Individual Case Study on Cerebrovascular Accident

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 lifestylea. smokingb. elevated serum cholesterolc. obesityd. heart disease

3. Modifiable by Medical meana. Transient Ischemic Attackb. Asymptomatic carotid bruitc. Diabetes Mellitusd. Increased blood viscositye. HPN

4. Non – modifiable risk factorsa. ageb. sexc. raced. 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

b. Subarachnoid (5%) – result from aneurismal rupture of a cerebral artery with blood loss into space surrounding the brain; evolve over 1 –2 hours.

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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 HEMORRHAGEIncidence 40 % 30 % 20 % 10 %

Mechanism - atheroscherostic sterosis or occlusion of a large blood vessel

- cholesterol other hematogenous material

- similar to thrombosis; small infarcts

- Hypertension – rupture of penetrating arterioles leading to hemorrhage

Onset and Progression

- gradual, slow stepwise progression of symptoms; may be hours to days

- abrupt - chronic progress; gradual onset

- sudden

Scenario - (+) warning signscommonly occurs at night with > 15 % with TIA

- most occur in setting of MI

Sites - internal carotid or MCA

- cortical small vessels - small, perforating arterioles

- sites of Lacunes

Clinical manifestation - aphasia visual- fields cuts- hemiparesis- hemisensory

- Cortical deficits (hallmark)

- Descrite & specific subortical deficits

- Inc. ICP; subcortical deficits (more extensive)

Prognosis - severe impairment - Repeated in same vascular territory

- Excellent; 85 % same vascular teritory

- - poor; initial mental retardation – 50% - 70%

- if blood is reabsorbed- mild deficit

Comparison Between Right and Left Hemisphere Stroke

Right Hemisphere Lesion Left Hemisphere Lesion- no deficits in ability to understand and express language - aphasia- impaired ability to assess position in space and to safety interact with environment; neglect of (L) side may be present

- usually unimpaired

- verbal memory interact (+) perceptual memory impairment

- impaired ability to retain verbal information, remote memory likely impaired

- careless and oblivious of mistakes; impulsive and decreased ability to anticipate consequence of behavior

- appropriate emotion

- 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 obvious because of intact verbal fluency

- (+) visuomotor perception- (+) 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

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- 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

Stage Muscle Tone Limb Movement Others1 flaccid None2 Beginning spasticity - minimal voluntary movement - basic limb synergies or some

of their components appear as associated reactions

3 Increased spasticity; may be severe (PEAK)

- voluntary control of movement synergies

Full range of all synergy components does not necessarily develop

4 Spasticity begins to decline - can master some movement combinations deviate from synergy

- full range of all synergy components does not necessarily develop

5 - more difficult movement patterns learned

- basic limb synergies lose their dominance over motor acts

6 Spasticity disappears (present only during rapid movement)

- individual joint movement possible coordination approaches normal- normal motor function restored in some

Synergy Patterns of the Upper Extremity: Stroke

FLEXION EXTENSIONScapula Retraction / elevation or hypertension ProtractionShoulderElbowForearmWrist and fingers

Abduction, external rotationFlexionSupinationFlexion

Abduction, internal rotationExtensionPronationFlexion

Synergy Patterns of the Lower Extremity: Stroke

FLEXION EXTENSIONHipKneeAnkleToe

Flexion; abduction; external notationFlexionDorsiflexion; inversiondorsiflexion

Extension, adduction; internal rotationExtensionPlantarflexion; 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.

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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 Malnutrition Falls and injuries Dysphagia Medication overuse

Shoulder dysfunction; RSD Deconditioning and endurance limitations

Depression Fatigue Sexual dysfunction Insomia Seizure

Basal ganglia (As per patients CT Scan result)

Basal ganglia labeled at top right.Latin nuclei basalesNeuroNames hier-206MeSH Basal+GangliaNeuroLex 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.

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http://en.wikipedia.org/wiki/File:Basal_Ganglia_and_Related_Structures.svg

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 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

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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

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.

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http://en.wikipedia.org/wiki/File:Basal-ganglia-coronal-sections-large.png

http://en.wikipedia.org/wiki/File:Basal-ganglia-classic.png

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 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.

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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 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

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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.

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.

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Neurotransmitters

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.

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

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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).

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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 Parts1. 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 Divides the cerebral hemispheres into right and left halves.

