Case Report
ECLAMPSIA
ANDALAS UNIVERSITY
By:
dr. Aswin Boy Pratama, SpOG
Trainee of Fetomaternal Subspeciality Education
Program
Mentor:
Prof. Dr. dr. Hj. Yusrawati, SpOG, Subs-KFM
(K)
Dr. Dr. dr. Joserizal Serudji SpOG, Subs-KFM
(K)
FETOMATERNAL SUBSPECIALITY EDUCATION PROGRAM
OBSTETRICS AND GYNECOLOGY
MEDICAL FACULTY OF ANDALAS UNIVERSITY
2024
PROGRAM STUDI SUBSPESISALIS OBSTETRI DAN
GINEKOLOGI PEMINATAN KEDOKTERAN FETOMATERNAL
FAKULTAS KEDOKTERAN UNIVERSITAS ANDALAS
RSUP Dr. M. DJAMIL PADANG
LEMBAR PENGESAHAN
Nama : dr. Aswin Boy Pratama, SpOG
Semester : I (Satu)
Telah menyelesaikan kasus Kehamilan
dengan Penyulit Eclampsia
Padang, Maret 2024
Pembimbing Peserta Pendidikan Subspesialis Obgyn
Peminatan Kedokteran Fetomaternal
Dr.Dr.dr.Joserizal Serudji SpOG(K) dr. Aswin Boy Pratama,SpOG
MENGETAHUI
KPS SUBSPESIALIS OBGYN
PEMINATAN KEDOKTERAN
FETOMATERNAL FK UNAND
Prof.Dr.dr.Hj.Yusrawati,SpOG(K)
CHAPTER I
Case: Mrs. Fidiawati 29 years old 01173589 with P 2A0H2 post CS o.i impending
eclampsia control to fetomaternal. Her blood pressure is 144/97 mmHg. BMI 29
kg/ m2. This blood pressure when her gestational age is below 20 weeks gestation.
She is referrals from another hospital with severe preeclampsia and have
complaint about headache, blurred vision and right upper quadrant abdominal
pain
CHAPTER II
LITERATURE REVIEW
2.1 Background
Preeclampsia and eclampsia are 2 of the most serious complications following
pregnancy and are the main causes of death of pregnant and delivering women
[1,2]. Although preeclampsia affects 3–8% of pregnancies, the mortality rate of
young mothers is 5–20% [1–7]. Coma, Hemolysis, Elevated Liver enzymes and
Low Platelets syndrome (HELLP syndrome), disseminated intravascular
coagulation (DIC), sudden cardiac arrest, pulmonary oedema, acute respiratory
distress syndrome (ARDS), kidney failure, central nervous system hemorrhage,
and mechanical ventilation complications constitute the main causes of death in
pregnant women associated with severe preeclampsia or eclampsia. About 50–
70% of mortality of women with pregnancy, complicated by hypertension, is due
to cerebrovascular incidents, and preeclampsia itself is associated with a 4-fold
increase in stroke during pregnancy, childbirth, and puerperium.
The mortality rate of this severe pregnancy complication in fetuses and
infants is estimated at 7–40%, and this is mainly the result of complications such
as preterm placental abruption, placental insufficiency, intrauterine death of fetus,
and complications arising from prematurity. This review aims to present an
overview of the current prevalence, diagnosis, and management of preeclampsia
and the need for improved maternal care.
2.2 Proceedings in the Case of Eclampsia
Eclampsia seizure involves 3 parallel pathways of clinical proceedings
administered simultaneously (3 equivalent therapeutic goals): (1) Drug treatment
aims at stopping eclampsia seizures (management of convulsions) and preventing
reoccurrence of eclampsia seizure and its complications; (2) Treatment with
antihypertensive drugs and management of hypertensive crisis; and (3)
Emergency treatment undertaken immediately during eclampsia seizure for life-
saving and health maintenance of mother and fetus.
Treatment involves oxygen therapy, prevention of injuries and hypoxia, fetal
surveillance, termination of pregnancy (labor) in the safest and least traumatic
manner (after stabilizing the patient’s condition), and prevention of complications.
Although patients with eclampsia should be treated at an intensive care medical
unit, every gynecologist-obstetrician and specialist in maternal-fetal medicine
should be ready to save the life of a mother and a fetus in the event of this life-
threatening complication of pregnancy [12].
