INTRODUCTION

Patients with medically refractory ulcerative colitis (UC) or colitis-associated neoplasia most likely require colectomy, as do those with familial adenomatous polyposis (FAP). Restorative proctocolectomy (RPC) and ileal pouch-anal anastomosis (IPAA) are the preferred surgical treatment due to the maintenance of the natural route of defecation. While RPC and IPAA significantly improve patients’ health-related quality of life, structural, inflammatory, functional, neoplastic, or metabolic adverse sequelae can occur, compromising short- or long-term surgical outcomes. Pouchitis is the most common long-term complication of IPAA. Earlier studies consistently showed that pouchitis mainly occurs in patients with underlying UC and is rare in patients with FAP. The exact etiology and pathogenesis of pouchitis are largely unknown. Since the initial acute episodes of pouchitis usually respond to broad-spectrum antibiotics, such as ciprofloxacin and metronidazole, the early hypothesis holds that acute pouchitis results from bacterial etiology. Although certain pathogens (such as Clostridium difficile and cytomegalovirus) may contribute to the pathogenesis in a small number of patients, microbial evaluation in the majority of patients fails to identify gastrointestinal (GI) pathogens. Therefore, pouchitis may be caused by dysbiosis of the commensal gut microbiome. However, microbiome theory alone cannot explain the disease course of chronic antibiotic-dependent pouchitis (CADP) or chronic antibiotic-refractory pouchitis (CARP). The latter two phenotypes of pouchitis often require and respond to induction and maintenance therapy with budesonide and biological agents. Clinical evidence suggests that other factors contribute to the etiology and pathogenetic pathway in pouchitis. Weight gain, accumulation of mesenteric or parapouch fat, ischemia, and autoimmunity play a role in the pathogenesis of CADP and CARP. ^,

The ileal pouch is made from the distal small intestine, which converts the small bowel’s function as an absorptive organ to a reservoir as a storage organ. “Physiolological” fecal stasis of aerobic and anaerobic organisms plays an important role in the maturation of the ileal pouch with colonic metaplasia and associated microbiota profile and immunological reactions. However, excessive fecal stasis can be pathological. An animal model study showed that ileal stasis resulted in increases in both mucosal myeloperoxidase activity and urinary 8-isoprostane levels, suggesting the role of oxidative stress associated with stasis. ^, In fact, fecal stasis-associated pouchitis (FSAP) is a newly described phenotype of pouchitis. Patients with FSAP often present with the clinical course of CADP, that is, symptoms responding to and depending on antibiotic therapy. Patients with FASP may have mild or no endoscopic inflammation and have been diagnosed as having irritable pouch syndrome or small intestinal bacterial overgrowth. In contrast to previous observations and publications, some investigators reported a high frequency of pouchitis in patients with FAP. Investigators from the Mayo Clinic performed a retrospective cohort study of 115 patients with IPAA for FAP and found that 25 patients (22.1%) developed pouchitis (mean time to pouchitis, 4.1 years) with 72% having acute pouchitis and 28% having chronic pouchitis. FAP pouchitis in this study was diagnosed based on the presence of typical pouchitis symptoms (increased frequency and looser consistency of bowel movements compared with baseline, abdominal and/or pelvic cramping, rectal bleeding, urgency, and/or fecal incontinence) and endoscopic inflammation (mucosal edema, granularity, friability, erythema, exudate, erosions, ulcerations, and/or loss of vascular pattern) during at least one symptomatic episode. A Cleveland Clinic study of 250 patients with FAP and IPAA reported that 38 (15.2%) had been labeled as having “pouchitis.” The investigators further evaluated these with “pouchitis” with more stringent clinical, endoscopic, and histologic criteria and found that no patient had nonspecific, acute pouchitis as defined by the criteria. Nine patients initially labeled as having pouchitis had benign ulcers that were common in ileal pouches. Frequent bowel movement was the most common symptom for which patients were labeled as “pouchitis.” Further evaluation showed that actual causes for the frequency included poor pouch emptying, poor eating habits, poor bowel habits, and the presence of afferent limb syndrome (ALS). Therefore, the pathogenesis of FAP-associated pouchitis is likely different from that of UC-associated pouchitis. Structural and functional pouch obstruction may cause FSAP in patients with underlying UC or FAP. Common causes of structural pouch outlet obstructions are anastomotic strictures, distal pouch or cuff inflammatory polyps, and floppy pouch complex (FPC). Bowel narrowing or stricture has been classified into intraluminal (such as blocking bezoars and pedunculated inflammatory polyps), intramural (such as ischemic anastomotic stricture), and extraluminal (such as pouch twist and pouch folding). These structural complications of IPAA can be initially managed by endoscopic therapy. Common etiologies for functional pouch outlet obstruction are dyssynergic defecation and sawtooth pattern. The treatment of structural and/or functional pouch outlet obstruction helps relieve symptoms and endoscopic inflammation of FSAP.

