backup bowel tumor RADIOLOGY PRESENTATION .pptx

gargshivansh14 7 views 77 slides Oct 26, 2025
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About This Presentation

Bowel tumor


Slide Content

Small and LARGE BOWEL TUMORS Dr Arpit Garg JR Dept. of Radiodiagnosis AIIMS Bathinda

Small bowel tumors

IMAGING MODALITIES USG Barium Meal & Follow Through Conventional Enteroclysis Conventional CT abdomen with I/V Contrast CT Enteroclysis MR Enteroclysis PET Scan Endoscopy

Enteroclysis TECHNIQUE OF ENTEROCLYSIS: For CT/MR enteroclysis we usually give neutral contrast (water or methylcellulose). Low signal on T1-weighted images. High signal on T2-weighted images. HU values of fluid on CT.

T2W T1W with fatsat

Tumors of small bowel Tumors of the small bowel both benign and malignant are quite uncommon. It also lies between two areas of high cancer risk, i.e. the colon and the stomach yet only about 3–5% of all GI tumors and less than 2% of all gastrointestinal malignancies arise in the small bowel.

Tumors of small bowel Epithelial (Adenoma, Adenocarcinoma) Non epithelial/Mesenchymal (Lipoma, Liposarcoma, Haemangioma, GIST, Leiomyoma, Leiomyosarcoma) Lymphoid tissue (Lymphoma) Neurogenic (Neurofibroma, Schwannoma) Secondary tumors /metastasis NET(Carcinoid) Polyps

adenoma M/c benign tumor of small intestine. Histology can be tubular, villous or tubulovillis . Pedunculated/Sessile Barium Studies: Appear as smooth or lobulated lesion appearing as filing defect and pedicle may be seen in pedunculated lesion. On CT enteroclysis : Well defined soft tissue lesion with moderate enhancemet and clear surrounding fat planes. On MRI : T1W Fatsat Post contrast – Homogenously enhancing mass lesion T2W – Low signal intensity intraluminal masses They usually don’t cause upstream dilatation of bowel loops.

Image from a barium study shows a sessile intraluminal filling defect with a typical lobulated surface pattern (arrows).

Small bowel adenoma: Axial (A) and coronal (B) CT enteroclysis images reveal a sessile polypoid moderately enhancing mass lesion in the ileum (arrows) with normal surrounding fat planes suggestive of an adenoma.

Lipoma 15-20 percent of all small intestine tumors Most of them are submucosal. CT: Shows fat attenuation MRI: T1/T2 Hyperintense and get suppressed on fatsat images. Many times act as lead point for intussusception.

Hemangioma Rare Mostly arise from submucosal plane and grows intraluminal. Imaging: 1. CT Scan Pre-contrast : Iso- to hypoattenuating soft tissue lesion May contain phleboliths (small calcifications) – diagnostic clue Post-contrast (especially arterial phase): Strong early peripheral nodular enhancement with centripetal fill-in (similar to hepatic haemangiomas).

Hemangioma MRI Appearance T1-weighted (pre-contrast): Hypointense relative to muscle T2-weighted: Hyperintense lesion (due to blood-filled vascular spaces) May have internal septations or flow voids Post-contrast (Gadolinium-enhanced) : Early peripheral nodular enhancement Delayed fill-in toward center , mimicking liver hemangiomas No restriction on DWI (typically).

Polyposis syndromes involving small bowel Familial Adenomatous Polyposis (FAP) Gene involved : APC Inheritance : Autosomal dominant Small intestine tumors : Especially duodenal and periampullary adenomas → may progress to adenocarcinoma. Extra points : Hundreds to thousands of adenomatous polyps throughout colon and small intestine. Risk of duodenal cancer is the second leading cause of death in FAP patients. Surveillance : Upper GI endoscopy recommended every 1–3 years.

