INTRODUCTION — Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) is performed for treating patients with ulcerative colitis (UC) or familial adenomatous polyposis (FAP). However, patients with IPAA are at risk for pouchitis, an inflammatory disorder that typically presents with increased stool frequency and urgency and is a common complication of IPAA or a continent ileostomy (eg, Kock pouch).

The focus of this topic is management of acute pouchitis and chronic pouchitis. The epidemiology, pathogenesis, clinical manifestations, and diagnosis of pouchitis are discussed in detail, separately. (See "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis".)

Surgical management of UC is discussed separately. (See "Surgical management of ulcerative colitis".)

Management of FAP is discussed separately. (See "Familial adenomatous polyposis: Screening and management of patients and families".)

Surgical complications and outcomes associated with proctocolectomy and IPAA are discussed separately. (See "Restorative proctocolectomy with ileal pouch-anal anastomosis: Laparoscopic approach".)

SPECTRUM OF DISEASE — Pouchitis has been classified based on several disease characteristics including the duration of symptoms, response to antibiotics, frequency of flares, etiology, and disease activity. Many patients with ileal pouches have some degree of endoscopic inflammation of the ileal pouch reservoir, and pouchitis likely represents a disease spectrum with a range of presentations that may evolve over time. As an example, acute antibiotic-responsive pouchitis may evolve into chronic antibiotic-refractory pouchitis. (See "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Spectrum of disease'.)

TREATMENT GOALS — The goal of pouchitis therapy is to alleviate symptoms and achieve clinical and endoscopic remission by demonstrating mucosal healing. Histologic improvement (ie, resolution of acute inflammatory cell infiltrate) is emerging as an additional component of disease remission [1,2].

Assessing treatment response for patients with pouchitis includes recognizing that the normal stool pattern for patients with an ileal pouch is four to seven formed stools daily without seepage, and typically without nocturnal bowel movements.

Endoscopic healing is an important goal of therapy because symptoms alone may not reflect the inflammatory status of the pouch [1,3-5]. However, the definition of mucosal healing varies among clinical studies. For example, endoscopic mucosal healing has been defined as completely normal mucosa [6], the absence of erosions or ulcers [7], or Pouchitis Disease Activity Index (PDAI) endoscopy subscores of 0 or 1 as well as no ulcers [8]. The PDAI and other scoring systems are described separately. (See "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Scoring systems for assessing disease activity'.)

PRIMARY PREVENTION — For primary prevention of pouchitis and to promote optimal pouch function, patients with an ileal pouch are advised to:

●Avoid nonsteroidal anti-inflammatory drugs (NSAIDs), because NSAIDs are associated with increased risk for chronic pouchitis [9].

●Maintain ideal body weight, because weight gain is a risk factor for pouch failure, and this is discussed separately (see "Restorative proctocolectomy with ileal pouch-anal anastomosis: Laparoscopic approach", section on 'Risk factors for pouch failure').

We do not routinely use probiotics or other pharmacologic agents for primary prevention of acute pouchitis. Studies on probiotics for primary prevention of acute pouchitis after pouch construction are uncertain and are limited by small trials [10]. Probiotics are organisms belonging to the gut flora that may have health benefits. Probiotics that have been studied for pouchitis include VSL#3 (Lactobacillus spp, Bifidobacterium spp, Streptococcus salivarius spp, and Thermophilus spp) and other composite agents; however, probiotics are used for secondary prevention of active pouchitis [11,12]. (See "Probiotics for gastrointestinal diseases", section on 'Pouchitis' and 'Maintenance therapy' below.)

ACUTE IDIOPATHIC POUCHITIS

General measures — Patients with acute idiopathic pouchitis have endoscopic evidence of active pouch inflammation without a clear cause based on histology, stool studies, and blood tests, and the following measures apply to such patients (algorithm 1) (see "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Evaluation'):

●Avoid nonsteroidal anti-inflammatory drugs (NSAIDs) – We advise patients with pouchitis to avoid NSAIDs, because NSAIDs are associated with increased risk for chronic pouchitis [9].

●Dietary adjustments – The author advises patients with normal pouches or active pouchitis to adhere to a diet that is low in poorly digested carbohydrates and low in fiber, as fermentation of dietary carbohydrates or fiber by small intestinal bacterial overgrowth in the pouch can cause increased stool frequency and bloating. Of note, dietary modification is used for symptomatic relief, rather than healing of pouch inflammation. The dietary approach is similar to the low fermentable oligo-, di-, monosaccharides and polyols diet. (See "Treatment of irritable bowel syndrome in adults", section on 'Dietary modification'.)

