Possible Complications

• Lung problems may occur after a D and C if the woman's uterus is bigger than 16 weeks
gestational size.

invasive moles.

These moles may grow so far into the uterine wall and cause bleeding or other
complications. A condition where a molar pregnancy, such as a partial hydatidiform mole or
complete hydatidiform mole, invades the wall of the uterus, potentially spreading and
metastasizing to other parts of the body (such as the vagina or lungs).

Invasive moles occur in about 20% of molar pregnancies but are more common in
complete molar pregnancies than in partial molar pregnancies. Invasive moles can develop both
before and after treatment by D & C. Treatment of an invasive mole may include chemotherapy.

choriocarcinoma,

a fast-growing cancerous form of gestational trophoblastic disease.

is quick-growing form of cancer that occurs in a woman's uterus (womb). The abnormal
cells start in the tissue that would normally become the placenta, the organ that develops during
pregnancy to feed the fetus. Choriocarcinoma is a type of gestational trophoblastic disease.

Choriocarcinoma may recur, usually within several months but possibly as late as 3 years
after treatment ends. Complications associated with chemotherapy or surgery can also occur. If a
hysterectomy is performed, infertility will result. Menopause will begin if the ovaries are also
removed.

is a malignant and aggressive cancer, usually of the placenta. It is characterized by early

hematogenous spread to the lungs. It belongs to the far end of the spectrum of gestational
trophoblastic disease (GTD), a subset of germ cell tumors.

Gestational trophoblastic disease

(GTD) refers to a group of abnormalities in which tumors grow inside a woman's uterus
(womb). The abnormal cells start in the tissue that would normally become the placenta, the
organ that develops during pregnancy to feed the fetus.

A baby may or may not develop during these types of pregnancies.

Alternative Names (Chorioblastoma; Choriocarcinoma; Trophoblastic tumor; Chorioepithelioma;
Invasive/malignant mole; Gestational trophoblastic neoplasia)

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Anatomy

The trophoblast is the outer covering of the early blastocyst. It provides nourishment between the
maternal endometrium and the embryo. The trophoblast eventually develops into the functional
part of the placenta, covering the placental villi and serving as a surface for the exchange of
oxygen and nutrients. The trophoblast is composed of 3 parts. From inner to outer, these parts are
the cytotrophoblast, the syncytiotrophoblast, and the intermediate trophoblast. The
syncytiotrophoblast is responsible for producing beta-hCG. Proliferation of this layer accounts
for the marked beta-hCG elevation seen in hydatidiform mole.

Pathophysiology

CHMs have a diploid chromosomal pattern, with all chromosomes being derived from the father
by means of either monospermic or dispermic fertilization. In monospermic fertilization, a single
haploid sperm fertilizes an ovum lacking a nucleus and then duplicates its chromosomes.
Monospermic fertilization always results in a 46XX karyotype, because 46YY zygotes lack
certain X-linked genes that are essential for development (Larsen, 1997). In dispermic
fertilization, 2 sperm fertilize an ovum lacking a nucleus. Dispermic fertilization may result in
either a 46XX or a 46XY karyotype. A 46XX karyotype is found in 90% of CHMs. This finding
indicates that monospermic fertilization is the dominant genetic mechanism (Szulman, 1978).

CHMs develop without the formation of fetal tissue, a feature that distinguishes them from
PHMs. On pathologic evaluation, CHMs demonstrate swollen chorionic villi with a grapelike
appearance and with hyperplastic trophoblastic tissue.

PHMs usually have a triploid karyotype (69XXX, 69XXY, or 69XYY) resulting from
fertilization of a normal egg by 2 sperm. Therefore, triploid PHMs consist of 2 sets of paternal
chromosomes and 1 set of maternal chromosomes. About 10% of PHMs have tetraploid or
higher karyotypes consisting of multiple sets of paternal chromosomes combined with 1 set of
maternal chromosomes. Fetal tissue is often present in PHMs, but the fetus is nonviable, it is
severely growth restricted, or it has multiple anomalies. On pathologic analysis, PHMs show
unpronounced swelling of chorionic villi and unpronounced trophoblastic hyperplasia.

Prognosis

A woman with a molar pregnancy often goes through the same emotions and sense of loss as
does a woman who has a miscarriage. Most of the time, she truly believed she was pregnant and
now has suffered a loss of the baby she thought she was carrying. In addition, there is the added
worry that the tissue left behind could become cancerous.

In the unlikely case that the mole is cancerous the cure rate is almost 100%. As long as the uterus
was not removed, it would still be possible to have a child at a later time.

