CEREBRO VASCULAR ACCIDENT

1. Definition
CVA (Cerebral Vascular Accident)/stroke is associated with permanent
neurological damage. CVA may be due to cerebral ischemia, infarction or
intracranial hemorraghe. True syncope is rare. However, intracranial
hemorraghe invariably result in sudden loss of consciousness and is associated
with am increase morbidity and mortality rate (Ganda, Kanchan. (2008).
Cerebral Vascular Accident (CVA) or stroke involves a sudden onset of
neurological deficit because of insufficient blood supply to a part of the brain,
leading to cellular damage and cellular death (Parker-Frizzel, 2005 in
Carpenito, Linda Juall. (2008)
CVA (Cerebral Vascular Accident) is a disorder of brain function that
arise due to sudden occurrence of circulatory disorders of the brain and can
happen to anyone and at anytime with symptoms lasting for 24 hours or more
a defect causing a paralysis of the limbs, disturbance speech, thought
processes, memory and other forms of disability to cause death (Muttaqin,
2008:234).
According to the WHO stroke is the presence of clinical signs rapidly
growing brain function due to disturbance of focal (or global) with symptoms
lasting 24 hours or more a cause of death without any other obvious cause
other than vascular. (Hendro Susilo, 2000)

2. Etiology
There are several causes of CVA infarction (Muttaqin, 2008: 235)
a. cerebral thrombosis
Occurs in blood vessel occlusion causing ischemic brain tissue that can
lead to edema and congestion around him. Thrombosis usually occurs in
older people who are sleeping or waking. Occurs due to decreased
sympathetic activity and blood pressure drop. Cerebral thrombosis is
caused due to:
b. Aterosklerostis: hardened / reduced flexibility and elasticity of blood
vessel walls
c. Hypercoagulable: thick blood that will lead to increased hematocrit
increases viscosity so that it can slow the cerebral blood flow

d. Arteritis: inflammation of the arteries

e. Embolism
Can occur due to blockage of blood brain vessel by a blood clot, fat, and
air. Emboli usually originate from thrombus in the heart of the system
apart and clog the middle cerebral artery. Circumstances that can lead to
embolism:
1) Rheumatic Heart Disease
2) Myocardial infarction
3) Atrial arrhythmias and state: can form small clots that can cause
cerebral embolism
4) Endocarditis: causes interference with the endocardial
5) Risk factors for stroke
There are several risk factors for CVA infarction (Muttaqin, 2008: 236):
1) Hypertension.
2) Cardiovascular disease-cerebral embolism from the heart: coronary
artery disease, congestive heart failure, left ventricular hypertrophy,
abnormal rhythms (especially atrial fibrillation), congestive heart
3)
4)
5)
6)
7)

disease.
High Cholesterol
Obesity
Increased hematocrit
Diabetes Mellitus
Smoking

3. Patophysiology
According to Ehrman, Jonathan K. et.al (2013), The artherosclerosis that
causes cerebrovascular disease and ultimately an ishchemic stroke, proceedsin
the same fashion as plaque progression in coronary artery disease (CAD). For
this reason the sama traditional and non traditional risk factor that are related
to the development and progression of CAD and peripheral arterial disease
(PAD) are associated with the developmentof ischemic cerebrovascular
disease. Ischemic strokes can be futher categorized as thrombotic, embolic,
and hemodynamic. In the case of thrombotic strokes, in which an occlusive
thrombus develops in or outside an ulcerated plaque, hipercoagulable states
due to increased coagulation potential or decreased fibrinolitic potential are
particularry importantant risk factor. Emboli that cause embolic strokes are
tipically from the carotid or other arteries. In the cases. The thrombus is not
large enough to acclude the large vessel, but the embolus that breaks off

