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INFLAMMATORY BOWEL DISEASE
-Dr Rahul Arya
(MD Medicine)
INTRODUCTION
 IBD is an immune mediated chronic intestinal condition.
 Two major types-
1. Ulcerative colitis (UC)
2. Crohn’s Disease (CD)
EPIDEMIOLOGY
Ulcerative Colitis Crohn’s Disease
Incidence 0-19.2 per 100000 0-20.2 per 100000
Age of onset 2nd to 4th decades and 7th to 9th decades
Ethnicity Jewish> non Jewish white
Female/male ratio 0.51-1.58 0.34-1.65
Smoking May prevent disease May cause disease
Oral contraceptive No increased risk Increased risk (odds ratio 1.4)
Appendectomy Protective Not protective
Monozygotic twins 6-18% concordance 38-58% concordance
Dizygotic twins 0-2% concordance 4% concordance
Antibiotic use in first year of life 2.9 times increased risk of developing childhood IBD
PATHOGENESIS
PATHOLOGY
 Ulcerative Colitis:- Macroscopic features
 Usually involves rectum and extends proximally to involve all or part of
colon.
 Rectum and Recto-sigmoid - 40-50%.
 Beyond sigmoid but not involving whole colon- 30-40%.
 Total colitis- 20%.
 Continuous spread
 Backwash ileitis- 10-20%.
 Mild disease- erythema & sand paper appearance(fine granularity)
 Moderate-marked erythema, coarse granularity, contact bleeding & no
ulceration.
 Severe- spontaneous bleeding, edematous & ulcerated.
 Long standing-epithelial regeneration so pseudopolyps , mucosal
atrophy & disorientation leads to a precancerous condition.
 Eventually can lead to shortening and narrowing of colon.
 Fulminant disease-Toxic colitis/megacolon.
 Ulcerative colitis :- Microscopic Features
 The process is limited to the mucosa and superficial submucosa,
with deeper layers unaffected except in fulminant disease.
 Ileal changes-villous atrophy and crypt regeneration with increased
inflammation, increased neutrophil and mononuclear inflammation in
the lamina propria, and patchy cryptitis and crypt abscesses.
 Crohn’s disease:- Macroscopic features
 Can involve any part of GI tract- from mouth to anus.
 Small bowel disease- 30-40%
 Both small and large intestine- 40-55%
 Colitis- 15-25%
 Rectum is often spared.
 Segmental involvement with skip areas.
 Perirectal fistulas, fissures, abscesses and anal stenosis are present in one-
third of patients.
 Transmural involvement
 Cobblestone appearance- characteristic of CD
(normal island of mucosa demarcated by stellate ulcerations that fuse
longitudinally and transversely).
 Active disease resolve by fibrosis leading to stricture formations
leading to bowel obstruction.
 Creeping fat- projection of thickened mesentry that encase the bowel.
 Crohn disease:- Microscopic features
 Aphatoid ulcerations
 Focal crypt abscesses
 Non caseating granulomas- pathogonomic
 Submucosal or subserosal lymphoid aggregates.
ULCERATIVE COLITIS:-CLINICAL PRESENTATION
 Diarrhea
 Rectal bleeding
 Tenesmus
 Passage of mucus
 Crampy abdominal pain
 Patient with proctatis-pass fresh or blood stained mucus with formed or semi
formed stool.
 Disease extends beyond the rectum:-blood mixed with stool or grossly bloody
diarrhea.
 Diarrhoea- usally nocturnal and/or postprandial.
 Physical signs
 Proctitis – Tender anal canal & blood on rectal examination.
 Extensive disease-tenderness on palpation of colon
 Toxic colitis-severe pain &bleeding
 If perforation-signs of peritonitis
ULCERATIVE COLITIS:-DIAGNOSIS
 Laboratory tests
 C-reactive protein is increased
 ESR is increased
 Platelet count-increased
 Hemoglobin-decreased
 Fecal lactoferrin- highly sensitive and specific marker for intestinal
inflammation.
