studies of the colon wall showed thinning of the circular muscle associated with early diverticula. Gaps

in the circular muscle were observed with larger diverticula.7

Figure 69-1. Cross section of the colon illustrating the relation of diverticula to the blood vessels penetrating the circular muscle

layer, the taeniae, and the appendices epiploicae.

Figure 69-2. Postevacuation film of barium enema, demonstrating a giant colonic diverticulum (arrows) partially filled with

barium. (Reproduced with permission from McNutt R, Schmitt D, Schulte W. Giant colonic diverticula. Dis Colon 1988;31:625.)

In contrast to typical pseudodiverticula, giant colonic diverticula almost always arise from the

antimesenteric border of the colon. They are assumed to be a complication of ordinary colonic

diverticulosis, possibly developing after inflammatory narrowing of the neck of a pseudodiverticulum

causes a ball-valve mechanism that entraps gas in the diverticulum, causing it to enlarge (Fig. 69-2).13

The observation of colonic diverticula in young patients with connective tissue disorders such as

Marfan disease and Ehlers–Danlos syndrome raises the question of whether connective tissue genetic

derangements play a role in diverticulosis development.14,15 Ordinary senescent connective tissue

change may be a factor as well. Cross-linkage of collagen fibrils in the colon wall increases with age,

rising markedly after age 40, and appears to decrease compliance of the colon wall. In comparison with

age-matched controls, this cross-linkage is exaggerated in patients with diverticulosis.16

Thickening of the colon wall in diverticulosis was originally attributed to muscle hypertrophy.12,17

This was disproven by histologic studies, but increased elastin deposition in the taeniae coli of patients

with uncomplicated diverticulosis has been shown. The taeniae are shortened as a result, causing the

circular muscle to be accordioned in the two intertaenial zones, the same areas where pseudodiverticula

more commonly form.18 The functional significance of this is not known, but it has been speculated that

muscle contractions may be stronger in these areas.

Motility Factors

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Four unusual colonic motility patterns have been observed in the setting of diverticulosis: segmentation,

high-pressure waves, slow-wave motility pattern, and disorganized propulsive activity.

Segmentation

Painter et al.19 used cineradiography and manometry to study colonic motility and reported that when

simultaneous haustral contractions occur in the same segment of colon, high pressure is generated in the

intervening bowel, causing ballooning of the colon wall and distention of diverticula (Fig. 69-3).

Figure 69-3. The role of segmentation in colonic physiology. A: Interhaustral ring contraction (“segmentation”) leads to increased

luminal pressure when there is simultaneous segment wall contraction. B: Relaxation of an interhaustral ring allows passage of

colon contents from the high-pressure segment to a neighboring low-pressure segment. C: Resistance to colon content flow can be

imposed by interhaustral ring contraction that functions as a baffle. Resultant interruption of flow can also significantly increase

luminal pressure in that segment. D: Diverticula always arise from the segment wall between interhaustral rings and never at the

rings.

High-Pressure Waves

High-pressure waves are independent of normal peristalsis and have an amplitude of 10 mm Hg in

normal patients but have higher amplitude (up to 90 mm Hg) and longer duration in patients with

diverticulosis.20

Slow-Wave Motility Pattern

The normal slow-wave pattern in the colon is altered in DD.21,22

Disorganized Propulsive Activity

High-amplitude propulsive contractions occurred more frequently and were more likely to be

disorganized in patients with DD than normal subjects. Retropulsive contractions occurred more

frequently in segments of colon with diverticulosis.23

Diet

Decreased dietary fiber is the most consistent factor associated with the high incidence of diverticulosis

in Western populations. Painter and Burkitt first elucidated this connection after noting the striking

disparity in incidence between British society and sub-Saharan populations. They measured colon transit

time and stool weights in over 1,000 individuals in the United Kingdom and sub-Saharan Africa. The rise

in the incidence of DD coincident with the rise in refined food products in diets in the West was also

noted.24 Painter and Burkitt25 also reported improvement of DD symptoms in patients who increased

dietary fiber and recrudescence of symptoms once fiber intake decreased again. There is now a rising

