Introduction
• Hypertension is one of the common medical
complications of pregnancy and contributes
significantly to maternal and perinatal morbidity
and mortality.
• According to WHO systematic review,
hypertensive disorders of pregnancy contribute
to 16% of maternal mortality which is more
than other leading causes of maternal mortality.
• Hypertensive disorders are also the cause of
fetal and neonatal morbidity and mortality.
• Hypertensive disorders complicate about 5 –
10% of all pregnancies and eclampsia may
occurs 1 in 2000 deliveries.
• The incidence is higher in primi gravida and in
the lower socioeconomic group.
• Furthermore, HDP lead to preterm delivery,
fetal intrauterine growth restriction, low birth
weight and perinatal death.
• Early identification and effective management
of this condition play a significant role in the
outcome of the pregnancy both for mother
and baby.
Hypertensive disorders during pregnancy
Definition
• Systolic blood pressure greater than or equal
to 140 mmHg and diastolic blood pressure
greater than or equal to 90 mmHg. These
measurements should be confirmed by
repeated readings over several hours (over 4
hours).
• If the diastolic blood pressure is 90 mm Hg or
more on two consecutive readings taken four
hours or more apart, diagnose hypertension.
• Diagnose hypertension in pregnancy if on two
consecutive readings taken four hours or more
apart:
• systolic blood pressure is 140 mmHg or
higher and/or
• diastolic blood pressure is 90 mmHg or
higher.
• Note: Blood pressure is in the severe range if
the systolic blood pressure is 160 mmHg or
higher and/or diastolic blood pressure is 110
mmHg or higher.
• If hypertension occurs for the first time after 20
weeks of gestation, during labour and/or within
48 hours of giving birth, it is gestational
hypertension, pre-eclampsia or eclampsia,
depending on the presence of other features.
• If hypertension occurs before 20 weeks of
gestation, it is most likely chronic
hypertension. Because some women’s blood
pressure might not be measured before 20
weeks of gestation, chronic hypertension may
be identified for the first time during
pregnancy after 20 weeks of gestation.
• Chronic hypertension will persist beyond 12
weeks postpartum.
• Elevations of both systolic and diastolic blood
pressures have been associated with adverse
fetal outcome and therefore both are
important .
• Perinatal mortality rises with diastolic blood
pressures above 90 mmHg
Classification
The old term such as pregnancy induced
hypertension(preeclampsia),preeclamptic
toxemia (PET) toxemia in pregnancy have
been replaced by hypertensive disorder of
pregnancy.
• The
terminology
used
to
describe
hypertension during pregnancy is inconsistent
and confusing. Commonly used classification
are:
Contd…




Gestational hypertension
Preeclampsia and eclampsia syndrome
Chronic hypertension
Preeclampsia superimposed on chronic
hypertension (superimposed
preeclampsia or eclampsia)
Risk Factors
•
•
•
•
Nulliparity or primigravida
Preeclampsia in a previous pregnancy
Age >40 years or <18 years
Family
history
of
pregnancy-induced
hypertension (mother and sister)
• Chronic hypertension
• Chronic renal disease
• or inherited thrombophilia
• Vascular or connective tissue disease
(systemic lupus erythematosus
and
antiphospholipid antibody syndrome )
• Diabetes mellitus (pregestational and
gestational)
• Multifetal gestation
• High body mass index
• Male partner whose previous partner had
preeclampsia
• Hydrops fetalis
• Unexplained fetal growth restriction
Gestational hypertension
• It is defined as blood pressure more than
140/90 mm Hg observed on at least two
occasions 6 hours apart, after 20 weeks of
gestation in a woman with previously
normal blood pressure.
• Formerly
called
Pregnancy-Induced
Hypertension.
• Mild hypertension without proteinuria or
other signs of preeclampsia.
• Develops in late pregnancy, after 20 weeks
gestation.
• Returning to normal 12 weeks after delivery
• It can progress into preeclampsia. Almost half
of these develop preeclampsia syndrome
Often when hypertension develops <30
weeks gestation.
• Indications for and choice of antihypertensive
therapy are the same as for women with
preeclampsia.
Preeclampsia
Definition:
• Pre-eclampsia is a multisystem disorder of
unknown etiology characterized by development
of hypertension to the extent of 140/90mm Hg
or more with proteinuria after the 20th week of
gestation in a previously normotensive and
nonproteinuric woman.
• Pre-eclampsia is pregnancy specific syndrome
that affects all most all the organ of the body.
Protein urea is an objective marker and reflect
system wide endothelial leak.
• The main diagnostic criteria of pre eclampsia
are
– Hypertension (an absolute rise of blood
pressure of at least 140/90 mm Hg)
– Proteinuria (>300 mg/24hr or >1+ dipstick)
– Oedema (pitting edema over the ankle after 12
hour of bed rest)
• The presence of proteinuria changes the
diagnosis from gestational hypertension to
pre-eclampsia.
• Diagnostic criteria for proteinuria include: two
urine dipstick measurements of at least 2+ (30
mg per dL) taken six hours apart; at least 300
mg of protein in a 24-hour urine sample; or a
urinary protein/creatinine ratio of 0.3 or
greater.
Epidemiology
• Preeclampsia complicates nearly 6% - 10% of
all pregnancies.
• The incidence of pre-eclampsia in hospital
practice varies widely from 5 to 15%.
• The incidence in primi gravida is about 10%
and in multi gravida 5%.
Risk Factors of Preeclampsia
•
•
•
•
•
•
•
•
•
Nulliparity or primigravida ( primipaternity)
Advanced maternal age: age > 40 years
History of preeclampsia in previous pregnancy
Maternal obesity, BMI>35kg/m2 :doubles the risk
Family history of hypertension and pre
eclampsia.
