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Table of Contents
Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 24-29

Transfusion-related acute lung injury

1 Department of Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
2 Department of Immunohaematology and Blood Transfusion, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

Date of Web Publication8-Jan-2019

Correspondence Address:
J Harikrishna
Associate Professsor, Department of Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517 507, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCSR.JCSR_9_18

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Transfusion-related acute lung injury (TRALI), an important non-infectious risk of blood transfusion is a leading cause of morbidity and mortality. Activation of polymorphonuclear (PMN) leucocytes by the mediators released due to the interaction of donor antibodies against the recipient monocytes is thought to trigger TRALI. Major histocompatibility complex Class II antibodies have been implicated in the direct causation of TRALI by direct activation of PMN leucocytes. TRALI has been reported in patients receiving all blood components that contain plasma. Awareness regarding TRALI among clinicians and a high index of suspicion will facilitate early diagnosis of the condition. TRALI is a clinical diagnosis that is suspected when new acute lung injury (ALI) develops within six hours of a transfusion. Diagnostic work-up should focus on ruling out other risk factors for ALI like sepsis, aspiration, among others. TRALI mitigation strategies are helpful to ensure blood safety and facilitate lessening of other transfusion reactions transfusion associated circulatory overload as well. The treatment for TRALI is symptomatic and supportive and is similar to that administered for ALI.

Keywords: Diagnosis, transfusion-associated circulatory overload, transfusion-related acute lung injury

How to cite this article:
Raja V A, Rahul C, Kumar M K, Pradeep V, Sreedhar Babu K V, Harikrishna J. Transfusion-related acute lung injury. J Clin Sci Res 2018;7:24-9

How to cite this URL:
Raja V A, Rahul C, Kumar M K, Pradeep V, Sreedhar Babu K V, Harikrishna J. Transfusion-related acute lung injury. J Clin Sci Res [serial online] 2018 [cited 2021 Jan 24];7:24-9. Available from: https://www.jcsr.co.in/text.asp?2018/7/1/24/249631

  Introduction Top

In the early 1800s, the first successful blood transfusion was done by James Blundell in a patient with post-partum haemorrhage.[1],[2] Since then, transfusion of blood products has become a major part in treating patients, especially the critically ill. Over the period of the next decade, blood transfusions have become commonplace; however, with an increase in blood transfusions, there was an increase in multiple transfusion-related infections. This complication was a major setback but was effectively overcome by screening procedures. As the incidence of transfusion-related infections began to fall, a new entity emerged which was a syndrome of acute lung injury (ALI) associated with transfusion. The term transfusion-related ALI (TRALI) was coined by Popovsky et al. in Mayo Clinic in 1985.[3]

TRALI was once regarded as an obscure complication of blood transfusion. However, over the past few years with the development of international consensus definition, there has been an increase in number of cases of TRALI. This has been in part due to the inclusion of cases which were previously diagnosed as volume overload and cardiogenic pulmonary oedema due to the common presentation of dyspnoea and hypoxia observed during transfusions. Sepsis has emerged as a leading risk factor for TRALI. This has altered our perception of this disease from a mere diagnosis of exclusion to one of the leading causes of mortality.

The French in 1993 initiated haemovigilance, which is a data reporting system that tracked and analysed blood transfusion safety, outcomes and quality.[4] Programmes similar to these have observed that TRALI is the leading cause of transfusion-related death worldwide. It is important to identify the aetiological factors in the development of TRALI as it is associated with several adverse outcomes. Moreover, learning the pathophysiological mechanisms behind this dreadful complication will alert the clinicians to take steps in preventing it without compromising the required management. This article is an insight into the recent epidemiological data, aetiopathogenesis and clinical presentation of TRALI.

