The classic procedure for ulcerative colitis is IPAA, where all the colorectum is removed and a storage pouch is made from the terminal small intestine and anastomosed to the anal canal. The procedure usually takes 2-3 stages to complete, and the temporary stoma is usually in place for 3-6 months. Since the anal sphincter is preserved, the patient can control bowel movements. There may be 10 bowel movements in the immediate postoperative period, which can then be reduced to 6 during the day and 1-2 at night, and anti-defecation medication can be taken to adjust the frequency of bowel movements. Because IPAA removes all of the colon, most patients do not require postoperative ulcer-related medications and the risk of colon cancer is greatly reduced. the vast majority (95%) of patients have a very good quality of life after IPAA. The most common postoperative complication in patients is storage pouchitis, which presents as abdominal pain and diarrhea, with an incidence of about 40%. These patients are usually treated with antibiotics and most of them may resolve, but about 20% develop chronic pouchitis, requiring several repeated doses of medication. The pathogenesis of pouchitis remains unclear and may be related to the NOD2/CARD15 gene, total colon type ulceration, inverted ileitis, primary sclerosing cholangitis, p-ANCA+, chronic ischemia, and NSAID use. Most patients after IPAA can develop chronic reservoir pouch inflammation regardless of symptoms, which manifests as twisted villi and mucosal hyperplasia of the colon. Clinical manifestations of pouch inflammation include increased stool volume, bleeding, etc. Fecal incontinence, systemic symptoms, and dehydration may also occur. Extra-intestinal manifestations such as skin diseases and rheumatic diseases are rare. Pouchitis can be acute (<4 weeks), or chronic (>4 weeks). Most acute patients do not progress to chronicity, but 60% of patients have at least one recurrence. Recent postoperative acute pouchitis has a high probability of becoming chronic. 15C19% of acute pouchitis will become chronic refractory pouchitis. However, the chances of heterogeneous growth and carcinoma of the pouch are low, with a 25-year incidence of 5% reported in the literature. Secondary pouch infections include Clostridium difficile infection, IgG4-associated, autoimmune, CD-associated, NSAID use, and structural abnormalities of the pouch. Endoscopic and pathological examination is important, with endoscopic manifestations of brittle tissue, erythema, inflammatory exudate, and erosive ulceration; and histological manifestations of acute inflammation (centrilobular infiltration, crypt abscess, mucosal ulceration) or chronic inflammation (blunted mucosa, crypt distortion/proliferation, chronic inflammatory cell infiltration, pyloric adenoid hyperplasia, etc.). Usually the first-line treatment is 14 days of ciprofloxacin, and if this does not work metronidazole or rifaximin can be used, or even an additional 4-week course. Some literature suggests that probiotics may reduce the incidence and recurrence of postoperative reservoir pouchitis. Patients who relapse from antibiotic withdrawal may be treated with topical mesalachin, hydrocortisone or budesonide enemas, and those who remain ineffective may be treated with oral budesonide or hormones. In contrast, immunomodulators and biologics are generally used in patients who have failed 8 weeks of oral hormone therapy or in patients with CD-associated storage pouchitis. Ultimately all medications are ineffective only in patients with surgical removal of the reservoir pouch and permanent stoma, which is generally <5% of patients.