Aspiration Prevention and Prophylaxis: Preoperative Considerations for the Full Stomach Patient

Key Points

The incidence of pulmonary aspiration in the general surgical population is low, but it is slightly increased among obstetric, pediatric, and trauma patients. It remains the leading cause of death related to airway management.
Regurgitation and aspiration can result from “light” anesthesia, coughing, or gagging in the patient whose airway is not protected with a cuffed endotracheal tube (ETT).
Patients manifesting no evidence of respiratory impairment for 2 hours after a known or suspected aspiration episode are highly unlikely to become significantly symptomatic later.
Preoperative ultrasonography of the gastric antrum may be used to screen patients at risk for perioperative pulmonary aspiration of regurgitated gastric contents.
Both pain and opioids significantly delay gastric emptying.
Aspiration of particulate antacids can induce a severe granulomatous pneumonitis.
Ingestion of clear liquids 2 to 3 hours before anesthetic induction does not appear to increase the risk of gastric content aspiration in patients with no gastrointestinal pathology.
Cricoid pressure can compromise ventilation by either face mask or supraglottic airway and can interfere with direct laryngoscopy, thus requiring discontinuation in certain circumstances.
Routine preoperative use of gastrointestinal stimulants, H ₂ -receptor antagonists, and proton pump inhibitors is not recommended in patients with no increased risk of pulmonary aspiration.
Meticulous attention to airway management during induction, through emergence, and after extubation is crucial for patients at risk for pulmonary aspiration. Approximately 50% of all cases of perioperative aspiration occur at times other than anesthetic induction.

Introduction

Pulmonary aspiration is a rare event. Yet, it is still about 10 times more common as an airway management complication than is the failure to oxygenate. Prevention of pulmonary aspiration is thus one of the basic goals of anesthetic care. In this chapter we will provide a thorough review of risk factors for pulmonary aspiration, preventive techniques, medical prophylaxis, and management strategies. The need for conscious adherence to deliberate practice principles and to development and maintenance of expertise in airway management as a key for the anesthesia provider to minimize the risk of pulmonary aspiration is highlighted.

Perioperative Aspiration

Perioperative pulmonary aspiration of regurgitated gastric contents is conceptually defined as the presence of gastric or bilious secretions or particulate matter in the tracheobronchial tree. In research and clinical practice, the method of diagnosis differs substantially: from visual confirmation (either direct visual or bronchoscopic confirmation), biochemical analysis of tracheal aspirate (pepsin A or pH), or postoperative imaging that demonstrates lung infiltrates not previously identified on a preoperative chest radiograph. The pulmonary aspiration of gastric contents has generated a body of research and recrimination that might seem disproportionate to its reported incidence. Yet, it remains one of the leading causes of mortality and morbidity related to the management of the airways.

Most cases of pulmonary aspiration occur during induction of anesthesia and initial airway management (50%) or during and after emergence from anesthesia. The basic tenet of a safe anesthesia management plan for reducing the incidence of pulmonary aspiration of gastric contents is preoperative fasting, which, in the past, led to prolonged rituals that have been more recently challenged, at least with respect to fluids. Crucial to pulmonary aspiration prevention is identifying those at risk and applying appropriate airway management techniques that may reduce the risk of pulmonary aspiration.

Incidence

The overall incidence of perioperative pulmonary aspiration is between 1 and 5 per 10,000 anesthetics. A multicenter, prospective study of almost 200,000 surgeries performed in France found the overall incidence of clinically apparent aspiration to be 1.4 per 10,000 anesthetics. Warner and colleagues retrospectively reviewed more than 215,000 general anesthetics and found an incidence of aspiration of 3.1 per 10,000 cases. Olsson and colleagues examined the records of more than 175,000 anesthetics administered at one hospital over more than 13 years and reported an incidence of aspiration of 4.7 per 10,000. In their 1999 review of 133 Australian cases, Kluger and Short reported that the incidence of passive regurgitation was three times that of active vomiting and that a majority of aspiration episodes accompanied anesthetics delivered by face mask or supraglottic airway (SGA). Among those who aspirated, 38% developed radiographic infiltrates, more often in the right lung than in the left. The authors also noted that a recurring theme in many incidents was inadequate depth of anesthesia leading to coughing/straining and subsequent regurgitation/vomiting.

