P009: REFRACTORY VASOPLEGIA IN LIVER TRANSPLANTATION: SUCCESSFUL USE OF HYDROXOCOBALAMIN AS RESCUE THERAPY
Nicolas P Caram, MD; Mariana Acosta, MD; Daniel Schmidt, MD; Marianfeli Landino, MD; Fouad Souki, MD; Ramona Nicolau-Raducu, MD, PhD
Jackson Memorial Hospital / University of Miami
Background: Vasoplegic syndrome is characterized by severe hypotension unresponsive to volume resuscitation or vasopressors. It is marked by low systemic vascular resistance (SVR) and high cardiac output (CO), likely due to splanchnic vasodilation, insufficient endogenous vasopressin production, and nitric oxide dysregulation (1).
Case Presentation: A 30-year-old man with a history of fulminant hepatic failure underwent orthotopic liver transplantation at age 4 and re-transplantation at age 20 due to chronic rejection. He presented for a third liver transplant. He had no history of coronary disease, and preoperative echocardiography demonstrated normal left ventricular function. His MELD-Na score was 45. The donor liver was preserved overnight using the OrganOx perfusion system.
Following induction, standard monitoring was established, including 9Fr and 14Fr double-lumen catheters in the left internal jugular vein, brachial and radial arterial lines, transesophageal echocardiography, and FloTrac®. Veno-venous bypass was initiated via right internal jugular and left femoral vein cannulation.
The 6-hour surgery was notable for an estimated blood loss of 50 liters. Intraoperatively, the patient received 130 units of pRBC, 111 units of FFP, 10 units of platelets, and 7 units of cryoprecipitate, along with fibrinogen, prothrombin complex concentrate (PCC). At reperfusion, 600 mcg of epinephrine was administered. Despite escalating vasopressor support (phenylephrine 100 mcg/min, norepinephrine 20 mcg/min, epinephrine 20 mcg/min, and vasopressin 0.08 u/min), he developed progressively worsening hypotension (mean arterial pressure [MAP] 40-50 mmHg). One-hour post-reperfusion, 100 mg of methylene blue was administered, with brief improvement, followed by 5 g of hydroxocobalamin over 15 minutes. During that period, the patient experienced ventricular tachycardia requiring 7 cycles of cardiopulmonary resuscitation (CPR) for 15 minutes before return of spontaneous circulation (ROSC) was achieved. By the end of surgery, the patient’s condition had improved with a decrease in vasopressor support (MAP 80-90 mmHg on phenylephrine 50 mcg/min, norepinephrine 10 mcg/min, epinephrine 10 mcg/min, and vasopressin 0.04 u/min).
Postoperatively, the patient developed atrial fibrillation, multifocal strokes, and respiratory failure requiring tracheostomy. Following a prolonged 110-day recovery, he was discharged to rehabilitation neurologically intact and asymptomatic.
Discussion: Vasoplegic syndrome during the neohepatic phase of liver transplantation presents a significant challenge. Its incidence is difficult to determine due to varying definitions and overlap with post-reperfusion syndrome. This case clearly met the criteria for vasoplegic syndrome, characterized by severe hypotension, low SVR, and high CO refractory to vasopressor support. High-dose vasopressors proved ineffective. Methylene blue provided temporary partial benefit (2). Hydroxocobalamin offered a promising alternative due to its ability to interrupt the cascade of events leading to vasoplegia by modulating nitric oxide (NO) pathways. Furthermore, hydroxocobalamin exerts a dual mechanism of action, increasing blood pressure while simultaneously inhibiting vasodilation (3). Its administration in this case appears to have been crucial in stabilizing the patient and potentially preventing further ischemic complications.
Conclusion: This case highlights the successful use of hydroxocobalamin as rescue therapy for severe vasoplegia during liver re-transplantation. This suggests its potential as a valuable treatment option in this challenging clinical setting. Further research is needed to optimize dosing and evaluate long-term outcomes in high-risk patients.