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. 2020 Dec 8;34(2):81–85. doi: 10.1055/s-0040-1716698

Pathophysiology and Epidemiology of Diverticular Disease

Stephanie D Talutis 1, F Angela H Kuhnen 2,
PMCID: PMC7904337  PMID: 33642946

Abstract

Diverticular disease exists on a spectrum, ranging from asymptomatic diverticulosis to complicated diverticulitis. Incidence of diverticulitis in western nations has increased in recent years, although the factors that influence the progression from diverticulosis to diverticulitis are unknown. Geographic/environmental influences, lifestyle variables, and microbiota of the gastrointestinal tract are some of the factors implicated in diverticular disease.

Keywords: diverticulitis, diverticulosis, colon, inflammation, risk factors, microbiome


Diverticular disease exists on a spectrum, ranging from asymptomatic diverticulosis to complicated diverticulitis. The incidence of diverticulitis in the United States and Europe has increased in recent years, although the exact triggers that induce progression from diverticulosis to diverticulitis remain unknown. 1 Symptomatic disease can be categorized into uncomplicated and complicated. 2 3 Those with uncomplicated diverticular disease typically have self-limited episodes of abdominal pain and change in bowel habits. These patients are managed with courses of antibiotics and lifestyle modifications and rarely require surgery. Complicated diverticulitis presents with abscess, perforation, peritonitis, fistulae, bleeding, stricture, or obstruction, and requires hospitalization and often surgical intervention. 2 4

Pathophysiology

Colonic diverticulae are pseudodivertiulae that develop as outpouchings where the vasa recta penetrate the colonic musculature. 3 In western nations, they most commonly occur in the descending and sigmoid colon, whereas right-sided diverticulosis is more common in the East. This regional difference is likely multifactorial, including genetic, environmental, and lifestyle factors. 3 Functionally, the cecum and ascending colon are the primary location of bacterial fermentation of carbohydrates and proteins. This region of the colon remains distended along longitudinal (teniae coli) and circular (plicae circulares) muscle layers for prolonged time periods to allow for microbial action. Reabsorption of water and electrolytes reduces the bulk of fecal matter by the time it reaches the descending colon. The descending colon functions as a reservoir for feces prior to defecation. 3

Diverticulitis has long been understood as a progression from luminal stasis to obstruction within diverticula and eventual ulceration/perforation ( Table 1 ). 4 The absence of dietary fiber increases colonic transport time, increasing colonic water absorption. 3 4 The resultant inspissated stool does not move easily through the colon, resulting in an increase in luminal pressure with each peristaltic contraction. 5 Stool trapped within diverticulae further cause increased pressure along the pseudodiverticulae wall, which, if persistent, can progress to ulceration and perforation. 6

Table 1. Pathophysiology and risk factors for diverticulitis.

Pathophysiology of diverticulitis 3,4 Risk factors for diverticulitis
Absence of dietary fiber
      ↓
↑ Colonic transport time
      ↓
↑ Colonic water absorption
      ↓
↑ Luminal pressure with peristalsis
      ↓
↑ Pressure on pseudodiverticular wall
      ↓
Ulceration and perforation
Advanced age 6 12 13 14
Obesity 20 21 22 24
Smoking 23 25 28 29
NSAID use 31
Sedentary lifestyle 22 32
Summer season 1
Western diet 6 19

Abbreviations: NSAID, nonsteroidal anti-inflammatory drug; down arrow, causation; up arrow, increase.

Alterations in the colonic musculature occur in diverticulosis. The plicae circularis thickens while the teniae coli shortens. 3 Similar changes occur with aging and inflammatory bowel disease (IBD). 3 6 Histological analysis of muscle fibers in those with diverticulosis shows accumulation and irregular deposition of elastin and collagen. Additionally, the ratio of types I and III collagen is altered in both serosal and submucosal layers as a result of scarring; some of these changes are also seen in IBD and are linked to inflammation. 3 Possible causes of these changes can be attributed to matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs). 5 7 Small studies have found increased expression of MMPs and TIMPs in patients with symptomatic diverticulitis to support this hypothesis. 5 8

