1. 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

2. 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

3. Let’s Play: Separated at birth? Example: “Teenage Mutant Ninja tic?”

4. 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.

5. Prevalence increasing over time (worldwide)
Jun S, Stollman N. Epidemiology of Diverticular Disease. Ballieres Clin Gastroenterol 2003

6. Epidemiology: Increasing over time (US)
Nationwide inpatient sample (NIS) data (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

7. 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.

8. Diverticula form at sites of vascular penetration

9. Pathologic Anatomy II Western individuals: Asian 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.

10. Sigmoid Diverticula: BE

11. Pan-colonic diverticula: BE

12. Separated at birth?

13. 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)

14. Etiology / Pathogenesis II Disordered 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)

15. 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.

16. 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

17. Etiology: dietary fiber
Stool weights & transit times (n=1200)
UK patients: western low-fiber diet
Rural Ugandans: high fiber diet
Transit time Weight
UK 80 hours 110 gm/d
Ugandans hours 450 gm/d
Painter NS, Burkitt DP. Br Med J 1971;2:450–54

18. 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

19. Fiber as RISK FACTOR for developing DD
Cross section study of >2000 screening colonoscopies, 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 ( )
BMs: >15/week vs <7/week
prevalence ratio for diverticulosis: 1.7 ( )
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

20. 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

21. 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, , no prior colonic dz
RR for symptomatic disease in highest vs lowest fiber groups = 0.63 ( ) (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: ( )
Vegetarians vs meat eaters: ( )
Aldoori WH et al. J Nutr 1998;128:714-19
Crowe FL et al. BMJ 2011;343:

22. 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 [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: (0.63 – 1.01), P = 0.04
Popcorn: (0.56 – 0.92), P = 0.007
Not only ‘no association’ but nuts and popcorn may actually have inverse / protective effect
MODIFIED
1. Stollman NH, Raskin JB. Diagnosis and management of diverticular disease of the colon in adults. Ad Hoc Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol Nov;94(11):
2. Strate LL, Liu YL, Syngal S, Aldoori WH, Giovannucci, EL. Nut, corn and popcorn consumption and the incidence of diverticular disease. JAMA August 27; 300(8): 907–914.
EDITED SOME ABOVE
1. Stollman NH, Raskin JB. Am J Gastroenterol. 1999;94(11):3110.
2. Strate LL et al. JAMA. 2008;300(8):907.

23. Separated at birth?

24. 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.

25. 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
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

26. 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

27. Predicting recurrent pain / SUDD
261 patients with diverticulosis on barium enema
136 provided bowel / psych symptoms
170 eligible for follow up
Excluded 91
Deceased 61
Declined FU 21
Misc 9
Recurrent pain 45
Asymptomatic 79
Pain 42 27 15
Pain free 18 64
1999
2006
Those with recurrent pain more likely to have history of diverticulitis (prolonged pain / antibiotics) more likely to be anxious HAD > 7 and had a higher PHQ15 score
Humes et al. British Journal of Surgery. 2008;95:

28. 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)
Cortesini et al Dis Colon Rectum 1991;34(4):339-42

29. 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
Simpson et al Neurogastroenterol Motil 2009;21:

30. 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

31. Visceral hypersensitivity in SUDD
Rectal barostat study in healthy volunteers (HV), asymptomatic DD (DDA) and symptomatic DD (DDS)
P<0.002
DDS vs DDA
No difference in compliance All groups showed increase in tone postprandially both is rectum and sigmoid
Colonoscopy study showed pain related to looping except in DD
Humes et al Neurogastroenterol Motil 2012;24:318-e163

32. 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 ( , P=0.005)
Supports hypothesis that AD might trigger long-term IBS/functional GI Sxs
Cohen ER et al. DDW 2012, abstract 1363

33. 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

34. 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 %)
p< NNT=3
All Complications (1 year) 2% (CI %)
p=0.03 NNT=59
Recurrent diverticulitis 2% (CI %)
p= NNT=50
Bianchi M et al. Aliment Pharmacol Ther 2011;33:902-10

35. Scopes trial?

36. 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

37. DIVA Trial 12 week Rx with 40 week additional f/u (52 week total)
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

38. Median Global Symptom Score
All results NS vs placebo

39. Global Symptom Score Responders
# Significant difference vs. placebo # # #
Responder = score of 0 or 1 for all symptoms

40. 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

41. 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?

