Crohn disease

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

Crohn disease is heterogeneous. Mucosal ulceration may coexist with full-thickness inflammation, mesenteric change, fistulae and fibrosis. Typical presentations include chronic diarrhoea, abdominal pain, weight loss, anaemia, perianal sepsis or obstructive episodes, but isolated small-bowel disease can be subtle. Granulomas support the diagnosis when present but are neither necessary nor entirely specific. The initial assessment should establish extent and behaviour, screen for complications, quantify inflammatory burden and identify factors that make cumulative bowel damage more likely. Smoking is associated with worse outcomes and should be addressed supportively.

The therapeutic target is sustained control without corticosteroids, alongside preserved nutrition, growth, function and bowel integrity. Clinical improvement alone may leave ongoing inflammation, so biomarkers, imaging and endoscopy are used proportionately to confirm response. Conversely, persistent pain or diarrhoea with normal objective activity should prompt evaluation for structural or functional causes before increasing immunosuppression. Shared decisions compare medicines with nutrition, endoscopic dilation or surgery and include fertility, pregnancy, infection, malignancy, vaccination and monitoring implications. Local commissioning determines access to specific advanced therapies, but urgent complications must not wait for routine approval.

Key points

Crohn disease causes discontinuous transmural inflammation anywhere from mouth to anus, most often involving terminal ileum or colon, and may produce strictures, fistulae or abscesses.
Diagnosis requires compatible clinical, endoscopic, histological and imaging evidence after excluding infection and other mimics; no single blood or stool marker is diagnostic.
At diagnosis document location, inflammatory versus stricturing or penetrating behaviour, perianal involvement, upper gastrointestinal disease, growth or nutrition and extra-intestinal manifestations.
Ileocolonoscopy with segmental biopsies and small-bowel cross-sectional imaging are complementary because normal colonic appearances do not exclude proximal transmural disease.
Symptoms may arise from active inflammation, fixed fibrosis, bile-acid diarrhoea, bacterial overgrowth, infection, irritable bowel physiology or medication effects; escalation only helps when the mechanism is right.
Corticosteroids or exclusive enteral nutrition can induce remission in selected disease but are not maintenance treatments; repeated steroid exposure signals treatment failure.
Early advanced therapy is considered when prognostic risk is high, disease is extensive or severe, or conventional therapy is unlikely to prevent damage, following current BSG and NICE pathways.
Abscess needs drainage and infection control, obstruction needs urgent structural assessment, and surgery can be the best disease-modifying option for localised complications rather than a failure of care.

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

Genetic immune susceptibility

Multiple genetic variants alter epithelial defence and innate or adaptive immune regulation, increasing susceptibility without determining disease in isolation.

Microbial and environmental interaction

An altered response to intestinal microbiota in a susceptible host sustains inflammation; diet, antibiotics and other exposures may modify risk.

Smoking and host factors

Smoking worsens incidence, recurrence and complication risk, while age, family history and prior appendicectomy patterns influence epidemiology but are not diagnostic.

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

1
Barrier and immune dysregulation
Defective epithelial handling of luminal organisms triggers persistent cytokine-driven inflammation rather than a self-limited response after mucosal exposure.
2
Discontinuous transmural injury
Patchy inflammation extends through the full bowel wall anywhere from mouth to anus, producing deep ulcers and thickening.
3
Fibrosis and penetration
Repeated healing causes strictures, while deep ulceration tracks through adjacent structures to form fistulae, phlegmon and abscess.

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

Luminal inflammation

Chronic diarrhoea, cramping, fatigue, fever, weight loss, aphthous oral ulcers, right iliac fossa tenderness and inflammatory anaemia form a common but non-specific presentation.

Stricturing disease

Postprandial colic, distension, vomiting, dietary avoidance and intermittent obstruction suggest luminal narrowing; inflammation and fixed fibrosis often coexist and respond differently.

Penetrating disease

Persistent fever, focal mass, recurrent urinary infection, pneumaturia, vaginal passage of gas or enterocutaneous drainage may indicate abscess or internal fistulation.

Perianal phenotype

Pain, swelling, discharge, complex fistulae, fissures away from the midline or anal stenosis can precede luminal diagnosis and require examination plus pelvic imaging.

Nutritional phenotype

Low body mass, sarcopenia, iron or vitamin B12 deficiency, hypoalbuminaemia, delayed puberty or impaired growth may be more prominent than diarrhoea.

Extra-intestinal signal

Peripheral arthritis, axial pain, erythema nodosum, pyoderma gangrenosum, uveitis and hepatobiliary disease can accompany or occasionally precede intestinal symptoms.

