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Preeclampsia and eclampsia

Uterine Vascular Changes
The human placenta receives its blood supply from numerous uteroplacental
arteries that are developed by the action of migratory interstitial and
endovascular trophoblasts into the walls of the spiral arterioles. This transforms
the uteroplacental arterial bed into a low-resistance, low-pressure, high-flow
system.
It is suggested that these vascular changes are effected in two stages, “the
conversion of the decidual segments of the spiral arterioles by a wave of
endovascular trophoblast migration in the first trimester and the myometrial
segments by a subsequent wave in the second trimester.”This process is
reportedly associated with extensive fibrinoid formation and degeneration of
the muscular layer in the arterial wall.
It has been postulated that this defective vascular response to placentation is
due to inhibition of the second wave of endovascular trophoblast migration that
normally occurs from about 16 weeks’ gestation onward. These pathologic
changes may have the effect of curtailing the increased blood supply required
by the fetoplacental unit in the later stages of pregnancy and may correlate with
the decreased uteroplacental blood flow seen in most cases of preeclampsia.
Vascular Endothelial Activation
and Inflammation
Soluble fms-like tyrosine kinase 1 (sFlt-1) is a protein produced by the placenta.
It acts by binding to the receptor-binding domains of vascular endothelial
growth factor (VEGF), and it also binds to placental-like growth factor (PLGF).
Increased levels of this protein in the maternal circulation results in reduced
levels of free VEGF and free PLGF with resultant endothelial cell dysfunction
 Criteria for Preeclampsia or Gestational Hypertension
With Severe Features

The ACOG Task Force report on hypertension in pregnancy recommended that

superimposed preeclampsia be stratified into two groups to guide management:
(1) superimposed preeclampsia, defined as a sudden increase in blood pressure
that was previously well controlled or escalation of antihypertensive
medications to control BP, or (2) new-onset proteinuria (>300 mg/24-hour
collection or a P/C ratio >0.3), or a sudden and sustained increase in proteinuria
in a woman with known proteinuria before conception or early in pregnancy.
A diagnosis of superimposed preeclampsia with severe features should be made
in the presence of any of the following:
(1) severe-range BP (>160 mm Hg systolic or >110 mm Hg
diastolic) despite escalation of antihypertensive therapy; (2) persistent cerebral
symptoms such as headaches or visual disturbances; (3) significant increase in
liver enzymes (at least two times the ULN concentration for a particular
laboratory);
(4) thrombocytopenia (platelet count <100,000/µL); or
(5) new-onset and/or worsening renal insufficiency

The incidence of preeclampsia ranges between 2% and 7% in healthy

nulliparous women. In these women, PE is generally mild, with the onset near
term or during labor(75% of cases), and the condition conveys only a minimally
increased risk for adverse fetal outcome. In contrast, the incidence and severity
of PE are substantially higher in women with multifetal gestation,chronic
hypertension, previous PE, pregestational diabetes mellitus, or preexisting
thrombophilias.

Atypical Preeclampsia
The criteria for atypical preeclampsia include gestational proteinuria or FGR plus
one or more of the following symptoms of preeclampsia: hemolysis,
thrombocytopenia, elevated liver enzymes, early signs and symptoms of
preeclampsia-eclampsia earlier than 20 weeks, and late postpartum
preeclampsiaeclampsia (>48 hours postpartum).

Hypertension is considered to be the hallmark for the diagnosis

of preeclampsia. However, in some patients with PE, the
disease may manifest as either a capillary leak (proteinuria,
facial and vulvar edema, ascites, pulmonary edema); excessive
weight gain, particularly during the second and early third
trimester; or a spectrum of abnormal hemostasis with
multiple-organ dysfunction. These women usually present with
clinical manifestations of atypical preeclampsia, such as
proteinuria with or without facial edema, vulvar edema (Fig.
31-4), excessive weight gain (>4 lb/wk), ascites, or pulmonary
edema in association with abnormalities in laboratory values or
presence of symptoms but without hypertension.32 Therefore
we recommend that women with capillary leak syndrome with
or without hypertension be evaluated for platelet, liver enzyme,
and renal abnormalities. Those with symptoms such as new
onset of unrelenting severe headache, severe visual
disturbances, or abnormal blood tests should be considered to
have PE.
COMPLICATION N (%)
Disseminated intravascular coagulation 92 (21)
Abruptio placentae 69 (16)
Acute renal failure 33 (8)
Severe ascites 32 (8)
Pulmonary edema 26 (6)
Pleural effusions 26 (6)
Cerebral edema 4 (1)
Retinal detachment 4 (1)
Laryngeal edema 4 (1)
Subcapsular liver hematoma 4 (1)
Adult respiratory distress syndrome 3 (1)
Death, maternal
Eclampsia is the occurrence of convulsions or coma unrelated to other
cerebral conditions with signs and symptoms of preeclampsia.or
Eclampsia is defined as the development of convulsions or
unexplained coma during pregnancy or postpartum in
patients with signs and symptoms of PE.
The diagnosis of eclampsia is secure in the presence of generalized edema,
hypertension, proteinuria, and convulsions. However, women in whom
eclampsia develops exhibit a wide spectrum of signs that range from severe
hypertension, severe proteinuria, and generalized edema to absent or minimal
hypertension, no proteinuria, and no edema.
Abnormal weight gain in excess of 2 lb/wk (with or without clinical edema)
during the third trimester might be the first sign before the onset of eclampsia.
Several clinical symptoms are potentially helpful in establishing the diagnosis of
eclampsia. These include persistent occipital or frontal headaches, blurred
vision, photophobia, epigastric or right upper quadrant pain, and altered mental
status. Women had at least one of these symptoms in 59% to 75% of the cases
Late postpartum eclampsia is defined as eclampsia that
occurs more than 48 hours but less than 4 weeks after delivery. Historically,
eclampsia was believed not to occur more
than 48 hours after delivery. However, several recent reports
have confirmed the existence of late postpartum eclampsia.
Although eclamptic patients may initially manifest
a variety of neurologic abnormalities—including cortical
blindness, focal motor deficits, and coma—fortunately, most
have no permanent neurologic deficits
Several neurodiagnostic tests—such as electroencephalography (EEG), CT,
cerebral Doppler velocimetry, MRI, and
cerebral angiography (both traditional and MRI angiography)—
have been studied in women with eclampsia. In general, the
EEG is acutely abnormal in most eclamptic patients; however,
these abnormalities are not pathognomonic of eclampsia. In
addition, the abnormal EEG findings are not affected by the
use of magnesium sulfate
Hypertensive disorders include preeclampsia, gestational hypertension, and
chronic hypertension and complicate up to 10 percent of pregnancies. As a
group, they are one member of the deadly triad—along with hemorrhage and
infection—that contributes greatly to maternal morbidity (
yed below 140/90 mm Hg (Alexander, 2006). In other cases, mean arterial
pressures that suddenly rise but that still lie in normal range—“delta
hypertension”—may signify preeclampsia.This increase from the 25th to 75th
percentile can be termed“delta hypertension.
Preeclampsia is best described as a pregnancy-specific syndrome that can
affect virtually every organ system