MANAGEMENT OF PRE-

ECLAMPSIA/
ECLAMPSIA. BY DR. ADDAH
A.O.
INTRODUCTION.
Pre- eclampsia is associated with
significant morbidity and mortality for both
mother and baby.
Morbidity will remain high in our
enviroment until there is general
improvement in maternity services.
 Trials on prevention disappointing.
 Mainstays of mgt –
 integrated antenatal care
 access to fetal monitoring services,
 Stabilisation of the maternal condition
 Delivery of the baby on the best day in the
best way to benefit mother and child.
Antenatal screening.
 Screening of women for the risk or signs of hypertension
at the antenatal clinic.
 Regular BP and analysis of urine – do not forget other
signs and symptoms of this disease.
 Majority of women with PIH i.e. hypertension and no
proteinuria usually have BP’s between 90 and 95 mmHg.
In the absence of other obstetric problems, follow-up can
best be achieved in an outpatient setting.
 Ideally women with PIH should be seen weekly (difficult
in our setting).
 Admit if:
 they need to attend ANC more than twice weekly.
 If pre- eclampsia or severe hypertension develops.
Risk of progression dependent
on GA and whether a
nulliparous woman.
None of the laboratory tests are
reliable predictors of
progression to pre- eclampsia
or severe hypertension.
However normal values are
reassuring.
 The role of antihypertensive in this group
controversial
 Rx
 Decreased incidence of severe
hypertension and hospital admission
 No reduction in development of protenuria
or risk of preterm delivery of perinatal
death.
 PIH not usually an indication for preterm
delivery unless severe hypertension
cannot be controlled.
 Induction at usually ≥ 37 wks gestation
Management of Pre-Eclampsia
 Definitive treatment of PE is delivery.
 Strike a balance between prematurity
and maternal state.
 Follow protocol enumerated earlier:
 Screening, those at risk are monitored
 Maternal condition is stabilized.
 Monitoring is continued.
 Delivery is initiated at the best time for the
baby and the mother.
 Usually Bp is the signpost for further mgt.
Assessment of the mother
 A Mild Pre-eclampsia
 Hospitalisation on diagnosis for bed rest
 Decrease possibility of convulsions
 Enhances chances of fetal survival
 Daily urine dipstick measurements of
proteinuria
 Bp monitoring every four hours
 24 hour urine protein measurement and total
creatinine clearance twice wkly.
 Daily weighing
 LFT, uric acid, electrolytes and serum albumin
on admission and wkly.
 GA assessment and fetal wt on
admission and every 2 wks on USS
 Antihypertensive therapy if DBp ≥ 100
mmHg or GA < 30 wks.
 Discourage sedatives
 Interfere with fetal heart rate
 Phenoborbital – impairment of vit K
dependant cloting factors.
 B Severe pre-eclampsia
 Goals of mgt –
 prevention of convulsions
 Control of maternal BP
 Initiation of delivery.
 Delivery definite mode of treatment if:
 Severe PE beyond 36 wks
 Evidence of fetal lung maturity
 Evidence of fetal jeopardy
 Mgt of severe PE < 36 wks controversial.
 Institutional variations
 Some institutions use antihypertensives to
control natural BP until fetal lung maturity
is reached.
 Anyone at 32-34 wks with severe PE
should be considered for delivery. Give
steroids.
 In patients 23-32 wks with severe PE,
delivery may be delayed. Transfer Pt to
tertiary centre.
 Mother should be placed on magnesium
sulphate for a minimum 24 hrs while the
diagnosis is made.
 BP should be controlled by the
antihypertensive to be discussed.
 Close observation with frequent laboratory
evaluations.
 See below for indications for delivery.
 If GA is < 23 wks, offer patient induction for
termination of pregnancy.
 Vaginal delivery is preferable to CS and
induction should be aggressive.
 Clear end point for induction should be
determined, usually within 24 hrs.
Assessment of the fetus
 Main disease process affecting the fetus is
placental insufficiency – IUGR
 Therefore test for growth and fetal wellbeing
 Methods of assessment:
 USS assessment of fetal size at time of diagnosis
 Usually asymmetrical growth
 Look for evidence of low liquor volume
 Serial liquor vol. estimations to detect fetal
compromise.
 Umbilical-artery Doppler assessment
 Cardiotocography (non-stress test)
mainstay of monitoring, because of
availability but of poor predictive value.
 Non-reactive non-stress tests require
further evaluation with Biophysical
profile.
 L/S ratio for only fetuses near term.
 continuous fetal monitoring in rapidly
worsening PE because of the risk of
abruptio placental and utero-placenta
insufficiency.
Indications for delivery in patients
with severe PE
 Severe uncontrolled hypertension ≥ DBp 110 mmHg.
 Thrombocytopenia
 Rising serum creatinine
 HELLP syndrome
 Persistent or severe headache
 Epigastric pain
 Abnormal LFTs
 Eclampsia
 Pulmonary oedema
 Abnormal antepartum fetal heart rate testing
 SGA fetus on serial USS
 A ratio of serum alanine aminotransferase to serum
aspartate aminotransferase (ALT/AST) twice normal.
Antihypertensive Therapy
 Controversy as to whether uterine blood flow is
auto regulated.
 Therefore, any precipitate reduction in Bp,
decrease uterine blood flow. Reduce Bp slowly.
 Goal of treatment is to bring DBp into 90-100
mmHg range.
 Decrease Bp only prevents complications
directly related to maternal hypertension. Auto
regulation lost in cerebral blood vessels above
MAP of 140 mmHg (risk of CVD)
 No evidence that reducing Bp influences
other aspects of disease progression.
 B-Blockers esp. has shown increased
risk of SGA infants
 Benefits of antihypertensives are in early
onset PE.
 All antihypertensive drugs seems to be
effective. Avoid Atenolol, inhibitors of
ACE, diuretics.
Antihypertensives
 Early treatment of antihypertensives decrease
incidence of hypertensive crisis
 Little evidence as choice of antihypertensives or
threshold of blood pressure that requires
therapy.
 Once Bp is controlled, expectant mgt is
beneficial to the baby by reducing risk of
prematurity.
 Average extension of pregnancy is 14 days.
 No single therapy can be successful in all
patients- increasing doses plus combination
therapy.
 A Hydrallazine – drug of choice
 Direct arteriolar vasodilator
 Reflex tachycardia and increased Co
(beneficial to uterine blood flow)
 If fetal heart decelerations occurs after
adm, give
 Adm. Fluid loading
 O2
 Turn patient on the left side
 Discontinue oxytocin

