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We were fascinated to read the paper by
describing cases of mucosal tearing at colonoscopy in patients subsequently found to have collagenous colitis. We were particularly interested in their postulated mechanism for these tears being a disruption of colonic mural integrity by the submucosal collagen layer. We would like to present two cases which add further weight to this theory as well as possibly providing information as to the pathogenesis of diarrhoea in this condition.
A 60 year old woman presented to her general practitioner with a two month history of profuse watery diarrhoea. A barium enema examination was reported as showing evidence of a mild colitis only. The general practitioner commenced corticosteroids resulting in complete resolution of her symptoms. On referral to our department, a gastrointestinal radiologist reviewed her radiographs. It was noticed that throughout the films there was a radiolucent border outlining the colonic mucosa (see fig 1) suggesting the presence of a submucosal layer of gas for which no explanation could be found. Although endoscopic examination of the colon was macroscopically normal, serial biopsies revealed the presence of a subepithelial collagen band up to 100 µm thick and a diagnosis of collagenous colitis was made. There was no evidence of pneumatosis or of submucosal barium on the small amount of submucosa included. She has since remained well on mesalazine.
The second patient was a 68 year old woman with a four week history of profuse watery diarrhoea. An emergency admission was required as a result of deranged clotting secondary to warfarin, which she was taking for a mechanical aortic valve. Following correction of her coagulopathy she underwent a colonoscopy. The instrument was advanced to the caecum without difficulty by a very experienced endoscopist who had performed in excess of 10 000 procedures. Macroscopically, there was evidence of a mild colitis. Standard serial biopsies were taken. Shortly following the procedure she complained of right shoulder tip pain. On examination she was neither distressed nor haemodynamically compromised. Her abdomen was soft. Chest and abdominal radiographs showed significant free gas under the diaphragm and in the peritoneum. At laparotomy she was found to have pneumoperitoneum without faecal contamination. No perforation was identified but there was considerable emphysema within the caecal wall extending proximally along the terminal ileum and distally to the mid ascending colon. No further operative procedure was performed. Endoscopic biopsies showed mild active inflammation and a subepithelial collagen band. None of the biopsies was full thickness. A diagnosis of collagenous colitis was made and her symptoms settled on a short course of corticosteroids.
We suggest that the complications seen in the investigation of these two patients result from a weakness within the colonic wall caused by the collagen layer. In the first case it appears that cleavage or dissection of the colonic wall alongside the collagen layer may have occurred. It is unclear whether this happened as a result of air insufflation at the time of examination or whether it was already present. In the second case we postulate that air insufflated at the time of the colonoscopy tracked alongside the collagen layer perforating into the peritoneum remote from its original point of entry; possibly a proximal biopsy site.
If a true weakness in the integrity of adhesion of the elements of the colonic wall does exist and such “dissection” can happen spontaneously, then it may provide some insight into the pathogenesis of the diarrhoea in this condition, especially as there appears to be no correlation between the width of the collagen band and the severity of symptoms.