Postoperative pulmonary complications



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REVIEW Postoperative pulmonary complications J., V. MAZO Department of Anesthesiology, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain ABSTRACT Postoperative pulmonary complications (PPC) account for a substantial portion of the risks related to surgery and anesthesia and are a source of postoperative morbidity, mortality and longer hospital stays. The current basis for our understanding of the nature of PPC is weak; only a small number of high-quality studies are available, a uniform definition has not emerged, and studies have focused on specific patients and kinds of surgeries. Current evidence suggests that risk factors for PPC are related to the patient s health status and the particular anesthetic and surgical procedures chosen. Age, general co-morbidity, pre-existing respiratory and cardiac diseases, the use of general anesthesia and the overall surgical insult. are the most significant factors associated with complications. Election of anesthetic technique, postoperative analgesia and physical therapy seem to be the preventive measures that are best supported by evidence. (Minerva Anestesiol 2010;76:138-43) Key words: Postoperative complications, Pulmonary atelectasis, Smoking, Continuous positive airway pressure, Analgesia. Postoperative pulmonary complications (PPC) account for a substantial proportion of morbidity and mortality related to surgery and anesthesia and lead to longer hospital stays. 1 The aim of this review is to describe the current evidence underpinning our understanding of PPC and to highlight measures that might become necessary at different points during the course of perioperative care. Definition and incidence of PPC There is no standard definition of PPC.Most investigators include postoperative pneumonia (confirmed or suspected), respiratory failure (usually defined as the need for ventilatory support) and bronchospasm, but analysis of the literature shows that other complications, such as unexplained fever, excessive bronchial secretions, productive cough, abnormal breath sounds, atelectasis or hypoxemia, may also be included. The incidence of PPC varies depending on the clinical treatment setting, the kind of surgery studied, and the definition of PPC used. For all of these reasons, incidence rates vary dramatically, ranging from 2% to 40%. 2 Causes of PPC The factors affecting the development of PPC are related to the prior health status of the patient and the effects of anesthesia and surgical trauma. The synergy between these factors determines risk. 3 General health status The patient s overall health has a strong influence on the development of complications. Preexisting disorders that affect normal respiratory and cardiovascular function and those associated with an abnormal immune response favor the development of complications. 138 MINERVA ANESTESIOLOGICA February 2010

General anesthesia General anesthesia has biological effects on the respiratory system and also results in mechanical and functional changes that enhance those effects. These effects begin with anesthetic induction and can extend into the postoperative period. General anesthesia reduces functional residual capacity, with an immediate and universal development of atelectasis in the dependent regions of the lung through three mechanisms: compression of lung tissue, absorption of alveolar air, and impairment of surfactant function. The resulting ventilationperfusion mismatch leads to increased shunt, dead space and hypoxemia. Anesthetics, analgesics and other perioperative drugs affect the central regulation of breathing, changing the neural drive of the upper airway and chest wall muscles and further contributing to PPC. Overall, the intensity and coordination of the activities of several muscle groups and the preservation of biological mechanisms in the lung are the keys to shifting the balance toward recovery rather than severe respiratory complications. 4, 5 Additionally, immunosuppressive effects due to anesthesia 6 and intraoperative transfusion have also been invoked as contributors to poor postoperative outcome. 7 Surgical trauma The type of surgical insult contributes greatly to the development of PPC. 3 All thoracic and abdominal surgery involves trauma near the diaphragm, resulting in at least three types of trauma. The first is functional disruption of respiratory muscle movements, caused by incisions. The second is the effect of postoperative pain in limiting respiratory motion. The third is the reflex inhibition of the phrenic nerve and other nerves that innervate respiratory muscles, a result of stimulating the viscera by mechanical traction. As a consequence, in the postoperative period, normal respiratory muscle activity, particularly that of the diaphragm, is disrupted. 