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Platelet function in acute respiratory failure
Author(s) -
Carvalho Angelina C.,
Quinn Deborah A.,
Demarinis Sandra M.,
Beitz Julie G.,
Zapol Warren M.
Publication year - 1987
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830250404
Subject(s) - medicine , acute respiratory failure , respiratory failure , platelet , respiratory system , intensive care medicine , cardiology , mechanical ventilation
To assess the role of platelets in thrombohemorrhagic complications of acute respiratory failure (ARF), we studied platelet function in 13 ARF patients admitted for intensive care, in six acutely ill intensive care patients without evidence of acute lung injury (non‐ARF), and in 10 normal subjects. Platelet counts in ARF and non‐ARF patients were similar to the normal range. The bleeding time of the ARF patients (8.5 ± 0.9 min) was significantly longer (p < 0.01) than the normal (4.8 ± 0.2 min) but similar to non‐ARF patients (5.4 ± 0.8 min). The bleeding time prolongations in ARF patients were unrelated to platelet concentration. Platelet aggregation induced by ADP and thrombin was normal in both ARF and non‐ARF patient groups. The epinephrine response was impaired in one non‐ARF patient and in three ARF patients; collagen‐induced aggregation was absent in two ARF patients, with a prolonged bleeding time. Levels of VIII:C and vWF in both groups of patients were similar to the normal level, but VIIIR:Ag levels in ARF patients (407 ± 45% of normal) were higher (p < 0.01) than in both non‐ARF patients (210% ± 10%) and normal subjects (106% ± 4). The electrophoretic mobility of VIIIR:Ag was abnormal in ARF patients. The prolonged bleeding time in ARF patients appears to result from the qualitative and quantitative VIIIR:Ag defect. β‐Thromboglobulin levels were greater (p < 0.01) in ARF patients (87.6 ± 6.9 ng/ml; p < 0.001) than in non‐ARF patients (46.2 ± 3.1 ng/ml) or in normal subjects (25.3 ± 2.5 ng/ml p < 0.0001). However, platelet factor 4 plasma levels in ARF patients (18 ± 1.6 ng/ml) did not differ from those in non‐ARF patients (15.0 ± 3.0 ng/ml), but both were significantly different from normal (6.1 ± 0.8 ng/ml). Plasma thromboxane B 2 (T × B 2 ) levels were not different from normal values in either ARF or non‐ARF patients, but 6‐keto‐PFG 1α levels were significantly reduced (p < 0.01) in ARF patients (215 ± 43 pg/ml) compared to normal values (381 ± 34 pg/ml). Non‐ARF patients had 6‐keto‐PGF 1α levels (285 ± 111 pg/ml) midway between the normal values and those of ARF patients. Our results suggest that in vivo platelet activation occurs in ARF. ARF patients have quantitative and qualitative platelet defects that may contribute to thrombotic and hemorrhagic complications.