AACN Advanced Critical Care
Volume 29, Number 3, pp 316-326
Preeclampsia: Acute Complications
and Management Priorities
Patricia M. Witcher, MSN, RNC-OB
ABSTRACT
Acute complications of preeclampsia con-
tribute substantially to maternal and fetal
morbidity and mortality. The considerable
variation in onset, clinical presentation, and
severity of this hypertensive disease that is
unique to pregnancy creates challenges in
identifying risk factors for clinical deteriora-
tion. Delivery of the fetus remains the only
definitive treatment for preeclampsia. Sur-
veillance of signs and symptoms and labora-
tory parameters consistent with progression
P reeclampsia is a multisystem disease
unique to pregnancy that complicates
3% to 8% of all pregnancies.1-3 The incidence
of this disease has increased by 25% in the
past 20 years, and hospitalization for the
condition is associated with substantial risk
for maternal and fetal morbidity and mor-
tality.4,5 Traditionally, preeclampsia is diag-
nosed by the presence of both hypertension
and proteinuria; however, multisystem involve-
ment in the absence of proteinuria also ful-
fills the criteria for diagnosis. The clinical
course of preeclampsia can lead to sudden
deterioration, which warrants vigilant surveil-
lance for onset of severe features.6,7 In the
United States, up to 30% of maternal deaths
during hospitalization for childbirth are attrib-
uted to complications from preeclampsia.8
Many of these deaths could have been pre-
vented through timely and appropriate inter-
ventions, including surveillance for clinical
manifestations that indicate progression in
severity and appropriate timing of delivery.9
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© 2018 AACN
in severity requires an appreciation of the
dynamic and progressive nature of the dis-
ease. This article provides a comprehensive
overview of the pathophysiology of preec-
lampsia, setting the foundation for discus-
sion of management priorities for acute
complications that pose the greatest risks to
maternal health.
Keywords: preeclampsia, hypertensive disor-
ders of pregnancy, maternal mortality, mater-
nal morbidity, pregnancy-induced hypertension
Stabilizing interventions should be guided by
a thorough understanding of the pathophysi-
ology of the disease.
Hypertensive Disorders
During Pregnancy
Hypertension during pregnancy encompasses
a broad continuum of acute and chronic dis-
ease processes with significant variation in clini-
cal presentation. During pregnancy, hypertensive
disorders are categorized based on the timing
of symptom onset before or during the preg-
nancy and the cause of the disorder. Hyper-
tensive disorders of pregnancy include the
following diagnoses: chronic hypertension,
gestational hypertension, preeclampsia, and
Patricia M. Witcher is Clinical Outcomes Manager, Women’s
Services, Northside Hospital, 1000 Johnson Ferry Road,
Atlanta, GA 30342 (trish.witcher@northside.com).
The author declares no conflicts of interest.
DOI: https://dx.doi.org/10.4037/aacnacc2018710
VO L U M E 2 9 • N U M B E R 3 • FA L L 2 018 PREECLAMPSIA

Table 1: Diagnostic Criteria for Hypertensive Disorders in Pregnancy

Preeclampsia
• New-onset hypertension after 20 weeksʼ gestation (systolic blood pressure 140 mm Hg or diastolic blood
pressure > 90 mm Hg on at least 2 occasions, 4 hours apart)
Plus
• Proteinuria ( 300 mg of protein in a 24-hour urine specimen, or protein-to-creatinine ratio of 0.3 mg/dL)
Or (in the absence of proteinuria)
• Thrombocytopenia (platelets < 100 000 per microliter)
• Impaired liver function (increased serum transaminases twice their normal value)
• New-onset renal insufficiency (serum creatinine > 1.1 mg/dL or doubling of serum creatinine)
• Pulmonary edema
• New-onset cerebral or visual disturbance
Gestational hypertension
• New onset of hypertension after 20 weeksʼ gestation
• Absence of proteinuria
• Absence of multisystem disturbances consistent with preeclampsia
Chronic hypertension
• Preexisting hypertension (before pregnancy)
• Onset of hypertension before 20 weeksʼ gestation
• Hypertension that persists after postpartum period
Chronic hypertension with superimposed preeclampsia
• Fulfills the diagnostic criteria for chronic hypertension
• Preeclampsia
Severe Features of Preeclampsiaa
• Systolic BP > 160 mm Hg, on at least 2 occasions, 4 hours apartb
• Diastolic BP > 110 mm Hg, on at least 2 occasions, 4 hours apartb
• Thrombocytopenia (platelets < 100 000 per microliter)
• Impaired liver function (increased serum transaminases twice their normal value)
• New-onset renal insufficiency (serum creatinine > 1.1 mg/dL or doubling of serum creatinine)
• Pulmonary edema
• New-onset cerebral or visual disturbance
Abbreviation: BP, blood pressure.
a
To be a severe form of disease, only one of the features must be present.
b
Antihypertensive therapy should be initiated for acute, severe hypertension before the criteria for diagnosis are met.

