INTRODUCTION — Diversion colitis is characterized by inflammation of the defunctionalized, bypassed colon following surgery [1,2]. Most patients with diversion colitis are asymptomatic, but in a small proportion of patients, symptoms can significantly impact quality of life [3].

This topic will review the epidemiology, pathogenesis, clinical manifestations, diagnosis, and management of diversion colitis. The epidemiology, clinical manifestations, diagnosis, and management of ulcerative colitis and Crohn disease are discussed in detail, separately. (See "Definitions, epidemiology, and risk factors for inflammatory bowel disease" and "Medical management of low-risk adult patients with mild to moderate ulcerative colitis" and "Management of the hospitalized adult patient with severe ulcerative colitis" and "Management of moderate to severe ulcerative colitis in adults" and "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults" and "Overview of the medical management of mild (low risk) Crohn disease in adults" and "Overview of medical management of high-risk, adult patients with moderate to severe Crohn disease".)

DEFINITION — Diversion colitis or diversion proctitis is a nonspecific inflammatory disorder that occurs in segments of the colon and rectum that are diverted from the fecal stream by surgery (eg, creation of a loop colostomy/ileostomy or an end colostomy/ileostomy with closure of the distal colon segment [eg, Hartmann's procedure]).

EPIDEMIOLOGY — The true incidence of diversion colitis is unknown. Several small observational studies have demonstrated histologic changes of diversion colitis in the distal colonic segment of 70 to 100 percent of patients with fecal diversion, and endoscopic evidence in 70 to 91 percent of patients [4-12]. Diversion colitis or proctitis is more common in patients with underlying inflammatory bowel disease (IBD; ie, Crohn disease and ulcerative colitis) than those with colon malignancy and diverticular diseases. (See 'Endoscopy and biopsy' below.)

In a retrospective pathology-registry-based study of 191 patients with diverted rectum for more than one year for underlying IBD who had undergone endoscopic follow-up, 161 (88.5 percent) had endoscopic mucosal inflammation. A total of 115 (71.4 percent) had diversion colitis, and 12 (7.5 percent) had a combination of diversion colitis and IBD in the diverted rectum [12]. (See 'Endoscopy and biopsy' below.)

ETIOLOGY AND PATHOGENESIS — Diversion colitis typically occurs in diverted segments of the colon following surgery for congenital, inflammatory, or neoplastic disorders. Patients usually have a loop colostomy (or ileostomy) or an end colostomy (or ileostomy) with closure of the distal colon segment (eg, Hartmann's procedure). Diversion of the fecal stream results in a deficiency of short-chain fatty acids (SCFAs) and other luminal nutrients in colonocytes in the diverted segment of the colon. It is hypothesized that the lack of these compounds or interference with their metabolism by alterations in gut flora may have a role in the development of colitis [13,14].

SCFAs, predominantly acetate, propionate, and n-butyrate, are derived from anaerobic bacterial metabolism of unabsorbed dietary carbohydrates. They are absorbed from the lumen by a combination of simple diffusion and ion exchange and oxidized by colonocytes [15]. In addition to supplying 70 percent of the fuel used by mucosal cells, luminal SCFAs have a number of other effects, including modulation of fluid and electrolyte transport, colonic motility, mucosal blood flow, and production of inflammatory cytokines [16,17]. Other luminal nutrients for colonocytes, such as glutamine, may also play a role in the pathogenesis of diversion colitis.

Detailed bacteriologic studies have also demonstrated that the diverted segment has fewer anaerobic flora and a higher percentage of nitrate-reducing strains than controls, which may in turn result in a lack of fermentation metabolites of carbohydrates and proteins [18-20]. However, no specific pathogens have been identified. In addition, the inconsistent response of certain patients to SCFAs in some studies and the response to restoration of fecal continuity suggest that other factors are involved in the pathogenesis of diversion colitis [21].

