Journal: Can J Anesth 54(12):1011-1016, 2007. 20 References
Reprint: Toronto General Hospital, University Health Network, Dept of Anesthesia, 3 Eaton North, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada (K Karkouti, MD)
Faculty Disclosure: Abstracted by T. Tilton, who has nothing to disclose.
A case report is made of a 62-yr-old man (95 kg) who underwent urgent coronary artery bypass grafting for known coronary artery disease. His history included two remote myocardial infarctions and several cardiac stents. His medications included clopidogrel, aspirin, metoprolol, simvastatin, remipril, amlodipine, indapamide, and oxazepam. Before initiation of bypass, he received IV tranexamic acid 100 mg/kg. At the time of closure, activated clotting time was normalized and hemostasis was adequate but, given the recent anti-platelet drug use, he received DDAVP 20 mcg IV. After heparin reversal, hemoglobin was 119 g/L, platelet count 154 x 109/L, international normalized ratio 1.5, activated partial thromboplastin time 24 sec, and fibrinogen 2.23 g/L.
Approximately 50 min after ICU admission, 70 mL of blood was in the chest drains and because he had been on anti-platelet drugs, the decision was made to transfuse 5 units of platelets over 15 min; 25 min later, the patient experienced acute hypoxia (trough SpO2 65%) and hypotension (trough BP 55/35 mmHg). Copious frothy pulmonary edema exuded from the endotracheal tube, and bilateral rales were heard with auscultation. Central venous pressure was only 10 mmHg and transesophageal echocardiography showed normal functioning with both ventricles underfilled. Chest x-ray (which was clear preoperatively) showed bilateral, diffuse airspace consolidation. Blood cultures and hemolytic indices were unremarkable so a diagnosis of transfusion-related acute lung injury (TRALI) was made.
Treatment consisted of increasing FIO2 to 100%; increasing positive end-expiratory pressure to 15 mmHg; initiating 20 ppm of inhaled nitric oxide (NO); aggressive fluid administration; infusions of epinephrine, norepinephrine, and dopamine. IV furosemide was administered twice; after each dose the patient’s urinary output increased but was accompanied with decreased blood pressure but no improvement in oxygenation; and prophylactic diphenhydramine and hydrocortisone.
The Canadian Blood Service screened the platelet pool for leukocyte antibodies by granulocyte and lymphocyte immunofluorescence (GIFT and LIFT) using flow cytometry. LIFT was positive and GIFT was negative, which was interpreted as the presence of anti-human leukocyte antigen (HLA). Plasma from 2 of the 5 pooled units demonstrated anti-HLA antibody.
Further blood loss was minimal and no additional transfusions were required. Inhaled NO was discontinued within 48 hours; ventilatory and hemodynamic support was gradually weaned. X-ray findings resolved and the patient was successfully extubated 6 days after the TRALI. He was discharged in good condition 14 days postoperatively.
The pathophysiology of TRALI is not clear and treatment is supportive. According to the Food and Drug Administration and the Canadian Consensus Conference mortality due to TRALI was 16.3% and 17%, respectively. Since no specific treatment exists, the focus must be on prevention. Clinicians should report all TRALI reactions to the source blood banks so that appropriate investigations can identify donors with antibodies who may potentially cause reactions in future recipients. Implicated donors may be excluded from future donations of high plasma-containing components (although TRALI has been reported with blood products containing low plasma volumes such as red blood cells and cryoprecipitate). Other primary prevention policies include using predominantly male plasma (females with prior pregnancy are at higher risk for developing leukocyte antibodies) and avoiding donors with a history of transfusion. The continued recommendation remains to use blood products only when absolutely necessary. |
