A high index of suspicion is needed to make the diagnosis of TRALI. The diagnosis of TRALI is primarily clinical and radiographic. As per the Canadian consensus conference, the diagnosis of TRALI is “not dependent on the results of laboratory tests or any proposed pathophysiologic mechanisms”
The symptoms commonly occur within 2 hours after the start of transfusion, with almost all reactions occurring by 6 hours. These symptoms may be rather severe and include dyspnea, hypoxemia, cyanosis, bilateral pulmonary edema, cough, fever, and chills. Both hypertension and hypotension have been reported in the presence of normal cardiac function. The hypotension may be unresponsive to intravenous fluid administration. Production of voluminous frothy secretions and an increase in airway pressures in intubated patients have also been noted. Radiographs of the chest show findings typical of ARDS. The pulmonary edema may be initially localized to the dependent or perihilar areas of the lungs, but more often it becomes generalized relatively rapidly with both alveolar and interstitial infiltrates, without cardiac enlargement or engorged
pulmonary vessels, also noted on radiography are the absence of cardiac enlargement and pulmonary vascular engorgement. Occasionally, a florid radiologic picture exists. This is described as “white out” of the lungs. The radiographic severity of lung injury often contrasts dramatically with the minimal auscultatory findings physical examination.
The central principle for diagnosing TRALI is exclusion of hydrostatic (cardiogenic) pulmonary edema. In the setting of blood transfusion, hydrostatic pulmonary edema occurring within 6 hours is referred to as transfusion-associated cardiac overload. The clinical manifestations of transfusion-associated cardiac overload include tachypnea/respiratory distress, cyanosis, tachycardia, and hypertension. Other conditions that are considered in the differential diagnosis of TRALI include allergic/anaphylactic reactions and transfusion of contaminated blood products.
The central venous and wedge pressures are typically low or
normal in TRALI but may be elevated if TRALI occurs in the setting of heart failure. Serum B type natriuretic peptide (BNP) levels may or may not be helpful in excluding cardiogenic edema, as elevated BNP levels have been reported in patients with ALI in the absence of left ventricular dysfunction. Finally, sampling of pulmonary edema fluid, shortly after lung injury, from the endotracheal tube (if present) may help in determining the etiology of the fluid. Pulmonary edema fluid in TRALI, like other causes of pulmonary capillary leak, has an elevated protein content.
Arterial blood gas analysis shows hypoxia, where a PaO2/FiO2 ratio less than 300 is consistent with ALI. Laboratory findings may also include hemoconcentration, leukopenia, neutropenia, hypocomplementemia, and hypoalbuminemia. The leukopenia is transient and thought to result from aggregation of circulating leukocytes in the pulmonary vasculature.
Serologic tests are important in confirming the diagnosis of TRALI. The basic principle is examination of sera from the donor for anti-HLA or anti-HNA antibodies. HLA antibody testing methods include lymphocytotoxicity, leuko-agglutination, and the flow panel reactive antibody assays. This latter method can detect antibodies as well as identify their specificities and is more sensitive than other techniques. Evaluation of neutrophil specific antibodies entails granulocyte agglutination and granulocyte immunofluorescence assays; notably, this latter assay does not necessarily distinguish between HLA I and HNA antibodies. DNA typing of granulocyte antigens may also be done. Although testing for neutrophil-priming activity and for antibodies in the recipient may provide important information about TRALI etiogenesis, they are not considered as part of the routine work-up.
Notification of the blood bank is advised to further evaluate the donor and their blood products for future donation or transfusion. Per the Canadian consensus conference, a donor can be considered as implicated in a TRALI reaction only if they are found to have anti-HLA or anti-HNA antibodies that are specific for antigens on the recipient’s leukocytes or via a positive cross-match.
Ref : Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008
My mother was recently diagnosed with this. Currently, she is intubated in ICU and waiting for her lungs to heal, if they will heal. She is only receiving male blood products since this has happened. As if battling Lymphoma wasn't enough, now this. I know sometimes blood products can be short supply... but prevention goes a long way. Why not have precautionary measures, and only give male blood products to someone who is already immunocompromised? This just adds insult to injury. More people should be aware of this, especially female recipients of blood transfusions.
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