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Preventing Postoperative Pulmonary Complications the Role of the Anesthesiologist David O

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Preventing Postoperative Pulmonary Complications the Role of the Anesthesiologist David O 1467 Ⅵ CLINICAL CONCEPTS AND COMMENTARY Richard B. Weiskopf, M.D., Editor Anesthesiology 2000; 92:1467–72 © 2000 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Preventing Postoperative Pulmonary Complications The Role of the Anesthesiologist David O. Warner, M.D.* THE Confederate General “Stonewall” Jackson was one widely. Nonetheless, it is still clear that PPCs occur of the earliest known victims of a respiratory complica- relatively frequently. In studies of noncardiac surgery, tion after surgery, dying of pneumonia 10 days after an the frequency of PPCs and cardiac complications (which otherwise successful ether anesthetic in 1863. Despite historically have attracted more attention from the anes- subsequent advances in anesthesia and surgical care, thesia community) are comparable.1 For example, in a postoperative pulmonary complications (PPCs) still are a series of adult men undergoing elective abdominal sur- significant problem in modern practice. This commen- gery, PPCs occurred significantly more frequently than tary examines why PPCs occur and how the anesthesi- cardiac complications (estimated rates of 9.6% and 5.7%, ologist can help prevent them. respectively) and were associated with significantly longer hospital stays.1 Significance of Perioperative Pulmonary Causes of Perioperative Pulmonary Complications Complications Determination of the frequency and clinical impact of A basic understanding of mechanism guides rational PPCs in modern practice is hampered by the lack of a practice. Many PPCs, such as atelectasis and pneumonia, uniform definition of a PPC among studies. Nearly all seem to be related to disruption of the normal activity of investigators include in this definition pneumonia (defi- the respiratory muscles, disruption that begins with the nite or suspected), respiratory failure (usually defined as induction of anesthesia and that may continue into the the need for mechanical ventilatory support), and bron- postoperative period. Breathing is a complex behavior chospasm. Others include unexplained fevers, excessive requiring the coordinated activity of several muscle bronchial secretions, abnormal breath sounds, “produc- groups, both in the upper airway and in the chest wall. tive” cough, atelectasis (often not defined), and hypox- Anesthetics and many other drugs used in the perioper- emia. Even within these categories, definitions vary ative period affect the central regulation of breathing, changing the neural drive to respiratory muscles such as * Professor of Anesthesiology. the diaphragm. At high doses, anesthetics attenuate the Received from the Mayo Medical School, Mayo Clinic, Rochester, activities of all respiratory muscles. However, at moder- Minnesota. Submitted for publication September 8, 1999. Accepted for ate depths of anesthesia, anesthetics may produce respi- publication December 2, 1999. Supported in part by grants no. GM- ratory depression by altering the distribution and timing 40909 and HL-45532 from the National Institutes of Health, Bethesda, of neural drive to the respiratory muscles, rather than by Maryland, and by the Mayo Foundation, Rochester, Minnesota. producing a global depression of activity. For example, Address reprint requests to Dr. Warner: Mayo Medical School, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905. Address at 1.2 minimum alveolar concentration, halothane anes- electronic mail to: [email protected] thesia depresses activity in some respiratory muscles Key words: Atelectasis; epidural analgesia; pneumonia; respiratory (such as the parasternal intercostals) but actually in- failure; respiratory muscles. creases activity in others (such as the transversus abdo- 2 The illustrations for this section are prepared by Dimitri Karetnikov, minis). Thus, perioperative respiratory muscle dysfunc- 7 Tennyson Drive, Plainsboro, New Jersey 08536. tion is, in some cases, more a matter of a lack of Anesthesiology, V 92, No 5, May 2000 1468 DAVID O. WARNER Fig. 1. Model showing how incoordina- tion of respiratory muscles impairs lung function. The position of the midpoint of a horizontal bar, suspended between fixed surfaces by inspiratory and expira- tory muscles, represents lung volume as denoted on a scale from low (residual volume, RV) to high (total lung capacity, TLC) volumes. During awake, coordi- nated inspiration (lower left), the bar re- mains horizontal (representing normal chest wall expansion), and lung volume changes efficiently. When anesthetized, muscle activity becomes incoordinated, such that the bar tilts during inspiration (representing chest wall distortion), im- pairing lung expansion. Incoordination