2.3 Actions Performed Ad Hoc Directly During Eclampsia for Life-Saving
and Supervision of the Fetus and Continuous Fetal Heart Rate
Monitoring
The most urgent part of the treatment is the lifesaving procedure, with airways
patency assessment, maintenance of breathing and blood circulation of the mother
(cardiopulmonary resuscitation), securing an adequate oxygen level of the mother
and thereby of the fetus, and the prevention of injuries. Appropriate procedure and
immediate therapy will reduce the morbidity and mortality rates in mothers and
infants. Engagement of a larger number of trained medical personnel is essential –
call for help and clear the airways, and place the patient in the left lateral position
to reduce the risk of aspiration. Eclampsia is always an immediate life-threatening
condition.
Combatting hypoxia and acidosis and reducing the risk of aspiration is
essential. The delivery of oxygen therapy is important to maintain proper
saturation level. Oxygen flow with a speed over 8–10 liters per min through the
facial mask provides an oxygen concentration over 60% in the breathing mixture
and reduced the risk of respiratory acidosis as a result of hyperventilation or even
apnea, which accompanies the eclampsia attacks and therefore prevents multi-
organ damage [1,13–15]. Control of blood oxygen saturation and its appropriate
level maintenance is essential. Percutaneous pulse oximetry is a simple and
essential tool for control of blood oxygen saturation.
In the event of a drop in oxygen saturation (SpO2) below 93%, the evaluation of
arterial blood gas test is essential, and bicarbonates should be administered if there
is acidosis [13,14]. In justified cases, intubation can be essential. In pregnant
women, ventilation through the endotracheal tube provides better gas exchange
than through a bag valve mask [15]. During intubation, it is often essential to use
an intubation tube of a smaller diameter than that used in non-pregnant woman
(0.5–1 mm) [15]. SpO2 ≤93% is linked to a 30-fold higher risk of maternal
adverse outcomes compared with patients with SpO2 over 97% [13,14]. An
increase in PCWP (pulmonary capillary wedge pressure) with correct CVP
(central venous pressure) is a symptom of the dysfunction of the left ventricle, and
as a result carries a risk of pulmonary edema [13–15].
The essential parts of a clinical procedure are appropriate positioning of
the patient in a lateral position with a slightly lifted right hip (for example, with
the use of a cushion) to minimize risk of aspiration of gastric contents into the
respiratory system, and to prevent patient injuries, lockjaw, and tongue bite, and
also to provide adequate blood flow in the utero-placental-fetal unit and to prevent
inferior vena cava syndrome. It is also essential to maintain safe patient
positioning during Caesarean section, which can be obtained through slight tilting
of an operating table to the left by 15°. Left lateral position is very important not
only for the mother but also for the baby. It improves the hemodynamics of the
circulatory system, and reduces the preload of the heart by reducing the
compression of an inferior vena cava. It may be necessary to remove saliva,
vomit, and alimentary contents from the patient’s mouth. The medical staff has to
be very careful while performing the procedure to not provoke vomiting (risk of
gag reflex), which additionally increases the risk of aspiration of stomach
contents, Mendelson syndrome, and death of a patient.
An essential step is obtaining access to the vein with 1 or more venous
catheter insertions required. The 3F Rule has to be followed: Fetus, Foley
catheter, and assessment of rehydration and kidney function (Fluids).
Additionally, reduction of stimuli such as light, sound, touch, and pain should be
reduced, as they can cause consecutive seizure attacks or even status eclampticus.
Approximately 1/10 to 1/3 of patients experience further eclampsia seizures [1].
Stabilizing the mother and appropriate resuscitation procedure have a direct
impact on the state of a fetus [1]. Maternal hypoxia and hypercapnia can lead to
fetal heart rate disturbances in the form of bradycardia, decreased short-term
variation in fetal heart rate (oscillation), late decelerations, and compensatory
tachycardia.
Pulmonary edema is a very rare but life-threatening complication [12,16].
Iatrogenic fluid overload, acute severe course of disease, cardiogenic causes, and
reduced oncotic pressure are the most common causes. It has to be emphasized
that the risk of maternal pulmonary edema additionally increases in the period of
increased workload of the circulatory system after labor. After stabilizing the
patient, it is recommended to terminate the pregnancy, most often through
Caesarean section. Vaginal birth is possible only when the mother’s and the
fetus’s state is stabilized and also when the cervix is well prepared for labor
(Bishop’s score over 5 points) [1].
