22 - Stroke Flashcards

1
Q

Pathophysiology of stroke

A
  • Abrupt onset focal neurologic deficit that lasts > 24 h and is of presumed vascular origin (separates this from seizure or other cause)
  • Majority are ischemic, caused by interruption of blood flow to brain due to clot
  • 13% are hemorrhagic, caused by uncontrolled bleeding in brain
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2
Q

Other names for stroke

A
  • Cerebral vascular accident (CVA)
  • Cerebral vascular insult (CVI)
  • Cerebral infarction
  • Brain attack
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3
Q

Definition of ischemic stroke

A

Occlusion of cerebral artery causing abrupt development of focal neurologic deficit due to inadequate blood supply to an area of the brain

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4
Q

Difference between thrombotic and embolic ischemic stroke

A
  • Thrombotic = thrombus formation inside an artery in the brain (ie: atherosclerosis of cerebral vasculature)
  • Embolic = emboli from intra or extracranial arteries
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5
Q

What are the 2 types of embolic ischemic strokes? What is the difference between each?

A
  • Carotid stenosis = atherosclerotic plaque ruptures -> thrombus formation -> local occlusion or dislodge as emboli & causes downstream cerebral vessel occlusion
  • Cardiogenic (means from heart) embolism = secondary to valvular heart disease, or nonvalvular atrial fibrillation; atrial blood stasis (blood isn’t flowing properly) -> emboli -> occlusion of cerebral circulation
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6
Q

Describe a transient ischemic attack (TIA)

A
  • Temporary focal neurologic deficit lasting < 24 h (typically < 30 min) as a result of diminished or absent blood flow
  • Commonly result from small clots breaking away from larger, distant clots; blood flow re-established as emboli are dissolved by fibrinolytic system
  • No residual neurologic deficit
  • Absence of acute infarction on imaging
  • At high risk for infarction or recurrent TIA (risk of stroke after definite TIA = 10% at 2 days, 17% at 90 days)
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7
Q

Describe hemorrhagic strokes

A
  • Escape of blood from cerebral vasculature into surrounding brain structure
  • Initial neurologic deficit attributable to direct irritant effects of blood in contact w/ brain tissue
  • Subsequent dysfunction due to anoxia (absence of oxygen) similar to ischemic stroke/TIA
  • Ex: subarachnoid hemorrhage (SAH), intracranial hemorrhage (ICH)
  • Causes = cerebral artery aneurysm, hypertensive hemorrhage, trauma, drugs
  • Prognosis poor
  • Predictors for worsened outcomes = higher clot volume, early & late edema
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8
Q

Modifiable risk factors for stroke

A
  • HTN, dyslipidemia, diabetes, heart disorders
  • Smoking
  • Hypercoagulability
  • Lifestyle (obesity, physical inactivity, diet)
  • Psychosocial stress
  • Intracranial aneurysms
  • Drugs, alcohol use
  • Carotid stenosis
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9
Q

Non-modifiable risk factors for stroke

A
  • Age (risk doubles for each decade > 55 y/o)
  • Male sex
  • Family history
  • Prior stroke
  • Race (African Americans, Asian-pacific islanders, Hispanics)
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10
Q

Clinical presentation of stroke

A
  • One sided weakness – sudden loss of strength or sudden numbness in face, arm, or leg
  • Trouble speaking – sudden difficulty speaking or understanding or sudden confusion
  • Vision problems – trouble seeing in one or both eyes, photophobia
  • Headache – sudden, severe, & unusual w/ no explainable cause
  • Dizziness – sudden loss of balance, vertigo, N/V
  • Altered level of consciousness
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11
Q

What is considered the acute and hyperacute phase of a stroke? What are the goals of therapy for acute phase?

