Cardiovascular Collapse During Living-Directed Orthotopic Liver Transplantation Associated With the Transfusion of Contaminated Red Blood Cells

LOOD TRANSFUSION HAS many documented risks. Anesthesiologists administer more than half of the transfusions in the United States. In 2004, about 22 million blood components were transfused in the United States. Patients undergoing liver transplant often require multiple blood components. A fatal complication of transfusion during liver transplantation because of Klebsiella contamination of a unit of red blood cells is reported. CASE REPORT A 53-year-old man with end-stage liver disease secondary to hepatitis C virus and alcoholic cirrhosis presented for living-directed orthotopic liver transplantation (OLTx). Physical examination revealed a 109-kg man with blood pressure of 101/70 mmHg, heart rate of 72 beats/min, and respiratory rate of 18 beats/min. The patient was mildly jaundiced and appeared chronically ill. Secondary to his cirrhosis, he also had ascites, hepatic encephalopathy, and esophageal varices. The patient had undergone a splenectomy many years ago after a motor vehicle accident. His end-stage liver disease score was 17. The patient’s younger brother was in excellent health and would serve as the liver donor. General anesthesia was induced with sodium thiopental and fentanyl, and endotracheal intubation was facilitated by rocuronium. Anesthesia was maintained with isoflurane, fentanyl, and pancuronium. Femoral and radial artery catheters were placed, and pulmonary artery catheterization was performed with an oximetric catheter using the right internal jugular vein. Vital signs before incision were unremarkable. The patient’s abdomen was opened through a bilateral subcostal incision, and multiple dense adhesions were encountered. With portal hypertension, the subsequent adhesionolysis was associated with significant blood loss, and the patient received 16 U of packed red blood cells (PRBCs) and 38 U of fresh frozen plasma. Eventually, the porta hepatis was isolated, and the hepatectomy was completed without incident. After hepatectomy, a temporary end-to-side portocaval shunt was constructed to decompress the portal venous system while work on the right lobe liver graft was completed. Hemostasis at this point in the procedure was excellent, and the patient’s hemodynamic status was unremarkable with blood pressure of 100/70 mmHg, heart rate of 90 beats/min, and pulmonary artery pressure of 28/15 mmHg. Significant laboratory studies revealed a hemoglobin of 6.1 g/dL, and the patient was transfused an additional unit of PRBCs. During the administration of this last unit of PRBCs, the patient became abruptly tachycardic with profound systemic hypotension (to 40/20 mmHg) and pronounced pulmonary hypertension (to 70/40 mmHg) consistent with acute biventricular failure and massive peripheral vasodilatation. On examination, the patient also had a mottled appearance. After several seconds, the patient’s heart rate slowed, and he became asystolic. The blood transfusion was stopped, and resuscitation was initiated with epinephrine. The patient did not respond to a total of 3 mg of epinephrine and 20 units of vasopressin administered over approximately 3 minutes so a midline sternotomy was urgently performed and the patient was placed on cardiopulmonary bypass (CPB). The authors estimate that the patient was without perfusion for 15 minutes. Despite flow of greater than 6 L/min and aggressive pharmacologic support including norepinephrine, 15 g/min, and vasopressin, 0.04 U/min for 5 hours, the patient remained profoundly hypotensive and acidotic (final pH 7.0, base deficit 18) despite treatment with sodium bicarbonate. The patient died secondary to refractory hypotension and the inability to establish a cardiac rhythm. A culture of the blood remaining in the unit of PRBCs at the time of the patient’s cardiovascular collapse revealed Klebsiella pneumoniae in less than 14 hours. An endotoxin assay on the donor blood was markedly positive at 632 EU/mL. A culture of the patient’s blood also revealed K pneumoniae. A transfusion of pooled platelets at another hospital that included the platelet concentrate derived from the same donor unit resulted in a transfusion reaction of an increase in temperature greater than 3°C. Although the fever was attributed to the platelet transfusion, no further evaluation of the platelets was performed. Unfortunately, the platelets were not cultured. The local collection facility contacted the donor who did not report any recent infections and remained asymptomatic. No other follow-up studies were performed on the donor.