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Cerebral Vascular Cerebral Vascular Accident Accident STROKE STROKE

Cerebral Vascular Accident

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Cerebral Vascular Accident. STROKE. Nonmodifiable Age- incidence ↑ with age until age 75. Race- higher in African Americans Gender- higher in men Heredity- family history increases risk. Potentially Modifiable - PowerPoint PPT Presentation

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Page 1: Cerebral Vascular Accident

Cerebral Vascular Cerebral Vascular AccidentAccident

STROKESTROKE

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RISK FACTORS FOR STROKESRISK FACTORS FOR STROKES

►NonmodifiableNonmodifiable Age- incidence Age- incidence ↑ ↑

with age until age with age until age 75.75.

Race- higher in Race- higher in African AmericansAfrican Americans

Gender- higher in Gender- higher in menmen

Heredity- family Heredity- family history increases riskhistory increases risk

► Potentially ModifiablePotentially Modifiable Lifestyle- excessive Lifestyle- excessive

alcohol, cigarette alcohol, cigarette smoking, obesity, high smoking, obesity, high fat diet, drug abuse.fat diet, drug abuse.

Pathologic conditions- Pathologic conditions- cardiac disease, DM, cardiac disease, DM, HTN, migraine HTN, migraine headaches, headaches, hypercoagulability hypercoagulability states.states.

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ETIOLOGY AND PATHOETIOLOGY AND PATHO

►Extra-cranial factors- related to the Extra-cranial factors- related to the circulatory system.circulatory system. Systemic blood pressure- <70 and >160Systemic blood pressure- <70 and >160 cardiac output- when reduced by 30% cardiac output- when reduced by 30%

cerebral blood flow is reduced.cerebral blood flow is reduced. Blood viscosity- anemia increases cerebral Blood viscosity- anemia increases cerebral

blood flow and polycythemia reduces it.blood flow and polycythemia reduces it.

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INTRACRANIAL FACTORSINTRACRANIAL FACTORS

►A. Metabolic factorsA. Metabolic factors Increased CO2 and low O2 results in Increased CO2 and low O2 results in

vasodilation to restore blood flow to vasodilation to restore blood flow to normal.normal.

CO2 is the most potent regulator of CO2 is the most potent regulator of cerebral blood flow.cerebral blood flow.

Increased Hydrogen ion concentration Increased Hydrogen ion concentration increases cerebral blood flow.increases cerebral blood flow.

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Intracranial factors, cont’dIntracranial factors, cont’d

►B. Blood vesselsB. Blood vessels The condition of the blood vessels The condition of the blood vessels

supplying the brain is important!!!supplying the brain is important!!!►Potential problems- congenital anomalies Potential problems- congenital anomalies

(tortuosity, coiling, kinking, and AV (tortuosity, coiling, kinking, and AV malformations).malformations).

►The malformations interfere with cerebral blood The malformations interfere with cerebral blood flow and contribute to atherosclerotic diseaseflow and contribute to atherosclerotic disease

►Collateral circulation developsCollateral circulation develops►Circle of WillisCircle of Willis

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Intracranial factors, cont’dIntracranial factors, cont’d

►C. Intracranial pressureC. Intracranial pressure ICP increases with an assault to brain.ICP increases with an assault to brain. Causes of ICP: stroke, neoplasms, Causes of ICP: stroke, neoplasms,

inflammation, trauma, and hydrocephalus.inflammation, trauma, and hydrocephalus. ICP compresses the brain and reduces ICP compresses the brain and reduces

cerebral blood flow, which may lead to cerebral blood flow, which may lead to infarct.infarct.

Both extracranial and intracranial factors Both extracranial and intracranial factors may lead to strokemay lead to stroke

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AtherosclerosisAtherosclerosis

► An abnormal accumulation and infiltration of An abnormal accumulation and infiltration of in the intima of the arteries.in the intima of the arteries.

► Plaques develop in an area of high Plaques develop in an area of high turbulence; which may later damage the turbulence; which may later damage the plaque.plaque.

► Platelets and fibrin aggregate or collect on Platelets and fibrin aggregate or collect on the surface of the plaque.the surface of the plaque.

