Transfusion-related acute lung injury: Difference between revisions
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== | ==Epidemiology== | ||
* | *Leading cause of transfusion related mortality in the US – 5-8% <ref>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</ref><ref><Looney MR, et al. Transfusion-related acute lung injury: a review. Chest. 2004;126:249</ref> | ||
* | *Occurs at a rate of 0.04-0.1%, or 1/5000, transfused blood components <ref name="four">Silliman CC, et al. Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. Blood. 2003;101:454</ref><ref>Popovsky MA, et al. Diagnostic and pathogenietic considerations in transfusion-related acute lung injury. Transfusion. 1985;25:573</ref><ref>Wallis JP. Transfusion-related acute lung injury (TRALI) - under-diagnosed and under-reported. Br J Anaesth. 2003;90:573</ref><ref>Rana R, et al. Transfusion-related acute lung injury and pulmonary edema in critically ill patients: a retrospective study. Transfusion. 2006;46:1478</ref> | ||
** | **Higher in critically ill | ||
==Pathophysiology== | |||
*Two-hit mechanism <ref name="four"></ref><ref>Sillman CC. The two-event model of transfusion-related acute lung injury. Crit Care Med. 2006;34:S124</ref><ref>Bux J, et al. The pathogenesis of transfusion-related acute lung injury (TRALI). Br J Haematol. 2007;136:788</ref> | |||
**'''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''' <ref>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</ref><ref>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</ref><ref name="fifteen">Toy P, et al. Transfusion-related acute lung injury: incidence and risk factors. Blood. 2012;119:1757</ref><ref>Benson AB, et al. Transfusion-related acute lung injury in ICU patients admitted with gastrointestinal bleeding. Intensive Care Med. 2010;36:1710</ref> | |||
**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''' <ref name="fifteen"></ref> | |||
**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== | ==Clinical Features== |
Revision as of 17:38, 26 July 2016
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]
- Higher in critically ill
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
- Neutrophils release cytokines, reactive oxygen species, etc. that damage pulmonary capillary endothelium
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
Transfusion Reaction Types
- Acute
- Delayed
Acute allergic reaction
- Allergic reaction/urticaria
- Anaphylaxis
- Angioedema
- Anxiety attack
- Asthma exacerbation
- Carcinoid syndrome
- Cold urticaria
- Contrast induced allergic reaction
- Scombroid
- Shock
- Transfusion reaction
Evaluation
TRALI vs TACO
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