Scott B. Simpson
Colonic distension is not only the main trigger of functional colonic pain, but also activates multiple different reflexes affecting both upper and lower gastrointestinal (GI) motility. Irritable bowel syndrome (IBS) patients have been documented with increased colonic faecal loading on abdominal x-ray. Medications, reduced mobility and probably hereditary factors which promote colonic stasis along with poorly digested fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) which increase colonic distension are known to trigger colonic symptoms. Colonic decompression has been shown to improve both functional colonic and upper gut symptoms as well as reducing typical gastro-oesophageal reflux disease (GORD) and laryngopharyngeal reflux (LPR) symptoms. The right colon appears to play an important role in regulating whole gut motility. GI smooth muscle functions according to the Frank-Starling principle where progressive distension initially promotes and later impairs motility and must be taken into account when selecting appropriate medical therapy. Colonic stasis is associated with the more benign form of acute ischaemic colitis. In mouse studies, colonic distension from a high FODMAP diet may well induce low-grade mucosal ischaemia, barrier dysfunction and ongoing low-grade inflammation causing IBS symptoms. Gut physiology suggests that occult constipation or proximal colonic faecal loading acts as a functional obstruction, which must be addressed by medical therapy to treat functional upper GI symptoms and refractory reflux optimally. Improvement in functional colonic symptoms with simple laxative therapy and other agents which promote colonic motility such as prucalopride correlates strongly with improvement in dyspeptic, refractory GORD and LPR symptoms.
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