1. Growths of colon
A PRESENTATION FROM DEPARTMENT OF SURGERY, RGKMC
EDITED BY PRITHWIRAJ MAITI
FINAL YEAR MBBS
R.G.KAR MEDICAL COLLEGE

2. Tumours of colon
• Polyp/ tumour/ swelling arises from mucosal
surface with a stalk/ pedicle- a mass
projecting into the bowel lumen beyond the
surface epithelium.

3. Classification
• Inflammatory – Ulcerative colitis
– Segmental colitis
– Dysenteric colitis
– Crohn’s disease
– Diverticulitis
• Metaplastic - Hyperplastic
polyps
• Harmartomatous • Peutz–Jeghers polyp
• Juvenile polyp
• Cronkhite-Canada
syndrome
• Neoplastic – Adenoma
• Tubular
• Tubulovillous
• Villous
– Adenocarcinoma
– Carcinoid tumour
• Others – Lipoma
– Haemangioma
– Leiomyoma

4. • Metaplastic polyp- Not premalignant
• Hamartomatous polyp
– Peutz-Jegher’s polyp•
•
•
•
Autosomal dominant, familial
Multiple
Premalignant
Melanosis of oral mucosa, lips, and digits

5. – Juvenile polyp• Commonest in infant and children
• Cause intussusception, prolapse,
bleeding PR
• Colonoscopic polypectomy
• Not premalignant

6. Colonic Adenoma
• Neoplastic
– Adenoma
• Tubular-70%
• Tubulovillous-25%
• Villous-5%
– Solitary/ multiple
– Sessile/ pedunculated
– Premalignant
•
•
•
•
Size
Sessile
Villous
Dysplasia

7. Clinical features
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•
•
Asymptomatic
Anaemia
Bleeding P/R
Prolapse
Diarrhoea, spurious diarrhoea
Colicky abdominal pain
Tenesmus

8. Investigation and treatment
Investigations:
• Hb
• Serum electrolyte
• Colonoscopy–
–
–
–
Size
Texture
Colour
ulceration
Treatment:
• Colonoscopic
polypectomy
• Per anal polypectomy
• Resection anastomosis
• Total polypectomy if
FAP

9. Familial adenomatous polyposis (FAP)
Extracolonic manifestations of FAP
• Endodermal derivatives:
Younger age group- 15-20 years.
– Adenomas and carcinomas of the
80 % with a positive family
duodenum, stomach, small intestine,
thyroid and biliary tree.
history. The remainder arise as a
– Fundic gland polyps.
result of new mutations in the
– Hepatoblastoma.
adenomatous polyposis coli (APC)
• Ectodermal derivatives:
gene.
– Epidermoid cysts.
This has been identified on the
– Pilomatrixoma.
short arm of chromosome 5.
– Congenital hypertrophy of the retinal
pigment epithelium (CHRPE).
Clinical features– Brain tumours.
Pain abdomen,
• Mesodermal derivatives:
Loose stool with blood and
– Desmoid tumours.
mucous,
– Osteomas.
Weight loss.
– Dental problems.
• Autosomal dominant.
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•

10. SPECIAL NOTE
 FAP + Benign mesodermal tumours (such as
desmoid tumours)+ Osteomas+ Epidermoid cysts
can also occur= Gardner’s syndrome.
• FAP+ Brain tumor= Turcot’s syndrome.

11. Investigations and treatment
Investigations:
– Double contrast barium
enema
– Colonoscopy
Treatment:
– Proctocolectomy with
ileo-anal anastomosis

13. Screening policy
• At-risk family members are offered
– Genetic testing in early teens.
– Should be examined at the age of 10–12 years, repeated
every year.
• Who are going to get polyps will have them at 20 years,
require operation.
• If there are no polyps at 20 years, 5 yearly
colonoscopy upto 50 years.
• If still no polyps, there is probably no inherited gene.
• Carcinomatous change may exceptionally occur before
the age of 20 years

14. Hereditary non-polyposis colorectal cancer
(HNPCC: Lynch syndrome)
• Increased risk of colorectal cancer and also cancers of
the endometrium, ovary, stomach and small intestines.
• Autosomal dominant condition.
• Cause-a mutation in one of the DNA mismatch repair
genes. ( MLH1 and MSH2).
• The lifetime risk of developing colorectal cancer 80%.
• Mean age of diagnosis is 45 years.
• Most cancers develop in the proximal colon.
• Females with HNPCC have a 30–50% lifetime risk of
developing endometrial cancer.

15. COLORECTAL CARCINOMA (CRC)
• One of the most common cancers in the world.
• US:
4th most common cancer (after lung,
prostate, and breast cancers).
2nd most common cause of cancer death
(after lung cancer).
• 2001
130,000 new cases of CRC
56,500 deaths caused by CRC

16. AETIOLOGY
 Older age,
 Male gender,
 High intake of fat, alcohol, red meat;
 Obesity,
 Sedentary life style,
 Smoking,
 Inflammatory bowel disease,
 HNPCC,
 FAP,
 Family history of colorectal cancer.

17. Development of CRC
• Result of interplay between environmental and
genetic factors.
• Central environmental factors.
• Diet and lifestyle.
• 35% of all cancers are attributable to diet.
• 50%-75% of CRC in the US may be preventable
through dietary modifications.

18. Colon cancers result from a series of pathologic changes that
transform normal colonic epithelium into invasive carcinoma.
Specific genetic events, shown by vertical arrows, accompany this
multistep process. The various chemopreventive agents exert their
effects at different steps in this pathway, and this is depicted on
the basis of the available epidemiologic evidence.

