Department of Medical Nursing, Faculty of Nursing, Chiang Mai University

Teaching Material for 561314: Adult Nursing II

For International Program Nursing Students

Semester I Academic Year 2007

Principle of Holistic of Nursing Care for Adult with Common Problem in the

Patients with Neurological System and Family

Dr. Pratoom Soiwong

Assist. Prof. Dr. Nitaya Pinyokham

Objectives: At the end of this session the students would be able to

1. Identify the causes and pathophysiology of common problems in

neurological system

2. Pinpoint the nursing assessment of patients with common problems in

neurological system

3. Identify nursing diagnosis of patients with common problems in neurological

system

4. Specify nursing activities and reasons of each common problem in

patients with neurological system

CONTENT

1. Cognitive system

Cognition and memory, the ability to concentrate and attend, elaboration of

thought are controlled by prefrontal area. The "Gatekeeper"; (judgment, inhibition),

personality and emotional traits.

A cognitive system response for the control and integration of the body’s

many activities, including memory, using and understanding language, and intellectual

function. Common problems in the cognitive system include alteration of

consciousness, seizure, alteration cognitive function and thought process, impaired

verbal communication. The details will be described as follows:

1.1 Unconsciousness

Consciousness involves two aspects: arousal and content. The arousal

component of consciousness refers to a state of wakefulness dependent of the activity of

the reticular activating system (RAS), a network of nerve fibers and cell bodies that is

located in the reticular formation in the central part of brainstem and has neural

connections to many parts of the nervous system. An intact RAS can maintain a state of

wakefulness, even in the absence of a function cortex. The content component of

consciousness refers to the ability to reason, think, and feel and to react to stimuli with

purpose and awareness. These activities are mediated by the cerebral hemispheres,

commonly called the higher centers. Intellect and emotional function are also controlled

by these centers. Interruption of impulses from the RAS or alteration of the functioning

of the cerebral hemispheres can cause unconsciousness. Any condition that markedly

alters the function of the hemispheres or that depresses or destroys the upper brainstem

events can result in unconsciousness.

Unconsciousness can be brief, lasting for a few seconds, to an hour or so, or

sustained, lasting for a few hours or longer. To produce unconsciousness, a disorder

must (1) disrupt the ascending reticular activating system, which extends the length of

the brainstem and up into the thalamus; (2) significantly disrupt the function of both

cerebral hemispheres; or (3) metabolically depress overall brain function, such as drug

overdose. Three kinds of disorder produce sustained unconsciousness.

1.1.1 Structural causes of unconsciousness include brain tumors, head

trauma, and cerebral hemorrhage including epidural and subdural hematomas. These

types of lesions destroy the reticular activating system or place pressure on brain tissues.

1.1.2. Metabolic cause. Metabolic disorder and diffuse lesions that impair the

cerebrum and arousal functions by reducing the supply of oxygen or allowing waste

products to accumulate. There are many metabolic cause of coma. The term metabolic is

used to describe problems that do not originate in the brain but begin in another system

and eventually cause a disorder in the nervous system. Hypoxia is a common cause of

metabolic brain disorder Blood loss, height above sea level, or carbon monoxide

poisoning may deprive the brain of oxygen. Ischemia, inadequate tissue levels of

oxygen, may occur with cardiac disorders in which cardiac output is decreased, such as

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cardiac arrest or even fainting. Disorder of the liver, lungs, and kidney may produce

coma because of the accumulation of metabolic wasted product. Finally, there are many

agents that affect the metabolism of neurons, They included toxins; hypoglycemia;

fever; infections, such as encephalitis; and fluid electrolyte, or acid-base imbalance.

1.1.3 Psychogenic causes, in which case the patients looks comatose but his

or her self-awareness is usually intact, as is in catanotnia and hysteria.

Pathophysiology

Only physiologic causes of coma are described here.

Masses within the brain alter the function of the brain in many ways. Masses

or lesions, whether they are growing tumors, edema, or bleeding, place pressure on the

brain. Because the brain is enclosed in the cranium, there is no space with in the skull

for the expending brain. Pressure slows blood and cerebrospinal fluid flow in than out to

the brain and reduces cerebral function. The level of consciousness and ability to move

purposefully are affected. When pressure reaches the diencephalons or brainstem, vital

function such as heart rhythm and respiration are affected The patients’ outcome

depends on the location of the mass, the size and rate of enlargement, and the amount of

edema and necrosis in brain tissues. A blow to the head can cause brain lacerations or

contusions because the brain is hit and strikes the bony cranium. In addition, the brain

can suffer diffuse injury as tissues are torn and sheared.

Metabolic disorders producing coma do so through various mechanisms,

Infections for the brain, such as encephalitis, cause inflammations of the meninges and

brain tissues. Hyperglycemia and hypoglycemia starve the cells of needed glucose for

metabolism. Overdoses of sedative drugs suppress the control nervous system (CNS),

special the center for breathing. Failure of the liver, kidney, and lungs allows

metabolic waste to accumulate; this wasted poisons the neurons.

Clinical manifestations

1. Changing in level of consciousness. From the normal alert state,

consciousness deteriorates in stage, with each stage having its own definition.

Fully consciousness. A patient who is awake, alert, and fully oriented to self,

other, place, and time is considered to be fully consciousness.

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Confusion is the loss of the ability to think rapidly and clearly; an impairment

in judgment and decision-making.

Lethargy or drowsiness is restriction in activity related to a decreased level of

alertness. The patient is easily aroused by speech or touch by returns to lying quietly or

sleep when not stimulated.

Stupor is a condition of deep sleep or unresponsiveness from which a patient

may be aroused only with forceful or shouting stimulation. Patients response by

withdrawing from or capture at the source of pain.

Semicoma is condition of unresponsiveness from which a patient may be

aroused only with painful stimulation, such as placing a pencil or pen across the

fingernail bed and applying firm pressure produces a constant noxious stimulus and a

minimal amount to tissue trauma, sternal rub, or compression, supraorbital pressure,

pinching various parts of the extremity or trunk.

Coma is condition of no motor or verbal response to the environment or any

stimuli, even deep pain or suctioning or other noxious (irritating, hurtful) stimuli.

2. Breathing pattern. Disorder causing coma and decreased levels of

consciousness commonly caused respiratory abnormal. Rapidly expanding lesions in the

cerebrum, brainstem, or cerebellum may lead to compression of the pons and medulla,

which leads to respiratory failure.

3. Eye movement and pupillary changes. Eye movements in the comatose

patient are uncoordinated, and pupillary response is abnormal.

4. Motor response. The patient may exhibit some abnormal motor movement

and postures. When the intracranial pressure is increased at the cortical level, abnormal

flexion (decorticate) posturing is seen as flexion of the arms, wrists, and finger with the

arm adducted at the shoulder. The legs are fully extended and internally rotated. As the

pressure increase to the level of the upper pons, abnormal extension (decereration)

posturing occurs. In this posture, the legs are extended abnormally, similar to decorticate

posturing. The arm are extended stiff and adducted and the hands are hyperpronated.

