Group 12

Case Analysis

I. IINTRODUCTION

PRE-ECLAMPSIA

Hypertensive disorders of pregnancy are a heterogeneous group of conditions that include

chronic hypertension, gestational hypertension, preeclampsia, and preeclampsia superimposed on

chronic hypertension. Hypertension in pregnancy is defined as a systolic BP of 140 mm Hg and a

diastolic BP of 90 mm Hg on two separate measurements at least 4–6 hours apart. Diagnose

women who develop hypertension after 20 weeks' gestation and who do not have proteinuria or

other criteria for preeclampsia with gestational hypertension. Preeclampsia is a multiorgan

disease process characterized by hypertension and proteinuria or one of the following features,

which are diagnostic when they develop in the setting of new-onset hypertension after 20 weeks'

gestation.

Preeclampsia is a multiorgan disease process characterized by new-onset elevated blood

pressure and proteinuria or one of its severe features after 20 weeks' gestation. Eclampsia is

preeclampsia complicated by generalized tonic-clonic convulsions. The progression of

preeclampsia to eclampsia is sudden and without prediction. The onset of eclamptic convulsions

can be antepartum (38% to 53%), intrapartum (18% to 36%), or postpartum (11% to 44%).

Onset is by definition after 20 weeks and although delivery usually resolves the

condition, symptoms can present as late as 4-6 weeks postpartum.

 Patients who meet the criteria for preeclampsia are at an increased risk of cerebral edema,

stroke, pulmonary edema, disseminated intravascular coagulation, liver failure, and renal failure.

Fetal risks include intrauterine demise, neonatal demise, placental abruption, prematurity,

ischemic encephalopathy, and intrauterine growth restriction.

II. ANATOMY AND PHYSIOLOGY

In the initial stages of pregnancy, the fertilized egg implants itself into the wall of the womb.

The womb is the organ a baby grows inside during pregnancy. The fertilized egg produces root-

like growths called villi, which help to anchor it to the lining of the womb. The villi are fed

nutrients through blood vessels in the womb and eventually grow into the placenta. During the

early stages of pregnancy, these blood vessels change shape and become wider. If the blood

vessels don't fully transform, it's likely that the placenta won't develop properly because it won't

get enough nutrients. This may lead to pre-eclampsia. It's still unclear why the blood vessels
don't transform as they should. It's likely that inherited changes in your genes have some sort of

role, as the condition often runs in families. But this only explains some cases.

When you have preeclampsia, your blood pressure is elevated (higher than 140/90 mmHg),

and you may have high levels of protein in your urine. Preeclampsia puts stress on your heart and

other organs and can cause serious complications. It can also affect the blood supply to your

placenta, impair liver and kidney function or cause fluid to build up in your lungs. The protein in

your urine is a sign of kidney dysfunction.

Preeclampsia can develop gradually, or come on quite suddenly, even flaring up in a

matter of hours, though the signs and symptoms may have gone undetected for weeks or months.

Most women with preeclampsia will deliver healthy babies and fully recover. However,

some women will experience complications, several of which may be life-threatening to mother

and/or baby. A woman’s condition can progress to severe preeclampsia very quickly.

Preeclampsia and other hypertensive disorders of pregnancy can be devastating diseases,

made worse by delays in diagnosis or management, seriously impacting or even killing both

women and their babies before, during or after birth.

 III. ETIOLOGY AND SYMPTOMATOLGY

There is no definitive known cause of pre-eclampsia, though it is likely related to a number of

factors. Some of these factors include; Immunologic factors, Abnormal placentation, Factors

from the outside, like pollution in the air, Dietary factors, e.g. calcium supplementation in areas

where dietary calcium intake is low has been shown to reduce the risk of pre-eclampsia, And

lastly, pre-eclampsia is more likely to occur in people who already have hypertension, obesity,

antiphospholipid antibody syndrome, or a history of pre-eclampsia. The risk is seven to eight

times higher for people with long-term high blood pressure than for those without it.
Physiologically, pre-eclampsia has been linked to the following changes: placental injury,

alterations in the interaction between the maternal immune response and the placenta, endothelial

cell injury, altered vascular reactivity, oxidative stress, an imbalance in vasoactive substances,

decreased intravascular volume and disseminated intravascular coagulation are all examples of

these changes.

