PRE ECLAMPSIA.pptx

Pre eclampsia management

1. PRE ECLAMPSIA PRESENTED BY : DR. DEEPIKA AGARWAL MODERATOR: DR. MONIKA RAMOLA

2. DEFINITION Hypertension in pregnancy is defined as a systolic blood pressure (bp) >/ 140 mmhg and / or diastolic BP >/90 mmhg . The measurement confirmed bt two or more readings in 4 hours apart.

3. PREVALENCE Hypertension and pre eclampsia contributes 5-10% of pregnancies globally and 7-8% in india . Hypertensive disorders contribute 5% of maternal deaths in india .

4. CLASSIFICATION ACOG CLASSIFICATION OF HYPERTENSION IN PREGNANCY 1. GESTATIONAL HYPERTENSIOM 2. PRE ECLAMPSIA AND ECLAMPSIA 3. CHRONIC HYPERTENSION 4. PRE ECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION

5. GESTATIONAL HYPERTENSION When hypertension ( BP of 140/90 mmhg or more) develops for the first time after 20 weeks gestation, documented on two occasions at least 4 hours apart in previously normotensive woman, and there is no proteinuria, or signs of end organ dysfunction, it is called gestational hypertension. As the disease progresses it may be reclassified into Pre eclampsia , if protienuria or no new signs of end organ damage Chronic hypertension : if hypertension persists 12 weeks after delivery Transient hypertension: if blood pressure is normal by 12 weeks after delivery

6. PRE ECLAMPSIA Pre eclampsia syndrome is a new onset hypertension (>140/90 mmhg ) on 2 occasions, 4 hours apart, that develop after 20 weeks gestation and is associated with Protienuria or Evidence of multiorgan dysfunction with or without protienuria . Protienuria is defined as : A value of >/300 mg or more in 24 hour urine sample or Spot urine protein: creat ratio of >/0.3 or A value of 30 mg/dl protien in a random urine sample or A urine dipstick reading of >/1+ in a single random urine sample if the other quantative methods are not available. A cut off >/2+ is reccomended by acog .

7. PROTIENURIA Protienuria is defined as : A value of >/300 mg or more in 24 hour urine sample or Spot urine protein: Creat ratio of >/0.3 or A value of 30 mg/dl protien in a random urine sample or A urine dipstick reading of >/1+ in a single random urine sample if the other quantative methods are not available. A cut off >/2+ is reccomended by acog .

8. CLASSIFICATION OF PRE ECLAMPSIA SEVERE PRE ECLAMPSIA NON SEVERE ECLAMPSIA

9. NON SEVERE PREECLAMPSIA The BP is >140/90 mmhg but less than <160/110 mmhg . this is confirmed by repeat examination 4 hours apart. Protienuria is usually present. In some women , proteinuria may be absent, but one or more features of end- organ involvement are usually present: Platelet count:<100,000/ cumm Serum creatinine >1.1 mg/dl Liver transaminase twice the upper limit of normal Pulmonary edema Cereberal or visual symptom- headache, blurring of vision,and scotoma

10. SEVERE PREECLAMPSIA It is diagnosed when : 1.The BP >160/110 mmhg 2. There is protienuria and/ or 3. There is evidence of multiorgan involvement The essential difference between non severe and severe pre eclampsia is the blood pressure. Non severe pre eclampsia can progress rapidly to severe pre eclampsia.

11. RISK FACTORS Primiparity Age,18 years Advanced maternal age (>35 years) High body mass index (>30 kg/m2) Multiple pregnancy Hydatidiform mole Maternal medical problems : diabetes, hypertension,renal disease,connective tissue disorder, antiphospholipid syndrome Past or family history of preeclampsia

12. ETIO PATHOGENESIS Complex multifactorial etiology Many theories have been put forward often referred to as a “Disease of Theories” It is a late manifestation of a multifactorial, multisystem disease, initiated very early in pregnancy, suggesting an inadequate maternal response to pregnancy. The most favored recent theory about etiopathogenesis talks about a two-stage theory Stage I –defective Placental invasion of maternal blood vessels in first trimester Stage II- toxic consequences of stage I leading to vascular spasm and endothelial damage

