Overview of the management of postoperative pulmonary complications

INTRODUCTION — Pulmonary complications are a major cause of morbidity and mortality during the postoperative period [1]. The reported incidence of postoperative pulmonary complications ranges from 5 to 80 percent, depending upon the patient population and the criteria used to define a complication [2]. The incidence also varies across hospitals, with one study reporting lower rates of complications in hospitals with a high volume of patients than in hospitals with a lower volume following esophagectomy, pancreatectomy, and intact abdominal aortic aneurysm repair [3].

Traditional definitions of postoperative pulmonary complications include atelectasis, bronchospasm, pneumonia, and exacerbation of chronic lung disease. However, the list can be expanded to include acute upper airway obstruction, complications from obstructive sleep apnea, pleural effusions, chemical pneumonitis, pulmonary edema, hypoxemia due to abdominal compartment syndrome, and tracheal laceration or rupture. Recognition and management of these postoperative pulmonary complications are reviewed here. Their prevention is discussed separately. (See "Strategies to reduce postoperative pulmonary complications in adults".)

ATELECTASIS — Atelectasis is one of the most common postoperative pulmonary complications, particularly following abdominal and thoracoabdominal procedures [4]. Measures to prevent atelectasis have become an integral part of routine postoperative care, as described separately. (See "Strategies to reduce postoperative pulmonary complications in adults", section on 'Lung expansion'.) This section focuses on the management of postoperative atelectasis.

Clinical presentation — Postoperative atelectasis can be asymptomatic or it may manifest as increased work of breathing and hypoxemia. The onset of hypoxemia due to postoperative atelectasis tends to occur after the patient has left the post-anesthesia care unit. It typically becomes most severe during the second postoperative night and continues through the fourth or fifth postoperative night [5,6].

Hypoxemia that develops earlier (ie, in the post-anesthesia care unit) should prompt the consideration of postoperative complications other than atelectasis, such as hypoventilation due to residual anesthetic effects and upper airway obstruction due to airway tissue edema. The latter may be due to the accumulation of pharyngeal secretions, prolapse of the tongue posteriorly, or tongue edema due to either surgical manipulation or an allergic reaction [4].

Pathogenesis — Postoperative atelectasis is usually caused by decreased compliance of lung tissue, impaired regional ventilation, retained airway secretions, and/or postoperative pain that interferes with spontaneous deep breathing and coughing [7,8]. These complications usually do not develop immediately following surgery, which explains why the onset of hypoxemia due to postoperative atelectasis tends to occur later, after the patient has left the post-anesthesia care unit. (See "Atelectasis: Types and pathogenesis in adults".)

Management — The initial approach to managing postoperative atelectasis depends upon whether the patient has abundant secretions, which we define as frequent expectoration, the expectoration of large amounts of sputum, and/or prominent rhonchi on auscultation. For patients without abundant secretions, continuous positive airway pressure (PAP) may be beneficial. For patients with abundant secretions, chest physiotherapy and suctioning are appropriate. Some patients with abundant secretions may also benefit from bronchoscopy; the absence of air bronchograms may help identify patients who are more likely to benefit from bronchoscopy, as described below. The use of mechanical devices to improve mucus clearing in the setting of chronic obstructive pulmonary disease and bronchiectasis is discussed separately. (See "Role of mucoactive agents and secretion clearance techniques in COPD" and "Bronchiectasis in adults: Treatment of acute and recurrent exacerbations".)

No option has proven benefit over another. One small study on an oscillating (vibratory) positive end-expiratory pressure (PEEP) device in the postoperative period, presumably for already-established increased mucus secretions and/or atelectasis in comparison with chest physiotherapy with incentive spirometry, looked specifically at hospital readmissions and cost. The overall existing data are not strong enough to recommend one device over another in the postoperative period following noncardiothoracic procedures [9].

Few respiratory secretions — Continuous PAP (CPAP) may be beneficial to patients who develop hypoxemia and/or increased respiratory effort due to postoperative atelectasis in the setting of few secretions. This was demonstrated by a multicenter trial in which 209 patients with hypoxemia (an arterial oxygen tension to inspiratory oxygen fraction ratio [PaO₂/FiO₂] of ≤300 mmHg) due to postoperative atelectasis following elective major abdominal surgery were randomly assigned to receive supplemental oxygen plus CPAP or supplemental oxygen alone [10]. CPAP decreased the incidence of endotracheal intubation (1 versus 10 percent), pneumonia (2 versus 10 percent), infection (3 versus 10 percent), and sepsis (2 versus 9 percent). The study aimed to include only patients with hypoxemia due to postoperative atelectasis, by excluding patients who were more likely to have an alternative cause of postoperative hypoxemia (eg, patients with cardiac or pulmonary comorbidities, hypercapnia and respiratory acidosis, acute respiratory distress syndrome, hypotension, or impaired consciousness). Important limitations to this evidence are that the trial was unblinded and terminated early due to benefit.

Although these findings have not been universal [11,12], we believe the potential benefits of a trial of CPAP outweigh the risks in most patients who have hypoxemia and/or increased respiratory effort due to postoperative atelectasis without abundant respiratory secretions. We monitor patients closely during the trial of CPAP so that intubation can be performed if it becomes clinically indicated. (See "The decision to intubate".)

Abundant respiratory secretions — All patients with clinically significant postoperative atelectasis and abundant respiratory secretions should be suctioned frequently and receive chest physiotherapy (ie, postural drainage and percussion). Oral suctioning is appropriate for patients who are able to expectorate their secretions, but many patients are unable to expectorate their secretions and require nasotracheal suctioning. Suctioning and chest physiotherapy are relatively low risk, inexpensive interventions with important potential benefits. The notion that there are potential benefits is based upon clinical experience and indirect evidence from patients with lung diseases characterized by abundant secretions (eg, cystic fibrosis, bronchiectasis), since there is a lack of data among postoperative patients. (See "Cystic fibrosis: Overview of the treatment of lung disease", section on 'Chest physiotherapy'.)

The role of flexible bronchoscopy is uncertain. We believe that flexible bronchoscopy should not be performed routinely prior to or instead of chest physiotherapy but may have a role in cases that are unresponsive to suctioning and chest physiotherapy. This approach is supported by the following evidence.

Several studies evaluated the use of flexible bronchoscopy to extract secretions from patients with atelectasis [13-16]. The results were variable, but overall, bronchoscopy had little benefit. These results may have been due to a true lack of effect (perhaps secretions reaccumulate, rendering the bronchoscopy ineffective) or due to the study design. With respect to the study design, many studies combined patients with and without air bronchograms (air bronchograms indicate airways that are free of secretions). Flexible bronchoscopy is least effective when air bronchograms exist and it is possible that the lack of effect among patients with air bronchograms could obscure a beneficial effect among patients without air bronchograms [15,17-19].

An illustrative trial randomly assigned 31 patients with acute lobar atelectasis following thoracic or abdominal surgery to immediate bronchoscopy followed by chest physiotherapy or chest physiotherapy alone without the initial bronchoscopy [17]. Chest physiotherapy was performed every four hours and consisted of five minutes of chest percussion, five minutes of postural drainage, deep breathing to total lung capacity for three minutes with an incentive spirometer (or multiple 1 to 2 liter inflations using an anesthesia bag if the patient was intubated), coughing (or tracheal suctioning if the patient was either intubated or had an ineffective cough), and inhalation of ten breaths of isoetharine (an inhaled bronchodilator):

●When patients who underwent flexible bronchoscopy followed by chest physiotherapy were compared to those who received chest physiotherapy alone, the mean percentage of resolution of volume loss following bronchoscopy was nearly identical to that following the first chest physiotherapy session, suggesting that flexible bronchoscopy did not add any initial benefit to chest physiotherapy alone.

●When patients with air bronchograms were compared to patients without air bronchograms, those without air bronchograms had better resolution of volume loss at 24 hours regardless of which intervention they received. This suggests that air bronchograms predict slower spontaneous resolution of the atelectasis.

CPAP and the mucolytic, N-acetylcysteine, do not have a role in the routine management of patients with abundant respiratory secretions. Regarding CPAP, the excess secretions are a contraindication to CPAP because the patient-device interface tends to impede suctioning. Regarding N-acetylcysteine, it has not been studied as a therapy for postoperative atelectasis, but it seems unlikely that it would be beneficial given its lack of effect in preventing postoperative atelectasis [20-22]. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Contraindications'.)

BRONCHOSPASM — Bronchospasm is common during the postoperative period. Clinical manifestations include dyspnea, wheezing, chest tightness, tachypnea, small tidal volumes, a prolonged expiratory time, and hypercapnia. Postoperative bronchospasm can be caused by aspiration, histamine release incited by medications (eg, opiates, tubocurarine, or atracurium), an allergic response to medications, or an exacerbation of a chronic pulmonary condition, such as asthma or chronic obstructive pulmonary disease. It can also be caused by reflex constriction of bronchial smooth muscles due to tracheal stimulation by secretions, suctioning, endotracheal intubation, or other surgical stimulation. Reflex bronchoconstriction is particularly common when the bronchodilatory effects of inhalational anesthetics wane [23].

Treatment of postoperative bronchospasm consists of treating the underlying cause, removing potential contributors (eg, medications), and pharmacotherapy. Short-acting inhaled beta-2-agonists (eg, albuterol) are bronchodilators that are considered first-line pharmacotherapy. The short-acting inhaled anticholinergic agent, ipratropium bromide, is also a bronchodilator that may have an additive effect on the degree of bronchodilation. The decision about whether to use an inhaled beta-2-agonist alone or to add ipratropium bromide is made on a case-by-case basis, depending upon the severity of bronchospasm. Patients who do not improve after one or two doses of the inhaled bronchodilators may benefit from the addition of systemic glucocorticoids.

Methylxanthines (ie, aminophylline, theophylline) and systemic beta-2-agonists are generally not used for the management of postoperative bronchospasm because the inhaled agents provide comparable or greater bronchodilation with fewer side effects [24].

Generally speaking, the approach to managing postoperative bronchospasm is similar to management of an exacerbation of asthma or chronic obstructive pulmonary disease (COPD), which are discussed in detail separately. (See "Acute exacerbations of asthma in adults: Home and office management" and "COPD exacerbations: Management" and "Beta agonists in asthma: Acute administration and prophylactic use" and "Delivery of inhaled medication in adults".)

PNEUMONIA — Postoperative pneumonia has clinical manifestations and a diagnostic approach that is nearly identical to other types of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP). However, it has some unique risk factors and treatment considerations [25]. This section focuses on postoperative pneumonia following noncardiothoracic surgery; other types of HAP and VAP are discussed separately [26]. (See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults" and "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

Clinical presentation — Postoperative pneumonia tends to occur within five postoperative days [25]. It may present with fever, leukocytosis, increased secretions, and pulmonary infiltrates on chest radiographs. Hypoxemia may develop, or the patient may require more supplemental oxygen to maintain the same oxyhemoglobin saturation. Respiratory distress, dyspnea, tachypnea, small tidal volumes, and hypercapnia may also occur. The minute ventilation often increases prior to the development of any blood gas abnormalities, a consequence of the patient becoming more catabolic due to the developing infection.

Diagnosis — The optimal strategy to diagnose postoperative pneumonia is uncertain and controversial. However, it is important because diagnosis based upon clinical criteria alone may result in over-diagnosis and inappropriate antibiotic therapy (resulting in the selection of resistant organisms), whereas stringent diagnostic criteria may lead to under-diagnosis, inadequate antibiotic coverage, and a worse prognosis [27].

Generally speaking, postoperative pneumonia should be suspected in any patient who has clinical signs of infection (eg, fever, purulent sputum, leukocytosis or leukopenia, and worsening oxygenation) and a new radiographic infiltrate. Patients with suspected postoperative pneumonia may be evaluated using the same diagnostic approach that is used for patients with suspected VAP, which is described in detail separately. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia".)

The diagnosis of postoperative pneumonia can be difficult because there are many other postoperative causes of fever and/or pulmonary infiltrates, such as atelectasis, pulmonary edema, pulmonary embolism, and acute lung injury. This was illustrated in a prospective cohort study of 129 consecutive surgical intensive care unit (ICU) patients with abnormal chest radiographs [28]. Forty-eight percent of the patients were recovering from operative procedures and causes of pulmonary infiltrates in this population included pneumonia (30 percent), pulmonary edema (29 percent), acute lung injury (15 percent), and atelectasis (13 percent).

Persistent PCT elevation on postoperative day 2 and beyond following abdominal surgery is more common in individuals developing hospital-acquired pneumonia versus those who do not develop hospital-acquired pneumonia. Nonetheless, the utility of elevated postoperative PCT levels as an early biomarker in aiding in the diagnosis of hospital-acquired pneumonia following abdominal surgery is unclear [29]. The utility of an elevated serum procalcitonin (PCT) level in aiding in the evaluation of postoperative fever is discussed separately. (See "Fever in the surgical patient", section on 'Laboratories'.)

Pathogens — Postoperative pneumonia is frequently caused by resistant organisms. This was demonstrated by a series of 837 patients with suspected postoperative pneumonia, occurring within the first 14 days following surgery [25]. Microbiologic sampling was performed in 718 of the patients (86 percent), including bronchoscopic sampling in 367 of the patients (44 percent):

●Most cases of pneumonia occur within five postoperative days (61 percent).

●Organisms were cultured from the respiratory samples of almost half of the patients (46 percent).

●More than one organism was cultured from some patients (29 percent).

●Most of the positive cultures were obtained from patients in whom pneumonia was diagnosed before the fifth postoperative day.

●Gram-negative bacteria and Staphylococcus aureus were the most commonly cultured microorganisms, while the most frequent bacterial combinations were Enterobacteriaceae plus either Staphylococcus aureus or streptococci. Haemophilus influenzae and Streptococcus pneumoniae accounted for 19 percent and 10 percent, respectively, of the microorganisms isolated from respiratory and blood cultures.

There are risk factors for postoperative pneumonia caused by particular microorganisms:

●Haemophilus influenzae or Streptococcus pneumoniae – Traumatically injured patients appear to be at increased risk for postoperative pneumonia due to Haemophilus influenzae or Streptococcus pneumoniae [28].

●Staphylococcus aureus – Neurosurgical patients (particularly those who are mechanically ventilated), victims of blunt trauma and coma, and patients who have sustained closed head injuries seem to be at increased risk for postoperative pneumonia due to Staphylococcus aureus (S. aureus) [30,31]. Additional risk factors for Staphylococcus pneumonia include: chronic kidney disease, diabetes mellitus, a history of injection drug use, and recent influenza [32]. Previous antibiotic use, a positive nasal screen for methicillin resistant S. aureus (MRSA), long operations (>300 minutes), and emergency surgery are risk factors for MRSA [26,33,34].

