Pregnancy Induced Hypertension: Mariano Marcos State University

Mariano Marcos State University
Republic of the Philippines

Batac, Ilocos Norte
College of Health and Sciences
Department of Nursing
PREGNANCY INDUCED
HYPERTENSION
BSN II-D Group 1

Aurelio, Lyca Mae M.
May 21, 2021
1
I. DEFINITION
https://nurseslabs.com/pregnancy-induced-hypertension/
• Pregnancy induced hypertension (PIH) is a condition wherein vasospasm

occurs during pregnancy in both the small and large arteries in the body.
Pregnancy induced hypertension (PIH) is defined as BP ≥ 140/90 mmHg, taken after a period
of rest on two occasions or ≥160/110 mmHg on one occasion in a previously normotensive
woman
• Also known as gestational hypertension.

• Pregnancy Induced Hypertension is a form of high blood pressure in pregnancy.
• It occurs in about 5 percent to 8 percent of all pregnancies.
• It is a condition in which vasospasm occurs during pregnancy in both small and
large arteries. With high blood pressure, there is an increase in the resistance of
blood vessels. This may hinder blood flow in many different organ systems in the
expectant mother including the liver, kidneys, brain, uterus, and placenta.
• Originally, it was called toxaemia because researchers pictured a toxin of some
kind being produced by the woman in response to the foreign protein of the growing
fetus, the toxin leading to the typical symptoms. No such toxin has ever been
identified.
https://www.hindawi.com/journals/tswj/2018/6268276/
History
According to some German authors, the first reports referring to eclampsia date from 2200
BC, observed in papyri of ancient Egypt [1]. The word eclampsia originates from the
Greek éklampsis and means “bright light” [1]. For about 2000 years, eclampsia was
understood as a disease characterized by convulsive seizures, typical of late gestation, that
ended at the childbirth. Scientists from the late 19th century, true enthusiasts of caregiver
empiricism, recognized the similarity between the swollen appearance of women who had
seizures and the edema of Bright’s disease, an abrupt glomerulonephritis onset characterized
by proteinuria. Thereafter, urinary alterations in childbearing women with seizures were
searched, which culminated in finding proteinuria in them. With the advent of noninvasive
blood pressure measurement, it was observed that these women had increased blood
2
pressure levels. It was not long before the understanding came that proteinuria and arterial
hypertension preceded the onset of the seizures. Thus, it was defined the “preeclampsia”
hypertensive condition, already understood at the time in its progressive character of severity
and which could lead, and led in a grim way, to series of consequences for the maternal and
fetal live
https://www.medicinenet.com/pregnancy-
induced_hypertension_symptoms_and_signs/symptoms.htm
Pregnancy-induced hypertension is high blood pressure that occurs during pregnancy.

Medical professionals also refer to the condition as gestational hypertension. In some
cases, hypertension during pregnancy can lead to a more dangerous condition known
as preeclampsia. Preeclampsia is a condition that usually starts after the 20th week of
pregnancy and is due to increased blood pressure and protein in the urine. Preeclampsia
affects the placenta, and it can affect the mother's kidney, liver, and brain. Preeclampsia is
a major cause of fetal complications, which include low birth weight, premature birth, and
stillbirth.
II. CLASSIFICATIONS
Gestational Hypertension
• A woman is said to have Gestational Hypertension when she develops an elevated

blood pressure (140/90 mmHg) but has no proteinuria or edema.
• Perinatal mortality is not increased with simple gestational hypertension, so no drug
therapy is necessary.
• Systolic blood pressure greater than 30 mmHg and diastolic blood pressure greater
than 15 mmHg above pregnancy values.
• No edema, no proteinuria and blood pressure returns to normal after birth.
Mild Preeclampsia
• A woman is said to be mildly preeclamptic when her blood pressure rises to 140/90
mmHg, taken on two occasions at least six (6) hours apart.
3
• Systolic blood pressure greater than 30 mmHg and diastolic blood pressure greater
than 15 mmHg above pregnancy values.
• In addition to hypertension, a woman has proteinuria (1+ or 2+ on a reagent test
strip on a random sample).
• A weight gain of more than 2 lbs/week in the second trimester or 1 lb/week in the
third trimester usually indicates abnormal tissue fluid retention.
Severe Preeclampsia
• A woman has passed from mild to severe preeclampsia when her blood pressure
has risen to 160 mmHg systolic and 110 mmHg diastolic or above on at least two
occasions 6 hours apart at bed rest.
• Marked proteinuria. 3+ or 4+ on a random urine sample or more than 5 g in a 24-
hour sample and extensive edema are also present.
• With the severe preeclampsia, the extreme edema will be noticeable as puffiness
in a woman’s face and hands.
• It is most readily palpated over bony surfaces. The woman may manifest oliguria
(altered renal function), elevated serum creatinine (more than 1.2 mg/dL); cerebral
or visual disturbances (blurred vision); thrombocytopenia and epigastric pain.
Eclampsia
This is the most severe classification of PIH. A woman has passed into this stage when
cerebral edema is so acute that seizure or coma occurs. With eclampsia, the maternal
mortality is high from cause such as cerebral hemorrhage, circulatory collapse or renal failure.
The fetal prognosis in eclampsia is poor because of hypoxia and consequent fetal acidosis.
The manifestations are the same accompanied by seizures.
https://www.mdedge.com/clinicianreviews/article/79478/cardiology/pregnancy-induced-
hypertension
Classification, Definitions
Pregnancy-induced hypertension (PIH) is classified as mild or severe. Mild PIH is defined as
new-onset hypertension (systolic blood pressure ≥ 140 mm Hg and/or diastolic blood
pressure ≥ 90 mm Hg), occurring after 20 weeks’ gestation. The majority of cases of mild PIH
4
develop beyond 37 weeks’ gestation, and in these cases, pregnancy outcomes are
comparable to those of normotensive pregnancies.2,7,8
Severe PIH is defined as sustained elevated blood pressures of ≥ 160 mm Hg systolic and ≥
110 mm Hg diastolic. In prospective cohort studies in which calcium supplementation and
low-dose aspirin use were being investigated for prevention of preeclampsia in healthy
pregnant women, those who were severely hypertensive were found to be at increased risk
for certain maternal comorbidities (eg, cesarean delivery, renal dysfunction, elevated liver
enzymes, placental abruption) and perinatal morbidities (delivery before 37 weeks’ gestation,
low birth weight, fetal growth restriction, and neonatal ICU admission), compared with patients
who were normotensive or mildly hypertensive.7,8
The diagnosis of PIH may later be amended or replaced by one of the following
diagnoses: preeclampsia, if proteinuria (to be defined and discussed later) develops; chronic
hypertension, if blood pressure remains elevated past 12 weeks postpartum; or transient
hypertension of pregnancy, if blood pressure normalizes by 12 weeks postpartum.5,6,10
III. RISK FACTORS
There are certain factors that contribute to the occurrence of pregnancy

induced hypertension.
• Women of color. Hypertension is most common to these women due to genetic

makeup of their race.
• Multiple pregnancies. Women who have undergone multiple pregnancies are
more compromised with hypertension.
• Primiparas who are 20 years and older. This group has an increased risk for
pregnancy induced hypertension than women who are 40 years old and above.
• Women from low socioeconomic backgrounds. These women may have a poor
diet due to their low socioeconomic background, which could contribute greatly to
hypertension.
• Underlying disease. This disease might contribute to the occurrence of pregnancy
induced hypertension.
5
2
https://emedicine.medscape.com/article/261435-overview#a4
Preeclampsia is more common at the extremes of maternal age (< 18 y or >35 y). The
increased prevalence of chronic hypertension and other comorbid medical illnesses in women
older than 35 years may explain the increased frequency of preeclampsia among older
gravidas. In addition, black women have higher rates of preeclampsia complicating their
pregnancies compared with other racial groups, mainly because they have a greater
prevalence of underlying chronic hypertension. Among women aged 30-39 years, chronic
hypertension is present in 22.3% of black persons, 4.6% of non-Hispanic white persons, and
6.2% of Mexican Americans. Hispanic women generally have blood pressure levels that are
the same as or lower than those of non-Hispanic white women.
Women who develop preeclampsia during pregnancy have an increased risk of recurrent
preeclampsia during subsequent pregnancies. The overall risk is about 18%. The risk is
higher (50%) in women who develop severe early preeclampsia (ie, before 27 weeks'
gestation). These women are also at increased risk for cardiovascular disease later in life.
Whether the preeclampsia increases cardiovascular risk or the 2 conditions share a common
underlying cause remains unclear. [11]
Maternal personal risk factors for preeclampsia
The following are maternal personal risk factors for preeclampsia:
• First pregnancy
• New partner/paternity
• Age younger than 18 years or older than 35 years
• History of preeclampsia
• Family history of preeclampsia in a first-degree relative
• Black race
• Obesity (BMI ≥30)
• Interpregnancy interval less than 2 years or longer than 10 years
Maternal medical risk factors for preeclampsia

