Diverticular Disease Update 2012

New Approaches to
Diverticulosis and
Diverticulitis Management
Neil Stollman MD, FACG
Chairman, Department of Medicine
Alta Bates Summit Medical Center
Oakland, CA
Associate Clinical Professor of Medicine
University of California San Francisco
San Francisco, CA
Anatomy / Etiology
Fiber as risk factor for DD (Diverticular Disease)
Fiber as treatment for DD
Other risk factors: nuts/seeds?
SUDD: a new paradigm of chronic DD?
Diverticulitis: 5-ASA, antibiotics, probiotics
Surgical timing change?
Diverticular Bleeding
Let’s Play: Separated at birth?
Example: “Teenage Mutant Ninja tic?”
• True incidence difficult to measure as most
patients asymptomatic
• No sex predilection generally
• “Disease of Western Civilization”
– Rare in rural Africa & Asia, common in US, Europe,
– Japanese migrating to Hawaii have rate intermediate
b/w native Japanese and mainland born, suggesting
‘westernization’ of colon.
Prevalence increasing over time
Rate (%)
Hong Kong
Jun S, Stollman N. Epidemiology of Diverticular Disease. Ballieres Clin Gastroenterol 2003
Epidemiology: Increasing over time (US)
• Nationwide inpatient sample
(NIS) data 1998-2005 (HCUP)
• 26% increase in admissions
– 82% increase in ages 18-44
• 29% increase in surgeries
– 73% increase in ages 18-44
• M>F for patients <45 years
• F>M for patients >45 years
• Lower rates in west, c/w rest
of country (?diet, ?obesity)
Etzioni DA et al. Ann Surg 2009;249:210-17
Nguyen GC et al. World J Gastroenterol 2011;28:1600-5
Pathologic Anatomy I
• Typically arise in 2 or 4 parallel rows:
– Along the mesenteric sides of the antimesenteric taenia and along both sides of the
mesenteric taenia
– Corresponds to sites of arterial penetration
through smooth muscle
– Pseudo-diverticula in that mucosa and
submucosa herniate through the muscle, but tic
does not include all layers of wall.
Diverticula form at sites of vascular
Pathologic Anatomy II
• Western individuals:
– 90% left-sided
15% right-sided
• Asian individuals:
– 25% left-sided
75% right-sided
• Vary in number from solitary to hundreds
• Typically 5-10mm in diameter, although
‘giant’ diverticula described.
Sigmoid Diverticula: BE
Pan-colonic diverticula: BE
Separated at birth?
Etiology / Pathogenesis I
Colonic Wall Resistance
• No evidence that atherosclerosis or
venous changes predispose
• >200% increase in elastin deposition, laid
down in contracted form, Þ shortening of
taenia and bunching of circular muscle
• Precocious diverticulosis occurs in
patients with connective tissue disorders
(Ehlers-Danlos, Marfan’s)
Etiology / Pathogenesis II
Disordered Motility
•  resting, post-prandial, & neostigmineinduced luminal pressures demonstrated in
patients with tics vs. controls without
• Symptomatic pts have higher motility indices
than asymptomatic patients
• Higher right-sided pressures seen in Asian
patients with right-sided diverticula
• Wynne-Jones: westernized urban lifestyle
“impermissive of flatus”  air retention 
increased intraluminal pressures & tic
formation (Lancet 1975;2:211-12)
Etiology / Pathogenesis III:
Painter’s “Little Bladders” Theory:
• Simultaneous manometry & cineradiography.
• Contractions by haustra cause ‘segmentation’ in
which colon is not continuous tube but series of
discrete ‘little bladders’, which can attain
‘locally’ high pressures, favoring herniation.
• Might have physiologic role in delaying transit
and augmenting water reabsorption.
• Western diet may enhance this occurrence.
