Chapter 12 Aspiration Prevention and Prophylaxis
The pulmonary aspiration of gastric contents has generated a body of research and recrimination that might seem disproportionate to its reported incidence. Aspiration pneumonitis is an anesthetic complication whose consequences can be formidable but whose prevention would seem, at least in theory, to be readily attainable. The desire to minimize risks long ago led to rituals of fasting that were later challenged, at least with respect to fluids. Any experience with aspiration and its dire sequelae may, however, inspire rigid adherence to conservative nil per os (NPO) standards and avid administration of prophylactic preoperative medications.
The statistical incidence of perioperative aspiration has been examined in long-term case reviews. A multicenter, prospective study of almost 200,000 operations performed in France found the overall incidence of clinically apparent aspiration to be 1.4 per 10,000 anesthesias.1 Leigh and Tytler’s 5-year survey of almost 110,000 anesthesias found 6 cases of aspiration requiring unplanned critical care.2 Warner and colleagues retrospectively reviewed more than 215,000 general anesthesias and found an incidence of aspiration of 3.1 per 10,000 cases.3 Olsson and associates examined the records of more than 175,000 anesthesias administered at one hospital over more than 13 years and reported an incidence of aspiration of 4.7 per 10,000.4 Kallar and Everett’s multicenter survey of more than 500,000 outpatient anesthesias found the incidence of aspiration to be 1.7 per 10,000.1
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 anesthesias delivered by face mask or laryngeal mask airway (LMA). Thirty-eight percent of those who aspirated 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 one of inadequate anaesthesia leading to coughing/straining and subsequent regurgitation/vomiting.”5 In their 1999 survey of pediatric aspiration, Warner and coauthors also wrote that “nearly all cases of pulmonary aspiration … occurred in patients who gagged or coughed during airway manipulation or during induction of anesthesia.”6
Several authors have observed that only about 50% or fewer of the episodes of perioperative aspiration occur during anesthetic induction and intubation, perhaps because concern is less heightened at other times.1–9 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.
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.4 Warner and coworkers reported that 64% of patients did not manifest coughing, wheezing, radiographic abnormalities, or a 10% decrease in arterial oxygen saturation (Sao2) 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 less than 5% of all aspirations.3
Mortality rates resulting from perioperative pulmonary aspiration have ranged from less than 5% to more than 80% in other reports.10,11 In the studies of Warner and Olsson and their coworkers, there were no deaths in healthy patients undergoing elective surgery.3,4 In their 1999 survey of 133 perioperative aspirations in Australia, Kluger and Short wrote that “the deaths following aspiration events occurred in sicker patients … although mortality can occur in healthy, younger patients.”5 Reviewing more than 85,000 Scandinavian anesthesias, Mellin-Olsen and associates noted that only 3 of 25 patients who aspirated developed serious morbidity, 2 of whom endured a prolonged course of illness but all of whom survived.8 In general, most healthy patients who aspirate only gastric fluid can expect to survive without residual respiratory impairment, albeit sometimes after a stormy postoperative course.
