CARCINOMA COLON DEFINITION It is commonly adenocarcinoma. Very rarely adenosquamous, squamous carcinoma can occur. Adenocarcinoma

1. en love da Homoeopathy
CARCINOMA
COLON

2. CARCINOMA
COLON

3. CARCINOMACOLON
DEFINITION
• It is commonly
adenocarcinoma.
• Veryrarely adenosquamous,
squamous carcinoma can
occur.
• Adenocarcinoma
COMMONSITES
• Sigmoid colonis the most
commonsite of malignancy
after rectum
• In caecum

4. AETIOLOGY
• Diet
 Red meat and saturatedfat
(Cholesterol)
↓
increases the bile acid
concentration(acts as
cocarcinogen).
 High fibre diet & Calcium
protects the colonagainst
cancer.
↓
It directlyacts on the colonic
mucosal cells
↓
to reduce their proliferative
potential
 Diet withlack of fibre &
highfat increases the risk.
 Dietaryvitamins A,C, E and
zinc reduces the risk.
• Genetic:
 individuals with
adenoma colon
 familial adenomatous
polyposis (FAP)
 Gardner’s syndrome,
 Turcot’s syndrome.

5. • Long standing ulcerative
colitis & Crohn’s disease
• Alcohol and cigarette
smoking increases the risk.
• Hereditary nonpolyposis
coloniccancer (HNCC)
• After cholecystectomy and
ileal resectionthere is
increasedbile salts and so
more prone for carcinoma
colon.
• Radiationincreases the
risk(mucinous type).
• Ureterosigmoidostomy
• Acromegaly
PATHOGENESIS
• Adenoma—carcinoma
sequence
• Most of the colonic
carcinoma develops from
polyp/adenoma pathway.
Normal epithelium
→initiation by 5q loss APC
gene → dysplasia
(hyperproliferative) →
DNA methylation→ early
adenoma → 12p activation
K ras → intermediate
adenoma

6. →18q loss DCC→ late
adenoma → actionby 17p loss
p53 →carcinoma → spread .
• 80% of colorectal cancer
arises fromloss of
heterozygosity (LOH)
pathway.
• LOH pathway
↓
APC gene defects (inFAP)
↓
K ras mutation altering the
cell cycle
↓
K ras binds to GTP(guanosine
triphosphate)
↓
hydrolyse to GDP which
inactivates G proteinnormally
↓
K ras mutation blocks GTP
hydrolyse
↓
leading intopermanently active
formof G protein causing
carcinoma

7. ↓
loss of DCCtumour suppressor
gene
↓
mutationof tumour suppressor
gene p53.
↓
LOH pathway is microsatellite
stable (MSS)and carries poor
prognosis compared with MSI.
• 20% of colorectal cancer
develops frommutation
fromRER (Replication Error
Repair) pathway
↓
whereinrepair mechanismof
DNA replication error is lost.
↓
It causes microsatellite regions of
genome to have repeated
sequences

8. ↓
leading intoerror and is called
as microsatellite instability
(MSI)
↓
In colon, it is seenin right side
growths & is associated with
better prognosis
• Colonic cancer may be:
Nonhereditary colon
cancer
• It can be sporadiccolon
cancer—60%.
• It canbe familial colon
cancer. Commonin
Ashkenazi– Jewish
population.
• Hereditary colon cancer
• FAP
• HNCC.
• PeutzJeghers syndrome—
2–3%risk of cancer colon.
• Cronkite—Canada
syndrome.

9. • Juvenilepolyposis
syndrome—it differs
fromisolated juvenile
polyps discussedearlier. It
is an autosomal dominant
condition
TYPES
• Patient can have de novo
multiple primary
carcinomas in different parts
of the colon at the same time,
i.e. synchro nous (5–10%)
• can present with growthin
different partsof the colon
in different periods, i.e. meta
chronous (10–20%).
• Gross types:
• Annular,
• Tubular
• ulcerative
• cauliflower like.

