transfusion-related acute lung injury

1
Pediatr Blood Cancer 2006;46:831 LETTER TO THE EDITOR Transfusion-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 and Moore [1,2]. Even so, we have yet 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]. The BNP is a biochemical marker 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 Francisco San Francisco California REFERENCES 1. Popovsky MA, Abel MD, 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. ß 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

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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