Pathogenesis, Diagnosis, and Treatment of Intestinal Gas Complaints
Authors: Fabrizis L. Suarez, MD, PhD, Research Associate, University of Minnesota School of Medicine, Minneapolis, MN; and Michael D. Levitt, MD, ACOS for Research, VA Medical Center, Professor of Medicine, University of Minnesota, Minneapolis, MN.
Peer Reviewers: Michael J. La Penta, MD, Medical Staff President, Anne Arundel Medical Center, Annapolis, MD; Kevin J. Roache, MD, FRCP(C), FACG, Associate Medical Director, Internal Medicine & Gastroenterology, Sterling Rock Falls Clinic, Ltd., Sterling, IL.
Editor’s NotePatients frequently attribute a variety of symptoms to the presence of excessive gastrointestinal gas. These symptoms may take the form of excessive eructation, bloating and abdominal distention, or abnormal volume, or malodor of flatus. Unfortunately, objective verification of the existence of these problems is difficult, if not impossible. Thus, the physician must commonly rely upon the patient’s self-perception that there is an abnormality. This unfortunate situation is further complicated by the lack of scientific information concerning the appropriate diagnostic and therapeutic approach to gaseous complaints. As a result, the physician usually treats gaseous problems without clear-cut evidence that a problem actually exists and with treatments of highly questionable efficacy.
In this issue, the authors review what is known about the origin, diagnosis, and treatment of gaseous complaints. Although many of these problems may not be susceptible to therapy, it is hoped that this review will allow the physician to respond to the complaint of "too much gas" in a cost-effective, rational fashion.
An understanding of the factors that deliver gas to and remove gas from the gut facilitates a rational response to gaseous complaints. Five gases are present in quantitatively important volumes in the human gut: N2, O2, H2, CO2, and CH4 (methane).1,2 None of these gases has an odor. The characteristic unpleasant odor of intestinal gas, as will be discussed, appears to result primarily from the presence of trace quantities of sulfur-containing compounds such as H2S.3
Figure 1 summarizes the mechanisms by which gas enters and leaves the human gut. The four mechanisms that deliver gas to the lumen and the specific gases delivered by these mechanism are: 1) air swallowing ® O2 and N2; 2) interaction of bicarbonate and acid ® CO2; 3) diffusion from the blood ® CO2, N2, and O2; and 4) bacterial fermentation reactions ® CO2, H2, CH4, and a wide variety of trace gases including gases containing sulfur such as H2S. Gases can be removed from the gut via: 1) eructation and passage per anus; 2) diffusion into the blood; and 3) consumption of gas by bacteria. The net of these processes proximal to a given site in the gut determines the volume and composition of gas passing that site; the net of these processes throughout the entire gut determines the volume and composition excreted per rectum.
It is apparent from the above that diffusion can contribute to or reduce the volume of gut gas. The direction of net diffusion of gas (i.e., into or out of the lumen) is determined by the partial pressure difference of the gas in the lumen and the blood. Gases whose sole source in the body is intraluminal production such as H2 and CH4 always diffuse from lumen to blood.4 Following absorption, these gases are carried by the blood to the lungs, where they are efficiently cleared in expired air. To determine the fractions of these gases that are absorbed and passed per rectum, subjects have been housed in airtight rooms for several-day periods.5 The total excretion rate of H2 and CH4 (via lungs and anus) was determined from the difference in concentration of the gas in the air entering and leaving the room. Measurements of the gases in expired air permitted determination of the rates that the gas was absorbed and excreted by the lungs. Usually, about 50% of each gas was absorbed and excreted on the breath, although when gas passage was very rapid, a smaller fraction was absorbed. Measurements of the excretion rate of H2 and CH4 on the breath provide a simple, noninvasive means of assessing the gut production of these gases.
Nitrogen and CO2 are normally present in the blood; thus, these gases have the potential to diffuse from the blood into the lumen as well as from lumen to blood. For example, air contains very little CO2; therefore, when air is swallowed, CO2 diffuses from the blood perfusing the stomach into the lumen. However, in the duodenum, acid reacts with duodenal bicarbonate producing very high concentrations of CO2, and this gas now diffuses from lumen to blood.6 Because CO2 diffuses very rapidly, virtually all this CO2 is probably absorbed in the small bowel. In the colon, the bacteria often produce large amounts of CO2 that is not totally absorbed, and flatus often contains sizable quantities of CO2.2,3
The patient uses the terminology "gas" to refer to a variety of complaints including excessive eructation, abdominal discomfort and bloating, or passage of excessively voluminous or malodorous gas per rectum. A crucial aspect of the patient’s history is to determine exactly which of these complaints is the problem since they have different origins and different treatments.
