|Year : 2008 | Volume
| Issue : 2 | Page : 126-131
TRALI - A Less Commonly Known Complication of Transfusion
Pradeep Bhatia1, KL Tulsiani2
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 Acceptance||22-Feb-2010|
|Date of Web Publication||19-Mar-2010|
A 54/3, Arvind Nagar, Golf Link Road, Jodhpur 342011
Source of Support: None, Conflict of Interest: None
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
| Introduction|| |
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 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|| |
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"  and by "National Heart, Lung, and Blood Institute (NHLBI) Working Group on TRALI"  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  or as an oxygen saturation measured by pulse oximetry of less than 90 percent when a patient is breathing room air  . 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  .
| Incidence|| |
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  . 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  . TRALI may be insufficiently investigated  , and mild or moderate cases may not be investigated or reported at all  . 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  . 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 , . Finlay et al  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  , 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 ,, and, rarely, after intravenous immunoglobulin treatment , ,cryoprecipitate9, granulocytes  and stem cell preparations 
| Risk factors|| |
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  , 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  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  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  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  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 
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  . Additionally, depletion of nitric oxide in stored blood products may also result in pulmonary vasoconstriction and increase in hydrostatic pressure leading to TRALI  .
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|| |
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  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  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  . 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  . 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  .
Laboratory findings may include unexpected haemoconcentration and a sudden fall in serum albumin  .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 , . Additionally, leukocyte antibody to recipient antigen and increased neutrophil priming activity in the lipid fraction of plasma in stored blood products  may also be found. It should be remembered that the diagnosis of TRALI is not made on the basis of laboratory test results  .
| Pathogenesis|| |
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 
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  .
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  .
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 , .
Two event hypothesis - A "two-event" hypothesis combines the two above theories. It states that TRALI is the result of two independent events , . 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  . 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  . Monocyte antibodies and/or monocyte activation have been identified in some TRALI cases  . 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  .
| Management|| |
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 ,. Extracorporeal membrane oxygenation has been used successfully in a severe case of TRALI following coronary artery bypass surgery  .
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  . 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  Intravenous corticosteroids have been advocated by some authors diminish complement-mediated granulocyte activation, aggregation, and degranulation  . 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 , . Thus, the routine use of corticosteroids is not recommended.
| Prevention|| |
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  .
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)  .
Popovsky and Moore  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  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  , TRALI reactions were significantly reduced by prestorage WBC reduction, while in another study  , prestorage WBC reduction was ineffective in inhibiting TRALI. Leukoreduction is currently mandated in Canada  and throughout most of Europe but not in the United States, where its merits are still being debated  . 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  . 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  .
There are presently insufficient evidence to support these recommendations since such strategies risk further limiting the availability of blood. 
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