Investigated were the haemostasis of 45 patients with histologically confirmed liver cirrhosis. The patients were subdivided into three groups according to the extent of their porto caval collateral circulation as proved by laparoscopy, gastroscopy and radiology: I = no porto caval shunts (n = 10); II = moderate porto caval shunts (n = 13); III = distinct porto caval shunts (n = 14). A 4th group consisted of 8 patients with bleeding from oesophageal varices. The results indicated a significant decrease in the stages I-III of the coagulation factors produced in the liver (incl. factor XIII and AT III) and the thrombocytes. Unchanged remained the concentration of factor VIII, whereas the factor VIII associated antigen showed an increased activity depending on the severity of the disease (stages I-III). In patients with bleeding from oesophageal varices, values of about 300% of normal could be demonstrated. Depending on the stage of the porto caval collateral circulation, the concentration of fibrin(ogen) split products were also increased. For comparison, patients with pre- and posthepatic blockage were investigated, whose portal hypertension was not caused by liver cirrhosis. Besides a mild thrombopenia they only showed a secondary hyperfibrinolysis. The results, above all in the cases of liver cirrhosis, can be explained by pathophysiological mechanism: a decreased synthesis of clotting factors-a disturbed portal microcirculation with fibrin deposition-an impaired function of the liver RES.