Diverticulosis and diverticular disease

1. DIVERTICULAR DISEASE
Dr Doha Rasheedy Ali
Assistant Professor of Geriatrics and
Gerontology
Faculty of Medicine- Ain Shams University

2. Diverticulosis
• Diverticula are acquired herniations of the colonic
mucosa and submucosa through the muscularis
propria.(psuedo/ false diverticulae)
• Uninflamed and non-bleeding diverticula are
asymptomatic.
• They occur most commonly in the sigmoid colon and
can vary in size and number, although typically they
are between 5 and 10 mm in diameter.
• Diverticulosis refers to the presence of diverticula in
an individual who is asymptomatic, whereas
diverticular disease refers to the presence of
diverticula associated with symptoms, which occurs
in 20% of individuals with diverticula.

4. Epidemiology
• Affects 5% to 10% of the population older than
45 years, and 80% of those older than 85 years.
• Approximately 20% of patients with diverticula
have an episode of symptomatic diverticulitis.
• Diverticular hemorrhage is the second most
common cause of colonic bleeding after
vascular lesions.
• Acute diverticulitis: There is a male
predominance in patients younger than 50
years of age, with equal gender distribution
after age 60 years

5. Saint’s triad
• Cholelithiasis, diverticulitis, and hiatal hernia
frequently occur together.

6. Pathophysiology
1. Site: mainly the sigmoid colon but may involve the
entire colon but never the rectum.
• Pathogenesis
A. Colonic Motility
1. Increased intraluminal pressure by segmentation
movement, push mucosa through week point were
vasa recta penetrate muscularis propria between the
taeniae coli
2. The interstitial cells of Cajal are thought to be
responsible for the generation of slow waves
myoelectrical activity increases segmentation
movement.

7. B. Colonic Wall Changes
– As individuals age, the tensile strength of the collagen and
muscle fibers of the colonic wall decreases due to increased
cross-linking of abnormal collagen fibers and deposition of
elastin in all layers of the colonic wall.
– Extracellular matrix degradation and remodeling is
mediated in part by matrix metalloproteinases. Activation of
matrix metalloproteinases results in the degradation of the
extracellular matrix, including collagens, noncollagenous
glycoproteins, and proteoglycans
– Patients with diverticular disease have been shown to have
an increase in collagen synthesis, an increase in tissue
inhibitors of metalloproteinases, and a decrease in the
expression of a matrix metalloproteinase subtype that is
responsible for the degradation of collagen

8. C. Visceral Hypersensitivity
– there is a generalized state of visceral hypersensitivity in
symptomatic diverticular disease that is similar to that
seen in irritable bowel syndrome. is not limited to areas of
the sigmoid with diverticula
D. Inflammation
– may exhibit low-grade colonic inflammation that may
resemble inflammatory bowel disease histologically.
– nonspecific mucosal inflammation, crypt abscesses, a
mononuclear cell infiltrate in the lamina propria, and
occasional submucosal inflammation or granulomas. When
these findings are present, the term segmental colitis is
applied. Possible causes include ischemia, changes in
bacterial flora, mucosal prolapse, and the presence of
intraluminal antigens.

9. E. Fiber
• Higher fiber in the diet leads to increased stool
bulk and decreased colonic transit times.
Individuals from countries with high-fiber diets
tend to have larger diameter colons, compared
with those from countries with low fiber intake.
Having a larger colonic diameter may impair the
segmental contractions of the colon that lead to
higher intraluminal pressures

10. Visceral
hypersensitivity
Colonic wall
changes
Inflammation,
low fiber
Colonic
motility:
increased
segmentation
Slow wave
myoelectrica
l activity

11. Etiology  fibre diet
 stool volume
 intraluminal pressure
 colonic wall tension
muscular hypertrophy,
pulsion diverticula
 tensile strength
 elasticity
 age