●Specialty consultation – We suggest that patients with pouchitis are referred to an inflammatory bowel disease center or pouch clinic for long-term management.

Initial therapy — First-line therapy for acute pouchitis consists of an oral antibiotic for two weeks (ciprofloxacin 500 mg every 12 hours). Alternatives to ciprofloxacin for initial therapy include metronidazole 500 mg every 12 hours or tinidazole 500 mg every 12 hours.

Selecting initial therapy for acute idiopathic pouchitis has been guided by clinical experience and few small trials [10,13,14]. In a systematic review that included one trial of 16 patients with acute pouchitis, ciprofloxacin resulted in higher rates of remission after two weeks compared with metronidazole (100 versus 33 percent, risk ratio 2.68 [95% CI 1.13 to 6.35]) [10,13]. In addition, patients treated with ciprofloxacin had lower rates of adverse events (eg, vomiting, dysgeusia, peripheral neuropathy) (0 versus 33 percent). We consider tinidazole to be a reasonable alternative to ciprofloxacin, based on the author's experience and limited indirect data [14].

The use of antibiotic therapy has been supported by studies that have linked intestinal microbiota to the development of pouchitis. (See "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Intestinal microbiota'.)

Most patients with acute pouchitis have symptomatic improvement (eg, improved stool frequency, no urgency) within three days after the initiating antibiotic therapy [13,15].

Patients who respond to initial treatment but have frequent relapses (≥3 episodes per year) are described as having antibiotic-dependent chronic pouchitis. For such patients, we suggest maintenance therapy with a probiotic. (See 'Managing relapse' below.)

Subsequent management — For patients with acute pouchitis who do not respond to initial antibiotic treatment, we perform stool culture and susceptibility testing of bacterial flora and select a single active antibiotic based on those results for a four-week course [16,17]. If such testing is not available, we give four weeks of dual oral antibiotic therapy consisting of ciprofloxacin (500 mg every 12 hours) combined with metronidazole (500 mg every 12 hours) or tinidazole (500 mg every 12 hours) or rifaximin (550 mg every 12 hours).

For patients who respond to ≥4 weeks of antibiotic therapy (based on susceptibility testing of bacterial flora or empiric treatment), we give maintenance therapy to prevent relapse, similar to the approach for patients with antibiotic-dependent chronic pouchitis. (See 'Managing relapse' below.)

For patients with persistent symptoms despite ≥4 weeks of antibiotic therapy, we reassess the patient before proceeding with additional treatment options. (See 'Managing nonresponders' below.)

Dual antibiotic therapy has been associated with symptomatic and endoscopic improvement in patients with pouchitis. In four observational studies including a total of 86 patients with patients with active pouchitis, dual antibiotic therapy (ciprofloxacin plus tinidazole or rifaximin or metronidazole) was associated with clinical response or remission in 73 patients (85 percent) [16,18-20].

Assessing response — For patients with acute idiopathic pouchitis, response to antibiotic therapy is typically assessed clinically (symptomatic improvement) and endoscopically (pouchoscopy with biopsy) after completing therapy. While endoscopic mucosal healing may lag behind symptomatic improvement, mucosal healing is a treatment target for patients with pouchitis [6].

MANAGING RELAPSE

Patients with infrequent relapse — For patients with acute pouchitis who have a clinical relapse of pouchitis after achieving remission with <4 weeks of antibiotic therapy, we begin another course of antibiotic monotherapy for two weeks. When treating relapse, the single antibiotic agent that was effective initially may be used again. (See 'Initial therapy' above.)  

For patients who have infrequent relapses (ie, <3 episodes of acute pouchitis per year), we do not use maintenance therapy.

Patients with frequent relapse — Patients with acute pouchitis who respond initially to antibiotic therapy (ie, <4 weeks) but who relapse ≥3 times per year are given long-term maintenance therapy, typically with a probiotic. (See 'Maintenance therapy' below.)

Patients who develop symptoms of active pouchitis while on maintenance therapy are reassessed before proceeding with additional treatment options. (See 'Managing nonresponders' below.)

Maintenance therapy — For patients with pouchitis who respond initially to antibiotic therapy but who relapse ≥3 times per year or who required ≥4 weeks of antibiotic therapy (dual or monotherapy) initially, we typically use maintenance therapy with a probiotic. Initial maintenance therapy consists of the probiotic VSL#3 (Lactobacillus spp, Bifidobacterium spp, Streptococcus salivarius spp, and Thermophilus spp; 6 to 9 g daily) with the rationale that changes in the microflora have been demonstrated in patients with pouchitis [21,22].