 Dose 5 mg IV every 15-20 minutes. Onset

of action is 15 minutes, peak effect 30-60
minutes, duration of action 4-6 hours.
 B Labetalol
 Combine a and B blockade
 More rapid effect than hydrallazine
 Decreased VR, no change in CO.
 Dosage – given every 10 minutes.
 1st dose 20mg, 2nd dose 40mg and
subsequent doses 80mg to a max 300 mg
or until blood pressure is controlled.
 C Methyl Dopa –
 1st choice for long term treatment.
 Reduces central sympathetic outflow.
 D Nifedipine –
 Calcium channel blocker
 Can be adm. by bite and swallow to lower
Bp acutely.
 Avoid in IUGR and abn. fetal ht rate
patterns.
 Reverse hypotensive effects with fluid
loading or IV calcium
 E Sodium Nitropruside
 F Trimethaphan
 G Nitroglycerin – venular vasodilator
Planning of Delivery
 Timing of delivery is critical
 Rushed delivery in an unstable patient
 Or delay in delivery in a side patient
 Delivery < 32 wks (CS in the UK) – many
centres would opt for vaginal delivery.
 Be cautious. Labour aggravates fluid
overload and Bp control.
 Vaginal del is successful in < 50%
 Caution.
Postpartum Treatment

 Constraints of therapy no longer exists –

diuretics can be used.
 Maintain anticonvulsants (Mg2SO4 for
24 hrs after the delivery.
 If there is hypreflexia with Mg2SO4, give
diuretics.