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Platelet Transfusion Associated With Acute Lung Injury After Coronary Artery Bypass Grafting

2011; Elsevier BV; Volume: 91; Issue: 6 Linguagem: Inglês

10.1016/j.athoracsur.2010.11.076

1552-6259

Gerard J. Fitzmaurice, Haralabos Parissis,

Cardiac Arrest and Resuscitation

Transfusion-related acute lung injury is a potentially fatal complication of blood and plasma transfusion; however, the incidence relating to platelet use in cardiac surgery is uncommon. In the presence of normal left ventricular function, an acute increase in pulmonary capillary permeability leads to a high protein content pulmonary edema, which leads to a dramatic reduction in pulmonary function due to acute lung injury and also intravascular fluid depletion. The clinical picture is acute and the condition is associated with considerable mortality. Although the exact mechanism of transfusion-related acute lung injury is unknown, it may be due to an antibody-mediated reaction caused by preformed leukocyte antibodies or activation of inflammatory mediators. The signs, diagnosis, and therapeutic interventions are discussed with reference to a case report. Transfusion-related acute lung injury is a potentially fatal complication of blood and plasma transfusion; however, the incidence relating to platelet use in cardiac surgery is uncommon. In the presence of normal left ventricular function, an acute increase in pulmonary capillary permeability leads to a high protein content pulmonary edema, which leads to a dramatic reduction in pulmonary function due to acute lung injury and also intravascular fluid depletion. The clinical picture is acute and the condition is associated with considerable mortality. Although the exact mechanism of transfusion-related acute lung injury is unknown, it may be due to an antibody-mediated reaction caused by preformed leukocyte antibodies or activation of inflammatory mediators. The signs, diagnosis, and therapeutic interventions are discussed with reference to a case report. Transfusion-related acute lung injury (TRALI) is a potentially fatal complication of blood, and blood product transfusion, and it is estimated to be a leading cause of transfusion-related mortality [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar]. All types of blood products have been associated with TRALI; however, the plasma-rich components, such as fresh frozen plasma and apheresis platelets, have been most frequently implicated [2Triulzi D.J. Transfusion-related acute lung injury: current concepts for the clinician.Anesth Analg. 2009; 108: 770-776Crossref PubMed Scopus (144) Google Scholar]. In contrary, previous reports have demonstrated that platelet transfusions are not associated with an increased morbidity or mortality among cardiac surgical patients [3Karkouti K. Wijeysundera D.N. Yau T.M. et al.Platelet transfusions are not associated with increased morbidity or mortality in cardiac surgery.Can J Anesth. 2006; 53: 279-287Crossref PubMed Scopus (63) Google Scholar]. There is only one previous report in the literature that associated platelet transfusion alone with TRALI postcardiac surgery [4Lin Y. Kanani N. Naughton F. Pendergast J. Karkouti K. Case report: transfusion-related acute lung injury (TRALI) – a clear and present danger.Can J Anesth. 2007; 54: 1011-1016Crossref PubMed Scopus (13) Google Scholar]. We report the case of a patient who underwent uneventful coronary artery bypass grafting, but became profoundly unstable approximately 20 minutes after completion of the transfusion of a single unit of platelets due to TRALI. We present the case of a previously well 49-year-old man who was referred for inpatient coronary artery bypass grafting. His preoperative medications included aspirin, clopidogrel (stopped 7 days prior to surgery), and enoxaparin. His pulmonary function tests and coagulation profile were normal, and the echocardiogram demonstrated normal left ventricular function with no valvular disease. The patient underwent a standard coronary artery bypass grafting procedure with core cooling to 34°C, and antegrade and retrograde myocardial protection with warm and cold blood cardioplegia. The grafts used were pedicle left internal mammary artery to mid-left anterior descending coronary artery, and long saphenous vein right coronary artery–posterior descending artery, right coronary artery, and obtuse marginal artery. The clamp time was 67 minutes and the pump time was 121 minutes. He was weaned from cardiopulmonary bypass on the first attempt and transferred to the cardiac intensive care unit in a stable condition, intubated and ventilated. In the first 2 hours postoperatively, he had a chest drain output of 460 