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
•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
🥇 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)