Radiology - all small bowel tumours benign and malignant and tumour like lesions, ct and MRI enterography techniques and acquiring protocol, ct enteroclysis also , all lesion pathognomic imaging findings and pathophysiology associated syndromes and radiology aspect of treatment. 1 adenoma 2 FAP 3 polyp and it's types 4 peutz jegher syndrome 5 lipoma 6 benign and malignant gist 7 lieomyoma and liomyosarcoma 8 adenocarcinoma, 9 lymphoma, 10 carcinoma 11 mets , choi criteria,recist criteria includes differentiating features of each pathology form other with close dd 11 diverticulitis mackels diverticulitis , morphological forms of lymphoma
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Here is a complete, structured review covering everything you asked. All content is drawn from Grainger & Allison's Diagnostic Radiology 7e, Yamada's Textbook of Gastroenterology 7e, Sabiston Textbook of Surgery, and Fischer's Mastery of Surgery 8e.
Small Bowel Tumours - Complete Radiology Review
IMAGING TECHNIQUES
CT Enterography (CTE)
CTE is the primary modality for SB tumour evaluation. The key principle is adequate luminal distension with neutral oral contrast - positive agents would mask wall enhancement and small lesions.
Protocol:
- Oral preparation: ~1500 mL neutral agent (VoLumen 0.1% barium, methylcellulose, or PEG solution) over 45-60 min; additional water immediately before scanning
- IV contrast: Weight-based iodinated contrast, 100-150 mL at 3-4 mL/s
- Phases:
- Single enterographic phase (~50-70 s post-injection): standard
- Biphasic (arterial ~25-35 s + enterographic): detects hypervascular tumours (carcinoid/NET), vascular malformations
- Triphasic (arterial + enterographic + delayed ~5 min): maximal sensitivity for subtle mural enhancement
- Reconstructions: Thin collimation (0.5-1 mm), axial + coronal/sagittal MPR, MIP for vessels
- Spasmolytic agents: IV glucagon or buscopan reduce peristaltic artefact; less essential with modern rapid-acquisition scanners
Strength: Superb for eccentric neoplasms, extraluminal extension, lymphadenopathy, mesenteric disease, liver metastases. CT enterography and especially CT enteroclysis are proven effective tools for SB tumour detection and characterisation.
CT Enteroclysis
Achieves higher and more uniform luminal distension than CTE via nasojejunal tube infusion.
Protocol:
- Nasojejunal tube under fluoroscopic guidance (tip past duodenojejunal flexure)
- Infuse neutral agent (0.5% methylcellulose, 1.5-2 L) at 80-120 mL/min via pump; or CO2/air for double-contrast technique
- IV contrast + thin-section CT acquisition follows as above
- Advantage: Superior uniform distension, better for flat/subtle mucosal lesions, strictures, small flat polyps - tumour nodules <5 mm may be missed even on MRE
- Disadvantage: More invasive, radiation dose (relevant for FAP/Crohn's surveillance with repeated imaging)
MR Enterography (MRE)
No ionising radiation - preferred for younger patients, FAP surveillance, Crohn's disease, pregnancy.
Protocol:
- Same oral preparation as CTE
- Spasmolytics: IV buscopan or glucagon
- Sequences:
- Coronal bSSFP/True FISP: rapid, bright-lumen technique for bowel wall and lumen
- Coronal T2 HASTE: morphology, wall thickness
- Coronal fat-suppressed T2 / STIR: oedema, active inflammation
- Pre + post-Gd T1 FS (VIBE/THRIVE): arterial + portal phase enhancement
- DWI (b=50, 400, 800 s/mm²): restricted diffusion indicates cellularity - useful in lymphoma, metastases
- In-phase/opposed-phase T1: confirms fat in lipoma (signal dropout on opposed-phase)
- Advantage over CT: Characterises lipoma definitively; detects cystic transformation of GIST liver metastases earlier; no radiation for serial follow-up
EPIDEMIOLOGY
Primary SB neoplasms = 3-6% of all GI neoplasms, <2% of all malignant tumours (despite SB comprising 75% of GI length). Two-thirds of SB neoplasms are malignant. Mean diagnosis delay: ~3 years benign, ~2 years malignant.