 Epidemiology: Incidence

1. North America and Europe: 1:1000 to 1:1500 pregnancies

2. Asia and Latin America: 1:400 to 1:200 pregnancies
3. Philippines: 1:250

 Risk Factors

1. Prior molar pregnancy

2. Extremes of reproductive age
1. Age under 20 years
2. Age over 45 years
3. Twin Gestation
4. High parity
5. Malnutrition

 Pathophysiology

1. Form of Trophoblastic Neoplasia

1. Benign proliferation of chorionic villi
2. Fetus absent
2. Choriocarcinoma (risk: 10-20%) predisposing factors
1. Complete hydatiform mole
2. Abnormally proliferative trophoblast
3. Pitocin or Hysterectomy for mole evacuation
4. Oral Contraceptive use after mole evacuation

 Types

1. Complete Mole
1. Total hydatidiform change
2. Marked proliferation of trophoblastic cells
3. No evidence of fetal vessels
4. Karyotype: 46XX (all paternally derived)
1. Derived from haploid 23X sperm
2. Sperm duplicates chromosomes without cell division
5. Higher risk for malignant change
2. Partial Mole
1. Associated with non-viable fetus or vessels only
2. Moderate trophoblastic proliferation
 3. Karyotype: Triploid (69XXX or 69XXY)
1. Fertilization by more than one sperm
4. Malignant change less likely than in complete mole

 Symptoms

1. Vaginal Bleeding during pregnancy in 3rd-4th month

2. Hyperemesis Gravidarum
3. Passage of grapelike villi from the uterus
4. Abdominal Pain early in pregnancy
5. Pallor or Dyspnea
1. Associated with Anemia
6. Anxiety and Tremor
1. Due to weak Thyroid stimulation by HCG

 Signs

1. Excessive Uterine enlargement

1. Larger than expected for gestational age
2. Fetus absent
1. Fetal Heart Tones absent
2. Absent fetal parts
3. Ovarian enlargement (10%)
1. Related to theca-lutein cysts
4. Onset Hypertension early in pregnancy
1. Occurs before Pregnancy Induced Hypertension
2. Occurs in first or second trimester

 Histology

1. Gross Examination
1. Whitish grape-like cluster
2. Interspersed blood clots
2. Microscopic changes of villi
1. Trophoblastic proliferation
1. Cytotrophoblast (Langerhans Cell) proliferation
1. Cuboid cells
2. Prominent nuclei
2. Syncytiotrophoblast proliferation
1. Sheets of cytoplasm proliferate
2. Dark oval nuclei
2. Hydropic changes to central stroma
1. Cystic spaces form (cisterns)
2. Avascular edematous spaces form
3. Fetal Vessels absent
 Labs

1. Quantitative bhCG
1. Excessively elevated above expected levels
2. Level may exceed 1 Million IU
3. Directly reflects tumor volume
2. Complete Blood Count
1. Anemia
2. Platelets decreased
3. Liver Function Testing
4. Thyroid Function Testing
1. Thyroid Stimulating Hormone
2. Free T4

 Radiology

1. Molar pregnancy screening: Pelvic Ultrasound

1. Mass of Vesicles appears like snowstorm
2. Differential diagnosis
1. Septic Abortion
2. Fibroma
2. Molar Pregnancy confirmed
1. Chest XRay
2. Consider CT Head and Abdomen

 Complications

1. Malignant transformation to Choriocarcinoma in 10-20%

1. Locally Invasive Mole: Chorioadenoma destruens (66%)
2. Gestational Choriocarcinoma (33%)
2. Hyperthyroidism
3. Pregnancy Induced Hypertension

 Management

1. Evacuation of uterus
1. Dilatation and Evacuation
2. Dilatation and Curettage
2. Avoid Hysterectomy, Hysterotomy, or Pitocin
1. Increased risk of metastasis (relative risk: 3.0)
2. Clamp uterine vessels early if Hysterectomy needed
3. Chemotherapy Indications after D&C
1. Quantitative bhCG persistently elevated
2. Persistent uterine bleeding
3. Evidence of trophoblastic metastasis
1. Brain
 2. Lungs

 Monitoring

1. Follow Quantitative bhCG levels until 0

2. Serial bHCG for 6 months to 1 year
1. Use Contraception during this time
3. Chemotherapy if bHCG rises or does not fall to 0
1. Methotrexate usually used

 Prognosis

1. Recurrence rate of complete mole: 20%

1. May recur as locally invasive or metastatic
2. Recurrence rate in future pregnancies: 1-2%