Red flags requiring action

Peritonism, sepsis, a tender mass or free perforation requires emergency surgical and gastroenterology assessment rather than empiric steroid escalation.
Persistent vomiting, distension, absolute constipation or escalating colic suggests obstruction and needs urgent imaging with intravenous fluids and surgical input.
Painful perianal swelling with fever is an abscess until assessed; do not wait for biologic optimisation before securing drainage.
Major bleeding, severe dehydration, venous thromboembolism, toxic dilatation or acute kidney injury warrants inpatient multidisciplinary care.
Before attributing deterioration to a flare, exclude enteric infection, including Clostridioides difficile where relevant, and assess for abscess.

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
Blood count, CRP, renal, liver and nutrition profileFirst step
Why
Quantify inflammation, complications and treatment readiness.
Interpretation and limitations
Anaemia, thrombocytosis, low albumin or raised CRP support inflammatory burden but normal results do not exclude isolated active disease, especially in an individual low-CRP responder.
02
Faecal calprotectin and stool microbiology
Why
Support intestinal inflammation assessment and exclude infectious diarrhoea.
Interpretation and limitations
Calprotectin is sensitive but not disease-specific and can rise with infection or other inflammation; interpret against symptoms, phenotype, medicines and the local assay pathway.
03
Ileocolonoscopy with segmental biopsies
Why
Define mucosal distribution, severity and histological chronicity while excluding mimics.
Interpretation and limitations
Document ulceration and skip pattern and biopsy both involved and uninvolved segments; inability to intubate the ileum does not exclude small-bowel disease.
04
MR enterography or intestinal ultrasound
Why
Assess small bowel and transmural inflammation without repeated ionising radiation.
Interpretation and limitations
Wall thickening, oedema and hyperenhancement support activity, while prestenotic dilatation, fistula or abscess identifies damage; fibrosis cannot be inferred from one feature alone.
05
CT abdomen and pelvis
Why
Rapidly assess suspected obstruction, perforation, severe sepsis or abscess.
Interpretation and limitations
CT is valuable in an emergency despite radiation; identify a drainable collection and transition to radiation-sparing monitoring after stabilisation.
06
Capsule endoscopy
Why
Investigate persistent small-bowel suspicion after non-diagnostic conventional assessment.
Interpretation and limitations
Use only when stenosis risk has been assessed, often with cross-sectional imaging or patency testing; minor erosions can arise from NSAIDs and require context.

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

Ulcerative colitis

Continuous rectum-based mucosal inflammation supports UC, whereas skip lesions, small-bowel disease, granulomas and fistulising or stricturing behaviour favour Crohn disease.

Infectious enterocolitis

Acute exposure, positive stool tests and resolution after infection support an infectious mimic; infection should be excluded before escalating immunosuppression.

Coeliac or functional disease

Positive coeliac serology with villous atrophy identifies coeliac disease, while IBS lacks endoscopic, histological and cross-sectional evidence of chronic inflammation.

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

01DIAGNOSEConfirm and phenotype diseaseFirst stepPersistent gastrointestinal, perianal, nutritional or extra-intestinal features suggest Crohn disease.

1Assess symptom pattern, weight, smoking, family history, medicines, infection exposure, perianal symptoms, growth and extra-intestinal features, with examination for complications.
2Obtain blood, faecal inflammatory and microbiological tests, arranging urgent imaging first when obstruction, abscess or perforation is possible.
3Complete ileocolonoscopy with biopsies and small-bowel imaging, adding upper endoscopy or capsule selectively when the suspected distribution remains unresolved.
4Record anatomical extent, behaviour, perianal disease, objective activity, nutrition and prognostic risk in a shared baseline plan.

02INDUCEControl active luminal inflammationObjective assessment confirms active inflammatory Crohn disease without an undrained abscess or fixed mechanical emergency.

1Match induction to location, severity, prognostic risk and preference, considering corticosteroid, exclusive enteral nutrition or appropriately selected advanced therapy under specialist care.
2Provide nutrition support, venous-thromboembolism assessment, infection screening, vaccination review and smoking-cessation help at the same time as anti-inflammatory treatment.
3Define early failure and response checks before starting, using symptoms plus CRP, calprotectin, imaging or endoscopy rather than symptom relief alone.
4Move promptly to a steroid-sparing maintenance strategy once response is achieved; repeated induction courses indicate that the maintenance plan is inadequate.

03COMPLICATIONSeparate inflammation from damageObstruction, fistula, abscess, persistent pain or discordant symptoms complicate the expected treatment response.

1Use cross-sectional imaging to identify inflammatory thickening, fixed narrowing, penetrating tracts, collection and proximal dilatation, involving colorectal surgery early.
2Drain sepsis where feasible and provide local microbiology-led antibiotics; immunosuppression decisions follow source control rather than replacing it.
3For short accessible strictures, discuss endoscopic dilation in an experienced service; for fibrotic, long, recurrent or penetrating disease, discuss surgery and bowel preservation.
4After intervention, reassess residual inflammatory activity and establish recurrence prevention rather than assuming resection or drainage has cured the underlying disease.

