Republic of the Philippines

UNIVERSITY OF EASTERN PHILIPPINES

University Town, Northern Samar
Web: http://uep.edu.ph Email: [email protected]

COLLEGE OF NURSING AND ALLIED HEALTH SCIENCES

PREECLAMPSIA
(OB WARD CASE STUDY)

Norla May A. Sevillano

Jessyl O. Siervo
Ryan James A. Snay
Myra Isabelle S. Solayao
Daniel Andre S. Somoray
Steffany Sopia Suarez
Czarina Mae Q. Tadeo
Christopher Angelo D. Tafalla
Hannah Marie A. Tagaban
Shanetelle Mae P. Tan

BSN-2D Group 3

Submitted to:
PROF. DANHILL C. DONOGA, PhD
Clinical Instructor
 Table of Contents

Cover Page …………………………………………………………………………………………………………………………… 1

Table of Contents ………………………………………………………………………………………………………………… 2

Case Scenario Summary 3

Overview ……………………………………………………………………………………………………………………………
…………………………………………………………………………………………………… 3

Anatomy and Physiology …………………………………………………………………………………………………… 5

Pathophysiology ………………………………………………………………………………………………………………… 8

Clinical Manifestations ………………………………………………………………………………………………………… 12

Nursing Management …………………………………………………………………………………………………………… 12

Medical Management …………………………………………………………………………………………………………… 14

Prognosis …………………………………………………………………………………………………………………………… 15

Resources …………………………………………………………………………………………………………………………… 18

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CASE SCENARIO SUMMARY

A 35-year-old female is 36 weeks pregnant and arrives to labor and delivery for a headache
that won’t go away with acetaminophen. The nurse gets the patient’s vitals.

The nurse notes that the patient’s blood pressure is 156/98 mm hg and asks the patient “have
you had any blurred vision, floaters or changes to that? Any sudden swelling, sudden weight
gain?” The patient responds, “Yes, I keep seeing floaters and have even thrown up from it. I
do have some swelling and my upper abdomen has really been hurting. My head is really
hurting.” The nurse goes to call the doctor. Nurse to Dr. “Hey Dr. Smith your patient, Maria
Evans is here with some symptoms of preeclampsia. She has a BP of 156/98 mm hg,
epigastric pain, bad headache, and some vision changes.

The nurse calls for help and nurses enter the room. They call the patient’s name, get fetal
heart tones, apply oxygen, and protect the patient. A nurse calls the doctor again and explains
the patient is having seizure. – Eclampsia.

OVERVIEW

What is Hypertension in Pregnancy?

Blood pressure is the force of blood pushing against blood vessel walls and the
heart pumps blood into the arteries (blood vessels) that carry the blood throughout the
body. High blood pressure, also called hypertension, means that the pressure in the
arteries is greater than the normal range or equal to 130/80 mm Hg which can impact the
body in different ways than it normally would and Mothers with high blood pressure
during pregnancy are at a higher risk of complications before, during and after the birth.

 Hypertension during pregnancy can be classified as one of the following:

— Chronic Hypertension: Blood pressure is high before pregnancy or before 20

weeks gestation. Chronic hypertension complicates about 1 to 5% of all
pregnancies.
— Gestational: Hypertension: develops after 20 weeks gestation (typically after
37 weeks) and remits by 6 weeks postpartum; it occurs in about 5 to 10% of
pregnancies, more commonly in multifetal pregnancy.

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What are the consequences of hypertension to maternal and fetal health?

 Maternal Impact:

Women with hypertension during pregnancy develops superimposed

preeclampsia, which carries higher maternal morbidity and mortality rates about 25%
and also the risk of abrupto placentae is increased threefold and this can lead to life-
threatening maternal hemorrhage. Other risks include accelerated hypertension with
potential target organ damage and cerebrovascular catastrophes, Preeclampsia also
confers increased risk of fatal intracerebral hemorrhage and the development of
Eclamptic seizures, HELLP syndrome, Hepatic rupture, pulmonary edema, and renal
failure and more likely the risks of having a cesarean birth section.

 Fetal Impact:

The perinatal outcome is strongly influenced by gestational age and the

severity of hypertension as expressed by the need for antihypertensive treatment,
irrespective of the underlying syndrome which is associated with different degrees of
fetal injury. The main impact on the fetus is under nutrition as High blood pressure
may reduce blood flow to the placenta. As a result, the fetus may not get enough of
the nutrients and oxygen needed to grow causing utero-placental vascular
insufficiency, which leads to growth retardation and the immediate impact observed is
altered fetal growth resulting in greater fetal liability. Fetal health as well as its weight
are highly compromised, leading to various degrees of fetal morbidity, and fetal
damage causing Premature birth, Fetal growth restriction, Low birth weight, and fetal
death.