Aspiration of gastric contents was the primary adverse event in 17% of major complications as reported in the Fourth National Audit Project (NAP4) of the Royal College of Anaesthetists and the Difficult Airway Society, which examined records for major complications among 2.9 million general anesthetics and airway management procedures across the United Kingdom. The audit revealed 184 serious airway-related complications that led to unanticipated admission to or prolonged stay in the intensive care unit, emergency invasive airway access, brain damage, and/or death. The report showed that pulmonary aspiration remains a serious issue and was responsible for 50% of anesthesia-related deaths related to airway management.

Several authors have observed that only 50% or less of episodes of perioperative aspiration occur during anesthetic induction and intubation, perhaps because concern is less heightened at other times. These potentially catastrophic events also take place before induction (when the unguarded patient may be excessively sedated), during anesthesia maintenance, and during or after emergence and extubation. Interestingly, the incidence of pulmonary aspiration rises to 50 per 10,000 anesthetics for patients who are managed with rapid sequence induction and intubation (RSI) and to 280 per 10,000 when RSI is performed outside the operating room. ^,

Consequences

When aspiration does occur, the subsequent clinical course can range from benign to fatal. Olsson and colleagues reported that 18% of patients who aspirated perioperatively required mechanical ventilatory support and 5% died; all those who died had a poor preoperative physical status. Warner and colleagues reported that 64% of patients did not exhibit coughing, wheezing, radiographic abnormalities, or a 10% decrease in arterial oxygen saturation from preoperative room air values during the first 2 hours after aspiration. Such patients, who remained asymptomatic for 2 hours, developed no respiratory sequelae. Of the patients who did manifest signs or symptoms of pulmonary aspiration within 2 hours after the event, 54% required mechanical ventilatory support for 6 hours or longer, and 25% were ventilated for more than 24 hours. Approximately 50% of those ventilated for 24 hours or longer died, generating an overall mortality rate of up to 5% of all aspiration events.

Mortality rates resulting from perioperative pulmonary aspiration have ranged from less than 5% to more than 80% in other reports. ^, ^, In the aforementioned studies of Warner and Olsson, there were no deaths in healthy patients undergoing elective surgery. ^, In a review of more than 85,000 Scandinavian anesthetics, only 3 of 25 patients who aspirated developed serious morbidity, 2 of whom endured a prolonged course of illness but all of whom survived. In general, most healthy patients who aspirate only gastric fluid can expect to survive without residual respiratory impairment, as long as aspiration is promptly recognized and adequately managed.

Risk Factors

Demographic

Published surveys have associated some patient characteristics or circumstances with an increased incidence of aspiration. Warner and colleagues noted that the relative risk of aspiration was more than four times higher for emergency surgeries compared with elective surgeries. A higher American Society of Anesthesiologists (ASA) physical status classification also was associated with a higher risk of aspiration. The incidence of aspiration increased from 1.1 per 10,000 elective anesthetics in ASA class I patients to 29.2 per 10,000 emergency anesthetics in ASA class IV and V patients. Age, gender, pregnancy, concurrent administration of opioids, obesity, experience of anesthesia provider, and types of surgical procedure—contrary to conventional wisdom—were not independent risk factors for pulmonary aspiration. In Warner’s study, the most common predisposing condition in all patients was gastrointestinal obstruction. In a retrospective review of pediatric cases, aspiration occurred significantly more often in patients with greater severity of underlying illness ( Box 14.1 ).

Box 14.1

Risk Factors for Aspiration of Gastric Contents

Regurgitation or vomiting

Hypotension

Opioids

Increased intragastric volume and pressure

Decreased lower esophageal barrier pressure

Incompetent laryngeal protective reflexes

Neurologic disease

Neuromuscular disease

Central nervous system depressants

Advanced age or debility

Olsson and colleagues found that children and the elderly were more likely than patients of intermediate ages to aspirate perioperatively. Statistically, the risk of aspiration was more than three times higher in emergency surgeries than in elective operations. The incidence of aspiration was increased more than sixfold when surgery was performed at night rather than during daylight hours. More recent studies of both adult and pediatric cases have confirmed an impressive increase in the incidence of perioperative aspiration in emergency situations. ^, ^, ^,

Pulmonary aspiration has been demonstrated to occur more frequently after difficulty with airway management. In Olsson’s study, 15 of 83 aspirations occurred in patients with no known risk factors; of these, 10 were associated with airway difficulty, suggesting that unanticipated difficult airway may be an important risk factor for pulmonary aspiration.