Decerebrate posturing is a serious sign than decorticate.

5. Change in vital sign. Some changes related directly to cause of the

unconsciousness. Some conditions causing coma produce autonomic nervous system

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instability because impairment of the hypothalamus. These disorders may cause a wide

variations in blood pressure, pulse, and body temperature.

Nursing management

Nursing diagnoses for patient with unconsciousness

Altered tissue perfusion related to cerebral tissue swelling (as manifested

by mental state, intracranial pressure > 20 mmHg, decreased cerebral blood flow or

oximetry).

Ineffective airway clearance related to unconsciousness and inability to

mobilized secretions (as manifested by ineffective cough, inability to clear secretion,

crackles on auscultation, thick secretions).

Risk for aspiration related to lack of effective airway clearance and loss

of gag reflex.

Risk for impaired skin integrity related to nutrition deficit, immobility,

self-care deficit.

Altered nutrition: less than body requirements related to inability to eat

or swallow.

Risk for injury related to unconsciousness and inability to immobilize.

Risk for fluid volume deficit

Risk for contractures related to disuse.

High risk fro impaired skin integrity related to fecal incontinence.

Risk of infection related to immobility, invasive monitoring devices and

lines, and compromised immune system.

Altered family processes related to uncertain future or coming death of

a family member.

Nursing Interventions

Initial

Ensure patent airway.

Administration oxygen via nasal canular or non-rebreather mask.

Establish IV access with one large-bore catheter and normal saline.

Administration IV naloxone if narcotic overdose suspected.

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Administration Thiamine to malnourished or known alcoholic patient

to prevent Wernicken’s encephalopathy.

Administration one vial 50 % dextrose if blood glucose < 60 mg/dl

Elevate head of bed or position on side to prevent aspiration (unless

trauma involved).

Ongoing monitoring

Monitoring vital signs, level of consciousness, oxygen saturation,

cardiac rhythm, Glasgow Coma Score, pupil size and reactivity, respiratory status.

Anticipate need for intubation if gag is absent.

Anticipate gastric lavage if drug overdose in suspected.

1.2 Seizure disorder and epilepsy

A seizure is an involuntary behavior that occurs abnormally and is generally

associated with epilepsy, but can come from other sources. Epileptic seizures are

categorized by the location in the brain from which they originate and the two main

categories of epileptic seizures are "partial" and "generalized." Partial seizures begin in a

discreet area of the brain. A simple partial seizure causes no change in consciousness.

The patient may have weakness, numbness and unusual smells or tastes. Sometimes,

there is twitching of the muscles or limbs, head turning from side to side, paralysis, sight

changes or vertigo.

Complex partial seizures occur in the temporal lobe and consciousness is altered.

The patient usually has a change in their ability to interact with their environment and

may exhibit automatic behaviors such as walking in a circle, sitting and standing, or

smacking their lips. Often, odd thoughts occur to the patient, such as a feeling of déjà vu

or uncontrollable laughing or odd smells.

Generalized seizures take place in larger areas of the brain and there are many

sub-types. Grand mal seizures include specific movements of the arms and legs or face

and may occur with a loss of consciousness. Sometimes there is yelling or crying before

the person faints. They may also experience an aura, which is an unusual feeling that

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often warns the patient that seizure is coming on. The patient abruptly falls and begins to

jerk and may become incontinent or drool or bite their tongue. This type of seizure

usually lasts between 5 and 20 minutes and the patient may awake in a confused state or

may sleep for a while. Sometimes, the patient has prolonged weakness after the event.

Petit mal seizures include a brief loss of consciousness but there is not associated

motor dysfunction and there is no aura prior to the seizure. Sometimes it just seems that

the person is briefly stopping what they were doing, staring for a few seconds, and then

continuing with their activity. The patient does not even have any memory of the event

(http://www.wisegeek.com/how-is-epilepsy-treated.htm).

Pathophysiology: Seizures are paroxysmal manifestations of the electrical

properties of the cerebral cortex. A seizure results when a sudden imbalance occurs

between the excitatory and inhibitory forces within the network of cortical neurons in

favor of a sudden-onset net excitation. If the affected cortical network is in the visual

cortex, the clinical manifestations are visual phenomena. Other affected areas of primary

cortex give rise to sensory, gustatory, or motor manifestations. The pathophysiology of

partial-onset seizures differs from the mechanisms underlying generalized-onset

seizures. Overall, cellular excitability is increased, but the mechanisms of

synchronization appear to substantially differ and are therefore discussed separately.

Complications

Status epilepticus is a state in which seizures recur in rapid succession

and the patient does not regain consciousness or normal function between seizures. It is

the most serious complication of epilepsy and a neurologic emergency. Status

epilepticus can involve any type of seizures. During repeated seizures, the brain use

more energy than can be supplied. Neuron become exhausted and cease to function.

Permanent brain damage may result.

Tonic-clonic status epilepticus is the most dangerous because it can

cause ventilatory and systemic acidosis, all of which can be fatal. Another complication

of epilepsy is severe injury and even death from trauma suffered during seizure. Patient

who lose consciousness during a seizure are at greatest risk. Death can result from head

injury incurred in a fall, from sinking in the bathtub, or from severe burns.

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Nursing management

Nursing diagnosis

Nursing diagnoses for the patient with seizure may include, but are not

limited to, these are presented as follow:

1. Ineffective breathing related to neuromuscular impairment secondary to

prolonged tonic phase of seizure or during postictal (as manifested by abnormal

respiratory rate, rhythm, or depth).

2. Ineffective airway clearance related to tracheobronchial obstruction (as

manifested by ineffective cough, inability to remove secretions, absence or abnormal

breath sound).

3. Risk for injury related to seizure activity and subsequent impaired physical

mobility secondary to postictal weakness or paralysis.

4. Ineffective individual coping related to perceived loss of control and denial

of diagnosis as manifested by verbalizations about not having epilepsy, lack of truth-

telling regarding seizure frequency, noncompliant behavior.

5. Self-esteem disturbance related to diagnosis of epilepsy as manifested by

anxiety, fear, social isolation, depression, role disturbance, altered family dynamics.

6. Ineffective management of therapeutic regimen related to lack of

knowledge about management of epilepsy as manifested by verbalization of lack of

knowledge, inaccurate perception of health status, noncompliance with prescribed health

behavior.

Nursing interventions

Nursing intervention for a hospitalized patient or a patient who has had

seizures as a results of metabolic factors should focus on observation and treatment of

the seizure, education, and psycholosocial intervention.

When a seizure occurs, the nurse should carefully observe and record

details of the event because the diagnosis and subsequent treatment depend on the

seizure description.