The Effects of Hypertension to Pregnancy Outcomes:

Hypertension is one of the leading causes of increased pregnancy complications in

reproductive-aged women. Hypertensive pregnancies have increased risks of fetal growth
restriction, placental abruption, preterm birth, cesarean delivery, and preeclampsia, which
is a dangerous complication, accompanied by proteinuria and may result in serious
adverse consequences for the mother and fetus.

Pregnancy-induced hypertension, pre-eclampsia and eclampsia are parts of the

hypertensive syndrome which is a life-threatening condition both for mother and fetus.
Apart from being associated with unpredictable onset, it is incurable, except by ending

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 the pregnancy. Its incidence is approximately between 6 - 10% of pregnant women.
Although the incidence of eclampsia has declined in recent years, mainly due to the of
healthcare, serious adverse outcomes still exist. Five percent of patients with hypertension
develop severe preeclampsia, and about 25% of women with eclampsia have hypertension
in subsequent pregnancies. About 2% of women with eclampsia develop eclampsia with
future pregnancies. Multiparous women with eclampsia have a higher risk for the
development of essential hypertension; they also have a higher mortality rate in
subsequent pregnancies than do primiparous women.

The most significant maternal complication of eclampsia is permanent Central

Nervous system damage secondary to recurrent seizures or intracranial bleeding which
has a maternal mortality rate of 8-36% in these cases. and by administration of a loading
dose of magnesium sulfate followed by maintenance doses for 12-24 hours may be
effective in preventing recurrent seizures for eclamptic patients.

ANATOMY AND PHYSIOLOGY

Hypertension in pregnancy affects almost all parts of the body. However, there are 3
main players to which preeclampsia and eclampsia generally first takes place:

 Cardiovascular system specifically the vascular endothelial cells

 Renal system specifically the glomerular filtration
 And the Placental

Cardiovascular System – Vascular Endothelial Cells

The vascular endothelium, a monolayer of

endothelial cells, constitutes the inner cellular lining
of arteries, veins and capillaries and therefore is in
direct contact with the components and cells of
blood. The endothelium is not only a mere barrier
between blood and tissues but also an endocrine
organ. It actively controls the degree of vascular
relaxation and constriction, and the extravasations of
solutes, fluid, macromolecules and hormones, as well
as that of platelets and blood cells. Through control

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of vascular tone, EC regulate the regional blood flow. They also direct inflammatory cells to
foreign materials, areas in need of repair or defence against infections. In addition, EC are
important in controlling blood fluidity, platelet adhesion and aggregation, leukocyte
activation, adhesion, and transmigration. They also tightly keep the balance between
coagulation and fibrinolysis and play a major role in the regulation of immune responses,
inflammation and angiogenesis. To fulfill these different tasks, EC are heterogeneous and
perform distinctly in the various organs and along the vascular tree. Important morphological,
physiological and phenotypic differences between EC in the different parts of the arterial tree
as well as between arteries and veins optimally support their specified functions in these
vascular areas.

Renal System – Glomerular Filtration

The role of the glomerular filtration is to selectively filter the blood by allowing small
molecules through but preventing plasma proteins from leaving the blood. This filtration
occurs extracellular and is done by what is known as the glomerular filtration barrier. This
structure is made up of three layers:

 Fenestrated capillary endothelium

 Glomerular basement membrane
 Podocytes

Fenestrated Capillary Endothelium

 There are small gaps called fenestrate

in the cytoplasm of the capillary
endothelium.
 They account for approximately 10%
of the surface area of the cells
 They allow water and non-cellular
components of the blood to pass through
 They act mainly as a barrier to the cells of the blood

Glomerular Basement Membrane

 Also known as the basal lamina

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  This is the main barrier to proteins
o Restricts all but the smallest plasma proteins from passing through
 Made up of a protein mesh in a gelatinous matrix
o Composed of collagen and other matrix proteins
 Prevents filtration of compounds >7,000 Da
 Lower permeability to anions compared to cations. This allows for further selective
filtration

