Hypertensive Disorders in Pregnancy

Zhou Wenhui ( 周雯慧 )

Department of Obstetrics and Gynecology

Zhongnan Hospital of Wuhan University

Email: wenhh_fr@yahoo.com.cn
Hypertensive disorders in pregnancy are
leading causes of maternal, fetal and neonatal
morbidity and mortality worldwide.
 Classification

 Gestational hypertension ( 妊娠期高血压 )

 Preeclampsia ( 子痫前期 )
 Eclampsia ( 子痫 )
 Preeclampsia superimposed on chronic
hypertension( 慢性高血压并发子痫前期 )
 Chronic Hypertension complicating
pregnancy ( 妊娠合并慢性高血压 )
Gestational hypertension is confirmed if
preeclampsia has not developed and the blood
pressure has returned to normal by 12 weeks
postpartum.

Transient hypertension ， without proteinuria

or pathologic oedema
Pre-eclampsia:
Mild: Hypertension (BP≥140/90 mmHg) with proteinuria
(≥0.3g/24hs) after 20 weeks of pregnancy

Severe: Hypertension (BP≥160/110 mmHg), proteinuria

(≥2.0g/24hs), increased serum creatinine, oliguria
(≤500ml /24hs), elevated liver enzymes, cerebral or
visual disturbances, platelet count <100.100/ml,
The exact incidence of preeclampsia is
approximately 5-8% of all pregnancies
depending of the population studied.
Preeclampsia is classified as mild (75%) or
severe (25%) according to clinical findings. It is
essential to note that the distinction of mild and
severe preeclampsia does not indicate different
diseases. It can lead to multiple organ
dysfunction syndrome, multi-system organ
Eclampsia:
Pre-eclampsia + convulsions
Eclampsia is defined as seizure activity with or
without coma unrelated to epilepsy or other
cerebral conditions in an obstetrical patient.
Approximately 2% of preeclamptic pregnancies
develop eclampsia. Eclampsia complicates
about 1 in 2000 pregnancies; the onset of
eclampsia can be antepartum/intrapartum
(60%), or postpartum (40%). While most cases
present in the third trimester of pregnancy or
within the first 48 hours following delivery
Preeclampsia superimposed on chronic
hypertension Superimposed preeclampsia is
diagnosed when a woman with chronic
hypertension develops new-onset proteinuria
after 20 weeks of pregnancy. The maternal and
perinatal outcome is worse than with the de
novo preeclampsia
Chronic hypertension is defined as blood pressure
exceeding 140/90 mm Hg before pregnancy or before
20 weeks' gestation. When hypertension is first
identified during a woman's pregnancy and she is at
less than 20 weeks' gestation, blood pressure
elevations usually represent chronic hypertension
 Gestational hypertension Hypertension detected for the first time after 20 weeks'
gestation in the absence of proteinuria. Hypertension resolves within 12 weeks after
the birth.

. Preeclampsia Hypertension and proteinuria detected for the first time after 20
weeks' gestation Proteinuria defined as 300 mg/day.

Eclampsia is the occurrence of seizures superimposed on the syndrome of

preeclampsia. If eclampsia is diagnosed, preeclampsia is accepted as severe.

Chronic hypertension Hypertension is known to be present before pregnancy or

detected before 20 weeks' gestation. essential hypertension (no underlying cause);
secondary hypertension ( underlying disease).

Preeclampsia superimposed on chronic hypertension Preeclampsia is

accepted as superimposed on chronic hypertension in the presence of new signs or
symptoms of preeclampsia after 20 weeks' gestation in a woman with chronic
hypertension.
 Predisposing Factors

 Primigravidae more than multigravidae.

