Stroke_Treatment
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Transcript Stroke_Treatment
Medical Management of
Stroke
Stroke Code!
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Rapid Assessment. (NIH Stroke Scale)
Non-con CT
CTA/CTP
Call Duty Neurologist
Is patient t-PA candidate?
– Or candidate for other acute therapies?
• See Neurology Sharepoint for Stroke Protocols
• Stroke registry
• Stroke review meetings
Stroke Definitions
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Focal Neurologic
Negative Symptoms
Vascular Origin
Sudden Onset
• Sudden Headache (SAH)
Cerebral Blood Flow
• Normal CBF 50 – 55 ml/100gm/min
• About 18 - 20 ml/100gm/min – Failure of neuronal
function
• About 8 -10 ml/100gm/min – cellular death
• Hypoperfused area = ischemic penumbra
• Restore perfusion to ischemic penumbra
• Protect neurons until perfusion restored
• Rapid Diagnosis and intervention
Transient Ischemic Attack
• < 24 hours by definition
• Most last 10 – 20 minutes
• Warning sign of Stroke: like unstable
angina and MI
• Expedite work-up
• Typically present with rapid-onset deficits
maximal at onset.
• Compare with “march” of Migraine or
Seizure
Signs of TIA
• Anterior circulation
– Aphasia, neglect, Amaurosis, isolated leg
weakeness, abulia
• Posterior circulation
– Diplopia, ataxia, dysphagia,hiccups, vertigo,
crossed signs
• Either
– Hemiplegia, visual field cuts, hemisensory
loss, dysarthria
TIA evaluation
• Carotid imaging
• Intracranial vessel imaging
• Cardiac source eval
TIA Rx
• CEA for symptomatic Carotid Stenosis
>70%
– Stenting, if surgical contraindications
• Cardiac source: Coumadin. ASA if not
able to give coumadin.
• Atherosclerosis: ASA, Statins, Clopidogrel.
ASA + dipyridimole
• Lacunar: ~ Same. Antihypertensive Rx.
MATCH Trial
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Management of Atherothrombosis with Clopidogrel in High-Risk Patients with Recent Transient
Ischemic Attack (MATCH) study,
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Clopidogrel + aspirin for secondary prevention of stroke
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The efficacy of any antiplatelet therapy, including aspirin, is modest when it is used as
monotherapy, and combination therapy with 2 antiplatelet agents has shown promise in reducing
the risk for secondary stroke in patients who have had a previous transient ischemic attack (TIA)
or ischemic stroke.
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MATCH trial indicated that the reduction in risk achieved by adding aspirin to clopidogrel is not
significantly greater than that achieved with clopidogrel alone.
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Significant increase in life-threatening bleeding complications was associated with the
combination of clopidogrel + aspirin.
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Clopidogrel + aspirin cannot be recommended at this time for the secondary prevention of stroke
in patients who have had a previous ischemic stroke or TIA.
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(? 3 month short term Rx after ominous stroke)
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From American Journal of Medicine
ESPS-2
• Second European Stroke Prevention
Study (ESPS-2)
• Demonstrated a significant reduction in
risk for secondary stroke with aspirin +
extended-release dipyridamole versus
aspirin alone
PRoFESS Trial
(Full results yet to be published)
• Prevention Regimen for Effectively
avoiding Second Strokes.