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incidence of diverticulosis among previously low-risk populations in concert with changes to a Westernstyle diet as a consequence of economic development or immigration. Japanese immigrants to the

United States acquire diverticulosis risk comparable to other Westerners, although the right-sided

predominance of diverticulosis seen among Asians persists.5,26 The exact protective mechanism of stool

bulk is not understood. Evidence that contradicts the role of low-fiber diet or constipation as

contributing factors to DD is provided by a study of 2813 patients enrolled in a vitamin D and colon

polyp colonoscopy study. Five hundred and thirty-nine patients aged 45 to 75 who had the incidental

colonoscopic finding of diverticulosis without antecedent history of it were compared to 1569 controls.

The control group had a higher self-reported history of less frequent or lumpy stools, and there was no

difference in dietary fiber intake. However, inaccuracies of bowel and diet habit self-reports, the

evaluation of individuals with asymptomatic diverticulosis versus symptomatic DD, and the imperfect

sensitivity of colonoscopy for detection of diverticulosis should be considered in the interpretation of

these findings.27

While the focus on dietary fiber has emphasized insoluble fiber, soluble fiber may also be of value.

Soluble fiber is processed by intestinal flora, which may in turn affect diverticulosis.26,28 Finally, despite

the long-held admonition to avoid eating nuts and seeds, there is no evidence to support this

recommendation.29

Other Factors

Other neurologic and chemical mediators of colonic motility may play a role in pseudodiverticula

genesis. Vasoactive intestinal peptide levels are increased in the bowel wall of patients with

diverticulosis.30 Age-related vagal attrition has been postulated to contribute to colonic smooth muscle

dysmotility.31 Alterations of serotonin expression and function are noted after resolution of acute

diverticulitis and may contribute to lasting symptoms.32

Emerging Concepts

Two observations have focused interest in the possibility of a primary inflammatory etiology of

diverticulitis. One is that a subset of patients with uncomplicated diverticulitis are unresponsive to

antibiotic therapy as would be expected in the case of a smoldering, focal bowel-wall infection due to

diverticular sepsis or microperforation (see below). The other is that anti-inflammatory medications

appear to reduce flares of diverticulitis in some patients. Shifts in the microbiome have also been

detected in other lower gastrointestinal system disorders including colon cancer and IBD.33–36 Subtle

peridiverticular inflammatory changes have been noted in some patients with asymptomatic DD.37

Whether diverticulosis results from or causes inflammation and whether progression to diverticulitis

likewise results from or causes inflammation is an open question. Similar questions have existed

regarding an interrelation between IBS and DD. A longitudinal study of administrative and clinical data

from the Veterans’ Association found the hazard ratio for developing IBS after an episode of

diverticulitis was 4.7 compared to controls even though the study group of older males (mean age 62

years) is generally a lower risk group for IBS.38 Whether these “new IBS” cases should actually be

regarded as segmental diverticulitis that could be managed by resection as opposed to a pan-colonic

phenomenon has not been demonstrated.

Pathogenesis of Diverticulitis

4 The process by which a subset of people with diverticulosis develop diverticulitis has yet to be

explained. Overwhelming inflammatory changes that develop with perforation or other complications of

diverticulitis likely obscure subtle histologic details that might explain the pathogenesis of the disease.

Traditionally, it has been postulated that mechanical obstruction by food or fecal material of a

diverticulum leads to bacterial proliferation, gas, and toxin production in the occluded diverticulum,

causing diverticulitis. However, the largely extracolonic manifestations of diverticulitis (phlegmon,

abscess, and free perforation) suggest micro- or macroperforation as the inciting event, possibly as a

kind of diverticular “blow-out” secondary to segmentation-type contractions or high-pressure waves. In

recent years (and perhaps with the rising number of patients undergoing screening colonoscopy),

peridiverticular inflammation has been identified, often in asymptomatic patients. Diverticulitisassociated colitis is of unrecognized clinical significance, partly because so many patients with these

findings are asymptomatic and partly because the findings are not uniformly evident in patients

requiring surgical therapy for diverticulitis. It has been suggested that low-grade inflammation could

alter bowel motility and thereby contribute to diverticular perforation risk. Endoscopists are cautioned

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