Diverticular Disease
Introduction
Background
Diverticular disease is a common disorder, yet it was not
recognized as a pathologic entity until the mid-19th
century. Diverticulitisand lower
gastrointestinal
(GI)
bleeding secondary to diverticulosis are the main
complications of clinical importance to emergency
physicians.
Pathophysiology
Diverticular disease may involve any part of the GI tract.
Typically, acquired, diverticular disease may be congenital,
such as Meckel's diverticulum (although this is rare).
Diverticula are herniations of the mucosa and submucosa or
the entire wall thickness through the muscularis (as seen in
congenital diverticula). The sigmoid is the most commonly
affected segment (95-98%); however, diverticular disease
may also involve the descending, ascending, and transverse
colon as well as the jejunum, ileum, and duodenum.
The images below depicting sigmoid diverticulitis are of the
same patient.
Sigmoid diverticulitis
in a 50-year-old man
with history of
diverticulosis and left
lower abdominal pain
and tenderness. This
image and the
images below are
sections from the
same patient.
Sigmoid diverticulitis
in a 50-year-old man
with history of
diverticulosis and left
lower abdominal pain
and tenderness.
Phlegmon. Sigmoid
diverticulitis in a 50year-old man with
history of
diverticulosis and left
lower abdominal pain
and tenderness. This
image and the one
below are
consecutive sections
of the same patient.
Phlegmon. Sigmoid
diverticulitis in a 50year-old man with
history of
diverticulosis and left
lower abdominal pain
and tenderness.
Precise etiology of this disease is unknown. High intraluminal
pressure and a weak colonic wall at the sites of nutrient
vessel penetration into the muscularis may lead to
herniation. The condition may also be caused by abnormal
colonic motility, defective muscular structure, defects in
collagen consistency (ie, increased cross-linking of collagen),
and aging.
Diverticulitis is an abscess or peridiverticular inflammation
initiated by the rupture of a microscopic mucosal abscess
into the mesentery. The infection may progress, fistulize,
obstruct, or spontaneously resolve. Acute diverticulitis results
from the inspissation of fecal material in the neck of the
diverticulum and resultant bacterial replication. Infection is
generally contained by pericolonic fat or adjacent organs, at
which point a local phlegmon develops. Macroperforation
may cause peritonitis and may erode locally.
Lower GI bleeding from diverticulosis results from rupture of
the small blood vessels that are stretched while coursing over
the dome of the diverticula.
Frequency
United States
Diverticular disease affects primarily those in developed
countries. Eighty years ago, the approximate prevalence of
diverticular disease was between 5% and 10%. A large study
performed in 2002 of 9,086 consecutive patients undergoing
colonoscopies revealed a prevalence of 27%, in which
prevalence increased with age.1
International
Diverticular disease has been dubbed the "disease of
Western civilization." In developed countries, the rate of
diverticular disease is between 5% and 45%, depending on
age and sex. In Africa and Asia, the prevalence is around 0.2%
and is typically right sided.
Mortality/Morbidity
Morbidity and mortality associated with diverticular disease
is primarily related to acute lower gastrointestinal bleeding,
diverticulitis, and perforated diverticulum. Fifteen percent of
persons with diverticular disease will develop acute GI
bleeding. Of those, one third will develop massive GI
bleeding. Risk of mortality with perforated diverticulum
increases with age, comorbid conditions, and onset of
perforation within the first year of diagnosis. Studies have
reported mortality rates between 22% and 39% for free
perforation and fecal peritonitis. Furthermore, multiple series
have noted that perforation may be the first manifestation of
complicated diverticulitis with a range in mortality of 50-70%.
Race
Diverticular disease primarily affects those in developed
countries. However, the incidence of diverticular disease is
increasing in Asian countries. In Asian and African countries,
the prevalence of diverticular disease is approximately 0.2%
and predominantly on the right side.
Sex
Gender variation occurs by age group. Diverticular disease is
more prevalent in men than in women younger than 50
years. Between the ages of 50-70 years, a slight female
predominance exists. In those older than 70 years, there is a
female predominance.
