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PATHOLOGY OF INFLAMMATORY BOWEL DISEASE
AND DIVERTICULAR DISEASE OF THE COLON
Moderator: Dr. Zelalem Assefa
(Consultant Colorectal and General Surgeon)
Presenter: Dr. fikreyohanis .s (GSR1)
Aug , 2021
OUTLINE
INFLAMMATORY BOWEL
DISEASE(IBD)
 Introduction
 Epidemiology
 Etiology and Pathophysiology
 Extra Intestinal Manifestation
of IBD
 Crohn’s Disease(CD)
 Ulcerative Colitis(UC)
 Indetereminate Colitis
DIVERTICULAR DISEASE OF
THE COLON (DDC)
 Introduction
 Epidemiology
 Pathophysiology
 Uncomplicated DDC
 Complicated DDC
Inflammatory Bowel Disease
• IBD is a chronic condition resulting from complex interactions between
intestinal microbiota and host immunity in genetically predisposed
individuals resulting an inappropriate mucosal immune activation
It comprises :
» Ulcerative colitis
» Crohn’s disease, and
» Indeterminate colitis
Epidemiology:
• UC - 8 to15 /100,000 and CD - 1 to 5/100,000 in USA and Northern
Europe, Lower in Asia, Africa and South America
Bimodal age distribution
• UC - Peaks in 3rd - 7th decades
• CD - peaks in 15- 30 then 60 -70 years
• Higher among Caucasians and White than Blacks, Hispanics and
Asians
Pathophysiology
 Under physiologic conditions, homeostasis normally exists between
• The commensal microbiota
• Epithelial cells
• Immune cells within the tissues
A consensus hypothesis is that each of these three major host
compartments that function together are affected by
 specific environmental (e.g., smoking, antibiotics, enteropathogens)
 genetic factors that, in a susceptible host, cumulatively and interactively
disrupt homeostasis
Genetics
• Risk for disease is increased when there is an affected family
member
• In Crohn disease, the concordance rate for monozygotic
twins is approximately 50% and only 16% in UC
• over 200 genes associated with IBD identified Among
these, NOD2, ATG16L1 and IRGM
• The presence of NOD2 gene on IBD1 locus on chromosome
16 has been linked to Crohn’s disease
• Persons with allelic variants on both have a 40-fold relative
risk of Crohn’s disease
COMMENSAL MICROBIOTA AND IBD
• The endogenous commensal microbiota within the intestines plays a
central role in the pathogenesis of IBD
• The establishment and maintenance of the intestinal microbiota
composition and function is under the control of host, environmental &
genetic (e.g., NOD2)
• The commensal microbiota in patients with both UC and CD is
demonstrably different from non-affected individuals, a state of
dysbiosis
DEFECTIVE IMMUNE REGULATION IN IBD
• The mucosal immune system does not normally elicit an inflammatory
immune response to luminal contents due to oral (mucosal) tolerance
• Oral tolerance may be responsible for the lack of immune
responsiveness to dietary antigens and the commensal microbiota in the
intestinal lumen
• In IBD this suppression of inflammation is altered, leading to
uncontrolled inflammation. The mechanisms of this regulated immune
suppression are incompletely known
Cont…
3/25/2024 Tesfaye.N 10
• Epithelial defects - a variety of epithelial defects have
been described in Crohn disease, ulcerative colitis. For
example, defects in intestinal epithelial tight barrier function
occur in patients with Crohn
CROHN’S DISEASE
• Crohn’s disease is a chronic, idiopathic transmural
inflammatory disease with skip lesions that may affect any
part of the GI tract,
 Small intestine alone - 30% of cases
 Small intestine and colon - 40%
 The colon alone - 30%
• CD may involve the duodenum, stomach, esophagus,
GROSS PATHOLOGY
 The earliest lesion characteristic of Crohn’s disease is the aphthous
ulcer. These superficial ulcers are up to 3 mm in diameter and are
surrounded by a halo of erythema. In the small intestine, aphthous ulcers
typically arise over lymphoid aggregates
 As disease progresses, aphthae coalesce into larger, stellate shaped
ulcers. Linear or serpiginous ulcers may form when multiple ulcers fuse
in a direction parallel to the longitudinal axis of the intestine. With
transverse coalescence of ulcers, a cobblestone appearance of the
mucosa may arise
 A pathognomonic feature of Crohn’s disease that is grossly evident
and helpful in identifying affected segments of intestine during surgery is
the presence of fat wrapping, which represents encroachment of
mesenteric fat onto the serosal surface of the bowel
Features that allow for differentiation between Crohn’s disease
of the colon and ulcerative colitis include
 The layers of the bowel wall affected in UC is limited to the
mucosa and sub mucosa but may involve the full-thickness in
Crohn’s disease
 The longitudinal extent of inflammation is continuous and
characteristically affects the rectum in UC but may be
discontinuous and spare the rectum in Crohn’s disease
Microscopic feature
 crypt abscess
 distortion of mucosal architecture
 Paneth cell metaplasia
 Non- caseating granulomas(hallmark)
- only found in 35 %
Clinical presentation CD
Depending on :-
o The segment of intestine involved
o Features of the disease:
 Fibrostenotic
 Inflammatory
 fistulizing
Fibrostenotic patterns
 occurs in any location, most commonly in the terminal ileum
 patients present with obstructive symptoms such as nausea,
vomiting, and decreased oral intake
 medical management is unsuccessful and surgical
intervention is required
Inflammatory
 It is characterized by mucosal ulceration and bowel wall
thickening
 This pattern often gives rise to obstructive symptoms in the