Etiology IV:
Fiber as RISK FACTOR for DD
• Historically, felt to be ‘fiber deficiency’ disease
– Worldwide striking geographic correlation with low
dietary fiber intake (eg Africans with high fiber diet
less DD c/w British with lower fiber intake)
– Develops in the west after the introduction of milling
– Humans & domesticated animals on low-fiber diets
are only species to develop diverticula
– Suggest preventable and/or correctable by ↑ fiber
• Problems: assumes uniform diets within
population, uncontrolled for other confounding
factors such as lifespan
Etiology: dietary fiber
• Stool weights & transit times (n=1200)
– UK patients: western low-fiber diet
– Rural Ugandans: high fiber diet
Transit time
80 hours
34 hours
Painter NS, Burkitt DP. Br Med J 1971;2:450–54
110 gm/d
450 gm/d
Etiology: dietary fiber
•  transit-times &  stool volume may 
intraluminal pressures and lead to diverticula
• Supported by rats fed diets of varying fiber
content over natural lifespan:
– Low-fiber diet:
45% developed diverticula
– High-fiber diet:
9% developed diverticula
– Histologically similar to human diverticula, but
mainly right-sided
Fiber as RISK FACTOR for developing DD
• Cross section study of >2000 screening colonoscopies,
30-80 years old, captured dietary / lifestyle info
• 42% overall had diverticulosis, increasing with age
• Fiber intake: highest quartile vs lowest:
– prevalence ratio for diverticulosis: 1.3 (1.13-1.50)
• BMs: >15/week vs <7/week
– prevalence ratio for diverticulosis: 1.7 (1.24-2.34)
• Physical activity, fat or red meat intake: no association
• “Hypotheses regarding risk factors for asymptomatic
diverticular disease should be reconsidered”
Peery AF et al. Gastroenterology 2012;142:266-72
Peery: Limitations
• Diet history taken after pts told they had DD
– Possible recall bias if aware of fiber/DD hypothesis
– Dietary hx one year only, lifetime intake most relevant
(is current diet reflective of lifelong habits?)
– Perhaps instructed to take fiber from prior dx
– Perhaps taking more fiber because having symptoms
• Even if accurate, data do not undermine possible
benefit of fiber in Rx of symptomatic DD
Fiber: risk for Sxs or complications?
• 2 large prospective cohort studies have shown inverse
relationship b/w fiber intake and diverticular complications
• HPFU study, >43K men, US, 1988-1992, no prior colonic dz
– RR for symptomatic disease in highest vs lowest fiber
groups = 0.63 (.44-.91) (insoluble fiber, esp cellulose)
• EPIC Oxford Study, 47K M & F, UK, 12 year f/u
– 812 cases (806 hospitalizations, 6 deaths)
Adjusted Relative Risk
– Highest vs lowest fiber intake:
0.59 (.46-.78)
– Vegetarians vs meat eaters:
0.69 (.55-.86)
Aldoori WH et al. J Nutr 1998;128:714-19
Crowe FL et al. BMJ 2011;343:
Does Evidence Support a
Restriction on Nuts, Corn, and Popcorn?
• ACG Practice Guidelines 19991
– “Controlled studies that support this belief are lacking….no
role for ‘elimination’ diet”
• Strate et al 20082 [US Health Professionals Study follow-up]
– 47,000 men free of DD on entry, followed 18 years
– 801 incident cases of diverticulitis
– Hazard ratio for highest vs lowest consumption
• Nuts:
0.80 (0.63 – 1.01), P = 0.04
• Popcorn: 0.72 (0.56 – 0.92), P = 0.007
• Not only ‘no association’ but nuts and popcorn may actually
have inverse / protective effect
1. Stollman NH, Raskin JB. Am J Gastroenterol. 1999;94(11):3110.
2. Strate LL et al. JAMA. 2008;300(8):907.
Separated at birth?
Natural History
• Majority of patients (+/-80%) will never
have symptomatic disease
• Serial barium studies reveal that
disorder is generally not progressive, ie.
pattern develops early and remains
fairly static.
Rate of progression to AD in
incidentally found diverticulosis?
• Risk of AD widely quoted at 15-25% in reviews,
texts and ACG guidelines. Based on older data
when true denominator unknown
• Retrospective review LA-VAMC 1996-2011
• 2127 pts with baseline diverticulosis (97% men)
• 130 month follow up:
– Liberal criteria dx AD: 4.3%
– Strict criteria dx AD: 1.0% (CT or surgery confirmed)
• Risk highest in younger patients
• Likely lower than we’ve thought
Shahedi K et al. DDW 2012, Plenary Presentation, #847
SUDD: a new paradigm?
• We’ve historically thought of DD as all or none,
(asymptomatic or complicated) but now conceptualizing a
“middle ground” of SUDD (Symptomatic Uncomplicated
Diverticular Disease), and evidence accumulating
demonstrating subclinical inflammation in such patients
• Possible mechanisms:
– Inflammatory damage to enteric nerves (and aberrant reinnervation leading to hypersensitivity, enhanced afferent
response to stimuli)
– Altered neuropeptides
– Subacute obstruction secondary to fibrotic reaction
– Muscle hypertrophy with increased intraluminal pressure
Predicting recurrent pain / SUDD
261 patients with diverticulosis on barium enema
170 eligible for follow up
136 provided bowel / psych symptoms
Recurrent pain 45
Pain free
Asymptomatic 79
Pain 42
Humes et al. British Journal of Surgery. 2008;95:195-198.
