported that the retinopathy associated with cancer occurs due to antibodies against the tumor antigens that cross-react with retinal cell layers. We present the case of a young male who came to the emergency department with sudden onset of bilateral vision loss. He had a large-sized testicular seminoma with metastatic retroperitoneal lymphadenopathy. Several primary ophthalmological and systemic conditions were considered. He had multiple, positive anti-retinal antibodies. The cancer was felt to be the cause of the vision loss based on the clinical presentation and the presence of anti-retinal antibodies. He was treated with intravenous steroids, plasmapheresis, and curative chemotherapy, but there was no improvement in vision. Unfortunately, he died due to multiorgan failure. Our case is the second on seminoma-associated retinopathy in the literature.

Hepatic hydrothorax: clinical review and update on consensus guidelines.

Hepatic Hydrothorax (HH) is defined as a pleural effusion greater than 500 ml in association with cirrhosis and portal hypertension. It is an uncommon complication of cirrhosis, most frequently seen in association with decompensated liver disease. The development of HH remains incompletely understood and involves a complex pathophysiological process with the most acceptable explanation being the passage of the ascetic fluid through small diaphragmatic defects. Given the limited capacity of the pleural space, even the modest pleural effusion can result in significant respiratory symptoms. The diagnosis of HH should be suspected in any patient with established cirrhosis and portal hypertension presenting with unilateral pleural effusion especially on the right side. Diagnostic thoracentesis should be performed in all patients with suspected HH to confirm the diagnosis and rule out infection and alternative diagnoses. Spontaneous bacterial empyema and spontaneous bacterial pleuritis can complicate HH and increase morbidity and mortality. HH can be difficult to treat and in our review below we will list the therapeutic modalities awaiting the evaluation for the only definitive therapy, which is liver transplantation.

Congenital pulmonary airway malformation (CPAM) with initial presentation in an adult: a rare presentation of a rare disease.

Congenital pulmonary airway malformation (CPAM) is a rare congenital abnormality with unknown exact aetiology or clear genetic association. It is characterised by a failure of bronchial development and localised glandular overgrowth. Typically, it is diagnosed on prenatal ultrasound, only infrequently in children, and even less commonly in adults. We present a case of a 25-year-old man, with no previous lung diseases who presented with right-sided chest pain, fever and cough suggestive of pulmonary infection. Chest imaging, including CT scan, showed a large focal cystic mass within the right lower lobe along with ground glass opacities suggestive of CPAM. He was started on intravenous antibiotics. Bronchoscopy showed a large amount of pus in the right lung and bronchoalveolar lavage confirmed the microbiological diagnosis of methicillin-resistant Staphylococcus aureus. He improved with antibiotic treatment. He was discharged with 6-week course of antibiotics and follow-up afterward.

Cocaine induced pleural and pericardial effusion syndrome.

A 42-year-old African American female with chronic cocaine use for 20 years, presented with two-day history of exertional shortness of breath and pleuritic chest pain. She was admitted three years back with acute kidney injury and skin rashes. At that time, skin biopsy was consistent with leukocytoclastic vasculitis and renal biopsy revealed proliferative glomerulonephritis. She responded to oral prednisone and mycophenolate with complete recovery of her kidney functions. Skin rash was waxing and waning over the last two years. On the second admission, patient was found to have large pleural effusion on computerized tomography scan and pericardial effusion on echocardiogram as shown in the figures. Pleural fluid analysis was exudative. Her serology was negative for ANA (antineutrophilic antibody) and anti-dsDNA (double stranded DNA). Complements levels were normal. She had positive low titers of ANCA levels. The patient was started on a course of prednisone for 6 months. Her pleural and pericardial effusion resolved completely on follow-up imaging with computerized tomography scan and echocardiogram. This case is unique since the pericardial and pleural effusions developed without any other etiology in the setting of cocaine; hence, we describe this clinical syndrome as cocaine induced pleural and pericardial effusions syndrome (CIPP).

Working memory capacity is decreased in sleep-deprived internal medicine residents.

BACKGROUND: Concerns about medical errors due to sleep deprivation during residency training led the Accreditation Council for Graduate Medical Education to mandate reductions in work schedules. Although call rotations with extended shifts continue, effects on resident sleep-wake times and working memory capacity (WMC) have not been investigated. OBJECTIVES: The objective of this study was to measure effects of call rotations on sleep-wake times and WMC in internal medicine residents. METHODS: During 2 months of an internal medicine training program adhering to ACGME work-hour restrictions (between April 2006 and June 2007), residents completed daily WMC tests, wore actigraphy watches, and logged their sleep hours. This observational study was conducted during a call month requiring 30-hour call rotations every fourth night, whereas the noncall month, which allowed sleep/wake cycle freedom, was used as the control. MAIN OUTCOME MEASURES: Sleep hours per night and WMC testing. RESULTS: Thirty-nine residents completing the study had less sleep per night during their call month (6.4 vs 7.3 h per night noncall, p < 0.001) and sleep per night varied from 3.7 to 10.1 hours. Call rotation caused greater self-assessed sleepiness and reduced WMC recall scores (-2.6/test, p < 0.05), and more math errors occurred when on call (+1.07/test, p < 0.04). Full recovery of WMC did not occur until the fourth day after call. On-call rotation on the first month had a confounding detrimental effect on WMC. CONCLUSION: A month of call rotations reduced overall sleep per night; sleep hours per night were variable, and WMC was adversely affected. Decreased WMC could explain impaired judgment during sleep deprivation, although clinical error rates were not evaluated.