Pathophysiological Mechanisms of Postrevascularization Hyperkalemia in Orthotopic Liver Transplantation

Abstract

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.

Opposite acute potassium and sodium shifts during transplantation of hypothermic machine perfused donor livers

“…[1][2][3][4] To counteract an anticipated acute rise of potassium after graft reperfusion, anesthesiologists may take preventive measures, such as the administration of glucose/insulin, bicarbonate, calcium, or measures as hyperventilation. Several factors are known to contribute to hyperkalemia during liver transplantation, including the release of potassium rich preservation solution, cell lysis during graft reperfusion, metabolic acidosis, and massive transfusion of red blood cells.…”

“…Several factors are known to contribute to hyperkalemia during liver transplantation, including the release of potassium rich preservation solution, cell lysis during graft reperfusion, metabolic acidosis, and massive transfusion of red blood cells. [1][2][3][4] To counteract an anticipated acute rise of potassium after graft reperfusion, anesthesiologists may take preventive measures, such as the administration of glucose/insulin, bicarbonate, calcium, or measures as hyperventilation. 5,6 Recently, end-ischemic hypothermic (oxygenated) machine perfusion of donor livers has been introduced into clinical practice as a new method of organ preservation.…”

Anesthesia in Liver Transplantation

“…High recipient potassium concentrations were found to be an independent predictor of death within the first year after liver transplantation (Dawwas et al, 2009). Bank blood transfusion imposes a severe potassium increase, and hyperkalemia may complicate the status of the transplant patient, especially in the presence of renal impairment and acidemia (Nakasuji& Bookallil, 2000). Serum potassium concentrations must be checked periodically and prereperfusion hyperkalemia must be corrected aggressively.…”

Liver transplantation

“…Independent predictors of hyperkalemia are the number of red blood cells (RBCs) transfused and higher initial values, especially in acidemic patients with renal insufficiency (Naksuji & Bookallil, 2000). Hyperkalemia is ominous and may cause fatal arrhythmias, particularly after reperfusion.…”