2. Molar pregnancy
Presented By
Nirsuba Gurung
Masters in nursing
Women health and development

3.  Gestational Trophoblastic disease
comprises a spectrum of interrelated
conditions originating from the placenta.

4.  Gestational trophoblastic disease is a
prolifirative disorder of trophoblastic cells
 It can be benign, premalignant or malignant

5. Classification of gestational Trophoblastic disease
WHO Classification
Malignant neoplasms
of various types of
trophoblats
Malformations of the
chorionic villi that are
predisposed to
develop trophoblastic
malignacies
Benign entities that
can be confused with
with these other
lesions
Choriocarcinoma
Complete
Hydatidiform moles
Placental site nodule
Exaggerated placental s
Epithilioid trophoblastic
tumors
Placental site
trophoblastic tumor Partial
Invasive

6.  Non-metastatic disease: confined to the
uterus
 Metastatic
 A- low risk-good prognosis
 B – high risk-poor prognosis

7. 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

8. 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

10. 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)

12. Macroscopic of Hydatidiform
mole
Hydropic villi
Grapelike vesicles
filled clear material
usually 1 to 3cm
diameter
proliferation of the
trophoblast

13. 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.

14. It is an abnormal condition of the
placenta where there are partly
degenerative and partly proliferative
changes in the young chorionic
villi.

15.  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

16. 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.

17. 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)

18. In the United States,
•1in 600
therapeutic
abortions
•1 in 1,500
pregnancies
In Asian countries,
•The rate is 10 times
higher than in
Europe and North
America
In Saudi Arabia;,
•1.48 in 1000 live births
(hospital-based study;
Felemban AA, et al;
1969)

19. Contd…….
 It is prevalent among teenage and elderly
patient with high parity.

20. TYPES
1. COMPLETE
2. PARTIAL

21. 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.

22. 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

23. 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

24. 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

25.  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

26.  An ethnic predisposition
 Diet (Deficiencies of protein or)
(Vitamin A deficiency)
 Animal fat
 Smoking
 Increased paternal age

27.  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

28. Pathogenesis and Cytogenetics of HM
Genetic
Constituti
on
Diploid Triploid/ teraploid
Patho-
genesis
4%
Fertilization
of an empty
ovum by two
sperms
“Diandric
dispermy”
90%
Triploid
fertilization of
a normal
ovum by two
sperms
“Dispermic
triploidy”
96%
Fertilization
of an empty
ovum by one
sperms that
undergoes
duplication
“Diandric
diploidy”
10%
Tetraploid
fertilization of a
normal ovum
by three
sperms
“Dispermi
c triploidy”
Karyotype46XX
69XXX
69YXX
69YYX
46XX
46XY
Complete Partial

29. Complete Mole, Pathogenesis
Duplication 46XX
Empty ovum
23X
Diandric diploidy
Androgenesis
Paternal
chromosomes only

30. Complete Mole, Pathogenesis
46XX
Empty ovum
23X
Dispermic diploidy
Paternal
chromosomes only
23X 23X
23X

31. Partial Mole, Pathogenesis
69XXY
Normal ovum
23X
Dispermic triploidy
Paternal extra set
23Y 23X
23Y 23X
23X

32. 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
factor and cytokine mediated
pathways, and antiapoptosis
genes
Trophoblastic hyperplasia
e.g. Down-regulation of insulin
growth factor binding proteins
and tumor necrosis factor
receptor

33. 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

34.  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

35. 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

37. Microscopic appearance
 Marked prolifiration of syncitial and
cytotrophoblastic epithelium
 Marked thining of the sromal tissue due to
hydropoc degeneration
 Absence of blood vessels

38. FEATURES COMPLETE
MOLE
PARTIAL MOLE
karyotype 46XX, paternal Triploid or quadriploid
Embryo/fetus absent Present
Villious edema All villi Some villi
Trophoblastic
proliferation
Diffuse, circumferential Focal, slight
Uterine size More than the date Less than the date
Beta hCG High(>50000) Slight elevation
Behaviour 2% choriocarcinoma Rare