Age
The prevalence of diverticular disease increases with age:
 Less than 5% by age 40 years
 Approximately 30% by age 60 years
 65% by age 85 years
Clinical
History
1. Clinical historical features of inflammatory disease
include the following:
 Abdominal pain - Occurs mostly in the left lower
quadrant and tends to be steady, severe, and deep
 History of fever suggestive of diverticulitis
 Previous episodes of dull, colicky, and diffuse abdominal
pain accompanied with flatulence, distention, and
change in bowel habits (diverticulosis)
 Altered bowel habits including diarrhea, increased
constipation, and tenesmus (physician may note
obstipation when treating a complicating bowel
obstruction)
 Nausea and vomiting
 Dysuria, pyuria, and urinary frequency if bladder or
ureter are irritated
 History of pneumaturia or recurrent urinary tract
infections (colovesicular fistulas)
 Feculent vaginal discharge (fistulas with the uterus or
vagina)
 Severe and generalized abdominal pain (diffuse
peritonitis)
 Back or lower extremity pain (perforation)
2. Establish history of hemorrhagic disease, including the
following:
 Lower GI bleeding from diverticulosis occurs in the form
of bright red-colored or wine-colored stools.
 Onset of bleeding typically is sudden, painless, and
accompanied by an urge to defecate.
 Amount of bleeding typically is massive and tends to
stop spontaneously.
 Ascertain a previous history of gastric or duodenal
ulcers, liver disease, or GI bleeding.

Discomfort
and
pain
upon
defecation
indicate hemorrhoids or anal fissures.
 History of weight loss and mucus in the stools
indicates inflammatory bowel disease.
 Establish list of medications used (nonsteroidal antiinflammatory drugs [NSAIDs], steroids) and of alcohol
abuse.
 Establish bleeding tendencies.
Physical
1. Establish localized tenderness, rebound tenderness,
and/or guarding. This is essential in the clinical
management of diverticular disease. Their presence
indicates diverticulitis.
2. When associated with GI bleeding, tenderness is not
typical of diverticular etiology; it indicates other disease
processes.
3. Assess vital signs to determine hemodynamic stability
and profile of presentation.
4. Low-grade fever commonly is found in diverticulitis.
5. Rectal examination identifies tenderness, establishes the
color of stools, and determines the presence and extent
of GI bleeding. A mass may be seen in the cul-de-sac.
6. Diffuse abdominal tenderness, rebound, absent bowel
sounds, and/or high-grade fever may be elicited. These
indicate possible complications of perforation and/or
peritonitis.
7. Pelvic and rectal examinations establish the correct
diagnosis.
8. Palpate for any mass or fullness, particularly in the left
iliac fossa.
9. Abdomen may be distended and tympanic.
10. Pain may be acute and located mainly in the left lower
quadrant.
Causes
1. Low-fiber diet is the highest risk factor for diverticular
disease. Common in industrialized nations, a low-fiber
diet forms low-bulk stool that leads to increased
segmentation of the colon during propulsion, causing
increased intraluminal pressure and formation of
diverticula.
2. High fat and beef diets also cause diverticular disease,
probably for the same reasons as above.
3. Genetic causes exist. Asians have right-sided diverticula
preponderance. In westerners, diverticula develop
mostly on the left side.
4. Aging leads to change in collagen structure such as
increased cross-linking and acid solubility.
5. Colonic motility disorders are a cause.
6. Corticosteroid therapy but not nonsteroidal antiinflammatory therapy has recently been shown to
increase the risk of diverticulitis.2
7. Colonic segmentation: Nonpropulsive contractions
produce isolated segments or little chambers with high
pressure within.
8.
Defects in colonic wall strength can cause diverticular
disease.
