Transcript Hypertensive Disorder of Pregnancy Final [PPT]

HYPERTENSIVE DISORDER OF
PREGNANCY- AN OVER VIEW
Prof. S.P.Jaiswar
Department of Obst. & Gynae.
K.G. Medical University,
Lucknow
INTRODUCTION

Commonest medical disorders
diagnosed by obstetrician
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Spectrum of severity ranges mild to
severe
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There is controversy and lack of
clarity about mild to moderate HDP
INTRODUCTION

Despite of years of research in this
field still there is lack of consensus
about
Definition

Classification
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Level of blood pressure at which
antihypertensive therapy needs to be
started
INTRODUCTION
Responsible for a high proportion of
- hospital admission
- labour inductions
- fetal morbidity and mortality (20-25%)
- major cause - maternal mortality (15-20%)
Incidence:
8-10%
INTRODUCTION
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Hypertension in pregnancy complicates
5% of all pregnancies & 11% of first
pregnancies
Leading cause of Maternal Mortality
Account for 40,000 maternal deaths
annually
In India 30% maternal deaths due to preeclampsia & eclampsia (Chhabra et al)
Measuring Blood Pressure
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At every visit
Woman should be sitting with back & arm
support without crossing legs for 5 min
BP is lowest in lateral recumbent position, & the
BP of the superior arm in this position is 10-12
mm Hg lower than the inferior arm
Remove all tight clothing
Always measure in right arm
Instrument at level of heart
Diastolic BP at Korotkoff V
DEFINITION
According to Working Group (2000) of High
Blood Pressure Education Programme
hypertension is diagnosed when:
Blood pressure >140/90 mm of Hg
- >30 mm of Hg or more in SBP.
- >15 mm of Hg or more in DBP.
This rise of BP is observed at interval of 4-6
hrs.
Classification of Hypertensive
disorder of Pregnancy
Gestational hypertension (PIH and transient HT)
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B.P. > 140/90 mm of Hg for first time during
pregnancy.
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NO proteinuria
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B.P. return to normal <12 wks post-partum.
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Final diagnosis made only in post-partum.
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May be associated with other signs of preeclampsia- headache, epigastric pain,
thrombocytopenia.
Pre-eclampsia
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B.P. > 140/90 mm of Hg. After 20 wks of gestation.
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Proteinuria >300 mg/24 hrs or >1 + dip stick.
Classification of Hypertensive
disorder in Pregnancy (Contd.)
Eclampsia- Convulsion in patients having preeclampsia. It may occur during ante-partum intrapartum, post-partum (upto 10 days).
Pre-eclampsia superimposed on chronic
hypertension- Chronic hypertension or
hypertension with proteinuria after 20 wks gestation
or platelet count <100,000mm3.
Chronic hypertension- B.P. >140/90 mm of Hg
before 20 wks of gestation or persists after 12 wks of
post-partum.
Classification ACOG 2013
Gestational hypertension – evidence for
pre-eclampsia syndrome does not
develop & hypertension resolves 12 wks
postpartum
 Pre-eclampsia & eclampsia syndrome
 Chronic hypertension of any etiology
 Pre-eclampsia superimposed on chronic
hypertension
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Pre-eclampsia
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Hypertension (≥140/90 mmHg) on 2 occasions 4 hours apart
after 20 wks gestation)
+
Proteinuria
− ≥300mg/24 hr or
− Protein ceratinine ratio ≥ 0.3 or
− Dipstick 1+ persistent
OR
Thrombocytopenia – Platelets < 1,00,000/µl
Renal insufficiency – creatinine >1.1 mg% or doubling of
baseline (no prior renal disease)
Liver involvement – Serum transaminase levels (AST or ALT)
twice normal)
Pulmonary edema
Cerebral Symptoms – Headache, Visual, disturbances,
convulsions
Severity of Pre-eclampsia
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ACOG
 Severe
 Non
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Severe
NICE
Mild Hypertension
Moderate Hypertension
Systolic BP Diastolic BP
140-149
90-99
150-159
100-109
Severe Hypertension
≥ 160
≥ 110
Severity of Pre-Eclampsia
Abnormality
Mild
Severe
SBP
<160mm of Hg
>160mm of Hg
Diastolic BP
<100 mm of Hg
>110 mm of Hg (BP > 160/110
Proteinuria
<2+
Persistent (>3+)
Headache
Absent
Present
Visual disturbances
Absent
Present
Upper abdominal pain
Absent
Present
Oliguria
Absent
Present
Convulsion
Absent
Present (Eclampsia)
Serum creatinine
Normal
Elevated (>1.2 mg/dl)
Thrombocytopenia
Absent
Present (<100,000/mm3)
Liver enzyme elevation
Minimal
Marked ( LDH, ALT or AST)
Fetal growth restriction
Absent
Obvious
Pulmonary edema
Absent
Present
ACOG Criteria (2013)
Abnormality
Non-severe
Severe
Diastolic BP