Assessment of the postictal period should be include a detailed

description of the level of consciousness, vital signs, memory loss, muscle soreness,

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speech disorder, weakness or paralysis, sleep period, and the duration of each sign or

symptoms.

During the seizure, it is important to maintain a patent airway. This may

involve supporting and protecting the head, turning the patient to the side, loosening

constrictive clothing, suctioning as needed, or easing the patient to the floor if sitting in

a chair. The patient should not be restrained and no objects should be placed in the

mouth. After the seizure the patient may require, suctioning and oxygen.

A seizure can be a frightening experience for the patient and for other

who may witness. The nurse should assess the level of their understanding and provide

information about how and why the event occurred.

Health promotion.

Many case of seizure can be prevented by promotion of generally safety

measures, such as the wearing of helmets in situations involving risk of health injury.

The patient with epilepsy should

The patient with epilepsy should practice good general health habits,

including maintaining a proper diet, getting adequate rest, and exercising.

The patients should be helped to identify events or situations that

precipitate the seizures and should be given suggestions for avoiding them or handling

them better.

Excessive alcohol intake, fatigue, and loss of sleep should be avoid, and

the patient should be helped to handle stress constructively.

1.3 Impaired verbal communication

Aphasia is a defect in using and interpreting the symbols of language.

Aphasia may involve any or all aspects of language use, such as speaking, reading,

writing, and understanding spoken language. There are about 50 types of aphasia, only a

few of the most common are described here. Aphasia may be categorized as follows:

1.4.1 Sensory (receptive aphasia), which affects speech

comprehension or understanding. Receptive aphasia is also called Wenicke’s aphasia.

Patients with fluent aphasia (Wernicke’s) have speech that is well articulated and

grammatically corrects but lacks content. The cell that function in understanding

language are found in the group of cells called Wernicke’s area, which is located at the

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temporal lobe. Damage to these temporal lobe area leaves the person unable to

understand spoken or written language or to recognize music or other environmental

sounds.

1.4.2 Motor (expressive aphasia or executive aphasia), which affects

speech production. Expressive aphasia is also called Braoca’s aphasia. Patients with

nonfluent aphasia (Broca’s) produce very little speech, and what words are spoken are

completely slowly, with great effort and poor articulation. Broca’s area lies anterior to

the primary motor cortex and superior to the lateral sulcus. These cells coordinate the

complex muscular activity of mouth, tongue, and larynx, which makes expressive

(motor) speech possible. Damage to this area leaves the patients unable to speak clearly.

1.4.3 Global, which affects both. Patients with global aphasia typically

repeat the same sounds they hear and have poor understand. Global aphasia (total

aphasia) is so extensive that neither expressive nor receptive language abilities are

retained.

Aphasia may occur if blood supply to a patient’s speech center is cut off.

Aphasia is associated with hemiplegia involving the dominant hemisphere. The speech

center of a right-handed patient is usually located in the left cerebral hemisphere. The

speech center for a left-handed patient may be in the brain’s right or left side. Thus,

right-handed patient with right-sided hemiplegia usually has aphasia, because the speech

center is in the damaged left hemiplegia. Most people have left-sided speech dominance.

Nursing management

Nursing diagnosis

Impaired verbal communication related to residual aphasia as manifested by

refusal or inability to speak, word-finding, use of inappropriate words, inability to

follow verbal direction.

Nursing intervention

Assess exact communication deficits and strengths to determine type of

communication problem and plan appropriate interventions.

Intervene as appropriate.

Nursing intervention for patient with motor aphasia

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A picture board may be helpful.

Use every encounter to encourage and support communication, yet be

careful not to cause fatigues. In general, when working with an aphasia patient, practice

expanded speech (a slower rate) and self-pacing (give the patient time to respond).

Listen and watch carefully when an aphasia patient attempts to

communicate. Try hard to understand. This reduces the patients’ frustration. Anticipate

an aphasia patient’s needs, to reduce feelings of communication helplessness.

Use short, simple questions that show up “yes” and “no” answer, speak

slowly and allow adequate time for response to avoid overwhelming patient with verbal

stimuli

Use gesture to support verbal cues.

Speak slowly and use visual aids such as flash cards to avoid frustration

and anger from worsening problem.

When a patient cannot identify objects by name, give practice in

receiving word images. For example, point to an object and clearly state its name, such

as hand, glass. Then have the patient repeat the word.

When a patient has difficulty with verbal expression, give practice in

repeating words after you. Begin with simple words and then progress to simple

sentences, such as Yes. No. Here is breakfast.

Nursing intervention for patient with sensory aphasia

When a patient cannot understand spoken words, repeat simple

directions until they are understood, such as drink this juice. Do not shout. The patient

can hear. Speak slowly and clearly. Talk without pressing for a response. Also use

nonberbal methods of communication.

When taking to a patient with receptive difficulty, stand within six feet

and face the patient directly. Gradually shift topics of conversation and say when you

are going to change the topic.

2. Motor system

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Motor system controls initiation of movement on opposite side of body,

facilitates proximal muscle activity, including activity for posture and gait, and

spontaneous movement and coordination. Only upper motor and lower motor neuron

lesion and Parkinson’s disease are described here.

2.1 Upper motor and lower motor neuron lesion. Upper motor neurons

influence skeletal muscle movement. Upper motor neurons originate in the cerebral

cortex and projected downward. The corticobulbar tract ends in the brainstem, and the

corticospinal tract descends into the spinal cord. Upper motor neurons lesion generally

cause weakness or paralysis, disuse atrophy, hyperreflexia, and increase muscle tone

(spasticity). On the other hand, lower motor neurons (LMNs) are the final common

pathway through which descending motor tracts influence skeletal muscle, the effectors

organ for movement. The cell bodies of LMNs, which send axons to innervate the

skeletal muscles of the arm, trunk, and legs, are located in the anterior horn of the

corresponding segments of the spinal cord such as cervical segment contain LMNs for

the arms. LMNs for skeletal muscles of the eyes, face, mouth, and throat are located in

the corresponding segment of brainstem. There cell bodies and their axons make up the

somatic more components of the cranial nerves. LMN lesions generally cause weakness

or paralysis, denervation atrophy, hyporeflexia or areflexian, and decreased muscle tone

(flaccidity).

2.2 Parkinson’s disease. Parkinsonism is a syndrome that consists of a

slowing down in the initiation and completing of movement (bradykinesia), increase

muscle tone (rigidity), tremor, and impaired postural reflexes. There are many causes of

Parkinsonism consisting of; encephalitis; intoxication, such as carbon monoxide and

manganese, drug such as reserpine, aldomet, haldol, thorazine. Many of manifestrations

of Parkinson’s disease are due to the side effects of drugs, particularly prolonged

levodopa (L-dopa) therapy.

