OBSTETRICS 2 GESTATIONAL

1S-3 | CEU-SOM A & B TROPHOBLASTIC

RONALDO ANTONIO R. SANTOS, MD, FPOGS
DISEASE
OUTLINE U These are vesicular tissues. If you puncture those, it is filled with
hCG – the hormone which is very similar to LH
I. SPECTRUM OF PLACENTAL-RELATED TUMORS U hCG is a pseudo-LH. It is not an LH but it acts on FSH. Their alpha
II. MOLAR PREGNANCY and beta subunits are very similar. If you track the levels of hCG in
A. Histologic Abnormality the serum, it will start at the time when there is trophoblast
B. Complete H. mole proliferation. It will then peak on the first trimester. Then after 12 to
C. Partial H. mole 14 days, it will begin to go down because the placenta is now
D. Twin Molar Pregnancy capable of producing its own progesterone.
E. Theca-lutein Cysts (Ovary) U In the first trimester, the placenta does not produce progesterone.
F. Epidemiology and Risk Factors The corpus luteum produces progesterone which is stimulated by
G. Clinical Course the LH.
H. Clinical Presentation U The hCG is directly proportional to the amount of blastocysts or
I. Trophoblastic Deportation of Embolization trophoblasts. The bigger the number of trophoblasts, the higher the
J. Management level of hCG.
III. GESTATIONAL TROPHOBLASTIC NEOPLASIA
A. Invasive mole HISTOLOGIC ABNORMALITY______________________________
B. Gestational Choriocarcinoma
C. Placental Site Trophoblastic Tumor
D. Epithelioid Trophoblastic Tumor
E. Clinical Course
F. Diagnosis
G. Treatment
IV. REFERENCES
V. APPENDIX

Legends: 2 - speaker’s notes Figure 2. Normal Figure 3. H. mole

U recording Chroionic villi:

Ÿ Trophoblastic proliferation
“Women are the stronger sex...” – Dr. Santos Ÿ Edema of villous stroma

I. SPECTRUM OF PLACENTAL-RELATED TUMORS

A. COMPLETE H. MOLE
U Trophoblast refers to the placenta. After implantation, the tissues
will know invade the endometrium – trophoblast GROSS__________________________________________________
U Trophoblast will proliferate without a baby – only placenta

MOLAR
Ÿ Hydatidiform moles
§ Complete, partial, invasive
U all of these three will invade the myometrium
U Molar refers to the chorion or chorionic villi

NONMOLAR
Ÿ Choriocarcinoma
Ÿ Placental site trophoblastic tumor
Ÿ Epithelioid trophoblastic tumor Figure 4. Vesicles of variable sizes with thin pedicles

GTN (Gestational Trophoblastic Neoplasia) 2 Mass of clear vesicles of variable size from barely visible to a few
Cm and hang in clusters from thin pedicles
U The characteristics of malignancy are: (1) uncontrolled growth and
(2) propensity to metastasize or invade body organs HISTOLOGY______________________________________________
U When the above tumors will appear, they will be referred as
gestational trophoblastic neoplasia because they are malignant

II. MOLAR PREGNANCY

Figure 5. Generalized edema and cistern formation

2 Hydropic degeneration and villous edema

Figure 1. Hydatidiform Mole 2 Absence of blood vessels

1S-3 GESTATIONAL TROPHOBLASTIC DISEASE ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA

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2 Trophoblastic epithelium proliferation of varying degrees
2 Absence of embryonic elements (fetus and amnion)
KARYOTYPE_____________________________________________
Ÿ Diploid, paternal origin
85% are 46 XX (both from father) ® ANDROGENESIS
Ÿ
2 Ovum if fertilized by haploid sperm which duplicates its own
chromosomes after meiosis while that of the ovum is absent
or inactivated
2 Minority are 46 XY from dispermic fertilization
Ÿ Some are 46 XY (dispermic fertilization or Dispermy)
Figure 6. Typical Pathogenesis of Complete and Partial Moles
U Figure 6-A: The sperm found an egg. Unfortunately, the egg does
not contain the 23,x chromosome. The sperm, on the other hand,
has either the 23,x or 23,y chromosome which will impregnate the
empty egg. In result, there will be no baby. The 46,xx are all
paternal. No human is produced because all of these
chromosomes came from the father. So, without the egg, there will
be no life. This is called a complete mole.
U Figure 6-B: 2 sperms impregnate an egg. This resulted to 69,xxy.
One of them has 46 chromosomes and that is alive human with
trophoblastic proliferation which is an H-mole. This is called a
partial mole.
MALIGNANT POTENTIAL___________________________________
Ÿ 15-20%
Ÿ Higher than partial mole
Ÿ Early evacuation: no role in lowering risk
B. PARTIAL H. MOLE
Figure 7. Partial H. mole
GROSS__________________________________________________
Ÿ Some elements of fetal tissues
Ÿ Less advanced or focal hydatidiform change
U As long as you will find fetal components in the placenta, that is
already considered as a partial mole.
U Can a fetus of a partial mole grow in maturity as a live fetus? It is
very rare because the placenta is not functioning well to provide the
1S-3 GESTATIONAL TROPHOBLASTIC DISEASE
necessary nutrients for the fetus so eventually, they die of
prematurity.
U Malignant potential is very low.
HISTOLOGY______________________________________________
Ÿ Slowly progressive
swelling of stroma of
avascular chronic villi
Ÿ Normal vascular villi with
functional fetal-placental
circulation
Figure 8. Histologic appearance of Partial H. mole
KARYOTPYE_____________________________________________
Ÿ Triploid: 69 XXX, 69XXY, 69XYY (diandry)
Ÿ One maternal and two paternal haploid sets of chromosomes
(dispermy)
Ÿ Fetus is nonviable with multiple malformations or with severe
growth restriction
Figure 9. Pathogenesis of Partial H. Mole
MALIGNANT POTENTIAL___________________________________
Ÿ Much lower risk of persistent disease
Ÿ Persistent disease is seldom choriocarcinoma
Ÿ Higher postevacuation bHCG correlates with increased risk of
persistent disease*
2 Levels ³ 200 mIU/ml in the 3rd to 8th week post evacuation: at
least 35% risk of persistent disease
C. TWIN MOLAR PREGNANCY
Ÿ Complete diploid molar pregnancy + a normal pregnancy (not
uncommon)
Ÿ Must be differentiated to Partial Mole by fetal karyotyping
Ÿ Variable survival of the normal coexisting fetus*
Ÿ Affected mothers have a higher risk pf preeclampsia, hemorrhage
and subsequent gestational trophoblastic neoplasia**
Ÿ NEITHER MATERNAL RISKS NOR LIKELIHOOD OF A HEALTHY
OFFSPRING HAVE BEEN PRECISELY ESTABLISHED IF
PREGANCY CONTINUED***
2 * Survival of fetus depends on whether condition is detected
and concomitant complications such as preeclampsia or
hemorrhage develops
** compared to those with partial mole but not greater than
those with singleton complete mole
*** PROBLEMATIC
U Mothers die due to hemorrhage – postpartum hemorrhage
secondary to uterine atony (failure to contract)
U What is your other consideration aside from H. mole if there is
bleeding and the uterus is larger than usual? Hindi pwedeng
gestational diabetes kasi wala namang bleeding and the growth
spurt usually happen at 2nd and 3rd trimesters. Siguro pwedeng
abortion pag may bleeding. Pupwedeng nagkamali ng bilang ng
LMP kaya naman malaki, o kaya baka twin pregnancy kaya malaki.
U Anong gagawin? First, do a pregnancy test to document that the
patient is pregnant, then second, request for an ultrasound.
ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA
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 Ultrasound can determine or rule out multiple pregnancy and
identify snowstorm appearance.
Figure 10. Features of Partial and Complete Hydatidiform Moles
D. THECA-LUTEIN CYSTS (OVARY)
Ÿ 25-60% of complete mole
Ÿ Variable sizes (micro to 10cm)
Ÿ Smooth, yellow surface, lined by