History of placental abruptio, IUGR, fetal death
Placental abnormalities (hyperplacentosis,
placental ischemia)
Multiple gestation
Molar pregnancy
•
•
•
•
•
•
Thrombotic vascular diseases
Chronic renal disease
Chronic hypertension
Diabetes milletus
Thrombophilias (antiphospholipid syndrome)
Smoking
Clinical Classification
A. Mild preeclampsia
• Mild preeclamsia has cases of sustained rise of
blood pressure of more than 140/90 mm Hg but
less than 160 mm Hg systolic or 110 mm Hg
diastolic without significant proteinuria.
B. Severe preeclampsia
• Persistent systolic BP >= 160/110 mmHg or
diastolic BP > 110mm Hg
• Oliguria (<400 ml/24 hr)
• Proteinuria 5 g/24hr or >= 2+ dipstick (persistent)
Cr > 1.2 mg/dl
• Platelets < 100,000 /mm3
•
•
•
•
•
•
•
•
Microangiopathic hemolysis
Elevated ALT or AST
Persistent headache
Persistent visual disturbance
Persistent severe epigastric pain
Retinal hemorrhages
IUGR
Pulmonary oedema
Classification of Preeclampsia
Mild PE
Severe PE
Blood pressure
>140/90
>160/110
Proteinuria
On 2 occasions, >4hrs
apart
>0.3gm/ 24 hrs
Dip stic > 1+
>5gm/24 hrs
Dipstic > 3+
S. creatinine
normal
elevated
Pulmonary edema
_
+
oliguria
_
+
IUGR
_
+
headache
_
+
Visual disturbance
_
+
Epigastric pain
_
+
HELLP syndrome
_
+
Pathophysiology
• Exact aetiology of preeclampsia has been elusive
and continues to challenge the researcher.
• Preclampsia is a result of generalized
vasoconstriction and vasospasm resulting
multiple system organ failure
disease in
pregnancy.
• The primary pathologic process of hypertension
is vasoconstriction, where as the underlying
cause of vasospasm remain unknown.
• In normal pregnancy vascular volume, cardiac
output increase significantly. Despite these
increases, blood pressure does not rise in normal
pregnancy. Pregnant women develop resistance
to the effect of vasoconstrictors such as
angiotensin II.
• Peripheral vascular resistance decreases because
of the effects of certain vasodilators such as
prostacyclin (PGI2) and endothelium derived
relaxing factor (EDRF).
• In preclampsia, peripheral vascular resistance
increases because preeclamptic women are
sensitive to angiotensin II.
• They also may have decrease in vasodilation. For
instance, the ratio of thromboxane (TXA2) to PGI2
increases.
• TXA2 produce by kidney and trophoblastic tissue,
cause vaso constriction and platelet aggregation.
• PGI2 produced by placental tissue and endothelial
cells causes vasodilation and inhibit platelet
aggregation.
• Vasospasma decreases the diameter of blood
vessels, which result in endothelial cells damage,
decreasing EDRF and increases the capillary
permeability.
• Vasoconstriction also results in impeded blood
flow and elevated blood pressure.
• As a result, circulation of all body organs includes
kidney, liver, brain and placenta is decreased.
• The changes are most significant in various
systems and organs which are as follows.
Uteroplacental circulation
• Vasospasm and hypovolaemia compromise
uteroplacental perfusion.
• Uteroplacental insufficiency
• Fetal complications:
- hypoxia
-IUGR
-Prematurity
-IUD
-Placental abruptio
- Increased perinatal morbidity
- Oligohydramnios
CVS
•
•
•
•
•
•
•
•
•
Increased vascular permeability
Intravascular volume deficit
Increased cardiac output and stroke volume
Increased systemic vascular resistance
Decrease colloid osmotic pressure
Hypertension
Hypovolemia
Endorgan ischemia
Total body water is increased (generalized
edema
Haematology
• Hemoconcentration (pts with anemia may appear
to have normal hematocrit)
• There is increased hemotocrit due to
hemoconcentration and thombocytopaenia.
• Thombocytopaenia  most common, but fewer
than 10% have platelet count < 100,000
• There is low platelet count and decreased
fibrinogen.
• Alteration in coagulation profile occurs and
haemolytic anaemia may be present due to
haemolysis.
• Platelet count correlates with disease severity
and incidence of abruptio placentae
• DIC due to activation of coagulation cascade
overconsumption of coagulants and platelets
spontaneous haemorrhage.
Hepatic
• When liver involved the disease is usually severe.
• It often occurs along with other abnormalities known
as HELLP Syndrome comprising hemolysis, elevated
liver enzymes and a lowered platelet count.
• Sometimes there is periportal haemorrhagic necrosis
giving rise to elevated enzyme level.
• RUQ pain is a serious complaint
– warrants imaging, especially when accompanied by
 liver enzymes
– caused by liver swelling, periportal hemorrhage,
subcapsular hematoma, hepatic rupture (30%
mortality)
• HELLP syndrome occurs in 20% of severe
preeclamptics.
Renal
• Decreased GFR due to hypovolaemia
– oliguria
–
blood urea, nitrogen,uric acid and creatinine is
elevated
– Urine sodium elevated
• Glomerulopathy
- proteinuria
• Acute renal failure may be developed due to
acute tubular necrosis. Renal function recovers
quickly postpartum or rarely renal cortical
necrosis which remains irreversible.
Respiratory
– Airway is edematous;
– ↓ internal diameter of trachea
– Pharyngolaryngeal edema
–  risk of pulmonary edema; 3% women with
preeclampsia.
CNS
• The brain is affected in severe cases of preclampsia and
eclampsia.
• Lesion seen in the brain include oedema, infracts,
thrombosis and haemorrhage.