Differential Diagnoses
Abdominal Hernias
Irritable Bowel Syndrome
Abdominal Trauma, Blunt
Lower Gastrointestinal Bleeding
Inflammatory Bowel Disease
Lower Gastrointestinal Bleeding,
Surgical Treatment
Adnexal Tumors
Lymphogranuloma Venereum
Appendicitis
Mesenteric Artery Ischemia
Cholangitis
Ovarian Cysts
Cholecystitis
Ovarian Torsion
Cholelithiasis
Pancreatitis, Acute
Syphilis
Colon Cancer, Adenocarcinoma
Inflammatory Disease
Perforated Peptic Ulcer
Crohn Disease
Peritonitis and Abdominal Sepsis
Duodenal Ulcers
Proctitis and Anusitis
Ectopic Pregnancy
Chronic Mesenteric Ischemia
Endometriosis
Tuberculosis
Endometritis
Ulcerative Colitis
Gastric Ulcers
Urinary Tract Infection, Females
Gastritis, Acute
Urinary Tract Infection, Males
Hemorrhoids
Volvulus, Sigmoid and Cecal
Acalculous Cholecystitis
Intestinal Perforation
intestinal irritation (ileus) and two thirds of visceral
perforations (free air). Radiographs can identify volvulus,
bowel obstruction, renal stones, and occasionally
suggest the existence of intra-abdominal masses. Chest
radiographs can identify free air to rule out perforation.
Radiographs are shown below.
o
"Thumbprinting" (seen in left mid quadrant) on a
plain abdominal radiograph (close-up image).
o
WorkupPelvic
Laboratory Studies
1. Complete blood count: CBC identifies leukocytosis
and/or a left shift in acute diverticulitis; however, 60% of
patients may have a normal white blood cell count,
particularly elderly and immunocompromised patients.
Manage GI bleeding by establishing hematocrit.
2. Type and cross-match blood; also obtain coagulation and
bleeding time profiles in patients with lower GI bleeding
or frank peritonitis.
3. Urinalysis/urine culture: This identifies urinary tract
infections and hematuria. It indicates existence of
colovesicular fistulas or if diverticular disease is the
etiology.
4. Serum electrolytes: In the absence of a prerenal picture,
an elevated BUN/creatinine ratio indicates the presence
of blood in the GI tract.
5. Lipase/amylase and liver function tests: These may help
establish other etiologies or features in the presentation
of abdominal pain. This is particularly important when
patients present atypically (eg, steroid therapy, elderly
patients, those with diabetes) or relatively late in the
course of an inflammatory process with generalized
tenderness or frank peritonitis.
6. Perform blood cultures if acute diverticulitis is suspected
prior to infusion of empiric antibiotic therapy.
Imaging Studies
1. Plain radiographs: An acute abdominal series, with flat
and upright abdominal imaging, identifies signs of
2.
o
o
o
o
Thickening of the bowel wall in the descending
colon due to bowel edema can be seen in the left
lower quadrant on this plain abdominal
radiograph. Note the narrowed colonic lumen. Note
the CT scan images in this article are from the same
62-year-old patient with diverticulitis.
CT scan: This is the test of choice for acute diverticulitis.
Look for diverticula, localized colonic wall thickening (>5
mm), abscesses, fistulas, and pericolic fat inflammation,
and exclude other pathologies, such as a tubo-ovarian
abscess or aortic or other vascular blood leakage.
Administering rectal contrast with no intravenous
contrast has been shown in one study to be equally as
sensitive as CT scans where oral contrast was
administered; however, the test of choice is a CT scan
that includes intravenous and oral contrast. Ten percent
of CT scans are unable to determine between
diverticular disease and carcinoma. Other findings
include the following:
Thickened fascia, 78.9%
Colonic diverticula, 84%
Soft tissue masses representing phlegmon, pericolic fluid
collections, representing abscesses, 35%
Muscular hypertrophy, 26.3%
o
Arrowhead sign (focal thickening of colonic wall with an
arrowhead-shaped lumen pointing to inflamed
diverticula), 23.7%
3. Double-contrast enema: This is useful in the diagnosis of
diverticulosis yet contraindicated in acute diverticulitis
because of the fear of perforation, leak of barium and
intestinal content, and subsequent severe peritonitis.
4. Water-soluble contrast enema: Water-soluble contrast is
safe in intraluminal imaging and useful in the workup of
patients with suspected diverticular disease. However, a
prospective study in 2000 has shown CT scanning to have
a 97% sensitivity rate as compared to 92% sensitivity rate
for water-soluble contrast enema. CT scanning was also
superior in detecting abscesses.
5. Ultrasonography: Ultrasonography is a noninvasive test
used by a number of investigators and has been reported
to have a specificity as high as 99.8%. 3 When using highresolution graded compression ultrasonography, a
sensitivity of 85-98% has been reported and a specificity
of 80-98%. Findings when used at the point of maximal
tenderness can reveal bowel wall thickening of 4-5 mm,
target appearance, and abscess formation.
