ECLAMPSIA

Arranged by:

Johannes Ephan Bagus K G99152087

Dika Arista Putra G99162035
Beby Talisa Salafi G99162038
Safira Nurullita G99162026
Elizabeth Agnes Sidabuntar G99162040

OBSTETRICS AND GYNECOLOGY DEPARTMENT

MEDICAL FACULTY OF SEBELAS MARET UNIVERVITY
RSUD DR. MOEWARDI
SURAKARTA
2017
 ECLAMPSIA

A. Overview

Ten percent of all pregnancies are complicated by hypertension. Eclampsia and

preeclampsia account for about half of these cases worldwide, and these conditions have
been recognized and described for years despite the general lack of understanding of the
disease.1 In the fifth century, Hippocrates noted that headaches, convulsions, and
drowsiness were ominous signs associated with pregnancy. In 1619, Varandaeus coined
the term eclampsia in a treatise on gynecology. 2,3

B. Eclampsia
1. Definition
Eclampsia, which is considered a complication of severe preeclampsia, is
commonly defined as new onset of grand mal seizure activity and/or unexplained
coma during pregnancy or postpartum in a woman with signs or symptoms of
preeclampsia. 4,5 It typically occurs during or after the 20th week of gestation or in the
postpartum period. Nonetheless, eclampsia in the absence of hypertension with
proteinuria has been demonstrated to occur in 38% of cases reported in the United
Kingdom.6 Similarly, hypertension was absent in 16% of cases reviewed in the United
States.4
The clinical manifestations of maternal preeclampsia are hypertension and
proteinuria with or without coexisting systemic abnormalities involving the kidneys,
liver, or blood. There is also a fetal manifestation of preeclampsia involving fetal
growth restriction, reduced amniotic fluid, and abnormal fetal oxygenation. 6 HELLP
syndrome is a severe form of preeclampsia and involves hemolytic anemia, elevated
liver function tests (LFTs), and low platelet count.
Most cases of eclampsia present in the third trimester of pregnancy, with
about 80% of eclamptic seizures occurring intrapartum or within the first 48 hours
following delivery. Rare cases have been reported before 20 weeks' gestation or as
late as 23 days’ postpartum. Other than early detection of preeclampsia, no reliable
test or symptom complex predicts the development of eclampsia. In developed
countries, many reported cases have been classified as unpreventable.
2. Course of eclamptic seizures
 Eclampsia manifests as 1 seizure or more, with each seizure generally lasting
60-75 seconds. The patient’s face initially may become distorted, with protrusion of
the eyes, and foaming at the mouth may occur. Respiration ceases for the duration of
the seizure.
Eclamptic seizures may be divided into 2 phases. Phase 1 lasts 15-20 seconds
and begins with facial twitching. The body becomes rigid, leading to generalized
muscular contractions. Phase 2 lasts about 60 seconds. It starts in the jaw, moves to
the muscles of the face and eyelids, and then spreads throughout the body. The
muscles begin alternating between contracting and relaxing in rapid sequence.
A coma or period of unconsciousness, lasting for a variable period, follows
phase 2. After the coma phase, the patient may regain some consciousness, and she
may become combative and very agitated. However, the patient will have no
recollection of the seizure.
A period of hyperventilation occurs after the tonic-clonic seizure. This
compensates for the respiratory and lactic acidosis that develops during the apneic
phase. Seizure-induced complications can include tongue biting, head trauma, broken
bones, and aspiration.
3. Etiologic for Preeclampsia/Eclampsia
The mechanism(s) responsible for the development eclampsia remain(s)
unclear. Genetic predisposition, immunology, endocrinology, nutrition, abnormal
trophoblastic invasion, coagulation abnormalities, vascular endothelial damage,
cardiovascular maladaptation, dietary deficiencies or excess, and infection have been
proposed as etiologic factors for preeclampsia/eclampsia. Imbalanced prostanoid
production and increased plasma antiphospholipids have also been implicated in
eclampsia. In murine models, placental ischemia appears to be associated with an
increased susceptibility to seizures and cerebrospinal fluid (CSF) inflammation.
4. Risk factors for eclampsia
The following are considered risk factors for eclampsia:
a. Nulliparity
b. Family history of preeclampsia, previous preeclampsia and eclampsia [2]
c. Poor outcome of previous pregnancy, including intrauterine growth
retardation, abruptio placentae, or fetal death
d. Multifetal gestations, hydatid mole, fetal hydrops, primigravida
e. Teen pregnancy
f. Primigravida
g. Patient older than 35 years
 h. Lower socioeconomic status

The following preexisting medical conditions are also considered risk factors [4] :

a. Obesity
b. Chronic hypertension
c. Renal disease
d. Thrombophilias-antiphospholipid antibody syndrome
e. Protein C deficiency and protein S deficiency
f. Antithrombin deficiency
g. Vascular and connective tissue disorders
h. Gestational diabetes
i. Systemic lupus erythematosus
5. Multiorgan System Effects
Preeclampsia/eclampsia produces multiple systemic derangements that can
involve a diversity of organ systems including hematologic, hepatic, renal, and
cardiovascular systems as well as the central nervous system. The severity of these
derangements often correlates with maternal medical (eg, preexisting renal or
vascular pathology) or obstetric factors (eg, multifetal gestations or molar pregnancy).
a. Cardiovascular concerns
Eclampsia is associated with cardiovascular derangements such as generalized
vasospasm, increased peripheral vascular resistance, increased left ventricular
stroke work index, decreased central venous pressure, and decreased pulmonary
wedge pressure.
b. Hematologic concerns
Hematologic problems associated with eclampsia can include decreased plasma
volume, increased blood viscosity, hemoconcentration, and coagulopathy.
c. Renal concerns
Eclampsia-associated renal abnormalities can include decreases in glomerular
filtration rate, renal plasma flow, and uric acid clearance.
d. Hepatic concerns
Hepatic derangements associated with eclampsia can include periportal necrosis,
hepatocellular damage, and subcapsular hematoma.
e. Central nervous system concerns
Eclampsia can result in central nervous system (CNS) abnormalities such as
cerebral overperfusion due to loss of autoregulation, cerebral edema, and cerebral
hemorrhage.
6. Pathophysiology of Eclampsia

