In this pattern, two (double halo sign) or three (the target sign) concentric and symmetric layers of alternating densities are recognised on the thickened bowel wall after intravenous contrast administration.
This pattern indicates inflammation or ischaemia of the bowel where the inner and outer high-density layers correspond to the hyperemic mucosa and serosa, respectively, while the low-density layer presumably represents the oedematous submucosa [2–4, 6, 7, 11, 21].
Although generally indicative of benign conditions, these signs are not specific and may be present in several acute conditions. Clinical presentation and adjacent findings such as perienteric findings help in narrowing the differential diagnosis:
Bowel ischaemia
Thickening of the bowel wall is the most common but least specific CT sign of bowel ischaemia [5, 22]. The extent of involvement, degree of thickness and pattern of attenuation of the ischaemic bowel vary according to three main factors: (1) pathogenesis of the ischaemia (arterial-occlusive, veno-occlusive or hypoperfusion); (2) severity of the ischaemia (transient ischaemia of the mucosa and/or submucosa versus transmural bowel wall necrosis); (3) superimposed haemorrhage or infection [5].
Although bowel wall thickening is a common finding in cases of bowel ischaemia, the ischaemic bowel wall may also appear paper thin, particularly in cases of acute arterial occlusion [5].
When the ischaemic bowel wall is thickened, it may present with one or more of the three above-mentioned attenuation patterns referred [3, 5, 23]. The stratified pattern of attenuation may be an early finding of bowel ischaemia. This results from oedema of the submucosa and hyperaemia or hyperperfusion of the mucosa and/or muscularis propria [5, 6, 21, 24]. This finding should be judged in the clinical context and associated imaging findings of bowel ischaemia, such as occlusion of the mesenteric artery or vein, bowel dilatation, engorgement of the mesenteric veins, and mesenteric oedema and ascites [3, 11, 21, 22, 25] (Fig. 11). Intestinal pneumatosis and gas in the mesenteric or portal veins are indicative of severe ischaemia and are usually associated with the thinning rather than thickening of the small bowel wall due to bowel wall necrosis [24].
Vasculitides are rare causes of gastrointestinal ischaemia with the highest prevalence in polyarteritis nodosa and usually present with thickening of the affected bowel wall with a stratified appearance [3, 24]. Distinguishing between ischaemia due to vasculitides and other causes of mesenteric ischaemia may be difficult based on radiologic findings alone (Fig. 12). This diagnosis, however, should be considered whenever mesenteric ischaemic changes occur in young patients; involve unusual sites such as the stomach, duodenum and rectum, and is not confined to a single vascular territory. In addition, systemic clinical manifestations (i.e. fever, weakness, malaise, myalgia and headache) point to the correct diagnosis [24].
Idiopathic inflammatory bowel disease
Bowel wall thickening with a stratified pattern may be also seen in both ulcerative colitis (UC) and Crohn’s disease, indicating acute, active disease [2, 7, 26].
Crohn’s disease may occur in any part of the gastrointestinal tract but predominantly affects the small bowel, particularly the ileum and right colon [2, 7]. CT signs favouring Crohn’s disease include discontinuous involvement of the bowel wall (“skip areas”), prominent vasa recta (“comb sign”) and signs of transmural inflammation such as fistulas and abscesses, and proliferation of the fat along the mesenteric border of the bowel [2, 3, 7] (Fig. 13).
By contrast, UC is typically left sided, involves the rectum in 95 % of cases, and shows contiguous, circumferential and proximal extension through the colon [27]. The inflammatory process in UC is superficial, predominantly affecting the mucosa [7]. Thus, wall thickening and pericolonic involvement are not as extensive in ulcerative colitis as they are in Crohn’s disease [27].
Infectious enteritis or colitis and pseudomembranous colitis
In most cases of infectious enteritis the small bowel wall appears normal or mildly thickened [3]. By contrast, infectious colitis typically manifests with significant wall thickening, which may demonstrate either homogeneous enhancement or a striated pattern due to intramural oedema. Stranding of the pericolic fat and ascites are also commonly seen [7, 28, 29]. Although the affected portion of the colon may suggest a specific organism, there is a considerable overlap of the appearances. Thus, laboratory studies are needed to achieve a definitive diagnosis [7].
Pseudomembranous colitis results from toxins produced by an overgrowth of the organism Clostridium difficile and usually presents as a pancolitis. The degree of bowel wall thickness in pseudomembranous colitis and cytomegalovirus colitis is usually greater than in any other inflammatory or infectious disease of the colon, while the pericolic fat stranding is often disproportionately mild [2, 9] (Fig. 14). After intravenous contrast administration, the thickened bowel wall may show low attenuation due to oedema, hyperenhancement due to hyperaemia or a striated appearance. When haustral folds are significantly thickened and protrude into the bowel lumen, they can trap the positive oral contrast material, an appearance known as the “accordion sign”. This sign suggests the diagnosis, although it may also occur from other causes of colitis [26].
Specific clinical entities
The striated attenuation may also be seen in specific clinical situations, such as graft-versus-host disease in patients submitted to allogeneic bone marrow transplantation, acute radiation enteritis or colitis in patients submitted to radiation therapy, bowel wall oedema in patients with a history of angioedema, and oedema of the right colon in cirrhotic patients [3, 7] (Figs. 15 and 16). In each of these conditions the appropriate clinical history is essential for establishing the correct diagnosis.
Other causes of stratified appearance
Stratification of the bowel wall may also be caused by infiltration of the submucosa by tumour or fat. The rare infiltrating scirrhous carcinomas (linitis plastica) of the stomach or rectosigmoid may present with symmetric wall thickening, regular contours and stratification of the bowel wall [4, 11]. Narrowing of the intestinal lumen, regional adenopathy and distant metastasis point to the correct diagnosis [11].
A target appearance may also be caused by deposition of fat in the submucosa, indicating past or chronic inflammation [2, 7]. It is more common in patients with idiopathic inflammatory bowel disease, especially ulcerative colitis (Fig. 17). Occasionally this sign can also be seen in patients with a history of radiation enteritis and even in patients with no history of gastrointestinal disease, where the intramural fat layer is usually much thinner than that seen in inflammatory bowel disease [3, 6, 27].