This document discusses polyps and malignancy of the large bowel. It begins by providing anatomy of the colon and rectum. It then discusses various types of colonic polyps including hyperplastic, adenomatous, and polyposis syndromes. Imaging features of polyps on colonoscopy, barium enema, CT, and MRI are presented. Characteristics of different polyposis syndromes such as FAP, Gardner's syndrome, Turcot syndrome, and Peutz-Jeghers syndrome are summarized. The document emphasizes the premalignant potential of adenomatous polyps and importance of recognizing polyposis syndromes.

1. Polyps and malignancy
of large bowel
Dr. Gobardhan Thapa
Resident, MD RD
NAMS, Bir hospital

2. ANATOMY OF COLON
• Length - 120 to 200 cm.
• Extraperitoneal – AC, DC, rectum
• Intraperitoneal- cecum, TC, sigmoid
• Transverse and sigmoid colon– mesentery (mesocolon)–
more mobility.
• Distinguishing feature — 3 taenia coli -- haustral
sacculations.

3. Rectum
– Rectosigmoid junction at Third sacral
segment
– Sigmoid mesocolon ends - Rectum begins
– 15-18 cm long
– No haustra
– Two or three full thickness folds – valves of
Houston.

4. Arterial supply of
colon
Venous drainage of colon

5. Lymphatic drainage of colon
• Lymph from large intestine passes from
four sets of lymph nodes
– Epicolic LN on the wall of the colon
– Paracolic LN on the medial side of AC and DC
and near the mesocolic border of sigmoid and
TC.
– Intermediate LN on the main branches of the
vessels
– Terminal nodes on the SMA and IMA.

6. Landmarks and measurements related to colon
• S3 segment- rectosigmoid junction
• Presacral space 0.7 to 1.5 cm
• Maximum diameter of cecum – 9 cm and
transverse colon – 5.5 cm
• Colon wall thickness
– With distension by oral contrast
• 3 mm or less normal
• 4 to 6 mm s/o pathology
• > 6mm definitely abnormal
– With distension by per rectal air
• 3mm upper limit for rectum
• 2mm upper limit for colon

7. COLONIC POLYPS
• Localized mass that
projects from the mucosa
into the lumen.
• Pathologically mucosal
overgrowth.
• Subdivisions traditionally:
– Hyperplastic(harmless)
– Adenomatous(premalignant)
– Others: juvenile,
inflammatory, lymphoid other
rare polyps

8. Classification of polyps and
polyposis syndrome

9. IMAGING OF POLYPS:
• Fibreoptic Colonoscopy
– Highest detection rate for polyps
even those < 1 cm in size.
– Biopsy and polypectomy at the
same sitting possible.
– Disadvantage:
• Cost
• High perforation rate than Ba enema
(1 in 1700)
• Failure to reach the cecum in 5-30%
of cases.

10. • Double contrast Ba enema (DCBE)
• Filling defects on dependent
surface
• Etched in white when on
nondependent surface
• Small non-pedunculated polyps-
Bowler Hat sign when seen on
oblique view.
• Pedunculated polyps - target or
Mexican hat sign on end on
view.
• Has to be differentiated from
diverticula, feces, flexural
pseudotumors and other pitfalls.
Fig. Bowler hat sign
Fig. pedunculated polyp

11. • Double contrast Ba enema( contd)
– Frequently impossible to say benign or malignant. Size and
morphology may help.
Size Histology Risk of
Malignancy
<5mm Almost all hyperplastic 0.5%
5-10 mm 90%adenoma 1%
10-20 mm Usually adenomas 10%
>20 mm Usually adenomas 50%
•Morphology- can’t reliably predict histology. But in case of villous
adenoma typical fronds or cauliflower like appearance will be
there.

12. Features which favor the polyp is most
likely malignant
1. Large size >2cm
2. Irregular lobulated surface (frond-like
surface)
3. Base wider than height
4. Base retracted.
5. sessile
Size alone is the best predictor of malignancy radiologically.