Published surveys have associated some characteristics of patients 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 was also associated with a higher risk of aspiration. The incidence of aspiration increased from 1.1 per 10,000 elective anesthesias in ASA class I patients to 29.2 per 10,000 emergency anesthesias in ASA class IV and V patients. Contrary to conventional wisdom, “Age, gender, pregnancy … concurrent administration of opioids, obesity … experience … of anesthesia provider, and types of surgical procedure were not independent risk factors for pulmonary aspiration. … The most common predisposing condition in all patients was gastrointestinal obstruction.”3 Borland and coauthors also wrote that “aspiration occurred significantly more often in patients with greater severity of underlying illness.”12
Olsson and colleagues found that children and elderly persons were more likely than patients of intermediate ages to aspirate perioperatively.4 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 operations,6,8 but Borland and coauthors found this increase to be only “marginally significant.”12
In Kallar and Everett’s outpatient survey,1 aspiration occurred most frequently in patients younger than 10 years of age. They also reported, “In patients with no other identifiable risk factors, 67% of aspirations occurred after difficulties in airway management or intubation.”1 In the study of Olsson and colleagues, 15 of 83 aspirations occurred in patients with no known risk factors.4 In 67% (10/15) of these cases, aspiration accompanied airway problems. In contrast to Kluger and Short’s findings,5 no patient aspirated while intubated. 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 subarachnoid anesthesia. Hypotension resulting from neuraxial sympathectomy can induce nausea and vomiting, and supplemental analgesics and sedatives given during lengthy operations can seriously obtund protective airway reflexes.4,13,14
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) are traditionally considered to be at increased risk for perioperative pulmonary aspiration (Boxes 12-1 and 12-2).10,15 As discussed later, pregnancy combines several of these likely risk factors. Although a lengthy NPO period before elective surgery is intended to minimize the volume of gastric contents, up to 90% of fasted patients have a gastric fluid pH level lower than 2.5.11 Recent ethanol ingestion or hypoglycemic episodes stimulate gastric acid secretion, whereas tobacco inhalation temporarily lowers LES tone. LES tone has also been found to be reduced by gastric fluid acidity, caffeine, chocolate, and fatty foods.11
Box 12-1 Risk Factors for Aspiration of Gastric Contents
Box 12-2 Factors That Increase Intragastric Volume and Pressure
Surgical outpatients have traditionally been thought to carry gastric contents of expanded volume and reduced pH, possibly because of preoperative anxiety. Clinical studies, however, have not consistently confirmed this expectation.1 Furthermore, Hardy and associates contradicted several conventional notions by finding that neither gastric content volume nor pH correlated with preoperative anxiety, body mass index (BMI), ethanol or tobacco intake, or reflux history.15
Obese patients were traditionally thought to pose a relatively high risk for aspiration because of their greater gastric fluid volume and acidity, intragastric pressure, and incidence of gastroesophageal reflux (GER).16 This assumption has been challenged. In 1998, Harter and colleagues studied 232 fasted, nondiabetic surgical patients who had received no relevant preoperative medication. Using conventional arbitrary criteria, they found that only 27% of obese patients, compared with 42% of the nonobese, had gastric contents of high volume and acidity. Grading obesity by BMI, they also found no association between degree of obesity and gastric fluid volume or pH.16 The presumed sluggishness of gastric emptying in obese patients has also been denied. Verdich and coworkers reported that obese and lean patients did not differ in rate of gastric emptying during the first 3 hours after a test meal.17 Lower esophageal pressure has also been shown not to differ significantly between obese and nonobese patients.16
On the other hand, the laryngoscopic challenges that arise with corpulence, along with the association between airway difficulties and aspiration episodes, appear to increase the risk of aspiration in obese patients regardless of their gastrointestinal motility. Clinical studies have both confirmed and denied a demonstrable increase in the incidence of difficult intubation (DI) in the obese.18–21 In a review of the topic, Freid noted that “obese patients … develop oxygen desaturation faster than the nonobese, and the safe apneic period is reduced from more than five minutes to less than two to three minutes in the preoxygenated state.” Importantly, he observed that “far more morbidity occurs owing to hypoxemia during difficult or failed intubation than from aspiration.”7
Patients with connective tissue, neurologic, metabolic, or neuromuscular disease may be imperiled by esophageal dysfunction or laryngeal incompetence. Progressive systemic sclerosis and myotonia dystrophica have been specifically mentioned in case reports.22–24 Hardoff and coworkers found that “gastric emptying time in patients with Parkinson’s disease was delayed compared with control volunteers [and] was even slower in patients treated with levodopa.”25 Advanced age may be associated with attenuated cough or gag reflexes.
