Molar pregnancy

Presented By
Nirsuba Gurung
Masters in nursing
Women health and development
 Gestational Trophoblastic disease
comprises a spectrum of interrelated
conditions originating from the placenta.
 Gestational trophoblastic disease is a
prolifirative disorder of trophoblastic cells

 It can be benign, premalignant or malignant

 Classification of gestational Trophoblastic disease

WHO Classification

Malformations of the
Benign entities that
Malignant neoplasms chorionic villi that are
can be confused with
of various types of predisposed to
with these other
trophoblats develop trophoblastic
lesions
malignacies

Choriocarcinoma Hydatidiform moles Exaggerated placental s

Placental site
Complete Partial Placental site nodule
trophoblastic tumor
Epithilioid trophoblastic Invasive
tumors
 Non-metastatic disease: confined to the
uterus
 Metastatic
 A- low risk-good prognosis
 B – high risk-poor prognosis
Low risk
 Disease present in less than 4 mooths
duration
 Initial serum hCG level < 40,000 IU/ml
 Metastasis limited to lung and vagina
 No prior chemotherapy
 No preceding term pregnancy
High risk
 Long duration of disease
 Initial serum hCG level > 40,000 IU/ml
 Brain or liver metastasis
 Failure of prior chemotherapy
 Following term pregnancy
Hydatidiform Mole
 Definition:
 In latin
"hydatid" means "drop of water”
"mole" means "spot”
 Pathologically,
Hydatidiform moles represents placentas with
abnormally developed chorionic villi (enlarged,
edematous and vesicular villi with variable
amounts of proliferative trophoblast)
 Macroscopic of Hydatidiform
mole
Hydropic villi
Grapelike vesicles
filled clear material
usually 1 to 3cm
diameter

proliferation of the
trophoblast
Hydatidiform mole(molar
pregnancy)
 Molar pregnancy is an abnormal form
of pregnancy, wherein a non viable ,
fertilized egg implants in the uterus, and
thereby converts pregnancy process into
pathological ones.

 It is characterized by presence of
hyadatidiform moles.
It is an abnormal condition of the
placenta where there are partly
degenerative and partly proliferative
changes in the young chorionic
villi.
 These results in the formation of clusters
of small cysts of varying size

 It is regarded as a begin neoplasia of the

chorion with malignant potential
INCIDENCE
 There is considerable geographical
and environmental influences in
incidence.

 The incidence is higher in eastern than

western countries. Its incidence in
India is 1:160 and 1:2000 in UK.
 Hydatidiform Mole
 Incidence:
 In the United States,
 1in 600 therapeutic abortions
 1 in 1,500 pregnancies
 Internationally:
 In Japan & China, 1-2 in 1,000 pregnancies
 In Indonesia & India, 12 in 1,000 pregnancies
 In the United Arab of Emirates,
 2 in 1000 deliveries (population-based study; Graham IH,
Fajardo AM; 1988)
 In Saudi Arabia;
 1.48 in 1000 live births (hospital-based study; Felemban AA,
et al; 1969)
In the United States,
•1in 600 In Asian countries,
therapeutic •The rate is 10 times
abortions higher than in
•1 in 1,500 Europe and North
pregnancies America

In Saudi Arabia;,
•1.48 in 1000 live births
(hospital-based study;
Felemban AA, et al;
1969)
Contd…….
 It is prevalent among teenage and elderly
patient with high parity.
TYPES
1. COMPLETE
2. PARTIAL
Complete mole
 A complete mole is caused by a single
sperm combining with an egg which has
lost its DNA.

 The genotype is typically 46XX due to

subsequent mitosis of fertilizing sperm but
can also be 46XY.
Partial mole
 Partial mole occurs when an egg is
fertilized by 2 sperm or by ,sperm which
reduplicates itself yielding the genotype of
69 XXY or 92XXXY
 Hydatidiform mole

Complete mole Partial mole Partial mole

Partial mol ( fetal tissue)

Grossly placenta a mixture of normal and
hydropic villi

Fetus Severe growth restriction

Multiple congenital anomalies
Risk Factors hydatidiform
mole
 Strongest risk factors are
Age and a history of prior hydatidiform
mole