The pathology of Parkinson’s disease is associated with the degeneration of

the dopamine-producing neurons in the substantial nigra of the midbrain. Damage or

loss of the dopamine-producing cells of the substantial nigra in the midbrain leads to

reduction of dopamine that influences the initiation, pronunciation, and completing of

movement and regulates unconscious autonomic movement. In case of drug-induced

Parkinsonism the dopamine receptor in the brain are blocked. It is hypothesized that

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there is normally a balance between acetylcholine (ACh) and dopamine (DA) in a basal

ganglia. Any shift in the balance of activity (an increase in ACh or a decrease in DA)

seems to lead to parkinsonism-like syndromes. Dopamine is a neurotransmitter that is

essential for normal functioning of the extrapyramidal motor system, including control

of posture, support, and voluntary motion. In Parkinson’s disease the level of DA-

synthesizing enzymes and metabolites are reduced, and postmortem analysis of cress

section of the mid brain show loss of the normal melain picment in the substain

midbrain shows loss of neurons. In addition deficient amounts of gamma-aminoburyic

acid)(GABA), serotonin, and norepinephrine have been found in basal ganglia and in the

substantial nigra.

Clinical manifestations

Because there is no specific diagnosis test for Parkinson’s disease, the

diagnosis is based on solely on the history and the clinical features. A firm diagnosis can

be made only when there are at least two of the three characteristic signs of the classic

triad: tremor, rigidity, and bradykinesia. The ultimate confirm of Parkinson’s disease is a

positive response to antiparkinsonian medication.

Tremor. Parkinosonian tremor is more prominent at rest and is aggravated by

emotional stress or increased concentration. The hand tremor is dexreibed as “pillin

rolling” because the thumb and forefinger apperar to move in a rotary fashion as if

rolling a pill, coin, or other small object. Tremor can involve the diaphragm, tongue,

lips, and jaw but rarely caused shaking of the head.

Rigidity is increased resistance to passive motion when the limbs are moved

through their range of motion. Parkinsonian rigidity is typified by a jerky quality, as if

there were intermittent catches in the movement of a cogwheel, when the joint is moved.

The rigidity is caused by sustained muscle contraction and consequently elicits a

compliant of muscle soreness; feeling tried and ache or pain in the head, upper body,

spine, or legs. Another consequence of rigidity is slowness of movement, because it

inhibits the alternating of contraction and relaxation in opposing muscle groups.

Bradykinesis (slow and retarded movement) is particularly evident in the loss

of automatic movements, which is secondary to the physical and chemical alteration of

the basaly ganglia. In the unaffected patient, autonomic movements are involuntary and

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occur subconsciously; these includes blinking of the eyelids, swinging of the arms

while walking, swallowing of saliva, self-expression with facial and hand movements,

and minor movement of postural adjustment. The characteristic of a person with

Parkinson’s disease are the stooped posture, masked facies (“deadpan” expression), leak

of saliva, and drag feet. There is difficulty in initiating movement.

Swallowing may become very difficulty (dysphagia) in severe cause, leading

to malnutrition or aspiration. Generally weaken may lead to pneumonia, urinary tract

infection, and skin breakdown.

Mobility is greatly decreased. The gait slows and turning is especially

difficult. The purposed is that of the old man image, with the head and trunk bent

forward and the legs constantly flexed. The lack of mobility may lead to constipation,

ankle edema, and more seriously, contractures.

Orthostatic hypotension may occur and, along with the loss of postural

reflexes, may result in falls or other injury.

Seborrhea, excessive sweating, conjunctivitis, insomnia, incontinence, and

depression may also occur.

Dementia occurs in up to 40 % of patients with Parkinson’s disease.

Nursing management

Goals

The patient with Parkinson’s disease will maximize neurologic function,

maintain independence in activities of daily living for as long as possible, and optimize

psychosocial well-being.

Nursing diagnoses

Impaired physical mobility related to rigidity, bradykinesia, and

akinesia as manifested by difficulty in initiation of volitional movement.

Self-care deficits related to parkinsonian symptoms.

Impaired verbal communication related to dysarthia and tremor or

bradykinesia as manifested by decreased amount of communication, slow and slurred

speech, inability to move facial muscles, decreased tongue mobility, inability to write.

Constipation related to weakness of abdominal and perineal muscles,

lack of excise, and side effect of medication.

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Altered nutrition: less than body requirements related to dysphagia

Deficient diversional activity relate to inability to perform usual

recreational activities

Sleep pattern disturbance related to medication side effects, anxiety,

rigidity, and muscle discomfort.

Nursing interventions.

Assist with ambulation. Perform activity range-of-motion exercise to

all extremities. Evaluation tremor in relation to medication. Instructions for patients who

tend to “freeze” while walking include these; think consciously about stepping over

imagery lines on the floor, drop rice kernels (most important part) and step over them,

rock from side to side to initiate leg movement.

Encourage activities of daily living within limit of mobility. Arrange

patient’s room for facilitate optimal self-care. Offer emotional support to encourage

patient’s effort in coping with a chronic degenerative disease.

Allow sufficient time for communication. Encourage deep breaths

before speaking. Consult speech therapist. Provide alternative communication, massage

patient’s facial and neck muscles.

Increase fluid intake to 3000 ml/day. Increase fiber in diet every meal.

Give stool softeners, laxatives, suppositories.

Carefully monitors swallowing ability during medication

administration and mealtime. Provide sofl-solid and thick-liquid diet. Massage patient’s

facial and neck muscles before meals. Maintain patient in upright position for all meals.

Consult speech therapist and dietician in order to provide specific plan to improve

swallowing and intake. Maintain caloric counts and weekly weights. Suction to remove

pooled secretion and prevent choking and aspiration.

3. Sensory system

Sensory system registers body sensations, such as temperature, touch,

pressure, pain, from opposite side of body, registers visual images, registers auditory

inputs, integrates somatic and special sensory inputs, integrates visual and auditory

inputs for language comprehensive, integrates past experience, and control higher-order

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process such as judgment, insight, reasoning, problem solving, planning. Sensory

system dysfunctions related to unilateral neglect and sensory-perceptual alteration are

described in this section.

3.1 Unilateral neglect is pattern of lack of awareness of body part, such as

paralyzed arms or legs. The patient behaves as if the part is simply not there. He or she

does not look for the paralyzed limb when moving about. It is caused by damage to

portions of the nondominat cerebral hemisphere (usually the right hemisphere).

Obviously unilateral neglect creates increase risk for injury. It is possible to relearn to

look for and to move the limb.

Nursing diagnosis

Unilateral neglect related to sensory loss on one side of body

Nursing intervention

Assess and document amount of visual field impairment to determine

extent of problem and plan appropriate interventions

Teaching patient to turn head and scan environment

Initially, approach patient on unaffected side. Adapt the environment

to the deficit by focusing on the patient unaffected side. Keep personal care items

and a bedside chair and commode on the unaffected side. Position patient’s extremities

in correct alignment. Gradually, approach patient on affected side. Move the personal

items, bedside chair, and commode to the affected side. Assist patient form the affected

side. Have the patient clean the affected side first.