Current frequency (malignant): Carcinoid 44% > Adenocarcinoma > Lymphoma 20% > GIST
Regional predilection: Adenocarcinoma: duodenum/proximal jejunum | Carcinoid: distal ileum | Lymphoma: distal/terminal ileum (except IPSID: proximal) | Lipoma: ileum
BENIGN TUMOURS AND TUMOUR-LIKE LESIONS
1. Adenoma
Pathophysiology: Neoplastic glandular epithelial tumour. Tubular (most common, throughout SB); villous (periampullary duodenum, highest malignant potential). Villous adenomas carry significant cancer risk.
CT/MRI:
- Tubular: pedunculated or sessile polypoid intraluminal mass, soft tissue density, mild enhancement; can act as lead point for intussusception
- Villous adenoma (typically >3 cm): broad-based, lobulated "cauliflower-like" filling defect with multiple radiolucent striations and frond-like surface projections (best demonstrated on enteroclysis with water contrast); mild-moderate enhancement
- No calcification or extraluminal extension
DD from adenocarcinoma: Adenoma lacks shouldered/overhanging margins, no luminal narrowing/obstruction, no lymphadenopathy.
2. Familial Adenomatous Polyposis (FAP)
Pathophysiology: Autosomal dominant APC gene mutation (chromosome 5q21). Hallmark: >100 colonic adenomatous polyps. Extracolonic features: SB adenomas/periampullary carcinoma (90%), desmoid tumours (15-20%), osteomas, epidermoid cysts, CHRPE. Duodenal/ampullary carcinoma is the leading cause of death in post-colectomy FAP patients.
CT/MRI:
- Multiple duodenal/periampullary polyps (subtle on routine CT; best detected on CTE or CT enteroclysis)
- Spigelman scoring (I-IV) based on polyp number, size, histology and dysplasia guides surveillance
- Desmoid tumours: mesenteric or abdominal wall soft-tissue masses, low T1/intermediate T2 on MRI, can mimic carcinoid desmoplasia but lack calcification and stellate pattern
- No universally endorsed protocol for SB beyond the duodenum; CTE, push enteroscopy, or capsule endoscopy used if anaemia, protein-losing enteropathy, or SB symptoms develop
3. Polyp Types
| Type | Origin | Location | Malignant Potential |
|---|---|---|---|
| Tubular adenoma | Neoplastic | Duodenum > proximal SB | Low-moderate |
| Villous adenoma | Neoplastic | Periampullary duodenum | High |
| Hamartoma (Peutz-Jeghers) | Developmental | Jejunum >> ileum | Low intrinsically; syndrome = elevated cancer risk |
| Hyperplastic | Reactive | Rare in SB | Very low |
| Inflammatory pseudopolyp | IBD-related | Terminal ileum | Low |
| Lymphoid polyp | Reactive lymphoid hyperplasia | Terminal ileum | Very low |
| Juvenile polyp | Hamartoma | SB in juvenile polyposis | Moderate syndrome risk |
CT common to all polyps: Intraluminal filling defects. Pedunculated polyps can act as intussusception lead points - CT shows "target sign" (concentric rings of fat, soft tissue, bowel wall). Hamartomatous and adenomatous polyps are indistinguishable on CT/MRI.
4. Peutz-Jeghers Syndrome (PJS)
Pathophysiology: Autosomal dominant STK11/LKB1 mutation (chromosome 19p13.3). Hamartomatous (not adenomatous) polyps throughout GI tract, most numerous in jejunum. Mucocutaneous hyperpigmentation: lips, buccal mucosa, perioral skin. Despite hamartomatous nature, carries ~13x elevated risk of GI adenocarcinoma and elevated extra-GI cancer risk (breast, pancreas, ovary, cervix, testis). Cancer risk thought to arise from adenomatous foci within/adjacent to hamartomas.
