Etiology
Physiologic mechanisms that normally reduce the risk of aspiration include the gastroesophageal junction, upper esophageal sphincter, and protective laryngeal reflexes. These protective mechanisms can be affected by several conditions, age, or drugs.[26]
Aspiration of food and liquids is more common in:[27]
Patients with oropharyngeal dysphagia, especially when it is due to stroke, Parkinson disease, dementia, or cervical spine surgery[28][29][30]
Older patients
Patients who are taking sedatives
Patients being fed by a gastric tube[29]
Patients who depend on others for feeding
Current smokers
Patients taking >8 drugs
Pregnant women.
Among critically ill patients, the major risk factors for aspiration include:[31]
Documented previous episode of aspiration
Decreased level of consciousness (Glasgow coma scale score <9 or a high level of sedation)
Neuromuscular disease, or congenital or acquired structural abnormalities of the aerodigestive tract
Endotracheal intubation
Vomiting
Persistently high gastric residual volume
Supine positioning.
Additional risk factors include the presence of a nasoenteric tube, intermittent feeding, abdominal/thoracic surgery or trauma, delayed gastric emptying, older age, inadequate nursing staff, large size or diameter of feeding tube in children, malpositioning of the feeding tube, and transport.
In the perioperative period, factors that increase the likelihood of aspiration include:[8]
A high urgency of surgery
Difficult airways
Inadequate depth of anesthesia
Use of the lithotomy position
Gastrointestinal problems such as delayed gastric emptying, gastroesophageal reflux, ileus, acute abdomen, or bowel obstruction[12]
Depressed consciousness
Increased severity of illness
Obesity
Use of drugs that reduce lower esophageal sphincter pressure or delay gastric emptying.
Certain drugs reduce the lower esophageal sphincter pressure and promote gastroesophageal reflux in anesthesia and disease states, and thereby increase the risk for aspiration. These drugs include atropine, glycopyrrolate, dopamine, nitroprusside, ganglion blockers, thiopental, tricyclic antidepressants, beta-adrenergic stimulants, halothane, opioids, and propofol.
Certain drugs delay gastric emptying. Opioids can significantly delay gastric emptying and promote ileus. Glucagon-like peptide-1 (GLP-1) receptor agonists and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonists are known to delay gastric emptying, and because of retained gastric contents, their use is a risk factor for aspiration during procedures requiring general anesthesia or deep sedation.[32][33][34]
Pathophysiology
A higher prevalence of cerebrovascular and degenerative neurologic disease in people ages >70 years explains why increased age is a risk factor for aspiration. These conditions result in dysphagia and an impaired cough reflex, both of which increase the risk for aspiration of foreign bodies, food, liquids, and barium contrast.[4][35]
Anticholinergics, antipsychotics, or anxiolytics may also impair the cough reflex and/or swallowing.
Tachypnea, resulting from various medical conditions, alters the coordination between deglutition and respiration, and increases the risk for aspiration.[36]
The lower and upper esophageal sphincter tone is decreased in GERD, by certain drugs (anticholinergics, antipsychotics, and anxiolytics), and by indwelling endotracheal, tracheostomy, gastric, or nasogastric tubes. This decrease in sphincter tone increases the risk for gastric content aspiration.[8]
The loss or impairment of protective laryngeal reflexes during the perioperative period contributes to the increased risk for anesthesia-related pulmonary aspiration. In addition to the obtunded reflexes from anesthesia and sedation, the supine position during diagnostic, surgical, and dental procedures aligns the trachea and the oropharynx, thereby increasing the risk for aspiration.[37]
Altered physiologic states such as pregnancy, gastrointestinal disorders, and diabetes mellitus are associated with delays in the rate of gastric emptying, which increase the gastric volume. Opioids can significantly delay gastric emptying and promote ileus. Glucagon-like peptide-1 (GLP-1) receptor agonists and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonists have been shown to delay gastric emptying.[32][33]
Pregnancy increases the risk of aspiration because progesterone decreases the tone of the lower esophageal sphincter and delays gastric emptying, in addition to the increase in intra-abdominal pressure secondary to the gravid uterus. Gastric juice aspiration and the resulting pneumonitis occurring in the context of pregnancy and anesthesia was first described by the eponymous Mendelson and is the basis for the wide practice of preoperative fasting.[38]
Aspiration of different gastric materials may have different effects. Low pH (acidic) material leads to neutrophil-predominant lung injury. There is apoptosis of type I alveolar epithelium caused by direct acid contact, and release of proinflammatory mediators secondary to activation of capsaicin-sensitive (TRPV-1) receptors. Alternatively, aspiration of small nonacidified gastric particles (SNAP) or bacteria directly stimulates alveolar macrophages to release innate immune/proinflammatory mediators through activation of polyanionic scavenger receptors or Toll-like receptors. Even without particulate or acid-related injury, gastric juice can contain digestive enzymes such as pepsin and bile salts that are caustic to the respiratory epithelium and likely to influence the type and severity of the respiratory presentation.[39] Most patients aspirate complex gastric contents, which are a combination of gastric food particles, bacterial products, cytokines, and acid, referred to as CASP (combined acid and small food particles). Aspiration of CASP may exacerbate damage due to the synergistic effect of acid and small gastric particles. The volume, viscosity, force of inhalation during aspiration, and host defenses contribute to the variable presentation that can manifest as bronchitis, bronchiolitis, pneumonitis/pneumonia, and ultimately acute respiratory distress syndrome.
Regardless of the type of aspiration material, there is an acute inflammation in the lung characterized by neutrophil infiltration, alveolar hemorrhage, intra-alveolar and interstitial edema, and impairment of alveolar fluid clearance. This is followed by a repair process characterized by scavenging of alveolar detritus by macrophages and proliferation of type II alveolar epithelial cells.[40]
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