IBD

1. Inflammatory Bowel Inflammatory Bowel
DiseaseDisease
Crystal M. Byerly, PA-CCrystal M. Byerly, PA-C
Seton Hill University PA ProgramSeton Hill University PA Program
Grant from Centocor, Inc.Grant from Centocor, Inc.

2. Learning ObjectivesLearning Objectives
Describe the disease process of Crohn’s versus Describe the disease process of Crohn’s versus
Ulcerative ColitisUlcerative Colitis
Identify the clinical presentation of a patient Identify the clinical presentation of a patient
with Crohn’s Disease and Ulcerative Colitiswith Crohn’s Disease and Ulcerative Colitis
Discuss the various diagnostic workups and how Discuss the various diagnostic workups and how
they may differentiate Crohn’s from other GI they may differentiate Crohn’s from other GI
ailmentsailments
Select appropriate treatments for a patient with Select appropriate treatments for a patient with
Crohn’s Disease and Ulcerative ColitisCrohn’s Disease and Ulcerative Colitis

3. Inflammatory Bowel DiseaseInflammatory Bowel Disease
Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center, Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,
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4. IBDIBD= Crohn’s Disease and = Crohn’s Disease and
Ulcerative ColitisUlcerative Colitis
Both are chronic inflammatory disorders of the GI tract Both are chronic inflammatory disorders of the GI tract
that currently have no real cure.that currently have no real cure.
disorders of unknown cause involving genetic and disorders of unknown cause involving genetic and
immunological influence on the gastrointestinal tract's immunological influence on the gastrointestinal tract's
ability to distinguish foreign from self-antigens.ability to distinguish foreign from self-antigens.

5. Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,
www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.

6. Ulcerative ColitisUlcerative Colitis

7. Disease Process of Ulcerative ColitisDisease Process of Ulcerative Colitis
Disorder in which Disorder in which
inflammation affects the inflammation affects the
mucosa and submucosa mucosa and submucosa
of the colon and terminal of the colon and terminal
ileum.ileum.
Peak incidence in ages Peak incidence in ages
15-30 years old.15-30 years old.
Artwork is reproduced, with permission, from www.medicinenet.inc all rights
reserved. 2007

8. Ulcerative ColitisUlcerative Colitis
Ulcerative ProctitisUlcerative Proctitis refers to inflammation that is limited refers to inflammation that is limited
to the rectum.to the rectum.
 In many patients with ulcerative proctitis, mild In many patients with ulcerative proctitis, mild
intermittent rectal bleeding may be the only symptom.intermittent rectal bleeding may be the only symptom.
–If no bloody stools (ever), its not UCIf no bloody stools (ever), its not UC
Other symptoms:Other symptoms:
–rectal pain rectal pain
–urgency urgency
sudden feeling of having to defecate and a need to rush to the sudden feeling of having to defecate and a need to rush to the
bathroom for fear of soilingbathroom for fear of soiling
–tenesmus tenesmus
ineffective, painful urge to move one's bowels ineffective, painful urge to move one's bowels

9. Ulcerative ColitisUlcerative Colitis
Universal ColitisUniversal Colitis or or PancolitisPancolitis refers to refers to
inflammation affecting the entire coloninflammation affecting the entire colon
–right colon, left colon, transverse colon and the right colon, left colon, transverse colon and the
rectum. rectum.
Symptoms of Pancolitis include:Symptoms of Pancolitis include:
– bloody diarrheabloody diarrhea
– abdominal pain and cramps abdominal pain and cramps
–weight lossweight loss
– fatigue fatigue
–fever fever
–night sweatsnight sweats
–Extraintestinal disease Extraintestinal disease

10. Ulcerative ColitisUlcerative Colitis
Clinical presentation:Clinical presentation:
A 26 year old woman gives a history of A 26 year old woman gives a history of
increasing abdominal pain with blood and mucus increasing abdominal pain with blood and mucus
in the stool. in the stool.
The plain film shows visible gas-filled colon with The plain film shows visible gas-filled colon with
variable mucosal thickening, giving typical variable mucosal thickening, giving typical
thumb-printingthumb-printing appearance. appearance.
The colon appears shorter than normal and has The colon appears shorter than normal and has
lost its usual haustral pattern giving the lost its usual haustral pattern giving the lead lead
pipe appearancepipe appearance term. term.

