New Approaches to Diverticulosis and

Diverticulitis Management

Neil Stollman MD, FACGChairman, Department of MedicineAlta Bates Summit Medical Center

Oakland, CAAssociate Clinical Professor of Medicine

University of California San FranciscoSan Francisco, CA

Outline• Epidemiology• 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?”

Epidemiology

• 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, Australia

– Japanese migrating to Hawaii have rate intermediate b/w native Japanese and mainland born, suggesting ‘westernization’ of colon.

Prevalence increasing over time (worldwide)

0

5

10

15

20

25

30

1960 1965 1970 1975 1980 1985 1990 1995 2000

Year

Ra

te (

%)

Finland Israel Jordan Kenya Singapore Hong Kong Japan

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;249:210-17Nguyen 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 anti-

mesenteric 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 penetration

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 IColonic 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 IIDisordered Motility

• Ý resting, post-prandial, & neostigmine-induced 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 WeightUK 80 hours 110 gm/dUgandans 34 hours 450 gm/d

Painter NS, Burkitt DP. Br Med J 1971;2:450–54

Etiology: dietary fiber

• Ý transit-times & ß stool volume may Ý 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;128:714-19Crowe 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 re-

innervation 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

Humes et al. British Journal of Surgery. 2008;95:195-198.

261 patients with diverticulosis on barium enema

136 provided bowel / psych symptoms

170 eligible for follow up

Excluded 91Deceased 61

Declined FU 21Misc 9

Recurrent pain 45 Asymptomatic 79

Pain 42

27 15

Pain free Pain free

18 641999

2006

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)

Controls ADD SUDD SCDD0

500

1000

1500

2000

Basal

Postcibal

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

questionnaire– 17 symptomatic – 15 asymptomatic DD pts

• Unprepared flexible sigmoidoscopy– Mucosal biopsy

peridiverticular & rectal• Normal appearance on

routine histology• No evidence of

inflammation Galanin Substance P Neuropeptide K0

0.05

0.1

0.15

0.2Sympt

Asympt

Simpson et al Neurogastroenterol Motil 2009;21:847-858.

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

P<0.002 DDS vs DDA

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 long-term 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 anti-spasmodics, although data in support is weak

• ? Antibiotics, ? Anti-inflammatories, ? Probiotics

Meta-analysis: 4 PRCTs, 1660 patientsPooled 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%)p=0.03 NNT=59

Recurrent diverticulitis 2% (CI -3.4 - -0.6%)p=0.0057 NNT=50

Bianchi M et al. Aliment Pharmacol Ther 2011;33:902-10

Cyclic Rifaximin in SUDD (400mg BID, 7 days/month)

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, double-

dummy, 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

Day 10 Week 12 Week 26 Week 39 Week 520

1

2

3

4

5

6

7

8

9

Placebo

Mesalamine

Mesalamine + probiotic

Med

ian

Glo

bal S

ympt

om S

core

(IT

T)

All results NS vs placebo

Global Symptom Score Responders

Day 10 Week 12 Week 26 Week 39 Week 520

10

20

30

40

50

60

70

80

Placebo

Mesalamine

Mesalamine + probiotic

Perc

ent R

espo

nder

s (IT

T)

Responder = score of 0 or 1 for all symptoms

# Significant difference vs. placebo#

#

#

Recurrent Diverticulitis (ITT)PLACEBO

(n=41)5-ASA (n=40)

5-ASA + Probiotic (n=36)

Withdrew due to surgery

1 (2.4%) 2 (5.0%) 0 (0%)

Recurrent Diverticulitis

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 DiverticulitisProtocol DD Stage Follow up

(N)Outcome

E. Coli Nissle plus antibiotic plus active charcoal1

SUDD 2.4 (15) Prolonged remission period, improved symptoms

L. casei, 5-ASA, or both2 SUDD 12 mos (90) Increased remission rate

L. casei plus 5-ASA3 SUDD 24 mos (75) Increased remission rate

VSL#3 plus balsalazide4 SUDD 2 mos (30) Improved symptoms

L. Acidophilus plus L. helviticus plus Bifidobacterium5

SUDD 6 mos (45) Prevented recurrence, improved symptoms

B. infantis6 AD 12 mos (40) 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 Diverticulitis Div Bleeding-ASA >2x/wk 1.25 1.70-NSAID >2x/wk 1.72 1.74

Strate L et al. Gastroenterology 2011; 140: 1427.

Tic’d off?

Complicated diverticulosisDiverticulitis

• Inflammation and/or infection associated w/ diverticula

• 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 diverticulosisDiverticulitis – 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• Ý WBC common; no other labs

routinely useful

• Differential Diagnosis• Acute Appendicitis• Crohn’s Disease• Colonic carcinoma• Pseudomembranous or ischemic

colitis• Ovarian cyst / abscess / torsion• Ectopic pregnancy

Complicated diverticulosisDiverticulitis - 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

prognosis.

Sigmoid (L) & Desc Colon (R) Diverticulitis: CT

Complicated diverticulosisDiverticulitis - 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 diverticulosisDiverticulitis - 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:

Augmentin• IV: aminoglycoside/aztreonam/3rd gen ceph plus

metronidazole or clindamycin. Single agents: Unasyn, Timentin, Cefoxitin.

• Sxs should ß 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 diverticulosisDiverticulitis - 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

Recurrence is infrequent and not more complicated

Broderick-Villa G et al. Arch Surg. 2005;140:576.

81% (n=2551)No surgery

7% (n=178) had elective colectomy,

typically young or had abscess

13% (n=314) Recurrence

• <2% per year• Younger age had

slightly higher risk• 1st recurrence

predicted re-recurrence

• All re- recurrences treated non-operatively

3.9% (n=92) 2 or more

recurrences

9.4% (n=222) single

recurrence

3165 patients hospitalized with acute diverticulitis

(Kaiser NorCal)

19% (n=601)Required surgery

during index admission

2366 followed 9 years (mean)

Sarcas-tic?

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

Chabok A et al. British Journal of Surgery. 2012;99:532.

Abscess, perforation(P = 0.3)

Recurrent diverticulitis

(P = 0.88)

No antibiotics 6 (1.9%) 47 (16.2%)

Antibiotics 3 (1.0%) 46 (15.8%)

Complicated diverticulosisDiverticulitis - 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 Ý 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 diverticulosisAbscess

• 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

Fistulas

• 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

Artis-tic?

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.

Artery Artery

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 diverticulosisHemorrhage III

• Diagnosis / Management– Fluid & blood product resuscitation– Exclude UGIB with NGT or EGD– Urgent Flex Sig, if negative for source:

• Tagged RBC Nuclear Scan Þ 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 diverticulosisHemorrhage 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 diverticulosisHemorrhage V

Surgical (’86-’92) Colonoscopic (’94-’98)

DEFINITE Div Hemorrhage 17 (23%) 10 (21%)ENDOSCOPIC FINDINGS Active bleeding 6 (35%) 5 (50%) Non-bleeding VV 4 (24%) 2 (20%)

Adherent Clot 7 (41%) 3 (30%)Additional bleeding 9 (53%) 0 (0%)Emergency colectomy 6 (35%) 0 (0%)Median time to discharge 5 days 2 daysComplications 2 (12%) 0 (0%)Late re-bleeding 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: Endoclips

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