ANATOMIC STRICTURES

Anastomotic stricture is a common form of intramural narrowing of the bowel in patients with IPAA who have handsewn or stapled anastomosis. The etiology of anastomotic stricture can be ischemia, Crohn’s disease (CD), the use of nonsteroidal antiinflammatory drugs (NSAIDs), or distal pouch prolapse or intussusception. Patients with anastomotic strictures often present with abdominal cramps, bloating, urgency, dyschezia, straining, and stool frequency. Further evaluation of frequency and diarrhea may yield the symptoms of incomplete evacuation. Anastomotic stricture is often associated with perianal excoriation of the skin, even perianal fistula, or vaginal fistula. The patients frequently report that their abdominal cramps and bloating improve with antibiotic therapy. The mucosa of the pouch body may show a loss of vascular pattern and excessive exudates ( Fig. 40.1 ). There appears to be an association between the diameter of anastomosis and the risk for pouchitis in a small cohort study. In a rat model of the ileal pouch, the creation of anastomotic stricture increased the intensity of pouchitis and stimulated the production of interleukins.

Anastomotic stricture in ileal pouch-anal anastomosis for familial adenomatous polyposis with fecal stasis. (A) The anastomotic stricture being treated with endoscopic stricturotomy; (B) associated fecal stasis in the pouch lumen before the endoscopic therapy.

In our clinical practice, endoscopic balloon dilation (EBD) and endoscopic stricturotomy (ESt) are routinely performed for the treatment of anastomotic strictures ( Fig. 40.1 ). The author found that for the treatment of stricture, endoscopic therapy, especially ESt, is more effective than digital dilation and safer than bougie dilation. We also noticed that endoscopic treatment of the anastomotic stricture may reduce the use of antibiotics and improve endoscopic and histologic inflammation of the pouch body. In patients with concurrent anastomotic strictures and perianal disease, the endoscopic treatment of stricture helps with perianal symptoms.

LUMEN-BLOCKING POLYPS

Benign lumen-blocking polyps can occasionally be seen in the distal pouch, anastomosis, or cuff, causing mechanical outlet obstruction. While the polyps have generally been classified into inflammatory types resulting from chronic inflammation, ischemia, and mucosal or full-thickness prolapse may also be contributing factors. Any polyps greater than 10 mm should be removed endoscopically for the concern of dysplasia and relief of symptoms of pouch outlet obstruction and anemia. Sometimes, these lumen-blocking inflammatory polyps from prolapse have extensive fibrosis in the stalk ( Fig. 40.2 ). The inflammatory polyps and diffuse pouchitis often coexist. It is possible that chronic inflammation can lead to inflammatory polyps or lumen-blocking inflammatory polyps may contribute to FSAP. The author has used endoscopic needle-knife to remove the polyp. We noticed that endoscopic polypectomy helps dyschezia symptoms, reduces stool frequency, and improves endoscopic inflammation in the pouch body ( Fig. 40.2 ).

Distal pouch polyp and fecal stasis-associated pouchitis. (A) A large pedunculated inflammatory polyp at the distal pouch, blocking the pouch outlet; (B) fecal stasis-associated pouchitis with diffuse mild pouch inflammation and mucosal exudates; (C) the large polyp was removed with endoscopic hot-snare polypectomy.

BEZOARS

Fecal bezoars may form in patients with structural or functional outlet obstruction, further exacerbating fecal stasis-associated pouchitis ( Fig. 40.3 ). A combined treatment of dyssynergic defecation with biofeedback, anastomotic stricture with EBD or stricturotomy, and bezoars with endoscopic basket helps relieve structural and functional pouch outlet obstruction, along with fecal stasis-associated mucosal inflammation. ^,

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