case cva by dr guruprasad shetty

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By….. Dr Guruprasad By….. Dr Guruprasad shetty. shetty. Padubidri.. Padubidri.. Cerebro vascular Cerebro vascular accident accident

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Page 1: Case cva by dr guruprasad shetty

By….. Dr Guruprasad shetty.By….. Dr Guruprasad shetty.

Padubidri..Padubidri..

Cerebro vascular Cerebro vascular accidentaccident

Page 2: Case cva by dr guruprasad shetty

DefinitionsDefinitions

Cerebro vascular accident (CVA): Cerebro vascular accident (CVA): a syndrome characterized by the a syndrome characterized by the gradual or rapid, onset of gradual or rapid, onset of neurological deficits that fits a neurological deficits that fits a known vascular territoryknown vascular territory

– Transient ischemia attack (TIA): Transient ischemia attack (TIA): – Stroke in evolution:Stroke in evolution:

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Blood Supply to the BrainBlood Supply to the Brain

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Anterior Anterior CirculationCirculation

Int. CarotidInt. Carotid– Arises from common Arises from common

carotid carotid – BranchesBranches: : Anterior cerebral, Anterior cerebral, Anterior communicating,Anterior communicating,Middle cerebral,Middle cerebral,Posterior Posterior

communicating.communicating.

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Posterior CirculationPosterior Circulation

VerebralVerebral– arises from arises from

subclavian and joins subclavian and joins at lower border of at lower border of pons to form basilar pons to form basilar

– BranchesBranches: : posterior cerebral, posterior cerebral, superior cerebellar, superior cerebellar, posterior inferior posterior inferior

cerebellar,cerebellar, anterior spinal anterior spinal

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Circle of WillisCircle of Willis – Anastomosis of Anastomosis of

arteries at base of arteries at base of brainbrain

– Permits collateral Permits collateral circulationcirculation

– Formed by 6 vesselsFormed by 6 vessels Internal carotid A. Internal carotid A. Anterior and posterior Anterior and posterior

cerebral A.cerebral A. Anterior Anterior

communicating Acommunicating A Two posterior Two posterior

communicating A.communicating A.

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Anterior Cerebral (blue)Anterior Cerebral (blue)– Basal ganglia, corpus Basal ganglia, corpus

callosum, medial surface of callosum, medial surface of cerebral hemispheres; superior cerebral hemispheres; superior surface frontal and parietal surface frontal and parietal lobes lobes

Middle Cerebral (red)Middle Cerebral (red)– Frontal lobe, parietal Frontal lobe, parietal

lobe, cortical surface lobe, cortical surface of the temporal lobe of the temporal lobe

Posterior Cerebral (green)Posterior Cerebral (green)– Part of diencephalon and Part of diencephalon and

temporal lobe, occipital lobe temporal lobe, occipital lobe

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Conditions Caused by Conditions Caused by OcclusionOcclusion

Anterior CerebralAnterior Cerebral

Middle CerebralMiddle Cerebral

Posterior CerebralPosterior Cerebral

Contralateral hemiplegia Contralateral hemiplegia (leg greater than arm) (leg greater than arm)

Aphasia Aphasia (dominant (dominant hemisphere)hemisphere)

Contralateral hemiplegia Contralateral hemiplegia (arm, face greater than (arm, face greater than leg), sensory loss, visual leg), sensory loss, visual loss loss

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SMAPrimaryMotorcortex

PrimaryVisualcortex

(Broca’s area)

Primaryauditory ortex

(Wernicke’s area) Angular gyrus

(ArcuateFasciculus)

Brain areas involved

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Corticospinal Damage Hemiparesis : Weakness

Cerebellar Damage Ataxia Timing Issues Motor Learning

Basal Ganglia Damage Parkinson’s Disease Huntingdon’s Chorea

Cortical Damage Apraxia: loss of ability to carry loss of ability to carry

out purposeful movements in the absence of out purposeful movements in the absence of sensory or motor impairmentsensory or motor impairment

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Classification of Classification of Stroke Stroke

StrokeStroke

Primary Hemorrhagic (20% of Strokes)

Primary Ischemic (80% of Strokes)

Thrombotic

53%

Embolic

31%

Intracerebral Hemorrhage 10%

Subarachnoid Hemorrhage 6%

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Primary Ischemic Primary Ischemic StrokeStroke

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ObstructionObstruction– Hypertension,Hypertension,– Diabetes,Diabetes,– Cardiac disease, Cardiac disease, – HypercholesterolemHypercholesterolem

ia,ia,– Atherosclerosis,Atherosclerosis,– Vasculitis Vasculitis

ThrombusThrombus

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EmbolusEmbolus

Atrial fibrillation, Atrial fibrillation, Valvular heart Valvular heart

disease,disease, Cardiomyopathy, Cardiomyopathy, Heart disease, Heart disease, Air/Fat/Infectious Air/Fat/Infectious

fragmentsfragments

Debris detaches Debris detaches flows and lodges in artery flows and lodges in artery

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CEREBRAl

ANEURYSMs

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PathogenesisPathogenesisIschemic CascadeIschemic Cascade

