Hematology Oncology · Year 2 · from Hematology Oncology

Case 1: Acute Hemolytic Transfusion Reaction

Patient Presentation

Demographics: 45-year-old female

Chief Complaint: Fever, back pain, and dark urine during blood transfusion

History of Present Illness: The patient is receiving her second unit of packed red blood cells for symptomatic anemia following GI bleeding. Fifteen minutes into the transfusion, she develops sudden onset fever (39.2C), rigors, severe lower back pain, and chest tightness. The nurse notices her urine in the Foley bag has turned dark red.

Past Medical History:

  • Peptic ulcer disease with acute GI bleed
  • Type A Rh-positive (per hospital records)
  • Prior transfusion 2 years ago without complications

Pre-transfusion Labs:

  • Hemoglobin: 6.8 g/dL
  • Blood type: A positive (documented)

Workup and Results

During Reaction:

  • Blood pressure: 88/52 mmHg (was 118/72)
  • Heart rate: 124 bpm
  • Temperature: 39.2C
  • Dark red urine (hemoglobinuria)

Immediate Investigation:

  • Clerical check reveals error: Unit labeled B positive was issued to A positive patient
  • Direct antiglobulin test (DAT): 4+ positive
  • Plasma: Pink (free hemoglobin)
  • LDH: 1,850 U/L (elevated)
  • Haptoglobin: <10 mg/dL (depleted)
  • Bilirubin: 4.2 mg/dL (rising)
  • PT/PTT: Prolonged (DIC developing)

Clinical Image

Comparison of normal plasma (left) with hemolyzed plasma from acute hemolytic transfusion reaction (right), showing characteristic pink discoloration from free hemoglobin release.

Diagnosis

ABO-Incompatible Acute Hemolytic Transfusion Reaction

Due to clerical error: Type B blood transfused into Type A recipient

  • Anti-B antibodies in recipient immediately attacked donor B red cells
  • Resulting in massive intravascular hemolysis

Discussion

This case illustrates acute hemolytic transfusion reaction:

  • Clerical Error: The lecture emphasizes that ABO incompatibility (clerical error) is the most common cause of acute hemolytic transfusion reactions. This underscores the importance of bedside verification.
  • ABO Antibodies: The lecture explains that naturally occurring ABO antibodies are primarily IgM, which efficiently activate complement causing rapid intravascular hemolysis.
  • Intravascular Hemolysis Markers: The lecture identifies elevated LDH, depleted haptoglobin, hemoglobinemia, and hemoglobinuria as markers of intravascular hemolysis.
  • DIC Risk: The lecture notes that massive hemolysis releases tissue factor and red cell contents, triggering disseminated intravascular coagulation.

Treatment Plan

  1. Immediate Actions:
  • STOP the transfusion immediately
  • Keep IV line open with normal saline
  • Return blood bag and tubing to blood bank
  • Recheck patient identification and unit label
  1. Supportive Care:
  • Aggressive IV fluid resuscitation
  • Maintain urine output >1 mL/kg/hour (preserve renal function)
  • Vasopressors if hypotension refractory to fluids
  1. Laboratory Workup:
  • Recheck ABO/Rh typing
  • Direct antiglobulin test
  • Free hemoglobin (plasma and urine)
  • Coagulation studies (DIC panel)
  • Renal function
  1. Monitoring:
  • ICU admission
  • Serial creatinine (acute kidney injury risk)
  • Serial coagulation studies

Teaching Points

  1. ABO incompatibility from clerical error is the most common cause of acute AHTR
  2. ALWAYS stop transfusion immediately when reaction suspected
  3. ABO antibodies (IgM) cause complement-mediated intravascular hemolysis
  4. Hemoglobinuria indicates intravascular hemolysis
  5. Goal: maintain urine output to prevent hemoglobin-induced AKI

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