small intestine and diarrhea in the colon
 Inflammatory pattern is much more likely to respond to
medical therapy
penetrating or fistulizing
• Patients may be completely asymptomatic, as in the case of
many entero-enteral fistulas, present with anorectal
abscesses or fistulas
• Symptom depend on Involvement of the secondarily organ –
» recurrent UTI or pneumaturia
» vaginal discharge
» diarrhea
» cutaneous feculent drainage
Classification of CD
ILEOCOLITIS
Terminal ileum is the most common site of inflammation
o presented with -:
 Right lower quadrant pain and Palpable mass
 Diarrhea
 Fever
 Leukocytosis
 Pain is usually colicky relieved by defecation
 Weight loss
o persistent inflammation, gradually progresses to fibrostenotic
narrowing , stricture and chronic bowel obstruction
o Severe inflammation may lead to localized wall thinning, with
microperforation and fistula formation
JEJUNOILEITIS
• Extensive inflammatory disease is associated with a loss of
digestive and absorptive surface, resulting in malabsorption
and steatorrhea
• Intestinal malabsorption can cause anemia,
hypoalbuminemia, hypocalcemia, hypomagnesemia,
coagulopathy
COLONIC
 Distribution
– 1/3 total colonic involvement,
– 40% segmental disease
– 30% left-sided only
 Patients with colitis present with low grade fevers, malaise,
diarrhea, crampy abdominal pain, and sometimes
hematochezia
Anorectal
• perianal involvement is clearly more common in those with
concomitant rectal or colonic disease
• CD patients may also manifest
 edematous (elephant ear) skin tags
 blue discoloration of the anus
 abscesses and fistulas that are often recurrent, multiple
INVESTIGATION
Serologic marker
• The most commonly tested antibodies are (pANCA) and (ASCA)
• ASCA+/pAaNCA–, is associated with a diagnosis of Crohn’s disease
• ASCA–/pANCA+, correlates with ulcerative colitis
• Although these antibody tests have high specificity, their use has been
hampered by low test sensitivities
Plain Films
 plain films is often a routine part of the diagnosis
 An abdominal plain film may help in the setting of –
» Bowel obstruction
» To exclude toxic megacolon, or
» To evaluate for pneumoperitoneum
CONTRAST STUDIES
 barium studies helped diagnose CD by identifying longitudinal and
transverse linear ulcerations that create cobblestone and nodular
patterns, skip lesions, fistulas, and strictures
 with newer studies such as CT and MRE traditional barium studies are
becoming less favorable
Computed Tomography
 In many centers, CT has now largely replaced the barium studies
 with the added ability to identify the extent of the disease and
involvement of surrounding structures, manifested by
 segmental bowel thickening
 mesenteric fat stranding
 intra-abdominal fluid &
 presence of fistula
Magnetic Resonance Imaging
• MRE is over 85% accurate in predicting stenosis, abscess, and fistula
• Its sensitivity (85–90%), specificity (100%), and negative predictive
value (77%)
• MRI has also been particularly useful in the evaluation of complex
perianal fistulas seen in CD
Endoscopy
• To identify the extent and severity of the disease and perform biopsies to
aid in diagnosis
• Endoscopic evaluation includes colonoscopy,
esophagogastroduodenoscopy (EGD), enteroscopy, and capsule
endoscopy
Ulcerative colitis
• It is characterized by recurring episodes of inflammation
limited to the mucosal layer of the colon
• It commonly involves the rectum and may extend in a proximal
and continuous fashion to involve other parts of the colon
Gross pathology
 Early UC - the mucosa grossly appear edematous, with confluent
erythema and a loss of vascular markings
 Intermediate - the mucosa will develop granularity with micropurulence
and bleeding
 Advanced UC - will be marked by pseudo-polyp formation, deep
ulcerations, gross purulence, mucosal bridging, and varied mucosal
thickness
Microscopic feature
• Early disease - characterized by mucosal inflammation, crypt distortion,
goblet cell mucin depletion, and vascular congestion
• Intermediate disease - is associated with crypt abscesses and loss of
mucosa with preservation of the crypts themselves
• Advanced disease- hallmarks are Crypt destruction, pseudopolyps, and
deeper invasion of inflammation
• It is in late disease where we tend to identify dysplasia;
however, it can only be interpreted when identified in non-
inflamed bowel, as many dysplastic features are similar to
inflammation
• The risk of colorectal carcinoma among UC patients is approximately
3.7%, with pancolitis conferring an even higher risk of 5.4%
• The same study found the cumulative risk of colorectal carcinoma by
decade was 2% at 10 years, 8% at 20 years, and18% at 30 years
Clinical Manifestations
Signs and symptoms depend on the severity and location
The most common findings are -:
 Blood and mucus in the stools
 Tenesmus
 Urgency
 Increased stool frequency
 Fecal incontinence, and
 pain with defecation
 Fecal incontinence
systemic symptoms including-
• fever, fatigue, weight loss, and anemia from blood loss
Physical examination
Mild disease- it is often normal
Moderate to severe UC - have abdominal tenderness, fever,
hypotension, tachycardia, and pallor, evidence of blood on DRE
DIAGNOSIS
Serologic Testing
 CRP and ESR are the only two widely used tests for assessing general
systemic inflammation
 pANCA and ASCA, may help differentiate CD from UC
 pANCA is more frequently identified in UC patients(50–70% of UC vs.
