Inflammatory Bowel Disease (IBD)

1. Clinical Overview

Summary

Inflammatory Bowel Disease (IBD) comprises two principal chronic, immune-mediated inflammatory disorders of the gastrointestinal tract: Ulcerative Colitis (UC) and Crohn's Disease (CD). These conditions are characterised by relapsing-remitting inflammation leading to significant morbidity and, if inadequately managed, life-threatening complications. [1,2]

Ulcerative Colitis presents with continuous mucosal inflammation invariably starting from the rectum and extending proximally in a contiguous pattern to involve variable lengths of colon (proctitis, left-sided colitis, extensive/pancolitis). The inflammation remains confined to the mucosa and submucosa, sparing deeper layers. [3,4]

Crohn's Disease is distinguished by its capacity to affect any segment of the GI tract from mouth to anus (though most commonly the terminal ileum and colon), characterised by skip lesions (discontinuous areas of inflammation interspersed with normal mucosa) and transmural inflammation (full-thickness bowel wall involvement). This transmural nature predisposes to structuring disease, penetrating complications (fistulae, abscesses), and perianal disease. [5,6]

Both conditions demonstrate a genetically complex, multifactorial aetiology involving dysregulated immune responses to intestinal microbiota in genetically susceptible individuals, influenced by environmental factors. [7,8]

Treatment strategy follows a stepwise escalation paradigm:

• 5-ASA (Aminosalicylates) remain first-line for mild-moderate UC (ineffective in Crohn's)
• Corticosteroids (oral prednisolone, IV hydrocortisone, topical budesonide) induce remission but unsuitable for maintenance
• Immunomodulators (thiopurines, methotrexate) maintain steroid-free remission
• Biologic agents (anti-TNF antibodies, anti-integrin vedolizumab, anti-IL-12/23 ustekinumab, anti-IL-23 risankizumab) and small molecules (JAK inhibitors: tofacitinib, upadacitinib, filgotinib; S1P modulators: ozanimod) for moderate-severe or refractory disease
• Surgical intervention when medical therapy fails or complications arise (curative in UC via proctocolectomy; non-curative in Crohn's with high recurrence rates) [1,2,9]

Acute Severe Ulcerative Colitis (ASUC) represents a medical emergency requiring immediate hospital admission, IV corticosteroids, thromboprophylaxis, and surgical consultation, with rescue therapy (ciclosporin or infliximab) if no improvement within 3-5 days. [10,11]

Clinical Pearls

UC = Continuous, Mucosal, Rectum-First: Think "Rectum is Certain" in UC. Rectal involvement is mandatory; proximal extension is contiguous. Crohn's = Skip lesions, Transmural, Anywhere (commonly terminal ileum).

Bloody Diarrhoea = UC, Abdominal Pain + Diarrhoea = Crohn's: Classical presentation patterns differ. UC typically presents with visible rectal bleeding and urgency. Crohn's more commonly presents with cramping abdominal pain (especially RLQ), non-bloody diarrhoea, and constitutional symptoms.

5-ASA is Cornerstone of UC, Useless in Crohn's: Mesalazine (oral + topical) is first-line induction and maintenance for UC. Multiple studies show no efficacy in Crohn's disease for inducing or maintaining remission.

Toxic Megacolon = Surgical Emergency: Colonic dilatation > 6cm on AXR with systemic toxicity. High risk of perforation and mortality. Requires urgent surgical review and potential emergency colectomy.

Smoking: Protective in UC, Harmful in Crohn's: One of medicine's paradoxes. Smoking reduces UC flares (though still discouraged); exacerbates Crohn's and accelerates need for surgery.

PSC Screening in UC: Primary Sclerosing Cholangitis occurs in 2-7.5% of UC patients, increases colorectal cancer risk, and may present before colitis symptoms. Annual LFT surveillance recommended.

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2. Epidemiology

Incidence and Prevalence

IBD demonstrates highest incidence in industrialised nations, with a notable North-South and urban-rural gradient. Incidence is rising in newly industrialised countries undergoing westernisation. [12,13]

Demographics

Risk Factors

Genetic Factors

• Family History: First-degree relatives have 10-15-fold increased risk
• Twin Concordance: Monozygotic twins 10-15% for UC, 30-50% for Crohn's
• Susceptibility Genes: > 200 IBD-associated loci identified through GWAS
  • "NOD2/CARD15: Strongest association with Crohn's (ileal disease)"
  • "IL23R, ATG16L1, IRGM: Autophagy and innate immunity pathways"
  • "HLA-DRB1*0103: Associated with extensive UC and primary sclerosing cholangitis [7,8]"

Environmental Factors

• Smoking: Paradoxical effects
  • "UC: Protective effect; disease often flares after smoking cessation"
  • "Crohn's: Harmful; doubles risk, increases severity, accelerates need for surgery"
• Diet: Western diet (high fat, refined carbohydrates, processed foods) increases risk
• Antibiotics: Early-life antibiotic exposure associated with increased IBD risk
• Hygiene Hypothesis: Reduced microbial exposure in childhood may impair immune tolerance
• Appendectomy: Protective for UC if performed for appendicitis before age 20
• NSAIDs: May trigger flares in established IBD
• Urban Environment: Higher incidence in urban vs rural settings [12,13]

Microbiome

• Dysbiosis: Reduced microbial diversity, decreased Firmicutes, increased Proteobacteria
• Loss of barrier function: Increased intestinal permeability ("leaky gut")
• Aberrant immune response: Failure of immune tolerance to commensal bacteria [8]

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3. Pathophysiology

Fundamental Differences: UC vs Crohn's Disease

Molecular Pathophysiology

Immune Dysregulation

Ulcerative Colitis:

• Predominantly Th2-mediated immune response
• Increased IL-5, IL-13 production
• NK T-cell activation
• Neutrophil infiltration with crypt abscesses
• Impaired epithelial barrier function
• Abnormal mucin production [7,8]

Crohn's Disease:

• Predominantly Th1 and Th17-mediated immune response
• IL-12, IL-23 drive Th1/Th17 differentiation
• TNF-α, IFN-γ, IL-17, IL-21 promote transmural inflammation
• M1 macrophage polarisation
• Defective autophagy (ATG16L1, IRGM, NOD2 mutations)
• Impaired bacterial clearance [7,8]

Cytokine Networks

Both conditions demonstrate elevated pro-inflammatory cytokines:

• TNF-α: Central mediator; target of anti-TNF biologics
• IL-12/IL-23: Drive pathogenic Th1/Th17 responses; targets of ustekinumab and risankizumab
• Integrin α4β7: Mediates lymphocyte trafficking to gut; target of vedolizumab
• JAK-STAT pathway: Intracellular signalling; target of tofacitinib, upadacitinib [14,15]

Montreal Classification

Standardised disease classification for phenotyping and prognostication:

Ulcerative Colitis (E Classification)

• E1: Proctitis (limited to rectum)
• E2: Left-sided colitis (distal to splenic flexure)
• E3: Extensive colitis/pancolitis (proximal to splenic flexure)

Crohn's Disease

Age at Diagnosis (A):

• A1: less than 16 years
• A2: 17-40 years
• A3: > 40 years

Location (L):

• L1: Ileal (terminal ileum ± limited caecal involvement)
• L2: Colonic
• L3: Ileocolonic
• L4: Isolated upper GI (modifier; can be added to L1-L3)

Behaviour (B):

• B1: Non-stricturing, non-penetrating (inflammatory)
• B2: Stricturing (obstructive)
• B3: Penetrating (fistulising, abscess formation)
• p: Perianal disease modifier (add to any B category) [5,6]

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4. Differential Diagnosis

Distinguishing IBD from Other Causes of Colitis

Red Flags Requiring Urgent Investigation

• Age > 50 with new-onset symptoms: Increased risk of colorectal malignancy
• Unintentional weight loss > 5% body weight
• Nocturnal symptoms: Suggests organic pathology over functional disorder
• Rectal bleeding: Always investigate
• Unexplained iron deficiency anaemia
• Palpable abdominal or rectal mass
• Family history: First-degree relative with colorectal cancer or IBD

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5. Clinical Presentation

Ulcerative Colitis

Cardinal Symptoms

Disease Extent Patterns

• Proctitis (E1): Rectal bleeding, urgency, tenesmus. Constipation may occur (paradoxically) due to rectal inflammation.
• Left-sided Colitis (E2): As above plus left-sided abdominal pain, more frequent diarrhoea.
• Extensive/Pancolitis (E3): Severe diarrhoea (> 6 stools/day), systemic symptoms (fever, tachycardia, weight loss), risk of acute severe colitis.

Systemic Features

• Fatigue and malaise
• Weight loss (severe disease)
• Low-grade fever
• Anorexia
• Dehydration (severe flares)

Crohn's Disease

Presentation by Phenotype

Inflammatory (B1):

• Chronic diarrhoea (often non-bloody)
• Cramping abdominal pain (particularly post-prandial)
• Weight loss and malnutrition
• Low-grade fever
• Aphthous oral ulcers

Stricturing (B2):

• Colicky abdominal pain
• Post-prandial pain and bloating ("food fear")
• Intermittent obstructive symptoms (nausea, vomiting)
• Weight loss
• Palpable mass (thickened bowel loop)

Penetrating/Fistulising (B3):

• Enteroenteric fistula: May be asymptomatic or cause malabsorption
• Enterovesical fistula: Pneumaturia (air in urine), faecaluria, recurrent UTIs
• Enterocutaneous fistula: Discharge of bowel content through skin (often post-operative)
• Perianal fistula: Purulent perianal discharge, pain, swelling

Common Presentations

Complications at Presentation

• Abscess: Fever, tender abdominal mass, leukocytosis
• Obstruction: Colicky pain, vomiting, absolute constipation, distension
• Growth failure (paediatric): Often presenting feature in children

Extraintestinal Manifestations (EIMs)

Present in 25-40% of IBD patients. Some correlate with intestinal disease activity; others are independent. [16,17]

Musculoskeletal (Most Common EIM)

Dermatological

Ophthalmological

Hepatobiliary

Haematological and Vascular

• Anaemia: Iron deficiency (chronic bleeding), anaemia of chronic disease, B12/folate deficiency (Crohn's with ileal disease/resection)
• Venous Thromboembolism (VTE): 2-3-fold increased risk due to hypercoagulable state, especially during flares. Requires thromboprophylaxis during hospitalisation.
• Osteoporosis/Osteopenia: Due to chronic inflammation, malabsorption (vitamin D, calcium), corticosteroid use. DEXA scanning recommended.

Renal and Urological

• Nephrolithiasis: Calcium oxalate stones (ileal Crohn's due to increased oxalate absorption); uric acid stones (dehydration)
• Obstructive uropathy: Inflammatory mass or abscess compressing ureter
• Amyloidosis: Rare complication of chronic inflammation (AA amyloidosis)

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6. Investigations

Initial Assessment

Blood Tests

Stool Tests

Endoscopic Evaluation

Gold standard for diagnosis. Requires direct visualisation and histological confirmation.

Colonoscopy with Ileoscopy and Multiple Biopsies

Ulcerative Colitis Findings:

• Macroscopic: Loss of vascular pattern, erythema, granularity, friability (bleeds with light contact), continuous inflammation from rectum proximally, pseudopolyps (islands of regenerating mucosa)
• Severe disease: Spontaneous bleeding, deep ulceration, mucosal sloughing
• Histology: Crypt architectural distortion, basal plasmacytosis, crypt abscesses, goblet cell depletion, lamina propria chronic inflammatory infiltrate. No granulomas.

Crohn's Disease Findings:

• Macroscopic: Aphthous ulcers (small, discrete, punched-out), serpiginous/linear deep ulcers, cobblestone appearance (oedematous mucosa between ulcers), skip lesions, rectal sparing (common), strictures, fistula openings
• Histology: Non-caseating epithelioid granulomas (20-30% of biopsies), transmural lymphoid aggregates, focal (discontinuous) inflammation, preserved crypt architecture between lesions
• Ileoscopy: Terminal ileal intubation essential; ileal disease confirms Crohn's diagnosis

Biopsy Protocol:

• Minimum 2 biopsies from at least 5 sites (rectum, sigmoid, descending, transverse, ascending colon, terminal ileum)
• Label each site separately
• Even from normal-appearing mucosa (may show microscopic inflammation in Crohn's)

Other Endoscopic Procedures

Imaging

Cross-Sectional Imaging

Plain Radiography

Severity Assessment

Truelove and Witts Criteria for Acute Severe Ulcerative Colitis (ASUC)

Presence of > 6 bloody stools per day AND at least one of:

• Heart rate > 90 bpm
• Temperature > 37.8°C
• Haemoglobin less than 10.5 g/dL
• ESR > 30 mm/hr

Fulminant colitis: ASUC + one or more of:

• Toxic megacolon
• Hypotension
• Altered mental status
• Peritoneal signs [10,11]

Travis Criteria (Day 3 of IV Steroid Therapy)

Predicts need for colectomy in ASUC:

• Stool frequency > 8/day OR
• Stool frequency 3-8/day + CRP > 45 mg/L

Sensitivity 75%, specificity 85% for predicting colectomy requirement. [10]

Harvey-Bradshaw Index (Crohn's Disease Activity)

Simple clinical scoring (no endoscopy):

• General well-being (0-4)
• Abdominal pain (0-3)
• Number of liquid stools per day
• Abdominal mass (0-3)
• Complications (arthralgia, uveitis, erythema nodosum, etc.)