The following are maternal medical risk factors for preeclampsia:
• Chronic hypertension, especially when secondary to such disorders as
hypercortisolism, hyperaldosteronism, pheochromocytoma, or renal artery stenosis
• Preexisting diabetes (type 1 or type 2), especially with microvascular disease
• Renal disease
• Systemic lupus erythematosus
• Obesity
• Thrombophilia
• History of migraine [12]
• Use of selective serotonin uptake inhibitor antidepressants (SSRIs) beyond the first
trimester
6
Placental/fetal risk factors for preeclampsia
The following are placental/fetal risk factors for preeclampsia:
• Multiple gestations
• Hydrops fetalis
• Gestational trophoblastic disease
• Triploidy
https://www.uptodate.com/contents/preeclampsia-clinical-features-and-diagnosis
A past history of preeclampsia increases the risk of developing preeclampsia in a

subsequent pregnancy eightfold compared with women without this history (RR 8.4, 95%
CI 7.1-9.9) [15].
The severity of preeclampsia strongly impacts this risk. Women with severe features of
preeclampsia in the second trimester are at greatest risk of developing preeclampsia in
a subsequent pregnancy: Recurrence rates of 25 to 65 percent have been reported [16-
19]. By comparison, women without severe features of preeclampsia in their first
pregnancy develop preeclampsia in 5 to 7 percent of second pregnancies [20,21].
Women who had a normotensive first pregnancy develop preeclampsia in less than 1
percent of second pregnancies.
●Preexisting medical conditions:
•Pregestational diabetes (RR 3.7, 95% CI 3.1-4.3) [15] – This increase has been
related to a variety of factors, such as underlying renal or vascular disease, obesity,
high plasma insulin levels/insulin resistance, and abnormal lipid metabolism [22].
•Chronic hypertension (RR 5.1, 95% CI 4.0-6.5) [15] – Although chronic
hypertension (when defined as blood pressure ≥140/90 mmHg) increases the risk
of preeclampsia fivefold compared with women without this risk factor, chronic
hypertension is uncommon in reproductive-age women and thus accounts for only
5 to 10 percent of preeclampsia cases [23].
Increasing data suggest that women with contemporary definitions of hypertension
are also at increased risk for preeclampsia [14,24-27]. There appears to be a dose-
response relationship between blood pressure and preeclampsia that becomes
clinically significant when blood pressure reaches the elevated level (systolic blood
pressure 120 to 129 mmHg and diastolic blood pressure <80 mmHg), increases
with stage 1 hypertension (systolic blood pressure 130 to 139 mmHg and/or diastolic
blood pressure 80 to 89 mmHg), and increases further with stage 2 hypertension
(systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg) [26,27].
•Some autoimmune disorders, such as systemic lupus erythematosus (RR 1.8,
95% CI 1.5-2.1) and antiphospholipid syndrome (RR 2.8, 95% CI 1.8-4.3),
increase the risk for developing preeclampsia [15]. The reasons for this relationship
7
are not clear but may include multiple mechanisms involving inflammation,
microangiopathy, increased platelet turnover, and kidney dysfunction.
•Prepregnancy overweight or obesity (body mass index >25 kg/m2 [RR 2.1, 95%
CI 2.0-2.2] and >30 kg/m2 [RR 2.8, 95% CI 2.6-3.1]) [15] – The risk of preeclampsia
doubles with each 5 to 7 kg/m2 increase in prepregnancy body mass index [28]. This
relationship persisted in studies that excluded women with chronic hypertension,
diabetes mellitus, multiple gestations, or after adjustment for other confounders.
Although overweight and obesity increase the risk of preeclampsia only two- to
threefold, overweight and obesity are highly prevalent worldwide and thus
cumulatively account for over 40 percent of preeclampsia cases [23].
•Chronic kidney disease (RR 1.8, 95% CI 1.5-2.1) [15] – The risk varies depending
on the degree of reduction of glomerular filtration rate and the presence or absence
of hypertension. In some studies, as many as 40 to 60 percent of women with
advanced chronic kidney disease (stages 3, 4, 5) were diagnosed with
preeclampsia in the latter half of pregnancy [29,30].
●Multifetal pregnancy (RR 2.9, 95% CI 2.6-3.1) [15] – In three large series,
preeclampsia occurred in 5 percent of singleton, 8 to 13 percent of twin, and 11 percent
of triplet gestations [31-34], although rates over 20 percent in multiple gestations are
commonly reported in small series [35].
●Nulliparity (RR 2.1, 95% CI 1.9-2.4) [15] – It is unclear why the nulliparous state is
consistently found to be the most prevalent predisposing factor for preeclampsia [15].
One theory is that the immune system of nulliparous women has had limited exposure
to paternal antigens, and this lack of desensitization may play a role in the pathogenesis
of the disease. Epidemiologic data support this theory: Protection from preeclampsia in
subsequent pregnancies is either reduced or eliminated if there is a change in paternity,
women using barrier methods of contraception are at increased risk, and risk is reduced
with increased duration of sexual activity before pregnancy [36]. However, the notion
that the risk of preeclampsia is increased in a subsequent pregnancy with a new partner
has been challenged by data suggesting that a longer interval between pregnancies may
be the reason for the increased risk with a new partner [37].
●A family history of preeclampsia in a first-degree relative (RR 2.90, 95% CI 1.70-
4.93) [14], suggesting a heritable mechanism in some cases [38,39]. The occurrence
and severity of the disease appear to be influenced primarily by maternal factors, but the
paternal contribution to fetal genes may play a role in defective placentation and
subsequent preeclampsia. (See "Preeclampsia: Pathogenesis", section on 'Genetic
factors'.)
●Prior pregnancy complications associated with placental insufficiency – Fetal
growth restriction (RR 1.4, 95% CI 0.6-3.0), abruption (RR 2.0, 95% CI 1.4-2.7), and
stillbirth (RR 2.4, 95% CI 1.7-3.4) can be different manifestations of placental
insufficiency [15]. They are risk factors for preeclampsia, and preeclampsia is a risk
factor for developing these disorders.
8
●Advanced maternal age (maternal age ≥35: RR 1.2, 95% CI 1.1-1.3; maternal age
≥40: RR 1.5, 95% CI 1.2-2.0) [15] – Older women tend to have additional risk factors,
such as obesity, diabetes mellitus, and chronic hypertension, that predispose them to
developing preeclampsia.
Whether adolescents are at higher risk of preeclampsia is more controversial. One
systematic review estimated that the prevalence of preeclampsia/eclampsia in
adolescent pregnancies was 6.7 percent [40] and another did not find an association
between adolescence and risk for preeclampsia [14], but the results are not conclusive
given the heterogeneity of the included studies. (See "Effects of advanced maternal age
on pregnancy".)
●Use of assisted reproductive technology is a risk factor in large cohort studies
(pooled rate 6.2 percent, 95% CI 4.7-7.9; RR 1.8, 95% CI 1.6-2.1) [15]. However,
multivariate logistic regression analysis attenuates this association, and propensity
analysis further weakens it [41]. In addition, one study reported the risk for hypertensive
disorders of pregnancy was increased with both autologous or donor oocyte frozen
embryo transfer and fresh donor oocyte embryo transfer, but not with autologous oocyte-
fresh embryo transfer [42].
IV. INCIDENCE
Muti, M., Tshimanga, M., Notion, G.T. et al. Prevalence of pregnancy induced hypertension
and pregnancy outcomes among women seeking maternity services in Harare,
Zimbabwe. BMC Cardiovasc Disord 15, 111 (2015). https://doi.org/10.1186/s12872-015-
0110-5
• Worldwide, 10 % of all pregnancies are complicated by hypertension, with pre-

eclampsia and eclampsia being the major causes of maternal and prenatal morbidity
and mortality
• It is also estimated that pregnancy induced hypertension (PIH), one of the
hypertensive disorders of pregnancy, affects about 5 – 8 % of all pregnant women
worldwide
• Pre-eclampsia affects 5-7 % of all pregnancies. It is broadly defined by hypertension
and proteinuria [4]. Eclampsia includes pre-eclampsia with the presence of
convulsions not attributable to other neurologic disease.
• Fifty percent of women diagnosed with gestational hypertension between 24 and 35
weeks develop preeclampsia
• PIH is a major pregnancy complication associated with premature delivery, intra-
uterine growth retardation (IUGR), abruptio placentae, and intra-uterine death, as well
as maternal morbidity and mortality [5, 6]. It is estimated that 9.1 % of maternal deaths
in Africa are due to hypertensive disorders of pregnancy
9
2
https://psa.gov.ph/content/deaths-philippines-2015-0
Hypertensive disorders of pregnancy account for 36.7% of all maternal deaths in the
Philippines [1], which is much higher than the worldwide rate of 18%
Eclampsia the number one leading cause of maternal death
The top leading cause of maternal deaths in 2015 was eclampsia with 337 (19.6%) out
of 1,721 deaths. It was followed by gestational hypertension with significant proteinuria with
292 (17.0%) deaths, and by abnormality of forces of labour with 206 (12.0%) deaths
J. Mayrink, M. L. Costa, J. G. Cecatti, "Preeclampsia in 2018: Revisiting Concepts,

Physiopathology, and Prediction", The Scientific World Journal, vol. 2018, Article
ID 6268276, 9 pages, 2018. https://doi.org/10.1155/2018/6268276
• Preeclampsia and eclampsia rank second or third in the world ranking of maternal
morbidity and mortality causes
• In an analysis implemented by the World Health Organization, which evaluated the
causes of maternal death occurred between 2003 and 2009, the hypertensive causes
appear in the second place, occurring in 14% of the cases, preceded only by
hemorrhagic causes, responsible for 27.1% of the maternal deaths
• Recently, Abalos et al., in a systematic review involving 40 countries with 39 million
women, showed an estimated rate of preeclampsia and eclampsia of 4.6% and 1.4%,
respectively
• In the last 50 years, there has been a decreasing trend in the incidence of these
aggravations in high-income countries, alongside an opposite movement in middle-
and low-income countries, which is basically due to access to quality prenatal care as
well as adequate management of cases of preeclampsia and eclampsia, with better
maternal and perinatal outcomes
hypertension
•
The risk for preeclampsia in patients with PIH is approximately 15% to 25% 12,16;
according to Magee et al,6 35% of women with PIH onset before 37 weeks’ gestation
develop preeclampsia.
10
• The risk for recurrence of PIH in subsequent pregnancies is about 26%, whereas
women who experience preeclampsia in one pregnancy have a comparable risk for
PIH or preeclampsia (about 14% each) in subsequent pregnancies.
V. MANIFESTATIONS
These signs and symptoms, once detected, would indicate pregnancy induced hypertension.
• Hypertension. An increase in the usual blood pressure of the woman is the first
indicator of this disease.
• Proteinuria. Protein leaks out during this condition and can be detected in the
urine.
• Edema. Since protein has already leaked out and it is responsible for containing
water inside the vessels, edema starts to occur.
hypertension
Clinical Presentation and Diagnostic Evaluation
Blood pressure should be measured and recorded at every prenatal visit, using the correct-
sized cuff, with the patient in a seated position.5 Gestational hypertension is a clinical
diagnosis confirmed by at least two accurate blood pressure measurements in the same arm
in women without proteinuria, with readings of ≥ 140 mm Hg systolic and/or ≥ 90 mm Hg
diastolic. It should then be determined whether the patient’s hypertension is mild or severe
(ie, blood pressure > 160/110 mm Hg). The patient with severe PIH should be evaluated for
signs of preeclampsia, as discussed below.
Patients with mild PIH are often asymptomatic, and the diagnosis is made at a prenatal visit
as a result of routine blood pressure monitoring; this is one of many reasons to encourage
early and regular prenatal care. Blood pressure may be higher at night in hypertensive
disorders of pregnancy
11
In contrast to patients with mild PIH, the clinical presentation of those with severe PIH or
preeclampsia (and the potential for impending eclampsia) may include the following
symptoms and signs:
• Generalized edema, including that of the face and hands