11. Classifications of UC SeverityClassifications of UC Severity
MILDMILD
–< 4 loose BM/day with small amounts of blood< 4 loose BM/day with small amounts of blood
–No sign of toxicity: No fever or tachycardiaNo sign of toxicity: No fever or tachycardia
–Mild anemiaMild anemia
– Normal ESR<30 mm/hrNormal ESR<30 mm/hr
MODERATEMODERATE
–> 4 stools/d> 4 stools/d
–Minimal signs of toxicityMinimal signs of toxicity
SEVERESEVERE
–>6 bloody stools/d>6 bloody stools/d
–Fever, tachycardiaFever, tachycardia
–AnemiaAnemia
–Elevated ESRElevated ESR
FULMINANTFULMINANT
–>10 stools/d with continuous bleeding>10 stools/d with continuous bleeding
–ToxicityToxicity
–Abdominal tenderness/distentionAbdominal tenderness/distention
–Transfusion requirement due to anemiaTransfusion requirement due to anemia
–Colonic dilatation on xrayColonic dilatation on xray

12. Complications of Severe UCComplications of Severe UC
Toxic MegacolonToxic Megacolon
–The inflammatory complications extend beyond the The inflammatory complications extend beyond the
submucosa into the muscularis, the colon dilates and submucosa into the muscularis, the colon dilates and
produces a toxic patientproduces a toxic patient
HR>120bpm, fever, hypotension, electrolyte disturbances, HR>120bpm, fever, hypotension, electrolyte disturbances,
MS changes, abdominal distentionMS changes, abdominal distention
Perforation of colonPerforation of colon
–As a result of toxic megacolon or severe UC As a result of toxic megacolon or severe UC
Strictures Strictures
–12% patients will develop between 5-25 yrs. after dx12% patients will develop between 5-25 yrs. after dx

13. Crohn’s DiseaseCrohn’s Disease

14. Crohn’s Crohn’s
Three Main Patterns of DistributionThree Main Patterns of Distribution
40% Ileum and Cecum40% Ileum and Cecum
30% confined to small intestine30% confined to small intestine
25% of colon only25% of colon only
–2/3 pancolonic2/3 pancolonic
–1/3 segmental1/3 segmental
About 80% of patients have small bowel involvementAbout 80% of patients have small bowel involvement

15. Crohn’s DiseaseCrohn’s Disease
Can involve any part of the GI tract.Can involve any part of the GI tract.
The esophagus, mouth, and liver can also The esophagus, mouth, and liver can also
become inflamed.become inflamed.
Peak incidence 15-25 y.o, but often <10 Peak incidence 15-25 y.o, but often <10
yrs. oldyrs. old

16. Crohn’s Disease SymptomsCrohn’s Disease Symptoms
Diarrhea Diarrhea
Abdominal painAbdominal pain
–From serosal inflammationFrom serosal inflammation
–Intermittent partial obstructionsIntermittent partial obstructions
Weight lossWeight loss
–Can be up to 20% of body weightCan be up to 20% of body weight
–Malabsorption and decreased oral intakeMalabsorption and decreased oral intake
Relapsing and remitting symptoms that Relapsing and remitting symptoms that
can spontaneously improve in 30% casescan spontaneously improve in 30% cases

17. Crohn’s DiseaseCrohn’s Disease
Thickened bowel wall Thickened bowel wall
with secondary narrowing with secondary narrowing
of the bowel lumen of the bowel lumen
occurs.occurs.
Discontinuous Discontinuous (skip)(skip)
lesionslesions are a are a
characteristic feature.characteristic feature.
““Cobblestone”Cobblestone”
appearance comes from appearance comes from
the confluent ulcers.the confluent ulcers.
Transmural thickening Transmural thickening
and ultimate fibrosis and ultimate fibrosis
produces the produces the “string sign” “string sign”
on CT = strictureson CT = strictures..

