This is comprehensive Presentation about IBD, its Classification, major subtypes, eitology, genetics, presentation, diagnosis and treatment. it Includes Both Crohn's Disease And Ulcerative Colitis in detail Pathology, Diagnosis, Medical Therapy, Surgical Management of Both the diseases are described

1. INFLAMMATORY BOWEL DISEASE
DR. VIKAS V
SUGERY PG
DEPT OF GENERAL SURGERY
MMCR&I, MYSORE

2. DEFINITION
• Conditions characterized by presence of IDIOPATHIC Intestinal Inflammation.
- Bailey & Love
• Chronic Condition resulting from Inappropriate Mucosal Immune Activation
- Robbins & Cotran
• Inflammatory Bowel Disease includes :
A] Crohn's Disease B] Ulcerative Colitis C] Indeterminate Colitis

3. INTRODUCTION
• In 85 % cases IBD can be differentiated into Ulcerative Colitis (UC) or
Crohn's Disease(CD) based on :
• Distribution of Affected Sites
• Morphological expression of Disease
• In 15% cases, differentiation is impossible; these patients are classified as
having Indeterminate Colitis.

4. MAJOR TYPES OF IBD
CROHN'S DISEASE
• CROHN’S DISEASE is a Chronic,
Idiopathic Transmural Inflammatory
disease with Skip Lesions that may affect
ANY part of the alimentary tract,
although there is propensity to affect the
Distal Small Bowel.
- Schwartz Principles of Surgery 11th edition
ULCERATIVE COLITIS
• ULCERATIVE COLITIS is a Chronic
Inflammatory disease that affects the
Mucosa and Superficial Submucosa of
the Rectum and colon
-Maingot‘s Abdominal Operations 13th edition

6. 1612
W.H Fabry (Germany) - Autopsy -
Fever & Pain Abdomen- Thickened
& obstructed Ileum
1769
G. B. MORGAGNI (ITALY)
Ulceration & Perforation of
inflamed, thickened distal ileum and
enlarged mesenteric lymph nodes
Early 20th Century
Cases similar to recently described
Johne’s mycobacterial infection of
cattle (M.paratuberculosis) Or
dismissed as INOPERABLE
Neoplasms
1913
KENNETH DALZIEL (Scotland) -
13 Patients – Chronic Intestinal
Enteritis & Not TB – Considered as
FIRST CASE SERIES OF CD
Later part of 20th Century
Retrospective Study (IRELAND) -
29 Cases of CD
1932
Dr. BURRILL B CROHN introduced
the term 'Regional Ileitis'
1932
American Medical Association -
CROHN & Oppenheimer excluding
Intestinal TB, Described similar
findins in 14 patients
HISTORY OF CROHN’S

7. EARLIEST
BONA-FIDE CASE
OF CD IN
SWEDEN
• 1913
• 13 Y/M Operated for Suspected Appendicitis
• Bypass Procedure – due to Stenosis Of Terminal
Ileum
• Dismissed Diagnosis of TB
• 1969
• Admitted For Perianal Fistulas - Barium Enema –
Difficult to Interpret
• Laparotomy + Resection of Bypassed Segment of
Ileum
• Subsequent HPE – Changes Typical of
CROHN'S Disease

8. EPIDEMIOLOGY
Source : Harrison Prinicples of
Internal Medicine 20th Edition

9. BACKGROUND OF THE DISEASE
• IBD exact Cause UNKNOWN. But believed to be a combination of :
Genetic Factors Mucosal Immune Response Environmental Factors
• Inappropriate Inflammatory Response to Intestinal bacteria in Genetically Susceptible
Individuals leading to a Sustained Mucosal Inflammatory Response that the Host is Unable
to Downregulate.
• Some evidence - Bacterial & Viral infections are a/w IBD, BUT No Specific Species
implicated.
• There are 2 Basic Components to the Immune Response: Innate & Adaptive

10. INNATE IMMUNITY
• Initial Response to invading pathogens
• Main Components: Epithelial barrier &
Phagocytes within the lamina propria
• Protective effect is limited because NO
MEMORY
• Immune Response- Not sed on Reinfection
• Initial response - Inadequate and Initiates This
Process In IBD
ADAPTIVE IMMUNITY
• Mediated by Lymphocytes, T and B cells, that
express antigen receptors on their surface
• Cytokines - produced by T cells - Eradicate
infection and also give rise to Memory Cells -
Prevent Reinfection
• In IBD, different subset of T Cells produce -
Interleukin 13 (IL-13) & IFN- Gamma
resulting in Epithelial dysfunction, Antibody
production, and Immune complex formation

11. • Tridirectional relationship
between Commensal
Flora (microbiota),
Intestinal Epithelial
cells (IECs), Mucosal
Immune System is
dysregulated, leading to
Chronic Inflammation
• Affected by Genetic and
Environmental factors
PATHOGENESIS
OF IBD

13. CD
UC

14. CROHN'S DISEASE

15. GENETIC FACTORS - CROHN’S
• CARD15/NOD2 gene mapped to chromosome 16q12. -BACT SENSING & AUTOPHAGY
• CARD15 - Innate immunity - Preferentially expressed to Paneth’s cells of the Ileum.
• CARD 15 - Production of proinflammatory cytokines in response to gut microbes.
• Mutations of CARD15 are neither necessary nor sufficient to contract this disease.
• ATG16L1 gene - Immune response to muramyl dipeptide, a component of both GRAM +VE
and GRAM -VE bacteria – AUTOPHAGY
Gene NOD2 polymorphisms ATG16L1
Strong Association With Fibro-Stenosing CD Fistulizing CD

16. CROHN'S DISEASE - REGIONAL ENTERITIS
• Involvement : Can affect ANY part of the GI tract from MOUTH to ANUS
• 80% of patients small bowel involvement : Terminal ileum is involved in 90%.
• 30–40% of patients have small bowel disease alone
• 40-55% - Involves Both Small & Large Bowel
• 30% having Terminal Ileitis Alone
• 15–25% have Colitis alone Rectum is often spared in CD
• Higher socioeconomic status - Increased risk of Crohn’s disease
• Breastfeeding - Protective against the development of Crohn’s disease.
• Crohn’s disease is More Prevalent among Smokers.
• Furthermore, Smoking is associated with the Increased risk for both the Need for Surgery and
the Risk of Relapse after Surgery for Crohn’s disease.

17. PATHOLOGY
• Pathological hallmark - Focal, Transmural inflammation with Multiple Lymphoid
Aggregates in a thickened edematous fibrotic Submucosa & Muscularis Propria .
• Noncaseating granulomas - valuable Diagnostic Feature
• Seen only in 50% of resected specimens (Maingot's) ; 70% of resected specimens
(Schwartz)
• Rarely seen on Endoscopic Biopsies
• Earliest Gross Manifestation - small mucosal ulcerations call Aphthous Ulcers.
• 3 mm in diameter and surrounded by a Halo of Erythema
• Typically Arise Over Lymphoid Aggregates
• Aphthae coalesce into larger, stellate shaped ulcers
• Longitudinal Fusion - Linear / Serpenginous Ulcers
• Transverse Fusion - Cobblestone Appearance of Mucosa

18. NORMAL

19. Fig : Gross : The middle portion of bowel seen here has a
thickened wall, and the mucosa has lost the regular folds and
contains deep fissures. The serosal surface shows reddish
indurated adipose tissue that creeps over the surface.

