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Preeclampsia: An update

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Preeclampsia : an update

G. LAMBERT (*, **), J. F. BRICHANT (**), G. HARTSTEIN (**), V. BONHOMME (*, **) and
P. Y. DEWANDRE (*, **)

Abstract : Preeclampsia was formerly defined as a mul- patients. Antenatal corticosteroids should be adminis-
tisystemic disorder characterized by new onset of hyper- tered to less than 34 gestation week preeclamptic
tension (i.e. systolic blood pressure (SBP) ≥ 140 mmHg women to promote fetal lung maturity. Termination of
and/or diastolic blood pressure (DBP) ≥ 90 mmHg) and pregnancy should be discussed if severe preeclampsia
proteinuria (> 300 mg/24 h) arising after 20 weeks of occurs before 24 weeks of gestation. Maternal end organ
gestation in a previously normotensive woman. Recent- dysfunction and non-reassuring tests of fetal well-being
ly, the American College of Obstetricians and are indica- tions for delivery at any gestational age.
Gynecolo- gists has stated that proteinuria is no longer Neuraxial anal- gesia and anesthesia are, in the absence
required for the diagnosis of preeclampsia. This of thrombocyto- penia, strongly considered as first line
complication of pregnancy remains a leading cause of anesthetic techniques in preeclamptic patients. Airway
maternal morbidity and mortality. edema and tracheal intubation-induced elevation in
Clinical signs appear in the second half of pregnancy, blood pressure are important issues of general
but initial pathogenic mechanisms arise much earlier. anesthesia in those patients. The major adverse
The cytotrophoblast fails to remodel spiral arteries, outcomes associated with preeclampsia are related to
leading to hypoperfusion and ischemia of the placenta. maternal central nervous system hemorrhage, hepatic
The fetal consequence is growth restriction. On the rupture, and renal failure. Preeclampsia is also a risk
maternal side, the ischemic placenta releases factors that factor for developing cardio- vascular disease later in
provoke a gen- eralized maternal endothelial life, and therefore mandates long-term follow-up.
dysfunction. The endothe- lial dysfunction is in turn
responsible for the symptoms and complications of Key words : Hemodynamic ; hypertension ; manage-
preeclampsia. These include hyper- tension, proteinuria, ment ; preeclampsia ; pregnancy.
renal impairment, thrombocytope- nia, epigastric pain,
liver dysfunction, hemolysis-elevat- ed liver enzymes-
low platelet count (HELLP) syndrome, visual
disturbances, headache, and seizures. Despite a better
understanding of preeclampsia pathophysiology and INTRODUCTION
maternal hemodynamic alterations during pre-
eclampsia, the only curative treatment remains placenta Preeclampsia remains a leading cause of ma-
and fetus delivery.
ternal and fetal morbidity and mortality (1, 2). De-
At the time of diagnosis, the initial objective is the
spite a better understanding of its pathophysiology
assessment of disease severity. Severe hypertension
(SBP ≥ 160 mm Hg and/or DBP ≥ 110 mmHg), throm- and some improvements in the ability of
bocytopenia < 100.000/µL, liver transaminases above monitoring
twice the normal values, HELLP syndrome, renal
failure, persistent epigastric or right upper quadrant
pain, visual or neurologic symptoms, and acute
pulmonary edema are all severity criteria. Medical G. LAMBERT, M.D. ; J.F. BRICHANT, Ph.D. ; G. HARTSTEIN, M.D. ;
treatment depends on the se- verity of preeclampsia, and V. BONHOMME, Ph.D. ; P. Y. DEWANDRE, M.D.
(*) University Department of Anesthesia & Intensive Care
relies on antihypertensive medications and magnesium
Medicine, CHR de la Citadelle, Liege, Belgium.
sulfate. Medical treatment does not alter the course of (**) Department of Anesthesia & Intensive Care Medicine,
the disease, but aims at preventing the occurrence of CHU Liege, Belgium.
intracranial hemorrhages and seizures. The decision of Correspondence address : Geraldine Lambert, University
terminating pregnancy and perform delivery is based on Department of Anesthesia & ICM, CHR de la Citadelle,
gestational age, maternal and fetal conditions, and 4000 Liège. Tel. : +32 42256111.
E-mail : [email protected]
severity of preeclampsia. Deliv- ery is proposed for Funding and support : This review paper is in relation with
patients with preeclampsia without severe features after the 2012 SARB Grant awarded to the authors by the Society
37 weeks of gestation and in case of severe for Anesthesia and Resuscitation of Belgium.
preeclampsia after 34 weeks of gestation. Between 24 This work was also supported by the Department of Anes-
and 34 weeks of gestation, conservative management of thesia & Intensive Care Medicine, CHU Liege, Belgium. The
authors have no conflict of interest to disclose.
severe preeclampsia may be considered in selected
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
138 G. LAMBERT et al.
the hemodynamic alterations in this population, the two measurements at least four hours apart.
only curative treatment remains fetus and placenta Protein- uria is defined as the excretion of at least
delivery. Medical treatment aims at avoiding 300 mg of protein in a 24 hour urine collection.
mater- nal complications such as seizures, Alternatively, a urine protein (mg/dL)/creatinine
hemorrhagic stroke, renal failure, or pulmonary ratio (mg/dL)
edema. Adequate timing of delivery is of ≥ 0.3 has good sensitivity (98.2%) and specificity
paramount importance, as well as the optimization (98.8%) as a diagnostic tool (3). Conversely, a
of obstetric analgesia or an- esthesia during posi- tive qualitative dipstick test for proteinuria
delivery. Preeclampsia is also a risk factor for provides too variable results to be considered as a
developing cardiovascular diseases later in life, reliable diagnostic tool of proteinuria. It can be
and an adequate long term follow up is there- fore used if no other method is readily available. In that
advised. Maternal end organ dysfunction and non- case only, a 1+ dipstick result is considered as the
reassuring tests of fetal well-being are indications cut-off for the diagnosis of proteinuria.
for delivery at any gestational age. This review Since recently, in recognition of the
will focus on recent de- velopments in the syndromic nature of preeclampsia, proteinuria is
definition of preeclampsia and severe no longer considered as mandatory for the
preeclampsia, pathophysiology of the dis- ease, diagnosis of pre- eclampsia (4, 5). Consequently,
recent advances in hemodynamic monitoring, and in the absence of proteinuria, preeclampsia can be
progresses in the medical, obstetrical, and diagnosed as new- onset hypertension associated
anesthetic management of those parturient patients. with (Table 1) :
– thrombocytopenia < 100.000/µL,
NOSOLOGY – elevated liver transaminases ( > twice the
normal values),
Hypertension during pregnancy is defined as a – impaired renal function (with serum creatinine
sys- tolic blood pressure (SBP) ≥ 140 mmHg > 1.1 mg/dL or doubling of serum creatinine
and/or a diastolic blood pressure (DBP) ≥ 90 level in the absence of any other renal disease),
mmHg and is classified into four categories : – pulmonary edema,
preeclampsia, chron- ic hypertension, chronic – new-onset visual or cerebral disturbances.
hypertension with super- imposed preeclampsia,
and gestational hyperten- sion. Hypertension is Severe preeclampsia was usually defined as pre-
considered to be mild, moderate or severe when eclampsia associated with any of the following :
SBP is ≥ 140, 150 or 160 mmHg or DBP is ≥ – severe hypertension (i.e. SBP ≥ 160 mmHg and/
90,100 or 110 mmHg, re- spectively. or DBP ≥ 110 mmHg),
Preeclampsia was usually defined as new-onset – thrombocytopenia < 100.000/µL,
hy- pertension (i.e. SBP ≥ 140 mmHg and/or – impaired liver function with liver transaminases
DBP higher than twice the normal values,
≥ 90 mmHg) and proteinuria (> 0.3 g/day) arising
after 20 weeks of gestation in a previously normo-
tensive woman. Elevated BP should be recorded on

