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GS II Presentation
A report by Block 6
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General Information This is the case of a 58 year old female, presenting with
a chief complaint of epigastric pain
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History of Present Illness
10 months
PTC
Pt felt epigastric pain, VAS 3/10.Sought consult and was prescribedomeprazole which she took daily.
(+) vomiting, anorexia
5 monthsPTC
Pt felt a hard fixed mass on R flank
with pain upon movement (+) directtenderness
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Targeted Review of Systems (+) increased bowel movements, hematochezia,
mucus mixed with stool, stool more malodorous,watery stools, abdominal pain, anorexia, weight loss
(-) vomiting, fever, chills,
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Past Medical History (-) TB, BA, Hpn, DM, Blood dyscracias
Has had no previous operations
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Family Medical History (+) bukol sa bituka in the mother
(-) TB, BA, Hpn, DM, Blood dyscracias
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Personal/Social History (+) prior OCP use
(+) occasional alcoholic beverage drinker
(-) smoking, illicit drug use
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OB History G4P4 (4004)
All 4 kids born full term, at home via a midwife andencountered no fetomaternal complications
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Targeted Physical ExaminationFindings HEENT: Pink conjunctivae, anicteric sclerae, pink oral
mucosa, thyroid not enlarged, (-) ANM, NVE, CLAD,trachea midline
Chest and lungs: ECE, CBS, (-) crackles, wheezes
Cardiac: AP, DHS, NRRR, (-) murmurs
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Targeted Physical ExaminationFindings HEENT: Pink conjunctivae, anicteric sclerae, pink oral
mucosa, thyroid not enlarged, (-) ANM, NVE, CLAD,trachea midline
Chest and lungs: ECE, CBS, (-) crackles, wheezes
Cardiac: AP, DHS, NRRR, (-) murmurs
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Targeted Physical ExaminationFindings Abdomen: Flat, soft, HABS, (+) direct tenderness on R
waist, (+) firm, tender mass on R waist.
GU: IE deferred
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Targeted Physical ExaminationFindings HEENT: Pink conjunctivae, anicteric sclerae, pink oral
mucosa, thyroid not enlarged, (-) ANM, NVE, CLAD,trachea midline
Chest and lungs: ECE, CBS, (-) crackles, wheezes
Cardiac: AP, DHS, NRRR, (-) murmurs
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Targeted Physical ExaminationFindings Abdomen: Flat, soft, HABS, (+) direct tenderness on R
waist, (+) firm, tender mass on R waist.
GU: IE deferred
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Targeted Physical ExaminationFindings HEENT: Pink conjunctivae, anicteric sclerae, pink oral
mucosa, thyroid not enlarged, (-) ANM, NVE, CLAD,trachea midline
Chest and lungs: ECE, CBS, (-) crackles, wheezes
Cardiac: AP, DHS, NRRR, (-) murmurs
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Targeted Physical ExaminationFindings Abdomen: Flat, soft, HABS, (+) direct tenderness on R
waist, (+) firm, tender mass on R waist.
GU: IE deferred
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Targeted Physical ExaminationFindings HEENT: Pink conjunctivae, anicteric sclerae, pink oral
mucosa, thyroid not enlarged, (-) ANM, NVE, CLAD,trachea midline
Chest and lungs: ECE, CBS, (-) crackles, wheezes
Cardiac: AP, DHS, NRRR, (-) murmurs
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Targeted Physical ExaminationFindings Abdomen: Flat, soft, HABS, (+) direct tenderness on R
waist, (+) firm, tender mass on R waist.
GU: IE deferred
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Targeted Physical ExaminationFindings Abdomen: Flat, soft, HABS, (+) direct tenderness on R
waist, (+) firm, tender mass on R waist.
