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Anaphylactic Reactions

Anaphylactic reactions can be associated with almost any type of blood component and are life-threatening.
 
Etiology: Absolute IgA deficiency ( < 0.05 mg/dL) or an IgA subclass deficiency puts a patient at higher risk of having an anaphylactic reaction. Approximately 1 in 1200 people are IgA deficient. Such persons may form IgE antibodies against IgA. When anti-IgA antibody binds to IgA in transfused plasma, complement is activated and severe anaphylaxis can occur.


Although IgA deficiency is the most well known cause of anaphylactic reactions, other causes have also been reported.

  • The recipient may have preformed antibodies to transfused allergens, drugs or chemicals
  • Bedside leukoreduction of components for patients receiving ACE inhibitors
  • Transfusion of plasma or platelets to patients with Chido or Rogers antibodies
  • Accumulation of bioactive lipids, CD40 ligand and cytokines in stored products
  • Passive transfer of IgE antibodies or high concentrations of histamine
  • Haptoglobin deficiency

In many cases the cause of the anaphylactic reaction is not identified.

Symptoms: Sudden onset of flushing and hypertension followed by hypotension, tachycardia, widespread edema, laryngeal edema, bronchospasm, shock, and sometimes GI symptoms such as abdominal cramping, nausea, vomiting, and diarrhea can occur within minutes of starting the transfusion.

Consequences: Potentially fatal due to shock or respiratory failure. Early recognition and treatment are critical.

Lab Data: TierOne testing should be performed to rule out a hemolytic reaction. No evidence of RBC serological incompatibility will be found in an anaphylactic reaction. IgA deficiency is diagnosed by measuring quantitative immunoglobulin levels on a pretransfusion specimen. Unfortunately, most nephelometric methods for measuring IgA have a lower limit of detection of 5 mg/dL, which is not sensitive enough to diagnose absolute IgA deficiency. A measureable amount of IgA, rules out an absolute deficiency, which practically excludes the likelihood of an anti-IgA mediated anaphylactic reaction. If IgA is deficient, serum can be sent to a reference laboratory for anti-IgA antibody determination.

Treatment:

  • When an anaphylactic reaction is recognized, the transfusion must be stopped immediately and not restarted
  • The patient should receive airway management and supportive care. Blood pressure and volume should be maintained with crystalloid infusions
  • The attending physician may need to prescribe medications to treat hypotension and bronchospasm

Prevention: Patients with a history of anaphylactic reactions or IgA deficiency with documented anti-IgA antibody should receive only washed red blood cells and platelets. If plasma is needed, it must be obtained from a known IgA deficient donor.

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