Diverticular disease

Diverticular disease is thought to be of multi-factorial aetiology. Both genetic and environmental factors are described as causative, especially a low dietary fibre intake, which in Western populations is deemed as the predominant contributing factor.[13][20][21]

Other predisposing factors described include decreased physical activity, obesity, increased red meat consumption, tobacco smoking, excessive alcohol and caffeine intake, steroids, and non-steroidal anti-inflammatory drugs.[2][22][23][24][25]

Other suggested aetiologies include:

alterations in colonic wall structure (increased type III collagen synthesis, elastin deposition), abnormal colonic motility, and colonic neurotransmitter dysfunction (decreased choline acetyltransferase, increased serotonin expression)[26][27]
connective tissue abnormalities such as Ehlers-Danlos syndrome, or herniosis, which have been implicated in the concurrence of disorders referred to as Saint's triad (hiatus hernia, colonic diverticulosis, gallstones)[28][29]
infection of the diverticula, which may be the cause of inflammation that results in diverticulitis
deregulation of the host immune response and the microbiome, which may contribute to diverticulosis and diverticulitis.[30]

There is no evidence to support the theoretical concern that ingested seeds and nuts could become trapped within a diverticulum and result in an episode of diverticulitis.

A low-fibre diet increases intestinal transit time and decreases stool volume resulting in increased intraluminal pressure and colonic segmentation, which predispose to diverticular formation.[31][32] However, the precise mechanism is not completely understood and this concept does not easily explain the right-sided disease seen in Asia. The sigmoid colon is commonly affected because of its small diameter.

Colonic diverticula are ‘pseudo diverticula’ (consisting only of mucosa and muscularis mucosa) and commonly occur between the tenia coli at presumed sites of weakness, where the vasa recti penetrate the colonic wall. Thickening of circular muscles and shortening of tenia without actual muscle hypertrophy is caused by increased elastin deposition between muscle cells and tenia coli. Nitric oxide is thought to be responsible for the segmentation of colonic wall in diverticulosis, by influencing the compliance of the circular muscle layer.[33] Inspissated food particles or faecal material may contribute to the development of infection, which when combined with increased intraluminal pressure, may cause inflammation, ischaemia, and necrosis of the wall of a diverticulum, leading to perforation. Microperforation of one or more diverticula may result in a localised phlegmon, a small confined abscess (stage I), a distant abscess (stage II), generalised peritonitis (stage III) or free perforation, and faecal peritonitis (stage IV).[3]

Clinical classification

Currently, there is no universally accepted clinical classification for diverticular disease. However, the following clinical distinctions are commonly used.[1][2]

Asymptomatic diverticulosis: usually an incidental finding on colonoscopy or radiological investigation.
Symptomatic uncomplicated diverticular disease: also referred to as painful diverticular disease and often characterised by episodic left-lower abdominal colicky pain with or without other non-specific symptoms of bloatedness, constipation, or diarrhoea. The symptoms may become recurrent.
Complicated diverticular disease: the most common complication is acute diverticulitis. Other complications include haemorrhage, abscess, segmental colitis, diverticular phlegmon, perforation, peritonitis, fistula, stricture, and obstruction.

The severity of acute diverticulitis is graded using the Hinchey classification:[3]

Stage I: small or confined pericolic or mesenteric abscess.
Stage II: large paracolic abscess often extending into pelvis.
Stage III: perforated diverticulitis where a peri-diverticular abscess has perforated resulting in purulent peritonitis.
Stage IV: perforated diverticulitis where there is free perforation and is associated with faecal peritonitis.

In recent years, both classification and management of acute colonic diverticulitis has changed dramatically. Computed tomography (CT) imaging has become a primary diagnostic tool in the diagnosis and staging of patients with colonic diverticulitis, and more detailed information provided by CT scans led to several modifications of the Hinchey classification.[4][5]

In 2015, a simplified classification system based on CT scan findings was proposed by the World Society of Emergency Surgery (WSES) acute diverticulitis working group.[6] This system has been designed to help guide clinicians in the management of acute diverticulitis, and may be universally accepted for day-to-day practice. The WSES classification divides acute diverticulitis into uncomplicated and complicated groups. In uncomplicated acute diverticulitis, the infection only involves the colon and does not extend to the peritoneum. In complicated acute diverticulitis, the infectious process proceeds beyond the colon. Complicated acute diverticulitis is divided into four stages, based on the extension of the infectious process:

Uncomplicated:

0 - Diverticula, thickening of the wall, increased density of the pericolic fat.

Complicated:

1A - Pericolic air bubbles or small amount of pericolic fluid without abscess (within 5 cm from inflamed bowel segment)

1B - Abscess ≤4 cm

2A - Abscess >4 cm

2B - Distant gas (>5 cm from inflamed bowel segment)

3 - Diffuse fluid without distant free gas

4 - Diffuse fluid with distant free gas.

Pathophysiology

Classification

Clinical classification