Colorectal Tumors

Download as pdf or txt
Download as pdf or txt
You are on page 1of 62

Colo-rectal tumors

Mohammad Al-Haj Qasem, MD


General & laparoscopic Surgeon
Specialized Arab hospital
o Anatomy
o Arterial supply
o Venous return
Non-neoplastic epithelial
polyps

Neoplastic epithelial
Benign tumors polyps

Mesenchymal tumors
 A polyp is a well circumscribed tissue mass that protrudes
into the lumen of the colon.
o Pedunculated, sessile, flat or depressed

o Non-neoplastic may be formed as a result of abnormal


mucosal maturation, inflammation or architecture.
o Neoplastic as the result of proliferative dysplasia
(premalignant lesions).
Non-neoplastic polyps

Hyperplastic Hamartomatous Inflammatory Lymphoid


polyps polyps polyps polyps
 Juvenile polyps
 Peutz-Jeghers’
polyps
Non-neoplastic polyps

 The majority of occur on a sporadic basis and increase in


frequency with age.

 Hyperplastic polyps: (metaplastic)


o usually a diameter of less than 5 mm.
o Found in the rectum and sigmoid in a multiple manner
o grow more slowly and have a longer lifespan than adjacent
normal mucosa cells.
 Hamartomas:
o is composed of an abnormal mixture of normal tissue.
o may occur sporadically or be associated with the rare
autosomal dominant juvenile polyposis syndrome.

 Juvenile polyps:
o congenital polyp, retention polyp, juvenile adenoma.
o usually occurs in children under 10 years of age, M>F.
o It is the most frequent colorectal tumor in children.
o Nearly 80% occur in the rectum but they may be scattered
throughout the colon.
o The majority of these polyps are larger than 1 cm in
diameter.
 Juvenile polyposis syndrome:

o multiple juvenile polyps arise in the colon but also in the


intestinal tract.
o Symptoms and signs are hematochezia, iron deficiency
anemia, hypoproteinemia, hypokalemia, anergy.
o There are extracolonic congenital and acquired
manifestations as macrocephaly, alopecia, bony swellings,
cleft lip, cleft palate, double renal pelvis and ureter, acute
glomeronephritis, undescended testicle and bifid uterus and
vagina.
o As juvenile polyposis is considered a potential premalignant
condition an aggressive management is indicated.
 Peutz-Jeghers’ polyps:
o occur singly or multiple in the Peutz-Jeghers’ syndrome which is a
rare autosomal dominant disease.
o Multiple polyps scattered throughout the entire gastrointestinal
tract and melanotic mucosal and cutaneous pigmentation around
the lips, oral mucosa, face, genitalia and palmar surfaces of the
hands.
o Diagnosis of the syndrome is based on family history, skin
pigmentation and gastrointestinal symptoms.
o The most common signs are abdominal pain often due to intestinal
obstruction (polyps or intussusception) and rectal bleeding.
o These patients have an increased risk of developing carcinomas of
the pancreas, breast, lung, ovary and uterus.
 Inflammatory polyps:
o Inflammatory (pseudo-) polyps representing inflamed
regenerating mucosa surrounded by ulceration,
o seen in patients with long standing inflammatory bowel
disease (ulcerative colitis or Crohn’s disease).

 Lymphoid polyps:
o occur typically where clusters of lymphoid follicles are
present (terminal ileum, rectum).
o Rectal lesions may lack symptoms while colonic polyps may
cause bleeding, abdominal pain, changing bowel habits and
intussusception above all in children.
o Removal is important in order to differentiate the condition
from other polyps.
Neoplastic epithelial polyp

Tubular Tubulovillous Villous


adenoma adenoma adenoma
Neoplastic epithelial polyps
 Benign, but have the potential to develop into cancer.

