Platelet consumption and sequestration in severe acute respiratory failure.

To evaulate alterations in platelek kinetics and organ sequestration patterns during acute lung injury, we studied the fate of autologous radiolabeled platelets in 15 patients with severe acute respiratory failure (ARF) of diverse etiology. Thrombocytopenia (< 100,000 platelets/microliters) occurred in 10 patients. Platelet lifespan was reduced (2.30 +/- 0.39 days; mean +/- SEM) compared with normal volunteers (6.29 +/- 0.69; p < 0.01). Platelet turnover rate during ARF (251,100 +/- 90,000 platelets/microliters x day) was twice normal and never below the normal range. Platelet sequestration, determined by surface scintillation counting, occurred in the lungs, liver, and spleen. Although our measurements in patients with severe ARF did not determine whether platelets cause or exacerbate acute lung disease, the increased platelet consumption and pulmonary sequestration we detected suggests that platelets are directly involved in the pathophysiology of acute lung injury.