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Dr. Mohammad Rehan
• It includes a group of chronic disorders that cause
inflammation or ulceration in large and small intestines.
• 2 major types: Ulcerative colitis (UC) and Crohn’s disease
(CD)
INCIDENCE-
 Highest incidence in Europe, the United Kingdom, and North
America.
 Urban areas > rural areas.
 high socioeconomic classes > lower socioeconomic classes.
INFLAMMATORY BOWEL DISEASE
• Recently two studies, both from northern India,
reported a population prevalence of ulcerative colitis
(UC) of approximately 42 per 100,000 .
• No such population based study is available for
crohn’s disease.
EPIDEMIOLOGY
ETIOPATHOGENESIS
 Exact cause is
unknown.
• Genetic factors
• Immunological factors
• Microbial factors
• Psychosocial factors
GENETIC FACTORS
• Ulcerative colitis is more common in DR2-related genes.
• Crohn’s disease is more common is DR5 DQ1 alleles.
• 3-20 times higher incidence in first degree relatives.
IMMUNOLOGIC FACTORS
• Defective regulation of immunosuppression.
• Activated CD+4 cells activate other inflammatory cells
like macrophages & B-cells or recruit more inflammatory
cells by stimulation of homing receptor on leucocytes &
vascular epithelium resulting in inflammation of mucosa
and sub mucosa.
PATHOGENESIS OF IBD
American Gastroenterological Association Institute, Bethesda,
MD. Sartor RB. Nat Clin Pract Gastroenterol Hepatol. 2006;3:390-
407.
Normal
Gut
Tolerance-
controlled
inflammation
(Infection, NSAID, other)
Complete Healing
Chronic Inflammation
Genetically
Susceptible
Host
Acute Inflammation
↓ Immunoregulation, failure of
repair or bacterial clearance
Acute injury
Environmental
triggers
PATHOLOGY
Macrocopic features
•Ulcerative colitis
 Usually involves rectum & extends proximally to involve all
or part of colon.
 Spread is in continuity.
 About 40–50% of patients have disease limited to the rectum and
rectosigmoid.
 30–40% have disease extending beyond the sigmoid but not
involving the whole colon, and
 20% have a total colitis (10–20% patients have backwash ilietis).
 Mild disease- erythematous & sand paper appearance
(fine granular surface) of mucosa.
 Moderate-marked erythema, coarse granularity, contact
bleeding & no ulceration.
 Severe- spontaneous bleeding, edematous & ulcerated
(collar button ulcer) mucosal surface.
 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/ perforation
ULCERATIVE
COLITIS
Ulcer
Pseudopolyps
MICROSCOPIC FEATURES
 Limited to mucosa & sub mucosa
 Crypts atrophy & irregularity
 Superficial erosion
 Diffuse mixed inflammation
 Basal lymphoplasmacytosis
Crypt
distortion
Diffuse
inflammation
MACROSCOPIC FEATURES
• Crohn’s disease
Can affect any part of GIT.
Transmural involvement.
Segmental with skip lesions.
Cobblestone appearance of mucosa.
Creeping fat- adhesions & fistula.
MICROSCOPIC
FEATURES
• Aphthous ulcerations.
• Focal crypt abscesses.
• Granuloma formation- pathognomic.
• Submucosal or subserosal lymphoid
aggregates.
• Transmural involvement with fissure
formation.
CLINICAL FEATURES
• Ulcerative colitis
Diarrhea
Rectal bleeding
Tenesmus
Passage of mucus
Crampy abdominal pain
 Systemic symptoms fever, weight loss
 Extra intestinal manifestations
• 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.
1. Truelove SC, et al. Br Med J. 1955;2:1041-1045.
2. Sandborn WJ. Curr Treat Options Gastroenterol.1999;2:113-118.
CLINICAL SEVERITY OF UC
Mild Moderate Severe Fulminant
Bowel movement <4/day Intermediate >6 >10
Blood in stool Intermittent moderate Frequent Continuous
Temperature Normal <37.5° >37.5° >37.5°
Pulse Normal <90bpm >90 bpm >90 bpm
Hemoglobin Normal >75% <75% Transfusion
required
ESR <30 mm/hour >30 mm/hour >30 mm/hour
Clinical signs Abdominal
tenderness
Abdominal
distension and
tenderness
EXTRA INTESTINAL MANIFESTATIONS OF
ULCERATIVE COLITIS
DIAGNOSIS
• Laboratory tests
• Endoscopy
• Radiography
• Tissue Biopsy
LABORATORY TESTS
• Hemogram
 ESR is increased
 Platelet count-increased
 Hemoglobin-decreased
• C-reactive protein is increased
• Fecal Calprotectin levels correlate with histological
inflammation, predict relapses & detect pouchitis.