 These polyps are classified by histology into three types:


1. Tubular adenomas (75% of adenomas) have a smooth,
firm surface and are often on a stalk.
2. Villous adenomas (10% of adenomas) are soft, sessile
lesions. Large villous adenomas may cause watery
diarrhea and potassium loss.
3. Tubulovillous adenomas (15% of adenomas) have
elements of both tubular and villous adenomas.
 At least 3 characteristics of polyps are associated with malignancy:

1. Size
o Polyps <1 cm: 1% malignant
o Polyps 1–2 cm in size: 10% malignant
o Polyps >2 cm in size: 50% malignant

2. Histologic type
o Tubular: 5% malignant
o Tubulovillous: 20% malignant
o Villous: 40% malignant

3. Grade of atypia
o Mild: 5% malignant
o Moderate: 20% malignant
o Severe: 35% malignant
Lipoma

Leiomyoma

Mesenchymal tumors

Neuroma

 Hemangioma
Angioma  Lymphangioma
Mesenchymal lesions
 Lipoma:
o the second most common benign tumor of the colon after
adenomatous polyps.
o The most common intramural tumor.
o They are mostly diagnosed with colonoscopy (cushion sign).
o As long as asymptomatic they do not require treatment.
o However with size in excess of 2 cm they give rise to some
symptoms: constipation, diarrhea, abdominal pain, rectal
bleeding and intussusception
o Colonoscopic resection is the treatment of choice.
 Leiomyoma:
o The tumor may be an incidental finding in asymptomatic
individual.
o Patients sometimes present with pain, intestinal
obstruction, hemorrhage or resistance in the abdomen.
o The mitotic rate is the single most important criterion for a
diagnosis of malignancy.
o Recurrences are frequent, mostly due to malignant
transformation
 Neuroma:
o Neuroma, neurofibroma are rare histologies found in the
colon and rectum.
o Visceral involvement in disseminated neurofibromatosis von
Recklinhausen is an extremely rare appearance of the
disease.
o Gastrointestinal bleeding or intestinal obstruction are the
main symptoms.
o Treatment has been local excision, if possible or resection.
 Angioma
 Hemangioma
o The pathogenesis is probably congenital.
o Capillary hemangiomas consist of small, thin walled.
o Cavernous hemangiomas are composed of large thin
vessels.
o Thrombosis is common in cavernous hemangiomas;
calcification frequently occurs.
o The most common complication of colonic hemangiomas is
bleeding (60 to 90%).
o Resection of a bleeding one is the optimal treatment, rectal
hemangiomas may be treated by sclerosing therapy.
o Radiation therapy in the rectum may be an alternative
approach.

 Lymphangioma:
o Lymphangiomas may be pedunculated, can be safely
removed via the colonoscope.
o Limited resection should be considered for all sessile
tumors.
Colo-rectal cancer
Incidence
 Most common malignancy in GIT
 Third most common cancer over all
 Second most common cause of cancer death
 Incidence increases with age starting at age 40, rapid
increase at 50 years and peak at 60–79 years of age.
 The lifetime risk is about 5%.
 This risk is slightly higher in male than in female.
Types
 Adenocarcinomas: represents more than 95% of colorectal
cancers.

 less common types include:


o Carcinoid tumors: These tumors start from specialized
hormone-producing cells in the intestine, neuroendocrine
cells [APUD] tumors).
o Gastrointestinal stromal tumors (GISTs): arise from
interstitial cells of Cajal in the colonic wall. Some are
benign; others are malignant, can be found anywhere in the
digestive tract, but unusual in the colon.
 Lymphomas: These are cancers of immune system cells that
typically start in lymph nodes, but they may also start in the
colon, rectum, or other organs
 Sarcomas: These tumors can start in blood vessels as well as in
muscle and connective tissue in the wall of the colon and
rectum. Sarcomas of the colon or rectum are rare.
Risk factors
 A family history of colorectal cancer:
o People who have two or more close relatives with colorectal
cancer make up about 20% of all people with colorectal
cancer
 FAP and HNPCC: accounts for 5%–10% of patients with colorectal
cancer.
 Ethnic background: Ashkenazi Jews.
 Age: increase markedly after age 50
 Diet: high fat diets, low Fiber diets, low Calcium diets.
 Obesity
 Personal history of colorectal polyps
 Personal history of chronic inflammatory bowel disease:
o UC higher risk than CD for malignancy
o In ulcerative pancolitis, the risk of carcinoma is 2% after 10
years, 8% after 20 years, and 18% after 30 years
 Diabetes increases the chance of cancer by 30%–40%.
 Smoking: Smokers are 30%–40% more likely than nonsmokers to
die from colorectal cancer.
 Alcohol intake.
 Familial adenomatous polyposis (FAP):