CNS manifestations include:
• headache,
• visual disturbances,
• seizures
• hyperexcitability,
• hyperreflexia,
• coma
Cause: cerebral edema and hypoperfusion
Clinical Features
Symptoms
• Mild:
• Slight swelling over the ankle which persist in the morning.
Gradually may extend to the face, abdominal wall and even
the whole body.
• Alarming symptoms: usually associated with acute
onset of the syndrome.
•
•
Headache : either located over the occipital or frontal
region. Headache is of new onset and may be described as
frontal, throbbing, or similar to a migraine headache.
However, no classic headache of preeclampsia exists.
Distrubed sleep
• Diminished urinary output : less than 400ml in 24
hours
• Epigastric pain : acute pain in the epigastric region.
Epigastric pain is due to hepatic swelling and
inflammation, with stretch of the liver capsule. Pain
may be of sudden onset, it may be constant, and it
may be moderate-to-severe in intensity.
• Eye symptoms : blurring vision ,dimness of vision or
at times complete blindness. Visual disturbances
typical of preeclampsia are scintillations and
scotomata. These disturbances are presumed to be
due to cerebral vasospasm.
Signs
1. Abnormal
weight gain: rapid weight gain is a result
of edema due to capillary leak as well as renal
sodium and fluid retention.
2.Rise of blood pressure: the diastolic pressure usually
tends to rise first followed by the systolic pressure
3.Edema: while mild lower extremity edema is
common in normal pregnancy, rapidly increasing or
nondependent edema may be a signal of developing
preeclampsia. However, this signal theory remains
controversial and recently has been removed from
most criteria for the diagnosis of preeclampsia.
4.Pulmonary edema: due to leaky capillaries and low
oncotic pressure
Investigation
• Urine: protein urea is the last feature of
preeclampsia.
• Opthalmoscopic examination
• Blood value : Haemoglobin and haematocrit,
platete count, a serum uric acid level of more than
4.5mg/dl indicates the presence of preclampsia.
• Renal function test
• Liver function test: elevated liver enzymes.
• Serum albumin estimation
• Serum electrolyte
• Coagulation profile
• Antenatal fetal monitoring for assessing fetal well
being
Diagnosis
• The clinical diagnosis is based mainly on
presence of high blood pressure, oedema
and proteinuria.
• Other clinical manifestation i.e. headahce,
epigastric pain.
• Laboratory investigation report
Prevention
• Regular Antenatal checkup: Early detection of
– rapid gain in weight
– rising blood pressure specially a diastolic one
– edema
– proteinuria/deranged liver or renal profile
• Antithrombotic agents:
• Low dose Aspirin (60mg daily) in High risk
group: ↑PGs and↓TXA2
• Calcium supplementation: no effects unless
women are calcium deficient
• Antioxidants- Vitamin C and E
• Nutritional
supplementation:
zinc,
magnesium, fish oil, low salt diet
• Balance diet rich in protein may reduce the
risk.
Management
• The ultimate and definitive treatment of
preclampsia is delivery.
• The urgency to deliver the patient depends
primarily on the maternal and fetal condition
and their mutual well being and the relative
gestational maturity.
GENERAL MANAGEMENT
• If the woman is not breathing or is
unconscious or convulsing, SHOUT FOR HELP.
Urgently mobilize all available personnel.
• Perform a rapid evaluation of the woman’s
general condition while simultaneously asking
her or her relatives about the history of her
present and past illnesses.
• If the woman is not breathing or her
breathing is shallow:
• Check airway and intubate if required.
• If she is not breathing, assist ventilation using
an bag and mask, or give oxygen at 4 – 6 L
per minute by endotracheal tube.
• If she is breathing, give oxygen at 4 – 6 L per
minute by mask or nasal canula.
• If the woman is unconscious:
• check airway, pulse and temperature;
• position her on her left side;
• check for neck rigidity.
• If the woman is convulsing:
• Position her on her left side to reduce the risk
of aspiration of secretions, vomit and
blood.
• Protect her from injuries (fall), but do not
attempt to restrain her. When managing the
woman’s problem, apply basic principles
when providing care.
• Never leave the woman alone.
• Provide constant supervision. A convulsion
followed by aspiration of vomit may cause
death of the woman and fetus.
• If eclampsia is diagnosed , give magnesium
sulfate.
• If the cause of convulsions has not been
determined, manage as eclampsia and continue
to investigate other causes.
SPECIFIC MANAGEMENT OF HYPERTENSIVE
DISORDERS OF PREGNANCY
A. GESTATIONAL HYPERTENSION
• Manage on an outpatient basis:
• Monitor blood pressure, urine (for proteinuria)
and fetal condition weekly.
• If blood pressure worsens or the woman develops
features of pre-eclampsia, manage as preeclampsia.
• If there are signs of severe fetal growth restriction
or fetal compromise, admit the woman to the
hospital for assessment and possible expedited
birth.
• Counsel the woman and her family about
danger signs indicating severe pre-eclampsia
or eclampsia.
• If all observations remain stable, allow to
proceed with spontaneous labour and
childbirth.
• In women with gestational hypertension, if
spontaneous labour has not occurred before
term, induce labour at term.
B. MILD PRE-ECLAMPSIA
I GESTATION LESS THAN 37 + 0/7 WEEKS
• As long as the well-being of the mother and
fetus remains stable, the goal is for the woman
to reach 37 + 0/7 weeks of gestation while
monitoring of maternal and fetal status
continues.
• However, it is important to remain vigilant
because pre-eclampsia may progress rapidly to
severe pre-eclampsia.
• The risk of complications, including eclampsia,
increases greatly once pre-eclampsia becomes
severe.
• Close monitoring and a high suspicion for
worsening disease are important.
• If blood pressure and signs of pre-eclampsia
remain unchanged or normalized, follow up
with the woman as an outpatient twice a
week:
• Monitor blood pressure, reflexes and fetal
condition.
