Inflammatory Bowel Disease

1. Inflammatory Bowel Disease Dr Lawrence Axten

2. IBD IBD is the term used to describe a group of idiopathic chronic inflammatory intestinal bowel diseases. Two main categories- Ulcerative colitis Crohn�s disease (Indeterminate colitis)

3. IBD Pathogenesis is unknown. Many overlapping histological, endoscopic, radiological and clinical findings. But...clear differences in distribution and depth of inflammation in the bowel. Crohn�s is transmural affecting any part of the GI tract. UC affects the colonic mucosa only.

4. Crohn�s Disease (CD) Relapsing and remitting. Characterised by focal asymmetrical transmural bowel wall granulomatous inflammation. Commonly affects the terminal ileum but can appear anywhere in GI tract. Complications-strictures, abscesses and fistulae. Montreal classfication-score using age of diagnosis, pattern and location of disease.

5. Crohn�s Aetiology Cause unknown but risk factors identified. Genetic-HLA-DR1 and 20% FH of UC/CD. Environmental-western lifestyle, smoking and diet. Occupation- white collar>blue collar. Infection-(none proven) suggestions- measles virus, paratuberculosis, listeria etc. Immune response. Apendicectomy. OCP (association). NSAID�s (weak evidence).

6. Appearance of Crohn�s Macroscopic Microscopic Skin lesions Cobblestone ulceration Lead pipe thickening Narrow lumen strictures Fistulae Rose thorn mouth ulcers Enlarged nodes around mesenteric nodes Terminal ileum 50% of cases Transmural ulceration Granulomas Lymphocyte inflitration

7. Clinical features Relapsing and remitting. Typically chronic onset but can be acute. Diarrhoea-chronic or nocturnal. Abdo pain, weight loss and fatigue. Anorexia and fever. Abdo mass or tenderness. Secondary obstruction. Adolescents can present with weight loss alone. Extraintestinal manifestation-clubbing, skin tags, arthritis (B27), erythema nodosum & anaemia.

8. Investigation of Crohn�s Primary care investigations- FBC, CRP & ESR, U&E & LFT�s Stool culture & microscopy (rule out infection) Investigations aimed at diagnosis and monitoring. Secondary care investigations- Bloods, endoscopy (upper & lower), histology (fissuring, full thickness inflammation, granulomata, ulceration, erosion) LFT�s and imaging.

9. Crohn�s Investigations (2) FBC-iron deficiency anaemia (often), B12/folate deficiency (rarely), leucocytosis. CRP-rasied good for monitoring activity. ESR-elevated. Biochem-in severe disease-hypoalbuminaemia (malabsorption), hyponatraemia, hyperkalaemia & abnormal LFT�s if chronic active hepatitis. Imaging-CT, AXR, contrast studies, large bowel enema, labelled WC scan, radionucleotide scanning & MRI. Endoscopic appearances-not continuous, rectum not always involved (50%). Fissures often seen. Skin lesions, cobblestone appearance and strictures are often present. Small bowel capsule endoscopy when high suspicion but other imaging unequivocal.

10. Management of Crohn�s depends on several factors- Disease Location Behaviour of Disease Medication Response Management Disease Location Medication Side Effects Extra intestinal problems

11. Medical Management-difficult? The basis of treatment rests on aminosalicylates (mesalazine, sulfasalazine, olsalazine & balsalazide) and corticosteroids (prednisolone, budesonide & hydrocortisone). And.... Effective management of nutrition (elemental diet) and surgery (in chronic and severe disease).

12. Acute moderate to mild treatment- Local application of corticosteroid or aminosalicylate for proctitis or distal colitis. Available in foam and suppositories for those patients who have problems retaining liquid. Diffuse crohn�s or local crohn�s not responding needs systemic treatment with an aminosalicylate such as budesonide. Refractive or moderate disease may need a course of corticosteriods.

