Cerebrovascular

Accident

Case Presentation
I. INTRODUCTION

The world as a whole has been facing

different constant changes not only in the
environment but also in people’s lives. As
changes occur, the more people become in
need to adopt with these changes, thus, and
we expose ourselves to illness that could
even lead to unwanted events in our lives.
Our nursing case presentation is about
Cerebrovascular Accident discussing
Ischemic stroke. The content includes the
patient’s general data and physical
assessment, anatomy, physiology and
pathophysiology, review of related
literature, laboratory and pharmacology.
The highlight if the presentation deals with the
nursing care presentation deals with the nursing
care plan of our patient revolving on his priority
nursing problems, goals of care, appropriate
nursing intervention and its feedback evaluation.

Our group is composed of 11 Nursing students.

We have chosen this case as a help for studies
and eliminating and prevention in the enlarging
occurrence of Cerebrovascular diseases like this.

We greatly acknowledge the cooperation

extended by the patient. We also appreciate the
effort of Our Lady of Fatima University Medical
Center staff and the guidance provided to us by
our Clinical Instructor, Mrs. Morales, and most
importantly we thank our God Almighty for all
the graces he bestowed on us.
II. GENERAL DATA
Name: Remedios, Salazar Estrellia
Age: 54
Civil Status: M
Date of Birth: October 25 1956
Place of Birth: Valenzuela City
Nationality: Filipino
Religion: Roman Catholic
Address: 618 Caloong I, Valenzuela City
Date of Admission: December 6 2010
Date of Discharge: December 10 2010
Admitting Diagnosis: Cerebrovascular
Accident
Chief Complaint: HEADACHE
• History of Present Illness: One day prior to admission,
patient complained of headache, associated with nape
pain and dizziness. There was also a noted limitation of
motion of the neck area. There was no associated
vomiting, blurring of vision and loss of consciousness.
No medications taken and no consult were done.
Few hours prior to admission, above symptoms have
persisted which prompted patient to seek consult of his
physician’s clinic. Patient was advised to be admitted for
further evaluation and management, hence the
subsequent admission.

 
 
 
Review of Systems:
>No yellowish discoloration of the skin and sclera
>No cough, no colds, slight difficult of breathing
>No chest pain, no palpitations
>No pain urination
>No diarrhea
 
Review of Systems:
>No yellowish discoloration of the skin and
sclera
>No cough, no colds, slight difficult of
breathing
>No chest pain, no palpitations
>No pain urination
>No diarrhea
Past Medical History:
(+) HPN- DX 2002
-on maintenance medication
(-) DM
(-) Asthma
(+) Previous hospitalization 2007 FUMC
(+) CVO Bleed –CVD bleed vs. infarct

 
 
Personal/ Social History:
(-) Smoker
(-) Alcoholic drinker
 
Family History:
(+) HPN on both sides
(+) DM on mother side
(+) CA both sides
-Cervical CA, Breast CA
III.PHYSICAL ASSESSMENT
Done on Admission: December 6 2010
General Assessment: Conscious, coherent, ambulatory, NICRD.
General Survey: Vital Signs:
Musculoskeletal disorder BP: 100/90
R/to CVD re-intant PR: 81
S/p CVD infarct RR: 18
Left with sensory deficit Temp: 36.8
Right extremely.
Skin:
Warm, with good skin turgor and
skin texture, moist
HEENT:
• PPC, AS.
• (-) CLAD
• (-) TPC

Neck:
(+) Limitation of the RAM of neck
Chest:
• SCE,
• (-) Retractor CBS

Abdomen:
• Flabby, nabs, soft
• (-) tenderness

Extremities:
The client cannot resist force when asked to
resist specially the left arm. Muscle strength
is 3/5 on the right and 2/5 on the left. The
peripheral pulses are equal. Lymph nodes
are not palpable. The IV site is in her left
arm.
 
IV. ANATOMY AND PHYSIOLOGY

A. Anatomy of the Brain

The cranium
The brain is protected by a bony
covering called the cranium (which,
along with the bones of the face, makes
up the skull). Inside the cranium, the
brain is surrounded by the meninges.
The meninges are made up of 3 layers
of tissue:

• Pia mater – the layer closest to the

surface of the brain
• Arachnoid membrane – the middle layer
of tissue
• Dura mater – the outer-most layer
The cerebrum – the front of the brain
The largest part of the brain located in the
front is called the cerebrum. The cerebrum
is responsible for:

• Movement
• Body temperature
• Touch
• Vision
• Hearing
• Judgment
• Reasoning
• Problem solving
• Emotions
• Learning
The cerebrum has 2 parts:
the right cerebral hemisphere and
the left cerebral hemisphere. They
are connected at the bottom and
have a deep groove running between
them. In general, the right cerebral
hemisphere controls the left side of
the body, and the left cerebral
hemisphere controls the right. The
right side is involved with creativity
and artistic abilities. The left side is
important for logic and rational
thinking.
The hemispheres of the cerebrum are
divided into lobes, or broad regions
of the brain. Each lobe is
responsible for a variety of bodily
functions:
• Frontal lobes are involved with
personality, speech, and motor
development
• Temporal lobes are responsible for
memory, language and speech
functions
• Parietal lobes are involved with
sensation
• Occipital lobes are the primary
vision centers
The surface of the cerebrum appears
wrinkled and is made up of deep
grooves (called sulci) and bumps or
folds (called gyri). The outer part of
the cerebrum is called gray matter
and contains nerve cells. The inner
part is called white matter and
contains connections of nerves.
The brainstem – the middle of the brain
The brainstem is located in front of the cerebellum.
The brainstem is like the hard-drive of a computer. It is
the main control panel for the body that passes
messages back and forth between the brain and other
parts of the body. The cerebrum, the cerebellum, and
the spinal cord are all connected to the brainstem. The
brainstem has three main parts, the midbrain, the pons,
and the medulla oblongata.