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Blockage of a Blockage of a cerebral blood vessel cerebral blood vessel reduces CBFreduces CBF

Ischemic-hypoxic Ischemic-hypoxic brain damage brain damage

Disturbance in Disturbance in glucose utilizationglucose utilization

Depletion of ATPDepletion of ATP Depletion of Depletion of

neurotransmitter neurotransmitter substances substances

Membrane Membrane depolarizationdepolarization

Influx of sodium and Influx of sodium and water and calciumwater and calcium

Release of glutamateRelease of glutamate Cell death Cell death

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Effects of Reduced CBFEffects of Reduced CBF

Normal ml/100g/min

50 – 55 25 20 15 8

Ischemia

Edema Loss of Na/K+ pump

↑lactate electrical failure; ↓ ATP

activity

PenumbraInfarction

Cell Death

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Cerebral InfarctionCerebral Infarction

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Facial Weakness? Spinal cordNo

Yes

FW same side as limb W? PonsNo

Internal CapsuleYes

Yes

Leg and arm equal?

No

Cortical signs?

Ipsilateral damage

Contralateraldamage

Where is my lesion: summary?

Cortex

Corona Radiata

Yes

No

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Stroke ManagementStroke Management

Patient presents with change in LOC, Patient presents with change in LOC, focal neurological deficit and severe focal neurological deficit and severe headacheheadache

Obtain history and physicalObtain history and physical– Duration of symptomsDuration of symptoms– Time from onsetTime from onset

Evaluate airway, breathing and Evaluate airway, breathing and circulationcirculation

Emergency non-contrast head Ct scanEmergency non-contrast head Ct scan

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Stroke MimickersStroke Mimickers

Seizures Seizures HypoglycemiaHypoglycemia Systemic infectionsSystemic infections Toxic encephalopathyToxic encephalopathy Presyncope or syncopePresyncope or syncope Vertigo Vertigo

– Benign positional vertigoBenign positional vertigo Intracranial tumors/ hematomasIntracranial tumors/ hematomas Migraine Migraine

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Diagnostic StudiesDiagnostic Studies

Laboratory: PT/PTT, CBC, serum glucoseLaboratory: PT/PTT, CBC, serum glucose Cerebral angiography: identifies Cerebral angiography: identifies

aneurysms, vasospasm and vessel aneurysms, vasospasm and vessel abnormalitiesabnormalities

MRI: identifies hemorrhage, edema or MRI: identifies hemorrhage, edema or causative factors depending on etiologycausative factors depending on etiology

Doppler Studies: reveals carotid diseaseDoppler Studies: reveals carotid disease EEG: reveals focal areas of decreased EEG: reveals focal areas of decreased

function around lesionfunction around lesion ECG: arrhythmias, myocardial infarctionECG: arrhythmias, myocardial infarction

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Initial Initial ManagementManagement

Ischemic StrokeIschemic Stroke– Begin IV hydrationBegin IV hydration– Supplemental O2Supplemental O2– Manage BPManage BP– Treat Treat

hyperglycemia hyperglycemia – Treat Treat

hyperthermiahyperthermia– Treat seizuresTreat seizures– Treat if T-PA Treat if T-PA

therapy plannedtherapy planned

Hemorrhagic StrokeHemorrhagic Stroke– SAH vs. ICHSAH vs. ICH

Neurosurgical consultNeurosurgical consult

– Begin IV hydrationBegin IV hydration– Supplemental O2Supplemental O2– Treat intracranial Treat intracranial

pressurepressure– Manage BPManage BP– Treat hyperglycemiaTreat hyperglycemia– Treat hyperthermiaTreat hyperthermia– Treat seizuresTreat seizures– Begin Nimodipine (SAH)Begin Nimodipine (SAH)– Angiogram (SAH)Angiogram (SAH)

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Management of Blood Management of Blood PressurePressure

IschemicIschemic– Treat SBP > 220 Treat SBP > 220

or DBP > 120 or DBP > 120 mmHg after mmHg after repeated repeated measurements measurements

– Treat if cardiac Treat if cardiac ischemia, heart ischemia, heart failure or aortic failure or aortic dissection is dissection is presentpresent

– Treat if T-PA Treat if T-PA therapy plannedtherapy planned

HemorrhagicHemorrhagic– Treat severe Treat severe

elevations with IV elevations with IV dripdrip SBP > 230 or DBP > SBP > 230 or DBP >

120 mmHg120 mmHg– Treat moderate Treat moderate

elevations with IVPelevations with IVP SBP > 180 or DBP > SBP > 180 or DBP >

105 mmHg105 mmHg– Treat elevated Treat elevated

blood pressure to blood pressure to approximate approximate premorbid BPpremorbid BP

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Intravenous ThrombolysisIntravenous Thrombolysis Tissue Plasminogen Activator Tissue Plasminogen Activator

(tPA)(tPA) Inclusion CriteriaInclusion Criteria

– Age < 18Age < 18– Ischemic stoke by Ischemic stoke by

clinical presentationclinical presentation– Persistent deficits Persistent deficits

beyond an isolated beyond an isolated sensory deficit or sensory deficit or ataxiaataxia

