Anaphylactic Transfusion Reaction

Anaphylactic transfusion reaction is a severe immediate hypersensitivity reaction to a blood component, with hypotension, bronchospasm, laryngeal oedema and urticaria, beginning within seconds to minutes of starting a transfusion (usually after under 100 mL).

Epidemiology. Severe anaphylaxis occurs in about 1 in 20,000 to 1 in 50,000 transfusions, and milder allergic reactions (urticaria alone) in 1 to 3%. Plasma containing products (plasma, platelets) are implicated more than red cells.

Causes.

• Anti-IgA antibodies in IgA-deficient recipients (selective IgA deficiency affects about 1 in 500 to 1 in 700 people, and only a minority have anti-IgA).
• Antibodies to other plasma proteins (haptoglobin deficiency, C4, albumin, other), and passive transfer of allergen or antibody from the donor (for example peanut).
• Allergens in components, including drugs and ethylene oxide residues.

Pathophysiology. Antigen antibody complexes or immunoglobulin E activate mast cells and complement, releasing histamine, tryptase and leukotrienes, with vasodilation, bronchospasm, mucosal oedema and cardiovascular collapse.

Presentation is flushing, urticaria, angioedema, wheeze, stridor, abdominal pain, vomiting, diarrhoea, hypotension, tachycardia and collapse. Fever may be absent. Early mild features may progress.

Red flags.

• Stridor, wheeze or hypotension within minutes of starting transfusion.
• Known IgA deficiency or previous severe reaction.
• Reaction during anaesthesia (hypotension and bronchospasm only).

Diagnosis is clinical. Stop the transfusion, recheck the identity of the patient and the component, and keep the bag. Measure serum tryptase (at 1 to 2 hours, with a baseline after 24 hours) and send a direct antiglobulin test, haemolysis screen and full blood count to exclude haemolysis. Later, measure IgA level and anti-IgA antibodies, haptoglobin and specific plasma protein antibodies.

Differential diagnosis. Acute haemolytic reaction, transfusion related acute lung injury, transfusion associated circulatory overload, bacterial contamination, hypotensive reaction and unrelated anaphylaxis (drug, latex, contrast).

Stop the transfusion and keep IV access with 0.9% sodium chloride.

Adrenaline. 0.5 mg IM into the anterolateral thigh (0.5 mL of 1 mg/mL) for adults and children over 12 years, 0.3 mg for 6 to 12 years, 0.15 mg for 6 months to 6 years, repeated every 5 minutes if needed. Give oxygen 10 to 15 L/min and lay the patient flat with legs raised.

Fluids. Rapid IV crystalloid 500 to 1000 mL (20 mL/kg in children), with reassessment.

Refractory shock. Adrenaline infusion 0.05 to 0.1 microgram/kg/min, nebulised adrenaline 5 mg for stridor, salbutamol 5 mg nebulised for bronchospasm, and early intubation for airway oedema.

Adjuncts. Chlorphenamine 10 mg IV slowly and hydrocortisone 200 mg IV, which do not replace adrenaline.

Mild reactions (isolated urticaria or itch). Pause, give chlorphenamine 10 mg IV, and resume the transfusion at a slower rate only if symptoms settle fully and no airway, respiratory or circulatory sign has appeared. Stop permanently for any systemic feature.

Future transfusions.

• Washed red cells and platelets, or IgA-deficient donor plasma products, for confirmed anti-IgA.
• Premedication has limited evidence. Allergy and transfusion specialists decide the plan.
• Carry an alert card, and give a written report to the patient.

Reporting. Notify the transfusion service and haemovigilance system.

Monitoring. Continuous ECG, blood pressure and oximetry. Observe for at least 6 hours, and 12 to 24 hours for severe reactions, because biphasic reactions occur.

Referral and escalation. Intensive care for refractory shock or airway oedema, haematology or immunology for follow up.

Special groups. In patients with known IgA deficiency, flag the record and arrange washed components in advance. In children, weight based adrenaline (0.01 mg/kg IM).