chronic hypertension with superimposed pre-
eclampsia. The classification schema is sum-
marized in Table 1.6
Chronic hypertension is defined as hyper-
tension that precedes pregnancy or has an
onset before the 20th week of pregnancy.
Hypertension that persists after the postpar-
tum period also fulfills the criteria for chronic
hypertension. Gestational hypertension or
preeclampsia is diagnosed when new onset
of hypertension occurs after 20 weeks of
gestation. Gestational hypertension is differ-
entiated from preeclampsia by the absence
of new-onset proteinuria and organ system
involvement from ischemia. Preeclampsia that
complicates chronic hypertension is classified
as superimposed preeclampsia.6
Physiologic adaptations of the cardiovascu-
lar system directed at meeting the increased
metabolic demands of pregnancy constitute a
significant physiologic stressor that may reveal
a preexisting condition that was not evident
before pregnancy.10,11 Furthermore, transient
elevations in blood pressure are common in
the postpartum period because of volume
redistribution, alterations in vascular tone,
or administration of intravenous crystalloid
fluid or nonsteroidal anti-inflammatory medi-
cations.12 Therefore, distinguishing chronic
hypertension from gestational hypertension
often is difficult when the onset of hyperten-
sion occurs during pregnancy or after deliv-
ery without prior history. Differentiating organ
system consequences of chronic hypertension
(eg, renal insufficiency) from superimposed pre-
eclampsia can also be challenging. The prog-
nosis for the woman and for the fetus is worse
with superimposed preeclampsia than when
hypertension presents alone, which supports
an erroneous diagnosis of superimposed pre-
eclampsia when the underlying cause of organ
system dysfunction is unclear. Hypertensive