Teach family and patient to stimulate paralyzed limbs using touch and

warm and cold stimuli to promote regeneration with the whole body.

Encourage patients to use cue cards and mirrors as reminder to survey

his or her whole body for position, cleanliness, and appropriate dress.

3.2 Sensory-perceptual alteration. Homonymous hemianopsia (blindness in

the same half of each visual field) is an common problem after a stroke. Ischemia of

visual pathways can lead to some bizarre changes in vision. A thorough assessment of

visual field is usually needed for this diagnosis. Sometimes you will notice that the

patient fails to notice you on one side of the bed or the other or fails to eat food from one

side of the food tray. Use that cue to do a compete visual field assessment. In the clinical

situation, it is often difficulty to distinguish between a visual field cut and a neglect

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syndrome. Both problems may occur with stroke affecting either the right side or the left

side of the brain.

Nursing diagnosis

Unilateral neglect related to visual field cut

Risk for injury

Nursing interventions

Approach the patient from the side that is not visually impaired.

Position the call light and phone on that side.

If possible, position the bed so that the side that is not visually

impaired is toward the center to the room.

Teach patient to position the head to increase the visual field. Provide

visual stimulation to promote use of full range of visual capabilities

Warn hemiplegic patient to be very careful when crossing streets

because the may not see traffic approaching form the affected side.

Place object in patient’s field of vision; give physical and verbal cues

to aid in path finding to compensate for visual field deficits.

An eye patch over one eye in patient with diplopia removes the second

image and assist vision.

If corneal reflex is absent, protect affected eye to prevent injury.

A patients with perceptual defects benefits from simplicity. A busy or

noisy environment is difficult to interpret and may increase confusion. Reduced

complexity and the need for decision making. For example, obtain clothing that is

simple designed and easy to put on. Give brief, simple direction. Prepare food trays with

a minimum number of utensils, dishes, and foods.

Nursing management for the patient with a stroke and family

Stroke (also referred to Cerebrovasuclar accident [CVA] or “brain attack” is

a broad term that includes a variety of disorder that influence blood flow to the brain and

result in neurological deficits. Stroke occurs when there is ischemia to a part of the brain

or hemorrhage into the brain that result in brain cell death. Regardless of the cause, the

damaged brain no longer performs cognitive, sensory, motor, or emotional functions.

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The severity of the loss of function varies according to the location and extent to the

brain involved.

Risk factors for strokes

Risk factors associated with stroke can be divided into nonmodifiable and

potential modifiable.

Nonmodifiable risk factors include age, race, and heredity. The incident

of stroke is higher in man than women. The increases of stroke increases with age until

age 75. African American experience a higher incidence of stroke, which is associated

with an increased incidence of hypertension, obesity, and diabetes mellitus. Persons with

a family history of stroke or transient ischemic attacks (TIAs) are also at higher risk for

stroke.

Modifiable risk factors are hypertension, cardiac disease, DM, sickle

cell disease, and certain lifestyle habits, such as cigarette smoking, a diet heigh in fat,

and heavy alcohol consumption. Approximately 25 % of strokes in patients over 80

years old are due to atrial fibrillation. Control of hypertension is the most significant

contributor to the prevention of stroke.

Type of stroke

Strokes are classified as ischemic stroke or hemorrhagic stroke based on their

underlying pathology.

1. Ischemic stroke result from a decreased blood flow to the brain secondary

to partial or complete occlusion of an artery. They occur much more frequently than

hemorrhagic strokes. The most common type of ischemic stroke are thrombotic and

embolic.

1.1 Thrombotic stroke is the formation of a blood clot or coagulation that

results in the narrowing of the lumen of a blood vessel with eventual occlusion. It is the

most common cause of cerebral infarction. Two thirds of the strokes caused by

thrombosis are associated with hypertension or diabetes mellitus, both of which

accelerate the atherosclerotic process. Additional risk factors associated with thrombotic

strokes include oral contraceptives, coagulating disorders, polycythemia vera, arteritis,

chronic hypoxia, and dehydration. Thrombotic strokes may be preceded by a TIA, which

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is characterized by brief episodes of neurologic manifestations, which clear completely

in less than 24 hours. The extend of the stroke depends on rapidly of onset, size of

lesion, and presence of collateral circulation. Most patient do not have a decreased level

of consciousness in the first 24 hours unless it is due to a brainstem stroke or other

conditions such as seizure, increase intracranial pressure, or hemorrhage. Ischemic

stroke symptoms may progress in the first 72 hours as infarctions and cerebral edema.

1.2 Embolic stroke. Cerebral embolism is the occlusion of a cerebral artery by

an embolus, resulting in necrosis and edema of the area supplied by the involved blood

vessel. Embolism is the second most common cause of stroke. The majority of emboli

originate in the endocardial (inside) layer of the heart, with plagues or tissue breaking

off from endocardium and entering the circulation. The emboli travel to smaller vessels

and become a source of obstruction a areas of vascular narrowing or junction. Emboli

are associated with heart conditions, such as atrial fibrillation, myocardial infarction,

infective endocarditis, rheumatic heart disease, valvular prostheses, and atrial septal

defects. In general, the patient with an embolic stroke commonly has a rapid occurrence

of severe clinical manifestation and may or may not be related to activity. The patient

usually remains conscious, although a headache may develops. Recurrence is common

unless the underlying cause is aggressively treated.

2. Hemorrhagic strokes result from bleeding into the brain tissue itself

(intracerebral or introparenchymal hemorrhage) or into the subarachnoid space or the

ventricles (subarachnoid hemorrhage).

2.1 Intracerebral hemorrhage is bleeding with the brain casued by a rupture of

a vessel. Hypertension is the most important cause of intracerebral hemorrhage. Other

cause include vascular malformation, coagulation disorders, and anticoagulation drugs,

trauma, and ruptured aneurysms.

Hemorrhage commonly occurs during periods of activity. There is most

often a sudden onset of symptoms, and progression over minutes to hours as a result of

ongoing bleeding.

Symptoms include neurologic deficit, headache, nausea, vomiting,

decreased level of consciousness, and hypertension. Extent of the symptoms varies

depending on amount and duration of bleeding.

Prognosis of patient with intracerebral hemorrhage is poor, with more

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than 50% of patients dying soon after the hemorrhage occurs andn only about 20%

being function independent at 6 months.

2.2 Subarachonoid hemorrhage occurs when there is intracrainial

bleeding into the cerebrospinal fluid-filled spaced between the arachnoid and pia mater

membranes on the surface of the brain. Subarachnoid hemorrhage is commonly caused

by rupture of a cerebral aneurysms (congenital or acquired weakness and ballooning of

vessels). Other causes of subarachnoid hemorrhage include arteriovenous

malformations, trauma, and illegal drug cocaine abuse.