GU: IE deferred
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Differential Diagnoses
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Colorectal Cancer R/I
(+) change in bowel movements, hematochezia, waterystools, abdominal pain, anorexia, weight loss, FMH of
abdominal tumor
R/o
Cannot be ruled out
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Crohns Disease R/I
(+) increased bowel movements, hematochezia,watery stools, abdominal pain, anorexia, weight loss
R/o
Cannot be entirely ruled out
Diarrhea of patient is of acute onset
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Ulcerative Colitis R/I
(+) increased bowel movements, watery stools,abdominal pain, anorexia, weight loss
R/O
Incontinence, urgency
No specific trigger for diarrhea
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Colonic Diverticulitis R/I
(+) increased bowel movements, watery stools,abdominal pain, anorexia, weight loss
R/o
(-) fever, chills, nausea, vomiting,
constipation/diarrhea pattern, urinary symptoms
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Colonic Polyps R/I
(+) increased bowel movements, watery stools,decreased caliber of stools, abdominal pain, >50 yo,
R/o
(-) fever, chills, nausea, vomiting,
constipation/diarrhea pattern, urinary symptoms
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Colon Cancer
Pathophysiology
F d t
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From adenoma tocarcinoma
carcinomas evolve through a progression of benignpolyps to invasive carcinoma
the larger the polyp, the higher the risk for cancer
tubular adenoma 2 cm 35%
villous adenomas carry a higher risk
than tubular adenomas villous adenoma >2 cm 50%
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Hereditary
(+) family history young age at onset presence of other
specific tumors anddefects
genetic mutation/spresent in all cells ofthe affectedindividual.
Sporadic
(-)family history older population (60-
80 y.o.) usually presents as
an isolated colon orrectal lesion
genetic mutation/slimited to the tumoritself.
Familial
Higher risk for familymembers: index case is young
(
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Mutation
Activationof
oncogenes(K-RAS)
Inactivation oftumor-
suppressorgenes (APC,
DCC, p53)
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APCgene tumor suppressor gene
located on chromosome 5q21
regulates the intracytoplasmic pool of -catenin
-catenin is a multifunctional protein which activates
transcription of genes like c-myc and others that regulatecellular growth and proliferation.
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also influences cell cycleproliferation by regulatingWnt expression
As -catenin levels rise,Wnt is activated.
Overexpression of Wntleads to activation of Wnttarget genes such ascyclin D1 and Myc, whichdrive cell proliferationand tumor formation.
APCgene
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K-ras gene proto-oncogene
mutation of only one allele will perturb the cell cycle
The K-ras gene product is a G protein involved inintracellular signal transduction
mutation G protein remains
in active formuncontrolled cell division
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DCC gene tumor suppressor gene
loss of both alleles is required for malignantdegeneration
role is poorly understood
may be involved in differentiationand cellular adhesion incolorectal cancer
more than 70% of colorectal
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p53 gene most frequently mutated tumor suppressor gene
occur rather late in the adenoma-carcinoma sequence
induces apoptosis in response to cellular damage
causes G1
cell-cycle arrest, allowing DNA repairmechanisms to occur
75% of colorectal cancers
prognostic significance
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MYH gene
Recently, a number of families were characterized with aphenotype resembling that of FAP or AFAP, but without adiscoverable APCgene defect.
Autosomal recessive inheritance
mutations in the gene responsible for base excision-repair and used to repair oxidative DNA damage
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Genetic Pathways
Loss of heterozygosity (LOH)pathway
chromosomal deletions andtumor aneuploidy
80% of colon CA
microsatellite stable
tend to occur in the moredistal colon, often have
chromosomal aneuploidy,and are associated with apoorer prognosis
Replication error
(RER) pathway
errors in mismatch repair
during DNA replication 20% of colon CA
associated withmicrosatellite instability(MSI)
tumors with MSI are morelikely to be right sided,possess diploid DNA, andare associated with a betterprognosis
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Mismatch repair genes
hMSH2, hMLH1, hPMS1,hPMS2, and hMSH6/GTBP
caretaker genes
police the integrity of thegenome and correct DNAreplication errors
mutations result in in the
HNPCC syndrome
microsatellite instability
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Incidence & risk factors
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Incidence
Most common malignancy of the GI tract
In 2003, the World Health Organization estimatedthat approximately 940,000 individuals werediagnosed with colorectal cancer worldwide and492,000 died from it that year.
Colorectal cancer is the third leading cause of
cancer deaths in the Philippines. In 2005, there were2,657 deaths due to colorectal cancer.
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Risk Factors
Aging
dominant risk factor for colorectal cancer
>90% of cases diagnosed in people older than 50
years
Hereditary Risk Factors
~ 80% sporadic
~ 20% with (+) family history
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Risk Factors
Environmental and DietaryFactors
Risk
Saturated or polyunsaturated fats Increase
Oleic acid (olive oil, coconut oil, fishoil) No increaseVegetable fiber Appears to be
protective
Alcohol IncreaseCalcium, selenium, vitamins A, C,and E, carotenoids, and plantphenols
May decrease
Obesity and sedentary lifestyle Increase dramatically
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Risk Factors
Inflammatory bowel disease
increased risk for the development of colorectal cancer
Other factors thought to increase risk include the
presence of primary sclerosing cholangitis and familyhistory of colorectal cancer.