 Fecal Calprotectin levels correlate with histological inflammation, predict
relapses &detect pouchitis.
 Sigmoidoscopy and colonoscopy-
 To assess disease activity and extent
 Erythema
 Loss of vascular patterns
 Granularity
 Friability
 ulceration
 Barium Enema
 Fine mucosal granularity
 Superficial ulcers seen
 Collar button ulcers
 Pipe stem appearance-loss of haustrations
 Narrow & short colon
 CT and MRI are not as helpful as endoscopy and barium enema.
CROHN’S DISEASE:- CLINICAL PRESENTATION
 Ileocolitis- most common site.
 recurrent episodes of right lower quadrant pain and diarrhea.
 Palpable mass, fever, and leukocytosis.
 Pain is usually colicky; it precedes and is relieved by defecation.
 Weight loss.
 Radiographic "string sign" of a narrowed intestinal lumen.
 Jejunoileitis
 Malabsorption and steatorrhea.
 Nutritional deficiencies.
 Colitis and Perianal Disease
 low-grade fevers, malaise, diarrhea, crampy abdominal pain,
sometimes hematochezia.
 Gross bleeding-not as common as in UC.
 Gastroduodenal Disease
 Nausea, vomiting, and epigastric pain.
CROHN’S DISEASE:- DIAGNOSIS
 Laboratory tests
 CRP-elevated
 ESR-elevated
 Anemia
 Leukocytosis
 hypoalbuminemia
 Endoscopy and Colonoscopy
 Rectal sparing, Aphthous ulcerations, fistulas, and skip lesions.
 Biopsy of mass lesions.
 Wireless capsule endoscopy (WCE)
 Allows direct visualization of the entire small bowel mucosa .
 The diagnostic yield is higher than CT enterography .
 WCE cannot be used in the setting of a small bowel stricture.
 Radiographic Features
 Aphthous ulcerations.
 Cobblestone appearance.
 Advanced disease-strictures,
fistulas, inflammatory masses,
and abscesses.
 string sign.
 CT enterography
 Mural hyperenhancement
 Stratification
 Engorged vasa recta
 Perienteric inflammatory changes
 Serological markers-
 Perinuclear antineutrophil cytoplasmic antibodies (pANCA).
 Anti saccharomyces cerevisiae antibodies.
EXTRAINTESTINAL MANIFESTATION
 Dermatologic- Erythema Nodosum, Pyoderma Gangrenosum
 Rheumatologic- Ankylosing spondylitis, sacroilitis
 Ocular- Uveitis, Conjuctivitis
 Hepatobiliary- Hepatic steatosis, Primary Sclerosing Cholingitis
 Urologic- calculi, ureteral obstruction and ileal bladder fistulas.
 Metabolic bone disorders- low bone mass, fractures, osteonecrosis
 Thromboembolic- venous and arterial thrombosis
 Other- endocarditis, myocarditis, ILD
TREATMENT
DRUGS
 5-ASA agents
 Glucocorticoids
 Antibiotics
 Immunosuppresants
 Biological therapy
5-ASA AGENTS
 Sulfasalazine (5-aminosalicylic acid and sulfapyridine as carrier
substance)
 Mesalazine (5-ASA), e.g. Asacol, Pentasa
 Balsalazide (prodrug of 5-ASA)
 Olsalazine (5-ASA dimer cleaves in colon)
 Use
 In mild to moderate UC- for inducing and maintaining remission.
 Limited role in inducing remission in CD but no clear role in
maintanence of CD.
 Adverse effects
 Nausea, headache, epigastric pain, diarrhoea,hypersensitivity,
pancreatitis
 Caution in renal impairment, pregnancy, breast feeding
GLUCOCORTICOIDS
 Anti inflammatory agents for moderate to severe UC and CD.
 Inhibition of inflammatory pathways
 Budesonide- 9mg/dl used for 2-3 months & then tapered.