Pain free
Excluded 91
Deceased 61
Declined FU 21
Misc 9
SUDD: Association between symptoms &
postprandial contractions
• 30 healthy volunteers
• 115 patients with
colonic diverticula
– 30 asymptomatic (ADD)
– 30 symptomatic
uncomplicated (SUDD)
– 55 symptomatic
complicated (SCDD)
Motility index
Cortesini et al Dis Colon Rectum 1991;34(4):339-42
Increased expression of galanin & tachykinins in SUDD
• Prospective study
• Detailed bowel symptom
– 17 symptomatic
– 15 asymptomatic DD pts
• Unprepared flexible
– Mucosal biopsy
peridiverticular & rectal
• Normal appearance on
routine histology
• No evidence of
Simpson et al Neurogastroenterol Motil 2009;21:847-858.
Substance P
Neuropeptide K
Inflammation in DD
• Fecal calprotectin (FC) levels
in healthy controls, IBS pts,
asymptomatic DD, SUDD,
acute diverticulitis (AD)
• FC values normal in healthy
controls, IBS & asymptomatic
DD; higher in SUDD and AD
• FC levels correlated with
inflammatory infiltrate
• FC levels decreased with Rx
in AD and SUDD
Tursi A, et al. Int J Colorectal Dis 2009;24:49-55
Visceral hypersensitivity in SUDD
Rectal barostat study in healthy volunteers (HV), asymptomatic
DD (DDA) and symptomatic DD (DDS)
Humes et al Neurogastroenterol Motil 2012;24:318-e163
Post – diverticulitis IBS?
• Retrospective review of
1102 pts LAVAMC with AD
b/w 1996 and 2011,
without prior Dx of IBS
(96% men, mean 64 years)
• Hazard Ratio for
subsequent Dx IBS or FBD
=4.6 (1.6-13.6, P=0.005)
• Supports hypothesis that
AD might trigger longterm IBS/functional GI Sxs
Cohen ER et al. DDW 2012, abstract 1363
Emerging Treatments for SUDD
• If there is indeed a symptomatic state of DD
marked by low-grade inflammation, and/or
visceral hypersensitivity and/or abnormal motor
function, can we intervene in such patients?
• Historically, we’ve prescribed fiber or antispasmodics, although data in support is weak
• ? Antibiotics, ? Anti-inflammatories, ? Probiotics
Cyclic Rifaximin in SUDD (400mg BID, 7 days/month)
Meta-analysis: 4 PRCTs, 1660 patients
Pooled Rate Difference (RD)
Sx relief (1 year)
29% (CI 24 - 34%)
p<0.0001 NNT=3
All Complications (1 year) 2% (CI -3.2 - -0.1%)
Recurrent diverticulitis
2% (CI -3.4 - -0.6%)
p=0.0057 NNT=50
Bianchi M et al. Aliment Pharmacol Ther 2011;33:902-10
Scopes trial?
Mesalamine in DD
• At least 6 Italian studies have evaluated 5-ASA
either after acute diverticulitis (3) or in SUDD (3)
• Generally favorable results
– Daily superior to cyclic
– But data very heterogeneous
– Not double blinded, not placebo controlled
– Subjective endpoints
– Dose / regimen unclear
DIVA Trial
• 52 week, randomized, multi-center, double-blind, doubledummy, placebo-controlled, proof-of-concept study (first in US)
• Required CT scan confirmed acute diverticulitis, excluded IBS Dx
• Patients randomized to:
– Standard care (abx, dietary advice as per local MD)
– Standard care, plus mesalamine 2.4gm QD
– Standard care, plus mesalamine 2.4gm QD plus B. infantis QD
(after Abx completed)
• 12 week Rx with 40 week additional f/u (52 week total)
Stollman N et al. American College of Gastroenterology 2010 Annual Scientific Meeting (ACG 2010). Abstract 49. Accepted Journal Clinical
Gastroenterology, publication pending
Median Global Symptom Score
Median Global Symptom Score (ITT)
All results NS vs placebo
+ probiotic
Day 10
Week 12
Week 26
Week 39
Week 52
Global Symptom Score Responders
# Significant difference vs. placebo
Percent Responders (ITT)
+ probiotic
Day 10
Week 12
Week 26
Week 39
Week 52
Responder = score of 0 or 1 for all symptoms
Recurrent Diverticulitis (ITT)
5-ASA + Probiotic
Withdrew due to
1 (2.4%)
2 (5.0%)
0 (0%)
8 (20%)
5 (12.5%)
4 (11.8%)
-Secondary Endpoints only, study not powered for this
-Recurrent Diverticulitis diagnosed by patient and
physician assessment, without CT scan documentation
-No statistical significance for any comparisons
DIVA Conclusions
• Treatment with mesalamine after an attack of
CT-confirmed acute diverticulitis led to:
– Lower (but NS) GSS at all time points
– Significant increase in responders (GSS=0 or 1) at
some (but not all) time points
– No effect on recurrence rates or surrogate markers
• Limitations: relatively underpowered, short
treatment duration, GSS not validated
previously, probiotic / mesalamine interaction?