• Monitor for danger signs associated with
features of severe pre-eclampsia .
• Counsel the woman and her family about
danger signs associated with severe preeclampsia or eclampsia.
• Encourage the woman to eat a normal diet.
• Do
not
give
anticonvulsants
or
antihypertensives unless clinically indicated.
• Do not give sedatives or tranquilizers.
• If follow-up as an outpatient is not possible,
admit the woman to the hospital:
• Provide a normal diet.
• Monitor blood pressure (four to six times
daily) and urine for daily output.
• Do not give anticonvulsants unless blood
pressure increases or other signs of severe
pre-eclampsia appear.
• Do not give sedatives or tranquilizers.
• Do not administer diuretics. Diuretics are
harmful and only indicated for use in women
with pre-eclampsia who have indications for a
diuretic (such as pulmonary oedema).
• Monitor for danger signs associated with
severe pre-eclampsia
• If blood pressure decreases to normal levels
or her condition remains stable, tell the
woman that she can go home:
• Advise her to watch for symptoms and signs of
severe pre-eclampsia.
• See her twice weekly to monitor blood
pressure and fetal well-being and to assess for
symptoms and signs of severe pre-eclampsia.
• If systolic blood pressure is 160 mmHg or
higher and/or diastolic blood pressure is 110
mmHg or higher, or if signs of severe preeclampsia appear, even if her blood pressure
is normal, admit the woman and follow
recommendations for management of severe
pre-eclampsia and eclampsia.
• A key factor in anticonvulsive therapy is timely
and adequate administration of anticonvulsive
drugs. Convulsions in hospitalized women are
most frequently caused by under-treatment.
• Magnesium sulfate is the drug of choice for
preventing and treating convulsions in severe
pre-eclampsia and eclampsia.
• An intramuscular or intravenous regimen can
be used.
II. GESTATION AT OR MORE THAN 37 + 0/7 WEEKS
• In women with mild pre-eclampsia at term (37 +
0/7 weeks or more), induction of labour is
recommended.
• Assess the cervix and induce or augment labour.
• Note: Do not give ergometrine to women with preeclampsia, eclampsia or high blood pressure
because it can increase blood pressure and increase
the risk of stroke or convulsions.
C. Medical management while awaiting delivery:
– use of steroids X 48 hours if fetus < 34 wks
– antihypertensives to maintain DBP < 105-110
– magnesium sulfate for seizure prophylaxis
Oral antihypertensive medications for nonsevere hypertension
1. Alpha methyldopa
• Administer 250 mg every six to eight hours.
• The maximum dose is 2000 mg per 24 hours.
2. Nifedipine:
• Administer 10–20 mg every 12 hours.
• The maximum dose is 120 mg per 24 hours.
3. Labetalol:
• Administer 200 mg every six to 12 hours.
• The maximum dose is 1200 mg per 24 hours.
Note: Women with congestive heart failure,
hypovolaemic shock or predisposition to
bronchospasm (asthma) should not receive
labetalol.
13/12/2003
Eclampsia
Scientific Evolution - Past

17th AD : Eclampsia - a Greek word
meaning ' to shine forth '-related to visual
phenomenon associated with PE.
 Alexander Hamilton (1781) described
eclampsia as a condition associated with
seizures.
13/12/2003
 Bright in 1827 recognized albuminurea in
addition, dropsy, relating it to renal
disease and eclampsia.
 In 1896 when the sphygmomanometer
was invented, arterial hypertension was
found associated with eclampsia
Eclampsia is among the
leading causes of
maternal mortality
worldwide
Causes of maternal mortalitya
71
Introduction
• The word eclampsia if derived from the Greek
word meaning“like a flash of lighting”.
• Eclampsia complicates 1 in 200-300 cases of
preeclampsia in Australia.
• Seizures may occur antenatally, intra-partum or
postnatally, usually within 24 hours of delivery
but occasionally later.
• Hypertension and proteinuria may be absent
prior to the seizure and not all women will
have warning symptoms such as headache,
visual disturbances or epigastric pain
• Seizures are generalized and 10% develop
after 48 hr postpartum
• Women older than 40 years with preeclampsia
have 4 times the incidence of seizures
compared to women in their third decade of
life.
– Twenty-five percent of eclampsia cases
occur before labor (ie, antepartum).
– Fifty percent of eclampsia cases occur
during labor (ie, intrapartum).
– Twenty-five percent of eclampsia cases
occur after delivery (ie, postpartum).
– Patients with severe preeclampsia are at
greater risk to develop seizures.
– Twenty-five percent of patients with
eclampsia have only mild preeclampsia
prior to the seizures
• It is extremely difficult to predict which
women with pre-eclampsia will develop
eclamptic seizures.
• The “Magpie” trial which showed clear
advantages in the use of Magnesium Sulfate in
severe pre-eclampsia reduced the relative risk
of eclampsia by 58% (0.8% vs. 1.9%, P < .0001)
and of maternal death by 45% (0.2% vs. 0.4%).
• However, the cornerstone of therapy for this
multisystem disorder is delivery of the baby
Definition
• Pre eclampsia when complicated with
generalized tonic – clonic convulsions and/or
coma is called eclampsia.
• It is the new onset of seizures or unexplained
coma during pregnancy or postpartum period
in patients with pre-existing PE and without
pre-existing neurological disorder.
• Two or more of the following features must also
be present within 24 hours of the seizure:
• hypertension
• proteinurea
• thrombocytopenia
• elevated serum AST levels.
Incidence of Eclampsia
 The incidence of eclampsia in the developed
countries is 1:2000 deliveries. While in
developing countries estimate vary widely, from
1 in 100 to 1 in 1700 deliveries (According to
Dr.Mazin Daghestani).
 Forty-four percent of seizures occur postnatally,
the remainder being antepartum (38%) or
intrapartum (18%).