Fig 1. Pathophysiology of Eclampsia

7. Inhibition of uterovascular development

Many uterovascular changes occur when a woman is pregnant. It is believed
that these changes are due to the interaction between fetal and maternal allografts and
result in systemic and local vascular changes. It has been shown that in patients with
eclampsia, the development of uteroplacental arteries is hindered.
a. Hindrance of cerebral blood flow regulation
It is believed that in eclampsia there is abnormal cerebral blood flow in the setting
of extreme hypertension. The regulation of cerebral perfusion is inhibited, vessels
become dilated with increased permeability, and cerebral edema occurs, resulting
in ischemia and encephalopathy. In extreme hypertension, normal compensatory
vasoconstriction may become defective. Several autopsy findings support this
model and consistently reveal swelling and fibrinoid necrosis of vessel walls.2
b. Endothelial dysfunction
 Factors associated with endothelial dysfunction have been shown to be increased
in the systemic circulation of women suffering from eclampsia. These include the
following1:
i. Cellular fibronectin
ii. Von Willebrand factor
iii. Cell adhesion molecules (ie, P-selectin, vascular endothelial adhesion
molecule-1 [VCAM-1]
iv. Intercellular adhesion molecule-1 [ICAM-1])
v. Cytokines (ie, interleukin-6 [IL-6])
vi. Tumor necrosis factor-α [TNF-α]

In addition, it is believed that antiangiogenic factors, such as placental protein

fms-like tyrosine kinase 1 (sFlt-1) and activin A, antagonize vascular endothelial
8
growth factor (VEGF). Elevated levels of these proteins cause a reduction of
VEGF and induce systemic and local endothelial cell dysfunction. 1 Leakage of
proteins from the circulation and generalized edema are sequelae of the
endothelial dysfunction and thus a defining factor associated with preeclampsia
and eclampsia.

c. Oxidative stress
Evidence indicates that leptin molecules increase in the circulation of women with
eclampsia, inducing oxidative stress, another factor in eclampsia, on cells. (The
leptin increase also results in platelet aggregation, most likely contributing to the
coagulopathy associated with eclampsia). 2,9
Oxidative stress has been found to stimulate the production and secretion of the
antiangiogenic factor activin A from placental and endothelial cells.8 Studies in
pregnant mouse models have proposed that there is a dysregulation in the reactive
oxygen species (ROS) signaling pathway.9, 10
Studies also suggest that increased systemic leukocyte activity plays a role in the
mediation of oxidative stress, inflammation, and endothelial cell dysfunction.
Histochemistry studies indicate that there is predominantly an increase in
neutrophil infiltration of vasculature in patients with eclampsia.10
8. Evaluation
Eclampsia always should be considered in a pregnant patient with a seizure
episode. A pregnant patient who has been involved in an unexplained trauma (such as
a single-vehicle auto accident) and has exhibited seizure activity should be evaluated
for eclampsia. Eclampsia can occur during the antepartum, intrapartum, and
postpartum periods. Ninety percent of eclampsia cases occur after 28 weeks'
gestation.2
Preeclampsia can quickly develop into eclampsia. The natural progression of
the disease is from symptomatic severe preeclampsia (differentiated from
preeclampsia by specific vital signs, symptoms, and laboratory abnormalities) to
seizures.
Features of eclampsia include the following:
a. Seizure or postictal state (100%)
b. Headache (80%), usually frontal
c. Generalized edema (50%)
d. Vision disturbance (40%), such as blurred vision and photophobia
e. Right upper quadrant abdominal pain with nausea (20%)
f. Amnesia and other mental status changes
The incidences of signs or symptoms before seizure include the following:
a. Headache (83%)
b. Hyperactive reflexes (80%)
c. Marked proteinuria (52%)
d. Generalized edema (49%)
e. Visual disturbances (44%)
f. Right upper quadrant pain or epigastric pain (19%)
The absence of signs or symptoms before seizure include the following:
a. Lack of edema (39%)
b. Absence of proteinuria (21%)
c. Normal reflexes (20%)
The relation of seizure to delivery is as follows:
a. Before delivery (>70%)
b. Before labor (antepartum) (25%)
c. During labor (intrapartum) (50%)
d. After delivery (postpartum) (25%)
Although patients with severe preeclampsia are at greater risk for seizures, 25%
of patients have symptoms consistent with mild preeclampsia (i.e., preeclampsia
without severe features) before the seizures.
A study by Cooray et al found that the most common symptoms that immediately
precede eclamptic seizures are neurologic symptoms (ie, headache, with or
without visual disturbance), regardless of degree of hypertension. This suggests
 that closely monitoring patients with these symptoms may provide an early
warning for eclampsia. 11
9. Physical findings
Most patients with eclampsia present with hypertension and seizures, along with
some combination of proteinuria and edema. Findings at physical examination
may include the following:
a. Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than
110 mm Hg
b. Tachycardia
c. Tachypnea
d. Rales
e. Mental status changes
f. Hyperreflexia
g. Clonus
h. Papilledema
i. Oliguria or anuria
j. Localizing neurologic deficits
k. Right upper quadrant or epigastric abdominal tenderness
l. Generalized edema
m. Small fundal height for the estimated gestational age
10. Diagnosis
Classification of hypertensive disorders in pregnancy. 11

Gestational hypertension Hypertension that 6–7 % of

(1) develops beyond 20 weeks of gestation pregnancies
(2) returns to normal within 42nd postpartum
day and is not associated with any other
features of preeclampsia

Preeclampsia/eclampsia Hypertension presenting beyond 20 weeks of 5–7 % of

gestation with >300 mg protein in a 24-h urine pregnancies
collection or 1 + (0.3 g/l) on urine dipstick
Eclampsia is the occurrence of seizures in a
pregnant woman with preeclampsia
 Chronic hypertension Blood pressure 140/90 mmHg present before 1–5 % of
pregnancy, before the 20th week of gestation, pregnancies
or persisting beyond the 42nd postpartum day

Preeclampsia The onset of features diagnostic of 20–25 % of chronic

superimposed on chronic preeclampsia in a woman with chronic hypertension
hypertension hypertension beyond 20 weeks of gestation pregnancies

