HaematologyTier 1Disease (DEADMAN)

Febrile non-haemolytic transfusion reaction

Description

The commonest transfusion reaction
Temperature rise >=1 C from baseline (to >=38 C) during or within 4 hours of transfusion, with rigors/chills, +/- mild dyspnoea or headache
No haemolysis, no hypotension, no organ dysfunction
*A diagnosis of exclusion* - benign in itself, but indistinguishable at onset from a septic or acute haemolytic reaction
- Every febrile reaction must be treated as potentially serious until those are excluded

~0.1-1% of red cell transfusions; higher with platelets (~1-3%) - platelets are stored at room temperature, so cytokines accumulate
Incidence fell substantially with universal leucodepletion
Risk rises with:
- Number of previous transfusions (alloimmunisation)
- Previous pregnancy
- Longer component storage age

Two mechanisms

1. Passively transfused cytokines (the dominant mechanism for platelets)

Residual donor leucocytes in the stored component release IL-1, IL-6, IL-8 and TNF during storage
-> infused directly -> pyrogenic response
Explains why the reaction rate rises with storage age, and why platelets (22 C) are worse than red cells (4 C)
*And why pre-storage leucodepletion works*

2. Recipient antibody against donor leucocyte antigens

Anti-HLA or anti-granulocyte antibodies formed after previous transfusion or pregnancy
-> bind residual donor white cells -> complement activation -> endogenous pyrogen release
This mechanism also underlies platelet refractoriness in the same patients

*Stop the transfusion first, then think.*

Definition

Temperature >=38 C AND a rise of >=1 C from pre-transfusion baseline, during or within 4 h of transfusion
+/- chills, rigors, headache, nausea, mild dyspnoea
In the absence of haemolysis, hypotension, hypoxia or any other explanation

What must be excluded before accepting the label

Alternative	Discriminator
Acute haemolytic transfusion reaction	Hypotension, loin/back pain, haemoglobinuria, DAT positive, free plasma haemoglobin, LDH up, haptoglobin down
Bacterial contamination / septic reaction	High fever with rigors, hypotension, shock, often within minutes. Platelets are the highest-risk component
TRALI	Hypoxaemia + bilateral infiltrates + hypotension
Allergic/anaphylactic	Urticaria, angioedema, bronchospasm; usually afebrile
Underlying infection	Fever pattern predates the transfusion

Investigation of every febrile reaction

Recheck the patient's identity against the unit label (the single most important step)
Return the unit and giving set to the blood bank
Repeat group and screen, DAT, FBE, LDH, bilirubin, haptoglobin, UEC, coagulation screen
Free plasma haemoglobin; urine for haemoglobinuria
Blood cultures from the patient AND culture of the unit
Notify the transfusion service; report to haemovigilance

A. Immediate

Stop the transfusion, maintain IV access with 0.9% sodium chloride
Full set of observations; check identity; examine for hypotension, rash, bleeding, haemoglobinuria
Paracetamol for fever; pethidine for severe rigors
Send the investigations above

B. Restarting

Mild, isolated fever with a completely reassuring assessment: the transfusion may be recommenced slowly with close observation
*Fever with hypotension, rigors, back pain, dyspnoea or haemoglobinuria: do NOT restart. The unit is discarded and worked up.*

C. Preventing recurrence

*Universal leucodepletion is the primary preventive measure* - already standard for all Australian cellular components
Routine pre-medication with paracetamol and antihistamine is NOT recommended
- No evidence of benefit; it masks the early fever of a septic or haemolytic reaction
- Reserve for patients with recurrent, documented febrile reactions
For repeated reactions despite leucodepletion:
- Use fresher components
- Washed (plasma-reduced) platelets - removes accumulated cytokines
- Consider HLA-matched platelets if refractoriness coexists
Slower infusion rate; transfuse where the patient can be observed

Multiply transfused patients - haematological malignancy, marrow failure, chronic transfusion programmes
Multiparous women (anti-HLA antibodies)
Platelet transfusion (room-temperature storage)
Platelet refractoriness - the same anti-HLA alloimmunisation
Post-transfusion purpura, transfusion-associated GVHD (other leucocyte-mediated hazards)
Bacterial contamination and acute haemolytic reaction - the differentials, not associations, but always considered together

Self-limiting - fever settles within a few hours
No long-term sequelae; no organ damage; not life-threatening in itself
Recurrence is common in the same patient - the tendency reflects their alloimmunisation and transfusion burden

The real hazard

*The danger of an FNHTR is diagnostic, not physiological* - assuming it and missing a septic or acute haemolytic reaction
Repeated reactions cause avoidable delays and cancellations of needed transfusions
Suppressing the fever pre-emptively removes the earliest warning sign of a dangerous reaction

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