Inflammatory Bowel Disease

Chronic, relapsing, immune-mediated inflammatory bowel disease with a range of possible extra-intestinal manifestations. Genetic and environmental factors both contribute. Left untreated, can lead to malnutrition, loss of bowel function, gut ischaemia, and death. Three recognised subtypes: ulcerative colitis (UC), Crohn disease (CD), and IBD-unclassified (IBD-U), which accounts for 10–15% of cases. Australian prevalence is estimated at ~4 per 1000 and rising — have a high index of suspicion, since diagnostic delay of 1–8 years is common (often because chronic diarrhoea is attributed to gastroenteritis or IBS).

Differentiating IBD from its main mimics

IBS is ~50× more common than IBD and is the most important differential to exclude. Features favouring IBD over IBS: weight loss, elevated CRP, elevated faecal calprotectin, nocturnal diarrhoea (especially if it wakes the patient), rectal bleeding, fever, obstructive symptoms, anaemia, iron deficiency, low albumin.

Also consider: infectious gastroenteritis; coeliac disease (more common than IBD, often non-specific symptoms); colorectal cancer (rectal bleeding, abdominal pain, weight loss, sometimes urgency — more common ≥50yrs, but EOCRC incidence is rising in <50s and is often diagnosed later-stage, so maintain a high index of suspicion even in young adults — see bowel-cancer-screening.md).

Ask specifically about family history, smoking (paradoxical relationship — smoking increases Crohn’s risk but reduces UC risk, and smoking cessation can precipitate UC), travel, vaccination history, and medications (NSAIDs can cause an IBD-mimicking enteropathy).

Assessment

Look for extra-intestinal manifestations (erythema nodosum, pyoderma gangrenosum, arthritis, episcleritis/iritis, mouth ulcers, night sweats, primary sclerosing cholangitis) and complications (obstruction from strictures — more Crohn’s; malabsorption/nutritional deficiency — Crohn’s; anaemia; acute abdomen from perforation; intra-abdominal sepsis/abscess — more Crohn’s; colorectal cancer). Examine perianal region for tags/fissures/fistulae/abscesses in suspected Crohn’s.

Initial investigations (no single test is diagnostic): FBC (anaemia; leukocytosis/thrombocytosis suggest inflammation), CRP/ESR (a normal result doesn’t exclude inflammation), EUC/LFT (low albumin from inflammation/ malnutrition), calcium/magnesium/phosphate, coeliac screen, stool culture ± C. difficile toxin, iron studies, TSH, and faecal calprotectin once an infective cause is excluded (MBS-funded since Nov 2021 if aged <51yrs, symptoms >6 weeks, no red flags — highly sensitive but non-specific; won’t be elevated in IBS, but rectal bleeding of any cause can elevate it, so it isn’t specific in that setting; don’t check if diarrhoea has been present <6 weeks). Imaging is rarely needed unless a surgical complication is suspected — barium studies are no longer recommended.

Triage and referral urgency

Severely unwell — emergency assessment: suspected/known IBD flare with fever, haemodynamic compromise, significant abdominal pain, suspected megacolon, perforation, obstruction, or abscess uncontrollable in the community. Acute severe colitis specifically: >6 bloody bowel motions/24h plus at least one of temperature >37.8°C, pulse >90bpm, Hb <105g/L, or raised ESR (>30mm/hr)/CRP (>30mg/L).

Moderately unwell — urgent gastroenterology assessment (seek phone advice from the gastroenterology service first; do not send a referral without discussion): suspected IBD with chronic diarrhoea/suspicious symptoms >6 weeks and elevated faecal calprotectin (>100µg/g), plus any of new/progressive symptoms, a critical laboratory factor (anaemia, low albumin, raised ESR/CRP, iron deficiency, ≥5% unexplained weight loss in 1 month or ≥10% in 6 months), or abnormal imaging suggesting IBD. Continue close monitoring while awaiting the appointment — escalate to ED if symptoms worsen.

