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 mm Hg or diastolic ࣙ 110 mm Hg).5 Table 1 presents the
pregnancy, which is a 25% increase in incidence in the past diagnostic criteria for hypertensive disorders in pregnancy.
2 decades. This increase in the incidence of hypertensive
disorders in pregnant women has been attributed to factors Gestational Hypertension
such as the increases in obesity, advanced maternal age,
and women who have associated comorbidities.1,2 Women Within the cohort of women who have gestational hyper-
who have hypertensive disorders during pregnancy are at tension, 25% to 50% will develop preeclampsia.6 Gestational
risk for intrauterine growth restriction, placental abruption, hypertension is more likely to progress to preeclampsia
preterm birth, and cesarean birth.2 The risk of fetal demise in women who develop hypertension prior to 32 weeks’
is 3.6 per 1000 pregnancies; however, the risk of fetal demise gestation. Women with mild gestational hypertension may
for women with preeclampsia is 5.2 per 1000 pregnancies.3 progress to preeclampsia within 7 to 21 days of diagnosis.5
Hypertensive disorders of pregnancy are also associated with Although some biomarkers such as increased uric acid levels
increased maternal morbidity and mortality, predominantly are associated with progression to preeclampsia, none have
because of maternal stroke.1,4 This article reviews definitions sufficient predictive value yet to be used in clinical practice.7,8
of hypertensive disorders in pregnancy, pathophysiology
of preeclampsia, diagnostic criteria, evaluation, treatment, Preeclampsia-Eclampsia
hypertensive crisis, and maternal complications. Counsel-
ing women about future pregnancies and ongoing health Preeclampsia is a disorder unique to pregnancy,9 affecting 2%
maintenance will be addressed. to 8% of pregnant women.10 In the past, preeclampsia without
severe features was characterized as mild. This terminology is
DEFINITION AND DIAGNOSTIC CRITERIA FOR no longer used as it is recognized that preeclampsia is a spec-
HYPERTENSIVE DISORDERS IN PREGNANCY trum and can progress in severity quite rapidly.5 Even in the
absence of symptoms of severe disease, morbidity and mor-
In 2013, the American College of Obstetricians and Gyne- tality are increased in women with preeclampsia compared
cologists (ACOG) published the results of a task force that with women who do not have a hypertensive disorder during
reexamined the management of hypertension in pregnancy. pregnancy.5
Four categories defining hypertension during pregnancy The classic triad of signs and symptoms that were used
were established, including 1) gestational hypertension, to make the diagnosis of preeclampsia were hypertension,
2) preeclampsia-eclampsia, 3) chronic hypertension (any edema, and proteinuria. Although edema and proteinuria are
cause), and 4) chronic hypertension with superimposed often present in women with preeclampsia, they are no longer
preeclampsia.5 During pregnancy, hypertension is classified essential components of the diagnostic criteria. Edema was re-
as mild or moderate (systolic 140-159 millimeters of mercury moved from diagnostic criteria years ago, as edema is a com-
mon finding in the third trimester of pregnancy.6 The use of
Address correspondence to Diane M. Folk, CNM, DNP, NP, Vanderbilt proteinuria as one of the diagnostic criteria for preeclamp-
University School of Nursing, 461 21st Avenue South, 358 Frist Hall, sia has also been reassessed. If proteinuria is present, it is in-
Nashville, TN 37240. Email: [email protected] 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 Chronic Hypertension with Superimposed
who do not have proteinuria but do have thrombocytopenia, Preeclampsia
renal insufficiency, pulmonary edema, or cerebral or visual The frequency of superimposed preeclampsia is 13% to 40%
symptoms. among women with chronic hypertension.5 Women who have
Severe preeclampsia is characterized by findings in chronic hypertension and superimposed preeclampsia are at
addition to the principal criteria for diagnosis. Because increased risk for significant maternal-fetal morbidity and
