Mola Hidatidosa

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Gestational Trophoblastic Disease (GTD) Dr. Swati Singh Department of Obs and Gyn UDUTH

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Mola Hidatidosa

Transcript of Mola Hidatidosa

  • Gestational Trophoblastic Disease (GTD)Dr. Swati SinghDepartment of Obs and GynUDUTH

  • Molar Pregnancy

  • It is a spectrum of trophoblastic diseases that includes:Complete molar pregnancyPartial molar pregnancies Invasive moleChoriocarcinoma Placental site trophoblastic tumourThe last 2 may follow abortion, ectopic or normal pregnancy.

    DefinitionsGestational Trophoblastic Disease (GTD)

  • ChoriocarcinomaI-Pathologic ClassificationII-Clinical ClassificationhCG based: WHO, FIGO, ACOG 2004 & RCOG 2010 Benign G.T.D. G.T. NeoplasiaMalignant G.T.D.Partial moleComplete moleInvasivemoleMetastaticNon metastaticLow riskHigh riskGestational Trophoblastic Disease (GTD)Placental site trophoblastic tumourPersistent GTDClassifications

  • -Hydatidiform Mole(H. MOLE)=Vesicular Mole

  • Hydatidiform Moles (H.M.)Hydatidiform moles are abnormal pregnancies characterized histologically by :Trophoblastic proliferation (Both syncitiotrophoblast & cytotrophoblast)Edema of the villous stroma (Hydropic) . Based on the degree and extent of these tissue changes, hydatidiform moles are categorized as either Complete hydatidiform mole.Partial hydatidiform mole.

  • Features Of Partial And Complete Hydatidiform Moles

    FeaturePartial moleComplete moleKaryotypeMost commonly69, XXX or - XXYMost commonly46, XX or -,XYPathologyFetusOften presentAbsentAmnion, fetal RBCUsually presentAbsentVillous edemaVariable, focalDiffuseTrophoblastic proliferationFocal, slight-moderateDiffuse, slight-severeClinical presentationDiagnosisMissed abortionMolar gestationUterine sizeSmall for dates50% large for datesTheca lutein cystsRare25-30%Medical complicationsRare10-25%Postmolar CTN2.5-7.5%6.8-20%

  • Epidemiology& Risk FactorsIncidence:USA 1/1000 South East 1/500 (Hospital) and in Nigeria 1/379.Risk Factors:Age: 40y(10 fold) & >50y (50% V.mole)Prior Molar PregnancySecond molar: 1% - Third molar : 20%!Diet: in low fat Vit. A or carotene diet (complete mole)Contraception :COC double the incidencePrevious spontaneous abortion: double the incidenceRepetitive H. moles in women with different partners

  • Partial moles have been linked to:Higher educational levelsSmokingIrregular menstrual cyclesOnly male infants are among the prior live birthsEpidemiology & Risk Factors

  • Homozygous 90%Pathogenesis of complete H. MoleKaryotype

  • Pathogenesis of complete H. MoleHeterozygous 10%Karyotype

  • Pathogenesis of Partial H. MoleKaryotype

  • Complete H. MoleMicroscopically Enlarged, edematous villi and abnormal trophoblastic proliferation that diffusely involve the entire villiNo fetal tissue, RBCs or amnion are producedMacroscopically, these microscopic changes transform the chorionic villi into clusters of vesicles with variable dimensions like bunch of grapes" No fetal or embryonic tissue are producedUterine enlargement in excess of gestational age .Theca-lutein cyst associated in 30%

  • Complete hydatidiform mole: Macroscopically, these microscopic changes transform the chorionic villi into clusters of vesicles with variable dimensions the name hydatidiform mole stems from this "bunch of grapes"

  • Partial H. MoleMicroscopically: The enlarged, edematous villi and abnormal trophoblastic proliferation are slight and focal and did not involve the entire villi.There is a scalloping of chorionic villi Fetal or embryonic or fetal RBCsMacroscopically: The molar pattern did not involve the entire placenta.Uterine enlargement in excess of gestational age is uncommon. Theca-lutein cysts are rare Fetal or embryonic tissue or amnion

  • Partial Hydatiform MoleVesiclesMaternal side

  • Partial H. mole.

  • The classic features areIrregular vaginal bleedingHyperemesisExcessive uterine enlargement &Early failed pregnancy.Breathlessness due to anaemiaAbdominal painPresentationSome women will present early with passage of molar tissue

  • Rarer presentations include:HyperthyroidismEarly onset pre-eclampsia Abdominal distension due to theca lutein cystsVery rarelyAcute respiratory failure Neurological symptoms such as seizures (?metastatic disease).

  • Clinical FindingsAnemiaBreathlessnessPseudo- Toxemia which consist of Systolic hypertension edema and proteinuriaThe Uterus is doughy in consistenceAbsence of fetal partEnlarged Cystic Ovaries

  • Complete Molar Pregnancy

  • Complete hydatidiform mole. The classic "snowstorm" appearance is created by the multiple placental vesicles.

  • Complete H.Mole (High-resolution) U/S Complex intrauterine mass containing many small cysts.Complete H.Mole Associated theca-lutein cysts. U/S Power Doppler

  • In most patients with a partial mole, the clinical and U/S diagnosis is Usually missed or incomplete abortion.This emphasizes the need for a thorough histopathologic evaluation ofall missed or incomplete abortions

  • Classically: A thickened, hydropic placenta with fetal or embryonic tissue Multiple soft markers, including:Cystic spaces in the placenta andTransverse to AP dimension a ratio of the gestation sac of > 1.5, is required for the reliable diagnosis of a partial molar pregnancy

  • Differential diagnosis

    Multiple pregnancy. Hydatidiform mole.Threatened abortion.Ectopic pregnancy.