• The brainstem controls vital functions of the body,

including:
• Breathing
• Consciousness
• Cardiac function
• Involuntary muscle movements
• Swallowing
• Movement of the eyes and mouth
• Relaying sensory messages (pain, heat, noise, etc.)
• Hunger
The cerebellum – the back of the brain
Behind the cerebrum at the back of the head is
the cerebellum. In Latin, cerebellum means
“little brain.” However, the cerebellum contains
more nerve cells than both hemispheres
combined. The cerebellum is primarily a
movement control center, responsible for:

• Voluntary muscle movements

• Fine motor skills
• Maintaining balance, posture, and equilibrium
• Unlike the cerebrum, the left cerebellum
controls the left side of the body, and the right
cerebellum controls the right side of the body.
 
Figure 4.2. The Motor, Sensory and Association Areas of
the Cerebral Cortex.
 
Other important parts of the brain

Ventricular system. The brain is not a

solid organ. There are fluid-filled
cavities within the brain called
ventricles. The ventricles are
important in providing nourishment
to the brain. The ventricular system
produces and processes
cerebrospinal fluid – a clear, watery
substance that flows around the
brain and helps cushion and protect
it.
Cranial nerves. The brain also contains 12
pairs of cranial nerves each responsible for
specific functions in the body:

• Olfactory nerve – smell

• Optic nerve – vision
• Oculomotor – eye movements, eyelid
opening
• Trochlear – eye movements
• Trigeminal – facial sensations, chewing
• Abducens – eye movements
• Facial – taste, facial expressions
• Vestibulocochlear – hearing, balance
• Glossopharyngeal – taste, swallowing
• Vagus – swallowing, taste
• Accessory – neck and shoulder muscles
• Hypoglossal – tongue movement
Pituitary gland. The pituitary gland
is located in the center of the brain
and is about the size of a dime. The
pituitary gland, often referred to as
the “master gland,” is responsible
for a number of functions including
producing hormones for the thyroid
and adrenal glands, as well as the
hormones responsible for normal
growth and sexual maturation.
B. Cerebral Circulation

The cerebral circulation receives

approximately 15% of the cardiac output,
or 750 ml per minute. The brain does not
store nutrients and has a high metabolic
demand that requires the high blood flow.
The brain’s blood pathway is unique
because it flows against gravity; its arteries
fill from below and the veins drain from
above. In contrast to other organs that may
tolerate decrease in blood flow because of
their adequate collateral circulation, the
brain lacks additional collateral blood flow,
which may result in irreversible tissue
damage when blood flow is occluded for
even short periods of time.
Arteries.
Two internal carotid arteries and vertebral
arteries and their extensive system of
branches provide the blood supply to the
brain. The internal carotids arise from the
bifurcation of the common carotid and
supply much of the anterior circulation of
the brain. The vertebral arteries branch
from the subclavian arteries, flow back to
and upward on either side of the cervical
vertebrae, enters the cranium through the
foramen magnum. The vertebral arteries
join to become the basilar artery at the level
of the brain stem; the basilar artery divides
to form the two branches of the posterior
cerebral arteries. The vertebrobasilar
arteries supply most of the posterior
circulation of the brain.
At the base of the brain surrounding the
pituitary gland, a ring of arteries is formed
between the vertebral and internal carotid
artery chains. This ring is called the circle
of Willis and is formed from the branches
of the internal carotid artery, and anterior
and middle cerebral arteries, and anterior
and anterior and posterior communicating
arteries. Functionally, the posterior portion
of the circulation and the anterior or carotid
circulation usually remain separate. The
arteries of the circle of Willis can provide
collateral circulation if one or more of the
four vessels supplying to become occluded
or are ligated.
The arterial anastomoses along the circle of
Willis are frequent sites of aneurysms.
Theses can be formed when the pressure at
a weakened arterial wall causes the artery
to balloon out. Aneurysms may be
congenital or the result of degenerative
changes in the vessel wall associated with
atherosclerotic vascular disease. If an artery
with an aneurysm bursts or becomes
occluded by vasospasm, an embolus, or a
thrombus, the neurons distal to the
occlusion are deprived f their blood supply
and the cells die quickly. The result is
hemorrhagic stroke (cerebrovascular
accident or infarction). The effects of the
occlusion depend on which vessels are
involved and which areas of the brain these
vessels supply.
Veins.
Venous drainage for the brain does not
follow the arterial circulation as in other
body structures. The veins reach the brain’s
surface, join larger veins, then cross the
subarachnoid space and empty into the
dural sinuses, which are vascular channels
lying within the tough Dura mater. The
network of sinuses carries venous outflow
from the brain and empties into the internal
jugular vein, returning the blood to the
heart. Cerebral veins and sinuses are unique
because, unlike other veins in the body,
they do not have valves to prevent blood
from flowing backward and depend on both
gravity and blood pressure.
Figure 4.3. The Arterial Blood Supply of the
Brain, including the Circle of Willis, as viewed
from ventral surface.
 
V. REVIEW OF RELATED
LITERATURE
A. Incidence
Stroke could soon be the most common cause of death
worldwide. Stroke is currently the second leading
cause of death in the Western world, ranking after heart
disease and before cancer, and causes 10% of deaths
worldwide. Geographic disparities in stroke incidence
have been observed, including the existence of a
"stroke belt" in the southeastern United States, but
causes of these disparities have not been explained.