Seizures in the first trimester or well into the postpartum period probably are
due to CNS pathology and warrant full evaluation, including computed tomography
(CT) scanning of the head, lumbar puncture (if clinical evidence of meningitis or
concern for hemorrhage exists), determination of electrolyte levels, and urine or
serum toxicologic screening. Do not overlook other neurologic causes of seizure,
particularly if the seizure occurs more than 24 hours after delivery. In addition, rule
out hypoglycemia as cause of seizure or result of seizure, and rule out hyperglycemia
as cause of mental status changes.
When preeclampsia occurs in the early second trimester (ie, 14-20 weeks'
gestation), the diagnosis of hydatiform mole or choriocarcinoma should be
considered. Ruling out eclampsia in an obstetric patient who has been involved in an
unexplained trauma is important.
11. Laboratory Findings and Imaging Studies
No single laboratory test or set of laboratory determinations is useful in
predicting maternal or neonatal outcome in women with eclampsia. Imaging studies
may be indicated after initial stabilization, especially if there is doubt about the
diagnosis or possible injuries secondary to seizure activity.
a. Urinalysis and Uric Acid levels
Proteinuria is typically one of the presenting symptoms in patients with
eclampsia. A timed collection has been the criterion standard for urinalysis to
detect proteinuria (>300 mg/24 h or >1 g/L). Protein per unit time measured
over 24 hours has been used traditionally; however, 12-hour collections have
proved to be as accurate.12
 Although investigational, Baweja et al suggest that when measuring intact
urinary albumin levels using high-performance liquid chromatography in an
early and uncomplicated pregnancy, spot urinary albumin:creatinine ratio
(ACR) values are higher. If measured early in the second trimester, an ACR of
35.5 mg/mmol or higher may predict preeclampsia before symptoms arise.13
b. Hematologic Studies
A complete blood cell (CBC) count may reveal the following:
1) Anemia due to microangiopathic hemolysis, hemoconcentration due to
third spacing, or physiologic hemodilution of pregnancy
2) Peripheral smear (schistocytes, burr cells, echinocytes)
3) Increased bilirubin (>1.2 mg/dL)
4) Thrombocytopenia (< 100,000) due to hemolysis and low platelet count
associated with HELLP syndrome (seen in 20-25% of patients with
eclampsia) 4
5) Low serum haptoglobin levels
6) Elevated lactate dehydrogenase (LDH) levels (threshold of 180–600 U/L)
The coagulation profile may reveal normal prothrombin (PT) and activated
partial thromboplastin (aPTT) times, fibrin split products, and fibrinogen
levels. Rule out associated disseminated intravascular coagulation (DIC).
c. Serum Creatinine level
The serum creatinine level is elevated in eclampsia because of a decreased
intravascular volume and a reduced glomerular filtration rate (GFR).
Creatinine clearance (CrCl) may be less than 90 mL/min/1.73 m2.
d. Liver Function Tests
Liver function test results may reveal the following (20-25% of patients with
eclampsia):
1) Aspartate aminotransferase (SGOT) level higher than 72 IU/L
2) Total bilirubin levels higher than 1.2 mg/dL
3) LDH level higher than 600 IU/L [2]
4) Elevated levels due to hepatocellular injury and HELLP syndrome
e. CT Scanning and MRI of the Head
Computed tomography (CT) scanning of the head, with or without contrast,
can exclude cerebral venous thrombosis, intracranial hemorrhage, and central
nervous system lesions, all of which can occur in pregnancy and present with
seizures.
Although obtaining a CT scan in eclampsia is not routine, abnormalities have
been observed in up to 50% of women imaged.
 Characteristic CT scan findings include cortical hypodense areas, particularly
in the occipital lobes, and diffuse cerebral edema, which is believed to
correspond to petechial hemorrhages and diffuse edema noted in postmortem
studies.
f. Transabdominal Ultrasonography
Transabdominal ultrasonography is used to estimate gestational age. This may
also be used to rule out abruptio placentae, which can complicate eclampsia.
12. Medical Therapy

