case study info :

  • A 25 year old female suffered a broken femur in a car accident, underwent surgery the next day and received 2 units of packed red blood cells.
  • Patient was extubated after adequate spontaneous ventilation was established. Approximately 3 hours after transfusion and 15 minutes after extubation,
  • Patient’s respiratory rate increased from 12 to 32breaths/minute.
  • Temperature rose from 36.7 to 38.7 C.
  • blood pressure dropped from 120/70 to 101/74.
  • Blood oxygen saturation (Spo2) dropped from 100% to 90%.
  • chest x-ray showed severe pulmonary edema.
  • Patient’s arterial blood gas (ABG) showed hypoxemia With PaO2 of 60 mmHG.
  • Patient’s oxygen saturation was not maintained above 90% with O2 supplementation and patient was reintubated.

laboratory result:

  • Suspected disease : pulmonary/fat embolism, aspiration pneumonitis, pulmonary edema, fluid overload, ARDS and TRALI.
  • Chest X-ray showed massive pulmonary congestion with diffuse infiltrates.
  • hemolysis urine.
  • ETT suction showed blood stained secretions.
  • Supportive measures were taken in the ICU and patient showed improvement clinically.
  • By Post-operative day two, chest x-ray became clear and patient was weaned and extubated.
  • Laboratory studies at the blood transfusion service confirmed the diagnosis of TRALI at a later date.

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Discussion:
There are two distinct mechanisms have been suggested to have caused TRALI which are:-

  1. An antibody-mediated reaction between recipient granulocytes and anti-granulocyte antibodies from donors who were sensitized during pregnancy.
  2. An antibody-mediated reaction between recipient granulocytes and anti-granulocyte antibodies from donors who were sensitized during previous transfusion.
  • TRALI is caused most often when anti-HLA class I and anti-neutrophil antibodies from blood products are passively transfused to a recipient.
  • Less frequent is the recipient antibody reacting to the white blood cells in the transfused blood product.
  • The subsequent antibody-antigen reaction in the recipient activates complement, and C5a produced during complement activation promotes neutrophil aggregation, margination, and sequestration in pulmonary microvasculature.
  • The entry of neutrophils into the lung damages and increases permeability of the pulmonary microvasculature, leading to pulmonary edema. This reaction is likely to occur in multiparous women.
  • Another theory suggest accumulation of lipid product resulting from cell degradation. This pro-inflammatory molecules accumulate during storage of cellular blood products.
  • Suspicion of TRALI should be reported to the blood transfusion service so appropriate action can be taken to prevent future morbidity and mortality in other patients
  • symptoms of TRALI:(Early diagnosis of TRALI is important in the supportive treatment measures)
    • -Dypsnea
    • -Hypoxemia
    • -hypotension
    • -fever along with physical findings of bilateral pulmonary edema, even many hours after the actual transfusions.

Treatment:

  • Treatment of TRALI is largely supportive, and oxygen supplementation is needed in almost all cases. Intubations and mechanical ventilation might be necessary for severe hypoxemia.

Prevention :

  • Donors who have been implicated in TRALI should be permanently deferred or subsequent donations should be limited to the production of frozen-deglycerolized or washed red blood cells.
  • Multiparous donors should be prospectively identified and their blood should be screened for HLA and neutrophil antibodies or diverted for uses other than whole blood, fresh frozen plasma or single-donor apheresis platelets.