Abstract

Dear Editor, A 41-year-old overweight (body mass index 35 kg/m) woman was admitted from home to the intensive care unit (ICU) for acute respiratory distress with fever. Her medical history mainly included a neurosarcoidosis treated with corticosteroids, methotrexate and six courses of cyclophosphamide. The computed tomography scan revealed a diffuse alveolar–interstitial syndrome without any mediastinal adenopathy. She received an initial antibiotherapy (cephalosporine, rovamycin) after an examination for infectious diseases. No infectious process or cause for an acute exacerbation of pulmonary sarcoidosis was found in the bronchoalveolar lavage fluid, and antibiotherapy was stopped after 5 days. There was no acute cardiac dysfunction on echocardiography. No diagnosis was made and her respiratory state worsened. She required, after 6 days of evolution, invasive mechanical ventilation to treat an acute respiratory distress syndrome (ARDS). After 3 days of lung protective ventilation [normal tidal volume (Vt) 5 ml/kg, respiratory rate (RR) 30/min, positive end expiratory pressure (PEEP) 12 cmH2O, plateau pressure (PP) 30 cmH2O, static compliance (SC) 20 ml/cmH2O) with neuromuscular blockade, she remained with a severe ARDS [partial pressure of oxygen in the blood (PaO2)/fraction of inspired oxygen (FiO2) 85 mmHg]. Two 24-h sessions of prone positioning failed to improve the PaO2/FiO2. No evolutive infectious process was found, and corticosteroids were maintained at 1 mg/kg/day to treat the ARDS inflammatory process. Her respiratory function worsened (Vt 5 ml/kg, RR 35/min, PEEP 10 cmH2O, PP 30 cmH2O, SC 20 ml/cmH2O) with refractory hypoxia on arterial gasometry [FiO2 100 %, pH 7.45; partial pressure oxygen (PO2) 75 mmHg; PCO2 40 mmHg; HCO3 -

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