Abdominal Distention: Old Hypotheses and New Concepts
Article Outline
See “Relationship of abdominal bloating to distention in irritable bowel syndrome and effect of bowel habit” by Houghton LA, Lea R, Agrawal A, Reilly B, and Whorwell PJ, on page 1003.
In a paper published in this issue of Gastroenterology,1 Houghton and Whorwell’s group elegantly shows that in healthy subjects’ girth changes relatively little over the day, whereas in patients complaining of abdominal bloating, girth variations become significantly more pronounced. They further demonstrate that in a considerable proportion of patients, but not all, bloating sensation is a real issue related to objective abdominal distention.
The study by Houghton et al1 was performed in patients who complained of bloating as part of an irritable bowel syndrome (IBS), and the measurements were performed on a predetermined date, independent of the severity of symptoms on that day. Usually, the intensity of bloating in IBS patients is not constant, and some days are much worse than others. Characteristically, the bloating sensations become really uncomfortable during discrete time intervals, that may last a few hours, and that occur episodically at variable frequency, usually not daily.2, 3 Whorwell’s observations on the circadian variations of bloating may explain the mechanisms of severe, clinically relevant bloating episodes; it is likely that the relation of subjective bloating to objective distention is much stronger during these episodes.
Bloating is an ambiguous term that may mean different things to different patients. Indeed, a large proportion of patients—about 24%—report bloating without visible abdominal distention,2 an observation corroborated in the present study. These patients may use the term bloating to refer to sensation of a full belly, feeling of abdominal pressure or wall tension, or even sensation of excess gas and/or abdominal rumbling. The sensation of bloating in the absence of objective abdominal distention may originate by different mechanisms. In the first place, the sensation may originate at the abdominal wall itself. This possibility has been poorly explored so far, but in case of abdominal wall traumas, injuries, or scars, the patient may perceive a sensation of abdominal wall tension interpreted as bloating. This mechanism may be particularly relevant in postoperative bloating after laparotomy. A prospective study reported that patients with bloating were more likely to have experienced recent weight gain than healthy controls.4 Thus, fat accumulation in the abdomen may favor the development or awareness of a bloating sensation.
Second, a bloating sensation without objective distention may originate from the viscera and may be related to impaired gut motility. Some studies have shown that patients complaining of bloating have impaired propulsion and delayed clearance of intraluminal gas5, 6, 7 owing to abnormal reflex control of gas transit.8, 9 This motor dysfunction cannot be identified by conventional techniques, such as intestinal manometry or scintigraphic measurement of solid/liquid chyme transit. Probably the dysfunction is more subtle, and may be related to increased resistance to flow and/or impaired accommodation in discrete disorders of gut segments, resulting in focal pooling without an increment in total gas content. Indeed, previous studies have shown that intestinal gas content is not, or only marginally, increased in patients complaining of bloating.5, 7, 10, 11, 12, 13
Alternatively, other components of chyme may be the offending element that triggers bloating. Indeed, Levitt et al14 illustrated how different intraluminal elements (gas or not gas) may induce bloating. In a group of healthy subjects, they showed that lactulose, which is not absorbed in the small intestine and is fermented into the colon, releasing hydrogen, induced flatulence and bloating. Interestingly, nonfermentable methylcellulose produced no hydrogen release detectable by breath test and did not induce flatulence, but still induced a sensation of abdominal bloating. Hence, probably little amounts of either gas or fiber, not likely to induce changes in girth, are sufficient to trigger the bloating sensation. Gut hypersensitivity, a characteristic feature of IBS patients, could explain the intolerance, sensed as bloating, of physiologic stimuli in the gut. Experimental studies have shown that probe stimuli, such as gut distention, tend to reproduce the customary symptoms in patients complaining of abdominal bloating, and this can be triggered by small volume balloon distention.15, 16 In patients with functional gut disorders, altered sensitivity combines with impaired control of gut motility, and both dysfunctions may interact to produce their bloating sensation.17 Basically, intraluminal trapping of contents, causing focal distention in a hypersensitive area, induces symptoms.
