27.1 Introduction

The term “diverticulum” indicates an abnormal pouch or sac, opening from a hollow organ such as the intestine. It is derived from the Latin verb divertere, which means “to turn aside.” Credit for the first description of diverticular disease has been given to Cruveilhier, ¹ who in 1849 described a series of small, pear-shaped, hernia protrusions of mucosa through the muscle coat of the sigmoid colon. From a historical perspective, diverticula were initially regarded as nothing more than a curiosity of pathology, defined as mucosa protruding through the muscular wall of the bowel. The advent of contrast radiology revealed a growing prevalence of this disease. These protrusions, or pseudodiverticula, are commonly associated with a muscular abnormality of the sigmoid colon. Over time, it became evident that diverticula could be associated with inflammation, perforation, adhesions, fistulas, and stenosis. When inflammation develops, the term diverticulitis is used. Initially, diverticulosis was not treated unless complications supervened. As anesthesia and surgical techniques became safer, however, physicians began to refer patients with diverticulosis for elective operation in an effort to prevent complications. Because many patients with this condition exhibit no evidence of inflammation, the encompassing term “diverticular disease” is used for the entire spectrum of the clinical consequences of colonic diverticulosis.

27.2 History and Anatomy

In a detailed study of the anatomy and pathology of diverticular disease, Slack ² compared the large intestine of 141 cadavers in which consecutive autopsies were performed with 36 consecutive operative specimens removed because of diverticulitis. Diverticula had broken through the circular muscle in four main positions (▶ Fig. 27.1). In approximately 40% of the cases, protrusions were also noted between the antimesenteric teniae. A sizable blood vessel was seen to course around the bowel on each side outside the muscular coat and penetrate through the mesenteric side of the antimesenteric teniae. In some cases, this vessel appeared to divide into deep and superficial branches, with the deeper one piercing the circular muscle coat and the more superficial one passing directly through the teniae. Small vessels arose from the main circumferential vessels and penetrated the circular muscle coat and the mesenteric teniae. In each case, small vessels passed along the neck of the diverticulum toward the lumen of the bowel.

27.3 Incidence

The prevalence of diverticulosis in the United States has increased dramatically since it was first described, and increases substantially with age. It is estimated that approximately 20% of patients with diverticulosis develop diverticulitis over the course of their lifetime ³ and that 30% of the population over the age of 60 years, and 60% of the population over the age of 80, may be affected. ⁴ Connell ⁵ estimated the risk of the aging population developing diverticular disease to be nearly 50%. In fact, it is impossible to estimate the precise incidence of diverticular disease in the general population. Data on the incidence and prevalence of diverticular disease of the colon represent a crude overall blend of numbers derived from radiologic, surgical, and autopsy reports on both hospitalized and ambulatory populations. In any review of statistics, autopsy studies will underestimate the incidence of diverticulosis because of the care needed to demonstrate all diverticula. Radiologic studies will overestimate the occurrence because people have colonoscopy and other imaging studies for various symptoms. What is evident is that the incidence has gradually increased in the past 100 years. For example, in 1930, Rankin and Brown ⁶ reported that of 24,620 barium enema examinations, 5.7% had diverticulosis, as did 5.2% of 1,925 autopsy cases at the Mayo Clinic. Heller and Hackler ⁷ reported that between 1909 and 1975, the autopsy incidence of diverticulosis increased from 5 to 50%. The incidence of diverticular disease is typically reported as more common in men. ^{8 , 9} Geographic location is also important, for it appears that diverticulosis is a disease of Western people. A close relationship exists between the prevalence of diverticular disease, economic development, and adoption of Western eating habits. Diverticula are common in Europe, North America, and Australia, less common in South America, and rare in Africa and Oriental countries. ^{10 , 11 , 12} Right-sided diverticulosis is found almost exclusively in Oriental people, and is more common than left-sided diverticula in Japan, Hawaii (among Japanese and Chinese individuals), China, Korea, Thailand, and Singapore. ⁶ Even so, right-sided diverticular disease of the colon seems to produce fewer clinical problems when compared with left-sided diverticular disease.

Diverticular disease currently accounts for approximately 300,000 hospitalizations per year in the United States, resulting in 1.5 million days of inpatient care. ¹³ Additionally, roughly 1.5 million outpatient visits each year are due to diverticular disease. ¹⁴ Over the past several years, research on natural biology of diverticulitis has been incorporated into the management recommendations for this challenging disease. Although diverticulitis may affect any location in the colon, this chapter will focus on left-sided disease.

