Liver Transplant IV

The liver synthesizes most of the proteins involved in coagulation or blood clotting. While we think of most cirrhotic patients as coagulopathic - unable to form clot - they are also paradoxically hypercoagulable. The liver also synthesizes proteins that break down clots so sometimes the balance tips towards formation of thrombi and emboli. We further perturb the system during surgery with local inflammatory mediators triggered by trauma, the transplant of a liver which has been synthesizing pro- and anti-coagulant proteins, transfusions of plasma to help reduce surgical bleeding.

This was most prominent in one of my liver transplants where after reperfusion of the new liver, clots were noted by transesophageal echocardiogram in the heart. There was a period of time when the heart was stunned during reperfusion, and I wonder if these low flow states in combination with procoagulants released from the liver lead to clot formation. Furthermore, the focus of the clot seemed to start from a central line tip sitting in the atria. However, when we checked coagulation tests, the patient's INR was 8 and PTT was over 300, both suggestive that the patient's blood was too thin.

This is the paradox of coagulation in liver disease. The patient was bleeding and clotting at the same time; somehow, the normal system of checks and balances had failed. This is disseminated intravascular coagulation, and in the middle of surgery, this is life-threatening. Even though it doesn't make much physiologic sense, we gave a small bolus of heparin to dissolve the clot while transfusing products to decrease the bleeding. Over the course of the surgery, the clot melted away. We didn't see any changes in our pulmonary artery pressures or oxygenation so we didn't think the clot emobolized from the heart to the lungs. Such situations show me the complexity of managing coagulopathy especially in the setting of a major surgery with vascular components in a cirrhotic patient.