In anesthesia, the term “full stomach” applies to patients that have recently ingested foods and/or have pharmacologic, metabolic, anatomic, or hormonal conditions, which impair gastric emptying. Full stomach patients are at a greater risk for pulmonary aspiration of gastric contents during all phases of an anesthetic.

The most important factors leading to complications from aspiration are the gastric volume and pH. Studies point to gastric volumes around 20 cc/kg (←check this number) and a pH <2.5 correlating to more severe complications of aspiration.

As an example, pregnant patients in the third trimester are considered “full stomach” even if they have obeyed fasting criteria.

Risk factors that increase the likelihood of gastric aspiration include anatomic, pharmacologic, metabolic, autonomic, and hormonal states that impair gastric emptying or impair protective airway reflexes. These include, but are not limited to:

A diabetic patient with profound autonomic neuropathy may have impaired gastric emptying. In addition, patients with large hiatal hernias, morbid obesity, and pregnancy may have a higher likelihood of gastric aspiration because of the cephalad displacement of the gastroesophageal junction and loss of lower esophageal sphincter (LES) tone [1].

Morbidly obese patients with large truncal adiposity may have displacement of their gastroesophageal junction cephalad, altering LES pressure and increasing the risk for gastric aspiration. In addition, obese patients are at greater risk for developing type 2 diabetes-induced autonomic neuropathy, which could slow gastric emptying. Patients with GERD generally are NOT at greater risk for gastric aspiration, unless their GERD is secondary to a large hiatal hernia or another process which has altered LES tone. Patients with well-controlled GERD are generally considered low risk for gastric aspiration [1].

While there are no agents that have demonstrated a decrease in the risk of gastric aspiration, some pharmacologic interventions can be employed to potentially mitigate any sequelae. The only agents available that BOTH decrease gastric volume and increase gastric pH are proton pump inhibitors (PPI) and histamine-2 blockers, such as famotidine (H2-blocker) or esomeprazole (PPI). Other agents that can be considered in high risk patients include metoclopramide, a gastric pro-kinetic agent that works by blocking dopamine receptors. This agent both increases LES tone and promotes gastric motility. Sodium citrate is a non-particulate antacid which can be used to increase gastric pH.

The LES is a 2–4 cm high pressure region at the gastroesophageal junction. Different from the remainder of esophagus, the LES maintains an increased resting tone secondary to cholinergic influences and calcium influxes. However, many ingestible, pharmacologic, and anatomic factors can alter this relationship. The following is a list of the most common factors:

Foods:

Hormones:

Others:

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