18. Crohn’s ComplicationsCrohn’s Complications
Extension of a mucosal breach through the intestinal Extension of a mucosal breach through the intestinal
wall into extraintestinal tissue results in:wall into extraintestinal tissue results in:
AbcessesAbcesses
–Occur in 15-20% of patientsOccur in 15-20% of patients
–Most commonly terminal ileum but not exclusivelyMost commonly terminal ileum but not exclusively
FistulasFistulas
–During a Crohn’s pt.’s lifetime ~1/2 will develop a fistulaDuring a Crohn’s pt.’s lifetime ~1/2 will develop a fistula
–83% of fistulas require surgical intervention83% of fistulas require surgical intervention
–can be multiple sites:can be multiple sites:
EnteroentericEnteroenteric
EnterocutaneousEnterocutaneous
EnterovesicalEnterovesical
EnterovaginalEnterovaginal

19. Extraintestinal manifestations of Extraintestinal manifestations of
IBDIBD
Colitic arthritisColitic arthritis
SacroiliitisSacroiliitis
Ankylosing spondylitisAnkylosing spondylitis
Hepatobiliary Hepatobiliary
complicationscomplications
Osteopenia, osteoarthritisOsteopenia, osteoarthritis
Avascular necrosisAvascular necrosis
Renal stonesRenal stones
UTI due to fistulaeUTI due to fistulae
Pyoderma gangrenosumPyoderma gangrenosum
Erythema nodosumErythema nodosum
Sweet syndromeSweet syndrome
UveitisUveitis
EpiscleritisEpiscleritis
DVT/PE, intracranial, DVT/PE, intracranial,
intraocular intraocular
thromboembolic eventsthromboembolic events

20. Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center, Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,
www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.

21. Genetics of IBDGenetics of IBD
IBD is a polygenic disorder. Not all of the IBD is a polygenic disorder. Not all of the
genes have been identified.genes have been identified.
Phenotypes change throughout the course Phenotypes change throughout the course
of diseaseof disease
10-15% of IBD is familial10-15% of IBD is familial
–Smokers get Crohn’sSmokers get Crohn’s
–Nonsmokers get UCNonsmokers get UC

22. ColoRectal Cancer and IBDColoRectal Cancer and IBD
Both CD and UC are known risk factors for Both CD and UC are known risk factors for
colorectal cancer. colorectal cancer.
The risk of development of colorectal cancer is The risk of development of colorectal cancer is
related to the severity and duration of the related to the severity and duration of the
disease. disease.
IBD patients should undergo colonoscopic IBD patients should undergo colonoscopic
surveillance for epithelial dysplasia, a precursor surveillance for epithelial dysplasia, a precursor
to cancer, at routine intervals. to cancer, at routine intervals.
–Surveillance should be performed every 1–2 years in Surveillance should be performed every 1–2 years in
patients with 8-10 years duration of disease patients with 8-10 years duration of disease
–annually in those with disease history of over 15 annually in those with disease history of over 15
yearsyears

23. Diagnosing IBDDiagnosing IBD

24. Differential Diagnosis of IBDDifferential Diagnosis of IBD
Chronic infectious colitisChronic infectious colitis
Ischemic colitisIschemic colitis
DiverticulitisDiverticulitis
Irritable Bowel SyndromeIrritable Bowel Syndrome
Small Bowel Bacterial OvergrowthSmall Bowel Bacterial Overgrowth
Crohn’s DiseaseCrohn’s Disease
Ulcerative ColitisUlcerative Colitis
Colon CancerColon Cancer

