Hypertensive Disorders Of Pregnancy by

Dr

Zainab
Mohamed Yaseen
Gestational hypertension

Preeclamsia
and
Eclamsia

MBBS.,DGO.,

 Superimposed preeclamsia (on chronic

hypertension)

Chronic hypertension

Pre Eclampsia
Essentials of Diagnosis

Blood pressure of - 140 mm Hg systolic or -90 mm Hg diastolic after

20 weeks of gestation.
Proteinuria of -0.3 g in 24 hours. 1+on dip stick

Severe Preeclampsia

Blood pressure of
diastolic.

Proteinuria
>2 g in 24 hours or 3+ on dipstick.
Oliguria of < 500 mL in 24 hours.
Thrombocytopenia.
Hemolysis, elevated liver enzymes, low platelets (HELLP).

Pulmonary edema.
symptoms
Fetal growth restriction. Rapid weight gain, 4 - 5 lbs in a single

160 mm Hg systolic or

week

A rise in blood pressure

Protein in urine
Severe headaches
Blurry vision
Seeing spots in eyes
Severe epigastric pain
Decrease in the amount of urine

110 mm Hg

Eclampsia

All of the above plus seizures.

General Considerations
Preeclampsia is defined as the presence of elevated blood pressure and
proteinuria during pregnancy. Eclampsia occurs with the addition of seizures.
Classically, the presence of three elements was required for the diagnosis of
preeclampsia-eclampsia: hypertension, proteinuria, and edema.
Edema was difficult to objectively quantify and is no longer a required element.

Preeclampsia-eclampsia can occur any time after 20 weeks of

gestation and up to 6 weeks postpartum. It is a disease unique to
pregnancy, with the only cure being delivery of the fetus and
placenta. Preeclampsia-eclampsia develops in approximately 7% of pregnant
women. Primiparas are most frequently affected; however, the incidence
of preeclampsia-eclampsia is increased with

multiple
pregnancies, chronic hypertension, diabetes, renal
disease, collagen-vascular and autoimmune
disorders, and gestational trophoblastic disease. 5%of
women with preeclampsia progress to eclampsia. Uncontrolled
eclampsia is a significant cause of maternal death.
The basic cause of preeclampsia-eclampsia is not known. Epidemiologic
studies suggest an immunologic cause for preeclampsia, since it occurs
predominantly in women who have had minimal exposure to sperm or have, in
primigravidas, and in women both of whose parents have similar HLA antigens.
Preeclampsia is an endothelial disorder resulting from poor placental perfusion,
which releases a factor that injures the endothelium, causing activation of
coagulation and an increased sensitivity to pressors. Before the syndrome
becomes clinically manifest in the second half of pregnancy, there has been
vasospasm in various small vessel beds, accounting for the pathologic changes
in maternal organs and the placenta with consequent adverse effects on the
fetus. Recently, investigators have suggested an etiologic role for circulating
angiogenic factors in preeclampsia based on studies in an animal model and in
women with preeclampsia.
The use of diuretics, dietary restriction or enhancement, sodium restriction,

aspirin, and vitamin-mineral supplements such as calcium or vitamin C and E

have not been confirmed to be useful in clinical studies. The only cure is

termination of the pregnancy at a time as favorable as possible

for fetal survival.

Clinical Findings
Clinically, the severity of preeclampsia-eclampsia can be measured with
reference to the six major sites in which it exerts its effects: the central
nervous system, the kidneys, the liver, the hematologic and
vascular systems, and the fetal-placental unit. By evaluating each of
these areas for the presence of mild to moderate versus severe preeclampsiaeclampsia, the degree of involvement can be assessed, and an appropriate
management plan can be formulated that is integrated with gestational age
assessment (Table 192).
Table 192. Indicators of mild to moderate versus severe preeclampsiaeclampsia.

