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COLON CANCER PRESENTED BY:
RAHAF HASANEIN
ANATOMY+ BLOOD SUPPLY
COLON ARTERIAL SUPPLY
SMA branches into :
Ileocolic artery (terminal ileum and proximal ascending colon).
Right colic artery (ascending colon).
Middle colic artery (transverse colon).
IMA branches into:
Left colic artery (descending colon).
Several sigmoidal branches (sigmoid colon)
Superior rectal artery (proximal rectum).
The terminal branches of each artery form anastomoses with the terminal branches of the adjacent artery and communicate via the marginal artery of Drummond.
VENOUS DRAINAGE
The veins of the colon parallel their corresponding arteries and bear the same
terminology.
IMV ascends in the retroperitoneal plane over the psoas muscle and
continues posterior to the pancreas to join the splenic vein.
THE LYMPHATIC DRAINAGE
Lymphatic vessels and lymph nodes follow the regional arteries.
COLON NERVE SUPPLY
The Sympathetic nerves arise from T6-T12 and L1-L3.
The parasympathetic innervation to the right and transverse colon is from the vagus nerve; the
parasympathetic nerves to the left colon arise from sacral nerves S2-S4.
POLYPS
Nonspecific clinical term that describes any projection from the surface of the intestinal mucosa
regardless of its histologic nature.
Most colorectal carcinomas evolve from adenomatous polyps.
ADENOMATOUS POLYPS
25% of the population older than 50 years of age.
Increase risk of malignancy?
Classification:
(acc. To histology)
Tubular adenomas (5%).
villous adenomas (40%).
Tubulovillous adenomas (22%).
(Acc. To shape)
Pedunculated -> colonoscopic snare
excision.
Sessile
Complications of polypectomy
include perforation and bleeding.
HYPERPLASTIC POLYPS
Extremely common.
These polyps are usually small (<5 mm) -> hyperplasia without any dysplasia.
Large hyperplastic polyps (>2 cm) -> foci of adenomatous tissue and dysplasia
Hyperplastic polyposis is a rare disorder in which multiple large hyperplastic polyps
occur in young adults. These patients are at slightly increased risk for the development of
colorectal cancer.
SERRATED POLYPS
Some of these polyps will develop into invasive cancers.
A familial serrated polyposis syndrome.
Serrated polyps should be treated like adenomatous polyps.
HAMARTOMATOUS POLYPS (JUVENILE)
Not premalignant.
Associated with mutation in PTEN.
Bleeding is a common symptom, and intussusception and/or obstruction may occur.
Treated by polypectomy.
FAMILIAL JUVENILE POLYPOSIS
AD disorder in which patients develop hundreds of polyps in the colon and rectum.
Annual screening should begin between the ages of 10 and 12 years.
Treatment is surgical and depends on the degree of rectal involvement
If the rectum is relatively spared, a total abdominal colectomy with ileorectal anastomosis.
If the rectum is carpeted with polyps, total proctocolectomy is the more appropriate operation and ileal
pouch–anal reconstruction to avoid a permanent stoma
PEUTZ-JEGHERS SYNDROME
polyposis of the small intestine, the colon and rectum.
Characteristic melanin spots on the buccal mucosa and lips of these patients..
Carcinoma may develop.
Surgery for symptoms.
Screening consists of a baseline colonoscopy and upper endoscopy at age 20 years, followed by annual flexible
sigmoidoscopy thereafter.
CRONKITE-CANADA SYNDROME
GI polyposis in association with alopecia, cutaneous pigmentation, and atrophy of the
fingernails and toenails.
Diarrhea is a prominent symptom, and vomiting, malabsorption, and protein-losing
enteropathy may occur.
Most patients die of this disease.
Surgery for complications.
COWDEN’S SYNDROME
AD.
Hamartomas of all three embryonal cell layers.
Facial trichilemmomas, breast cancer, thyroid disease and gastrointestinal polyps.
Patients should be screened for cancers.
Treatment is otherwise based on symptoms.
INFLAMMATORY POLYPS
Not premalignant.
In inflammatory bowel disease
After amebic colitis, ischemic colitis, and schistosomal colitis.
Microscopic examination shows islands of normal, regenerating mucosa (the polyp) surrounded by areas of mucosal loss.
Polyposis may be extensive, especially in patients with severe colitis, and may mimic FAP.
INHERITED COLORECTAL CARCINOMA
FAMILIAL ADENOMATOUS POLYPOSIS
AD, 1% of all colorectal adenocarcinomas.
Mutation in the APC gene, on chromosome 5q (positive in 75% of cases).
Up to 25% present without other affected family members.
Hundreds to thousands of adenomatous polyps shortly after puberty.
Risk of colorectal cancer 100% by age 50 years.