25. Current Diagnostic Tools for Initial Current Diagnostic Tools for Initial
IBD DiagnosisIBD Diagnosis
History and Physical History and Physical
Exam=clinical Exam=clinical
suspicionsuspicion
Stool studiesStool studies
ColonoscopyColonoscopy
Serology studiesSerology studies
Small Bowel Small Bowel
Series/SBFTSeries/SBFT
Barium EnemaBarium Enema
WCE=Wireless WCE=Wireless
Capsule EndoscopyCapsule Endoscopy
EUS=Endoscopic EUS=Endoscopic
UltrasoundUltrasound
Pelvic MRIPelvic MRI
MRI EnterographyMRI Enterography
CT EnterographyCT Enterography
PET ScanPET Scan
WBC ScanningWBC Scanning

26. There is no ONE single test to dx There is no ONE single test to dx
IBD.IBD.
Historically the two main tests used:Historically the two main tests used:
–ColonoscopyColonoscopy
–SBFTSBFT
Lab studies have become an additional Lab studies have become an additional
tooltool

27. Common Bloodwork Common Bloodwork
in diagnosing IBDin diagnosing IBD
C-Reactive ProteinC-Reactive Protein
–Inflammation reflects inflammatory disease Inflammation reflects inflammatory disease
activity initiallyactivity initially
–Can be used as a marker to treatment Can be used as a marker to treatment
responseresponse
pANCApANCA= Anti-neutrophil cytoplasmic = Anti-neutrophil cytoplasmic
antibody with perinuclear stainingantibody with perinuclear staining
ASCAASCA= anti-saccharomyces cerevisiae= anti-saccharomyces cerevisiae

28. Differentiating type of IBDDifferentiating type of IBD
LAB TESTLAB TESTSENSITIVITYSENSITIVITYSPECIFICITYSPECIFICITYTYPE IBDTYPE IBD
+ pANCA+ pANCA50-65%50-65% 85-92%85-92% UCUC
+ASCA+ASCA 55-61%55-61% 88-95%88-95% CROHN’SCROHN’S
+pANCA+pANCA & &
ASCA -ASCA -
44-57%44-57% 81-97%81-97% UCUC
-pANCA-pANCA & &
ASCA+ASCA+
38-56%38-56% 94-97%94-97% CROHN’SCROHN’S
Sandborn WJ et al, Inflamm Bowel Dis 2001;7:192-201
Peeters M et al, AM J Gastroenterology 2001; 96:730-4

29. Immune Markers being Immune Markers being
studied for diagnosing IBDstudied for diagnosing IBD
Anti-12Anti-12 = antibody to pseudomonas = antibody to pseudomonas
flourescens transcription factorflourescens transcription factor
Omp COmp C = antibody to Escherichia coli = antibody to Escherichia coli
outer membrane porin Couter membrane porin C
PABPAB = Pancreatic antibodies = Pancreatic antibodies
Fecal lactoferrinFecal lactoferrin = fecal inflammation iron- = fecal inflammation iron-
binding glycoproteinbinding glycoprotein
Anti-flagellinAnti-flagellin = CBir 1 antigen = CBir 1 antigen

30. IBD ManagementIBD Management
Management Management
can be divided can be divided
intointo
–Acute Acute
exacerbationexacerbation
–Maintenance of Maintenance of
remission: remission:
conventional conventional
and biologic and biologic
therapiestherapies
–SurgicalSurgical
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Gastroenterology and Hepatology Resource Center, Gastroenterology and Hepatology Resource Center,
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reserved.reserved.

31. Acute Management of IBDAcute Management of IBD
IV->PO Hydrocortisone or MethylprednisoloneIV->PO Hydrocortisone or Methylprednisolone
–Fast symptom reliefFast symptom relief
–Not advised for prolonged use (120 day max)Not advised for prolonged use (120 day max)
–No mucosal healingNo mucosal healing
–Does not improve long term surgery ratesDoes not improve long term surgery rates
Cipro +/- Metronidazole Cipro +/- Metronidazole
–Effectiveness arguable but often seen used anywayEffectiveness arguable but often seen used anyway
IV Cyclosporine 2-4 mg/kgIV Cyclosporine 2-4 mg/kg
–Effective for induction of remission but not long-term Effective for induction of remission but not long-term
maintenancemaintenance
Bowel RestBowel Rest
Rectal +/- Oral 5-ASA; SulfasalazinesRectal +/- Oral 5-ASA; Sulfasalazines

