case cva by dr guruprasad shetty
TRANSCRIPT
By….. Dr Guruprasad shetty.By….. Dr Guruprasad shetty.
Padubidri..Padubidri..
Cerebro vascular Cerebro vascular accidentaccident
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:
Blood Supply to the BrainBlood Supply to the Brain
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.
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
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.
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
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
SMAPrimaryMotorcortex
PrimaryVisualcortex
(Broca’s area)
Primaryauditory ortex
(Wernicke’s area) Angular gyrus
(ArcuateFasciculus)
Brain areas involved
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
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%
Primary Ischemic Primary Ischemic StrokeStroke
ObstructionObstruction– Hypertension,Hypertension,– Diabetes,Diabetes,– Cardiac disease, Cardiac disease, – HypercholesterolemHypercholesterolem
ia,ia,– Atherosclerosis,Atherosclerosis,– Vasculitis Vasculitis
ThrombusThrombus
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
CEREBRAl
ANEURYSMs
PathogenesisPathogenesisIschemic CascadeIschemic Cascade
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
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
Cerebral InfarctionCerebral Infarction
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
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
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
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
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)
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
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
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
Complications of t-PAComplications of t-PA
Intracranial Intracranial hemorrhagehemorrhage
Systemic bleedingSystemic bleeding Reocclusion Reocclusion New stroke New stroke DeathDeath
Surgical TreatmentSurgical Treatment
Craniotomy
Aneurysm Clipping
Aneurysm Coiling
Endovascular Procedures
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
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%
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
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
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
Treatment is planned according to –
Causation of illness Pathological factors involved & Clinical presentation
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