HOLY ANGEL UNIVERSITY

College of Nursing

In Partial Fulfilment of Requirements for RLE 104

“ PREGNANCY INDUCED HYPERTENSION”

A Book-Based Case Study

Presented To:

Teacher’s Full Name MAN, RN

Submitted By:
Gueco, Daryl C.

GROUP 2 of N-407
 Pregnancy-Induced Hypertension: A Case Study 2

September 29, 2010

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TABLE OF CONTENTS

INTRODUCTION

BRIEF DESCRIPTION OF THE DISEASE 3

REASONS FOR CHOOSING THE CASE 5

STATISTICS 6

STUDENT NURSE-CENTRED OBJECTIVES 7

DIAGNOSTIC & LABRATORY PROCEDURES 8

PHYSICAL ASSESSMENT 16

ANATOMY & PHYSIOLOGY 29

PATHOPHYSIOLOGY

SYNTHESIS OF THE DISEASE 44

DEFINITION OF THE DISEASE 46

PREDISPOSING & PRECIPITATING FACTORS 47

SIGNS AND SYMPTOMS WITH RATIONALE 48

MEDICAL MANAGEMENT

IVF 50

PHARMACOTHERAPY 52

DIET 61

NURSING CARE PLAN 62

DISCHARGE PLANNING 72

LEARNING DERIVED 73

REFERENCES

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 Pregnancy-Induced Hypertension: A Case Study 4

“W e learn more by looking for the answer to a question

.”
and not finding it than we do from learning the answer itself

~Lloyd Alexander, American Author, 1924

In the field of nursing, one encounters a wide-array of various diseases and conditions. In

order to give adequate and holistic care to individuals, it is necessary that nurses be equipped

with the proper knowledge and skills for dealing with different health states. It is only through

continuous learning that nurses acquire the necessary skill. A case study is a means of continuing

such learning. In doing a case study, the students delve into the question, “what is this disease

condition?” Student nurses learn actively and will be able to handle patients and experience what

it means to care for a patient with that particular condition. They learn, from continuous

interaction with the patients along side with inquires into books and informative journals of the

disease process, it symptoms, and corresponding treatments.

Pregnancy-induced hypertension is one of the conditions which student-nurses encounter

during their exposure at the clinical setting. The disease comprises of complexities of the

anatomical concepts that surveys a thorough description to understand its manifestations and

formulate interventions. It is interesting on our part to learn its definition, causes, and proper

management. The student-nurses chose the case to be able to have an insight about the

condition.

Brief Description

Pregnancy induced hypertension (PIH) is a condition in which vasospasms occurs

during pregnancy. In this condition signs of hypertension, proteinuria and edema develop in

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pregnant and postpartum women. Despite years of research and studies investigating the disease,

the cause of the disorder is still seemingly idiopathic. Originally, this condition has been called

the toxemia of pregnancy because researchers depicted and hypothesized that a toxin of some

kind being produces by a woman in response to the foreign protein of the growing fetus, the

toxin leading to the symptoms. Still, despite the efforts in finding an explanation to the cause of

pregnancy induced hypertension, no such toxin has ever identified.

Pregnancy –induced hypertension is an alarming condition which can affect both the

welfare of the mother and the child. Women who develop high blood pressure in pregnancy

appear to have an elevated risk high blood pressure and stoke in later life. Women with a history

of high blood pressure in pregnancy, known as gestational hypertension, were more likely than

women with no history to develop high blood pressure in later years. In terms of the welfare of

the child in-utero, the fetus may be placed in distress due to the presence of the condition, and

complications from high blood pressure such as convulsions can cause dire consequences. The

case of pre-eclampsia, the condition can strike without warning causing blood pressure to risk to

dangerously high levels. Pre-eclampsia may progress to eclampsia in which high blood pressure

and convulsions could be fatal to the mother or child. Pre-eclampsia is a leading cause of

maternal death. It strikes about five percent of first time mothers and one to two percent of

mothers during subsequent pregnancies.

Classification of Hypertensive Diseases in Pregnancy

Chronic Hypertension is defined as blood pressure >140/90 at <20 weeks of gestation.

Pregnancy Induced Hypertension is defined as a sustained blood pressure increase to 140/90 at

>20 weeks gestation.

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Superimposed Pregnancy-Induced Hypertension is defined as coexistence of chronic

hypertension and pregnancy-induced hypertension.

Clinical Manifestations of Severe Disease in Patients with PIH

Blood pressure >160-180 mm Hg systolic or >110 mm Hg diastolic

Proteinuria >5 g/24 h or > 1+ on dipstick (normal <300 mg/24 h)

Elevated serum creatinine

Generalized seizures (eclampsia)

Pulmonary edema

Oliguria <500 mL/24 hours

Microangiopathic hemolysis

Thrombocytopenia

Hepatocellular dysfunction (elevated alanine toxemia preeclampsia, aminotransferase, aspartase

aminotransferase)

Intrauterine growth restriction or oligohydramnios

Symptoms suggesting significant end-organ involvement: headache, visual disturbances, or

epigastric or right-upper quadrant pain

REASONS FOR CHOOSING THE CASE

The student nurses have chosen this study because of different reasons such as, it is a

very common disease at the obstetric ward as well as the delivery room. There are a lot of cases

of pre-eclampsia, the topic is interesting and most especially, for us to learn more about the

disease and in return, we will gain more knowledge about the study.

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STATISTICS

Pregnancy induced hypertension is a condition which effects many women in the world.

This is true even for those expecting mothers in the Philippines. Studies of preeclampsia report

about 5 percent of nulliparous women develop preeclampsia and 40 to 50 percent of these

women develop severe disease worldwide. In the Philippines, according to Department of

Health, Maternal Mortality Rate (MMR) is 162 out of 10,000 live births (Family Planning

Survey 2006). Maternal deaths account for 14% of deaths among women. For the past five years

all of the causes of maternal deaths exhibited an upward trend. Preeclampsia showed an

increasing trend of 6.89%; 20%; 40%; and 100%. Ten women die every day in the Philippines

from pregnancy and childbirth related causes but for every mother who dies, roughly 20 more

suffer serious disease and disability. The UNFPA office in the Philippines declared that family

planning can help prevent maternal deaths by 35%.

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STUDENT NURSE-CENTRED OBJECTIVES

G E N E R A L
O B J E C T I V E S


After the completion of this book-based case study, the student nurses will be able to:

❖ Know and understand the disease process and concept of pregnancy-induced

hypertension.

S P E C I F I C
O B J E C T I V E S


After the completion of this book-based study on pregnancy-induced hypertension, the student
nurses will be able to:

Cognitive

➢ Review the proper physical assessment (IPPA) and expected findings in a woman with pregnancy
induced hypertension.
➢ Understand the disease process: the causes, effects, management, treatment, and possible
preventions.
➢ Determine the pathophysiology of the condition with their rationale for occurrence of each
manifestation.
➢ Determine why certain management and medications are given and provided for the condition.
➢ Understand how and why certain diagnostic tests are done for the condition.
➢ Review the concepts about the anatomy and physiology with regards to the condition.
Psychomotor

➢ Identify the appropriate health teachings in which to provide to future patients with the said
condition.
Affective

➢ Share the learning acquired to co-student-nurses to increase awareness and help them if ever they
will encounter patient with the same condition.

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DIAGNOSTIC & LABRATORY PROCEDURES

COMPLETE BLOOD COUNT

Diagnostic Procedure Indications or Purpose Possible Results Normal Values

HGB (g/dL) To measure the total May be elevated due 120-160 g/dl
amount of hemoglobin in to hemoconcentration
the blood. of blood.

HCT (%) To aid diagnosis of May be elevated due 36.0 – 47.0

abnormal states of to hemoconcentration
hydration, polycythemia of blood.
and anemia and aids in
calculation of
erythrocyte indices.
Platelet Count To evaluate platelet Thrombocytocpenia 150 – 400
production or decreased platelet
(x10 9/L) states are often found
in PIH

WBC (x10 9/L) To determine for WBC and differential 4.8 – 10.8
presence of for further counts may be
tests such as WBC elevated depending
differential infection and upon the presence of
also for determination infection for the
count individual case of the
patient.
Differential Count: To provide a numeric WBC and 55-65%
estimate of the client’s differential counts
Segmenters (%) immune status. may be elevated
depending upon the
presence of

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infection for the

individual case of the
patient.

Lymphocytes (%) To check for immune WBC and 25-35%

responses differential counts
may be elevated
depending upon the
presence of infection
for the individual
case of the patient.
Eosinophils (%) To determine presence of WBC and 2-4%
multicellular parasites differential counts
and certain infections may be elevated
depending upon the
presence of infection
for the individual
case of the patient.
Monocytes (%) To determine presence of WBC and 2-6%
Chronic inflammatory differential counts
disease, Parasitic may be elevated
infection, Viral infection depending upon the
presence of infection
for the individual
case of the patient.

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COMPLETE BLOOD COUNT

NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER PROCEDURE

Before the Procedure

 Explain the procedure to the pt. and why it is indicated

 Inform the patient that fluid and food restriction is not required

 Inform the patient that a blood sample will be taken.

 Tell the patient that he may experience transient discomfort from the needle puncture

 Fill up laboratory request form properly and send it to the laboratory technician during

the collection of sample/specimen.

During the Procedure

 Inform the patient that pain may be felt through prick in the needle

 Instruct the patient to calm down to avoid uneasiness.

After the Procedure

 Apply brief pressure to prevent bleeding

 Apply warm compress if Hematoma will develop at the venipuncture site.

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BLOOD CHEMISTRY

Diagnostic Procedure Indications or Purpose Possible Findings Normal Values

Creatinine This test measures the Often normal but 0.5-1.69 mg/dl
amount of creatinine in may be increased in
the blood. It is used to cases of severe
diagnose impaired renal preeclampsia.
function and assess
glomerular filtration.

To check for water Normal in PIH, but 137-145 mmo/l

Sodium (Na+)
balance. may differ due to
comorbid existing
conditions for the
patient

Potassium (K+) Normal in PIH, but 3.6-5.0 mmo/l

To measure acid base
balance and normal may differ due to
muscle activity. comorbid existing
conditions for the
patient

Tests for the presence of Usually below 5

Bilirubin liver disease or 0.2-1.9 mg/dL
mg/dL
dysfunction through
evaluation of bilirubin
levels in the blood.

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AST is usually below 6-34 IU/L

500 IU
Aspartate The aspartate
Aminotransferase (AST) aminotransferase (AST)
test can be used
specifically to check for
liver or heart problems,
or it can be part of
standard medical test
screening.
Alkaline phosphotase 20-140 IU/L
may increase 2 to 3
Alkaline Phosphotase A test which evaluates fold in PIH
the alkaline phosphotase
levels in blood. This is
an enzyme that is
normally present in high
concentrations in
growing bone and in
bile. It is essential for
the deposition of
minerals in the bones
and teeth.