2.4 Antihypertensive Medications/Treatment for Hypertensive Urgencies
According to the World Health Organization (WHO), hypertension in pregnancy
and its complications cause 16% of deaths of pregnant women, even in developed
countries [2,3,5]. Clinical studies indicate that proper blood pressure control of
pregnant women is one of the most important factors effectively reducing the risk
of deaths or acute complications and poor pregnancy outcomes. It is important to
highlight the necessity of individual hypertension management treatment in
pregnant women and those in labor, keeping in mind not only the conscious
choice of the antihypertensive drug, clinical situation, and adverse effects of
drugs, but also its effect on maintaining optimal maternal-placental and fetal
circulation.
In patients with eclampsia, it is necessary to administer antihypertensive drugs
with rapid effect by venous infusion. The increase of blood pressure and
hypertensive orifice constitute a risk of increase in intracranial pressure, or
intracranial hemorrhage, development of hypertensive encephalopathy, and risk of
severe complications and deaths of mothers and infants. Proper pharmacological
control of blood pressure prevents vascular complications, CNS hypoxia, kidney
damage, heart attack, and threats to the fetus.
However, it is important to remember not to reduce blood pressure too
rapidly due to the risk of a sudden drop of blood flow in maternal organs,
including the uteroplacental blood flow and risk of fetal hypoxia, and even
intrauterine fetal death. The aim of antihypertensive drug treatment is the gradual
reduction in blood pressure to achieve systolic pressure of less than 150–140
mmHg and a diastolic pressure of 90–105 mmHg, and MAP II of 126–105
mmHg, with constant surveillance of fetus heart rate through cardiotocography
(CTG) recording.
Sibai [1,11] advised systolic BP values lower than 160 mmHg but not lower than
140 mmHg, and a diastolic BP lower than 110 mmHg but not lower than 90
mmHg for maintenance of proper maternal cerebral perfusion pressure and
uteroplacental blood flow. It is not recommended to lower BP below 10–15% of
initial BP value throughout 1 h.
It has to be kept in mind that blood flow across the placenta is proportional to the
average blood pressure (perfusion pressure) and reversely proportional to vascular
resistance.
Additional unfavorable factors decreasing organ and tissue blood flow occurring
in preeclampsia and eclampsia are contraction of the small blood vessels
(prearteriol), which to a large extent are responsible for blood supply to tissues
and organs, and “blood thickening” linked to movement of fluids from an
intravascular space to interstitial space resulting from loss of protein, increase in
hypertension, damage to vessel endothelium, and fluid gathering in tissues in the
form of edema.
International guidelines indicate drugs such as Hydralazine, Labetalol, and
Nifedipine as first-line drugs in the treatment of hypertensive crisis and severe
hypertension [2,11,17–20]. In unconscious patients with eclampsia, it is necessary
to administer drugs intravenously.
Hydralazine and Labetalol are among the most commonly-used
intravenous antihypertensive drugs recommended by the American College of
Obstetricians and Gynecologists [2,19] as first-line therapies in patients with
eclampsia. The choice of an antihypertensive drug should be individual and based
on the patient’s clinical condition, drug accessibility, the impact of the drug on a
growing fetus, as well as on the medical staff’s experience [17,18,20].
Hydralazine causes dilation of blood vessels, provides systemic reduction of
vessel resistance, reduces the vessel’s afterload, and relaxes precapillary arterioles
by immediately affecting the smooth muscles of these blood vessels. At the same
time, it shows a minimal effect on post-capillary capacitive (extra-capillary)
vessels, leading to a reduction of resistance of the systemic vessels and blood
pressure [21]. Reversely affecting the pathological mechanism of preeclampsia
and eclampsia, Hydralazine improves maternal and fetal circulation, which
contributes greatly to organ protection. Hydralazine increases umbilical vein
blood flow, which additionally suggests that vasodilation properties also act on
umbilical vessels and lead to an increase in intervillous-space blood flow
regardless of maternal blood pressure value or heart rate [22,23]. It is argued that
the improvement in placental circulation is a consequence of the vasodilation of
blood vessels [22].
After administration of Hydralazine, 50% of patients showed non-life-
threatening short-term adverse effects in the form of reflex tachycardia and heart
pounding, and an increase in cardiac output may appear. Rarely, patients display
symptoms of chest pain, dizziness, sudden fall in blood pressure, state of fear,
face redness, headaches, lower abdominal pain, and fluid retention [24].
