Vesicular Mole

Dr. MOHAMMED ABDALLA

EGYPT, DOMIAT G. HOSPITAL
It is a benign neoplasm
of the chorionic villi
Incidence: 1:2000 pregnancies in United States and Europe

1:200 in Asia

10 times more in women over 45 years old.

The increasing use of ultrasound in early pregnancy has

probably led to the earlier diagnosis of molar pregnancy
 RISK FACTORS:

1-Maternal age :
Young mothers (under age 20 years) have a slightly
higher prevalence of GTD, although not nearly so great
as those mothers over age 35 years.
2-Women who have had a previous molar gestation
3-The risk increases with the number of spontaneous
abortions.
4- Women with blood type A may be more likely to
develop choriocarcinoma (but not hydatidiform mole);
 What Is A Hydatidiform Mole?
A hydatidiform mole is an abnormality of fertilization

COMPLETE MOLE PARTIAL MOLE

It is the result of It is the result of

fertilisation of anucleated
fertilisation of an
ovum ( has no chromosomes)
with a sperm which will
ovum by 2 sperms so
duplicate giving rise to 46 the chromosomal
chromosomes of paternal number is 69
origin only. chromosomes
 Differentiation Between Complete And Partial
Mole

Partial Mole Complete Mole Feature

Present Absent Embryonic or
foetal tissue
Focal Diffuse Swelling of the villi
Focal Diffuse Trophoblastic
hyperplasia
Paternal and maternal Paternal 46 XX (96%) Karyotype
69 XXY or 69 XYY or 46 XY (4%)

Rare 5-10% Malignant Changes

 Three components make up the trophoblast:

cytotrophoblast, intermediate trophoblast syncytiotrophoblast

The cytotrophoblast is The intermediate

trophoblast has features
The syncytiotrophoblast,
a stem cell with high which constitutes the
mitotic activity but of the other two
components and is villous trophoblast, has low
without hormonal
synthesis. responsible for mitotic activity. The
endometrial invasion and syncytiotrophoblast is
implantation responsible for the
synthesis of the (beta-hCG)
and can be identified with
immunohistochemical
stains.
 Pathology
There is trophoblastic proliferation, with mitotic
activity affecting both syncytial and
cytotrophoblastic layers. This causes excessive
secretion of hCG,chorionic thyrotrophin and
progesterone.
.

microscopic evaluation shows trophoblastic

hyperplasia
 Pathology
(hydropic) villi The uterus is distended
by thin walled, translucent, grape-like
vesicles of different sizes.

,At histologic analysis

Uniformly edematous (hydropic) villi with
dissolution of central stroma (cavitation/cistern
 Pathology
There is no vasculature in the
chorionic villi leads to early
death and absorption of the
embryo.

At histologic analysis Occasionally, necrosis is seen

 Pathology
High hCG causes:
multiple theca lutein exaggeration of the
cysts in the ovaries normal early
in about 50% of pregnancy symptoms
cases.
and signs
 Pathology
1.Uniformly edematous (hydropic) villi
with dissolution of central stroma
(cavitation/cistern)
2.Villous vessels absent (usually)
3.Trophoblastic hyperplasia –
circumferential, haphazard, involves
CT/ST/IT
4.Trophoblastic atypia
 Symptoms and Signs
Usually occur in first 20 ­24 weeks of gestation.

•Bleeding.
• pain.
• toxemia (25% ).
•hyperemesis (25%) .
•absent fetus, LGA, SGA.
•hyperthyroidism (7%).
• passage of tissue with vesicles.
•bilateral thecalutein cysts (30%).
 :MOST COMMON
GTD
•complete hydatidiform mole,
•invasive mole,
•choriocarcinoma.

LESS COMMON:
•Partial hydatidiform moles
•placental site trophoblastic tumor
 Complete Hydatidiform Mole

U/S evaluation.
allows identification of numerous,
discrete, anechoic (cystic) spaces
within a central area of
heterogeneous echotexture
 Complete Hydatidiform Mole

U/S evaluation.
The coexistence of a fetus with a complete
hydatidiform mole is uncommon (in contrast to the
partial hydatidiform mole), occurring in 1%-2% of
cases .as a result of dizygotic twinning; thus, the
fetus is chromosomally normal. but, fetal survival
until term is unlikely because of the maternal
complications of the mole itself
 Complete Hydatidiform Mole

U/S evaluation.

