HYPERTENSIVE

DISORDERS OF
PREGNANCY

General Classification

Preeclampsia or Eclampsia (hypertension

and proteinuria unique to pregnancy)
Chronic hypertension
Chronic hypertension with superimposed
preeclampsia
Gestational or transient hypertension

(National Institutes of Health Working Group

Report on High Blood Pressure in Pregnancy,2000.
Adopted by ACOG ,2002)

Diagnosis of Hypertension

Blood pressure readings vary depending

on maternal position and the gestational
age of the pregnancy.
Tends to be lower in the LLD position,
higher in the sitting position.
In the supine position some elevated
pressure, some have supine hypotension
due to compression of the vena cava by
the uterus.

Arterial blood pressure normally declines

during 1st and 2nd trimester
The diagnosis of hypertension should be
reserved for patients with a systolic
greater than or equal to 140 mmHg or a
diastolic greater than or equal to 90
mmHg.
BP should be taken in the sittting or lateral
decubitus position after woman has rested
at least 10 minutes.

PREECLAMPSIA

A syndrome unique to pregnancy, characterized by

the new onset of hypertension and proteinuria in the
latter half of gestation divided into mild and severe
preeclampsia.
Classically affecting the first pregnancy, but also
occurs in multiparas or change in husband
Two criteria for diagnosis of preeclampsia : the BP
140/90 mmHg and development of new onset
proteinuria after 20th wks AOG.
Proteiunuria defined as 0.3 gram protein in a 24
hour urine collection ,
usually correlates 30 mg/dl (+1 on dipstick)

Criteria for Severe Preeclampsia

BP 160/110 mmHg at rest on two

occasions at least 6 hr apart
Proteinuria 5 gram in a 24 h urine
collection or qualitative +3
Oliguria (< 500 ml in 24 hr)
Cerebral or visual disturbances
Pulmonary edema or cyanosis

Epigastric or right upper quadrant pain

Impaired liver function (elevated liver
enzyme)
Thrombocytopenia
Fetal growth restriction

(ACOG, Practice Bulletin No.33, Washington,DC,2002)

Eclampsia

Is the presence of tonic clonic seizures in

a woman with preeclampsia that cannot
be attributed to other causes.

Chronic Hypertension

The diagnosis of chronic hypertension

requires at least one of the following :
known hypertension before pregnancy,
development of hypertension before 20
weeks gestation, or, in cases in which
hypertension is first noted during
pregnancy, persistence of elevated
blood pressures greater than 12 weeks
postpartum.

Chronic Hypertension with Superimposed

Preeclampsia

The diagnosis of superimposed preeclampsia

should be reserved for those women with chronic
hypertension who develop new onset proteinuria
(0.3 g in a 24 hour collection) after 20th week of
gestation.
In pregnant women with preexisting hypertension
and proteinuria, the diagnosis of superimposed
preeclampsia should considered if they experience
sudden significant increases in blood pressure or
proteinuria or any of the other signs and
symptoms consistent with severe preeclampsia.

Gestational Hypertension

The diagnosis of gestational hypertension is

made if hypertension without proteinuria first
appears after 20 weeks gestation or within 48
to 72 hours after delivery and resolves by 12
weeks postpartum.
The diagnosis of gestational hypertension can
only be made in retrospect, if the pregnancy
has been completed without the development
of proteinuria and if the blood pressure has
returned to normal before the 12 week
postpartum.

Etiology Preeclampsia /
Eclampsia

Preeclampsia is called a disease of

theories, because
genetic,immunologic,vascular, hormonal,
nutritional, and behavioral factors have
all been proposed as causes. No single
definitive cause has been identified and
the origins of the disease are considered
to be multifactorial.

Placental ischemia, or hypoxia appears

to be central to the development of the
disease and has been attributed to
failure of the cytotrophoblasts to
adequately invade the uterine spiral
arteries and establish the low resistance
uteroplacental circulation characteristic
of normal pregnant

It is postulated that uteroplacental

ischemia results in oxidative stress leading
to production and release of toxins that
enter the circulation and cause widespread
inflammation, endothelial dysfunction and
activation of the coagulation system.
Endothelial dysfunction leads to imbalance
between different classes of locally
produced vasoconstrictors and
vasodilators.

Endothelial changes also appear to involve a

relative deficiency in the production of nitric
oxide, a vasodilator and inhibitor of platelet
aggregation along with increased production of
endothelin-1. Endothelin 1 is an extremely potent
vasoconstrictor and activator platelets.
The net effect of these processes would be
spread vasoconstriction leading to hypoxic and
ischemic damage in different vascular
beds,systemic hypertension, the HELLP syndrome
or DIC and worsening placental ischemia.