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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 LobeArea 4 - primary motor areaArea 6 - premotor areaArea 8 - frontal eye movement and papillary change areaArea 44 - motor speech (Brocas Area)

2. Parietal LobeArea 3, 1, 2 - primary sensory areasArea 5, 7 - sensory association areasArea 39 – 40 - Wernicke’s areaArea 5, 7, 39 – 40 - Gnostic areaArea 43 - primary gustatory area

3. Occipital LobeArea 17 - primary visual cortexArea 18 – 29 - visual association areas

4. Temporal LobeArea 41 - primary auditory cortexArea 42 & 22 - auditory association areas

AREA 4: PRIMARY MOTOR AREALocation : precental gyrus and paracentral lobuleFunction : contralateral voluntary motor activityClinical findings when damaged:

Irritative lesions will present with convulsive seizures Gross lesions will result in flaccid paralysis and areflexia

AREA 6: PREMOTOR AREALocation : 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

Location : Medial aspect of Area 6

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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 AREALocation : Frontal lobeFunction : 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 AREALocation : OCCIPITAL LOBE specifically along the lips of the calcarine sulcus; this is

called the visual or striate area.Function : visionClinical 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 AREALocation : TEMPORAL LOBE specifically at the transverse gyriFunction : hearingClinical 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 AREAThe 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 in consciousness and arousal)

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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 & 83. 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 viscera3. Regulates and controls the pituitary gland4. Center for mind-over-body phenomena5. Secrets regulating hormones6. Functions in rage and aggression 7. Controls normal body temperature, food intake

and thirst8. Helps maintain the walking state and sleep9. Functions as a self-sustained oscillator 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.

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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 AnatomyBlood

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

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COMPUTED TOMOGRAPHY SCANPlain 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 sinus, bilateral. Opacified left ethmoid sinus, left which can be due to sinusitis. Sclerotic mastoid, right.

VI. LABORATORY

COMPUTED TOMOGRAPHY SCANDate: July 13, 2009

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 PROTEINTRANSPARENCY Sl. Turbid SUGARPH/REACTION 6.5 (4.5-8.0) ACETONESPECIFIC GRAVITY 1.015 (1.005-1.030) BILE PIGMENTSCAST/LFP CRYSTALSHayline Cast Amorp. Urate/Phospates FewCELLS/HPF EPITHELIAL CELLSWBC/Pus Cell 3-6 (0-4) Squamous RareRBC/Red Blood Cell >50 (<2) RenalYeast Cells MUCUS THREADS RarePregnancy 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.

HEMATOLOGYDate: July 7, 2009

EXAMINATIONS REFERENCE VALUESHEMOGLOBIN 132 120-160 g/LHEMATOCRTI (HCT) 39 34-47 vol %LEUKOCYTE COUNT (WBC) 13.1 5.0-10.0DIFFERENTIAL COUNT:Nuetrophils 84 50-70 %Lymphocytes 15 20-40 %Eosinophils 1 1-3 %Toxic Granules NegativeClotting Time 2-6 minutesBleeding Time 1-4 minutesMalarial 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 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.

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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 CHEMISTRYDate: July 8, 2009

EXAMINATIONS RESULT S.I. UNITS NORMAL VALUESGlucose (Fasting) 3.26 mmol/L 3.85-6.05Total Cholesterol 7.52 mmol/L 3.9-5.1Blood Urea Nitrogen 9.0 mmol/L 1.7-9.3Serum 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.

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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

Occlusion of affected blood vessels

Narrowed lumen Break off

Emboli

Vertebral arteries Vertebrobasilar arteries Internalcarotid arteries

Dysphagia

Numbness Weakness

Vertigo

Ataxia Hemiparesis

Paralysis

Lower facial Sensory lossDysarthria

Gait problem

Headache

Syncope

weaknessNumbness

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VIII. PHYSICAL ASSESSMENT

PSYCHOSOCIAL PATHOPHYSIOLOGICAL BASISSignificant others The patient is visited by her

daughter’s and niece’s. A very supportive family who shows comfort and care that can relieve stress that is felt by the patient

Coping Mechanism Interacting with SO and Laughing trip.

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.

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 Health Care

Patient’s older sister working in Dubai and patient’s first cousin working in London.

Occupation Bakery ManagerGeneral appearance LOC: Conscious

GCS: Eyes 3Verbal 2Motor 4 . TOTAL 9

Weak in appearance

Brain damage not that severe.

Due to decreased O2 supply and perfusion in the brain.

Due to illness.