ultimately lodges in a smaller cerebral artery or arteriole. Often, major stroke

are preceeded by transient ischemic attack (TIAs), which are considered a
major predictor of impending stroke. In a study of patients who reported to an
emergency room with a TIA, approximately 10% experienced a stroke with in
90d. perhaps even more compelling is the fact that 5% experienced a stroke
with in 2d. All older populations should be screened for possible prior TIA
because about 50% of patients who experience a TIA do not report it to a
clinician.
Hypertentsions is the major risk factor for hemorrhagic stroke, which
makes up approximately 10% of strokes. Hemorrahagic strokes can also be
caused by aneurysm, drug use, brain tumor, congenital arteriovenous
malformations, and anticoagulant medications. Hemorrhagic strokes are
classified as either itracerebral, which refers to bleeding inside the brain, or
subarachnoid, which refers to bleeding in and around the spaces that surround
the brain. Unfortunately, there is usually little warning for a hemorrhagic
stroke. Acute signs or symptomps include altered consciousness, headache,
vomiting, and large elevations in blood pressure. Additionally, patients with
subarachnoid hemorrhage may develop neck stiffness.

Risk Factors for

4. WOC

Damaged heart valves,

myocardial infarction,
atrial endocarditis
Blockage of a brain blood
vessel by a blood clot, fat &
Air

Aterosklerosis,
Hiperkoagulasi, Artesis
Thrombosis Serebral
Vascular occlusion
Ischemic Brain Edema
Network & network
congestion around

Aneurysms,
malformations,
arterivenous
intracerebral hemorrhage
Oozing of blood in the
brain parenchyma
suppression of brain
tissue edema and
herniation of brain

cerebral
embolism
Stroke (Cerebro
Vaskuler Accident)
Deficit
neurologis

Serebral Infark
Decrease in
cerebral

loss of
controlvolunteer

Risk of
increased ICP

Hemiplegic &
hemiparasis

Herniasa taks
cerebral and
into the
foramen
magnum

Damage to
physical

Inadequate
nutritional
intake
Changes in
nutrient
intake
inadequate

Brainstem
compression

COMA

Cardiovascular
and respiratory
depression

General
physical
weakness

Death

Inability of
adequate selfcare
Self-care

risk of

Cognitive impairment
and psychological
effects

Disartia,
dysphasia /
aphasia, apraxia

Limited field of vision,

difficulty
understanding,
forgetfulness, lack of
motivation,
frustration, instability.
Emotional, hostile,
vindictive, less
cooperation and

Damage
verbal

Decreased
level of
consciousness
Emphasis local
network

Risk of
damage to

Decreased
cough ability,
lack of physical
mobility and
production
secret

Dysfunction of
the bladder and
the digestive
tract
Alvi & uri
elimination

Risk of
ineffective
airway

Dysfunction of
visual spatial
perception and
sensory loss

Changes in
sensory
perception

1.
2.
3.
4.

psychological
disorders
change the role
of family
Anxiety clients &
families
Implementation
of risk reduction
worship

4
Muttaqin (2008)

5. Classification (Arief Mansjoer, et al, 2000)

a. Based Clinic
1) Haemorrhagic Stroke (SH)
Strokes that occur because of sub arachnoid hemorrhage, probably caused by
the rupture of cerebral blood vessels in certain areas, usually occurs when the
patient or activity when active. But may also occur at rest, patient awareness is
generally declining
2) Non Hemorrhagic Stroke (SNH)
May include ischemia, cerebral embolism and thrombosis, usually happens
after a long rest, sleep or just woken up in the morning. Not occur ischemia
causes hypoxia and subsequent edema may occur secondary, patient awareness
is generally good.
b. Travel by Disease
1) Trancient Ischemic Attack (TIA) or ischemic attacks at a glance
A focal neurological disorder that arises suddenly and disappear within a few
minutes (average duration 10 minutes) to several hours (24 hours).
2) Stroke Involution or Progressive
Course of the disease is going slowly though acute stroke. Emergence of
symptoms grew worse, progressive process several hours to several days.
3) Complete Stroke
Neurological disorders that arise are settled or permanent, the maximum since
the beginning of the attack and showed little parbaikan be preceded by a TIA
are recurrent.

