Paediatrics chapters
Inflammatory bowel disease in children
Crohn disease and ulcerative colitis in children and teenagers: causes, how the two differ, growth failure and extraintestinal features, tests such as colonoscopy and calprotectin, and stepwise treatment.
- IBD has two main types: Crohn disease (any part from mouth to anus, transmural, skip lesions, granulomas, fistulas, perianal disease) and ulcerative colitis (colon only, starts at the rectum, continuous, mucosal); peak onset is in the second decade.
- Children with Crohn disease often present subtly with abdominal pain, weight loss, growth failure and delayed puberty; UC presents with bloody diarrhoea, urgency and tenesmus; toxic megacolon is the dangerous complication of severe colitis.
- Diagnose with CBC, ESR/CRP, albumin, faecal calprotectin, and colonoscopy with biopsy plus small bowel imaging; treat with 5-ASA (mainly UC), steroids for flares, azathioprine/6-MP to spare steroids, anti-TNF (infliximab) for resistant disease, and surgery (curative in UC only).
On this page
Overview
Inflammatory bowel disease (IBD) is chronic, relapsing, idiopathic inflammation of the gut. Its two main forms in children are Crohn disease (CD) and ulcerative colitis (UC). In children the incidence peaks in the second decade of life. Children differ from adults because growth and puberty are at stake, so treatment aims to control inflammation, restore growth and keep steroid exposure low.
Types and aetiology
Types
| Type | Extent |
|---|---|
| Crohn disease | Any part of the GI tract from mouth to anus; often terminal ileum and colon; patchy (skip lesions) |
| Ulcerative colitis | Colon only, starting at the rectum and spreading continuously upward |
| IBD unclassified | Colitis with features of both |
Aetiology
The cause is unknown. The current model is an abnormal, uncontrolled immune response, in a genetically prone host, to an environmental trigger (possibly gut bacteria or a virus).
| Factor | Evidence |
|---|---|
| Genetic | A first-degree relative with IBD raises risk about 30-fold; links with some HLA types and several susceptibility genes |
| Environmental | Identical twins are often not both affected; incidence is rising in industrialised countries; less common in tropical countries |
| Ethnic | More common in Jewish populations |
| Smoking | Doubles the risk of Crohn disease and halves the risk of UC |
| Diet | Not proven as a trigger |
Smoking has opposite effects: harmful in Crohn disease, protective in UC. It is a favourite MCQ.
Clinical features
Shared features
Diarrhoea, abdominal pain, fever, weight loss and blood loss. When colitis is present (either type): blood and mucus in stool, urgency, tenesmus, and waking at night to pass stool.
Ulcerative colitis
- Bloody diarrhoea is almost universal (Akbar: blood in stool in nearly all, abdominal pain about 95%, tenesmus about 75%).
- Symptoms of colitis are always present, so UC is usually recognised early.
- Severity (Akbar):
| Severity | Features |
|---|---|
| Mild (most children) | Fewer than 4 stools/day, no fever |
| Moderate | More than 6 stools/day, fever, anaemia, low albumin |
| Severe | More than 10 stools/day, high fever, tenderness, distension, tachycardia, leucocytosis, bleeding, severe anaemia |
Crohn disease
- Often subtle and diagnosed late.
- Crampy, post-meal abdominal pain, often periumbilical or right lower quadrant; anorexia.
- Weight loss, growth failure, delayed puberty: may precede gut symptoms.
- Fever of unknown origin, anaemia, lethargy.
- Perianal disease: skin tags, fissures, fistulas, abscesses.
- Oral aphthous ulcers; arthritis may come before gut symptoms.
- Fibrotic strictures can cause partial or complete small bowel obstruction; a right lower quadrant mass may be felt.
A teenager with short stature, delayed puberty and anaemia but few gut symptoms may have Crohn disease. Check inflammatory markers and growth charts.