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Other Risk Factors
Cigarette smoking
increased risk especially after >35 years of use
Patients with ureterosigmoidostomy
Acromegaly increased human growth hormone and IGF-I
Pelvic irradiation
Obesity
F t With D d Ri k f C l
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Factors With Decreased Risk of ColonCancer
Physical activity
Relative reduction risk of 40-50% for people with highenergy expenditure
NSAIDS
Postmenopausal female supplement
Diet Modification
Dietary fat and meat intake
Dietary fiber, vegetables,fruit
Vitamin E, Calcium
Statins
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Screening
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Screening
Preferred CRC screening recommendations:
Cancer prevention tests should be offered first. The
preferred CRC prevention test is colonoscopy every 10
years, beginning at age 50. Screening should begin at age 45 years in African
American
Cancer detection test. This test should be offered topatients who decline colonoscopy or another cancer
prevention test. The preferred cancer detection test isannual FIT for blood.
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Screening
Alternative CRC prevention tests:
Flexible sigmoidoscopy every 5 10 years
CT colonography every 5 years
Alternative cancer detection tests:
Annual Hemoccult Sensa
Fecal DNA testing every 3 years
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Screening
Recommendations for screening when family history ispositive but evaluation for HNPCC considered not indicated
Single first-degree relative with CRC or advanced
adenoma diagnosed at age 60 years Recommended screening: same as average risk
(colonoscopy every 10 years beginning at age 50 years)
Single first-degree with CRC or advanced adenomadiagnosed at age
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Screening
FAP
Patients with classic FAP (>100 adenomas) shouldbe advised to pursue genetic counseling and genetic
testing, if they have siblings or children who couldpotentially benefit from this testing
Patients with known FAP or who are at risk of FAPbased on family history (and genetic testing has not
been performed)should undergo annual flexiblesigmoidoscopy or colonoscopy, as appropriate, untilsuch time as colectomy is deemed by physician andpatient as the best treatment
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Screening
FAP
Patients with retained rectum after subtotalcolectomy should undergo flexible sigmoidoscopy
every 6 12 months
Patients with classic FAP, in whom genetic testing isnegative, should undergo genetic testing for bi-allelic
MYH mutations. Patients with 10 100 adenomascan be considered for genetic testing for attenuatedFAP and if negative, MYH associated polyposis
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Screening
HNPCC
Patients who meet the Bethesda criteria shouldundergo microsatellite instability testing of their
tumor or a family members tumor and/or tumorimmunohistochemical staining for mismatch repairproteins
Patients with positive tests can be offered genetic
testing. Those with positive genetic testing, or thoseat risk when genetic testing is unsuccessful in anaffected proband, should undergo colonoscopyevery 2 years beginning at age 20 25 years, untilage 40 years, then annually thereafter
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Work-up
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Laboratory Studies
Goal of assessing patients organ function (liver,
kidneys) in anticipation of diagnostic and therapeuticprocedures
Estimate tumor burden (carcinoembryonic antigen[CEA] level)
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Laboratory Studies
Complete blood cell count
Chemistries and liver function tests
Serum CEA
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Imaging Studies
Adequate imaging of the chest and abdomen should
be obtained for the purpose of staging.
Chest radiograph or chest CT scan
Abdominal barium study Abdominal/pelvic computerized tomography (CT
scan)
Contrast ultrasound of the abdomen/liver
Abdominal/pelvic MRI Positron emission tomography (PET) scans
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Procedures
Rectal examination
Colonoscopy
Sigmoidoscopy
Double contrast barium enema
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Histologic Findings
Microscopic appearance of colon adenocarcinomas
well-differentiated or
poorly differentiated glandular structures
Normal topological architecture of colonicepithelium in terms of a crypt-villous axis is lost.
N l Hi l
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Normal Histology
P l Diff i d
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Poorly Differentiated
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Colon cancer staging
TNM S i
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TNM Staging
International standard for staging colorectal cancer
3 descriptors:
T for primary tumor
N for lymph nodal involvement
M for metastasis
P i T (T)
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Primary Tumor (T)
NCCN: Clinical Practice Guidelines in Oncology: Colon Cancer. 2011.
R i l L h N d (N)
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Regional Lymph Nodes (N)
NCCN: Clinical Practice Guidelines in Oncology: Colon Cancer. 2011.
