Benign diseases of the colon: diverticulosis, polyps and polyposis syndromes
DIVERTICULOSIS
Colonic diverticula are mucosal and submucosal herniations through weak points in the muscular wall, commonly where vasa recta penetrate. They are most frequent in the sigmoid colon in Western populations. Risk increases with age and is associated with low-fibre dietary patterns, obesity, smoking and inactivity. Diverticulosis is often asymptomatic but may cause painless lower GI bleeding.
DIVERTICULITIS
Diverticulitis is inflammation, sometimes with microperforation, of a diverticulum. Features include constant left lower-quadrant pain, fever, altered bowel habit and local tenderness; right-sided disease can mimic appendicitis. CT with contrast is the preferred investigation in uncertain or complicated cases and identifies abscess, perforation, fistula or obstruction. Colonoscopy is generally avoided during acute inflammation and arranged after recovery when indicated to exclude malignancy. Uncomplicated disease may be managed as an outpatient with analgesia, diet as tolerated and selective antibiotics according to severity and local guidance. Abscess may require antibiotics and image-guided drainage; generalised peritonitis, free perforation, fistula or obstruction may require surgery. Elective resection is individualised, not based solely on a fixed number of episodes.
COLONIC POLYPS
Polyps are mucosal projections and may be neoplastic or non-neoplastic. Adenomas (tubular, tubulovillous, villous) are premalignant; risk rises with size, villous architecture, high-grade dysplasia and multiplicity. Sessile serrated lesions are also precursors to colorectal cancer. Hyperplastic polyps are usually low risk when small and distal. Most polyps are asymptomatic; larger lesions may bleed or cause iron-deficiency anaemia. Colonoscopy allows detection, biopsy and polypectomy. Histology determines surveillance interval; incomplete excision, large lesions or high-grade dysplasia require closer follow-up.
POLYPOSIS SYNDROMES
Familial adenomatous polyposis (FAP) is an autosomal dominant APC mutation causing hundreds to thousands of adenomas and near-certain colorectal cancer risk without prophylactic management. Attenuated FAP has fewer, later polyps. Lynch syndrome is mismatch-repair deficiency with microsatellite instability; it is not a classic polyposis syndrome but confers high colorectal and extracolonic cancer risk. MUTYH-associated polyposis is autosomal recessive. Peutz–Jeghers causes hamartomatous polyps and mucocutaneous pigmentation; juvenile polyposis also increases cancer risk. Recognise family history and refer for genetic counselling/testing.