The histological changes of diverticular disease produce physiological alterations in colonic function. 3 Endoscopic manometry shows similar resting pressures in colons affected by diverticular disease and normal colons; however, contractions are increased in number and amplitude in areas with disease. 9 Additionally, electrophysiological evaluation of the colonic wall show increased activity in early stage diverticulosis and low or absent tone in those with advanced disease. 10 These structural and mechanical alterations further contribute to pressure-induced damage to the colonic wall. 3

Incidence

It is difficult to estimate the number of people affected by diverticular disease due to the asymptomatic nature of early-stage diverticulosis. It is estimated that 20% of patients with diverticulosis develop symptomatic diverticulitis over the course of a lifetime. 6 11 Diverticulitis is among the top five gastrointestinal admission diagnoses in the United States, 2 with approximately 200,000 people hospitalized annually. 1 This accounts for US$2.5 billion per year in direct and indirect healthcare costs. 2

Risk Factors

Age

It has long been believed that the prevalence of diverticulosis increases with age. Under the age of 40, fewer than 10% of adults are found to have diverticulosis; however, up to 30% of those aged 40 to 60 years and 50 to 70% of those >80 years of age are affected by diverticulosis. 6

In recent years, symptomatic diverticulitis has been increasing in younger populations. In the United States, from 1998 to 2005, the number of patients treated for diverticulitis increased by 26%. The incidence increased greatest in those aged 18 to 44 years (151–251 per one million people) followed by those aged 45 to 64 years (659–771 per one million). Stable rates were observed in those aged 65 to 74 years (659 per one million), whereas rates of diverticulitis admissions decreased in those aged ≥ 75 years (2,247 per one million) over the same time period. 12 The average age of patients with diverticulitis also decreased from 64.6 years to 61.8 years. 12 Other studies have found similar trends in admission age group distributions for diverticulitis among western nations. 13 14

Historically, elective resection was recommended after the first attack of complicated diverticulitis in those under the age of 40 due to the belief that young patients with diverticulitis have more aggressive pathology. 15 16 Recent work has challenged this view, however. 14 15 17 18 In a retrospective review of all abdominopelvic computed tomography (CT) scans in those with diverticulitis over a 5-year period in a single institution, young patients (age ≤ 50 years) were more likely to be male, have extraluminal air, and have greater colonic wall thickness. However, there were no differences in the rates of free perforation, abscess formation, or fistula formation between the older and younger age groups. When controlling for gender, males had a higher incidence of extraluminal air on CT, suggesting that the pathophysiology of disease may be more severe in this group. 15 Similar findings were observed in an Israeli cohort; although younger patients were more likely to have extraluminal air on CT, the intraoperative Hinchey score and the need for emergency or multiple surgeries did not differ between the older and younger groups. 16 There were no differences in disease complexity, peritonitis, laboratory findings, and presence of fistula or abscess among older (> 50 years) and younger patients. Younger patients were more likely to have readmissions or diverticular complications, possibly due to their earlier discharge compared with those > 50 years of age. 16

Those with certain genetic syndromes have a predisposition for colonic diverticulosis and often present with symptoms at a younger age. These syndromes commonly include defects in collagen or extracellular matrix components, such as Marfan's syndrome, Ehlers-Danlos' syndrome, Williams–Beuren's syndrome, Coffin–Lowry's syndrome, and polycystic kidney disease. 6 These patients may be offered earlier elective surgery as a result.

Obesity

Obesity is a known risk factor for many pathologies of the gastrointestinal tract, such as cancer of the esophagus, pancreas, and colon, cirrhosis, cholelithiasis, and gastroesophageal reflux disease (GERD). 19 Obesity produces a low-grade inflammatory state, which may increase the risk of diverticulitis. 20 21 Cytokines are secreted by adipose tissue, which may promote diverticular inflammation and altered intestinal flora. 22 23 24

Studies in male and female cohorts have demonstrated increased incidence of diverticulitis in obese patients (body mass index [BMI] ≥ 30) compared with lean patients. 22 24 A cohort of Swedish women found that overweight (BMI 25–29.99) and obese (BMI ≥ 30) patients were 29% and 33%, respectively, more likely to be hospitalized for diverticulitis compared with lean women (BMI < 25). Additionally, overweight and obese women had 41% increased risk of perforation and abscess compared with their lean counterparts. 22