Eclamptic convulsions are life-threatening emergencies and require the proper

treatment to decrease maternal morbidity and mortality. Delivery is the only
definitive treatment for eclampsia. The patient should be advised and educated on
the course of the disease and any residual problems. She should also be educated on
the importance of adequate prenatal care in subsequent pregnancies.
Several organizations have developed screening, treatment, and prevention
guidelines for preeclampsia and eclampsia. 15,16,17 The American College of
Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal
Medicine (SMFM) continue to support the short-term (usually <48 hours) use of
magnesium sulfate in obstetric care for conditions and treatment durations that
include the following :17
a. For prevention and treatment of seizures in women with preeclampsia
or eclampsia: Recent recommendations suggest that magnesium sulfate be
utilized for seizure prophylaxis in severe preeclampsia and for controlling
seizures in eclampsia, though magnesium sulfate is not required for
preeclampsia without severe features
b. For fetal neuroprotection before anticipated early preterm (<32 weeks of
gestation) delivery
 c. For short-term prolongation of pregnancy (≤48 hours) to allow for the
administration of antenatal corticosteroids in pregnant women who are at risk
of preterm delivery within 7 days
Holistic theraphy
a. Consultations and/or transfer
An experienced obstetrician or maternal-fetal medicine specialist should
be consulted. Patients with eclampsia require immediate obstetric consultation
and admission to a labor and delivery unit capable of providing intensive care
until delivery of the neonate. In the event of premature delivery or fetal
compromise, a pediatrician or neonatologist should be consulted.
When initially evaluating a patient with eclampsia, become familiar with
the level of care that the medical center can offer the patient, as eclampsia
clearly poses a risk of considerable maternal and neonatal morbidity and
mortality. Patients with eclampsia may benefit from management at a tertiary
care center, a high-risk obstetric facility that provides neonatal and maternal
intensive care.
b. Supportive care
Emergency medical services personnel should (1) secure an intravenous
(IV) line with a large-bore catheter, (2) initiate cardiac monitoring and administer
oxygen, and (3) transport the patient in the left lateral decubitus position.
Supportive care for eclamptic convulsions includes the following:
1) Close monitoring (invasive, if clinically indicated)
2) Airway support
3) Adequate oxygenation
4) Anticonvulsant therapy
5) Blood pressure (BP) control
Place the patient in the left lateral position. This positioning decreases the
risk of aspiration and will help to improve uterine blood flow by relieving
obstruction of the vena cava by the gravid uterus. Protect the patient against injury
during the seizure by padding and raising guardrails, using a padded tongue blade
between the teeth, and suctioning the oral secretions as needed.
After the seizure has ended, a 16- to 18-gauge IV line should be established
for drawing specimens and administering fluids and medications. (Fluid
management is critical in patients with eclampsia.) IV fluids should be limited to
 isotonic solutions to replace urine output plus about 700 mL/d to replace
insensible losses.
c. Pharmacologic considerations for convulsions and hypertension
Pharmacotherapy goals are to reduce morbidity, prevent complications, and
correct eclampsia. The drug of choice to treat and prevent eclampsia is
magnesium sulfate.17,18 Familiarity with second-line medications phenytoin and
diazepam/lorazepam is required for cases in which magnesium sulfate may be
contraindicated (eg, myasthenia gravis) or ineffective. Control of hypertension is
essential to prevent further morbidity or possible mortality. The most commonly
used antihypertensive agents are hydralazine, labetalol, and nifedipine.
IV magnesium sulfate is the initial drug administered to terminate seizures.
Seizures usually terminate after the loading dose of magnesium. A loading dose of
4-6 g (15-20 min) and a maintenance dose of 1-2 g per hour as a continuous IV
solution should be administered. Alternatively, lorazepam (Ativan; 4 mg IV over
2-5 minutes) or diazepam (Valium; 5-10 mg IV slowly) can be used to terminate
the seizure, after which magnesium sulfate is administered. Once the seizures
terminate, 85% of patients note improved BP control. 16,19 Note: Magnesium
toxicity can cause coma, and, if mental status changes with these infusion rates,
this should be considered.2
Benzodiazepines or phenytoin can be used for seizures that are not
responsive to magnesium sulfate. Avoid the use of multiple agents to abate
eclamptic seizures, unless necessary. Severe hypertension must be addressed after
magnesium infusions. Hydralazine or labetalol can be administered IV for BP
control. The goal is to maintain systolic BP between 140 and 160 mm Hg and
diastolic BP between 90 and 110 mm Hg. An IV bolus of hydralazine (5-10 mg
q20min prn) or labetalol (20-40 mg q15min prn) is recommended. Other potent
antihypertensive medications, such as sodium nitroprusside or nitroglycerin, can
be used but are rarely required.2
Diuretics are used only in the setting of pulmonary edema. Care must be
taken not to decrease the BP too drastically; an excessive decrease can cause
inadequate uteroplacental perfusion and fetal compromise. 18 A dose of antenatal
 steroids may be administered in anticipation of emergent delivery when
gestational age is less than 32 weeks. Betamethasone (12 mg IM q24h × 2 doses)
or dexamethasone (6 mg IM q12h × 4 doses) is recommended.
About 10% of women with eclampsia will have an additional seizure after
receiving magnesium sulfate. Another 2 g bolus of magnesium may be given in
these cases. For the rare patient who continues to have seizure activity while
receiving adequate magnesium therapy, seizures may be treated with sodium
amobarbital, 250 mg IV over 3-5 minutes. 20 Alternatively, lorazepam or diazepam
may be administered (as described above) for status epilepticus. However, these
drugs can be associated with prolonged neonatal neurologic depression.
BP should be assessed with the goal of maintaining the diastolic BP at less
than 110 mm Hg with administration of antihypertensive medications as needed
(eg, hydralazine, labetalol, nifedipine).
Keep nothing by mouth (including medications) until the patient is
medically stabilized or delivered, because she is at risk for aspiration when
postictal and may have recurrent seizures. Anjum et al reported that following a
loading dose of magnesium sulfate, a reduced duration of maintenance doses (12
hours vs 24 hours) for women with eclampsia may be effective for preventing
recurrent seizures. 21
d. Maternal monitoring
Depending on the clinical course, regularly check the patient’s neurologic
status for signs of increased intracranial pressure or bleeding (eg, funduscopic
examination, cranial nerves). Monitor fluid intake and urine output, maternal
respiratory rate, and oxygenation, as indicated, and continuously monitor fetal
status. Pulmonary arterial pressure monitoring is rarely indicated but may be
helpful in patients who have evidence of pulmonary edema or oliguria/anuria.
Once the seizure is controlled and the patient has regained consciousness,
the patient’s general medical condition should be assessed to identify any other
causes for seizures.Induction of labor may be initiated when the patient is stable.
e. Fetal monitoring
 Fetal heart rate and uterine contractions should be continuously monitored.
Fetal bradycardia is common following the eclamptic seizure and has been
reported to last from 30 seconds to 9 minutes. The interval from the onset of the
seizure to the fall in the fetal heart rate is typically 5 minutes or less. Transitory
fetal tachycardia may occur following the bradycardia. Typically, emergent
cesarean delivery is not indicated for this postseizure transient bradycardia; it
spontaneously resolves.
After the initial bradycardia, during the recovery phase, the fetal heart rate
tracing may reveal a loss of short- and long-term variability and the presence of
late decelerations. These abnormalities are most likely due to the decrease in
uterine blood flow caused by the intense vasospasm and uterine hyperactivity
during the convulsion. If the fetal heart tracing does not improve following a
seizure, further evaluation should be undertaken. Growth-restricted and preterm
fetuses may take longer to recover following a seizure. Placental abruption may
be present if uterine hyperactivity remains and fetal bradycardia persists.
f. Delivery (antepartum or intrapartum eclampsia)
Delivery is the treatment for eclampsia after the patient has been stabilized.
No attempt should be made to deliver the infant either vaginally or by cesarean
delivery until the acute phase of the seizure or coma has passed. The mode of
delivery should be based on obstetric indications but should be chosen with an
awareness that vaginal delivery is preferable from a maternal standpoint.
Adequate maternal pain relief for labor and delivery is vital and may be
provided with either systemic opioids or epidural anesthesia.In the absence of
fetal malpresentation or fetal distress, oxytocin or prostaglandins may be initiated
to induce labor.
Cesarean delivery may be considered in patients with an unfavorable cervix
and a gestational age of 30 weeks or less, as induction under these circumstances
may result in a prolonged intrapartum course and is frequently unsuccessful in
avoiding cesarean delivery, given the high rate of intrapartum complications.
When emergent cesarean delivery is indicated, substantiating the absence of
coagulopathy before the procedure is important. (See Surgical Therapy.) 22
 Intrapartum complications include the following:
1) Fetal growth retardation (30%)
2) Nonreassuring fetal heart rate patterns (30%)
3) Placental abruption (23%)
Irrespective of gestational age, a prolonged induction with clinically
significant worsening of maternal cardiovascular, hematologic, renal, hepatic,
and/or neural status is generally an indication for cesarean delivery when the
anticipated delivery time is remote.
g. Surgical Therapy
Cesarean delivery may be necessary for obstetric indications or a
deteriorating maternal condition. The patient should be stabilized with respect to
seizures, oxygenation, and hemodynamic status before the initiation of cesarean
delivery. BP should be controlled and coagulopathies monitored or corrected.
13. Postpartum Outpatient Monitoring
Follow up 1-2 weeks after delivery to evaluate the patient for BP control and
any residual deficits from the eclamptic seizure. Patients with persistent hypertension
past 8 weeks' puerperium or neurologic changes may need medical referral. Al-Safi et
al suggest that the first week after discharge is the most critical period for the
development of postpartum eclampsia. Discussing the risks and educating patients
about the possibility of delayed postpartum preeclampsia is important, regardless of
whether they develop hypertensive disease prior to discharge. 23
14. Prevention of Preeclampsia/Eclampsia
Preventing the development of preeclampsia in high-risk patients could
theoretically decrease the risk of eclampsia and its complications later in pregnancy.
Aspirin blocks platelet aggregation and vasospasm in preeclampsia, and it may be
effective in preventing preeclampsia. Studies have shown that low-dose aspirin in
women at high risk for preeclampsia can contribute to a decreased risk of
preeclampsia, a reduction in preterm delivery rates, and a reduction in fetal death
rates, without increasing the risk of placental abruption. An obstetrician should
directly supervise low-dose aspirin therapy in high-risk patients.
 If the patient has preexisting hypertension, she should have good control before
conception and throughout her pregnancy. Her case should be followed for
recognition and treatment of preeclampsia.
A study by Vadillo-Ortega et al suggests that in a high-risk population (eg,
