P080: POST-REPERFUSION HYPERKALEMIA IN MULTIVISCERAL TRANSPLANTATION: A CASE OF CARDIAC ARREST AND SUCCESSFUL RESUSCITATION
Marianfeli C Landino Delgado, MD; Nicolas Caram, MD; Mariana Acosta, MD; Daniel Schmidt, MD; Ramona Nicolau Raducu, MD, PhD; Marina Gitman, MD
Jackson Memorial Hospital-University of Miami
Background: Multivisceral transplantation (MVTx) involves grafting multiple intra-abdominal organs, including the pancreas, liver, stomach and intestine. Common indications are intestinal failure or extensive thrombosis. A major perioperative risk is post-reperfusion hyperkalemia, a potentially fatal complication triggered by ischemia-reperfusion injury, preservation solutions, cell lysis, metabolic acidosis, and massive transfusion. Severe hyperkalemia can lead to life-threatening arrhythmias and cardiac arrest, requiring aggressive intervention.
Case Presentation: A 50-year-old male with metastatic neuroendocrine tumor of the pancreas, underwent MVTx. His MELD-Na score was 8, with no coronary disease and a normal preoperative echocardiogram (EF >60%).
Following induction, 9Fr and 12Fr double-lumen catheters were placed in the left internal jugular vein, along with brachial and radial arterial lines. Continuous hemodynamic monitoring was performed using transesophageal echocardiography and FloTrac®. Vasopressor and inotropic agents, including vasopressin, phenylephrine, norepinephrine and epinephrine were readily available for administration as needed.
Pre-reperfusion vasopressin and epinephrine drips were administered at 0.04 U/min and 0.05 mcg/kg/min, respectively. Arterial blood gas (ABG) values were within acceptable limits, with potassium at 3.6 mEq/L. However, immediately after reperfusion, the patient developed bradycardia and hypotension, progressing to cardiac arrest with ventricular fibrillation. Cardiopulmonary resuscitation was initiated, with administration of epinephrine (4 mg), calcium chloride (2,000 mg), sodium bicarbonate (100 mEq), heparin (5,000 UI), and amiodarone (300 mg). Two defibrillation shocks were required to restore circulation.
The post-reperfusion ABG at 8 minutes revealed severe hyperkalemia (K+ 8.6 mEq/L); however, potassium levels were likely even higher at the time of cardiac arrest. The patient received 9 units of RBCs, 4 units of FFP, 2 units of platelets, 2 units of cryoprecipitate, 5L of crystalloid, and 2L of albumin. Transfusion of blood products was guided by thromboelastography. Estimated blood loss was 3L, with a total surgical time of 9 hours and cold ischemia time of 7 hours.
Discussion: Post-reperfusion hyperkalemia is an unpredictable complication in transplantation, particularly in MVTx, where massive ischemic organ load and potassium-rich preservation solutions can cause extreme potassium shifts. Despite adequate pre-reperfusion potassium levels, the patient experienced sudden hemodynamic collapse, highlighting this condition’s unpredictability. Key risk factors include potassium in preservation solutions, high serum lactate, and metabolic acidosis. Additionally, low cardiac index post-reperfusion, donation after cardiac death, and storage-aged red blood cells contribute to severe hyperkalemia. However, lowering potassium below 3 mEq/L increases dysrhythmia risk, making significant pre-reperfusion reduction neither feasible nor safe. Although prompt calcium, bicarbonate, and insulin administration is standard, this case underscores the need for early recognition, aggressive resuscitation, and preemptive measures to mitigate hyperkalemia.
Conclusion: Post-reperfusion hyperkalemia is associated with increased intraoperative mortality and poor postoperative outcomes in transplantation. Identifying pre-revascularization risk factors—including baseline potassium levels, metabolic acidosis, and impaired hepatic lactate clearance—is essential for anticipating and mitigating this life-threatening event. Further studies are needed to refine prevention strategies, optimize intraoperative potassium management, and improve patient survival following MVTx.