Diverticular disease - Clinical Tree

Historical perspectives

Colonic diverticulosis is a common anatomical disorder characterised by acquired, sac-like mucosal protrusions (diverticula) through the muscle wall. They are false diverticula because they do not involve all colonic layers. The term ‘ diverticulum’ (‘divertikel’ in German) was originally used to describe what was an anatomical curiosity in the early 1800s and was not in widespread use until the recognition of ‘perisigmoiditis’ and related colovesical fistulae by the latter half of the 19th century. It was Lord Berkeley Moynihan (1865–1936 Leeds) who propagated the term ‘ diverticulitis’ at the turn of the 20th century while more latterly, diverticulosis was proposed as an umbrella term for asymptomatic individuals as well as symptomatic patients. For decades much of what was written was based on erroneous assumption; a lack of evidence created a knowledge vacuum that was filled with the dogma of the era. We were left with variable terminology and a multiplicity of management protocols.

Terminology

According to the European Society of Coloproctology (ESCP) guidelines, the following terminology is used to define the various clinical scenarios with which colonic diverticula may be associated ( Box 9.1 ).

Box 9.1

Terminologies used to define the various clinical scenarios with which colonic diverticula may be associated

Diverticulosis – the presence of colonic diverticula.
Diverticular disease – clinically significant and symptomatic diverticulosis and may be caused by:
- Diverticulitis or
- Other less well-described manifestations (e.g., visceral hypersensitivity without evidence of inflammation).
Symptomatic uncomplicated diverticular disease (SUDD) – persistent abdominal symptoms attributed to diverticula without diverticulitis or bleeding.
Diverticulitis – acute or chronic symptoms in the presence of inflamed diverticula.
- Uncomplicated – Computed tomography (CT) shows only colonic wall thickening with fat stranding.
- Complicated – CT shows abscess, peritonitis, obstruction, fistula or haemorrhage.
Diverticular bleeding – haemorrhage from diverticula (right- or left-sided)
Segmental colitis associated with diverticulosis (SCAD) – inflammation resembling inflammatory bowel disease isolated to areas marked by diverticulosis.

Anatomical and physiological perspectives

Colonic diverticulosis and related disorders are traditionally thought to be a western world, industrialised country, mature age-group phenomenon with clearly defined origins in meat-rich, fibre-poor diets. Some of the earliest descriptions date only to the early 20th century and the scientific basis for our current understanding is still limited. Parks described his findings on diverticulosis based on 300 cadaveric dissections in 1968. He noted that diverticula tended to form rows in the lateral inter-taenial (rather than anti-mesenteric) areas that they were mainly in the sigmoid but could be anywhere in the colon, and that frequently, a blood vessel pierced the wall at the neck of the diverticulum. Much of what was determined about the incidence of diverticulosis was from this and other mid-20th century post-mortem studies. Population-based studies confirm diverticula are rare before 30 years, more common after 40 years, found in one third after 60 years and over 50% of those older than 70 years of age. The age-related phenomenon gives clues to the aetiology and points to general ageing processes including declining collagen strength or repair.

Incidence and geographical differences

Race and geography

Geographic disparities in the incidence of diverticulosis imply that it is predominantly in industrialised societies associated with an ageing population and western diet. Moreover, the incidence has increased in North America by up to 50% in the past two decades, and more so in younger people. In contrast, diverticulosis is uncommon in Asia and Africa compared to Europe and the USA with a reported prevalence as low as 0.5–1.7% in China and Korea. ^, Industrialisation or immigration to western countries results in a higher prevalence. ^, This has been best described in Japanese immigrants to Hawaii where necropsy studies demonstrate a dramatic increase in diverticulosis compared to age-matched mainland Japanese controls (52% vs. 0.5–1%). Similar increases are apparent among the urban, industrialised, black population in South Africa compared with their rural counterparts.

However, the increasing incidence is not solely due to adoption of a western lifestyle and genetic factors may play a role. There are distinct differences in prevalence within ethnic groups living in the same region. For example, studies of ethnic groups living in Israel demonstrate differences in Ashkenazi Jews (16.2%), Sephardic Jews (3.8%) and Arabs (0.7%). ^, Aside from variances in prevalence between different ethnicities, anatomical variations also exist with a reported frequency of right-sided diverticulosis of 20% in patients <40 years increasing to 40% in patients >60 years old in Asian populations. ^, Furthermore, while the incidence of diverticular disease increases as these countries become more westernised, the anatomical location (right colon) remains the same. ^,

Age and gender

Recent studies point towards age- and gender-related differences in patients presenting with diverticulitis. Males are more likely to develop diverticulitis at a younger age whereas there is a female predominance in older patients. ^, In western populations, approximately one fifth of patients with diverticulitis are under the age of 50 years (reported incidence 18–34%). There was a trend towards a more aggressive surgical approach in younger patients based on the hypothesis that the disease was more virulent in this subgroup. ^, Younger age may be a risk factor for recurrent disease rather than an indication for early intervention in the acute setting, as these patients are just as likely to settle with conservative management. ^,

Diet

Painter and Burkitt described diverticular disease as a deficiency of dietary fibre proposing that consumption of a refined western diet led to longer colonic transit times, decreased stool volume and increased intra-luminal pressures. Although a role for dietary fibre in the pathogenesis of diverticular disease is plausible, there is little evidence to support this hypothesis. Conclusions are drawn from several randomised controlled trials with small patient numbers producing conflicting results ^, and do not demonstrate an improvement in symptoms or diverticulitis recurrence overall. Residue refers to any indigestible food substance that remains in the intestinal tract and contributes to stool bulk. Historically, low residue diets were recommended because indigestible remnants were thought to clog in diverticula leading to diverticulitis or perforation. These concerns were dismissed by conclusive evidence from the healthcare professionals follow-up study.

Low fibre diet has an epidemiological association with the development of diverticular disease. However, recommending fibre as a treatment for diverticulosis is largely based on outdated, poorly controlled studies.

Young patients (<50 y) may be more likely to suffer from recurrent diverticulitis. There is no evidence to support aggressive surgical intervention in cases of uncomplicated diverticular disease. ^,

Aetiology and pathogenesis

There are several theories as to the pathogenesis of diverticular disease. Aside from luminal trauma, potential aetiological factors include elevated colonic pressures, compromised colon wall integrity, and altered bacterial flora. Colonic wall abnormalities (specifically mural thickening, increased collagen cross-linking, muscle atrophy and shortening of taeniae coli ) are thought to produce a ‘stiffer’ less compliant colon predisposing to diverticular herniation. In addition, abnormalities in cholinergic smooth muscle excitation and neurohumoral signalling (serotonin, nitric oxide, VIP) may contribute to disordered contractions and increased intra-luminal pressures.

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