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 Every minute, at least 1 woman dies from

complications related to pregnancy or childbirth

 That means 529,000 women a year

 In addition, for 1 woman dying in childbirth,


around 20 more suffer injury, infection or disease –
approximately 10,000,000 women each year

 5 direct complications account for more than 70%


of maternal deaths:
 Haemorrhage (25%)
 Infection (15%)
 Unsafe abortion (13%)
 Eclampsia (12%)
 Obstructed labour (8%)
WHERE DO WE STAND?

• More women die due to pregnancy-related


causes in India than anywhere else in the
world
• Not something to be proud of

• Make up almost 1/4th of the maternal


deaths that occur annually worldwide

• Roughly one maternal death occurs every


five minutes
WHERE DO WE STAND?
Causes of maternal death (%)

> 100,000 women die each year from pregnancy


related problems
• Haemorrhage - 30
• Anaemia - 19
• Sepsis - 16
• Obstructed labor - 10
• Abortion - 8
• Toxemia - 8
• Others - 8
HYPERTENSION IN PREGNANCY
Dr. Rupak Ranjan Roy
MD, DNB, FRCOG (London)
QUESTION ON HYPERTENSION IN
PREGNANCY CAME IN……

 1998 – long question


 2001 – long question
 2002 – short note
 2003 – long question
 2008 – long question
 2009 – short note
 2011 – short note
 2012 – long question
 2013 – short note
 2017 - long question
 2018 – short note
NORMAL BLOOD PRESSURE CHANGES IN PREGNANCY

 Blood pressure is dependent on


 Systemic vascular resistance
 Cardiac output
 Blood pressure falls by about 30/15 mm. of
Hg in the 2nd trimester
 Occurs in normotensives
 Occurs in hypertensives
 Pressure rises again to the pre-pregnant level by
term

 Hypertension in pre-eclampsia is mainly


due to increase in systemic vascular
resistance
DEFINITIONS

 Hypertension:
 Systolic BP  140 mm. of Hg (or a rise
of 30 mm. of Hg)
 Diastolic BP  90 mm. of Hg. (or a
rise of 15 mm. of Hg)

 Either or both

 Proteinuria:
 Urinary protein excretion > 300 mg. in 24
hours
 Or >1g/l in a random sample
HYPERTENSION

 Blood pressure
 ≥ 140/90 mm. of Hg
 Two readings taken six hours apart with
the woman
 Comfortably resting
 At 45 degrees

 With an appropriately sized cuff

 Taken with the instrument at the level of


the heart
 Korotkow V (sometimes IV) as the
diastolic
PROTEINURIA
 Proteinuria
 Often develops later in the course of the
disease
 Dipstick is a common screening test, but
is inaccurate
 + - 300mg/l
 ++ - 1g/l
 +++ - 3g/l
 Protein-creatinine ratio on a random spot
sample is fairly accurate
 30mg / mmol is equivalent of 300mg / 24 hours of
proteinuria
CLASSIFICATION
 Pregnancy induced hypertension (PIH):
usually manifests AFTER 20 weeks
 Pre-eclampsia / Eclampsia
 Transient hypertension
 Occurs near term or early puerperium
 Rapid resolution
 Pre-existing (or chronic) hypertension:
usually present BEFORE 20weeks
 Essential hypertension
 Secondary to renal or other causes
 Pre-eclampsia superimposed on chronic
hypertension
 Unclassified
PRE-ECLAMPSIA

 Peculiar to pregnancy

 Of placental origin

 Cured by delivery
PRE-ECLAMPSIA
 Hypertension after 20 weeks = PIH
 PIH + proteinuria = Pre-eclampsia

 Pre-eclampsia + epileptiform seizures =


Eclampsia
 Pre-eclampsia is a multisystem disease in
pregnancy, usually manifest as
hypertension and proteinuria after 20
weeks of gestation
EPIDEMIOLOGY OF PRE-ECLAMPSIA

 Occurs in about 10% of pregnant women


 5 - 8% of all pre-eclamptics will have eclampsia in
under-developed countries
 1 in 2000 will have eclampsia in developed countries
 More common in nulliparous women
 Can occur in multiparous women if
 She had pre-eclampsia in the past (30% recurrence)
 She changes her partner
 Worldwide, 50,000 women die each year from
pre-eclampsia
 In India – accounts for 12% of all mothers dying
from pregnancy (Indian MMR 167 / 100,000)
PATHOLOGY
 In normal pregnancy the trophoblast
invades the muscular coat of the spiral
arterioles in the placental bed