Characteristic presentation of a ruptured aneurysm is the sudden onset

of a severe headache different from a previous headache and typically the worst

headache of one’s life. Loss of consciousness may or may not occur and the patient’s

level of consciousness may range from alert to comatose, depending on the severity of

the bleeding.

Other symptoms include focal neurological deficits including cranial

nerve deficits, nausea, vomiting, seizures, and stiff neck.

Despite improvements in surgical techniques and management, many

patients with subarachnoid hemorrhage die or are left with significant morbidity.

Table 1

Types of stroke

Type Gender/Age Warning Time of onset Course/Prognosis

Ischemic

Thorombotic Men more

than women,

oldest

TIA (30 %

to 50% of

cases

During or

after sleep

Stepwise progressive, signs

and symptoms develop

slowly, usually some

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median age improvement, recurrence in

20% to 25% of survivors

Embolic Men more

than women

TIA

(uncommon)

Lack of

relationship to

activity,

sudden onset

Single event, signs and

symptoms develop quickly,

usually some improvement,

recurrence common without

aggressive treatment of

underlying disease

Hemorrhagic

Intracerebral Slightly

higher in

women

Headache

(25% of

cases)

Activity

(often)

Progression over 24 hr; poor

prognosis, fatality more

likely with presence of coma

Subarachnoid Slightly

higher in

women,

youngest

median age

Headache

(common)

Activity

(often),

sudden onset

Most common

related to head

trauma

Single sudden event usually,

fatality more likely with

presence of coma

Temporal development of stroke

The classification of temporal development of CVAs includes transient

ischemic attacks (TIA), reversible ischemic neurologic deficit, stroke-in-evolution or

progressive strokes, and completed stroke (stable stroke). Knowledge of this

classification is useful in planning.

Transient ischemic attack. The TIA is characterized by brief episodes of

neurologic manifestations, which clear completely in less than 24 hours. The

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neurological deficit present with TIAs disappear leaving no residual effects. Persons

experiencing TIAs fall into three categories: one third never have another TIA, one third

will have more than on TIA, and one third will experience a stroke.

Reversible ischemic neurologic deficit. The term reversible ischemic

neurologic deficit is sometimes used if the neurologic deficit remains after 24 hours but

leaves no residual signs or symptoms after days to weeks. This is considered by some to

be a completed stroke with minimal to no residual deficit.

Stroke-in-evolution. A stroke-in-evolution, or a progressing stroke, develops

over a period of hours or days. This pattern of progression is most characteristic of an

enlarging intraarterial thrombus. A stepwise or intermittent progression of deterioration

of neurologic findings is common. The progression occurs because ischemic tissue

becomes infracted tissue. The manifestations of stroke-in-evolution do not resolve (as

compared with TIAs) and leave residual neurologic effects.

Completed stroke. When the neurologic deficit remains unchanged over a 2-

to-3 day period, the stroke is termed a completed stroke (stable storke). An embolic

stroke may demonstrate this characteristic from the onset. With the exception of stroke

secondary to a ruptured aneurysm, a completed stroke signals readiness for more

aggressive rehabilitative treatment. If a ruptured aneurysm is the suspected cause,

activity may be restricted for as long as 3 to 4 weeks to reduced the possibility of

rebleeding.

Clinical manifestations

A stroke affects many body functions, including neuromotor activity,

elimination, intellectual function, spatial-perceptual alterations, personality and affect,

sensation and communication. The functions affected are directly related to the brain

area perfuse by the affected artery.

Neuromotor function. Motor deficits are the most obvious effect of stroke

and are caused by destruction of motor neurons in the pyramidal. Problems associated

with neuromotor function deficits include impairment of (1) mobility, (2) respiratory

function, (3) swallowing, (4) gag reflex, and (5) self-care abilities. The symptom are

caused by the destruction of motor neuron in the pyramidal pathway (nerve fibers from

the brain and passing through the spinal cord to the motor cell). The characteristic motor

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deficit include loss of skilled voluntary movement (akinesia), impairment of integration

of movement, alteration in muscle tone, and alteration in reflex. The initial hyporeflexia

(depressed reflexes) progress to hyperreflex (hyperactivities reflexs) for most patients.

Because of the pyramidal pathway crossing at the level of the medulla, a lesion on one

side of the brain affects the motor function on the opposite side of the brain.

Manifestations related to right-and left-brain damage are show as follows:

Right brain damage

(Stroke on right side of the brain)

Left brain damage

(Stroke on left side of the brain)

Paralyzed left-side: hemiplegia

Left-sided neglect

Spatial-perceptual deficits

Tends to deny or minimize problems

Rapid performance, short attention

span

Impulsive, safety problems

Impaired judgment

Impaired time concepts

Paralyzed right side: hemiplegia

Impaired speech/language aphasias

Impaired right/left discrimination

Slow performance, cautious

Impaired speech/language

Aware of deficits: depression,

anxiety

Impaired comprehensive related to

language, math

Communication. The left hemisphere is dominate for language skill in all

right-handed persons and in most left-handed persons.

When the stroke involve Wernick’s area of the brain, the patient

experiences receptive aphasia; neither the sounds of speech nor its meaning can be

understood, and comprehension of both written and spoken language is impaired.

The stroke causing expressive aphasia affects Broca’s area, the motor

area for speech. The patient has difficulty in speaking and writing.

Most stroke patients also experience dysarthria, a disturbance in the

muscle control of speech.

Affect. Patient with a stroke may have difficulty expressing their emotions;

emotional responses may be exaggerated or unpredictable. Additional manifestations

include impairment of memory and judgment, deficits in spatial-perceptual orientation,

and transient problems with bowel and bladder function.

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Diagnosis studies

When symptom of a stroke occurs, diagnostic studies are done to confirm that

it is a stroke, not another brain lesion, and to identify the likely cause of the stroke.

Diagnostic tests include CT scan, CT angiography, MRI, Magnetic resonance

angiography (MRA).

Collaborative care.

Prevention

The goals of stroke prevention include management of modifiable risk factors

to prevent a primary or secondary stroke.

Patients with known risk factors, such as DM, hypertension or cardiac

dysfunction, should b monitored closely. Measures designed to prevent the development

of a thrombus or embolus are used; low-dose aspirin or dipyramdamole (persantine) or

combined dipyridamole and aspirin can reduced the risk for stroke. The platelet-

aggregation inhibitor called ticlopidine hydrochloride (ticlid) has been shown to be as

effective as aspirin in reducing the incidence of stroke.

Surgery therapy for the patients with TIAs include carotid

endarterectomy, transluminal angioplasty, and extracranial intracranial by pass.