► Parts of the plaque breaks off and travel to a Parts of the plaque breaks off and travel to a narrower distal arterynarrower distal artery

► Cerebral infarct occurs.Cerebral infarct occurs.

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TYPES OF STROKETYPES OF STROKE

► Ischemic: Most common type of stroke!Ischemic: Most common type of stroke! Occurs due to decreased blood flow to an Occurs due to decreased blood flow to an

area of the brain due to partial or complete area of the brain due to partial or complete occlusion of and artery due to thrombosis.occlusion of and artery due to thrombosis.

This lack of blood, oxygen and nutrients to This lack of blood, oxygen and nutrients to an area of the brain causes necrosis of an area of the brain causes necrosis of cerebral tissue.cerebral tissue.

Two types: thrombotic and embolicTwo types: thrombotic and embolic See Lewis, page 1648; table 55-1.See Lewis, page 1648; table 55-1.

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Thrombotic strokeThrombotic stroke

►Most common cause of cerebral infarct!Most common cause of cerebral infarct!►Cause: Due to formation of a blood clot Cause: Due to formation of a blood clot

or coagulation of blood that results in or coagulation of blood that results in narrowing of blood vessel or occlusion.narrowing of blood vessel or occlusion.

►2/3 of strokes due to HTN or DM. 2/3 of strokes due to HTN or DM. (accelerate the atherosclerotic process)(accelerate the atherosclerotic process)

►May also be due to oral contraceptives, May also be due to oral contraceptives, coagulation disorders, polycythemia, coagulation disorders, polycythemia, arteritis, chronic hypoxia and arteritis, chronic hypoxia and dehydration.dehydration.

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Thrombotic StrokeThrombotic Stroke

►Thrombotic strokes are usually Thrombotic strokes are usually proceeded by prodromal episodes proceeded by prodromal episodes (warnings) called TIA’s (transient (warnings) called TIA’s (transient ischemic attacks).ischemic attacks).

►TIA’s last from 5 to 30 minutes.TIA’s last from 5 to 30 minutes. Include- paresis or decreased strength and Include- paresis or decreased strength and

motion of an extremity.motion of an extremity. Aphasia or disturbance of language function,Aphasia or disturbance of language function, Paralysis, mental confusion, or visual Paralysis, mental confusion, or visual

disturbances.disturbances.

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Thrombotic strokeThrombotic stroke

► The extent of the stoke depends on rapidity The extent of the stoke depends on rapidity of onset, size of lesion, and presence of onset, size of lesion, and presence collateral circulation.collateral circulation.

► There is a pattern to thrombotic stroke!There is a pattern to thrombotic stroke! 1. single attack; symptoms occur over several 1. single attack; symptoms occur over several

hourshours 2. intermittent progression toward a stroke over 2. intermittent progression toward a stroke over

hours or days.hours or days. 3. partial stroke with permanent neuro deficits3. partial stroke with permanent neuro deficits 4. series of TIA’s followed by a stroke with 4. series of TIA’s followed by a stroke with

permanent neuro deficits.permanent neuro deficits.

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Thrombotic strokeThrombotic stroke

►Symptoms at 72 hours are usually due Symptoms at 72 hours are usually due to resulting edema to tissues; to resulting edema to tissues; symptoms improve after edema symptoms improve after edema subsides (@ 2 weeks).subsides (@ 2 weeks).

►This type of stroke occurs during or This type of stroke occurs during or after stroke.after stroke.

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EMBOLIC STROKEEMBOLIC STROKE

►Cerebral embolism results from Cerebral embolism results from occlusion of cerebral artery by an occlusion of cerebral artery by an embolus. embolus.

►Necrosis and cerebral edema results.Necrosis and cerebral edema results.►Embolus is the second most common Embolus is the second most common

cause of stroke.cause of stroke.►Most emboli originate in the Most emboli originate in the

endocardium with plaques or tissue endocardium with plaques or tissue breaking off and entering circulation.breaking off and entering circulation.