Inflammation in the diverted segment of the large bowel may also set the stage for the development of symptomatic "ulcerative colitis"-like condition in the in-stream colon proximal to the diverted segment [22-24]. This was illustrated in a report of two patients who had undergone sigmoid colostomies who developed diversion colitis [22]. Neither had a family history of inflammatory bowel disease (IBD), but both patients later developed bleeding through the colostomy, with endoscopic and histologic features of ulcerative colitis in the previously normal colon proximal to the colostomy. It appears that both innate and adaptive immunities of diverted colon mucosa are altered [25,26]. A plausible hypothesis for the pathogenesis of proximal colitis is that leukocytes sensitized and activated in the vasculature of the diverted segment are recruited to the genetically susceptible proximal mucosa.

CLINICAL MANIFESTATIONS — Fewer than 50 percent of patients with histologic evidence of diversion colitis have symptoms [4-11]. In patients who are symptomatic, the onset usually occurs 3 to 36 months after colonic exclusion [27]. The most common symptoms in adults are tenesmus, urgency, bloody and/or mucus discharge, abdominal pain, and pelvic pain or pressure [12,28]. Symptoms are mild in up to 50 percent of patients [3,11]. In rare cases, patients have severe bleeding that requires transfusion, diarrhea, or sepsis from deep ulceration and marked mucosal inflammation [11,29-32].

The likelihood of symptoms may at least in part be associated with the underlying disease. In a series of 73 patients with a diverted colorectum, 87 percent of those with ulcerative colitis had symptoms as compared with 30 percent of those with Crohn disease, and 28 percent of those without inflammatory bowel disease (IBD) [33]. In a study of 36 children with Hirschsprung disease, only one child (3 percent) with an ileostomy for six years developed diversion colitis [7]. By contrast, in another study that included 14 children who underwent diversion because of chronic intestinal pseudoobstruction, 11 (79 percent) developed diversion colitis between four months to seven years after surgery [34].

Persistent inflammation and long-term non-use may result in mild to severe stricture of the diverted bowel. In the study of 191 IBD patients with ostomies for more than one year, 57 (29.8 percent) were found to have strictures in the diverted rectum [12]. The stricture can also occur in the diverted ileal pouch (picture 1). In addition, accumulation of mucus materials may cause the formation of a bezoar. The stricture can cause symptoms of abdominal or pelvic pain and discomfort, and sensation of incomplete evacuation (picture 1).

EVALUATION — Evaluation of a patient with suspected diversion colitis serves to exclude other causes of colitis and establish the diagnosis of diversion colitis.

Diagnosis — Diversion colitis should be considered in an individual with or without preexisting inflammatory bowel disease (IBD) who complains of cramping abdominal pain with a mucoid or bloody discharge from the defunctionalized, diverted distal colon. As the clinical manifestations, endoscopic and histologic findings of diversion colitis are nonspecific, the diagnosis requires exclusion of other disorders that can have similar clinical manifestations. (See 'Endoscopy and biopsy' below and 'Differential diagnosis' below.)

History — A history of risk factors for other causes of colitis should be sought. This includes a history of recent travel to areas endemic for bacterial or parasitic infections including amebiasis, recent antibiotic use that might predispose to an infection with Clostridioides difficile, and a history of or risk factors for sexually transmitted diseases (eg, Neisseria gonorrhea and herpes simplex virus [HSV]) that are associated with proctitis. Atherosclerotic disease or prior ischemic episodes are suggestive of chronic colonic ischemia. A history of abdominal/pelvic radiation and nonsteroidal antiinflammatory drug (NSAID)/medication exposure should be sought, as these may also be associated with colitis. In an immunocompromised patient, cytomegalovirus (CMV) infection can mimic ulcerative colitis or Crohn disease. (See "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults", section on 'Differential diagnosis' and "Radiation proctitis: Clinical manifestations, diagnosis, and management" and "NSAIDs: Adverse effects on the distal small bowel and colon" and "Colonic ischemia".)