intrauterine growth restriction is managed in the same mortality.
manner with or without preeclampsia, the presence of growth
restriction has been eliminated as a diagnostic finding in
severe preeclampsia.5 Related Disorders: HELLP Syndrome, Acute Fatty
Headache is included in the definition of the visual and Liver of Pregnancy, and Thrombotic
Thrombocytopenia Purpura/Hemolytic Uremic
cerebral disturbances associated with severe preeclampsia.
Syndrome
The descriptors of headache associated with preeclampsia
include “severe,” “persistent,” “worst headache ever experi- The spectrum of systemic involvement present in
enced,” or “not relieved with analgesics.”11 Benign headache preeclampsia-eclampsia, such as thrombocytopenia, ab-
symptoms occur in up to 60% of women of reproductive age normal liver enzyme concentrations, and hemolysis, can
and in 25% to 59% of women experiencing a normal preg- be confused with other conditions that can complicate the
nancy during the antepartum period. However, 50% to 80% of diagnosis and management of preeclampsia-eclampsia.
women who experience an eclamptic seizure have a headache Severe preeclampsia can be complicated by a syndrome
prior to the seizure.11 of hemolysis, elevated liver enzymes, and low platelets,
Atypical preeclampsia, defined as the onset of signs or or HELLP syndrome. HELLP syndrome occurs in nearly
symptoms of preeclampsia-eclampsia at either less than 20 10% to 20% of women affected by severe preeclampsia or
weeks’ gestation or more than 48 hours after birth, can present eclampsia.13 Signs of preeclampsia may be subtle or missing,
several weeks after birth.6 Eclampsia is the development of although hypertension is usually present.14 The clinical
new-onset seizures in a pregnant or postpartum woman with development of HELLP syndrome is often one of progressive
preeclampsia.5 Women who present with seizures may not and frequently abrupt worsening of maternal and fetal status.5
have been previously diagnosed with preeclampsia. Adverse outcomes, such as placental abruption, acute renal
failure, pulmonary edema, subcapsular liver hematoma,
stroke, coagulopathy, acute respiratory distress syndrome,
Chronic Hypertension
renal failure, and sepsis, have been reported.15
Chronic hypertension affects approximately 5% of women For women with HELLP syndrome who are at 34 0/7
during pregnancy. Hypertension that persists for more than weeks’ gestation or more, birth is facilitated as soon as the
12 weeks after birth is also considered chronic hypertension.2 woman is stable.5 The syndrome may worsen after birth. Ap-
In the last 20 years, the incidence of chronic hypertension proximately 20% to 30% of women with HELLP syndrome ex-
in the United States has increased in all ethnic and racial perience initial symptoms more than 48 hours after birth.6
groups, with the greatest increase among non-Hispanic black Acute fatty liver of pregnancy is a rare, potentially fa-
women.1 tal complication of pregnancy. This disorder occurs in ap-
There are 2 types of chronic hypertension. Primary or es- proximately one in 6700 to 13,000 women during pregnancy.
sential hypertension is defined as elevated blood pressure in Acute fatty liver of pregnancy is typically diagnosed in the
the absence of end-organ damage or attributable to a cause. third trimester and is more common in nulliparous women
Secondary hypertension is defined as elevated blood pres- and women with a multiple gestation.16,17 Historically, women
sure resulting from a renal or endocrinologic cause.5,12 Most with acute fatty liver of pregnancy had a maternal mortality
women with chronic hypertension have primary (essential) rate of nearly 70%. Because of advances in care and manage-
hypertension. Some women with chronic hypertension (as ment, maternal mortality is currently less than 10%. Perina-
many as 10%) may have underlying renal or endocrine dis- tal mortality is 13.1%. Neonatal morbidity continues to be ap-
orders responsible for secondary hypertension.5 proximately 74% because of the high rate of preterm birth.17