• Rapid weight gain
• Blurred vision or scotomata (ie, areas of diminished vision in the visual field)
• Severe, throbbing or pounding headaches
• Epigastric or right upper quadrant pain
• Oliguria (urinary output < 500 mL/d)
• Nausea, with or without vomiting
• Hyperactive reflexes
• Chest pain or tightness
• Shortness of breath
Laboratory Testing
In patients with PIH, laboratory evaluation should be focused to rule out preeclampsia. The
potential for proteinuria (defined as ≥ 0.3 g/d in a 24-hour urine sample1,14) must be
investigated at diagnosis and at regular visits during the pregnancy.1 At least two random
urine samples, collected at least 6 hours apart, should be evaluated for protein. A spot
(random) urine sample with a result of 2+ protein or greater is highly suggestive of proteinuria;
a 24-hour urine collection is the gold standard by which such findings should be confirmed
and protein levels in the urine quantified.1,14
Elevated blood pressure and proteinuria are the hallmarks of preeclampsia.6 Patients affected
by these developments must be evaluated for signs and symptoms of severe preeclampsia.
However, those with only mild elevations in blood pressure and little or no proteinuria may
complain of sudden-onset throbbing or pounding headache, blurry vision, and severe
epigastric pain—possibly indicating severe preeclampsia.5,10
In addition to laboratory evaluation for urinary protein excretion, the following tests are
recommended by the American College of Obstetricians and Gynecologists (ACOG)14 to
assess for end organ involvement, which is consistent with severe preeclampsia:
• Hematocrit, which may be either high, to suggest hemoconcentration; or low,

indicating hemolysis
• Platelet count, which is normal in women with PIH and low in those with severe
preeclampsia; if results are abnormal, this test should be followed by coagulation
12
testing (international normalized ratio, activated partial thromboplastin time,
fibrinogen)
• Renal function testing (blood urea nitrogen and creatinine may be elevated in severe
preeclampsia), and random urine testing for proteinuria, as explained earlier
• Liver enzymes (which are elevated in severe preeclampsia), and
• Lactate dehydrogenase (which is elevated in severe preeclampsia).1,14
https://childrenswi.org/medical-care/fetal-concerns-center/conditions/pregnancy-
complications/pregnancy-induced-hypertension
What are the symptoms of pregnancy-induced hypertension?
The following are the most common symptoms of high blood pressure in pregnancy.
However, each woman may experience symptoms differently. Symptoms may include:
• increased blood pressure

• protein in the urine
• edema (swelling)
• sudden weight gain
• visual changes such as blurred or double vision
• nausea, vomiting
• right-sided upper abdominal pain or pain around the stomach
• urinating small amounts
• changes in liver or kidney function tests
VI. COMPLICATIONS
https://emedicine.medscape.com/article/261435-overview#a23
Several complications that affect different organ systems need to be considered in gestational
hypertension.
Life-threatening complications in preeclampsia
Superimposed preeclamptic disorders on hypertension during pregnancy may lead to severe
maternal complications, including eclamptic seizures, intracerebral hemorrhage, pulmonary
edema (due to capillary leak, myocardial dysfunction, excess IV fluid administration), acute
13
renal failure (due to vasospasm, acute tubular necrosis [ATN], or renal cortical necrosis),
proteinuria greater than 4-5 g/d, HELLP syndrome (microangiopathic hemolysis, elevated
liver enzymes, and thrombocytopenia [platelets < 100/µL]), hepatic swelling with or without
liver dysfunction, hepatic infarction/rupture and subcapsular hematoma (which may lead to
massive internal hemorrhage and shock), DIC and/or consumptive coagulopathy (rare).
Consumptive coagulopathy is usually associated with placental abruption and is uncommon
as a primary manifestation of preeclampsia.
Fetal complications include abruptio placentae, intrauterine growth restriction, premature
delivery, and intrauterine fetal death.
Acute fatty liver of pregnancy
Although a distinct and rare disorder, acute fatty liver has some clinical features similar to,
and often overlapping with, severe preeclampsia.
Thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome
Although unrelated to preeclampsia, consider TTP and HUS important disorders in the setting
of presumed severe HELLP syndrome.
https://www.cdc.gov/bloodpressure/pregnancy
Complications from high blood pressure for the mother and infant can include the following:
• For the mother: preeclampsiaexternal icon, eclampsiaexternal icon, stroke, the need
for labor induction (giving medicine to start labor to give birth), and placental abruption
(the placenta separating from the wall of the uterus).1,4,5
• For the baby: preterm delivery (birth that happens before 37 weeks of pregnancy)
and low birth weight (when a baby is born weighing less than 5 pounds, 8
ounces).1,6 The mother’s high blood pressure makes it more difficult for the baby to
get enough oxygen and nutrients to grow, so the mother may have to deliver the baby
early. PIH has also been found to be a risk factor for low birth weight. Rahman et al
found PIH to be an independent risk factor for low birth weight. Women who delivered
low birth weight babies were 5 times more likely to have had pregnancy-induced
hypertension
https://www.marchofdimes.org/complications/high-blood-pressure-during-pregnancy.aspx
High blood pressure can cause problems for you and your baby during pregnancy, including:
Problems for moms include:
14
• Preeclampsia. This is when a pregnant woman has high blood pressure and signs
that some of her organs, like her kidneys and liver, may not be working properly.
Signs and symptoms of preeclampsia include having protein in the urine, changes
in vision and severe headaches. Preeclampsia can be a serious medical condition.
Even if you have mild preeclampsia, you need treatment to make sure it doesn’t
get worse. Without treatment, preeclampsia can cause serious health problems,
including kidney, liver and brain damage. In rare cases, it can lead to life-
threatening conditions called eclampsia and HELLP syndrome. Eclampsia causes
seizures and can lead to coma. HELLP syndrome is when you have serious blood
and liver problems. HELLP stands for hemolysis (H), elevated liver enzymes (EL),
low platelet count (LP).
• Gestational diabetes. This is a kind of diabetes that only pregnant women get.
It’s a condition in which your body has too much sugar (also called glucose). Most
women get a test for gestational diabetes at 24 to 28 weeks of pregnancy.
• Heart attack (also called myocardial infarction).
• Kidney failure. This is a serious condition that happens when the kidneys don’t
work well and allow waste to build up in the body.
• Placental abruption. This is a serious condition in which the placenta separates
from the wall of the uterus before birth. If this happens, your baby may not get
enough oxygen and nutrients in the womb. You also may have serious bleeding
from the vagina. The placenta grows in the uterus and supplies the baby with food
and oxygen through the umbilical cord.
• Postpartum hemorrhage (also called PPH). This is when a woman has heavy
bleeding after giving birth. It’s a serious but rare condition. It usually happens 1
day after giving birth, but it can happen up to 12 weeks after having a baby.
• Pulmonary edema. This is when fluid fills the lungs and leads to shortness of
breath.
• Stroke. This is when blood flow to your brain stops. Stroke can happen if a blood
clot blocks a vessel that brings blood to the brain or when a blood vessel in the
brain bursts open.
• Pregnancy related death. This is when a woman dies during pregnancy or within
1 year after the end of her pregnancy from health problems related to pregnancy.
If you have high blood pressure during pregnancy, you’re also more likely have a cesarean
birth (also called c-section). This is surgery in which your baby is born through a cut that your
doctor makes in your belly and uterus.
Problems for babies include:
• Premature birth. This is birth that happens too early, before 37 weeks of
pregnancy. Even with treatment, a pregnant woman with severe high blood
15
pressure or preeclampsia may need to give birth early to avoid serious health
problems for her and her baby.
• Fetal growth restriction. High blood pressure can narrow blood vessels in the
umbilical cord. This is the cord that connects the baby to the placenta. It carries
food and oxygen from the placenta to the baby. If you have high blood pressure,
your baby may not get enough oxygen and nutrients, causing him to grow slowly.
• Low birthweight. This is when a baby is born weighing less than 5 pounds, 8
ounces.
• Fetal death. When a baby dies spontaneously in the womb at any time during
pregnancy.
• Neonatal death. This is when a baby dies in the first 28 days of life.
Kattah, A. G., & Garovic, V. D. (2013). The management of hypertension in

pregnancy. Advances in chronic kidney disease, 20(3), 229–239.
https://doi.org/10.1053/j.ackd.2013.01.014
Complications of hypertensive pregnancy
The most significant short term complications of hypertensive pregnancy in the mother are
cerebrovascular complications, including cerebral hemorrhage and seizures, renal
impairment and cardiovascular complications, such as pulmonary edema (Table 2). Women
with chronic hypertension and evidence of end-organ damage prior to pregnancy are at
increased risk of pulmonary edema, hypertensive encephalopathy, retinopathy, cerebral
hemorrhage and acute renal failure
HELLP syndrome occurs in 10–20% of severe preeclamptic/eclamptic pregnancies.32,33 The