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Embolic StrokeEmbolic Stroke

►Emboli are associated with heart Emboli are associated with heart conditions such as;conditions such as; A fibA fib MIMI Infective endocarditisInfective endocarditis Rheumatic heart diseaseRheumatic heart disease Valvular prosthesesValvular prostheses ASDASD

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Embolic strokeEmbolic stroke

►Less common causes of emboli:Less common causes of emboli: AirAir Fat from long bone fractureFat from long bone fracture Amniotic fluid postpartumAmniotic fluid postpartum tumorstumors

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Embolic strokeEmbolic stroke

►Prodromal warning less likely; single Prodromal warning less likely; single eventsevents

►sudden onsetsudden onset►Most commonly related to head Most commonly related to head

traumatrauma►High rate of re-occurrence if cause is High rate of re-occurrence if cause is

not treated.not treated.

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Hemorrhagic strokeHemorrhagic stroke

► Intracerebral hemorrhageIntracerebral hemorrhage is bleeding is bleeding within the brain caused by rupture of a within the brain caused by rupture of a blood vessel that lasts from minutes to blood vessel that lasts from minutes to days.days.

►Most commonly caused by HTNMost commonly caused by HTN►May be caused by brain tumors, May be caused by brain tumors,

trauma, thrombolytic drugs, and trauma, thrombolytic drugs, and ruptured aneurysms.ruptured aneurysms.

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Hemorrhagic strokeHemorrhagic stroke

►Blood within the closed area of the Blood within the closed area of the brain imposes pressure on the brain brain imposes pressure on the brain tissue and displaces brain tissue and tissue and displaces brain tissue and decreases blood flow to brain.decreases blood flow to brain.

►Clinical manifestations depends on the Clinical manifestations depends on the site and amount of hemorrhage and site and amount of hemorrhage and resultant damage.resultant damage.

►Poor prognosis; 70% die Poor prognosis; 70% die

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Subarachnoid strokeSubarachnoid stroke

►Caused by aneurysms, AV Caused by aneurysms, AV malformations, trauma, and HTN.malformations, trauma, and HTN.

►May have prodromal symptoms if May have prodromal symptoms if ballooning or dilation applies pressure ballooning or dilation applies pressure to brain tissue.to brain tissue.

►May suddenly rupture, causing neuro May suddenly rupture, causing neuro changeschanges

►Majority of aneurysms are in the Majority of aneurysms are in the Circle Circle of Willisof Willis

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Subarachnoid hemorrhage, Subarachnoid hemorrhage, cont’dcont’d

► If aneurysm leaks, pt may have a headache!If aneurysm leaks, pt may have a headache!► Rupture of aneurysm causes pressure in Rupture of aneurysm causes pressure in

subarachnoid space due to bleeding. Clinical subarachnoid space due to bleeding. Clinical manifestations: manifestations: Headache, lethargy, confusion, nausea, vomiting, Headache, lethargy, confusion, nausea, vomiting,

fever, neck pain, and backaches, paralysis, coma and fever, neck pain, and backaches, paralysis, coma and death.death.

Massive hemorrhage is defines as 30 to 50 ml of blood.Massive hemorrhage is defines as 30 to 50 ml of blood.

Watch for re-bleeding when clot starts to dissolve. Watch for re-bleeding when clot starts to dissolve. (usually within first 2 weeks post rupture). Reduce (usually within first 2 weeks post rupture). Reduce activity and prevent straining.activity and prevent straining.

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Temporal Development of Temporal Development of CVACVA

►Transient Ischemic Attacks (TIA’s)- Transient Ischemic Attacks (TIA’s)- Brief episodes of neuro manifestations Brief episodes of neuro manifestations

(less than 24 hours).(less than 24 hours). Leaves no residual effectsLeaves no residual effects Three categories:Three categories:

►1/3 never have another TIA1/3 never have another TIA►1/3 will have more than one TIA1/3 will have more than one TIA►1/3 will have a stroke 1/3 will have a stroke

WARNING SIGNS OF PROGRESSING CVA!WARNING SIGNS OF PROGRESSING CVA!

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TIA’sTIA’s

►s/s vary depending on the part of brain s/s vary depending on the part of brain affected.affected.

►Treatment:Treatment: Medications such as aspirin, Persantine Medications such as aspirin, Persantine

(dipyridamole), Ticlid, and anticoagulant (dipyridamole), Ticlid, and anticoagulant medication.medication.

