Difference between revisions of "Transfusion-related acute lung injury"

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===Pathophysiology===
 
===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>
 
*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'''
+
**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.)
+
**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
 
***Neutrophils release cytokines, reactive oxygen species, etc. that damage pulmonary capillary endothelium
****Leads to '''inflammatory pulmonary edema'''
+
****Leads to inflammatory pulmonary edema
  
 
===Risk factors===
 
===Risk factors===

Revision as of 18:02, 26 July 2016

Background

Abbreviation: TRALI

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

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 Presentation

  • Acute onset hypoxemic respiratory failure due to non-cardiogenic pulmonary edema occurring during or shortly after transfusion
    • Majority of cases present within minutes of initiating transfusion [3]
    • Some present 1-2 hours post-transfusion and up to 6 hours after [13][14]
  • Most common signs/symptoms [15]
    • Hypoxemia
    • New pulmonary infiltrates
    • Pink frothy secretions via ETT
    • Fever
    • Hypotension
    • Cyanosis
  • Other
    • Tachypnea
    • Tachycardia
    • Elevated peak/plateau pressures on ventilator
    • Transient drip in peripheral neutrophil count (from neutrophil sequestration in lung)

Differential Diagnosis

Transfusion Reaction Types

Acute allergic 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

  1. 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
  2. <Looney MR, et al. Transfusion-related acute lung injury: a review. Chest. 2004;126:249
  3. 3.0 3.1 3.2 Silliman CC, et al. Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. Blood. 2003;101:454
  4. Popovsky MA, et al. Diagnostic and pathogenietic considerations in transfusion-related acute lung injury. Transfusion. 1985;25:573
  5. Wallis JP. Transfusion-related acute lung injury (TRALI) - under-diagnosed and under-reported. Br J Anaesth. 2003;90:573
  6. Rana R, et al. Transfusion-related acute lung injury and pulmonary edema in critically ill patients: a retrospective study. Transfusion. 2006;46:1478
  7. Sillman CC. The two-event model of transfusion-related acute lung injury. Crit Care Med. 2006;34:S124
  8. Bux J, et al. The pathogenesis of transfusion-related acute lung injury (TRALI). Br J Haematol. 2007;136:788
  9. 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
  10. 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. 11.0 11.1 Toy P, et al. Transfusion-related acute lung injury: incidence and risk factors. Blood. 2012;119:1757
  12. Benson AB, et al. Transfusion-related acute lung injury in ICU patients admitted with gastrointestinal bleeding. Intensive Care Med. 2010;36:1710
  13. Kleinman S, et al. Toward an understanding of transfusion-related acute lung injury: statement of a consensus panel. Transfusion. 2004;44:1774
  14. Sillman CC, et al. Transfusion-related acute lung injury. Blood. 2005;105:2266
  15. van Stein D, et al. Transfusion-related acute lung injury reports in the Netherlands: an observational study. Transfusion. 2010;50:213