Site

Indicator

Central
nervous
system

Symptoms and
signs

Kidney

Proteinuria

Uric acid

Mild to Moderate

Severe

Hyperreflexia
Headache

0.35 g/24 h

Seizures
1
Blurred
vision 2
Scotomas
3
Headache
4
Clonus
5
Irritability
6
> 5 g/24 h or
catheterized urine
with 4+ protein

> 4.5 mg/dL

> 4.5
mg/dL

Liver

Urinary output

> 2030 mL/h

AST, ALT, LDH

Normal

< 2030 mL/h

Elevated

Site

Indicator

Mild to Moderate

Severe
LFTs
Epigastric
pain
Ruptured
liver

Platelets
Hemoglobin

Hematologic

Vascular
Fetalplacental
unit

>
>100,000/mc
L
Normal range

<
100,000/m
cL
Elevated

Blood pressure

< 160/110 mm Hg

> 160/110 mm Hg

Retina

Arteriolar spasm

Retinal
hemorrhages

Growth restriction

Absent

Present

Oligohydramnios

May be present

Present

Fetal distress

Absent

Present

AST, aspartate aminotransferase; ALT, alanine aminotransferase; LDH, lactate

dehydrogenase; LFTs, liver function tests.

Preeclampsia
Mild to moderate
Precise differentiation between mild and moderate preeclampsia is difficult
because the abnormalities that define the disease are quite variable and fail to
accurately predict progression to more severe disease. Symptoms are generally
minimal or mild. With mild preeclampsia, patients usually have few
complaints, and the diastolic blood pressure is less than 90100 mm Hg.
Edema is usually more pronounced with moderate disease, and diastolic
blood pressures are in the range of 90110 mm Hg. The platelet count is
over 100,000/mcL, antepartum fetal testing is reassuring, central nervous
system irritability is minimal, epigastric pain is not present, and liver
enzymes are not elevated.

Severe
Symptoms are more dramatic and persistent. The blood pressure is often
quite high, with readings over 160/110 mm Hg. Thrombocytopenia (platelet
counts < 100,000/mcL) may be present and progress to disseminated

intravascular coagulation. Severe epigastric pain may be present

from hepatic subcapsular hemorrhage with significant stretch or rupture of
the liver capsule. The HELLP syndrome (hemolysis, elevated liver enzymes,
low platelets) is a form of severe preeclampsia.

Eclampsia
The occurrence of seizures defines eclampsia. It is a manifestation of
severe central nervous system involvement. The other abnormal findings
of severe preeclampsia are also observed with eclampsia.

Differential Diagnosis
Preeclampsia-eclampsia can mimic and be confused with many other diseases,
including chronic hypertension, chronic renal disease, primary

seizure disorders, gallbladder and pancreatic disease, immune or

thrombotic thrombocytopenic purpura, and hemolytic-uremic
syndrome. It must always be considered a possibility in any pregnant woman
beyond 20 weeks of gestation. It is particularly difficult to diagnose when
preexisting disease such as hypertension is present. Uric acid values can be
quite helpful in such situations, since hyperuricemia is uncommon in
pregnancy except with gout, renal failure,or preeclampsia,eclampsia..

Treatment
Preeclampsia
Early recognition is the key to treatment. This requires careful
attention to the details of prenatal careespecially subtle changes in blood
pressure and weight. The objectives are to prolong pregnancy if possible, to
allow fetal lung maturity while preventing progression to severe disease and
eclampsia. The critical factors are the gestational age of the fetus, fetal
pulmonary maturity status, and the severity of maternal disease. Preeclampsiaeclampsia at 36 weeks or more of gestation is managed by delivery regardless of
how mild the disease is judged to be. Prior to 36 weeks, severe preeclampsiaeclampsia requires delivery except in unusual circumstances associated with
extreme fetal prematurity, in which case prolongation of pregnancy may be
attempted. Epigastric pain, thrombocytopenia, and visual
disturbances are strong indications for delivery of the fetus. For
mild to moderate preeclampsia-eclampsia, bed rest is the cornerstone of
therapy. This increases central blood flow to the kidneys, heart, brain, liver, and

placenta and may stabilize or even improve the degree of preeclampsiaeclampsia for a period of time.
Bed rest may be attempted at home or in the hospital. Prior to making this
decision, the provider should evaluate the six sites of involvement and make an
assessment about the severity of disease.

Home management
Home management with bed rest may be attempted for patients with mild
preeclampsia and a stable home situation. This requires homemaking assistance,
rapid access to the hospital, a reliable patient, and the ability to obtain frequent
blood pressure readings. A home health nurse can often provide frequent
home visits and assessment.

