After reading this note you will be able to describe the clinical approach to IBD, list relevant tropical differentials, interpret key investigations and outline safe initial and definitive management – remembering to verify doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
Inflammatory bowel disease (IBD) comprises chronic, relapsing inflammatory disorders of the gastrointestinal tract, principally Crohn’s disease (CD) and ulcerative colitis (UC). Both are characterised by mucosal ulceration, crypt architectural distortion and a propensity for extra‑intestinal manifestations.
Anatomy and physiology you need
| Structure | Relevance to IBD |
|---|---|
| Terminal ileum | Common CD site; B12 absorption |
| Colon (rectum to cecum) | UC involves continuous mucosa, starts in rectum |
| Mesenteric lymph nodes | Site of granuloma formation in CD |
| Submucosal plexus | Autonomic dysregulation contributes to motility symptoms |
| Hepatobiliary tree | Primary sclerosing cholangitis linked to UC |
| Perianal region | Fistulae, abscesses frequent in CD |
Understanding the layered gut wall (mucosa → submucosa → muscularis → serosa) helps explain why CD can be transmural while UC remains mucosal.
Causes and risk factors
| Category | Specific factors in Kenya |
|---|---|
| Genetic | NOD2, IL23R variants; family history |
| Infectious (tropical) | Prior intestinal TB, chronic schistosomiasis, HIV (immune dysregulation) |
| Environmental | High‑fat Western diet, smoking (worsens CD, may protect UC), urbanisation |
| Immunologic | Dysregulated Th1/Th17 response, loss of regulatory T‑cell control |
| Other comorbidities | Sickle cell disease (vascular compromise), rheumatic diseases (e.g., ankylosing spondylitis) |
| Medication | Long‑term NSAIDs, antibiotics altering gut flora |
Pathophysiology
Genetic susceptibility → impaired epithelial barrier → ↑ intestinal permeability → luminal antigens (bacterial, dietary) penetrate → aberrant innate immune activation → cytokine cascade (TNF‑α, IL‑12/23, IL‑17) → chronic adaptive Th1/Th17 response → tissue injury (ulceration, fibrosis) → clinical disease.
Crohn’s: transmural granulomatous inflammation → strictures, fistulae.
Ulcerative colitis: mucosal ulceration limited to colon → continuous lesions, pseudopolyps.
Clinical features
| Aspect | Key questions / findings | Why it occurs |
|---|---|---|
| Onset & duration | “When did the symptoms start? Have they been continuous or episodic?” | IBD is chronic; flares may be intermittent, whereas infection is often acute. |
| Stool pattern | Frequency, consistency, presence of blood or mucus, nocturnal stools, urgency, tenesmus | Ulceration of colonic mucosa → bloody mucus; rectal involvement → urgency and tenesmus; small‑bowel disease (Crohn’s) often watery, non‑bloody. |
| Abdominal pain | Location (right lower quadrant, periumbilical, left lower), character (cramping vs. constant), relation to meals or bowel movements | Crohn’s ileocolitis → RLQ or periumbilical pain; colonic disease → left‑sided cramping; pain improves after defecation in ulcerative colitis. |
| Weight & appetite | Unintentional weight loss, reduced appetite, early satiety | Chronic inflammation, malabsorption (especially in Crohn’s), and cytokine‑mediated catabolism. |
| Systemic symptoms | Fever, night sweats, fatigue, arthralgia, skin lesions, eye symptoms | Extra‑intestinal manifestations driven by immune dysregulation; systemic inflammation can cause low‑grade fever and fatigue. |
| Growth & development (pediatrics) | Change in growth velocity, delayed puberty | Chronic disease and steroid exposure impair growth; relevant for younger trainees. |
| Medication & infection history | Recent antibiotics, NSAIDs, anti‑TB therapy, HIV status, malaria episodes, sickle‑cell crises | Certain drugs and infections can mimic or trigger colitis; HIV/TB are important mimics in Kenya. |
| Family history | Relatives with IBD, psoriasis, ankylosing spondylitis | Genetic predisposition (NOD2, IL23R) increases risk. |
| Social & dietary factors | Smoking status, diet high in processed foods, travel history | Smoking worsens Crohn’s, may protect ulcerative colitis; travel raises suspicion for infectious colitis. |
