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Nonspecific ulcerative colitis.
Medical expert of the article
Last reviewed: 12.07.2025
Ulcerative colitis is a chronic ulcerative inflammatory disease of the colon mucosa, most often characterized by bloody diarrhea. Extraintestinal symptoms of nonspecific ulcerative colitis, especially arthritis, may be observed. The long-term risk of colon cancer is high. Diagnosis is made by colonoscopy. Treatment of nonspecific ulcerative colitis includes 5-ASA, glucocorticoids, immunomodulators, anticytokines, antibiotics, and sometimes surgery.
What causes ulcerative colitis?
The causes of non-specific ulcerative colitis are unknown. The suspected etiologic factors are infection ( viruses, bacteria ), poor nutrition (low-fiber diet). Many consider the latter factor to be predisposing to the development of the disease.
Ulcerative colitis usually begins in the rectum. The disease may be limited to the rectum (ulcerative proctitis) or progress proximally, sometimes involving the entire colon. Rarely, the entire colon is affected at once.
Inflammation in ulcerative colitis involves the mucous membrane and submucous layer, and a clear boundary is maintained between normal and affected tissue. Only in severe cases is the muscular layer involved. In the early stages, the mucous membrane appears erythematous, finely granulated and friable, with loss of the normal vascular pattern and often with irregular areas of hemorrhage. Large ulcerations of the mucous membrane with abundant purulent exudate characterize the severe course of the disease. Islands of relatively normal or hyperplastic inflamed mucous membrane (pseudopolyps) protrude above the zones of ulcerated mucous membrane. Fistulas and abscesses do not form.
Fulminant colitis occurs when transmural ulceration occurs, causing local ileus and peritonitis. Over a period of hours to days, the colon loses muscle tone and begins to dilate.
Toxic megacolon (or toxic dilation) refers to an emergency in which severe transmural inflammation leads to colonic dilation and sometimes perforation. It most often occurs when the transverse diameter of the colon exceeds 6 cm during an exacerbation. It usually occurs spontaneously during very severe colitis but may be precipitated by opiates or anticholinergic antidiarrheal drugs. Colonic perforation significantly increases mortality.
Symptoms of ulcerative colitis
Bloody diarrhea of varying intensity and duration alternates with asymptomatic intervals. Usually, the exacerbation begins acutely with frequent urge to defecate, moderate cramping pain in the lower abdomen, blood and mucus are found in the stool. Some cases develop after infections (e.g., amebiasis, bacterial dysentery).
If ulceration is limited to the rectosigmoid region, the stool may be normal, firm, and dry, but between bowel movements, mucus mixed with red and white blood cells may be released from the rectum. General symptoms of ulcerative colitis are absent or mild. If ulceration progresses proximally, the stool becomes more liquid and more frequent, up to 10 times a day or more, with severe spasmodic pain and disturbing tenesmus, including at night. The stool may be watery and contain mucus, and often consists almost entirely of blood and pus. In severe cases, patients may lose a lot of blood within a few hours, requiring urgent transfusion.
Fulminant colitis presents with sudden severe diarrhea, fever up to 40 C, abdominal pain, signs of peritonitis (eg, guarding, peritoneal signs) and severe toxemia.
Systemic symptoms of ulcerative colitis are more characteristic of severe disease and include malaise, fever, anemia, anorexia, and weight loss. Extraintestinal manifestations (especially joint and skin manifestations) are always present in the presence of systemic symptoms.
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Diagnosis of non-specific ulcerative colitis
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Initial manifestations of ulcerative colitis
The diagnosis is suggested by the development of typical symptoms and signs, especially if the disease is accompanied by extraintestinal manifestations or a history of similar attacks. Ulcerative colitis should be differentiated from Crohn's disease and other causes of acute colitis (eg, infection; in elderly patients, ischemia).