Hospital care
Hospitalization is required for women with moderate or severe preeclampsia
or those with unreliable home situations. Regular assessment of blood
pressure, reflexes, urine protein, and fetal heart tones and activity are
required. A complete blood count, platelet count, and electrolyte panel
including liver enzymes should be checked every 1 or 2 days. A 24-hour
urine collection for creatinine clearance and total protein should be
obtained on admission and repeated as indicated. Sedatives and opioids
should be avoided because the fetal central nervous system depressant
effects interfere with fetal testing. Magnesium sulfate is not used until the
diagnosis of severe preeclampsia-eclampsia is made or until labor occurs.
Fetal evaluation should be obtained as part of the workup. If the patient is
being admitted to the hospital, fetal testing must be performed on the same day
to make certain that the fetus is safe. This may be done by fetal heart rate
testing with nonstress or stress testing or by biophysical profile. A regular
schedule of fetal surveillance must then be followed. Daily fetal kick counts
can be recorded by the patient herself. Consideration should be given to
amniocentesis to evaluate maturity status if hospitalization occurs at 3037
weeks of gestation. If immaturity is (betamethasone 12 mg or
dexamethasone 16 mg, two doses intramuscularly 1224 hours apart) can
be administered to the mother. Fetuses between 26 and 30 weeks of
gestation can be presumed to be immature, and corticosteroids should be
given.
The method of delivery is determined by the maternal and fetal status.
Cesarean section is reserved for the usual fetal indications.

Eclampsia

Emergency care A B C D
If the patient is convulsing, she is turned on her
side to prevent aspiration and to improve blood
flow to the placenta. Fluid or food is aspirated from the glottis or
trachea. The seizure may be stopped by giving an intravenous bolus of either
magnesium sulfate, 4 g, or lorazepam, 2-4 mg over 4 minutes or until the
seizure stops. A continuous intravenous infusion of magnesium sulfate is then
started at a rate of 23 g/h unless the patient is known to have significantly
reduced renal function. Magnesium blood levels are then checked every 46
hours and the infusion rate adjusted to maintain a therapeutic blood level (46
mEq/L). Urinary output is checked hourly and the patient assessed for signs of
possible magnesium toxicity such as loss of deep tendon reflexes

or decrease in respiratory rate and depth, which can be reversed

with calcium gluconate, 1 g intravenously over 2 minutes.C-

ABCD
A-prevent Aspiration B- Blood flow to the
placenta C-control Convulsion&D-Delivery.
control convulsion,D-delivery. Treatment of Eclamsia

1. Control of convulsions using an intravenously administered loading dose

of magnesium sulfate. This is followed either by a continuous infusion
of magnesium sulfate or by an intramuscular loading dose and periodic
intramuscular injections.
2. Intermittent intravenous or oral administration of an antihypertensive
medication to lower blood pressure whenever the diastolic pressure is
considered dangerously high. Some clinicians treat at 100 mm Hg, some
at 105 mm Hg, and some at 110 mm Hg.
3. Avoidance of diuretics and limitation of intravenous fluid administration
unless fluid loss is excessive. Hyperosmotic agents are avoided.
4. Delivery.
Magnesium Sulfate to Control Convulsions
In more severe cases of preeclampsia, as well as eclampsia, magnesium sulfate
administered parenterally is an effective anticonvulsant agent without producing
central nervous system depression in either the mother or the infant. It may be

given intravenously by continuous infusion or intramuscularly by intermittent

injection (Table 347). The dosage schedule for severe preeclampsia is the same
as for eclampsia. Because labor and delivery is a more likely time for
convulsions to develop, women with preeclampsiaeclampsia usually are given
magnesium sulfate during labor and for 24 hours postpartum. Magnesium
sulfate is not given to treat hypertension.

Continuous Intravenous Infusion

1. Give 4- to 6-g loading dose of magnesium sulfate
diluted in 100 mL of IV fluid administered over 1520
min.
2. Begin 2 g/hr in 100 mL of IV maintenance infusion.
3. Measure serum magnesium level at 46 hr and adjust
infusion to maintain levels between 47 mEq/L (4.88.4
m/dL).
4. Magnesium sulfate is discontinued 24 hr after
delivery.

