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Cerebral Vascular

Accident
STROKE

RISK FACTORS FOR STROKES


Nonmodifiable

Age- incidence
with age until age
75.
Race- higher in
African Americans
Gender- higher in
men
Heredity- family
history increases risk

Potentially

Modifiable

Lifestyle- excessive
alcohol, cigarette
smoking, obesity, high
fat diet, drug abuse.
Pathologic conditionscardiac disease, DM,
HTN, migraine
headaches,
hypercoagulability
states.

ETIOLOGY AND PATHO


Extra-cranial

factors- related to the


circulatory system.
Systemic blood pressure- <70 and >160
cardiac output- when reduced by 30%
cerebral blood flow is reduced.
Blood viscosity- anemia increases cerebral
blood flow and polycythemia reduces it.

INTRACRANIAL FACTORS
A.

Metabolic factors

Increased CO2 and low O2 results in


vasodilation to restore blood flow to
normal.
CO2 is the most potent regulator of
cerebral blood flow.
Increased Hydrogen ion concentration
increases cerebral blood flow.

Intracranial factors, contd


B.

Blood vessels

The condition of the blood vessels


supplying the brain is important!!!
Potential

problems- congenital anomalies


(tortuosity, coiling, kinking, and AV
malformations).
The malformations interfere with cerebral blood
flow and contribute to atherosclerotic disease
Collateral circulation develops
Circle of Willis

Intracranial factors, contd


C.

Intracranial pressure

ICP increases with an assault to brain.


Causes of ICP: stroke, neoplasms,
inflammation, trauma, and hydrocephalus.
ICP compresses the brain and reduces
cerebral blood flow, which may lead to
infarct.
Both extracranial and intracranial factors
may lead to stroke

Atherosclerosis
An

abnormal accumulation and infiltration of


in the intima of the arteries.
Plaques develop in an area of high turbulence;
which may later damage the plaque.
Platelets and fibrin aggregate or collect on the
surface of the plaque.
Parts of the plaque breaks off and travel to a
narrower distal artery
Cerebral infarct occurs.

TYPES OF STROKE
Ischemic:

Most common type of stroke!

Occurs due to decreased blood flow to an


area of the brain due to partial or complete
occlusion of and artery due to thrombosis.
This lack of blood, oxygen and nutrients to
an area of the brain causes necrosis of
cerebral tissue.
Two types: thrombotic and embolic
See Lewis, page 1648; table 55-1.

Thrombotic stroke
Most

common cause of cerebral infarct!


Cause: Due to formation of a blood clot or
coagulation of blood that results in
narrowing of blood vessel or occlusion.
2/3 of strokes due to HTN or DM.
(accelerate the atherosclerotic process)
May also be due to oral contraceptives,
coagulation disorders, polycythemia,
arteritis, chronic hypoxia and dehydration.

Thrombotic Stroke
Thrombotic

strokes are usually


proceeded by prodromal episodes
(warnings) called TIAs (transient
ischemic attacks).
TIAs last from 5 to 30 minutes.
Include- paresis or decreased strength and
motion of an extremity.
Aphasia or disturbance of language function,
Paralysis, mental confusion, or visual
disturbances.

Thrombotic stroke
The

extent of the stoke depends on rapidity of


onset, size of lesion, and presence collateral
circulation.
There is a pattern to thrombotic stroke!
1. single attack; symptoms occur over several hours
2. intermittent progression toward a stroke over
hours or days.
3. partial stroke with permanent neuro deficits
4. series of TIAs followed by a stroke with
permanent neuro deficits.

Thrombotic stroke
Symptoms

at 72 hours are usually due


to resulting edema to tissues;
symptoms improve after edema
subsides (@ 2 weeks).
This type of stroke occurs during or
after stroke.

EMBOLIC STROKE
Cerebral

embolism results from occlusion


of cerebral artery by an embolus.
Necrosis and cerebral edema results.
Embolus is the second most common
cause of stroke.
Most emboli originate in the
endocardium with plaques or tissue
breaking off and entering circulation.

Embolic Stroke
Emboli

are associated with heart


conditions such as;

A fib
MI
Infective endocarditis
Rheumatic heart disease
Valvular prostheses
ASD

Embolic stroke
Less

common causes of emboli:

Air
Fat from long bone fracture
Amniotic fluid postpartum
tumors

Embolic stroke
Prodromal

warning less likely; single

events
sudden onset
Most commonly related to head
trauma
High rate of re-occurrence if cause is
not treated.

Hemorrhagic stroke
Intracerebral

hemorrhage is bleeding
within the brain caused by rupture of a
blood vessel that lasts from minutes to
days.
Most commonly caused by HTN
May be caused by brain tumors,
trauma, thrombolytic drugs, and
ruptured aneurysms.