6. Clinical Consideration
According to Ehrman, Jonathan K. et.al (2013), Medical and clinical
considerations for stroke include signs and symptoms spesific to whether damage
occurs on the right or leftside of the brain. The clinician needs tobe aware of the
acute signs of the stroke and the clinical manifestation that occur after the event.
5

Finally, the method of determining the definitive diagnosis of stroke is amother

important clinical decision.
Memory loss and paralysis are two of the more consistent symptomps of
stroke. In the case of paralysis, the brain damage causes paralysis on the opposite side
of the body. Furthermore, right-brain damage can result in vision problems and
awkward or inappropriate behavior, where as left-brain damage causes speech and
language problems and slow or cautious behavior. A patient suffering from acute
stroke can have one of the following symptomps;
1. Numbness or weakness of the face, arm, or leg
2. Confusion, speech problem, and cognitive defects
3. Impaired bilateral or unilateral vision
4. Impaired coordination and walking
5. headache
Clinical manifestations depend on the neuroanatomical and vaskularization . Clinical
symptoms and neurologic deficits were found to be useful for assessing the location
of ischemia
a. Circulatory disorders of the anterior cerebral artery causing contralateral
hemiparesis and hemihipestesi mainly involving the limbs
b. Arteri circulatory disorders causing cerebral hemiparesis and contralateral
hemihipestesi especially on the arm with a sublime dysfunction aphasia ( if the
dominant area of the brain ) or a hemispatial negalect ( when the nondominant
brain area )
c. Blood Circulation disorder causing posterior cerebral artery hemianopsi
kuadrantanopsi

homonym

or

without

contralateral

motor

and

sensory

disturbances. Memory disorders occur in the event of infarction in the medial

temporal lobe. Aleksia without agrafia arise when infarction occurs in the
dominant visual cortex and corpus callosum splenium. Agnosia and prosopagnosia
( inability to recognize faces ) result from infarction of the inferior cortex
temporooksipitalis
d. Circulatory disorders of the brain stem causing cranial nerve disorders such as
dysarthria, and vertigo diplopic; cerebellar disorders, such as ataxia or loss of
balance ; impairment of consciousness
e. Lacunar infarction is a clinical disorder kecildengan infarction pure motor or
sensory function of the sublime without interruption
7. Diagnostic tests
According to Ehrman, Jonathan K. et.al (2013), Ultrasound, magnetic
resonance imaging (MRI), and angiography are the main diagnostic test use to assess
6

impending occusions that could cause an ischemic stroke. The major diagnostic tool
for determining hemorrhagic stroke is noncontrast computerized tomography (CT).
CT can also be used to diagnose ischemic stroke, although the sensitivity of this
technique varies across research studies. Recently, diffusion weighted MRI has been
shown to be more effective than CT for diagnosing ischemic stroke, making this a
promising diagnostic tool.
Examination of supporting the CVA infarction patients:
a. laboratory:
1) On examination packet stroke : blood viscosity at CVA apsien no increase in
VD > 5.1 cp , Platelet Aggression Test ( TAT ), arachidonic acid ( AA ),
Platelet Activating Factor ( PAF ), fibrinogen ( Muttaqin , 2008: 249-252 )
2) Standard laboratory analysis include urinalysis, CVA infarction patients HDL
HDL decreased below the normal value of 60 mg/dl, erythrocyte
sedimentation rate ( LED ) in patients with CVA aims to measure the velocity
of red blood cells settle in a tube LED high blood indicate an inflammation .
But LEDs do not indicate whether the long -term inflammation, such as
arthritis, basic metabolic panel ( sodium ( 135-145 nmol / L ), potassium ( 3.6
to 5.0 mMol / l ) , chloride , ) ( Prince , et al , 2005 : 1122 )
b. X -ray examination of the thorax : can detect an enlarged heart ( cardiomegaly )
and pulmonary infiltrates associated with congestive heart failure ( Prince, et al ,
2005:1122 )
c. Ultrasonography ( USG ) karaois : an evaluation standard for the detection of
carotid blood flow disturbances and possible movement memmperbaiki stroke
(Prince , et al , 2005:1122).
d. Cerebral angiography : help determine the specific cause of the stroke -like lesions
ulseratrif, stenosis, displosia fibraomuskular, arteriovenous fistulas, vasculitis and
thrombus formation in large vessels (Prince, et al , 2005:1122) .
e. Scanning with Positron Emission Tomography ( PET ) : identify how large an area
of the brain to receive and metabolize glucose as well as extensive injury (Prince,
et al , 2005:1122)
f. Transesofagus echocardiogram (TEE) : detects potential kardioembolus (Prince ,
et al, 2005:1123).
g. CT scan : This scan shows the specific location of edema , hematoma position ,
the brain tissue infarction or ischemia and its position with certainty . Test results
are usually obtained hiperdens focal , sometimes seen in ventricular compaction or
spread to the brain surface (Muttaqin, 2008:140).
7

h. MRI uses magnetic waves to examine the position and large / regional extent of
infarction (Muttaqin, 2008:140).
8. Medical management