Table 1
Diagnostic criteria for preeclampsia (4)
Blood pressure  ≥ 140 mmHg systolic or ≥ 90 mmHg diastolic on two occasions at least 4 hours apart after 20 weeks of
gestation in a woman with a previously normal blood pressure.
 ≥ 160 mmHg systolic or ≥ 110 mmHg diastolic can be confirmed within a short interval (minutes) to
facilitate timely antihypertensive therapy.
and
Proteinuria  ≥ 300 mg/24 h urine collection.
or
 Protein/creatinine ratio ≥ 0.3 (each measured as mg/dL).
 Dipstick reading of 1 + (if other methods not available).
Or in the absence of proteinuria, new-onset hypertension with the new onset of any of the following :
Thrombocytopenia  Platelet count < 100 000/µL
Renal insufficiency  Serum creatinine level > 1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of
other renal disease.
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 PREECLAMPSIA 139
Impaired liver function  Elevated blood concentrations of liver transaminases to twice normal concentration.
Pulmonary edema
Cerebral or visual symptoms

© Acta Anæsthesiologica Belgica, 2014, 65, n° 4

 140 G. LAMBERT et al.
Table 2
Eclampsia is defined as generalized tonico-clonic
Severe features of preeclampsia (any of these findings)[4] seizure that is not attributable to another cause, and
 SBP ≥ 160 mmHg or DBP ≥ 110 mmHg on two occasions at least occurring within the course of preeclampsia. Ec-
4 hours apart while the patient is on bed rest (unless antihyper-
tensive therapy is initiated before this time). lampsia generally spontaneously resolves within
 Thrombocytopenia (platelet count < 100 000/µL) approximately 60 sec, or within less than 3 to 4
 Impaired liver function as indicated by abnormally elevated blood min. Eclampsia has a recurrence rate of about 10%
concentrations of liver enzymes (to twice normal concentration),
severe persistent right upper quadrant or epigastric pain
with- out appropriate treatment.
unrespon- sive to medication and not accounted for by alternative HELLP is the acronym for Hemolysis, Elevated
diagnosis, or both. Liver enzymes, and Low Platelets count. It is a
 Progressive renal insufficiency (serum creatinine concentration
> 1.1 mg/dL or a doubling of the serum creatinine concentration
com- mon complication of severe preeclampsia
in the absence of other renal disease). (10- 20%). Even if HELLP should be suspected
 Pulmonary edema. when confronted with clinical signs such as
 New-onset cerebral or visual disturbances.
epigastric or RUQ pain, nausea, and vomiting, the
diagnosis of HELLP syndrome relies on laboratory
findings. These include microangiopathic
– severe and persistent right upper quadrant (RUQ) hemolysis with schizocytes, increased lactate
or epigastric pain not accounted for by any other dehydrogenase (LDH) (twice the normal value),
diagnosis, bilirubin > 1.2 mg/ dL, low haptoglobin, liver
– renal insufficiency defined as serum creatinine transaminases > twice the normal values, and
> 1.1 mg/dL or a doubling of serum creatinine in platelet count (PC)
the absence of other renal disease, < 100.000/µL (Table 3).
– massive proteinuria > 5 g/day, PRES is the acronym for Posterior Reversible En-
– pulmonary edema, cephalopathy Syndrome, and is commonly seen in
– new-onset cerebral or visual disturbances, patients with eclampsia.
– fetal growth restriction (FGR).

