[Thrombocytic hemostasis in patients with severe craniocerebral trauma]

Platelet vascular hemostasis was assessed in 32 patients with slight craniocerebral injuries (SCCI) (Glasgow coma score 14-15) (group 1) on days 1, 3, 5, and 7 and in 84 patients (score 3-8) (group 2) in the same terms and on days 9, 14, and 21 after the injury. Under study were platelet count, spontaneous platelet aggregation and that induced by ADP, adrenalin, and ristomicin. Moderate disorders of platelet vascular hemostasis were revealed in all the patients; they were most of all expressed on day 5 and were mainly due to moderate disorders of the athrombogenicity of the vascular endothelium. The injury caused a manifest dysfunction of platelets connected with the developing disseminated intravascular blood coagulation and, specifically, with injury to the vascular endothelium. Spontaneous aggregation of platelets was the maximum on day 5 and coincided in time with an increase in Willebrand factor-dependent ristomicin-induced platelet aggregation (Willebrand factor is a marker of injury to the vascular endothelium). An increase of ristomicin-induced platelet aggregation was more often observed in the patients who died than in the survivors, and in those developing the respiratory distress syndrome (stages II-IV) and that combined with pneumonia.