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*Department of Intensive Care Medicine and
Department of Hematology and Central Hematology Laboratory, Division of Transfusion Medicine, University Hospital-Inselspital, Bern, Switzerland; and
Blood Transfusion Service, SRC Bern Ltd., Bern, Switzerland
Address correspondence to Lukas Brander, MD, Department of Intensive Care Medicine, University Hospital, Inselspital, 3010 Bern, Switzerland. Address e-mail to lukas.brander{at}insel.ch.
| Abstract |
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| Introduction |
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| Case Report |
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Auscultation of the chest revealed rales, and a chest radiograph was obtained (Fig. 1). Cardiac auscultation and an electrocardiogram were normal. Transesophageal echocardiography performed 45 min after transfusion showed normal myocardial function, intact heart valves, and no evidence of pericardial tamponade. The reaction started after the transfusion and when the FFP bags were no longer available for culture. Blood cultures remained sterile.
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Initial resuscitation procedures comprised mechanical ventilation with positive end-expiratory pressure (15 cm H2O), epinephrine (Table 1), 3000 mL IV fluids, muscle paralysis with vecuronium, meropenem, methylprednisolone, ranitidine, and clemastine. His mean arterial blood pressure increased from 40 mm Hg to more than 60 mm Hg within 30 min and Pao2 increased from 34 mm Hg to 94 mm Hg (Fio2 of 1.0) within 2 h. Bleeding was controlled without any further intervention. The patients condition improved within 25 h of transfusion and he was in excellent condition 1 yr after surgery.
Granulocyte-reactive and agglutinating alloantibodies were detected in the serum of one of the two FFP donors using granulocyte and lymphocyte immunofluorescence and granulocyte agglutination tests. The cross-match with the patients granulocytes and lymphocytes revealed antibodies specific for human leukocyte antigens (HLA) class I. Antibody specificity was confirmed by a glycoprotein-specific enzyme immunoassay (MAIGA).
| Discussion |
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Based on the close timely correlation with FFP transfusion, the acute development and the severity of the oxygenation disturbance, the diffuse bilateral pulmonary infiltrates, the normal echocardiography findings, and the lack of a gradient between diastolic pulmonary artery pressure and pulmonary artery occlusion pressure suggesting increased pulmonary capillary permeability without increased capillary pressure, our initial differential diagnosis included TRALI and septic or anaphylactic shock with acute lung injury. Aspiration of gastric contents was unlikely and extracorporeal circulation, as well as cardiac surgery, were considered as possible predisposing factors.
TRALI was later confirmed by laboratory studies and the FFP donor, a multiparous, never-transfused woman, was precluded from future blood donation.
With TRALI, respiratory impairment normally occurs within 30 minutes to 2 hours, but it may develop as late as 6 hours after transfusion (1,8,9). Symptoms and signs range from mild dyspnea to full-blown respiratory failure, severe hypoxemia, and fever, and may develop suddenly and fulminantly. Severe forms are indistinguishable from the acute respiratory distress syndrome. The most consistent manifestations are dyspnea, cough, fever, diffuse bilateral pulmonary edema on chest radiograph, hypoxemia, leukopenia, and no evidence of heart failure (1).
Acute, severe leukopenia and restoration to marked leukocytosis within 24 hours was present in our case. With TRALI, leukopenia is assumed to be the result of sequestration of leukocytes in the pulmonary circulation, and leukocytosis might result from consecutive activation of the bone marrow to restore the circulating leukocyte pool. Unexplained leukopenia after transfusion may suggest TRALI.
Multiple factors may help explain the marked transient decrease in systemic blood pressure in our patient, such as intravascular hypovolemia (as a result of rewarming after surgery in conjunction with acute, increased permeability pulmonary edema), temporarily impaired systemic vasoregulation after extracorporeal circulation, and, possibly, cardiac dysfunction. We speculate that the initial increase in mean pulmonary artery pressure with normal or only slightly decreased cardiac output (increased pulmonary vascular resistance) might be explained by factors such as hypoxic pulmonary vasoconstriction, positive pressure ventilation, and potentially pulmonary capillary obstruction by agglutinated leukocytes.
Respiratory impairment in conjunction with transfusion of blood products should heighten the clinicians suspicion of TRALI, and cardiogenic pulmonary edema must be excluded. Treatment is nonspecific and includes oxygen supplementation, mechanical ventilation, and hemodynamic support. Local transfusion facilities should trace the donor of suspect blood products and restrict transfusion of blood products from donors with leukocyte-reactive antibodies.
The pathogenesis of TRALI is not completely clear, but alloimmune mechanisms, including donor alloantibodies, have been identified to be directed against granulocytes or human leukocyte antigens (anti-HLA) (1). Implicated blood donors are usually multiparous women with antibodies produced after exposure to paternally derived alloantigens on the fetal leukocytes. In the antigen-positive recipient, leukocytes coated with recipient-type antibodies agglutinate and compartmentalize in the microvasculature of the lungs (10). As transfusion rates of antibody-containing blood components exceed the reported prevalence of TRALI, recipient-related predisposing factors and nonimmunologic mechanisms are currently under investigation (9,11). In the absence of antibodies against neutrophils, biologically active lipids may play an important role in the activation of neutrophils (12).
The true incidence of TRALI is likely to be underestimated (5). Mild to moderate cases might be misdiagnosed as volume overload, and acute lung injury from concomitant circumstances (such as trauma, sepsis, and hemorrhagic shock) might confuse recognition of TRALI. The combination of lack of awareness, high numbers of plasma containing blood products transfused, and the potential severity of the respiratory failure renders patients at risk. Reducing the numbers of blood products transfused by adhering to transfusion guidelines, timely tracing of implicated blood donors, and preclusion of donors with granulocyte-reactive antibodies from future blood donation, may prevent TRALI and potentially saves the lives of future transfusion recipients.
The authors are indebted to J. Wurz for assistance in the preparation of the manuscript.
| Footnotes |
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Accepted for publication February 1, 2005.
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