2 Volume 00, No. 0, xxxx 2018

 Table 1. Diagnostic Criteria Hypertensive Disorders in Pregnancy
Condition Diagnostic Criteria
Gestational SBP ࣙ140 mm Hg and/or DBP ࣙ90 mm Hg in a previously normotensive woman
hypertension Two BP readings at least 4 hours apart
Presents after 20 weeks’ gestation
Absence of proteinuria, laboratory abnormalities, pulmonary edema, or CNS signs
Preeclampsia without SBP ࣙ140 mm Hg and/or DBP ࣙ90 mm Hg in a previously normotensive woman
severe features 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)
Preeclampsia with Same as preeclampsia without severe features, with the addition of at least one of the following (proteinuria not
severe features 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 proteinuria, edema, low-grade fever, jaundice, ascites, bleed-
include malaise, anorexia, nausea, vomiting, epigastric or ing, and bright yellow urine. Laboratory abnormalities may
right upper quadrant pain, headache, and jaundice.16,17 Some include hemoconcentration, elevated white blood count,
women may present with preterm labor or decreased fe- elevated transaminases, hypoglycemia, elevated bilirubin,
tal movement. Examination findings include hypertension, 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- Although these disorders are not common during preg-
tithrombin levels consistent with disseminated intravascular nancy or the postpartum period, midwives should be aware of
coagulation.16,17 them because women who are affected by HELLP syndrome,
Another disorder that mimics preeclampsia is throm- acute fatty liver of pregnancy, or TTP/HUS may present with
botic thrombocytopenia purpura/hemolytic uremic syn- symptoms that suggest they have preeclampsia.
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- PATHOPHYSIOLOGY OF PREECLAMPSIA
cytopenia, hemolytic anemia, neurologic abnormalities, fever,
Abnormal Placentation
and renal dysfunction. The complete constellation of symp-
toms is seen in only 40% of patients, whereas 50% to 75% Preeclampsia is characterized by abnormal placentation and
demonstrate the initial 3 findings.16 failed remodeling of the spiral arteries that occurs early in
Presenting symptoms of TTP/HUS may also include ab- gestation. Normally, cytotrophoblast cells invade the decidual
dominal pain, nausea, vomiting, gastrointestinal bleeding, segment of the spiral arteries first, and then later, in a second
epistaxis, petechiae, or purpura. Neurologic symptoms are of- wave, they invade the myometrial portion of the arteries. This
ten vague but may include headache, visual disturbances, con- process causes the vessels to lose the muscular tunica media
fusion, aphasia, weakness, and seizures. Physical findings may so they become large, low-resistance vessels that can accom-
include hematuria, proteinuria, and tea-colored urine. Hyper- modate increased flow. The cytotrophoblast does not infiltrate
tension may be present or absent. Laboratory abnormalities the myometrial portion of the spiral arteries in women with
include thrombocytopenia (platelet count ⬍100,000/mm3 , of- preeclampsia.18 The vessels remain small and narrow with
ten ⬍20,000/mm3 ), acute anemia, and severe elevation of lac- the ability to constrict, which results in placental hypoperfu-
tate dehydrogenase. Liver enzyme transaminase findings may sion and hypoxia19–21 (Figure 1). This first stage of preeclamp-
be normal or elevated, whereas coagulation study findings are sia occurs prior to the appearance of clinical manifestations
usually normal.16 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- Table 2. Risk Factors for Preeclampsia
velop preeclampsia, but vascular, immunologic, and genetic Risk Factors
factors have all been implicated.19
African American race
The second stage of preeclampsia is due to maternal
inflammatory response to abnormal placentation and sub- Advanced maternal age (⬎40 years)
sequent placental hypoxia. This is referred to as maternal Chronic hypertension, chronic renal disease, or both
systemic endothelial activation.22 The resulting hypoxia and Family history of preeclampsia
subsequent oxidative stress lead to endothelial cell dysfunc- History of thrombophilia
tion in the maternal spiral arteries.23 The placenta releases
In vitro fertilization
excessive antiangiogenic factors, such as soluble fms-like ty-
rosine kinase 1 (sFlt-1) and soluble endoglin (sEng), which Multifetal gestation
are increased in the maternal circulation weeks before the Nulliparity
