Hematology · Transfusion Medicine
The facts most likely to be tested
Acute hemolytic transfusion reaction (AHTR) is caused by ABO incompatibility resulting in intravascular hemolysis mediated by preformed IgM antibodies.
The classic clinical triad of AHTR consists of fever, flank pain, and hemoglobinuria occurring within minutes to hours of transfusion.
Hypotension, disseminated intravascular coagulation (DIC), and acute kidney injury (AKI) are the most severe life-threatening complications of AHTR.
The immediate first step in any suspected transfusion reaction is to stop the transfusion and maintain IV access with normal saline.
Direct Coombs test (direct antiglobulin test) will be positive in cases of hemolytic transfusion reactions due to antibody-coated donor red blood cells.
Delayed hemolytic transfusion reaction (DHTR) typically occurs 3–10 days post-transfusion and is caused by an anamnestic response to minor red cell antigens (e.g., Kidd, Rh).
Laboratory findings in AHTR include elevated LDH, elevated indirect bilirubin, decreased haptoglobin, and positive plasma hemoglobin.
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A 45-year-old female is undergoing a routine blood transfusion for symptomatic anemia. Ten minutes after the infusion begins, she develops chills, rigors, and severe flank pain. Physical examination reveals a temperature of 102.4°F (39.1°C), a blood pressure of 88/52 mmHg, and a heart rate of 118 bpm. A Foley catheter is placed, and the urine appears dark red/cola-colored. Laboratory studies reveal elevated LDH and decreased haptoglobin.
What is the most likely diagnosis?
Acute hemolytic transfusion reaction (AHTR)
The patient's presentation of fever, flank pain, and hemoglobinuria (cola-colored urine) shortly after transfusion is pathognomonic for AHTR, which is tested by the classic triad of symptoms and the mechanism of ABO incompatibility.
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High yield triage
Etiology / Epidemiology
Caused by ABO incompatibility due to clerical error. Results in acute intravascular hemolysis.
Clinical Manifestations
Classic triad: fever, flank pain, and dark urine. Hypotension and DIC are red flags.
Diagnosis
Confirmed by Direct Coombs test. Look for hemoglobinemia and hemoglobinuria.
Treatment
Stop transfusion immediately and initiate aggressive IV fluids to maintain renal perfusion.
Prognosis
Risk of acute kidney injury (AKI) and multi-organ failure. Mortality is high if unrecognized.
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Epidemiology & Etiology
Most cases result from clerical error (wrong blood to wrong patient). It is a type II hypersensitivity reaction occurring within minutes to hours of transfusion.
Pertinent Anatomy
The reaction involves the renal tubules, where filtered free hemoglobin precipitates, leading to obstruction and tubular necrosis.
Pathophysiology
Preformed recipient antibodies (IgM) bind to donor RBC antigens, activating the complement cascade. This leads to massive intravascular hemolysis, release of cytokines, and activation of the coagulation cascade.
Clinical Manifestations
Patients present with fever, flank pain, and dark urine (hemoglobinuria). Watch for hypotension, tachycardia, and signs of DIC (oozing from IV sites). Back pain is a classic board buzzword.
Diagnosis
The Direct Coombs test is the gold standard for diagnosis. Laboratory findings include elevated LDH, decreased haptoglobin, and hemoglobinemia.
Treatment
Stop the transfusion immediately and maintain venous access with normal saline. Administer IV fluids to promote diuresis and prevent renal failure. Do not use diuretics until volume status is stabilized.
Prognosis
Primary concern is acute kidney injury (AKI) due to hemoglobin-induced tubular toxicity. Early recognition is critical to prevent multi-organ failure.
Differential Diagnosis
Febrile non-hemolytic: fever without hemolysis or flank pain
TRALI: respiratory distress and pulmonary edema within 6 hours
TACO: volume overload with hypertension and JVD
Delayed hemolytic: occurs days to weeks post-transfusion
Anaphylactic reaction: rapid onset of wheezing and angioedema