22. cervical cancer

Cervical Cancer
Hale Teka, M.D., OB-GYN Resident
Mekelle University,
College of Health Sciences, Dep't of OB-GYN

Part – I: Preinvasive Lesions of the Cervix
Hale T., M.D., Resident PhysicianFriday, December 30,
2016
2

• Contents
1. The Squamocollumnar Junction
2. Squamous Metaplasia
3. Human Papillomavirus
4. Cervical Intraepithelial Neoplasia
5. Differential Diagnosis and Evaluation of
Cervical Lesions
6. Management of Cervical Intraepithelial
Neoplasia
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2016
4

The Squamocolumnar Junction
(SCJ)
• The location of the SCJ varies with age
and hormonal status
• It everts outward onto the ectocervix
during
1. Adolescence,
2. Pregnancy, and
3. With the use of combination hormone
contraceptives
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5

• It regresses into the endocervical canal
with low estrogen states such as
1. Menopause and
2. Prolonged lactation
3. Use of progestin-only contraceptives,
4. Natural process of squamous metaplasia
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2016
7

Friday, December 30,
2016
Hale T., M.D., Resident Physician 8

Squamous Metaplasia
• Lower vaginal pH is the suspected
stimulus for squamous metaplasia
– Ongoing replacement of columnar
epithelium by squamous epithelium on the
cervix
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• Undifferentiated reserve cells are the
precursors of the new metaplastic cells,
which differentiate further into squamous
epithelium
• This normal process creates a
progressively widening band of
metaplastic epithelium termed the
transformation zone (TZ), lying
between the original SCJ and the present
columnar epithelium
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• Cervical reserve and immature metaplastic
cells appear particularly vulnerable to the
oncogenic effects of HPV and cocarcinogens
• Squamous metaplasia is most active during
adolescence and pregnancy
• This may explain why early age at
sexual activity onset and at first pregnancy are
known risk factors for cervical cancer
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2016
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• Human Papilloma Virus
– Double-stranded DNA virus with a protein capsid
– Cause of genital and extragenital cancers
– Responsible for approximately 5 percent of all
cancers
– Approximately 130 genetically distinct HPV types
have been identified
– Of these types, 30 to 40 primarily infect the lower
anogenital tract
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• Two types of genes
– Early genes
• Six “early” (E) genes govern functions early in the viral
life cycle, including DNA maintenance, replication, and
transcriptions
– Late genes
• The two “late” genes encode the major (L1) and minor (L2)
capsid proteins and are expressed in the more superficial
layers
• These proteins are needed late in the viral life cycle to
complete assembly into new, infectious viral particles
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• HPV gene expression occurs in
synchrony with and is dependent upon
squamous epithelial differentiation
• Therefore, completion of the viral life
cycle takes place only within an intact,
fully differentiating squamous epithelium
• The completely assembled viral particles
are shed within the superficial squames
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• HPV is a nonlytic virus, and therefore
infectiousness depends upon the normal
desquamation of infected epithelial cells
• A new infection is initiated when the L1
and L2 capsid proteins bind to the
epithelial basement membrane and/
or basal cells, permitting entry of HPV
viral particles into new host cells
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• HPV Types
– 130 types
– 30-40 anogenital
– High risk (oncogenic)
• 15-20 oncogenic types
• 16, 18, 31, 33, 35,39, 45, 51, 52 and 58
• 16 the most oncogenic type mainly because of its
persistence
• 16 and 18 account for about 70% of cervical cancer
cases
– Low risk (nononcogenic)
• 6, 11, 40 42, 43, 44, and 54
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• Infection with high risk HPV does not
result in neoplasia in most infected
women
• This indicates that additional host and
environmental factors determine whether
or not high risk HPV will cause neoplasia
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• HPV Transmission
– Transmission of genital HPV results from
direct, usually sexual, contact with the
genital skin, mucous membranes, or body
fluids of a partner with either warts or
subclinical HPV infection
– Little is known regarding the infectivity of
subclinical HPV, but it is assumed to be
high, especially in the presence of high
viral counts
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• HPV gains access to the basal cell layer
and basement membrane through
microabrasions of the genital epithelium
during sexual contact
• Once infected, these basal cells become
a viral reservoir
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• Genital HPV infection is multifocal, involving
more than one lower reproductive tract site in
most cases
• Therefore, neoplasia at one genital site
increases the risk of neoplasia elsewhere within
the lower genital tract, although the cervix
appears most vulnerable
• Also, simultaneous or sequential infection with
multiple HPV types is common
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• Most genital HPV infections result from
sexual intercourse.
• High-risk HPV cervical infection is
generally limited to women who have
experienced penetrative sexual contact
• Sexually naïve women occasionally test
positive for nononcogenic types at the
vulva or vagina, perhaps due to vaginal
tampon use or digital penetration
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• Women prior to coitarche can become
infected with high-risk types as well, but
this is uncommon
– Fomite transmission, known to occur
with nongenital warts, is unproven but likely
explains some of these cases
• The role of nonsexual transmission of
HPV remains unclear and requires further
study
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• Oral-to-genital and hand-to-genital HPV
transmissions are possible, but appear to
be far less common than with genitalto-
genital transmission, particularly penile-
vaginal penetrative contact
• Women who have sex with women
frequently report past sexual experiences
with men
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• This subgroup of women has rates of
– high risk HPV positivity,
– abnormal cervical cytology, and
– high-grade cervical neoplasia similar to
those of heterosexual women, but
undergoes cervical cancer screening less
often
• Those who have never had sex with
men appear to be at similar risk,
implying that digital, oral, and object
contact places them at risk of HPV
infection
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• Therefore, all women who are sexually
active should undergo cervical cancer
