Transfusion Related-Acute Lung Injury

A Case Study

Dawn Barten MT(ASCP)

barten@yahoo.com
Dawn.Barten@und.edu

1
Objectives:

1. Obtain a basic understanding of the clinical presentation and

treatment of transfusion-related acute lung injury (TRALI) in a
transfused patient.

2. Obtain a basic understanding of which laboratory tests will aid the

clinician in their diagnosis.

3. Obtain a brief introduction into the pathophysiology of TRALI and

the current proposed mechanisms of TRALI.

4. Review the laboratory work-up of TRALI.

5. Obtain a brief overview of how to prevent TRALI.

2
Patient History:

 A 69 year old male recently diagnosed with

refractory anemia with excess blasts (RAEB) is
returning to his oncologist for a follow up visit.
 Current Treatment(s): Induction phase with
supportive care
 Chief Complaint(s): Weakness and fatigue which
has been increasing during the last week.
 Physician Order(s):
 Complete blood count (CBC)
 Basic metabolic panel (BMP)

3
Laboratory Results:
Test : CBC Patient Reference Test: BMP Patient Reference
Results Range Results Range
2.6x103 /μL 4.5-11.0 Glucose 128 mg/dl 65-99 mg/dl
WBC
x103/μL Creatinine 1.0 mg/dl 0.7-1.20
mg/dl
RBC 2.46x106/μL 4.5-5.9
x106/μL Bun 15.0 mg/dl 8.0-23 mg/dl

7.4 g/dL 13.5-17.5 Calcium 8.5 mg/dl 8.8-10.2

Hemoglobin mg/dl
g/dL
Sodium 138 mmol/L 136-145
Hematocrit 21.8 % 41.0-53.0 % mmol/L
Platelet 7.0x103/μL 150-450 Potassium 3.9 mmol/L 3.5-5.1
x103/μL mmol/L

Neutrophil 63% 40-75 % Chloride 100 mmol/L 98-107

mmol/L
Lymphocyte 27% 20-45 % Bicarbonate 25 mmol/L 22-29
mmol/L
Monocyte 8% 0-12 %
Anion Gap 17 mmol/L 9-18 mmol/L
Eosinophil 1% 0-5 %
Basophil 1% 0-2%
4
Physician Order(s):

 Patient to be admitted for short term observation.

 Type and Cross match for 2 units of leukoreduced packed
red blood cells (LPRBC’s) and one unit of aphaeresis
platelets to be transfused the same day.
 Pre-medicate with Acetaminophen 325 mg and Benadryl
5mg both to be taken orally.
Test Patient Results
ABO/Rh O Positive
Antibody Screen Negative
LPRBC’s 2 units O Pos LRPBC’s are
cross-match compatible and
available
Aphaeresis Platelets 1 unit O Pos platelets available

5
RN Admission Work-up:

 While the blood bank is setting up the blood the

patient goes to the medical floor to be admitted.
After proper identification the nurse proceeds
with her admission work-up.
Assessment Patient results

Blood Pressure 130/85

Pulse 74 beats/ min
Temperature 38.0 °C
Pulse oximetry 99%
Lung sounds Clear
Intravenous line Left forearm
6
Time-line:

 The blood is signed out in the blood bank and per protocol
,the patient is properly identified at the bedside by two
nurses and the transfusion is started.
 He is monitored for the first fifteen minutes. The patient is
tolerating the transfusion well so the nurse continues her
rounds.
 Approximately two and a half hours later the first unit has
finished and the nurse obtains the platelet unit from the
blood bank and the transfusion is started again per protocol.
 After the platelet transfusion is complete there is a delay for
the second unit of LPRBC’s as the nurse is taking care of
another admission.
7
Time-line:
 Thirty minutes post platelet transfusion the patient starts
to complain of shortness of breath. Seeing the patient
struggling for his breath the nurse administers
supplemental oxygen by nasal prongs.
 Re-checking the patients vital signs the nurse finds the
following and the physician is notified.
Vital Sign Patient Results
Blood Pressure 110/70
Pulse 90 beats/minute
Temperature 39.0°C
Pulse Oximetry 90 %
Skin appearance No reddening, rash or
hives
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 Time-line:
After the physician is notified the last unit of LPRBC’s is placed on hold and a
transfusion reaction is initiated.
After another 10 minutes the patient is continuing to deteriorate, vitals are
now:

Vital Sign Patient Results

Blood Pressure 90/50
Pulse 110 (tachycardic)
Pulse Oximetery 85 %
PhysicianLung
orderssounds Rales
the patient to be moved to the critical care unit for possible
initiation of mechanical support.
Orders the following tests: EKG, portable chest x-ray, arterial blood gas
(ABG), creatine kinase-muscle brain (CK-MB), troponin (cTnI), B-natriuretic
peptide (BNP) and d-dimer.

