The prevalence of a heparin-like effect shown on the thromboelastograph in patients undergoing liver transplantation

✍ Scribed by Seema Agarwal; Marco Senzolo; Clare Melikian; Andrew Burroughs; Susan V. Mallett

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 129 KB
• Volume: 14
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.21437

✦ Synopsis

It has been known for several decades that thromboelastographic analysis of the blood of patients undergoing liver transplantation may show a heparin-like effect (HLE) at the time of reperfusion. However, the prevalence of HLE and the origin of these heparin-like substances remain largely unstudied. The primary aim of this retrospective observational analysis was to determine the prevalence of the HLE in 211 consecutive patients having liver transplantation in our institution at various stages throughout the transplant. One of the secondary aims was to analyze the prevalence of HLE with respect to the various etiologies of liver disease. Paired Thromboelastograph traces (native and heparinase) were examined at 5 stages of the transplant: the baseline stage, dissection stage, anhepatic stage, reperfusion stage, and end of the case. HLE was defined as a reduction in the reaction and coagulation times of greater than 50% by the addition of heparinase to the sample. Thirty-one percent of patients had evidence of an HLE at baseline, and this increased to 75% after reperfusion of the donor graft. This HLE resolved spontaneously in 47% by the end of the case. Patients with fulminant liver failure were more likely to demonstrate HLE at baseline than those with chronic liver disease (45.8% compared to 29%). There was no difference in the prevalence of HLE after reperfusion. In conclusion, prior to transplantation, there is a significant difference in the prevalence of HLE with respect to etiology. However, this difference disappears after reperfusion as the majority of patients then develop HLE. Although it is clear that there are both endogenous and exogenous sources of heparin contributing to the HLE, the clinical significance of these findings remains unclear.