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BLOOD CHEMISTRY

NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER PROCEDURE

Before the Procedure

 Explain the procedure to the pt. and why it is indicated

 Inform the patient that fluid and food restriction is not required

 Inform the patient that a blood sample will be taken.

 Tell the patient that he may experience transient discomfort from the needle puncture

 Fill up laboratory request form properly and send it to the laboratory technician during

the collection of sample/specimen.

During the Procedure

 Inform the patient that pain may be felt through prick in the needle

 Instruct the patient to calm down to avoid uneasiness.

After the Procedure

 Apply brief pressure to prevent bleeding

 Apply warm compress if Hematoma will develop at the venipuncture site.

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URINALYSIS

Diagnostic Procedure Indications or Purpose Possible Findings Normal Values

Urinalysis For general health Urinalysis reveals Color: Straw

screening to detect renal Proteinuria (positive yellow to
and metabolic disease; albumin levels) and amber.
diagnosis of disease or occasional hyaline
disorders of the kidney casts. Transparency:
or urinary tract; transparent
monitoring patient’s with Sugar: negative
diabetes.
Albumin:
negative

Specific
Gravity: 1.015 –
1.025

Pus cells: 5-
10/HPF

RBC: o-2 HPF

Epithelial cells:
Moderate

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URINALYSIS

NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER PROCEDURE

Before the Procedure

 Explain to the significant others the test, it’s purpose and how it done.

 Inform the significant others that the test will require urine specimen.

 Provide a clean container for the specimen.

During the Procedure

 Label the specimen cup before giving it to the client

 Assist the client in the comfort room

 Instruct the client to take the middle urine

After the Procedure

 The specimen should be delivered to the lab within 1 hour.

 Obtain result and secure it to the chart

Refer result to the physician

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PHYSICAL EXAMINATION & ASSESSMENT

the following physical assessment guide has been created to create a full picture of what a nurse
may find in the course of assessment of a patient with pregnancy induced hypertension. The
findings are hypothetical and based on the signs and symptoms lifted from authors such as
Pilliteri and Black. The actual signs and symptoms of the disease may vary from case to case.

Assessment of the Central Nervous System

Tissues are capable of regulating their own blood flow; this process is known as autoregulation.

Cerebral perfusion is maintained by autoregulation at a constant level of about 55 mL/min/100 g

at a wide range of blood pressures (Fig 19-1). However, blood pressure may rise to levels at

which autoregulation cannot function. When this occurs, the endothelial tight junctions open,

causing plasma and red blood cells to leak into the extravascular space. This may result in

petechial hemorrhage or gross intracranial hemorrhage. The upper limit of autoregulation varies

from one person to another; eg, chronic hypertension may cause medial hypertrophy of the

cerebral vessels, resulting in a shift of the curve to the right (Fig 19-1). This explains the paradox

of 2 patients with equally severe hypertension who have markedly different clinical

presentations. The young primigravida whose blood pressure is normally 110/70 mm Hg may

convulse with a blood pressure of 180/120 mm Hg, while a chronic hypertensive may be

asymptomatic or have only a headache at the same pressure.

The mechanism of the cerebral damage in eclampsia is unclear. The pathologic findings are

similar to those of hypertensive encephalopathy. These abnormalities include fibrinoid necrosis

and thrombosis of arterioles, microinfarcts, and petechial hemorrhages. In both hypertensive

encephalopathy and eclampsia, the lesions are widely distributed throughout the brain, but the

brainstem is more severely affected in the former, while the cortex is more severely affected in

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the latter. Other differences in the two conditions are that eclampsia may be seen in the absence

of hypertension and that retinal hemorrhages and infarcts are rare in eclampsia. Two theories

have been proposed to explain the pathogenesis of hypertensive encephalopathy, vasospasm, and

forced dilation. In the first, vasospasm causes local ischemia, arteriolar necrosis, and disruption

of the blood-brain barrier. According to the second, as blood pressure rises above the limit of

autoregulation, cerebral vasodilation occurs. Initially, some vessel segments dilate, and some

remain constricted. Overdistention of the dilated segments results in necrosis of the medial

muscle fibers and damage to the vessel wall. It is possible that both mechanisms are operant.

The presence of cerebral edema in preeclampsia-eclampsia is controversial. One set of

researchers stated that cerebral edema was not present in eclamptic patients when autopsy was

performed within 1 hour of death and that such edema was a late postmortem change. In contrast,

some others found generalized cerebral edema in some autopsy specimens and confirmed

increased intracranial pressure in eclamptics with prolonged coma (> 6 hours). Early studies of

cerebrospinal fluid opening pressure showed elevated pressures; however, more recent studies

have failed to confirm this.

Head computed tomographic (CT) scans in women with eclampsia have shown abnormalities in

about one-third. By using fourth-generation equipment and with a short interval from seizure to

CT scan, abnormalities may be detected in half the patients. The main findings are focal

hypodensities in the white matter in the posterior half of the cerebral hemispheres with

occasional lesions in the gray matter, temporal lobes, and brainstem. One researcher suggested

that these areas of radiographic hypodensity represented petechial hemorrhages accompanied by

local edema. Subarachnoid or intraventricular hemorrhages may be seen in the most severe

cases.

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Magnetic resonance imaging (MRI) is more sensitive at demonstrating abnormalities than CT

scan, but it is not as widely available. T2-weighed MRI scans show high signal in the cortical

and subcortical white matter. Most of the abnormalities lie in the occipital and parietal areas in

watershed areas where the anterior, middle, and posterior circulations meet. Basal ganglia and

brainstem abnormalities occur in more critically ill patients.

Cerebral angiography has been performed in a few patients with eclampsia, revealing diffuse

arterial vasoconstriction.

Electroencephalograms (EEGs) show nonspecific abnormalities in about 75% of patients after

eclamptic seizures. The pattern is usually a diffuse slowing of activity (theta or delta waves),

sometimes with focal slow activity and occasional paroxysmal spike activity. These

abnormalities may be seen in other conditions, such as hypoxia, renal disease, polycythemia,

hypocalcemia, and water intoxication. The electroencephalographic pattern is unaffected by

magnesium sulfate. It gradually returns to normal 6-8 weeks postpartum. Uncomplicated

eclampsia causes no permanent neurologic deficit.

Assessment of the Eyes

Both serous retinal detachment and cortical blindness may occur.

Assessment of the Pulmonary System

Pulmonary edema may occur with severe preeclampsia or eclampsia. It may be cardiogenic or

noncardiogenic and usually occurs postpartum. In some cases it may be related to excessive fluid

administration or to delayed mobilization of extravascular fluid. It may also be related to

decreased plasma colloid oncotic pressure from proteinuria, use of crystalloids to replace blood

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loss, and decreased hepatic synthesis of albumin. Pulmonary edema is particularly common in

patients with underlying chronic hypertension and hypertensive heart disease, which may be

manifested by systolic dysfunction, diastolic dysfunction, or both. Aspiration of gastric contents

is one of the most dreaded complications of eclamptic seizures. This may result in death because

of asphyxia from particulate matter plugging major airways or in chemical pneumonitis from

aspirated gastric acid. Aspiration may cause various types of pneumonia, ranging from patchy

pneumonitis to full-blown adult respiratory distress syndrome.

Assessment of the Cardiovascular System

Plasma volume is reduced in patients with preeclampsia. Normal physiologic volume expansion

does not occur, possibly because of generalized vasoconstriction, capillary leak, or some other

factor. Because the cause of the reduced volume is unknown, management is controversial. One

theory is that the decreased volume is a primary event causing a chronic shocklike state.

Hypertension is thought to be the result of release of a pressor substance from the hypoperfused

uterus or of compensatory secretion of catecholamines. Proponents of this theory advocate

avoidance of diuretics and use of volume expanders. Another theory is that decreased volume is

secondary to vasoconstriction. Proponents of this theory advocate the use of vasodilators and

warn that volume expanders may aggravate hypertension or cause pulmonary edema.

Studies using the Swan-Ganz catheter have demonstrated a spectrum of hemodynamic findings

in preeclampsia ranging from a low-output, high-resistance state to a high-output, low-resistance

state. One study found a low wedge pressure, low cardiac output, and high systemic vascular

resistance in untreated nulliparous preeclamptic women, while patients who received various

therapies and were usually referred, a wide range of hemodynamics was found. The conclusion

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was that the untreated preeclamptic patient was significantly volume-depleted and that the wide

spectrum of hemodynamic findings in the treated group resulted from prior therapy and the

presence of other variables such as labor, multiparity, and preexisting hypertension.

In another study of a heterogeneous population of pretreated and nonpretreated patients, a

generally consistent profile emerged. Preeclampsia was in general a high cardiac output state

associated with an inappropriately high peripheral resistance. Although the systemic vascular

resistance was within the normal range for pregnancy, it was still inappropriately high for the

elevated cardiac output. The failure of the circulation to dilate in the setting of increasing cardiac

output appeared to be a characteristic feature of preeclampsia. The normal wedge and central

venous pressures found in their study suggested venoconstriction with central relocation of

intravascular volume if the generally accepted reports of decreased plasma volume in

preeclampsia are correct. They postulated splanchnic venoconstriction as the mechanism of this

volume shift.

Normal pregnant women are resistant to the vasoconstrictor effects of angiotensin II. Pregnant

women require about 21/2 times the amount of angiotensin II required by nonpregnant women to

raise the diastolic blood pressure 20 mm Hg. Patients who will develop superimposed

preeclampsia lose their refractoriness to angiotensin II many weeks before hypertension

develops. These patients may be identified as early as 18-24 weeks' gestation by infusion of

angiotensin II.

Normal pregnant women lose their refractoriness to angiotensin II after treatment with

prostaglandin synthetase inhibitors such as aspirin or indomethacin; this suggests that

prostaglandin is involved in mediating vascular reactivity to angiotensin II in pregnancy.

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Refractoriness to angiotensin II can be restored in patients with preeclampsia by the

administration of theophylline, a phosphodiesterase inhibitor that increases intracellular levels of

cAMP. Therefore, prostaglandins synthesized in the arteriole may modulate vascular reactivity to

angiotensin II by altering the intracellular level of cAMP in vascular smooth muscle.

Assessment of the Liver

The spectrum of liver disease in preeclampsia is broad, ranging from subclinical involvement

with the only manifestation being fibrin deposition along the hepatic sinusoids to rupture of the

liver. Within these extremes lie the HELLP syndrome (hemolysis, elevated liver enzymes, and

low platelets) and hepatic infarction.

Assessment of the Kidneys

The characteristic lesion of preeclampsia, glomeruloendotheliosis, is a swelling of the

glomerular capillary endothelium that causes decreased glomerular perfusion and glomerular

filtration rate. Fibrin split products have been found on the basement membrane by some

observers, who have suggested that intravascular coagulation may be secondary to

thromboplastin released from the placenta. However, the fibrin split products are found

infrequently and only in small amounts. Other investigators have detected IgM, IgG, and

complement in the glomeruli of some patients and have suggested an immunologic mechanism.