Di t t M t t i (M)
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Distant Metastasis (M)
NCCN: Clinical Practice Guidelines in Oncology: Colon Cancer. 2011.
Anatomic Stage/Prognostic
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Anatomic Stage/PrognosticGroups
NCCN: Clinical Practice Guidelines in Oncology: Colon Cancer. 2011.
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Management of
Colorectal Cancers
A report by Block 6
References:
Sabiston, Textbook of Surgery 18th ed
Schwartz, Principles of Surgery, 9th ed
NCCN Guidelines for Colon Cancer
P i i l f R ti
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Principles of Resection
TumorRemoval
Identify FieldDefects
Lymph NodeResections
Lymphovascular supply
Vessels, omentum,adjacent organs
Strong family history ofcolonic neoplasms
Subtotal versusComplete colectomies
Oncologic adequacy ofresection
12-node minimum
St S ifi Th
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Stage Specific Therapy
No risk of lymph node metastasis
Excision with assuranceStage 0
Based upon the risk of local recurrence andthe risk of lymph node metastasis.
Depends primarily on depth of invasion
Stage 1Malignant
Polyp
Cured with surgical resection Up to 46% of patients cured, die of colon
cancer, hence neoadjuvant therapy is advised.
Stage 1Localized
Carcinoma
St S ifi Th
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Stage Specific Therapy
Neoadjuvant therapy based on 5-FU reducesrecurrence.
New chemotherapeutic agents, capecitabine,irinotecan, oxaliplatin, angiogenesis inhibitors, andimmunotherapy are promising
Stage III
Tany, N1,M0
All patients require neoadjuvant chemotherapy
Survival is extremely limited, but highly selectedpatients with isolated, resectable metastases (usuallyin the liver or lungs) may benefit from metastectomy.
In those who cannot be cured surgically, palliation isthe focus of therapy.
Stage IVTany, N1, M1
M li t P l
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Malignant Polyp
A malignant polyp is defined as one with cancerinvading the submucosa
Classified as carcinoma in-situ, and therefore they
have not penetrated the submucosa and do notmetastasize.
In patients with invasive cancer or adenoma(tubular, tubulovillous, or villous), no additionalsurgery is required if the polyp has been completelyresected and has favorable histological features.
Favorable features: grade 1 or 2 lesion, nolymphovascular space invasion, negative resection
margins
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Malignant Polyp
Colectomy with en bloc removal of lymph nodes is recommended if: The polyp is fragmented
The margins cannot be assessed
There is unfavorable histology
All patients who have resected polyps should undergo total colonoscopyto rule out other synchronous polyps, as well as appropriate follow-up
surveillance endoscopy.
Non-metastatic Invasive
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o etastat c as eCarcinoma
A complete staging workup is mandatory, including:
Pathologic tissue review
Total colonoscopy
CBC
Blood chemistry profile
Carcinoembryonic antigen (CEA) determination
Baseline computed tomographic (CT) scans of the
chest, abdomen, and pelvis.
Non-metastatic Invasive
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Carcinoma
Surgical procedure of choice (if resectable):
Colectomy with en bloc removal of the regional lymphnodes.
Extent should be based on the tumor location,resecting the portion of the bowel and arterial arcadecontaining the regional lymph nodes.
Other nodes, such as those at the origin of the vesselfeeding the tumor, as well as suspicious lymph nodesoutside the field of resection, should also be biopsiedor removed if possible.
Non-metastatic Invasive
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Carcinoma
For resectable colon cancer that is causing overtobstruction, resection with diversion, stent insertionfollowed by colectomy, or diversion followed bycolectomy are options.
If the cancer is locally unresectable or medicallyinoperable, chemotherapy is recommended with thegoal of converting the lesion to a resectable state.
Chemotherapy in Colon
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pyCancer
Choices for adjuvant therapy for patients with resectednonmetastatic colon cancer are dependent on the stage ofdisease:
Stage 2 (high risk) & Stage 3
6 mos. 5-FU/LV/oxaliplatin capecitabine
Stage 2 (low risk)
5-FU capecitabine
Stage 1
No need for adjuvant therapy
Chemotherapy in Colon
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Chemotherapy in Colon
Cancer Relapses occur within 2 years following surgery Relapse rates (
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Types of Chemotherapy
FOLFOX (infusional 5-fluorouracil (5-FU), leucovorin(LV), oxaliplatin)
Regimen of choice in both adjuvant and metastaticchemotherapy.
