Management of Patients

With Cerebrovascular
Disorders

ARIEL M. ORTUOSTE, RN, MAN

LEARNING OBJECTIVES

1. Describe the incidence and social impact of

cerebrovascular disorders.
2. Identify the risk factors for cerebrovascular
disorders and related measures for prevention.
3. Compare the various types of cerebrovascular
disorders: their causes, clinical manifestations, and
medical management.
4. Relate the principles of nursing management to
the care of a patient in the acute stage of an
ischemic stroke.
5. Use the nursing process as a framework for
care of a patient recovering from an ischemic
stroke.
6. Use the nursing process as a framework for
care of a patient with a cerebral aneurysm.
7. Identify essential elements for family teaching
and preparation for home care of the stroke
patient
Cerebrovascular disorders

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

 isdefined to as an abrupt loss of

consciousness with resulting
paralysis that may be temporary or
permanent
STROKE
 ..\EDUCATIONAL VIDEOS\Stroke.mp4

 ..\EDUCATIONAL VIDEOS\What Is A Stroke_ -

Narration and Animation by Cal Shipley,
M.D..mp4
 Stroke is the primary cerebrovascular
disorder in the world.
 Although preventive efforts have brought about
a steady decline in incidence over the last
several years, stroke is still the third leading
cause of death. Approximately 500,000
people experience a new stroke, 100,000
experience a recurrent stroke, and
approximately 160,000 die of a stroke each
year.
Strokes can be divided into two
major categories:

A. Ischemic (85%), in which vascular

occlusion and significant
hypoperfusion occur, and
B. Hemorrhagic (15%), in which there
is extravasation of blood into the
brain

(American Heart Association, 2000).

ISCHEMIC
STROKE
..\EDUCATIONAL VIDEOS\Ischemic Stroke.mp4
A. ISCHEMIC STROKE

 Anischemic stroke, cerebrovascular

accident (CVA), or what is now
being termed “brain attack” is a
sudden loss of function resulting
from disruption of the blood
supply to a part of the brain.
five different types according
to their cause:

1. large artery thrombosis (20%),

2. small penetrating artery
thrombosis (25%),
3. cardiogenic embolic stroke (20%),
4. cryptogenic (30%) and
5. other (5%)
1. Large artery thrombotic strokes

 Large artery thrombotic strokes are

due to atherosclerotic plaques in the
large blood vessels of the brain.
 Thrombus formation and
occlusion at the site of the
atherosclerosis result in ischemia
and infarction
2. Small penetrating artery
thrombotic strokes

 Small penetrating artery thrombotic strokes

affect one or more vessels and are the most
common type of ischemic stroke.
 Small artery thrombotic strokes are also called
lacunar strokes because of the cavity that is
created once the infarcted brain tissue
disintegrates.
3. Cardiogenic embolic strokes

 Cardiogenic embolic strokes are

associated with cardiac
dysrhythmias, usually atrial
fibrillation.
 Emboli originate from the heart and
circulate to the cerebral vasculature,
most commonly the left middle
cerebral artery, resulting in a stroke.
 The last two classifications of ischemic strokes
are cryptogenic strokes, which have no
known cause, and other strokes, from causes
such as cocaine use, coagulopathies,
migraine, and spontaneous dissection of the
carotid or vertebral arteries
 Advanced age, gender, and race are well-known
non-modifiable risk factors for stroke (American Heart
Association, 2000).
 Specifically, high-risk groups include people over the
age of 55, because the incidence of stroke more than
doubles in each successive decade, and men, who
have a higher rate of stroke than women (due to the
higher prevalence of women in the elderly population,
however, the absolute numbers of men and women
with stroke are similar).
Modifiable Risk Factors for
Ischemic

 Hypertension (controlling hypertension, the

major risk factor, is the key to preventing
stroke)
 High cholesterol levels
 Obesity
 Elevated hematocrit (increases the risk of
cerebral infarction)
Cardiovascular disease (cerebral
emboli may originate in the heart)

• Atrial fibrillation
• Coronary artery disease
• Heart failure
• Left ventricular hypertrophy
• Myocardial infarction (especially
anterior)
• Rheumatic heart disease
 Diabetes mellitus (associated with
accelerated atherogenesis)
 Oral contraceptive use (increases risk,
especially with coexisting hypertension,
smoking, and high estrogen levels)
 Smoking
 Drug abuse (especially cocaine)
 Excessive alcohol consumption
Pathophysiology

