HYPERTENSION

IN PREGNANCY
Dr. CUCUK SANTOSO, SpOG
2019
 OVERVIEW
■ complicating up to 10% of pregnancies.
■ Hypertensive disorders during pregnancy are classified into
4 categories:
– Chronic hypertension
– Preeclampsia-eclampsia
– Preeclampsia superimposed on chronic hypertension
– Gestational hypertension/ transient hypertension/
chronic hypertension identified in the latter half of
pregnancy/ pregnancy-induced hypertension (PIH)
 Definitions
■ Chronic hypertension
– blood pressure exceeding 140/90 mm Hg before
pregnancy or before 20 weeks' gestation.
■ Pre-eclampsia
– new onset of elevated blood pressure readings after 20
weeks' gestation mandates the consideration and
exclusion of preeclampsia.
– occurs in 3-6% of all pregnancies.
– the incidence is 1.5 to 2 times higher in first time
pregnancies.
– a leading source of maternal mortality.
 CHRONIC
HYPERTENSION
 Chronic Hypertension
■ Underlying causes:
– renal parenchymal disease
– renal vascular disease
– endocrine disorders (eg, adrenocorticosteroid or
mineralocorticoid excess, pheochromocytoma,
hyperthyroidism or hypothyroidism, growth hormone
excess, hyperparathyroidism)
– coarctation of the aorta.
– oral contraceptive use.
■ About 20-25% of women with chronic hypertension develop
preeclampsia during pregnancy.
PRE-ECLAMPSIA
 Preeclampsia
■ the exact pathophysiologic mechanism is not clearly
understood.
– a disorder of placental dysfunction
■ endothelial dysfunction
■ associated vasospasm
– demonstrates evidence of placental insufficiency with
associated abnormalities
■ diffuse placental thrombosis
■ an inflammatory placental decidual vasculopathy
■ abnormal trophoblastic invasion of the endometrium
■ central to the development of this disorder is placental
damage from diffuse microthrombosis.
 Preeclampsia
■ The widespread endothelial dysfunction may manifest as:
– a maternal syndrome
– fetal syndrome
– Both maternal + fetal syndrome
■ The pregnant woman may manifest dysfunction of multiple
organ systems, including:
– the central nervous
– Hepatic
– Pulmonary
– Renal
– hematologic systems.
 Preeclampsia
■ Endothelial damage leads to pathologic capillary leak that
can present in the mother as:
– rapid weight gain
– nondependent edema (face or hands)
– pulmonary edema
– Hemoconcentration
– a combination
 Preeclampsia

■ The diseased placenta can also affect the fetus via

decreased uteroplacental blood flow.
■ This decrease in perfusion can manifest clinically as:
– nonreassuring fetal heart rate testing
– low scores on a biophysical profile
– Oligohydramnios
– fetal growth restriction.
 Preeclampsia
■ The hypertension occurring in preeclampsia is due primarily
to:
– Vasospasm
■ with arterial constriction and relatively reduced intravascular
volume compared with that of a normal pregnancy.
– Hyper-responsiveness to vasoactive peptides
■ The vasculature of normal pregnant women typically
demonstrates decreased responsiveness to vasoactive
peptides such as angiotensin-II and epinephrine.
– increased arterial stiffness
■ treatment with alpha methyldopa significantly improved the
vascular stiffness in preeclampsia but did not normalize it.