Long-standing diabetes mellitus is commonly considered to delay gastric emptying and may also compromise LES function.26 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.27–30 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 imposes a constellation of potential risk factors. The enlarging uterus increases intragastric pressure by compressing the stomach, physically delays gastric emptying by pushing the pylorus cephalad and posteriorly, and promotes GER by altering the angle of the gastroesophageal junction. Progesterone decreases the tone of the LES, and excess gastrin, produced by the placenta, promotes gastric acid secretion.26,31,32 The alterations in physique that are typical of late pregnancy can interfere with laryngoscopy and endotracheal intubation. Laryngeal and upper airway edema is also common in the parturient and can be exaggerated by preeclampsia.33
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 and wrote that “recent studies of gastric emptying in nonlaboring term women … suggest that gastric emptying is not delayed during pregnancy.”34 Chiloiro and coworkers found that gastric emptying time did not become slower with the progress of gestation but that total orocecal transit time did.35 A more common clinical concern is the parturient in labor. Scrutton and associates reported that laboring patients who consumed a light solid meal had significantly greater gastric volumes than those allowed only water.36 Although pain, in any circumstance, is thought to delay gastric emptying, Porter and coauthors stated that “pain does not appear to be the sole cause of gastric slowing in late labour since [there was] a similar delay in women in late labour who had received either epidural local anesthetic alone or no analgesia.”37
Pain and its treatment are considered to be risk factors for aspiration, notably in patients presenting with trauma. As stated by Crighton and colleagues, “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.”38 Patients with spinal cord or brain injuries have also been shown to manifest delayed gastric emptying of both liquid and solid contents.39–41
Administration of opioids to alleviate pain is an essential act of kindness but 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 retard gastric emptying.42 Even modest intravenous doses of morphine demonstrably prolong gastric transit times in clinical studies.38,43–45
Neuraxial opioids can also prolong gastric emptying. In obstetric anesthesia, Kelly and associates “conclude[d] that the administration of fentanyl 25 mg intrathecally delays gastric emptying in labor compared with both extradural fentanyl 50 mg with bupivacaine and extradural bupivacaine alone.”46 Older reports indicated that epidural fentanyl boluses of 50 or 100 mg would retard gastric emptying. On the other hand, the addition of fentanyl (2 or 2.5 mg/mL) to dilute bupivacaine for epidural infusion during labor was not found to affect gastric motility.37,47
Agnew and colleagues continuously monitored esophageal and tracheal pH in thoracotomy patients “considered to be at low risk of GER.” Twenty-eight percent of their patients not treated with a histamine2 (H2)-receptor antagonist were found to have acid reflux into the esophagus while in the lateral decubitus position, and almost 8% had acid in the trachea. Although the authors did not correlate clinical outcomes with their findings, they did advise that patients undergoing thoracotomy be considered for routine preoperative aspiration chemoprophylaxis.48
When gastric contents enter the lungs, the resultant pulmonary pathology depends on the nature of the material aspirated (Box 12-3). 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.32,49 Acid aspiration induces an inflammatory response that begins within minutes and progresses over 24 to 36 hours.49,50 In 1940, Irons and Apfelbach wrote that the “characteristic microscopic changes are intense engorgement of the alveolar capillaries, … edema, and hemorrhage into the alveolar spaces.… Another outstanding characteristic is the extensive desquamation of the lining of the bronchial tree.”51 Other authors have also described hemorrhagic pulmonary edema, intense inflammation, and derangement of the pulmonary epithelium.50,52 The membranous epithelial cells that produce surfactant are damaged or destroyed by the acid and replaced by granular epithelial cells.14 As surfactant production fails, lung units progressively collapse. Fibrin and plasma leak from the capillaries into the pulmonary interstitium and alveoli, producing the noncardiogenic pulmonary edema often referred to as adult (or acute) respiratory distress syndrome (ARDS).14,50,53,54 With effective supportive care, the acute inflammation can diminish, and epithelial regeneration can begin, within 72 hours.
