Ulcerative colitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

UC is diagnosed from a compatible pattern of chronic colitis after exclusion of infection and mimics such as drug injury, ischaemia and Crohn disease. Ileocolonoscopy defines extent and permits biopsies from affected and apparently normal segments. In a severe flare, full colonoscopy and bowel preparation may increase risk; limited flexible sigmoidoscopy with careful sampling is usually more appropriate. Histology supports chronicity but early disease can be non-specific. A stool culture and Clostridioides difficile test are important during an apparent flare because infection and inflammation may coexist.

Treatment aims for clinical remission without corticosteroid and objective control of inflammation. Extent guides the route of 5-ASA: suppositories reach proctitis, enemas reach further and oral therapy treats more proximal colon. Adherence often matters more than unnecessary switching, so ask about formulation, routine and barriers without blame. Patients with persistent activity, adverse prognostic features or steroid dependence need timely advanced therapy or surgical review. Longstanding colonic inflammation increases dysplasia risk; surveillance is risk-stratified by duration, extent, inflammatory burden, family history, post-inflammatory polyps and primary sclerosing cholangitis.

Key points

Ulcerative colitis is chronic mucosal inflammation beginning in the rectum and extending proximally in a usually continuous pattern; extent can change over time or appear modified by treatment.
Bloody diarrhoea, urgency, tenesmus and nocturnal stool are typical, but diagnosis still requires stool infection assessment, endoscopy and histology rather than symptoms alone.
Record proctitis, left-sided or extensive disease and quantify activity because topical reach, systemic risk, surveillance and treatment selection all depend on them.
For mild to moderate disease, mesalazine delivered to the involved mucosa is foundational; combined oral and rectal delivery is often more effective than ignoring distal treatment.
Corticosteroids induce remission when 5-ASA is insufficient but should not maintain it; relapse during taper or repeated courses requires escalation to steroid-sparing therapy.
Moderate to severe disease may require biologic or small-molecule therapy selected through current NICE and BSG guidance, individual safety assessment and shared decision-making.
Increasing bloody stool frequency, tachycardia, fever, anaemia or raised inflammatory markers can indicate acute severe ulcerative colitis and requires hospital assessment, not an outpatient prescription change.
Colectomy removes colitis and colorectal cancer risk from retained colon, but surgery creates new functional, fertility, stoma or pouch considerations and should be discussed before emergency circumstances.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Genetic immune susceptibility

Polygenic variants alter epithelial and immune regulation, increasing risk within families without following a simple Mendelian inheritance pattern.

Microbiome and barrier interaction

An inappropriate immune response to intestinal microbiota develops across a susceptible colonic barrier and sustains chronic mucosal inflammation.

Environmental modifiers

Age, prior enteric exposure, smoking history, medicines and other environmental factors influence risk or activity, but no single trigger explains most cases.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Rectal mucosal inflammation
Inflammation begins in the rectum and usually extends proximally in a continuous pattern limited primarily to mucosa and superficial submucosa.
2
Ulceration and impaired absorption
Crypt inflammation, epithelial loss and friability cause blood, mucus, urgency, diarrhoea and reduced colonic water absorption.
3
Chronic remodelling and dysplasia
Repeated inflammatory injury alters architecture and can produce dysplastic clones, with cancer risk related to duration, extent and inflammatory burden.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Distal colitis

Rectal bleeding, mucus, urgency, tenesmus and frequent small stools may occur without substantial systemic illness and can respond particularly well to topical therapy.

Extensive active disease

Frequent bloody diarrhoea, nocturnal symptoms, cramping, weight loss, anaemia and raised inflammation suggest a larger mucosal burden and higher systemic risk.

Acute severe physiology

High stool frequency with fever, tachycardia, anaemia or marked inflammatory response should prompt hospital admission and formal severe-colitis assessment.

Extra-intestinal disease

Peripheral arthritis, axial spondyloarthritis, uveitis, skin inflammation and hepatobiliary disease may track intestinal activity or follow an independent course.

Treatment toxicity

Renal impairment on mesalazine, steroid effects, cytopenia on immunomodulators and infection on immune therapy can mimic or compound an intestinal deterioration.

Cancer and dysplasia signal

New altered pattern, unexplained iron deficiency, weight loss, stricture or visible lesion in longstanding colitis needs high-quality colonoscopic assessment rather than attribution to routine flare.