12. Quiz
Explain:
• Diverticula are not seen in the rectum while so
common in the sigmoid colon
• the early formation of diverticula in patients with
connective tissue disorders, such as Marfan
syndrome, Ehlers-Danlos syndrome, and polycystic
kidney disease

13. Pathogenesis of complications
1. If the neck of a diverticulum is obstructed, it may distend and lead to bacterial
overgrowth and invasion, often with perforation, which is generally walled off by the
adjacent mesocolon or appendices epiploicae.
2. Factors that favor increased colonic pressures are altered autonomic activity (seen with
decreased exercise and neostigmine), activation of opioid receptors, and decreased
mechanical stretching of the colon due to a low-fiber diet.
3. Altered microbial composition within the gut, resulting in chronic low-grade
inflammation.
4. Nonsteroidal anti-inflammatory medications (NSAIDs) have been associated with
diverticulitis and perforation. The association of NSAIDs with diverticulitis is postulated
to be related to decreased prostaglandin synthesis and direct topical mucosal damage.
prostaglandins aid in maintaining the colonic mucosal barrier by stimulating mucin and
bicarbonate secretion and increasing mucosal blood flow, In addition, NSAIDs are weak
acids that may denude epithelial cells, resulting in increased mucosal permeability,
ulceration, and the translocation of bacteria and toxins
5. a diet low in fiber; fibers protection by increasing stool weight and water content, fiber
helps reduce colonic segmentation pressures, which may protect against perforation
6. Red meat: predispose to perforation as associated with apoptosis of colonic epithelial
cells
7. Nut, corn and popcorn consumption did not increase the risk of diverticulosis or
diverticular complications

14. Riskofperforation
obstruction
Increased
pressure
Low fiber
Red meat
NSAIDs
Altered flora

15. The clinical presentation of diverticulosis
Depends on:
1. the location of the affected diverticulum,
2. The severity of the inflammatory process
3. the presence of complications
includes
• Left lower quadrant pain (70% of patients),
• Change in bowel habits(typically diarrhea)
• Nausea and vomiting
• Constipation
• Diarrhea
• Flatulence
• Bloating
• The stool may contain trace blood, but profuse bleeding is very
uncommon

16. The clinical presentation of Acute
diverticulitis
• Left lower quadrant pain (70% of patients), fever,
leucocytosis= diverticulitis
• can be either complicated or uncomplicated.
• results from the micro- or macroperforation of a
diverticulum, resulting in anything from
subclinical inflammation to feculent peritonitis
• Patients may also complain of nausea and
vomiting (20–62%), constipation (50%), diarrhea
(25–35%), and urinary symptoms (10–15%).

17. Physical findings
1. In simple diverticulitis, localized abdominal tenderness in the
area of the affected diverticula and fever
2. Left lower quadrant tenderness is most common, as most
diverticula occur in the sigmoid colon
3. Right lower quadrant tenderness, mimicking acute appendicitis,
can occur in right sided diverticulitis
4. In complicated diverticulitis with abscess formation, a tender
palpable mass
5. Elderly patients and some patients taking corticosteroids may
have unremarkable findings, even in the presence of severe
diverticulitis.
6. Diffuse tenderness suggests free perforation and peritonitis.
Abdominal distention and hypoactive bowel sounds may be
present if an ileus has developed. In cases of free perforation,
hemodynamic instability may develop, along with a rigid
abdomen.

18. Complicated acute diverticulitis
1. Haemorrhage:which occurs when the arteriole associated
with the diverticulum erodes
2. Perforation:
– Generalized tenderness with rebound and guarding on
abdominal examination
– The abdomen may be distended and tympanic to percussion
– Bowel sounds can be diminished or absent
3. Fistula: Colovesical and, less frequently, colovaginal and
colocutaneous fistulas may occur
– colovaginal fistulas may present with a purulent
vaginal discharge
– Colovesicular fistulas may present as urinary tract
symptoms (eg, suprapubic, flank, or costovertebral
angle tenderness)(urosepsis)
– Coloenteric (malabsorption bacterial overgrowth)

19. • 3. Repeated episodes of acute diverticulitis
may lead to colonic obstruction
• 4. Jaundice or hepatic abscesses suggest
pylephlebitis.