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disorders of pregnancy typically progress in
severity as gestation advances. Gestational
hypertension can progress to preeclampsia
within days to weeks, and preeclampsia may
manifest with severe features quickly. Appro-
priate management requires an understanding
of the syndromic nature and pathophysiology
of the disease.6
Pathophysiology
Although the precise mechanism is unknown,
preeclampsia is believed to originate from a
complex interaction of maladaptive cardio-
vascular and uteroplacental responses to
pregnancy.10,11,13-16 In normal pregnancy, ade-
quate uteroplacental perfusion depends on
normal physiologic development of the pla-
cental vascular system through trophoblast
invasion of the uterine spiral arteries. The
placental vasculature is subsequently con-
verted into a dilated, low-resistance system,
through a process termed angiogenesis.11,17-19
Early in pregnancy, the placenta develops
under low oxygen tension. As the placenta
matures and maternal blood invades the
uterine spiral arteries, oxygen tension
increases, generating oxygen free radicals
and initiation of lipid peroxidation. Fortu-
nately, antioxidants are upregulated to pre-
vent oxidative damage.19
In preeclampsia, trophoblast invasion of
uterine spiral arteries is shallow, which pro-
hibits dilation of the uterine spiral arteries.
The placenta is inadequately perfused as a
result of the high-resistance state in the pla-
cental vasculature.2,5,10,13,15,20,21 Reduced utero-
placental perfusion likely generates oxygen
free radicals in the intervillous space, and
placental ischemia is further exacerbated by
diminished antioxidant activity.19,22 Leukocyte
adhesion to the endothelium and resultant
neutrophil activation may contribute to vascu-
lar injury and endothelial damage.23 Placental
ischemia leads to the release of inflammatory
and antiangiogenic factors into the systemic
circulation, perpetuating widespread endo-
thelial dysfunction and decreased end-organ
perfusion.4,5,20,24 Antiangiogenic proteins, such
as soluble fms-like tyrosine kinase 1 (sFlt-1)
and soluble endoglin (sEng), antagonize pro-
angiogenic proteins, such as vascular endo-
thelial growth factor and placental growth
factor.6,13-15,25,26 Increased circulating levels of
sFlt-1 and sEng and decreased placental growth
factor and vascular endothelial growth factor
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W W W. A AC N AC C O N L I N E . O R G
levels precede the development of preeclampsia
by weeks to months.6,13
Pathophysiologic consequences of decreased
end-organ perfusion may be revealed through
derangements in one or multiple organ sys-
tems. Clinical manifestations of underlying
organ system abnormalities that arise from
placental ischemia and endothelial vascular
damage are not unique to preeclampsia.15
Overexpression of the antiangiogenic proteins
sFlt-1 and sEng has an increased association
with endothelial dysfunction, myocardial dys-
function, and other adverse cardiovascular
outcomes in the general population.11,14 Endo-
thelial dysfunction plays a significant role in
the pathophysiology of coronary artery dis-
ease, as with preeclampsia. The acute athero-
sis of the placental vasculature in pregnancies
complicated by preeclampsia is similar to ath-
erosclerosis.6,15 Therefore, it is unclear whether
antiangiogenic proteins cause endothelial dam-
age and myocardial dysfunction in preeclamp-
sia or reflect cardiac dysfunction that becomes
evident with failure of cardiovascular system
adaptations directed at meeting the increased
metabolic demands of pregnancy.16,27
Perhaps the most significant cardiovascular
physiologic adaptation in normal pregnancy
is an increase in cardiac output, largely as a
result of intravascular volume expansion.10,28,29
Increased vascular compliance and decreased
systemic vascular resistance (SVR) accommo-
date the expanded intravascular volume and
contribute to uteroplacental blood flow and
increased maternal end-organ perfusion.28,30
Investigative reports on hemodynamic findings
in preeclampsia using invasive and noninvasive
technology demonstrate large variability in
hemodynamic profiles.31-36 Hemodynamic pro-
files range from elevated cardiac output with
decreased SVR to normal or decreased cardiac
output with increased SVR.37,38
Different hemodynamic profiles in pre-
eclampsia have been hypothesized to arise
on the basis of the timing of disease onset.35,38,39
Early-onset preeclampsia (before 34 weeks’
gestation) typically is associated with elevated
placental vascular resistance from poor pla-
cental implantation and widespread endothelial
dysfunction as previously described.19,35,38,40
Cardiac output is low with elevated SVR.41
Increased capillary permeability from endo-
thelial injury promotes a shift of fluids from
the intravascular compartment to the inter-
stitium, decreasing intravascular volume and
VO L U M E 2 9 • N U M B E R 3 • FA L L 2 018
cardiac output.42 Late-onset preeclampsia
(after 34 weeks’ gestation) is associated with
predisposing cardiovascular or metabolic risk
factors. In this preeclampsia subset, the hemo-
dynamic profile varies from normal cardiac
output with increased SVR to high cardiac
output with low SVR secondary to compen-
satory vasodilation to accommodate increased
blood flow.38,39 Some women may be unable
to accommodate intravascular volume expan-
sion of pregnancy without developing hyper-
tension.30 Autonomic adaptive response may
fail with progression of the disease process or
impaired baseline cardiovascular function.10,43
As a result, these women may develop fluid
volume overload.10
Whether preeclampsia predisposes women
to cardiovascular disease or manifests in
women with a predisposition to cardiovascu-
lar disease is unclear.24,38 Early-onset preeclamp-
sia increases the risk of stroke 5-fold compared
with later-onset preeclampsia, suggesting an
accelerated course to severe cardiovascular
and cerebrovascular disease from endothelial
dysfunction.12 Despite normalization of blood
pressure typically by the sixth week postpar-
tum, cardiac changes do not revert to the
prepregnancy state.4 Asymptomatic left ven-
tricular cardiac dysfunction or hypertrophy
persists for a few years after delivery.38 Over-
all, women with preeclampsia have a higher
risk of chronic hypertension, renal disease,
and cardiovascular disease later in life.4
Progression in Severity
Hypertension is the central feature of pre-
eclampsia.6 Disturbances in hematologic, renal,
and hepatic systems are most frequently
encountered.15 Preeclampsia is typically diag-
nosed by new-onset hypertension (systolic
blood pressure of ≥ 140 mm Hg or diastolic
blood pressure of ≥ 110 mm Hg) with pro-
teinuria (≥ 300 mg protein in 24-hour urine
specimen or protein-to-creatinine ratio of ≥
0.3 mg/dL). Some women present with signs
and symptoms consistent with multisystem
involvement that usually indicate disease sever-
ity in the absence of proteinuria. Therefore,
in the absence of proteinuria, preeclampsia is
diagnosed when one of the following severe
features accompanies new-onset hypertension:
thrombocytopenia (platelets < 100 000 per
microliter), impaired liver function (increased
serum transaminases twice their normal value),
new development of renal insufficiency (serum
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PREECLAMPSIA
creatinine > 1.1 mg/dL or doubling of serum
creatinine), pulmonary edema, or new-onset
cerebral or visual disturbance (headache, sco-
tomata, photopsia, diplopia, blurred vision,
or amaurosis fugax).6,44
Although not included in the diagnostic
criteria for preeclampsia, persistent, severe
right upper quadrant (RUQ) or epigastric
pain is a significant finding in preeclampsia
because it may suggest impaired perfusion to
the liver.45 Further evaluation for thrombocy-
topenia and elevated serum transaminases is
indicated, and these laboratory abnormalities
may support the diagnosis of HELLP (hemo-
lysis, elevated liver enzymes, low platelet)
syndrome. Whether HELLP syndrome is a
preeclampsia subtype or a separate disorder
is a subject of debate.46,47 Regardless, the diag-
nostic criteria for preeclampsia encompass
features of HELLP syndrome, and appropri-
ate timing of delivery is similarly recom-
mended for HELLP syndrome to optimize
maternal-fetal outcomes.22
Once the diagnosis of preeclampsia is estab-
lished, gestational age, maternal and fetal sta-
tus, and/or progression in severity determines
the appropriateness of expectant treatment
versus delivery of the fetus.6 Women without
severe features who are remote from term ges-
tation are often treated expectantly; antepar-
tum management focuses on close observation
for progression in organ system involvement.
Absence of severe features supports delivery
of the fetus at 37 weeks of gestation.6,15,48
However, the potentially catastrophic mater-
nal and fetal outcomes often necessitate pre-
term birth.49 In anticipation of preterm birth,
women with severe features should receive a
48-hour antenatal course of corticosteroids
(betamethasone or dexamethasone) to pro-
mote fetal lung maturation and reduce other
complications of prematurity, such as intra-
ventricular hemorrhage or necrotizing entero-
colitis. However, some complications warrant
delivery after initiation and before completion
of a full course of corticosteroids.
Eclampsia, pulmonary edema, disseminated
intravascular coagulation (DIC), severe hyper-
tension refractory to antihypertensive therapy,
abnormal fetal surveillance findings, and pla-
cental abruption are indications for delivery
immediately after initial maternal stabilization,
regardless of gestational age. Intrauterine fetal
demise and nonviable fetus also are indications
for delivery at an earlier gestational age because
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Table 2: : Indications for Preterm Delivery
Immediate deliverya following stabilization
• Eclampsia
• Pulmonary edema
• DIC
• Severe hypertension refractory to treatment
• Abnormal fetal surveillance (inability to rule
out fetal acidemia at the time of observation)
• Placental abruption
• Nonviable fetus
• Intrauterine fetal demise
Abbreviations: DIC, disseminated intravascular coagulation; HELLP, hemolysis, elevated liver enzymes, and low platelets.
a
Immediate delivery incorporates supporting labor and vaginal birth. The mode of delivery is individualized for the specific circumstances.
b
Oligohydramnios or persistent biophysical profile score of 6/10 or less may indicate impaired uteroplacental perfusion. Abnormal fetal heart
rate parameters that could reflect fetal acidemia require delivery at any gestational age.
the risks to the woman of continuing the preg-
nancy outweigh any fetal benefit.6 Indications
for preterm delivery in the setting of preeclamp-
sia are summarized in Table 2.6
The decision to manage expectantly versus
deliver the fetus is challenged by the consid-
erable variation in onset, clinical presentation,
and severity of the disease, and data are scarce
regarding identification of risk factors that
predict progression from mild to severe presen-
tation.7 The need for evidence-based criteria
that evaluate maternal risk for severe morbid-
ity or mortality has led to development of mod-
els to predict risk for adverse outcome. One
such model is the Preeclampsia Integrated
Estimate of Risk (fullPIERS), which was devel-
oped and validated to identify risk for life-
threatening complications of preeclampsia.50
The fullPIERS investigators concluded that
a combination of gestational age, chest pain
or dyspnea, arterial hemoglobin oxygen satu-
ration, platelet count, serum creatinine level,
and aspartate transaminase level predicted
adverse outcome within 48 hours of determi-
nation of eligibility of study participants. The
miniPIERS includes systolic blood pressure
along with the parameters in fullPIERS and
has demonstrated ability to identify maternal
risk for adverse outcome within 48 hours of
admission in low-resourced areas. The purpose
of both these risk-prediction models is to iden-
tify women who would benefit most from
interventions, such as magnesium sulfate or
antihypertensives, and/or transition to a higher
level of care.51
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Delivery after 48 hours of antenatal corticosteroids
• Persistent symptoms of severe disease
• HELLP syndrome
• Significant renal dysfunction, excluding proteinuria
• Intrauterine fetal growth restriction less than the fifth
percentile
• Reversal of umbilical artery end-diastolic flow
• Any woman at 34 weeksʼ gestation who is stable with
one of the following:
• Labor
• Rupture of membranes
• Fetal oligohydramnios or persistent biophysical profile
score of 6/10 or lessb
A systematic review of 32 studies that
explored prediction of adverse outcomes of
preeclampsia revealed inconsistent results,
likely due to heterogeneity in study popula-
tions.52 Individual laboratory or clinical tests
were not clinically useful in prognosticating
adverse outcome in this systematic review,
except for oxygen saturation less than 93%.
Rather, combined abnormal assessment find-
ings of headache, visual disturbances, elevated
aspartate aminotransferase, chest pain, or
dyspnea and early gestational age were more
likely to identify risk for adverse outcome.
Although delivery of the infant remains the
only definitive treatment for preeclampsia,
resolution is not immediate, and women
may require critical care during the intrapar-
tum and postpartum periods. A list of acute
complications of preeclampsia is provided
in Table 3.7,53 Eclampsia, intracranial hemor-
rhage, and pulmonary edema are the most
common complications of preeclampsia
that predispose women to mortality and
severe morbidity.44,54-56
Acute Complications of
Preeclampsia
Eclampsia
Eclampsia is the most common neurologic
complication of preeclampsia and is defined
as convulsions or unexplained coma in a
woman with preeclampsia.15,28 Eclampsia
complicates about 1 in 1000 deliveries in
the United States and can present before,
during, or after delivery.57,58 It manifests
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Table 3: Acute Complications of Table 4: Administration Guidelines for