Polyposis syndromes involving small bowel 2. Peutz-Jeghers Syndrome (PJS) Gene involved : STK11 (LKB1), chromosome 19p13.3 Inheritance : Autosomal dominant Polyp type : Hamartomatous polyps, mainly in small intestine (especially jejunum) Cancer risk : Increased risk of GI (especially small bowel, pancreas, colon) and non-GI cancers (e.g., breast, ovary). Clinical clue : Mucocutaneous pigmentation (lips, oral mucosa, hands, feet) Complications : Intussusception due to large polyps

Coronal T2W MR enteroclysis images reveal multiple round to oval T2 iso to hypointense polyps in the jejunum. Jejuno -jejunal intussusception due to a polyp acting as a lead point is also well seen (arrow)

Polyposis syndromes involving small bowel 3. Juvenile Polyposis Syndrome (JPS) Gene involved : SMAD4 or BMPR1A Inheritance : Autosomal dominant Polyp type : Hamartomatous polyps; can be in small bowel Cancer risk : Increased risk of colorectal and gastric cancers; small bowel cancer less common but possible. Age group : Presents in childhood or adolescence.

Polyposis syndromes involving small bowel 4. Cowden Syndrome (PTEN Hamartoma Tumor Syndrome) Gene involved : PTEN (chromosome 10q23) Inheritance : Autosomal dominant Polyp type : Hamartomatous polyps throughout GI tract including small intestine Cancer risk : Breast, thyroid (follicular), endometrial, and sometimes GI malignancies. Other features : Trichilemmomas, oral papillomas , macrocephaly

Adenocarcinoma Feature Details Common symptoms Pain, weight loss, vomiting, anemia, obstruction, melena Best imaging tools CT enterography , MRI enterography , endoscopy Common site Duodenum > jejunum > ileum Complications Obstruction, perforation, metastasis

Imaging Features 1. CT Enterography / CT Abdomen (with contrast): Irregular asymmetric wall thickening Apple-core lesion (constrictive, circumferential mass) Polypoid or exophytic masses Shouldering margins at transition zones Proximal dilatation (sign of obstruction) Enlarged mesenteric lymph nodes 2. MRI Enterography : Better soft tissue contrast

Imaging Features 3. Barium Follow-Through (older technique): Annular constricting lesions Filling defects Displaced or narrowed loops 4. Endoscopy (especially for duodenal tumors ): Direct visualization and biopsy Capsule endoscopy For deeper small bowel 5. PET-CT: Useful in staging and detecting distant metastases

The images show a short obstructing circular mass in the jejunum (yellow arrow) with enlarged lymph node (red arrow). This proved to be an adenocarcinoma.

Post-contrast T1W-image with fatsat (left) and T2W-image (right) show an obstructing mass in the jejunum with shouldering (arrow). There is prestenotic dilatation.

Lymphoma Small bowel is second most common site of GI lymphoma (after stomach) Most commonly involves ileum > jejunum > duodenum Usually Non-Hodgkin B-cell lymphomas. Can be primary (arising in bowel) or secondary from systemic disease.

CT Features Feature Description Wall thickening Long segment, symmetric or asymmetric, homogeneous Aneurysmal dilatation Classic feature; tumor infiltrates nerves → loss of muscular tone Polypoid mass May protrude into lumen, sometimes lead to intussusception Soft tissue mass Bulky, exophytic or circumferential Minimal obstruction Despite large mass, obstruction is uncommon Lymphadenopathy Mesenteric and retroperitoneal nodes; may be bulky Enhancement Mild to moderate; typically homogeneous

MRI Features Sequence Appearance T1-weighted Hypointense mass T2-weighted Mildly hyperintense Post-contrast Homogeneous moderate enhancement DWI Restricted diffusion

Morphologic Type Description / Imaging Features Polypoidal Form - Discrete intraluminal mass- May be single or multiple- Can cause intussusception Endoexoenteric Mass - Large mass involving all layers- Both luminal and exophytic extension- May displace loops Mesenteric Invasive Type - Infiltration into mesentery- Soft tissue strands into surrounding fat- Bulky nodes Infiltrative / Wall Thickening - Long segment homogeneous thickening- May cause aneurysmal dilatation - Minimal obstruction Ulcerative / Necrotic Type - Central necrosis or ulceration- Cavitation or fistula formation Stenosing / Annular Form - Concentric narrowing with short segment involvement- May resemble carcinoma

There is irregular wall thickening of the terminal ileum with aneurysmatic dilatation.

Homogenously enhancing lesion with avid FDG uptake

Reversed fold pattern indicating celiac disease Ileal-ileal intussusception (yellow arrow), in a patient with multifocal small bowel lymphoma. Mesenteric lymphadenopathy (red arrows).