All patients should have their stool examined for enteric pathogens, and Entamoeba histolytica should be excluded by immediate post-void stool examination. If amebiasis is suspected in travelers from epidemiological areas, serologic titers and biopsy should be performed. In patients with a history of antibiotic use or recent hospitalization, stool should be tested for Clostridium difficile toxin. Patients at risk should be tested for HIV, gonorrhea, herpes virus, chlamydia, and amebiasis. In patients taking immunosuppressive agents, opportunistic infections (eg, cytomegalovirus, Mycobacterium avium-intracellulare) or Kaposi's sarcoma should be excluded. Colitis may occur in women using oral contraceptives; such colitis usually resolves spontaneously after discontinuation of hormonal therapy.
Sigmoidoscopy should be performed; this test allows visual confirmation of colitis and direct culture for microscopic and bacterial evaluation, as well as biopsy of the affected areas. However, both visual inspection and biopsy may be nondiagnostic because similar lesions occur in different types of colitis. Severe perianal lesions, impaired rectal function, lack of bleeding, and asymmetric or segmental colonic involvement suggest Crohn's disease rather than ulcerative colitis. Colonoscopy should not be performed immediately; it should be done when indicated if inflammation extends proximally beyond the reach of the sigmoidoscope.
Laboratory tests should be performed to detect anemia, hypoalbuminemia, and electrolyte abnormalities. Liver function tests may reveal elevated alkaline phosphatase and γ-glutamyl transpeptidase levels, which suggest the possibility of primary sclerosing cholangitis. Perinuclear antineutrophil cytoplasmic antibodies are relatively specific (60-70%) for ulcerative colitis. Anti-Saccharomyces cerevisiae antibodies are relatively specific for Crohn's disease. However, these tests do not clearly differentiate between the two diseases and are not recommended for routine diagnostics.
Radiographic studies are not diagnostic but may sometimes reveal abnormalities. Plain abdominal radiography may show mucosal edema, loss of haustration, and absence of formed stool in the affected bowel. Barium enema shows similar changes but more clearly and may also demonstrate ulceration, but should not be performed in the acute phase of the disease. A shortened, rigid colon with atrophic or pseudopolyposis mucosa is often seen after several years of disease. Radiographic thumbprinting and segmental involvement are more suggestive of bowel ischemia or possibly Crohn's colitis than ulcerative colitis.
Recurrent symptoms of ulcerative colitis
Patients with established disease and recurrence of typical symptoms should be investigated, but extensive workup is not always necessary. Depending on the duration and severity of symptoms, sigmoidoscopy or colonoscopy and complete blood count may be performed. Stool cultures for microflora, eggs and parasites and C. difficile toxin testing should be performed in cases of atypical features of relapse or worsening of symptoms after prolonged remission, during an infectious illness, after antibiotic use, or if there is clinical suspicion of disease.
Fulminant symptoms of ulcerative colitis
Patients require further evaluation in severe acute exacerbations. Supine and upright abdominal radiographs should be performed; these may reveal megacolon or intraluminal gas that completely fills the entire length of the paralytic colon as a result of loss of muscle tone. Colonoscopy and barium enema should be avoided due to the risk of perforation. Complete blood count, ESR, electrolytes, prothrombin time, APTT, blood group, and cross-match should be performed.
The patient should be monitored for peritonitis or perforation. The appearance of a "resolving hepatic dullness" sign on percussion may be the first clinical sign of free perforation, especially in patients in whom the abdominal symptoms of ulcerative colitis may be obscured by the use of high doses of glucocorticoids. Abdominal radiographs should be obtained every 1 or 2 days to monitor for colonic dilation, intraluminal gas, and free air in the peritoneal cavity.
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Treatment of non-specific ulcerative colitis
General treatment of ulcerative colitis
Avoidance of raw fruits and vegetables limits trauma to the inflamed colonic mucosa and may reduce symptoms. Avoidance of milk may be effective but should not be continued if ineffective. Loperamide 2.0 mg orally 2-4 times daily is indicated for relatively mild diarrhea; higher oral doses (4 mg in the morning and 2 mg after each bowel movement) may be needed for more severe diarrhea. Antidiarrheal drugs should be used with extreme caution in severe cases because they may precipitate toxic dilation.
