Colonic Diverticular Disease
Colonic diverticulosis is among the most common diseases in developed Western countries. In the United States, diverticulosis occurs in approximately one third of the population older than age 45 and in up to two thirds of the population older than 85 years,1,2 and it also affects a significant proportion of younger adults.
DEFINITION AND CAUSES
A diverticulum is a saclike protrusion in the colonic wall that develops as a result of herniation of the mucosa and submucosa through points of weakness in the muscular wall of the colon. The colonic diverticulum is a false or pulsion diverticulum-that is, it does not contain all layers of the colonic wall. Diverticulosis indicates the presence of multiple diverticula and generally implies an absence of symptoms (Fig. 1). Diverticular disease implies any clinical state caused by diverticula, including hemorrhage, inflammation, or their complications. Diverticulitis describes the presence of an inflammatory process associated with diverticula. Its pathogenesis is attributed to genetic and environmental factors (Box 1).
PREVALENCE
The actual prevalence of diverticulosis is difficult to measure because most individuals are asymptomatic. Comparisons of the earliest and most recent autopsies and barium enema studies have indicated that the worldwide prevalence is increasing over time (Box 2).1,3,4
Studies so far include barium examinations and necropsy series. These may be misleading for determining the actual prevalence rate, however, mainly because barium studies may overestimate the prevalence of diverticulosis in people who have been referred for gastrointestinal (GI) symptoms, and necropsy series may either overestimate the frequency of diverticula in older age groups or miss the presence of small diverticula in younger populations.5,6 Whether these findings are the results of increased numbers of older individuals in the population, increased screening, or an actual increase in prevalence is unknown. Younger patients presenting earlier than age 40 years have a prevalence rate of 5% and are more commonly male.7–9
PATHOPHYSIOLOGY
Colonic diverticulosis in general is an acquired disease, developing as mucosal and submucosal herniations through the circular muscle layer at vulnerable weak points of the colonic wall. Diverticula are covered only by serosa, and tend to develop at four well-defined points around the circumference of the colon, where the vasa recta penetrate the muscular layer.10,11 These vessels enter the colonic wall on either side of the mesenteric teniae and on the mesenteric border of the two antimesenteric teniae. Diverticula do not develop in the rectum, presumably because of the coalescence of the teniae with the longitudinal muscle layer that marks the junction between the sigmoid colon and the rectum. In the colon, the presence of anatomic and physiologic changes contributes to the development of diverticula (Box 3). Mycosis, a set of findings consisting of the thickening of the muscular layer, shortening of the teniae, and luminal narrowing, is found in most patients with sigmoid diverticula.
The mechanical features of the colonic wall change with increasing age.12,13 Combined barostat-manometry studies of the entire colon have demonstrated that compliance is lowest in the sigmoid and descending colon and greatest in the transverse and ascending colon.13 This difference in mechanical properties between the right and left sides might partly account for the left-sided predominance of diverticulosis.14
Structural components of the extracellular matrix of the colonic wall, including collagen, elastin, and proteoglycans, are likely to be important in maintaining the strength and integrity of the colonic wall.15,16 Changes in these components of the bowel wall, such as damage and breakdown of mature collagen, and consequently its immature synthesis can lead to a change in bowel consistency.17 These changes may be related to a genetic predisposition such as that seen in Ehlers-Danlos and Marfan’s syndromes, which may be responsible for the occurrence of diverticula at an early age, or to the natural course of the aging process itself. In one study, it has been reported that collagen fibrils in the left colon are smaller and more tightly packed than those in the right colon with increasing age, and that this difference is accentuated in diverticular disease.16
The thickening of longitudinal and circular muscles in diverticular disease is neither hyperplastic nor hypertropic, but appears to be related to a contractile state. An increase in the number of elastic fibers has been observed only in the longitudinal muscle.18 It has been suggested that this process is responsible for longitudinal contraction, with subsequent thickening of both muscle layers.18 All these changes, along with elastin deposition in the teniae coli, lead to an irreversible state of contracture, with substantial bowel shortening, which may result in decreased resistance of the colon wall to persistent intraluminal pressure.19
The fiber content of the diet plays a large role in the pathogenesis of diverticular disease. Fiber has been found to be protective. Most fiber in the human diet is of plant origin and this type of fiber binds water and salt in the colon, leading to bulkier and more voluminous stools. Therefore, fiber decreases the frequency of contractions and prevents an exaggerated form of segmentation.6,20,21 In addition, dietary fiber influences the content of colonic bacterial flora, forms the main substrate for bacterial carbohydrate fermentation, and produces energy-yielding substrates—short-chain fatty acids—for growth and maintenance of colonic cellular function. Consequently, a fiber-deficient diet increases the chances of intense, more frequent segmentation, thus predisposing to herniation of mucosa by allowing isolated increases of intraluminal pressure.6,22
After the development of colonic diverticula, a spectrum of inflammatory changes or bleeding caused by the traumatic injury to penetrating vessels may occur.20,21 Changes within these vessel walls, such as eccentric intimal thickening and thinning of the media of the vessel facing the bowel lumen, result in segmental weakness of these vessels and render them vulnerable to injury and bleeding.
