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Epidemiology and pathophysiology of colonic diverticular disease

Official reprint from UpToDate

www.uptodate.com 2013 UpToDate

Epidemiology and pathophysiology of colonic diverticular disease

Authors
Tonia Young-Fadok, MD
John H Pemberton, MD

Section Editor
Lawrence S Friedman, MD

Deputy Editor
Shilpa Grover, MD, MPH

Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2013. | This topic last updated: abr 18, 2013.
INTRODUCTION Diverticular disease of the colon is common. This topic review will focus on the epidemiology and pathophysiology of the disorder. It is useful to begin with a
series of definitions of the terms that are commonly used:
A diverticulum is a sac-like protrusion of the colonic wall.
Diverticulosis merely describes the presence of diverticula.
Diverticulitis refers to inflammation of diverticula.
Diverticular disease is a term encompassing diverticulosis and diverticulitis. Symptomatic diverticular disease includes hemorrhage, inflammation (diverticulitis), or complications of
diverticulitis such as abscess, fistula, obstruction, or free perforation.
EPIDEMIOLOGY Diverticular disease was uncommonly encountered at the beginning of the twentieth century. The first report of surgical resection for complicated diverticulitis
was by Mayo in 1907 [1]. The prevalence of diverticular disease is age-dependent, increasing from less than 20 percent at age 40, to 60 percent by age 60 [2,3]. A nationwide
inpatient study of hospitalizations in the United States showed an increase of 26 percent in admissions for acute diverticulitis from 1998 to 2005 [4]. The largest increase (82 percent)
was in patients aged 18 to 44 years. Elective operations for diverticulitis also increased by 29 percent with the most rapid increase (73 percent) in patients aged 18 to 44 years.
A male preponderance was noted in early series, but other studies have suggested either equal distribution or a female preponderance [5]. This may be explained by a gender
distribution which varies with age; in one series, men were more often affected under age 50, there was a slight female preponderance between the ages of 50 and 70, and a marked
female preponderance over age 70 [6]. An excess number of males has also been noted for acute diverticulitis in patients under 40 years of age [7,8].
There are geographic variations in both the prevalence and pattern of diverticulosis.
"Westernized" nations have prevalence rates of 5 to 45 percent, depending upon the method of diagnosis and age of the population [9,10]. Diverticular disease in these
countries is predominantly left-sided, with right-sided diverticulitis being present in only 1.5 percent of cases [11].
The findings are different in Asia, where the prevalence is between <1 and 5 per million population [12], and diverticulosis is usually right-sided [13].
Japan, after adopting a more Western lifestyle, has experienced an increase in the prevalence of right-sided diverticulosis. In one report of 615 patients with colonic diverticular
disease, right-sided diverticula were present in approximately 70 percent of all patients and were responsible for approximately 75 percent of cases of diverticulitis [14]. A
review of 13,947 barium enema examinations performed over a 15-year period in Japan revealed a steady increase in the incidence of diverticulosis of the right colon [15]. Leftsided diverticula did not increase in frequency over time. The increase in the incidence of right-sided diverticula in Japan is similar to the increase in the incidence of left-sided
diverticula in westernized countries. A right-sided predominance has also been noted in Singapore, where 70 percent of cases occur in patients less than 40 years old [16],
and in Hong Kong [17,18].
ETIOLOGY The increase in incidence in the developed nations suggests environmental and lifestyle factors play an important role in the pathogenesis of diverticular disease.
Dietary fiber intake Several studies have suggested that low dietary fiber predisposes to the development of diverticular disease [2,19,20] although this hypothesis has not been
confirmed in all studies [21-26]. One report that evaluated a cohort of over 47,000 men provided strong evidence for the role of dietary fiber [20]. After adjustment for age, energyadjusted total fat intake, and physical activity, total dietary fiber intake was noted to be inversely associated with the risk of symptomatic diverticular disease. The relative risk was
0.58 for men in the highest quintile compared to those in the lowest quintile for fiber intake. The observation that diverticular disease is less common in vegetarians than
nonvegetarians is also compatible with a role for dietary fiber, since vegetables and fruits are important sources of fiber (table 1) [27].
If it is beneficial, dietary fiber may act by producing a large bulky stool, resulting in a wider-bore colon that is less likely to permit efficient segmentation and therefore less likely to
develop diverticula (see 'Pathophysiology of diverticula formation' below) [2]. In addition, increasing dietary fiber is often used as first-line therapy for treatment of constipation.
However, there is no clear correlation between constipation and diverticular disease, probably stemming from the retrospective nature of most studies and the difficulties in defining
constipation in a large series of patients.
Other dietary factors Other dietary factors that might contribute to the pathogenesis of diverticular disease have been examined. There is no substantially increased risk
associated with smoking, caffeine, or alcohol [28]. On the other hand, an association has been noted between obesity in men under 40 years and acute diverticulitis. This finding is
compatible with observations that the risk of symptomatic diverticular disease is particularly increased (relative risk 2.35 to 3.32) by a diet characterized by a high intake of total fat or
red meat and a low intake of dietary fiber [20]. Issues related so consumption of seeds and nuts are discussed separately. (See "Treatment of acute diverticulitis", section on 'Seeds
and nuts'.)
Physical activity Lack of vigorous exercise also may be a risk factor for diverticular disease. In a prospective study of almost 48,000 American men aged 40 to 75 who were free
of known colonic disease, the risk of developing symptomatic diverticular disease was inversely related to overall physical activity (0.63 for highest versus lowest extremes) after
adjustment for age and dietary fat and fiber [29]. Most of the decrease in risk with exercise was associated with vigorous activity such as jogging and running. An interaction was
noted between physical activity and dietary fiber; men in the lowest quintile for both had a relative risk of 2.56 compared to men in the highest quintile for both. How physical activity
might prevent diverticular disease is not known.
Obesity Obesity has been linked to the development of diverticulitis and diverticular bleeding in several reports. In a large, prospective cohort study, for example, there were 801
incident cases of diverticulitis and 383 cases of diverticular bleeding during 18 years of follow-up in a cohort of 47,228 male health professionals [30]. The relative risk of diverticulitis in
those with the highest quintile of waist circumference was 1.56 (95% CI 1.18-2.07). A similar increase was noted for diverticular bleeding (RR 1.96, 95% CI 1.30-2.97).
Possible relation with colon cancer There may also be a relation between diverticulosis and colon cancer. One series of 7000 patients found an excess number of colon and
rectal cancers in the first two years after the diagnosis of diverticular disease but not with more prolonged follow-up [31]. There was, however, a long-term excess of left-sided colon
cancers, suggesting a possible relation between these tumors and diverticular disease.
LOCATION A typical colonic diverticulum is a "false" or pulsion diverticulum, eg, it does not contain all layers of the wall as a true (congenital) diverticulum does; instead, mucosa
and submucosa herniate through the muscle layer, covered only by serosa (picture 1). Diverticula develop at four well-defined points around the circumference of the colon, sites at
which the vasa recta penetrate the circular muscle layer. These vessels enter the wall on each side of the mesenteric taenia and on the mesenteric border of the two antimesenteric
taeniae (figure 1).
Diverticula are distributed unevenly in the colon. Ninety-five percent of patients have sigmoid diverticula, while 35 percent also have more proximal disease. Among the latter group, 7
percent have diverticula throughout the colon, and 4 percent have diverticula limited to a segment proximal to the sigmoid [32]. The location of diverticular disease requiring surgery is
similar, with 95 percent of all operative cases involving the sigmoid [6].