Although the exact cause of pre-eclampsia is still unknown, there is strong evidence that an

abnormally implanted placenta is a major factor that puts a woman at risk for the condition. This

abnormally implanted placenta may lead to inadequate uterine and placental perfusion, resulting

in hypoxia, elevated oxidative stress, and the maternal plasma's release of anti-angiogenic

proteins and inflammatory mediators. The generalized endothelial dysfunction that results from

this sequence of events is a major consequence. The mother's immune system's reaction to the

placenta, specifically a lack of established immunological tolerance during pregnancy, may be

the cause of the abnormal implantation. Hypertension and many of the other symptoms and

complications of pre-eclampsia are caused by endothelial dysfunction.

IV. PATHOPHYSIOLOGY

The villous cytotrophoblast invades the inner third of the myometrium during a typical

pregnancy, causing the spiral arteries to lose most of their muscle fibers and endothelium. By

becoming low-resistance vessels and subsequently less sensitive or even insensitive to

vasoconstrictive agents due to these anatomical adaptations, spiral arteries also undergo

functional changes.
 Pre-eclampsia has a complicated pathophysiology, with an aberrant placentation as its main

cause. Pre-eclampsia is accompanied with defective cytotrophoblast cell invasion of the spiral

arteries. Recent research has revealed that the invasion of the uterus by cytotrophoblasts is

actually a special differentiation route in which the fetal cells adopt some characteristics of the

maternal endothelium they normally replace. This differentiation mechanism malfunctions in

pre-eclampsia. The irregularities may be connected to the nitric oxide pathway, which

significantly affects the regulation of vascular tone. Increased uterine arterial resistance causes

higher sensitivity to vasoconstriction and, as a result, chronic placental ischemia and oxidative

stress. Additionally, it prevents implantation of the embryo by inhibiting the mother’s production

of nitric oxide. Fetal problems brought on by this persistent placental ischemia include

intrauterine growth restriction and intrauterine mortality. Parallel to this, oxidative stress causes

chemicals including free radicals, oxidized lipids, cytokines, and serum-soluble vascular

endothelial growth factor to be released into the mother’s circulation. These anomalies cause

vascular hyperpermeability, thrombophilia, and hypertension to make up for the decreased flow

in the uterine arteries brought on by peripheral vasoconstriction, which is the cause of

endothelial dysfunction.

Understanding that improper placentation is the main cause of pre-eclampsia is vital. Two

widely held theories—a genetic theory and an immunological theory—seem to be connected.

Pre-eclampsia may be caused by a number of susceptibility genes. These genes likely interact

with one another in the cardiovascular, inflammatory, and hemostatic systems. Angiotensinogen

on 1-q42-43 and eNOS on 7q36 are just two of the many genes they have been linked to in

candidate gene studies. Other significant loci include 2p12, 2p25, 9p13, and 10q22.1.
 Pre-eclampsia might be thought of as a defect in the mother’s immune system that inhibits

the fetoplacental unit from being recognized. Tumor necrosis factor alpha is secreted when

immune cells are produced in excess, which causes the extravillous cytotrophoblast to undergo

apoptosis. Given that women with pre-eclampsia had lower levels of HLA-G and HLA-E, the

human leukocyte antigen (HLA) system also appears to be involved in the faulty invasion of the

spiral arteries. The interaction between these cells and the trophoblast occurs during healthy

pregnancies as a result of natural killer cells secreting vascular endothelial growth factor and

placental growth factor. Women with pre-eclampsia have been discovered to have high levels of

the antagonist of placental growth factor and vascular endothelial growth factor, soluble fms-like

tyrosine kinase 1 (sFlt-1), which is present throughout the body. As a result, tests for sFlt-1,

placental growth factor, endoglin, and vascular endothelial growth factor, all of which rise 4–8

weeks before to the onset of the illness, may be helpful in predicting pre-eclampsia. A potential

target for the therapy of pre-eclampsia, according to recent findings, is heme oxygenase 1 and

carbon monoxide, which have a protective function in pregnancy.

