Hypertension

in
Pregnancy
Jhon Philip Fuego
Clinical Clerk
WVSU-Medical Center
 Hypertension
• Appropriately taken blood pressure exceeding 140 mm Hg systolic or
90 mm Hg diastolic.
 Four Types of Hypertensive Disease
1. Gestational hypertension—evidence for the preeclampsia
syndrome does not develop and hypertension resolves by
12 weeks postpartum
2. Preeclampsia and eclampsia syndrome
3. Chronic hypertension of any etiology
4. Preeclampsia superimposed on chronic hypertension.
 Gestational Hypertension
New-onset of BP elevation after 20 weeks AOG without proteinuria.
BP returns to normal by 12 weeks postpartum
May have other signs or symptoms of preeclampsia

Transient hypertension
 PREECLAMPSIA
New onset hypertension + new onset proteinuria
• 24-hour urinary excretion >300mg
• Urine protein:creatinine ratio ≥ 0.3 or
• Persistent 30mg/dL protein (dipstick 1+)

BP elevation occurs after 20 weeks AOG and most

often near term
 PREECLAMPSIA
In the absence of proteinuria, preeclampsia is diagnosed as
hypertension with the following:
Thrombocytopenia Platelet count: <100,000/uL

Renal Insufficiency S. Creatinine >1.1 mg/dL, or doubling of baseline

Liver Involvement Serum Transaminase levels (AST/ALT) twice normal

Cerebral Symptoms Headache, Visual Disturbances, convulsions

Pulmonary Edema
 Severe Features of Preeclampsia

• BP ≥160/110 mmHg on 2 occasions at least 4 hours

apart while the patient is on bedrest
• Thrombocytopenia- platelet count <100,000/uL
• Impaired liver function- abnormally elevated liver
enzymes to 2x normal), severe right upper quadrant pain
 Severe Features of Preeclampsia

• Progressive renal insufficiency- serum creatinine

>1.1mg/dl or doubling
• Pulmonary edema
• New onset of cerebral/visual disturbances
 SEVERITY
GESTATIONAL
HYPERTENSION
DISORDERS
 ECLAMPSIA
• Convulsive phase of the disorder
• New-onset grand mal seizures in a woman with preeclampsia
• It can occur before, during and after labor
• Often preceded by premonitory events, but it can occur in the
absence of warning signs and symptoms
• Ominous signs: severe headache, epigastric distress,
hyperreflexia
• If seen in a patient, give MgSO4
 CHRONIC HYPERTENSION

• Blood pressures ≥ 140/90 mm Hg before pregnancy or

detected before 20 weeks or both
• Failure of BP to normalize postpartum
• If patient has taken anti-hypertensives before pregnancy,
chronic HPN is most likely
• Usual causes: chronic kidney disease (most common),
primary aldosteronism or phaeochromocytoma
 Categories of Chronic Hypertension Based on
Blood Pressure Levels

Mild to Severe
Moderate
Systolic 140-159 ≥160

Diastolic 90-109 ≥110

 CHRONIC HYPERTENSION WITH SUPERIMPOSED
PREECLAMPSIA
• Patients with chronic hypertension who develop
preeclampsia
• Usually earlier and more severe than pure
preeclampsia
• Associated with fetal growth restriction
 CHRONIC HYPERTENSION WITH SUPERIMPOSED
PREECLAMPSIA
• Includes patients with hypertension in early gestation
with the following findings:
• Proteinuria develops after 20 weeks
• Proteinuria present before 20 weeks with:
• Sudden exacerbation of hypertension
• RUQ pain and severe headache, increase in
liver enzymes
• Pulmonary congestion/edema
• Renal insufficiency
• Sudden, substantial and sustained increase in protein excretion
RISK FACTORS
 RISK FACTORS OF
PREECLAMPSIA SYNDROME
• Young and nulliparous women are vulnerable to developing preeclampsia,
• Older women are at greater risk for chronic hypertension with
superimposed preeclampsia
• Obesity, multifetal gestation, maternal, age, hyperhomocysteinemia, and
metabolic syndrome are associated with preeclampsia
• Environmental, socioeconomic, and even seasonal influences
• Smoking has been associated with a reduced risk for hypertension during
pregnancy probably due to upregulation of placental adrenomedullin
expression, which regulates volume homeostasis.
 ETIOLOGY OF
PREECLAMPSIA
 ETIOLOGY OF PREECLAMPSIA
• Abnormal trophoblastic invasion
• Placental implantation with abnormal trophoblastic invasion of uterine
vessels
• Immunologic Factors
• Maladaptive tolerance between maternal, paternal (placental) and fetal
tissues
• Endothelial Cell Activation
• Maternal maladaptation to cardiovascular or inflammatory changes of
normal pregnancy
• Genetic Factors
• Inherited predisposing genes as well as epigenetic influences
 ABNORMAL TROPHOBLASTIC INVASION
• Defective remodeling of spiral arteries
Normal Placental implantation In Preeclampsia
Proliferation of extravillous Defective implantation characterized
trophoblasts from the anchoring by incomplete invasion of spiral
villous arteriolar wall by extravillous
trophoblasts
Trophoblasts invade the deciduas and This results in a small caliber vessel
the walls of the spiral arteriole to with high resistance to flow
replace the endothelium and
muscular wall to create a dilated low
resistance vessel
 IMMUNOLOGICAL FACTORS
• Loss or dysregulation of tolerance of paternally derived placental and fetal
antigens
• Immune maladaptation – extravillous trophoblasts early in pregnancy
expressed reduced amounts of immunosuppressive nonclassic HLA G →
defective placental vascularization
• Women with 1597ΔC allele are predisposed to develop preeclampsia
• Possibly shared susceptibility genes with diabetes and
chronic hypertension
• Histological changes at the maternal-placental interface are suggestive of
acute graft rejection
 ENDOTHELIAL CELL ACTIVATION