9
Test Results:
Test Patient Results Reference Range
EKG Normal Sinus tachycardia; no Normal Sinus rhythm
evidence of ischemic changes
X-ray extensive bilateral pulmonary Heart and lungs look normal;
infiltrates seen no infiltrates seen
ABG pH
7.312 7.35-7.45

paCO2 47.2 35-45 mmHg

paO2 62.0 80-100 mmHg

SpO2 86.1 95-100%

HCO3 22.3 22-26 mEq/L

B.E -3.9 -2.0-2.0 mEq/L

CK-MB
26 0-23 IU/ml
Troponin
0.252 0-0.2 ng/ml
BNP
61.4 5-100 pg/ml
D-Dimer
0.2 0-0.5 mcg/ml
Transfusion Work-up
Negative Negative

10
Treatment:
 Due to the rapid decline in the patients respiratory
status, the following was initiated.
 Mechanical support
 Ventilator using positive end expiratory pressure (PEEP) of 10
mmHg.
 Invasive hemodynamic monitoring
 Arterial blood pressure of 65/30 mmHg with normal being
110/70 mmHg.
 Central venous pressure (CVP) of 15 mmHg with normal range
being 2-8 mmHg.
 Vasopressure support (agent that produces
vasoconstriction and a rise in blood pressure)
 Dopamine
 Dobutamine
 Non adrenaline 11
Patient Response to Treatment:

 After 48 hours from the onset of respiratory distress his

hemodynamics stabilized and he was removed from
vasopressor support.
 Within 72 hours the patient had responded to
symptomatic measures.
 It took another 2 days for the pulmonary infiltrates to
clear and at this point he was weaned from the ventilator.
 He was then transferred back to a medical room 24 hours
after having been weaned from the ventilator to
continue is recovery under medical supervision.

12
 Transfusion-Related Acute Lung
Injury
 2003 FDA lists it as the leading cause of transfusion
related morbidity and mortality.
 A working group was formed in 2003 by the National
Heart Lung and Blood Institute to arrive at a consensus
definition.
 “TRALI is an acute lung injury temporarily related to
transfusion and is not physiologically different from other
forms of acute lung injury (ALI) or acute respiratory distress
syndrome (ARDS).”
 The plasma fraction of the blood or blood products
appears to cause TRALI rather than the cellular
components.

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 Transfusion-Related Acute Lung
Injury
 Incidence 1/1333- 1/5000 transfusion
 Mortality rates of 5-35% with lower rates of 5-10% being
more common.
 Implicated blood products
 Whole blood–derived platelet concentrates (WB-PLTs)
Fresh frozen plasma (FFP)
Packed red blood cells (PRBCs)
Whole blood (WB)
Apheresis platelet concentrates (A-PLTs)
Granulocytes
Stem cell preparations
Intravenous gamma globulin
Cryoprecipitate

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Clinical Presentation:
 Occurs within 6 hours of the start of the transfusion.
 Usually within 1-2 hours after the start of the transfusion.
 Present with rapid onset of:
 Tachypnea, cyanosis, dyspnea and fever (≥ 1°C)
 Hypotension is commonly reported but not always
consistently found.
 Diffuse crackles and decreased breath sounds.
 Chest x-ray confirms bilateral fluffy infiltrate consistent
with pulmonary edema.
 Other Symptoms include:
 Acute hypoxia and decreased pulmonary compliance even
given near normal cardiac function.
 IDENTICAL TO THAT OF ACUTE LUNG INJURY (ALI)
15
Differential Diagnosis:

 Transfusion associated circulatory overload (TACO).

 Occurs minutes to hours of the start of the
transfusion.
 Similar symptoms: tachypnea, tachycardia and
cyanosis with hypertension. Hypertension is rare in
TRALI but has been reported.
 Responds quickly to aggressive diuretic therapy and
ventilator support.
 Brain natriuretic peptide (BNP) and n-terminal pro-
brain natriuretic peptide (NT-proBNP) are markers for
congestive heart failure.