 Both extremes of reproductive age

adolescents twofold risk
Older than 40 tenfold risk
 History of Prior mole
 High parity
 Disturbed maternal immune mechanism
suggested by:
 Rise in gammaglobulin level in absence of
hepatic disease
 Increased association with AB blood group
which possess no ABO antibody
 An ethnic predisposition
 Diet (Deficiencies of protein or)
(Vitamin A deficiency)
 Animal fat
 Smoking
 Increased paternal age
 The risk of another mole
 Complete mole is 1.5 percent
 Partial mole is 2.7 percent

Two prior molar pregnancies

 the risk is 23 percent
 Pathogenesis and Cytogenetics of HM
Complete Partial
Genetic
Diploid Constituti Triploid/ teraploid
on
4% 90% 10%
96%
Fertilization Triploid Tetraploid
Fertilization
of an empty fertilization of fertilization of a
of an empty
ovum by two a normal normal ovum
ovum by one
sperms Patho- ovum by two by three
sperms that
undergoes
“Diandric genesis sperms sperms
dispermy” “Dispermic “Dispermi
duplication
triploidy”
“Diandric c triploidy”
diploidy”

69XXX
46XX Karyotype
46XX 69YXX
46XY
69YYX
Complete Mole, Pathogenesis
Paternal
Empty ovum chromosomes only

Duplication 46XX

23X

Diandric diploidy
Androgenesis
 Complete Mole, Pathogenesis
Paternal
Empty ovum chromosomes only

23X 23X
46XX
23X

23X

Dispermic diploidy
 Partial Mole, Pathogenesis
Paternal extra set
Normal ovum

23Y 23X
23X 69XXY
23Y 23X

23X

Dispermic triploidy
 Hydatidiform Mole
Alterations in gene
expression profiles

Up-regulation and down-regulation of

proteins committed to cell growth
control

e.g. Up-regulation of growth e.g. Down-regulation of insulin

factor and cytokine mediated growth factor binding proteins
pathways, and antiapoptosis and tumor necrosis factor
genes receptor

Trophoblastic hyperplasia
Pathogenesis
 Principally a disease of the chorion
 Death of the ovum ir failure of the embryo
to grow is essential to develop complete H.
mole
 The secretion from the hyperplastic cells
and transferred substances from the
maternal blood accumulates in the stroma
of the villi which are deviod of blood
vessels
 This results in distension of the villi to
form small vesicles
 The distension may also be due to edema
and liquification of the stroma
 Vesicle fluid is interstitial fluid and is
almost similar to ascitic or edema fluid but
rich in hCG
Naked eye appearance
 The mass filling the uterus is made of
multiple chains and clusters of cysts of
varying sizes
 No trace of embryo or the amniotic sac
 Hemorrhage, if occurs, takes place in the
decidual space
Microscopic appearance
 Marked prolifiration of syncitial and
cytotrophoblastic epithelium
 Marked thining of the sromal tissue due to
hydropoc degeneration
 Absence of blood vessels
FEATURES COMPLETE PARTIAL MOLE
MOLE

karyotype 46XX, paternal Triploid or quadriploid

Embryo/fetus absent Present

Villious edema All villi Some villi

Trophoblastic Diffuse, circumferential Focal, slight

proliferation

Uterine size More than the date Less than the date

Beta hCG High(>50000) Slight elevation

Behaviour 2% choriocarcinoma Rare

Clinical features
 Amenorrhea 8-12 weeks with following
manifestation
 Vaginal bleeding
 Varying degree of abdominal pain
 Constitutional symptoms
 Patient become sick without any apparent reason
 Vomiting of pregnancy becomes excessive
 Breathlessness
 Thyrotoxic symptoms
 Expulsion of grape like vesicles per
vaginum

 History of quickening absent

Clinical Presentation:
Complete mole:

Vaginal
bleeding

Passage of
Severe
hydropic
anemia
villi
Signs
 Features suggestive of early pregnancy
 Pallor
 Features of pre-eclampsia
 Per abdomen
 Uterus –more than gestational period (70%)
 Uterus feels firm elastic(doughy )
 Fetal parts not palpable
 Absence of fetal movement and FHS
Vaginal examination
 Internal ballotement cannot be elicited
 Unilaternal or bilaternal enlargement of
ovary (25-50%)
 Finding of vesicles in the vaginal discharge
 Open cervical os
Classical symptom of a complete
mole
 Abnormal vaginal bleeding
 Lower abdominal pain
 Hyperemesis gravidarum
 Features of early onset of pre-eclampsia
 Uterus > dates
 No fetal parts and FHS
 Classical symptoms
contd….
 Expulsion of vesicular tissues
 Theca lutein cyst of ovaries
 Hyperthyriodism
 Serum hCG >1,00,000 IU/ml
 USG –snow strom appearance
Hydatidiform Mole
 Diagnosis:
 History
 Clinical examination
 Ultrasound examination
 Serum hCG levels
 Histopathological examination
 Cytogenetic and molecular biological
examination
 Hydatidiform Mole
 Diagnosis:
 Ultrasonography:
* The diagnosis of molar pregnancy is nearly always
made by ultrasonography
•The classical finding is a
Complete mole “snow storm" pattern
•Theca lutein cysts are frequent
findings on ultrasound
The snow storm appearance of complete hydatidiform mole
Theca lutein cysts, a frequent finding on ultrasound
 Hydatidiform Mole
 Diagnosis:
 Ultrasonography:
Abnormal gestational sac
The classic vesicular sonographic
findings of a complete mole are
usually not seen
Partial mole Focal sonographic cystic changes
and/or hydropic changes in the
placenta are significantly associated
with the diagnosis of a partial molar
pregnancy
Hydatidiform Mole
 Diagnosis:
 Ultrasonography:
 However, based on ultrasound, correct diagnosis
can be suspected in only:
• 84% of patients with complete mole and
• 30% of patients with partial mole

(Lindholm and Flam, 1999)

 The accuracy of ultrasonogrophy is gestational age
dependent
In comlete mole:
• 100% of cases cane be diagnosed at a gestational age of
13 weeks or more
• 50% of cases cane be diagnosed in earlier pregnancies

(Lazarus et al, 1999)

Hydatidiform Mole
 Diagnosis:
 Serum hCG levels:
 Serum hCG levels of greater than 92 000 IU/l
associated with absent fetal heart beat indicate a
diagnosis of complete hydatidiform moles
(Romero et al, 1985)

 Serum hCG level decreases quickly if the patient

has an abortion, but it does not in molar pregnancy
Hydatidiform Mole
 Diagnosis:
 Histopathological examination:
 It should always be done as far as possible and
samples should be kept for DNA analysis for a
final diagnosis when histology can not
differentiate molar pregnancy from abortion
Table3: Pathological features of complete and partial
hydatidiform mole
Complete Mole Partial Mole
Macro- A mass of large, The placental tissue is
scopically edematous villi that are less bulky
diffusely distributed, A few enlarged villi with
typically described as a focal distribution
resembling a cluster of A fetus may be
grapes identified grossly that
often has multiple
congenital anomalies
including syndactyly of
the fingers & toes
The grape like vesicles in gross appearance
Table3: Pathological features of complete and partial
hydatidiform mole
Complete Mole Partial Mole
Micro- Enlarged edematous Two distinct populations
scopicall villi which show a of villi. One with large,
y central acellular fluid- edematous villi with
filled space referred to central cisterns. The other
as a “central cistern” contains small villi that
Abnormal show some degree of
trophoblastic stromal fibrosis
proliferation that is Abnormal circumferential
circumferential in trophoblastic proliferation
contrast to normal villi Fetal tissue, RBSs
in which trophoblastic
proliferation is at one
end of the villus
Absence of fetal tissue
DIFFERENTIAL DIAGNOSIS
1. THREATENED ABORTION
2. FIBROID OR OVARIAN TUMOR WITH
PREGNANCY.
3. MULTIPLE PREGNANCY
4. MISTAKEN DATE
5. ACUTE HYDRAMINOS
 Complications associated with molar
pregnacy:
 Those related to the increased trophoblastic
tissue volume:
 Theca-lutein cysts
 Pregnancy-induced hypertension,

 hyperthyroidism,

 Respiratory distress

 Hyperemesis

 Those related to its management:

 Uterine perforation
Hydatidiform Mole, complications
 Theca-lutein cysts:
 Prevalence:
 Clinically evident theca lutein cysts (usually >5–6 cm) are
detected in about 25-35% of women with molar pregnancies
 Association:
 They usually correlate with marked elevation of serum hCG
levels above 100,000 IU/l
 Complications:
 Pain or pressure that may require percutaneous aspirations.
 Torsion, rupture, or bleeding are rare complications that can
require oophorectomy
 Bilateral theca letein cysts increase the risk of post-molar GTD
 Course:
 The mean time for theca luteal cysts to regress is approximately
8 weeks
Hydatidiform Mole, complications
 Respiratory distress syndrome:
 Prevalence:
 Rare
 Pathophysiology:
 Embolization of trophoblastic tissue
 Transient impairment of left ventricular function
during induction of anesthesia for suction D&C of
molar pregnancy
 coexisting conditions such as anemia,
hyperthyroidism, hypertension from preeclampsia
 Risk factors:
 Uterine size larger than 14 to 16 weeks’
 High levels of hCG
Hydatidiform Mole, complications
 Respiratory distress syndrome:
 Presentation:
 Tachypnia and tachycardia following evacuation
 Bilateral pulmonary infiltrates on chest x-ray

 Management:
 Central venous monitoring
 Ventilatory support

 Course:
 It should resolve within 24 to 48 hours after molar
evacuation
Hydatidiform Mole, complications
 Hyperthyroidism:
 Prevalence:
 Clinical hyperthyroidism is seen in less than 10%
of patients with molar pregnancies
 A small number of patients may have elevated
thyroid function tests without clinical evidence of
disease
 Management:
 Beta-blockers should be administered prior to
molar evacuation to prevent thyroid storm that may
be induced by anesthesia and surgery.
 A hydatidiform mole and a co-existent fetus:
 Prevalence:
 Rare (1 in 22,000–100,000)
 partial moles and twin gestations with co-existent fetuses
and molar gestations
 Diagnosis:
 Usually, by ultrasound
 Few, after examination of the placenta following delivery
 Complications:
 Increased risk of medical complications
 Increased risk for postmolar gestational trophoblastic disease
 Management:
 No clear guidelines for management
 Risk Factors for post-molar gestational trophoblastic
disease:
 Advanced maternal age
 Factors that reflect the volume of trophoblastic tissue:Clinical
factors that are associated with
 high hCG levels (>100,000 mIU/mL)
 uterus large for date,
 bilateral theca lutein cysts,
 Respiratory distress syndrome after molar evacuation,
 eclampsia,
 hyperthyroidism,
 Uterine subinvolution with post evacuation hemorrhage.
(With any one of these factors or a combination of many, the risk of
post-molar GTD has ranges from 25% to 100%)
Hydatidiform Mole
 Risk Factors for post-molar gestational trophoblastic disease:
 The presence of “invasive trophoblast antigen (ITA)”
which has 100% sensitivity and specificity for invasive
trophoblastic tumors
(Cole et la, 2003)

*There is no correlation between the degree of anaplasia and

the risk of post-molar GTD
COMPLICATIONS

 IMMEDIATE
1. Hemorrhage and shock
2. Sepsis
3. Perforation of uterus
4. Pre-eclampsia
5. Acute pulmonary insufficiency
6. Coagulation failure
 LATE
Development of choriocarcinoma (2 to 20%)

Risk factors of malignant change:

 Patient’s age>40 or <20
 Parity >3
 Serum hCG> 100000 mIU/mL
 Uterine size> 20 wk
 Previous history of molar pregnancy
 Thece leutin cysts: large(>6cm diameter)
MANAGEMENT
 The principle of the management:
1. Suction evacuation of the uterus
2. Supportive therapy
3. Counselling for regular follow up
The patient are grouped into two:
 Group A:the mole is in the process of
expulsion
 Group B:the uterus remains inert
Management
1 Complete history and physical examination

2 Investigations

3 Medical and surgical care

 History and physcal examination:
 Should aim to rule out the classic symptoms and
signs that would lead to a diagnosis of:
 severe anemia
 dehydration
 preeclampsia
 thyrotoxicosis

The patient should be stabilized hemodynamically

 Management:
 Investigations:
 Laboratory:
 Pre-evacuation hCG
 Complete blood count
 Electrolytes, BUN, creatinine
 Liver function tests
 Thyroid function tests
 Imaging:
 Pelvic ultrasound
 Chest x-ray
Hydatidiform Mole
 Management:
 Medical care:
 Correction of:
 Anemia
 Dehydration
 Hyperthyroidism
 hypertension
Management:Surgical
Suction curettage
(with oxytocin or •The method of choice
prostaglandin
infusion)
•Increased risk of
Hysterectomy medical complications

