Dilla University College of Medicine and

Health Science
Department of Obstetric and Gynaecology

SEMINAR ABOUT MANAGEMENT OF

ECLAMPSIA

Moderator:- Dr.Melese (Obstetrician and Gynecologist)

Prepared by:- Tadele.Y (Intern)
 Out line
• Introduction
• Epidemology
• Definition
• Classification
• Pathogenesis
• Diagnosis
• Management
• Complications
• Reference
 Introduction
• The term eclampsia is derived from a Greek word,
meaning “like a flash of lightening”. It may occur
quite abruptly, without any warning manifestations.
• In majority (over 80%), however,the disease is
preceded by features of severe preeclampsia.
• Thus, it may occur in patients with preeclampsia or in
patients who have preeclampsia superimposed on
essential hypertension
 Definition

• Eclampsia is the occurrence of convulsions or

coma unrelated to other cerebral conditions
with signs and symptoms of PE.
• Eclampsiais defined as the development of
convulsions or unexplained coma during
pregnancy or postpartum in patients with
signs and symptoms of PE.
 Pathogenesis
• Several theories and pathologic mechanisms
have been implicated as possible etiologic
factors, but none of these has been proven
conclusively. It is not clear whether the
pathologic features in eclampsia are a cause
or an effect of the convulsions.
 Diagnosis