20. PATHOLOGY - CROHN'S CONTINUED
• Focal inflammation → Fistula Tracts → Resolves by Fibrosis → Stricturing of Bowel
• Skip Lesions - Separated by intervening Normal-appearing intestine
• Bowel wall → Thickened , Fibrotic → Chronic Recurrent Bowel Obstruction
• Thickened mesentery → Projections into bowel (‘Creeping Fat’) / Fat Wrapping (pathognomonic)
• Serosa & Mesentery inflammation → Adhesion of the Inflamed bowel to other loops of Bowel
or Other Adjacent Organs.
• Transmural Involvement : Lead to : Intra-Abdominal Abscesses, Fistulas, and, rarely, free
perforation

21. FIG : Histology Showing Mucosal Ulceration & Destruction FIG : Histology Shows Non Caseating Granuloma

22. Source : Maingot's abdominal
Operations 13th edition

23. CLINICAL PRESENTATION
• Vary greatly depending on the Segment of Intestine involved.
• Crohn’s disease can be categorized into three general manifestations:
A] Inflammatory disease B] Stricturing disease C] Perforating disease.
• Do not represent truly distinct forms of disease; used to describe the predominant
gross manifestation of the disease
• More than one pattern tends to occur in same patient or even same segment of
intestine.
• Even so, one pattern tends to predominate.

24. INFLAMMATORY PATTERN
• Mucosal ulceration and Bowel Wall Thickening
• Edema - lead to an Adynamic segment of Intestine
and Luminal narrowing.
• Obstructive symptoms in the Small Intestine
• Diarrhea in the Colon .
• Of the three patterns of Crohn’s disease, the
Inflammatory pattern is much more likely to respond to
Medical Therapy.

25. STRICTURING PATTERN
• Chronic inflammation → Fibrotic scar tissue →
constricts the intestinal lumen with cicatricial
strictures [“Fibrostenotic lesions.”]
• Develop Partial or Complete Intestinal
Obstruction, and hence their symptoms are
primarily obstructive in nature.
• Not Reversible with Medical Therapy
• Once Fibrostenotic areas become symptomatic,
significant improvement rarely occurs and
Surgical intervention is often required

26. PERFORATING PATTERN
• Development of Sinus tracts, Fistulas, and Abscesses .
• Penetrating Sinus tracts - deep mucosal ulcerations.
• Abscess - Penetrate through the muscularis propria
• Fistulas -When Penetrate into surrounding structures
• Free perforation with spillage of intestinal contents into
the abdominal cavity is NOT a common phenomenon.
• Perforating disease is accompanied by a degree of
Stricture Formation.

27. CROHN'S
DISEASE -
DISTINGUISING
FEATURES

28. AGGRESSIVE FISTULIZING DISEASE
• Fistulas are manifestations of the Transmural Nature of CD
• Perianal Fistulas are common and occur in 15% to 35% of patients.
• Enterovaginal fistulas occur in women.
• Entero-Vesicular - recurrent polymicrobial UTI or as Frank Pneumaturia and Fecaluria.
• Entero-Cutaneous fistula after Appendectomy.
• Other types-
• Entero-Enteric, Entero-Colonic, and Colo-Colonic fistulas

30. BLADDER

31. LOCATION OF DISEASE
• GASTRODUODENAL AND ESOPHAGEAL CROHN'S
• CROHN’S DISEASE OF THE SMALL INTESTINE
• CROHN’S COLITIS
• EXTRAINTESTINAL CROHN’S DISEASE
• Occular : Uveitis & Episcleritis
• Dermatological : Erythema Nodosum & Pyoderma Gangrenosum
• Hepatobiliary : Primary Sclerosing Cholangitis, Gallstones
• Joint disorders : Ankylosing Spondylitis , Sacroilitis
Seronegative Polyarteritis,

32. GASTRODUODENAL AND OESOPHAGEAL CROHNS
DISEASE
• Esophageal - < 2% of patients.
• Dysphagia, Odynophagia, Substernal Chest pain, and Heartburn
• Mouth ulcers - aphthous ulcers - Hard Palate, Esophageal Ulcers.
• Esophageal stricture and esophagobronchial fistula
• Gastroduodenal - (Focal gastritis, Duodenitis with or without granulomas)
• H-pylori-negative peptic ulcer disease, dyspepsia or epigastric pain as the
primary symptoms.
• Symptoms usually related to the Obstructive nature of the disease with delayed
gastric emptying, a sense of postprandial gastric fullness, nausea, and vomiting.

33. FIG :“notching” of the duodenal folds protruding lesions in the
bulb and second duodenal portion a “bamboo-joint-like (BJL)”
appearance.
FIG :Pre-pyloric gastric ulcer in pt with Crohn’s disease

34. CROHNS DISEASE OF SMALL INTESTINE
• Pain abdomen - 90% of cases
• Result of obstructive or septic complications.
• Partial obstruction - Pain Abd - Postprandial and Crampy in nature
• Septic complications - Pain Abd - Steady and Associated with fevers.
• Weight loss
• Food avoidance / Result of Malabsorption
• RLQ Palpable mass -
• Abscess or Phlegmon in Perforating disease
• Thickened loop of intestine in Obstructive disease
• Evidence of Fistulization to the skin, urinary bladder, or vagina

35. CROHNS DISEASE OF SMALL INTESTINE
• Ileocolitis
• Recurrent Right Lower Quadrant Pain and non bloody diarrhoea
• Tender palpable mass in RIF , fever and leucocytosis
• Pain is colickly and Relieved by defecation
• May Present as Small Bowel Obstruction
• Jejunoileitis
• A/W loss of digestive and absorptive surface
• Malabsorption and steatorrhoea
• Anemia, Hypoalbuminemia, Hypocalcemia, Hyperoxaluria

36. CROHN’S COLITIS
• Diarrhea that may or may not be bloody.
• Acute Flares : fever and Abdominal Pain Excacerbated by
Bowel Movements
• Stricturing - Advanced disease - Colonic Obstruction.
• Abscess Formation + Fistula Formation
• Very Rarely - Toxic MegaColon can occur ( Less Frequent
than UC)

37. PERINEAL CROHN’S DISEASE
• 40% of patients will develop perineal manifestations .
• Isolated Perineal and Anorectal disease occurs in 5% to 10% of affected patients
• Frequently affects the Anal Crypts and gives rise to Perianal Fistulas, Abscesses, and
Anal Strictures.
• Associated with Hypertrophic Perianal Skin Tags, Fissures, and Perineal Scarring

39. EXTRA INTESTINAL MANIFESTATIONS OF CROHNS
• Peripheral Polyarteritis, Episcleritis, Uveitis and Erythema Nodosum → correlate
with the activity of Intestinal Crohn's disease
• These Regress with complete surgical resection of the affected segment of intestine or
with successful medical control of the intestinal inflammation
• Clinical course of Ankylosing Spondylitis and Primary Sclerosing Cholangitis →
Independent of the level of disease activity → Do not improve with Surgical Resection of
affected Segment of Bowel
• Pyoderma gangrenosum - Inconsistent Data.