lutein cells
Ÿ Overstimulation from large
amounts of bHCG
Ÿ Persistent disease more likely if
these are present esp. if bilateral*
Ÿ Torsion, infarction, hemorrhage
Ÿ Regression after evacuation
Ÿ Only indication for oophorectomy -
infarction after untwisting Figure 11. Theca-Lutein Cyst
2 * higher B hCG- worse prognosis
** Regresses with evacuation as beta hCG lowers so
oophorectomy is not indicated unless there is complication
of ovarian infarction
U Theca-lutein cysts are enlarged cysts of the ovary.
U What stimulates the growth of corpus luteum? It is LH. Since there
is no LH but you have pseudo-LH which is hCG, the cysts will grow.
U What is the danger of theca-lutein cysts? Rupture then
hemorrhage. Hemorrhage happens inside and there is no signs for
that. But you can determine if there is rebound tenderness.
U when you palpate the abdomen and then release, there would be
pain – that is rebound tenderness. What is the significance of
rebound tenderness? The peritoneum is irritated with blood, pus,
or acidic fluid. The tendency of having rebound tenderness is there
might be a rupture.
U but if there are no signs and symptoms, just let it go. Because these
cysts will regress inside the moment you deliver the placenta. The
moment you evacuate the trophoblast, the hCG titers will go down.
So simply observe if there are poor signs of complications.
E. EPIDEMIOLOGY AND RISK FACTORS
EPIDEMIOLOGY
Ÿ US and Europe: 1-2 per 1000 pregnancies
Ÿ Appeear to be more common among Hispanics, Americans
Indians, Asians
RISK FACTORS
Ÿ Age – extremes of age (adolescent and >40 years old)
2 Age-pregnancy at extreme of reproductive age: adolescents,
those 36-40 have two-fold risk;>40 tenfold risk
Ÿ Prior Molar Pregnancy
§ Complete Mole – 1.5%
§ Partial Mole – 2.7%
§ Prior Molar Pregnancy – 23%
2 Prior molar pregnancy- substantive increased risk
1S-3 GESTATIONAL TROPHOBLASTIC DISEASE
2 OCP use and previous miscarriage-increase chances by as much
as two-fold
2 smoking, vta def., increased paternal age-implicated in certain
studies
U what are the signs and symptoms of early pregnancy? Nausea and
vomiting – rising titers of hCG and estrogen – large amount of
trophoblast.
F. CLINICAL COURSE
Ÿ Has changed due to earlier diagnosis
Ÿ Early prenatal care and ultrasonographic exam ® earlier
detection
Ÿ Symptoms more pronounced in complete moles
U Vigilant post-evacuation surveillance by always monitoring βhCG
weekly until it becomes negative. So, expect that there is a
regression every week in the titer of βhCG.
U When do you say that there is a plateau? It is constant and it is
within plus or minus 10%. If there is greater than 10% decrease,
there is reduction. But if there is more than 10% increase, that is
trophoblastic proliferation – may naiwan pa or baka may malignant
transformation. So when you find an increase, suspect gestational
trophoblastic neoplasia.
U Also order for Chest X-ray. Why? Because it is the number one
organ where malignant transformation will metastasize. So you will
find the lesion in the lungs and also in the vagina.
G. CLINICAL PRESENTATION
Ÿ 1-2 months of amenorrhea
Ÿ Nausea and vomiting (maybe significant)
Ÿ Uterine bleeding (58%)
2 Universal, varying degrees: spotting to profuse hemorrhage,
may even be concealed with moderate IDA, may begin just
before a molar abortion or occur intermittently over a period
of weeks to months
Ÿ Enlarged uterus (50% of cases in complete mole) – soft
Ÿ No fetal motion
Ÿ Thyrotoxicosis (possible but not common) – TSH and FT4
2 Thyrotropin effect of hCGàelevated plasma T4 and low
TSH, rapidly normalizes after evacuation
Ÿ Early onset preeclampsia – hypoxic trophoblast releases anti-
angiogenic factors ® endothelial damage
2 Preeclampsia developing BEFORE 24 weeks AOG should
raise the suspicion of molar pregnancy
H. TROPHOBLASTIC DEPORTATION OR EMBOLIZATION
Ÿ Escape of trophoblast into pelvic venous system during molar
evacuation
Ÿ May invade pulmonary embolism or edema
Ÿ Acute pulmonary embolism or edema
Ÿ Fatalities uncommon but possible
CLINICAL DIAGNOSIS
Ÿ Clinical manifestations – amenorrhea, bleeding
Ÿ Ultrasonography
Ÿ Spontaneous expulsion
Ÿ Beta HCG
§ Elevated about the expected AOG
§ False negative urine PT is common (oversaturation of test
assay due to high HCG)
ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA
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 I. ULTRASONOGRAPHY Ÿ Creatinine
Ÿ Consider hygroscopic dilators

