Expert Commentary -- Bloating, Distension, and the Irritable Bowel Syndrome

Richard Lea, MD; Peter J. Whorwell, MD

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In This Article

The Pathophysiology of Bloating

Patients and some physicians believe that excessive quantities of intestinal gas are the reason for bloating and/or distension. However, studies attempting to measure gas volumes have not consistently supported this theory. One such study, by Lasser and colleagues,[26] using a gas washout technique, found no differences in gas volumes between patients with bloating and their volunteer counterparts; several more recent studies using labeled sulfurhexafluoride have supported this finding.[27] Using CT scanning to estimate gas volumes, Maxton and colleagues[21] also found no definitive evidence of excess gas in IBS patients, despite demonstrating increased lateral abdominal profiles in these patients. In contrast, Koide and coworkers[28] used plain abdominal radiographs to show that gas volumes were greater in patients with IBS compared with controls. In another study, King and colleagues[29] found that although patients with IBS produced more hydrogen, total gas production was not significantly increased. Thus, the balance of evidence is against excessive gas being the sole cause of abdominal distension.

An alternative approach to determining whether bloating/distension is related to excessive amounts of intestinal gas is to assess whether attempting to modify gas volumes alters the severity of these complaints. One such study administered lactulose, a fermentable fiber (psyllium), and a nonfermentable fiber (methylcellulose) to healthy volunteers. Although lactulose ingestion resulted in an increase in flatus, all 3 materials resulted in an increase in bloating. Gas production as measured by breath hydrogen concentrations only increased following lactulose. This interesting study suggests that whereas gaseous symptoms (ie, passage of flatus) are probably related to an increase in gas production, bloating may not be.[30] Another approach to altering gas production is the modification of colonic flora. Two studies found that treatment with antibiotics improved gastrointestinal symptoms other than bloating in patients with IBS thought to have bacterial overgrowth,[31,32] and another reported similar results in patients with functional gastrointestinal disorders without bacterial overgrowth.[33] Other studies using probiotics have also failed to demonstrate any improvement in bloating, although one study did report an improvement in flatus production.[34,35] Taken together, these studies also suggest that excessive quantities of intestinal gas may be associated with gas-related complaints (flatus volume and frequency), although not necessarily be related to the symptom of bloating.

Accumulating evidence from the Barcelona group, headed by Professors Azpiroz and Malegalada, has suggested that while gas volumes may be normal in bloated patients, intestinal gas handling is abnormal. Following a study validating their "gas challenge" technique (the gas challenge test involves infusing gas at 12 mL/min into the subject's jejunum, while recording symptoms, abdominal girth, and gas volumes) in healthy volunteers,[36] Serra and colleagues[27] found that during jejunal gas infusion, 18 of 20 IBS patients retained gas, had distention, or developed abdominal symptoms, whereas 16 of 20 healthy volunteers failed to do so. These changes could be augmented by enteral infusion of lipid, providing one possible rationale as to why bloating frequently worsens in the postprandial period.[37] Another study by the same investigators suggested that the physical component of a meal (simulated by an intragastric balloon) may induce bloating, but the chemical component (simulated with an enteral lipid infusion) causes distension.[38] This is of considerable importance because it lends experimental support to questionnaire data suggesting that bloating and distension are not always synonymous, and that each may arise from distinct but overlapping pathophysiologic mechanisms. This idea was also supported by another study showing that bloating could be induced by voluntary inhibition of gas passage, while gut relaxation (induced using glucagon) caused asymptomatic distension.[39] Using abdominal inductance plethysmography, we have recently shown that patients with IBS, who complain of bloating in the absence of distension of the abdomen, have lower rectal sensitivity thresholds to balloon distension compared with patients who have both bloating and distension.[40] These patients with bloating alone may have primary perceptual abnormalities, and attempts to modify gas volumes therefore may not be expected to affect their symptoms. In contrast, patients with bloating who exhibit marked abdominal distension, as defined using abdominal inductance plethysmography, may have reduced gut sensitivity (hyposensitivity),[41] and taken together, these 2 observations may provide a possible explanation for the studies inducing bloating in the absence of distension or vice versa.

Several additional non-gas-related mechanisms have been suggested as being relevant to the pathogenesis of bloating and/or distension. Two studies have examined abdominal muscle function and reached different conclusions. One found that patients with bloating were able to perform fewer sit-ups compared with controls,[12] and the other used the more sophisticated technique of surface electrode electromyography (EMG) to show that there were no significant differences in recordings taken from IBS patients and volunteers.[42] A more recent study from the Barcelona group also used EMG recordings; these investigators found subtle changes in recordings from the abdominal oblique muscles in patients with experimentally induced bloating and distension.[43] Although the exact clinical significance of surface EMG recordings on the abdominal wall remains unclear, it does seem reasonable to assume that some form of "accommodation reflex" involving relaxation of the anterior abdominal musculature is likely to be associated with the consumption of a meal. Thus, an exaggeration or abnormality of such a reflex might partly explain the phenomenon of distension in patients with IBS. Therefore, abdominal wall function is certainly worthy of further investigation to assess its possible role in this setting.

Carbohydrate malabsorption is also sometimes cited as a possible factor causing bloating in a subgroup of patients with IBS. Whereas lactase deficiency is relatively prevalent, and therefore frequently found when specifically looked for in patients with IBS, whether this is of clinical importance is disputed. One placebo-controlled study supplementing patients' diet with lactase found that IBS symptoms were independent of treatment with this enzyme,[44] suggesting that there was no causal link between lactose intolerance and IBS symptomatology. Sorbitol and fructose have also been implicated in some patients,[45] although malabsorption of these sugars is also probably equally common in healthy controls. Finally, fluid retention has been proposed as a possible cause of bloating; however, no changes in body weight have been found during bloating episodes, and therefore this mechanism seems unlikely to be of major importance.[12] The study by Maxton and colleagues[21] using CT scanning largely excluded the previously "popular" theories of abnormal diaphragmatic descent, increased lumbar lordosis, or voluntary abdominal protrusion. A study that directly compared anxiety levels between patients with functional bloating and inflammatory bowel disease suggested that anxiety was also an unimportant factor.[46]

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