40. DERMATALOGICAL
• Pyoderma gangrenosum
• Erythema nodosum
• Granulomatous inflammation of the skin
• Aphthous ulcers of the mouth
• Angular cheilitis

41. PYODERMA
GANGRENOSUM
Fig: Pyoderma gangrenosum presents
as ulcerated lesions that appear
independent of disease activity, and is
more difficult to treat
PYODERMAGANGRENOSUM
Fig : Typically appears as Painful,
Red, Subcutaneous Nodules on
Extensor Surfaces and mirrors
disease activity
ERYTHEMANODOSUM

42. MUSCULOSKELETAL
• Clubbing
• Arthritic manifestations
• Peripheral Arthropathy - 16% to 20%
• Pauciarticular arthropathy (type I, affecting four or fewer joints)
• Polyarticular arthropathy (type II, with five or more joints affected)
• Axial arthropathies - 3% to 10%
• Metabolic bone disease
• Granulomatous vasculitis, periostitis and amyloidosis

43. OCULAR MANIFESTATIONS
• Occur in 6% of patients .
• Episcleritis
• Scleritis
• Uveitis - the anterior segment
• Keratopathy and night blindness
FIG: Episcleritis -
Inflammation of
the Vascular layer
directly beneath
the Conjunctiva
Fig : Scleritis -
Inflammation of
Deeper Scleral
vessels.
May involve
Vision changes

44. HEPATOBILIARY
• Gallstones
• Asymptomatic and mild elevations of
liver biochemical tests
• PSC more often is associated with UC >
CD (RARE)
• Autoimmune hepatitis.
• Venous thromboembolism
• Arterial thrombosis.
VASCULAR
PRIMARY SCLEROSING CHOLANGITIS
• Intra-hepatic & extrahepatic bile duct
inflammation & fibrosis.
• In 5% UC pts., less in CD.
• Both PSC & IBD are usually pANCA (+)ve.
• Gold standardis ERCP.
• MRCP is more sensitive, specific & safer.
• Gallbladder polyps have high risk of
malignancy.
• Symptomatic patients develop liver failure
within 5-10 yrs needing transplant

45. RENAL AND GENITOURINARY
• Inflammatory entrapment of the ureter
• Uric acid and oxalate stones.
• Membranous nephropathy & Glomerulonephritis
• Renal amyloidosis.
• Penile and vulvar edema

46. DIAGNOSIS
• No single symptom, sign, or diagnostic test establishes the diagnosis of Crohn’s disease.
• Serologic and Inflammatory markers are typically elevated and correlate with disease
activity . Ex : C- Reactive Protein , Calprotectin , ESR
• Fecal calprotectin and Lactoferrin levels have been used to distinguish IBD from irritable
bowel syndrome (IBS), assess whether CD is active.
• 2% to 28% of patients : p - ANCA Positive ; ASCA Positive found in 39% to 69% patients
• Should be excluded :
• Acute ileitis caused by Campylobacter and Yersinia species
• Typhoid enteritis caused by Salmonella typhosa
• Mycobacterium tuberculosis - Terminal Ileum Involvement
• Cytomegalovirus (CMV) can cause Intestinal ulcers, bleeding, and perforation

47. DIAGNOSIS
• Colonoscopy - with intubation of Terminal Ileum
is the main diagnostic tool.
• Cobblestone appearance - Focal Ulcerations
adjacent to areas of Normal Appearing Mucosa
along with polypoid mucosal changes
• Skip areas of involvement, Rectal Sparing
• Pseudopolyps, as seen in ulcerative colitis, are also
often present.
• Opportunity for a biopsy for histologic evaluation

49. IMAGING
• Barium small bowel follow-through, CT enterography, or MR enterography - contrast
examinations of small bowel to Reveal Strictures , Ulcers & Fistulas .
• Early Disease : Mucosal Granulations with Ulceration and Nodularity
• Progression of Disease : Thickening of Mucosal Folds and Edema of the bowel wall.
• Advanced Disease : Cobblestone Appearance
• CT - Helps in identifying Abscess / Inflammatory mass / Other Intra Abd disorders
• Enteric fistulas including ileosigmoid and ileovesical fistulas are not typically demonstrated
on contrast radiography - Demosstrated well in CT-Entergraphy
• CTE combined with Ileocolonoscopy as a First-line Test for Diagnosis & Staging of Crohn’s .

50. Fig: Small bowel radiograph demonstrating Crohn’s
disease of the terminal ileum
Fig: Small bowel radiograph demonstrating Crohn’s
disease of the terminal ileum with high-grade
strictures and ulcerations.

51. Fig: CobbleStone Appearance :Small bowel
radiograph demonstrating Crohn’s disease with
strictures in the jejunum.
Fig: String Sign of Kantour : Long segment of
narrowed terminal ileum in a 'string like'
configuration in keeping with long stricture segment

52. MR ENTEROGRAPHY
• Intestinal wall thickening, Submucosal edema, Vasa recta engorgement,
and lymphadenopathy are signs of Active disease
• FIESTA (Fast Imaging Employing Steady-state Acquisition) images can
add information regarding the functional status of fibrotic segment.
• MRI images yield a diagnostic accuracy of 91%.

53. CAPSULE ENDOSCOPY
• Patient Swallows encapsulated video camera
• Transmits an image to a receiver outside the pt.
• It is most commonly used for finding Obscure sources of GI blood loss,
• The images can find Ulcerations associated with CD if endoscopy and
colonoscopy are unrevealing.
• The major risk is the potential to get lodged at the point of a stricture!

