Ulcerative Colitis
Background
Pathophysiology
- Continuous area of inflammation in rectum ± colon.
- Inflammed, friable mucosa, with crypt changes, reduced goblet cells, and pseudopolyps. Submucosal inflammation and ulceration if severe.
Epidemiology
- Prevalence: 1/1000.
- Bimodal onset: 15-25 years (commoner) and 55-65 years.
Signs and symptoms
- Diarrhoea: bloody in 75%. May contain mucus.
- Lower abdo cramps.
- Rectal symptoms: urgency, tenesmus.
- Relative to Crohn's, it is more likely to present gradually.
Attacks:
- Tender distended abdo.
- Fever
- Anorexia and weight loss.
- May be triggered by infection.
Non-intestinal:
- Eyes: uveitis, episcleritis, conjunctivitis.
- Aphthous ulcers, though much less than in Crohn's.
- Clubbing
- Erythema nodosum, pyoderma gangrenosum.
- MSK: entero-arthritis (usually large joints such as knee), ankylosing spondylitis.
Hepatobiliary:
- Primary sclerosing cholangitis.
- Chronic hepatitis, NAFLD, and cirrhosis.
Risk factors
- Not-smoking i.e. it is less common in smokers.
- Family history.
- HLA-B27.
Investigations
- ↑CRP/ESR in active disease. Other signs of inflammation e.g. ↑platelets, ↓albumin.
- Hb and haematinics (iron studies, B12, folate): ⅓ patients have anaemia, usually anaemia of chronic disease or iron deficiency. Less commonly, ↓B12 or ↓folate anaemia.
- U+E, Mg2+, and Ca2+ for nutritional deficiencies.
- LFT for associated hepatobiliary disease.
- Immunological: pANCA (70% in UC), ASCA (70% in Crohn's). Not routinely checked.
Stool:
- Culture to rule out infection.
- Faecal calprotectin as a marker of inflammation, 93% sensitive and 96% specific for IBD.
- C. diff toxin. Presence is a poor prognostic marker.
Endoscopy with biopsy:
- Sigmoidoscopy usually sufficient. Colonoscopy if poor response to treatment.
- Endoscopy shows mucosal granularity, and biopsy shows crypt architecture changes, including cryptitis and crypt abscesses.
Abdominal XR:
- May show perforation or gross dilatation in a flare up or toxic megacolon (transverse colon dilation >6 cm).
Management
Medical
- Mild-moderate: 1st line is mesalazine PR if distal (descending colon, rectosigmoid) plus PO if proximal or refractory. 2nd line add prednisolone PO +/or PR. Usually managed as outpatient.
- Severe: {≥6 stools/day, usually bloody} plus one of {fever, ↑HR, ↓Hb, or ESR >30}. Admit and give corticosteroids IV, then ciclosporin, biologic, or subtotal colectomy if refractory.
Maintain remission:
- Mesalazine PO +/or PR if rectosigmoid: 1st line after mild-moderate attack.
- Azathioprine or mercaptopurine PO: 1st line after a severe attack, or if steroids needed twice in 1 year.
Biologics and Janus kinase inhibitors:
- Can be used for induction and maintenance in refractory moderate-severe disease.
- Anti-TNFα: infliximab, adalimumab, golimumab.
- Other agents: vedolizumab (anti α4β7-integrin), tofacitinib (anti JAK1 and JAK3).
Surgical
- Medically-refractory chronic or acute UC.
- Toxic megacolon or perforation.
- Dysplasia or malignancy.
Elective:
- Proctocolectomy with ileo-anal pouch anastomosis or end ileostomy.
- Ileo-anal pouch avoids a stoma but is technically harder and carries higher morbidity in terms of functional and quality-of-life outcomes. The pouch is formed from several loops of ileum which are sutured side to side.
- Ileo-anal pouch complications include pouchitis (50%), nocturnal seepage (15%), urgency (10%), and impaired fertility in women (due to adhesions). Pouchitis presents with loose and frequent stools; treat it with metronidazole PO.
Acute:
- Subtotal colectomy – sparing the rectum – with end ileostomy and long rectal stump. Ileorectal anastomosis is also possible.
- Complications: sepsis, poor healing due to high dose steroids.
Complications
- Perforation
- Toxic megacolon
- Colorectal carcinoma. Screen with colonoscopy every 3 years, starting 10 years after onset, and consider removal if dysplasia found.
- VTE
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