  • Partial Molar Pregnancies

  • There are 2 important basic lines :1-Evacuation of the mole2-Regular follow-up to detect persistent trophoblastic diseaseIf both basic lines are done appropriately, mortality rates can be reduced to zero.

    Management

  • For Partial mole: It depends on the fetal partsSmall fetal parts :Suction curettageLarge fetal parts: Medical (oxytocics) In partial mole the oxytocics is safe ,as the hazard to embolise and disseminate trophoblastic tissue is very low Also, the needing for chemotherapy is 0.1- 0.5%.Is That The Same For Partial Mole?

  • Post-evacuation Surveillance Why? To determine when pregnancy can be allowed To detect persistent trophoblastic disease (i.e. GTN)

  • The Post-evacuation Surveillance. How?A baseline serum -hCG level is obtained within 48 hours after evacuation.Levels are monitored every 1 to 2 weeks while still elevated to detect persistent trophoblastic disease (GTN). These levels should progressively fall to an undetectable level (
  • What Is The Optimum Follow-up Period Following Normalization of hCG?For 6 months from the date of uterine evacuation.For 6 months from normalization of the hCG level. BFor 12 months from the date of uterine evacuation. (For Nigeria)

  • Barrier methods until normal hCG level.Once hCG level have normalized:Combined oral contraceptive (COC ) pill may be used. If oral COC was started before the diagnosis of GTD ,COC can be continue as its potential to increase risk of GTN is very lowIUCD should not be used until hCG levels are normal to reduce uterine perforation.What Is Safe Contraception Following GTD?

  • Part II: Gestational Trophoblastic Neoplasia (GTN)

  • Nonmetastatic disease

    Locally invasive GTT develops in about 15%Patient usually present with Irregular vaginal bleedingTheca lutein cystsUterine subinvolution or asymptomatic enlargement Persistently elevated serum hCG level Persistent GTT After hydatiaiform mole

  • Invasive Mole Villus formation preserved Trophoblast cells invade myometrium and blood vessels Myometrium invadedMyometrium Villus

  • Invasive H. MoleMyometrial invasionSometimes involving the peritoneum, parametrium, or vaginal vault. Originate almost always from H. moleVesicles

  • Placental-site trophoblastic tumor Uncommon but important variant of choriocarcinoma Characteristic Produce small amount of hCG and hPLRemain confined to the uterusMetastasizing late in their course Relatively insensitive to chemotherapy

  • Gestational ChoriocarcinomaAneuploidy (not multiplication of 23 )1 in 30,000 pregnancies in western world 1 in 300 to 1000 in Nigeria40% after molar pregnancy: Easily Diagnosed60% non-molar pregnancy: Difficult Diagnosis The main presentations are often non-gynecologic including hemoptysis or pulmonary embolism, cerebral hemorrhage, gastrointestinal or urologic hemorrhage.

  • Gestational ChoriocarcinomaSheets of anaplastic cytotrophoblast and syncytiotrophoblast cells with hemorrhage & necrosis.Myometrial & B. vessels invasion and early metastasesNo Villus formationCytotrophoblastSyncytiotrophoblast

  • Metastatic disease

    Metastatic GTT occur in about 4% after complete mole Symptom of metastases may result from spontaneous bleeding at metastatic foci The common site of metastases areLung(80%)vagina(30%) pelvis(20%) liver(10%) brain(10%)

  • GTN Vaginal Metastasis

  • Cranial MRI scan: Large metastasis on the left (black arrows)Brain MRI of a patient with a solitary brain metastasis in remission

  • Autopsy specimen Multiple hemorrhagic hepatic metastasisCT Scan: Liver metastsis

  • FIGO Anatomic Staging Of GTN

  • Staging : FIGO

    Risk factor affecting staging hCG level > 100,000 mIU/mlDuration of disease longer than 6 months from termination of pregnancy Stage 1-4Without risk factors a 1 risk factorbWith 2 risk factorsc

  • FIGO Prognostic Scoring For GTN (2000(Total Score Survival : 6 = Low risk (100%) 7 = High risk. (95%)

  • Non metastatic GTD Metastatic Single agent ChemotherapyMethotrexate or Actinomycen DMulti-agent ChemotherapyLow Risk ( 6) High Risk (7)What Is The Optimum Treatment For GTN?GTN

  • What is the best methotrexate regimen? MTX:1mg/kg IM D:1, 3 ,5 ,7 alternating with Folinic acid 0.1mg/kg IM D 2 , 4 , 6 , 8 followed by 6 rest daysTreatment is continued, until the hCG level has returned to normal and then for a further 6 consecutive weeks.As any chemotherapy treatment is reevaluated if FBC, liver or kidney FT are affected or at drug resistance

  • Chemotherapy

    Combination chemotherapy Triple therapy : MTX, Act-D, cyclophosphamide EMA-CO : etoposide, MTX, Act-D, cyclophosphamide, vincristine EMA-EP : etoposide and cisplatin on day 8

    Duration of therapy Until 3 normal hCG level

    After that, at least 2 additional course are administered

  • Follow UpStage 1-3 receive follow-up with Weekly hCG level until normal for 3 wks Monthly hCG level until normal for 12 monthsEffective contraception during the entire interval of hormonal follow-up Stage 4 receive follow-up with Weekly hCG level until normal for 3 wksMonthly hCG level until normal for 24 months

  • What Is The Survival of GTN By FIGO Stage?Disaia &Creasman Clinical Gynecological Oncology 2007

    StageSurvivalPercent %I424/424100II27/27100III130/13199IV14/1878

  • **********************FIGO Anatomic Staging **