colorectal_ca- COG.ppt

Dr Kuku Kapenda Kapasu
Bsc.HB, MBChB UNZA,
MBA-HCM UNILUS (understudy)
DPPPR ZIDIS (understudy)
Colorectal Cancer
5/23/2023 Dr Kuku Kapenda Kapasu

It is commonly adenocarcinoma.
Very rarely adenosquamous, squamous carcinoma can
occur.
Adenocarcinoma
Sigmoid colon (21%) is the most common site of
malignancy after rectum (38%).
In caecum it is 12% common.

Aetiology
Diet:
Red meat and saturated fat increases the incidence of
colonic cancer.
Cholesterol increases the bile acid concentration in the
intestinal lumen which acts as cocarcinogen.
High fibre diet protects the colon against cancer.
Calcium in diet prevents colonic cancer by combining
with bile salts and reducing bile salt concentration in the
colon. It directly acts on the colonic mucosal cells to reduce
their proliferative potential.
Diet with lack of fibre increases the risk. Diet with high fat
increases the risk.
Dietary vitamins A,C, E and zinc reduces the risk.

Genetic:
Carcinoma colon is more common in individuals with
adenoma colon or with familial adenomatous polyposis
(FAP), Gardner’s syndrome, Turcot’s syndrome.
Relatives of colonic cancer patient have got 2-4 times
increased risk of developing carcinoma of colon.
Long standing ulcerative colitis, Crohn’s disease has high
risk of colonic cancer. Crohn‘s disease is a premalignant
condition but not as much as ulcerative colitis.

• Alcohol and cigarette smoking increases the risk.
• Hereditary nonpolyposis colonic cancer (HNCC) has
• got high incidence (25%) of synchronous and
metachronous growth, so total colectomy is needed.
After cholecystectomy and ileal resection there is
increased bile salts and so more prone for carcinoma
colon.
• Radiation increases the risk (mucinous type). _
Ureterosigmoidostomy increases the risk by 100-500
times.
Acromegaly may increase the risk.
Note:
Aspirin, calcium and other NSAIDs protect against colonic
cancer.

• Colonic cancer may be:
• Nonhereditary colon cancer
• It can be sporadic colon cancer—60%.
• It can be familial colon cancer—30%. Common in
Ashkenazi
• Jewish population.

Hereditary colon cancer
FAP.
HNCC.
Peutz Jeghers syndrome—2-3% risk of cancer colon.
Cronkite—Canada syndrome.
Juvenile polyposis syndrome—it differs from isolated
juvenile polyps discussed earlier. It is an autosomal
dominant condition, occurs in children and adolescent.
Germ line mutation of SMAD-4 gene is observed. It
increases the risk
• of colonic cancer.

Types
Patient can have de novo multiple primary carcinomas in
different parts of the colon at the same time,
i.e. synchronous
(5-10%), or can present with growth in different parts of the
colon in different periods, i.e. metachronous (10-20%).
Gross types: Annular, tubular, ulcerative, cauliflower like.
Annular (stenosing) type:
It is more common on left side.
Here the growth spreads round the internal wall and so it
often presents with intestinal obstruction.

Ulcerative type:
It is common on right side.
Proliferative type:
Common in right side. It is fl eshy, bulky and
polypoid. It is less malignant

SMA
MCA
Rt CA
Ileocolic a

Epicolic LN
Paracolic LN
Intermediate
colic LN
Central
colic LN

Rt Colon
Tr colon
Lt colon
Sigmoid
colon
Rectum
5 segments of the colon

Distribution of colorectal cancer by site

Classification of colorectal polyps
• Neoplastic
Adenoma:-
Tubular
Tubulovillous
Villous
• Hamartomatous
Juvenile polyp
Peutz-Jeghers
• Inflammatory
e.g.ulcerative colitis &bilharzial polyps
• Metaplastic

1- Annular 2- Tubular
3- Ulcer 4- Cauliflouer
The four common macroscopic varieties of carcinoma

Dukes’ classification

Staging of carcinoma colon
Duke’s
• A. Confirned to bowel wall, mucosa and submucosa
• B. Extends across the bowel wall to the muscularis
propria with no lymph nodes involved
• C. Lymph nodes are involved

Modified Duke’s
A. Growth limited to rectal wall
B. Growth extending into extrarectal tissues but no lymph
node spread
B1: Invading muscularis mucosa
B2: Invading into or through the serosa
C. Lymph node secondaries
D. Distant spread to liver, lungs, bone, brain

Ca of the Right colon
oAnaemia (3A)
oMass in the right
iliac fossa

CA of the Lt colon
o Progressive intestinal
obstruction
oProgressive constipation
o Pain
oDistension
oAttacks of diarrhea may follow
constipation
o Acute intestinal obstruction
o No mass is felt, if a mass is
felt it is faecal impaction above
the tumour.