Serial renal biopsies have shown that the lesion is totally reversible over about 6 weeks.

Assessment of the Blood

Most patients with preeclampsia-eclampsia have normal clotting studies. In some, a spectrum of

abnormalities may be found, ranging from isolated thrombocytopenia to microangiopathic

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hemolytic anemia to disseminated intravascular coagulation (DIC). Thrombocytopenia is the

most common abnormality; a count of less than 150,000/uL is found in 15-20% of patients.

Fibrinogen levels are actually elevated in preeclamptic women as compared with normotensive

patients. Low fibrinogen levels in preeclampsia-eclampsia are usually associated with abruptio

placentae or fetal demise. Elevated fibrin split products are seen in 20% of patients (usually in

the range of 10-40 uL/mL). Microangiopathic hemolytic anemia without other signs of DIC may

be seen in about 5% of patients, and evidence of DIC is also present in about 5%. In the past,

DIC was thought to be the cause of preeclampsia; now it is regarded as a sequela of the disease.

The HELLP syndrome describes patients with hemolytic anemia, elevated liver enzymes, and

low platelet count. Criteria for the diagnosis at the authors' institution are schistocytes on the

peripheral blood smear, lactic dehydrogenase > 600 U/L, total bilirubin > 1.2 mg/dL, aspartate

aminotransferase > 70 U/L, and platelet count < 100,000/mm3. This syndrome is present in about

10% of patients with severe preeclampsia-eclampsia. It is frequently seen in Caucasian patients

with delay in diagnosis or delivery and in patients with abruptio placentae. The syndrome may

occur remote from term (eg, at 31 weeks) and with no elevation of blood pressure. The syndrome

is frequently misdiagnosed as hepatitis, gallbladder disease, idiopathic thrombocytopenic

purpura, or thrombotic thrombocytopenic purpura. Most hematologic abnormalities return to

normal within 2-3 days after delivery, but thrombocytopenia may persist for a week.

Assessment of the Endocrine System

The role of the renin-angiotensin-aldosterone system in the regulation of blood pressure during

normal and hypertensive pregnancy has not been clearly defined. In normal pregnancy,

estrogen's effect on the liver markedly increases production of renin substrate. This increases

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plasma renin activity, plasma renin concentration, and angiotensin II levels. Plasma aldosterone

levels rise even higher than can be accounted for by the prevailing plasma renin activity. Despite

the high plasma concentration of aldosterone, there is no blood pressure increase or hypokalemia

in normal pregnancy; indeed, blood pressure falls in the midtrimester. This may be due to

counterregulatory factors such as the natriuretic effect of progesterone or activation of

vasodepressor systems such as kinins or prostaglandins.

Interpreting renin, angiotensin, and aldosterone levels in studies of preeclampsia is difficult

because of differences in the definition of preeclampsia (parity, degree of proteinuria, early- or

late-onset disease), differences in taking of blood samples (values may be affected by bed rest,

sodium intake, labor, etc), and differences in assay techniques. In the majority of studies, renin,

angiotensin, and aldosterone are all suppressed in preeclampsia, but they are still above

nonpregnant levels. The available evidence suggests that the renin-angiotensin system is only

secondarily involved in preeclampsia.

Atrial natriuretic peptide (ANP) is a volume regulatory hormone synthesized by cardiac

myocytes, which has potent natriuretic, diuretic, and vasorelaxant properties. ANP secretion is

stimulated by increased atrial pressure and alterations in sodium balance. Elevated

concentrations of ANP accompany pathologic states characterized by fluid overload such as

Cirrhosis, congestive heart failure, and chronic renal failure. However, ANP is elevated in

preeclampsia, a disorder supposedly characterized by hypovolemia. It is even elevated in the

second trimester before the onset of clinical evidence of preeclampsia. The mechanism for the

elevation is unknown. It may be that endothelin or another vasoactive peptide is stimulating

release of ANP. It may also be that the widely accepted concept of central hypovolemia in

preeclampsia is incorrect.

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Assessment of the Catecholamines

Urinary and blood catecholamine levels are the same in normotensive pregnant women, women

with preeclampsia, and nonpregnant controls. However, it cannot be ruled out that sympathetic

activity is of pathogenetic importance for initiation or maintenance of hypertension in patients

with preeclampsia. Catecholamine levels increase during labor, presumably owing to stress. The

vascular refractoriness to catecholamines is lacking in preeclampsia, as is the refractoriness to

other endogenous vasopressors such as antidiuretic hormone and angiotensin II.

Assessment of the Prostacyclin

Prostacyclin is a prostaglandin discovered in 1976. It increases intracellular cAMP in smooth

muscle cells and platelets resulting in vasodilator and platelet antiaggregatory effects. Its half-life

is about 3 minutes, breaking down in plasma to 6-keto-PGF1α, which is stable and can be

measured as an indication of prostacyclin levels. These plasma levels are low, indicating that

prostacyclin acts physiologically at the local level rather than as a circulating hormone.

Prostacyclin is made primarily in the endothelial cell from arachidonic acid, catalyzed by the

enzyme cyclooxygenase. Cyclooxygenase can be inhibited by aspirin-like drugs. Mechanical or

chemical perturbation of the endothelial cell membrane stimulates formation and release of

prostacyclin. For example, pulsatile pressure or chemicals such as bradykinin or thrombin

stimulate prostacyclin generation in the vessel wall.

Thromboxane A2 generated by platelets from arachidonic acid via cyclooxygenase induces

vasoconstriction and platelet aggregation. Thus, prostacyclin and thromboxane have opposing

roles in regulating platelet-vessel wall interaction.

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Aspirin irreversibly inhibits cyclooxygenase. Cyclooxygenase must be produced continuously by

endothelial cells, because they recover their ability to synthesize prostacyclin within a few hours

after a dose of aspirin. On the other hand, platelets do not have a nucleus and therefore cannot

make fresh cyclooxygenase. Thromboxane synthesis recovers only as new platelets enter the

circulation. Platelet life span is about 1 week. Thus, daily treatment with low-dose aspirin results

in chronic inhibition of thromboxane metabolites and decreased excretion of prostacyclin

metabolites in preeclamptic patients. Low-dose aspirin therapy is aimed at restoring the

presumed thromboxane-prostacyclin imbalance in preeclampsia.

Assessment of the Nitric Oxide

Nitric oxide (NO) is an endogenous vasodilator and inhibitor of platelet aggregation and acts

synergistically with prostacyclin. It is produced by endothelial cells from L-arginine. Synthesis

can be inhibited by arginine analogs such as NG-monomethyl-L-arginine and NG-nitro-L-

arginine. Intravenous injection of one of these inhibitors into rats, rabbits, or guinea pigs causes

an immediate rise in blood pressure that is reversed by L-arginine. This indicates that continual

basal release of NO from endothelial cells keeps the vasculature in a dilated state. NO acts only

in the immediate vicinity of the cell that releases it. Any that escapes into the bloodstream decays

chemically to form nitrite or is immediately inactivated by hemoglobin.

NO plays an important role in several pathologic processes. It is one of the mediators of

hypotension in septic shock. A deficiency of NO contributes to the cause of hypertension and

Atherosclerosis. Currently it is thought that the NO system may be more important than the

prostaglandins in the pathogenesis of preeclampsia. Chronic blockade of the endogenous NO

system produces a model of hypertension and renal damage in pregnant and nonpregnant rats.

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 Pregnancy-Induced Hypertension: A Case Study 27

Some studies have shown that there is decreased excretion of NO in the urine of pregnant

preeclamptic women, but whether NO plays an important pathophysiologic role in the

development of preeclampsia remains unknown.

Assessment of the Endothelin-1

In addition to the relaxing factors prostacyclin and NO, the vascular endothelium releases

vasoconstrictor substances. The vasoconstrictor endothelin was discovered in 1988. There are 3

different isopeptides: endothelin 1, 2, and 3. Endothelin-1 is the only endothelin manufactured by

endothelial cells. Endothelins are also synthesized by kidney cells and nervous tissue. There are

widespread endothelin-binding sites including those in the brain, lung, kidney, adrenal, spleen,

intestine, and placenta. It is thought that endothelins act as endogenous agonists of

dihydropyridine-sensitive calcium channels. The most striking property of endothelin-1 is its

long-lasting vasoconstrictor action. It is 10 times more potent than angiotensin II. Endothelin

may play a role in constriction of placental vessels after delivery and may regulate closure of the

ductus arteriosus in the newborn. The mitogenic effects of endothelin-1 may cause vascular wall

hypertrophy in Atherosclerosis and hypertension. Endothelin-1 may play a role in renal

vasoconstriction in acute renal failure. A 3-fold elevation of plasma endothelin 1 and 2 has been

found in women with preeclampsia compared with gestation-matched controls.

One hypothesis is that prostacyclin is an antiplatelet and vasodilator mechanism held in reserve

to reinforce the NO system when endothelial damage occurs. Lack of NO may be a causative

factor in hypertension. Endothelin-1 is released by endothelial cells to constrict the underlying

smooth muscle in an emergency such as laceration. Excess endothelin-1 may also be involved in

the genesis of hypertension.

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 Pregnancy-Induced Hypertension: A Case Study 28

Assessment of the Placenta

In normal pregnancy, the proliferating trophoblast invades the decidua and the adjacent

myometrium in 2 forms: interstitial and endovascular. The role of the interstitial form is not clear

but it may serve to anchor the placenta. The endovascular trophoblastic cells invade the maternal

spiral arteries, where they replace the endothelium and destroy the medial elastic and muscular

tissue of the arterial wall. The arterial wall is replaced by fibrinoid material. This process is

complete by the end of the first trimester, at which time it extends to the deciduomyometrial

junction. There appears to be a resting phase in the process until 14 to 16 weeks' gestation, when

a second wave of trophoblastic invasion extends down the lumen of the spiral arteries to their

origin from the radial arteries deep in the myometrium. The same process is then repeated, ie,

replacement of the endothelium, destruction of the medial musculoelastic tissue, and fibrinoid

change in the vessel wall. The end result is that the thin-walled, muscular spiral arteries are

converted to saclike, flaccid uteroplacental vessels, which passively dilate to accommodate the

greatly augmented blood flow required in pregnancy.

Preeclampsia develops following a partial failure in the process of placentation. First, not all the

spiral arteries of the placental bed are invaded by trophoblast. Second, in those arteries that are

invaded, the first phase of trophoblastic invasion occurs normally, but the second phase does not

occur, and the myometrial portions of the spiral arteries retain their reactive musculoelastic

walls.

In addition, acute atherosis (a lesion similar to Atherosclerosis) develops in the myometrial

segments of the spiral arteries of patients with preeclampsia. The lesion is characterized by

fibrinoid necrosis of the arterial wall, the presence of lipid and lipophages in the damaged wall,

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 Pregnancy-Induced Hypertension: A Case Study 29

and a mononuclear cell infiltrate around the damaged vessel. Acute atherosis may progress to

vessel obliteration with corresponding areas of placental infarction.

