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* From the Departments of Anesthesia and
Community Health Sciences, University of Calgary, Calgary, Alberta, Canada.
Address correspondence to: Dr. Saul Pytka, Department of Anesthesia, Rockyview General Hospital, 7007 - 14 Street N.W., Calgary, Alberta T2V 1P9, Canada. Phone: 403-943-3410; Fax: 403-943-3360/3434; E-mail: spytka{at}telusplanet.net
| Abstract |
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Methods: A single-blind, randomized study of 126 adult patients, age
18 yr, ASA physical status I or II, BMI > 30 kgm2 who were scheduled for elective surgery under general anesthesia. Patients were excluded if they had diabetes mellitus, symptoms of gastroesophageal reflux, or had taken medication within 24 hr that affects gastric secretion, gastric fluid pH or gastric emptying. All patients fasted from midnight and were randomly assigned to fasting or fluid group. Two hours before their scheduled time of surgery, all patients drank 10 mL of water containing phenol red 50 mg. Those in the fluid group followed with 300 mL clear liquid of their choice. Immediately following induction of general anesthesia and tracheal intubation, gastric contents were aspirated through a multiorifice Salem sump tube. The fluid volume, pH and phenol red concentration were recorded.
Results: Median (range) values in fasting vs fluid groups were: gastric fluid volume 26 (3107) mL vs 30 (3187) mL, pH 1.78 (1.317.08) vs 1.77 (1.277.34) and phenol red retrieval 0.1 (030)% vs 0.2 (015)%. Differences between groups were not statistically significant.
Conclusion: Obese patients without comorbid conditions should follow the same fasting guidelines as non-obese patients and be allowed to drink clear liquid until two hours before elective surgery, inasmuch as obesity per se is not considered a risk factor for pulmonary aspiration.
| Introduction |
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In 1999 a task force of the ASA, after an exhaustive review of randomized clinical trials and other scientific evidence, recommended that healthy patients undergoing elective surgery could safely drink clear liquids until two hours preoperatively and that routine pharmacologic antacid prophylaxis was not indicated.4 The task force cautioned that the guidelines may need to be modified for patients with co-existing disease that might affect gastric emptying or fluid volume (e.g., pregnancy, obesity, diabetes, hiatal hernia, gastroesophageal reflux disease, ileus or bowel obstruction, emergency care or enteral tube feeding) and patients in whom airway management might be difficult.5 No randomized clinical trials of fasting vs drinking on residual gastric fluid volume (RGV) and pH had been conducted in these conditions on which to give an evidence-based recommendation.
Obese patients have been considered to be at increased risk of pulmonary aspiration since Vaughan et al. in 19755 observed that the risk factors of RGV > 25 mL and pH < 2.5 were present in a higher proportion of fasting [npo from midnight] morbidly obese than non-obese surgical patients. More recently, Harter et al. found a lower incidence of these risk factors in otherwise healthy, fasting obese than non-obese patients.6 Furthermore, Warner et al. were unable to identify obesity as a risk factor in their analysis of 67 cases of pulmonary aspiration in 215,000 general anesthetics.2
The prevalence of obesity among adults is 15% in Canada7 and 27% in the United States.8 Anesthesiologists may currently choose to include or exclude these patients from the ASA4 and similar Canadian Anesthesiologists Society (CAS) fasting guidelines.9 In morbidly obese volunteers, the dual isotope technique for measuring gastric emptying of solids and liquids demonstrates delayed emptying of solids, but no delay for clear liquids.1014 The purpose of this study was to determine, in obese patients, the effect of drinking 300 mL clear liquid two hours before elective surgery on the volume and pH of gastric contents at induction of anesthesia.
| Methods |
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18 yr, ASA I or II, with body mass index (BMI) > 30 kgm2 who were scheduled for elective surgery under general anesthesia. We excluded patients who had diabetes mellitus, proven hiatus hernia, symptoms of gastroesophageal reflux, those who had taken medication within 24 hr that affects gastric secretion or emptying. All data from eight patients whose surgery was delayed more than four hours from the time of phenol red ingestion were excluded from analysis. Our research nurse explained the study to patients by telephone on the day before surgery. Those who agreed to participate had nothing to eat or drink after midnight. When they were admitted on the day of surgery, their demographic data and time of last oral intake were recorded. They were then randomized to the "drinking" or "fasting" group, using a computer-generated table of random numbers. Two hours before their scheduled time of surgery, all patients drank 50 mg phenol red (phenolsulfonphthalein, Sigma Chemicals, Oakville, ON, Canada, P4758 a non-toxic marker dye that is not absorbed from the stomach)15 in 10 mL water, followed in the drinking group by 300 mL clear liquid (water, apple juice, black coffee, clear tea, carbonated beverage) while those in the fasting group resumed their overnight fast. No premedication was given unless the patient requested an anxiolytic agent.