previous pregnancy complicated by preeclampsia, preeclampsia in a first-degree
relative), supplementation during pregnancy with a special food (eg, bars) containing
L-arginine and antioxidant vitamins may reduce the risk of preeclampsia. Notably, the
beneficial effect was greatest when supplementation was started prior to 24 weeks'
gestation. Antioxidant vitamin supplementation alone did not protect against
preeclampsia. More studies performed on low-risk populations are needed.24
15. Complications of Eclampsia
As many as 56% of patients with eclampsia may have transient deficits,
including cortical blindness. However, studies have failed to demonstrate evidence of
persisting neurologic deficits after uncomplicated eclamptic seizures during the
follow-up period. 25 Studies suggest that there is an increased risk for cerebrovascular
accidents (CVAs) and coronary artery disease (CAD) in eclamptic mothers later in
life. Other potential complications of eclampsia include the following:
a. Permanent neurologic damage from recurrent seizures or intracranial bleeding
b. Renal insufficiency and acute renal failure
c. Fetal changes – IUGR, abruptio placentae, oligohydramnios
d. Hepatic damage and rarely hepatic rupture
e. Hematologic compromise and DIC
f. Increased risk of recurrent preeclampsia/eclampsia with subsequent pregnancy
g. Maternal or fetal death: Eclampsia is associated with approximately 13% of
maternal deaths worldwide.5
Although some women who have had eclampsia or preeclampsia have reported
subsequent cognitive difficulties even years later, a long-term follow-up study by
Postma et al utilizing standardized testing was unable to find objective evidence of
such problems. The reported neurocognitive difficulties have seemingly been
associated with concentration and memory, as well as with vision-related tasks of
daily living. In the study, 46 women who had been eclamptic and 51 who had been
 preeclamptic were given neurocognitive tests an average of about seven years
following the index pregnancy; 48 controls, who had normotensive pregnancies, were
also involved. 26,27
The eclamptic and preeclamptic women in the study did not perform as well as
the controls on motor-function tests. (They also performed more poorly on the
Hospital Anxiety and Depression Scale.) However, they scored similarly to the
control subjects with regard to attention, executive functioning, visual perception, and
working and long-term memory. The investigators suggested that the reported
cognitive difficulties in previously eclamptic or preeclamptic women occur during
complex, stressful situations of daily life and may be exacerbated by anxiety and
depression. 26,27
B. HELLP Syndrome
HELLP syndrome, named for 3 features of the disease (hemolysis, elevated
liver enzyme levels, and low platelet levels), is a life-threatening condition that can
potentially complicate pregnancy. HELLP was once known as edema-proteinuria-
hypertension gestosis type B in the early 20th century and was later renamed in 1982
by Louis Weinstein.
Although the idea is controversial, some propose that HELLP is a severe form
of preeclampsia, which, in turn, is defined as gestational hypertension accompanied
by proteinuria after the 20th week of gestation. Others believe that HELLP syndrome
is an entity of its own. Although the cause of HELLP syndrome is unknown, certain
risk factors, including a maternal age of older than 34 years, multiparity, and
European descent, have been described. 1, 2, 3
1. Pathophysiology
HELLP is a syndrome characterized by thrombocytopenia, hemolytic
anemia, and liver dysfunction believed to result from microvascular endothelial
activation and cell injury. The pathophysiology of HELLP syndrome is ill-
defined. Some theorize that, because HELLP is a variant of preeclampsia, the
pathophysiology stems from a common source. In preeclampsia, defective
placental vascular remodeling during weeks 16-22 of pregnancy with the second
wave of trophoblastic invasion into the decidua results in inadequate placental
perfusion. The hypoxic placenta then releases various placental factors such as
 soluble vascular endothelial growth factor receptor-1 (sVEGFR-1), which then
binds vascular endothelial growth factor (VEGF) and placental growth factor
(PGF), causing endothelial cell and placental dysfunction by preventing them
from binding endothelial cell receptors. The result is hypertension, proteinuria,
and increased platelet activation and aggregation.
Furthermore, activation of the coagulation cascade causes consumption of
platelets due to adhesion onto a damaged and activated endothelium, in addition
to microangiopathic hemolysis caused by shearing of erythrocytes as they traverse
through capillaries laden with platelet-fibrin deposits. Multiorgan microvascular
injury and hepatic necrosis causing liver dysfunction contribute to the
development of HELLP. 4, 1, 5, 5, 6, 7, 8, 9
Another hypothesis proposes acute maternal immune rejection due to
immunocompetent maternal cells coming into contact with a genetically distinct
fetus, altering the maternal-fetal immune balance and causing endothelial
[10]
dysfunction, platelet activation and aggregation, and arterial hypertension.
Other theories include inborn errors of fatty acid oxidative metabolism secondary
to long- and medium-chain fatty acid mutations, which cause liver damage
secondary to insufficient mitochondrial oxidation of fatty acids required for
ketogenesis.11,12 Yet another theory suggests a placental-instigated acute
inflammatory condition targeting the liver.13 In addition, dysfunction in the
complement system via excessive activation or defective regulation for a given
amount of endothelial injury has been proposed to cause damage to hepatic
vessels in HELLP.14 Many hypotheses attempt to define the pathogenesis of
HELLP syndrome, but the true pathology remains a mystery.
2. Etiology
The cause of HELLP syndrome is currently unknown, although theories as
described in Pathophysiology have been proposed.
3. Risk Factors
Risk factors for HELLP syndrome include the following:
a. Maternal age older than 34 years
b. Multiparity
c. White race or European descent
d. History of poor pregnancy outcome 1, 15
4. Epidemiology
 HELLP syndrome occurs in 0.1%-0.6% of all pregnancies and in 4%-12%
of patients with preeclampsia. HELLP syndrome typically occurs between week
16,
27 of gestation and delivery, or immediately postpartum in 15%-30% of cases.
17, 18, 19
The incidence of HELLP syndrome is significantly higher in whites and
women of European descent. 18 HELLP has been shown to occur in older maternal
age groups, with a mean age of 25 years. In contrast, preeclampsia is most
common in younger patients (mean age, 19 years). 18
5. Prognosis
Most patients with HELLP syndrome stabilize within 24-48 hours, with
[2]
the most protracted postpartum recovery time in patients with class 1 disease.
The recurrence rate is 2%-27% in subsequent pregnancies. 20, 21
Patients are at
increased risk of preeclampsia or pregnancy-induced hypertension, in addition to
preterm delivery, fetal growth restriction, and placental abruption in future
pregnancies.20, 2
Women with HELLP syndrome are also at increased risk of
developing hypertension and cardiovascular disease.7
a. Maternal
Maternal mortality ranges from 1%-3%, with a perinatal mortality rate of
35%. 22 Class 1 or complete HELLP (see Stages) is associated with the highest
incidence of perinatal morbidity and mortality. Sixty percent of deaths occur
in patients with class 1 disease; cerebral hemorrhage is the most common
autopsy finding. 23, 24 Morbidity includes the following:
1) Disseminated intravascular coagulation (DIC) (20%)
2) Placental abruption (16%)
3) Acute renal failure (7%)
4) Pulmonary edema (6%) 22
b. Neonatal
Fetal morbidity and mortality rates range from 9%-24%25 and usually result
from placental abruption, intrauterine asphyxia, or prematurity. 26
6. Clinical Presentation
a. History
HELLP syndrome typically occurs between 27 weeks’ gestation and delivery
in women with a mean age of 25 years. A complete review of systems may
reveal malaise, nausea, vomiting, weight gain, and various other nonspecific
symptoms. A wide range of symptoms, none of which are diagnostic, may be
present in persons with HELLP syndrome. For instance, nausea, vomiting, and
 epigastric and right upper quadrant pain has been reported in 30%-90% 18, 27, 28
of patients, headache in 33%-68%,29, 27
visual changes in 10%-20%,30 and
jaundice in 5%.22 In a series by Sibai et al, most patients with HELLP
syndrome presented preterm with complaints of epigastric or right upper
quadrant pain and nonspecific viral syndrome types of symptoms.18 In earlier
studies by Weinstein, nausea, vomiting, and epigastric pain were found to be
the most common symptoms in patients with HELLP symptoms.31, 3
Common history findings are as follows:
1) Malaise
2) Nausea and vomiting
3) Edema with secondary weight gain
4) Epigastric or right upper quadrant pain
5) Dyspnea (if pulmonary edema present)
b. Physical Examination
A complete physical examination may reveal signs of dehydration,
including dry mucous membranes, sunken eyes, weakness, and imbalance
secondary to dizziness from excessive vomiting. Vital signs may reveal
tachycardia, tachypnea, and hypertension. Patients with HELLP syndrome show
various signs and symptoms, many of which are synonymous with
preeclampsia. Proteinuria is shown to be present in 86%-100% of patients and
hypertension in 80%.22 However, it should be noted that 15% of patients do not
present with either.18, 16, 30
In addition, 55%-67% of patients present with nondependent edema,
which can be periorbital or in the upper and lower extremities .2 Right upper
quadrant tenderness is found in 65%-90% of patients, while jaundice is evident
in 5% of patients.22 A lung examination may reveal crackles if pulmonary edema
is present.
Vital signs may include the following:
1) Hypertension
2) Tachycardia
3) Tachypnea
Generalized findings may include the following:
1) Fatigue or weakness
2) Distress due to pain
3) Jaundice
 Head, ears, eyes, nose and throat (HEENT) findings may include the
following:
1) Signs of dehydration including sunken eyes
2) Edema leading to puffy eyes
3) Dry mucous membranes
Pulmonary findings may include crackles secondary to noncardiogenic
pulmonary edema. Abdominal findings may include right upper quadrant to
epigastric tenderness. Extremities findings may include edema.
c. Diagnostic criteria
At present, there are two major definitions for diagnosing the HELLP
syndrome. In the Tennessee Classification System. The Tennessee classification
describes HELLP as either complete or partial. Complete HELLP is defined as
hemolysis with an abnormal peripheral smear finding and an LDH level greater
than 600 IU/L or bilirubin level greater than 1.2 mg/dL. Patients with complete
HELLP have platelet counts less than 100,000/µL and AST levels over 70 IU/L.
Partial HELLP describes severe preeclampsia plus some features of
HELLP. These features are further defined as LP, or low platelet syndrome
(slightly thrombocytopenic but no hemolysis or liver dysfunction); EL, or
elevated liver enzyme syndrome (mildly elevated liver enzymes but no
hemolysis or thrombocytopenia); HEL syndrome (hemolysis, elevated liver
enzyme levels, but no thrombocytopenia); and ELLP syndrome (elevated liver
enzyme levels and low platelet counts, no hemolysis). 38
Complete HELLP syndrome is characterized by the following:
1) Platelet count of 100,000/μL or less
2) AST or ALT levels of 70 IU/L or more
3) LDH (or bilirubin) (with hemolysis as evidenced on abnormal peripheral
smear) levels of 600 IU/L (≥0.2 mg/dL) or more
Partial HELLP syndrome is characterized by severe preeclampsia plus one of
the following:
1) ELLP: Elevated liver enzyme levels, thrombocytopenia, no hemolysis
2) EL: Mildly elevated liver enzyme levels, no thrombocytopenia, no
hemolysis
3) LP: Thrombocytopenia, no hemolysis, normal liver enzyme levels
4) HEL: Hemolysis, liver dysfunction, no thrombocytopenia
Main diagnostic criteria of the HELLP syndrome
Table 2: Mississippi Classification of HELLP Syndrome
 Class 1 (Severe) Class 2 (Moderate) Class 3 (Mild)