< 110mmhg
≥ 110mmHg
Systolic BP
< 160mmhg
≥ 160mmHg
Proteinuria
None to positive
None to positive
Headache
Absent
Present
Visual Disturbance
Absent
Present
Upper Abdominal Pain
Absent
Present
Oliguria
Absent
Present
Convulsion (eclampsia)
Absent
Present
Serum creatinine
Normal
Elevated
Thrombocytopenia
(<100,000/µl)
Absent
Present
Serum transminase elevation
Minimal
Marked
Fetal Growth restriction
Not included
Not included
Pulmonary edema
Absent
Present
HIGH RISK GROUP
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Young age < 18 yrs,
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Primi gravida, obese
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Multiple pregnancy, new paternity
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Racial genetic factor
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Poor socioeconomic status
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H/o chronic hypertension, family, past H/O PET
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Maternal age >35 yrs
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Pre-existing vascular disease, DM, APLA, Thrombophilic
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PET may appear before 20 wks in-hydatidform mole
-acute polyhyromnioss
-multiple pregnancy
Preconceptional Risk Factors
Rates of preeclampsia depend on: severity of underlying complications&
combinations of risk factors.
Risk factors
Risk %
Chronic hypertension/renal disease
15-40
Pre gestational DM
10-35
Connective tissue disease (lupus, rheumatoid arthritis)
10-20
Thrombophilia (acquired or congenital)
10-40
Obesity/insulin resistance
10-15
Age older than 40 y
10-20
Limited sperm exposure
10-35
Family history of preeclampsia/ cardiovascular disease
10-15
Woman born as SFGA
1.5 fold
Adverse outcome in a previous pregnancy: IUGR, ab placentae,
IUFD
2-3 fold
Pregnancy-Related Factors
Regular antenatal care is mandatory for the prevention & early
detection of PE.
Risk factors: Magnitude of risk depends on the number of factors
Multifetal gestation
Unexplained FGR
Gestational hypertension
Hydrops/hydropic
degeneration of the
placenta
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Incidence of Pre-eclamsia- 5-15%
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Primi-gravida- 3-10%
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Multi-gravida- 5%
PATHOPHYSIOLOGY OF PRE-ECLAMSIA
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The exact pathophysiology is not clear.
Pre-eclampsia is a disorder of endothelial
function with vasospasm.
Histopathology of placenta shows Diffuse placental thrombosis
 Inflammatory placental decidual
vasculopathy
 Abnormal trophoblastic invasion of end
arteries.
Altered maternal immune response to fetal/
placental tissue.
Pathogenesis:
•unknown (Barton& Sibai, 2008).
Impaired trophoblast differentiation&
invasion
Placental & endothelial dysfunction
Immune maladaptation to paternal ages.
Exaggerated systemic inflammatory
response.
In PE:
Impaired trophoblast differentiation &
invasion
PATHOPHYSIOLOGY OF PREECLAMSIA
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Increase vascular sensitivity to angiotensin II.
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Imbalance between prostacyclin and
thromboxane A2
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Increase oxygen free radicals
Abnormal calcium metabolism
Vit E, C, Antioxidant and micronutrient
deficiency
Genetic predisposition
Inhibition of Nitric Oxide synthesis- increases main
arterial pressure
PATHOGENESIS OF PRE-ECLAMPSIA
Pathological deterioration of function in a number of
organs and systems presumably as a consequences of
vasospasm and ischemia has been identified.
Changes in Mother
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Vasospasm  Resistance to blood flow  arterial
hypertension.
Release of Angiotensin II  endothelial cell to contract
endothelial cell damage  interendothelial cell leaks 
subendothelial deposition of platelets and fibrinogen.
Vascular changes  local hypoxia  hemorrhage and
necrosis of tissue  end organ disturbances in mother.
Fetus
Reduced uteroplacental perfusion  fetal compromise 
growth retardation, oligohydromnios, IUD
Placenta : Placental infarction, calcification, abruptio placentae
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PATHOLOGICAL CHANGES
Cardiovascular System
Increased cardiac after load caused byHypertenison,
endothelial injury,
extravasation- especially in lungs (pulm edema)
Haemodynamic Changes
Marked reduction in cardiac output
Increased peripheral resistance
Blood Volume
Haemoconcentration
Increased vascular permeability
Patients is sensitive to vigorous fluid therapy,
even sensitive to blood loss at delivery.
PATHOLOGICAL CHANGES
Haematological Changes
Thrombocytopenia- Platelets count
<100,000/l, delivery is indicated because
platelet count continues to decrease
HELLP Syndrome- Haemolysis, Elevated
Liver enzyme, Low Platelets count.
