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‡  
‡
  
‡   
! 
‡  
  

‡ Hypertension is defined as elevation either

of systolic BP to 140 mm Hg or higher or
of diastolic BP to 90 mm Hg or higher.
‡ Chronic hypertension is defined as
hypertension diagnosed before pregnancy
or before 20 weeks' gestation, or elevated
BP that is first diagnosed during
pregnancy and persists after 42 days
postpartum.


‡ is defined as elevated BP and proteinuria
after 20 weeks' gestation (except in the
presence of trophoblastic disease or
multiple gestation, in which cases
preeclampsia may appear before 20
weeks' gestation).
   
! 
‡ is defined as preeclampsia that occurs in a
patient with preexisting chronic
hypertension. It is often difficult to
differentiate chronic hypertension with
superimposed preeclampsia from an
exacerbation of chronic hypertension.
  

‡ Transient hypertension, also known as

"#! , is defined
as elevated BP during pregnancy or the first 24
hours postpartum without other signs of
preeclampsia or chronic hypertension.
‡ Transient hypertension must be differentiated
from preeclampsia because transient
hypertension is associated with an increased
risk of chronic hypertension, whereas
preeclampsia or eclampsia is not associated
with such a risk.

$"
$ Preeclampsia is reported to occur in 7±
10% of all pregnancies extending beyond 20
weeks. It is the third leading cause of maternal
mortality, responsible for over 17% of maternal
deaths. It is also a major cause of neonatal
morbidity and mortality, both directly, via
intrauterine growth restriction, and indirectly,
through its association with abruptio placentae
and the need for preterm delivery. Preeclampsia
has been implicated in 10% of perinatal deaths,
20% of labor inductions, 15% of cesarian
sections, and 10% of medically indicated
preterm deliveries.
 % 
± for preeclampsia and eclampsia include age
younger than 20 years or older than 40 years;
nulliparous status; presence of chronic
hypertension, lupus erythematosus, diabetes,
or renal disease; history of previous
eclampsia as primigravida, previous
preeclampsia as multipara, or previous
superimposed preeclampsia; and positive
family history of preeclampsia or eclampsia,
multiple gestation, hydatidiform moles, and
fetal hydrops.

"

‡ The development of preeclampsia requires the

presence of trophoblastic tissue but not
necessarily a fetus.
‡ There are a number of prominent "
! of preeclampsia. Derangements are
noticed in vascular reactivity, volume
homeostasis, thrombogenesis, and regulation of
a number of synthetic processes.
‡ The temporal sequence of these alterations, and
which are causal and which consequences of
the disorder, are as yet undetermined.

"
‡ &
'! should be recorded with the
woman sitting or in a semireclining
position. Her right arm should be held
consistently, roughly horizontally at heart
level. Early measurement of the baseline
BP is important because BP normally
declines in the second trimester.
 
of preeclampsia or eclampsia may include the following:
1. Headache
2. Visual symptoms: blurred vision, scotomata, and
blindness (retinal detachment)
3. Epigastric or right upper quadrant pain
4. Nausea and vomiting
5. Dyspnea (from pulmonary edema)
6. Decreased urine output, hematuria, or rapid weight gain
(greater than 5 lb in 1 week)
7. Constant abdominal pain (resulting from abruptio
placentae)
8. Absence of fetal movement (resulting from fetal
compromise)
9. Premature labor

 "
may include the following:
1. Elevated BP
2. Proteinuria
3. Retinal vascular spasm on funduscopic
examination
4. Bibasilar rales on cardiovascular examination
5. Right upper quadrant tenderness (secondary to
hepatic edema causing stretching of the liver
capsule)
6. Uterine tenderness, or uterine tetany secondary
to abruptio placentae on abdominal
examination
7. Nondependent edema (face and hands)
 •( "
‡ Increase in hematocrit (resulting from decreased
intravascular volume)
‡ Proteinuria greater than 300 mg/dL in a 24-hour
collection (or score of 1+ or higher on dipstick test)
‡ Uric acid level higher than 5 mg/dL, which is abnormal in
pregnancy but is not used to diagnose preeclampsia
‡ Creatinine level of 0.9 mg/dL or higher, which is
abnormal in pregnancy
‡ Elevated liver enzyme levels, indicated by AST level
higher than 70 U/L
‡ Platelet count lower than 100,000/mm3
‡ Prolonged prothrombin and partial thromboplastin times,
which may be a result of primary coagulopathy or
abruptio placentae
‡ Decreased fibrinogen, fibrin degradation products, or
both as a result of coagulopathy or abruptio placentae

'
‡ ! !$ Ingestion of 2 g of
elemental calcium per day has not been shown
to be beneficial in the general population;
however, in populations at risk with low calcium
intake, supplementation may lower the risk of
preeclampsia.
‡ $ Multicenter randomized clinical trials
with aggregate enrollment of more than 27,000
women have demonstrated minimal to no benefit
to low-dose aspirin therapy in preventing
preeclampsia; therefore, it is not recommended
at this time.
‡
!    have no role in
the prevention of preeclampsia.
 ×"$
‡
'    
   
