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Transfusion-related acute lung injury

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Title: Transfusion-related acute lung injury


1
Transfusion-related acute lung injury
  • Presented by Intern ???
  • Intern ???

2
Transfusion-related acute lung injury
  • Case report
  • Med Sci Monit, 2005 11(5) CS19-22
  • Transfusion-related acute lung injury
  • a literature review
  • Anaesthesia, 2006, 61, pages 777785

3
Case report (I)
  • 56-year-old woman
  • She had undergone a low anterior resection in
    2002 because of a Dukes stage D adenocarcinoma
    of the rectum.
  • In June 2003 she was referred to our department,
    presenting symptoms and signs of ileus.

4
Case report (II)
  • Abdominal radiograph revealed multiple air-fluid
    levels, while a computed tomography scan showed
    disease dissemination.
  • Colonoscopic control verified recurrent disease
    in the anastomotic area.
  • At surgery, a palliative loop ostomy was
    generated.

5
Case report (III)
  • In the 4th postoperative day it was decided that
    one unit of pRBCs be transfused (Hb 7.6 g/dL).
  • Within 35 minutes of the onset of transfusion,
    and having received 40 ml of RBCs, she
    experienced sudden onset of respiratory distress,
    dyspnea, severe hypoxemia (SpO2 lt70), a rise in
    body temperature from 37.2C to 38.4C,
    shivering, tachycardia (120/min), and
    hypertension (190/120 mmHg).

6
Case report (IV)
  • She underwent chest radiograph within the first 8
    h of the episode.

7
Case report (V)
  • After cardiac catheterization, the patients
    cardiac pressures were normal and a
    transesophageal echocardiogram showed normal
    function, with no evidence of left ventricular
    failure or volume overload.
  • A clinical diagnosis of a non-cardiogenic
    pulmonary edema was made.

8
Case report (VI)
  • Hemodynamic stabilization and resuscitation
    required diuretics and a high concentration of
    inspired oxygen in combination with
    bronchodilators.
  • Clinical improvement occurred 12 hours later.

9
Case report (VII)
  • Full recovery of the syndrome was observed in 6
    days, while chest X-ray returned to normal
    findings within 4 days.

4 days after transfusion
8 hrs after transfusion
10
Transfusion-related acute lung injuryN. A.
Barrett and P. C. A. KamAnaesthesia, 2006, 61,
pages 777785
11
Transfusion-related acute lung injury
  • Introduction
  • Definition
  • Incidence
  • Aetiology
  • Pathology
  • Clinical manifestations
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • Conclusion

12
Introduction (I)
  • Transfusion-related acute lung injury (TRALI) is
    a serious and potentially fatal complication of
    transfusion of blood and blood components.
  • The United States Food and Drug Administration
    (FDA) currently estimates it to be the leading
    cause of transfusion-related mortality.

13
Introduction (II)
  • TRALI is under-diagnosed and under-reported
    because of a lack of awareness.
  • Despite the fact that it is estimated to be the
    leading cause of transfusion-associated death,
    little research towards optimising management
    strategies has been undertaken because it is a
    relatively rare condition.

14
Definition (I)
  • Respiratory complications following blood
    transfusion that resemble the syndrome of TRALI
    have been reported since the 1950s.
  • The term transfusion-related acute lung injury
    was proposed in 1983 by Popovsky to refer to
    pulmonary edema complicating blood transfusion.

15
Definition (II)
  • A definition emerged from the TRALI consensus
    conference in 2004 and from the US National
    Heart, Lung and Blood Institute.
  • Acute lung injury (ALI) is defined by the the
    American-European Consensus Committee (AECC) as a
    syndrome based on clinical and radiological
    findings rather than a pathological or a
    pathophysiological diagnosis.

16
Definition (III)
  • The AECC definition of ALI is characterised by
  • Acute onset
  • Hypoxemia (PaO2 / FiO2 300 mmHg at sea level
    regardless of level of positive end-expiratory
    pressure or SpO2 lt 90 on room air)
  • Bilateral pulmonary infiltrates on the frontal
    chest
  • radiograph
  • No clinical evidence of left atrial-hypertension
    or circulatory overload

17
Definition (IV)
  • Risk factors associated with the development of
    ALI include increased age, ethanol or tobacco
    abuse, severe illness, and the presence of the
    variant surfactant B Gene.