Bloating sensation without distention may be also related to a distorted interpretation. Levitt’s group showed that people who regarded themselves as severely lactose intolerant and complained of bloating after consumption of even small amounts of diary products, when specifically tested in a double-blind fashion, recorded negligible symptoms when consuming 250 mL milk, regardless of whether it was lactose hydrolyzed or not.18 Thus, despite their conviction, the experimental evidence proved that customary milk-related symptoms in these patients were psychosomatic. Some patients with a normal or fatty abdomen believe, sometimes to the point of obsession, that their abdomen is distended. These patients may interpret IBS-like symptoms as secondary to gut distention.
As reviewed, various mechanisms may explain the origin of bloating sensation in the absence of abdominal distention. However, probably the most relevant point in Whorwell’s report is that subjective claims of distention represent true perception of a real event in a significant proportion of patients. The volume of intra-abdominal contents exhibits physiologic variations in relation to ingestion and bladder/rectal evacuation. For that purpose the abdominal walls, particularly the anterior wall and the diaphragm, adapt to intra-abdominal contents featuring a true abdominal accommodation reflex. Some recent work from our laboratory shows that a considerable intra-abdominal overload of 1.4 L colonic gas infusion produces a relatively small increment in girth in healthy subjects because the muscles in the anterior abdominal wall contract and the diaphragm relaxes. This abdominophrenic coordination controls the intra-abdominal distribution of the volume load.19 Obviously, a very large intra-abdominal volume increment will result in visible abdominal distention with significant girth increment, and this can be seen in patients with massive intestinal retention due to intestinal obstruction or pseudo-obstruction or in patients with ascites, but this is not the case in the usual IBS patient that complains of bloating. Interestingly, recent data show that in these functional patients the abdominal accommodation reflex is abnormal. In them intra-abdominal volume increments in the physiologic range, induce a paradoxical relaxation of the anterior abdominal wall and a contraction of the diaphragm, and this abdominophrenic incoordination is associated to exaggerated abdominal distention.20, 21 Abnormal wall responses to intra-abdominal volume increments may explain the characteristic meal-related abdominal distention documented in 24% of patients in Whorwell’s study.
Careful studies using an original program for volumetric measurements by computed tomographic (CT) analysis have demonstrated that in a considerable proportion of patients, bloating and objective abdominal distention are not related to intra-abdominal volume increments.22 But, if it is not within the belly, where is it coming from? By comparing CT images from the same patients during basal conditions and during episodes of severe bloating, the same studies showed that the protrusion of the anterior abdominal wall is related to a significant diaphragmatic descent. Hence, after all it may not even be the abdomen, but a thoracic displacement that causes abdominal distention.
The mechanism of this abdominophrenic dysfunction, whether a subcortical reflex or a behavioral attitude, has not been demonstrated yet. Because these patients exhibit abnormal viscerovisceral reflexes,17 subcortical impairment of viscerosomatic reflexes is conceivable. However, other uncontrolled observations suggest that abdominophrenic incoordination and abdominal wall dystony may be related to learned responses. In a classic article, Alvarez23 described in great detail a series of patients in whom pronounced abdominal distention was, in his view, related to the muscular activity of the abdominal wall. In a very graphic way, he used for this very specific subgroup of patients the term hysterical type of nongaseous abdominal bloating. This hypothesis is substantiated by the fact that in some patients visible abdominal distention has a very rapid onset3, 23 and resolves instantaneously with gentle abdominal palpation while asking the patients to relax or by anesthesia.23 In Whorwell’s own experience, severe abdominal distention also resolves during hypnotic induction, further sustaining a cognitive mechanism. Following this reasoning, abdominal bloating, and distention should perhaps be treated with behavioral techniques, and in analogy to abdominoperineal dyssynergia in constipation, abdominophrenic incoordination may finally resolve with biofeedback therapy.
Data collected over the past 10 years with different methodologies, including the inductance plethysmography developed by Whorwell’s group, have provided experimental evidence in support to the abdominal wall hypothesis. However, contrary to Alvarez’s idea, this mechanism may not apply only to a specific subgroup of patients, but rather, abnormal activity of the abdominal walls may be part of a broader and more comprehensive concept of impaired abdominal accommodation that may contribute to bloating/distention in a much larger proportion of patients than initially postulated. This model may help to finally understand bloating, a frequent and elusive clinical problem,24, 25 and may provide a basis to develop effective management strategies.
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PII: S0016-5085(06)01924-X
doi:10.1053/j.gastro.2006.08.046
© 2006 American Gastroenterological Association (AGA) Institute. Published by Elsevier Inc. All rights reserved.

