Terminology and Classification

Four types of hypertensive disease:

•Gestational hypertension—evidence for the
preeclampsia syndrome does not develop and
hypertension resolves by 12 weeks postpartum
•Preeclampsia and eclampsia syndrome
•Chronic hypertension of any etiology
•Preeclampsia superimposed on chronic
hypertension.
 Diagnosis
• Hypertension is diagnosed empirically when
appropriately taken blood pressure exceeds
140 mm Hg systolic or 90 mm Hg diastolic.
 Gestational Hypertension
• Diagnosis is made in women whose blood
pressures reach 140/90 mm Hg or greater for
the first time after midpregnancy, but in
whom proteinuria is not identified.
• Gestational hypertension is reclassifed as
transient hypertesion if evidence for
preeclampsia does not develop and the blood
pressure returns to normal by 12 weeks
postpartum.
 Preeclampsia Syndrome
• Preeclampsia is best described as a
pregnancy-specific syndrome that can affect
virtually every organ system.
• Appearance of proteinuria remains an
important diagnosis criterion.
• Proteinuria is an objective marker and reflects
the system-wide endothelial leak, which
characterizes the preeclampsia syndrome.
 Eclampsia
• In a woman with preeclampsia, a convulsion
that cannot be attributed to another cause is
termed eclampsia.
• May appear before, during, or after labor.
 Preeclampsia Superimposed on
Chronic Hypertension
• Chronic hypertensive disorder predisposes a woman to
develop superimposed preeclampsia syndrome
• Blood pressures ≥ 140/90 mm Hg before pregnancy or
before 20 weeks’ gestation, or both.
• In some women with chronic hypertension, their blood
pressure increases to obviously abnormal levels, and this is
typically after 24 weeks.
• If new-onset or worsening baseline hypertension is
accompanied by new-onset proteinuria or other findings,
then superimposed preeclampsia is diagnosed.
• Compared with “pure” preeclampsia, superimposed
preeclampsia commonly develops earlier in pregnancy. It
also tends to be more severe and often is accompanied by
fetal-growth restriction.
 Etiology
Those currently considered important include:
• Placental implantation with abnormal
trophoblastic invasion of uterine vessels
• Immunological maladaptive tolerance between
maternal, paternal (placental), and fetal tissues
• Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancy
• Genetic factors including inherited predisposing
genes and epigenetic influences.
Abnormal Trophoblastic Invasion
 Immunological Factors
• Loss of maternal immune tolerance to paternally
derived placental and fetal antigens
• The histological changes at the maternal-placental
interface are suggestive of acute graft rejection.
• Some of the factors possibly associated with
dysregulation include “immunization” from a previous
pregnancy, some inherited human leukocyte antigen
(HLA) and natural killer (NK)-cell receptor haplotypes,
and possibly shared susceptibility genes with diabetes
and hypertension
 Nutritional Factors
• A diet high in fruits and vegetables with
antioxidant activity is associated with
decreased blood pressure.
• Incidence of preeclampsia was doubled in
women whose daily intake of ascorbic acid
was less than 85 mg
 Genetic Factors
• Incident risk for preeclampsia of 20 to 40
percent for daughters of preeclamptic
mothers;
• 11 to 37 percent for sisters of preeclamptic
women;
• 22 to 47 percent for twins.
 Management
Basic management objectives for any pregnancy
complicated by preeclampsia are:
• termination of pregnancy with the least possible
trauma to mother and fetus
• birth of an infant who subsequently thrives
• complete restoration of health to the mother.
In many women with preeclampsia, especially those
at or near term, all three objectives are served
equally well by induction of labor. One of the most
important clinical questions for successful
management is precise knowledge of fetal age.
 Management
• Termination of pregnancy is the only cure for
preeclampsia.
• When the fetus is preterm, the tendency is to
temporize in the hope that a few more weeks in
utero will reduce the risk of neonatal death or
serious morbidity from prematurity.
• With moderate or severe preeclampsia that does
not improve after hospitalization, delivery is
usually advisable for the welfare of both mother
and fetus.
Management for suspected severe
preeclampsia
 Early Diagnosis of Preeclampsia
• Women with new-onset diastolic blood pressures > 80
mm Hg but < 90 mm Hg or with sudden abnormal
weight gain of more than 2 pounds per week includes,
at minimum, return visits at 7-day intervals.
• Outpatient surveillance is continued unless overt
hypertension, proteinuria, headache, visual
disturbances, or epigastric discomfort supervene.
• Women with overt new-onset hypertension— either
diastolic pressures ≥ 90 mm Hg or systolic pressures ≥
140 mm Hg—are admitted to determine if the increase
is due to preeclampsia, and if so, to evaluate its
severity.
 Evaluation
A systematic evaluation is instituted to include the following:
• Detailed examination, which is followed by daily scrutiny
for clinical findings such as headache, visual disturbances,
epigastric pain, and rapid weight gain
• Weight determined daily
• Analysis for proteinuria or urine protein:creatinine ratio on
admittance and at least every 2 days thereafter
• Blood pressure readings in the sitting position with an
appropriate-size cuff every 4 hours, except between 2400
and 0600 (unless previous readings had become elevated )
• Measurements of plasma or serum creatinine and hepatic
aminotransferase levels and a hemogram that includes
platelet quantification
• Evaluation of fetal size and well-being and amnionic fluid
volume, with either physical examination or sonography.
 Eclampsia Management
• Control of convulsions using an intravenously administered
loading dose of magnesium sulfate that is followed by a
maintenance dose, usually intravenous, of magnesium
sulfate
• Intermittent administration of an antihypertensive medica-
tion to lower blood pressure whenever it is considered
dangerously high
• Avoidance of diuretics unless there is obvious pulmonary
edema, limitation of intravenous uid administration unless
uid loss is excessive, and avoidance of hyperosmotic agents
• Delivery of the fetus to achieve a remission of
preeclampsia.
 Management of Severe Hypertension
Hydralazine
• administered intravenously with a 5-mg initial
dose, and this is followed by 5- to 10-mg doses at
15- to 20-minute intervals until a satisfactory
response is achieved
• target response antepartum or intrapartum is a
decrease in diastolic blood pressure to 90 to 110
mm Hg
• target response antepartum or intrapartum is a
decrease in diastolic blood pressure to 90 to 110
mm Hg
Labetalol
•target response antepartum or intrapartum is a
decrease in diastolic blood pressure to 90 to 110
mm Hg
•10 mg intravenously initially
•If the blood pressure has not decreased to the
desirable level in 10 minutes, then 20 mg is given.
The next 10-minute incremental dose is 40 mg and
is followed by another 40 mg if needed. If a salutary
response is not achieved, then an 80-mg dose is
given. (max dose 220mg)
 Hydralazine versus Labetalol
• Hydralazine caused significantly more
maternal tachycardia and palpitations,
whereas labetalol more frequently caused
maternal hypotension and bradycardia.
• Both drugs have been associated with a
reduced frequency of fetal heart rate
accelerations
Nifedipin
• Randomized trials that compared nifedipine
with labetalol found neither drug de nitively
superior to the other. However, Nifedipin
lowered blood pressure more quickly
• Recommend a 10-mg initial oral dose to be
repeated in 30 minutes if necessary