Describe the incidence and social impact of cerebrovascular disorders.

Identify the risk factors for cerebrovascular disorders and related measures for prevention.

Compare the various types of cerebrovascular disorders: their causes, clinical manifestations, and medical management.

Relate the principles of nursing management to the care of a patient in the acute stage of an ischemic stroke.

Use the nursing process as a framework for care of a patient recovering from an ischemic stroke.

Use the nursing process as a framework for care of a patient with a cerebral aneurysm.

Identify essential elements for family teaching and preparation for home care of the stroke patient.

Your patient had symptoms of an ischemic stroke approximately 2 hours ago and is undergoing a confirmatory CT scan in 30 minutes. You know t-PA must be administered within 3 hours of the symptoms What actions would you take? What is your rationale for these actions?

Your patient has expressive aphasia following an ischemic stroke.

How would you explain this phenomenon to the patient and family?

Describe appropriate techniques for communicating with a patient with this type of aphasia.

Your patient is admitted with hemorrhagic stroke and exhibits homonymous hemianopsia How would you explain this phenomenon

to the patient and family? How would you modify your care for this

patient? Describe ways that the patient and family

may work together to compensate for this problem

A 50-year-old patient is expected to be discharged to home today following a 5-day stay for an ischemic stroke. He tells you that he lives alone in a small apartment and knows none of his neighbors. He has some residual right-sided weakness. What teaching would be indicated to

prevent another stroke? What resources may be needed to enable

him to go home as scheduled?

“Cerebrovascular disorders” is an umbrella term that refers to any functional abnormality of the central nervous system (CNS) that occurs when the normal blood supply to the brain is disrupted.

Stroke is the primary cerebrovascular disorder in the United States and in the world.

Strokes can be divided into two major categories: ischemic (85%), in which vascular

occlusion and significant hypoperfusion occur

hemorrhagic (15%), in which there is extravasation of blood into the brain

(American Heart Association, 2000).

CLASSIFICATION CAUSES

Ischemic

Hemorrhagic

Large artery thrombosis

Small penetrating artery thrombosis

Hypertension (controlling hypertension, the major risk factor, is the key to preventing stroke)

Cardiovascular disease (cerebral emboli may originate in the heart) • Atrial fibrillation• Coronary artery disease• Heart failure• Left ventricular hypertrophy• Myocardial infarction (especially anterior) • Rheumatic heart disease

High cholesterol levels Obesity Elevated hematocrit (increases the risk of cerebral infarction) Diabetes mellitus (associated with accelerated atherogenesis) Oral contraceptive use (increases risk, especially with

coexisting hypertension, smoking, and high estrogen levels) Smoking Drug abuse (especially cocaine) Excessive alcohol consumption Hock, 1999; Summers et al., 2000.

An ischemic stroke, cerebrovascular accident (CVA), or what is now being termed “brain attack” is a sudden loss of function resulting from disruption of the blood supply to a part of the brain.

Strokes using the time course are commonly classified in the following manner: (1) transient ischemic attack (TIA); (2) reversible ischemic neurologic

deficit; (3) stroke in evolution; and (4) completed stroke (Hock, 1999)

The ischemic cascade begins when cerebral blood flow falls to less than 25 mL/100 g/min.

At this point, neurons can no longer maintain aerobic respiration.

The mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in the pH level.

This switch to the less efficient anaerobic respiration also renders the neuron incapable of producing sufficient quantities of adenosine triphosphate (ATP) to fuel the depolarization processes.

Thus, the membrane pumps that maintain electrolyte balances begin to fail and the cells cease to function.

Early in the cascade, an area of low cerebral blood flow, referred to as the penumbra region, exists around the area of infarction.

The penumbra region is ischemic brain tissue that can be salvaged with timely intervention.

The ischemic cascade threatens cells in the penumbra because membrane depolarization of the cell wall leads to an increase in intracellular calcium and the release of glutamate (Hock, 1999).

The penumbra area can be revitalized by administration of tissue plasminogen activator (t-PA), and the influx of calcium can be limited with the use of calcium channel blockers.

