Pulmonary Kaposi Sarcoma as an Unusual Etiology of Acute Hypoxemic Respiratory Failure in the Era of Highly Active Antiretroviral Therapy: A Case Report.

Kaposi sarcoma (KS) is caused by human herpesvirus 8 (HHV-8). Epidemic KS is described in the human immunodeficiency virus (HIV) population with acquired immune deficiency syndrome (AIDS). It primarily affects the skin, but it may uncommonly disseminate to involve extracutaneous sites such as the gastrointestinal (GI) tract, liver, and lungs. In this case report, the authors report a 26-year-old homosexual male who was admitted with acute hypoxemic respiratory failure. He was diagnosed with an HIV infection about five months before index presentation, and he was commenced on highly active antiretroviral therapy (HAART). Physical examination was remarkable for diffuse cutaneous nodules over the lower extremities, back, and oropharynx. Chest imaging revealed diffuse bilateral infiltrates, mediastinal adenopathy, and a persistent bilateral pleural effusion. Extensive diagnostic workup was negative for underlying infectious etiology. Transbronchial biopsy demonstrated proliferated spindle cells that stained positive for HHV-8 in keeping with pulmonary KS. Skin biopsies also concurred with the diagnosis of cutaneous KS. Interestingly, the cluster of differentiation 4 (CD4) count was 647 cells/mm3, and HIV viral load (VL) was 500 copies/ml. This case demonstrated an atypical natural history of pulmonary KS in an HIV patient as pulmonary and disseminated mucocutaneous KS occurred with a relatively higher CD4 count (≥500 cells/mm3). It also reminds pulmonologists and infectious disease specialists to consider pulmonary KS as a differential diagnosis of acute hypoxemic respiratory failure in HIV patients, even in the absence of other clinical and laboratory criteria that define the AIDS stage.

Targeted temperature management after cardiac arrest: Updated meta-analysis of all-cause mortality and neurological outcomes.

BACKGROUND: Cardiac arrest carries high mortality and morbidity burden. Different studies showed conflicting data regarding outcomes of targeted temperature management (TTM) for cardiac arrest. The purpose of this meta-analysis is to systematically determine the effect of TTM on all-cause mortality and neurological outcomes after cardiac arrest. METHODS: We conducted a systematic search for randomized controlled trials in Pubmed, Cochrane & ScienceDirect. Primary outcomes were neurological outcome and all-cause mortality. RESULTS: Nine randomized controlled trials utilizing data for in-hospital and out-of-hospital cardiac arrest were selected for meta-analysis. Total number of patients included was 1592. Mortality was lower in targeted temperature management group (OR 0.637, 95% CI 0.436-0.93, p-value 0.019, I2 = 44.78%, n = 1592). Therapeutic hypothermia group also demonstrated reduction in poor neurological outcomes (OR 0.582, 95% CI 0.363-931, p-value 0.024, I2 = 56.79%, n = 1567). Subgroup analysis was conducted, after excluding in-hospital cardiac arrest patients, and demonstrated reduction in poor neurological outcome (OR 0.562, 95% CI 0.331-0.955, p-value 0.033, I2 = 61.78%, n = 1480) and mortality in out-of-hospital cardiac arrest patients (OR 0.674, 95% CI 0.454-999, p-value 0.049, I2 = 43.8%, n = 1505). CONCLUSION: Targeted temperature management after cardiac arrest may be associated with improvement in all-cause mortality and reduction in poor neurological outcome.