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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 30’s 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.

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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

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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

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Different Pathogenesis of Stroke

CRITERIA THROMBOTIC EMBOLIC LACUNAR HEMORRHAGE


Incidence 40 % 30 % 20 % 10 %
Mechanism – - - cholesterol - similar to - Hypertension –
ath other thrombosis; small rupture of
ero hematogenous infarcts penetrating
sch material arterioles leading
ero to hemorrhage
stic
ste
rosi
s
or
occ
lusi
on
of
a
lar
ge
blo
od
ves
sel
Onset and – - - abrupt - chronic - sudden
Progression gra progress; gradual
du onset
al,
slo
w
ste
pwi
se
pro
gre
ssi
on
of
sy
mp
to
ms
;
ma
y
be
ho
urs
to
da
ys
Scenario – - - most occur in
(+) setting of MI
wa
rni
ng
sig
ns
– co
m
mo
nly
occ
urs

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at
nig
ht
wit
h>
15
%
wit
h
TIA
Sites – - - cortical small - small, - sites of Lacunes
int vessels perforating
ern arterioles
al
car
oti
d
or
MC
A
Clinical – - - Cortical deficits - Descrite & - Inc. ICP;
manifestation ap (hallmark) specific subcortical
has subortical deficits deficits (more
ia extensive)
vis
ual
– -
fiel
ds
cut
s
– -
he
mi
par
esi
s
– -
he
mis
ens
ory
Prognosis – - - Repeated in - Excellent; 85 % – -
sev same vascular same vascular po
ere territory teritory or;
im init
pai ial
rm me
ent nta
l
ret
ard
ati
on

50
%-
70
%
– if
blo
od
is
rea
bso
rbe

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d
– m
ild
def
icit

Comparison Between Right and Left Hemisphere Stroke

Right Hemisphere Lesion Left Hemisphere Lesion


- no deficits in ability to understand and - aphasia
express language
- impaired ability to assess position in space - usually unimpaired
and to safety interact with environment;
neglect of (L) side may be present
- verbal memory interact (+) perceptual - impaired ability to retain verbal information,
memory impairment remote memory likely impaired
- careless and oblivious of mistakes; impulsive - appropriate emotion
and decreased ability to anticipate
consequence of behavior
- impaired visual motor perception - able to communicate property
- loss of visual memory - decreased vocabulary and auditory retention
span
- lack of insights and judgement but not - (+) visuomotor perception
obvious because of intact verbal fluency - (+) visuomotor memory
- difficult to rehabilitate - 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 Muscle Tone Limb Movement Others


tag
e
1 flaccid None
2 Beginning spasticity - minimal voluntary - basic limb synergies or

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movement some of their
components appear as
associated reactions
3 Increased spasticity; may be - voluntary control of Full range of all synergy
severe (PEAK) movement synergies components does not
necessarily develop
4 Spasticity begins to decline - can master some - full range of all synergy
movement combinations components does not
deviate from synergy necessarily develop
5 - more difficult movement - basic limb synergies
patterns learned lose their dominance
over motor acts
6 Spasticity disappears - individual joint movement
(present only during rapid possible coordination
movement) approaches normal
- normal motor function
restored in some

Synergy Patterns of the Upper Extremity: Stroke

FLEXION EXTENSION
Scapula Retraction / elevation or Protraction
hypertension
Shoulder Abduction, external rotation Abduction, internal rotation
Elbow Flexion Extension
Forearm Supination Pronation
Wrist and fingers Flexion Flexion

Synergy Patterns of the Lower Extremity: Stroke

FLEXION EXTENSION
Hip Flexion; abduction; external Extension, adduction; internal
Knee notation rotation
Ankle Flexion Extension
Toe Dorsiflexion; inversion Plantarflexion; inversion
dorsiflexion

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 LATE
➢ Urinary tract infection ➢ Spasticity
➢ Pressure sore ➢ Contracture
➢ Dehydration ➢ Central post-stroke pain
syndrome
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➢ Malnutrition ➢ Falls and injuries
➢ Dysphagia ➢ Medication overuse

➢ Shoulder dysfunction; ➢ Deconditioning and


RSD endurance limitations
➢ Depression ➢ Fatigue
➢ Sexual dysfunction ➢ Insomia
➢ Seizure

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

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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 areas—the striatum
in particular—also 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 obsessive–compulsive 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 median-
parafascicular) 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
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have distinguished two main circuits, known as the "direct" and
"indirect" pathways. The direct pathway runs
cortex→striatum→GPi→thalamus→cortex. 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
cortex→striatum→GPe→STN→GPi→thalamus→cortex. 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,
however—perhaps 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
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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.

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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
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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.

