CEREBROVASCULAR DISEASE

CEREBROVASCULAR INSUFFICIENCY
Cerebrovascular insufficiency is an interruption or inadequate blood flow to a focal area of the
brain resulting in transient or permanent neurologic dysfunction. Transient ischemic attack (TIA)
lasts less than 24 hours. Ischemic stroke is similar to myocardial infarction, in that the
pathogenesis is loss of blood supply to the tissue, which can result in irreversible damage if
blood flow is not restored quickly.

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 (STROKE, BRAIN ATTACK)

Stroke, cerebrovascular accident (CVA), or brain attack is the onset and persistence of
neurologic dysfunction lasting longer than 24 hours and resulting from disruption of blood
supply to the brain and indicates infarction rather than ischemia.

Stroke is the term used to describe neurological changes caused by an interruption in the blood
supply to a part of the brain

Strokes can be divided into two major categories: ischemic (85%), in which vascular occlusion
and significant hypoperfusion occur, and hemorrhagic (15%), in which there is extravasation of
blood into the brain (American Heart Association, 2000).

incidence

Stroke is the leading cause of long-term disability and the third leading cause of death in the
United States, with an annual incidence of 700,000.

Ischemic Stroke

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

Ischemic attack occurs when blood supply to a part of the brain is suddenly interrupted by a
thrombus (blood clot) , embolus (foreign material travelling through the circulation or stenosis.

Hemorrhagic Stroke
Bleeding into the brain tissue or the subarachnoid space causes the cause a hemorrhagic stroke.

The neurologic defect caused by ischemia and the resultant necrosis of cells in the brain vary
according to the area of the brain involved , the size of the affected area, and the length of the
time blood flow is decreased or stopped . A major loss of the blood supply to the brain can cause
severe disability or death. When the duration of the decrease blood flow is short and the
anatomic area involved is small, the person may not be aware that damage has been done.

Causes and Risk Factors

Thrombosis: A thrombus starts with damage to the endothelial lining of the vessels.
Atherosclerosis is the primary reason. Atherosclerosis causes fatty material to deposit and to
form plaques on vessels walls. These plaque continue to enlarge and cause stenosis of the artery.
Blood swirls around the irregular surface of the plaques, causing platelets to adhere to the
plaque. Eventually the vessel lumen becomes obstructed. Thrombotic stroke s the most common
type of the stroke in people with diabetes.

Embolism: The occlusion of a cerebral artery by an embolus causes an embolic stroke.

An embolus forms outside the brain, detaches and travels through the cerebral circulation until it
lodges in and occlude a cerebral artery. A common embolus is plaque. Chronic arterial
fibrillation is associated with a high incidence of embolic stroke.

Mechanical prosthetic heart valve have a rougher surface than the normal endocardium so there
is a increase risk of blood clots.

Bacterial and non bacterial endocarditis can be source of emboli.

Other sources of emboli include tumor, fat, bacteria and air. The incidence of cerebral embolism
increase with age.

Hemorrhage: most intracerebral hemorrhage are caused by the rupture of artherosclerotic and
hypertensive vessels which causes bleeding into the brain tissue.intracerebral hemorrhage is most
often secondary to hypertension and most common after the age of 50.

Aneurysms are another cause of hemorrhage.

Stroke secondary to bleeding often produces spasm of cerebral vessels and cerebral ischemia
because the blood outside the vessels acts as irritant to the tissues.

The overall mortality of intracerebral hemorrhage varies between 25% and 60%. The volume of
the hemorrhage is the single most important predictor of the patient outcomes.
Other causes

 Cerebral arterial spasm, caused by irritation, reduces blood flow to the area of the brain
supplied by the constricted vessels
 Hypercoagulable states, including protein C and protein S deficiency and disorders of the
clotting cascade, can cause thrombosis and ischemic stroke.
 Compression of cerebral vessels may result from a tumor, large blood clot, swollen brain
tissue, brain abscess or other disorders.