Crohn disease versus ulcerative colitis
| Feature | Crohn disease | Ulcerative colitis |
|---|---|---|
| Site | Mouth to anus, ileum common | Colon only (rectum always) |
| Pattern | Skip lesions | Continuous |
| Depth | Transmural | Mucosal |
| Rectal bleeding | Sometimes | Usual |
| Abdominal mass | Common | Rare |
| Perianal disease | Common | Rare |
| Ileal involvement | Common | None (only "backwash ileitis") |
| Strictures | Common | Unusual |
| Fistulas | Common | Very rare |
| Granulomas | Common | Rare |
| Crypt abscesses | Variable | Usual |
| Mouth ulcers, erythema nodosum | Common | Less common |
| Osteopenia at onset | Yes | No |
| Sclerosing cholangitis, autoimmune hepatitis | Rare | More common |
| Colon cancer risk | Increased | Greatly increased |
| p-ANCA | Few | Most (Akbar about 70%) |
| ASCA | About half | Few |
Crohn = "Can Skip Anywhere, Through the wall" (any site, skip lesions, transmural, fistulas). UC = "Up from the rectum, Continuous, Colon only".
Extraintestinal manifestations
| System | Features |
|---|---|
| Growth | Growth failure, delayed puberty (much more common in Crohn disease) |
| Joints | Arthralgia, peripheral arthritis, sacroiliitis |
| Skin | Erythema nodosum, pyoderma gangrenosum |
| Eyes | Uveitis, episcleritis |
| Mouth | Aphthous stomatitis |
| Liver and biliary | Primary sclerosing cholangitis (mainly UC), chronic hepatitis, gallstones |
| Kidney | Kidney stones |
| Blood | Anaemia, raised platelets |
Toxic megacolon
A life-threatening complication of severe colitis (mainly UC): fever, abdominal distension and pain, a massively dilated colon, anaemia and low albumin from protein loss in stool. Akbar notes about 5% of UC patients present this way and need urgent colectomy.
Investigations
| Test | Finding |
|---|---|
| CBC | Anaemia, raised platelets, raised white count |
| ESR, CRP | Raised in most (not all) |
| Albumin | Low (faecal protein loss) |
| Faecal calprotectin | Screening test for gut inflammation (Akbar) |
| Stool microscopy and culture, C. difficile toxin | To exclude infection (Campylobacter, Yersinia, amoebiasis, giardiasis) |
| p-ANCA / ASCA | p-ANCA favours UC, ASCA favours Crohn disease; neither is absolute |
| Colonoscopy with biopsy | Preferred test. UC: diffuse fine ulcers, loss of haustra, no skip areas. Crohn: larger linear or aphthous ulcers, skip areas, granulomas on histology |
| Upper endoscopy | Detects proximal Crohn disease |
| Small bowel imaging | Barium follow-through (Crohn: string sign, skip lesions), MR enterography (no radiation), CT for abscesses, capsule endoscopy |
| Double-contrast barium enema | UC: diffuse lesions, pseudopolyps (largely replaced by colonoscopy) |
Differential diagnosis
- Chronic infections: amoebiasis, giardiasis, Yersinia, Campylobacter, C. difficile; abdominal tuberculosis should also be kept in mind in our setting
- Coeliac disease, lymphoma
- Henoch-Schönlein purpura, SLE, juvenile arthritis
Yersinia infection of the terminal ileum can mimic Crohn disease or appendicitis (Nelson). Always exclude infection with stool tests before labelling a child as IBD.
Management
Aims: induce remission, maintain remission, restore growth and puberty, limit steroid use.
Nutrition
- High-protein, high-energy diet with normal fat; less roughage in active disease; lactose may be poorly tolerated in flares.
- Vitamins, iron, zinc, calcium and vitamin D.
- Nutritional support is central for growth in Crohn disease.