54. DIFFERENTIAL DIAGNOSIS : SMALL BOWEL CROHN'S
• Irritable Bowel syndrome ; Acute appendicitis ; Intestinal Ischemia ; Pelvic
Inflammatory Disease ; Gynecologic malignancies
• Radiation enteritis, Yersinia Infections, Intestinal injury from NSAIDs ; Intestinal
Tuberculosis, Small Bowel Tumors
• Most important : A] Small Bowel Malignancy B] Intestinal TB
• Small Bowel Malignancy suspected - Resection should be undertaken to make certain
the diagnosis.
• TB - Exposure to TB, PPD Skin test, Chest X ray .
• If Latent Tb + Crohn's → should be treated for TB prior to Immmunosuppresive
Therapy for CROHN'S

55. DIFFERENTIAL DIAGNOSIS : CROHN'S DISEASE OF COLON
• Ulcerative colitis ; Infectious Colitis ; Collagenous Colitis ; Ischemic colitis ;
Diverticular Disease ; Colonic Neoplasm ; Solitary Rectal Ulcer Syndrome ;
NSAID colopathy
• Difficult to Differentiate from Ulcerative Colitis
• As it is Possible for Crohn’s disease of the colon to Reproduce all the features of
ulcerative colitis
• After a complete history and Physical examination complemented by appropriate
radiologic, endoscopic, Blood investigations - Differentiated in 85% case
• Rest Cases - 15% - Inderminate Colitis

56. MEDICAL MANAGEMENT
• Approach to Luminal CD over the past decade:
1. Symptoms in CD correlate poorly with endoscopic activity;
2. More severe endoscopic activity predicts worse outcomes.
3. Endoscopic healing is associated with improved short and long-term outcomes.
• Goals of therapy should include Endoscopic, as well as clinical remission.
• “Conventional” Sequential therapy - Steroids, followed by Immunomodulators, followed by Anti-TNF
agents.
• Anti-TNF-α agents -- most effective in inducing and maintaining clinical remission, achieving endoscopic
healing, and decreasing hospitalizations and surgeries in CD.
• Recent Advances - Therapy for CD is more effective in disease of shorter duration.
• Trend - using anti-TNF-α mAbs Earlier in course of CD.

57. MEDICAL MANAGEMENT
5-ASAAGENTS
• Action :
• Inhibit LT production by inhibition of 5-LOX Activity.
• Inhibits Production of IL-1 and TNF.
• Limited role in Inducing Remission. Useful in Mild to Moderate CD . No clear role in
Maintenance.
• Controlled-release preparation is also effective as maintenance therapy to prevent recurrence after
a flare of disease has been effectively managed either medically or surgically .
• [Patients with Crohn’s disease avoid NSAIDs - powerful inhibitors of COX-1 and COX-2.
NSAIDs may exacerbate Crohn’s disease]

58. Oral 5-ASA Preparations

59. MEDICAL MANAGEMENT
• Antibiotics (Ciprofloxacin/Metronidazole)
• In Management of abscesses or wound infections.
• Maintenance therapy of chronic perineal septic complications.(with Anti TNF-Alpha)
• Bacterial overgrowth associated with chronic obstructive disease.
• Corticosteroids
• Most effective agents for controlling Acute Exacerbations
• Remission in active small bowel Crohn’s - Oral Prednisone - 0.25 and 0.5 mg/kg/d
• Or Methylprednisolone 40 to 60 mg given as a daily infusion.

60. MEDICAL MANAGEMENT
• Immunomodulators (Azathioprine and 6-Mercaptopurine)
• Inhibit cytotoxic T-cell and NK cell function
• effective in treating Mild to Moderate Crohn’s disease REMISSION
• Azathioprine given at 2.0 to 2.5 mg/kg/d or 6-MP in doses of 1.0 to 1.5 mg/kg/d
• 50% to 60% response rate in patients with Active Crohn’s disease
• Biologic Therapies (Anti-TNF Therapies and Anti-Integrin Antibodies)
• Infliximab -80% response rate with a single dose of infliximab
• 5 mg/kg iv at weeks 0, 2, and 6, & then 5 mg/kg every 8 weeks thereafter
• Increased risk for infectious complications and intra-abdominal abscesses
• Natalizumab (anti-alpha-4 integrin) ; Vedolizumab (anti-α4-β7 ntegrin)

61. Shackelford's SURGERY of the ALIMENTARY TRACT 8th Ed

62. Shackelford's SURGERY of the ALIMENTARY TRACT 8th Ed
The combination of a thiopurine
and infliximab is the most
effective inductive therapy
Use Methotrexate for patients who do not
tolerate thiopurine.
American Gastroenterological Association (AGA) Risk Stratification for Assessment and Medical Therapy of CD

63. SURGICAL TREATMENT
• Goal : Provide Long-lasting Symptomatic Relief while avoiding Excessive Morbidity
• Complete extirpation of disease should NOT be the primary goal of surgery, as it does
not produce cure and is frequently counterproductive.
• Main aims of Surgical Management:
• Treatment of Complications
• Palliation of Symptoms
• Avoiding Excessive Loss of Intestine
• OPTIMAL SURGICAL THERAPY :
• Leaving behind segments of intestine with Mild but Asymptomatic disease
• Resection of only the areas of Severe and Symptomatic Disease

64. INDICATIONS FOR
SURGICAL
INTERVENTION IN
CROHN’S DISEASE
• Acute onset of severe disease:
• Crohn’s colitis +/− Toxic megacolon (rare)
• Failure of medical therapy:
• Persistent symptoms despite long-term steroid use
• Recurrence of symptoms when high-dose steroids are tapered
• Drug-induced complications (Cushing’s disease, hypertension)
• Development of disease complications:
• Obstruction
• Perforation
• Complicated fistulas
• Hemorrhage
• Malignancy risk

65. SURGICAL MANAGEMENT
• Most common Indications : Intestinal Obstruction
• Abscesses and fistulas are frequently encountered during surgery
• Most abscesses : Amenable to Percutaneous drainage
• Fistulas: unless a/w symptoms or metabolic derangements, do not require surgical
intervention
• C/o Presumed Appendicitis : Intraop discovery of Inflammation limited to Terminal Ileum
• Can be caused by Acute Crohn's OR Acute Ileitis caused by Yersinia or Campylobacter
• Both conditions should be TREATED MEDICALLY; Ileal Resection NOT indicated
• Appendix, even if normal appearing, Should Be Removed - TO exclude from D/D

66. SURGICAL MANAGEMENT
• When the diagnosis of Crohn’s is known
and Surgery is planned :
• Thorough examination of the Entire Intestine should be performed.
• Characteristics of Active Disease to be appreciated Intra Operatively :
• Thickening of the bowel wall Narrowing of the lumen
• Serosal inflammation and coverage by Creeping Fat
• Thickening of mesentery Skip lesions are present in approx 20% Cases
• Segmental Intestinal Resection of grossly evident disease followed by
Primary Anastomosis is the usual procedure of choice

67. SURGICAL MANAGEMENT - RESECTION MARGINS & TECHNIQUE
OF ANASTOMOSIS
• Microscopic evidence of CD at resection margins DOES NOT Compromise Safe Anastomosis
• In a RCT the effects of achieving 2-cm resection margins V/S 12-cm resection margins:
• NO evident differences with respect to Clinical Recurrence rates or Anastomotic
Recurrences
• Recurrence rates similar whether margins - Histologically Free of OR Involved with CD
• Ideal Anastomotic technique after Intestinal Resection. - A RCT of 139 patients:
• Reconstructed using end-to-end sutured (2-0 PDS) anastomosis V/S Side-to-side Staples
Anastomosis
• No differences in Endoscopic or Symptomatic disease Recurrence
• Alternative to Segmental resection for Obstructing lesions is Stricturoplasty

68. STRICTUROPLASTY
• Planned for cases with
• Extensive disease and Fibrotic strictures
• Undergone Previous Resection
• At risk for developing Short Bowel Syndrome
• Depending on the length of the stricture
• < 12cm - Reconstruction Similar to Heinecke-Mickulicz pyloroplasty
• 12 - 25 cm - Similar to Finney pyloroplasty
• Mean lenghts 50 cm - Side-to-side Isoperistaltic enteroenterostomy
• Stricturoplasty is contraindicated in patients with intra-abdominal abscesses or intestinal fistulas.
• Bypass procedures (gastrojejunostomy) are also used in the presence of duodenal strictures, for which
stricturoplasty and segmental resection can be technically difficult.

