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I.

INTRODUCTION:
Preeclampsia is defined as a pregnancy-specific syndrome observed after the 20th week
of pregnancy with systolic blood pressure of >= 140 mm Hg or diastolic blood pressure of >= 90
mmHg, accompanied by significant proteinuria. Previous definitions included edema as part of
the diagnosis, but this has subsequently been dropped as being too non-specific. Likewise, the
criteria of a 30-point change in systolic blood pressure or a 15-point change in diastolic blood
pressure have been eliminated for the same reason in favor of an absolute blood pressure
threshold.

Differentiating between worsening hypertension and preeclampsia superimposed on


chronic hypertension is challenging especially to those mother who present pregnancy late for
OB care. The Preeclampsia superimposed is classified by this facts. Hypertension in pregnancy
with onset of proteinuria of more than 300 mg. protein in a 24- hour collection. Hypetension and
proteinuria before 20 weeks age of gestation. A sudden increase in the proteinuria in a woman
with chronic hypertension. a sudden increase in BP who has been controlled.
Thrombocytopenia(platelet count less than 100,000), increase SGOT (AST) or SGPT (ALT)

Preeclampsia is the most common hypertensive disorder during pregnancy, affecting an


estimated 5-8% of pregnant women annually in the United States, and has the greatest effect on
maternal and infant outcome. Chronic hypertension affects an increasing proportion of
pregnancies, and confers significant risk for the development of preeclampsia. Preeclampsia
occurs more frequently and is more severe in women with preexisting hypertension than in
women who are normotensive prior to pregnancy. From a public health perspective, it is
alarming that the rate of preeclampsia has increased by nearly one-third over the past decade,
likely due to a rise in the number of older mothers and multiple births, scenarios that predispose
to preeclampsia. Older maternal age during pregnancy also contributes to an increased frequency
of chronic hypertension and thus preeclampsia complicating pregnancy.

Maternal complications acutely can include pulmonary edema, thrombotic complications,


renal failure, and death. Preeclampsia can evolve into eclampsia, leading to maternal seizures.
One specific subset of signs and symptoms known as the HELLP Syndrome (Hemolysis,
Elevated Liver Enzymes, and Low Platelets) is a cause of extensive morbidity. The vague nature
of the presenting complaints can make the diagnosis of HELLP syndrome frustrating to
physicians. Approximately 90 percent of patients present with generalized malaise, 65 percent
with epigastric pain, 30 percent with nausea and vomiting, and 31 percent with headache.
Because early diagnosis of this syndrome is critical, any pregnant woman who presents with
malaise or a viral-type illness in the third trimester should be evaluated with a complete blood
cell count and liver function tests.

In the United States, hypertensive disorders of pregnancy account for nearly 15 percent of
maternal mortality; throughout the world these conditions are responsible for more than a third of
maternal deaths. The vast majority of these deaths and most infant deaths are due to
preeclampsia and eclampsia, arising either de novo or superimposed on chronic hypertension.
Long-term sequelae may also result. Women with chronic hypertension have an obvious long-
term risk from the persistent hypertension. However, women with preeclampsia, despite the
resolution of the disorder postpartum, are also at increased risk of cardiovascular disease in later
life compared to women with pregnancies without preeclampsia.

Two millennia ago, Celsus described puerperal seizures, termed eclampsia. In the late
19th century, it was recognized that increased blood pressure and proteinuria preceded the
seizures. Soon thereafter, physicians realized that these findings constituted the syndrome of
preeclampsia, which increased maternal and infant mortality and morbidity even if seizures did
not occur. Over the past decade, a great deal of attention has been focused on understanding the
pathophysiology of preeclampsia to assist in devising therapeutic interventions for subsequent
assessment. This has resulted in a better understanding of the pathophysiological mechanisms,
but many details remain unclear. In addition, clinical trials testing two promising therapies,
calcium supplementation and aspirin, to prevent preeclampsia or improve its outcome,
demonstrated at most minor benefits. Progress has been limited by the lack of animal models
with placental physiology comparable to humans. In contrast to preeclampsia, in chronic
hypertension where prior knowledge of pathophysiology of the disease in nonpregnant women
provides useful insight to treatment, little work has been done to apply these insights to therapy
for women with hypertension who become pregnant.

Infections of the urinary tract are the second most common type of infection in the body.
Urinary tract infections (UTIs) account for about 8.3 million doctor visits each year. Women and
pregnant mothers are especially prone to UTIs for reasons that are not yet well understood. One
woman in five develops a UTI during her lifetime. UTIs in men are not as common as in women
but can be very serious when they do occur.

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%.

This study wants to lessen the prevalence of this complication among pregnant woman in
order to decrease maternal and newborns mortality rate in our country. Nurses who play an
important role in the health care delivery system should expand and reach out people in the
community about the preeclampsia, HELLP Syndrome and their complications. By pursuing the
government’s project on Information, Education and Communication (IEC) about this disease,
surely will decrease the statistics of its incedence not only in our country but worldwide.

Our study focused in a case of a Chronic Hypertension with Superimposed Preeclampsia


Severe T/C CVA Bleed; HELLP Syndrome UTI of patient Liza. A 27 year old woman who has a
poor OB history for her 4 pregnancies. This study will enlighten and clarify questions and
misconceptions about the disease. It also very helpful especially to the members of health team
in rendering quality services to both the mother and the newborn.
II. PATIENT’S PROFILE

NAME: Liza

ADDRESS: San Francisco De Asis, Matina Crossing, Davao City


AGE: 27 years old

RELIGION: Roman Catholic

BIRTHDAY: March 25,1983

SEX: Female

NATIONALITY: Filipino

DATE OF ADMISSION: March 16, 2011

TIME: 11:00 pm

INSTITUTION: Southern Philippines Medical Center

DATE DISCHARGED:?

TIME:?

DIAGNOSIS: Pregnancy Uterine 21 5/7 Weeks Age of Gestation Cephalic In PreTerm labor
Gravida 4 Para 3 (1201), Chronic Hypertension with Superimposed Preeclampsia Severe T/C
CVA Bleed, Poor OB History; HELLP Syndrome;UTI
OBJECTIVES OF THE STUDY

GENERAL OBJECTIVES

Client Centered

• To assess the health of the patient

• To develop, implement, and evaluate plans for health promotion

• To provide client education and involve patient in implementing therapeutic regimen to


promote understanding and compliance.