13. CT Scan
–Not used for dx
–Help to depict any malignant
transformation and complications
(perforation, fistula, mets in liver
and adjacent structures)
–Polyps are seen as intraluminal
filling defects.

14. CT COLONOGRAPHY
– Rapidly emerging alternative to invasive
fibreoptic colonoscopy.
– Pre-requisites:
• Cleansed bowel
• optimal bowel distension with air or CO2
• use of MDCT,
• prone and supine imaging in single breath
hold (for each position),
• 1.25 to 2.5mm collimation and
reconstruction interval of 1mm,
• software programmes that provide
endoluminal display and “fly through”
capabilities provide 3D volume rendering
image processing.
• both 2D axial CT reconstructions and 3D
volume-rendered image.
Fig. Surface reconstruction of
images can identify the colonic
wall in a manner that appears like
optical endoscopy of the colon.
The triangular appearance is
characteristic of folds in the
transverse colon; hence, some
practitioners term these methods
virtual colonoscopy

15. Fig. (A) Endoluminal CTC image depicting a polyp (arrow) growing on a
haustral fold just above residual colonic fluid (B) corresponding 2D image
shows a stalked lesion (arrow) coated by a thin rim of tagged fluid.

16. Fig. (A) 3D CT colonogram – polypoid lesion simulating a sessile polyp. (B)
2D view shows a tiny locule of gas (arrow) demonstrating that this is a
retained fecal residue.
• Fecal residue – may mimic a polyp
- has variable attenuation due to internal gas content
unlike homogeneous soft tissue attenuation of a polyp
- fecal tagging using oral contrast

17. • MRI
– Not a primary modality for polyps
– show polyp signal intensity
comparable to that of bowel on
non-enhanced images. After
gadolinium, enhancement is
similar to that of bowel on early
and late images.
• MR colonoscopy
– Studies have shown that MR-
based endoluminal assessment
of colon is possible.
Fig. sagittal image post
contrast FS MR colonogram –
an enhancing sigmoid polpyp
(arrow)

18. • Ultrasound
–Insensitive for polyp scanning due to
bowel gas.
–May be used to assess polyps and
mass after retrograde instillation of
warm sodium chloride solution into
the colon – polyp appear as
hyperechoic structures projecting into
the lumen.
–Can be used to screen thyroid, abd,
breast etc in polyposis syndrome
cases/relatives.

19. HYPERPLASTIC POLYPS
• 90% Colonic polyps (autopsy)
• 20% surgically removed polyps
• Recto-sigmoid common site. May occur
anywhere.
• Any age group. Diagnosed most commonly at 50-
70 yrs.
• Size – 90% < 0.5cm 10% > 0.5cm
• Larger polyps - rarely develop adenomatous foci
(serrated adenoma)
• Significance - No malignant potential except in
rare instances.

20. Adenomatous polyps
• 10%
• Malignant potential.
• 90% < 1.5cm– small
potential for malig.
• 10% larger– greater
potential ,,
• 3 divisions
1. Tubular
2. Tubulovillous
3. Villous

21. Tubular Tubulo-villous Villous
Incidence Most common (75%) - Least common
Site Anywhere in colon 1.Distal colon and
rectum(75%) 2. Cecum
n AC
Propensity for
Rectosigmoid
Morphology Pedunculated or
sessile
Mixed pattern broad based, sessile,
cauliflower-like(frond-like)
surface, Large,
Malignant
potential
Least among 3. Depends upon degree
of villous component.
Greatest malignant
potential
Symptoms Asymptomatic mostly.
Rectal bleeding
Asymptomatic to rectal
bleeding.
Symptomatic more often than
other 2.
Rectal bleeding.
Electrolyte imbalance d/t
hypersecretion—hypokalemia
and profuse mucus
discharge.