69. Fig: Heineke-Mikulicz strictureplasty
Fig: Finney strictureplasty

70. Segment of
intestine
affected
divided,2
limbs are
drawn
onto each
other
Longitudinal enterotomies are made along the
Antimesenteric borders of the 2 limbs
2 limbs are anastomosed together in a lengthy
side-to-side fashion.
A
C
B

71. MANAGEMENT OF COMPLICATED CROHN’S
DISEASE
• Crohn’s Disease of the Duodenum
• Almost always manifests with stricturing disease that can be managed by strictureplasty or with
bypass procedures
• Distal segment (typically the terminal ileum or neoterminal ileum) that fistulizes into an otherwise
normal duodenum
• Strictures:
• First 3 parts : Heinecke-Mikulicz strictureplasties
• Last Part : Finney strictureplasty
• If Duodenal stricture is lengthy or the tissues around the stricture are too rigid or unyielding, an
Intestinal Bypass procedure should be undertaken

72. INTESTINAL BYPASS FOR STRICTURE DUODENUM
• M/C : simple Side-to-side Retrocolic Gastrojejunostomy
• Risk for Stomal ulcerations + : Highly Selective Vagotomy done
• Stricture limited to the third or fourth portions :
• Roux-en-Y duodenojejunostomy to the proximal duodenum Preferred

73. DUODENAL FISTULAS :
• Most duodenal fistulas located AWAY from the Pancreaticoduodenal margin, and thus,
these fistulas can be managed by :
• Resection with Primary closure of the Duodenal Defect.
• Larger fistulas or fistulas that are involved with a large degree of inflammation:
• Roux-en-Y Duodenojejunostomy or with a Jejunal Serosal patch
• Duodenal resections are almost never necessary for Crohn’s disease, and they should be
considered the surgical option of last resort.

74. COMPLETE INTESTINAL OBSTRUCTION
• Rarely requires urgent surgical intervention
• Vascular supply to the intestinal loop is never compromised.
• Almost all cases of Complete or High-grade Partial small bowel obstruction - respond to
Conservative management
• Nasogastric Decompression, Intravenous hydration, and Steroid Therapy. - Rx
• High risk for Recurrent episodes and persistent symptoms.
• Elective surgery should be considered once episode of Complete obstruction has resolved
• If obstruction fails to respond to appropriate conservative treatment, surgery is required.
• High index of suspicion for Small Bowel Cancer as the cause of the obstruction needed

75. ILEOSIGMOID FISTULAS
• Asymptomatic ileosigmoid fistulas do usually require operative management.
• Large Ileosigmoid Fistulas can result in bypass of the intestinal contents from the terminal
ileum to the distal colon and thus give rise to Debilitating Diarrhea .
• Rx :
• Simple division of Fistulous adhesion & Resection of the ileal disease .
• Defect in the Sigmoid colon is then debrided, and Simple closure is undertaken
• Sigmoid colon resection is necessary when primary closure of the fistula is at risk for
poor healing .

76. ILEOVESICAL FISTULA
• 5% of Crohn’s disease patients
• Indicator of complex fistulizing disease, as most ileovesical fistulas occur along with other enteric
fistulas.
• Can be managed medically for extended periods of time without significant complications
• Surgery is indicated when
• Recurring Urinary infections occur,
• Particularly Pyelonephritis,
• Concomitant potential for worsening of renal function
• Surgical treatment of ileovesical fistulas requires Resection of the Ileal disease with closure of the
bladder defect
• Cystogram taken on postoperative day 5 - Only then Foley's to be Removed

77. ABSCESS
• Small intraloop or Intramesenteric Abscesses.
• Resection of the Defective segment and its Mesentery and Primary Anastomosis
• Large abscesses : best managed with CT-guided percutaneous drainage
• Enterocutaneous fistula often occurs : Spontaneously close or it may persist
• Such a fistula may spontaneously close or it may persist, and the intestine may continue to
be a source of sepsis.
• Initial nonoperative management after successful percutaneous drainage can be undertaken
in carefully selected patients
• If Drainage through the fistula continues, Surgical Resection of the Affected Segment of
intestine becomes necessary.

78. CROHN’S DISEASE OF THE COLON
• CECAL DISEASE
• Terminal Ileitis - predominant component - With extension into Cecum
• Surgical Resection should encompass the Margins of Gross Disease
• Anastomosis b/w Neoterminal Ileum and the Proximal Ascending Colon
• Recurrence - Common at Anastamosis Site - At the Preanastomotic Ileum
• Risk for Recurrent disease within the Distal colon or the rectum is low.
• EXTENSIVE COLITIS WITH RECTAL SPARING
• Approximately 20% Cases of Crohn’s colitis.
• Total Abdominal Colectomy with Ileorectal Anastomosis .
• Upto 50% - Recurrence within Rectum- Require a Proctectomy with Permanent Ileostomy

79. CROHN’S DISEASE OF THE COLON
• PROCTOCOLITIS
• Total Proctocolectomy with Permanent Ileostomy
• Severe Perianal Disease - 2 staged procedure
• First stage - Resection of Colon and Majority of the Rectum with Short Rectal Stump created
- Perineal Abscesses - drained and Fistulas are laid open
• Once the Perineal Sepsis is cleared & Perineum Healed - Short anorectal stump removed
through perineal approach .
• Second stage - primary closure of the perineum
- without the high risk of persistent perineal wounds.
• First step removes the diseased colon and rectum without creating a perineal wound that
may be difficult to heal in the presence of active perineal sepsis

80. PERIANAL DISEASE
• Perianal Disease - Abscess, Fistulas, Fissures, Anal Stenosis, Hypertrophic Skin Tag.
• Originates from Inflammation within the Anal Crypts.
• Inflammation - Sepsis & Fistulization
• Usually A/w Active or Quiescent disease elsewhere within the GI tract
• Controversial :
• Disease activity parallels with Intestinal Disease .
• Surgical control of Intestinal Disease - Ameliorate - Perianal Manifestations
• Perianal Crohn’s disease tends to be Recurrent, Complex, and Progressive.
• Surgical Incision and Drainage - Incision closed to Anal Margin. Pack with Ribbon Gauze
• If Fistula Tract - Loose Seton . Low Lying Fistulas - Fistulotomy

