ETIOLOGY

3 Neither the etiology of diverticulosis nor factors causing progression to symptomatic disease have been rigorously defined, but lack of dietary fiber, colonic dysmotility, and colonic structural abnormalities and age-related changes have all been implicated. There may be an association between irritable bowel syndrome (IBS) and diverticulitis, the microbiome may be a mediator in diverticular inflammation, and idiopathic inflammation may also contribute to the DD spectrum.

Structural/Anatomic Factors

In the colon, the outer, longitudinal layer of the muscularis propria is condensed in three longitudinal bands called the taeniae coli. One of these runs along the mesenteric aspect of the colon; the other two are antimesenteric in location (Fig. 69-1). Mesenteric blood vessels encircle the colon and penetrate the circular muscle in the intertaenial areas between the mesenteric taenia and the two antimesenteric taeniae. Pseudodiverticula develop at areas where these vessels pass through muscle.¹² Postmortem 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

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

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).

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 incidence of diverticulosis among previously low-risk populations in concert with changes to a Western-style 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. Diverticulitis-associated 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 to avoid confusing diverticulitis-associated colitis with inflammatory bowel disease. Probiotics and nonsteroidal anti-inflammatory medications are being explored as potentially protective agents.^26,39,40

Diagnosis

Noninflammatory Diverticular Disease

Most patients with diverticulosis noted on barium study, colonoscopy, or abdominal CT scan are asymptomatic. In patients who have vague, crampy, left lower quadrant pain in the absence of fever, leukocytosis, or CT findings of focal inflammation, other causes of pain must also be considered. Additional symptoms reported may include nausea, flatulence, bloating, and change of bowel habit. The differential diagnosis includes colonic adenocarcinoma, constipation, inflammatory bowel disease, and IBS. There are no peritoneal signs on examination, the rectal examination is unrevealing, and proctoscopy shows no inflammation. Postinflammatory neurogenic alteration has been postulated as a cause of visceral hypersensitivity.^41–43 Nonspecific, mild mucosal inflammation and muscle spasm may also contribute. There is considerable overlap with IBS. In addition to high-fiber modification of the diet and bulk-forming agents such as psyllium or flaxseed, anticholinergics, analgesics, and antibiotics can be prescribed to manage symptoms.

Hemorrhagic Diverticular Disease. Like bleeding from colonic angiodysplasia, diverticular hemorrhage is classically asymptomatic until presentation with lower gastrointestinal hemorrhage that can be massive. This differs from hemorrhage from inflammatory bowel disease or ischemic colitis where there are typically symptoms before bleeding begins. A foregut source of bleeding must be excluded by nasoenteric recovery of bilious, nonbloody aspirate or upper endoscopy. Likewise, an anorectal source of bleeding must be excluded by examination. Localization of lower gastrointestinal hemorrhage of any cause is necessary to help guide appropriate colon resection should that be required. Although most cases of diverticular hemorrhage are self-limited, recurrence or failure of bleeding to stop spontaneously determines the need for resection. Colonoscopy, tagged red blood cell scan, or, if bleeding is brisk enough, angiography is used to localize bleeding (Fig. 69-4).

Giant Colonic Diverticula. Symptoms and signs of giant colonic diverticula may be noninflammatory (pain, bloating, nausea, vomiting, diarrhea, abdominal tenderness and mass) or inflammatory, resulting from perforation (pain, leukocytosis, fever, localized or generalized peritonitis).¹³

Inflammatory Diverticular Disease

The constellation of inflammatory signs and symptoms corresponds to the spectrum of inflammatory complications of DD. The Hinchey classification⁴⁴ categorized the severity of acute diverticulitis and has been modified to reflect refinements of diagnosis enabled by improved CT scan quality (Table 69-2).⁴⁵ The modified classification also includes manifestations of chronic inflammation such as fistula formation and stricture/obstruction.