Examination findings
| Finding | Interpretation |
|---|---|
| General – pallor, low‑grade fever, tachycardia | Anemia of chronic disease or iron deficiency; systemic inflammation. |
| Abdominal – tenderness (RLQ or left lower), palpable mass, distension, guarding | Local inflammation (Crohn’s ileitis → RLQ), colonic spasm (ulcerative colitis), strictures or abscesses (Crohn’s). |
| Perianal – fissures, fistulae, skin tags, abscess | Typical of Crohn’s perianal disease; absent in ulcerative colitis. |
| Rectal exam – friable mucosa, blood, ulceration | Direct visualization of ulcerative colitis; may be normal in isolated small‑bowel Crohn’s. |
| Skin – erythema nodosum, pyoderma gangrenosum | Immune‑mediated extra‑intestinal manifestations; help differentiate from infection. |
| Joint – swelling of large joints, sacroiliac tenderness | Arthropathy associated with IBD; helps support diagnosis. |
| Eye – uveitis, episcleritis | Extra‑intestinal sign, more common in Crohn’s. |
| Growth parameters (children) – height/weight centiles | Chronic disease impact; useful for severity assessment. |
Differential diagnosis
| Condition | Points toward it | How to separate from IBD |
|---|---|---|
| Infectious colitis (Shigella, Salmonella, Entamoeba, CMV) | Acute onset, recent travel, fever, stool leukocytes, HIV | Stool culture, PCR, ova‑parasite exam; resolves with antimicrobial therapy, no chronic relapsing pattern. |
| Intestinal tuberculosis | Weight loss, night sweats, TB exposure, ileocecal mass | Chest X‑ray, Mantoux/IGRA, TB PCR on tissue; granulomas with caseation, response to anti‑TB drugs. |
| Ischemic colitis | Elderly, vascular disease, sudden LLQ pain, bloody diarrhea | Colonoscopy shows segmental, sharply demarcated lesions; CT angiography shows vascular compromise. |
| Irritable bowel syndrome | Pain improves with defecation, no bleeding, normal labs | Absence of inflammation on labs/endoscopy; symptom pattern linked to stress. |
| Microscopic colitis | Chronic watery diarrhea, normal colonoscopy, elderly | Biopsy shows lymphocytic or collagenous changes; no gross ulceration. |
| Drug‑induced colitis (NSAIDs, antibiotics) | Recent drug exposure, temporal relation | Discontinuation leads to improvement; histology may mimic IBD but lacks chronic architectural distortion. |
| Sickle cell vaso‑occlusive gut crisis | Known sickle cell disease, pain crises, abdominal pain | Hemoglobin electrophoresis, crisis pattern; colonoscopy usually normal. |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| CBC + ESR/CRP | Inflammation, anemia, leukocytosis | Elevated CRP/ESR supports active disease; anemia may be iron deficiency or anemia of chronic disease. |
| Stool studies (culture, PCR, ova‑parasite, C. difficile toxin) | Infectious exclusion | Negative results favour IBD; positive C. difficile may coexist – treat accordingly. |
| Serology (ASCA, pANCA) | Phenotypic clues | ASCA positive → Crohn’s tendency; pANCA positive → ulcerative colitis tendency; not diagnostic alone. |
| Colonoscopy with ileoscopy & biopsies | Mucosal pattern, extent, histology | Continuous ulceration → ulcerative colitis; skip lesions, transmural inflammation, granulomas → Crohn’s. |
| CT/MRI enterography | Small‑bowel involvement, strictures, fistulae, abscesses | Cross‑sectional imaging delineates extraluminal disease; helps stage Crohn’s. |
| Upper GI endoscopy (if upper symptoms) | Esophageal, gastric, duodenal involvement | Skip lesions in upper gut suggest Crohn’s; rule out other causes of anemia. |
| Fecal calprotectin | Presence of intestinal inflammation | High levels indicate active IBD; low levels suggest functional disorder. |
| TB screening (IGRA, chest X‑ray) | Rule out intestinal TB | Positive IGRA or chest lesion → consider TB before immunosuppression. |
| HIV test (if risk) | Co‑infection risk, therapy implications | Positive HIV influences choice of biologics and infection prophylaxis. |
Diagnosis and severity
- Establish diagnosis
- Clinical picture + objective inflammation (elevated CRP/fecal calprotectin) + endoscopic/histologic confirmation.