Preeclampsia Magnesium Sulfate

• Maternal mortality Indications • Prophylaxis: severe features of

• Neurologic preeclampsia
• Eclampsia • Treatment: eclampsia
• Stroke
• Posterior reversible encephalopathy syndrome Loading dose • 4 to 6 g IV over 15 to 30 minutes
• Transient ischemic attack • Assessment
• Cardiopulmonary • Heart rate, respirations, BP, SaO2,
• Heart failure every 15 minutes for 2 hours
• Pulmonary edema • DTRs 1 hour after initiation of
• Hypertensive crisis loading dose
• Acute myocardial infarction or ischemia • Intake and output every 1 to 2 hours
• Need for inotropic support Maintenance • 2 g IV per hour
• Hepatic infusion • 1 g IV per hour may be indicated
• Subcapsular hematoma for abnormal renal function or oliguria
• Hepatic rupture • Assessment
• Hematologic • Heart rate, respirations, BP, SaO2,
• Postpartum hemorrhage every 1 to 2 hours
• Placental abruption • DTRs every 1 to 2 hours
• Disseminated intravascular coagulation • Intake and output every 1 to 2 hours
• Thrombocytopenia
• Ophthalmologic Additional • 2 g IV over 5 minutes
• Cortical blindness bolus dose
• Retinal detachment Suspected • Suspected: absent DTRs, decreased
• Uteroplacental toxicity level of consciousness, respiratory
• Intrauterine fetal growth restriction depression
• Abnormal Doppler studies • Confirmed: serum magnesium
• Intrauterine fetal death level > 7 mEq/L or > 8.4 mg/dL
• Renal • Discontinue infusion and obtain
• Acute kidney injury serum magnesium level
• Renal insufficiency • Calcium gluconate 1 g IV over
3 minutes

suddenly and often without premonitory symp- Abbreviations: BP, blood pressure; DTRs, deep tendon reflexes; IV,
toms, which makes it difficult to predict. This intravenous; SaO2, oxygen saturation.

warrants seizure prophylaxis with magnesium

sulfate in women with severe features of pre-
eclampsia.6,15,44,59,60 The etiology of eclampsia
is undetermined, but proposed mechanisms
include a cerebrovascular response to hyper-
tension that leads to vasospasm, ischemia,
and intracellular edema; hyperperfusion
from loss of cerebral autoregulation with
subsequent extracellular or vasogenic edema;
and cerebral edema from endothelial dam-
age.15,44 Eclampsia is a severe feature that
requires delivery of the infant following
maternal stabilization.6,44
Although eclamptic seizure typically lasts
only 1 to 2 minutes, up to 10% of women
experience recurrent seizures.22,61 Therefore,
magnesium sulfate is indicated to prevent
repeated seizure activity before or during
exploration for other causes of seizure (eg,
intracranial bleeding, severe hypoglycemia
or electrolyte imbalance, drug withdrawal).15,22
An intravenous (IV) loading dose of magne-
sium is required to increase serum levels,
followed by a maintenance IV infusion to
maintain a therapeutic serum magnesium
level. The initial loading dose is typically
administered as a 4- to 6-gram bolus IV
infusion over 15 to 30 minutes followed by
a maintenance IV infusion of 1 to 2 gram
per hour.22 The maintenance infusion should
be continued during the intrapartum period
and for 24 hours after delivery.6 When initi-
ated in the postpartum period, magnesium
sulfate typically is continued for 24 hours
after initiation of the loading dose.44
A serum magnesium level of 3 to 7 mEq/L
or 4.8 to 8.4 mg/dL is presumed to be thera-
peutic. Recurrent seizure during the mainte-
nance infusion of magnesium sulfate indicates
a subtherapeutic serum magnesium level and
is typically treated with an additional 2-gram

