Pathophysiological Mechanisms of Postrevascularization Hyperkalemia in Orthotopic Liver Transplantation

The underlying mechanisms of hyperkalemia occurring immediately after revascularization in orthotopic liver transplantation (OLT) are unknown. We investigated the possible pathophysiological mechanisms of hyperkalemia in relation to the donor and recipient. The study included 64 consecutive patients undergoing OLT. Recipients were divided into two groups: Group 1 consisted of 47 patients with serum K+ concentration <5.5 mmol/L at 1-min postrevascularization, and Group 2 consisted of 17 patients with serum K+ exceeding 5.5 mmol/L. Increased serum K+ concentration, more progressive metabolic acidosis, and decreased mean arterial blood pressure and cardiac index during the anhepatic phase were recognized in Group 2. Multiple regression analysis showed that cardiac index, serum lactate, and serum K+ concentration during the anhepatic phase were independent and significant factors that could predict serum K+ concentration 1-min postrevascularization. Hyperkalemia at 1-min postrevascularization did not correlate with the extent of preservation injury of the graft liver (represented by the peak value of aspartate aminotransferase measured within the first 72 h after OLT) or the duration of cold ischemia. We conclude that hyperkalemia occurring immediately after revascularization in OLT is mainly caused by metabolic acidosis as a result of insufficient cardiac output during the anhepatic phase. Implications We demonstrate that serum K+ concentration, serum lactate, and cardiac index during the anhepatic phase predict K+ concentration just after revascularization in orthotopic liver transplantation and that the extent of preservation injury of graft liver and duration of cold ischemia do not contribute significantly to the induction of hyperkalemia.