The incidence of stroke increases exponentially from

30 years of age, and etiology varies by age. Advanced
age is one of the most significant stroke risk factors.
95% of strokes occur in people age 45 and older, and
two-thirds of strokes occur in those over the age of 65.
A person's risk of dying if he or she does have a stroke
also increases with age. However, stroke can occur at
any age, including in childhood.
Family members may have a genetic tendency for
stroke or share a lifestyle that contributes to
stroke. Higher levels of Von Willebrand factor are
more common amongst people who have had
ischemic stroke for the first time. The results of
this study found that the only significant genetic
factor was the person's blood type. Having had a
stroke in the past greatly increases one's risk of
future strokes.
Men are 25% more likely to suffer strokes than
women, yet 60% of deaths from stroke occur in
women. Since women live longer, they are older
on average when they have their strokes and thus
more often killed (NIMH 2002). Some risk factors
for stroke apply only to women. Primary among
these are pregnancy, childbirth, menopause and
the treatment thereof (HRT).
 B. Clinical Presentation and Medical
Management
An ischemic stroke can cause a wide variety of
neurologic deficits, depending on the location of
the lesion (which vessels are obstructed), the
size of the area of inadequate perfusion, and the
amount of collateral (secondary or accessory)
blood flow. The patient may present with any of
the following signs and symptoms:
-Numbness or weakness of the face, arm, or leg,
especially on ne side of the body;
-Confusion or change in mental status;
-Trouble speaking or understand speech;
-Visual disturbances;
-Difficulty walking, dizziness, or loss of balance or
coordination;
-Sudden severe headache
-Motor sensory, cranial nerve, cognitive and other
functions may be disrupted.
Table 5-1. Neurologic Deficits of Stroke: Manifestations and
Nursing Implications
Nursing Implication/
Neurologic Deficit Manifestation Patient Teaching
Application

Visual field deficits

Homonymous hemianopsia -Unaware of the persons or -Place objects within intact field
(loss of half of the visual objects on side of the visual of vision.
field) loss. -Approach the patient from side
-Neglect of one side of the of the intact field of vision
body. -Instruct/remind the patient to
-Difficulty judging turn the head in the direction of
distances. visual loss to compensate for
loss of visual field
-Encourage the use of eye
glasses if available
-when teaching the patient, do
so within the patient’s intact
visual field.
Loss o peripheral >Difficulty seeing at night -Avoid night driving or
other risky activities in
vision >Unaware of objects or the darkness
the borders of objects -Place objects in center of
patient’s intact visual
field.
-Encourage the use of a
cane or other object to
identify objects in the
periphery of visual field.
Diplopia >Double of vision -Explain to the patient
the location of an object
when placing it near the
patient.
-Consistently place
patient care items in the
same location.
Motor Deficits
Hemiparesis -Weakness of the face, arm, -Place objects within
and leg on the same side
(due to a lesion in the the patient’s reach
opposite hemisphere) on the non affected
site.

Hemiplegia -Paralysis of the face, arm, -Encourage the patient to provide

range-of-motion exercises to the
and leg on the same side
affected site.
(due to a lesion in the
-Provide immobilization as needed
opposite hemisphere) on the affected site.
_-Maintain body alignment in
functional position.
-exercise unaffected limb to
increase mobility, strength and use.
Ataxia -Staggering, unsteady gait -Support patient during the
-Unable to keep feet initial ambulation phase
together; needs a broad -Provide supportive device for
base to stand ambulation (walker, cane).
Instruct the patient not to walk
without assistance or
supporting device.
Dysarthria -Difficulty in forming -Provide the patient with
words alternative methods of
communicating.
-Allow the patient
sufficient time to respond
to verbal communication.
-Support patient and
family to alleviate
frustration relate to
difficulty communicating.

Dysphagia Difficulty swallowing -Test the patient’s

pharyngeal reflexes
before offering food or
fluids.
-Assist the patient with
meals.
-Place food on the
affected site of the
mouth.
-Allow ample time to
eat.
Sensory deficit
Paresthesia (occurs on the Numbness and tingling of -Instruct the patient to avoid
site opposite to the lesion) extremity using this extremity as the
Difficulty with dominant limb due to altered
proprioception sensation.
-Provide range of motion to
affected areas and apply
corrective devices as needed.

Verbal deficits
Expressive aphasia Unable to form words that -Encourage patient to
are understandable; may repeat sounds of the
be able to speak in single alphabet.
word responses

Receptive aphasia Unable to comprehend the -Speak slowly and clearly

spoken word; can speak to assist the patient in
but may not make sense. forming sounds.
Global (mixed) aphasia Combination of both -Speak clearly and in simple
receptive and expressive sentences; use gestures or
aphasia pictures when able.
-Establish alternative means
of communication.
Cognitive Deficits

-Short and long term -Reorient patient to time, place

memory loss and situation frequently.
-Decreased attention span -Use verbal and auditory cues
-Impaired ability to to orient patient.
concentrate Provide familiar objects ( family
-Poor abstract reasoning photographs, favorite objects)
Altered judgment -Use no complicated language.
-Match visual tasks with a
verbal cue; holding a
toothbrush, stimulate brushing
of teeth while saying, “I would
like you to brush your teeth
now.)
-Minimize distracting noises
and views when teaching the
patient.
-Repeat and reinforce
instructions frequently.
Emotional Deficits