1. there is disruption of the cerebral

blood flow due to obstruction of a
blood vessel.
2. This disruption in blood flow
initiates a complex series of cellular
metabolic events referred to as the
ischemic cascade
3. The ischemic cascade begins when cerebral
blood flow falls to less than 25 mL/100 g/min. At
this point, neurons can no longer maintain
aerobic respiration.
4. The mitochondria must then switch to
anaerobic respiration, which generates large
amounts of lactic acid, causing a change in the
pH level
5. This switch to the less efficient anaerobic
respiration also renders the neuron incapable of
producing sufficient quantities of adenosine
triphosphate (ATP) to fuel the depolarization
processes
6. Thus, the membrane pumps that maintain
electrolyte balances begin to fail and the cells
cease to function.
Clinical Manifestations

 Numbness or weakness of the face, arm, or

leg, especially on one side of the body
 Confusion or change in mental status
 Trouble speaking or understanding speech
 Visual disturbances
 Difficulty walking, dizziness, or loss of balance
or coordination
 Sudden severe headache
motor loss

 A stroke is a lesion of the upper motor neurons

and results in loss of voluntary control over
motor movements.
 Because the upper motor neurons decussate
(cross), a disturbance of voluntary motor
control on one side of the body may reflect
damage to the upper motor neurons on the
opposite side of the brain.
 The most common motor dysfunction is
hemiplegia (paralysis of one side of the
body) due to a lesion of the opposite side
of the brain. Hemiparesis, or weakness
of one side of the body, is another sign.
 In the early stage of stroke, the initial
clinical features may be flaccid
paralysis and loss of or decrease in
the deep tendon reflexes.
 When these deep reflexes reappear
(usually by 48 hours), increased tone is
observed along with spasticity (abnormal
increase in muscle tone) of the
extremities on the affected side.
communication loss

 Dysarthria (difficulty in speaking),

caused by paralysis of the muscles
responsible for producing speech
 Dysphasia or aphasia (defective
speech or loss of speech), which
can be expressive aphasia,
receptive aphasia, or global
(mixed) aphasia
 Apraxia (inability to perform a previously
learned action), as may be seen when a
patient picks up a fork and attempts to
comb his hair with it
perceptual disturbances

 Homonymous hemianopsia (loss of half

of the visual field) may occur from stroke
and may be temporary or permanent.
The affected side of vision corresponds
to the paralyzed side of the body.
 Loss of peripheral vision
- Difficulty seeing at night
- Unaware of objects or the borders of
objects
 Diplopia
– Double vision
Motor Deficits

 Hemiparesis
– Weakness of the face, arm, and leg on the
same side (due to a lesion in the opposite
hemisphere)
 Hemiplegia
– Paralysis of the face, arm, and leg on the
same side (due to a lesion in the opposite
hemisphere)
 Ataxia
– Staggering, unsteady gait
– Unable to keep feet together; needs a broad base to
stand
 Dysarthria
– Difficulty in forming words
 Dysphagia
– Difficulty in swallowing
Sensory Deficits

 Paresthesia (occurs on the side opposite

the lesion)
– Numbness and tingling of extremity
– Difficulty with proprioception
Verbal Deficits

 Expressive aphasia
– understandable; may be able to speak in single-
word responses
 Receptive aphasia
– Unable to comprehend the spoken word; can speak
but may not make sense
 Global (mixed) aphasia
– Combination of both receptive and expressive
aphasia
Cognitive Deficits

 • Short- and long-term memory loss

 • Decreased attention span
 • Impaired ability to concentrate
 • Poor abstract reasoning
 • Altered judgment
Emotional Deficits

 • Loss of self-control
 • Emotional lability
 • Decreased tolerance to stressful situations
 • Depression
 • Withdrawal
 • Fear, hostility, and anger
 • Feelings of isolation
The Stroke Continuum: Time
Course Classification

 Strokes are commonly classified using the time

course in the following manner:
 (1) transient ischemic attack (TIA),
 (2) reversible ischemic neurologic deficit,
 (3) stroke in evolution, and
 (4) completed stroke
– (Hock, 1999).
1. Transient Ischemic Attack