PREVENT: MMX Mesalamine in
Recurrent Diverticulitis (Shire, Lialda)
• Two identical Phase III RCTs
– PREVENT 1 and 2: both worldwide
– Intended 590 pts enrolled each, both completed enrollment
– Mesalamine 1.2, 2.4, 4.8 gm/day vs placebo, 2 year follow-up
• Press Release 3/30/12: “PREVENT 2 did not meet the
primary endpoint in reducing the rate of recurrence of
diverticulitis over a 2-year treatment period. In addition,
mesalamine did not show a significant difference compared
to placebo on the key secondary endpoint of the
study…..Although the results of the second trial are
pending, it is our current intention not to pursue a
regulatory filing for this indication for MMX® mesalamine.”
Other Mesalamine Trials
• Dr. Falk Pharma, Mesalazine, Germany
– Mesalazine Granules vs. Placebo for the
Prevention of Recurrence of Diverticulitis
• “Terminated” according to clinicaltrials.gov
– Two Doses Mesalazine Granules Versus Placebo
for the Prevention of Recurrence of Diverticulitis
• “currently recruiting”
• Conclusions still unclear as to role of 5-ASA in
DD, but reasonable for challenging cases
Probiotics for Diverticulitis
DD Stage
Follow up
E. Coli Nissle plus antibiotic
plus active charcoal1
2.4 (15)
Prolonged remission period,
improved symptoms
L. casei, 5-ASA, or both2
12 mos (90) Increased remission rate
L. casei plus 5-ASA3
24 mos (75) Increased remission rate
VSL#3 plus balsalazide4
2 mos (30)
Improved symptoms
L. Acidophilus plus L.
helviticus plus
6 mos (45)
Prevented recurrence,
improved symptoms
12 mos (40)
B. infantis6
No effect + 5-ASA
1. Fric P, Zavoral M. Eur J Gastroenterol Hepatol. 2003;15:313-315; 2. Tursi A et al. J Clin Gastroenterol. 2006;40:312-316;
3. Tursi A et al. Hepatogastroenterology. 2008;55:916-920; 4. Tursi A et al. Int J Colorectal Dis. 2007;22:1103-1108.
5. Lamiki P et al. J Gastrointestin Liver Dis. 2010;19:31-36. 6. Stollman N et al. ACG 2010 Annual Scientific Meeting Abstract 49
Can we prevent diverticular complications?
• Many studies have implicated ASA and NSAIDs
but small and non-detailed
• Follow up of US Health Professionals study;
>45K men, followed since 1986
Relative Risk
Div Bleeding
-ASA >2x/wk
-NSAID >2x/wk
Strate L et al. Gastroenterology 2011; 140: 1427.
Tic’d off?
Complicated diverticulosis
• Inflammation and/or infection associated w/
Affects 15-20% of patients with diverticula
450,000 US admissions / year
2 million outpatient visits US / year
Generally the result of perforation of a single
diverticulum, probably due to obstruction by
inspissated stool.
Bacteria breach mucosa, extend process through
wall, and cause (often limited) perforation.
Impacted fecolith with inflammation
Complicated diverticulosis
Diverticulitis – Clinical Features
• Clinical Features
Pain and tenderness, usually LLQ,
but in Asians or those with
redundant sigmoids, can be RLQ
or suprapubic.