– CT scan negative CT scan negative for hemorrhagefor hemorrhage

– Treatment initiated Treatment initiated within 3 hours of within 3 hours of symptom onsetsymptom onset

Exclusion CriteriaExclusion Criteria– More than 3 hours since More than 3 hours since

symptom begansymptom began– Rapidly improving deficitsRapidly improving deficits– CT scan shows substantial CT scan shows substantial

edema, mass effect or shiftedema, mass effect or shift– PT > 15 seconds; INR > PT > 15 seconds; INR >

1.7 or prolonged PTT1.7 or prolonged PTT– Platelet count < 100, 000Platelet count < 100, 000– SBP > 185 or DBP > 110SBP > 185 or DBP > 110– Prior stoke or serious head Prior stoke or serious head

trauma within 3 monthstrauma within 3 months– Prior ICHPrior ICH– History of GI/GU bleedingHistory of GI/GU bleeding– Seizures at onset of strokeSeizures at onset of stroke– Symptoms suggest SAHSymptoms suggest SAH

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Administration of t-PAAdministration of t-PA

Treatment should begin immediatelyTreatment should begin immediately Dosing: 0.9 mg/kg IV over one hourDosing: 0.9 mg/kg IV over one hour

– 10% IV bolus over 1 minute10% IV bolus over 1 minute– Maximum dose is 90 mgMaximum dose is 90 mg

Aspirin recommended 160 – 325 Aspirin recommended 160 – 325 mg/day for those unable to receive t-mg/day for those unable to receive t-PAPA

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Complications of t-PAComplications of t-PA

Intracranial Intracranial hemorrhagehemorrhage

Systemic bleedingSystemic bleeding Reocclusion Reocclusion New stroke New stroke DeathDeath

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Surgical TreatmentSurgical Treatment

Craniotomy

Aneurysm Clipping

Aneurysm Coiling

Endovascular Procedures

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ComplicationsComplications NeurologicalNeurological

– Seizures 10%Seizures 10%– Increased ICPIncreased ICP

PulmonaryPulmonary– AspirationAspiration– PneumoniaPneumonia

CardiovascularCardiovascular– Cardiac arrhythmiasCardiac arrhythmias– DVTDVT

GIGI– GI bleedingGI bleeding– Urinary tract infectionUrinary tract infection– Bowel impactionBowel impaction– MalnutritionMalnutrition

MusculoskeletalMusculoskeletal– Impaired mobilityImpaired mobility– ContracturesContractures– Heterotrophic Heterotrophic

ossificationossification– SpasticitySpasticity

PsychosocialPsychosocial– Depression – Depression –

60%60%– Loss of self Loss of self

esteemesteem

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Major Risk FactorsMajor Risk Factors

Risk FactorRisk Factor PrevalencePrevalence

HTNHTN

Heart DiseaseHeart Disease35%35%

10 – 120 %10 – 120 %

Previous CVAPrevious CVA

Carotid BruitCarotid Bruit2%2%

4%4%

DiabetesDiabetes

SmokingSmoking4-6%4-6%

25%25%

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Unmodifiable Risk Factors for Unmodifiable Risk Factors for StrokeStroke

AgeAge Incidence of stroke Incidence of stroke more than doubles more than doubles each decade after each decade after age 55age 55

SexSex Incidence is about Incidence is about 30% higher for men 30% higher for men than womenthan women

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RehabilitationRehabilitation GoalsGoals

– Regain patient Regain patient independenceindependence

– Maximize abilities in all ADLMaximize abilities in all ADL Assessment of disabilityAssessment of disability

– Cognition and level of Cognition and level of consciousnessconsciousness

– Swallow and nutritional Swallow and nutritional statusstatus

– SpeechSpeech– Motor strength and Motor strength and

coordinationcoordination– GaitGait

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Emerging TherapiesEmerging Therapies Intra-arterial t-PAIntra-arterial t-PA Other antithrombotic agentsOther antithrombotic agents

– IV heparinIV heparin– Abciximab: platelet glycoprotein antagonistAbciximab: platelet glycoprotein antagonist– Argatroban: direct thrombin inhibitorArgatroban: direct thrombin inhibitor

Neuroprotective agentsNeuroprotective agents– Glutamate antagonistsGlutamate antagonists - Calcium antagonists- Calcium antagonists– Opiate antagonistsOpiate antagonists - GABA-A - GABA-A

agonistsagonists– AntioxidantsAntioxidants - Neuroperfusion- Neuroperfusion– Mild hypothermiaMild hypothermia - Blood substitutes- Blood substitutes

- Kinase inhibitors- Kinase inhibitors

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Treatment is planned according to –

Causation of illness Pathological factors involved & Clinical presentation

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Remember…….Remember…….

Stroke is preventableStroke is preventable Neural damage after stroke is Neural damage after stroke is

progressiveprogressive There is a therapeutic window for There is a therapeutic window for

optimal treatmentoptimal treatment Stroke is an emergencyStroke is an emergency Effective therapies currently existEffective therapies currently exist New therapies are currently being New therapies are currently being

developeddeveloped

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