• Plavix (clopidogrel) ~= Aggrenox (ASA +
DP)
• (Micardis not better than Placebo)
CT scan of early stroke
Types of Stroke
• Ischemic
– Arterial
– Venous
• Headache, lethargy, Seizure
• Hemorrhagic
– Intra-parenchymal
– Sub-arachnoid
Stroke etiologies
Stroke risks
Ischemic Stroke
• Destructive cascade induced by ischemia
• Decreased O2 and glucose
– ATP insufficiency
– Ca++ influx
– Increase Glutamate
– Membrane degradation
– Free radical increase
– Apotosis
Large MCA Stroke
Sources of stroke
Stroke Syndromes
• Carotid
– ACA: Leg > Arm, Frontal lobe symptoms
– MCA: Face, Arm > Leg; gaze preference,
Aphasia, hemineglect etc
• Vertebrobasilar
– PCA: Hemianopsia, etc
– Brain stem Stroke: Crossed signs, diplopia,
vertigo, dysphagia, Horner’s Syndrome, etc
Right PICA stroke
Lacunar Syndromes
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Pure Motor
Pure Sensory
Sensorimotor
Ataxia-hemiparesis
Dysarthria Clumsy Hand
Hemichorea
Arteriopathies
• Atherosclerosis
• Non-Atherosclerotic
– Inflamatory
• Angiitis
• GCA
• Syphilis etc
– Non-inflamatory
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Dissection
FMD
Moya Moya
Homocysteinuria
CADASIL
– cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy
• Drugs etc
Stroke Risk Factors
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Age
Race
Gender
Family History
Prior Stroke
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HTN
DM
Heart Disease
Smoking
Hyperlipidemia
Carotid bruits
Excessive EtOH
BCP
Obesity and inactivity
Embolic Stroke
• High Risk vs Low Risk Cardiac sources
Hematological Diseases
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Antiphospholipid Antibody Syndrome
Protein C deficiency
Protien S deficiency
Factor V Leiden
Other hypercoagulable states
Venous Ischemic Stroke
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Post partum
Hypercoagulable States
Infections
Dehydration
Tumors
Post-op
Hemorrhagic Strokes
• Hypertensive
– Putamen
– Thalamus
– Cerebellar
– Pontine
• Aneurysmal
• AVM
• Amyloid Angiopathy
Stroke Rx decision tree
Ischemic Stroke Strategies
• “Time is Brain”
• Reperfusion
• Ancillary Care
– Systemic
– Avoid Complications
• Neuro-protection
• Secondary Prevention
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Anti-platelet agents
Statins
Hypertension Rx
Smoking cessation
Weight Control
Initial Stabilization and Monitoring
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Assess airway maintenance
Level of Arousal
Evaluation for MI
Dysrhythmia monitoring
Diagnostic Eval for Stroke
• Urgent, for all: CT or MRI, Electrolytes, glucose,
BUN, Creatinine, CBC, PT/PTT, O2 Sat
• Urgent, for some: Tox screen, Blood alcohol,
LFTs, HCG, CXR, ABG, LP, EEG
• Non-urgent, for etiologic eval: TEE or TTE,
Carotid Doppler, MR angiogram, CT angiogram,
Catheter angiogram, RPR, ESR, homocysteine,
lipids.
• Selected patient eval: Coag panel, TSH, MR
imaging and MRA of intracranial vessels
Stroke Rx
• Anticoagulation ~doesn’t benefit
• Consider anticoagulation
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Known large vessel disease with fluctuating symptoms
Mechanical Heart valves
LV Thrombus
Prothrombotic states
Cerebral Venous Thrombosis
• Prone to Hemorrhage:
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Large infarcts
Extensive Occipital Lobe involvement
Early Petechial Conversion
Uncontolled hypertension, Hyperglycemia
Stroke Rx
• Induced hypertension might help salvage
ischemic Penumbra
• Double edge sword
Fluid management
• May need to be NPO
• Avoid hypotonic solutions if risk of cerebral
edema
• Monitor electrolytes
• Prevent hyperglycemia – leads to worse
outcome
Prevent Complications
• DVT prophylaxis
– Pneumatic compression stockings
– SQ Low Molecular Weight Heparin
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GI Prophylaxis
Feeding
Chest PT/positioning
Stool softeners
Prevent infection - UTI
MRIs before and after t-PA
Thrombolytic Therapy
• Goal – preserve ischemic penumbra
• 3 hour window for IV t-PA
– 6% bleed.
– Outcome: 12 % > placebo
• Intra-arterial t-PA – not FDA approved –
“investigational”, 6 hour window.
• Abciximab – disappointing result
• ASA acute Rx – some value
• Hypothermia – shows promise, but technically
difficult
• “Merci” clot retriever – FDA approved
Absolute contraindications to t-PA
• Presenting symptoms and signs should not suggest acute
subarachnoid hemorrhage
• Head trauma or prior stroke within the previous 3 months
• Myocardial infarction within the previous 3 months
• Gastrointestinal or urinary tract hemorrhage within the previous 21
days
• Major surgery within the previous 14 days
• Arterial puncture at a noncompressible site within the previous 7
days
• History of previous intracranial hemorrhage
• Active bleeding or acute trauma (fracture) on examination
• Platelet count <100,000 mm3
• Blood glucose <50 mg/dL
• Seizure or postictal neurologic impairments
Relative contraindications to t-PA
• Oral anticoagulation (international
normalized ratio must be ≤1.5)
• Heparin within the previous 48 hours
(activated partial thromboplastin time must
be in the normal range)
Stroke with hemorrhage s/p t-PA
Protocol for thrombolytic therapy in patients with of
acute ischemic stroke
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1. Determine if the patient is a candidate for thrombolytic therapy.
