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Inflammatory bowel disease- Lower gi hemorrhage

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LOWER GI HEMORRHAGE- PLAYLIST OF 6 VIDEOS
Dear Viewers,
Greetings from “Surgical Educator”.
I have made a playlist for Lower GI Hemorrhage which consists of six videos on various causes of Lower GI Hemorrhage. They are Introduction, diverticular disease, haemorrhoids, fissure-in-ano, colorectal carcinoma and inflammatory bowel disease. If you watch all these videos together you will become confident to tackle the clinical problem of Lower GI Hemorrhage. You can watch these videos in the following link: https://www.youtube.com/playlist…
Thank you for watching the videos.

Published in: Health & Medicine
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Inflammatory bowel disease- Lower gi hemorrhage

  1. 1. LOWER GI HEMORRHAGE INFLAMMATORY BOWEL DISEASE Dr.B.SELVARAJ MS;Mch;FICS: PROFESSOR OF SURGERY MELAKA MANIPAL MEDICAL COLLEGE MELAKA 75150 MALAYSIA
  2. 2. INFLAMMATORY BOWEL DISEASE Causes of Lower GI Hemorrhage Epidemiology Etiology Pathology Clinical Features Investigations Complications Medical Treatment Surgical Treatment Comparision of Crohn’s & Ulcerative Colitis Diagnostic Algorithm Management Algorithm
  3. 3. Causes for Lower GI Hemorrhage Diverticular disease Angiodysplasia- AV Malformation Colorectal carcinoma Hemorrhoids Fissure-in-ano Ischemic colitis Inflammatory bowel disease Meckel’s diverticulum Upper GI hemorrhage
  4. 4. IBD-CROHN’S- ETIOLOGY Crohn’s disease is a trans mural IBD that can affect any part of the GI tract from the mouth to the anus. The incidence is about 3 new cases/ 100,000 people, with a prevalence of about 30 cases/100,000 people. Both genetic and environmental factors are implicated Genetic: The IBD1 locus on chromosome 16 is strongly associated with Crohn disease. Environment: Infective agents implicated measles virus and Mycobacterium para tuberculosis Cigarette smoking and intake of refined sugars
  5. 5. IBD-CROHN’S- PATHOLOGY Macroscopic: Classically segmental with areas of normal bowel separating areas of involved bowel- ‘skip’ lesions. Thickening of wall, which becomes firm and rigid. Encroachment on mesenteric fat “Creeping fat” Linear mucosal ulceration. A ‘cobble-stone’ pattern of islands of surviving mucosa. Deep linear ulceration.
  6. 6. IBD-CROHN’S- PATHOLOGY Microscopic: Transmural inflammation from mucosa to serosa. Marked edema of submucosa. Lymphoid aggregates Patchy mucosal ulceration and fissuring. Presence of non-caseating granulomas (found in only 60% of cases).
  7. 7. CROHN’S-CLINICAL FEATURES Three distinct types of disease are seen: inflammatory, stricturing and perforating Patients are young and present with abdominal pain, weight loss, and diarrhea. Abdominal pain is colicky. Some patients present with frequent bloody stools with mucus . These patients are indistinguishable from those with ulcerative colitis. Extraintestinal manifestations include erythema nodosum, pyoderma gangrenosum, uveitis and sacroiliitis, large joint involvement, and clubbing. Perianal Crohn diseaseRectal examination reveals evidence of ulceration, edematous skin tags, perianal abscess and/or fistulation, and stricture.
  8. 8. CROHN’S- INVESTIGATIONS Colonic disease is best diagnosed by colonoscopy. The distribution of colitis is discontinuous with rectal sparing. Terminal ileum can be visualized and biopsied to confirm small bowel disease. Upper GI series with small bowel follow-through or CT enterography may be useful in identifying small bowel involvement. Definitive imaging of perineal disease may require examination under anesthesia with proctoscopy or sigmoidoscopy. Transrectal ultrasonography and magnetic resonance imaging of the anal canal can also reveal perineal disease
  9. 9. CROHN’S- INVESTIGATIONS STRING SIGN OF KANTOR ROSE THRON APPEARANCE COBBLE STONE APPEARANCE
  10. 10. CROHN’S- COMPLICATIONS  Intestinal obstruction. Fistula formation. Abscess formation. Malabsorption syndrome. Toxic dilatation. Haemorrhage. Perianal complications. Gallstones (reduction of entero hepatic circulation of bile in terminal ileum).
  11. 11. CROHN’S- Medical Treatment Aim is symptom relief and maintenance of well-being Patients should have a well-balanced diet and maintain weight. An acute flare-up of obstructive symptoms can be managed with a short, high-dose regimen of oral steroids. Azathioprine may allow maintenance at a lower steroid dosage. Budesonide is an enteric-coated steroid that is released into the terminal ileum averts the side effects of oral steroids In a patient with remission, sulfasalazine derivatives may also be used (e.g.mesalazine or Pentasa) . Immune suppressants such as azathioprine and cyclosporine have been shown to be effective The anti-TNF antibody infliximab has been shown to promote healing in complex cases of P C D .