Laboratory studies — Although the sensitivity and specificity of assays for pathogens in specimens from a diverted colorectum are not known, stool studies should still be performed. These include stool C. difficile toxins, routine stool cultures (Salmonella, Shigella, Campylobacter, Yersinia), and specific testing for E. coli O157:H7. Microscopy for ova and parasites (three samples) and a Giardia stool antigen test should also be performed, particularly if the patient has risk factors such as recent travel to endemic areas.

In addition, testing for sexually transmitted infections, including C. trachomatis, N. gonorrhoeae, HSV, and Treponema pallidum, may be warranted, particularly in men who have sex with men or patients with severe rectal symptoms including urgency and tenesmus. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents" and "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus in patients with HIV" and "Syphilis: Screening and diagnostic testing".)

We also check a complete blood count, electrolytes, albumin, and markers of inflammation C-reactive protein (CRP) and fecal calprotectin may be used to assess disease severity.

Endoscopy and biopsy — The mucosa of diverted bowel is normally friable (image 1). To minimize the risk of bleeding or perforation, gentle air or carbon dioxide insufflation during endoscopy is preferred. In addition, deep or jumbo biopsy should be avoided [35,36].

Endoscopic features of diversion colitis are nonspecific and include erythema, friability, edema, granularity of the colorectal mucosa. In more severe cases, patients may have ulcers, nodularity, edema, or inflammatory and filiform polyps and strictures [37]. In some patients, endoscopy may show a "cat scratch" pattern with bright erythematous linear marks. In some patients with outlet stricture, there might be an accumulation of large quantity of exudates, which can cause symptoms of fever, pelvic discomfort, and urgency (image 2).

Histopathological features of diversion colitis are not diagnostic, but biopsies of the colon are necessary to exclude other causes of colitis. The most common pathological features of diversion colitis include expanded lymphoid aggregates and inflammation in the lamina propria with lymphocytes and plasma cells (picture 2) [1,7]. Although crypt architecture is usually preserved, features that mimic IBD, including crypt distortion and basal lymphoplasmacytosis, may be seen [5,11,27]. In cases with marked lymphoid hyperplasia, the crypts may appear atrophic, short, and displaced by the lymphoid infiltrate imparting a false appearance of crypt architectural abnormalities of IBD [38].

Imaging — The diverted bowel may have nonspecific thickened wall and hypermucosal enhancement on contrasted cross-sectional imaging regardless of the presence of inflammation. Therefore, the value of computed tomography or magnetic resonance imaging for the assessment of inflammation is limited. Water soluble contrasted enemas via stoma or anus may help delineate the presence and nature of strictures of the diverted bowel (image 3).

DIFFERENTIAL DIAGNOSIS — In order to diagnose diversion colitis, it is important to distinguish it from other disorders that can have similar clinical manifestations [39]. The clinical history provides important information to narrow the differential diagnosis, but additional evaluation may be needed. There are distinct and shared features on clinical, endoscopic, and histologic features between ulcerative proctitis, chronic radiation proctopathy, and diversion proctitis (table 1).

●Infectious colitis – Infectious colitis may have a similar clinical presentation and endoscopic appearance to diversion colitis (table 2). Infectious colitis can be excluded with stool and tissue cultures, stool studies, and on biopsies of the colorectum. (See 'Laboratory studies' above.)

●Inflammatory bowel disease – The documentation of the presence or absence of inflammatory bowel disease (IBD) in the diverted colon segment prior to surgery is helpful in distinguishing recurrent IBD in the diverted colon from diversion colitis.

In patients with distal colonic involvement of IBD prior to surgery, it is difficult to differentiate recurrent active IBD in the diverted colon from diversion colitis. However, certain histological features may be helpful:

•The histology pattern of enterocolic lymphocytic phlebitis, characterized by artery-sparing and venulocentric lymphoid infiltration, is more commonly seen in patients with IBD and superimposed diversion colitis as compared with those with IBD alone [40].

•The presence of noncaseating, nonmucinous granulomas in the defunctionalized rectum is suggestive of the presence of Crohn disease [41].

