Introduction: It has been reported that abnormalities in the coagulation and fibrinolytic system can be developed after severe head injury. α2-plasmin inhibitor (α2-PI) is the most important inhibitor of fibrinolysis, and α2-PI inhibits plasmin activity on the surface of fibirin clot. Deficiency of α2-PI is known to cause excessive fibrinolysis and plasmin-induced endothelial injury. Factor XIII (XIII), a key player for fibrin crosslinking, also has an antifibrinolytic property by means of crosslinking α2-PI and fibrin. In this study we focused on α2-PI and XIII, and evaluated whether alteration of fibrinolytic activities is associated with the clinical course of patients with severe head injury. Methods: Blood samples were obtained from 23 consecutive patients with isolated head injury within 3 hr after insult (GCS≤8, 13 cases; GCS≥9, 10 cases; 8 cases died). Coagulation and fibrinolytic parameters, including plasma levels of α2-PI, XIII, and thrombin-antithrombin III complex (TAT; a parameter of coagulation activation), were measured. Results: TAT levels were elevated more than 300μg/L in 18 patients. α2-PI levels were lower in non-survivors than in survivors (48.1 ±21.8 vs. 82.5 ±18.3 p<.001, by Mann-Whiteney U test), and were decreased less than 60% in patients with TAT>500μg/L. Reduced levels of α2-PI less than 60% were observed in 6 non-survivors, but not in good outcome patients. All patients with both α2-PI<60% and XIII>60% survived, while all non-survivors with α2-PI<60% showed XIII<55% and suffered from marked bleeding tendency, severe brain edema or severe hypotension within several hours after injury. Conclusion: These preliminary data suggest that excessive fibrinolysis induced by secondary α2-PI deficiency may contribute to the pathophysiology and outcome of severe head injury, and is exacerbated by XIII deficiency.
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine