Clinically significant aspiration is a relatively rare complication of anesthesia. The reported incidence is 1 to 5 per 10,000 patients, although it is more common in certain situations, such as traumatic brain injury. About half of the cases of perioperative aspiration occur during induction of anesthesia. Although an emergency indication for surgery is a major risk factor for aspiration, the majority of cases occur during elective procedures. Increased gastric pressure, decreased lower esophageal sphincter tone, and blunted protective airway reflexes promote aspiration. Therefore, risk factors for aspiration include full stomach, pregnancy, bowel obstruction, gastroesophageal reflux, obesity, gastrointestinal motility disorders, and neurologic conditions. Airway manipulation in an unfasted patient or an inadequate depth of anesthesia may increase the risk of aspiration. Many anesthetics reduce lower and upper esophageal sphincter tone and diminish protective airway reflexes. The appropriate use of laryngeal mask airways does not increase the risk of aspiration, although it may induce gastroesophageal reflux. Certain surgical procedures such as laparoscopic insufflation of the abdomen and bowel manipulation are associated with increased rates of aspiration.

Aspiration of gastric and oropharyngeal contents causes three overlapping syndromes. First, aspiration of large particulate matter may obstruct the airways and lead to atelectasis. Acute aspiration pneumonitis is more common and is a result of chemical burning of the tracheobronchial tree and pulmonary parenchyma by gastric and oral fluids. Finally, aspiration of bacteria from the oropharynx or a superinfection of the chemical pneumonitis may result in aspiration pneumonia.

Mendelson originally described aspiration pneumonitis in 66 obstetrical patients who aspirated gastric contents during anesthesia. Respiratory distress and cyanosis developed
within 2 hours after aspiration event. All patients (except two who had airway obstruction from solid food particles) recovered within 24 to 36 hours without antibiotics and had radiographic resolution. Signs and symptoms of aspiration pneumonitis include cough, wheeze, dyspnea, hypoxia, fever, tachypnea, and crackles on lung auscultation. Radiography usually demonstrates diffuse bilateral infiltrates.

Aspiration pneumonitis may be mild and elude clinical detection. Rarely, aspiration is fulminant and rapidly fatal. Most patients rapidly improve after aspiration and have clearing of radiographic lung infiltrates. Occasionally, patients initially improve but then develop progressive lung infiltrates on chest radiograph. These infiltrates probably represent secondary bacterial infection or ARDS. The volume and pH of the aspirated fluid are important factors affecting the degree of lung injury. In adults, approximately 25 mL of gastric acid with pH <2.5 is considered a clinically relevant threat. Smaller volumes may produce a milder syndrome. Bile may elicit a potent inflammatory response and has been identified in patients’ endotracheal tubes. Atelectasis, peribronchial hemorrhage, pulmonary edema, and degeneration of bronchial epithelial cells all develop within minutes of aspiration. By 4 hours, the alveoli fill with polymorphonuclear leukocytes and fibrin and hyaline membranes form. Hyaline membranes form within 4 hours. The lung becomes grossly edematous and hemorrhagic with alveolar consolidation.

Aspiration pneumonia may result from a superimposed infection of the chemical injury or inhalation of microorganisms from the oropharynx. Poor dentition is a risk factor for aspiration pneumonia. Common bacteria include Haemophilus influenzae, Streptococci, and other anaerobes. The oral flora changes in chronically ill patients and those in health care settings for greater than 48 to 72 hours. In these patients, gramnegative bacteria and resistant Staphylococcus may colonize the oropharynx and cause pneumonia.

Awake patients capable of airway protection should be placed in the upright or recovery position and encouraged to cough. However, clinicians may need to suction or rescue the airway if the patient has impaired protective airway reflexes. Supplemental oxygen should be administered for hypoxemia. Clinicians should avoid noninvasive ventilation because of the risk of gastric insufflation unless there is no further risk of additional vomiting. There is no evidence supporting lavage with saline or sodium bicarbonate. Gastric acid is rapidly neutralized by the physiologic response. When possible, the stomach should be emptied with a nasogastric tube. A chest radiograph should be ordered. In select circumstances, a bronchoscopy may be necessary for airway clearance and evaluation especially if airway obstruction is suspected. Bronchoscopy can provide quantitative lower respiratory tract cultures from bronchoalveolar lavage or protected brushings. These techniques can distinguish aspiration pneumonitis from pneumonia.

Although some animal studies support the use of corticosteroids in aspiration pneumonitis, there is no evidence of benefit in human studies. Moreover, the literature does not support the routine use of antibiotics immediately after aspiration. However, patients should be followed closely to identify the development of a secondary infection. If the clinicians diagnose aspiration pneumonia, they should choose antibiotics that provide coverage against oral flora including gram-negative coverage for patients with nosocomial
colonization. This may include extended spectrum beta lactamases inhibitors such as piperacillin-tazobactam.

Certain measures may help reduce the risk of perioperative aspiration. These include adequate fasting, prophylactic antiemetics, rapid sequence intubation (RSI), limited tidal volumes if bag ventilation used, and extubation when patient has return of laryngeal reflexes. Anti-acid medications can increase gastric pH; however, their use is only supported by expert opinion.

RSI involves preoxygenation followed by intubation using an induction agent and neuromuscular blockade without face-mask ventilation. There are no prospective randomized controlled trials that show whether RSI reduces the incidence of aspiration. However, RSI has been shown to decrease the time to achieve successful intubation, which may be beneficial when the risk of aspiration is high. The value of cricoid pressure during intubation remains controversial.

Respiratory failure commonly complicates the postoperative period and is strongly associated with an increased mortality. A number of clinical prediction rules exist to predict the risk of postoperative pulmonary complications. Predisposing factors include a high American Society of Anesthesiologists (ASA) Physical Status Classification, poor functional status, and hypoalbuminemia. Lung diseases such as obstructive airways dysfunction and extrapulmonary diseases such as liver cirrhosis, congestive heart failure, and renal failure also predispose patients to respiratory failure. Additional risk factors include emergency indications for surgery, prolonged procedural time, and the requirement for large volume fluid and blood product resuscitation. Because of their effects on respiratory mechanics,
thoracoabdominal surgeries, especially aortic aneurysm repair, are particularly high-risk procedures.

An extensive literature has evaluated the role of limiting tidal volumes to prevent VILI. Ventilation with tidal volumes greater than 8 mL per kg ideal body weight (IBW) is a risk factor for postoperative pulmonary complications in thoracic and abdominal surgery. Moreover, a randomized controlled trial in major abdominal surgery demonstrated that restricting tidal volumes from 6 to 8 mL per kg IBW decreased the incidence of postoperative respiratory failure. This intervention was part of a lung-protective strategy, which combined restricted tidal volumes with PEEP as compared to large tidal volumes without PEEP. Because the intervention also included PEEP, we cannot ascribe the full benefit to tidal volume restriction. In sum, the current data support targeting tidal volumes to less than 8 mL per kg IBW. The optimum dose of intraoperative PEEP is less clear. A meta-analysis revealed that a no PEEP approach was a risk factor of postoperative pulmonary complications in thoracic and abdominal surgery. However, a randomized trial during high-risk abdominal surgery did not demonstrate a benefit from high PEEP and recruitment maneuvers. As a whole, the current evidence supports the use of moderate PEEP (approximately 5 cm H₂O) during surgery and using higher PEEP and recruitment maneuvers when the patient’s physiology suggests derecruitment.

Numerous mechanisms contribute to the pathogenesis of postoperative respiratory failure (Fig. 3.1). A combination of postoperative pain, recumbent position, anesthetics, and impaired secretion clearance leads to collapse of dependent lung regions. Atelectasis increases shunt fraction, diminishes respiratory system compliance, and commonly contributes to postoperative respiratory failure.

Treating postoperative patients with high concentrations of inspired oxygen can lead to absorption atelectasis. Normally, the consumption of oxygen by peripheral tissues creates a small gradient between the gas tensions in the alveoli and pulmonary capillary blood. The gradient is normally small compared to the total gas tensions because nitrogen is the most abundant gas in both compartments. Nitrogen acts as a pneumatic splint in the lung by limiting the magnitude of the gas tension gradient between the alveoli and pulmonary capillary. Breathing high FIO₂ denitrogenates the body and increases the partial pressure of oxygen in alveolar gas much more than in mixed venous blood. Without nitrogen, venous blood becomes very hypobaric relative to alveolar gas. Therefore, high FIO₂ increases the gas tension gradient, which drives gas from the alveoli to the pulmonary capillary blood. This promotes the collapse of poorly ventilated alveoli (Fig. 3.2).

In the postoperative period, bronchospasm and impaired mucociliary clearance can decrease the rate of expiratory airflow and increase the work of breathing. Residual sedation and neuromuscular blockade may weaken respiratory muscles and diminish protective
muscle tone in the upper airway. Shock causes acidosis and hypoperfusion of respiratory muscles leading to respiratory failure. In particular, clinicians should consider the diagnosis of occult hemorrhage in any postoperative patient who develops respiratory failure. However, the clinician must also consider the opposite problem of fluid overload. Fluid accumulation in the lungs, chest wall, pleura, and peritoneum is a common problem and may decrease respiratory compliance and worsen gas exchange.

The systemic inflammatory response to major surgery or an acute illness will increase rates of tissue oxygen consumption and carbon dioxide (CO₂) production. The increased ventilatory requirement may impose an unsustainable burden on a respiratory system impaired by the aforementioned factors. This is especially true in the setting of debility, malnutrition, and chronic lung disease.

The history of the patient’s illness provides key evidence for determining the cause of respiratory failure. The clinician should review the past medical history, anesthesia record, operative reports, and perform a careful physical examination. The integration of these data should generate a short list of diagnostic possibilities (Table 3.1). Laboratory testing can help exclude or confirm diagnoses.

Arterial blood gas analysis can help triage disease severity and identify alveolar hypoventilation, increased alveolar-arterial oxygen gradient, and acid-base status. Additional labs including complete blood count, metabolic profile, and coagulation parameters are important part of the early evaluation. Chest x-rays are an essential part of the diagnostic approach to respiratory failure. However, their interobserver variability is high and their diagnostic accuracy is limited in acute respiratory failure.

Point-of-care diagnostic ultrasound can aid the diagnosis of acute respiratory failure (Table 3.2). In critically ill patients, pulmonary ultrasound is superior to chest x-ray in identifying pneumothorax, consolidation, pleural effusion, and lung edema. The use of basic echocardiography to identify right or left heart dysfunction can improve diagnostic accuracy. This approach can help distinguish cardiogenic from noncardiogenic causes of pulmonary edema and raise the suspicion for pulmonary embolism. Ultrasonography, like all clinical skills, requires expert training.

Pulmonary emboli (PE) are common in the postoperative period. PE cause tachycardia, tachypnea, and mildly reduce SpO₂. Large PE may cause shock. An abrupt increase in arterial to end-tidal PCO₂ gradient can be a sign of increased alveolar dead space from PE. If a clinician suspects PE, a computed tomography (CT) angiography is the best test. Ventilation-perfusion scintigraphy is an alternative if CT angiography cannot be performed. Given the
high-case fatality rate of untreated PE, therapeutic anticoagulation is indicated when PE is strongly suspected or confirmed. Clinicians must carefully consider the risk of bleeding from surgery sites or neuraxial anesthesia.

Pneumonia is the most important postoperative infection. Surgery, hospitalization, and illness alter the host’s bacterial flora and lead to pneumonia with antibiotic-resistant organisms. A chest x-ray, arterial blood gas, and blood cultures should be obtained in all patients suspected of having health care-associated pneumonia. In the case of ventilatorassociated pneumonia, clinical diagnosis may be inaccurate. Quantitative cultures of the lower respiratory tract obtained from bronchoalveolar lavage or protected brushings can assist the diagnosis.

NIPPV may be an alternative to endotracheal intubation in some situations. NIPPV can deliver high flow rates of oxygen, maintain PEEP, stent open the upper airway, and unload the work of breathing. Careful patient selection and recognition of contraindications to its use are essential. In this patient, the vomiting due to bowel obstruction is likely a contraindication to a trial of noninvasive ventilation (Table 3.3). Generally, the etiology of the respiratory failure and the type of mask interface are more important determinants of treatment success than the mode of NIPPV. The clinical indications with the best supporting evidence for NIPPV are acute cardiogenic pulmonary edema, obstructive sleep apnea, and exacerbations of chronic obstructive pulmonary disease. In cardiogenic pulmonary edema, the application of positive pressure can markedly reduce left ventricular preload and afterload. Bilevel and continuous positive airway pressure (CPAP) modes are both effective in cardiogenic pulmonary edema. Although there is little data from randomized controlled trials, there is a compelling physiologic rationale for the use of noninvasive ventilation for respiratory failure due to neuromuscular weakness and obesity-hypoventilation syndrome.

The clinical trial data for NIPPV in other causes of postoperative respiratory failure are mixed. Clinicians must exercise caution when using NIPPV for acute hypoxemic respiratory failure. Although it can help avoid intubation in some situations, about half of the patients treated with NIPPV for ARDS or pneumonia ultimately require intubation. Patients with multiorgan dysfunction are more likely to require intubation. Unfortunately, the largest randomized trial of NIPPV for acute hypoxemic respiratory found no benefit. This trial used CPAP mode, which improved gas exchange. However, there was a markedly increased mortality rate among patients who failed NIPPV. There was also an alarmingly high rate of cardiac arrest during rescue intubation in this setting. This risk is likely due to the sudden derecruitment and loss ventilation during the intubation process.