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Abstract
Transfusion-related acute lung injury is a life-threatening clinical syndrome. In the last 3 years, it has become the leading cause of reported transfusion-related deaths in the United States. This syndrome is characterized by acute hypoxemia and noncardiogenic pulmonary edema directly linked in time to a blood transfusion. All types of blood products have been implicated in transfusion-related acute lung injury, but transfusion of plasma-containing products from multiparous women seems to carry the highest risk. The purpose of this article is to raise awareness of this syndrome for the critical care nurse. This article discusses the widely accepted clinical features of transfusion-related acute lung injury, its pathogenesis, differential diagnosis, and treatment.
Transfusion-related acute lung injury (TRALI) is a life-threatening clinical syndrome. In the last 3 years, it has become the leading cause of reported transfusion-related deaths in the United States.1 All types of blood products, including red blood cells, platelets, and fresh frozen plasma, have been implicated.1 Despite its increasing notoriety, much about the pathogenesis, treatment, and prevention of TRALI is poorly understood. Clinically and pathologically, TRALI seems to be closely related to acute respiratory distress syndrome (ARDS), but with a shorter course of illness and a lower mortality rate. Preventive strategies now focus on improved education of clinicians about TRALI, an increased awareness of the syndrome, and emerging new approaches to manage the blood supply. The purpose of this article is to raise awareness of TRALI for the critical care nurse. The widely accepted clinical features of TRALI, its pathogenesis, differential diagnosis, and treatment are presented. New blood management strategies are also summarized.
CASE STUDY
A 44-year-old white male with newly diagnosed acute promyelocytic leukemia was transferred to the medical intensive care unit with melena, hematochezia, hemoglobin 6.7 g/dL, platelets 16,000/[mu]L, and severe coagulopathy. He arrived awake and alert to person, place, and time, with supplemental oxygen administered via 2 L/min by nasal cannula. He was pale, febrile at 39.6[degrees]C, and tachycardic; however, the patient was hemodynamically stable. A transthoracic echocardiogram performed earlier in the day showed an ejection fraction of 65% with normal filling pressures. Red blood cells, platelets, and fresh frozen plasma were transfused before performing an upper endoscopy.
After the endoscopy, the patient became increasingly tachypneic and tachycardic. As he remained profoundly coagulopathic, emergent transfusions of blood products continued. By midnight, the patient was placed on a 100% nonrebreather mask for dropping peripheral oxygen saturation (SpO2) levels. His respiratory condition continued to worsen. An arterial blood gas drawn at 2:30 am revealed an arterial partial pressure of oxygen (PaO2) of 67 mm Hg. With a chest radiograph that showed new bilateral interstitial infiltrates and a worsening clinical picture that included new hypotension, the patient was intubated. Between arrival in the medical intensive care unit and intubation, a period of 6 hours, the patient received 4 units of red blood cells, 6 units of fresh frozen plasma, 4 units of platelets, and 4 units of cryoprecipitate.
The healthcare team considered multiple differential diagnoses for the patient's acute respiratory decompensation: Transfusion-associated circulatory overload, pulmonary hemorrhage, and TRALI were considered. As work ruling out the differential diagnoses continued, at 3 am the senior medical resident contacted the hospital's blood bank regarding this patient who now had a probable diagnosis of TRALI. All blood tubing and bags had already been discarded. Because no clear link to one blood product was able to be made, all further blood transfusions the patient received had to avoid blood products from the donors of the 18 blood products already transfused.
The patient remained intubated 4 days, eventually improving. He was discharged from the medical intensive care unit 6 days after admission.
CLINICAL PRESENTATION
Transfusion-related acute lung injury is characterized by acute hypoxemia and noncardiogenic pulmonary edema directly linked in time to a blood transfusion. The key clinical presentation is an acute onset of respiratory compromise or severe hypoxemia within 6 hours of beginning a transfusion. The symptoms typically appear between 1 and 2 hours of the start of transfusion.2 The most common associated signs and symptoms are progressive dyspnea, cyanosis, fever, tachycardia, hypotension, and frothy sputum.2-5 Pulmonary edema may first be seen in dependent areas of the lung or in the perihilar area with more diffuse, generalized edema appearing in a few hours.3 Auscultation reveals decreased breath sounds and diffuse crackles.6 Consistent with a mandatory finding of noncardiogenic pulmonary edema for a clinical diagnosis of TRALI, the central venous pressure is normal, and there is no S3 gallop. Supportive oxygen is necessary in virtually all cases, with up to 70% of patients requiring mechanical ventilation.3 Even when initial hypoxemia has been severe, resolution of clinical symptoms occurs rapidly in most cases with proper identification and prompt treatment. Patients requiring mechanical ventilation can usually be extubated within 48 hours. Clinical signs and symptoms can be found in Table 1.