onset of clinical symptoms.24 Meanwhile, levels of proan- Obesity
giogenic factors, such as placental growth factor (PlGF) and
Previous preeclamptic pregnancy
vascular endothelial growth factor (VEGF), are decreased.20
Antiangiogenic factors counteract the effects of the proan- Systemic lupus erythematosus
giogenic factors, which are key in the maintenance of the Type I or type II diabetes mellitus
vascular endothelium.24 The shedding of placental debris into
Sources: Lo et al,1 American College of Obstetricians and Gynecologists.5
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- acid level is greater than 5.2 mg/dL (309 ␮mol/L). Although
tivation in preeclampsia.23 these findings are promising, prospective trials are needed
The vascular endothelium has many essential functions. It before clinical recommendations about use of uric acid lev-
is responsible for control of smooth muscle tone via the release els can be proposed.5,7,8 More recently, antiangiogenic pro-
of vasoconstrictor and vasodilatory chemicals as well as con- teins (sFlt-1 and sEng) and proangiogenic proteins (PlGF
trol of anticoagulation, antiplatelet activity, and fibrinolysis.25 and VEGF) have been investigated. Although the results are
The endothelium lines the entire circulatory system; thus, en- promising, more research is needed. Currently there are no
dothelial dysfunction in the placenta manifests itself in ev- biochemical markers that are recommended for use in clinical
ery organ system. Examples include edema due to capillary practice.26
leaking, proteinuria due to altered tubular protein filtration, The value of uterine artery Doppler velocimetry to pre-
pulmonary edema due to leakage of fluid into alveoli, and dict preeclampsia has also been studied. Resistance to flow in
liver dysfunction due to damage to the lining of small ves- the uterine circulation offers indirect information about faulty
sels causing hemolysis and fibrin deposition. The central ner- trophoblast invasion. Studies have demonstrated that predic-
vous system is also affected as the endothelium lining cerebral tion accuracy in low-risk women is minimal to moderate, and
blood vessels exhibits increased permeability, with resulting in high-risk populations it is minimal. Current evidence does
headache and visual disturbances.9 not support the use of uterine artery Doppler velocimetry for
the prediction of preeclampsia.5,27
Combinations of biomarker testing and uterine Doppler
RISK FACTORS FOR PREECLAMPSIA
artery velocimetry are encouraging and may prove useful as
Risk factors for preeclampsia are listed in Table 2. A woman research continues. However, no one test has been found to
has a 2- to 4-fold risk of preeclampsia if a first-degree rela- predict the development of preeclampsia, and there is no evi-
tive had a pregnancy affected by preeclampsia. Her risk is in- dence that accurate prediction of preeclampsia improves ma-
creased 7-fold if she experienced preeclampsia in a previous ternal and/or fetal outcomes.9 Therefore, ACOG does not rec-
pregnancy.5 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-
PREDICTION AND PREVENTION
curate selection of women who would benefit from referral
OF PREECLAMPSIA
for intensive surveillance or application of strategies to reduce
Recently there has been an effort to identify first-trimester the risk for developing severe preeclampsia-eclampsia.28 A re-
biomarkers to predict the development of preeclampsia. Fe- cent meta-analysis by the United States Preventive Services
toplacental proteins, such as human chorionic gonadotropin, Task Force (USPSTF) published in 2017 also states that evi-
estriol, alpha fetoprotein, inhibin A, pregnancy-associated dence is lacking to support any specific risk-based screening
plasma protein A, and placental protein 13, have been stud- approach or strategy for women during pregnancy because of
ied. Elevated uric acid has also been proposed as a marker the complex pathophysiology and clinical unpredictability of
for identifying women with gestational hypertension that may preeclampsia.29,30
progress to preeclampsia.5 A 2011 study that followed women
with gestational hypertension (N = 163) after measuring uric
Prevention
acid levels found that uric acid may be an accurate predictor
of progression from gestational hypertension to preeclamp- Interventions proposed for preventing preeclampsia include
sia, with a positive predictive value of 91.4% when the uric calcium supplementation in women with insufficient calcium