 The arterioles become


 Low resistance vessels
 Resistant to vasopressor agents

 In pre-eclampsia – this invasion is


incomplete and probably, is the starting
point for all the terrible things that follow
Incomplete
Acute
trophoblastic
invasion
atherosis

Spiral
artery flow
reduction

Abnormal
Uteroplacental uterine
flow reduction artery
waveform

Exaggerated
inflammatory
response
Exaggerated
inflammatory
response

Endothelial
cell damage

↑ vascular
permeability Vasoconstriction

Clotting
abnormality

Oed Protei HT
Eclampsi
a
ema nuria IUGR

Liver
damage
PATHOPHYSIOLOGY

 Vasospasm – in all the vessels

 Extravasation

 Absent pregnancy hypervolaemia –


haemoconcentration occurs

 Haemolysis, low platelets, altered clotting

 Reduced GFR, reduced clearance of


metabolites, proteinuria, ATN in severe
cases
PATHOPHYSIOLOGY

 Liver involvement indicates severe disease

 Elevated liver enzymes

 Subcapsular haemorrhages

 Cerebral edema, infarcts, thrombosis,


haemorrhage

 Papilloedema, retinal vascular spasm,


narrowing, haemorrhage
TO SUMMARIZE THE PATHOPHYSIOLOGY

 Stage 1:
 Development of the disease
 Occurs before 20 weeks
 No symptoms
 Incomplete trophoblastic invasion
Impaired materno-fetal interaction may
be caused by altered immune responses
+ spiral arterioles may have
atheromatous lesions
TO SUMMARIZE THE PATHOPHYSIOLOGY
 Stage 2:
 Manifestation of the disease
 Occurs after 20 weeks
 The ischaemic placenta, via an
exaggerated maternal inflammatory
response causes the clinical
manifestations
 Vascularendothelial damage with
vasospasm, transudation of plasma,
and ischemic & thrombotic sequelae
AETIOLOGY
 Exact “Cause” – still unknown: possible altered
immune response
 Predisposing factors
 Nulliparity
 Previous history of pre-eclampsia
 Large placenta (twins, molar pregnancy, hydrops
fetalis)
 Family history of pre-eclampsia
 New partner
 Extremes of maternal age (particularly older age)
 Long inter-pregnancy interval
 Obesity
 PCOS
 Pre-existing microvascular diseases
 Chr. HT/chr. renal dis, diabetes, antiphospholipid syndrome
SEVERITY OF PRE-ECLAMPSIA
 Mild:
 Systolic: 140 – 149
 Diastolic BP 90 – 99

 Moderate:
 Systolic BP 150 - 159
 DBP 100 – 109

 Severe
 Systolic BP 160
 DBP 
 Proteinuria - > 1g/l
CLINICAL FEATURES
 Symptoms
 Usually asymptomatic
 Headache, visual disturbances, epigastric pain,
nausea, vomiting in severe disease
 Signs
 Oedema
 But, is common in most pregnant women
 Therefore, is of little diagnostic value
 But, in pre-eclampsia
 May develop suddenly
 May be massive
 Not postural
 Hypertension
 Urine shows proteinuria
CLINICAL FEATURES OF “SEVERE” PRE-ECLAMPSIA

 In addition to HT & proteinuria


 Severe headache
 Visual disturbance
 Blurring
 Flashing lights
 Epigastric pain and/or vomiting
 Liver tenderness
 Brisk reflexes, clonus
 Papilloedema
 Occipital lobe blindness
 Platelet count falling to below 100 x 106/l
 Abnormal liver function test
 HELLP syndrome
COMPLICATIONS OF PRE-ECLAMPSIA
 Early onset disease tends to be more severe
 Maternal complications
 Eclampsia
 Cerebrovascular haemorrhage
 HELLP syndrome
 Hemolysis
 Elevated liver enzymes
 Low platelets
 Placental abruption
 Renal failure
 Pulmonary edema
 Coma and death
COMPLICATIONS OF PRE-ECLAMPSIA
 Fetal complications