Long term therapy post TIALong term therapy post TIA Surgical treatment- carotid endartarectomy, Surgical treatment- carotid endartarectomy,

extra-cranial- intracranial bypass (EC-IC extra-cranial- intracranial bypass (EC-IC bypass), and transiluminal angioplasty.bypass), and transiluminal angioplasty.

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Reversible ischemic Neurologic Reversible ischemic Neurologic DeficitDeficit

►A neuro deficit which remains 24 hours A neuro deficit which remains 24 hours after onset; but leaves no residual after onset; but leaves no residual signs or symptoms.signs or symptoms.

►Considered a completed stroke with Considered a completed stroke with minimal to no residual deficitsminimal to no residual deficits

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Stroke –In- EvolutionStroke –In- Evolution

►A progressive stroke which develops A progressive stroke which develops over hours or days.over hours or days.

►Characteristic of an enlarging intra-Characteristic of an enlarging intra-arterial thrombus.arterial thrombus.

►A stepwise or intermittent progression A stepwise or intermittent progression of deterioration of neurological of deterioration of neurological symptoms.symptoms.

►Manifestations do not resolve and leave Manifestations do not resolve and leave residual damage.residual damage.

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Completed StrokeCompleted Stroke

►Neuro defects unchanged over 2 to 3 Neuro defects unchanged over 2 to 3 days.days.

►Usually embolic in natureUsually embolic in nature►Also called “stable stroke”.Also called “stable stroke”.►Signals readiness for aggressive rehab Signals readiness for aggressive rehab

therapy. (unless an aneurysm is therapy. (unless an aneurysm is involved).involved).

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Clinical ManifestationsClinical Manifestations

►All deficits are directly related to area All deficits are directly related to area of brain that is involved.of brain that is involved.

►See Lewis, page 1650, Table 55-2.See Lewis, page 1650, Table 55-2.

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Neuromotor FunctionNeuromotor Function

►Destruction of motor neurons in the Destruction of motor neurons in the pyramidal pathway causes:pyramidal pathway causes: MobilityMobility Respiratory functionRespiratory function Swallowing and speechSwallowing and speech Gag reflexGag reflex Self-care abilitiesSelf-care abilities

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Motor deficitsMotor deficits

►Loss of skilled voluntary movement Loss of skilled voluntary movement (akinesia).(akinesia).

► Impairment of integration of Impairment of integration of movementsmovements

►Alterations in muscle tonesAlterations in muscle tones►Alteration in reflexesAlteration in reflexes► Initial hypo-reflexia which progresses Initial hypo-reflexia which progresses

to hyper-reflexia for most patients. to hyper-reflexia for most patients.

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Patterns of deficitsPatterns of deficits

►Contralateral deficitsContralateral deficits A lesion on one side of the brain affects the A lesion on one side of the brain affects the

motor function on the other side of the motor function on the other side of the brain.brain.

The arms and legs on the affected side may The arms and legs on the affected side may be weak or paralyzed to different degrees be weak or paralyzed to different degrees depending the degree of cerebral depending the degree of cerebral circulation compromised.circulation compromised.

See Lewis, Page 1651; Table 55-5See Lewis, Page 1651; Table 55-5

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►The affected shoulder tends to rotate The affected shoulder tends to rotate internally; the hip rotates externally.internally; the hip rotates externally.

►The affected foot is plantar flexed and The affected foot is plantar flexed and inverted.inverted.

►An initial period of flaccidity may lasts An initial period of flaccidity may lasts for several days to weeks.for several days to weeks.

►Spasticity of muscles follows the Spasticity of muscles follows the flaccid stage and is related to flaccid stage and is related to interruption of upper neuron influence.interruption of upper neuron influence.

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CommunicationCommunication

► Aphasia- total loss of comprehension and Aphasia- total loss of comprehension and use of language due to damage to the use of language due to damage to the dominant hemisphere (left hemisphere).dominant hemisphere (left hemisphere).

