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A 69-year-old Caucasian male with a past medical history remarkable for hypertension and testicular nonHodgkin's lymphoma (NHL) presented to the emergency department with a 1-week history of fatigue and new onset lower extremity edema. For the past 8 months, the patient was having a nonproductive cough. Work up by his primary care physician was negative, and the patient was switched from enalapril to losartan 1 week before presentation. The cough resolved, however, 2 days later the patient began to experience fatigue and lightheadedness that persisted despite decreasing the dose of losartan. He continued to develop lower extremity edema and was again seen by his primary care physician who noted the patient to be hypotensive. He was referred to the emergency department for evaluation.In a 69-year-old male presenting with fatigue, lower extremity edema, and hypotension, our first concern was for a cardiac process such as heart failure. The differential for his hypotension also included sepsis, adrenal insufficiency, hemorrhage, or possibly an adverse drug reaction. We suspected that his cough was secondary to the enalapril as his symptoms had resolved with discontinuation of this medication; however, we remained concerned that an underlying pulmonary process could also be present.The patient denied chest pain, orthopnea, paroxysmal nocturnal dyspnea, fever, weight loss, or night sweats. His testicular NHL was treated 16 years prior with orchiectomy and four cycles of CHOP without evidence of recurrence. In addition to losartan, the patient also took a daily aspirin. He was a retired carpenter who had a 19-pack year smoking history and had quit 37 years before presentation. He occasionally drank alcohol. He denied illicit drug use. On examination, he was not in distress. His weight was 80.2 kg. His temperature was 36.48C, pulse 130 and regular, respiratory rate 18, blood pressure 78/46, and oxygen saturation was 97% while breathing ambient air. Physical examination was remarkable for a normal jugular venous pressure, tachycardia without extra heart sounds and generalized anasarca including 2+ pitting edema of his lower extremities. There was no lymphadenopathy, palpable masses, or cutaneous lesions. His neurologic examination was normal.The patient's review of systems was negative for symptoms of an acute coronary syndrome or heart failure, as well as for B-symptoms or a rapidly progesssive infectious process. On physical examination, his vital signs suggested intravascular volume depletion with tachycardia and hypotension; however, he appeared to have a component of fluid overload or third spacing of fluids with the marked degree of anasarca. His normal jugular venous pressure suggested normal right heart pressure making a cardiac cause of his anasarca less likely.The patient's white cell count was 12,300/mm 3 , with 93% neutrophils, 1% bands, and 6% monocytes. The hemoglobin level was 11.3 g/dl, with a mean corpuscular volume of 78.8 mm 3 . The platelet count was 554,000/ mm 3 . The serum sodium level was 126 mmo...

Recurrent transfusion-related acute lung injury after fresh frozen plasma in a patient with hereditary factor V deficiencyTo the Editor: Transfusion-related acute lung injury (TRALI) can be a serious complication resulting from the transfusion of plasma that contains antibodies against recipient white blood cells. There have been only four previously reported cases of recurrent TRALI [1][2][3]. We describe a patient with recurrent TRALI, emphasizing potential strategies to prevent this disease. A 25-year-old man with hereditary factor V deficiency and a baseline FV level of <2% received five units of fresh frozen plasma after a spontaneous axillary hematoma and developed TRALI. The patient recovered fully and was discharged 48 hr later. Five months later, he received two units of plasma after a trauma-induced right foot hematoma and suffered a recurrent episode of TRALI. Donors associated with the initial and recurrent TRALI episodes were tested for anti-HLA class I, anti-HLA class II, and antigranulocyte antibodies. Sera from three female donors from the first transfusion episode and one female donor from the second transfusion episode showed antibodies against HLA class I, class II, or both (Table I). None showed antigranulocyte antibodies. The patient could not be HLA-typed because of relocation. Both TRALI episodes of our patient met American-European Consensus Conference criteria, including a new episode of acute lung injury occurring within 6 hr of transfusion, bilateral pulmonary infiltrates on chest X-ray, and no evidence of an alternative risk factor for acute lung injury nor of circulatory overload [4]. Our patient was in good health, did not have any of the known associated antecedent ''first events'' such as major surgery, active infection, or massive transfusion, and the presence of anti-HLA antibodies in the transfused plasma appeared adequate, in itself, to cause the clinical entity. Our case study emphasizes the observation that the risk of recurrent TRALI may persist for longer periods (months, years) than previously thought, and raises the question of whether certain previously unrecognized populations (such as patients with FV deficiency) are vulnerable to TRALI. Our patient received 309 plasma units over a 13-year period, and the only registered transfusion reactions are the recurrent TRALI episodes reported herein. This amounts to an observed prevalence of $1 TRALI episode per 150 units, which is higher than the estimated risk for the general population (1:1,120 to 1:5,000). Strategies to reduce TRALI, such as the British experience using male gender plasma, suggest a positive impact of this strategy in decreasing the incidence of TRALI [5]. On the other hand, it must be recognized that some recent observations do not support the disqualification of multiparous female donors, and such a policy may prove problematic for blood centers in which this population constitutes up to 30% of the donor pool [6]. On account of this, our approach in this patient, and in Rhode Island, is be to screen dono...

Acute pancreatitis (AP) remains the most common reason for hospital admission of all the gastrointestinal illnesses in the United States. Since the last narrative review in the Journal of Hospital Medicine in 2010, new developments in regard to diagnosis and classification, fluid resuscitation, antibiotic use, nutritional support, and management of complications have helped refine the approach and improve outcomes in this disease. Whereas there is still no proven pharmacologic therapy to specifically combat the inflammatory consequences of AP, recent interventions have led to increased survival, shorter length of stay, and more appropriate transfer criteria for pancreatitis patients. This case‐oriented review will highlight these developments and emphasize the primary role of the hospitalist in managing AP over the course of the admission. It will focus on when to coordinate with subspecialists, how to deliver effective yet efficient hospitalized care, and how to optimize appropriate discharge planning. Journal of Hospital Medicine 2016;11:724–729. © 2016 Society of Hospital Medicine