10. Annular (stenosing) type:
• It is more common on left
side.
• Here the growthspreads
roundthe internal wall and
so it oftenpresents with
intestinal obstruction.
Ulcerative type:
• It is common on right side
Proliferative type
• Common in right side.
• It is fleshy, bulky and
polypoid. It is less
malignant.
Histology (WHO)
• Adenocarcinoma—90%.
• Mucinous
adenocarcinoma—5–10%.
• Signet ring cell carcinoma.
• Small cell/oat cell
carcinoma—rare—
extremely poor prognosis.
• Squamous cell carcinoma.
• Undifferentiated carcinoma

11. Duke’s histological grading of
carcinoma colon (nowmodified
Morson-Dawson)
• Grade I—low grade.
• Grade II—average grade.
• Grade III—highgrade.
• Grade IV—anaplastic.
Carcinoma confined to
muscularis mucosadoes not
metastasize.
Sessile MalignantPolyp
• InvasionSm 1: Submucosal
invasion into upper 1/3rd
(superficial/ inner)
• Sm 2: Submucosal invasion
into middle 1/3rd (inner
2/3rd)
• Sm3: Submucosal invasion
lower 1/3rd(deep).

12. SPREAD
• Direct spread:
• Locallyit can invade the
bladder, obstruct ureter
and so cause
hydronephrosis.
• Canperforate and cause
peritonitis/pericolic
abscess/faecal fistula.
• Growth may get
adherent to psoas
muscle posteriorly.
• Carcinoma sigmoid
colon caninfiltrateand
cause colovesical or
colovaginal fistula.
• It can infiltrate ureter,
ovary, uterus etc. It can
cause pericolicabscess
or abscess in lateral
abdominal wall.

13. • Lymphatic spread:
• Growththrough
lymphatics spreads to
pericolic, epicolic,
intermediate and
principal group of
lymph nodes. Groups of
lymph nodes draining
colon
• N1: Nodes immediately
adjacentto bowel wall.
• N2: Nodes along
ileocolic/right
colic/middle colic/ left
colic/ sigmoidarteries.
• N3: Nodes near the
originof SMA and IMA.
• Nodal spreadin
carcinoma colon is
sequential fromN1 →
N2 → N3

14. TNMCLASSIFICATION- Blood
spread
• 40%of carcinoma colon
spreads to liver via portal
veins.
• Secondaries may be either
solitaryor multiple, present
as liver with hard,
umbilicatednodules.
• Rarelyit spreads to bone,
lung, skin.
TNMstaging of colorectal cancer
Tumour—T
• Tx – Primary tumour
cannot be assessed
• T0 – No evidence of tumour
• Tis – Carcinoma in situ—
intraepithelial/invasioninto
lamina propria
• T1 – Invasion into
submucosa
• T2 – Invasion into
muscularis propria
• T3 – Invasion into
pericolorectal tissues/fat

15. • T4a – Invasionintosurface
of the visceral peritoneum
T4b – Direct Invasion or
adherent to adjacent
structures/organs
Regional nodes—N
• Nx – Nodes cannot be
assessed
• N0 – No nodal spread
• N1 – Regional nodes 1–3
involved –
• N1a – 1 regional node
• N1b – 2 to 3 regional
nodes
• N1c – Tumour deposits
in serosa/mesentery/
nonperitonealised
pericolic or perirectal
tissues without regional
nodes

16. • N2 – Regional nodes 4 or
more involved
• N2a – 4-6 regional nodes
• N2b – 7 or more regional
nodes .
Distant metastases—M
• M0 – No distantspread
• M1 – Distant spread present
• M1a – Spread confined
to one organ or site—
liver/lung/ovary/
nonregional nodes;
• M1b – Spread to more
than one organor
site/peritoneum.

17. Histological grade—G
• Gx – Grade cannot be
assessed
• G1 – Well differentiated
• G2 – Moderately
differentiated
• G3 – Poorly differentiated
• G4 – Undifferentiated
CLINICALFEATURES
• Occurs usually after 50
years.
• Familial type can present in
younger age group.
• loss of appetite& weight
• Anaemia
• abdominal discomfort and
mass per abdomen.
• 20% - acuteintestinal
obstruction.
• 20% of colonic/colorectal
cancer has stageIV
disease at the time of first
presentation

18. • Right sided growth
commonly presents with
• Anaemia
• palpable mass in the
rightiliacfossa, which is
not moving
• with respiration
• Mobile
• Nontender
• hard, well-localised with
impairedresonant note.
• Carcinoma caecum
occasionallypresents
• Acuteappendicitis/
• intusscepion with
intestional
obstruction

19. • Left sided growth presents
• colicky pain
• alteredbowel habits
(alternating
constipationand
diarrhoea)
• palpable lump
• distensionof
abdomendue to sub
acute/chronic
obstruction.
• Later may presentlike
• complete colonic
obstruction
• Tenesmus, with passage
of blood and mucus
• with alternate
constipation&
diarrhoea, is common.
• Bladder symptoms may
warn colovesical fistula.
• Features of pericolic
abscess/obstruction
/perforation/ peritonitis
maybe the first
presentation