Score less than 5 = Remission; 5-7 = Mild; 8-16 = Moderate; > 16 = Severe

Crohn's Disease Activity Index (CDAI)

More complex; includes symptoms, haematocrit, weight. Score > 450 = severe; 150-220 = mild; less than 150 = remission. Less used clinically (research trials).

Pre-Treatment Screening

Before commencing immunosuppression or biologics:

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7. Management

Treatment Paradigm: Treat-to-Target Strategy

Modern IBD management emphasises mucosal healing (not just symptom control) and tight disease control to prevent complications, hospitalisation, and surgery. [1,2,9]

Targets:

• Clinical remission: Symptom resolution
• Biochemical remission: Normal CRP, faecal calprotectin
• Endoscopic remission: Mucosal healing on colonoscopy (Mayo 0-1 for UC; absence of ulcers in Crohn's)
• Histological remission: Increasingly recognised goal (no active inflammation on biopsy)

Monitoring: Regular assessment every 3-6 months with clinical symptoms, CRP, faecal calprotectin; colonoscopy at 6-12 months post-treatment escalation and annually/biannually for dysplasia surveillance.

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Ulcerative Colitis Management

Induction of Remission

Mild-Moderate Disease (Proctitis/Left-sided):

1. First-line: 5-ASA (Mesalazine)

   • Proctitis: Rectal therapy (suppository 1g once daily OR enema 1-2g once daily) more effective than oral alone
   • Left-sided colitis: Combination oral mesalazine (2.4-4.8g/day) + rectal mesalazine (1-2g/day) superior to either alone
   • Duration: 8 weeks for induction

2. If inadequate response at 4 weeks:

   • Increase oral mesalazine to maximum dose (4.8g/day)
   • Ensure adherence to rectal therapy
   • Consider adding topical corticosteroid (prednisolone 20mg suppository/enema)

3. If still no response:

   • Add oral corticosteroid: Prednisolone 40mg once daily, taper over 8 weeks
   • OR consider switching to oral budesonide MMX 9mg OD (fewer systemic effects; UC-specific formulation)

Moderate-Severe Disease:

1. Oral corticosteroid (Prednisolone 40mg OD) + 5-ASA (oral + rectal)
2. Prednisolone taper: Reduce by 5mg weekly once remission achieved (usually 8-week course)
3. Do not use corticosteroids for maintenance (ineffective; unacceptable side effects)

Extensive Disease/Refractory:

• Consider early biologics or small molecules (see below)

Acute Severe Ulcerative Colitis (ASUC) – MEDICAL EMERGENCY [10,11]

Immediate Management (Day 0):

1. Admit to hospital with surgical consultation at admission
2. IV corticosteroids: Hydrocortisone 100mg QDS OR methylprednisolone 60mg OD (IV)
3. IV fluids: Correct dehydration and electrolyte abnormalities (especially potassium)
4. Thromboprophylaxis: LMWH (high VTE risk)
5. Stool cultures: C. difficile toxin, bacterial pathogens, consider CMV if steroid-refractory
6. Abdominal X-ray: Assess for toxic megacolon (colon > 6cm)
7. Daily examination: Stool frequency, abdominal signs, temperature, HR
8. Avoid: Opiates (mask symptoms, increase megacolon risk), NSAIDs, anticholinergics, anti-diarrhoeals
9. Nutrition: Enteral/oral nutrition as tolerated (NBM not required unless surgical intervention planned)

Day 3 Assessment (Travis Criteria):

• Stool frequency > 8/day OR 3-8/day + CRP > 45 mg/L predicts 85% colectomy risk
• Improving (stool frequency decreasing, apyrexial, CRP falling): Continue IV steroids to Day 5-7, then switch to oral prednisolone taper + 5-ASA maintenance
• Not improving: Commence rescue therapy

Rescue Therapy (if no response by Day 3-5):

Two options (equipotent efficacy):

1. Ciclosporin (Calcineurin inhibitor)

   • IV 2mg/kg/day continuous infusion
   • Monitor levels (target 200-400 ng/mL)
   • Monitor BP, renal function, magnesium
   • Risk: Seizures (check cholesterol, Mg), opportunistic infection (PCP prophylaxis with co-trimoxazole)
   • Bridge to thiopurine maintenance (start azathioprine during ciclosporin therapy)
   • Duration: 7 days IV, then oral ciclosporin for 3 months while thiopurine loading

2. Infliximab (Anti-TNF antibody)

   • 5mg/kg IV infusion at Week 0, 2, 6, then 8-weekly maintenance
   • Advantages: Can continue as long-term maintenance; faster acting
   • Screen for TB, HBV, HCV before use
   • Consider combination with thiopurine (reduces immunogenicity, increases efficacy)

If rescue therapy fails (Day 7-10): Colectomy

Surgical options:

• Subtotal colectomy with end ileostomy (emergency): Preserves rectum for future restorative surgery
• Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) (elective, staged): Curative; preserves continence [18]

Maintenance of Remission

Thiopurine Monitoring:

• TPMT genotype/phenotype before starting (avoid if deficient; reduce dose if intermediate)
• FBC, LFTs: Weekly for 4 weeks, then fortnightly for 4 weeks, then 3-monthly
• Warn about infection risk, bone marrow suppression, hepatotoxicity

Advanced Therapies for Moderate-Severe UC

1. Anti-TNF Antibodies

• Efficacy: 60-70% clinical response; 40-50% remission at 1 year
• Combination therapy: Infliximab + azathioprine superior to monotherapy (reduces immunogenicity)
• Monitoring: Drug levels and anti-drug antibodies (therapeutic drug monitoring) to optimise dosing
• Contraindications: Active TB, heart failure (NYHA III/IV), demyelinating disease, malignancy [19]