screening according to current
recommendations regardless
of sexual orientation
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• Congenital HPV Infection
– Uncommon
– Not related to the presence of maternal
genital warts or route of delivery
– Manifestations
• Conjunctival, laryngeal, vulvar, or perianal
warts present at birth or that develop within 1 to
3 years of birth
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• Indications for cesarean section
– Large genital warts that would likely
obstruct delivery or
– Warts that would avulse and bleed with
cervical dilation or vaginal delivery
– Otherwise CS not always indicated in HPV
infection and for the presence of warts
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• Warts in pediatric age group
– Sexual abuse
– Fomite
– Nonsexual contact,
– Autoinoculation
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2016
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• 3 possible outcomes of HPV infection
– Latent HPV infection
• Virus not integrated and its oncogenes not expressed
– Productive HPV infection
• Low level oncogene expression but no integration
• Manifestations
– Subclinical infection
– Genital warts  Condyloma acuminata
– Neoplastic HPV infection
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– Neoplastic HPV infection
• HPV genome integrates with the host genome
• Early genes supress p53 and pRB
• Infected cells vulnerable to malignant
transformation by loss of cell-cycle control,
cellular proliferation, and accumulation of DNA
mutations over time
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• Natural History of HPV Infection
– HPV infection is a marker of the initiation
of sexual activity and is not necessarily
evidence of promiscuity
– Most HPV lesions, whether clinical or
subclinical, spontaneously regress, especially
in adolescents and young women
– The risk of progression to high-grade
neoplasia increases with age, as HPV
infection in older women is more likely to
be a persistent infection
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• HPV Prevalence
– Genital HPV is the most common sexually
transmitted infection.
– Inapparent (subclinical) infection is far more
common than clinically apparent infection
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• Risk Factors for HPV Infection
– The most important risk factors for the
acquisition of genital HPV infection are the
number of lifetime and recent sexual
partners and early age at first sexual
intercourse
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• Diagnosis of HPV Infection
– A sure diagnosis can be made only by the
direct detection of HPV DNA
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• Treatment of HPV Infection
– Indications for treatment
• Symptomatic warts that cause physical or
psychologic discomfort,
• High-grade neoplasia, or
• Invasive cancer
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• Prevention of HPV Infection
– Behavioral interventions
– Condoms
– HPV Vaccines
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• Immunology of HPV Infection
– How does the HPV evade the immune
system?
1. Limitation of the infection to the epithelium
and therefore absence of a viremic phase
2. Low level expression of early genes;
3. The nonlytic, noninflammatory nature of the
infection; and
4. Delayed production of the highly immunogenic
capsid proteins within the superficial squames
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• Prophylactic HPV Vaccines
– They prevent the establishment of new and
persistent infection and subsequent development of
neoplasia
– They do not prevent transient HPV positivity or
resolve preexistent infection
– Two types FDA approved
• Gardasil is a quadrivalent vaccine against HPV types 6,
11,16, and 18
• Cervarix is a bivalent vaccine against HPVs 16 and 18.
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• Vaccines are expected to prevent
approximately 70 percent of cervical cancers,
but they will not protect against the
approximately 30 percent caused by oncogenic
HPV types not covered in the vaccine
• HPV vaccination, therefore, does not negate
the need for cervical cancer screening
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• Therapeutic Vaccines
– Todate no therapeutic vaccine has
developed for established HPV infection
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Cervical Intraepithelial Neoplasia
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2016
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• The two most important risk factors
– Multiple sexual partners
– Early coitarche
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• Tobacco smoking
– The biologic plausibility of a link between
tobacco and cervical neoplasia is supported
by several points:
1. cervical mucus of smokers contains carcinogens
and is mutagenic;
2. genetic alterations in the cervical tissue of
smokers are similar to those seen in smoking-
related neoplasias at other sites;
3. risk is dose-dependent, increasing with both
duration and amount of tobacco use; and
4. risk decreases with cessation of smoking
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• Dietary deficiencies
– Although data are inconclusive, dietary
deficiencies of certain vitamins such as A,
C, E, beta carotene and folic acid may alter
cellular resistance to HPV infection and
thus may promote viral infection persistence
and cervical neoplasia
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• Exogenous hormones
– There is an increased risk of cervical cancer
in current users of combination oral
contraceptives (COCs) that is related to
duration of use.
– Moreover, the relative risk nearly doubles at
5 years of COC use
– The increased risk declines after COC use
ceases, and risk returns to that of nonusers
10 years after use stops
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• Parity
– Increasing parity has been correlated with cervical
cancer risk, but it is unclear if this is related to
earlier sexual activity, a progestin exposure effect,
or other factors
– Immune suppression during pregnancy,
hormonal influences on cervical epithelium, and
physical trauma related to vaginal deliveries have
been suggested as etiologic factors associated with
the development of cervical neoplasia
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• Immunosuppression
– Immunosuppressed women in general show
increased severity, multifocal lesion
pattern, treatment failure, persistence, and
recurrence of lower genital tract disease
compared with those who are
immunocompetent
• Human immunodeficiency virus (HIV)-positive
women
• Transplant recipients
• Women on immunosuppressive medications
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• Inadequate screening
– Cervical cancer prevention requires
identification and eradication of precursor or
early invasive lesions through cytologic
screening
– Lack of screening is a major contributor to