Coagulation failure occurs when
associated consumptive coagulopathy like
Placental abruption, profound
haemorrhage.
Haemoconcentration
PATHOLOGICAL CHANGES
Kidney
Decrease glomerular filtration
Decrease renal perfusion
Increase plasma uric acid concentration
Increased plasma creatinine level (>0.5 mg/dl)
Proteinuria >300 mgdl/24 hrs of + 1.
Renal failure- tubular necrosis- oliguria, anuria
Liver
Alteration in hepatic function test
Periportal haemorrhagic necrosis in periphery of liver lobuleIncreased serum liver enzyme
Hepatic rupture
Sub-capsular haemorrhage- abdominal pain and hepatic
haemorrhage.
HELLP syndrome
HELLP syndrome- characterized by
H- haemolysis
EL- elevated liver enzyme
LP- low platelet count
It occurs in 20% of women with sever PET
associated with placental abruption,
renal failure, sub capsular hematoma
Increase fetal and maternal mortality.
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PATHOLOGICAL CHANGES
Brain- Hypertension is responsible for
Oedema
Hyperemia
Visual disturbances
Thrombosis
Convulsions
Haemorrhage
Confusion and coma
Eye- Retinal haemorrhage, papilioedema
Retinal detachment- retinal ischemia and infarction
Visual loss- cortical blindness
Prognosis is good, changes usually return to normal
within a week.
PREDICTION OF PRE-ECLAMPSIA
Prediction of pre-eclampsia depends on variety of
biochemical and biophysical markers based on rationale
implicated in the pathology and pathophysiology of
hypertensive disorder.
Role over test- 28-32 wks lateral to supine DBP >20mmHg.
Angiotensin II infusion Test- 28-32 wks rise of 20 mm of Hg,
DBP with < 8 ng/kg/min
Mean arterial Pressure- >90 mm of Hg in 2nd trimester
Doppler ultrasound- Persistent of diastolic notch at 18-24 wks.
None of the prediction test has been found to be very useful.
Uterine artery doppler
velocimetry
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Increased impedance to flow in the uterine arteries as
indicated by:
Diastolic Notch in uterine artery waveform
Increase in uterine artery pulsatility index .
is associated with increased risk of preeclampsia.
UTERINE ARTERY DOPPLER
VELOCIMETRY
Development of preeclampsia overall was
associated with increased PI, but not the
presence of notch before 21 weeks of
gestation
 The sensitivity was 43% and specificity
67% .
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(ACOG 2012).
FETOPLACENTAL UNIT
DYSFUNCTION
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Human chorionic gonadotrophin
Alphafetoprotein
Estriol
Inhibin A
Pregnancy associated plasma protein A
Activin A
Corticotrophin release hormone
PREVENTION
As exact etiology is not known, it can not be prevented,
only severity of the condition can be prevented by regular
ante-natal check-up (BP, urine albumin.).
No drug prevents pre-eclampsia as it has no definite
cause of its origin.
But following drugs may prevent severity of disease.
High dose calcium
2gm/day
Decrease intracellular ion
Smooth muscle relaxant
Decrease responsiveness to pressure stimuli
Low dose aspirin
-
50-100mg/day
Prevents platelets aggregation
Decrease thromboxane A2 synthesis
Fish oil
-
4-9 cap./day
Antioxidants
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Vit. C, E reduce
oxidative stress
MANAGEMENT
Basic aim of management
Termination of pregnancy at appropriate time only
curative treatment.
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Birth of alive and healthy baby.
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Complete restoration of health of mother.
Investigations
Antenatal Investigation
Specific Investigation
•Hb
•Complete Haemogram
•ABO RH
•General blood picture
•Urine Routine Microscopy
•Pletelet Count
•Screening blood sugar
•24 hrs urinary protein
•VDRL
•Liver function test
•HbsAg
•Kidney function test
•HIV
•Serum Uric Acid
•Coagulation profile
•Fundus Examination
•Doppler USG
•Obst USG
Biochemical Parameters-Value in pregnancy
and Preeclampsia
Investigation
Normal pregnancy
Severe Preeclampsia
S. Bilirubin
< 1 mg/dl
>1.2 mg/ dl
SGPT
5-40 U/L
>70 IU/L
SGOT
5-40 U/L
>70 IU/ L
Alkaline phosphatase
100-280 U/L
>300 U/ L
LDH
135-225 IU/L
> 600 IU/ L
B. Ureas
15 mg/dl
>20-25 mg/dl
S. Creatinine
0-8 mg/dl
>1 mg/ dl
Biochemical Parameters-Value in pregnancy and
Preeclampsia contd..
S. Uric acid
2-5 mg/ dl
>6 mg/ dl
General blood picture
Normocytic,
Normochromic
Haemolytic cells- burr
cells, schistocytes
Platelet count
>200000
<100000
24 hrs urinary protein
<300 mg
>500 mg
Fundus examination
Normal
Constriction of the
arterioles, increase in vein
to artery ratio, segmental
vasospasm retinal
MANAGEMENT
For early detection
Increase antenatal visit especially 3rd trimester
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Blood pressure >140/90 mm of Hg- to be admitted
to the hospital for evaluation of severity.
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Mild disease may often manage as out patient.
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Hospitalizationhypertension,