 Prednisone-40-60mg/day
 No role in maintainence therapy.
 Side effects- fluid retention,abdominal striae,
hyperglycemia,subcapsular cataract, osteoperosis, myopathy.
ANTIBIOTICS
 No role in active/quienscent UC
 Metronidazole is effective in active inflammatory,fistulous & perianal
CD.
 Dose-15-20mg/kg/day in 3 divided doses.
 Side effects- metallic taste, nausea, disulfiram like reaction,
peripheral neuropathy.
 Ciprofloxacin- 500mg BD.
 S/E- Achiles Tendinitis.
IMMUNOSUPPRESANTS
 Azathioprine
 6-mercaptopurin
 Methotrexate
 Cyclosporine
 Azathioprines and 6-MP- for steroid dependent IBD
 For maintanence therapy in UC and CD.
 Side effect- Pancreatitis, bone marrow suppression.
 Methotrexate- for inducing and maintaining remission
 Side effects- leukopenia, hepatic fibrosis, hypersensitivity
pneumonitis.
 Cyclosporine
 Prevent clonal expansion of T cell subsets
 Use
 Steroid sparing
 Active and chronic disease
 Side effects
 Tremor, paraesthesiae, malaise, headache, gingival hyperplasia,
hirsutism Major: renal impairment,infections, neurotoxicity.
 Biological therapy
 Infliximab-Anti TNF alpha monoclonal antibody.
 For mod to severe active UC and active CD refractory to
glucocorticoides.
 Other- adalimumab, certolizumab, golimumab.
 Side effects- NHL,infusion reaction, skin lesions, infections.
SURGICAL THERAPY
 Indications:
 Intractable disease
 Fulminant disease
 Toxic megacolon
 Colonic perforation
 Colonic obstruction
 Risk of neoplastic change
 Extraintestinal manifestations
 Severe hemorrhage or stenosis
 Refractory fistula
 Abscess
 In UC:-Ileoanal J pouch
anastomosis (IPAA)- operation of
choice
 In CD- resection of disease
segment and strictureplasty.
Inflammatory bowel disease
Inflammatory bowel disease

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Inflammatory bowel disease

  • 1. INFLAMMATORY BOWEL DISEASE -Dr Rahul Arya (MD Medicine)
  • 2. INTRODUCTION  IBD is an immune mediated chronic intestinal condition.  Two major types- 1. Ulcerative colitis (UC) 2. Crohn’s Disease (CD)
  • 3. EPIDEMIOLOGY Ulcerative Colitis Crohn’s Disease Incidence 0-19.2 per 100000 0-20.2 per 100000 Age of onset 2nd to 4th decades and 7th to 9th decades Ethnicity Jewish> non Jewish white Female/male ratio 0.51-1.58 0.34-1.65 Smoking May prevent disease May cause disease Oral contraceptive No increased risk Increased risk (odds ratio 1.4) Appendectomy Protective Not protective Monozygotic twins 6-18% concordance 38-58% concordance Dizygotic twins 0-2% concordance 4% concordance Antibiotic use in first year of life 2.9 times increased risk of developing childhood IBD
  • 5.
  • 6. PATHOLOGY  Ulcerative Colitis:- Macroscopic features  Usually involves rectum and extends proximally to involve all or part of colon.  Rectum and Recto-sigmoid - 40-50%.  Beyond sigmoid but not involving whole colon- 30-40%.  Total colitis- 20%.  Continuous spread  Backwash ileitis- 10-20%.
  • 7.
  • 8.  Mild disease- erythema & sand paper appearance(fine granularity)  Moderate-marked erythema, coarse granularity, contact bleeding & no ulceration.  Severe- spontaneous bleeding, edematous & ulcerated.  Long standing-epithelial regeneration so pseudopolyps , mucosal atrophy & disorientation leads to a precancerous condition.  Eventually can lead to shortening and narrowing of colon.  Fulminant disease-Toxic colitis/megacolon.