Risk Factors

Hypertension: HTN is the greatest risk factors for a stroke. Increase systolic and diastolic blood
pressure is associated with damage to all blood vessels, including cerebral vessels. People with
hypertension have 4 to 6 times greater risk for stroke.

Heart disease: arterial fibrillation is the second greatest risk factor for stroke. Others risk heart
disease includes mitral valve stenosis patent foramen ovale and cardiac surgery.

Diabetes mellitus: diabetes leads to vascular changes in both the systemic and cerebral
circulation and increase the risk of hypertension ( the prevalence of HTN is 40% hyper in people
with diabetes). People with diabetes are three times more likely to have stroke compared to those
without diabetes.

Sleep apnea: considered a major risk factor for Stroke. Sleep apnea increase blood pressure and
cause decrease oxygen and increase carbon dioxide in the blood.

Blood cholesterol levels: increase blood cholesterol levels contribute to the risk of
artherosclerosis including arteries in the cerebral circulation

Smoking : cigarette smoking doubles a person’s risk for ischemic stroke and increase the risk for
cerebral hemorrhage upto 3.5%.

Sickle cell disease: changes in the shape of the red blood cells (RBCs) increase blood viscosity
and produce erythrocyte clumps that occlude small cerebral vessels.

Substance abuse: the injection of unpurified substance increase the risk factors for stroke, and
abuse of the certain drugs can increase cerebral blood flow and increase the risk for intracranial
hemorrhage. Substance associated with stroke include marijuana, anabolic steroids, heroin,
amphetamines and cocaine.

Living in the stroke belt: people living in the southeastern united state have the highest stroke
mortality rate in the country.
Other risk factor includes: family history of stroke, obesity, a sedentary life style, recent viral
and bacterial infections, oral contraceptive user, pregnancy, childbirth, menopause, migraine
headache, autoimmune disorder ( such as diabetes and lupus) and clotting disorders.

Pathophysiology

Ischemic Stroke
Blood supply

Ischemia

Energy failure

Acidosis Ion imbalance

Intracellular calcium increased

Cell membranes and proteins break down

Formation of free radicals

Cell injury and death

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

Early in the cascade, an area of low cerebral blood flow, referred to as the penumbra region,
exists around the area of infarction. The penumbra region is ischemic brain tissue that can be
rescue with timely intervention. The ischemic cascade threatens cells in the penumbra because
membrane depolarization of the cell wall leads to an increase in intracellular calcium and the
release of glutamate (Hock, 1999). The penumbra area can be revitalized by administration of
tissue plasminogen activator
(t-PA), and the invasion of calcium can be limited with the use of calcium channel blockers. The
influx of calcium and the release of glutamate, if continued, activate a number of damaging
pathways that result in the destruction of the cell membrane, the release of more calcium and
glutamate, vasoconstriction, and the generation of free radicals. These processes enlarge the area
of infarction into the penumbra, extending the stroke.
Each step in the ischemic cascade represents an opportunity for intervention to limit the extent of
secondary brain damage caused by a stroke. Medications that protect the brain from secondary
injury are called neuroprotectants (Reed, 2000). A number of clinical trials are focusing on
calcium channel antagonists that block the calcium influx, glutamate antagonists, antioxidants,
and other neuroprotectant strategies that will help prevent secondary complications

Clinical Manifestations

An ischemic stroke can cause a wide variety of neurologic deficits, depending on the location of
the lesion of the area of inadequate perfusion, and the amount of collateral blood flow.
 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, sensory, cranial nerve, cognitive, and other functions may be disrupted

MOTOR LOSS
A stroke is a lesion of the upper motor neurons and results in loss of voluntary control over
motor movements
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: Unable to form words that are 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

