Cva

I.
PERSONAL DATA
Name: Mrs. Celie Ara Apostle
Sex: Female
Address: Tallungan, Reina, Mercedez
Birth date: July 26, 1960
Birth place: Luna, Isabella
Age: 49y/o
Occupation: House Keeper
Religion: Roman Catholic
Civil Status: Widow
Nationality: Filipino
II. HISTORY OF PAST ILLNESS
The daughter of the patient reported that the patient already has
diabetes and hypertension during her 30s and has no other sickness other
than those. Visual problems were also verbalized by the patient. Also, the
daughter verbalized of no surgery was done to the patient.
III. HISTORY OF PRESENT ILLNESS
Prior to admission, patient is having a slurred speech and an elevated
blood pressure. According to her daughter, the patient suddenly fell from her
seat and speech became incomprehensive, hand and feet movements
became imprecise.
Patient was then admitted in General Faustino M. Dy, Sr, Memorial
Hospital by her attending physician, Dr. Paguirigan, at exactly 08:50 in the
afternoon of July 7, 2009. She was admitted with the admitting diagnosis of
CVA probable infarct vs. hemorrhage.
Page 1 of 53
IV. BRIEF DESCRIPTION OF THE DISEASE

Cerebrovascular Accident
Definition:
It is characterized by a relatively abrupt onset of persisting
neurological symptoms due to the destruction of brain tissue (infarction)
cause by ischemia (thrombus or embolism) or hemorrhage resulting from
disorders in blood vessels that supply the brain. Also called stroke
Stroke any sudden onset focal neurological deficit
Causes:
Intracerebral hemmorhage (rupture of a blood vessel in the pia
mater or brain
Emboli (blood clots)
Atherosclerosis (formation of plaque) of the cerebral arteries.
Risk Factor:
1. Hypertension leading risk factor for coronary heart disease and stroke
treatable and can be controlled.
2. Modifiable by change in lifestyle
a. smoking
b. elevated serum cholesterol
c. obesity
d. heart disease
3. Modifiable by Medical mean
a. Transient Ischemic Attack
b. Asymptomatic carotid bruit
c. Diabetes Mellitus
d. Increased blood viscosity
e. HPN
4. Non modifiable risk factors
a. age
b. sex
c. race
d. previous stroke
Types of Stroke by Etilogy:
1. Hemorrhage stroke (intracranial hemorrhage)
5% of all strokes
two division
a. Intracerebral (10%) due to rupture of weakened vessels
within brain parenchyma as result of Hypertension,
arteriovenous malformation or tumor
Page 2 of 53
b. Subarachnoid (5%) result from aneurismal rupture of a

cerebral artery with blood loss into space surrounding the
brain; evolve over 1 2 hours.
2. Ischemic Strokes (remaining 85%)
Large (40%) or small (20%) vessel thrombosis
-most
commonly
occur
in
presence
of
atherosclerotic
cerebrovascular disease
-vascular changes or lipohyalinosis found in small deep penetrating
arteries as associated with chronic hypertension can lead to small
vessel thrombosis.
-rapid or prolonged interval of onset and may lead last many hours
Cerebral embolism (20%)
-usually a cardiac origin
-frequently result of chronic ischemic cardiovascular disease with
secondary ventricular wall hypokinessis or artial arrhythmia both
conditions increase risk of intracardiac thrombus formation
-quick onset and fully develop in a matter of minutes
Temporal Classification of Stroke
1. Transient ischemic attack (TIA)
neurologic symptoms develop and disappear over several
minutes and completely resolve in 24 hours
most frequently associated with atherosclerotic carotid artery
disease
2. Reversible Ischemic Neurologic Deficit
etiology unknown
likely the result from small infarctions (Lacunes) of the deep
subcortical gray and white matter resulting in only temporary
impairment
3. Stroke in Evolution
describe an unstable ischemic event characterized by the
progressive development of more severe neurologic impairment
often associated with active occlusive thrombosis of a major
cerebral artery.
Once stable called Complete Stroke
Most important sign Intellectual Regression
Page 3 of 53
Different Pathogenesis of Stroke

CRITERIA
Incidence
Mechanism
Onset and
Progression
Scenario
THROMBOTIC
40 %
ath
ero
sch
ero
stic
ste
rosi
s
or
occ
lusi
on
of
a
lar
ge
blo
od
ves
sel
gra
du
al,
slo
w
ste
pwi
se
pro
gre
ssi
on
of
sy
mp
to
ms
;
ma
y
be
ho
urs
to
da
ys
(+)
wa
rni
ng
sig
ns
co
m
mo
nly
occ
urs
EMBOLIC
30 %
- cholesterol
other
hematogenous
material
LACUNAR
20 %
- similar to
thrombosis; small
infarcts
HEMORRHAGE
10 %
- Hypertension
rupture of
penetrating
arterioles leading
to hemorrhage
- abrupt
- chronic
progress; gradual
onset
- sudden
- most occur in
setting of MI
Page 4 of 53
Sites
Clinical
manifestation
Prognosis
at
nig
ht
wit
h>
15
%
wit
h
TIA
int
ern
al
car
oti
d
or
MC
A
ap
has
ia
vis
ual
fiel
ds
cut
s
he
mi
par
esi
s
he
mis
ens
ory
sev
ere
im
pai
rm
ent
- cortical small
vessels
- small,
perforating
arterioles
- sites of Lacunes
- Cortical deficits
(hallmark)
- Descrite &
specific
subortical deficits
- Inc. ICP;
subcortical
deficits (more
extensive)
- Repeated in
same vascular
territory
- Excellent; 85 %
same vascular
teritory
po
or;
init
ial
me
nta
l
ret
ard
ati
on
50
%70
%
if
blo
od
is
rea
bso
rbe
Page 5 of 53
d
m
ild
def
icit
Comparison Between Right and Left Hemisphere Stroke

Right Hemisphere Lesion
- no deficits in ability to understand and
express language
- impaired ability to assess position in space
and to safety interact with environment;
neglect of (L) side may be present
- verbal memory interact (+) perceptual
memory impairment
- careless and oblivious of mistakes; impulsive
and
decreased
ability
to
anticipate
consequence of behavior
- impaired visual motor perception
- loss of visual memory
- lack of insights and judgement but not
obvious because of intact verbal fluency
- difficult to rehabilitate
Left Hemisphere Lesion

- aphasia
- usually unimpaired
- impaired ability to retain verbal information,
remote memory likely impaired
- appropriate emotion
- able to communicate property
- decreased vocabulary and auditory retention
span
- (+) visuomotor perception
- (+) visuomotor memory
- learn by visual demonstration step by step;
imitation
Typical Deficits Artery Involved

1. Anterior Cerebral Artery
paralysis and cortical hypersthesia of contralateral lower limb
mild involvement contralateral arm
impaired judgement / insight
apraxia of gait
sucking / grasp reflex contralateral side
bowel bladder incontinence
2. Middle Cerebral Artery
contralateral hemiplegia
hemianopsia
visual agnosia
loss sensation
dysphasia
4. Posterior Cerebral Artery
alexia
mental change with memory impairment
inability to recognize people and things (visual agnosia) often
temporary
3rd nerve palsy
Sequential Recovery Stages in Hemiplegia
S
tag
e
1
2
Muscle Tone
flaccid
Beginning spasticity
Limb Movement
None
- minimal voluntary
Others
- basic limb synergies or
Page 6 of 53
movement
some of their
components appear as
associated reactions
Full range of all synergy
components does not
necessarily develop
- full range of all synergy
components does not
necessarily develop
- basic limb synergies
lose their dominance
over motor acts
Increased spasticity; may be

severe (PEAK)
- voluntary control of
movement synergies
Spasticity begins to decline
- can master some

movement combinations
deviate from synergy
- more difficult movement
patterns learned
Spasticity disappears
(present only during rapid
movement)
- individual joint movement

possible coordination
approaches normal
- normal motor function
restored in some
5
6
Synergy Patterns of the Upper Extremity: Stroke

Scapula
Shoulder
Elbow
Forearm
Wrist and fingers
FLEXION
Retraction
/
elevation
or
hypertension
Abduction, external rotation
Flexion
Supination
Flexion
EXTENSION
Protraction
Abduction, internal rotation
Extension
Pronation
Flexion
Synergy Patterns of the Lower Extremity: Stroke

FLEXION
Flexion; abduction; external
notation
Flexion
Dorsiflexion; inversion
dorsiflexion
Hip
Knee
Ankle
Toe
EXTENSION
Extension, adduction; internal
rotation
Extension
Plantarflexion; inversion
Thrombotic Stroke
Is caused by occlusion of a large cerebral vessel by a thrombus (blood
clot).
Sit is most often occur in older people who are resting or sleeping. The
blood pressure is lower during sleep, so there is less pressure to push the
blood through an already narrowed arterial lumen, and ischemia may result.
Thrombi tend to form in large arteries that bifurcate and have
narrowed lumens as a result of deposits of atherosclerotic plaque.
The most common locations of thrombi are the internal carotid
artery, the vertebral arteries and the junction of the vertebral and
basilar arteries.
Occurs rapidly but progresses slowly.
COMMON SECONDARY POST-STROKE PROBLEMS
(EARLY & LATE)
EARLY
Urinary tract infection
Pressure sore
Dehydration
LATE
Spasticity
Contracture
Central post-stroke pain
syndrome
Page 7 of 53
Malnutrition
Dysphagia
Falls and injuries

Medication overuse
Shoulder dysfunction;
RSD
Depression
Sexual dysfunction
Seizure
Deconditioning and
endurance limitations
Fatigue
Insomia
Basal ganglia (As per patients CT Scan result)
Basal ganglia labeled at top right.