Podocytes

The cells of the visceral layer of the Bowman’s capsule possess finger like foot processes
called pedicels. These wrap around the outer layer of the basal lamina. Filtration occurs
through small gaps between pedicels called slit diaphragms. This is the final barrier against
proteins

Placental Development and Perfusion

The placenta undergoes consistent change throughout the course of pregnancy;

between week 0 and 13 after conception, the fertilized blastocyst (what the embryo becomes
once its cells start differentiating at about five days after the egg is fertilized) embeds itself in
the mucous membrane (endometrium) of the uterine wall, allowing for the fetus and placenta
to start forming. By the fourth or fifth month of pregnancy, the placenta takes up about half
of the uterine surface, though this percentage shrinks as the fetus grows. At birth, the placenta
is also ejected from the body.

Crucial to placenta development is the formation of small, finger-like structures

called chorionic villi, which are composed of two types of cells—cytotrophoblasts and
syncytiotrophoblasts. The former of these
interact with arteries and veins in the walls of
the uterus to ensure the fetus gets the
nutrients and oxygen it needs.

One important feature in the

development of the placenta is the spiral
arteries as they play a vital role in supplying
nutrients to the placenta and fetus. The spiral
arteries in the placental bed are normally

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transformed into large dilated vessels undergoing dramatic structural changes in their vessel
wall. The spiral arteries are also known as the utero-placental arteries. The terms
“physiologic changes” or “physiologic transformation” of the spiral arteries were first
introduced by Brosens, Robertson and Dixon in 1967 to emphasize that these changes were
part of normal pregnancy.

The key findings of physiologic transformation are:

1. dilatation of the lumen

2. Trophoblast invasion of the vessel wall, which includes both the media and
endothelium
3. Replacement of the muscular and elastic tissue of the arterial wall by a thick layer of
fibrinoid material

Current studies also investigated that these structural changes, particularly the destruction
of muscle in the media, would lead to loss in vasomotor control. Collectively, these changes
are thought to maximize the delivery of maternal blood to the intervillous space by making
the arterial lumen wider as well as reducing the responsiveness of these vessels to
vasoconstrictor agents. Invasion of the utero-placental veins has been implicated as a
mechanism responsible for the lateral placental growth.

PATHOPHYSIOLOGY

Abnormal Placentation and Vasospasm

 Preeclampsia is linked to abnormal placentation. In a normal pregnancy, fetal

cytotrophoblasts migrate into the maternal uterus and cause remodeling of the
endometrial vasculature for the blood supply of the placenta. In preeclampsia, there is
an inadequate invasion of
the cytotrophoblasts, thus
leading to poor remodeling
of the spiral arteries, which
reduces the blood supply to
the placenta. When there is
poor blood supply,
maternal circulation makes

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 up to this abnormality and increase uterine arterial resistance and induces
vasoconstriction, ultimately causing placental ischemia and oxidative stress.
 Endothelial dysfunction
o Due to oxidative stress induced by ischemic placenta, free radicals and
cytokines, such as vascular endothelial growth factor 1 or VEGF, are released
in hopes to increase
blood flow in the
placenta. These
substances however, are
toxic to endothelial cells
and causing damage.
Normally, endothelial
cells in circulation
control the tone of a blood vessel, how it constricts or relaxes. Damage
endothelial cells, in turn, have no tone, thus vasospasm occurs or constriction
of that particular vessel. Endothelial disruption occurs not only at the site of
the uterus but also at different parts of the body. As vasoconstriction occur,
blood pressure increases dramatically.
o Endothelial cells
also control the
permeability of the
blood vessels.
Normally,
endothelial cells are
tightly binded to
each other, when
damaged, however,
permeability increases and substances that tends to leak out such as protein,
passes through it. As protein leaks, water follows, causing edema and
proteinuria.
 Proteinuria and Edema – Vasospasm in the kidney increases blood
flow resistance. Degenerative changes develop in kidney glomeruli
because of the back-pressure. This leads to increased permeability of

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 the glomelular membrane, allowing the serum protein albumin and
globulin escape into the urine (PROTEINURIA). Degenerative
changes also results in decreased glomelular filtration, so there is
lowered urine output and clearance of creatinine. There also is an
increased tubular reabsorption of sodium. Because sodium retains
fluid, edema results. Moreover, edema is further increased as more
protein is lost, the osmotic pressure of the circulating blood falls and
fluid diffuses from the circulatory system into denser interstitial spaces
to equalize the pressure.
 As there is increased permeability of blood vessels in brain tissues,
cerebral edema occurs. Swelling in the brain, neurological changes
happens as the CNS is irritated. As fluid also collects in the woman’s
lung, pulmonary edema might also occur which might cause breathing
disruption such as shortness of breath. Abdominal edema and/or
ischemia in the pancreas or liver might also occur causing severe
epigastric pain, nausea, and vomiting.