20–30% of CD)
 ASCA is more frequently associated with CD, although it may be present
in 10 to 15% of UC patients as well
Endoscopy
 Endoscopy is the GOLD STANDARD for diagnosis of UC
 Colonoscopic examination alone is generally enough to diagnose UC ,
allows for tissue biopsy as well as assessment of the gross appearance
and specific pattern of inflammation
 The entire extent of the disease process can effectively be surveyed
Mucosal Biopsies
• During the procedure, multiple biopsies are necessary for diagnosing UC
and from six segments (the terminal ileum, the ascending, transverse,
descending and sigmoid colon and the rectum) should be obtained
Plain Film X-Rays
 X-rays still play a role when considering the patient who presents acutely
with abdominal pain
 We may see presence of free air or toxic megacolon
CT- SCAN
In UC, the indications for CT enterography and colonography are
currently
• strictures precluding endoscopic assessment
• patients with severe comorbidities where colonoscopy is contraindicated
• It also allows excluding small bowel involvement for the differential
diagnosis of CD or in the case of indeterminate colitis
Magnetic Resonance
• The role of MRI in IBD is still evolving. While less efficient
and more costly than CT for an abdominal survey
Indetereminate Colitis
• In 15% of patients with IBD, differentiating UC from CD is impossible
“indeterminate colitis”
• Their symptoms similar to ulcerative colitis
• Endoscopic and pathologic findings usually include features common to
both diseases
Serologic markers have been employed to differentiate UC from CD
• pANCA- 60% to 70% in UC, compared to 2% to 28% in CD
• ASCA-39% to 69% in CD, but only 5% to 15% of UC
Diverticular Disease of the Colon
• A diverticulum is a sac-like protrusion of the colonic wall
• Diverticulosis is defined by the presence of diverticula without
inflamation
• Diverticular disease - is defined as clinically significant and
symptomatic diverticulosis due to diverticular bleeding, diverticulitis,
segmental colitis
• The majority of colonic diverticula are false diverticulum which
the mucosa and muscularis mucosa have herniated through
the colonic wall
• These diverticula occur at the teniae coli, at points where
nutrient artery penetrate the colonic wall
EPIDEMOLOGY
The distribution of diverticulosis within the colon varies by geography
 Western and industrialized nations have prevalence rates of 50 %
above the age of 50
• Approximately 95 % of patients with diverticula have sigmoid diverticula
 In Asia, the prevalence of diverticulosis is between 13 and 25 % and
diverticulosis is predominantly right-sided
Pathophysiology
MORPHOLOGY
• Colonic diverticula are small, flasklike outpouchings, usually 0.5-1 cm in
diameter
• They are most common in the sigmoid colon, but other regions of the
colon may be affected
• Colonic diverticula have a thin wall composed of a flattened or atrophic
mucosa, compressed submucosa, and attenuated muscularis propria
RISK FACTORS
 Diet - Low fiber, high fat, and red meat
 Physical inactivity
 Obesity
Clinical Features
Uncomplicated Diverticulitis
 It is characterized by LLQ pain and tenderness
 CT findings include pericolic soft tissue stranding, colonic wall
thickening, and/or phlegmon
 Most patients will respond to outpatient therapy with broad-spectrum oral
antibiotics (7 to 10 D) and a low-residue diet
 10% to 20% of patients with more severe pain, tenderness, fever, and
leukocytosis are treated in the hospital with parenteral antibiotics
Complicated Diverticulitis
Abscess
 It occur in 17 % of patients hospitalized with acute diverticulitis
 The symptoms of a diverticular abscess are similar to acute diverticulitis
 CT is the imaging modality of choice
 It should be suspected in patients with uncomplicated diverticulitis who
have no improvement of symptoms despite of antibiotic treatment
FISTULA
 Acute diverticulitis may result in the formation of a fistula between the
colon and adjacent viscera
 Fistulas most commonly involve the bladder, and may have
pneumaturia, fecaluria, or dysuria
 Patients with a colovaginal fistula may report vaginal passage of feces or
flatus
Perforation
 Generalized peritonitis may result from rupture of a diverticular abscess
or free rupture of an inflamed diverticulum
 only 1 to 2 % of patients with acute diverticulitis have a perforation, but
mortality rates is about 20 %
 The abdomen is distended and diffusely tender to light palpation. There
is diffuse guarding, rigidity, and rebound tenderness, and bowel sounds
are absent
Hemorrhage
• Bleeding results from erosion of the peri-diverticular arteriole and may
result in massive hemorrhage
• Most significant LGIB occurs in elderly patients is due to diverticulosis
• The exact bleeding source may be difficult to identify, Fortunately, in 80%
of patients, bleeding stops spontaneously
Hinchey classification of Diverticulitis
REFERENCES
• Marvin L. Corman..etal,corman’s Colon And Rectal
Surgery,6th edition
• Jeffrey H. Peters…etal,Shackelford’s Surgery of the
Alimentary Tract,7th edition
• Brunicardi FC, Schwartz’s Principles of Surgery, 11th
edition
• Michael J. …etal,maingot’s Abdominal Surgery,13th
edition
• Uptodate 2018
THANK YOU

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  • 1. PATHOLOGY OF INFLAMMATORY BOWEL DISEASE AND DIVERTICULAR DISEASE OF THE COLON Moderator: Dr. Zelalem Assefa (Consultant Colorectal and General Surgeon) Presenter: Dr. fikreyohanis .s (GSR1) Aug , 2021