Immediately following induction of general anesthesia and tracheal intubation, a #18 multiorifice Salem sump® tube (Sherwood Medical, St. Louis, MO, USA) was passed orally through a Williams airway intubator (Anesthesia Associates Inc., San Marcos, CA, USA) into the stomach. An assistant massaged the patients epigastrium while the tube was moved backwards and forwards in the stomach and the investigator aspirated gastric contents blindly into a 60-mL syringe. Gastric fluid volume was recorded and its pH measured using a calibrated Corning 150 pH meter. The phenol red concentration was measured using a Beckman DU-50 spectrophotometer at 560, 520 and 600 nm.16 The amount of phenol red retrieved in the gastric fluid was its concentration (mgmL-1) x RGV (mL). The ingested amount of phenol red was 50 mg. The portion of 300 mL ingested liquid in the gastric fluid samples in the drinking group was therefore (mg phenol red retrieved ÷ 50) x 300.
We based our sample size on RGV results in non-obese patients.17 If RGV was 25 ± 10 mL in the fasting group and 35 ± 20 mL in the drinking group, then a two-sided test with
= 0.05 would have a power (1-ß) greater than 80% chance of detecting a statistically significant difference with 63 patients in each group. An independent groups t test was initially used to compare mean volume in the two groups. However, RGV within both groups showed such a skewed distribution with such a wide range that comparison of means was inappropriate. We therefore compared median values using a least absolute value model. As a secondary analysis, we used the same model to compare pH in the two groups. Covariates such as weight, BMI and ingestion-sampling interval were explored using the analysis of covariance.
| Results |
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| Discussion |
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The stomach is a very distensible organ that accommodates 1,000 to 1,500 mL before the resting intragastric pressure rises.18 Despite the wide range of RGV in this study, the maximum RGV in each group was far below the volume at which intragastric pressure starts to rise. Gastric pressure must exceed the barrier pressure of the lower esophageal sphincter (LES) for regurgitation to occur. The barrier pressure of the LES does not appear to be as easily overcome under general anesthesia as is generally believed. Furthermore, a rise in intragastric pressure causes a reflex rise in barrier pressure. A rise in mean gastric pressure from 12.1 to 24.9 cm water, produced by external abdominal pressure, caused a rise in LES barrier pressure from 35.6 to 54.8 cm water in normal subjects.19 Similarly, a rise in mean gastric pressure from 5.2 to 15.7 cm water, during peritoneal insufflation for laparoscopy, caused a rise in LES barrier pressure from 31.2 to 47.0 cm water.20
OMullane measured intragastric pressure with 500 to 1,000 mL saline in the stomachs of patients under anesthesia with neuromuscular blockade.21 The pressure remained -5 to +5 cm water in supine, foot-down, Trendelenburg or lithotomy position in lean individuals. It ranged from +2 to +18 cm water in those with a distended abdomen including pregnancy. Neither sand bags placed on the abdominal wall to maintain intragastric pressure 15 to 20 cm water, nor the surgeons manual compression of the stomach caused regurgitation. Plourde and Hardy demonstrated in anesthetized cats, whose LES is similar to that in humans, that a mean (range) intragastric volume of 21 (841) mLkg-1 was required to overcome LES barrier pressure and produce regurgitation of water tinted with methylene blue into the pharynx.22 This volume was at least 20 times greater than the volume (0.4 mLkg-1, pH
2.5) required to produce pulmonary damage by intratracheal injection. Hartsilver et al. measured gastric pressure and RGV in 20 women during emergency Cesarean section under general anesthesia.23 Baseline mean gastric pressure following 30 mL sodium citrate 0.3 molL-1, rapid sequence induction and tracheal intubation, was 11 mmHg (15 cm water), rising to 19 mmHg (25 cm water) during delivery. In one patient, gastric pressure rose to 65 mmHg (85 cm water) during fundal pressure. At the end of surgery, RGV was 112 (20350 mL). There was no correlation between gastric pressure and gastric volume.