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

HYPERTENSION DURING PREGNANCY
Physical examination is one of the most informative compo-
nents in the evaluation for preeclampsia. Reported symptoms Midwives may collaborate in the care of women with medical
such as headache, visual disturbances, shortness of breath, conditions such as chronic hypertension. Midwifery manage-
chest pain, nausea, vomiting, heartburn, or abdominal pain ment of women with hypertensive disorders of pregnancy will
(right upper quadrant or epigastric) are concerning.6 Often, vary depending on state regulations, practice protocols, prac-
blood pressure measurement is the primary initial evaluation, tice setting, and consulting physician relationships.
followed by a test for proteinuria and assessment of weight to The major goals of treatment of hypertensive disorders of
determine if the woman has experienced a sudden increase in pregnancy are to prevent severe hypertension and maternal
weight that is larger than normal. Fundoscopic examination cerebrovascular events.5
can provide valuable information, as at least 50% of women
with preeclampsia will demonstrate retinal vascular changes.
Chronic Hypertension
Deep tendon reflexes are often increased prior to an eclamp-
tic seizure. Tremulousness may be present. Evaluation of the Women with chronic hypertension benefit from a compre-
abdomen for right upper quadrant tenderness, indicating hep- hensive evaluation early in pregnancy that includes serum cre-
atic capsular distension, should be performed.34 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 Fetal
Recurrent severe HTN Gestational age of 34 0/7 weeks
Recurrent symptoms of severe preeclampsia Severe IUGR (ultrasound estimate of fetal weight less
Progressive renal insufficiency (serum creatinine greater than 1.1 mg/dL or than 5th percentile)
doubling of the serum creatinine in the absence of other renal disease) Persistent oligohydramnios (maximum vertical
Persistent thrombocytopenia or HELLP syndrome pocket less than 2 cm)
Pulmonary edema BPP 4/10 or less on at least 2 occasions, 6 hours apart
Eclampsia Reversed end-diastolic flow on umbilical artery
Suspected placental abruption Doppler studies
Progressive labor or ROM Recurrent variable or late decelerations during NST
IUFD
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 ultrasound monitoring, may be indicated for women with ges-
chronic hypertension of greater than 4 years’ duration, an tational hypertension.6
electrocardiogram and/or echocardiogram to differentiate es- Antihypertensive medication is not recommended for
sential versus secondary hypertension and hypertension with women with mild gestational hypertension or preeclampsia
end-organ damage is recommended.5 without severe features with a systolic blood pressure less than
The precise goal ranges for blood pressure in pregnancy 160 mm Hg or diastolic less than 110 mm Hg.5 The ACOG
for women with chronic hypertension are not established, and task force advises twice weekly blood pressure measure-
there is considerable debate about when to initiate antihyper- ments, daily fetal movement counting, assessment of maternal
tensive therapy. Antihypertensive therapy has been shown to symptoms, weekly platelet counts, and liver enzyme moni-
reduce maternal morbidity by limiting episodes of severe hy- toring. For women without severe hypertension and mater-
pertension but has not been demonstrated to reduce the in- nal symptoms, magnesium sulfate is not recommended for
cidence of superimposed preeclampsia, placental abruption, seizure prophylaxis in the intrapartum setting.5
or intrauterine growth restriction.2 Furthermore, there is con-
cern that aggressively lowering maternal blood pressure may Preeclampsia with Severe Features
compromise uteroplacental perfusion.2
The National Institute for Health and Care Excellence in Maternal complications, such as severe renal failure, pul-
the United Kingdom recommends a blood pressure goal of monary edema, stroke, coagulopathy, and acute respiratory
less than 150/100 mm Hg for women with uncomplicated hy- distress syndrome, are more likely to occur in women who
pertension without comorbidities. In this population, it is rec- have preexisting comorbidities, such as obesity, renal disease,
ommended that diastolic blood pressure should not be less chronic hypertension, diabetes mellitus, acquired throm-
than 80 mm Hg because lower diastolic pressures may impede bophilia, and connective tissue disease. Most fetal and neona-
uteroplacental perfusion.38 The goal for pregnant women with tal complications are secondary to uteroplacental insuffi-
comorbidities related to hypertension is to maintain blood ciency and preterm birth.5
pressure at less than 140/90 mm Hg. Expectant management may be undertaken if the woman
The ACOG task force recommends different target blood is at less than 34 0/7 weeks’ gestation and both maternal and
pressure guidelines as well as individual recommendations for fetal conditions are stable. Administration of corticosteroids
the specific hypertensive disorders of pregnancy. For women to expedite fetal lung maturity is recommended. For women
with chronic hypertension with blood pressure values less with severe preeclampsia at 34 0/7 weeks’ gestation and be-
than 160/105 mm Hg and no end-organ damage, antihyper- yond, birth is advised as soon as maternal stabilization is
tensive therapy is not recommended during pregnancy. For achieved.5 Maternal and fetal indications for birth are listed
treating women with antihypertensive medications, the tar- in Table 3.
get blood pressure is 120 to 160 mm Hg systolic and 80 to
105 mm Hg diastolic. Women who have poorly controlled Acute Hypertensive Crisis
chronic hypertension are advised to use home blood pressure
monitoring.5 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
Gestational Hypertension and Preeclampsia without hypertension that persists for 15 minutes or more is a hy-
Severe Features
pertensive emergency.39,40 Treatment should not be delayed
Surveillance, such as more frequent prenatal visits, assess- pending laboratory results. The Consensus Bundle on Severe
ment of new maternal symptoms, serial laboratory evalua- Hypertension During Pregnancy and the Postpartum Period,
tion of platelets and liver enzymes, and interval fetal growth published in 2017, is a landmark collaboratively developed