• Fecal lactoferrin- high levels indicate intestinal
inflammation.
BARIUM ENEMA
BARIUM ENEMA
• Fine mucosal granularity-
earliest radiological change.
• Superficial ulcers seen
• Collar button ulcers- s/o
mucosal penetration
• Pipe stem appearance- loss of
haustrations
• Narrow & short colon-
• Ribbon contour colon
SIGMOIDOSCOPY
• Always abnormal
• Loss of vascular patterns
• Granularity
• Friability
• Ulceration
Colonoscopy with acute ulcerative colitis: severe
colon inflammation with erythema, friability, and
exudates.
CLINICAL FEATURES
ILEAL CROHN’S DISEASE
 Abdominal pain
 Diarrhea
 Weight loss
 Low grade fever
JEJUNOILEITIS - associated with a loss of digestive
and absorptive surface, resulting in
 Malabsorption
 Steatorrhea
Colitis and perianal disease
• Bloody diarrohea
• Passage of mucus
• Lethargy
• Malaise
• Anorexia
• Weight loss
Contd. Clinical features
GASTRODUODENAL DISEASE –
• Symptoms and signs of upper GI tract disease include
nausea, vomiting, and epigastric pain.
• The second portion of the duodenum is more commonly
involved than the bulb.
• Patients with advanced gastro duodenal CD may develop a
chronic gastric outlet obstruction.
DIAGNOSIS
• Laboratory tests
• Endoscopy
• Radiography
• Biopsy
• CT enterography
LABORATORY TESTS
• Anemia
• Leukocytosis
• ESR-elevated
• CRP-elevated
• Hypoalbuminemia
BARIUM ENEMA
String sign
Represents long areas of
circumferential inflammation and
fibrosis, resulting in long segments
of luminal narrowing.
COLONOSCOPY
• Endoscopic features of CD include rectal sparing,
aphthous ulcerations, fistulas, and skip lesions.
• Colonoscopy allows examination and biopsy of
mass lesions or strictures and biopsy of the
terminal ileum.
• Upper endoscopy is useful in diagnosing
gastroduodenal involvement in patients with
upper tract symptoms
CT- ENTEROGRAPHY
• Mural hyper
enhancement.
• Stratification.
• Engorged vasa recta.
• Perienteric inflammatory
changes.
TREATMENT
LIFE STYLE CHANGES
DIET CHANGE
DRUGS
SURGERY
DIETARY
CHANGES
 Eating :
 Low-fat foods.
 Smaller, more
frequent meals.
 Avoiding :
 foods high in
undigestible fiber.
 Refined sugars .
LIFESTYLE CHANGES
NO SMOKING
REDUCING STRESSDOING EXERCISE
TAKING REST
Therapeutic approach for IBD
DRUGS
• 5-ASA agents
• Glucocorticoids
• Antibiotics
• Immunosuppresants
• Biological therapy
5-ASA AGENTS
• Sulfasalazine – combination of 5-aminosalicylic acid( anti
inflammatory ) + sulfapyradine-antibacterial).
 Partially absorbed in jejunum but remainder passes in colon
 Therapeutic action –inhibition of P.G.s & leukotriene
synthesis, free radical scavanging, free radical scavanging,
impairement of white cell adhesion and function, inhibition
of cytokine synthesis.
• Mesalamine group (coating 5-ASA with acrylic resins), e.g.
Asacol, Pentasa, Balsalazide (prodrug of 5-ASA).
• Olsalazine (5-ASA dimer cleaves in colon).
