10 - Strokes Flashcards
1
Q
A
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
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
9
Q
Ischemic Stroke: Mechanisms
* Cardioembolism
A
10
Q
Ischemic Stroke: Mechanisms
* Uncommon causes – 5-10%
A
- 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
11
Q
Ischemic Stroke: Mechanisms
* Cryptogenic (unknown cause) – 20-25%
A
- 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
12
Q
Stroke/TIA Mimics
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13
Q
TIA (Transient Ischemic Attack): Definition
A
- 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
14
Q
ABCD^2 Score
A
15
Q
TIA: Why do we care?
A
16
Q
Approach to Acute Stroke
A
- 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
17
Q
NIH Stroke Scale
A
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
A
- Thrombolysis
- 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
A
- 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
A
- 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
Acute stroke treatment - Endovascular Thrombectomy
26
Stroke Workup
* 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
Stroke Imaging - MRI
28
Localizing the Lesion
* Right or Left?
* Anterior or posterior circulation?
* Cortical vs subcortical?
* Which specific vessel?
* 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
Secondary Stroke Prevention
**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
Secondary Stroke Prevention
* 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
Antiplatelet Therapy
32
Anticoagulation Therapy
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
Recovery
34
Hemorrhagic Stroke: Definition
A non-traumatic rupture of a cerebral blood vessel
leading to intraparenchymal hemorrhage
35
Intraparenchymal Hemorrhage – “Hemorrhagic Stroke”
* Acute hemorrhage appears hyperdense on head CT
* 40% 1-year survival, 12 – 39% functional independence at follow-up
36
Intraparenchymal Hemorrhage (IPH)
* Clinical symptoms
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
strokes - hypertension
* 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
CEREBRAL AMYLOID ANGIOPATHY
39
Imaging Features of CAA (Cerebral Amyloid Angiopathy)
Superficial Siderosis
40
imaging features of IPH induced by hypertension
41
Treatment - Prevent Hemorrhage Expansion!
* 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
