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Chest, Vol 97, 923-926, Copyright © 1990 by American College of Chest Physicians
ARTICLES |
PQ Eichacker, JH Shelhamer, M Brenner and JE Parrillo
Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Md. 20892.
Pulmonary platelet sequestration has been implicated in the pathophysiology of ARDS. Since HPTs are frequently given therapeutically to patients with ARDS, a serious concern clinically has been the possibility that platelet transfusions might worsen pulmonary function in such patients. To prospectively evaluate this issue, we assessed the effects of HPT on two parameters of pulmonary function: (1) Qs/Qt; and (2) PVR. Measurements were made immediately before and at 1 hour and 4 hours after HPT in 16 patients during 18 separate episodes of ARDS and in 11 control patients. The ARDS had been present for at least 48 hours in all patients at the time of study. Prior to HPT, patients with ARDS had significantly worse pulmonary function compared to control subjects. Although a small number of patients with ARDS had large changes in PVR and Qs/Qt after HPT, no group showed significant changes in any pulmonary parameter following transfusion. Neither individual changes in the platelet count after HPT nor the duration of ARDS before HPT was associated with changes in pulmonary function after platelet administration. We concluded that therapeutically required HPT did not significantly worsen pulmonary function at up to four hours after transfusion in this group of patients with well-defined and fully evolved (greater than 48-hour duration) ARDS. The reason for this absence of effect was not known, but the pathogenesis of ARDS might only be susceptible to alteration during the early developmental stage.
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