o FAP is caused by mutations in the APC gene.


o About 1% of all colorectal cancers are due to FAP
o Patients develop hundreds or thousands of polyps in their
colon and rectum, usually in their teens or early adulthood.
o Cancer usually develops in 1 or more of these polyps as early
as age 20. By age 40, almost all people will develop colon
cancer if the colon isnt removed first to prevent it.
o In attenuated FAP, which is a subtype of FAP, patients have
fewer polyps (<100) and colorectal cancer tends to occur at
a later age
o Gardner syndrome is a type of FAP that also has benign
(non-cancerous) tumors of the skin, soft tissue, and bones.
 Hereditary non-polyposis colon cancer (HNPCC):

o Lynch syndrome, accounts for about 2% to 4% of all colorectal


cancers.
o In most cases, is caused by an inherited defect in either the gene
MLH1 or MSH2, and other genes, which normally help repair DNA
damage.
o The cancers develop when people are relatively young, but not as
young as in FAP.
o People with HNPCC may also have polyps, but few.
o The lifetime risk of colorectal cancer may be as high as 80%.
o Women with HNPCC also have a very high risk of developing
endometrial cancer.
o Other cancers linked with HNPCC: cancer of the ovary, stomach,
small bowel, pancreas, kidney, brain, ureters, and bile duct.
 can be diagnosed by genetic testing or the Amsterdam II
criteria:
o Three or more family members with an HNPCC-related cancer
(colorectal, endometrial, small bowel, ureter, renal pelvis), one of
whom is a first-degree relative of the other two;
o Two successive affected generations;
o At least one colorectal cancer diagnosed before the age of 50
years;
o FAP excluded;
o Tumors verified by pathological examination.

 Patients with HNPCC are subjected to regular (every one to two


years) colonoscopic surveillance.
 MUTYH-associated polyposis (MAP):

o Autosomal recessive syndrome.


o colon polyps will become cancerous if the colon is not
removed.
o They also have an increased risk of cancers of the small
intestine, skin, ovary, and bladder.
o This syndrome is caused by mutations in the gene MUTYH
Prevention

 Increase fiber in diet


 Decrease animal fat and red meat,
 Decrease smoking and EtOH
 Increase exercise and decrease BMI
 Secondary prevention with screening
Screening