Orientation The patient still knows where she is, when she was admitted and who are the SO present.

An abnormal orientation can be a symptom of brain damage caused by CVA

Memory Patient still has a good memory thus she recalls diet prescribed her physician and thus still remembers a lot things.

Damaged cause by the infarct is not yet that severe to affect the memory of the patient.

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.

ELIMINATIONStool Frequency: Once a day

Pattern: Every morningConsistency: Normal StoolAmount: Approximately 9-10 inches in length, 1.5 in diameterColor: Light BrownOdor: Normally foul stool odor

Abdomen: contour palpation Rounded, (-) palpable massUrine Quantity: 500cc to 1300cc per

shift

Pattern: On IFC

Color: Lt. Yellow

Transparency: Sl. Turbid

Spc. Gravity: 1.015

Due to oral and IV fluid intake.

Patient is on IFC to decrease BP.

Due to the general liquid diet of the patient.Due to the general liquid diet of the patient.Still within normal range.

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REST AND ACTIVITYCurrent activity level Lie and sit on bed Patient moment varies due to body

weaknessSleep 8-9 hours a day during the

confinement periodPain/relief measures Patient tries to position himself

on a comfortable position.

Patient also verbalized that upon having a headache she takes Biogesic.

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.

SAFETYAllergic Reaction Sea foodsMedications Gentamicin 160 mg IV OD

Cefuroxime 750 mg IV q8hClonidine 1 tab SL nowImidapril 1 tab OD/ NGT

Bactoban ointment to wound TID

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.

Eye/vision Glasses: Pupils:

With a 120 reading glassRight pupil is dilated non-reactive to light. Left Pupil constricted with minimal reaction to light.

Due to an infarct in the brain, vision and normal eye function can be affected.

Hearing/hearing aid Patient has normal hearingSkin integrity Lesion scars

Intact SkinWith scars on left hand Due to an accident caused by bakery

machineries.Mucus membrane Moist and intactTemperature Temperature, via axillary, of the

patient varies from 36.0°C to 37.4°C

OXYGENActivity Tolerance Can move minimally Patient has general weaknessAirway clearance

NoseMouth

With no secretionsClear

Respiration rateDepthRhythm

28 cycle per minuteNormalRegular

ColorSkinNailsLips

PalePinkishSomewhat dry

Patient has a low hemoglobin count.

Capillary refill 1-2 seconds Normal Oxygenation of tissue cellsPulses Within normal range Blood pressure 140-210/70-110 mmHg Patient is having an elevated BP due to

illness.Edema NoneHoman’s Sign Negative

NUTRITIONHospital Diet/Restrictions OR feeding of 1600 calories in 4

equally divided feedingIVFs (according to chart) PNSS 1L x 20-21 gtt/min

D5NSS 1L x 20-21 gtt/minD5W ½L x 20 µgtt/min

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Site Left posterior forearmTissue turgor Good skin turgorAbility to:

ChewSwallow

AbleAble

Feed self With SO’s assistance Due to decreased hand movement accuracy.

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IX. DRUG ANALYSIS

DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATION Generic Name:-Clonidine Hydrochloride Brand Name:-Catapres, Dixaril Classification:-Cardiovascular Agent, General acting anti-hypertensive, analgesic Stock:-75mg tab SL Doctor’s order:-75mg Sl q8 x BP >150/100

Date started:-July 7, 2009

Date consumed:-July 14, 2009

-Elevated systolic and diastolic BP

ACTION- Central-acting anti-adrenergic derivative. Stimulates alpha2-adrenergic receptors in CNS to inhibit sympathetic vasomotor centers. Also inhibits rennin release from kidneys.

-Hypersensitivity to drug regimen -Pregnancy -Lactation

-CV: Hypotension, peripheral edema, ECG changes, tachycardia, bradycardia -GI: Dry mouth, constipation, N/V, hepatitis -CNS: drowsiness, sedation, dizziness, headache, fatigue, weakness, sluggishness, nervousness -Skin: rashes, pruritus -UG: impotence, loss of libido

-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 -Instruct patient not to breastfeed while taking this drug(for mothers)

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DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATION Generic Name:- Captopril Brand Name:- Capoten, Captale, Captril Classification:-Cardiovascular Drug Stock:- 25mg tab Doctor’s order:- 25mg tab BID



-Elevated systolic and diastolic BP

ACTION- Central-acting anti-adrenergic derivative. Stimulates alpha2-adrenergic receptors in CNS to inhibit sympathetic vasomotor centers. Also inhibits rennin release from kidneys.