proteinuria
Persistent or worsening of
Patient develops
MANAGEMENT
In Hospital
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For systemic evaluation detailed history of
headache, visual disturbance, epigastric pain,
rapid weight gain.
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Daily weight recording
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Urine for protein- every 2nd day
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Blood pressure recording 4 hrly in sitting position
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Estimation of S. creatinine, hematocrit, platelets
count, S. liver enzyme
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Evaluation of fetal size, ammniotic fluid- clinically,
USG.
MANAGEMENT
Care to be taken
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Reduced activity is beneficial
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Absolute bed rest is not necessary
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Adequate protein and calories should be given
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Sodium and fluid intake should be adequate
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Do not give diuretics to correct oliguria or anuria
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Do not give diazepam to stop convulsion- apnea,
aspiration
Maternal Surveillance in mild Preeclampsia
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Measure BP-4 times per day
Measure body weight- weekly
Daily urine dipstick evaluation of protein in urine
Proteinuria in a 24 hr specimen every week
CBC with platelet count, LDH, AST, ALT twice per
week
Inquire in each contact about fetal movements,
development of scotoma, headache, epigastric pain.
Maternal Surveillance in sever Preeclampsia
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Measure BP 4 times per day
Measure body weight every day
Daily input and output
Daily urine dipstick evaluation of urine protein
Proteinuria in 12 hr specimen
CBC with platelet count, LDH, AST, ALT, KFT every
other day or more frequent
Inquire in each contact about fetal movements,
development of scotoma, headache, epigastric pain.
Fetal Surveillance in mild Preeclampsia
Daily fetal heart rate monitoring
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Daily fetal movement count
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Modified biophysical profile every week
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Fetal biometry every 3 weeks
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Umbilical and cerebral doppler every week
Fetal surveillance
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Baseline USG for AFI, fetal weight, Doppler
DFMC
Weekly NST
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NICE guidelines recommend 2 weekly
Doppler for mild PE
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No large prospective studies comparing
frequency of monitoring
Fetal Surveillance in sever PreeclampsiaDaily fetal heart rate monitoring
 Daily fetal movement count
 Daily NST
 Amniotic fluid volume twice every week
 Fetal biometry every 2 weeks
 Umbilical and cerebral doppler twice every week
Initial Recommended Management of Severe
PET
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Immediate hospitalization
Detailed history taken to assess severity – Headache,
visual disturbance, epigastric pain, rapid weight gain,
bleeding P/V or labor
Detailed examination done for – edema, brisk reflexes &
clonus, Chest auscultation for basal crepts, fetal growth &
well being
IV magnesium sulfate started to prevent convulsions
Anti hypertensive medication administered to lower BP (
iv Labetalol plus oral nifedipine)
Aim is to keep systolic BP between 140-155 /150 and
diastolic BP between 90-105/100 mm Hg
Corticosteroids given between 26-34 weeks gestation
Indications for Delivery in PreeclampsiaMaternal indications• BP persistently 160/100 or greater despite treatment
• Platelet count 50,000/ cubic mm
• Urine output <400 ml in 24 hrs
• Progressive deterioration in liver function
• Progressive deterioration in renal function
• Suspected abruptio placentae
• Persistent severe headaches, or visual changes
• Persistent severe epigastric pain, nausea or vomiting
Fetal indication
Severe growth restriction
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Nonreassuring fetal cardiotocography
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Oligohydramnios
There is general agreement that all such
patients should be delivered if the disease
develops after 34 weeks gestation
There is disagreement about
management of patients with
severe PET before 34 weeks
gestation
Prompt delivery is
indicated
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Imminent eclampsia
Multi-organ dysfunction
Severe IUGR < 5th
percentile
Suspected abruption
placentae
Non reassuring fetal
testing
