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 strokeo Atherosclerosis is the primary causeo 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 stenosiso 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 shouldero Pronation of forearmo Flexion of fingerso Extension of hip and kneeo 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 aphasiao Receptive, sensory or fluent aphasiao Sensory speech problem in which one cannot

understand spoken or written wordo Speech may be fluent but with inappropriate

contento Result of infarction in the temporal lobe

Broca’s aphasiao Expressive, motor or nonfluent aphasiao 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 losto Result of infarction in the frontal lobe

Mixed or global aphasiao Affects both speech comprehension and

speech productiono 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 rateo Give client time to respondo Do not shout and always put client at easeo Repeat simple directions until they are

understoodo Give client practice in repeating words after youo The family should not do all the talking for the

client Provide emotional support and health education to the client and

family