The influx of calcium and the release of glutamate, if continued, activate a number of damaging pathways that result in the destruction of the cell membrane, the release of more calcium and glutamate, vasoconstriction, and the generation of free radicals.

These processes enlarge the area of infarction into the penumbra, extending the stroke.

Each step in the ischemic cascade represents an opportunity for intervention to limit the extent of secondary brain damage caused by a stroke.

Medications that protect the brain from secondary injury are called neuroprotectants (Reed, 2000).

A number of clinical trials are focusing on calcium channel antagonists that block the calcium influx, glutamate antagonists, antioxidants, and other neuroprotectant strategies that will help prevent secondary complications

(NINDS, 1999; Reed, 2000).

An ischemic stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion (which vessels are obstructed), the size of the area of inadequate perfusion, the amount of collateral (secondary or accessory) blood

flow

The patient may present with any of the following signs or symptoms: Numbness or weakness of the face, arm, or leg,

especially on one side of the body Confusion or change in mental status Trouble speaking or understanding speech Visual disturbances Difficulty walking, dizziness, or loss of balance or

coordination Sudden severe headache

A stroke is a lesion of the upper motor neurons and results in loss of voluntary control over motor movements. Because the upper motor neurons decussate (cross), a disturbance of voluntary motor control on one side of the body may reflect damage to the upper motor neurons on the opposite side of the brain.

The most common motor dysfunction Hemiplegia (paralysis of one side of the body) due to a

lesion of the opposite side of the brain. Hemiparesis, or weakness of one side of the body, is

another sign. In the early stage of stroke, the initial clinical features

may be flaccid paralysis and loss of or decrease in the deep tendon reflexes.

When these deep reflexes reappear (usually by 48 hours), increased tone is observed along with spasticity (abnormal increase in muscle tone) of the extremities on the affected side

Other brain functions affected by stroke are language and communication. In fact, stroke is the most common cause of aphasia.

The following are dysfunctions of language and communication: Dysarthria (difficulty in speaking), caused by

paralysis of the muscles responsible for producing speech

Dysphasia or aphasia (defective speech or loss of speech), which can be expressive aphasia, receptive aphasia, or global (mixed) aphasia

Apraxia (inability to perform a previously learned action), as may be seen when a patient picks up a fork and attempts to comb his hair with it

Perception is the ability to interpret sensation. Stroke can result in visual-perceptual dysfunctions, disturbances in visual-spatial relations, and sensory loss.

Visual-perceptual dysfunctions are due to disturbances of the primary sensory pathways between the eye and visual cortex. Homonymous hemianopsia (loss of half of the visual field) may occur from stroke and may be temporary or permanent. The affected side of vision corresponds to the paralyzed side of the body.

Disturbances in visual-spatial relations (perceiving the relation of two or more objects in spatial areas) are frequently seen in patients with right hemispheric damage.

The sensory losses from stroke may take the form of slight impairment of touch or may be more severe, with loss of proprioception (ability to perceive the position and motion of body parts) as well as difficulty in interpreting visual, tactile, and auditory stimuli.

THROMBOLYTIC THERAPY Enhancing Prompt Diagnosis Dosage and Administration Side Effects

Age 18 years or older Clinical diagnosis of stroke with NIH stroke

scale score under 22 Time of onset of stroke known and is 3 hours or less

BP systolic ≤ 185; diastolic ≤ 110 Not a minor stroke or rapidly resolving

stroke No seizure at onset of stroke Not taking warfarin (Coumadin) Prothrombin time ≤ 15 seconds or INR ≤ 1.7 Not receiving heparin during the past 48

hours with elevated partial thromboplastin time

Platelet count ≥ 100,000 Blood glucose level between 50 and 400

mg/dL No acute myocardial infarction No prior intracranial hemorrhage, neoplasm,

arteriovenous malformation, or aneurysm No major surgical procedures within 14 days No stroke or serious head injury within 3

months No gastrointestinal or urinary bleeding

within last 21 days Not lactating or postpartum within last 30 days

The acute phase of an ischemic stroke may last 1 to 3 days, but ongoing monitoring of all body systems is essential as long as the patient requires care.