Distribution of 5-ASA Preparations
Oral
•Varies by agent: may be released in the
• distal/terminal ileum, or colon1
Suppositories
• Reach the upper rectum2,5
• (15-20 cm beyond the anal verge)
Liquid Enemas
• -May reach the splenic flexure2-4
• -Do not frequently concentrate in the
rectum3
Topical Action of 5-ASA: Extent of Disease
Impacts Formulation Choice
1. Sandborn WJ, et al. Aliment Pharmacol Ther. 2003;17:29-42; 2. Regueiro M, et al. Inflamm Bowel Dis. 2006;12:972–978; 3. Van Bodegraven AA,
et al. Aliment Pharmacol Ther. 1996; 10:327-332; 4. Chapman NJ, et al. Mayo Clin Proc. 1992;62:245-248; 5. Williams CN, et al. Dig Dis Sci. 1987;32:71S-75S.
 Use
• Mainstay of OPD treatment for mild to moderate active
UC & Crohns colitis.
• Maintaining remission
• May reduce risk of colorectal cancer
 Adverse effects
• Nausea, headache, epigastric pain, diarrhoea,
hypersensitivity, pancreatitis
• Caution in renal impairment, pregnancy, breast feeding
GLUCOCORTICOIDS
• Anti inflammatory agents for moderate to severe
relapses (including IV treatment; enemas for
acute proctitis)
• Inhibition of inflammatory pathways.
• No role in maintenance therapy
• Prednisone-40-60mg/day
• Budesonide- 9mg/dl used for 2-3 months & then
tapered.
ANTIBIOTICS
• Metronidazole is effective in active inflammatory,
fistulous & perianal Crohn’s Disease.
 Dose-15-20mg/kg/day in 3 divided doses.
• Ciprofloxacin 500mg BD.
• Rifaximin.
• No role of antibiotics in active/quiescent UC.
IMMUNOSUPPRESANTS
• Thiopurines- Azathioprine, 6-mercaptopurine.
• Methotrexate
• Cyclosporine
 Reduce inflammation by suppressing immune system’s
response (which might damage digestive tissue) invading
virus or bacterium.
• Used in patients unresponsive to steroid &
amino salicylates
CYCLOSPORINE
 Preventing clonal expansion of T cell subsets.
Use
• Steroid sparing
• Active and chronic disease
Side effects
 Minor: tremor, paresthesias, malaise, headache
gingival hyperplasia, hirsutism.
 Major: renal impairment, infections, neurotoxicity
BIOLOGICAL THERAPY
Infliximab
 Anti TNF monoclonal antibody.
 Binds to TNF trimers with high affinity, preventing cytokine from
binding to its receptors.
 It also binds to membrane-bound TNF- a and neutralizes its activity
& also reduces serum TNF levels.
• Use
• Fistulizing CD
• Severe active CD
• Refractory/intolerant of steroids or immunosuppression
• Side effects
• Infusion reactions
• Sepsis
• Reactivation of Tuberculosis
• Increased risk of Tuberculosis
• Newer Biologics
1) Adalimumab
2) Certolizumab
3) Golimumab
OTHER MEDICATIONS
 Anti- diarrheal - Loperamide
(Imodium)
 Laxatives - senna, bisacodyl
 Pain relievers- acetaminophen
(Tylenol).
 Iron supplements
SURGERY
Ulcerative colitis
Indications:
• Fulminating disease.
• Chronic disease with anemia, frequent stools,
urgency & tenesmus.
• Steroid dependent disease.
• Risk of neoplastic change.
• Extra intestinal manifestations.
• Severe hemorrhage or stenosis.
• Reconstructive Proctocolectomy with ileoanal
pouch.
• Proctocolectomy & ileostomy.
• Rectal & anal dissection.
• Colectomy with ileorectal anastomosis.
• Ileostomy with intra abdominal pouch.
Surgery in ulcerative colitis
OTHERS
• Proctocolectomy & ileostomy.
• Rectal & anal dissection.
• Colectomy with ileorectal anastomosis.
• Ileostomy with intra abdominal pouch.
SURGERY IN CROHN’S
DISEASE
• Ileocaecal resection.
• Segmental resection.
• Colectomy & ileorectal anastamosis.
• Temporary loop ileostomy.
• Proctocolectomy.