Symptoms of acute diverticulitis include steady, left lower-quadrant abdominal pain; fever; change in bowel habits (constipation or diarrhea); anorexia; nausea; vomiting; bloating; and urinary tract symptoms such as urinary frequency or retention. Examination will reveal left lower-quadrant tenderness that may be appreciable only with deep palpation in stage 0 inflammation. In stage I or II inflammation, focal peritoneal signs in the left lower quadrant are likely, and there may be a tender mass. Digital rectal examination may also reveal pelvic tenderness or a tender mass in the cul-de-sac. Generalized peritoneal signs would be expected for stage III or IV inflammation. Dehydration with earlier stages or evolving sepsis with later stages may cause tachycardia and hypotension. Leukocytosis is more likely with advancing stage of inflammation. The differential diagnosis includes perforated colon cancer, acute appendicitis, perforated peptic ulcer, acute ischemic colitis, pancreatitis, and flare of Crohn disease or ulcerative colitis. Normal serum amylase and lipase help exclude a diagnosis of pancreatitis. Imaging studies and endoscopy help to distinguish diverticulitis from the other diagnoses. However, active inflammation or contained perforation may limit the utility of rectal contrast CT, barium enema studies, and endoscopy in the acute setting. Distinguishing perforated colon cancer from DD can be especially challenging, even in the operating room.

Diverticular fistula formation represents internal drainage of an abscess (or external drainage in the case of colocutaneous fistulas). Approximately half of diverticular fistulas are colovesical fistulas. Women with colovesical or colovaginal fistulas have usually had a hysterectomy.^46,47 Urinary tract infection symptoms, pneumaturia, and fecaluria are common complaints. Recurrent urinary tract infection in elderly men should raise concern for the presence of a colovesical fistula, which is often secondary to DD. Passage of feces or flatus from the vagina is a characteristic symptom of a colovaginal fistula. Colocutaneous fistulas are a rare complication of DD.

Thirteen percent of large-bowel obstructions are due to DD. The concurrent incidence of colon carcinoma in 7% of patients with symptomatic sigmoid DD confounds diagnosis and treatment.⁴⁸ CT scan is not as reliable for distinguishing these diagnoses as colonoscopy or contrast enema studies.

Right-sided diverticulitis frequently is confused with appendicitis, and misdiagnosis is common. The duration of symptoms is usually longer than appendicitis. Patients are usually older than those with appendicitis (late 30s or 40s) but younger than patients with typical left-sided diverticulosis (over 50 years of age).^49,50

Imaging and Diagnostic Studies for Diverticular Disease

Plain Radiographs. While seldom useful in the diagnosis of uncomplicated diverticulitis, a three-way abdominal series that includes an upright chest radiograph, an abdominal flat plate, and a left lateral decubitus view is useful for demonstrating free air. An ileus pattern or soft tissue mass may also be detected.^51,52

5 Computed Tomography Scan. CT scanning has revolutionized the diagnosis of acute diverticulitis and, sometimes, by way of percutaneous abscess drainage, its treatment. The accuracy of CT scans in the acute setting is central to the trend toward converting what formerly were surgical emergencies into elective, often single-stage operations. Intravenous and water-soluble oral and rectal enteric contrast should be administered. Water-soluble contrast is used to avoid barium peritonitis that may result if barium leaks from a perforated diverticulum into the peritoneal cavity.

A CT scan can reveal the presence and extent of diverticulosis, but its real strength is characterizing extracolonic inflammatory change. Signs of inflammation include colon wall thickening, pericolic fat stranding, or phlegmon formation. Pericolic abscess size and location can be detected (Fig. 69-5). Perforation is evidenced by free air; contained perforation may be identified by loculated extraluminal pericolic air. CT more accurately demonstrates diverticular abscesses and severity of inflammation than contrast enema studies.⁵³ Air in the bladder or contrast in the vagina may indicate the presence of a fistula (Fig. 69-6).

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