8 Factors related 4 to the degree of surgical insult, such as level of aggressiveness, procedure duration or amount of blood lost, may by themselves increase the risk of PPC or may interact with the local effects described above. The postoperative immune response is extremely complex and has detrimental procoagulant and immunosuppressive effects. Proinflammatory cytokines, especially tumor necrosis factor α and interleukin-6, are major players because of their roles in the systemic inflammatory response syndrome and multiple organ dysfunction after trauma. Again, immune depression, in this case provoked by the surgical insult, may be invoked as a mediator that increases the risk of postoperative respiratory infection and other complications. 4 Preoperative management Preoperative assessment includes taking a medical history, paying close attention to preexisting respiratory diseases, smoking, respiratory symp- TABLE I. Significant risk factors according the systematic review of the American College of Physicians. 6 Level of evidence Patient Procedure Laboratory test A (good evidence) Cardiac failure ASA class 2 Advanced age COPD Functional dependence Aortic aneurysm Thoracic surgery Abdominal surgery Upper abdominal surgery Neurosurgery Prolonged surgery (>3h) Head and neck surgery Emergency surgery Vascular surgery General anaesthesia Low serum albumin B (fair evidence) Weight loss Impaired sensorium Cigarette use Alcohol use Transfusion Chest X-ray Blood urea Vol. 76 - No. 2 MINERVA ANESTESIOLOGICA 139

TABLE II. Postoperative Pneumonia Risk Index. Perioperative risk factor point value Type of surgery Abdominal aortic aneurysm repair 15 Thoracic 14 Upper abdominal 10 Neck 8 Neurosurgery 8 Vascular 3 Age >80 yr 17 70-79 yr 13 60-69 yr 9 50-59 yr 4 Functional status Totally dependent 10 Partially dependent 6 Weight loss >10% in past six months 7 History of chronic obstructive pulmonary disease 5 General anesthesia 4 Impaired sensorium 4 History of cerebrovascular accident 4 Blood urea <8 mg/dl 4 22-30 mg/dl 2 30 mg/dl 3 Blood transfusion >4 U 3 Emergency surgery 3 Steroid use for chronic condition 3 Current smoker within one year 3 Alcohol intake >two drinks/day in past two weeks 2 Pneumonia risk: 0-15 points, 0.24%; 16-25 points, 1.18%; 26-40 points, 4.6%; 41-55 points, 10.8%; >55 points, 15.9%. From Arozullah AM et al. 12 toms and any medications that have been given for respiratory disorders. A positive cough test (performed by having the patient take a deep breath and cough once, with a positive finding defined as repeated coughing after the first cough) has been demonstrated as a predictor of PPC. 9 The cough test is easy to perform and could possibly indicate some degree of airway hyperreactivity and hypersecretion. With the exception of assessment prior to lung resection surgery, there is no evidence that routine chest radiographs 10 or pulmonary function tests are beneficial. 11 The first step in respiratory management is to identify the preoperative risk factors associated with PPC. Table I shows factors with good (level A) or fair (level B) evidence according to a systematic review by the American College of Physicians. 11 The same meta-analysis shows that there is fair or good evidence that diabetes, obesity, asthma, and hip, gynecological and urologic surgery do not increase the risk of PPC. Obstructive sleep apnea syndrome has also not been definitively implicated in an increased risk of PPC. Predictive indices for postoperative pneumonia 12 (Table II) and respiratory failure 13 have been developed within the context of the US National Veterans Affairs Improvement Program for identifying high-risk patients. However, although these studies included the largest known samples with regard to PPC, the patients were mostly male veterans who were far from representative of a general surgical population. Preventive measures SMOKING CESSATION Several studies have analyzed the beneficial effects of preoperative smoking cessation as well as how long before surgery the patient should quit smoking. 14 This is an important step, and patients should be informed about how quitting will decrease their perioperative risk. The degree of benefit will depend on three factors: the amount of lifetime smoking (pack-years), how long the patient has been abstinent, and age at the moment of smoking cessation. There is no clear evidence regarding whether risk for PPC derives from smoking per se or is due to the comorbidity that smoking generates. Nonetheless, preoperative abstinence should be recommended and an abstinence period of at least 4-6 weeks seems to be the most beneficial. 15 The following evidence and pathophysiologic reasoning supports this advice: 16 the effects that are attributable to carbon monoxide and nicotine disappear during the first 12-48 hours of abstinence; at one week after smoking cessation, airway reactivity is significantly reduced; at two weeks after smoking cessation, sputum volume is reduced by half and declines steadily over a six-week period. It is not clear whether the transient increase in cough and sputum production during the first two weeks increases the risk for PPC. In addition, observational studies suggest that patients are more prone to quitting smoking permanently after undergoing surgery. 17 For this reason, it is very important to be aware that the preoperative visit is a window of opportunity for encouraging patients to quit smoking through counseling. 18 Parents should also be warned about 140 MINERVA ANESTESIOLOGICA February 2010

