1. Definition and clinical relevance
Inflammatory bowel disease (IBD) encompasses two distinct chronic relapsing-remitting conditions: Crohn's disease (CD) and ulcerative colitis (UC). Both involve non-infectious gut inflammation driven by an environmental trigger acting on a genetically susceptible host, though they differ fundamentally in distribution, depth of inflammation, and clinical behaviour. IBD predominantly strikes people aged 15 to 40 years, affects both sexes equally, and carries significant morbidity including malnutrition, extraintestinal complications, colorectal cancer risk, and surgical need. For an Australian intern, recognising a severe acute flare and initiating timely escalation is a critical time-sensitive skill, as roughly half of all severe UC attacks occur in patients without a prior IBD diagnosis.
2. Key values, thresholds, scoring systems
UC Severity Classification
| Severity | Stool frequency | Rectal bleeding | Systemic features | Action |
|---|---|---|---|---|
| Mild | Fewer than 4 liquid stools per day | Minimal or absent | None | Primary care management |
| Moderate | 4 to 6 liquid stools per day | Moderate | Mild systemic disturbance | Specialist review; escalate if no response |
| Severe | More than 6 liquid stools per day | Frequent | Fever, tachycardia, anaemia | Hospital admission, IV therapy |
Admission thresholds
| Trigger | Threshold |
|---|---|
| Fever | Above 37.5 degrees C |
| Tachycardia | Heart rate above 90 bpm |
| Diarrhoea duration | Persistent beyond 4 weeks warrants urgent investigation |
Colorectal cancer surveillance
| UC extent | Surveillance start |
|---|---|
| Proctitis only | Low risk; standard intervals |
| Left-sided or extensive colitis | Colonoscopy from 7 to 10 years after symptom onset |
Montreal Classification of UC extent
| Code | Description |
|---|---|
| E1 | Proctitis: rectum only |
| E2 | Left-sided: rectum, sigmoid, descending colon |
| E3 | Pancolitis: entire colon and rectum |
3. Approach: presentation and differential
History
Both CD and UC cause recurrent bloody diarrhoea with mucus, urgency, and cramping abdominal pain. Weight loss, fever, and malaise are more prominent in CD. Oral aphthous ulcers and perianal disease (fistulae, abscesses, indolent fissures, skin tags) point strongly toward CD. Ask about smoking: active smoking is associated with CD flares, whereas UC disproportionately affects non-smokers and ex-smokers. A family history of IBD raises pre-test probability. In patients from regions where ileocolonic tuberculosis is prevalent (for example, migrants from South or Southeast Asia), TB must be actively excluded before attributing ileocaecal disease to CD.
Distinguishing features
| Feature | Crohn's disease | Ulcerative colitis |
|---|---|---|
| Distribution | Mouth to anus; skip lesions; any segment | Rectum upward; continuous; colon only |
| Depth of inflammation | Transmural | Mucosal only |
| Granulomas on histology | Present | Rare |
| Goblet cells | Preserved | Depleted |
| Crypt abscesses | Occasional | Prominent |
| Perianal disease | Common | Rare |
| Smoking association | Risk factor | Protective |
| Colonoscopic appearance | Aphthoid or deep serpiginous ulcers, cobblestoning | Diffuse mucosal friability, continuous ulceration |
Extraintestinal manifestations (both conditions)
Joints: pauciarticular (type I) or polyarticular (type II) peripheral arthropathy, sacroiliitis, ankylosing spondylitis. Eyes: uveitis, episcleritis, conjunctivitis. Skin: erythema nodosum, pyoderma gangrenosum. Hepatobiliary: primary sclerosing cholangitis (more common in UC), fatty liver, gallstones. Renal: nephrolithiasis. Vascular: venous thromboembolism risk is elevated, especially during active disease.
Enteropathic arthritis occurs in up to 10 to 15 percent of IBD patients. It is asymmetric and predominantly affects lower limb joints. Notably, joint symptoms can precede bowel diagnosis. In UC, colectomy often induces joint remission; in CD, arthritis may persist despite good bowel control.
Differential diagnosis (in order of clinical importance)
- Infective colitis (Salmonella, Campylobacter, Shigella, Clostridioides difficile, CMV)
- Irritable bowel syndrome
- Colorectal malignancy
- Ischaemic colitis
- Microscopic colitis (lymphocytic or collagenous)
- Coeliac disease
- Diverticulitis
- Pseudomembranous colitis
- Ileocaecal tuberculosis (in at-risk populations)
4. Investigations
Bedside
Observations including temperature, heart rate, and blood pressure to assess severity. Stool chart. Abdominal examination for tenderness, distension, or peritonism (the last suggesting toxic megacolon, which is a surgical emergency visible on plain film or CT).
Bloods
| Test | Purpose |
|---|---|
| FBC | Anaemia (iron deficiency or megaloblastic), leucocytosis in severe disease |
| CRP and ESR | Markers of inflammatory activity |
| LFTs and albumin | Nutritional status, hepatobiliary complications |
| Iron studies, B12, folate | Deficiencies common in CD with ileal involvement |
| Coagulation | VTE risk assessment |
| Blood cultures | If febrile and systemically unwell |
Stool
Microscopy, culture, and sensitivity to exclude infective cause. Clostridioides difficile toxin. Faecal calprotectin is useful in primary care for distinguishing IBD from IBS in patients under 40 years; a raised result supports referral for colonoscopy.
Imaging and endoscopy
Colonoscopy with ileoscopy and biopsies is the diagnostic standard. During a severe attack, full colonoscopy carries an unacceptable perforation risk; an unprepared flexible sigmoidoscopy is safer and sufficient for diagnosis and CMV biopsy. MRI of the small bowel (MR enterography) is preferred for assessing CD extent and complications such as fistulae, strictures, and abscesses. CT abdomen is used acutely when perforation or obstruction is suspected. Plain abdominal X-ray can identify toxic megacolon (colonic diameter above 6 cm with systemic toxicity).