There are several treatment in patients with CVA infarction ( Muttaqin, 2008:14 ):
a. To treat acute conditions, trying to stabilize TTV by:
1) Maintain a patent airway
2) Control of blood pressure
3) Taking care of the bladder, do not wear the verge of defeat
4) Position the right, the position changed every 2 hours, passive motion
exercises
b. Conservative therapy
1) Improve the flow of cerebral vasodilators
2) Anti aggregation trombolis : aspirin to inhibit the release reaction that occurs
after aggregation thrombosis alteroma ulceration
3) Anti-coagulant to prevent the occurrence or severity of trombosis or
embolization from other places to the cardiovascular system .
4) If there is an increase in ICT, it is done:
a) Hyperventilation with ventilator so that PaCO2 30-35 mmHg
b) osmotherapy among others:
(1) 20 % mannitol infusion of 100 ml or 0.25-0.5 g / kg aBW / times

c)
d)
e)
f)

within 15-30 minutes, 4-6 times/day.

(2) Infusion of 250 ml 10% glycerol in 1 hour , 4 times / day
The position of head of head-up ( 15-30 )
Avoid straining at BAB
Avoid cough
Minimize hot environment

9. Complication
There are some complications CVA infarction (Muttaqin, 2008: 253)
a. In terms of immobilization:
1) respiratory infections (pneumonia)
2) Tenderness on pressure sores
3) Constipation
b. In terms of paralysis
1) Pain in the back,
2) joint dislocation, deformity
c. In terms of brain damage:
1) Epilepsy
2) Headache
d. cerebral hypoxia
e. brain herniation
f. contractures

10. Nursing Process

a. Assessment
1) Identity
Usually experienced by old age, but did not rule can also he experienced by
younger age, gender, and race can also affect.
2) The main complaint
Limb weakness next to the body, speech pelo, can not communicate, and the
patient's loss of consciousness.
3) Medical history now
Infarction sudden stroke at rest or wake up in the morning.
4) Past medical history
A history of hypertension , history of previous stroke , diabetes mellitus , heart
disease ( especially arrhythmias ), the use of anti- coagulant drugs, aspirin ,
vasodilators, obesity. A history of smoking, use of alcohol and drug abuse
(cocaine).
5) Family history of disease
Presence of a family history of hypertension, diabetes mellitus, or a history of
stroke in the previous generation.
6) Psychosocial - spiritual history
Fees for examination, treatment and care of the family finances that may
confound these cost factors can affect the stability of the emotions and minds
of the clients and families . Changes occur because of the relationship and the
role of patient difficulty communicating due to tough talk . Anxiety and fear of
disability and impaired self-image
7) Needs
(a) Nutrition: the symptoms decreased appetite, nausea and vomiting in the
acute phase, loss of sensation (ketchup flavor) on the tongue, cheeks,
throat, dysphagia characterized by difficulty swallowing, obesity
(b) Elimination: shows the change patterns of urinary incontinence as urine,

anuria. Abdominal distension (bladder distesi excess), negative bowel

(paralytic Ilius), bowel habit constipation usually occurs due to decreased
intestinal peristalsis
(c) Activities: shows the difficulty of the move as weakness, sensory loss or

paralise/hemiplegi, tiredness, muscle tone disorders, paralytic (hemiplegia)