-Loss of self control -Support patient during

-Emotional lability uncontrollable outbursts.
-Decreased tolerance to -Discuss with the patient
stressful situations and family that the outbursts
-Depression are due to the disease
Withdrawal process.
-Fear, hostility, and anger -Encourage the patient to
Feelings of isolation participate in group activity.
-Provide stimulation for the
patient.
-Control stressful situations,
if possible.
-Provide a safe
environment.
-Encourage patient to
express feelings and
frustrations related to
disease process.
C. Laboratory and Radiologic Examination
Any patient with neurologic deficits needs a careful history and a complete physical
and neurologic examination. Initial assessment will focus on airway patency, which
may be compromised by loss of gag or cough reflexes and altered respiratory pattern;
cardiovascular status (including blood pressure, cardiac rhythm and rate, carotid
bruit), and gross neurologic losses.
Stroke patients may present to the acute care facility at any point along a continuum
of neurologic involvement. A system that uses the time course to classify patients
along this continuum may be used to guide treatment. Strokes use the time course is
commonly classified in the following manner: (1) transient ischemic attack; (2)
reversible ischemic neurologic disease; (3) stroke in involution; and (4) compensated
stroke.
The initial diagnostic test for a stroke is a non contrast computed therapy (CT) scan
performed emergently to determine of the event is ischemic or hemorrhagic (which
determines treatment). Further diagnostic work up for ischemic stroke involves
attempting to identify the source of thrombi or emboli. A 12-lead electrocardiogram
and a carotid ultrasound are standard tests. Other studies may include Cerebral
Angiography, transcranial flow studies, transthoracic or transesophagel
echocardiography, magnetic resonance imaging of the brain and/or neck, xenon CT,
and single photon emission CT.
Remarkable advances in technology now make it possible to examine how the brain
looks, works and gets its blood supply. These tests can outline the affected part of the
brain and help define the problem created by stroke. Most of these tests are safe,
painless and can be done as an outpatient. However, in many cases these tests are
ordered when a patient is hospitalized with a stroke. A doctor must decide on a case-
by-case basis whether such tests will be useful, and if so, which ones to use. The
following tests are described in this section:
i. Carotid phonoangiography
ii. Computerized axial tomographic
scan (CT or CAT scan)
iii. Digital subtraction angiography
(DSA)
iv. Doppler ultrasound test
v. Electroencephalogram (EEG)
vi. Evoked response test
vii. Magnetic resonance imaging
scanning (MRI)
viii. Radionuclide angiography
What imaging tests are done on the
brain?
• Computerized axial tomographic scan
(CT or CAT scan) — Uses X-rays to
generate an image of the brain. Doctors
use CT to determine whether a stroke
has occurred and, if so, what
kind. (Ischemic strokes are caused by a
clot that blocks an artery. Hemorrhagic
strokes result from a ruptured blood
vessel in the brain causing bleeding into
brain tissue.) CT scanning takes from 5
to 10 minutes to complete (mostly less
than 5 minutes). The test causes no
discomfort.
• Magnetic resonance imaging scanning
(MRI) — The stroke patient is placed into
the MRI scanner. This scanner has a
magnetic field in which the head is
subjected to bursts of energy of a known
magnetic frequency. The response of the
brain cells to these bursts of energy is
detected as signals that ultimately generate
an image of the brain. MRI can give very
accurate images of the brain. These are used
to determine the presence, location and size
of aneurysms and arteriovenous
malformations, which are potential sources
for hemorrhagic stroke. This test is
performed in 40 minutes to one hour, and
causes no discomfort.
• Radionuclide
angiography — Radioactive compounds
are injected into a vein in the arm; the
bloodstream then carries them toward the
head. As the radioactive compound
circulates in the bloodstream, it
constantly emits bursts of radiation. Once
the radioactive compound reaches the
brain, these bursts of radiation are
detected and used to form an image of
the brain. This imaging procedure can
show areas where the brain has been
deprived of blood flow and is damaged.
What tests show the brain's electrical activity?
• Electroencephalogram (EEG) — Small metal
disks (electrodes) are placed at strategic
locations on a person's scalp. The electrodes
can detect the electrical activity in the form of
impulses that are then transcribed to paper. By
observing such impulse characteristics as
intensity (the size of the impulse), duration (the
width of the impulse), frequency (how often
impulses occur during a given time) and
location (what region of the brain produces
these impulses), an EEG can provide valuable
information about underlying problems in the
brain. Some people who have strokes are prone
to seizures, and this test will help doctors
determine if seizures are present and if
treatment with medications is needed.
• Evoked response test — a diagnostic
procedure that provides a measurement
of the brain's ability to process and
react to different sensory stimuli. A
doctor evokes a visual response by
flashing a light or checkerboard pattern
in front of a patient. For auditory
evoked responses, a doctor produces a
sound in one of the patient's ears. For
bodily evoked responses, one of the
nerves in an arm or leg is electrically
stimulated. The responses from these
sensory stimuli can indicate abnormal
areas of the brain.
What tests show blood flow?
• Doppler ultrasound test — Uses high-
frequency sound waves to detect blockages
in the carotid artery. A Doppler probe or
instrument capable of generating ultrasound
waves is placed on the neck very near to the
carotid artery. Ultrasound waves from the
probe travel through the neck and bounce
off the moving blood cells. The reflected
sound wave, now returning to the probe at a
different frequency, is then detected by the
same probe. The change in frequency of the
sound waves relates to the speed of the
blood cells and thus the blood flow. This
test takes an hour or more, and causes no
discomfort.
• Carotid phonoangiography — a
sensitive microphone is placed on the
neck, very close to the carotid artery, to
record sounds. Ordinarily, in a normal
artery, blood flows in a smooth and
controlled manner. However, the
presence of blockages, such as those
caused by atherosclerosis, causes the
blood flow to become turbulent. This
turbulent blood flow can create a sound,
called a bruit (BROO'e), which can be
detected and registered by the
microphone. The presence of a bruit
may indicate a blockage in the carotid
artery and is cause for more tests.
• Digital subtraction angiography
(DSA) — gives an image of the brain's major
blood vessels. A thin plastic tube (a catheter)
is inserted into a major artery of the leg and
advanced through the body's major vessels
until it reaches the brain's blood vessels. A
contrast dye is injected through the catheter
and allowed to circulate in the bloodstream.
At that point, an X-ray machine quickly takes
a series of pictures of the head and neck. The
images track the movement of the contrast
dye as it moves through the brain's blood
vessels. This imaging technique lets the
doctor identify and localize the source of a
blocked blood vessel that caused the stroke.
Some people may feel a warm sensation as
the contrast medium is injected into the blood
vessels.
In patient with TIA, a bruit (abnormal sound
heard on auscultation resulting from
interference with normal blood flow) may be
heard over the carotid artery. There are
diminished or absent of carotid pulsationsin
the neck. Diagnostic tests for TIA may
include carotid phonoangiography; this
involves auscultation, direct visualization,
and photographic recording of carotid bruits.
Oculoplethysmography measures the
pulsation of blood flow through the
ophthalmic artery. Carotid angiography
allows visualization of intracranial and
cervical vessels. Digital subtraction
angiography is used to define carotid artery
obstruction and provides information on
patterns of cerebral blood flow.
D.NIH Stroke Scale
The National Institute of Health (NIH) stroke scale
(NIHSS) is a standardized method used by physicians
and other health care professionals to measure the level
of impairment caused by a stroke. The NIH stroke
scale serves several purposes, but its main use in
clinical medicine is during the assessment of whether
or not the degree of disability caused by a given stroke
merits treatment with tPA. Another important use of
the NIHSS is in research, where it allows for the
objective comparison of efficacy across different stroke
treatments and rehabilitation interventions. The NIH
stroke scale measures several aspects of brain function,
including consciousness, vision, sensation, movement,
speech, and language. A certain number of points are
given for each impairment uncovered during a focused
neurological examination. A maximal score of 42
represents the most severe and devastating stroke.
Current guidelines as of 2008 allow strokes with scores
greater than 4 points to be treated with tPA.
VI.PATHOPHYSIOLOGY
 