Latin
nuclei basales
NeuroNames
hier-206
MeSH
Basal+Ganglia
NeuroLex ID
birnlex_826
The basal ganglia (or basal nuclei) are a group of nuclei in the
brain interconnected with the cerebral cortex, thalamus and brainstem.
The mammalian basal ganglia are associated with a variety of
functions, including motor control and learning.
Currently popular theories implicate the basal ganglia in action
selection, that is, the decision of which of several possible behaviors to
execute at a given time. Anatomical studies show that the basal
ganglia exert an inhibitory influence on a number of motor systems,
and physiological studies show that a release of this inhibition permits
a motor system to become active. The "behavior switching" that takes
place within the basal ganglia is influenced by signals from many parts
of the brain, including the prefrontal cortex, which is widely believed to
play a key role in executive functions.
The main components of the basal ganglia are the striatum,
pallidum, substantia nigra, and subthalamic nucleus. The striatum, a
large neural mass at the base of the forebrain, receives input from
many brain areas but sends output only to other components of the
basal ganglia. The pallidum receives its most important input from the
striatum (either directly or indirectly), and sends inhibitory output to a
Page 8 of 53
number of motor-related areas, including the part of the thalamus that

projects to the motor-related areas of the cortex. The substantia nigra
consists of two parts, one that functions similarly to the pallidum, and
another that is the source of dopamine input to the striatum. The
subthalamic nucleus receives input mainly from the striatum and
cortex, and projects to the pallidum. Each of these areasthe striatum
in particularalso has a very complex internal anatomical and
neurochemical organization.
The basal ganglia play a central role in a number of neurological
conditions, including several movement disorders. The most notable
are Parkinson's disease, which involves degeneration of the dopamine
cells in the substantia nigra, and Huntington's disease, which primarily
involves damage to the striatum. Basal ganglia disfunction is also
implicated in some other disorders of behavior control such as
Tourette's syndrome and obsessivecompulsive disorder, although the
neural mechanisms underlying these are not well understood.
The basal ganglia have a limbic sector whose components are
assigned distinct names: the nucleus accumbens (ventral striatum),
ventral pallidum, and ventral tegmental area (VTA). The VTA supplies
dopamine to the nucleus accumbens and prefrontal cortex. This
dopaminergic projection has attracted a great deal of attention,
because there is much evidence that it plays a central role in reward
learning. A number of highly addictive drugs, including cocaine,
amphetamines, and nicotine, act to increase the efficacy of the VTA
dopamine signal. There is also evidence implicating overactivity of the
VTA dopaminergic projection in schizophrenia.
Terminology
The nomenclature of the basal ganglia system and its
components has always been problematic. Early anatomists, seeing
the macroscopic structure but knowing nothing of the cellular
architecture or functional organization, grouped together components
that are now believed to have distinct functions (such as the internal
and external segments of the globus pallidus), and give distinct names
to components that are now thought to be functionally parts of a single
structure (such as the caudate nucleus and putamen).
The term "basal" comes from the fact that most of its elements
are located in the basal part of the forebrain. The term ganglia is an
anomaly: in modern usage, neural clusters are only called "ganglia" in
the peripheral nervous system; in the central nervous system they are
referred to as "nuclei". For this reason, the basal ganglia are also
occasionally known as the "basal nuclei". Terminologia anatomica
(1998), the international authority for anatomical naming, retained
"nuclei basales", which is not commonly used.
The International Basal Ganglia Society (IBAGS) informally
considers the basal ganglia to be made up of the striatum, the
pallidum (with two nuclei), the substantia nigra (with its two distinct
parts) and the subthalamic nucleus. Percheron et al. in 1991 and
Parent and Parent in 2005 included the central region (centre medianparafascicular) of the thalamus as part of the basal ganglia, while
Mena-Segovia et al. in 2004 included the pedunculopontine complex as
well.
Anatomy
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Coronal slices of human brain showing the basal ganglia. White matter is shaded darkly, gray
matter lightly.
ANTERIOR: striatum, globus pallidus (GPe and GPi)
POSTERIOR: subthalamic nucleus (STN), substantia nigra (SN)
Main article: Anatomical subdivisions and connections of the basal ganglia
The basal ganglia form a fundamental component of the

vertebrate telencephalon (forebrain). In contrast to the pallial or
cortical layer that lines the surface of the forebrain, the basal ganglia
are a collection of distinct masses of gray matter lying in the interior,
not far from the junction with the thalamus. Like most parts of the
brain, the basal ganglia consist of left and right sides that are virtual
mirror images of each other.
At the highest level, the basal ganglia are divided by anatomists
into four distinct structures. Two of them, the striatum and pallidum,
are relatively large; the other two, the substantia nigra and
subthalamic nucleus, are smaller. In the illustration to the right, two
coronal sections of the human brain show the location of the basal
ganglia. The subthalamic nucleus and substantia nigra lie farther back
in the brain than the striatum and pallidum.
Connections
Connectivity diagram showing excitatory glutamatergic pathways as red,

inhibitory GABAergic pathways as blue, and modulatory dopaminergic as magenta.
The flow of neural signals through the basal ganglia is strongly

directional. The striatum is the primary recipient of input from other
brain areas, most notably the cerebral cortex. The internal segment of
the globus pallidus (GPe), together with the reticular part of the
substantia nigra (SNr), give rise to the primary output, most notably to
the thalamus. The striatum projects to the pallidum both directly and
indirectly via the subthalamic nucleus, which also receives cortical
input. The substantia nigra consists of two parts, one of which
functions similarly to the pallidum, the other of which sends a
modulatory dopaminergic input to the striatum and other structures.
The adjoining figure shows some of the most important
connections between components. On the largest scale, the basal
ganglia form a loop that begins and ends in the cortex. Anatomists
Page 10 of 53
have distinguished two main circuits, known as the "direct" and

"indirect"
pathways.
The
direct
pathway
runs
cortexstriatumGPithalamuscortex. Two of these links are
excitatory, and two inhibitory, so the net effect of the whole sequence
is excitatory: the cortex excites itself via the direct pathway. The
indirect
pathway
runs
cortexstriatumGPeSTNGPithalamuscortex. Three of these
links are inhibitory and two excitatory, so the net effect of the
sequence is inhibitory: the cortex inhibits itself via the indirect
pathway. The total effect of basal ganglia upon the cortex is believed to
result from a complex interplay between these two pathways.
Striatum
The striatum is the largest component of the basal ganglia. The
term "striatum" comes from the observation that this structure has a
striped appearance when sliced in certain directions, arising from
numerous large and small bundles of nerve fibers (white matter) that
traverse it. Early anatomists, examining the human brain, perceived
the striatum as two distinct masses of gray matter separated by a
large tract of white matter called the internal capsule. They named
these two masses the "caudate nucleus" and "putamen". More recent
anatomists have concluded, on the basis of microscopic and
neurochemical studies, that it is more appropriate to consider these
masses as two separated parts of a single entity, the "striatum", in the
same way that a city may be separated into two parts by a river.
Numerous functional differences between the caudate and putamen
have been identified, but these are taken to be consequences of the
fact that each sector of the striatum is preferentially connected to
specific parts of the cerebral cortex.
The internal organization of the striatum is extraordinarily
complex. The great majority of neurons (about 96%) are of a type
called "medium spiny neurons". These are GABAergic cells (meaning
that they inhibit their targets) with small cell bodies and dendrites
densely covered with dendritic spines, which receive synaptic input
primarily from the cortex and thalamus. Medium spiny neurons can be
divided into subtypes in a number of ways, on the basis of
neurochemistry and connectivity. The next most numerous type
(around 2%) are a class of large cholinergic interneurons with smooth
dendrites. There are also several other types of interneurons making
up smaller fractions of the neural population.
Numerous studies have shown that the connections between
cortex and striatum are generally topographic; that is, each part of the
cortex sends stronger input to some parts of the striatum than to
others. The nature of the topography has been difficult to understand,
howeverperhaps in part because the striatum is organized in three
dimensions whereas the cortex, as a layered structure, is organized in
two. This dimensional discrepancy entails a great deal of distortion and
discontinuity in mapping one structure to the other.
Pallidum
The pallidum consists of a large structure called the globus
pallidus ("pale globe") together with a smaller ventral extension called
the ventral pallidum. The globus pallidus appears as a single neural
mass, but can be divided into two functionally distinct parts, called the
internal (sometimes "medial") and external (sometimes "lateral")
segments, abbreviated GPi and GPe. Both segments contain primarily
Page 11 of 53
GABAergic neurons, which therefore have inhibitory effects on their

targts. The two segments participate in distinct neural circuits. The
external segment, or GPe, receives input mainly from the striatum, and
projects to the subthalamic nucleus. The internal segment, or GPi,
receives signals from the striatum via two pathways, called "direct"
and "indirect". The direct pathway consists of direct projections from
the striatum to the GPi. The indirect pathway consists of projections
from the striatum to the GPe, followed by projections from the GPe to
the subthalamic nucleus (STN), followed by projections from the STN to
the GPi. These pathways have opposite net effects: striatal activity
inhibits the GPi via the direct pathway because striatal outputs are
GABAergic, but has a net excitatory effect on the GPi via the indirect
pathway because this three-link pathway consists of two inhibitory
links plus one excitatory link.
Pallidal neurons operate using a "disinhibition" principle. These
neurons fire at steady high rates in the absence of input, and signals
from the striatum cause them to "pause". Because pallidal neurons
themselves have inhibitory effects on their targets, the net effect of
striatal input to the pallidum is a reduction of the tonic inhibition
exerted by pallidal cells on their targets.
Subthalamic nucleus
Function
The greatest source of insight into the functions of the basal
ganglia has come from the study of two neurological disorders,
Parkinson's disease and Huntington's disease. For both of these
disorders, the nature of the neural damage is well understood and can
be correlated with the resulting symptoms. Parkinson's disease
involves major loss of dopaminergic cells in the substantia nigra;
Huntington's disease involves massive loss of medium spiny neurons in
the striatum. The symptoms of the two diseases are virtually opposite:
Parkinson's disease is characterized by gradual loss of the ability to
initiate movement, while Huntington's disease is characterized by an
inability to prevent parts of the body from moving unintentionally. It is
noteworthy that although both diseases have cognitive symptoms,
especially in their advanced stages, the most salient symptoms relate
to the ability to initiate and control movement. Thus, both are
classified primarily as movement disorders. A different movement
disorder, called hemiballismus, may result from damage restricted to
the subthalamic nucleus. Hemiballismus is characterized by violent and
uncontrollable flinging movements of the arms and legs.
Role in motivation
Although the role of the basal ganglia in motor control is clear,
there are also many indications that it is involved in the control of
behavior in a more fundamental way, at the level of motivation. In
Parkinson's disease, the ability to execute the components of
movement is not greatly affected, but motivational factors such as
hunger fail to cause movements to be initiated or switched at the
proper times. The immobility of Parkinsonian patients has sometimes
been described as a "paralysis of the will". These patients have
occasionally been observed to show a phenomenon called kinesia
paradoxica, in which a person who is otherwise immobile responds to
an emergency in a coordinated and energetic way, then lapses back
into immobility once the emergency has passed.
Page 12 of 53
The role in motivation of the "limbic" part of the basal ganglia