syndrome was first described in 1982 by Weinstein and colleagues34 as being characterized
by hemolysis, low platelets and elevated liver enzymes. It is associated with significant
maternal morbidity and mortality. In a prospective study of 442 patients with HELLP
syndrome, there were 5 maternal deaths, 3 attributed to diffuse hypoxic encephalopathy, and
significant morbidity – including placental abruption (16%), acute renal failure (7.7%),
pulmonary edema (6%) and subcapsular hematoma (0.9%). 32 Hypertension and proteinuria
may not be present,32 and so providers must be alert to the deceptive signs and symptoms
of HELLP syndrome – including midepigastric or right upper quadrant pain, nausea, vomiting
and general malaise. Women with HELLP syndrome should typically be delivered as soon as
possible due to the significant morbidity and mortality. They are not candidates for expectant
management. 35,36 HELLP syndrome must be differentiated from hemolytic uremic syndrome
(HUS) and thrombotic thrombocytopenia purpura (TTP), two forms of thrombotic
microangiopathy that may present during pregnancy. 33 TTP and HUS, either typical or
16
atypical, are not characterized by elevated liver enzymes and, in addition, TTP is associated
with deficiency in the enzyme ADAMTS13, a metalloproteinase that degrades von Willebrand
factor multimers.
Eclampsia is the convulsive form of preeclampsia and occurs in 0.5% of patients with mild
preeclampsia, and in 2–3% of those with severe preeclampsia.37 The most feared
complication and cause of maternal death in eclampsia is stroke. 38 In a population-based
study in France in 1995, 31 cases of stroke in pregnancy were identified and eclampsia
accounted for nearly half of both hemorrhagic and non-hemorrhagic strokes. 39 A more recent
study by Martin and colleagues looked at 28 women who had suffered strokes in the setting
of severe preeclampsia and eclampsia 40 and found that their systolic blood pressures were
> 155 mm Hg immediately before their cerebrovascular accidents. Only 5 patients reached a
diastolic blood pressure of 105 mm Hg, and therefore would not necessarily be candidates
for treatment according to the current NHBPEP and ACOG guidelines. 1 In this study,
maternal mortality was 53.6%, and only 3 of the 28 patients had no residual deficits post-
stroke. The authors concluded that a paradigm shift is needed toward treatment of SBP of
155–160 mm Hg in severe preeclamptic and eclamptic patients.
Posterior reversible encephalopathy syndrome (PRES) was first described in the setting
of eclampsia in 1996. 41 PRES is a syndrome characterized by neurologic signs and
symptoms, such as headache, impaired consciousness, visual changes and seizures, in
combination with neuroimaging findings of vasogenic edema in the posterior circulation. In a
retrospective study of patients with eclampsia at Mayo Clinic, Rochester, 13 cases of
eclampsia were identified, of which 7 had neuroimaging studies, and all of the women had
characteristic findings of PRES syndrome. Importantly, pregnant patients developed PRES
at lower peak systolic BPs (mean 173 mm Hg) than the non-pregnant PRES subjects. 42 The
authors hypothesize that the reduction in BP in these women may delay progression of
vasogenic to cytotoxic edema and cerebral infarction. The true incidence of PRES in
eclampsia, or even in severe preeclampsia, has not been established, but the association is
one that requires future study.
Long-term complications
It was long believed that if hypertension and proteinuria resolve after delivery, there would
not be any long term risk of cardiovascular or renal complications in the mother. However,
recent studies have shown that a history of hypertensive pregnancy is a risk factor for
hypertension, 43,44 as well as cardiovascular disease, 44,45 with an approximate relative risk of
2, compared to those without hypertensive pregnancies. The risk of future kidney disease is
not clear, although several studies have suggested an association. It has been shown that a
history of preeclampsia is associated with a higher frequency of microalbuminuria up to 5
years after delivery. 46 A study using registry data from Norway found that preeclampsia
occurring during a first pregnancy increased the risk of future end-stage renal disease
(ESRD). 47 The study population consisted of women with a first singleton birth between 1967
and1991, and follow-up extended until December 2005. The absolute risk of ESRD after any
17
preeclamptic pregnancy was low, 14.5/100,000 person-years, but the adjusted relative risk
was 4.3 (95% CI 3.3–5.6), and in women with greater than 2 preeclamptic pregnancies, the
adjusted relative risk increased to 10.9 (95% CI 5.0–23.8). It should be noted that as this was
a registry study, and patients with renal disease prior to pregnancy were not able to be
excluded, which would certainly impact the associated risk. As to the mechanisms that
underlie this association, it is not clear whether it is the hypertensive pregnancy itself that
leads to the increased risk of these complications, or whether there is underlying endothelial
dysfunction in the mother that manifests differently at varying stages of life. Either way,
women with a history of preeclampsia should be advised regarding life style modifications
and should be monitored closely for traditional risk factors.
https://www.who.int/healthinfo/statistics/bod_hypertensivedisordersofpregnancy.pdf
Hypertensive disorders of pregnancy (HDP) represent a group of conditions associated with

high blood pressure during pregnancy, proteinuria and in some cases convulsions. The most
serious consequences for the mother and the baby result from pre-eclampsia and eclampsia.
These are associated with vasospasm, pathologic vascular lesions in multiple organ systems,
increased platelet activation and subsequent activation of the coagulation system in the
micro-vasculature1 . Eclampsia is usually a consequence of pre-eclampsia consisting of
central nervous system seizures which often leave the patient unconscious; if untreated it
may lead to death. The long-term sequelae of both preeclampsia or eclampsia are not well
evaluated, and the burden of hypertensive disorders of pregnancy stems mainly from deaths.
VII. PROGNOSIS
Marín, R., Gorostidi, M., Portal, C. G., Sánchez, M., Sánchez, E., & Alvarez, J. (2000). Long-
term prognosis of hypertension in pregnancy. Hypertension in pregnancy, 19(2), 199–209.
https://doi.org/10.1081/prg-100100136
After an average of 13. 6 years since the index pregnancy, women with hypertensive
pregnancies have an increased risk of subsequent hypertension. Gestational hypertension is
the hypertensive disorder of pregnancy with the highest incidence of subsequent
hypertension. Women with preeclampsia have a greater tendency to develop hypertension
than women with normotensive pregnancies. By contrast, women with eclampsia do not.
18
hypertension/page/0/3
Follow-Up and Prognosis

Patients with PIH should be evaluated postpartum for persistent hypertension. Blood
pressure in patients with PIH usually normalizes by day 7 postpartum.32 If blood pressure
elevation persists past 12 weeks postpartum, the patient’s diagnosis is revised to chronic
hypertension and managed accordingly.
In the patient with persistent hypertension who chooses breastfeeding, it is important to select
an antihypertensive medication with low transfer into breast milk. Many β-adrenergic
antagonists and calcium channel antagonists are considered “compatible” with breastfeeding
by the American Academy of Pediatrics.33
In addition to the potential for recurrent PIH in subsequent pregnancies, women with PIH are
at increased risk for hypertension later in life, and findings from several large cohort studies
suggest increased cardiovascular risk in patients with hypertensive
pregnancies. 16,34 9
Magnussen et al, who followed more than 15,000 mothers of singleton
infants for several years postpartum, found that those who experienced hypertensive
disorders (particularly recurrent hypertensive disorders) during pregnancy were more likely
than normotensive women to subsequently develop diabetes, dyslipidemia, and
hypertension. Women who remained normotensive while pregnant generally had lower BMI
measurements than those who experienced PIH or preeclampsia.
VIII. PATHOPHYSIOLOGY
• Increased cardiac output occurs with pregnancy, and it can injure the epithelial cell
of the arteries.
• Prostaglandin, a vasodilator, may also contribute to the injury.
• Reduced responsiveness of the blood vessels to the blood pressure is lost.
• There is vasoconstriction, and blood pressure increases.
Braunthal, S., & Brateanu, A. (2019). Hypertension in pregnancy: Pathophysiology and

treatment. SAGE open medicine, 7, 2050312119843700.
https://doi.org/10.1177/2050312119843700
19
Any hypertensive disorder of pregnancy can result in preeclampsia. It occurs in up to 35% of
women with gestational hypertension32 and up to 25% of those with chronic
hypertension.17,33 The underlying pathophysiology that upholds this transition to, or
superposition of, preeclampsia is not well understood; however, it is thought to be related to
a mechanism of reduced placental perfusion inducing systemic vascular endothelial
dysfunction.34 This arises due to a less effective cytotrophoblastic invasion of the uterine
spiral arteries.35 The resultant placental hypoxia induces a cascade of inflammatory events,
disrupting the balance of angiogenic factors, and inducing platelet aggregation, all of which
result in endothelial dysfunction manifested clinically as the preeclampsia
syndrome.35,36 Angiogenic imbalances associated with the development of preeclampsia
include decreased concentrations of angiogenic factors such as the vascular endothelial
growth factor (VEGF) and placental growth factor (PIGF) and increased concentration of their
antagonist, the placental soluble fms-like tyrosine kinase 1 (sFlt-1).37,38 Impeding the binding
of VEGF and PIGF to their receptors is a factor in the reduction of nitric oxide synthesis, a
crucial factor in vascular remodeling and vasodilation, which may otherwise be able to
ameliorate placental ischemia.39 Early-onset preeclampsia (EOPE), occurring before 34
weeks of gestation, is thought to be primarily caused by the syncytiotrophoblast stress leading
to poor placentation, whereas late-onset preeclampsia (LOPE), occurring at or after 34
weeks, is understood to be secondary to the placenta outgrowing its own circulation. 40 It is
worth mentioning that EOPE is more frequently associated with fetal growth restriction than
LOPE, due to a longer duration of placental dysfunction.29
During the postpartum period, up to 27.5% of the women may develop de novo hypertension.
This is due to several factors, including mobilization of fluid from the interstitial to intravascular
space, administration of fluids and vasoactive agents. The shift of fluids increases the stroke
volume and cardiac output up to 80%, followed by a compensatory mechanism of diuresis
and vasodilation, which softens the rise in blood pressure.35
The pathophysiology of hypertension in pregnancy becomes particularly relevant when

reviewing the current state of adjunct therapies to antihypertensives that may help prevent
preeclampsia.
hypertension
Pathophysiology and Risk Factors

