The most comprehensive analysis of this event in adults is contained in a retrospective study published by Warner and colleagues [1]. They defined pulmonary aspiration as “either the presence of bilious secretions or particulate matter in the tracheobronchial tree” or “a postoperative chest X-ray with infiltrates not identified by preoperative chest X-ray or physical examination”. Pulmonary aspiration occurred in 67 of 172,335 patients who underwent 215,488 general anesthetics, which gives an incidence of 1:3216 anesthetics.

However, the chances of pulmonary aspiration increase for anesthesia providers who have a larger than usual number of emergency anesthetics (1:895) or patients rated as ASA IV or V (1:1401), but for most providers that would still mean less than one aspiration per year. This study and others all indicate that pulmonary aspiration is an infrequent occurrence . Of the patients in the Warner study who aspirated, about half (24 of 52) of those undergoing elective surgery and all of the emergency patients (15) had one or more preoperative conditions that are thought to predispose to aspiration, including bowel obstruction, obesity, preoperative opiate administration, depressed consciousness, and ingestion of a meal within 3 h. Aspiration occurred during induction of anesthesia or endotracheal intubation in 57 of the 67 cases, despite the use of cricoid pressure in all cases where aspiration was considered a possibility. Does this mean that cricoid pressure was ineffective in preventing aspiration? This issue will receive greater consideration later in this chapter.

In many cases, pulmonary aspiration causes little or no sequellae. In the Warner study 64 % (42 of 66) patients did not develop any symptoms related to the event, and their recovery was uneventful. The remainder (24) developed symptoms and signs of pulmonary aspiration within 2 h of the event. These included cough, wheezing, decrease in arterial oxygen saturation breathing room air, and X-ray evidence of pulmonary aspiration. Of the 24 patients, 18 required special respiratory or intensive care, and 13 required mechanical ventilation. Six patients developed adult respiratory distress syndrome (ARDS), and three died of respiratory failure. While the incidence of death was only 1:71,829 anesthetics, when severe, aspiration can be fatal. The four factors that increase the likelihood of death from aspiration are: age and general health; volume of aspiration; acidity of the aspirate; and contents of the aspirate. Patients who are elderly and have existing pulmonary or cardiovascular diseases are at increased risk of death if pulmonary aspiration occurs. Obviously, the greater the volume of aspirate, which is rarely quantifiable in clinical practice, the greater is the risk of death or severe disability. Likewise, the greater the acidity of the aspirate below pH 2.5, the more severe is the damage to the lungs. Finally, aspiration of solid matter that obstructs major airways, or aspiration of highly infectious material such as fecal matter carries a high mortality in any age group.

Of all the measures designed to prevent aspiration of gastric contents during anesthesia, fasting is the most universal and the most important. Recognizing that the rate of gastric emptying after a meal is highly variable, the ASA Practice Guidelines recommend that anesthesia providers advise adults and children not to ingest a light meal within 6 h, a heavy meal within 8 h, and clear liquids within 2 h of an elective operation. For infants, the fasting recommendations are 2 h for clear liquids, 4 h for breast milk, and 6 h for infant formula and non-human milk [2] (Table 8.1).

The use of prophylactic medications such as antacids (sodium citrate), H₂ receptor antagonists (cimetidine, ranitidine), antiemetics (ondansetron, dolasetron), or drugs to enhance gastric emptying or increase lower esophageal sphincter tone (metoclopromide) to prevent or lessen the severity of pulmonary aspiration is controversial. In the Warner study only half of the patients who aspirated had received any prophylactic medication, and the incidence and severity of the aspiration was no different from those who did not receive the medications. Other studies have shown similar results. The ASA Task Force on Preoperative Fasting concluded from their analysis of existing data that there is insufficient evidence that decreasing gastric acidity or gastric volume, or use of antiemetics decreases either the incidence or sequellae of pulmonary aspiration. While existing evidence challenges the value of prophylactic medication with antacids, H₂ receptor antagonists, and drugs that enhance gastric emptying , it is probably advisable to continue to use one or more of them because of the medicolegal consequences of not doing so.

This condition has come into prominence in the practice of anesthesiology. Whether the patient has symptoms of GERD is asked of everyone who is about to undergo anesthesia. It is defined as the passive movement of gastric contents into the esophagus, and occasionally into the throat causing irritation of the esophageal and oropharyngeal mucosa. Patients may feel a substernal burning sensation, which in the past was often called “heartburn”.

What is known about GERD? Unfortunately, not very much! We do know that GERD is very common. Most, if not all patients experience GERD at one time or another, especially going to bed just after overeating, eating fried, fatty or spicy foods, or after excessive consumption of alcohol. According to the National Institutes of Health, more than 60 million American adults experience GERD at least once a month, and 25 million have daily attacks. However, there are no clear criteria to delineate when GERD changes from being a casual, inconsequential event to becoming a disease. Furthermore, GERD is often referred in the anesthesia literature as being mild, moderate or severe, but there are no data to document what constitutes each category. Is severity based on frequency of attacks, volume of reflux, intensity of symptoms, response to medications, or some combination of these?

Gastroenterologists classify GERD on the basis of findings of mucosal damage at esophagoscopy, or by esophageal findings at roentgenography using double contrast barium swallow examinations. However, most patients reporting GERD have never undergone either of these studies. Finally, while the incidence of pulmonary aspiration in patients with GERD has not been studied in detail, history and clinical experience would certainly indicate that these patients rarely have clinically significant aspiration during anesthesia.

Since there is no scientifically established linkage between GERD and pulmonary aspiration during induction of anesthesia, how should we deal with the patient who has a history of GERD? When interviewing such a patient, two questions are key. First, does the patient have GERD when he/she does not eat? If the answer is no, then it becomes a non-issue for those patients who are NPO prior to surgery. Second, are the symptoms of GERD controlled by diet and/or medications (antacids, H₂ receptor blockers or proton pump inhibitors)? If the answer is yes then one should advise the patient to take their usual medication the day of surgery. Most patients with GERD will fall into one or both of these categories, and other measures to prevent aspiration are unnecessary. To do otherwise would mean that almost all patients are candidates for aspiration prevention.