9

(d) Rest: rest client has difficulty because of muscle spasms / muscle pain

b. Physical Examination
1) Respiratory System (Breathing): cough, increased sputum production,
shortness of breath, muscle use breathing aids, as well as changes in the speed
and depth of breathing. Ronchi any secretions due to increased production and
decreased ability to cough due to decreased awareness of the client. On both
the conscious clients often found abnormalities on examination of the
respiratory system.
2) Cardiovascular system (Blood): can hypotension or hypertension, irregular
heart rate, presence of murmurs
3) neurological system
(a) The level of awareness: conscious could well until there is a comma . GCS
assessment to assess the client's level of consciousness
(b) Pathological Reflexes
Positive Babinski reflex showed the presence of bleeding in the brain /
intracerebral hemorrhage and to distinguish the type of stroke that is
whether bleeding or infarction
(c) Examination of the cranial nerves
(1) Nerve I: usually in clients with stroke no abnormalities in olfactory
function
(2) Nerve II: visual perception dysfunction due to impaired primary
sensory distance between the corner of the eye and visual cortex.
Visula-spatial relations disorder often seen in clients with left
hemiplegia . Clients may not be able to wear clothes without assistance
because of the inability to match the dress to the body.
(3) Nerves III , IV and VI when a stroke resulting in paralysis of the
muscles of the whole okularis obtained conjugates decreased ability of
the unilateral hand movements are sick
(4) Nerve VII of taste perception in the normal range , facial asymmetry,
facial muscles attracted to the healthy side
(5) Nerve XII asymmetrical tongue , there is a deviation on one side and
(d)
(e)
(f)
(g)

fasciculations . Normal sense of taste.

Urinary System (Bladder): urinary incontinence occurs
Reproductive system: hemiparese can cause sexual fulfillment
The endocrine system: the enlargement of the thyroid gland gland
Gastrointestinal System (Bowel): the complaint difficulty swallowing, loss
of appetite, nausea and vomiting in the acute phase. May experience faecal
incontinence or constipation occurs due to decreased peristalsis
10

usus.Adanya V nerve disorders that cause stroke in some circumstances

the trigeminal nerve paralysis, showed decreased ability to coordinate the
movement of chewing, mandibular deviation on the ipsilateral side and
paralysis of the whole pterigoideus muscles and the nerves IX and X are
less good swallow ability, difficulty opening the mouth.
(h) Musculoskeletal system and integument: Volenter lost control motor
movements. There is hemiplegia or hemiparesis or hemiparese extremities.
Assess the presence of pressure sores due to physical immobilization.

11

c. Intervensi Keperawatan
NURSING CARE PLAN

NURSING DIAGNOSE
Ineffective cerebral tissue perfusion related
to of bleeding, edema or cerebral vascular
occlusion.

cerebral tissue perfusion ineffective .........

OD:

NOC
Circulation status
Neurologic status
Tissue Prefusion: cerebralAfter care for

Impaired

mental

status,

behavioral

changes,

change

motor

response,

resolved with the expected outcomes:

Pressure systole and diastole within the

expected range
pupillary reaction changes, difficulty No ortostatikhipertensi
swallowing, weakness or paralysis Communication clearly
Demonstrate concentration and orientation
ekstremitas, speech abnormalities
balanced and reactive pupils
free from seizure activity
Ineffective Airway Clearance related to:
Respiratory Status: Ventilation
accumulation of sputum (due to Respiratory Status: Airway patency
weakness, loss of cough reflex) Patient is Aspiration Control After nursing actions for
patients
..............
demonstrate
the
able to maintain a patent airway.
SD:- dyspnoea
OD:
Decreased breath sounds, Orthopneu,

effectiveness of airway evidenced with

sounds were clean, there was no cyanosis

sounds (rales, wheezing), difficulty

and dyspnea (capable of removing sputum,

Abnormalities

of

speaking, Cough, not efekotif or no,

sputum production, Restless, change
frequency and rhythm of breath

NIC
Monitor vital signs
Monitor AGD, pupil size, sharpness, symmetry and

reaction
Monitor the diplopia, blurred vision, headache
Monitor the level of confusion and orientation
Monitor the movement of muscle tone
Monitor pressure and response intrkranial nerologis
Record changes patients in response to stimulus
Monitor fluid status
Keep parameterhemodinamik
Elevate the head of 0-45 depending on konsisi patients
and medical orders

Ensure the needs of oral / tracheal suctioning.