 Preeclampsia
=risk factors=
■ Maternal personal risk factors for preeclampsia
1. First pregnancy 5. Family history of
2. New partner/paternity preeclampsia
3. Age younger than 18 6. Black race
years or older than 35 7. Obesity (BMI ≥30)
years 8. Interpregnancy interval
4. History of less than 2 years or
preeclampsia longer than 10 years
 Preeclampsia
=risk factors=
Maternal personal Maternal medical
risk factors risk factors
1. First pregnancy 1. Chronic hypertension
2. New partner/paternity 2. Preexisting diabetes
3. Age younger than 18 years or older 3. Renal disease
than 35 years 4. Systemic lupus erythematosus
4. History of preeclampsia 5. Obesity
5. Family history of preeclampsia in a 6. Thrombophilia
first-degree relative 7. History of migraine
6. Black race 8. Use of selective serotonin uptake
7. Obesity (BMI ≥30) inhibitor antidepressants (SSRIs)
8. Interpregnancy interval less than 2 beyond the first trimester
years or longer than 10 years
 Preeclampsia
=risk factors=
Placental/fetal risk factors
1. Multiple gestations

2. Hydrops fetalis

3. Gestational trophoblastic disease

4. Triploidy
 GESTATIONAL
HYPERTENSION
 Gestational Hypertension
■ Definition
– hypertension with onset in the latter part of pregnancy (>20
weeks' gestation) without any other features of preeclampsia
– followed by normalization of the blood pressure postpartum.
– about one third develops the syndrome of preeclampsia.
– superimposed preeclamptic disorders cause most of the
morbidity due to chronic hypertension during pregnancy.
■ The pathophysiology of gestational hypertension is unknown.
■ Gestational hypertension may, however, be a harbinger of chronic
hypertension later in life.
 Gestational Hypertension
■ the leading causes of maternal mortality:
– Pre-eclampsia
– Thromboembolism
– Hemorrhage
– nonobstetric injuries
– Infections.
■ hypertension before pregnancy or during early pregnancy is associated
with a twofold increased risk of gestational diabetes mellitus.
■ maternal diastolic blood pressure (DBP) greater than 110 mm Hg is
associated with an increased risk for:
– placental abruption
– fetal growth restriction.
EVALUATION
 EVALUATION
■ Determining whether elevated blood pressure identified during
pregnancy is due to chronic hypertension or to preeclampsia is
sometimes a challenge, especially if no recorded blood
pressures from the first half of the gestation are available.
– Clinical characteristics obtained via history
– physical examination
– certain laboratory investigations
 may be used to help clarify the diagnosis.
 EVALUATION
=Gestational age=
■ Hypertension before 20 weeks' gestation is almost always
due to chronic hypertension;
■ new-onset or worsening hypertension after 20 weeks'
gestation should lead to a careful evaluation for
manifestations of preeclampsia.
■ preeclampsia is rare before the third trimester.
 EVALUATION
=Symptoms of preeclampsia=
■ Symptoms of preeclampsia may include:
– visual disturbances, typically scintillations and scotomata, presumed to be
due to cerebral vasospasm.
– new-onset headache that is frontal, throbbing, or similar to a migraine
headache.
– gastrointestinal complaints of sudden, new-onset, constant epigastric pain
that may be moderate to severe in intensity and due to hepatic swelling and
inflammation, with stretch of the liver capsule.
– rapidly increasing or nondependent edema may be a signal of developing
preeclampsia.
■ edema is no longer included among the criteria for the diagnosis of preeclampsia.
■ rapid weight gain is a result of edema due to capillary leak as well as renal sodium and
fluid retention
 EVALUATION
=Cardiovascular findings in preeclampsia=
■ edema in nondependent areas (such as the face and hands), or rapid weight
gain suggest a pathologic process and warrant further evaluation for
preeclampsia.
■ Preeclampsia is a multisystem disease with various physical signs.
■ How to measure the blood pressure in pregnancy in order to detect pre-
eclampsia ?
– Women should be allowed to sit quietly for 5-10 minutes before each blood
pressure measurement.
– Blood pressure should be measured in the sitting position, with the cuff at
the level of the heart.
■ Inferior vena caval compression by the gravid uterus while the patient is supine can
alter readings substantially, leading to an underestimation of the blood pressure.
 EVALUATION
=Ophthalmologic findings in preeclampsia=
■ Retinal vasospasm is a severe manifestation of maternal
disease
– consider delivery.
– retinal edema is known as serous retinal detachment.
■ This can manifest as severely impaired vision.
■ It generally reflects severe preeclampsia
■ lead to prompt consideration of delivery.