Data supporting the use of VSL#3 for maintaining remission are mixed [23-26]. In a trial including 40 patients with chronic pouchitis, maintenance therapy with VSL#3 (6 g daily) resulted in lower relapse rates after nine months compared with placebo (15 versus 100 percent) [23]. However, in open-label studies, the response rate to VSL#3 was lower than that reported in randomized trials and the discontinuation rate was high [24,26]. In a study of 31 patients with antibiotic-dependent pouchitis who received VSL#3 as maintenance therapy, 25 patients (81 percent) discontinued the probiotic at eight months due to lack of efficacy or the development of adverse effects [24]. It is unclear if these conflicting results are due to differences in study population characteristics, inclusion criteria, induction therapy with antibiotics, and/or the composition and dosage of the probiotic agents.

An alternative to chronic probiotic therapy for maintenance is a nonabsorbable antibiotic or low-dose systemic antibiotic; however, risk of adverse effects, antibiotic resistance, and cost are limitations of this strategy. We do not routinely use antibiotic therapy for long-term maintenance therapy (ie, >3 months). Options for maintenance therapy include rifaximin (in doses ranging from 200 mg once daily to 600 mg every eight hours) and low-dose ciprofloxacin (250 to 500 mg daily) [24]. Rifaximin, a nonabsorbable antibiotic, has the advantage of a favorable safety profile; however, its long-term use may be limited by cost. Adverse effects of ciprofloxacin and other fluoroquinolones (eg, risk of tendinopathy, Clostridioides difficile infection, aortic dissection) are discussed separately. (See "Fluoroquinolones", section on 'Adverse effects'.)

Data on efficacy of antibiotic maintenance therapy for chronic pouchitis are limited to small observational studies [24,27,28]. As an example, in a case series including 39 patients with chronic antibiotic-dependent pouchitis who had been maintained on antibiotics for at least one year, symptomatic remission was achieved by eight patients (21 percent) over a mean duration of six years [28]. Adverse effects from long-term antibiotic use (ie, ciprofloxacin, metronidazole) developed in 11 patients (28 percent).

Some patients continue to have frequent episodes of acute pouchitis despite maintenance therapy with probiotics or antibiotics, and such patients have developed chronic antibiotic-refractory pouchitis. (See 'Managing nonresponders' below.)

MANAGING NONRESPONDERS

Pretreatment evaluation — Patients with pouchitis who do not have symptomatic improvement despite at least four weeks of antibiotic therapy are regarding as having chronic antibiotic-refractory pouchitis (CARP). Therapy for CARP is guided by pretreatment evaluation that includes (see "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis" and 'Special populations' below):

●Pouchoscopy with biopsy to reassess mucosal healing of the pouch following antibiotic therapy and to exclude infection (eg, cytomegalovirus)

●Laboratory testing to confirm that secondary causes and coexisting conditions have been excluded (eg, infection, primary sclerosing cholangitis [PSC]). Blood tests include aspartate aminotransferase, alanine aminotransferase, total bilirubin, alkaline phosphatase, celiac disease serology, antinuclear antibody, immunoglobulin G4 level, and stool specimen for Clostridioides difficile is also obtained. (See "Diagnosis of celiac disease in adults", section on 'Serologic evaluation'.)

Patients with elevated liver biochemical tests in a cholestatic pattern (predominantly elevated alkaline phosphatase) are evaluated for primary sclerosing cholangitis with liver ultrasound or magnetic resonance cholangiopancreatography, and the diagnosis of PSC is discussed separately. (See "Primary sclerosing cholangitis in adults: Clinical manifestations and diagnosis".)

Immune-mediated chronic pouchitis — Patients with CARP who do not have PSC, IgG4 disease, or a secondary cause for inflammatory changes of the pouch (eg, infection, ischemia, Crohn disease), are managed as immune-mediated CARP. (See "Pouchitis: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Differential diagnosis'.)

The management approach for patients with CARP is generally similar to management of ulcerative colitis. (See "Medical management of low-risk adult patients with mild to moderate ulcerative colitis".)