 Temporary episode of neurologic

dysfunction manifested by a sudden
loss of motor, sensory, or visual
function.
 It may last a few seconds or minutes
but not longer than 24 hours..
 Complete recovery usually occurs
between attacks.
 The symptoms result from temporary
impairment of blood flow to a specific
region of the brain due to atherosclerosis,
obstruction of cerebral microcirculation
by a small embolus, a decrease in
cerebral perfusion pressure (CPP), or
cardiac dysrhythmias
 A TIA may serve as a warning of impending
stroke, which has its greatest incidence in the
first month after the first attack.
 Lack of evaluation and treatment of a patient
who has experienced previous TIAs may result
in a stroke and irreversible deficits.
2. Reversible Ischemic Neurologic
Deficits

 Signs and symptoms are consistent

with but more pronounced than a
TIA and last more than 24 hours.
 Symptoms resolve in days with no
permanent neurologic deficit.
3 Stroke in Evolution

 Worsening of neurologic signs and

symptoms over several minutes or
hours. This is a progressing stroke.
4. Completed Stroke

 Stabilization of the neurologic signs

and symptoms. This indicates no
further progression of the hypoxic
insult to the brain from this particular
ischemic event.
Assessment and Diagnostic
Findings

 history and a complete physical and

neurologic examination.
 noncontrast computed
tomography (CT) scan performed
emergently to determine if the event
is ischemic or hemorrhagic
 12-lead electrocardiogram
 carotid ultrasound
 cerebral angiography,
 Transcranial Doppler flow studies,
 transthoracic or transesophageal
echocardiography,
 magnetic resonance imaging of the brain
and/or neck, xenon CT, and single photon
emission CT
Prevention

 Stroke risk screenings

Medical Management

 warfarin sodium (Coumadin)

 When warfarin is contraindicated, aspirin is
used
 Platelet-inhibiting medications (aspirin,
dipyridamole [Persantine], clopidogrel [Plavix],
and ticlopidine [Ticlid]) decrease the incidence
of cerebral infarction in patients who have
experienced TIAs
thrombolytic therapy

 Thrombolytic agents are used to treat ischemic

stroke by dissolving the blood clot that is
blocking blood flow to the brain.
 Recombinant t-PA is a genetically engineered
form of t-PA, a thrombolytic substance made
naturally by the body.
Enhancing Prompt Diagnosis

 After being notified by emergency medical

service personnel, the emergency department
calls the appropriate staff (neurologist,
neuroradiologist, radiology department, nursing
staff, and electrocardiogram technician) and
informs them of the patient’s imminent arrival
at the hospital
Dosage and Administration

 The patient is weighed to determine the dose

of t-PA. The minimum dose is 0.9 mg/kg; the
maximum dose is 90 mg. The loading dose is
10% of the calculated dose and is administered
over 1 minute
 The remaining dose is administered over 1
hour via an infusion pump. After the infusion is
completed, the line is flushed with 20 mL of
normal saline solution to ensure that all the
medication is administered.
Side Effects.

 Bleeding is the most common side effect of t-

PA administration, and the patient should be
closely monitored for any bleeding (intracranial,
intravenous [IV] insertion sites, urinary catheter
site, endotracheal tube, nasogastric tube,
urine, stool, emesis, other secretions)
 Note: Not all patients are candidates for t-
PA therapy.
 Other treatments include anticoagulant
administration (IV heparin or low-molecular
weight heparin) for ischemic strokes and
careful maintenance of cerebral
hemodynamics to maintain cerebral perfusion.
 ENDARTERECTOMY FOR PREVENTION OF
ISCHEMIC STROKE
 The main surgical procedure for managing
TIAs and small stroke is carotid
endarterectomy, currently the most frequently
performed peripheral vascular procedure in the
United States
 EDUCATIONAL VIDEOS\3D Medical
Animation (HD) - Stroke Management.mp4
NURSING PROCESS:
Assessment