•The presence of a diffuse cellular infiltrate and prominent lymphoid follicular hyperplasia is suggestive of diversion colitis [7,27,33,40].

In some cases, this distinction may still not be possible. In such cases, a response to a trial of short-chain fatty acid enemas is suggestive of diversion colitis. On the other hand, a favorable response to systemic corticosteroid or anti-tumor necrosis factor (TNF) biologics in a patient with diverted colorectum suggests the dominant role of underlying IBD in symptomatology. (See 'Short-chain fatty acid enemas' below.)

●Radiation colitis/proctitis – Endoscopic and histologic features of diversion colitis can mimic those seen in radiation colitis/proctitis. Radiation colitis may be seen weeks to years after abdominal or pelvic irradiation. Although not specific for radiation colitis/proctitis, histologic findings suggestive of radiation colitis include eosinophilic infiltrates, epithelial atypia, fibrosis, and capillary telangiectasia. (See "Radiation proctitis: Clinical manifestations, diagnosis, and management", section on 'Clinical suspicion' and "Radiation proctitis: Clinical manifestations, diagnosis, and management", section on 'Clinical manifestations'.)

●Medication associated colitis – Nonsteroidal antiinflammatory drugs (NSAIDs) can cause chronic diarrhea and bleeding [42]. Other drugs associated with a similar clinical presentation include retinoic acid and gold. Immune checkpoint inhibitors, which block the co-inhibitory receptors on T cells to activate their cytotoxic immune function, are growingly used for the treatment of malignancies. Those agents, including cytotoxic T lymphocyte antigen 4 (CTLA-4) inhibitors (such as ipilimumab), and programmed cell death protein 1 (PD-1) and programmed cell death protein ligand 1 (PD-L1) inhibitors (such as pembrolizumab and nivolumab), are associated with colitis [43]. The diagnosis is established by a history of medication use and the presence of nonspecific mucosal inflammation or mucosal erosions on endoscopy and biopsy, and in some cases, resolution of symptoms and mucosal inflammation after the cessation of the insulting medications. (See "NSAIDs: Adverse effects on the distal small bowel and colon".)

●Ischemic colitis – Patients with ischemic colitis have a history of underlying vascular disease or other risk factors (eg, aortic surgery, cardiopulmonary bypass, myocardial infarction, hemodialysis, dehydration, thrombophilia). Colonoscopic findings include pale mucosa with petechial bleeding. Bluish hemorrhagic nodules may be seen. More severe disease is marked by cyanotic mucosa and hemorrhagic ulcerations. Ischemia colitis is segmental in distribution with abrupt transition between injured and non-injured mucosa, and rectal sparing. A single linear ulcer running along the longitudinal axis of the colon may also be suggestive of ischemic colitis [44]. Biopsies taken from affected areas may show nonspecific changes such as intra- and/or submucosal hemorrhage, crypt destruction or crypt drop-out, capillary thrombosis, granulation tissue with crypt abscesses, and pseudopolyps, which may mimic Crohn disease [45,46]. In the chronic phase of ischemic colitis, mucosal atrophy and areas of granulation tissue may be seen. Chronic ischemic colitis may manifest as colonic strictures. Biopsy of a post-ischemic stricture is marked by extensive transmural fibrosis and mucosal atrophy. The clinical presentation and diagnosis of ischemic colitis is discussed in detail, separately. (See "Colonic ischemia", section on 'Clinical features'.)

The clinical, endoscopic and histologic features of ulcerative proctitis, chronic radiation proctopathy, and diversion proctitis are listed in the table (table 1) [47].

TREATMENT — Surgical reanastomosis is the treatment of choice in symptomatic patients with diversion colitis. Medical therapy (eg, short-chain fatty acid [SCFA] enemas, topical 5-aminisalicylic acid, and topical glucocorticoids) should be reserved for symptomatic patients who are not candidates for surgery or in whom diversion colitis cannot be distinguished from active distal inflammatory bowel disease (IBD). Surgical proctectomy or sigmoidoproctectomy is an ultimate treatment modality for the disorder, despite the risk of procedure-associated modalities, such as persistent perineal sinus.