higher rates of cervical cancer in
socioeconomically disadvantaged women
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• Differential Diagnosis and Evaluation
of Cervical Lesions
– Cervical Cytology
• Pap test screening test of choice in
asymptomatic women
• Pap test’s specificity is consistently
high, approximating 98 percent
• However, estimates of its sensitivity are lower
and more variable
• Pap test being less sensitive for the detection of
adenocarcinomas than for squamous lesions.
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– False-negative Pap test results
may be caused by
• Sampling error, in which abnormal cells are not
present in the Pap test;
• Screening error, in which the cells are present
but missed by the screener; or
• Interpretation error, in which abnormal cells are
misclassified as benign
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• Performing a Pap Test
– Patient Preparation
• Avoid menstruation
• Abstain from vaginal intercourse, douching,
and use of vaginal tampons and medicinal or
contraceptive creams for a minimum of 24 to
48 hours before a test
• Treatment of cervicitis or vaginitis prior to Pap
testing is optimal
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– Location
• Sampling of the transformation zone is
paramount to the sensitivity of the Pap test
– Sampling devices
• Spatula, the broom, and the endocervical brush
• A spatula predominantly samples the ectocervix.
An endocervical brush samples the endocervical
canal and is used in combination with a spatula.
• A broom samples both endo- and ectocervical
epithelia simultaneously, but can be
supplemented by an endocervical brush
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– Conventional slide collection
• Avoid air drying of cells, which is a leading cause of poor
slide quality
• The spatula sample should be held while the
endocervical brush sampling immediately follows.
• The spatula sample is then quickly spread as evenly as
possible over one half to two thirds of a glass slide
• The endocervical brush is firmly rolled over the remaining
area of the slide, after which fixation is quickly carried out
by spraying with or immersing in fixative
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• Liquid-Based Test Collection
– Currently, two liquid-based Pap tests are
FDA approved
• BD SurePath
• ThinPrep
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• Initiation of Screening
– Screening should begin at age 21 years regardless
of sexual history
– Exceptions to this
• Immune compromise, including
– HIV infection,
– Use of immunosuppressive medications, and
– Organ transplantation
• In such cases, screening should begin at sexual activity
onset, even if before age 21, and should consist of two
Pap tests at 6-month intervals during the first year, then
annually
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• Screening Interval
– ACOG recommendation
• Between ages 21 and 29, ACOG (2009)
recommends Pap testing at 2-year intervals
using either conventional or liquid-based
methods
• At age 30, women at average risk for cervical
cancer can be screened at 3-year intervals if
three previous, consecutive, Pap tests have been
documented as negative
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– Women with HIV infection should receive
annual screening for life
– Women with prior treatment for CIN 2, CIN
3, or cervical cancer should receive annual
screening for at least 20 years as they
remain at increased long-term risk of
cervical cancer
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• Discontinuation of Screening
– Screening may be stopped at age 65 or 70 in
women with average risk for cervical cancer after
three consecutive, negative Pap results during the
prior 10 years
– ACOG (2009) alone recommends that older women
who are sexually active and have multiple partners
continue routine screening because it is unclear if
the postmenopausal cervix remains at increased risk
of neoplasia when exposed to new HPV infection
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• Screening after hysterectomy
– For supracercial hysterectomy
– Women with histories of high-grade cervical
neoplasia or cancer
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• Colposcopy
– This is an outpatient procedure that
examines the lower anogenital tract with a
binocular microscope
– The colposcope consists of a stereoscopic
lens or digital imaging system that has
magnification settings ranging from 3- to
40-fold and that is attached to a moveable
stand
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• Solutions
– Normal saline
• Used at the beginning of the colposcopic
examination, saline helps remove cervical mucus
and allows initial assessment of vascular patterns
and surface contours
• Abnormal vessels, especially when viewed with
green-filtered light, may be more prominent
than after acetic acid application
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– Acetic Acid
• Acetic acid 3- to 5-percent is a mucolytic agent
that is thought to exert its effect by reversibly
clumping nuclear chromatin
• This causes lesions to assume various shades of
white depending on the degree of abnormal
nuclear density.
• Applying acetic acid to abnormal epithelium
results in the acetowhite change characteristic of
neoplastic lesions as well as some nonneoplastic
conditions.
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– Lugol Solution
• Lugol iodine solution stains mature squamous
epithelial cells a dark brown color in
estrogenized women as a result of high cellular
glycogen content
• Due to poor cellular differentiation, dysplastic
cells have lower glycogen content, fail to fully
stain, and appear various shades of yellow
• Lugol solution should not be used in patients
allergic to iodine, radiographic contrast, or
shellfish.
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• This solution is particularly useful when abnormal
tissue cannot be found using acetic acid alone
• It is also used to define the limits of the active
transformation zone, as immature squamous
metaplasia does not stain as strongly as mature
(fully differentiated) squamous epithelium
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• Excissional Biopsy
– Ectocervical biopsy
– Endocervical sampling
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Hale T., M.D., Resident Physician
1. Endocervical curette,
2. Endocervical speculum,and
3. Cervical biopsy forceps.
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The 2001 Bethesda System
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The 2001 Bethesda System: Epithelial Cell Abnormalities
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Cervical Cytology:
Initial Management of Epithelial Cell
Abnormalities
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Surveillance of Abnormal Cervical Cytology
in the Absence of Histologic High-Grade Neoplasia
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2016