-Hypersensitivity to drug regimen -Pregnancy -Lactation

-CV: Hypotension, peripheral edema, ECG changes, tachycardia, bradycardia -GI: Dry mouth, constipation, N/V, hepatitis -CNS: drowsiness, sedation, dizziness, headache, fatigue, weakness, sluggishness, nervousness -Skin: rashes, pruritus -UG: impotence, loss of libido

-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 -Instruct patient not to breastfeed while taking this drug(for mothers)

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DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATIONSGeneric name:-Mannitol

Brand name:-Osmofundan 20%

Classification:-Osmotic Diuretic

Doctor’s order:-Manitol 100cc IV q8 / IV q4

Date started :-July 8, 2009 (IV q8)-July 10, 2009 (IV q4)

Date Consumed:-July 14, 2009

Reduction of elevated intracranial pressure, cerebral edema or increased intraocular pressure.

ACTIONElevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma.

-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.

-CNS: dizziness, headache, fever

-CV: edema, hypotension, tachycardia, vascular overload

-EENT: blurred vision, rhinitis

-GI: thirst, dry mouth, nausea, vomiting, diarrhea

-GU: urine retention

-Metabolic: dehydration

-Other: chills

-Assess patient’s blood pressure history before therapy. Monitor pulse and blood pressure regularly

-Check weight, renal function, fluid balance and serum urine sodium and potassium daily

-Monitor CNS symptoms and changes in mental status.

-To relieve thirst, give frequent mouth care or fluids-monitor allergic reaction: rash,fever, pruritus,and urticaria.

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DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATIONSDrug name-Citicholine

Brand name:-Somazine

Classification:-Belongs to the class of other agents used as CNS stimulant.

Doctor’s order:-Citicoline 1gm IV q8



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.

ACTIONIt 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 tyrosine-hydroxylase.

-Must not be administered to patients with hypertonia of the parasympathetic.

-Gastrointestinal disorders

-Fleeting and discrete hypotensive effect

-Elevated body temperature

-Restlessness

-May be taken with or without food

-Should be administered slowly for patients with intracranial hemorrhage

-Monitor vital signs specifically the BP

-Provide frequent rest periods

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DRUG INDICATION CONTRAINDICATION SIDE EFFECTS NURSING CONSIDERATIONSDrug name:-Cefuroxime sodium

Brand name:-Zinacef

Doctor’s order:-Cefuroxime 750 mg IV q8 ANST



-Secondary bacterial infection of acute bronchitis.

ACTION -Second generation cephalosporin that inhibits cell wall synthesis, promoting osmotic instability; usually bactericidal.

-Contraindicated in patients hypersensitive to drug or other cepghalosporins.

-Use cautiously in patients hypersensitive to penicillin because of possible cross-sensitivity with other beta-lactam antibiotics

-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, anaphylaxis

-Ask patient if he is allergic to penicillins or cephalosporins.

-Obtain specimen for culture and sensitivity test before giving first dose.

-Tablet and suspension aren’t bioequivalent and can’t be substituted milligram-for-milligram.

-monitor patient for signs and symptoms of superinfection.

-tell pt. to take drug as prescribed even after he feels better

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DRUG INDICATION SIDE EFFECTS ADVERSE EFFECTS NURSING CONSIDERATIONGeneric Name:-Ranitidine Hydrochloride

Brand Name: -Zantac

Classification:-H2 receptor blocker

Doctor’s order:-Ranitidine 50mg IV q8



-Active duodenal and gastric ulcer-Gastro-esophageal reflux disease (GERD)-Heartburn

ACTIONCompetitively inhibits action of histamine on the h2 at receptor sites of parietal cells, decreasing gastric acid secretion.

-Headache, malaise, nausea, vomiting, dizziness, skin rash.

-Bradycardia, constipation, diarrhea, blurred vision, cardiac arrhythmias, burning and itching at injection site, headache and fatigue.

-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.

