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We investigated platelet count, bleeding time, platelet aggregation, prothrombin time, activated partial thromboplastin time, and fibrinogen level in 58 very low-birth-weight infants during the first postnatal day to determine the relationship between hemostatic disorders and intraventricular hemorrhage. Thirty-two of the 58 infants (55%) were found to have periventricular-intraventricular hemorrhage by computerized tomography or autopsy. Nine patients (16%) had subarachnoid hemorrhage only and 17 (29%) had no evidence of intracranial hemorrhage. Infants with IVH had a significantly lower mean platelet count than did infants with no SAH/IVH. However, only five patients with IVH had initial thrombocytopenia. The IVH group had a mean bleeding time which was significantly prolonged compared to that of the group without SAH/IVH. Similarly, patients with IVH had a mean platelet aggregation response which was significantly diminished in comparison to that of patients with no SAH/IVH. Infants with IVH had a significantly longer mean PT than did infants with no SAH/IVH. In addition, babies with IVH had a significantly longer mean APTT compared to that of babies without SAH/IVH. The groups did not differ significantly with respect to fibrinogen levels. Three infants with IVH had disseminated intravascular coagulation in the early neonatal period. These data suggest that disorders of platelet-capillary interaction and defects in the intrinsic and extrinsic coagulation pathways may play important roles in intraventricular hemorrhage in the premature infant.

Marked platelet hyperaggregability to adenosine diphosphate, epinephrine, and collagen was demonstrated in two children with vitamin E deficiency, with complete reversal following E supplementation. No clinical thrombotic tendency was observed during the E-deficient state. The action of vitamin E in the schema of platelet arachidonate peroxidation appears to be at the step of phosphilpase A activation, or the conversion of arachidonic acid into the cyclic endoperoxides, since the peroxidation product malonaldehyde was increased during the E-deficient state with normalization following E sufficiency.

The effects of transfusion of whole blood clot emboli and aged citrated platelet-poor plasma on pulmonary capillary permeability were investigated in anesthetized sheep by continuous collection of pulmonary lymph. Changes in lymph flow and lymph-to-plasma ratios (CL/CP) for albumin and globulin were utilized to detect changes in permeability. Infusion of 0.5 cc/kg of finely (less than or equal to 1 mm) diced autologous whole blood clot resulted in a 170% increase in lymph flow over control with no change in CL/CP for albumin or globulin. Infusion of 1 cc/kg of autologous clot increased lymph flow 180% over control and increased CL/CP for albumin and globulin. Infusion of homologous platelet-poor plasma caused greater increases in lymph flow without changes in CL/CP. Changes in each of these three groups were consistent with increased permeability. Balloon occlusion of one main pulmonary artery was induced without a fall in cardiac output and resulted in no change in lymph flow of CL/CP despite a rise in pulmonary vascular resistance (PVR). Femoral arteriovenous fistulas were created to increase cardiac output, but no change in lymph flow or CL/CP occurred. The results in these latter two experiments suggest that increased perfusion per unit lung capillary bed or increased PVR were not primarily responsible for the changes observed in the emboli-treated and plasma-infused animals. Since both emboli and aged platelet-poor plasma increased pulmonary capillary permeability, the permeability increasing factor appears to be humoral in origin. Similar humoral factors may be important in the pathogenesis of the adult respiratory distress syndrome in man.