Journal of Midwifery & Women’s Health r www.jmwh.org 7

patient safety bundle guideline that addresses the appropri- nant women, careful screening, and early diagnosis are cru-
ate response to severe hypertension identified in a pregnant cial. Women are less likely to seek care if they do not know or
or postpartum woman.39 Acute-onset severe hypertension understand the symptoms of preeclampsia.47 Lack of knowl-
should be confirmed within 15 minutes. If severe hyperten- edge about the severity of symptoms has been identified as a
sion is confirmed, treatment with antihypertensive medica- factor in maternal preeclampsia deaths.48 Women who are di-
tion should be initiated immediately to prevent maternal cere- agnosed and treated for preeclampsia have fewer unfavorable
bral hemorrhage or stroke.39 Institutional protocols should outcomes than those with delayed diagnoses.47
be in place and used. Systolic rather than diastolic hyper- Prompt recognition, evaluation, and treatment of hyper-
tension may be the most relevant predictor of cerebral hem- tensive emergencies are essential to prevent potentially dev-
orrhage or infarction.40,41 The goal of treatment is not to astating outcomes.39,40 Management of women with hyper-
reduce blood pressure to a normal range but to prevent repeti- tensive disorders of pregnancy will always include physician
tive or prolonged exposure to severe systolic hypertension and consultation, collaboration, and possibly referral depending
the ensuing loss of cerebral autoregulation.40 First-line thera- on institutional guidelines, the practice setting, and consult-
pies for acute hypertensive crisis include intravenous labetalol ing physician relationships.
(Normodyne) and hydralazine (Apresoline). An immediate-
release oral formulation of nifedipine (Procardia) is now a TIMING OF BIRTH
first-line therapy option, especially if the woman does not
One of the major changes in the management of women with
have intravenous access.5
gestational hypertension and preeclampsia is the timing of
Stroke is a known complication of severe preeclampsia-
birth. Preterm birth is associated with neonatal respiratory
eclampsia.41 Many maternal deaths from hypertensive
complications, neonatal intensive care unit admission, and
disease (38.7%) are due to cerebrovascular complications.42,43
higher incidence of neonatal death compared with neonates
Cerebral autoregulation, the process by which blood flow
born at 37 0/7 weeks’ gestation and beyond. However, ex-
to the brain is maintained at an appropriate level despite
pectant management in women with gestational hypertension
changes in blood pressure, is impaired in preeclampsia.44–46
and preeclampsia without severe features can increase the risk
This physiologic alteration is thought to explain why some
of development of severe hypertension, eclampsia, HELLP
women develop cerebral edema, cerebral hemorrhage, and
syndrome, placental abruption, and fetal death.5
seizures despite a lack of significant hypertension.43 It is also
For women with mild gestational hypertension or
theorized that severe acute hypertension causes cerebrovas-
preeclampsia without severe features, birth at or beyond 37
cular overregulation, triggering vasospasm.46
0/7 weeks’ gestation is recommended. Women experiencing
In a study published in 2008, the Dutch Maternal Mor-
preeclampsia with severe features at 34 0/7 weeks’ gestation
tality Committee reported findings reviewing the standard of
or beyond and women with unstable maternal or fetal status,
care in 27 cases of maternal mortality during the years 2000
regardless of gestational age, should give birth as soon as
to 2004 due to hypertensive disorder in pregnancy. Substan-
maternal stabilization is achieved. For women with HELLP
dard care was present in 96% of the cases. The cause of death
syndrome at 34 0/7 weeks’ gestation, birth should also occur
in 71% of the cases was cerebrovascular accident.42
upon maternal stabilization.5
Martin et al41 conducted a retrospective review of 28 med-
Studies have shown the amount or change in protein-
ical records of women with pregnancy-related stroke occur-
uria does not indicate the severity of preeclampsia or pre-
ring between 1980 and 2003. The most common signs present
dict maternal or fetal outcome.5,9 Therefore, a decision to in-
prior to stroke included headache (95.6%), nausea and vomit-
duce labor should not depend on the amount of proteinuria
ing (62.5%), epigastric pain (54.2%), and visual disturbances
or change in proteinuria.5
(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 ANTIHYPERTENSIVE MEDICATIONS USED
women. Diastolic blood pressure of 110 mm Hg or higher was TO TREAT HYPERTENSIVE DISORDERS
IN PREGNANCY
present only 12.5% of the time, but diastolic blood pressure of
105 mm Hg was present in 20.8% of this cohort. Protein- Midwives are increasingly caring for women during preg-
uria levels of 3+ to 4+ were present in only 58.3% of the nancy with medical complications. State regulations, practice
women. The maternal mortality rate in the 28 medical records protocols, practice setting, and consulting physician relation-
reviewed was 53.6%. Antihypertensive medications were ad- ships determine prescribing practices by midwives of anti-
ministered prior to stroke in 12.5% of cases, and magnesium hypertensive agents. Although some midwives may not pre-
sulfate was given in 50% of cases. The authors concluded that scribe antihypertensive medications, it is ideal for midwives to
withholding antihypertensive therapy in the presence of se- have knowledge of these agents, as they may continue to care
vere systolic hypertension is inadvisable.41 for these women. Common maintenance medications used to
treat hypertensive disorders of pregnancy are listed in Table 4.