32. Chronic Therapy of IBDChronic Therapy of IBD
Goals: Goals:
–remission of bowel inflammationremission of bowel inflammation
–1-4 BM/day with mucosal healing1-4 BM/day with mucosal healing
–Prevention of strictures, fistulas, other Prevention of strictures, fistulas, other
complicationscomplications
–Prevention of need for surgeryPrevention of need for surgery
Hopefully feeling NORMAL, not just betterHopefully feeling NORMAL, not just better

33. CorticosteroidsCorticosteroids
Severe IBD with hospitalization should be Severe IBD with hospitalization should be
treated with IV steroids for rapid symptom treated with IV steroids for rapid symptom
relief.relief.
Not a long-term solutionNot a long-term solution
Convert IV to PO then taper off advisedConvert IV to PO then taper off advised
Steroid dependence occurs in 28% pts.Steroid dependence occurs in 28% pts.
Should be used in combination with AZA/ Should be used in combination with AZA/
6-MP +/- cyclosporine for severe IBD 6-MP +/- cyclosporine for severe IBD
symptomssymptoms

34. Cyclosporine Cyclosporine
IV dosing effective for induction of IV dosing effective for induction of
remission in severe UCremission in severe UC
Little efficacy for maintenance of Little efficacy for maintenance of
remissionremission
No data on mucosal healingNo data on mucosal healing
Nephrotoxicity, seizures rare SENephrotoxicity, seizures rare SE

35. Mesalamines:Mesalamines:
5-ASA/Aminosalicylates5-ASA/Aminosalicylates
Aminosalicylates Aminosalicylates has been the mainstay of has been the mainstay of
therapy because of its anti-inflammatory therapy because of its anti-inflammatory
activities. activities.
50-70% response in high doses for UC.50-70% response in high doses for UC.
Some mucosal healing found.Some mucosal healing found.
Excellent safety profile.Excellent safety profile.
Not always beneficial. Be quick to move on if Not always beneficial. Be quick to move on if
patient is not seeing benefit.patient is not seeing benefit.
No fistula closure benefits to treatment found.No fistula closure benefits to treatment found.

36. Mesalamines continuedMesalamines continued
Different formulations have been released and Different formulations have been released and
are thought to target specific regions of the are thought to target specific regions of the
bowel in oral and rectal formulations:bowel in oral and rectal formulations:
Sulfasalazine and BalsalazideSulfasalazine and Balsalazide
–Are primarily released in the colonAre primarily released in the colon
–Folic acid supplement advised with sulfasalazineFolic acid supplement advised with sulfasalazine
Dipentum and AsacolDipentum and Asacol
–Releases in the distal ileum and colonReleases in the distal ileum and colon
PentasaPentasa
–Releases in the distal colonReleases in the distal colon
RowasaRowasa
–Primarily effective in the distal colon and rectumPrimarily effective in the distal colon and rectum

37. ThiopurinesThiopurines
Azathioprine/ 6-MP (mercaptopurine)Azathioprine/ 6-MP (mercaptopurine)
– up to 6-12 weeks until effectiveup to 6-12 weeks until effective
–Has been shown beneficial in both induction and Has been shown beneficial in both induction and
maintenance of remissionmaintenance of remission
–NOT as beneficial a 5-ASA for UCNOT as beneficial a 5-ASA for UC
–Not as many trials for data with UC as with CDNot as many trials for data with UC as with CD
–Some chance of fistula closure with useSome chance of fistula closure with use
–Must monitor CBC and LFTs with useMust monitor CBC and LFTs with use
Bone marrow suppressionBone marrow suppression
Liver toxicity possibleLiver toxicity possible