 | TABLE 1 Clinical Symptoms and Common Associated Events |
The radiographic features of TRALI are nonspecific.1 Chest films show bilateral patchy or diffuse infiltrates consistent with pulmonary edema. A discrepancy between the severity of the bilateral alveolar and interstitial infiltrates by x-ray and the relatively benign physical findings by ausculatory examination has been described.1,3,7 Radiographically, at its most severe, TRALI is indistinguishable from acute respiratory distress syndrome. Unlike acute respiratory distress syndrome, the chest infiltrates are usually transient, clearing within 96 hours in just more than 80% of patients diagnosed with TRALI.7
PATHOGENESIS
The pathophysiology of TRALI is not well understood. It is a complex clinical syndrome that does not seem to be caused by a single pathogenic event. Two basic mechanisms have been proposed. Increased permeability within the pulmonary microcirculation allows fluid high in protein to enter the interstitum and alveolar spaces resulting in impaired diffusion of oxygen. There is a close similarity with acute respiratory distress syndrome, most notably in the pathogenic role of neutrophils.8
One of the 2 proposed pathogenic mechanisms involves an antibody-mediated reaction.9 Specifically, antibody-antigen interactions cause complement-mediated pulmonary sequestration and activation of neutrophils resulting in TRALI.8 In most cases that have been explained by this hypothesis, donor antibodies in the transfused blood are directed against antigens on the surface of the recipients' leukocytes.10,11 More rarely, cases have been described with donor antigens and recipient antibodies12 (see Figure 1). Human leukocyte antigen class I and II and neutrophil-specific antibodies have been implicated.11,13,14 An interesting clinical exemplar supporting antibody-mediated TRALI is the case of a 34-year-old woman with a right, single lung transplant. This patient developed unilateral TRALI after receiving antibodies from a transfusion of red blood cells that reacted to the transplanted lung tissue but not to her native lung.15
 | Figure 1. Antibody-mediated reaction. |
A second mechanism proposes that TRALI is caused by 2 independent events, the so-called "two-hit" model.16 The first event is a predisposing inflammatory condition that leads to endothelial activation resulting in pulmonary sequestration and priming of neutrophils.2 Transfusion of blood comprises the second event. The two-hit model theorizes that the infusion of biologically active lipids from cell membranes in older blood products causes the already primed neutrophils to become activated. In support of this hypothesis is the report of an individual receiving an autologous blood transfusion resulting in TRALI. In this report, 2 units of autologous blood had been stored 18 and 25 days. After infusion of the second unit, the patient became hypoxic and hypotensive and was diagnosed with suspected TRALI. The presence of biolipids from the storage of blood was later documented.17
As biologically active lipids are the result of the breakdown of cell membranes that can accumulate in stored blood, this theory does not account for cases of TRALI resulting from infusion of products with few cellular components such as fresh frozen plasma.2 More recently, a modified two-hit model has been developed where both the antigen-antibody reaction and the action of biologically active lipids are complementary rather than competing theories. This combined theory suggests that TRALI is the result of polymorphonuclear leukocyte activation from either antigen or biolipid (degraded cell membrane) exposure.18
DIAGNOSTIC CRITERIA AND DIFFERENTIAL DIAGNOSIS
A diagnosis of TRALI is supported by clinical and radiographic evidence and is not dependent on laboratory tests.19 There must be new, acute lung injury within 6 hours of a completed transfusion, hypoxemia (partial pressure of oxygen in arterial blood [PaO2]/fraction of inspired oxygen [FiO2] <= 300 mm Hg or SpO2 < 90% on room air), new bilateral infiltrates on chest radiograph, and no evidence of left atrial hypertension (eg, pulmonary occlusion pressure <18 mm Hg). The National Heart, Lung, and Blood Institute working group20 and, more recently, the North American-European Consensus Conference panel19 have detailed the criteria for a clinical diagnosis of TRALI.