2. Vedolizumab (Anti-α4β7 Integrin – Gut-Selective)

• Mechanism: Blocks lymphocyte trafficking to GI tract; minimal systemic immunosuppression
• Dosing: 300mg IV Week 0, 2, 6, then every 8 weeks (SC formulation available: 108mg every 2 weeks)
• Efficacy: Slower onset than anti-TNF (12 weeks to response); 45-50% remission at 1 year
• Advantages: Gut-selective (lower infection risk, safe in elderly); no TB reactivation risk
• Preferred in: Older patients, prior malignancy, recurrent infections, failed anti-TNF [20]

3. Ustekinumab (Anti-IL-12/IL-23)

• Dosing: Weight-based IV loading (260mg if less than 55kg, 390mg if 55-85kg, 520mg if > 85kg), then 90mg SC every 8 weeks
• Efficacy: 60% clinical response; 40-45% remission at 1 year
• Use: Approved for UC after anti-TNF failure [14]

4. JAK Inhibitors (Small Molecules – Oral)

• Advantages: Oral, rapid onset (2-4 weeks), no immunogenicity
• Risks: Herpes zoster (consider vaccination), VTE, hyperlipidaemia, infections [21]

5. S1P Modulators

• Efficacy: 37% remission at 1 year
• Monitoring: First-dose cardiac monitoring (bradycardia risk), ophthalmic exam (macular oedema), LFTs

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Crohn's Disease Management

Induction of Remission

Ileocaecal Mild-Moderate:

1. Budesonide (Entocort) 9mg once daily for 8 weeks

   • Ileal-release formulation: High first-pass metabolism (fewer systemic steroid effects than prednisolone)
   • Efficacy 50-60% remission
   • Taper to 6mg for 2 weeks, then 3mg for 2 weeks

2. If inadequate response or contraindication: Prednisolone 40mg OD (as per UC protocol)

Colonic/Extensive Moderate-Severe:

1. Prednisolone 40mg OD, taper over 8 weeks
2. Consider early biologics (anti-TNF) if high-risk features:
   • Extensive small bowel disease
   • Deep ulceration on endoscopy
   • Perianal disease
   • Young age at diagnosis (less than 40)
   • Stricturing or penetrating behaviour

5-ASA NOT Effective in Crohn's Disease (multiple RCTs show no benefit for induction or maintenance)

Maintenance of Remission

First-line Immunomodulators:

1. Azathioprine (2-2.5mg/kg/day) or Mercaptopurine (1-1.5mg/kg/day)

   • Slow onset (3-6 months to full effect)
   • Monitoring: TPMT pre-treatment, FBC/LFTs as per UC protocol
   • Efficacy: 60-70% maintain remission at 1 year
   • Continue for at least 4 years if effective

2. Methotrexate (SC 25mg once weekly + folic acid 5mg 48h post-dose)

   • Alternative if thiopurine intolerance/failure
   • Teratogenic: Contraception mandatory (males and females)
   • Monitoring: FBC, LFTs, baseline CXR (pneumonitis risk)
   • Efficacy: 65% maintain remission at 1 year [5,6]

Top-Down Strategy (Early Biologics):

Increasingly used for high-risk Crohn's rather than step-up approach. Achieves better long-term outcomes (less surgery, fewer complications). [9]

Biologic and Advanced Therapies for Crohn's Disease

1. Anti-TNF Antibodies

• Efficacy: 60-70% clinical response; 40-50% remission at 1 year
• Fistula Closure: Infliximab achieves 30-50% complete fistula closure
• Loss of Response: ~10-20%/year develop secondary loss of response (anti-drug antibodies). Manage with dose escalation or switch to alternative biologic.
• Therapeutic Drug Monitoring (TDM): Measure trough levels and anti-drug antibodies to guide dose optimisation or switch decisions [19]

2. Vedolizumab

• Dosing: 300mg IV Week 0, 2, 6, then 8-weekly (SC available)
• Efficacy: 39% remission at 1 year (GEMINI 2 trial)
• Preferred in: Anti-TNF failure, infections, elderly, extraintestinal manifestations (less effective for EIMs than anti-TNF) [20]

3. Ustekinumab

• Dosing: Weight-based IV loading, then 90mg SC every 8 weeks
• Efficacy: 53% clinical response; 40% remission at 1 year (UNITI trials)
• Use: Second-line after anti-TNF failure; effective in refractory disease [14]

4. Risankizumab (Anti-IL-23)

• Dosing: 600mg IV Week 0, 4, 8, then 360mg SC every 8 weeks
• Efficacy: Superior to placebo in anti-TNF-experienced patients (ADVANCE, MOTIVATE trials)
• Latest addition: Recently approved; potent option for refractory Crohn's [15]

Sequential Biologic Use:

• After first biologic failure: ~40-50% respond to second biologic (same class or different mechanism)
• Consider switching mechanism after anti-TNF failure (e.g., vedolizumab, ustekinumab)
• TDM informs decision: Low drug levels + no antibodies → dose escalation; high antibodies → switch drug

Perianal Crohn's Disease [22]

Stepwise Approach:

1. Assessment: MRI pelvis (essential to map fistula anatomy and exclude abscess)
2. Examination Under Anaesthesia (EUA): Drain abscesses, place setons (non-cutting drains to maintain drainage and prevent abscess formation)
3. Medical Therapy:
   • Antibiotics: Metronidazole 400mg TDS + Ciprofloxacin 500mg BD for 6-8 weeks (symptom improvement; not curative)
   • Anti-TNF: Infliximab is most effective medical therapy (30-50% complete fistula closure at 1 year). Combination with azathioprine improves outcomes.
4. Surgical Options (complex; require specialist colorectal surgery):
   • Fistulotomy: For simple, low fistulae (risk of incontinence)
   • Advancement flaps: For complex fistulae
   • Diverting stoma: For refractory disease to allow healing
   • Proctectomy: Last resort for destroyed rectum/sphincters

Stricturing Crohn's Disease

Fibrotic vs Inflammatory Stricture:

• MRI Enterography: Differentiates active inflammation (T2 hyperintense, enhancing) from fibrotic stricture (T2 hypointense, no enhancement, prestenotic dilation)

Management:

1. Inflammatory stricture: Optimise medical therapy (biologics)
2. Fibrotic stricture:
   • Endoscopic balloon dilation (if short less than 4cm, accessible)
   • Surgery: Stricturoplasty (preserves bowel length) or resection (if long/multiple strictures)
3. Avoid repeated resections: "Bowel-sparing" approach; preserve intestinal length to avoid short bowel syndrome [5,6]

Surgery for Crohn's Disease [18]

NOT curative – postoperative recurrence ~70% at 10 years (endoscopic recurrence earlier).