●Pseudomonas aeruginosa – No particular type of surgery has been convincingly shown to increase the likelihood of postoperative Pseudomonas pneumonia. However, risk factors for Pseudomonas pneumonia include: intubation >8 days, structural lung disease (eg, bronchiectasis, cystic fibrosis, and chronic obstructive pulmonary disease [COPD]), corticosteroid therapy, malnutrition, and prolonged exposure to antibiotics [35,36]. Prolonged exposure to antibiotics has been defined as receipt of antibiotics for more than 48 hours during the 10 days preceding the episode of pneumonia [37]. (See "Pseudomonas aeruginosa pneumonia".)

●Acinetobacter species – Acinetobacter species are a well-recognized cause of postoperative pneumonia, although no particular type of surgery has been shown to predispose patients to postoperative Acinetobacter pneumonia. The most important risk factor for Acinetobacter pneumonia is mechanical ventilation. Multidrug resistance is an increasing problem and Acinetobacter pneumonia is associated with a high mortality rate [38-40]. (See "Acinetobacter infection: Treatment and prevention", section on 'Pneumonia'.)

●Anaerobic species – The role of anaerobes in the pathogenesis of postoperative pneumonia is uncertain. Abdominal surgery is generally considered a risk factor for pneumonia due to anaerobic organisms [26], but several studies suggest that anaerobes may not be important pathogens in this setting. As an example, studies that cultured bronchoscopy specimens or mini-bronchoalveolar lavage (mini-BAL) specimens for anaerobic bacteria identified no such organisms [41-45].

Treatment — The management of postoperative pneumonia involves the collection of respiratory specimens for microbiological analysis, followed by the prompt initiation of empiric antimicrobial therapy. Once the microbiological data has been reported and the patient's response to empiric therapy assessed, the antimicrobial regimen should be tailored.

The collection of respiratory specimens, selection of an empiric antimicrobial regimen, and subsequent adjustments to the antimicrobial regimen are similar to that for other types of HAP and VAP. These interventions are discussed separately. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia", section on 'Noninvasive respiratory sampling' and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

The following considerations are specific for postoperative pneumonia and should be incorporated into the selection of an appropriate empiric antibiotic regimen:

●The most common pathogens reported in postoperative pneumonia are gram-negative bacilli (eg, Pseudomonas aeruginosa, Klebsiella pneumoniae, and Acinetobacter species) and Staphylococcus aureus. Haemophilus influenzae or Streptococcus pneumoniae are also common [25].

●Postoperative pneumonia is often polymicrobial in origin. The most frequent bacterial combinations appear to be Enterobacteriaceae plus either Staphylococcus aureus or streptococci [25].

●Victims of trauma are particularly susceptible to pneumonia caused by Haemophilus influenzae, Streptococcus pneumoniae, or Staphylococcus aureus. Neurosurgical patients, especially those requiring mechanical ventilation, are also at increased risk for pneumonia due to Staphylococcus aureus.

●Anaerobic coverage may be considered following thoracoabdominal surgery, although its value is uncertain. Antimicrobial coverage of aerobic bacteria should be continued if anaerobic coverage is added.

ACUTE UPPER AIRWAY OBSTRUCTION — Acute upper airway obstruction typically occurs during the immediate postoperative period. It usually manifests as stridor if the obstruction is incomplete or aphonia if the obstruction is complete. Patients also may develop respiratory distress with dyspnea, tachypnea, tachycardia, and diaphoresis. Causes of acute upper airway obstruction include laryngeal edema, iatrogenic vocal cord paralysis, laryngospasm, and obstruction from the tongue or other soft tissues.

Acute upper airway obstruction is a medical emergency that requires immediate evaluation by a clinician who is capable of performing endotracheal intubation. Ideally, the clinician should have significant experience in airway management, including the ability to intubate the patient using a fiberoptic laryngoscope. Inhaled bronchodilating medications or helium-oxygen mixtures may be beneficial to patients who do not require immediate intubation, while the cause of the acute upper airway obstruction is evaluated and treated. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults" and "Physiology and clinical use of heliox".)

EXACERBATION OF OBSTRUCTIVE SLEEP APNEA — Obstructive sleep apnea (OSA) is a common disorder characterized by apneas and hypopneas due to repetitive complete or partial collapse of the upper airway during sleep. The repetitive upper airway collapse may lead to frequent awakenings and/or episodic oxyhemoglobin desaturation. The pathogenesis, clinical presentation, diagnosis, natural history, and management of OSA are discussed in detail separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "Obstructive sleep apnea: Overview of management in adults".)

OSA can be exacerbated during the postoperative period, which manifests as more frequent, more severe, or more prolonged episodes of oxyhemoglobin desaturation during sleep. This is often accompanied by new or worse hypercapnia. The frequency of oxyhemoglobin desaturation was demonstrated by a series of 438 patients with known or suspected OSA who underwent surgery [46]. Oxyhemoglobin desaturation to less than 90 percent during sleep occurred in 16 percent of patients, while oxyhemoglobin desaturation to less than 80 percent during sleep occurred in 7 percent of patients. These episodes usually occurred within the first 24 to 48 hours after the surgical procedure. The propensity of patients with OSA to develop postoperative hypoxemia and/or hypercapnia increases the likelihood of an adverse clinical outcome, such as reintubation, myocardial ischemia, cardiac arrhythmias, hypoxic encephalopathy, or death [47].

