Postreperfusion syndrome is a recognized complication of liver transplant, characterized by acute cardiovascular instability following graft reperfusion . We present a case series of 2 deceased-donor liver transplant recipients who developed distinct patterns of reperfusion injury: a patient with early reperfusion syndrome and another patient with delayed (late) reperfusion instability. Both cases manifested significant hypotension and bradycardia or low cardiac output, requiring prompt anesthetic intervention with vasopressors and inotropes. Timely recognition, vigilant intraoperative monitoring, and tailored anesthetic management resulted in hemodynamic stabilization and favorable graft outcomes. This series highlights the importance of proactive anesthetic strategies for management of ischemia-reperfusion injury during liver transplant.

Key words : Intraoperative anesthetic management, Ischemia-reperfusion injury, Liver transplantation, Postreperfusion syndrome

Introduction
Postreperfusion injury is characterized as a state of cardiovascular failure subsequent to the reperfusion of the freshly transplanted liver.¹ It is a clinical syndrome of profound cardiovascular impairment that includes bradycardia, a reduction in mean arterial pressure, and a reduction in systemic vascular resistance, accompanied by a concurrent elevation in pulmonary filling pressures.^3,4,5 We present a case series of 2 patients who experienced early and late reperfusion injury while undergoing transplant with a focus on anesthetic strategies to manage these complications intraoperatively.

Case Report

Patient 1
Patient 1 was a 52-year-old man from Ethiopia with chronic hepatitis B-related end-stage liver disease complicated to cirrhosis on treatment with tenofovir, scheduled for deceased-donor liver transplant. Model for End-Stage Liver Disease score was 17, and Child Pugh score was C. The patient had experienced a recent acute progression of ascites in 1 month. His blood group was A-positive, and serology was positive for hepatitis B surface antigen. The 40-year-old female donor had the A-positive blood group and had experienced intracerebral hemorrhage. The patient underwent uncomplicated conventional liver transplant. Antibiotics and immunosuppressive agents were given according to protocol. There was 1500 mL of blood loss for which 4 U of allogeneic leukocyte-depleted packed red blood cells and 600 mL of fresh-frozen plasma were transfused. Prereperfusion urine output was 60 mL/h. During transplant there was an episode of bradycardia as low as 40 beats/min and hypotension with mean arterial pressure down to 50 mm Hg for 30 seconds, indicating early reperfusion syndrome, which was promptly managed intraoperatively with 40 μg of adrenaline and 200 μg of phenylephrine with good response. Reperfusion of the portal vein and hepatic artery was uneventful. Urine output was 100 mL/h after reperfusion. Lactate levels shifted between 1.6 to 2.1 mmol/L. Cold ischemia time was 265 minutes, and warm ischemia time was 30 minutes. Postoperative liver enzyme levels were initially elevated, with alanine transaminase (ALT) at 311 IU/L and aspartate aminotransferase (AST) at 690 IU/L. These values demonstrated a downward trend, reaching ALT 66 IU/L and AST 41 IU/L by day 4, which normalized by day 5 in the intensive care unit. Postoperative creatinine was mildly elevated at 1.54 mg/dL and showed a rising trend, possibly attributable to tacrolimus levels.

Patient 2
Patient 2 was a 68-year-old man from India with metabolic dysfunction-associated steatohepatitis (previously called nonalcoholic steatohepatitis), chronic liver disease, hepatocellular carcinoma who underwent deceased-donor liver transplant. Model for End-Stage Liver Disease score was 20, and Child Pugh score was C. He presented with decompensated liver failure and minimal portal hypertension. The donor was a 42-year-old laborer with intracerebral hemorrhage after a fall from a height. The patient underwent uncomplicated conventional liver transplant. Antibiotics and immunosuppressive agents were given according to protocol. Six units of leukocyte-depleted packed red blood cells were given to offset blood loss. Prereperfusion urine output was 100 mL/h. During transplant, reperfusion was uneventful. However, during artery anastomosis, after 1 hour the recipient exhibited intraoperative hemodynamic instability showing hypotension with low cardiac index, indicating late reperfusion syndrome, which was managed intraoperatively with 30 μg of adrenaline and 300 μg of phenylephrine. Postreperfusion urine output was 70 to 90 mL/h. Lactate shifted between 2.3 mmol/L with peaks of 3.8 mmol/L. Cold infusion time was 210 minutes, and warm infusion time was 36 minutes. Postoperative liver enzyme levels were elevated, with ALT at 1504 IU/L and AST at 4040 IU/L, but both showed a downward trend from day 2 onwards. Postoperative creatinine was 0.83 mg/dL.

Conclusions
This case series underscores the importance of vigilant intraoperative monitoring and prompt anesthetic intervention for management of both early and late reperfusion injury during liver transplant.^1,2 Tailored fluid management and timely double inotropic/vasopressor support were crucial for stabilization of hemodynamics and optimization of graft function.^3,4 These cases highlight the need for continued refinement of anesthetic strategies to improve outcomes in transplant patients who develop ischemia-reperfusion injury.⁵