Transfusion-related acute lung injury following ...

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TRALI has been defined as new acute lung injury (ALI)/ acute respiratory distress syndrome (ARDS) occurring during or within 6 hours after blood product ...
568367 research-article2015

PRF0010.1177/0267659114568367PerfusionBitargil et al.

Original Paper

Transfusion-related acute lung injury following coronary artery bypass graft surgery

Perfusion 2015, Vol. 30(8) 626­–628 © The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0267659114568367 prf.sagepub.com

M Bitargil,1 C Arslan,2 HS Başbuğ,1 H Göçer,1 Y Günerhan1and YY Bekov2

Abstract Blood transfusion is sometimes a necessary procedure during or following coronary artery bypass graft (CABG) surgery. However, transfusion-related acute lung injury (TRALI)/possible TRALI is a rare and fatal complication and characterized by acute hypoxemia and non-cardiogenic pulmonary edema that occurs within 6 hours following a transfusion. Antileukocyte antibodies or, possibly, other bioactive substances cause inflammation and capillary endothelial destruction in susceptible recipients’ lungs. Prompt diagnosis and mechanical ventilatory support are important. A successful treatment of two male patients following CABG surgery, compatible with TRALI/possible TRALI, is presented here. Keywords coronary artery bypass; blood transfusion; acute lung injury; cardiac surgery; complication

Introduction TRALI has been defined as new acute lung injury (ALI)/ acute respiratory distress syndrome (ARDS) occurring during or within 6 hours after blood product administration. It is a rare, but potentially fatal complication of the blood product transfusions.1 TRALI occurs at an approximate rate of 1 in 5000 transfused blood components. When an alternative risk factor for ALI/ARDS coexists, such as recent surgery, massive blood transfusion and active infection, the diagnostic terminology to be used is “possible TRALI”.2 It is the leading cause of transfusion-related mortality and TRALI/possible TRALI - associated mortality has ranged from 5 to 58 percent.3 In this article, two reports of possible TRALI cases following CABG surgery are presented.

Case Report Case 1 A 55-year-old man was referred to our department for CABG. Echocardiography showed a left ventricular ejection fraction (LVEF) of 60% and no valve pathology. His physical examination was normal. Cardiopulmonary bypass (CPB) commenced in a standard way. Myocardial protection was achieved via both antegrade and retrograde cardioplegia. Triple bypass was performed and the patient was weaned from the CPB. The postoperative

course was problem free and the patient was extubated in the intensive care unit (ICU) on the same night as the surgery. His hemodynamic parameters were normal. Oxygen pressure (PO2) was 110 mmHg and oxygen saturation (SO2) was 98 percent. His control chest x-ray was normal (Figure 1). During the second day of his stay in the ICU, blood transfusion was decided due to a low hematocrit (Hct) level. Four hours after the blood transfusion (fresh whole blood), the patient’s blood pressure (BP), SO2 and PO2 gradually decreased (PO2: 87-47-41 mmHg, SO2: 90-89-78%, BP: 85/45 mmHg), with tachypnea and dyspnea. Control echocardiography showed an LVEF of 55-60%. Urgent chest x-ray revealed infiltrations in the lung tissues (Figure 2). TRALI was suspected. The patient’s response to continuous positive airway 1Cardiovascular

Surgery Department, Kafkas University Medical Faculty, Kars, Turkey 2Cardiovascular Surgery Department, Istanbul University Cerrahpasa Medical Faculty, Istanbul, Turkey Corresponding author: Macit Bitargil Kafkas University Medical Faculty Cardiovascular Surgery Department 36000 Kars Turkey. Email: [email protected]

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Figure 1.  Postoperative chest roentgenogram of Case 1.

Figure 2.  Chest roentgenogram 4 hours after completion of blood transfusion, demonstrating diffuse lung infiltrates (Case 1).

pressure (CPAP) was not good, so he was intubated. The tidal volume was kept low and the peak lung pressure was kept under 30 mmHg via pressure-controlled ventilation. After the achievement of hemodynamic stability, diuretic and steroid therapy were applied. The patient was kept intubated for 48 hours. His general condition became better in days and PO2, SO2 and chest x-ray findings returned to normal (Figure 3). He was discharged on the tenth postoperative day fully recovered.

Case 2 A 44-year old man was referred to our department for CABG. His LVEF was 60% and his physical examination was normal. CABG was scheduled electively. Triple

Figure 3.  Chest roentgenogram 4 days after completion of blood transfusion, demonstrating recovery from infiltration. (Case 1).

bypass was performed. He was transferred to the ICU in a stable condition, intubated and ventilated. The first night of the ICU stay was problem free and the patient was extubated. His PO2 was 120 mmHg, his SO2 was 99%, the blood pressure was normal and a control chest x-ray was problem free. The patient’s Hct was 21% on the next day in the ICU and a blood transfusion was decided. Severe dyspnea and tachypnea developed within one hour after the administration of the erythrocyte suspension. The patient’s arterial blood gas, hemodynamic parameters and chest x-ray revealed respiratory distress (PO2: 57 mmHg, SO2: 85%, BP: 90/50 mmHg, pulse: 120/min, chest x-ray: bilateral infiltration). He was intubated and inotropic drug support was initiated. Steroid and diuretic therapy were applied. He was kept intubated for 48 hours, with a low tidal volume. His general condition became better on the following days and the PO2, SO2 and chest x-ray findings returned to normal. The remainder of his postoperative course was uneventful and he was discharged in good condition on the seventh postoperative day.

