transfusion-related acute lung injury
TRANSCRIPT
Pediatr Blood Cancer 2006;46:831
LETTER TO THE EDITORTransfusion-Related Acute Lung Injury
To the Editor: It has been about 20 years since the first
reports of transfusion-related acute lung injury (TRALI) by
Popovsky andMoore [1,2]. Even so,we haveyet to determine
the incidence and mechanisms responsible for the develop-
ment of TRALI, a potentially fatal transfusion reaction. It is
important for clinicians to recognize that TRALI should be
considered in the differential diagnosis in the setting of new
or worsening acute lung injury within 6 hr of a plasma-
containing blood product. Most importantly, one needs to
differentiate TRALI, a non-cardiogenic pulmonary edema
syndrome, from transfusion-associated circulatory overload
(TACO). TACO usually occurs within 2 hr of transfusion.
Infants and recipients over the age of 60 are at increased risk.
The clinical presentation is respiratory distress [3]. The
patient may have increased blood pressure, heart rate, and
central venous pressure as well as an increased wedge
pressure. Unlike TRALI, patients with TACO respond to
diuretics. Clinically useful tests to differentiate between
cardiogenic pulmonary edema and TRALI include B-type
natriuretic peptide (BNP) and determination of the protein
concentration in the pulmonary edema fluid and serum. A
ratio greater than or equal to .75 indicates the fluid to be an
exudate (acute lung injury and permeability edema) rather
than a transudate indicative of cardiogenic pulmonary edema
[4]. TheBNP is a biochemicalmarker of volume and pressure
overload [5,6].
Reporting to the blood bank is imperative for full
evaluation of the suspected TRALI case and potential
work-up, including anti-leukocyte and anti-granulocyte
antibodies in the donor(s) and the recipient, as indicated by
the clinical presentation. In reporting such cases, the blood
banks will be able to keep databases of TRALI evaluations
and will continue to contribute to our understanding of
TRALI. We need more data to establish the mechanism(s)
responsible for TRALI, demonstration of the correlation of
laboratory tests, and prevention of such a potentially fatal
transfusion reaction.
In the case report presented by Koussi et al., the patient
manifested the most common presenting symptom of
respiratory distress (76% in 46 TRALI cases evaluated) [7].
Hypotension and hypertension were each seen in 15% of the
cases [7]. In the case presented, the absence of fluid overload
and marked recovery support a clinical diagnosis of TRALI.
The authors do not mention the human leukocyte antigen
type of the recipient or the anti-leukocyte antibody found in
the multiparous donor. It would be interesting to know
if there was an antigen and antibody match, although even if
there was not, the clinical picture is consistent with TRALI
once cardiogenic edema is ruled out.
Rosa Sanchez, MD*Department of Pediatric Hematology-Oncology
University of California San FranciscoSan Francisco
California
REFERENCES
1. PopovskyMA,AbelMD,Moore SB. Transfusion-related acute lung
injury associated with passive transfer of antileukocyte antibodies.
Am Rev Respir Dis 1983;128:185–189.
2. Popovsky MA, Moore SB. Diagnostic and pathogenetic considera-
tions in transfusion-related acute lung injury. Transfusion
1985;25:573–577.
3. Popovsky M. Circulatory overload. In: Popovsky M, editor.
Transfusion reactions. Bethesda: AABB Press; 2001. pp 255–
260.
4. Fein A, Grossman RF, Jones JG, et al. The value of edema fluid
protein measurement in patients with pulmonary edema. Am J
Med 1979;67:32–38.
5. Tabbibizar R, Maisel A. The impact of B-type natriuretic peptide
levels on the diagnoses and management of congestive heart failure.
Curr Opin Cardiol 2002;17:340–345.
6. Morrison LK, Harrison A, Krishnaswamy P, et al. Utility of a rapid
B-natriuretic peptide assay in differentiating congestive heart failure
from lung disease in patients presenting with dyspnea. J Am Coll
Cardiol 2002;39:202–209.
7. Popovsky MA, Haley NR. Further characterization of transfusion-
related acute lung injury: Demographics, clinical and laboratory
features, and morbidity. Immunohematology 2000;16:157–159.
� 2006 Wiley-Liss, Inc.DOI 10.1002/pbc.20778
——————*Correspondence to: Rosa Sanchez, Department of Pediatric
Hematology-Oncology, University of California San Francisco, 505
Parnassus Avenue, M649 San Francisco, CA 94143.
E-mail: [email protected]
Received 24 December 2005; Accepted 30 December 2005