PLATELET CONSUMPTION AND SEQUESTRATION IN SEVERE ACUTE RESPIRATORY-FAILURE

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Abstract
To evaluate alterations in platelet kinetics and organ sequestration patterns during acute lung injury, the fate of autologous radiolabeled platelets was studied in 15 patients with severe acute respiratory failure (ARF) of diverse etiology. Thrombocytopenia (< 100,000 platelets/.mu.l) occurred in 10 patients. Platelet lifespan was reduced (2.30 .+-. 0.39 days; mean .+-. standard error of the mean) compared to normal volunteers (6.29 .+-. 0.69; P < 0.01). Platelet turnover rate during ARF (251,000 .+-. 90,000 platelets/.mu.l .times. day) was twice normal and never below the normal range. Platelet sequestration, determined by surface scintillation counting, occurred in the lungs, liver and spleen. Measurements in patients with severe ARF did not determine whether platelets cause or exacerbate acute lung disease. The increased platelet consumption and pulmonary sequestration suggest that platelets are directly involved in the pathophysiology of acute lung injury.