Acute care

The goal of acute care are preserving life, prevention of further brain damage,

and reducing disability. Treatment differs according to the type of stroke and as the

patient progresses from the acute to rehabilitation phase.

The first goal is to maintain a patent airway, which may be

compromised as a result of decreased consciousness. Oxygen administration, an

artificial airway, intubation, and mechanical ventilation may be indicated.

The patient is monitored closely for sign of increasing neurologic

deficit.

Patients with ischemic strokes may be treated with hypervolemic

hemodilution and volume expansion with crytalloids or colloid. The goal is to decrease

blood viscosity, which promotes blood flow to the area of stroke.

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Fluid and electrolyte balance must be controlled carefully. Although

the goal is to maintain perfusion to the brain, overhydration may compromise perfusion

by increasing cerebral edema. Adequate fluid intake during acute care via oral, IV

administration, or tube feeding should be 1500 to 2000 ml/day. Patient monitored for

urine output.

Management of increased intracranial pressure focuses on improving

venous drainage, including elevation of the head of the bed ordered, maintaining head

and neck in alignment, and avoiding hip flexion.

Other measure include pain management, avoidance of

hypervolemia, and management of constipation. Diuretic medication , such as mannitol

and furosemide may be used to decrease cerebral edema.

Surgical therapy for stroke may include an immediate evacuation of blood

occurring with a stroke resulting from an aneurysm-induced hematoma or a

cerebellar hematoma > 3 cm in size.

Drug therapy

Thrombolytic therapy. Recombinant tissue plasminogen activator (tPA) is

used to reestablish blood flow and prevent cell death for patient with ischemic strokes.

This drug must be administrated within 3 hours of onset of clinical signs. Patient are

screened carefully before tPA can be given, including a CT or MRI scan to rule out

hemorrhagic stroke, blood test for coagulation disorder, and screening of recent history

of GI bleeding.

The major side effect of tPA is cerebral hemorrhage. During infusion

the patient’s vital signs are monitored to assess for improvement or deterioration related

to intracerebral hemorrhage.

Control BP is critical during treatment and for 24 hours after treatment.

Platelet inhibition/anticoagulation therapy. Patient with stroke cause by

thrombi and emoboli may also be treated with platelet inhibitors and anticoagulants

(after the first 24 hours if treated with tPA) to prevent the formation of more clots.

Common anticoagulants include heparin and warfarin (Coumadin). Platelet inhibitors

include aspirin and ticlopidine.

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Other durg therapies. Aspirin or acetaminophen is given to treat

hyperthermia. Cooling blankets may be used cautiously to lower core temperature. The

nurse must closely monitor the patient’s temperature. Antiseizure medication such as

phenytoin (dilatin) may be administered if a seizure is present.

Nutritional therapy.

The stress of illness contributes to a catabolic state that can interfere with

recovery.

The patient may initially be receiving IV fluid. The first oral feeding

should be approached with caution because the gag reflex may be impaired. Before

initiation of feeding, the gage must be assessed. The patient should remain in a high

fowler’s position, preferely in a chair wt the head flexed forward for the feeding and for

30 minutes after feeding. After the acute phase, the dietitian can assist in determine

the appropriate daily caloric intake for the patient. If the patient is unable to take in an

adequate oral diet, enteral feeding via a nasogastric tube may be used.

Rehabilitation care

After stroke has stabilized for 12 to 24 hours, care shifts for preserving life to

lessening disability and attaining of optimal function. Depending on the patient status,

the patient’s rehabilitation potential, and the available resources, the patient may be

transferred to a rehabilitation facility or unit. Other option for rehabilitation included

outpatient therapy or home care-based rehabilitation.

Nursing management

Goals

The patients who has experienced a stroke will maintain a stable or improved

level of consciousness, attain maximum physical functioning, maintain stable body

functions (such as bladder control), maximize communication abilities, attain maximum

self-care abilities and skill, maintain adequate nutrition, avoid complications of strokes,

and maintain effective personal and family coping.

Nursing diagnoses

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Ineffective tissue perfusion (cerebral) related to decreased cerebral

blood flow secondary to thrombus, embolus, hemorrhage, edema, or spasm. As

Risk for ineffective airway clearance related to inability to raise

secretions.

Impaired physical mobility related to generalized weakness, muscle

atrophy, or paralyzed extremities.

Impaired verbal communication related to residual aphasia

Self-care deficits related to motor weakness, paralysis, and loss of

ability to effectively perform activities of daily living as manifested by observation or

verbal report of inability to eat, bathe, use toilet, dress, or clean independently.

Unilateral neglect related to visual field cut and sensory loss on one

side of body as manifested by consistent inattention to stimuli on affected side.

Altered urinary elimination relate to impaired impulse to void or

inability to reach toilet or manage tasks of voiding as manifested by incontinence and

flow of urine at unpredictable times.

Impaired swallowing related to weakness or paralysis of affected

muscles as manifested by drooling difficulty in swallowing, choking.

Self-esteem disturbance related to actual or perceived loss of function

as manifested by expression of shame or guilt, increasing dependence on others, refusal

to participate in self-care.

Risk for ineffective management to therapeutic regimen related to

functional, cognitive, or communication limitations.

See nursing care plan 55-1 for the patient with a stroke, Lewis and others,

Medical-surgical nursing, edition 5, pp. 1659-1661.

Acute nursing interventions

Respiratory system. During the acute phase of a stroke the nursing priority is

management of respiratory function.

An orpharyngeal airway may be used in comatose patients to hold the

tongue in place, prevent airway obstruction, and make suctioning accessible.

Interventions include frequent assessment airway patency and function, suctioning,

patient mobility, positioning of the patient to prevent aspiration, and encouragement of

deep breathing.

27

Neurologic system. The patient’s neurologic status needs to be monitored

closely to detect change suggesting extension of the stroke, increased intracranial

pressure (IICP), and vasospasm.

Neurologic assessment includes the Glasgow Coma Scale, mental

status, pupillary responses, and extremity movement and strength.

A decreasing level of consciousness may indicate IICP. Vital signs are

closely monitored and documented.

Cardiovascular system. Nursing goals for the cardiovascular system are

aimed at maintaining homeostasis.

Fluid retention plus overhydration can result in fluid overload. It can

also increase cerebral edema and ICP. The nurse should closely monitor

intake and output. IV therapy is also carefully regulated.

After a stroke the patient is at risk for thrombophebitis and deep vein

thrombosis in the weak or paralyzed lower extremity.

Other measures used to prevent thrombophebitis include positioning to

minimize the effects of dependent edema and the use of elastic compression gradient

stocking.

Musculoskeletal system. The goal for the musculoskeletal system is to

maintain optimal function, which is accomplished by prevention of join contractions and

muscle atrophy.

In the acute phase, ROM exercise and positioning are important

intervention. Passive ROM exercise is begun on the first day of hospitalization. Muscle

atrophy secondary to lack of innervations (nerve impulse) and to inactivity can develop

within a month after stroke.

