Mural hyperenhancement refers to segmentally increased attenuation of bowel loops compared to adjacent loops, and this correlates histologically with areas of active inflammation in Crohn’s patients [21]. Mural hyperenhancement is the most sensitive sign of bowel inflammation, and it can be an isolated finding in mild inflammation. Hyperenhancement alone is a nonspecific finding in the small bowel, but asymmetric and patchy hyperenhancement, particularly along the mesenteric border, is indicative of Crohn’s disease (Figs. 19.1 and 19.5).

Mural hyperenhancement is often accompanied by bowel wall thickening, which in the small bowel wall is greater than 3 mm in thickness in a bowel loop that is distended with luminal contrast. Wall thickening in Crohn’s disease is often asymmetric and more prominent along the mesenteric border as well. As mural inflammation increases, wall thickening is often accompanied by mural stratification, which refers to a bilaminar and trilaminar appearance to the bowel wall (Fig. 19.5). The presence of both segmental mural hyperenhancement and wall thickening in the presence of asymmetric bowel involvement yields the best combination of imaging criteria for diagnosing mural inflammation in Crohn’s disease [10, 22].

Several CT findings indicate more severe inflammation. Penetrating ulcers can also be seen in severely inflamed bowel loops, and they may appear as filling defects in the inflamed bowel wall; however, they are more frequently seen at MR enterography. Stranding in the perienteric fat is correlated with C-reactive protein elevation [23]. The “comb sign” refers to engorged vasa recta, which supply inflamed bowel loops and penetrate the gut wall perpendicular to the gut lumen, resembling the shape of a comb [24]. The comb sign is associated with increased serum C-reactive protein, length of hospitalization, and response to anti-inflammatory treatment (Fig. 19.5) [20, 23, 25]. Successful response to treatment following medical therapy is evidenced primarily by decreasing length of inflammatory bowel involvement along the length of the GI tract, but also a reduction in wall thickness and hyperenhancement [26].

CT enterography can also display findings of chronic inflammation. Intramural fat can be seen in actively and uninflamed small bowel loops in the colon, indicating chronic inflammation, but intramural fat in the terminal ileum is a normal finding. Alternatively, pseudopolyps are frequently seen throughout the colon after healing of acute inflammation [27]. Fibrofatty proliferation is seen as proliferation of fat, usually allowing the mesenteric aspect of the bowel loop, displacing nearby abdominal loops; however, in the rectum fibrofatty proliferation is circumferential, mimicking pelvic lipomatosis, except that there are prominent perirectal vessels and reactive lymphadenopathy. Crohn’s strictures generally possess both an inflammatory and fibrotic component [28, 29], and while CT findings of inflammation correlate histologically with inflammation in these strictures, the absence of CT findings of inflammation does not correlate with fibrosis [28]. CT enterography can be used to estimate the length of strictures to evaluate for potential endoscopic dilation or plan surgical treatment, and to evaluate for complications such as obstruction, enterolith, fistula, or malignancy.

Findings of intestinal inflammation in ulcerative colitis are similar to Crohn’s colorectal involvement, but differ in some respects. The pattern of inflammation in ulcerative colitis that is most typical is continuous inflammation from the rectum proximally, whereas patchy inflammation will be typical of Crohn’s colitis. Ulcerative colitis typically involves both the mesenteric and antimesenteric colonic wall to a similar degree, and does not cause penetrating complications. A patulous ileocecal valve is often seen when inflammation extends to the cecum (Fig. 19.6), as well as backwash ileitis, which involves the terminal ileum symmetrically without penetration. Inflammation can be mild to severe, often with loss of haustral markings. Rectal sparing can be seen when patients utilize steroid enemas. As inflammation becomes chronic, foreshortening of the colon is also often seen. As inflammation diminishes and becomes chronic, intramural fat is deposited throughout the colon, but this finding is not unique to ulcerative colitis. While surveillance of disease activity in ulcerative colitis is performed with endoscopy, CT enterography is often used to exclude small bowel inflammation in indeterminate colitis or symptomatic patients (that may have extraintestinal IBD manifestations) [30]. It is also used to evaluate for complications of severe acute colitis such as toxic megacolon, perforation or septic thrombosis (Fig. 19.7) [31, 32]. CT findings of toxic megacolon are only described in small retrospective series, but include marked colonic distension with loss of haustral markings and segmental colonic wall thinning [31].

The most subtle findings of perienteric inflammation in Crohn’s disease are perienteric fat stranding [23]. Fistulas appear as hyperenhancing extraenteric tracts, which may or may not contain air and fluid [33], and are named by the structures that they connect (e.g., entero-enteric, entero-colic, entero-vesical, entero-cutaneous , and perianal). They generally arise from or proximal to an inflammatory stricture [34] or inflamed bowel segment, and cause tethering of the involved loops, frequently forming asterisk-shaped fistulae complexes (Fig. 19.8). Fistulas may extend to other bowel loops or organs and structures, e.g., the bladder and iliopsoas muscle. CT enterography has been shown to be highly accurate for the detection of penetrating complications such as abscesses and fistulae [35]. CT enterography can be used for surgical planning in patients with known fistulizing disease, and several studies have shown that fistulizing Crohn’s disease is often clinically unsuspected [33, 36], so the principal benefit of the enterography examination is often to identify unsuspected fistulas in symptomatic patients. Every CT enterography exam should image the perineum, as CT exam can identify an unsuspected perianal fistula or abscess in patients with indeterminate colitis, a key finding likely indicating that colonic inflammation is due to Crohn’s disease. Fistulas may also arise from surgical anastomoses and leaks. Postoperative and some perianal fistulas are often not hyperenhancing due to their chronic nature.

Mural inflammation often causes luminal narrowing of the small bowel. Luminal narrowing alone at CT enterography does not imply lack of distensibility or stricturing disease. Distensibility can be observed fluoroscopically, for example, using peroral pneumocolon. At CT enterography assessment, lack of distensibility is only indicated with certainty when proximally located small bowel loops are unequivocally dilated. Small bowel dilation can occur proximal to an inflamed bowel segment or stricture. At histopathologic assessment, most Crohn’s strictures demonstrate a spectrum of inflammatory and fibrotic changes [29], and most Crohn’s strictures will demonstrate some degree of hyperenhancement at imaging, consistent with the histopathologic observation that some degree of inflammation is present. In contradistinction , however, lack of is not a good indicator of fibrosis [28].

CT enterography can detect Crohn’s-related extra-enteric findings in addition to penetrating complications. In one retrospective series of over 300 Crohn’s patients, nearly 20 % of Crohn’s patients had extraintestinal IBD manifestations, and in about two-thirds of these patients, the findings were previously unknown [36]. Common extraintestinal, non-penetrating complications detected at CT enterography include primary sclerosing cholangitis, mesenteric vascular thromboses or occlusions, cholelithiasis and nephrolithiasis, sacroiliitis, and avascular necrosis of the femoral heads. Chronic mesenteric venous occlusions, which are associated with Crohn’s related inflammation (Fig. 19.9), are rarely seen in the acute setting, have recently been described and correlate with subsequent stricture and surgery [7, 8]. While acute portal and superior mesenteric vein thrombi typically resolve completely, peripheral chronic mesenteric vein thromboses often result in chronically narrowed mesenteric veins with dilated collateral veins and potentially varices.