Indications:

• Failed medical therapy (refractory symptoms despite biologics)
• Stricturing disease with obstructive symptoms
• Penetrating disease (abscess drainage, fistula management)
• Dysplasia/cancer
• Growth failure in children

Common Procedures:

• Ileocaecal resection (most common): For terminal ileal disease
• Stricturoplasty: Widen stricture without resection (Heineke-Mikulicz, Finney techniques)
• Abscess drainage: Percutaneous or surgical
• Segmental colonic resection: For localised colonic disease

Postoperative Prophylaxis:

• Anti-TNF (adalimumab or infliximab) started within 4 weeks post-op reduces endoscopic recurrence by 50%
• Thiopurines: Less effective than biologics but reduce clinical recurrence
• Colonoscopy at 6-12 months post-op to assess anastomosis (Rutgeerts score); escalate therapy if recurrence detected [5]

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Supportive and Adjunctive Therapies

Nutrition

Crohn's Disease:

• Exclusive Enteral Nutrition (EEN): Polymeric formula (sole nutrition for 6-8 weeks). Effective for inducing remission in paediatric Crohn's (efficacy comparable to steroids; preferred in children). Less effective in adults (adherence issues).
• Malnutrition: Common due to malabsorption (ileal disease), inflammation. Nutritional supplementation (vitamins B12, D, iron, calcium, zinc, folate).
• Low FODMAP diet: May reduce symptoms but does not alter inflammation.

UC:

• Nutritional deficiencies less common (colon does not absorb nutrients)
• Iron supplementation for anaemia (IV if intolerant to oral)
• Maintain adequate hydration during flares

Symptom Management

• Diarrhoea: Loperamide (use cautiously; avoid in severe flares/toxic megacolon risk)
• Pain: Paracetamol (first-line). Avoid NSAIDs (may trigger flares). Opiates only short-term (addiction risk, ileus).
• Bile salt malabsorption (ileal Crohn's/resection): Cholestyramine 4-8g/day

Psychological Support

• Anxiety, depression common (30-40% prevalence)
• Cognitive behavioural therapy, support groups, psychological input improve quality of life

Smoking Cessation (Crohn's)

• Smoking doubles relapse risk, accelerates disease progression, increases surgery need
• Smoking cessation should be strongly encouraged (improves outcomes)

Vaccinations

• Before immunosuppression: Pneumococcal (PCV13 + PPSV23), influenza (annual), hepatitis B, HPV
• Avoid live vaccines on immunosuppression: MMR, varicella, yellow fever, BCG
• Inactivated vaccines safe: Influenza, pneumococcal, COVID-19

Bone Health

• DEXA scan: At diagnosis if risk factors (corticosteroid use, postmenopausal, low BMI)
• Calcium + Vitamin D supplementation: All patients on corticosteroids
• Bisphosphonates: If osteoporosis confirmed

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8. Complications

Acute Complications

Chronic Complications

Colorectal Cancer (CRC) Risk [23]

Increased Risk in Long-Standing Extensive IBD:

Surveillance Colonoscopy Protocol (BSG/ECCO Guidelines):

• Start surveillance: 8 years after symptom onset (earlier if PSC: start at diagnosis)
• Frequency:
  • "High risk (extensive colitis + PSC, stricture, dysplasia in last 5 years, family history): Annual"
  • "Intermediate risk (extensive colitis, post-inflammatory polyps): 2-3 yearly"
  • "Low risk (left-sided colitis, no other risk factors): 5 yearly"
• Technique: High-definition white-light endoscopy with chromoendoscopy (dye spray: indigo carmine/methylene blue) preferred over random biopsies. Target biopsies of visible lesions.
• Dysplasia Management:
  • "Low-grade dysplasia (LGD): If visible, polypoid, completely resectable → Endoscopic resection + intensive surveillance (6 months, then annually). If flat/invisible → Colectomy discussion."
  • "High-grade dysplasia (HGD): Colectomy recommended (30-40% have synchronous cancer)."
  • "Indefinite for dysplasia: Repeat colonoscopy in 3-6 months after optimising inflammation control. [23]"

Strictures (Crohn's)

• Occur in 30-40% of Crohn's patients
• Fibrostenotic (non-inflammatory) strictures: Require endoscopic dilation or surgery
• Inflammatory strictures: May respond to medical therapy (biologics)
• Symptoms: Intermittent obstructive symptoms, post-prandial pain, bloating

Fistulae (Crohn's)

• Present in ~30% of Crohn's patients over disease course
• Perianal (most common): Managed as per section above
• Enterovesical: Recurrent UTIs, pneumaturia, faecaluria. Requires surgical repair.
• Enterocutaneous: Often post-operative. May require surgical revision.
• Enteroenteric: Often asymptomatic; may cause bacterial overgrowth/malabsorption.

Malnutrition and Deficiencies

Crohn's (especially ileal):

• Vitamin B12 deficiency: Terminal ileum affected → pernicious anaemia. Requires 3-monthly IM hydroxocobalamin.
• Fat-soluble vitamins (A, D, E, K): Ileal disease/resection → bile salt malabsorption.
• Iron deficiency: Chronic bleeding, malabsorption, dietary restriction.
• Zinc, selenium: Chronic diarrhoea.

Monitoring: Annual micronutrient levels (B12, folate, vitamin D, iron, zinc, selenium).

Osteoporosis

• Prevalence: 40-50% have low bone mineral density
• Causes: Chronic inflammation, corticosteroids, malabsorption (calcium, vitamin D), smoking, low BMI
• Screening: DEXA scan at diagnosis if risk factors; repeat every 2-3 years
• Treatment: Calcium + vitamin D supplementation; bisphosphonates if T-score < -2.5

Venous Thromboembolism (VTE)

• 2-3-fold increased risk due to hypercoagulable state (inflammation, platelet activation)
• Higher during flares and hospitalisation
• Prophylaxis: LMWH during hospitalisation, post-operative; consider extended prophylaxis in high-risk patients

Drug-Related Complications

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9. Prognosis and Outcomes

Natural History

Ulcerative Colitis:

• Chronic relapsing-remitting course: 50% in remission at any time; 30% mild activity; 20% moderate-severe.
• 10-year colectomy rate: ~10-15% (decreasing with biologic era).
• CRC risk: Increases with disease duration and extent (surveillance reduces mortality).
• Life expectancy: Near-normal if well-controlled; small excess mortality in severe uncontrolled disease.