18
Definition (V)
  • For a diagnosis of TRALI to be made there must be
    no pre-existing ALI before transfusion, the onset
    of signs and symptoms must occur during or within
    6 h of transfusion and there must be no temporal
    relationship to an alternative risk factor for
    ALI.

19
Definition (VI)
  • If both transfusion and another cause for ALI are
    temporally related, the consensus conference
    recommended that the term possible TRALI be
    used in these cases.

20
Incidence (I)
  • Estimates of the incidence of TRALI include
  • 1 in 5000 blood and blood components transfused
  • 1 in 2000 plasma-containing components
  • 1 in 7900 units of fresh frozen plasma
  • 1 in 432 units of whole blood-derived platelet
    concentrates
  • 1 in 1323 blood components transfused

21
Incidence (II)
  • The FDA estimated that TRALI is the leading cause
    of transfusion-related death in the US.
  • TRALI was a leading cause of transfusion-related
    morbidity and mortality in the UK.
  • The French haemovigilance network reported that
    15 of transfusion related fatalities were caused
    by TRALI.
  • In Germany, 101 out of 765 cases associated with
    complications of blood transfusion that were not
    related to infections were caused by TRALI.

22
Aetiology
  • The antibody-mediated model
  • The two-event (biologically active mediator)
    model
  • Combined model

23
The antibody-mediated model (I)
  • The antibody-mediated model postulates that the
    reaction is secondary to antibodies in donor
    plasma against antigens present on the
    recipients leucocytes.
  • These may be antibodies to the human leucocyte
    antigen (HLA) or to other leucocyte antigens.

24
The antibody-mediated model (II)
  • HLA antibodies may be directed against either HLA
    class I antigens that are present in all
    leucocytes or HLA class II antigens found on B
    lymphocytes and monocytes or infusion of donor
    leucocytes into a recipient whose antibodies are
    directed against these donor leucocytes.

25
The antibody-mediated model (III)
  • The antibodyantigen interaction causes
    complement activation, resulting in the pulmonary
    sequestration and activation of neutrophils,
    endothelial cell damage and a capillary leak
    syndrome in the lungs leading to TRALI.

26
The antibody-mediated model (IV)
  • Rabbit and rat models for antibody-mediated TRALI
    have been developed.
  • This study demonstrated granulocyte sequestration
    within the pulmonary capillaries, extravasation
    of granulocytes into the alveoli and pulmonary
    edema with proteinaceous material in the alveoli.

27
The antibody-mediated model (V)
  • Clinical studies of patients who experienced
    TRALI have demonstrated the presence of either
    anti-HLA or anti-granulocyte antibodies in donor
    plasma.
  • Several look-back studies followed up
    recipients of blood components from a donor
    implicated in a TRALI reaction to determine the
    risk associated with subsequent transfusions from
    such donors.

28
The antibody-mediated model (VI)
  • These look-back studies demonstrated that
    single donors could cause TRALI reactions in more
    than one patient, lending support for the
    antibody-mediated hypothesis.
  • However, blood containing anti-leucocyte
    antibodies may be transfused without causing
    TRALI, indicating that the antibody alone is
    insufficient to cause the syndrome.

29
The antibody-mediated model (VII)
  • There is also evidence that TRALI is commoner in
    recipients of blood products from multiparous
    donors who are more likely to possess anti-HLA
    and anti-HNA antibodies.

30
The two-event model (I)
  • The first event is the clinical condition of the
    patient, resulting in pulmonary endothelial
    activation and neutrophil sequestration.
  • The second event is the transfusion of
    biologically active mediators (lipids,
    anti-granulocyte antibodies) that activate
    adherent neutrophils leading to endothelial
    damage, capillary leak and TRALI.

31
The two-event model (II)
  • The first event can be caused by a variety of
    insults to the pulmonary vascular endothelium
    such as sepsis, cardiopulmonary bypass,
    haematological malignancy, thermal injury and
    trauma.

32
The two-event model (III)
  • Isolated rat lung model
  • Non-cardiogenic pulmonary edema developed
    after the pulmonary vasculature was primed by
    lipo-polysaccharide with subsequent infusion of
    supernatant from 42-day-old red cell concentrates
    and from 5-day-old platelet concentrates.

