A Transfusion Reaction During an Outpatient Infusion
A 68-year-old woman with myelodysplastic syndrome receiving a unit of packed red cells in the infusion clinic develops fever to 39.1°C, chills, and flank pain 15 minutes into the transfusion. Her baseline blood pressure is 128/76 mmHg; now it is 96/58 mmHg with a heart rate of 118. The unit is stopped immediately. The transfusion service receives the returned bag and a post-transfusion EDTA sample. Pretransfusion and post-transfusion plasma samples are both grossly pink. The unit was crossmatched electronically; no antibody screen was performed because the patient had a historical type and screen with no antibodies 2 years ago. She has no history of prior transfusion reactions.
1. What is the most likely category of reaction, and what immediate bedside and laboratory actions are indicated?
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The combination of fever, chills, flank pain, hypotension, and pink plasma in both pre- and post-transfusion samples points to an acute hemolytic transfusion reaction, most likely ABO incompatibility from a clerical or wrong-blood-in-tube error. Immediate actions: stop the transfusion, maintain IV access with normal saline, support blood pressure, monitor urine output, and notify the transfusion service and physician. Laboratory actions: repeat ABO/Rh typing on a new post-transfusion sample and on the returned unit, repeat the antibody screen and crossmatch, perform a direct antiglobulin test, and send a post-transfusion sample for plasma free hemoglobin, haptoglobin, LDH, bilirubin, and urinalysis for hemoglobinuria. The returned bag and tubing should be cultured only if bacterial contamination is suspected. The key judgment is to treat this as acute hemolysis until disproven.
2. The repeat type on the post-transfusion sample is A positive, but the unit label reads B positive. Explain the mechanism and the process failure.
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The patient is group A and received group B red cells. Group A recipients have anti-B antibodies in plasma; transfused group B red cells are coated with B antigen and are rapidly destroyed intravascularly by complement-fixing anti-B, producing fever, flank pain, hemoglobinemia, hemoglobinuria, and hypotension. The process failure is that the unit was issued by electronic crossmatch without a current antibody screen and without a bedside or clerical check that would have caught the ABO mismatch. Electronic issue requires at least two concordant ABO determinations and a valid current antibody screen; relying on a 2-year-old type and screen and skipping the immediate spin or bedside verification defeated the safety barriers. The corrective action is a root-cause review of sample labeling, unit issue, and bedside identification.
3. Two days later the patient's creatinine rises from 0.9 to 2.4 mg/dL and urine output falls. Explain the pathophysiology and the expected laboratory trend.
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Intravascular hemolysis releases free hemoglobin, which is filtered by the glomerulus and precipitates in tubules, causing acute tubular injury and hemoglobinuric acute kidney injury. The kidney also suffers from hypoperfusion during the hypotensive episode and from disseminated intravascular coagulation that can accompany acute hemolysis. Expected laboratory trend: peak hemoglobinemia and hemoglobinuria within hours, falling haptoglobin, rising LDH and indirect bilirubin, a positive DAT (usually IgG and/or C3), and a rising creatinine over 24-72 hours. The direct antiglobulin test may become negative as the incompatible cells are cleared, so a negative DAT does not exclude the diagnosis. Management is supportive: fluids, monitoring, and dialysis if needed; the patient should receive a transfusion alert card and future units must be ABO-identical with a full crossmatch.