81. PERIANAL DISEASE
• Since Introduction of Anti-TNF-α agents, Need for aggressive surgical intervention, such as Proctectomy,
has significantly decreased.
• Level I evidence from two RCT using Anti-TNF-α agents demonstrated upto 50% 1-year fistula closure
rate for CD with perianal fistulas .
• Drainage of any Undrained Infection and placement of Noncutting Seton drains - Symptomatic Relief
• Seton drain will :
• Preserve the Integrity of Anal Sphincter,
• Drain the fistula tracts.
• Limit the chances of abscess formation or perineal sepsis during medical therapy.
• Within 12 months - Rectum reexamined & if no luminal disease - complex fistulas - considered for repair.
• M/c Procedure - Endorectal Advancement Flap with healing rates ranging between 55% and 72%.
• *Emerging Alternative to Surgical Repair* - Injection of Allogenic or Native Stem Cells into Tract .
- Mesenchymal stem cells (MSCs) & Gore Plugs
- Success rate less than 50% in 1 yr

82. Photograph of a patient with multiple perianal
fistulas secondary to Crohn’s disease
An 18-year-old
male Crohn's
disease patient.
A: A rubber
band was
placed during
the surgery for
drainage;
B: Thirty
weeks after the
surgery

83. PERIANAL DISEASE
• Complex Fisutlas - Risk for Surgical Complications - higher.
• Aggressive Medical therapy is warranted Before Surgery
• Infliximab treatment - Healing of Complex Perianal Fistulas is seen in 60% of cases.
• Use of Setons with infliximab therapy - Improves overall effectiveness of Infliximab.
• Rectal Advancement Flap - Closure of the Internal Opening of the fistula
• Incision made at the Dentate Line ---> Flap of Mucosa and Muscularis Undermined.
• Advanced down Over the internal opening of the fistula & Sutured.
• Severe Disease - Fecal Diversion with a Stoma may be necessary.
• Proctectomy - Damage to Sphincters + Incontinence .

84. CONCLUSION
• Management of Crohn’s disease is complex and requires a Multidisciplinary Team
Approach.
• Initial management is typically Medical and has had several advances.
• Surgical intervention is typically reserved for Refractory disease or complications of the
disease .
• With Proper history, Utmost Clinical Suspicion and adequate Diagnostic confirmation,
Crohn's Disease can be diagnosed early and treated appropriately.

85. ULCERATIVE COLITIS

86. ULCERATVE COLITIS
• Ulcerative colitis (UC) is a Chronic Relapsing and Remitting intestinal disorder plagued
by diffuse and continuous mucosal inflammation involving the rectum, and extending
proximally throughout the colon.
• Inflammatory hallmark in UC is limited to the mucosa.
• Infection with Salmonella or Campylobacter has been associated with an 8- to 10-fold
Increased risk of developing of UC the following year .
• Patients who have undergone an Appendectomy are at decreased risk of developing UC.

87. PATHOLOGY (CONTD)
• Mild Inflammation – Mucosa is erythematous and
has granular surface. (Sandpaper appearance)
• Severe inflammation – Mucosa Hemorrhagic, Edematous
and Ulcerated.
• Long standing disease – Pseudopolyps
• Pseudopolyps, Inflammatory polyps - Regeneration of Inflamed Mucosa
• Toxic megacolon –Transverse or right colon with diameter > 6cm with loss
of haustrations in severe UC.
Pseudopolyps in UC.

88. PATHOLOGY - ULCERATIVE COLITIS
• Macroscopic Appearance
• Involves rectum and extends proximally to involve Entire Colon.
40 – 50 % - Disease Limited to Rectum and Rectosigmoid
30 – 40 % - Extends Beyond Sigmoid but not involving whole colon
20 % - Pancolitis
• No skip lesions. - Continous Involvement
• Backwash ileitis – Inflammation extends 2 – 3 cm into terminal ileum in 10 -20 %

89. Fig : Endoscopic image of a sigmoid colon afflicted
with ulcerative colitis. Note the vascular pattern of the
colon granularity and focal friability .
Fig : Colonic pseudopolyps of a patient with intractable
ulcerative colitis. Colectomy specimen

90. MICROSCOPY
• Limited to Mucosa and Submucosa.
• Deeper layers may be affected in fulminant
disease.
• Distortion of Crypt Architecture
• Basal plasma cells and lymphoid aggregates.
• Mucosal vascular congestion with edema
and focal hemorrhage.
• Cryptitis and Crypt abscess – Neutrophils invade the epithelium in the crypts & expand
Individual Crypts of Lieberkühn.
• Mucosal infiltration by Neutrophils, Lymphocytes, Plasma cells and Macrophages.

91. CRYPT ABSCESS
Fig : Active ulcerative colitis. The glands are irregular
with branching, and focally, the long axis of the gland is
horizontal rather than perpendicular. A central crypt
abscess is present. There are increased numbers of chronic
infl ammatory cells throughout the lamina propria

92. Fig: H&E stain of a colonic biopsy showing a Crypt
abscess, a classic finding in ulcerative colitis
Fig: Biopsy sample (H&E stain) that demonstrates
marked lymphocytic infiltration (blue/purple) of the
intestinal mucosa and architectural distortion of crypts.

94. CLINICAL FEATURES OF UC
• Diarrhoea Tenesmus Passage of mucus
• Rectal bleeding Crampy abdominal pain
Proctitis –
• Fresh blood and blood stained mucus, either with stool or streaked onto the
surface of normal or hard stool. Sense of incomplete evacuation and
urgency
Proctosigmoiditis – May have constipation

95.  SEVERE COLITIS
• Grossly Bloody Diarrhea Anorexia
• Liquid stool containing Blood, Pus and fecal matter
• Nausea Vomiting
• SIGNS –
• Tender anal canal Blood on DRE
• Tenderness on palpation over colon in severe disease

96. PRIMARY SCLEROSING CHOLANGITIS
• Primary sclerosing cholangitis (PSC) occurs in 5% to 8% of patients with UC
• Patients with UC with HLA-B8 or HLA-DR3 --> 10 times more likely to develop PSC.
• PSC & Ulcerative Colitis typically have a more quiescent disease course.
• PSC + UC --> Risk of Colon Cancer 5 times > than with patients with UC alone.
• PSC Presentation :
• Asymptomatic - Diagnosed on AbN Laboratory Studies
• May present with Obstructive Jaundice + Abdominal Pain.
• PSC - Disease - progressive and ultimately fatal. Unless Liver Transplant done.
• Colectomy - No role / Effect in Course of PSC .