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PATHOPHYSIOLOGY OF DIVERTICULA FORMATION The points at which diverticula develop, eg, where vasa recta penetrate the bowel wall, are considered areas of weakness
[33]. Most patients with sigmoid diverticula exhibit mycosis, which consists of thickening of the circular muscle layer, shortening of the taeniae, and luminal narrowing. There is no
hypertrophy or hyperplasia of the bowel wall, but increased elastin deposition is found in the taeniae [34]. There are also structural changes in collagen that are similar to, but greater
in magnitude than, those that occur because of aging [35].
These changes may decrease resistance of the wall to intraluminal pressure. Structural changes in the wall may also be responsible for the appearance of diverticula at an early age
in connective tissue disorders such as Ehlers-Danlos and Marfan's syndromes and in autosomal dominant polycystic kidney disease [36]. (See "Extrarenal manifestations of
autosomal dominant polycystic kidney disease".)
The law of Laplace explains the development of diverticula. The law states that pressure P is proportional to wall tension T, and inversely proportional to bowel radius R:
P = kT R
where k is a conversion factor. Since the sigmoid colon is the segment of the colon with the smallest diameter, it will tend to be the site of the highest pressure. This is not true
under normal circumstances because pressure should be the same throughout the colon. However, segmentation of the colon (a motility process in which segmental muscular
contractions separate the lumen into chambers) is exaggerated in diverticulosis, occluding both ends of the chamber during muscular contraction [37]. This increases intraluminal
pressure and may predispose to herniation of mucosa. The neural basis for the abnormal motility observed in patients with diverticulosis remains unclear. One report found that a
central event appeared to be upregulation of smooth muscle M3 receptors [38].
Thus, abnormal colonic motility may predispose to the development of diverticula. It has been suggested that dietary fiber, by producing a large bulky stool, results in a wider-bore
colon that is less likely to permit efficient segmentation and therefore less likely to develop diverticula [2].
Pathophysiology of diverticulitis Diverticulitis, eg, inflammation of diverticula, produces variable clinical manifestations, ranging from subclinical inflammation to generalized
peritonitis. The underlying cause is micro- or macroscopic perforation of a diverticulum. It was previously believed that obstruction of diverticula, eg, by fecaliths, increased
diverticular pressure and caused perforation; such obstruction is now thought to be rare (picture 2 and picture 1) [21]. The primary process is thought to be erosion of the diverticular
wall by increased intraluminal pressure or inspissated food particles. Inflammation and focal necrosis ensue, resulting in perforation.
The inflammation is frequently mild, and a small perforation is walled off by pericolic fat and mesentery. This may lead to a localized abscess or, if adjacent organs are involved, a
fistula or obstruction. In comparison, poor containment results in free perforation and peritonitis.
Pathophysiology of diverticular bleeding As a diverticulum herniates, the penetrating vessel responsible for the wall weakness at that point becomes draped over the dome of
the diverticulum, separated from the bowel lumen only by mucosa (picture 3) [33]. Over time, the vasa recta is exposed to injury along its luminal aspect, leading to eccentric intimal
thickening and thinning of the media. These changes may result in segmental weakness of the artery, predisposing to rupture into the lumen. Diverticular bleeding typically occurs in
the absence of diverticulitis [33]. (See "Colonic diverticular bleeding".)
The anatomic relationship between diverticula and vasa recta is similar in both the right and left colon; however, right-sided diverticula have wider necks and domes. This could
expose the vasa recta to injury over a greater length, which could explain the higher incidence of right-sided hemorrhage [33].
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patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed.