Thus, in preeclampsia there is an area of vascular resistance in the spiral artery because of

failure of the second wave of trophoblastic invasion. In addition, acute atherosis further

compromises the vascular lumen. Consequently, the fetus is subjected to poor intervillous blood

flow from the time of early gestation; this may result in intrauterine growth retardation or

stillbirth. Antihypertensive therapy may be detrimental because peripheral vasodilatation may

further reduce the already compromised placental blood flow.

Representation of the relationship between cerebral blood flow and mean arterial blood

pressure. Cerebral blood flow normally remains constant at mean arterial pressures of 60-140

mm Hg. In chronically hypertensive patients, medial hypertrophy causes the lower and upper

limits of autoregulation to be shifted to higher blood pressure values. (Modified and reproduced,

with permission, from Donaldson JO: Neurology of Pregnancy. Saunders, 1978.)0

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 Pregnancy-Induced Hypertension: A Case Study 30

ANATOMY & PHYSIOLOGY

The female reproductive system

consists of the ovaries, uterine

tubes (or fallopian tubes), uterus,

vagina, external genitalia, and

mammary glands. The internal

reproductive organs of the

female are located within the

pelvis, between the urinary

bladder and the rectum. The

uterus and the vagina are in the midline , with an ovary to each side of the organ. The internal

reproductive organs are held in place within the pelvis with ligaments. The most conspicuous is

the brad ligament, which spreads out on both sides of the uterus and to which the ovaries and the

uterine tubes attach.

Ovaries

The two ovaries are small organs suspended in the pelvic

cavity by ligaments. The suspensory ligament extends

from each ovary to the lateral body wall, and the ovarian

ligament attaches the ovary to the superior margin of the uterus. In addition, the ovaries are

attached to the posterior surface of the broad ligament by folds of the peritoneum called the

mesovarium. The ovarian arteries, veins, and nerves transverse the suspensory ligament and

enter the ovary through the mesovarium.

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 Pregnancy-Induced Hypertension: A Case Study 31

A layer of visceral peritoneum covers the surface of the ovary. The outer part of the ovary is

made up of dense connective tissue and contains the ovarian follicles. Each of the ovarian

follicles contains an oocyte, the female sex cell. Loose connective tissue makes up the inner part

of the ovary, where blood vessels, lymphatic vessels, and nerves are located.

Uterine Tubes

A uterine tube, fallopian tube, or oviduct (named after the italian anatomist, Gabriele Fallopio) is

associated with each ovary. The uterine tubes extend from the area of the ovaries to the uterus.

The open directly into the peritoneal cavity near each ovary and receive an oocyte. The opening

of each uterine tube is surrounded by long, thin processes called fimbriae.

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 Pregnancy-Induced Hypertension: A Case Study 32

The fimbriae nearly surround the surface of the ovary. As a result, as soon as the oocyte is

ovulated, it comes into contact with the surface of the fimbriae. Cilia on the fimbriae surface

sweep the oocyte into the uterine tube. Fertilization usually occurs in the part of the uterine tube

near the ovary known as the ampulla.

Uterus

The uterus is as big as the size of a medium-sized pear. It is oriented in the pelvic cavity with the

larger, rounded portion directed superiorly. The part of the uterus superior to the entrance of the

fallopian tubes is called the fundus. The main part of the uterus is called the body, and the

narrower part is termed the cervix and is directed inferiorly. Internally, the uterine cavity in the

fundus and uterine body continues through the cervix as the cervical canal, which opens into the

vagina. The cervical canal is lined by mucous glands.

The Uterine wall is composed of three layers: a serous layer or perimetrium of the uterus,

consists of smooth muscle is quite thick and accounts for the bulk of the uterine wall. The inner

most layer of the uterus is called the endometrium. The endometrium consists of simple

columnar epithelium tissues with an underlying connective tissue layer. Simple tubular glands,

called endometrial glands, are formed by folds of the endometrium. The superficial part os the

endometrium is sloughed off during menstruation.

The uterus is supported by the broad ligament and the round ligament. In addition to these

ligaments that support the uterus, much support is provided inferiorly to the uterus by skeletal

muscles of the pelvic floor. If ligaments that support the uterus or the muscles of the pelvic floor

are weakened such as in childbirth, the uterus can extend inferiorly into the vagina, a condition

termed as a prolapsed uterus. Severe cases require surgical correction.

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 Pregnancy-Induced Hypertension: A Case Study 33

Vagina

The vagina is the female organ of copulation and functions to receive the penis during

intercourse. It also allows menstrual flow and childbirth. The vagina extends from the uterus to

outside the body. The superior portion of the vagina is attached to the sides of the cervix so that a

part of the cervix extends into the vagina.

The wall of the vagina consists of an outer muscular layer and an inner mucous layer. The

muscular layer is smooth muscle and contains many elastic fibers. Thus the vagina can increase

in size to accommodate the penis during intercourse, and it can stretch greatly during childbirth.

The mucous membrane is moist stratified squamous epithelium that forms a protective surface

layer. Lubricating fluid passes through the vaginal epithelium into the vagina.

In young females, the vaginal opening is covered by a thin mucous membrane known as the

hymen. The hymen can completely close the vaginal orifice in which case it must be removed to

allow menstrual flow. More commonly, the hymen is perforated by one or several holes. The

openings of the hymen are usually greatly enlarged during the first sexual intercourse. The

hymen can also be perforated during a variety of activities including strenuous exercise. The

condition of the hymen is therefore not a reliable indicator of virginity.

The External Genitalia

The external female genitalia, also called the vulva, or pudendum, consists of the vestibule and

its surrounding structures. The vestibule is the space into which the vagina and urethra open. The

urethra opens just anterior to the vagina. The vestibule is bordered by a pair of thin, longitudinal

skin folds called the labia minora. A small erectile structure called the clitoris is located in the

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 Pregnancy-Induced Hypertension: A Case Study 34

anterior margin of the vestibule. The two labia minora unite over the clitoris to form a fold of

skin known as the prepuce.

The clitoris consists of a shaft and a distal glans. Like the glans penis, the clitoris is well

supplied with sensory receptors, and it is made up of erectile tissue. An additional erectile tissue

is located on either side of the vaginal opening.

On each side of the vestibule, between the vaginal opening and the labia minora, are openings of

the greater vestibular glands. These glands produce a lubricating fluid that helps maintin the

moistness of the vestibule.

Lateral to the labia minor are two prominent rounded folds of skin called the labia majora. The

two labia majora unite anteriorly at the elevation of tissue over thepubic symphysis calle dthe

mons pubis. The lateral surfaces of the labia majora and the surface of the mons pubis are

covered with coarse hair. The medial surfaces of the labia minora are covered with numerous

sebaceous and sweat glands. The space between the labia minor is called the pudendal cleft.

Most of the time, the labia minora are in contact with each other across the midline , closing the

pudendal cleft and covering the deeper structures within the vestibule.

The region between the vagina and the anus is the clinical perineum. The skin and muscle of this

region can tear during childbirth. To preven such tearing, an incision called an episiotomy is

sometimes made in the clinical perineum. Traditionally, this clean, straight incision is thought to

result in less injury, and less trouble in healing, and less pain. However, many studies indicate

that there is less injury and pain when no episiotomy is performed.

Mammary Glands

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 Pregnancy-Induced Hypertension: A Case Study 35

Mammary glands are located inside the breasts of sexually mature female body. They are in

actuality modified sweat glands which are in fact comprised of secretory mammary alveoli and

the appropriate ducts. Mammary glands are considered to be part of the integumentary system

rather than the reproductive system. The glands are associated with the female reproductive

system in part due to their assistance in attracting a mate as well as their role in nourishing a

baby. Size and shape of the female breast are different for every human body and factors such as

race, age, body fat, and pregnancy can make a large difference in these variations.

The release of estrogen during puberty releases hormones that stimulate the growth of the

breasts and the functions of the mammary glands. Pregnant women as well as nursing women

experience hypotrophy of the breasts while it is not uncommon for atrophy of the breasts to

occur after menopause.

Breasts are situated over ribs 2 through 6 and overlap the pectoral muscle as well as some

portions of the oblique muscles. The lateral margin of the sternum creates an unintentional

margin for the edge of each breast. Each breast also follows the anterior margin of the respective

axilla. Coming within very close proximity to the Axillary vessels, the breasts upward and

laterally toward the axilla, which contributes to the high incidence of breast cancer due to the

axillary process’ lymphatic drainage.

15 to 20 lobes compose the mammary gland, and each lobe is equipped with its own duct to the

outside of the body. Adipose tissue in varying amounts segregates each lobe. While this tissue

controls the size and shape that the breast takes, there is no determination by this tissue when it

comes to the woman’s ability to suckle her young. Lobules are subdivisions of each lobe. These

subdivisions contain mammary alveoli. The milk of a lactating female are produced within the

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 Pregnancy-Induced Hypertension: A Case Study 36

mammary alveoli. Suspensory ligaments support the breasts which are attached between the

lobules and run deep into the fascia which overlap the pectoral muscles. Breast milk is secreted

into a network of mammary ducts which receive the milk from the clusters of mammary alveoli.

These mammary ducts converge to form lactiferous ducts. Near the nipple, each lactiferous duct

expands into the lumen to allow for outward flow of milk. The lactiferous sinuses store the milk

before the suckling action, or additional pressure, releases it from the body. The milk leaves the

body from the tip of the nipple.

The nipple contains some erectile tissue that protrudes into a cylindrical projection. The circular

area around the nipple that contrasts in color is the areola. Sebaceous areola glands create a

bumpy surface around the areola which resides just under the surface of the areola’s skin. These

glands secrete fluids during lactation as well as when a woman is not lactating, which keep the

nipple supple. The complexion of the areola is based on the complexion of the skin that covers

the rest of the body, varying in pigments and tints. During gestation most areola surfaces darken.

It also becomes larger in most cases. This is thought to be more obvious for a nursing infant to

find.

Branches of the internal thoracic artery are responsible for supplying blood flow to the nipple as

well as the rest of the breast and mammary glands. Between the second, third, and forth

intercoastal spaces these braches of the thoracic artery enter the mammary glands. These spaces

are positioned laterally to the sternum and offer entry to the mammary artery, which only

supplies supportive blood. The return veins run alongside the initial arteries which supply the

blood. During pregnancy and lactation, and sometimes during other periods, a superficial venous

plexus can be seen through the surface of the skin.

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 Pregnancy-Induced Hypertension: A Case Study 37

The fourth, fifth, and sixth thoracic nerves innervate the breast principally through sensory

somatic neurons. These neurons are derivative of the anterior and lateral branches of the thoracic

nerves. The release of milk is dependant upon the sensory innervations as stimulus is the only

natural release an infant can provide to be nourished.

Menstrual Cycle

Menstruation is the shedding of the lining of the uterus (endometrium) accompanied by bleeding.

It occurs in approximately monthly cycles throughout a woman's reproductive life, except during

pregnancy. Menstruation starts during puberty (at menarche) and stops permanently at

menopause.