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Some consider delivery as
the definite treatment
regardless of gestational
age
Others recommend
prolonging pregnancy for
fetal lung maturity till 34
weeks
Although delivery is beneficial to mother , it
must be weighed against the risk for
prematurity
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It was believed that
premature infants of
severe PET have
accelerated lung and
neurological maturation as
a result of stress in utero
Had lower rates of
morbidity and mortality
with similar gestation age
of normal infants
This has been
revealed wrong
 They have higher
rates of admission
in neonatal
intensive care unit
Sibai 2007
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Timing and mode of Delivery
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Continue pregnancy till 37weeks
Expectant management vs Induction of
labor (Hypitat trial 2010)
Reduced rates of severe HT (induction
group).
No difference in CS delivery and neonatal
outcome.
Induction prevents complications however
little they are
MANAGEMENT
Control of blood pressure
Anti-hypertensive drug therapy
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To prolong pregnancy to get better fetal outcome
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To reduce blood pressure in severe hypertension.
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Sudden fall in blood pressure must be avoided.
Drugs
Methyl dopa- 250 mg 8 hrly – 2 gm/day orally
Hydralazine- 5 mg I.V. stat. 5 mg ½ hrly.
Nifedipine- 10 mg 6 hrly – 20 mg/4 hrly orally
Labetalol- 250 mg – 8 hrly or 6 hrly. orally
ACE inhibitor are contraindicated during pregnancy.
Antihypertensives safe in pregnancy
Drug
Starting dose
Maximum dose
Methyldopa
250 mg TDS/QID
4 g / day
Labetalol
100 mg BD
2400 mg/ day
Nifedipine
10 mg BD
120 mg / day
Thiazide diuretic 12.5 mg BD
50 mg/day
Antihypertensives for
Hypertensive emergency
Drug
Starting dose
Maximum Contraindications
dose
Labetalol
20 mg IV every
15min
Dose doubled to 4080 mg according to
effect
220 mg
Hydralazin
e
5-10 mg every 20 min 20 mg
Tachycardia, persistent
headache
Nifedipine
10-20 mg every 30
min
Tachycardia,
palpitations & headache
50 mg
Asthma, CHF, cardiac
conduction abnormality
MANAGEMENT
Prevention of convulsion
Anti-convulsant drug therapy- in severe preeclampsia to prevent convulsion
Magnesium Sulphate
 Loading Total dose 4+10= 14 gm
4 gm (20 ml of 20% solu.) I.V. within 3-5 mins.
5 gm (10 ml of 50% solu.) deep I.M. in each buttock
with 1 ml of 1% of xylocain
If recurrent fits after 30 min of loading dose- repeat 2 gm
20% (4 ml drug with 6 ml NS) slow in 5 min.
Prevention of convulsion
Maintenance dose5 gm deep IM (50%) alternate buttocks after
monitoring every 4 hrs.
Monitoring of toxicity
Presence of patellar reflex- > 10meq/lit, disappear
 Respiratory rate> 16 min- > 12 meq/lit- respiratory
paralysis
 Urine output>30 ml/hr in last 4 hrs
Continue till 24 hrs after last fit/ delivery which ever is
later
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Management of Magsulf toxicity
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If patellar jerk is absent or urine output < 30 ml/hrstop magsulf and monitor hourly- restart maintenance
dose if criteria is fulfilled.
RR<16 / min- with hold magsulf.
Give antidote- Calcium gluconate 1 gm IV 10 ml of 10%
solution in 10 min
Mechanical ventilation if respiratory paralysis(>15
meq/lit)
Convulsion prevents- when magnesium level
maintained at 4 to 7 meq/lit
Diuretics in Pregnancy
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Use throughout pregnancy controversial
Commonly prescribed to women with
Essential hypertension prior to pregnancy
Here diuretics may be continued alone or in
combination with other Antihypertensives in
pregnancy because increase in plasma
volume during pregnancy lesser than normal
but not associated with adverse fetal
outcome
Discontinue in case of superimposed preeclampsia or
IUGR
MANAGEMENT
Obstetrical management
Termination of Pregnancy
Indications
 Patient develops signs of imminent eclampsia
 Severe pre-eclampsia does not respond to
conservative treatment.
 Eclampsia
Method of Termination
 Induction of labour at term if favorable cervix.
 LSCS in unfavorable cervix or other indication.
Obstetrical management> 37 weeks Termination of pregnancy.
 Induction of labour as per the bishop score.
> 34-< 37 weeksTreatment should be individualized BP controlled- explain maternal and fetal adverse effect to
relatives.
 Regular fetal and maternal surveillance.
 Terminate at 37 weeks.
 BP uncontrolled, worsening clinical and biochemical
parameters- terminate the pregnancy.
Obstetrical management>24- <34 weeks
 corticosteroid coverage
 BP controlled- continue maternal and fetal surveillanceterminate at 37 weeks.
 BP uncontrolled, worsening clinical and biochemical
parameters- terminate the pregnancy.
< 24 weeks Fetal salvage difficult- terminate the pregnancy.
MANAGEMENT
During Labour