 The maternal case fatality rate is 1.8% and 35%
of women will have at least one major
complication.
Risk factors
•
•
•
•
•
•
•
•
Maternal age less than 20 years
Multigravida
Molar pregnancy
Triploidy
Pre-existing hypertension or renal disease
Previous severe Preeclampsia or Eclampsia
Nonimmune hydrops fetalis
Systemic Lupus Erythematosus
Clinical Features
• A eclamptic patients have previous manifestation
of acute fulminating pre eclampsia (manifestation
of severe preeclampsia).
• Eclamptic convulsions are epileptic form and
consist of four stages
Premonitory stage: twitching of muscles of
face, tongue, limbs and eye. Eyeballs rolled or
turned to one side, 30s
Tonic stage: opisthotonus, limbs flexed, hands
clenched, 30s
Clonic stage: 1-4 min, frothing, tongue bite,
stertorous breathing
Stage of coma: variable period.
• The patient may have 1 or more seizures.
• Respiration ceases for the duration of the
seizure.
Contd....
• Prior to the seizures,
Symptoms include the
following:
– Headache (82.5%)
– Hyperactive reflexes
(80%)
– Marked proteinuria
(52%)
• Sometimes, there is:
.
– Normal reflexes
(20%)
– Absence of
proteinuria (21%)
– Generalized edema
(49%)
– Visual disturbances
(44.4%)
– Right upper
quadrant pain or
epigastric pain
(19%)
• Lack of edema (39%)
• Investigation of severe preeclampsia with
frequent monitoring of haemoglobin, platelet
count, Liver enzymes (transaminases), urea
and creatinine together with oxygen
saturation is recommanded
• Cerebral imaging (MRI or CT) is not indicated
in uncomplicated eclampsia. However,
imaging is necessary to exclude haemorrhage
and other serious abnormalities in women
with focal neurological deficits or prolonged
coma
Management of Severe Pre-eclampsia and
Eclampsia
• Severe pre-eclampsia and eclampsia are managed
similarly, except that birth must occur within 12
hours of onset of convulsions in eclampsia.
• Once symptoms consistent with severe preeclampsia begin, expectant management is not
recommended.
Note: All cases of severe pre-eclampsia should be
managed actively. Symptoms and signs of
“impending eclampsia” (e.g. blurred vision,
hyperreflexia) are unreliable.
General Management
• Provide supportive care:
– Protect from injury (mainly fall)
– Prevent aspiration: keep in the lateral position
– Maintain airway: oral suction frequently
– To ensure adequate oxygenation: maintained
through oxygen administration by face mask 8- 10
L/min to prevent respiratory acidosis, and monitor
by using transcuataneous pulse oximeter.
• Detail history is to be taken from relatives
regarding eclampsia.
• Examination: After stabilization, perform quick
general, abdominal and vaginal examination.
• Monitoring : monitor vital signs (pulse, blood
pressure, respiration and pulse oximetry), reflexes
and fetal heart rate hourly.
• Monitor urinary output on hourly basis.
• If the patient is undelivered monitor fetal heart
rate regularly. Immediately after convulsion fetal
bradycardia is common.
• If the patient is in labour, monitor progress of
labour.
• If systolic blood pressure remains at 160
mmHg or higher and/or if diastolic blood
pressure remains at 110 mmHg or higher, give
antihypertensive drugs .
• Antibiotics for prevention of infection.
Note: An important principle is to maintain
blood pressures above the lower limits of
normal.
• Fluid balance : Start an IV infusion and infuse
IV fluids . Crystalloid solution (Ringer’s
solution) is started as a first choice. Total fluid
should not exceed the previous 24 hours
urinary output plus 1000ml.
• Catheterize the bladder to monitor urine
output.
• Maintain a strict fluid balance chart (monitor
the amount of fluids administered and urine
output) to prevent fluid overload.
- If urine output is less than 30 mL per hour:
Withhold magnesium sulfate and infuse IV fluids
(normal saline or Ringer’s lactate) at 1 L in eight
hours.
Monitor for the development of pulmonary oedema
(increased respiratory rate and/or work of
breathing, rales on auscultation of lungs).
• Never leave the woman alone. A convulsion
followed by aspiration of vomit may cause death
of the woman and fetus.
• Auscultate the lung bases hourly for rales
indicating pulmonary oedema.
 If rales are heard, withhold fluids and administer
furosemide 40 mg IV once.
• Assess clotting status with a bedside clotting test
. Failure of a clot to form after seven minutes or a
soft clot that breaks down easily suggests
coagulopathy.
Specific Management
ANTICONVULSIVE THERAPY FOR SEVERE PREECLAMPSIA OR ECLAMPSIA
• A key factor in anticonvulsive therapy is timely
and adequate administration of anticonvulsive
drugs. Convulsions in hospitalized women are
most frequently caused by under-treatment.
• Magnesium sulfate is the drug of choice for
preventing and treating convulsions in severe
pre-eclampsia and eclampsia.
• An intramuscular or intravenous regimen can be
used .
• Intramuscular Regimen
A. Loading dose (IV and IM):
• Give 4 g of 20% magnesium sulfate solution IV over
five minutes.
• Follow promptly with 10 g of 50% magnesium sulfate
solution: Give 5 g in each buttock as a deep IM
injection with 1 mL of 2% lidocaine in the same
syringe.
• Ensure aseptic technique when giving magnesium
sulfate deep IM injection.
• Warn the woman that she will have a feeling of
warmth when the magnesium sulfate is given.
B. Maintenance dose (IM):
• Give 5 g of 50% magnesium sulfate solution
with 1 mL of 2% lidocaine in the same syringe
by deep IM injection into alternate buttocks
every four hours.
• Continue treatment for 24 hours after birth
or the last convulsion, whichever occurs last.
