INTRODUCTION

Pregnancy-induced hypertension is a condition in which vasospasm occurs

during pregnancy. Signs of hypertension, proteinuria, and edema develop.

PIH, a condition separate from chronic hypertension tends to occur most

frequently in primiparas younger than age 20 years or older than 40 years, women who
have had five or more pregnancies, women of color, women with a multiple pregnancy,
women with hydramnios and women with underlying disease such as heart disease,
diabetes with vessel or renal involvement and essential hypertension. The condition may
be associated with poor calcium or magnesium intake.

A woman has passed from mild to Severe Preeclampsia when her blood pressure
has risen to 160mmHg systolic and 110mmHg diastolic or above on at least two
occasions 6 hours apart at bed rest or her diastolic pressure is 30mmHg above the
prepregnancy level. Marked proteinuria, 3+ or 4+ on a random urine sample, or more
than 5g in a 24 hours sample, and extensive edema are also present.

The hypertension, albuminuria and edema of preeclampsia, usually arise 32 weeks

into a first pregnancy, and are often accompanied by headache and disruptions of vision.
Preeclampsia seems to originate from an implantation abnormality that affects placental
blood vessels. The resulting placental ischemia may be severe enough to produce
placental infarcts.

Complications of hypertension are the third leading cause of pregnancy-related

deaths, superseded only by hemorrhage and embolism. Preeclampsia is associated with
increased risks of placental abruption, acute renal failure, cerebrovascular and
cardiovascular complications, disseminated intravascular coagulation, and maternal
death.

In the case of Mrs. Geanette Tamargo, 38 years old from Pudoc San Vicente,
Ilocos Sur, she was admitted to Gabriela Silang General Hospital ( OB ward ) last August
23, 2006 at 1:27 pm with diagnosis of Post-op and severe preeclampsia.
OBJECTIVES OF THE STUDY

1. Gather factual health assessment of the patient.

2. Perform proper assessment of the patient.

3. To gain new facts and ideas about the disease.

4. To gain better and clearer understanding on the nature, course, physical and
emotional changes and signs and symptoms relevant to this disease.

5. To disseminate information to the patient as well as his relative about the illness
and how to care for the patient.

6. To be able to formulate related nursing diagnosis from the patients health data and
to the current problems the patient experiences and to come out with different
nursing interventions effective for the patient to improve and progress on the most
possible time.

7. Set realistic objectives of care.

 PATIENT’S PROFILE

NAME: Geanette Tamargo

ADDRESS: Pudoc Sur, San Vicente, Ilocos Sur

HOME ADDRESS: Pudoc Sur, San Vicente, Ilocos

AGE: 34 years old

RELIGION: Iglesia ni Kristo

BIRTHDAY: July 14, 1972

SEX: Female

NATIONALITY: Filipino

DATE OF ADMISSION: August 23, 2006 TIME: 1.27 pm

INSTITUTION: GSGH

WARD: WBC

DATE DISCHARGED: September 2, 2006 TIME: 3:00PM

DIAGNOSIS: Post-operative, Preeclampsia

NURSING HISTORY OF PAST AND PRESENT ILLNESS

Geanette Agpoon Tamargo, was 8 months pregnant; a resident of Pudoc Sur, San
Vicente Ilocos Sur.

During my interview with her, last August 28, 2006, she states that in her
previous pregnancy, she had a normal delivery with her first baby.

It was in the morning of August 23, 2006 when she went to Gabriela hospital for
her scheduled check up while she was being check by doctor Trilles the patient instantly
suffered a blurred vision. Her blood pressure was 160/90. After being checked, the doctor
told her then that she will be delivering her baby through C.S operation in the afternoon.
She was then formally admitted and confined at the hospital on that same date.

During the operation the doctor was surprised for she found out that the patients
have twin babies. It’s so good the operation was successful and the babies are both
females and they are alive and that they were placed at the incubator for they are pre-
mature babies. But then the mother suffered from preeclampsia where in her blood
pressure was high.
ANATOMY AND PHYSIOLOGY OF THE ORGAN INVOLVED
PATHOPHYSIOLOGY

A. ALGORITHM

Pregnant woman with blood pressure higher than 140/90mmHg

↓ ↓

Before 20 weeks of Gestation After 20 weeks of Gestation

↓ ↓ ↓ ↓

No/stable New/ ↑ proteinuria, dev’t of Proteinuria No Proteinuria

Proteinuria ↑ blood pressure/ HELLP syndrome

↓ ↓

Preeclampsia Gestational HPN

↓

Preeclampsia Super Imposed

On Chronic Hypertension
B. EXPLANATION

The current concepts regarding the pathophysiology of preeclampsia recognize

that preeclampsia is a multisystem disorder characterized by vasoconstriction, metabolic
changes, endothelial dysfunction, and activation of the coagulation cascade in
conjunction with an inflammatory response. A 2-stage model of preeclampsia has been
proposed in which failure of placental vascular remodeling results in reduced placental
perfusion and initiates a cascade of events that result in serious maternal illness with the
potential for significant perinatal morbidity and death. Women with underlying
microvascular disease, such as diabetes, hypertension, and collagen vascular disease,
have a higher incidence of preeclampsia.