 IUGR
 Fetal distress
 Prematurity
 Fetal death
DIAGNOSIS AND MONITORING
 Clinical features
 Symptoms
 Signs
 Investigations
 Confirm proteinuria – Dipstick / P:C ratio
 If proteinuria - exclude urinary infection
 Serum uric acid – whether high (pregnancy normal range
is lower)
 To monitor maternal wellbeing
 Platelet count – whether low
 Clotting studies – whether deranged
 Liver enzymes – AST, ALT, LDH – whether high / rising
 Renal function – creatinine – whether high
 To monitor fetal wellbeing (whether IUGR)
 Ultrasound scan (+ Doppler studies)
 CTG
MANAGEMENT
 DELIVERY CURES
 Timing of delivery depends on
 Severity of the disease
 Gestational age
 Till then…..
 Outpatient management possible in
 Women with mild disease
 No proteinuria
 Check BP twice weekly
 Check urine for protein twice weekly
 Ultrasound scans for fetal growth
 Check blood for uric acid, platelet count
 Antihypertensives if appropriate
 Admit if
 Moderate or severe disease
 Proteinuria - ++ or more
 Anytime the disease worsens or fetal compromise appears
MANAGEMENT IN HOSPITAL
 Rest
 Traditionally adviced, benefits doubtful
 Family disruption, expensive, stressful
 Risk of DVT
 Regular BP check
 Check proteinuria daily
 Salt restriction
 Should not be done
 Antihypertensives
 Severe disease - Mandatory
 Milder disease – Often given, but role uncertain
 Monitor the baby
 Ultrasound scan
 CTG
DRUGS USED
 Antihypertensives
 These do not modify the course of the disease
 These are given to try and prevent maternal
complications (cerebral haemorrhage) and may
help in prolonging the pregnancy
 Given if BP > 160/110 mm.of Hg
 Methyl dopa
 Nifedipine
 Labetalol
 Hydralazine
 Magnesium sulphate
 Treatment of eclampsia
 Prevention of eclampsia
DRUGS USED
 Role of antihypertensives in mild disease is
debatable
 Some use it while some don’t

 Steroids (Betamethasone)
 For fetal lung maturity if delivery < 36 weeks is
anticipated
DRUGS TO AVOID
 Avoid
 ACE inhibitors
 Captopril, lisinopril
 Angiotensin receptor antagonists
 Losartan

 These can cause


 Birth defects in first trimester
 Fetal growth restriction, oligohydramnios, pulmonary
hypoplasia
 Fetal renal disorders
 Joint contractures
 Incomplete ossification of the fetal skull
 Fetal death
DRUGS TO AVOID
 Avoid diuretics
 Reduces blood volume further
 Can cause fetal compromise
 Only used if there is pulmonary edema

 Avoid lowering the pressure


 Too much
 Too quickly
 Can cause fetal distress
DELIVERY
 Depends on the severity of the disease and the
gestational age

 Balance must be struck between


 Risks of prematurity – if pregnancy is
terminated too soon
 Risks of the disease - if pregnancy is allowed
to continue
DELIVERY
 As a general rule
 Aim to take the pregnancy to as close as 37
weeks as possible

 > 37 weeks – deliver


 < 34 weeks – conservative if appropriate
 34 – 37 weeks – conservative, but with a low
threshold for delivery

 Deliver – if  1 fetal or maternal complications


are likely to arise within 2 weeks of the onset of
proteinuria
DELIVERY
 Mild hypertension without fetal compromise
 Monitor for deterioration
 Deliver at term (around 37 weeks)
 Moderate or severe pre-eclampsia
 > 34 – <36 weeks
 Consider delivery as problems of prematurity are less
 BP > 170/110mm. Of Hg. - control BP first
 < 34 weeks
 Conservative management in specialist unit with full neonatal
facilities
 Give steroids
 Treat hypertension
 Intensive maternal and fetal surveillance
 Clinical deterioration in either deliver
 Severe pre-eclampsia with complications or
fetal distress deliver whatever the
gestation
MODE OF DELIVERY
 < 34 weeks – usually caesarean section
 > 34 weeks – induction of labour
 Close observation of BP in labour
 Close observation of fluid balance
 Continuous fetal monitoring
 Epidural anaesthesia where available
 Antihypertensives – sometimes given IV
 Avoid pushing in second stage if BP > 170/110
 Cut short the second stage by forceps / ventouse
 Use oxytocin the third stage
 NOT ergometrine – can cause severe hypertension
POSTNATAL CARE
 Condition may worsen in the first 24 hours
 Monitor
 Liver enzymes
 Platelet count
 Renal function
 Strict fluid balance
 Excessive IV fluid may lead to pulmonary edema
 Consider a CVP line
 Use frusemide if pulmonary edema
 Watch out for renal failure
 Aim to keep BP around 140 / 90
 Nifedipine
 Betablocker
 Captopril
 Methyl dopa can cause postnatal depression, so not favoured
 Antihypertensive treatment may need to be continued for
upto 6 weeks, sometimes up to 3 months
ECLAMPSIA
 IT IS A MEDICAL EMERGENCY

