Journal of Midwifery & Women’s Health www.jmwh.

org
Review

Hypertensive Disorders of Pregnancy: Overview

and Current Recommendations
CEU
Diane M. Folk, CNM, DNP, NP

Hypertensive disorders of pregnancy include chronic hypertension, gestational hypertension, preeclampsia-eclampsia, and chronic hypertension
with superimposed preeclampsia. These disorders are an important cause of maternal and fetal morbidity and mortality. Although advances in ef-
fective treatments have been made, current research has yet to identify a biochemical or diagnostic imaging marker to reliably predict preeclampsia.
Despite current guidelines that address diagnosis and management of hypertensive disorders in pregnancy, health care providers may overlook or
be unaware of signs that require immediate evaluation and treatment. This article reviews the definitions of hypertensive disorders of pregnancy,
diagnosis, pathophysiology of preeclampsia, indications for treatment, neurologic sequelae, and counseling about the implications of hypertension
in pregnancy for subsequent health.
J Midwifery Womens Health 2018;00:1–12  c 2018 by the American College of Nurse-Midwives.

Keywords: pregnancy, hypertension, preeclampsia, eclampsia, chronic hypertension, gestational hypertension, postpartum hypertension,
antihypertensive medications

INTRODUCTION [mm Hg] or diastolic 90-109 mm Hg) or severe (systolic ࣙ160

Hypertensive disorders affect 5% to 10% of women during
pregnancy, which is a 25% increase in incidence in the past
2 decades. This increase in the incidence of hypertensive
disorders in pregnant women has been attributed to factors
such as the increases in obesity, advanced maternal age,
and women who have associated comorbidities.1,2 Women
who have hypertensive disorders during pregnancy are at
risk for intrauterine growth restriction, placental abruption,
preterm birth, and cesarean birth.2 The risk of fetal demise
is 3.6 per 1000 pregnancies; however, the risk of fetal demise
for women with preeclampsia is 5.2 per 1000 pregnancies.3
Hypertensive disorders of pregnancy are also associated with
increased maternal morbidity and mortality, predominantly
because of maternal stroke.1,4 This article reviews definitions
of hypertensive disorders in pregnancy, pathophysiology
of preeclampsia, diagnostic criteria, evaluation, treatment,
hypertensive crisis, and maternal complications. Counsel-
ing women about future pregnancies and ongoing health
maintenance will be addressed.
DEFINITION AND DIAGNOSTIC CRITERIA FOR
HYPERTENSIVE DISORDERS IN PREGNANCY
In 2013, the American College of Obstetricians and Gyne-
cologists (ACOG) published the results of a task force that
reexamined the management of hypertension in pregnancy.
Four categories defining hypertension during pregnancy
were established, including 1) gestational hypertension,
2) preeclampsia-eclampsia, 3) chronic hypertension (any
cause), and 4) chronic hypertension with superimposed
preeclampsia.5 During pregnancy, hypertension is classified
as mild or moderate (systolic 140-159 millimeters of mercury
Address correspondence to Diane M. Folk, CNM, DNP, NP, Vanderbilt
University School of Nursing, 461 21st Avenue South, 358 Frist Hall,
Nashville, TN 37240. Email: diane.m.folk@vanderbilt.edu
mm Hg or diastolic ࣙ 110 mm Hg).5 Table 1 presents the
diagnostic criteria for hypertensive disorders in pregnancy.
Gestational Hypertension
Within the cohort of women who have gestational hyper-
tension, 25% to 50% will develop preeclampsia.6 Gestational
hypertension is more likely to progress to preeclampsia
in women who develop hypertension prior to 32 weeks’
gestation. Women with mild gestational hypertension may
progress to preeclampsia within 7 to 21 days of diagnosis.5
Although some biomarkers such as increased uric acid levels
are associated with progression to preeclampsia, none have
sufficient predictive value yet to be used in clinical practice.7,8
Preeclampsia-Eclampsia
Preeclampsia is a disorder unique to pregnancy,9 affecting 2%
to 8% of pregnant women.10 In the past, preeclampsia without
severe features was characterized as mild. This terminology is
no longer used as it is recognized that preeclampsia is a spec-
trum and can progress in severity quite rapidly.5 Even in the
absence of symptoms of severe disease, morbidity and mor-
tality are increased in women with preeclampsia compared
with women who do not have a hypertensive disorder during
pregnancy.5
The classic triad of signs and symptoms that were used
to make the diagnosis of preeclampsia were hypertension,
edema, and proteinuria. Although edema and proteinuria are
often present in women with preeclampsia, they are no longer
essential components of the diagnostic criteria. Edema was re-
moved from diagnostic criteria years ago, as edema is a com-
mon finding in the third trimester of pregnancy.6 The use of
proteinuria as one of the diagnostic criteria for preeclamp-
sia has also been reassessed. If proteinuria is present, it is in-
cluded as one component of the diagnostic criteria. However,