 Screening: is the process of looking for cancer or pre-cancer in


people who have no symptoms of the disease.
 From the time the first abnormal cells start to grow into polyps,
it usually takes about 10 to 15 years for them to develop into
colorectal cancer.
Screening Tools
 Digital rectal exam (DRE): most common exam, but not
recommended as a screening tool
 Fecal occult blood test (FOBT):
• proper test requires 3 samples of stool
• still recommended annually by the World Health Organization
(WHO)
• results in 16-33% reduction in mortality in RCTs
• Minnesota Colon Cancer Study: RCT showed that annual FOBT can
decrease mortality rate by 1/3 in patients 50-80 years old
 Sigmoidoscopy:
• can identify 30-60% of lesions
• sigmoidoscopy + FOBT misses 24% of colonic neoplasms
 Colonoscopy:
• can remove or biopsy lesions during procedure
• can identify proximal lesions missed by sigmoidoscopy
• used as follow-up.
• Risk of perforation 0.2%
 Virtual colonoscopy (CT colonography): 91% sensitive, 17%
false positive rate
 Air contrast barium enema: 50% sensitive for large (>1 cm)
adenomas, 39% for polyps
 Carcinogenic embryonic antigen (CEA): to monitor for
recurrence q3 months
Signs and symptoms
 Colorectal cancer may cause one or more of the symptoms
below.
o A change in bowel habits
o Rectal bleeding
o Blood in the stool which may make it look dark
o Cramping or abdominal pain
o Weakness and fatigue
o Unintended weight loss
Presentation
 Emergency, chronic symptoms.
 Right side lesions:
o Anaemia, mass, diarrhoea, appendicitis like symptoms, and
small bowel obstructions.
 Left side lesions:
o Change in bowel habit,
o colicky abdominal pain,
o progressive constipation,
o blood in stool.
 NB: Non specific abdominal pain 50%.
Diagnosis
 Medical history and physical exam:
o Complete medical history to check for symptoms and risk
factors, including family history
o As part of a physical exam, examination of abdomen for
masses or enlarged organs and the rest of body, DRE

 Blood tests:
o Complete blood count (CBC): to look if there is anemia.
o Liver enzymes: to look for liver metastasis.
 Tumor markers:
o The most common tumor markers for colorectal cancer are
carcinoembryonic antigen (CEA).
o Used to monitor patients who already have been diagnosed
with or treated for colorectal cancer.
o These tumor markers are not used to screen for or
diagnose colorectal cancer.
o can sometimes be normal in a person who has cancer
o higher levels may be found in patients with ulcerative
colitis, non-cancerous tumors of the intestines, or some
types of liver disease or chronic lung disease
 If symptoms/signs or blood tests suggest that colorectal cancer
might be present:
o Colonoscopy+Biopsy: Usually if a suspected colorectal
cancer is found by any diagnostic test, it is biopsied during a
colonoscopy.
o Computed tomography (CT) scan: can help tell if colon
cancer has spread into your liver or other organs.
o Ultrasound: can be used to look for tumors in liver,
gallbladder, pancreas, or elsewhere in abdomen, it is often
done if the CT shows tumors in the liver.
 Two special types of ultrasound exams are sometimes used to
evaluate colon and rectal cancers.
o Endorectal ultrasound: used to see how far cancer
penetration through the rectal wall and whether it has
spread to nearby organs or tissues such as lymph nodes.
o Intraoperative ultrasound: This exam is done intra-
operatively to look for liver spread.
 Magnetic resonance imaging (MRI) scan: can be helpful in
rectal cancers to look for nearby structures spread, also
sometimes useful in looking at abnormal areas in the liver.
 Chest x-ray: to see if cancer has spread to the lungs.
 Positron emission tomography (PET) scan A PET scan can help
give the doctor a better idea of whether an abnormal area seen
on another imaging test is a tumor or not. also be useful if
doctor thinks the cancer may have spread but doesn't know
where.
 PET/CT scan: This allows to compare areas of higher
radioactivity on the PET with the more detailed picture of that
area on the CT.
 Angiography: can help to decide if the liver tumors can be
removed and also planning other treatments, like embolization
Staging

