TRALI

OVERVIEW

Transfusion related acute lung injury (TRALI) is defined as hypoxia and bilateral pulmonary edema occurring during or within 6h of a transfusion in the absence of other causes such as cardiac failure or intravascular volume overload

  • incidence is 1 in 5,000 U of plasma containing products (FFP, platelets or whole blood)

CAUSE

Theories

  1. donor anti-granulocytic antibodies called leukoagglutinins in plasma target recipient leucocyte antigens on neutrophils sequestered in the lungs, resulting in an immune reaction
  2. “biological response modifiers” (BRMs) such as cytokines and biologically active lipids (e.g. in aged cellular components) cause a lung-mediated response

Pathophysiology

“2 hit” model: lung capillaries are primed by an underlying illness  then triggered by exposure to irritant in blood transfusion

  • Step 1: underlying illness -> complement activation -> pulmonary sequestration of neutrophils
  • Step 2: transfusion -> neutrophil activation -> endothelial cell damage and capillary leak syndrome

CLINICAL FEATURES

  • dyspnea
  • hypoxia
  • fever
  • hypotension or hypertension

DIAGNOSIS

  • acute onset ALI(within 6 hours of a transfusion
  • hypoxia (PaO2/FiO2 <= 300mmHg regardless of PEEP or SpO2)
  • bilateral pulmonary infiltrates
  • not cardiogenic in origin (PAWP < 18mmHg)

DIFFERENTIAL DIAGNOSIS

  • acute pulmonary oedema e.g. TACO (transfusion associated circulatory overload), LVF, negative pressure pulmonary edema, neurogenic
  • aspiration pneumonitis
  • inhalational injury
  • ALI/ ARDS due to sepsis or other causes
  • fat embolism
  • diffuse alveolar haemorrhage (expect hemoptysis)

INVESTIGATIONS

  • haemoconcentration
  • hypoalbuminaemia
  • neutropenia or neutrophilia
  • pulmonary fluid analysis (hydrostatic versus capillary leak)

MANAGEMENT

  • stop transfusion
  • respiratory support (may require NIV or intubation)
  • lung protective ventilation if intubated
  • haemodynamic support if needed e.g. noradrenaline
  • supportive care and monitoring
  • no evidence for steroids
  • inform blood bank and haematology

PROGNOSIS

  • most recover within 48-96 hours
  • radiological changes often last 7 days
  • mortality 5%

PREVENTION

  • limit transfusion of blood products
    • preoperative optimization of blood volume (dietary supplements, Fe2+, EPO), prevent hypothermia, use antifibrinolytics, cell salvage
  • avoid donations (especially FFP) from multiparous women

References and Links

  • Gajic O, Gropper MA, Hubmayr RD. Pulmonary edema after transfusion: how to differentiate transfusion-associated circulatory overload from transfusion-related acute lung injury. Crit Care Med. 2006 May;34(5 Suppl):S109-13. PMID: 16617253.
  • Sayah DM, Looney MR, Toy P. Transfusion reactions: newer concepts on the pathophysiology, incidence, treatment, and prevention of transfusion-related acute lung injury. Crit Care Clin. 2012 Jul;28(3):363-72 PMC3380279.
  • Shaz BH, Stowell SR, Hillyer CD. Transfusion-related acute lung injury: from bedside to bench and back. Blood. 2011 Feb 3;117(5):1463-71. PMID: 20944069.
  • Triulzi DJ. Transfusion-related acute lung injury: current concepts for the clinician. Anesth Analg. 2009 Mar;108(3):770-6. PMID: 19224781.

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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