  Definition and Diagnosis Top

Suspected TRALI is defined as development of ALI within 6 h of transfusion of blood or blood products in the absence of other risk factors.[5] This definition was developed by the National Heart Lung and Blood Institute (NHLBI), in patients who had no ALI immediately before transfusion, and no other risk factor for ALI is present. It is important to note that this definition excludes patients with ALI before transfusion even though existing ALI could be worsened following transfusions. Prospective studies have shown that the incidence of ALI in patients with ALI risk factors is <50%. Development of ALI in a patient with ALI risk factor could be due to either transfusion or risk factor or both. To diagnose TRALI in such patients, the NHLBI has recommended critical care experts to judge, whether the new ALI is temporally associated with risk factor or temporally associated with transfusion. However, the Canadian consensus conference proposed the term “possible TRALI,” which is the development of new TRALI in patients with a pre-existing risk factor.

  Epidemiology Top

The exact incidence of TRALI is not well documented. TRALI has been documented in all age groups and both genders.[6],[7],[8] It has been estimated that TRALI occurs in 0.014%–0.08% per allogeneic blood product unit transfused (0.04%–0.16% per patient transfused).[9],[10],[11],[12],[13] The incidence rate of TRALI varies widely for various blood products, ranging from 1 in 432 to 1 in 88,000 per unit of whole blood platelets; 1 in 1224 per unit of apheresis platelets; 1 in 4000 to 1 in 557,000 per unit of red blood cells (RBCs) and 1 in 7896 to 1 in 74,000 per unit of fresh frozen plasma (FFP) transfused.[7],[8],[13],[14] In most reported cases of TRALI, the implicated blood product usually has contained >60 mL of plasma; occurrence of TRALI after transfusion of products containing <60 mL of plasma, such as cryoprecipitate and platelet concentrates, has been reported.[15]

TRALI has been frequently reported when multiparous women or women who have had at least three live births were the donors.[8] The frequency of anti-human leucocyte antigen (HLA) antibodies among female donors has been demonstrated to increase with the number of pregnancies, ranging from 7.8% in nulliparous women to 26.3% in women who have had three or more pregnancies.[16] It has been recently reported that 12.9% of female platelet donors were found to be positive for either HLA Class I or Class II antibodies.[17]

  Pathogenesis Top

The mechanisms underlying pathophysiology of TRALI are unclear. A two-hit hypothesis has been proposed.[18],[19],[20] In this, the first hit refers to the condition of the patient which results in adherence of primed neutrophils to the pulmonary endothelium, and the second hit refers to the transfused product which activates the pulmonary neutrophils and endothelial cells resulting in ALI. The second hit includes TRALI mediated by either antibodies or biological response modifiers.

  Antibody-Mediated Transfusion-Related Acute Lung Injury Top

Majority of the cases of TRALI have been associated with HLA or human neutrophil antigen (HNA) antibodies in plasma-rich transfusions products. The relationship between the strength of HLA and HNA antibody and the development of TRALI has been studied which might enlighten the existence of TRALI even when small amounts of blood products are transfused.[21],[22],[23],[24] Initial clinical trials implicated donor antibodies against HLA Class 1 antigens and granulocyte antigens in 89% and 72% of the cases, respectively.[9] The donor antibodies bind to the cognate antigen in the host. This results in sequestration of the polymorphonuclear (PMN) leucocytes in the lung, followed by their activation. This results in the release of microbicidal substances, endothelial damage capillary leak and ALI.[8],[9],[25] The pathogenesis was supported by the fact that human volunteers developed TRALI on being exposed to HLA and HNA antibodies. This theory has been further confirmed when monoclonal antibodies (H2Kd) when administered in mice at a concentration of 4.5 g/kg produced ALI.[26] This, however, requires the presence of Fc receptor and PMN. Granulocyte depletion or Fc receptor knockout has shown to prevent TRALI.[26] In situ animal models were done which showed that antibody-specific HNA also causes TRALI. Initial experiments showed infusion of specific antibodies (HNA-3a), human PMNs and plasma, which acted as a complement source, induced ALI.[17] Further experiments obviated the need for complement source. Antibodies specific for HLA Class 2 antigens have been implicated in large number of TRALI cases. Binding of these antibodies against their antigens on PMNs or monocytes results in the synthesis of interleukins 1β, interleukin,[6],[8] tissue factors, chemokines and tumour necrosis factor-alpha (TNF-α), which result in pro-inflammatory action of endothelial cells and PMNs which lead to TRALI.[10],[27],[28],[29],[30],[31] This was confirmed in animal experiments. Rats were treated with lipopolysaccharide (LPS) which resulted in expression of MHC Class 2 antigens on PMNs and endothelial cells. Infusion of antibodies against HLA Class 2 antibodies resulted in the development of TRALI in such animals.