Carcinoid Tumors Well-differentiated neuroendocrine tumor (NET), often slow-growing, commonly found in the GI tract (especially ileum and appendix) and lungs. May produce hormones → carcinoid syndrome if metastatic (esp. to liver). Common Locations GI Tract: Ileum > appendix > rectum > stomach Lung: Central bronchial carcinoid Others: Pancreas, ovary, thymus

Carcinoid Tumors Small Bowel Carcinoid (most common GI site) Primary tumor : Often small, hard to see; best seen with CT enterography or MRI Mesenteric mass : Classic finding: Spiculated mass with desmoplastic reaction Causes retraction , angulation of adjacent bowel loops May contain calcifications Bowel wall thickening or narrowing from fibrosis

Carcinoid Tumors 2. Liver Metastases Hypervascular lesions on contrast-enhanced imaging: CT (arterial phase) : Bright enhancing lesions MRI : T1 hypointense T2 hyperintense Arterial enhancement Functional Imaging: Ga68 Dotatate PET/CT- Lights up somatostatin receptor-positive tumors (most sensitive).

Small intraluminal mass in the ileum (yellow arrow). Associated spiculated mesenteric mass with adjacent desmoplastic reaction in small bowel carcinoid.

A typical carcinoid presenting as a large mesenteric mass with desmoplastic reaction and retraction of adjacent small bowel loops with wall thickening (arrows).

Hyper vascular enhancement pattern in the late arterial phase.

Metastasis to small bowel Uncommon , but important to recognize. Usually via hematogenous spread , peritoneal seeding, or direct invasion Can present with obstruction, bleeding, perforation , or intussusception

Metastasis to small bowel Primary Tumor Route Notes Melanoma Hematogenous Most common; may present as multiple polypoid masses Lung carcinoma Hematogenous Especially small cell and adenocarcinoma Breast carcinoma Hematogenous Infiltrative or nodular pattern Renal cell carcinoma Hematogenous Hypervascular metastasis Gastric / colon carcinoma Direct or peritoneal Often late-stage, serosal deposits Ovarian / pancreatic Peritoneal seeding Serosal involvement and implants

Metastasis to small bowel Pattern Description Polypoid lesions Discrete, nodular, endoluminal masses → can lead to intussusception Infiltrative thickening May mimic primary small bowel adenocarcinoma or lymphoma Serosal implants Plaque-like masses along bowel surface; from peritoneal spread Hypervascular masses Especially in melanoma or RCC metastases (avid enhancement) Ulceration / cavitation May occur in necrotic metastases (e.g., lung) Bowel obstruction Can be caused by mass effect or intussusception

Desmoid Desmoid is a rare, benign, locally aggressive mass composed of fibrous tissue. It is the most common primary tumor of the mesentery and can mimic a malignant bowel- or mesenteric neoplasm. Most desmoids are sporadic tumors , but some occur in the setting of Gardner syndrome. There is often a history of previous abdominal surgery. Desmoid tumors do not metastasize, but do tend to recur. The high recurrence rate favors the use of nonsurgical therapy. Mesenteric desmoids usually show minimal enhancement. Small bowel or mesenteric vessels can be displaced or encased. Because these tumors can be very hard, percutaneous biopsy can be challenging.

Large well defined enhancing heterogenous lesion (proven case of desmoid)

Large bowel tumors

Large bowel tumors Epithelial lesions(Adenoma, Adenocarcinoma) Mesenchymal(Lipoma, Leiomyoma, GIST, Leiomyosarcoma) Polyps(Hyperplastic and hamartomatous ) Others(Lymphoma, Metastasis)

Adenocarcinoma 3rd most common cancer worldwide 2nd leading cause of cancer-related death. Incidence is higher in developed countries (e.g., U.S., Europe, Australia) Age: Risk increases sharply after age 50 Median age at diagnosis: ~66 years Sex: Slightly more common in men than women

Risk Factors Modifiable Risk Factor Details Diet High in red and processed meats; low in fiber , fruits, and vegetables Physical inactivity Sedentary lifestyle increases risk Obesity Especially abdominal obesity Alcohol use Excessive intake linked to increased risk Smoking Long-term tobacco use is associated with CRC