Surgical reanastomosis — In symptomatic patients with diversion colitis, restoring intestinal continuity by surgical reanastomosis is first-line treatment with a high chance of complete resolution of inflammation resulting from fecal diversion (image 4) [48]. While there are no randomized trials, in small observational studies reanastomosis has been reported to be uniformly curative within three months [21]. In patients who are candidates for surgery, early reanastomosis is preferred because, with a delay in reestablishment of bowel continuity, symptoms often become more frequent and severe, and there is a progressive decrease in capacity and involution of the defunctionalized anorectum [4,49]. In patients with Crohn disease, if the distal segment was not involved endoscopically and histologically before diversion, early reanastomosis will improve symptoms and may help avert stricture formation in the lumen of diverted colorectum [4].

In patients with known distal colonic IBD in whom it is unclear if the symptoms are due to diversion colitis or active IBD in the diverted colon, a symptomatic response to SCFA enemas supports the diagnosis of diversion colitis and should be followed by surgical reanastomosis [13]. Despite advances in medical and surgical treatment, surgical reanastomoses may not be feasible in some patients, particularly in those with IBD [12]. (See 'Differential diagnosis' above and 'Short-chain fatty acid enemas' below.)

Surgical proctectomy — Proctectomy or sigmoidoproctectomy has been performed in patients with refractory or symptomatic diversion proctitis or colitis, or dysplasia-associated neoplasia in the diverted bowel as an ultimate solution for the disorder [12].

Short-chain fatty acid enemas — SCFA enemas are used as initial therapy in patients with diversion colitis who are unable or unwilling to undergo surgery and in patients with known distal IBD in whom the diagnosis of diversion colitis is unclear. In patients with underlying IBD, we use SCFA enemas in combination with topical antiinflammatory drugs [50]. (See '5-aminosalicylic acid (5-ASA)' below and 'Glucocorticoids' below.)

SCFA enemas require preparation at compounding pharmacies [13]. In addition, they are not readily available and can be expensive. The use of coconut oil enema containing fatty acids with comparatively short chain length has been described to treat diversion proctitis in a patient with refractory Crohn disease [51].

●The enema solution consists of sodium acetate (60 mmol), sodium propionate (30 mmol), and sodium n-butyrate (40 mmol) with additional sodium chloride (22 mmol) to yield an osmolality of 280 to 290 mosmol/L, which is similar to plasma. The pH is adjusted to 7.0 with sodium hydroxide.

●A dose of 60 mL should be instilled into the diverted rectum twice daily for up to six weeks. Once improvement occurs, it can usually be maintained by a less frequent schedule (eg, one enema daily and then three times a week at bedtime).

The initial observation that the diverted segment of the colorectum contained negligible concentrations of SCFAs, and response in four patients to administration of D-glucose in a pilot study provided the rationale for the use of SCFA [13]. However, most studies in adults have had a small sample size and results have been conflicting [13,52-54]. As examples:

●In a prospective study that included 13 patients with diversion colitis, treatment with SCFA for 14 days was not associated with endoscopic or histologic remission [53]. However, this study was limited by the short duration of treatment and the fact that most patients had only mild endoscopic and histologic changes of diversion colitis at baseline.

●A randomized crossover trial included 10 patients with IBD (nine Crohn disease and one ulcerative colitis) who had undergone colectomy with creation of a Hartmann pouch a median of 15 months prior to the start of the trial. Patients were treated with SCFA instillation or placebo for three weeks. In this study, treatment with SCFA was not associated with an improvement in inflammation [52]. However, most patients had severe inflammation by endoscopy and histology that might have been more consistent with the underlying IBD than with diversion colitis.

