General internists practicing in the inpatient setting are frequently called upon to provide perioperative care to a broad spectrum of surgical patients, in either a consultative or a comanagement role. Although historically much emphasis has been placed on postoperative cardiac complications, postoperative pulmonary complications are known to occur with equal frequency. The Confederate general, Thomas “Stonewall” Jackson, wounded in the Battle of Chancellorsville in 1863, was perhaps the earliest recorded victim of a postoperative pulmonary complication, dying of pneumonia eight days after the successful amputation of his left arm. Postoperative pulmonary complications contribute significantly to morbidity, mortality, and healthcare costs. It is estimated that over 1 million patients undergoing nonthoracic surgery in the United States annually experience postoperative pulmonary complications. Pulmonary complications produce the highest attributable costs among common categories of postoperative complications and can result in a fivefold increase in the median cost of an operation. The presence of pulmonary complications after major surgery increased 30-day mortality from 2% to 22%, and 1-year mortality from 8.7% to 45.9% based on data from the National Surgical Quality Improvement Program (NSQIP). The most important postoperative pulmonary complications are atelectasis, pneumonia, respiratory failure, and exacerbation of underlying chronic lung disease, although earlier studies have also included transient and self-limited clinical findings. A general principle is that the closer the operative site is to the diaphragm, the higher the likelihood of postoperative pulmonary complications. Interventions to reduce the incidence of these complications depend on the aggressive application of preventive measures to high-risk patients. A recent systematic review characterized patient-related and procedure-related risk factors and provided evidence-based guidelines on preventive strategies.1 This chapter focuses on the pathogenesis, early recognition, and evidence-based treatment of common postoperative pulmonary complications.

Atelectasis, or reversible alveolar collapse, is a common perioperative phenomenon and occurs in 90% of patients receiving general anesthesia. Computed tomographic (CT) studies have demonstrated collapse of 15–20% of the lung volume near the diaphragm. Dr. William Pasteur, a Swiss physician practicing in England in the early part of the last century, wrote extensively on the postoperative lung and noted, “when the true history of postoperative lung complications comes to be written, active collapse of the lung from deficiency of inspiratory power will be found to occupy an important position among determining causes.” Most atelectasis appearing during general anesthesia resolves within 24 hours after surgery in normal subjects and is of little clinical significance. Atelectasis can persist for two days or longer after major surgery, including abdominal and thoracic surgery, and is thought to represent the starting point in a cascade of events that leads to the more serious complications of pneumonia and acute respiratory failure.

Pathophysiology

The formation of perioperative atelectasis can be understood by considering the effect of surgery on normal respiratory mechanics as well as the mechanisms involved in alveolar collapse. The induction of anesthesia alters the distribution and timing of neural drive to the respiratory muscles, interfering with coordination of activity. The supine position and use of positive pressure ventilation alter the distribution of ventilation and lead to hypoventilation of dependent areas. Surgical trauma can produce reflex inhibition of the phrenic nerve from stimulation of the viscera, mechanical disruption of the intercostal or abdominal respiratory muscles, and voluntary limitation of respiratory motion from postoperative pain. The characteristic postoperative mechanical abnormality is a restrictive pattern with severely reduced inspiratory capacity, vital capacity (VC), and functional residual capacity (FRC), clinically demonstrated by rapid shallow respirations.

Pulmonary atelectasis occurs by three mechanisms: compression atelectasis, absorption (resorption) atelectasis, and loss of surfactant. Compression atelectasis results when the transmural pressure distending the alveolus is reduced, allowing the alveolus to collapse. During anesthesia, change in diaphragmatic function and chest geometry causes pressure from the abdomen to be transmitted into the thorax, resulting in compression of lung tissue. Resorption atelectasis describes collapse of alveoli related to absorption of gas from occluded or hypoventilated areas of the lung. Since oxygen is absorbed more rapidly than nitrogen, air with high inspired FiO2 will be absorbed more rapidly, resulting in collapse. Surfactant function, important in stabilizing the alveoli, may be disrupted by anesthesia and mechanical ventilation. The physiologic consequence is ventilation-perfusion (V/Q) mismatch resulting in hypoxemia.

Diagnosis—Does This Patient Have Atelectasis?

Atelectasis is recognized by the finding of hypoxemia in an appropriate clinical scenario in the absence of other plausible diagnoses. The patient demonstrates dyspnea or tachypnea, and physical findings can include basilar rales and decreased breath sounds in the affected area. Atelectasis is often cited as a cause of postoperative fevers, but studies have demonstrated no association between atelectasis and fever and suggest that early postoperative fevers are more likely due to the inflammatory response to surgery.2 Atelectasis is detected radiographically by opacification of a lobe or lobar segment and evidence of volume loss. The most reliable sign is displacement of the interlobar fissure, but other signs include elevation of the hemidiaphragm, mediastinal shift, and compensatory overinflation of adjacent aerated segments. There may be linear opacities (“plate-like”) in the parenchyma in dependent portions of the lungs. Silhouette sign can be positive, with obliteration of adjacent boundaries. Posteroanterior (PA) and lateral images of the chest are preferred, and the ability of plain radiographs to detect atelectasis in recumbent critically ill patients is less certain. CT is sensitive in detecting areas of collapse, and may also reveal other pathology.