There are several factors that probably contribute to postoperative exacerbation of OSA [47]. Anesthetic agents, sedatives, and opioids promote relaxation of pharyngeal muscles during sleep, which may increase the frequency, severity, and duration of upper airway collapse. Anesthetic agents may also blunt the hypoxic and hypercapnic respiratory centers, thereby compromising the protective arousal response. Finally, patients are often supine following surgery, and this position may predispose some patients to worse OSA.

The postoperative management of patients with known or suspected OSA is reviewed in detail separately (see "Postoperative management of adults with obstructive sleep apnea").

PLEURAL EFFUSION — Small pleural effusions are common during the immediate postoperative period following abdominal surgery. This was demonstrated by a series of 200 abdominal surgery patients who had posteroanterior, left lateral, and bilateral decubitus radiographs performed 48 to 72 hours after surgery [48]. Pleural effusions were found in 97 patients (49 percent). Among the pleural effusions, 52 percent were <4 mm, 27 percent were 4 to 10 mm, and 22 percent were >10 mm (on the decubitus radiographs). Most effusions were exudates. A pleural effusion was more common after upper abdominal surgery, among patients with postoperative atelectasis, and among patients with free abdominal fluid. All of the effusions resolved without specific therapy with the exception of one, in which the pleural fluid culture grew Staphylococcus aureus.

Most postoperative pleural effusions resolve spontaneously within a few days and, therefore, do not require intervention. However, atypical characteristics of either the pleural effusion or the patient's clinical course warrant diagnostic evaluation of pleural effusions. Postoperative pleural effusions are evaluated in the same way that other pleural effusions are evaluated. The diagnostic evaluation of a pleural effusion is reviewed separately. (See "Pleural fluid analysis in adults with a pleural effusion".)

Subphrenic abscess is a complication of surgery that may induce pleural effusions; however, the effusions associated with a subphrenic abscess are distinct from the usual postoperative pleural effusion in that they usually become apparent about 10 days after surgery and are typically associated with signs and symptoms of systemic infection [49].

Pleural effusions that develop following cardiac surgery are discussed separately. (See "Evaluation and management of pleural effusions following cardiac surgery".)

CHEMICAL PNEUMONITIS — Surgical patients are at risk for chemical pneumonitis resulting from the aspiration of acidic gastric contents during the perioperative period. The clinical features of chemical pneumonitis include the abrupt onset of dyspnea and tachycardia. Patients may also exhibit fever, bronchospasm, hypoxemia, cyanosis, and/or pink frothy sputum. Infiltrates may appear in one or both lower lobes, usually within the first 24 hours. In a series of more than 172,000 consecutive adults who underwent procedures involving general anesthesia, aspiration of gastric contents occurred in 1 of every 3216 procedures with an overall mortality of 1 in 71,829 procedures [50]. While the incidence of aspiration is infrequent in healthy adults, aspiration is more common in pediatric and obstetric patients [51]. Most aspirations occurred during tracheal extubation or laryngoscopy; a high American Society of Anesthesiologists (ASA) class and emergency surgery were each associated with greater risk of aspiration (table 1). The increased risk for aspiration and chemical pneumonitis during the perioperative period is probably related to ineffective upper airway reflexes due to the induction of anesthesia and the use of muscle relaxants and central respiratory depressant medications.

The clinical course of chemical pneumonitis varies. Full recovery is the usual outcome. In the series above, patients who did not develop a cough, wheeze, >10 percent oxyhemoglobin desaturation, or radiological abnormalities within two hours of aspiration or completion of the procedure, had no respiratory sequelae [50]. However, some patients develop a secondary bacterial infection (ie, aspiration pneumonia) or acute respiratory distress syndrome (ARDS). In a series of more than 300,000 adult surgical patients, the prevalence of aspiration pneumonia was 0.8 percent, which varied among hospitals and by surgical procedure [52]. The following patient characteristics were independently associated with the development of aspiration pneumonia: male gender, not being from a White population, age >60 years, dementia, chronic obstructive pulmonary disease, renal disease, malignancy, moderate-to-severe liver disease, and emergency department admission. (See "Aspiration pneumonia in adults" and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".)

Witnessed aspiration of gastric secretions in the pharynx should prompt the clinician to immediately turn the patient's head to the side (ie, lateral head positioning), assuming integrity of the cervical spine, and then to suction the patient's oropharynx. Endotracheal intubation should be considered if airway reflexes are absent or compromised [23]. If there is suspicion of an unwitnessed intraoperative or postoperative aspiration event, the patient should be monitored closely over the ensuing 24 to 48 hours for the development of aspiration pneumonitis. Treatment is supportive, which may include supplemental oxygen, noninvasive mechanical ventilation, or conventional mechanical ventilation. Prophylactic administration of corticosteroids or antibiotics is not indicated. However, if the clinical findings have not resolved after 48 hours, antibiotic therapy may be considered [53]. Specific antibiotic therapy should be instituted in the setting of a secondary bacterial infection. (See "Aspiration pneumonia in adults", section on 'Chemical pneumonitis' and "Aspiration pneumonia in adults", section on 'Bacterial pneumonia'.)