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A thorough reconsideration by Cécile and Oskar Vogt Cécile 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 Déjerine to Burdach (1822). For this,
the Vogts proposed the simpler "pallidum". The term "locus niger" was
introduced by Félix Vicq-d'Azyr as tache noire in (1786), though that
structure has since become known as the substantia nigra, due to Von
Sömmering 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 médian-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


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➢ 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 Brodmann’s 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 - primary motor area
Area 6 - premotor area
Area 8 - frontal eye movement and papillary change
area
Area 44 - motor speech (Brocas Area)

2. Parietal Lobe
Area 3, 1, 2 - primary sensory areas
Area 5, 7 - sensory association areas
Area 39 – 40 - Wernicke’s area
Area 5, 7, 39 – 40 - Gnostic area
Area 43 - primary gustatory area

3. Occipital Lobe
Area 17 - primary visual cortex
Area 18 – 29 - visual association areas
4. Temporal Lobe
Area 41 - primary auditory cortex
Area 42 & 22 - 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

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

MIDBRAIN 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.
DIENCEPHALON
Thalamus 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.
Hypothalamus 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
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that drives many biological rhythms.
Cerebrum 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.

CEREBELLUM 1. Controls subconscious skeletal muscle


contraction’s 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.
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➢ Blood supply to choroids plexuses of III & IV ventricles
➢ With calcarine artery and perforating branches to posterior thalamus
and subthalamus.

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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 SO’s.
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 it’s 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.

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URINALYSIS
Date: July 13, 2009
COLOR Lt. Yellow PROTEIN
TRANSPARENCY Sl. Turbid SUGAR
PH/REACTION 6.5 (4.5-8.0) ACETONE
SPECIFIC GRAVITY 1.015 (1.005-1.030) BILE PIGMENTS
CAST/LFP CRYSTALS
Hayline Cast Amorp. Few
Urate/Phospates
CELLS/HPF EPITHELIAL CELLS
WBC/Pus Cell 3-6 (0-4) Squamous Rare
RBC/Red Blood Cell >50 (<2) Renal
Yeast Cells MUCUS THREADS Rare
Pregnancy Test Bacteria 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 REFERENCE VALUES
HEMOGLOBIN 132 120-160 g/L
HEMATOCRTI (HCT) 39 34-47 vol %
LEUKOCYTE COUNT (WBC) 13.1 5.0-10.0
DIFFERENTIAL COUNT:
Nuetrophils 84 50-70 %
Lymphocytes 15 20-40 %
Eosinophils 1 1-3 %
Toxic Granules Negative
Clotting Time 2-6 minutes
Bleeding Time 1-4 minutes
Malarial Smear 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 client’s 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 RESULT S.I. UNITS NORMAL VALUES
Glucose (Fasting) 3.26 mmol/L 3.85-6.05
Total Cholesterol 7.52 mmol/L 3.9-5.1
Blood Urea Nitrogen 9.0 mmol/L 1.7-9.3
Serum Creatinine 167.4 µmol/L 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 client’s 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 RISK FACTOR


➢ Subacute Infarct, righ basal ➢ Age
ganglia and right perventricular ➢ Hypertension
white matter region ➢ Diet (LDL)
➢ Lacunar Infarct, left basal ganglia ➢ DIC
➢ Sclerotic Mastiod, right

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 Narrowed lumen Break off


thrombus
Emboli
Occlusion of affected
blood vessels

Vertebral arteries Vertebrobasilar arteries Internalcarotid arteries

Dysphagia Vertigo Paralysis

Numbness Weakness Ataxia Lower facial Sensory


Hemiparesis loss
Dysarthria Headache weakness
Numbness

Gait problem Syncope

Page 25 of 53
VIII. PHYSICAL ASSESSMENT

PSYCHOSOCIAL PATHOPHYSIOLOGICAL
BASIS
Significant others The patient is visited by A very supportive family who
her daughter’s and shows comfort and care that
niece’s. can relieve stress that is felt by
the patient
Coping Mechanism Interacting with SO and Being happy during treatment
Laughing trip. can contribute to patients fast
recovery and interaction with in
the family can be a diversion
activity thus reducing pain and
stress.
Religion Roman Catholic It is important to know, for
there might be beliefs of a
certain religion that has a
conflict with a health
intervention.
Primary Language Ibanag/ Ilocano/ Tagalog 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.
Financial Source of Patient’s older sister
Health Care working in Dubai and
patient’s first cousin
working in London.
Occupation Bakery Manager
General appearance LOC: Conscious Brain damage not that severe.