1526-9523/09/$36.00 doi:10.1111/jmwh.12725 
c 2018 by the American College of Nurse-Midwives 1
 ✦ Hypertensive disorders complicate 5% to 10% of all pregnancies, which is an increase of 25% in the past 2 decades.
✦ Superimposed preeclampsia occurs in 13% to 40% of women with chronic hypertension.
✦ Proteinuria is unnecessary for the diagnosis of preeclampsia.
✦ Patient and provider factors can contribute to severe complications of preeclampsia.
✦ Prior to hospital discharge, all women should be educated about the signs of preeclampsia, not only those women with
known hypertension.
preeclampsia is also diagnosed in women with hypertension
who do not have proteinuria but do have thrombocytopenia,
renal insufficiency, pulmonary edema, or cerebral or visual
symptoms.
Severe preeclampsia is characterized by findings in
addition to the principal criteria for diagnosis. Because
intrauterine growth restriction is managed in the same
manner with or without preeclampsia, the presence of growth
restriction has been eliminated as a diagnostic finding in
severe preeclampsia.5
Headache is included in the definition of the visual and
cerebral disturbances associated with severe preeclampsia.
The descriptors of headache associated with preeclampsia
include “severe,” “persistent,” “worst headache ever experi-
enced,” or “not relieved with analgesics.”11 Benign headache
symptoms occur in up to 60% of women of reproductive age
and in 25% to 59% of women experiencing a normal preg-
nancy during the antepartum period. However, 50% to 80% of
women who experience an eclamptic seizure have a headache
prior to the seizure.11
Atypical preeclampsia, defined as the onset of signs or
symptoms of preeclampsia-eclampsia at either less than 20
weeks’ gestation or more than 48 hours after birth, can present
several weeks after birth.6 Eclampsia is the development of
new-onset seizures in a pregnant or postpartum woman with
preeclampsia.5 Women who present with seizures may not
have been previously diagnosed with preeclampsia.
Chronic Hypertension
Chronic hypertension affects approximately 5% of women
during pregnancy. Hypertension that persists for more than
12 weeks after birth is also considered chronic hypertension.2
In the last 20 years, the incidence of chronic hypertension
in the United States has increased in all ethnic and racial
groups, with the greatest increase among non-Hispanic black
women.1
There are 2 types of chronic hypertension. Primary or es-
sential hypertension is defined as elevated blood pressure in
the absence of end-organ damage or attributable to a cause.
Secondary hypertension is defined as elevated blood pres-
sure resulting from a renal or endocrinologic cause.5,12 Most
women with chronic hypertension have primary (essential)
hypertension. Some women with chronic hypertension (as
many as 10%) may have underlying renal or endocrine dis-
orders responsible for secondary hypertension.5
2 Volume 00, No. 0, xxxx 2018
Chronic Hypertension with Superimposed
Preeclampsia
The frequency of superimposed preeclampsia is 13% to 40%
among women with chronic hypertension.5 Women who have
chronic hypertension and superimposed preeclampsia are at
increased risk for significant maternal-fetal morbidity and
mortality.
Related Disorders: HELLP Syndrome, Acute Fatty
Liver of Pregnancy, and Thrombotic
Thrombocytopenia Purpura/Hemolytic Uremic
Syndrome
The spectrum of systemic involvement present in
preeclampsia-eclampsia, such as thrombocytopenia, ab-
normal liver enzyme concentrations, and hemolysis, can
be confused with other conditions that can complicate the
diagnosis and management of preeclampsia-eclampsia.
Severe preeclampsia can be complicated by a syndrome
of hemolysis, elevated liver enzymes, and low platelets,
or HELLP syndrome. HELLP syndrome occurs in nearly
10% to 20% of women affected by severe preeclampsia or
eclampsia.13 Signs of preeclampsia may be subtle or missing,
although hypertension is usually present.14 The clinical
development of HELLP syndrome is often one of progressive
and frequently abrupt worsening of maternal and fetal status.5
Adverse outcomes, such as placental abruption, acute renal
failure, pulmonary edema, subcapsular liver hematoma,
stroke, coagulopathy, acute respiratory distress syndrome,
renal failure, and sepsis, have been reported.15
For women with HELLP syndrome who are at 34 0/7
weeks’ gestation or more, birth is facilitated as soon as the
woman is stable.5 The syndrome may worsen after birth. Ap-
proximately 20% to 30% of women with HELLP syndrome ex-
perience initial symptoms more than 48 hours after birth.6
Acute fatty liver of pregnancy is a rare, potentially fa-
tal complication of pregnancy. This disorder occurs in ap-
proximately one in 6700 to 13,000 women during pregnancy.
Acute fatty liver of pregnancy is typically diagnosed in the
third trimester and is more common in nulliparous women
and women with a multiple gestation.16,17 Historically, women
with acute fatty liver of pregnancy had a maternal mortality
rate of nearly 70%. Because of advances in care and manage-
ment, maternal mortality is currently less than 10%. Perina-
tal mortality is 13.1%. Neonatal morbidity continues to be ap-
proximately 74% because of the high rate of preterm birth.17
 Table 1. Diagnostic Criteria Hypertensive Disorders in Pregnancy
Condition
Gestational
hypertension
Preeclampsia without
severe features
Preeclampsia with
severe features
Diagnostic Criteria
SBP ࣙ140 mm Hg and/or DBP ࣙ90 mm Hg in a previously normotensive woman
Two BP readings at least 4 hours apart
Presents after 20 weeks’ gestation
Absence of proteinuria, laboratory abnormalities, pulmonary edema, or CNS signs
SBP ࣙ140 mm Hg and/or DBP ࣙ90 mm Hg in a previously normotensive woman
Two BP readings at least 4 hours apart
Presents after 20 weeks’ gestation
Proteinuria:
ࣙ300 mg per 24-hour urine collection, total protein-to-creatinine ratio ࣙ0.3, or urine dipstick proteinuria of
ࣙ1+ if quantitative method not available
In the absence of proteinuria, HTN plus any of the following:
Thrombocytopenia ⬍100,000 per mL
Impaired liver function: transaminases 2 × normal
Renal insufficiency: In the absence of other renal disease, serum creatinine ⬎1.1 mg/dL or 2 × baseline
Pulmonary edema
CNS signs (HA, visual changes, etc)
Same as preeclampsia without severe features, with the addition of at least one of the following (proteinuria not
required for diagnosis):

SBP ࣙ160 mm Hg and/or DBP ࣙ110 mm Hg measured twice at least 15 minutes apart
Thrombocytopenia ⬍100,000 per mL
Impaired liver function: transaminases 2 × normal, severe RUQ or epigastric pain
Renal insufficiency: In the absence of other renal disease, serum creatinine ⬎1.1 mg/dL or 2 × baseline
Pulmonary edema
New-onset cerebral or visual disturbances
Chronic hypertension SBP ࣙ140 mm Hg and/or DBP ࣙ90 mm Hg
Two BP readings, at least 4 hours apart
Presents pre-pregnancy or prior to 20 weeks’ gestation
Laboratory testing not applicable to diagnosis
Chronic HTN with Sudden increase in previously well-controlled BP
superimposed New-onset proteinuria or abrupt increase in proteinuria in a woman with known proteinuria prior to or in early
preeclampsia pregnancy
Chronic HTN with Any of the following:
superimposed Severe-range blood pressures
preeclampsia with Thrombocytopenia ⬍100,000 per mL
severe features Impaired liver function: transaminases 2 × normal
Renal insufficiency: In the absence of other renal disease, serum creatinine ⬎1.1 mg/dL or 2 × baseline
Pulmonary edema
CNS signs (HA, visual changes, etc)