Instruct the patient to rest and breath in Position the

patient to maximize ventilation

Perform chest physiotherapy if necessary
Remove secretions by coughing or

breathing easily, no pursed lips)

Demonstrate a patent airway (the client
does not feel suffocated, breathing rhythm,

suctioning

Auscultation of breath sounds, note the presence of an

expected outcomes:
Demonstrate effective cough and breath

breath

Cyanosis,

additional voice
Give bronchodilators
Monitor hemodynamic status
Provide humidifier Kassa wet Moist NaCl Give

antibiotics:
Adjust fluid intake to optimize the balance.
Monitor the status of respiration and O2
12

respiratory rate within normal range, no

nutritional imbalance less of a body

requirement related to

inadequate nutrient intake nutritional

requirements are met

DS:
Abdominal pain
Vomiting
Seizures stomach
The full flavor of a suddenafter meals
DO:
Diarrhea
Loss of hairexcess
Lack of appetite
Bowel excess
Pale conjunctiva
The pulse is weak

abnormal breath sounds)

Able to identify and prevent the factors that

cause.
O2 Saturation within normal limits
Photos thoracic within normal limits
Nutritional status: Adequacy of nutrient
Nutritional status: food and Fluid Intake
Weight ControlAfter the act of nursingfor
nutrients .... less resolved with expected

outcome:
Serum Albumin, Pre serum albumin,
Hematocrit, Hemoglobin, Total iron binding
capacity, The number of lymphocytes

Maintain adequate hydration to dilute secret

Explain to the patient and family about use of
equipment: O2, Suction, Inhalation

Assess the food allergy

Collaboration with a nutritionist to determine the

amount of calories and nutrients it needs patients

Make sure you eat a diet containing high fiber to prevent

constipation
Teach patients how to make food diaries
Monitor the weight loss and blood sugar
Monitor the environment for eating
Schedule of treatment and no action during a meal
Monitor skin turgor
Monitor dryness, dull hair, total protein , hemoglobin

and hematocrit levels

Monitor nausea and vomiting
Monitor pale , redness , and dryness of the conjunctival

tissue
Monitor intake nutrition
Inform the client and family about the benefits of

nutrition
Collaboration with the doctor about the need for dietary
supplements such as NGT / TPN so that adequate fluid

intake can be maintained .

Set -Fowler position semi-Fowler or higher during
13

decreased motor function of (specify)

secondary to damage to upper motor

neurons
Impaired physical mobility related to:

OD:
- Decreased reaction time
- Difficulty to change position- Changes
in
-

movement(decline

to

run,speed,

difficultystart a short step)

Limitations gross motorand smoothLimitations ROM
Movement with breathShort or tremor
Instability positionduring ADL
The movement is very slow and

Joint Movement: Active

Mobility Level
Self care: ADLs
Transfer PerformanceAfter the act of

disorders,

decreased muscle strength, decreased

muscle coordination, depression, pain,
self-care

increases

persepsiKemampuan

damage

tongue papillae and oval cavity

Exercise therapy: ambulation
Monitoring vital signs sebelm / after practice and see the

patient's response during exercise

Consult with a physical therapy plan of ambulation as

needed
Assist clients to use
cane when walking and prevent against injuries Teach

nursing for impaired physical mobility

resolved ....the outcome criteria:

Client increases in physical activity
Understand the purpose of increasing

mobility
Memverbalisasikan feeling in Improving

ambulation techniques
Assess the patient's ability to mobilize Train the patient

strength and ability to move

Demonstrate the use of

in meeting the needs of ADLs independently according

tool

mobilization (walker)

Self care: Activity of Daily Living (ADLs)

After the act of nursing for .... Top with

self-care deficit outcome criteria:

Client rid of body odor
Stating comfort in their ability to perform
ADLs

the

for

uncoordinated
self-care deficit related to :
Weakness, neuromuscular

feeding Manage pemberan anti- emetic : .....

Encourage a lot of drinking Maintain IV line therapy
Note the presence of edema, hiperemik, hypertonic

patient

or

other

health professionals

about

to ability
Mentor and Help the patient as mobilization and help

meet the needs of ADLs ps.