These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
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articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
Basics topics (see "Patient information: Diverticulitis (The Basics)")
Beyond the Basics topics (see "Patient information: Diverticular disease (Beyond the Basics)")
SUMMARY Diverticula occur at points of weakness in the bowel wall where blood vessels penetrate. The development of diverticula is probably multifactorial, involving both
increases in intraluminal pressure and abnormalities in the bowel wall. Raised intraluminal pressure may be caused by abnormalities in motility that predispose to segmentation, and
is likely to be exacerbated by a low fiber diet.
Histologic changes in the muscle and collagen of the bowel wall decrease the tensile strength of the wall; these changes are similar to, but more pronounced than, the changes that
occur with age. Trauma to diverticula may produce either inflammation, which results in perforation, or changes in the vasa recta in the diverticular wall, which predisposes to
weakness and rupture of the vessel.
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REFERENCES
1. Mayo, WJ, Wilson, LB, Giffin, HZ. Acquired diverticulitis of the large intestine. Surg Gynecol Obstet 1907; 5:8.
2. Painter NS, Burkitt DP. Diverticular disease of the colon, a 20th century problem. Clin Gastroenterol 1975; 4:3.
3. Peery AF, Barrett PR, Park D, et al. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology 2012; 142:266.
4. Etzioni DA, Mack TM, Beart RW Jr, Kaiser AM. Diverticulitis in the United States: 1998-2005: changing patterns of disease and treatment. Ann Surg 2009; 249:210.
5. Parks TG. Natural history of diverticular disease of the colon. Clin Gastroenterol 1975; 4:53.
6. Rodkey GV, Welch CE. Changing patterns in the surgical treatment of diverticular disease. Ann Surg 1984; 200:466.
7. Acosta JA, Grebenc ML, Doberneck RC, et al. Colonic diverticular disease in patients 40 years old or younger. Am Surg 1992; 58:605.
8. Schauer PR, Ramos R, Ghiatas AA, Sirinek KR. Virulent diverticular disease in young obese men. Am J Surg 1992; 164:443.
9. Hughes LE. Postmortem survey of diverticular disease of the colon. I. Diverticulosis and diverticulitis. Gut 1969; 10:336.
10. Manousos ON, Truelove SC, Lumsden K. Prevalence of colonic diverticulosis in general population of Oxford area. Br Med J 1967; 3:762.
11. Fischer MG, Farkas AM. Diverticulitis of the cecum and ascending colon. Dis Colon Rectum 1984; 27:454.
12. Delvaux M. Diverticular disease of the colon in Europe: epidemiology, impact on citizen health and prevention. Aliment Pharmacol Ther 2003; 18 Suppl 3:71.
13. Chan CC, Lo KK, Chung EC, et al. Colonic diverticulosis in Hong Kong: distribution pattern and clinical significance. Clin Radiol 1998; 53:842.
14. Sugihara K, Muto T, Morioka Y, et al. Diverticular disease of the colon in Japan. A review of 615 cases. Dis Colon Rectum 1984; 27:531.
15. Miura S, Kodaira S, Shatari T, et al. Recent trends in diverticulosis of the right colon in Japan: retrospective review in a regional hospital. Dis Colon Rectum 2000; 43:1383.
16. Ngoi SS, Chia J, Goh MY, et al. Surgical management of right colon diverticulitis. Dis Colon Rectum 1992; 35:799.
17. Markham NI, Li AK. Diverticulitis of the right colon--experience from Hong Kong. Gut 1992; 33:547.
18. Lo CY, Chu KW. Acute diverticulitis of the right colon. Am J Surg 1996; 171:244.
19. Painter NS. The cause of diverticular disease of the colon, its symptoms and its complications. Review and hypothesis. J R Coll Surg Edinb 1985; 30:118.
20. Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of diet and the risk of symptomatic diverticular disease in men. Am J Clin Nutr 1994; 60:757.
21. Rege RV, Nahrwold DL. Diverticular disease. Curr Probl Surg 1989; 26:133.
22. Talbot JM. Role of dietary fiber in diverticular disease and colon cancer. Fed Proc 1981; 40:2337.
23. Mendeloff, AI. A critique of "fiber deficiency". Dig Dis 1976; 21:109.
24. Ornstein MH, Littlewood ER, Baird IM, et al. Are fibre supplements really necessary in diverticular disease of the colon? A controlled clinical trial. Br Med J (Clin Res Ed) 1981;