 During the acute phase, a neurologic flow

sheet is maintained to provide data about the
following important measures of the patient’s
clinical status:
 Change in the level of consciousness or
responsiveness as evidenced by movement,
resistance to changes of position, and
response to stimulation; orientation to time,
place, and person
 Presence or absence of voluntary or
involuntary movements of the extremities;
muscle tone; body posture; and position of the
head
 Stiffness or flaccidity of the neck
 Eye opening, comparative size of pupils and
pupillary reactions to light, and ocular position
 Ability to speak
 Volume of fluids ingested or administered;
volume of urine excreted each 24 hours
 Presence of bleeding
 Maintenance of blood pressure within the
desired parameters
NURSING DIAGNOSES

 Impaired physical mobility related to

hemiparesis, loss of balance and coordination,
spasticity, and brain injury
 Acute pain (painful shoulder) related to
hemiplegia and disuse
 Self-care deficits (hygiene, toileting, grooming,
and feeding) related to stroke sequelae
 Disturbed sensory perception related to altered
sensory reception, transmission, and/or
integration
 Impaired swallowing
 Incontinence related to flaccid bladder,
detrusor instability, confusion, or difficulty in
communicating
 Disturbed thought processes related to brain
damage, confusion, or inability to follow
instructions
 Impaired verbal communication related to brain
damage
 Risk for impaired skin integrity related to
hemiparesis/ hemiplegia, or decreased mobility
 Interrupted family processes related to
catastrophic illness and caregiving
burdens
 Sexual dysfunction related to neurologic
deficits or fear of failure
Nursing Interventions

 IMPROVING MOBILITY AND PREVENTING

JOINT DEFORMITIES
 A hemiplegic patient has unilateral paralysis
(paralysis on one side). When control of the
voluntary muscles is lost, the strong flexor
muscles exert control over the extensors. The
arm tends to adduct (adductor muscles are
stronger than abductors) and to rotate
internally.
 Preventing Shoulder Adduction
 To prevent adduction of the affected shoulder
while the patient is in bed, a pillow is placed in
the axilla when there is limited external
 rotation; this keeps the arm away from the
chest. A pillow is placed under the arm, and
the arm is placed in a neutral (slightly flexed)
position, with distal joints positioned higher
than the more proximal joints.
 Positioning the Hand and Fingers
 The fingers are positioned so that they are
barely flexed. The hand is placed in slight
supination (palm faces upward), which is its
most functional position. If the upper extremity
is flaccid, a volar resting splint can be used to
support the wrist and hand in a functional
position.
 Changing Positions
 The patient’s position should be changed every
2 hours. To place a patient in a lateral (side-
lying) position, a pillow is placed between the
legs before the patient is turned. To promote
venous return and prevent edema, the upper
thigh should not be acutely flexed.
 Establishing an Exercise Program
 The affected extremities are exercised
passively and put through a full range of
motion four or five times a day to maintain joint
mobility, regain motor control, prevent
contractures in the paralyzed extremity,
prevent further deterioration of the
neuromuscular system, and enhance
circulation
 Preparing for Ambulation
 As soon as possible, the patient is assisted out
of bed. Usually, when hemiplegia has resulted
from a thrombosis, an active rehabilitation
program is started as soon as the patient
regains consciousness; a patient who has had
a cerebral hemorrhage cannot participate
actively until all evidence of bleeding is gone.
 PREVENTING SHOULDER PAIN
 A flaccid shoulder joint may be overstretched
by the use of excessive force in turning the
patient or from over strenuous arm and
shoulder movement. To prevent shoulder pain,
the nurse should never lift the patient by the
flaccid shoulder or pull on the affected arm or
shoulder.
 ENHANCING SELF-CARE
 As soon as the patient can sit up, personal
hygiene activities are encouraged. The patient
is helped to set realistic goals; if feasible, a
new task is added daily. The first step is to
carry out all self-care activities on the
unaffected side
 MANAGING SENSORY-PERCEPTUAL
DIFFICULTIES
 Patients with a decreased field of vision should
be approached on the side where visual
perception is intact. All visual stimuli (clock,
calendar, and television) should be placed on
this side. The patient can be taught to turn the
head in the direction of the defective visual
field to compensate for this loss.
THANK YOU…
Hemorrhagic
Stroke
..\EDUCATIONAL VIDEOS\Hemorrhagic Stroke
(Brain Hemorrhage).mp4
 Hemorrhagic strokes account for 15% of
cerebrovascular disorders and are primarily
caused by an intracranial or subarachnoid
hemorrhage.
 Hemorrhagic strokes are caused by bleeding
into the brain tissue, the ventricles, or the
subarachnoid space.
 Primary intracerebral hemorrhage from a
spontaneous rupture of small vessels accounts
for approximately 80% of hemorrhagic strokes
and is primarily caused by uncontrolled
hypertension (Qureshi et al., 2001).
 Secondary intracerebral hemorrhage is
associated with arteriovenous malformations
(AVMs), intracranial aneurysms, or certain
medications (eg, anticoagulants and
amphetamines) (Qureshi et al., 2001).
CAUSES