Although the pathophysiology of PIH is not well understood, the pathogenesis
of preeclampsia likely involves abnormalities in the development, implantation, or perfusion
of the placenta, and often leads to impaired maternal organ function.6,11 It is not clear whether
PIH and preeclampsia are two different diseases that share a manifestation of elevated blood
pressure or whether PIH represents an early stage of preeclampsia.4,12 However, women with
20
preexisting hypertension, especially severe hypertension, are at increased risk for
preeclampsia, placental abruption, and fetal growth restriction. 2
There are some similarities and some distinct differences among the clinical features and risk
factors associated with PIH, compared with those of preeclampsia. Risk factors for PIH
include a pre-pregnancy BMI of 25 or greater, PIH and/or preeclampsia in previous
pregnancies, and history of renal disease, cardiac disease, or diabetes. The most important
risk factors for preeclampsia include preexisting diabetes or nephropathy, chronic
hypertension, PIH or preeclampsia in a previous pregnancy, maternal age younger than 18
or older than 34, African-American ethnicity, first pregnancy, multiple pregnancy, history of
preeclampsia in the patient’s mother or sister, obesity, autoimmune disease, and an interval
between pregnancies longer than 10 years.4-6,13-15
The risk for preeclampsia in patients with PIH is approximately 15% to 25%12,16; according to
Magee et al,6 35% of women with PIH onset before 37 weeks’ gestation develop
preeclampsia.6,12,17 The risk for recurrence of PIH in subsequent pregnancies is about 26%,
whereas women who experience preeclampsia in one pregnancy have a comparable risk for
PIH or preeclampsia (about 14% each) in subsequent pregnancies.18
Luger RK, Kight BP. Hypertension In Pregnancy. [Updated 2020 Oct 11]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK430839/
The pathophysiology of hypertension in pregnancy is not completely understood. Current

research demonstrates that improper trophoblast differentiation during endothelial invasion
due to abnormal regulation and/or production of cytokines, adhesion molecules, major
histocompatibility complex molecules, and metalloproteinases plays a key role in the
development of a gestational hypertensive disease. Abnormal regulation and/or production
of these molecules leads to abnormal development and remodeling of spiral arteries in the
deep myometrial tissues. This leads to placental hypoperfusion and ischemia. More recent
research shows role of antiangiogenic factors that are released by placental tissue cause
systemic endothelial dysfunction which can result in systemic hypertension. Organ
hypoperfusion from endothelial dysfunction is most commonly seen in the eyes, lungs, liver,
kidneys and peripheral vasculature. Overall, most experts agree underlying reason is
multifactoria
IX. DIAGNOSTIC PROCEDURES
https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/hospital-
medicine/pre-eclampsia-eclampsia-and-pregnancy-induced-hypertension/
21
What diagnostic tests should be performed?
The first diagnostic test would be blood pressure measurement. To diagnose hypertension
in pregnancy, an elevated reading of 140/90 mm Hg or greater must be obtained on two
separate occasions at least 4 hours apart but within a period of 7 days.
Caution must be taken to measure the blood pressure appropriately. A properly-sized cuff
must be used on the right arm at the level of the heart on a seated patient (in an ambulatory
setting) or in a semi-reclining position (in a hospital setting). Of note, it is not recommended
to take the blood pressure in the upper arm of a woman lying in a left lateral position because
the blood pressure would then be falsely lowered.The patient should rest quietly for 10
minutes and abstain from tobacco or caffeine for 30 minutes prior to having the blood
pressure taken. The same technique should be used on all measurements to ensure
consistency of readings. Diastolic pressure should be measured with the Korotkoff V sound
whenever possible. If it is absent, this should be noted and the Korotkoff IV sound may be
substituted, although the two sounds may be as much as 10 mmHg apart. Automatic devices
can be used as long as they are able to record the Korotkoff V sound, although a mercury
sphygmomanometer is the more accurate device.
The other required diagnostic test is the collection of all urine during a 24-hour period for
determination of the degree of proteinuria. The diagnostic threshold for preeclampsia is 300
mg of protein in a 24-hour urine collection. A spot protein/creatinine ratio cut-off level of 0.3
mg/dL can be used instead of the 24-hour urine collection for protein. Urine dipstick analysis
has low accuracy and is not recommended for determination of proteinuria; if there is no other
available alternative then a cut-off value of 1+ indicated proteinuria diagnostic of
preeclampsia.
These diagnostic criteria (hypertension and proteinuria) would apply to the majority of women
with pre-eclampsia. However, some women have developed pre-eclampsia and eclampsia
without either hypertension or proteinuria, although they may present with other signs and
symptoms or laboratory abnormalities of pre-eclampsia. For example, a parturient with pre-
eclampsia might not have elevation of blood pressure at the onset but she may present with
manifestations of a capillary leak (such as proteinuria, ascites, or pulmonary edema) or
abnormalities in laboratory values suggestive of multiorgan dysfunction. Conversely, the
absence of proteinuria should not negate the diagnosis of pre-eclampsia syndrome,
particularly in the setting of gestational hypertension with persistent symptoms and laboratory
abnormalities. Recently, in the absence of proteinuria, new-onset hypertension along with
these manifestations (thrombocytopenia, elevated liver enzymes, elevated serum creatinine,
cerebral symptoms, and pulmonary edema) have been recognized as pre-eclampsia with
severe features.
What laboratory studies should be ordered to help establish the diagnosis? How
should the results be interpreted?
22
New-onset hypertension in a pregnant woman should be evaluated with: complete blood
count (CBC), serum ALT and AST, serum creatinine, serum uric acid levels, and a 24-
hour urine collection for protein. If HELLP syndrome is suspected, the addition of a
peripheral smear, serum lactate dehydrogenase (LDH) and indirect bilirubin is recommended.
A coagulation profile consisting of a prothrombin time (PT), activated partial thromboplastin
time (aPTT) and fibrinogen is not indicated unless the platelet count is less than 100,000
cells/microliter
or if there is evidence of bleeding.
A finding of at least 300 mg of protein in a 24-hour urine collection fulfills the laboratory criteria
for the diagnosis of pre-eclampsia. Current literature reports variance in threshold levels to
indicate end-organ involvement in pre-eclampsia with severe features or HELLP syndrome.
In general, the accepted values are as follows:
Hematologic changes:
• Abnormal peripheral blood smear (schistocytes, burr cells, or echinocytes)
• Indirect bilirubin >1.2 mg/dL
• Platelet count <100,000 cells/ microliter
• Low serum haptoglobin
• Disseminated intravascular coagulation (DIC): thrombocytopenia, plasma fibrinogen <

300 mg/dL, fibrin split products above 40 mg/mL.
• LDH >600 international units/liter (IU/L)
Renal function abnormalities:
• Serum creatinine >1.1 mg/dL or twice of her baseline serum creatinine
Hepatic function abnormalities:
• Serum AST and ALT > 72 IU/L
Of note, massive proteinuria of >5 grams/ 24 hours is no longer a diagnostic criteria for
preeclampsia with severe features because the severe degree of proteinuria has recently
been found not to be associated with worse maternal and neonatal outcomes.
What imaging studies should be ordered to help establish the diagnosis? How should
the results be interpreted?
23
Ultrasound examination to evaluate fetal growth and amniotic fluid volume as well as a non-
stress test (NST) to evaluate fetal well-being are necessary. If the diagnosis of fetal growth
restriction is made, Doppler ultrasound evaluation of the umbilical artery should be performed
to rule out uteroplacental insufficiency.
In certain situations after an eclamptic seizure, maternal imaging may include computed
tomography (CT) scanning or magnetic resonance imaging (MRI) of the head. These studies
may show posterior reversible encephalopathy syndrome in women with eclampsia. In
approximately 50% of cases of eclampsia, CT and MRI can show edema and infarction in the
parieto-occipal subcortical white matter and adjacent gray matter. Cerebral imaging findings
in eclampsia are similar to those seen in hypertensive encephalopathy.
Imaging is unnecessary to make the diagnosis in most eclamptic women. Indications for
cerebral imaging include focal neurological deficits or prolonged coma in which other treatable
processes (hemorrhage or abnormalities requiring medical or surgical intervention) must be
excluded. Women with atypical presentation of eclampsia, either before 20 weeks or greater
than 48 hours after delivery, or with eclampsia refractory to medical therapy with magnesium
sulfate may also benefit from imaging to assist in diagnosis. Unfortunately there are no
pathognomonic imaging findings for eclampsia.
Physical Examination
The clinician performing the physical exam should be attentive to accurate blood pressure
measurements and any signs that suggest preeclampsia. Weight should be measured and
BMI calculated at each prenatal visit.
If the patient’s blood pressure is markedly elevated, the focused physical examination should
include an ophthalmologic examination for jaundice and for evidence of hypertensive
retinopathy or papilledema; pulmonary and cardiac examination; abdominal examination,
including palpation of the liver; examination of the face and extremities for edema; and a
complete neurologic examination, including assessment of deep tendon reflexes and
examination for clonus.
X. PREVENTION
24
1
https://rmob.coloradowomenshealth.com/pregnancy/preeclampsia-and-high-blood-pressure
High blood pressure prevention during pregnancy
As with most medical concerns, prevention is better than treatment if it is an option. We can
assist a woman in taking steps to help prevent high blood pressure during pregnancy and
preeclampsia. For women who want to get pregnant and already have hypertension,
managing that condition is a great first step.
Managing other pre-existing conditions is another important step in successful pregnancy

planning. If the woman is overweight, we will likely recommend weight loss. Medical
conditions such as diabetes should also be properly managed before pregnancy. Speaking
with one of our doctors at a preconception counseling appointment is an opportunity to learn
how to manage these risk factors.
For some mothers, we may recommend a low-dose aspirin regimen to help prevent
preeclampsia. This treatment is not effective for all women and should be discussed with a
doctor before adopting.

