Asian Cardiovasc Thorac Ann 2006;14:e65-e67
© 2006 Asia Publishing EXchange Ltd
Transfusion Related Acute Lung Injury in Cardiac Surgery
Maninder S Kalkat, FRCS,
Uday Dandekar, FRCS,
Vijay Jegannath, MD,
Adrian Levine, FRCS
University Hospital of North Staffordshire, Stoke on Trent, United Kingdom
For reprint information contact: Maninder S Kalkat, FRCS Tel: 44 192 262 4653 Fax: 44 121 627 5736 Email: mankalkat{at}hotmail.com, Department of Cardiothoracic Surgery, University Hospital of North Staffordshire, Stoke on Trent , ST4 7LN, United Kingdom.
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ABSTRACT
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Transfusion related acute lung injury (TRALI) is an uncommon complication following administration of blood products. It is often difficult to differentiate from other commoner causes of cardio-respiratory instability. However, prompt diagnosis and management is associated with favorable outcome.
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INTRODUCTION
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There are various reasons for postoperative respiratory insufficiency in patients undergoing cardiopulmonary bypass including pump lung, underlying cardiac disease, volume overload, reaction to drugs and blood products. Transfusion related acute lung injury is an under-reported complication of blood product transfusion, the diagnosis of which requires a high degree of suspicion and exclusion of others causes. Treatment is supportive, with prognosis substantially better than most causes of lung injury.
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CASE REPORT
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A 62-year-old man with unstable angina underwent emergency coronary artery bypass surgery. Postoperatively he was transferred to the intensive care unit in a hemodynamically stable condition. However, during the early postoperative period he had excessive drainage from the chest drains. After reviewing the coagulation results, fresh frozen plasma (FFP) was administered. Soon after infusion of the first unit, the patient became hypoxic, his airway pressures increased and a frothy fluid appeared in the endotracheal tube. He became hypotensive with a fall in the central venous pressure. A Swan Ganz catheter was floated, which revealed low filling pressures and high cardiac output. A chest X-Ray demonstrated extensive bilateral pulmonary infiltrates (Figure 1
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In view of the relationship between the clinical picture and administration of FFP, a presumptive diagnosis of transfusion reaction was considered. The patient was ventilated for the next 24 hours, given corticosteroids, intravenous fluids, and norepinephrine. The patient’s condition improved rapidly overnight and a repeat X-Ray showed marked resolution of the pulmonary infiltration (Figure 2). The patient was extubated a few hours later and had an uneventful stay in the hospital. The used FFP bag and patient’s blood were sent for analysis, and a diagnosis of TRALI was made on the basis of HLA antibodies detected in the donor’s plasma.
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DISCUSSION
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Transfusion related acute lung injury is an under-diagnosed complication of transfusion therapy and is the second most common cause of transfusion related mortality.1 Popovsky in 1983 coined the term "transfusion related acute lung injury" (TRALI) to define noncardiogenic pulmonary edema complicating blood transfusion.2 The condition is characterized by a sudden onset of pulmonary edema, often with marked systemic hypovolemia and hypotension, occurring within hours of transfusion. Most cases occur within 1–2 hours, and almost all occur within 6 hours of transfusion.3,4 Fever and rigors are reported, but may be absent or mild. There is rapid onset of severe hypoxia, chest radiographs demonstrate bilateral pulmonary infiltrates and copious frothy yellow or pink fluid in the tracheobronchial tree.5 The diagnosis of TRALI relies on excluding other causes such as cardiogenic pulmonary edema, sepsis, volume overload, adult respiratory distress syndrome and acute hemolytic transfusion reaction. While all plasma containing blood products have been implicated in the pathogenesis of TRALI, the majority of cases are associated with whole blood, packed red blood cells, fresh frozen plasma, and platelets. The incidence of TRALI varies from 0.02%2 to 0.08%4 per unit transfused.