INTRAOPERATIVE
Ÿ Large bore Intravenous Catheter(s)
Ÿ Regional or General Anesthesia
Ÿ Oxytocin 20 units in 1L of D5LR
Ÿ Karman Cannula – size 10, 12 or 14
Ÿ Sonography machine
Ÿ Other uterotonics:
§ Methylgonovine - .2mg/ml every 2 hours
§ Carbopost (PGF2a) 250 ug/ml every 15.90 minutes
§ Misoprostol (PGE1) – 200 mg/tab (800-1000 mg once)

SUCTION CURETTAGE

Figure 12. Complete H. mole Ÿ TREATMENT OF CHOICE

Ÿ Adequate anesthesia
Ÿ Snowstorm pattern Ÿ Blood availability
Ÿ Echogenic mass with anechoic cystic spaces without cystic Ÿ Preoperative dilatation if cervix is
spaces without fetus or amnionic sac closed (osmotic dilators)
2 complex, echogenic uterine mass with numerous cystic Ÿ Oxytocin AFTER evacuation of most
spaces and no fetus or amnionic sac of the molar tissues
Ÿ Thorough gentle curettage with
sharp curette AFTER myometrium
has contracted
Ÿ Intraoperative ultrasonography*
2 helps determine if uterus Figure 14. Suction curettage
has been emptied

PROPHYLACTIC CHEMOTHERAPY
Ÿ Not routinely recommended because of significant toxicities and
the fact that this has not improve long-term prognosis