13. Pregnancy Two stage theory

14. Pathogenesis Defective placental invasion leads to an imbalance between angiogenic(PIGF) and anti-angiogenic factors(soluble fts-like tyrosine kinase 1(sFlit-1) + releases of toxic cytokines in circulation Along with immunological, environmental and genetic factors- Leads to vasospasm and endothelial damage in the blood vessels all over the vascular tree Vaso spasm  reduced organ perfusion Endothelial damage  platelet aggregation  thrombocytopenia

15. Pathogenesis of Preeclampsia

16. Organ-specific Complication of PE Brain  reduced perfusion cerebral edema , infracts, Intracranial haemorrhage, CVE, PRES headaches, convulsions(eclampsia), hemiplegia Retina  Hypertensive retinopathy, papilledema, retinal detachment blurring of vision, blindness RETINOPATHY CLASSIFICATION Liver reduced perfusion- hepatocellular damage, subcapsular haemorrhage,  raised hepatic enzymes (transaminases, Alk Po4), epigastric pain, hepatic rupture Kidney—reduced perfusion  glomerular damage(leaky glomeruli) protein excretion hypoproteinaemia , proteinuria ARF, ATN Placenta—reduced perfusion reduced uteroplacental circulation  FGR , oligohydramnios, fetal hypoxia, IUGD, Placental abruption Coagulation system –DIC ,

17. Complications of Pre eclampsia Maternal Complication Eclampsia CVE Retinal detachment Hepatic haemorrhage ARF DIC CCF Pulmonary edema PRES Hypertensive/hypoxic encephalopathy HELLP syndrome—Haemolysis+ elevated live enzymes + low platelet

18. Complications of Preeclampsia Fetal Complication Placental abruption FGR Oligohydramnios IUFD SFD Iatrogenic prematurity

19. Clinical features Primigravida, elderly gravida (>40years) Obese Diabetic H/O PE in a previous pregnancy , F/O HT Symptoms  of headache, blurring of vision epigastric pain Signs  BP > 140/90 –150/100 mm of Hg  Mild PE BP > 160/110mm of Hg  Severe PE Pedal edema , puffy face, pallor, Brisk DTR Abdominal wall edema Obstetric examination ---FGR, reduced liquor

20. Investigations ANC profile, CBC, FBS , Viral markers, HPLC, Thyroid profile Urinary protein estimation Spot—dipstick –qualitative estimation 24-hour urinary protein- quantitative estimation Protein creatinine ratio-Spot quantitative estimation LFT RFT Coagulation profile Fundoscopy USG for fetal gestational age, feat weight, FGR, liquor amount, Doppler for uteroplacental circulation Tests for fetal well-being –NST, Biophysical profile

21. Principles of Management Pre-pregnancy counselling Prevention Early detection Treatment – Aims of treatment- Control of Blood pressure Prevention of complications Monitor fetal growth/well-being Judicious timely delivery

22. Pre-pregnancy counselling Identify High-risk women Normalise BP Treat thyroid disorder Optimize weight Treat anaemia Investigate for CKD Investigate for ALPA syndrome –especially in women with H/O- RPL Early onset, severe PE BOH H/O placental abruption

23. Tests for Early detection of PE Detailed history High free beta HCG in DUAL marker test, high PAPP-A High inhibin A, Activin A in Quadruple test Persistent diastolic notch in uterine artery Doppler after 14 weeks Role over test sFlt-1/ PIGF ratio

24. Prevention Routine supplementation with calcium, magnesium, omega-3 fatty acids, or antioxidant vitamins is ineffective. Calcium+ Vit D reduces the risk of developing preeclampsia Low-dose aspirin 150mg at bedtime is effective for women at increased risk of preeclampsia from 11 weeks to 36weeks Low-dose aspirin is effective for women at highest risk from previous severe preeclampsia, diabetes, chronic hypertension, or renal or autoimmune disease LMWH in women with Biochemically detected APLA syndrome—to be stared in first trimester after appearance of cardiac activity

25. Treatment The ultimate cure is DELIVERY. Assess gestational age Assess cervix Fetal well-being Laboratory assessment Rule out severe disease