In an ischemic brain attack, there is disruption of the cerebral blood flow due to
obstruction of blood vessel. This disruption in blood flow initiates a complex series of
cellular metabolic events referred to as the ischemic cascade.
The ischemic cascade begins when cerebral blood flow falls less than 25 ml/100
g/min. at this point, neurons can no longer maintain anaerobic respiration. The
mitochondria must then switch to anaerobic respiration, which generates large
amounts of lactic acid, causing a change in pH level. This switch to the less efficient
anaerobic respiration also renders the neuron incapable of producing sufficient
quantities of adenosine triphosphate (ATP) to fuel the depolarization process. Thus
membrane pumps that maintain electrolyte balances begin to fail and the cells cease
to function.
Early in the cascade, an area of low cerebral blood flow, referred to as penumbra
region, exists around the area of infarction. The penumbra region is ischemic brain
tissue that can be salvaged with timely intervention. The ischemic cascade threatens
cells in the penumbra because membrane depolarization of the cell walls leads to an
increase in intracellar calcium and the release of glutamate. The penumbra area can
be revitalized with the administration of tissue plaminogen activator (t-PA), and the
influx of calcium can be limited with the use of cacium channel blocker. The influx of
calcium and release of glutamate, if continued, activate a number of damaging
pathways that result in the destruction of the cell membrane, the release of more
calcium and glutamate, vasoconstriction, and the generation of free radicals. These
processes enlarge the area of infarction into the penumbra, extending the stroke.
 Ischemia

Energy failure

Acidosis Ion imbalance

Increase Depolarization
Glutamate

Intracellular calcium
increased

Cell injury and death

Figure 6-1. Pathophysiology of the Cerebrovacular Accident. Process

contributing to ischemic brain iinjury. Courtesy of National Stroke
Association, Englewood, Colorado
VII. LABORATORY RESULTS

A. COMPLETE BLOOD COUNT

Dec 06 2010 Normal values Interpretation

Hemoglobin 117 g/L 123-152 g/ L Lower

Hematocrit 0.36 0.37-0.42 % Slightly lower

WBC count 11.9 5.0-10.0 x 10 g/L Higher

Differential Count
Lymphocytes 0.22 0.20-0.40 Normal

Monocytes 0.07 0.02-0.08 Normal

Eosinophils 0.01 0.01-0.03 Normal

Basophils 0.01 0-0.02 Normal

Neutrophils 0.69 0.40-0.60 Higher
RBC 4.98 4.5-5.5x10/2 L Normal
MCV 73 88-96 Lower
MCH 23.5 27-33 pg Lower
MCHC 321 330-360 g/L Lower
RDW 14.3 12.7-22.7 % Normal
Platelet 210 150-450x 10 g/L Normal

MPV 9.47 4.5-7.5 Higher

PDW 3.17-39.1
CT 2-4 mins.
BT 1-3 mins.
Reticular Count 05-1.5%

ESR 0-20 mm/hr

B. Electrolytes

Creatinine 88.2mmol/L
Sodium 135 mmol/L
Potassium 4.3 mmol/L
Calcium 1.12 mmol/L
Chloride 92 mmol/L

C.Clinical Chemistry

Cholesterol 5.0 mmol/L

Triglycerides 0.32 mmol/L
Didevet HDL Cholesterol 1.9 mmol/L
LDL Cholesterol 3.66 mmol/L
CT Scan
December 7 2010:
Impression: Cortical cerebral atrophy.
 
