Acute hemolytic transfusion reaction (AHTR) is a potentially serious complication associated with the transfusion of ABO incompatible blood. It results in disseminated intravascular coagulation (DIC), shock, renal failure and death. Patient misidentification, sample mislabeling are some of the causes of an AHTR. To-date there is no data available on the use of RBCET in the management of an AHTR. We report the clinical course and successful management of an AHTR following massive ABO incompatible blood transfusion. The patient is a 68-year-old female with known coronary artery disease and type O Rh negative blood, who presented to the emergency room with unstable angina. She was taken emergently to the operating room for a quadruple coronary artery bypass graft. Due to sample mislabeling, she received 7 units of incompatible type A Rh negative packed red blood cells (PRBC) intra-operatively. During the immediate post-operative period, she was noted to have increased drainage from the surgical site, decreased urine output, hematuria and a precipitous drop in hemoglobin to 6.5 g/dL. She underwent re-exploration and received an additional 2 units of incompatible type A Rh negative PRBC and other blood products including fresh frozen plasma (FFP), platelets and cryoprecipitate that were ABO incompatible. In the recovery room, family members confirmed her blood type as type O Rh negative. Immediate re-typing utilizing pre-transfusion blood samples collected for CBC and chemistry, and obtaining blood bank records from her previous admission from another hospital a diagnosis of ABO incompatible AHTR was established. Further work-up revealed a strong positive DAT (3+ IgG) with a positive eluate (patient’s anti-A antibodies coating the transfused type A RBC’s). Hemolysis parameters showed elevated LDH 753 IU, bilirubin 2.1 mg/dL, and decreased haptoglobin 29.4 mg/dL. Her urine output continued to decrease with increase in serum creatinine to 2.4mg/dL. A continuous veno-venous hemodialysis (CVVHD) was started along with fluid resuscitation and urine alkalinization. A RBCET was performed within 11 hours after the transfusion of the last incompatible unit, which was followed by a second RBCET 24 hours later. Each RBCET consisted of 8 units of type O Rh negative blood. Following the two RBCET her blood type became type O Rh negative. Hemolysis parameters improved over the next several days and became normal. Serum creatinine progressively improved with increasing urine output. Dialysis was discontinued on day 13. Patient continued to do well and was discharged home in good condition with a normal renal function three weeks after her initial admission. The severity and course of an AHTR is dictated by the load of incompatible blood cells in the circulation. The high mortality rate associated with an AHTR warrants an aggressive approach in addition to supportive care. RBCET is used in the management of severe hemolytic disease of the new born, complications of sickle cell disease, and to lower the parasite load in malaria and babesiosis. The role of RBCET in AHTR is not established. There are two case reports in the Japanese literature where a RBCET was performed in the management of an AHTR with successful outcome. The course of this patient suggests that aggressive management including supportive care, timely RBCET, and renal replacement treatment may prevent DIC, organ damage and alter the grave prognosis associated with AHTR following incompatible blood transfusion.
Disclosure: No relevant conflicts of interest to declare.