12 Pathophysiology of IBDnnnnnnnnnnnnnnnnnnnnnn and Diverticular Disease (1).pptx
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
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
By contrast, concordance of monozygotic twins for ulcerative colitis is only 16%, suggesting that genetic factors are less dominant in this form of IBD
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
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
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)
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
Bowel movements may either be diarrhea or conversely follow an obstructive pattern due to luminal narrowing or extrinsic compression from the phlegmon
While medical management continues to
be a major component of each of the latter two patterns, surgery is often required for resolution of symptoms
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
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
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
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
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
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
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
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
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
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
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.
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
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
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