●In another randomized trial, 20 patients with fecal diversion (more than 30 days) for IBD, colorectal cancer, or diverticular disease were assigned to sodium butyrate enemas or saline enemas [55]. Of the 17 patients with diversion colitis/proctitis who completed the trial, there was in endoscopy scores in both treatment and control groups. The improvement was greater in the study group as compared with the placebo group. Histologic scores of inflammation in both groups were numerically increased at the end of the trial. However, mucosal atrophy scores were reduced or unchanged in the study group and increased in the control group suggesting that SCFA may prevent atrophy of the diverted colon/rectum.

It has been suggested that children diverted for reasons other than IBD seem to respond more consistently to SCFA enemas than adults; however, few observational studies have been published and the long-term response to SCFAs is unknown [48,54].

5-aminosalicylic acid (5-ASA) — We suggest topical 5-aminosalicylic acids (ASAs; mesalamine) in patients whose symptoms fail to improve after two to four weeks of treatment with SCFA enemas. In patients with diversion colitis who have underlying IBD, regardless of whether IBD involves the diverted segment, we use topical 5-ASAs in conjunction with SCFAs. Topical 5-ASAs are widely available as suppositories or enemas (eg, mesalamine suppository 1 gram twice daily, mesalamine retention enema 4 grams twice daily). However, evidence to support topical 5-ASA use in diversion colitis is limited to case reports [56].

Glucocorticoids — The use of glucocorticoids should be limited to patients with diversion colitis who do not respond to or only partially respond to two to four weeks of therapy with SCFA enemas and topical mesalamine. For patients who completely fail to respond to SCFA and/or topical 5-ASA agents, topical corticosteroids can be used as the sole agent. For patients who have a partial response to SCFA and/or topical 5-ASA agents, topical corticosteroids can be used in addition to the existing regimen [57].

Topical preparations of glucocorticoids include enemas, suppositories, and foam (eg, hydrocortisone enema 100 mg twice daily, hydrocortisone suppository 30 mg twice daily, hydrocortisone foam 10 percent 90 mg twice daily). Topical steroids have not been systemically studied for the treatment of diversion colitis and their use is based on their efficacy in patients with other forms of colitis. In this author’s experience, patients with diversion colitis/proctitis along with underlying IBD may have a more favorable response to the topical glucocorticoid therapy than those without underlying IBD. However, it is important to note that adrenal suppression and other systemic adverse effects do occur in patients with long-term use of topical glucocorticoids. (See "Major side effects of systemic glucocorticoids", section on 'Organ-based toxicity of systemic glucocorticoids'.)

Other — Although the use of a solution containing soluble and insoluble soybean fiber has associated with improvement in the endoscopic and histological appearance of diversion colitis in a small prospective study of 11 patients with loop colostomies, additional studies are needed to confirm these findings [58]. Some experts have used high-concentration dextrose (50 percent) (picture 3) [59] or leukocytapheresis [60]. There was a case report on autologous fecal microbiota transplantation for chronic diversion colitis [61]. Other topical agents, which showed efficacy in reduction of mucosal inflammation or pro-inflammatory mediators in animal models, include sucralfate [62], heparin [63], dietary fibers [58], and curcumin enema [64].

Endoscopic therapy of stricture in the diverted bowel — Stricture at diverted bowel can be short or long with a cut-off of 4 to 5 cm (image 3), with the most common location at the distal rectum, pouch, anus, or anastomosis. Purely diversion-associated stricture often results in web-like strictures. The stricture can be inflammatory, fibrotic, or both. Fibrotic strictures mainly occur in the ileal pouch-anal anastomosis, ileorectal anastomosis, or colorectal anastomosis in patients with diverting ostomies. In severe cases, the outlet of diverted bowel can be completely sealed (image 3) [65].

Diversion-associated strictures can be managed by digital dilatation, bougie dilation, endoscopic balloon dilatation, or endoscopic stricturotomy [65].

CANCER SURVEILLANCE — The risk of dysplasia or cancer in the diverted colorectum appears to be low in patients with diversion colitis in the absence of a history of colorectal cancer (CRC) or inflammatory bowel disease (IBD) [66], therefore, surveillance for CRC in the diverted segment is not required unless the underlying condition for which the surgery was performed is associated with an increased risk of CRC (eg, preoperative diagnosis of CRC or a long history of IBD involving the colon and rectum) [12,67-69]. (See "Post-treatment surveillance after colorectal cancer treatment" and "Surveillance and management of dysplasia in patients with inflammatory bowel disease".)