 '$
‡ For patients presenting at more than 34
weeks' gestation with these conditions,
delivery should be considered. The
urgency of delivery depends on severity.
 × $
‡ If the gestation is remote from term when
mild preeclampsia is discovered, the
patient may be managed expectantly. Salt
restriction, use of sedatives, and
antihypertensive therapy do not improve
fetal outcome.
  management
‡ Bed rest
‡ Regular diet (no salt restriction)
‡ BP measurement every 4 hours while awake
‡ Daily review of weight, urine output, and symptoms, with
examination for edema, deep tendon reflex check, and
fetal movement count
‡ Every-other-day 24-hour urine protein measurement
‡ Twice weekly hematocrit measurement, platelet count,
and measurement of AST level
‡ Fetal growth sonogram no more frequently than every 2
weeks
‡ Fetal surveillance with weekly or semiweekly nonstress
test (NST) or biophysical profiles
 ' 
‡ The mother's safety must be considered above
all. The first priority is to assess and stabilize
maternal condition, particularly coagulation
abnormalities.
‡  )* %+ "  , delivery is the
optimal treatment. Immediate delivery by
cesarean section is not indicated in every case.
Patients in labor, or with a cervical condition
favorable to the initiation of labor with oxytocin,
can deliver vaginally. Both maternal and fetal
conditions must be monitored continuously,
however, with hourly assessments and careful
attention to intake and output.
  " of severe
preeclampsia
‡ Patients who are eligible to be followed expectantly
should receive the following:
‡ Bed rest
‡ Seizure prophylaxis for the first 24 hours of
hospitalization BP measurement every 4 hours
‡ Daily examination to assess weight, review systems,
check for edema, and check deep tendon reflexes;
evaluation of 24-hour urine specimen for volume and
protein level measurement; CBC with platelet count; and
measurement of AST, LDH, and bilirubin levels
‡ Daily fetal surveillance including fetal movement counts
and NST or biophysical profile
 |••
 ,
‡ which consists of hemolysis, elevated liver
enzymes, and low platelet count, is a form
of severe preeclampsia.


± ($ A platelet count of less
than 100,000/mm3 is the most consistent
finding in HELLP syndrome.
± | is defined as the presence of
abnormal peripheral smear results with burr
cells and schistocytes, bilirubin level of 1.2
mg/dL or higher, or LDH level higher than 600
U/L.
± ' ' !  !$ AST
level is 70 U/L or higher.

$
‡ Typically, HELLP syndrome occurs in a white
multiparous patient older than 25 years, but it is
not limited to such patients. It may develop
antepartum or postpartum. The majority of cases
appear to develop antepartum. The patient
frequently is remote from term and complains of
epigastric or right upper quadrant pain (90%),
nausea and vomiting (50%), and sometimes a
nonspecific virus-like syndrome. Ninety percent
of patients give a history of malaise of several
days' duration before presentation. Patients may
present with hematuria or GI bleeding.
Hypertension may be absent (20%), mild (30%),
or severe (50%).

 ,
‡ may reveal right upper quadrant
tenderness (80%) and significant weight
gain with edema (60%).

 "
‡ include benign thrombocytopenia of
pregnancy, idiopathic thrombocytopenic
purpura, thrombotic thrombocytopenic
purpura, hemolytic uremic syndrome,
gallbladder disease, viral hepatitis,
pyelonephritis, acute fatty liver of
pregnancy, kidney stones,
glomerulonephritis, and gastroenteritis.
 |••
$
‡ Management is the same as for severe
preeclampsia²'. The average
time for resolution of symptoms is 4 days.
‡ If no response is seen by 24±48 hours or
the patient's condition worsens, the patient
should be delivered.
 -! ,
‡ during labor and for 24 hours postpartum
is necessary for all patients with
preeclampsia. Some patients with severe
preeclampsia need seizure prophylaxis for
longer periods before and after delivery
than do patients with less severe
preeclampsia.
 -! ,
‡ ×"! ! .×"*/
‡
 .
/
 
  ' '  " "

‡ Eclampsia
‡ Thrombocytopenia with a platelet level of less
than 100,000/mm3
‡ Hemolysis (seen on peripheral blood smear)
‡ Elevated liver enzyme levels
‡ Pulmonary edema
‡ Oliguria
‡ Persistent need for antihypertensive medication,
except in selected cases between 25 and 27
weeks' gestation
 ' 
‡ is indicated for antepartum, intrapartum,
and postpartum patients with a diastolic
BP of 105 mm Hg or higher. Acute
treatment for severe hypertension in
pregnancy involves reducing BP in a
controlled manner without reducing
uteroplacental perfusion.
 ' 
‡ The goal is not to make the patient
normotensive but rather to reduce the
patient's diastolic BP to 90±100 mm Hg. A
rapid or significant drop in BP interferes
with uteroplacental perfusion and results in
fetal heart rate decelerations.
 ' 
‡ |- , administered
IV, is the drug of choice for acute BP
control.
‡ •( , administered
IV, is an alternative therapy to IV
hydralazine for women who cannot be
given or have not responded to
hydralazine.
 ' 
‡ '!  ./
‡ Trimethaphan can be used to treat
sudden-onset extreme hypertension
requiring minute-to-minute titration.
 ! "$
‡ Patients with preeclampsia frequently are
hypovolemic because of loss of fluid into
the interstitial spaces due to low serum
oncotic pressure and because of
increased capillary permeability. These
same abnormalities, however, also put
these patients at increased risk for
pulmonary edema. IV fluids should be
restricted to 84±125 mL/hour.
 "!
‡ is defined as urine output of less than 100
mL in 4 hours; it is treated with a 500-mL
bolus of crystalloid fluid if the lungs are
clear. If no response to this treatment
occurs, then another 500-mL bolus can be
given. If there is still no response after a
total of 1 L has been administered, central
hemodynamic monitoring should guide
further management.