Abbreviations: BP, blood pressure; CNS, central nervous system; DBP, diastolic blood pressure; HA, headache; HTN, hypertension; mm Hg, millimeters of mercury; RUQ,
right upper quadrant; SBP, systolic blood pressure.
Source: American College of Obstetricians and Gynecologists.5

Presenting symptoms of acute fatty liver of pregnancy
include malaise, anorexia, nausea, vomiting, epigastric or
right upper quadrant pain, headache, and jaundice.16,17 Some
women may present with preterm labor or decreased fe-
tal movement. Examination findings include hypertension,
proteinuria, edema, low-grade fever, jaundice, ascites, bleed-
ing, and bright yellow urine. Laboratory abnormalities may
include hemoconcentration, elevated white blood count,
elevated transaminases, hypoglycemia, elevated bilirubin,
and elevated ammonia. Coagulation changes include low

Journal of Midwifery & Women’s Health r www.jmwh.org 3

 Figure 1. Abnormal Placentation in Preeclampsia
The top illustration depicts normal placental development during pregnancy. Note the large capacitance vessels to provide adequate placental per-
fusion and the diminished tunica media. The bottom illustration depicts the abnormal placentation present in preeclampsia. The tunica media is
maintained, allowing vessels to remain narrow with the ability to constrict.
Reprinted with permission from Lam et al.21

fibrinogen, prolonged prothrombin time, and low an-
tithrombin levels consistent with disseminated intravascular
coagulation.16,17
Another disorder that mimics preeclampsia is throm-
botic thrombocytopenia purpura/hemolytic uremic syn-
drome (TTP/HUS). The incidence of TTP/HUS is estimated
to be one in 25,000 women during pregnancy. The disorder
is characterized by a classic constellation of 5 signs: thrombo-
cytopenia, hemolytic anemia, neurologic abnormalities, fever,
and renal dysfunction. The complete constellation of symp-
toms is seen in only 40% of patients, whereas 50% to 75%
demonstrate the initial 3 findings.16
Presenting symptoms of TTP/HUS may also include ab-
dominal pain, nausea, vomiting, gastrointestinal bleeding,
epistaxis, petechiae, or purpura. Neurologic symptoms are of-
ten vague but may include headache, visual disturbances, con-
fusion, aphasia, weakness, and seizures. Physical findings may
include hematuria, proteinuria, and tea-colored urine. Hyper-
tension may be present or absent. Laboratory abnormalities
include thrombocytopenia (platelet count ⬍100,000/mm3 , of-
ten ⬍20,000/mm3 ), acute anemia, and severe elevation of lac-
tate dehydrogenase. Liver enzyme transaminase findings may
be normal or elevated, whereas coagulation study findings are
usually normal.16
Although these disorders are not common during preg-
nancy or the postpartum period, midwives should be aware of
them because women who are affected by HELLP syndrome,
acute fatty liver of pregnancy, or TTP/HUS may present with
symptoms that suggest they have preeclampsia.
PATHOPHYSIOLOGY OF PREECLAMPSIA
Abnormal Placentation
Preeclampsia is characterized by abnormal placentation and
failed remodeling of the spiral arteries that occurs early in
gestation. Normally, cytotrophoblast cells invade the decidual
segment of the spiral arteries first, and then later, in a second
wave, they invade the myometrial portion of the arteries. This
process causes the vessels to lose the muscular tunica media
so they become large, low-resistance vessels that can accom-
modate increased flow. The cytotrophoblast does not infiltrate
the myometrial portion of the spiral arteries in women with
preeclampsia.18 The vessels remain small and narrow with
the ability to constrict, which results in placental hypoperfu-
sion and hypoxia19–21 (Figure 1). This first stage of preeclamp-
sia occurs prior to the appearance of clinical manifestations
of the disease. It is not known why normal development of