mL. Thromboelastography was completed, which demonstrated a short maximum amplitude time with a postoperative platelet count of 91; consequently he received 1 unit of platelets through a standard filtered, giving set (Table 1). Approximately 20 minutes after the completion of the platelet transfusion, he became profoundly hypotensive and hypoxic with a raised pulmonary artery pressure. An urgent transoesphagheal echocardiogram demonstrated no evidence of cardiac tamponade with good left ventricular function; however, a chest roentgenogram demonstrated significant lung infiltrates (Fig 1). His arterial blood gas showed a respiratory acidosis with a pO2:FiO2 ratio of 131 mm Hg (Table 1).Table 1Postoperative Arterial Blood Gas Measurements and Coagulation ProfileaPlatelet transfusion commenced at 15.45.Time15:0016:1516:4416:5818:28FiO270%55%100%100%80%pH7.2967.3327.267.2557.294pO2 (kPa) (mm Hg)51.8 (389)9.7 (72)11.4 (86)13.5 (101)32.1 (241)pCO2 (kPa)5.865.546.176.415.44Lactate1.51.51.51.93.0pO2 : FiO255613186101301Platelet count91————Prothrombin time21.00————APTT37.40————Fibrinogen1.19————APTT = activated partial thromboplastin time.a Platelet transfusion commenced at 15.45. Open table in a new tab APTT = activated partial thromboplastin time. The patient was treated as a suspected case of TRALI and was managed with supportive care, including nitric oxide, steroids, intravenous fluids, and continued inotropic support. He made a steady recovery as inotropic support was weaned, and he was extubated 48 hours after the onset of TRALI. The remainder of his postoperative course was uneventful, and he was discharged from the hospital in good condition. Analysis of the used platelet bag and the patients own blood demonstrated no evidence of antibodies or bacterial contamination. The platelets were pooled from 4 female donors, all parous with a history of between 2 and 5 pregnancies each, and who had been well at the time of donation. Two of the female donors were found to be human lymphocyte antigen and Human Neutrophil Antigen antibody positive. In addition, the donor who had provided the plasma that was used to suspend the platelet pool was found to have both class I and II human lymphocyte antigen antibodies, whereas the patient had the cognate antigen, specifically A*25 and DR51. Transfusion-related acute lung injury is a potentially fatal complication of blood and blood product transfusion, and it is estimated to be a leading cause of transfusion-related mortality [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 2Triulzi D.J. Transfusion-related acute lung injury: current concepts for the clinician.Anesth Analg. 2009; 108: 770-776Crossref PubMed Scopus (144) Google Scholar]. Diagnosis is based on clinical and radiologic findings, which include acute onset (during or within 6 hours of transfusion), hypoxia (pO2:FiO2 ratio < 300 mm Hg), respiratory distress, and bilateral pulmonary infiltrates with no clinical evidence of intravascular fluid overload [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 4Lin Y. Kanani N. Naughton F. Pendergast J. Karkouti K. Case report: transfusion-related acute lung injury (TRALI) – a clear and present danger.Can J Anesth. 2007; 54: 1011-1016Crossref PubMed Scopus (13) Google Scholar]. Although the incidence of TRALI is biased, due to under-reporting, it ranges from 0.001% to 0.16% [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 5Rubenfeld G.D. Caldwell E. Peabody E. et al.Incidence and outcomes of acute lung injury.N Engl J Med. 2005; 353: 1685-1693Crossref PubMed Scopus (2973) Google Scholar]. Transfusion-related acute lung injury has been associated with all plasma containing blood product transfusions, but it is more likely to occur with large plasma volumes such as fresh frozen plasma [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar]. Treatment is supportive involving respiratory support with the possible addition of inotropes as required [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar]. Although the use of diuretics is contentious, there has been some evidence supporting the use of steroids [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 4Lin Y. Kanani N. Naughton F. Pendergast J. Karkouti K. Case report: transfusion-related acute lung injury (TRALI) – a clear and present danger.Can J Anesth. 2007; 54: 1011-1016Crossref PubMed Scopus (13) Google Scholar]. Prognosis is good with early diagnosis and intervention, and the time-course ranges from 48 to 96 hours with a mortality of 5% to 10% [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar]. The exact mechanism behind TRALI is unknown, but two theories have been postulated [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 2Triulzi D.J. Transfusion-related acute lung injury: current concepts for the clinician.Anesth Analg. 