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Background
Epidemiology
- Leading cause of transfusion related mortality in the US – 5-8% [1][2]
- Occurs at a rate of 0.04-0.1%, or 1/5000, transfused blood components [3][4][5][6]
Pathophysiology
- Two-hit mechanism [3][7][8]
- Neutrophil sequestration and priming in lung microvasculature
- Recipient neutrophil activation by factor in the blood product (i.e. antibodies in blood component directed at recipient antigens, bioactive lipids, etc.)
- Neutrophils release cytokines, reactive oxygen species, etc. that damage pulmonary capillary endothelium
- Leads to inflammatory pulmonary edema
Risk factors
- Recipient factors [9][10][11][12]
- Liver disease
- Hematologic malignancy
- Alcohol abuse
- High peak airway pressures on mechanical ventilation
- Current smoking
- Positive fluid balance
- Massive transfusion
- Critical illness
- Sepsis
- Shock
- Blood component factors [11]
- Plasma or whole blood from female donor
- Volume of HLA class II antibody reactive to recipient HLA antigen
- Volume of transfused anti-human neutrophil antigen antibody
- Highest risk components (though can occur with any, including PRBC)
- Plasma
- Apheresis platelet concentrates
- Whole blood
Clinical Features
- Time Frame: abrupt to within 6 hours of transfusion initiation
- ARDS-like symptoms
Differential Diagnosis
Evaluation
|
TRALI
|
TACO
|
Onset |
Acute, within 6hrs |
Often more gradual
|
BP |
Low |
High
|
Temp |
Febrile |
Normal
|
JVD/pedal edema |
Unlikely |
Likely
|
CVP/PAWP |
Normal |
Elevated
|
BNP |
Normal |
Elevated
|
Resp |
Dyspneic |
Dyspneic
|
CXR |
B/l infiltrates |
B/l infiltrates
|
Management
- Strop transfusion
- Treat like ARDS
- Avoid diuresis
Disposition
- Bilateral pulmonary infiltrates due to noncardiogenic pulmonary edema within 6h of transfusion
See Also
External Links
References
- ↑ Fatalities Reported to FDA Following Blood Collection and Transfusion: Annual Summary for Fiscal Year 2011. Available at www.fda/gov/biologicsbloodvaccines/safetyavailability/reportaproblem/transfusiondonationfatalities/ucm302847.htm
- ↑ <Looney MR, et al. Transfusion-related acute lung injury: a review. Chest. 2004;126:249
- ↑ 3.0 3.1 Silliman CC, et al. Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. Blood. 2003;101:454
- ↑ Popovsky MA, et al. Diagnostic and pathogenietic considerations in transfusion-related acute lung injury. Transfusion. 1985;25:573
- ↑ Wallis JP. Transfusion-related acute lung injury (TRALI) - under-diagnosed and under-reported. Br J Anaesth. 2003;90:573
- ↑ Rana R, et al. Transfusion-related acute lung injury and pulmonary edema in critically ill patients: a retrospective study. Transfusion. 2006;46:1478
- ↑ Sillman CC. The two-event model of transfusion-related acute lung injury. Crit Care Med. 2006;34:S124
- ↑ Bux J, et al. The pathogenesis of transfusion-related acute lung injury (TRALI). Br J Haematol. 2007;136:788
- ↑ Vlaar AP, et al. Risk factors and outcome of transfusion-related acute lung injury in the critically ill: a nested case-control study. Crit Care Med. 2007;176:886
- ↑ Gajic O, et al. Transfusion-related acute lung injury in the critically ill: prospective nested case-control study. Am J Respir Crit Care Med. 2007;176:886
- ↑ 11.0 11.1 Toy P, et al. Transfusion-related acute lung injury: incidence and risk factors. Blood. 2012;119:1757
- ↑ Benson AB, et al. Transfusion-related acute lung injury in ICU patients admitted with gastrointestinal bleeding. Intensive Care Med. 2010;36:1710