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

Leading to arteriosclerosis and stenosis 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

o o

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 Wernickes 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 Brocas 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

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