27.4 Etiology

It is generally agreed that colonic diverticula are acquired. They are considered pulsion diverticula, which, under the influence of increased intraluminal pressure, are mucosal herniations that protrude through points of the bowel wall weakened by entry of blood vessels. Recognition of the segmentation mechanism of pressure production and its role in the localization of high intracolonic pressures has led to some understanding of the pathogenesis of diverticular disease, but the etiology of the disease to a great degree remains a mystery. Painter ¹⁵ hypothesized that it is a deficiency disease caused by inadequacy of fiber brought about by the refining of carbohydrates. In the past half century, the amount of cereal fiber consumed by individuals in the Western world has declined dramatically. Painter ¹⁵ believed that this dietary change is the most probable cause of the emergence of diverticular disease in Westernized populations in the 20th century. A colon with a wide lumen is less able to form segments efficiently, and large-bore colons are found wherever individuals eat a diet containing plenty of roughage. By contrast, consuming the over-refined, fiber-deficient diet of the industrial countries produces small hard stools that pass through a narrower colon that can segment more easily. Higher pressures are needed to transport these stiff stools, and because the fecal stream is more viscous by the time it reaches the distal colon, it causes the sigmoid to segment excessively. Thus, segmentation is postulated to be the mechanism responsible for the pathogenesis of diverticula, and a fiber-deficient diet is the likely cause of the disease. Burkitt et al ¹⁶ studied the fiber intake of African natives and compared it to that of British subjects. They found that the Africans had a higher stool weight and a shorter transit time. They attributed the low incidence of diverticular disease to this high fiber intake. Bingham ¹⁷ provided an excellent summary of the dietary fiber intake of general populations and found that Africans consume 60 to 150 g/d; Europeans, 15 to 25 g/d; Japanese, 20 g/d; Canadian vegetarians, 30 g/d; and people in the United States, 13 to 20 g/d. In a study of barium enema examinations in vegetarians and nonvegetarians, Gear et al ¹⁸ found a 12% incidence of diverticular disease in vegetarians, compared with a 33% incidence among nonvegetarians. Manousos et al ¹⁹ found that patients with diverticula consumed significantly less brown bread and vegetables but more meat than controls.

Nakaji et al ²⁰ compared the etiology of right-sided diverticula in Japan with that of left-sided diverticula in the West. Diverticula occur predominantly in the right-sided colon (> 70%) in Japanese patients, and even among Japanese who emigrate, in contrast with the diverticula in Western patients. The increased detection rate over time is higher in urban areas than in rural areas, and it corresponds to the distribution of dietary fiber intake. Furthermore, the significant relationship of right-sided diverticula with intraluminal pressure in Japan is similar to that of left-sided diverticula in the West, and the pathological features of these diverticula are similar. The etiology of right-sided diverticula in Japan (and perhaps other Mongolian peoples) is very similar to that of left-sided diverticula in the West. The location may represent a difference in morphology of the large intestine between Mongolians (including Japanese) and West-erners, rather than environmental differences.

Other lifestyle habits also appear to have an influence on the development of symptomatic diverticular disease. In a prospective study of 47,678 American men, Aldoori et al ²¹ found that physical activity was inversely associated with the risk of symptoms, with a relative risk of 0.60 for individuals engaged in vigorous activity such as jogging and running. From the same cohort of men, Aldoori et al ²² found that smoking, caffeine, and alcohol intake are not associated with any substantial increase in the risk of symptomatic disease. They further examined dietary fiber calculated from food composition values from a prospective cohort of 43,881 U.S. male health professionals in the 40 to 75 years age group. ²³ Their findings suggest that the insoluble component of fiber was significantly associated with a decreased risk of diverticular disease (relative ratio [RR] = 0.63), and this inverse association was particularly strong for cellulose (RR = 0.52).

Advancing age has an effect on mechanical strength of the colon wall, likely a consequence of changes in collagen structure. Wess et al ²⁴ measured collagen from unaffected human colons and compared it to those with colonic diverticulosis obtained at necropsy. The total collagen content was constant with age. The acid solubility of the collagen, however, increased after the age of 40 years. After 60 years of age, colonic diverticulosis was associated with an increased acid solubility ratio compared with values in unaffected colons (15:3 compared with 9:2). Stumpf et al ²⁵ showed decreased levels of mature collagen type I and increased levels of collagen type III, with a resulting lower collagen ratio I/III, in patients with diverticulitis. The expression of matrix metalloproteinase-I was significantly reduced in the diverticulitis group, while the expression of matrix metalloproteinase-13 did not differ significantly between the two groups. Their findings support the theory of structural changes in the colonic wall as one of the major pathogenic factors in the development of diverticular disease. Bode et al ²⁶ reported the contents of types I and III collagen telopeptides and total collagen were similar in diverticulosis and healthy tissue and that type III collagen synthesis was increased in diverticulosis, but not in malignancy.

