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Gestational trophoblastic disease

Novak 2003. Gestational trophoblastic disease. Hydatidiform Mole Persistent Gestational Trophoblastic Tumor Chemotherapy. Hydatidiform mole. Epidemiology Complete versus partial mole Clinical picture Natural history Diagnosis

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Gestational trophoblastic disease

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  1. Novak 2003 Gestational trophoblastic disease

  2. Hydatidiform Mole • Persistent Gestational Trophoblastic Tumor • Chemotherapy

  3. Hydatidiform mole

  4. Epidemiology • Complete versus partial mole • Clinical picture • Natural history • Diagnosis • Treatment • Follow up

  5. GTD is among the rare tumors that can be cured even if metastasized Types: • Complete mole • Partial mole • Placental site mole • Choriocarcinoma Persistent GTT: Most commonly follow molar pregnancy May also follow: abortion, ectopic or term pregnancy introduction

  6. % varies in different sites: Japan = 2 : 1000 pregnancies USA = 0.6 – 1.1 : 1000 pregnancies In pathological studies: Complete mole 1 : 945 Partial mole 1 : 695 epidemiology

  7. Risk factors in complete mole: 1 – nutritional: ↓ carotene ↓ vit A 2 – Age: > 35 years = X 2 > 40 years = X 7.5 Risk factors in partial mole: 1 - OCCP 2 - H/O irregular menstruation

  8. Complete mole Pathology: • No fetal or embryonic tissue • Villi show: Diffuse hydropic swelling Diffuse trophoblastic hyperplasia Chromosome: 90% 46XX 10% 46XY Complete versus partial mole

  9. Chromosomes are entirely paternal Mitochondria DNA is maternal in origin 1 - Absent or inactivated ovum nucleus + 1 haploid sperm  endoredublication  homozygous mole 2– Absent or inactivated ovum nucleus + 2 haploid sperms  heterozygous mole

  10. Partial mole Villi vary in size and show: • Focal hydropic swelling • Focal trophoblastic hyperplasia • Focal cavitation • Stromaltrophoblastic inclusion • Scalloping Fetal or embryonic tissues

  11. Chromosomes: Absent or inactivated ovum nucleus + 3 haploid sperms  triploid in 90% = 69XXX, 69XXY, 69XYY The fetus shows triploidy stigmata: • GR • Multiple congenital anomalies as: Syndactyly - Hydrocephalus

  12. Complete Partial Fetus absent present Karyotype 46XX(90%) 69XXX 46XY (90%) Hydropic swelling diffuse focal Trophoblastic diffuse focal hyperpleasia Scalloping no present Stromal inclusions no present

  13. Complete Partial past now Vaginal bleeding 97% 84% 74% Anemia 50% 5% Excessive uterine size 50% 28% 4% Preeclampsia 50% 1.5% Hyperemesis 27% 8% Hyperthyroidism 7% 0% Trophoblastic embolism 2% 0% Theca lutein cysts 50% HCG > 100,000mIU/mL 6% Clinical picture

  14. Excessive uterine size: = ↑ trophoblastic tissue  ↑ hCG  ↑ preeclampsia  ↑ hyperthyroidism  ↑ hyperemesisgravidarum  ↑ trophoblasticembolization  ↑ theca lutein cyst size

  15. Preeclampsia: Early preeclampsia = hydatidiform mole Hyperthyroidism: Due to ↑ free T3, T4 C/P: • tachycardia • warm skin • tremor

  16. Thyroid storms: Give β–blockers before anesthesia to avoid thyroid storms C/P: ↑ pulse, ↑ temp, ↑ COP + delirium + convulsions may  HF

  17. Trophoblasticembolization: C/P: • dyspnea • cough • tachypnea • ↑ P • chest pain • asymptomatic

  18. Chest examination diffuse rales Chest X ray bilateral infiltrates Causes of respiratory distress: • Trophoblastionembolization • Complications of: • preeclampsia • thyroid storm • excessive fluid intake

  19. Theca lutein ovarian cysts • Due to ovarian overstimulation by ↑ hCG • May not be felt with oversized uterus • May  pressure symptoms  treated by decompression by laparoscopic or U/Sguided aspiration • If ruptured or torsion occur acute pain  laparoscope

  20. Complete mole • Invasive = 15% • Metastatic = 4% Risk factors: • hCG > 100,000 mIU/mL • Excessive uterine size • Theca lutein cysts = 6 cm Natural history

  21. Low risk = 60%  3.4% persistent mole 0.6% metastatic High risk = 40%  31% persistent mole 9% metastatic Age: > 40 years = 37% > 50 years = 56%

  22. Complete mole U/S  vesicular pattern Partial mole U/S  focal cystic spaces in placenta + ↑ transverse diameter of GS Both together  90% +ve predictive value diagnosis

  23. I – Hystrectomy + aspiration of CL cyst + follow up as usual 2 - Suction evacuation Preferred ttt for hydatidiform mole Give oxytocine before anesthesia Use 12 canula If > 14 weeks support the fundus + do fundal massage treatment

  24. Dilatation  ↑ bleeding Suction evacuation  ↓ bleeding If RH –ve  give Anti RH Ig 3 - Prophylactic chemotherapy ↓ invasive mole to 4% after 1stcourse ↓ “””””””””””””””””” 0% after 2nd course Controversial : Why to expose all patients to chemotherapy while only 20% will need it?