• Treatment of CIN
– Ablative procedures
• Cryosurgery,
• Electrofulguration, and
• Carbon dioxide (CO2) laser
– Excisional procedures
• Cold-knife conization
• Laser conization
• LEEP
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– Hysterectomy
• Recurrent high-grade cervical disease if
childbearing has been completed or
• When a repeat cervical excision is strongly
indicated but technically not feasible
• Otherwise unacceptable as primary therapy for
CIN 1, 2, or 3
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Part – II: Cervical Cancer
2016
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• Contents
1. Incidence
2. Risks
3. Pathophysiology
4. Histologic Types
5. Diagnosis
6. Staging
7. Workup
8. Management
9. Prognosis
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Introduction
• Incidence
– Cervical cancer is the most common
gynecologic cancer in women and is
mostly attributed to HPV infection
– Compared with other gynecologic
malignancies, cervical cancer develops in a
younger population (median age at
diagnosis 48 years of age) of women and
screening should begin in young adulthood
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• Mostly early cancers are asymptomatic
• Symptoms of advanced cancer include
– Bleeding
– Watery discharge
– Sings associated with venous, lymphatic,
neural or ureteral compression
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• Biopsy is diagnostic
• Staging is clinical and it dictates the
management and is the most important
indicator of long term survival
– Early stages
• Effectively erradicated surgically by either
conization or radical hysterectomy
– Late stages
• Chemoradiation is primarily selected
2016