•Associated with a
markedly decreased rate
of malignant sequelae
(3.5%) when compared
with suction evacuation.
Hysterectomy
Hysterectomy: is indicated in:
a)Patient with over 35,
b)Patient complete her family
irrespective of age,
c)Uncontrolled hemorrhage or
perforation during surgical evacuation,
Counselling
Counselling for follow up:
Routine follow up is mandatory for
all cases for at least 1 year.
Intervals: initially the check up must be made
at an interval of 1 week till the serum hCG
levels become negative.This usually happen
by 4-8 weeks.
once negative within 56 days,the patient
is followed up at every 1 month intervals
for 6 months.
Women undergone chemotherapy should be
followed up for 1 year after hCG has
been normal.
Methods employed in each visit:
a)enquire about each symptoms
b)abdomino vaginal examination
c)investigations:hCG,chest x-ray
PROPHYLACTIC
CHEMOTHERAPY
 If the hCG levels fails to normal by
the stipulated time(10-12) weeks or
relevation at 4-8 weeks.
 Post evacuation hemorrhage.
 Where follow up facilities are not
adequate.
 Evidence of metastasis irrespective of
the level of hCG.
 Prophylactic Chemotherapy:
 In one randomized clinical trial, a single
course of methotrexate and folinic acid
reduced the incidence of postmolar
trophoblastic disease from 47.4% to
14.3% (P <.05) in patients with high-risk
moles:
 hCG levels greater than 100,000
mIU/mL,
 uterine size greater than gestational age,
 ovarian size greater than 6 cm),
 However, the incidence was not reduced in
patients with low-risk moles

 On the other hand, the use or prophylactic

chemotherapy increases the risk of drug resistance

 Because of the excellent primary cure rates among

women with post-molar GTD, and mortality
achieved by monitoring patients with serial hCG
determinations and instituting chemotherapy only
in patients with postmolar gestational
trophoblastic disease outweighs the potential risk
and small benefit of routine prophylactic
chemotherapy.
Pregnancy after Hydatidiform Mole:
 Risk of another molar pregnancy:
 Increased by 10-fold (1–2% incidence)

 Current recommendations for management of

subsequent pregnancies:
 an early ultrasound to confirm normal gestational

development and dates

 A chest x-ray to screen for occult metastasis
masked by the hCG rise of pregnancy
 Examination of the placenta or products of
conception histologically at the time of delivery or
evacuation for evidence of occult trophoblastic
disease
 An hCG level should be obtained 6 weeks post
evacuation or delivery to confirm normalization.
CONTRACEPTIVE ADVICE

 The patient is advised not to be

pregnant for at least 1 year.

 Use of contraception
IUD is contraindicated.
OCP:after hCG value have been
normal.
Barrier method.
Hydatidiform Mole
 Prognosis:
 Post-molar gestational trophoblastic disease:
 Risk:
 Following complete mole: 20%
 Following partial mole: 5%
 Type:
 70% to 90% are persistent or invasive moles
 10% to 30% are choriocarcinomas
 Diagnosis:
 A rising, plateauing, or persistent elevation of human chorionic
gonadotropin after evacuation of a hydatidiform mole or an
ectopic or term pregnancy
PROGNOSIS
 More than 80% of H. moles are benign. The
outcome after treatment is usually excellent.
Highly effective means of contraception are
recommended to avoid pregnancy for at least 6 to
12 months.

 About 15 to 20% of cases may develop into

persistent GTD.
 In 2 to 10% of cases it may change into
choriocarcinoma.
 Over 90% of women with malignant, non
spreading cancer are able to survive and retain
their ability to conceive and bear children.

 In those with metastatic cancer, remission

remains at 75 to 85%, although their childbearing
ability is usually lost.
NURSING DIAGNOSIS
 Acute pain related to uterine contraction.
 Risk for fluid volume deficit related to
execessive vascular loss.
 Ineffective uteroplacental tissue perfusion
related to abnormal trophoblastic
proliferation.
 Risk for maternal injury related to blood
loss,abnormal blood profile,impaired immune
system.
 Fear related to fetal loss and outcome
of pregnancy.