Red flags requiring action

Suspected acute severe colitis requires same-day hospital assessment with gastroenterology and colorectal surgery involvement from admission.
Abdominal distension, tenderness, systemic toxicity or reduced stool passage can indicate toxic megacolon or perforation and needs urgent imaging and surgical review.
Major haemorrhage, shock, severe electrolyte disturbance or venous thromboembolism is an emergency and should not await elective IBD clinic contact.
A painful red eye with photophobia or reduced vision suggests uveitis and requires urgent ophthalmology assessment rather than routine optometry alone.
Worsening symptoms during immunosuppression require infection testing and medicine-toxicity assessment before assuming uncontrolled UC.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Stool culture and Clostridioides difficile testingFirst step
Why
Exclude treatable infection at diagnosis and during clinically important flares.
Interpretation and limitations
A positive result can coexist with UC activity and requires coordinated antimicrobial and IBD decisions; a negative panel does not itself prove inflammatory relapse.
02
Faecal calprotectin
Why
Estimate neutrophilic intestinal inflammation and support non-invasive follow-up.
Interpretation and limitations
Interpret trends with symptoms and local assay thresholds; infection, NSAIDs and other bowel inflammation can raise it, while very distal mild disease may produce less marked elevation.
03
Ileocolonoscopy with mapped biopsies
Why
Confirm chronic colitis, define extent and exclude Crohn disease or another mimic.
Interpretation and limitations
Continuous inflammation from the rectum supports UC, but treatment can create patchiness; histological chronicity and terminal ileal findings require integrated interpretation.
04
Blood count, CRP, renal, liver and albumin profile
Why
Assess severity, anaemia, dehydration, nutrition and treatment safety.
Interpretation and limitations
Anaemia, thrombocytosis, low albumin and inflammatory response indicate burden; renal function also provides a mesalazine baseline and liver tests may reveal associated hepatobiliary disease.
05
Limited flexible sigmoidoscopy
Why
Assess active severe colitis and obtain biopsies with less procedural burden.
Interpretation and limitations
Describe ulceration and extent reached, and request cytomegalovirus assessment when clinically relevant; avoid excessive insufflation or a full prepared colonoscopy in toxic severe disease.
06
Surveillance colonoscopy
Why
Detect dysplasia in patients with long-standing colonic disease at increased risk.
Interpretation and limitations
Use high-quality inspection by an experienced service and a risk-based interval; visible lesions, invisible dysplasia and active inflammation require different MDT pathways.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Infectious colitis

Acute exposure and positive stool testing support infection; Clostridioides difficile can also trigger a flare and should be sought before immunosuppression escalation.

Crohn disease

Skip lesions, small-bowel or perianal involvement and transmural stricturing or fistulation favour Crohn disease over continuous mucosal UC.

Ischaemic or microscopic colitis

Abrupt segmental pain and bleeding after low flow suggests ischaemia, while normal mucosa with watery non-bloody stool and diagnostic biopsies suggests microscopic colitis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01CONFIRMEstablish diagnosis and extentFirst stepPersistent bloody diarrhoea, urgency or tenesmus raises suspicion of new ulcerative colitis.

1Assess haemodynamic and systemic severity first, admitting suspected acute severe disease rather than progressing through a routine outpatient pathway.
2Obtain blood and stool tests, including infection assessment, medication and travel history, and examine for abdominal, perianal and extra-intestinal findings.
3Perform ileocolonoscopy with systematic biopsies when safe, using limited sigmoidoscopy instead if severe colitis makes full examination hazardous.
4Document activity, proctitis versus left-sided or extensive involvement, nutrition, extra-intestinal disease and individual cancer-surveillance factors.

02MILD-MODERATEDeliver mesalazine to the inflamed colonObjective mild to moderate activity is present without systemic severe-colitis criteria.

1Select rectal suppository or enema according to distal extent and add appropriate oral mesalazine when disease is left-sided, extensive or insufficiently controlled.
2Explain administration, formulation and expected response, addressing adherence barriers and monitoring renal function according to product and local guidance.
3If response is inadequate, confirm adherence and infection status, then optimise 5-ASA and consider a time-limited topical or systemic corticosteroid strategy.
4After remission, continue an effective maintenance 5-ASA plan and reassess objectively when symptoms, biomarkers or adherence change.

03ESCALATEAchieve steroid-free controlEscalationDisease is moderate to severe, steroid dependent, frequently relapsing or objectively active despite optimised conventional therapy.

1Restage activity and extent, exclude infection, review adherence and quantify prior steroid burden before declaring the current mechanism ineffective.
2Screen for infection, update vaccination and discuss reproductive, thrombotic, cardiovascular and malignancy factors before advanced treatment selection.
3Choose a biologic or small molecule using current NICE access, likely efficacy, speed, route, safety, patient preference and extra-intestinal needs.
4DefinitiveSet an early objective response target and bring colorectal surgery into discussion when disease remains refractory, dysplasia develops or quality of life favours a definitive option.