Assessment and Diagnostic Findings

 careful history and a complete physical and neurologic examination.
 The initial diagnostic test for a stroke is a noncontrast computed tomography (CT) scan
performed emergently to determine if the event is ischemic or hemorrhagic
 Further diagnostic workup for ischemic stroke involves attempting to identify the source
of the thrombi or emboli
 A 12-lead electrocardiogram and a carotid ultrasound are standard tests.
 Other studies may include 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
 In a patient with a TIA, a bruit may be heard over the carotid artery
  Diagnostic tests for TIA may include carotid phonoangiography; this involves
auscultation, direct visualization, and photographic recording of carotid bruits
 Oculoplethysmography measures the pulsation of blood flow through the ophthalmic
artery.
 Carotid angiography allows visualization of intracranial and cervical vessels

Medical Management

 Patients who have experienced a TIA or mild stroke from atrial fibrillation or from
suspected embolic or thrombotic causes are candidates for nonsurgical medical
management.

 Those with atrial fibrillation are treated with dose-adjusted warfarin sodium (Coumadin)
unless contraindicated.

 When warfarin is contraindicated, aspirin is used in doses between 50 and 325 mg/d

 Platelet-inhibiting medications (aspirin, dipyridamole [Persantine], clopidogrel [Plavix],

and ticlopidine [Ticlid]) decrease the incidence of cerebral infarction in patients who
have experienced TIAs from suspected embolic or thrombotic causes
 Currently the most cost-effective antiplatelet regimen is aspirin 50 mg/d and
dipyridamole 400 mg/d

Acute Treatment
1. Support of vital functions maintain airway, breathing, oxygenation, circulation
2. Reperfusion and hemodilution with colloids and volume expanders (albumin).
3. Thrombolytic therapy: recombinant tissue plasminogen (t-PA) given I.V. 0.9 mg/kg
within 3 hours of onset of symptoms; transarterially within 6 hours of onset of symptoms.
(Recombinant t-PA is a genetically engineered form of t-PA, a thrombolytic substance
made naturally by the body. It works by binding to fibrin and converting plasminogen to
plasmin, which stimulates fibrinolysis of the atherosclerotic lesion)
 Delays make the patient ineligible for thrombolytic therapy because
revascularization of necrotic tissue (which develops after 3 hours) increases the
risk for cerebral edema and hemorrhage.

Eligibility Criteria for t-PA Administration

 Age 18 years or older
 Clinical diagnosis of stroke with NIH stroke scale score under 22
 Time of onset of stroke known and is 3 hours or less
 BP systolic ≤185; diastolic ≤110
 Not a minor stroke or rapidly resolving stroke
 No seizure at onset of stroke
 Not taking warfarin (Coumadin)
 Prothrombin time ≤15 seconds or INR ≤1.7
  Not receiving heparin during the past 48 hours with elevated
 Platelet count ≥100,000
 Blood glucose level between 50 and 400 mg/dL
 No acute myocardial infarction
 No prior intracranial hemorrhage, neoplasm, arteriovenous
 malformation, or aneurysm
 No major surgical procedures within 14 days
 No stroke or serious head injury within 3 months
 No gastrointestinal or urinary bleeding within last 21 days
 Not lactating or postpartum within last 30 days

Dosage and Administration 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.

The patient is admitted to the intensive care unit, where continuous cardiac monitoring is
implemented.

Vital signs are obtained every 15 minutes for the first 2 hours, every 30 minutes for the next 6
hours, then every hour for 16 hours. Blood pressure should be maintained with the systolic
pressure less than 180 mm Hg and the diastolic pressure less than 100 mm Hg.