CT Scan: Cervical Spine with settings for the soft tissues
and bone detail revealed.
December 7 2010
Findings:
-Scannogram shows mild reversal of the cervical lordesis
most likely due to muscular spasm.
-Thecal sac is intact.
-There is no evidence of canal stenosis
-Osteophytic formation is ruled at C5 and C6 vertebral
bodies.
-Visualized soft tissue planes within normal.
-No other findings noted.
VIII.PHARMACOLOGY
A. Mannitol

Brand name Osmitrol

Patient’s Dosage 75 mg prn
Classification Diagnostic agent; osmotic diuretic, urinary irrigant
Indication  Prevention and treatment of oliguric phase of renal
disease
 Reduction of intracranial pressure and treatment of
cerebral edema; of elevated IOP when the pressure
cannot be lowered by other means
 Promotion of the urinary excretion of toxic
substances
 Diagnostic use: measurement of GFR
 Irrigant in transurethral prostatic resection or other
transurethral precedures
Action Elevates the osmolarity of the glomerular filtrate,
thereby hindering the reabsorption of water and
leading to a loss of water, sodium, chloride (used
for diagnosis of glumerular filtration rate);
creates an osmotic gradient in the eye between
plasma and oclular fluids, thereby reducing IOP;
creates an osmotic effect, leading to decreased
swelling in posttransurethral prostatic resection.

Pharmacokinetics
Route Onset Peak Duration
IV 30-60 minutes 1 hour 6-8 hours
Irrigant Rapid Rapid Short
Metabolism T 1/2 : 15-100 minutes
Distribution Crosses placenta; may enter breast milk
Excretion Urine
Dosage and Administration
Adults:
IV infusion only; individualized concentration and rate of administration. Dosage is 50-
200g/day. Adjust dosage to maintain urine flow of 30-50 ml/hr.
•Prevention of oliguria: 50-100 g IV as a 5% -25% solution
•Treatment of oliguria: 50-100 g IV of a 15%-25% solution.
•Reduction of intracranial pressure and cerebral edema: 1.5-2g/kg IV as a 15%-25%
solution over 30-60 minutes. Evidence of reduced pressure should be seen in 15
minutes.
•Reduction of IOP: infuse 1.5-2 g/kg as a 25% solution, 20% solution. Or 15% solution
over 30 minutes. If used preoperatively, use 60-90 minutes before surgery for maximal
effect.
•Adjunctive therapy to promote dieresis in intoxications: maximum of 200 g IV of
mannitol with other fluids and electrolytes.
•Measurement of glumerular filtration rate: dilute 100 ml of a 20% solution with 108
ml of sodium chloride injection. Infuse this 280 ml of 702% solution IV at rate of 20
ml/ min. collect urine with a catheter for the specified time for measurement of
mannitol in mg/min. draw blood at the start and at the end of the time for
measurement of mannitol in mg/ml plasma.
•Test dose of mannitol for patients with inadequate renal function: 0.2 g/kg IV (about 50
ml of 25% solution, 75 ml of a 20% solution) in 3-5 minutes to produce urine flow of
30-50 ml/hour. If urine flow does not increase, repeat dose. If no response to second
dose, reevaluate patient situation.
•Urologic irrigation: use prepared 5g/ 100ml distilled water solution; irrigate as
needed.
Contraindications Contraindicated with anuria due to severe
renal disease
Precaution Use cautiously with pulmonary congestion,
active intracranial bleeding (except during
crainiotomy), dehydration, renal disease,
heart failure, pregnancy, lactation.
Adverse Reactions and Side effects
Central Nervous Dizziness, headache, blurred vision, seizzures
System
Cardiovascular Hypotension, hypertension, edema, HF,
thromboplebitis, tachycardia, chest pain
Dermatologic Urticaria, skin necrosis with infiltration
Gastrointestinal Nausea, anorexia, dry mouth, thirst
Genitourinary Diuresis, urine retention
Hematologic Fluid and electrolyte imbalances
Respiratory Pulmonary congestion, rhinitis
Nursing Considerations
Assessment
 History Pulmonary congestion, active intracranial bleeding,
dehydration, renal disease, heart failure, pregnancy, lactation
 Physical Skin color, lesions, edema, hydration, orientation, muscle
strength , reflexes, pupils, pulses, BP, perfusion; Respiratory
pattern, adventitious sounds, urinary output patterns, serum
electrolytes, urinalysis , renal function tests
Interventions
Warning: Do not give electrolyte free mannitol with blood. If blood must be given, add at
least 20 mEq of sodium chloride to each liter of mannitol solution
Do not exposesolutions to low temperatures; crystallization may occur. If crystals are seen,

warm the bottle in a hot water bath, then cool to body tempearature before administering.
Make sure the infusion set contains a filter if giving concentrated mannitol.

Monitor serum electrolyte periodically with prolonged therapy.

