Complete hydatidiform mole results from fertilization of an egg by two sperm cells (dispermy), resulting in a triploid fetus. Partial molar pregnancies occur when a normal egg is fertilized by two sperm, resulting in an abnormal placenta. Diagnosis is made through clinical exam, blood tests showing elevated hCG levels, ultrasound findings, and pathological examination. Treatment involves surgical evacuation of the uterus followed by monitoring of hCG levels to ensure no remaining molar tissue.

1. 1
HYDATIDIFORM MOLE
Presentor: Dr. Kajal Gupta
Moderator: Dr. Namita

2. WHO CLASSIFICATION
Gestational trophoblastic disease:
 Premalignant Diseases
Complete Hydatidiform Mole
Partial Hyadatidiform Mole
 Malignant Diseases (Gestational Trophoblastic Neoplasia)
Nonmetastatic
 Invasive Mole
 Placental site trophoblastic tumor ( PSTT )
 Epitheloid tumour
Metastatic
Gestational Choriocarcinoma

3.  Hydatidiform
Definition
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condition of
moles (V
esicular Moles) are abnormal
the placenta where there are partly
degenerative and partly proliferative changes in the
chorionic villi.
 These include the complete hydatidiform mole and partial
hydatidiform mole.

4. Grossly,
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 Grossely- uterus is filled with small multiple vesicles
 No trace of embryo or amniotic sac

5. The classic histological findings of molar pregnancy include
 Villous stromal edema
 Trophoblast proliferation
 Absence of blood vessels in the villi
 Villous pattern is distinctly maintained
Villous
stromal edema
Haphazard
trophoblast
proliferation
5

6.  Ethnic predisposition to hydatidiform mole, which has
increased prevalence in Asians, Hispanics, and American
Indians.
 Incidence : 1 to 2 per 1000 deliveries
Epidemiology
6

7.  Age:
 Both extremes of reproductive age are most vulnerable.
 Adolescents and women aged 36 to 40 years have a
twofold risk.
 Older than 40 have an almost tenfold risk
Risk Factors
7

8.  History of prior hydatidiform mole.
 Prior complete mole, the risk of another mole is 0.9
percent.
 With a previous partial mole, the rate is 0.3 percent
 After two prior molar pregnancies, it is reported that
20 percent of women had a third mole.(berkowitz et al 1998)
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9. Pathogenesis
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a. Complete Mole (46,XX)
• 23,X Haploid sperm penetrates a 23,X containing haploid
egg whose genes have been “inactivated’.
• Here Paternal chromosomes duplicate to create a 46,XX
diploid solely of paternal origin.

10. b. Incomplete Mole (69,XXY)
• Two Haploid sperms either 23,X or 23,Y fertilizes
(Dispermy)a 23,X containing haploid egg whose genes
have not been “inactivated’.
• Here, the resulting egg is triploid with two chromosome
sets being donated by the father (Diandry)
10

11. Twin Molar Pregnancy
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• Rarely, in twin pregnancies , one chromosomally normal
foetus is paired with a complete diploid molar
pregnancy.

12.  The clinical presentation has changed remarkably over the
past several decades due to early diagnosis as
 Prenatal care is sought much earlier and
 Sonography is virtually universal.
 As a result, most molar pregnancies are detected when they
are small and before complications ensue.
Symptoms and Signs
12

13. In early stage of pregnancy, women typically present to their
obstetric clinician with
 Missed menstrual periods,
 Apositive pregnancy test, and
 Signs and symptoms consistent with early pregnancy or early
pregnancy complications
 Spot bleeding,
 Pelvic and breast discomfort,
 Hyperemesis gravidarum and Anemia are reported only in 2
to 8% of cases.
Symptoms and Signs
13

14.  As gestation advances,
symptoms in Complete mole > Uncomplete mole
14
always cause
 Untreated molar pregnancies will almost
abnormal vaginal bleeding
“white currant in red currant juice”

15. Bleeding may proceeds to spontaneous molar abortion with
expulsion of vesicular tissues,
 Varying degree LowerAbdominal Pain
 Overstretching of uterus
 Concealed hemorrhage
 Infection
 Uterine contractions to expel out contents
 Rarely perforation of uterus 15

16.  Nausea and vomiting may become significant
 Severe preeclampsia and eclampsia are relatively common with
large molar pregnancies and twin molar pregnancy.
 Hypoxic trophoblastic mass, which releases antiangiogenic
factors that activate endothelial damage
16

17. to pulmonary embolization of
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 Breathlessness due
trophoblastic cells (2%)
 Thyrotoxic features: Tremors and Tachycardia (2%)
 Due to thyrotropin like effects of HCG which increases free T4..
Usually normalize after uterine evacuation.

18. P/A
 Fundal Height more than expected.
 The enlarged uterus has a soft consistency,
 Fetal part cannot be felt
 No fetal heart motion is detected.
18

19. Vaginal Examination
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 Internal Ballottement cannot be elicited
 Unilateral or Bilateral enlargement (Theca Lutein cyst) of
ovary(25-50% cases)
• Due to overstimulation of lutein elements by sometimes
massive amounts of hCG.

