Gastrointestinal Gas: Eructation, Borborygmus, and Flatulence

Chapter 15 Gastrointestinal Gas

Eructation, Borborygmus, and Flatulence

Pathophysiology and Mechanisms

Gastrointestinal gas is derived from four sources: (a) aerophagia, (b) luminal chemical reactions, (c) bacterial fermentation, and (d) diffusion from circulation into the lumen. The majority of intestinal gas is composed of nitrogen, oxygen, hydrogen, methane, and carbon dioxide, all of which are odorless. Most intestinal nitrogen and oxygen is derived from ingested air. The predominant gases in flatus are CO2, H2, and N2, with lesser quantities of CH4 and H2S.2 Odiferous compounds identified in canine flatus include carboxylic acids, phenols, ammonia, hydrogen sulfide, indole, skatole, mercaptans, volatile amines, ketones, alcohols, and short-chain fatty acids, which together comprise less than 1% of intestinal gas.3

Aerophagia and Eructation

Some air is inevitably swallowed during normal feeding, although individual dogs and cats differ in volumes of swallowed air. Variables affecting the volume of air swallowed have not been defined but likely involve the size of the food bolus, rate of ingestion, physical characteristics of food, and head and neck posture during eating. In the stomach, gas bubbles coalesce and accumulate in the dorsal fundus and cardia, which activates stretch receptors in the wall of the gastric cardia.4 Afferent vagal fibres arising from the cardia of the stomach induce transient relaxations of the gastroesophageal sphincter (GES).5 These are relatively prolonged relaxations of the GES that have a pattern distinctly different from swallow-induced gastroesophageal sphincter relaxation. This reflex, induced by gastric gas, has been termed the belch or eructation reflex. As gas is refluxed through the relaxed GES postprandially, reflux of gastric contents and acid may occur simultaneously.6

Disease processes that disrupt stretch receptors, sensory vagal afferents, or vagal inhibition of the GES may impede sphincteric response to gastric gaseous distention. Development of gastric dilation–volvulus syndrome in dogs is believed to depend upon such defects. Indeed, gastric volvulus has been reported in dogs with a prior history of eructation, borborygmus, and flatuluence.7 When chronic gastric bloating is a prominent sign, excessive aerophagia and defective eructation should be considered as underlying mechanisms. Aerophagia during eating may account for large amounts of intestinal gas, although dogs described as “greedy eaters” by their owners are not reported to have an increased incidence of flatulence.1

Aerophagia and gastric gaseous distention can also occur secondary to respiratory tract disease. Dyspnea resulting from brachycephalic airway disease can culminate in excessive aerophagia and gastric distention.8

Intestinal Gas Transit and Borborygmus

Gas that is present in the small and large intestine can originate from aerophagia or be endogenously formed. Intestinal CO2 is mostly formed from the reaction between bicarbonate (HCO3) and gastric acid producing water and CO2 in the upper small intestine. For each mole of H+ neutralized by pancreatic HCO3, 1 mole of CO2 is produced. In the 3 hours following a meal a dog may produce 6 mEq H+, which will result in production of 134 mL CO2.9 Most of the CO2 diffuses into circulation but some remains within the luminal contents. The remaining gases are produced from microbial fermentation, predominantly in the distal small intestine and colon.

Gas is moved along the intestine independently of solids and liquids, and gas transit is more effective in the erect than supine position illustrating active propulsion of gas.10 Rate of gas passage is influenced by dietary fat, but not by dietary moisture content.11 Intestinal gas can be rapidly propelled aborally in normal dogs such that infusion of air at 2 mL/min does not produce obvious abdominal discomfort.12 In humans, up to 30 mL/min can be infused jejunally without discomfort.11 Gas is actively propelled by a sustained contraction proximal to the gas but it is still not known if intestinal gas induces classical peristaltic waves responsible for movement of liquid and solid ingesta.13 Consumption of solid food, but not water, increases volume and rate of transit of gas through the gastrointestinal tract.11 Duodenal lipid has the most profound inhibitory effect on gas transit times; fiber slows intestinal gas transit, as well as increases volume of gas produced from fermentation.14

Physical exercise is known to reduce the retention of gastrointestinal gas.15 Although not directly studied in dogs, flatulence is reported less frequently by owners of dogs that exercise frequently than by owners of sedentary dogs.1

Borborygmus can result from excessive intestinal gas or altered gastrointestinal motility. Patients with irritable bowel syndrome develop intestinal gas retention and pain in response to gas loads that are otherwise well tolerated by normal individuals.16 In those patients, proximal intestinal gas rather than large intestinal gas is responsible for clinical symptoms.16


Ingested atmospheric gases form the largest component of flatulence, but odiferous compounds resulting from microbial fermentation of luminal content are the most notable to pet owners. Flatulence that occurs within 2 hours of feeding is more likely related to rapid transport of aerophagic gases following feeding.3,17 Fermentative by-products accumulate at other times and are not necessarily related to feeding. Malodor is strongly correlated with presence of hydrogen sulphide, although production of hydrogen sulphide is highly variable amongst animals fed the same diet.3 Sulphur gases are produced by sulphate-reducing bacteria such as the genera Desulfotomaculum, Desulfobacter, Desulfomonas, and Desulfobulbus, and differences in sulphur gas production between animals likely represents differences in these microflora.18 Sources of sulphur for fermentation include endogenously derived amino acids in mucin, sulphate in cruciferous vegetables and nuts, and poorly digestible sulphated polysaccharides such as the gelling agent carrageenan.

In addition to inhibiting gas transit, fermentable fibers are a significant substrate for luminal production of intestinal gases. In normal humans fiber intake increases the number of daily flatus emissions.11,19 Thus normal humans high-fiber diets increase gas production by colonic flora and inhibit gas transit leading to gas retention, notable borborygmus, abdominal pain, and flatulence.11 Ingestion of a “fiber-free” diet for 48 hours significantly reduces the total volume of flatus. Highly purified, highly fermentable fibers will increase flatus volumes more so than nonfermentable fiber, as well as altering the composition of flatus. For example, xylan and pectin diets induce much higher volumes of flatus, including hydrogen, carbon dioxide, and methane content than cellulose or corn bran diets.20 Intestinal and/or microbial adaptation to changes in fiber content may take several days and flatus volumes may not stabilize until 2 to 5 days postfeeding.20 Significant differences in intestinal microflora exist between individual dogs and cats, and some of that difference may even be related to breed.21

Methane production varies greatly between individuals, and is dependent upon diet, fiber content, and specific methanogenic bacteria.22 Physiologic concentrations of methane slow ileal transit by augmenting ileal circular muscle contractions.12 Consequently, inflammatory bowel disease (IBD) patients in whom methane is produced almost universally suffer from constipation and ileal discomfort.12 Induction of nonpropulsive segmental contractions by methane may trigger dysmotility and discomfort in dogs and cats. Consequently, it is prudent to consider this side effect when supplementing fiber in the diet.

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Jul 10, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Gastrointestinal Gas: Eructation, Borborygmus, and Flatulence
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