The patient who has had a stroke is at risk for multiple complications, including deconditioning and other musculoskeletal problems, swallowing difficulties, bowel and bladder dysfunction, inability to perform self-care, and skin break- down.

After the stroke is complete, management focuses on the prompt initiation of rehabilitation for any deficits.

During the acute phase, a neurologic flow sheet is maintained to provide data about the following important measures of the patient’s clinical status: Change in the level of consciousness or

responsiveness as evidenced by movement, resistance to changes of position, and response to stimulation; orientation to time, place, and person

Presence or absence of voluntary or involuntary movements of the extremities; muscle tone; body posture; and position of the head

Stiffness or flaccidity of the neck

Eye opening, comparative size of pupils and pupillary reactions to light, and ocular position

Color of the face and extremities; temperature and moisture of the skin

Quality and rates of pulse and respiration; arterial blood gas values as indicated, body temperature, and arterial pressure

Ability to speak Volume of fluids ingested or administered;

volume of urine excreted each 24 hours Presence of bleeding Maintenance of blood pressure within the

desired parameters

Based on the assessment data, the major nursing diagnoses for a patient with a stroke may include: Impaired physical mobility related to hemiparesis, loss of balance and

coordination, spasticity, and brain injury Acute pain (painful shoulder) related to hemiplegia and disuse Self-care deficits (hygiene, toileting, grooming, and feeding) related to

stroke sequelae Disturbed sensory perception related to altered sensory reception,

transmission, and/or integration Impaired swallowing Incontinence related to flaccid bladder, detrusor instability, confusion, or difficulty in communicating Disturbed thought processes related to brain damage, con- fusion, or inability to follow instructions Impaired verbal communication related to brain damage Risk for impaired skin integrity related to hemiparesis/ hemiplegia, or decreased mobility Interrupted family processes related to catastrophic illness and caregiving burdens Sexual dysfunction related to neurologic deficits or fear of failure

Potential complications include: Decreased cerebral blood flow due to increased ICP Inadequate oxygen delivery to the brainPneumonia

Nursing care has a significant impact on the patient’s recovery.

Often many body systems are impaired as a result of the stroke, and conscientious care and timely interventions can prevent debilitating complications.

During and after the acute phase, nursing interventions focus on the whole person.

In addition to providing physical care, nurses can encourage and foster recovery by listening to patients and asking questions to elicit the meaning of the stroke experience

(Eaves, 2000; Pilkington, 1999).

IMPROVING MOBILITY AND PREVENTINGJOINT DEFORMITIES Preventing Shoulder Adduction Positioning the Hand and Fingers Changing Positions Establishing an Exercise Program Preparing for Ambulation

PREVENTING SHOULDER PAIN ENHANCING SELF-CARE MANAGING SENSORY-PERCEPTUAL

DIFFICULTIES MANAGING DYSPHAGIA

Managing Tube Feedings ATTAINING BOWEL AND BLADDER

CONTROL

IMPROVING THOUGHT PROCESSES IMPROVING COMMUNICATION MAINTAINING SKIN INTEGRITY IMPROVING FAMILY COPING HELPING THE PATIENT COPE

WITH SEXUAL DYSFUNCTION

PROMOTING HOME AND COMMUNITY-BASED CARE Teaching Patients Self-Care Continuing Care

A hemiplegic patient has unilateral paralysis (paralysis on one side).

When control of the voluntary muscles is lost, the strong flexor muscles exert control over the extensors.

The arm tends to adduct (adductor muscles are stronger than abductors) and to rotate internally.

The elbow and the wrist tend to flex, the affected leg tends to rotate externally at the hip joint and flex at the knee, and the foot at the ankle joint supinates and tends toward plantar flexion.

Correct positioning is important to prevent contractures; measures are used to relieve pressure, assist in maintaining good body alignment, and prevent compressive neuropathies, especially of the ulnar and peroneal nerves.