■ The condition typically resolves upon completion of
pregnancy and resolution of the hypertension and fluid
retention.
 EVALUATION
=Gastrointestinal findings in preeclampsia=
■ Right upper quadrant (RUQ) abdominal tenderness
– liver swelling
– Liver capsular stretch.
– Consider delivery.
 EVALUATION
=Central nervous system findings in preeclampsia=
■ Brisk, or hyperactive, reflexes are common during
pregnancy.
■ Clonus is a sign of neuromuscular irritability that usually
reflects severe preeclampsia.
 ROUTINE TEST
=PRE-ECLAMPSIA=
■ Blood tests to order when evaluating eclampsia include those suggested to evaluate for
preeclampsia.
■ Such studies include: Spot urine specimens for
– urinalysis; obtaining protein/creatinine ratio
– complete blood cell (CBC) count can fulfill the proteinuria
– serum sodium, potassium, calcium diagnostic criteria for pre-
– uric acid
eclampsia.
– Creatinine
A ratio of greater than 0.3
– glucose levels
(when each is measured as
mg/dL) is an acceptable
– creatinine clearance
equivalent to 24 urine protein
– blood urea nitrogen (BUN)
greater than 300mg/day for
– Albumin
diagnosis of pre-eclampsia.
– liver enzymes and bilirubin
– urine dip for protein
 ROUTINE TEST
=CHRONIC HYPERTENSION=
■ For a woman with chronic hypertension in her first trimester, obtain
the following laboratory studies (to serve as baseline values, to be
referred to later in the pregnancy if a concern regarding superimposed
preeclampsia arises)
– CBC count
– Electrolytes
– BUN
– Creatinine
– liver enzymes
– urine dip for protein and a 24-hour urine collection for creatinine
clearance and protein excretion.
 Fetal Monitoring
■ Close fetal monitoring under the direction of an obstetrician is
essential in pregnant women with preeclampsia.
■ Preeclampsia is a disease of the placenta.
– hypoperfusion of the fetus
– manifest as a consequence of placental insufficiency :
■ a decrease in the amniotic fluid level (oligohydramnios)
■ fetal growth restriction
■ intrauterine fetal death
 an indication for delivery.
■ Monitoring ultrasounds to assess fetal growth after viability and fetal
surveillance by biophysical profile weekly or non-stress test twice
weekly.
 Medical Therapy
■ Acute severe hypertension in pregnancy is:
– a medical emergency
– requiring treatment to lower blood pressures within 30 minutes of
confirmation to reduce risk of maternal stroke.
■ According to the February 2015 ACOG Committee Opinion #623
“Emergent Therapy for Acute-Onset, Severe Hypertension During
Pregnancy and the Post-Partum Period,” first line options for
treatment include:
– oral immediate-release nifedipine
– IV labetalol
– IV hydralazine.
 Medical Therapy
■ Bedrest and hospitalization
– often are placed on bed rest or restricted activity
– no scientific evidence demonstrates that this is beneficial in
prolonging gestation or reducing maternal or fetal
morbidity/mortality.
■ Women with hypertension and suspected preeclampsia are typically
admitted to a hospital for close observation and investigation.
– Those with established preeclampsia must be observed very
closely, either in hospital or in a comprehensive home
monitoring program under the care of an obstetrician.
 Medical Therapy
■ no evidence suggests that pharmacologic treatment of mild
hypertension reduces the incidence of preeclampsia in this population
although the primary risk of chronic hypertension in pregnancy is
development of superimposed preeclampsia.
■ In normal pregnancy, women's mean arterial pressure drops 10-15
mm Hg over the first half of pregnancy.
– Most women with mild chronic hypertension (ie, SBP 140-160 mm
Hg, DBP 90-100 mm Hg) have a similar decrease in blood
pressures and may not require any medication during this period.
■ Women with preexisting end- organ damage from chronic hypertension
should have a lower threshold for starting antihypertensive medication
(ie, >139/89) and a lower target blood pressure (< 140/90). [3]
 Medical Therapy
■ DBP greater than 110 mm Hg has been associated with an
increased risk of:
– placental abruption
– intrauterine growth restriction
■ SBP greater than 160 mm Hg increases the risk of maternal
intracerebral hemorrhage.
