Introduction

The origin of the word diverticulum is suggested to come from the Latin de-verto – to turn aside, at that time implying a by-road (Google, 2008), although perhaps more memorably it has been suggested that it related to a ‘wayside house of ill repute’ (Tjandra et al., 2008). Nowadays, it is associated with a benign sac-like protuberance that arises from a hollow organ.

Colonic diverticula are more correctly pseudodiverticula as it is the mucosa that invaginates through the circular muscle bound by muscularis mucosae and a thin layer of connective tissue. Asymptomatic colonic diverticula identified as an incidental finding are referred to as diverticulosis. If diverticula become symptomatic this is known as diverticular disease. Inflammation associated with diverticular disease is called diverticulitis. During the double contrast barium enema examination, mild uncomplicated diverticula may be noted and ignored except for a short comment in the report.

In this chapter, it is intended to bring to life the humble colonic diverticulum and to provide the reader with an insight into how and why it develops and the complications that can arise.

History

Diverticula of the colon were first described by Littre in 1700. The possibility of diverticula as a site of infection and perforation was first raised in 1849 by Jean Cruveilhier, an eminent Parisian anatomist (Painter and Burkitt, 1971; Mimura et al., 2002). In 1912, George Haenisch, a roentgenologist, was the first to recognize and describe diverticulitis radiologically.

When considering the etiology of diverticular disease, the most substantiated theory is that of a deficiency in dietary fiber. Following his work as a surgeon in central Africa in the 20th century, Dennis Burkitt appreciated the connection between dietary fiber and the volume and soft nature of feces produced with negligible discomfort by the Africans who lived largely on a vegetarian diet. In 1971, Painter and Burkitt put forward their belief that a low-residue diet was the cause of diverticular disease. It was also noted at that time that, in the central parts of Africa, a number of diseases common in the West, including diverticulitis, were rarely observed (Painter and Burkitt, 1971; Story and Kritchersky, 1994; Netter, 2000; Mimura et al., 2002; Stollman and Raskin, 2004).

Anatomy: colon structure as it relates to diverticular disease

To understand the mechanism of how and why diverticula can form, the musculature and blood supply of the colon need to be reviewed. The colon is made up of four layers: mucosa, submucosa, muscularis and serosa. The muscular layer consists of an inner circular muscle and external longitudinal muscle. The circular muscle forms a thin layer over the cecum and colon, forming a thicker layer covering the rectum. The external longitudinal muscle forms a coating of muscle fiber much thinner than that of the circular muscle it covers. On three aspects of the circumference of the colon, the muscle thickens to form three longitudinal bands, the teniae coli. Individually, the muscle bands are known as tenia mesocolica, libera and omentalis. The three teniae are shorter than the length of circular muscle causing the colon to concertina and become sacculated. These sacculations are called haustral folds between which circular muscle fiber becomes thicker. The three teniae have their origin of attachment at the base of the appendix. In most cases, the bands are spaced equidistant around the circumference of the cecum (Davies, 1969; Netter, 1975) (see also Chapter 4).

In the distal colon, the three teniae fan out at the level of the peritoneal reflection, completely encasing the rectum but forming a thickened portion still recognizable as bands on the anterior and posterior aspects of the rectum (Wolf et al., 2000). Diverticula do not occur distal to the peritoneal reflection, as the anatomical and pathophysiological features are different to that of the colon.

The English physician, Sir David Drummond, described an arterial ring around the colon, the ‘marginal artery of Drummond’ (Gunasekera et al., 2003; Floch and Bina, 2004). The vasa recta arise at frequent intervals around the marginal artery. Dividing at the tenia mesocolica, the vasa recta branches into nutrient vessels that supply the colon. The nutrient vessels pass deep via a canal either side of mesocolica and on the mesenteric side of teniae libera and omentalis (Bassotti et al., 2003; Floch and Bina, 2004). Along these canals the nutrient artery passes through the circular muscle fiber to its origin. In the right circumstances, these canals constitute the weak points through which the mucosa can protrude creating a diverticulum (Figures 15.1 and 15.2).