Although regional techniques are often favored for patients at increased risk for aspiration, elderly patients, in particular, have been reported to vomit and aspirate during spinal anesthesia. Hypotension resulting from neuraxial sympathectomy can induce nausea and vomiting, and supplemental analgesics and sedatives given during lengthy operations can significantly obtund protective airway reflexes. ^, ^,

Barrier Pressure

Patients who are likely to have gastric contents of increased volume or acidity, elevated intragastric pressure, or decreased tone of the lower esophageal sphincter (LES) traditionally are considered to be at increased risk for perioperative pulmonary aspiration ( Boxes 14.1 and 14.2 ). ^, The LES forms a boundary between the stomach and the esophagus, creating a sling around the abdominal esophagus to prevent reflux of gastric contents into the esophagus. Intragastric pressure is normally less than 7 mm Hg; the difference between LES pressure and gastric pressure is the barrier pressure , which is typically 15 to 25 mm Hg in conscious individuals. An incompetent LES reduces barrier pressure, increasing the risk of regurgitation of gastric contents, such as in patients with gastroesophageal reflux disease (GERD). Likewise, elevated intragastric pressure, such as when the stomach is distended postprandially, reduces barrier pressure and increases the risk of regurgitation. Gastric distention with increased intragastric pressure causes reflex relaxation of the LES with resultant reflux.

Box 14.2

Factors That Increase Intragastric Volume and Pressure

Increased gastric filling

Air insufflation during mask ventilation

Increased gastric acid production

Gastrin

Histamine ₂ (H ₂ ) receptor stimulation

Recent ethanol ingestion

Recent hypoglycemic episode

Decreased gastric emptying

Intestinal obstruction

Diabetic gastroparesis

Opioids

Anticholinergics

Sympathetic stimulation (pain and anxiety)

Anesthetic agents relax the LES, reduce barrier pressure, and predispose the patient to regurgitation. Cricoid pressure (CP) application and laryngoscopy during anesthesia also decrease LES tone. Drugs that lower LES tone include anticholinergics, benzodiazepines, dopamine, sodium nitroprusside, thiopental, tricyclic antidepressants, β-adrenergic stimulants, opioids, and propofol. Inhalational anesthetic agents can reduce the LES pressure below the intragastric pressure, depending on the degree of relaxation. Recent ethanol ingestion or hypoglycemic episodes stimulate gastric acid secretion, whereas tobacco inhalation temporarily lowers LES tone. LES tone also has been found to be reduced by gastric fluid acidity, caffeine, chocolate, and fatty foods. Drugs that increase LES pressure include antiemetics, cholinergic drugs, succinylcholine (also increases the intragastric pressure), pancuronium, metoclopramide, neostigmine, metoprolol, α-adrenergic stimulants, and antacids.

Surgical outpatients traditionally have been thought to have increased gastric volume and reduced gastric pH, possibly because of preoperative anxiety. Clinical studies, however, have not consistently confirmed this expectation and have failed to confirm an increased risk of pulmonary aspiration in the outpatient, with no correlation between anxiety or outpatient status and gastric residual. Furthermore, Hardy and colleagues contradicted several conventional notions by finding that neither gastric volume nor pH correlated with preoperative anxiety, body mass index (BMI), ethanol or tobacco intake, or history of GERD.

Obesity

Obese patients traditionally have been thought to pose a relatively high risk for aspiration because of increased gastric volume and acidity, increased intragastric pressure, and a higher incidence of GERD ; however, this assumption has been challenged. In 1998, Harter and colleagues studied 232 fasted, nondiabetic surgical patients who had received no relevant preoperative medication; they found that obese patients had a lower incidence of elevated gastric volume and acidity compared with nonobese patients. Grading obesity by BMI, they also found no association between degree of obesity and gastric fluid volume or pH. Verdich and colleagues reported that obese and lean patients did not differ in rate of gastric emptying during the first 3 hours after a test meal. LES pressure also has been shown not to differ significantly between obese and nonobese patients.