4 Volume 00, No. 0, xxxx 2018

uteroplacental circulation does not occur in women who de-
velop preeclampsia, but vascular, immunologic, and genetic
factors have all been implicated.19
The second stage of preeclampsia is due to maternal
inflammatory response to abnormal placentation and sub-
sequent placental hypoxia. This is referred to as maternal
systemic endothelial activation.22 The resulting hypoxia and
subsequent oxidative stress lead to endothelial cell dysfunc-
tion in the maternal spiral arteries.23 The placenta releases
excessive antiangiogenic factors, such as soluble fms-like ty-
rosine kinase 1 (sFlt-1) and soluble endoglin (sEng), which
are increased in the maternal circulation weeks before the
onset of clinical symptoms.24 Meanwhile, levels of proan-
giogenic factors, such as placental growth factor (PlGF) and
vascular endothelial growth factor (VEGF), are decreased.20
Antiangiogenic factors counteract the effects of the proan-
giogenic factors, which are key in the maintenance of the
vascular endothelium.24 The shedding of placental debris into
the maternal circulation has been implicated in the release of
proinflammatory cytokines such as tumor necrosis factor-␣
and interleukin-6, important mediators of endothelial cell ac-
tivation in preeclampsia.23
The vascular endothelium has many essential functions. It
is responsible for control of smooth muscle tone via the release
of vasoconstrictor and vasodilatory chemicals as well as con-
trol of anticoagulation, antiplatelet activity, and fibrinolysis.25
The endothelium lines the entire circulatory system; thus, en-
dothelial dysfunction in the placenta manifests itself in ev-
ery organ system. Examples include edema due to capillary
leaking, proteinuria due to altered tubular protein filtration,
pulmonary edema due to leakage of fluid into alveoli, and
liver dysfunction due to damage to the lining of small ves-
sels causing hemolysis and fibrin deposition. The central ner-
vous system is also affected as the endothelium lining cerebral
blood vessels exhibits increased permeability, with resulting
headache and visual disturbances.9
RISK FACTORS FOR PREECLAMPSIA
Risk factors for preeclampsia are listed in Table 2. A woman
has a 2- to 4-fold risk of preeclampsia if a first-degree rela-
tive had a pregnancy affected by preeclampsia. Her risk is in-
creased 7-fold if she experienced preeclampsia in a previous
pregnancy.5
PREDICTION AND PREVENTION
OF PREECLAMPSIA
Recently there has been an effort to identify first-trimester
biomarkers to predict the development of preeclampsia. Fe-
toplacental proteins, such as human chorionic gonadotropin,
estriol, alpha fetoprotein, inhibin A, pregnancy-associated
plasma protein A, and placental protein 13, have been stud-
ied. Elevated uric acid has also been proposed as a marker
for identifying women with gestational hypertension that may
progress to preeclampsia.5 A 2011 study that followed women
with gestational hypertension (N = 163) after measuring uric
acid levels found that uric acid may be an accurate predictor
of progression from gestational hypertension to preeclamp-
sia, with a positive predictive value of 91.4% when the uric
Journal of Midwifery & Women’s Health r www.jmwh.org
Table 2. Risk Factors for Preeclampsia
Risk Factors
African American race
Advanced maternal age (⬎40 years)
Chronic hypertension, chronic renal disease, or both
Family history of preeclampsia
History of thrombophilia
In vitro fertilization
Multifetal gestation
Nulliparity
Obesity
Previous preeclamptic pregnancy
Systemic lupus erythematosus
Type I or type II diabetes mellitus
Sources: Lo et al,1 American College of Obstetricians and Gynecologists.5
acid level is greater than 5.2 mg/dL (309 ␮mol/L). Although
these findings are promising, prospective trials are needed
before clinical recommendations about use of uric acid lev-
els can be proposed.5,7,8 More recently, antiangiogenic pro-
teins (sFlt-1 and sEng) and proangiogenic proteins (PlGF
and VEGF) have been investigated. Although the results are
promising, more research is needed. Currently there are no
biochemical markers that are recommended for use in clinical
practice.26
The value of uterine artery Doppler velocimetry to pre-
dict preeclampsia has also been studied. Resistance to flow in
the uterine circulation offers indirect information about faulty
trophoblast invasion. Studies have demonstrated that predic-
tion accuracy in low-risk women is minimal to moderate, and
in high-risk populations it is minimal. Current evidence does
not support the use of uterine artery Doppler velocimetry for
the prediction of preeclampsia.5,27
Combinations of biomarker testing and uterine Doppler
artery velocimetry are encouraging and may prove useful as
research continues. However, no one test has been found to
predict the development of preeclampsia, and there is no evi-
dence that accurate prediction of preeclampsia improves ma-
ternal and/or fetal outcomes.9 Therefore, ACOG does not rec-
ommend screening for the prediction of preeclampsia beyond
obtaining a thorough medical history to assess individual risk
factors, as the current state of screening will not allow ac-
curate selection of women who would benefit from referral
for intensive surveillance or application of strategies to reduce
the risk for developing severe preeclampsia-eclampsia.28 A re-
cent meta-analysis by the United States Preventive Services
Task Force (USPSTF) published in 2017 also states that evi-
dence is lacking to support any specific risk-based screening
approach or strategy for women during pregnancy because of
the complex pathophysiology and clinical unpredictability of
preeclampsia.29,30
Prevention
Interventions proposed for preventing preeclampsia include
calcium supplementation in women with insufficient calcium
5
intake, supplemental vitamin C or vitamin E, strict dietary salt Laboratory Evaluation
consumption, and bed rest. None of these interventions has
Laboratory assessment for preeclampsia includes a complete
been shown to be effective to date.5,9
blood count including platelet count, liver enzymes (alanine
Low-dose aspirin therapy has generated interest because
transaminase and aspartate transaminase), renal function
preeclampsia is a state of increased inflammation and aspirin
tests (creatinine concentration), urinalysis with microscopy,
is an anti-inflammatory agent that blocks the production of
assessment for proteinuria, lactate dehydrogenase, and evalu-
thromboxanes. An analysis by the USPSTF of 15 randomized
ation of coagulation factors. Important findings that support
controlled trials (RCTs) concluded that low-dose aspirin de-
a diagnosis of severe preeclampsia include evidence of
creased the risk of preeclampsia, preterm birth, and intrauter-
hemolysis, thrombocytopenia, abnormally high liver enzyme
ine growth restriction by 24%, 14%, and 20%, respectively.31
values, compromised renal function, and/or consumptive
The USPSTF recommends that low-dose aspirin be initiated
coagulopathy.6,34
between 12 and 28 weeks’ gestation in women with one or
more high-risk factors (eg, multifetal gestation, chronic hy-
pertension, type 1 or 2 diabetes, renal disease, autoimmune Proteinuria
disease, history of preeclampsia). Low-dose aspirin may ben-
One of the most significant paradigm shifts in the diagno-
efit women with several moderate risk factors (eg, nullipar-
sis of preeclampsia is the use of proteinuria as a diagnos-
ity, obesity, family history of preeclampsia, an age of 35 years
tic criterion. Proteinuria may be a late finding in the disease
or older, African American race, previous low birth weight or
process or not be present at all. Dipstick urine assessments
adverse pregnancy outcome); however, the evidence for use in
for proteinuria have a high rate of false-negative and false-
this population is less clear.31–33
positive results because the test relies on the concentration of
The timing of discontinuation of aspirin therapy is less
the urine tested. A 2015 prospective observational study (N =
clearly defined. Most RCTs included in the USPSTF recom-
2212 urine specimens from 1033 women) compared the
mendation recommended continuing aspirin therapy until
urinary protein-to-creatinine ratios in pregnant women af-
birth.31 ACOG updated its recommendation in July 2016 to
ter urine dipstick testing. The researchers found that false-
consider the use of low-dose aspirin (81 mg per day), initi-
negative results occurred in 8.8% of samples. False-positive
ated at 12 to 28 weeks’ gestation, using the high-risk factors
test results occurred in 59% of samples. The false-positive rate
suggested by the USPSTF.31,33
was 78%, 21%, and 1.3% for a 1+, 2+, and 3+ dipstick test,
Counseling women about lifestyle modifications to pre-
respectively.35
vent preeclampsia, including exercise and diet, should be
Considered the gold standard, timed urine (24-hour
undertaken.5 Because many pregnancies are unplanned, all
urine) samples can be quite challenging for a pregnant woman
women of childbearing age with chronic hypertension should
to collect. The high collection error rate (13%-54%) suggests
receive counseling that addresses how to improve their health
the results may be of limited value.36 The International Soci-
and reduce risk of pregnancy-related complications, such as
ety for the Study of Hypertension in Pregnancy recommends
superimposed preeclampsia, fetal growth restriction, placen-
use of the protein-to-creatinine ratio as an alternate method
tal abruption, preterm birth, and cesarean birth.2
to detect significant proteinuria.37 A protein-to-creatinine ra-
tio of at least 0.3 mg/dL is an acceptable threshold for the di-
CONSIDERATIONS IN MAKING THE DIAGNOSIS agnosis of preeclampsia, as this ratio closely approximates a
OF PREECLAMPSIA 24-hour urine collection of 300 mg of protein. The urine dip-
The diagnosis of preeclampsia is made based on symptoms, stick method is unreliable and not to be used unless other
blood pressure values, and laboratory indices of liver and renal quantitative methods are not available.5 That said, a dipstick
function. reading of greater than 1+ protein may be used if other tests
are not accessible.

