Overview
Recognise paediatric Crohn disease and ulcerative colitis before growth failure advances, stage intestinal and extra-intestinal disease and coordinate nutrition, medicines, surgery and developmental monitoring through specialist care.
History covers stool frequency, blood, urgency, nocturnal waking, pain, vomiting, mouth ulcers, perianal symptoms, fever, joints, eyes and skin. Plot weight, height and growth velocity and assess puberty. Examine pallor, mouth, clubbing, abdomen, liver, spleen and perianal region with consent and chaperoning. In younger children, poor growth and anaemia may dominate while bowel symptoms are understated.
Request FBC, CRP or ESR, albumin, renal and liver profiles, ferritin and stool pathogen testing. Faecal calprotectin helps demonstrate intestinal inflammation but rises during infection and is age sensitive. Normal CRP does not exclude limited disease. Urgent referral is appropriate when blood, growth failure, anaemia, hypoalbuminaemia or perianal disease persists; primary care should not delay for repeated empirical diets.
Specialist diagnosis maps distribution and behaviour. Ileocolonoscopy with terminal ileal and segmental biopsies plus upper endoscopy is the reference mucosal assessment. MR enterography or intestinal ultrasound evaluates small bowel and transmural complications without routine ionising radiation. Histology separates chronic IBD from infection and other enteropathy. Very-early-onset or atypical disease may need immunology and genomic investigation.
Aetiology
Genetic susceptibility
Polygenic epithelial and immune variants raise risk, with very-early-onset disease sometimes reflecting an identifiable monogenic immune dysfunction.
Dysregulated mucosal immunity
An inappropriate sustained response to intestinal microbes drives tissue injury in a genetically susceptible child through persistent cytokine signalling.
Environmental interaction
Antibiotic exposure, diet, smoking exposure and geography influence risk, but no single behaviour explains an individual child's disease.
Very early onset immune disease
Presentation under six years, severe perianal disease or unusual infection can signal an underlying primary immune disorder requiring genomic assessment.
Pathophysiology
- 1Crohn transmural inflammation
Patchy full-thickness inflammation may affect mouth to anus, producing strictures, fistulas, abscesses and impaired nutrient absorption.
- 2Ulcerative mucosal inflammation
Continuous colonic inflammation begins at the rectum and causes friable bleeding mucosa, urgency and high stool frequency.
- 3Systemic inflammatory burden
Cytokines suppress appetite and growth pathways, increase energy demand and drive anaemia, bone loss and extra-intestinal disease.
- 4Growth and puberty disruption
Malnutrition, inflammation and corticosteroid exposure impair linear growth and pubertal progression, sometimes preceding dramatic bowel symptoms.
Clinical features and red flags
Patchy mouth-to-anus disease, weight loss, right-sided pain, perianal lesions and stricturing or fistulation support Crohn disease.
Continuous rectal and colonic inflammation produces bloody diarrhoea, urgency and tenesmus without small-bowel transmural complications.
Falling height velocity or delayed puberty can precede obvious diarrhoea and is a central paediatric severity marker.
Arthritis, erythema nodosum, pyoderma gangrenosum, uveitis and hepatobiliary disease may track or diverge from gut activity.
Frequent bloody stool plus systemic upset, anaemia, low albumin or colonic dilatation requires inpatient rescue planning.
Investigations
- 01
First-line inflammatory and nutritional profileFirst stepFirst line - Why
- Detect anaemia, inflammation, hypoalbuminaemia, organ involvement and treatment baseline abnormalities.
- Interpretation and limitations
- Normal individual markers do not exclude IBD; combine trends with growth, stool and examination.
- 02
Stool pathogen testing - Why
- Exclude bacterial, C difficile and selected parasitic mimics before immunosuppressive escalation.
- Interpretation and limitations
- Positive results need clinical correlation because infection can coexist with established IBD.
- 03
Faecal calprotectin - Why
- Support the presence and follow-up of intestinal neutrophilic inflammation in an age-appropriate context.
- Interpretation and limitations
- It is not disease specific and cannot replace endoscopy for initial classification.
