Colitis is inflammation of the mucosal lining of the colon which may be acute or chronic. Colitis is common and increasing in prevalence worldwide. Patients with colitis present with watery diarrhea, abdominal pain, tenesmus, urgency, fever, tiredness, and blood in the stool. However, colitis has different types and results from several mechanisms including infection, autoimmunity, ischemia, and drugs. Also, it may occur secondary to immune deficiency disorders or secondary to exposure to radiation. Because the clinical presentation can be the same across different types of colitis, there is a need for a review presenting an approach to assess patients presenting with colitis. Searching the literature reveals that this area is deficient, and nearly most publications are focused on one aspect of colitis or are disease-based articles. This review discusses the etiology, epidemiology, pathophysiology, clinical presentation, evaluation, differential diagnosis, complications and management of patients with colitis.
In adults, colitis may be the result of infection, inflammatory bowel disease, microscopic colitis, ischemia, drugs, secondary to immune deficiency disorders, or radiation.
Campylobacter jejuni is the number one bacterial cause of diarrheal illness worldwide with an estimated prevalence of 25 to 30 per 100000 population. For Salmonella and Shigella, the prevalence estimates are 20 cases per 100000 population.
Inflammatory bowel disease has been increasing in incidence and prevalence in various regions in the globe with the highest rates in North America and Europe.[1] The prevalence of inflammatory bowel disease in the USA is 263 per 100000 for adults.
Microscopic colitis is most commonly present in older adults with an average age between 50 and 70 years. Microscopic colitis is more common in women than in men with a female-to-male ratio typically higher in CC ranging up to 9 to 1. The incidence of MC is between 1 and 30 per 100000 person-year.
The incidence of ischemic colitis has risen from 6.1 cases per 100000 person-year in 1976 to 1980 to 22.9 per 100000 in 2005 to 2009.[2] While the reason for such increase may be related to several reasons including the improvement in medical intervention and the use of endoscopy in diagnosis, the prevalence of this condition increases with age and comorbidity and hence the increases in incidence as the population ages.
M. tuberculosis colitis is endemic in many countries, and there has been a resurgence of tuberculosis in the Western world. The annual global incidence of tuberculosis is estimated to be 9.4 million cases. The global case fatality rate was 23 to 25% and exceeded 50% in some African countries with high HIV prevalence rates.[3]
The pathologic basis includes:
While there is no specific approach for assessing histological changes associated with colitis, the histological pattern approach described by Jessurun seems to be practical and the current recommendation. The patterns include (1) acute colitis associated with colonic infections and drug-induced injuries, inflammation may be patchy or diffuse, and mixed inflammatory cells and abundant neutrophils are usually present (2) focal active colitis, mostly seen in drug-induced injuries, but maybe a manifestation of inflammatory bowel disease especially Crohn disease. (3) Pseudomembranous colitis pattern associated with C. difficile infection, although it can result from other infections such as Shigella, drugs, and radiation injury, (4) hemorrhagic colitis is associated with the entero-hemorrhagic strain of E. coli 0157: H7. The lamina propria appears hemorrhagic and edematous. Fibrin thrombi are present within capillaries, and crypts show ischemic injury, and (5) ischemic colitis associated with acute ischemic colitis. The extent of mucosal injury determines the clinical presentation; however, colonoscopy and biopsies are seldom necessary for patients presenting with acute abdomen due to embolic occlusion, or intestinal obstruction.[5]
Patients with colitis present with abdominal pain, watery diarrhea, fever, urgency, and blood in the stool. Examining doctor should look for red flags such as patient’s age, hemodynamic changes, nocturnal diarrheas, tenesmus, urgency, weight loss, comorbidities, history of heart failure, arrhythmias, autoimmune disorders, detailed history of patient’s medication, signs suggestive of toxic megacolon, and anemia.
In ulcerative colitis, extraintestinal manifestations associated with colitis and disease activity include arthropathies, eye changes (episcleritis, scleritis, uveitis), skin changes (erythema nodosum and pyoderma gangrenosum). Other extraintestinal manifestations reported in colitis include sacroiliitis, ankylosing spondylitis, hepatic dysfunction, and primary sclerosing cholangitis.[6]
Diagnosis of colitis has its basis in clinical findings, laboratory tests, endoscopy, and biopsy. Endoscopy and biopsy should not be the primary investigations and may be arranged after a critical evaluation of the patient’s condition and the results from the initial examinations.