16
Differential Diagnosis:

 Transfusion associated circulatory overload

 BNP
 They measured the BNP of 80 respiratory failure
patients who also underwent pulmonary catheter
placement.
 BNP level was ≤200 pg/ml it was 91% specific for acute
lung injury. Values ≥1200 pg/ml were 92% specific for
cardiogenic pulmonary edema.

17
Differential Diagnosis:

 Transfusion associated circulatory overload

 BNP
 Zhou et. al. measured BNP levels in 21 patients with
suspected transfusion related cardiac overload. They
obtained pre and post transfusion levels.
 The BNP was considered significant if the post transfusion
to pre transfusion ration was ≥1.5 and the post transfusion
BNP level was ≥200 pg/ml.
 Absence of jugular venous distension and S3 gallop.
 Central venous pressure (CVP) and pulmonary wedge
pressure are normal.

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Differential Diagnosis:

 Anaphylactic transfusion reaction

 Respiratory distress related to bronchospasms
manifested by tachypnea, wheezing, cyanosis and
severe hypotension.
 Facial and truncal reddening of the skin with a rash or
hives is present which are not seen in TRALI.
 Related to laryngeal and bronchial edema rather than
the pulmonary edema seen in TRALI.

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Differential Diagnosis:

 Bacterial contamination of blood components

 Transfusion-related bacterial sepsis.
 Fever, hypotension, vascular collapse which may include
respiratory distress.
 Culturing of implicated blood component will give
negative results and rule this out.
 Hemolytic transfusion reactions
 Some signs and symptoms can mimic TRALI
 Hemolysis noted in the plasma and urine will rule this
out.

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Treatments:

 Identical to Acute lung injury

 Aggressive respiratory support.
 Use of supplemental oxygen and mechanical
ventilation
 Corticosteroids and diuretics do not play a role in
the treatment of TRALI.
 Diuretics may harm the patient by decreasing their
vascular volume.

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Pathophysiology

 Not well understood but they have proposed two

basic mechanisms.
 Most reported cases involve an immune
(antibody) mediated mechanism
 In rare cases where no antibody has been found,
a non-immune mechanism has been proposed.
 A newer third mechanism involving neutropenic
patients is now emerging.

22
 Pathophysiology:
(A) Single clinical event,
infusion of donor
antibodies directed
against host
leukocytes.
(B) Two clinical events, the
first is health condition
of the host which
causes endothelial
activation and
adherence in the lung.
Second the transfusion
of biologic response
modifiers.
(C) Neutropenic patients,
agents that cause
endothelial
fenestration.
http://bloodjournal.hematologylibrary.
org/cgi/reprint/105/6/2266.pdf
23
Pathophysiology:
 Immune (antibody)-mediated TRALI
 In 1970, Ward proposed infusion of donor antibodies to
explain TRALI. Popovsky and Moore confirmed this in 1985.
 89% of cases had donor antibodies to granulocytes and 72%
were antibodies to Human leukocyte antigens (HLA).
 Most granulocyte antibodies did not exhibit specificity, but 59% of
HLA class I antibodies did.
 10% of cases involved binding of recipient antibodies to
cognate antigens on transfused donor granulocytes.
 Infusion of specific HLA antibodies has been confirmed in 50-
60% of documented cases of TRALI.
 This mechanism requires that antibodies bind to the
cognate antigen in the host.
 Causes pulmonary sequestration and activation of PMNs
resulting in the release of cytotoxic agents, endothelial
damage, capillary leak and ALI.
24
Pathophysiology:
 Immune (antibody)-mediated TRALI
 Dykes et al demonstrated a case in which a
women underwent a lung transplant.
 Post transplant she was given two units of packed
red blood cells (PRBC’s).
 Became dyspneic, had marked hypoxia and chest x-ray
revealed a unilateral “white-out” of the transplanted
lung.
 HLA-B44 antibodies were present in the donor of the
second unit of PRBC’s and the cognate antigen was
present in the transplanted lung, but not in the uninvolved
lung.