The term diverticulitis represents a spectrum of inflammatory changes that ranges from localized subclinical inflammation to generalized peritonitis, with free perforation (Fig. 2). In turn, this leads to hyperplasia of the lymphoid tissue within the mucosa at the base of the diverticulum, one of the earliest signs of diverticulitis. Inflammation usually begins at the apex of the diverticulum and seldom involves the neck or mucosa proximal to the neck. However, there is active inflammation of the pericolic and mesenteric fat, with peridiverticular abscess formation. These peridiverticular abscesses often involve areas of subserosa and are closely related to the outer aspect of the muscularis propria; they can spread circumferentially and longitudinally and may be responsible for the pathologic picture of diverticular colitis. Longitudinal tracking, especially, may result in fissuring, along with the lymphoid aggregates, which resembles the distinctive feature of colonic colitis in Crohn’s disease.23 This may cause misinterpretation of the pathologic study of the specimen. Therefore, the differential diagnosis of these two conditions in terms of pathologic interpretation of the resected specimen is important. Persistent localized inflammation after diverticular rupture results in a phlegmon, a thickened, firm segment of bowel wall, which ultimately may manifest as acute or subacute large bowel obstruction. If left untreated or treated inadequately, it may result in extensive fibrosis around the affected segment of the colon, giving it a mass appearance indistinguishable macroscopically from that of a neoplasm.
Another pathologic entity that may be encountered during progression of the disease, with recurrent attacks of diverticulitis, is the formation of a localized abscess with chronic inflammation and involvement of other neighboring luminal organs, such as the bladder, small and large bowel loops, uterus, and vagina. Fistulae may develop within this contained area, between involved segment(s) of colon and these organs. Fistulae occur in 2.4% to 20% of cases; 65% of these fistulae are colovesical and 20% are colovaginal fistulae.24–26
SIGNS AND SYMPTOMS
Most people with uncomplicated colonic diverticulosis are asymptomatic. A small fraction of these patients may have troublesome symptoms, such as colicky abdominal pain, bloating, flatulence, or altered bowel habit. The symptoms characteristically disappear after defecation or passage of flatus. On clinical examination, they may have tenderness in the left iliac fossa with no signs or symptoms of peritonitis or systemic illness, and all laboratory values may be within normal limits. The clinical picture of symptomatic uncomplicated diverticulosis often overlaps with that of irritable bowel syndrome (IBS), because these two clinical entities are usually diagnosed after other pathologies are excluded. IBS-type symptoms are independent of the presence or absence of diverticulosis on double-contrast barium enema studies. Bleeding alone can sometimes be the only sign of diverticulosis.27
Signs and symptoms of acute diverticulitis may vary from local findings and manifestations to a wide variety of clinical pictures, with signs and symptoms of intra-abdominal sepsis, depending on the stage of disease (Box 4).
Patients with acute uncomplicated diverticulitis classically present with left-sided lower abdominal pain, fever, and leukocytosis.28 The site of pain often depends on the segment of colon affected. Right-sided symptoms may occur in the presence of right-sided diverticulosis, as well as in redundant sigmoid colon lying on the right side of the abdomen. Patients with left-sided pain may also have right-sided symptoms. Other common manifestations are frequently related to GI disturbances, with alteration in bowel habits, constipation, either alone or alternating with bouts of diarrhea, anorexia, and nausea and vomiting. Urinary symptoms such as dysuria, frequency, and urgency may develop in a minority of patients, probably because of the proximity of the bladder to the inflamed sigmoid colon. In acute presentations, fever is almost always present, but high fever must suggest the possibility of advanced disease and sepsis from generalized peritonitis caused by perforation and spreading of inflammation in the peritoneum.
DIAGNOSIS
The initial assessment of patients with suspected acute diverticulitis is comprised of a thorough history and physical examination, including abdominal, rectal, and pelvic examinations. Useful initial examinations may include a complete blood cell count, urinalysis, and flat and upright abdominal radiography. If the clinical picture is clear enough to diagnose diverticulitis, no other tests are indicated.1 When the diagnosis is in question, other tests such as computed tomography (CT), water-soluble contrast enema, cystography, endoscopy, and ultrasound may be performed. The differential diagnosis of acute diverticulitis should also be considered,29 not only during examination of the patient but also while ordering the tests (Box 5). In particular, the differential diagnosis of colorectal cancer, as well as the detection of its possible coexistence, is important.30,31 A barium enema examination should be avoided in acute presentations in patients with suspected acute diverticulitis and localized peritoneal signs because of a possible extravasation of barium into the peritoneal cavity, which can increase the morbidity and mortality related to barium-induced chemical peritonitis.31 In the emergency setting, water-soluble enemas are safer.