the nucleus accumbens (NA), ventral pallidum, and ventral tegmental
area (VTA)is particularly well established. Thousands of experimental
studies combine to demonstrate that the dopaminergic projection from
the VTA to the NA plays a central role in the brain's reward system.
Animals with stimulating electrodes implanted along this pathway will
bar-press very energetically if each press is followed by a brief pulse of
electrical current. Numerous things that people find rewarding,
including addictive drugs, good-tasting food, and sex, have been
shown to elicit activation of the VTA dopamine system. Damage to the
NA or VTA can produce a state of profound torpor.
Although it is not universally accepted, some theorists have
proposed a distinction between "appetitive" behaviors, which are
initiated by the basal ganglia, and "consummatory" behaviors, which
are not. For example, an animal with severe basal ganglia damage will
not move toward food even if it is place a few inches away, but if the
food is placed directly in the mouth, the animal will chew it and
swallow it.
Comparative anatomy and naming
The basal ganglia form one of the basic components of the
forebrain, and can be recognized in all species of vertebrates. Even in
the lamprey (generally considered one of the most primitive of
vertebrates), striatal, pallidal, and nigral elements can be identified on
the basis of anatomy and histochemistry.
The names given to the various nuclei of the basal ganglia are different
in different species:
For example, the "internal segment of the globus pallidus" in

primates is called the "entopenduncular nucleus" in rodents.
The "striatum" and "external segment of the globus pallidus" in

primates are called the "paleostriatum augmentatum" and
"paleostriatum primitivum" respectively in birds.
A clear emergent issue in comparative anatomy of the basal

ganglia is the development of this system through phylogeny as a
convergent cortically re-entrant loop in conjunction with the
development and expansion of the cortical mantle. There is
controversy, however, regarding the extent to which convergent
selective processing occurs versus segregated parallel processing
within re-entrant closed loops of the basal ganglia. Regardless, the
transformation of the basal ganglia into a cortically re-entrant system
in mammalian evolution occurs through a re-direction of pallidal (or
"paleostriatum primitivum") output from midbrain targets such as the
superior colliculus, as occurs in sauropsid brain, to specific regions of
the ventral thalamus and from there back to specified regions of the
cerebral cortex that form a subset of those cortical regions projecting
into the striatum. The abrupt rostral re-direction of the pathway from
the internal segment of the globus pallidus into the ventral thalamus-via the path of the ansa lenticularis--could be viewed as a footprint of
this evolutionary transformation of basal ganglia outflow and targeted
influence. The evolutionary emergence of cortical re-entrant systems in
the brain has been postulated by Gerald Edelman as a critical basis for
the emergence of primary consciousness in the theory of Neural
Darwinism.
Neurotransmitters
Page 13 of 53
In most regions of the brain, the predominant classes of neurons

use glutamate as neurotransmitter and have excitatory effects on their
targets. In the basal ganglia, however, the great majority of neurons
use GABA as neurotransmitter and have inhibitory effects on their
targets. The inputs from the cortex and thalamus to the striatum and
STN are glutamatergic, but the outputs from the striatum, pallidum,
and substantia nigra pars reticulata all use GABA. Thus, following the
initial excitation of the striatum, the internal dynamics of the basal
ganglia are dominated by inhibition and disinhibition.
Other neurotransmitters have important modulatory effects. The
most intensively studied is dopamine, which is used by the projection
from the substantia nigra pars compacta to the striatum, and also in
the analagous projection from the ventral tegmental area to the
nucleus accumbens. Acetylcholine also plays an important role, being
used both by several external inputs to the striatum, and by a group of
striatal interneurons. Although cholinergic cells make up only a small
fraction of the total population, the striatum has one of the highest
acetylcholine concentrations of any brain structure.
Other disorders linked with the basal ganglia
Attention-deficit hyperactivity disorder (ADHD)
Athymhormic syndrome (PAP syndrome)
Cerebral palsy: basal ganglia damage during second and third

trimester of pregnancy
Dystonia
Fahr's disease
Foreign accent syndrome (FAS)
Huntington's disease
Lesch-Nyhan syndrome
Obsessive-compulsive disorder
Parkinson's disease
Tourette's disorder
Tardive dyskinesia, caused by chronic antipsychotic treatment
Stuttering
Spasmodic dysphonia
Wilson's disease
Blepharospasm
History
The acceptance that the basal ganglia system constitutes one
major cerebral system took long to arise. The first anatomical
identification of distinct subcortical structures was published by
Thomas Willis in 1664. For many years, the term corpus striatum was
used to describe a large group of subcortical elements, some of which
were later discovered to be functionally unrelated. For many years, the
putamen and the caudate nucleus were not associated with each other.
Instead, the putamen was associated with the pallidum in what was
called the nucleus lenticularis or nucleus lentiformis.
Page 14 of 53
A thorough reconsideration by Ccile and Oskar Vogt Ccile and

Oskar Vogt (1941) simplified the description of the basal ganglia by
proposing the term striatum to describe the group of structures
consisting of the caudate nucleus, the putamen and the mass linking
them ventrally, the nucleus accumbens. The striatum was named on
the basis of the striated (striped) appearance created by radiating
dense bundles of striato-pallido-nigral axons, described by anatomist
Samuel Alexander Kinnier Wilson (1912) as "pencil-like".
The anatomical link of the striatum with its primary targets, the
pallidum and the substantia nigra was discovered later. The name
globus pallidus was attributed by Djerine to Burdach (1822). For this,
the Vogts proposed the simpler "pallidum". The term "locus niger" was
introduced by Flix Vicq-d'Azyr as tache noire in (1786), though that
structure has since become known as the substantia nigra, due to Von
Smmering in 1788. The structural similarity between the substantia
nigra and globus pallidus was noted by Mirto in 1896. Together, the two
are known as the pallidonigral ensemble, which represents the core of
the basal ganglia. Altogether, the main structures of the basal
ganglia are linked to each other by the striato-pallido-nigral bundle,
which passes through the pallidum, crosses the internal capsule as the
"comb bundle of Edinger", then finally reaches the substantia nigra.
Additional structures that later became associated with the basal
ganglia are the "body of Luys" (1865) (nucleus of Luys on the figure) or
subthalamic nucleus, whose lesion was known to produce movement
disorders. More recently, other areas such as the central complex
(centre mdian-parafascicular) and the pedunculopontine complex
have been thought to be regulators of the basal ganglia.
Near the beginning of the 20th century, the basal ganglia system
was first associated with motor functions, as lesions of these areas
would often result in disordered movement in humans (chorea,
athetosis, Parkinson's disease).
Page 15 of 53
V. ANATOMY AND PHYSIOLOGY

The Brain
BRAIN
Made up of 1000 billion neurons and is one of the largest organs of the
body, weighing about 1300 kg (3 lbs).
It is a mushroom shaped
4 Principal Parts
1. Brain Stem
Stalk of the mushroom
Consist of medulla oblongata, pons and midbrain
2. Diencephalon
Consisting primarily of the thalamus and hypothalamus
3. Cerebrum
Spreads over the diencephalons
Constitute about seven-eights of the total weight of the brain and
occupies most of the cranium.
4. Cerebellum
Inferior to the cerebrum and posterior to the brain stem
Protection and Coverings
The brain is protected by the cranial bones. Like the spinal cord. The
brain is also protected by meninges. The cranial meninges surround the
brain are continues with the spinal meaninges and have the same basic
structure and bear the same names as the spinal meninges.
1. Dura meter
pachymenix, tough fibrous tissue

- outermost covering
2. Arachnoid - together with the pia meter is called Leptomeninges
- middle, delicate thin cob-web like membrane
3. Pia meter - innermost
- soft thin membrane which closely lines brain and spinal
cord extending into all fissures and sulci.
- extends around blood vessels throughout the brain.
Main Sulci and Fissures of Cerebral Cortex
1. Lateral or Sylvian Fissure
Divided the temporal lobe from the frontal and parietal lobe
Buried under the posterior part of the SYLVIAN FISSURE is the
TRANSVERSE TEMPORAL gyri which contains the AUDITORY
RECEPTIVE AREA.
2. Rolandic or Central Sulcus
Separates the frontal lobe from the parietal lobe
It separates the precentral gyrus from the Postcentral gyrus, thus
separating the motor from the somasthetic area.
3. Longitudinal Cerebral Fssure
Page 16 of 53
Divides the cerebral hemispheres into right and left halves.

4. Parietooccipital Fissure
Separates the parietal lobe from the occipital lobe.
5. Calcarine Sulcus
This sulcus is surrounded by the visual receptive area.
Lobes of Cerebral Cortex and Brodmanns Classification
The function of the cerebral cortex has been mapped out into areas by
Broadmann. These two major types of cortical areas are:
1. Primary Cortical Area regions directly related to a specific function
2. Secondary Cortical Area/ Association Area these lie adjacent to the
primary area and are concerned with a higher level of organization and
integration.
The Major Primary and Association Areas
1. Frontal Lobe
Area 4
Area 6
Area 8
area
Area 44
- primary motor area

- premotor area
- frontal eye movement and papillary change
- motor speech (Brocas Area)
2. Parietal Lobe
Area 3, 1, 2
- primary sensory areas
Area 5, 7
- sensory association areas
Area 39 40
- Wernickes area
Area 5, 7, 39 40 - Gnostic area
Area 43
- primary gustatory area
3. Occipital Lobe
Area 17
Area 18 29
4. Temporal Lobe
Area 41
Area 42 & 22
- primary visual cortex

- visual association areas
- primary auditory cortex
- auditory association areas
AREA 4: PRIMARY MOTOR AREA