CT/MRI:
- Multiple lobulated intraluminal polyps throughout SB; variable and often large size (>3 cm)
- Enteroclysis: smooth lobulated filling defects with a "tree-trunk" branching stalk pattern
- CTE/MRE: lobulated soft-tissue filling defects, indistinguishable from adenomas
- Most important complication: intussusception - CT: "target sign" or sausage-shaped mass with mesenteric fat and vessels dragged in; usually transient but can be sustained/obstructing
- Also shows gastric and colonic polyps
- Surveillance: CTE or MRE for SB; MRCP/EUS for pancreatic cancer surveillance
5. Lipoma
Pathophysiology: Benign submucosal tumour of adipocytes. Most common in ileum. Third most common benign SB neoplasm. Usually asymptomatic; large lesions (>4 cm) can cause obstruction, haemorrhage, intussusception.
CT - PATHOGNOMONIC:
- Smooth, ovoid, well-defined submucosal/intramural mass
- Fat attenuation: -80 to -120 HU (unenhanced CT) - diagnostic
- No internal enhancement
- "Squeeze sign" on fluoroscopy: deformation with peristalsis/compression
MRI - also pathognomonic:
- High signal on T1 and T2
- Signal dropout on fat-saturated T2/T1 FS and STIR - confirms fat
- Chemical shift artefact (signal dropout) on opposed-phase T1 - confirms intracytoplasmic fat
- No restricted diffusion on DWI
DD: Leiomyoma (solid, soft tissue density, no fat signal); GIST (enhancing, no fat); duplication cyst (fluid density, -10 to +20 HU, does not dropout on fat suppression).
MALIGNANT TUMOURS
6. GIST (Benign and Malignant)
Pathophysiology: Mesenchymal tumours of the interstitial cells of Cajal (bowel pacemaker cells), arising within muscularis propria. Hallmark: KIT (CD117) positivity by IHC - distinguishes GIST from leiomyoma, leiomyosarcoma, schwannoma. ~60% gastric; SB GISTs arise mostly in jejunum/ileum. KIT mutations in ~85% (exons 9, 11, 13, 17); PDGFRA mutations in ~10% (D842V = imatinib-resistant); wild-type in ~5%.
Benign vs. Malignant - Imaging Features:
| Feature | Low-risk (Benign) | High-risk (Malignant) |
|---|---|---|
| Size | <2 cm | >5 cm |
| Margins | Smooth | Irregular, lobulated |
| Enhancement | Homogeneous | Heterogeneous |
| Necrosis/cystic | Absent | Central necrosis - common |
| Calcification | Absent | Coarse, irregular |
| Ulceration | Uncommon | Common (central) |
| Growth direction | Intramural | Exophytic (large lesions) |
| Metastases | None | Liver (cystic/hypodense), peritoneum |
CT findings:
- Small lesions: smooth, rounded, homogeneous enhancing intramural mass (40-60 HU pre-contrast, moderate post-contrast enhancement)
- Large lesions: exophytic (most common pattern), heterogeneous, central necrosis/haemorrhage, fistulation, coarse calcification; can grow to >30 cm
- Site of origin can be unclear for large exophytic masses (may mimic adrenal, pancreas, colon) - MPR/3D reconstructions needed
- Liver metastases: Hypodense/cystic lesions; become progressively more cystic under imatinib (do NOT interpret as progression)
- Peritoneal metastases: nodular implants
GIST vs. Leiomyoma: Radiographically indistinguishable; CD117 (IHC) is the gold standard. Large size, necrosis, and exophytic growth favour GIST.
7. Leiomyoma and Leiomyosarcoma
Pathophysiology: True smooth muscle tumours (SMA+, desmin+, CD117-). Leiomyomas are benign; leiomyosarcomas are aggressive with haematogenous metastases (liver, lungs; no lymph node spread).