Lesions of the left flank of the colon
For patients with proctitis or colitis extending proximally no higher than the splenic flexure, 5-aminosalicylic acid (5-ASA, mesalamine) enemas are used once or twice daily, depending on the severity of the process. Suppositories are effective for more distal lesions and are usually preferred by patients. Glucocorticoid and budesonide enemas are less effective but should also be used if treatment with 5-ASA is ineffective and tolerated. When remission is achieved, the dosage is slowly tapered to a maintenance level.
Theoretically, continued oral 5-ASA may be effective in reducing the likelihood of dissemination of the disease to the proximal colon.
Moderate or widespread damage
Patients with inflammation extending proximal to the splenic flexure or the entire left flank that is unresponsive to topical agents should be given oral 5-ASA in addition to 5-ASA enemas. High-dose glucocorticoids are added for more severe manifestations; after 1 to 2 weeks, the daily dose is reduced by about 5 to 10 mg each week.
Severe course of the disease
Patients with bloody stools more than 10 times a day, tachycardia, high fever, and severe abdominal pain should be hospitalized for high-dose intravenous glucocorticoid therapy. Treatment of ulcerative colitis with 5-ASA may be continued. Intravenous fluids should be given for dehydration and anemia. Patients should be monitored for the development of toxic megacolon. Parenteral hyperalimentation is sometimes used as nutritional support, but it has no value as primary therapy; patients who are not intolerant to food should be fed orally.
Patients who do not show a treatment effect within 3-7 days are given intravenous cyclosporine or surgical treatment. If the treatment is effective, patients are transferred to oral prednisolone 60 mg once a day for approximately one week, and depending on the clinical effect, the dose can be gradually reduced when transferred to outpatient treatment.
Fulminant colitis
If fulminant colitis develops or toxic megacolon is suspected:
- all antidiarrheal drugs are excluded;
- food intake is prohibited and intestinal intubation is performed with a long tube with periodic aspiration;
- Active intravenous transfusion of fluids and electrolytes is prescribed, including 0.9% NaCI solution and potassium chloride; if necessary, blood transfusion;
- high doses of glucocorticoids are administered intravenously and
- antibiotics (eg, metronidazole 500 mg IV every 8 hours and ciprofloxacin 500 mg IV every 12 hours).
The patient should be turned over in bed and rotated to the prone position every 2-3 hours to redistribute gas throughout the colon and prevent progression of distension. Insertion of a soft rectal tube may also be effective, but this should be done with extreme caution to avoid perforation of the colon.
If intensive care does not result in significant improvement within 24 to 48 hours, surgical treatment is necessary; otherwise, the patient may die from sepsis due to perforation.
Maintenance therapy for ulcerative colitis
After effective treatment of an exacerbation, the dose of glucocorticoids is reduced and, depending on the clinical effect, discontinued; they are ineffective as maintenance therapy. Patients should take 5-ASA orally or rectally, depending on the localization of the process, since interruption of maintenance therapy often leads to a relapse of the disease. The intervals between rectal administration of the drug can be gradually increased to once every 2-3 days.
Patients who cannot be discontinued from glucocorticoids should be switched to azathioprine or 6-mercaptopurine.
Surgical treatment of nonspecific ulcerative colitis
Almost 1/3 of patients with widespread ulcerative colitis eventually require surgical treatment. Total colectomy is a cure: life expectancy and quality of life are restored to statistical norms, the disease does not recur (unlike Crohn's disease) and the risk of colon cancer is eliminated.
Emergency colectomy is indicated for massive bleeding, fulminant toxic colitis, or perforation. Subtotal colectomy with ileostomy and suturing of the rectosigmoid end of the bowel or fistula repair are the usual procedures of choice, as most critically ill patients cannot tolerate more extensive intervention. The rectosigmoid fistula may be closed later if indicated or used to create an ileorectal anastomosis with an isolated loop. The normal rectal area should not be left unmonitored indefinitely due to the risk of disease activation and malignant transformation.