PULMONARY EDEMA — Postoperative pulmonary edema can be cardiogenic, noncardiogenic, or a combination of both.

Postoperative cardiogenic pulmonary edema occurs most often within the initial 36 postoperative hours when fluid retention exceeds 67 mL/kg per day according to a series of 13 patients who died from pulmonary edema following elective noncardiac surgery [54]. Cardiogenic pulmonary edema was identified by chest radiography and elevated pulmonary artery pressures, and then confirmed at autopsy. The diagnosis and management of cardiogenic pulmonary edema are discussed separately. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Treatment of acute decompensated heart failure: General considerations".)

An important cause of postoperative noncardiogenic edema is negative pressure pulmonary edema, which can result from laryngospasm or other forms of upper airway obstruction following extubation [55,56]. Patients usually present with signs of acute upper airway obstruction following extubation and, upon relief of the obstruction, immediately develop dyspnea with pink frothy sputum and bilateral infiltrates on their chest radiograph. Less often, the development of pulmonary edema can be delayed for several hours [57]. Thus, it is important that patients who experience postanesthetic laryngospasm be monitored longer than usual [57,58]. The recommended postanesthetic monitoring period in this patient population ranges from 2 to 12 hours [59,60]. Pulmonary hemorrhage and frank hemoptysis have also been reported [61].

It is estimated that negative pressure pulmonary edema follows 0.05 to 0.1 percent of all procedures involving intubation and general anesthesia but is often attributed to other etiologies [56]. Patients with a predisposition to upper airway obstruction are at the greatest risk for negative pressure pulmonary edema; however, laryngospasm-induced pulmonary edema following extubation has also been reported in young, healthy, athletic adults [62-65]. Risk factors for upper airway obstruction include obesity and having a short neck, obstructive sleep apnea, or acromegaly [66]. It also includes previous ear, nose, and throat surgery. In one case series, patients who were extubated during Stage 2 anesthesia (as opposed to being fully awake [Stage 1 anesthesia]) were at increased risk of laryngospasm [62].

The etiology of negative pressure pulmonary edema is multifactorial but appears to be related to the generation of markedly negative intrathoracic pressure due to forced inspiration against a closed glottis, referred to as a Mueller (or reverse Valsalva) maneuver. As the intrathoracic pressure becomes more negative, blood flow to the right heart increases. This causes the pulmonary vascular bed to dilate, the interstitial pressure around the capillaries to become more negative, and intravascular fluid to be drawn into the interstitial space. This worsens gas exchange and triggers a cascade of hypoxemia, catecholamine release, and systemic and pulmonary hypertension. The result is an acute increase in afterload, which worsens transcapillary fluid efflux and increases interstitial and alveolar edema [62].

Treatment of negative pressure pulmonary edema is supportive. All patients receive supplemental oxygen, and some may benefit from diuresis if they are hypervolemic [62]. Bronchodilators and/or noninvasive continuous positive airway pressure may be helpful [62], although some patients will require reintubation [67]. Most cases resolve spontaneously in a relatively short period of time with no long-term sequelae [62].

PULMONARY EMBOLISM — Acute pulmonary embolism is a well-known postoperative pulmonary complication. The clinical manifestations, diagnosis, and treatment of pulmonary embolism are reviewed separately. (See "Epidemiology and pathogenesis of acute pulmonary embolism in adults" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults".)

ABDOMINAL COMPARTMENT SYNDROME — Progressive hypoxemia may be the initial manifestation of abdominal compartment syndrome (ACS). ACS refers to symptomatic organ dysfunction resulting from an increase in the intraabdominal pressure. It is most common in trauma patients who require massive fluid resuscitation following injury or emergent abdominal surgery [68]. The incidence of ACS in trauma patients is estimated to be between 2 and 9 percent [69,70]. ACS may also be due to tight surgical closures or burn scars that reduce abdominal compliance [71]. The diagnosis and management of ACS are reviewed separately. (See "Abdominal compartment syndrome in adults".)

TRACHEAL LACERATION OR RUPTURE — Laceration or rupture of the upper airway is an unusual but well-described complication of endotracheal intubation [72-75]. Clinical and radiographic signs of the injuries include respiratory compromise, subcutaneous emphysema, pneumomediastinum, and unilateral or bilateral pneumothorax [76].

Laceration or rupture of the upper airway may result in immediate respiratory compromise, or it may not be recognized until after extubation if the injury causes only a slow air leak or is masked by the endotracheal tube. In one series of 14 patients with iatrogenic airway lacerations, only two patients (14 percent) were diagnosed intraoperatively [74]. The median duration until diagnosis for the remaining patients was 24 hours.

Surgical management is generally required and may involve sternotomy, thoracotomy, or cervicotomy. Conservative management may be considered in clinically stable patients with small (<2 cm) tears, minimal air leaks, or prohibitively high operative mortality [72,73,77]. Other complications of intubation are presented separately. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients".)