1. Intravenous Regimen
• Intravenous administration can be considered,
preferably using an infusion pump, if available:
A. Loading dose:
• Give 4g of 50% magnesium sulfate solution IV.
• If convulsions recur after 15 minutes, give 2 g of
50% magnesium sulfate solution IV over five
minutes.
B. Maintenance dose (IV):
• Give intravenous infusion 1g/ hour. Continue
treatment for 24 hours after childbirth or the last
convulsion, whichever occurs last.
• Although magnesium toxicity is rare, a key
component of monitoring women with severe preeclampsia and eclampsia is assessing for signs of
magnesium toxicity.
• Before repeat administration, ensure that:
respiratory rate is at least 16 per minute;
patellar reflexes are present;
urinary output is at least 30 mL per hour over four
hours.
• If there are signs of toxicity, delay the next IM dose or
withhold the IV infusion of magnesium sulfate.
• If there are no signs of toxicity, give the next IM dose
or continue the IV infusion of magnesium sulfate.
Signs indicating the need to withhold or delay
maintenance dose of magnesium sulfate
• Closely monitor the woman for signs of magnesium
toxicity.
To prevent magnesium intoxication, it is important to
evaluate respiratory rate, deep tendon reflexes and
urinary output before administering an additional
dose.
• Withhold or delay drug if:
respiratory rate falls below 16 breaths per minute;
patellar reflexes are absent;
urinary output falls below 30 mL per hour over
preceding four hours.
• Keep antidote ready. In case of respiratory
arrest:
assist ventilation (mask and bag, anaesthesia
apparatus, intubation);
 give calcium gluconate 1 g (10 mL of 10%
solution) IV slowly over three minutes, until
respiration begins to counteract the effect of
magnesium sulfate.
ANTIHYPERTENSIVE MEDICATIONS
• Antihypertensive medications should be
started if the systolic blood pressure is 160
mmHg or higher and/or the diastolic blood
pressure is 110 mmHg or higher.
• The choice and route of administration of an
antihypertensive drug for severe hypertension
during pregnancy should be based primarily on
the prescribing clinician’s experience with that
particular drug and its cost and local
availability, while ensuring that the medication
has no adverse fetal effects.
• If antihypertensive medication for acute
treatment of severe hypertension cannot be
given intravenously, oral treatment can be
given
Antihypertensive medications and dosing
options for acute treatment of severe
hypertension
• Hydralazine
Intravenous treatment:
– Administer 5 mg IV, slowly.
– Repeat every five minutes until the blood pressure
goal has been achieved.
– Repeat hourly as needed or give 12.5 mg IM
every two hours as needed.
– The maximum dose is 20 mg per 24 hours.
• Labetalol
Oral treatment:
• Administer 200 mg.
• Repeat dose after one hour until the treatment
goal is achieved.
• The maximum dose is 1200 mg in 24 hours.
Labetalol cont..
Intravenous treatment:
– Administer 10 mg IV.
– If response is inadequate after 10 minutes, administer 20
mg IV.
– The dose can be doubled to 40 mg and then 80 mg with
10 minute intervals between each increased dose until
blood pressure is lowered below threshold.
– The maximum total dose is 300 mg; then switch to oral
treatment.
Note: Women with congestive heart failure,
hypovolaemic
shock
or
predisposition
to
bronchospasm (asthma) should not receive labetalol.
• Nifedipine immediate-release capsule
Oral treatment:
• Administer 5–10 mg orally.
• Repeat dose after 30 minutes if response is
inadequate until optimal blood pressure is
reached.
• The maximum total dose is 30 mg in the acute
treatment setting.
• Alpha methyldopa
Oral treatment:
• Administer 750 mg orally.
• Repeat dose after three hours until the treatment
goal is achieved.
• The maximum dose is 3 g in 24 hours.
• Other treatment options should be considered
if blood pressure is not lowered within the
acute treatment phase of 90 minutes with 30
mg immediate-release nifedipine.
• Once blood pressure is reduced to non-severe
levels (lower than 160/110 mmHg), ongoing
treatment should be continued using oral
medication.
OPTIMAL TIMING FOR BIRTH
• Birth should be considered as soon as the
woman’s condition has stabilized.
• The decision about the optimal timing of
childbirth should be made on an individual
basis, gestational age, maternal and fetal status
and well-being, cervical favourability, and
urgency.
Note: Following an eclamptic convulsion, birth of
the baby should occur within 12 hours of the
onset of convulsions.
Gestation Less than 24 Weeks (PreViable Fetus)
• Induction of labour is recommended for women
with severe pre-eclampsia if the fetus is not
viable or is unlikely to achieve viability within one
or two weeks.
• Assess the cervix and induce labour as per
medical management of inevitable abortion if the
gestational age is less than 24 weeks or offer
dilatation and evacuation for expedited birth.
• Hysterotomy (incision of the uterus through the
abdominal wall at less than 24 weeks of
gestation) should be avoided.
Gestation between 24 and 34 Weeks
• In women with severe pre-eclampsia and a viable
fetus before 34 weeks of gestation, expectant
management is recommended, provided that
uncontrolled maternal hypertension, maternal
danger signs (e.g. severe headache, visual
changes and abdominal pain) and fetal distress
are absent and can be monitored.
• When laboratory services are available, it is
advisable to monitor the maternal laboratory
values (creatinine, liver enzymes and platelets).
• Give antenatal corticosteroids to accelerate fetal
lung maturation.
• Antenatal
corticosteroid
therapy
is
recommended for women with pregnancies at a
gestational age of 24–34 weeks for whom
preterm birth is considered imminent (due to
severe pre-eclampsia or eclampsia). If the
following conditions are met:
- Gestational age assessment can be accurately
undertaken.
- There is no clinical evidence of maternal infection.