Non-pharmacological therapeutic approach
Lifestyle interventions, such as weight loss and a reduction in salt intake, are of proven benefit
in non-pregnant hypertensive patients. There is currently no evidence from prospective,
randomized trials that instituting an exercise program during pregnancy is effective in
preventing preeclampsia in at risk individuals,1,48, although some benefit has been seen in an
animal model.49 Similarly, there is no current evidence that instituting a weight loss program
in pregnancy can prevent preeclampsia,48 although obesity is a risk factor for gestational
hypertension and preeclampsia.50 In 2009, the Institute of Medicine revised their guidelines
for gestational weight gain and recommended that women who are overweight prior to
pregnancy (body-mass index (BMI) 25–29.9) gain only 15–25 lbs during pregnancy, as
opposed those with normal weight (BMI 18.5–24.9) prior to pregnancy, who should gain 25–
35 lbs.51 Obese women with a BMI > 30 should gain only 11–20 lbs, according to the new
recommendations.
25
As volume contraction is common in preeclampsia, salt restriction is not routinely
recommended. However, bed rest is frequently advised, and has been shown to lower blood
pressure, promote diuresis, and reduce premature labor
https://www.everydayhealth.com/hypertension/preventing/tips/hypertension-during-
pregnancy.aspx
How to Prevent Pregnancy Hypertension
• Know your blood pressure level before getting pregnant. Make an appointment for a
checkup with your primary care doctor or ob-gyn and make a note of your blood pressure.
You can also stop by a health fair for a free evaluation, or check you blood pressure at a
pharmacy that has a self-service machine.
• Kick the salt habit. High salt, or sodium, intake can raise blood pressure. If you typically
sprinkle salt on every dish, now is the time to break the habit. Most adults should keep salt
intake to 1 teaspoon per day — that includes what comes out of the shaker as well as the
hidden sodium in processed foods.
• Get off the couch. Get up and get moving before you conceive. If you’re already pregnant,
ask your doctor about starting a regular exercise program. Sedentary women are likely to
gain weight, which can increase the risk of hypertension during pregnancy, as well as before
and after. Try to start your pregnancy at a healthy body weight.
• Pay attention to medication. Make sure you aren't taking medication that can raise blood
pressure levels — check with your doctor to see what's safe. You may not realize that popping
a decongestant, such as pseudoephedrine (Sudafed and others), for something minor like a
stuffy nose can cause an increase in blood pressure. Think twice about using any medication
unless your doctor approves.
If you already have high blood pressure, talk to your doctor about medication use before and
during pregnancy. It is very important to have your blood pressure under control and stable
before becoming pregnant, as those nine months are not the best time to try new or additional
medication. Work with your doctor to make sure that you are taking a medication that will be
safe to continue during pregnancy.
• Get regular prenatal checkups. If your blood pressure starts to rise during pregnancy, you
want to catch it early. Make sure to keep all appointments and consider buying a home blood
pressure monitor to check your blood pressure more frequently.
• Don't smoke or drink alcohol. Tobacco and alcohol aren't safe for your unborn child and
will do no favors for your blood pressure.
26
4
Luger RK, Kight BP. Hypertension In Pregnancy. [Updated 2020 Oct 11]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK430839/
Enhancing Healthcare Team Outcomes
The management of hypertension in pregnancy is best done in an interprofessional team that

consists of a cardiologist, obstetrician, dietitian, physical therapist, and nurse. The key is to
prevent hypertension in the first place. While there is no one absolute way to prevent
hypertension during pregnancy, it should encourage the patient to change lifestyle and
become more physically active. The patient should eat healthy and avoid excess gain in
weight. Regular follow up with the obstetrician is recommended and the patient should be
taught how to monitor blood pressure at home. Smoking and alcohol should be avoided and
the patient should try and avoid eating too many sugary foods. [14][19](Level V)
XI. NEW TRENDS AND ISSUES

Future Directions
Over the last several years, evidence has emerged suggesting that women with hypertensive
pregnancy disorders are at an increased risk for both immediate and long-term cardiovascular
disease. On the other hand, current recommendations for the treatment of hypertension in
pregnancy, unlike those for the general population, have remained the same for many years,
mainly due to a lack of studies that address the safety and benefits of lowering BP in
pregnancy. At present, several interventional studies for the treatment of hypertension in
pregnancy are underway (ClinicalTrials.gov
– NCT01192412, NCT01351428, NCT00293735, NCT00194974, NCT01361425) that may
provide long needed information, with respect to therapeutic targets and preferred agents in
pregnant hypertensive patients. 24 While awaiting the results of these trials, a recent editorial
by Moser and colleagues suggested using a new approach to the treatment of hypertension
in pregnancy, whereby women with a history of chronic hypertension should continue their
anti-hypertensive medications throughout pregnancy, provided that they are safe, with careful
monitoring of BP and dose adjustments, as necessary. 24 The authors suggest that a new
target BP in previously normotensive women should be 140/90 mm Hg, with beta-blockers,
diuretics or calcium-channel blockers as first line therapies. The emphases of this proposal
are to simplify the classification of hypertensive pregnancy disorders into chronic
27
hypertension and de novo hypertension after 20 weeks, simplify the target BP goal to less
than 140/90 mm Hg, and recommend specific pharmacologic agents. The authors suggest
that the currently available methods for monitoring fetal well-being and safety should be
instrumental in this approach, and applied during both the introduction and titration of anti-
hypertensive medications. The studies currently underway may help address what the
appropriate targets for BP should be in pregnancy, and which anti-hypertensive agents are
most effective.
Current guidelines for the prevention of cardiovascular disease in women recommend referral
of patients with a history of hypertensive pregnancy to primary care or cardiology, in order to
facilitate monitoring and control of risk factors, 68 and though there are currently no guidelines,
routine screening for renal disease with blood urea nitrogen, serum creatinine and urinalysis
may be indicated in affected women. Future research should address the question as to
whether more aggressive BP control during hypertensive pregnancies may result in the
reduction of the future cardiovascular disease outcomes and renal disease in the affected
women.
XII. MEDICAL MANAGEMENT
Medical Management
Medications and other therapies are instituted by the physician to reverse pregnancy induced
hypertension.
• Antiplatelet therapy. There is an increased tendency for platelets to cluster along

the vessel walls, so a mild antiplatelet agent is ordered by the physician.
• Administer medications to prevent eclampsia. To avoid progression of the
disease to eclampsia, hydralazine, nifedipine, and labetalol may be prescribed to
reduce hypertension.
Treatment/Management and Follow-Up
Regular prenatal monitoring to assess for worsening of PIH and/or development of
preeclampsia is key to management. Figure 12 outlines an algorithm for managing PIH, which
28
is guided by the severity of the condition. Patients with mild PIH can be managed with weekly
outpatient visits and assessed for signs and symptoms of preeclampsia, monitoring of fetal
movements, weight, blood pressure measurements, and urine and blood tests. 2
At each visit, it is important to instruct patients to report immediately any of the following
symptoms: new-onset severe headache, visual changes, epigastric or right upper quadrant
pain, nausea or vomiting, difficulty breathing or chest tightness, as well as vaginal bleeding,
decreased fetal movements, or uterine contractions.6,14
Generally, expectant management with delivery at term is recommended for women with mild
PIH.2 Vaginal delivery (or cesarean delivery, if indicated) is recommended at 37 weeks or
when fetal maturity is confirmed; and at 34 weeks if fetal or maternal distress is evident. 2,6
Findings from the Hypertension and Preeclampsia Intervention Trial At Term (HYPITAT),22 an
open-label, randomized clinical trial in women with PIH or mild preeclampsia, suggested an
association between induction of labor between 36 and 41 weeks’ gestation and improved
maternal outcomes (specifically, reduced risk for severe hypertension), compared with
expectant management. Similarly, in a literature review by Caughey et al,23 results from nine
randomized controlled trials indicated a reduced risk for cesarean delivery in women who
underwent induction of labor, compared with expectant management. Rates of “successful”
induction of labor (ie, procedures resulting in vaginal rather than cesarean delivery) were
greater in women with higher parity, a favorable cervix, and earlier gestational age.
Based on data from the HYPITAT trial,22 a cost-effectiveness analysis of induction of labor
compared with expectant management revealed an 11% reduction in the average cost in
delivery that followed induction of labor, compared with expectant management, in women
with PIH or mild preeclampsia.24 Caughey et al23 reported similar savings, particularly when
induction of labor was performed at 41 weeks’ gestation.
If induction of labor is being considered in a woman with an unfavorable cervix, administration

of prostaglandins is recommended to enhance cervical ripening.6
Medication
Pregnant women should be advised to discontinue previously prescribed ACE inhibitors,
angiotensin receptor blockers, or thiazide diuretics, which are associated with congenital
abnormalities, intrauterine growth restriction, and/or neonatal nephropathy. 5,6,13,21
Antihypertensive medication is not recommended for women with mild to moderate PIH, as it
does not appear to improve outcomes. Evidence was found insufficient in a 2007 Cochrane
review to determine the potential impact of antihypertensive medications for treatment of mild
to moderate PIH on clinical outcomes such as preterm birth, infant mortality, and infant size
relative to gestational age.25 A similar review conducted in 2011, with primary outcomes that
included severe preeclampsia, eclampsia, and maternal death or perinatal death, concluded
29
only that further study was needed to determine how tightly blood pressure must be controlled
to improve maternal and fetal outcomes in patients with PIH. 26
ACOG14 recommends antihypertensive therapy (eg, hydralazine, labetalol) only for women
with diastolic blood pressure of 105 to 110 mm Hg or higher.1,2 There are several
recommendations from different organizations regarding the choice of antihypertensive
medications for PIH. In the UK’s NICE guidance,21 it is recommended that patients with
moderate to severe PIH take oral labetalol as first-line treatment to keep systolic blood
pressure below 150 mm Hg and diastolic blood pressure between 80 and 100 mm Hg.
Like severe preeclampsia, severe PIH should be managed in an inpatient setting.6,14 IV