POSTOPERATIVE RESPIRATORY FAILURE — Postoperative respiratory failure accounts for more than 20 percent of all patients receiving ventilatory support [78,79]. Respiratory failure requiring unplanned reintubation in the postoperative period is associated with high morbidity, leading to a longer hospital stay, and increase in 30-day mortality [80-82]. The incidence of unanticipated reintubation in the first 72 hours is, in general, low (<1 percent) but higher in older patients (up to 3 percent) [80,81]. As an example, in one study that reviewed 29,924 patients who underwent surgery, the reintubation rate was less than 1 percent [82]. Reintubation was associated with an increased likelihood of death (odds ratio 72). The risk of reintubation was greatest within the first six hours (after primary extubation) with pulmonary edema, atelectasis, pneumonia, impaired brain function, aspiration, and airway obstruction cited as the most common reasons for reintubation.

Other than low-flow oxygen, there is no single intervention in this population that is routinely used to prevent or treat postoperative acute respiratory failure. Other options include noninvasive ventilation (NIV) and oxygen delivered high flow nasal cannula (HFNC) [10,83-87]:

●NIV – NIV has been studied in the postoperative population. Although it is not routinely applied as a primary prevention strategy, it is typically used as a secondary intervention for the treatment of hypoxemic respiratory failure that is refractory to or not suitable for low-flow or high-flow oxygen [88].

Best supporting the use of NIV in this population is a trial of 293 patients with hypoxemic respiratory failure following abdominal surgery [87]. Compared with patients treated with low-flow oxygen only, patients who received NIV delivered via a face mask had fewer reintubations (33 versus 45 percent). NIV was also associated with more ventilator-free days (25 versus 23 days), and fewer healthcare-associated infections (31 versus 49 percent) but was not associated with a mortality benefit. Methodologic flaws such as the exclusion of patients requiring immediate reintubation and a lower-than-expected rate of reintubation in the oxygen alone group limits interpretation of this study.

Data that support this approach as well as strategies that prevent postoperative atelectasis are discussed in detail separately. (See "Strategies to reduce postoperative pulmonary complications in adults", section on 'Lung expansion'.)

●HFNC – High-flow nasal oxygen, which can oxygenate patients as well as provide a small amount of positive airway pressure (PAP) and reduce dead space. Randomized trials evaluating the efficacy of HFNC are lacking such that HFNC is not routinely used as first line therapy for the treatment or prevention of postoperative respiratory failure. However, it may be an alternative to NIV, particularly in those in whom NIV is not tolerated. HFNC has been studied in the treatment and prevention of respiratory failure in the postoperative setting [85,86,89-91]. Most of these trials compared HFNC with conventional low-flow oxygenation strategies and were performed in patients following thoracic surgery. Studies were flawed by low event rates, heterogeneity, imprecision, and indirectness.

•One study of 830 patients who were at risk of or who developed acute respiratory failure following cardiothoracic surgery were randomly assigned to receive either continuous HFNC (50 L/minute; fraction of inspired oxygen 50 percent) or NIV with bilevel PAP delivered for at least four hours per day (pressure support 8 cm H₂O and positive end expiratory pressure 4 cm H₂O) [85]. HFNC and NIV had similar rates of treatment failure (reintubation, switch to the other treatment, or treatment discontinuation; 21 and 22 percent, respectively). Similarly, mortality was unaffected (7 and 6 percent, respectively). However, skin breakdown, as expected, was more commonly encountered with NIV (10 versus 3 percent). Methodologic flaws in study design (eg, lack of comparison with usual care, variable level of pressure support, premature extubation as an inclusion criterion) and wide noninferiority boundaries in this trial may have affected the outcome.

•In another study of 527 patients, half of whom were postsurgical, the immediate application of HFNC post-extubation was associated with a lower risk of respiratory failure and reintubation at 72 hours when compared with conventional oxygen therapy [86]. This study is discussed separately. (See "Extubation management in the adult intensive care unit", section on 'Postextubation management'.)

•In a meta-analysis of seven randomized trials involving 2781 patients, HFNC had a similar reintubation rate compared with either conventional oxygen therapy (COT; RR 0.58, 95% CI 0.21-1.60) or NIV (RR 1.11, 95% CI 0.88-1.40) [92]. However, in a subgroup analysis, critically ill patients treated with HFNC had a lower reintubation rate compared with the COT group (RR 0.35, 95% CI 0.19-0.64). In another meta-analysis of 14 studies, HFNC resulted in a reduction in intubation rate that was not significant and a reduction in the hospital length of stay [90]. In contrast, in a subsequent meta-analysis of nine trials, compared with COT, use of HFNC post-operatively lowered reintubation rates (RR 0.32, 95% CI 0.12-0.88) and decreased the need to escalate respiratory support (eg, cross over to NIV; RR 0.54, 95% CI 0.31-0.94) [91]. HFNC had no effect on mortality, ICU and hospital length of stay, or rate of postoperative hypoxia.

HFNC is not routinely available in all institutions for adult use, and it should only be administered by staff educated in its application. Technical details regarding its application and the use of HFNC as a treatment for acute respiratory failure in medical patients are discussed separately. (See "Continuous oxygen delivery systems for the acute care of infants, children, and adults", section on 'Nasal cannula'.)

