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Clients with Cerebrovascular Disease

Cerebrovascular Accident (CVA)

 Commonly known as stroke or brain attack
 A condition in which neurologic deficits result from decreased blood
flow to localized area of the brain
 Neurologic deficits determined by the area of brain involved, size of
affected area, length of time blood flow is decreased or stopped
 Major loss of blood supply to brain can cause severe disability or death; if
short or small area involved client may not be aware
 Pathophysiology
 Characterized by gradual, rapid onset of neurologic deficits due to
compromised cerebral blood flow
 Blood flow and oxygenation of cerebral neurons decreased or
interrupted; changes occur in 4 – 5 minutes
 Cells swell and cerebral blood vessels swell decreasing blood flow;
vasospasm and increased blood viscosity further impede blood flow
 Penumbra is a central core of dead or dying cells surrounded by
band of minimally perfused cells
 Cells of the penumbra receives marginal blood flow and their
metabolic activities are impaired
 These cells may survive if adequate circulation is re-
 Neurologic deficits occur on opposite side where stroke occurred in
brain: contralateral deficit
 Causes
 Ischemia
 Occurs when the blood supply to a part of the brain is
interrupted or totally occluded
 Commonly due to thrombosis or embolism
• Thrombotic (large vessel) stroke
o The most common cause of ischemic stroke
o Atherosclerosis is the primary cause
o Fatty materials deposit on large vessel walls
(especially at arterial bifurcations) and
eventually these plaques causes stenosis of the
o Blood swirls around the irregular surface of the
plaques causing platelets to adhere and the
vessel becomes obstructed
o These causes infarcts usually affecting the
o Most common type of stroke in people with
• Lacunar (small vessel) stroke
o Endothelium of smaller vessel is primarily
affected due to hypertension
o Leading to arteriosclerosis and stenosis
o Infarcts are usually located in the deeper,
noncortical parts of the brain or in the brainstem
• Embolic stroke
o Occlusion of a cerebral artery by an embolus or
blood clot
o Embolus forms outside the brain, detaches and
travels through the cerebral circulation where it
lodges and causes an obstruction
o Chronic atrial fibrillation is associated with a
high incidence
o Other sources of emboli include tumor, fat,
bacteria and air
o Usually has a sudden onset with immediate
maximum deficit
 Hemorrhage
 Results from rupture of a cerebral vessel causing bleeding
into the brain tissues
 Bleeding results with edema, compression of the brain
contents or spasm of the adjacent blood vessels
 Often secondary to hypertension and most common after age
 Other factors includes ruptured intracranial aneurysms,
trauma, erosion of blood vessels by tumors, arteriovenous
malformations, anticoagulant therapy, blood disorders
 Usually produce extensive residual functional loss and
slowest recovery
 Risk factors
 Hypertension
 Diabetes mellitus
 Atherosclerosis
 Substance abuse including alcohol, nicotine, heroin, amphetamines,
 Obesity, sedentary life-style, hyperlipidemia, atrial fibrillation, cardiac
disease, cigarette smoking, previous transient ischemic attacks
 Women: oral contraceptive use, pregnancy, menopause
 Clinical manifestations
 Stroke manifestations can be correlated with the cause and with the
area of the brain in which perfusion is affected
 Manifestations of thrombotic stroke develop over minutes to
hours to days (slow onset is related to increasing size of the
 Embolic strokes occur suddenly and without warning
 Hemorrhagic stroke occurs rapidly with manifestations
developing over minutes to hours
 General findings unrelated to specific vessel sites includes
headache, vomiting, seizures and changes in mental status
 Early warnings of impending ischemic stroke includes
 Transient hemiparesis
 Loss of speech
 Hemisensory loss
 Specific deficits after stroke
 Motor deficits
 Affects connections involving motor areas of cerebral cortex,
basal ganglia, cerebellum, peripheral nerves
 Produce effects in contralateral side ranging from mild
weakness to severe limitation
 Hemiplegia (paralysis of half of body)
 Hemiparesis (weakness of half of body)
 Apraxia (inability to perform a previously learned skilled task
in the absence of paralysis)
• Able to conceptualize the content of the message to
send to muscles but motor patterns necessary to
convey the impulse cannot be reconstructed
• Instructions do not reach the limb from the brain and
desired action cannot happen
• E.g. dressing and bathing
 Flaccidity (absence of muscle tone or hypotonia)
 Spasticity (increased muscle tone usually with some degree
of weakness)
 Affected arm and leg are initially flaccid and become spastic
in 6 – 8 weeks, causes characteristic body positioning
• When voluntary muscle control is lost, strong flexor
muscles overbalance the extensors
• Imbalance can cause serious contractures
o Adduction of shoulder
o Pronation of forearm
o Flexion of fingers
o Extension of hip and knee
o Foot drop, outward rotation of leg, with
dependent edema
 Muscles of the thorax and abdomen are usually not affected
because they are innervated from both cerebral hemispheres
 Communication disorders
Usually result of stroke affecting dominant hemisphere (left
hemisphere dominant in 95% right-handed persons; 70% left-
handed persons)
 Aphasia (deficit in the ability to communicate or inability to
use or understand language)
• Involve any or all aspects of communication including
speaking, reading, writing and understanding spoken
• Wernicke’s aphasia
o Receptive, sensory or fluent aphasia
o Sensory speech problem in which one cannot
understand spoken or written word
o Speech may be fluent but with inappropriate
o Result of infarction in the temporal lobe
• Broca’s aphasia
o Expressive, motor or nonfluent aphasia
o Motor speech problem in which client
understands what is said but can only respond
verbally in short phases or inability to combine