Teaching Points
 You may experience these side effects: Increased urination; GI upset (eat frequent small
meals); dry mouth (suck sugarless lozenges); headache, blurred vision (use caution when
moving for assistance).
 Report difficulty of breathing, pain in the IV site, chest pain.
B.Tramadol hydrochloride

Brand name Ultral, Ultral ER

Patient’s Dosage 50 mg PO q 6h
Classification Analgesic (centrally acting)
Opoid Analgesic
Indication  relief of moderate to moderately severe pain
 relief of moderate to severe chronic pain
in adults who need RTC Treatment for
extended periods (ER tablets)
 Unlabelled uses: Premature ejaculation;
restless leg syndrome
Action Binds to mu-opiod receptors and inhibits the
reuptake of norepinephrine and serotonin;
causes many effects similar to opoids- dizziness,
somnolence, nausea, constipation - but does not
have the respiratory depressant effects.
Pharmacokinetics
Route Onset Peak
Oral 1 hour 2 hours
Metabolism Hepatic; t ½ : 6-7 hours
Distribution Crosses placenta; enters breast milk
Excretion Urine
Dosage and Administration
Adults:
Patients who require rapid analgesic effect: 50-100mg PO every 4-6 hr; do not exceed 400

mg/day
Patients with moderate to moderately severe chronic pain: Initiate at 25 mg /day in the morning,

and titrate in 25-mg increments every 3 days to reach 100 mg/day. Then increase every 3 days
to reach 200 mg/day. After titration, 50-100mg every 4-6 hours; do not exceed 400 mg/day.
Alternatively, 100-mg ER tablet once daily, titrated by 100-mg increments every 5 days; do not
exceed 300 mg/day.
Geriatric Patients or patients with hepatic or renal impairment
Older than 75 years old: do not exceed 300 mg/day
Patients with cirrhosis: 50 mg every 12 hour ER tablets should not be used in severe hepatic
impairment
Patients with creatinine clearance less than 30ml/min: 50-100 mg PO every 12 hours. Maximum
200 mg/day. ER tablets should not be used in patients with creatinine clearance less than 30
ml/min.
Contraindications Contraindicated with allergy to tramadol, or opoids
or acute intoxication with alcohol opoids and
psychoactive drugs.
Precaution Use cautiously with pregnancy, lactation; seizures;
concomitant use of CNS depressants, MAOIs, SSRIs,
TCAs; renal impairment; hepatic impairment.
Adverse Reactions and Side effects
Central Nervous Sedation, dizziness or vertigo, headache, confusion,
System dreaming, sweating, anxiety, seizures
Cardiovascular Hypotension, tachycardia, bradycardia
Dermatologic Sweating, pruritus, rash, pallor, urticaria
Gastrointestinal Nausea, vomiting, dry mouth, constipation,
flatulence
Others Potential abuse, anaphylatoid reactions
Drug Interactions
 Devreased effectiveness with carbamazepine
 Increased risk of tramadol toxicity with MAOIs or SSRIs
Nursing Considerations
Assessment
 History Hypersensitivity to tramadol; pregnancy; acute
intoxication with alcohol, opoids, psychotropic
drugs or other centrally acting analgesics;
lactation; seizures; concomitant use of CNS
depressants or MAOIs; renal ore hepatic
impairment; past or present history of opoid
addiction

 Physical Skin color, texture, lesions; orientation, reflexes,

bilateral grip strength, affect; Pulmonary
auscultation, BP; bowel sounds, normal output;
LFTs, renal function tests
Interventions
 Control environment (temperature, lighting,) if sweating or
CNS effects occur.
Warning: Limit use in patients with past or present history of
addiction to or dependence on opoids.

Teaching points
 You may experience these side effects: dizziness, sedation,
drowsiness, impaired visual acuity (avoid driving or
performing tasks that require alertness); nausea, loss of
appetite, (lie quietly, eat frequent small meals)
 Repot severe nausea, dizziness, severe constipation.
 C. Celecoxib
Brand name Celebex
Patient’s Dosage 100 mg PO bid
Classification Analgesic (nonopoid)
NSAID
Specific COX-2 enzyme inhibitor
Indication  acute and long term treatment of Signs and
symptoms of rheumatoid arthritis and
osteoarthritis
 reduction of the number of colorectal polyps
in familial adenomatous polyposis (FAP)
 management acute pain
 treatment of primary dysmenorrhea
 relief of signs and symptoms of ankylosing
spondylitis
 Relief of signs and symptoms of juvenile
rheumatoid arthritis.
Action Analgesic and anti-inflammatory activities related to
inhibition of the COX-2 enzyme, which is activated I
inflammation to cause the signs and symptoms
associated with inflammation; does not affect the
COX-1 enzyme, which protects the lining of the GI
tract and has blood clotting and renal functions.
Pharmacokinetics
Peak
Route Onset
3 hours
Oral Slow
Metabolism Hepatic; t ½ : 11 hours
Distribution Crosses placenta; may enter breast milk
Excretion Bile, urine
Dosage and Administration
Adults
Initially, 100mg PO bid; may increase to 200 mg/day PO bid as needed.
acute pain, dysmenorrheal: 400mg, then 200mg PO bid

