Cerebrovascular accident(Stroke)

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Cerebrovascular accident(Stroke)

 It refers to any functional abnormality of the CNS that occurs

when the normal blood supply to the brain is disrupted.
 Sudden loss of neurological function is the hallmark of
cerebrovascular disease
 It is the third commonest cause of death in developed world
 Following Coronary heart diseases and cancer.
 It is a leading cause of disability
 Approximately 500,000 people experience a new stroke.
 Approximately 160,000 die of a stroke each year
 The prevalence and incidence of stroke is also on the rise in
developing countries

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Classification of Stroke

A. Based on Etiology
1.Ischemic stroke (85%)- It is termed “brain attack” is a sudden loss
of function. Ischemic stroke can be:
 Thrombotic
 Cardiogenic embolic stroke
 Cryptogenic
 Other strokes
2.Hemorrhagic Stroke(15%) : it can be caused by
 Intracranial hemorrhage: unrecognized or poorly controlled
hypertention.
 Subarachnoid hemorrhage : ruptured intracranial aneurysm, or
certain medications (eg, anticoagulants and amphetamine)
 Subdural hematomas
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B. Classification based on duration of stroke
A. Transient Ischemic attack/TIA/: -
 focal neurologic deficit lasting < 24hrs
 Confined to an area of brain perfused by specific artery.
B. Reversible Ischemic neurologic deficit:
 Sudden onset focal neurologic deficit which lasts for more than
24hrs, but the neurologic deficit recovers/resolves/.
C. Stroke in evolution:
 A focal neurologic deficit and the degree of which is progressing
over a couple of hours or days.
D .Complete Stroke:
 Sudden onset of focal neurologic deficit, in which the deficit

neither improves nor gets worse over time.

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 It is often associated with infarction of whole part of the brain.
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Causes stroke
 Ischemic stroke occurs when the occlusion evolves from partial to
complete due to thrombosis formation and Embolic from cardiac
origin
 A hemorrhagic stroke
 A ruptured
 Leaking aneurysm
 An arteriovenous malformation
 A bleeding disorder
 Trauma
 An arterial rupture (as caused by hypertension)

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 Pathophysiology of Ischemic stroke

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 Clinical manifestations

 Symptoms are determined by the circulatory vessel that

is obstructed or affected.
 Most commonly the middle cerebral arteries are
affected
 Supply to the lateral portion of the cerebral hemispheres
that house the motor and sensory areas for the upper
extremities and face, as well as the speech center.
(Contra lateral face and arm)

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Clinical Manifestations….
 Of all strokes, those due to cerebral embolism develop
most rapidly
Affects many body functions
o Motor activity
o Elimination
o Intellectual function
o Perceptual alterations
o Personality
o Affect
o Sensation
o Communication

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 Clinical Manifestations….
Visual Field Deficits
o Homonymous hemianopsia (loss of half of the visual field)
o Loss of peripheral vision
o Diplopia
Motor Deficits
o Hemiparesis
o Hemiplegia
o Ataxia
o Dysarthria
o Dysphagia
Sensory Deficits
o Paresthesia (occurs on the side opposite the lesion)
Verbal Deficits
18 Aphasia
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 Clinical Manifestations….
Emotional Deficits
Cognitive Deficits
 Loss of self-control
 Short- and long-term
 Emotional lability/altered
memory loss
 Decreased tolerance to
 Decreased attention span
 Impaired ability to
stressful situations
 Depression
concentrate
 Withdrawal
 Poor abstract reasoning
 Fear, hostility, and anger
 Altered judgment
 Feelings of isolation

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 Diagnostic Studies
 Diagnostic studies are done to confirm and identify likely
causes.
 CT is the primary diagnostic test used after a stroke.
 CT identifies or exclude hemorrhage as the cause of
stroke, and they identify extra parenchymal hemorrhages,
neoplasms, abscesses, and other conditions
 MRI- reliably documents the extent and location of
infarction in all areas of the brain

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Diagnostic Studies…
Additional studies
CBC
Platelets, PT, PTT
Electrolytes, blood glucose
Renal and hepatic studies
Lipid profile:- LDL, HDL

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Managemet of stroke
 Interruption of further brain damage.

 Management of complication.

 Control progression

 To allow the brain to recover from the initial insult (bleeding)

 To prevent or minimize the risk of re-bleeding and

 To prevent or treat other complications.