Similar trends were seen in a cohort of American men. Obese men had 78% increased risk of developing diverticulitis and a threefold increased incidence of diverticular bleeding compared with lean men (BMI < 21). Based on these findings, in a 10-year period, 14.7 cases of diverticulitis and 8.2 cases of diverticular bleeding would be expected to occur per 1,000 obese men compared with 6.6 cases of diverticulitis and 2.6 cases of diverticular bleeding in 1,000 men with BMI < 21. A positive association of diverticulitis with waist-to-hip ratio and weight gain was also observed; those who gained > 45 lbs since the age of 21 were more likely to be hospitalized for diverticulitis compared with those who gained < 5 lbs in the same time period. 24

Smoking

Multifactorial effects of smoking and nicotine may promote inflammatory conditions of the gastrointestinal tract, such as diverticulitis. 25 26 27 Smoking alters the pro-oxidant and antioxidant balance in tissues, causing increases in free radical production and decreases in the levels of protective antioxidants. 26 Smoking decreases colonic mucosa growth, resulting in impaired endothelial function and altered colonic bacterial composition. 28 It also increases secretion of vasointestinal polypeptide, increasing colonic motility and intraluminal pressure, furthering damage to the colonic mucosa. 25 27 Nicotine adds to the effect of smoking by decreasing colonic and systemic immunity. Nicotine inhibits synthesis of cytokines causing inflammation, such as interleukin-1 and tumor necrosis factor-α in colonic mucosa. 25 26 Smoking and nicotine both impair colonic blood supply. Potential for ischemia is further augmented by smoking-induced serotonin-mediated endothelial vasoconstriction. 27

Large-scale cohort studies have shown increased incidence of diverticulitis in smokers. Compared with never-smokers, current and former smokers have increased odds of requiring surgery for diverticulitis after adjusting for age and disease severity. 23 28 29 Additionally, there is a dose-dependent effect of the number of daily cigarettes smoked 25 and the number of pack-years on the risk of hospitalization for diverticulitis. 11 For former smokers, the increased risk of diverticulitis persists until 10 years after cessation, at which point the patient's risk is equal to that of nonsmokers. 29 Smokers additionally have been found to have more complicated diverticulitis, with higher rates of perforation and stricture, making them more likely to require surgery for diverticulitis at an earlier age than nonsmokers. Postoperatively, smokers also have higher rates of perforation and recurrent diverticulitis. 27

Nonsteroidal Anti-Inflammatory Drugs

Cyclooxygenase (COX) is an enzyme responsible for the production of prostaglandins, which are implicated in inflammation and pain. COX-1 and COX-2 isoenzymes also regulate intestinal motility. These enzymes play a role in altered gastrointestinal motility in inflammatory states. In normal colonic tissue, COX-1 and COX-2 inhibitors have been shown to downregulate cholinergic motility and enhance tachykinergic activity. In colonic tissue affected by diverticular disease, the effect of COX-1 and COX-2 inhibitors is lost, but COX-2 inhibitors maintain and control tachykinergic activity. 30 The etiology of these effects could be through direct colonic endothelial damage or through impaired prostaglandin synthesis. Impaired prostaglandin synthesis results in compromised mucosal integrity and increased bacterial and toxin translocation. 31

Regular nonsteroidal anti-inflammatory drug (NSAID) use is strongly associated with both complicated and uncomplicated diverticulitis, as well as increased risk of diverticulitis-related complications. To a lesser extent, regular aspirin use also increases the risk of complicated and uncomplicated diverticulitis even when adjusting for the presence of comorbidities. For both NSAIDs and aspirin, habitual users are at greater risk of diverticulitis, with a duration-dependent effect. 31

Physical Activity

Long-term physical activity has benefits on the gastrointestinal tract and may reduce the risk of cancers, cholelithiasis, and gastrointestinal bleeding. 22 32 Exercise results in hormonal changes, which influence motility and secretions. Increased colonic activity may decrease intracolonic pressure and transit time, preventing bacterial stasis. Additionally, exercise may prevent chronic vascular changes at sites of diverticular bleeding. 32

The benefits of physical activity on diverticulitis and diverticular bleeding have been shown with ≥ 30 minutes of exercise per day. 22 32 One study found that men with the highest quintile of physical activity had 25 to 46% risk reduction compared with those in the lowest quintile. Importantly, the effect of physical activity persisted even when controlling for obesity. 32 Conversely, those with sedentary lifestyles, classified by sitting for ≥ 5 hours per day, are at increased risk of symptomatic diverticulitis. 22 Nonvigorous activity and sedentary time are not associated with increased risk of perforation or complications. 22 32