On the other hand, the difficulties with airway management that arise from obesity, along with the association between airway difficulty and aspiration, appear to increase the risk of aspiration in obese patients regardless of their gastrointestinal motility. Clinical studies on the incidence of difficult intubation in the obese have been contradictory. In a review of the topic, it has been reported that obese patients develop oxygen desaturation faster than the nonobese, and the safe apneic period is reduced from more than 5 minutes to less than 2 to 3 minutes in the preoxygenated state. In addition, because obese patients are at a high risk for difficult mask ventilation, gastric insufflation may occur as a result of increased airway pressures during mask ventilation. Thus, the risk of regurgitation in an obese patient may be increased because of intragastric pressure increases. Nevertheless, morbidity in obese patients occurs more often from hypoxemia related to decreased functional residual capacity during difficult or failed intubation than from aspiration. With the increased frequency of bariatric procedures, clinicians should recognize that patients who have previously undergone bariatric surgery are at particular risk for aspiration because of their gastric dysfunction.

Systemic Diseases

Patients with connective tissue, neurologic, metabolic, or neuromuscular disease may be at risk for esophageal dysfunction or laryngeal incompetence. Progressive systemic sclerosis and myotonic dystrophy have been specifically mentioned in case reports. Gastric emptying time in patients with Parkinson disease was shown to be delayed compared with control volunteers and was even slower in patients treated with levodopa. Advanced age may be associated with attenuated cough or gag reflexes.

Long-standing diabetes mellitus is well known to delay gastric emptying and also may compromise LES function. Several authors have reported a high incidence of gastroparesis and prolonged mean gastric emptying times, at least for solid foods, in diabetic patients compared with control subjects. Impairment of gastric motility was usually found to correlate with findings of autonomic neuropathy but not with peripheral neuropathy or with indices of glycemic stability.

Pregnancy

Pregnancy imposes a constellation of potential risk factors for regurgitation of gastric contents. The enlarging uterus increases intragastric pressure by compressing the stomach, physically delays gastric emptying by pushing the pylorus cephalad and posteriorly, and promotes gastroesophageal reflux by altering the angle of the gastroesophageal junction. Progesterone decreases LES tone, and excess gastrin produced by the placenta promotes gastric acid secretion. ^, ^, The alterations in anatomy that are typical of late pregnancy can interfere with laryngoscopy and tracheal intubation. It has been observed that the incidence of Mallampati classes III and IV increases during labor compared with the prelabor period. Laryngeal and upper airway edema are also common in the parturient and can be exaggerated by preeclampsia.

Studies of gastric emptying in pregnancy have produced somewhat inconsistent results. Wong and colleagues found that water was readily cleared from the stomachs of nonobese, nonlaboring parturients at term. Other recent studies of gastric emptying in nonlaboring term women also suggest that gastric emptying is not delayed during pregnancy. Chiloiro and colleagues found that gastric emptying time did not become slower with the progress of gestation but that total orocecal transit time did.

A more common clinical concern is the parturient in labor. Laboring patients who consumed a light solid meal had significantly greater gastric volumes than those allowed only water. Although pain, in any circumstance, is thought to delay gastric emptying, Porter and colleagues suggest that pain does not appear to be the sole cause of gastric slowing in late labor because there was a similar delay in women in late labor who had received either epidural local anesthetic alone or no analgesia.

Pain and Analgesics

Pain and its treatment are risk factors for aspiration, notably in patients presenting with trauma. Crighton and colleagues found that circulating catecholamines have an inhibitory effect on gastric emptying, and noradrenaline release in response to painful stimuli may cause inhibition of gastric tone and emptying. Trauma patients, especially those in acute pain who are scheduled for emergency surgery, have decreased gastrointestinal motility and increased gastrointestinal secretion despite fasting preoperatively. The incidence of pulmonary aspiration increases markedly after trauma because of recent ingestion of food, depressed consciousness, diminished or absent airway reflexes, or gastric stasis induced by increased levels of catecholamines. Patients with spinal cord or brain injuries also have been shown to manifest delayed gastric emptying of both liquid and solid contents. ^,

Administration of opioids to alleviate pain may further impair gastrointestinal function. Opioid receptors can be found throughout the gastrointestinal tract; human and animal studies suggest that there are central and peripheral mechanisms by which these drugs delay gastric emptying. Even modest intravenous doses of morphine demonstrably prolong gastric transit times in clinical studies. ^,

Neuraxial opioids also can prolong gastric emptying. In parturients, the administration of fentanyl 25 µg intrathecally delayed gastric emptying in labor compared with both extradural fentanyl 50 µg with bupivacaine and extradural bupivacaine alone. On the other hand, the addition of fentanyl (2 or 2.5 µg/mL) to dilute bupivacaine for epidural infusion during labor was not found to affect gastric motility. ^,