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WITCHER
IV bolus. Administration guidelines are sum-
marized in Table 4.6,22,45 Seizure activity that
is refractory to magnesium sulfate may require
the administration of other anticonvulsant
medications, such as diazepam, midazolam,
or lorazepam.62 Use of additional anticonvul-
sants increases the risk of apnea upon resolu-
tion of the seizure and warrants preparation
for endotracheal intubation as soon as possi-
ble after onset of seizure.15
Magnesium toxicity can produce central
nervous depression, respiratory depression,
and cardiopulmonary arrest that are associ-
ated with serum magnesium levels of greater
than 7 mEq/L, 10 mEq/L, and 25 mEq/L,
respectively. Loss of deep tendon reflexes
precedes respiratory depression and other
adverse system effects and warrants assess-
ment of deep tendon reflexes and respiratory
rate at least every 1 to 2 hours.22 Magnesium
is excreted by the kidneys, and impaired renal
function predisposes the woman to magne-
sium toxicity. Therefore, urine output requires
hourly measurement or with each void if an
indwelling urinary retention catheter is not
inserted. Oliguria and/or elevated serum cre-
atinine may warrant a maintenance infusion
of 1 g per hour to prevent magnesium toxic-
ity. Immediate access to the antidote, calcium
gluconate, is an additional precaution against
magnesium toxicity. When magnesium toxic-
ity is suspected or confirmed, 1 gram of cal-
cium gluconate should be administered IV
over 3 minutes.45
Intracranial Hemorrhage
About 90% of strokes in preeclampsia are
hemorrhagic, resulting from pressure-induced
capillary rupture of the cerebral vasculature.44
Cerebral hemorrhage from uncontrolled, severe
hypertension is the leading cause of death in
women with preeclampsia, prompting nation-
ally recognized guidelines for antihypertensive
therapy for hypertensive emergencies.44,54,55,63,64
Severe, acute hypertension is defined as either
systolic blood pressure of ≥ 160 mm Hg or
diastolic blood pressure of ≥ 110 mm Hg,
sustained for 15 minutes.55,56,63,64 Immediate
treatment, within 30 to 60 minutes of onset
of severe hypertension, is directed at reduc-
ing the risk of intracranial hemorrhage and
other end-organ complications, primarily pla-
cental abruption and pulmonary edema.63,64
An abrupt decline in blood pressure may pre-
cipitate decreased maternal cerebral perfusion
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W W W. A AC N AC C O N L I N E . O R G
or decreased uteroplacental perfusion.65 There-
fore, acute antihypertensive treatment targets
a threshold of 140 to 159 mm Hg systolic or
90 to 100 mm Hg diastolic.3,6,63
Acute antihypertensive treatment for severe,
acute hypertension in preeclampsia typically
involves escalation of doses of IV hydralazine,
IV labetalol, or oral nifedipine until the target
blood pressure threshold is achieved. Admin-
istration of antihypertensive agents for acute,
severe hypertension is summarized in Table
5.63 Although often the first-line treatment
for hypertension in the general population,
angiotensin-converting enzyme inhibitors are
not recommended during pregnancy because
of the increased risk of fetal renal dysgenesis,
oligohydramnios, and intrauterine growth
restriction.28 Nicardipine, nitroglycerin, and
sodium nitroprusside are reserved for severe
hypertension that is refractory to obstetric
first-line antihypertensive agents. Decreased
preload and adverse fetal effects of decreased
maternal cardiac output with the administra-
tion of nitroglycerin in the antepartum or
intrapartum period warrant fetal heart rate
evaluation. Sodium nitroprusside is typically
reserved for postpartum administration or
for a limited duration prior to delivery because
of concerns about fetal cyanide and thiocya-
nate toxicity.37
Pulmonary Edema
Pulmonary edema is the most common car-
diopulmonary complication of preeclampsia.
It occurs in about 3% of women with pre-
eclampsia and is a severe feature of the dis-
ease.38,66 A multicenter case-control study of
women with preeclampsia during hospital-
ization for delivery in 2 Toronto hospitals
evaluated risk factors for pulmonary edema.67
Women with laboratory markers consistent
with severe features of preeclampsia, specifi-
cally thrombocytopenia and elevated serum
uric acid concentration, were at higher risk
for developing pulmonary edema.
Administration of magnesium sulfate
was associated with more than a 10-fold
increase in the risk for developing pulmo-
nary edema. Magnesium sulfate is indicated
for seizure prophylaxis for those who man-
ifest with severe features of preeclampsia;
thus, the investigators concluded that mag-
nesium sulfate was a marker of preeclamp-
sia severity rather than a direct contributor
to pulmonary edema because of the low
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Table 5: Administration of First-Line Antihypertensives for Acute, Severe Hypertension