History and Physical Examination INDICATIONS FOR THE TREATMENT OF

Physical examination is one of the most informative compo-
nents in the evaluation for preeclampsia. Reported symptoms
such as headache, visual disturbances, shortness of breath,
chest pain, nausea, vomiting, heartburn, or abdominal pain
(right upper quadrant or epigastric) are concerning.6 Often,
blood pressure measurement is the primary initial evaluation,
followed by a test for proteinuria and assessment of weight to
determine if the woman has experienced a sudden increase in
weight that is larger than normal. Fundoscopic examination
can provide valuable information, as at least 50% of women
with preeclampsia will demonstrate retinal vascular changes.
Deep tendon reflexes are often increased prior to an eclamp-
tic seizure. Tremulousness may be present. Evaluation of the
abdomen for right upper quadrant tenderness, indicating hep-
atic capsular distension, should be performed.34
HYPERTENSION DURING PREGNANCY
Midwives may collaborate in the care of women with medical
conditions such as chronic hypertension. Midwifery manage-
ment of women with hypertensive disorders of pregnancy will
vary depending on state regulations, practice protocols, prac-
tice setting, and consulting physician relationships.
The major goals of treatment of hypertensive disorders of
pregnancy are to prevent severe hypertension and maternal
cerebrovascular events.5
Chronic Hypertension
Women with chronic hypertension benefit from a compre-
hensive evaluation early in pregnancy that includes serum cre-
atinine, electrolytes, uric acid, liver enzymes, platelet count,

