Perianal Crohn disease: predictors of need for permanent diversion.

OBJECTIVE: Fissures, fistulas, abscesses, and anal canal stenosis are manifestations of perianal Crohn disease (CD). There are no known predictors of which patients will fail sphincter-sparing surgical therapy and ultimately require fecal diversion. METHODS: Of 356 consecutive patients with CD, 24% (86) had perianal CD (age range, 14-83 years), and women were slightly more frequently affected. Clinical variables were examined for factors predictive of the need for permanent fecal diversion. RESULTS: CD associated with perianal CD was limited to the small bowel and/or ileocolic area in 23% of patients; the remainder had colorectal CD. Eighty-six patients underwent 344 operations. Forty-two patients (49%) ultimately required permanent diversion; among them were 21 of 32 patients (66%) with anal stricture and 12 of 20 women (60%) with rectovaginal fistula. Univariate analyses of clinical variables were performed with respect to need for permanent fecal diversion. Significant univariate predictors were the presence of colonic CD (P = 0.0045, odds ratio [OR] 5.4), avoidance of ileocolic resection (P = 0.0147, OR 0.4), and the presence of an anal stricture (P = 0.0165, OR 3.0). In multivariate logistic regression, the presence of colonic disease and anal canal stricture were predictors of permanent diversion. The OR associated with the risk of permanent diversion in the presence of colonic disease and in the absence of anal stricture was 10 (P = 0.0345). In the presence of both colonic disease and anal canal stenosis, the OR associated with permanent stoma was 33 (P = 0.0023). CONCLUSIONS: The management of perianal CD continues to be challenging. Roughly half of patients required permanent fecal diversion, which was even more frequently true for patients with colonic CD and anal stenosis. Recognizing these tendencies will assist both patients and surgeons in planning optimal treatment.

A case of enterolith small bowel obstruction and jejunal diverticulosis.

We reported a case of 79-year old woman with known large bowel diverticulosis presenting with small bowel obstruction due to stone impaction - found on plain abdominal X-ray. Contrast studies demonstrated small bowel diverticulosis. At laparotomy, the gall bladder was normal with no stones and no abnormal communication with small bowel - excluding the possibility of a gallstone ileus. Analysis of the stone revealed a composition of bile pigments and calcium oxalate. This was a rare case of small bowel obstruction due to enterolith formation - made distinctive by calcification (previously unreported in the proximal small bowel).

Evidence for incorporation of free-floating mesothelial cells as a mechanism of serosal healing.

Regeneration of the mesothelium is unlike that of other epithelial-like surfaces, as healing does not occur solely by centripetal migration of cells from the wound edge. The mechanism of repair of mesothelium is controversial, but it is widely accepted, without compelling evidence, that pluripotent cells beneath the mesothelium migrate to the surface and differentiate into mesothelial cells. In this study we examined an alternative hypothesis, using in vivo cell-tracking studies, that repair involves implantation, proliferation and incorporation of free-floating mesothelial cells into the regenerating mesothelium. Cultured mesothelial cells, fibroblasts and peritoneal lavage cells were DiI- or PKH26-PCL-labelled and injected into rats immediately following mesothelial injury. Implantation of labelled cells was assessed on mesothelial imprints using confocal microscopy, and cell proliferation was determined by proliferating cell nuclear antigen immunolabelling. Incorporation of labelled cells, assessed by the formation of apical junctional complexes, was shown by confocal imaging of zonula occludens-1 protein. Labelled cultured mesothelial and peritoneal lavage cells, but not cultured fibroblasts, implanted onto the wound surface 3, 5 and 8 days after injury. These cells proliferated and incorporated into the regenerated mesothelium, as demonstrated by nuclear proliferating cell nuclear antigen staining and membrane-localised zonula occludens-1 expression, respectively. Furthermore, immunolocalisation of the mesothelial cell marker HBME-1 demonstrated that the incorporated, labelled lavage-derived cells were mesothelial cells and not macrophages as it had previously been suggested. This study has clearly shown that serosal healing involves implantation, proliferation and incorporation of free-floating mesothelial cells into the regenerating mesothelium.