22. Polyposis syndrome
• Multiple polyps within gi tract.
• Types
– Familial inherited (autosomal dominant)
– Nonfamilial

23. • Familial inherited polyposis syndromes– 2
subtypes
1. Adenomatous polyposis syndromes
1. FAP coli
2. Gardner syndrome
3. Turcot syndrome
2. Hamartomatous polyposis syndromes
1. Peutz-Jeghers syndrome
2. Juvenile polyposis syndrome

24. • Non-inherited polyposis syndrome
– Cronkhite-Canada syndrome
• Polyps with nail atrophy, brownish skin
pigmentation and alopecia.
• Watery diarrhea and protein losing enteropathy.

25. • Syndrome recognition important as the
adenomatous polyposis is premalignant.
• Should be considered when-
–Intestinal polyp in young patient
–2 or more polyps in any patient
–Colonic Ca in < 40 yrs of age
–Related extra-intestinal manifestations.

26. Familial adenomatous polyposis coli
• AD inheritance
• Mutation in APC gene
(chromosome 5q21).
• 2/3rd
of ptt– family h/o FAP
or colonic Ca
• 1/3rd
of ptt– disease occurs
as spontaneous mutation
• All affected family members
exhibit polyps by the age of
35 yrs.

27. FAP coli( contd.)
• 1-2mm to 1cm to larger
polyps—150 to over 1000;
carpeting the colon
• Mostly diffuse
involvement, occasionally
segmental.
• Associations
– Hamartomatous polyps in
stomach(49%)
– Adenomatous polyps of
duodenum(25%) and
– Periampullary carcinoma
Fig. FAP syndrome. Colonic mucosa
carpeted with innumerable small
polyps seen as tiny filling defects.

28. FAP coli (contd.)
• Malignant potential
– All pt develop colonic Ca by 20 yrs of dx.
• Attenuated adenomatous polyposis
syndrome – variant of AFP; fewer
polyps(<100, as few as 5-10 polyps).

29. GARDNER SYNDROME
• Variant of FAP with prominent skeletal and
skin manifestations.
• FAP and Gardner syndrome may occur in
the same family.
• Polyps - histologically adenomatous as in
FAP.
• 100% pt – malignant transformation.

30. Soft tissue tumours
Epidermoid inclusion cysts of the skin, Dermoid
tumours, Fibroma, Lipoma, Neurofibroma,
Leiomyoma
GI tumours
Colonic polyposis(100%), gastric adenomatous
polyps(5-68%), Gastric hamartomatous polyps,
Duodenal adenomatous polyps(90%)
GARDNER SYNDROME

31. Osseous abnormalities – exostosis, bone
islands.
Endocrine tumours – papillary Ca thyroid,
Carcinoid tumor of small bowel, parathyroid
adenoma
CNS - medulloblastoma
Abnormal dentition – supernumary teeth,
impacted teeth

32. • Desmoplastic tendency of fibrous
tissues in pt with Gardner syndrome
results in
– Desmoid tumours
– Keloids
– Mesenteric fibrosis and Peritoneal adhesions
– Retroperitoneal fibrosis and
– Mammary fibromatosis

33. TURCOT SYNDROME
• Turcot syndrome is an association between
colonic polyps (adenomatous), colonic
carcinoma and brain tumors.
• Most brain tumours are supra-tentorial
glioblastoma; occasionally medulloblastoma.
• Other reported abnormalities
– Sebaceous cysts
– Papillary Ca of thyroid
– Leukemia and
– Spinal cord tumours

34. TURCOT SYNDROME(contd.)
• Mutations in two types of genes:
– Mutation in APC gene– mostly a/w brain tumors.
Recent study- APC gene mutation and FAP ptt 90 x
more risk of developing brain tumours than general
populations.
– Mutation of 1 of 2 mismatch repair genes, hMLH1 and
hPMS2--- higher risk of developing Ca. This mutation
also cause hereditary non-polyposis colorectal cancer
(HNPCC or LYNCH SYNDROME).

