MANAGEMENT OF

PREECLAMPSIA

Zamzuri Hudaya Hezal

 INTRODUCTION

There are four major hypertensive disorders that occur in

pregnant women:
Preeclampsia/ Eclampsia : PE : syndrome of new onset of
hypertension and either proteinuria or end organ dysfunction
most often after 20 weeks of gestation in a previously
normotensive woman. Eclampsia is diagnosed when seizures
have occurred
Chronic (preexisting) hypertension : defined as systolic 140
mmHg and/or diastolic 90 mmHg that antedates pregnancy, is
present before the 20 week of pregnancy, or persists longer
than 12 weeks postpartum.
 INTRODUCTION

PE superimposed upon chronic hypertension : when a woman

with chronic hypertension develops worsening hypertension
with new onset proteinuria or other features of preeclampsia
(eg, elevated liver enzymes, low platelet count)
Gestational hypertension : BP >20 weeks g a in the absence
of proteinuria or other diagnostic features of preeclampsia.
Over time, some patients with gestational hypertension will
develop proteinuria or endorgan dysfunction characteristic of
preeclampsia and be considered preeclamptic, while others will
be diagnosed with preexisting hypertension because of
persistent blood pressure elevation postpartum
 INTRODUCTION

EARLY ONSET LATE ONSET

PREECLAMPSIA PREECLAMPSIA

34 WGA

The Differences are: RISK

Biochemical Markers FACTOR
Clinical Manifestation
Maternal and Fetal Outcome
Prognosis and Complication OVERLAP
PATHOPHYSIOLOGY
CONCEPT
EARLY-ONSET LATE-ONSET

Fetus/ Placental Maternal

Factor Constitution

Pregnancy-
Specific Changes

PREECLAMPSIA
 RISK FACTORS

o No evidence of associations of preeclampsia with maternal educational

attainment, marital status, or employment during pregnancy

o Women with a prior history of pregnancy-associated hypertensive disorders

had a statistically significant increasing risk of preeclampsia (OR=10.17,
95%CI:1.26 - 82.02).This association was particularly strong for early onset
preeclampsia (OR=21.45, 95%CI: 2.19 - 210.57)
 RISK FACTORS
o Women who were 30-34 years of age (OR=2.23, 95%CI: 1.06 - 4.71) and >35
years of age (OR=2.69, 95%CI: 1.27 - 5.70) were more likely to have late-
onset preeclampsia compared to women 25-29 years of age.

o Family history of hypertension had a 2.14-fold increasing risk of late onset of

preeclampsia (95%CI: 1.04, 4.40)

o Women who were underweight (<18.5 kg/m2) had a 62% reducing risk of
late onset preeclampsia (OR=0.38, 95%CI: 0.18, 0.81) obese women (>30
kg/m2) had a 4.76-fold increasing risk of late onset preeclampsia (OR=4.76,
95%CI: 1.73, 13.12)

Consistent with prior reports the vast majority of preeclampsia cases

(81%) were classified into the late-onset cases while 19% were
classified into early-onset cases
 Profile of Preeclampsia in Dr. Moewardi Hospital
Surakarta 2010 2014

Parity : Multigravida
Age : 18 35 years old
Gestasional age : >34 weeks g a
Educational level : Senior High School
Ocupation : Housewife
Marrital : Married
History of Hypertension : Non
Previous of PE : Non
BMI : <35
Complication : Hellp Syndrome, IUGR
Decidual Immun Adaptation Process
Decidual Immun Adaptation Process
LOCAL SYSTEMIC
Pathophysiology

In normal placental development,

invasive cytotrophoblasts of fetal origin
invade the maternal spiral arteries,
transforming
them from small-caliber resistance
vessels to high-caliber capacitance
vessels capable of providing placental
perfusion adequate to sustain the
growing fetus.
During the process of vascular invasion,
the cytotrophoblasts differentiate from
an epithelial phenotype to an
endothelial phenotype, a process
referred to as pseudovasculogenesis
or vascular mimicry (top).
In preeclampsia, cytotrophoblasts fail to
adopt an invasive endothelial
phenotype. Instead, invasion of the
spiral arteries is shallow, and they
remain small caliber, resistance vessels
(bottom).
 Pathophysiology of
Late-Onset PE
Predisposed maternal
Normal placenta constitution reflecting
microvascular disease as
occurs with long-term:
Angiogenesis
hypertension
diabetes
obesity
Endothelial hyperlipidemia
Dysfunction hyperhomosisteinemi
maternal genetic
metabolic dysbalance

Preeclampsia
 Pathophysiology
of Late-Onset PE

Late-onset PE is associated with the maternal pathway,

but that its association with the placental pathway is
weak or non-existent.

