10 - Strokes Flashcards

1
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2
Q

Symptoms of stroke

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3
Q

Symptoms of stroke

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4
Q

Stroke: two major subtypes

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5
Q

Ischemic Stroke: Definition

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6
Q

Ischemic Stroke: Mechanisms (overview)

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  • Small Vessel Disease
  • Large Vessel Stenosis
  • Cardioembolism
  • Other Determined Etiology
    – Hypercoagulable state, Dissection, Vasculitis, etc.
  • Cryptogenic/Idiopathic
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7
Q

Ischemic Stroke: Mechanisms - Small Vessel Occlusive Disease

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8
Q

Ischemic Stroke: Mechanisms
* Large Artery Stenosis

A
  • ~20% of ischemic strokes
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9
Q

Ischemic Stroke: Mechanisms
* Cardioembolism

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10
Q

Ischemic Stroke: Mechanisms
* Uncommon causes – 5-10%

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  • Autoimmune or infectious vasculitis
  • Drugs/toxins (cocaine)
  • Dissections
  • Vasospasm
  • Paradoxical embolism from venous thrombus (i.e. through a patent foramen ovale in the heart)
  • Hypercoagulable conditions
    -Ex: APLAS, malignancy
  • Genetic disorders
    -Ex: CADASIL, Moyamoya
  • Mitochondrial disorders
    -Ex: MELAS
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11
Q

Ischemic Stroke: Mechanisms
* Cryptogenic (unknown cause) – 20-25%

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  • A major goal of stroke evaluation is to determine the cause of the stroke in patients whose underlying stroke mechanism is not known at first
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12
Q

Stroke/TIA Mimics

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13
Q

TIA (Transient Ischemic Attack): Definition

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  • Transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without infarction on neuroimaging
  • The typical duration of a TIA is < 1 or 2 hours, but occasionally, prolonged episodes occur.
  • Can sometimes be challenging to be certain it was a TIA because, by definition, the symptoms have resolved and imaging is
    normal
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14
Q

ABCD^2 Score

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15
Q

TIA: Why do we care?

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16
Q

Approach to Acute Stroke

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  • Time-line (last known normal)
  • Examine the patient
    – NIH Stroke Scale
    – Do they have a vascular syndrome
  • Data
    – Vital signs
    – Blood glucose
    – Non-contrast head CT, CT angiogram
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17
Q

NIH Stroke Scale

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18
Q

Imaging - CT

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  • 60% of infarcts are seen within 3-6 hrs and
    virtually all are seen in 24 hours.
  • What to look for on head CT?
  • Blood, mass, early infarct signs
  • Obtain a CT angiogram to evaluate for large vessel occlusion
19
Q

Imaging – early infarct signs

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20
Q

Imaging – Large Vessel Occlusion

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21
Q

Acute stroke treatment

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  1. Thrombolysis
  2. Endovascular therapy
    Address acute treatment first, then proceed
    with stroke etiology workup and secondary
    stroke prevention next
22
Q

Alteplase/Tenecteplase (tPA/TNK)

A

– Binds fibrin and converts plasminogen -> plasmin (active form), which degrades fibrin clot
– Tenecteplase is a modified form of alteplase with
higher selectivity for fibrin, longer half-life, and
administered as a single bolus

23
Q

tPA: The Evidence

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  • Benefit seen in all stroke subtypes, if disabling deficits present
  • Overall 28% reduction in disability at 90 days, 1.9 times as likely to have favorable outcome
  • 3-6% risk of symptomatic hemorrhage
  • Can be given up to 4.5 hrs from last known normal time in most cases (off-label if age>80, hx stroke and DM, severe stroke)
24
Q

Thrombolysis: Main Contraindications

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  • Stroke, severe head trauma, neurosurgery in past 3 months
  • ICH at ANY point
  • Coagulopathy
    – Plts <100k, Anticoagulation within 48 hrs, or on
    Vit K antag with INR >1.7
  • Systemic bleeding in prior 3 weeks
  • Intra-axial tumor, vascular malformation, infective endocarditis
  • Uncontrolled hypertension (needs to be lowered to <185/110 to administer)
25
Q