  12. 12. CROHN’S- Surgical Treatment Surgery is used when drug therapy cannot achieve optimal relief. Ileocecal disease resection to grossly normal bowel with primary anastomosis Recurrence tends to occur Extensive colitis with rectal sparing urgent colectomy with ileorectal anastomosis  Segmental Crohn colitis also lends itself to segmental resection and reanastomosis  Rectal Crohn disease Crohn colitis require panproctocolectomy and the ileal pouch is not generally accepted because of the tendency of Crohn disease to affect the pouch, leading to its failure.
  13. 13. Ulcerative Colitis- Etiology This diffuse inflammatory disease affects the mucosa of the colon and rectum. Incidence: 1to15 new cases per 100,000 population. Bimodal distribution, with most cases occurring in the teen years followed by a second peak in the 40s. Etiology is uncertain. Abnormal immune response to gut microorganisms Autoimmunity against colonic epithelial cells Genetic factors: -familial clustering occurs; - association with HLA- DR2; - higher concordance rate in monozygotic twins Geographic factors: much commoner in western countries than in developing world
  14. 14. Ulcerative Colitis- Pathology Macroscopic: Proctitis: inflammation of mucosa limited to rectum.  Colitis extending for a variable distance proximally from the rectum. Total colitis with or without backwash ileitis. The mucosal surface is ulcerated with areas of heaped regenerating mucosa called pseudopolyps Fistulae do not occur
  15. 15. Ulcerative Colitis- Pathology Microscopic: Diffuse, mixed inflammatory cell infiltrate. Crypt abscess formation. Distortion of glandular architecture. Mucosal ulceration.
  16. 16. Ulcerative Colitis- Types
  17. 17. Ulcerative Colitis Clinical Features Clinical severity is extremely variable Frequent passage of blood-stained stools or diarrhea that contains mucus Mild lower abdominal pain, fever, and tenesmus Rectal examination reveals blood and, on sigmoidoscopy, there is evidence of proctitis A severe attack, usually with pancolitis results bloody diarrhea ( 10 to 24 times a day) , colicky lower abdominal pain, and weight loss. Extraintestinal features: Pyoderma gangrenosum, Erythema nodosum, Scleritis/episcleritis, Uveitis, Iritis, Ankylosing spondylitis and Sclerosing cholangitis.
  18. 18. Ulcerative Colitis- Investigations Colonoscopy is a definitive imaging technique. A full examination to the cecum is performed. Visualization of the terminal ileum during colonoscopy to rule out Crohn disease. A barium enema is used less frequently in the imaging of ulcerative colitis Lead pipe appearance, Thumb print sign and Rose thorn appearance are classical radiological signs  Upto 10% of patients, the differentiation between ulcerative colitis and Crohn’s disease may not be complete, and the colitis is thus labelled indeterminate.
  19. 19. Ulcerative Colitis- Investigations Lead Pipe Appearance
  20. 20. Ulcerative Colitis- Investigations
  21. 21. Ulcerative Colitis- Complications Toxic dilatation. Perforation. Increased risk of colorectal cancer. Electrolyte disturbances with severe diarrhoea.
  22. 22. Ulcerative Colitis- Medical Treatment Medical management of the stable patient consists of drug therapy Such a patient may be maintained for months or years on minimal medication, with occasional periods of high-dose steroid therapy for exacerbations. 5-Aminosalicylic acid (5-ASA) induces remission and prevents recurrence, and it is the mainstay of medical treatment. Antidiarrheal drugs may be used to reduce bowel frequency Bowel rest and total parenteral nutrition (TPN) are indicated in severe colitis. Cyclosporine or tacrolimus , are used for refractory colitis. Azathioprine and 6-mercaptopurine are used to facilitate remission induced by cyclosporine Anti- TNF antibody infliximab and monoclonal antibodies, such as anti- interleukin-2 receptor antibody
  23. 23. Ulcerative Colitis- Surgical Treatment Most common indication is intractability of disease and failure of medical management to control symptoms. Other indications include bleeding, perforation, toxic colonic dilatation, and infection. Total proctocolectomy involves excising all colon, rectum, and anus with closure of perineal wound. A permanent right lower quadrant spouted (Brooke) ileostomy is created. The ileal pouch (0,W,or S pouch) or neorectum to replace diseased rectum offers the chance of surgical cure without the need for a permanent ileostomy. Long-term sequelae include pouchitis , anastomotic stricture, pouch failure , and sexual dysfunction.
  24. 24. Ulcerative Colitis VS Crohn’s Disease
  25. 25. Diagnostic Algorithm
  26. 26. Treatment Algorithm
  27. 27. THANK YOU LIKE SHARE SUBSCRIBE

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