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low dose Aspirin in obstetrics

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low dose Aspirin
in obstetrics

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low dose Aspirin in obstetrics

  1. 1. low dose Aspirin in obstetrics Aboubakr Elnashar Benha University Hospital, Egypt Aboubakr Elnashar
  2. 2. Contents I. SAFETY II. Mechanism of action III.USES: 1.Prevention of 1.PET 2. IUGR 3.PTL 4.hypertension in multiple pregnancy 5.repeated miscarriage 6.DVT 2.Treatment of antiphysolipid syndrome Aboubakr Elnashar
  3. 3. I. SAFETY Fetal and neonatal complications stillbirths, neonatal death, birth defects: Similar (Ahren et al, 2016). No increased risk of hemorrhage either before or after delivery (HR: .57, 95% CI: .25-1.33; p = .194). (Ayal et al, 2013) Aboubakr Elnashar
  4. 4. SCH LDA: 40.2% Control: 10.9% LDA may be associated with an increased risk of developing a SCH during the first trimester. (Truong et al, 2016) Vaginal bleeding: LDA: 22% Control: 17%, P=0.02 (Ahren et al, 2016). Aboubakr Elnashar
  5. 5. Placental abruption LDA increases the incidence of placental abruption (OR, 1.35; 95% CI, 1.05-1.73) not other major complications LDA is effective in preventing: PET PTL IUGR in high-risk pregnancies without posing a major safety risk to mothers or fetuses. (XU et al, 2015) Aboubakr Elnashar
  6. 6. No adverse effects on infants Decrease behavioral difficulties (Vinod et al, 2009) Aboubakr Elnashar
  7. 7. Aboubakr Elnashar
  8. 8. II. MECHANISM OF ACTION diminishes platelet thromboxane A2 synthesis maintaining vascular wall prostacyclin synthesis: altering the balance in favor of prostacyclin Aboubakr Elnashar
  9. 9. Aboubakr Elnashar
  10. 10. III. USES 1. Prevention of PET Rationale PE: increased platelet turnover increased platelet derived thromboxane levels LDA: diminishes platelet thromboxane A2 synthesis while maintaining vascular wall prostacyclin synthesis: altering the balance in favor of prostacyclin Aboubakr Elnashar
  11. 11. I. Studies on moderate and high risk women low dose aspirin: effective modest reduction in risk of PE (0-3% in treated vs 12-35% in controls) other adverse pregnancy outcome: PTL, IUGR (by 10-20%). [Dekker et al, 2001].level 2 evidence (Cochrane SR, 2007 ) Aboubakr Elnashar
  12. 12.  When to start? ≤16 w, at 12 w significant reduction in: PE (RR 0.47, 95% CI 0.360.62; 7.6 vs 17.9%)  severe PE (RR 0.18, 95% CI 0.080.41; 1.5 vs 12.3%) IUGR (RR 0.46; 8.0 vs 17.6%) PTL (RR 0.35, 95% CI 0.220.57; 4.8 vs 13.4%) [Roberge et al, 2013; Meher et al, 2013; XU et al, 2015; Roberge et al, 2016} Aboubakr Elnashar
  13. 13. Dose: 75-80 mg seems to be the right dosage for about two thirds of the women [Rey et al, 2011] 1/3: need higher dosages up to 160 mg Aspirin resistance test: woman is resistant to 75-80 mg: increase the dose. (Bujold, 2013) 100 mg/d should be the minimum dose for prevention of complications in pregnancy (Ayal et al, 2013) Aboubakr Elnashar
  14. 14. Aspirin non-responsiveness= Aspirin resistance= Aspirin treatment failure Significant proportion of aspirin-treated individuals exhibit suboptimal platelet response inability of aspirin to reduce platelet production of thromboxane A2 and thereby platelet activation and aggregation. Determination: Measurements of whole blood TXA2 formation urinary excretion of TXA2 metabolites Aboubakr Elnashar
  15. 15. Causes inadequate dose drug interactions genetic polymorphisms of COX-1 and other genes involved in thromboxane biosynthesis upregulation of non-platelet sources of thromboxane biosynthesis increased platelet turnover. can be overcome by treating the cause or causes  minimising thromboxane production and activity blocking other pathways of platelet activation. Aboubakr Elnashar
  16. 16.  At bed time:  Not upon awakening  significantly regulates ambulatory BP  reduces the incidence of  Preeclampsia  gestational hypertension  preterm delivery, and  IUGR. (Ayal et al, 2013) Aboubakr Elnashar
  17. 17. II. Unselected nulliparous women little or no benefit [Sibai et al, 1993] no effect on incidence of FGR, or length of gestation [Subtil et al, 2003]. 1. Although nulliparity is a risk factor for PE, prevalence rates are relatively low (4%) compared with moderate to high risk groups (8-30%) [Henderson et al, 2014]. 2. Pathogenesis of PE in nulliparous is different from that in women with previous PE or preexisting vascular disease [Sibai et al, 2005]. Aboubakr Elnashar