42. 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.”

43. 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

44. Probiotics for Diverticulitis
Protocol
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
12 mos (90)
Increased remission rate
L. casei plus 5-ASA3
24 mos (75)
VSL#3 plus balsalazide4
2 mos (30)
Improved symptoms
L. Acidophilus plus L. helviticus plus Bifidobacterium5
6 mos (45)
Prevented recurrence, improved symptoms
B. infantis6 AD
12 mos (40)
No effect + 5-ASA
One study compared an antibiotic/active charcoal to an antibiotic/active charcoal/probiotic (E. coli, Nissle strain) regimen. The addition of the probiotic produced longer intervals of disease quiescence and a greater degree of symptom relief than the antibiotic/absorbent regimen alone [Fric 2003]. The second study investigated the efficacy of Lactobacillus casei DG in combination with mesalamine in patients with symptomatic uncomplicated diverticular disease that was in remission. [Tursi 2006] The third study evaluated a high-potency probiotic in combination with balsalazide. in patients with acute uncomplicated diverticulitis in remission, respectively. [Tursi 2007] In both studies, the probiotic/5‑ASA combination was associated with greater symptom improvement and fewer relapses compared to the 5-ASA regimen. [Tursi 2006]
1. Fric P, Zavoral M. Eur J Gastroenterol Hepatol. 2003;15: ; 2. Tursi A et al. J Clin Gastroenterol. 2006;40: ;
3. Tursi A et al. Hepatogastroenterology. 2008;55: ; 4. Tursi A et al. Int J Colorectal Dis. 2007;22:
5. Lamiki P et al. J Gastrointestin Liver Dis. 2010;19: Stollman N et al. ACG 2010 Annual Scientific Meeting Abstract 49

45. 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
-NSAID >2x/wk
Strate L et al. Gastroenterology 2011; 140: 1427.

46. Tic’d off?

47. Complicated diverticulosis Diverticulitis
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.

48. Impacted fecolith with inflammation

49. Complicated diverticulosis Diverticulitis – 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

50. 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 prognosis.

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

52. 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.

53. 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: 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

54. 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.

55. 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?

56. 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: Salem L et al. J Am Coll Surg 2004;199:904-12

57. Recurrence is infrequent and not more complicated
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) 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)
Rafferty J, Shellito P, Hyman NH, Buie WD, et al. Practice parameters for sigmoid diverticulitis. Dis Colon Rectum. 2006; 49: 939–944. Available at
Broderick-Villa G et al. Arch Surg. 2005;140:576.

58. Sarcas-tic?

59. 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%)
Antibiotics
3 (1.0%)
46 (15.8%)
Chabok A et al. British Journal of Surgery. 2012;99:532.

60. 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 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.

61. Complicated diverticulosis Abscess
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.

62. 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.

63. BE and CT with Diverticular Abscess

64. 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

65. Colo-enteric and colo-vesicular fistulas: BE

66. Artis-tic?

67. 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.

68. Artery
Artery

69. 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.

70. 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 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.

71. Complicated diverticulosis Hemorrhage IV
121 pts w/ severe hematochezia & diverticulosis
Rapid oral purge with PEG solution
Colonoscopy within 6-12 hours
: 73 patients treated medically and surgically, if recurrent or severe bleeding
: 48 patients treated medically and with colonoscopic therapy for select stigmata
Jensen DM et al. NEJM 2000; 342: 78-82

72. Complicated diverticulosis Hemorrhage 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 days
Complications 2 (12%) 0 (0%)
Late re-bleeding 0 (0%) 0 (0%)
Issues: historical cohort only, small number of patients (n=10)

73. 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

74. Endoscopic control of bleeding: Endoclips
Patient with LGIB, ‘visible vessel’ within diverticulum, tx’d with endoclip Courtesy of T Hargrave MD

75. Quaker Oats?

76. 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