• Strictureplasty.
DIFFERENTIAL DIAGNOSIS OF UC AND CD
Inflammatory bowel disease
Inflammatory bowel disease

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Inflammatory bowel disease

  • 2. • It includes a group of chronic disorders that cause inflammation or ulceration in large and small intestines. • 2 major types: Ulcerative colitis (UC) and Crohn’s disease (CD) INCIDENCE-  Highest incidence in Europe, the United Kingdom, and North America.  Urban areas > rural areas.  high socioeconomic classes > lower socioeconomic classes. INFLAMMATORY BOWEL DISEASE
  • 3. • Recently two studies, both from northern India, reported a population prevalence of ulcerative colitis (UC) of approximately 42 per 100,000 . • No such population based study is available for crohn’s disease.
  • 5. ETIOPATHOGENESIS  Exact cause is unknown. • Genetic factors • Immunological factors • Microbial factors • Psychosocial factors
  • 6.
  • 7. GENETIC FACTORS • Ulcerative colitis is more common in DR2-related genes. • Crohn’s disease is more common is DR5 DQ1 alleles. • 3-20 times higher incidence in first degree relatives.
  • 8. IMMUNOLOGIC FACTORS • Defective regulation of immunosuppression. • Activated CD+4 cells activate other inflammatory cells like macrophages & B-cells or recruit more inflammatory cells by stimulation of homing receptor on leucocytes & vascular epithelium resulting in inflammation of mucosa and sub mucosa.
  • 9.
  • 10.
  • 11. PATHOGENESIS OF IBD American Gastroenterological Association Institute, Bethesda, MD. Sartor RB. Nat Clin Pract Gastroenterol Hepatol. 2006;3:390- 407. Normal Gut Tolerance- controlled inflammation (Infection, NSAID, other) Complete Healing Chronic Inflammation Genetically Susceptible Host Acute Inflammation ↓ Immunoregulation, failure of repair or bacterial clearance Acute injury Environmental triggers
  • 12. PATHOLOGY Macrocopic features •Ulcerative colitis  Usually involves rectum & extends proximally to involve all or part of colon.  Spread is in continuity.  About 40–50% of patients have disease limited to the rectum and rectosigmoid.  30–40% have disease extending beyond the sigmoid but not involving the whole colon, and  20% have a total colitis (10–20% patients have backwash ilietis).
  • 13.
  • 14.  Mild disease- erythematous & sand paper appearance (fine granular surface) of mucosa.  Moderate-marked erythema, coarse granularity, contact bleeding & no ulceration.  Severe- spontaneous bleeding, edematous & ulcerated (collar button ulcer) mucosal surface.  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/ perforation
  • 16. MICROSCOPIC FEATURES  Limited to mucosa & sub mucosa  Crypts atrophy & irregularity  Superficial erosion  Diffuse mixed inflammation  Basal lymphoplasmacytosis
  • 18.
  • 19. MACROSCOPIC FEATURES • Crohn’s disease Can affect any part of GIT. Transmural involvement. Segmental with skip lesions. Cobblestone appearance of mucosa. Creeping fat- adhesions & fistula.
  • 20.
  • 21.
  • 22. MICROSCOPIC FEATURES • Aphthous ulcerations. • Focal crypt abscesses. • Granuloma formation- pathognomic. • Submucosal or subserosal lymphoid aggregates. • Transmural involvement with fissure formation.
  • 23.
  • 24.
  • 25. CLINICAL FEATURES • Ulcerative colitis Diarrhea Rectal bleeding Tenesmus Passage of mucus Crampy abdominal pain  Systemic symptoms fever, weight loss  Extra intestinal manifestations
  • 26. • 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.
