Ulcerative colitis is a chronic idiopathic inflammatory disease of unknown origin. Depending on the extension and activity, the presence and severity of leading symptoms of the disease such as diarrhoea, rectal blood loss, abdominal pain and fever, can vary and laboratory parameters of the acute phase response (e.g. C-reactive protein, erythrocyte sedimentation rate, faecal calprotectin) may be normal or abnormal. These findings usually depend on the severity and extent of colonic involvement.

Ulcerative colitis involves the rectum and extends proximally to all or different portions of the colon (ulcerative proctitis, sigmoiditis, left-sided colitis or pancolitis). Rectosigmoid involvement is present in almost all patients at endoscopy, with approximately 40–50 % of patients having disease limited to the rectum and rectosigmoid, 30–40 % disease extending beyond the sigmoid colon but not involving the entire colon and 20 % total colitis. Mucosal inflammation of the terminal ileum, the so-called backwash ileitis, is observed in up to 20 % of patients with pancolitis, but rarely in patients without caecal involvement. However, involvement of the appendix as a skip lesion is reported in up to 75 % of patients with UC, and the patchy inflammation in the caecum (the so-called “caecal patch”) may also be observed in patients with left-sided colitis, but both these conditions do not seem to be associated with a worse disease outcome.

Proximal spread of the disease, from the rectum to the caecum, occurs in continuity without areas of uninvolved mucosa. However, macroscopical sparing of the rectum has been described in children presenting with UC prior to treatment. In adults, normal or patchy inflammation of the rectum is likely to be due to topical therapy and although macroscopic activity may suggest skip areas, endoscopic biopsies from mucosa with a normal appearance are usually abnormal.

Indeed, the mucosa may appear normal when disease is in remission, whereas with mild and moderate inflammation it is erythematous and of granular appearance. In more severe cases, the mucosa is ulcerated and haemorrhagic (Fig. 1). In long-standing disease, the mucosa may appear atrophic and inflammatory polyps or pseudopolyps may be present as a result of epithelial regeneration.

In UC, histological changes are limited to the mucosa and superficial submucosa with deeper layers being unaffected, except in fulminant colitis. The major changes are distortion of crypt architecture and basal plasma cells and basal lymphoid cell infiltrate. Mucosal vascular congestion with oedema, focal haemorrhage and inflammatory cell infiltration may also be present (Fig. 2).

These histological changes, as well as endoscopic features, correlate well with sonographic images. However, since the disease is confined to the inner layers of the colon, endoscopy alone may be sufficient to detect and assess the extent and activity of the disease in UC, unlike CD. In this context, the role of cross sectional imaging, US included, may be marginal although useful, in some instances, since it can be repeated and is non-invasive.

The US features of UC include bowel wall thickening, alterations of the bowel wall echopattern, hyperaemia and loss of haustra coli. Occasionally mesenteric hypertrophy and mesenteric lymph nodes, or complications such as stenosis or toxic megacolon, can be found.

Ultrasonographic features of bowel wall, and particularly bowel wall thickening, largely depend on the activity of the disease. In active UC patients, US frequently reveals thickened bowel walls, usually >4 mm, frequently ranging from 5 to 7 mm, rarely >10 mm (Worlicek et al. 1987; Valette et al. 2001; Fig. 3).

However the abnormal thickening of bowel walls at US (bowel wall thickness >4 mm) is not specific, since several intestinal disorders, including UC, are characterised by US thickening of bowel walls. The degree of thickness in UC depends on disease activity, being greater in active disease and normal in the quiescent phases (Fig. 4).

Sonographic diagnosis of UC relies on different features of the bowel wall. In UC, the thickness of the bowel wall is usually homogeneous and continuous, predominates in the left colon and is, therefore, usually found in the left iliaca fossa and in the hypogastric region and extends throughout the entire colon in pancolitis (Fig. 5). Loss of haustration is a frequent finding in active and extensive disease. The thickness of the bowel wall is circumferential and symmetrical.

Since inflammation involves the mucosa and the superficial submucosa, the stratified echopattern of the bowel wall is usually preserved (Fig. 5). However, in cases of acute inflammation, the thickening involves the submucosa which may appear slightly hypoechoic and dishomogeneous, sometimes giving the bowel wall the US appearance of pathological wall thickening with loss of stratification, with increased bowel wall vascularity (Fig. 6).

The muscularis propria, which is imaged at US as an external hypoechoic line is preserved, therefore external profiles of the bowel walls in UC are usually linear and regular (Fig. 5).

Unlike CD, ulcerations are superficial and, therefore, not usually revealed by US. No deep or penetrating ulcers are present, except in severe UC in which a pre-perforative laceration of the submucosa is found. Therefore, in mild to moderate active UC, the inner layers of the colonic wall are usually regular. On the contrary, in severe active disease, the inner layer may be regular or even irregular with fine multiple hyperechoic spots, representing deep penetrating ulcers, but within a severely thickened and hypoechoic bowel wall (Fig. 7).

Since the colon returns, at endoscopy, to a normal appearance after resolution of inflammation, US also reveals a normal colonic wall. Indeed, after several recurrences, in quiescent disease, as well as in some cases with mild inflammation, the colonic wall shows normal or only slight thickening with a predominant echogenic submucosa contrasting with the hypoechoic inner mucosa and outer muscularis (Fig. 8).

Particular US findings may be observed in UC patients with extensive pseudopolyposis. Pseudopolyps may be observed as small echogenic nodules visible at the surface of the mucosa or echogenic indentations into the fluid-filled intestinal lumen. However, while isolated inflammatory polyps can be detected (Fig. 9), better imaged by hydrocolonic sonography, extensive pseudopolyposis appears as an increased and inhomogeneous thickness of the bowel wall (up to 15 mm) without the typical wall stratification (at least in inactive UC), markedly irregular internal margins and/or as a dilated incompressible bowel with echogenic inhomogeneous content (Fig. 10). To obtain confirmation of the pseudopolypoid nature of the intestinal content, colour-power Doppler can be used to assess the blood flow within the echogenic material.

The US diagnosis of UC relies upon the above-mentioned findings, mainly upon visualisation of bowel wall thickening greater than 4 mm.