Figure 15.1 Cross-section of the colon with the site of diverticular outpouching.

Figure 15.2 Apparent haphazard formation of diverticula at barium enema. Sillhouette margin showing diverticula arising from the apex of the haustral folds.

Pathogenesis

Papers by Painter and Burkitt (1971), Smith (1986), Aldoori et al. (1998), Frieri et al. (2006) and Blackwood and Salter (2000) are among the many that support the hypothesis that dietary fiber reduces the risk of diverticular disease and, conversely, the risk being increased by a lack of fiber, particularly the insoluble fiber hydrocolloid cellulose.

The dietary fiber hydrocolloid cellulose is a non-digestible carbohydrate found in plant material. Although this cellulose itself has a low water content, it is porous and has a significant capability to retain water within its pores. Hydrocolloid cellulose is also resistant to the effects of enzymes in the small bowel and it can provide support for the growth of microflora in the colon as fermentation takes place. It is the high water-retaining capability of the insoluble element of cellulose that is responsible for the (beneficial) formation of a more bulky stool. This results in the maintenance of colonic lumen diameter commensurate with the stool volume. The fluid retained within the stool as a result of dietary fiber intake reduces fecal viscosity and results in a reduced transit time (Prosky and Dreher, 1999; Bassotti et al., 2003). Painter and Burkitt (1971) reported that, in areas of Africa where the population has a high fiber intake, normal colonic transit time was half that common in the West at that time.

Understanding the widely accepted hypothesis as to what provides and constitutes a good stool enables an understanding of the converse, that a lack of dietary fiber results in a reduction in fecal water content. This leads to the stool being more compact and smaller in diameter and with an increased viscosity. The denser less viscous stool, in conjunction with the reduced diameter of the colon, results in a higher intraluminal pressure requirement to pass the fecal column through the bowel. The slower passage of the stool though the colon allows more fluid to be absorbed maintaining the vicious circle that supports the pathogenesis of diverticular disease (Table 15.1).

Table 15.1 Pathogenesis of diverticular disease

Pathophysiology

The high intraluminal pressure directed towards the bowel wall identifies the points of least resistance. At the apex of the arc-like haustral folds where the tensile strength is least, the weak points are the canals either side of tenia mesocolica and on the mesenteric side of teniae libera and omentalis through which the nutrient vessels pass.

Pierre-Simon Laplace (1749–1827), a French mathematician, gave his name to a law that provides an explanation as to how the intra- and extraluminal pressure difference, the radius of the colonic lumen and the nature and thickness of the bowel wall can affect the bowel wall tension (Smith, 1986; West, 2006).

Basford (2002) considers the law of Laplace and its relevance today. One area in which Laplace’s law can be demonstrated is fecal transit in the colon. The wider diameter of the colonic lumen resulting from a bulky fluid retentive stool provides for a relatively low fecal viscosity and a reduced transit time which together assist in maintaining a low intraluminal pressure requirement for the movement of stool through the large bowel. Normally, the sigmoid region has the narrowest lumen within the colon and thereby lends itself to having the highest intraluminal pressure and thus the greatest propensity towards colonic diverticular disease anywhere where a low fiber diet is usual.

Contractions occur in the colon to help propel fecal material through the lumen and aid its mixing for fluid absorption. These contractions cause segmentation in the lumen that are not normally of any clinical relevance when a diet includes a significant proportion of insoluble dietary fiber creating the optimum stool form.

When segmentation becomes occlusive, the likelihood of diverticulosis is increased. Occlusive segmentation happens when the structural changes in the connective tissue shortens the longitudinal muscle, thickening the circular muscle layer. Efforts from increased work requirement from the circular muscle results in concertina-like folds narrowing the lumen. In conjunction with these factors, there are associated pathogenetic factors (high intraluminal pressure and high fecal viscosity) which predispose to strong muscular contraction that divides the lumen into segments that can be exaggerated to the point of causing occlusive capsules. Within the occlusive capsule, additional intraluminal pressure is generated that is directed towards the colonic wall.