  • 27. 1. Truelove SC, et al. Br Med J. 1955;2:1041-1045. 2. Sandborn WJ. Curr Treat Options Gastroenterol.1999;2:113-118. CLINICAL SEVERITY OF UC Mild Moderate Severe Fulminant Bowel movement <4/day Intermediate >6 >10 Blood in stool Intermittent moderate Frequent Continuous Temperature Normal <37.5° >37.5° >37.5° Pulse Normal <90bpm >90 bpm >90 bpm Hemoglobin Normal >75% <75% Transfusion required ESR <30 mm/hour >30 mm/hour >30 mm/hour Clinical signs Abdominal tenderness Abdominal distension and tenderness
  • 28. EXTRA INTESTINAL MANIFESTATIONS OF ULCERATIVE COLITIS
  • 29. DIAGNOSIS • Laboratory tests • Endoscopy • Radiography • Tissue Biopsy
  • 30. LABORATORY TESTS • Hemogram  ESR is increased  Platelet count-increased  Hemoglobin-decreased • C-reactive protein is increased • Fecal Calprotectin levels correlate with histological inflammation, predict relapses & detect pouchitis. • Fecal lactoferrin- high levels indicate intestinal inflammation.
  • 32. BARIUM ENEMA • Fine mucosal granularity- earliest radiological change. • Superficial ulcers seen • Collar button ulcers- s/o mucosal penetration • Pipe stem appearance- loss of haustrations • Narrow & short colon- • Ribbon contour colon
  • 33. SIGMOIDOSCOPY • Always abnormal • Loss of vascular patterns • Granularity • Friability • Ulceration
  • 34. Colonoscopy with acute ulcerative colitis: severe colon inflammation with erythema, friability, and exudates.
  • 35.
  • 36. CLINICAL FEATURES ILEAL CROHN’S DISEASE  Abdominal pain  Diarrhea  Weight loss  Low grade fever JEJUNOILEITIS - associated with a loss of digestive and absorptive surface, resulting in  Malabsorption  Steatorrhea
  • 37. Colitis and perianal disease • Bloody diarrohea • Passage of mucus • Lethargy • Malaise • Anorexia • Weight loss Contd. Clinical features
  • 38. GASTRODUODENAL DISEASE – • Symptoms and signs of upper GI tract disease include nausea, vomiting, and epigastric pain. • The second portion of the duodenum is more commonly involved than the bulb. • Patients with advanced gastro duodenal CD may develop a chronic gastric outlet obstruction.
  • 39. DIAGNOSIS • Laboratory tests • Endoscopy • Radiography • Biopsy • CT enterography
  • 40. LABORATORY TESTS • Anemia • Leukocytosis • ESR-elevated • CRP-elevated • Hypoalbuminemia
  • 41. BARIUM ENEMA String sign Represents long areas of circumferential inflammation and fibrosis, resulting in long segments of luminal narrowing.
  • 43. • Endoscopic features of CD include rectal sparing, aphthous ulcerations, fistulas, and skip lesions. • Colonoscopy allows examination and biopsy of mass lesions or strictures and biopsy of the terminal ileum. • Upper endoscopy is useful in diagnosing gastroduodenal involvement in patients with upper tract symptoms
  • 44.
  • 45. CT- ENTEROGRAPHY • Mural hyper enhancement. • Stratification. • Engorged vasa recta. • Perienteric inflammatory changes.
  • 46.
  • 47.
  • 48. TREATMENT LIFE STYLE CHANGES DIET CHANGE DRUGS SURGERY
  • 49. DIETARY CHANGES  Eating :  Low-fat foods.  Smaller, more frequent meals.  Avoiding :  foods high in undigestible fiber.  Refined sugars .
  • 50. LIFESTYLE CHANGES NO SMOKING REDUCING STRESSDOING EXERCISE TAKING REST
  • 52. DRUGS • 5-ASA agents • Glucocorticoids • Antibiotics • Immunosuppresants • Biological therapy
  • 53. 5-ASA AGENTS • Sulfasalazine – combination of 5-aminosalicylic acid( anti inflammatory ) + sulfapyradine-antibacterial).  Partially absorbed in jejunum but remainder passes in colon  Therapeutic action –inhibition of P.G.s & leukotriene synthesis, free radical scavanging, free radical scavanging, impairement of white cell adhesion and function, inhibition of cytokine synthesis. • Mesalamine group (coating 5-ASA with acrylic resins), e.g. Asacol, Pentasa, Balsalazide (prodrug of 5-ASA). • Olsalazine (5-ASA dimer cleaves in colon).
  • 54.
