1 / 47

Screening for P reeclampsia and IUGR

Screening for P reeclampsia and IUGR . Prof Dr Rıza Madazlı Istanbul University Cerrahpaşa Medical Faculty. Pre-eclampsia. %2-7 M ajor cause of maternal and perinatal mortality and morbidity 50 000 maternal death/year ¼ of obstetric admissions to intensive care units.

ann
Download Presentation

Screening for P reeclampsia and IUGR

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Screening for Preeclampsia and IUGR Prof Dr Rıza Madazlı Istanbul University Cerrahpaşa Medical Faculty

  2. Pre-eclampsia • %2-7 • Major cause of maternal and perinatal mortality and morbidity • 50 000 maternal death/year • ¼ of obstetric admissions to intensive care units

  3. Fairly restricted to humans • Pregnancy specific / PLACENTA • Brain is energetically expensive and requires adeeply invasive placenta / RISKY PROCESS • Cost of Evolution / To be human • Discover secrets of pregnancy

  4. Maternal Syndrome / Endothelial Dysfunction • All clinical manifestations can be explained by endothelial dysfunction

  5. Placentation - Inadequate Trophoblastic Invasion Madazlı et al, BJOG, 2000

  6. ImmuneGeneticTrophoblastic MaladaptationPredisposition Defect Placentation Defect Cytokines Leukocyte Activation Lipid Peroxidation Apoptosis/ Microparticule Compleman Activation Maternal Endothelial Dysfunction Pre-eclampsia

  7. GestationalAge at Presentation

  8. Early and Late PE • Associated with different • Maternal and fetal outcomes • Biochemical markers • Heritability • Clinical features • Predictability • Have different etiologies • Differentforms of the disease

  9. Late Onset PE • (≥34 GW) • Early Onset PE • (<34 GW) • Placental PE • Abnormal UtA Doppler • High FGR • Highfetal andmaternal mortality, morbidity • Maternal PE • NormalUtA Doppler • Low FGR • Perinatal outcome favourable • Exaggerated systemic inflamatory response

  10. Screening Placentation • Disease • 1. Trm • 3. Trm • Prediction • Early diagnosis • Preclinic diagnosis

  11. Prophylactic low-dose aspirin < 16 weeks • reducesthe prevalence by about 50% • reduce the prevalence of preterm PE byabout 90% • no significant effect on the risk of term PE

  12. Screening at 11–13 weeks • define the high-risk group for prophylactic treatment with low-dose aspirin • Screening at 20–24 weeks • improve the prediction provided by the firsttrimesterassessment • closer surveillanceof the maternal and fetal condition • define the best time for delivery

  13. Biochemical markers • products of trophoblast or decidua and reflect the placental dysfunction • inflammatory or metabolic responses of maternal systems to abnormal pregnancy • Maternal Characteristics • BMI • MAP • Uterine Artery Doppler

  14. Maternal Characteristics +LR • Age >40 1.96 • Nulliparous 2.91 • Previous PE 7.19 • Family history of PE 2.90 • Multiple pregnancy 2.83 • APL Syndrome 9.72 • Diabetes 3.56 • Chronic hypertension ↑ • SLE ↑ • DR 30- 45% / FPR 10–25% • Morethan ½ the women develop pre-eclampsia have norisk factors

  15. BodyMass Index (BMI) • BMI ≥25 BMI ≥35 • Sensitivity 47% (33–61) 21% (12–31) • Specificity 73% (64–83) 92% (89–95) • +LR 1.7 (0.3–11.9) 2.7 (1.0–7.3)

  16. Mean arterial pressure (MAP) +LR • MAP>90mm Hg 3.5 • 10% FPR, DR 37.5% MAP • Poon, Hypertension. 2008 • Cnossen, BMJ,2008

  17. Biochemical markers • Endothelial Dysfunction • Fibronectin • PTX3 • Selectin • Oxidative stress markers • Insulin resistance • TNF-α • SHBG • Adiponectin • Leptin • Genomic, Metabolomics • C-free DNA • AngiogenicProteins • PIGF • VEGF • sFLT1 • sENG • Serum Analytes • HCG • PAPP-A • AFP • uE3 • İnhibin • ADAM12 • PP13

  18. AngiogenicProteins (Factors) • Placental growth factor (PlGF) ↓ • Vascular endothelial growth factor (VEGF) ↓ • Solublefms-like tyrosine kinase-1 (sFLT1) ↑ • Soluble endoglin (sENG) ↑ • imbalance in circulating angiogenic factors

  19. sFLT1 • 17 studies • PlGF • 18 studies

  20. sENG - 9 studies • Test accuracy is too poor for accurate identificationin clinical practice • Should not be used alone for the prediction of pre-eclampsia.

  21. PIGF Andraweera et al. VEGF family in adverse pregnancy outcomesHuman Reproduction Update, 18, 436–457, 2012

  22. Downs Screening • HCG ↑ • PAPP-A ↓ • AFP↑ • uE3 ↓ • İnhibin ↑

  23. PAPP-A

  24. Placental protein 13 (PP13) • First trimester PP13 inadequate for screening

  25. Fibronectin

  26. Uterine Artery Doppler Madazlı et al, Placenta, 2003

  27. Second Trimester UtA Doppler • PE • +LR : 7.5 • FGR • overall (+LR: 9.1) • severe (+LR: 14.6)

  28. First Trimester UtA Doppler

  29. Useful for predicting early-onset pre-eclampsia, aswell as other adverse pregnancy outcomes • AbnormalUtA Doppler in low-riskwomen sufficiently high performance to justifyaspirin prophylaxis

  30. C-free DNA

  31. Combination

  32. 11-14 weeks

  33. 1. and 2. Trimester

  34. Screening at 11–13 weeks / Prophylaxis • Combination tests more effective • More effective / Early onset preeclampsia

  35. Screening

  36. Thank you

More Related