The two-stage theory may thus be irrelevant for the

pathophysiology of late-onset PE
 Pathophysiology
of Late-Onset PE

A weak or non-existent association between a dysfunctional/

hypoxic placenta (the placental pathway) and late-onset
PE is supported by following findings:

Late-onset PE was not associated with small for gestational

age / IUGR
Management of PE
 Management of Eclampsia
Airway-Breathing-Circulation

Overcome and prevent seizures / anticonvulsants

Fluid management

Controlling blood pressure

Supporting Examination

Delivery

Postpartum care
Note GCS

GCS 14 (compos mentis) : Regular management

GCS 9-13 (decreased consciousness) : Blood Gass Analysis,

CVP, born in the 6-8 hours immediately after the state
emergency is resolved
GCS 8 (not aware) : CVP, intubation and ventilation, C.
Section with G.A soon after controlled blood pressure and
corrected thrombocytopenia, treatment in ICU
 Fluid management

Iatrogenic fluid overload major cause of maternal death in

preclampsia / eclampsia
More fluid restriction is recommended for intrapartum and
postpartum
80 ml / hour or 1 ml / kg bw/ hour, or urine output in the
previous hour + 30 ml
Loading 500 ml of crystalloid: before antihypertensive,
epidural anesthesia, early management of oliguria
 Anticonvulsant

Diazepam

dose : 5 mg IV

Contraindications: Hypersensitivity to diazepam, narrow-angle

glaucoma.

Safety in pregnancy category D, not safe to use in pregnant

women (in the first trimester)

Warning: May cause maternal apnea and cardiac arrest if given too quickly. In neonates
can cause respiratory depression, hypotonia and poor appetite.
 Anticonvulsant

NIMODIPINE
Calcium channel blocker vasodilator cerebral
Minimal toxicological
Anti hypertensi
Dose 60 mg/oral/4 hours
Increase cerebral perfusion pressure cytotoxic
/ vasogenic edema
 Anticonvulsant

Phenytoin
Initial dose: 10 mg / kg BW IV per drip (<50 mg / min), followed
by a maintenance dose (5 mg / kg 2 hours later).
Contraindications: Hypersensitivity to phenytoin, sinoatrial block, AV
block second and third degree, sinus bradycardia, Adams-Stokes
syndrome.

Safety in pregnancy categories: D-not safe for pregnancy

(trimester 1)

Warning: It takes the examination and analysis of urine counts when

therapy is initiated to determine the presence of blood dyscrasia
 Anticonvulsant
MgSO4

Initials
Initials dose:
dose: 4-6
4-6 grams
grams IV
IV bolus
bolus in
in 15-20
15-20 minutes,
minutes, ifif seizures
seizures occur
occur after
after bolus
bolus
administration,
administration, may
may bebe added
added 22 grams
grams IVIV in
in 3-5
3-5 minutes.
minutes. Approximately
Approximately 10-15%
10-15%
of
of patients
patients have
have seizures
seizures again
again after
after loading
loading dose
dose administration.
administration.

Maintenance
Maintenance dose:
dose: 2-4
2-4 gg // hh per
per drip
drip IV.
IV. When
When magnesium
magnesium levels>
levels> 10
10 mg
mg // dl
dl within
within
44 hours
hours after
after administration
administration of of aa bolus
bolus then
then maintenance
maintenance dose
dose can
can be
be lowered.
lowered.

Contraindications:
Contraindications: Hypersensitivity
Hypersensitivity to
to magnesium,
magnesium, the
the heart
heart block,
block, Addison
Addison
disease,
disease, heart
heart muscle
muscle damage,
damage, severe
severe hepatitis
hepatitis or
or myasthenia
myasthenia gravis.
gravis.

