The singular is diverticulum and the plural diverticula.

Note: The frequently used plurals of diverticulae and diverticuli are both incorrect and should therefore not be used, especially by pathologists and clinicians purporting to have a gastrointestinal (GI) interest or expertise! We all have too many areas of relative ignorance to make overt errors over simple things. Diverticular disease is fine as, of course, is diverticulitis and diverticulosis.

Diverticula occur in all parts of the GI tract, specifically the duodenum, jejunum, the ileum including Meckel’s diverticulum, in the appendix, and large bowel. Meckel’s diverticulum is described in Chapter 16 and diverticula of the appendix in Chapter 15.

The prevalence of diverticulosis varies greatly in different geographic areas of the world. It is most common in the Western Hemisphere and rare in Africa, Asia, and many parts of South America. In the Western Hemisphere, diverticular disease has an overall frequency of 15% to 35% using barium studies and is primarily left sided⁵, ⁶ and up to 50% to 70% by age 75. In the West, about 95% of patients have disease involving the sigmoid and left colon, but with age, they occur progressively more proximally. Right-sided diverticular disease is therefore found in older patients with pan-diverticular disease.⁷

In Southeast Asia, right sided diverticular disease is the most frequent form of diverticular disease and has a barium enema frequency of 8% to 22% and affects the right side of the colon in 70% to 98% of patients.⁸, ⁹ In sub-Saharan Africa, diverticular disease is uncommon and affects mostly the right colon.¹⁰, ¹¹, ¹²

Interestingly, the risk of diverticular disease in black Africans living in Western countries is higher than that in their indigenous counterparts.⁴ The risk of diverticular disease is related to a patient’s age and ethnicity.⁴ Men and women are equally affected.⁴ In Western countries, diverticulosis is uncommon before the age of 40. Diverticular disease incidence increases progressively,⁴ so that by age 90 about 50% of the population have it. Men and women are equally affected.

The pathogenesis of diverticulosis is not well understood and is likely multifactorial. Evidence suggests dietary fiber may be protective as one of the major differences between the populations of areas of low and high incidence is diet. In the Western Hemisphere, diets tend to be highly refined and fiber deficient, compared with those of African countries, which have a diet high in vegetable fiber and low in refined carbohydrates.¹³ The incidence of diverticula increases when people migrate from low-prevalence areas to Westernized communities, for example, among Japanese migrants to Hawaii.², ⁴ Also it has been found that the prevalence of diverticulosis in vegetarians is three times less than in nonvegetarians.¹⁴ Even rats fed with low-fiber diet seem to develop diverticulosis more frequently compared to controls.¹⁵, ¹⁶ The question is: How does a low-residue diet result in diverticulosis? For diverticula to develop, two requirements are necessary: (1) increased intraluminal pressure of the colon and (2) points of relative weakness in the bowel wall through which the bowel mucosa protrudes to form diverticula:

1. It has been postulated that people with high-fiber diets have increased stool bulk, which increases the tone of the bowel wall, resulting in faster intestinal transit with more frequent stools and less fecal stasis. In contrast, lack of dietary residue (i.e., fecal bulk) has been postulated to produce irregular and uncoordinated peristalsis, which converts the colon into a series of saccules sealed off from one another by a valvular mechanism produced by alternating and overlapping semicircular arcs of thickened circular muscle. This is thought to result in a markedly increased intraluminal pressure, hypertrophy of the muscularis propria, and consequent diverticular outpouchings.¹⁷ Another interesting hypothesis put forward for increased intraluminal pressure is related to the posture during defecation. It has been suggested that the natural position for defecation for human is squatting, where the rectum and sigmoid are more aligned in a straight line requiring less intraluminal pressure for the passage of stools from sigmoid to rectum. In contrast, in the sitting position, the rectosigmoid angle is close to 90 degrees requiring higher intraluminal pressure for defecation. This would also explain the lower rates of diverticulosis in parts of the world where defecation in sitting position is still the preferred mode, while diverticulosis is far more common in Western societies or
in populations in developing countries who have been increasingly adopting Western lifestyle.¹⁸, ¹⁹, ²⁰ Muscular thickening of the bowel wall usually accompanies diverticulosis, but it is still unclear whether this is a secondary phenomenon resulting from a need for increased intraluminal pressure or is a primary pathology.

2. The points of diminished resistance of the bowel wall occur at those sites where the nutrient arteries pass through the muscularis propria into the sub-mucosa, between the mesenteric and antimesenteric tenia. These areas are covered by connective tissue. It has been suggested that the collagen in these areas gradually loses its flexibility and tensile strength with age, resulting in weakening of the bowel wall and a predisposition to diverticula formation. This mechanism may help to explain the presence of diverticula in those cases of left-sided diverticulosis in which increased luminal pressure, reduced fecal weight, and prolonged intestinal transit are not found.²¹ What is less clear is the role that veins play as these accompany the arterioles or whether the outpouchings are really along the tracts created by the veins. And if so, does this create local congestion? Which shows how little we know about this disease.