GCS: Due to decreased O2 supply


Eyes 3 and perfusion in the brain.
Verbal 2
Motor 4 .
TOTAL 9
Due to illness.
Weak in appearance
Orientation The patient still knows An abnormal orientation can be
where she is, when she a symptom of brain damage
was admitted and who caused by CVA
are the SO present.
Memory Patient still has a good Damaged cause by the infarct is
memory thus she recalls not yet that severe to affect the
diet prescribed her memory of the patient.
physician and thus still
remembers a lot things.
Speech Slurred speech Dysarthria resulting from
lacunar infarcts, right and left
basal ganglia
Non-verbal behavior Silence Patient expresses his feeling
through not speaking especially
when she is feeling bad.
ELIMINATION
Stool Frequency: Once a day
Pattern: Every morning
Consistency: Normal Stool
Amount: Approximately 9-
10 inches in length, 1.5 in
diameter
Color: Light Brown
Odor: Normally foul stool
odor
Abdomen: contour Rounded, (-) palpable

Page 26 of 53
palpation mass
Urine Quantity: 500cc to 1300cc Due to oral and IV fluid intake.
per shift

Pattern: On IFC Patient is on IFC to decrease BP.

Color: Lt. Yellow Due to the general liquid diet of


the patient.
Transparency: Sl. Turbid Due to the general liquid diet of
the patient.
Spc. Gravity: 1.015 Still within normal range.
REST AND ACTIVITY
Current activity level Lie and sit on bed Patient moment varies due to
body weakness
Sleep 8-9 hours a day during
the confinement period
Pain/relief measures Patient tries to position Patient usually positions himself
himself on a comfortable on his back and sometimes lie
position. left laterally or right laterally,
depending on patients choice of
comfort.
Patient also verbalized Patient assumes analgesics for
that upon having a pain relief measure in
headache she takes addressing headache.
Biogesic. Sudden headache is one of the
s/sx of CVA.
SAFETY
Allergic Reaction Sea foods
Medications Gentamicin 160 mg IV OD Antibiotics were administered
Cefuroxime 750 mg IV so as to stop, or if not, lessen
q8h infection which caused the
Clonidine 1 tab SL now disease.
Imidapril 1 tab OD/ NGT CV agent drugs were ordered to
lower the blood pressure of the
Bactoban ointment to patient.
wound TID Antibacterial ointment was
ordered to prevent infection of
the wound.
Eye/vision
Glasses: With a 120 reading glass
Pupils: Right pupil is dilated non- Due to an infarct in the brain,
reactive to light. Left Pupil vision and normal eye function
constricted with minimal can be affected.
reaction to light.

Hearing/hearing aid Patient has normal


hearing
Skin integrity Intact Skin
Lesion scars With scars on left hand Due to an accident caused by
bakery machineries.
Mucus membrane Moist and intact
Temperature Temperature, via axillary,
of the patient varies from
36.0°C to 37.4°C
OXYGEN
Activity Tolerance Can move minimally Patient has general weakness
Airway clearance
Nose With no secretions
Mouth Clear
Respiration rate 28 cycle per minute
Depth Normal
Rhythm Regular

Color
Skin Pale Patient has a low hemoglobin
Nails Pinkish count.
Lips Somewhat dry
Page 27 of 53
Capillary refill 1-2 seconds Normal Oxygenation of tissue
cells
Pulses Within normal range
Blood pressure 140-210/70-110 mmHg Patient is having an elevated BP
due to illness.
Edema None
Homan’s Sign 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 ½L x 20 µgtt/min
Site Left posterior forearm
Tissue turgor Good skin turgor
Ability to:
Chew Able
Swallow Able
Feed self With SO’s assistance Due to decreased hand
movement accuracy.

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

NURSING
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION
CONSIDERATION
Generic Name: -Elevated systolic and -Hypersensitivity to -CV: Hypotension, -Monitor BP frequently
-Clonidine diastolic BP drug regimen peripheral edema, ECG
Hydrochloride changes, tachycardia, -Instruct client to
-Pregnancy bradycardia change position slowly.
Brand Name:
-Catapres, Dixaril ACTION -Lactation -GI: Dry mouth,
- Central-acting anti- constipation, N/V, -Instruct patient to
Classification: adrenergic derivative. hepatitis avoid potentially
-Cardiovascular Agent, Stimulates alpha2- hazardous activities
General acting anti- adrenergic receptors in -CNS: drowsiness, until reaction to drug
hypertensive, analgesic CNS to inhibit sedation, dizziness, has been determined
sympathetic vasomotor headache, fatigue,
Stock: centers. Also inhibits weakness, -Instruct patient not to
-75mg tab SL rennin release from sluggishness, omit doses without
kidneys. nervousness consulting the
Doctor’s order: physician
-75mg Sl q8 x BP -Skin: rashes, pruritus
>150/100 -Instruct patient not to
-UG: impotence, loss of breastfeed while taking
Date started: libido this drug(for mothers)
-July 7, 2009

