Transfusion-Associated Acute Lung Injury (TRALI)

(aka Leukoagglutinin-Mediated Pulmonary Edema)

Epidemiology

Incidence: about 8% of critically ill patients develop TRALI in response to blood products (when a 6 hr latency period is used to define TRALI)
Risk Factors
- Sepsis
- History of ETOH Abuse
- Transfusion of Products from Multiparous Females: females with >3 pregnancies
  - 7% of all multiparous females have anti-leukocyte antibodies
- Inceased Number of Blood Products Transfused
- Presence of Anti-Human Leukocyte Antigen Class II Antibodies in Product
- Concentration of Phosphatidylcholine in Product

Has been reported with all blood products
- Probably related to plasma, so is seen more commonly with high plasma volume products, such as FFP and platelets

Mechanism: probably due to donor antibody + recipient antigen in most (95% of) cases
- HLA I antibodies are the most commonly implicated Ab
- Can occur with transfusion of blood or blood products (as little as 50 mL)
- However, in about 5% of cases, recipient’s anti-leukocyte antibodies react against the donor WBC instead
- TRALI does not involve hemolytic transfusion or anaphylactic reactions

Acute Lung Injury-ARDS (see [[Acute Lung Injury-ARDS]])
- Clinical: occurs within 30 min-few hrs after transfusion (as long as 6 hrs after infusion)
  - Dyspnea
  - Cough
  - Fever (see [[Fever]])
  - Hypotension (see [[Hypotension]])
  - Urticarial rash (see [[Urticaria-Angioedema]]): 50% of cases
- Treatment: supportive care

Transfusion-related acute lung injury: Definition and review. Crit Care Med 2005;33:721-26
Transfusion-related acute lung injury in the critically ill. Am J Respir Crit Care Med 2007;176:886-91