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Gastric content aspiration responsible for pneumonia is a rare but severe complication of general anesthesia (1). Risk factors include induction of anesthesia in nonfasted patients and conditions associated with slow gastric emptying (2). Obese patients are believed to be prone to aspiration pneumonia. This vulnerability has been ascribed to abnormal gastric emptying, based on an early study in which gastric content in the fasting state was both more abundant and more acid in obese than in lean individuals (3). A more recent study failed to replicate this finding (4). However, methodological limitations call into question the validity of the findings from both studies (3,4). In the present study, we compared the volume and pH of gastric content in fasting obese and lean individuals. Patients and Methods Approval of the study was obtained from the appropriate ethics committee and informed consent from the patients. Twenty-three lean (body mass index [BMI] <30 kg/m2) and 25 obese (BMI >35 kg/m2) consecutive patients scheduled for fiberoptic gastric endoscopy without premedication, general anesthesia, or sedation were included prospectively. Endoscopy was routinely performed before bariatric surgery in obese patients. In lean patients, endoscopy was indicated for abdominal pain. Exclusion criteria were age older than 60 yr, pregnancy, presence of a gastric tube, and a history of reflux, diabetes mellitus, or medication use within the last 7 days. Finally, only the patients with normal endoscopy were included. Endoscopy was performed after an 8-h fast, with the patient lying on the left side. Local anesthesia of the pharynx and larynx was achieved by application of viscous lidocaine gel. The fiberoptic endoscope was inserted through the mouth and immediately pushed into the gastric antrum. The gastric content was aspirated completely under visual guidance and collected in a volumetric container. A sample was taken for pH measurement using a pH meter. The required sample size was calculated. We calculated the sample size such that gastric volume of 20 mL in lean and 26 mL in obese would produce a Type 1 error rate of two-tailed α = 2.5% and, under the alternate hypothesis, would retain the null hypothesis with a Type 2 error of β = 0.05% (yielding a power of 99.5%). Results are reported as mean ± sd or median (range). Patient characteristics and gastric content volume and pH in the lean and obese subjects were compared using a Mann-Whitney U-test. P values <2.5% were considered statistically significant. Results BMI was 46 ± 8 kg/m2 in the obese subjects and 22 ± 2 kg/m2 in the lean subjects. The groups were similar for age (35 ± 12 yr and 40 ± 16 yr in the obese and lean subjects, respectively), gender (5/25 obese men and 7/23 lean men), and smoking status (6 smokers in each group). ASA grade was I or II in all subjects. Gastric content volume was identical in the obese and lean subjects (26 ± 13 mL and 26 ± 8 mL, respectively). The values of pH were 2.3 (1.3–7.1) and 2.8 (1.6–7.1) in obese and lean patients, respectively. Discussion We found identical gastric content volumes in fasting obese and lean subjects, with a lower pH in the obese individuals. An early study suggested that gastric content in the fasting state was both more abundant and more acid in obese than in lean individuals (3). However, in this previous study, gastric content was collected through a gastric tube, without visual control, leaving some doubt as to whether all the fluid was aspirated. Furthermore, some of the patients received premedication with diphenhydramine and a combination of droperidol and fentanyl (Innovar®), and the gastric content was collected after anesthesia induction and tracheal intubation. All these factors may alter gastric acid secretion and gastric emptying. Despite these methodological shortcomings, this study was considered conclusive for >20 yr and was the main foundation of the belief that obese patients are prone to aspiration pneumonia. A study of subjects who received no premedication has been published (4). Gastric content was both smaller and less acidic in the obese than in the lean subjects. However, in this study, gastric content was collected via a tube without visual control. The findings from our study of gastric content collected during endoscopy disagree with those of both earlier studies. This discrepancy may be explained by the difference in the collection technique. Although a few studies suggest that collection via a gastric tube may be reliable (5), the amounts of gastric fluid found are so small that failure to aspirate even a tiny proportion of the fluid could invalidate the results. This is probably what happened in the two earlier studies. Only aspiration of the fluid under endoscopic control, as in our study, ensures that all the gastric fluid is collected and tested. The pH and volume of residual gastric content may be important for defining populations at high risk for aspiration pneumonia. Although this remains controversial in humans (6), large gastric content volume and low gastric content pH in animal models produce significant pulmonary injury after pulmonary aspiration of gastric fluid (2). The exact level of gastric content pH and volume above which the risk of pulmonary injury becomes significant is not agreed on (6). In addition, there is no proof that such a specific value does exist. Thus, the mechanism underlying the increased risk of aspiration pneumonia in obese subjects is not an increase in gastric content volume because this volume is the same as in lean subjects, as presently demonstrated. Other factors such as intragastric, abdominal, and lower esophageal sphincter pressures probably play a key role in the pathophysiology of pulmonary aspiration. However, they were not investigated in the present study. Our study was prospective and descriptive. The fact that the patients have not been randomized may have introduced some degree of bias. Randomization was obviously impossible. Thus, in contradistinction to the results of several earlier studies, fasting gastric content is not more abundant in obese patients than in lean patients after an eight-hour fast. However, because other factors potentially implicated in the pathophysiology of pulmonary aspiration (i.e., abdominal and lower esophageal sphincter pressures) have not been investigated in the present study, premedication with citrate and an antihistamine before general anesthesia induction is still appropriate in obese patients. The risk of aspiration pneumonia in obese patients and the factors underlying this risk remain to be determined.
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Juvin et al. (2001) studied this question.
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