6. Magnetic resonance imaging (MRI): MRI was evaluated
in one study and found that it accurately identified
diverticulitis in 10 out of 11 patients.4 Larger studies are
needed to further evaluate the modality of MRI in aiding
in diagnosis of diverticulitis.
Procedures
1. Endoscopy: Endoscopy is useful in diagnosing diverticular
disease and in establishing the source of lower GI
bleeding. Endoscopy is avoided in acute diverticulitis
because of the fear of perforation and peritonitis. A
nasogastric tube is usually inserted first to exclude most
upper GI causes of rectal bleeding. A 2000 study found
that aggressive urgent colonoscopy performed by a
dedicated endoscopy team with experience in
interventional procedures uses colonoscopy as both a
diagnostic measure and a therapeutic measure.5
2. Technetium-99m-blood cell scan: Technetium-99m
labeled RBC scan has a sensitivity of 97%, specificity of
85%, and a positive predictive value of 94% to identify
active bleeding at a rate of 0.1 mL/min.6 It does,
however, have a poor ability to localize the source of
bleeding. Follow with a selective mesenteric arteriogram
to identify the source.
Treatment
Prehospital Care
1. Start intravenous fluids and oxygen, particularly during
lengthy prehospital periods.
2. Scenarios that usually require mobilization of prehospital
resources are severe abdominal pain, GI bleeding, or
hemodynamic instability with a diagnosis that has not
yet been established.
Emergency Department Care
1. When a patient presents with classic signs and
symptoms of uncomplicated diverticulosis, discharge on
antispasmodics and a high-fiber diet with a follow-up
sigmoidoscopy at a later time. Typically, no fever,
leukocytosis, palpable mass, or other evidence of acute
diverticulitis is present.
2. For patients who present with signs and symptoms of
acute diverticulitis, take the following actions:
 Administer intravenous fluid resuscitation as indicated.
 Give the patient nothing by mouth (NPO).
 In a recent retrospective study, patients who underwent
surgical therapy after an initial episode of acute
diverticulitis had less recurrence than those who were
managed medically.
 Analgesic pain control should be given. Although studies
have indicated that analgesics do not mask peritoneal
signs, consider general surgery consultation prior to
analgesic pain control.
 Insert a nasogastric tube if the patient is vomiting or
colonic obstruction is suspected.
 Administer empiric broad-spectrum intravenous (IV)
antibiotics. Antibiotics should target anaerobes such
as Bacteroides
fragilis and Peptostreptococcus, Peptococcus,
and Clostridium species, as well as aerobes such
as Escherichia coli and Klebsiella, Proteus, Streptococcus,
and Enterobacterspecies. If an abscess is suspected,
coverage also should include Pseudomonas aeruginosa.
3. Most patients diagnosed with acute diverticulitis should
be hospitalized; most improve in 48-72 hours.
4. Patients with mild-to-moderate acute diverticulitis and
no systemic signs or localized peritonitis may be
discharged home on a low-residue food diet and oral
antibiotics covering gram-negative organisms and
anaerobes. Instruct patients to return if the pain
increases or signs of systemic infection develop,
assuming the patient is a normal host with no clinical
evidence of other morbid conditions requiring admission
or additional workup.
5. Perform the following if the patient presents with signs
and symptoms of acute GI bleeding:
 Address standard ABCs appropriately.
 Administer supplemental oxygen.
 Maintain hemodynamic stability.
 Secure 2 large-bore IV lines.
 Administer lactated Ringer or normal saline solution.
Once 2 liters of intravenous fluids are administered,
transfuse blood.
 Insert a nasogastric tube to exclude potential upper GI
source for the bleeding.
 Search for comorbid conditions such as an acute
myocardial infarction from the hypovolemic state.

Insert a urinary catheter to monitor output, which
reflects adequacy of resuscitation.
 Secure the appropriate emergent consultations quickly.
 Admit the patient to an intensive care setting.
6. Subsequent management centers on identifying the
source of bleeding.