Box 12-3 Pathophysiology of Aspiration
The clinical features of aspiration pneumonitis have been well described for more than 60 years. Even earlier, in 1887, Becker referred to bronchopneumonia as a postoperative complication related to the inhalation of gastric contents.51 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.55 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.56 (Subsequent reports have not found wheezing to be so 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.11,50,57
Refractory hypoxemia can ensue almost immediately as bronchospasm, airway edema or obstruction, and alveolar collapse or flooding increase the effective intrapulmonary shunt fraction (Box 12-4). The awake patient may experience intense dyspnea and may cough up the pink, frothy sputum characteristic of pulmonary edema.11,32,50 More modest aspirations may not become clinically evident for several hours.32,58,59
Box 12-4 Aspiration and Hypoxemia
Hemodynamic derangements can also demand therapeutic attention. As the alveolar-capillary membrane loses its integrity, plasma leaks out of the pulmonary vasculature. If the leak becomes a flood, the loss of circulating fluid volume can produce hemoconcentration, hypotension, tachycardia, and even shock.11,32 Pulmonary vasospasm may also contribute to right ventricular dysfunction.11
The radiographic evidence of pulmonary aspiration may become evident promptly, if aspiration is massive, or after a delay of several hours. There is no pattern on the chest roentgenogram 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. Because of bronchial anatomy, aspiration occurring in the supine patient affects the right lower lobe most commonly, the left upper lobe least often.11,32 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.32
In his 1946 report, Mendelson undertook to determine the relationship between gastric fluid acidity and pulmonary morbidity. When liquid containing hydrochloric acid (HCl) was instilled into rabbits’ tracheas, the animals developed a syndrome “similar in many respects to that observed in the human following liquid aspiration,”56 with cyanosis, dyspnea, and pink, frothy sputum. On the other hand, when neutral liquid was instilled into the trachea, the rabbits endured a brief symptomatic period, “but within a few hours they [were] apparently back to normal, able to carry on rabbit activities uninhibited.”56 (Mendelson maintained a discreet silence about the nature of these uninhibited rabbit activities.)
Since Mendelson’s report, numerous attempts (and assumptions) have been made to define the “critical” volume and pH of gastric contents required to inflict significant damage on the lungs. Such neatly defined threshold values may be illusory objects of desire rather than features of clinical reality. Nonetheless, almost all researchers in the field of aspiration pneumonitis have made some use of critical values to define the success or failure of drug therapies in the modification of gastric contents.
In 1952, Teabeaut injected HCl solutions of different volumes and acidities into rabbits’ tracheas. He found that solutions with a pH higher than 2.4 caused a relatively benign tissue response similar to that induced by the intratracheal injection of water. As the pH of the injectate was reduced from 2.4 to 1.5, a progressively more severe tissue reaction was elicited. At pH 1.5, the damage was maximal and equal to that found at lower pH values.60 From this study stemmed the popular concept of the pH value of 2.5 as a threshold for chemical pneumonitis.
The determination of a critical volume of gastric contents required to produce severe aspiration pneumonitis has been even more contentious than that of a critical pH. Two teams of investigators each found that, in dogs, pulmonary injury became independent of pH as the volume of aspirate was increased from 0.5 to 4.0 mL/kg.11 A preliminary experiment by Roberts and Shirley, involving gastric fluid instillation into the right main stem bronchus of a single monkey, long ago led to the acceptance, in some quarters, of 0.4 mL/kg as the volume of gastric fluid that places a subject at risk for development of aspiration pneumonitis.61–63 Subsequent researchers challenged this number. James and colleagues demonstrated that aspirate volumes as low as 0.2 mL/kg could induce pulmonary injury if the pH of the aspirate were reduced to 1.09.64 On the other hand, Raidoo and coworkers, also studying monkeys, found that the aspiration of 0.4 to 0.6 mL/kg of fluid with a pH of 1.0 produced mild or moderate pulmonary injury, and 0.8 to 1.0 mL/kg at pH 1.0 produced severe pneumonitis, with a 50% mortality rate (3/6) at 1.0 mL/kg.61
Clearly, the volume of aspirate that is considered hazardous depends on how much morbidity or pathology must be produced to be considered significant. Arguments have also been made concerning the experimental instillation of gastric fluid into one lung versus both lungs and the reliability of gastric fluid volume measurements. In addition, even if a critical volume for aspiration pneumonitis could be reliably determined, it cannot be known how much fluid must be present in the stomach in order to deposit this critical volume into the lung or lungs.61,65 However, studies of therapeutic interventions must have criteria for defining success or failure, and threshold values for gastric fluid volume and pH are typically employed, regardless of their validity.