 Staging is the process of finding out how far a cancer has


spread. This involves a physical exam, biopsies, and imaging
tests (CT or MRI scan, x-rays, PET scan, etc).
 If the stage is based on the results of the physical exam, biopsy,
and any imaging tests, it is called a clinical stage
 If surgery has been done the results can be combined with
clinical stage factors, called a pathologic stage
 Pathologic staging is likely to be more accurate than clinical
one.
AJCC (TNM) Staging System
 Tis: The cancer is in the earliest stage (in situ). It involves only the
mucosa. It has not grown beyond the muscularis mucosa (thin inner
muscle layer).
 T1: The cancer has grown through the muscularis mucosa and extends
into the submucosa.
 T2: The cancer has grown through the submucosa and extends into
the muscularis propria.
 T3: The cancer has grown through the muscularis propria and into the
outermost layers of the colon or rectum but not through them. It has
not reached any nearby organs or tissues.
 T4a: The cancer has grown through the serosa (visceral peritoneum).
 T4b: The cancer has grown through the wall of the colon or rectum
and is attached to or invades into nearby tissues or organs.
 N categories: indicate if the cancer has spread to nearby lymph
nodes.
 To get an accurate idea about lymph node involvement, most doctors
recommend that at least 12 lymph nodes be removed during surgery
and looked at under a microscope.
 N0: No cancer in nearby lymph nodes.
 N1: Cancer cells are found in or near 1 to 3 nearby lymph nodes
o N1a: Cancer cells are found in 1 nearby lymph node.
o N1b: Cancer cells are found in 2 to 3 nearby lymph nodes.
o N1c: Small deposits of cancer cells are found in areas of fat near
lymph nodes, but not in the lymph nodes themselves.
 N2: Cancer cells are found in 4 or more nearby lymph nodes
o N2a: Cancer cells are found in 4 to 6 nearby lymph nodes.
o N2b: Cancer cells are found in 7 or more nearby lymph nodes.
 M categories: indicate whether or not the cancer has spread
(metastasized) to distant organs
o M0: No distant spread is seen.
o M1a: The cancer has spread to 1 distant organ or set of
distant lymph nodes.
o M1b: The cancer has spread to more than 1 distant organ or
set of distant lymph nodes, or it has spread to distant parts
of the peritoneum.
o M1c: Metastasis to the peritoneal surface is identified alone
or with other site or organ metastases
Cancer spread
 Direct spread:

 Lymphatic spread:
Epicolic, paracolic, para aortic lymph nodes.

 Blood borne spread:


Liver 50%, lung10%.

 Transcoelomic spread
Grades of colorectal cancer
 It describes how closely the cancer looks like normal tissue
when seen under a microscope, affect outlook for survival
 The scale used for grading colorectal cancers goes from 1 to 4.
o Grade 1 (G1) means the cancer looks much like normal
colorectal tissue.
o Grade 4 (G4) means the cancer looks very abnormal.
o Grades 2 and 3 (G2 and G3) fall somewhere in between.
 The grade is often simplified as either low grade (G1 or G2) or
high grade (G3 or G4).
 Low-grade cancers tend to grow and spread more slowly than
high-grade cancers.
Clinicopathological staging
 Dukes’ staging:
o A ic not breaching muscularis propria
o B ic breaching muscularis propria
o C ic involving lymph nodes
o D ic with distant metastasis
Treatment

 SURGERY (indicated in potentially curable or symptomatic


cases - not always in stage IV)
o Curative: wide resection of lesion (5 cm margins) with nodes
and mesentery
o Palliative: if distant spread, then local control for
hemorrhage or obstruction
 80% of recurrences occur within 2 years of resection
 Improved survival if metastasis consists of solitary hepatic mass
that is resected
 Colectomy:
 most patients get primary anastomosis (e.g. hemicolectomy,
low anterior resection (LAR)-
 if cancer is below levators in rectum, patient may require an
abdominal perineal resection (APR) with a permanent end
colostomy, especially if lesion involves the sphincter
complex.
 Complications: anastomotic leak or stricture, recurrent
disease, pelvic abscess, enterocutaneous fistula
 RADIOTHERAPY & CHEMOTHERAPY:
 Chemotherapy (5-FU based regimens): for patients with
node-positive disease
 Radiation: for patients with node-positive or transmural
rectal cancer (pre ± post-op), not effective in treatment of
colon cancer
 Adjuvant therapy – chemotherapy (colon) and radiation
(rectum)
 Palliative chemotherapy/radiation therapy for improvement
in symptoms and survival
Operative technique
 Right hemicolectomy

 Extended right hemicolectomy

 Lt hemicolectomy

 Sigmoid colectomy

 Anterior resection

 Low anterior resection

 Abdomino-perineal resection (APR)


Thanks

You might also like