By definition, the menstrual cycle begins with the first day of bleeding, which is counted as day

1. The cycle ends just before the next menstrual period. Menstrual cycles normally range from

about 25 to 36 days. Only 10 to 15% of women have cycles that are exactly 28 days. Usually,

the cycles vary the most and the intervals between periods are longest in the years immediately

after menarche and before menopause.

Menstrual bleeding lasts 3 to 7 days, averaging 5 days. Blood loss during a cycle usually ranges

from ½ to 2½ ounces. A sanitary pad or tampon, depending on the type, can hold up to an ounce

of blood. Menstrual blood, unlike blood resulting from an injury, usually does not clot unless the

bleeding is very heavy.

The menstrual cycle is regulated by hormones. Luteinizing hormone and follicle-stimulating

hormone, which are produced by the pituitary gland, promote ovulation and stimulate the ovaries

to produce estrogen and progesterone stimulates the uterus and breasts to prepare for possible

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 Pregnancy-Induced Hypertension: A Case Study 38

fertilization. The cycle has three phases: follicular (before release of the egg), ovulatory (egg

release), and luteal (after egg release).

HORMONES AND FEMALE CYCLES

The ovarian cycle is

hormonally regulated in two phases.

The follicle secretes estrogen before

the ovulation; the corpus luteum

secretes both estrogen and

progesterone after ovulation.

Hormones from the hypothalamus and

anterior pituitary control the ovarian

cycle. The ovarian cycle covers events

in the ovary; the menstrual cycle

occurs in the uterus.

Menstrual cycles vary from between 15 and 31 days. The first day of the cycle is the

first day of blood flow (day 0) known as menstruation. During menstruation, the uterine lining is

broken down and shed as menstrual flow. FSH and LH are secreted on day 0, beginning both the

menstrual cycle and the ovarian cycle. Both FSH and LH stimulate the maturation of a single

follicle in one of the ovaries and the secretion of estrogen. Rising levels of estrogen in the blood

trigger secretion of LH, which stimulates follicle maturation and ovulation (day 14, or mid

cycle). LH stimulates the remaining follicle cells to form the corpus luteum, which produces

both estrogen and progesterone.

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 Pregnancy-Induced Hypertension: A Case Study 39

Estrogen and progesterone stimulate the development of the endometrium and

preparation of the uterine lining for implantation of a zygote. If pregnancy does not occur, the

drop in FSH and LH causes the corpus luteum to disintegrate. The drop in hormones also causes

the sloughing off of the inner lining of the uterus by a series of muscle contractions of the uterus.

Fertilization and Pregnancy

If a female and male have sex within several days of the female's ovulation (egg release),

fertilization can occur. When the male ejaculates (which is when semen leaves a man's penis),

between 0.05 and 0.2 fluid ounces (1.5 to 6.0 milliliters) of semen is deposited into the vagina.

Between 75 and 900 million sperm are in this small amount of semen, and they "swim" up from

the vagina through the cervix and uterus to meet the egg in the fallopian tube. It takes only one

sperm to fertilize the egg.

About a week after the sperm fertilizes the egg, the fertilized egg (zygote) has become a multi-

celled blastocyst (pronounced: blas-tuh-sist). A blastocyst is about the size of a pinhead, and it's

a hollow ball of cells with fluid inside. The blastocyst burrows itself into the lining of the uterus,

called the endometrium (pronounced: en-doh-mee-tree-um). The hormone estrogen causes the

endometrium to become thick and rich with blood. Progesterone, another hormone released by

the ovaries, keeps the endometrium thick with blood so that the blastocyst can attach to the

uterus and absorb nutrients from it. This process is called implantation (pronounced: im-plan-

tay-shun).

As cells from the blastocyst take in nourishment, another stage of development, the embryonic

stage, begins. The inner cells form a flattened circular shape called the embryonic disk, which

will develop into a baby. The outer cells become thin membranes that form around the baby. The

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 Pregnancy-Induced Hypertension: A Case Study 40

cells multiply thousands of times and move to new positions to eventually become the embryo

(pronounced: em-bree-o). After approximately 8 weeks, the embryo is about the size of an

adult's thumb, but almost all of its parts — the brain and nerves, the heart and blood, the

stomach and intestines, and the muscles and skin — have formed.

During the fetal stage, which lasts from 9 weeks after fertilization to birth, development

continues as cells multiply, move, and change. The fetus (pronounced: fee-tus) floats in

amniotic (pronounced: am-nee-ah-tik) fluid inside the amniotic sac. The fetus receives oxygen

and nourishment from the mother's blood via the placenta (pronounced: pluh-sen-tuh), a disk-

like structure that sticks to the inner lining of the uterus and connects to the fetus via the

umbilical (pronounced: um-bih-lih-kul) cord. The amniotic fluid and membrane cushion the

fetus against bumps and jolts to the mother's body.

Pregnancy lasts an average of 280 days — about 9 months. When the baby is ready for birth, its

head presses on the cervix, which begins to relax and widen to get ready for the baby to pass

into and through the vagina. The mucus that has formed a plug in the cervix loosens, and with

amniotic fluid, comes out through the vagina when the mother's water breaks.

When the contractions of labor begin, the walls of the uterus contract as they are stimulated by

the pituitary hormone oxytocin (pronounced: ahk-see-toh-sin). The contractions cause the cervix

to widen and begin to open. After several hours of this widening, the cervix is dilated (opened)

enough for the baby to come through. The baby is pushed out of the uterus, through the cervix,

and along the birth canal. The baby's head usually comes first; the umbilical cord comes out with

the baby and is cut after the baby is delivered.

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 Pregnancy-Induced Hypertension: A Case Study 41

The last stage of the birth process involves the delivery of the placenta, which is now called the

afterbirth. After it has separated from the inner lining of the uterus, contractions of the uterus

push it out, along with its membranes and fluids.

The renin-angiotensin-aldosterone system

The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood

volume and systemic vascular resistance, which together influence cardiac output and arterial

pressure. As the name implies, there are three important components to this system: 1) renin, 2)

angiotensin, and 3) aldosterone. Renin, which is primarily released by the kidneys, stimulates the

formation of angiotensin in blood and tissues, which in turn stimulates the release of aldosterone

from the adrenal cortex.

Renin is a proteolytic enzyme that is released into the circulation primarily by the kidneys. Its

release is stimulated by:

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 Pregnancy-Induced Hypertension: A Case Study 42

1. sympathetic nerve activation (acting via β1-adrenoceptors)

2. renal artery hypotension (caused by systemic hypotension or renal artery stenosis)

3. decreased sodium delivery to the distal tubules of the kidney.

Juxtaglomerular (JG) cells associated

with the afferent arteriole entering the

renal glomerulus are the primary site of

renin storage and release in the body. A

reduction in afferent arteriole pressure

causes the release of renin from the JG

cells, whereas increased pressure inhibits

renin release. Beta1-adrenoceptors

located on the JG cells respond to

sympathetic nerve stimulation by releasing renin. Specialized cells (macula densa) of distal

tubules lie adjacent to the JG cells of the afferent arteriole. The macula densa senses the amount

of sodium and chloride ion in the tubular fluid. When NaCl is elevated in the tubular fluid, renin

release is inhibited. In contrast, a reduction in tubular NaCl stimulates renin release by the JG

cells. There is evidence that prostaglandins (PGE2and PGI2) stimulate renin release in response

to reduced NaCl transport across the macula densa. When afferent arteriole pressure is reduced,

glomerular filtration decreases, and this reduces NaCl in the distal tubule. This serves as an

important mechanism contributing to the release of renin when there is afferent arteriole

hypotension.

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 Pregnancy-Induced Hypertension: A Case Study 43

When renin is released into the blood, it acts upon a circulating substrate, angiotensinogen, that

undergoes proteolytic cleavage to form the decapeptide angiotensin I. Vascular endothelium,

particularly in the lungs, has an enzyme,angiotensin converting enzyme (ACE), that cleaves off

two amino acids to form the octapeptide, angiotensin II (AII), although many other tissues in the

body (heart, brain, vascular) also can form AII.

AII has several very important functions:

• Constricts resistance vessels (via AII [AT1] receptors) thereby increasing systemic

vascular resistance and arterial pressure

• Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to

increase sodium and fluid retention

• Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior

pituitary, which increases fluid retention by the kidneys

• Stimulates thirst centers within the brain

• Facilitates norepinephrine release from sympathetic nerveendings and inhibits

norepinephrine re-uptake by nerve endings, thereby enhancing sympathetic adrenergic function

• Stimulates cardiac hypertrophy and vascular hypertrophy

The renin-angiotensin-aldosterone pathway is regulated not only by the mechanisms that

stimulate renin release, but it is also modulated by natriuretic peptides (ANP and BNP) released

by the heart. These natriuretic peptides acts as an important counter-regulatory system.

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 Pregnancy-Induced Hypertension: A Case Study 44

Therapeutic manipulation of this pathway is very important in treating hypertension and heart

failure. ACE inhibitors, AII receptor blockers and aldosterone receptor blockers, for example, are

used to decrease arterial pressure, ventricular afterload, blood volume and hence ventricular

preload, as well as inhibit and reverse cardiac and vascular hypertrophy.

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 Pregnancy-Induced Hypertension: A Case Study 45

BOOK-BASED PATHOPHYSIOLOGY

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 Pregnancy-Induced Hypertension: A Case 4

Endothelial damage Vasospasms

Increased
Fluid shifts endothelin & Increased
Intravascular
Increased from sensitivity to
coagulation
thromboxane to intravascular to decreased nitric angiotensin II
prostacydin intracellular oxide
space

Generaliz
ed Glomerul
vasoconst Uteroplacen ar Cortical
Pulmonar
riction tal arteriole damage brain
y edema
lesions spasms

Proteinur
-IUGR ia
Hypertensi Headach
-Abruption Edema of Dyspnea
on of
e
the
placenta hands Hyperrefl
face and exia
-increased abdomen
uterine
contractili (depende Seizure
ty nt)

Platelet Hepatic
Retinal aggregati micro
arteriolar Haemolys on and emboli;
spasms is of RBCs fibrin
depositio Liver
n d-
aelmevaagtee
-Blurred Thrombocytop d liver
-Decreased enzymes
vision enia
haemoglobin
-Nausea and vomiting
-Maternal
Disseminated
hyperbilirubin -Epigastric pain
intravascular
emia
coagulation -Right Upper
Quadrant Pain

-Decreased blood
glucose

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 Pregnancy-Induced Hypertension: A Case 4

B O O K - B A S E D :
SY N T H E S I S O F T H E D I S E A S E

Definition of the Disease

Pre-eclampsia is a medical condition where hypertension arises in pregnancy (pregnancy-

induced hypertension) in association with significant amounts of protein in the urine. Because

pre-eclampsia refers to a set of symptoms rather than any causative factor, it is established that

there are many different causes for the syndrome. It also appears likely that there is a substance

or substances from the placenta that may cause endothelial dysfunction in the maternal blood

vessels of susceptible women.