20. Complications
Hemorrage
Perforation.
peritonitis
fistula
Repeated
attacks
Colonic
obstruction
Hepatic
abscess

21. • Dysuria, urinary frequency, and urgency
reflect bladder irritation, whereas
pneumaturia, fecaluria, or recurrent urinary
tract infection suggests a colovesical fistula.

22. Clinical staging of acute diverticulitis
by Hinchey's classification
• Stage I: Diverticulitis with phlegmon or localized
pericolic or mesenteric abscess
• Stage II: Diverticulitis with walled off pelvic,
intraabdominal, or retroperitoneal abscess
• Stage III: Perforated diverticulitis causing
generalized purulent peritonitis
• Stage IV: Rupture of diverticula into the
peritoneal cavity with fecal contamination
causing generalized fecal peritonitis

24. Hinchey's classification
• Stage I diverticulitis is characterized by small
confined pericolonic abscesses,
• stage II diseaseincludes larger confined
pericolonic collections.
• Stage III involves generalized suppurative
peritonitis (perforateddiverticulitis); because the
diverticular neck isgenerally obstructed by a
fecolith, peritoneal contaminationby feces may
not occur.
• Stage IV indicates fecal peritonitis.

27. Diagnosis
• history and physical examination
• laboratory tests
• Computed tomography (CT) scanning of the
abdomen
• Contrast enema, using water- soluble medium
• Plain abdominal radiograph series with supine
and upright films

28. laboratory tests
1. The white blood cell count may show leukocytosis
and a left shift (can be normal)
2. Blood cultures should be obtained prior to the
administration of empiric parenteral antimicrobial
therapy for severe complicated cases
3. If the amylase is elevated, it is suggestive of possible
peritonitis or a perforation.
4. A pregnancy test must be performed in any female
of childbearing age with abdominal pain
In uncomplicated diverticulosis, laboratory values,
including the hematocrit, hemoglobin, and white blood
cell count, are normal and Hemoccult testing of the
stool is negative.

29. Plain abdominal radiographs
• are typically normal in patients with mild diverticulitis,
• but in the setting of severe disease, there may be an
ileus pattern, or, if obstruction is present, proximal
bowel dilation. A large abscess may be associated with
an air-fluid level on upright films. If there is perforation
into the retroperitoneal space, the psoas shadow may
be obliterated due to air diffusing along the psoas
muscle. Free air under the diaphragm may be seen on
upright films in the setting of intraperitoneal
perforation, especially if there is feculent peritonitis.

30. Air in the bowel wall

31. ileus Air under diaphragm

32. Massive retroperitoneal and peritoneal
free-air from ascending colon rupture
Notice that the kidney and psoas muscle
outlined by the free-air below.
the contour of the iliopsoas muscle
(short arrows) and the right kidney
(long arrows) extremely well, much
better than normal. They are
outlined by air that originated from
a traumatic rupture of the
duodenum.

33. Ultrasound
• Ultrasound is a noninvasive method with
limited utility.
• It is highly operator dependent, and in the
setting of an ileus may be limited due to
distention of the bowel by gas. It may identify
a phlegmon, abscess, or bowel wall
thickening. It can be helpful in guiding the
drainage of intra-abdominal abscesses.