  • 2. OUTLINE INFLAMMATORY BOWEL DISEASE(IBD)  Introduction  Epidemiology  Etiology and Pathophysiology  Extra Intestinal Manifestation of IBD  Crohn’s Disease(CD)  Ulcerative Colitis(UC)  Indetereminate Colitis DIVERTICULAR DISEASE OF THE COLON (DDC)  Introduction  Epidemiology  Pathophysiology  Uncomplicated DDC  Complicated DDC
  • 3. Inflammatory Bowel Disease • IBD is a chronic condition resulting from complex interactions between intestinal microbiota and host immunity in genetically predisposed individuals resulting an inappropriate mucosal immune activation It comprises : » Ulcerative colitis » Crohn’s disease, and » Indeterminate colitis
  • 4. Epidemiology: • UC - 8 to15 /100,000 and CD - 1 to 5/100,000 in USA and Northern Europe, Lower in Asia, Africa and South America Bimodal age distribution • UC - Peaks in 3rd - 7th decades • CD - peaks in 15- 30 then 60 -70 years • Higher among Caucasians and White than Blacks, Hispanics and Asians
  • 5. Pathophysiology  Under physiologic conditions, homeostasis normally exists between • The commensal microbiota • Epithelial cells • Immune cells within the tissues A consensus hypothesis is that each of these three major host compartments that function together are affected by  specific environmental (e.g., smoking, antibiotics, enteropathogens)  genetic factors that, in a susceptible host, cumulatively and interactively disrupt homeostasis
  • 6. Genetics • Risk for disease is increased when there is an affected family member • In Crohn disease, the concordance rate for monozygotic twins is approximately 50% and only 16% in UC
  • 7. • over 200 genes associated with IBD identified Among these, NOD2, ATG16L1 and IRGM • The presence of NOD2 gene on IBD1 locus on chromosome 16 has been linked to Crohn’s disease • Persons with allelic variants on both have a 40-fold relative risk of Crohn’s disease
  • 8. COMMENSAL MICROBIOTA AND IBD • The endogenous commensal microbiota within the intestines plays a central role in the pathogenesis of IBD • The establishment and maintenance of the intestinal microbiota composition and function is under the control of host, environmental & genetic (e.g., NOD2) • The commensal microbiota in patients with both UC and CD is demonstrably different from non-affected individuals, a state of dysbiosis
  • 9. DEFECTIVE IMMUNE REGULATION IN IBD • The mucosal immune system does not normally elicit an inflammatory immune response to luminal contents due to oral (mucosal) tolerance • Oral tolerance may be responsible for the lack of immune responsiveness to dietary antigens and the commensal microbiota in the intestinal lumen • In IBD this suppression of inflammation is altered, leading to uncontrolled inflammation. The mechanisms of this regulated immune suppression are incompletely known
  • 11. • Epithelial defects - a variety of epithelial defects have been described in Crohn disease, ulcerative colitis. For example, defects in intestinal epithelial tight barrier function occur in patients with Crohn
  • 12. CROHN’S DISEASE • Crohn’s disease is a chronic, idiopathic transmural inflammatory disease with skip lesions that may affect any part of the GI tract,  Small intestine alone - 30% of cases  Small intestine and colon - 40%  The colon alone - 30% • CD may involve the duodenum, stomach, esophagus,
  • 14.  The earliest lesion characteristic of Crohn’s disease is the aphthous ulcer. These superficial ulcers are up to 3 mm in diameter and are surrounded by a halo of erythema. In the small intestine, aphthous ulcers typically arise over lymphoid aggregates  As disease progresses, aphthae coalesce into larger, stellate shaped ulcers. Linear or serpiginous ulcers may form when multiple ulcers fuse in a direction parallel to the longitudinal axis of the intestine. With transverse coalescence of ulcers, a cobblestone appearance of the mucosa may arise
  • 15.  A pathognomonic feature of Crohn’s disease that is grossly evident and helpful in identifying affected segments of intestine during surgery is the presence of fat wrapping, which represents encroachment of mesenteric fat onto the serosal surface of the bowel
  • 16. Features that allow for differentiation between Crohn’s disease of the colon and ulcerative colitis include  The layers of the bowel wall affected in UC is limited to the mucosa and sub mucosa but may involve the full-thickness in Crohn’s disease  The longitudinal extent of inflammation is continuous and characteristically affects the rectum in UC but may be discontinuous and spare the rectum in Crohn’s disease
  • 17. Microscopic feature  crypt abscess  distortion of mucosal architecture  Paneth cell metaplasia  Non- caseating granulomas(hallmark) - only found in 35 %
  • 18. Clinical presentation CD Depending on :- o The segment of intestine involved o Features of the disease:  Fibrostenotic  Inflammatory  fistulizing
  • 19. Fibrostenotic patterns  occurs in any location, most commonly in the terminal ileum  patients present with obstructive symptoms such as nausea, vomiting, and decreased oral intake  medical management is unsuccessful and surgical intervention is required