Location
: precental gyrus and paracentral lobule
Function
: contralateral voluntary motor activity
Clinical findings when damaged:
Irritative lesions will present with convulsive seizures
Gross lesions will result in flaccid paralysis and areflexia
AREA 6: PREMOTOR AREA
Location
: Superior Frontal Gyrus (lateral aspect)
Function
: Sensorially guided movements this refers to voluntary
motor activity dependent on sensory, inputs; these movements
are activated in response to visual, auditory and somatosensory
stimuli.
SUPPLEMENTARY MOTOR AREA
Page 17 of 53
Location
: Medial aspect of Area 6
Function
: Programming and planning of motor activities and
perhaps their imitation.
Has presentation for both right and left sides as well as
proximally and distally.
AREA 8: FRONTAL EYE FIELD AREA
Location
: Frontal lobe
Function
: Center of voluntary movements of the eye INDEPENDENT
of visual stimuli such as the conjugate eye movements.
All three areas with motor function (4, 6 & 8) receive inputs
from the thalamus, cerebellum, other cortical regions and other
peripheral receptors.
AREA 17: PRIMARY VISUAL AREA
Location
:
OCCIPITAL LOBE specifically along the lips of the
calcarine sulcus; this is called the visual or striate area.
Function
: vision
Clinical findings when damanged:
an irritative lesion will present with visual hallucinations
a destructive lesion will cause contralateral homonymous defects
of visual fields and visual disorganization.
Area 18 & 19 secondary visual areas
AREA 41: PRIMARY AUDITORY AREA
Location
: TEMPORAL LOBE specifically at the transverse gyri
Function
: hearing
Clinical findings when damaged:
irritative lesion will cause buzzing and roaring sensation
unilateral destructive lesion will lead to a mild hearing loss
bilateral destructive lesion will lead to a complete hearing loss
SECONDARY AUDITORY AREA: AREA 42 & 22, HESCHIL AREA
The auditory association area is involved in the comprehension of
language and lesions in this area results in auditory agnosia or the inability
to recognize what he hears but patient has intact hearing).
FRONTAL LOBE: additional notes
lie interior to the central sulcus and lateral fissure
main function: motor, cognition, speech, affective behavior
PREFRONTAL CORTEX (Area 9, 10, 11, 12) is essential for abstract
thinking, foresight and judgement
A lesion in the prefrontal cortex results in behavior at changes and
changes in cognitive function.
Functions of Principal Parts of the Brain
PARTS
FUNCTION
BRAIN STEM
Medulla
1. Relays motor & sensory impulses

between other parts of the brain and the
spinal cord.
2. Reticular formation (also in pons,
midbrain and diencephalons) functions
Page 18 of 53
3.
4.
5.
6.
Pons
1.
2.
3.
MIDBRAIN
DIENCEPHALON
Thalamus
Hypothalamus
in consciousness and arousal)

Vital reflex centers regulate heartbeat,
breathing (together with pons) and
blood vessel diameter.
Nonvital
reflex
centers
coordinate
swallowing, coughing, sneezing and
hiccupping.
Contains nuclei of origin for CN 8, 9, 10,
11 and 12.
Vestibular
nuclear
complex
helps
maintain equilibrium.
Relay impulses with in the brain and
between parts of the brain and spinal
cord.
Contains nuclei of origin of CN 5, 6, 7 &
8
Pneumotoxic area and apneustic area,
together with the medulla, help control
breathing.
1. Relay motor impulses from the cerebral

cortex to the pons and spinal cord and
relays sensory impulses from the spinal
cord to the thalamus.
2. Superior
colliculi
coordinates
movements of the eyeballs in response
to visual and other stimuli and the
inferior colliculi coordinate movements
of the head and trunk in response to
auditory stimuli.
3. Contains nuclei of origin for cranial
nerves III & IV.
1. Several nuclei serve as relay stations for
all sensory impulses, except small, to
the cerebral cortex.
2. Relays motor impulses from the cerebral
cortex to the spinal cord.
3. Interprets pain, temperature, light
touch, and pressure sensations.
4. Anterior nucleus functions in emotions
and sensory.
1. Controls and integrates the autonomic
nervous system.
2. Receives impulses from viscera
3. Regulates and controls the pituitary
gland
4. Center for mind-over-body phenomena
5. Secrets regulating hormones
6. Functions in rage and aggression
7. Controls normal body temperature,
food intake and thirst
8. Helps maintain the walking state and
sleep
9. Functions as a self-sustained oscillator
Page 19 of 53
Cerebrum
CEREBELLUM
that drives many biological rhythms.

1. Sensory
areas
interprets
sensory
impulses, motor areas function in
emotional and intellectual processes.
2. Basal ganglia control gross muscle
movements and regulate muscle tone.
3. Limbic system functions in emotional
aspects of behavior related to survival.
1. Controls subconscious skeletal muscle
contractions required for coordination,
posture and balance.
2. Assume
a
role
in
emotional
development, modulating sensations of
anger and pleasure.
Vascular Anatomy
Blood
Transport oxygen, nutrients and other substances for brain functioning
Carries away metabolites
Approximately 18% of total blood volume in brain.
Brain uses 20% of oxygen absorbed in the lungs
Two major arteries supplying blood to the brain are the INTERNAL
CAROTID ARTERY & VERTEBRAL ARTERY.
Branches of ICA: ophthalmic, middle cerebral and anterior cerebral
artery.
Vertebral artery unites to form the basilar artery in the pons.
Branches of vertebrobasilar artery: posterior cerebral, posterior and
anterior inferior cerebellar, pontine and internal auditory arteries.
The circle of Willis is formed by the PCA, ACA, anterior communicating
and posterior communicating arteries.
The MIDDLE CEREBRAL ARTERY does not form part of the circle of Willis
The venous drainage of the cerebrum includes the veins of the brain
itself, dural venous sinuses, meningeal veins (dura) and diploic veins.
CEREBRAL ARTERIES
1. MIDDLE CEREBRAL ARTERY (MCA)
From internal carotid artery
Blood supply to deep structures
Enters lateral fissure sends cortical branches to lateral aspect of
FRONTAL, TEMPORAL, PARIETAL, & OCCIPITAL LOBES.
Basal MCA sends small penetrating lenticulo striate arteries to supply
internal capsule and adjacent structures.
2. ANTERIOR CEREBRAL ARTERY (ACA)
Also branch of the internal carotid artery
Internal carotid artery to longitudinal fissure to genes of corpus
callosum - sends branches to medial frontal and parietal lobes and
adjacent cortex, extending posteriorly.
3. POSTERIOR CEREBRAL ARTERY (PCA)
Basilar artery sends branch to medial and inferior surface of the
temporal lobe and medial occipital lobe.
Page 20 of 53
Blood supply to choroids plexuses of III & IV ventricles

With calcarine artery and perforating branches to posterior thalamus
and subthalamus.
Page 21 of 53
VI. LABORATORY
COMPUTED TOMOGRAPHY SCAN
Date: July 13, 2009
COMPUTED TOMOGRAPHY SCAN
Plain Study
Non contrast CT scan using 5mm in the posterior fossa and
10mm contiguous slices in the supratentorial region show the
following findings:
- There is a focus of low attenuation density seen in the right
basal ganglia extending into the ispilateral internal capsule.
Hypodense focus is seen on the right frontal perventricular
white matter region.
- Small foci on low attenuation density are also noted on the
left basal ganglia.
- No definite evidence of intracranial hemorrhage noted.
- Midline stuctures are not displaced.
- Ventricles are not dilated or displaced.
- Cortical sulci and cisterns are not unusual.
- Posterior fossa structures are remarkable.
- Visualized osseous structures are intact.
- Both frontal sinus are aplastic. There is opacification of the
left ethmoid sinus.
- Calcifications are seen in the pineal gland which are
physiologic in nature.
- Paucity of pnuemonized air cells are noted on the right
mastoid compared to the cotralateral side.
IMPRESSION:
Impression of the CT scan: Acute to subacute infarcts,
right basal ganglia periventricular white matter region
as described.
Lacunar infarcts, left basal ganglia.
Negative intracranial hemorrhage. Aplastic frontal
Interpretation:
From the result of the CT scan and from its plain study, it shows that
there is a sub acute infarct at the right basal ganglia periventricular white
matter region as described and a lacunar infarcts on the left basal ganglia.
This causes the slurred speech symptom of the patient as well as its
decreased motor responses. The plain study also indicates that there is a
negative intracranial hemorrhage thus proving the diagnosis CVA probable
infarct vs hemorrhage. It also shows a sclerosis on the right mastoid.
Nursing consideration:
1. Ensure a signed consent and explain the procedure to the patient as
well with the SOs.
2. Check hospital policy on withholding food and fluids. Clients are
usually on NPO status
3. (Except for medications ordered as part of the test) for 8 hours
before the test if its done in the morning. If the test is done in the
afternoon the client may have a liquid breakfast.
4. Give medications up to 2 hours before test.
5. Asses for possible reaction to iodine dye (by asking about allergy to
seafood). Document any allergy and inform the physician and
radiography department.
6. Remove metal hairpins, clips and earrings.
Page 22 of 53
URINALYSIS
Date: July 13, 2009
COLOR
TRANSPARENCY
PH/REACTION
SPECIFIC GRAVITY
CAST/LFP
Hayline Cast
CELLS/HPF
WBC/Pus Cell
RBC/Red Blood Cell
Yeast Cells
Pregnancy Test
Lt. Yellow
Sl. Turbid
6.5 (4.5-8.0)
1.015 (1.005-1.030)
3-6 (0-4)
>50 (<2)
PROTEIN
SUGAR
ACETONE
BILE PIGMENTS
CRYSTALS
Amorp.
Urate/Phospates
EPITHELIAL CELLS
Squamous
Renal
MUCUS THREADS
Bacteria
Few
Rare
Rare
Occasional
Interpretation:
The urinalysis of the above patient shows that there is an increase in
RBC. This suggest that RBC cast indicates hemorrhage in the nephron thus
suggesting acute glomerolonephritis. This might be due to the prolonged
catheterization, increasing the ascending infection causing damage to the
nephron. With regards to this, it indicates that there is an acute bacterial
infection within the urinary tract, supported by the U/A laboratory result with
an increase WBC.
Nursing consideration before Urinalysis:
1. Instruct patient to collect urine early in the morning (Clean catch
technique).
2. Collect midstream urine.
3. Bring obtained specimen to the laboratory no more than 30
minutes.
HEMATOLOGY
Date: July 7, 2009
EXAMINATIONS
HEMOGLOBIN
HEMATOCRTI (HCT)
LEUKOCYTE COUNT (WBC)
DIFFERENTIAL COUNT:
Nuetrophils
Lymphocytes
Eosinophils
Toxic Granules
Clotting Time
Bleeding Time
Malarial Smear
132
39
13.1
84
15
1
REFERENCE VALUES
120-160 g/L
34-47 vol %
5.0-10.0
50-70 %
20-40 %
1-3 %
Negative
2-6 minutes
1-4 minutes
No Malarial Parasite Seen (NMPS)
Intrepretation:
Leukocytosis is a raised white blood cell count (the leukocyte count)
above the normal range. This increase in leukocytes (primarily neutrophils) is
usually accompanied by a "left shift" in the ratio of immature to mature
neutrophils. The increase in immature leukocytes increases due to
proliferation and release of granulocyte and monocyte precursors in the bone
marrow which is stimulated by several products of inflammation including
C3a and G-CSF. Although it may be a sign of illness, leukocytosis in-and-of
itself is not a disorder, nor is it a disease. It is simply a laboratory finding. A
leukocyte count above 25 to 30 x 109/L is termed a leukemoid reaction,
which is the reaction of a healthy bone marrow to extreme stress, trauma, or
infection. (It is different from leukemia and from leukoerythroblastosis, in
Page 23 of 53
which immature blood cells are present in peripheral blood.) Leukocytosis is