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X. COURSE IN THE WARD

ADMISSION DAYJuly 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 FLUIDSCatapres 75mg SL q8 x BP >150/100Captopril 25mg tab BIDManitol 100cc IV now then q8Citicholine 2 drops BID

PNSS 1L x 12°

Attending Physician: Dr. Paguirigan

2nd DAY OF HOSPITALIZATIONJuly 8, 2009

Medical Ward

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 FLUIDSCatapres 75mg SL q8 x BP >150/100Captopril 25mg tab BID Manitol 100cc IV now then q4Ranitidine 50mg IV q8Citicholine 1g IV q8Cefuroxime 750mg IV q8

PNSS 1L x 12°

Attending Physician: Dr. Paguirigan

3rd DAY OF HOSPITALIZATIONJuly 9, 2009

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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. Salvador with orders carried out. Patients BP as of this time is 190/110.

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 FLUIDSCaptopril 25mg tab BID Catapres 75mg SL q8 x BP >150/100Cefuroxime 750mg IV q8Citicholine 1g IV q8Manitol 100cc IV now then q8Ranitidine 50mg IV q8

PNSS 1L x 12°D5NSS 1L x q 12° (Hooked at 9:50am)D5W ½L x 20 µgtt/min + 4 amps Hydralazine

Attending Physician: Dr. PaguiriganConsultant: Dr. Salvador

4th DAY OF HOSPITALIZATIONJuly 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.


MEDICATIONS INTRAVENOUS FLUIDS

Captopril 25mg tab BID Catapres 75mg SL q8 x BP >150/100Cefuroxime 750mg IV q8Citicholine 1g IV q8Manitol 100cc IV now then q8Ranitidine 50mg IV q8

D5NSS 1L x q 12°D5W ½L x 20 µgtt/min + 4 amps Hydralazine



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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.



D5NSS 1L x q 12°D5W ½L x 20 µgtt/min + 4 amps Hydralazine



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

Captopril 25mg tab BID Catapres 75mg SL q8 x BP >150/100Cefuroxime 750mg IV q8Citicholine 1g IV q8Manitol 100cc IV now then q8

D5NSS 1L x q 12°D5W ½L x 20 µgtt/min + 4 amps HydralazinePNSS 1L x q12°

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Ranitidine 50mg IV q8



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.


PNSS 1L x q12°D5W ½L x 20 µgtt/min + 4 amps HydralazineD5NSS 1L x q12°



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.

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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 FLUIDSAspirin 80mg 2 tab Now then 1 tab ODCaptopril 25mg tab BID Catapres 75mg SL q8 x BP >150/100Cefuroxime 750mg IV q8Citicholine 1g IV q8Manitol 100cc IV now then q8Ranitidine 50mg IV q8

D5NSS 1L x q12°D5W ½L x 20 µgtt/min + 4 amps Hydralazine


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XI. COMPREHENSIVE NURSING CARE PLAN

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ASSESSMENT NURSING DIAGNOSIS SCIENTIFIC ANALYSIS NURSING GOAL INTERVENTION RATIONALE EVALUATIONSUBJECTIVE: “hindi namin maintindihan ang sinasabi niya” as verbalized by the daughter.

OBJECTIVE:Inspection:-With slurred speech-Right eye dilated-↓ in muscle strength:-Arms: L= 3/5R= 1/5-Legs:L= 3/5R= 1/5-GCS: E= 3V=2M=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.-Difficulty in chewing and swallowing-With pale nail beds-Level 3 physical mobility

Lab/Diagnostic Tests:CT Scan: HEMORRHAGE IN THE LEFT AND RIGHT BASAL GANGLIA

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.

Deposition of fatty materials on vessel walls

Narrowing of atherosclerosis plaque

SHORT-TERM GOAL:After 8 hours of nursing intervention, the patient will be able to: a) Manifest an improved nail beds from pale to pinkishb) Manifest a normal papillary response LONG-TERM GOAL:After 1 week of nursing intervention, the patient will be able to:a) Manifest an improved participation in performing ADL’s with or without support.b) Manifest an improved speechc) 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 bodye) Improved physical mobility from level 3 to level 2 and improved GCS scale

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 atmosphere6. Reposition pt every 2 hours 7. Patient in comfortable position8. Provide support on affected body part such as pillows and assistance to do ADL’s 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 drinking liquor, smoking, improper exercise and too much fatty foods.

COLLABORATIVE:1. Administer medications as ordered:- Citicoline 2 drops BID / 1gm IV q8

-To gain the patient’s 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 data and monitor any further complications/ deviations from normal.-To promote circulation and venous drainage and to maintain a patent airway.-For conservation of energy and lowers oxygen demand-To promote circulation and oxygen distribution-To promote optimal level of functioning-To maintain position of function and reduce discomforts.