The paralyzed or weak side needs special attention when the patient is

positioned. Each joint should be positioned higher than joint proximal to it. Specific

deformities on the affected side of the patient with stroke are shoulder adduction; flexion

contractures of the hand, wrist, and elbow; external rotating of the hip; and plantar

flexion of the foot.

Integument system. The patient’s skin is particularly susceptible to breakdown

because of the loss of sensation, diminished circulation, and immobility.

The patient should not be left in any position longer than 2 hours. Time

28

spent lying on the paralyzed or weak side should be limited to 30 minutes at a time.

GI system. The most common bowel problem is constipation. The patient

should be checked every 2 days for fecal impaction.

Depending on the patient’s fluid balance status and swallowing ability,

fluid intake should include 1800 to 2000 ml/day and fiber intake up to 25 g/day.

Physical activity also promotes bowel function.

Urinary system. In the acute stage of stroke, the primary urinary problem is

poor bladder control, resulting in incontinence.

Effort should be mad to promote normal bladder function and avoid the

use of an indwelling catheter.

Long-term use of an indwelling catheter is associated with urinary tract

infections and delayed bladder retraining. An intermittent catheterization program may

be used for patients with urinary retention.

Communication. During the acute stage the nurse’s role in meeting the

psychologic needs of the patient is primarily supportive.

An alert patient is usually anxious because of a lack of understanding of

what has happened and the inability to communicate. If the patient cannot understand

words, gesture may be used to support verbal cues. It may help to speak slowly and to

calmly use relatively simple words.

Sensory-perceptual alterations. Homonymous hemianopsia (blindness in the

same half of each visual field) is a common problem after a stroke.

Initially, the nurse helps the patients to compensate by arranging the

environment within the patient’s perceptual field, such as arranging the food tray so that

all food is on right side or the left side to accommodate for field of vision.

Later, the patient is instructed to consciously attend to the neglected

side. The weak or paralyzed extremities are carefully noted for adequacy of dressing,

hygiene, and trauma.

Visual problems may include diplopia (double vision), loss of the

corneal reflex, and ptosis (drooping eyelid), particularly if the stroke is in the vertebro

basilar distribution. Diplopia is often treated with the use of eye patch. If the corneal

reflex is absent the patient is a risk for a corneal abrasion and should be observed closely

and protected against eye injuries with artificial tears or gel to keep the eyes moist.

29

Coping. A stroke is usually a sudden, extremely stressful event for the patient,

close family members, and significant others.

Reactions vary considerably but may involve fear, anxiety, denial of

severity of the stroke, depression, and anger.

During the acute phase of caring for the patient and family, nursing

intervention designed to facilitate coping involve providing information and emotional

support.

Explanations to the patient about what has happened and about

diagnosis and therapeutic procedures should be clear and understandable. It will be

particularly challenging to keep the aphasic patient adwequately informed.

Because family members usually have not had time to prepare for the

illness, they may need assistance in arranging care for family members or pets and in

arranging transpiration and finance.

Home care and rehabilitation.

Nurse have an excellent opportunity to prepare the patient and family for

hospital discharge through education, demonstration and return demonstration, practice,

and evaluation of self-care skills before discharge. Total care is considered in discharge

planning in relation to medication, nutrition, mobility, exercise, hygiene, and toileting.

Follow-up care is carefully planned to permit continuing nursing,

physical, occupational, and speech therapy, as well as medical care. Community

resources should also be identified.

The goals of rehabilitation are to prevent deformity and to maintain and

improve function. These goals are mutually set by the patient, family, nurse and other

members of the rehabilitation team. The goals typically include (1) learning techniques

to self-monitoring and maintain physical wellness; (2) demonstrating self-care skills; (3)

exhibiting problem-solving skills with self-care; (4) avoiding complications associated

with stroke; (5) establishing and maintaining a useful communication system; (6)

maintaining nutritional and hydration status; (7) listing community resources for

equipment, supplies, and support; and (8) establishing flexible role behaviors to promote

family cohesiveness.

30

Rehabilitation and long-term management of the stroke patient are further

described in chapter 55 of Lewis and other, Medical-surgical nursing, ed 5.

Patient and family teaching

The care providers needs instruction and practice in necessary areas of

home care while the patient is hospitalized. This allows for support and encouragement,

as well as opportunities for feedback. Adjustment in the home environment, such as the

removal of a door to accommodate a wheelchair, can be made before discharge.

Specific areas for instruction related to home care include exercise and

ambulation techniques; dietary requirements; recognition of signs indicating the

possibility of another stroke, such as headache, vertigo, numbness, visual disturbances;

understanding of emotional changes and possibility of depression; medication routine;

and time, place, and frequency of follow-up activities such as occupational therapy and

physical therapy.

To assist the caregiver to stay healthy after the patient is discharged. It

is important to plan for respite or time away from caregiving activities on a regular

basis.

References

Brillhart, B. (2000). Nursing manage patient with a stroke in S. M. Lewis, M. M.

Heitkemper & S. R. Dirksen Medical-surgical nursing: Assessment and

management of clinical problems (5th ed.) (pp.1645-1671). St. Louis:

Mosby.

Dirksen S.R., Lewis, S.M., & Heitkemper, M.M. (2004). Clinical companion to

Medical-surgical nursing (3th ed.). St. Louis: Mosby.

Kerr, M. R. (2000). Nursing manage intracranial problems in S. M. Lewis, M. M.

Heitkemper & S. R. Dirksen (Eds.), Medical-surgical nursing: Assessment

and management of clinical problems (5th ed.) (pp.1608-1644). St. Louis:

Mosby.

Ozuna, J. M. (2000). Nursing manage chronic neurologic problems in S. M. Lewis, M.

M. Heitkemper & S. R. Dirksen (Eds.), Medical-surgical nursing:

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Assessment and management of clinical problems (5th ed.) (pp.1672-1712).

St. Louis: Mosby.

Schnell, S. S. (1997). Nursing care of clients with cerebral disorder in J, M. Black, & E.

Matassarinl-Jacobs (Eds.), Medical-surgical nursing: Clinical

management for continuity of care (4th ed.) (pp.834-889). Philadelphia:

W.B.Saunders.

Schnell, S. S. (1997). Nursing care of clients with cerebravascular disorder in J, M.

Black, & E. Matassarinl-Jacobs (Eds.), Medical-surgical nursing: Clinical

management for continuity of care (4th ed.) (pp.771-833). Philadelphia:

W.B.Saunders.

Schnell, S. S. (1997). Nursing care of comatose or confusion clients in J, M. Black, & E.

Matassarinl-Jacobs (Eds.), Medical-surgical nursing: Clinical

management for continuity of care (4th ed.) (pp.743-770). Philadelphia:

W.B.Saunders.

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