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Liver Transplantation
The liver is the manufacturer and clearinghouse of most of the coagulation proteins. Liver disease disrupts all phases of the hemostasis process that depend on proper hepatic function. It follows then, that patients with liver disease are affected by low levels of procoagulant and inhibitors produced by the liver and by high concentrations of circulating tissue plasminogen activator (TPA), which is produced by the endothelium and metabolized by the healthy liver. Clearly, in the presence of a non-functional liver, the hemostasis balance shifts towards hypocoagulability due to low coagulation protein, dysfunctional platelets, and hyperfibrinolysis. It has also been shown that heparin-like activity can be detected in the blood of many patients in the post-reperfusion phase, even when there is no known source of exogenous heparin (donor or recipient).
Post liver transplantation, the imbalance shifts towards hypercoagulability, especially in children, due to exposure of tissue factor (TF) due to traumatic injury to a large capillary bed, venous stasis during clamping of the portal vein and inferior vena cava, ischemic insult to the intestines, activator release from the grafted liver, and massive blood transfusion.
In all three stages of liver transplantation: dissection, anhepatic, and reperfusion, there is a shift in the imbalance in patient hemostasis as shown in the figures below.
Clinical example
This clinical example shows the hypocoagulable state in the pre- and early operative period, then the shift into hyperfibrinolysis during the anhepatic phase, and finally the shift into hypercoagulability post-operatively.
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TEG® tracings