Normal placental development involves progressive loss of the musculoelastic

tissue in the spiral arteries that feed the vessels of the intervillous spaces, which results in
uterine blood flow increases of nearly 25% during the first trimester. This process of
remodeling the maternal spiral arteries that branch from the uterine artery is typically
completed by 18-20 weeks' gestation.

In women destined to develop preeclampsia (and in infants who are small for
gestational age or whose mothers have diabetes mellitus), this physiologic dilatation of
the spiral arteries does not occur because the placental trophoblast cells do not invade the
spiral arteries, resulting in maintenance of narrow vessels with resultant placental
hypoperfusion and ischemia. In severe cases, not only do the spiral arteries maintain their
muscular structure, but other pathologic changes also occur. Accumulation of fat-laden
macrophages with fibrinoid necrosis (ie, acute atherosis), disruption of the basement
membranes, platelet deposition, mural thrombi, and proliferation of intimal and smooth
muscle cells all decrease the luminal diameter.

The narrowed and damaged spiral arteries become thrombosed, resulting in

placental infarction and necrosis. Uteroplacental blood flow is then reduced by 50-75%.
The anatomical reduction in blood flow may be complicated by vasospasm of the
uteroplacental bed.

The primary defect in preeclampsia appears to originate at the maternal-fetal

interface (the placenta). Decreased placental perfusion is thought to lead to fetoplacental
ischemia. The ischemic placenta may produce circulating antiangiogenic factors that
promote generalized maternal vascular endothelium dysfunction, leading to systemic
manifestations of preeclampsia. Associated abnormalities in clotting and platelet function
contribute to vasoconstriction and platelet adhesion and aggregation, as well as to the
activation of coagulation factors that increase the risk of thromboembolic formation.

The primary feature of preeclampsia, development of hypertension, occurs when

normally extreme vasodilatation does not occur. Although cardiac output increases 30-
50%, the decreased peripheral vascular resistance (PVR) results in decreased BP, even in
women with chronic hypertension. Women who develop preeclampsia experience an
increase in PVR and alterations in vascular sensitivity to endogenous hormones (eg,
angiotensin II, catecholamines, vasopressin). This increase in vascular reactivity to
pressor hormones may be mediated, at least in part, through damage to vascular
endothelial cells, disrupting the normal prostaglandin balance.

The normal expansion of blood volume by 50% that occurs with pregnancy is
decreased by 15-20% in patients with preeclampsia. This is the result of diminished
plasma volume, leading to the relative hemoconcentration observed in preeclampsia. The
plasma volume abnormality involves a redistribution of extracellular fluid, such that
interstitial fluid volume is increased while the plasma volume is decreased. The
hematocrit increases as the severity of preeclampsia increases. Circulating blood volume
is maintained by the increased vascular tone. Whether the vasospasm is the cause or
effect of the vascular endothelial injury is not known. Regardless, this injury likely
results in the microangiopathic hemolysis and disseminated intravascular coagulation that
accompanies severe preeclampsia.

The increased circulating blood volume and cardiac output of normal pregnancy
results in increased renal blood flow and glomerular filtration rates (GFRs). Women with
preeclampsia have markedly decreased renal blood flow and GFRs. Renal biopsies of
these women show a constellation of lesions, termed glomerular capillary endotheliosis.
Some consider glomerular capillary endothelial swelling that is accompanied by deposits
of fibrinogen degradation products within and under the endothelial cells as
pathognomonic of the disease. These lesions resolve within a month of delivery.
MANAGEMENT

MADICAL SURGICAL INTERVENTIONS

A. MEDICAL CARE

Incomplete understanding of the genesis and underlying pathophysiology in

preeclampsia has impeded attempts at prevention. Empiric approaches of dietary
manipulations, low-dose aspirin, use of diuretics or antihypertensives, and manipulations
of mineral and electrolyte concentrations have not produced consistent results. Resolution
of the disease only occurs after delivery of the placenta. Antepartum management is
fraught with controversies before 37 weeks' gestation. In mild cases, fetal and maternal
surveillance may allow pregnancy to proceed toward maturity, while prevention of CNS
effects, control of hypertension, and management of fluid balance is attempted. Timing
and mode of delivery are obstetrical decisions generally based on the maternal and fetal
condition.

Maternal treatment often includes magnesium sulfate infusions. Depending on the

duration of infusion and maternal blood levels, this may result in symptomatic neonatal
hypermagnesemia. Although the hypotonia and apnea are transient, they may result in the
need for respiratory support in the infant.

Among infants born to women with preeclampsia who exhibited absent or reverse
end-diastolic umbilical artery Doppler flow velocity on fetal monitoring, an increased
frequency of hypoglycemia and polycythemia that is independent of the degree of
gestational age and fetal growth restriction has been found.

B. SURGICAL CARE
Preeclampsia is not a surgical disease of the mother or affected newborn.
However, cesarean delivery may be required to address increasing maternal disease
severity and minimize maternal and fetal-neonatal morbidity and mortality.