The belief that > 25 mL RGV with pH < 2.5 in the stomach is a surrogate marker for an increased risk of pulmonary aspiration was based on false premises. In their experiment on one monkey Roberts and Shirley did not measure volume or pH of the animals stomach contents.24,25 They prepared their test liquids and injected them directly into the monkeys right main bronchus from a syringe. To be a valid surrogate marker, the incidence of > 25 mL RGV in the stomach must correlate with the true end-point, clinically significant pulmonary aspiration. The incidence of clinically significant pulmonary aspiration occurs in 0.014% (1 in > 7,000) of healthy patients undergoing elective surgery2 whereas RGV > 25 mL with pH < 2.5 occurs in 40 to 80% (approximately one in two).2628
Schreiner marked the 25th anniversary of Roberts and Shirleys original paper by systematically challenging their surrogate marker.29 Median RGV in fasting adults is 25 to 35 mL or 0.4 to 0.5 mLkg-1 with an upper limit of approximately 2 mLkg-1. He argued that, because high RGV is so common and clinically significant aspiration so rare, other pathways or mechanisms must be important. Warner et al.s prospectively gathered data support this view. Sixty-seven aspirations occurred in their 215,488 general anesthetics. Increasing ASA physical status and emergency surgery were associated with greater incidence of aspiration. The commonest predisposing condition was intestinal obstruction. There was no correlation with age, pregnancy, obesity with BMI
35 kgm2 or individual comorbid conditions. Furthermore, in patients undergoing elective procedures, risk factors were present in less than half (24 of 52) of those who aspirated.
Pulmonary aspiration coincided with gagging and vomiting (not passive regurgitation) in two-thirds of Warner et al.s cases,2 during airway manipulations of either laryngoscopy (33%) or tracheal extubation (36%). Vomiting differs from passive regurgitation because the squeezing action of the diaphragm and abdominal muscles causes a sudden increase in intragastric pressure to > 60 cm water.30 This is accompanied by reflex relaxation of the LES and upper esophageal sphincter,18 to allow unimpeded flow of gastric contents. Herein lies the significance of Warner et al.s analysis. During vomiting, relaxation of the sphincters facilitate escape of gastric contents, at all other times the barrier pressure of the normal LES prevents it. Other investigators have shown that episodes of gastroesophageal reflux (GER) during anesthesia are related to airway stimulation from straining on the endotracheal tube,31 and that the incidence of GER (not risk of aspiration) at induction of anesthesia is independent of RGV.32
Gastric emptying of solids in obese subjects is faster, slower, or no different1014 from non-obese patients. The rate may vary according the content of the test meal. There is no difference in the rate of gastric emptying of liquids between obese and non-obese subjects.1014 A wide variation in RGV may be expected in obese patients as in non-obese patients.
In conclusion, obesity alone is an unproven risk factor for pulmonary aspiration during induction of anesthesia on the basis of RGV. However, associated GER may be present in some patients and coincidental difficult laryngoscopy may lead to gagging and vomiting. Median RGV in otherwise healthy obese patients who drink 300 mL of clear liquid two hours before their scheduled surgery is not statistically significantly greater than in those who remain npo from midnight. This study does not exclude the possibility that obese patients have a higher risk of aspiration. It merely shows that drinking according to the ASA and CAS guidelines does not increase that risk. Obese patients may therefore follow the same fasting guidelines as non-obese patients for clear liquids.
| Acknowledgments |
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| Footnotes |
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| References |
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2 Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration in the perioperative period. Anesthesiology 1993; 78: 5962.
3 Fasting S, Gisvold SE. Serious intraoperative problems a five-year review of 83,844 anesthetics. Can J Anesth 2002; 49: 54553.
4 Anonymous. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures: a report by the American Society of Anesthesiologist Task Force on Preoperative Fasting. Anesthesiology 1999; 90: 896905.[Medline]
5 Vaughan RW, Bauer S, Wise L. Volume and pH of gastric juice in obese patients. Anesthesiology 1975; 43: 6869.[Medline]
6 Harter RL, Kelly WB, Kramer MG, Perez CE, Dzwonczyk RR. A comparison of the volume and pH of gastric contents of obese and lean surgical patients. Anesth Analg 1998; 86: 14752.[Abstract]
7 Katzmarzyk PT. The Canadian obesity epidemic: an historical perspective. Obes Res 2002; 10: 66674.[Medline]
8 Wadden TA, Brownell KD, Foster GD. Obesity: responding to the global epidemic. J Consult Clin Psychol 2002; 70: 51025.[Medline]
9 2001 CAS Guidelines to the practice of anesthesia. Can J Anesth 2001; 48(Suppl).
