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-
established
 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
artery
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
cortex
o Most common type of stroke in people with
diabetes
 • 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
50
 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,
cocaine
 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
thrombus)
  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
language
• 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
content
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
speaking)
• 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
control
 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
eye
• 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
side
 Elimination disorders
 Partial loss of sensation that triggers bladder and bowel
elimination
• Urinary frequency, urgency and incontinence are
common
 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
cooperate)
• Decreased tolerance for stress (anger, depression)
 • Intellectual changes: memory loss, decreased
attention span, poor judgment, inability to think
abstractly
 Diagnostic tests
 CT scan without contrast: determine hemorrhage, tumors,
aneurysms, ischemia, edema, tissue necrosis, shifting in intracranial
contents
 Arteriography of cerebral vessels: reveals abnormal vessel
structures, vasospasm, stenosis of arteries
 MRI: detect shifting of brain tissues resulting from hemorrhage or
edema
 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
identification
 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
manifestations
• E.g. streptokinase, urokinase and tissue plasminogen
activator (alteplase)
 Antiplatelet and anticoagulants are given to prevent clot
formation
• 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
hours
 • 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
avoided
• 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
helpful
 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
smoothly
• Allow client to work on balance and proprioception
skills
 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
communication
• 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
understood
o Give client practice in repeating words after you
o The family should not do all the talking for the
client
 Provide emotional support and health education to the client and
family

10/4/96 2100. 86 y.o. male admitted 10/3/96 for L CVA. V/S 99.2 T, 100, 20, 140/76.
Vital signs assessed q 2 hrs, Nursing Assessments every 4 hours, Neuro Checks q 4 hrs.
Alert and oriented x 3. Responds appropriately to verbal stimuli. PERL, 2-3 mm bilateral.
No slurring of speech. At risk for injury related to dysphagia, on soft-thick dysphagia diet,
feeds self with assistance. No JVD. Grips unequal, strong on right, weak on left. Left arm
has limited mobility due to weakness secondary to CVA. At risk for injury (falls) related
to limited mobility, side rails up x 4, call light in reach, patient needs assessed q 2 hours.
Has a saline lock R forearm, flush q 8 hours, patent and intact, site free from redness or
drainage. (If your patient has an infusing IV, make sure you record the fluid and rate in
your assessment). Lung sounds clear in all lung fields. (If your patient is on O2, make sure
you record the O2 rate and delivery system here, along with pulse ox readings). Heart
sounds clear and regular, patient has a history of heart disease and has an implanted
pacemaker (If your patient is on a heart monitor, record the rhythm here - such as normal
sinus rhythm, A-fib ect.). Bowel sounds active in all 4 quads, abd non-tender to palpation.
(If your patient has an abdominal incision, record the condition of it here). Last BM 17:15
today, brown, soft formed. Has a history of constipation. Urine clear yellow. Uses urinal,
has occasional episodes of incontinence. Peri-area skin currently clear and intact, with no
areas of redness. At risk for skin breakdown related to limited mobility and incontinence,
at risk for pneumostatic pneumonia due to limited mobility, TCDB q 2 hr, up in chair TID
with assist of 2 people. Limited mobility L leg, weakness due to CVA. At risk of DVT
due to immobility, TEDS on bilateral, Active ROM Right leg, Passive ROM left leg, q 4
hours. Calf pumps x 5 bilateral encouraged every 2 hours while awake. Homans sign
negative bilateral. Pedal pulses palpable bilateral. Feet cool, dry, intact, with thick toenails
bilateral. Capillary refill toes < 2 Sec. Shift Intake 850, Output 750 cc Fluid balance
Positive 100 cc for this shift.