Elective surgery is indicated for high-grade mucinous dysplasia confirmed by two pathologists, overt cancer, clinically evident stricture of the entire bowel, growth retardation in children, or, most commonly, severe chronic disease leading to disability or glucocorticoid dependence. Occasionally, severe extraintestinal manifestations associated with colitis (eg, pyoderma gangrenosum) are also an indication for surgical treatment. The elective procedure of choice in patients with normal sphincter function is restorative proctocolectomy with ileorectal anastomosis. This procedure creates a pelvic intestinal reservoir or pouch from the distal ileum, which is connected to the anus. The intact sphincter retains obturator function, typically with 8 to 10 bowel movements per day. Pouch inflammation is a consequence of the inflammatory reaction observed after this procedure in approximately 50% of patients. It is thought to be due to bacterial overgrowth and is treated with antibiotics (eg, quinolones). Probiotics have protective properties. Most cases of pouch inflammation respond well to treatment, but 5-10% fail to respond due to intolerance to drug therapy. Alternative surgical options include ileostomy with intestinal reservoir (Koeck) or, more commonly, a traditional ileostomy (Brooke).
The physical and psychological problems associated with any type of colon resection must be addressed and care must be taken to ensure that the patient follows all recommendations and receives the psychological support that is necessary before and after surgery.
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What is the prognosis for ulcerative colitis?
Ulcerative colitis is usually chronic with recurrent exacerbations and remissions. In approximately 10% of patients, the first attacks of the disease develop acutely with massive bleeding, perforation, or sepsis and toxemia. Complete regeneration after a single episode is observed in 10%.
Patients with localized ulcerative proctitis have a more favorable prognosis. Severe systemic manifestations, toxic complications, and neoplastic degeneration are unlikely, and in the long term, disease dissemination occurs in only about 20-30% of patients. Surgical intervention is rarely required, and life expectancy is within the statistical norm. The course of the disease, however, may be persistent and poorly responsive to treatment. In addition, since the disseminated form of ulcerative colitis may begin in the rectum and progress proximally, proctitis cannot be considered a localized process for more than 6 months. A localized process that progresses later is often more severe and more intolerant to treatment.
Colon cancer
The risk of developing colon cancer is proportional to the duration of the disease and the extent of colonic involvement, but not necessarily to the activity of the disease. Cancer usually begins to manifest itself 7 years after the onset of the disease in patients with widespread colitis. The overall probability of cancer is approximately 3% at 15 years from the onset of the disease, 5% at 20 years, and 9% at 25 years, with an annual increase in the risk of cancer of approximately 0.5-1% after 10 years of disease. There is probably no risk of cancer among patients who have had colitis since childhood, despite a longer duration of disease.
Regular colonoscopic surveillance, preferably during remission, is indicated in patients with disease duration greater than 8–10 years (except for isolated proctitis). Endoscopic biopsy should be performed every 10 cm along the entire length of the colon. Any degree of established dysplasia within the colitis-affected area is prone to progression to more advanced neoplasia and even cancer and is a strict indication for total colectomy; if dysplasia is strictly limited to a single area, the polyp should be completely removed. It is important to differentiate established neoplastic dysplasia from reactive or secondary regenerative atypia in inflammation. However, if dysplasia is clearly defined, delaying colectomy in favor of further surveillance is a risky strategy. Pseudopolyps have no prognostic value but may be difficult to differentiate from neoplastic polyps; thus, any suspicious polyp should be excisional biopsied.
The optimal frequency of colonoscopic surveillance has not been defined, but some authors recommend screening every 2 years for 2 decades of disease and then annually.
Long-term survival after diagnosis of ulcerative colitis-related cancer is approximately 50%, which is comparable to colorectal cancer in the general population.
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