Volume and acidity are not, of course, the only determinants of sequelae when gastric contents enter the lungs. Since the report of Bond and coworkers in 1979, it has been appreciated that gastric fluid containing particulate antacids can produce severe aspiration pneumonitis, even at near-neutral pH, with wheezing, pulmonary edema, and hypoxemia requiring mechanical ventilatory support.66 Animal studies confirmed that nonparticulate gastric acid and particulate antacid solutions have similar potentials for pulmonary mischief if aspirated.58 Although blood and digestive enzymes do not appear to induce chemical pneumonitis, feculent gastric contents with a high bacterial density readily produce pneumonitis and death in animals. (Acidic gastric contents are normally sterile.) Another study demonstrated that the mucus present in the gastric fluid of dogs with intestinal obstruction produced diffuse small airway obstruction and pulmonary injury when aspirated.11
The clinical challenges of perioperative pulmonary aspiration are prevention, prophylaxis, and treatment. Ideally, gastric contents can be physically prevented from entering the lungs in the first place. Should prevention fail, pharmacologic prophylaxis may modify the volume and character of gastric contents so that they inflict minimal damage on the lungs. Least desirably, aspiration pneumonitis can require intensive medical treatment and ventilatory support.
The most common means of keeping gastric contents out of the lungs is to minimize the volume of such contents through preoperative fasting. However, both the utility and the necessity of adhering to traditional NPO regimens for clear liquids have been challenged. As noted by Sethi and coauthors, “the stomach can never be completely empty even after a midnight fast since it continues to secrete gastric juices.”67 The issue has been studied in both pediatric and adult surgical patients and has become particularly contentious and emotional regarding obstetric anesthesia.
Conventional preoperative fasting can impose physical and emotional discomfort on children and their parents and may be difficult to enforce reliably in outpatients. Dehydration in infants and hypoglycemia in neonates may also result from prolonged NPO times.1,10 The normal stomach can empty 80% of a clear liquid load within 1 hour after ingestion. Whereas the stomach continues to secrete and reabsorb fluid throughout NPO time, ingested clear liquids are completely passed into the duodenum within 2.25 hours.68 Several researchers have therefore sought to demonstrate that children may safely be allowed to drink clear liquids until just 2 to 3 hours before elective surgery.
Van der Walt and Carter, as well as other groups, determined that healthy infants could drink limited volumes of clear liquids 3 to 4 hours before surgery with no effect on gastric content volumes.69 Splinter and colleagues found that healthy infants could drink clear liquids ad libitum until 2 hours before anesthetic induction without altering gastric fluid volume or pH. (Gastric fluid pH was quite variable, and mean pH was less than 2.5 in all groups of patients studied, regardless of NPO time.) On the other hand, milk or formula intake on the morning of surgery (4 to 6 hours before induction) was associated with the presence of curds in many of the gastric aspirates. This was considered to represent an unacceptable risk of particulate aspiration. The authors therefore concurred with previous recommendations that infants not be allowed milk or formula on the morning of surgery.70
More recently, Cook-Sather and associates studied 97 healthy infants undergoing elective surgery and found that gastric fluid volume was not increased when the fasting time for formula was reduced from 8 hours to either 6 or 4 hours.71 Schreiner and colleagues compared the gastric contents of children subjected to conventional preoperative fasting (mean NPO time, 13.5 hours) with those of children permitted clear liquids until 2 hours before anesthetic induction (mean NPO time, 2.6 hours). Gastric fluid volumes actually tended to be somewhat smaller in the children allowed to drink clear liquids up to 2 hours preoperatively, and almost all children in both groups had gastric content pH values of 2.5 or less.72 Sandhar and coauthors, studying children 1 to 14 years old, also found that clear liquid ingestion 2 to 3 hours preoperatively did not significantly increase the mean volume of gastric contents and did not increase the number of patients with gastric contents more voluminous than 0.4 mL/kg.68 Reports by Splinter, Moyao-Garcia, Maekawa, and Gombar and their colleagues all concluded that permitting children to drink nonparticulate fluids 2 to 3 hours before surgery had either no effect or a small beneficial influence on the quantity and acidity of their gastric contents.73–76
