Ulcerative colitis (UC) is the most common form of inflammatory bowel disease.
It is most prevalent amongst the Caucasian population – with the age at presentation following a bimodal distribution of peak incidence of onset between 15-25yrs and a smaller peak of incidence between 55-65yrs.
Prevalence in the UK is approximately 0.2%, with males and females affected equally.
The disease typically follows a remitting and relapsing course. A severe fulminant exacerbation may be life-threatening, resulting in severe systemic upset, toxic megacolon, colonic perforation and even death.
In this article, we shall look at the risk factors, clinical features and management of ulcerative colitis.
Although the exact aetiology of ulcerative colitis is unknown, current theories suggest it develops as an interaction between genetic factors and environmental triggers.
Smoking is protective against ulcerative colitis, whilst a positive family history of inflammatory bowel disease is a strong risk factor.
It is characterised by diffuse continual mucosal inflammation of the large bowel, beginning in the rectum and spreading proximally – potentially affecting the entire bowel. A portion of the distal ileum can become affected in a small proportion of cases, termed ‘backwash ileitis’ (if the ileocaecal valve is not competent).
Histological changes include inflammation of the mucosa and submucosa, crypt abscesses, and goblet cell hypoplasia. Repeated cycles of ulceration and healing may lead to raised areas of inflamed tissue termed ‘pseudopolyps’.
|Ulcerative Colitis||Crohn’s Disease|
|Site Involvement||Large bowel||Entire GI tract|
|Microscopic Changes||Crypt abscess formation
Reduced goblet cells
|Macroscopic Changes||Continuous inflammation (proximal from rectum)
Pseudopolyps and ulcers may form
|Discontinuous inflammation (‘skip lesions’)
Fissures and deep ulcers (‘cobblestone appearance’)
Table 1 – Characteristic Features of Inflammatory Bowel Disease
Ulcerative colitis is typically insidious in onset. The cardinal feature is bloody diarrhoea; visible blood in stool is reported in more than 90% of cases of UC.
The most common manifestation of ulcerative colitis is proctitis – where the inflammation is confined to the rectum. Patients will complain of PR bleeding and mucus, increased frequency and urgency of defecation, and tenesmus.
Patients presenting with more widespread colonic involvement are more likely to experience bloody diarrhoea with clinical features of dehydration and electrolyte imbalance. Systemic symptoms also include malaise, anorexia and low-grade fever.
Unless there is a severe exacerbation, clinical examination is generally unremarkable. Fulminant colitis, toxic megacolon, or colonic perforation should be suspected if the patient complains of severe abdominal pain and on examination demonstrates systemic upset or signs of peritonism.
The severity of an exacerbation can be graded using the Truelove and Witt criteria.
The severity degree is based on the presence of any one of the criteria as shown in Table 2:
|Bowel movements (no. per day)||<4||4-6||>6|
|Blood in stool||Minimal||Mild-severe||Visible blood|
|Pulse >90 bpm||No||No||Yes|
Table 2 – Truelove and Witt Criteria
Ulcerative colitis, much like Crohn’s disease, is associated with extra intestinal manifestations of disease:
- Musculoskeletal – Enteropathic arthritis (typically affecting sacroiliac and other large joints), nail clubbing, or metabolic bone disease (secondary to malabsorption).
- Skin – Erythema nodosum (Fig. 1, tender red/purple subcutaneous nodules, typically found on the patient’s shins) or apthous ulcers (shallow ulcers in mouth or on tongue).
- Eyes – Episcleritis, anterior uveitis, or iritis.
- Hepatobiliary – Primary sclerosing cholangitis (chronic inflammation and fibrosis of the bile ducts).
The primary differential diagnosis for ulcerative colitis is Crohn’s disease, as this can present in a similar fashion – however patients with UC typically experience a more bloody diarrhoea.
Alternative forms of colitis include chronic infections (schistosomiasis, giardiasis and TB), mesenteric ischaemia, or radiation colitis. Other differentials to consider include colorectal carcinoma or coeliac disease.
Routine bloods (FBC, U&Es, CRP, LFTs, and clotting) are required to examine for anaemia, low albumin (secondary to malabsorption), and raised CRP and WCC.
Liver function tests may become deranged in patients on treatment and clotting can become deranged in severe attacks due to the large inflammatory response affecting the coagulation cascade.