- Distinguish Crohn’s disease (skip lesions, transmural, granulomas, perianal disease) from ulcerative colitis (continuous colonic involvement, mucosal disease, rectal sparing rare).
- Assess disease extent
- Ulcerative colitis: proctitis, left‑sided, extensive (pancolitis).
- Crohn’s disease: ileal, colonic, ileocolonic, upper GI, isolated small bowel.
- Determine activity (severity) – use a combination of clinical indices (e.g., Mayo score for UC, CDAI for Crohn’s), laboratory markers, and endoscopic findings.
| Severity | Clinical clues | Objective markers |
|---|---|---|
| Mild | <4 stools/day, no systemic signs, no weight loss, no anemia | CRP normal‑low, fecal calprotectin modestly raised, endoscopy shows limited ulceration |
| Moderate | 4–6 stools/day, mild anemia, low‑grade fever, abdominal pain | CRP moderately raised, calprotectin high, endoscopy shows larger ulcerated areas |
| Severe/fulminant | >6 stools/day, gross bleeding, high fever, tachycardia, significant weight loss, toxic megacolon risk | CRP markedly high, calprotectin very high, endoscopy shows deep ulceration, possible perforation on imaging |
- Risk stratification – consider age, extra‑intestinal manifestations, perianal disease, growth failure (children), and comorbid infections (HIV, TB). These influence choice of therapy and monitoring intensity.
Management pathway (brief)
- Induction – oral/rectal 5‑ASA for mild UC; corticosteroid (systemic or budesonide) for moderate‑severe disease; exclusive enteral nutrition or steroids for Crohn’s.
- Maintenance – 5‑ASA (UC), immunomodulators (azathioprine, methotrexate) for steroid‑sparing, biologic agents (anti‑TNF, anti‑integrin, IL‑12/23 inhibitors) for refractory or high‑risk disease.
- Adjuncts – iron supplementation for anemia, calcium/vitamin D, vaccination updates, prophylaxis for opportunistic infections when on biologics.
Monitoring
- Clinical review every 4–8 weeks during induction, then every 3–6 months.
- Labs: CBC, CRP, liver function, drug levels where applicable.
- Fecal calprotectin every 3 months to detect subclinical relapse.
- Endoscopic reassessment at 1 year or earlier if symptoms worsen.
Safety
- Screen for latent TB and hepatitis B before biologics.
- Vaccinate against pneumococcus, influenza, HPV, and consider COVID‑19 boosters.
- Counsel on infection signs, especially in HIV‑positive patients.
Prepared for Year 4 MBChB clinical rotations – Kenya.