Contraception, pregnancy and IBD

• COCP: absorption may be reduced with small bowel Crohn’s involvement (large bowel involvement doesn’t affect absorption); avoid in patients prone to severe exacerbations requiring hospitalisation (increased VTE risk in this group).
• IBD increases osteoporosis risk, and DMPA’s effect on bone density may be additive — progestogen-only methods that don’t affect bone density may be preferred.
• Methotrexate is teratogenic — both partners need effective contraception during treatment and for at least 3 months after stopping.
• Fertility is generally unaffected by UC itself, but can be reduced by scarring after J-pouch (ileoanal anastomosis) surgery in women. Good disease control improves the chance of conceiving — aim for three months of corticosteroid-free remission before conception, since roughly one-third of patients who conceive in remission flare during pregnancy, against over half of those with active disease at conception.
• Mode of delivery: vaginal delivery is safe for most women with IBD. Caesarean section is specifically recommended for active perianal fistulising Crohn’s disease, and after a J-pouch (IPAA), given the risk of sphincter/pouch damage; otherwise mode of delivery follows usual obstetric indications and preference.
• Thiopurines in pregnancy: continuing an established dose is safe (see below), but starting or increasing the dose during pregnancy is not recommended, given its slow onset of action and an associated risk of liver injury.
• Preconception planning: continue all medications except methotrexate before and during pregnancy (methotrexate absolutely contraindicated — delay pregnancy ≥3 months after stopping, for both partners). Pregnancy is safe on all biologics except tofacitinib; most women can continue biologics throughout pregnancy. Sulfasalazine has a mild antifolate effect (avoid if planning fertility) and can cause reversible male infertility. Involve the gastroenterologist early, and request urgent gastroenterology assessment once pregnancy is planned or confirmed.
• Medication safety in pregnancy/breastfeeding: 5-ASAs are safe throughout. Steroids may be associated with cleft palate in the first trimester but should still be used if needed to control disease. Thiopurines (azathioprine, mercaptopurine) are safe in pregnancy despite a TGA category D listing — no discernible increase in congenital abnormality risk, and they don’t affect spermatogenesis. Biologics can generally continue throughout pregnancy (seek specialist advice); babies exposed in utero should avoid live vaccines (particularly rotavirus) for 6–12 months, with MMR still given on schedule at 12 months. All these medications (except methotrexate) are safe while breastfeeding.

Ulcerative colitis

Idiopathic, chronic relapsing/remitting inflammation of the colon — continuous from the rectum proximally, mucosal only (doesn’t involve the full bowel-wall thickness), and with no extra-colonic disease.

Demographics: onset typically in the 20s; higher incidence in European/ developed-nation populations.

History: long-standing (generally >6 weeks) diarrhoea, usually bloody — diarrhoea that wakes the patient from sleep is highly suggestive. Weight loss; fever (more common in CD); urgency and tenesmus with more severe disease; colicky pain/bloating can occur from faecal overload proximal to the active segment. Generally a gradual, insidious onset.

Examination: not particularly helpful in UC; abdominal distension may indicate severe disease with toxic megacolon.

Crohn disease

Idiopathic, chronic relapsing/remitting inflammation that can affect any part of the GI tract, with non-continuous (skip) lesions that tend to stay stable in location over a patient’s lifetime. Inflammation is transmural (full thickness), with extra-colonic disease (abscesses, fistulae, perianal disease).

Demographics: onset typically in the 20s; higher incidence in European/ developed-nation populations.

History: more varied symptoms than UC, with a gradual, insidious onset over a long period — abdominal pain, diarrhoea, weight loss. Diarrhoea is less likely to be bloody than in UC unless there’s active colonic inflammation, but diarrhoea that wakes the patient from sleep remains highly suggestive. Systemic symptoms (malaise, anorexia, fever) and nutritional deficiencies are common.

Examination: look for extra-intestinal manifestations — perianal fistulae, oral ulceration.

Investigations (both UC and CD)

Diagnosis is based on the combination of clinical symptoms, blood/stool tests, and colonoscopy/endoscopy findings — there is no single diagnostic test.

• FBC (anaemia); UEC (electrolyte disturbance); iron studies (deficiency from malabsorption).
• CRP/ESR — helpful if elevated, but a normal result doesn’t exclude significant inflammation.
• Coeliac serology, to exclude coeliac disease as a differential/comorbidity.
• Faecal calprotectin — positive with gut inflammation, but also positive in infective diarrhoea (especially bacterial), so isn’t specific to IBD alone.
• Stool MCS/OCP/PCR + C. difficile toxin, to exclude an infective cause.
• If IBD is suspected on this basis, refer to gastroenterology for colonoscopy and endoscopy to confirm the diagnosis.