labetalol or hydralazine is recommended to lower the blood pressure to less than 160/110
mm Hg, although current evidence is insufficient to identify a target blood pressure.6,26 A 2002
ACOG practice bulletin recommends one of the following:
• Hydralazine 5 to 10 mg IV every 15 to 20 minutes until the desired response is

achieved; or
• Labetalol 20 mg IV bolus, followed by 40 mg if not effective within 10 minutes, then 80
mg every 10 minutes with maximum total dose of 220 mg.1,14
In women who have severe PIH or who develop severe preeclampsia or eclampsia,
magnesium sulfate is administered to prevent or treat seizures.14 This agent should be used
during labor and for at least 24 hours postpartum.2 Dosing of magnesium sulfate for this
indication is 4 g IV bolus, followed by infusion of 1 g/h. It is important to monitor treated
patients for signs of toxicity, including muscle weakness, loss of patellar reflexes,
hypoventilation, pulmonary edema, hypotension, and bradycardia. IV calcium gluconate
should be readily available for use as an antidote to life-threatening hypermagnesemia
https://rmob.coloradowomenshealth.com/pregnancy/preeclampsia-and-high-blood-pressure
Treatment for mild preeclampsia
Mothers with mild features of preeclampsia may seek treatment at a hospital, by visiting her
OB-GYN or through close health monitoring at home. Monitoring and treatment include:
• Monitoring the baby: Our obstetrician may recommend keeping track of the baby’s
movements. This includes keeping a kick count to identify any changes in the baby’s
activity. It may also be recommended to perform monitoring of the baby through fetal
heart rate monitoring and/or ultrasounds to assess fetal growth and amniotic fluid
levels.
30
• Monitoring the mother: Frequently measuring mom’s blood pressure can help spot
an unhealthy trend before it gets severe. Doctors will also do urine analyses regularly
to monitor for any increase in protein, as well as monitor the kidneys, liver and lungs
for any changes. There will likely be weekly, or sometimes twice weekly, appointments
with a health care professional.
• Preterm birth: Based on the ongoing tests and monitoring, scheduling an early birth
could be the best option for the baby and mother to limit the impact of preeclampsia.
Treatment for severe preeclampsia
For women with more serious preeclampsia symptoms, also known as preeclampsia with
severe features, the treatment typically takes place in the hospital. This allows the obstetrician
the opportunity to monitor the mother’s and baby’s health and adjust the treatment plan
should the condition worsen.
Ultimately, the treatment for preeclampsia with severe features is to have the baby as soon
as possible.
If the pregnancy is at least 34 weeks along, our physicians will often recommend proceeding
with preterm delivery (or induced labor) as soon as it’s deemed safe for the baby’s health and
development. If the pregnancy is less than 34 weeks and stable, the obstetrician may
prescribe corticosteroids, which help the baby’s lungs mature faster in preparation for a
possible early birth after 34 weeks. The mother may also receive medication to help prevent
seizures and lower blood pressure.
Labor & delivery with gestational hypertension or preeclampsia
While giving birth, mothers with severe preeclampsia may be treated with intravenous (IV)
magnesium, which is safe for the baby. This medication is a potent muscle relaxer that
decreases the likelihood of the mother having a seizure, or eclampsia. This treatment typically
continues for 24 hours after delivery. It usually takes two weeks for the mother’s blood
pressure to return to normal levels after giving birth.
Gestational hypertension and complications resulting from high blood pressure are both
common and manageable. At CU Medicine OB-GYN East Denver (Rocky Mountain), we work
closely with parents to understand the risks and options, should the mother develop high
blood pressure in pregnancy or preeclampsia.
31
α-adrenergic agonists
One of the medications with the longest track record in pregnancy is methyldopa. A long-term
follow-up study on children born to women treated with methyldopa during pregnancy could
find no increased incidence of general health problems or cognitive problems. 54 This record
of safety makes it the first line agent recommended by the NHBPEP working
group. 1 Methyldopa acts centrally by decreasing sympathetic tone, and therefore can have
many side effects, including sedation and impaired sleep patterns. One potential side effect
is that it may cause mild elevations of liver enzymes, which can lead to diagnostic confusion
with HELLP syndrome. Although it is relatively safe, methyldopa is not a potent BP lowering
agent and side effects, which are commensurate with the dose, can limit its use. Methyldopa
can be combined with other anti-hypertensives, such as a diuretic (discussed below), to
achieve target blood pressure values.
Clonidine has a similar mode of action to methyldopa, but has a much stronger effect in
lowering BP. Clonidine may impair fetal growth, especially if the mother has a reduction in
heart rate after therapy is initiated. 21 It can cause significant rebound hypertension and does
not have as strong a record of safety as methyldopa. It should be considered in cases of
intolerance to methyldopa.
Beta-blockers
Beta-blockers are generally well-tolerated and safe in pregnancy. Labetalol is becoming one
of the favored therapies for hypertension in pregnancy. It is a non-selective beta blocker that
antagonizes both beta and alpha-1 receptors. Its side effects include fatigue, decreased
exercise tolerance, as well as bronchospasm in individuals with reactive airway disease.
Labetalol has been compared to methyldopa in prospective trials and neither medication was
associated with adverse maternal or fetal outcomes. 25,55 It is available in both oral and
intravenous forms, so it may be used for both outpatient and inpatient management.
Atenolol has been shown to have minimal effects on systolic BP in preeclamptic women, and
it is also associated with intrauterine growth retardation.56 Given the availability of other more
effective medications, including labetalol, atenolol should be avoided in pregnancy.
Calcium channel blockers
In a small trial of preeclamptic mothers who received nifedipine versus placebo, there were
significant reductions in maternal BP, serum creatinine and urea values, and 24-hour urinary
protein measurements, without a reduction in umbilical artery blood flow. 57 According to a
prospective, multicenter cohort study of 78 women exposed to calcium channel blockers in
32
the first trimester, mainly nifedipine and verapamil, there was no increase in major congenital
malformations. There was an increase in preterm delivery in those who received calcium
channel blockers versus controls, matched for age and smoking status (28% vs. 9%,
p=0.003), although this was attributed to underlying maternal disease by stepwise
regression.58 There is little data available on diltiazem, although it may be used as a rate
control agent in pregnancy,59 and has been shown to lower BP and proteinuria in pregnant
patients with underlying renal disease in a small study of 7 patients.60 Calcium channel
blockers are also potent tocolytics and can affect the progression of labor. A major concern
with calcium channel blockers in pregnancy is the concurrent use of magnesium sulfate for
seizure prophylaxis, as co-administration of these agents has been reported to cause
circulatory collapse and neuromuscular blockade.16 Despite these issues, calcium channel
blockers, nifedipine in particular, as there is more data available for it, is an effective and safe
alternative to methyldopa as a first-line agent for the treatment of hypertension in pregnancy.
Diuretics
As noted above, diuretics are the most commonly used medication among women of child-
bearing age with chronic hypertension. 19 A possible side effect of any diuretic is vascular
volume contraction, which may paradoxically cause further elevations of BP in preeclamptic
women. Women with preeclampsia have lower plasma volumes compared to those with
normal pregnancies, and volume contraction may stimulate the renin-angiotensin-
aldosterone axis, causing further increases in peripheral vascular resistance, thus worsening
hypertension. 24,61 However, the 2000 NHBPEP Working Group report on High BP in
Pregnancy recognized that the major concern for diuretic use in pregnancy is mainly
theoretical, as supporting evidence for their adverse effects is lacking. Therefore, if a woman
is on a diuretic prior to pregnancy, this can be continued during pregnancy, with the exception
of spironolactone, which may have fetal anti-androgen effects.
Hydralazine
Hydralazine is a direct vasodilator that can be administered orally or intravenously, and is

often used in the setting of hypertensive urgency, given its fast onset of action. However,
hydralazine has been associated with hypotension, oliguria and fetal distress. 62 It is also
associated with a lupus-like syndrome and peripheral neuropathy. The lupus-like syndrome
is usually seen with higher oral daily doses (> 200 mg daily)63, though has been seen with
doses as low as 50 mg daily when the exposure is prolonged (months to years)64. Due to
these potential side effects, labetalol is increasingly viewed as a safer agent for inpatient
management of hypertension. Hydralazine remains, however, commonly used when other
treatment regimens have failed to achieve adequate BP control, as most obstetricians are
quite familiar with its pharmacological actions and find its side-effect profile acceptable.
Renin-Angiotensin-Aldosterone System Blockade
33
Renin-Angiotensin-Aldosterone System (RAAS) blockers, including most commonly ACE
inhibitors and ARBs, are extremely effective in lowering BP and have significant benefit in
proteinuric diseases. Initially, these medications were considered to be relatively safe during
the first trimester, and only associated with defects when taken in the second trimester,
potentially leading to oligohydramnios, anuria, and fetal renal failure. However, a study
published in 2006 by Cooper and colleagues demonstrated that exposure to ACE inhibitors
in the first trimester can be associated with significant congenital malformations affecting both
the cardiovascular and central nervous systems. 65 The relative risk of major congenital
malformations after a first trimester exposure was 2.71 (95% CI 1.72–4.27) as compared to
infants with no exposure to anti-hypertensives. A 2011 study of over 400,000 women-infant
pairs in the Northern California Kaiser Permanente region did find an increased risk of
congenital heart defects in the offspring after exposure to ACE inhibitors in the first trimester
as compared to healthy controls (OR 1.54, CI 0.9–2.62), but not as compared to women on
other anti-hypertensive agents
XIII. NURSING MANAGEMENT
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279097/
General measures include:
• Care for respiratory system by:
• head-down tilt to help drainage of bronchial secretion,
• frequent change of patient position,
• keep upper respiratory tract clear by aspiration of mucous through a plastic