20. • Closedloop obstruction can
occur in transverse colon
growth(stricture type
causing block) with
competent ileocaecal valve.
• Enormouslydilated right
sided colonis prone for
• stercoral ulcer
• Perforation& faecal
peritonitis.
• Enlargedliver with multiple
umbilicatedhard
secondaries
• Ascites
• rectovesical secondaries
• palpable left supraclavicular
lymph nodes are other
presentations.
• Faecal strength of
Streptococcus bovisbacteria
increases many fold in
patients with coloniccancer
compared to individuals
without coloniccancer

21. INVESTIGATION
• Bariumenema
• Shows irregular filling
defect and ‘apple core’
lesion (inleft sided
carcinoma)
• It also helps in finding
colonicpolyps (air-
contrast barium
enema).
• Colonoscopy and biopsy
confirms the diagnosis.
Virtual colonoscopy (CT
colonography) is also useful to
visualize entirecolon

22. • CT scanabdomenand
pelvis—to see local spread,
invasion, size and extent,
stage, nodal status and liver
secondaries.
• Left supraclavicular lymph
nodeif palpable, its FNAC
may clinchthe histological
diagnosis.
• Hb%, PCV, haematocrit,
ESR. Look for occult blood in
stool is the initial test for
anaemia.
• LFT—mainlyenzyme
studies like alkaline phos
phatase
• SGPT.
• US
• secondaries in liver
• Peritoneum
• lymph nodestatus
• rectovesical secondaries.
• CEA(carcinoembryonic
antigen):
• It is a cell surface
glycoprotein
-- discovered by
Gold and Freedman

23. SURGERY
Right-sidedearly growth:
• Right radical hemicolec
tomy with ileo-transverse
anastomosis is done.
• Structures removedare
terminal 6 cm of ileum,
caecumand appendix,
ascending colon, 1/3 of
transversecolon, lymph
nodes (epicolic, paracolic,
intermediate).
• In inoperable rightsided
growth, ileotransverse
anastomosis is done as a by-
pass procedure.

24. Transverse colon growth:
• An extended right
hemicolectomyis the
procedure done for
transversecolon growth
Left-sided early growth:
• Left radical
hemicolectomyis done,
where in left ½ of
transversecolon and des
cending colon is removed
along withlymph nodes.
• Left-sided stenosing type
of growthcan present
with acuteintestinal
obstruction, in which case
initially colostomyis done

25. • Oftengrowthin the
transverseor left sided
colon, whichis stenosing or
obstructive type, can cause
closed loop obstruction
Multiple synchronous primaries
in the colon:
• Total abdominal colectomy
with ileorectal anastomosis
is done
• Surgical treatment of liver
secondaries:
• In solitaryliver secondary,
segmental hepaticresection
is useful
• Adjuvant Therapy
Chemotherapy

26. Indications for chemotherapy
• Positive nodes.
• T4 lesions.
• Venous (microscopic)
spread.
• Signet cell type.
• Poorlydifferentiated
tumour/aneuploidy.
• Changes in CEAlevel.
• Postoperative
chemotheraphy
• Radiotherapy (RT)
• Usually there is no role for
RT as tumour is
radioresistant.

27. • It is often usedin locally
advancedtumour,
infiltrating the psoas major
muscle or lateral abdominal
wall, left sided colonic
growth.
COMPLICATION
• Intestinal obstruction ™
• Closedloop obstruction ™
• Perforation& peritonitis ™
• Vesicocolicfistula ™
• Invasionof ureter ™
• Pericolic abscesss
PROGNOSIS
• Site—left sidedtumours
has got better prognosis as
theypresent early.
• Type—colloid carcinoma
has got poorer prognosis.
• Size of the tumour.
• Lymph nodes status:
Number of lymph nodes
involved decides the
prognosis.
• Liver secondaries has poor
prognosis.
• Age of the patient.

28. • Associateddiseases like HIV.
• Stage of the tumour.
• Presence of complications
• perforation
• peritonitis.
• On the whole, it is a
curable malignancy with
proper surgeryand
adjuvant therapy.
5 yearsurvival is:
• Stage I – 90%.
• Stage II – 75%.
• Stage III – 50%.
• Stage IV – less than 5%.
REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

29. A
Special Thanks
To A Very
Special Doctor