  • 20. Inflammatory  It is characterized by mucosal ulceration and bowel wall thickening  This pattern often gives rise to obstructive symptoms in the small intestine and diarrhea in the colon  Inflammatory pattern is much more likely to respond to medical therapy
  • 21. penetrating or fistulizing • Patients may be completely asymptomatic, as in the case of many entero-enteral fistulas, present with anorectal abscesses or fistulas • Symptom depend on Involvement of the secondarily organ – » recurrent UTI or pneumaturia » vaginal discharge » diarrhea » cutaneous feculent drainage
  • 23. ILEOCOLITIS Terminal ileum is the most common site of inflammation o presented with -:  Right lower quadrant pain and Palpable mass  Diarrhea  Fever  Leukocytosis  Pain is usually colicky relieved by defecation  Weight loss
  • 24. o persistent inflammation, gradually progresses to fibrostenotic narrowing , stricture and chronic bowel obstruction o Severe inflammation may lead to localized wall thinning, with microperforation and fistula formation
  • 25. JEJUNOILEITIS • Extensive inflammatory disease is associated with a loss of digestive and absorptive surface, resulting in malabsorption and steatorrhea • Intestinal malabsorption can cause anemia, hypoalbuminemia, hypocalcemia, hypomagnesemia, coagulopathy
  • 26. COLONIC  Distribution – 1/3 total colonic involvement, – 40% segmental disease – 30% left-sided only  Patients with colitis present with low grade fevers, malaise, diarrhea, crampy abdominal pain, and sometimes hematochezia
  • 27. Anorectal • perianal involvement is clearly more common in those with concomitant rectal or colonic disease • CD patients may also manifest  edematous (elephant ear) skin tags  blue discoloration of the anus  abscesses and fistulas that are often recurrent, multiple
  • 28. INVESTIGATION Serologic marker • The most commonly tested antibodies are (pANCA) and (ASCA) • ASCA+/pAaNCA–, is associated with a diagnosis of Crohn’s disease • ASCA–/pANCA+, correlates with ulcerative colitis • Although these antibody tests have high specificity, their use has been hampered by low test sensitivities
  • 29. Plain Films  plain films is often a routine part of the diagnosis  An abdominal plain film may help in the setting of – » Bowel obstruction » To exclude toxic megacolon, or » To evaluate for pneumoperitoneum
  • 30. CONTRAST STUDIES  barium studies helped diagnose CD by identifying longitudinal and transverse linear ulcerations that create cobblestone and nodular patterns, skip lesions, fistulas, and strictures  with newer studies such as CT and MRE traditional barium studies are becoming less favorable
  • 31. Computed Tomography  In many centers, CT has now largely replaced the barium studies  with the added ability to identify the extent of the disease and involvement of surrounding structures, manifested by  segmental bowel thickening  mesenteric fat stranding  intra-abdominal fluid &  presence of fistula
  • 32. Magnetic Resonance Imaging • MRE is over 85% accurate in predicting stenosis, abscess, and fistula • Its sensitivity (85–90%), specificity (100%), and negative predictive value (77%) • MRI has also been particularly useful in the evaluation of complex perianal fistulas seen in CD
  • 33. Endoscopy • To identify the extent and severity of the disease and perform biopsies to aid in diagnosis • Endoscopic evaluation includes colonoscopy, esophagogastroduodenoscopy (EGD), enteroscopy, and capsule endoscopy
  • 34.
  • 35. Ulcerative colitis • It is characterized by recurring episodes of inflammation limited to the mucosal layer of the colon • It commonly involves the rectum and may extend in a proximal and continuous fashion to involve other parts of the colon
  • 36. Gross pathology  Early UC - the mucosa grossly appear edematous, with confluent erythema and a loss of vascular markings  Intermediate - the mucosa will develop granularity with micropurulence and bleeding  Advanced UC - will be marked by pseudo-polyp formation, deep ulcerations, gross purulence, mucosal bridging, and varied mucosal thickness
  • 37. Microscopic feature • Early disease - characterized by mucosal inflammation, crypt distortion, goblet cell mucin depletion, and vascular congestion • Intermediate disease - is associated with crypt abscesses and loss of mucosa with preservation of the crypts themselves • Advanced disease- hallmarks are Crypt destruction, pseudopolyps, and deeper invasion of inflammation
  • 38. • It is in late disease where we tend to identify dysplasia; however, it can only be interpreted when identified in non- inflamed bowel, as many dysplastic features are similar to inflammation
  • 39. • The risk of colorectal carcinoma among UC patients is approximately 3.7%, with pancolitis conferring an even higher risk of 5.4% • The same study found the cumulative risk of colorectal carcinoma by decade was 2% at 10 years, 8% at 20 years, and18% at 30 years
  • 40. Clinical Manifestations Signs and symptoms depend on the severity and location The most common findings are -:  Blood and mucus in the stools  Tenesmus  Urgency  Increased stool frequency  Fecal incontinence, and  pain with defecation  Fecal incontinence
  • 41. systemic symptoms including- • fever, fatigue, weight loss, and anemia from blood loss Physical examination Mild disease- it is often normal Moderate to severe UC - have abdominal tenderness, fever, hypotension, tachycardia, and pallor, evidence of blood on DRE
  • 42.