very common in acutely ill patients. It occurs in response to a wide variety of
conditions, including viral, bacterial, fungal, or parasitic infection, cancer,
hemorrhage, tissue necrosis(for this case, brain tissue death or infarct)
and exposure to certain medications or chemicals including steroids.
Leukocytosis can also be the first indication of neoplastic growth of
leukocytes.
Nursing consideration:
1. Explain the procedure and the purpose of the test.
2. Assess the clients knowledge of the test.
3. Adhere standard precaution.
4. Apply pressure to the venipuncture site.
5. Explain that some bruising, discomfort, and swelling may appear
at
the site and that moist compress can alleviate this.
6. Monitor signs of infections.
BLOOD CHEMISTRY
Date: July 8, 2009
EXAMINATIONS
Glucose (Fasting)
Total Cholesterol
Blood Urea Nitrogen
Serum Creatinine
RESULT
3.26
7.52
9.0
167.4
S.I. UNITS
mmol/L
mmol/L
mmol/L
mol/L
NORMAL VALUES
3.85-6.05
3.9-5.1
1.7-9.3
53-106
Interpretation:
Too much cholesterol in the blood, however, can cause deposits of
cholesterol inside arteries. These plaques can narrow the artery enough to
block blood flow. This process known as atherosclerosis commonly occurs in
the coronary arteries which nourish the heart. For this case, an increase in
the Total Cholesterol is just a proof supporting the atherosclerosis and the CT
scan result having an impression of a sclerotic right mastoid.
Measuring serum creatinine is a simple test and it is the most
commonly used indicator of renal function. A rise in blood creatinine levels is
observed only with marked damage to functioning nephrons. Therefore, this
test is not suitable for detecting early stage kidney disease. The increase
serum createnine is only indicative that due to the ischemic stroke there is a
renal failure and the damaged nephrones are caused by bacterial infections.
Nursing Considerations:
1. Explain the procedure and the purpose of the test.
2. Assess the clients knowledge of the test.
3. Adhere standard precaution.
4. Apply pressure to the venipuncture site.
5. Explain that some bruising, discomfort, and swelling may appear
at
the site and that moist compress can alleviate this.
6. Monitor signs of infections.
Page 24 of 53
VII. PATHOPHYSIOLOGY
ETIOLOGY
Subacute
Infarct,
righ
basal
ganglia and right perventricular
white matter region
Lacunar Infarct, left basal ganglia
Sclerotic Mastiod, right
RISK FACTOR
Age
Hypertension
Diet (LDL)
DIC
Deposition of atherosclerotic
Plaque in intima of arteries
Elastic lamina become thin and frayed
Platelet adhere to rough surface
Release of adenosine diphosphate enzyme
Thrombus form
Enlargement of
thrombus
Narrowed lumen
Break off
Emboli
Occlusion of affected
blood vessels
Vertebral arteries
Vertebrobasilar arteries
Dysphagia
Numbness
Weakness
Dysarthria
Gait problem
Vertigo
Ataxia
Hemiparesis
Headache
Internalcarotid arteries
Paralysis
Lower facial
Sensory
loss
weakness
Numbness
Syncope
Page 25 of 53
VIII. PHYSICAL ASSESSMENT

PSYCHOSOCIAL
Significant others
The patient is visited by

her daughters and
nieces.
Coping Mechanism
Interacting with SO and

Laughing trip.
Religion
Roman Catholic
Primary Language
Ibanag/ Ilocano/ Tagalog
Financial Source of
Health Care
Patients older sister

working in Dubai and
patients first cousin
working in London.
Bakery Manager
LOC: Conscious
Occupation
General appearance
GCS:
Eyes
Verbal
Motor
TOTAL
3
2
4 .
9
Speech
Weak in appearance
The patient still knows
where she is, when she
was admitted and who
are the SO present.
Patient still has a good
memory thus she recalls
diet prescribed her
physician and thus still
remembers a lot things.
Slurred speech
Non-verbal behavior
Silence
Orientation
Memory
PATHOPHYSIOLOGICAL
BASIS
A very supportive family who
shows comfort and care that
can relieve stress that is felt by
the patient
Being happy during treatment
can contribute to patients fast
recovery and interaction with in
the family can be a diversion
activity thus reducing pain and
stress.
It is important to know, for
there might be beliefs of a
certain religion that has a
conflict with a health
intervention.
Language can be a barrier for
an effective nursing
intervention thus it is important
for a nurse to know what
language to use to have an
effective communication.
Brain damage not that severe.

Due to decreased O2 supply
and perfusion in the brain.
Due to illness.
An abnormal orientation can be
a symptom of brain damage
caused by CVA
Damaged cause by the infarct is
not yet that severe to affect the
memory of the patient.
Dysarthria resulting from
lacunar infarcts, right and left
basal ganglia
Patient expresses his feeling
through not speaking especially
when she is feeling bad.
ELIMINATION
Frequency: Once a day
Pattern: Every morning
Consistency: Normal Stool
Amount: Approximately 910 inches in length, 1.5 in
diameter
Color: Light Brown
Odor: Normally foul stool
odor
Abdomen: contour
Rounded, (-) palpable
Stool
Page 26 of 53
palpation
Urine
mass
Quantity: 500cc to 1300cc
per shift
Due to oral and IV fluid intake.
Pattern: On IFC
Patient is on IFC to decrease BP.
Color: Lt. Yellow
Due to the general liquid diet of

the patient.
Due to the general liquid diet of
the patient.
Still within normal range.
Transparency: Sl. Turbid

Spc. Gravity: 1.015
REST AND ACTIVITY
Current activity level
Lie and sit on bed
Sleep
Pain/relief measures
8-9 hours a day during

the confinement period
Patient tries to position
himself on a comfortable
position.
Patient also verbalized
that upon having a
headache she takes
Biogesic.
Allergic Reaction
Medications
SAFETY
Sea foods
Gentamicin 160 mg IV OD
Cefuroxime 750 mg IV
q8h
Clonidine 1 tab SL now
Imidapril 1 tab OD/ NGT
Bactoban ointment to
wound TID
Eye/vision
Glasses:
Pupils:
Hearing/hearing aid
Skin integrity
Lesion scars
Mucus membrane
Temperature
Activity Tolerance
Airway clearance
Nose
Mouth
Respiration rate
Depth
Rhythm
Color
Skin
Nails
Lips
With a 120 reading glass

Right pupil is dilated nonreactive to light. Left Pupil
constricted with minimal
reaction to light.
Patient has normal
hearing
Intact Skin
With scars on left hand
Moist and intact
Temperature, via axillary,
of the patient varies from
36.0C to 37.4C
OXYGEN
Can move minimally
Patient moment varies due to

body weakness
Patient usually positions himself
on his back and sometimes lie
left laterally or right laterally,
depending on patients choice of
comfort.
Patient assumes analgesics for
pain relief measure in
addressing headache.
Sudden headache is one of the
s/sx of CVA.
Antibiotics were administered
so as to stop, or if not, lessen
infection which caused the
disease.
CV agent drugs were ordered to
lower the blood pressure of the
patient.
Antibacterial ointment was
ordered to prevent infection of
the wound.
Due to an infarct in the brain,
vision and normal eye function
can be affected.
Due to an accident caused by

bakery machineries.
Patient has general weakness
With no secretions
Clear
28 cycle per minute
Normal
Regular
Pale
Pinkish
Somewhat dry
Patient has a low hemoglobin

count.
Page 27 of 53
Capillary refill
1-2 seconds
Pulses
Blood pressure
Within normal range

140-210/70-110 mmHg
None
Negative
NUTRITION
Hospital
OR feeding of 1600
Diet/Restrictions
calories in 4 equally
divided feeding
IVFs (according to chart) PNSS 1L x 20-21 gtt/min
D5NSS 1L x 20-21 gtt/min
D5W L x 20 gtt/min
Site
Left posterior forearm
Tissue turgor
Good skin turgor
Ability to:
Chew
Able
Swallow
Able
Feed self
With SOs assistance
Normal Oxygenation of tissue

cells
Patient is having an elevated BP
due to illness.
Edema
Homans Sign
Due to decreased hand

movement accuracy.
Page 28 of 53
Page 29 of 53
IX. DRUG ANALYSIS

DRUG
Generic Name:
-Clonidine
Hydrochloride
INDICATION
-Elevated systolic and
diastolic BP
CONTRAINDICATION
-Hypersensitivity to
drug regimen
-Pregnancy
Brand Name:
-Catapres, Dixaril
Classification:
-Cardiovascular Agent,
General acting antihypertensive, analgesic
Stock:
-75mg tab SL
Doctors order:
-75mg Sl q8 x BP
>150/100
Date started:
-July 7, 2009
ACTION
- Central-acting antiadrenergic derivative.
Stimulates alpha2adrenergic receptors in
CNS to inhibit
sympathetic vasomotor
centers. Also inhibits
rennin release from
kidneys.
-Lactation
ADVERSE REACTION
-CV: Hypotension,
peripheral edema, ECG
changes, tachycardia,
bradycardia
-GI: Dry mouth,
constipation, N/V,
hepatitis
-CNS: drowsiness,
sedation, dizziness,
headache, fatigue,
weakness,
sluggishness,
nervousness
NURSING
CONSIDERATION
-Monitor BP frequently
-Instruct client to
change position slowly.
-Instruct patient to
avoid potentially
hazardous activities
until reaction to drug
has been determined
-Instruct patient not to
omit doses without
consulting the
physician
-Skin: rashes, pruritus

