NCP Cerebro Vascular Accident (CVA) / Stroke


Cerebrovascular disease refers to any functional or structural abnormality of the brain caused by a pathological condition of the cerebral vessels or of the entire cerebrovascular system. This pathology either causes hemorrhage from a tear in the vessel wall or impairs the cerebral circulation by a partial or complete occlusion of the vessel lumen with transient or permanent effects. Over 700,000 Americans are affected by a CVA annually. CVA is the third leading cause of death after heart disease and cancer and is the leading cause of disability cost to the nation (approximately $30–$40 billion/year.)

Thrombosis, embolism, and hemorrhage are the primary causes for CVA, with thrombosis being the main cause of both CVAs and transient ischemic attacks (TIAs). The most common vessels involved are the carotid arteries and those of the vertebrobasilar system at the base of the brain. A thrombotic CVA causes a slow evolution of symptoms, usually over several hours, and is “completed” when the condition stabilizes. An embolic CVA occurs when a clot is carried into cerebral circulation and causes a localized cerebral infarct. Hemorrhagic CVA is caused by other conditions such as a ruptured aneurysm, hypertension, arteriovenous (AV) malformations, or other bleeding disorders. Symptoms depend on distribution of the cerebral vessel(s) involved. Ischemia may be (1) transient and resolve within 24 hours, (2) reversible with resolution of symptoms over a period of 1 week (reversible ischemic neurological deficit [RIND]), or (3) progress to cerebral infarction with variable effects and degrees of recovery.


Although the patient may initially be cared for in the intensive care unit (ICU), this phase of care focuses on the step-down or medical unit and subacute/rehabilitation units to community level.


Hypertension: severe

Craniocerebral trauma (acute rehabilitative phase)

Psychosocial aspects of care

Seizure disorders

Total nutritional support: parenteral/enteral feeding

Patient Assessment Database

Collected data are determined by location, severity, and duration of pathology.


May report:
Difficulties with activity due to weakness, loss of sensation, or paralysis (hemiplegia) tires easily; difficulty resting (pain or muscle twitching)

May exhibit:
Altered muscle tone (flaccid or spastic); paralysis (hemiplegia); generalized weakness
Visual disturbances
Altered level of consciousness


May report:
History of postural hypotension, cardiac disease (e.g., myocardial infarction [MI], rheumatic/valvular heart disease, HF, bacterial endocarditis), polycythemia

May exhibit:
Arterial hypertension (common unless CVA is due to embolism or vascular malformation)
Pulse rate may vary (preexisting heart conditions, medications, effect of stroke on vasomotor center)
Dysrhythmias, electrocardiogram (ECG) changes
Bruit in carotid, femoral, or iliac arteries, or abdominal aorta


May report:
Feelings of helplessness, hopelessness

May exhibit:
Emotional liability and inappropriate response to anger, sadness, happiness
Difficulty expressing self


May exhibit:
Change in voiding patterns, e.g., incontinence, anuria
Distended abdomen (overdistended bladder); absent bowel sounds (paralytic ileus)


May report:
Lack of appetite
Nausea/vomiting during acute event (increased ICP)
Loss of sensation in tongue, cheek, and throat; dysphagia
History of diabetes, elevated serum lipids

May exhibit:
Mastication/swallowing problems (palatal and pharyngeal reflex involvement)
Obesity (risk factor)


May report:
Dizziness/syncope (before CVA/transient during TIA)
Severe headache (intracerebral or subarachnoid hemorrhage)
Tingling/numbness/weakness (commonly reported during TIAs, found in varying degrees in other types of stroke); involved side seems “dead”
Visual deficits, e.g., blurred vision, partial loss of vision (monocular blindness), double vision (diplopia), or other disturbances in visual fields
Touch: Sensory loss on contralateral side (opposite side) in extremities and sometimes in ipsilateral side (same side) of face
Disturbance in senses of taste, smell
History of TIA, RIND (predisposing factor for subsequent infarction)

May exhibit:
Mental status/LOC: Coma usually present in the initial stages of hemorrhagic disturbances; consciousness is usually preserved when the etiology is thrombotic in nature; altered behavior (e.g., lethargy, apathy, combativeness); altered cognitive function (e.g., memory, problem-solving, sequencing)
Extremities: Weakness/paralysis (contralateral with all kinds of stroke), unequal hand grasp; diminished deep tendon reflexes (contralateral)
Facial paralysis or paresis (ipsilateral)
Aphasia: Defect or loss of language function may be expressive (difficulty producing speech); receptive (difficulty comprehending speech); or global (combination of the two)
Loss of ability to recognize or appreciate import of visual, auditory, tactile stimuli (agnosia), e.g., altered body image awareness, neglect or denial of contralateral side of body, disturbances in perception
Loss of ability to execute purposeful motor acts despite physical ability and willingness to do so (apraxis)
Pupil size/reaction: Inequality; dilated and fixed pupil on the ipsilateral side (hemorrhage/herniation)
Nuchal rigidity (common in hemorrhagic etiology); seizures (common in hemorrhagic etiology)