Several centuries ago, postprandial belching indicated appreciation for the meal; today, however, eructation is generally socially unacceptable. One socially acceptable form of eructation is esophageal speech, which allows laryngectomized patients to form words via controlled belching.7
The mechanism of belching has been studied using radiological and manometric techniques.8-10 McNally et al demonstrated that the pressure in the human stomach plateaued at 4-7 mmHg during distention of the stomach with air.8 This finding suggests relaxation of both the gastric and abdominal musculature in response to increasing intragastric volume. At intermittent intervals, the lower esophageal sphincter (LES) opened, a common gastroesophageal cavity was established, and the subject belched. The requirement for relaxation of LES in belching is supported by the frequently observed inability of subjects to belch following fundoplication.11 A belch also requires relaxation of the upper esophageal sphincter (UES). Kahrilas et al proposed that gaseous distention of the esophageal body induces relaxation of the UES.10 Interestingly, UES pressure increases in response to fluid distention of the esophagus,10 suggesting that the characteristics of esophageal contents may influence UES function.
Virtually every analysis of gas aspirated from the stomach has demonstrated that the predominant components are N2 and O2, the atmospheric gases.12 Gases produced in the gutCO2, H2, and CH4usually represent a minor fraction of this gas, although with gastric outlet obstruction, bacterial overgrowth in the stomach can lead to appreciable bacterial gas production. Thus, ordinarily, a belch is derived from swallowed air rather than gas produced in the stomach.
Using ultrafast computerized tomography, it was recently demonstrated that a mean of 17 mL of air accompanied each swallow of a 10 mL bolus of liquid.13 Thus, 1700 mL of air (1350 mL of N2) will be swallowed each day with the roughly one liter of liquid ingested per 24 hours. The swallowing of saliva and food will deposit additional N2 in the stomach, and it seems likely that over 2000 mL of N2 is swallowed each day. However, healthy subjects were found to excrete a mean of only about 250 mL of N2 per 24 hours in flatus.14 It is not possible to establish an appreciable positive N2 gradient between lumen and blood; therefore, N2 absorption from the gut is negligible. It follows that the vast majority of swallowed N2 must be eliminated via recognized or unrecognized eructation.
In addition to the air swallowing that accompanies food and liquid ingestion, some subjects unconsciously aspirate air into the esophagus, often in an attempt to initiate an eructation. All or most of this air is immediately eructed from the esophagus, although the patient believes that the gas is emanating from the stomach. This maneuver results in a what might be termed a "pseudo" belch (i.e., a belch that clears gas from the esophagus, as opposed to the "true" belch that removes gas from the stomach).
Occasional belching is a normal phenomenon usually observed postprandial. Excessive and uncontrollable belching reflects excessive air swallowing or aspiration. The belching patient virtually never recognizes that excessive air swallowing is occurring, and conscious efforts to stifle air swallowing are seldom effective.
