Postperfusion lung syndrome following coronary artery bypass grafting: the timing of extubation Running title: Postperfusion lung syndrome Shi-Min Yuan Department of Cardiothoracic Surgery, Affiliated Hospital of Taishan Medical College, Taian 271000, Shandong Province, People’s Republic of China. Correspondence to: Shi-Min Yuan, MD, PhD, Professor of Surgery & Head, Department of Cardiothoracic Surgery, Affiliated Hospital of Taishan Medical College, 706 Taishan Street, Taishan District, Taian 271000, Shandong Province, People’s Republic of China. Tel: +86 538 6237167; Fax: +86 538 8420042; E-mail: s.m.yuan@v.gg 1 Abstract The postperfusion lung syndrome is an uncommon event after open-heart surgery. However, the timing of tracheal extubation after the operation remains controversy. A 58-year-old female patient underwent coronary artery bypass grafting. She developed postperfusion lung syndrome after the operation. In spite of stable cardiopulmonary condition, her SaO2 and PaO2 were low. After 42 hours' intubation, she was successfully weaned and extubated. She was doing well after the operation. Patients with postperfusion lung syndrome may benefit from early extubation after the operation. Non-invasive ventilation support can be an adjunct to the respiratory management if necessary. Keywords: Coronary artery bypass; Heart-lung machine; Lung injury; Ventilation. 2 Introduction The postperfusion lung syndrome is an uncommon event after open-heart surgery with an incidence of 1-2% [1]. In spite of the development of minimally invasive surgery and off-pump coronary artery bypass techniques, pulmonary complications remain a leading cause of early postoperative morbidity and mortality [2]. On the one hand, general anesthesia, thoracotomy and sternotomy may inevitably cause respiratory function impairment; on the other hand, aged patients may have innate lung diseases (asthma, emphysema, COPD or pulmonary artery hypertension, etc.) may exacerbate the pulmonary complications [2]. Cardiopulmonary bypass leads to systemic inflammatory response, which may involve pulmonary, renal, gut, central nervous system, and myocardial dysfunction; coagulopathy; vasoconstriction; capillary permeability; vasodilatation; accumulation of increased interstitial fluid; hemolysis; pyrexia; and increased susceptibility to infections and leukocytosis [3]. When this pathological course progresses prevailing with an acute lung inflammation, it is called postperfusion lung syndrome [4]. Even though the treatment strategies for this syndrome have been described, the timing of tracheal extubation remains controversy. This article aims to discuss this topic in connection with a recent case. Case Report A 58-year-old female patient was admitted to the Department of Cardiology due to exertional chest distress for 20 years. She had a history of hypertension and cerebral infarction. At the initial admission, her blood pressure was 160/100 mmHg. Physical examination revealed no rales over both lungs. Her heart rate was 68 beats/min, no heart murmur was audible. Electrocardiogram revealed depressed S-T segment in leads I, aVL, and V4-6 and inverted T 3 waves in leads V4-6 . Roentgenogram showed clear lung field (Fig. 1). She was diagnosed of old myocardial infarction, acute coronary syndrome, primary hypertension, and cerebral infarction. She received coronary angiography which showed a diffuse stenosis of LAD 60-80%, the first diagonal branch 70%, and mid-right coronary artery 90% (Fig. 2). She underwent coronary artery bypass with the left internal mammary artery grafted to the LAD, and a saphenous vein grafted sequentially to the first diagonal branch and the posterior descending artery. The bypass time was 102 min and the crossclamp time was 72 min. Prebypass blood-gas analysis revealed SaO2 was 91% and PaO2 was 64 mmHg. At 8:30 AM of the first day after the operation, the module of the ventilator was changed into CPAP, PEEP was decreased to 2 cmH2O, FiO2 to 40%, and the SaO2 was kept at 87%. At 9 o'clock, the mechanical ventilator was weaned from the patient, inspired with high concentration of oxygen (5 L/min), and the SaO2 of the patient was kept at 82-83%. PaO2 was 51 mmHg. Meanwhile, the patient had a stable blood pressure 122/70 mmHg. She complained no respiratory symptoms. The patient was conscious and demanded an extubation by shaking her head. However, she was refused according to the guild line of extubation of an SaO2 of 85% at the ICU. She was given sediment and the module of the ventilator was changed back into PEEP 6, SIMV 10, and FiO2 60%. The patient's temperature was normal, and no rales was audible. Blood examinations were normal for the electrolytes and the proteins. Chest roentgenogram revealed small patchy shadows over both lungs (Fig. 3), suggesting a diagnosis of postperfusion lung syndrome. Till then, she was