25
Pathophysiology:
 Immune (antibody)-mediated TRALI
 Animal models
 Ex vivo rabbit model
 Infused a mixture of human PMN’s (HNA-3a (5b) positive),
human HNA-3a antibodies and rabbit plasma for
complement source .
 Pulmonary edema occurred within 3-6 hours post infusion.
 However, if on of the 3 components were missing, the lung
pulmonary edema would not occur.
 Also they found if immunoglobulins with indeterminate antigen
specificity were infused with complement and human PMN’s,
acute lung injury was not reported.
 This study has been recently updated by Brux et al and
demonstrates that using antigranulocyte antibodies and PMN’s
that have cognate antigen does cause pulmonary edema without
the addition of complement.
26
Pathophysiology:
 Immune (antibody)-mediated TRALI
 Constraints with HLA class I and granulocyte
antibodies.
 59% of immunoglobulin's identified demonstrated
antigen specificity.
 50% of the implicated antibodies demonstrated specificity
for recipient antigens.
 Precise mechanism for immune (antibody)-mediated
TRALI is not know.
 Antibodies have been transfused into patients with
cognate antigen on their leukocytes and many did not
acquire TRALI.

27
Pathophysiology:

 Immune (antibody)-mediated TRALI

 HLA class II antibodies have also been implicated.
 Kopko et al and several other groups have postulated
that TRALI can also be caused by infusion of HLA class II
antibodies that have specificity for HLA class II antigens
in the recipient.
 They have also found that these HLA class II antibodies
could activate circulating monocytes that express these
antigens which will cause the synthesis of Tumor necrosis
Factor – α (TNF-α), Interlukin -1β and tissue factor.

28
Pathophysiology:
 Immune (antibody)-mediated TRALI
 HLA class II antigens can be expressed on
endothelial cells, especially after inflammatory
stimuli.
 Researchers question if the infused HLA class II
antibodies into a recipient with cognate antigen
expressed on their pulmonary endothelium will
actually manifest in TRALI.

29
Pathophysiology:
 Immune (antibody)-mediated TRALI
 Constraints with HLA class II antibodies.
 Time delay for the production of the cytokines by
circulating monocytes (4 hours).
 Must have recognition of antibody to specific antigen.
 Resting PMN’s do express HLA class II antigens at a very low
level, or not at all.
 Cytokine-activated PMN’s do express high levels of HLA
class II antigens.

30
Pathophysiology:
 Non Immune (Two-event) model of TRALI
 There are cases documented in which antibodies have
not been detected, either in the recipient or the donor.
 If infusion of specific anti-leukocyte antibodies is
sufficient to cause TRALI, than blood from donors with
specific antibodies against common leukocyte
antigens should cause TRALI in recipients who express
the cognate antigen.
 “Look-back” study of donors who have high titer
“TRALI-implicated” antibodies.
 HLA class I alone, HNA-3a, HLA class I and HLA class II or
HLA class II alone.

31
Pathophysiology:
 Non-Immune (two-event) model of TRALI
 Two-event model was postulated
 First event: Condition of the patient.
 Second event: Is inherent in the blood product.
 Biologic response modifiers
 During storage you have accumulation of lipids.
 Lysophophatdylcholines accumulate in the plasma portion.
 Reach maximal concentration on the day of the components
outdate.

32
Pathophysiology:
 Non-Immune (two-event) model of TRALI
 Two-event model
 Initially verified in an isolated perfused lung model and
then reconfirmed in an in vivo rat model.
 Infused with saline or endotoxin (LPS) as the first event
 Infusion of plasma from stored PRBC’s or antibodies (OX18
and OX27) against HLA class I antigens as second event.
 Both the plasma and the antibodies directed against HLA
class I antigens caused ALI.
 In the saline injected rats neither the plasma from stored
PRBC’s nor the antibodies caused ALI.
 Even if a high titer of monoclonal antibody was used.

33
Pathophysiology:
 Non-Immune (two-event) model of TRALI
 Clinical studies supporting the two-event model.
 The first study identified 4 separate first events.
 Active infection, recent surgery, cytokine therapy and
massive transfusion.
 These have been documented by others in both antibody-
mediated TRALI and TRALI caused by BMR’s.
 Nested case control study also documented involved two
patient groups that were at particular risk for TRALI.
 Those were cardiac surgery patients and those with
hematological malignancies in the induction phase of therapy.
 The second event for the nested case control study was the
infusion of bioactive lipids from the stored products.

34
Pathophysiology:
 Non-Immune (two-event) model of TRALI
 Two-event constraints
 PMNs need to be sequestered in the pulmonary
vasculature.
 “Healthy” patients who experience TRALI would seem to
disprove the two-event mechanism.
 Study of the PMNs from 5 “healthy” donors , by history
demonstrated that their PMNs were grossly primed.
 Determined by the appearance and activity of these PMNs.
 All these donors acquired infections (viral or bacterial) over the
next 24 hours.
 So the question remains, is someone who is receiving a
transfusion considered healthy?

