P061: C-ING IS BELIEVING: ASCORBIC ACID TO THE RESCUE AFTER LIVER TRANSPLANT REPERFUSION
Kyle H Chan, MD; Asad H Bashir, MD, FAAP
University of Florida College of Medicine
Introduction: Post-reperfusion syndrome (PRS) during liver transplantation was first defined in 1987 as a fall in mean arterial pressure (MAP) of more than 30% within the first five minutes after liver reperfusion, with a duration of at least one minute (1). This definition has since been further divided into categories such as mild, significant, prolonged, and recurring by various authors (2,3). Treatment typically involves administration of fluids, vasopressors, and calcium chloride, along with other options such as methylene blue (4) and hydroxocobalamin (5). We describe a case of PRS during liver transplantation unresponsive to these standard treatments which responded well to intravenous (IV) ascorbic acid (vitamin C) administration.
Case presentation: The patient was a 50-year-old female with alcohol-associated cirrhosis (MELD score of 39) who presented for liver transplant. Preoperatively, the patient was hospitalized for decompensated liver cirrhosis on dual vasopressor therapy and continuous renal replacement therapy for hepatorenal syndrome. Clinical features of hepatopulmonary syndrome were present, evidenced by elevated mean pulmonary artery pressures with right sided heart dysfunction noted on transthoracic echocardiography.
The patient tolerated the initial five minutes post-reperfusion uneventfully, maintaining MAPs in 70s-90s on baseline triple vasopressor infusions of epinephrine, vasopressin and norepinephrine, along with bolus doses of 20 mcg epinephrine, 10 mg ephedrine, 1000 mg calcium chloride, and 50 mEq sodium bicarbonate. After five minutes, the patient was noted to have decreased MAPs, drifting into the 50s. This decrease in MAPs was refractory to 200mg methylene blue, repeated boluses of vasopressor medications, and increased rates on vasopressor medication drips. An institutional shortage of hydroxocobalamin precluded its use during this case. At this stage, the patient was treated with 50 mg IV hydrocortisone and 6 g IV ascorbic acid. Gradual improvement in MAPs was noted in the next 30-60 minutes, even with cessation of the epinephrine infusion and decrease in the rates of the vasopressin and norepinephrine infusions.
Discussion: PRS can lead to deep hemodynamic instability with associated hyperfibrinolysis immediately after reperfusion of the liver graft. Ascorbic acid contributes to increases in blood pressure by reducing the production of nitric oxide and serving as a co-factor in catecholamine synthesis (6). For its antioxidant and anti-inflammatory properties, its use has been explored in the setting of septic shock (6) and after cardiac surgery with cardiopulmonary bypass (7). A randomized control trial protocol for using vitamin C for prevention of PRS in orthotopic liver transplantation has been proposed (8), providing a stepping stone for transplant anesthesiologists. Our experience with IV ascorbic acid provides further insight into an additional option available to counter hypotension due to refractory vasoplegia after liver reperfusion.
Conclusion: Ascorbic acid has been documented as a potential treatment for vasoplegia in the setting of sepsis, burns, and post cardiopulmonary bypass. PRS occurs in 12-77% of liver transplants (3), with an increased predisposition in patients with high MELD scores. In such instances, ascorbic acid serves as a promising alternative for management of hypotension in the post-reperfusion period, particularly in the age of medication shortages.