Most cases of TRALI occur in the setting of an operating room or intensive care unit. Various experimental studies have supported a "two-hit" hypothesis of the pathogenesis of TRALI. The first "hit" is thought to be the underlying condition of the patient and the second "hit" is hypothesized to be associated with the transfusion of blood products. The first insult is priming and adherence of the neutrophils to pulmonary endothelium, which occurs commonly in patients undergoing cardiopulmonary bypass. There are two theories explaining the second insult in TRALI – passively transfused antibodies, and biologically active lipids. The antibody theory is the most plausible etiology of TRALI.5 Antibodies in the plasma of a single donor unit attach to specific antigens on primed neutrophils, leading to their activation and release of pro-inflammatory granule contents and reactive oxygen species that cause capillary leak and pulmonary edema.6 These antibodies may also attach and activate pulmonary endothelial cells and monocytes.7 There are isolated reports of recipient antibodies attacking donor white blood cells and producing a TRALI-like picture, albeit in a milder form.7
In approximately 10% of cases of TRALI, no neutrophil antibodies can be found in the donor or recipient plasma.8 The biologically active lipid theory explains the occurrence of TRALI in these cases. Biologically active lipids are breakdown products of cell membranes that normally accumulate in older, cellular blood components. Lysophosphatidylcholines have been identified as a component of these lipids and have been shown to prime neutrophils.5
The diagnosis of TRALI requires a high degree of suspicion, and exclusion of commoner etiologies of respiratory insufficiency.5 Transfusion related acute lung injury should be suspected and excluded in cases presenting with respiratory insufficiency, typical radiological features, and appearance of pulmonary edema soon after blood product transfusion. Cardiac causes of pulmonary edema should be ruled out with the aid of a Swan Ganz catheter and if necessary, echocardiography. Pulmonary edema fluid can be collected and protein measurements compared with a matched plasma sample. An edema fluid/plasma protein ratio less than 0.65 favors hydrostatic pulmonary edema whereas a ratio greater than 0.75 is compatible with increased permeability pulmonary edema.5 However, confirmatory and definitive evidence for the diagnosis of TRALI requires presence of donor and/or recipient leukocyte antibodies using lymphocyte cross match, which can be performed retrospectively.
In the majority of cases, TRALI is a self-limiting condition and carries better prognosis than most of the usual causes of acute lung injury. In a series from the Mayo clinic the pulmonary infiltrates resolved rapidly in 81% of patients within four days with a mortality of 6%.8 For mild cases, supplemental oxygen and supportive care may be sufficient. In severe cases, continued ventilatory support with low ventilatory pressure is useful. Diuretics are not recommended, as the pulmonary edema is not due to fluid overload, but a result of "capillary leak syndrome". In addition, corticosteroids have no demonstrable role in the management of TRALI.5 The best results are obtained in cases where the diagnosis is made early, and treatment instituted promptly. Limiting the amount of blood product transfusion can reduce the incidence of TRALI. This can be achieved by adhering to surgical principles, guidelines for transfusion of blood products, and use of cell saver techniques. It is prudent to avoid older blood products.5
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CONCLUSION
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Transfusion related acute lung injury is a serious, potentially life threatening condition as a consequence of blood product transfusion which is under-diagnosed, especially in patients undergoing cardiopulmonary bypass. Early diagnosis and management is associated with favorable outcome.
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REFERENCES
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- Sazama K. Reports of 355 transfusion-associated deaths: 1976 through 1985. Transfusion 1990;30:583–90.[Medline]
- Popovsky MA, Abel MD, Moore SB. Transfusion-related acute lung injury associated with passive transfer of antileukocyte antibodies. Am Rev Respir Dis 1983;128:185–9.[Medline]
- Kopko PM, Marshall CS, MacKenzie MR, Holland PV, Popovsky MA. Transfusion-related acute lung injury: report of a clinical look-back investigation. JAMA 2002;287:1968–71.[Abstract/Free Full Text]
- Silliman CC, Boshkov LK, Mehdizadehkashi Z, Elzi DJ, Dickey WO, Podlosky L, et al. Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. Blood 2003:101:454–62.[Abstract/Free Full Text]
- Looney MR, Gropper MA, Matthay MA. Transfusion-related acute lung injury: a review. Chest 2004;126:249–58.[Medline]
- Wyman TH, Bjornsen AJ, Elzi DJ, Smith CW, England KM, Kelher M, et al. A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release. Am J Physiol Cell Physiol 2002;283: C1592–603.[Abstract/Free Full Text]
- Kopko PM, Paglieroni TG, Popovsky MA, Muto KN, MacKenzie MR, Holland PV. TRALI: correlation of antigen-antibody and monocyte activation in donor-recipient pairs. Transfusion 2003;43:177–84.[Medline]
- Popovsky MA, Moore SB. Diagnostic and pathogenetic considerations in transfusion-related acute lung injury. Transfusion 1985;25:573–7.[Medline]
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ABSTRACT
INTRODUCTION
