Acute haemolytic transfusion reaction

Overview

Caused by ABO-incompatible blood - almost always human error (mislabelled sample, failed identity check)
Preformed IgM anti-ABO antibodies → classical complement activation → intravascular haemolysis + macrophage cytokine release → fever, pain, shock

Presentation

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Classic exam triad: fever + pain (abdominal/chest/back) + hypotension during active transfusion. Pain is the discriminating feature - separates AHTR from febrile non-haemolytic reaction (fever only) and TACO (hypertension + pulmonary oedema).
Fever and rigors - cytokine-mediated; rise ≥1.5°C
Pain - abdominal, chest, back/flank, or infusion site; hallmark distinguishing feature
Hypotension and tachycardia - cytokine-mediated vasodilation and shock
Haemoglobinuria - dark red/brown urine; hallmark of intravascular haemolysis
Feeling of apprehension - early symptom; patient reports 'something is wrong' before objective signs
Oozing from wounds/puncture sites - indicates evolving DIC
Symptoms can begin after as little as 5-10 mL of incompatible blood

Investigations

Bedside identity check - most important immediate step; verify patient against blood unit label
Direct antiglobulin test (DAT/direct Coombs) - detects antibodies/complement on red cells; typically positive in AHTR
Repeat ABO typing and crossmatch - discrepancy confirms mismatch
FBC - falling Hb confirms haemolysis
LDH and unconjugated bilirubin - both rise with red cell destruction
Urine dipstick - haemoglobinuria
U&E and clotting screen - detect evolving AKI and DIC

Management

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Do NOT wait for results - stop the transfusion immediately and resuscitate. Investigations run in parallel.

🥇 First-line

Stop transfusion immediately - keep IV access patent; return unit and giving set to blood bank
IV 0.9% sodium chloride - maintain circulating volume and renal perfusion; target urine output ≥100 mL/hour
Urinary catheterisation - monitor urine output and detect haemoglobinuria
Notify blood bank urgently - repeat identity checks, withdraw associated components

🥈 Second-line

Mannitol (forced diuresis) - if urine output inadequate despite adequate fluid resuscitation
Vasopressors - distributive shock unresponsive to fluids

🥉 Third-line

Renal replacement therapy - if established oliguric/anuric AKI
FFP, cryoprecipitate, or platelets - if DIC develops

Complications

AKI - free haemoglobin directly toxic to renal tubules; tubular obstruction and renal vasoconstriction
DIC - complement/cytokine activation triggers coagulation cascade; thrombocytopaenia, elevated PT/APTT, low fibrinogen, wound oozing
Distributive shock - massive cytokine-driven vasodilation; may require vasopressors and ITU
Death - up to 10% mortality in severest reactions (e.g. group O receiving group A blood)