Arising at the apex of the haustra (where the tensile strength is least), diverticula become manifest in a linear array contrary to their apparent irregular distribution demonstrated at barium enema examination (Box 15.1) (Figures 15.2,15.3A, 15.3B) (Netter, 1975; Whiteway and Morson, 1985; Smith, 1986; Bassotti et al., 2003; Eastwood, 2003; Stollman and Raskin, 2004; Floch and Bina, 2004; West, 2004, 2006; West and Losada, 2004; Ye et al., 2005; Parra-Blanco, 2006).

BOX 15.1 Pathophysiology of diverticular disease

Reduction in tensile strength

High intraluminal pressure

Law of Laplace explains effect of pressure on colonic wall

Increased deposits in connective tissue of (e.g.) elastin

Shortening of the longitudinal muscle

Thickening of the circular muscle

Muscular contraction causes segmentation

Diverticula form through tract of the vasa recta

Figure 15.3 (A) Longitudinal dissection of colon demonstrating uniformity of formation; (B) dissection through the bowel wall showing cross-section through diverticula.

Epidemiology of right-sided colonic diverticula

The Western tendency towards sigmoid diverticular disease is not reflected in Asian populations where diverticular disease predominantly affects the right colon (Gunasekera et al., 2003). West (2006) reports the suggestion that diverticula of the cecum and ascending colon, as commonly found in Asia, differ from the diverticula found in the West, occurring at an earlier age and associated with a genetic predisposition. The predisposition of right-sided diverticula in Asians is supported by others (Mimura et al., 2002; Stollman and Raskin, 2004; Kang et al., 2004; Rajendra and Ho, 2005). Etiology of the predominantly right-sided diverticula found in Japan was reported by Nakaji et al. (2002) as similar to left-sided diverticula in the West.

Age

Asymptomatic diverticular disease in the Western world is rare under the age of 40 but is widely recognized as increasing in prevalence with age. A number of papers suggest that diverticulosis might be present in up to 60% of the population, however, there is a variance in the reported age range to which this percentage relates between 60 years and over 80 years of age (Carter and Whelan, 2000; Mimura et al., 2002; Floch and Bina, 2004; West and Losada, 2004).

In a 10-year UK study of diverticular disease hospitalizations, Jeyarajah et al. (2008) reported 1 219 480 patients hospitalized with a diagnosis of diverticular disease with the disease being the primary cause of admission in 567 423 cases and a comorbidity in 652 057 admissions.

With age, structural changes occur in the connective tissue, including increase in submucosal deposits of collagen, elastin and reticular tissue. The association between this and the increased chance of diverticulosis is discussed in the section on pathophysiology in this chapter (Aldoori et al., 1998; Carter and Whelan, 2000; Basford, 2002; Mimura et al., 2002; Eastwood, 2003; Floch and Bina, 2004; West and Losada, 2004; Parra-Blanco, 2006).

Complications

Between 75 and 85% of patients with diverticula will remain asymptomatic (West, 2004; Salzman and Lillie, 2005). The complications that are associated with diverticular disease include bleeding and inflammation, which itself can lead to perforation, abscess formation, obstruction and peritonitis.

Diverticulitis

Colecchia and Sandri (2003) suggest that diverticulitis will affect 10–25% of patients with diverticular disease. Floch and Bina (2004) advanced further evidence to support the suggestion that fiber deficiency not only leads to the formation of diverticula but is also associated with changes in the colonic microflora. This may be associated with a decrease in the colonic mucosal immune response, supporting referenced evidence that chronic segmental colitis is associated with diverticula. The presented hypothesis was that the chronic inflammation occurs in the mucosa associated with the diverticula and is the cause of diverticulitis (Smith, 1986).