continues into the postoperative period after thoracic and abdominal surgery. Dashed lines in lower panels denote end- expiratory position of the bar. coordination than a lack of overall activity. As with other nisms (fig. 2). First, functional disruption of respiratory complex systems, this lack of coordination reduces effi- muscles (such as the intercostal or abdominal muscles) ciency (fig. 1), in this instance producing hypoventila- by incisions, even after surgical repair, may impair their tion. In addition, deformation of the chest wall alters the effectiveness. Second, postoperative pain may cause vol- underlying lung, decreasing the functional residual ca- untary limitation of respiratory motion. Finally, stimula- pacity and producing atelectasis in dependent lung re- tion of the viscera, such as provided by mechanical gions. These regions of atelectasis develop in nearly all traction on the gallbladder or esophageal dilation, mark- patients after a few minutes of anesthesia and may sig- edly decreases phrenic motoneuron output and changes nificantly impair pulmonary gas exchange.3 Chest wall the activation of other respiratory muscles, generally distortion and atelectasis also occur when the respira- acting to minimize diaphragmatic descent. These effects tory muscles are inactive during mechanical ventilation are only partially attenuated by vagotomy, suggesting and persist even with positive end-expiratory pressure. that multiple afferent pathways mediate this reflex.4 These intraoperative changes in the pattern of breath- Thus, like anesthesia, surgical trauma can also disrupt ing can persist in the postoperative period as additional normal coordination of respiratory muscle action, lead- effects of surgical trauma come into play. Residual anes- ing to persistent decreases in functional residual capacity thetic effect may also contribute to postoperative and vital capacity, with lung atelectasis that can last for changes in breathing, although the importance of this several days after surgery. The clinical impression is that factor has not been studied. The effects of surgical this atelectasis leads to pneumonia, although this pro- trauma are most pronounced after thoracic and abdom- gression has not been conclusively shown. These post- inal surgery, and they arise from at least three mecha- operative changes in pulmonary function can be partially Anesthesiology, V 92, No 5, May 2000 1469 POSTOPERATIVE PULMONARY COMPLICATIONS Fig. 2. Factors producing respiratory muscle dysfunction after surgical trauma. From left to right: (1) surgical trauma stimulates central nervous system (CNS) reflexes mediated by both visceral and somatic nerves that produce reflex inhi- bition of the phrenic and other nerves innervating respiratory muscle; (2) me- chanical disruption of respiratory mus- cles impairs efficiency; and (3) pain pro- duces voluntary limitation of respiratory motion. These factors all tend to reduce lung volumes and can produce hypoven- tilation and atelectasis. ameliorated by using endoscopic techniques to mini- barotrauma and gas exchange abnormalities. Anesthetic mize surgical trauma.5 However, because procedures gasses and tracheal intubation may impair normal muco- such as laparoscopic cholecystectomy still stimulate ab- ciliary transport. Recent studies suggest that prolonged dominal viscera (e.g., through gallbladder traction), pul- anesthesia and surgery may impair the function of lung monary mechanics are still affected; this is probably also inflammatory cells, which could increase susceptibility true for thoracoscopy. to postoperative infections.6 Finally, other respiratory Other factors may also contribute to PPCs. Reflex stim- outcomes are related specifically to surgical or anes- ulation during airway instrumentation and release of thetic interventions, such as acute lung injury after car- inflammatory mediators by drug administration can pro- diopulmonary bypass, pneumothorax caused by baro- duce bronchoconstriction. This increased airway resis- trauma or surgical trauma, negative pressure pulmonary tance limits especially expiratory gas flow from the lung, edema after airway obstruction during spontaneous which, if severe, can produce hyperinflation with risk of breathing, and aspiration pneumonitis. Anesthesiology, V 92, No 5, May 2000 1470 DAVID O. WARNER Assessment of Risk factor for PPCs. The optimal timing of quitting is not known and should be the focus of future investigations. Consistent risk factors for PPCs among extant studies Of interest, some studies find that recent cessation or include surgical site (with thoracic and abdominal sur- reduction of smoking (within approximately 2 months gery posing the highest risk), smoking, and the presence before surgery) may actually increase the risk of PPCs.11 of pulmonary disease. Although the results of pulmonary However, these studies are not
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