NEONATAL EFFECTS
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Transcript NEONATAL EFFECTS
Eclampsia
Dr Soraya Saleh Gargari
Fellowship feto- maternal medicine
from Royal College of England
Shahid Beheshti university
Mahdyeh Hospital
— Eclampsia is the occurrence of
convulsions or coma unrelated to
other cerebral conditions with
signs and symptoms of
preeclampsia
INCIDENCE AND EPIDEMIOLOGY
— An eclamptic seizure occurs in 2 to
3 % of severely PIH women not
receiving anti-seizure prophylaxis; the
seizure rate is estimated to be
between 0 and 0.6 % in women with
“mild” PIH .
The incidence of eclampsia has been
relatively stable at 1.6 to 10 cases per
10,000 deliveries in developed
countries .
In developing countries, however, the
incidence varies widely: from 6 to 157
cases per 10,000 deliveries
Risk factors for eclampsia are similar to those for
preeclampsia .
Peak incidence is in the teenage years and low twenties,
but there is also an increased incidence in women over 35
years of age.
Timing: antepartum, intrapartum, postpartum
— the timing and frequency of eclampsia
is antepartum (38 to 55%), intrapartum
(13 to 36 %), less than or equal to 48
hours postpartum (5 to 39 %), and
greater than 48 hours postpartum (5 to
17 %)
)
Almost all cases (91%) of eclampsia develop
in the third trimester (≥28 weeks)
The remaining cases occur between 21 and
27 weeks’ gestation (7.5%) or at or before
20 weeks’ gestation (1.5%)
Late postpartum eclampsia is
defined as eclampsia that occurs
more than 48 hours but less than 4
weeks after delivery.
Historically, eclampsia was
believed not to occur more than 48
hours after delivery.
However, several recent reports
have confirmed the existence of
late postpartum eclampsia.
These women have signs and
symptoms consistent with
preeclampsia in association with
convulsions.
Some of these women demonstrate
a clinical picture of preeclampsia
during labor or immediately
postpartum (56%), whereas others
demonstrate these clinical findings
for the first time more than 48
hours after delivery (44%).
Therefore, women in whom
convulsions develop in association
with hypertension or proteinuria or
with headaches or blurred vision
after 48 hours of delivery should be
considered to have eclampsia and
initially treated as such.
Cerebral Pathology
Autoregulation of the cerebral
circulation is a mechanism for the
maintenance of constant cerebral blood
flow during changes in BP and may be
altered in eclampsia.
Through active changes in
cerebrovascular resistance at the
arteriolar level, cerebral blood flow
normally remains relatively constant
when cerebral perfusion pressure
ranges between 60 and 120 mm Hg.
PATHOGENESIS OF SEIZURES
— The exact cause of seizures in women with
eclampsia is not known.
The following two hypotheses have been proposed :
●Cerebral overregulation in response to high systemic
blood pressure results in vasospasm of cerebral
arteries, underperfusion of the brain, localized
ischemia/infarction, and cytotoxic (intracellular)
edema.
●Loss of autoregulation of cerebral blood flow in
response to high systemic pressure (ie,
hypertensive encephalopathy) results in
hyperperfusion, endothelial damage, and
vasogenic (extracellular) edema.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
Maternal —
Eclampsia is a clinical diagnosis based upon evidence of
one or more generalized convulsions and/or coma in a
preeclamptic woman and in the absence of other
neurologic conditions.
Eclamptic seizures are almost always self-limiting and
seldom last longer than 3 to 4 min (usual duration 60 to
75 seconds).
Symptoms that may occur in the hours before the
seizure include persistent frontal or occipital
headaches or thunderclap headaches, visual
disturbances , right upper quadrant or epigastric
pain, altered mental status, and shortness of
breath.
The relationship between the level of blood
pressure elevation and onset of seizures is
unclear.
The diagnosis of preeclampsia may not be suspected prior
to the development of seizures in women with relative
hypertension (ie, blood pressure elevated compared with
patient's baseline, but less than 140/90 mmHg) and no
proteinuria
In general, women with typical eclamptic seizures
who do not have focal neurologic deficits or
prolonged coma do not require diagnostic
evaluation with either electroencephalographic or
cerebral imaging studies .
If cerebral imaging is performed, MRI is the
optimal study.
Fetal — Fetal bradycardia lasting at least 3 to 5 min is a
common finding during and immediately after an
eclamptic seizure, and does not necessitate emergent
cesarean delivery.
Stabilizing the mother by administering anticonvulsant
drugs and oxygen and treating severe hypertension (if
present) can help the fetus recover in-utero from the
effects of maternal hypoxia, hypercarbia, and uterine
tachysystole.
Resolution of maternal seizure activity is
associated with compensatory fetal tachycardia
and loss of variability, sometimes associated with
transient FHR decelerations.
If the FHR tracing remains nonreassuring
for more than 10 to 15 min with no
improvement despite maternal and fetal
resuscitative interventions,
then the possibility of an occult abruption
should be considered and emergent
delivery may be indicated.
