• DYSPEPSIA
• ELECTROPHYSIOLOGY
• IRRITABLE BOWEL SYNDROME
• NEUROGASTROENTEROLOGY

The symptom of bloating means a feeling of being puffed up in the abdomen. Bloating can have many different causes and is also part of the normal spectrum of signals from the alimentary tract. Bloating can be felt, for example, after eating a little too much. A population survey in the USA reported that 16% of healthy individuals experienced bloating at least once a month.1 The origin of such ‘physiological’ bloating is likely the stomach or the upper small intestine.2 ,3 Abnormal bloating occurs in functional gastrointestinal disorders, in particular, the irritable bowel syndrome (IBS), functional dyspepsia and functional bloating. Bloating is perceived as the most frequent and bothersome symptom by patients with IBS.4 There is considerable overlap between bloating, as defined above, and abdominal distension. The latter is sometimes specified as measurable or visible distension, thus implying that abdominal distension is a clinical sign rather than a symptom.5 Abdominal distension was found in 76%–85% of IBS patients with bloating.4 ,6 A study that employed an objective method for measuring abdominal girth found abdominal distension in 48% of patients with IBS and bloating.7 Contrary to many other symptoms in patients with functional gastrointestinal disorders, neither bloating nor abdominal distension seems to have a relation to psychological factors.7 ,8 An interesting observation is that bloating with abdominal distension is a frequent finding also in patients with opioid-induced dysmotility.9

The mechanisms leading to bloating and abdominal distension have been much debated. The interested reader is referred to an excellent review of pathophysiological mechanisms in abdominal bloating by Azpiroz and Malagelada.10 Abdominal distension can have four different causes: increased amounts of abdominal fluid (ascites), increased tissue volume of abdominal contents, increased volume of luminal contents, and displacement of abdominal contents. Ascites is not a feature of functional abdominal distension, and fluid retention as a cause for abdominal distension was rejected because no weight gain could be found during episodes of bloating.11 Intestinal oedema can contribute to abdominal distension in patients with an acute attack of hereditary angioneurotic oedema,12 but intestinal oedema has not been reported in patients with functional abdominal distension. Many patients and also some physicians believed that bloating and distension followed from increased amounts of gas in the gastrointestinal tract. Patients with IBS were found to have impaired transport of gas and retained more gas in the intestines following gas infusion into the jejunum.13 Bloating and distension were associated with increased amounts of intestinal gas in patients with manometry-defined intestinal dysmotility.14 However, several studies using different techniques were unable to demonstrate an excess of intestinal gas in patients with functional bloating and abdominal distension compared with healthy controls.13–15 The role of luminal fluids and chyme in the development of abdominal distension is yet unclear.10

Voluntary displacement of abdominal contents by contraction of the diaphragm and increased lumbar lordosis was reported from a case series by Alvarez in 1949,16 and this remained an explanatory model for functional abdominal distension until it was disproved using plain x-ray and CT of the abdomen.17

The possibility of involuntary displacement of abdominal contents became a leading hypothesis after the seminal work by Accarino et al,14 who showed that functional abdominal distension resulted from caudoventral redistribution of contents. The key component of this redistribution was diaphragmatic descent. In order to accommodate abdominal contents when the upper border of the abdominal cavity descends, the muscles of the abdominal wall have to relax. Interestingly, when abdominal wall muscles and diaphragm were studied using electromyography (EMG), healthy controls relaxed the diaphragm and increased abdominal muscle tone during intraluminal gas infusion, whereas patients with IBS contracted the diaphragm and relaxed the internal oblique muscle of the abdominal wall.18 Burri et al19 further enhanced our understanding of functional abdominal distension. They recorded EMG from abdominal wall muscles and the diaphragm in patients with functional dyspepsia and healthy controls before and during controlled nutrient intake. Healthy controls responded to the nutrient challenge by relaxing the diaphragm and increasing the tone of abdominal muscles, whereas patients with functional dyspepsia relaxed their upper abdominal muscles and increased the tone in the diaphragm. The two studies clearly point at viscerosomatic reflex disturbances being involved in the pathogenesis of functional abdominal distension.

It is yet unclear if such a disturbance is confined to the diaphragm, or if abdominal wall muscles are included as well. Given that the contraction of the diaphragm increases the intra-abdominal pressure, the relaxation of abdominal wall muscles could be a normal response. The reverse would be more unlikely as it is difficult to envisage a reflex that would contract the diaphragm in response to relaxation of abdominal wall muscles. The discrepancies between IBS and functional dyspepsia regarding muscle groups in the abdominal wall are difficult to interpret. IBS and functional dyspepsia are believed to affect different segments of the gut and conditioning of reflex systems may differ between the two diagnoses. The analogy of paradoxical diaphragm contraction with paradoxical puborectalis contraction is thought provoking, and so is the biofeedback approach to treatment.19 We will look forward to seeing the results of biofeedback therapy for functional abdominal distension, in particular, since our current therapeutic modalities leave a substantial unmet need. Since opioid therapy can induce abdominal distension, it would be of great interest to find out if opioid-induced distension is associated with a similar pattern of abnormal viscerosomatic reflexes. The patient samples are limited in both studies, and findings need to be confirmed by other research groups but my gut feeling is that Burri et al19 have taken us at least one level up in our understanding of abdominal bloating.