  25. Useful if follow up is: Unreliable Unavailable Study: Prophylactic chemotherapy in high risk patients ↓ persistent mole from 47% to 14%

  26. 1 - HCG Average time needed to return to normal values = 9 weeks Measure hCG/week  3 consecutive normal results /month  6 consecutive normal R 2 - Contraception: OCCP or barrier methods IUD is C/I  perforation Follow up

  27. Persistent gestational trophoblastictumor

  28. Nonmetastatic disease • Placental-site TT • Metastatic D • Staging • Prognostic scoring systems • Diagnostic evaluation • Management

  29. Invasive mole = 15% after evacuation C/P: • Irregular vaginal bleeding • Uterine subinvolution • Theca lutein cysts • ↑hCG • Perforation of myometrium internal Hg • Perforation of uterine vessels  vaginal Hg • Infection  acute pain purulent discharge Nonmetastatic disease

  30. Histology: • After molar pregnancy  hydatidiform mole or choriocarcinoma • After nonmolar pregnancy  choriocarcinoma = sheets of anaplastic cytotrophoblast and syncytiotrophoblast + no villi

  31. Uncommon Variant of choriocarcinoma Consists of intermediate trophoblast Produce small amounts of hCG & hPL Tends to be confined to the uterus Metastasize late Resistant to chemotherapy Placental-site tt

  32. = 4% after molar pregnancy More often after nonmolar pregnancy Usually associated with choriocarcinoma Highly vascular  spontaneous bleeding Early vascular spreading Sites: Pulmonary 80% Hepatic 10% Vaginal 30% Brain 10% Pelvic 20% Metastatic disease

  33. 1 – Pulmonary metastases: Symptoms: dyspnea cough hemoptysis chest pain asymptomatic May be acute of chronic

  34. Chest X ray: • Snowstorm pattern • Discrete rounded densities • Pleural effusion • Pulmonary artery embolism May be misdiagnosed as 1ry pulmonary disease and only recognized as GTD after thoracotomy

  35. Pulmonary embolism may  pulmonary HTN Early RF + intubation = bad prognosis 2 – Vaginal metastasis highly vascular biopsy may  excessive bleeding Symptoms: Vaginal bleeding Purulent discharge Site: fornices/suburethral

  36. 3 – Hepatic metastasis Usually in advanced cases Symptoms: Epigastric or upper RT ¼ pain due to stretching subcapsular hematoma Rupture  internal Hg 4 – Brain metastasis Usually in advanced cases Spontaneous bleeding  acute focal neurological defects

  37. Stage I confined to uterus Stage II confined to genital structures Stage III pulmonary metastasis Stage IV other metastasis At any stage: A= no risk factors B= 1 risk factor C= 2 risk factors staging

  38. 0 1 2 4 Age ≤39 >39 Pregnancy mole abortion term Duration <4m 4-6 7-12 >12 hCG <1000 <10000 <100000 > Largest size <3cm 3-5 >5 Site of met 0 kidney/spleen GIT/liver brain Number <3 1-3 4-8 >8 ABO group 0 A/O B/AB Chemotherapy 1 ≥2 Prognostic scoring systems

  39. H/O • Examination • hCG • Liver function tests • Kidney function tests • Thyroid function tests • WBCs • Platelet count Diagnostic evaluation

  40. Chest  X-ray -- CT Abd & pelvis  U/S -- CT Brain  MRI -- CT If no pulmonary or vaginal metastasis  metastasis are rare Chest CT  for micrometastasis Liver CT  for abnormal LFTs Brain CT  for asymptomatic lesions imaging

  41. If brain CT is normalmeasure CSF hCG If serum hCG/CSF hCG = < 60% then there is brain metastasis Pelvic U/S for: • Extent of uterine lesion • Localization of resistant lesions • Identifying patients who will benefit from hystrectomy

  42. Stage I • Stage II & III • Stage IV management

  43. If the patient does not wish to preserve fertility  Hystrectomy + Chemotherapy to: • ↓ dissemination of GTD • Treat dissemination of GTD • Treat occult metastasis • ↓ bleeding • ↓ sepsis Stage I

  44. If the patient wish to preserve fertility: Low risk  Single agent High risk  Combined chemotherapy Resistant  Local uterine resection after localization of resistant sites by U/S, MRI, or arteriography

  45. Placental site GTD: - Only curative ttt for nonmetastatic cases is hystrectomy - Resistant to chemotherapy  few metastatic cases reported complete remission after chemotherapy

  46. Pulmonary metastasis Low risk  single agent  82% CR High risk  combined chemotherapy Resistant  thoracotomy after localization of and exclusion of other resistant sites Stage ii & iii

  47. Vaginal metastasis Low risk  single agent  84% CR High risk  combined chemotherapy Resistant  wide local excision Vaginal bleeding: • Packing of the vagina • Wide local excision • Embolization of hypogastric arteries

  48. Hystrectomy - In metastatic disease  - to control Hg - to control sepsis - In extensive uterine disease  - to ↓ GTT burden - to ↓ chemotherapy courses

  49. Follow up of stage I, II, III: hCG/week  3 consecutive normal results hCG/month  12 consecutive normal results + effective contraception

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