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282:1353.
25. Brodribb AJ. Treatment of symptomatic diverticular disease with a high-fibre diet. Lancet 1977; 1:664.
26. Hodgson WJ. The placebo effect. Is it important in diverticular disease? Am J Gastroenterol 1977; 67:157.
27. Nair P, Mayberry JF. Vegetarianism, dietary fibre and gastro-intestinal disease. Dig Dis 1994; 12:177.
28. Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of alcohol, smoking, caffeine, and the risk of symptomatic diverticular disease in men. Ann Epidemiol 1995;
5:221.
29. Aldoori WH, Giovannucci EL, Rimm EB, et al. Prospective study of physical activity and the risk of symptomatic diverticular disease in men. Gut 1995; 36:276.
30. Strate LL, Liu YL, Aldoori WH, et al. Obesity increases the risks of diverticulitis and diverticular bleeding. Gastroenterology 2009; 136:115.
31. Stefnsson T, Ekbom A, Sparn P, Phlman L. Increased risk of left sided colon cancer in patients with diverticular disease. Gut 1993; 34:499.
32. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. Br Med J 1969; 4:639.
33. Meyers MA, Alonso DR, Gray GF, Baer JW. Pathogenesis of bleeding colonic diverticulosis. Gastroenterology 1976; 71:577.
34. Whiteway J, Morson BC. Elastosis in diverticular disease of the sigmoid colon. Gut 1985; 26:258.
35. Wess L, Eastwood MA, Wess TJ, et al. Cross linking of collagen is increased in colonic diverticulosis. Gut 1995; 37:91.
36. Scheff RT, Zuckerman G, Harter H, et al. Diverticular disease in patients with chronic renal failure due to polycystic kidney disease. Ann Intern Med 1980; 92:202.
37. PAINTER NS, TRUELOVE SC, ARDRAN GM, TUCKEY M. SEGMENTATION AND THE LOCALIZATION OF INTRALUMINAL PRESSURES IN THE HUMAN COLON, WITH
SPECIAL REFERENCE TO THE PATHOGENESIS OF COLONIC DIVERTICULA. Gastroenterology 1965; 49:169.
38. Golder M, Burleigh DE, Belai A, et al. Smooth muscle cholinergic denervation hypersensitivity in diverticular disease. Lancet 2003; 361:1945.
Topic 1379 Version 9.0