Hydralazine should not be used when a patient has maternal tachycardia of more
than 100 beats per minute. Sudden hypotensive reaction and increased risk of
hypotension and oliguria may appear. Hypotension can be dangerous, especially
in patients with preeclampsia and eclampsia at decreased intravascular volume. It
may lead to hypoperfusion (ischemia) of the utero-placental unit, reduction of
utero-placental blood flow, pulse disruption, and fetal bradycardia, which can be
risky for patients with hypovolemia [21,23]. This is why Hydralazine has to be
taken carefully, starting with a small dose, and any decision in regard to an
increase has to be made very cautiously. A change in a patient’s position may be
indicated, along with a possible increase in the intravascular volume of the patient
and appropriate management of the patient’s fluid supply.
Labetalol is a non-selective beta blocker and postsynaptic inhibitor of
alpha 1 receptors. It inhibits neuronal uptake of norepinephrine and dilates blood
vessels. Labetalol causes a significant drop in peripheral systemic vascular
resistance, slows the heart rate and reduces blood pressure while maintaining
peripheral circulation at normal levels, including uteroplacental circulation,
without significant impacts on maternal cerebral, renal, and coronary circulation.
Labetalol is an effective drug and generates relatively minor adverse effects. This
drug is well tolerated by patients with congestive heart failure and after
myocardial infarction. Labetalol almost immediately decreases blood pressure,
mostly by vasodilation and a drop in heart rate. It is a cardio-selective drug that
does not generate endogenous sympathomimetic activity. It is mostly
recommended in patients displaying hypertension accompanied by tachycardia
and myocardial ischemia [17,18,24]. Labetalol may cause bradycardia in mother
and fetus [24].
The literature suggests similar effectiveness of Hydralazine and Labetalol
in severe hypertension treatment in patients with a pregnancy complicated by
preeclampsia or eclampsia. Sometimes Labetalol is perceived as safer than others
in hospital treatment. However, Hydralazine is still the most commonly-used
antihypertensive drug, especially in cases of lack of stabilized blood pressure
during Labetalol treatment. Hydralazine is a drug well known in obstetrics and its
adverse effects are usually acceptable. Apart from this, it seems that its influence
on a mother’s and placental blood circulation is not insignificant. The choice of
antihypertensive medication depends on the clinician’s experience, knowledge of
the drug, and knowledge on its adverse effects, but one should be very careful
with the drug’s activity assessments, as there have been few randomized clinical
studies.
Regardless of the first choice of drug being administered (Labetalol or
Hydralazine), a change of drug should be considered when the first choice has not
brought desired results after 3 doses [21]. At the same time, in the event of
medication change, an interval between the dose of a newly-chosen drug and
administration of the last dose of a first-choice drug should be maintained [27].
The lower effectiveness of Hydralazine compared to Nifedipine and worse
maternal and perinatal results suggest that Hydralazine should not be used as a
first-choice drug in treatment of preeclampsia. However, Vigil-De Gracia’s
research did not indicate that one of the drugs provides better results than another
[20,28]. Similar results were obtained by Duley and Arulkumaran [17,18].
Research suggests that atenolol has minimal impact on systolic blood
pressure in patients with severe preeclampsia [31,32]. Furthermore, taking into
account its association with the induction of intrauterine fetal growth restriction
(FGR) and the availability of other effective drugs from the same group, use of
atenolol during pregnancy should be avoided [31–36]. In the event of
hypertension complicated by heart rhythm disturbances, especially to achieve the
desired reduction of heart rate, it may be beneficial to administer Metoprolol at a
dose of 25–50 mg. Sodium nitroprusside is used only in exceptional
circumstances, as a last resort, in a life-threatening hypertension crisis, when other
drugs cannot overcome this condition. Complications such as violent vasodilation
in women with a reduced volume of circulating blood have been observed.
Another concern is the risk of sodium nitroprusside toxicity (related to toxic
metabolites: cyanides and thiocyanates).
Diuretics have to be avoided because they can cause intravascular volume
depletion. Use of diuretics may lead to worsening of the utero-placental and
placental-fetal blood flow, and may worsen thromboembolic risk, and thus
increase the threat to the life of the mother and fetus [36]. Exceptions in which the
use of diuretics such as Furosemide in pregnant women is acceptable are the risk
of pulmonary edema or cerebral edema.
More possibilities of diuretics administration appear after birth, and also in certain
conditions. Diuretic drugs intensify the pathogenic mechanism of preeclampsia,
leading to additional thickening of the blood at already disturbed organ perfusion,
including the kidneys (it is allowed to be administered when the glomerular
filtration rate [GFR] is over 30 ml/min).