Drugs
| Drug | Use | Notes (doses from Akbar) |
|---|---|---|
| Aminosalicylates (5-ASA): sulfasalazine, mesalazine | First-line in mild to moderate UC; less effective in Crohn disease | Sulfasalazine is split by colonic bacteria into sulfapyridine (side effects) and 5-ASA (active); 50 to 75 mg/kg/day in 2 to 4 doses |
| Corticosteroids (prednisolone) | Induce remission in moderate to severe flares; not for long-term use | 1 to 2 mg/kg/day (maximum 40 to 60 mg) |
| Azathioprine / 6-mercaptopurine | Steroid-sparing maintenance; often started early in Crohn disease | Azathioprine 2 to 2.5 mg/kg/day; 6-MP 1 to 1.5 mg/kg/day |
| Methotrexate | Difficult Crohn disease | Subcutaneous |
| Metronidazole (or ciprofloxacin) | Perianal and colonic Crohn disease | 15 to 30 mg/kg/day in 3 doses |
| Anti-TNF (infliximab) | Resistant Crohn disease and rescue in severe UC | Intravenous; most effective biologic in Nelson |
| Ciclosporin | Severe steroid-resistant UC, often as a bridge to surgery | High relapse after stopping |
| Probiotics | Help maintain remission in UC, do not induce it | — |
Surgery
| Ulcerative colitis | Crohn disease |
|---|---|
| Colectomy is curative | Not curative; disease recurs |
| For uncontrolled bleeding, toxic megacolon, intractable symptoms, growth failure, dysplasia or cancer, or electively to remove cancer risk | For obstruction (strictures), abscess, fistula, or severe unremitting disease; resect as little bowel as possible |
| Usually colectomy with ileoanal pouch | About 70% need surgery at some point (Akbar) |
Surgery cures UC but not Crohn disease. In Crohn disease, keep resections short to avoid short bowel syndrome.
Prognosis, monitoring and complications
- Both are lifelong relapsing conditions with periods of remission.
- Crohn disease: low mortality but high morbidity; growth failure, strictures, fistulas, repeated surgery.
- UC: generally good prognosis; Akbar notes 20 to 40% eventually need colectomy (pancolitis, anaemia, low albumin).
- Colon cancer risk rises with duration and extent of colitis (much higher in UC), so surveillance colonoscopy is needed in long-standing disease.
- Monitor height, weight and puberty, haemoglobin, inflammatory markers, liver tests (sclerosing cholangitis), bone density, drug side effects (blood counts on azathioprine; infection risk on immunosuppressants).
Expect: peak age in adolescence; Crohn disease (mouth to anus, transmural, skip lesions, granulomas, fistulas, perianal disease, growth failure) versus UC (colon only, rectum, continuous, mucosal, bloody diarrhoea, crypt abscesses); smoking's opposite effects; p-ANCA in UC and ASCA in Crohn; sclerosing cholangitis with UC; toxic megacolon; colonoscopy with biopsy as the key test; 5-ASA for UC, steroids to induce remission, azathioprine to spare steroids, infliximab for resistant disease; metronidazole for perianal Crohn; and surgery being curative only in UC.
Quick revision
- Peak onset second decade; genetic plus environmental; smoking worsens Crohn, protects UC.
- Crohn: mouth to anus, skip, transmural, granulomas, fistulas, perianal disease, growth failure.
- UC: rectum upward, continuous, mucosal, bloody diarrhoea, tenesmus.
- Toxic megacolon: fever, distension, dilated colon, anaemia, low albumin.
- Tests: CBC (anaemia, high platelets), ESR/CRP, albumin, calprotectin, colonoscopy with biopsy.
- p-ANCA = UC; ASCA = Crohn.
- 5-ASA (UC), steroids for flares, azathioprine/6-MP maintenance, infliximab rescue.
- Colectomy cures UC; surgery does not cure Crohn disease.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
What is the single most useful test to diagnose IBD?
Colonoscopy with biopsies (often with upper endoscopy), because it shows the pattern of disease and gives tissue for histology.
Why does Crohn disease cause poor growth?
Chronic inflammation, poor appetite, malabsorption and steroid treatment all reduce growth; poor growth and delayed puberty can be the first signs.
Which IBD is linked to sclerosing cholangitis?
Mainly ulcerative colitis, so liver tests should be monitored in children with UC.
Can probiotics treat a UC flare?
No. They may help keep UC in remission but do not induce remission during an active flare.