 Intracerebral
haemorrhage
 Subarachnoid haemorrhage
 Cerebral aneurysm
 Arteriovenous malfunction
Pathophysiology

 INTRACEREBRAL HEMORRHAGE
 An intracerebral hemorrhage, or bleeding into
the brain substance, is most common in
patients with hypertension and cerebral
atherosclerosis because degenerative
changes from these diseases cause rupture of
the vessel.
 They also may be due to certain types of
arterial pathology, brain tumor, and the use of
medications (oral anticoagulants,
amphetamines, and illicit drugs such as crack
and cocaine).
 The bleeding is usually arterial and occurs
most commonly in the cerebral lobes, basal
ganglia, thalamus, brain stem (mostly the
pons), and cerebellum (Qureshi et al., 2001).
 Occasionally, the bleeding ruptures the wall of
the lateral ventricle and causes intraventricular
hemorrhage, which is frequently fatal
 INTRACRANIAL (CEREBRAL) ANEURYSM
 An intracranial (cerebral) aneurysm is a
dilation of the walls of a cerebral artery that
develops as a result of weakness in the arterial
wall.
 The cause of aneurysms is unknown,
although research is ongoing.
 An aneurysm may be due to atherosclerosis,
resulting in a defect in the vessel wall with
subsequent weakness of the wall; a congenital
defect of the vessel wall; hypertensive vascular
disease; head trauma; or advancing age.
 ARTERIOVENOUS MALFORMATIONS
 An AVM is due to an abnormality in embryonal
development that leads to a tangle of arteries
and veins in the brain without a capillary bed.
The absence of a capillary bed leads to dilation
of the arteries and veins and eventual rupture.
 They are commonly a cause of hemorrhage in
young people.
 SUBARACHNOID HEMORRHAGE
 A subarachnoid hemorrhage (hemorrhage into
the subarachnoid space) may occur as a result
of an AVM, intracranial aneurysm, trauma, or
hypertension.
 The most common cause is a leaking
aneurysm in the area of the circle of Willis or a
congenital AVM of the brain.
Clinical Manifestations

 Many of the same motor, sensory, cranial

nerve, cognitive, and other functions that are
disrupted following ischemic stroke are
altered following a hemorrhagic stroke
Assessment and Diagnostic
Findings

 CT scanning to determine the size and

location of the hematoma as well as the
presence or absence of ventricular blood and
hydrocephalus
 Cerebral angiography confirm the diagnosis
of an intracranial aneurysm or AVM.
 Lumbar puncture is performed if there is no
evidence of increased ICP
Prevention

 Primary prevention of hemorrhagic stroke is

the best approach and includes managing
hypertension and ameliorating other significant
risk factors
 Control of hypertension, especially in
individuals over 55 years of age, clearly
reduces the risk for hemorrhagic stroke
 Stroke risk screenings provide an ideal
opportunity to lower hemorrhagic stroke risk
 prevention effort unique to hemorrhagic stroke
is to increase the public’s awareness
Medical Management

 The goals of medical treatment of hemorrhagic

stroke are to
 allow the brain to recover from the initial
insult (bleeding),
 to prevent or minimize the risk for
rebleeding, and
 to prevent or treat complications
 bed rest
 management of vasospasm
 Surgical or medical treatment to prevent
rebleeding.
 Analgesics (codeine, acetaminophen) may be
prescribed for head and neck pain.
 The patient is fitted with elastic compression
stockings to prevent deep vein thrombosis
COMPLICATIONS

