Crohn disease is a chronic transmural granulomatous inflammatory bowel disease that can affect any part of the gastrointestinal tract. Colorectal involvement is seen in 30-50% of cases. Characteristic findings include skip lesions (segmental involvement), transmural inflammation, fistula, and stricture formation. Most commonly begins between ages 15-35. CT enterography and MR enterography are primary imaging modalities for diagnosis and follow-up. Terminal ileum is the most commonly affected site, but isolated colonic involvement may also occur.
Age Range
15-50
Peak Age
30
Gender
Equal
Prevalence
Uncommon
Crohn disease results from inappropriate immune response triggered by environmental factors (gut microbiome changes, smoking) on a background of genetic susceptibility (NOD2/CARD15 mutation is the strongest risk factor). Inflammation is transmural — affecting all layers from mucosa to serosa. This transmural inflammation forms the basis of Crohn complications: fistulae (inflammation extending beyond the wall), abscesses (infection in fistula tracts), strictures (chronic inflammation resulting in fibrosis), and perforation. On CT, transmural inflammation appears as wall thickening, increased mucosal enhancement (active inflammation), and perienteric fat stranding. Comb sign (vasa recta engorgement) is the CT correlate of active mesenteric inflammation and hyperemia — engorged straight vessels resemble comb teeth. Skip lesions reflect the segmental nature of the disease and distinguish from ulcerative colitis.
The combination of segmental wall thickening between normal bowel segments (skip lesions) with engorged vasa recta on the mesenteric side (comb sign) is the signature finding of Crohn disease. Skip lesions reflect the segmental nature, comb sign reflects active transmural inflammation.
Segmental wall thickening (>4 mm) between normal bowel segments. Skip lesions are pathognomonic for Crohn and distinguish from continuous involvement of ulcerative colitis.
Report Sentence
Segmental wall thickening in a skip lesion pattern between normal bowel segments is seen, consistent with Crohn disease.
Engorged vasa recta on the mesenteric side of the inflamed bowel segment — comb-teeth appearance. Indicates active mesenteric inflammation and hyperemia.
Report Sentence
Comb sign is seen on the mesenteric side of the inflamed bowel segment, suggesting active inflammation.
Fistula tracts originating from inflamed bowel segment — may be enteroenteric, enterocutaneous, enterovesical, or perianal. Sinus tracts are blind-ending tracts. Appear as enhancing linear tracts on CT.
Report Sentence
A ___ type fistula tract originating from the inflamed bowel segment is seen.
Mural edema on T2W — submucosal edema appears as hyperintense layer (stratification). MR indicator of active inflammation. MR enterography preferred in young patients due to radiation advantage over CT.
Report Sentence
Submucosal edema and mural stratification on T2W in the inflamed bowel segment is seen, consistent with active Crohn disease.
Mesenteric fat proliferation — fat accumulation on the mesenteric side of the inflamed bowel segment (creeping fat). Characteristic finding of chronic Crohn disease.
Report Sentence
Creeping fat is seen on the mesenteric side of the inflamed bowel segment, consistent with chronic Crohn disease.
Diffusion restriction in actively inflamed bowel segment on DWI. Valuable for differentiating active inflammation from fibrotic stricture. ADC value decreases in active inflammation.
Report Sentence
Diffusion restriction on DWI is seen in the thickened bowel segment, suggesting active inflammation.
Criteria
Montreal B1. No stricture or fistula. Wall thickening and inflammation predominate.
Distinct Features
Wall thickening, fat stranding, comb sign on CT. Good response to medical therapy. T2 hyperintensity and DWI positivity on MR confirm active inflammation.
Criteria
Montreal B2. Luminal narrowing and proximal dilation. No fistula.
Distinct Features
Luminal narrowing, proximal dilation (obstruction) on CT. Low T2 signal on MR suggests fibrotic stricture, high T2 + DWI positivity suggests active inflammatory stricture. Treatment determined by active vs fibrotic distinction.
Criteria
Montreal B3. Fistula, sinus tract, or abscess present. Most aggressive phenotype.
Distinct Features
Fistula tracts, perienteric abscesses, free fluid on CT/MR. Requires anti-TNF therapy (infliximab) and/or surgery. Perianal fistulae best evaluated by MRI.
Distinguishing Feature
Ulcerative colitis shows continuous (no skip lesions), symmetric mucosal involvement extending proximally from rectum. Crohn shows segmental, asymmetric, transmural involvement and fistulae.
Distinguishing Feature
Ischemic colitis affects vascular watershed areas (splenic flexure), sudden onset, common in elderly. Crohn characterizes young patients, terminal ileum involvement, and fistulae.
Distinguishing Feature
Adenocarcinoma shows focal mass/annular narrowing, shouldered margins, and lymphadenopathy. Crohn shows long-segment involvement, skip lesions, and inflammatory changes.
Distinguishing Feature
Lymphoma shows aneurysmal dilation, homogeneous wall thickening, and luminal widening. Crohn shows luminal narrowing (stricture), fistulae, and comb sign.
Urgency
urgentManagement
medicalBiopsy
NeededFollow-up
6-monthTreatment in Crohn disease is determined by disease phenotype and activity. Active inflammatory disease uses 5-ASA (mild), corticosteroids (moderate), anti-TNF (infliximab, adalimumab — moderate-severe), vedolizumab, or ustekinumab. Stricturing disease: active inflammatory stricture → medical therapy, fibrotic stricture → endoscopic balloon dilation or surgical resection. Penetrating disease: perienteric abscess → percutaneous drainage + antibiotics, fistula → anti-TNF + surgery. Perianal fistulae: MR-guided seton placement + anti-TNF is standard treatment. Follow-up: CT/MR enterography every 6-12 months for activity assessment, fecal calprotectin and CRP for laboratory monitoring.
Chronic, relapsing disease. Requires immunosuppressive therapy. Complications (stricture, fistula, abscess) may require surgery. Long-standing colitis increases colorectal cancer risk.