10 Horowitz M, Collins PJ, Harding PE, Shearman DJ. Abnormalities of gastric emptying in obese patients. Int J Obes 1983; 7: 41521.[Medline]
11 Wright RA, Krinsky S, Fleeman C, Trujillo J, Teague E. Gastric emptying and obesity. Gastroenterology 1983; 84: 74751.[Medline]
12 Dubois A. Obesity and gastric emptying (Editorial). Gastroenterology 1983; 84: 8756.[Medline]
13 Christian PE, Datz FL, Moore JG. Gastric emptying studies in the morbidly obese before and after gastroplasty. J Nucl Med 1986; 27: 168690.
14 Maddox A, Horowitz M, Wishart J, Collins P. Gastric and oesophageal emptying in obesity. Scand J Gastroenterol 1989; 24: 5938.[Medline]
15 Schedl HP. Use of polyethylene glycol and phenol red as unabsorbed indicators for intestinal absorption studies in man. Gut 1966; 7: 15963.
16 Bloom DS, Jacobson ED, Grossman MI. Validation of dilution indicators in the stomach. Gastroenterology 1967; 52: 20510.[Medline]
17 Scarr M, Maltby JR, Jani K, Sutherland LR. Volume and acidity of residual gastric fluid after oral fluid ingestion before elective ambulatory surgery. CMAJ 1989; 141: 11514.[Abstract]
18 Guyton AE, Hall JE. Textbook of Medical Physiology, 10th ed. Philadelphia: WB Saunders Company; 2000: 72833.
19 Lind JF, Warrian WG, Wankling WJ. Responses of the gastroesophageal junctional zone to increases in abdominal pressure. Can J Surg 1966; 9: 328.[Medline]
20 Jones MJ, Mitchell RW, Hindocha N. Effect of increased intra-abdominal pressure during laparoscopy on the lower esophageal sphincter. Anesth Analg 1989; 68: 635.
21 OMullane EJ. Vomiting and regurgitation during anaesthesia. Lancet 1954; 1: 120912.
22 Plourde G, Hardy JF. Aspiration pneumonia: assessing the risk of regurgitation in the cat. Can Anaesth Soc J 1986; 33: 3458.[Medline]
23 Hartsilver EL, Vanner RG, Bewley J, Clayton T. Gastric pressure during emergency caesarean section under general anaesthesia. Br J Anaesth 1999; 82: 7524.
24 Roberts RB, Shirley MA. Reducing the risk of acid aspiration during cesarean section. Anesth Analg 1974; 53: 85968.[Medline]
25 Roberts RB, Shirley MA. Antacid therapy in obstetrics (Letter). Anesthesiology 1980; 53: 83.
26 Manchikanti L, Colliver JA, Marrero TC, Roush JR. Assessment of age-related acid aspiration risk factors in pediatric, adult, and geriatric patients. Anesth Analg 1985; 64: 117.
27 Sutherland AD, Stock JG, Davies JM. Effects of preoperative fasting on morbidity and gastric contents in patients undergoing day-stay surgery. Br J Anaesth 1986; 58: 8768.
28 Lam AM, Grace DM, Manninen PH. The effects of cimetidine and ranitidine with and without metoclopramide on gastric volume and pH in morbidly obese patients. Can Anaesth Soc J 1986; 33: 7739.[Medline]
29 Schreiner MS. Gastric fluid volume: is it really a risk factor for pulmonary aspiration? Anesth Analg 1998; 87: 7546.
30 Marchand P. A study on the forces productive of gastroesophageal regurgitation and herniation through the diaphragmtic hiatus. Thorax 1957; 12: 189202.
31 Illing L, Duncan PG, Yip R. Gastroesophageal reflux during anaesthesia. Can J Anaesth 1992; 39: 46670.
32 Hardy JF, Lepage Y, Bonneville-Chouinard N. Occurrence of gastroesophageal reflux does not correlate with the volume of gastric contents. Can J Anaesth 1990; 37: 5028.
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