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)

 Intracranial bleeding is a major complication that occurs in approximately 6.5% of

patients

4. anticoagulant administration (IV heparin or low-molecularweight heparin) for ischemic

strokes and patient not receiving t-PA therapy
5. Management of increased ICP such as administering an osmotic diuretic (eg, mannitol),
maintaining PaCO2 within the range of 30 to 35 mm Hg, and positioning to avoid
hypoxia.
6. Elevation of the head of the bed to promote venous drainage and to lower increased ICP
7. Intubation with an endotracheal tube to establish a patent airway, if necessary
8. Continuous hemodynamic monitoring. Systolic pressure should be maintained at less
than 180 mm Hg, diastolic pressure at less than 100 mm Hg. Maintaining the blood
pressure within this range reduces the potential for additional bleeding or further
ischemic damage.
 9. Neurologic assessment to determine whether the stroke is evolving or whether other acute
complications are developing,
10. A rehabilitation program, including physical therapy, occupational therapy, speech
therapy (as soon as stable), and counseling as needed.
11. Treatment of poststroke depression with antidepressants such as selective serotonin
reuptake inhibitors.

Eligibility Criteria for t-PA

Prevention

Primary prevention of ischemic stroke is the best approach. Stroke risk screenings are an ideal
opportunity to lower stroke risk by identifying high-risk individuals or groups and educating the
patients and the community about recognition and prevention of stroke

Modifiable Risk Factors for Ischemic and Hemorrhagic Stroke

 Hypertension (controlling hypertension, the major risk factor, is the key to preventing
stroke)
Cardiovascular disease (cerebral emboli may originate in the heart)
• Atrial fibrillation
• Coronary artery disease
• Heart failure
• Left ventricular hypertrophy
• Myocardial infarction (especially anterior)
• Rheumatic heart disease
• High cholesterol levels
• Obesity
• Elevated hematocrit (increases the risk of cerebral infarction)
• Diabetes mellitus (associated with accelerated atherogenesis)
• Oral contraceptive use (increases risk, especially with coexisting hypertension, smoking, and
high estrogen levels)
• Smoking
• Drug abuse (especially cocaine)
• Excessive alcohol consumption

 For people at high risk, interventions that alter modifiable factors, such as treating
hypertension and hyperglycemia and stopping smoking, will reduce stroke risk.
 Many health promotion efforts involve encouraging a healthy lifestyle, including eating a
low-fat, low-cholesterol diet and increasing exercise.
 Recent evidence suggests that eating fish two or more times per week reduces the risk of
thrombotic stroke for women (Iso et al., 2001).
 Patients with moderate to severe carotid stenosis are treated with carotid endarterectomy
 In patients with atrial fibrillation, which increases the risk of emboli, administration of
warfarin (Coumadin), an anticoagulant that inhibits clot formation, may prevent both
thrombotic and
embolic strokes.
 Platelet-inhibiting medications (aspirin, dipyridamole [Persantine], clopidogrel [Plavix],
and ticlopidine [Ticlid]) decrease the incidence of cerebral infarction in patients who
have experienced TIAs from suspected embolic or thrombotic causes
Complications

 Aspiration pneumonia
 Dysphagia in 25% to 50% of patients after stroke
 Spasticity, contractures
 Deep vein thrombosis, pulmonary embolism
 Brain stem herniation
 Poststroke depression

Hemorrhagic Stroke
Hemorrhagic strokes account for 15% of cerebrovascular disorders and are primarily caused by
an intracranial or subarachnoid hemorrhage. Patients generally have more severe deficits and a
longer recovery time compared to those with ischemic stroke

Causes
 Hypertension is the most important cause of intracerebral hemorrhage
 Ruptured aneurysm
 Arteriovenous malformations (avms
 Medications (eg, anticoagulants and thrombolytic drugs)
 Coagulation disorders

.
Pathophysiology

Hemorrhagic strokes can bleeding into the brain tissue ( intracerebral hemorrhage), the
ventricles( intraventricular), or the subarachnoid space( subarchnoid hemorrhage

Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for
approximately 80% of hemorrhagic strokes and is primarily caused by uncontrolled hypertension
Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVMs),
intracranial aneurysms, or certain medications (eg, anticoagulants and thrombolytic drugs