Date consumed:
-July 14, 2009

Page 30 of 53
NURSING
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION
CONSIDERATION
Generic Name: -Elevated systolic and -Hypersensitivity to -CV: Hypotension, -Monitor BP frequently
- Captopril diastolic BP drug regimen peripheral edema, ECG
changes, tachycardia, -Instruct client to
Brand Name: -Pregnancy bradycardia change position slowly.
- Capoten, Captale,
Captril ACTION -Lactation -GI: Dry mouth,
- Central-acting anti- constipation, N/V, -Instruct patient to
Classification: adrenergic derivative. hepatitis avoid potentially
-Cardiovascular Drug Stimulates alpha2- hazardous activities
adrenergic receptors in -CNS: drowsiness, until reaction to drug
Stock: CNS to inhibit sedation, dizziness, has been determined
- 25mg tab sympathetic vasomotor headache, fatigue,
centers. Also inhibits weakness, -Instruct patient not to
Doctor’s order: rennin release from sluggishness, omit doses without
- 25mg tab BID kidneys. nervousness consulting the
physician
Date started: -Skin: rashes, pruritus
-July 7, 2009 -Instruct patient not to
-UG: impotence, loss of breastfeed while taking
Date consumed: libido this drug(for mothers)
-July 14, 2009

Page 31 of 53
NURSING
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION
CONSIDERATIONS
Generic name: Reduction of elevated -Contraindicated in -CNS: dizziness, -Assess patient’s blood
-Mannitol intracranial pressure, patients hypersensitive headache, fever pressure history before
cerebral edema or to drug therapy. Monitor pulse
Brand name: increased intraocular -CV: edema, and blood pressure
-Osmofundan 20% pressure. -Contraindicated in hypotension, regularly
patients with anuria, tachycardia, vascular
Classification: ACTION severe pulmonary overload -Check weight, renal
-Osmotic Diuretic Elevates blood plasma congestion, frank function, fluid balance
osmolality, resulting in pulmonary edema, -EENT: blurred vision, and serum urine sodium
Doctor’s order: enhanced flow of water severe heart failure, rhinitis and potassium daily
-Manitol 100cc IV q8 / from tissues, including severe dehydration,
IV q4 the brain and metabolic edema or -GI: thirst, dry mouth, -Monitor CNS symptoms
cerebrospinal fluid, into active intracranial nausea, vomiting, and changes in mental
Date started : interstitial fluid and bleeding. diarrhea status.
-July 8, 2009 (IV q8) plasma.
-July 10, 2009 (IV q4) -GU: urine retention -To relieve thirst, give
frequent mouth care or
Date Consumed: -Metabolic: fluids
-July 14, 2009 dehydration -monitor allergic
reaction: rash,fever,
-Other: chills pruritus,and urticaria.

Page 32 of 53
DRUG INDICATION CONTRAINDICATION ADVERSE NURSING
REACTION CONSIDERATIONS
Drug name Cerebrovascular -Must not be -Gastrointestinal -May be taken with or
-Citicholine accident in acute administered to patients disorders without food
recovery phase, with hypertonia of the
Brand name: symptoms and signs of parasympathetic. -Fleeting and discrete -Should be administered
-Somazine cerebral insufficiency hypotensive effect slowly for patients with
such as dizziness, intracranial hemorrhage
Classification: memory loss, poor -Elevated body
-Belongs to the class concentration, temperature -Monitor vital signs
of other agents used disorientation and specifically the BP
as CNS stimulant. recent cranial -Restlessness
traumatism and their -Provide frequent rest
Doctor’s order: sequelae. periods
-Citicoline 1gm IV q8
ACTION
Date started: It increases the
-July 7, 2009 neurotransmission
levels because it favors
Date consumed: the synthesis and
-July 14, 2009 production speed of
dopamine in the
striatum, acting then
as a dopaminergic
agonist thru the
inhibition of tyrosine-
hydroxylase.

Page 33 of 53
DRUG INDICATION CONTRAINDICATION SIDE EFFECTS NURSING
CONSIDERATIONS
Drug name: -Secondary bacterial -Contraindicated in -CV: phlebitis, -Ask patient if he is
-Cefuroxime sodium infection of acute patients hypersensitive thrombophlebitis allergic to penicillins or
bronchitis. to drug or other cephalosporins.
Brand name: cepghalosporins. -GI: nausea,
-Zinacef ACTION anorexia,vomiting, -Obtain specimen for
-Second generation -Use cautiously in diarrhea culture and sensitivity
Doctor’s order: cephalosporin that patients hypersensitive test before giving first
-Cefuroxime 750 mg IV inhibits cell wall to penicillin because of -Hematologic: dose.
q8 ANST synthesis, promoting possible cross-sensitivity Eosinophilia, hemolytic
osmotic instability; with other beta-lactam anemia, -Tablet and suspension
Date started: usually bactericidal. antibiotics thrombocytopenia aren’t bioequivalent
-July 7, 2009 and can’t be
-Skin: urticaria, substituted milligram-
Date consumed: maculopapular and for-milligram.
-July 14, 2009 erythematous rashes,
temperature elevation -monitor patient for
signs and symptoms of
-Other: superinfection.
Hypersensitivity
reactions, serum -tell pt. to take drug as
sickness, a prescribed even after
naphylaxis he feels better