Platelets ≤50,000/µL 50,000-100,000/µL 100,000-150,000/µL

AST or ALT ≥70 IU/L ≥70 IU/L ≥40 IU/L

LDH ≥600 IU/L ≥600 IU/L ≥600 IU/L

Incidence of
13% 8% No increased risk
bleeding

BMC Pregnancy Childbirth. 2009; 9: 8.

The Mississippi-Triple Class System, a further classification of the
disorder is based on the nadir PLT count any time during the course of the disease
(Table 1). 7 Class 1 and class 2 are associated with haemolysis (LDH > 600 U/L)
and elevated AST (≥ 70 U/L) concentration, while class 3 requires only LDH >
7,33,34
600 U/L and AST ≥ 40 U/L in addition to the specific PLT count . Class 3
HELLP syndrome is considered as a clinical significant transition stage or a phase
of the HELLP syndrome which has the ability of progression. 34
The diagnosis of the HELLP syndromes has often been based on different
criteria.9 The condition can be diagnosed simply on biochemical evidence. 4,9,14,35-37

Some authors require the presence of severe preeclampsia together with

biochemical substantiation to diagnose HELLP.5,38-42 Others deal with the HELLP
syndrome as partial or incomplete HELLP.43,44 A number of studies have included
women with lack of suspicion or evidence of haemolysis. The syndrome ELLP
has been described where there has been no haemolysis.15,45 The use of different
definitions makes comparison of published data difficult.9 According to Smulian
et al. the threshold of normal LDH values may be much lower than 600 U/L
depending on the laboratory method adopted.41 Visser and Wallenburg used ALAT
> 30 U/L to define abnormality (2 SD above mean in hospital).20 Clearly, the
analytical method used is important for the diagnostic reference range.
d. Differential diagnosis
The HELLP syndrome may be misdiagnosed as viral hepatitis, cholangitis
and other acute diseases (Table 2).6,46 Other less common, but serious conditions
that may mimic HELLP, include ITP, acute fatty liver of pregnancy (AFLP),
haemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura
(TTP) and systemic lupus erythematosus (SLE).21,32 These conditions are
associated with high maternal mortality and may cause long-term squeals.32 They
may be mistaken for a HELLP syndrome and a careful diagnostic evaluation is
required as their therapy is quite different.
Table II. BMC Pregnancy
Differential diagnosis of the HELLP syndrome.