APC
gene t
est
ing
+
annual flexible sigmoidoscopy beginning at
age 10 to 15 years is done until polyps are identified.
-
Refused or unavailable
annual flexible sigmoidoscopy beginning at
age 10 to 15 years is performed until age 24 years.
every 2 years until age 34 years
every 3 years until age 44 years
then every 3 to 5 years.
Risk for the development of adenomas anywhere in the gastrointestinal tract, particularly in the
duodenum.
Upper endoscopy (every 1 to 3 years beginning at age 25 to 30 years).
Treatment is surgical.
Three operative procedures can be considered:
1. Total proctocolectomy with an end (Brooke) ileostomy
2. Total abdominal colectomy with ileorectal anastomosis
3. Restorative proctocolectomy with ileal pouch–anal anastomosis with or without a temporary ileostomy.
FAP may be associated with extraintestinal manifestations such as congenital hypertrophy of the
retinal pigmented epithelium, desmoid tumors, epidermoid cysts, mandibular osteomas (Gardner’s
syndrome)
central nervous system tumors (Turcot’s syndrome).
Desmoid tumors are often hormone responsive, and growth may be inhibited in some patients with
tamoxifen. COX-2 inhibitors and nonsteroidal, anti-inflammatory drugs may also be beneficial in
this setting.
ATTENUATED FAMILIAL ADENOMATOUS POLYPOSIS
Variant of FAP.
Present later in life with fewer polyps (usually 10–100) predominantly in the right colon.
CRca develops in more than 50% of these patients, but occurs later (average age, 55 years).
Patients are also at risk for duodenal polyposis.
APC gene mutations are present in only about 30% (AD)
Mutations in MYH also result in the(AR).
Genetic testing.
When positive, screen at-risk family members.
If the family mutation is unknown, screening colonoscopy is recommended beginning at age 13 to 15
years, then every 4 years to age 28 years, and then every 3 years.
These patients are often candidates for a total abdominal colectomy with ileorectal anastomosis
because the limited polyposis in the rectum can usually be treated by colonoscopic snare excision.
Prophylaxis with COX-2 inhibitors.
HEREDITARY NONPOLYPOSIS COLON CANCER (LYNCH’S SYNDROME).
HNPCC (Lynch’s syndrome) is more common than FAP.
(1%–3% of all colon cancers).
AD, Errors in mismatch repair.
Development of colorectal carcinoma at an early age (average age, 40–45 years). Approximately 70%
Cancers appear in the proximal colon and have a better prognosis regardless of stage.
The risk of synchronous or metachronous colorectal carcinoma is 40%.
May also be associated with extracolonic malignancies, including endometrial carcinoma, which is
most common, and ovarian, pancreas, stomach, small bowel, biliary, and urinary tract carcinomas.
The diagnosis is made based on family history.
The Amsterdam criteria for clinical diagnosis of HNPCC are:
Three affected relatives with histologically verified adenocarcinoma of the large bowel (one must be
a first-degree relative of one of the others) in two successive generations of a family with one
patient diagnosed before age 50 years.
The presence of other HNPCC-related carcinomas should raise the suspicion of this syndrome.
Screening colonoscopy is recommended annually for at risk patients beginning at either age 20 to 25
years or 10 years younger than the youngest age at diagnosis in the family, whichever comes
first.
Because of the high risk of endometrial carcinoma, transvaginal ultrasound or endometrial aspiration
biopsy is also recommended annually after age 25 to 35 years.
Because there is a 40% risk of developing a second colon cancer, total colectomy with ileorectal
anastomosis is recommended once adenomas or a colon carcinoma is diagnosed.
Annual proctoscopy is necessary because the risk of developing rectal cancer remains high. Similarly,
prophylactic hysterectomy and bilateral salpingo-oophorectomy should be considered in women
who have completed childbearing.
FAMILIAL COLORECTAL CANCER
10% to 15% of patients with colorectal cancer.
Diagnosis before the age of 50 years is associated with a higher incidence in family members.
Screening colonoscopy is recommended every 5 years beginning at age 40 years or beginning 10 years
before the age of the earliest diagnosed patient in the pedigree.
ADENOCARCINOMA AND POLYPS
Most common malignancy of the GIT.
Third most common cancer in women and men.
Third leading cause of cancer-related deaths.
F:M 1:1
RISK FACTORS
Aging
Hereditary Risk Factors
Environmental and Dietary Factors
Inflammatory Bowel Disease
Cigarette smoking
Patients with ureterosigmoidostomy
Acromegaly
Pelvic irradiation
CLINICAL FEATURES
Depend on: Site, Presence of complications and metastases.
SPREAD
Direct extension
Hematogenous
lymphatic
DIAGNOSIS
Hx+ PE
Colonoscopy to obtain biopsy and evaluate for synchronous tumors (5%)
OR flexible sigmoidoscopy and barium enema.