Note: Stroke management is the most effective patient arrive less

than three hours within hospital especially thrombolytic agent
treatment
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 Managemet of stroke….
The goal for the emergent management of stroke is to
complete the following within 60 minutes or less of patient
arrival:
 Assess (ABCs) and stabilize the patient as necessary
 Complete the initial evaluation and assessment, including
imaging and laboratory studies
 Initiate reperfusion therapy, if appropriate
Critical treatment decisions focus on the following:
 The need for airway management
 Optimal blood pressure control
 Identifying potential reperfusion therapies

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 Collaborative Care-Acute Care
Initial intervention
Ensure patient airway
Remove dentures
Perform pulse oximetry
Maintain adequate oxygenation
IV access with normal saline
Maintain BP according to guidelines

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 Collaborative Care-Acute Care…
Initial Interventions
Remove clothing
Obtain CT scan immediately
Perform baseline laboratory tests
Position head midline
Elevate head of bed 30 degrees if no symptoms of
shock or injury
Frequent Monitoring of vital signs and neurologic
status

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 B. Management of Specific Etiologies
1) Atherosclerotic stroke (Thrombotic stroke )
i) Thrombolytic therapy: tpA, to patients who present within
3 hrs of onset of stroke, helps to lyse the thrombus and
restore perfusion to the affected brain.
ii) Anticoagulants: Low dose heparin can be given for
prevention of thromboembolism.
iii) Anti-platelet aggregation agents:
o Aspirin reduces the incidence of stroke and vascular
mortality.
o General recommendation is to give 325 mg of ASA once
daily.
o It may not help to resolve the already formed thrombus, but
26 ASA prevents recurrence of stroke.
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 Cont…
2) Embolic stroke: (Cardiogenic embolus)
 Anticoagulation is indicated to prevent recurrent embolic
stroke.
 Anticoagulation with heparin should be initiated when the
acute phase of stroke is over.
 Warfarin is used for chronic anticoagulation.
3) Intra-cerebral hemorrhage
 Continue supportive measures
 Control very high blood pressure
 Surgical consultation is indicated for removing cerebellar
hematoma, as it may compress vital centers in the
brainstem.
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 Con’t…..
4) Subarachnoid Hemorrhage
 Medical therapy:
(a) Supportive measures include bed rest, sedatives,
analgesic, laxative,
(b) Control of hypertension and
(c) Nimodipin (calcium channel blocker) is given to
prevent neurologic deterioration due to vasospasm.

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 Surgical intervention
 To relieve pressure and control bleeding if hemorrhage is
present.
 Carotid endarterectomy

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 Prevention
Primary stroke prevention refers to the treatment of
individuals with no previous history of stroke. Measures
may include use of the following:
 Platelet antiaggregants
 Statins
 Exercise
 Lifestyle interventions (eg, smoking cessation, alcohol
moderation)

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 Nursing process
Assessment
 Weigh patients
 Level of consciousness or responsiveness, ability to speak,
and orientation
 Muscle tone, body posture, and head position
 Stiffness or flaccidity of the neck
 Volume of fluids ingested or administered and volume of
urine excreted per 24 hours
 Blood pressure maintained within normal limits
 nursing assessment on impairment of function in patient’s
daily activities.
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 Nursing diagnosis
 Impaired physical mobility related to hemiparesis, loss of
balance and coordination, spasticity, and brain injury
 Acute pain related to hemiplegia and disuse
 Deficient self-care (bathing, hygiene, toileting, dressing,
grooming, and feeding) related to stroke sequelae
 Disturbed sensory perception (kinesthetic, tactile, or
visual) related to altered sensory reception, transmission,
and/or integration.
 Disturbed thought processes related to brain damage
 Impaired verbal communication related to brain damage
 Risk for impaired skin integrity related to hemiparesis or
hemiplegia, decreased mobility
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 Planning and Goals
 Improved mobility,
 Achievement of self-care,
 Relief of sensory and perceptual deprivation,
prevention of aspiration,
 Continence of bowel and bladder,
 Improved thought processes,
 Achieving a form of communication,
 Maintaining skin integrity,
 Restored family functioning,
 Improved sexual function, and absence of
complications.
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 Nursing Intervention
Improving Mobility and Preventing Deformities
 Apply a splint at night to prevent flexion of affected
extremity.
 Assist in maintaining good body alignment
 Elevate affected arm to prevent edema and fibrosis.
 Change position every 2 hours; place patient in a prone
position for 15 to 30 minutes several times a day

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 Nursing intervention…
 Establishing an Exercise Program
o Provide full range of motion 4 – 5 times a day
o Encourage patient to exercise unaffected side
o Preparing for Ambulation. Sit, stand and walk slowly, if
dizziness use wheel chair
o Elevate arm and hand to prevent dependent edema of
the hand

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 Nursing intervention…
 Enhancing Self-Care
 Encourage personal hygiene activities as soon as the
patient can sit up;
 Assist with dressing activities (e.g. clothing)
 Improving Family Coping
 Provide counseling and support to family
 Encourage everyone to approach patient with a
supportive and optimistic attitude,

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 Differential diagnosis
 TIA
 Seizure
 Migraine
 Brain abscess,
 Meningioma,
 Glioblastoma ,
 Hypoglycemia:-
 HHNC
 Metastatic brain tumors.