Some women with preeclampsia don’t have any symptoms, so it’s important to see your

doctor for regular blood pressure checks and urine so here are the factors and symptoms is also

called “edema” protein in the urine and blood pressure over 140/90, preeclampsia symptoms

include:

Weight gain over 1 or 2 days because of a large increase in bodily fluid such as Shoulder

pain,Belly pain, especially in the upper right side ,Severe headaches,Change in reflexes or

mental state,Peeing less or not at all

Dizziness,Trouble breathing,Severe vomiting and nausea

 Vision changes like flashing lights, floaters, or blurry vision

Unlike the Preeclampsia of Factors things that can increase your chance of getting

preeclampsia include:Being a teen or woman over 40.Being

Being pregnant for the first time

Having babies less than 2 years apart or more than 10 years apart

Pregnancy with a new partner instead of the father of your previous children

High blood pressure before getting pregnant

A history of preeclampsia

A mother or sister who had preeclampsia

A history of obesity

Carrying more than one baby

In-vitro fertilization

A history of diabetes, kidney disease, lupus, or rheumatoid arthritis .Preeclampsia

Complications

Preeclampsia can keep your placenta from getting enough blood, which can cause your baby

to be born very small. This is called fetal growth restriction.

V. MEDICAL MANAGEMENT
 Your healthcare provider will advise you on the best way to treat preeclampsia. Treatment

generally depends on how severe your preeclampsia is and how far along you are in pregnancy.

If you're close to full term 37 weeks pregnant or greater, your baby will probably be delivered

early. You can still have a vaginal delivery, but sometimes a Cesarean delivery (C-section) is

recommended. Your healthcare provider may give you medication to help the fetus's lungs

develop and manage your blood pressure until the baby can be delivered. Sometimes it is safer to

deliver the baby early than to risk prolonging the pregnancy. When preeclampsia develops earlier

in pregnancy, you'll be monitored closely in an effort to prolong the pregnancy and allow for the

fetus to grow and develop. You'll have more prenatal appointments, including ultrasounds, urine

tests and blood draws. You may be asked to check your blood pressure at home. If you are

diagnosed with severe preeclampsia, you could remain in the hospital until you deliver your

baby. If the preeclampsia worsens or becomes more severe, your baby will need to be delivered.

During labor and following delivery, people with preeclampsia are often given magnesium

intravenously (directly into the vein) to prevent the development of eclampsia (seizures from

preeclampsia). There isn't a cure for preeclampsia. Preeclampsia can only be cured with delivery.

Your healthcare provider will still want to monitor you for several weeks after delivery to make

sure your symptoms go away.

 VI. NURSING MANAGEMENT

NURSING CARE PLAN

CUES NEED NURSING SCIENTIFI GOALS NURSING RATIONAL EVALUATIO

S DIAGNOSI C BASIS OBJECTIVE INTERVENTION E N
S S S
CRITERIA

Subjective:
“Nabantaya
n nko nga
nibugat
akong
timbang ug
permi ko
malipong ug
sakit akong
batok”
verbalized
by
the patient