38. MethotrexateMethotrexate
Used with patients who are allergic or Used with patients who are allergic or
unresponsive to trial of Thiopurines (6-MP or unresponsive to trial of Thiopurines (6-MP or
AZA) at adequate dosing.AZA) at adequate dosing.
Has been shown to induce and maintain Has been shown to induce and maintain
remission. remission.
Little data to prove fistula closure on this drugLittle data to prove fistula closure on this drug
1mg Folate supplementation advised1mg Folate supplementation advised
Monitor CBC and LFTsMonitor CBC and LFTs
–Bone marrow suppressionBone marrow suppression
–Risk of hypersensitivity pneumonitisRisk of hypersensitivity pneumonitis
–Liver toxicityLiver toxicity

39. Biologic Therapy –vs- Conventional Biologic Therapy –vs- Conventional
Therapy in IBDTherapy in IBD
Conventional therapyConventional therapy
–Aimed at symptom Aimed at symptom
reliefrelief
–Reduces Reduces
hospitalizationshospitalizations
–Doesn’t reduce long Doesn’t reduce long
term surgery ratesterm surgery rates
–Doesn’t maintain Doesn’t maintain
mucosal healingmucosal healing
Biologic therapyBiologic therapy
–25-50% remission sx 25-50% remission sx
at 1 monthat 1 month
–Reduces Reduces
hospitalizationshospitalizations
–Lowers surgery ratesLowers surgery rates
–Maintains long term Maintains long term
mucosal healingmucosal healing
–Fistula closures more Fistula closures more
oftenoften

40. Biologic Therapy with CDBiologic Therapy with CD
If patients are not able to be in complete If patients are not able to be in complete
remission on Azathioprine with mucosal remission on Azathioprine with mucosal
healing, and off steroids, the clinician healing, and off steroids, the clinician
should consider starting biologic therapy should consider starting biologic therapy
and discuss this with their patient as an and discuss this with their patient as an
effective treatment option.effective treatment option.

41. Biologic TherapyBiologic Therapy
Infliximab is currently approved for use in Infliximab is currently approved for use in
Crohn’s Disease.Crohn’s Disease.
–CD mucosal healing has been confirmed with CD mucosal healing has been confirmed with
endoscopyendoscopy
–Lower rates of hospitalization and surgeryLower rates of hospitalization and surgery
–Lessened fistulas Lessened fistulas
–800,000 patients treated with NO infusion 800,000 patients treated with NO infusion
reaction deathsreaction deaths
–Some delayed hypersensitivity reactionsSome delayed hypersensitivity reactions

42. AdalimumabAdalimumab
Recombinant human IgG1 monoclonal Recombinant human IgG1 monoclonal
antibody directed against tumor necrosis antibody directed against tumor necrosis
factorfactor
Approved for tx of CDApproved for tx of CD
Subcutaneous injectionSubcutaneous injection

43. Combination Therapy for Crohn’sCombination Therapy for Crohn’s
AZA + Biologic combinationsAZA + Biologic combinations
–Slightly higher benefitSlightly higher benefit
–Higher blood concentrations with Higher blood concentrations with
demonstrated lower C-Reactive Proteindemonstrated lower C-Reactive Protein
–Tolerated wellTolerated well
–Lower rates of antibody formation to the drugLower rates of antibody formation to the drug

44. Biologic therapy with UCBiologic therapy with UC
Infliximab approved for moderate-severe Infliximab approved for moderate-severe
Ulcerative Colitis who have had Ulcerative Colitis who have had
inadequate response to steroids and AZA.inadequate response to steroids and AZA.
–Best results in overall sx reduction and healing Best results in overall sx reduction and healing
with remission for UC.with remission for UC.
Future therapiesFuture therapies
–VisilizumabVisilizumab
–MLN-02MLN-02
–NatalizumabNatalizumab

45. IBD Surgery TreatmentIBD Surgery Treatment

46. Crohn’s SurgeryCrohn’s Surgery
Probability of needing surgery increases Probability of needing surgery increases
with timewith time
By 30 years post-diagnosis nearly 100% of By 30 years post-diagnosis nearly 100% of
patients will have had one surgerypatients will have had one surgery
Previous to biologic therapy the rate of Previous to biologic therapy the rate of
surgery increased 10% per year with CDsurgery increased 10% per year with CD
Studies are looking at ways to predict Studies are looking at ways to predict
future surgery needs based on new tx and future surgery needs based on new tx and
serologies.serologies.