04MAINTAINPursue steroid-free durable controlInduction has achieved clinical response or remission and long-term strategy is required.

1Select immunomodulator or advanced therapy from prior response, phenotype, immunogenicity, safety, reproductive plans and current NICE commissioning criteria.
2Monitor symptoms and objective inflammation at planned intervals, optimising adherence and drug exposure before declaring mechanistic failure when appropriate.
3Address iron, vitamin B12, vitamin D, bone, mental health, vaccination, cancer surveillance and smoking as part of disease control.
4Review therapy when deep control is sustained or toxicity emerges through shared specialist decisions; abrupt unplanned withdrawal risks relapse and antibody formation.

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

Rapidly suppresses active inflammatory Crohn disease when infection and undrained sepsis have been excluded.

Systemic corticosteroid

Time-limited oral or intravenous induction regimen tapered through the specialist pathway.

Not a maintenance therapy; infection, hyperglycaemia, psychiatric effects, osteoporosis and adrenal suppression require prevention and monitoring, while repeated exposure demands strategy change.

Can induce remission, especially in children and selected adults, while improving nutritional state.

Exclusive enteral nutrition

Complete formula-based nutrition course supervised by the IBD dietetic team.

Adherence, food restriction, refeeding risk and psychosocial burden need active support; partial unsupervised formula use is not equivalent to a prescribed exclusive course.

Achieves steroid-free control in moderate to severe, high-risk, fistulising or refractory disease.

Advanced immune therapy

Agent-specific induction and maintenance prescribed by an experienced IBD specialist service.

Screen infection and vaccination status, consider malignancy, thrombosis and pregnancy factors, and follow current NICE eligibility plus class-specific laboratory and clinical monitoring.

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

Stricture and obstruction

Inflammatory swelling or fixed fibrosis narrows bowel, causing pain, vomiting and nutritional compromise; the distinction determines medical, endoscopic or surgical treatment.

Fistula and abscess

Transmural penetration creates enteroenteric, enterocutaneous, perianal or organ fistulae and sepsis that requires drainage before intensified immunosuppression.

Malnutrition and systemic risk

Reduced intake, malabsorption and inflammation cause anaemia and deficiency, while active disease increases thrombosis, osteoporosis and colorectal cancer risk.

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

Track stool pattern, pain, weight, function, steroid exposure and complications, but pair symptoms with CRP, calprotectin or phenotype-appropriate imaging.
Confirm response after induction within a predefined timeframe and change strategy when objective inflammation persists rather than extending corticosteroids indefinitely.
Use MR enterography or intestinal ultrasound for transmural small-bowel follow-up and endoscopy when mucosal healing or dysplasia surveillance will alter care.
Monitor medicine-specific bloods, infection, skin, vaccination, reproductive plans and adherence under a written shared-care arrangement.
Review nutrition, iron, vitamin B12 after ileal disease or resection, vitamin D, bone health and sarcopenia throughout the disease course.
After surgery, perform risk-stratified recurrence assessment because endoscopic recurrence may precede symptoms by a considerable interval.

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

Transmural disease needs cross-sectional assessment

Colonoscopy describes mucosa but cannot map an extraluminal abscess, fistula or the full length of a small-bowel stricture. Imaging answers that separate question.

Symptoms and inflammation can diverge

Ongoing diarrhoea after inflammatory control may reflect bile-acid malabsorption or functional disease, while silent ulceration can progress despite feeling well.

Steroid response is not success

A patient who improves repeatedly but relapses during taper is steroid dependent and needs a safer maintenance or surgical strategy.

Surgery can preserve bowel

Timely limited resection or strictureplasty may prevent emergency sepsis and prolonged malnutrition; delayed repeated operations are more likely to sacrifice bowel length.

Smoking is modifiable disease biology

Smoking is linked to recurrence and adverse Crohn outcomes. Offer evidence-based cessation support without blame or implying that smoking caused the disease.

11Common pitfallsFrequent interpretation and management errors.

01
Making the diagnosis from a raised faecal calprotectin without endoscopic, histological and imaging correlation or infection exclusion.
02
Escalating immunosuppression for obstruction before determining whether fixed fibrosis or an abscess is the dominant mechanism.
03
Using corticosteroids as maintenance because symptoms recur during every taper.
04
Assuming normal CRP excludes active ileal disease in a patient whose previous inflammation produced little CRP response.
05
Calling surgery a treatment failure and delaying referral until malnutrition, sepsis or emergency obstruction worsens operative risk.
06
Starting capsule endoscopy when a stricture has not been excluded.