HYPERTENSIVE

DISORDERS OF
THE PREGNANCY
LAIBA AMIR
2018/085
Contents
• Introduction
• Classification
• Non- proteinuric pregnancy-induced
hypertension
• Pre-eclampsia
• Chronic hypertension
• Fetal Growth Restriction
Introduction
• Approximately 1 in 10 women have one or more
episodes of raised blood pressure prior to delivery.
• About 1/3rd of these women will develop pre-
eclampsia, which is a leading cause of maternal
death.
• According to the WHO, between 50000-75000 women
die of pre-eclampsia each year.
• It is frequently accompanied by fetal growth
restriction (FGR) which can lead to perinatal
morbidity and mortality.
CLASSIFICA
TION
Non-proteinuric
pregnancy–induced
hypertension

Pre-eclampsia

Chronic hypertension
 NON-PROTEINURIC
PREGNANCY-INDUCED
HYPERTENSION
Hypertension that arises for the first time in the second
half of pregnancy and in the absence of proteinuria.
Also known as gestational hypertension.

• Not associated with adverse pregnancy outcome.

• Mild and moderate increases in blood pressure in this
setting do not require treatment.
• 1/3rd of women who present with gestational
hypertension will progress to pre-ecalmpsia.
 PRE-
ECLAMPSIA
Defined as:
• Hypertension of at least
140/90 mmHg recorded on at
least 2 separate occasions
and at least 4 hours apart
• In the presence of at least
300 mg protein in a 24-hour
collection of urine
• Arising de novo after the 20th
week of pregnancy in a
previously normotensive
woman
>300
• Resolving completely by the
mg
sixth postpartum week.
 RISK
• First pregnancy.
FACTORS
• Multiparous with a previous history of pre-eclampsia.
• Pre-eclampsia in any previous pregnancy.
• 10 years or more since last baby.
• Age 40 years or more.
• Body mass index (BMI) of 35 or more.
• Family history of pre-eclampsia (in mother or sister).
• Booking diastolic blood pressure of 80 mmHg or more.
• Booking proteinuria ( of ≥1+ on more than one occasion or
quantified at ≥0.3g/24 h).
• Multiple pregnancy.
• Certain underlying medical conditions:
1. pre-existing hypertension;
2. pre-existing renal disease;
3. pre-existing diabetes;
4. antiphospholipid antibodies.
 PATHOPHYSIOL
OGY
In the first stage, trophoblast invasion is patchy and the
spiral arteries retain their
muscular walls. This is thought to prevent the development
of a high-flow low-
impedance utero-placental circulation and leads to utero-
placental ischemia.

The reason why trophoblasts invade less effectively in

these pregnancies is not
known but may reflect an abnormal adaptation of the ma-
ternal immune system.

In the second stage, uteroplacental ischemia results in ox-

idative and inflammatory stress, with the involvement of
secondary mediators leading to endothelial
dysfunction, vasospasm and activation of the coagulation
system.
 MULTISYSTEM
INVOLVEMENT
Cardio- Renal Liver
vascular

• Glomeru- • Subendothelial
• Marked
loend-othelio- fibrin deposition.
peripheral sis.
vasoconstriction • Elevation of liver
• Impaired enzymes.
• High intravascu-
glomerular • Hemolysis and a
lar pressure and filtration.
loss of endothe- low platelet count
lial cell integrity due to platelet
• Selective loss consumption.
results of proteins.
in generalized • HELLP Syndrome
edema. • Generalized
edema.
 HELLP SYN-
•
DROME
HELLP syndrome is an acronym for hemolysis, eleva-
tion of liver
enzymes and low platelets.

• Women with HELLP syndrome typically present with

epigastric pain,
nausea and vomiting.

• Hypertension may be mild or even absent.

• HELLP syndrome is associated with a range of seri-

ous complications
including acute renal failure, placental abruption and
stillbirth.

• The management of HELLP syndrome involves stabi-

lizing the mother,
 Hemato- Neurologi-
logical cal
• Development of
• Increased fibrin de-
convulsions= Eclampsia.
position.
• Vasospasm.
• Reduction in the
platelet count. • Cerebral edema.

• Hypertensive
encephalopathy(Retinal
hemorrhages, exudates
and papilloedema).
 CLINICAL
PRESENTATION
The classical symptoms include frontal headache, visual distur-
bance and epigastric pain.
However, the majority of women with pre-eclampsia are asymp-
tomatic or merely
complain of general vague ‘flu-like’ symptoms.

• Hypertension is usually the first sign but occasionally is absent

or transient until the late
stages of the disease.

• Dependent oedema of the feet is very common in healthy

pregnant women. However,
rapidly progressive oedema of the face and hands may suggest
pre-eclampsia.

• Epigastric tenderness is a worrying sign and suggests liver in-

volvement.