Page 34 of 53
DRUG INDICATION SIDE EFFECTS ADVERSE EFFECTS NURSING
CONSIDERATION
Generic Name: -Active duodenal and -Headache, malaise, -Bradycardia, -Assess patient for
-Ranitidine Hydrochloride gastric ulcer nausea, vomiting, constipation, abdominal pain.
-Gastro-esophageal dizziness, skin rash. diarrhea, blurred
Brand Name: reflux disease (GERD) vision, cardiac -Remind patient to take
-Zantac -Heartburn arrhythmias, burning once daily prescription drug
and itching at at bedtime for best results.
Classification: ACTION injection site,
-H2 receptor blocker Competitively inhibits headache and -Take the drug with foods.
action of histamine on fatigue.
Doctor’s order: the h2 at receptor -Advice patient to report
-Ranitidine 50mg IV q8 sites of parietal cells, abdominal pain and blood
decreasing gastric in stool or emesis.
Date started: acid secretion.
-July 7, 2009 -Assess potential for
interactions with other
Date consumed: pharmacological agents the
-July 14, 2009 patient may be taking.

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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 INTRAVENOUS FLUIDS


Catapres 75mg SL q8 x BP >150/100 PNSS 1L x 12°
Captopril 25mg tab BID
Manitol 100cc IV now then q8
Citicholine 2 drops BID

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 INTRAVENOUS FLUIDS


Catapres 75mg SL q8 x BP >150/100 PNSS 1L x 12°
Captopril 25mg tab BID
Manitol 100cc IV now then q4
Ranitidine 50mg IV q8
Citicholine 1g IV q8
Cefuroxime 750mg IV q8

Attending Physician: Dr. Paguirigan

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 ½L + 4 amp Hydralzine was hooked regulated at 20 µgtt/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


Captopril 25mg tab BID PNSS 1L x 12°
Catapres 75mg SL q8 x BP >150/100 D5NSS 1L x q 12° (Hooked at 9:50am)
Cefuroxime 750mg IV q8 D5W ½L x 20 µgtt/min + 4 amps
Citicholine 1g IV q8 Hydralazine
Manitol 100cc IV now then q8
Ranitidine 50mg IV q8

Attending Physician: Dr. Paguirigan


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 ½L x 20
µgtt/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
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


Captopril 25mg tab BID D5NSS 1L x q 12°
Catapres 75mg SL q8 x BP >150/100 D5W ½L x 20 µgtt/min + 4 amps
Cefuroxime 750mg IV q8 Hydralazine
Citicholine 1g IV q8
Manitol 100cc IV now then q8
Ranitidine 50mg IV q8

Attending Physician: Dr. Paguirigan


Consultant: Dr. Salvador
5th DAY OF HOSPITALIZATION
July 11, 2009

At 8:00 in the morning patient was received with an IVF of D5NSS 1L X 20gtt/min at 600cc level, side drip of D5W ½L x 20
µgtt/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.

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


Captopril 25mg tab BID D5NSS 1L x q 12°
Catapres 75mg SL q8 x BP >150/100 D5W ½L x 20 µgtt/min + 4 amps
Cefuroxime 750mg IV q8 Hydralazine
Citicholine 1g IV q8
Manitol 100cc IV now then q8
Page 39 of 53
Ranitidine 50mg IV q8
Attending Physician: Dr. Paguirigan
Consultant: Dr. Salvador
6th DAY OF HOSPITALIZATION
July 12, 2009

At 8:00 in the morning patient was received with an IVF of D5NSS 1L X 20gtt/min at 700cc level, side drip of D5W ½L x 20
µgtt/min + 4 amps Hydralazine at 100cc and with a patent IFC draining to approximately 1300cc of yellowish urine.

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.

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 and a physical therapist.

MEDICATIONS INTRAVENOUS FLUIDS

Page 40 of 53
Captopril 25mg tab BID D5NSS 1L x q 12°
Catapres 75mg SL q8 x BP >150/100 D5W ½L x 20 µgtt/min + 4 amps
Cefuroxime 750mg IV q8 Hydralazine
Citicholine 1g IV q8 PNSS 1L x q12°
Manitol 100cc IV now then q8
Ranitidine 50mg IV q8

Attending Physician: Dr. Paguirigan


Consultant: Dr. Salvador

7th DAY OF HOSPITALIZATION


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 ½L x 20
µgtt/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


Captopril 25mg tab BID PNSS 1L x q12°
Catapres 75mg SL q8 x BP >150/100 D5W ½L x 20 µgtt/min + 4 amps

Page 41 of 53
Cefuroxime 750mg IV q8 Hydralazine
Citicholine 1g IV q8 D5NSS 1L x q12°
Manitol 100cc IV now then q8
Ranitidine 50mg IV q8

Attending Physician: Dr. Paguirigan


Consultant: Dr. Salvador

8th DAY OF HOSPITALIZATION


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 ½L x 20
µgtt/min + 4 amps Hydralazine at 250cc and with a patent IFC draining to approximately 520cc 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.