  Non-Antibody Mediated Transfusion-Related Acute Lung Injury Top

This is thought to be caused due to accumulation of pro-inflammatory mediators during the storage of blood products. The mechanism behind this is still not clear. Two mechanisms have been proposed, which includes either the soluble mediators or the cellular mediators.

  Soluble Mediators Top

Bio-active lipids

Bio-active lipids accumulate in stored transfusion products. Both polar and non-polar lipids get accumulated. The polar lipids include lysophosphatidylcholines, lipids structurally similar to platelet activating factor and to ligand of G2A receptor.[32],[33] The non-polar lipids are arachidonic acid, 5-hydroxeicosatetranoic acid (HETE), 12-HETE and 15-HETE.[34] Polar lipids accumulate in both whole-blood RBCs and platelets and to a lesser extent in leucoreduced RBCs. Non-polar lipids can be isolated in platelets but not in RBCs. This was confirmed in a murine model when rats were stimulated with LPS, which acted as a first hit. The lungs were then perfused ex vivo with plasma from 42-day-old RBCs which acted as a second hit. The plasma was preheated to 56°C to prevent the action of human complement. This caused an evident lung injury in the mice.[20],[32]

Soluble CD40L

Endothelial and epithelial cells, monocytes and macrophages express CD40, which is a member of TNF receptors. It has a ligand CD40L, produced by the platelets, which gets accumulated in the stored blood as soluble forms or cell-associated forms.[35],[36],[37] The CD40L activates the macrophages and also stimulates the production and release of many pro-inflammatory cytokines. An increase in sCD40L found in stored platelets has been associated with transfusion reactions and increased respiratory burst in PMNs.[38],[39]

  Cellular Mediators Top

The ageing of the erythrocyte

As the blood is stored for a long time, the RBCs undergo certain changes such as decreased deformability, depletion of 2,3diphosphoglycerate and reduction in nitric oxide along with other changes. These effects have been connected to poorer outcomes of transfusion. The stored RBCs also lose Duffy antigen expression, which has a chemokine scavenging function. The chemokines bound to the RBC are inaccessible for the neutrophils in the blood.[40] The absence of Duffy antigen is associated with increased chances of ALI.

The ageing platelet

The platelets also undergo certain changes when they are stored. They shrink and show cytoplasmic condensation, plasma membrane blebbing and extension of filopodia.[41] The stored platelets which were illuminated with ultraviolet-B caused ALI in animal models.[42],[43],[44],[45] However, similar studies done in recent times could not replicate these findings which may be attributed to the difference in storage conditions. In recent studies, the platelets were illuminated in a closed system, whereas in older studies, the platelets were illuminated in an open system which could have caused enhanced reactive oxygen species production.[46]

  Clinical Features Top

Definition of TRALI states that the clinical features develop within 6 h of blood transfusion. However, most of the times, it usually presents during the period of transfusion or in the first 1–2 h of transfusion. It is characterised by sudden onset of tachypnoea, cyanosis, dyspnoea and fever (1°C or higher). Hypotension unresponsive to intravenous fluid therapy[8] is common. Sometimes, hypertension may be present. On auscultation of the lungs, there are diffuse crackles with decreased breath sounds more in the dependent areas.