6 Volume 00, No. 0, xxxx 2018

 Table 3. Severe Preeclampsia: Maternal and Fetal Indications for Birth
Maternal
Recurrent severe HTN
Recurrent symptoms of severe preeclampsia
Progressive renal insufficiency (serum creatinine greater than 1.1 mg/dL or
doubling of the serum creatinine in the absence of other renal disease)
Persistent thrombocytopenia or HELLP syndrome
Pulmonary edema
Eclampsia
Suspected placental abruption
Progressive labor or ROM
Abbreviations: BPP, biophysical profile; HELLP, hemolysis, elevated liver enzymes and low platelets; HTN, hypertension; IUFD, intrauterine fetal demise; IUGR, intrauterine
growth restriction; NST, non-stress test; ROM, rupture of membranes.
Source: American College of Obstetricians and Gynecologists.5
and urine protein determination. For women who have
chronic hypertension of greater than 4 years’ duration, an
electrocardiogram and/or echocardiogram to differentiate es-
sential versus secondary hypertension and hypertension with
end-organ damage is recommended.5
The precise goal ranges for blood pressure in pregnancy
for women with chronic hypertension are not established, and
there is considerable debate about when to initiate antihyper-
tensive therapy. Antihypertensive therapy has been shown to
reduce maternal morbidity by limiting episodes of severe hy-
pertension but has not been demonstrated to reduce the in-
cidence of superimposed preeclampsia, placental abruption,
or intrauterine growth restriction.2 Furthermore, there is con-
cern that aggressively lowering maternal blood pressure may
compromise uteroplacental perfusion.2
The National Institute for Health and Care Excellence in
the United Kingdom recommends a blood pressure goal of
less than 150/100 mm Hg for women with uncomplicated hy-
pertension without comorbidities. In this population, it is rec-
ommended that diastolic blood pressure should not be less
than 80 mm Hg because lower diastolic pressures may impede
uteroplacental perfusion.38 The goal for pregnant women with
comorbidities related to hypertension is to maintain blood
pressure at less than 140/90 mm Hg.
The ACOG task force recommends different target blood
pressure guidelines as well as individual recommendations for
the specific hypertensive disorders of pregnancy. For women
with chronic hypertension with blood pressure values less
than 160/105 mm Hg and no end-organ damage, antihyper-
tensive therapy is not recommended during pregnancy. For
treating women with antihypertensive medications, the tar-
get blood pressure is 120 to 160 mm Hg systolic and 80 to
105 mm Hg diastolic. Women who have poorly controlled
chronic hypertension are advised to use home blood pressure
monitoring.5
Gestational Hypertension and Preeclampsia without
Severe Features
Surveillance, such as more frequent prenatal visits, assess-
ment of new maternal symptoms, serial laboratory evalua-
tion of platelets and liver enzymes, and interval fetal growth
Journal of Midwifery & Women’s Health r www.jmwh.org
Fetal
Gestational age of 34 0/7 weeks
Severe IUGR (ultrasound estimate of fetal weight less
than 5th percentile)
Persistent oligohydramnios (maximum vertical
pocket less than 2 cm)
BPP 4/10 or less on at least 2 occasions, 6 hours apart
Reversed end-diastolic flow on umbilical artery
Doppler studies
Recurrent variable or late decelerations during NST
IUFD
ultrasound monitoring, may be indicated for women with ges-
tational hypertension.6
Antihypertensive medication is not recommended for
women with mild gestational hypertension or preeclampsia
without severe features with a systolic blood pressure less than
160 mm Hg or diastolic less than 110 mm Hg.5 The ACOG
task force advises twice weekly blood pressure measure-
ments, daily fetal movement counting, assessment of maternal
symptoms, weekly platelet counts, and liver enzyme moni-
toring. For women without severe hypertension and mater-
nal symptoms, magnesium sulfate is not recommended for
seizure prophylaxis in the intrapartum setting.5
Preeclampsia with Severe Features
Maternal complications, such as severe renal failure, pul-
monary edema, stroke, coagulopathy, and acute respiratory
distress syndrome, are more likely to occur in women who
have preexisting comorbidities, such as obesity, renal disease,
chronic hypertension, diabetes mellitus, acquired throm-
bophilia, and connective tissue disease. Most fetal and neona-
tal complications are secondary to uteroplacental insuffi-
ciency and preterm birth.5
Expectant management may be undertaken if the woman
is at less than 34 0/7 weeks’ gestation and both maternal and
fetal conditions are stable. Administration of corticosteroids
to expedite fetal lung maturity is recommended. For women
with severe preeclampsia at 34 0/7 weeks’ gestation and be-
yond, birth is advised as soon as maternal stabilization is
achieved.5 Maternal and fetal indications for birth are listed
in Table 3.
Acute Hypertensive Crisis
Acute-onset severe systolic hypertension (systolic ࣙ160 mm
Hg and/or diastolic ࣙ110 mm Hg) can occur during preg-
nancy, labor and birth, or the postpartum period. Severe
hypertension that persists for 15 minutes or more is a hy-
pertensive emergency.39,40 Treatment should not be delayed
pending laboratory results. The Consensus Bundle on Severe
Hypertension During Pregnancy and the Postpartum Period,
published in 2017, is a landmark collaboratively developed
7
patient safety bundle guideline that addresses the appropri-
ate response to severe hypertension identified in a pregnant
or postpartum woman.39 Acute-onset severe hypertension
should be confirmed within 15 minutes. If severe hyperten-
sion is confirmed, treatment with antihypertensive medica-
tion should be initiated immediately to prevent maternal cere-
bral hemorrhage or stroke.39 Institutional protocols should
be in place and used. Systolic rather than diastolic hyper-
tension may be the most relevant predictor of cerebral hem-
orrhage or infarction.40,41 The goal of treatment is not to
reduce blood pressure to a normal range but to prevent repeti-
tive or prolonged exposure to severe systolic hypertension and
the ensuing loss of cerebral autoregulation.40 First-line thera-
pies for acute hypertensive crisis include intravenous labetalol
(Normodyne) and hydralazine (Apresoline). An immediate-
release oral formulation of nifedipine (Procardia) is now a
first-line therapy option, especially if the woman does not
have intravenous access.5
Stroke is a known complication of severe preeclampsia-
eclampsia.41 Many maternal deaths from hypertensive
disease (38.7%) are due to cerebrovascular complications.42,43
Cerebral autoregulation, the process by which blood flow
to the brain is maintained at an appropriate level despite
changes in blood pressure, is impaired in preeclampsia.44–46
This physiologic alteration is thought to explain why some
women develop cerebral edema, cerebral hemorrhage, and
seizures despite a lack of significant hypertension.43 It is also
theorized that severe acute hypertension causes cerebrovas-
cular overregulation, triggering vasospasm.46
In a study published in 2008, the Dutch Maternal Mor-
tality Committee reported findings reviewing the standard of