Pre-treatment screening (before immunosuppression/biologic therapy)

Because most IBD therapy beyond 5-ASAs is immunosuppressive, a structured pre-treatment screen is needed:

History: infection history (bacterial, fungal, viral including HSV/VZV, parasitic, latent/active TB treatment); vaccination history (including BCG); environmental/travel risk for TB, Strongyloides stercoralis, or Burkholderia pseudomallei (melioidosis).

Examination: look for signs of active infection — pyoderma, scabies, chronic lung/dental/sinus infection.

TB screening: history as above, plus a tuberculin skin test or TB-specific interferon-gamma release assay (IGRA).

Other tests: hepatitis B serology; Strongyloides serology (if epidemiological risk); varicella-zoster serology; HPV screening (as per routine cervical screening); B. pseudomallei serology if significant immunosuppression planned and prior residence in a melioidosis-endemic area.

Vaccination:

• Ideally at IBD diagnosis: confirm routine vaccinations are up to date (diphtheria, tetanus, inactivated polio, pertussis); hepatitis B vaccine if seronegative; varicella vaccine if seronegative with no reliable chickenpox/ shingles history (zoster vaccine instead if seropositive).
• Before starting immunomodulation: inactivated influenza (then annually); pneumococcal vaccine (booster as indicated).

Patient advice: hygiene advice (avoid raw egg/meat, unpasteurised dairy, walking barefoot); refer to infectious diseases/travel medicine for any travel plans once immunosuppressed.

Management of ulcerative colitis

Severity and site of disease determine drug choice and route of administration.

Active proctitis or distal colitis

Initial therapy: rectal mesalazine plus an oral 5-aminosalicylate (5-ASA). Rectal preparation choice depends on the extent of disease — suppositories reach ~20cm, foam reaches the sigmoid colon, and liquid enemas reach the splenic flexure.

Mesalazine rectal dosing:

Preparation	Acute (induction) dose	Maintenance dose
Enema (1g/100mL, or 2g/60mL–4g/60mL)	1–4g daily, single or divided dose	1–4g, 2–3×/week
Foam enema (1g/applicator)	1–4g (1–4 applications) daily	1–4g, 2–3×/week
Suppository (1g)	1g once or twice daily	1g, 2–3×/week

Oral 5-ASA dosing:

Drug	Adult acute (induction)	Adult maintenance
Sulfasalazine	2–4g daily	1–2g daily
Mesalazine	2–4.8g daily	1–3g daily
Balsalazide	6.75g daily	3g daily
Olsalazine	1.5–3g daily	1–2g daily

If 5-ASA alone is ineffective, add a rectal corticosteroid — budesonide 2mg foam once daily, hydrocortisone acetate 10% foam once–twice daily, prednisolone 20mg/100mL enema once–twice daily, or (for isolated proctitis) prednisolone 5mg suppository once–twice daily. If rectal mesalazine isn’t tolerated, a rectal corticosteroid can be used alone. Continue until symptoms resolve, then taper over several weeks; rectal mesalazine can be used for maintenance in patients with repeated relapses.

If unresponsive: add prednisolone 40–50mg daily (child 1–2mg/kg, max 50mg) until response, then taper over 6–8 weeks. Use budesonide MMX instead if there’s a known adverse reaction to systemic steroids. Check for constipation proximal to the inflamed segment — this can prevent topical medication reaching the site adequately. Repeated/prolonged steroid courses should prompt escalation to the moderate-severe pathway below.

Mild-moderate extensive UC

Oral 5-ASA at induction dose is often sufficient. If no response, add prednisolone 40–50mg daily until clinical response, then taper over 6–8 weeks (MMX budesonide if steroids are contraindicated).

Moderate-severe, chronically active, or frequently relapsing UC

Add an immunomodulatory drug if not contraindicated — onset of effect can be delayed by weeks to months; dosing can be optimised by monitoring metabolite levels.

• Azathioprine 2–2.5mg/kg orally daily, or mercaptopurine 1–1.5mg/kg orally daily.
• Methotrexate (for patients who can’t tolerate thiopurines) 25mg subcutaneously/IM/orally once weekly, plus folic acid 5–10mg orally weekly (preferably not on the methotrexate day).