Geography/Environment

In western societies, diverticulosis is commonly observed in older individuals; however, it is less common outside these regions. 1 Within Europe, rates of diverticulitis vary by region; those in the north have a higher prevalence of diverticulitis than those in the south. 3

Seasonal variation in the rates of hospitalization for diverticulitis has been observed in the United States, the United Kingdom, and Australia. Highest rates of admission for diverticulitis were seen in summer months for each region; rates were highest in May to September in the United States, August to October in the United Kingdom, and December to February in Australia. Seasonal change was represented by 22 to 24% maximal increase in admissions during peak months. Using length of stay as a surrogate for disease severity, there were no significant differences observed in length of stay between peak and low-volume months. 1 Similar seasonal variation has also been observed for appendicitis. 2 Plausible explanations include dietary variation, dehydration leading to fecal stasis, altered colonic motility, infectious etiologies, and seasonal variation in vitamin D levels. 1 2 Consumption of fresh fruits and vegetables increases in the summer months. Climate changes, migration/vacation variation, and lifestyle factors are also affected by seasonal variation and could explain this relationship. 2

Numerous population studies have highlighted the fiber-poor Western diet as a risk factor for diverticulitis. In Asia and Africa where diets are fiber-rich, there is a low incidence of diverticulitis, but immigrants from these areas to the United States and Europe develop diverticulitis following adoption of the Western diet. 6 Immigrants from Asia and Africa to westernized countries have lower rates of diverticulitis. However, risk of diverticulitis increases with the amount of time since emigration, indicating acculturation and adoption of western diet as possible factors. 6 19 This finding supports that diverticulitis is related to environmental factors and less influenced by genetics. 19 The dietary link to diverticulitis has been challenged in recent years, however, as this relationship is difficult to prove due to the long duration between symptom-free development of diverticula and later symptomatic diverticulitis. 6

The impact of socioeconomic status on admission for diverticulitis has been studied with conflicting results. 17 19 Those with lower socioeconomic status are at high risk of numerous diseases but also to not utilize health care resources to the same extent as those with higher socioeconomic status. One study supported this theory, finding higher rates of diverticulitis outside urban areas, where hospital access is likely more limited. 19

Microbiome

Recently, the gut microbiome has been hypothesized to play a major role in intestinal health, including diverticulitis. 4 20 The human gastrointestinal tract contains microorganisms with a combined 10 12 –10 14 genes, more than the human genome. The bacteria of the gastrointestinal tract exist in a symbiotic relationship with the host impacting the morphology of the gut epithelium and contributing to the mucosal protective barrier and resistance to pathogens. Additionally, the microbiome functions to ferment indigestible dietary substrates into short-chain fatty acids, which have anti-inflammatory properties and provide the primary energy source for colonic cells. 4

Ninety-five percent of bacteria in the gut are of the phyla Bacteroides and Firmicutes , specifically genera bacteroides , bifidobacterium , eubacterium , clostridium , peptococcus , peptostreptococcus , and ruminococcus . The stability of the microbiome is maintained by pH, temperature, bacterial interactions, peristalsis, bile acids, medications, and immune responses, allowing for fluctuation due to environmental conditions and diet. In diverticulitis, Bifidobacterium longum and B. animalis are found in higher frequencies. 4

Changes in bacterial flora, occurring as a result of slow colonic transit and fecal stasis, result in diverticulae-related pathology, such as appendicitis, pouchitis, and diverticulitis. 33 Fiber deficiency is thought to play a role in diverticulitis by producing smaller volume stool. This results in reduced colonic motility and increased intraluminal pressure and alteration in microbiome. 4 Additionally, the interaction with intestinal bacteria and mucosa can produce inflammation. The symptoms of diverticulitis (abdominal pain, bloating, tenesmus, diarrhea) may be caused by inflammation similar to that in IBD. 4

Conclusion

The pathology of diverticulitis is complex and is influenced by a variety of risk factors. Minimization of known risks can help reduce progression of diverticulitis admissions. Awareness of nonmodifiable risk factors can be used to counsel patients who are more likely to develop complex pathology requiring surgery.

Footnotes

Conflict of Interest None.

References

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