7. Diagnosis and treatment guidelines for sigmoid
diverticulitis are available from the American Society of
Colon and Rectal Surgeons.7
Consultations
Consult with a general surgeon if the patient presents with
any of the following:
1. Sepsis, fistula, or obstruction
2. Clinical evidence of perforation of viscus
3. Failure of medical therapy or clinical deterioration
4. Inability to exclude carcinoma or recurrence of the
disease
5. Young age, use of steroids, immunocompromised
patients, and right-sided diverticulitis (relative
indications for surgical intervention)
Consult for further workup and management as well as the
arrangement of follow-up colonoscopy.
Medication
Goals of pharmacotherapy are to treat the infection and
prevent complications. Organisms that should be covered by
antimicrobial therapy include the following:
1. Anaerobes -Bacteroides fragilis, Peptostreptococcus,
Clostridium species
2. Aerobes
-Escherichia
coli,
Klebsiella,
Proteus,
Streptococcus, Enterobacter organisms
Typical antimicrobial therapy is divided into inpatient and
outpatient regimens.
1. Outpatient therapy (one of the following):
 Metronidazole plus ciprofloxacin or levofloxacin or
TMP/SMX
 Amoxicillin/clavulanate
 Moxifloxacin
2. Inpatient therapy - Mild-to-moderate disease (one of the
following):
 Metronidazole plus
ciprofloxacin or levofloxacin
(intravenous)
 Ampicillin/sulbactam
 Ertapenem
 Piperacillin/tazobactam
 Ticarcillin/clavulanate
 Tigecycline
3. Inpatient therapy - Severe disease (one of the following):
 Imipenem
 Doripenem
 Meropenem
 Ampicillin
plus
metronidazole
plus
ciprofloxacin or levofloxacin or gentamicin
4. For penicillin-allergic patients: Metronidazole plus
aztreonam or ciprofloxacin or levofloxacin
Antibiotics
Therapy should cover all likely pathogens in the context of
the clinical setting.
Ciprofloxacin (Cipro)
Fluoroquinolone that inhibits bacterial DNA synthesis and,
consequently, growth, by inhibiting DNA gyrase and
topoisomerases, which are required for replication,
transcription, and translation of genetic material. Quinolones
have broad activity against gram-positive and gram-negative
aerobic organisms. Has no activity against anaerobes.
Continue treatment for at least 2 d (7-14 d typical) after signs
and symptoms have disappeared.
Adult
500 mg or 750 mg PO bid 400 mg IV bid
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
Amoxicillin and clavulanate (Augmentin)
Amoxicillin inhibits bacterial cell wall synthesis by binding to
penicillin-binding proteins. Addition of clavulanate inhibits
beta-lactamase
producing
bacteria.
Good alternative antibiotic for patients allergic or intolerant
to the macrolide class. Usually well tolerated and provides
good coverage to most infectious agents. Not effective
against Mycoplasma and Legionella species. Half-life of oral
dosage form is 1-1.3 h. Has good tissue penetration but does
not
enter
cerebrospinal
fluid.
For children >3 months, base dosing protocol on amoxicillin
content. Because of different amoxicillin/clavulanic acid
ratios in 250-mg tab (250/125) vs 250-mg chewable-tab
(250/62.5), do not use 250-mg tab until child weighs >40 kg.
Adult
500-875 mg PO q12h or 250-500 mg PO q8h for 7-10 d
Pediatric
<3 months: 125 mg/5 mL PO susp; 30 mg/kg/d (based on
amoxicillin component) divided bid for 7-10 d
>3 months: If using 200 mg/5 mL or 400 mg/5 mL susp, 45
mg/kg/d PO divided q12h; if using 125 mg/5 mL or 250 mg/5
mL susp, 40 mg/kg/d PO divided bid for 7-10 d
>40 kg: Administer as in adults
Ertapenem (Invanz)
Bactericidal activity results from inhibition of cell wall
synthesis and is mediated through ertapenem binding to
penicillin-binding proteins. Stable against hydrolysis by a
variety of beta-lactamases including penicillinases,
cephalosporinases, and extended-spectrum beta-lactamases.
Hydrolyzed by metallo-beta-lactamases.