Establish and confirm acute, severe hypertension
• Assess BP every 5 minutes for 15 minutes
• Sustained systolic BP 160 mm Hg OR diastolic 110 mm Hg for 15 minutes
• Initiate fetal monitoring if undelivered
• Initiate first-line antihypertensive in accordance with providerʼs order immediately (within 30 to 60 minutes)
or immediately notify provider if an order needs to be obtained
First-line antihypertensive
• Administer antihypertensive in escalating doses as noted below until BP is no longer in severe range:
Target threshold: systolic BP 140-159 mm Hg and diastolic BP 90-100 mm Hg
• Assess BP 10 minutes after each dose of labetalol
• Assess BP 20 minutes after each dose of hydralazine or nifidepine

IV Hydralazine IV Labetalol Oral Nifedipine

1. Initial dose: 5-10 mg 1. Initial dose: 20 mg 1. Initial dose: 10 mg
2. Subsequent dose: 10 mg 2. Subsequent dose: 40 mg 2. Subsequent dose: 20 mg
3. Labetalol 20 mg 3. Subsequent dose: 80 mg 3. Subsequent dose: 20 mg
4. Labetalol 40 mg 4. Hydralazine 10 mg 4. Labetalol 40 mg
Interventions when medication is effective in treating blood pressure
• Assess BP every 10 minutes x 1 hour, every 15 minutes x 1 hour, every 30 minutes x 1 hour, every 4 hours
• Confirm orders for subsequent severe elevation (ie, start with initial dose versus dose previously effective
in lowering blood pressure)
• Notify provider of dose required to lower blood pressure and obtain additional orders
Intervention for severe hypertension that is refractory to treatment:
• Obtain emergency consultation: MFM, internal medicine, anesthesia, or critical care

Abbreviations: BP, blood pressure; IV, intravenous; MFM, maternal-fetal medicine.

volume of magnesium sulfate infusions in presentation and treatment of cardiogenic

this study population.
Preventive measures include judicious
administration of IV fluid at a rate of 75 to
125 mL per hour during labor and the first
12 to 24 hours after delivery.42 However,
varying hemodynamic profiles of preeclamp-
sia present challenges in fluid management.
Intravascular volume depletion and decreased
colloid oncotic pressure from increased capil-
lary permeability predispose women to non-
cardiogenic pulmonary edema.38,67 Decreased
circulating blood volume may negatively
affect cardiac output, producing hypotension
or impairing fetal oxygenation because of
decreased uteroplacental perfusion. Intravas-
cular volume expansion for epidural-mediated
hypotension or oliguria or intrauterine fetal
supportive measures may be required before
or during delivery.42 Alternatively, increased
cardiac afterload and left ventricular dysfunc-
tion predispose women to cardiogenic pulmo-
nary edema.38,67 These women may require IV
fluid restriction or inotropic support. Mobili-
zation of interstitial fluids after delivery further
contributes to the risk of pulmonary edema
in the postpartum period.42 Clinical
pulmonary edema in women with preeclamp-
sia are similar to those in the general popula-
tion, and most women respond to intravenous
furosemide and fluid restriction. Antepartum
treatment of pulmonary edema often requires
evaluation of the fetal heart rate because of
the risk of decreased uteroplacental perfusion
if intravascular volume status becomes com-
promised.38 Pulmonary edema that is unre-
sponsive to initial treatment with diuresis
and inspired oxygen warrants further diag-
nostic evaluation to determine the etiology,
which will guide further management.42
Hemorrhagic Complications
Preeclampsia is associated with an increased
risk of hemorrhagic complications, including
DIC.52 Hypertension is a well-established risk
factor for placental abruption, increasing the
risk 5-fold compared with pregnancies with-
out hypertension.68 Shallow trophoblastic
invasion of uterine spiral arteries and subse-
quent poor placental implantation predispose
women with preeclampsia to premature sepa-
ration of the placenta (placental abruption),
likely as a result of decidual necrosis from