COVID-19 — While coronavirus disease 2019 (COVID-19) is not a complication of surgery per se, patients with perioperative COVID-19 experience significant complications from surgery.

Two cohort studies reported data on 30-day mortality and postoperative pulmonary complications. In the smaller matched cohort study from Italy in which 41 patients with COVID-19 were matched with 82 control patients, 30-day mortality was higher in the COVID-19 group versus the control group (19.5 versus 2.5 percent). Pulmonary complications, most often pneumonia or acute respiratory failure, were also more frequent in patients with COVID-19 compared with the control group (58.5 versus 3.7 percent) [93].

A larger international multicenter cohort study extended these findings. This observational cohort reported pulmonary complications in 51 percent of patients who had surgery (835 had emergency surgery and 280 had elective surgery) and in whom severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was detected within 7 days before or 30 days after surgery [94]. Among those with pulmonary complication, the 30-day mortality was higher than the group as a whole (38 versus 24 percent). Treatment is similar to nonsurgical patients with COVID-19 (see "COVID-19: Management in hospitalized adults" and "COVID-19: Management of the intubated adult"). Increased awareness of the possibility of SARS-CoV-2 infection preoperatively and also postoperatively is important in the management of postoperative pulmonary complications and in minimizing spread of SARS-CoV-2 in-hospital transmission.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Atelectasis (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Pulmonary complications are a major cause of morbidity and mortality during the postoperative period. (See 'Introduction' above.)

●Atelectasis is one of the most common postoperative pulmonary complications. It can be asymptomatic or manifest as increased work of breathing and hypoxemia. Postoperative atelectasis tends to develop after the patient has left the post-anesthesia care unit. The initial approach to managing postoperative atelectasis depends upon whether the patient has abundant secretions, which we define as frequent expectoration, the expectoration of large amounts of sputum, and/or prominent rhonchi on auscultation (see 'Atelectasis' above):

•For patients without abundant respiratory secretions who have hypoxemia and/or increased respiratory effort due to postoperative atelectasis, we suggest a trial of continuous positive airway pressure (Grade 2C).

•For patients with abundant respiratory secretions and clinically significant postoperative atelectasis, we suggest frequent suctioning and chest physiotherapy (ie, postural drainage and percussion) (Grade 2C). In addition, we suggest that bronchoscopy not be routinely performed as a first-line intervention prior to suctioning and chest physiotherapy (Grade 2B). Bronchoscopy should be reserved for patients who are unresponsive to suctioning and chest physiotherapy.

●Bronchospasm is common during the postoperative period. Treatment involves treating the underlying cause, removing potential contributors (eg, medications), and pharmacotherapy. For patients with postoperative bronchospasm, we recommend short-acting inhaled beta-2-agonists (eg, albuterol, metaproterenol) as first-line therapy (Grade 1A). The addition of a short-acting inhaled anticholinergic, ipratropium, may be beneficial if the bronchospasm is severe. (See 'Bronchospasm' above.)

●Postoperative pneumonia tends to occur within five postoperative days. It has clinical manifestations and a diagnostic approach that is nearly identical to other types of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP). Postoperative pneumonia is frequently caused by resistant organisms, such as gram-negative bacteria and Staphylococcus aureus, or multiple organisms. The management of postoperative pneumonia involves collection of respiratory specimens for microbiological analysis, followed by the initiation of empiric antimicrobial therapy. Once the microbiological data has been reported and the patient's response to empiric therapy assessed, the antimicrobial regimen should be tailored. (See 'Pneumonia' above.)

●Acute upper airway obstruction typically occurs during the immediate postoperative period. It usually manifests as stridor if the obstruction is incomplete or aphonia if the obstruction is complete. Acute upper airway obstruction is a medical emergency that requires immediate evaluation by a clinician who is capable of performing endotracheal intubation. (See 'Acute upper airway obstruction' above.)

●Obstructive sleep apnea (OSA) can be exacerbated during the postoperative period, which manifests as more frequent, more severe, or more prolonged episodes of oxyhemoglobin desaturation during sleep. (See 'Exacerbation of obstructive sleep apnea' above.) The postoperative management of patients with known or suspected OSA is reviewed in detail separately. (See "Postoperative management of adults with obstructive sleep apnea".)

●Small pleural effusions are common during the immediate postoperative period following abdominal surgery. Most resolve spontaneously within a few days and, therefore, do not require intervention. However, atypical characteristics of either the pleural effusion or the patient's clinical course (eg, signs of infection [fevers, chest infiltrate, worsening productive cough]) warrant diagnostic evaluation of the effusion. (See 'Pleural effusion' above.)

●Additional postoperative pulmonary complications include chemical pneumonitis due to aspiration, pulmonary edema, pulmonary embolism, abdominal compartment syndrome, tracheal laceration or rupture, and respiratory failure. (See 'Chemical pneumonitis' above and 'Pulmonary edema' above and 'Pulmonary embolism' above and 'Abdominal compartment syndrome' above and 'Tracheal laceration or rupture' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Michael Johnson, MD, who contributed to earlier versions of this topic review.