26. Treatment mild PE Admission for BP charting, investigation OPD treatment –frequent visits –every visit –measure BP, Weight , Urinary protein assess fetal growth Dietary salt restriction has no effect Bedrest has no effect Start antihypertensive drugs only if BP is persistently at 150/100 Investigate periodically to see the worsening of the disease Fetal monitoring by USG, Doppler, and Biophysical profile Deliver at term Gestational hypertension (HT without proteinuria ) deliver at 38Weeks

27. Severe PE (BP > 160/110) Admission Investigate –CBC, LFT, RFT, Coagulation, urinary proteins, and fundoscopy. USG + Doppler Anti hypertensives MGSO4 for prevention of eclampsia IF > 37 weeks  deliver –IOL If 34-37weeks  Antihypertensive ,MGSO4 + IOL If less than 34 weeks Steroids for fetal lung maturity Monitor FWB by Doppler +USG + NST IOL and delivery

28. Mode of delivery Vaginal delivery is preferred Pt in labour –Augment labour Poor bishop –induce labor Caesarean section For obstetric indication Fetal distress Deranged fetal Doppler Eclampsia –poor bishop score

29. Mild PE Expectant treatment{BP 140/90- 150/100} Maternal monitoring ; Frequent ANC visits Measure BP twice weekly Obtain lab tests weekly: CBC, Platelets, AST, ALT, LDH , uric acid , creatinine Urinary protein by urine protein creatinine ratio/24-hour urinary protein Fetal monitoring NST Biweekly, AFI weekly or twice weekly Biophysical profile weekly USG for fetal biometry every three weeks

30. Management in Severe PE Admit in LR If gestation 37weeks or more – Investigate, obstetric assessment ‘ Antihypertensives MGSO4 for eclampsia prevention Induce labor ---Deliver 34-37 weeks obstetric assessment Deliver <34 weeks Steroids +IOL after 48hours <32weeks Steroids + MGSO4 for neuroprotection Deliver after 48 hours

31. Severe Preeclampsia Indications for delivery irrespective of gestational age- Uncontrolled HT Development of complication Severe FGR with Doppler changes IUFD

32. Antihypertensive Start antihypertensives if BP is persistently 140/100-150/100mm of Hg Labetalol is the drug of choice Start at 100-200 mg TDS can be increased to 800 mg TDS Very high BP (160/110 mm of Hg) IV labetalol 20mmg IV  40mg IV --80mg IV --80 mg every 10-15 minutes (maximum 220 mg in 24 hours) 20 mg /hr IV infusion BP monitoring every 15-20 minutes Other antihypertensives – Nifedipine, alpha-methyl dopa, hydralazine, Nitro-glycerine (NTG) Avoid ace inhibitors –cause fetal malformations if taken in the first trimester Fetal renal damage in the second, and third trimesters

33. MGSO4 in severe PE Prevention and /or treatment of eclampsia in severe PE or impeding eclampsia Offers Maternal and fetal neuroprotection Acts on neuro-muscular junction Indication Severe PE Impending eclampsia –(severe headache, blurring of vision, epigastric pain , brisk DTR) Eclampsia MHSO4 regimes IV/IM injections Pritchard’s - 14 Dhaka Zuspan

34. Pritchard regime –most commonly used Loading dose : 4gram IV diluted as 20 % solution IV slowly + 10gram IM injection (5 grams in each buttock) Maintenance dose: 5 gram IM every 4 hours in alternate buttocks to be continued for 24 hours after delivery Monitoring : Urine output -30ml/hour Respiratory rate DTR Toxicity Absent DTR Respiratory paralysis—needing Intubation and mechanical ventilation Antidote Calcium gluconate- 10 ml of 10% solution iv slowly over 10 minutes

35. Management in labour Frequent monitoring of BP, Respiration, Pulse Routine monitoring of Progress of labour FHR monitoring by CTG Maintain hydration nutrition Cut short 2 nd stage AMTSL Avoid methyl ergometrine Careful monitoring of 4 th stage of labour

36. Post partum management After delivery continue MGSO4 for 24 hours Continue anti-hypertensive for 1 week Monitor vitals, urine output , look out for complications Counsel for contraception Foll0w-up for chronic HT

37. THANKYOU