323
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WITCHER
placental ischemia.24 Disseminated intravascu-
lar coagulation occurs in 10% of placental
abruptions.69 Endothelial disruption that
accompanies placental abruption promotes
the release of tissue factor, which is abundant
in placental tissue, into the maternal circula-
tion, thereby activating widespread imbalance
between procoagulants and anticoagulants
that can lead to DIC.69,70 Placental abruption
and DIC that are severe enough to cause
intrauterine fetal death are associated with
more extensive depletion of coagulation fac-
tors, which increases the risk of profound
hemorrhage. Abnormal fetal heart rate typi-
cally prompts emergency delivery.71 Signifi-
cant blood loss may not be evident before
delivery if blood pools behind the site of pla-
cental detachment, and the amount of blood
loss may not be fully appreciated after deliv-
ery. Therefore, postpartum onset of hypoten-
sion or blood pressure that appears to have
normalized from an elevated baseline may
reflect hemodynamic instability that accompa-
nies hemorrhage. Hemodynamic stabilization
should include evaluation of complete blood
count and coagulation profile with anticipa-
tion that blood and blood component therapy
may be necessary to promote hemodynamic
stability and correct coagulopathy.45
Hepatic rupture is a life-threatening com-
plication of preeclampsia. Decreased perfusion
to the liver may lead to hepatic infarction
with potential progression to subcapsular
hematoma from portal capillary rupture
beneath the Glisson capsule and subsequent
hepatic rupture, or hemorrhage into the
peritoneal cavity. The most common clinical
manifestation of hepatic rupture is profound
hypovolemic shock that is often preceded by
shoulder pain or severe epigastric or RUQ
pain. Aggressive hemodynamic support, includ-
ing blood and blood component therapy, and
surgical intervention are warranted. The clini-
cal manifestation of persistent, severe epigastric
or RUQ pain that is accompanied by eleva-
tion in serum transaminases in the woman
with preeclampsia may indicate decreased
hepatic perfusion and may present an indica-
tion for delivery owing to concerns about
subcapsular hematoma or hepatic rupture.15
Acute Kidney Injury
Acute kidney injury is a rare complication
of preeclampsia and is typically associated
with an underlying medical condition or
324
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W W W. A AC N AC C O N L I N E . O R G
hemorrhagic complication, such as placen-
tal abruption or postpartum hemorrhage.72
Decreased renal perfusion arises from intra-
vascular volume depletion, increased after-
load, or renal artery vasoconstriction.
Oliguria is typically the first sign of renal
compromise. Management should be deter-
mined by the etiology.
In a report by Clark and colleagues,31 pul-
monary artery catheterization in 9 preeclamp-
tic women with oliguria that failed to respond
to an initial IV fluid challenge revealed 3
hemodynamic subsets. Most of the women
were determined to be oliguric from intravascu-
lar volume depletion, as evidenced by decreased
pulmonary capillary wedge pressure (PCWP),
elevated cardiac output, and moderately ele-
vated SVR. In this subset, oliguria resolved
with intravascular volume expansion. A few
women in the second subset had normal or
elevated PCWP and cardiac output with nor-
mal SVR and were determined to have selec-
tive renal artery vasoconstriction. Oliguria
resolved in this subset with vasodilator therapy
and preload reduction. One woman had mark-
edly elevated PCWP and SVR with depressed
cardiac output. She required fluid restriction
and aggressive afterload reduction. Oliguria
may be a consequence of anemia from blood
loss. Evaluation of complete blood count and
coagulation profile is warranted when oliguria
fails to respond to an initial IV fluid challenge.
Red blood cell transfusion may be necessary.
Renal replacement therapy is rarely required
but may be used to correct fluid volume over-
load unresponsive to diuretics, azotemia, and
electrolyte and acid-base abnormalities.72
Summary
Variation in the clinical presentation of
preeclampsia and progression in severity
presents challenges in accurately identifying
risk factors for adverse outcome. Manage-
ment is determined by early identification
of preeclampsia, particularly onset of severe
features, and gestational age. The potentially
devastating maternal and fetal outcomes
often necessitate preterm delivery. Delivery
remains the only definitive treatment. The
progressive and dynamic nature of the disease
process requires vigilant assessment for onset
of severe features and stabilizing treatment
during the antepartum, intrapartum, and
postpartum periods. Complications from
preeclampsia remain a significant contributor
VO L U M E 2 9 • N U M B E R 3 • FA L L 2 018
to severe maternal morbidity and mortality.
Management priorities aimed at averting
adverse maternal outcome focus on preven-
tion and treatment of eclampsia, control of
severe hypertension, and timely diagnosis
and management of pulmonary edema.
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 Preeclampsia: Acute Complications and Management Priorities
Patricia M. Witcher
AACN Adv Crit Care 2018;29 316-326 10.4037/aacnacc2018710
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