intravenously infused 310 ml, and her urinary output was 280 ml. She thus received intravenous furosemide and high doses of methylprednisolone. She was stable and the SaO2 was 86-88% with 4 intubation on the second day. She was with successfully weaned and further extubated, and her SaO2 was 85-94% with low flow oxygen with nasal cannula. Non-invasive ventilation was not needed. The ventilatory support time was 42 hours. Since then, she had an uneventful course, and was discharged home 11th day after the operation. Discussion Postperfusion lung syndrome is a breathing complication developed within hours of cardiac operation performed with the aid of cardiopulmonary bypass. The pathophysiological changes may include ventilatory alcalosis, hypocapnia, hypoxemia and the rise in the alveolar arterial oxygen gradient is increased during the second postoperative day [5]. Mitochondrial and lamellar body damages and endothelial and alveolar swelling were major observations following cardiopulmonary bypass under an electron microscope [6]. Postperfusion lung syndrome seems to be related to the types of oxygenator used in the cardiac surgery, as the clinical observations of the early years have revealed that Travenol bubble oxygenator may bring about more severe pulmonary injury than with a membrane oxygenator [7]. Age of patients, severity of disease, preoperative pulmonary function, prolonged duration of extracorporeal circulation and myocardial ischemia have been found to be predisposing factors responsible for the postoperative cardiopulmonary morbidities [8]. Patients with this syndrome may present with constitutional symptoms including weakness, anorexia, fever, hypoventilation except for breathing problems like shortness of breath [9]. Apart from the usual management strategies, to treat the downstream, neutrophil-derived effectors was proved to be an alternative way of therapy [10]. Invasive mechanical ventilation is associated with numerous complications and the return to 5 spontaneous ventilation has many physiological benefits. Therefore, early weaning and extubation have been proposed following trauma control surgery for these well-known reasons in particular in those patients with stable cardiopulmonary conditions [11]. Protracted ventilatory support may bring about mechanical damage to the patient's respiratory tract and may alleviate the patient's immunity leading to infections and multiple organ dysfunction. If the the patient remains hypo-oxygenation after extubation, non-invasive ventilation support can be an adjunct to the respiratory management if necessary. In conclusion, patients with postperfusion lung syndrome may benefit from early extubation after the operation. Non-invasive ventilation support can be an adjunct to the respiratory management if necessary. 6 References 1. Luciani GB, Pessotto R, Mazzucco A. Adrenoleukodystrophy presenting as postperfusion syndrome. N Engl J Med. 1997;336(10):731-2. 2. 1Weissman C. Pulmonary complications after cardiac surgery. Semin Cardiothorac Vasc Anesth. 2004;8(3):185-211. 3. Utley JR. Pathophysiology of cardiopulmonary bypass: a current review. Aust J Cardiac Thorac Surg 1992;1:46–52. 4. Fujii M, Miyagi Y, Bessho R, Nitta T, Ochi M, Shimizu K. Effect of a neutrophil elastase inhibitor on acute lung injury after cardiopulmonary bypass. Interact Cardiovasc Thorac Surg. 2010;10(6):859-62. 5. Foliguet B. Pulmonary complications after extracorporeal circulation. ECC lung syndrome. Ann Anesthesiol Fr. 1977;18(1):134-49. 6. Anyanwu E, Dittrich H, Gieseking R, Enders HJ. Ultrastructural changes in the human lung following cardiopulmonary bypass. Basic Res Cardiol. 1982;7(3):309-22. 7. Byrick RJ, Noble WH. Postperfusion lung syndrome. Comparison of Travenol bubble and membrane oxygenators. J Thorac Cardiovasc Surg. 1978;76(5):685-93. 8. Gattiker R, Pescia R. Cardio-pulmonary complications, respiratory treatment and PaO2 after open heart surgery. Herz. 1978;3(3):191-7. 9. Postperfusion lung syndrome. http://www.rightdiagnosis.com/p/postperfusion_lung_syndrome/intro.htm. 10. Carney DE, Lutz CJ, Picone AL, Gatto LA, Ramamurthy NS, Golub LM, Simon SR, Searles B, Paskanik A, Snyder K, Finck C, Schiller HJ, Nieman GF. Matrix 7 metalloproteinase inhibitor prevents acute lung injury after cardiopulmonary bypass. Circulation. 1999;100(4):400-6. 11. Thornhill R, Tong JL, Birch K, Chauhan R. Field intensive care--weaning and extubation. J R Army Med Corps. 2010;156(4 Suppl 1):311-7. 8 Legends of Figures Fig. 1. Preoperative chest roentgenogram showed clear lung field. Fig. 2. Coronary angiography which showed (A) a diffuse stenosis of the left anterior descending coronary artery 60-80%, the first diagonal branch 70%, and (B) mid-right coronary artery 90%. Fig. 3. Postoperative chest roentgenogram revealed small patchy shadows over both lungs. 9 Fig. 1. 10 Fig. 2 11 Fig. 3 12