The most characteristic feature of this presentation is wall edema and the presence of ulcers.
Initially, mucosal edema and lymphoid follicle hyperplasia are observed.
The follicles may experience superficial ulceration, giving rise to aphthous ulcers, which in principle would not be detectable by MRE. In the case of greater activity, mucosal thickening increases and in some cases becomes digitiform. Any wall thickening > 3 mm should be regarded as abnormal.
When involvement becomes transmural, submucosal edema appears, leading to irregular wall thickening (with distortion of the Kerckring folds or connivent valves), with hyperintensity in T2-weighted sequences and decreased motility.
In many cases a laminar pattern is detected after intravenous gadolinium contrast administration.
The presence of edema and granulation tissue causes nodular elevations of the mucosa, making up the inflammatory pseudopolyps responsible for the nodular pattern. In these cases there usually is no bowel luminal narrowing as in the case of the cobblestone presentation.
Deepening and coalescence of the aphthous lesions in the mesenteric margin of the loops causes thickening, fibrosis and retraction, with the development of antimesenteric pseudo-saccular structures.
In some cases a number of aphthous lesions may become larger and deeper, showing a spiculate appearance.
Another effect of transmural involvement is mesenteric fat proliferation, i.e., the presence of hypertrophic white adipose tissue surrounding the damaged loops; this occurs from the start and represents a “brand mark” of Crohn’s disease.
In more advanced stages the inflammation spreads to the entire intestinal wall, the serosa, or even beyond. The “cobblestone” or ulcerous-nodular pattern appears, due to the presence of deep longitudinal and transverse ulcerations delimiting “islets” of inflamed mucosa and submucosa.
Marked reduction of the intestinal lumen is characteristic. In addition, circulatory changes occur, with vasa recta ingurgitation or hyperemic thickening, conforming the so-called “comb sign”.
Collagen accumulation, occurring mainly in the submucosa, is the cause of the development of strictures and even small bowel obstruction.
The wall appears thickened and usually iso- or hyperintense with respect to the rest of the intestine in T2-weighted sequences.
The lumen is reduced, with prestenotic dilatation in some cases. In Cine-MRI sequences the affected segments appear rigid and with diminished motility. The affected long segments with diminished luminal diameter and loss of the mucosal pattern conform the so-called “string sign”.
In some cases several stenotic segments separated by radiologically normal segments can be seen.
In penetrating disease, the ulcers reach deep layers of the wall and even the mesenterium, producing so-called deep ulcerations or “sinus tracts”.
Once ulceration has spread beyond the wall, cul de sac formations or abscesses can develop, or other organs can be affected. Fistulas are abnormal communications between epithelial surfaces (opening to other parts of the intestine, the bladder, vagina, or skin).
Complex fistulas between bowel loops usually have a stellate appearance, with multiple trajectories that converge towards a central point.
Inflammatory masses or phlegmons are poorly-defined mesenteric lesions which in some cases encompass bowel loops or extend to other organs. Homogeneous enhancement is observed after contrast administration.
Abscesses usually appear confined to a given bowel segment, though in some cases they may extend towards other zones such as the psoas muscle, etc. After gadolinium administration, peripheral capsule enhancement is observed, with the restriction of contrast diffusion.
In some cases regenerative changes can be observed in chronic disease. Small mucosal polyps are typical in this evolutive stage. It is also possible to observe fat deposits or fibrosis in the submucosa.