 Potential complications include

– rebleeding;
– cerebral vasospasm resulting in cerebral ischemia;
– acute hydrocephalus, which results when free
blood obstructs the reabsorption of cerebrospinal
fluid (CSF) by the arachnoid villi; and
– seizures.
COMPLICATIONS

 Cerebral Hypoxia and Decreased Blood

Flow
 Immediate complications of a hemorrhagic
stroke include cerebral hypoxia, decreased
cerebral blood flow, and extension of the area
of injury.
– Providing adequate oxygenation of blood to the
brain minimizes cerebral hypoxia
 Vasospasm.
– The development of cerebral vasospasm (narrowing
of the lumen of the involved cranial blood vessel) is
a serious complication of subarachnoid hemorrhage
and accounts for 40% to 50% of the morbidity and
mortality of those who survive the initial intracranial
bleed.
 Increased ICP
– An increase in ICP can follow either an ischemic or
hemorrhagic stroke but almost always follows a
subarachnoid hemorrhage, usually because of
disturbed circulation of CSF caused by blood in the
basal cisterns.
 Systemic Hypertension
– Preventing sudden systemic hypertension is critical
in hemorrhagic stroke management. The goal of
therapy is to maintain the systolic blood pressure at
about 150 mm Hg.
SURGICAL MANAGEMENT

– Many patients with a primary intracerebral

hemorrhage are not treated surgically.
– However, surgical evacuation is strongly
recommended for the patient with a cerebellar
hemorrhage if the diameter exceeds 3 cm and the
Glasgow Coma Scale score is below 14
 An extracranial-intracranial arterial bypass
may be performed to establish collateral blood
supply to allow surgery on the aneurysm.
 endovascular treatment (occlusion of the
parent artery) and
 aneurysm coiling (obstruction of the
aneurysm site with a coil).
NURSING DIAGNOSES

 • Ineffective cerebral tissue perfusion related to

bleeding
 • Disturbed sensory perception related to
medically imposed restrictions (aneurysm
precautions)
 • Anxiety related to illness and/or medically
imposed restrictions (aneurysm precautions)
Nursing Interventions

 OPTIMIZING CEREBRAL TISSUE

PERFUSION
– The patient is closely monitored for neurologic
deterioration occurring from recurrent bleeding,
increasing ICP, or vasospasm
 Implementing Aneurysm Precautions
– Cerebral aneurysm precautions are implemented for
the patient with a diagnosis of aneurysm to provide
a nonstimulating environment, prevent increases in
ICP pressure, and prevent further bleeding.
 RELIEVING SENSORY DEPRIVATION AND
ANXIETY
– Sensory stimulation is kept to a minimum for
patients on aneurysm precautions. For patients who
are awake, alert, and oriented, an explanation of the
restrictions helps reduce the patient’s sense of
isolation. Reality orientation is provided to help
maintain orientation
 MONITORING AND MANAGING POTENTIAL
COMPLICATIONS
 Vasospasm
– The patient is assessed for signs of possible
vasospasm: intensified headaches, a decrease in
level of responsiveness (confusion, disorientation,
lethargy), or evidence of aphasia or partial paralysis.
 Seizures
– Seizure precautions are maintained for every patient
who may be at risk for seizure activity. Should a
seizure occur, maintaining the airway and
preventing injury are the primary goals
 Hydrocephalus
– Hydrocephalus can occur within the first 24 hours
(acute) after subarachnoid hemorrhage or days
(subacute) to several weeks (delayed) later
 Rebleeding
– Aneurysm rebleeding occurs most frequently in the
first 2 weeks after the initial hemorrhage and is
considered a major complication.
– Symptoms of rebleeding include sudden severe
headache, nausea, vomiting, decreased level of
consciousness, and neurologic deficit.
Evaluation

 Expected patient outcomes may include:

1. Demonstrates intact neurologic status and
normal vital signs and respiratory patterns
2. Demonstrates normal sensory perceptions
 a. States rationale for aneurysm precautions
 b. Exhibits clear thought processes
 3. Exhibits reduced anxiety level
 a. Is less restless
 b. Exhibits absence of physiologic indicators of
anxiety (eg, normal vital signs; normal
respiratory rate; absence of excessive, fast
speech)
THANK YOU…