Acute stroke treatment - Endovascular Thrombectomy

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26
Q

Stroke Workup

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  • After acute management, focus on etiology
  • Clinical Work-up
    – Brain MRI
    – Echocardiogram (TTE and/or TEE)
    – Cardiac rhythm monitoring (EKG, short/long-term telemetry)
    – Vessel imaging (CTA/MRA/Carotid Ultrasound,
    Cather Angiogram)
    – Labs (Lipid panel, Hemoglobin A1C)
    Determining the mechanism is key to determining appropriate treatment for secondary stroke prevention
27
Q

Stroke Imaging - MRI

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28
Q

Localizing the Lesion
* Right or Left?
* Anterior or posterior circulation?
* Cortical vs subcortical?
* Which specific vessel?

A
  • Cortical or Subcortical?
    – Cortical signs:
  • Aphasia – Typically left frontal or temporal cortex
  • Neglect – Right parietal cortex
  • Apraxia – Different cortical locations depending on type
  • Agraphesthesia– Parietal cortex
  • Gaze preference – Frontal eye fields (look “toward” stroke)
  • Visual field cut – Occipital cortex
  • Isolated face/arm or hand weakness – Motor cortex
29
Q

Secondary Stroke Prevention

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Vascular risk factor control
* Treatment of hypertension, diabetes,
hyperlipidemia (LDL goal<70), smoking and
excessive alcohol cessation
* Diet (Mediterranean) and exercise

Antithrombotics (blood thinners)
* Anti-platelet or anticoagulant agents – choice depends on stroke etiology

30
Q

Secondary Stroke Prevention

A
  • Vascular risk factor control
  • Treatment of hypertension, diabetes,
    hyperlipidemia (LDL goal<70), smoking and
    excessive alcohol cessation
  • Diet (Mediterranean) and exercise
  • Antithrombotics (blood thinners)
  • Anti-platelet or anticoagulant agents – choice depends on stroke etiology
31
Q

Antiplatelet Therapy

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32
Q

Anticoagulation Therapy

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Choice depends on indication for
anticoagulation (i.e. atrial fibrillation, clotting
disorder, etc.)
* Factor Xa inhibitors (apixaban, rivaroxaban)
* Direct thrombin inhibitors (dabigatran)
* Vitamin K antagonists (warfarin)
* Antithrombin III activators (heparinoids)

33
Q

Recovery

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34
Q

Hemorrhagic Stroke: Definition

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A non-traumatic rupture of a cerebral blood vessel
leading to intraparenchymal hemorrhage

35
Q

Intraparenchymal Hemorrhage – “Hemorrhagic Stroke”

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  • Acute hemorrhage appears hyperdense on head CT
  • 40% 1-year survival, 12 – 39% functional independence at follow-up
36
Q

Intraparenchymal Hemorrhage (IPH)
* Clinical symptoms

A
  1. may be the exact same as
    ischemic stroke
    * Other symptoms/signs common in IPH:
    * Nausea and vomiting
    Sudden, severe headache
    * Diminished level of consciousness
    * Significant BP elevation
37
Q

strokes - hypertension

A
  • Strongest risk factor and most common cause of IPH
  • Chronically high pressures leads to
    vascular remodeling, lipohyalinosis, and vessel
    wall weaking and risk of rupture
  • Deep brain structures
  • Basal ganglia
  • Thalamus
  • Brainstem
  • Deep Cerebellum
38
Q

CEREBRAL AMYLOID ANGIOPATHY

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39
Q

Imaging Features of CAA (Cerebral Amyloid Angiopathy)

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Superficial Siderosis

40
Q

imaging features of IPH induced by hypertension

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41
Q

Treatment - Prevent Hemorrhage Expansion!

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  • Reversal agents if patient on anticoagulation (no role for platelet transfusion if on antiplatelet agent unless thrombocytopenic)
  • INR < 1.5, platelets>100
  • Reduce blood pressure immediately to at least < 160 systolic
  • Head of bed 30 degrees
  • Consider surgical hemorrhage evacuation, esp if expanding