Discussion TRALI/possible TRALI is characterized by acute hypoxemia and non-cardiogenic pulmonary edema that occur within 6 hours following a transfusion;1 it is estimated to be a leading cause of transfusion-related mortality. The diagnosis of TRALI/possible TRALI is made clinically. The most common signs and symptoms are hypoxemia (SO2≤ 90% and it is seen in 100% of patients), pulmonary infiltrates on chest radiography (100%), pink

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frothy airway secretion from the endotracheal tube (56%), fever (33%), hypotension (32%) and cyanosis 25%. Tachypnea, tachycardia and a transient drop in peripheral neutrophil count are also common symptoms.4 Hypoxemia occurred within 6 hours following a transfusion in both of cases. Pulmonary infiltrates on chest x-ray, hypotension, tachypnea and tachycardia were present in both cases. There was no fever or transient drop in peripheral neutrophil blood count. Pink frothy airway secretion from the endotracheal tube and cyanosis were present in Case 1 and absent in Case 2. When an alternative risk factor for ALI/ARDS coexists, such as recent surgery, massive blood transfusion and active infection, the diagnostic terminology to be used is “possible TRALI”. The reason why this case was diagnosed as “possible TRALI” is the possibility of ALI via CABG. Differential diagnosis of TRALI/possible TRALI includes situations such as transfusionassociated circulatory overload (TACO), hemolytic transfusion reactions (HTR), anaphylaxis and sepsis. These are other conditions that can manifest with respiratory distress following transfusion. TACO is more likely to be associated with signs suggesting volume overload, such as elevated central venous pressure and positive fluid balance with hypertension that were absent in both of these cases. Sepsis is generally associated with leukocythemia, positive microbiology and fever. There were no such findings in either of the cases. Chills and fever and hemoglobinuria, which were absent in both of the cases, tend to predominate in HTR. This situation generally occurs due to ABO incompatibility. Anaphylaxis is associated with a new rash and gastrointestinal symptoms such as nausea and vomiting, which were also absent in both cases. All blood products may cause TRALI/possible TRALI. Plasma-rich components, such as apheresis platelet concentrates, fresh frozen plasma and whole blood carry the greatest risk.5 A unit of fresh whole blood was responsible for the reaction in Case 1 as was an erythrocyte suspension in Case 2. The exact mechanism is unknown, but it may be due to an antibody-mediated reaction caused by preformed leukocyte antibodies or the activation of inflammatory mediators, which cause an increase in pulmonary capillary permeability, high protein content pulmonary edema and a dramatic reduction in pulmonary function.6 The treatment of TRALI/possible TRALI is supportive. The transfusion should be stopped immediately. In less severe cases, oxygen supplementation via continuous positive airway pressure (CPAP) may be sufficient. However, endotracheal intubation is often required (80%).7 The use of diuretics is contentious, but there has been some evidence supporting the use of

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steroids.6 Patient responses to CPAP were not good, so they were intubated. The tidal volume was kept low and peak lung pressure was kept under 30 mmHg via pressure-controlled ventilation. After hemodynamic stability achievement, diuretic and steroid therapy were applied. The patients were kept intubated for 48 hours. Their general condition became better within a few days and the PO2, SO2 and chest x-ray findings returned to normal in both cases. Possible outcomes for patients with TRALI and/or possible TRALI remain incompletely defined. Although limited information is available, it appears that most survivors will recover to their baseline pulmonary function and they can safely receive additional blood products in the future.8 Since blood transfusions are sometimes necessary during or following CABG, the probability of TRALI/ possible TRALI occurrence should be kept in mind. Declaration of Conflicting Interest The authors declare that there is no conflict of interest.

Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

References 1. Toy P, Popovsky MA, Abraham E, et al. Transfusionrelated acute lung injury: definition and review. Crit Care Med 2005; 33: 721–726. 2. Silliman CC, Boshkov LK, Mehdizadehkashi Z, et al. Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. Blood 2003; 101: 454–462. 3. Vlaar AP, Binnekade JM, 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: 771–778. 4. Van Stein D, Beckers EA, Sintnicolaas K, et al. Transfusionrelated acute lung injury reports in the Netherlands: an observational study. Transfusion 2010; 50: 213–220. 5. Eder AF, Herron RM Jr, Strupp A, et al. Effective reduction of transfusion- related acute lung injury risk with male-predominant plasma strategy in the American Red Cross (2006–2008). Transfusion 2010; 50: 1732–1742. 6. Fitzmaurice GJ, Parissis HD. Platelet transfusion associated with acute lung injury after coronary artery bypass grafting. Ann Thorac Surg 2011; 91: 1977–1979. 7. Gajic O, Rana R, Winters JL, et al. Transfusion-related acute lung injury in the critically ill: prospective nested case-control study. Am J Respir Crit Care Med 2007; 176: 886–891. 8. Silliman CC, Ambruso DR, Boshkov LK. Transfusionrelated acute lung injury. Blood 2005; 105: 2266-2273.

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