the consequences of smoking for their children who are about to undergo surgery. PATIENTS WITH A CHRONIC PULMONARY DISEASE Patients with a chronic pulmonary disease, especially those with some degree of bronchial hyperreactivity, might benefit from starting preoperative bronchodilator therapy or increasing the therapy dosage. 19 Extra vigilance is needed for patients who have suffered an acute respiratory exacerbation, including influenza; in cases of elective surgery, cancellation might be advisable. PREOPERATIVE PHYSICAL THERAPY There is no clinical evidence supporting routine preoperative physiotherapy, even in high-risk patients. 3 However, therapy may be advisable in specific cases to reduce bronchial secretions and to teach breathing techniques that can be used postoperatively. NUTRITION A low preoperative albumin concentration has been shown to be a good predictor of PPC; 20, 21 for this reason, it would seem advisable for patients who are severely undernourished to receive preoperative nutritional supplements. However, there is no proven advantage to total parenteral nutrition over enteral nutrition or even no supplementation. 21 Intraoperative management Anesthetic technique No evidence currently provides strong support for recommending one anesthetic technique over another in order to reduce the incidence of PPC. If avoidance of general anesthesia is feasible, this precaution might be advisable in patients at high risk for PPC in order to reduce the formation of atelectases. The only measure proven to be beneficial is the avoidance of long-acting neuromuscular blocking drugs (e.g., pancuronium), 21,22 the likely mechanism being the association between residual muscle paralysis and PPC. 22 Ventilatory management There is no consensus on how to ventilate patients during surgery to reduce the risk of PPC. In general, a low tidal volume strategy is advised for all patients 23, and therapeutic strategies for preventing and treating atelectasis should be planned for those at higher risk. 24, 25 It has been shown that the incidence of atelectasis can be reduced by using positive airway pressure, either as positive end-expiratory pressure (PEEP) 26 or continuous pressure (CPAP), even before anesthetic induction 27 and intraoperative recruitment maneuvers. 28 The application of intraoperative positive pressure in obese patients 26 or in specific surgical procedures 29 also reduces the incidence of atelectasis. No clear recommendation regarding intraoperative ventilatory management for reducing the incidence of PPC has emerged, however. Further prospective studies are needed. Fluid therapy It has been suggested that perioperative fluid overloading might increase the risk of PPC, but no evidence has been found to support this assumption in a general surgical population. 30 An association between transfusion and PPC has been demonstrated, 12 however; therefore, it seems advisable to avoid transfusion if possible. Surgical management Risk factors related to the type of surgery play a large role in promoting PPC. 3, 11 To some extent, these factors can be mitigated by surgeons, and this possibility should be discussed whenever patients are at high risk for complications. Measures to apply might include: 1) avoiding emerging surgical techniques whenever possible; 2) reducing surgical aggressiveness and duration if possible; and 3) using minimally invasive surgery (e.g., laparoscopic surgery) whenever possible. Postoperative management Postoperative analgesia The most important measure to implement postoperatively to reduce the incidence of PPC is the provision of adequate analgesia. Postoperative epidural or intravenous patient-controlled analgesia both seem to be superior to on-demand delivery of opioids in preventing PPCs. 21, 31 The epidural route of administration seems to be superior to Vol. 76 - No. 2 MINERVA ANESTESIOLOGICA 141

others for delivering opioids in terms of preventing PPCs, and epidural analgesia by itself may further reduce PPC. 32 Evidence regarding postoperative epidural analgesia remains insufficient, however. A greater number of high-quality trials are needed to accurately assess the whether this modality is superior to others in reducing PPC rates. Postoperative lung expansion measures Lung expansion techniques include incentive spirometry, chest physical therapy, deep breathing exercises, postural drainage, and CPAP. There is evidence that for patients undergoing thoracic and abdominal surgery, any type of lung expansion intervention is better than none. 21, 33 However, no single modality is better than any other, and combining methods does not provide additional risk reduction. 