Association Between Flushed Fluid Potassium Concentration and Severe Postreperfusion Syndrome in Deceased Donor Liver Transplantation

Abstract

BackgroundsPredicting the occurrence of severe postreperfusion syndrome (PRS) is clinically challenging. We investigated whether the flushed fluid potassium concentration (FFK) was associated with severe PRS in deceased donor liver transplantation (DDLT).Material/MethodsForty adult DDLT recipients were enrolled in this retrospective study. Effluent solution samples were collected at the end of the portal vein flush, and the FFK was determined using a point-of-care blood gas analyzer. The risk factors associated with severe PRS and the clinical outcomes in 2 groups were compared.ResultsSevere PRS occurred in 22 out of 40 patients (55.0%). The FFK of the severe PRS group was significantly higher than that of the non-severe PRS group (median, 9.6 vs. 5.8, P<0.001). Other variables associated with severe PRS included the donor risk index (DRI), Child-Turcotte-Pugh score, donor type, donor warm ischemia time, and Model for End-stage Liver Disease score. The area under the receiver operator characteristic curve for the FFK was 0.982, and the best cut-off value of the FFK for predicting severe PRS was 6.75 mmol/L (100.0% sensitivity and 88.9% specificity). A significant positive correlation was observed between the FFK and DRI (R=0.714). Patients who experienced severe PRS had a higher early allograft dysfunction rate (63.6% vs. 22.2%, P=0.019) and a longer hospital stay (median, 33.0 vs. 24.0, P=0.034).ConclusionsBoth the severity of the recipient’s liver disease and the donor graft factors play an important role in the development of severe PRS in DDLT. An FFK of more than 6.75 mmol/L was associated with severe PRS after reperfusion.

Postreperfusion syndrome, hyperkalemia and machine perfusion in liver transplantation

“…After graft reperfusion, hyperkalemia can result from acute metabolic acidosis, causing and extracellular potassium ions shift in exchange of H + , from exogenous potassium administration associated with red blood cells transfusion, and from the flush of potassium-rich preservation solution (like University of Wisconsin solution) from the graft into recipient circulation. This last has been particularly emphasized, and some studies have detected an association between potassium concentration of effluent flush fluid and severe PRS (9). However, two facts should be acknowledged.…”

Risk factors of the post-reperfusion syndrome during orthotopic liver transplantation: a clinical observational study

“…It occurs within the first 5 min after reperfusion of the donor’s liver with the recipient’s blood during the transition from the anhepathic phase to the neohepathic phase, which lasts for at least 1 min [ 4 , 8 , 9 ]. It is associated with poor patient and transplanted liver outcomes [ 3 , 10 , 11 ]. Although the definitive mechanism of this syndrome is complex and not fully understood [ 7 , 9 , 12 – 14 ], it is attributed to the release of oxygen free radicals, endotoxin, inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), IL-2, vasoactive, hyperkalemic, cold, and acidotic substances of maintenance solution, donor’s liver, and recipient ischemic intestine [ 6 , 9 , 14 , 15 ].…”

Elevated effluent potassium concentrations predict the development of postreperfusion hyperkalemia in deceased liver transplantation: a retrospective cohort study

“…The surgical procedures have been described in detail previously [ 14 ]. Briefly, liver grafts were implanted using the conventional caval replacement technique without venovenous bypass.…”

“…Perioperative anesthetic care was carried out according to the standard of care at our institution [ 14 ]. During the study period, intraoperative sK + levels were generally monitored by performing blood gas measurements at the following fixed time points: 1) before incision; 2) immediately before portal vein clamping; 3) immediately before reperfusion; 4) at one minute following reperfusion; 5) at 5 min following reperfusion; 6) at one hour following reperfusion; 7) at 2 h following reperfusion; and 8) at the end of the surgery.…”

“…However, most of these predisposing factors are often unmodifiable, and the exact pathophysiological mechanism of PRHK caused by ECD liver grafts has not been fully elucidated. Given that effluent potassium (eK + ) concentrations following a standard portal vein flush (PVF) are generally elevated during LT using ECD liver grafts [ 13 , 14 ], we conducted this retrospective cohort study to assess the association between eK + concentrations and the development of PRHK in adult patients undergoing deceased LT.…”