• Continuation of defective placentation that leads to

inflammatory and ischemic changes that provokes endothelial
cell injury
• Results from extreme activated state of leukocytes in the
maternal circulation
• Oxidative stress generates toxic radicals that injure endothelial
cells
• The toxic radicals from oxidative stress can spread to the
maternal circulation
 GENETIC FACTORS
• Multifactorial, polygenetic

• Predisposition is likely the result of interactions of

literally hundreds of inherited genes – both
paternal and maternal that controls metabolic and
enzymatic functions on every organ systems
PATHOGENESIS AND
PATHOPHYSIOLOGY
SCREENING TESTS
SCREENING TESTS
 SCREENING TESTS
• Attempts have been made to identify early markers of faulty
placentation, impaired placental perfusion, endothelial cell
activation and dysfunction, and activation of coagulation.

• Currently, no screening tests are predictably reliable, valid,

and economical

• However, combinations of tests may be promising

 SCREENING TESTS
• Mean Arterial Pressure (MAP)
-defined as 1/3 systolic BP plus 2/3 the diastolic BP
-MAP value in the second trimester of >90mmHg and a MAP value in the 3rd
trimester of >105mmHg has resulted in an increase incidence of preeclampsia
• Supine pressor test/ Roll over Test
-done between 28-32 weeks (increased plasma volume)
-an increase of at least 20mmHg in diastolic pressure constitutes a Positive
Roll over Test
-positive predictive value is only 33%
• Combination of MAP and roll over test
-prediction rate increased to 78%
 SCREENING TESTS
Predictor Specificity (%) Sensitivity (%)

AFP 96 9
Fibronectin 94 65
Total Fetal DNA 88 50
hCG 89 24
Inhibin A 95 30
Activin A 89 61
PAPPA 94 10
Kallikreinuria 98 83
MANAGEMENT
 Basic management objectives:

• Termination of pregnancy with the least trauma to

mother and fetus
• Consider the safety of the mother first then
delivery of the baby
• Birth of an infant who subsequently thrives
• Complete restoration of health to the mother
 MATERNAL EVALUATION
• A. Laboratory Exam
a. CBC with Platelet
b. S. Creatinine
c. Lactic dehydrogenase
d. Liver enzymes
e. 24-hour urine protein or protein/creatinine ratio
B. Assess for symptoms of severe preeclampsia
 FETAL EVALUATION

• Sonographic Estimated Fetal Weight

• Non stress test
• Biophysical profile
• Doppler velocimetry
• Fetal weight – to check for presence of IUGR
• Amniotic Fluid – to check for oligohydramnios
 MANAGEMENT OF SEVERE PREECLAMPSIA

Aggressive
• High neonatal mortality and
morbidity due to prematurity
• Prolonged NICU stay
• Long term disability
Expectant
• Fetal death
• Asphyxial damage in utero
• Increased maternal morbidity
Schematic Clinical
Management Algorithm For
Suspected Severe
Preeclampsia At < 34 Weeks
 PHARMACOLOGY
• The following drugs are given to immediately lower BP:
• Labetalol – first line because it has decreased S/E of
tachycardia; not available locally; Contraindicated in asthma,
heart disease
• Hydralazine – aka apresoline; available in the Philippines;
maximum dose: 20-25 mg
• Nifedipine – if both drugs are not available