For a diagnosis of TRALI, there should be no preexisting or coexisting evidence of acute lung injury such as that from sepsis, shock, aspiration, or pneumonia. If a second risk factor for acute lung injury appears within the 6-hour window of transfusion onset, a diagnosis of "possible TRALI" can be made.19 Using the option of "possible TRALI" diagnosis allows differential tracking of more complex cases, an important consideration in determining the true incidence of TRALI versus other acute lung injury conditions (see Table 2). It is important to stress that although the blood component workup for antibody-antigen reactions is an imperative part of the workup in all suspected cases of TRALI, a positive finding is not required to make a diagnosis.21
 | TABLE 2 Criteria for TRALI Diagnosis |
In considering the differential diagnosis for respiratory insufficiency temporally related to a blood transfusion, diagnoses considered must include circulatory overload, infusion of a bacterial contaminated blood product, an anaphylactic transfusion reaction, a hemolytic transfusion reaction, and TRALI.6 A transient neutropenia secondary to lung sequestration has been reported and may support diagnosis. The duration of neutropenia during TRALI is in hours.22 Also, high protein content in the pulmonary fluid can help differentiate TRALI from fluid overload and cardiogenic pulmonary edema.2,23 Sampling the fluid in distal airways soon after intubation may provide a diagnostic clue. An undiluted endotracheal aspirate fluid to plasma protein ratio of greater than 0.75 is seen in TRALI. A ratio of less than 0.65 identifies a transudative process and suggests hydrostatic pulmonary edema.2,24
INCIDENCE, PREVALENCE, AND IMPLICATED BLOOD PRODUCTS
Transfusion-related acute lung injury is often under diagnosed. Patients who develop TRALI have no common demographics such as sex, age, or previous transfusion history.25,26 Two groups of patients, however, have been identified to be at particular risk: (1) patients in the induction phase of treatment of hematological malignancies and (2) patients with cardiovascular disease who require bypass surgery.27 It is difficult to determine the true incidence of TRALI largely because the defining characteristics are evolving. The overall frequency of antibody-mediated TRALI has been reported at 1 in 5,000 transfused units and 1 in 625 patients transfused. The in-hospital mortality rate of recognized TRALI is estimated to be between 5% and 10%.28
All types of blood products in all types of anticoagulant/preservative solutions have been implicated in TRALI.1,2,20 In some cases, only a small amount of plasma has been involved; both red blood cells packaged with additive solution and cryoprecipitate have been linked to TRALI reactions. Although a blood product made up of 10% plasma is enough to trigger a reaction, most cases involve blood components of more than 50% plasma. The Serious Hazards of Transfusion Scheme, a UK-wide hemovigilance project started in 1996, determined that fresh frozen plasma and platelet concentrates accounted for 47% of the reported TRALI cases.1
TREATMENT
The first step in treatment is arriving at the correct diagnosis, a challenge in what can sometimes be a very complicated clinical picture as demonstrated in the case study. The critical care nurse plays an important role in the correct diagnosis and prompt subsequent treatment. Treatment involves immediate management of respiratory compromise in the patient by the clinical team and later management of the blood supply by the transfusion specialists. There must be a working partnership and excellent communication between those at the bedside and those in the blood bank.1 In all cases of suspected TRALI, the blood transfusion must be stopped, the bag and blood tubing saved, and the blood bank notified. Workup for alternative diagnoses should proceed accordingly.
The critical care nurse is key to patient care because management is supportive. Supplemental oxygen delivery with mechanical ventilation is often needed. If the patient is placed on a mechanical ventilator, low-volume and low-plateau pressure protocols are recommended. The hypotension associated with TRALI may not completely respond to intravenous fluid resuscitation,1 and vasopressor support may be needed in cases with sustained hypotension. There is no role for steroids or diuretics.2 Most cases of TRALI are self-limiting. In nonfatal TRALI, there is little evidence of structural damage to lung parenchyma evidenced by fibrosis or chronic lung disease.8 Long-term lung function seems no different than from patients who never had TRALI and patient prognosis is good.3
Critical care nurses must accurately assess the patient for signs and symptoms of TRALI. During the recovery period, monitoring the effects of vasopressors and intravenous fluid resuscitation is crucial. Other possible treatments include the administration of prostanglandins and nonsteroidal antiinflammatory medications.
Blood supply management begins with identifying the implicated blood product and then the associated donor. All blood products from the donor of the implicated blood product must be sequestered. The blood transfusion facility will decide if testing for antibody-antigen reactions is warranted.21 The American Association of Blood Banks (AABB) advocates temporary disqualification of donors implicated in TRALI reactions until leukocyte testing has been completed.29
All reactions involving a diagnosis of TRALI or possible TRALI should be reported to the US Food and Drug Administration. The responsibility for notification, whether by bedside clinician or transfusion specialist, is institution specific. Transfusion-related deaths are to be reported to the Food and Drug Administration's Center for Biologics Evaluation and Research.30 The Food and Drug Administration has now started tracking the incidence of nonfatal TRALI and has requested that all nonfatal reactions also be reported.25
PREVENTION
The lack of a clear understanding on the mechanism underlying the development of TRALI makes the task of a designing a comprehensive prevention strategy complex.31 Patients with a preexisting inflammatory condition should receive the freshest blood product. Based on the two-hit model, this intervention will minimize contact with bioactive lipids and thus, theoretically, decrease risk of contracting TRALI. There is no research to date on the validity of this intervention. Using the antibody-antigen model, the blood supply should be limited primarily to donors with the least risk of being alloimmunized. Complex management strategies, however, may limit supply and will certainly increase costs related to blood products.