Adult
1 g qd for 7- 14 d if IV; infuse over 30 min if IV CrCl <30
mL/min/1.73 m2: 500 mg IV qd
Pediatric
<3 months: Not established
3 months to 12 years: 15 mg/kg IV q12h; not to exceed 1 g/d
>12 years: Administer as in adults
Gentamicin sulfate
Aminoglycoside antibiotic for gram-negative coverage
bacteria including Pseudomonas species. Synergistic with
beta-lactamase against enterococci. Interferes with bacterial
protein synthesis by binding to 30S and 50S ribosomal
subunits.
Dosing regimens are numerous and are adjusted based on
CrCl and changes in volume of distribution, as well as body
space into which agent needs to distribute. Dose of
gentamicin may be given IV/IM. Each regimen must be
followed by at least trough level drawn on third or fourth
dose, 0.5 h before dosing; may draw peak level 0.5 h after 30min infusion.
Adult
5 mg/kg IV/IM qd
Pediatric
<5 years: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose IV/IM q8h or 6-7.5 mg/kg/d
divided q8h; not to exceed 300 mg/d; monitor as in adult
Tigecycline (Tygacil)
A glycylcycline antibiotic that is structurally similar to
tetracycline antibiotics. Inhibits bacterial protein translation
by binding to 30S ribosomal subunit, and blocks entry of
amino-acyl tRNA molecules in ribosome A site. Complicated
intra-abdominal infections caused by C freundii, E cloacae, E
coli, K oxytoca, K pneumoniae, E faecalis (vancomycinsusceptible isolates only), S aureus (methicillin-susceptible
isolates only), S anginosusgroup. (includes S anginosus, S
intermedius, and S constellatus), B fragilis, B
thetaiotaomicron,
B
uniformis,
B
vulgatus,
C
perfringens, and P micros.
Adult
Infuse each dose over 30-60 min 100 mg IV once, then 50 mg
IV q12h Severe hepatic impairment (ie, Child Pugh class C):
100 mg IV once, then 25 mg IV q12h
Pediatric
<18 years: Not established
>18 years: Administer as in adults
Imipenem and cilastatin (Primaxin)
For treatment of multiple organism infections in which other
agents do not have wide-spectrum coverage or are
contraindicated due to potential for toxicity.
Adult
Base initial dose on severity of infection, and administer in
equally divided doses; dose may range from 250-500 mg q6h
IV for a maximum of 3-4 g/d
Alternatively, 500-750 mg q12h IM or intra-abdominally
Pediatric
Infants >3 months and children
<12 years: 15-25 mg/kg/dose IV q6h
Fully susceptible organisms: Not to exceed 2 g/d
Infections with moderately susceptible organisms: Not to
exceed 4 g/d
>12 years: Administer as in adults
Doripenem (Doribax)
Carbapenem antibiotic. Elicits activity against a wide range of
gram-positive and gram-negative bacteria. Indicated as a
single agent for complicated intra-abdominal infections
caused by susceptible strains of Escherichia coli, Klebsiella
pneumoniae, Pseudomonas aeruginosa, Bacteroides caccae,
Bacteroides
fragilis,
Bacteroides
thetaiotaomicron,
Bacteroides uniformis, Bacteroides vulgatus, Streptococcus
intermedius,
Streptococcus
constellatus,
and
Peptostreptococcus micros.
Adult
500 mg IV q8h infused over 1 h
CrCl> 50: No dosage adjustment necessary
CrCl≥ 30 to ≤ 50: 250 mg IV q8h
CrCl> 10 to < 30: 250 mg IV q12h
Pediatric
<18 years: Not established
>18 years: Administer as in adults
Aztreonam (Azactam)
A monobactam, not a beta-lactam antibiotic that inhibits cell
wall synthesis during bacterial growth. Active against gramnegative bacilli but very limited gram-positive activity and not
useful for anaerobes. Lacks cross-sensitivity with beta-lactam
antibiotics. May be used in patients allergic to penicillins or
cephalosporins.
Duration of therapy depends on severity of infection and
continued for at least 48 h after patient asymptomatic or
evidence of bacterial eradication obtained. Doses smaller
than
indicated
should
not
be
used.
