Year : 2012 | Volume
: 15 | Issue : 1 | Page : 86--87
TRALI: A volley of caution
Department of Internal Medicine/Critical Care, Medwin Hospital, Nampally, Hyderabad, Andhra Pradesh, India
AMC, 3rd Floor, Medwin Hospital, Chirag Ali Lane, Nampally, Hyderabad, Andhra Pradesh 500 001
|How to cite this article:|
Gude D. TRALI: A volley of caution.Ann Card Anaesth 2012;15:86-87
|How to cite this URL:|
Gude D. TRALI: A volley of caution. Ann Card Anaesth [serial online] 2012 [cited 2019 Oct 14 ];15:86-87
Available from: http://www.annals.in/text.asp?2012/15/1/86/91471
Having read with great interest the article by Scott BH on blood transfusion,  I would like to focus on a potentially dangerous complication- Transfusion-related acute lung injury (TRALI). The incidence of TRALI has been estimated to be 0.014%-0.02% per unit transfused (mortality rate of 5%-8%). A study showed that in critically ill medical patients, development of TRALI, apart from prolonged mechanical ventilation, ICU and hospital lengths of stay, is independently associated with decreased long-term survival (74.3% mortality at 2 years).  Plasma from female donors [relative risk (RR) of 19] is associated with an increased risk of TRALI, compared to RBCs from female donors (RR of 1.2). Maternal donation of blood products in paediatric surgeries is a potential risk factor for TRALI because of the development of antileukocyte antibodies during pregnancy. Leucoreduction is shown to cause a substantial reduction in TRALI rate (83%), especially for red blood cell (RBC) and platelet (PLT) transfusions.
Significantly greater accumulation of pulmonary granulocytes and higher serum MIP-2 in mice with severe combined immunodeficiency, upon infusion of anti-MHC (H-2K d ) class I antibody clone34-1-2s, points to the protective role of recipient T and B lymphocytes in suppressing TRALI (perhaps by modulating recipient chemokine production).  Passive transfer of donor antibodies [HLA class I or II or neutrophil antibodies directed against antigens carried on the recipient's (patient's) leukocytes] causes an antigen/antibody interaction resulting in the recipient's neutrophils to be deposited in the alveolar capillaries. The subsequent damage causes fluid leakage into the air spaces resulting in respiratory distress. Neutrophil antibodies (HNA-3a) predominate (22%) TRALI compared to HLA class I or HLA class II antibodies (1%). The "2-hit" model, activation and sequestration of neutrophils in the pulmonary vasculature followed by transfusion of a biologic response modifier such as antileukocyte antibodies, is supported in many studies.
A retrospective cohort study showed that the risk factors for TRALI were emergency cardiac surgery, hematologic malignancy, massive transfusion, sepsis, mechanical ventilation, and high acute physiology and chronic health evaluation II score whereas pneumonia was a negative predictive factor. Also, 90-day survival was lower compared with transfused control subjects and acute lung injury control subjects (53% vs. 75% and 83%).  Another study showed that ICU patients with end-stage liver disease (ESLD) presenting with GI bleed develop TRALI more frequently than those without ESLD (29% versus 1%). Fresh frozen plasma (FFP) is temporally associated with TRALI in 86% of the cases. Patient-specific risk factors include MELD score, admission serum albumin level, and presence of ALI risk factors. 
Three life-threatening (refractory to standard therapy) cases of TRALI are reported to have been successfully treated with ECMO (Extracorporeal membrane oxygenation).
The longer duration of neutrophil sequestration in the lung without concomitant pulmonary capillary damage may cause absence of CXR (Chest X-ray) infiltrates and hence demands higher index of suspicion in all cases of transient acute leukopenia post transfusion (regardless of CXR findings). TRALI could be a devastating complication of transfusions and appropriate preventive strategies and utmost vigilance can help escape its catastrophes.
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