Rahaf Hasanein Anatomy Blood supply Colon arterial Supply SMA branches into I leocolic artery terminal ileum and proximal ascending colon Right colic artery ascending colon M iddle colic artery ID: 909411
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Slide1
Colon Cancer
Presented by:
Rahaf Hasanein
Slide2Anatomy+ Blood supply
Slide3Slide4Colon arterial SupplySMA 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.
Slide5Venous drainageThe 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.
Slide6The lymphatic drainageLymphatic vessels and lymph nodes follow the regional arteries.
Slide7Colon Nerve SupplyThe 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.
Slide8PolypsNonspecific 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.
Slide9Adenomatous polyps25% 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%).
Slide10(Acc. To shape)
Pedunculated -> colonoscopic snareexcision.
Sessile
Complications of polypectomyinclude perforation and bleeding
.
Slide11Hyperplastic polypsExtremely common.
These polyps are usually small (<5 mm) -> hyperplasia without any dysplasia.L
arge hyperplastic polyps (>2 cm) -> foci of adenomatous tissue and dysplasiaHyperplastic 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.
Slide12Serrated polypsSaw-toothed appearance under the microscope.
Some of these polyps will develop into invasive cancers.A familial serrated polyposis syndrome
.Serrated polyps should be treated like adenomatous polyps.
Slide13hamartomatous polyps (juvenile)Not premalignant.
Associated with mutation in PTEN.Bleeding
is a common symptom, and intussusception and/or obstruction
may occur. Treated by polypectomy.
Slide14Familial juvenile polyposisAD 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
Slide15Peutz-Jeghers syndromepolyposis 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.
Slide16Cronkite-Canada syndromeGI 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.S
urgery for complications.
Slide17Cowden’s syndromeAD.
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.
Slide18Inflammatory polypsNot premalignant.
In inflammatory bowel diseaseAfter 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.
Slide19Inherited Colorectal Carcinoma
Slide20Familial Adenomatous PolyposisAD, 1% of all colorectal adenocarcinomas. M
utation in the APC gene, on chromosome 5q (positive in 75% of cases).Up to 25% present without other affected family members.H
undreds to thousands of adenomatous polyps shortly after puberty.Risk of colorectal cancer 100% by age 50 years.
Slide21Slide22Risk 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:
Total proctocolectomy with an end (Brooke) ileostomyTotal abdominal colectomy with ileorectal anastomosisR
estorative proctocolectomy with ileal pouch–anal anastomosis with or without a temporary ileostomy.
Slide23FAP 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.
Slide24Attenuated Familial Adenomatous PolyposisVariant 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).
Slide25Genetic 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.
Slide26Hereditary 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.
Slide27The 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.
Slide28Screening 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.
Slide29Because 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.
Slide30Familial Colorectal Cancer10% 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.
Slide31ADENOCARCINOMA AND POLYPSMost common malignancy of the GIT.
Third most common cancer in women and men.Third leading cause of cancer-related deaths.F:M 1:1
Slide32Risk FactorsAging
Hereditary Risk FactorsEnvironmental and Dietary FactorsInflammatory Bowel Disease
Cigarette smoking
Patients with ureterosigmoidostomyAcromegalyPelvic irradiation
Slide33Slide34Slide35Clinical featuresDepend on: Site, Presence of complications and metastases.
Slide36SpreadDirect extension Hematogenouslymphatic
Slide37Slide38DiagnosisHx+ PEColonoscopy
to obtain biopsy and evaluate for synchronous tumors (5%)OR flexible sigmoidoscopy and barium enema.CBC, LFTWater-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
Slide39Slide40staging
Slide41Slide42Managementsurgical resection: Remove the primary tumor along with its lymphovascular
supply➢ Surgeries could be curative or palliativeAdjuvant chemotherapy: stage III / VI or locally advanced stage IIcombination of 5-fluorouracil/leucovorin with either irinotecan (FOLFIRI) or oxaliplatin (FOLFOX).
Slide43Stage-Specific TherapyStage 0 (Tis, N0, M0):
PolypectomySegmental resection.
Slide44Stage 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
Slide45Stages 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).
Slide46Stage III: Lymph Node Metastasis (T
any, N1, M0)Adjuvant chemotherapy has been recommended routinely in these patients.
Slide47Stage IV: Distant Metastasis (T
any, Nany, M1).Highly selected patients with isolated,
resectable metastases may benefit from resection (metastasectomy
).All patients require adjuvant chemotherapy.
Slide48colonic 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.
Slide49Right hemicolectomy
Carcinoma of the caecum or ascending colon.
The ileocolic vessels, right colic vessels, and right branches of the middle colic vessels are ligated.
I
leal-transverse colon anastomosis
Slide50Extended right colectomyLesions 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
Slide51Transverse colectomy
Lesions in the mid and distal transverse colon
R
esecting the transverse colon
L
igating the middle colic vessels.
Colocolonic
anastomosis.
E
xtended right may be a safer anastomosis with an equivalent functional result.
Slide52Left colectomy
L
esions 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.
Slide53Extended left colectomyOption 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.
Slide54Sigmoid colectomy
Lesions in the sigmoid colon
L
igation of the sigmoid branches of the inferior mesenteric artery.
anastomosis created between the descending colon and upper rectum.
Slide55Total 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).
Slide56Hartmann procedure.
Slide57proctocolectomyTotal 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.A
nastomosis of an ileal reservoir to the anal canal
Slide58Follow-upStool guaiac testAnnual CT scan of abdomen/pelvis and CXR for up to 5 yearsColonoscopy 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.
Slide59Other typesCarcinoid Tumors. Lipomas.
Lymphoma.Leiomyoma and Leiomyosarcoma.
Slide60References:Schwartz’s Principles of Surgery.Bailey and love’s short practice of surgery
Surgical recall.The washington manual of surgery.
Slide61Thank you