However, recent studies have demonstrated EPIDEMIOLOGY, MORBIDITY, AND MORTALITY ASSOCI-
minimal to no influence of the severity of protein- ATED WITH PREECLAMPSIA.
uria on pregnancy outcome in preeclampsia ; man-
agement of FGR is similar in pregnant women with Preeclampsia complicates 5 to 8% of all preg-
or without preeclampsia (4, 6). Therefore, massive nancies. This represents 8.5 million cases a year
proteinuria (> 5 g/day), and FGR are no longer cri- worldwide. This pathology remains one of the
teria of severe preeclampsia (Table 2). Diagnosing three leading causes of maternal death. The
severe preeclampsia is of paramount importance, majority of these maternal deaths are related to
insofar as it has a major impact on medical treat- cerebral hemor- rhage that is secondary to poorly
ment and timing of delivery as compared to pre- controlled hyper- tension (SBP > 160 mmHg) (1,
eclampsia without severe features. Recently, and 2). Renal failure, pulmonary edema, liver failure or
according to the dynamic character of rupture, seizures (eclampsia), disseminated
preeclampsia, the American College of intravascular coagulation (DIC), retinal
Obstetricians and Gynae- cologists (ACOG) has detachment, cortical blindness, ab- ruptio
discouraged the diagnosis of “mild preeclampsia”, placentae, and hemorrhage represent other
and proposed the diagnosis of “preeclampsia complications of preeclampsia. All contribute to
without severe features”. preeclampsia-associated maternal morbidity and
Gestational hypertension is defined as SBP mortality. Five percent of severe preeclamptic pa-
≥ 140 mmHg and/or DBP ≥ 90 mmHg after 20
ges- tation weeks in the absence of proteinuria, or
any of the aforementioned systemic findings, and
resolv- ing before 12 postpartum weeks. Table 3
Chronic hypertension corresponds to hyperten- Diagnosis criteria for HELLP syndrome
sion existing before pregnancy, or appearing
before 20 gestation weeks, and persisting more
than 12 postpartum weeks.
Superimposed preeclampsia is new-onset
protein- uria appearing after 20 gestation weeks in
a previ- ously hypertensive woman.
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 PREECLAMPSIA 141
Hemolysis •  lactate dehydrogenase > 600 UI/L
•  bilirubin level > 1.2 mg/dL
• schizocytes

Elevated liver transaminases •  twice normal value

• ASAT > 70 UI/L
Platelet count < 100 000/µL

© Acta Anæsthesiologica Belgica, 2014, 65, n° 4

142 G. LAMBERT et al.
tients are admitted to an ICU. Finally, The underlying mechanism of hypertension in
preeclampsia is known to increase the risk of preeclampsia remains somewhat controversial. Dif-
developing a cardio- vascular disease later in life
by a factor of 2.
Regarding the fetus and the neonate, pre-
eclampsia is responsible for 5% of stillbirths in
infants without congenital abnormalities, accounts
for 8-10% of the overall preterm birth rate, and for
15-20% of the overall FGR and very low birth
weight (VLBW) (7).

PATHOPHYSIOLOGY OF PREECLAMPSIA

a. Abnormal placental development

As opposed to normal pregnancy, preeclamp-

sia is characterized by an immunologically-
initiated impaired trophoblast invasion of the spiral
arteries between 8 and 16 gestation weeks. This
abnormal invasion of placenta nourishing arteries
leads to a failure of their remodeling. Failed
remodeling im- pairs the transformation of small
high resistance muscular arteries into large
capacitance vessels. Consequently, the utero-
placental blood flow pro- gressively fails to meet
the needs. Placental isch- emia ensues, with
oxidative stress, inflammation, apoptosis, and
structural damage (8).

b. Angiogenic imbalance

As a consequence of placental ischemia, sec-

ondary mediators are released. During normal
preg- nancy, placental growth factor (PlGF) and
vascular endothelial growth factors (VEGF) are
potent pro- angiogenic substances. They enhance
the vasodilat- ing properties of prostaglandins (PG)
and nitrous oxide (NO), and promote endothelial
health. In pre- eclampsia, several anti-angiogenic
factors are pro- duced. They are responsible for
angiogenic imbal- ance, impaired vasodilation and
an endothelial dysfunction. The soluble fms-like
tyrosinekinase (sFlt-1) antagonises VEGF and PlG.
Soluble endog- lin (sEng) antagonises TGF-β, and
blocks NO. This imbalance between pro and anti-
angiogenic factors produces generalized
endothelial dysfunction, mi- croangiopathy, and
vasospasm. These rise to the various signs and
symptoms of this multisystemic disease, which
become clinically evident after 20 gestation weeks
(8, 9).

c. Hemodynamic alterations in preeclampsia

© Acta Anæsthesiologica Belgica, 2014, 65, n° 4

 PREECLAMPSIA 143
ferent hemodynamic states have been described in may induce hy- pertensive encephalopathy, and
preeclamptic patients. These range from low vasogenic ede- ma (23, 24). Reversibility of
cardi- ac output (CO) with increased systemic neurologic signs and
vascular resistance (SVR) to a hyperdynamic state
with in- creased CO associated with an increased
stroke vol- ume and a moderate increase in SVR
(10-15). These different hemodynamic situations
might be related to the early or late onset of
preeclampsia, as well as to its severity (16). Use
of cardiac output, and not only blood pressure, as
an endpoint when treating severe preeclampsia
might improve the hemody- namic management
of these patients (17, 18). The routine use of
invasive hemodynamic monitor- ing (arterial
line, pulmonary artery catheter, or de- vices
estimating CO from the invasive arterial pres-
sure waveform such as LiDCO® (LiDCO Group
PLc, London, UK) PiCCO® (Pulsion Medical
Sys- tems, Munich, Germany), or Vigileo®
(Edwards Lifesciences, Irvine, CA, USA)) is not
common practice for preeclampsia management.
Invasive techniques estimating CO do not have
any proven benefits on maternal outcome, and
may be associ- ated with adverse events (19).
Echocardiography may provide useful
information but necessitates a trained operator,
and does not allow continuous measurement (20).
Recent non-invasive techniques based on pulse
wave analysis for continuous assess- ment of CO
and SVR might be associated with a better
hemodynamic management and a better risk/
benefit profile (17, 18, 21). Their impact on
overall outcome needs to be evaluated on a larger
scale.