For patients not responding to an adequate 5-ASA trial (≥3 months) and a corticosteroid (± an immunomodulator): biologic therapy — infliximab 5mg/kg IV over 2 hours at weeks 0/2/6 (then 8-weekly maintenance if responding), or vedolizumab 300mg IV over 30 minutes at weeks 0/2/6 (then 8-weekly maintenance). Combination therapy with infliximab plus a thiopurine/methotrexate may be needed. Secondary care now has further options beyond these two — ustekinumab, risankizumab and the JAK inhibitors upadacitinib and tofacitinib — with network meta-analyses suggesting upadacitinib, risankizumab and ozanimod rank highest for inducing remission in biologic-naive patients, and upadacitinib, tofacitinib and ustekinumab rank highest after prior biologic exposure; agent selection remains a specialist decision. Surgery (proctocolectomy with ileal pouch-anal anastomosis, or end-ileostomy) is an option for chronic refractory disease.

Acute severe UC (medical emergency)

Affects up to 25% of UC patients at some point. Defined by the Truelove & Witts criteria: temperature >37.8°C, HR >90bpm, Hb <105g/L, ESR >30mm/hr (≥6 bloody stools/day plus ≥1 systemic toxicity sign). Refer to ED for high-dose IV corticosteroids (methylprednisolone 100mg daily, or hydrocortisone 100mg four times daily). Give routine chemical VTE thromboprophylaxis — ASUC carries an 8-fold increased VTE risk despite the bloody diarrhoea. Antibiotics do not improve outcomes outside severe sepsis, per a recent RCT — don’t add them routinely.

Salvage therapy if unresponsive to high-dose IV steroids by day 3–5: ciclosporin 2mg/kg IV as a 24-hour continuous infusion, or infliximab 5mg/kg over 2 hours at weeks 0/2/6 (medical salvage — reduces colectomy rate by up to 80% when given promptly), or colectomy (surgical salvage). The Travis criteria predicts need for surgery: >8 stools/ day, or 3–8 stools plus CRP >45, after 3 days of IV steroids. Emergency surgery indications: toxic megacolon, haemodynamically unstable bleeding, perforation.

UC maintenance

Usually 5-ASA ± an immunomodulator. Patients responding to rectal mesalazine continue at reduced-frequency maintenance dosing; patients with severe initial disease or frequent relapses despite 5-ASA go onto immunomodulator maintenance dosing.

Management of Crohn disease

Similar treatment aims to UC.

Induction therapy, mild-moderate CD

Corticosteroids are most effective here (60–70% respond within 12–16 weeks): prednisolone 40–50mg daily (child 1–2mg/kg, max 50mg) each morning until response, then taper over 6–8 weeks. For ileocaecal disease, consider controlled- ileal-release budesonide 9mg daily each morning for 6–8 weeks (then taper over 2–4 weeks) instead — particularly for patients with a history of, or precautions against, systemic corticosteroid adverse effects (e.g. diabetes). Antibiotics have no role unless there’s confirmed infection.

May need to switch to or add an immunomodulator (azathioprine, mercaptopurine, or methotrexate — delayed onset by several months) if response is inadequate; if still minimal response, escalate to a biologic (infliximab, adalimumab, or vedolizumab).

Induction therapy, severe CD

Initial therapy is an IV corticosteroid: hydrocortisone 100mg (child 2–4mg/kg, max 100mg) IV 6-hourly, or methylprednisolone sodium succinate 100mg (child 1mg/kg, max 50mg) IV daily — optimal duration isn’t established, but typically 3–7 days. Antibiotics have no role unless a transmural complication (abscess, complex fistula) is present.

Complications: abscesses need radiological drainage or surgery; surgery may be needed for perforation, bowel obstruction, or fistulae.

CD maintenance

A relapsing/remitting condition — most patients need ongoing therapy to maintain remission, using the same immunomodulator/biologic options as above, without the prednisolone. Smoking makes CD worse — smoking cessation is an active part of management (unlike UC, where smoking has a more complex/less clearly harmful relationship).

