Crohn's disease is a chronic idiopathic relapsing form of inflammatory bowel disease that can affect the whole gastro-intestinal tract from the mouth to the anus.
2. Epidemiology
More common in those of European origin and Western societies
Incidence - 5-10 new cases/100,000 per year
Prevalence - 50-100/100,000
Can affect any age group. Bimodal distribution - first largest peak at 15-30, next smaller peak at 60-80.
3. Risk Factors
Exact aetiology is unknown - many theories including genetic, infective, environmental and immunological causes.
Smoking increases risk
Family history
4. Symptoms and Signs
Many patients have had symptoms for years before presentation.
Unlike ulcerative colitis, symptoms can be insidious, making diagnosis difficult
Symptoms can be classified in to systems
Click here to see the National Association for colitis and Crohn's disease
4.1 Gastrointestinal System
4.1.1 Symptoms
Abdominal pain - crampy, intermittent pain is most common symptom
Chronic diarrhoea - can vary according to which segment of bowel is affected. Ileitis leads to high volumes of watery diarrhoea, colitis leads to smaller volumes but higher frequency
Nocturnal diarrhoea
Bloody diarrhoea - less common than in UC
Symptoms of intestinal strictures -
bloating
distension
vomiting
nausea
obstruction
Symptoms of intestinal fistulae -
pneumaturia
vaginal discharge
Peri-anal symptoms
pain on defaecation
itching
incontinence
4.1.2 Signs
Abdomen
Palpable mass
Fistulae - click here to see a picture of complex intestinal fistulae
Peri-anal signs
fistulae - can be multiple
fissures
abscesses
Mouth - apthous ulcers
Hands -clubbing
4.2 Systemic symptoms + signs
Fever
Weight loss
Growth failure in children
Anorexia
Cachexia
4.3 Extra-intestinal symptoms + Signs
4.3.1 Related to underlying disease activity
Erythema nodosum
Peripheral Arthritis
Apthous ulcers
Pyoderma Gangrenosum
Episcleritis
4.3.2 Unrelated to underlying disease activity
Uveitis
Spondylarthropathy - Ankylosing spondylitis
4.3.3 Extra-intestinal diseases
Gallstones
Primary Sclerosing Cholangitis
Nephrolithiasis
Thromboembolism
5. Diagnosis + Investigation
Can be difficult to reach the diagnosis of Crohn's in some patients
History and Examination
Bloods -
Hb - may demonstrate anaemia due to multiple causes - from either blood loss or B12 deficiency (due to terminal ileal disease reducing absorption) or anaemia of chronic disease
ESR + CRP - elevated due to inflammation. Correlate closely with disease activity.
Serum Albumin - hypoalbuminaemia due to malabsorption
Stool culture - MC&S + C-Diff toxin
AXR - may demonstrate small bowel dilatation due to stricture formation
Colonoscopy - best test as allows visualisation of colon + terminal ileum + allows biopsies to be taken for tissue diagnosis
Barium enema - allows diagnosis of colonic fistulae + stricture. Does not allow biopsies to be taken and may underestimate extent of disease.
Barium follow through - May suggest the diagnosis by identification of small bowel strictures esp. terminal ileum, fistulae, ulcers, cobblestoning
Diagnosis is made by the combination of the above tests with history and examination findings, demonstrating the typical pathological findings and manifestations of CD
MR Enteroclysis - small bowel mri - allows good imaging of the small bowel without the use of ionising radiation and will replace small bowel follow through as a small bowel investigation
6. Pathology (see table comparing to UC)
6.1 Macroscopic
Can involve anywhere in the gastrointestinal tract from mouth to anus
Three commonest sites of involvement are
ileocolic
ileal
colic
Perianal disease, particularly fissures and fistulae, is common
reddened mucosa + small apthous ulcers
superficial spreading ulcers
deep narrow ulcers
fistulation
extensive fissuring leaves islands of raised mucosa - cobblestoning
Segments of bowel that are affected are known as "skip" lesions
Areas of advanced disease, inflammation becomes fibrotic
stricture + "hosepipe" segments
6.2 Microscopic
Begins as a focal inflammatory infiltrate around crypts
Inflammatory cells (macrophages and giant cells) invade deeper layers and organize into noncaseating granulomas (absence of granulomas does not exclude the diagnosis of Crohn's and is found in 70% of cases).
7. Management
7.1 Medical Management
Clinical course of CD characterized by exacerbations and remission
Treatment is primarily medical
7.1.1 Aminosalicylates
5-aminosalicylic acid derivatives (e.g. mesalazine) - less effective in Crohn's than UC
7.1.2 Corticosteroids
Used for in short courses and for patients with severe symptoms and in those unresponsive to aminosalicylates
Steroids tapered slowly once remission achieved
NOT indicated for maintenance due to complications of prolonged use
7.1.3 Antibiotics
Useful in co-existing infection
7.1.4 Thiopurines (azathioprine)
Used if steroid withdrawal is proving difficult
Main role is steroid sparing
Careful monitoring required to look for evidence of bone marrow suppression and hepatotoxicity.
7.1.5 Infliximab
Anti-TNF monoclonal antibody
Use limited to people with severe active UC refractory or intolerant to steroids and immunosuppression, who are not appropriate for surgery.
7.2 Indications for Surgery
Patients requiring surgery for IBD should be under joint care of a gastroenterologist and a colorectal surgeon.
Unlike UC, surgery for patient's with Crohn's disease is NOT curative and is aimed at bowel conservation
Surgery should only be offered to patients with symptomatic disease including Crohn's patients with anal and peri-anal CD rather than patients with asymptomatic, radiologically identified disease or asymptomatic anal and peri-anal CD.
Bowel resection is limited to macroscopic disease - features of which are
thickened hyperaemic bowel wall
fat encroachment
8. Suggested further reading
National Assocation for Colitis and Crohn's http://www.nacc.org.uk
BSG guidelines for management of IBD http://www.bsg.org.uk/pdf_word_docs/ibd.pdf
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