35
Pathophysiology:

 Autologous TRALI case

 No leukocyte antibodies were detected, but there
were measureable amounts of biologic response
modifiers (BRMs) present.
 Neutropenic patients
 Etiology is thought to involve the transfusion of
permeability agents.
 Vascular endothelial growth factor (VEGF) .
 Effective permeability factor.
 Infusion of antibodies against HLA antigens.
 Reside on the pulmonary endothelium.
 Endothelial shape change, and fenestration.
36
Laboratory Work-up:
 Granulocyte immunofluorescence test (GIFT) and
granulocyte agglutination test (GAT) in combination is an
effective approach for detecting PMN reactive antibodies
in serum or plasma.
 Detect both HNA and HLA class I , but further work is
necessary for detection of HLA class II.
 If HNA antibodies are suspected than it is necessary to include
GAT.
 The combination of GIFT and GAT applied to a panel of
phenotyped PMNs allows identification of HNA antibody
specificity.
 These techniques are limited to reference laboratories in
the Granulocyte Working Party (GWP) of the ISBT (
www.isbt-web.org).

37
Laboratory Work-up:
 HLA class I and class II antibody screening methods are
highly sensitive techniques .
 Will detect any antibodies in donor or recipient sera that
could be clinically important leading to graft rejection
and/or graft versus host disease.
 Because HLA antibody screening is widely available it is
often the first step in many TRALI investigations.
 Reports have reveal that only a small number of HLA class I
antibodies actually induce TRALI.
 One questions the clinical relevance of all of the HLA antibodies
detected in TRALI.
 Current flow-based assays are so sensitive that a high percentage of non-
transfused males have demonstrated antibodies
 Also flow-based assays used to detect HLA class II antigens are designed
to detect very small amounts of antibodies and may overestimate the
role of antibodies to HLA class II antigens in TRALI.
38
Laboratory Work-up:
 Investigation of the cognate antigen.
 It is important to do this, but there is great variability in
how TRALI cross-matches are performed.
 Lymphocytotoxicity test (LCT), GIFT alone or GIFT and GAT
combination.
 LCT is based on stable and storable lymphocytes which make them
investigator friendly.
 Are not the primary target cell in TRALI and do not express PMN-
specific antigens (HNA1-2) so will not detect incompatibilities
with these antigens.
 Must interpret the results of this test, if done alone, with these
limitations in mind.
 Confirmation of cognate antigen implies the donor
antibody has a target or substrate to react with, but does
NOT confirm the antibody contributed etiologically to the
TRALI reaction.
39
Laboratory Work-up:
 Investigation of cognate antigen
 Testing of associated donor serum/plasma with the
recipient’s effector cells (PMNs).
 Should employ the incubation using both the GIFT and GAT
techniques.
 If the case involves the antibody being in the recipient than the
cross match should also test recipient serum/plasma with the
donor’s PMNs.
 Especially for granulocyte transfusions.
 PMN cross-match is very valuable.
 Positive cross-match or incompatibilities provide in vitro
evidence of a reaction between recipient PMNs and associated
donor serum/plasma antibodies.

40
Laboratory Work-up:

 Important points to consider

 In determining if an donor antibody did cause TRALI a few
points need to be considered and should continued to be
researched.
 Method of detection
 Antibody titer
 Epitope specificity
 Antibody isotype
 Ability to prime PMN’s that express cognate antigen.
 This detailed antibody information may shed more light on
the role of allo-antibodies in the TRALI mechanism.

