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REVIEW ARTICLE
Year : 2008  |  Volume : 52  |  Issue : 2  |  Page : 126-131 Table of Contents     

TRALI - A Less Commonly Known Complication of Transfusion


1 Associate Professor, Department of Anaesthesiology & Critical Care, S. N. Medical College, Jodhpur, India
2 Professor and Head, Department of Anaesthesiology & Critical Care, S. N. Medical College, Jodhpur, India

Date of Acceptance22-Feb-2010
Date of Web Publication19-Mar-2010

Correspondence Address:
Pradeep Bhatia
A 54/3, Arvind Nagar, Golf Link Road, Jodhpur 342011
India
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Source of Support: None, Conflict of Interest: None


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Transfusion Related Acute Lung Injury (TRALI) has been recently recognized as one of the serious risks associated with transfusion, presenting as respiratory distress during or after transfusion of blood products. The symptoms can be confused with other transfusion-related events such as anaphylaxis, haemolysis, or circulatory overload, or with non-transfusion-related co­morbidities such as cardiac failure. TRALI varies in severity, and mortality is not uncommon. TRALI is now the leading cause of transfusion-associated mortality, even though it is probably still under-diagnosed and under-reported due to lack of awareness of its entity.

Keywords: Transfusion; Complication; Lung injury; TRALI


How to cite this article:
Bhatia P, Tulsiani K L. TRALI - A Less Commonly Known Complication of Transfusion. Indian J Anaesth 2008;52:126-31

How to cite this URL:
Bhatia P, Tulsiani K L. TRALI - A Less Commonly Known Complication of Transfusion. Indian J Anaesth [serial online] 2008 [cited 2019 Dec 15];52:126-31. Available from: http://www.ijaweb.org/text.asp?2008/52/2/126/60610


   Introduction Top


Although the blood transfusion has become safer with regard to transmission of infectious agents, Trans­fusion-Related Acute Lung Injury (TRALI) is now rec­ognized as an important and potentially preventable clini­cal syndrome. The first case series describing TRALI was published by Popovsky and Moore in 1985[1] and describe it as a constellation of clinical and laboratory features (respiratory distress, hypoxemia and bilateral parenchymal infiltrates, in absence of congestive heart failure) seen within 6 hrs of the transfusion of plasma­containing blood products. Many clinicians are still un­aware of TRALI and may not recognize it when it oc­curs.


   Definition Top


A Consensus Conference was convened in Toronto, Canada, in April 2004, titled "Towards an Un­derstanding of TRALI". Canadian Blood Services and Hma-Qubec sponsored the conference, with support from the International Society of Blood Transfusion's Biomedi­cal Excellence for Safer Transfusion (BEST) subcom­mittee. Numerous experts presented data to approxi­mately 240 international attendees, including a Consen­sus Panel of 11 members representing a wide range of medical and other disciplines including specialists in trans­fusion medicine, epidemiology, immunology, anaesthesiology, critical care medicine, and ethics, as well as a regular blood donor and a chronic transfusion recipient.

TRALI, as defined by the "Canadian Consensus Conference Panel on TRALI" [2] and by "National Heart, Lung, and Blood Institute (NHLBI) Working Group on TRALI" [3] is new acute lung injury (ALI) within six hours of a completed transfusion. Applying this definition, TRALI is a clinical syndrome, rather than a disease with a single aetiology. The ALI criteria for the definition of hypoxemia have been expanded in the Consensus Panel definition of TRALI. For clinical investigations hypox­emia is defined as a ratio of the partial pressure of oxy­gen to the fractional inspired oxygen concentration (PaO2/FiO2) of less than 300 mmHg [4] or as an oxygen saturation measured by pulse oximetry of less than 90 percent when a patient is breathing room air [2] . More re­cent data suggest that the process of lung injury may develop more rapidly than previously thought, within one hour of transfusion in up to 90% of cases [2] .


   Incidence Top


TRALI is now the most commonly reported cause of transfusion-related death in the United States, sur­passing deaths caused by ABO incompatibility and bac­terial contamination [5] . The incidence of TRALI has not been well established. The syndrome is severely under­recognized and under-reported because of a lack of sen­sitive and specific diagnostic criteria and poor aware­ness of the syndrome outside blood banks [6] . TRALI may be insufficiently investigated [7] , and mild or moderate cases may not be investigated or reported at all [8] . Since 1985, the number of TRALI cases reported in the literature has increased significantly with improved recognition of the syndrome.