Careful BP monitoring
Close watch on fetal heart sound
Early ARM to accelerate the labour
Analgesia – epidural
Early intervention in IInd stage- forceps, ventouse
Inj. Oxitocin 10 IU Im. with delivery of baby as active
management of 3rd stage of labour prevent PPH.
Watch for PPH- patient does not tolerate slight blood loss.

Methyl ergometrine is not to be given
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Decision to perform cesarean section is
based on
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Gestational age, FHR tracing, Doppler studies, AFI, fetal
presentation
Condition of cervix (Bishops score)
Maternal condition specially uncontrolled BP and developing
complications
In general the presence of severe PET is not an indication for
cesarean delivery and decision has to be individualized
In severe PET for LSCS, GA carries a risk for aspiration and failed
intubation owing to airway edema and is associated with marked
increase in cerebral pressure during intubation & extubation
These patients may need intubation under fiberoptic observation
with the availability of immediate tracheostomy
Regional anesthesia is contraindicated in presence of coagulopathy
or severe thrombocytopenia
MANAGEMENT
Post-natal Period
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Dose of antihypertensive is usually reduced

Methyl dopa is discontinued- causes post-partum
depression
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ACE inhibitor may be started- if required

Patient must be counseled for recurrence in future
pregnancy or develop hypertension in later life.
Antihypertensives in Postpartum
period
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Should be started if SP > 150 mm Hg & DP > 100 mm
Hg
Discontinued if BP remains below hypertensive level
for atleast 48 hours
Causes of exacerbation of Hypertension in Postpartum
period:
- IV fluids given in labour
- IV Oxytocin in labour
- Mobilization of extracellular fluid to intravascular
compartment
Antihypertensives in Postpartum
period & Breast feeding
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All antihypertensives are found in breast milk but
plasma: milk ratio of drugs is different

Long term effects of these drugs on
breastfeeding infants not studied
Choice of Antihypertensives in
Postpartum period
•Labetalol & Nifedipine drug of choice
•Labetalol/ Hydralazine (IV)- in Hypertensive
emergency
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Diuretics- only indicated in Pulmonary edema,
decrease milk production
ACE inhibitors - adverse effect on neonatal renal
function
Methyldopa- Postpartum depression
Amlodipine- also a calcium channel blocker but
not used due to limited studies in literature
supporting use
Eclampsia
Dr. S.P. Jaiswar
Professor
Dept. of Obst. & Gynae
KGMU Lucknow
Introduction

Convulsive state of pre-eclampsia is
called eclampsia.

Pre-eclampsia is complicated by
generalized tonic and clonic convulsions
and coma .
Incidence
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1 in 500 to 1 in 30
More common in primi-gravida
Five time more common in twins
50% occur in late pregnancy
According to time of onset of convulsions  Ante- partum- 50%
 Intra- partum- 30%
Intercurrent
 Post- partum- 20%
Cause of Convulsions

Cerebral irritation- due to cerebral hypoxia
- due to spasm of cerebral vessels

Cerebral oedema- perivascular oedema

Cerebral dysarrythmia
- Following anoxia or oedema
Cerebral Pathology
Cortical and sub- cortical oedema

Infarction

Haemorrhage
Hypoxia, ischaemia or oedema
Clinical featuresSometimes patient shows premonitory
symptoms before developing convulsions
Divided into four stages Pre monitory Stage
 Tonic Stage
 Clonic Stage
 Stage of Coma
Premonitory Stage
Patient become unconscious

Twitching of muscles of face, tongue, limbs
Eyeballs roll or turned to one side, become
fixed
 Its last for 30 sec.