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2. Infuse alteplase (rt-PA) 0.9 mg/kg (maximum of 90 mg) over 60 minutes with 10%
of the dose given as a bolus over 1 minute.
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3. Admit the patient to an intensive care unit or stroke unit for monitoring.
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4. Neurologic assessment to be performed every 15 minutes during the infusion of rtPA and every 30 minutes for the first 2 hours for the next 6 hours, then every hour for
24 hours from the time of initial treatment.
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5. If the patient develops a severe headache, acute hypertension, nausea, or
vomiting, discontinue the infusion and perform and emergency CT brain scan.
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6. Measure blood pressure every 15 minutes for the first 2 hours, every 30 minutes
for the next 6 hours, and then every hour until 24 hours from the time of initial
treatment.
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7. Increase the frequency of blood pressure measurements if a systolic blood
pressure ≥180 mm Hg systolic or ≥105 mm Hg diastolic is recorded. Administer
antihypertensive medications to maintain the blood pressure at or below these levels
Antihypertensive Rx in acute stroke
• Avoid Rx unless planned thombolysis and
SBP > 185 or DBP >110
• Evidence of end organ damage
• Excessively high BP: SBP > 220 ; DBP >
110
• Labetolol or Nicardipine Drip for BP Rx
with thombolysis
Antihypertensive Rx
Drug
Mechanism Dose
Cautions
Labetolol
a-1, b-1, b-2
antagonist
0.5 – 2.0
mcg/min
infusion
Bradycardia,
Bronchospasm
Esmolol
b-1 antagonist
50 -300
mcg/kg/min
infusion
Bradycardia,
Bronchospasm
Nicardipine
CCB
5 -15 mg/ hour
infusion
Reflex
tachycardia, LV
Failure, AS
Fenoldopam
DA-1 agonist
0.1 – 0.3
mg/kg/min
infusion
Tachycardia,
Glaucoma, Liver
disease
Nitroprusside
Vasodilator
0.25 – 10
mg/kg/min
infusion
Increase ICP, N/V,
sweating, Toxicity
Vasopressor Rx
Drug
Mechanisms Dose
Cautions
Phenylephrine
a-1 agonist
40 -180 mcg/min
Bradycardia or
tachycardia, MI
Norepinephrine
a-1, b-1 agonist
2 -40 mcg/mim
Tachycardia, site
necrosis, MI,
Sulfa
Dopamine
DA -1 agonist
a-1, DA -1 agonist
a-1, b-1, DA-1 agonist
1 -2.5 mcg/kg/min
2.5 –10mcg/kg/min
>10mcg/kg/min
H/A, Tachycardia,
CAD, Sulfa
Dobutamine
b-1, b-2 agonist
2 – 20 mcg/kg/min
Tachycardia, MI,
cardiac ectopy
Vasopressin
ADH analog
0.01 – 0.1 units/min
Arrythmia, MI,
seizures, H20
intoxication
Massive stoke with trans-falcine
herniation
Cerebral Edema Rx
• First prevention
• Higher risk
– Large hemispheric stroke in younger person
(little room to swell)
– Cerebellar Stroke
– H/o Hypertension
Cerebral Edema Rx
• HOB elevation, Fluid restriction, Treat fever
• Hyperventilation – causes vasoconstriction: brief
effect, may get rebound vasodilation, ?worsens
ischemia
• Osmotic agents – mannitol vs hypertonic saline
vs furosemide
• Barbiturates – decrease cerebral metabolic rate.
Not really effective.
• Steroids do not work for cytotoxic stroke edema
• Hypothermic Rx?
• Hemicranectomy/Surgical Decompression
Large stroke s/p hemicraniectomy
Hemorrhagic Stroke Strategies
• Stop Bleeding
• Ancillary Support
• Neuro-protection
Parenchymal Hemorrhage in
Basal Ganglia
Intracerebral Hemorrhage
• May be difficult clinically to distinguish
Ichemic Stroke from Hemorrhage
• More likely to be Headache, vomiting,
Loss of Consciousness
• CT scan
• Prognosis: size of hematoma, clinical
status, age, intraventricular blood.