Theca lutein cysts multiloculated,

often bilateral

resolve after treatment of the

intrauterine process

Occasionally seen in twin gestations, fetal hydrops,

pharmacologic stimulation (especially with human
maternal gonadotropin)
 Partial Hydatidiform Mole

U/S evaluation.
Ultrasound has limited value in detecting partial molar
pregnancies.
Grade C recommendations

• the ultrasound diagnosis of a complete mole is often reliable, the diagnosis of a

partial molar pregnancy is more complex. The finding of multiple cystic spaces in the
placenta is suggestive of a partial molar pregnancy. *
• When there is diagnostic doubt about the possibility of a combined molar pregnancy
with a viable fetus then ultrasound examination should be repeated before
intervention.

RCOG/Fine C, Bundy A L, Berkowitz R S et al. Sonographic diagnosis of partial hydatidiform

mole. Obstet Gynecol 1989; 73:414-8.
In twin pregnancies with
a viable fetus and a
molar pregnancy, the
pregnancy can be
allowed to proceed.

(Grade C recommendation
twin pregnancies with a viable fetus and a molar
pregnancy are associated with:

reduced live birth rate of 25%

risk from complications such as pre-eclampsia and haemorrhage.

The subsequent need for chemotherapy, about 20%, is the same whether
*/**
the pregnancy is terminated, or allowed to proceed to term.

1. Evans A C Jr, Soper J T, Hammond C B. Clinical features of molar pregnancies and gestational
trophoblastic tumours. In: Hancock B W, Newlands E S, Berkowitz R S, editors. Gestational Trophoblastic
Disease. London: Chapman and Hall 1997: 109-25.
2. Foskett M A, Seckl M J, Paradinas F J, et al. A review of 126 cases registered at Charing Cross Hospital as
twin-multiple pregnancies complicated by a complete hydatidiform mole (CHM) IX World Congress of
Gestational Trophoblastic Disease, Jerusalem, November 1998.
 Partial Hydatidiform Mole

U/S evaluation.
The clues for the sonographer in this
diagnosis are the presence of a
fetus (although usually with severe,
but nonspecific, abnormalities) in
combination with a formed
placenta containing numerous
cystic spaces
 • When Sonography alone is not sufficient.To
differentiate between twin pregnancy with a
normal fetus and a coexistent complete mole,
AND partial molar pregnancy,

In twin pregnancy with a normal fetus and a coexistent complete

mole maternal serum AFP levels are within the normal range.
in partial molar pregnancy, elevated levels of AFP are found in
the maternal serum and normal levels of AFP in the amniotic
fluid
Jauniaux E, Campbell S. Placenta and Cord. In: Dewbury K, Meire H, Cosgrove D, eds.
Ultrasound in Obstetrics and Gynecology. London, United Kingdom. Churchill Livingstone
1993;448-9.
Freeman SB, Priest JH, Macmahon WC, Fernhoff PM, Elsas LJ. Prenatal ascertainment of
triploidy by maternal serum alpha-fetoprotein screening. Prenat Diagn 1989;9:339-47.
 RCOG Recommendations

1. Ultrasound has limited value in detecting partial molar pregnancies.

2. In twin pregnancies with a viable fetus and a molar pregnancy, the
pregnancy can be allowed to proceed.
3. Surgical evacuation of molar pregnancies is advisable.
4. Routine repeat evacuation after the diagnosis of a molar pregnancy is
not warranted.
5. Registration of any molar pregnancy is essential.
6. The combined oral contraceptive pill and hormone replacement therapy
are safe to use after hCG levels have reverted to normal.
7. Women should be advised not to conceive until the hCG level has been
normal for six months or follow-up has been completed (whichever is
the sooner).

Grade C recommendation
 Evacuation of Molar Pregnancies

Suction curettage is the method of

choice of evacuation for
complete molar pregnancies.