2.5 Anticonvulsant Therapy and Prophylaxis of the Recurrence of Eclampsia
All patients suffering from seizure of unknown etiology during pregnancy, labor,
or after childbirth at postpartum should be treated like patients with eclampsia
seizure until a diagnosis is made. Magnesium sulphate (MgSO4) is the drug of first
choice and is the criterion standard in treatment of eclampsia. It effectively
overcomes eclampsia seizure and prevents subsequent eclamptic convulsions.
Despite the strong effectiveness of magnesium sulphate in treatment and
prophylaxis of eclampsia, the mechanism of its functioning is not yet fully known
[1,40]. Magnesium sulphate is not a typical anti-convulsive drug against. It shows
significant vasodilation properties decreasing peripheral resistance and dilating
peripheral vascular system and cerebral vessels. It leads to a fall in systemic blood
pressure, dilating small distal brain capillaries, and reverses brain hypoxia caused
by contraction of the blood vessels. It protects the vascular endothelium,
contributing to increased production of prostacyclin and nitric oxide. It also
protects the blood–brain barrier, limiting cerebral edema, and has central activity
through inhibition of NMDA (N-methyl-D-aspartate) receptors, leading to
reduced convulsive readiness [40]. In addition, magnesium sulphate, through the
reduction of acetylcholine secretion, blocks neuromuscular transmission [41,42].
It stops and prevents convulsions, decreasing the risk of death in patients with
eclampsia and severe preeclampsia.
Clinical research analysis and literature data confirm that magnesium
sulphate treatment in patients with eclampsia is essential and not just an option to
consider. The loading dose of magnesium sulfate is equal to 4–6 g applied within
15–20 minutes, with a subsequent intravenous magnesium sulfate infusion with a
dose of 1–2 g per hour [1,19,43]. Sibai [1] recommends an intravenous infusion of
2 g magnesium sulphate per hour after administering the loading dose. An
intravenous infusion should be maintained for at least 24 h postpartum, or at least
24 h after the last eclampsia seizure. Kidney functioning has to be monitored as
well. In the event of kidney dysfunction, there is a risk of magnesium sulphate
adverse effects. A level of creatinine over 1.2 mg/dL or oliguria defined as below
30 mL of excreted urea per hour for the next 4 h constitutes an indication for the
administration of MgSO4 in the form of intravenous infusion at a smaller
therapeutic dose of 1 g/h.
In the case of a lack of access to a vein or difficulties with intravenous
administration of this drug, it is possible to administer magnesium sulphate via
intramuscular injection to each buttock up to a maximum dose of 10 g, and then a
dose of 5 g every 4 h [44]. However, possible symptoms suggesting HELLP
syndrome or bleeding diathesis have to be considered (these are contraindications
of this drug’s use via intramuscular injection). In this method of administration,
increased fluctuation of magnesium and decreased stability of drug level in the
patient’s blood are observed. The author’s clinical experience shows that a dose of
1 g magnesium sulphate per hour infused after a loading dose of 4 g can be
effective in the treatment of eclampsia, or even in a cessation eclamptic state and
prophylaxis of a recurrence of eclampsia seizure [45]. At the same time, it limits
the risk of adverse effects and possible overdose of magnesium sulfate.
It must be emphasized that systolic BP below 140–150 mmHg and
diastolic BP below 90 mmHg minimizes the risk of hemorrhagic stroke [17] and
that hypertensive encephalopathy (HE), a massive increase in intracranial
pressure, or intracerebral hemorrhage raises mothers’ morbidity and mortality
rates.
In the event of the lack of effectiveness of magnesium sulphate therapy in
therapeutic doses (which occurs in approximately 10% of patients), diazepam in a
dose of 5–10 mg can be administered or phenytoin at a dose of 250mg
intravenously (250-750-1250 mg) depending on the body mass, within 12 h. The
therapeutic level of phenytoin is 12 mg/ml. Vigil-De Gracia et al recommend a
dose of 100 mg of phenytoin every 6 h for 24 h [20,44]. Diazepam can have an
adverse effect on the fetus, such as risk of hypoxia and a lower Apgar score.
If eclampsia seizure reoccurs during therapy with magnesium sulphate at
therapeutic doses, Sibai recommends an application of 4 mg of Lorazepam within
3–5 min [1,11].