• ? No ischemic penumbra
Medical Rx of Intracerebral
Hemorrhage
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ABCs
Blood Pressure Management
Increased BP may be response to the acute event
Controversy - ?ischemic penumbra
MAP vs SBP
– MAP goal 100 – 120 mm Hg
– SBP goal 130 – 160 mm Hg
• Obstuctive hydrocephalus
• Surgical evacuation
– Particularly for cerebellar hematoma
• Euvolemia, Euthermia, Normal glucose
Intracranial Pressure
• CPP = MAP – ICP
• CPP > 60 mm Hg
• Acute Rx of increase ICP
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Raise HOB > 30 degrees
* Hyperventilate to Pco2 of 25 -30 mm Hg
* Diuretics: Lasix
* Mannitol 1gm/Kg IV to get serum osmolarity of 300 –
320 mOsm
– * for acutely deteriorating patient
– No steroids
Seizure prophylaxis
• Risk highest in first 24 hours
• Risk higher if cortical hemorrhage
• Prophylaxis options
– Phenytoin
– Fosphenytoin
– Valproate
SAH
SAH data
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“Worst headache of my life”
Sentinel Bleeds
~ 10/100,000 person-years
~30,000 cases per year in USA
Increased risk with EtOH intake, hypertension, smoking,
1st degree relative with SAH
• Prevalence of unrupture intracranial aneurysm about
1%.
• SAH - ~80% reach hospital alive, ~30% in-hospital
mortality, ~16% with full recovery without defecits
• Outcome predicted by: Neuro status at admission, age,
amount of sub-arachnoid blood.
Hunt-Hess Grading scale for SAH
Grade
Criteria
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Asymptomatic or minimal headache and
slight nuchal rigidity
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Moderate-to-severe headache, nuchal
rigidity, no neurologic deficit other than
cranial nerve palsy
Drowsiness, confusion, or mild focal deficit
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Stupor, moderate-to-severe focal deficit
(hemiparesis); vegetative disturbances
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Deep coma, decerebrate posturing
SAH Medical Rx
• Early clipping of aneurysms now standard.
• Previously: rebleeding was major cause of
mortality and morbidity.
• Now: vasospasm and delayed ischemic
deficits are primary concerns.
SAH Medical Rx
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ABCs
Pain Control
IV access
Fever control
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Prevent vasospasm with Nimodipine
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Rebleeding vs reduced perfusion
Respiratory
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30 -34% is ideal
Blood Pressure
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Cerebral salt wasting vs SIADH
Maintain normall intravascular volume
Hematocrit
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60mg q4hr po
Seizure prophylaxis
Fluids
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“central fever” vs infection
Supplemental Oxygen
DVT prophylaxis
Bowel care
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NPO initial 24 – 48 hrs
Ulcer prophylaxis
Nausea Rx
SAH complications
• Vasospasm
• Cerebral Salt Wasting
• Hydrocephalus
Vasospasm in SAH
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Documented in ~60%, ~ 50% symptomatic
Delayed ischemic deficits in ~16%
Onset about 3 -5 days post-bleed
Peaks 7 – 10 days
Resolves spontaneously over 2 – 4 weeks
Manifest clinically by: decreased responsiveness, abulia,
focal deficits
• Transcranial Doppler
• “Triple-H therapy”: Hypervolemia, hemodilution,
hypertension.
• Angiography suite for Rx
Hyponatremia in SAH
• Hyponatremia in ~30%/
• Cerebral Salt Wasting
– Hypovolemia
– Natriuresis
– Hyponatremia
• Contrast with SIADH
• Volume repletion and maintenance of
positive Sodium balance
Hydrocephalus
• Noncomunicating – usually acute
• Communicating (non-obstructive) – usually subacute or
delayed.
• Signs: decline in alertness, confusion, disorientation,
inattention.
• CT scan – enlarged ventricles
• Noncommunicating
– Intraventricular catheter to drain CSF
• Communicating
– Lumbar drain
– Serial LPs
– If chronic, ventriculoperitoneal shunt. (About 20% of patients will
require)
JCAHO Performance Measures for
Stroke Centers
• 1* Deep Vein Thrombosis (DVT) Prophylaxis
• 2* Discharged on Anti-thrombotics
• 3* Patients with Atrial Fibrillation Receiving Anticoagulation
Therapy
• 4* Tissue Plasminogen Activator (t-PA) Considered
• 5 Anti-thrombotic Medication Within 48 Hours of Hospitalization
• 6 Lipid Profile During Hospitalization
• 7 Screen for Dysphagia
• 8 Stroke Education
• 9 Smoking Cessation
• 10 A Plan for Rehabiliation was Considered
• *Initial standardized stroke measure set
• Note: All ten measures comprise set for pilot testing.