41
Laboratory Work-up:

 Investigation of BRMs
 Very few laboratories world wide.
 Research Department at Bonfils Blood Center,
Denver, CO and Australian Red Cross Blood Service,
Brisbane, Australia.
 Have their inherent quirks and require trained
personnel, but are not difficult assays to perform.
 Usually you test samples as part of their research
endeavors.
 If priming activity is found, further identification is
required including lipid identification or measurement of
chemokines by commercial ELISA.
42
TRALI Prevention
 Blood product manipulation
 Washing of cellular blood products does remove all of the
implicated mediators in TRALI.
 Located in the plasma portion.
 Expensive, time consuming and time constraints for critically ill
patients may not allow for the time to remove the plasma from
stored cellular components.
 For scheduled surgical procedures this may be an option.
 In some cases decreases in plasma in the cellular blood
products has been tried but in a number of TRALI cases only
small amounts of plasma are required.
 Pre-storage leukoreduction.
 Does decrease a number of leukocyte and platelet derived
mediators it was NOT effective in inhibiting BRM-mediated
TRALI in vivo.
43
TRALI Prevention:
 Blood product manipulation
 Solvent-detergent plasma (SDP)
 Manufactured from enormous pools of plasma in which
leukocyte antibodies are thought to be diluted and neutralized
during processing, and cellular fragments are removed during
the filtration.
 No cases of TRALI have been reported in Norway since the use of
SDP.
 The use of fresher products
 Used for high risk patients who are not neutropenic.
 PRBCs for less than 14 days and platelet concentrates for less
than 2 days may avert the BRMs.
 Donor selection
 Male predominant plasma.
 Great Britain has had a significant decrease in the total cases of
TRALI, particularly in the cases of fatal TRALI. 44
TRALI Prevention:
 Donor Selection
 Male predominant plasma.
 Disqualification of multiparous females.
 Plasma from females has not been disproportionately
implicated .
 Most data does not support the disqualification of
multiparous females.
 May be disastrous to blood centers where 20-30% of the donor
pool comes from these females.
 Disqualification of donors implicated in TRALI.
 American Association of Blood Banks (AABB) advocates
this until antibody testing can be completed.
 If have antibodies to high frequency leukocyte antigens
 HNA-3a, HLA-A2, HLA-B12. Disqualify from plasma and platelet
donation. 45
TRALI Prevention:
 Donor selection
 Disqualification of donors implicated in TRALI.
 AABB recommendations
 If antibody testing comes back negative
 Reinstate donor.
 Questions that remain
 What is the expense of testing donor s implicated in
TRALI? Who will pay? What will the effect of
deferring all donors in a whole blood platelet pool
and the cost of testing all of them be?
 Multi-institutional prospective studies will help to
answer these and many other questions that exist.

46
TRALI Prevention:

 Donor selection
 Rapid methods of screening for donor HLA and
HNA antibodies appears pertinent, especially for
apheresis donors.
 Cost and time required is not insignificant and many
of the assays employed have a level of sensitivity
related to organ transplantation and have not been
validated for Transfusion Medicine.
 Also, HNA antibody testing is a major hurdle since
there are currently no mass screening technology
available.

47
TRALI Prevention:

 Decreasing blood usage

 This will likely diminish the cases o f TRALI.
 There are a number of unpleasant clinical outcomes
related to transfusion and these must be considered
to maximize patient outcome especially for the
critically ill patients that require transfusions.
 Apply consistent transfusion guidelines.
 Decreases unnecessary transfusions and the
morbidity associated with needless exposure to
blood products.

48
Conclusion
 Transfusion-related acute lung injury
 Causes
 Passive infusion of antibodies against recipient leukocytes.
 Infusion of biological response modifiers (BRMs).
 Infusion of permeability factors.
 Single event antibody mediated mechanism
 Reasonable but questions still remain.
 Occurs without the infusion of specific antibodies against recipient
leukocytes.
 Does not occur when we have an antibody infused in a patient known to
have the cognate antigen.
 Two-event mechanism
 Activation of pulmonary endothelium.
 Sequestration of PMN.
 Activation of those primed sequestered PMN’s.
 Endothelial damage, capillary leak and ALI.

49
Conclusion:

 Transfusion-related acute lung injury

 Variety of testing options to determine TRALI
after the initial reaction.
 Necessary to confirm the presence of an antibody
and cognate antigen.
 Blood product manipulation and donor selections.
 Many options are available, you need to chose what
will work best in your institution.
 Obviously having a consistent transfusion guideline
will help decrease the amount of needless
transfusions and exposure to many adverse
transfusion reactions. 50
 References
1. Haji AG, Sharma S, Vijaykumar DK, Paul J. Transfusion-related acute
lung injury presenting with acute dyspnea: A case report. J. med
Case Reports 2008; 2:336-341.
2. Erol DD, Ahinel L. Transfusion-related acute lung injury (TRALI) in a
multipara patient. The Internet Journal of Anesthesiology 2005;
9(2). Available from:
http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ija/vol
9n2/trali.xml
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