Complications
Fulminant or severe colitis is seen in up to 15% of patients.[131]
The overall lifetime incidence of toxic megacolon in patients with UC is 1% to 2.5%, which carries with it the risks of perforation and death.[132]
Treatment is with supportive care, bowel rest, and broad-spectrum antibiotics.
Colectomy is indicated if the patient does not respond within 24 to 48 hours.
Perforation with peritonitis has been associated with 50% mortality in patients with UC.
Cytomegalovirus (CMV) and Clostridium difficile may complicate UC. Cowdry inclusions seen on biopsies are typical of CMV colitis.
Treatment of CMV is with systemic therapy with ganciclovir, valganciclovir, foscarnet, or cidofovir for 4 to 6 weeks.
Massive hemorrhage occurs in up to 3% of patients.
Treatment is with supportive care and blood transfusion. Urgent colectomy may be necessary.
Develops in 3% to 5% of patients with UC. The risk increases with the duration of disease. Risk increases with younger age at onset, longer duration of disease, presence of primary sclerosing cholangitis, and greater extent of colonic involvement.
Patients with longstanding colitis have a 5-fold to 10-fold higher risk of colorectal cancer than age-matched controls.
Studies report that the incidence of colorectal cancer in colitis is falling.[133][134] This might be a result of more rigorous adherence to maintenance mesalamine. Agents shown to be protective include cyclooxygenase 2 inhibitors and ursodeoxycholic acid (ursodiol) in UC patients with primary sclerosing cholangitis. The 5-aminosalicylate (5-ASA) compounds have been reported to reduce the risk as well.[135][136][137]
These strictures can rarely cause intestinal obstruction.
These pseudopolyps are irregularly shaped islands of residual intact colonic mucosa that are the result of the mucosal ulceration and regeneration.
The polyps are typically multiple and scattered throughout the colitic region of the colon. They can be recognized by their histologic features. A biopsy can help make the diagnosis.
They are not dysplastic and are not a risk factor for colon cancer. However, their presence can complicate the recognition of true adenomas and a dysplasia-associated lesion or mass.
PSC is a chronic progressive disorder of unknown etiology that is characterized by inflammation, fibrosis, and stricturing of medium-sized and large ducts in the intrahepatic and extrahepatic biliary tree.
Between 3% and 7% of UC patients develop PSC.[139]
More than 70% of patients with PSC have underlying UC.[140]
Liver tests should be checked yearly and PSC considered in patients with abnormal results.
Some patients with UC who have dysplasia associated with a nonadenoma-like DALM may have an underlying invasive carcinoma. This may not be detectable by endoscopic biopsy and warrants colectomy (60% on surgical specimens).
Some clinical, histologic, and molecular features have been studied to help make this distinction. Patients with nonadenoma-like DALM: are more likely to be younger and have a longer duration of disease, more extensive disease, and larger lesions (1.8 versus 0.5 cm in 1 study); have lesions that appear endoscopically as adenomas (pedunculated or sessile) rather than having other characteristics (e.g., flat, ulcerated, or plaque-like appearance); and have a favorable prognosis with endoscopic removal and close follow-up.[138]
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