Risk Factors Factor Details Age Risk rises sharply after age 50 Personal history of CRC or adenomatous polyps Increased recurrence risk Inflammatory bowel disease (IBD) Especially ulcerative colitis and Crohn's disease (long-standing) Family history of CRC Especially in first-degree relatives Genetic syndromes Lynch syndrome (HNPCC) – high lifetime risk Familial adenomatous polyposis (FAP) – nearly 100% risk if untreated

Polyp Type Histology Malignant Potential Features/Notes Adenomatous Polyps (Adenomas) Dysplastic epithelium (tubular, villous, tubulovillous) Premalignant (risk varies) Most common precursors to CRC; villous have highest risk; size >1cm increases risk - Tubular adenoma Tubular glands Low to moderate Most common, usually <1 cm, lower risk - Villous adenoma Villous (finger-like) High Larger, higher malignant potential - Tubulovillous adenoma Mixed Intermediate Features between tubular and villous Serrated Polyps Saw-tooth glandular pattern Variable Includes hyperplastic polyps (usually benign), sessile serrated adenomas (premalignant) - Hyperplastic polyp No dysplasia Benign Common, usually left colon - Sessile serrated adenoma (SSA) Dysplasia may develop Premalignant Right colon, associated with MSI pathway Inflammatory Polyps Granulation tissue None Seen in IBD, no malignant potential Hamartomatous Polyps Disorganized but benign tissue Low/variable Seen in syndromes ( Peutz-Jeghers ), risk depends on syndrome

Pathogenesis Colorectal carcinoma (CRC) develops through a multistep process involving genetic mutations , epigenetic changes , and environmental/lifestyle influences , progressing from normal mucosa → adenoma → carcinoma .

Pathogenesis Chromosomal Instability (CIN) – Most common (~70-80%) Stepwise mutation: APC → KRAS → TP53 Associated with classic adenoma-carcinoma sequence Microsatellite Instability (MSI) – ~15% Due to defective DNA mismatch repair Seen in Lynch syndrome and some sporadic cases CpG Island Methylator Phenotype (CIMP) – ~15-20% Epigenetic silencing of tumor suppressor genes via methylation Often overlaps with BRAF mutation and serrated polyps

Clinical features General Symptoms: Change in bowel habits ( diarrhea , constipation, or alternating) Blood in stool (bright red or occult) Abdominal pain or discomfort Unexplained weight loss Fatigue, weakness (due to anemia ) Tenesmus (feeling of incomplete evacuation)

Clinical features Location Common Features Right-sided (cecum, ascending colon) Occult bleeding, iron-deficiency anemia , vague abdominal pain, weight loss Left-sided (descending colon, sigmoid) Change in bowel habits , blood-streaked stool, crampy pain, obstruction more common Rectal cancer Rectal bleeding, tenesmus , sensation of mass, pain on defecation

Category Stage Description Primary Tumor (T) Tx Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1 Tumor invades submucosa T2 Tumor invades muscularis propria T3 Tumor invades through muscularis propria into subserosa or non- peritonealized pericolic/perirectal tissues T4a Tumor penetrates visceral peritoneum T4b Tumor invades or adheres to adjacent organs or structures Regional Lymph Nodes (N) Nx Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis N1a Metastasis in 1 regional lymph node N1b Metastasis in 2–3 regional lymph nodes N1c Tumor deposits in subserosa or non- peritonealized tissue without regional nodal metastasis N2a Metastasis in 4–6 regional lymph nodes N2b Metastasis in ≥7 regional lymph nodes Distant Metastasis (M) Mx Distant metastasis cannot be assessed M0 No distant metastasis M1a Metastasis confined to one organ (e.g., liver, lung, ovary, or non-regional lymph node), without peritoneal metastases M1b Metastases to more than one organ , but without peritoneal metastases M1c Metastases to the peritoneum , with or without metastases in other organs

Staging

Screeening Should commence at 50 yrs of age: 1. Yearly fecal occult blood test (FOBT) or fecal immunochemical test (FIT) 2. Flexible sigmoidoscopy every 5 years 3. Yearly FOBT or FIT, plus flexible sigmoidoscopy every 5 years 4. Double contrast barium enema every 5 years 5. Colonoscopy every 10 years.

imaging Barium Enema CT(Virtual colonoscopy could be performed) MRI(Used in rectal cancer) Endorectal USG Colonoscopy

Barium enema Double contrast barium enema use to be performed. Not used routinely for colorectal cancer now days Detects mucosal irregularities, masses, polyps, and stricturing lesions. Classic finding: “ Apple-core ” lesion indicating an annular constricting tumor .