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 Intracranial pressure

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Intracranial pressure
 ICP is a measure of the pressure in the cranial cavity
 0 to 15 mm Hg is normal
 16 to 20 mm Hg is mildly elevated
 21 to 30 mm Hg is moderately elevated
 31 mm Hg or more is severely elevated
 The adult skull has a fixed volume of intracranial components
 80% brain tissue
 10% blood
 10% CSF

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 Intracranial pressure ….
 Increase in ICP is a serious medical problem
 The pressure itself can damage the brain or spinal cord
by pressing on important brain structures and by
restricting blood flow into the brain.
 The degree to which these factors increase ICP
depends on the ability of the brain to accommodate to
the changes
 Sustained increases in ICP result in brainstem
compression and herniation of the brain from one
compartment to another.
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 Regulation and Maintenance for ICP
If the volume in any one of the components (brain
tissue, blood, and CSF)
 increases within the cranial vault and the volume from
another component is displaced, the total intracranial
volume will not change
Normal compensatory adaptations
Alteration of CSF absorption or production
Shunting of CSF into spinal subarachnoid space
Shunting of venous blood out of the skull

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Increase in CSF result from
 Decreased absorption
 Obstructed circulation of CSF
 Normal fluctuation in intracranial Pressure occurs when
coughing, sneezing & straining.

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 Factors that influence ICP
 Arterial pressure
 Venous pressure
 Intraabdominal and intrathoracic pressure
 Posture
 Temperature
 Blood gases (CO2 levels)

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 Causes of increased ICP
 ICP can become elevated for various reasons in response to disease,
environment, emotion and normal bodily functions
 rising in CSF pressure
 increased pressure in brain matter
 bleeding into the brain
 bleeding into the fluid around the brain
 swelling within the brain matter

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Elevated ICP----

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Elevated ICP----

 Why is it Important to keep ICP in normal value ?

 Maintaining cerebral perfusion pressure is the main focus in
management of cerebral injuries that impact the 3 components in the
central system such as brain/blood/CSF
 CPP is calculated using the Mean Arterial Pressure (MAP) and
Intracranial Pressure (ICP) : CPP = MAP – ICP
 Normal CPP 60 to 100 mmHg
 Goal is to maintain a minimum of 60mmHg for brain injuries
 Cerebral Perfusion Pressure (CPP) values of
 CPP >150 mmHg disrupts the blood brain barrier and causes hyper
perfusion and potentially brain edema / swelling. This could
potentially lead to herniation syndrome
 CPP <50 mmHg causes hypoperfusion and brain ischemia
 CPP <30 mmHg Causes irreversible ischemia and damage
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S & S of Increased ICP depend on
 Compartmental location of lesion (supratentorial or

infratentorial)
 Specific location of mass (cerebral hemispheres, brain stem or

cerebellum)
 Degree of intracranial compensation (compliance)

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 Clinical
Change
Manifestations
in level of consciousness
 Abnormal respiratory and vasomotor response
 The earliest sign of ICP is
 Lethargy
 Slowing of speech and delay in response to verbal
suggestions
 Confusion
 Restlessness Results from compression of brain
 Drowsiness
 As pressure increase pt. reacts only to loud auditory or
painful stimuli
 Abnormal motor response
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Cushing’s Triad

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 Diagnosis
 History taking
 Neurological examination
 taking vital signs
 laboratory investigation
 Advanced diagnostic imaging tools
 observation of traids signs of ICP
 hypertension with wide pulse ,
 Bradycardia ,
 irregular respirations and Seizure

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 Management
 Osmotic Diuretics to decrease the volume of brain
and ECF-Mannitol
 Corticosteroid - Decrease edema secondary to brain
tumor
 Dobutamine hydrochloride – to improve cardiac out
put
 Reducing metabolic demand – barbiturates
 Controlling fever -antipyretics

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 Management…..
 Hyperventilation therapy: suctioning →hyperventilate
with 100% oxygen
 Adequate oxygenation
 PaO2 maintenance at 100 mm Hg or greater
 ABG analysis guides the oxygen therapy
 May require mechanical ventilator

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 Management ………
 Nutritional therapy
 Patient is in hypermetabolic and hypercatabolic state-
Need for glucose
 Keep patient normovolemic
 IV 0.45% or 0.9% sodium chloride

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 Management …….
 Maintain patent airway
 Normal fluid and electrolyte balance
 No complications secondary to immobility
 Respiratory function
 Fluid and electrolyte balance
 Body position maintained in head-up position: elevate
HOB 30°
 Protection from injury: positioning/turning
 Pain control
 Psychological considerations

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 Complications
 Brain stem herniation
 Diabetes Insipidus /DI/ ADH

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