Aspiration Prophylaxis and Rapid Sequence Induction for Elective Cesarean Delivery

Abstract

Aspiration of gastric contents is a rare but feared and potentially fatal complication of anesthesia. In Mendelson’s landmark article on the pathophysiology of pulmonary aspiration in obstetric patients, he recognized that the clinical presentation is different depending on whether the aspirate is solid or liquid. Solid material resulted in suffocation and death, whereas liquid material resulted in “asthma-like” symptoms. Subsequently, he not only demonstrated that lung injury is secondary to gastric acid but also made 2 critical observations: gastric emptying time is delayed during labor, and aspiration occurs when airway reflexes are obtunded by anesthesia. Since 1946, these observations have been considered valid for every parturient who presents for labor and delivery; however, a question arises when caring for the fasted patient who presents for elective cesarean delivery. Does she have the same risk of aspiration as her laboring counterpart? We suggest that she may not be at as high risk as previously thought. This issue emerged when we cared for a primigravida with cardiomyopathy, severe global biventricular hypokinesis, and a left ventricular ejection fraction of 20%. Our decision to proceed with general anesthesia forced us to confront the issue of airway management. Traditional and contemporary teaching considers all obstetric patients to be at increased risk for pulmonary aspiration compared with patients scheduled for nonobstetric elective surgical procedures, mandating pharmacological prophylaxis as well as rapid sequence induction of anesthesia with cricoid pressure. However, the requirements of a patient at risk for aspiration are difficult to reconcile with a judicious, titrated induction of anesthesia that is ideal for a patient with severely compromised cardiac function. Faced with this choice, we opted for a careful induction of anesthesia with mask ventilation before endotracheal intubation, omitting cricoid pressure. This case made us reconsider long-held beliefs about the risk of aspiration in a subset of obstetric patients and specifically ask ourselves whether an appropriately fasted patient presenting for elective cesarean delivery is indeed at increased risk for aspiration compared with patients scheduled for non-obstetric elective procedures. Defining the full stomach has proven difficult. Many investigators have shown that lung injury increases markedly when the pH of the aspirate is 3. The oft-quoted threshold values for defining a full stomach and increased risk of aspiration are gastric volume 0.4 mL/kg with a pH 2.5. These data come from an experiment in a single rhesus monkey in which the investigators directly instilled liquid of varying volumes and acidity into the mainstem bronchus. Lung injury occurred with a volume 0.4 mL/kg and a pH 2.5. This experiment has led to considerable confusion about gastric volume and the risk of aspiration. The authors defined only the amount of aspirate necessary to cause lung injury if the pH was suitably low. The value 0.4 mL/kg has been erroneously interpreted as the amount of gastric volume that puts a patient at risk of aspiration when in fact it is the volume that produced lung injury in a highly contrived laboratory experiment. The more important question is what amount of gastric volume results in regurgitation. Animal data suggest that the residual gastric volume required to produce regurgitation under general anesthesia is much larger than 0.4 mL/kg. As the volume of liquid gastric contents increases, the risk of regurgitation also increases. At some currently unknown volume, this risk may become unacceptably high. There is, however, much evidence showing that if gastric emptying is normal and patients are appropriately fasted, the risk of significant aspiration is extremely low. The critical question to be answered is whether obstetric patients have normal gastric emptying. Mendelson studied laboring patients whom he correctly identified as having delayed gastric emptying. Since then, delayed gastric emptying has frequently been attributed to all obstetric patients. The presumed mechanisms are a hormonally induced decrease in gastric motility and the mechanical and anatomic effect of cephalad displacement of the stomach with distortion of the gastroesophageal From the Department of Anesthesiology, University of Virginia, Charlottesville, Virginia.