Ca of the Rectum
•Bleeding per rectum
•Spurious diarrhea ( sense
of incomplete defecation)
•Pain=extra rectal spread

Ca of the caecum treated by right hemicolectomy

Ca of transverse colon treated by transverse
colectomy or extended right hemicolectomy

Ca of left colon treated by left hemicolectomy

Ca of sigmoid treated by sigmoid colectomy

Ca of upper2/3 treated
by anterior resection
Ca of lower 1/3 treated by
abdominoperineal resection
Ca of the rectum

Competent
ileocaecal valve
Closed loop syndrome
Carcinomatous stricture (X) of the hepatic loop obstruction

Malignant
stricture

Absolute
constipation
Vomiting
Pain
Distension
Pathophysiology of intestinal obstruction

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.
Duke’s histological grading of carcinoma colon (Now
modified Morson-Dawson)
• Grade I—low grade.
• Grade II—average grade.
• Grade III—high grade.
• Grade IV—anaplastic.
Carcinoma confined to muscularis mucosa does not
metastasize.

Spread
Direct spread:
Locally it can invade the bladder, obstruct ureter and so
cause hydronephrosis.
Can perforate and cause peritonitis/pericolic/
Abscess/faecal Fistula.
Growth may get adherent to psoas muscle posteriorly.
Carcinoma sigmoid colon can infiltrate and cause
colovesical or colovaginal fistula. It can infiltrate ureter,
ovary, uterus etc. It can cause pericolic abscess or abscess
in lateral abdominal wall.

Lymphatic spread:
Growth through lymphatics spreads to pericolic, epicolic,
intermediate and principal group of lymph nodes.
Groups of lymph nodes draining colon
N1: Nodes immediately adjacent to bowel wall.
N2: Nodes along ileocolic/right colic/middle colic/ left colic/
sigmoid arteries.
N3: Nodes near the origin of SMA and IMA.
Nodal spread in carcinoma colon is sequential from N1 →
N2 → N3.

Blood spread:
40% of carcinoma colon spreads to liver via portal veins.
Secondaries may be either solitary or multiple, present as
liver with hard, umbilicated nodules.
Rarely it spreads to bone, lung, skin.

Clinical Features
Occurs usually after 50 years. Familial type can present in
younger age group. Common in males (M : F :: 3 : 2).
Commonly present with loss of appetite and
weight,anaemia, abdominal discomfort and mass per
abdomen.
20% of cases present as an acute intestinal obstruction.
20% of colonic/colorectal cancer has stage IV disease at
the time of first presentation.
Right sided growth commonly presents with anaemia,
palpable mass in the right iliac fossa, which is not moving
with respiration, mobile, nontender, hard, well-localised
with impaired resonant note.

Differential diagnosis for mass in the right iliac fossa
• Ileocaecal tuberculosis
• Appendicular mass
• Actinomycosis
• Ectopic kidney
• Mesenteric lymph nodes
• Ovarian tumour in females
• Retroperitoneal tumour
• Amoeboma

Carcinoma caecum occasionally presents like acute
appendicitis or intussusception with intestinal obstruction.
Left sided growth presents with colicky pain, altered
bowel habits (alternating constipation and diarrhoea),
palpable lump, distension of abdomen due to sub
acute/chronic obstruction. Later may present like complete
colonic obstruction. Tenesmus, with passage of blood and
mucus,with alternate constipation and diarrhoea, is
common.
Bladder symptoms may warn colovesical fistula.
Features of pericolic abscess/obstruction
(15%)/perforation/peritonitis may be the first presentation.

Closed loop obstruction can occur in transverse colon
growth (stricture type causing block) with competent
ileocaecal valve. Enormously dilated right sided colon is
prone for stercoral ulcer, perforation and faecal peritonitis.
Enlarged liver with multiple umbilicated hard secondaries,
ascites, rectovesical secondaries, palpable left
supraclavicular lymph nodes are other presentations.
Faecal strength of Streptococcus bovis bacteria increases
many fold in patients with colonic cancer compared to
individuals without colonic cancer.