The importance of an intact connective tissue in maintaining the structural integrity of the colon is further attested to by the following observations:

a. Cases of diverticulosis occurring primarily in the cecum and right colon with luminal pressures that are lower than normal and do not show muscular thickening

b. The finding of diverticulosis in young patients with connective tissue disorders, such as Marfan’s disease²², ²³ and Ehlers-Danlos syndrome²⁴

c. Acromegaly is also associated with an increased prevalence of diverticular disease.²⁵

However, the notion that interplay between muscle fibers, nerves, interstitial cells of Cajal (ICC), neurotransmitters, and possibly inflammatory cells plays a part in the development of diverticula is increasingly recognized. In one study, ICC and glial cells were decreased in colonic diverticular disease, whereas enteric neurons appear to be normally represented.²⁶ Mast cells have also shown to be increased,²⁷ but how these all fit together is not entirely clear and many of the histologic changes in the neuromuscular apparatus reported are likely secondary in nature.

Diverticulitis has been attributed to trapped fecaliths in diverticula.²⁸ Since these have at most a muscularis mucosae, impacted feces cannot be ejected so become hard and they cannot pass back into the lumen. Subsequently, edema and inflammation may further narrow the diverticula necks and impede the outflow of feces from diverticula.²⁸ Mucosal inflammation can readily extend to the submucosa of the diverticula, which is directly subjacent to either the peritoneal cavity or the retroperitoneum where further extension of the inflammation admixed with fecal contents may occur, and can result in fistula tracts.

Diverticular disease increases with age and is found in approximately one-third to one-half of the patients over 60. Men and women are equally affected.²⁹, ³⁰ Though presumed to be a rare entity, diverticulitis in patients younger than 40 years old has gradually risen.³¹, ³² Uncomplicated diverticular disease (diverticulosis) is often asymptomatic³³ but may be associated with crampy abdominal pain and diarrhea alternating with constipation.³³ In this setting, symptoms may be attributed to diverticula, but this is usually difficult to prove.³³, ³⁴, ³⁵

Diverticulosis may be present for months or years before complications ensue. Complications in diverticulosis occur in only about 20% to 25% of patients,³⁶ and only a small minority develop severe or life-threatening complications.²

Diverticulitis or its complications may be confined to a single attack with permanent remission or may consist of repeated episodes over many years. The symptoms and signs of diverticulitis are left lower abdominal pain, fever and, commonly, a palpable, tender, rope-like mass. Acute diverticulitis almost invariably results from perforations that are often quite small at the tip of the diverticulum. This area usually becomes walled off, with local abscess formation, fever, and abdominal tenderness. Generalized peritonitis is very uncommon.³⁷ Sometimes adjacent structures, such as the bladder, intestinal loops, vagina, anterior abdominal wall, and, rarely, adjacent vascular structures, become adherent to the inflamed colon, resulting in fistula formation. In 5% to 10% of cases, resolution of diverticulitis results in severe scar formation with large bowel obstruction, which may mimic carcinoma clinically.³⁸

Hemorrhage is an uncommon complication of diverticular disease and is not usually associated with acute diverticulitis clinically,³⁸ although necrosis of arteriolar walls must occur, which presumably results from inflammation. Interestingly, often arterioles adjacent to the diverticula have marked luminal obliteration resulting from reactive intimal proliferation, even in the absence of active inflammation. Vascular injection studies have shown a close relation between blood vessels and diverticula, as well as features of vascular ectasia.³⁹ It has been estimated that diverticular hemorrhage accounts
for between 20% and 48% of lower GI bleeding,⁴⁰, ⁴¹ but these figures are likely erroneous, since endoscopic experience has shown that many patients with GI hemorrhage previously thought to be due to diverticular disease on clinical and radiologic grounds are due to other patients such as vascular ectasia. Clinically, bleeding from diverticula is usually abrupt and painless but, in some patients may be massive and life threatening. The blood is usually bright red and arteriolar, being most overt if the hemorrhage occurs from disease in the sigmoid colon.³⁸ The site of origin of hemorrhage can be difficult to localize. Selective arteriography may be helpful, especially in those patients with persistent, life-threatening hemorrhage in whom surgery is contemplated.⁴²

Some patients develop inflammation indistinguishable from IBD in the segment of colon with diverticula, also referred to as diverticular colitis or segmental colitis associated with diverticular disease (SCAD). Prolapse-type polyps may also develop at the orifices of diverticula. Its differential diagnosis is Crohn’s disease especially if the rectum is spared and ulcerative colitis when the disease extends into the rectum. Thus, demonstration of a normal rectal biopsy is intrinsic in the diagnosis, as is the presence of proximal lack of involvement.

At colonoscopy, diverticula are characterized by 3- to 5-mm-wide orifices lying in shallow haustral pouches commonly separated by ridgelike elevations (Fig. 6-1).⁴³ The mucosa around the mouths of the diverticula may be inflamed, with patchy erythema, and may sometimes be raised above adjacent mucosa mimicking polyps. Only rarely is blood or purulent material seen extruding from the diverticulum. In diverticular strictures, the lumen becomes quite distorted and narrowed, but overlying mucosa is intact, and the valvulae appear symmetrical and regular, in contrast to their appearance with carcinoma.