Crohn's Disease:

• Progressive disease in majority: Transition from inflammatory (B1) to stricturing (B2) or penetrating (B3) behaviour over time.
• Surgery rate: 50-70% require surgery within 10 years of diagnosis (decreasing with early biologics).
• Post-operative recurrence: 70% endoscopic recurrence at 1 year; 30-50% clinical recurrence at 5 years (reduced with biologic prophylaxis).
• Disability: 15-20% experience significant work disability over disease course.
• Life expectancy: Slightly reduced in population studies (mainly from surgical complications, malignancy, VTE).

Predictors of Poor Prognosis (Crohn's)

• Young age at diagnosis (less than 40, especially less than 25)
• Extensive small bowel disease
• Perianal disease at presentation
• Need for steroids at diagnosis
• Deep ulceration on index endoscopy
• Stricturing or penetrating behaviour
• Smoking

"Accelerated Step-Up" or "Top-Down" Therapy: Early biologic use in high-risk patients improves long-term outcomes (mucosal healing, reduced surgery, hospitalisations). [9]

Pregnancy and Fertility [24]

Fertility:

• UC/Crohn's in remission: Fertility comparable to general population
• Active disease: Reduced fertility (inflammation, tubal adhesions)
• Post-IPAA surgery (UC): Temporary reduction in female fertility (pelvic adhesions)
• Male fertility: Sulfasalazine reduces sperm count/motility (reversible; switch to mesalazine)

Pregnancy Outcomes:

• Disease in remission: Normal pregnancy outcomes
• Active disease at conception: Higher risk of miscarriage, preterm birth, low birth weight, flares during pregnancy
• Recommendation: Conceive during remission; continue most IBD medications during pregnancy (benefits outweigh risks)

Medication Safety in Pregnancy:

Mode of Delivery:

• Vaginal delivery safe in most cases
• Caesarean section if: Active perianal Crohn's, IPAA pouch (to protect pouch/sphincters)

Postpartum:

• Restart/continue medications (safe during breastfeeding except methotrexate)
• Monitor for flares (common in postpartum period)

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10. Evidence and Guidelines

Key Clinical Guidelines

Landmark Trials

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11. Patient and Layperson Explanation

What is Inflammatory Bowel Disease (IBD)?

IBD is a term for two conditions: Ulcerative Colitis (UC) and Crohn's Disease. Both cause long-term inflammation in the digestive system, leading to symptoms like diarrhoea, abdominal pain, and fatigue.

Ulcerative Colitis affects only the large bowel (colon), starting at the rectum and spreading upwards. The inflammation stays in the inner lining of the bowel.

Crohn's Disease can affect any part of the digestive system, from mouth to bottom, but usually affects the end of the small intestine (terminal ileum). The inflammation goes deeper through the bowel wall and can cause complications like narrowing (strictures) or abnormal connections (fistulae).

What Causes IBD?

The exact cause is unknown, but IBD develops when the immune system mistakenly attacks the bowel. This happens in people who are genetically susceptible, often triggered by environmental factors (diet, infections, smoking).

IBD is NOT caused by stress or eating the wrong foods, though these may worsen symptoms.

What Are the Symptoms?

Ulcerative Colitis:

• Bloody diarrhoea (main symptom)
• Urgency to go to the toilet
• Cramping tummy pain
• Feeling tired

Crohn's Disease:

• Diarrhoea (may not be bloody)
• Tummy pain (often right lower side)
• Weight loss
• Tiredness
• Mouth ulcers
• Problems around the back passage (fissures, abscesses)

How is it Diagnosed?

• Blood tests: Check for anaemia and inflammation
• Stool tests: Rule out infection; measure inflammation (faecal calprotectin)
• Colonoscopy: Camera test to look inside the bowel and take small tissue samples (biopsies)
• Scans (CT or MRI): For Crohn's to check the small bowel

How is IBD Treated?

Treatment aims to:

1. Control inflammation (get into remission)
2. Keep inflammation under control (stay in remission)
3. Avoid complications

Medications:

• Anti-inflammatory drugs (5-ASA like Mesalazine): First treatment for mild-moderate Ulcerative Colitis (taken as tablets or suppositories/enemas)
• Steroids (Prednisolone): To quickly reduce inflammation during flare-ups (short-term only; not for long-term use)
• Immunosuppressants (Azathioprine, Methotrexate): Reduce immune system activity to keep disease under control
• Biologics (Infliximab, Adalimumab, Vedolizumab, Ustekinumab): Advanced treatments given by injection or drip; very effective for moderate-severe disease
• JAK inhibitors (Tofacitinib): Tablets for moderate-severe disease

Surgery:

Sometimes needed if medicines don't work or complications develop.

• Ulcerative Colitis: Removing the colon (colectomy) cures UC. Surgeons can often create an internal pouch from small bowel to replace the colon.
• Crohn's Disease: Surgery does not cure Crohn's (it can come back), but may be needed to remove damaged sections, drain abscesses, or fix narrowings.

Can I Live a Normal Life?

Yes! With modern treatments, most people with IBD can live full, active lives. The disease typically has "flare-ups" (active symptoms) and "remission" (no symptoms). The goal is to keep you in remission as long as possible.

What About Pregnancy?

Women with IBD can have healthy pregnancies. It's important to:

• Keep disease controlled before getting pregnant
• Continue most medications during pregnancy (they are safe; stopping them is riskier)
• Work closely with your IBD team and obstetrician

Long-Term Monitoring

• Regular check-ups: Blood tests, stool tests
• Colonoscopy surveillance: After 8-10 years (to check for bowel changes/cancer risk)
• Bone health: Scans if on steroids long-term
• Vaccinations: Keep up to date (flu, pneumonia, etc.)

Where Can I Get Support?

• Crohn's & Colitis UK (charity): Information, support groups, helpline
• IBD nurse specialists: Available at most hospitals
• Patient forums and online communities

Key Messages

• IBD is a lifelong condition, but not life-threatening with good treatment
• Modern treatments are very effective
• Surgery can be curative for UC
• Most people with IBD can work, travel, exercise, and have families
• Never stop medications without discussing with your doctor (flare-ups are dangerous)

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12. References

Primary Sources

1. Raine T, Bonovas S, Burisch J, et al. ECCO Guidelines on Therapeutics in Ulcerative Colitis: Medical Treatment. J Crohns Colitis. 2022;16(1):2-17. doi:10.1093/ecco-jcc/jjab178. PMID: 34635910.

