Abstract

We have experienced two cases of DIC following infusion of ascitic fluid from the peritoneal cavity to the vascular system. We have studied the etiology of this DIC. So, FDP, endotoxin, coagulant factors and procoagulant activity were investigated in ascitic fluid of 11 hepatic cirrhosis cases and 15 cancer cases.Method and Result; FDP in ascites were more included than in plasma. Endotoxin were positive in about 60% of ascitic fluid. The coagulant factors were recognized a littile except VUI-factor. Only ascitic fluid ded not clott the fibrinogen and did not affect the platlate aggregation. The procoagulant activities were measured by clotting times which the normal plasma (0.lcc) was added with the ascitic fluid or buffer (0.1cc), after 3 minutes incubation, and then added with 1/40 M Cacl2 (0.1cc).The clotting time was shortened in the ascitic fluid than buffer (buffer 120.7 ± 7.9 sec, Cancer 82 ± 23.8 sec., cirrhosis 91.4 ± 16.5 sec), and both VII and VIII deficient plasma was shortened too, but X dificient plasma was not coagulated. Also FDP and endotoxin did not shorten the clotting time of normal plasma. Experimentally, the ascitic fluid in dog by binding vena cava in ferior and the ascitic fluid in rat by transplantation of tumor cells shortened the clotting time. Conclusion; Coagulant, fibrinolytic and procoagulant factors were existed in ascitic fluid. We think that DIC induced by ascitic fluid are due to this procoagulant factor and this procoagulant factor may be not tissue - thromboplastin only.

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