– Cervical cancer is common worldwide and
ranks third among all malignancies for
women
– In general, higher incidences are found in
developing countries, and these countries
contribute 85 percent of reported cases
annually and this high incidence is
attributed to lack of screening
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• Risk Factors
– Invasive cervical cancer shares the same risk
factors as cervical preinvasive lesions
• HPV infection
– 99.7% of cervical cancers are associated with an
oncogenic HPV subtype
– HPV 16 accounts for 57% and HPV 18 for 16% of
cervical cancers
• Lower socioeconomic predictors
– Lower educational attainment, older age, obesity,
smoking, neighborhood poverty and lack of screening
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– Cigarette Smokign
• Increases the risk of SCC
• May alter high risk HPV clearance
– Reproductive behavior
• Multiparity
• Use of combined oral contraceptives
– Sexual activity
• Early coitarche
• Multiple sexual partners
2016

Pathophysiology
• Tumorigenesis
– HPV infection to the cells of SCJ 
dysplastic lesion  SCC of the cervix
– HPV oncoproteins are critical component of
continued cancer cell proliferation
• HPV infection  E1 and E2 (early replication
proteins) enable the virus to replicate within
cervical cells  LSIL
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2016
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– E7 bind to Rb (retinoblastoma tumor
suppressor protein)
– E6 bind to p53 tumor suppressor protein
– In both instances bidning leads to
degradation of these suppressor protiens
and immortalization of cervical cells
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2016

Tumor Spread
2016
Paracervical and parametrial LNs
Obturator LN  Internal, external
LN Common illiac LN 
Paraaortic LN
In contrast, lymphatic channels from
the posterior cervix course
through the rectal pillars and the
uterosacral ligaments to the rectal
lymph nodes. These nodes are
encountered during radical
hysterectomy and are removed with
the uterosacral ligaments