- Adequate childbirth care is available (including the
capacity to recognize and safely manage preterm
labour and birth), and the preterm newborn can
receive adequate care if needed (including
resuscitation, thermal care, feeding support,
infection treatment and safe oxygen use).
• Corticosteroids dosing and timing of birth:
- Give two doses of betamethasone 12 mg IM,
24 hours apart, or four doses of
dexamethasone 6 mg IM, 12 hours apart.
- If the maternal or fetal condition is rapidly
deteriorating, expedite birth after the first
dose of antenatal corticosteroids.
- Do not wait to complete the course of
antenatal corticosteroids before the woman
gives birth.
• Monitor the woman and fetus.
• Monitor fetal growth by symphysis-fundal
height (weekly) or ultrasound, if available.
• Give magnesium sulfate
- If the clinical picture is not worsening,
premonitory signs of eclampsia are absent
and signs of severe pre-eclampsia are not
persistent, stop magnesium sulfate after 24
hours.
• Monitor blood pressure at least every four hours
and give antihypertensive medications if systolic
blood pressure is 160 mmHg or higher and/or
the diastolic blood pressure is 110 mmHg or
higher.
• If severe pre-eclampsia or eclampsia persists (e.g.
uncontrolled
hypertension
despite
antihypertensive medications, deterioration in
blood tests or non-reassuring fetal status),
expedite the birth.
Gestation 34 to 36 6/7 Weeks
• In women with severe pre-eclampsia and a viable
fetus that is between 34 and 36 + 6/7 weeks of
gestation, a policy of expectant management may
be recommended, provided that uncontrolled
maternal hypertension, worsening maternal status
and fetal distress are absent and can be closely
monitored.
• Note: If any features of worsening severe preeclampsia or eclampsia are present, or if close
monitoring of the woman and fetus is not feasible,
transfer to a higher-level facility. If transfer is not
possible, the birth should be expedited.
• Monitor the woman and fetus.
• Monitor fetal growth by symphysis-fundal height
(weekly) or ultrasound, if available.
• Give magnesium sulfate
- If the clinical picture is not worsening,
premonitory signs of eclampsia (e.g. increased
reflexes associated with clonus, severe headache
or visual disturbance) are absent and signs of
severe pre-eclampsia (diastolic blood pressure is
110 mmHg or higher, systolic blood pressure is
160 mmHg or more, elevated liver transaminases,
elevated creatinine, low platelets) are not
persistent, stop magnesium sulfate after 24
hours.
• Monitor blood pressure at least every four hours
and give antihypertensive medications if systolic
blood pressure is 160 mmHg or higher and/or the
diastolic blood pressure is 110 mg Hg or higher.
• If severe pre-eclampsia or eclampsia persists (e.g.
uncontrolled hypertension despite antihypertensive
medications, deterioration in blood tests or nonreassuring fetal status), expedite the birth.
• Note: After 34 completed weeks of gestation,
corticosteroids are not recommended for the
indication of fetal lung maturation.
Gestation after 37 + 0/7 Completed
Weeks
• For women with pre-eclampsia at term (37 + 0/7
weeks), regardless of pre-eclampsia severity, giving
birth is recommended.
• Assess the cervix and induce labour .
• If vaginal birth is not anticipated within 12 hours
(eclampsia) or 24 hours (severe pre-eclampsia),
perform a caesarean.
• If there are fetal heart rate abnormalities (less than
100 or more than 180 beats per minute), perform a
caesarean .
• If safe anaesthesia is not available for
caesarean or if the fetus is dead:
– Aim for vaginal birth.
– If the cervix is unfavourable (firm, thick, closed),
ripen the cervix.
Note: Before performing a caesarean, ensure
that:
 coagulopathy has been ruled out;
 safe general or regional anaesthesia is available.
Spinal anaesthesia is associated with a risk of
hypotension. This risk can be reduced if
adequate IV fluids (500–1000 mL) are infused
prior to administration of the spinal
anaesthesia.
REFERRAL FOR TERTIARY LEVEL CARE
• Consider referral of women who have:
• HELLP-syndrome (haemolysis, elevated liver
enzymes and low platelets) coagulopathy;
• persistent coma lasting more than 24 hours after
convulsion;
• severe pre-eclampsia and maternal and fetal wellbeing cannot be adequately monitored;
• uncontrolled hypertension despite treatment with
antihypertensives;
• oliguria that persists for 48 hours after giving
birth.
SERIOUS COMPLICATIONS
• HELLP syndrome
• Abruptio placentae
• Pulmonary oedema
• Acute renal failure
• Cerebral haemorrhage
• Visual disturbances & blindness
• Hepatic rupture
• Electrolytic imbalance
• Postpartum collapse
Prevention
• Majority of the eclampsia is preceded by
severe pre-eclampsia. Thus the prevention of
eclampsia rests on early detection and
effective treatment and judicious termination
of pregency during preclampsia
• It is not always preventable condition,
because it may present in atypical ways, hence
it is the time to difficult to predict.
• Use of antihypertensive drugs, prophylactic
anticonvulsant therapy and timely delivery are
important step of prevention.
• Close monitoring during labour and 24 hours
postpartum are also important in prevention
of eclampsia.
• Magpie trial showed prophylactic use of
magnesium sulphate lowers the risk of
eclampsia.
• For the treatment and prophylaxis of
seizures, magnesium sulphate is the
anticonvulsant of choice for women with
eclampsia.
• Magnesium sulphate versus diazepam
for eclampsia
• Magnesium sulphate appears to be
substantially more effective than diazepam
for treatment of eclampsia.