d. Eclampsia

Eclampsia occurs in 0.5% of preeclamptic

pa- tients without severe features, and in 2-3% of
severe preeclampsia. This corresponds up to
10/10000 de- liveries in developed countries, and
up to 157/10000 deliveries in developing
countries (22). Eclamptic seizures contribute
substantially to maternal mor- bidity and
mortality. Several prodromal symptoms such as
severe headache, altered mental status, blurred
vision, and hyperreflexia with clonus may
precede the onset of seizures. However, in 40% of
eclampsia cases, no prodromal signs are present.
Two different pathophysiologic mechanisms may
underlie these neurologic symptoms. Vasospasm
associated with hypertension and cerebrovascular
overregulation might induce localized ischemia
and cytotoxic edema. Alternatively, loss of
cerebral au- toregulation, hyperperfusion, and
increased blood brain barrier (BBB) permeability
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 144 G. LAMBERT et al.
radiologic findings is in favor of the latter hypothe- or garlic), nor drugs such as pro- gesterone, nitric
sis. Radiologic findings have been described as the oxide donors, diuretics, or low mo-
posterior reversible encephalopathy syndrome
(PRES). A recent study has evidenced PRES in al-
most every eclamptic patient. Furthermore, PRES
has been identified in multiple areas of the brain in
a series of cases where severe hypertension was
not a constant feature (25, 26).

RISK FACTORS, PREDICTION AND PREVENTION OF PRE-

ECLAMPSIA

Several factors are associated with an in-

creased risk of preeclampsia : antiphospholipid
syn- drome (risk ratio (RR) : 9.72), past history of
pre- eclampsia (RR : 7.19), pregestational
diabetes (RR :3.56), multiple gestation (RR : 2.93),
nullipar- ity (RR : 2.91), family history of
preeclampsia (RR :2.90), body mass index (BMI)
> 30 before pregnancy (RR : 2.47), age ≥ 40 years
(RR :1.96), pre-existing hypertension (RR : 1.5),
pre-existing renal disease, and pregnancy interval >
10 years (27, 28). Use of risk factors as predictive
tools for pre- eclampsia has only modest success.
Biomarkers of preeclampsia and its severity have
also been pro- posed (8, 29). Placental expression
and serum levels of sFlt-1 in preeclamptic women
are increased dur- ing active disease, as compared
with normal preg- nancy. Serum levels of sFlt-1
are directly correlated with the severity of the
disease. PlGF is low during preeclampsia. This is
due to its binding to sFlt-1. A plasma sFlt-1/PlGF
ratio ≥ 85 is associated with ad- verse outcomes
and delivery within two weeks of presentation
(30). The sFlt-1/PlGF ratio could allow classifying
the severity of the disease. Similarly, B- natriuretic
peptide has been suggested as a marker of
preeclampsia. Preeclamptic patients have higher
levels of natriuretic peptide than non preeclamptic
patients. Larger prospective studies are needed to
determine if elevated concentrations predict devel-
opment of preeclampsia and its complications (31).
Up to now, the use of these biomarkers as parts of
a screening test remains investigational.
Women at high risk of preeclampsia should
re-
ceive low dose aspirin daily from gestation week
12 to 37. Its prophylactic effect may be the result
of the inhibition of thromboxane production.
Studies indi- cate a small reduction in the
incidence and morbid- ity of preeclampsia, with no
difference in bleeding complication rates.
Conversely, neither nutritional supplements (such
as calcium, folic acid, vitamins C and E, fish oils,
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 PREECLAMPSIA 145
lecular weight heparin (LMWH) have shown Antihypertensive treatment re- mains controversial
effi- cacy at preventing preeclampsia. in patients with mild to moder- ate hypertension
Restriction of dietary salt and restriction of (33). Prevention of eclampsia with MgSO4 is not
physical activity in addition to bed rest during recommended in preeclamptic pa-
pregnancy have no effect on preeclampsia
prevention (4). Statins, by stimu- lating
hemoxygenase expression, inhibit sFlt-1 re-
lease and promote VEGF. Studies to explore a
pos- sible benefit of statins are currently being
carried out (9).

MANAGEMENT OF PREECLAMPSIA

The only etiologic treatment of

preeclampsia is fetus and placenta delivery.
Timing of delivery must take into account the
gestational age, severity of preeclampsia, as well
as maternal and fetal con- ditions. Current
treatments aim at avoiding maternal
complications such as cerebral hemorrhage,
pulmo- nary edema, and eclampsia. Treatment is
essentially based on antihypertensive therapy
and magnesium sulfate (MgSO4).
During the last 6 years, guidelines aiming
at improving outcome of women with
preeclampsia have been published by several
scientific societies. They provide a robust
common basis with minor between-societies
differences (4, 6, 7, 27, 32).
At the time of diagnosis, the initial
objective is to assess the severity of the disease.
In addition to blood pressure and proteinuria
measurement and re- cording, clinical signs of
severity must be searched for. Neurological
symptoms such as headache, blurred vision, or
altered mental status must be con- sidered, as
well as epigastric pain or RUQ pain, nausea
and vomiting, oliguria, and dyspnea. Labo-
ratory evaluation must assess platelet count,
schizo- cytes count, serum creatinine, liver
transaminases, bilirubin, LDH, haptoglobin, and
coagulation tests. Fetal assessment relies on fetal
heart rate, fetal weight, amniotic fluid volume,
biophysical profile,
and umbilical artery Doppler velocimetry.