Not all infectious colitis requires antibiotic therapy; patients with mild to moderate C. jejuni or Salmonella infections do not need antibiotic therapy because the infection is self-limited. Treatment with quinolinic acid antibiotics is reserved for patients with dysentery and high fever suggestive of bacteremia. Also, patients with AIDS, malignancy, transplantation, prosthetic implants, valvular heart disease or extreme age will require antibiotic therapy. For mild to moderate cases of C. difficile infection metronidazole is the preferred treatment. In severe cases of C. difficile infection oral vancomycin is recommended. In complicated cases, oral vancomycin with intravenous metronidazole is recommended. Cytomegalovirus colitis is treated with valganciclovir; the duration of treatment should be individualized depending on the clinical picture and laboratory parameters.[11]
5-aminosalicylic acid (5-ASA) drugs are the standard treatment in ulcerative colitis for induction and maintenance of remission of mild and moderate cases. The place of 5-ASA in the management of Crohn disease is controversial. Immunomodulators including azathioprine, 6-mercaptopurine, and methotrexate, are the mainstay of treatment in maintenance therapy for patients with mild to moderately severe Crohn disease and frequently relapsing ulcerative colitis where 5-ASA drugs failed. Biological therapies, tumor necrosis factor-oe, such as infliximab, adalimumab, and certolizumab are available for the management of Crohn disease, to get the disease under control and long-term maintenance. Corticosteroids are effective in reducing remission in inflammatory bowel disease and are cheap. However, they are not recommended for maintenance therapy and are associated with serious side effects. Surgery is recommended in patients not responding to medical therapy.[6][12][13]
In microscopic colitis, discontinuation of any offending medication and smoking cessation are vital. While anti-diarrheal medications, bismuth subsalicylate or cholestyramine may help, budesonide is effective in inducing remission and should be the first medication to start.[14] Patients in whom budesonide therapy is not feasible, bismuth salicylate or mesalamine is an option.
Patients with ischemic colitis without peritoneal signs, medical management may be safely employed including intravenous fluid resuscitation, optimizing cardiac output, use of supplementation of oxygen, placing the bowel on rest, parenteral nutrition, the use of broad-spectrum antibiotics to cover both aerobic and anaerobic coliform bacteria and close monitoring. Failure of medical management and the development of peritoneal signs or intestinal perforation necessitates surgical intervention and bowel resection.[10][15]
Anti-tuberculous treatment comprising isoniazid, rifampin, pyrazinamide, and ethambutol for 2 months is recommended in tuberculous colitis followed by isoniazid and rifampin for 7 months. The duration of treatment is nine months, and patients should be regularly followed up for assessing their response to the treatment.[16]
Complications include:
Toxic megacolon is an uncommon complication of colitis, characterized by total or segmental nonobstructive colonic dilatation, associated with systemic toxicity and has an overall mortality of 19%.[17] Diseases such as ulcerative colitis and pseudomembranous colitis are well-known to be complicated and develop toxic megacolon for over 60% of cases.[18] Other conditions associated with inflammation of colon including Campylobacter and shigella colitis may develop toxic megacolon.
The symptoms of colitis are non-specific, detailed medical, examination and laboratory workup are needed; however, endoscopic evaluation and mucosal biopsy are essential to confirm the diagnosis and exclude inflammatory bowel disease-associated colitis.
Colitis, depending on its cause, may be self-limited, life-threatening, chronic or recurrent. Patients with chronic and recurrent colitis need lifelong monitoring. The general practitioners have key roles in early diagnosis of the disease, support of the patients and assisting them with smoking cessation and management of their disease. The patients should be encouraged by nursing to take responsibility for their condition and provide knowledge of their pathology and drugs used. The pharmacists should be aware of the disease and drugs that could cause colitis and assist in explaining the potential complications. The nurse and pharmacist should report untoward complications to the clinical team. Other healthcare professionals including nurses need to be mindful of the clinical picture, common presentations, management, and care of patients with chronic and recurrent colitis. The surgeons play a key role with specific aspects of colitis in emergencies and in cases that failed to respond to medical therapy. Patients with chronic colitis develop depression and anxiety and need mental health support. All these various disciplines need to work together collaboratively in an interprofessional team to bring about the best outcomes for patients who have colitis. [Level V]
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