ROLE OF THE MIDWIFE IN CARING FOR WOMEN

WITH HYPERTENSION DURING PREGNANCY Antihypertensive Medications Contraindicated
in Pregnancy
Hypertensive disorders of pregnancy are common, and mid-
wives are likely to be involved in the care of women who Angiotensin-converting enzyme (ACE) inhibitors and
develop hypertension during pregnancy. Education of preg- angiotensin-receptor blockers (ARBs) are contraindicated in

8 Volume 00, No. 0, xxxx 2018

 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 constriction due to the inhibition of prostaglandin produc-
second or third trimester of pregnancy has been associated tion. NSAIDs can also mitigate the effectiveness of sev-
with fetal hypotension, renal failure and oligohydramnios eral antihypertensive medications, including beta blockers.45
with resultant intrauterine growth restriction, joint contrac- NSAIDs should be avoided postpartum in women with
tures, pulmonary hypoplasia, and fetal demise. Hypocalvaria, known hypertension.53,54
wherein the cranial bones are hypoplastic, has also been re-
ported. First-trimester exposure to ACE inhibitors and ARBs COUNSELING FOR THE FUTURE
has been studied with inconsistent results.49,50 In a recent
study by Bateman et al,51 the authors concluded that after Recurrence Risk
adjusting for confounders representing known risk factors Women who experience gestational hypertension have a 16%
for congenital malformations, exposure to ACE inhibitors to 47% risk of developing gestational hypertension in a subse-
in the first trimester of pregnancy was not associated with quent pregnancy, and the risk of developing preeclampsia in
an increased risk of congenital malformations. The authors a future pregnancy is 2% to 7%. The risk of developing gesta-
stated that any conclusions must be made cautiously and that tional hypertension in a future pregnancy, for a woman who
women should be placed on alternate hypertensive therapy has had preeclampsia in a prior pregnancy, is 13% to 53%,
early on to prevent known late-pregnancy exposure. Few with a 16% possibility of a subsequent pregnancy being af-
studies have specifically investigated first-trimester exposure fected by preeclampsia. A previous pregnancy affected by se-
to ARBs. Because of inconsistent results and the lack of vere preeclampsia, eclampsia, or HELLP syndrome with birth
studies of the use of ARBs, it is recommended that women prior to 34 weeks’ gestation confers a 25% recurrence risk;
who are planning a pregnancy be changed to an alternate however, if birth was necessary prior to 28 weeks’ gestation,
antihypertensive.49,50 the recurrence risk is 55%.3