5. Management
Acute severe UC: inpatient
Admit immediately. Start intravenous hydrocortisone 100 mg every 6 hours. Commence subcutaneous low molecular weight heparin at prophylactic doses for VTE prevention. Do not delay corticosteroids while awaiting stool culture results, though if Clostridioides difficile is strongly suspected, add oral vancomycin concurrently. Flexible sigmoidoscopy should be performed early to confirm diagnosis and obtain biopsies to evaluate for CMV colitis.
Reassess response at 72 hours with input from both a gastroenterologist and a colorectal surgeon. Patients not responding to IV steroids at 3 days require either salvage medical therapy (infliximab or ciclosporin) or colectomy. Responders can transition to oral prednisolone after approximately 5 days, with a weaning course over 8 to 10 weeks.
All patients admitted with severe colitis should be assessed for long-term maintenance therapy: thiopurines (azathioprine or mercaptopurine), anti-TNF biologics (infliximab, adalimumab), or newer immunomodulatory agents.
Mild to moderate UC: outpatient
Aminosalicylates (mesalazine) are first-line for induction and maintenance in mild to moderate UC. Topical preparations (suppositories for proctitis, enemas for left-sided disease) are effective and reduce systemic exposure. Oral prednisolone is added for moderate flares not responding to aminosalicylates.
Crohn's disease
Management requires gastroenterology input with IBD expertise and is highly individualised based on disease location, behaviour (inflammatory, stricturing, or penetrating), and complications. Key principles:
Early nutritional assessment is essential. CD commonly causes malabsorption, iron deficiency, B12 deficiency (terminal ileal disease), and protein-energy malnutrition. Enteral nutrition has a particular role in paediatric CD and in adults where steroids are to be avoided.
Inpatient CD patients require prophylactic subcutaneous LMWH. Corticosteroids (oral prednisolone or IV hydrocortisone) induce remission but do not maintain it. Thiopurines and methotrexate are used for maintenance. Anti-TNF agents (infliximab, adalimumab) are used for moderate to severe disease, fistulising disease, and steroid-dependent or steroid-refractory cases. Ustekinumab (IL-12/23 inhibitor) and JAK inhibitors are options in refractory disease.
Surgery is reserved for complications: obstruction, abscess, fistula, perforation, or failure of medical therapy. Unlike UC, surgery is not curative in CD.
Microscopic colitis
Budesonide is first-line. Aminosalicylates and bismuth preparations have supporting evidence. Refractory cases may need prednisolone or azathioprine. Coeliac disease must be excluded given the strong association.
Enteropathic arthritis
Treat the underlying IBD. NSAIDs help joint symptoms but may worsen diarrhoea. Intra-articular corticosteroids are preferred for monoarthritis. Sulfasalazine may benefit both bowel and joint disease. Anti-TNF agents (infliximab, adalimumab, golimumab, certolizumab) address both conditions simultaneously.
6. Australian-specific considerations
Aboriginal and Torres Strait Islander peoples: IBD is less prevalent in First Nations communities than in non-Indigenous Australians, but presentations may be delayed due to geographic barriers, health system distrust, and symptom normalisation. When managing IBD in First Nations patients, involve Aboriginal Liaison Officers early, use interpreters where needed, and ensure follow-up plans are culturally safe and practically achievable. Chronic disease management plans (GPMP and TCA, MBS items 721 and 723) can support coordinated specialist access. The 715 health assessment (MBS item 715) for Aboriginal and Torres Strait Islander adults provides an opportunity to screen for undiagnosed chronic conditions including IBD.
Rural and remote: Access to colonoscopy and gastroenterology is limited outside major centres. Faecal calprotectin in primary care helps triage who needs urgent referral. Telehealth gastroenterology is increasingly available. For acute severe colitis in a rural setting, stabilise with IV hydrocortisone and arrange urgent retrieval to a centre with gastroenterology and colorectal surgery. Do not delay treatment pending transfer.
Migrant and refugee populations: Ileocaecal TB can mimic CD clinically, endoscopically, and radiologically. In patients from high-prevalence regions (South Asia, Southeast Asia, sub-Saharan Africa), obtain tissue for TB microscopy and culture before committing to a CD diagnosis. A supervised trial of anti-TB therapy may be warranted where the distinction cannot be made confidently.
PBS access: Biologics for IBD (infliximab, adalimumab, ustekinumab, vedolizumab) are PBS-listed under specific criteria requiring specialist initiation and documented failure of conventional therapy. Ensure specialist review before initiating or continuing these agents.
VTE: IBD is an independent VTE risk factor. Hospitalised patients should receive pharmacological thromboprophylaxis unless there is active major haemorrhage.
Clinical pearls
- Perianal disease (fistulae, multiple fissures, skin tags) is a hallmark of CD and should prompt targeted investigation even before bowel symptoms are prominent.
- Faecal calprotectin is a practical, non-invasive tool for distinguishing IBD from IBS in patients under 40 in the primary care setting; a normal result makes active IBD unlikely.
- In a severe UC flare, the 72-hour IV steroid response is the key decision point: no improvement by day 3 means escalation to salvage therapy or surgery, not more time on steroids alone.
- Active smoking worsens CD and is associated with higher relapse rates; smoking cessation is a meaningful therapeutic intervention in CD management.
- All IBD patients admitted to hospital carry elevated VTE risk and require prophylactic LMWH unless actively bleeding.
- In patients from TB-endemic regions presenting with ileocaecal disease, always obtain tissue for TB culture before labelling the diagnosis as CD, as the two conditions can be indistinguishable without microbiological confirmation.