Transient or persistent renal insufficiency may prolong serum
levels. After initial loading dose of 1 or 2 g, reduce dose by
one half for estimated ClCr of 10-30 mL/min/1.73 m2. When
only serum creatinine concentration available, the following
formula (based on sex, weight, and age) can approximate
ClCr. Serum creatinine should represent a steady state of
renal function.
Males: ClCr = [(weight in kg)(140 - age)] divided by (72 X
serum creatinine in mg/dL)
Females:
0.85
X
above
value
In patients with severe renal failure (ClCr <10 mL/min/1.73
m2), those supported by hemodialysis, usual dose of 500 mg,
1 g, or 2 g, is given initially.
Maintenance dose is one fourth of usual initial dose given at
usual fixed interval of 6, 8, or 12 h.
For serious or life-threatening infections, supplement
maintenance doses with one-eighth of initial dose after each
hemodialysis session.
Elderly persons may have diminished renal function. Renal
status is a major determinant of dosage in these patients.
Serum creatinine level may not be an accurate determinant
of renal status. Therefore, as with all antibiotics eliminated
by kidneys, obtain estimates of ClCr, and make appropriate
dosage modifications. Insufficient data are available
regarding IM administration to pediatric patients or dosing in
pediatric patients with renal impairment. Administered IV
only to pediatric patients with normal renal function.
Adult
500-2000 mg IV/IM q6-8h
Pediatric
90-120 mg/kg/d IV/IM divided q6-8h
Metronidazole (Flagyl)
Active against various anaerobic bacteria. Enters cell, binds
DNA, and inhibits protein synthesis, causing cell death.
Adult
500 mg PO/IV qid
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Piperacillin and tazobactam sodium (Zosyn)
Antipseudomonal penicillin plus beta-lactamase inhibitor.
Inhibits biosynthesis of cell wall mucopeptide and is effective
during stage of active multiplication.
Adult
3/0.375 g (piperacillin 3 g and tazobactam 0.375 g) IV q6h
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Levofloxacin (Levaquin)
For pseudomonal infections and infections due to multidrug
resistant gram-negative organisms.
Adult
500-750 mg PO/IV qd for 7-14 d
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
Moxifloxacin (Avelox)
Inhibits the A subunits of DNA gyrase, resulting in inhibition
of bacterial DNA replication and transcription.
Adult
400 mg PO/IV qd
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
Ticarcillin and clavulanate potassium (Timentin)
Inhibits biosynthesis of cell wall mucopeptide and is effective
during
stage
of
active
growth.
Antipseudomonal penicillin plus beta-lactamase inhibitor that
provides coverage against most gram-positive organisms,
most gram-negative organisms, and most anaerobes.
Adult
3.1 g IV q4-6h
Pediatric
75 mg/kg IV q6h
Meropenem (Merrem I.V.)
Bactericidal broad-spectrum carbapenem antibiotic that
inhibits cell wall synthesis. Effective against most grampositive
and
gram-negative
bacteria.
Has slightly increased activity against gram-negatives and
slightly decreased activity against staphylococci and
streptococci compared with imipenem.
Adult
1 g IV q8h
Pediatric
40 mg/kg IV q8h
Ampicillin (Principen)
Broad-spectrum penicillin. Interferes with bacterial cell wall
synthesis during active replication, causing bactericidal
activity against susceptible organisms. Alternative to
amoxicillin when unable to take medication orally.
Until recently, the HACEK bacteria were uniformly
susceptible to ampicillin. Recently, however, beta-lactamase–
producing strains of HACEK have been identified.
Adult
2 g IV q6h; not to exceed 12 g/d
Pediatric
50-100
mg/kg/d
PO
divided
q4-6h
100-400 mg/kg/d IV/IM divided q4-6h
Follow-up
Further Inpatient Care
1. Modalities used to stop bleeding include the following:
 Intra-arterial vasopressin
 Embolization was successful in 85% of cases based on a
recent meta-analysis.
 Endoscopic homeostasis by epinephrine injection, heater
probe, or bipolar coagulation
2. If bleeding persists or clinical condition does not permit
the above modalities, perform emergency surgery.
Further Outpatient Care
1. If the patient is not admitted and the diverticular disease
episode resolves, arrange for colonoscopy and/or barium
contrast enema.