  • 43. DIAGNOSIS Serologic Testing  CRP and ESR are the only two widely used tests for assessing general systemic inflammation  pANCA and ASCA, may help differentiate CD from UC  pANCA is more frequently identified in UC patients(50–70% of UC vs. 20–30% of CD)  ASCA is more frequently associated with CD, although it may be present in 10 to 15% of UC patients as well
  • 44. Endoscopy  Endoscopy is the GOLD STANDARD for diagnosis of UC  Colonoscopic examination alone is generally enough to diagnose UC , allows for tissue biopsy as well as assessment of the gross appearance and specific pattern of inflammation  The entire extent of the disease process can effectively be surveyed
  • 45. Mucosal Biopsies • During the procedure, multiple biopsies are necessary for diagnosing UC and from six segments (the terminal ileum, the ascending, transverse, descending and sigmoid colon and the rectum) should be obtained
  • 46. Plain Film X-Rays  X-rays still play a role when considering the patient who presents acutely with abdominal pain  We may see presence of free air or toxic megacolon
  • 47. CT- SCAN In UC, the indications for CT enterography and colonography are currently • strictures precluding endoscopic assessment • patients with severe comorbidities where colonoscopy is contraindicated • It also allows excluding small bowel involvement for the differential diagnosis of CD or in the case of indeterminate colitis
  • 48. Magnetic Resonance • The role of MRI in IBD is still evolving. While less efficient and more costly than CT for an abdominal survey
  • 49. Indetereminate Colitis • In 15% of patients with IBD, differentiating UC from CD is impossible “indeterminate colitis” • Their symptoms similar to ulcerative colitis • Endoscopic and pathologic findings usually include features common to both diseases Serologic markers have been employed to differentiate UC from CD • pANCA- 60% to 70% in UC, compared to 2% to 28% in CD • ASCA-39% to 69% in CD, but only 5% to 15% of UC
  • 50. Diverticular Disease of the Colon • A diverticulum is a sac-like protrusion of the colonic wall • Diverticulosis is defined by the presence of diverticula without inflamation • Diverticular disease - is defined as clinically significant and symptomatic diverticulosis due to diverticular bleeding, diverticulitis, segmental colitis
  • 51. • The majority of colonic diverticula are false diverticulum which the mucosa and muscularis mucosa have herniated through the colonic wall • These diverticula occur at the teniae coli, at points where nutrient artery penetrate the colonic wall
  • 52. EPIDEMOLOGY The distribution of diverticulosis within the colon varies by geography  Western and industrialized nations have prevalence rates of 50 % above the age of 50 • Approximately 95 % of patients with diverticula have sigmoid diverticula  In Asia, the prevalence of diverticulosis is between 13 and 25 % and diverticulosis is predominantly right-sided
  • 54. MORPHOLOGY • Colonic diverticula are small, flasklike outpouchings, usually 0.5-1 cm in diameter • They are most common in the sigmoid colon, but other regions of the colon may be affected • Colonic diverticula have a thin wall composed of a flattened or atrophic mucosa, compressed submucosa, and attenuated muscularis propria
  • 55. RISK FACTORS  Diet - Low fiber, high fat, and red meat  Physical inactivity  Obesity
  • 57. Uncomplicated Diverticulitis  It is characterized by LLQ pain and tenderness  CT findings include pericolic soft tissue stranding, colonic wall thickening, and/or phlegmon  Most patients will respond to outpatient therapy with broad-spectrum oral antibiotics (7 to 10 D) and a low-residue diet  10% to 20% of patients with more severe pain, tenderness, fever, and leukocytosis are treated in the hospital with parenteral antibiotics
  • 58. Complicated Diverticulitis Abscess  It occur in 17 % of patients hospitalized with acute diverticulitis  The symptoms of a diverticular abscess are similar to acute diverticulitis  CT is the imaging modality of choice  It should be suspected in patients with uncomplicated diverticulitis who have no improvement of symptoms despite of antibiotic treatment
  • 59. FISTULA  Acute diverticulitis may result in the formation of a fistula between the colon and adjacent viscera  Fistulas most commonly involve the bladder, and may have pneumaturia, fecaluria, or dysuria  Patients with a colovaginal fistula may report vaginal passage of feces or flatus
  • 60. Perforation  Generalized peritonitis may result from rupture of a diverticular abscess or free rupture of an inflamed diverticulum  only 1 to 2 % of patients with acute diverticulitis have a perforation, but mortality rates is about 20 %  The abdomen is distended and diffusely tender to light palpation. There is diffuse guarding, rigidity, and rebound tenderness, and bowel sounds are absent
  • 61. Hemorrhage • Bleeding results from erosion of the peri-diverticular arteriole and may result in massive hemorrhage • Most significant LGIB occurs in elderly patients is due to diverticulosis • The exact bleeding source may be difficult to identify, Fortunately, in 80% of patients, bleeding stops spontaneously
  • 62. Hinchey classification of Diverticulitis
  • 63. REFERENCES • Marvin L. Corman..etal,corman’s Colon And Rectal Surgery,6th edition • Jeffrey H. Peters…etal,Shackelford’s Surgery of the Alimentary Tract,7th edition • Brunicardi FC, Schwartz’s Principles of Surgery, 11th edition • Michael J. …etal,maingot’s Abdominal Surgery,13th edition • Uptodate 2018

Editor's Notes

  1. By contrast, concordance of monozygotic twins for ulcerative colitis is only 16%, suggesting that genetic factors are less dominant in this form of IBD