care in 27 cases of maternal mortality during the years 2000
to 2004 due to hypertensive disorder in pregnancy. Substan-
dard care was present in 96% of the cases. The cause of death
in 71% of the cases was cerebrovascular accident.42
Martin et al41 conducted a retrospective review of 28 med-
ical records of women with pregnancy-related stroke occur-
ring between 1980 and 2003. The most common signs present
prior to stroke included headache (95.6%), nausea and vomit-
ing (62.5%), epigastric pain (54.2%), and visual disturbances
(37.5%). Systolic blood pressure of 160 mm Hg or higher
was present in 95.8% of women, and a systolic blood pres-
sure of 155 mm Hg or higher was present in 100% of these
women. Diastolic blood pressure of 110 mm Hg or higher was
present only 12.5% of the time, but diastolic blood pressure of
105 mm Hg was present in 20.8% of this cohort. Protein-
uria levels of 3+ to 4+ were present in only 58.3% of the
women. The maternal mortality rate in the 28 medical records
reviewed was 53.6%. Antihypertensive medications were ad-
ministered prior to stroke in 12.5% of cases, and magnesium
sulfate was given in 50% of cases. The authors concluded that
withholding antihypertensive therapy in the presence of se-
vere systolic hypertension is inadvisable.41
ROLE OF THE MIDWIFE IN CARING FOR WOMEN
WITH HYPERTENSION DURING PREGNANCY
Hypertensive disorders of pregnancy are common, and mid-
wives are likely to be involved in the care of women who
develop hypertension during pregnancy. Education of preg-
8 Volume 00, No. 0, xxxx 2018
nant women, careful screening, and early diagnosis are cru-
cial. Women are less likely to seek care if they do not know or
understand the symptoms of preeclampsia.47 Lack of knowl-
edge about the severity of symptoms has been identified as a
factor in maternal preeclampsia deaths.48 Women who are di-
agnosed and treated for preeclampsia have fewer unfavorable
outcomes than those with delayed diagnoses.47
Prompt recognition, evaluation, and treatment of hyper-
tensive emergencies are essential to prevent potentially dev-
astating outcomes.39,40 Management of women with hyper-
tensive disorders of pregnancy will always include physician
consultation, collaboration, and possibly referral depending
on institutional guidelines, the practice setting, and consult-
ing physician relationships.
TIMING OF BIRTH
One of the major changes in the management of women with
gestational hypertension and preeclampsia is the timing of
birth. Preterm birth is associated with neonatal respiratory
complications, neonatal intensive care unit admission, and
higher incidence of neonatal death compared with neonates
born at 37 0/7 weeks’ gestation and beyond. However, ex-
pectant management in women with gestational hypertension
and preeclampsia without severe features can increase the risk
of development of severe hypertension, eclampsia, HELLP
syndrome, placental abruption, and fetal death.5
For women with mild gestational hypertension or
preeclampsia without severe features, birth at or beyond 37
0/7 weeks’ gestation is recommended. Women experiencing
preeclampsia with severe features at 34 0/7 weeks’ gestation
or beyond and women with unstable maternal or fetal status,
regardless of gestational age, should give birth as soon as
maternal stabilization is achieved. For women with HELLP
syndrome at 34 0/7 weeks’ gestation, birth should also occur
upon maternal stabilization.5
Studies have shown the amount or change in protein-
uria does not indicate the severity of preeclampsia or pre-
dict maternal or fetal outcome.5,9 Therefore, a decision to in-
duce labor should not depend on the amount of proteinuria
or change in proteinuria.5
ANTIHYPERTENSIVE MEDICATIONS USED
TO TREAT HYPERTENSIVE DISORDERS
IN PREGNANCY
Midwives are increasingly caring for women during preg-
nancy with medical complications. State regulations, practice
protocols, practice setting, and consulting physician relation-
ships determine prescribing practices by midwives of anti-
hypertensive agents. Although some midwives may not pre-
scribe antihypertensive medications, it is ideal for midwives to
have knowledge of these agents, as they may continue to care
for these women. Common maintenance medications used to
treat hypertensive disorders of pregnancy are listed in Table 4.
Antihypertensive Medications Contraindicated
in Pregnancy
Angiotensin-converting enzyme (ACE) inhibitors and
angiotensin-receptor blockers (ARBs) are contraindicated in
 Table 4. Common Maintenance Antihypertensive Medications Used to Treat Hypertensive Disorders in Pregnancy
Medication Dosage
Generic (Brand) Dosage Range Frequency Action Comments
Methyldopa 250-500 mg orally 2-4 times Centrally acting alpha-2 adrenergic May reduce mental alertness and
(Aldomet) MDD 3000 mg/day5,57 daily57 agonist. Reduces sympathetic increase fatigue. Dry mouth
tone; decreases systemic possible.58 May consider adding
vascular resistance. Acts on sites a second agent if BP control
in the brainstem.58 suboptimal.
Labetalol 100-400 mg orally; usual 2-3 times Blocks alpha-1 vascular receptors Use cautiously in women with
(Normodyne) maintenance dosage daily57,58 and beta-1 and -2 receptors. BP severe asthma because of beta-2
200-600 mg reduction due to dilation of receptor blocker properties.58
MDD 2400 mg/day57,58 arterioles and veins, decreased
heart rate and inotropy, and
reduced renin release.58
Hydralazine Initially 10 mg for 2-4 4 times Direct vasodilation of arteriolar Vasodilatory effects lead to reflex
(Apresoline) days; titrate to 25 mg daily57 smooth muscle.58,59 stimulation of the sympathetic
for an additional 3-5 nervous system, increase in
days for a total of plasma renin, and compensatory
7 days. May titrate to fluid retention. Myocardial
50 mg until desired ischemia or infarction can be
blood pressure precipitated in women with
control achieved coronary atherosclerosis. These
MDD 300 mg/day 57 reflex mechanisms rapidly offset
the hypotensive effect of
hydralazine, causing rebound
hypertension and necessitating
additional antihypertensive
agents. May use beta blocker to
treat reflex tachycardia and
renin release.58,59 Side effects
may include headache, nausea,
flushing, or palpitations.57
Nifedipine Immediate release: Immediate Calcium channel blocker; prevents The increase in heart rate and
(Procardia) initially 10 mg; usual release: 3 calcium ions from entering cells inotropy is temporary, typically
maintenance dosage times daily with greatest effect on the heart seen with immediate-release
10-20 mg Extended and vascular smooth muscle. form.58 Historically a theoretical
MDD 120 mg/day release: Blockage of calcium in concern about the use of
Extended release: once peripheral arterioles produces magnesium sulfate and
30-60 mg daily 58 vasodilation, thus decreasing BP. nifedipine simultaneously. The
MDD 120 mg/day58 Decreased BP activates estimated incidence of
baroreceptor reflex, causing neuromuscular blockade with
sympathetic stimulation of the the use of both agents together is
heart.57 less than 1%.60 Do not chew or
crush immediate release
nifedipine because of risk of
severe hypotension.