35. Peutz-Jeghers syndrome
• Multiple hamartomatous intestinal
polyps associated with
mucocutaneous melanotic
pigmentation.
• Mutations of STK11 gene (location
19p).
• Polyps occur mainly in the
stomach and small bowel; large
bowel polyps are fewer, but are
larger often pedunculated, and
may bleed.

36. • GI polyps
– Small bowel-------- 95% ptt—may carpet it.
– Stomach and du– 25% ptt
– Colon n rectum---- 25% ptt – no carpeting
usually.
• Non-GI polyps
– Nose, larynx, bronchial tree
– Urinary tract (particularly UB)
Peutz-Jeghers syndrome(contd.)

37. • Malignant change rare. Risk of developing
other neoplasm 18 times > general pop.
• Variety of malignant tumours associated:
– In 13 % cases pancreatic Ca
– Breast Ca (mainly ductal) commonly B/L
– Ovarian cyst and neoplasms in 5% cases.
– Neoplasms in thyroid, lung, skin, uterus and
testicles has also been reported.
Peutz-Jeghers syndrome(contd.)

38. JUVENILE POLYPOSIS SYNDROME
• Most common cause of colonic polyposis in
children - rare.
• 3 forms
– Familial juvenile polyposis of stomach
– Familial ,, ,, coli- rectosigmoid
common.
– Generelised ,, ,, - polyps through out GI tract.
• Variable penetrance of the disease, variable no.
of polyps.
• Polyps invariably possess stalk.

39. Screening and surveillance of patient with
adenomatous polyposis coli syndrome
• First degree relative with FAP:
– Flexible sigmoidoscopy
– Start at puberty(10-12 yrs) or sooner in
symptomatic patient.
– Do annually until adenomas detected or until
genetic testing done along with index patient
or until found not to have mutant gene that
caused the disease in index patient.
– After 25 yrs if no polyps, do every 2 yrs till the
age of 35 yr by when almost all exhibit polyps.

40. Colonic malignancy
• Primary Adenocarcinoma - almost 99%
of colorectal carcinoma.
• Mucinous Adenocarcinoma
• Primary signet ring cell carcinoma (linitis
plastica)
• Metastatic tumours
• GISTs
• Lymphoma

41. Colonic adenocarcinoma
• 3rd
most common Ca in
men and women in
North America and
West Europe.
• Most common GI Ca
• Best prognosis. 5 yr
survival rate of ~50%
can be improved by
screening -
polypectomy.

42. • Origin
– Majority adenoma-carcinoma sequence from adenomatous polyps
and polyposis.
– Some from non-polypoid dysplastic mucosa as in inflammatory
bowel disease.
• Polyp dwell time
– Initiated polyp grow for 10-15 yrs before becoming frankly
malignant.

43. • Distribution of adenomatous polyps and
cancer
Site Polyp % Cancer %
rectosigmoid 52 55
DC 18 6
TC 11 11
AC 13 9
Cecum 7 13

44. RISKS FOR COLONIC CARCINOMA
– High fat low fiber diet
– Age >50 yrs
– Personal h/o colorectal adenomatous polyps
– First degree relative with colorectal Ca (3-fold risk).
– Adenomatous polyposis coli ( FAP, Gardner S, Turcot
S) - 100% risk if no colectomy.
– Juvenile polyposis syndrome, PJS: slightly increased
risk.
– Inflammatory bowel disease
• UC( risk 30% after 25 yrs)
• CD( 4-to 10-fold risk).

45. • Male and female equally affected.
• 90% >50 yrs patient
• 10% < 50 yrs patient
• Peak incidence: 70 – 85 yrs
Colon, adenocarcinoma (contd.)