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 P

Figure 1. Pathophysiology of Preeclampsia

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CLINICAL MANIFESTATION

 Gestational Hypertension
 Blood pressure of 140/90; no proteinuria or edema; blood pressure returns to
normal after birth.
 Preeclampsia
 Elevated blood pressure of 140/90
 Proteinuria of 1–2 on a random sample
 Weight gain over 2 lb per week in second trimester and 1 lb per week in third
trimester
 Mild edema in upper extremities or face.
 Severe Preeclampsia
 Blood pressure of 160/110
 Proteinuria 3–4 on a random sample and 5 g on a 24-hour sample
 Oliguria
 Elevated serum creatinine more than 1.2 mg/dL)
 Eerebral or visual disturbances
 Pulmonary or cardiac involvement
 Extensive peripheral edema
 Hepatic dysfunction
 Thrombocytopenia
 Epigastric pain.
 Eclampsia
 Seizure or coma accompanied by signs and symptoms of pre-eclampsia.

NURSING MANAGMENT

For Preeclampsia:

1. Promote bed rest – When body is in a recumbent position, sodium tends to be

excreted at a faster rate than during activity. Bed rest, therefore, is the best method of
aiding increased evacuation of sodium and encouraging dieresis.
2. Promote good nutrition – the woman needs to continue her usual pregnancy diet. At
one time, stringent restriction of salt was advised to reduce edema. This, however is

12
 no longer true as stringent sodium restriction may activate the RAAS and result in
increased blood pressure
3. Provide emotional support to mother and family – A mother on bed rest is a stress on
the total family, so other family member may need support as well
4. Enforced bed rest – loud environmental stimuli such as a tray falling could trigger
seizures especially in severe preeclampsia. Thus, the mother should be admitted to a
private room where she can rest as undisturbed ad possible.
5. Monitor Maternal well-being – the woman’s blood pressure should be taken
frequently or with a continuous monitoring device to detect any increase, which is a
warning that her condition is worsening
6. Obtain blood studies as ordered – to assess renal and liver functions and the
development of DIC, which often accompanies severe vasospasm.
7. Obtain daily hematocrit levels as ordered – to monitor blood concentration. This level
will rise if increased fluid is leaving the bloodstream for interstitial tissue.
8. Monitor fetal well being – Single Doppler auscultation at approximately 4 hour
intervals is sufficient. However, fetal heart rate may be assessed continuously. The
woman may have a nonstress test or biophysical profile done daily to assess
uteroplacental sufficiency
9. Support a Nutritious diet – woman needs a moderate to high protein, moderate sodium
diet to compensate for the protein loss. An intravenous line should be initiated and
maintained to serve as an emergency rout for drug administration as well as to
administer fluid to reduce hemoconcentration and hypovolemia
10. Administer medications to prevent eclampsia – a hypotensive drug such as
hydralazine or labetalol may be prescribed to reduce hypertension, and magnesium
sulphate to act as an anticonvulsant.

For Eclampsia:

1. Tonic-clonic seizures
a. Priority is to maintain patent airway. Administer oxygen by mask to protect
the fetus during this interval. Assess oxygen saturation via pulse oxymeter.
Apply an external fetal heart monitor if one is not already in place to assess
fetal condition. To prevent aspiration, turn the woman on her side to allow
secretions to drain from her mouth

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 b. Third stage of seizure – extremely close observation is needed as the woman is
in semicomatose. Premature separation of placental may occur, labor may
begin during this period and the woman may not be able to report sensation of
contractions. Moreover, pain may stimulate another seizure. Keep the patient
on her side so secretions can be drained from the mouth
c. Continuously assess fetal heart sounds and uterine contractions. Check for
vaginal bleeding every 15 minutes. Evidence for placental separation may
have occurred will first appear on the fetal heart record. vaginal bleeding will
strengthen the presumption.
2. Birth
a. Decision about delivery will be made as soon as the woman’s condition
stabilizes, usually 12 to 24 hours after seizure. Induction in labour may be
instituted if there is no rupture of membranes or poor progression of labor. If
ineffective and the fetus appears to be in imminent danger, caesarean birth is
indicated.
3. Postpartal hypertension
a. May occur up to 14 days after birth. Monitoring blood pressure in postpartal
period is essential to detect residual hypertensive or renal disease. Woman
who had an elevation of blood pressure during pregnancy should be instructed
to return for postpartal check up to have their postpregnancy blood pressure
evaluated to be retain it has returned to normal.