2009; 108: 770-776Crossref PubMed Scopus (144) Google Scholar, 4Lin Y. Kanani N. Naughton F. Pendergast J. Karkouti K. Case report: transfusion-related acute lung injury (TRALI) – a clear and present danger.Can J Anesth. 2007; 54: 1011-1016Crossref PubMed Scopus (13) Google Scholar]. The first describes an antibody-mediated reaction in which preformed leukocyte antibodies in the donor plasma cause activation of the complement system; however, in many cases, neither the donor nor the recipient's plasma has demonstrated an antibody to cause activation of the cascade [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 2Triulzi D.J. Transfusion-related acute lung injury: current concepts for the clinician.Anesth Analg. 2009; 108: 770-776Crossref PubMed Scopus (144) Google Scholar, 4Lin Y. Kanani N. Naughton F. Pendergast J. Karkouti K. Case report: transfusion-related acute lung injury (TRALI) – a clear and present danger.Can J Anesth. 2007; 54: 1011-1016Crossref PubMed Scopus (13) Google Scholar]. Hence, the second “double-hit” theory that describes the administration of biologically active mediators to unwell patients, which causes activation of inflammatory mediators that can damage the pulmonary vascular endothelium [1Barrett N.A. Kam P.C.A. Transfusion-related acute lung injury: a literature review.Anaesthesia. 2006; 61: 777-785Crossref PubMed Scopus (48) Google Scholar, 2Triulzi D.J. Transfusion-related acute lung injury: current concepts for the clinician.Anesth Analg. 2009; 108: 770-776Crossref PubMed Scopus (144) Google Scholar, 4Lin Y. Kanani N. Naughton F. Pendergast J. Karkouti K. Case report: transfusion-related acute lung injury (TRALI) – a clear and present danger.Can J Anesth. 2007; 54: 1011-1016Crossref PubMed Scopus (13) Google Scholar]. This “double-hit” theory is particularly relevant to cardiac surgeons because cardiopulmonary bypass is one mechanism by which the pulmonary vasculature may be initially damaged. The impact of blood product transfusion on lung injury after cardiopulmonary bypass poses a unique challenge when attempting to apply standard definitions of TRALI, in part, because measures of pulmonary morbidity may not reflect injury but cardiac events that prolong ventilatory support [6Koch C. Li L. Figueroa P. Mihalijevic T. Svensson L. Blackstone E.H. Transfusion and pulmonary morbidity after cardiac surgery.Ann Thorac Surg. 2009; 88: 1410-1418Abstract Full Text Full Text PDF PubMed Scopus (128) Google Scholar]. Nevertheless, blood product transfusion in cardiac surgery is associated with pulmonary morbidity. Despite this, TRALI is an uncommon complication of cardiac surgery; however, in 2010, Vlaar and colleagues [7Vlaar A.P. Binnekade J.M. Prins D. et al.Risk factors and outcome of transfusion-related acute lung injury in the critically ill: a nested case-control study.Crit Care Med. 2010; 38: 771-778Crossref PubMed Scopus (162) Google Scholar] demonstrated emergency cardiac surgery as an independent risk factor for TRALI. Cardiopulmonary bypass has previously been established as an independent cause of pulmonary injury through activation of the systemic inflammatory response [8Clark S.C. Lung injury after cardiopulmonary bypass.Perfusion. 2006; 21: 225-228Crossref PubMed Scopus (105) Google Scholar]. Although numerous methods to alleviate this insult exist, such as off-pump surgery, it highlights the fact that postoperative cardiac surgical patients are at risk of acute lung injury prior to any competing transfusion-related insult [8Clark S.C. Lung injury after cardiopulmonary bypass.Perfusion. 2006; 21: 225-228Crossref PubMed Scopus (105) Google Scholar]. Although this case was related to platelet administration, previous reports have demonstrated that platelet transfusions are not associated with an increased morbidity or mortality among cardiac surgical patients [3Karkouti K. Wijeysundera D.N. Yau T.M. et al.Platelet transfusions are not associated with increased morbidity or mortality in cardiac surgery.Can J Anesth. 2006; 53: 279-287Crossref PubMed Scopus (63) Google Scholar]. With this in mind, it is important to be vigilant with regard to TRALI in these patients. For the cardiac surgeon, it is important to be aware of the potential for TRALI, particularly in patients who have received platelets. It is also important to be aware of the increased risk in emergency cardiac surgical cases. Early recognition and institution of the best supportive care can lead to positive outcomes. In the interim, research is ongoing into the exact mechanism behind TRALI, and efforts continue to alter both blood products and donor criteria to limit the risks of TRALI to our patients.