Safety
Safety in
in pregnancy
pregnancy categories:
categories: A-safe
A-safe in
in pregnancy
pregnancy

Warning:
Warning: always
always monitor
monitor the
the loss
loss of
of reflexes,
reflexes, respiratory
respiratory depression
depression and
and decreased
decreased
urine
urine output.
output.
 Regimen magnesium sulfat

Intramuscular regimen according to Pritchard:

Loading dose: 4 g IV + 10 grams of IM
Maintenance dose: 5 g IM every 4 hours
Regimen Zuspan : Loading dose: 4 g IV
Maintenance dose: 1-2 g IV per hour
Intravenous regimens according to Sibai : Loading
dose: 6 g IV
Maintenance dose: 2-3 g IV per hour
In the event of a seizure,

Loading dose of 4 g in infusion pump within 5-10

minutes, followed by 1-2 g / hour to 24 hours of last
seizure.

If repeated seizures
bolus infusion of 2 g or raise to a 1.5-2g / hour
 Antihypertension

GENERAL APPROACH

The decision consider the risks and benefits for both mother
and fetus. The level of BP is the most important factor. Tx of
severe hypertension (systolic BP 160 mmHg and/or diastolic BP
110 mmHg) is always recommended because it is believed to
reduce the risk of maternal stroke.

Antihypertensive therapy in women with mild (systolic 140 to

150 mmHg, diastolic 90 to 100 mmHg) to moderate (systolic 150
to 159 mmHg, diastolic 100 to 109 mmHg) is less clear in
some women, aggressive lowering of blood pressure, or even the
medications themselves, can inhibit fetal growth and expose the
fetus to potentially harmful physiological effects of these drugs
 Antihypertension

2002 : fetal weight, fetal growth significantly / 10

mmHg;
2014 : did not increase the frequency of delivery of a small
for gestational age infant. It also did not significantly reduce
perinatal mortality or frequency of prematurity,
preeclampsia, or abruptio placentae.
2015 : There were no adverse fetal effects in those
randomized to the lower target blood pressure
 Antihypertension

All antihypertensive drugs cross the placenta.

Women with chronic hypertension, either treated or untreated,

are at increased risk of congenital malformations :
particularly cardiac malformations.
 Antihypertension

Options :
Methyldopa
Betablockers
Labetalol
Calcium channel blockers
Hydralazine
Thiazide diuretics
Clonidine
 Antihypertension

1. Antepartum and intrapartum

Persistent rise in blood pressure at least 1 hour
Sistole 160 mmHg/diastole 110 mmHg/ MAP 130 mmHg
Persistent rise in blood pressure at least 30 minutes
Sistole 200 mmHg/diastole 120 mmHg/ MAP 140 mmHg
Thrombocytopenia or congestive heart failure
Sistole 160 mmHg/diastole 105mmHg/ MAP 125 mmHg

2. Postpartum (persistent at least 30 minutes)

Sistole 160 mmHg/diastole 105 mmHg/ MAP 125 mmHg
 Antihypertension
Onset Peak
Class Medicine (Min) (Min)
Dose

5 -10 mgIV/ 15-30 min

10 20 mg PO/ 30 min

20-40-80 mg IV/
10-20 min-300 mg

0, 2-5, 0 g/ kg/ min

Nifedipin
Inhibit platelet aggregation (Am J Hypertens (1988)1:175-7)

Improve urine output in 24 hours postpartum (Am J Obstet Gynecol

(1990)162: 788-92)

Has an effect equivalent to hydralazine and labetalol

(Obstet Gynecol (1991)77:331-4; Br J Obstet Gynaecol (1988)95:868-76)

Decreasing blood pressure and provide a good

perinatal outcome (Am J Obstet Gynecol (1992)167:879-84)

MgSO4 did not increase the side effects when used

together (Am J Obstet Gynecol (2005)193:153-163)
 Management of Obstetric

1. Expectative/ Concervative (<35 weeks

of gestasional age)

Maintained pregnancy until the fetus is viable

Term: gestational age <35 weeks without
complications.

2. Active termination of pregnancy

 Termination of Pregnancy
Vaginal or C. Section

The mode of delivery should determined after considering the

presentation of the fetus and the fetal condition, together with
the likelihood of success of induction of labour after assssment
of the cervix

Both of them is availability possible

 Termination of Pregnancy
Vaginal

In the active phase, there are no other complications,

a full awareness / minimal neurological disorders
C. Section

Impairment of consciousness, uncooperative,

complications, vaginal will be more than 8 hours,
there are obstetric indications, fetal distress
TERIMA KASIH