• Neurological examination may reveal hyperreflexia and clonus

Testing for Proteinuria
 MANAGEMENT &
TREATMENT
There is no cure for pre-eclampsia other than to end the
pregnancy by delivering the baby (and placenta).
Management strategies are aimed at minimizing risk to the
mother in order to permit continued fetal growth. In severe
cases this is often not possible.
The principles of management of pre-eclampsia are:
• Early recognition of the symptomless syndrome.
• Awareness of the serious nature of the condition in its
severest form.
• Adherence to agreed guidelines for admission to hospital,
investigation and the use of antihypertensive and
anticonvulsant therapy.
• Well-timed delivery to pre-empt serious maternal or fetal
complications.
• Postnatal follow-up and counselling for future pregnancies.

A diagnosis of pre-eclampsia usually requires admission.

MANAGE-
MENT
 INVESTIGATIONS

To monitor maternal complications:

• Full blood count (with particular emphasis on falling platelet
count and rising hematocrit).
• If platelet values are normal, additional clotting studies are
not indicated.
• Serum renal profile (including serum uric acid levels).
• Serum liver profile.
• Frequent repeat proteinuria quantification is probably
unhelpful once a diagnosis of pre-eclampsia has been made.
To monitor fetal complications: Ultrasound assessment of:
• fetal size;
• amniotic fluid volume;
• maternal and fetal Dopplers.
• Antenatal cardiotocography, used in conjunction with
ultrasound surveillance, provides a useful but by no means
infallible indication of fetal well-being. A loss of baseline
variability or decelerations may indicate fetal hypoxia.
 TREATMENT OF
HYPERTENSION
• Methyldopa is a centrally acting antihypertensive agent. It can only be
given orally and takes up to 24 hours to take effect and has a range of
unpleasant side-effects including sedation and depression. These
properties limit its usefulness.

• Labetalol is an alpha-blocking and beta-blocking agent. It has a good

safety record
in pregnancy and can be given orally and intravenously. It is the first drug
of choice
in most national guidelines including the current (NICE) guidelines.

• Nifedipine is a calcium-channel blocker with a rapid onset of action. It can,

however, cause severe headache that may mimic worsening disease.

• In severe cases of fulminating disease, an intravenous infusion of

hydralazine or labetalol can be titrated rapidly against changes in the
blood pressure.
 ECLAMPSIA TREATMENT
AND PREVENTION
The drug of choice for the treatment of eclampsia is
magnesium sulphate. This is given intravenously and has
been shown to reduce the incidence of further convulsions in
women with eclampsia.
Magnesium sulphate should also be used in women with
severe pre-eclampsia to prevent the onset of convulsions.
• Loading Dose: Give 4 g of magnesium sulfate (20 ml of 20%
MgSo4 Solution) IV SLOWLY over 5 to 10 min (patient may
feel warmth during injection)
• Maintenance Dose: Infusion of 1 g/hour maintained for 24
hours after the last seizure.
• Recurrent seizures should be treated with either a further
bolus of 2 g magnesium sulfate or an increase in
the infusion rate to 1.5 g or 2.0 g/hour.
Watch out for TOXICITY:
1. Urine output <30 ml/hr
2. Loss of deep tendon reflexes
 SCREENING AND
PREVENTION
Doppler ultrasound uterine artery waveform analysis to
identify women at risk of pre-eclampsia (and other adverse
pregnancy outcomes).
• In pregnancies with incomplete trophoblast remodelling of
the spiral arteries, a characteristic ‘notch’ can often be seen
in the waveform pattern that frequently also demonstrates
high resistance. This screening test may have a role in
women who have already been identified as being at risk of
the disease because of their medical or past obstetric
history. However, it is not of value in screening low-risk
women.
• Established preventive interventions include low-dose
aspirin (typically 75 mg daily), which modestly reduces the
risk of pre-eclampsia in high-risk women.
• Calcium supplementation may also reduce risk, but only in
women with low dietary intake.
 MANAGE-
MENT
• Premature delivery of the fetus is often required in severe pre-
eclampsia. If her condition allows, the mother should be transferred
to a centre with adequate facilities to care for her baby.
• Prior to 34 weeks’ gestation steroids should be given intramuscularly
to the mother to reduce the chance of neonatal respiratory distress
syndrome.
• Delivery before term is often by caesarean section, such patients are
at particularly high risk for thromboembolism and should be given
prophylactic subcutaneous heparin and issued with
antithromboembolic stockings.
• In the case of spontaneous or induced labor and if clotting studies
are normal, epidural anesthesia is indicated as it helps control blood
pressure.
• Ergometrine is avoided in the management of the third stage as it
can significantly increase blood pressure.
• Postnatally, blood pressure and proteinuria will resolve. However, in
a minority of cases one or both persist beyond 6 weeks and this
suggests the presence of underlying chronic hypertension or renal
disease.
• Additionally, a careful search should be made postnatally for
underlying medical disorders in women who present with severe pre-
eclampsia before 34 weeks’ gestation.
 CHRONIC
HYPERTENSION

Maternal risks of pre-existing hypertension include:

1. Pre-eclampsia
2. Abruption
3. Heart Failure
4. Intracerebral hemorrhage

Pre-eclampsia develops in around one-third of women

with
pre-existing hypertension and is more likely to affect
those with
severe hypertension and/or renal disease.
 MANAGEM
ENT
Mild cases (<150/100
mmHg)
• No immediate indication to treat.
• Pregnancy should be monitored carefully to detect:
Changes in blood pressure
Signs of pre-eclampsia
Fetal growth restriction (serial ultrasound scans)

• Antihypertensive medication taken before pregnancy

can often be discontinued in the first half of pregnancy
as there is a physiological reduction in blood pressure.
• ACE inhibitors, ARBs and Atenolol should be
discontinued due to teratogenicity.
 MANAGEM
ENT
Blood pressure is consistently >150/100 mmHg
• Antihypertensive medication should be offered to reduce the risk of
severe hypertension and the attendant risks of intracerebral hemorrhage.
• The treatment does not prevent placental abruption or superimposed
pre-eclampsia, nor does it influence perinatal outcome.

Preferred antihypertensive agents include labetalol, nifedipine and

methyldopa (centrally acting agent). The aim of antihypertensive
medication is to maintain the blood pressure below 160 mmHg systolic
and
80–100 mmHg diastolic.

Following delivery, the maternal blood pressure often decreases, but care-
ful
surveillance is required as it tends to increase again on the third or fourth
postpartum day.

Breastfeeding is encouraged and medication should be changed to those

drugs that are considered safe.
 SUPERIMPOSED PREECLAMPSIA

Risk factors for developing superimposed pre-

eclampsia:
• Renal disease.
• Maternal age >40 years.
• Pre-existing diabetes.
• Multiple pregnancy.
• Connective tissue disease (e.g. antiphospholipid
syndrome).
• Coarctation of the aorta.
• Blood pressure ≥160/100 mmHg in early pregnancy.
• Pre-pregnancy BMI >35.
• Previous pre-eclampsia.
• Antiphospholipid syndrome.
 FETAL GROWTH
RESTRICTION
Fetal Growth Restriction is defined as a failure of a fetus to
achieve its genetic growth potential. This usually results in
a fetus that is small for gestational age (SGA).
SGA means that the weight of the fetus is less than the
10th centile for its gestation. Other cut-off points (e.g. the
third centile) can be used.
The terms SGA and FGR are not synonymous. It is
important to remember that most SGA fetuses are
constitutionally small and are not compromised.
FGR indicates that there is a pathological process
operating to restrict the growth rate of the fetus.
Consequently, some FGR fetuses may not actually be SGA,
but nevertheless will have failed to fulfil their growth
potential.
 CAUSES

1. Maternal undernutrition is globally the major cause

of FGR.
2. Low maternal oxygen saturation will reduce fetal
pO2 levels and fetal metabolism.
3. Smoking, by increasing the amount of
carboxyhemoglobin in the maternal circulation,
effectively reduces the amount of oxygen available to
the fetus causes FGR.
4. A wide variety of drugs can affect fetal growth
including alcohol and cocaine, through multiple
mechanisms affecting fetal enzyme systems, placental
blood flow and maternal substrate levels.
5. Poor placental function secondary to inadequate
trophoblast invasion of the spiral arteries. This results
in reduced perfusion of the intracotyledon space,
which in turn leads to abnormal development of the
terminal villi and impaired transfer of oxygen and
CAUSES
PATHOPHYSIOLOGY
 RISK FACTORS
Serial ultrasounds performed for at risk pregnancies.
 MANAGEM
ENT
The detection of an SGA infant contains two elements: first the accurate
assessment of gestational age and second, the recognition of fetal
smallness.

When a diagnosis of SGA has been made, the next step is to clarify
whether the baby is normal and simply constitutionally small or whether
it is
FGR.

There are no widely accepted treatments available for FGR related to

uteroplacental insufficiency. Low-dose aspirin may have a role in the
prevention of FGR in high-risk pregnancies but is not effective in the
treatment of established cases.

When growth restriction is severe and the fetus is too immature to be

delivered safely, bed rest in hospital is usually advised in an effort to
Maximize placental blood flow. The aim of these interventions is to gain
as much maturity as possible before delivering the fetus, thereby reduc-
ing the
 NEW
DEVELOPMENTS
• Placental growth factor (PlGF) belongs to the
vascular endothelial growth factor (VEGF) family and
represents a key regulator of angiogenic events in
pathological conditions. PlGF is low in pregnancy-
complicated pre-eclampsia and early data suggest
that a low PlGF has a high sensitivity for predicting
adverse outcomes in women presenting with
suspected pre-eclampsia. The results of a larger trial
are awaited.

• There is also an urgent need to develop treatments

for FGR. Sildenafil citrate potentiates the effect of
nitrous oxide (NO) and thus may cause vasodilatation
of vessels responsive to NO. The incomplete
remodeling of maternal spiral arteries in FGR results
in vessels with intact or partially intact muscular
layers, which remain responsive to regional vascular
control. Sildenafil has the potential to increase
uteroplacental circulation and perfusion, resulting in
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