CBC, LFT
Water-soluble contrast enema is performed to assess the degree and level of obstruction and to “clear”
the colon proximal to the obstruction.
A chest/abdominal/pelvic CT.
PET scan (It is routinely performed prior to concurrent colectomy and liver resection for hepatic
metastases)
CEA
STAGING
MANAGEMENT
surgical resection: Remove the primary tumor along with its lymphovascular supply
➢ Surgeries could be curative or palliative
Adjuvant chemotherapy: stage III / VI or locally advanced stage II
combination of 5-fluorouracil/leucovorin with either irinotecan (FOLFIRI) or oxaliplatin (FOLFOX).
STAGE-SPECIFIC THERAPY
Stage 0 (Tis, N0, M0):
Polypectomy
Segmental resection.
Stage I: The Malignant Polyp (T1, N0, M0):
Invasive carcinoma in pedunculated polyp polypectomy or Segmental colectomy.
Invasive carcinoma arising in a sessile polyp extends into the submucosa and is usually
best treated with segmental colectomy
Stages I and II: Localized Colon Carcinoma (T1-3, N0,M0):
Surgical resection.
Adjuvant chemotherapy has been suggested for selected patients with stage II disease
(young patients, tumors with “high-risk” histologic findings).
Stage III: Lymph Node Metastasis (Tany, N1, M0)
Adjuvant chemotherapy has been recommended routinely in these patients.
Stage IV: Distant Metastasis (Tany, Nany, M1).
Highly selected patients with isolated, resectable metastases may benefit from resection
(metastasectomy).
All patients require adjuvant chemotherapy.
colonic stenting for obstructing lesions of the left colon also provide good palliation.
More limited surgical intervention such as a diverting stoma or bypass procedure may be appropriate in
patients with stage IV disease who develop obstruction.
Hemorrhage in an unresectable tumor can sometimes be controlled with angiographic embolization.
External beam radiation also has been used for palliation.
RIGHT HEMICOLECTOMY
Carcinoma of the caecum or ascending colon.
The ileocolic vessels, right colic vessels,
and right branches of the middle colic
vessels are ligated.
Ileal-transverse colon anastomosis
EXTENDED RIGHT COLECTOMY
Lesions located at the hepatic flexure or proximal transverse colon.
Right hemicolectomy + reminder of transverse colon and splenic flexure.
resection of right colic artery, iliocecal artery and middle colic artery.
Anastomosis relies on the marginal artery of Drummond
TRANSVERSE COLECTOMY
Lesions in the mid and distal transverse
colon
Resecting the transverse colon
Ligating the middle colic vessels.
Colocolonic anastomosis.
Extended right may be a safer anastomosis
with an equivalent functional result.
LEFT COLECTOMY
Lesions in distal transverse colon, splenic
flexure, or descending colon.
The left branches of the middle colic
vessels, the left colic vessels, and the first
branches of the sigmoid vessels are ligated.
A colocolonic anastomosis.
EXTENDED LEFT COLECTOMY
Option for removing lesions in the distal transverse colon.
In this operation, the left colectomy is extended proximally to include the right branches of the middle
colic vessels.
SIGMOID COLECTOMY
Lesions in the sigmoid colon
Ligation of the sigmoid branches of the
inferior mesenteric artery.
anastomosis created between the
descending colon and upper rectum.
TOTAL OR SUBTOTAL
COLECTOMY
The superior rectal vessels are preserved.
If the sigmoid is to be resected (total abdominal colectomy with ileorectal anastomosis).
preserve the sigmoid, the distal sigmoid vessels are left intact (subtotal colectomy with ileosigmoid anastomosis).
HARTMANN PROCEDURE.
PROCTOCOLECTOMY
Total Proctocolectomy. In this procedure, the entire colon, rectum, and anus are removed, and the
ileum is brought to the skin as a Brooke ileostomy.
Restorative Proctocolectomy (Ileal Pouch–Anal Anastomosis). The entire colon and rectum are
resected, but the anal sphincter muscles and a variable portion of the distal anal canal are preserved.
Anastomosis of an ileal reservoir to the anal canal
FOLLOW-UP
Stool guaiac test
Annual CT scan of abdomen/pelvis and CXR for up to 5 years
Colonoscopy at 1 year and then every 3 years until negative then every 5 years.
CEA levels are checked periodically (every 3 months in the first year) and then every 6 months the next 4 years.
OTHER TYPES
Carcinoid Tumors.
Lipomas.
Lymphoma.
Leiomyoma and Leiomyosarcoma.
REFERENCES:
Schwartz’s Principles of Surgery.
Bailey and love’s short practice of surgery
Surgical recall.
The washington manual of surgery.
THANK YOU