Altered bowel habits
Anorexia, nausea, vomiting
Hematochezia rare
Dysuria: sympathetic cystitis
Fever common; shock or
hypotension unusual
WBC common; no other labs
routinely useful
• Differential Diagnosis
Acute Appendicitis
Crohn’s Disease
Colonic carcinoma
Pseudomembranous or ischemic
Ovarian cyst / abscess / torsion
Ectopic pregnancy
Complicated diverticulosis
Diverticulitis - Diagnostic Modalities
• CT scanning - most accurate
– Abd & Pelvic scans; oral / rectal / IV contrast
– Findings: pericolic infiltration of fatty tissues,
wall thickening, abscess
– Sensitivity and Specificity: 85-95%
– Severe disease predicts complications and poor
Sigmoid (L) & Desc Colon (R) Diverticulitis: CT
Complicated diverticulosis
Diverticulitis - Treatment I
• Determine need for hospitalization:
– Mild sxs, no peritoneal signs, tolerating POs, &
supportive home networks may be candidates for
outpatient Rx.
– Elderly, immunosuppressed, comorbid illness, or
evidence of severe disease (high WBC or fevers):
inpatient Rx.
Complicated diverticulosis
Diverticulitis - Treatment II
• Antibiotics: cover gut organisms (eg GNRs &
anaerobes, esp E. coli and bacteroides)
Little data to guide choice.
Oral: consider T/S or cipro plus flagyl, Single agent:
IV: aminoglycoside/aztreonam/3rd gen ceph plus
metronidazole or clindamycin. Single agents:
Unasyn, Timentin, Cefoxitin.
Sxs should w/in 2-3 days, advance diet.
Continue Rx for 7-10 days
Complicated diverticulosis
Diverticulitis - Treatment III
• Inpatients: NPO, IVF, IV Abx
• Consider: Gram(-) coverage with
aminoglycoside/aztreonam/3rd gen ceph plus
metronidazole or clindamycin. Reasonable
single agents: Unasyn, Timentin, Cefoxitin.
• Expect improvement in in 2-4 days, then
advance diet; outpatient Abx X7-10 days.
Complicated diverticulosis
Diverticulitis - Treatment Outcome I
• Majority will respond to medical Rx; up to 25%
will require surgery during admission.
• For those who respond, a complete colonic
evaluation is required after resolution of
clinically diagnosed case, to exclude other
diagnoses, such as CA.
• Surgery to prevent recurrence?
When to consider surgery?
• Prior guidelines, including ASCRS and ACG recommended
‘considering’ prophylactic surgical resection after 2nd attack
• Most recent ASCRS recommendations1
– “The number of attacks of uncomplicated diverticulitis is
not necessarily an overriding factor in defining the
appropriateness of surgery.”
– Advocate a case-by-case individualized approach
• Markov Model (WA State database)2
– Colectomy after fourth (rather than 2nd) episode → 0.5%
fewer deaths and saved $1,035/patient.
– Expectant management through 3 recurrent episodes with
colectomy after the 4th was the dominant strategy across
the variables tested in the sensitivity analysis
1. Rafferty J et al. Dis Colon Rectum. 2006;49:939. 2. Salem L et al. J Am Coll Surg 2004;199:904-12
3165 patients hospitalized
with acute diverticulitis
(Kaiser NorCal)
81% (n=2551)
No surgery
7% (n=178) had
elective colectomy,
typically young
or had abscess
Recurrence is infrequent
and not more complicated
19% (n=601)
Required surgery
during index
2366 followed
9 years (mean)
Broderick-Villa G et al. Arch Surg. 2005;140:576.
13% (n=314)
• <2% per year
• Younger age had
slightly higher risk
• 1st recurrence
predicted rerecurrence
• All re- recurrences
treated nonoperatively
9.4% (n=222)
3.9% (n=92)
2 or more
Are Antibiotics Obligate?
• First RCT: 623 Swedish patients
• CT-confirmed acute diverticulitis without complications
• No antibiotics vs antibiotics at MD’s discretion for >7 days
Abscess, perforation
(P = 0.3)
Recurrent diverticulitis
(P = 0.88)
No antibiotics
6 (1.9%)
47 (16.2%)
3 (1.0%)
46 (15.8%)
Chabok A et al. British Journal of Surgery. 2012;99:532.
Complicated diverticulosis
Diverticulitis - The Young Patient
• Historically, 2-4% of episodes occur in pts <40 y/o
(but might be increasing)
• M>F and worse outcome, with 30-80% requiring
urgent surgery during initial attack, and  risk of
recurrences & complications.
• This, plus low operative risk in younger patients,
suggests considering elective resection earlier after
well-documented diverticulitis in younger patients.