33
Combined model
  • They suggested that TRALI occurred in patients
    when the pulmonary vascular bed was primed by
    sepsis, trauma or transfusion followed by the
    activation of primed neutrophils by either
    biologically active mediators or by
    anti-granulocyte antibodies leading to pulmonary
    vascular endothelial damage.

34
Pathology
  • Dilation of pulmonary capillaries
  • - Sequestration of granulocytes within the
    capillaries
  • - Extravasation of granulocytes into the
    alveoli
  • - Interstitial and intra-alveolar edema
  • - Presence of proteinaceous material

Blood, Vol. 105, Issue 6, 2266-2273
35
Clinical manifestations and diagnosis
  • Common symptoms and signs
  • - progressive dyspnea
  • - tachypnea
  • - frothy sputum
  • - hypoxemia
  • - hypotension or (rarely) hypertension
  • CXR
  • - Bilateral pulmonary infiltrates
  • - Without cardiogenic pulmonary edema

36
Clinical manifestations and diagnosis
  • Criteria for the diagnosis of TRALI AECC
  • 1. ALI as evidenced by
  • - acute onset of S/S
  • - hypoxemia
  • - bilateral infiltrates on CXR w/o
    cardiomegaly
  • - no clinical evidence of left atrial
    hypertension
  • 2. no preexisting ALI before transfusion
  • 3. within 6 h of transfusion
  • 4. no temporal relationship with an
  • alternative risk factor for ALI

37
Clinical manifestations and diagnosis
  • Laboratory
  • - no specific markers
  • Neutropenia, antileucocyte AbAg pairs
  • ? support the diagnosis
  • high protein in pulmonary edema fluid
  • ? D/D

38
Management
  • Supportive
  • Ceasing transfusion immediately
  • Respiratory support -- varying
  • Hemodynamic support required
  • Diuretics and Corticosteroids -- unproven

39
Prognosis
  • Most patients recover within 4896 h
  • Hypoxemia and CXR change can persist for 7 days
  • Mortality 510

40
Prevention
  • To limit the transfusion of blood products using

41
  • A multicenter, randomised, controlled clinical
    trial of transfusion requirements in critical
    care (NEJM 1999 340 40917.)

42
Prevention
  • For pre-operative strategies
  • - Dietary supplements or erythropoietin
  • - Prevention of hypothermia
  • - Antifibrinolytic drugs

43
Prevention
  • British Committee for Standard in Hematology
  • Red cell transfusion
  • British Journal of Hematology 2001 113 2431
  • FFP transfusion
  • British Journal of Haematology 2003 122 1023
  • Platelet transfusion
  • British Journal of Haematology 2004 126 1128

44
Prevention
  • To donors
  • - permanently disqualified?
  • Multiparous donors
  • - More likely to possess antileucocyte
    antibodies
  • - Higher incidence of TRALI

45
Prevention
  • Shorter periods of blood product storage
  • No evidence support

46
Conclusion
  • TRALI presenting as a spectrum
  • largely unrecognized

47
Complications of Blood Transfusion
  • IMMUNE COMPLICATIONS
  • Hemolytic reactions
  • Acute vs. delayed
  • Nonhemolytic reactions
  • Febrile reactions
  • Urticarial reactions
  • Anaphylactic reactions
  • TRALI (noncardiogenic pulmonary edema)
  • Graft-versus-host disease
  • Posttransfusion purpura
  • Immune supression
  • INFECTIOUS COMPLICATIONS
  • MASSIVE BLOOD TRANSFUSION

48
A Woman Who Developed Acute Pulmonary Edema
During Operation -- A Case Report
  • By R2 ???
  • August 2002

49
(No Transcript)
50
Differential Diagnosis
  • Transfusion-associated circulatory overload
  • Anaphylactic transfusion reactions
  • Transfusion-related bacterial sepsis
  • Immediate hemolytic transfusion reaction

51
Final Thought
The disgnosis of TRALI should be considered in
all cases of respiratory distress with
significant hypoxemia temporally related to a
transfusion and should satisfy the criteria for
diagnosis of ALI.
52
Thanks for Your Attention
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