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:
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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.
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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
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the person faints. They may also experience an aura, which is an unusual feeling that
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
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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.
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 truthtelling 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.
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
Assessment of the postictal period should be include a detailed
description of the level of consciousness, vital signs, memory loss, muscle soreness,
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.
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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
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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
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
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communication problem and plan appropriate interventions.

Intervene as appropriate.
Nursing intervention for patient with motor aphasia

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
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and face the patient directly. Gradually shift topics of conversation and say when you
are going to change the topic.

2. Motor system
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.
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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
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 DAsynthesizing 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
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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
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.
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
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.

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.
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
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
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.
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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
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.
18

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.
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.
19
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
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.
20

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
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.
21
Table 1
Types of stroke
Type
Gender/Age
Warning
Time of onset
Course/Prognosis
Ischemic
Thorombotic
Men
more TIA (30 % During
or Stepwise progressive, signs
than women, to 50% of after sleep
and
oldest
slowly,
cases
median age
symptoms
develop
usually
some
improvement, recurrence in
20% to 25% of survivors
Embolic
Men
more TIA
than women
Lack
of Single
event,
signs
and
(uncommon) relationship to symptoms develop quickly,
activity,
usually some improvement,
sudden onset
recurrence common without
aggressive
treatment
of
underlying disease
Hemorrhagic
Intracerebral
Slightly
higher
Subarachnoid
Headache
in (25%
women
cases)
Slightly
Headache
Activity
of (often)
Progression over 24 hr; poor
prognosis,
fatality
more
likely with presence of coma
Activity
Single sudden event usually,
(often),
fatality more
women,
sudden onset
presence of coma
youngest
Most common
median age
related to head
higher
in (common)
trauma
likely
with
22
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
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 2to-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,
23
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
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
Left brain damage
(Stroke on right side of the brain)
(Stroke on left side of the brain)

Paralyzed left-side: hemiplegia

Paralyzed right side: hemiplegia

Left-sided neglect

Impaired speech/language aphasias

Spatial-perceptual deficits

Impaired right/left discrimination

Tends to deny or minimize problems

Slow performance, cautious

Rapid performance, short attention 

span

Impulsive, safety problems

Impaired judgment

Impaired time concepts
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.
24

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.
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 plateletaggregation 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.
25

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

Patients with ischemic strokes may be treated with hypervolemic
deficit.
hemodilution and volume expansion with crytalloids or colloid. The goal is to decrease
blood viscosity, which promotes blood flow to the area of stroke.

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
26
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.
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.
27
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

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.
28
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.
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.
29

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
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.
30

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.
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
31
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.
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
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Heitkemper & S. R. Dirksen Medical-surgical nursing: Assessment and
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Mosby.
32
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.
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Schnell, S. S. (1997). Nursing care of clients with cerebral disorder in J, M. Black, & E.
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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.
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File: neuro17October07