-UG: impotence, loss of
libido

breastfeed while taking
this drug(for mothers)
Date consumed:
-July 14, 2009
Page 30 of 53
DRUG
Generic Name:
- Captopril
Brand Name:
- Capoten, Captale,
Captril
Classification:
-Cardiovascular Drug
Stock:
- 25mg tab
Doctors order:
- 25mg tab BID
Date started:
-July 7, 2009
Date consumed:
-July 14, 2009
INDICATION
-Elevated systolic and
diastolic BP
CONTRAINDICATION
-Hypersensitivity to
drug regimen
-Pregnancy
ACTION
- Central-acting antiadrenergic derivative.
Stimulates alpha2adrenergic receptors in
CNS to inhibit
sympathetic vasomotor
centers. Also inhibits
rennin release from
kidneys.
-Lactation
ADVERSE REACTION
-CV: Hypotension,
peripheral edema, ECG
changes, tachycardia,
bradycardia
-GI: Dry mouth,
constipation, N/V,
hepatitis
-CNS: drowsiness,
sedation, dizziness,
headache, fatigue,
weakness,
sluggishness,
nervousness
NURSING
CONSIDERATION
-Monitor BP frequently
-Instruct client to
change position slowly.
-Instruct patient to
avoid potentially
hazardous activities
until reaction to drug
has been determined
omit doses without
consulting the
physician
-Skin: rashes, pruritus

-UG: impotence, loss of
libido

breastfeed while taking
this drug(for mothers)
Page 31 of 53
DRUG
Generic name:
-Mannitol
Brand name:
-Osmofundan 20%
Classification:
-Osmotic Diuretic
Doctors order:
-Manitol 100cc IV q8 /
IV q4
Date started :
-July 8, 2009 (IV q8)
-July 10, 2009 (IV q4)
Date Consumed:
-July 14, 2009
INDICATION
Reduction of elevated
intracranial pressure,
cerebral edema or
increased intraocular
pressure.
ACTION
Elevates blood plasma
osmolality, resulting in
enhanced flow of water
from tissues, including
the brain and
cerebrospinal fluid, into
interstitial fluid and
plasma.
CONTRAINDICATION
-Contraindicated in
patients hypersensitive
to drug
-Contraindicated in
patients with anuria,
severe pulmonary
congestion, frank
pulmonary edema,
severe heart failure,
severe dehydration,
metabolic edema or
active intracranial
bleeding.
ADVERSE REACTION
-CNS: dizziness,
headache, fever
-CV: edema,
hypotension,
tachycardia, vascular
overload
NURSING
CONSIDERATIONS
-Assess patients blood
pressure history before
therapy. Monitor pulse
and blood pressure
regularly
-EENT: blurred vision,

rhinitis
-Check weight, renal

function, fluid balance
and serum urine sodium
and potassium daily
-GI: thirst, dry mouth,

nausea, vomiting,
diarrhea
-Monitor CNS symptoms

and changes in mental
status.
-GU: urine retention
-To relieve thirst, give

frequent mouth care or
fluids
-monitor allergic
reaction: rash,fever,
pruritus,and urticaria.
-Metabolic:
dehydration
-Other: chills
Page 32 of 53
DRUG
Drug name
-Citicholine
Brand name:
-Somazine
Classification:
-Belongs to the class
of other agents used
as CNS stimulant.
Doctors order:
-Citicoline 1gm IV q8
Date started:
-July 7, 2009
Date consumed:
-July 14, 2009
INDICATION
CONTRAINDICATION
Cerebrovascular
accident in acute
recovery phase,
symptoms and signs of
cerebral insufficiency
such as dizziness,
memory loss, poor
concentration,
disorientation and
recent cranial
traumatism and their
sequelae.
-Must not be
administered to patients
with hypertonia of the
parasympathetic.
ADVERSE
REACTION
NURSING
CONSIDERATIONS
-Gastrointestinal
disorders
-May be taken with or
-Fleeting and discrete

hypotensive effect
-Should be administered
-Elevated body
temperature
-Restlessness
without food
slowly for patients with

intracranial hemorrhage
-Monitor vital signs

specifically the BP
-Provide frequent rest

periods
ACTION
It increases the
neurotransmission
levels because it favors
the synthesis and
production speed of
dopamine in the
striatum, acting then
as a dopaminergic
agonist thru the
inhibition of tyrosinehydroxylase.
Page 33 of 53
DRUG
Drug name:
-Cefuroxime sodium
Brand name:
-Zinacef
Doctors order:
-Cefuroxime 750 mg IV
q8 ANST
Date started:
-July 7, 2009
Date consumed:
-July 14, 2009
INDICATION
-Secondary bacterial
infection of acute
bronchitis.
ACTION
-Second generation
cephalosporin that
inhibits cell wall
synthesis, promoting
osmotic instability;
usually bactericidal.
CONTRAINDICATION
-Contraindicated in
to drug or other
cepghalosporins.
-Use cautiously in
to penicillin because of
possible cross-sensitivity
with other beta-lactam
antibiotics
SIDE EFFECTS
-CV: phlebitis,
thrombophlebitis
-GI: nausea,
anorexia,vomiting,
diarrhea
-Hematologic:
Eosinophilia, hemolytic
anemia,
thrombocytopenia
-Skin: urticaria,
maculopapular and
erythematous rashes,
temperature elevation
-Other:
Hypersensitivity
reactions, serum
sickness, a
naphylaxis
NURSING
CONSIDERATIONS
-Ask patient if he is
allergic to penicillins or
cephalosporins.
-Obtain specimen for
culture and sensitivity
test before giving first
dose.
-Tablet and suspension
arent bioequivalent
and cant be
substituted milligramfor-milligram.
-monitor patient for
signs and symptoms of
superinfection.
-tell pt. to take drug as
prescribed even after
he feels better
Page 34 of 53
DRUG
Generic Name:
-Ranitidine Hydrochloride
Brand Name:
-Zantac
Classification:
-H2 receptor blocker
Doctors order:
-Ranitidine 50mg IV q8
Date started:
-July 7, 2009
Date consumed:
-July 14, 2009
INDICATION
-Active duodenal and
gastric ulcer
-Gastro-esophageal
reflux disease (GERD)
-Heartburn
ACTION
Competitively inhibits
action of histamine on
the h2 at receptor
sites of parietal cells,
decreasing gastric
acid secretion.
SIDE EFFECTS
ADVERSE EFFECTS
-Headache, malaise,
nausea, vomiting,
dizziness, skin rash.
-Bradycardia,
constipation,
diarrhea, blurred
vision, cardiac
arrhythmias, burning
and itching at
injection site,
headache and
fatigue.
NURSING
CONSIDERATION
-Assess patient for
abdominal pain.
-Remind patient to take
once daily prescription drug
at bedtime for best results.
-Take the drug with foods.
-Advice patient to report
abdominal pain and blood
in stool or emesis.
-Assess potential for
interactions with other
pharmacological agents the
patient may be taking.
Page 35 of 53
X. COURSE IN THE WARD

ADMISSION DAY
July 7, 2009
Emergency Room
At 08:50 pm, a 49- year old female patient was admitted with history of slurred speach and body weakness few hours prior
to admission. She was assessed to have a BP of 150/100 mmHg. She was then seen and examined by Dr. Paguirigan with orders
made and carried out by the nurse on duty. A request of CXR, ECG, CBS, U/A, BUN, Total Cholesterol, Createnin and FBS was sent
to the Laboratory and for a Cranial CT Scan. IFC was inserted aseptically and connected to urine bag. An IVF of PNSS 1L x 12 was
also inserted at left hand. Stat medications were given. An ECG was done immediately.
At 9:35 pm, she was sent to the medical ward per wheelchair with same IVF on.
At 9:40 pm, patient was received at the medical ward per wheelchair with an IVF of same. She was placed on bed
comfortable and was assessed to be conscious, weak and with slurred speech with a v/s of q 1
MEDICATIONS
Catapres 75mg SL q8 x BP >150/100
Captopril 25mg tab BID
Manitol 100cc IV now then q8
Citicholine 2 drops BID
INTRAVENOUS FLUIDS
PNSS 1L x 12
Attending Physician: Dr. Paguirigan

2nd DAY OF HOSPITALIZATION
July 8, 2009
Medical Ward
Page 36 of 53
At 7 am, patient was received on bed with same IVF at left hand. He was seen to have an intact IFC which is connected to a
urine bag. Seen and examined by Dr. Paguirigan at around 8:00 am, with new orders and carried out. Manitol was increase from q8
to q4 with TF of PNSS. A Cranial CT scan and neurologist referral was ordered by Dr. Paguirigan.
At 1:20 am, the patient was given a Catapres due to a recorded BP of 200/110.
At 5:15pm a Blood serum result was also attached and referred to AP but with no further orders. BP as of this time is
180/110.
MEDICATIONS
Ranitidine 50mg IV q8
Citicholine 1g IV q8
Cefuroxime 750mg IV q8
INTRAVENOUS FLUIDS
PNSS 1L x 12

3rd DAY OF HOSPITALIZATION
July 9, 2009
At 8:00 in the morning patient was received with an IVF of PNSS 1L X 20gtt/min at 80cc level and with a patent IFC draining
to approximately 300cc of yellowish urine.
At 9:00am, patient was seen and examined by Dr. Salvadorwith orders carried out. Patients BP as of this time is 190/110.
Page 37 of 53
At 9:50am, above IVF was consumed. Due to infiltration, IFV was reinserted on the right radial vein with D5NSS 1L x q 12
regulated at 20-21 gtt/min.
For additional care and second opinion the patient was then referred to Dr. Salvador with orders carried out. Manitol was
decrease from q4 to q8. At 12:15pm a side drip of D5W L + 4 amp Hydralzine was hooked regulated at 20 gtt/min.
Monitoring of v/s is carried all throughout the day as well as due meds were given. Patient is still for CT scan and still for
referral to a neurologist.
MEDICATIONS
INTRAVENOUS FLUIDS
PNSS 1L x 12
D5NSS 1L x q 12 (Hooked at 9:50am)
D5W L x 20 gtt/min + 4 amps
Hydralazine

Consultant: Dr. Salvador
4th DAY OF HOSPITALIZATION
July 10, 2009
At 8:00 in the morning patient was received with an IVF of D5NSS 1L X 20gtt/min at 920cc level, side drip of D5W L x 20
gtt/min + 4 amps Hydralazine and with a patent IFC draining to approximately 560cc of yellowish urine.
At 11:00am, patient was seen and examined by Dr. Salvador with orders carried out.
Page 38 of 53
MEDICATIONS
INTRAVENOUS FLUIDS
D5NSS 1L x q 12
Hydralazine

