D. Magnetic resonance imaging

 

Magnetic resonance imaging (MRI) is becoming the first-line option for the study of patients with Crohn’s disease (CD). Since this technique does not involve the use of ionizing radiations, it appears to be ideal for patients of this kind, with chronic disease starting in youth. Magnetic resonance enterography (MRE) is well tolerated, rapid and easy to interpret, and moreover allows evaluation of both the bowel loops and of the peri-intestinal structures in the same exploratory procedure.

Magnetic resonance imaging allows us to identify each of the clinical patterns of the disease. In addition, the analysis of certain factors may help us to assess the degree of disease activity.

 

MANIFESTING PATTERNS IN CROHN’S DISEASE

Non-stricturing – non-penetrating

The most characteristic feature of this presentation is wall edema and the presence of ulcers.
Initially, mucosal edema and lymphoid follicle hyperplasia are observed.

 
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Figure 1. B-FFE axial sequence showing minimal ileal wall thickening and signs of lymphoid follicle hyperplasia.
 

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.

 
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Figure 2. B-FFE axial sequence showing filiform mucosal hypertrophy.
 

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.

 
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Figure 3. T2-weighted axial sequence with fat saturation. Increased signal intensity of the ileal wall and peri-intestinal tissues is seen, attributable to edema.
 

 

Video 1. Reduced intestinal motility in Cine-MRI
 

In many cases a laminar pattern is detected after intravenous gadolinium contrast administration.

 
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Figure 4. T1-weighted coronal sequence obtained after intravenous gadolinium administration. The stratified enhancement (arrows) is due to increased uptake by the mucosa and serosa, while the submucosa remains hypointense.
 

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.

 
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Figure 5. Nodular elevations of the mucosa due to submucosal edema (nodular pattern). T2-weighted coronal sequence.
 

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.

 
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Figure 6. B-FFE coronal sequence showing retraction of the ileal mesenteric margin and the development of antimesenteric sacculations.
 

In some cases a number of aphthous lesions may become larger and deeper, showing a spiculate appearance.

 
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Figure 7. B-FFE axial sequence showing deep fissures in the bowel wall, exhibiting 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.

 
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Figure 8. T2-weighted coronal sequence. Thickened ileal loops and mesenteric adipose tissue proliferation (“ghost fat”).
 

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.

 
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Figure 9. Severe involvement of the terminal ileum in the form of a “gross cobblestone” pattern. T2-weighted coronal sequence (a) and B-FFE axial sequence (b).
 

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”.

 
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Figure 10. B-FFE coronal sequence showing vasa recta ingurgitation conforming the so-called “comb sign”.
 

In many cases enlarged, enhanced uptake lymph nodes are seen after gadolinium administration in the vicinity of the affected loops.

 
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Figure 11. T1-weighted coronal sequence obtained after intravenous gadolinium administration. Several adenopathies are observed in the ileocecal region.
 

 

Stricturing

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.

 
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Figure 12. B-FFE axial sequence showing ileal stricture with prestenotic dilatation.
 

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.

 
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Figure 13. Multiple stenotic jejunal segments of different lengths (T2-weighted coronal sequence).

 

Penetrating

In penetrating disease, the ulcers reach deep layers of the wall and even the mesenterium, producing so-called deep ulcerations or “sinus tracts”.

 
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Figure 14. Deep, transmural ulcer, in the wall of the ileum (arrow) (T2-weighted axial sequence).
 

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).

 
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Figure 15. Enterocutaneous fistula (T1-weighted axial sequence obtained after intravenous gadolinium administration).
 

Complex fistulas between bowel loops usually have a stellate appearance, with multiple trajectories that converge towards a central point.

 
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Figure 16. B-FFE coronal sequence showing the typical “stellate” appearance of entero-enteral fistulas.
 

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.

 
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Figure 17. Lesion in the right iliac fosse, showing irregular margins, with no central abscessification, corresponding to a phlegmon or “inflammatory mass” (T1-weighted coronal sequence obtained after intravenous gadolinium 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.

 
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Figure 18. Abscesses between ileal loops. In T1-weighted coronal sequencing following gadolinium injection: (a) peripheral enhancement of the abscess is observed (black arrows). In T2-weighted axial sequencing: (b) two small collections are seen (arrows), with restriction in the diffusion sequence (c).

 

Other findings

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.

 
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Figure 19. Small regenerative polyps (arrows) in the region of an ileal segment lacking inflammatory signs (T2-weighted sequence).

 
 

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