2. Torres J, Bonovas S, Doherty G, et al. ECCO Guidelines on Therapeutics in Crohn's Disease: Medical Treatment. J Crohns Colitis. 2020;14(1):4-22. doi:10.1093/ecco-jcc/jjz180. PMID: 31711158.

3. Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol. 2019;114(3):384-413. doi:10.14309/ajg.0000000000000152. PMID: 30840605.

4. Ko CW, Singh S, Feuerstein JD, et al. AGA Clinical Practice Update on Diet and Nutritional Therapies in Patients With Inflammatory Bowel Disease: Expert Review. Gastroenterology. 2024;166(3):521-532. doi:10.1053/j.gastro.2023.11.303. PMID: 38276922.

5. Lichtenstein GR, Loftus EV, Isaacs KL, et al. ACG Clinical Guideline: Management of Crohn's Disease in Adults. Am J Gastroenterol. 2018;113(4):481-517. doi:10.1038/ajg.2018.27. PMID: 29610508.

6. Feuerstein JD, Ho EY, Shmidt E, et al. AGA Clinical Practice Guidelines on the Medical Management of Moderate to Severe Luminal and Perianal Fistulizing Crohn's Disease. Gastroenterology. 2021;160(7):2496-2508. doi:10.1053/j.gastro.2021.04.022. PMID: 33885977.

7. de Lange KM, Moutsianas L, Lee JC, et al. Genome-wide association study implicates immune activation of multiple integrin genes in inflammatory bowel disease. Nat Genet. 2017;49(2):256-261. doi:10.1038/ng.3760. PMID: 28067908.

8. Roda G, Chien Ng S, Kotze PG, et al. Crohn's disease. Nat Rev Dis Primers. 2020;6(1):22. doi:10.1038/s41572-020-0156-2. PMID: 32467580.

9. Colombel JF, Panaccione R, Bossuyt P, et al. Effect of tight control management on Crohn's disease (CALM): a multicentre, randomised, controlled phase 3 trial. Lancet. 2018;390(10114):2779-2789. doi:10.1016/S0140-6736(17)32641-7. PMID: 29096949.

10. Lamb CA, Kennedy NA, Raine T, et al. British Society of Gastroenterology consensus guidelines on the management of inflammatory bowel disease in adults. Gut. 2019;68(Suppl 3):s1-s106. doi:10.1136/gutjnl-2019-318484. PMID: 31562236.

11. Turner D, Walsh CM, Steinhart AH, Griffiths AM. Response to corticosteroids in severe ulcerative colitis: a systematic review of the literature and a meta-regression. Clin Gastroenterol Hepatol. 2007;5(1):103-110. doi:10.1016/j.cgh.2006.09.033. PMID: 17142106.

12. Ng SC, Shi HY, Hamidi N, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies. Lancet. 2017;390(10114):2769-2778. doi:10.1016/S0140-6736(17)32448-0. PMID: 29050646.

13. Kaplan GG, Windsor JW. The four epidemiological stages in the global evolution of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2021;18(1):56-66. doi:10.1038/s41575-020-00360-x. PMID: 33028996.

14. Feagan BG, Sandborn WJ, Gasink C, et al. Ustekinumab as Induction and Maintenance Therapy for Crohn's Disease. N Engl J Med. 2016;375(20):1946-1960. doi:10.1056/NEJMoa1602773. PMID: 27959607.

15. Ferrante M, Panaccione R, Baert F, et al. Risankizumab as maintenance therapy for moderately to severely active Crohn's disease: results from the multicentre, randomised, double-blind, placebo-controlled, withdrawal phase 3 FORTIFY maintenance trial. Lancet. 2022;399(10340):2031-2046. doi:10.1016/S0140-6736(22)00466-4. PMID: 35525255.

16. Harbord M, Annese V, Vavricka SR, et al. ECCO Guidelines on Extraintestinal Manifestations in Inflammatory Bowel Disease. J Crohns Colitis. 2023;17(8):1179-1211. doi:10.1093/ecco-jcc/jjad025. PMID: 37351850.

17. Vavricka SR, Schoepfer A, Scharl M, et al. Extraintestinal Manifestations of Inflammatory Bowel Disease. Inflamm Bowel Dis. 2015;21(8):1982-1992. doi:10.1097/MIB.0000000000000392. PMID: 25993694.

18. Lightner AL, Vogel JD, Carmichael JC, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Surgical Management of Crohn's Disease. Dis Colon Rectum. 2020;63(8):1028-1052. doi:10.1097/DCR.0000000000001716. PMID: 32692071.

19. Feagan BG, Rutgeerts P, Sands BE, et al. Vedolizumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2013;369(8):699-710. doi:10.1056/NEJMoa1215734. PMID: 23964932.

20. Sandborn WJ, Feagan BG, Rutgeerts P, et al. Vedolizumab as induction and maintenance therapy for Crohn's disease. N Engl J Med. 2013;369(8):711-721. doi:10.1056/NEJMoa1215739. PMID: 23964933.

21. Sandborn WJ, Su C, Sands BE, et al. Tofacitinib as Induction and Maintenance Therapy for Ulcerative Colitis. N Engl J Med. 2017;376(18):1723-1736. doi:10.1056/NEJMoa1606910. PMID: 28467869.

22. Gecse KB, Bemelman W, Kamm MA, et al. A global consensus on the classification, diagnosis and multidisciplinary treatment of perianal fistulising Crohn's disease. Gut. 2014;63(9):1381-1392. doi:10.1136/gutjnl-2013-306709. PMID: 24951257.

23. Laine L, Kaltenbach T, Barkun A, et al. SCENIC international consensus statement on surveillance and management of dysplasia in inflammatory bowel disease. Gastroenterology. 2015;148(3):639-651. doi:10.1053/j.gastro.2015.01.031. PMID: 25702852.

24. European Crohn's and Colitis Organisation. ECCO Guidelines on Sexuality, Fertility, Pregnancy, and Lactation in Inflammatory Bowel Disease. J Crohns Colitis. 2022;16(Supplement 2):ii1-ii31. doi:10.1093/ecco-jcc/jjac035. PMID: 36005814.

25. Maaser C, Sturm A, Vavricka SR, et al. ECCO-ESGAR Guideline for Diagnostic Assessment in IBD Part 1: Initial diagnosis, monitoring of known IBD, detection of complications. J Crohns Colitis. 2019;13(2):144-164. doi:10.1093/ecco-jcc/jjy113. PMID: 30137275.