Nurse Centered

• To apply the nursing process in the care of the hospitalized patient

• To describe effects of illness on individuals and family members’ roles and functions

SPECIFIC OBJECTIVES

Client-Centered

• Discuss indications for and management of pregnant clients

• Discuss nursing implications for medications commonly prescribed for pregnant

• Describe nursing care for the client

• Use the nursing process to provide individualized care for clients who has experienced pre-
eclampsia, HELLPS Syndrome and UTI

• Support client and family, and encourage them to ask questions so that information could be
clarified and understood

Nurse-Centered

• Identify major risk factors influencing the said condition.

• Identify the risk factor contributing to the occurrence of the disease.

• Learn the pathophysiology and manifestations of pre-eclampsia, HELLPS Syndrome and UTI

• Identify common diagnostic tests used for the said condition and their nursing implications.

• Identify and describe nursing measure to promote awareness in the condition


III. NURSING HISTORY

PAST HEALTH HISTORY

Liza experienced measles, mumps, and chickenpox as a child. She also experienced
diarrhea, fever, cough, colds and self-medicates with over the counter medications like
paracetamol and cough medications before she became pregnant. She has completed all her
immunizations and including three shots of tetanus toxoid during her prenatal visits. She has no
known allergies. She was never been hospitalized before. This was the first time patient she was
admitted in the hospital. She has taken prescribed ferrous sulfate regularly at home.

On June 1998, when she was 5 years old, patient had Dengue Hemorrhagic Fever and had
been hospitalized for 2 weeks at Montero Hospital in Malita.

On September 2007, she gave birth to her first baby through Normal Spontaneous
delivery at Malita Provincial Hospital. She was diagnosed to have Pregnancy Induced
Hypertension with a blood pressure of 160/ 120 mmHg and confined at the said hospital for
about 2 weeks.

On July 2009, she gave birth to her second baby at Davao Regional Hospital; the baby
was delivered preterm by 28 weeks AOG. She was diagnosed again to have Pregnancy Induced
hypertension with a blood pressure of 260/ 120 mmHg and confined at the said hospital for 2
weeks. Other than this she has no known chronic illnesses and endures only an occasional cough
and cold.

History of Present Illness

2 months prior to admission, patient visited their health center for her prenatal check up
and found out her Blood pressure of 180/110 mmHg. The Physician referred her to SPMC for
further evaluation but the patient refused due to fear of hospitalization.
1 month prior to admission, patient visited their health center for her 2nd prenatal check
up, her BP shoot up to 190/130 mmHg, Physician prescribed Nifedipine and Captopril and
patient complied with those medications but no BP monitoring done after the prenatal check up.
1 week prior to admission, patient fell down from the table due to an accident. Her head
hit the floor and caused severe headache and experienced tinnitus. No medications taken and
patient continued to do her activities of daily living such as managing her own “sari-sari” store.
1 day prior to admission, patient experienced facial asymmetry, sudden paralysis of the
left side of the body, sudden troubled speaking, numbness, dizziness, orbital edema and loss of
blinking reflex. No consultation done due to fear of hospitalization.
1 hour prior to admission, the patient’s neighbor took the patient’s BP and the result was
260/150. Then the family rushed the patient to SPMC OB-ER.
Family History and Socio-cultural Background

Patient X is the eldest among seven siblings. Her mother passed away due to
cerebrovascular accident. Her father was known hypertensive and died also due to cerebral
vascular accident. The eldest, 4th, 5th and her youngest siblings are currently in good condition
while the 2nd and her 3rd siblings are known hypertensive. Based on the genogram, the patient has
higher risk to acquire hypertensive disorder.

The patient is High School graduate and she is self employed. She has her own small
sari-sari store that supports their daily needs. She got married at the age of 24 years old and have
____ children. Her husband is a tricycle driver who earns 200-300 pesos per day.

Patient X was raised as Roman Catholic, were she learned about religious values but she
still believes in super natural forces and superstitious beliefs. When it comes to health matters,
she seeks the help of an albularyo and uses herbal medicines to treat their illnesses. But when
serious matters arise they still refer to medical professionals for help.

Lifestyle

The patient does not smoke. Her husband and relatives that share the same residence as
her are heavy smokers, consuming approximately 1-2 packs per day. She has sedentary lifestyle.
Her hobbies are watching t.v, taking charge with her small sari-sari store and playing mahjong
with her friends. Her diet consists frequently of her favorite dish “bulad” and “ginamus” with
tomatoes. She catches sleep at 8 in the evening and usually wakes at 6 in the morning.

Community Resources

Patient X resides in an urban type of community. Her home is located near the Matina
Health Center, where she usually goes for pre-natal check up. The modes of transportation in
their community are jeepneys and tricycles.
IV. ANATOMY AND PHYSIOLOGY
Central Nervous System
Cerebrum; is the largest and most developmentally advanced part of the human brain. It is
responsible for several higher functions, including higher intellectual function, speech, emotion,
integration of sensory stimuli of all types, initiation of the final common pathways for
movement, and fine control of movement.
The cerebrum is divided into a right and a left hemisphere and is composed of pairs of frontal,
parietal, temporal, and occipital lobes.
The left hemisphere controls the majority of functions on the right side of the body, while the
right hemisphere controls most of functions on the left side of the body The crossing of nerve
fibers takes place in the brain stem. Thus, injury to the left cerebral hemisphere produces sensory
and motor deficits on the right side, and vice versa.
Cerebellum; the second largest area, is responsible for maintaining balance and further control
of movement and coordination.
Brain stem; is the final pathway between cerebral structures and the spinal cord. It is responsible
for a variety of automatic functions, such as control of respiration, heart rate, and blood pressure,
wake-fullness, arousal and attention.
Medulla Oblongata; relays motor and sensory impulses between other parts of the brain and the
spinal cord. Reticular formation (also in pons, midbrain, and diencephalon) functions in
consciousness and arousal. Vital centers regulate heartbeat, breathing (together with pons) and
blood vessel diameter.
Hypothalamus; controls and intergrates activities of the autonomic nervous system and pituitary
gland. Regulates emotional and behavioral patterns and circadian rhythms. Controls body
temperature and regulates eating and drinking behavior. Helps maintain the waking state and
establishes patterns of sleep. Produces the hormones oxytocin and antidiuretic hormone.
Cardiovascular System
Heart; lies in the mediastinum, behind the body of the sternum. The shape of the heart tends to
resemble the chest. The heart has chambers divided into four cavities with the right and left
chambers (atria and the ventricles) separated by the septum. It pumps the blood to circulate
properly.

