IBD - Mosaiced.org

IBD – Crohn’s Disease (Gastroenterology):
Example case:
A chronic inflammatory disease of the bowel causing lesions throughout any part of the GIT from mouth
to anus.
150/100,000 Australians
Commonly diagnosed between 15-30yoa
More common in Western countries
Female > male
Increases risk of colorectal & small bowel cancer
Associated with sclerosing cholangitis in ~10% of ppl
Risk/Protective factors:
Family Hx
Other GIT disorders e.g. coeliac, food intolerance
There are 3 major patterns of involvement in Crohn’s disease including:
 Disease in the ileum and cecum, occurring in 40% of patients.
 Disease confined to the small intestine, occurring in 30% of patients.
 Disease confined to the colon, occurring in 25% of patients.
Unknown cause. Genetic link with 8-10% of sufferers having other family members with Crohn’s while
parents with Crohn’s have a 3-5% chance of an offspring with Crohn’s. Disease can be
aggravated/stimulated by bacterial infection. Factors believed to influence disease expression:
 Smoking (x2 ↑ risk)
 Breastfeeding for >3 months reduces risk
 Exposure to antibiotics as a child increases risk
 “hygiene hypothesis” i.e. overly sterile upbringing  Crohn’s
Normal physiology/anatomy:
Transmural (across wall) inflammation i.e. layers from the mucosa to muscle level leading to
discontinuous lesions (i.e. patches), most commonly affecting the ileum area, but again can affect any
part of the GIT. The cause is inappropriate activation of the innate immune system by natural gut flora
 neutrophil mediation  T cell activation  cytokine release.
Can cause fistulas, scarring, strictures
Clinical Features (signs & symptoms):
Ulcers (aphthous mouth)
Fistulas – anorectal, enterorectal, enterocutaneous fistulas are most common
Liver inflammation – pain, jaundice
Pyoderma gangernosum – necrosis of tissue  deep ulcer most common in legs
Erythema nodosum – painful, red nodules mostly on limbs that last ~2 weeks and can change colour
and texture
 Uveitis/Iritis – inflammation of the uvea (layer of the eye made up of iris, ciliary bodies and choroid)
 pain, tearing, redness, sensitivity to light and blurred vision.
Rectal bleeding - melena, haematochezia
Abdo/rectal pain
Tenesmus (constant feeling of needing to defecate)
Joint pathology – arthralgia & arthritis, ankylosing spondylitis
Neurological – lack of B12 absorption mainly  headaches, depression, myopathy, peripheral
 Malabsorption  weight loss
 Fever
NB: Crohn’s is less associated with systemic manifestations than UC.
 All forms of Crohn
- Diarrhea occurs in most patients
- Abdominal pain in 2/3
- Weight loss, malaise
- Abdominal tenderness
- Low-grade fever
- Abdominal mass (occasionally)
- Fistula: Perirectal, bladder, skin, vagina
- Extraluminal disease (10%): Skin, iritis, arthritis, sclerosing cholangitis
 Small-bowel disease only (15-30%)
- Diarrhea prominent, including nocturnal
- Vague abdominal pain frequent
- Intestinal obstruction (1/3): Cramping abdominal pain precedes for months.
- Bleeding in 20%, rarely massive
- Perianal disease, including fistulae
- Internal fistulae
 Colon disease only (25-30%)
- Diarrhea prominent, including nocturnal
- Hematochezia
- Abdominal pain in 50%, relieved by stooling
- Perianal disease in 40%, fistulae
- Weight loss prominent
- Megacolon in 10%
- Intestinal obstruction occasional
 Colon and small-bowel disease (40-60%)
- Intestinal obstruction much more common than in other types
UC – only occurs in mucosa layers of colon and rectum with less extra-intestinal s/s.
Appendicitis – if near ileocecal area, RIF pain, fever, fatigue
Intermediate colitis
Ischaemic colitis
Investigations & relevant findings:
 Magnetic resonance enterography – type of MRI with contrast (usually gadolinium) to produce
detailed images of intestine
 Scopes + biopsy – colonoscopy, sigmoidoscopy, endoscopy – see cobblestone appearance, apthous &
linear ulcers, friability
 Small bowel enema
 Capsule endoscopy (pillcam)
 Barium enema – barely used
 Stool MSC – to exclude infectious diarrhoea
 Blood tests – inflammatory markers (ESR, CRP), malnutrition (FBE, vitamin levels, iron studies) and gut
& liver functions (UEC, LFTs)
 Serum ASCA (anti-saccharomyces cerevisiae antibodies) +ve in 50% of patients.
 Lifestyle – maintaining weight and nutrition (reduce intake of intolerant substances e.g. protein, fats,
fibre), relieve stress, quit smoking, reduce alcohol.
 Drugs
o Mild attacks – aminosalicylates (anti-inflammatory drugs) or corticosteroids (prednisolone) PO
(per oral) 30mg for 1 wk, then 20mg for 2-4wks, if improved, taper off 5mg/2-4wks, stop when
normal again.
o Immunosuppresants in patients with frequent relapse
o Severe disease – IV steroids (hydrocortisone), nil by mouth, IVI (infusions - saline, dextrose), if
improving after 5 days, change to oral prednisolone, if no improvement = infliximab &
adalimumab(TNF-α inhibitors)
o Antibiotics – metronidazole if infection or perianal disease
 Surgery – if drug therapy fails or complications occur. Bowel resection, stricturoplasty or closer of
fistulae and drainage abscesses can be done.
No cure is available, 15% of patients are unable to work after 5-10yrs. Slightly higher mortality rate than
 Small bowel obstruction
 Toxic dilatation (>6cm colon diameter)
 Abscess (buildup of pus and inflammation), fistulae (e.g. colovesical aka. Bladder, colovaginal, perianal
etc), perforation, rectal haemorrhage
 CA colon
 fatty liver
 PSC, cholangiocarcinoma
 renal stones
 osteomalacia, malnutrition (B12)
 amyloidosis
NB: perianal disease i.e. any condition affecting the rectal/anal area affect 50% of patients.