C. NURSING CARE

> Monitor v/s and report to the doctor if there is an abnormal findings.

> Give antihypertensive medicines as ordered. Monitor therapeutic effect and side

effects.

> Implement no added no salt diet.

> Provide educational teaching related to hypertension.

 > Assess, monitor and document type, duration of seizure activity.

> Support head on side to prevent aspiration.

> Assess weight daily.

> Assess breath sounds, monitor I&O.

PREVENTION

There currently are no well-established measures for preventing preeclampsia.

Both low-dose aspirin therapy and daily calcium supplementation have been studied as
preventive measures but have not been shown to be beneficial in the general pregnant
population and are not recommended for primary prevention of preeclampsia. Some
evidence does support the use of low-dose aspirin therapy and daily calcium
supplementation in certain high-risk women. Calcium supplementation has been shown
to produce modest blood pressure reductions in pregnant women who are at above-
average risk for hypertensive disorders of pregnancy and in pregnant women with low
dietary calcium intake. An optimum calcium dosage for these women has not been
established. Low-dose aspirin therapy (100 mg per day or less) has been shown to reduce
the incidence of preeclampsia in women who were found to have an abnormal uterine
artery on Doppler ultrasound examination performed in the second trimester.

Research on the use of antioxidants in the prevention of preeclampsia is

promising. However, further study is needed, and antioxidant therapy currently is not
recommended.

Although preeclampsia is not preventable, many deaths from the disorder can be
prevented. Women who do not receive prenatal care are seven times more likely to die
from complications related to preeclampsia-eclampsia than women who receive some
level of prenatal care. Some studies indicate that preeclampsia-related fatalities occur
three times more often in black women than in white women. Although the precise
reasons for the racial differences remain elusive, the differences may be indicative of
disparities in health status, as well as access to, and quality of, prenatal care. To decrease
preeclampsia-related mortality, appropriate prenatal care must be available to all women.
Early detection, careful monitoring, and treatment of preeclampsia are crucial in
preventing mortality related to this disorder.
TREATMENT

Delivery remains the ultimate treatment for preeclampsia. Although maternal and
fetal risks must be weighed in determining the timing of delivery, clear indications for
delivery exist. When possible, vaginal delivery is preferable to avoid the added
physiologic stressors of cesarean delivery. If cesarean delivery must be used, regional
anesthesia is preferred because it carries less maternal risk. In the presence of
coagulopathy, use of regional anesthesia generally is contraindicated.

Women with preeclampsia and preterm pregnancy can be observed on an

outpatient basis, with frequent assessment of maternal and fetal well-being. Women who
are noncompliant, who do not have ready access to medical care, or who have
progressive or severe preeclampsia should be hospitalized. Women whose pregnancy is
remote from term should be cared for in a tertiary care setting or in consultation with an
obstetrician or family physician who is experienced in the management of high-risk
pregnancies.

During labor, the management goals are to prevent seizures and control
hypertension.4 Magnesium sulfate is the medication of choice for the prevention of
eclamptic seizures in women with severe preeclampsia and for the treatment of women
with eclamptic seizures. One commonly used regimen is a 6-g loading dose of
magnesium sulfate followed by a continuous infusion at a rate of 2 g per hour.
Magnesium sulfate has been shown to be superior to phenytoin (Dilantin) and diazepam
(Valium) for the treatment of eclamptic seizures.1 Although magnesium sulfate
commonly is used in women with preeclampsia, studies to date have been inadequate to
show that it prevents progression of the disorder.

Antihypertensive drug therapy is recommended for pregnant women with systolic

blood pressures of 160 to 180 mm Hg or higher24 and diastolic blood pressures of 105 to
110 mm Hg or higher. The treatment goal is to lower systolic pressure to 140 to 155 mm
Hg and diastolic pressure to 90 to 105 mm Hg. To avoid hypotension, blood pressure
should be lowered gradually.

Although evidence about the potential adverse effects of most antihypertensive

drugs has been poorly quantified, use of many of these agents is contraindicated during
pregnancy. Hydralazine (Apresoline) and labetalol (Normodyne, Trandate) are the
antihypertensive drugs most commonly used in women with severe preeclampsia
Nifedipine (Procardia) and sodium nitroprusside (Nitropress) are potential alternatives,
but significant risks are associated with their use. Note that labetalol therapy should not
be used in women with asthma or congestive heart failure. Use of angiotensin-converting
enzyme inhibitors is contraindicated in pregnant women

In women with preeclampsia, blood pressure usually normalizes within a few

hours after delivery but may remain elevated for two to four weeks. As previously noted,
a diagnosis of chronic hypertension is made if blood pressure remains elevated at 12
weeks postpartum.

Women with preeclampsia should be counseled about future pregnancies. In

nulliparous women with preeclampsia before 30 weeks of gestation, the recurrence rate
for the disorder may be as high as 40 percent in future pregnancies. Multiparous women
have even higher rates of recurrence.