Management
Immediate stabilisation
| Problem | Immediate action | Rationale |
|---|---|---|
| Severe anaemia or active GI bleed | Give packed red cells (type‑specific) and tranexamic acid if bleeding is brisk | Restores oxygen delivery; antifibrinolytic reduces ongoing loss |
| Hypovolaemia / electrolyte loss | Rapid IV crystalloids (e.g. normal saline) + replace potassium & magnesium as labs dictate | Prevents shock and arrhythmias |
| Acute severe colitis (≥6 bloody stools/day, fever, tachycardia, anaemia) | Start IV corticosteroid (e.g. methylprednisolone) within 24 h, nil per os, nasogastric tube if vomiting, broad‑spectrum IV antibiotics if perforation risk | Steroid is first‑line rescue; bowel rest limits perforation; antibiotics cover translocation |
| Toxic megacolon suspicion (diameter > 6 cm, systemic toxicity) | Nil per os, broad‑spectrum IV antibiotics, IV steroids, urgent surgical consult | Prevents perforation; early surgery if no response in 24‑48 h |
Definitive treatment – choose according to disease type, severity, and extra‑intestinal manifestations (EIMs).
| Disease | First‑line oral/IV agents | When to step‑up | Role of biologics / small molecules |
|---|---|---|---|
| Mild‑moderate Crohn’s (ileocaecal) | Oral 5‑ASA (mesalamine) ± budesonide | Persistent symptoms after 8 weeks → azathioprine/6‑mercaptopurine | Anti‑TNF (infliximab/adalimumab) if refractory; ustekinumab for stricturing disease |
| Moderate‑severe Crohn’s | Systemic steroids → taper | Failure to taper or steroid dependence → immunomodulators (azathioprine) ± anti‑TNF | Anti‑TNF or vedolizumab; consider combination with immunomodulator |
| Mild‑moderate ulcerative colitis (UC) | Oral 5‑ASA + topical 5‑ASA (enema/suppository) | Inadequate response → oral steroids (short course) | Anti‑TNF or vedolizumab if steroid‑dependent; tofacitinib for refractory UC |
| Moderate‑severe UC | Oral steroids → taper | Steroid non‑response after 3 days → infliximab or ciclosporin (IV) | Anti‑TNF, vedolizumab, or tofacitinib as maintenance; consider colectomy if no response |
Monitoring & safety
- Clinical: stool frequency, blood, weight, pain score daily while inpatient; weekly in the first month of steroids.
- Laboratory: CBC, electrolytes, CRP, ESR, liver function, renal function at baseline, then 2‑weekly for steroids, 4‑weekly for immunomodulators, 8‑weekly for biologics.
- Therapeutic drug monitoring: azathioprine/6‑MP metabolites, anti‑TNF trough levels when loss of response suspected.
- Infection surveillance: screen for TB, hepatitis B/C before biologics; vaccinate (influenza, pneumococcal, HPV) prior to immunosuppression.
- Bone health: DEXA after 6 months of chronic steroids; calcium/vit D supplementation.
Contra‑indications / safety alerts
- Active systemic infection → hold steroids/biologics.
- Latent TB without treatment → treat TB first.
- Severe hepatic impairment → avoid azathioprine/6‑MP.
- Pregnancy: 5‑ASA safe; steroids acceptable; anti‑TNF considered if benefits outweigh risks.
Complications and prognosis
- Intestinal: strictures, fistulae, perforation, toxic megacolon, colorectal cancer (risk rises after 8‑10 years of extensive colitis).
- Extra‑intestinal: primary sclerosing cholangitis, ankylosing spondylitis, uveitis, thromboembolic events, nutritional deficiencies (vit B12, iron, folate).
- Medication‑related: steroid‑induced osteoporosis, cataracts, hyperglycaemia; immunomodulator‑related marrow suppression; biologic‑related opportunistic infections (CMV, PCP).
- Prognosis: Variable; many achieve remission with step‑up therapy, but up to 30 % will need surgery (resection for Crohn’s, colectomy for UC). Early aggressive therapy in high‑risk patients improves long‑term outcomes and reduces cancer risk.
High‑yield exam points
- Look‑alikes: Infectious colitis (Shigella, amoebiasis), intestinal TB, drug‑induced colitis (NSAIDs), ischemic colitis.
- Common wrong first step: Jumping to surgery without a trial of steroids in acute severe UC.
