Diverticulitis: A Primer for Primary Care Providers

PATHOPHYSIOLOGY

Diverticula tend to occur in areas where the colonic wall is weak: namely, between the mesenteric and antimesenteric taeniae, where the vasa recta penetrate the muscle—points of entry of blood vessels through the colonic wall.^1,4 The exact pathogenesis of diverticular disease is not completely understood but is thought to be multifactorial. Microscopic studies have shown muscular atrophy at the sites of diverticula, making them more susceptible to mucosal herniation in the setting of increased intraluminal pressure.¹ Additional potential contributing factors include alterations in colonic microbiota, muscular dysfunction or dysmotility, lifestyle, and genetics.

Diverticulitis is the result of microscopic and macroscopic perforation of diverticula. Historically, the perforations were thought to result from obstruction of a diverticulum by a fecalith, leading to increased pressure within the outpouching, followed by perforation.³ Such obstruction is now thought to be rare. A more recent theory suggests that increased intraluminal pressure is due to inspissated food particles that lead to erosion of the diverticular wall, causing focal inflammation and necrosis and resulting in perforation.³ Microperforations can easily be contained by surrounding mesenteric fat; however, progression to abscess, fistulization, or intestinal obstruction can occur. Frank bowel wall perforation is not contained by mesenteric fat and can lead quickly to peritonitis and death if not treated emergently.

RISK FACTORS

Dietary fiber

In 1971, Burkitt was the first to posit that diverticular disease developed due to small quantities of fiber in the diet that led to increased intracolonic pressures.⁸ His theory was based on the observation that residents of several African countries, who ate a high-fiber diet, had a low incidence of diverticular disease. Burkitt hypothesized that this was due to shorter colonic transit time induced by high dietary fiber.

Several studies conducted since Burkitt made his observations have examined the association of dietary fiber and diverticular disease, with conflicting results. In 1998, Aldoori et al found that a low-fiber diet increases the incidence of symptomatic diverticular disease.⁹ However, in 2012, a large cohort study of patients undergoing colonoscopy found that those who reported the highest fiber intake were at highest risk for diverticulosis.¹⁰ In 2013, Peery et al examined the relationship among bowel habits, dietary fiber, and asymptomatic diverticulosis and found that less-frequent bowel movements and hard stools were associated with a decreased risk for diverticulosis.¹¹ In 2017, a prospective cohort study of nearly 50,000 men without a known history of diverticulosis showed that diets high in red meat were associated with a higher incidence of diverticulitis over nearly three decades of follow-up, whereas a diet high in fiber was associated with a decreased incidence of diverticulitis.¹²

Although no definitive association has been found between dietary fiber intake and risk for diverticulosis, some studies have demonstrated an association between dietary fiber and diverticular complications. In 2014, Crowe et al found that consumption of a high-fiber diet was associated with a lower risk for hospital admission and death from diverticular disease.¹³ Recent guidelines from the American Gastroenterological Association (AGA) on diverticulitis recommend high dietary fiber intake in patients with a history of acute diverticulitis.¹⁴ However, no study has shown a reversal of the process or a reduction in the number of episodes of diverticulitis after adoption of a high-fiber diet.

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