Normal brain metabolism is disrupted by the brain being exposed to blood; by an increase in ICP
resulting from the sudden entry of blood into the subarachnoid space, which compresses and
injures brain tissue;
or by secondary ischemia of the brain resulting from the reduced perfusion pressure and
vasospasm.
Clinical Manifestations
 The patient with a hemorrhagic stroke can present with a wide variety of neurologic
deficits, similar to the patient with ischemic stroke
 Rupture of an aneurysm or AVM usually produces a sudden, unusually severe headache
and often loss of consciousness for a variable period
 There may be pain and rigidity of the back of the neck (nuchal rigidity) and spine due to
meningeal irritation
 Visual disturbances (visual loss, diplopia, ptosis) occur when the aneurysm is adjacent to
the oculomotor nerve
 Tinnitus, dizziness, and hemiparesis may also occur.

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, the CT scan
results are negative, and subarachnoid hemorrhage must be confirmed.

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 with sedation to prevent agitation and stress,
 management of vasospasm, and surgical or medical treatment to prevent rebleeding.
Management of vasospasm remains difficult and controversial. Based on one theory that vasospasm is caused by an
increased influx of calcium into the cell, medication therapy may be used to block or antagonize this action and
prevent or reverse the action of vasospasm already present. Calcium-channel blockers may include nimodipine
(Nimotop), verapamil (Isoptin), and nifedipine (Procardia). Other therapy for vasospasm is aimed at minimizing the
deleterious effects of the associated cerebral ischemia and includes fluid volume expanders and induced arterial
hypertension, normotension, or hemodilution.
 Analgesics (codeine, acetaminophen) may be prescribed for head and neck pain.
 The patient is fitted with elastic compression stockings to prevent deep vein thrombosis, a
threat to any patient on bed rest.

SURGICAL MANAGEMENT
 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. Surgical
evacuation is most frequently accomplished via a craniotomy
 intracranial aneurysm is prepared for surgical intervention as soon as the condition is
considered stable. An extracranial-intracranial arterial bypass may be performed to
establish collateral blood supply to allow surgery on the aneurysm
  less invasive endovascular treatments for aneurysm include endovascular treatment
(occlusion of the parent artery) and aneurysm coiling (obstruction of the aneurysm site
with a coil).

NURSING PROCESS WITH STROKE PATIENT

Nursing Assessment

 Maintain neurologic flow sheet (the Modified Rankin scale or NIH Stroke Scale may be
used).
 Assess for voluntary or involuntary movements, tone of muscles, presence of deep tendon
reflexes (reflex return signals end of flaccid period and return of muscle tone).
 Also assess mental status, cranial nerve function, sensation/proprioception.
 Monitor bowel and bladder function/control.
 Monitor effectiveness of anticoagulation therapy.
 Frequently assess level of function and psychosocial response to condition.
 Assess for skin breakdown, contractures, and other complications of immobility.

Nursing Diagnoses
 Ineffective cerebral tissue perfusion related to decrease cerebral blood flow secondary to
thrombus, embolus, hemorrhage, or edema as evidenced by ICP 15 mm Hg for 15-30
second or longer, decrease GCS, and altered respiratory pattern
 Ineffective airway clearance related to inability to raise secretion as evidenced by
adventitious breath sounds, diminished breath sounds and ineffective cough

 Risk for Injury related to neurologic deficits

 Impaired Physical Mobility related to motor deficits
 Disturbed Thought Processes related to brain injury
 Impaired Verbal Communication related to brain injury
 Self-Care Deficit: Bathing, Dressing, Toileting related to hemiparesis/paralysis
 Imbalanced Nutrition: Less Than Body Requirements related to impaired self-feeding,
chewing, swallowing
 Impaired Urinary Elimination related to motor/sensory deficits
 Disabled Family Coping related to catastrophic illness, cognitive and behavioral sequelae
of stroke, and caregiving burden