Treatment

Treatment of postoperative atelectasis centers on lung expansion techniques, shifting from supine position when possible, and adequate postoperative analgesia. The FRC has been identified as the single most important postoperative lung volume parameter, and efforts to restore normal pulmonary mechanics are beneficial. A simple posture change from supine to seated will increase FRC by 0.5 to 1.0 liters. Standing and early ambulation are also helpful when tolerated.

The goal of lung expansion maneuvers is to produce a large and sustained increase in transpulmonary pressure that distends the lung and reexpands the collapsed lung units. Techniques include incentive spirometry, deep breathing exercises, chest physical therapy, intermittent positive-pressure breathing (IPPB), and continuous positive airway pressure (CPAP). A recent systematic review found that for patients undergoing abdominal surgery, any type of lung expansion intervention improved outcome, with no one modality being superior. Incentive spirometry was the least labor intensive. IPPB is the most costly and was associated with unacceptable abdominal distension in a significant number of cases. CPAP is beneficial for patients unable to participate in incentive spirometry or deep breathing exercises. Another systematic review also found evidence that use of CPAP in patients undergoing abdominal surgery led to lower rates of postoperative atelectasis and pneumonia.

The effect of different types of analgesia in decreasing postoperative atelectasis has been examined. Studies have been heterogeneous and small, but a recent meta-analysis found a trend toward decreased postoperative atelectasis and pneumonia with the use of postoperative epidural analgesia in patients undergoing abdominal surgery. Postoperative epidural and patient-controlled intravenous analgesia both seem superior to on-demand delivery of opioids in preventing postoperative pulmonary complications. The potential benefit of epidural anesthesia must be weighed against bleeding risk from deep vein thrombosis (DVT) prophylaxis.

Complications

Mild hypoxemia from atelectasis is usually well tolerated, but more severe hypoxemia can affect end organs. Atelectasis itself may cause mild acute lung injury. Left untreated, atelectasis likely predisposes to the development of pneumonia and potentially respiratory failure

Pneumonia ranks as the third most common postoperative infection behind urinary tract infection (UTI) and wound infection. The incidence of pneumonia following major abdominal surgery ranges between 2% and 19% and is a principal factor in increased mortality. Development of hospital-acquired pneumonia is associated with a 30–50% increased risk of developing acute respiratory failure requiring mechanical ventilation and increases hospital stays by an average of 7–9 days at an excess cost of $40,000 per patient.

Postoperative pneumonia is a subset of hospital-acquired pneumonia (HAP), which is pneumonia occurring 48 hours or more after admission and not incubating at the time of admission. The major early management goal for postoperative pneumonia is to provide appropriate antibiotics in adequate doses based on the best prediction of suspected pathogens and resistance pattern.

The timing of onset of HAP is an important epidemiologic variable. Early-onset HAP, less than five days into admission, is more likely to be caused by antibiotic-sensitive bacteria unless other risk factors for multidrug-resistant (MDR) pathogens are present. Late-onset HAP, five or more days after admission, is more likely to be associated with MDR pathogens. Additional risk factors for MDR pathogens include acute care hospitalization for two or more days or antimicrobial therapy within the preceding 90 days, nursing home or long-term care facility residence, home infusion therapy, chronic dialysis, wound care, family member with an MDR pathogen, and immunosuppression (Table 56-1). Hospital- and unit-specific microbiologic data are also very important in selecting appropriate treatment.

The recent American Thoracic Society/Infectious Diseases Society of America (ATS/IDSA) guideline emphasizes ventilator-associated pneumonia (VAP) because it is more readily studied, but suggests it is reasonable to extrapolate the conclusions regarding risk factors for infection with specific pathogens to nonintubated, nonventilated HAP patients.

Pathophysiology

The sequence of events in HAP begins with colonization of the oropharynx with pathogens, which can occur within 48 hours of admission. Sources of pathogens include contaminated healthcare devices, the environment, and transfer from other patients or staff. These pathogens must be aspirated from the oropharynx into the lower respiratory tract, and then overwhelm the natural host defense mechanisms. Microaspiration is known to occur in up to 45% of healthy subjects during sleep and can be worsened in postsurgical patients by decreased gag reflex, ineffective coughing, sedation, supine posture, especially during enteral feeds, and routine (rather than selective) use of nasogastric (NG) tubes. The host defenses are also affected in multiple ways by general anesthesia, including mechanical impairment of normal mucociliary transport and interference with function of alveolar inflammatory cells, including polymorphonuclear leukocytes, macrophages, lymphocytes, cytokines, antibodies, and complement.

The microbiology of early-onset HAP without MDR risk factors tends to mirror community-acquired pneumonia and includes Streptococcus pneumoniae, Haemophilus influenzae, methicillin-sensitive Staphylococcus aureus, and antibiotic-sensitive Enterobacteriaceae (Table 56-2). Pathogens in late-onset HAP or the presence of MDR risk factors also include methicillin-resistant S. aureus (MRSA), Pseudomonas aeruginosa, extended-spectrum beta-lactamase (ESBL) -producing Klebsiella, and Acinetobacter baumannii (Table 56-3).