  • 9.  Ulcerative colitis :- Microscopic Features  The process is limited to the mucosa and superficial submucosa, with deeper layers unaffected except in fulminant disease.  Ileal changes-villous atrophy and crypt regeneration with increased inflammation, increased neutrophil and mononuclear inflammation in the lamina propria, and patchy cryptitis and crypt abscesses.
  • 10.
  • 11.  Crohn’s disease:- Macroscopic features  Can involve any part of GI tract- from mouth to anus.  Small bowel disease- 30-40%  Both small and large intestine- 40-55%  Colitis- 15-25%  Rectum is often spared.  Segmental involvement with skip areas.  Perirectal fistulas, fissures, abscesses and anal stenosis are present in one- third of patients.
  • 12.  Transmural involvement  Cobblestone appearance- characteristic of CD (normal island of mucosa demarcated by stellate ulcerations that fuse longitudinally and transversely).  Active disease resolve by fibrosis leading to stricture formations leading to bowel obstruction.  Creeping fat- projection of thickened mesentry that encase the bowel.
  • 13.  Crohn disease:- Microscopic features  Aphatoid ulcerations  Focal crypt abscesses  Non caseating granulomas- pathogonomic  Submucosal or subserosal lymphoid aggregates.
  • 14. ULCERATIVE COLITIS:-CLINICAL PRESENTATION  Diarrhea  Rectal bleeding  Tenesmus  Passage of mucus  Crampy abdominal pain  Patient with proctatis-pass fresh or blood stained mucus with formed or semi formed stool.  Disease extends beyond the rectum:-blood mixed with stool or grossly bloody diarrhea.  Diarrhoea- usally nocturnal and/or postprandial.
  • 15.  Physical signs  Proctitis – Tender anal canal & blood on rectal examination.  Extensive disease-tenderness on palpation of colon  Toxic colitis-severe pain &bleeding  If perforation-signs of peritonitis
  • 16. ULCERATIVE COLITIS:-DIAGNOSIS  Laboratory tests  C-reactive protein is increased  ESR is increased  Platelet count-increased  Hemoglobin-decreased  Fecal lactoferrin- highly sensitive and specific marker for intestinal inflammation.  Fecal Calprotectin levels correlate with histological inflammation, predict relapses &detect pouchitis.
  • 17.  Sigmoidoscopy and colonoscopy-  To assess disease activity and extent  Erythema  Loss of vascular patterns  Granularity  Friability  ulceration
  • 18.  Barium Enema  Fine mucosal granularity  Superficial ulcers seen  Collar button ulcers  Pipe stem appearance-loss of haustrations  Narrow & short colon  CT and MRI are not as helpful as endoscopy and barium enema.
  • 19. CROHN’S DISEASE:- CLINICAL PRESENTATION  Ileocolitis- most common site.  recurrent episodes of right lower quadrant pain and diarrhea.  Palpable mass, fever, and leukocytosis.  Pain is usually colicky; it precedes and is relieved by defecation.  Weight loss.  Radiographic "string sign" of a narrowed intestinal lumen.
  • 20.  Jejunoileitis  Malabsorption and steatorrhea.  Nutritional deficiencies.  Colitis and Perianal Disease  low-grade fevers, malaise, diarrhea, crampy abdominal pain, sometimes hematochezia.  Gross bleeding-not as common as in UC.  Gastroduodenal Disease  Nausea, vomiting, and epigastric pain.
  • 21. CROHN’S DISEASE:- DIAGNOSIS  Laboratory tests  CRP-elevated  ESR-elevated  Anemia  Leukocytosis  hypoalbuminemia
  • 22.  Endoscopy and Colonoscopy  Rectal sparing, Aphthous ulcerations, fistulas, and skip lesions.  Biopsy of mass lesions.  Wireless capsule endoscopy (WCE)  Allows direct visualization of the entire small bowel mucosa .  The diagnostic yield is higher than CT enterography .  WCE cannot be used in the setting of a small bowel stricture.