Cerebral perfusion promotion

 Monitor neurologic status to detect change indicative of worsening or improving

condition
  Monitor respiratory status ( rate , rhythm, depth, Pao2, Paco2, PH and bicarbonate
level) to assess changes in neurologic status
 Monitor patients ICP and neurological responses to care activities as ICP can
increase with change in positioning and movements.
 Administered vasopressin, calcium channel blocker, anticoagulant medication,
anti platelet medication, thrombolytic medications as order to increase tissue
perfusion
 Administered volume expander as order to maintain hemodynamic parameters
 Avoid neck flexion or extreme hip/knee flexion to avoid obstruction of arterial or
venous blood flow

Enhance airway clearance

 Auscultate breath sounds, noting area of decreased/ absent ventilation and

presence of adventitious sounds to obtain ongoing data on patient’s response to
therapy
 Removing secretion by encouraging coughing or by suctioning to clear airway.
 Assist patient to a sitting position with head slightly flexed, shoulder relaxed and
knee flexed to provide optimal positioning for generating maximum intra-thoracic
pressure during cough
 Instruct patient to inhale deeply, bend forward slightly and perform three to four
huffs to expel secretions
 Encourage incentive spirometry to open collapsed alveoli, promote deep breathing
and prevent atelectasis.

Preventing Falls and Other Injuries

 Maintain bed rest during acute phase (24 to 48 hours after onset of stroke) with head of
bed slightly elevated and side rails in place.
 Administer oxygen as ordered during acute phase to maximize cerebral oxygenation.
 Frequently assess respiratory status, vital signs, heart rate and rhythm, and urine output to
maintain and support vital functions.
 When patient becomes more alert after acute phase, maintain frequent vigilance and
interactions aimed at orienting, assessing, and meeting the needs of the patient.
 Try to allay confusion and agitation with calm reassurance and presence.
 Assess patient for risk for fall status.

Optimizing Cognitive Abilities

 Be aware of the patient's cognitive alterations, and adjust interaction and environment
accordingly.
 Participate in cognitive retraining program reality orientation, visual imagery, cueing
procedures as outlined by rehabilitation nurse or therapist.
 In patients with increased awareness, use pictures of family members, clock, calendar;
post schedule of daily activities where patient can see it.
 Focus on patient's strengths, and give positive feedback.
 Be aware that depression is common and therapy should include psychotherapy and
pharmacological agents.

Facilitating Communication

 Speak slowly, using visual cues and gestures; be consistent, and repeat as necessary.
 Speak directly to the patient while facing him.
 Give plenty of time for response, and reinforce attempts as well as correct responses.
 Minimize distractions.
 Use alternative methods of communication other than verbal, such as written words,
gestures, or pictures

Fostering Independence

 Teach patient to use nonaffected side for activities of daily living (ADLs) but not to
neglect affected side.
 Adjust the environment (eg, call light, tray) to side of awareness if spatial neglect or
visual field cuts are present; approach patient from uninvolved side.
 Teach the patient to scan environment if visual deficits are present.
 Encourage family to provide clothing a size larger than patient wears, with front closures,
Velcro, and stretch fabric; teach patient to dress while sitting to maintain balance.
 Make sure personal care items, urinal, and commode are nearby and that patient obtains
assistance with transfers and other activities as needed.
 Be aware that ADLs require anticipatory (automatic coordination of multiple muscle
groups in anticipation of a specific movement) and reactive (adjustment of posture to
stimuli) postural adjustments.
 Be aware that patients usually have clear goals in relation to functional abilities, against
which all success and forward progress will be measured; help them set realistic short-
and long-term goals