The first step in prevention of TRALI is to minimize blood product transfusions. Bedside clinicians can use evidence-based transfusion guidelines.1 Conservative transfusion thresholds have not been shown to adversely affect patient outcomes.32 A second step in prevention is improved physician and nurse education on the symptoms and diagnosis of TRALI. This will increase surveillance of the blood supply and help identify donors implicated in fatal and nonfatal cases.1 Washing cellular products has also been proposed as a preventive action. This will remove most donor antibodies but is time-consuming and costly, and there are few data on the efficacy of washing to remove biologically active lipids.33
It is essential to balance the safety needs of the patient with the adequacy of the blood supply. Several studies have established that multiparous donors are more likely to possess antileukocyte antibodies.34,35 Female donors often have leukocyte antibodies stemming from pregnancy; pregnancy exposes women to fetal antigens inherited from the father. The more pregnancies, the greater the opportunity a woman will have to form leukocyte antibodies.2
It is impossible to predict, however, which multiparous donor will be sensitized and of those sensitized, which will be implicated in a case of TRALI.2 In one randomized controlled trial, transfusion of plasma from multiparous donors with a history of 3 or more pregnancies was associated with impaired pulmonary function as compared with plasma from male or nonparous female donors.34 The impaired pulmonary function was evidenced by transient, significantly lower oxygen saturation. Of the hundred patients enrolled, 1 had a reaction typical of a TRALI diagnosis related to a plasma unit from a multiparous donor. Analysis of the donor sample revealed immunoglobulin G antibodies. Interestingly, the donor plasma/patient granulocyte compatibility test was negative.
The exclusion of multiparous donors from all blood donations would significantly reduce the donor pool. Based on the results of a Canadian Blood Service survey of 6,000 donors quoted in Goldman et al,1 deferral of women from donation who have had 3 or more pregnancies would result in a loss of 12% of donors. As not all blood that contains leukocyte antibodies causes TRALI, a 12% drop in what is already a very tight supply is not acceptable given the associated low risk.
Management of the blood supply centers around 2 strategies. The first is to identify those donors with antibodies through testing and exclude them from further donation. The second is to identify those donors at most risk for carrying antibodies and divert their blood products. Both are important strategies to maintain blood supply safety. The first strategy would be costly and unmanageable if implemented at the time of collection but is essential in the workup of implicated donors after a patient with TRALI has been identified. Most transfusion specialists and blood supply agencies recommend permanent deferment for donors implicated in serious or fatal cases of TRALI who have demonstrable antibodies.1,19
The second strategy for blood supply safety calls for the identification of at-risk donor groups and subsequent diversion of their blood products. This strategy was adopted by the National Blood Service in England in 20031 and recently endorsed by the American Association of Blood Banks.36 In Britain, the National Blood Service has implemented a policy of minimizing the transfusion of fresh frozen plasma and buffy-coat-derived platelets from female donors. Subsequent to implementation, the number of cases of TRALI arising from these components has dropped substantially.37 More than 90% of fresh frozen plasma produced by the National Blood Service in England is now derived exclusively from male donors.1
In the United States, recommendations from the American Association of Blood Banks have called for national and institutional interventions to minimize high plasma-volume blood components from donors thought to be alloimmunized. Recommended strategies for implementation include preparing high-volume blood components from male donors and to divert plasma from female donors to fractionated products.
SUMMARY
Transfusion-related acute lung injury is an infrequent but clinically important potential complication of transfusion therapy. Characterized by respiratory compromise and related symptoms, the etiology has not yet been fully elucidated. Although most patients with TRALI recover, supportive management can be complex and expensive; a 5% to 10% mortality has been reported. When TRALI occurs, bedside clinicians must work closely with blood bank experts to identify and, ultimately, defer donors associated with confirmed cases. Clinicians reporting fatal TRALI cases, as well as nonfatal TRALI and possible TRALI reactions to the Food and Drug Administration, with help track prevalence. As the pathogenic mechanisms are clarified, more approaches for TRALI prevention may become evident. Until that time, there may be an increase in the reported incidence of TRALI as clinicians become more knowledgeable about TRALI and consider this clinical syndrome in the differential diagnosis for respiratory distress temporally associated with blood transfusion. Blood agencies in the United States are preparing to adopt gender-driven blood donor management strategies in an effort to minimize this rare but serious transfusion risk. It will be important to evaluate the impact on the reported incidence of TRALI in the United States once female-derived plasma is diverted from high-volume blood components.
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