a. Management of preeclampsia without severe

features

Recommendations for the management of

pre- eclampsia without severe features before 37
weeks of gestation are mainly based on expert
opinion. Fluorinated steroids should be
administered in pa- tients before 34 weeks of
gestation, in order to favor fetal maturation.
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
146 G. LAMBERT et al.
tients with no severe features. Bed rest does not end-diastolic flow in the umbilical artery as assessed
im- prove outcome. Preeclamptic patients with no by Doppler ultrasound, new-onset or increasing re-
se- vere features should be closely monitored.
Monitoring includes several evaluations of
maternal condition and fetal well-being. Maternal
condition is assessed through inventory of clinical
symptoms, at least twice weekly. Blood pressure
should be measured frequently, and lab tests
should be per- formed weekly, including platelet
count and liver enzyme levels. Fetal well-being
should be assessed daily by the mother herself
(screening of fetal move- ments), fetal heart rate
monitoring, at least twice a week, and ultrasound
scanning to evaluate amniotic fluid volume, fetal
growth, and umbilical artery ve- locimetry.

b. Management of severe preeclampsia

Women with severe preeclampsia must be ad-

mitted to a maternal high dependency unit, a labor
and delivery ward, or a regular intensive care unit.
Severe preeclampsia is an indication for
prompt delivery in women with gestational age
above 34 weeks. Before 24 weeks, it is
recommend- ed to terminate the pregnancy
immediately. In women with severe preeclampsia
between 24 and 34 weeks, steroids are
recommended to favor fetal maturation. In that
case, delivery must be delayed for 48 hours,
whenever possible.
In selected women who are cared for in spe-
cialized units, expectant management of
preeclamp- sia can be considered. Expectant
management in- cludes antihypertensive treatment
in patients with severe hypertension, and MgSO4
to prevent eclamp- tic seizures.
However, it must be kept in mind that, while
expectant management of severe preeclampsia im-
proves neonatal outcome, it is not associated with
any benefit to the future mother.
Delaying delivery in women with severe pre-
eclampsia can be associated with several complica-
tions such as ICU admission (27.6%), HELLP syn-
drome (11%), recurrent severe hypertension
(8.5%),
pulmonary edema (2.9%), eclampsia (1.1%), and
sub-capsular hematoma of the liver (0.5%).
Regard- ing fetal and neonatal complications,
delaying de- livery can lead to non-reassuring fetal
heart rate (50%), fetal growth retardation
(37%), prenatal
death (7.3%) and/or abruptio placentae (5.1%)
(34). Contra-indications to expectant management
beyond 48 hours include fetal growth retardation
(< 5th percentile), severe oligohydramnios, reverse
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 PREECLAMPSIA 147
nal dysfunction, liver disease, coagulation disor- agreement exists on the need to avoid precipitous
ders, preterm rupture of membranes (PROM), and decreases in blood pressure, which could affect
preterm labor. ute- ro-placental blood flow. A decrease of
In case of uncontrollable severe 10 to
hypertension, eclampsia, pulmonary edema,
disseminated intra- vascular coagulation, abruptio
placentae, non-reas- suring fetal status, or fetal
demise, it is recommend- ed to proceed to
delivery as soon as possible after maternal
stabilization.
Expectant management of severe preeclamp-
sia can be considered in pregnancy between 24
and 34 gestation weeks, with controlled
hypertension, moderately and transiently
abnormal lab tests and fetal weight above the 5th
percentile.

c. Antihypertensive treatment in preeclampsia

Antihypertensive therapy of non-severe hyper-

tension : a controversy
The purpose of treating severe hypertension
is to prevent complications such as intracranial
hem- orrhage, hypertensive encephalopathy, and
pulmo- nary edema. There is no worldwide
consensus re- garding the management of non-
severe hypertension, insofar as the evidence of an
improvement of mater- nal and neonatal outcome
by treatment is lack- ing (33). Society of
Obstetric Medicine of Australia and New Zealand
(SOMANZ) guidelines consider that
antihypertensive treatment can be initiated when
blood pressure ranges from 140/160 mmHg SBP
and/or 90/100 mmHg DBP (27). National In-
stitute for Health and Clinical Excellence (NICE)
guidelines recommend treating hypertension
when SBP > 150 mmHg and DBP > 100 mmHg
(7), and the last ACOG task force report on
hypertension in pregnancy recommend treating
women with SBP
≥ 160 mm Hg or DBP ≥ 110 mm Hg (4). In 2010,
a Cochrane review concluded that the benefit of
treat- ing mild to moderate hypertension was
unclear (33). Oral labetalol, nifedipine or
nicardipine, methyldo- pa, and clonidine can be
used for the treatment of non-severe hypertension
(Table 4). Angiotensin- converting-enzyme
(ACE)-inhibitors and angioten- sin receptor (AR)-
blockers are contraindicated.