CT Condition CT Scan Findings Notes Colorectal Cancer - Irregular circumferential bowel wall thickening (“apple-core” or “napkin-ring” lesion) Classic imaging sign - Focal or diffuse asymmetric wall thickening(Initial T stages not well differentiated of CT) Helps differentiate tumor from inflammatory thickening - Loss of normal bowel wall layers Tumor infiltration - Pericolonic fat stranding (inflammation or tumor invasion) Suggests local spread - Enlarged regional lymph nodes Suggests nodal metastasis - Distant metastases (commonly liver, lung, peritoneum) Helps in staging and treatment planning - Signs of complications: bowel obstruction, perforation May require urgent management EMVI( Extramural Vascular Invasion) Direct invasion of a blood vessel (usually a vein) by a tumour.

Abdominal Ct showing an apple-core lesion of the transverse colon (arrow) in an 86 years-old male patient .

Virtual colonoscopy Bowel Preparation Clear liquid diet for 24 hours before the exam Laxatives: Typically a polyethylene glycol (PEG) solution or bisacodyl is used to cleanse the colon. Day of Exam Nothing by mouth (NPO) except necessary medications. Colon Insufflation During the exam, the colon is inflated with carbon dioxide or room air via a small rectal tube. This distension is necessary to fully visualize the colon wall.

MRI It is gold standard for local staging of rectal cancer. In T1W SE images, rectosigmoid tumors are seen as wall thickening with signal intensity similar to or higher than skeletal muscles (long T1). Perirectal fat has short T1 and hence appears bright on T1WI and rectal air has no signal, thus these tumors are very well delineated on T1W images and their extension beyond the colonic wall is well visualized. The different layers comprising the bowel wall on gadolinium-enhanced T1-weighted fat- suppressed spin echo images are the high-signal intensity mucosa, low-signal intensity muscularis mucosa and lamina propria, high-signal intensity submucosa and low-signal intensity muscularis propria.

Feature MRI Finding Tumor (T) Stage T1–T2 Tumor confined to submucosa or muscularis propria; preserved outer muscular layer T3 Tumor extends through muscularis propria into mesorectal fat T4a Tumor invades peritoneal reflection T4b Tumor invades adjacent organs or structures (e.g., prostate, bladder, uterus) Circumferential Resection Margin (CRM) Measured as distance between tumor and mesorectal fascia Involved CRM ≤1 mm between tumor and mesorectal fascia → high risk of incomplete resection Clear CRM >1 mm → favorable for surgical resection Nodal (N) Involvement Suspicious lymph nodes Round shape, irregular border, heterogeneous signal, >5 mm short axis Nodal location Mesorectal, internal iliac, or superior rectal nodes commonly involved Extramural Vascular Invasion (EMVI) Tumor signal extending into adjacent blood vessels (irregular, expanded veins) Positive EMVI Associated with higher recurrence and poor prognosis Distance from Anal Verge MRI can measure exact distance (important for sphincter-saving surgery decisions) Response to Neoadjuvant Therapy Reduction in tumor size, fibrosis, and signal intensity suggest downstaging

Solid and Mucinous The distinction between solid and mucinous tumor types is relevant because mucinous adenocarcinomas have a poorer prognosis and typically show a poorer response to neoadjuvant treatment.  Mucinous tumors show distinct bright signal on T2-weighted MRI compared to the more intermediate signal of solid type tumors .

A semicircular rectum tumor with invasion into the mesorectum from approximately 1 to 4 o’clock. It does not grow within 1mm of the mesorectal fascia. Hypointense line of muscularis propria is breached.

EMVI Extramural vascular invasion is a risk factor for recurrent disease, metastases and impaired overall survival. A n EMVI+ tumor with tumor signal extending into an adjacent vessel structure, expanding and disrupting the vessel contour.    

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