  2. over 200 genes associated with IBD identified Among these, NOD2, ATG16L1 (autophagy-related16–like-1) and IRGM (immunity-related GTPase M) Molecular linkage analyses of affected families have identified NOD2(nucleotide oligomerization binding domain 2) as a susceptibility gene in Crohn disease. NOD2 encodes a protein that binds to intracellular bacterial peptidoglycans and subsequently activates NF-κB. Some studies suggest that the disease-associated form of NOD-2 is ineffective at defending against intestinal bacteria. The result is that bacteria are able to enter through the epithelium into the wall of the intestine, where they trigger inflammatory reactions. It should, however, be recognized that disease develops in less than 10% of individuals carrying specific NOD2polymorphisms, and these polymorphisms are uncommon in African and Asian patients with Crohn disease
  3. The endogenous commensal microbiota within the intestines plays a central role in the pathogenesis of IBD The establishment and maintenance of the intestinal microbiota composition and function is under the control of host (e.g., immune and epithelial responses), environmental (e.g., diet and antibiotics), & genetic (e.g., NOD2) The commensal microbiota in patients with both UC and CD is demonstrably different from non-afflicted individuals, a state of dysbiosis
  4. Mucosal immune responses. Although the mechanisms by which mucosal immunity contributes to the pathogenesis of UC and CD are still being deciphered, immunosuppressive and immunomodulatory agents remain mainstays of IBD therapy Defects in regulatory T cells, especially the IL-10-producing subset, are believed to underlie the inflammation especially in Crohn disease. Mutations in the IL-10 receptor are associated with severe, early-onset colitis. Thus, some combination of excessive immune activation by intestinal microbes and defective immune regulation likely is responsible for the chronic inflammation in both forms of IBD Multiple mechanisms are involved in the induction of oral tolerance and include deletion or anergy of antigen-reactive T cells or induction of CD4+ T cells that suppress gut inflammation (e.g., T-regulatory cells expressing the FoxP3 transcription factor) that secrete anti-inflammatory cytokines such as IL-10, IL-35, and transforming growth factor β(TGF-β)
  5. Fibrostenotic patterns may occur in any location, though these occur most commonly in the terminal ileal region, where patients present with obstructive-type symptoms such as nausea, vomiting, and decreased oral intake. Due to the recurrent chronic nature that results in progressive thickening of the bowel wall, medical management is typically unsuccessful and surgical intervention is required
  6. Bowel movements may either be diarrhea or conversely follow an obstructive pattern due to luminal narrowing or extrinsic compression from the phlegmon
  7. While medical management continues to be a major component of each of the latter two patterns, surgery is often required for resolution of symptoms
  8. Terminal ileum is the most common site of inflammation and presented with chronic history of recurrent episodes of right lower quadrant pain and diarrhea Sometimes the initial presentation mimics acute appendicitis with pronounced right lower quadrant pain, a palpable mass, fever, and leukocytosis. Pain is usually colicky; it precedes and is relieved by defecation. A low-grade fever is usually noted. High-spiking fever suggests intraabdominal abscess formation. Weight loss is common—typically 10–20% of body weight—and develops as a consequence of diarrhea, anorexia, and fear of eating
  9. Bowel obstruction may take several forms. In the early stages of disease, bowel wall edema and spasm produce intermittent obstructive manifestations and increasing symptoms of postprandial pain. Over several years, persistent inflammation gradually progresses to fibrostenotic narrowing and stricture. Diarrhea will decrease and be replaced by chronic bowel obstruction. Acute episodes of obstruction occur as well, precipitated by bowel inflammation and spasm or sometimes by impaction of undigested food or medication. These episodes usually resolve with intravenous fluids and gastric decompression
  10. Extensive inflammatory disease is associated with a loss of digestive and absorptive surface, resulting in malabsorption and steatorrhea Nutritional deficiencies can also result from poor intake and enteric losses of protein and other nutrients Intestinal malabsorption can cause anemia, hypoalbuminemia, hypocalcemia, hypomagnesemia, coagulopathy, Many patients need to take oral and often intravenous iron. Vertebral fractures are caused by a combination of vitamin D deficiency, hypocalcemia, and prolonged glucocorticoid use. Pellagra from niacin deficiency can occur in extensive small-bowel disease, and malabsorption of vitamin B 12 can lead to megaloblastic anemia and neurologic symptoms. Other important nutrients to measure and replete if low are folate and vitamins A, E, and K. Levels of minerals such as zinc, selenium, copper, and magnesium are often low in patients with extensive small-bowel inflammation or resections, and these should be repleted as well. Most patients should take a daily multivitamin, calcium, and vitamin D supplements
  11. Within the colon, the distribution is somewhat variable, with approximately one-third of patients having total colonic involvement, 40% showing segmental disease, and left-sided only in up to 30%.60 Regardless of the exact location within the large intestine, patients with colonic involvement may experience abdominal pain and, in some cases, malnutrition. Diarrhea is often of smaller volume and may be from several sources—salt/water and bile acid malabsorption, infection (CMV), or as a result of an enterocolonic fistula. 61,62 Unlike ulcerative colitis, rectal bleeding is not routine, and bowel movements are often nonbloody, except in those with moderate-to-severe Crohn’s colitis. In addition, similar to disease in the small bowel, patients can experience hip pain from fistulas, cramping, and obstructive symptoms. Patients with chronic disease may also demonstrate pseudopolyps on endoscopic examination
