Ulcerative colitis (UC) is a chronic idiopathic inflammatory bowel disease affecting the mucosal layer of the colon and rectum. It starts from the rectum and spreads proximally in a continuous (uninterrupted) pattern — this 'continuous involvement' pattern is the key differentiating feature from Crohn's disease skip lesion pattern. On CT and CT enterography, diffuse, symmetric, continuous colonic wall thickening, mucosal hyperemic enhancement ('target sign'), pericolonic fat infiltration, and loss of haustrations ('lead-pipe colon') are observed. In acute flares, toxic megacolon (transverse colon diameter >6 cm), perforation, and massive bleeding are life-threatening complications. Colorectal cancer risk significantly increases in long-standing UC — surveillance colonoscopy is initiated after 8-10 years of disease duration. Primary sclerosing cholangitis (PSC) association is seen in 5%.
Age Range
15-55
Peak Age
35
Gender
Equal
Prevalence
Uncommon
Ulcerative colitis develops through dysregulation of mucosal immune response to environmental triggers in genetically predisposed individuals. NOD2/CARD15, IL-23R, and HLA-DRB1 gene polymorphisms increase disease risk. The pathological process is limited to mucosa and submucosa — transmural involvement is a differentiating criterion from Crohn's. Disruption of mucosal epithelial barrier allows luminal antigens to cross into the lamina propria, activating Th2-dominant immune response. Proinflammatory cytokines (IL-5, IL-13, TNF-alpha) stimulate neutrophilic infiltration — crypt abscesses form and mucosal ulceration develops. Prolonged crypt destruction leads to loss of crypt architecture, followed by mucosal atrophy and pseudopolyp formation. The 'target sign' on CT reflects three-layered wall structure: mucosal hyperemic enhancement (inner ring), submucosal edema (middle hypointense ring), and serosal/muscularis enhancement (outer ring). In the chronic phase, loss of haustrations ('lead-pipe colon') results from muscularis mucosae fibrosis and colonic shortening — fibrotic contracture of smooth muscle layer due to chronic inflammation rigidifies the colonic wall. Colorectal cancer risk derives from chronic inflammation disrupting DNA repair mechanisms, initiating dysplasia-carcinoma sequence through p53 and APC mutation accumulation and microsatellite instability.
In chronic UC, the colon takes a straight, featureless 'lead-pipe' appearance due to loss of haustrations, colonic shortening, and tubular straightening. This finding is considered pathognomonic for chronic UC and results from years of mucosal inflammation + fibrosis.
In portal venous phase, symmetric colonic wall thickening starting from rectum and continuing proximally without interruption is observed. 'Target sign': three-layered structure with inner hyperdense mucosal enhancement, middle hypodense submucosal edema, and outer hyperdense muscularis/serosal enhancement.
Report Sentence
Continuous symmetric colonic wall thickening extending from rectum to [location] is identified with 'target sign' pattern — consistent with ulcerative colitis.
On non-contrast or contrast-enhanced CT, loss of haustrations and colonic shortening ('lead-pipe colon') is observed in chronic UC. Colon takes a tubular, straight, haustration-free appearance. This finding is particularly prominent in the left colon and is the fibrotic result of years of inflammation.
Report Sentence
Loss of haustrations and colonic shortening in the [left/transverse/entire] colon is identified, consistent with chronic ulcerative colitis findings.
In acute flare, transverse colon diameter reaches >6 cm (toxic megacolon). Wall thinning (<2 mm), intramural air (pneumatosis), pericolonic free fluid, and free intraperitoneal air (perforation sign) may accompany. Toxic megacolon is a surgical emergency.
Report Sentence
Transverse colon diameter measures [value] cm with [wall thinning/pneumatosis/free air] findings, consistent with toxic megacolon — EMERGENCY surgical consultation.
In chronic UC, regenerative mucosal islands ('pseudopolyps') appear as small, multiple polypoid protrusions in the colonic lumen. Preserved mucosal islets between ulcerated mucosa show higher density than surrounding ulcer craters.
Report Sentence
Multiple small pseudopolyps in the colonic mucosa are identified, consistent with chronic ulcerative colitis sequelae.
On MRI T2-weighted sequences, hyperintense submucosal edema is observed in the colonic wall. Wall thickening and T2 signal increase are prominent in active inflammation areas. Active inflammation may show diffusion restriction on DWI.
Report Sentence
On MRI T2-weighted sequence, hyperintense submucosal edema and wall thickening in the [location] colon wall is identified, consistent with active inflammation.
In chronic UC, presacral space widening (>15 mm) and perirectal fat tissue increase are observed. Proliferative adipose tissue ('creeping fat' — though less prominent than Crohn's) reflects the effect of chronic inflammation on mesenteric fat.
Report Sentence
Presacral space is widened to [value] mm, consistent with chronic ulcerative colitis.
Criteria
Involvement limited to rectum only. Mildest form.
Distinct Features
Isolated rectal wall thickening on CT. Best prognosis. High topical treatment response rate.
Criteria
Involvement from rectum to splenic flexure. Most common pattern.
Distinct Features
Left colon wall thickening on CT, right colon normal. Intermediate cancer risk.
Criteria
Form involving entire colon from rectum to cecum. Most severe involvement.
Distinct Features
Diffuse wall thickening throughout colon on CT. Highest cancer risk. Greatest toxic megacolon risk. Highest colectomy need.
Distinguishing Feature
Crohn's skip lesions, transmural involvement, fistula/abscess, ileal involvement; UC continuous from rectum, mucosal-limited, no fistula
Distinguishing Feature
Ischemic colitis segmental, watershed distribution, rectum usually spared; UC starts from rectum, continuous
Distinguishing Feature
Carcinoma focal mass/stricture, asymmetric; UC diffuse, symmetric, continuous wall thickening
Distinguishing Feature
Lymphoma segmental wall thickening, aneurysmal dilatation, obstruction rare; UC continuous involvement, luminal narrowing, obstruction possible
Urgency
urgentManagement
medicalBiopsy
NeededFollow-up
specialist-referralUC treatment is planned with stepwise approach based on disease extent and severity: 5-ASA (mesalamine) for mild-moderate flares, corticosteroids and immunomodulators (azathioprine, anti-TNF) for moderate-severe flares, biological agents (vedolizumab, tofacitinib) for refractory cases. Toxic megacolon is a surgical emergency — urgent colectomy is life-saving. Dysplasia surveillance (chromo-endoscopy + biopsy) every 1-2 years in pancolitis patients >8-10 years. Colectomy indicated if high-grade dysplasia or DALM (dysplasia-associated lesion or mass) detected. Cholangiocarcinoma risk also increased in PSC association.
Increased colorectal cancer risk in chronic disease (screening recommended after 10 years). Toxic megacolon is a life-threatening complication. Colectomy can be curative.