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Zareh.F.MD

Zareh.F.MD. Third trimester bleeding. All bleeding during pregnancy should be investigated by examination and imaging studies. 1/4 of women who bleed at 14-26 w had pp or ap.

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Zareh.F.MD

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  1. Zareh.F.MD Third trimester bleeding

  2. All bleeding during pregnancy should be investigated by examination and imaging studies

  3. 1/4 of women who bleed at 14-26 w had pp or ap. • 1/3 of pregnancy with vag bleeding after 26 w had poor outcome. Unexplained vag.bleeding at term must be considered for delivery.

  4. etiologies • Placenta previa • Placenta abruption • Vasa previa • Cervical lesions (carcinoma,polyps) • Vaginal laceration (trauma,carcinoma) • Uterine rupture or dehiscence

  5. Placenta previa

  6. Placenta previaincidece • 0.5-1% of all pregnancies • Fatal 0.03% of cases • Incidence in multipar :1/20 • Incidence in nulipar : 1/1500

  7. difinition • Dillated cervix: complete previa partial previa marginal previa low lying • Closed cervix: complete partial / marginal <1 cm from int.os 1-2 cm from int.os >2 cm from int.os

  8. pathophysiology • Abnormal endometrial tissue less favorable location for implantation: poor vascularization thinner myometrium • Uterine trauma from c/s (6 fold)

  9. Risk factors • Perior c/s • Black , minority • Older women >35 y • High gravidity & parity • Cigarette smoking 2.6-4.4 fold • Previous abortion

  10. diagnosis • Abdominal sonography misdiagnosis : full distended bladder lower ut segment contraction pp in 2nd trimester 90-95% resolved by the 3rd trimester (but no central) • 3 dimensional scanning • transvaginal scan • Transperineal scan • Double set up examination • MSAFP>2 MoM

  11. Clinical features • Asymptomatic • Vaginal bleeding variable intermittent red to brownish maternal origin • thefetus usually not in jeopardy

  12. complication • Hospital stay • c/s • Abruptio placenta • Malpresentation • Post partum hemorrhage • Growth restriction • Placenta accreta pp+previous c/s10-35% +multiple c/s 60-65% • Coagulation defect

  13. Other complications • A.T.N • Sheehan syndrome • Maternal mortality<1% • Perinatal mortality <5%

  14. outcome • IUGR ? • Preterm birth • Congenital anomaly • Respiratory distress syndrome • Anemia • Recurrence rate 2-3%(6-8 fold)

  15. management no bleeding • 2nd trimester intercourse avoid usual activity repeat sonography • 3rd trimester decrease physical activity travel away from home prolonged bed rest

  16. management with Bleeding • Evaluation of the patient • Fetal status • IV fluid • Blood cross match • RHoGam if necessary • Steroid if 24-34 W • Delivery after 34-36W

  17. management Severe hemorrhage • Medical team for immediate delivery • 2 large bore IV line • Blood cross match • Foley catheter • Coagulation panel • Continuous Fetal monitoring • delivery

  18. Placenta abruption

  19. Premature separation of placenta. • 0.5-1% of deliveries • Perinatal mortality is 20-25% • Preterm birth is 40% • Cause of 15% of stillbirth

  20. Definition Preplacentalor subamniotic

  21. retroplacental

  22. Risk factors Socioeconomic: • High parity • low education • infertility

  23. Risk factors Uterine: • ut.malformation • ut.septum • Myoma

  24. Risk factors Medical: • Diabete pregestational • Hypertension _chronic&gestational • PROM with chorioamnionitis

  25. Risk factors Thrombophilias • Antiphospholipid syndrome • Prothrombin 20210A mutation • Hyperhomocysteinemia • Factor V leiden mutation • Activated protein C resistance • Protein C and S deficiency • dysfibrinogenemia

  26. Risk factor iatrogenic • Sudden decompression(amniocentesis) • External cephalic version • Cigarette smoking • Cocaine abuse • Blant trauma • Heavy physical activity

  27. pathophysiology • Blunt trauma : forceful shearing effort • Majority of other case : cell death (apoptosis) induced through ischemia ,hypoxia. • Thrombophilia : thrombose in decidua basalis • Chorioamnionitis: infectious agents (lipopolysacharids & endotoxins) cytokines,superoxide ischemia and hypoixia

  28. Pathophysiologycont. • Nicotine(cigarete) and cocaine vasoconstriction ischemia placental lesions(infarction,oxidative stress,appoptosis and necrosis) • Circumvalateplacenta(chorion leave don’t insert at the edge of placenta) A.P,IUGR,PROM,preterm labor

  29. diagnosis Clinically • vaginal bleeding • Uterine pain • tetanic contraction • fetal heart abnormality sinusoidal pattern

  30. diagnosis Paraclinic • Ultrasound • MRI • Doppler • Biochemical test Unexplained elevated of MSAFP AP>10 fold Preterm labor+AFP>2MoM = AP (67%) Preterm labor+AFP>2MoM+bleeding= AP (100%) HCG Inhibin A Fetal Hb

  31. management • Marginal Abruptio hospitalize a patient with any bleeding after fetal viability • Large retroplacental usually require acute & aggressive management

  32. Large bleeding • Continues fetal monitoring • Foley catheter • Frequent maternal v/s • Steroid therapy (24-34w , membrane intact) • Folic acid 1mg ,vit B12 ,vit B6

  33. discharge • Mild bleeding : 2-5 days without any further bleeding • Large bleeding :decision is difficult with any bleeding ,pain , contraction no discharge

  34. Tocolytic use • Now become acceptable to consider a short course of tocolytictherapy for: stable patient, limited abruptio , establishedfetal well being, preterm G.age

  35. Which tocolytic • B mimetics (terbut,ritod): mask cardiovascular response to volume depletion • Ca channel blockers(nifidipine): reduce BP • Mgso4 : most acceptable agents

  36. delivery Vaginal or c/s Depending on the: Degree of bleeding Presence or absence of: Active labor Fetal distress

  37. complications • c/s 50% of case • Shock • DIC • Renal failure • Couvelaire uterus • Recurrence : 10 fold

  38. Fetal outcome • Mortality: term babies 25 fold • Prematurity: 40%

  39. Thrombophilia defects • Anticardiolipin antibodies • Lupus anticoagulant • Pr c, Pr s and antithrombin 3deficiencies • Factor v leiden “activated pr c resistance” • Metilentetrahydrofulate reductase gene mutation • Prothrombin 20210A gene mutation • Congenital dysfibrinogenemia

  40. Factor V leiden • Activated protein C resistance • Most common genetic factor predisposing to thrombosis • Most common identifiable causes • Substitution of adenine for guanine • “ Amino acid arginine for glutamine • Increased tendency to form clots

  41. hyperhomocysteinemia Methionine metabolise homocysteine damage vascular Remethylate MTHFR endothelium folate vit.B12 , vit. B6 Methionine

  42. Thank you

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