Presentation on Hydatidiform mole. Consists of pathological basics, approach, management and patient counselling.

1. AN ACADEMIC PRESENTATION ON
HYDATIDIFORM MOLE
Dr. Sharad Prasad Dahal
MBBS (TU)
2075/09/17
1st January, 2019
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2. Objectives of Presentation
 To define risk factors, pathogenesis of H. mole
 To clarify approach according to C/F and different
investigations
 To describe different approaches of treatment and follow up
 To discuss different queries of patient and counselling.
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3.  Hydatidiform moles (Vesicular Moles) are abnormal
condition of the placenta where there are partly
degenerative and partly proliferative changes in the young
chorionic villi.
 These include the complete hydatidiform mole and partial
hydatidiform mole.
Definition
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4. Grossly,
 Mass filling the uterus made of multiple chains and clusters of
cyst of varying size,
 No trace of embryo or amniotic sac,
 Hemorrhage, if occurs, is in decidual space.
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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
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6.  Ethnic predisposition to hydatidiform mole, which has
increased prevalence in Asians, Hispanics, and American
Indians.
 Incidence : 1 to 2 per 1000 deliveries
Epidemiology
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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
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8.  History of prior hydatidiform mole.
 Prior complete mole, the risk of another mole is 1.5
percent.
 With a previous partial mole, the rate is 2.7 percent
 After two prior molar pregnancies, it is reported that
23% of women had a third mole.(berkowitz et al 1998)
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9. Pathogenesis
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.
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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)
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11. Twin Molar Pregnancy
• Not rare
• Vejerslev (1991) found that of 113 such pregnancies, 45 %
progressed to 28 weeks, and 70 % neonates survived
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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
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13. In early stage of pregnancy, women typically present to their
obstetric clinician with
 Missed menstrual periods,
 A positive 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
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14.  As gestation advances,
symptoms in Complete mole > Uncomplete mole
 Untreated molar pregnancies will almost always cause
abnormal vaginal bleeding
“white currant in red currant juice”
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15.  Bleeding may presage spontaneous molar abortion with
expulsion of vesicular tissues,
 Varying degree Lower Abdominal Pain
 Overstretching of uterus
 Concealed hemorrhage
 Infection
 Uterine contractions to expel out contents
 Rarely perforation of uterus
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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
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17.  Breathlessness due to pulmonary embolization of
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.
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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.
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19. Vaginal Examination
 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.
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20. Diagnosis
 Clinical
 Serological
 Radiological
 Pathological
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21. Clinical Diagnosis
 Amenorrhea followed by irregular vaginal bleeding with
excessive nausea and vomiting
 Spontaneous passage of molar tissue.
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22. Differential Diagnosis
 Spontaneous Abortion with Hydropic changes
 Hydropic chorionic villi not accompanied by trophoblastic
hyperplasia
 Gestational Trophoblastic Neoplasia
 Causes of enlarged uterus:
 Benign or malignant pathologies like leiomyomas,
adenomyosis or uterine malignancy
 Ovarian theca Lutein cyst
 Multiple Pregnancy 22

23. Serological Diagnosis
Definitive Investigations
 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.
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24. Supportive Tests
 Type and Rh; group and screen or crossmatch
 Creatinine and Hepatic aminotransferase levels
 TSH, free T4 levels
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25. Radiological Diagnosis
Sonography
 Complete mole
 Echogenic uterine mass with
numerous anechoic cystic
spaces but without a fetus or
amnionic sac.
 Described as a “snowstorm”
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26.  Partial mole
 Thickened, multicystic
placenta along with a
fetus or at least fetal
tissue.
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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.
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28. 28

29. Correlations,
 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.
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30. Pathological Diagnosis
 Histological
 Ploidy analysis
 p57KIP2 immunostaining
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31. Histological
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
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32. Ploidy Analysis
 Partial moles are Triploid.
 Complete Moles and Non molar pregnancies with hydropic
placental degeneration are both diploid.
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33.  Gene that expresses p57KIP2 is paternally imprinted, only
maternally donated genes are expressed.
 Complete moles do not produce p57KIP2; as it contains only
paternal genetics
 A complete mole
Diploid/p57KIP2-Negative
 A partial mole
Triploid/p57KIP2-Positive
 Spontaneous abortion with hydropic placental degeneration
Diploid/p57KIP2-Positive
p57KIP2 immunostaining Analysis
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34. Management
 Management of Complications
 Termination of Pregnancy
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35. Management of complications
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.
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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
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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
 Regardless of uterine size, Suction Evacuation is usually
the preferred treatment.
 Intraoperative bleeding are usually greater than non molar
evacuation
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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
 Methergine 0.2mg Im every 2 hour
 Carboprost PGF2α: 250 μg IM every 15–90 min
 Misoprostol (PGE1) :200 mg tablets for rectal
administration, 800–1000 mg once
Blood loss is minimized by
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40.  Intraoperative sonography ensure uterine cavity is emptied.
 In some cases, pelvic arterial embolization or hysterectomy
may be necessary
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41. Following curettage
 Anti-D immunoglobulin for Rh D-negative women
 fetal tissues with a partial mole may include red cells with
D-antigen.
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42. Place of Medical termination of pregnancy in H mole
 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
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43. Place of Hysterectomy following evacuation
 Preferable for women who have completed
childbearing
 Markedly reduces this Likelihood of GTN
 40 and older, approximately a third will subsequently
develop GTN,
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44. Place of Curettage following vaginal evacuation
 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.
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45. Post evacuation Follow up
The follow-up protocols include:
 History and clinical examination and
 hCG assay
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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
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48. Chest X-ray
 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
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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).
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50. However, It is indicated if,
 If the hCG level fails to become normal by the stipulated time (10–12
weeks) or there is re-elevation at 4–8 weeks.
 Rising β-hCG after reaching normal levels or Plateau level.
 Post evacuation hemorrhage (presence of trophoblastic activity).
 Where follow-up facilities are not adequate.
 Evidences of metastases irrespective of the level of hCG.
 Cases with higher rate of malignant sequelae (Risk Factors) 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 every 7 days. 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.
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52. Patient’s Querries and
Counselling
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53. -There is a chance that it will.
 Prior complete mole, the risk of another mole is 1.5 percent.
 With a previous partial mole, the rate is 2.7 percent
 After two prior molar pregnancies, it is reported that 23% of
women had a third mole.(berkowitz et al 1998)
Will it re-occur in my next pregnancy?
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54. Is there anything different that I should do to avoid
recurrence?
 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.
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55. How soon can I be pregnant again?
: Not until 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.
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56. What contraception is best for me?
 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.
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57. What about my 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
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58.  Early recognition of risk factors that precipitate H. Mole is
important.
 Prompt diagnosis can be achieved by correlation with clinical
evaluation, serological and histopathological test
 Suction evacuation is main stay of treatment. However other
modalities of treatment must be kept in mind.
 Regular follow up is an integral part of H. Mole management
 It is necessary to address patient queries and proper counselling is of
upmost importance.
Conclusion of presentation
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59. THANK YOU
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