Because flexor muscles are stronger than extensor muscles, a posterior splint applied at night to the affected extremity may prevent flexion and maintain correct positioning during sleep.

Hemorrhagic strokes account for 15% of cerebrovascular disorders and are primarily caused by an intracranial or subarachnoid hemorrhage.

Each year in the United States there are approximately 50,000 intracerebral hemorrhages and 25,000 cases of subarachnoid hemorrhage from ruptured intracranial aneurysm

(Pfohman & Criddle, 2001; Qureshi et al., 2001).

Hemorrhagic strokes are caused by bleeding into the brain tis- sue, the ventricles, or the subarachnoid space.

Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for approximately 80% of hemorrhagic strokes and is primarily caused by uncontrolled hypertension (Qureshi et al., 2001).

Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVMs), intracranial aneurysms, or certain medications (eg, anticoagulants and amphetamines)

(Qureshi et al., 2001).

The pathophysiology of hemorrhagic stroke depends on the cause and type of cerebrovascular disorder.

Symptoms are produced when an aneurysm or AVM enlarges and presses on nearby cranial nerves or brain tissue or, more dramatically, when an aneurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space).

Normal brain metabolism is disrupted by the brain being exposed to blood; by an increase in ICP resulting from the sudden entry of blood into the subarachnoid space, which compresses and injures brain tissue; or by secondary ischemia of the brain resulting from the reduced perfusion pressure and vasospasm that frequently accompany subarachnoid hemorrhage.

Hemorrhagic Stroke INTRACEREBRAL HEMORRHAGE INTRACRANIAL (CEREBRAL) ANEURYSM ARTERIOVENOUS MALFORMATIONS SUBARACHNOID HEMORRHAGE

The patient with a hemorrhagic stroke can present with a wide variety of neurologic deficits, similar to the patient with ischemic stroke.

A comprehensive assessment will reveal the extent of the neurologic deficits.

Many of the same motor, sensory, cranial nerve, cognitive, and other functions that are disrupted following ischemic stroke are altered following a hemorrhagic stroke.

In addition to the neurologic deficits that are similar to ischemic stroke, the patient with an intracranial aneurysm or AVM can have some unique clinical manifestations.

Rupture of an aneurysm or AVM usually produces a sudden, unusually severe headache and often loss of consciousness for a variable period.

There may be pain and rigidity of the back of the neck (nuchal rigidity) and spine due to meningeal irritation. Visual disturbances (visual loss, diplopia, ptosis) occur when the aneurysm is adjacent to the oculomotor nerve.

Tinnitus, dizziness, and hemiparesis may also occur.

Cerebral Hypoxia and Decreased Blood Flow

Vasospasm Increased ICP Systemic Hypertension

Many patients with a primary intracerebral hemorrhage are not treated surgically. However, surgical evacuation is strongly recommended for the patient with a cerebellar hemorrhage if the diameter exceeds 3 cm and the Glasgow Coma Scale score is below 14

Assessment A complete neurologic assessment is performed initially and should include evaluation for the following: Altered level of consciousness Sluggish pupillary reaction Motor and sensory dysfunction Cranial nerve deficits (extraocular eye movements, facial droop, presence of ptosis) Speech difficulties and visual disturbance Headache and nuchal rigidity or other neurologic deficits

Based on the assessment data, the patient’s major nursing diagnoses may include the following: Ineffective cerebral tissue perfusion related to bleeding Disturbed sensory perception related to medically imposed restrictions (aneurysm precautions) Anxiety related to illness and/or medically imposed restrictions (aneurysm precautions)

Based on the assessment data, potential complications that may develop include the following: • Vasospasm• Seizures• Hydrocephalus • Rebleeding

OPTIMIZING CEREBRAL TISSUE PERFUSION Implementing Aneurysm Precautions

MONITORING AND MANAGING POTENTIAL COMPLICATIONS Vasospasm Seizures Hydrocephalus Rebleeding