What are the cross sectional imaging features of Crohns disease in the GI tract?
Findings of active inflammatory Crohn’s disease include a “target” sign or increased mural T2-weighted signal intensity relative to skeletal muscle due to submucosal edema, mural restricted diffusion due to inflammatory cell infiltration, increased mural enhancement (either homogeneously in the wall or with mural stratification to predominantly involve the mucosal layer ± serosal layer), mural ulcerations, and inflammatory pseudopolyps (seen as polypoid intraluminal filling defects secondary to islands of residual bowel mucosa surrounded by areas of ulceration). Ancillary findings include surrounding fat stranding, a “comb” sign, and enlarged or hyperenhancing reactive lymph nodes.
Findings of inactive or quiescent Crohn’s disease include lack of a “target” sign, presence of low to intermediate mural T2-weighted signal intensity relative to skeletal muscle, lack of mural restricted diffusion, presence of a “fat halo” sign, normal mural enhancement, and lack of the ancillary findings of active inflammatory disease listed above.
Fibrostenotic Crohn’s disease is present when there is a bowel stricture (seen as an area of bowel wall thickening that is associated with fixed luminal narrowing and upstream bowel dilation). This may occur either with mixed fibrostenotic and active inflammatory Crohn’s disease or in the setting of inactive Crohn’s disease.
Penetrating Crohn’s disease (which may occur in the setting of active inflammatory Crohn’s disease or mixed fibrostenotic and active inflammatory Crohn’s disease) is present when there is fistula formation (seen as linear or curvilinear enhancing soft tissue tracts that connect two epithelial surfaces, such as enterocutaneous, enteroenteric, enterocolic, enterovesical, and enterovaginal fistulae), sinus tract formation (seen as linear or curvilinear enhancing soft tissue tracts that extend from mural defects but blindly end in the surrounding fat without connection to adjacent epithelial surfaces), abscess formation, or uncommonly, bowel perforation.
Wall thickening (focal or segmental, circumferential or asymmetric) and fibrofatty proliferation (seen as increased fat adjacent to abnormal segments of bowel) may be seen with active inflammatory, inactive, or fibrostenotic Crohn’s disease. Luminal narrowing may be seen with active inflammatory or fibrostenotic Crohn’s disease
