Septic transfusion reaction
Overview
Symptoms begin during or within hours of transfusion. Speed and severity reflect bacterial load and endotoxin concentration.
•Fever - usually >38.5°C, often with rigors
•Hypotension - key distinguishing feature from non-haemolytic febrile reaction (NHFTR); reflects distributive shock
•Tachycardia - compensatory response
•Abdominal pain, nausea, vomiting - visceral manifestation of systemic inflammatory response
•Rigors - intense shivering from cytokine-mediated hypothalamic resetting
•Confusion/reduced GCS - sign of cerebral hypoperfusion; indicates severity
•Progression to septic shock and multi-organ failure if untreated
Investigations
🥇 First-line
•Stop transfusion immediately and retain the blood unit - send for urgent Gram stain and culture
•Blood cultures (x2 peripheral) - before antibiotics if possible, but do not delay treatment
•ABG with lactate - elevated lactate confirms tissue hypoperfusion
•FBC - leucocytosis or leucopenia both possible in sepsis
•U&E/creatinine - AKI is an early complication
•Clotting screen including fibrinogen - DIC can complicate severe reactions
•DAT and repeat group and screen - to exclude concurrent haemolytic reaction
•Urinalysis - haemoglobinuria (pink/red urine) would suggest haemolytic rather than purely septic reaction
🏆 Gold standard
•Culture and Gram stain of the blood product unit - confirms bacterial contamination and identifies organism
Differential diagnosis
Management
Immediate
- 1Stop the transfusion immediately
- 2Retain unit and giving set - return to blood bank for Gram stain and culture
- 3Call for senior/medical help
Resuscitation
- 1IV fluid resuscitation - crystalloid bolus for hypotension
- 2High-flow oxygen
- 3Draw blood cultures x2 peripheral before antibiotics if possible
Treatment
- 1Start broad-spectrum antibiotics promptly - do not delay for cultures if patient is deteriorating
- 2Transfer to HDU/ICU if septic shock (lactate >2 mmol/L, persistent hypotension)
Complications
•Septic shock with multi-organ failure - primary cause of death; occurs rapidly if untreated
•AKI - hypoperfusion and direct bacterial toxin effects
•DIC - endotoxin activates coagulation cascade; bleeding and thrombosis simultaneously
•ARDS - diffuse alveolar damage from systemic inflammation
•Death - significant case fatality rate, particularly with Gram-negative organisms and delayed recognition