97. ULCERATIVE
COLITIS
Clinical Presentation

98. INVESTIGATIONS
• Elevated acute phase reactants like CRP and elevated ESR
• Low Hemoglobin
• Leukocytosis may be seen
• Fecal lactoferrin and Fecal Calprotectin levels – Correlate with histologic
inflammation and predict relapses
• Stool examination for bacteria, C. difficile toxin and ova and parasites.
• P-ANCA is positive in 60 -70 %. ASCA positive in 5 – 15 %.
• Anti-goblet cell antibodies (GAB) is +ve in UC

99. IMAGING DIAGNOSIS
• Computed Tomography, Ultrasound, MRI, and Endoscopy reveal
• Acute Mucosal Wall Thickening,
• Fat Stranding,
• Perforation
• Leukocyte scintigraphy is an uncommon imaging technique used to quantify leukocytes
in the Intestinal wall
• Useful in Ascertaining the distribution (continuous vs discontinuous) of disease
• Response to Treatment
• Endoscopy remains the Gold Standard for imaging in Diagnosis of UC.

100. Fig: MRI. Yellow arrows point to segments of
visualized colon which are narrowed, ahaustral, and
foreshortened
Fig: CT. Lead Pipe Appearance in both descending
and ascending colon (yellow arrows) thick red arrow
demonstrates post-inflammatory polyps

101. Fig: CT, Pancolitis. A. This cross-section demonstrates
pancolitis with a striated wall appearance from mucosal enhancement andintramural edema (yellow arrows).
B. Acute on chronic UC flare. Striated appearance is due to chronic submucosal fat deposition.

102. Fig: Toxic Megacolon. Abdominal plain radiograph,
Grossly dilated transverse colon with
“thumbprinting” due to mucosal edema
Fig: Stricture in Chronic Ulcerative Colitis.

103. SIGMOIDOSCOPYAND COLONOSCOPY
• With biopsy – to assess disease activity and confirm diagnosis
• Sampling of the ileum, four colonic sites, and the rectum, with a minimum of two biopsies
from each site
• Mild disease – Mild erythema and friability with mucosal inflammation
• Severe disease – Ulcerations & Spontaneous bleeding starting at Rectum with proximal
extension
• In addition, there is often loss of vascularity, loss of haustral folds, mucosal erosions,
mucosal friability, and evidence of mucopurulent exudates.
• Longstanding disease - Pseudopolyps are often observed

104. Figure : An
endoscopic view
of ulcerative
colitis.
A. Mild
ulcerative colitis.
B. Moderate
ulcerative colitis.
C. Severe
ulcerative colitis.
The mucosa is
plagued with
white exudative
granularities

105. COMPLICATIONS
• Only 15% present with catastrophic illness
• Massive bleeding → 1% patients, if > 6-8 units of blood needed within 24-48 hrs.,
colectomy indicated
• Toxic Megacolon → If diameter > 6 cm, seen in 5%, triggered by electrolyte abnormalities
& narcotics
• Perforation → most dangerous complication, symptoms may be masked by glucocorticoids
• Strictures occur in 5-10% patients, if impassable with colonoscope,must be assumed
malignant until proven otherwise.

106. COLONIC STRICTURE
• Occur in 5% to 12% of patients with Chronic Ulcerative Colitis
• Most often Benign and caused by hypertrophy of the muscularis
• Cancer Must be Excluded in All Colonic Strictures of UC
• Colonic stricture in a patient with ulcerative colitis must be presumed carcinoma until
proved otherwise. - Sabiston Textbook of Surgery 18th Edition
• If malignancy cannot be ruled out by Endoscopy, the Presence of a stricture is an Indication
for operative intervention. - Sabiston Textbook of Surgery 18th Edition
• Three important features are suggestive of Malignant Strictures :
1. Appearance Later in course of UC (60% after 20 yrs v/s 0% before 10 yrs)
2. Location Proximal to the Splenic Flexure (86% malignant)
3. Large Bowel Obstruction caused by the Stricture .

107. RISK FOR CARCINOMA
• Risk Factors : Prolonged duration of disease, Pancolonic disease, Continuously Active disease, &
Severity of the Inflammation.
• Cumulative Risk for cancer : 25% at 25 yrs; 35% at 30 yrs; 45% at 35 yrs ; 65% at 40 yrs
• Involvement of Left side of the colon - Lower risk < Entire Colon - High Risk
• Surveillance Colonoscopy :
• Every 1 to 2 years beginning 8 years after the onset of Pancolitis.
• 12 to 15 years after the onset of Left-Sided Colitis.
• At least 30 Random Biopsy Specimens obtained. ( Traditionally - 10 )
• Risk of Ca with degree of dysplasia
• 10% of colons displaying low grade dysplasia,
• 30% to 40% with high-grade dysplasia,
• More than 50% of colons - Dysplasia Associated with Lesion or Mass ( DALM )

108. TOXIC MEGACOLON
• Serious, Life-threatening condition
• Can occur in Ulcerative colitis, Crohn’s colitis, and Infectious Colitides - Pseudomembranous Colitis.
• Bacterial Infiltration of walls of the colon ---> creates a Dilation of Colon ---> Progresses to Point of
Imminent Perforation
• Necrotic, Thin-walled bowel in which Pneumatosis can often be seen radiographically.
• Medical Therapy - Some cases Reported - High Rate of Recurrance with Subsequent Surgery
• Aggressive Preoperative Stabilization
• Volume Resuscitation with Crystalloid solutions to prevent Dehydration 2o to 3rd Space Fluid Loss.
• Stress Dose Steroids for patients previously on Steroid therapy.
• Broad-Spectrum Antibiotics.
• Surgical : Mainstay in Toxic Megacolon.
• Total Abdominal Colectomy with Ileostomy and Preservation of the Rectum for Anastamosis at a later date

109. Shackelford's SURGERY of the ALIMENTARY TRACT 8th Ed

110. Shackelford's SURGERY of the ALIMENTARY TRACT 8th Ed

111. MEDICAL MANAGEMENT
• No medication cures ulcerative colitis, many can reduce symptoms. The goals of
medication therapy are:
• Inducing and Maintaining Remission.
• Improving the person's quality of life.
• 5-ASAAgents
• Induces & maintains clinical remission in mild to moderate UC
• Patient usually improves symptoms by 2 to 4 weeks

113. GLUCOCORTICOIDS
• Prednisone (oral) started at 40 – 60 mg/ day for active UC unresponsive to
5-ASA therapy
• Parenteral → Hydrocortisone 300 mg / day (or) Methylprednisolone 40
– 60 mg / day
• New → Budesonide → released entirely in colon, no side-effects,dose = 9
mg / day for 8 weeks, no taper required
• Topical route may be used for distal colitis & rectal involvement

114. TNF INHIBITORS
• Infliximab, adalilumab, and golilumab are effective in inducing and maintaining
clinical remission in UC
• Infliximab - intravenously every 8 weeks after induction dosing.
• Adalilumab and golilumab - subcutaneous injection every 2 weeks
• Can exacerbate Latent Tuberculosis or Hepatitis B, leading to Disseminated TB
or Fulminant Hepatitis B.
• Should be evaluated for these infections Prior to therapy

115. MANAGEMENT OF ACUTE COLITIS
• Severe Acute Colitis presents a potential surgical emergency.
• Acute colitis may be initially treated with Medical Therapy and daily re-
evaluation
• Deterioration or failure of symptoms to resolve within the first 3 days triggers
the need for urgent colectomy .
• The Main Goals of operative intervention include
• Achieving Definitive Cure by Resection of the Colon and Rectum,
• Reconstructing a Route of Elimination
• Minimizing morbidity and improving quality of life.