Preeclampsia is a disorder that occurs only during pregnancy and the postpartum period

and affects both the mother and the unborn baby. Affecting at least 5-8% of all pregnancies, it is

a rapidly progressive condition characterized by high blood pressure and the presence of protein

in the urine. Swelling, sudden weight gain, headaches and changes in vision are important

symptoms; however, some women with rapidly advancing disease report few symptoms.

Preeclampsia has been described as a disease of theories, because the cause is unknown.

Some theories include (1) endothelial cell injury, (2) rejection phenomenon (insufficient

production of blocking antibodies), (3) compromised placental perfusion, (4) altered vascular

reactivity, (5) imbalance between prostacyclin and thromboxane, (6) decreased glomerular

filtration rate with retention of salt and water, (7) decreased intravascular volume, (8) increased

central nervous system irritability, (9) disseminated intravascular coagulation, (10) uterine

muscle stretch (ischemia), (11) dietary factors, and (12) genetic factors. The relatively new

theory of endothelial injury explains many of the clinical findings in preeclampsia. The theory

emphasizes that there is more to preeclampsia than hypertension. The vascular endothelium

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 Pregnancy-Induced Hypertension: A Case 4

produces a number of important substances including endothelial-derived relaxing factor or nitric

oxide, endothelin-1, prostacyclin, and tissue plasminogen activator. Thus, endothelial cells

modify the contractile response of the underlying smooth muscle cells, prevent intravascular

coagulation, and maintain the integrity of the intravascular compartment. Several findings

suggest endothelial injury in preeclampsia.

Predisposing / Precipitating Factors

Women with preeclampsia have abnormal blood vessels feeding the placenta, although the

exact cause of this abnormality is not know. There are no tests that can reliably predict who will

get preeclampsia, and there is no way to prevent it. Women with one or more of the following

characteristics have an increased risk of developing preeclampsia:

 First pregnancy (excluding miscarriages)

 High blood pressure, kidney disease, lupus, or diabetes prior to pregnancy

 Gestational diabetes

 Multiple gestation (eg, twins or triplets)

 A family history of preeclampsia in a sister or mother

 A previous history of preeclampsia

 Age under 20 years and possibly age over 35 to 40 years

 Obesity

Conversely, women who do not develop preeclampsia in their first pregnancy are at low risk of

developing it in a subsequent pregnancy.

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 Pregnancy-Induced Hypertension: A Case 4

Other precipating factors may include: pregnancy, long interval pregnancy and urinary tract

infection.

Other predisposing factors may include: genetics, low socioeconomic status, race and heart

disease.

Signs and Symptoms

Signs of severe preeclampsia — Mild preeclampsia can worsen and become severe. This usually

occurs over several days to weeks, but may occur more quickly. Severe preeclampsia may be

characterized by one or more of the following signs or symptoms. However, the signs of both

mild and severe preeclampsia may be subtle, and patients should not hesitate to mention any

concerns about possible signs of preeclampsia to their provider:

 Blood pressure ≥160/110 mmHg. Women with blood pressures in this range have an

increased risk of stroke

 Persistent severe headache

 Visual problems (blurred or double vision, blind spots, flashes of light or squiggly lines,

loss of vision)

 Abnormal kidney tests or decreased urination (urinating less than 500 mL in 24 hours)

 Fluid in the lungs, which may cause new shortness of breath

 Low platelet count; platelets help the blood to clot, which may cause easy bruising or

bleeding

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 Pregnancy-Induced Hypertension: A Case 5

 Liver abnormalities (detected by blood tests); symptoms may include nausea, vomiting,

or pain in the mid- or right upper abdomen (similar to heartburn)

 Destruction of red blood cells (hemolysis, which is detected by blood tests).

Partial or complete separation of the placenta from the uterus (called abruption); symptoms

include vaginal bleeding, uterine pain, and/or decreased fetal activity

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 Pregnancy-Induced Hypertension: A Case 5

MEDICAL MANAGEMENT

In t r a v e n o u s
T h e r a p y

INTRAVENOUS FLUID THERAPY

Medical Management General Description Indication or Purposes

5% Dextrose in Lactated Hypertonic Solution  To replace fluids and

Ringer’s Solution electrolytes loss
A solution containing sodium  To increase vascular/
(30gtts/min) chloride, potassium chloride, plasma volume necessary
calcium chloride and sodium during bleeding or blood
lactated in distilled water, loss
referred to Lactated Ringer’s  To replenish fluid loss of
solution calories from dextrose the body, maintain
nutritional intake when
patient is unable to tolerate
feedings, also serves as
medium for administration
of medications.

INTRAVENOUS THERAPY

NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER

Before the Procedure

 Check the doctor’s order regarding to what type of IVF to be used and also its volume
and rate.
 Explain the procedure to the patient.
 Gather all materials needed for the insertion of IVF to save time and not to waste time for
looking for other materials.
 Wash hands before and after the procedure to prevent contamination from insertion site.
During the Procedure

 Place patient in a comfortable position to facilitate easy insertion of IV line and to

decrease patient’s fear about the procedure.

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 Pregnancy-Induced Hypertension: A Case 5

 Make sure that we give the proper IV fluid and drop rate accurately because patient may
experience fluid overload or dehydration.
 Check for its patency by observing the backflow of blood upon insertion.
After the Procedure

 Press the site where the needle was inserted and secure it with micropore.
 Check the site of hand where the needle is inserted if bulging is not visible. If so,
reinsertion is to be undertaken.
 Advice patient to avoid scratching the site less movement of the hand where the needle
was inserted to keep it in place.
 Instruct patient and significant others to inform the nurse on duty if bulging of the site is
visible, if there is back flow of blood of if IVF is not infusing well.
 Observe the IV site at least every hour for signs of infiltration or other complications
fluid or electrolyte overload and air embolism.
 IVF regulation should be checked and monitored upon receiving patient.
 Always check the doctor’s order for new orders regarding the IVF supplement of the
patient.
 Always check if the IVF is infusing well and intact.
 Monitor the patient’s skin integrity.
 Provide comfort for the patient.
 Remove and dispose used items.
 Report and record as appropriate.
 Place IV tag

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 Pregnancy-Induced Hypertension: A Case 5

P h a r m a c o l o g i c a l ,
M a n a g e m e n t

Drugs Given Before Delivery

Generic Name Indication or Side effects &

General Action Dose and Route Contraindications
(Brand Name) Purposes Adverse Reactions

Magnesium Mineral/ For Eclampsia: the most Flushing, Magnesium sulfate

Anticonvulsant Initially 1 to 2 g common sweating, sharply should be given
Sulfate Injection in 25% or 50% medicine used lowered blood very cautiously in
Magnesium is the solution is given for preventing pressure, the presence of
(Magnesium second most intramuscularly. eclampsia hypothermia, serious impairment
Sulfate/ Epsom plentiful cation of Subsequently, 1 (seizures) stupor and of renal function
the intracellular g is given every during ultimately, since it is excreted
Salt) fluids. It is 30 minutes until pregnancy respiratory almost entirely by
essential for the relief is depression. the kidneys. This
activity of many obtained. The product contains
enzyme systems blood pressure aluminum that
and plays an should be may be toxic.
important role with monitored after Aluminum may
regard to each injection. reach toxic levels
neurochemical with prolonged
transmission and parenteral
muscular administration if
excitability. kidney function is
Deficits are impaired.
accompanied by a
variety of Magnesium sulfate
structural and should not be
functional administered
disturbances. parenterally in
patients with heart
block or
myocardial
damage.

Hydralazine Anti-hypertensive Start with 10 an intravenous (Common)\ MAO inhibitors

mg four times medicine for Headache, should be used
Hydralazine daily for the quickly anorexia, nausea, with caution in
(Apresoline) apparently lowers first 2-4 days, lowering vomiting, diarrhea, patients receiving
blood pressure by increase to 25 severely high palpitations, hydralazine. Used
exerting a mg four times blood pressure tachycardia, angina with caution in
peripheral daily for the during pectoris. patients with
vasodilating effect balance of the pregnancy suspected coronary
through a direct first week. For artery disease.
relaxation of the second and Apresoline should
vascular smooth subsequent be used with
muscle. weeks, increase caution in patients
Hydralazine, by dosage to 50 mg with advanced
altering cellular four times daily. renal damage
calcium For
metabolism, maintenance,
interferes with the adjust dosage to
calcium the lowest
movements within effective levels.
the vascular

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 Pregnancy-Induced Hypertension: A Case 5

smooth muscle that

are responsible for
initiating or
maintaining the
contractile state

Methyldopa Anti-hypertensive starting dosage an oral edation, usually With active hepatic
of ALDOMET medicine for transient, may disease, such as
ALDOMET is an is 250 mg two controlling high occur during the acute hepatitis and
(Aldomet) aromatic-amino- or three times a blood pressure initial period of active cirrhosis.
acid decarboxylase day in the first during therapy or With liver
inhibitor in 48 hours. When pregnancy whenever the dose disorders
animals and in ALDOMET is is increased. previously
man. Although the given with Headache, associated with
mechanism of antihypertensive asthenia, or methyldopa
action has yet to be s other than weakness may be therapy. With
conclusively thiazides, the noted as early and hypersensitivity to
demonstrated, the initial dosage of transient any component of
antihypertensive ALDOMET symptoms. these products.
effect of should be
methyldopa limited to 500 On therapy with
probably is due to mg daily in monoamine
its metabolism to divided doses; oxidase (MAO)
alpha- when inhibitors.
methylnorepinephr ALDOMET is
ine, which then added to a
lowers arterial thiazide, the
pressure by dosage of
stimulation of thiazide need
central inhibitory not be changed.
alpha-adrenergic daily dosage of
receptors, false ALDOMET is
neurotransmission, 500 mg to 2 g in
and/or reduction of two to four
plasma renin doses. Although
activity. occasional
Methyldopa has patients have
been shown to responded to
cause a net higher doses, the
reduction in the maximum
tissue recommended
concentration of daily dosage is 3
serotonin, g
dopamine,
norepinephrine,
and epinephrine.