The incidence reported in 1985 was 1 in 5000 U transfused at the Mayo Clinic [1] . Rates reported in the literature vary widely from 1 in 432 to 1 in 88,000 per platelet transfusion, and 1 in 4,000 to 1 in 557,000 per unit of red blood cells [9],[10] . Finlay et al [11] developed and tested a computer screening system to detect potential or unreported cases of transfusion-related acute lung injury (TRALI). They used retrospective computer blood gas data after transfusions during a 45-day period at a tertiary care academic hospital. During this period, 820 patients received 6,888 blood products. Seven cases of TRALI were diagnosed, whereas only 2 had been re­ported. The system had 99% accuracy and 26% posi­tive predictive value for detecting potential TRALI. These investigators, and others [12] , reported the incidence of TRALI to be one case for every 1000 to 2400 units transfused. Additional research is needed to better de­termine the actual incidence of TRALI.

TRALI has been associated with transfusions of all blood products, most commonly with whole blood, RBCs, fresh frozen plasma (FFP) and platelets [13],[14],[15] and, rarely, after intravenous immunoglobulin treatment [16],[17] ,cryoprecipitate9, granulocytes [18] and stem cell prepara­tions [19]


   Risk factors Top


No definite risk factor is known for the develop­ment of TRALI. This syndrome has been reported in paediatric to old age population, and in both sexes.

Nulliparous vs. multiparous donors: During preg­nancy mothers are exposed to alloantigens that prime their immune system. The rate of alloimmunization cor­relates directly with parity as reported by Insunza et al [20] , where percentage of female donors with anti-leukocyte antibodies after one, two or three prior pregnancies was approximately 9%, 18% and 23% respectively. In a study Palfi et al [21] found patients receiving blood from multipa­rous donors had a greater decrease in their PaO2/FiO2 ratio as compared to patients who received blood from nulliparous donors.

Blood components: Bray et al [22] in a study found highest incidence of Anti-leukocyte antibodies in FFP and cryoprecipitate (29% and 24% respectively) while packed red blood cells had the lowest (12%). Gajic et al [23] reported that transfusion of FFP but not packed red cells was

independently associated with development of TRALI.

Massive transfusion: There seems to be a strong relationship between exposure to multiple transfusions and development of TRALI. The evidence of this asso­ciation is shown in a study done by the Canadian Critical Care Trial Group [24] in which 838 critically ill patients were randomized to either a liberal strategy (Hb threshold for transfusion 10g/dl) or restrictive strategy (Hb threshold for transfusion 7g/dl). On average 2.6 units were trans­fused in restrictive group compared to 5.6 units in the liberal group. TRALI developed in 11.4% of patients in the liberal group as compared to 7.7% patients from re­strictive group. In another study, the risk of TRALI did not correlate with the volume of plasma infused or the titer of the anti-leukocyte antibody [2]

Stored blood products: Inflammatory mediators like cytokines accumulate during storage of blood prod­ucts, which trigger an inflammatory cascade leading to injury to alveolar-capillary membrane and consequently pulmonary oedema [25] . Additionally, depletion of nitric oxide in stored blood products may also result in pulmo­nary vasoconstriction and increase in hydrostatic pres­sure leading to TRALI [26] .

Underlying clinical condition: Factors such as trauma, major surgery, sepsis may serve as initial prim­ing event in the development of TRALI (Two event hypothesis)


   Diagnosis Top


The diagnosis is clinical and radiographic. TRALI should be considered whenever dyspnoea, hypoxemia, and pulmonary infiltrates occur during or within six hours after transfusion of any blood product, in the presence of normal cardiac function [8] It is important for the clini­cian to differentiate ALI with cardiogenic pulmonary oedema, associated with increased left atrial pressure, although, the two conditions can coexist. If undiluted oedema fluid is obtained at the time of endotracheal in­tubation, the oedema fluid to plasma protein ratio can be determined. A ratio of 0.6 suggests permeability (ALI) rather than hydrostatic pulmonary oedema [27] The NHLBI Working Group recognized that ALI in patients with other recognized risk factor (such as trauma, sepsis) would be difficult to classify as TRALI and such cases would be designated as "indeterminate." The Consensus Panel designate these "indeterminate" cases as "possible TRALI," a category used by the Consensus Panel for cases in which ALI is temporally related to a transfu­sion in the presence of one other risk factor for ALI. The guidelines recommend classifying each suspected case in one of the following 3 categories: (1) "TRALI,"(2) "Possible TRALI," or (3) "Not TRALI."