46. – mutation of mismatch repair (MMR) genes
– Life time risk of CRC is 70-85%; occur at
earlier age (mean 45 years) - More common
in rt side
“Amsterdam” criteria {3-2-1 rule}:
– colorectal cancer in at least 3 family members
spanning 2 generations, with at least 1 case
diagnosed before the age of 50 yrs.
Lynch syndrome (HNPCC)

47. • Preferred examinations
– Digital rectal examination
– Stool inspection and occult blood test
– CBC, LFT, CEA level.
– Sigmoidoscopy or colonoscopy
– DCBE study
– CT scan and CTC
– MRI and MRC
Imaging Adenocarcinoma Colon

48. • DCBE
– Gold standard to see mucosal
detail
– Early carcinoma looks like
polypoidal mass.
– Advanced Ca gives one or more of
the 3 morphological appearances
• Polypoid lesions - contour deformity
along one margin of bowel wall/ filling
defect.
• Annular lesions - apple-core lesions
(narrow lumen, mucosal irregularity
and overhanging edges - shouldering)
• Flat lesions are rare.

49. Annular carcinoma sigmoid colon-
circumferential mass causing lumen
narrowing & mucosal destruction
and the overhanging edges or
shouldering at the tumor margins
Apple core lesion in ascending colon
Apple core sigmoid cancer

50. • Plain x-ray
–Large bowel obstruction
–Perforation
–Calcifications in mucin-producing
colon carcinoma.

51. Conventional CT:
–Area of focal wall
thickening (>3 mm),
usually homogeneous
but can be
heterogeneous in large
adenoCa or mucinous
tumors or when
associated with abscess
formation.
Fig. Cecal carcinoma with
circumferential involvement of
the cecal wall.

52. – CT has higher sensitivity and lower specificity than
MRI in T staging.
– Overall T, N and M staging accuracy are comparable
to both CT and MRI.( 60%, 60%, 90% for TNM
respectively)
For staging and to assess recurrence.
Goal is to predict 3 factors which affect prognosis
Depth of tumour penetration in colon wall
Regional or distant lymph node mets
Distant mets to other sites.

53. Enlarged portal nodes (between
inferior vena cava and portal
vein) & hepatic metastases Recurrent colon Ca invades sacrum

54. • CT Colonography and
MR Colonography
– Can be used to
diagnose the colonic
ca.
– Sensitivity and
specificity is higher for
advanced cases. For
small polypoidal
lesions role and
limitations are as
described previously.
Fig. Colon Ca – CT colonography

55. Fig. 2D axial CT colonogram image –
circumferential tumor (arrow)
Fig. sagittal oblique CT through
mid-sigmoid cancer showing an
irregular outer margin extending
into pericolic fat

56. • Ultrasound
– To detect hepatic mets (70-90 %
detection rate).
– Most hepatic mets are hyperechoic;
may be hypoechoic also.
– Tumour itself looks as a target sign
(hyperechoic centre surrounded by
echopoor mass) or as a localised
irregular colonic wall thickening, an
irregular contour , lack of normal
peristalsis and absence of normal
layered appearance of colonic wall.
– Endorectal US: for local invasion by
tumour. Competes with MRI to
detect local tumour invasion.
Fig. USG cecal
carcinoma-- concentric
thickening of the
hypoechoic bowel wall
by the tumor

57. Radionuclide study
–May be used to detect tumour
recurrence
• Radioimmunoscintigraphy with monoclonal
antibody that recognises CEA or tumour
associated glycoprotein-72 to detect
recurrence in pelvis and extrahepatic
abdomen.
• PET with fluorodeoxyglucose (FDG)

58. Role of intervention in Ca colon
• Stent placement across the obstructing Ca
– To improve general condition of the ptt before surgery
– In ptt unfit for surgery or in unresectable tumours– as
a palliative measure.
• Intra-arterial chemotherapy for unresectable
tumours
• Intra-arterial chemotherapy via hepatic artery for
hepatic mets from colon Ca.
• Radiofrequency thermal ablation in selected
patient with hepatic mets from colon Ca.