  18. 18. III. Studies on women with abnormal uterine artery Doppler (UAD) Abnormal UAD: identified women who are likely to develop PE and IUGR [Subtil et al, 2003]. PE: 6 vs 1% IUGR: 18 vs 8% LDA of abnormal UAD: Did not reduce the incidence of PE PE occurred in 2% of patients in each group. Did not reduce the incidence of IUGR. Aboubakr Elnashar
  19. 19. Guidelines ACOG, 2013 LDA: not recommended for women at low risk for PE. Recommend in high risk women: women with history of : early onset PE superimposed PE plus delivery at <34 w or PE in >1 pregnancy. Aboubakr Elnashar
  20. 20. NICE, 2010 low dose (75 mg) aspirin for  1 high risk factor for PE chronic hypertension kidney disease diabetes autoimmune disease hypertension in previous pregnancy OR 2 moderate risk factors for PE age ≥40 y first pregnancy multiple gestation >10 y between pregnancies, BMI≥35 kg/m at presentation family history of PE Aboubakr Elnashar
  21. 21. US Preventive Services Task Force (USPSTF) 2014 LDA: ≥1 high risk factors absolute risk for PE ≥ 8%. {No validated methods (biomarkers, clinical diagnostic tests, medical history) for identifying women at high risk for PE} 81 mg/d at 12 w Discontinue 5 to 10 days before expected delivery {diminish the risk of bleeding during delivery} [Hirsh et al, 2008} Aboubakr Elnashar
  22. 22. 2. Prevention of IUGR LDA: effective in preventing SGA birth in women at high risk of PET although the effect size is small (RR 0.51, 95% CI 0.28–0.92) number needed to treat = 10 (95%CI 5–50). should be commenced at, or before, 16 w of pregnancy. (NICE, 2011) It is not possible to determine to what extent the effect of LDA is due to the reduction of pre- eclampsia in these women. Aboubakr Elnashar
  23. 23. LDA: Started early pregnancy reduces the risk of placenta-mediated complications such as IUGR and perinatal death after 20 ws: not effective in reducing the risk of a SGA infant. Efficacy has been demonstrated in: abnormal first-trimester uterine artery Doppler Prior history of chronic hypertension or PET (Roberge et al, 2016) Aboubakr Elnashar
  24. 24. 3. Prevention of PTL LDA started early in pregnancy in high-risk women: prevent more than half of PET and IUGR significant decrease of PTL (relative risk 0.22, 95% confidence interval: 0.10-0.49). (Bujol et al, 2011) could become an additional weapon in the prevention of PTL Aboubakr Elnashar
  25. 25. LDA: Started at 15 and 18 w In singleton pregnant women, who had unexplained AFP >2.5 MOM reduces adverse pregnancy outcome delivery before 34 w (Khazardoos et al, RCT, 2014) Preconception LDA: not significantly associated with the overall rate of PTL (Silver et al, 2015) Aboubakr Elnashar
  26. 26. 4. Prevention of adverse pregnancy outcome In multiple pregnancy LDA: 75 mg daily from 12 w until the birth of the babies if they have one or more of the following risk factors for hypertension: 1. first pregnancy 2. age 40 years or older 3. pregnancy interval of more than 10 y 4. BMI of 35 kg/m2 or more at first visit 5. family history of PET. (NICE, 2011) Aboubakr Elnashar
  27. 27. 5. Prevention of RM Preconception initiated LDA: 1-2 previous losses: no significantly associated with live birth or pregnancy loss Single documented loss at less than 20 ws during the previous year: higher live birth rates Not recommended for the prevention of pregnancy loss (Schisterma et al, 2014; Mumfor et al, 2016) Aboubakr Elnashar
  28. 28. Preconception-initiated LDA history of 1-2 pregnancy losses: non significant increase in fecundability of 14% history of only one pregnancy loss of <20 w in the preceding year: significant increase of 28% Preconception-initiated LDA may increase fecundability in certain women with a recent early pregnancy loss (Schisterma et al, 2015) Aboubakr Elnashar
  29. 29. LDA+ LMWH: No reduction in pregnancy loss rate in pregnant women with 2 or more consecutive previous pregnancy losses. (SPIN (Scottish Pregnancy Intervention) multicenter, RCT; Clar et al, 2010) Aboubakr Elnashar
  30. 30. 6. Prevention of thrombosis Not recommended in: Any patient group (American College of Physicians) Obstetric patient: (RCOG, 2015) Postoperative (NICE,2013) Aboubakr Elnashar
  31. 31. 7. Treatment of APAS Improvement of fetal outcomes in APAS LDA in combination with heparin is the first line treatment (MRCOG, 2011) -Success: 70% (Rai et al,1997) -Reduces the miscarriage rate by 54% (Empson et al, Cochrane Database Syst Rev, 2005) Aboubakr Elnashar
  32. 32.  Baseline nonpregnant studies of aPLs:  CBC with platelets  PT, PTT  LA, aCL and aβ2GP LDA: 75-81 mg: initiated before conception discontinued 4 ws before EDD resumed postpartum continued for life unless otherwise contraindicated Aboubakr Elnashar
  33. 33. Thanks Aboubakr Elnashar

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