04SURVEILPrevent and detect colitis-associated cancerThe duration and extent of colitis place the patient within an IBD surveillance programme.

1Define risk from disease extent, duration, inflammatory burden, family history, post-inflammatory polyps, strictures, dysplasia and primary sclerosing cholangitis.
2Schedule high-quality surveillance at the risk-appropriate interval, aiming for good disease control and adequate bowel preparation before inspection.
3Manage visible dysplasia according to resectability and surrounding mucosa, and confirm invisible dysplasia through expert pathology and repeat expert assessment.
4Discuss colectomy or continued intensive surveillance in a specialist MDT when dysplasia risk cannot be managed safely by endoscopic resection alone.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Induces and maintains remission in mild to moderate UC by treating involved colonic mucosa.

Mesalazine

Oral and rectal regimen matched to extent, formulation and licensed product instructions.

Check renal function before and during treatment; rare nephrotoxicity, pancreatitis, blood dyscrasia or paradoxical worsening requires prompt review, and brands are not always dose-equivalent.

Controls active disease when optimised 5-ASA is insufficient or presentation is more severe.

Corticosteroid

Time-limited topical, oral or intravenous induction course selected by severity.

Never use for maintenance; infection, hyperglycaemia, mood effects, osteoporosis, thrombotic risk and adrenal suppression require mitigation, with a predefined taper and escalation plan.

Provides steroid-sparing control for moderate to severe or conventionally refractory ulcerative colitis.

Advanced immune therapy

Specialist induction and maintenance schedule under current NICE and local commissioning criteria.

Class-specific infection, malignancy, cardiovascular, thrombotic, hepatic and pregnancy considerations differ substantially; complete screening and avoid choosing solely by convenience.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute severe colitis and megacolon

Intense inflammation causes systemic toxicity, anaemia and colonic dilatation, with perforation risk and a need for timely rescue therapy or colectomy.

Thrombosis and nutritional loss

Active disease increases venous thromboembolism risk, while bleeding, protein loss and reduced intake cause anaemia and malnutrition.

Colorectal cancer

Longstanding extensive inflammatory burden increases dysplasia and cancer risk, supporting high-quality risk-based surveillance rather than symptom-led colonoscopy alone.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record bloody stool frequency, urgency, nocturnal symptoms, weight, function and cumulative steroid exposure at each clinically important review.
Use faecal calprotectin and CRP trends with symptoms, recognising that discordance may require endoscopic reassessment rather than automatic treatment escalation.
Monitor renal function for mesalazine and follow drug-specific blood, infection and safety schedules for immunomodulator or advanced therapy.
Assess iron deficiency, nutrition, bone health, mental wellbeing, vaccination, fertility and extra-intestinal manifestations as part of ongoing care.
Confirm mucosal response when it will guide de-escalation, switch or surveillance quality; absence of bleeding alone is not proof of healed disease.
Maintain a risk-based dysplasia-surveillance register with active recall, expert pathology access and clear ownership of every biopsy result.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Route is part of the prescription

An oral drug may not optimally treat the rectum. Suppositories and enemas place active treatment at the site producing urgency and bleeding.

Patchiness can be treatment-created

Although untreated UC is usually continuous, topical or systemic treatment can produce relative rectal sparing or uneven healing and should not automatically relabel disease as Crohn.

Infection and flare can coexist

Finding C. difficile does not exclude active UC. Antimicrobial, isolation and anti-inflammatory decisions need joint specialist assessment rather than a binary choice.

Colectomy changes the disease landscape

Removing colon cures colonic inflammation but not every extra-intestinal manifestation, and pouch or stoma function creates distinct long-term care needs.

Inflammation drives cancer risk

Duration and extent matter, but cumulative histological activity also influences dysplasia risk, making durable inflammatory control part of cancer prevention.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing UC from bloody diarrhoea without stool infection testing and histological confirmation.
02
Prescribing oral mesalazine for distressing proctitis without offering an effective rectal preparation or discussing how to use it.
03
Continuing systemic corticosteroids as maintenance because bleeding returns during taper.
04
Managing suspected acute severe colitis through routine outpatient messages and delayed blood tests.
05
Treating a raised calprotectin as UC-specific without considering infection, NSAID use or another inflammatory disorder.
06
Delaying surgical discussion until emergency colectomy removes time for stoma education, fertility counselling and shared choice.