Fecal material inspissated within a diverticulum can rasp, irritate and damage the mucosa. While the sac of the diverticulum is bounded by the muscularis, it is provided with extrinsic support. However, once through to the serosa the support is no longer present leading to the potential to perforate, particularly with the increased intraluminal pressure produced with the strain to evacuate. A resultant perforation may only be small, but such a microperforation makes it possible for bacteria to pass into the subserosa and create a local inflammatory reaction within close proximity to the bowel wall, this can result in small contained pericolic abscess formation (Figure 15.4).

Figure 15.4 Crumpled mucosa of an inflammatory diverticular stricture; large diverticulum, the remains of a pericolic abscess; colocolic fistula.

A local inflammatory process can extend through the full thickness of the bowel wall. The more serious macroperforation can lead to abscess and inflammatory mass formation within the peritoneum. Inflammatory mass and peritoneal abscess development can result in one or more of a number of complications including: adhesions, scarring, stricturing and free perforation into the peritoneum resulting in fecal peritonitis. Where there is inflammatory adhesion to an adjacent hollow organ, such as the bladder or vagina, there is the potential for fistula formation (Smith, 1986; Netter, 2000; Colecchia and Sandri, 2003; West and Losada, 2004).

Fistula

The term fistula originates from the Latin for pipe or tube and denotes a pathologically abnormal passage leading from an abscess cavity or hollow organ to another hollow organ or the skin surface. When a phlegmon or abscess extends from a diverticulum, it has the potential of rupturing into an adjacent hollow organ enabling a fistula to develop (Figure 15.5). Colovesical fistulae are the most common variety with a male to female predominance by a factor of 2:1, the female bladder being protected by the uterus. Colovaginal fistulae constitute 25% of all cases and are the next most common tract formation resulting from diverticulitis (Blackwood et al., 2000; Netter, 2000) (Figures 15.5 and 15.6).

Figure 15.5 Colovaginal fistula seen to arise from a small diverticulum.

Figure 15.6 Passage of rectal contrast passing directly through a fistulous tract into the vagina.

Stricturing and obstruction

Luminal narrowing or obstruction during an acute episode of diverticulitis can occur due to the pericolic inflammation (Figure 15.7) or compression from abscess formation. Diverticular abscess formation is easily diagnosed with CT.

Figure 15.7 Narrow segment associated with an acute diverticulitis.

Diverticulitis is often self-limiting and responds to drug therapy and with the therapeutic response the associated stricturing can resolve. It is possible for a patient to have recurrent bouts of diverticulitis which appear asymptomatic; these can trigger the development of fibrotic stricturing (Figures 15.8 and 15.9) (Box 15.2) (Netter, 2000; Blackwood et al., 2000).

Figure 15.8 Fibrotic stricture: the appearance of the stricture may also suggest a malignancy and will require further imaging to confirm or exclude.

Figure 15.9 Fibrotic stricture: complete obstruction to the retrograde flow of barium, although antegrade passage may still be possible.

BOX 15.2 Complications of diverticular disease

Bleeding

The vasa recta may be stretched over the forming diverticula

40% of lower GI bleeding is of diverticular origin

GI bleeding not necessarily related to inflammation

Diverticulitis

Affects 10–25% of patients with diverticular disease

Damaged diverticular mucosa can result in micro- or macroperforation

Microperforation can result in peridiverticular abscess

Macroperforation can lead to inflammatory mass, peritoneal abscess, free perforation, peritonitis, fistula colonic structuring

Additional information

Symptoms associated with diverticular disease and its complications (Chapter 10 – Symptoms of lower gastrointestinal disease).

Diagnosis of diverticular disease and its complications can be found in Chapter 13 – Fluoroscopic investigations of the large bowel; Chapter 17 – Cross-sectional investigations, nuclear medicine and ultrasound of the small and large bowel; Chapter 20 – Endoscopy of the upper and lower gastrointestinal tract.

Surgical management of diverticular disease and its complications (Chapter 21 – Common surgical procedures of the gastrointestinal tract).