- Bedside examiner questions:
- “What features on abdominal exam suggest toxic megacolon?”
- “How would you differentiate Crohn’s from ulcerative colitis on colonoscopy?”
- “Why is it important to screen for TB before starting infliximab?”
- “What is the role of 5‑ASA in Crohn’s disease?”
Clinical case
Case: 22‑year‑old male university student presents with 3 weeks of crampy abdominal pain, watery diarrhoea (6‑7 motions/day) with occasional blood, weight loss of 5 kg, and low‑grade fever. Examination: mild tachycardia, tender left lower quadrant, no perianal disease. Labs: Hb 10 g/dL, CRP 45 mg/L, ESR 38 mm/h. Colonoscopy shows continuous ulceration from rectum to sigmoid colon, pseudopolyps.
Questions
- What is the most appropriate next step in management?
Answer: Initiate oral 5‑ASA combined with a short course of oral prednisolone to induce remission, then taper steroids and continue 5‑ASA as maintenance.
- Which extra‑intestinal manifestation should be screened for in this patient?
Answer: Primary sclerosing cholangitis – obtain liver function tests and consider MRCP if cholestatic pattern emerges.
- If the patient fails to respond to steroids after 5 days, what is the recommended rescue therapy?
Answer: Administer intravenous infliximab (anti‑TNF) after confirming negative TB screen; alternatively, consider ciclosporin if infliximab unavailable.
Practice questions
Question 1
A 35‑year‑old woman with known ulcerative colitis presents with 8 bloody stools/day, temperature 38.5 °C, pulse 110 bpm, haemoglobin 9 g/dL. Abdomen is distended, tympanic, with guarding. What is the next best action?
A. Start oral mesalamine and discharge
B. Begin IV hydrocortisone and arrange urgent surgical review
C. Give oral metronidazole and observe
D. Perform immediate colonoscopy
Answer: B. Begin IV hydrocortisone and arrange urgent surgical review
Explanation: Features meet criteria for acute severe colitis; IV steroids are first‑line, and surgical input is needed early in case of toxic megacolon or perforation.
Question 2
A 28‑year‑old man from a malaria‑endemic area has chronic diarrhoea, weight loss, and a non‑healing perianal fistula. Colonoscopy shows skip lesions with cobblestoning. Which investigation is essential before starting anti‑TNF therapy?
A. Serum amylase
B. Quantiferon‑TB Gold test
C. HIV viral load
D. Stool ova and parasites
Answer: B. Quantiferon‑TB Gold test
Explanation: Anti‑TNF agents reactivate latent TB; screening is mandatory regardless of endemicity.
Question 3
A patient with Crohn’s disease on azathioprine develops leukopenia (WBC 2 × 10⁹/L). What is the safest immediate step?
A. Increase azathioprine dose
B. Continue same dose, monitor weekly
C. Stop azathioprine and switch to methotrexate
D. Add oral prednisone
Answer: C. Stop azathioprine and switch to methotrexate
Explanation: Azathioprine‑induced marrow suppression requires cessation; methotrexate is an alternative immunomodulator.
Question 4
Which of the following differentiates ulcerative colitis from Crohn’s disease on endoscopy?
A. Presence of granulomas
B. Continuous colonic involvement starting at the rectum
C. Transmural inflammation
D. Fistula formation
Answer: B. Continuous colonic involvement starting at the rectum
Explanation: UC characteristically begins in the rectum and progresses proximally in a continuous fashion; the other features are typical of Crohn’s.
Question 5
A 45‑year‑old patient with longstanding ulcerative colitis is being evaluated for colorectal cancer surveillance. How often should surveillance colonoscopy be performed?
A. Every 5 years
B. Every 2 years
C. Every 10 years
D. Only when symptoms change
Answer: B. Every 2 years
Explanation: After 8‑10 years of extensive colitis, biennial colonoscopy is recommended for dysplasia detection.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.