DIVERSION POUCHITIS — Diversion pouchitis is a variant of diversion colitis that develops following an ileal pouch-anal anastomosis (IPAA) (eg, patients with ulcerative colitis or familial adenomatous polyposis) (picture 4). The first stage of the IPAA procedure often consists of total proctocolectomy, IPAA, and a diverting loop ileostomy, which is followed by a second-stage procedure (ie, loop ileostomy closure three to six months later) [70,71]. The first-stage of surgery results in temporary diversion of the fecal stream from the ileal pouch reservoir, which can lead to mucosal inflammation. In some patients with an ileal pouch, diversion may be permanent (eg, if they develop pouch failure due to refractory pouchitis or Crohn pouchitis), predisposing these patients to diversion pouchitis [72,73]. The clinical manifestations, diagnosis, evaluation, and management of diversion pouchitis are the same as diversion colitis. (See 'Clinical manifestations' above and 'Evaluation' above and 'Treatment' above.)

DIVERSION MICROSCOPIC ILEITIS — De novo diversion-associated collagenous ileitis in the efferent limb of loop ileostomy for rectosigmoid cancer has been reported [74].

DIVERSION NEOVAGINITIS AFTER SIGMOID VAGINOPLASTY — A segment of colon is being used as pedicled graft in neovaginoplasty to surgically construct a neovagina. The diverted colon segment may become inflamed, with the term "diversion neovaginitis." The etiopathogenesis of diversion neovaginitis may be similar to that in diversion proctocolitis or diversion pouchitis. Patients with an inflamed neovagina may present discharge and malodor and a loss of vascular pattern, edema, granularity, friability, erythema, and stiffness on endoscopy [75]. Short-chain fatty acid enema has been used to treat this condition [76].

PROGNOSIS OF DIVERSION COLITIS, PROCTITIS, AND POUCHITIS — Proximal fecal diversion with ileostomy or colostomy remains a valid therapeutic modality for refractory disease in downstream bowel or perianal area, or for protection of anastomosis in the distal bowel. The fecal diversion can be temporary or permanent. For patients with temporary ileostomy or colostomy, the ultimate treatment for their diversion colitis, proctitis, or pouchitis is surgical reestablishment of bowel continuity. However, not all patients with temporary fecal diversion are able to have stoma closure. This is particularly true in patients with Crohn disease. In a study of 138 patients with fecal diversion for severe perianal Crohn disease, 30 (22 percent) achieved stoma closure, 45 (33 percent) kept a stoma with diverted rectum in place, and 63 (45 percent) had to have proctectomy with permanent stoma during a mean follow-up of 5.7 years [77]. The predictors for no-stoma closure surgery were disease involvement of the rectum and presence of setons of perianal disease [77]. In addition, the reestablishment of bowel continuity may not lead to complete resolution of endoscopic and histologic inflammation, even in non-inflammatory bowel disease patients. But clinical significance of residual endoscopic and histologic inflammation is not clear [78]. Nonetheless, the reestablishment of gut continuity was shown to restore anal sphincter function [79].