Complicated diverticulosis
• Suggested by persistent fever or WBC
• CT scan: diagnose & follow course
• Stage I (small pericolic abscesses): 70-80% success
with medical tx alone
• Stage II (distant abscesses):
– CT-guided percutaneous drainage
– Allows for rapid control of sepsis without operative risk,
allows for temporary drainage and single-stage
procedure in 3-4 weeks.
– 15-25% may still require primary surgical therapy if
multiloculated or inaccessible.
Complicated diverticulosis
Abscess II
• CT-guided percutaneous drainage
– Assuming primary management role
– Allows for rapid control of sepsis without risk of
anesthesia, allowing for temporary drainage and a
subsequent single-stage procedure in 3-4 weeks in
75-85% of cases.
– 15-25% may still require primary surgical therapy
if multiloculated or inaccessible.
BE and CT with Diverticular Abscess
Complicated diverticulosis
• Occur when phlegmon/abscess extends or
ruptures into adjacent organ.
Colovesicular: (65%) 2:1 M:F
– fecaluria - pathognemonic
– pneumaturia - suggestive
Colovaginal: (25%) stool / flatus per vagina
Coloenteric, colouterine, colocutaneous: rare
Treatment: single-stage resection / closure
Colo-enteric and colo-vesicular
fistulas: BE
Complicated diverticulosis
Hemorrhage I
• Most common cause of LGIB (30-50%)
• 5-10% of patients with diverticula bleed
• While most tics in left colon, bleeding may occur
more often from right colonic tics.
• Arterial bleed from vasa recta coursing over
dome of tic.
• Increased risk with NSAID use.
Complicated diverticulosis
Hemorrhage II
• Clinical Features:
– Rarely occurs with diverticulitis.
– Abrupt, painless onset of maroon / red blood or
clots; melena uncommon.
– Mild lower abd cramps / urge to defecate
– Never consider tics as cause of Heme+ stool
– 75-80% stop bleeding spontaneously.
– 25-35% recurrent bleeds; consider surgery
after recurrent episodes.
Complicated diverticulosis
Hemorrhage III
• Diagnosis / Management
– Fluid & blood product resuscitation
– Exclude UGIB with NGT or EGD
– Urgent Flex Sig, if negative for source:
• Tagged RBC Nuclear Scan  angiography OR
• “Rapid Purge” and colonoscopy; although endoscopic
Rx much less effective than in UGIB
– Surgery if endoscopy or angiography fails-
segmental vs. subtotal colectomy.
Complicated diverticulosis
Hemorrhage IV
• 121 pts w/ severe hematochezia & diverticulosis
• Rapid oral purge with PEG solution
• Colonoscopy within 6-12 hours
• 1986-1992: 73 patients treated medically and surgically,
if recurrent or severe bleeding
• 1994-1998: 48 patients treated medically and with
colonoscopic therapy for select stigmata
Jensen DM et al. NEJM 2000; 342: 78-82
Complicated diverticulosis
Hemorrhage V
Surgical (’86-’92)
DEFINITE Div Hemorrhage
Active bleeding
Non-bleeding VV
Adherent Clot
Additional bleeding
Emergency colectomy
Median time to discharge
Late re-bleeding
Colonoscopic (’94-’98)
17 (23%)
10 (21%)
6 (35%)
4 (24%)
7 (41%)
5 (50%)
2 (20%)
3 (30%)
9 (53%)
0 (0%)
6 (35%)
5 days
2 (12%)
0 (0%)
0 (0%)
2 days
0 (0%)
0 (0%)
Issues: historical cohort only, small number of patients (n=10)
Endoscopic control of bleeding:
Epinephrine injection
Patient with LGIB, ‘visible vessel’ in diverticulum, oozing with Epi injection but
ultimately, cessation of bleeding. Courtesy of F Ramirez MD
Endoscopic control of bleeding:
Patient with LGIB, ‘visible vessel’ within diverticulum, tx’d with endoclip Courtesy of T
Hargrave MD
Quaker Oats?
Summary / Key points
• Increasing problem
• Fiber: unsettled as to cause / etiology but likely
DOES help diminish complications, and seeds/nuts
need not be forbidden
• Is SUDD a real entity marked by subclinical
inflammation and/or visceral hypersensitivity?
– If so, can we treat it with probiotics, 5-ASA and/or Abx?
– Will this simply improve symptoms or actually lower
recurrent diverticulitis or complication rates?
• Surgery: increasingly less aggressive approach

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