FAP: 400mg PO bid

Anyklosing spondylitis: 200mg/day PO; after 6week,; if no effect, suggest

another therapy.
Contraindications Contraindicated with allergies to sulfonamides,
celecoxib, NSAID's or aspirin; significant renal
impairment; pregnancy (third trimester), lactation.
Precaution Use cautiously with impaired hearing, hepatic and CV
condition.
Adverse Reactions and Side effects
Central Nervous System Headache, dizziness, somnolence, insomnia, fatigue,
tiredness, dizziness, tinnitus, ophthalmologic effects
Cardiovascular MI, CVA
Dermatologic Rash, pruritis, sweating, dry mucous membranes,
stomatitis
Gastrointestinal Nausea, abdominal pain, dyspepsia, flatulence, GI bleed
Hematologic Neutropenia, eosinophilia, leucopenia, pancytopenia,
thrombocytopenia, agranulocytosis, granulocytopenia,
aplastic anemia, decreased Hgb or Hct, bone marrow
depression, menorrhagia
Others Peripheral edema, anaphylactoid reactions to
anaphylactic shock
Drug Interactions
 Increased risk of bleeding if taken concurrently with warfarin.
Monitor patient closely and reduce warfarin dose as appropriate.
 Increased lithium level and toxicity.
 Increased risk of GI bleeding with long term use of alcohol, smoking.
Nursing Considerations
Assessment
 History Renal impairment, impaired hearing, allergies
hepatic and CV conditions, lactation and
pregnancy.
 Physical Skin color and lesions; orientation, reflexes,
ophthalmologic and audiometric evaluation,
peripheral sensation; Pulmonary edema,
Respiratory, adventitious sounds; liver
evaluation; CBC, LFT’s, renal function tests;
serum electrolytes.
Interventions
Block Box warning: Be aware that the patient maybe at increased risk for
CV events, GI Bleeding; monitor accordingly.
Administer drug with food or after meals if GI upset occurs.

Establish safety measures if CNS or visual disturbances occur.

Arrange for periodic ophthalmologic examination during long term therapy.

Warning: If overdose occurs, institute emergency procedures-gastric lavage,

induction of emesis, supportive therapy.
Provide further comfort measures to reduce pain (e.g. positioning,

environmental control) and t reduce inflammation (e.g. warmth, positioning,

and rest).

Client/ Family Teaching

 Take only the prescribed dosage, do not increase dosage.
 You may experience these side effects: Dizziness, drowsiness (avoid
driving or the use of dangerous machinery while taking this drug).
 Report sore throat, fever, rash, itching, swelling in ankles or fingers;
changes in vision.
D. Olmesartan medoxomil

Brand name Benicar

Patient’s Dosage 20 mg/ day PO as a once-daily dose
Classification Angiotensin II receptor antagonist
Antihypertensive
Indication Treatment of hypertension, alone or in
combination with other hypertensives.
Action Selectively blocks the binding Angiotensin II to
specific tissue receptors found in the vascular
smooth muscle and adrenal gland; this action
blocks the vasoconstricting effect of the renin-
angiotensin system as well as the release of
aldosterone leading to decreased BP; may
prevent the vessel remodeling associated with
the development of atherosclerosis.
Pharmacokinetics
Route Onset Peak
Oral Varies 1-2 hours
Metabolism Hydrolyzed in GI tract; T 1/2 : 13hours
Distribution Crosses placenta; enters breast milk
Excretion Feces, urine
Dosage and Administration
Adults
20 mg/day as a once-daily dose; mat titrate to 40 mg/day if needed
after 2 weeks.
Pediatric Patients
Safety and efficacy not established.
Contraindications Contraindicated with hypersensitivity to any
component of drug, pregnancy (use during
the second or third trimester can cause injury
or death to the fetus.
Precaution Use cautiously with renal impairment,
hypovolemia, salt depletion.
Adverse Reactions and Side effects
Central Nervous Headache, dizziness, syncope, muscle
System weakness
Cardiovascular Hypotension, tachycardia
EENT Rash, inflammation, urticaria, pruritus,
alopecia, dry skin
Gastrointestinal Diarrhea, abdominal pain, nausea,
constipation, dry mouth, dental pain
Hematologic Increased CPK, hyperglycemia,
hypertriglycemia
Respiratory URI symptoms, bronchitis, cough, sinusitis,
rhinitis, pharyngitis.
Others Back pain, flulike symptoms, fatigue,
hematuria, arthritis
Nursing Considerations
Assessment
 History Hypersensitivity to any component of the drug, pregnancy,
lactation, hepatic or renal impairment hypovolemia, salt
depletion.
 Physical Skin lesions, turgor; body temp; reflexes, affect; BP, R,
respiratory auscultation; LFTs, renal function tests, serum
electrolytes.
Interventions
 Administer without regard to meals.
Black Box Warning: ensure that patient is not pregnant before beginning therapy. Suggest
the use of barrier birth control while using olmesartan; fetal injury and deaths have been
reported.
 Find an alternate method of feeding infant if given to a nursing mother. Depression of the
renin-angiotensin system in infants is potentially very dangerous.
Warning: alert the surgeon and mark the patient’s chart with notice that the olmesartan is
being taken. The blockage of the renin-angiotensin system following the surgery can
produce problems. Hypotension may be reversed with volume expansion.
 Monitor patient closely in any situation that may lead to decreased in BP secondary to
reduction in fluid volume- excessive perspiration, dehydration, vomiting, diarrhea;
excessive hypotension can occur.
Client/ Family Teaching
 Take drug without regard of meals. Do not stop taking this drug
without consulting your health care provider.
 Use barrier method of birth control while using this drug; if you
become pregnant or desire to become pregnant, consult your health
care provider.
 Take special precautions to maintain your fluid intake and safety
precautions in any situations that night cause a loss of fluid volume-
excessive perspiration, dehydration, vomiting, diarrhea; excessive
hypotension can occur.
 You may experience these side effects: Dizziness (avoid driving a
car or perform hazardous activitie0; headache (medications may be
available to help) nausea, vomiting diarrhea (proper nutrition is
important, consult dietician o maintain nutrition); symptoms of the
upper respiratory tract and cough (do not self medicate, consult
your health care provider if this becomes uncomfortable).
 Report fever, chills, dizziness, pregnancy, and swelling.