sounds into appropriate words and syllables
o Ability to write, make signs or speak is lost
o Result of infarction in the frontal lobe
• Mixed or global aphasia
o Affects both speech comprehension and
speech production
o Can be so extensive that neither expressive nor
receptive language abilities are retained
 Dysarthria (imperfect articulation that causes difficulty in
• Client understands language but has difficulty
pronouncing words
• No disturbance is evident in grammar and sentence
construction unlike in aphasia
• Caused by cranial nerve dysfunction resulting with
weakness or paralysis of the muscles of the lips,
tongue and larynx
• Often manifested with difficulty chewing and
swallowing (dysphagia) because of poor muscle
 Sensory-perceptual deficits
 Visual changes
• Parietal and temporal lobe strokes may cause visual
acuity impairment
• Depth perception and visual perception of horizontal
and vertical plane may also be impaired
• Diplopia (double vision) and ptosis (drooping of
eyelids) are also common
 Homonymous hemianopia
• Visual loss in the same half of the visual field of each
• Client may see clearly on one side of the midline but
see nothing on the other side
 Agnosia (inability to recognize one or more subjects that
were previously familiar through the senses)
• May be visual, tactile or auditory
• Client with visual agnosia sees objects but is unable to
recognize or attach meaning to them
• Disorientation is common due to inability to recognize
environmental cues, familiar faces or symbols
 Hemisensory loss (loss of sensation on one side of the body)
• Paresthesia is common
• Proprioception (ability to perceive the relationship of
body parts to the external environment) is impaired
 Unilateral neglect (inability to respond to stimulus on the
contralateral side of the cerebral infarct)
• Attention disorder in which client ignores affected part
of body
• Client cannot integrate or use perceptions from
affected side of body or from environment on affected
 Elimination disorders
 Partial loss of sensation that triggers bladder and bowel
• Urinary frequency, urgency and incontinence are
 Bowel elimination changes result from LOC changes,
immobility, dehydration
 May also relate to cognitive deficits
 Cognitive and behavioral changes
 Ranges from mild confusion to coma
 May result from actual tissue damage from stroke, cerebral
edema, or increased intracranial pressure
 May exhibit
• Emotional lability: laughing or crying inappropriately
• Loss of self-control (i.e. swearing, refusing to
• Decreased tolerance for stress (anger, depression)
• Intellectual changes: memory loss, decreased
attention span, poor judgment, inability to think
 Diagnostic tests
 CT scan without contrast: determine hemorrhage, tumors,
aneurysms, ischemia, edema, tissue necrosis, shifting in intracranial
 Arteriography of cerebral vessels: reveals abnormal vessel
structures, vasospasm, stenosis of arteries
 MRI: detect shifting of brain tissues resulting from hemorrhage or
 Positron emission tomography (PET), single-photon emission
computed tomography (SPECT): examine cerebral blood flow
distribution and metabolic activity of brain
 Management and Nursing care
 Medical management is directed at early diagnosis and early
 Maintain cerebral oxygenation and cerebral blood flow
 Maintain patent airway and turn patient to side if unconscious
 Elevate head and neck should not be flexed
 Hypertension may be reduced with vasodilators and calcium
channel blockers
 Thrombolytic agents are given to dissolve the clot
• Intracerebral hemorrhage should be ruled out first
• Must be given within 3 hours of onset of
• E.g. streptokinase, urokinase and tissue plasminogen
activator (alteplase)
 Antiplatelet and anticoagulants are given to prevent clot
• Heparin and warfarin
• Aspirin, clopidogrel (Plavix), ticlodipine (Ticlid) or
dipyridamole (Persantine)
 Corticosteroids to treat cerebral edema, diuretics to reduce
increased intracranial pressure and anticonvulsants to
prevent seizures
 Hyperthermia is treated immediately
• Temperature elevations lead to increased cerebral
metabolic needs which in turn cause cerebral edema
which can lead to further ischemia
• Antipyretics are used
• Causing the client to shiver should be avoided
 Aspiration precaution is done
• Oral food and fluids are generally withheld for 24-48
• Tube feeding is done
 Prevent valsalva maneuver
• Maneuver increases ICP
• Straining stool, excessive coughing, vomiting, lifting
and use of the arms to change position should be
• Mild laxatives and stool softeners are often prescribed
 Compensate for perceptual difficulties
 For clients with visual deficits
• Approach the client from the unaffected side
• Place articles on the unaffected side
• Teach client to turn the head from side to side to see
entire visual field
• Eye patch over one eye in clients with diplopia is
 Assist and support client
• Prevent injury and falls
• Promote self-care and prevent skin breakdown
 Prevent complications
 Physical therapy to prevent contractures and to improve
muscle strength and coordination
• Encourage bed exercise
• Facilitate ROM and isometric exercises
o Do not force extremities beyond the point of
initiating pain and spasm
o Always support the joint and move the extremity
• Allow client to work on balance and proprioception
 Occupational therapy
• Help client relearn ADLs and to use assistive devices
that promote independence
• Teach client how to use the wheelchair and promote
walking with assitance
 Speech therapy for clients with impaired verbal
• Most aphasic clients regain some speech through
spontaneous recovery or speech therapy
• Speech therapy should be started early
• For aphasic clients
o Speak at a slower rate
o Give client time to respond
o Do not shout and always put client at ease
o Repeat simple directions until they are
o Give client practice in repeating words after you
o The family should not do all the talking for the
 Provide emotional support and health education to the client and