1. Stone M, Bagshawe K D. An analysis of the influence of maternal age, gestational age, contraceptive
method and mode of primary treatment of patients with hydatidiform moles on the incidence of
subsequent chemotherapy. Br J Obstet Gynaecol 1979; 86:782-92.
 Evacuation of Molar Pregnancies

Medical termination of complete molar

pregnancies, including cervical
preparation prior to suction
evacuation should be avoided where
possible. because of the potential to
embolise and disseminate trophoblastic
tissue through the venous system.
1. Gillespie A M, Tidy J, Bright N, Radstone C R, Coleman R E and Hancock B W.
Primary gynaecological management of gestational trophoblastic tumours and the
subsequent development of persistent trophoblastic disease. Br J Obstet Gynaecol
1998; 107(suppl 17) Abs. No. 287, p. 95.
 Evacuation of Molar Pregnancies

oxytocic infusions are only

commenced once evacuation has
been completed. If the patient is
experiencing significant
haemorrhage prior to evacuation and
some degree of control is required
then use of these agents will be
necessary according to the clinical
condition.
1. Bagshawe K D, Dent J, Webb J. Hydatidiform mole in England and Wales
1973-1983. Lancet 1986; 2:673-7.
 Evacuation of Molar Pregnancies

In partial molar pregnancies where the size

of the fetal parts deters the use of suction
curettage, medical termination can be
used.
(Grade C recommendation.

Gillespie A M, Tidy J, Bright N, Radstone C R, Coleman R E and Hancock B W. Primary

gynaecological management of gestational trophoblastic tumours and the subsequent
development of persistent trophoblastic disease. Br J Obstet Gynaecol 1998; 107(suppl 17)
Abs. No. 287, p. 95.

Newlands E S. Presentation and management of persistent gestational trophoblastic disease and

gestational trophoblastic tumours in the UK. In: Hancock B W, Newlands E S, Berkowitz R S,
editors. Gestational Trophoblastic Disease. London: Chapman and Hall 1997; 143-56.
Therapy:
dilatation and suction curettage (at which time the diagnosis is confirmed).

of women with complete hydatidiform mole will develop recurrent disease in the form 15%
.of invasive mole or choriocarcinoma

SO

all patients are followed up with successive serum beta-hCG measurements to allow early
detection of persistent gestational trophoblastic neoplasia

Avoid pregnancy
IF serial testing shows progressive decrease in the serum beta-hCG level

The clinical diagnosis of complete hydatidiform mole is reached.

 Clinical management of persistent low level hCG elevation

At the Eleventh World Congress on Gestational Trophoblastic

Disease 2001, over 70 cases of persistent low level hCG elevation
were reported from four Trophoblast Centres. The majority view of
an expert panel was to refrain from immediate chemotherapy and/or
surgery but to monitor such patients carefully and repeatedly (even
over many years) looking for evidence of tumour or for a definite
rise in hCG values.

Hancock BW, Everard JE, Drew D. Quiescent gestational trophoblastic disease (FTD): how common is it and
what is its outcome? XIth World Congress on Gestational Trophoblastic Diseases, Santa Fe, 2001, abstract.
Kohorn EI. Persistent low level hCG: a clinical enigma. XIth World Congress on Gestational Trophoblastic
Disease, Santa Fe, 2001, abstract.
Newlands ES, Seckl MJ, Foskett M, Short D, Fuller S and Mitchell H. Problems of interpretation of persistent
low levels of hCG in patients suspected of having gestational trophoblastic disease (GTD). XIth World
Congress on Gestational Trophoblastic Diseases, Santa Fe, 2001, abstract.
 Evacuation of Molar Pregnancies

Because persistent trophoblastic disease may

develop after any pregnancy it is recommended
that all products of conception obtained after
repeat evacuation, performed because of
persisting symptoms, should undergo histological
examination. Grade C recommendation

Bagshawe K D, Dent J, Webb J. Hydatidiform mole in England and Wales 1973-

1983. Lancet 1986; 2:673-7.
 Evacuation of Molar Pregnancies

There is no clinical indication for the routine use of a second

uterine evacuation in the management of molar
pregnancies.
In cases where there are persisting symptoms after initial
evacuation, consultation with the Screening Centre
should be sought before surgical intervention. (Grade C
recommendation)

Newlands E S. Presentation and management of persistent gestational

trophoblastic disease and gestational trophoblastic tumours in the UK. In:
Hancock B W, Newlands E S, Berkowitz R S, editors. Gestational
Trophoblastic Disease. London: Chapman and Hall 1997; 143-56.