Baroreceptor, pressure-sensitive sensory receptors, are located in the aorta, internal carotid
arteries, and other large arteries in the neck and chest. They send impulses to the cardiovascular
center in the medulla oblongata to help regulate blood pressure. The two most important
baroreceptor reflexes are the carotid sinus reflex and the aortic reflex.
Chemoreceptors, sensory receptors that monitor the xhemical composition of blood, are located
close to the baroreceptors of the carotid sinus and the arch of the aorta in small structures called
carotid bodies and aortic bodies, respectively. These chemoreceptors detect changes in blood
level of O2, CO2, and H+.
Endocrine System

Renin-Angiotensin-Aldosterone system. When blood volume falls or blood flow to the kidneys
decreases, juxtaglomerular cells in the kidneys secrete renin into the bloodstream. In sequence,
renin and angiotensin converting enzyme (ACE) act on their substrates to produce the active
hormone angiotensin II, which raises blood pressure in two ways. First, angiotensin II is a potent
vasoconstrictor; it raises blood pressure by increasing systemic vascular resistance. Second, it
stimulates secretion of aldosterone, which increases reabsorption of sodium ions and water by
the kidneys. The water reabsorption increases total blood volume, which increases blood
pressure.
Antidiuretic hormone. ADH is produced by the hypothalamus and released from the posterior
pituitary in response to dehydration or decreased blood volume. Among other actions, ADH
causes vasoconstriction, which increases blood pressure.
Atrial Natriuretic Peptide. Released by cells in the atria of the heart, ANP lowers blood
pressure by causing vasodilation and by promoting the loss of salt and water in the urine, which
reduces blood volume.
Liver; is a reddish brown organ with four lobes of unequal size and shape. A human liver
normally weighs 1.4–1.6 kg (3.1–3.5 lb), and is a soft, pinkish-brown, triangular organ. It is both
the largest internal organ (the skin being the largest organ overall) and the largest gland in the
human body.

This organ plays a major role in metabolism and has a number of functions in the body,
including glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone
production, and detoxification. It lies below the diaphragm in the abdominal-pelvic region of the
abdomen. It produces bile, an alkaline compound which aids in digestion via the emulsification
of lipids. The liver's highly specialized tissues regulate a wide variety of high-volume
biochemical reactions, including the synthesis and breakdown of small and complex molecules,
many of which are necessary for normal vital functions. The various functions of the liver are
carried out by the liver cells or hepatocytes.

Reproductive System

Ovaries; it is an almond-shape organ. It contains the ova and is responsible in expelling the
ova. It also produces estrogen and progesterone.

Fallopian Tubes; is approximately 10-12 cm. It has three parts the isthmus, ampulla, and the
indifublum. Fertilization happen in the ampulla.

Uterus; is the organ for implantation and pregnancy. it is a pear shaped organ which has 3 parts;
fundus, corpus, and the isthmus. It gives nourishment to a growing fetus

Pathophysiology (Book Based)

Predisposing Factors: Precipitating Factors:

Multiparity Chronic renal disease

Age>25y.o Chronic hypertension

American race Antiphospholipid syndrome

Genetic (Family history) Diabetes mellitus


History of Poor Pregnancy out come Twin gestation

High body mass index

Angiotensinogen gene T235

Endothelial Injury ( Triggered by Pregnancy)---Continuation at the next page

Sensitivity to AngiotensinII

Peripheral and Vascular Vasospasm

O2 supply- Hypertension

Kidney Liver Eyes


Placenta

Tissue Ischemia Retinal Constriction


Placental

Glomerular Dec. GFR Liver Edema Blurred Vision Degeneration

Degeneration Epigastric Pain Scotoma-Spots IUGR

Inc. Permeability Inc. Na Reabsorption in the Eyes Preterm


Birth

Proteinuria Inc. Water Retention Convulsion Reversible Blindness

Fluid shift from Upper and Lower

Intracellular to Extremities Edema Inc. Cerebral Irritability

Extracellular Anasarca

(Generalized Body Edema) Cerebral Congestion


Lungs Heart Brain

Pulmonary Edema CHF Cerebral Edema

Endothelial Injury ( Triggered by Pregnancy)

Fibrin forms crosslinked networks in the small blood vessels

Microangiopathic Hemolytic Anemia d/t RBC is forced through a strainer

Platelet consumed

Liver cells suffers ischemia

DIC

Paradoxical Bleeding

CVA (Possible)

UTI

Predisposing factors: Precipitating factors:


• Age – UTI is a prevalent • Inadequate access to toilet facilities
disease among children and • Avoidance of the urge to void
elderly • Urinary catheterization
• Sex – it has a higher • Fistula between the intestine and
incidence rate with the bladder
female gender • Inadequate fluid intake
• Pregnancy, and DM

Bacterial invasion (i.e. E.coli)

Multiplication of the bacteria – causing


UTI in any part of the urinary tract

Change in Urine Color Immune response by the body (defense Inc. WBC subsequent
mechanism of the body to foreign bodies) to pus formation
Interruption in the normal homeostatic
environment of the urinary tract

Body induces the


action of the cytokines
and prostaglandins

Cytokine and
prostaglandin release

The body responds by Inflammation of the lining of Irritation of the lining of


producing physiologic the urinary tract urinary tract
changes aimed at elevating Urethritis and Spasm of the

body temperature Narrowed urine passage dysuria bladder

Fever Poor emptying of bladder


Frequent Urination, Urgency Urinary Incontinence
and nocturia

Pathophysiology (Problem Based)

Predisposing Factors: Precipitating Factors:

Multiparity(G4P3)

Age>25y.o Chronic hypertension

Genetic (Family history)

History of Poor Pregnancy out come

Endothelial Injury ( Triggered by Pregnancy)-----Continuation at the next page


Sensitivity to AngiotensinII

Peripheral and Vascular Vasospasm

O2 supply- Hypertension

Kidney Liver Eyes


Placenta

Tissue Ischemia Retinal Constriction


Placental

Glomerular Dec. GFR Liver Edema Blurred Vision Degeneration

Degeneration Epigastric Pain IUGR

Inc. Permeability Inc. Na Reabsorption Preterm Birth

Proteinuria Inc. Water Retention Convulsion

Fluid shift from Upper and Lower

Intracellular to Extremities Edema Inc. Cerebral Irritability

Extracellular Anasarca

(Generalized Body Edema) Cerebral Congestion

Lungs Heart Brain

Pulmonary Edema Cerebral Edema


Endothelial Injury ( Triggered by Pregnancy)