Initial therapy — Initial therapy for immune-mediated CARP is topical (rectal) mesalamine for four weeks [29,30]. Mesalamine is widely available in two forms: suppository or enema (table 1). We typically use mesalamine suppository 1 g once daily or mesalamine enema 4 grams once daily, and the dosing is similar to that used for patients with ulcerative proctitis. For patients without symptomatic relief (ie, decreased stool frequency) after two weeks of topical (rectal) mesalamine, we add oral mesalamine and continue topical mesalamine daily. We typically use oral mesalamine (ie, 2.4 to 4.8 g daily) for two to four weeks.

The use of mesalamine for chronic pouchitis has been supported by limited direct data and the author's experience. In an observational cohort of 10 patients with refractory pouchitis, oral or topical mesalamine was associated with clinical remission rates of 50 percent [16].

For patients with chronic pouchitis and coexisting arthritis, an alternative to oral mesalamine is sulfasalazine (2 to 4 g daily) and folic acid (1 mg daily) [31,32]. Adverse effects of mesalamine and sulfasalazine and treatment of arthritis associated with inflammatory bowel disease are discussed separately. (See "Treatment of arthritis associated with inflammatory bowel disease" and "Sulfasalazine and 5-aminosalicylates in the treatment of inflammatory bowel disease".)

Subsequent therapy — For patients who do not have symptomatic improvement after four weeks of topical (rectal) and oral mesalamine therapy, subsequent options include (table 1):

●Begin topical (rectal) hydrocortisone (suppository, foam, enema) once daily for two weeks.

●Begin topical (rectal) budesonide (eg, foam, 2 mg per application) once daily for two weeks [33,34].

●Begin oral budesonide (9 mg daily for eight weeks). Oral budesonide is typically used for patients who have not improved with topical mesalamine, oral mesalamine, and topical glucocorticoids. The dosing and pharmacology of budesonide is discussed separately. (See "Overview of budesonide therapy for adults with inflammatory bowel disease".)

An alternative to oral budesonide is oral beclomethasone dipropionate (10 mg daily for eight weeks), but oral beclomethasone dipropionate is not widely available [35,36].

For example, for patients on mesalamine therapy who have some symptomatic improvement but without symptom resolution, we typically add a topical glucocorticoid or oral budesonide while continuing mesalamine.

For patients who do not improve with mesalamine or glucocorticoids or who develop recurrent symptoms upon drug discontinuation, other options include biologic therapy. (See 'Other options' below.)

The use of topical and oral glucocorticoids for patients with antibiotic-refractory pouchitis is based on limited published data and the author's experience [33-35,37]. In an observational study of 20 patients with antibiotic-refractory pouchitis who were treated with oral budesonide, 15 patients (75 percent) achieved clinical remission based on Pouchitis Disease Activity Index (PDAI) score after eight weeks [37].

Other options — For patients with immune-mediated chronic pouchitis who fail mesalamine and glucocorticoid therapy, we begin biologic therapy and typically use vedolizumab as first-line therapy, followed by ustekinumab as the second choice (because of their efficacy and side effect profiles) [38,39]. We reserve anti-tumor necrosis factor (TNF) agents (eg, infliximab, adalimumab) for patients who fail vedolizumab and ustekinumab. The pretreatment evaluation, dosing, and administration of these agents for patients with chronic pouchitis are similar to the approach for patients with ulcerative colitis (UC), and this is discussed in more detail separately. (See "Overview of dosing and monitoring of biologic agents and small molecules for treating ulcerative colitis in adults" and "Management of moderate to severe ulcerative colitis in adults", section on 'Ustekinumab'.)

Most data on biologic agents for chronic pouchitis are based on small observational studies:

●Vedolizumab – Vedolizumab, a gut-selective anti-integrin agent, has been associated with symptom and endoscopic improvement in chronic pouchitis [6,39]. In a systematic review of seven studies including 44 patients with chronic pouchitis who were treated with vedolizumab, 33 patients (75 percent) had symptomatic improvement at 12 weeks, and 28 of 38 patients (74 percent) had endoscopic improvement at six months [39].

●Ustekinumab – Ustekinumab, an anti-interleukin 12/23 antibody has been used for chronic pouchitis [7,38,40]. In an observational study including 24 patients with CARP with a median follow-up time of 13 months, 12 patients (50 percent) had symptomatic response and four of nine patients (44 percent) had endoscopic improvement [38].

●Anti-TNF agents – The use of anti-TNF agents for chronic pouchitis may be limited by pre-colectomy exposure to the drug [41-46]. In a study including 23 patients with chronic pouchitis who were treated with infliximab, 10 patients (44 percent) achieved clinical remission at 14 weeks of therapy [41]. Adverse events associated with infliximab (eg, infusion reactions, hypersensitivity) led to discontinuation of the drug in nine patients (39 percent), possibly due to immunogenicity in patients with prior exposure to anti-TNF agents. In a cohort of 13 patients with chronic pouchitis who were treated with adalimumab, five patients (39 percent) achieved clinical remission at 14 weeks [41].

