Severe coagulopathies can occur during liver transplantation, particularly after reperfusion of the grafted liver. Heparin release has been proposed as one of the factors contributing to this coagulopathy. We have analysed the thrombelastograph (TEG) traces of 55 patients after reperfusion using native and heparinase-treated samples. In almost all cases an abnormal native TEG was improved in vitro by heparinase, demonstrating the presence of heparin or a heparin-like substance. The heparinase-modified TEG allowed assessment of the underlying coagulation status, providing a rational guide to blood component replacement or treatment of fibrinolysis.
Over the time scale of 24 hours, lactate derived from continuous dialysis circuits is efficiently cleared from the blood of most patients with multi-organ failure, but with less effect on systemic acidosis than is produced by equivalent amounts of bicarbonate.
Abstract. Aprotinin has been reported to reduce blood loss in difficult cases requiring cardiopulmonary bypass surgery and more recently in liver transplantation. Over a 9‐month period we compared the effects of an intra‐operative infusion of aprotinin on transfusion requirements and coagulation profiles in 12 patients undergoing liver transplantation for end‐stage cirrhosis with an equal number of consecutive transplants in patients with similar pathology who did not receive aprotinin. Transfusion of blood and blood products was reduced to one‐third in the aprotinin‐treated group. Operative time was also significantly reduced, as was ICU stay post‐operatively. Aprotinin profoundly inhibits fibrinolysis and this is likely to be the major effect by which blood loss is reduced. Thromboelastography revealed severe fibrinolytic changes in the anhepatic stage in 4 of 6 controlled patients; this accelerated in 3 following reperfusion of the new graft. By contrast, only 1 patient of 12 in the aprotinin‐treated group showed fibrinolytic activity in the anhepatic period, and none showed evidence of fibrinolysis following reperfusion of the new graft.
We describe the use of thrombelastography in HELLP syndrome (Haemolysis, Elevated Liver Enzymes, Low Platelets). It differentiated between two possible causes of significant haemorrhage and revealed an accompanying underlying fibrinolysis. This allowed specific therapy to be directed at both abnormalities and, we believe, helped prevent this patient from undergoing radical surgery to curb blood loss.
Thromboelastography evaluates the viscoelastic properties of blood coagulation. Using native blood, measurement must start soon after sampling. With normal coagulation, native and citrated blood values correlate well. No data exists from cirrhotic patients. We compared native and citrate thromboelastography parameters in 30 cirrhotic patients (20 Child-Pugh C class, two liver failure). Thromboelastography was performed within 4 min using native blood and after recalcification within 1-2 h of citrate storage. Thromboelastography variables (, alpha, ) were compared using the Mann-Whitney test, correlation investigated with the Pearson method and the degree of agreement with the Bland-Altman method. There was no significant difference between citrated and native blood for all variables. Median values for native and citrated were, respectively, 16.4 (range 2.3-22.5) and 15.1 (range 9.8-29.9); 6.3 (range 3.5-11.3) and 6.2 (range 2.8-10.9); 48.3 (range 30.7-62.9) and 46.2 (range 30.4-60.4); angle alpha 30.8 (range 18.7-46.8) and 33.2 (range 19.9-55.8). Correlation for each variable was significant ( 0.01). There was a good degree of agreement for all but two patients (both bleeding) for all variables. Citrated blood can substitute native blood using thromboelastography in cirrhotic patients, allowing more time between sampling and the thromboelastography measurement.
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