Pathophysiology

Generalized vasospasm
GFR and renal blood flow are
significantly lower
Damage of glomerular membranes ,
increasing their permeability to proteins
and leading to proteinuria.
Cerebral vascular resistance is high in
patients with PE and Eclampsia

Pathology

Lack of decidualization of the

myometrial segments of the spiral
arteries
Glomerular capillary endotheliosis
Ischemia, hemorrhage and necrosis in
many organs, presumably secondary to
arteriolar constriction.

Clinical and laboratory manifestations

Weight gain and edema

Elevation of blood pressure
Proteinuria
Increase serum uric acid concentration
Thrombocytopenia
Liver function : elevated serum enzyme
levels (alanine aminotransferase and
aspartate aminotransferase)

Retroplacental hemorrhage or abruptio

Visual disturbance
Laboratory : CBC, platelet count,LDH,
Ureum, creatinin and uric acid, urinalysis
24 hour urine for protein and creatinine,
liver function tests.

PREVENTION
1. BMI and diet.
Several authors have shown that women with
BMI> 30 had an increase risk of gestational
hypertension, preeclampsia, gestational diabetes
and fetal macrosomia. The influence maybe due
to inflammation.
2. Low dose Aspirin
In PIH patients circulating levels of Thromboxane
A2(TXL-A2 vasoconstrictor) increased and
Prostacyclin (PGI, vasodilator) decreased. Low
dose Aspirin effectively inhibit TXA2 .

Many Authors concluded that low dose aspirin

have moderate benefits when used for
prevention of preeclampsia.
3. High dose Calcium
Oral intake of high dose calcium (2 Gm/day) has
been proposed to prevent pre-eclampsia.
High dose calcium exerts a negative feedback
effect on parathyroid hormone > lowering
intracellular calcium ion levels > smooth
muscle relaxation and diminished
responsiveness to pres-sor stimuli.

Management of Mild Preeclampsia and

Gestational Hypertension
1.

2.

3.

4.

Initial hospitalization to obtain baseline data and

monitor feto-maternal status. The mother is also
instructed to perform fetal movement counts
daily and low salt, high calcium diet.
OPD follow up basically consist of review of fetal
movement, BP reading and NST (Non Stress Test)
We prefer to give oral methyldopa, low dose
aspirin and high dose calcium
We tend to push the mild preeclampsia patient
to near term as possible provided feto-maternal
status is not impaired.

Evaluation and
management

Delivery is the only definitive cure for

preeclampsia and eclampsia after a
period of stabilization, regardless of the
gestational age of the fetus.
Seizure prophylaxis : magnesium sulfate
Antihypertensive therapy : hydralazine,
labetalol, nifedipine, methyldopa

Management of Severe Preeclampsia and

Eclampsia
1.

Control of convulsions
The anti convulsant of choice is
Magnesium Sulfate although some
prefer diazepam. The RCT has shown
the superiority of MgSO4 over
diazepam and phenytoin.
Give a loading dose of 4 Gm slow IV
bolus over 5 minutes followed by a
maintenance dose of 1-2 Gms per hour
IV drip.

The safety of MgSO4 is monitored at the

bedside using the following points :
- the presence of deep tendon reflexes
- respiratory rate of > 12 per minute
- urine output of at least 100 cc/4 hours
- Serum magnesium for greater accuracy
- Antidote calcium gluconas 10 % is
prepared

2. Control of Hypertension
- Hydralazine initial dose 5 mg IV bolus
followed by 5 mg incremental increases
half hourly if diastolic BP does not
improve up to total dose of 20 mg
- Nifedipine
- Labetalol
- Methyldopa

3. Optimum time and Mode of Delivery

Immediate delivery may be done for the
following :
- all cases of eclampsia regardless of age
of gestation
- severe preeclampsia who are at least
34 weeks AOG in the presence of a
mature fetal lung and adequate nursery
facilities.

- evidence of uncontrollable
hypertension of 160/110 mmHg, oliguria
< 40 cc hours, trombocytopenia <
100.000, pulmonary edema and
impending eclampsia
- evidence of fetal compromise based on
abnormal fetal movement counting,
CTG, BPS monitoring

In the presence of clinical disease at <

34 weeks AOG , conservative
management should focus on the
evaluation of maternal and fetal status
plus therapy with anticonvulsant,
antihypertensive, corticosteroid for lung
maturity.
Mode of delivery : vaginal is more
preferable than CS.

THANK YOU.....