U If the patient’s compliance is poor for follow-up, magbigay ng

prophylactic chemotherapy. That is the practice in the Philippines.
Figure 13. Partial H. mole Give prophylactic chemotherapy in the form of oral Methotrexate.
U If there is bleeding and we cannot control it, do hysterectomy
Ÿ Thickened multicystic placenta with fetus especially if the patient has completed her reproductive career.
Ÿ Misdiagnosed as incomplete or missed abortion U If the cervix is already open, do a suction curettage.
2 Partial: thickened hydrophic placenta with fetal tissues
2 In early pregnancy, UTZ shows characteristic appearance in COMPLICATIONS: INTRAOPERATIVELY
only about 1/3 of women with partial H mole Ÿ Bleeding – uterotonics, surgical methods
Ÿ Trophoblastic deportation – respiratory insufficiency, pulmonary
PATHOLOGICAL DIAGNOSIS edema, embolism
Ÿ Histological characteristics
Ÿ Determination of Differing Ploidy, Diploid (complete), Triploid OTHER METHODS OF TERMINATION
(Partial) Ÿ Labor induction or hysterotomy
Ÿ Immunostaining (P57KIP2) Nuclear protein § NOT usually done – increase blood loss and persistent
§ Complete – Negative trophoblastic disease
§ Partial – Positive Ÿ Hysterectomy with ovarian preservation
§ Non Molar hydrophic change – positive § if no further pregnancy is desired
Ÿ Complete Mole – diploid (P57KIP2 – negative) Ÿ logical for women 40 and up, markedly reduces likelihood of
Ÿ Partial Mole - triploid (P57KIP2 – positive) persistent trophoblastic neoplasia, important adjunct to treatment
Ÿ Spontaneous abortion with Hydropic degeneration - diploid of chemo resistant tumors
(P57KIP2 – positive) Ÿ Do not remove theca lutein cyst
Ÿ Aspiration of large cyst to minimize pain or torsion
J. MANAGEMENT
POSTOPERATIVE
Emphasis is on Ÿ Anti D Immunoglobulin if Rh D NEGATIVE
Ÿ Early diagnosis Ÿ Initiate contraception
Ÿ Timely molar evacuation § OCP or medroxyprogesterone acetate (poor compliance)
Ÿ Vigilant postevacuation surveillance § IUD – perforation
Ÿ Barrier – high failure rates
PREOPERATIVE Ÿ Review Pathology Report
Ÿ Preoperative evaluation of complications Ÿ Median time of Beta HCG resolution: Partial – 7 weeks and
Ÿ Preoperative Chest X-ray Complete – 9 weeks
Ÿ MRI or CT scan: if chest X-ray is positive for lung lesions or if Ÿ Serum Beta HCG Surveillance – within 48 hrs, weekly until
extrauterine disease (liver or brain) is suspected undetectable the monthly for 6 months
Ÿ Hemogram (detection of anemia)
Ÿ ABO typing and Rh screen U Prevent sensitization because the succeeding pregnancy may
Ÿ Serum hepatic transaminase levels (assessment f liver carry an Rh negative baby.
involvement) U Initiate contraception because the woman should not get pregnant
Ÿ Baseline serum bhCG in the period of one year. Because if tumaas ang hCG niya, hindi
1S-3 GESTATIONAL TROPHOBLASTIC DISEASE ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA
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 mo alam baka malignant transformation or due to pregnancy. So A. INVASIVE MOLE
please initiate contraception for 1 year.
GROSS__________________________________________________
POSTEVACUATION SURVEILLANCE Ÿ Formerly called Chorioadenoma
Ÿ LONG TERM GOAL: complete resolution of trophoblastic disease destruens
Ÿ STEPS: Ÿ Excessive trophoblastic
1. Prevention of pregnancy for a minimum of 6 months with overgrowth with extensive tissue
hormonal contraception invasion by trophoblastic cells and
2. Obtain baseline βhCG within 48 hours postevacuation then whole villi
monitor levels every 1-2 weeks while still elevated (to detect
persistent disease). Levels should fall progressively to
undetectable levels
3. Chemotherapy is NOT indicated if levels continue to drop. A
rise or plateau warrants evaluation of persistent disease and
treatment. An increase in levels indicate significant Figure 15. Figure 15. Gross
trophoblastic proliferation unless the patient is pregnant. appearance of Invasive mole
4. Once serum βhCG levels normalize, levels are then
determine monthly for anther 6 months. If undetectable by HISTOLOGIC_____________________________________________
this time, surveillance is stopped and pregnancy is allowed.
Ÿ Deep penetration into the
Ÿ Usually in those with no persistent disease, serum beta hCG is myometrium (even at times the
undetectable by 7 weeks postevacuation in partial mole and by 9 peritoneum, parametrium or
weeks postevacuation in complete mole vaginal vault)
Ÿ Usually in those with no persistent disease, serum β hCG is Ÿ Almost always arise from a
undetectable by 7 weeks post evacuation in partial mole and by 9 partial or complete mole
weeks post evacuation in complete mole Ÿ Locally invasive but lacks the
tendency for widespread
metastasis
RISK FACTORS FOR DEVELOPING GTN FOLLOWING MOLAR
EVACUATION:
Ÿ Complete 15-20% Partial 1-5%
Ÿ Older Age
Ÿ Beta HCG > 100,000 μu/ml Figure 16. Histologic appearance
of Invasive mole
Ÿ Uterine size large for gestational age
Ÿ Theca Lutein cyst >6cm
B. GESTATIONAL CHORIOCARCINOMA
Ÿ Slow decline of β HCG
Ÿ Extremely malignant carcinoma of chorionic epithelium
Ÿ Myometrial nodules of hypervascularity by postevacuation
ultrasound Ÿ 2/3 follow a normal delivery, 1/3 follow molar gestation
Ÿ Considered anytime there is persistent bleeding after any
pregnancy event
III. GESTATIONAL TROPHOBLASTIC NEOPLASIA