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 INTRAVENOUS FLUIDS


Aspirin 80mg 2 tab Now then 1 tab D5NSS 1L x q12°
OD D5W ½L x 20 µgtt/min + 4 amps
Captopril 25mg tab BID Hydralazine

Page 42 of 53
Catapres 75mg SL q8 x BP >150/100
Cefuroxime 750mg IV q8
Citicholine 1g IV q8
Manitol 100cc IV now then q8
Ranitidine 50mg IV q8

Attending Physician: Dr. Paguirigan


Consultant: Dr. Salvador

Page 43 of 53
XI. COMPREHENSIVE NURSING CARE PLAN

NURSING SCIENTIFIC
ASSESSMENT NURSING GOAL INTERVENTION RATIONALE EVALUATION
DIAGNOSIS ANALYSIS
SUBJECTIVE: Ineffective cerebral Deposition of fatty SHORT-TERM GOAL: INDEPENDENT: SHORT-TERM GOAL:
“hindi namin tissue perfusion r/t materials on vessel After 8 hours of 1. Establish rapport to -To gain the patient’s After 8 hours of
maintindihan ang interruption of blood walls nursing intervention, the patient and S. O.’s and S.O.’s trust and nursing intervention,
sinasabi niya” as flow in the brain the patient will be cooperation during goal was met as
verbalized by the secondary to presence able to: the nursing care and evidenced by:
daughter. of subacute infarcts of Plaque formation a) Manifest an 2. Monitor V/S every procedures. a) Patient having an
the right basal ganglia improved nail beds 30 minutes -To gather baseline improved nail beds
OBJECTIVE: and lacunar infarct of from pale to pinkish data and monitor any from pale to pinkish in
Inspection: the left basal ganglia Narrowing of b) Manifest a normal further complications/ color
-With slurred speech of the brain. atherosclerosis plaque papillary response 3. Evaluate pupils, deviations from b) Patient having a
-Right eye dilated noting size, shape and normal. normal papillary
-↓ in muscle LONG-TERM GOAL: equity -To gather baseline response
strength: After 1 week of data and monitor any
Aneurysm formation
-Arms: nursing intervention, further complications/ LONG-TERM GOAL:
L= 3/5 the patient will be 4. Elevate HOB (15 deviations from After 1 week of
R= 1/5 able to: degrees) and maintain normal. nursing intervention,
Rupture of artery
-Legs: a) Manifest an head or neck in -To promote circulation goal was met as
supplying the brain
L= 3/5 improved participation midline and venous drainage evidenced by:
R= 1/5 in performing ADL’s 5. Provide quiet and and to maintain a a) Patient having an
-GCS: with or without restful atmosphere patent airway. improved participation
deprivation of blood
E= 3 support. 6. Reposition pt -For conservation of in performing ADL’s
supply in the brain
V=2 b) Manifest an every 2 hours energy and lowers with or without
M=4 improved speech 7. Patient in oxygen demand support.
-With poor muscle c) Manifest an comfortable position -To promote circulation b) Patient having an
Cerebral infarction
tone on the right and increase in muscle 8. Provide support on and oxygen improved speech with
left hand and foot strength of both arms affected body part distribution diminished slurred
- Limited ROM on the and legs of the such as pillows and -To promote optimal characteristics.
Impaired function of
right hand and patient. assistance to do ADL’s level of functioning c) Patient having an
the brain
foot(only able to d) Maintain functional as needed. -To maintain position increased muscle
carry out passive abilities of the right 9. Provide safety of function and reduce strength with a scale
ROM on this area) and left side of the precautions by raising discomforts. of:
Ineffective tissue
-Unable to carry out body up the side rails. Arms
perfusion
activities without e) Improved physical 10. Encourage the -To prevent fall and L=4/5 R=2/5
assistance such as mobility from level 3 patient and S.O.’s to injury Legs
feeding and changing to level 2 and avoid sedentary L=4/5 R=2/5
clothes. improved GCS scale lifestyle such as d) Patient having an

Page 44 of 53
-Difficulty in chewing drinking liquor, -These factors may improved functional
and swallowing smoking, improper affect them in ability of the right and
-With pale nail beds exercise and too much developing various left side of the body.
-Level 3 physical fatty foods. diseases as what like e) Patient having
mobility the patient is suffering level 2 physical
COLLABORATIVE: now. mobility and a GCS
Lab/Diagnostic Tests: 1. Administer scale of E=4, V=4,
CT Scan: medications as M=5.
HEMORRHAGE IN THE ordered:
LEFT AND RIGHT - Citicoline 2 drops
BASAL GANGLIA BID / 1gm IV q8 -It restores the activity
and functions of the
brain. It improves
neuromuscular
function.