►Dysphasia-dysfunction related to Dysphasia-dysfunction related to comprehension or use of language due to comprehension or use of language due to partial disruption or loss.partial disruption or loss. Non-fluent (minimal speech activity with slow Non-fluent (minimal speech activity with slow

speech that requires obvious effort)speech that requires obvious effort) Fluent- (speech is present, but contains little Fluent- (speech is present, but contains little

meaningful communication).meaningful communication).

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CommunicationCommunication

►Conductive aphasia- mixture of both Conductive aphasia- mixture of both expressive and receptive aphasiaexpressive and receptive aphasia

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

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Communication, cont’dCommunication, cont’d

►Wernicke’s area damageWernicke’s area damage Receptive aphasia where neither the sound or Receptive aphasia where neither the sound or

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

written language.written language.

Boca’s area damageBoca’s area damageExpressive aphasia (difficulty speaking and writing)Expressive aphasia (difficulty speaking and writing)

Dysarthria- disturbance in muscular control of Dysarthria- disturbance in muscular control of speech. (pronunciation, articulation, phonation) speech. (pronunciation, articulation, phonation) DOES NOT EFFECT COMPREHENSION OF DOES NOT EFFECT COMPREHENSION OF LANGUAGE.LANGUAGE.

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AffectAffect

►May be unable to control emotionsMay be unable to control emotions►May be depressed RT body image and May be depressed RT body image and

loss of functionloss of function►May be frustrated RT immobility and May be frustrated RT immobility and

communication issuescommunication issues

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Intellectual FunctionIntellectual Function

►Memory and judgment may be Memory and judgment may be impairedimpaired

►Left-sided stroke patients are more Left-sided stroke patients are more cautious in judgment and movement.cautious in judgment and movement.

►Right-sided stroke patients more Right-sided stroke patients more impulsive and move quicker.impulsive and move quicker.

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Spatial-Perceptual AlterationsSpatial-Perceptual Alterations

►Right sided stroke patient has more Right sided stroke patient has more spatial-perceptual orientation issues:spatial-perceptual orientation issues: Erroneous perception of self and illness Erroneous perception of self and illness

(may deny illness or body parts).(may deny illness or body parts). Erroneous perception of self in space (may Erroneous perception of self in space (may

ignore affected side; can’t judge distances)ignore affected side; can’t judge distances) Agnosia or inability to recognize an object Agnosia or inability to recognize an object

by sight, touch or hearing.by sight, touch or hearing. Apraxia or the inability to carry out learned Apraxia or the inability to carry out learned

sequential movements on command.sequential movements on command.

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EliminationElimination

►Most occur initially and are transient.Most occur initially and are transient.►Frequent constipation DT immobility, Frequent constipation DT immobility,

weak abdominal muscles, dehydration, weak abdominal muscles, dehydration, and diminished defecation reflexes.and diminished defecation reflexes.

►Urinary and bowel elimination may be Urinary and bowel elimination may be DT functional inabilities to express DT functional inabilities to express needs and manage clothing.needs and manage clothing.

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Diagnostic StudiesDiagnostic Studies

►CT Scan-CT Scan- indicate size and location of indicate size and location of lesion, differentiates between infarct lesion, differentiates between infarct and hemorrhage, effectiveness of and hemorrhage, effectiveness of treatment, and evaluate the course of treatment, and evaluate the course of healing.healing.

►MRI- considered best method to MRI- considered best method to differentiate between hemorrhage and differentiate between hemorrhage and infarct.infarct.

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DiagnosticsDiagnostics

►PET PET shows chemical activity and depicts shows chemical activity and depicts extent if tissue damage.extent if tissue damage.

►DDSASA- IV or arterial injection of contrast - IV or arterial injection of contrast material to visualize blood vessels.material to visualize blood vessels.

►TDA- TDA- transcranial doppler measures transcranial doppler measures velocity of cerebral blood flow in the velocity of cerebral blood flow in the arteries, also detects micro-emboli.arteries, also detects micro-emboli.