Magnesium sulphate should be given early to prevent seizures in
preeclampsia with severe features [17] and magnesium sulphate therapy should be
continued during labor and Caesarean section [42,46]. Discontinuation of
MgSO4 is linked to eclampsia seizure recurrence risk. Phenytoin and
benzodiazepines can be used if there are contraindications for the use of
magnesium sulphate or when MgSO4 is ineffective [1,17,47]. CNS (central
nervous system) imaging studies, such as MRI or CT, are not recommended for
routine use in eclamptic patients [1]. Most often, MRI or CT discloses
characteristics of cerebral oedema in white matter and closely-located grey matter,
mostly in the parietal and occipital lobe [48]. However, in seizures resistant to
treatment and concerning symptoms such as paralysis, vision impairment,
blindness, and prolonged coma or mental confusion, MRI or CT have to be
performed urgently [1,44,49,50]. Pulmonary edema is a very severe complication
that is estimated to occur in 3% of patients with severe preeclampsia. The risk of
pulmonary edema increases with the number of deliveries, age of the patient, and
fluid workload, and it has a high maternal mortality rate [1,2,11]. It is important to
perform an echocardiographic examination whenever cardiomyopathy is
suspected.
Pulmonary artery catheterization is rarely required, but it may be necessary in
patients with heart disorders, cardiac failure, and pulmonary hypertension. The
amount of excreted urine has to be monitored, and the 3-F rule has to be kept in
mind, which is Fluid, Fetus, and Foley catheter, reaching an hourly diuresis level
of over 25 mL, also in the postpartum period. Reaching hourly diuresis of over 25
mL, especially in the range of 25–40 mL, is a sign of a patient’s improvement. All
patients with eclampsia, and after eclamptic seizures, should be treated in an
intensive care unit (ICU). However, taking into account not only clinical realities,
especially in developing countries, and literature reviews, this is not always
possible.
In 1/5 of patients with preeclampsia, a very rapid course of the disease is
observed, although 1 week prior to the eclampsia seizure, these patients may not
show clinical symptoms of this condition at all [40]. It is necessary for all
gynecologists-obstetricians and maternal-fetal medicine specialists to be fully
prepared for eclampsia, although it is very rare. Stabilization of the patient’s
condition and maintenance of the patient’s blood pressure at normal levels are the
priority. The recovery of the patient and prevention of recurrent eclampsia
convulsions is not possible without reduction of blood pressure. However, lack of
blood pressure stabilization and its increase (uncontrolled jumps in BP) are one of
the main causes of eclampsia recurrence.
CHAPTER III
DISCUSSION
Labor is the only currently known causal factor and is the most effective treatment
for preeclampsia and eclampsia. Antihypertensive treatment is a symptomatic,
medical strategy that allows the postponement of pregnancy termination/delivery
until the stops fetus is maturity and the patient and fetus are prepared for delivery.
In the case of severe preeclampsia, delivery is always beneficial for the mother
and it constitutes the onset of causal therapy, but it is not always beneficial for the
fetus (especially when the due date is distant), because of prematurity and its
complications.
Better understanding of etiological and pathological mechanisms
underlying preeclampsia development has vital meaning for new methods of its
diagnosis and for treatment, and finally for the prevention of eclampsia. It is not
known why eclampsia occurs in some patients and not in others. Mahendra et al
emphasize that there is no existing evidence that an increase in intracranial
pressure precedes an eclampsia attack [51]. However, cerebral edema and the
occurrence of vascular abnormalities in Doppler’s method research in patients
with eclampsia, along with neurological symptoms, such as persistent headache,
vision impairment, hyperactivity or stroke, have been confirmed. It seems that
vasogenic edema is the main factor leading to abnormalities and results from an
increase in BP and from the increase in the permeability of vascular endothelium
and brain autoregulation disturbances. Cerebral edema and an increase in
intracranial pressure have crucial meaning for the occurrence of neurological
symptoms, and eclampsia as a result.
Recommended eclampsia prevention methods through the administration
of magnesium sulphate in all patients with severe preeclampsia can decrease the
risk of seizures by 10 times, from 3.4% to 0.3% [52]. Sullivan et al recommend
the extended use of magnesium sulphate for over 24 h because the risk of
eclamptic seizures is still high in the first 24 h postpartum [43]. Discontinuation of
magnesium sulphate and lack of blood pressure stabilization or uncontrolled
jumps in blood pressure are the main causes of eclamptic seizures recurrence.
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