Leiomyoma - CT:
- Well-defined, smooth, homogeneously enhancing submucosal mass; endoluminal, extraluminal or mixed growth
- Soft tissue density, no necrosis/calcification in small lesions; mild-moderate enhancement
- No lymphadenopathy
Leiomyosarcoma - CT:
- Typically large (>5 cm) at presentation
- Heterogeneous with central necrosis, exophytic growth
- Liver and lung metastases (no lymph node metastases - key differentiating feature from lymphoma and adenocarcinoma)
- Cannot be distinguished from malignant GIST on CT alone - CD117-negative IHC is required
8. Adenocarcinoma
Pathophysiology: Most common primary SB malignancy of duodenum and proximal jejunum. Associated with coeliac disease, Crohn disease (terminal ileum), FAP, Lynch syndrome (HNPCC), immunodeficiency. Aggressive, chemoresistant.
CT - PATHOGNOMONIC pattern: "annular-constricting" lesion:
- Circumferential wall thickening with irregular luminal narrowing
- Abrupt "overhanging"/"shouldered" margins - unlike the gradual tapering of Crohn stricture
- Mild-moderate contrast enhancement
- Proximal bowel obstruction (common - predominantly radial growth)
- Mucosal ulceration (not always visible on CT)
- Mesenteric infiltration in advanced disease
- Lymphadenopathy in ~50%
- Less commonly: small polypoid intraluminal mass (early stage)
Close DD:
- Lymphoma: Greater wall thickening; bulky distant LAP; aneurysmal dilatation (not obstruction); homogeneous enhancement; "soft" tumour
- Crohn stricture: Gradual tapering; skip lesions; comb sign; history of IBD
- Carcinoid: Ileal location; desmoplastic mesenteric mass; avid arterial-phase enhancement; calcification
9. Lymphoma
Pathophysiology: Most common GI site of extranodal lymphoma. Primary SB lymphoma criteria: no peripheral/mediastinal LAP, no hepatic/splenic involvement, normal WBC differential, predominantly GI disease. Predisposing conditions: coeliac disease (EATL - enteropathy-associated T-cell lymphoma), Crohn disease, HIV/AIDS, IPSID (Mediterranean lymphoma, involves proximal SB/duodenum/jejunum). Secondary GI involvement in ~10% limited-stage NHL, up to 60% advanced NHL.
4 Morphological Forms on Imaging:
| Pattern | CT Appearance | Key Notes |
|---|---|---|
| Multinodular | Multiple discrete nodules along SB | Multifocal involvement distinguishes from adenocarcinoma and carcinoid |
| Dominant mass | Single large mass; often causes intussusception as lead point | May present as acute SBO |
| Infiltrating | Short-segment wall thickening, fold destruction, occasional shouldering | Most common pattern |
| Exophytic | Extraluminal mass ± ulceration | Mimics GIST |
| Aneurysmal dilatation | Segmental paradoxical luminal widening | PATHOGNOMONIC of lymphoma - lymphomatous invasion of muscularis and neural plexuses destroys peristaltic function |
Additional CT features:
- Homogeneous low-attenuation enhancement (relative to muscle) - more uniform than adenocarcinoma
- Bulky lymphadenopathy, often confluent forming the "sandwich sign" - mesenteric lymphomatous tissue encases mesenteric vessels and bowel loops between two confluent nodal masses
- Lymph nodes may show low-attenuation centres (necrosis in high-grade)
AIDS-related lymphoma patterns:
- Homogeneous circumferential wall thickening (single or multiple segments)
- OR single/multiple cavitary lesions (large hollow necrotic masses)
- Otherwise similar morphology and distribution to non-AIDS lymphoma
Close DD vs. adenocarcinoma:
- Lymphoma: bulky distant LAP, aneurysmal dilatation, no obstruction, homogeneous enhancement, "soft" tumour
- Adenocarcinoma: shouldered margins, obstruction common, moderate enhancement, local mesenteric invasion but less distant LAP
10. Carcinoid / NET
Pathophysiology: Now the most common malignant SB tumour (44%). Arises from enterochromaffin cells (Kulchitsky cells) in the crypts of Lieberkühn. Secrete serotonin, histamine, kallikrein - carcinoid syndrome (flushing, diarrhoea, wheezing, palpitations) occurs only when liver metastases bypass hepatic clearance. 30% are multicentric. Desmoplastic reaction in mesentery is driven by serotonin/TGF-β. Metastatic risk: ~80% lymph node mets, ~50% liver mets for primaries >2 cm.