NURSING SCIENTIFIC
ASSESSMENT NURSING GOAL INTERVENTION RATIONALE EVALUATION
DIAGNOSIS ANALYSIS

Page 45 of 53
SUBJECTIVE: Impaired physical Deposition of fatty SHORT-TERM GOAL: INDEPENDENT: SHORT-TERM GOAL:
“Hindi siya ganong mobility r/t subacute materials on vessel After 8 hours of 1. Establish rapport to -To gain the pt’s & After 8 hours of
magkagalaw” as infarcts of the right walls nursing intervention, the patient and S. O.’s S.O.’s trust & nursing intervention,
verbalized by the basal ganglia and the patient will be cooperation during goal was met as
daughter. lacunar infarct of the able to: 2. Assess and the nsg care & evidenced by:
left basal ganglia of Plaque formation a) Participate in determine factors that procedures. a) Patient
OBJECTIVE: the brain. performing ADL’s with contribute to physical -To identify participated in
-Weak in appearance minimal assistance immobility contributing factors performing ADL’s with
-↓ in muscle Narrowing of from others that enable the nurse minimal assistance
strength: atherosclerosis plaque b) Do active and 3. Determine degree to focus on b) Patient having an
-Arms: passive ROM exercise of immobility & appropriate active and passive
L= 3/5 on the right side of his muscle strength interventions ROM exercise within
R= 1/5 body within physical 4. Assist patient in -To assess functional physical limitations
Aneurysm formation
Legs: limitations after hours comfortable position ability after hours of sleep
L= 3/5 of sleep. 5. Provide support on c) Patient having an
R= 1/5 c) Have an affected body parts adequate sleep of 4
Rupture of artery
-GCS: adequate rest and such as pillow -To promote optimal hours
supplying the brain
E= 3 sleep of about 4-5 6. Provide safety level of functioning
V=2 hours. precautions by raising -To maintain position LONG-TERM GOAL:
Intracranial
M=4 up the side rails. of function and reduce After 1 week of
hemorrhage
-Unable to carry out LONG-TERM GOAL: 7. Provide discomfort nursing intervention,
activities without After 1 week of environment free from -To prevent injury and goal was met as
assistance such as nursing intervention, noise and fall evidenced by:
Deprivation of blood
feeding and changing the patient will be disturbances
supply in the brain
clothes. able to: 8. Change position a) Patient having an
-With poor muscle a) Manifest an every 2 hours and -To have a good improved participation
tone on the right improved participation possibly more often if atmosphere in performing ADL’s
Cerebral
hand and foot in performing ADL’s placed on the affected conducive to the with or without
haemorrhage in the
-Difficulty in chewing with or without part recovery of the support.
motor area
and swallowing support. 9. Massage pressure patient b) Patient having an
-Limited ROM on the b) Maintain functional points after each -To reduce risk of improved functional
right hand and abilities of the right position changes tissue ischemia or abilities of the right
Impairment of gross
foot(only able to side of the body. 10. Assist in injury and side of the body
and motor function of
carry out passive c) Manifest an performing ADL to prevent pressure c) Patient having an
the brain
ROM on this area) increase in muscle 11. Assist in sores increased muscle
-Needs assistance strength of both arms performing ROM strength with a scale
when turning and legs of the exercise after hours of -To promote circulation of:
Impaired physical
-Level 3 physical patient. sleep & within and oxygen Arms
mobility
mobility d) Manifest an physical limitations. distribution L=4/5
improvement in 12. Encourage the pt -To promote optimal R=2/5
Lab/Diagnostic Tests: chewing and and S.O.’s to avoid level of functioning Legs
-CT Scan: swallowing abilities sedentary lifestyle -To minimize muscle L=4/5
HEMORRHAGE IN THE e) Improved physical such as drinking atrophy and promote R=2/5
LEFT AND RIGHT mobility from level 3 liquor, smoking, circulation d) Patient having an
BASAL GANGLIA to level 2 improved improper exercise and -These factors may improved chewing and
GCS scale too much fatty foods. affect them in swallowing abilities

Page 46 of 53
COLLABORATIVE: developing various e) Patient having
1. Administer diseases as what like level 2 physical
medications as the patient is suffering mobility and a GCS
ordered: now. scale of E=4, V=4,
- Citicoline 2 drops M=5.
BID / 1gm IV q8

-It restores the activity


and functions of the
brain. It improves
neuromuscular
function.