Labetalol Anti-hypertensive DOSAGE an intravenous Body as a Whole: The drug is

MUST BE medicine for Fever. contraindicated in
Labetalol HCl INDIVIDUALI quickly bronchial asthma,
(Trandate) combines both ZED. The lowering Cardiovascular: overt cardiac
selective, recommended severely high Hypotension, and failure, greater-
competitive, initial dosage is blood pressure rarely, syncope, than-first-degree
alpha1-adrenergic 100 mg twice in the hospital, bradycardia, heart heart block,
blocking and daily whether and also an oral block. cardiogenic shock,
nonselective, used alone or medicine for severe bradycardia,
competitive, beta- added to a controlling high Central and other conditions
adrenergic diuretic blood pressure Peripheral Nervous associated with
blocking activity in regimen. After 2 during Systems: severe and
a single substance. or 3 days, using pregnancy Paresthesia, most prolonged
In man, the ratios standing blood frequently hypotension, and
of alpha- to beta- described as scalp

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 Pregnancy-Induced Hypertension: A Case 5

blockade have pressure as an tingling. In most in patients with a

been estimated to indicator, cases, it was mild history of
be approximately dosage may be and transient and hypersensitivity to
1:3 and 1:7 titrated in usually occurred at any component of
following oral and increments of the beginning of the product
intravenous (IV) 100 mg b.i.d. treatment.
administration, every 2 or 3
respectively. days. The usual Collagen
Beta2-agonist maintenance Disorders:
activity has been dosage of Systemic lupus
demonstrated in labetalol HCl is erythematosus,
animals with between 200 and positive
minimal beta1- 400 mg twice antinuclear factor.
agonist (ISA) daily.
activity detected. Eyes: Dry eyes.
In animals, at
doses greater than Immunological
those required for System:
alpha- or beta- Antimitochondrial
adrenergic antibodies.
blockade, a
membrane Liver and Biliary
stabilizing effect System: Hepatic
has been necrosis, hepatitis,
demonstrated. cholestatic
jaundice, elevated
liver function tests.

Musculoskeletal
System: Muscle
cramps, toxic
myopathy.

Respiratory
System:
Bronchospasm.

Skin and
Appendages:
Rashes of various
types, such as
generalized
maculopapular,
lichenoid,
urticarial, bullous
lichen planus,
psoriaform, and
facial erythema;
Peyronie's disease;
reversible alopecia.

Urinary System:
Difficulty in
micturition,
including acute
urinary bladder
retention.

Hypersensitivity:
Rare reports of
hypersensitivity
(e.g., rash,

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 Pregnancy-Induced Hypertension: A Case 5

urticaria, pruritus,
angioedema,
dyspnea) and
anaphylactoid
reactions.

Nifedipine Anti-hypertensive Dosage should an oral Body as a Concomitant

be adjusted medicine for Whole/Systemic: administration with
The mechanism by according to controlling high chest pain, leg pain strong P450
(Adalat) which nifedipine each patient's blood pressure inducers, such as
reduces arterial needs. It is during Central Nervous rifampin, are
blood pressure recommended pregnancy System: contraindicated
involves peripheral that Adalat CC paresthesia, since the efficacy
arterial be administered vertigo of nifedipine
vasodilatation and, orally once daily tablets could be
consequently, a on an empty Dermatologic: rash significantly
reduction in stomach. Adalat reduced.
peripheral vascular CC is an Gastrointestinal:
resistance. The extended release constipation Nifedipine must
increased dosage form and not be used in
peripheral vascular tablets should be Musculoskeletal: cases of
resistance, an swallowed leg cramps cardiogenic shock.
underlying cause whole, not
of hypertension, bitten or Respiratory:
results from an divided. In epistaxis, rhinitis
increase in active general, titration Known
tension in the should proceed Urogenital: hypersensitivity to
vascular smooth over a 7-14 day impotence, urinary nifedipine.
muscle. Studies period starting frequency
have demonstrated with 30 mg once
that the increase in daily. Upward
active tension titration should
reflects an increase be based on
in cytosolic free therapeutic
calcium. efficacy and
safety. The
usual
maintenance
dose is 30 mg to
60 mg once
daily. Titration
to doses above
90 mg daily is
not
recommended.
Betamethasone Glucocorticoid/ Injectable To Accelarate Allergic Reactions: contraindicated in
Corticosteroid Suspension may the Anaphylactoid patients who are
vary from 0.25 development of reaction, hypersensitive to
(Diprolene/ Naturally to 9.0 mg per surfactant in anaphylaxis, any components of
Celestone) occurring day depending infants in angioedema. this product.
glucocorticoids on the specific mothers with
(hydrocortisone disease entity PIH Cardiovascular:
and cortisone), being treated. Bradycardia,
which also have cardiac arrest, Intramuscular
salt-retaining cardiac corticosteroid
properties, are arrhythmias, preparations are
used as cardiac contraindicated for
replacement enlargement, idiopathic
therapy in circulatory thrombocytopenic
adrenocortical collapse, purpura.
deficiency states. congestive heart

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 Pregnancy-Induced Hypertension: A Case 5

Their synthetic failure, fat

analogs are embolism,
primarily used for hypertension,
their anti- hypertrophic
inflammatory cardiomyopathy in
effects in disorders premature infants,
of many organ myocardial rupture
systems. A following recent
derivative of myocardial
prednisolone, infarction,
betamethasone has pulmonary edema,
a 16β-methyl syncope,
group that tachycardia,
enhances the anti- thromboembolism,
inflammatory thrombophlebitis,
action of the vasculitis.
molecule and
reduces the Dermatologic:
sodium- and Acne, allergic
water- retaining dermatitis,
properties of the cutaneous and
fluorine atom subcutaneous
bound at carbon 9. atrophy, dry scaly
skin, ecchymoses
and petechiae,
edema, erythema,
hyperpigmentation
,
hypopigmentation,
impaired wound
healing, increased
sweating, rash,
sterile abscess,
striae, suppressed
reactions to skin
tests, thin fragile
skin, thinning
scalp hair,
urticaria.

Endocrine:
Decreased
carbohydrate and
glucose tolerance,
development of
cushingoid state,
glucosuria,
hirsutism,
hypertrichosis,
increased
requirements for
insulin or oral
hypoglycemic
adrenocortical and
pituitary
unresponsiveness
(particularly in
times of stress, as
in trauma, surgery,
or illness),
suppression of
growth in pediatric

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 Pregnancy-Induced Hypertension: A Case 5

patients.

Fluid and
Electrolyte
Disturbances:
Congestive heart
failure in
susceptible
patients, fluid
retention,
hypokalemic
alkalosis,
potassium loss,
sodium retention.

Gastrointestinal:
Abdominal
distention,
bowel/bladder
dysfunction (after
intrathecal
administration),
elevation in serum
liver enzyme
levels (usually
reversible upon
discontinuation),
hepatomegaly,
increased appetite,
nausea,
pancreatitis, peptic
ulcer with possible
perforation and
hemorrhage,
perforation of the
small and large
intestine
(particularly in
patients with
inflammatory
bowel disease),
ulcerative
esophagitis.

Metabolic:
Negative nitrogen
balance due to
protein catabolism.

Musculoskeletal:
Aseptic necrosis of
femoral and
humeral heads,
calcinosis
(following intra-
articular or
intralesional use),
Charcot-like
arthropathy, loss of
muscle mass,
muscle weakness,
osteoporosis,

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 Pregnancy-Induced Hypertension: A Case 5

pathologic fracture
of long bones,
postinjection flare
(following intra-
articular use),
steroid myopathy,
tendon rupture,
vertebral
compression
fractures.

Neurologic/Psychi
atric:
Convulsions,
depression,
emotional
instability,
euphoria,
headache,
increased
intracranial
pressure with
papilledema
(pseudotumor
cerebri) usually
following
discontinuation of
treatment,
insomnia, mood
swings, neuritis,
neuropathy,
paresthesia,
personality
changes, psychic
disorders, vertigo.
Arachnoiditis,
meningitis,
paraparesis/paraple
gia, and sensory
disturbances have
occurred after
intrathecal
administration

Ophthalmic:
Exophthalmos,
glaucoma,
increased
intraocular
pressure, posterior
subcapsular
cataracts, rare
instances of
blindness
associated with
periocular
injections.

Other:
Abnormal fat
deposits, decreased
resistance to

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 Pregnancy-Induced Hypertension: A Case 6

infection, hiccups,
increased or
decreased motility
and number of
spermatozoa,
malaise, moon
face, weight gain.

Dexamethasone Glucocorticoid/ 0.75 to 9 mg a To Accelarate Anaphylactoid Contraindicated in

Corticosteroid day depending the reaction, systemic fungal
on the disease development of anaphylaxis, infections and
Glucocorticoids, being treated. surfactant in angioedema. patients with
naturally occurring infants in Bradycardia, known
and synthetic, are mothers with cardiac arrest, hypersensitivity to
adrenocortical PIH cardiac the product and its
steroids that are arrhythmias, consituents.
readily absorbed cardiac
from the enlargement,
gastrointestinal circulatory
tract. collapse,
Glucocorticoids congestive heart
cause varied failure, fat
metabolic effects. embolism,
In addition, they hypertension,
modify the body's hyper-trophic
immune responses cardiomyopathy
to diverse stimuli. in premature
Naturally infants, myocardial
occurring rupture following
glucocorticoids recent myocardial
(hydrocorti-sone infarction. Acne,
and cortisone), allergic dermatitis,
which also have dry scaly skin,
sodium-retaining ecchymoses and
properties, are petechiae,
used as erythema,
replacement impaired wound
therapy in healing, increased
adrenocortical sweating, rash,
deficiency states. striae, suppression
Their synthetic of reactions to skin
analogs including tests, thin fragile
dexamethasone are skin, thinning
primarily used for scalp hair,
their anti- urticaria.
inflammatory
effects in disorders
of many organ
systems.

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 Pregnancy-Induced Hypertension: A Case 6

Nursing Responsibilities for All Drugs

Before the administration of drug:

 Verify Doctor’s order

 Remember the 10R’s of Drug administration
During the administration of drug:

 Verify patient’s identification

 Inform the patient with regards to drug administration
 Clean the IV port prior to administration of the drug
After the administration of drug:

 Monitor patient for adverse effects

 Inform patient that easy bruising may occur
 Caution patient not to stop taking drug abruptly without first consulting prescriber

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 Pregnancy-Induced Hypertension: A Case 6

D i e t &
A c t i v i t y
M a n a g e m e n t

LOW SALT, LOW FAT DIET

Indication or Examples of
Type of Diet General Description
Purposes Restricted foods

Low Salt, Low Fat Reduced sodium and To prevent risk for -Fried foods
diet. cholesterol content of other complications -Salty Sauces (Fish
food which may arise from sauce and soy sauce)
hypertension. -Snack foods
-Processed foods

LOW SALT, LOW FAT DIET

NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER

Before the Procedure

 Check the doctor’s order.

 Check the right client.
 Be sure that the diet is properly instructed.
During the Procedure

 Monitor if the client complies with the given diet.

