Postreperfusion Syndrome In Liver Transplantation Research Articles

Administration of magnesium sulphate does not prevent post-reperfusion syndrome but is necessary during living donor liver transplantation.

Severe hemodynamic instability is observed during portal vein de-clamping in the form of post-reperfusion syndrome in liver transplantation. The protective effect of magnesium on inflammation and ischemia-reperfusion injuries of various organs is evident, but its role in the prevention of post-reperfusion syndrome in liver transplantation is not clear. We investigated the effect of magnesium sulphate on the incidence of post-reperfusion syndrome during living donor liver transplantation. The secondary outcomes were the requirement of vasopressor boluses and levels of serum magnesium, lactate and serum C-reactive protein. Seventy living donor liver transplant recipients were randomized into a magnesium (M) group (n=35) or normal saline (N) group (n=35). The patients in group M received 35mg/kg of magnesium sulphate, 30 minutes after the beginning of the anhepatic phase, and patients in group N received normal saline. The incidence of post-reperfusion syndrome in group M and group N was 34.29% and 40%, respectively, with no significant difference. The requirement for rescue vasopressor boluses and levels of C-reactive protein and lactate were also comparable between the two groups. However, the incidence of hypomagnesemia at the end of surgery was significantly higher in group N (37.1% vs. 14.28%, p=0.027). Magnesium does not appear to prevent post-reperfusion syndrome. However, hypomagnesemia is more frequently seen during liver transplantation. Hence, serum magnesium should be routinely monitored and administered during liver transplantation.

Postreperfusion syndrome in liver transplantation: Outcomes, predictors, and application for recipient selection.

This study aimed to identify risk factors for postreperfusion syndrome (PRS) and its impact on LT outcomes. Data analysis was performed in 1021 adult patients undergoing donation after brain death (DBD) LT to identify PRS incidence, the risk factors for PRS development, and its impact on LT outcomes. The overall incidence of PRS was 16.1%. Independent risk factors for PRS included donor age (odds ratio (OR) 1.01, P=.02), donor body mass index (BMI) (OR 1.04, P=.003), moderate macrosteatosis (OR 2.48, P=.02), and cold ischemia time (CIT) (OR 1.06, P=.02). On multivariable analysis for 30-day graft failure, PRS (hazard ratio (HR) 3.49; P<.001) and Model for End-stage Liver Disease (MELD) score (HR 1.01; P=.05) were independent risk factors. Patients were categorized into four distinct groups based on PRS risk groups and MELD groups, which showed different 1-year graft survival (P<.001). There were comparable outcomes between low PRS risk- high MELD and high PRS risk - low MELD group (P=.33). Donor age, donor BMI, moderate macrosteatosis, and CIT were identified as risk factors for the development of PRS in LT using DBD grafts. PRS risk evaluation may improve donor-to-recipient matching based on their MELD scores.

Post-Reperfusion Syndrome in Liver Transplantation: Does a Caval Blood Flush Vent Help?

BackgroundPost-reperfusion syndrome (PRS) during liver transplantation can range from a benign event to a profound hemodynamic excursion from baseline with significant morbidity. Multiple variables can be responsible for the diverse presentations. Over time, our group noticed that a blood flush of the liver graft via a caval vent (in addition to a standard chilled flush via the portal vein) appeared to result in a milder reperfusion effect. Attenuation of PRS via caval vent seemed to minimize hemodynamic instability and reduce metabolic derangements associated with reperfusion.Material/MethodsThis was a prospective observational pilot study of standard practice with the addition of lab values and hemodynamic evaluations. We methodically observed normal clinical flow in 20 adult orthotopic liver transplant recipients. We analyzed blood and fluid samples at set time intervals during the peri-reperfusion phase.ResultsSixteen out of 20 patients received a blood flush via caval venting. Mean arterial pressure (MAP) and heart rate were better preserved in the patient population that received a caval blood flush vent. Elevations in central venous pressure (CVP) were similar between the 2 groups. Lab values (blood gas, electrolyte, and hemoglobin) of the patients’ blood were similar, with no notable differences. Analysis of the initial blood flushed through the liver graft proved to be hypothermic, acidotic, and hyperkalemic.ConclusionsPre-reperfusion caval venting in liver transplantation (in addition to a portal vent and a chilled LR/albumin portal flush solution) appears to have favorable hemodynamic effects. The literature on this technique is sparse and larger studies are needed.