MANAGEMENT —
General principles — If the seizure is
witnessed, maintenance of airway patency and
prevention of aspiration should be the first
responsibilities of management.
The gravida should be rolled onto her left side.
A bed with raised, padded side rails provides
protection from trauma.
Supplemental oxygen (8 to 10 L/min) via a face
mask has been recommended to treat
hypoxemia due to hypoventilation during the
convulsive episode
Maternal hypoxemia and acidosis may
develop in women who have had repetitive
convulsions, in those with aspiration
pneumonia, in those with pulmonary edema,
or as a result of a combination of these
factors.
It is the author’s policy to use transcutaneous
pulse oximetry to monitor oxygenation in all
eclamptic patients.
Arterial blood gas analysis is required if the
pulse oximetry results are abnormal (oxygen
saturation ≤92%).
Sodium bicarbonate is not given unless the pH
is below 7.10.
The immediate issues in caring for an eclamptic
woman include:
●Prevention of maternal hypoxia and trauma
●Management of severe hypertension, if present
●Prevention of recurrent seizures
●Evaluation for prompt delivery
The definitive treatment of eclampsia is delivery,
irrespective of gestational age, to reduce the risk
of maternal morbidity and mortality from
complications of the disease.
Treatment of hypertension — Strokes account for 15
to 20 percent of deaths from eclampsia.
The general risk of stroke in the nonpregnant
population correlates directly with the degree of
elevation in systolic and diastolic pressures and
maternal age .
It is not clear whether there is a threshold pressure
above which emergent therapy should be instituted
in pregnant hypertensive women .
Most experts recommend aggressive
antihypertensive therapy for sustained diastolic
pressures greater than 105 to 110 mmHg or systolic
blood pressures ≥160 mmHg, although the validity of
thresholds has not been tested prospectively.
Options for initial treatment of hypertensive crisis include:
●Hydralazine beginning with 5 mg intravenously, followed by 5 to 10 mg
boluses as necessary every 20 minutes, or
●Labetalol beginning with 10 or 20 mg intravenously followed by doubling the
dose at 10-minute intervals up to 80 mg for a maximum total cumulative dose
of 220 to 230 mg (eg, 20-40-80-80 mg or 10-20-40-80-80 mg)
Although clinical trials have not adequately addressed the question of
how aggressively to lower an eclamptic patient's blood pressure, many
experts consider a reasonable goal to be a systolic pressure of 140 to
155 mmHg and diastolic pressure of 90 to 105 mmHg.
In women with extremely severe hypertension (≥180/120 mmHg), a
diastolic goal of 100 to 105 mmHg should be achieved within two to six
hours, with the maximum initial (within 10 to 20 minutes) fall in BP not
exceeding 25 percent of the presenting value .
An additional therapeutic option in these women is nicardipine beginning
with 5 mg/hour intravenously and increased by 2.5 mg/hour every 5 to 15
minutes to a maximum dose of 15 mg/hour.
The use of antihypertensive agents to control mildly elevated
blood pressure in the setting of preeclampsia/eclampsia has not
been shown to alter the course of the disease, nor to diminish
perinatal morbidity or mortality .
Pharmacologic treatment of mild hypertension is not
recommended, as neither maternal nor fetal benefits have been
demonstrated.
Treatment of convulsions
— The initial convulsion is usually of short
duration and often occurs in a setting where
intravenous access and drugs are not readily
available. Therefore, treatment is primarily
directed at prevention of recurrent convulsions
rather than control of the initial seizure. The
drug of choice is magnesium sulfate
Management of persistent
convulsions — Recurrent convulsions
occurring in patients on maintenance
magnesium sulfate therapy can be treated
with an additional bolus of 2 grams of
magnesium sulfate over 15 to 20 minutes,
with careful monitoring for signs of
magnesium toxicity .
If two such boluses do not control seizures,
then other measures should be instituted. A
number of options are included below,
although diazepam or lorazepam are used
most commonly.
●Diazepam — Intravenously administered diazepam (0.1
to 0.3 mg/kg over 60 seconds, maximum cumulative
dose 20 mg) rapidly enters the CNS, where it achieves
anticonvulsant levels within 1 min, and will control
seizures in greater than 80 % of patients within 5 min.
A diazepam gel for rectal administration is also available
(0.2 mg/kg).
Some experts recommend avoiding benzodiazepines for
management of eclamptic seizures because of
potentially profound depressant effects on the fetus and
mother.
The duration of diazepam's acute anticonvulsant effect is
typically less than 20 min.
Lorazepam 0.02 to 0.03 mg/kg intravenously,
allowing approximately 1 min to assess its
effect.
If seizures continue at this point, additional
doses of lorazepam (up to a cumulative dose
of 0.1 mg/kg) are infused at a maximum rate
of 2 mg/min for acute treatment. Lorazepam
is as effective as diazepam in terminating
seizures, but the time from its injection to its
maximum effect against seizures is as long as
2 min.