Patients with chronic pouchitis who fail medical therapy and whose quality of life is significantly compromised may be referred to a colorectal surgeon for consideration of surgical intervention (eg, fecal diversion with ileostomy). Risk of pouch failure is discussed separately. (See "Restorative proctocolectomy with ileal pouch-anal anastomosis: Laparoscopic approach" and "Surgical management of ulcerative colitis", section on 'Surgical complications'.)  

Investigational therapies — Therapies that have been studied for treating CARP but remain investigational include:

●Tofacitinib – Several case reports have shown that the small molecule tofacitinib was effective for treating patients with CARP who have failed anti-TNF agents, anti-interleukin agents, or anti-integrin agents [47,48]. Tofacitinib therapy for patients with UC is discussed separately. (See "Management of moderate to severe ulcerative colitis in adults", section on 'Tofacitinib'.)

●Intravenous immunoglobulin – In a small case series of 16 patients with refractory pouchitis, intravenous immunoglobulin infusion was associated with clinical and endoscopic improvement as measured by the modified Pouchitis Disease Activity Index (PDAI) [49].

●Topical alicaforsen – Topical application of alicaforsen has been associated with clinical improvement for some patients with CARP [50,51]. In an observational study including 12 patients with CARP, treatment with alicaforsen enema for six weeks was associated with clinical improvement as measured by reduction in PDAI score [51]. Alicaforsen is an antisense inhibitor of intercellular adhesion molecule-1 oligonucleotide.

●Topical tacrolimus – In an observational study of 10 patients with antibiotic-refractory pouchitis, topical tacrolimus for eight weeks was shown to reduce symptom, endoscopy, and histology scores [52].

●Therapies of no or uncertain benefit – Fecal microbiota transplantation (FMT) has been studied for treating non-Clostridioides difficile infection; however efficacy has not been established [53-57]. The use of FMT for treating Clostridioides difficile infection is discussed separately. (See "Fecal microbiota transplantation for treatment of Clostridioides difficile infection".)

Butyrate and glutamine suppositories [58] and bismuth carbomer foam [59] have been studied for treating chronic pouchitis but their efficacy has not been established.

SPECIAL POPULATIONS

PSC-associated chronic pouchitis — Patients with an ileal pouch and underlying primary sclerosing cholangitis (PSC) are at higher risk for CARP, and patients with PSC-associated chronic pouchitis are generally managed with therapies that target the resolution of mucosal inflammation in both the pouch body and afferent limb. The diagnosis of PSC is discussed in more detail separately. (See "Primary sclerosing cholangitis in adults: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

Patients with ileal pouch and coexisting PSC commonly have endoscopic and/or histologic inflammation of the pouch body, afferent limb, and cuff [60]. The author has also observed that patients often have mild symptoms in the presence of marked pouch inflammation and a long segment of enteritis (>10 cm). On endoscopy, the pouch inlet shows a patulous appearance. Patients with PSC-associated pouchitis are typically given antibiotic therapy initially, while oral mesalamine is an alternative option. (See 'Acute idiopathic pouchitis' above and 'Immune-mediated chronic pouchitis' above.).

For patients with PSC who do not respond to initial therapy, we typically use an eight-week course of oral budesonide (9 mg daily) or budesonide enema or foam daily [33,61]. Because symptomatic and endoscopic relapse is common, patients who respond to oral budesonide may require maintenance therapy with the same agent at a lower dose (eg, oral budesonide 3 mg daily). Dosing and adverse effects of budesonide are discussed separately. (See "Overview of budesonide therapy for adults with inflammatory bowel disease", section on 'Dosing'.)

For some patients who fail budesonide, the author has observed that oral vancomycin (500 to 1000 mg daily) may be beneficial for treating both pouchitis and enteritis [62,63].

For patients who achieved clinical remission with glucocorticoids, an alternative approach for maintenance therapy is to use an immunomodulator (eg, oral 6-mercaptopurine [6-MP] 25 to 50 mg daily or methotrexate 7.5 to 12.5 mg subcutaneously weekly). Pretreatment evaluation, dosing and monitoring for immunomodulators are discussed separately. (See "Overview of azathioprine and mercaptopurine use in inflammatory bowel disease" and "Major side effects of low-dose methotrexate".)