POSTPARTUM HYPERTENSION Future Cardiovascular Disease

Blood pressure tends to decrease immediately postpar- Pregnancy has traditionally been viewed as an isolated event
tum with a subsequent rise that generally peaks on post- unrelated to a woman’s lifetime medical history. After birth
partum days 3 to 6.50 Hypertension due to preeclampsia and the 6-week postpartum visit, the issues during preg-
may resolve within the first postpartum week; however, in nancy are often overlooked. However, hypertensive disorders
more severe cases, hypertension may not resolve until 2 to of pregnancy are associated with an increased risk of car-
4 weeks postpartum.44 Therefore, postdischarge follow-up for diovascular disease and stroke well beyond the reproductive
all women with preeclampsia should be within 3 to 7 days years. The risk of a cardiovascular event within 10 years in
if blood pressure medication was administered during la- women with a history of preeclampsia is 18.2% versus 1.7% for
bor and birth or postpartum. If no blood pressure medica- women with uncomplicated pregnancies. In 2011, the Amer-
tion was used, follow-up should be within 7 to 14 days after ican Heart Association included preeclampsia as a major risk
discharge.52 factor for future cardiovascular disease.49 The risk is further
Hypertension may present for the first time in the post- increased if a woman gave birth preterm or had a pregnancy
partum period, often after the woman has been discharged. complicated by intrauterine growth restriction.5 Women who
California pregnancy-related deaths from 2002 to 2005 were had preeclampsia should be counseled postpartum about
reviewed by a multidisciplinary committee. Out of the these risks and referred to a primary care provider or cardiol-
207 deaths, 36 (17%) were identified as caused by preeclamp- ogist for continued follow-up care after pregnancy. The Amer-
sia or eclampsia. Of those deaths, 60% were determined to ican Heart Association and the American Stroke Association
have had a good-to-strong chance of preventability. Con- suggest that women with preeclampsia be evaluated within 6
tributing maternity care provider and patient factors were to 12 months after birth of the affected pregnancy.55,56 The
identified.48 Women may not seek prompt medical care if ACOG task force recommends that women with preeclamp-
they lack understanding of the symptoms of preeclampsia.5 sia who gave birth preterm or who have a history or recurrent
Several retrospective studies have found that many women preeclampsia have yearly assessment of blood pressure, fasting
who presented postpartum with eclampsia and stroke expe- blood glucose, body mass index, and lipids.5
rienced symptoms for hours or even days prior to presenta-
tion for care. Furthermore, some providers are not aware that
CONCLUSION
preeclampsia and eclampsia can arise up to 4 weeks after birth.
It is recommended that all postpartum women, not only those Hypertensive disorders of pregnancy continue to be a leading
with known hypertension, be provided with education upon cause of maternal morbidity and mortality. Ongoing research
discharge about the signs and symptoms of preeclampsia and is advancing our understanding of preeclampsia; however, the
the importance of promptly contacting their maternity care search for a predictive test for the disease remains elusive.
providers.5 Currently, there are no proven biomarker or imaging tests for
Compounding the issue of postpartum preeclampsia- routine use to predict preeclampsia. Recent guidelines such
associated hypertension in the immediate postpartum period as those by the ACOG Task Force on Hypertension in Preg-
is the use of nonsteroidal anti-inflammatory drugs (NSAIDs) nancy assist in defining hypertensive disorders of pregnancy
for pain relief. Blood pressure may be increased with use and clarifying diagnostic criteria as well as providing rec-
of NSAIDs because of salt and fluid retention and vaso- ommendations for management. Severe acute hypertension

10 Volume 00, No. 0, xxxx 2018

can be a life-threatening emergency with potential lifelong on 28 consecutive cases. Am J Obstet Gynecol. 1999;181(2):389-
morbidity. Maternity care providers are vigilant for hyper- 395.
tension in pregnancy; however, they do not always recog- 18.Zhou Y, Fisher SJ, Janatpour M, et al. Human cytotrophoblasts adopt
a vascular phenotype as the differentiate: a strategy for successful en-
nize the presence of disease or its severity or take prompt
dovascular invasion? J Clin Invest. 1997;99(9):2139-2151.
action. Maternity care providers must use current guidelines 19.Fisher SJ. Why is placentation abnormal in preeclampsia? Am J Obstet
and evidence-based research to diagnose and treat suspected Gynecol. 2015;213(suppl 4):S115-S122.
preeclampsia to guard the health of women and fetuses. 20.Maynard SE, Karumanchi SA. Angiogenic factors and preeclampsia.
Semin Nephrol. 2011;31(1):33-46.
AUTHOR 21.Lam C, Lim KH, Karumanchi SA. Circulating angiogenic factors
in the pathogenesis and prediction of preeclampsia. Hypertension.
Diane M. Folk, CNM, DNP, NP, is a member of the faculty 2005;46(5):1077-1085.
at Vanderbilt University School of Nursing’s nurse-midwifery 22.Redman CW, Staff AC. Preeclampsia, biomarkers, syncytiotrophoblast
education program. stress, and placental capacity. Am J Obstet Gynecol. 2015;213(suppl
4):S9-S11.
23.Greer IA, Lyall F, Perera T, Boswell F, Macara LM. Increased concen-
CONFLICT OF INTEREST trations of cytokines interleukin-6 and interleukin-1 receptor antago-
The author has no conflicts of interest to disclose. nist in plasma of women with preeclampsia: a mechanism for endothe-
lial dysfunction? Obstet Gynecol. 1994;84(6):937-940.
24.Powe CE, Levine RJ, Karumanchi SA. Preeclampsia, a disease of the
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documents.s3.amazonaws.com/cmop/cmopresources/CMQCC_ article as a part of a continuing education theme issue. To
Preeclampsia_Toolkit_1.17.14.pdf. Accessed August 28, 2017. obtain CEUs online, please visit www.jmwhce.org. A CEU
48.Main EK, McCain CL, Morton CH, Holtby S, Lawton ES. Pregnancy- form that can be mailed or faxed is available in the print
related mortality in California: causes, characteristics, and improve- edition of this issue.
ment opportunities. Obstet Gynecol. 2015;125(4):938-947.

12 Volume 00, No. 0, xxxx 2018