This document discusses gestational trophoblastic disease (GTD), which includes complete and partial hydatidiform moles, invasive moles, choriocarcinoma, and placental site trophoblastic tumors. Complete moles are diploid and androgenic in origin with no fetal tissue, while partial moles are usually triploid. Clinical features may include irregular bleeding, hyperemesis, and uterine enlargement. Diagnosis involves hCG levels, ultrasound, and histological examination. Treatment is usually suction evacuation followed by hCG monitoring for persistent trophoblastic disease. Rarely, choriocarcinoma may develop and spread to distant organs requiring chemotherapy. Prognosis is generally good even

1. GESTATIONAL
TROPHOBLASTIC
DISEASE
Maryam Majid AL-Ezairej
Obstetrics and gynecology
Collage of medicine, RAKMHSU

2. objectives
 Introduction
 pathophysiology
 Clinical features
 Work up
 Management
 Follow up

3. Introduction
 Gestational trophoblastic disease (GTD) forms a group of disorders spanning
the conditions of complete and partial molar pregnancies through to the
malignant conditions of invasive mole, choriocarcinoma and the very rare
placental site trophoblastic tumour (PSTT).
 Molar pregnancies can be subdivided into complete (CM) and partial moles
(PM) based on genetic and histopathological features.

4. Background
 Complete moles are diploid and androgenic in origin, with no evidence of
fetal tissue.
 Complete moles usually (75–80%) arise as a consequence of duplication of a
single sperm following fertilisation of an ‘empty’ ovum.
 complete moles (20–25%) can arise after dispermic fertilisation of an ‘empty’
ovum.
 Partial moles are usually (90%) triploid in origin, with two sets of paternal
haploid genes and one set of maternal haploid genes.
 Partial moles occur, in almost all cases, following dispermic fertilisation of an
ovum. 10%of partial moles represent tetraploid or mosaic conceptions.
 In a partial mole, there is usually evidence of a fetus or fetal red blood cells.
 GTD (hydatidiform mole, invasive mole, choriocarcinoma, placental-site
trophoblastic tumour) is a rare event

7. CLINICAL FEATURES
 The classic features of molar pregnancy are irregular vaginal bleeding,
hyperemesis, excessive uterine enlargement and early failed pregnancy.
 Absence of Fetal parts & FHR
 Vaginal passage of hydropic vesicles (White Currant in red currant jelly-
passage of moles per vagina)
 Rarer presentations include hyperthyroidism, early onset pre-eclampsia or
abdominal distension due to theca lutein cysts.
 Clinicians should check a urine pregnancy test in women presenting with such
symptoms.

8. WORK UP
 URINE PREGNANCY TEST
 Base line HCG
 Baseline chest x-ray
 Complete blood count , Blood for ABO & Rh
 Clotting function studies
 Tests for associated medical complications
 IMAGING
 ultrasound
 Contrast CT scan of the abdomen and pelvis
 Chest CT
 MRI of the head (preferable to CT) – Only if lung metastasis or persistent mole

9. Diagnosis of molar pregnancy
 HCG levels
 Much Elevated compared to a normal pregnancy of
similar gestational age
 Ultrasound examination is helpful in making a pre-evacuation
diagnosis but the definitive diagnosis is made by histological
examination of the products of conception.

10. Ultrasound
 Complete mole:
 Ultrasound shows central
heterogeneous mass with
numerous anechoic spaces
(swelling of hydropic chorionic villi);
“snowstorm pattern”
 Partial mole:
 Fetus, often growth restricted,
reduced amniotic fluid, “swiss
cheese pattern” of chorionic villi .

11. Management
Principles-Immediate Evacuation
-Follow up
Termination methods
 Suction Evacuation (Treatment of choice)
• In combination with oxytocin
• Curettage is done at the end
• Intraoperative USG helps
 Hysterectomy:
 Age of the patient (>40 years)
 No desire to preserve fertility
 Malignant potential

12. Follow up
 Serum βHCG* tested
 Within 48 hours after evacuation
 Every 2 weeks till normal
 Then monthly for 6 months
*any rise/persistent plateau in levels should prompts evaluation &
treatment
 Contraception
 Abstinence or barrier before hCG normalization
 OCP is started after hCG normalizes
 Must be used during the entire follow-up period
 At least 6 months / preferred 1 year

13. FOLLOW UP

14. GTD
Benign
(Hydatidiform
mole)
Complete
Partial
Persistent (Invasive
mole)
Malignant
Non-metastatic
(PSTT)
Metastatic
(Choriocarcinoma)

15. INVASIVE MOLE
 Histologically identical to complete mole
 Invades myometrium without intervening stroma
 Diagnosis
 Persistence of HCG
 By MRI
 Best diagnosis: histology
 Treatment
 Chemotherapy
 Surgery

16. Choriocarcinoma
 Malignant form
 May follow
 Histologically: no villi structure
 Rapid myometrium invasion , uterine vessel invasion & systemic metastasis by
embolization
 Abnormal bleeding for >6 weeks after any pregnancy should be evaluated
 LOOK FOR SYSTEMIC METS (CT scan/PET scan)
 Most common sites of metastasis are lungs & genital tract
 If metastases are present, signs and symptoms associated with the metastatic
disease, such as hemoptysis, abdominal pain, hematuria, and neurologic
symptoms, may be present.

17. Investigation
 Serum quantitative hCG
 CBC
 Liver enzymes
 Pelvic ultrasonography
 Chest radiograph(staging)
 CT scan of the chest (optional): Micro-metastases detected
 CT scan of the abdomen and pelvis
 Contrast CT and MRI of the head

18. Staging and scoring
International Federation of Gynecology and Obstetrics staging
 Stage I – Confined to the uterus
 Stage II –Limited to the genital structures
 Stage III-Lung metastases
 Stage IV –Other metastases

19. FIGO SCORE

20. Management of choriocarcinoma
 Decided by revised FIGO scoring system
 Non-metastatic - by Methotrexate or Actinomycin D
 Score ≥7 needs multi agent chemotherapy
 Radiotherapy is added for brain or liver metastasis
 PROGNOSIS
 Cure rates for non metastatic & good prognosis choriocarcinoma ≈ 100%
 Poor prognosis is 80-90%
 Indications for surgery
 Control of hemorrhage
 Remove chemo resistant disease