Complication: grade 3 peripheral sensory neuropathy
FLOX (bolus 5-FU/LV/oxaliplatin)
No statistically significant difference in over survival.
Grade 3 neurotoxicity, diarrhea, and dehydration were higherin FLOX than FOLFOX.
Capecitabine
Single agent, at least equivalent to bolus 5- FU/LV
Adjuvant Chemoradiation
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Adjuvant Chemoradiation
Radiation therapy delivered concurrently with 5-FU-based chemotherapy may be considered for veryselect patients with disease characterized as T4tumors penetrating to a fixed structure or for patientswith recurrent disease.
Radiation therapy fields should include the tumorbed as defined by preoperative radiological imaging
and/or surgical clips. Intraoperative radiotherapy(IORT), if available, should be considered for thesepatients as an additional boost.1
Invasive Metastatic Colon
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Cancer 50%-60% of patients diagnosed with colorectal cancer
will develop colorectal metastases
80%-90% of these have unresectable metastatic liverdisease
over one-half of patients who die of colorectal cancer have
liver metastases at autopsy and that metastatic liver diseaseis the cause of death in the majority of these patients.
The criteria for determining patient suitability for resectionof metastatic disease are
the likelihood of achieving complete resection of all evidentdisease with negative surgical margins
maintaining adequate liver reserve
Incomplete resection or debulking has not been shown tobe beneficial.
Invasive Metastatic Colon
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Invasive Metastatic ColonCancer
Chemotherapy is recommended in conjunction withliver resection in those patients who arechemotherapy nave.
Potential advantages of preoperative chemotherapyinclude:
earlier treatment of micrometastatic disease
determination of responsiveness to chemotherapy(which can be prognostic and help in the planning of
postoperative therapy)
avoidance of local therapy for those patients with earlydisease progression.
Invasive Metastatic Colon
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Invasive Metastatic ColonCancer
Potential disadvantages include: chemotherapy-induced liver injury
missing the window of opportunity for resection making itdifficult to identify areas for resection.
potential for development of liver steatohepatitis and sinusoidalliver injury when irinotecan- and oxaliplatin-basedchemotherapeutic regimens are administered.
The current management of disseminated metastatic colon
cancer uses various active drugs, either in combination oras single agents: 5-FU/ LV, capecitabine; irinotecan,oxaliplatin, bevacizumab, cetuximab, and panitumumab.
Nonresectable Invasive
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Metastatic Colon Cancer
Primary treatment of unresectable synchronous liveror lung metastases by palliative colon resectionshould be considered only if the patient has anunequivocal imminent risk of obstruction or acutesignificant bleeding.
Symptomatic improvement in the primary is oftenseen with systemic chemotherapy even within the
first 1 to 2 weeks, and routine palliative resection ofa synchronous primary lesion should not beroutinely done in the absence of overt obstruction.
Post-treatment
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Surveillance
Evaluate:
possible therapeutic complications
discover a recurrence that is potentially resectable for
cure to identify new metachronous neoplasms at a
preinvasive stage
Increased rates of resectability and survival in
patients treated for local recurrence and distantmetastases of colorectal cancer in more recentyears, thereby providing support for more intensivepost-treatment follow-up in these patients.
Post-treatment
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Surveillance
Colonoscopy is recommended at approximately 1 yearfollowing resection (or at approximately 3 to 6 monthspost resection if not performed preoperatively due to anobstructing lesion).
Repeat colonoscopy is typically recommended at 3years, and then every 5 years thereafter, unless follow-upcolonoscopy indicates advanced adenoma.
CT scan is recommended to monitor for the presence ofpotentially resectable metastatic lesions, primarily in the
lung and the liver. CT Scan and CEA monitoring should be done from the
1st to 5th years but are not recommended after 5 years.
Post-treatment
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Surveillance
Initial follow-up office visits at 3 month intervals forhistory and physical examination may be moreuseful for patients diagnosed with stage III disease,whereas patients with a diagnosis of stage I diseasemay not need to be seen as frequently.
Recommendation First 3 years Years 4 and 5
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RECOMMENDATIONS
Patients should undergo regular surveillance for at
least 5 years following resection.
PhysicalExamination
q 3-6 months q 6 months
Serum CEA q 3 months q 6 months
Chest andAbdominal CT Scan
Annually
Follow-up
Colonoscopy
3rd Year q 5 years