Fibrin forms crosslinked networks in the small blood vessels

Microangiopathic Hemolytic Anemia d/t RBC is forced through a strainer

Platelet consumed

Liver cells suffers ischemia

DIC

Paradoxical Bleeding

CVA (Possible)

UTI

Predisposing factors: Precipitating factors:


•Sex – it has a higher • Inadequate access to toilet facilities
incidence rate with the • Avoidance of the urge to void
female gender • Urinary catheterization
• Inadequate fluid intake
• Pregnancy

Bacterial invasion (i.e. E.coli)

Multiplication of the bacteria – causing


UTI in any part of the urinary tract

Change in Urine Color Immune response by the body (defense Inc. WBC subsequent
mechanism of the body to foreign bodies) to pus formation

Interruption in the normal homeostatic


environment of the urinary tract

Body induces the


action of the cytokines
and prostaglandins

Cytokine and
prostaglandin release

The body responds by Inflammation of the lining of Irritation of the lining of


producing physiologic the urinary tract urinary tract
changes aimed at elevating Urethritis and Spasm of the

body temperature Narrowed urine passage dysuria bladder

Fever Poor emptying of bladder


Frequent Urination, Urgency Urinary Incontinence
and nocturia

Narrative Pathophysiology
The general consensus is that preeclampsia is an endothelial cell disorder resulting in
mild-to-severe microangiopathy of target organs such as brain, liver, kidney, and placenta.While
hypertension may be the most common presenting symptom, it should not be viewed as the
initial pathogenetic process. Evidence of other organ involvement before hypertension becomes
fulminant is not uncommon. Several circulating markers of endothelial cell injury have been
shown to be elevated in women who develop preeclampsia before they became symptomatic.
These include endothelin, cellular fibronectin, plasminogen activator inhibitor-1, and altered
prostacyclin/thromboxane profile.Evidence to date suggests that oxidative stress; circulatory
maladaptation; inflammation; and humoral, mineral, and metabolic abnormalities may all
contribute to endothelial dysfunction and pathogenesis of preeclampsia.
Furthermore, it shows that persisting symptoms will make patient’s body sensitive to
AngiotensinII thus presenting manifestations occurs.

Many investigators believe that the placenta is the trigger for endothelial cell injury.
Evidence suggests that hypoperfused placentas produce various factors that are capable of
injuring endothelial cells. Recent data suggest that circulating factors that interfere with the
action of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) play a
major role in maternal manifestation of the disorder.

Placental hypoperfusion or ischemia in preeclampsia has many causes. Preexisting


vascular disorders such as hypertension and connective tissue disorders can result in poor
placental circulation. In cases of multiple gestation or increased placental mass, it is not
surprising for the placenta to become underperfused. However, most women who develop
preeclampsia are healthy and do not have underlying medical conditions. In this group of
women, abnormally shallow placentation has been shown to be responsible for placental
hypoperfusion.

The shallow placentation noted in preeclampsia is a result of the inability of trophoblasts


to invade the decidual vessels. In normal pregnancies, a subset of cytotrophoblasts called
invasive cytotrophoblasts migrate through the implantation site and invade decidua tunica media
of maternal spiral arteries and replace its endothelium in a process called pseudovascularization.8
As a result of these changes, these vessels undergo transformation from small muscular arterioles
to large capacitance, low-resistance vessels. This allows increased blood flow to the maternal-
fetal interface. Remodeling of these arterioles probably begins in the first trimester and ends by
18-20 weeks' gestation. However, the exact gestational age at which the invasion stops is
unknown.

In preeclampsia, this invasion of the decidual arterioles is incomplete. The invasive


cytotrophoblasts fail to replace tunica media, resulting in mostly intact arterioles that are capable
of vasoconstriction. Histologic evaluation of the placental bed demonstrates few cytotrophoblasts
beyond the decidual layer. The trophoblast differentiation along the invasive pathway involves
alteration in the expression of a number of different classes of molecules, including cytokines,
adhesion molecules, extracellular matrix, metalloproteinases, and the class Ib major
histocompatibility complex molecule, HLA-G.

Primary cause for the failure of these invasive cytotrophoblasts to undergo


pseudovascularization and invade maternal blood vessels is not clear. However, immunologic
and genetic factors have been proposed. In addition, early hypoxic insult to differentiating
cytotrophoblasts has been proposed as a contributing factor. However, these hypotheses need to
be tested further.

Endothelium regulates vascular permeability, vassal tone, and coagulation cascade. While
not all the factors produced by the placenta responsible for endothelial dysfunction have been
characterized, recent data show that an imbalance of pro- and anti-angiogenic factors produced
by the placenta may play a major role in mediating endothelial dysfunction. The circulating
proangiogenic factors secreted by the placenta include VEGF and PlGF. Other substances that
have been proposed, but not proven, to contribute to this process include tumor necrosis factor,
interleukins, various lipid molecules, and syncytial knots.

Angiogenesis is critical for successful placentation. Both VEGF and PlGF promote
angiogenesis by interacing with the VEGF receptor family. While both growth factors are
produced by placenta, the serum level of PlGF rises much more significantly in pregnancy.
Taylor et al demonstrated that the serum level of PlGF decreased in women who later developed
preeclampsia. The fall in serum level was notable as early as the second trimester in women who
developed preeclampsia and intrauterine growth restriction. In 2003, Maynard et al observed that
the serum levels of both VEGF and PlGF were decreased in women with preeclampsia.
However, the magnitude of decrease was less pronounced for VEGF since its serum level was
not as high as PlGF, even in normal pregnancy. Others have confirmed this finding and showed
that the serum level of PlGF decreased in women before they developed preeclampsia.