The majority of patients with permanent stoma who have diverted colon, rectum, or ileal pouch in situ are likely to develop diversion bowel disease anytime and to a certain degree, which often requires topical medical therapy. Long-term fecal diversion may also result in stricture formation in the distal bowel, which may benefit from endoscopic therapy. In one study, the cumulative frequency of diversion-associated strictures in patients with underling inflammatory bowel disease (IBD) was 29 percent [12]. For patients with refractory diversion bowel disorder who are not candidates for stoma closure or those with neoplasia in the diverted bowel, surgical excision of the segment of bowel can be an option. However, completion colectomy, proctectomy, and pouch excision carries a risk for anal stump leak or abscess [80]. Therefore, management strategy of diversion bowel disorders should be based on the short- and long-term goal of fecal diversion and balance the risks and benefits of medical, endoscopic, and surgical therapies. It is not clear whether the presence of endoscopic or histologic inflammation increases the risk for the development of stricture or neoplasia. There is also a lack of consensus on whether asymptomatic patients with endoscopic and/or histologic inflammation need to be treated to prevent these complications. Nonetheless, the presence of inflammation of the diverted bowel in the patients at risk for the development of neoplasia, such as those with long-standing IBD or those with a history of colorectal neoplasia, warrant appropriate medical therapy regardless of symptomatology. Endoscopic and/or histologic inflammation may persists in non-IBD patients, even after bowel continuity is restored [78].

SUMMARY AND RECOMMENDATIONS

●Diversion colitis is an inflammatory process that occurs in segments of the colorectum that are diverted from the fecal stream by surgery. (See 'Definition' above.)

●Patients with diversion colitis have usually undergone a loop or end colostomy/ileostomy with closure of the distal colon segment (eg, Hartmann’s procedure). Diversion of the fecal stream results in a deficiency of short-chain fatty acids (SCFAs), along with other luminal nutrients needed by colonocytes in the diverted segment. It is hypothesized that the lack of these compounds or interference with their metabolism by alterations in gut flora may have a role in the development of colitis. However, the inconsistent response of patients to SCFAs and the almost uniform response to restoration of fecal continuity suggest that other factors are involved in the pathogenesis of diversion colitis. (See 'Etiology and pathogenesis' above.)

●Most patients with histologically evident diversion colitis are asymptomatic. The most common symptoms in adults are tenesmus, urgency, bloody and/or mucus discharge, and abdominal pain. Symptoms are mild in up to 50 percent of patients. In rare cases, patients have severe bleeding that requires blood transfusion, diarrhea, or sepsis from deep ulceration. Persistent inflammation and long-term non-use may result in mild to severe stricture of the diverted bowel, especially in the diverted ileal pouch. In addition, accumulation of mucus materials may cause the formation of a bezoar. The stricture can cause symptoms of abdominal or pelvic pain and discomfort, and sensation of incomplete evacuation. (See 'Clinical manifestations' above.)

●Diversion colitis should be considered in an individual with or without preexisting inflammatory bowel disease who complains of cramping abdominal pain with a mucoid or bloody discharge from the defunctionalized, bypassed distal colon. Since the clinical manifestations of diversion colitis are nonspecific, the diagnosis requires exclusion of other disorders by history, laboratory studies, and colonoscopy with biopsy. (See 'Evaluation' above and 'Diagnosis' above and 'Differential diagnosis' above.)

●In patients with symptomatic diversion colitis in whom restoration of intestinal continuity is feasible, we suggest reanastomosis as soon as possible after diversion (Grade 2C). (See 'Surgical reanastomosis' above.)

●For symptomatic patients who are not candidates for reanastomosis, we suggest a trial of SCFA enemas (Grade 2C). For patients who do not respond to a trial of SCFA enemas, we suggest the addition and/or substitution with topical 5-aminosalicylic acid (ASA) (Grade 2C). In patients who fail to respond completely to SCFA and/or topical 5-ASA agents, we use topical glucocorticoids. Topical glucocorticoids may be particularly useful in patients with underlying IBD. However, long-term use should be avoided to avoid glucocorticoid side effects. (See '5-aminosalicylic acid (5-ASA)' above.)

●The risk for the development of dysplasia or colorectal cancer (CRC) in the diverted colorectum in patients without a history of CRC or underlying inflammatory bowel disease (IBD) is low. We therefore do not perform routine CRC surveillance in the diverted segment unless the underlying condition for which the surgery was performed is associated with an increased risk of cancer (eg, preoperative diagnosis of CRC, the presence of primary sclerosing cholangitis, or a long history of IBD involving distal colon). (See 'Cancer surveillance' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Dr. Richard I. Breuer, who contributed to an earlier version of this topic review.