Intermittent Intramuscular Injections

1. Give 4 g of magnesium sulfate (MgSO4 7H2O USP)
as a 20% solution intravenously at a rate not to exceed
1 g/min.
2. Follow promptly with 10 g of 50% magnesium sulfate
solution, one-half (5 g) injected deeply in the upper
outer quadrant of both buttocks through a 3-inch-long,
20-gauge needle. (Addition of 1.0 mL of 2%lidocaine
minimizes discomfort.) If convulsions persist after 15
min, give up to 2 g more intravenously as a 20%
solution at a rate not to exceed 1 g/min. If the woman is
large, up to 4 g may be given slowly.
3. Every 4 hr thereafter give 5 g of a 50% solution of
magnesium sulfate injected deeply in the upper outer
quadrant of alternate buttocks, but only after ensuring

that:
a. the patellar reflex is present
b. respirations are not depressed
c. urine output the previous 4 hr exceeded 100 mL
Magnesium sulfate is discontinued 24 hr after delivery.

IV&IM injection of MgSo4 dosages for severe pre

eclampsia&eclampsia
magnesium toxicity such as loss of deep tendon reflexes or
decrease in respiratory rate and depth, which can be reversed
with calcium gluconate, 1 g intravenously over 2 minutes

extensive clinical observations, magnesium most likely

exerts specific anticonvulsant action on the cerebral, the
mother stops convulsing after the initial administration
of magnesium sulfate and, within an hour or two,
regains consciousness sufficiently to be oriented as to
place and time.
. When magnesium sulfate is given to arrest and prevent
recurrent eclamptic seizures, about 10 to 15 percent of
women have a subsequent convulsion. An additional 2-g
dose of magnesium sulfate in a 20-percent solution is
administered slowly intravenously. In a small woman, an
additional 2-g dose may be used once, and twice if
needed in a larger woman. Sodium amobarbital is given
slowly intravenously in doses up to 250 mg in women
who are excessively agitated in the postconvulsion phase.
Thiopental is suitable also. Maintenance magnesium
sulfate therapy for eclampsia is continued for 24 hours
after delivery. If eclampsia that develops postpartum,
magnesium sulfate is administered for 24 hours after the
onset of convulsions

General care
The occurrence of eclampsia necessitates delivery once the
patient is stabilized. It is important, however, that
assessment of the status of the patient and fetus take place
first. Continuous fetal monitoring must be performed and
blood typed and cross-matched quickly. A urinary catheter
is inserted to monitor urinary output, and blood is sent for
complete blood count, platelets, liver enzymes, uric acid,
creatinine or urea nitrogen, and electrolytes. If hypertension
is present with diastolic values over 110 mm Hg,
antihypertensive medications should be administered to
reduce the diastolic blood pressure to 90100 mm Hg.
Hydralazine given in 5- to 10-mg increments intravenously
every 20 minutes is frequently used to lower blood pressure.
Nifedipine, 10 mg sublingually or orally, or labetalol, 1020
mg intravenously, both every 20 minutes, can also be used.

Delivery
Except in unusual circumstances, delivery is mandated once eclampsia has
occurred. Vaginal delivery may be attempted if the patient has already been in
active labor or the cervix is quite favorable and the patient is clinically stable.
The rapidity with which delivery must be achieved depends on the fetal and
maternal status following the seizure and the availability of laboratory data on
the patient. Oxytocin may be used to induce or augment labor. Regional
analgesia or anesthesia is acceptable. Cesarean section is used for the usual
obstetric indications or when rapid delivery is necessary for maternal or fetal
indications.

Postpartum
Magnesium sulfate infusion (23 g/h) should be continued until preeclampsiaeclampsia has begun to resolve postpartum (which may take 17 days), but in
any case for at least 24 hours. The most reliable indicator of this resolution is
the onset of diuresis with urinary output of over 100200 mL/h. When this
occurs, magnesium sulfate can be discontinued. Late-onset preeclampsia-

eclampsia can occur during the postpartum period. It is usually manifested by

either hypertension or seizures. Treatment is the same as prior to deliveryie,
with magnesium sulfatealthough other antiseizure medications can be used
since the fetus is no longer present, we delivered already.

THANK
U

SO MUCH