A 23-year-old man with a bleeding femoral fracture is hypotensive and receives a blood transfusion. Immediately after the transfusion starts, he develops fever, chills, severe itching, dyspnoea, stridor, neck swelling, SpO2 75% and bilateral polyphonic rhonchi. EXAM TASKS Identify and justify the event causing deterioration. List the immediate measures. Provide a treatment plan. Give me the best brief answer

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Acute Anaphylactic Transfusion Reaction - Complete Management


1. IDENTIFICATION AND JUSTIFICATION

Diagnosis: Anaphylactic Transfusion Reaction (severe/grade IV)
This is NOT a simple febrile or haemolytic reaction. The clinical picture is anaphylaxis triggered by the blood transfusion, with features of angio-oedema + upper airway obstruction + lower airway bronchospasm + cardiovascular collapse + urticaria - all occurring within seconds to minutes of starting transfusion.
FeatureThis PatientSignificance
Fever + chillsPresentImmune activation
Severe itchingPresentIgE-mediated mast cell degranulation - urticaria
StridorPresentLaryngeal/supraglottic oedema - upper airway emergency
Neck swellingPresentAngioedema
Dyspnoea + bilateral polyphonic rhonchiPresentBronchospasm - lower airway obstruction
SpO2 75%PresentCritical hypoxaemia - life-threatening
Hypotension (pre-existing)PresentDistributive + haemorrhagic shock
Onset: immediately after transfusionPresentClassic anaphylaxis timing
Pathophysiology: Anaphylaxis occurs most commonly in IgA-deficient patients who possess IgA-specific antibodies of the IgE class. Transfused IgA (present in donor plasma) cross-links these IgE antibodies on mast cells and basophils, triggering massive release of histamine, tryptase, and leukotrienes. This causes: (1) systemic vasodilation and capillary leak → hypotension; (2) laryngeal and supraglottic oedema → stridor and neck swelling; (3) bronchial smooth muscle contraction → wheezing and bronchospasm. Haptoglobin deficiency is an alternative mechanism (anti-haptoglobin IgG/IgE). - Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 607
Why not other reactions?
  • Febrile non-haemolytic reaction: fever alone, NO stridor/bronchospasm/angioedema
  • Haemolytic reaction: flank/back pain, haemoglobinuria, DIC - no urticaria or airway oedema
  • TRALI: delayed pulmonary oedema, non-cardiogenic - no urticaria or stridor

2. IMMEDIATE MEASURES

Priority: STOP - CALL - AIRWAY - ADRENALINE
  1. STOP the transfusion immediately - first and non-negotiable step; do NOT resume
  2. Keep the IV line open with normal saline (new giving set)
  3. Call for help - activate resuscitation team / senior anaesthetist
  4. Airway assessment and positioning - sit the patient upright if tolerated; prepare for intubation
  5. High-flow oxygen - 15 L/min via non-rebreather mask targeting SpO2 >94%
  6. Epinephrine (Adrenaline) IM - first-line drug
    • 1 mg/mL (1:1,000) solution, 0.5 mg IM into the anterolateral thigh
    • Repeat every 5 minutes if no improvement
    • If in shock with no response: IV epinephrine infusion 0.1-1 mcg/kg/min
  7. Aggressive IV fluid resuscitation - normal saline boluses (caution in context of ongoing haemorrhage)
  8. Monitor: continuous ECG, SpO2, BP, urine output
  9. Send blood sample back to blood bank + patient identification check
  10. Notify blood bank immediately - return unused blood product for investigation

3. TREATMENT PLAN

Phase 1: Immediate (0-5 minutes)

DrugDoseRouteRationale
Epinephrine0.5 mg (1:1,000)IM (anterolateral thigh)Reverses bronchospasm, oedema, hypotension - first-line
Oxygen15 L/minNon-rebreather maskTreat SpO2 75%
0.9% NaCl500-1000 mL bolusIVVolume replacement for distributive shock

Phase 2: Adjunct Pharmacotherapy (5-15 minutes)

DrugDoseRouteRationale
H1 antihistamine (chlorphenamine)10 mgIV slowReduce urticaria, pruritus - adjunct only
H2 antihistamine (ranitidine)50 mgIVComplement H1 blockade
Corticosteroids (hydrocortisone)200 mgIVPrevent biphasic reaction, reduce oedema - delayed onset
Nebulised salbutamol2.5-5 mgInhaledEpinephrine-resistant bronchospasm
Critical note: Antihistamines and steroids do not act rapidly enough to treat acute anaphylaxis. Epinephrine is the only drug that works fast enough to reverse the life-threatening components. - Rosen's Emergency Medicine, p.3757

Phase 3: Airway Management

  • If stridor persists or worsens despite epinephrine: early endotracheal intubation (do not delay - laryngeal oedema can progress to complete obstruction)
  • Racemic epinephrine (nebulised) may help reduce supraglottic oedema as a bridge
  • RSI with ketamine (maintains BP) + succinylcholine preferred in this haemodynamically unstable patient
  • Have surgical airway (cricothyrotomy) kit at bedside

Phase 4: Haemorrhage Management (concurrent)

  • This patient still has a bleeding femoral fracture - once airway and anaphylaxis are being controlled, orthopaedic/surgical team must address haemostasis
  • Future blood transfusion (if still needed) must use washed red blood cells (plasma-depleted) or IgA-deficient blood products
  • Pre-medicate with corticosteroids + antihistamines 30-60 minutes before any future transfusion

Phase 5: Investigation and Monitoring

  • Serum tryptase: draw within 30 minutes - 6 hours of symptom onset (confirms anaphylaxis)
  • Blood bank: ABO/Rh crossmatch verification, direct antiglobulin test
  • Blood cultures (rule out septic transfusion reaction)
  • FBC, U&E, LFTs, coagulation screen
  • Admit to ICU/HDU for minimum 24 hours (risk of biphasic anaphylaxis)
  • Allergy/immunology referral after discharge: IgA level, anti-IgA antibodies

Future Transfusion Safety

  • Document reaction formally (haemovigilance reporting)
  • Patient requires IgA-deficient blood products or washed cellular products for all future transfusions
  • Provide medical alert bracelet

Summary mnemonic: SAEOC
  • S - Stop transfusion
  • A - Adrenaline (IM 0.5 mg, 1:1,000)
  • E - Epinephrine infusion if shock persists + Ensure airway
  • O - Oxygen + IV fluids
  • C - Corticosteroids + antihistamines (adjuncts)
Sources: Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 607; Rosen's Emergency Medicine, p. 3755-3757; Goldman-Cecil Medicine, Transfusion Reactions chapter
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