1. Diseases related to pregnancy

 Benign thrombocytopenia of pregnancy
 Acute fatty liver of pregnancy (AFLP)
2. Infectious and inflammatory diseases, not specifically
related to pregnancy:
 Virus hepatitis
 Cholangitis
 Cholecystitis
 Upper urinary tract infection
 Gastritis
 Gastric ulcer
 Acute pancreatitis
3. Thrombocytopenia
 Immunologic thrombocytopenia (ITP)
 Folate deficiency
 Systemic lupus erythematosus (SLE)
 Antiphospholipid syndrome (APS)
4. Rare diseases that may mimic HELLP syndrome
 Thrombotic thrombocytopenic purpura (TTP)
 Haemolytic uremic syndrome (HUS)
(Childbirth. 2009; 9: 8)

Clinical signs of AFLP vary and there is significant overlap in clinical and
biochemical features with the HELLP syndrome.47 AFLP typically occurs between
the 30th and 38th gestational weeks with a 1 to 2 week history of malaise,
anorexia, nausea, vomiting, mid epigastric or right upper abdominal pain,
headache and jaundice. Hypertension and proteinuria are usually absent. Further
examination reveals haemoconcentration, metabolic acidosis, acute liver failure
and low grade disseminated intravascular coagulation (DIC) with normal or
moderately subnormal PLT count, prolonged prothrombin time (PT) and partial
thromboplastin time (PTT), low serum fibrinogen and antithrombin
concentrations.32,47,48 Abnormal blood tests also include leucocytosis, increased
levels of creatinine, uric acid, ammonium and liver enzymes such as alkaline
phosphatase, AST, ALAT and bilirubin .32,49 Hypoglycemia and prolongation of
prothrombin time may distinguish AFLP from the HELLP syndrome.47 Ultrasound
examination of the liver may reveal increased echogenicity in severe cases of
AFLP. Computerized tomography (CT) can well show decreased or diffuse
attenuation in the liver. Liver biopsy is recommended as the standard procedure to
confirm the diagnosis, but requires an acceptable haemostatic function.32
Gastrointestinal bleeding, acute renal failure and pancreatitis may complicate
AFLP. Most women improve in the course of 1 to 4 weeks post-partum, but AFLP
may recur in next pregnancy.47
ITP is a clinical syndrome with thrombocytopenia which may be
manifested as a bleeding disorder with purpura and petechiae. Pregnancy does not
increase the incidence of ITP, nor does it exacerbate a preexisting disease. Even
with a very low platelet count there is in most cases neither maternal nor fetal
morbidity or mortality. 29,50,51
HUS and TTP are thrombotic microangiopathies which share some of the
pathophysiological characteristics of the HELLP syndrome including endothelial
injury, platelet aggregation, microthrombi, thrombocytopenia and anaemia.49
Abnormal blood smear, increased LDH and creatinine levels may help in the
differentiation. The microvascular injury in HUS affects mainly the kidneys.32
HUS develops usually in the post-partum period, with signs and symptoms of
renal failure.9 However, most cases arise in children and adolescents caused by a
specific enterotoxin produced by Escherichia coli O157:H7. Rare forms may be
due to a genetic abnormality in the complement system.52 TTP, which is an
extremely rare condition during pregnancy, is characterized by neurological
dysfunction, fever, abdominal pain and bleeding. The spectrum of neurological
abnormalities spans from headache to visual disturbances, confusion, aphasia,
transient paresis, weakness and seizures. High levels of high-molecular weight
von Willebrand factor in maternal serum reflect the virtual absence of the
metalloprotease ADAMTS13 enzyme which is required to control the level of the
factor.32,53 Specific tests for this hereditary condition are not readily available in
 routine clinical laboratories.32 The mortality of HUS and TTP has decreased due
to the use of plasma exchange and intensive care.52
SLE is an autoimmune disorder characterized by deposits of antigen-
antibody complexes in capillaries, with mild to severe clinical findings. SLE may
affect multiple organ systems (kidneys, lungs, heart, liver and brain). The clinical
and laboratory findings in women with lupus nephritis are similar to those with
severe preeclampsia. Antiphospholipid antibodies (lupus anticoagulant and/or
anticardiolipin antibodies) are present in 30–40% of the cases, while
thrombocytopenia occurs in 40–50% and haemolytic anaemia in 14–23% of the
women with SLE. Cerebral lesions and symptoms may develop because of
vasculitis and/or cerebro-vascular occlusion that might lead to seizures.32 In the
so-called antiphospholipid syndrome (APS) antiphospholipid antibodies are
associated with recurrent thrombosis (in arteries and veins) and pregnancy loss.
APS may also occur as a primary disease, unrelated to SLE. Development of
HELLP syndrome in women with an established APS syndrome may be more
frequent than previously thought.54
Folate deficiency is common in pregnancy, but its progression to
megaloblastosis is rare. Haemolytic anaemia, thrombocytopenia, and
coagulopathy due to folate deficiency may mimic the incomplete HELLP
syndrome.55
e. Complications
Maternal complications of HELLP syndrome may include the following:
1) Hematologic: DIC, bleeding, hematoma
2) Cardiac: Cardiac arrest, myocardial ischemia
3) Pulmonary: Pulmonary edema, respiratory failure, pulmonary embolism, adult
respiratory distress syndrome (ARDS)
4) CNS: Hemorrhage/stroke, cerebral edema, central venous thrombosis,
seizures, retinal detachment
5) Renal: Acute renal failure, chronic renal failure requiring dialysis
6) Hepatic: Hepatic (usually subcapsular) hematoma with possible rupture,
ascites, nephrogenic diabetes insipidus
7) Infection 16, 2
Neonatal complications of HELLP syndrome may include the following:
1) Prematurity
2) Intrauterine growth retardation (39%)2
 3) Thrombocytopenia (one third of neonates born to patients with HELLP; 4% of
these infants will have intraventricular hemorrhage) 26
f. Management of pregnant women with HELLP syndrome
In general, there are three major options for the management of women with
severe preeclampsia and HELLP syndrome7,9,72,98. These include:
1) Immediate delivery which is the primary choice at 34 weeks' gestation or later.
2) Delivery within 48 hours after evaluation, stabilization of the maternal clinical
condition and CS treatment. At 27 to 34 weeks of gestation, this option
appears appropriate and rational for the majority of cases.
3) Expectant (conservative) management for more than 48–72 hours may be
considered in pregnant women before 27 weeks' gestation. In this situation,
CS treatment is often used, but the regimens vary considerably.
g. Conservative management (> 48 hours)
Large randomized clinical trials aimed to compare conservative versus
aggressive management with immediate delivery of women with the HELLP
syndrome are missing. However, expectant management before completed 34
weeks' gestation may be an acceptable option in selected cases if it is performed
in tertiary care units under close maternal and foetal surveillance (e.g.
antihypertensive treatment, ultrasound and Doppler examination). Possible
advantages due to limited prolongation of pregnancy should be carefully weighed
against the increased risks for maternal and foetal complications (abruptio
placentae, acute renal failure, pulmonary oedema, DIC, perinatal and maternal
death).10 If the maternal condition worsens, immediate Caesarean section is
inevitable. Conservative treatment is contraindicated in women with DIC .
The benefit of temporizing management of HELLP syndrome is
questioned10; some authors warn against expectant management to optimize
maternal condition before delivery beyond 24–48 hours10 or conservative
management is disregarded. However, expectant management of pregnant women
with HELLP syndrome remote from term is common practice in the Netherlands,
conditional on the safety of the mother.20
 CASE ANALYSE