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


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

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


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

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

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

The exact cause of HELLP is unknown, but general activation of the coagulation cascade
is considered the main underlying problem. Fibrin forms crosslinked networks in the small blood
vessels. This leads to a microangiopathic hemolytic anemia: the mesh causes destruction of red
blood cells as if they were being forced through a strainer. Additionally, platelets are consumed.
As the liver appears to be the main site of this process, downstream liver cells suffer ischemia,
leading to periportal necrosis. Other organs can be similarly affected. HELLP syndrome leads to
a variant form of disseminated intravascular coagulation (DIC), leading to paradoxical bleeding,
which can make emergency surgery a serious challenge.

HELLP syndrome is a rare but serious illness in pregnancy. This illness can start quickly,
most often in the last 3 months of pregnancy (the third trimester). It can also start soon after you
have your baby. HELLP stands for Hemolysis, Elevated Liver enzyme levels and a Low Platelet
count. These are problems that can occur in women who have this syndrome.

Women who have HELLP syndrome may have bleeding problems, liver problems and
blood pressure problems that can hurt both the mother and the baby.

Infections of the urinary tract are the second most common type of infection in the body.
Urinary tract infections (UTIs) account for about 8.3 million doctor visits each year. Women are
especially prone to UTIs for reasons that are not yet well understood. One woman in five
develops a UTI during her lifetime. UTIs in men are not as common as in women but can be very
serious when they do occur. Pregnant women are at increased risk for UTIs. Beginning in week 6
and peaking during weeks 22 to 24, approximately 90 percent of pregnant women develop
ureteral dilatation, which will remain until delivery (hydronephrosis of pregnancy). Increased
bladder volume and decreased bladder tone, along with decreased ureteral tone, contribute to
increased urinary stasis and ureterovesical reflux. Additionally, the physiologic increase in
plasma volume during pregnancy decreases urine concentration. Up to 70 percent of pregnant
women develop glycosuria, which encourages bacterial growth in the urine. Increases in urinary
progestins and estrogens may lead to a decreased ability of the lower urinary tract to resist
invading bacteria. This decreased ability may be caused by decreased ureteral tone or possibly by
allowing some strains of bacteria to selectively grow.These factors may all contribute to the
development of UTIs during pregnancy.

The urinary tract, from the kidneys to the urethral meatus, is normally sterile and resistant
to bacterial colonization despite frequent contamination of the distal urethra with colonic
bacteria. Mechanisms that maintain the tract's sterility include urine acidity, emptying of the
bladder at micturition, ureterovesical and urethral sphincters, and various immunologic and
mucosal barriers.

About 95% of UTIs occur when bacteria ascend the urethra to the bladder and, in the case
of acute uncomplicated pyelonephritis, ascend the ureter to the kidney. The remainder of UTIs
are hematogenous. Systemic infection can result from UTI, particularly in the elderly. About
6.5% of cases of hospital-acquired bacteremia are attributable to UTI.

CAUSATIVE AND ETIOLOGIC FACTORS

PREECLAMPSIA AND HELLP SYNDROME

The etiology of preeclampsia and HELLP Syndrome is unknown. At present, 4 hypotheses are
the subject of extensive investigation, as follows:

(1) Placental ischemia-Increased trophoblast deportation, as a consequence of ischemia, may


inflict endothelial cell dysfunction.

(2) Very low-density lipoprotein versus toxicity-preventing activity-In compensation for


increased energy demand during pregnancy, nonesterified fatty acids are mobilized. In women
with low albumin concentrations, transporting extra nonesterified fatty acids from adipose tissues
to the liver is likely to reduce albumin's antitoxic activity to a point at which very-low density
lipoprotein toxicity is expressed.

(3) Immune maladaptation-Interaction between decidual leukocytes and invading


cytotrophoblast cells is essential for normal trophoblast invasion and development. Immune
maladaptation may cause shallow invasion of spiral arteries by endovascular cytotrophoblast
cells and endothelial cell dysfunction mediated by an increased decidual release of cytokines,
proteolytic enzymes, and free radical species.

(4) Genetic imprinting-Development of preeclampsia-eclampsia may be based on a single


recessive gene or a dominant gene with incomplete penetrance. Penetrance may be dependent on
fetal genotype. The possibility of genetic imprinting should be considered in future genetic
investigations of preeclampsia.

Urinary Tract Infection


Commensal colonic gram-negative aerobic bacteria cause most bacterial UTIs. In relatively
normal tracts, strains of E. coli with specific attachment factors for transitional epithelium of the
bladder and ureters are the most frequent causes. The remaining gram-negative urinary
pathogens are other enterobacteria, especially Klebsiella , Proteus mirabilis, and Pseudomonas
aeruginosa. Enterococci (group D streptococci) and coagulase-negative staphylococci (eg,
Staphylococcus saprophyticus) are the most frequently implicated gram-positive organisms.

SYMPTOMATOLOGY

PREECLAMPSIA AND HELLP SYNDROME

-Visual disturbances typical of preeclampsia are scintillations and scotomata. These disturbances
are presumed to be due to cerebral vasospasm.
-Headache is of new onset and may be described as frontal, throbbing, or similar to a migraine
headache.
-Epigastric pain is due to hepatic swelling and inflammation, with stretch of the liver capsule.
Pain may be of sudden onset, is typically constant, and may be moderate to severe in intensity.
-While mild lower extremity edema is common in normal pregnancy, rapidly increasing or
nondependent edema may be a signal of developing preeclampsia. Edema is no longer included
among the criteria for diagnosis of preeclampsia.
-Rapid weight gain is a result of edema due to capillary leak as well as renal sodium and fluid
retention.
-Retinal vasospasm is a severe manifestation of maternal disease; consider delivery.
-Retinal edema is known as serous retinal detachment. This can manifest as severely impaired
vision if the macula is involved. It generally reflects severe preeclampsia and should lead to
prompt consideration of delivery. The condition typically resolves upon completion of pregnancy
and resolution of the hypertension and fluid retention.
-Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular
stretch. Consider delivery.
-Brisk, or hyperactive, reflexes are common during pregnancy. Clonus is a sign of
neuromuscular irritability that usually reflects severe preeclampsia.
-In most normal pregnancies, the woman has some lower extremity edema by the third trimester.
In contrast, a sudden worsening in dependent edema, edema in nondependent areas (such as the
face and hands), or rapid weight gain suggest a pathologic process and warrant further evaluation
for preeclampsia. Common symptoms in women with the HELLP syndrome include a general
feeling of feeling unwell (malaise), nausea and/or vomiting, and pain in the upper abdomen.
Increased fluid in the tissues (edema) is also frequent. Protein is measurable in the urine of most
women with the HELLP syndrome. Blood pressure may be elevated. Occasionally, coma can
result from seriously low blood sugar
Urinary Tract Infection

Lower urinary tract infection (cystitis): The lining of the urethra and bladder becomes inflamed
and irritated.