39. 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

40.  Expulsion of grape like vesicles per
vaginum
 History of quickening absent

41. Clinical Presentation:
Complete mole:
Vaginal
bleeding
Severe
anemia
Passage of
hydropic
villi

42. 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

43. 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

44. 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

45. Classical symptoms
contd….
 Expulsion of vesicular tissues
 Theca lutein cyst of ovaries
 Hyperthyriodism
 Serum hCG >1,00,000 IU/ml
 USG –snow strom appearance

46. Hydatidiform Mole
 Diagnosis:
 History
 Clinical examination
 Ultrasound examination
 Serum hCG levels
 Histopathological examination
 Cytogenetic and molecular biological
examination

47. Hydatidiform Mole
 Diagnosis:
 Ultrasonography:
* The diagnosis of molar pregnancy is nearly always
made by ultrasonography
Complete mole
•The classical finding is a
“snow storm" pattern
•Theca lutein cysts are frequent
findings on ultrasound

48. The snow storm appearance of complete hydatidiform mole

49. Theca lutein cysts, a frequent finding on ultrasound

50. Hydatidiform Mole
 Diagnosis:
 Ultrasonography:
Partial mole
Abnormal gestational sac
The classic vesicular sonographic
findings of a complete mole are
usually not seen
Focal sonographic cystic changes
and/or hydropic changes in the
placenta are significantly associated
with the diagnosis of a partial molar
pregnancy

51. 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)

52. 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

53. 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

54. Table3: Pathological features of complete and partial
hydatidiform mole
Complete Mole Partial Mole
Macro-
scopically
A mass of large,
edematous villi that are
diffusely distributed,
typically described as
resembling a cluster of
grapes
The placental tissue is
less bulky
A few enlarged villi with
a focal distribution
A fetus may be
identified grossly that
often has multiple
congenital anomalies
including syndactyly of
the fingers & toes

55. The grape like vesicles in gross appearance

56. Table3: Pathological features of complete and partial
hydatidiform mole
Complete Mole Partial Mole
Micro-
scopicall
y
Enlarged edematous
villi which show a
central acellular fluid-
filled space referred to
as a “central cistern”
Abnormal
trophoblastic
proliferation that is
circumferential in
contrast to normal villi
in which trophoblastic
proliferation is at one
end of the villus
Absence of fetal tissue
Two distinct populations
of villi. One with large,
edematous villi with
central cisterns. The other
contains small villi that
show some degree of
stromal fibrosis
Abnormal circumferential
trophoblastic proliferation
Fetal tissue, RBSs

57. DIFFERENTIAL DIAGNOSIS
1. THREATENED ABORTION
2. FIBROID OR OVARIAN TUMOR WITH
PREGNANCY.
3. MULTIPLE PREGNANCY
4. MISTAKEN DATE
5. ACUTE HYDRAMINOS

58.  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

59. 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

60. 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

61. 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

62. 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.

63.  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

64.  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%)

65. 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

66. COMPLICATIONS
 IMMEDIATE
1. Hemorrhage and shock
2. Sepsis
3. Perforation of uterus
4. Pre-eclampsia
5. Acute pulmonary insufficiency
6. Coagulation failure

67.  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)

68. MANAGEMENT
 The principle of the management:
1. Suction evacuation of the uterus
2. Supportive therapy
3. Counselling for regular follow up

69. The patient are grouped into two:
 Group A:the mole is in the process of
expulsion
 Group B:the uterus remains inert

70. Management
Complete history and physical examination
Investigations
Medical and surgical care
1
3
2

71.  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

72.  Management:
 Investigations:
 Laboratory:
 Pre-evacuation hCG
 Complete blood count
 Electrolytes, BUN, creatinine
 Liver function tests
 Thyroid function tests
 Imaging:
 Pelvic ultrasound
 Chest x-ray

73. Hydatidiform Mole
 Management:
 Medical care:
 Correction of:
 Anemia
 Dehydration
 Hyperthyroidism
 hypertension

74. Management:Surgical
Suction curettage
(with oxytocin or
prostaglandin
infusion)
Hysterectomy
•The method of choice
•Increased risk of
medical complications
•Associated with a
markedly decreased rate
of malignant sequelae
(3.5%) when compared
with suction evacuation.

75. 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,

76. 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.

77. 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

78. 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.

79.  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),

80.  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.

81. 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.

82. 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.

83. 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

84. 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.

85.  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.

86. 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.

87.  Fear related to fetal loss and outcome
of pregnancy.