Objectives Patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) frequently present with a febrile illness that may progress to pneumonia and hypoxic respiratory failure. Aerosolized epoprostenol (aEPO) has been evaluated in patients with acute respiratory distress syndrome and refractory hypoxemia. A paucity of literature has assessed the impact of aEPO in patients with SARS-CoV-2 receiving oxygen support with high flow nasal cannula (HFNC). The objective of this study was to evaluate whether aEPO added to HFNC prevents intubation and/or prolong time to intubation compared to controls only treated with HFNC, guided by oxygen saturation goals. Methods This was a single-center, retrospective study of adult patients infected with coronavirus 2019 (COVID-19) and admitted to the medical intensive care unit. A total of 60 patients were included. Thirty patients were included in the treatment, and 30 in the control group, respectively. Among patients included in the treatment group, response to therapy was assessed. The need for mechanical ventilation and hospital mortality between responders vs. non-responders was evaluated. Results The primary outcome of mechanical ventilation was not statistically different between groups. Time from HFNC initiation to intubation was significantly prolonged in the treatment group compared to the control group (5.7 days vs. 2.3 days, P = 0.001). There was no statistically significant difference between groups in mortality or length of stay. Patients deemed responders to aEPO had a lower rate of mechanical ventilation (50% vs 88%, P = 0.025) and mortality (21% vs 63%, P = 0.024), compared with non-responders. Conclusion The utilization of aEPO in COVID-19 patients treated with HFNC is not associated with a reduction in the rate of mechanical ventilation. Nevertheless, the application of this strategy may prolong the time to invasive mechanical ventilation, without affecting other clinical outcomes.

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Acute respiratory distress syndrome is the result of an acute inflammatory response of the lungs, causing severe hypoxemia. A variety of therapeutic modalities have been extensively studied, with only a few demonstrating improvement in survival. Specifically, mechanical ventilation with use of low tidal volumes, prone positioning, and treatment with neuromuscular blocking agents have proven beneficial. This article focuses on the utilization of neuromuscular blocking agents in this entity. In particular, we briefly review the mechanism of action of neuromuscular blockades, the latest published evidence supporting their use in acute respiratory distress syndrome, and current recommendations for their utilization in clinical practice.

We describe a patient with history of dextro-transposition of the great vessels, ventricular septal defect, and pulmonary valve replacement who presented with fatigue, prolonged fever, and leg edema. He was found to have kidney injury, pancytopenia, and liver congestion. Echocardiogram revealed thickened leaflets with prolapsing vegetation on the pulmonary valve. Given the negative blood cultures, high Bartonella henselae immunogobulin G titer (1:1024) and positive immunoglobulin M titer (1:20), he was diagnosed with Bartonella endocarditis complicated with glomerulonephritis.KEYWORDS Bartonella henselae; culture-negative endocarditis; glomerulonephritis; prosthetic valve B artonella species are rare causes of infective endocarditis (IE).1,2 Patients with Bartonella endocarditis usually present with signs and symptoms of IE, but blood cultures are usually negative.2 Bartonella henselae usually affects patients with previous valvular disease, prosthetic or bioprosthetic valves, or congenital heart defects. 3,4 In rare instances, patients with Bartonella endocarditis may develop glomerulonephritis. 5,6 CASE DESCRIPTIONA 29-year-old man had complete transposition of the great arteries and ventricular septal defect, for which he received Rastelli repair at age 4 and right ventricle-to-pulmonary artery conduit replacement with a porcine valve at age 18 for conduit stenosis. He initially presented with fatigue, prolonged fever, and leg edema. His temperature was 101 F. A 5/6 harsh systolic murmur was heard over the left sternal border, his jugular veins were distended, his liver was enlarged, and his ankles were edematous. His erythrocyte sedimentation rate was 58 (normal range 0-15 mm/hr), C-reactive protein was 5.1 (normal range 0.0-0.3 mg/dL), creatinine was 3.3 mg/dL, red blood cells were 2.83 M/mL, white blood cells were 3.2 K/mL, and platelets were 105 K/mL. Echocardiogram showed a left ventricular ejection fraction of 35% to 40%. The pulmonic valve had thickened cusps and a prolapsing mass. He was treated with vancomycin, doxycycline, and piperacillin/tazobactam.The blood cultures, drawn at the time of presentation, showed no growth. The urine protein-creatinine ratio was 4.4 and his 24-hour urine protein was 6.4 g. C3 was 61.4 mg/dL (normal range 90-180 mg/dL), complement C4 was 9.4 mg/dL (normal range 10-40 mg/dL), and serum albumin was 2.3 g/ dL. Antineutrophil cytoplasmic antibody in the serum was positive. A kidney biopsy revealed focal segmental proliferative glomerulonephritis with incomplete crescent formation. Electron microscopy showed small mesangial electron-dense deposits and widespread foot process effacement. The mesangial regions were positive for the following immunofluorescence markers: immunoglobulin G (IgG), immunoglobulin M (IgM), C3, C1q, and kappa and lambda light chains. Though not specific, IgM immunofluorescence demonstrated the brightest signal, suggestive of a recent or ongoing infection (Figure 1).Brucella antibody, Coxiella burnetii IgG and IgM, and Ehrlichia IgG were negat...

We report a 67-year-old woman who presented with adrenal crisis as a manifestation of autoimmune polyglandular syndrome 2, a polygenic disorder characterized by concurrent primary adrenal insufficiency and either autoimmune thyroid disease or type 1 diabetes mellitus.