Promoting Adequate Oral Intake

 Initiate referral for a speech therapist for individuals with compromised LOC, dyspraxic
speech, or speech difficulties, to evaluate swallowing function at bedside or
radiographically to demonstrate safe and functional swallowing mechanisms before
initiation of oral diet.
 Help patient relearn swallowing sequence using compensatory techniques.
o Place ice on tongue and encourage sucking.
 o Progress to ice pops and soft foods.
o Make sure mechanical soft or pureed diet is provided, based on ability to chew.
 Encourage small, frequent meals, and allow plenty of time to chew and swallow. Dietary
consults can be helpful for selection of food preferences.
 Remind patient to chew on unaffected side.
 Encourage patient to drink small sips from a straw with chin tucked to the chest,
strengthening effort to swallow while chin is tucked down.
 Inspect mouth for food collection and pocketing before entry of each new bolus of food.
 Inspect oral buccosa for injury from biting tongue or cheek.
 Encourage frequent oral hygiene.
 Teach the family how to assist the patient with meals to facilitate chewing and
swallowing.
o Reduce environmental distractions to improve patient concentration.
o Provide oral care before eating to improve aesthetics and afterward to remove
food debris.
o Position the patient so he is sitting with 90 degrees of flexion at the hips and 45
degrees of flexion at the neck. Use pillows to achieve correct position.
o Maintain position for 30 to 45 minutes after meals to prevent regurgitation and
aspiration.

Attaining Bladder Control

 Insert indwelling bladder catheterization during acute stage for accurate fluid
management; remove as soon as status stabilizes.
 Establish regular voiding schedule every 2 to 3 hours, correlated with fluid intake when
bladder tone returns. If patient is unable to void, intermittent catheterization can be used
to empty bladder and prevent overstretching of bladder. The bladder scan device is useful
in monitoring bladder capacity and identifying individuals at risk.
 Assist with standing or sitting to void (especially males).

Strengthening Family Coping

 Encourage the family to maintain outside interests.

 Teach stress management techniques, such as relaxation exercises, use of community and
faith-based support networks.
 Encourage participation in support group for family respite program for caregivers, or
other available resources in area.
 Involve as many family and friends in care as possible.
 Provide information about stroke and expected outcome.
 Teach family that stroke survivors do show depression in the first 3 months of recovery

Patient Education and Health Maintenance

 Teach the patient and family to adapt home environment for safety and ease of use.
 Instruct the patient of the need for rest periods throughout day.
  Reassure the family that it is common for poststroke patients to experience emotional
lability and depression; treatment can be given.
 Encourage consistency in the environment without distraction.
 Assist family to obtain self-help aids for the patient.
 Instruct the family in management of aphasia (see Box 15 3).
 Educate those at risk for stroke about lifestyle modifications and medication therapy that
can lower risk (see page 490).
 Refer the patient/family for more information and support to such agencies as The
National Stroke Association

Risk Factors for Stroke

Medical Conditions

 Hypertension (30% to 40% risk reduction with treatment): goal BP is lower than 140/90;
if renal insufficiency or heart failure, less than 130/85; if diabetic, less than 130/80
 Cardiac disorders congenital heart disease, valvular conditions, endocarditis
 Atrial fibrillation (risk reduction is 68% with oral anticoagulant therapy; 21% with
aspirin therapy for nonvalvular causes)
 Diabetes mellitus (44% risk reduction in hypertensive diabetics with controlled BP)
 Hyperlipidemia (20% to 30% risk reduction with those with known coronary heart
disease [CHD] on statin therapy): goal LDL is less than 160 mg/dL if one or no risk
factor; less than 130 if two or fewer risk factors or 10-year CHD risk is less than 20%;
less than 100 if two or fewer risk factors and 10-year CHD risk greater than 20%
 Carotid stenosis
 Prior history of TIA or stroke
 Elevated homocysteine level in blood

Behaviors

 Cigarette smoking (50% risk reduction in 1 year; return to baseline in 5 years)

 Alcohol abuse
 Physical inactivity
 Cocaine use (hemorrhagic stroke)

Nonmodifiable factors

 Increasing age risk doubles for each decade over age 50

 Gender men are at greater risk than women
 Heredity increased risk with family history of stroke
 Ethnic background Blacks and Hispanics at higher risk than Whites
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