Local complications of carcinoma colon
• Intestinal obstruction
• Closed loop obstruction
• Perforation and peritonitis
• Vesicocolic fi stula
• Invasion of ureter
• Pericolic abscesss

Investigations
Screening and surveillance for colon cancer
• Faecal occult blood test (FOBT)—it is nonspecific test
for peroxidase contained in haemoglobin. It is simple but
with low specificity
• Flexible sigmoidoscopy—once in 5 years to identify the
adenoma; it is often combined with FOBT
• Colonoscopy is the most accurate and most complete
method for evaluating the entire colon. It allows
identification of small polyps (< 1 cm), allows biopsy,
polypectomy, control of bleeding, stricture dilatation if
needed. Problem as a screening method is—prior need
for mechanical bowel preparation

• Air contrast barium enema (ACBE) detects polyps
greater than 1 cm. Its accuracy is more in proximal colon
than in sigmoid colon as one may misinterpret a polyp
for diverticulosis
• CT colonography (Virtual colonoscopy)—it is helical CT
3 dimensional intraluminal colon imaging. It needs bowel
preparation, air insufflation, CT imaging
• Barium enema: Shows irregular filling defect and ‘apple
core’ lesion (in left sided carcinoma). It also helps in finding
colonic polyps (Air-contrast barium enema).
• Colonoscopy and biopsy confirms the diagnosis.
• Virtual colonoscopy (CT colonography) is also useful to
visualize entire colon.

CEA (Carcinoembryonic antigen): It is a cell surface
glycoprotein discovered by Gold andFreedman.
• It is normally produced by colonic epithelium.
• Its serum ½ life is up to 10 days and is cleared by liver
through Kupffer cells. So its ½ life prolongs in
cholestasis and hepatocellular dysfunction. Normal level
is < 2.5 ng/ml. Level > 5 ng/ml is significant. Even though
it is a widely used tumour marker, it has got low
sensitivity. CEA is primarily associated with colorectal
cancers, but it can also increase significantly in
pancreatic, gastric, lung, breast carcinomas. Often its
level also increases in non-malignant conditions like
pancreatitis, hepatitis, obstructive jaundice, BPH

Uses in colorectal cancers are:
a. Preoperative levels >7.5 ng/ml signifi es poor prognosis.
b. If postoperative level does not fall, it indicates either
incomplete resection, or occult metastasis elsewhere.
c. Increase CEA during follow-up indicates recurrence
or secondaries.

• Left supraclavicular lymph node if palpable, its FNAC
may clinch the histological diagnosis.
• Hb%, PCV, haematocrit, ESR. Look for occult blood in
stool is the initial test for anaemia.
• CT scan abdomen and pelvis—to see local spread,
invasion,size and extent, stage, nodal status and liver
secondaries.
• LFT—mainly enzyme studies like alkaline phos phatase,
SGPT.

TREATMENT
Mainly Surgical
• Right sided early growth:
Right radical hemicolectomy with ileo transverse
anastomosis is done. Structures removed are terminal 6
cm of ileum, caecum and appendix, ascending colon, 1/3
of transverse colon, lymph nodes (epicolic, paracolic,
intermediate).
• In inoperable right sided growth, ileotransverse
anastomosis is done as a by-pass procedure.
•

• Transverse colon growth
An extended right hemicolectomy is the procedure done
for transverse colon growth which includes division of right
colic, middle colic arteries at their origin, with removal of
terminal 6 cm ileum, ascending and transverse colon;
anastomosing terminal ileum and proximal part of the
descending colon—ileocolic.
Alternatively, in mid-transverse colon growth, transverse
colon with both flexures can be removed; anastomosing
cut ends of ascending and descending colon—colocolic.

• Left sided early growth:
Left radical hemicolectomy is done, where in left ½ of
transverse colon and descending colon is removed along
with lymph nodes.

Radiotherapy
Usually there is no role for RT as tumour is radioresistant.
It is often used in locally advanced tumour, infiltrating the
psoas major muscle or lateral abdominal wall, left sided
colonic growth. It is also used in inoperable recurrent
tumour.

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