20. Diagnosis
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 Clinical
 Serological
 Radiological
 Pathological

21. Clinical Diagnosis
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 Amenorrhea followed by irregular vaginal bleeding with
excessive nausea and vomiting
 Spontaneous passage of molar tissue.

22. Differential Diagnosis
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 SpontaneousAbortion with Hydropic changes
 Hydropic chorionic villi not accompanied by trophoblastic
hyperplasia
 Gestational Trophoblastic Neoplasia
like leiomyomas,
 Causes of enlarged uterus:
 Benign or malignant pathologies
adenomyosis or uterine malignancy
 Ovarian theca Lutein cyst
 Multiple Pregnancy

23. Serological Diagnosis
Definitive
Investigations
23
 Serum β-HCG measurements
 In Complete molar pregnancy serum β-HCG levels are
commonly elevated than partial mole.
 In advanced moles, as high as millions miU/ml (Usually
>100,000 miU/ml).
 High hCG titer in urine (positive pregnancy test) diluted up to 1 in
200 to 1 in 500 beyond 100 days of gestation is very much
suggestive.
 Rapidly increasing values of serum HCG is usual.

24. Supportive Tests
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 Type and Rh; group and screen or crossmatch
 Creatinine and Hepatic aminotransferase levels
 TSH, free T4 levels

25. Radiological Diagnosis
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Sonography
 Complete mole
 Echogenic uterine mass with
numerous anechoic cystic
spaces but without a fetus or
amnionic sac.
 Described as a “snowstorm”

26.  Partial mole
26
 Thickened, multicystic
placenta along with a
or at least fetal
fetus
tissue.

27.  However,
In early pregnancy, these sonographic characteristics are
seen in fewer than half of hydatidiform moles
 Chest Radiographs
 To rule out Pulmonary embolization even in benign mole.
27

28. 28

29. Correlation
s,
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 Initial high hCG level (>100,000 mIU/mL),a transvaginal
ultrasound will likely demonstrate molar disease, if
present.
 High hCG level and ultrasound showing normal
singleton gestation,
 Repeat USG and hCG in one week to exclude twin
conception with normal fetus and co-existent molar
pregnancy.

30. Pathological Diagnosis
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 Histological
 Ploidy analysis
 p57KIP2 immunostaining

31. Histological
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Features Partial Mole Complete Mole
Embryo-fetus Often present Absent
Amnion, fetal erythrocytes Often present Absent
Villous edema Focal Widespread
Trophoblastic
proliferation
Focal, slight to
moderate
Slight to severe
Trophoblast atypia Mild Marked

32. PloidyAnalysis
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 Partial moles are Triploid.
 Complete Moles and Non molar pregnancies with hydropic
placental degeneration are both diploid.

33.  Gene that expresses
p57KIP2 immunostainingAnalysis
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p57KIP2 is paternally imprinted, only
maternally donated genes are expressed.
 Complete moles do not produce p57KIP2; as it contains only
paternal genetics
 Acomplete mole
Diploid/p57KIP2-Negative
 Apartial mole
Triploid/p57KIP2-Positive
 Spontaneous abortion with hydropic placental degeneration
Diploid/p57KIP2-Positive

34. Management
 Management of Complications
 Termination of Pregnancy
34

35. Management of complications
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Immediate:
 Hemorrhage and shock
 Separation of the vesicles from its attachment to the decidua ( concealed or
revealed)
 Massive intraperitoneal hemorrhage
 During evacuation of the mole due to atonic uterus or uterine injury.
 Sepsis
 Absence of protective membranes leads ascend of vaginal organisms into
uterine cavity.
 Degenerated vesicles, sloughing decidua and old blood favors bacterial
growth.
 Increased operative interference.

36.  Perforation of the uterus
 Perforating mole
 During vaginal evacuation especially by conventional (D&E) method during
curettage following suction evacuation.
 Preeclampsia
 Acute pulmonary insufficiency
 Coagulation failure
 fibrin and platelets deposition within the vascular tree
36

37. Late complications
Choriocarcinoma following hydatidiform mole 2–10%.
Risk Factors
Complete moles 15 to 20 %
Partial moles 1 to 5 %
Patient’s age ≥ 40 or < 20 years irrespective of parity

•
•
Parity ≥ 3. Age is more important than the parity

•
•
β-hCG levels > 100,000 mIU/mL
low decline in β-hCG level
Uterine size that is large-for-gestational age,

•
•
Previous history of molar pregnancy

•
•
Theca-lutein cysts > 6 cm,
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38. Termination of Pregnancy
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 Regardless of uterine size, Suction Evacuation is usually
the preferred treatment.
 Intraoperative bleeding are usually greater than non molar
evacuation