May report:
Headache of varying intensity (carotid artery involvement)

May exhibit:
Guarding/distraction behaviors, restlessness, muscle/facial tension


May report:
Smoking (risk factor)

May exhibit:
Inability to swallow/cough/protect airway
Labored and/or irregular respirations
Noisy respirations/rhonchi (aspiration of secretions)


May exhibit:
Motor/sensory: Problems with vision
Changes in perception of body spatial orientation (right CVA)
Difficulty seeing objects on left side (right CVA)
Being unaware of affected side
Inability to recognize familiar objects, colors, words, faces
Diminished response to heat and cold/altered body temperature regulation
Swallowing difficulty, inability to meet own nutritional needs
Impaired judgment, little concern for safety, impatience, lack of insight (right CVA)


May exhibit:
Speech problems, inability to communicate


May report:
Family history of hypertension, strokes; African heritage (risk factor)
Use of oral contraceptives, alcohol abuse (risk factors)

Discharge plan considerations
DRG projected mean length of inpatient stay: 6.4 days
May require medication regimen/therapeutic treatments
Assistance with transportation, shopping, food preparation, self-care, and homemaker/ maintenance tasks
Changes in physical layout of home; transition placement before return to home setting
Refer to section at end of plan for postdischarge considerations.


CT scan (with/without enhancement): Demonstrates structural abnormalities, edema, hematomas, ischemia, and infarctions. Note: May not immediately reveal all changes, e.g., ischemic infarcts are not evident on CT for 8–12 hr; however, intracerebral hemorrhage is immediately apparent; therefore, emergency CT is always done before administering tissue plasminogen activator (t-PA). In addition, patients with TIA commonly have a normal CT scan.
PET scan: Provides data on cerebral metabolism and blood flow changes, especially in ischemic stroke.
MRI: Shows areas of infarction, hemorrhage, AV malformations; and areas of ischemia.
Cerebral angiography: Helps determine specific cause of stroke, e.g., hemorrhage or obstructed artery, pinpoints site of occlusion or rupture. Digital subtraction angiography evaluates patency of cerebral vessels, identifies their position in head and neck, and detects/evaluates lesions and vascular abnormalities.
Lumbar puncture (LP): Pressure is usually normal and CSF is clear in cerebral thrombosis, embolism, and TIA. Pressure elevation and grossly bloody fluid suggest subarachnoid and intracerebral hemorrhage. CSF total protein level may be elevated in cases of thrombosis because of inflammatory process. LP should be performed if septic embolism from bacterial endocarditis is suspected.
Transcranial Doppler ultrasonography: Evaluates the velocity of blood flow through major intracranial vessels; identifies AV disease, e.g., problems with carotid system (blood flow/presence of atherosclerotic plaques).
EEG: Identifies problems based on reduced electrical activity in specific areas of infarction; and can differentiate seizure activity from CVA damage.
X-rays (skull): May show shift of pineal gland to the opposite side from an expanding mass; calcifications of the internal carotid may be visible in cerebral thrombosis; partial calcification of walls of an aneurysm may be noted in subarachnoid hemorrhage.
Laboratory studies to rule out systemic causes: CBC, platelet and clotting studies, VDRL/RPR, erythrocyte sedimentation rate (ESR), chemistries (glucose, sodium).
ECG, chest x-ray, and echocardiography: To rule out cardiac origin as source of embolus (20% of strokes are the result of blood or vegetative emboli associated with valvular disease, dysrhythmias, or endocarditis).


1. Promote adequate cerebral perfusion and oxygenation.
2. Prevent/minimize complications and permanent disabilities.
3. Assist patient to gain independence in ADLs.
4. Support coping process and integration of changes into self-concept.
5. Provide information about disease process/prognosis and treatment/rehabilitation needs.


1. Cerebral function improved, neurological deficits resolving/stabilized.
2. Complications prevented or minimized.
3. ADL needs met by self or with assistance of other(s).
4. Coping with situation in positive manner, planning for the future.
5. Disease process/prognosis and therapeutic regimen understood.
6. Plan in place to meet needs after discharge.