2. Recommend a fiber-rich diet.
Transfer
1. Transfer patients if the medical center has no general
surgeons or radiologic facilities.
2. Do not transfer patients with active GI bleeding and
impending or actual peritonitis.
Deterrence/Prevention
1. High-fiber diet
2. Psyllium
3. Agar
4. Methylcellulose
Complications
1. Fistulas
 Fistulas occur secondary to chronic diverticulitis or
recurrent episodes of acute diverticulitis. Chronic
inflammatory process causes adhesions to form between
the colon and neighboring organs.
 Colovesicular fistulas are the most common (most occur
in men), followed by colovaginal fistulas (80% occur in
women who have undergone hysterectomies).
Additionally, fistulas to the integument, uterus, fallopian
tubes, and pelvic floor have been reported.
 Contrast enemas, retrograde dye studies, or CT scan
confirms the diagnosis.
 Treatment of fistulas consists of surgical resection of the
involved colon.
2. Hemorrhage
3. Perforation with peritonitis
 Clinical presentation typically is more severe than in
acute diverticulitis.
 It often is diagnosed by observing free air on plain
radiographs. Barium enemas and endoscopy are
contraindicated.
 Treat surgically. Laparoscopic resection has comparable
results to open resections when performed in
experienced institutions.
4. Abscess
o Suspect abscess when the patient fails to respond
to medical therapy. It may be palpable.
o CT scan or ultrasonography typically permits
diagnosis of abscess.
o Treat with percutaneous drainage. Some report
successful transrectal and transvaginal drainage in
selected situations.
5. Colonic obstruction
o Colonic obstruction results from repetitive
episodes of diverticulitis that cause mycosis coli or
colonic muscular wall thickening.
o Differentiate from other causes of obstruction,
such as ischemia, colitis, or carcinoma, by contrast
enemas or endoscopy.
o If diagnosis is uncertain or obstructive symptoms
develop, perform resection.
Prognosis
 The Hinchey staging system reflects surgical
outcome. It guides surgeons in selecting their
operative strategy and reflects the risk of secondary
complications after the acute episode is managed
successfully.
o Stage I - Pericolic abscess
o Stage II - Pelvic abscess
o Stage III - Purulent peritonitis
o Stage IV - Feculent peritonitis
 Stage I disease treated by primary resection has 0%
mortality, while stages II and III have 5% and 18%
mortality, respectively.
 Prognosis is good with early detection and
treatment of complications.

Of those with a first episode of diverticulitis who
successfully are treated medically, 67% do not have
subsequent attacks requiring hospitalization, and
33% have recurrences; 2-3 recurrences in 1-2 years
is an indication to electively remove the involved
segment of colon.
 Of those with diverticular bleeding, as many as 20%
rebleed within months to years.
Miscellaneous
Medicolegal Pitfalls
 Failure to promptly initiate empiric antibiotic
therapy with clinically evident diverticulitis
 Failure to promptly diagnose visceral perforation or
peritonitis
 Failure to adequately treat patients younger than 40
years
 Failure to appreciate that right lower quadrant pain
in an elderly patient or a premenopausal woman
may be caused by acute diverticulitis
Special Concerns
 Hemorrhage secondary to diverticulosis in elderly
persons carries a worse morbidity and mortality.
A Comparison of Laparoscopic Sigmoid Resection and Open
Sigmoid Resection in Managing Diverticular Disease
Summary
How does laparoscopic sigmoid resection (LSR) compare with
open sigmoid resection (OSR) in managing diverticular
disease? The authors conducted a trial with 52 patients
randomized into each group. The operating time for LSR was
about an hour longer than that with OSR. The results were
similar with respect to overall complication rate; however,
major complications such as leakage, bleeding, and abscess
formation were more frequent in the OSR group (P = .038).
Patients in the LSR group returned home earlier and had less
postoperative pain.
Viewpoint
This report found that LSR is at least as good as and possibly
better than OSR in managing diverticular disease that
requires surgery. The quality-of-life score was improved in
the LSR group, although it is possible that some patients
knew which operation had been performed despite the
covered incisional area. A larger trial might have
demonstrated a significant reduction in overall postoperative
complications in the LSR group.