Antihypertensive therapy of severe hypertension

Treatment is recommended for SBP
≥ 160 mmHg and/or DBP ≥ 110 mmHg with a
target between 130 and 150 mmHg for SBP, and
between 80 and 100 mmHg for DBP (7). General
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 148 G. LAMBERT et al.
Table 4
Example of oral antihypertensive agents
Drug Dose Action Contra-indications Secondary effects
Labetalol 200-1200 mg/d in two to three β-blocker with vascular Asthma Bradycardia, bronchospasm,
divided doses α-receptor blocking ability headache, nausea
Nifedipine 20-120 mg/d of a slow release Calcium channel antagonist Aortic stenosis Headache, flushing, tachycardia
preparation
Nicardipine 60 mg/d in three divided doses Calcium channel antagonist Aortic stenosis Headache, flushing, tachycardia
Clonidine 225-450 µg/d in three divided α2-agonist Dry mouth, sedation, bradycardia
doses
Methyldopa 0.5-3 g/d in two to three divided α2-agonist Dry mouth, sedation, bradycardia
doses

20 mmHg every 10 to 20 min has been suggested postpartum hours. A rise

by some authors (35). The most frequently recom-
mended medications for the treatment of severe
hypertension during pregnancy are hydralazine,
labetalol, calcium channel blockers and clonidine
(Table 5).
Among antihypertensive medications that are
considered to be safe in this context, no evidence
supports one drug over another. Consequently,
choice should be based on the clinician’s
experience and available resources. However,
nitroprusside, di- azoxide, ketanserin,
chlorpromazine should be avoided. MgSO4 is not
considered as an effective treatment for very high
blood pressure (although this is indicated for
prevention and treatment of eclampsia) (36).

d. Management of HELLP syndrome

Corticosteroid administration to favor fetal

maturation reverses HELLP-associated laboratory
abnormalities in subgroup of patients, and might
prolong pregnancy for 3-14 days. However, there
is no evidence for a maternal or perinatal
corticoste- roid-related improved outcome.
Expectant manage- ment of HELLP syndrome
beyond 48 hours remains an experimental
approach, and is not recommend- ed (37). Medical
treatment of HELLP syndrome re- lies on
antihypertensive treatment and MgSO4. Platelet
transfusion should be considered if PC falls below
20.000/µL, in case of bleeding, and to achieve a
PC of 40-50.000/µL in case of caesarean sec-
tion (6). Randomized controlled trials have provid-
ed evidence of improvement in platelet count with
corticosteroids, but no improved overall maternal
outcome. In clinical settings where an
improvement of platelet count is considered useful,
corticoste- roids could be used (38). Worsening of
hemolysis, thrombocytopenia, and liver
dysfunction is com- mon during the first 24-48
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 PREECLAMPSIA 149
in PC > 100.000/µL usually occurs at day 3 post
nadir, or day 6 postpartum.

e. Prevention and management of eclampsia

Treatment of eclamptic seizures consists in

the administration of MgSO4 (Table 6), and in
the treat- ment of hypertension (Table 5). The
Collaborative Eclampsia Trial showed a 67%
reduction of recur- rent seizures in eclamptic
women treated with MgSO4, as compared with
those treated by phenyt- oin. There was a 52%
reduction in recurrence as compared to
diazepam. For women with eclampsia, MgSO4
should be continued for at least 24 hours after
the last seizure (39).
Delivery is the only curative treatment. So
far, any other treatment is palliative. Expectant
manage- ment of eclampsia to prolong gestation
for fetal benefit is associated with a substantial
increase in maternal and perinatal morbidity and
mortality. De- laying delivery for 24-48 hours in
order to allow the administration of
corticosteroids prior to 34 gesta- tion weeks has
been reported in one retrospective study, but the
safety of such an approach has not been proved.
Induction of labor is sometimes pos- sible after
maternal stabilization, and in case of an expected
delivery within 24 hours. Cesarean section can
be considered before 32 gestation weeks, or in
case of unfavorable cervix. MgSO4 is the corner-
stone of the prevention and treatment of
eclampsia. Its use is associated with a 50%
reduction of ec- lampsia episodes in severe
preeclampsia. It also re- duces the risk of
maternal death. The number need- ed to treat
(NNT) to observe 1 beneficial effect is 50 for
severe preeclampsia patients, whereas it rises to
100 for patients with preeclampsia without
severe features (40). In case of severe
preeclampsia arising in the postpartum period,
the administration of MgSO4 is also
recommended for at least 24 hours. The effect of
MgSO4 is likely multifactorial, includ-

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150 G. LAMBERT et al.
Table 5
Antihypertensive agents used for severe hypertension treatment
Drug Dose Action Contra-indications Secondary effects
Labetalol IV 20 mg/10 min + 5-20 mg/h β-blocker with vascular Asthma Bradycardia, bronchospasm,
α-receptor blocking ability headache, nausea
Hydralazine IV 5 mg/20 min + 0.5-10 mg/h Vasodilator Flushing, headache, nausea
Nifedipine PO 10 mg/ 30 min Calcium channel antagonist Aortic stenosis Headache, flushing, tachycardia
Nicardipine IV 0.5 mg + 1-5 mg/h Calcium channel antagonist Aortic stenosis Headache, flushing, tachycardia
Clonidine IV 15-40 µg/h α2-agonist Dry mouth, sedation

Table 6 volume, submitting

Rules for the administration of magnesium sulfate
 Loading dose : 4-6 g over 30 minutes
 Infusion : 1-2 g/hour for 24 hours
 If recurrent seizure, 2-4 g over 5 minutes

ing both vascular and neurological mechanisms.