Perianal and fistulising CD

Perianal fissures, fistulae, and abscesses occur in up to 40% of CD patients — manage with specialist surgical exploration and drainage. Antibiotics for active perianal disease: metronidazole 400mg (child 10mg/kg, max 400mg) orally 12-hourly, or ciprofloxacin 500mg (child 12.5mg/kg, max 500mg) orally 12-hourly — may be needed for weeks to months (long-term metronidazole risks peripheral neuropathy). Add an immunomodulator for severe/refractory cases.

Post-operative relapse prevention

High relapse risk in smokers, those with a history of perforating disease (abscesses, fistulae, free perforation), or prior resections. Options: 5-ASA, or 3 months of metronidazole. With one or more risk factors, add a thiopurine and/or a TNF inhibitor (most effective post-operative prophylaxis) if the thiopurine isn’t tolerated. Colonoscopy at 6 months post-surgery guides the need for further treatment.

Ileal malabsorption

Extensive ileal disease or ileal resection can cause bile-salt malabsorption (bile-salt diarrhoea/steatorrhoea), which can occur even without active inflammation — manage as for short bowel syndrome:

• Small, frequent meals; separate solids from fluids.
• Long-term IM B12 and fat-soluble vitamin (A, D, E, K) supplementation.
• High-energy, high-protein diet (oral nutritional supplements as needed, but watch high osmolar loads worsening diarrhoea).
• Reduce insoluble fibre (particularly with no colon present) and, if steatorrhoea is present from excess fat intake, reduce fat intake.
• Appropriate glucose/electrolyte fluid replacement (avoid hypo-/hypertonic fluids); a low-lactose diet (lactose intolerance is common); added salt to meals.
• A low-oxalate diet if hyperoxaluria/renal stones are present — short bowel with an intact colon carries a ~25% risk of oxalate stones from increased colonic oxalate absorption.
• Antidiarrhoeal medication (loperamide/codeine) and high-dose twice-daily PPI as an antisecretory measure.

Disease affecting the small bowel can cause bacterial overgrowth, where antibiotic therapy is beneficial — seek expert advice before treating.

Monitoring for immunomodulatory/biologic therapy

Immunomodulatory drugs carry significant adverse-effect risk and need careful monitoring:

• TNF inhibitors — review effectiveness and adverse effects (especially infection) every 3–6 months.
• Azathioprine/mercaptopurine — baseline FBC and LFTs, then FBC weekly for 4 weeks, then every 2 weeks for 4 weeks, then every 12 weeks for the duration of therapy. LFTs every 3 months. Annual skin check for early skin cancer detection.
• Methotrexate — causes abnormal LFTs, especially in diabetic, obese, CKD, viral hepatitis, or excessive-alcohol patients; hepatotoxicity correlates with cumulative dose and can progress to fibrosis/cirrhosis. FBC, UEC, LFTs monthly for the first 6 months, then every 1–2 months; monitor more frequently if LFTs are abnormal. Consider transient elastography (FibroScan) or liver biopsy for persistently raised LFTs, even after stopping methotrexate.
• Ciclosporin — baseline FBC, UEC, LFTs, fasting lipids, and BP; specialist- guided ongoing monitoring, plus annual skin cancer checks. Blood concentration monitoring isn’t usually routine, but can be used at high doses, if toxicity is suspected, or for inadequate response (absorption/adherence issues).

Dietary measures

No evidence supports routine dietary restriction — avoiding insoluble fibre may give symptomatic diarrhoea relief during an acute flare. The main goal is meeting nutritional needs through normal food and supplements where possible; severe disease may need enteral or even parenteral feeding.

General IBD management

Fertility: avoid methotrexate, stopping ≥3 months before planning pregnancy (both men and women). No effect on female fertility; sulfasalazine may reduce sperm count/motility, reversible on stopping. Ideally delay pregnancy until remission is achieved — active disease carries a greater risk to mother and baby than continuing therapy through pregnancy. Manage pregnancy jointly with gastroenterology.

Osteoporosis: risk is increased by corticosteroid use and malabsorption. Prevent with regular weight-bearing exercise, adequate calcium intake, smoking cessation, and limiting alcohol. Give vitamin D ± calcium for patients on corticosteroids.

Iron deficiency: monitor frequently. Oral iron often worsens GI symptoms, so IV iron is generally preferred, though oral iron can be used when disease is inactive. Recheck iron studies regularly after stopping therapy (3-monthly, then 6–12-monthly) to catch recurrence.