-Dysuria: pain or burning during urination


-Frequency: more frequent urination (or waking up at night to urinate, sometimes referred to as
nocturia); often with only a small amount of urine
-Urgency: the sensation of having to urinate urgently
-Hesitancy: the sensation of not being able to urinate easily or completely (or feeling that you
have to urinate but only a few drops of urine come out)
-Cloudy, bad-smelling, or bloody urine
-Lower abdominal pain
-Mild fever (less than 101 F), chills, and "just not feeling well" (malaise)

Upper urinary tract infection (pyelonephritis): Symptoms develop rapidly and may or may not
include the symptoms for a lower urinary tract infection.

-Fairly high fever (higher than 101 F)


-Shaking chills

-Nausea
-Vomiting
-Flank pain: pain in your back or side, usually on only one side at about waist level

V. NURSING ASSESSMENT

Nursing Assessment (Problem-Based) -----WITH EMPHASIS ON ABNORMALITIES-


SAMPLE ONLY

Neurologic:
LOC: drowsy to stuporous, 3-4 mm pupil size anisocoric, with brisk reaction to light; GCS – 9
(E4- Spontaneous eye opening V1- none/mechanical ventilation M4 – withdraws to pain) (+)
doll’s eye reflex (+) babinski on right foot (-) corneal reflex, no visual threat
Respiratory
Patient is hooked to a mechanical ventilator through a tracheostomy. Ventilator set-up:
350/30/14/AC/5. (+) crackles on both lung fields. With equal breath sounds.

Cardiac
With atrial fibrillation; fine course, with occasional unifocal PVC’s. HR = 97 BP= 120’s-
130’s/60’s-70’s.

Musculo-Skeletal
No contractures noted but there was stiffness noted at the right wrists and both ankle joints; with
normal muscle tone and non-spontaneous movement; with severe weakness on both upper and
lower extremities.

Hematologic
Latest PTPA: INR = 1.02 Act = 98%

DIAGNOSTIC AND LABORATORY STUDIES (CP PREECLAMPSIA EXCEL)

CT scan of the brain


• Perform a CT scan to exclude cerebral hemorrhage in the setting of seizures, severe
headache, or altered level of consciousness, as depicted in the image below. The fetal
radiation exposure with abdominal shielding is well under the permissible 5 rads. CT
scan can also be used to exclude mass lesion.
(RESULT PLEASE)

NURSING THEORY

Florence Nightingale

Environmental Theory

Her Notes on Nursing emphasized that a clean environment, warmth, ventilation,


sunlight, and a quiet environment lead to good health.

Many elements in the patient’s environment must be maintain appropriately such as


ventilation, light, warmth, cleanliness and others. For our patient, any deviation may have a
crucial effect to them. Such as in newborn where keeping them thermoregulated and dry will free
them from cold stress. And for mothers, making the facilities available in their hygienic
practices is very necessary. Infections are a very crucial problem to anticipate for, since they are
very vulnerable to it.

A non-stimulating environment is essential especially for our patient, in a way that it


promotes faster recovery on our patient through minimizing external and stressful stimuli such as
limiting visitors during resting periods that may worsen the situation of our client. Especially that
our patient had suffered signs and symptoms of CVA. Meanwhile, we should be very careful in
any procedure and activities for our patient, because a simple mishandling will lead her in a
bleeding and seizure problem.

Jean Watson

( Human Caring Relationship Theory)

Jean Watson as one of our n ursing theorist emphasized the value of our
profession as being able to assist and help our patients in attaining there
optimal level of health. She adopts a view of the human being as: “….. a valued person in
and of him or herself to be cared for, respected, nurtured, understood and assisted; in general a
philosophical view of a person as a fully functional integrated self. He, human is viewed as
greater than and different from, the sum of his or her parts”.

1. The formation of a humanistic- altruistic system of values


• Begins developmentally at an early age with values shared with the parents.
• Mediated through ones own life experiences, the learning one gains and exposure to the
humanities.
• Is perceived as necessary to the nurse’s own maturation which then promotes altruistic
behavior towards others.
2. Faith-hope
• Is essential to both the carative and the curative processes.
• When modern science has nothing further to offer the person, the nurse can continue to
use faith-hope to provide a sense of well-being through beliefs which are meaningful to
the individual.
3. Cultivation of sensitivity to one’s self and to others
• Explores the need of the nurse to begin to feel an emotion as it presents itself.
• Development of one’s own feeling is needed to interact genuinely and sensitively with
others.
• Striving to become sensitive, makes the nurse more authentic, which encourages self-
growth and self-actualization, in both the nurse and those with whom the nurse interacts.
• The nurses promote health and higher level functioning only when they form person to
person relationship.
4. Establishing a helping-trust relationship
• Strongest tool is the mode of communication, which establishes rapport and caring.
• She has defined the characteristics needed to in the helping-trust relationship. These are:
• Congruence
• Empathy
• Warmth
• Communication includes verbal, nonverbal and listening in a manner which connotes
empathetic understanding.
5. The expression of feelings, both positive and negative
• “feelings alter thoughts and behavior, and they need to be considered and allowed for in a
caring relationship”.
• Awareness of the feelings helps to understand the behavior it engenders.
6. The systematic use of the scientific problem-solving method for decision making
• According to Watson, the scientific problem- solving method is the only method that
allows for control and prediction, and that permits self-correction.
• She also values the relative nature of nursing and supports the need to examine and
develop the other methods of knowing to provide an holistic perspective.
• The science of caring should not be always neutral and objective.
7. Promotion of interpersonal teaching-learning
• The caring nurse must focus on the learning process as much as the teaching process.
• Understanding the person’s perception of the situation assist the nurse to prepare a
cognitive plan.
8. Provision for a supportive, protective and /or corrective mental, physical, socio-cultural
and spiritual environment
• Watson divides these into eternal and internal variables, which the nurse manipulates in
order to provide support and protection for the person’s mental and physical well-being.
• The external and internal environments are interdependent.
• Watson suggests that the nurse also must provide comfort, privacy and safety as a part of
this carative factor.
9. Assistance with the gratification of human needs
• It is grounded in a hierarchy of need similar to that of the Maslow’s.
• She has created a hierarchy which she believes is relevant to the science of caring in
nursing.
• According to her each need is equally important for quality nursing care and the
promotion of optimal health. All the needs deserve to be attended to and valued.
10. Allowance for existential-phenomenological forces
• Phenomenology is a way of understanding people from the way things appear to them,
from their frame of reference.
• Existential psychology is the study of human existence using phenomenological analysis.
• This factor helps the nurse to reconcile and mediate the incongruity of viewing the person
holistically while at the same time attending to the hierarchical ordering of needs.
• Thus the nurse assists the person to find the strength or courage to confront life or death.
“Being a Nurse, is not only a profession but a also a vocation. It needs voluntary acceptance
of responsibilities without taking something in return. Having the courage to put your own
health in a risky situation of having exposde to the patient's diseases is not so easy. Taking
care other people, you just know now is a gift. For being an instrument of the Almighty God,
Nurses succeeded in rendering a quality service and overcome many problems along the way.
Nurses must not see the patient as having a physical problem since they are in the hospital
but rather be seen in a holistic approach. By that, Health care members can anticipated each
needs that should be addressed and resolved. The goal of the team is to assist the patient in
gaining a higher degree of harmony within mind, body and soul which generates self
knowledge, self reverence, self- healing and self care. It is the essence of Jean Watson
Theory which has 10 Carative Factors which will be an excellent guidelines in doing the
rightful and competent thing. Not only for the patient, but for the sake of the group.”