airway,
• prophylactic antibiotic and
• oxygen is administered during and after fits.
• a medical pro fessional skilled in performing intubations should be immediately

available (27).
• The tongue is protected from biting by a plastic mouth gauge.
• After sedation, a self-retained Foley’s catheter is applied. The hourly output of urine is
charted. Proteinuria, haematuria and specific gravity are noticed.
• Efficient nursing in a single quiet semi-dark room to prevent any auditory or visual
stimuli.
• Observation for maternal
34
• pulse
• temperature
• blood pressure
• respiratory rate
• tendon reflexes
• urine (see before)
• number of fits and duration of coma
• uterine contraction
• Observation for fetal:
• FHS.
Patient Education
Patient education is an important aspect of caring for women with PIH. The American
Academy of Family Physicians29,30 provides a comprehensive patient education resource that
defines the hypertensive disorders in pregnancy, explains the symptoms and signs of severe
hypertension or preeclampsia, and describes appropriate diagnostic tests, monitoring, and
treatment options. (See http://familydoctor.org/familydoctor/en/diseases-
conditions/pregnancy-induced-hypertension.printerview.all.html.)
Patients who are considering pregnancy should be counseled to maintain a healthy weight
prior to and during pregnancy. Adequate dietary calcium can reduce the risk for PIH, and
calcium supplementation has been shown to reduce the risk for preeclampsia, especially in
women at high risk.31 The Society of Obstetricians and Gynaecologists of Canada
recommends low-dose aspirin (75 mg/d) at bedtime for high-risk women, starting before
pregnancy, or upon diagnosis of pregnancy to prevent preeclampsia.6 Although there is
insufficient evidence to recommend dietary salt restriction, excess salt can increase fluid
retention and possibly blood pressure. Patients should be urged to attend all scheduled
prenatal visits and to review the warning signs and symptoms of severe hypertension and
preeclampsia at each visit.
Mode of delivery may be discussed and will depend on the severity of hypertension, presence
of preeclampsia, and fetal well-being. Vaginal delivery at term is considered optimal unless
35
there are indications for cesarean delivery. Induction of labor may be considered at term in
patients with PIH. Those with severe preeclampsia who may require preterm delivery must
be prepared for potential issues associated with prematurity.
https://www.nursingcenter.com/ce_articleprint?an=00000446-201711000-00026
The absence of definitive strategies to prevent preeclampsia limits nurses' ability to provide
anticipatory guidance and teach patients evidence-based approaches for reducing
preeclampsia risk. Nurses can, however, encourage all women planning pregnancy to work
toward achieving a healthy body weight and consume a healthy diet replete with
recommended nutrients. Current guidance is to limit foods with added sugars and those that
are high in fat and to eat a variety of fruits, grains, vegetables, low-fat or fat-free dairy, and
proteins, avoiding such sources of mercury as shark, swordfish, mackerel, and tilefish, and
limiting the consumption of another source, tuna, to less than six ounces per week.
Current screening approaches include preeclampsia risk identification through the

collection of demographic information and comprehensive personal and family history. Risks
related to a short time interval between exposure to paternal semen and pregnancy can be
assessed through a review of sexual history that includes duration of the sexual relationship
and use of a barrier birth control method. A personal or family history of preeclampsia may
provide an opportunity to discuss potential screening and diagnostic strategies.
Warning signs of preeclampsia can occur during the second half of pregnancy and in the
postpartum period. These include severe headache, right upper quadrant epigastric pain,
nausea, visual changes (such as loss of visual fields or seeing spots), difficulty breathing, and
swelling in areas such as the face or hands.40 Nurses play a key role in teaching pregnant
women about these subtle, subjective warning signs.
Accurate blood pressure measurement is crucial. Ask the patient to sit comfortably-with
her back supported, her feet flat on the floor, and her arm at heart level. Select the proper
cuff size based on the patient's arm circumference, and measure blood pressure on the same
arm each time.
Changes in body weight may indicate fluid imbalance associated with generalized edema.
A weight gain of more than three to five pounds in one week, reduced urine output, or the
presence of edema, including pulmonary edema, suggest preeclampsia-associated fluid
imbalance, especially during the second half of pregnancy.
36
Preeclampsia diagnosis and surveillance. Blood and urine tests may provide objective
evidence of preeclampsia during pregnancy and in the postpartum period. Upon diagnosis of
preeclampsia, maternal and fetal surveillance is initiated to determine progression and
severity. Maternal assessment includes evaluation of subjective symptoms, serial blood
pressure measurement, physical assessment, and laboratory analyses to guide intervention.
Fetal surveillance includes serial nonstress testing to evaluate fetal oxygenation, ultrasound
measurement of amniotic fluid volume as a proxy for fetal-placental perfusion, and estimation
of fetal growth and gestational age. The nonstress test may be accompanied by a biophysical
profile, scored based on ultrasound measurements of fetal breathing, body movements,
muscle tone, and amniotic fluid level. Umbilical artery Doppler velocimetry, which measures
blood flow in the umbilical cord or between the uterus and the placenta, may be indicated as
a follow-up if there are concerns related to reduced placental perfusion.
Determining optimal timing of delivery. Gestational age at diagnosis and severity of

preeclampsia are major factors in determining optimal timing of delivery, which is the only
way to reverse preeclampsia that occurs during pregnancy. The ACOG Task Force
recommends delivery for women with preeclampsia who are at or beyond 37 weeks' gestation
or who are between 34 and 37 weeks' gestation and have preeclampsia with severe
features.1 In women between 20 and 34 weeks' gestation, preeclampsia with severe features
is ideally managed in a facility with adequate maternal and neonatal intensive care resources.
Because of the risk of preterm birth, care includes corticosteroid administration to enhance
fetal lung maturity.
Pharmacologic treatment for severe sustained hypertension in pregnancy and the

postpartum period is instituted when systolic blood pressure rises to or above 160 mmHg or
when diastolic blood pressure rises to or above 110 mmHg. The goal is to stabilize blood
pressure at 140-150/90-100 mmHg (see Figure 241). If blood pressure is reduced to below
established goals, perfusion to maternal organs and the fetus may be insufficient. Nursing
management includes assessment of maternal response to antihypertensive therapy.
37

Pregnancy Induced Hypertension: Mariano Marcos State University

Uploaded by

Copyright:

Available Formats

Pregnancy Induced Hypertension: Mariano Marcos State University

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Pregnancy Induced Hypertension: Mariano Marcos State University

Uploaded by

Copyright:

Available Formats

Mariano Marcos State University

Republic of the Philippines

BSN II-D Group 1

May 21, 2021

• Pregnancy induced hypertension (PIH) is a condition wherein vasospasm

• Also known as gestational hypertension.

Pregnancy-induced hypertension is high blood pressure that occurs during pregnancy.

• A woman is said to have Gestational Hypertension when she develops an elevated

III. RISK FACTORS

There are certain factors that contribute to the occurrence of pregnancy

• Women of color. Hypertension is most common to these women due to genetic

Maternal medical risk factors for preeclampsia

A past history of preeclampsia increases the risk of developing preeclampsia in a

• Worldwide, 10 % of all pregnancies are complicated by hypertension, with pre-

Eclampsia the number one leading cause of maternal death

J. Mayrink, M. L. Costa, J. G. Cecatti, "Preeclampsia in 2018: Revisiting Concepts,

Clinical Presentation and Diagnostic Evaluation

• Generalized edema, including that of the face and hands

• Hematocrit, which may be either high, to suggest hemoconcentration; or low,

• increased blood pressure

Kattah, A. G., & Garovic, V. D. (2013). The management of hypertension in

Complications of hypertensive pregnancy

HELLP syndrome occurs in 10–20% of severe preeclamptic/eclamptic pregnancies.32,33 The

Hypertensive disorders of pregnancy (HDP) represent a group of conditions associated with

Follow-Up and Prognosis

Braunthal, S., & Brateanu, A. (2019). Hypertension in pregnancy: Pathophysiology and

The pathophysiology of hypertension in pregnancy becomes particularly relevant when

Pathophysiology and Risk Factors

The pathophysiology of hypertension in pregnancy is not completely understood. Current

IX. DIAGNOSTIC PROCEDURES

• Abnormal peripheral blood smear (schistocytes, burr cells, or echinocytes)

• Indirect bilirubin >1.2 mg/dL

• Platelet count <100,000 cells/ microliter

• Low serum haptoglobin

• Disseminated intravascular coagulation (DIC): thrombocytopenia, plasma fibrinogen <

• LDH >600 international units/liter (IU/L)

Renal function abnormalities:

• Serum creatinine >1.1 mg/dL or twice of her baseline serum creatinine

Hepatic function abnormalities:

• Serum AST and ALT > 72 IU/L

High blood pressure prevention during pregnancy

Managing other pre-existing conditions is another important step in successful pregnancy

Kattah, A. G., & Garovic, V. D. (2013). The management of hypertension in

Non-pharmacological therapeutic approach

How to Prevent Pregnancy Hypertension

Enhancing Healthcare Team Outcomes

The management of hypertension in pregnancy is best done in an interprofessional team that

XI. NEW TRENDS AND ISSUES

Kattah, A. G., & Garovic, V. D. (2013). The management of hypertension in

XII. MEDICAL MANAGEMENT

• Antiplatelet therapy. There is an increased tendency for platelets to cluster along

If induction of labor is being considered in a woman with an unfavorable cervix, administration

Like severe preeclampsia, severe PIH should be managed in an inpatient setting.6,14 IV

• Hydralazine 5 to 10 mg IV every 15 to 20 minutes until the desired response is

Treatment for mild preeclampsia

Treatment for severe preeclampsia

Labor & delivery with gestational hypertension or preeclampsia

Calcium channel blockers

Hydralazine is a direct vasodilator that can be administered orally or intravenously, and is