Villous adenoma is a premalignant neoplasm arising from colorectal mucosa, comprising 5-10% of all colorectal adenomas. It is distinguished from other adenoma types by its characteristic 'frond-like' structure composed of long papillary villi. Most commonly found in the rectum and sigmoid colon, typically presenting as broad-based (sessile), large (usually >2 cm), soft-consistency, 'carpet-like' growth pattern. Villous adenoma has the highest malignant transformation risk among adenoma types (30-40%). Secretory diarrhea with hypokalemia and dehydration (McKittrick-Wheelock syndrome) is a rare but characteristic complication. On CT colonography, it appears as intraluminal, smooth or lobulated surface, contrast-enhancing polypoid or carpet lesion. On MRI, T2 hyperintense villous projections and diffusion restriction correlate with dysplasia grade.
Age Range
45-80
Peak Age
65
Gender
Male predominant
Prevalence
Uncommon
Villous adenoma is part of the adenoma-carcinoma sequence initiated by APC tumor suppressor gene mutation in crypt base stem cells. APC mutation leads to constitutive Wnt/beta-catenin pathway activation, initiating uncontrolled cell proliferation. Villous adenoma histologically contains >75% villous component — long, thin papillary projections (villi) extend from mucosal surface intraluminally. This villous structure reflects disrupted normal mucosal gland architecture and dysplastic epithelium growing in papillary configuration. High malignancy risk derives from faster accumulation of genetic instability (microsatellite instability, KRAS mutation, p53 loss) in villous adenomas compared to tubular ones. Carpet-like growth pattern reflects the lesion covering a wide area on the mucosal surface while invasion depth remains shallow. McKittrick-Wheelock syndrome results from excessive mucin secretion by villous epithelium — increased mucosal surface area increases secretory capacity, causing 1.5-3 liters daily mucous diarrhea leading to severe electrolyte imbalance (hypokalemia, hyponatremia) and prerenal renal failure. CT enhancement derives from neovascular capillary network induced by dysplastic epithelium. T2 hyperintense villous projections on MRI reflect free fluid (mucin) accumulation between long papillary structures.
Wide-area covering, flat-spreading lesion on colonic mucosal surface, not thick but extensive — pathognomonic growth pattern for villous adenoma. Spreads like a carpet on the mucosal surface rather than forming a focal mass.
In CT portal venous phase, a broad-based, mucosal-spreading, contrast-enhancing 'carpet-like' lesion in rectum or sigmoid colon is observed. Lesion may cover the colonic wall circumferentially or semicircumferentially. Lobulated or papillary contour visible on surface.
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A [size] mm broad-based, mucosal-spreading, enhancing carpet-like lesion in the [rectum/sigmoid] is identified, consistent with villous adenoma.
On MRI T2-weighted sequences, villous projections show markedly hyperintense signal — mucinous fluid accumulating between villi produces long T2 signal. The 'frond-like' morphology is best evaluated on T2. Submucosal invasion depth is assessed from the relationship between T2 hypointense muscularis propria and the lesion.
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On MRI T2-weighted sequence, a carpet-like mucosal lesion with hyperintense villous projections in the [location] colon is identified.
On DWI, villous adenoma shows diffusion restriction and restriction degree correlates with dysplasia grade. ADC values are markedly decreased (<0.9 × 10⁻³ mm²/s) in high-grade dysplasia or invasive carcinoma foci. This feature makes DWI valuable for non-invasive dysplasia grade assessment.
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On DWI, the lesion demonstrates diffusion restriction with [focal/diffuse] signal decrease on ADC map — should be evaluated for dysplasia.
On non-contrast CT, low-density intraluminal material may be observed in rectal or colonic lumen due to mucin secretion of villous adenoma. Dense mucin accumulation may form 'mucin cap' on lesion surface.
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Low-density mucinous material accumulation on the lesion surface in the [rectum/colon] lumen is observed.
On transrectal US, a broad-based, heterogeneous echogenicity mucosal mass with papillary surface pattern is observed in the rectum. If muscularis propria is intact, non-invasive adenoma is considered. Submucosal invasion may appear as hypoechoic penetration.
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On transrectal US, a [size] mm broad-based mucosal mass with papillary surface pattern in the rectum with [intact/disrupted] muscularis propria is identified.
In arterial phase, villous adenoma shows early enhancement — dysplastic neovascular capillary network leads to arterial phase contrast uptake. Enhancement is more prominent than tubular adenomas.
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In arterial phase, the lesion shows early enhancement reflecting neovascular structure.
Criteria
Low-grade dysplasia, no invasion. Most villous adenomas in this category.
Distinct Features
Mild diffusion restriction on DWI. Endoscopic resection may be sufficient.
Criteria
High-grade dysplasia, basement membrane intact (no invasion). Carcinoma in situ.
Distinct Features
Prominent diffusion restriction on DWI. ADC <0.9 × 10⁻³ mm²/s. Surgical resection recommended.
Criteria
Basement membrane breached in dysplastic focus, submucosal invasion present.
Distinct Features
Focal wall thickening, submucosal invasion on CT/MRI. Most prominent restriction on DWI. Surgical resection mandatory.
Distinguishing Feature
Carcinoma wall invasion, irregular contour, LAP; villous adenoma mucosal-limited, carpet-like spread, muscularis propria intact
Distinguishing Feature
Tubular adenomatous polyp small, pedunculated, lobulated; villous adenoma large, sessile, carpet-like
Distinguishing Feature
Lipoma fat density (-80 to -120 HU), non-enhancing; villous adenoma soft tissue density, enhancing
Distinguishing Feature
UC diffuse continuous wall thickening, from rectum proximally; villous adenoma focal mucosal lesion, localized
Urgency
urgentManagement
surgicalBiopsy
NeededFollow-up
6-monthVillous adenoma is a premalignant lesion requiring mandatory complete excision and histopathological evaluation. Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) can be performed for small (<2 cm) lesions. Surgical resection preferred for large (>4 cm) or high-grade dysplasia-containing lesions. McKittrick-Wheelock syndrome requires emergency electrolyte replacement + surgical resection. Colonoscopic follow-up at 3-6 month intervals post-polypectomy — recurrence and metachronous lesion surveillance. All villous adenomas should be considered potentially premalignant due to 30-40% malignant transformation risk.
Villous adenomas carry the highest malignant transformation risk among all colorectal adenomas (up to 40%). Cancer risk increases with size. Requires complete endoscopic resection or surgery.