VI. NURSING CARE PLAN (CP PREECLAMPSIA EXCEL)

VII. DRUG STUDY (CP PREECLAMPSIA EXCEL)- LACK IV FLUIDS

A. MANAGEMENT

MEDICAL CARE

Incomplete understanding of the genesis and underlying pathophysiology in preeclampsia


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

Maternal treatment often includes magnesium sulfate infusions. Depending on the


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

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

Hematological findings include abnormalities in clotting and platelet function. In severe


preeclampsia, thrombocytopenia due to microthrombi formation and a mild consumptive
coagulopathy are frequent findings. Hemolysis, elevated liver enzymes, and low platelets
(HELLP) syndrome may accompany severe cases of preeclampsia. In these patients, hepatic
subcapsular hematomas may occur and result in life-threatening capsular rupture. Periportal
hemorrhagic necrosis in the periphery of the liver lobule probably results in the elevation of liver
enzymes and the site of hemorrhage. Once again, the endothelial damage is considered the
underlying etiology.

CNS effects of headache, dizziness, tinnitus, altered mental status, visual changes, and
seizures are thought to result from the increased vascular resistance and vasospasm of
preeclampsia. Although total cerebral blood flow and cerebral oxygen metabolism generally are
not altered in preeclampsia, regional changes certainly do occur. One third of patients who died
from eclampsia experienced cerebral hemorrhages of varying degrees. The visual changes may
result from vasospasm, ischemia, and hemorrhage in the occipital cortex, or from retinal artery
spasm, edema, or retinal detachment.

The therapy for this condition is to improve the platelet count by transfusion of fresh
frozen plasma or platelets. Complications associated with the syndrome are subcapsular liver
hematoma, hyponatremia, renal failure, and hypoglycemia. If hypoglycemia is present, this is
corrected by an intravenous dextrose infusion. Maternal hemorrhage may occur at birth because
of poor clotting ability. Epidural anesthesia is not possible because of a low platelet count and
possible bleeding in the site. Laboratory result returns to normal after birth.

Urinary Tract Infections medical treatment is the oral administration of antibiotic. In


addition the patient should drink a large quantity of fluid to “flush” the infection out of the
urinary tract. Cranberry Juice is often recommended as it acidify the urine and making it more
resistant to bacterial growth.

B. SURGICAL CARE

Preeclampsia is not a surgical disease of the mother or affected newborn. However,


cesarean delivery may be required to address increasing maternal disease severity and minimize
maternal and fetal-neonatal morbidity and mortality. A form of childbirth in which a surgical
incision is madethrough a mother's abdomen and uterus to deliver one or more babies. It is
usually performed when a vaginal delivery would put the baby's or mother's life or health at risk;
although in recent times it has been also performed upon request for births that would otherwise
have been natural. Low transverse cesarean section is a type of cesarean section that involves a
transverse cut just above the edge of the bladder and results in less blood loss and is easier to
repair.

In our patient, they had the following operations:

-Hysterotomy is a surgical incision of the uterus, performed as a method of abortion in a


pregnancy beyond the first trimester of gestation when a saline injection abortion was incomplete
or a tubal sterilization is to be done with the abortion. During surgery the lower segment of the
uterus is incised, and the products of conception are withdrawn. It requires small incision.
Postoperative care includes close observation for excessive vaginal bleeding.

-Peritoneal washing is a procedure used to look for malignant cells, i.e. cancer, in the
peritoneum. Peritoneal washes are routinely done to stage abdominal and pelvic tumours e.g.
ovarian cancer.

-Tubal ligation or tubectomy (informally known as getting one's "tubes tied") is a form of
female sterilization, in which the fallopian tubes are severed and sealed or "pinched shut", in
order to prevent fertilization

C. NURSING CARE

> Monitor v/s and report to the doctor if there is an abnormal findings.
> Give due medicines as ordered. Monitor therapeutic effect and side effects.
> Implement no added no salt diet.
> Provide educational teaching related to the disease.

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


> Support head on side to prevent aspiration.
> Assess weight daily.
> Assess breath sounds, monitor I&O.

PREVENTION

There currently are no well-established measures for preventing preeclampsia. Both low-
dose aspirin therapy and daily calcium supplementation have been studied as preventive
measures but have not been shown to be beneficial in the general pregnant population and are not
recommended for primary prevention of preeclampsia. Some evidence does support the use of
low-dose aspirin therapy and daily calcium supplementation in certain high-risk women.
Calcium supplementation has been shown to produce modest blood pressure reductions in
pregnant women who are at above- average risk for hypertensive disorders of pregnancy and in
pregnant women with low dietary calcium intake. An optimum calcium dosage for these women
has not been established. Low-dose aspirin therapy (100 mg per day or less) has been shown to
reduce the incidence of preeclampsia in women who were found to have an abnormal uterine
artery on Doppler ultrasound examination performed in the second trimester.