A patient, G2P1A0, 28 years old with 24 +3 weeks of gestation came from Islamic
Hospital of Klaten with eclampsia. Patient had been seizure once times in her house at
August 21, 2017. Patient complained that she got headache, nausea and vomiting, and
there was no double vision. Patient felt that she got 6 month of pregnancy, there was
neither uterus contraction nor amnionic water coming out from birth passage. She did not
feel there is blood and mucus coming out from birth passage. Patient routinely went to a
specialist in obstetrics and gynecology once a month, and has a good history of blood
pressure. High blood pressure was known after patient had seizure. She said that she did
not has hypertention, diabetes mellitus, cardiovascular disease, allergy, asthma before.
She also said that she did not has hypertention of gestation in her first pregnancy.
She had been get magnesium sulphate 40% 4gr intramuscular in 15 minutes and
maintenance with magnesium sulphate 1gr/hour for 12 hours, dopamet 2x250mg,
dexamethasone 1ampul/12hours from Islamic Hospital of Klaten. MgSO4 injection is
administered as an anti-seizure so that people with severe preeclampsia do not become
impending eclampsia / eclampsia by reducing interseluler calcium levels so that the
action potential is inhibited. MgSO4 injection may be administered intravenously by
injecting an initial dose of MgSO4 20% with a dose of 4 grams in 15 minutes then
followed by a maintenance dose of 1 gram per hour within 24 hours after initial dosing.
Intravenous administration is done through a syringe pump, up to 24 hours after delivery.
It should be noted that MGSO4 intoxication is present when a patellar reflex is lost,
decreased respiratory frequency <16x / min, slowing or cessation of heart rate. If
breathing occurs immediately resuscitate the patient or with ventilator installation. An
antidote given in case of intoxication is Ca gluconas 20% with an intravenous 1 g dose
inserted slowly until breathing begins again
When she came to hospital at first time, her general condition was good and
composmentis. Her blood pressure was 150/90 mmHg, heart rate was 92x/minutes,
respiratory rate was 18x/minutes, and temperature was 36,5 0C. There was no conjunctiva
anemia, no icteric sclera. Cor and pulmo in normal range. There was no distended
abdominal, no tender pain, ballottement (+), uterus contraction (-), fetal heart rate (+)
148x/minutes, fundal uterus height was 18cm. From ultrasonography examination, we’ve
got data that there was an intrauterine single fetus, fetal heart rate (+), estimated fetal
body weight was 615gr. Insertion of placenta in corpus, grade I. Amniotic fluid seems
normal. There was no major congenital anomaly. Fetus seems in good condition. Patient
was diagnosed as eclampsia free seizure partial HELLP syndrome in immature pregnancy
secundigravida, not in labor.
Diagnosis of eclampsia was estabilished by seizure history at August 21, 2017.
Eclampsia, which is considered a complication of severe preeclampsia, is commonly
defined as new onset of grand mal seizure activity during pregnancy or postpartum
woman with sign and symptom of preeclampsia. In this patient, there were sign and
symptom of preeclampsia, among others are high blood pressure during pregnancy
(150/90 mm Hg) and proteinuria (+3).

The hypertension occurring in these patients can be caused by vasoconstriction

occurring mainly in arterioles that is thought to be caused by increased vascular
reactivity. The mechanism of increased vascular reactivation is thought to be caused by
changes in the interactions between the vasodilator substances (prostacyclin, nitrit oxide)
and vasoconstrictive (thromboxane A2, endothelin). These changes increase arterial blood
pressure (afterload).
Proteinuria that occurs in these patients is caused by damage of glomerular
endothelium due to free radicals from the ischemic placenta. Glomerular damage causes
the protein that should be filtered out through the urine. The release of protein through
the urine results in decreased albumin in the blood vessels and causes hypoalbuminemia
(3.3). Albumin in the blood vessels serves to maintain the oncotic pressure of the blood
vessels. Hypoalbuminemia causes a decrease in oncotic pressure, resulting in leakage of
plasma that causes edema in various organs such as the extremities, lung, eyes and brain.
HELLP syndrome, named for 3 features of the disease (hemolysis, elevated liver
enzyme levels, and low platelet levels), is a severe form of preeclampsia and a life-
threatening condition that can potentially complicate pregnancy. Patient got increasing
level of LDH (976), eleveted level of liver enzyme (SGOT= 42, SGPT=39). Activation of
the coagulation cascade causes consumption of platelets due to adhesion onto a damaged
and activated endothelium, in addition to microangiopathic hemolysis caused by shearing
of erythrocytes as they traverse through capillaries laden with platelet-fibrin deposits
(low platelet levels). Multiorgan microvascular injury and hepatic necrosis causing liver
dysfunction and manifest in elevated liver enzyme.

Based of patient’s condition, she was planned to get termination of pregnancy

with misoprostol induction 25mcg/5hour pervaginam in 24 hours (max 4 times),
education and informed consent, severe pre-eclampsia procedure, injection of
dexamethasone 5mg/12 hour, injection of oxytoxin 10 IU in 500cc ringer lactate after
inpartu. Misoprostol is a synthetic prostaglandin E 1 analogue that is used off-label for a
variety of indications in the practice of obstetrics and gynecology, including medication
abortion, medical management of miscarriage, induction of labor, cervical ripening
before surgical procedures, and the treatment of postpartum hemorrhage . Severe pre-
eclampsia procedure include oxygenation 3 liters/minute, ringer lactate infuse 12
drops/minute, magnesium sulphate 20% 4 grams in 15 minutes, continued by magnesium
sulphate 20% 1 grams/hours in 24 hours, nifedipine if blood pressure is same or more
than 160/110, Dexamethasone is given to increase lung inflammation in infants. Oxytocin
is given to increase uterine contractions.
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