• Lymphovascular Space Involvement
– As tumor invades deeper into the stroma, it
enters blood capillaries and lymphatic
channels
– Not included in staging
– Poor prognostic indicator
– Indication for radiation therapy
2016

• Local and Distant Tumor Extension
– With extension through the parametria to
the pelvic sidewall, ureteral blockage
frequently develops, resulting in
hydronephrosis
– Additionally, the bladder may be invaded
by direct tumor extension through the
vesicouterine ligaments (bladder pillars)
2016

• The rectum is invaded less often because it is
anatomically separated from cervix by
the posterior cul-de-sac
• Distant metastasis results from hematogenous
dissemination, and the lungs, ovaries, liver, and
bone are the most frequently affected organs
2016

Histologic Types
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• The two most common histologic
subtypes of cervical cancer are
squamous cell and adenocarcinoma
2016

Squamous Cell Carcinoma
• 75% of cervical cancers
• Arise from ectocervix
• 3 histologic types
– Keratinizing
– Nonkeratinizing
– Papillary
Adenocarcinoma of Cervix
• Trends in increasing
incidence of
adenocarcinoma
• 20-25% of cervical
cancers
• Arises from endocervix
• Poorer overall survival
2016

Diagnosis
• Symptoms
– Usually asymptomatic
– Early symptoms
• Watery discharge
• Blood tignged vaginal discharge
2016

• Symptoms of advanced diseases
– Compression symptoms
• Compression of lymphatic drainage
– Lower extremity edema
• Sciatic nerve compression
– Low back pain
• Uretral compression
– Hydronephrosis and uremia
– Ureteral stenting or percutaneous nephrostomy
tube insertion are usually required
2016

– Hemorrhage
• Can be uncontrolled if from a tumor bed
• Can be treated with
– Packing
– Monsel solution
– Topical aceton
– Radiation
– Hypogastric artery ligation
2016

• Tumor invasion to local organs
– Bladder
• Hematuria
• Symptoms of vesicovaginal fistula
– Rectum
• Symptoms of rectovaginal fistula
• Constipation
2016

• Physical Examination
– Most have a normal general physical exam findings
– With advancing disease
• Enlarged supraclavicular or inguinal
lymphadenopathy,
• Lower extremity edema,
• Ascites, or
• Decreased breath sounds with lung auscultation
may indicate metastases
– Cervical growth can be exophytic or endophytic
2016

• During bimanual examination,
– a clinician may palpate an enlarged uterus resulting from
tumor invasion and growth
– Alternatively, hematometra or pyometra may
expand the endometrial cavity following obstruction
of fluid egress by a primary cervical cancer
– In this case, the uterus may feel enlarged and
boggy
• Advanced cervical cancer cases may have vaginal
involvement, and the extent of disease can be
appreciated on rectovaginal examination
2016

• In such cases, palpation of the rectovaginal
septum between the index and middle finger
of an examiner’s hand reveals a thick, hard,
irregular septum.
• The proximal posterior vaginal wall is most
commonly invaded
• In addition, during digital rectal examination,
parametrial, uterosacral, and pelvic sidewall
involvement may be palpated.
2016

• Either one or both parametria may be invaded,
and involved tissues feel thick, irregular, firm,
and less mobile
• A fixed mass indicates that tumor has probably
extended to the pelvic sidewalls
• However, a central lesion can become as large
as 8 to 10 cm in diameter before reaching the
sidewall
2016

• Pap Smear
– Its use for suspicious lesions is discouraged
– Sesitivity of a single Pap test
• For high grade lesions  55-80%
• For low grade lesions  30-50%
– Thus, the preventive power of Pap smear
testing lies in regular serial screening
2016

• Colposcopy and Biopsy
– If abnormal Pap smear findings are noted,
colposcopy is often performed
– Cervical punch biopsies or conization
specimens are the most accurate for
allowing assessment of cervical cancer
invasion
2016