Provide a tool if the client requires.
Teach patients how to change the position and provide

assistance if needed
Self Care assistane: ADLs
Monitor kemempuan clients for independent self-care.
Monitor the client's needs for assistive devices for

personal hygiene, dressing, ornate, toileting and eating.

Provide assistance to clients as a whole is able to

perform self-care.
Encourage the client to perform daily activities in
14

DO:
inability to bathe, inability to dress,

Can be done with the help of ADLS

inability to eat, inability to toileting

Risk
factors
internal:
Weakness,

visiondecreased, decreased sensationtactile,

decreased
coordinationmuscle

Knowledge: Personal Safety

Safety Behavior: Fall Prevention
Safety Behavior: Fall occurance
Safety Behavior: Physical Injury
Tissue Integrity: Skin and

external:environment

membranes
After the act

Risk of trauma related to

traumatized

of

clients

nursing
with

accordance normal capabilities.

Encourage to perform independently, but give

assistance when clients are not able to do

Teach clients / families to promote independence, to

provide assistance only if the patient is unable to do

Provide day-to-day routine activities according to

ability.
Consider the age of the client if it encourages the

with the physical and cognitive functions of patients and

mucous

not long
expected

outcomes:
Trauma patients free from physical

implementation of day-to-day activities.

Environmental Management safety
Provide a safe environment for patients
Identify the security needs of patients, in accordance
patient's history of previous illness
Avoid hazardous environments (eg moving furniture)
Install side rail bed
Provide a comfortable bed and clean Put light switches

within easy reach of patients.

Restrict visitors
Provide adequate lighting
Encourage families to accompany the patient
Controlling the environment from noise
Move items that can endanger
Provide a description of the patient and their family or

visitors
changes in health status and
the causes of disease

15

LITERATURE
Carpenito, Linda Juall. (2008) Nursing Diagnosis Application to Clinical Practise.
12th ed. Wolters Kluwer: USA
Dewanto, Goerge, dkk. (2009). Panduan Praktis Diagnosis & Tatalaksana Penyakit
Saraf. Jakarta;ECG
Ehrman, Jonathan K. et.al. (2013). Clinical Exercise Physiology. third edition. United
Stated: Human Kinetics
Ganda, Kanchan. (2008). Dentists Guide to Medical Condition, Medication &
Complication. 2th ed. Blackwell Publishing: USA
Hudak, C.M. Gallo, B.M. (1996). Keperawatan Kritis. Pendekatan holistic Edisi VI
volume II. EGC:Jakarta
Muttaqin, Arif (2008). Asuhan Keperawatan Klien dengan Gangguan Sistem
Persyarafan. Salemba Medika: Jakarta.
Susilo, Hendro. (2000). Simposium Stroke, Patofisiologi Dan Penanganan Stroke,
Suatu Pendekatan Baru Millenium III. Bangkalan.

16

ENGLISH IN NURSING PAPER

NEUROLOGY SYSTEM
(CEREBRO VASCULAR ACCIDENT)

BY
THIRD GROUP AJ-A B16
Dewi Agustina Ayu Ningsih

131311123014

Tia Kumala Dewi

131311123015

Anis Candra Dewi

131311123016

Rina Wahyuningsih

131311123018

Wilda Kharisma

131311123019

Stefani Angel K.

131311123020

Yosina Martha I. Tamonob

131311123021

Mubarokah Isnaeni

131311123059

FACULTY OF NURSING
AIRLANGGA UNIVERSITY
SURABAYA
2013

17

TABLE OF CONTENTS
COVER .............................................................................................................. i
TABLE OF CONTENTS ................................................................................... ii
CVA
1. Definition ...............................................................................................
2. Ethiology ................................................................................................
3. Pathophysiology .....................................................................................
4. WOC ......................................................................................................
5. Classification ..........................................................................................
6. Clinical Consideration ............................................................................
7. Diagnostic test ........................................................................................
8. Medical management .............................................................................
9. Complication ..........................................................................................
10. Nursing Process ......................................................................................

1
1
2
4
5
7
8
9
10
11

LITERATURE .................................................................................................... 15

18