►LP may be done to detect blood or LP may be done to detect blood or WBC’s (not done if increased ICP is WBC’s (not done if increased ICP is suspected)suspected)

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Collaborative careCollaborative care

►PREVENTIONPREVENTION Healthy dietHealthy diet Weight controlWeight control Regular exerciseRegular exercise No SMOKINGNo SMOKING Limiting alcoholLimiting alcohol Routine health assessmentRoutine health assessment

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DRUG THERAPYDRUG THERAPY

►Prophylactic low dose aspirin, daily.Prophylactic low dose aspirin, daily.►Persantine 50 mg 3 X day decreases Persantine 50 mg 3 X day decreases

platelet aggregation which helps to platelet aggregation which helps to decrease risk of thrombus and decrease risk of thrombus and embolus formation.embolus formation.

►TICLID or PLAVIX- platelet aggregation TICLID or PLAVIX- platelet aggregation inhibitorsinhibitors

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Surgical TherapySurgical Therapy

►Carotid endarterectomy (CEA)- the Carotid endarterectomy (CEA)- the atheromatous lesion is removed from atheromatous lesion is removed from the carotid artery to improve blood the carotid artery to improve blood flowflow Decreases stroke and death in patient Decreases stroke and death in patient

with TIA’s.with TIA’s. Done on patient with 70-99% occlusionDone on patient with 70-99% occlusion

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Transluminal AngioplastyTransluminal Angioplasty

► Insertion of balloon to open stenosed Insertion of balloon to open stenosed artery to permit blood flow.artery to permit blood flow. Patient with symptomatic stenosis of Patient with symptomatic stenosis of

vertebrobasilar or carotid arteriesvertebrobasilar or carotid arteries Risk of dislodging emboliRisk of dislodging emboli

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EC-IC BYPASSEC-IC BYPASS

►Extracranial-intracranial bypassExtracranial-intracranial bypass Used when obstruction cannot be Used when obstruction cannot be

removed directlyremoved directly A branch of extracranial artery is A branch of extracranial artery is

anastomosed to a branch of intracranial anastomosed to a branch of intracranial artery just beyond the area of obstruction.artery just beyond the area of obstruction.

Patients at high risk for stroke and require Patients at high risk for stroke and require close-long term assessment and close-long term assessment and management.management.

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ACUTE CAREACUTE CARE

►Table 55-5; Lewis page 1654.Table 55-5; Lewis page 1654.► InitiallyInitially

Ensure patent airway DT altered level of Ensure patent airway DT altered level of consciousness.consciousness.►Remove denturesRemove dentures

Administer oxygen via nasal cannula or Administer oxygen via nasal cannula or non-rebreather mask DT respiratory non-rebreather mask DT respiratory distressdistress

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Acute CareAcute Care

►Establish IV access with normal saline Establish IV access with normal saline to maintain BPto maintain BP

►Remove clothingRemove clothing►Obtain immediate CT ScanObtain immediate CT Scan►Monitor VS, LOC, O2 sats, cardiac Monitor VS, LOC, O2 sats, cardiac

rhythms, Glasgow Coma Scale, pupil rhythms, Glasgow Coma Scale, pupil size and reactivity.size and reactivity.

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Acute CareAcute Care

►Maintain patient warmthMaintain patient warmth►Reassure patient and familyReassure patient and family

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Ischemic CascadeIschemic Cascade

►Series of events in response to Series of events in response to thrombotic and embolic strokes.thrombotic and embolic strokes. Ischemic area becomes discolored and Ischemic area becomes discolored and

soft, initially. However, around the border soft, initially. However, around the border there is an area of perfusion called the there is an area of perfusion called the ischemic penumbraischemic penumbra that maintains that maintains perfusion for 3 to 6 hours post stroke. perfusion for 3 to 6 hours post stroke.

If adequate blood flow is reinitiated during If adequate blood flow is reinitiated during this period, less neuro damage resultsthis period, less neuro damage results

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TreatmentTreatment

►Control fluid and electrolyte balanceControl fluid and electrolyte balance Adequate hydration promotes perfusion to Adequate hydration promotes perfusion to

the brain; however over hydration may the brain; however over hydration may increase cerebral edema!increase cerebral edema!