19. Types of colon CA
• Synchrous- Multiple primary ca in different
parts of colon at the same time.
• Metachronus- Growth in different parts of
colon in different time.
• Gross type– Annular (left side)
– Tubular (left side)
– Ulcerative (right side)
– Cauliflower type (right side).

20. Histology (WHO)
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•
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•
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Adencarcinoma- 90%
Mucinous adenocarcinoma- 5-10%
Signet ring cell carcinoma
Small cell carcinoma
Squamous cell carcinoma
Undifferentiated carcinoma

21. Spread
Via blood
Via lymphatics
Liver
(40% via
portal vein;
Hard
umbilicated)
Lung
Brain
Bones
Direct
Lymph nodes
(Pericolic,
Epicolic
Intermediate
Principal)
Abdominal wall
Nerves
Vessels
Ureter, Bladder

22. Staging of CRC
Dukes staging system
A
B
C1
C2
D
Mucosa
invade Into (B1)/ through (B2) Muscularis propria
B1 + LN Involvement
B2 + LN Involvement
Distant metastatic spread

23. Staging of CRC
TNM system
Primary tumor (T)
Regional lymph nodes (N)
Distant metastasis (M)

24. TNM classification for colonic cancer
T-Tumour stage
T1: Into submucosa
T2: Into muscularis propria
T3: Into pericolic fat or sub-serosa but not breaching serosa
T4: Breaches serosa or directly involving another organ
N- Nodal stage
N0: No nodes involved
N1: 1–3 nodes involved
N2: ≥4 nodes involved
M- Metastases
M0: No metastases
M1: Metastases

25. Typical sites and incidence of colon cancer

26. Clinical feature
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After 50 years
M:F- 3:2
Weight loss
Loss of appetite
Night sweats, Fever
Abdominal pain & mass
Acute intestinal obstruction- 20%
Rt sided growth- anaemia, palpable mass in RIF.
LT sided growth- colicky pain, rectal bleeding,
change in bowel habits, sub acute obstruction.

27. Typical sites and incidence of colon cancer

28. Investigation
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BARIUM ENEMA
COLONOSCOPY AND BIOPSY
VIRTUAL COLONOSCOPY
USG W/A
CEA
Hb, PCV, ESR, FOBT
CT
LFT

29. • The barium enema of
colon• In this case, the
classic "apple core”
lesion is present,
representing an
encircling
adenocarcinoma that
constricts the lumen.

31. Therapy
Surgical resection the only curative treatment.
Likelihood of cure is greater when disease is
detected at early stage.
Early detection and screening is of pivotal
Importance.

32. SURGERY
• Rt sided early growth• Rt radical hemicolectomy– Terminal 6 cm of ileum
– Caecum
– Appendix
– Ascending colon
– 1/3rd of transverse colon
– Lymph node

33. • Transverse colon growth
• Extended Rt hemicolectomy- Rt.
hemicolectomy+ transverse colon
• Lt sided growth- Left hemicolectomy
• Sigmoid growth- Sigmoidectomy

34. •
•
•
•
Elective setting-prepared colon
Emergency setting
Type of anastomosis
colostomy

35. Adjuvant therapy
• Adjuvant chemotherapy
• Indication
• Node+
• Venous spread
• Poorly differentiated CA
• Change in CEA
– Regime
• 5FU + Folinic acid- 6 month.
• Preoperative neoadjuvant therapy.
• No role of radiotherapy as colonic tumour is radioresistant.

36. Follow up
• For 3 years regular interval once in 3-6 month
• By
– Regular CEA
– USG
– Barium enema
– Colonoscopy
– Serum Alkaline phosphatase (ALP)

37. Prognosis
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Site
Type
Size
Lymph node status
Liver secondaries
Age
Stage
Complication

38. Screening
What is screening?
A public health service in which members
of a defined population are examined to
identify those individuals who would benefit
from treatment to reduce the risk of a disease or
its complications.

39. Types of Screening
Fecal occult blood test (FOBT)
Chemical test for blood in a stool sample.
Annual screening by FOBT reduces colorectal cancer
deaths by 33%.
Flexible sigmoidoscopy can detect about 65%–75% of
polyps and 40%–65% of colorectal cancers.
Rectum and sigmoid colon are visually inspected.

40. Current Screening Guidelines
Regular screening for all adults aged 50 years or
older is recommended
FOBT every year
Flexible sigmoidoscopy every 5 years
Total colon examination by colonoscopy
every 10 years or by barium enema every
5–10 years

41. OGILVIE’S SYNDROME
• Colonic pseudoobstruction.
• Clinical features:
– Distention,
– Tympanic,
– Nontender.
• Cause:
– Scleroderma,
– Myotonic dystrophy,
– Hypothyroidism, DM,
– CRF,
– Poisoning,
– Retroperitoneal irritation
by blood fluid,
– Idiopathic.
• Investigation:
– X Ray –Dilated colon
– Barium- Normal
– CT
• Treatment:
– Conservative.
– Neostigmine,
– Tube cecostomy.

42. Colostomy
• A colostomy is a surgical procedure in which a
stoma is formed by drawing the healthy end
of the large intestine or colon through an
incision in the anterior abdominal wall and
suturing it into place. This opening, in
conjunction with the attached stoma
appliance, provides an alternative channel for
feces to leave the body.

44. Types
• Loop
• End
• Double barrel

45. Temporary Loop colostomy, Devine’s double barrel
 For diversion to facilitate distal healing
Permanent End
 APR

46. • Diversion
• Decompression
– Blow hole
– Tube caecostomy
– Loop transverse colostomy
• Irrigation

47. Complication
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Prolapse
Retraction
Necrosis
Stenosis
Herniation
Bleeding
Diarrhoea
Enteritis
Skin excoriation

48. THANK YOU