Objective:
 Variations
in blood
pressure
 Edema
 B/P
140/100
 DRUG STUDY

DATE BRAND ACTION INDICATIO ROUTE/ DRUG ADVERS PRECAUT NURSING

AND NAME NS DOSAGE/ INTERAC E ION INTERVENT
TIME TIME TIONS EFFECT S/ IONS
INTERVAL S CONTRAI
NDI
CATIONS
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7-3 ide reduced theraphy) bronchodilator eadache, drug drug masks
shift peripheral Once supine HALF LIFE: effect of these Paresthe component common
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NAME: resistance begun to rise IV/5½ in patients with nt, Scalp and in symptoms of
trandate s, Give 200mg hours. Bronchospasm. Syncope those shock. Keep
as a result PO, followed May need to vertigo with patient
CLASSIFI of By 200 to ABSORPTI increase dosage asthenia, bronchial supine while
CATION alpha and 400mg PO ON: Oral of this drug. tingling. to or its patient is
therapeutIc beta depending on Cardiacghyeosid asthma receiving IV
blockage BP response. e: may increase (history of therapy.
class: May increase risk of obstructive Monitor BP
Antihyperte 200 PO b.i.d brodycardia. airway closely
nsives At one day Monitor therapy. diseases before
intervals CV over allowing
usual dosage diuretics: drugs HIF greater patient to
range is 100 increase hypersen than first ambulate.
to 30mg PO sitive effects. degree Don't
b.i.d Monitor BP. heart routinely
block of withdraw
Drug-herb except long term
mahuang: in patient beta blocker
antihypertensive with therapy
Discourage use functioning before surgery.
together decrease pacemaker) In diabetic
effects . patient
Cardiogeni monitor
EXCRETION: e glucose
Urine Severe level closely
bradycardia because
, blocker beta
and other may masks
conditions certain.
shock, that Signs and of
may severe symptoms
and hypoglycemia.
prolonged
hypotensio
n cause.
Use
cautiously
 inpatients
with HF,
Hepatic
Chronic
failure,bron
chitis,
Emphysem
a, and
PVD,
Pheochrom
ocvtoma.

VII. HEALTH TEACHINGS

When it comes to identifying and reporting symptoms correctly, educating patients is the first

line of defense. Preeclampsia can be a rapidly progressing illness, with symptoms worsening in

the short time between routine prenatal visits. Preeclampsia is more seriously understood when

there is higher compliance and reporting. However, simply explaining preeclampsia to patients is

insufficient. Pregnant patients typically have little knowledge about preeclampsia, despite

obtaining information from their provider is linked to better understanding. When educating the

patients, take into account the following factors. Lay Terms - don't make assumptions about what

she needs to know. Use simple language. Instead of hypertension, say high blood pressure. Be

Specific - Make sure she understands the symptoms and what to do if she experiences any of

them. Assess Her Understanding - Instead of asking, "Do you have any symptoms to report?"

ask, "Have you noticed any changes in your vision?" Have you ever had a severe headache that

refused to go away despite medication? "Ask her what she would do if she experienced any of

those symptoms: should she call the nurse's hotline or go straight to labor and delivery?
 Women are more likely to report symptoms and comply with prescribed treatments when

they understand how to recognize the signs and symptoms and understand the explanations

provided. This has a direct impact on lowering negative outcomes. Most women who have

preeclampsia without severe symptoms will not have it again in a subsequent pregnancy. The

risk of recurrence is higher in women who have severe preeclampsia symptoms, especially if

they occur in the second trimester. Women who develop preeclampsia appear to be at an

increased risk of developing cardiovascular disease later in life, so routine health care may be

especially important in this patient group. Women who had high blood pressure during

pregnancy should have their blood pressure checked yearly. They can also lower their chances of

developing high blood pressure later in life by maintaining a healthy weight, limiting their salt

intake, avoiding excessive alcohol consumption, and exercising regularly.

VIII. REFERENCE

https://www.ncbi.nlm.nih.gov/books/NBK570548/

https://www.preeclampsia.org/faqs

https://my.clevelandclinic.org/health/diseases/17952-preeclampsia

https://www.nhs.uk/conditions/pre-eclampsia/causes/

https://www.preeclampsia.org/educating-patients

https://www.uptodate.com/contents/preeclampsia-beyond-the-basics