• The diagnosis of eclampsia is secure in the

presence of generalized edema, hypertension,
proteinuria, and convulsions.
• However, women in whom eclampsia
develops exhibit a wide spectrum of signs that
range from severe hypertension, severe
proteinuria, and generalized edema to absent
or minimal hypertension, no proteinuria, and
no edema.
• Several clinical symptoms are potentially
helpful in establishing the diagnosis of
eclampsia.
• These include persistent occipital or frontal
headaches, blurred vision, photophobia,
epigastric or right upper quadrant pain, and
altered mental status.
 Time of Onset of Eclampsia
 The onset of eclamptic convulsions can be
during :
• Antepartum (38% to 53%)
• Intrapartum(18%)
• postpartum period(11% to 44%)
• Late postpartum eclampsiais defined as
eclampsia that occurs more than 48 hours but
less than 4 weeks after delivery.
• late-postpartum eclampsia developed despite
the use of prophylactic magnesium sulfate
during labor and for at least 24 hours
postpartum in previously diagnosed
preeclamptic women.
 Cerebral Pathology
• Cerebral pathology in cortical and subcortical
white matter in the form of edema, infarction,
and hemorrhage (microhemorrhage and
intracerebral parenchymal hemorrhage) is a
common autopsy finding in patients who die
of eclampsia.
• Two theories have been proposed to explain
these cerebral abnormalities, forced dilation
and vasospasm and the forced dilation theory
suggests that the lesions in eclampsia are
caused by loss of cerebrovascular
autoregulation.
 Cerebral imaging is indicated for
• patients with focal neurologic deficits or
prolonged coma.
• In these patients, hemorrhage and other
serious abnormalities that require specific
pharmacologic therapy or surgery must be
excluded.
• an atypical presentation for eclampsia
 Differential Diagnosis
of Eclampsia
• Hypertensive encephalopathy
• • Seizure disorder
• • Hypoglycemia, hyponatremia
• • Posterior reversible encephalopathy syndrome
• • Vasculitis, angiopathy
• • Amniotic fluid embolism
• • Cerebrovascular accident
• • Ruptured aneurysm or malformation
• • Arterial embolism, thrombosis
• • Cerebral venous thrombosis
• • Hypoxic ischemic encephalopathy
 Management of Eclampsia
A. Treatment of Eclamptic Convulsion
Eeclampsia is so frightening, the natural
tendency is to attempt to abolish the
convulsion. However, drugs such as diazepam
should notbe given in an attempt to stop or
shorten the convulsion, especially if the
patient does not have an IV line in place and
someone skilled in intubation is not
immediately available.
B.Prevention of Maternal Injury During the
Convulsions
• The first priority in the management of eclampsia
is to prevent maternal injury and to support
cardiovascular function.
• During or immediately after the acute convulsive
episode, supportive care should be given to
prevent serious maternal injury and aspiration,
assess and establish airway patency, and ensure
maternal oxygenation.
C.Prevention of Recurrent Convulsions
• Magnesium sulfate is the drug of choice to treat and
prevent subsequent convulsions in women with
eclampsia.
• A loading dose of 6 g over 20 minutes is
recommended, followed by a maintenance dose of
2 g per hour as a continuous IV solution.
• Approximately 10% of eclamptic women have a
second convulsion after receiving magnesium
sulfate.
• In women who have only mild preeclampsia,
discontinuation of therapy after 12 hours may
be safe .
• In women with severe preeclampsia or
eclampsia, seizure prophylaxis is generally
continued for 24 to 48 hours postpartum,
after which the risk of recurrent seizures is
low.
 Mechanism of action
 reduced presynaptic release of the
neurotransmitter glutamate
 blockade of glutamatergic N-methyl D-
aspartate (NMDA) receptors
 potentiation of adenosine action improved
calcium buffering by mitochondria
 blockage of calcium entry via voltage-gated
channels
• complications and side effects — Rapid
infusion of magnesium sulfate causes
diaphoresis, flushing, and warmth, probably
related to peripheral vasodilation and a drop
in blood pressure.
• Nausea, vomiting, headache, muscle
weakness, visual disturbances, and
palpitations can also occur.
• Toxicity:
• loss of deep tendon reflexes occurs at 9.6 to
12.0 mg/dL (4.0 to 5.0 mmol/L),
• respiratory paralysis at 12.0 to 18.0 mg/dL (5
to 7.5 mmol/L), and
• cardiac arrest at 24 to 30 mg/dL (10 to
12.5 mmol/L).
How to prevent toxicity?
 Frequent evaluation of patellar reflex and respirations
 Maintenance of urine output at >25 ml/hr or 600 ml/d
Reversal of toxicity:
 Give Slowly intravenous calcium gluconate 1 g (10 mL of
10% solution)
 Oxygen supplementation
 Cardiorespiratory support
D.Control of Severe Hypertension
• The objectives of treating severe hypertension
are to avoid loss of cerebral autoregulation
and to prevent CHF without compromising
cerebral perfusion or jeopardizing
uteroplacental blood flow, which is already
reduced in many women with eclampsia.
• Thus maintaining systolic BP between 140 and
160 mm Hg and diastolic BP between 90 and
105 mm Hg is a reasonable goal. This can be
achieved with bolus 5- to 10-mg doses of
hydralazine every 20 minutes or labetalol(20
to 40 mg intravenously) every 10 minutes as
needed.
Intrapartum Management of Eclampsia
• The presence of eclampsia is not an indication
for cesarean delivery.
• The decision to perform a cesarean delivery
should be based on gestational age, fetal
condition, presence of labor, and cervical
Bishop score.
• Cesarean delivery is recommended for those
with eclampsia before 30 weeks’ gestation
who are not in labor with an unfavorable
cervix (Bishop score <5).
• Patients in labor or whose membranes have
ruptured are allowed to deliver vaginally in
the absence of obstetric complications.
• When labor is indicated, it is initiated with
either oxytocin infusions or prostaglandins in
all patients with a gestational age at or greater
than 30 weeks, irrespective of the Bishop
score.
• A similar approach is used for those before 30
weeks’ gestation if the cervical Bishop score is
at least 5.
Postpartum Management of Eclampsia
• Parenteral magnesium sulfate should be
continued for at least 24 hours after delivery
or for at least 24 hours after the last
convulsion.
• If oliguria is present(<100 mL/4 h), both the
rate of fluid administration and the dose of
magnesium sulfate should be reduce.
• Once delivery has occurred, other oral
antihypertensive agents such as labetalol or
nifedipine can be used to keep systolic BP less
than 155 mm Hg and diastolic BP less than105
mmHg.
 Maternal and Perinatal Outcome
• Eclampsia is associated with a slightly increased
risk for maternal death in developed
countries(0% to 1.8%),but the maternal
mortality rate may be as high as 14% in
developing countries.
• The high maternal mortality reported from
developing countries occurs primarily among
patients who have had multiple seizures outside
the hospital and those without prenatal care.
• In addition, lack of resources and intensive
care facilities needed to manage maternal
complications from eclampsia
 Pregnancies complicated by eclampsia are also
associated with increased rates of maternal
morbidities such as
 placental abruption(7% to 10%),
 DIC(7% to 11%), pulmonary edema(3% to 5%),
 acute renal failure(5% to 9%),
 aspiration pneumonia(2% to 3%),
 cardiopulmonary arrest(2% to 5%).
 ARDS and intracerebral hemorrhage are rare
complication
 Perinatal mortality and morbidity remain high
in eclamptic pregnancies.
 The reported perinatal death rate in recent
series ranged from 5.6% to 11.8%
 Prevention of Eclampsia
 prevention of eclampsia can be:
• Primary,by preventing the development
and/or progression of PE
• Secondary,by using pharmacologic agents that
prevent convulsions in women with
established PE.
• Tertiary,by preventing subsequent convulsions
inwomen with established eclampsia.
 Current management schemes designed to
prevent eclampsia are:
 early detection of GH or PE and subsequent
use of preventive therapy in such women.
 close monitoring(in-hospital or outpatient),
 use of antihypertensive therapy to keep
maternal BP less than a certain level(less than
severe range or to normal values),
 timely delivery
 prophylactic use of magnesium sulfate during
labor and immediately postpartum in those
considered to have PE.
 Overall, the percentage of eclampsia
considered unpreventable ranged from 31% to
87%.
Complications of Eclampsia
 Aspiration
 Trauma from fall accidents and tongue injury
 Preterm labor
 Higher risk of infections such as pneumonia
 Fetal distress and asphyxia
 Cerebral edema in prolonged or repetitive seizures
 hypoxic encephalopathy
 Subsequent Pregnancy Outcomes and
Remote Prognosis
• Women with a history of eclampsia are at
increased risk for all forms of PE in subsequent
pregnancies.
• In general, the rate of PE in subsequent
pregnancies is approximately 25%, with
substantially higher rates if the onset of
eclampsia was in the second trimester.
• The rate of recurrent eclampsia is
approximately 2%.
 Reference
• Gabbe obstetrics 7th edition
• Uptodate 21.6
• Obstetrics magement protocols for hospitals
 u !! !
k Yo
Than