CT findings (biphasic protocol is ideal):
- Primary tumour: Small (<2 cm), submucosal, avidly enhancing plaque-like intramural nodule in distal ileum - often occult; seen as asymmetric mural thickening; 30% are multicentric so the entire bowel must be scrutinised
- Mesenteric mass (PATHOGNOMONIC): Discrete mesenteric soft-tissue mass with dystrophic calcification (up to 70%); radiating spiculations/strands in the perimeteric fat - "spoke-wheel" or stellate desmoplastic pattern; kinking of adjacent bowel loops; vascular encasement
- Liver metastases: Hypervascular (best on arterial phase), ring-like peripheral enhancement; can calcify
- 68Ga-DOTA-TATE PET/CT: Now preferred over octreotide scintigraphy; somatostatin receptor-positive tumours show avid uptake; combined with enterography because of physiological gut uptake
Close DD vs. retractile mesenteritis: Both show a spiculated calcified mesenteric mass - virtually indistinguishable on CT; clinical context (carcinoid syndrome, urinary 5-HIAA, CgA) and 68Ga-DOTA-TATE PET are differentiating tools.
11. Metastases
Pathophysiology: Two routes - haematogenous and peritoneal/transcoelomic.
Haematogenous (common primaries: melanoma, Kaposi sarcoma, breast, lung, renal):
- CT: discrete eccentric masses from the bowel wall; characteristic "bull's-eye" or "target lesion" - central ulceration within a submucosal mass (especially melanoma)
- Melanoma: hypervascular, often multiple, can cavitate
Peritoneal/transcoelomic (common primaries: ovarian, colon, breast, lung, gastric):
- CT: tethering and serosal thickening of bowel loops; clumped/clustered bowel; mesenteric nodularity; omental caking; serosal implants; ascites
- Ovarian metastases: large serosal masses at mesenteric border causing mass effect on adjacent loops
- Bowel loops may be normal calibre but "tethered" - simulates SBO symptomatically without frank obstruction
- MRI DWI: restricted diffusion from dense peritoneal deposits; better than CT for small implants <5 mm
RESPONSE ASSESSMENT CRITERIA
RECIST 1.1
Designed for standard cytotoxic therapies. Based purely on unidimensional size.
- Measurable lesion: ≥10 mm on CT
- Target lesions: up to 5 (max 2 per organ)
- CR: All target lesions disappear
- PR: ≥30% decrease in sum of longest diameters
- SD: Neither PR nor PD criteria met
- PD: ≥20% increase AND ≥5 mm absolute increase; or new lesions
Limitation for GIST: GIST liver metastases under imatinib become cystic/hypodense (they enlarge while becoming less viable). RECIST would misclassify this as stable or progressive disease.
Choi Criteria (GIST on TKI Therapy)
Better correlates with disease-specific survival and PFS than RECIST.
Combines size + CT attenuation (density):
- Response: ≥10% decrease in longest diameter OR ≥15% decrease in CT attenuation (HU)
- PD: ≥10% increase in size AND failure to meet response criteria; OR new lesions; OR new intratumoral nodule within a cystic mass
Rationale: Imatinib causes myxoid degeneration and necrosis - responding tumours become less dense (more cystic/hypodense) even if maintaining size. Falling HU values = "metabolic switch-off" = surrogate of pathological response. Monitoring: CT or MRI every 8-12 weeks.
PET/CT (FDG): Detects early response within days (before anatomical changes) and detects secondary resistance ("nodule within a mass sign" - focal FDG-avid viable nodule within a cystic responding lesion).
DIVERTICULITIS AND MECKEL'S DIVERTICULUM
Diverticulitis
Jejunal diverticulitis: Acquired diverticula on the mesenteric border of the jejunum (at vessel entry points).