– Therefore, pregnant patients should be started on
antihypertensive therapy if the SBP is greater than 160 mm Hg
or the DBP is greater than 100-105 mmHg.
■ The goal of pharmacologic treatment should be a DBP of less than
100-105 mm Hg and an SBP less than 160 mm Hg.
 Medical Therapy
■ If a pregnant woman's blood pressure is sustained greater
than 160 mm Hg systolic and/or 110 mm Hg diastolic at
any time, lowering the blood pressure quickly with rapid-
acting agents is indicated for maternal safety. [4]
■ Anticonvulsant therapy may be undertaken in the setting
of:
– severe preeclampsia (primary prophylaxis)
– eclamptic seizures (secondary prophylaxis).
– The most effective agent is IV magnesium sulfate
(MgSo4)
■ phenytoin is an alternative, although less effective, therapy.
 Medical Therapy
■ Methyldopa
– an established safety record
– a mild antihypertensive with a slow onset of action
■ Labetalol
– alpha blocker and beta blocker
– rapid onset of action
– orally or parenterally
– preferred as a first-line agent.
■ Nifedipine (Long Acting) is a reasonable medication to treat
chronic hypertension
 Medical Therapy
■ ACE inhibitors
– should be avoided during pregnancy
■ associated with:
– fetal renal dysgenesis or death when used in the second and third
trimesters
– increased risk of cardiovascular and central nervous system
malformations when used in the first trimester.
 Medical Therapy
■ Diuretics
– do not cause fetal malformations
– generally avoided in pregnancy
– prevent the physiologic volume expansion seen in normal
pregnancy.
– may be used in states of volume-dependent hypertension, such as
renal or cardiac disease.
 Medical Therapy
=chronic hypertension=
■ do not require antihypertensive therapy during most of pregnancy.
– If maternal blood pressure exceeds 160/100 mm Hg, however,
drug treatment is recommended.
– no data support the use of medication in patients with blood
pressures less than 160/100 mm Hg
■ Pharmacologic treatment of mild hypertension does not reduce the
likelihood of developing preeclampsia later in gestation
■ increases the likelihood of intrauterine growth restriction.
 Medical Therapy
=Pre-eclampsia=
■ delivering the baby is always in the mother's best interest.
– Any delay in delivery should be due to uncertainty about the
diagnosis or immaturity of the fetus.
■ When preeclampsia develops remote from term (ie, < 34-36 weeks'
gestation)
– attempts are often made to prolong the pregnancy to allow for
further fetal growth and maturation.
– should be promptly transferred to a facility with adequate
resources to care for premature newborn infants
– both maternal and fetal status must be very closely monitored.
– the mode of delivery decided by obstetric indications.
 Medical Therapy
=Pre-eclampsia=
■ Other symptoms and signs of worsening preeclampsia must be sought routinely
and delivery facilitated if the maternal or fetal condition worsens.
■ Patients who are diagnosed with HELLP syndrome are typically delivered after
corticosteroids have been completed for fetal benefit.
– Occasionally, the patient may be too unstable to wait for the full benefit of
steroids, and immediate delivery should be considered.
■ Hypertension due to preeclampsia may worsen or even present in the
postpartum period.
■ Blood pressure changes due to preeclampsia usually resolve within days to
weeks after delivery but may persist for 3 months.
– Persistent hypertension beyond this point probably represents chronic
hypertension.
 Medical Therapy
=Pre-eclampsia=
■ Longterm monitoring:
– Laboratory abnormalities related to preeclampsia (eg,
proteinuria, thrombocytopenia, liver enzyme elevations) should
be followed until the abnormalities return to the reference range.
– Women with preeclampsia require follow-up after hospital
discharge to ensure normalization of blood pressure and any
noted laboratory abnormalities.
■ Preeclampsia and related disorders identify women at increase risk
for future cardiovascular disease.
THANK YOU