116. INDICATIONS FOR SURGERY
• Fulminating disease
• Chronic disease with anemia, frequent stools,urgency & tenesmus
• Steriod dependant disease
• Massive Colonic Bleeding
• Risk of Neoplastic change
• Dysplasia - Carcinoma
• Colonic Stricture - Malignancy cannot be ruled out in Endoscopy
• Extraintestinal manifestations

117. SURGICAL MANAGEMENT
• Removal of the entire colon "cures" Ulcerative colitis. Eliminates the long-term
risk of cancer .
• A surgeon can do that by two different types of surgery :
• Proctocolectomy and ileostomy.
• Proctocolectomy and ileoanal reservoir.(IPAA)
• Full recovery from both operations may take 4 to 6 weeks.
• Surgery of choice in urgent and emergent situations is Total Abdominal
Colectomy (TAC) with end ileostomy. - Later - Completion Proctectomy + IPAA
• Rectal stump - Hartmann pouch /closure with exteriorization into S/C tissue.

118. TOTAL COLECTOMY WITH ILEORECTAL
ANASTOMOSIS
• Following standard colectomy, Rectum - left intact ; obviating deep pelvic dissection and potential
injury to pelvic nerves.
• Rectal Remnant -
• Requires continued Medical therapy and Surveillance, - Chance Of Recurrance
• Risks of colitis and Later Cancer have not been eliminated.
• Anastomosis is at the level of the Sacral promontory, where the Superior Hemorrhoidal vessels are
left intact.
• Usually not Followed. Except in Patients with Significant debility who are poor operative
candidates.

119. TOTAL PROCTOCOLECTOMY WITH
ILEAL POUCH-ANAL ANASTOMOSIS
• Terminal ileum - Reconstructed to recreate a fecal reservoir in order to mimic anorectal
continence after colectomy.
• Single or Staged Procedure.
• Many variations to the Ileal Pouch - S, J, and W
• Adequate length of the Ileocolic Pedicle must be confirmed.
• Distal ileum is used to construct the J-pouch.
• Inflow and outflow limb - anastomosed together using a linear stapler.
• Apex of the Pouch is then anastomosed to the Rectal cuff.

120. RECONSTRUCTIVE
PROCTOCOLECTOMY WITH
ILEOANAL POUCH

121. SURGICAL OPTIONS IN SURGICAL MANAGEMENT OF UC
1. One-stage Total Proctocolectomy with ileal pouch–anal anastomosis (IPAA);
2. Two-stage approach - Total Proctocolectomy with IPAA + diverting Loop Ileostomy,
- Followed by Closure of Ileostomy
3. Modified Two-stage procedure - Total Abdominal Colectomy(TAC) + End Ileostomy
- Completion proctectomy with IPAA (without ostomy)
4. Three-stage - Total Abdominal Colectomy (TAC) + End Ileostomy
- Completion Proctectomy + IPAA
- Reversal of Ileostomy
• Modified 2 stage approach - Safe alternative to traditional two- & three-stage approaches
• Decreases the risk for an anastomotic complication - Lower Risk of Anastamotic Leak
• Without increasing the cost or the number of surgeries the patient has to undergo.

122. ELECTIVE OPERATIONS FOR
ULCERATIVE COLITIS

124. KOCK POUCH
(CONTINENT ILEOSTOMY)
• High-Volume, Low-Pressure Single Chambered Reservoir
• Made by Suturing several limbs of Ileum together after
the antimesenteric border has been divided.
• Outflow tract : Maintained by an Intussuscepted Nipple Valve
• Design of the pouch was
• Permit Fecal material to Accumulate
• Emptied at the Patient’s Convenience Several times a day.
• Inserting a tube at the Level of Stoma into the Reservoir to Release its Contents.
• Indication : Surgical rescue option following failed IPAA
• Major complications include Valve Dysfunction, the most common of which is valve de-intussusception

125. POSTOPERATIVE COMPLICATIONS
• Septic Complications
• Anastomotic Leak
• Abscess
• Fistulas
• Non-Septic Sequelae
• Intestinal Obstruction
• Stricture
• Cuffitis
• Pouchitis

126. POUCHITIS
• M/C complication following restorative proctocolectomy - 16% to 48%.
• More common in UC with primary sclerosing cholangitis.
• Other extraintestinal manifestations a/w 10-fold increase in risk after 5 yrs follow up.
• Mediated by Same Proinflammatory process underlying the Primary diagnosis.
• Symptoms :
• Increase in Fecal Frequency
• Bowel consistency is Looser Secondary to Exudative Inflammation with Blood staining or Mucus.
• Villous Atrophy and Crypt Hyperplasia are classified as Colonic Metaplasia - Response to
Inflammation.

127. Treatment
• Oral metronidazole at a dose of 750 to 1500 mg/day
for 7 to 14 days
• Not responding to Metronidazole :
• cyclic courses of three or four antibiotics, such as
ciprofloxacin, amoxicillin/ clavulanic acid,
erythromycin, and tetracycline, given at weekly
intervals
• Budesonide suppositories (1.5 mg/day)

128. CONCLUSION
• Patients with Ulcerative Colitis - Need High Suspicion of clinician and early diagnosis.
• Patients have Good improvement in symptoms and can be presented with a multitude of
Options when considering surgery.
• Emergency situations and othe important indications for surgery must be considered.
• Ulcerative Colitis - Surgery can Offer 'Cure' . But need appropriate medical and post
operative care.

129. DISTINGUISHING CHARECTERISTIC FEATURES b/w ULCERATIVE COLITIS & CROHN'S DISEASE

135. CONCLUSION
• Uncontrolled Immune Mediated Inflammatory response in Genetically predisposed individuals to a
still Unknown Environmental Trigger that interacts with the Intestinal flora.
• Enormous amount of information emanating from epidemiological studies providing expanded insight
into occurrence, distribution, determinants, and mechanisms of IBD.
• Evaluation, diagnosis, and monitoring of inflammatory bowel disease (IBD) has improved
significantly over the past few decades
• Evolution of serologic markers has improved our understanding of the pathogenesis and natural
history of IBD.
• Advancements in endoscopy and endoscopic scoring systems have improved the accuracy of
diagnosis and the efficacy of surveillance of IBD patients.

136. REFERENCES
• Maingot's Abdominal Operations 13th Edition
• Schwartz Principles of Surgery 11th Edition
• Sabiston Textbook Of Surgery 18th Edition
• Shackelford's Surgery of the Alimentary Tract 8th Edition
• Bailey & Love Textbook of Surgery 27th Edition
• Harrison's Principles of Internal Medicine 20th Edition
• Gastroenterology Clinics of North America Volume 33 , Issue 2
• Russel D.Cohen - Inflammatory Bowel Disease