Total intake (oral, tube feedings, IV etc., Total intake (oral, tube feedings, IV etc., 1500-2000 per day)1500-2000 per day)

Monitor urine output ( if ADH released Monitor urine output ( if ADH released urine output will decrease)urine output will decrease)

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TreatmentTreatment

► IV solutions with glucose and water are IV solutions with glucose and water are avoided. (hypertonic solutions may avoided. (hypertonic solutions may increase cerebral edema)increase cerebral edema)

► Increased ICP from cerebral edema Increased ICP from cerebral edema peaks in 72 hours and may cause peaks in 72 hours and may cause brain herniation.brain herniation.

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How to manage ICPHow to manage ICP

►Enhance venous drainage by:Enhance venous drainage by: Elevating HOBElevating HOB Maintain head and neck in alignmentMaintain head and neck in alignment Avoidance of hip flexionAvoidance of hip flexion

Limit cerebral tissue metabolism and Limit cerebral tissue metabolism and vasodilation by:vasodilation by:

avoiding hyperthermia, avoiding avoiding hyperthermia, avoiding hypervolemia, manage constipationhypervolemia, manage constipation

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MedicationsMedications

►Diuretics (decrease cerebral edema)Diuretics (decrease cerebral edema) Mannitol (Osmitrol)Mannitol (Osmitrol) Lasix, (Furosemide)Lasix, (Furosemide) Dexamethasone for patients with Dexamethasone for patients with

vasogenic edemavasogenic edema

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Drug TherapyDrug Therapy

►Thrombolytic therapyThrombolytic therapy Recombinant tissue plasminogen activator Recombinant tissue plasminogen activator

(t-PA)- to re-establish blood flow and (t-PA)- to re-establish blood flow and prevent cell death for patients with prevent cell death for patients with ischemic strokes.ischemic strokes.

Patients who receive t-PA within 3 hours Patients who receive t-PA within 3 hours after a stroke more likely to have 32% after a stroke more likely to have 32% less injury three months after stroke.less injury three months after stroke.

T-PA works by lysis thrombus/clot by T-PA works by lysis thrombus/clot by binding and digesting the fibrin and binding and digesting the fibrin and fibrinogen. fibrinogen.

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t-PAt-PA

Clot specificClot specific►Less likely to cause hemorrhage as Less likely to cause hemorrhage as

compared to streptokinase or compared to streptokinase or urokinase.urokinase.

►Single most important factor is Single most important factor is timing!!!timing!!!

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t-PAt-PA

►Patients are screened for coagulation Patients are screened for coagulation disorders, GI bleeding, and hemorrhagic disorders, GI bleeding, and hemorrhagic stroke before initiation of treatment.stroke before initiation of treatment.

►Major side effect is cerebral hemorrhage.Major side effect is cerebral hemorrhage.►Monitor VS during treatment/ control BPMonitor VS during treatment/ control BP►O anticoagulants or antiplatelet drug for O anticoagulants or antiplatelet drug for

25 hours post treatment.25 hours post treatment.

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Platelet inhibition/anticoagulant Platelet inhibition/anticoagulant therapytherapy

►Heparin, coumadin, aspirin, ticlipidine Heparin, coumadin, aspirin, ticlipidine (Ticlid), clopidrogel (Plavix), (Ticlid), clopidrogel (Plavix), dipyridamole (Persantine).dipyridamole (Persantine).

►Contraindicated for patients with Contraindicated for patients with hemorrhagic strokeshemorrhagic strokes

►Monitor PT/ PTTMonitor PT/ PTT►Monitor patient for bleedingMonitor patient for bleeding

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Drug therapyDrug therapy

►Calcium channel blockers are given for Calcium channel blockers are given for patients with hemorrhagic strokes.patients with hemorrhagic strokes.

►Excess intracellular calcium may be Excess intracellular calcium may be harmful to brain tissue.harmful to brain tissue.

►Nimodipine (Nimotop) decreases Nimodipine (Nimotop) decreases effects of vasospasm and minimizes effects of vasospasm and minimizes tissue damage.tissue damage.

►Aspirin decreases platelet aggregation Aspirin decreases platelet aggregation at site of plaque.at site of plaque.

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Drug therapyDrug therapy

►Tylenol treats hyperthermiaTylenol treats hyperthermia►Dilantin may be given for seizuresDilantin may be given for seizures