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


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

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

Because of the variable nature of the clinical presentation, the diagnosis of HELLP
syndrome is generally delayed for an average of eight days. Many woman with this syndrome are
initially misdiagnosed with other disorders, such as cholecystitis, esophagitis, gastritis, hepatitis
or idiopathic thrombocytopenia. In this one, early detection is a must especially in pregnancy
with complete blood count and liver test.

For Urinary Tract Infection, teach the patient about proper hygienic activities.
Encouraged to increase oral fluid intake and let the patient urinate every 4 hours in order to
prevent stasis of the urine. Wiping from the front to back when moving her bowels or urinating
must be practice. Wear cotton undergarment.

TREATMENT

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

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

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

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

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

In women with preeclampsia, blood pressure usually normalizes within a few hours after
delivery but may remain elevated for two to four weeks. As previously noted, a diagnosis of
chronic hypertension is made if blood pressure remains elevated at 12 weeks postpartum.

Women with preeclampsia should be counseled about future pregnancies. In nulliparous


women with preeclampsia before 30 weeks of gestation, the recurrence rate for the disorder may
be as high as 40 percent in future pregnancies. Multiparous women have even higher rates of
recurrence. Urinary Tract Infection needs antibiotic theraphy until atleast have a three sterile
urine specimen.
VIII. PROGNOSIS:

Usually the high blood pressure, protein in the urine, and other effects of preeclampsia
and HELLP Syndrome go away completely within 6 weeks after delivery. However, sometimes
the high blood pressure will get worse in the first several days after delivery.

A woman with a history of preeclampsia and HELLP Syndrome is at risk for the
condition again during future pregnancies. Often, it is not as severe in later pregnancies.

Women who have high blood pressure problems during more than one pregnancy have an
increased risk for high blood pressure when they get older.

One of the leading causes of maternal death is pre-eclampsia and HELLP Syndrome —
the rapid elevation of blood pressure during pregnancy—which, if untreated, can lead to seizures
(eclampsia), kidney and liver damage, and ultimately, death. Eclampsia and severe pre-eclampsia
claim the lives of an estimated 63,000 women each year, as well as the lives of many of their
babies. The infant's risk of death depends on the severity of the preeclampsia and how
prematurely the baby is born.

Superimposed Preeclampsia can develop into eclampsia if the mother has seizures. There
can be other severe complications for the mother, including bleeding problems, premature
separation of the placenta from the uterus before the baby is born (placental abruption), rupture
of the liver, stroke, death (rarely). However, these complications are unusual. Severe
preeclampsia may lead to HELLP syndrome.

Patients who have had HELLP syndrome should be counseled that they have a 19 to 27
percent risk of developing the syndrome in subsequent pregnancies. They also have up to a 43
percent risk of developing preeclampsia in another pregnancy. Patients with class I HELLP
syndrome have the highest risk of recurrence. When the syndrome recurs, it tends to develop
later in gestation and is generally less severe after two episodes. Patients who have had HELLP
syndrome may subsequently use oral contraceptive pills safely.Patients who develop atypical
early-onset preeclampsia or HELLP syndrome should be screened for the presence of
antiphospholipid antibodies. Urinary Tract Infection patient who has a good compliance in
medical intervention can be treated easily especially if early diagnosed. Possible recurrence can
be, depending on some factors mentioned above, severity and damage of the previous UTI.
IX. DISCHARGE PLANNING (METHODS)

MEDICATION
• Reinforce importance of medication compliance to patient and her relatives; its time,
frequency, duration dosage and route.
• Advice to report unusual manifestations and side effects of drugs to physician.
• Monitor and evaluate effectiveness of medication regimen.

ENVIRONMENT/ EXERCISE/ADL
• Instruct patients watcher to provide calm and non stressful environment to prevent stimuli that
could lead to seizures and an increase in Intracranial Pressure
• Advice to limit visitors
• Provide environment within normal room and body temperature.
• Maintain safe environment.
• Institute seizure precaution.
• Initiate positional precaution to prevent increase in intracranial pressure.
• Teach patient’s relative to perform passive range of motion exercises on patient’s extremities.
• Encouraged proper hygienic practices to avoid infections and further complications.

OUT PATIENT FOLLOW UP


• Inform relatives regarding importance of compliance on follow-up check up.

Diet
• Refer to dietician for dietary instructions.

SPIRITUAL / SEXUAL
• Encourage patient’s relatives to seek spiritual support.
• Encourage patient’s husband on alternative ways on showing affections such as hugs and
kisses.

X. INSIGHTS
XI. Bibliography

Human Anatomy and Physiology, Fifth Edition., 2000. ISBN: 0805349898

Maternal And Child Health Nursing, 4th Edition 2003. Adelle Pilliteri

http://www.nhlbi.nih.gov/resources/hyperten_preg/index.html

http://www.capefearvalley.com/outreach/outreach/peapods/hypertension Pregnancy/

American College of Obstetrician & Gynecologist (2001). ACOG practice bulletin; Chronic
hypertension in pregnancy (No. 29). Washington D.C.

Brooks, M. (2005). Pregnancy Preeclampsia. www. Emedine. Com/emerg.topic480.htm

http://3.bp.blogspot.com/E4VRTHYYpkY/5025
DUsKKKI/AAAAAAADmuw/kdJj8udoY7A/S1600-h/Patho+Preeclampsia.JPG

http:///emedecine. Medscape.com/article/1476919-overview

http://stevestakeshisfirststep.wordpress.com/2008/03/12/pathohysiology-of-preeclampsia

http://hb4110.net/wpcontent/uploads/KIT_MATERNAL%20HEALTH_BASIC
%20STATS.doc.

Payne TN, et al. A comparison of total laparoscopic hysterectomy to robotically assisted


hysterectomy: surgical outcomes in a community practice. J Minim Invasive Gynecol. 2008
May-June;15(3):286-91
http://medical-dictionary.thefreedictionary.com/hysterotomy
http://nursingcrib.com/case-study/hypertension/
http://emedicine.medscape.com/article/953579-overview

http://www.ncbi.nlm.nih.gov/pubmed/9822529

hypoglycemia).http://www.medicinenet.com/script/main/art.asp?articlekey=8430
http://emedicine.medscape.com/article/261435-overview

http://www.docstoc.com/docs/8981344/Case-Study-Pre-Eclampsia