July 11, 2009
gtt/min + 4 amps Hydralazine at 450cc and with a patent IFC draining to approximately 500cc of yellowish urine.
At 9:30am, patient was seen and examined by Dr. Salvador with orders carried out.
MEDICATIONS
INTRAVENOUS FLUIDS
D5NSS 1L x q 12
Hydralazine
Page 39 of 53
July 12, 2009
At 9:30am, patient was seen and examined by Dr. Paguirigan with orders to continue medications.
At 5:00pm the student nurse, Emmanuel D. Mania, noted, upon assessment, that the right pupil is dilated and non reactive
to light while the left eye pupil is reactive to light. Then at around 6:15pm the student also observed that the IV line is already
sludge. With the supervision of his clinical instructor, Ms. Arcalyd Rose A. Romos, RN, the IV catheter is removed aseptically and
temporarily stopped. Hot compress was applied to the affected site as to reduce swelling and pain. At 6:30, IV line was reinserted
on the right arm with same solution of D5NSS 1L properly regulated at 20 gtt/min.
At 6:50pm a BP recording is 150/100 thus a Catapres was administered SL as ordered.
At 9:00pm the student again observed that the IV line is again sludge. With the supervision of his CI, Ms. Arcalyd Rose A.
Romos, RN, the IV catheter is removed aseptically and temporarily stopped. Hot compress was applied on both hands to reduce
swelling and pain. At 9:30pm, IV line was reinserted on the left posterior forearm with same solution of D5NSS 1L properly
regulated at 20 gtt/min.
At 10:30pm, above IVF was consumed and replaced with PNSS 1L regulated properly at 20gtt/min.
referral to a neurologist and a physical therapist.
MEDICATIONS
INTRAVENOUS FLUIDS
Page 40 of 53

D5NSS 1L x q 12
Hydralazine
PNSS 1L x q12

July 13, 2009
At 8:00 in the morning patient was received with an IVF of PNSS 1L X 20gtt/min at 780cc level, side drip of D5W L x 20
gtt/min + 4 amps Hydralazine at 480cc, replaced before the 8:00am-4:00pm shift, and with a patent IFC draining to
approximately 1215cc of yellowish urine.
At 2:30 pm, patient was out for CT scan. CT scan results are available at this date.
At around 4:00pm, the patient is still having slurred speech, no disease progression and still appears weak.
At 8:30pm, above IVF consumed and replaced with D5NSS 1L properly regulated at 20 gtt/min.
Monitoring of v/s is carried all throughout the day as well as due meds were given, v/s q8 until stable. Patient is still for CT
scan and still for referral to a neurologist and a physical therapist.
MEDICATIONS
INTRAVENOUS FLUIDS
PNSS 1L x q12
Page 41 of 53
Hydralazine
D5NSS 1L x q12

July 14, 2009
At 8:00 in the morning patient was received with an IVF of D5NSS 1L x 20gtt/min at 850cc level, side drip of D5W L x 20
At 2:30 pm, patient was out for CT scan. CT scan results are available at this date.
At around 4:00pm, the patient is still having slurred speech, no disease progression and still appears weak.
At 8:30pm, above IVF consumed and replaced with D5NSS 1L properly regulated at 20 gtt/min.
At 9:30am, patient was seen and examined by Dr. Salvador with new orders and carried out.
At 10:00am SD was temporarily stopped due to a recording of a BP of 150/100mmHg.
Monitoring of v/s is carried all throughout the day as well as due meds were given, v/s q8 until stable. Patient is still for CT
scan and still for referral to a neurologist and a physical therapist.
MEDICATIONS
Aspirin 80mg 2 tab Now then 1 tab
OD
INTRAVENOUS FLUIDS
D5NSS 1L x q12
Hydralazine
Page 42 of 53

Page 43 of 53
XI. COMPREHENSIVE NURSING CARE PLAN
ASSESSMENT
SUBJECTIVE:
hindi namin
maintindihan ang
sinasabi niya as
verbalized by the
daughter.
OBJECTIVE:
Inspection:
-With slurred speech
-Right eye dilated
- in muscle
strength:
-Arms:
L= 3/5
R= 1/5
-Legs:
L= 3/5
R= 1/5
-GCS:
E= 3
V=2
M=4
-With poor muscle
tone on the right and
left hand and foot
- Limited ROM on the
right hand and
foot(only able to
carry out passive
ROM on this area)
-Unable to carry out
activities without
assistance such as
feeding and changing
clothes.
NURSING
DIAGNOSIS
Ineffective cerebral
tissue perfusion r/t
interruption of blood
flow in the brain
secondary to presence
of subacute infarcts of
the right basal ganglia
and lacunar infarct of
the left basal ganglia
of the brain.
SCIENTIFIC
ANALYSIS
Deposition of fatty
materials on vessel
walls
Plaque formation
Narrowing of
atherosclerosis plaque
Aneurysm formation
Rupture of artery
supplying the brain
deprivation of blood
supply in the brain
Cerebral infarction
Impaired function of
the brain
Ineffective tissue
perfusion
NURSING GOAL
SHORT-TERM GOAL:
After 8 hours of
nursing intervention,
the patient will be
able to:
a) Manifest an
improved nail beds
from pale to pinkish
b) Manifest a normal
papillary response
LONG-TERM GOAL:
After 1 week of
the patient will be
able to:
a) Manifest an
improved participation
in performing ADLs
with or without
support.
b) Manifest an
improved speech
c) Manifest an
increase in muscle
strength of both arms
and legs of the
patient.
d) Maintain functional
abilities of the right
and left side of the
body
e) Improved physical
mobility from level 3
to level 2 and
improved GCS scale
INTERVENTION
INDEPENDENT:
1. Establish rapport to
the patient and S. O.s
2. Monitor V/S every
30 minutes
3. Evaluate pupils,
noting size, shape and
equity
4. Elevate HOB (15
degrees) and maintain
head or neck in
midline
5. Provide quiet and
restful atmosphere
6. Reposition pt
every 2 hours
7. Patient in
comfortable position
8. Provide support on
affected body part
such as pillows and
assistance to do ADLs
as needed.
9. Provide safety
precautions by raising
up the side rails.
10. Encourage the
patient and S.O.s to
avoid sedentary
lifestyle such as
RATIONALE
-To gain the patients
and S.O.s trust and
cooperation during
the nursing care and
procedures.
-To gather baseline
data and monitor any
further complications/
deviations from
normal.
-To gather baseline
deviations from
normal.
-To promote circulation
and venous drainage
and to maintain a
patent airway.
-For conservation of
energy and lowers
oxygen demand
and oxygen
distribution
-To promote optimal
level of functioning
-To maintain position
of function and reduce
discomforts.
-To prevent fall and
injury
EVALUATION
SHORT-TERM GOAL:
After 8 hours of
goal was met as
evidenced by:
a) Patient having an
improved nail beds
from pale to pinkish in
color
b) Patient having a
normal papillary
response
LONG-TERM GOAL:
After 1 week of
goal was met as
evidenced by:
in performing ADLs
with or without
support.
b) Patient having an
improved speech with
diminished slurred
characteristics.
c) Patient having an
increased muscle
strength with a scale
of:
Arms
L=4/5 R=2/5
Legs
L=4/5 R=2/5
d) Patient having an
Page 44 of 53
-Difficulty in chewing
and swallowing
-With pale nail beds
-Level 3 physical
mobility
drinking liquor,
smoking, improper
exercise and too much
fatty foods.
COLLABORATIVE:
1.
Administer
medications as
ordered:
- Citicoline 2 drops
BID / 1gm IV q8
Lab/Diagnostic Tests:
CT Scan:
HEMORRHAGE IN THE
LEFT AND RIGHT
BASAL GANGLIA
ASSESSMENT
NURSING
DIAGNOSIS
SCIENTIFIC
ANALYSIS
NURSING GOAL
INTERVENTION
-These factors may

affect them in
developing various
diseases as what like
the patient is suffering
now.
improved functional
ability of the right and
left side of the body.
e) Patient having
level 2 physical
mobility and a GCS
scale of E=4, V=4,
M=5.
-It restores the activity

and functions of the
brain. It improves
neuromuscular
function.
RATIONALE
EVALUATION
Page 45 of 53
SUBJECTIVE:
Hindi siya ganong
magkagalaw as
verbalized by the
daughter.
OBJECTIVE:
-Weak in appearance
- in muscle
strength:
-Arms:
L= 3/5
R= 1/5
Legs:
L= 3/5
R= 1/5
-GCS:
E= 3
V=2
M=4
-Unable to carry out
activities without
assistance such as
feeding and changing
clothes.
-With poor muscle
tone on the right
hand and foot
-Difficulty in chewing
and swallowing
-Limited ROM on the
right hand and
foot(only able to
carry out passive
ROM on this area)
-Needs assistance
when turning
-Level 3 physical
mobility
Lab/Diagnostic Tests:
-CT Scan:
HEMORRHAGE IN THE
LEFT AND RIGHT
BASAL GANGLIA
Impaired physical
mobility r/t subacute
infarcts of the right
basal ganglia and
lacunar infarct of the
left basal ganglia of
the brain.
Deposition of fatty
materials on vessel
walls
Plaque formation
Narrowing of
atherosclerosis plaque
Aneurysm formation
Rupture of artery
supplying the brain
Intracranial
hemorrhage
Deprivation of blood
supply in the brain
Cerebral
haemorrhage in the
motor area
Impairment of gross
and motor function of
the brain
Impaired physical
mobility
SHORT-TERM GOAL:
After 8 hours of
the patient will be
able to:
a)
Participate in
performing ADLs with
minimal assistance
from others
b)
Do active and
passive ROM exercise
on the right side of his
body within physical
limitations after hours
of sleep.
c)
Have an
adequate rest and
sleep of about 4-5
hours.
LONG-TERM GOAL:
After 1 week of
the patient will be
able to:
a) Manifest an
in performing ADLs
with or without
support.
b) Maintain functional
side of the body.
c)
Manifest an
increase in muscle
strength of both arms
and legs of the
patient.
d)
Manifest an
improvement in
chewing and
swallowing abilities
e) Improved physical
mobility from level 3
to level 2 improved
GCS scale
INDEPENDENT:
1. Establish rapport to
the patient and S. O.s
2. Assess and
determine factors that
contribute to physical
immobility
3. Determine degree
of immobility &
muscle strength
4. Assist patient in
comfortable position
5. Provide support on
affected body parts
such as pillow
6. Provide safety
precautions by raising
up the side rails.
7.
Provide
environment free from
noise and
disturbances
8. Change position
every 2 hours and
possibly more often if
placed on the affected
part
9. Massage pressure
points after each
position changes
10. Assist in
performing ADL
11. Assist in
performing ROM
exercise after hours of
sleep & within
physical limitations.
12. Encourage the pt
and S.O.s to avoid
sedentary lifestyle
such as drinking
liquor, smoking,
improper exercise and
too much fatty foods.
-To gain the pts &