• Differential Diagnosis
1. Cervical leiomyoma,
2. Cervical polyp,
3. Prolapsing uterine leiomyoma or sarcoma,
4. Vaginitis,
5. Cervical eversion,
6. Cervicitis,
7. Threatened abortion,
8. Placenta previa,
9. Cervical pregnancy,
10. condyloma acuminata,
11. Herpetic ulcer, and
12. Chancre
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Staging
• Cervical cancers are staged clinically
• Allowable components of staging include
– Cold knife conization,
– Pelvic examination under anesthesia,
– Cystoscopy,
– Proctoscopy,
– Intravenous pyelogram
– Computed-tomography [CT] scan), and
– Chest radiograph
2016

MRI for Cervical Ca evaluation
Advantages
• Measures tumor size precisely
even for endocervical
lesions, and for delineating
cervical tumor boundaries
and surrounding invasions
• commonly performed in
patients being considered for
fertility-sparing radical
trachelectomy
Limitations
• Less accurate for diagnosing
microscopic or deep cervical
stromal invasion or
identifying minimal
parametrial extension
• False-negative findings occur
with small volumes
of disease and with tissue foci
in which cancer cannot be
differentiated from other
tissues such as scar or
necrosis
2016

CT for Cervcail Ca Evaluation
Advantages
• Can aid detection of enlarged
lymph nodes, ureteral
obstruction, or distant
metastasis
• High-resolution depiction of
anatomy, especially when
used with contrast
• evaluate tumor size and bulky
extension beyond the cervix
Limitations
• CT is not accurate for
assessing subtle parametrial
invasion
or deep cervical stromal
invasion
• This is because of its poor
soft-tissue contrast resolution
and thus its difficulty in
enhancing local tumor
invasion from normal
parametrium
• Internal node architecture is
often poorly defined by CT
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2016

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Work up
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Treatment
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Simple and Extended Hysterectomy
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2016

• Early Stage
– Stage IA1
• Conization
• Type I hysterectomy
• Radical trachelectomy with pelvic LN dissection
if they desire fertility
– Stage IA2 – IIA
• Radical hysterectomy (Type III ) and pelvic
lymphadenectomy
2016

• Adavanced Stage Primary Disease
–  Stage IIB -IVA
• Radical surgery at times pelvic exenteration
• Radiation therapy
– External beam radiation
– Extended field radiation
– Brachytherpay  Intracavitary radiation
• Chemoradiation
• IVB
– Palliation
2016

• Palliative Care
– Gastrostomy tube for persistent N & V
– Surgery for bowel obstruction
– Percutaneous nephrostomy tubes for urinary
fistulas or urinary tract obstruction
– Pain management
2016

Chemotherapy Regimens and
Response Rates of Cervical Cancer
2016

Prognosis
• Prognostic Factors
– Stage of the disease
– Nodal involvement
– Histologic grade
– Histologic type of the tumor
2016

2016

Management during Pregnancy
• Diagnosis
– Pap screening similar to the nonpregnant
population
– If Pap results show HSIL or suspected
malignancy  colposcopic–directed biopsy
should be obtained
– If colposcopic-directed biopsy fails to show
malignant cells  Cold-knife conization
should be performed in the second
trimester
2016

• Management in early stage
– IA1-IIA
• Intentional delay of treatment till 6 weeks
postpartum doesn’t pose harm
• IA1
– Vaginal delivery
• IA2-IIA1
– Delivery via C/S
• Management in advanced stage
– IIB-IVB
• Chemoradiation
• Classical C/S
2016

References
1. F. Gary Cunningham, 2012. Williams Gynecology, 2nd
edition, The McGraw-Hill Companies, Inc.
2. James R. Scott, 2008. Danforth’s Obstetrics and
Gynecology, 10th edition
3. UpToDate 21.8
2016
129

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