Page 47 of 53
SCIENTIFIC NURSING
ASSESSMENT DIAGNOSIS PLANNING RATIONALE EVALUATION
EXPLANATION INTERVENTION

Page 48 of 53
OBJECTIVE Risk for infection r/t Inadequate protective After 8hr. shift of INDEPENDENT: After 8hr. shift of
>not changing of IV prolonged of defense mechanism nursing interventions, nursing interventions,
site within 24-36hrs. catheterization the patient will: -Monitor and teach the - Any suspicious GOAL MET, the patient
pt. to the signs of drainage should be was:
- know the proper infection cultured
Bacterium, virus, hand washing as well - know the proper
fungus, or other as the significant -encouraged the pt. to - Washing between hand washing as well
parasites invades the others. wash hands before procedures reduces as the significant
susceptible pt. contact with the the risk of others.
- know the sign and patient transmitting
symptoms of infection pathogens from one - know the sign and
Breaks in the and when to report area of the body to symptoms of infection
integument these to the physician another and when to report
or nurse - Encourage intake of these to the physician
protein- and calorie- - This maintains or nurse
Invasion of pathogens -able to know what rich foods optimal nutritional
carried through bld. food he must eat status -able to know what
Stream or lymphatic - Encourage fluid food he must eat
system -able to increase his intake of 2000 ml to especially in taking of
fluid intake at the 3000 ml of water per - Fluids promote protein and calorie
range of 8-10 glasses day diluted urine and rich foods.
Risk for infection of water frequent emptying of
bladder; reducing -able to consumed
stasis of urine, in 9glasses of water
turn, reduces risk of
-able to take bladder infection or
antibiotics as urinary tract
prescribed - Teach patient to take infection (UTI). -instructed to take
antibiotics as antibiotics as
prescribed - Most antibiotics prescribed
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.

Page 49 of 53
NURSING SCIENTIFIC
ASSESSMENT NURSING GOAL INTERVENTION RATIONALE EVALUATION
DIAGNOSIS ANALYSIS
SUBJECTIVE: Fluid volume excess Deposition of fatty SHORT-TERM GOAL: INDEPENDENT: SHORT-TERM GOAL:
“Nagmamanas ang r/t accumulation of materials on vessel After 8 hours of 1. Establish rapport -To gain the patient’s After 8 hours of
paa nya” as fluids at interstitial walls nursing intervention, to the patient and S. and S.O.’s trust and nursing intervention,
verbalized by the spaces as evidenced the patient will be O.’s cooperation during goal was met as
niece. by bipedal swelling of able to: the nursing care and evidenced by:
patient’s skin above Plaque formation a) Exhibit normal skin procedures. a) Patient having a
OBJECTIVE: the ankle with skin and body condition -To gather baseline normal skin and body
-The patient has a indentation of particularly ↓ 2. Monitor V/S every data and monitor any condition puffiness of
skin indentation of 1+(about 2mm deep) Stenosis of the artery puffiness of the area 30 minutes further complications/ the area above the
about 2mm deep above the ankle deviations from ankle.
(1+) normal.
-Swelling of skin Alteration of usual LONG-TERM GOAL: -To relieve patient LONG-TERM GOAL:
above the ankle smooth flow of blood After 1 week of After 1 week of
-Area shiny through the artery nursing intervention, 3. Clean edematous -To avoid further nursing intervention,
-Cold to touch the patient will be ankle of patient with fluid accumulation goal was met as
-Skin area is pale in able to: warm saline wiper -To avoid to much evidenced by:
color Swirling of blood a) Have a skin 4. Regulate fluid expenditure of a) Patient having
aroung the irregular indentation on intake carefully energy an skin indentation
surface of the normal limits and will 5. Advise patient to on normal limits and
plaques be free from promote bed rest -To allow good venous negative for puffiness
puffiness of the area 6. Elevate patient’s circulation of the area affected.
affected legs for about half an -Because wearing
Vessel lumens hour constrictive clothes
become obstructed 7. Instruct the patient impedes lower
and occluded and S.O.’s that extremities’
constrictive clothes circulation of venous
should be avoided to return
↑ blood volume in the patient
the area proximal to
the obstructed vessel
COLLABORATIVE:
1.Administer -For diuresis and
↑ hydrostatic medications as subsequent
pressure ordered: mobilization of
Manitol 100cc IV q8 excess fluid
(Osmotic Diuretic)
Fluid extravasates
from intravascular to
interstitial spaces.

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

PPD’s Nursing Drug Guide 2nd Edition -


Nurse’s Pocket Guide – Doenges, Moorehouse & Murr

Documentation In Action – Lippincott

Pocket Dictionary – Mosby’s

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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