Magnesium is a calcium antagonist and induces
va- sodilation. In addition, MgSO4 may decrease
blood brain barrier (BBB) permeability and limit
vasogen- ic edema (41). In addition, MgSO4 has
anticonvul- sant properties, which may be related
to its N-meth- yl-D-aspartate (NMDA) glutamate
receptor antagonist activity. The adverse effects of
MgSO4 consist in flushing, palpitations, nausea,
vomiting, sedation, respiratory depression, and
cardiac ar- rest (42). These side effects follow a
dose-response relationship and occur more
frequently in patients with impaired renal function.
Close monitoring of the patellar reflex, oxygen
saturation, respiration rate, urine output, blood
pressure, heart rate and level of consciousness is
recommended to detect toxicity. Routine serum
magnesium measurement is not necessary. In case
of toxicity, calcium gluconate administration is
recommended (1g over 10 min- utes). MgSO4 must
be continued during labor or C- section, and during
the first 24 postpartum hours. Despite theoretical
concerns about potential syner- gistic cardiac
depression, the simultaneous adminis- tration of
MgSO4 with calcium channel blockers is not
contraindicated (43).

f. Fluid management

Pulmonary edema is a potential complication

of preeclampsia. Decreased colloid osmotic pres-
sure, increased capillary permeability, increased
hy- drostatic pressure, and cardiac diastolic
dysfunction may all contribute to this complication
(11, 44, 45). Preeclampsia is also regarded as a
hemodynamic state of depleted intravascular

© Acta Anæsthesiologica Belgica, 2014, 65, n° 4

 PREECLAMPSIA 151
the patient to a higher risk of renal failure. The in-
travenous administration of fluids to increase
plas- ma volume or to improve renal perfusion is
not rec- ommended in women with normal renal
function. In case of oliguria, variable invasive
monitoring has been proposed to guide fluid
therapy. This invasive monitoring may be
associated with several compli- cations.
Echocardiography and pulmonary ultra- sound,
allowing interstitial fluid imaging (B lines), may
provide useful information to guide fluid ther- apy
in this situation, where the risk of renal failure
must be balanced against the risk of
pulmonary edema.

g. Timing of delivery

For women with chronic hypertension and

no additional maternal or fetal complications,
delivery before 38 0/7 gestation weeks is not
recommended.
For women with mild gestational
hypertension or preeclampsia without severe
features, and no other indication for delivery,
expectant manage- ment with maternal and fetal
monitoring is suggest- ed until the 37 0/7
gestation week. At or beyond 37 0/7 WG,
delivery rather than continued observation is
suggested. Delivery should be planned within 24-
48 hours.
In case of severe preeclampsia at or beyond
34 0/7 gestation weeks, and in case of unstable
mater- nal or fetal conditions, irrespective of
gestational age, delivery is recommended soon
after maternal stabilization. In case of severe
preeclampsia before fetal viability (24 gestation
weeks), delivery after maternal stabilization
should be performed. In that case, expectant
management should not even be considered.
When gestation is less than 34 0/7, with stable
maternal and fetal conditions, expectant man-
agement can only be undertaken at facilities with
adequate maternal and neonatal intensive care re-
sources. In any case, for women with
preeclampsia, a decision of delivery should not be
based on the amount or change in the amount of
proteinuria.

© Acta Anæsthesiologica Belgica, 2014, 65, n° 4

 152 G. LAMBERT et al.
HELLP syndrome before fetal viability is an in the absence of other coagulation abnormalities is
indication of delivery, shortly after maternal
stabili- zation. When those patients are at or
beyond 34 ges- tation weeks, it is recommended to
proceed to deliv- ery soon after initial maternal
stabilization. In between gestational age of fetal
viability and 33 6/7 gestation weeks, it is suggested
to delay delivery for 24-48 hours, but only if
maternal and fetal condi- tions remain stable and
allow completing a course of corticosteroids for
fetal benefits.

h. Mode of delivery

For women with preeclampsia, the mode of

delivery should be determined by the fetal gesta-
tional age, fetal presentation, cervical status, and
maternal and fetal condition. Caesarean delivery is
therefore not mandatory. Cervix ripening with in-
duction of labor should be considered when possi-
ble. After 32 gestation weeks, a 60% vaginal birth
rate is achievable (46).

ANESTHESIA AND ANALGESIA FOR THE PREECLAMPTIC

PARTURIENT

a. Coagulopathy and regional techniques

The risk of spinal hematoma associated with a

coagulopathy has always been a concern in pre-
eclamptic women. Preeclampsia is associated with
an increased incidence of thrombocytopenia, and
potentially other coagulation abnormalities. On the
other hand, spinal hematoma is less frequent in
par- turient women as compared to the general
popula- tion. The very few cases reported in
obstetrics are associated with HELLP syndrome
(47). Several studies have addressed the incidence
of thrombocy- topenia and coagulopathy in
preeclampsia, and demonstrate a maximal 10%
incidence of thrombo- cytopenia (< 100.000/µL) in
preeclamptic patients. Increase in prothrombin
time (PT), partial thrombo- plastin time (PTT), or
decreased fibrinogen have only been described in
severe preeclampsia associ- ated with a
thrombocytopenia below 100.000/µL. These data
lead to the conclusion that, in preeclamp- sia, the
sole monitoring of platelet count, and re- serving
PT, PTT and fibrinogen monitoring for pa- tients
with thrombocytopenia, is a safe policy (48, 49).
Guidelines suggest that monitoring platelet count
in preeclamptic patients (as opposed to nor- mal
pregnancy) reduces maternal anesthesia com-
plications (50). A stable platelet count > 75.000/µL
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
 PREECLAMPSIA 153
usually considered safe for neuraxial techniques. cesarean de- livery. General anesthesia may lead to
Some authors consider a platelet count of several diffi- culties. Intubation can be complicated
50.000/ µL as acceptable for spinal anesthesia by airway edema, while a severe hypertensive
(32). response may

b. Neuraxial analgesia for labor

Unless contraindicated, preeclampsia is

con- sidered to be a medical indication for
epidural or combined spinal epidural analgesia
(CSE) during labor. These techniques not only
provide optimal analgesia, but also give better
maternal hemo- dynamic control. In addition, an
in situ epidural catheter during labor may avoid
the risks associated with general anesthesia,
should an emergency cesarean section become
necessary during labor.