  12. perianal involvement is clearly more common in those with concomitant rectal or colonic disease CD patients may also manifest edematous (elephant ear) skin tags blue discoloration of the anus abscesses and fistulas that are often recurrent, multiple, and located well away from the anal verge
  13. Serologic marker The most commonly tested antibodies are antineutrophil cytoplasmic antibody (pANCA) and antisaccharmyces cerevisiae antibody (ASCA). ASCA+/pAaNCA–, is associated with a diagnosis of Crohn’s disease, while ASCA–/pANCA+, correlates with ulcerative colitis. Although these antibody tests have high specificity, their use has been hampered by low test sensitivities
  14. In many centers, CT has now largely replaced the barium enema and small bowel follow-through, with the added ability to identify the extent of the disease and involvement of surrounding structures, manifested by segmental bowel thickening, mesenteric fat stranding, and intra-abdominal fluid. Additionally, CT is useful to identify secondarily involved organs or provide information that may be pertinent to preoperative planning, suchas bladder or vaginal air indicating presence of a fistula, an adjacent psoas abscess in ileocecal disease, or ureteral obstruction that may require stenting. CT and MR enterography provide improved detail of the mucosal surface and are esapecially useful in depicting fistulas and strictures, along with the added benefit of lower levels of radiation exposure. The latter benefit is especially relevant considering the generally younger patient population, body habitus, and potential need for lifelong repeat imaging associated with CD
  15. The colorectal mucosa in early UC may grossly appear edematous, with confluent erythema and a loss of vascular markings. As the disease progresses, the mucosa will develop granularity with micropurulence and bleeding. Advanced UC will be marked by the characteristic pseudopolyp formation, deep (even full-thickness) ulcerations, gross purulence, mucosal bridging, and varied mucosal thickness
  16. Meta-analysis of premillennial UC data suggested that the risk of colorectal carcinoma among UC patients is approximately 3.7%, with pancolitis conferring an even higher risk of 5.4%. The same study found the cumulative risk of colorectal carcinoma by decade was 2% at 10 years, 8% at 20 years, and 18% at 30 years
  17. Serologic Testing C-reactive protein (CRP) and ESR are the only two widely used tests for assessing general systemic inflammation. Neither measurement is sensitive or specific for IBD, but they may give an idea as to the level of inflammation in an IBD flare if other causes of inflammation are ruled out. ESR is felt to correlate more with colitis than small bowel disease irrespective of CD versus UC. The results of ESR and CRP may be misleading, as elevation can indicate anything from a perirectal abscess to pneumonia. A normal level can also be somewhat misleading, as the degree of inflammation may not correlate with a patient’s symptoms. Such a scenario could involve a symptomatic stricture without significant active inflammation antineutrophil cytoplasmic antibodies (pANCA) and anti-Saccharomyces cerevisiae antibodies (ASCA), which were the first two widely used markers. It is felt that the presence or absence of these markers may help differentiate CD from UC in cases that are clinically in question. pANCA is more frequently identified in UC patients (50–70% of UC vs. 20–30% of CD) and may indicate a more medically refractory phenotype. 152 ASCA is more frequently associated with CD, although it may be present in 10 to 15% of UC patients as well
  18. X-rays still play a role when considering the patient who presents acutely with abdominal pain We may see presence of free air or “toxic megacolon,”a term , colonic dilatation ≥ 6 cm or cecal diameter > 9 cm in the setting of fever, tachycardia, and abdominal pain is a grave concern that mandates urgent surgical intervention.
  19. A diverticulum is a sac-like protrusion of the colonic wall Diverticulosis is defined by the presence of diverticula without inflamation Diverticular disease is defined as clinically significant and symptomatic diverticulosis due to diverticular bleeding, diverticulitis, segmental colitis associated with diverticula, or symptomatic uncomplicated diverticular disease
  20. It is estimated that half of the population older than age 50 years has colonic diverticula The sigmoid colon is the most common site of diverticulosis Western and industrialized nations have prevalence rates of 5 to 45 percent, depending upon the method of diagnosis and age of the population [5,6]. Approximately 95 percent of patients with diverticula have sigmoid diverticula (image 1) [7]. Diverticula are limited to the sigmoid colon in 65 percent of patients; in 24 percent of patients diverticula predominantly involve the sigmoid, but are also present in other parts of the colon
  21. Bleeding results from erosion of the peri-diverticular arteriole and may result in massive hemorrhage Most significant lower gastrointestinal hemorrhage occurs in elderly patients due to both diverticulosis and angiodysplasia The exact bleeding source may be difficult to identify,Fortunately, in 80% of patients, bleeding stops spontaneously Clinical management should focus on resuscitation and localization of the bleeding site as described