Hypersalivation from gum chewing, smoking, oral irritation, a chronic postnasal drip, nervousness, and tension are alleged to be associated with aerophagia, and treatment of these conditions should presumably be beneficial. Repeated "pseudo" eructation may result from attempts to alleviate discomfort in the stomach or esophagus (most commonly reflux esophagitis), and, for some reason, this maneuver seems to temporarily alleviate the discomfort. Treatment designed to eliminate the cause of the discomfort often leads to a decrease in eructation. While it has been claimed that it is difficult to swallow air if a tongue blade or some other object is held between the teeth, the effectiveness of this treatment has not been objectively evaluated. There is little scientific evidence that drugs such as simethicone, antispasmodics, or sedatives are useful in the treatment of excessive eructation. Of interest is a recent report by Spiegel of a 71-year-old subject with incessant eructation of four months’ duration who was successfully treated with hypnosis.15
Abdominal bloating and distention
Frequently, the patient complaining of too much "gas" is referring to sensations of abdominal bloating or distention. In general, patients and health providers believe that excessive intestinal gas is the cause of such symptoms. However, using a washout technique, we found normal volumes of gas (< 200 mL) in the intestines of bloating subjects.2 In addition, a study using computerized tomography found no evidence of increased intestinal gas in patients complaining of bloating,16 and abdominal roentgenographs in patients complaining of bloating seldom demonstrate abnormal volumes of gas. Lastly, periods of high breath hydrogen excretion do not correlate with symptoms of discomfort in bloating patients.17 Thus, it appears that complaints of bloating and distention are usually indicative of an "irritable" bowel that causes the patient to perceive that the intestine is over-distended when no such distention actually exists. This concept is supported by the observation that bloating patients have an enhanced pain response to balloon-induced bowel distention.18 It is also possible that feelings of distention reflect increased volume of solid or liquid luminal contents. For example, we found that healthy subjects complained of mild distention and "gas" following ingestion of fiber.19 These subjects had no increase of flatus or breath H2 excretion, and it appeared that the fiber-induced increase in luminal bulk was responsible for the sensation of distention.
It should be stressed that partial bowel obstruction also presents with bloating and distention. Thus, the work-up required for these complaints depends upon the age of the patient, duration of the problem, and associated symptoms. The subject under 40 years of age with a multiple-year history and no systemic symptoms is unlikely to have an obstructing lesion, and a minimal workup is indicated. In contrast, an elderly patient with a brief history of symptoms requires a more thorough evaluation.
We are aware of no data to indicate that treatments designed to reduce bowel gas benefit patients with functional bloating and distention. Therapy should generally be directed toward treatment of the underlying irritable bowel.
Patients not infrequently complain that their passage of rectal gas represents a major social problem. This complaint can take the form of putative problems with excessive volumes of flatus or gas that has an abnormally bad odor. A rational approach to this complaint would presumably proceed as follows (see Figure 2): 1) objectively determine if there truly is abnormality of volume or odor; 2) if volume is excessive, determine if the major source of this gas is air swallowing or intraluminal production; if odor is excessive, identify the responsible gas; 3) prescribe treatment based on the origin of the problem. This simple scheme has never been implemented either in practice or in the research laboratory. Recent studies have increased our understanding of flatus problems, although effective therapy remains elusive.3,14
Objective verification that the patient actually is passing abnormal volumes of gas requires quantitative collection of all gas passed per rectum for several 24-hour periods. Such 24-hour collections require a rectal tube and a collecting reservoir. Rectal tubes are uncomfortable (particularly if the subject is ambulatory) and often plug with fecal material. Thus, long-term flatus collections have been obtained only rarely in research studies and never in the clinical situation. The best normal data for relatively long-term flatus excretion have recently been provided by Tomlin et al, who found that seven healthy subjects on their normal diets plus 200 g of baked beans passed from 476 mL to 1491 mL/24 hours (median, 705 mL/24 hours).14
Quantitative collections of rectal gas are only possible with highly motivated patients. A much simpler measure of flatus normality is a count of flatus passages, a technique we have used extensively in research studies designed to assess gas excretion after ingestion of lactose, lactulose, beans, and fiber.20-22 A study involving 20 healthy subjects ingesting their ad lib diets indicated that healthy controls pass gas an average of 10 times per day, with an upper limit of normal (mean ± SD) of 20 times per day.19 No statistically significant difference in the frequency of gas passage was observed with gender or age. The finding of statistically significant increases in gas passages when the diet was supplemented with lactulose or pinto beans, two stimuli known to increase gas production in the colon, supports the ability of this technique to identify a real increase in flatulence. However, since an individual passage of gas can vary in volume from 17 mL to 375 mL,4 flatulence frequency obviously is not a perfect quantitative indicator of gas passage.
In practice, patients generally complain of excessive frequency rather than excessive volume of gas passage. As the initial step in the evaluation of such a patient, we recommend that the subject maintain a meticulous recording of each flatus passage for a one-week period. There is a good deal of misunderstanding as to what constitutes normal for flatus frequency, and these recordings frequently show a normal frequency (i.e., < 20 passages per day). In this situation, no further diagnostic tests are indicated, and reassurance should be provided to the subject as to his or her "normality." While patients may not be completely satisfied by this reassurance, further evaluation is not indicated when no abnormality exists.