34. Computed tomography (CT)
• best imaging method to confirm the diagnosis
(helical CT and colonic contrast)
• Findings:
1. Pericolic fat stranding due to inflammation
2. Colonic diverticula
3. Bowel wall thickening
4. inflammatory masses
5. Phlegmon
6. Abscesses

35. Axial CT image demonstrates left
colonic wall thickening,
pericolonic fat stranding, fascial
thickening (arrowheads) and an
inflamed diverticulum (arrow).
Axial CT image shows an ileal
diverticulum (arrow) with
surrounding inflammation
(arrowheads). Thin arrow =
normal appendix

36. Axial CT image shows free
fluid (long arrow), jejunal
diverticula,thickened walls of
duodenal and jejunal loops
and mesenteric fat stranding
(both short arrows)

37. Investigations - CT
Air-filled diverticula
Mesenteric stranding

38. Ambrosetti CT criteria
• Mild diverticulitis
– Wall thickening (>5 mm)
– Pericolic fat stranding
• Severe diverticulitis
– Wall thickening (>5 mm)
– Pericolic fat stranding with
– Abscess
– Extraluminal air
– Extraluminal contrast

39. Contrast enema
• using water-soluble medium

41. • A contrast enema shows diverticula but not diverticular
inflammation. Moreover, contrast studies may cause
perforation.
• If the clinical features are highly suggestive of diverticulitis,
imaging studies are unnecessary. If the diagnosis is
uncertain or if an abscess is suspected, computed
tomography is preferred,
• If segmental spasm is present, a transient saw-tooth
pattern may be seen.
• In uncomplicated diverticulosis, there should be no
extravasation of contrast, nor should there be evidence of
fistulae, strictures, or persistent spasm, all of which suggest
diverticulitis.

42. • Findings on barium enema in the setting of acute
diverticulitis include;
• persistent spasm, saw-tooth pattern of the
involved segment
• , deformed diverticulum,
• sinus tract or fistula,
• extravasation of contrast,
• abscess, stricture, obstruction,
• mass effect from extraluminal compression,
• and pneumoperitoneum

45. • Single-contrast barium
enema study
demonstrates
diverticulitis of the
descending colon with
fistula formation in the
small bowel.

46. • Single-contrast barium
enema study
demonstrates sigmoid
diverticulitis with a
colovesical fistula. Note
the contrast material in
the bladder.

47. • Single-contrast barium
enema study
demonstrates sigmoid
diverticulitis with fistula
formation in the vagina.

48. Endoscopy
• Diverticulosis is frequently discovered during
colonoscopy as an incidental finding
• Flexible sigmoidoscopy is necessary only if
carcinoma or colitis is a concern
• Colonoscopy is relatively contraindicated in
patients in whom acute diverticulitis is
suspected, due to an increased risk of colonic
perforation.

49. • patients who have not previously had a
colonoscopy should have one to exclude an
underlying malignancy or other disorder, with
a waiting period of 6–8 weeks following
resolution of the episode of diverticulitis. If an
endoscopy is to be performed in order to
differentiate between acute diverticulitis and
cancer or colitis prior to surgery, it should only
be attempted by an experienced endoscopist,
with minimal insufflation.

51. Differential Diagnosis uncomplicated
diverticulosis
• nonspecific symptoms of uncomplicated
diverticulosis are also seen in irritable bowel
syndrome. The fact that both disorders are
common, and can coexist, makes
differentiation even more difficult. Irritable
bowel syndrome frequently causes diffuse
abdominal pain; thus, pain localized to the left
lower quadrant in the setting of demonstrated
diverticula supports a diagnosis of
uncomplicated diverticulosis

52. Differential Diagnosis diverticulitis
• Other pelvic infections, such as appendicitis
and pelvic inflammatory disease, can also
mimic diverticulosis. Other causes of lower
abdominal pain that need to be considered
are infectious colitis, inflammatory bowel
disease, ischemic colitis, colorectal cancer,
and endometriosis.

53. TREATMENT

54. uncomplicated diverticular disease
• Therapies used to treat uncomplicated
diverticular disease include:
• fiber-rich diets
• nonabsorbable antibiotics
• Mesalazine
• probiotics, and prebiotics.
• Contrary to popular teaching, there is no strong
evidence that seeds, nuts, or popcorn lead to an
increase in the frequency of complications from
diverticulosis.