34, 35 Local treatment protocols may already be available for specific high-risk patient groups. Simple measures (positioning, mobilization, hydration, cough stimulation, ambulation, sleep) are probably best for reducing the incidence of complications. Nasogastric tube Routine placement of nasogastric tubes refers to their use after surgery until the return of gastrointestinal motility. A meta-analysis examined evidence of selective versus routine nasogastric decompression after elective laparotomy, 36 finding that a tube should be introduced if the patient has postoperative nausea or vomiting, is unable to tolerate oral intake, or there is symptomatic abdominal distension. Patients receiving selective nasogastric decompression have been found to possess a significantly lower rate of pneumonia and atelectasis with no difference in aspiration rates. It should be noted, however, that nasogastric tube placement impairs the cough reflex and provides a more direct pathway for oro-pharyngeal bacteria to the lungs, thus potentially increasing respiratory tract infections. Treatment of PPC Early postoperative hypoxemia is very common, especially in those patients and surgical settings in which there is a greater risk of atelectasis. 37 Postoperative oxygen therapy should not be used routinely. Routine continuous pulse oximetry during the first postoperative hours, with a target of maintaining 92% or greater saturation, is one selective strategy. Any method of oxygen administration alleviates hypoxemia efficiently. 38 Late postoperative hypoxemia is a result of persistent atelectasis and the development of respiratory infection and failure. In high-risk patients, early application of CPAP may prevent the development of severe hypoxemia after elective major abdominal surgery. 39 If a PPC is suspected, arterial blood gas assessment, sputum culture, chest x-rays and an electrocardiogram should be ordered. Aggressive treatment is encouraged, to take advantage of the combination of antibiotics, physical therapy and ventilatory support. When acute postoperative respiratory failure develops, non-invasive continuous positive airway pressure is the first-choice method for ventilatory support, to avoid reintubation. 40 If respiratory failure progresses, however, and acute lung injury is demonstrated, invasive mechanical ventilation may be required. 40 Conclusions PPCs are often life threatening, as shown by PPC-associated mortality rates that can be as high as 20%. However, the level of evidence for implementing preventive measures is relatively low. Patient- and surgery-related factors have been identified, but many of them cannot be modified. The most important step is to identify high-risk patients. Few specific measures can be managed perioperatively. Election of anesthetic technique, postoperative analgesia and physical therapy seem to be the measures that are best supported by evidence at this time. Aggressive treatment of PPCs is mandatory if mortality is to be reduced. References 1. Smetana GW. Preoperative pulmonary evaluation. N Engl J Med 1999;340:937-44. 2. Rock P, Rich PB. Postoperative pulmonary complications. Curr Op Anaesthesiol 2003;16:123-32. 3. Warner DO. Preventing postoperative pulmonary complications. Anesthesiology 2000;92:1467-72. 4. Duggan M, Kavanagh BP. Pulmonary atelectasis. A pathogenic perioperative entity. Anesthesiology 2005;102:838-54. 5. Kavanagh BP. Perioperative atelectasis. Minerva Anestesiol 2008;74.285-7. 6. Ahlers O, Nachtigall I, Lenze J, Goldmann A, Schulte E, 142 MINERVA ANESTESIOLOGICA February 2010

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Anesthesiology 1999;91: 1221-31. 27. Rusca M, Proietti S, Schnyder P, Frascarolo P, Suter M, Spahn DR et al. Prevention of atelectasis formation during the induction of general anesthesia. Anesth Analg 2003;97:1835-9. 28. Magnusson L, Spahn DR. New concepts of atelectasis during general anesthesia. Br J Anaesth 2003;91:61-72. 29. Fernandez-Perez ER, Keegan MT, Brown DR, Hubmayr RD, Gajic O. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology 2006;105:14-8. 30. Grocott MP, Mythen MG, Gan TJ. Perioperative fluid management and clinical outcomes in adults. Anesth Analg 2005;100:1093-106. 31. Walder B, Schafer M, Henzi I, Tramer MR. Efficacy and safety of patient-controlled opioid analgesia for acute postoperative pain. A quantitative systematic review. Acta Anaesthesiol Scand 2001;45:795-804. 32. Liu SS, Block BM, Wu CL. 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Early postoperative arterial oxygen desaturation. Determinig factors and response to oxygen therapy. Anesth Analg 1989;69:207-12 38. McBrien ME, Sellers WFS. A comparison of three variable performance devices for postoperative oxygen therapy. Anaesthesia 1995;50:136-8. 39. Squadrone V, Coha M, Cerutti E, Schellino MM, Biolino P, OccellaP et al. Continuous positive airway pressure for treatment of postoperative hypoxemia: A randomized controlled trial. JAMA 2005;293:589-95. 40. Jaber S, Delay JM, Chanques G, Sebbane M, Jacquet E, Souche B et al. Outcomes of patients with acute respiratory failure after abdominal surgery treated with noninvasive positive pressure ventilation. Chest 2005;128:2688-95. Fundings. Supported by Fundació La Marató de TV3 grant 041610 (2003). Conflicts of interest. None. Acknowledgments. M. E. Kerans edited the English language in a version of the manuscript. Received on April 14, 2009 - Accepted for publication on October 13, 2009. Corresponding author: J. Canet, Department of Anesthesiology, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain. E-mail: jcanet.germanstrias@gencat.cat Vol. 76 - No. 2 MINERVA ANESTESIOLOGICA 143