If flatus frequency is appreciably greater than 20 times per day, the assumption is that the patient is passing excessive gas, and the next step should be to determine the origin of the gas. There are two possible sources of excessive bowel gas: intraluminal production and swallowed air. The quantitatively important gases produced in the lumen are CO2, H2, and CH4, whereas air swallowing delivers N2 and O2 to the gut. Thus, the analysis of a carefully collected flatus sample provides a quick means of determining the source of the gas.
The collection of a rectal gas sample is most easily achieved using a rectal tube attached to a syringe via a three-way stopcock.4 It should be stressed that the initial gas sample collected contains large amounts of air from the dead space of the tube. Thus, several gas samples must be collected and discarded via the free arm of the three-way stopcock before collecting the sample for analysis. The O2 content of the sample provides a simple internal control with regard to atmospheric contamination of the sample. Rectal gas always contains low levels of O2 (< 5%), whereas atmosphere contains 21% O2. Samples containing greater than 5% O2 are not a reliable indicator of flatus composition
While our laboratory is one of the few in the country capable of routinely carrying out a complete analysis of rectal gas, detectors used for analysis of breath H2, CH4, and CO2 are widely available. With appropriate dilution (H2 and CH4 may require dilutions of 5000-fold), the contribution of gases produced in the lumen can be measured with these detectors. If the analysis shows that H2, CO2, and CH4 represent the majority of flatus, the gas is being produced in the gut. If these gases comprise the minority of the flatus sample, it can be assumed that N2 must be the major component, and that air swallowing is the major source of the gas.
Excessive rectal gas is commonly assumed, both by physicians and the lay public, to result from intraluminal production as opposed to swallowed air. In reality, there have been too few studies of flatulent subjects to determine if this assumption is correct.23 We have recently studied a very flatulent patient (up to 120 passages of gas per day) who had been subjected to innumerable expensive diagnostic tests in the belief that the patient must have an abnormality of the gut that caused excessive gas production.24 Analysis of flatus samples on three occasions showed that virtually all the rectal gas was N2 (i.e., excessive air swallowing was the source of the flatus). In this situation, therapy should be directed toward the reduction of air swallowing (see eructation section). Given that eructation appears to be an important determinant of the quantity of swallowed air that enters the intestine, treatment with carminotives that enhance belching (i.e., peppermint water) theoretically could reduce rectal gas excretion.
When flatus consists of non-atmospheric gases, H2, CO2, and CH4, fermentation reactions carried out by the intestinal flora are the source of the rectal gas. The quantity of gas produced is a function of the availability of fermentable substrates (primarily carbohydrates) to the colonic flora and the gas-releasing ability of the flora.25
The colon contains bacteria that produce gas and other organisms that efficiently consume gas. The net of these two competing processes determines the amount of gas available for excretion. For example, fermentation of 10 g of carbohydrate can liberate 3400 mL of H2.26 Since healthy subjects are thought to malabsorb about 30 g of carbohydrate each day, over 10,000 mL of H2 should be produced in the colon per 24 hours. This volume of H2 would obviously produce very severe flatulence. However, only about 5% of the H2 that is produced in the colon is actually excreted;27 the other 95% is consumed by bacteria that use this gas for methane production or sulfate reduction.28-30
The substrate used by the colonic flora for gas production may be of endogenous or exogenous (dietary) origin. Mucin is a carbohydrate-rich compound that is produced endogenously. In order for a dietary carbohydrate to serve as substrate for fermentation reactions in the colon, the carbohydrate must be incompletely absorbed in the small bowel. In patients with diffuse intestinal disease (celiac disease, for example), all dietary carbohydrates may be malabsorbed. Healthy subjects may also incompletely absorb a variety of carbohydrates.