13. Acute severe treatment- Hospital admission. Treatment with intravenous corticosteroid and fluids/electrolytes. Possible blood transfusion. Possible parental nutrition and antibiotics. Possible metronidazole in perianal involvment. Crohn�s that is still unresponsive may benefit from azathioprine, mercaptopurine or once weekly methotrexate. NICE recommend only Infliximab prescribed by a gastroenterologist, only if other measure have failed & not in remission.

14. Maintenance of remission- Oral mesalazine for ileal disease, other aminosalicylates more value in UC. Not steriods due to their long term side effects. In resistant or frequent relapsing-azathioprine or mercaptopurine (specialist monitoring). 3 rd line-methotrexate.

15. Adjunctive Treatments- Low residual diet or high fibre. If IBS during remission avoid high fibre diet & possible antispasmodic. Laxatives in proctitis. Diarrhoea from end ileal disease resulting in loss of bile salts sometimes response to colestyramine (bile salt binder).

16. Ulcerative colitis (UC) Affects the large bowel only. Usually starts at rectum extending proximally in a symmetrical, circumferential and uninterrupted pattern. May effects parts of mucosa or whole surface. Excerbations and remissions. Classified by the Montreal system into ulcerative proctitis, left sided colitis or extensive colitis.

17. UC Epidemiology Onset often in adolescents-young adults. Also a small peak in 50�s. Male = Female. Family clustering. Western disease. Incidence 5-8/100,000 in North-Western Europe, Northern America and New Zealand. Prevalence-70-150/100,000.

18. Aetiology Unknown. Genetic factors. Environmental factors-non smokers and FH. NSAID�s can cause excerbations. Appendicectomy for true appendicitis has a protective affect. Pathological features-affect mucosa & submucosa, no skip lesions, inflammatory cell infiltrate, haustral loss, pseudopolyps, friable.

19. Clinical features Often insidious symptoms May present acutely Bloody diarrhoea or rectal bleeding >6 weeks. Frequency Approx 1 to 20 stools a day. 90% of UC pt�s present with rectal bleeding. Urgency, tenesmus, nocturnal defecation, abdo pain, ache in L IF and pain relieved after defecation. A child may present as �failure to thrive�. Pallor. Dehydration. Mouth ulcers. Abdo tenderness. Associated Features Erythema nodosum. Pyoderma gangrenosum. Uveitis. Arthritis.

20. Assessing Severity Mild �less than 4 stools daily with or without blood, no systemic disturbance and normal CRP/ESR values (<30)/Hb >11.0 Moderate -four to six stools a day with minimal systemic disturbance. Severe-more than six stools a day containing blood and systemic disturbance & Hb <10.5.

21. Investigation FBC, CRP, ESR, U&E and LFT�s. ANCA found in HLA-DR2 has association. Secondary care- barium enema, rectal biopsy, colonoscopy, white cell scan & molecular biology. No gold standard for diagnosis.

22. Management Aims to maintain remission. Aminosalicylates (1st line), thiopurines (2nd line) and infliximab (if previous response). Immunosuppresants used in Crohn�s-methotrexate/azathioprine are used by about 20% of UC sufferers. Excerbations-steriods can be used. Elemental diets are of no use, fish oils helpful, some early evidence for use of probiotics.

23. Complications of UC Local Systemic Haemorrhage . Malnutrition . Electrolyte imbalance . Toxic megacolon . Stricture formation � (rare) . Fistula formation � (rare). Perforation . Increased risk of malignancy - lymphoma, carcinoma. Weight loss, anaemia Hypoproteinaemia Arthropathy �large joints Liver pathology Sacro-iliitis and ankylosing spondylitis Carcinoma of the bile ducts-(rare)

24. Prognosis Primary care Secondary care Refer at 8-10 yrs of UC for reassessment of disease. Refer at 15 yrs for left sided UC. Proctitis no follow up. 1% risk of colon cancer at 10 yrs. 13% at 20 yrs. 34% at 30 yrs Stable pt�s -yearly FBC and LFT�s. 1-2 yearly colonoscopies and biopsies after 10 yrs. Normal life expectancy of general population due to improved treatments.

25. Questions?