 Pre-existing hypertension.
 Previous pre-eclampsia.
 Family history of pre-eclampsia.
 Hyperplacentosis i.e. excessive chorionic
tissue as in hydatidiform mole, multiple
pregnancy, uncontrolled diabetes mellitus and
foetal haemolytic diseases.
 Obesity
 Etiology

 The uteroplacental bed

 Immunological factor
 Endothelial cell
dysfunction
 Genetic factor
In early pregnancy, the extravillous
trophoblasts has the potential to invade into
the deep of the decidua and replace the uterine
spiral arterial endothelial cells, which is the key
step for the remodeling of maternal spiral
arteries and the formation of placenta. During
the second trimester of normal pregnancy, a
second wave of invasion occurs into the
myometrial segments of the spiral arteries. If
the second invasion does not occur pre-
After invasion into the decidual stroma,
trophoblasts, carrying paternal antigens, are in
close contact with maternal ICCs. The amazing
thing is that maternal lymphocytes do not attack
the embryo and even cooperate with
trophoblasts via production of some cytokines
and growth factors, to participate in the
establishment of a unique maternal-fetal
immunological microenvironment which help
fetus to survive and develop in uterus till
 The Materno-fetal Interface

A- Uterine spiral artery, CT- Cell columns, T- Interstitial trophoblast, F- Fibrinoid material, E- Endovascular
trophoblast, GC- Placental bed giant cell, S- Stromal cell, K- Uterine NK cells, M- macrophages, T- T cells
The release of a large amount of toxic factors
(tumor necrosis factor, IL, oxygen free radical )
can induce the injury of endothelial cells

Imbalance between prostacyclin (a vasodilator

and an inhibitor for platelets aggregation)
thromboxane (vasoconstrictor and platelets
aggregator)
A maternal autosomal recessive gene or a
foetal genetic component could be
responsible. An increase in HLA-DR4 (subtype
of human leucocyte antigen) has been noted in
pre-eclamptic women, their babies and their
sisters who developed hypertensive disorders.
In summary, the current hypothesis is that an
immunological disturbance causes abnormal
placental implantation resulting in decreased
placental perfusion. The abnormal perfusion
stimulates the production of substances in the
blood that injure endothelial cells.
 Pathophysiology

Vasospasm
The vascular changes and local hypoxia of the
surrounding tissues lead to haemorrhage,
necrosis and other pathological changes
Central nervous system: ischaemia, haemorrhages
and oedema

Liver: subcapsular haemorrhage, periportal necrosis

and infarctions

Endocrine glands: necrosis and haemorrhage in

pituitary, pancreas and adrenal glands

Heart and lungs: myocardial and endocardial

haemorrhage and necrosis. Lungs show haemorrhage
Kidney: decrease in renal blood flow → glomerular
damage (glomerular endotheliosis) leading to: decrease
glomerular filtration rate by about 50%, loss of protein
in urine, elevated serum levels of uric acid, urea and
creatinine. Serum uric acid level is diagnostic and
prognostic for severe preeclampsia.

Placenta: Reduced utero-placental blood flow leading to

intrauterine growth retardation (IUGR) and even death.
Placental thrombosis, infarction and abruptio placent
 Diagnosis

 History
 Physical Examination
 Laboratory Evaluation
Preeclampsia
Blood pressure: 140 mm Hg or higher systolic or 90
mm Hg or higher diastolic after 20 weeks of gestation
in a woman with previously normal blood pressure
Proteinuria: 0.3 g or more of protein in a 24-hour
urine collection
Severe preeclampsia
Blood pressure: 160 mm Hg or higher systolic or 110
mm Hg or higher diastolic on two occasions at least six
hours apart in a woman on bed rest

Proteinuria: 5 g or more of protein in a 24-hour urine

collection

Other features: oliguria (less than 500 mL of urine in

24 hours), cerebral or visual disturbances, pulmonary
edema or cyanosis, epigastric or right upper quadrant
pain, impaired liver function, thrombocytopenia,
 Treatment

 Physical Medication
 Control of Seizure
 Control of Hypertension
 Operation
Control of Seizure
Magnesium Sulfate
The mechanism of the anticonvulsant action of
magnesium sulfate is still unclear. Magnesium sulfate is
usually given intravenously as a loading dose of 6 g
over 20 minutes followed by a constant infusion of 2/h,

Maternal dose-related effects: 10 mg/dl loss of deep

tendon reflexes; 15 mg/dl respiratory paralysis; 25
mg/dl cardiac arrest
 Prevention

There currently are no well-established measures for

preventing preeclampsia. Both low-dose aspirin therapy
and daily calcium supplementation have been studied as
preventive measures.
Although preeclampsia is not preventable, many deaths
from the disorder can be prevented. Women who do not
receive prenatal care are seven times more likely to die
from complications related to preeclampsia-eclampsia
than women who receive some level of prenatal care