Since absorption of carbohydrates requires that these compounds be digested to the monosaccharide form, malabsorption may reflect the inability to digest a carbohydrate or the inability to absorb certain monosaccharides (i.e., sorbitol). Table 1 lists various foods that contain non-absorbable carbohydrates. Examples of foods that are malabsorbed due to incomplete digestion include lactose, in lactase-deficient subjects, and legumes, which contain oligosaccharides such as raffinose that are totally indigestible by humans. Of particular interest is the demonstration that the commonly ingested sources of starch, such as wheat, potatoes, corn, and oats, increase breath H2 excretion, indicating incomplete absorption.31 The resistance to digestion of these foodstuffs appears to result from the inability of amylase to gain access to the starch as opposed to an inherent indigestibility of the starch molecule. Refrigeration of cooked wheat products such as pasta aggravates this maldigestion by causing the starch to crystallize in a process called retrogradation.32
The vast majority of subjects complaining of excessive flatus have no recognizable disorder of the intestinal tract. Thus, extensive diagnostic studies are generally not indicated unless there is some other evidence of a malabsorptive disorder. In particular, there is no gross anatomical lesion that could cause excessive flatulence, and expensive endoscopic and radiological studies are not useful.
Theoretically treatment of excessive flatus due to gas production in the gut may involve: 1) enhancement of digestion of carbohydrates using exogenous enzymes; 2) removal of the offending foodstuff(s) from the diet; or 3) alteration of the colonic flora.
The most common situation in which exogenous enzymes are recommended for increased gas is when lactose is ingested by lactase-deficient subjects. However, our controlled studies showed that flatus frequency was only mildly but not statistically significantly increased when lactase-deficient subjects ingested one or two cups of milk with breakfast and dinner.33 Thus, the use of lactase preparations should be limited to the situation in which lactose is ingested in very appreciable quantities (i.e., > 2 cups per day). Lactase preparations can be added to milk, which is then incubated overnight, or taken as tablets with milk or milk products. A preparation that contains the enzyme required for digestion of the oligosaccharides in legumes (Beano) is available over-the-counter. Unfortunately, our studies have suggested that when this enzyme is used in accordance to the product insert, flatus frequency is not diminished.
Dietary alterations to reduce gas require elimination of most of the foods listed in Table 1. This is extremely difficult because of the multiple complex carbohydrates, such as wheat and potatoes, that are malabsorbed. Rice is the only complex carbohydrate that is completely absorbed.34 A diet that contains no complex carbohydrates markedly reduces gas production.14 Unfortunately, such a diet is found to be relatively unpalatable by the average American.
Lastly, induction of a flora that tends either to produce little gas or that efficiently consumes gas would be a useful therapeutic tool. There is some evidence that feeding subjects large quantities of nonabsorbable carbohydrates (such as lactose to lactose malabsorbers) induces a flora rich in lactobacilli, organisms that ferment carbohydrate via a non-gaseous pathway.35,36 As a result, less gas is produced following lactose ingestion.
There is no evidence that any known manipulation can induce a flora that more effectively consumes gas. Antibiotic therapy does not appear to be a useful means of reducing colonic gas production due either to a failure of antibiotics to reduce gas producing organisms or, more likely, to a reduction of gas-consuming organisms.
Despite the enormous amount of discussion devoted to the topic of flatus odor, there has been minimal study of the factors responsible for this odor.3 It was taught for many years that the offensive odor of flatus resulted from its content of aromatic breakdown products of proteins such as indole and skatole. However, Moore et al, in an elegant study of human feces, concluded that these aromatic compounds were present in very low concentration and that these compounds had an odor distinctly different from human feces.37 These workers concluded that three sulfur-containing gasesmethanethiol, dimethyldisulfide, and trimethylsulfidewere the major offensive gases elaborated by human feces.
We recently carried out the first systematic study designed to identify the odoriferous components of human flatus.3 In this study, 87 individual flatus passages obtained from healthy subjects were collected via rectal tube and analyzed for sulfur containing gases. In contrast to the findings of Moore et al with human feces, we found the predominant sulfur gases in flatus to be H2S, methanethiol, and dimethylsulfide (see Figure 3), with H2S being the predominant gas. The discrepancy between our findings and those of Moore et al appears to reflect the fact that the compounds we observed in flatus are all highly volatile and thus would rapidly leave the feces for the gas space. In contrast, two of the compounds observed by Moore and co-workers in feces, dimethyldisulfide and trimethylsulfide, have very low volatility. Thus, it is not surprising that these compounds are found in feces but not the surrounding gas phase (i.e., flatus).