The clinical presentation of TRALI is identical to ARDS, with at least two important exceptions. First, mortality resulting from TRALI is often approximated at 5 to 10%, occasionally higher (50%), but mostly well below the 40 to 70% mortality estimates associated with ARDS. Second, in contrast to ARDS, in which lung in­jury can be irreversible, TRALI is generally transient, with PO2 levels returning to pretransfusion levels within 48 to 96 h [8] . The time frame of symptom onset helps to identify the syndrome, as symptoms are always associ­ated with recent blood transfusion occurring during or shortly after transfusion, usually within 1 to 2 h, but al­ways within 6 h.

The entities in the differential diagnosis of this clini­cal presentation are acute intravascular volume over­load (TACO: transfusion-associated circulatory over­load), haemolytic transfusion reactions, or anaphylaxis due to the transfusion of IgA-containing products to a recipient with IgA deficiency. Differentiating between TRALI and TACO can be difficult [28] . Findings support­ing a diagnosis of TACO include physical findings sug­gesting volume overload (such as elevated jugular ve­nous pressure), elevated systolic blood pressure near the time when dyspnoea developed, a widened pulmonary vascular pedicle on chest radiography, and, if measured, an increase in the circulating level of B-type natriuretic peptide (BNP) shortly after transfusion [29] .

Laboratory findings may include unexpected haemoconcentration and a sudden fall in serum albumin [30] .As in other causes of acute alveolar capillary leak, the pulmonary exudate in TRALI has a high albumin content. Peripheral blood neutropenia has been reported but neu­trophilia is more common [31],[32] . Additionally, leukocyte antibody to recipient antigen and increased neutrophil priming activity in the lipid fraction of plasma in stored blood products [11] may also be found. It should be remembered that the diagnosis of TRALI is not made on the basis of laboratory test results [33] .


   Pathogenesis Top


The pathogenesis of TRALI remains controver­sial. There are three theories proposed to explain the underlying mechanism. All proposed mechanisms lead to a final common pathway of increased pulmonary cap­illary permeability, resulting in pulmonary oedema [34]

Anti-granulocyte antibodies - The antibody hy­pothesis states that an antigen-antibody reaction triggers a series of events leading to TRALI. Most often, the donor blood component contains antibodies against recipient white blood cell (WBC) antigens. Antibodies may be HLA Class I or HLA Class II or directed against HNAs. It is possible that transfused HLA antibodies may directly injure pulmonary endothelial cells. Alterna­tively, the transfused antibodies, by binding to circulating WBCs, particularly neutrophils, cause cellular activa­tion. Activated neutrophils, and possibly other WBCs, lodge in pulmonary capillaries either through cellular adhesive mechanisms or by physical trapping of WBC agglutinates. Such activated neutrophils release vasoac­tive substances, such as leukotrienes, or cytotoxic sub­stances such as reactive oxygen metabolites. These mediators cause pulmonary endothelial leakage or dam­age with consequent pulmonary edema [35] .

Evidence that the antibody hypothesis may not be sufficient to explain all cases of TRALI comes from observations that many cases of TRALI are not associ­ated with donor HLA or HNA antibodies and not all transfusions of components from donors with HLA or HNA antibodies cause TRALI [35] .

Granulocyte priming - This theory states that biologically active substances, such as lipids and cytokines contained within the transfusions, have the ability to prime the activity of granulocytes in the pulmo­nary vasculature, contributing to increased vascular per­ meability [9],[36] .

Two event hypothesis - A "two-event" hypoth­esis combines the two above theories. It states that TRALI is the result of two independent events [37],[38] . The first event is caused by the recipient's underlying clini­cal condition (surgery, infection or inflammation), that primes circulating neutrophils, sequestering them in the pulmonary circulation. The second event involves trans­fusion of anti-leukocyte antibodies or biological response modifiers in stored blood components, which in turn ac­tivate the primed neutrophils resulting in pulmonary en­dothelial damage and capillary leak.

Support for the neutrophil priming hypothesis comes from the investigation of TRALI cases in which WBC antibodies could not be demonstrated. The largest series of such cases involved 90 TRALI events in 81 patients [9] . Platelet concentrates or RBCs were judged to be the causative component in all but one of these cases. Of 28 cases investigated for antibodies, HLA or HNA antibodies were found in 7 patients only (7 positive donors in 104 tested donors). Elevated neutrophil priming activity was detected in implicated platelet concentrates and in the post-reaction plasma samples of TRALI patients compared to pre-reaction plasma samples (n = 34), but no such difference was found in control patients (n = 10).