The arterial blood gas reveals an arterial oxygen tension (PaO2) to fraction of inspired oxygen ratio <300; the frontal chest radiograph shows bilateral perihilar diffuse infiltrates.

  Differential Diagnosis Top

Clinical presentation of TRALI resembles that of acute respiratory distress syndrome (ARDS) and must be distinguished from ARDS and conditions causing cardiogenic pulmonary oedema.

Transfusion-associated lung injury versus transfusion-associated circulatory overload

The clinical features of transfusion-associated circulatory overload (TACO) are similar to other conditions which give rise to pulmonary oedema. Apart from dyspnoea and tachypnoea the characteristic features include jugular venous distension, S3 gallop and high systolic blood pressure [Table 1].[47],[48],[49],[50]
Table 1: Comparison of transfusion-related acute lung injury and transfusion-associated circulatory overload

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In the presence of new-onset hypoxemia and worsening bilateral infiltrates suggestive of pulmonary oedema, several tests help determine if it is TACO or TRALI. Oedema fluid/plasma protein concentration >0.65, pulmonary artery occlusion pressure >18 or brain natriuretic peptide <250 or any two of the following: (i) systolic ejection fraction >45 and no severe valvular heart disease; (ii) systolic blood pressure <160 mmHg; (iii) vascular pedicle width <65 mm and cardio-thoracic ratio <0.55, all indicate permeability pulmonary oedema suggestive of TRALI (39–42). The absence of the above-mentioned factors along with no electrocardiogram changes is suggestive of TACO.[47],[48],[49],[50]

  Prevention Top

TRALI mitigation strategies have been found to be important for blood safety and have also been known to lessen other transfusion reactions, such as TACO. Blood donors with evidence of demonstrable antibodies, who have been implicated in causation of TRALI, should be permanently deferred.[7],[14] Some workers have suggested that blood obtained from multiparous donors who have not been screened for leucocyte alloantibodies should not be used as whole blood, FFP or single-donor apheresis platelets.[6],[12] Biologically active lipids accumulate in blood products with storage. It has been suggested that the administration of fresh blood cell components would reduce the risk of TRALI by preventing exposure of recipient neutrophils to neutrophil priming agents.[7],[13] However, factors other than age of the blood products are thought to contribute to the risk of TRALI, and further research is needed before age of blood components can be used to mitigate the risk of TRALI.[51] Overall, reduction of blood product utilisation using evidence-based criteria for transfusion may be a safe and appropriate strategy to decrease the incidence of TRALI.[14]

  Treatment Top

There is no specific treatment for TRALI. Patients usually need additional oxygen, and mechanical ventilation is required in 70%–90% of the cases.[49] Restrictive tidal volume ventilation is done in these patients. There is no evidence for the use of corticosteroids in these patients. Animal experiments have shown promising response with aspirin but have still not been tried in patients with ARDS.

TRALI patients generally improve clinically within 48–96 h of onset.[6] Usually, a resolution of the pulmonary infiltrates, as assessed by chest radiographs, occurs within 1–4 days.[6],[52] However, in approximately 20% of patients, hypoxemia and pulmonary infiltrates may persist for longer than 7 days. In those patients who recover rapidly, no long-term sequelae are found.[6] Despite the usually excellent prognosis, it should be noted that TRALI can be a serious condition. TRALI is fatal in 5%–10% of reported cases.[6],[9],[53]

  Prognosis Top

Only in a minority of TRALI cases, an implicated alloantibody is evident in the recipient. An individual who has had TRALI in the past is thought to be at increased risk for the occurrence of recurrent TRALI with subsequent transfusions. There is no consensus regarding the optimal management strategy for these patients.

Patients with a history of TRALI have to be carefully monitored during and after the subsequent transfusion of allogeneic blood products. It has been suggested that repeated TRALI reactions in these patients may be prevented by leucoreduction of any cellular components transfused to a TRALI patient; however, no evidence supports or refutes this practice.[8],[54]

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Conflicts of interest

There are no conflicts of interest.

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