While sulfur-containing gases are present in very low concentrations (< 0.01%) in flatus, these compounds have a very powerful, offensive odor. To actually determine if these gases were responsible for flatus malodor, it was necessary to employ the only instrument capable of judging the offensiveness of an odorthe human nose. In what is known as the "sniff test,"38 two judges, previously shown to have excellent olfactory discrimination, blindly ejected a small amount of flatus contained in a syringe at a distance of about 5 cm from the nose. The offensiveness of the odor was rated on a linear scale. As shown in Table 2, a highly significant correlation was observed between the intensity of malodor and the concentrations of the sulfur gases. Such a correlation could indicate that the gases were associated with the presence of other odoriferous compounds as opposed to being cause of the odor. Thus, further experiments were carried out in which flatus samples were treated with zinc, which avidly binds the sulfhydryl components of H2S and methanethiol. This treatment markedly reduced the odor, indicating that the two sulfur-containing gases were very likely responsible for much of the offensive smell of flatus. Lastly, artificial flatus samples comprised of the three sulfur containing gases in concentrations typical of flatus were blindly presented to our judges. These mixture were rated to be offensive and to have a fecal-like odor.
On the basis of the above evidence, we concluded that the sulfur gases were the predominant, but probably not the only offensive malodorous component of flatus. This knowledge simplifies studies of flatus odor in that the objective measurement of the concentration of gases can be employed in place of the time-consuming subjective evaluation of odor. Studies of the sulfur gases showed, somewhat contrary to expectation, that flatus from males had a lower concentration of sulfur gases than did gas collected from females.3 However, the stimulation of the nose that results from flatus passage is a function of the amount of offensive gas released per passage as opposed simply to the concentration of these gases. When the larger volume of flatus passages in males vs. females (119 ± 11.9 mL vs 88 ± 8.9 mL) was taken into account, the actual volume of sulfur gas released per passage showed no gender difference.
We also indirectly investigated the "silent but deadly" concept, which proposes that quiet flatus passages are more offensive than noisy passages. While we did not employ an audiometer to measure the sound of the passages, it seems likely that large volume passages are more noisy than small passages. Thus, if the "silent but deadly" concept were correct, the quantity of sulfur gases should have been inversely correlated with the size of the passages. This was not the case, and, in fact, there was a strong positive correlation between the volume of sulfur gases and the volume of the passage.
The only treatment presently that has been claimed to reduce flatus odor is a fabric-covered, charcoal-lined cushion sold under tradename of "Toot Trapper" (UltraTech Products. Inc., Houston, TX). The manufacturer of this cushion claims that the cushion absorbs odoriferous gases in flatus, hence limiting the odor that escapes into the environment. Objective testing of the efficacy of this cushion requires a means of accurately determining the quantity of sulfur gases that escapes the cushion. To this end, we fabricated gas-tight mylar pantaloons that were sealed at the waist and the thighs with duct tape. The cushion was tested by inserting the active cushion, an identical appearing placebo cushion (charcoal encased in mylar), or no cushion into the pantaloons. The subjects sat on a wooden chair, and a small tube was situated at the anus. A mixture of the sulfur-containing gases was infused at the anus, and the quantity of gases escaping into the environment of the pants was determined. The cushion clearly was effective as evidenced by the more than 90% reduction in sulfur gases that occurred with the active cushion. The placebo cushion produced about a 50% reduction in sulfur gases, apparently due to reactivity of these gases with the fabric of the cushion. We conclude that the cushion is effective but unwieldy. Present experiments are being directed to miniaturizing the cushion and searching for compounds that bind sulfur gases in the colon.
References
1. Kirk E. The quantity and composition of human colonic flatus. Gastroenterol 1949;12:782-794.
2. Levitt MD. Volume and composition of human intestinal gas determined by means of an intestinal washout technique. N Engl J Med 1971;284:1394-1398.
3. Suarez FL, Furne JK, Springfield JR, Levitt MD. Identification of gases responsible for the odor of human flatus and evaluation of a device purported to reduce this odor. Gastroenterol 1997;112:A45.
4. Suarez FL, Furne JK, Springfield JR, Levitt MD. Insights into human colonic physiology obtained from study of flatus composition. Am J Physiol 1997;272:G1028-G33.
5. Christl SU, Murgatroyd PR, Gibson GR, Cummings JH. Quantitative measurement of hydrogen and methane from fermentation using a whole body calorimeter. Gastroenterol 1992;102:1269-1277.