59. Colon, adenocarcinoma-
STAGING
• Modified Dukes staging
Stage Description
A Limited to mucosa
B
B1
B2
Involvement of muscularis propria
Extension into mp
Extension through mp into serosa/mesenteric fat.
C
C1
C2
Lymph node metastasis
+ growth limited to bowel wall
+growth extending into adipose tissue
D Distant mets

60. TNM staging (7th
edition)
•T
• Tis - carcinoma in situ
• T1 - invasion of submucosa
• T2 - invasion of muscularis propria
• T3 - invasion outside muscularis
propria
• T4 - T4a invasion of visceral
peritoneum, T4b invasion of
other organs
•N
• N0 - no lymph node involvement
• N1 - 1 to 3 pericolic lymph node
involvement
• N2 - >/= 4 pericolic LN involvement
•M
• M0 - no distant mets
• M1 - distant mets M1a in one organ
M1b in > 1 organ or peritoneum
Fig. layers involved in T1 – T4
colorectal cancers according to the
TNM, 7th
edition

61. • TNM staging (contd.)
Stage Grouping 5-yr survival
0 TisN0M0 >95%
I T1N0M0
T2N0M0 75 to 100%
II T3N0M0
T4N0M0 50 to 75 %
III AnyT N1 M0
AnyT N2,3M0 30 to 50%
IV anyT anyN M1 < 10%

62. Other large bowel tumors
• Carcinoid tumors
• Mostly in cecum, rectum and appendix.
• May result in carcinoid syndrome.
• Non-specific imaging findings.

63. Primary appendiceal adenoCa:
•Rare, 0.5% of all neoplasms of GIT.
•Found in <2% of appendectomy
specimens.
•Cystic and colonic growth pattern

64. • Cystic type: mucin
producing –
tendency to rupture
and spread
throughout peritoneal
cavity –
pseudomyxoma
peritonei.
• Colonic type:
develop from tubular
and tubulovillous
adenoma, similar to
Fig. primary appendiceal
adenocarcinoma

65. • Colonic lymphoma
• Usually arises from nodal disease, rarely primary (0.5%).
• Lymphoid tissue mostly in cecum and rectum – majority
lymphoma site.
• B cell Hodgkin type
• Bulky polypoid lesions to diffuse annular infiltrating
forms.

66. • Mucosa intact: sub-mucosal spread and lumen patent
• CT: bulky soft tissue mass
Fig. axial CT – marked symmetrical bowel wall thickening (arrows)
secondary to primary colonic lymphoma. Note the lumen remains patent.

67. Metastatic disease to colon:
• Intra-peritoneal seedling:
–Ovarian, gastric, pancreatic
• Hematogeneous routes:
–Malignant melanoma, breast, lung
•Multiple bizarre, extrinsic lesions
•Particular site eg POD

68. • Contiguous spread:
–From prostate, bladder or ovary
• Spread along the mesentery:
–Pancreatic Ca to transverse
mesocolon

69. Summary
• Colonoscopy best method by sensitivity, specificity and
due to added adv of Bx and polypectomy. But has disadv
of invasiveness and occasional failure to reach cecum.
• DCBE - gold standard imaging modality to see mucosal
detail. high detection rate for >1cm polyps but low for <
1cm ones.
• CT and MRI - for staging
• CTC and MRC – emerging alternative for invasive
fibreoptic colonoscopy. Till date has not replaced it.
• USG - To detect mets in liver.
• TRUS - competes with MRI to accurately find out the
local invasion of Ca rectum.

70. Thank
you !!

71. References
• Text book of Radiology and Imaging,
David Sutton; 7/e.
• Fundamentals of diagnostic radiology,
Bryant and Helms; 4/e.
• Grainger and Allison’s diagnostic
radiology, 6/e.