ANTECEDENT PREGNANCIES TO GTN_________________ GROSS__________________________________________________

Ÿ H mole – 50% Ÿ Rapidly growing
Ÿ Abortion/Tubal Pregnancies – 25% Ÿ Invades myometrium and blood
Ÿ Preterm or Term Pregnancies – 25% vesselsà hemorrhage and
necrosis
CLINICAL FINDINGS_________________________________ Ÿ Dark red or purplish, ragged
Ÿ Aggressive myometrial invasion and friable
Ÿ Strong tendency to metastasize Ÿ Early bleeding, sloughing and
Ÿ Irregular bleeding with uterine subinvolution infection with involvement of
Ÿ Diagnosed only by persistent elevation of serum βhCG in most endometrium
cases Ÿ Dark irregular nodules with
Ÿ Myometrial Perforation – intraperitoneal hemorrhage involvement of peritoneum
Ÿ Some with lower genital tract metastasis or distant metastasis

HISTOLOGIC CLASSIFICATION OF GTN________________ Figure 17. Gestational

Choriocarcinoma (Gross app.)
Ÿ INVASIVE MOLE
Ÿ CHORIOCARCINOMA
Ÿ PLACENTAL SITE TROPHOBLASTIC TUMOR
Ÿ EPITHELIOID TROPHOBLASTIC TUMOR HISTOLOGIC_____________________________________________
Ÿ Involvement of
* The diagnosis of GTN is usually based on persistent elevation of serum cytotrophoblasts and syncytial
βhCG level without confirmation by pathological study. Management is elements (one or the other
NOT directed by histologic findings. may predominate)
Ÿ Columns or sheets of
CRITERIA FOR DIAGNOSIS OF GTN OR POSTMOLAR GTD (FIGO) trophoblasts penetrating
1. Plateau of serum βhCG level (± 10 %) for four measurements myometrium and blood
during a period of 3 weeks or longer-days 1,7,14,21 vessels
2. Rise of serum βhCG level > 10% during three weekly Ÿ Plexiform or disorderly
consecutive measurements or longer, during a period of two arrangement
weeks or more-days 1,7,14 Ÿ No villous patterns
3. The serum βhCG level remains detectable for 6 months or
longer Figure 18. Gestational Choriocarcinoma
4. Histologic criteria for choriocarcinoma

1S-3 GESTATIONAL TROPHOBLASTIC DISEASE ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA

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METASTASIS_____________________________________________
Ÿ Early and Hematogenous (affinity of trophoblasts to blood vessels)
Ÿ Lungs (75%), Vagina (50%)
Ÿ Vulva, kidneys, brain, bowel
Ÿ Ovarian theca lutein- cysts seen in over 1/3 of metastatic cases
Figure 19. Metastatic lesions
showed on Chest radiograph
Figure 21. MRI of abdomen showing
metastatic lesion
C. PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT)
Ÿ Rare variant
Ÿ GTN arising in placental
implantation site
Ÿ Follows term, abortion, ectopic,
or molar pregnancy
Ÿ Presents mainly as bleeding
Ÿ Locally invasive tumors are
resistant to chemotherapy
Ÿ HYSTERECTOMY: best
treatment
Ÿ High risk Stage 1 and later
stages: Adjunct chemotherapy
Figure 23. Gross appearance of PSTT
HISTOLOGIC_____________________________________________
Ÿ Intermediate trophoblastic cells
mostly producing prolactin
Ÿ Serum β hCG low relative to the
tumor mass
1S-3 GESTATIONAL TROPHOBLASTIC DISEASE
Figure 20. Metastatic lesion in
Vagina
Figure 22. Metastatic lesion in Brain
Figure 24. Histologic app. of PSTT
D. EPITHELIOID TROPHOBLASTIC TUMOR
GROSS__________________________________________________
Ÿ Rare
Ÿ Preceding pregnancy event
maybe remote or may not even be
confirmed
Ÿ Grossly nodular
Ÿ Hysterectomy-primary mode of
treatment because this tumor is
resistant to chemotherapy
Figure 25. Gross app. of
Epitheloid Trophoblastic Tumor
HISTOLOGIC_____________________________________________
Ÿ Develops from neoplastic
transformation of chorionic type
intermediate trophoblast
Ÿ Resembles PSTT but the cells are
smaller and there is less nuclear
pleomorphism
Figure 26. Histo app. of
Epitheloid Trophoblastic Tumor
E. CLINICAL COURSE
Ÿ Irregular bleeding with uterine subinvolution
Ÿ Bleeding: continuous or intermittent, maybe sudden and massive
Ÿ Intraperitoneal hemorrhage: myometrial perforation by invading
trophoblasts
Ÿ May initially present as vulvar or vaginal metastasis or other
distant mets with the uterine tumor disappearing
Ÿ Choriocarcinoma: fatal without treatment
F. DIAGNOSIS
Most important factor: consideration for possibility of GTN-
Ÿ Persistent bleeding after any pregnancy event: mandates
measurement of βhCG and consideration of diagnostic curettage
Ÿ Thorough pelvic assessment, hemogram, renal and liver function
tests, chest X-ray or CT
Ÿ +of pulmonary nodulesà further imaging of brain, abdomen and
pelvis (CT Scan, MRI, PET Scan)
Ÿ CSF β HCG
FIGO 2002 STAGING_______________________________________
Ÿ Stage l - confined to uterus
Ÿ Stage ll - extends outside uterus but limited to genital structures
(adnexae, vagina, broad ligament)
Ÿ Stage lll - extends to lungs with or without known genital
involvement
Ÿ Stage lV - other metastatic sites
WHO PROGNOSTIC SCORING, 2002_________________________
Ÿ ≤ 6: low risk disease treatable by single chemotherapeutic agent
Ÿ ≥7: high risk disease requiring combination chemotherapy
G. TREATMENT
Ÿ Best managed by Oncologist
Ÿ Single agent chemotherapy: nonmetastatic or low risk disease
§ Methotrexate (less toxic)
§ Actinomycin D
Ÿ Risk factors for additional chemotherapy beyond first course:
§ Metastatic disease
ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA
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 § Single-day methotrexate infusion
§ Complete mole histology
Ÿ Repeat curettage: avoided (increases risk of perforation, bleeding,
micturation and adhesion) unless there is bleeding or a
substantial amount of retained molar tissue*
Ÿ Tumor debulking by curettage on the otherhand may hasten
response to chemotherapy
Ÿ Hysterectomy (women who have completed childbearing)
Ÿ Subsequent chemotherapy is based on serial βhCG levels
Ÿ 1year GTN
Ÿ 2 years if GTN is with metastasis
Ÿ Fertility is not compromised and pregnancy can be achieved after
successful treatment
Ÿ 2% risk of developing trophoblastic disease in subsequent
pregnancy
Ÿ Sonographic evaluation on early pregnancy and subsequently
Ÿ Histopathology of placenta or products of conception
Ÿ Serum β HCG determination 6 week postpartum

Ÿ Combination chemotherapy for high risk cases: IV. REFERENCES

§ EMA-CO: Etoposide, Methotrexate, Actinomycin D, Ÿ Williams Obstetrics 25th ed
Cyclophosphamide, Oncovin (Vincristine) Ÿ Dr. Santos’ PPT
§ Surgery, Radiotherapy Ÿ Notes and Recordings of OB Trans Team

SUBSEQUENT PREGNANCY________________________________ “Women are the stronger sex...” – Dr. Santos

Ÿ Surveillance duration: (minimum)
Ÿ 6 months-molar pregnancy
V. APPENDIX

Figure 27. WHO Prognostic Diagnosis, 2002

Figure 28. Obstetrics (FIGO) Staging and Diagnostic Scoring System for Gestational Trophoblastic Neoplasia

1S-3 GESTATIONAL TROPHOBLASTIC DISEASE ESTUYE Ÿ HO Ÿ JAVIER Ÿ RAMOS Ÿ ROCHA

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