How to treat diversion colitis?: Current state of medical knowledge, own research and experience

Abstract

The aim of this study was to present current knowledge about a nospecific inflammation of mucosa within segments of colon excluded from normal bowel passage called as a "diversion colitis" (DC) and to try to determine the role of factors which might modify the clinical course of DC. We also unswered the question; how to treat DC: conservatively or surgically? Our own experience with DC concerns 145 patents (which is most numerous and well exactly examined series presented in literature). In the group of patients studied, clinical signs of DC were present in over 70% of patients (early signs were low abdominal pain and tenesmus, while anal oozing appeared later). Predominating endoscopic features of DC in the group of patients studied were: a. blurring of vascular pattern (in app. 90% of patients); b. contact bleeding (in app. 80% of patients); c. mucosal oedema (in app. 60% of patients). Results of own observations and literature data indicate, that morphologic alterations in the segment of bowel excluded from normal passage are probably vasogenic consisting in atrophy and inflammation of the allergic type (this would confirm the theory about vascular etiology of DC). In our material, we have not noticed any trend toward hyperproliferation or dysplasia in the excluded segment of colon, supporting the thesis that these disturbances are largely reversible. Clinical pathology of DC does not depend on age, sex, cause and type of surgical procedure performed, mode of surgery or concomitant diseases. Authors suggested an alternative algorithm of diagnostic work-up in patients suspected of DC, and proposed that patients with a segment of bowel excluded from normal passage be subdivided into three groups: 1. Patients with no clinical, endoscopic nor morphologic signs of DC. 2. Patients with moderate signs of DC. 3. Patients with severe signs of DC. Patients in the group 1 should remain under continuous specialised supervision, because they are at risk of developing DC, while patients in the groups 2 and 3 should undergo surgical restoration of bowel continuity. This applies particularly to group 3, where indications for surgery do not stem from risk of hyperproliferation, dysplasia or malignant transformation, but from that of a massive inflammation, which may constitute a danger for patientis health and even life. Authors also underline that DC can be treated conservatively but the best and most successful and remained method of treatment of DC is the operation of decolostomy, which means restoration continuity of digestive tract.

Evaluation of topical n-acetylcysteine in diversion colitis

“…As the pathogenesis of DC is related to deficient supply of SCFAs, the most obvious strategy is to apply enemas with SCFAs in the segment without fecal stream 18,19,33,34 . A series of studies confirmed that the irrigation of segments without fecal stream with SCFAs-rich solutions, particularly butyrate, can revert endoscopic and histological alterations related to the disease and reduce the levels of tissue oxidative stress [9][10][11][12][13]15,17,18,33,34 . The main action of SCFAs in the segment without fecal stream would be to restore homeostasis in the reactions that promote energy production by the cells, preventing the excessive formation of OFRs and, consequently, the tissue oxidative stress 34 .…”

“…The application of SCFAs in the excluded colon was experimentally demonstrated to improve the inflammatory process, while the interrupted application promoted the disease dissemination 10 . The deficient supply of SCFAs as a factor that triggers DC was confirmed with the results of clinical and experimental studies showing that the restoration of fecal stream or the application of butyrate-rich solutions, the main subtype of SCFAs metabolized by colonocytes, reverted the clinical symptoms and the characteristic endoscopic and histological alterations of the disease [11][12][13][14][15][16][17][18][19] . However, despite these evidences, the molecular mechanisms through which the deficient supply of SCFAs determines the tissue inflammation, have not been fully explained 20 .…”

“…DC is a chronic inflammatory disease developed in 100% of the patients 36 months after the intestinal stream interruption 5,6,[9][10][11][12][13][14][15][16][17][18][19][20] . Recent studies have demonstrated that the increased OFRs production by epithelial cells with deficient SCFAs supply and the recognized deficiency of colonic mucosa in antioxidant enzymatic systems, which makes the intestinal epithelium particularly vulnerable to oxidative stress, are mechanisms related to the pathogenesis of DC 20,27 .…”

“…Then, the early restoration of fecal stream, reestablishing the supply of SCFAs, prevents the disease development 9,10 . Studies have shown that fecal stream restoration reverts the disease symptoms in most cases, making it the most effective therapy for the prevention of DC 13 .However, fecal traffic recovery is not always possible, which promotes the evaluation of other therapeutic strategies 20 . As the pathogenesis of DC is related to deficient supply of SCFAs, the most obvious strategy is to apply enemas with SCFAs in the segment without fecal stream 18,19,33,34 .…”

Efeitos do butirato nos níveis de peroxidação lipídica em células da mucosa cólica sem trânsito fecal: estudo experimental em ratos

“…Essa possibilidade é reforçada ao se constatar que a reconstituição do trânsito, ou a irrigação dos segmentos exclusos com soluções nutricionais ricas em AGCC, restabelecendo o substrato energético à mucosa cólica, são capazes de reverter as alterações clínicas e histopatológicas encontradas nos portadores de CE [9][10][11] . Os AGCC são formados a partir da fermentação de carboidratos não absorvidos pelo intestino delgado pela flora bacteriana do interior do cólon.…”