The aggregation of human platelets by ascitic fluid. a mechanism for the disseminated intravascular coagulation (DIC) complicating leveen shunts

Abstract

Disseminated intravascular coagulation (DIC) is a common problem in patients with LeVeen shunts. There is little doubt that this is caused by the infusion of ascitic fluid into the systemic circulation since ligation of the shunt is associated with cessation of DIC and patients who do not develop this complication usually have non-functioning shunts. The factor in the ascitic fluid responsible for the precipitation of DIC has not been previously recognized. This study is concerned with the effects of ascitic fluid on human platelets and offers an explanation for the mechanism of DIC post-LeVeen shunts. The addition of ascitic fluid concentrated 5-fold to platelet rich plasma resulted in marked platelet aggregation which was inhibited by EDTA and adenosine. No aggregation was observed when aspirin treated platelets were used. The aggregating activity could be precipitated by high-speed ultracentrifugation at 100,000 g for 60 min. The pre-incubation of the aggregating fluid with collagenase resulted in . complete loss of aggregation. These findings suggested that the aggregating factor was collagen. This was confirmed by a hydroxyproline assay and the finding of a brand corresponding to type I collagen on SDS polyacrylamide gel electrophoresis. Besides its ability to activate platelets, collagen can also activate the contact clotting factors, namely factors XI and XII. This dual activation would result in significant thrombin generation with the development of DIC in vivo . Preliminary experiments in rabbits indicate that the infusion of collagen obtained from ascitic fluid precipitates DIC which is prevented by the prior use of aspirin. The role of aspirin in the prevention or modification of DIC post-LeVeen shunts in man needs to be explored.