CT: Air-fluid-filled diverticulum surrounded by acute inflammatory fat stranding; adjacent jejunal wall thickening and oedema; peritoneal free gas/fluid if perforated; abscess as complication. Must exclude appendicitis, Meckel's, perforated tumour, Crohn disease.
Meckel's Diverticulum and Meckel's Diverticulitis
Anatomy/Pathophysiology: Failure of the omphalomesenteric (vitello-intestinal) duct to close. "Rule of 2s": 2% population, 2 feet (60 cm) from ileocaecal valve, 2 inches long, 2 types of ectopic mucosa (gastric most common, pancreatic), 2:1 male preponderance, presents in first 2 years. Located on the antimesenteric border of the ileum. Ectopic gastric mucosa: 20% of adults, 95% of children presenting with bleeding.
Complications: Bleeding, ulceration, perforation, diverticulitis, intussusception, internal hernia, volvulus, adhesive SBO.
Imaging by modality:
-
Tc-99m Pertechnetate Scintigraphy (Meckel's scan):
- Detects ectopic gastric mucosa as focal tracer uptake in right lower quadrant (appears simultaneously with stomach)
- Most accurate in paediatric age group; less accurate in adults
- Pentagastrin or H2-blocker pretreatment enhances sensitivity
-
CT Enteroclysis:
- Blind-ending sac arising from antimesenteric border of ileum - key localising feature
- Triadiate pattern of mucosal folds at the base of the diverticulum
- Inverted Meckel's = polypoid filling defect (can cause intussusception)
-
CT in Meckel's Diverticulitis:
- Thickened, homogeneously enhancing diverticular wall with adjacent fat stranding
- Infrequently: intraluminal endolith (calcified vitelline remnant)
- Complications: abscess, perforation (free gas/fluid), SBO
- Normal appendix must be identified to exclude appendicitis
-
Angiography:
- Persistent vitelline artery is the PATHOGNOMONIC angiographic sign in chronic GI bleeding from Meckel's diverticulum
DIFFERENTIAL DIAGNOSIS MASTER TABLE
| Entity | Location | CT Key Feature | Pathognomonic Sign | Obstruction | LAP |
|---|---|---|---|---|---|
| Lipoma | Ileum | Fat density (-80 to -120 HU) | Fat attenuation; MRI signal dropout on fat sat | Rare | No |
| Leiomyoma | Any | Homogeneous soft tissue, no necrosis | CD117 negative (IHC) | Rare | No |
| Villous adenoma | Duodenum | Cauliflower frond-like filling defect | Frond-like projections on enteroclysis | No | No |
| PJS polyp | Jejunum >> | Multiple lobulated polyps | Intussusception; mucocutaneous pigmentation | Intussusception | No |
| Adenocarcinoma | Duodenum/jejunum | Annular constricting, shouldered margins | Abrupt shouldered margins + obstruction | Common | Yes ~50% |
| Lymphoma | Ileum | Homogeneous wall thickening, bulky LAP | Aneurysmal dilatation; sandwich sign | Rare | Yes (bulky, distant) |
| GIST | Jejunum/ileum | Exophytic, heterogeneous, necrosis | CD117+ (IHC); cystic on imatinib | Rare | No (liver/peritoneal) |
| Leiomyosarcoma | Any | Large, necrotic, exophytic | No LAP; lung/liver mets only; CD117- | Sometimes | No |
| Carcinoid/NET | Distal ileum | Avid arterial enhancement | Stellate desmoplastic mesenteric mass + calcification | Secondary (kinking) | Yes (calcified) |
| Mets (haematogenous) | Any | Eccentric submucosal masses | Bull's eye/target lesion (melanoma) | Occasionally | Variable |
| Mets (peritoneal) | Any (serosal) | Tethered/clumped loops, omental caking | Serosal implants, ascites | Functional | Variable |
| Meckel's diverticulitis | Ileum (antimesenteric) | Blind-ending diverticulum + fat stranding | Antimesenteric location; endolith; persistent vitelline artery | Occasionally | No |
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