6. Fordtran JS, Walsh JH. Gastric acid secretion rate and buffer content of the stomach after eating. Results in normal subjects and in patients with duodenal ulcer. J Clin Invest 1973;52:645-657.
7. Pope CE. II. Heartburn, dysphagia and other esophageal symptoms. In Sleisinger MH, Fordtran JS, (eds). Gastrointestinal diseases: Pathophysiology, diagnostic and management, 4th ed. Philadelphia, PA: WB Saunders Company 1989:200-203.
8. McNally FE, Kelly JE, Ingelfinger FJ. Mechanism of belching: effects of gastric distention with air. Gastroenterol 1964;46:254-259.
9. Castell CD. The lower esophageal sphincter: physiology and clinical aspects. Ann Intern Med 1975;83:390-401.
10. Kahrilas PJ, Dodds WJ, Dent J, Wyman JB, Hogan WJ, Arndorfer RC. Upper esophageal sphincter function during belching. Gastroenterol 1986;91:133-40.
11. DeMeester TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease. Evaluation of primary repair in 100 consecutive patients. Ann Surg 1986;204:9-20.
12. Maddock WG, Bell JL, Tremaine MJ. Gastrointestinal gas. Observation of belching during anesthesia, operations an pyelography and rapid passage of gas. Ann Surg 1949;130:512.
13. Pouderoux P, Gulchin AE, Shezhang L, Kahrilas PJ. Esophageal bolus transit imaged by ultrafast computerized tomography. Gastroenterol 1996;110:1422-1428.
14. Tomlin J, Lowis C, Read NW. Investigation of normal flatus production in healthy volunteers. Gut 1991;32:665-669.
15. Spiegel SB. Uses of hypnosis in the treatment of uncontrollable belching: A case report. Am J Clin Hypnosis 1996;38:263-270.
16. Maxton DG, Martin DF, Whorwell PJ, Godfrey M. Abdominal distention in female patients with irritable bowel syndrome: Exploration of possible mechanisms. Gut 1991;32:662-664.
17. Haderstorfer B, Psycholgin D, Whitehead WE, Schuster MM. Intestinal gas production from bacterial fermentation of undigested carbohydrate in irritable bowel syndrome. Am J Gastroenterol 1989;84:375-378.
18. Ritchie J. Pain from distention of pelvic colon by inflating a balloon, in the irritable bowel syndrome. Gut 1973;14:125-132.
19. Levitt MD, Furne J, Olsson S. The relation of passage of gas and abdominal bloating to colonic gas production. Ann Intern Med 1996;124:422-424.
20. Suarez FL, Savaiano DA, Levitt MD. A comparison of symptoms in people with self- reported severe lactose intolerance after drinking milk or lactose-hydrolyzed milk. N Engl J Med 1995;333:1-4.
21. Zumarraga LM, Levitt MD, Suarez FL. Absence of Gaseous Symptoms During Ingestion of Commercial Fiber Preparations. Aliment Pharmacol Therapeutics 1997 (in press).
22. Strocchi A, Corazza G, Ellis CJ, et al. Detection of malabsorption of low doses of carbohydrate: accuracy of various breath H2 criteria. Gastroenterol 1993;105:1404-1410.
23. Levitt MD, Lasser R, Schwartz J, Bond JH. Studies of a flatulent patient. N Engl J Med 1976;295:260-262.
24. Levitt MD, Furne J, Aeolus MR, Suarez FL. Evaluation of an extremely flatulent patient: Case report and proposed diagnostic and therapeutic approach. 1997. Submitted for publication.
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Physician CMEQuestions
46. Gases present in quantitatively important volumes in the human gut include all of the following except:
a. hydrogen.
b. carbon monoxide.
c. oxygen.
d. nitrogen.
e. methane.
47. "Normal" flatus frequency can be characterized as:
a. less than five passages per day.
b. up to 10 passages per day.
c. up to 20 passages per day.
d. up to 30 passages per day.
48. Examples of foods that are incompletely absorbed by the human body include:
a. potatoes.
b. legumes.
c. oats.
d. corn.
e. all of the above.
49. The only complex carbohydrate that is completely absorbed is:
a. wheat.
b. potatoes.
c. rice.
d. corn.
e. oats.
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