 Sometimes BP may rise later


 Sometimes proteinuria may appear later

 Sometimes may occur after delivery

 Antepartum – 50%

 Intrapartum – 25%

 Postpartum – 25% (upto 44% has been


reported)
ECLAMPSIA
 Seizure
 Four phases
 Aura followed by twitching around face
 Tonic phase where the entire body becomes

rigid, arms are flexed, fists clenched,


respiration ceases
 Clonic phase where jerky movements start,

there is frothing, patient is cyanosed


 Recovery, slumps into coma of variable

duration
ECLAMPSIA
 Management:
 Turn the patient to her side
 Avoids aspiration
 Secure the airway if possible
 Give oxygen by mask
 Control fits
 I.V. Magnesium sulphate – 4 g loading dose i.v.,
then 1 g/hour
 I.V. Diazepam – 10 mg slow i.v., repeat after 10
min if required
 Once the patient stabilizes, plan for
delivery
 Nurse in a quiet room
ECLAMPSIA
 Send bloods for
 Complete haemogram
 Platelet count

 Clotting screen
 PT / APTT
 Fibrinogen

 LFT

 Urea, creatinine, electrolytes


ECLAMPSIA

 Antihypertensive
 I.V. labetalol, hydralazine
 In hypertensive crisis – sodium nitroprusside,
nitroglycerine
 Anticonvulsants
 Magnesium sulphate – most commonly used
 Diazpam
 Pethidine+chlorpromazine+promethazine – Lytic
cocktail
 Phenytoin
ECLAMPSIA
 Mode of delivery
 Often caesarean section
 Labour may be induced if

 Cervix is favourable
 Maternal condition is stable

 There is no fetal distress

 Cephalic presentation

 No further fits occur


ECLAMPSIA
 Close monitoring of the mother

 Fluid balance (80 ml/hour or 1ml.kg/hour)


till there is diuresis

 Careful not to overload – pulmonary edema


 Hourly urine output

 Put in a central venous cannula if required

 BP every 15 min.
ECLAMPSIA
 Anaesthesia
 Epidural is okay if no clotting disorder
 Avoid hypotension as much as possible

 In labour
 Monitor maternal wellbeing
 BP, fluid balance, analgesia, progress of labour

 Continuous CTG to monitor the baby


 Epidurals if appropriate (check platelet count)
 Shorten second stage – use forceps
 Avoid ergometrine, use bolus oxytocin instead
ECLAMPSIA
 After delivery

 Continue the close observation


 Continue Magnesium sulphate x 24
hours after delivery or after the last
fit
 Continue antihypertensives
MAGNESIUM SULPHATE
 Magnesium sulphate is used to

 Treat eclampsia
 Prevent recurrent convulsions

 Prevent eclampsia in severe pre-eclamptics

 Possible cerebral vasodilator effect

 Safe drug
HOW MAG SULPH WORKS
 Still
obscure
 Possibly acts by
 Inducing cerebral vasodilatation
 Antagonising the excitatory glutamate
N-methyl-D aspartate receptors.
 Increasing the production of
prostacyclins which is an endothelial
vasodilator, inhibits platelet
activation and protects endothelial
cells form injury mediated by free
radicals.
MAGNESIUM SULPHATE REGIMENS
 ZUSPAN - Loading dose 4g (diluted in
normal saline) – slow i.v. over 10 – 15
mins
 Followed by i.v. infusion 1g/hour x 24
hours
 PRITCHARD - Loading dose 4g (diluted
in normal saline) – slow i.v. over 10 –
15 mins
 5g i.m. in each buttock followed by 5g
every 4 hours x 24 hours
MAGNESIUM SULPHATE
 How to monitor for toxicity
 Monitor knee jerk – whether present

 Monitor respiratory rate – whether < 16/min

 Monitor urine output – whether < 25 mls/min

 Checking blood magnesium level not


required

 Calcium
gluconate – 1 g (10 ml) i.v. if
magnesium toxicity
ECLAMPSIA
 Puerperium
 Reduce antihypertensives in a stepwise manner

 HT may take up to 3 months to resolve

 However, if proteinuria and HT persists after 6


weeks, further investigations are required
 Prevention
 30% recurrence rate
 Low dose aspirin started before 20weeks
pregnancy may help
 Anti oxidants, vitamin C, calcium have all been
tried, but not found to be truly effective