  • 55. Distribution of 5-ASA Preparations Oral •Varies by agent: may be released in the • distal/terminal ileum, or colon1 Suppositories • Reach the upper rectum2,5 • (15-20 cm beyond the anal verge) Liquid Enemas • -May reach the splenic flexure2-4 • -Do not frequently concentrate in the rectum3 Topical Action of 5-ASA: Extent of Disease Impacts Formulation Choice 1. Sandborn WJ, et al. Aliment Pharmacol Ther. 2003;17:29-42; 2. Regueiro M, et al. Inflamm Bowel Dis. 2006;12:972–978; 3. Van Bodegraven AA, et al. Aliment Pharmacol Ther. 1996; 10:327-332; 4. Chapman NJ, et al. Mayo Clin Proc. 1992;62:245-248; 5. Williams CN, et al. Dig Dis Sci. 1987;32:71S-75S.
  • 56.  Use • Mainstay of OPD treatment for mild to moderate active UC & Crohns colitis. • Maintaining remission • May reduce risk of colorectal cancer  Adverse effects • Nausea, headache, epigastric pain, diarrhoea, hypersensitivity, pancreatitis • Caution in renal impairment, pregnancy, breast feeding
  • 57. GLUCOCORTICOIDS • Anti inflammatory agents for moderate to severe relapses (including IV treatment; enemas for acute proctitis) • Inhibition of inflammatory pathways. • No role in maintenance therapy • Prednisone-40-60mg/day • Budesonide- 9mg/dl used for 2-3 months & then tapered.
  • 58. ANTIBIOTICS • Metronidazole is effective in active inflammatory, fistulous & perianal Crohn’s Disease.  Dose-15-20mg/kg/day in 3 divided doses. • Ciprofloxacin 500mg BD. • Rifaximin. • No role of antibiotics in active/quiescent UC.
  • 59. IMMUNOSUPPRESANTS • Thiopurines- Azathioprine, 6-mercaptopurine. • Methotrexate • Cyclosporine  Reduce inflammation by suppressing immune system’s response (which might damage digestive tissue) invading virus or bacterium. • Used in patients unresponsive to steroid & amino salicylates
  • 60. CYCLOSPORINE  Preventing clonal expansion of T cell subsets. Use • Steroid sparing • Active and chronic disease Side effects  Minor: tremor, paresthesias, malaise, headache gingival hyperplasia, hirsutism.  Major: renal impairment, infections, neurotoxicity
  • 61. BIOLOGICAL THERAPY Infliximab  Anti TNF monoclonal antibody.  Binds to TNF trimers with high affinity, preventing cytokine from binding to its receptors.  It also binds to membrane-bound TNF- a and neutralizes its activity & also reduces serum TNF levels. • Use • Fistulizing CD • Severe active CD • Refractory/intolerant of steroids or immunosuppression • Side effects • Infusion reactions • Sepsis • Reactivation of Tuberculosis • Increased risk of Tuberculosis
  • 62. • Newer Biologics 1) Adalimumab 2) Certolizumab 3) Golimumab
  • 63. OTHER MEDICATIONS  Anti- diarrheal - Loperamide (Imodium)  Laxatives - senna, bisacodyl  Pain relievers- acetaminophen (Tylenol).  Iron supplements
  • 64. SURGERY Ulcerative colitis Indications: • Fulminating disease. • Chronic disease with anemia, frequent stools, urgency & tenesmus. • Steroid dependent disease. • Risk of neoplastic change. • Extra intestinal manifestations. • Severe hemorrhage or stenosis.
  • 65. • Reconstructive Proctocolectomy with ileoanal pouch. • Proctocolectomy & ileostomy. • Rectal & anal dissection. • Colectomy with ileorectal anastomosis. • Ileostomy with intra abdominal pouch. Surgery in ulcerative colitis
  • 66. OTHERS • Proctocolectomy & ileostomy. • Rectal & anal dissection. • Colectomy with ileorectal anastomosis. • Ileostomy with intra abdominal pouch.
  • 67. SURGERY IN CROHN’S DISEASE • Ileocaecal resection. • Segmental resection. • Colectomy & ileorectal anastamosis. • Temporary loop ileostomy. • Proctocolectomy. • Strictureplasty.
  • 68.
  • 69.