c. Neuraxial anesthesia for cesarean delivery

Unless contraindicated, neuraxial

anesthesia is the technique of choice for
cesarean delivery. Neur- axial anesthesia
provides satisfactory hemodynamic stability, and
avoids the risks associated with gen- eral
anesthesia in preeclamptic patients. These risks
include the potential presence of a difficult
airway, and severe hypertension associated with
tracheal intubation. For many years, the fear of
profound hypotension caused by the sympathetic
blockade in patients with increased vascular
resistance and depleted intravascular volume
precluded the use of spinal anesthesia, and
favored the use of epidural anesthesia. However,
numerous studies have dem- onstrated that
spinal anesthesia in preeclamptic women is
associated with less hypotension, less
vasopressor requirement, and minimal changes
in CO (51-53). It has also been demonstrated
that re- gional anesthesia for cesarean section in
preeclamp- tic women is associated with a two
times higher stroke-free survival rate, as
compared to general anesthesia (54). Therefore,
spinal anesthesia can be safely used in this
population (55). Combined spi- nal-epidural
anesthesia is also an appropriate tech- nique for
these patients (56). Epidural anesthesia is the
technique of choice when a cesarean section is
required during labor under epidural analgesia.

d. General anesthesia for cesarean section

In case of contraindications to neuraxial

anesthesia (i.e. pulmonary edema, coagulopathy,
al- tered consciousness following eclamptic
seizures), general anesthesia may be required for
© Acta Anæsthesiologica Belgica, 2014, 65, n° 4
154 G. LAMBERT et al.
result from laryngoscopy and tracheal intubation. feeding. Conversely, clonidine is best avoided in
Opioids (remifentanil, fentanyl, sufentanil) must be the nursing mother. The use of methyldopa is con-
used in combination with antihypertensive drugs troversial during that period (Table 7). The choice
(labetalol, esmolol, MgSO4) in order to blunt the of the antihypertensive agent should be based on
blood pressure response to this noxious stimula- the clinician’s familiarity with the drug. The use of
tion (27). For women treated with MgSO4, fu- rosemide may decrease the need for other
monitor- ing neuromuscular blockade is necessary, antihy- pertensive therapy, but more data are
insofar as MgSO4 potentiates and prolongs the necessary be- fore recommending this treatment
effects of non- depolarizing muscle relaxants. (63). When blood pressure is adequately controlled
for at least 48 h, medication can be reduced
e. Uterotonic agents in preeclampsia. progressively. Resolu- tion may take several
weeks. During the postpartum period, non-steroidal
For patients with preeclampsia, slow adminis- anti-inflammatory drugs should be avoided.
tration of 3 IU of oxytocin is recommended as the
first line uterotonic measure. It must be followed b. Thromboprophylaxis
by an infusion at the lowest effective rate, in order
to avoid acute vasodilation, tachycardia, increased Preeclampsia is a risk factor for thrombosis,
cardiac output, and fluid retention (antidiuretic particularly if additional risk factors are present
hor- mone (ADH) effect) (57-59). Carbetocin is (BMI > 30, age > 35, multiparity). Unless contrain-
associ- ated with the same side effects as oxytocin dicated, postpartum thromboprophylaxis with low
(60). Given its vasoconstrictive effects, molecular weight heparins should be given,
ergometrine is usually considered to be contra- particu- larly in case of antenatal bed rest for more
indicated in pre- eclampsia (61). than four days, or after caesarean section (6, 27).

c. Medical follow-up
MANAGEMENT DURING THE POSTPARTUM PERIOD
Women with a history of preeclampsia or
a. Management of postpartum hypertension eclampsia are at higher risk (approximately two-
fold) of early cardiac, cerebrovascular, peripheral
In women with preeclampsia, blood pressure arterial disease, and cardiovascular mortality (64).
usually decreases within 48 hours after, but may For women with a history of preeclampsia, yearly
rise again after 3-6 postpartum days. Preeclampsia assessment of blood pressure, lipids, fasting blood
may also appear up to 4 weeks after delivery. It is glucose, and body mass index is suggested (4).
therefore recommended to closely follow blood
pressure after delivery (62). Antihypertensive treat-
ment is suggested if SBP remains above 150 CONCLUSION
mmHg and/or DBP persists above 100 mmHg, on
at least two occasions at least 4-6 hours apart. Preeclampsia remains a leading cause of ma-
Persistent SBP of 160 mmHg or DBP of 110 ternal and fetal morbidity and mortality. Despite a
mmHg or higher should be treated within 1 hour. better understanding of the pathophysiologic mech-
As opposed to dur- ing pregnancy, some ACE- anisms underlying the disease, the only curative
inhibitors (captopril and enalapril) are considered treatment is delivery. Medical treatment does not
to be safe during breast-

Table 7
Example of treatment of postpartum hypertension
Drug Dose Action Contra-indications Secondary effects
Nifedipine 20-120 mg/d Calcium channel antagonist Aortic stenosis Headache, flushing, tachycardia
Oral labetalol 200-1200 mgL/d in two or β-blocker with vascular Asthma Bradycardia, bronchospasm,
three didvides doses α-receptor blocking abiblty headache, nausea
Propanolol 120-240 mg/d in three β-blocker Asthma Bradycardia, bronchospasm, nausea
divided doses
Captopril 50 mg/d in two divided ACE inhibitor Pregnancy, renal artery Hyperkaliemia, angioneurotic
doses stenosis edema, reduced lactation?

© Acta Anæsthesiologica Belgica, 2014, 65, n° 4

 PREECLAMPSIA 155
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