Methods Used to Prevent Hypertensive Disorders of Pregnancy
Proper prenatal care
Low-salt diet
Diuretics
Antihypertensive drugs
Nutritional supplementation
Magnesium (365 mg/d)
Zinc (20 mg/d)
Calcium (1500–200 mg/d)
Fish oil
Antithrombotic agents Low-dose aspirin (50–150 mg/d)
Dipyridamole (225–300 mg/d)
Subcutaneous heparin (15,000 IU/d)
13/12/2003
Preventio
• Low doses of aspirin do help prevent
pre-eclampsia, but there is little
information about whether they are of
benefit for treatment of established
pre-eclampsia “ cochrane 22 April
2003
• “Calcium supplements may prevent
high blood pressure and help
prevent preterm labour” cochrane
22 April 2003
Chronic Hypertension
Introduction
• Majority of pregnant women have the “essential”
type of chronic hypertension and therefore it is
seen frequently in women who are of advanced
maternal age or obese .
• Approximately 1 – 3 % of pregnancies are
complicated by essential hypertension.
• A patient with chronic hypertension in pregnancy
run a risk of complication which leads to enhance
perinatal morbidity and mortality.
• Hypertension occurs before 20 weeks of
gestation is classified as essential/or chronic
hypertension in pregnancy.
• It is defined as the presences of hypertension
of any causes antedating or before 20 weeks
of gestation and its presence beyond the 42
days after delivery.
• In patients with sustained hypertension,
prospective
controlled
studies
have
demonstrated enhanced fetal survival when
the blood pressure was controlled with
antihypertensive medication.
• Such medication must be chosen carefully to
avoid fetal and material toxicity, and diuretics
and salt restriction during pregnancy should
be avoided.
Diagnostic Criteria
1. Rise of blood pressure to the extent of
140/90mm Hg or more during pregnancy
prior to the 20 weeks of gestation.
2. Cardiac enlargement on chest radiography
and ECG.
3. Presence of medical disorders.
4. Prospective follow up shows persistent rise of
blood pressure after 42 days following
delivery.
Women with essential hypertension who become
pregnant are at increased risk of:
1.Accelerated hypertension in the third trimester
2.superimposed pre-eclampsia- incidence is 10-50%
3.Placental abruption- the risk is 1-10% and
depends on the age,parity,severity & duration of
hypertension.
4.Complication due to increased blood pressureobserved in 3-6% of patients- CHF, Malignant
hypertension,CVA, Renal damage.
5.Premature delivery and stillbirth. The risk of
perinatal loss is double.
6.Intra-uterine growth restriction (IUGR)
Target blood pressure in chronic hypertension
in pregnancy
• In pregnant women with uncomplicated
chronic hypertension aim to keep blood
pressure lower than 150/100 mmHg
• If target-organ damage secondary to chronic
hypertension (for example, kidney disease)
– aim to keep blood pressure lower than 140/90
mmHg
Investigations
•
•
•
•
Routine investigations- urine albumin,protien,
Blood test
ECG,ECHO For mother
The fetus must be evaluated regularly with
USG,BPP, NST, kick counts, clinical growth
parameters.
Management
The principle of management are:
• To stabilize blood pressure to below 160/100
mm Hg
• To prevent super imposition of pre-eclampsia
• To monitor maternal and fetal wellbeing.
• To terminate the pregnancy at the optimal
time.
Management during pregnancy
• All essential hypertensive women must be evaluated
prior to pregnancy, when plan can be drawn up so as
optimize therapy.
• At this time the patient should receive information
regarding her illness, dietary advice ,advice regarding
lifestyle change , need for treatment and follow up and
exercise requirements.
• Investigation are best performed at this time.
• Bed rest. Hospitalization may be necessary to
investigation and control blood pressure.
Note: Blood pressure should not be lowered
below its pre-pregnancy level.
• In pregnant women with uncomplicated
chronic hypertension aim to keep blood
pressure lower than 160/100 mmHg.
• Clinicians should not offer pregnant women
with uncomplicated chronic hypertension
treatment to lower diastolic blood pressure
below 80 mmHg.
• Antihypertensive drugs
– Routine use of antihypertensive drugs is not
favored. It may lower the blood pressure and
there by benefit the mother but the diminished
pressure may reduce the placental perfusion
which may be detrimental to the fetus.
– Antihypertensive drugs should be used only when
the pressure is raised beyond 160/100 mm Hg.
– In pregnancy labetalol is the first line treatment.
Alternatives include methyldopa and nifedipine.
• If the woman was on an antihypertensive
medication before pregnancy and her blood
pressure is well-controlled, continue the same
medication if acceptable in pregnancy or transfer
to medication safely used in pregnancy.
• If the systolic blood pressure is 160 mmHg or
more or the diastolic blood pressure is 110
mmHg or more, treat with antihypertensive
medications .
• If proteinuria or other signs and symptoms of
pre-eclampsia
are
present,
consider
superimposed pre-eclampsia and manage as preeclampsia.
• Monitor fetal growth and condition.
• If there are no complications, induce labour at
term (after 37 week)
• If pre-eclampsia develops, manage as mild preeclampsia or severe pre-eclampsia .
• If there are fetal heart rate abnormalities (less
than 100 or more than 180 beats per minute),
suspect fetal distress.
• If fetal growth restriction is severe and pregnancy
dating is accurate, assess the cervix and induce
labour.
• If there is no complication terminate the
pregnancy in 37 weeks.
• Observe for complications, including abruptio
placentae and superimposed pre-eclampsia
• Offer pregnant women with secondary chronic
hypertension referral to a specialist in
hypertensive disorders.
• Prescribe aspirin from 12 weeks onwards in order
to prevent the development eclampsia
Note: Assessment of gestation by ultrasound in
late pregnancy is not accurate. Use a first
trimester ultrasound scan, if available, to date
the pregnancy.
Complication
• Superimposed preeclampsia: 30%
• Renal failure and/or CVA: 30%
• Perinatal mortality: over 40%