The traditional belief is that diverticula develop as a result of elevated intraluminal pressures that arise because of segmentation of the colon. Segmentation causes the colon to act not as a tube, but as a series of “little bladders,” each of which has narrowed outflow (▶ Fig. 27.2). ²⁷ High pressures develop in these segments and force the mucosa through the muscular wall of the colon. Segmentation plays a part in normal colonic physiology by shunting colon contents back and forth in the sigmoid colon, presumably to aid in the absorption of water from the fecal stream. Thus, Painter and Burkitt believe that diverticula are the outward visible sign of an inward disturbance of colonic motility, due to a diet low in fiber. ²⁷ Painter ²⁸ summarized his extensive studies of the role of segmentation as the cause of diverticular disease and its symptoms as follows. Segmentation of the colon is the mechanism by which the colon propels its contents or halts material moving through its lumen. It involves the production of increased intraluminal pressures and has been demonstrated by recording the intracolonic pressures with open-ended tubes, while simultaneous fluoroscopy recorded the behavior of the colon. The intracolonic pressures produced by segmentation may exceed 90 mm Hg. Cineradiography also has revealed high localized intraluminal pressures that are produced by segmentation of the colon, regardless of the stimulus that evokes them.

Another theory on the etiology of diverticular change proposes that there is no muscle abnormality, but there is likely a connective tissue abnormality causing a density of diverticula in the colon. This abnormality provides inadequate support for vessels in the wall of the colon, increasing the propensity for vascular malformations and bleeding. Clinical evidence suggests that both acute and chronic pain may be caused by either inflammation or muscle spasm. This theory also proposes that perforation may be due to abnormal intraluminal pressures rather than diverticular inflammation. ²⁹

Nonetheless, the muscle abnormality is the most consistent and important feature in diverticular disease of the sigmoid colon. ⁹ When the colonic wall is sectioned, the interior aspect reveals openings that may at times be inconspicuous and detected only when fecal matter is impacted. The muscular coat is thickened, and the mucosal layer is heaped into transverse folds that project into the lumen. The luminal diameter is reduced in size. The thickened longitudinal and circular muscle layers have been considered responsible for shortening the sigmoid colon and pleating the mucosa. Narrowing of the lumen may be due to these redundant folds but in part may be secondary to pericolic fibrosis. ⁹

Microscopically, pulsion diverticula are comprised of two of the four layers of the colon wall: an inner mucosal layer and an outer serosal layer. An artery, vein, and attenuated muscle may be seen close to the neck of the diverticulum (▶ Fig. 27.3). In patients with diverticular disease, both the muscularis mucosa and muscularis propria are greatly increased in thickness. There has been much conjecture about whether the muscle thickening is due to hypertrophy or hyperplasia. In their study of the thickened bowel, Whiteway and Morson ³⁰ failed to reveal evidence of cellular hypertrophy or hyperplasia. Instead, they attributed the thickening to the presence of elastic tissue, specifically in the teniae. ³¹ This progressive elastosis causes longitudinal foreshortening of the colon, accentuating the semicircular corrugations of the shortened circular muscle. The source of the elastosis is uncertain, but this abnormality precedes the development of diverticulosis. It is characteristic of diverticular disease in that it is never seen in other segmental or diffuse inflammatory conditions of the colon. Why the muscle abnormality occurs predominantly in the sigmoid colon is unclear. It is postulated that the muscle of the sigmoid colon is different from that of the more proximal colon because it appears thicker and shows an increased capacity for muscular spasm.

27.5 Natural History

Despite the significant prevalence of diverticulosis of the colon in western adults—estimated to be 15 to 37% ⁴ —it is an asymptomatic condition in most patients. It is estimated that 10 to 25% of patients with diverticulosis will develop diverticulitis. ³² Of patients with diverticulitis of the colon, 10 to 33% eventually require operative intervention. ³³ From his extensive personal studies and thorough review of the literature, Parks ⁴ summarized the following features of diverticular disease. The incidence increases with advancing years, with an increased risk of hemorrhage in the elderly. In young patients, the disease may pursue a more aggressive course. There seems to be an increasing incidence in women. Progression of disease relative to number and size of diverticula does not seem to occur. In the majority of patients with diverticula localized to the distal colon, the disorder will not necessarily progress relentlessly and involve additional segments; progression more often occurs within the segment of bowel initially affected. On an average, patients with extensive involvement may be younger than those with localized disease. Parks ⁴ also noted severe complications to occur equally in patients with distal disease and those with total colonic involvement, and after an operation to eradicate distal disease, it is unusual for inflammatory complications to develop in the proximal bowel. However, Parks described that hemorrhage occurred more readily from the proximal bowel, it was not necessarily of diverticular origin, and may be due to vascular ectasias, which are more common in the right colon.