Acquired haemostatic defects in the ill newborn.

Abstract

Summary. The kinetics and function of platelets and fibrinogen were studied in 22 ill newborns. Overall 51Cr‐platelet survival was considerably shortened (patients 2·6 d ± 1·7, adult normal 9·5 d ± 0·6, P < 0·001) while 125I‐fibrinogen surival was less severely decreased (patients 2·1 d ± 0·8, adult normal 5·1 d ± 0·4, P < 0·05).Three patients with bacterial sepsis and one with disseminated herpes simplex had the most severely reduced platelet survival times (1·3 d ± 0·9), causing thrombocytopenia (62 ±32 × 109/l) despite production rates averaging 2 1/2 times normal. Although fibrinogen survival times were comparably reduced in these patients to 1·4 d ± 0·4, fibrinogen concentrations were normal because of compensatory increased production.In three patients with necrotizing enterocolitis platelet and fibrinogen survival times were similarly reduced (platelets 1·6 d ± 0·6, fibrinogen 1·6 d ± 0·6) with platelet counts of 69 ± 27 × 109/l and platelet production rates of twice normal. Since their fibrinogen production was not increased, they had decreased fibrinogen concentration (1·0 ± 0·19 g/l).In six patients with respiratory distress syndrome the kinetic results were more variable. Platelet survival was less severely affected than in the other groups and production was approximately twice normal; hence, the platelet count was maintained (177 ± 107 × 109/l). Fibrinogen in this group was slightly reduced because of decreased production in the presence of mildly decreased survival (2·7 d ± 0·7).The two patients with cytomegalovirus infection had severe thrombocytopenia (23 × 109/l) due to a combination of decreased platelet survival (3·6 d), increased splenic pooling and no compensatory increase in marrow platelet production. Fibrinogen production was normal but its plasma concentration was moderately reduced because of a decrease in fibrinogen survival.In many of these patients, fibrinogen dysfunction was suggested by a prolonged thrombin time and a discrepancy between fibrinogen concentration as determined by a time dependent assay and an equilibrium total clottable protein assay. Likewise, platelet dysfunction, evidenced as a prolonged bleeding time, was found in patients with RDS; some of these infants had otherwise unexplained bleeding.