 Be sure patient is taking or eating food he can tolerate
After the Procedure

 Assess for patient’s condition; how he responds to the diet

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 Chronic Obstructive Pulmonary Disease: A Case 6

NURSING CARE PLAN

DECREASED CARDIAC OUTPUT

Nursing Scientific
Cues Objectives Nursing Interventions Rationale
Diagnosis Explanation

S=  Decreased A hypertensive Short 1. Assess other Enhances ideas to

cardiac pregnant Term: precipitating factors. prioritize things.
output r/t woman is
altered heart caused by After 2-3
O= pt. May hours oh
rate AEB sudden weight
manifest: nursing 2. Involve client in Enhances sense of
increased gain. This would
intervention formulation of plan of control and aids in
>pallor blood bring
s the pt. care at level of ability. cooperation and
pressure complications in
will be able maintenance of
>non- the body
to independence.
pitting/ because there is
pitting an inadequate demonstrat 3. Note presence, Bounding carotid,
edema blood pumped e stable quality of central and jugular, radial, femoral
by the heart to cardiac peripheral pulses. pulses may be
>hypertensi rhythm and
meet the observed or palpated.
on rate within
metabolic Pulses in the legs or
demands of the patient’s
>body feet may be
body, there is normal
malaise diminished, reflecting
an alteration of range. effects of
>variations her V/S vasoconstriction and
4. Monitor blood
in blood especially on venous congestion.
pressure of the patient.
pressure the blood Long
Measure in both
Term:
 Pregnancy-Induced Hypertension: A Case 6

>anxiety pressure and After 2-3 arms/thighs three Comparison of

and heart rate. As a days the pt. times, 3-5 min., then pressures provides a
restlessness result, a will be able sitting, then standing more complete picture
decreased to for initial evaluation. of vascular
volume blood participate Use correct cuff size involvement or scope
pumped by in activities and accurate technique. of the problem.
either ventricle that reduce
of the heart blood
each minute. pressure or 5. Observe skin color,
cardiac moisture, temperature
workload. and capillary refill Presence of pallor,
time. cool, moist skin and
delayed capillary refill
time may be due to
peripheral
6. Note independent or vasoconstriction.
general edema.
May indicate heart
failure, renal or
vascular impairment.
[Link] the
client with legs To promote venous
elevated return to the heart

8. Encourage leg
exercise such as flexion To improve blood flow
and extension of the and reduce venous
feet, active and stagnation
relaxation of the calf
muscles

9. Place the client in a

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 Pregnancy-Induced Hypertension: A Case 6

highfowler’s position

To decrease preload
and reduce pulmonary
10. Instruct the congestion
client the importance
of maintaining
regular physical
ability To promote circulation
and vascular health

11. Provide calm, restful

surroundings, minimize
environmental activity Can reduce stressful
or noise. stimuli produce
calming effect thereby
reduces blood
pressure.
12. Maintain activity
restrictions; provide
comfort measures, e.g.
back and neck Help reduce
massage, elevation of sympathetic
head. stimulation promotes
relaxation.

13. Instruct pt. in

relaxation technique
and guided imagery. Reduces physical
stress and tension that
affect blood pressure

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 Pregnancy-Induced Hypertension: A Case 6

and causes
hypertension.
14. Monitor response to
medications to control
high blood pressure.
Response to drug
therapy is dependent
on both individuals
well as the synergistic
effects of the drugs.
Because side effects,
drug interactions and
patient’s motivation
for taking
antihypertensive
medication, it is
important to use the
smallest number and
lowest dosage of
medications.

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 Chronic Obstructive Pulmonary Disease: A Case 6

INEFFECTIVE UTEROPLACENTAL TISSUE PERFUSION

Nursing Scientific
Cues Objectives Nursing Interventions Rationale
Diagnosis Explanation
S= Ineffective Preeclampsia is
uteroplacenta characterized
l tissue by an increased Short 1. Assist the patient in Decreases factors that
perfusion in blood Term: identifying lifestyle could lead to
O=patient adjustment (e.g., decreased perfusion of
related to pressure After 2
may avoiding prolonged oxygen to uterus,
vasospasm of resulting from hours of
manifest the sitting, sitting with placenta, and fetus
spiral arteries vasospasm of nursing
following: crossed legs, or
secondary to arteries (for this intervention
preeclampsia case, we are standing; developing
>edema s, the
pertaining to exercise plan for
patient will cardiovascular fitness
>maternal the spiral be able to during pregnancy;
blood artery) that verbalize avoiding wearing
pressure of causes understandi constrictive clothing;
160/100 vasoconstriction ng of maintaining a balance
mmHg . This then condition, diet with adequate
leads to therapy
>increased hydration) that may be
decrease in regimen
or needed because of
oxygen supply and side
decreased changes in physiologic
to the placenta effects of
fetal heart function during
which is medications Permits monitoring of
tone pregnancy.
otherwise cardiovascular
.
>positive known as response to illness
homan’s ineffective state and provides
sign uroplacental 2. Check and monitor early warning of
perfusion. Long vital signs hourly. perfusion problems.
 Pregnancy-Induced Hypertension: A Case 6

Term:

After 2-3 Provides early warning

days of of perfusion problems,
nursing 3. Monitor fetal heart and promotes early
intervention rate and well being. intervention.
, the
patient will
be able to It enhances
demonstrat uteroplacental
e increased 4. Institute O2, with an
initial volume of at least perfusion thereby
perfusion as decreasing fetal heart
individually 2L/min.
workload.
appropriate
(e.g. vital
signs,
especially
blood
To check for renal
pressure,
5. Monitor intake and perfusion and to
within
output every hour. determine fluid loss
client’s
and need for
normal
replacement or fluid
range and
excess which further
absence of
increases BP
edema)

6. Instruct the patient to

To promote placental
assume the left side
perfusion and prevent
lying position when
the compression of
lying down.
vena cava.

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 Pregnancy-Induced Hypertension: A Case 6

It reduces anxiety and

promotes rest. Both
7. Provide quiet, non- measures will assist in
stimulating maintaining peripheral
environment for the circulation by avoiding
patient. vasoconstriction.

It reduces anxiety and

provides teaching
opportunity.
8. Provide the patient
and family factual
information and support It assists in controlling
as needed. blood pressure.
Restriction of protein
helps limit BUN.
9. Provide low-sodium
diet (not more than 6g
daily or less than 2.5 g Provides support and
daily). Restrict intake fosters cost-effective
of protein. collaboration through
use of readily available
resources
10. Refer to other
health care
professionals as

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 Pregnancy-Induced Hypertension: A Case 7

necessary

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 Pregnancy-Induced Hypertension: A Case 7

ACTIVITY INTOLERANCE

Nursing Scientific
Cues Objectives Nursing Interventions Rationale
Diagnosis Explanation

S= Activity When there is a After 2-3 1. Assess for other Fatigue is a side effect
intolerance r/t high blood days the pt. precipitators or causes of some medications.
imbalance pressure, there will be able of treatment and pain. Pain and stressful
oxygen is an to achieve regimens also extract
O=
supply and inadequate measurable energy and produce
Pt. may demand AEB blood flow. increase in fatigue.
manifest abnormal Inadequate activity
heart rate or blood flow intolerance, 2. Involve client in
-pallor blood decreases the evidenced formulation of plan of Enhances sense of
pressure nutrients and by reduced care at level of ability control and aids in
>non-pitting
response oxygen in the fatigue and cooperation and
edema
tissues in the weakness maintenance of
>hypertensi body as well as and by V/S independence.
on in metabolic within
demands. By acceptable 3. Assess the patient’s
>body then, a person limits during response to activity,
malaise will not be able activity. nothing pulse rate more The stated parameters
to meet her than 20 beats/min. are helpful in
>variations assessing physical
desired faster than resting rate ;
in blood responses to the stress
activities marked increase in
pressure of activity and if
because of blood pressure during
depleted energy or after activity; present are indicators
>anxiety
that the body dyspnea or chest pain; of over exertion.
and
restlessness needs to sustain excessive fatigue and
normal weakness; diaphoresis;
metabolic rate. dizziness or syncope.

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 Pregnancy-Induced Hypertension: A Case 7

4. Determine current Comprehensive

cap[abilities and functional assessment
barriers to participation includes independent
in self care. performance of basic
ADLs, social activities,
sensory abilities,
cognition and ability to
ambulate.

5. Evaluate accelerating
activity intolerance. May denote increasing
cardiac
decompensation rather
than over activity.

6. Provide assistance
with self-care activity as Meets client’s personal
indicated, intersperse care needs without
activity period with rest undue myocardial
period. stress or excessive
oxygen demand.

7. Instruct client
energy-conserving Energy saving
techniques. techniques reduced
the energy
expenditures, thereby
assisting in

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 Pregnancy-Induced Hypertension: A Case 7

equalization of oxygen
supply and demand.

Gradual activity
8. Encourage intolerance
progressive activity progression prevents a
when tolerated. sudden increase in
cardiac workload.

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 Chronic Obstructive Pulmonary Disease: A Case 7

DISCHARGE PLANNING

M- Instructed the patient to take the following home medication as ordered by the physician.

E- Instructed patient to avoid strenuous activities and practice deep breathing exercise.

Instructed patient that she may resume regular exercise as tolerated.

T- n/a

H- Emphasized the importance of breast feeding.

Instructed patient to have proper hygiene.

Instructed patient to continue oral medication as prescribed by the physician.

O- Advice patient to have follow up check up after 1 week.

D- LSLF
 Pregnancy-Induced Hypertension: A Case 7

LEARNING DERRIVED

A case study is a requirement which all nursing students must complete in order to gain
the appropriate knowledge, skills, and attitude in the field of nursing. It allows the students to
delve into the synthesis and meaning of the disease, the signs and symptoms, as well as the
corresponding nursing care management for the case. A book-based case study is no different,
and in actuality, students are given the opportunity to learn beyond what clients may feel and
into the different dimensions of the disease. In short, the case is not limited to merely the
treatments of the patient to his or her signs and symptoms.

In the four days it took to complete this case study, it can be said that the students have
really learned alot about the “toxemia of pregnancy” or pregnancy induced hypertension. It eas
also beneficial on the part of the group because the case served as a review on previous lessons
discussed in NCM 101. In completing this case, however, the group encountered many
difficulties and one such difficulty was the creation of the pathophysiology.

Many books and researches have different theories on the development of PIH and the
etiology of the disease. Some theories explain the phenomenon as a result of a “toxin” whilst
others go into an explanation of the possibility of a “uterine stretch” from the growing fetus,
which in turn causes ischemia and vasoconstriction. In an effort to include these well-respected
theories of different doctors, the student nurses briefly explained each in order to bring to light a
possible explanation to the occurance of the disease process.

Although it remains true that his case study was difficult to accomplish due to a lack of
supporting evidence to elaborate the occurance of this disease, still, many learnings regarding the
case have been derived. Despite the sleepless nights sacrificed to complete the case study, the
efforts in the end have paid [Link] though the case had been done in such a busy and turbulent
time (CON days), still the manuscript serves as proof that with the belief and faith in God and
the unity of team work, all things are possible. PRAISE BE TO GOD!

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 Pregnancy-Induced Hypertension: A Case 7

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Gutierrez, K. J., Peterson, P.G. (2007). Saunders sursing survival guide pathophysiology.
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Stockley, R. A. (2007). Chronic obstructive pulmonary disease. Chicago, IL. Wiley-

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Spratto, G.R., Woods, A.L. (2004). PDR nurse’s drug handbook. Springfield, IL.
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Wallach, J.B. (2007). Interpretation of diagnostic tests: Doody’s all reviewed collection.
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Lam, M., (2010) Estrogen Dominance: The silent epidemic. The Authority on Natural
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