IgG4-associated chronic pouchitis — Patients with immunoglobulin G4-related pouchitis are at higher risk for antibiotic-refractory pouchitis, and such patients are primarily managed with therapies that target mucosal inflammation [64,65]. (See "Treatment and prognosis of IgG4-related disease".)

Initial therapy is typically oral budesonide (9 mg daily) for eight weeks [66]. (See "Overview of budesonide therapy for adults with inflammatory bowel disease".)

For patients who fail budesonide or who relapse with discontinuation, other options include low dose immunomodulator (eg, 6-MP 50 mg daily). Pretreatment evaluation, dosing and monitoring for immunomodulators are discussed separately. (See "Overview of azathioprine and mercaptopurine use in inflammatory bowel disease".)

Patients with coexisting prepouch enteritis — For patients with pouchitis and coexisting prepouch enteritis (≥10 cm), we begin with oral budesonide, 9 mg daily for eight weeks, followed by 3 mg daily for maintenance therapy. Pharmacology and safety of budesonide for patients with inflammatory bowel disease is discussed separately. (See "Overview of budesonide therapy for adults with inflammatory bowel disease".)

An alternative to oral budesonide is oral mesalamine (2 to 4 g daily) or mesalamine enemas daily (table 1). Biologic agents have been studied, but failed to achieve remission in most patients [67].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pouchitis".)

SUMMARY AND RECOMMENDATIONS

●Pouchitis is an inflammatory condition of the ileal pouch reservoir of an ileal pouch-anal anastomosis. Pouchitis has been classified based on disease characteristics such as the duration of symptoms, response to antibiotics, frequency of flares, etiology, and disease activity. Most patients with an ileal pouch have some degree of endoscopic or histologic inflammation, and pouchitis likely represents a disease spectrum with a range of presentations that may evolve over time. (See 'Spectrum of disease' above.)

●Goals of therapy for patients with acute pouchitis are to alleviate symptoms and to achieve clinical and endoscopic remission by demonstrating mucosal healing. Histologic improvement (ie, resolution of acute inflammatory cell infiltrate) is emerging as an additional component of disease remission. Assessing treatment response for patients with pouchitis includes recognizing that the normal stool pattern is typically four to seven formed stools daily without seepage. (See 'Treatment goals' above.)

●For patients with acute idiopathic pouchitis, we suggest initial therapy with ciprofloxacin rather than other antibiotics or observation (Grade 2C). We typically use ciprofloxacin 500 mg every 12 hours for two weeks, while alternatives to ciprofloxacin include metronidazole or tinidazole since these agents have also been associated with symptomatic improvement (algorithm 1). (See 'Initial therapy' above.)

●For patients with acute idiopathic pouchitis who do not respond to initial antibiotic treatment, we perform stool culture and susceptibility testing of bacterial flora and select a single active antibiotic based on those results for a four-week course. If such testing is not available, we suggest empiric, dual antibiotic therapy rather than antibiotic monotherapy (Grade 2C). We typically use ciprofloxacin combined with metronidazole or tinidazole or rifaximin for four weeks. (See 'Subsequent management' above.)

●For patients with pouchitis who respond to antibiotic therapy but who relapse ≥3 times per year or who required ≥4 weeks of antibiotic therapy to achieve remission, we suggest maintenance probiotic therapy rather than no maintenance or chronic antibiotic therapy (Grade 2C). We typically use the probiotic VSL#3; however, chronic antibiotic therapy (eg, rifaximin daily) is an alternative option. (See 'Managing relapse' above and "Probiotics for gastrointestinal diseases".)

●Patients with pouchitis who do not have symptomatic improvement despite at least four weeks of antibiotic therapy are regarded as having chronic antibiotic-refractory pouchitis. After confirming that secondary causes of pouchitis have been excluded, we suggest initial management with topical (rectal) mesalamine rather than further antibiotics (Grade 2C). If there is no symptomatic improvement in two weeks, we add oral mesalamine. For patients who fail topical or oral mesalamine, subsequent options include topical or oral glucocorticoids (eg, budesonide) or a biologic agent. (See 'Managing nonresponders' above.)

●The approach to surveillance for patients with inflammatory bowel disease including those with an ileal pouch is discussed separately. (See "Surveillance and management of dysplasia in patients with inflammatory bowel disease".)

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

We are saddened by the death of Paul Rutgeerts, MD, who passed away in September 2020. The UpToDate editorial staff acknowledges Dr. Rutgeerts' work as our Section Editor for Gastroenterology.