47. Surgical Therapies with FistulaSurgical Therapies with Fistula
I & D for abcessesI & D for abcesses
Seton- keeps open with permanent suture Seton- keeps open with permanent suture
material to prevent recurrent abcess.material to prevent recurrent abcess.
Fistulectomy-currative with superficial Fistulectomy-currative with superficial
fistulafistula
Diverting surgical proceduresDiverting surgical procedures
Rectal advancement flap or sleeveRectal advancement flap or sleeve
Proctectomy or total proctocolectomyProctectomy or total proctocolectomy

48. Ileal Resection in Crohn’s DiseaseIleal Resection in Crohn’s Disease
Indications:Indications:
–Failure of medical therapyFailure of medical therapy
–Recurrent obstructionRecurrent obstruction
–PerforationPerforation
–FistulaFistula
–AbcessAbcess
–HemorrhageHemorrhage
–Growth retardation (children)Growth retardation (children)
–carcinomacarcinoma

49. Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center, Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,
www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.

50. Post-Op Recurrence of CDPost-Op Recurrence of CD
Commonly see recurrence near the Commonly see recurrence near the
ileocolonic anastomosis from previous ileocolonic anastomosis from previous
surgery.surgery.
Endoscopic recurrence is found as high as Endoscopic recurrence is found as high as
73% only 1 year later.73% only 1 year later.
Prevention of recurrences usingPrevention of recurrences using
–Mesalamine/5-ASA, 6-MP, probiotics Mesalamine/5-ASA, 6-MP, probiotics
(lactobacillus), metronidazole(lactobacillus), metronidazole

51. Ulcerative Colitis Surgery Ulcerative Colitis Surgery
IndicationsIndications
ABSOLUTE ABSOLUTE
INDICATIONS:INDICATIONS:
–HemorrhageHemorrhage
–PerforationPerforation
–Cancer or dysplasiaCancer or dysplasia
–Unresponsive acute sxUnresponsive acute sx
RELATIVE RELATIVE
INDICATIONS:INDICATIONS:
–Chronic intractabilityChronic intractability
–Steroid dependencySteroid dependency
–Growth retardationGrowth retardation
–Systemic complications Systemic complications
associated with UCassociated with UC

52. Surgery types with UCSurgery types with UC
IPAA = Ileal pouch-anal anastomosisIPAA = Ileal pouch-anal anastomosis
–Gold standard as “cure” but not without its Gold standard as “cure” but not without its
own complicationsown complications
Incontinence, diarrhea, sexual dysfunction, Incontinence, diarrhea, sexual dysfunction,
decreased fertility, pouchitis, cuffitisdecreased fertility, pouchitis, cuffitis
Conventional Ileostomy (Brooke)Conventional Ileostomy (Brooke)
Continent ileostomy (Koch pouch)Continent ileostomy (Koch pouch)
Ileorectal anastomosisIleorectal anastomosis

53. Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center, Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,
www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.www.hopkins-gi.org,copyright 2006, Johns Hopkins University, all rights reserved.

54. Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center, Artwork is reproduced, with permission, from the Johns Hopkins Gastroenterology and Hepatology Resource Center,
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55. ConclusionConclusion
Review of Learning ObjectivesReview of Learning Objectives
Describe the disease process of Crohn’s versus Describe the disease process of Crohn’s versus
Ulcerative ColitisUlcerative Colitis
Identify the clinical presentation of a patient Identify the clinical presentation of a patient
with Crohn’s Disease and Ulcerative Colitiswith Crohn’s Disease and Ulcerative Colitis
Discuss the various diagnostic workups and how Discuss the various diagnostic workups and how
they may differentiate Crohn’s from other GI they may differentiate Crohn’s from other GI
ailmentsailments
Select appropriate treatments for a patient with Select appropriate treatments for a patient with
Crohn’s Disease and Ulcerative ColitisCrohn’s Disease and Ulcerative Colitis

56. Thank YouThank You