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13. Examination Focus

High-Yield MCQ/SBA Topics

1. UC vs Crohn's Differentiation: Pattern (continuous vs skip), depth (mucosal vs transmural), location (colon vs any GI), histology (no granulomas vs granulomas), complications (toxic megacolon vs fistulae).

2. Acute Severe Ulcerative Colitis: Truelove & Witts criteria (> 6 bloody stools + systemic toxicity). Management: IV hydrocortisone, fluids, thromboprophylaxis, surgical review. Travis criteria (Day 3 assessment).

3. First-Line Treatments:

   • Mild UC: 5-ASA (mesalazine) oral + rectal
   • Moderate UC: 5-ASA + oral steroids
   • Severe UC (ASUC): IV steroids → rescue therapy (ciclosporin or infliximab) → colectomy
   • Mild-moderate ileocaecal Crohn's: Budesonide
   • Moderate-severe Crohn's: Prednisolone OR biologics (early if high-risk)
   • Perianal Crohn's: MRI pelvis + EUA/seton + antibiotics + anti-TNF

4. Smoking: Protective in UC, harmful in Crohn's.

5. Histology:

   • UC: Crypt abscesses, basal plasmacytosis, NO granulomas
   • Crohn's: Non-caseating granulomas (20-30%), transmural inflammation

6. Extraintestinal Manifestations:

   • Correlate with disease activity: Peripheral arthritis, erythema nodosum
   • Independent of disease activity: Axial spondyloarthropathy, pyoderma gangrenosum, PSC

7. PSC: Strongly associated with UC. Elevated ALP. MRCP shows strictures. Increased cholangiocarcinoma and CRC risk.

8. Biologics:

   • Anti-TNF (infliximab, adalimumab): First-line for moderate-severe; best for fistulising Crohn's
   • Vedolizumab: Gut-selective; safer in elderly/infections
   • Ustekinumab: Anti-IL-12/23; effective in anti-TNF failures
   • Tofacitinib: Oral JAK inhibitor for UC; VTE and infection risk

9. Colorectal Cancer Surveillance: Start at 8 years (sooner if PSC). Frequency based on risk. Chromoendoscopy preferred.

10. Surgery:

    • UC: Colectomy is curative
    • Crohn's: NOT curative; 50-70% need surgery; high recurrence

OSCE/Clinical Scenarios

Station 1: History Taking – Bloody Diarrhoea

• Differentiate UC vs Crohn's vs infectious colitis
• Red flags: Weight loss, nocturnal symptoms, FH
• Assess severity and extraintestinal features

Station 2: Data Interpretation

• Bloods: Anaemia, raised CRP, low albumin
• Faecal calprotectin: Elevated (> 250 = IBD likely)
• Colonoscopy report: Continuous inflammation from rectum (UC) vs skip lesions (Crohn's)
• AXR: Toxic megacolon (> 6cm colon)

Station 3: Management Discussion

• Explain treatment ladder to patient
• Discuss biologic options and monitoring
• Explain need for surveillance colonoscopy

Station 4: Examination

• Abdominal examination: Scars, masses, stomas
• Perianal examination (Crohn's): Fissures, fistulae, skin tags
• Extraintestinal signs: Arthritis, erythema nodosum, oral ulcers

Viva Questions and Model Answers

Q1: How do you differentiate Ulcerative Colitis from Crohn's Disease?

A: Key differences:

• Location: UC affects colon only (rectum always involved, continuous proximally). Crohn's affects any part of GI tract (mouth to anus), commonly terminal ileum, with skip lesions and rectal sparing.
• Depth: UC is mucosal/submucosal. Crohn's is transmural (full thickness).
• Histology: UC has crypt abscesses, no granulomas. Crohn's has non-caseating granulomas in 20-30%.
• Complications: UC → toxic megacolon, haemorrhage. Crohn's → strictures, fistulae, abscesses.
• Surgery: UC → curative (colectomy). Crohn's → non-curative (high recurrence).

Q2: Describe the management of Acute Severe Ulcerative Colitis.

A: ASUC is defined by Truelove & Witts criteria: > 6 bloody stools/day + HR> 90 OR temp> 37.8 OR Hbless than 10.5 OR ESR> 30.

Immediate Management:

1. Hospital admission with surgical review
2. IV hydrocortisone 100mg QDS
3. IV fluids and electrolyte correction
4. VTE prophylaxis (LMWH)
5. Stool cultures (C. diff, bacterial)
6. AXR (exclude toxic megacolon > 6cm)
7. Avoid opiates, anticholinergics, NSAIDs

Day 3 Assessment (Travis Criteria):

• If > 8 stools/day OR 3-8 stools + CRP> 45 → 85% will need colectomy
• If improving → continue IV steroids; switch to oral prednisolone Day 5-7
• If not improving → Rescue therapy: Ciclosporin IV OR Infliximab IV

If rescue fails → Colectomy

Q3: What are the indications for surgery in Crohn's Disease?

A: Surgery is not curative but indicated for:

1. Failed medical therapy: Refractory symptoms despite biologics
2. Stricturing disease: Symptomatic obstruction not responsive to medical therapy or balloon dilation
3. Penetrating complications: Abscess (not amenable to drainage), symptomatic fistulae (enterovesical, enterocutaneous)
4. Dysplasia or cancer
5. Growth failure in children
6. Toxic megacolon (rare in Crohn's)

Common procedures: Ileocaecal resection, stricturoplasty (preserve bowel length), abscess drainage, segmental colonic resection.

Postoperative: Start anti-TNF within 4 weeks to reduce endoscopic recurrence. Colonoscopy at 6-12 months (Rutgeerts score).

Q4: Explain the colorectal cancer surveillance protocol in IBD.

A: Patients with long-standing extensive IBD have increased CRC risk.

Start surveillance: 8 years after symptom onset (sooner if PSC – at diagnosis).

Frequency:

• High risk (extensive colitis + PSC, stricture, dysplasia history, FH CRC): Annual
• Intermediate risk (extensive colitis, post-inflammatory polyps): 2-3 yearly
• Low risk (left-sided colitis): 5 yearly

Technique: High-definition colonoscopy with chromoendoscopy (dye spray: indigo carmine) + targeted biopsies of visible lesions.

Dysplasia management:

• LGD visible/polypoid: Endoscopic resection + intensive surveillance
• LGD flat/invisible: Discuss colectomy
• HGD: Recommend colectomy (30-40% have synchronous cancer)

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.