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Coagulopathy during ascites reinfusion: prevention by antiplatelet therapy
H H Tang1, H H Salem, L J Wood
1Department of Gastroenterology, Monash University, Alfred Hospital, Melbourne, Australia.
Insights
Infusing concentrated ascitic fluid in cirrhosis patients caused disseminated intravascular coagulation (DIC). Collagen in the fluid triggered DIC, which was prevented by antiplatelet therapy.
Area of Science:
- Gastroenterology
- Hematology
- Pathophysiology
Background:
- Cirrhosis patients with refractory ascites often undergo procedures involving ascitic fluid.
- Disseminated intravascular coagulation (DIC) is a serious complication that can arise in various clinical settings.
Purpose of the Study:
- To investigate the development of DIC during controlled intravenous infusion of concentrated ascitic fluid in patients with cirrhosis.
- To determine the role of ascitic fluid collagen in the pathogenesis of DIC.
Main Methods:
- Nine studies were conducted on patients with cirrhosis and refractory ascites who did not receive prophylactic antiplatelet therapy.
- Laboratory evidence of DIC was assessed, and collagen infusion was estimated by ascitic hydroxyproline concentration.
- Coagulation profiles were monitored during and after ascitic fluid infusion, and the effect of antiplatelet therapy (aspirin and dipyridamole) was evaluated.
Main Results:
- All nine patients developed laboratory evidence of DIC following ascitic fluid infusion.
- A significant correlation was found between the amount of collagen infused and the prolongation of partial thromboplastin time with kaolin (r = 0.8628; P < 0.005) and the decrease in platelet count (r = 0.5674; P < 0.05).
- Coagulation changes were reversible within 12 hours of ceasing infusion, and no DIC was observed in patients receiving antiplatelet therapy.
Conclusions:
- Intravenous infusion of concentrated ascitic fluid in cirrhosis patients induces DIC.
- The severity of DIC correlates with the quantity of collagen infused.
- Inhibiting collagen-induced platelet aggregation completely prevents DIC, supporting the role of ascitic fluid collagen in this complication.
Abstract:
The development of disseminated intravascular coagulation (DIC) during a controlled IV infusion of concentrated ascitic fluid was studied in a group of patients with cirrhosis and refractory ascites. Nine studies were performed on patients who had not received prophylactic antiplatelet therapy. All developed laboratory evidence of DIC. The total collagen infused, estimated by ascitic hydroxyproline concentration, correlated significantly with both the prolongation of the partial thromboplastin time with kaolin (r = 0.8628; P less than 0.005) and the decrease in platelet count (r = 0.5674; P less than 0.05). The changes in the coagulation profile were reversible on ceasing the infusion, returning to baseline levels within 12 hours. There were no changes in the coagulation profiles of four patients studied 48 hours after beginning antiplatelet therapy with aspirin and dipyridamole. It is concluded that the infusion of concentrated ascitic fluid into a peripheral vein of patients with cirrhosis results in DIC, the severity of which correlates with the amount of collagen infused and which is completely prevented by inhibiting collagen-induced platelet aggregation. The results support the hypothesis that the DIC that complicates ascites infusion into the systemic circulation is largely related to ascitic fluid collagen.
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