In the UK, NICE guidelines recommend that faecal calprotectin testing is carried out in patents with recent onset lower gastrointestinal symptoms: it is raised in inflammatory bowel disease, but unchanged in irritable bowel syndrome. A stool sample should be sent for microscopy and culture.
The definitive diagnosis for ulcerative colitis is via colonoscopy with biopsy. Characteristic macroscopic findings are of continuous inflammation with possible ulcers and pseudopolyps visible. A flexible sigmoidoscopy may be sufficient and in clinical practice full colonoscopy is only required if the diagnosis is unclear; colonoscopy should be avoided in acute severe exacerbations.
Note: At least two biopsies are required from five sites, including the rectum and the terminal ileum.
In acute exacerbations, an abdominal x-ray (AXR) is used to determine if toxic megacolon and/or bowel perforation has occurred. AXR features of ulcerative colitis also include mural thickening and thumbprinting, indicating a severe inflammatory process in the bowel wall. In chronic cases of UC, a lead-pipe colon is often described – but this is usually best seen on barium studies.
Patients with suspected IBD should be referred to a gastroenterologist for confirmation of the diagnosis and initiation of treatment; those with acute severe disease should be admitted on an emergency basis.
Anti-motility drugs, such as loperamide, should be avoided in acute attacks, as these can precipitate toxic megacolon.
The primary goal in the management of ulcerative colitis is to induce remission. NICE guidelines suggest that a stepwise approach is adopted, dependent upon the clinical severity of the exacerbation.
Any acute attacks will also warrant aggressive fluid resuscitation, nutritional support, and prophylactic heparin (due to prothrombotic state of IBD).
|Severity||Step 1||Step 2|
|Mild to Moderate (proctitis)||Topical mesalazine or sulfasalazine||Add oral prednisolone + oral tacrolimus if no response after 2-4 weeks.|
|Mild to Moderate (extensive inflammation)||High oral dose mesalazine or sulfasalazine|
|Severe (all spread of disease)||Intravenous corticosteroids and assess the need for surgery||Add IV ciclosporin + infliximab if no short-term response|
*Continue to step 2 if no improvement on step 1 for 4 weeks
Once any acute event has been controlled, remission of the disease can be maintained using oral aminosalicylates (mesalazine or sulfasalazine). Infliximab or alternative monoclonal antibody therapy can be used as next line therapies to maintain remission patients with recurrent symptoms despite optimisation of oral regimes.
Due to increased risk of colorectal malignancy, colonoscopic surveillance is offered to people who have had the disease for >10 years with >1 segment of bowel affected (follow-up time frame depends on risk stratification of disease following initial endoscopy).
Patients should be referred to IBD-nurse specialists and patient support groups. Enteral nutritional support should be considered in young patients with growth concerns, with close support from a nutritional team.
Antibiotics are only offered to those with obvious concurrent infection or perianal disease (typically ciprofloxacin or metronidazole).
Approximately 30% of those with ulcerative colitis will at some point require surgery.
Indications for acute surgical treatment include disease refractory to medical management, toxic megacolon, or bowel perforation. Any decision made for surgical intervention must be done so in concordance with the MDT, including IBD-nurses and gastroenterologists.
Total proctocolectomy is curative, with the patient requiring an ileostomy. Alternatively, a restorative proctocolectomy with ileal pouch-anal anastomosis may be undertaken; this procedure involves a pouch being created from loops of ileum to act as a reservoir for intestinal contents, then being anastamosed to the anus, with the aim to maintain faecal continence.
Surgery may also be undertaken to reduce the risk of colonic carcinoma, if dysplastic cells are detected on routine monitoring.
The complications of ulcerative colitis include:
- Toxic megacolon – serious complication of ulcerative colitis, characterised by dilatation of the colon (to at least 6 cm diameter on AXR) and associated systemic toxicity.
- Patients typically present with abdominal pain and distension, fever, and tachycardia.
- Decompression of the bowel is required as soon as possible, due to high risk of perforation, and failure to respond to medical management is an indication for surgery.
- Colorectal carcinoma
- Osteoporosis – patients should be regularly assessed for fracture risk and treated as appropriate.
- Pouchitis – inflammation of an ileal pouch (as described above). Typical symptoms include abdominal pain, bloody diarrhoea and nausea. Pouchitis should be treated with metronidazole and ciprofloxacin.
Patients with well-controlled UC can expect to have a similar life expectancy as those in the general population.