Pathophysiology

When gastric contents enter the lungs, the resultant pulmonary pathology depends on the nature of the material aspirated ( Box 14.3 ). Food particles small enough to enter the distal airways induce a foreign body reaction of inflammation and eventual granuloma formation. The aspiration of particulate antacids produces the same adverse response. ^, Acid aspiration induces an inflammatory response that begins within minutes and progresses over 24 to 36 hours. ^, In 1940, Irons and Apfelbach described the characteristic microscopic changes as intense engorgement of the alveolar capillaries, edema, hemorrhage into the alveolar spaces, and extensive desquamation of the lining of the bronchial tree. Other authors also have described hemorrhagic pulmonary edema, intense inflammation, and derangement of the pulmonary epithelium. ^, The membranous epithelial cells that produce surfactant are damaged or destroyed by the acid and replaced by granular epithelial cells. As surfactant production fails, lung units progressively collapse. Fibrin and plasma leak from the capillaries into the pulmonary interstitium and alveoli, producing noncardiogenic pulmonary edema often referred to as adult respiratory distress syndrome. ^, ^, ^, With effective supportive care, the acute inflammation can diminish, and epithelial regeneration can begin within 72 hours.

Box 14.3

Pathophysiology of Aspiration

Particulate aspiration → Airway obstruction →

Granulomatous inflammation → Acid aspiration →

Neutrophilic inflammation → Hemorrhagic pulmonary edema →

Destruction of airway epithelium → Loss of type I alveolar cells →

Loss of surfactant → Alveolar instability and collapse →

Disruption of alveolar-capillary membrane → Plasma leakage from pulmonary capillaries →

Noncardiogenic pulmonary edema → Hypovolemia

The clinical features of aspiration pneumonitis have been well described for more than 70 years. Even earlier, in 1887, Becker referred to bronchopneumonia as a postoperative complication related to the inhalation of gastric contents. Hall, in 1940, published the first description of gastric fluid inhalation in obstetric patients. He distinguished between the aspiration of solid material, which could quickly kill by suffocation, and the aspiration syndrome produced by gastric fluid, for which he coined the term chemical pneumonitis . Mendelson, in 1946, described the clinical features of 66 cases of peripartum aspiration observed from 1932 to 1945. Solid food produced airway obstruction, which was quickly fatal in two instances. Otherwise, wheezing, rales, rhonchi, tachypnea, and tachycardia were prominent. Subsequent reports have not found wheezing to be as universal a manifestation, occurring in about one-third of aspirations. When present, wheezing is thought to result from bronchial mucosal edema and from a reflex response to acidic airway irritation. ^, ^,

Refractory hypoxemia can ensue almost immediately as bronchospasm, airway edema, airway obstruction, and alveolar collapse or flooding increase the effective intrapulmonary shunt fraction ( Box 14.4 ). The awake patient may experience intense dyspnea and may cough up pink, frothy sputum characteristic of pulmonary edema. ^, ^, More modest aspirations may not become clinically evident for several hours. ^, ^,

Box 14.4

Causes of Hypoxemia in Aspiration

Upper airway obstruction

Increased lower airway resistance

Obstruction by airway debris

Airway edema

Reflex bronchospasm

Alveolar collapse and flooding

Hemodynamic derangements also can demand therapeutic attention. As the alveolar-capillary membrane loses its integrity, plasma leaks out of the pulmonary vasculature. With increasing volumes of fluid leaking into the lung, the loss of circulating volume can produce hemoconcentration, hypotension, tachycardia, and even shock. ^, Pulmonary vasospasm also may contribute to right ventricular dysfunction.

Radiographic evidence of pulmonary aspiration may become evident immediately, if aspiration is massive, or after a delay of several hours. There is no pattern on the chest radiograph that is specific for aspiration. The distribution of infiltrates depends on the volume of material inhaled and the patient’s position at the time of the event. As a result of bronchial anatomy, aspiration occurring in the supine patient affects the right lower lobe most commonly and the left upper lobe least often. ^, In most cases, infiltrates are seen in dependent parts of the lungs, predominating in the lower lobes ( Fig. 14.1 ). If pulmonary aspiration is not complicated by secondary events, improvement in symptoms can be anticipated within 24 hours, although the radiographic picture may continue to worsen for another day.

Fig. 14.1, Chest x-ray performed after tracheal intubation. Pulmonary infiltrates are seen in the dependent parts of the lungs (arrows) .

Determinants of Morbidity

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