Coagulation studies were performed on 104 hospital inpatients with acute infectious hepatitis. Patients with clinical evidence of liver failure were studied separately from those without liver failure. A coagulation defect was found in 57 of the 78 patients without liver failure. This consisted of a prolonged prothrombin time and reduced levels of factors V, VII and X, and plasminogen. The defect was mild in most patients and was not associated with bleeding. A severe coagulation defect was found in all 26 patients with liver failure. Factors II, V, VII and X were markedly reduced. Plasminogen was reduced in all patients, and a low plasma fibrinogen concentration and thrombo‐cytopenia were found in half. One third of the patients studied showed an increase in serum fibrin/ fibrinogen degradation products. It is suggested that in some of these patients disseminated intravascular thrombosis contributed to the coagulation defect. Two patients had evidence of increased fibrinolytic activity. Bleeding occurred in 15 patients with liver failure and required treatment in 10. Fifteen patients with liver failure died. Nine patients with liver failure were treated with exchange transfusions during which a significant improvement of the prothrombin time and a slight reduction in platelet count was observed. Bleeding stopped during exchange transfusions in six of eight patients. It is possible that the improvement of the coagulation defect during exchange transfusions contributed to improved haemostasis.
|Number of pages||22|
|Journal||British Journal of Haematology|
|Publication status||Published - Jun 1972|