Hemorrhagic stroke
Blood

within the closed area of the


brain imposes pressure on the brain
tissue and displaces brain tissue and
decreases blood flow to brain.
Clinical manifestations depends on the
site and amount of hemorrhage and
resultant damage.
Poor prognosis; 70% die

Subarachnoid stroke
Caused

by aneurysms, AV malformations,
trauma, and HTN.
May have prodromal symptoms if
ballooning or dilation applies pressure to
brain tissue.
May suddenly rupture, causing neuro
changes
Majority of aneurysms are in the Circle of
Willis

Subarachnoid hemorrhage,
contd
If

aneurysm leaks, pt may have a headache!


Rupture of aneurysm causes pressure in
subarachnoid space due to bleeding. Clinical
manifestations:
Headache, lethargy, confusion, nausea, vomiting,
fever, neck pain, and backaches, paralysis, coma and
death.
Massive hemorrhage is defines as 30 to 50 ml of blood.
Watch for re-bleeding when clot starts to dissolve.
(usually within first 2 weeks post rupture). Reduce
activity and prevent straining.

Temporal Development of
CVA
Transient

Ischemic Attacks (TIAs)-

Brief episodes of neuro manifestations


(less than 24 hours).
Leaves no residual effects
Three categories:
1/3

never have another TIA


1/3 will have more than one TIA
1/3 will have a stroke
WARNING SIGNS OF PROGRESSING CVA!

TIAs
s/s

vary depending on the part of brain


affected.
Treatment:
Medications such as aspirin, Persantine
(dipyridamole), Ticlid, and anticoagulant
medication.
Long term therapy post TIA
Surgical treatment- carotid endartarectomy,
extra-cranial- intracranial bypass (EC-IC
bypass), and transiluminal angioplasty.

Reversible ischemic Neurologic


Deficit
A

neuro deficit which remains 24 hours


after onset; but leaves no residual
signs or symptoms.
Considered a completed stroke with
minimal to no residual deficits

Stroke In- Evolution


A

progressive stroke which develops


over hours or days.
Characteristic of an enlarging intraarterial thrombus.
A stepwise or intermittent progression of
deterioration of neurological symptoms.
Manifestations do not resolve and leave
residual damage.

Completed Stroke
Neuro

defects unchanged over 2 to 3

days.
Usually embolic in nature
Also called stable stroke.
Signals readiness for aggressive rehab
therapy. (unless an aneurysm is
involved).

Clinical Manifestations
All

deficits are directly related to area


of brain that is involved.

See

Lewis, page 1650, Table 55-2.

Neuromotor Function
Destruction

of motor neurons in the


pyramidal pathway causes:

Mobility
Respiratory function
Swallowing and speech
Gag reflex
Self-care abilities

Motor deficits
Loss

of skilled voluntary movement


(akinesia).
Impairment of integration of
movements
Alterations in muscle tones
Alteration in reflexes
Initial hypo-reflexia which progresses
to hyper-reflexia for most patients.

Patterns of deficits
Contralateral

deficits

A lesion on one side of the brain affects the


motor function on the other side of the brain.
The arms and legs on the affected side may
be weak or paralyzed to different degrees
depending the degree of cerebral circulation
compromised.
See Lewis, Page 1651; Table 55-5

The

affected shoulder tends to rotate


internally; the hip rotates externally.
The affected foot is plantar flexed and
inverted.
An initial period of flaccidity may lasts
for several days to weeks.
Spasticity of muscles follows the
flaccid stage and is related to
interruption of upper neuron influence.

Communication
Aphasia-

total loss of comprehension and


use of language due to damage to the
dominant hemisphere (left hemisphere).
Dysphasia-dysfunction related to
comprehension or use of language due to
partial disruption or loss.
Non-fluent (minimal speech activity with slow
speech that requires obvious effort)
Fluent- (speech is present, but contains little
meaningful communication).

Communication
Conductive

aphasia- mixture of both


expressive and receptive aphasia
Global aphasia- results from a massive
lesion and there is virtual loss of all
language ability.

Communication, contd
Wernickes

area damage

Receptive aphasia where neither the sound or


speech or its meaning can be understood.
Impaired comprehension of both spoken and
written language.

Bocas area damage


Expressive aphasia (difficulty speaking and writing)
Dysarthria- disturbance in muscular control of
speech. (pronunciation, articulation, phonation)
DOES NOT EFFECT COMPREHENSION OF
LANGUAGE.

Affect
May

be unable to control emotions


May be depressed RT body image and
loss of function
May be frustrated RT immobility and
communication issues

Intellectual Function
Memory

and judgment may be


impaired
Left-sided stroke patients are more
cautious in judgment and movement.
Right-sided stroke patients more
impulsive and move quicker.

Spatial-Perceptual Alterations
Right

sided stroke patient has more


spatial-perceptual orientation issues:
Erroneous perception of self and illness
(may deny illness or body parts).
Erroneous perception of self in space (may
ignore affected side; cant judge distances)
Agnosia or inability to recognize an object
by sight, touch or hearing.
Apraxia or the inability to carry out learned
sequential movements on command.

Elimination
Most

occur initially and are transient.


Frequent constipation DT immobility,
weak abdominal muscles, dehydration,
and diminished defecation reflexes.
Urinary and bowel elimination may be
DT functional inabilities to express
needs and manage clothing.