-To prevent fall and injury -These factors may affect them in developing various diseases as what like the patient is suffering now.

-It restores the activity and functions of the brain. It improves neuromuscular function.

SHORT-TERM GOAL:After 8 hours of nursing intervention, goal was met as evidenced by:a) Patient having an improved nail beds from pale to pinkish in colorb) Patient having a normal papillary response LONG-TERM GOAL:After 1 week of nursing intervention, goal was met as evidenced by: a) Patient having an improved participation in performing ADL’s 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:ArmsL=4/5 R=2/5LegsL=4/5 R=2/5d) Patient having an 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.

ASSESSMENT NURSING DIAGNOSIS SCIENTIFIC ANALYSIS NURSING GOAL INTERVENTION RATIONALE EVALUATIONSUBJECTIVE: “Hindi siya ganong magkagalaw” as verbalized by the daughter.

OBJECTIVE:-Weak in appearance-↓ in muscle strength:-Arms: L= 3/5R= 1/5Legs:L= 3/5R= 1/5-GCS: E= 3V=2M=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.


Plaque formation

Narrowing of atherosclerosis plaque

SHORT-TERM GOAL:After 8 hours of nursing intervention, the patient will be able to:a) Participate in performing ADL’s with minimal assistance from othersb) 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 nursing intervention, the patient will be able to:a) Manifest an improved participation in performing ADL’s with or without support.b) Maintain functional abilities of the right 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 abilitiese) 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 strength4. Assist patient in comfortable position5. 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 disturbances8. Change position every 2 hours and possibly more often if placed on the affected part9. Massage pressure points after each position changes10. Assist in performing ADL11. 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. COLLABORATIVE:1. Administer medications as ordered:- Citicoline 2 drops BID / 1gm IV q8

-To gain the pt’s & 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 level of functioning -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 -To promote circulation and oxygen distribution-To promote optimal level of functioning-To minimize muscle atrophy and promote circulation-These factors may affect them in developing various diseases as what like the patient is suffering now.

-It restores the activity and functions of the brain. It improves neuromuscular function.

SHORT-TERM GOAL:After 8 hours of nursing intervention, goal was met as evidenced by:a) Patient participated in performing ADL’s with minimal assistanceb) Patient having an active and passive ROM exercise within physical limitations after hours of sleepc) Patient having an adequate sleep of 4 hours LONG-TERM GOAL:After 1 week of nursing intervention, goal was met as evidenced by: a) Patient having an improved participation in performing ADL’s with or without support.b) Patient having an improved functional abilities of the right side of the bodyc) Patient having an increased muscle strength with a scale of:ArmsL=4/5R=2/5LegsL=4/5R=2/5d) Patient having an improved chewing and swallowing abilitiese) Patient having level 2 physical mobility and a GCS scale of E=4, V=4, M=5.

ASSESSMENT DIAGNOSIS SCIENTIFICEXPLANATION

PLANNING NURSINGINTERVENTION

RATIONALE EVALUATION

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

-encouraged the pt. to wash hands before contact with the patient

- Encourage intake of protein- and calorie-rich foods

- Encourage fluid intake of 2000 ml to 3000 ml of water per day

- Teach patient to take antibiotics as prescribed

- Any suspicious drainage should be cultured

- Washing between procedures reduces the risk of transmitting pathogens from one area of the body to another

- 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

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ASSESSMENT NURSING DIAGNOSIS SCIENTIFIC ANALYSIS NURSING GOAL INTERVENTION RATIONALE EVALUATIONSUBJECTIVE:“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

Fluid volume excess r/t accumulation of fluids at interstitial spaces as evidenced by bipedal swelling of patient’s skin above the ankle with skin indentation of 1+(about 2mm deep)


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.

Edema

SHORT-TERM GOAL:After 8 hours of nursing intervention, 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 nursing intervention, the patient will be able to:a) Have a skin indentation on normal limits and will be free from puffiness of the area affected

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 wiper4. Regulate fluid intake carefully5. Advise patient to promote bed rest6. Elevate patient’s legs for about half an hour7. 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)

-To gain the patient’s 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 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

-For diuresis and subsequent mobilization of excess fluid

SHORT-TERM GOAL:After 8 hours of nursing intervention, 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 nursing intervention, goal was met as evidenced by:a) Patient having an skin indentation on normal limits and negative for puffiness of the area affected.

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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Individual Case Study on Cerebrovascular Accident

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