Rule of thumb: There should only be GRADUAL reduction of BP, never

abrupt to preserve adequate fetal circulation.
 PHARMACOLOGY

• Antihypertensive medications for urgent BP control during

pregnancy
• Labetalol – 10-20mg IV then 20-80mg q20-30min to
a maximum dose of 300mg
• Hydralazine – 5mg IV or IM then 5-10mg IV q15-20
min or constant infusion of .5-10mg/h
• Nifedipine – 10-20mg orally, repeat in 30 mins if
needed then 10-20mg q 2-6H
 PHARMACOLOGY

• Maintenance Medications
• Do NOT give methyldopa for the purpose of immediate
reduction of BP. It should only be for maintenance.
 OBJECTIVES FOR TREATMENT
A. Prevent complications B. Prevent and control
such as: Eclampsia
• Congestive heart failure • Premonitory S/Sx of
eclampsia
• Myocardial ischemia
• Presence of headache,
• Renal injury or failure
visual disturbances and
• Ischemic or hemorrhagic scotomata
stroke
• Epigastric or RUQ pain
• Hyperreflexia
 Magnesium Sulfate (MgSO4) Prophylaxis

• Can be given as an continuous IV infusion or intermittent IM injections

• Should be given up to 24Hours after delivery
• Monitor urine output, reflexes and respiration
• Loading dose: 4g IV diluted in 100 ml IVF given for 15 min
• Continuous infusion: 2g/hr
• 10g IM (5g per buttock)
• Maintenance: 5g every 4h or 1-2g IV

Do NOT stop MgSO4 after delivery because eclampsia may still occur!
 DELIVERY

• Termination of the pregnancy is the only cure for

preeclampsia
• AOG – preterm, term
• Presence or absence of severe features
• Presence of eclampsia, HELLP syndrome
• Presence of maternal or fetal compromise –
placental abruption, IUGR
If in the presence of eclampsia, you should DELIVER the baby
after the patient was stabilized.
Maternal Indications for Delivery in Women
With Severe Preeclampsia
• Oliguria (<500ml/24hr)
• HELLP syndrome
• Platelet counts <100,000/mm3
• Deterioration of renal function
• (Serum creatinine >/=1.5 mg/dl)
• Suspected abruptio placenta, progressive labor,
and/or rupture of membranes

Sibai et al AmJOG 2007

Fetal Indications For Delivery In Women With
Severe Preeclampsia
• Repetitive late or severe variable deceleration
• Biophysical profile </=4 on 2 occasions at 6 hours
apart
• IUGR (Estimated fetal weight <5th percentile)
• Umbilical artery Doppler with reverse end
diastolic flow
• Severe oligohydramnios
Sibai et al AmJOG 2007
 Mode of Delivery

Vaginal delivery
- Inducible cervix
- No fetal distress
Cesarean section
 GLUCOCORTICOIDS FOR LUNG MATURATION

• Steroids to improve fetal lung maturity in preterm

infants
• Decrease incidents of respiratory distress
• Improve fetal survival
 HOSPITALIZATION

• Recommendation for immediate hospitalization

(gestational hypertension and preeclampsia without
severe features)
• New S/Sx of severe preeclampsia
• Evidence of fetal growth restriction
• Elevation of liver enzymes
• Thrombocytopenia
COMPLICATIONS
 ECLAMPSIA

• Maternal complications
- Cerebrovascular accident – hemorrhage/infarction
- Abruption placenta and DIC
- Aspiration pneumonia
- Pulmonary edema
- Renal failure
- C-P arrest
 ECLAMPSIA

• Fetal Complications
- Fetal death
- Prematurity- in cases of preterm pregnancies
- Fetal complications may be due to placental
insufficiency or abruption placenta
 PREVENTION OF
HYPERTENSION IN
PREGNANCY
 PREVENTION OF HPN IN PREGNANCY
• Low dose aspirin – recommended in reducing the risk of
preeclampsia in patients who are moderate to high risk
• Dose – 60-80mg/day
• Calcium supplementation – may prevent preeclampsia in
patients with low dietary intake of calcium
• Dose – 1.5-2g elemental calcium/day
• Vit C, Vit E, selenium, Vit A, Fish oil – not effective
 PREVENTION OF HPN IN PREGNANCY

• Early and frequent prenatal check-ups and good

nutrition is still the most effective means of
decreasing the incidence and severity of HPN in
pregnancy