55. Fiber
• Fiber is slowly or completely fermented by gut
microflora, resulting in the production of short
chain fatty acids and gas. This in turn results in
shortened gut transit time, which reduces
intracolonic pressure and helps with constipation.
• The recommended daily fiber intake for adults is
20–35 g/day,
• increasing dietary fiber, often with fiber
supplements, is currently the mainstay of treating
uncomplicated diverticular disease.

56. Nonabsorbable Antibiotics
• Rifaximin is a broad-spectrum antibiotic that acts by
binding to the -subunit of bacterial DNA-dependent
RNA polymerase. Eighty to 90% of rifaximin remains
within the gut.
• Although the exact mechanism is unknown, rifaximin
has been shown in a few studies to improve the
symptoms of uncomplicated diverticular disease.
• Symptom improvement may be due to the ability of
rifaximin to influence the metabolic activity of gut flora
that degrade dietary fiber and produce gas. The drug
may also influence the gut flora responsible for
chronic, low-grade mucosal inflammation.

57. Mesalazine
• an anti-inflammatory drug that acts topically
on the gut mucosa and is typically used in the
treatment of inflammatory bowel disease.
Because some of the symptoms of diverticular
disease may be related to chronic mucosal
inflammation, mesalazine may have a role in
the treatment of patients with symptoms
related to diverticular disease.

58. Probiotics and Prebiotics
• Probiotics contain microorganisms with beneficial properties,
and the goal in using them is to alter the gut's microflora to
reestablish the normal bacterial flora. Bifidobacteria and
Lactobacilli are used most frequently. Some preparations also
contain other bacteria and nonbacterial organisms, such as
Escherichia coli and Saccharomyces boulardii.
• Prebiotics are substances that promote the growth and
metabolic activity of beneficial bacteria, especially
Bifidobacteria and Lactobacilli. Prebiotics are frequently
indigestible complex carbohydrates. Bacteria ferment these
substances, leading to a more acidic luminal environment,
which suppresses the growth of harmful bacteria. Substances
that have been shown to promote the growth of
Bifidobacteria and Lactobacilli include psyllium fiber,
lactulose, fructose, oligosaccharides, germinated barley
extracts, and inulin

59. Treatment of diverticulitis

60. Hinchey’s stage I disease first attack
• outpatient regimen
• A clear liquid diet
• 7-10 days of oral broad spectrum antimicrobial therapy
• Patients can advance the diet slowly as tolerated after
clinical improvement occurs, which should be within 48-
72hours
• After the acute attack has resolved, a high fiber diet and
colonoscopy (to exclude cancer) are advisable.
• 5% to 10% of patients will have a second attack within 2
years. the response rate to therapy drops with each
subsequent attack, from 70% for the first episode, to 6% for
the third episode

61. • Single agent or multiple agent antibiotic regimens
for outpatient therapy are equally effective,
provided that they provide both anaerobic and
aerobic coverage:
• Ciprofloxacin and metronidazole
• Trimethoprim- sulfamethoxazole and metronidazole
• Moxifloxacin
• Amoxicillin/clavulanic acid

62. When to hospitalize
• Severe pain, inability to tolerate oral intake, persistent symptoms
despite adequate outpatient therapy:
• Hospitalization,
• nothing by mouth,
• broad-spectrum intravenous antibiotics.
• Avoid Morphine (Increases Intracolonic Pressure) Merperidine
better than morphine
• Computed tomography to exclude abscess or perforation.
• Consider computed tomography guided percutaneous drainage of
an abscess to control systemic sepsis,
3 weeks later
• Endoscopy to rule out cancer
4-6 weeks later
• Elective resection, if appropriate

63. Surgery:
• Emergency operation is
indicated for
1. Peritonitis
2. uncontrolled sepsis
3. perforation,
4. clinical deterioration.
• Indications for elective
surgery include:
1. fistula formation
2. Stricture
3. recurrent diverticulitis.
4. After two episodes
one should seriously
consider elective
resection

64. Choice of surgery
1. If surgical treatment can be deferred until acute
inflammation heals, then a single-stage primary
resection and reanastomosis, perhaps
laparoscopically, can be accomplished with minimal
morbidity and mortality.
2. For emergency indications, the first stage of a two-
stage procedure involves resection of the diseased
segment and creation of an end colostomy with
oversewing of the distal colonic or rectal stump
(Hartmann’s procedure). Colonic continuity may be
reestablished in a second operation.