MEDICAL MANAGMENT

The only cure for preeclampsia is delivery of fetus and placenta.

 Oxytocin (Pitocin) is given intravenously to induce labor (stimulate the uterus to

contract). If labor does not progress, or if complications develop that require the fetus
to be delivered quickly, a cesarean birth may be indicated.

Regarding eclampsia, the drug of choice for prevention and management is magnesium
sulfate. This drug reduces the risk of seizures in patients with severe preeclampsia.

 The goal of treatment is to prevent significant cerebrovascular and cardiovascular

events in the mother without compromising fetal well-being.

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  The primary objective of magnesium sulfate prophylaxis in women with preeclampsia
is to prevent or reduce the rate of eclampsia and complications associated with
eclampsia.

The first line antihypertensives for preeclampsia/eclampsia include hydralazine, labetalol,

and nicardipine.

 Hydralazine-is an arteriolar dilator that reduces blood pressure

 Labetalol- a combined alpha and beta blocker, used to treat hypertension in
preeclamptic women, and is now known to reduce CPP in women with preeclampsia.
 Nicardipine- used to treat pressure and control to chest pain or angina and high blood
pressure.

Seizures are treated with IV magnesium as a loading dose of 4 grams oer 5 to 10 minutes,
followed by an infusion of 1g/hr maintained for 24 hours after the last seizure.

 Lorazepam and phenytoin may be used as second line of defense, but are avoided due
to fetal effects.

Also, other supportive measures include sparing use of diuretics and fluid restrictions to
avoid pulmonary cerebral edema.

PROGNOSIS

Most women with mild preeclampsia have good pregnancy outcomes. Eclampsia is a
serious condition with about a 2% mortality (death) rate.

The recurrence risk for preeclampsia varies according to the onset and severity
of the condition.

 Women with severe preeclampsia who had an onset of the condition early in
pregnancy have the highest recurrence risk.
 Studies show recurrence rates of 25% to 65% for this population.
 Only 5% to 7% of women with mild preeclampsia will have preeclampsia in a
subsequent pregnancy.

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 Women with preeclampsia may be at increased risk for cardiovascular disease later in
life. This risk is greatest in women with early onset of severe preeclampsia. Research is
ongoing to further clarify this potential risk.

Fetal

Fetal complication includes:

o Premature birth - a birth that takes place more than three weeks before the baby's
estimated due date. In other words, a premature birth is one that occurs before the
start of the 37th week of pregnancy. Premature babies, especially those born very
early, often have complicated medical problems.
o Fetal Growth Restriction - a condition in which an unborn baby (fetus) is smaller
than expected for the number of weeks of pregnancy (gestational age). It is often
described as an estimated weight less than the 10th percentile.
o Fetal hypoxia - occurs when the fetus is deprived of an adequate supply of oxygen.

Maternal

Maternal Complications includes:

o HELLP (Hemolysis, Elevated Liver enzymes and Low Platelets) syndrome - a

pregnancy complication that affects the blood and liver. It's a medical emergency
that needs quick treatment. Signs and symptoms of HELLP include blurry vision,
chest pain or pain in the upper right or middle part of the belly, swelling and
throwing up.
 A life-threatening pregnancy complication usually considered to be a
variant of preeclampsia.
o Pulmonary edema - a condition caused by too much fluid in the lungs. This fluid
collects in the many air sacs in the lungs, making it difficult to breathe.
o Seizures - a sudden, uncontrolled electrical disturbance in the brain. It can cause
changes in your behavior, movements or feelings, and in levels of consciousness.
o Renal failure - means one or both kidneys can no longer function well on their own.
Sometimes, kidney failure is temporary and comes on quickly. Other times, it is a
chronic condition that can get worse slowly over a long time.
o Disseminated intravascular coagulation (DIC) - a serious disorder in which the
proteins that control blood clotting become overactive.

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o Placental Abruption - Sudden complete/partial separation of a normally implanted
placenta after 20th weeks AOG
o Oligohydramnios - occurs during pregnancy when your amniotic fluid is lower than
expected for your baby’s gestational age.

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