  • 23.  Radiographic Features  Aphthous ulcerations.  Cobblestone appearance.  Advanced disease-strictures, fistulas, inflammatory masses, and abscesses.  string sign.
  • 24.  CT enterography  Mural hyperenhancement  Stratification  Engorged vasa recta  Perienteric inflammatory changes  Serological markers-  Perinuclear antineutrophil cytoplasmic antibodies (pANCA).  Anti saccharomyces cerevisiae antibodies.
  • 25. EXTRAINTESTINAL MANIFESTATION  Dermatologic- Erythema Nodosum, Pyoderma Gangrenosum  Rheumatologic- Ankylosing spondylitis, sacroilitis  Ocular- Uveitis, Conjuctivitis  Hepatobiliary- Hepatic steatosis, Primary Sclerosing Cholingitis  Urologic- calculi, ureteral obstruction and ileal bladder fistulas.  Metabolic bone disorders- low bone mass, fractures, osteonecrosis  Thromboembolic- venous and arterial thrombosis  Other- endocarditis, myocarditis, ILD
  • 27. DRUGS  5-ASA agents  Glucocorticoids  Antibiotics  Immunosuppresants  Biological therapy
  • 28. 5-ASA AGENTS  Sulfasalazine (5-aminosalicylic acid and sulfapyridine as carrier substance)  Mesalazine (5-ASA), e.g. Asacol, Pentasa  Balsalazide (prodrug of 5-ASA)  Olsalazine (5-ASA dimer cleaves in colon)
  • 29.  Use  In mild to moderate UC- for inducing and maintaining remission.  Limited role in inducing remission in CD but no clear role in maintanence of CD.  Adverse effects  Nausea, headache, epigastric pain, diarrhoea,hypersensitivity, pancreatitis  Caution in renal impairment, pregnancy, breast feeding
  • 30. GLUCOCORTICOIDS  Anti inflammatory agents for moderate to severe UC and CD.  Inhibition of inflammatory pathways  Budesonide- 9mg/dl used for 2-3 months & then tapered.  Prednisone-40-60mg/day  No role in maintainence therapy.  Side effects- fluid retention,abdominal striae, hyperglycemia,subcapsular cataract, osteoperosis, myopathy.
  • 31. ANTIBIOTICS  No role in active/quienscent UC  Metronidazole is effective in active inflammatory,fistulous & perianal CD.  Dose-15-20mg/kg/day in 3 divided doses.  Side effects- metallic taste, nausea, disulfiram like reaction, peripheral neuropathy.  Ciprofloxacin- 500mg BD.  S/E- Achiles Tendinitis.
  • 33.  Azathioprines and 6-MP- for steroid dependent IBD  For maintanence therapy in UC and CD.  Side effect- Pancreatitis, bone marrow suppression.  Methotrexate- for inducing and maintaining remission  Side effects- leukopenia, hepatic fibrosis, hypersensitivity pneumonitis.
  • 34.  Cyclosporine  Prevent clonal expansion of T cell subsets  Use  Steroid sparing  Active and chronic disease  Side effects  Tremor, paraesthesiae, malaise, headache, gingival hyperplasia, hirsutism Major: renal impairment,infections, neurotoxicity.
  • 35.  Biological therapy  Infliximab-Anti TNF alpha monoclonal antibody.  For mod to severe active UC and active CD refractory to glucocorticoides.  Other- adalimumab, certolizumab, golimumab.  Side effects- NHL,infusion reaction, skin lesions, infections.
  • 36. SURGICAL THERAPY  Indications:  Intractable disease  Fulminant disease  Toxic megacolon  Colonic perforation  Colonic obstruction  Risk of neoplastic change  Extraintestinal manifestations  Severe hemorrhage or stenosis  Refractory fistula  Abscess
  • 37.  In UC:-Ileoanal J pouch anastomosis (IPAA)- operation of choice  In CD- resection of disease segment and strictureplasty.