The clinical advantage of lorazepam is that
the effective duration of action against
seizures is as long as 4 to 6 hours.
●Sodium amobarbital 250 mg
intravenously over 3 to 5 min.
Delivery — The definitive treatment for eclampsia is prompt
delivery; however, this does not necessarily preclude
induction of labor and attempted vaginal delivery.
Induction is a reasonable option for women with a
favorable cervix at any gestational age or who are
greater than 32 to 34 weeks of gestation.
Cervical ripening agents can be used to improve the
Bishop score; however, in our opinion, long inductions
should be avoided and a clear endpoint for delivery
planned (eg, within 24 hours).
Because the fetus benefits from in utero
resuscitation before delivery, it is desirable
to wait 15 to 20 minutes and until the
mother and fetus show signs of recovery
(control of convulsions; mother oriented to
name, time, and place; fetal heart rate
reassuring) before proceeding to surgery, if
possible.
POSTPARTUM COURSE — Maternal vital signs, input,
and output should be monitored closely to detect large
changes in blood pressure and fluid imbalance AT LEAST
48 HOURS.
Anticonvulsant drugs are generally administered
for 24 to 48 hours postpartum, when the risk of
recurrent seizures is low.
Therapy is continued in women whose disease
has not begun to improve postpartum and
discontinued in women who are clearly improving
clinically (eg, diuresis of ≥100 mL/h for two
consecutive hours and the absence of symptoms).
Maternal complications occur in up to 70 %
of women with eclampsia and include :
abruptio placentae (7% to 10%),
DIC (7% to 11%), pulmonary
edema (3% to 5%), acute renal
failure (5% to 9%), aspiration
pneumonia (2% to 3%), and
cardiopulmonary arrest (2% to
5%).
Maternal
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, this high mortality rate could
be attributed to the lack of resources and
intensive care facilities needed to
manage maternal complications from
eclampsia.
Perinatal outcome —
Premature delivery, abruptio placenta,
and intrauterine asphyxia are the
primary causes of perinatal death in
eclamptic pregnancies.
Perinatal mortality ranges from 2 to 23
percent and is closely related to
gestational age.
Maternal Transport of the
Eclamptic Patient
During the past 20 years, there has
been a marked reduction in the
number of eclamptic patients.
Consequently, most obstetricians
have little or no experience in the
management of eclampsia.
Because management of the
eclamptic patient requires the
availability of neonatal and
obstetrical intensive care units and
personnel with special expertise, it
is recommended that eclamptic
women at term be cared for only at
level II or III hospitals with
adequate facilities and with
consultants from other specialties.
For those eclamptic patients who
are remote from term, referral
should be made to a tertiary care
center.
The following steps should be taken before
transfer of these critically ill patients:
1. The referring physician or nurse should consult with
the physician at the perinatal center regarding the
referral and appropriate treatment. All maternal
records, including prenatal data and a detailed
summary of the patient’s condition, should be
transmitted.
2. BP should be stabilized and convulsions controlled.
3. Adequate prophylactic anticonvulsive medications
should be given. An accepted regimen is 4 g
intravenous magnesium sulfate as a loading dose over
20 minutes
4. Maternal laboratory assessment (complete blood
count with platelet count, liver enzymes) and fetal
monitoring should be undertaken.
5- sent in an ambulance with medical personnel in
attendance for proper management in case of
subsequent convulsions
Recurrence risk —
Recurrent eclampsia occurs in 2 percent of
subsequent pregnancies .
The risk appears to be reduced by close
maternal monitoring and timely intervention if
preeclampsia develops. Preeclampsia,
however, cannot be prevented in most cases.
Subsequent pregnancies in women with a history of
severe PIH or eclampsia are also at increased risk of
other obstetric complications compared to women with
no such history.
These problems include :
●Abruptio placenta (2.5 to 6.5 versus 0.4 to 1.3 percent
of the general obstetrical population)
●PTL (15 to 21 versus 12 percent)
●IUGR (12 to 23 versus 10 percent)
●Perinatal mortality (4.6 to 16.5 versus 1 percent).
Women with a history of preeclampsia/eclampsia remote
from term (less than 28 weeks of gestation) are at
highest risk of developing these complications, as well as
recurrent preeclampsia .
PREVENTION
Can eclampsia be predicted? — The relationship
between hypertension, signs and symptoms of
cortical irritability and seizures remains unclear.
The magnitude of blood pressure elevation does
not appear to be predictive of eclampsia, although
it correlates well with the incidence of stroke .
20 to 38 % of eclamptic patients have a maximal
blood pressure less than 140/90 prior to their
seizure and about 20 % have no evidence of
proteinuria
Many cases of eclampsia do not appear to be
preventable, even among women receiving
regular prenatal care, or those who are
hospitalized
..
Overall, the percentage of eclampsia
considered unpreventable in these series
ranges from 31% to 87%.86