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

6. 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

7. 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.

8. 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.

9. CLASSIFICATION OF PRE ECLAMPSIA
• SEVERE PRE ECLAMPSIA
• NON SEVERE ECLAMPSIA

10. 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

11. 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.

12. 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

13. 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

14. Pregnancy Two stage theory

15. 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

16. Pathogenesis of Preeclampsia

17. 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 ,

18. 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

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

20. 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

21. 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

22. 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

23. 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

24. 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

25. 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

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

27. 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

28. 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

29. 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

30. 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

31. 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

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

33. 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

34. 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

35. 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

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

38. 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

39. THANKYOU