Acute kidney injury and post-reperfusion syndrome in liver transplantation.

In the past decades liver transplantation (LT) has become the treatment of choice for patients with end stage liver disease (ESLD). The chronic shortage of cadaveric organs for transplantation led to the utilization of a greater number of marginal donors such as older donors or donors after circulatory death (DCD). The improved survival of transplanted patients has increased the frequency of long-term complications, in particular chronic kidney disease (CKD). Acute kidney injury (AKI) post-LT has been recently recognized as an important risk factor for the occurrence of de novo CKD in the long-term outcome. The onset of AKI post-LT is multifactorial, with pre-LT risk factors involved, including higher Model for End-stage Liver Disease score, more sever ESLD and pre-existing renal dysfunction, either with intra-operative conditions, in particular ischaemia reperfusion injury responsible for post-reperfusion syndrome (PRS) that can influence recipient’s morbidity and mortality. Post-reperfusion syndrome-induced AKI is an important complication post-LT that characterizes kidney involvement caused by PRS with mechanisms not clearly understood and implication on graft and patient survival. Since pre-LT risk factors may influence intra-operative events responsible for PRS-induced AKI, we aim to consider all the relevant aspects involved in PRS-induced AKI in the setting of LT and to identify all studies that better clarified the specific mechanisms linking PRS and AKI. A PubMed search was conducted using the terms liver transplantation AND acute kidney injury; liver transplantation AND post-reperfusion syndrome; acute kidney injury AND post-reperfusion syndrome; acute kidney injury AND DCD AND liver transplantation. Five hundred seventy four articles were retrieved on PubMed search. Results were limited to title/abstract of English-language articles published between 2000 and 2015. Twenty-three studies were identified that specifically evaluated incidence, risk factors and outcome for patients developing PRS-induced AKI in liver transplantation. In order to identify intra-operative risk factors/mechanisms specifically involved in PRS-induced AKI, avoiding confounding factors, we have limited our study to “acute kidney injury AND DCD AND liver transplantation”. Accordingly, three out of five studies were selected for our purpose.

Hemodynamic recovery following postreperfusion syndrome in liver transplantation.

The authors' current understanding of the phenomenon of significant and sustained decrease in arterial pressure following liver graft reperfusion (postreperfusion syndrome [PRS]), is derived from relatively small observational reports, and no large scale analysis of PRS exists up to date. This study investigated its incidence, risk factors, temporal course of hemodynamic recovery, and its impact on functional graft outcome. Retrospective observational study of 1,024 electronic records of orthotopic liver transplant recipients. Major transplant center. Out of 1,024, 715 records satisfied the inclusion criteria. Data were analyzed by multivariable Cox's proportional hazard model to identify risk factors for PRS. Hemodynamic recovery patterns and functional graft outcomes were compared between the cohorts of interest (intraoperative PRS) and control (no intraoperative PRS) after propensity score-matching. Association between donor risk index and hemodynamic recovery after hepatic artery reperfusion was analyzed by a multivariable regression model. The overall incidence of PRS was 31.6% with associated mortality of 0.3%. Independent risk factors for PRS included older donor age, higher donor risk index, and lower central venous pressure at reperfusion. Hemodynamic recovery after PRS following portal vein reperfusion was delayed until hepatic artery reperfusion. The slope of hemodynamic recovery, expressed as %MAP/min, correlated negatively with donor risk index (p=0.014). Immediate and 1-year graft survival rates were similar in both cohorts. Host hemodynamic response to graft reperfusion appeared to be phasic: initial abrupt hypotension after portal vein reperfusion was followed by a period of gradual decline of blood pressure until hepatic artery reperfusion, and sustained hemodynamic recovery afterwards. The slope of hemodynamic recovery correlated negatively with the donor risk index. PRS was not associated with deterioration of post-transplant graft survival and function.

Atropine prophylaxis of the postreperfusion syndrome in liver transplantation

Atropine prophylaxis of the postreperfusion syndrome in liver transplantation

Phenylephrine treatment of the postreperfusion syndrome in liver transplantation

Phenylephrine treatment of the postreperfusion syndrome in liver transplantation