Tonic Stage
Whole body goes into a tonic spasm

Respiration ceases, tongue protrudes out

Cyanosis appears, eyeballs become fixed

This stage last for 30 sec
Clonic Stage
Voluntary muscles undergo alternative contraction and
relaxation

Twitching start from the face then involve one side of
extremities and ultimately the whole body

Biting of tongue

Breathing is laboured and blood stained frothy secretions

Cyanosis gradually disappear

Lasts for 1-4 min.
Stage of Coma-
Following fits patient passes in stage of coma
Status eclampticusMultiple recurring fits at varying intervals
Differential Diagnosis Epilepsy
 Hysteria
 Encephalitis
and Meningitis
 Puerperal cerebral thrombosis
 Poisoning
 Cerebral malaria
 Intra- cranial tumors
Prognosis
Immediate Mortality-2-30% maternal mortality
Causes of Maternal death Cardiac Failure
 Pulm oedema
 Aspiration septic pneumonitis
 Cerebral hemorrhage
 Acute renal failure
 Cardiopulmonary arrest
 Adult respiratory distress syndrome
 Post partum shock
 Puerperal sepsis
Fetal Complications
Peri natal mortality- 30-50%

Pre maturity- spontaneous, induced

Intra uterine asphyxia- Infarction, retroplacental, haemorrhage spasm

Effect of drugs

Trauma
Management-
Prevention To control blood pressure

Prophylactic magsulf therapy

Patient to be referred to tertiary centre
Hospital Management-

Shout for help
Maintain airway, breathing and circulation
Oxygen administration 8-10 L/min
Arrest convulsions
Ventilator support
Prevention of injury
Hemodynamic stabilization
Delivery within 6-8 hr, maximum 12 hrs
Prevention of complications

Post partum care








Specific ManagementAnti-convulsions-

Magnesium sulphate is the drug of choice
Pritchard regimen (Intramuscular)
4 gm I/V, over 3-5 min(20 ml of 20% solution)
10 gm I/M deep(5 gm in each buttock-50% solution)
Maintenance dose- 5 gm I.M. 4 hrly

Intravenous- Zuspan or Sibai

4-6 gm IV over 15-20 min 1-2 gm/hr IV infusion




INTRAMUSCULAR DOSAGE SCHEDULE




Magnesium sulphate 8 ml (50% weight by volume
= 4gm) dissolved in 12 ml of saline ( total=20 ml)
for 20 % w/v intravenous dose
Magnesium sulphate 10 ml (5gm) injected deep
intramuscular in each buttock.(50% w/v dose)
Addition of 1 ml of 2% lidocaine reduces pain.
LOADING DOSE : 4 gm of magnesium sulphate as
20% solution intravenously at rate of 1 gm/min +
10 gm of 50% magnesium sulphate solution , one
half (5 gm) injected deeply in upper outer
quadrant of each buttock.
INTRAMUSCULAR DOSAGE SCHEDULE
MAINTAINENCE DOSE
 Every four hour give 5 gm of 50% w/v solution
(10 ml= 5 gm) injected deep intramuscular in
upper outer quadrant of alternate buttocks
 BUT only after ensuring that :
1.Patellar reflex is present
2.Respiration not depressed
3.Urine output in previous 4 hour exceeded 100 ml.

In case of recurrent fits half loading dose :
2gm more intravenously as 20% solution
is given.
 4 ml of 50% w/v (2 gm of magnesium
sulphate) dissolved in 6 ml of saline to
make 2 gm of 20% w/v solution( 2gm in 10
ml)

ADVERSE EFFECTS OF
MAGSULPH






Fits controlled at blood levels of 4-7 meq/l
10 meq/l: patellar reflexes disappear
>= 10 meq/l : respiratory depression
>=12 meq/l : respiratory paralysis and
respiratory arrest
Neonatal respiratory depression only if severe
hypermagnesemia at delivery
Neonatal compromise usually not problematic
Antidote
Calcium gluconate or calcium chloride 1
gm intravenously and witholding further
magnesium sulphate reverses mild to
moderate respiratory depression
 For severe cases prompt tracheal
intubation and mechanical ventilation
required.