39.  Adequate anesthesia, sufficient IV access and arrangement
of blood products is necessary.
 Intraoperatively Oxytocin infusion can limit bleeding. (20U
in 100ml RL for continuous infusion)
 Other uterotonic agents, as need, may be added
Blood loss is minimized by
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for rectal
 Methergine 0.2mg Im every 2 hour
 Carboprost PGF2α: 250 μg IM every 15–90 min
 Misoprostol (PGE1) :200 mg tablets
administration, 800–1000 mg once

40.  Intraoperative sonography ensure uterine cavity is emptied.
 In some cases, pelvic arterial embolization or hysterectomy
may be necessary
40

41. Following curettage
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 Anti-D immunoglobulin for Rh D-negative women
NOT required in Complete Mole: because of poor vascularisation of the
chorionic villi and absence of the D-antigen.
Required in:
-partial mole: due to presence of RBCs
-complete mole: if diagnosis is not confirmed
histopathologically.

42. Place of Medical termination of pregnancy in H
mole
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 With Uterotonics , Uterine contractions will increase the
risk of trophoblastic embolization to the lungs or of
metastatic disease.
 More difficult to obtain a complete specimen with
medication-only evacuation

43. Place of Hysterectomy following
evacuation
 Preferable for women with
interactable bleeding who have
completed childbearing.
 Markedly reduces this Likelihood of
GTN
 40 years and older
, approximately one-
third of cases will subsequently develop 43

44. Curettage following vaginal evacuation
44
 Routine curettage is not recommended.
 Done in selected cases with persistent vaginal bleeding
(persistent GTN).
 Gentle curettage may be done 5–7 days following evacuation.
 In 5-7 days, Uterine wall gets thicker, firmer and the cavity
becomes smaller.

45. Post evacuation Follow up
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The follow-up protocols include:
 History and clinical examination and
 hCG assay

46. History Taking
Enquire about
 Irregular vaginal bleeding,
 persistent cough,
 breathlessness
 hemoptysis.
Abdominovaginal examination
Note about
 Involution of the uterus,
 Ovarian size and
 Malignant deposit if any, in the anterior vaginal wall.
Pelvic examination is done after one week of molar evacuation.
46

47. Investigations:
Serum hCG levels:
 within 48 hours of evacuation,
 1 to 2 weekly until undetectable,
 then monthly for 6 months
The median time for such resolution is 7 weeks for partial
moles and 9 weeks for complete moles
. 47

48. Chest X-ray
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 If the pre evacuation chest radiograph shows metastasis,
 should be repeated every 4 weeks until remission is
confirmed.
 Then repeated at 3 months interval during the rest of the
follow-up period.
 When pre-evacuation chest X-ray is normal,
 Repeated only when the hCG titer plateaus or rises

49. Prophylactic Chemotherapy
 About 80% of patients undergo spontaneous remission
 Following evacuation, the long-term prognosis for women
with a hydatidiform mole is not improved with
prophylactic chemotherapy (Goldstein, 1995).
49

50. However, It is indicated if,
 High levels of hCG for >4 weeks post evacuation.
 Rising β-hCG after reaching normal levels or Plateau level.
 Invasive mole
 Where follow-up facilities are not adequate.
 Evidences of metastases irrespective of the level of hCG.
 Histological evidence of choriocarcinoma. 50

51.  Methotrexate, 1 mg/kg/day IV or IM is given on days 1, 3, 5
and 7
With,
 Folic acid 0.1 mg/kg IM on days 2, 4, 6 and 8.
 It is to be repeated at interval of two weeks. A total three courses are given.
 β-hCG level should decrease by at least 15%, 4–7 days after methotrexate.
 Alternatively, intravenous actinomycin D 12 μg/kg body weight daily for 5
days may be given. 51

52. -There is a chance that it will.
 Prior complete mole, the risk of another mole is 0.9percent.
 With a previous partial mole, the rate is 0.3percent
 After two prior molar pregnancies, it is reported that 20%of
women had a third mole.(berkowitz et al 1998)
52

53. 53
 Recurrence NOT decreased by changing partners.
: Dietary Modification
 In the Oriental Countries, Faulty nutrition caused by inadequate
intake of protein, animal fat have shown association.
 Low dietary intake of carotene has shown association with
increased risk.

54. 54
Pregnancy should plan 6 - 12 months after β-hCG becomes
untraceable, or more if β-hCG levels rises again in the period of
follow up.
Rising β-hCG levels from a new pregnancy may create confusion with GTN in
follow up.

55. What contraception is best ?
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 Most recommend either combination hormonal
contraception or injectable medroxyprogesterone acetate.
 Intrauterine devices are not used until β-hCG levels are
undetectable
 Risk of uterine perforation in an invasive mole.
 Barrier and other methods are not recommended because
of their relatively high failure rates.

56. What about ovarian cysts?
 They spontaneously regress following
molar termination, Regular follow up is
necessary.
 Some recommend aspiration of larger
cysts to minimize pain and torsion risk
56

57. THANK YOU
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