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GRAPHICS
Fiber content of foods
Food

Average fiber per serving, g

Vegetables
Beans (navy, lima, kidney, baked)

8.5 to 10.0

Beans (string)

2.0

Broccoli

3.2

Brussels sprouts

2.3

Cabbage

2.0

Carrots

2.0

Celery

1.0

Corn

2.6

Corn on the cob

5.9

Lettuce

1.0

Potato (baked with skin)

3.0

Potato (french fries)

1.6

Peas (canned)

6.0

Rice

0.8

Fruit
Apple with peel

2.0

Apple juice

0.0

Banana

1.5

Grapefruit (fresh)

0.6

Orange

2.0

Peach

2.0

Raspberries

4.6

Strawberries

1.6

Bread
Whole wheat

1.3

White, rye, French

0.7

Cereal
All bran (100 percent)

8.4

Corn flakes

2.6

Wheaties

2.6

Other
Meats (chicken, liver, fish, lamb)

0.0

Cheese, milk, yogurt

0.0

Adapted from: Cheskin, LJ, Principles of Ambulatory Medicine, 4th ed, Williams & Wilkins, Baltimore, 1995, p. 479.

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Fecolith in diverticulum

Low power view shows a fecolith within a colonic diverticulum.

Courtesy of Robert Odze, MD.

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Location of colonic diverticula within the bowel wall

Diverticula develop at four well-defined points around the

circumference of the colon, the sites at which the vasa recta
penetrate the circular muscle layer. These vessels enter the wall
on each side of the mesenteric taenia and on the mesenteric
border of the two antimesenteric taeniae. The insets represent
the development of a diverticulum at one such point of
weakness.

Reproduced from Pemberton, JH, Armstrong, DN, Dietzen, CD. In: Textbook
of Gastroenterology, 2d ed, Yamada, T (Ed), 1995. By permission of Mayo
Foundation 1997.

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Diverticulum with nonobstructing fecolith

This nonobstructing fecolith within a large diverticulum could

predispose to the development of diverticulitis if the fecolith were
to obstruct the diverticulum, thereby increasing diverticular
pressure.

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Blood vessel within a colonic diverticulum

Endoscopy showing a blood vessel within a diverticulum. The blood

vessel is separated from the bowel lumen only by mucosa. Over
time, the vessel wall is exposed to injury along its luminal aspect,
possibly leading to segmental weakness which predisposes to
rupture into the lumen.
Courtesy of James B McGee, MD.

Normal sigmoid colon

Endoscopic appearance of the normal sigmoid colonic mucosa.

The fine vasculature is easily visible, and the surface is shiny
and smooth. The folds are of normal thickness.
Courtesy of James B McGee, MD.

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