Other possible mechanisms - Several other ex­planations for TRALI have been suggested, but these are not supported by clinical and experimental evidence. These include direct injury to pulmonary endothelium, immune complex formation with complement activation, and cytokine network activation [35] . Monocyte antibodies and/or monocyte activation have been identified in some TRALI cases [39] . Cytokines or other yet to be identified biologic response modifiers that are present in blood com­ponents and which may increase with blood component storage may directly or indirectly activate or injure pul­monary endothelium. One possible candidate for this lat­ter mechanism is IL-8, which has been shown to directly increase permeability of cultured endothelial cell monolayers [40] .


   Management Top


Management of the patient with TRALI is sup­portive involving haemodynamic and ventilatory support. Milder cases can be managed with supplemental oxy­gen alone. Mechanical ventilation may be required in severe cases. Ventilator management should be guided by the same principles (eg, low tidal volumes and pla­teau pressures) used in patients with ARDS. High con­centration of inspired oxygen and positive end-expira­tory pressure may be required. The resolution is typi­cally rapid, with most cases resolving within 96 hours [1],[3]. Extracorporeal membrane oxygenation has been used successfully in a severe case of TRALI following coro­nary artery bypass surgery [41] .

Other, less well-documented and unproven thera­pies (eg, diuretics, corticosteroids, prostaglandin E1) have also been used. Diuretics are said to have no role in TRALI treatment [42] . Administration of a diuretic should be considered when pulmonary oedema develops in as­sociation with blood product transfusion, particularly when the distinction between TRALI and TACO is uncertain. However, the absence of significant improvement after initial diuresis makes TRALI somewhat more likely. Accordingly, subsequent diuresis should be avoided be­cause hypotension can ensue in patients who are intra­vascularly volume depleted [43] Intravenous corticosteroids have been advocated by some authors diminish comple­ment-mediated granulocyte activation, aggregation, and degranulation [44] . However, the efficacy of corticosteroids has not been tested in prospective clinical studies, and anecdotal evidence is unconvincing in a condition in which patients tend to recover rapidly and completely with sup­portive care alone [45],[46] . Thus, the routine use of corticosteroids is not recommended.


   Prevention Top


Blood donated by multiparous women is more likely to contain anti-leucocyte antibodies, most likely due to sensitization to foetal antigens during pregnancy. As many as 20% of parous female donors have anti-leucocyte antibodies in their plasma [47] .

TRALI has also been attributed to inter-donor incompatibility when multiple or pooled blood products are given (ie, the recognition by one donor's antibodies of another donor's leukocytes) [8] .

Popovsky and Moore [1] stressed the importance of awareness in medical practice and urged blood banks to identify donors whose plasma is linked to TRALI cases in order to prevent recurrence. Several blood donor man­agement strategies have been proposed as ways to re­duce the incidence of TRALI. Wallis et al [48] suggested that multiparous women should be excluded from dona­tion of plasma-rich components, since many of the cases of TRALI observed in their institution were traceable to HLA class I or class II antibodies. Leukoreduction is yet another preventative measure that has been investigated and discrepant results found. In one study [49] , TRALI re­actions were significantly reduced by prestorage WBC reduction, while in another study [9] , prestorage WBC re­duction was ineffective in inhibiting TRALI. Leukoreduction is currently mandated in Canada [50] and throughout most of Europe but not in the United States, where its merits are still being debated [51] . The screening of all donors for all specific antibodies with the intent of eliminating them from the donor pool to prevent TRALI may be a costly, premature, and ultimately futile under­taking [9] . Patient screening and history as well as per­forming a cross-match procedure may or may not be helpful in preventing TRALI. Examples may be found in which TRALI occurred despite negative cross-match results [52] .

There are presently insufficient evidence to sup­port these recommendations since such strategies risk further limiting the availability of blood. [53]

 
   References Top

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50.Hebert PC, Fergusson D, Blajchman MA, et al Clinical out­comes following institution of the Canadian Universal Leukoreduction Program for Red Blood Cell Transfusions. JAMA 2003;289:1941-49.  Back to cited text no. 50      
51.Corwin HL, AuBuchon JP. Is leukoreduction of blood compo­nents for everyone? JAMA 2003;289:1953-55.  Back to cited text no. 51      
52.Win N, Montgomery J, Sage D, et al Recurrent transfusion­related acute lung injury. Transfusion 2001;41:1421-25.  Back to cited text no. 52      
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