S.O.s trust &
cooperation during
the nsg care &
procedures.
-To identify
contributing factors
that enable the nurse
to focus on
appropriate
interventions
-To assess functional
ability
-To promote optimal
-To maintain position
of function and reduce
discomfort
-To prevent injury and
fall
-To have a good
atmosphere
conducive to the
recovery of the
patient
-To reduce risk of
tissue ischemia or
injury and
to prevent pressure
sores
and oxygen
distribution
-To promote optimal
-To minimize muscle
atrophy and promote
circulation
-These factors may
affect them in
SHORT-TERM GOAL:
After 8 hours of
goal was met as
evidenced by:
a) Patient
participated in
performing ADLs with
minimal assistance
active and passive
ROM exercise within
physical limitations
after hours of sleep
adequate sleep of 4
hours
LONG-TERM GOAL:
After 1 week of
goal was met as
evidenced by:
in performing ADLs
with or without
support.
improved functional
side of the body
increased muscle
strength with a scale
of:
Arms
L=4/5
R=2/5
Legs
L=4/5
R=2/5
d)
Patient having an
improved chewing and
swallowing abilities
Page 46 of 53
COLLABORATIVE:
1. Administer
medications as
ordered:
- Citicoline 2 drops
BID / 1gm IV q8
developing various
diseases as what like
the patient is suffering
now.
e)
Patient having
level 2 physical
mobility and a GCS
scale of E=4, V=4,
M=5.
-It restores the activity

and functions of the
brain. It improves
neuromuscular
function.
Page 47 of 53
ASSESSMENT
DIAGNOSIS
SCIENTIFIC
EXPLANATION
PLANNING
NURSING
INTERVENTION
RATIONALE
EVALUATION
Page 48 of 53
OBJECTIVE
>not changing of IV
site within 24-36hrs.
Risk for infection r/t

prolonged
catheterization
Inadequate protective
of defense mechanism
Bacterium, virus,
fungus, or other
parasites invades the
susceptible pt.
Breaks in the
integument
Invasion of pathogens
carried through bld.
Stream or lymphatic
system
Risk for infection
After 8hr. shift of

nursing interventions,
the patient will:
- know the proper
hand washing as well
as the significant
others.
- know the sign and
symptoms of infection
and when to report
these to the physician
or nurse
-able to know what
food he must eat
-able to increase his
fluid intake at the
range of 8-10 glasses
of water
-able to take
antibiotics as
prescribed
INDEPENDENT:
-Monitor and teach the
pt. to the signs of
infection
- Any suspicious
drainage should be
cultured
-encouraged the pt. to

wash hands before
contact with the
patient
- Washing between
procedures reduces
the risk of
transmitting
pathogens from one
area of the body to
another
- Encourage intake of
protein- and calorierich foods
- Encourage fluid
intake of 2000 ml to
3000 ml of water per
day
- Teach patient to take

antibiotics as
prescribed
- This maintains
optimal nutritional
status
- Fluids promote
diluted urine and
frequent emptying of
bladder; reducing
stasis of urine, in
turn, reduces risk of
bladder infection or
urinary tract
infection (UTI).
- Most antibiotics
work best when a
constant blood level
is maintained; a
constant blood level
is maintained when
medications are
taken as prescribed.
The absorption of
some antibiotics is
hindered by certain
foods; patient should
be instructed
accordingly.
After 8hr. shift of

nursing interventions,
GOAL MET, the patient
was:
- know the proper
hand washing as well
as the significant
others.
- know the sign and
symptoms of infection
and when to report
these to the physician
or nurse
-able to know what
food he must eat
especially in taking of
protein and calorie
rich foods.
-able to consumed
9glasses of water
-instructed to take
antibiotics as
prescribed
Page 49 of 53
ASSESSMENT
SUBJECTIVE:
Nagmamanas ang
paa nya as
verbalized by the
niece.
OBJECTIVE:
-The patient has a
skin indentation of
about 2mm deep
(1+)
-Swelling of skin
above the ankle
-Area shiny
-Cold to touch
-Skin area is pale in
color
NURSING
DIAGNOSIS
Fluid volume excess
r/t accumulation of
fluids at interstitial
spaces as evidenced
by bipedal swelling of
patients skin above
the ankle with skin
indentation of
1+(about 2mm deep)
SCIENTIFIC
ANALYSIS
Deposition of fatty
materials on vessel
walls
Plaque formation
Stenosis of the artery
Alteration of usual
smooth flow of blood
through the artery
Swirling of blood
aroung the irregular
surface of the
plaques
Vessel lumens
become obstructed
and occluded
blood volume in
the area proximal to
the obstructed vessel
hydrostatic
pressure
Fluid extravasates
from intravascular to
interstitial spaces.
NURSING GOAL
SHORT-TERM GOAL:
After 8 hours of
the patient will be
able to:
a) Exhibit normal skin
and body condition
particularly
puffiness of the area
above the ankle
LONG-TERM GOAL:
After 1 week of
the patient will be
able to:
a)
Have
a
skin
indentation
on
normal limits and will
be
free
from
puffiness of the area
affected
INTERVENTION
INDEPENDENT:
1. Establish rapport
to the patient and S.
O.s
2. Monitor V/S every

30 minutes
3. Clean edematous
ankle of patient with
warm saline wiper
4. Regulate fluid
intake carefully
5. Advise patient to
promote bed rest
6. Elevate patients
legs for about half an
hour
7. Instruct the patient
and S.O.s that
constrictive clothes
should be avoided to
the patient
COLLABORATIVE:
1.Administer
medications as
ordered:
Manitol 100cc IV q8
(Osmotic Diuretic)
RATIONALE
-To gain the patients
and S.O.s trust and
cooperation during
the nursing care and
procedures.
-To gather baseline
deviations from
normal.
-To relieve patient
-To avoid further
fluid accumulation
-To avoid to much
expenditure of
energy
-To allow good venous
circulation
-Because wearing
constrictive clothes
impedes lower
extremities
circulation of venous
return
EVALUATION
SHORT-TERM GOAL:
After 8 hours of
goal was met as
evidenced by:
a) Patient having a
normal skin and body
condition puffiness of
the area above the
ankle.
LONG-TERM GOAL:
After 1 week of
goal was met as
evidenced by:
a)
Patient having
an skin indentation
on normal limits and
negative for puffiness
of the area affected.
-For diuresis and

subsequent
mobilization of
excess fluid
Page 50 of 53
Edema
Page 51 of 53
Page 52 of 53
XII. BIBLIOGRAPHY
Book Sources:
Fundamentals of Nursing Kozier
Medical-Surgical Nursing Brunner and Suddart
PPDs Nursing Drug Guide 2nd Edition Nurses Pocket Guide Doenges, Moorehouse & Murr
Documentation In Action Lippincott
Pocket Dictionary Mosbys
Essential of human anatomy - Marrieb
Pharmacology Kee, Hayes & McQuisition
Internet Sources:
http://www.siumed.edu/~dking2/ssb/neuron.htm#neuron
http://www.dls.ym.edu.tw/neuroscience/nsdivide.html
http://en.wikipedia.org/wiki/Human_brain
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I.

IV. BRIEF DESCRIPTION OF THE DISEASE

b. Subarachnoid (5%) result from aneurismal rupture of a

Different Pathogenesis of Stroke

Comparison Between Right and Left Hemisphere Stroke

Left Hemisphere Lesion

Typical Deficits Artery Involved

- basic limb synergies or

Increased spasticity; may be

Spasticity begins to decline

- can master some

- individual joint movement

Synergy Patterns of the Upper Extremity: Stroke

Synergy Patterns of the Lower Extremity: Stroke

Falls and injuries

Basal ganglia (As per patients CT Scan result)

Basal ganglia labeled at top right.

number of motor-related areas, including the part of the thalamus that

The basal ganglia form a fundamental component of the

Connectivity diagram showing excitatory glutamatergic pathways as red,

The flow of neural signals through the basal ganglia is strongly

have distinguished two main circuits, known as the "direct" and

GABAergic neurons, which therefore have inhibitory effects on their

The role in motivation of the "limbic" part of the basal ganglia

For example, the "internal segment of the globus pallidus" in

The "striatum" and "external segment of the globus pallidus" in

A clear emergent issue in comparative anatomy of the basal

In most regions of the brain, the predominant classes of neurons

Attention-deficit hyperactivity disorder (ADHD)

Athymhormic syndrome (PAP syndrome)

Cerebral palsy: basal ganglia damage during second and third

Foreign accent syndrome (FAS)

Tardive dyskinesia, caused by chronic antipsychotic treatment

A thorough reconsideration by Ccile and Oskar Vogt Ccile and

V. ANATOMY AND PHYSIOLOGY

pachymenix, tough fibrous tissue

Divides the cerebral hemispheres into right and left halves.

- primary motor area

- primary visual cortex

AREA 4: PRIMARY MOTOR AREA

1. Relays motor & sensory impulses

in consciousness and arousal)

1. Relay motor impulses from the cerebral

that drives many biological rhythms.

Blood supply to choroids plexuses of III & IV ventricles

which immature blood cells are present in peripheral blood.) Leukocytosis is

VIII. PHYSICAL ASSESSMENT

The patient is visited by

Interacting with SO and

Ibanag/ Ilocano/ Tagalog

Patients older sister

Brain damage not that severe.

Due to oral and IV fluid intake.

Patient is on IFC to decrease BP.

Color: Lt. Yellow

Due to the general liquid diet of

Transparency: Sl. Turbid

8-9 hours a day during

With a 120 reading glass

Patient moment varies due to

Due to an accident caused by

Patient has general weakness

Patient has a low hemoglobin