Ten percent of all pregnancies are complicated by hypertension.

Eclampsia
and preeclampsia account for about half of these cases worldwide and have been recognized and
described for years despite the general lack of understanding of the disease.

n the fifth century,
Hippocrates noted that headaches, convulsions, and drowsiness were ominous signs associated with
pregnancy. n 1619, Varandaeus coined the term 0.,258, in a treatise on gynecology.
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.

t 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.

Similarly, hypertension was absent in 16% of cases reviewed in the United States.
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.

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. n
developed countries, many reported cases have been classified as unpreventable.
Course of ecIamptic 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. t 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.
EtioIogic and Risk Factors for PreecIampsia/EcIampsia
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.

mbalanced prostanoid production and increased plasma antiphospholipids
have also been implicated in eclampsia.
Risk factors for ecIampsia
The following are considered risk factors for eclampsia:
O Nulliparity
O Family history of preeclampsia, previous preeclampsia and eclampsia
O Poor outcome of previous pregnancy, including intrauterine growth retardation, abruptio placentae,
or fetal death
O Multifetal gestations, hydatid mole, fetal hydrops, primigravida
O Teen pregnancy
O Primigravida
O Patient older than 35 years
O Lower socioeconomic status

The following preexisting medical conditions are also considered risk factors

:
O Obesity
O Chronic hypertension
O Renal disease
O Thrombophilias-antiphospholipid antibody syndrome
O Protein C deficiency and protein S deficiency
O Antithrombin deficiency
O Vascular and connective tissue disorders
O Gestational diabetes
O Systemic lupus erythematosus

uItiorgan 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).
CardiovascuIar 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.
HematoIogic concerns
Hematologic problems associated with eclampsia can include decreased plasma volume, increased
blood viscosity, hemoconcentration, and coagulopathy.
RenaI concerns
Eclampsia-associated renal abnormalities can include decreases in glomerular filtration rate, renal
plasma flow, and uric acid clearance.
Hepatic concerns
Hepatic derangements associated with eclampsia can include periportal necrosis, hepatocellular
damage, and subcapsular hematoma.
CentraI 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.
PathophysioIogy of EcIampsia
Inhibition of uterovascuIar deveIopment
Many uterovascular changes occur when a woman is pregnant. t is believed that these changes are
due to the interaction between fetal and maternal allografts and result in systemic and local vascular
changes. t has been shown that in patients with eclampsia, the development of uteroplacental
arteries is hindered.
Hindrance of cerebraI bIood fIow reguIation
t 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. n extreme
hypertension, normal compensatory vasoconstriction may become defective. Several autopsy findings
support this model and consistently reveal swelling and fibrinoid necrosis of vessel walls.
EndotheIiaI dysfunction
Factors associated with endothelial dysfunction have been shown to be increased in the systemic
circulation of women suffering from eclampsia. These include the following

:
O Cellular fibronectin
O Von Willebrand factor
O Cell adhesion molecules (ie, P-selectin, vascular endothelial adhesion molecule-1 [VCAM-1]
O ntercellular adhesion molecule-1 [CAM-1])
O Cytokines (ie, interleukin-6 [L-6])
O Tumor necrosis factor-d [TNF-d]
n addition, it is believed that antiangiogenic factors, such as placental protein fms-like tyrosine kinase
1 (sFlt-1) and activin A, antagonize vascular endothelial growth factor (VEGF).

Elevated levels of
these proteins cause a reduction of VEGF and induce systemic and local endothelial cell dysfunction.
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.
idative 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.)
Oxidative stress has been found to stimulate the production and secretion of the antiangiogenic factor
activin A from placental and endothelial cells. Studies in pregnant mouse models have proposed that
there is a dysregulation in the reactive oxygen species (ROS) signaling pathway.
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.
EvaIuation
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.
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:
O Seizure or postictal state (100%)
O Headache (80%), usually frontal
O Generalized edema (50%)
O Vision disturbance (40%), such as blurred vision and photophobia
O Right upper quadrant abdominal pain with nausea (20%)
O Amnesia and other mental status changes
The incidences of signs or symptoms before seizure include the following:
O Headache (83%)
O Hyperactive reflexes (80%)
O Marked proteinuria (52%)
O Generalized edema (49%)
O Visual disturbances (44%)
O Right upper quadrant pain or epigastric pain (19%)
The absence of signs or symptoms before seizure include the following:
O Lack of edema (39%)
O Absence of proteinuria (21%)
O Normal reflexes (20%)
The relation of seizure to delivery is as follows:
O Before delivery (>70%)
O Before labor (antepartum) (25%)
O During labor (intrapartum) (50%)
O After delivery (postpartum) (25%)
Although patients with severe preeclampsia are at greater risk for seizures, 25% of patients have
symptoms consistent with mild preeclampsia 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.
PhysicaI 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:
O Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg
O Tachycardia
O Tachypnea
O Rales
O Mental status changes
O Hyperreflexia
O Clonus
O Papilledema
O Oliguria or anuria
O Localizing neurologic deficits
O Right upper quadrant or epigastric abdominal tenderness
O Generalized edema
O Small fundal height for the estimated gestational age
O Apprehension

Cervical examination of the patient with eclampsia should not be overlooked, because the delivery
mode may largely depend upon the patient's cervical status.