Magnesium Sulphate- Preferred
Control fits without depression in mother and
foetus
Reduce of recurrent convulsions
Significantly reduce maternal death (3%)
Reduce perinatal mortality
Anti hypertensive drugs- BP >160/105 mm of
Hg (NHBPEP-2000)
Diuretics-In pulmonary oedema(20-40 mg IV)
Other Regimens
Lytic cocktail- Is a combination of
chlorpromazine, promethazine and
pethidine


Diazepam
Phenyton- in1000mg, iv infusion in one hour,
500mg oral after 10 hrs ,24hrs postpartum
Other Regimens
Lytic cocktail- Is a combination of
chlorpromazine, promethazine and
pethidine


Diazepam
Phenyton- in1000mg, iv infusion in one hour,
500mg oral after 10 hrs ,24hrs postpartum
ANTIHYPERTENSIVE
THERAPY








HYDRALAZINE- 5 to 10mg at 15 to 20 min till satisfactory
BP
Drug of choice during pregnancy act on periferal vessels.
LABETALOL- 10mg IV double the dose at every 10 min till
get satisfactory response or maximum-220mg
NIFEDIPINE-10mg oral, repeated in 30 min, if necessary
VERAPAMIL-5 to 10mg per hour
NIMODIPINE-continuous infusion or oral.
KETANSERIN
NITROPRUSSIDE
MANAGEMENT






DIURETICS - causes intravascular volume depletion
compromise placental perfusion.
HYPEROSMOTIC AGENTS- should be used in pulmonary
oedema only
FLUID THERAPY- Lactated Ringer solution-60-125ml/hr.
excessive fluid may cause pulmonary oedema.
INVASIVE HEMODYNAMIC MONITORING-to manage
oliguria and to avoid pulmonary oedema.
DELIVERY- prefer vaginal delivery. Less tolerant to blood
loss.
ANALGESIA & ANESTHESIA- Epidural is prefer then SA
or GA
Management of complicationsPulmonary oedema
 Heart failure
 Anuria
 Hyperpyrexia
 Psychosis

OTHER HYPERTENSIVE
DISORDERS



Chronic hypertension- Essential hypertension
Secondary hypertension- Renal, endocrinal vascular
Systolic hypertension- Thyrotoxicosis, Hyperkinetic
circulation
It should be managed
According to cause and severity- During antenatal,
intranatal and postnatal period to reduce maternal and
fetal complication and give better outcome.
CONCLUSION
Severe manifestation and
complication can be decreased byEarly detection
 Meticulous antenatal care
 Timely intervention.
To reduce maternal and fetal morbidity and
mortality and to get better outcome.

Hypertensive Disorders Of
Pregnancy
Questionaire
1) All are prognostic indicators of pregnancy
induced hypertension , except:
a.
Low platelets
b.
Serum sodium
c.
Elevated liver enzymes
d.
Serum uric acid
B (serum sodium levels)
2) All of the following can be used in pregnancy
associated hypertension except:
a.
Nifedipine
b.
Captopril
c.
Methyldopa
d.
hydralazine
B (captopril)
3) Which is the drug of choice for severe pre
eclampsia
a)
Labetalol
b)
Metaprolol
c)
Alpha methyl dopa
d)
Nifedipine
A ( labetalol)
4) Best drug for management of eclampsia is:
a)
MgSo4
b)
Lytic cocktail regimen
c)
Phenytoin
d)
diazepam
A (MgSO4)
5) Concentration of MgSo4 in the treatment of
eclampsia in meq/l:
a)
7-10
b)
10-15
c)
2-4
d)
4-7
D ( 4-7 meq/lt)
7) Earliest sign of magnesium toxicity:
a)
Depression of deep tendon reflexes
b)
Respiratory depression
c)
Cardiac arrest
d)
Anuria
A (depression of deep tendon reflexes)
8) Which is not a feature of HELLP syndrome:
a)
Thrombocytopenia
b)
Eosinophilia
c)
Raised liver enzymes
d)
Hemolytic anemia
B (eosinophilia)
9) A 28 year old eclamptic woman develop
convulsion. The first measure to be done is:
a)
Give MgSo4
b)
Sedation of patient
c)
Immediate delivery
d)
Care of airway
D ( care of airway)
10) In severe pregnancy induced hypertension
BP is
a)
160/110 mm Hg
b)
150/100 mm Hg
c)
260/100 mm Hg
d)
120/80 mm Hg
A ( 160/110 mm Hg)
11) Pregnancy induced hypertension is
hypertension that develops after:
a)
18 weeks of pregnancy
b)
20 weeks of pregnancy
c)
24 weeks of pregnancy
d)
28 weeks of pregnancy
B ( 20 weeks of pregnancy)
12) In a patient on magnesium sulphate therapy,
usually at what level the knee (patellar) reflex
disappears:
a)
6-8 meq/l
b)
10-12 meq/l
c)
12-14 meq/l
d)
>15 meq/l
B ( 10-12 meq/lt)
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