! $
‡ Pulmonary artery catheterization is
required to guide therapy for pulmonary
edema.
   '

‡ renal failure (acute tubular necrosis),
‡ acute cortical necrosis,
‡ cardiac failure,
‡ pulmonary edema,
‡ thrombocytopenia,
‡ disseminated intravascular coagulopathy,
and
‡ cerebrovascular accidents.

 !$
‡ Complication of pregnancy by severe
preeclampsia is associated with high
perinatal mortality and morbidity rates.
These high rates are attributable to
extreme prematurity, intrauterine growth
retardation (IUGR), abruptio placentae,
and perinatal asphyxia.
 
‡ is defined as the development of convulsions,
coma, or both in a patient with preeclampsia.
Eclampsia occurs in 1% of patients with
preeclampsia. Although many other conditions
can result in seizures during pregnancy,
obstetric patients with seizures should be
considered eclamptic until proven otherwise.
Perinatal mortality in one U.S. series was 12%,
attributable to extreme prematurity, abruptio
placentae, and IUGR.
‡ Although many other conditions can result
in seizures during pregnancy, obstetric
patients with seizures should be
considered eclamptic until proven
otherwise.
  $
‡ Maternal complications may include
pulmonary edema, aspiration pneumonitis,
abruptio placentae with hemorrhage,
cardiac failure, intracranial hemorrhage,
and transient blindness.

"$
‡ The etiology of eclamptic seizures is
unknown. It is thought that eclampsia
occurs when the patient's mean arterial
pressure exceeds the upper limit of
cerebral autoregulation. The arterioles
then fail to protect the cerebral capillaries
from the systemic hypertension. Increased
cerebral edema, increased intracranial
pressure, or both may play a role.
 ×"$
‡ Eclampsia is an obstetric emergency
requiring immediate treatment.
‡ Goals of therapy include the following:
± Control of seizures
± Correction of hypoxia and acidosis
± Control of severe hypertension
± Delivery
 ×  

‡   -!0
‡ ×"! !, administered
parenterally, is the treatment of choice for
eclamptic seizures.
‡ The alternative treatment is phenytoin.
‡ The magnesium maintenance dosage
should be decreased as indicated by
clinical factors (absent deep tendon
reflexes, decreased respiratory rate,
oliguria, or renal insufficiency) or plasma
magnesium levels.
‡ Duration of therapy is 24 hours
postdelivery or 24 hours after a
postpartum seizure.
‡ The loading dose of MgSO4 is 6 g over
15±20 minutes IV. If the patient has a
seizure after administration of the loading
dose, another bolus of 2 g of MgSO4 can
be administered over 3±5 minutes.
‡ ! ! is treated with
diazepam, administered IV at a rate of 1
mg/minute, or up to 250 mg of sodium
amobarbital, slowly administered IV.

    
 !" -!$
‡ The patient must never be left unattended.
Bedside rails should be elevated, and a
padded tongue depressor should be
available to prevent oral lacerations.
      
'$
‡ Pulse oximetry should be performed or
arterial blood gas levels obtained. The
patient may require oxygen administration
by mask or endotracheal tube. Difficulty in
oxygenating patients with repetitive
seizures warrants a chest radiographic
examination to rule out aspiration
pneumonia.
   $
‡ Treatment of hypertension in eclampsia is
the same as treatment in preeclampsia

'   !$
‡ Induction of labor may begin, or a cesarean
section may be performed, after the patient is
stabilized.
‡ Although prompt delivery is desirable, vaginal
delivery may be attempted in the absence of
other maternal or fetal complications.
‡ Preparation for emergency cesarean section
should always be made in case maternal or fetal
condition deteriorates.
 !$
‡ Long-term neurologic sequelae of
eclampsia are rare. CNS imaging with CT
or MRI should be performed if seizures are
of late onset (longer than 48 hours after
delivery) or if neurologic deficits are
clinically evident.
‡ The signs and symptoms of preeclampsia
usually resolve within 1±2 weeks
postpartum. Approximately 25% of
eclamptic patients develop preeclampsia
in subsequent pregnancies, with a
recurrence of eclampsia in 2% of cases.