What are the intraoperative risk factors for blood loss during liver transplantation?

Updated: Apr 19, 2019
  • Author: Vanessa A Olcese, MD, PhD; Chief Editor: Ron Shapiro, MD  more...
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Liver transplantation surgery may be divided into 3 stages. Stage I (preanhepatic period) begins with dissection of the inflow and outflow vascular structures of the liver and ends with removal of the diseased organ. Stage II (anhepatic phase) begins with implantation of the donor liver and ends with reperfusion of the new organ. Stage III (reperfusion and postreperfusion period) begins with reperfusion of the grafted liver and ends with completion of the surgery.

Blood loss in stage I occurs mainly from transection of the fragile collateral vessels that develop as a result of portal hypertension. In addition, extensive bleeding may occur from raw areas remaining after liver explantation.

Preexisting abnormalities of clotting, platelets, and fibrinolysis compound the problem. Addressing these abnormalities is crucial. The anesthesiologist must aggressively attempt to correct the international normalized ratio (INR) and platelet count by transfusing plasma and platelets early in the operative procedure. Furthermore, coagulation factors, especially factors V and VIII, may be degraded during transplantation as a result of enhanced proteolysis, and the degree of degradation correlates with the transfusion requirements during orthotopic liver transplantation (OLT). [2]

Transplantation of a healthy liver usually restores the patient's clotting function in the operating room. However, a dysfunctional graft may not immediately produce clotting factors. In severe cases, this may lead to nonfunction of the primary graft, which mandates retransplantation. However, in some patients this is temporary and the graft recovers and function improves.

Clotting function is assessed during liver transplantation with the standard coagulation tests (ie, PT, aPTT, fibrinogen level). In addition, the thromboelastogram and coagulation and platelet function analyzer (eg, Sonoclot) are used.

The thromboelastogram is used to monitor clot formation until an endpoint of clot lysis or retraction is determined. The thromboelastogram, which is performed using whole blood, analyzes the interactions of plasma coagulation proteins with platelets and fibrinogen. Specific details regarding the interpretation of the thromboelastogram are beyond the scope of this article, but its findings correlate with intraoperative hemorrhage and coagulopathy and can assist the anesthesiologist in treating intraoperative bleeding by helping identify the cause.

Fibrinolysis may be a problem during the anhepatic or postanhepatic phase of OLT. The cause of fibrinolysis is most likely diminished uptake of tissue plasminogen activator (t-PA), accumulation of fibrinolytic activators, and enhanced release of t-PA from the donor liver after reperfusion. Additionally, alpha-2 antiplasmin, the principal inhibitor of plasmin and plasminogen activity during this phase, is decreased.

Bleeding during the postanhepatic phase also may be related to disseminated intravascular coagulation (DIC) and platelet trapping. Platelet trapping has been documented by simultaneous measurement of arterial and venous platelet counts. Decreases as large as 55% have been described in the absence of any thrombus in the graft.

One study described extravasation of platelets into the space of Disse and the sinusoids, along with phagocytosis by Kupffer cells. Additionally, many platelets that remained were found to be degranulated or nonfunctional. DIC has been correlated with ischemic damage of the graft liver. Antithrombin III administration has not been shown to be effective for reversing reperfusion-related DIC.

Other potential causes of bleeding after reperfusion include the release of heparinlike factors from the allograft, release of preservative solution into the systemic circulation, and dysfunction of the graft.

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