65. Complicated Diverticulitis, Abscess
Hinchey Stages I (pericolic abscess) and II
(retroperitoneal or pelvic abscess)
• Pre-op CT-guided percutaneous drainage
• Elective resection, primary re-anastomosis
Hinchey Stage III (purulent peritonitis)
• Emergent Hartmann’s procedure, or
• Emergent resection, primary re-anastomosis
Hinchey Stage IV (feculent peritonitis)
• Emergent Hartmann’s procedure

66. Hartmann’s procedure
• Resection of the
sigmoid colon, bring up
proximal colon as on
ostomy. Leave rectal
stump.
• Sigmoid ends when
taenia converges, that’s
where you at rectum

67. • Indications operation for elective
• ≥ 2 acute attacks, successfully treated
medically
• one attack requiring hospitalization in patient
< 40 y.o.
• one complicated attack
• one attack in immunocompromised patient
• inability to rule out colonic carcinoma

68. • Prior to surgery, all patients should receive antibiotics. If possible, bowel
preparation is carried out, although in emergent situations it often is not feasible.
• An alternative to a two-stage procedure is an on-table lavage, in which the colon
is lavaged with 3–6 L of warm saline, with povidone–iodine being added to the
last liter of saline. This allows for resection of the diseased colon with a primary
anastomosis (a one-stage procedure). The infection rate associated with a one-
stage procedure following an on-table lavage is less than 20%, with an
anastomotic leakage rate of less than 6%.
• A three-stage procedure is the classic approach but is rarely used because of its
higher mortality rate (26% vs 7% for other procedures). In the first stage, the
diseased segment is drained and a proximal diverting stoma is created, but no
resection is carried out. During the second stage, the diseased colon is resected
and a primary anastomosis is created. Finally, in the third stage, the stoma is
closed. The first stage of the procedure can be carried out to stabilize a patient
who is unstable prior to transfer to a larger medical center, or when inflammation
prevents safe dissection of the ureters or iliac vessels.

69. • Patients requiring surgery for free perforation have a mortality rate of
30% compared with 1% for those undergoing elective surgery. Following
resolution of an initial episode of diverticulitis, up to 30% of patients
will go on to develop recurrent diverticulitis.
• Four to 30% of patients will have episodic cramps, without clinical signs
of diverticulitis, and 30–40% will be asymptomatic. Patients who have
recovered after having peritonitis may develop small bowel
obstructions due to adhesions. Patients with colovesical fistulas may
develop urosepsis, and those with coloenteric fistulas may develop
malabsorption due to bacterial overgrowth or due to short gut
syndrome (as a result of the bypassing of segments of small bowel).
Local irritation of the perineum or abdominal wall skin can be seen with
colovaginal and colocutaneous fistulas, respectively. These fistulas can
also be associated with fluid losses.
• For patients who have undergone a surgical resection, 1.0–10.4% will
develop recurrent diverticulitis, with 0–3.1% requiring an additional
resection. Twenty-seven to 33% will complain of persisting symptoms.

70. Emergency resection for perforation
• mortality rate of 30%
• Recurrence 30%

71. After resection
• Recurrence (1-10%)
• Recurrence need resection (0-3%)
• Persistent symptoms (33%)

73. Bleeding (lower GI)
• Massive
– Transfusions
– Angiography
– If + superselective embolization
– If - observe patient, RBC scanning. An RBC nuclear scan
is a group of tests using small amounts of radioactive
material to mark (tag) red blood cells (RBCs). The body is
then scanned to detect the location and flow of the tagged
RBC
• Moderate
– Observe patient
– Colonoscopy