Abbreviations: BP, blood pressure; MDD, maximum daily dose.

Journal of Midwifery & Women’s Health r www.jmwh.org 9

pregnancy. Prenatal exposure to these medications during the
second or third trimester of pregnancy has been associated
with fetal hypotension, renal failure and oligohydramnios
with resultant intrauterine growth restriction, joint contrac-
tures, pulmonary hypoplasia, and fetal demise. Hypocalvaria,
wherein the cranial bones are hypoplastic, has also been re-
ported. First-trimester exposure to ACE inhibitors and ARBs
has been studied with inconsistent results.49,50 In a recent
study by Bateman et al,51 the authors concluded that after
adjusting for confounders representing known risk factors
for congenital malformations, exposure to ACE inhibitors
in the first trimester of pregnancy was not associated with
an increased risk of congenital malformations. The authors
stated that any conclusions must be made cautiously and that
women should be placed on alternate hypertensive therapy
early on to prevent known late-pregnancy exposure. Few
studies have specifically investigated first-trimester exposure
to ARBs. Because of inconsistent results and the lack of
studies of the use of ARBs, it is recommended that women
who are planning a pregnancy be changed to an alternate
antihypertensive.49,50
POSTPARTUM HYPERTENSION
Blood pressure tends to decrease immediately postpar-
tum with a subsequent rise that generally peaks on post-
partum days 3 to 6.50 Hypertension due to preeclampsia
may resolve within the first postpartum week; however, in
more severe cases, hypertension may not resolve until 2 to
4 weeks postpartum.44 Therefore, postdischarge follow-up for
all women with preeclampsia should be within 3 to 7 days
if blood pressure medication was administered during la-
bor and birth or postpartum. If no blood pressure medica-
tion was used, follow-up should be within 7 to 14 days after
discharge.52
Hypertension may present for the first time in the post-
partum period, often after the woman has been discharged.
California pregnancy-related deaths from 2002 to 2005 were
reviewed by a multidisciplinary committee. Out of the
207 deaths, 36 (17%) were identified as caused by preeclamp-
sia or eclampsia. Of those deaths, 60% were determined to
have had a good-to-strong chance of preventability. Con-
tributing maternity care provider and patient factors were
identified.48 Women may not seek prompt medical care if
they lack understanding of the symptoms of preeclampsia.5
Several retrospective studies have found that many women
who presented postpartum with eclampsia and stroke expe-
rienced symptoms for hours or even days prior to presenta-
tion for care. Furthermore, some providers are not aware that
preeclampsia and eclampsia can arise up to 4 weeks after birth.
It is recommended that all postpartum women, not only those
with known hypertension, be provided with education upon
discharge about the signs and symptoms of preeclampsia and
the importance of promptly contacting their maternity care
providers.5
Compounding the issue of postpartum preeclampsia-
associated hypertension in the immediate postpartum period
is the use of nonsteroidal anti-inflammatory drugs (NSAIDs)
for pain relief. Blood pressure may be increased with use
of NSAIDs because of salt and fluid retention and vaso-
10
constriction due to the inhibition of prostaglandin produc-
tion. NSAIDs can also mitigate the effectiveness of sev-
eral antihypertensive medications, including beta blockers.45
NSAIDs should be avoided postpartum in women with
known hypertension.53,54
COUNSELING FOR THE FUTURE
Recurrence Risk
Women who experience gestational hypertension have a 16%
to 47% risk of developing gestational hypertension in a subse-
quent pregnancy, and the risk of developing preeclampsia in
a future pregnancy is 2% to 7%. The risk of developing gesta-
tional hypertension in a future pregnancy, for a woman who
has had preeclampsia in a prior pregnancy, is 13% to 53%,
with a 16% possibility of a subsequent pregnancy being af-
fected by preeclampsia. A previous pregnancy affected by se-
vere preeclampsia, eclampsia, or HELLP syndrome with birth
prior to 34 weeks’ gestation confers a 25% recurrence risk;
however, if birth was necessary prior to 28 weeks’ gestation,
the recurrence risk is 55%.3
Future Cardiovascular Disease
Pregnancy has traditionally been viewed as an isolated event
unrelated to a woman’s lifetime medical history. After birth
and the 6-week postpartum visit, the issues during preg-
nancy are often overlooked. However, hypertensive disorders
of pregnancy are associated with an increased risk of car-
diovascular disease and stroke well beyond the reproductive
years. The risk of a cardiovascular event within 10 years in
women with a history of preeclampsia is 18.2% versus 1.7% for
women with uncomplicated pregnancies. In 2011, the Amer-
ican Heart Association included preeclampsia as a major risk
factor for future cardiovascular disease.49 The risk is further
increased if a woman gave birth preterm or had a pregnancy
complicated by intrauterine growth restriction.5 Women who
had preeclampsia should be counseled postpartum about
these risks and referred to a primary care provider or cardiol-
ogist for continued follow-up care after pregnancy. The Amer-
ican Heart Association and the American Stroke Association
suggest that women with preeclampsia be evaluated within 6
to 12 months after birth of the affected pregnancy.55,56 The
ACOG task force recommends that women with preeclamp-
sia who gave birth preterm or who have a history or recurrent
preeclampsia have yearly assessment of blood pressure, fasting
blood glucose, body mass index, and lipids.5
CONCLUSION
Hypertensive disorders of pregnancy continue to be a leading
cause of maternal morbidity and mortality. Ongoing research
is advancing our understanding of preeclampsia; however, the
search for a predictive test for the disease remains elusive.
Currently, there are no proven biomarker or imaging tests for
routine use to predict preeclampsia. Recent guidelines such
as those by the ACOG Task Force on Hypertension in Preg-
nancy assist in defining hypertensive disorders of pregnancy
and clarifying diagnostic criteria as well as providing rec-
ommendations for management. Severe acute hypertension
Volume 00, No. 0, xxxx 2018
can be a life-threatening emergency with potential lifelong
morbidity. Maternity care providers are vigilant for hyper-
tension in pregnancy; however, they do not always recog-
nize the presence of disease or its severity or take prompt
action. Maternity care providers must use current guidelines
and evidence-based research to diagnose and treat suspected
preeclampsia to guard the health of women and fetuses.
AUTHOR
Diane M. Folk, CNM, DNP, NP, is a member of the faculty
at Vanderbilt University School of Nursing’s nurse-midwifery
education program.
CONFLICT OF INTEREST
The author has no conflicts of interest to disclose.
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