Ingestion of clear liquids alone therefore appears to pose no demonstrable hazard if taken no later than 2 hours before anesthesia by children without gastrointestinal pathology. However, solid or semisolid foods are not cleared from the stomach as rapidly as clear liquids. Meakin and associates found that a light breakfast of biscuits or orange juice with pulp, taken 2 to 4 hours before induction, did increase the volume of gastric aspirate in healthy children compared with those who had fasted for 4 hours or longer. In all fasted children, and in almost all of the fed children, the gastric content pH was 2.5 or less.77 Hyperosmolar glucose solutions are also associated with delayed gastric emptying.68
In 1999, the ASA issued the report of its Task Force on Preoperative Fasting, which included practice guidelines. These guidelines were intended to apply to healthy patients who have no known relevant risk factors or injuries and are scheduled for elective surgery. Within these limitations, the ASA Task Force “support[ed] a fasting period for clear liquids of two hours for all patients [and] a fasting period for breast milk of four hours for both neonates and infants” while considering it “appropriate to fast from intake of infant formula for six or more hours.”78
In adult surgical patients, too, considerable evidence has demonstrated that clear liquid intake within 2 to 3 hours of anesthetic induction does not increase the risk of gastric acid aspiration. It is important to note that these studies typically involved healthy, nonpregnant, nonobese patients who were free of known gastrointestinal pathology, were not receiving opioids or other medications known to interfere with gastric emptying, and were undergoing elective surgery. The results of such studies cannot, therefore, be reliably applied to any other groups of patients.79–82
With adults, as with children, the basic arguments favoring relaxed NPO regimens for clear liquids involve their normally rapid gastric clearance. More than 90% of a 750-mL bolus of isotonic saline was found to pass from the normal stomach within 30 minutes.83 After 2 hours of fasting, the fluid in the stomach primarily represents the acid secreted by the stomach itself. Exogenous clear liquids tend to dilute endogenous gastric acid and may even accelerate gastric emptying.65,72,81 Solids, lipids, and hyperosmotic liquids are thought to delay gastric emptying, and their intake would therefore be considered ill advised before anesthetic induction.65
Several researchers have sought to correlate these theoretical considerations with clinical situations. Maltby and colleagues studied outpatients who were either kept NPO from the previous midnight or given 150 mL of water 2.5 hours before anesthetic induction. Although the mean gastric pH did not differ significantly between the two groups, the mean gastric volume was significantly less in the patients who drank than in those who fasted.83 Read and Vaughan similarly found that permitting patients to drink water ad libitum until 2 hours before surgery had no impact on gastric volume or pH but did decrease preanesthetic anxiety. Many patients had gastric pH values less than or equal to than 2.5, regardless of the time elapsed since fluid intake.84
Phillips and colleagues also determined that patients who were allowed to drink clear liquids until 2 hours before surgery had gastric volume and pH values similar to those of patients who fasted for 6 hours. Other studies have also confirmed that the ingestion of 150 mL of (pulp-free) orange juice, coffee, tea, or apple juice 2 to 3 hours before surgery has no detrimental effect on gastric pH or volume in surgical outpatients.81 (Since the publication of these reports, one can only wonder how many hours of presurgical time have been consumed in speculation regarding the pulp content of orange juice that patients have admitted to consuming.)
The safety of clear liquid ingestion before surgery does not, of course, imply that solid food may also be taken with impunity. In an early study, Miller and coworkers compared 22 adults kept NPO overnight before surgery with 23 adults permitted a light breakfast (one slice of buttered toast and tea or coffee with milk) on the morning of surgery (mean NPO time, 3.8 hours). The two groups were found not to differ significantly in mean volume or median pH of gastric contents or in the percentage of patients with a gastric pH lower than 3.0.80 Soreide and coauthors reported that the particulate elements of a light breakfast had not completely exited after 4 hours.85 Reflecting a consensus of clinical comfort, the aforementioned ASA Task Force recommended a 6-hour preoperative fast following a “light meal” and a fast of 8 hours or longer “for a meal that included fried or fatty foods or meat.”78
As preoperative NPO standards became more relaxed, strenuous debate arose over the necessity of adhering to conventional NPO regimens for patients in labor. Obstetricians, nurse-midwives, and psychologists joined the fray. On the one hand, anesthesiologists have long recognized that advanced gestation increases the risk of gastric content aspiration. On the other hand, proponents of liberalizing oral intake for parturients cited the infrequency of aspiration pneumonitis in modern practice, the futility of fasting in ensuring an empty stomach, and the detrimental effects of fasting on maternal and fetal well-being. The fashionable battle cry of “patient autonomy” was also heard.