- 04
Ileocolonoscopy and upper endoscopy with biopsies - Why
- Provide reference diagnosis, histology and extent across the gastrointestinal tract.
- Interpretation and limitations
- Take segmental samples including apparently normal mucosa; chronicity and distribution inform Crohn versus ulcerative classification.
Differential diagnosis
Enteric infection
Campylobacter, Salmonella, Shigella, Yersinia, C difficile and parasites can mimic inflammatory diarrhoea and must be excluded appropriately.
Coeliac disease
Growth failure, anaemia and diarrhoea overlap, but coeliac serology and small-bowel histology distinguish gluten-driven enteropathy from IBD.
Functional bowel disorder
Functional pain lacks bleeding, nocturnal stool, growth failure, objective inflammation and destructive perianal disease on careful assessment.
Polyps or Meckel diverticulum
Painless lower gastrointestinal bleeding with less inflammatory illness may arise from a juvenile polyp or ectopic gastric mucosa.
Immune deficiency or allergy
Infantile colitis, unusual infection and severe eczema broaden assessment beyond conventional adolescent IBD toward immune deficiency or allergy.
Management
01SuspectProtect growth and referFirst stepBlood, nocturnal stool, growth failure, anaemia or perianal disease persists.+
- 1Assess severity, hydration and abdominal or perianal complication and admit if unstable.
- 2Obtain inflammatory, nutritional and stool tests without delaying specialist referral.
- 3Continue adequate nutrition and avoid empirical restrictive diets that impair growth.
02Confirm and induceClassify before treatment escalationEscalationSpecialist assessment clinically supports newly diagnosed IBD.+
- 1Complete endoscopy, histology and small-bowel assessment appropriate to phenotype.
- 2Use enteral nutrition or corticosteroid induction for Crohn disease with paediatric growth considerations.
- 3
Complications
Stricture fistula and abscess
Transmural Crohn disease can obstruct bowel, connect organs and form septic collections requiring drainage or surgery.
Toxic megacolon and perforation
Fulminant colitis can dilate and thin the colon, causing systemic toxicity, perforation and a possible need for emergency colectomy.
Malnutrition and bone disease
Reduced intake, malabsorption, inflammation and steroids impair growth, puberty, vitamin D status and peak bone mass.
Treatment toxicity
Infection, cytopenia, liver or pancreatic injury and infusion reactions require structured screening, laboratory monitoring and named clinical ownership.
Psychosocial and educational harm
Urgency, fatigue, admissions and treatment burden affect school, body image, independence and transition to adult services.
Monitoring and follow-up
- Plot weight, height velocity, BMI and puberty at every meaningful review.
- Track stool frequency, blood, nocturnal symptoms, pain, school and validated activity index.
- Monitor FBC, liver, renal and inflammatory markers according to disease and exact medicine.
- Review infection exposure, vaccines and live-vaccine restrictions before and during immunosuppression.
- Assess iron, vitamin D, nutrition and bone health during chronic activity or after systemic steroids.
- Maintain rapid contact routes for fever, severe pain, distension, bleeding and medication toxicity.
Special situations
Growth is an inflammatory marker
A falling height velocity may reveal active Crohn disease even when stool frequency appears modest.
Calprotectin has context
Infection and young age can elevate it, while a value cannot distinguish Crohn disease from ulcerative colitis.
Nutrition can induce remission
Exclusive enteral nutrition treats intestinal inflammation while supporting growth and avoiding corticosteroid toxicity.
Surgery is not treatment failure
Timely drainage, resection or colectomy can control complications and restore health when medicine cannot do so safely.
Common pitfalls
- 01
Reassuring from a normal CRP despite blood, growth failure or perianal disease.
- 02
Starting immunosuppression before relevant stool infection testing.
- 03
Using corticosteroids as maintenance treatment.
- 04
Ignoring height and puberty while recording weight only.
- 05
Delaying surgical involvement in acute severe colitis.
- 06
Allowing restrictive diets to worsen energy and micronutrient intake.