Diagnostic Studies
CT

Scan- indicate size and location of


lesion, differentiates between infarct
and hemorrhage, effectiveness of
treatment, and evaluate the course of
healing.
MRI- considered best method to
differentiate between hemorrhage and
infarct.

Diagnostics
PET

shows chemical activity and depicts


extent if tissue damage.
DSA- IV or arterial injection of contrast
material to visualize blood vessels.
TDA- transcranial doppler measures
velocity of cerebral blood flow in the
arteries, also detects micro-emboli.
LP may be done to detect blood or WBCs
(not done if increased ICP is suspected)

Collaborative care
PREVENTION

Healthy diet
Weight control
Regular exercise
No SMOKING
Limiting alcohol
Routine health assessment

DRUG THERAPY
Prophylactic

low dose aspirin, daily.


Persantine 50 mg 3 X day decreases
platelet aggregation which helps to
decrease risk of thrombus and
embolus formation.
TICLID or PLAVIX- platelet aggregation
inhibitors

Surgical Therapy
Carotid

endarterectomy (CEA)- the


atheromatous lesion is removed from
the carotid artery to improve blood
flow
Decreases stroke and death in patient
with TIAs.
Done on patient with 70-99% occlusion

Transluminal Angioplasty
Insertion

of balloon to open stenosed


artery to permit blood flow.
Patient with symptomatic stenosis of
vertebrobasilar or carotid arteries
Risk of dislodging emboli

EC-IC BYPASS
Extracranial-intracranial

bypass

Used when obstruction cannot be


removed directly
A branch of extracranial artery is
anastomosed to a branch of intracranial
artery just beyond the area of obstruction.
Patients at high risk for stroke and require
close-long term assessment and
management.

ACUTE CARE
Table

55-5; Lewis page 1654.


Initially
Ensure patent airway DT altered level of
consciousness.
Remove

dentures

Administer oxygen via nasal cannula or


non-rebreather mask DT respiratory
distress

Acute Care
Establish

IV access with normal saline


to maintain BP
Remove clothing
Obtain immediate CT Scan
Monitor VS, LOC, O2 sats, cardiac
rhythms, Glasgow Coma Scale, pupil
size and reactivity.

Acute Care
Maintain

patient warmth
Reassure patient and family

Ischemic Cascade
Series

of events in response to
thrombotic and embolic strokes.
Ischemic area becomes discolored and
soft, initially. However, around the border
there is an area of perfusion called the
ischemic penumbra that maintains
perfusion for 3 to 6 hours post stroke.
If adequate blood flow is reinitiated during
this period, less neuro damage results

Treatment
Control

fluid and electrolyte balance

Adequate hydration promotes perfusion to


the brain; however over hydration may
increase cerebral edema!
Total intake (oral, tube feedings, IV etc.,
1500-2000 per day)
Monitor urine output ( if ADH released
urine output will decrease)

Treatment
IV

solutions with glucose and water are


avoided. (hypertonic solutions may
increase cerebral edema)
Increased ICP from cerebral edema
peaks in 72 hours and may cause
brain herniation.

How to manage ICP


Enhance

venous drainage by:

Elevating HOB
Maintain head and neck in alignment
Avoidance of hip flexion
Limit cerebral tissue metabolism and
vasodilation by:
avoiding hyperthermia, avoiding
hypervolemia, manage constipation

Medications
Diuretics

(decrease cerebral edema)

Mannitol (Osmitrol)
Lasix, (Furosemide)
Dexamethasone for patients with
vasogenic edema

Drug Therapy
Thrombolytic

therapy

Recombinant tissue plasminogen activator


(t-PA)- to re-establish blood flow and prevent
cell death for patients with ischemic strokes.
Patients who receive t-PA within 3 hours
after a stroke more likely to have 32% less
injury three months after stroke.
T-PA works by lysis thrombus/clot by binding
and digesting the fibrin and fibrinogen.

t-PA
Clot specific
Less likely to cause hemorrhage as
compared to streptokinase or
urokinase.
Single most important factor is
timing!!!

t-PA
Patients

are screened for coagulation


disorders, GI bleeding, and hemorrhagic
stroke before initiation of treatment.
Major side effect is cerebral hemorrhage.
Monitor VS during treatment/ control BP
O anticoagulants or antiplatelet drug for
25 hours post treatment.

Platelet inhibition/anticoagulant
therapy
Heparin,

coumadin, aspirin, ticlipidine


(Ticlid), clopidrogel (Plavix),
dipyridamole (Persantine).
Contraindicated for patients with
hemorrhagic strokes
Monitor PT/ PTT
Monitor patient for bleeding

Drug therapy
Calcium

channel blockers are given for


patients with hemorrhagic strokes.
Excess intracellular calcium may be
harmful to brain tissue.
Nimodipine (Nimotop) decreases
effects of vasospasm and minimizes
tissue damage.
Aspirin decreases platelet aggregation
at site of plaque.

Drug therapy
Tylenol

treats hyperthermia
Dilantin may be given for seizures

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