A
  • Acute = 0-7 days
  • Hyperacute = 0-24 h
  • Goals = stabilization, reperfusion, supportive measures, prevent complications, & prevent recurrence
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12
Q

Acute phase tx – ischemic stroke

A
  • ABCs (airways, breathing, circulation)
  • BP (HTN common & transient in acute phase; treat only if SBP > 220/120 mmHg, have evidence of aortic dissection, acute MI, pulmonary edema, or hypertensive encephalopathy)
  • Fluids, electrolytes, temp
  • Glucose management
  • Neurological assessment
  • Early reperfusion – thrombolysis w/ r-tPA or endovascular therapy
  • Other issues – DVT prophylaxis (LMWH or UFH) & rule out cardioembolic source of ischemic stroke
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13
Q

Describe thrombolysis w/ r-tPA

A
  • Inclusion criteria = 18 years or older, ischemic stroke causing measurable neurologic deficit, given w/in 4.5 h before sx onset
  • Exclusion criteria = only minor or rapidly improving stroke sx, any source of active hemorrhage or any condition that could increase risk of major hemorrhage, any hemorrhage on brain imaging, recent major surgery, SBP > 185 or DBP > 110 refractory to antihypertensives
  • Dose = 0.9 mg/kg (max 90 mg)
  • Fibrinolytics (TNK) not yet proven as effective as tPA
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14
Q

Purpose of endovascular therapy for stroke

A
  • Used w/ r-tPA; 5 RCTs demonstrated benefit if done w/in 6 h of stroke onset
  • Criteria = age > 18, functionally disabling stroke, infarct in major cerebral artery
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15
Q

Other drugs for acute tx of ischemic stroke

A
  • Antiplatelets – reduce risk of early recurrent stroke; no effect on early mortality but significant decrease in death at 6 months; ASA should be given 24 h after tPA once post-thrombolysis hemorrhage ruled out
  • Combination antiplatelets (ASA + clopidogrel) – one study showed reduced risk of recurrent stroke w/o increased hemorrhagic stroke; has to be given w/in 12 h of sx onset
    • W/ results of CHANCE and POINT trials, combo ASA/clopidogrel are becoming standard of care for 3 weeks post minor stroke/TIA; beyond 3 weeks seems to increase bleeding w/ little stroke benefit
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16
Q

Acute phase monitoring for ischemic stroke

A
  • Neurologic sx – speech, extremity strength, facial symmetry; worsening sx indicate recurrence or extension
  • BP
  • Electrolytes
  • Complications (DVT, PE, infections)
  • Adverse effects = signs of bleeding (severe bruising, nose bleeds, blood in urine or stool, intracranial hemorrhage)
17
Q

Acute phase tx – hemorrhagic stroke

A

BP for intracranial hemorrhage w/ SBP 150-220 mmHg and w/o CI, acute lowering of SBP to 140 is safe & can be effective for improving functional outcome

18
Q

Secondary prevention – noncardioembolic ischemic stroke

A
  • Surgical intervention
    • Carotid endarterectomy (CEA) – indicated for carotid artery stenosis of > 70% on side of neurologic deficit; only performed in experienced stroke centre
    • Carotid artery angioplasty & stenting (CAS) – restricted to px refractory to medical therapy & not surgical candidates
  • For px w/ noncardioembolic ischemic stroke or TIA, use of antiplatelets rather than oral anticoagulation is recommended to reduce risk of recurrent stroke & other CV events (ASA alone first, then add on dipyridamole if had a stroke while on ASA; can use clopidogrel is ASA CI’d; ASA + clopidogrel not recommended b/c no benefit & increased risk of life-threatening bleeding)
  • Warfarin not recommended
19
Q

Secondary prevention – cardioembolic stroke

A
  • For px w/ first & recurrent stroke in nonvalvular atrial fibrillation – warfarin, apixaban, dabigatran, or rivaroxaban
  • Start warfarin w/in 1-2 weeks after cardioembolic stroke & use ASA until INR therapeutic
  • For px unable to take oral anticoagulants, ASA alone is recommended; addition of clopidogrel to ASA may be reasonable
20
Q

Anticoagulation in rate control

A
  • Oral anticoagulant – warfarin, dabigatran, rivaroxaban, apixaban
  • EC ASA 81-325 mg/day
21
Q

Toxicity endpoints – anticoagulation

A
  • Signs of bleeding, Hgb < 100 or drop of 20%
  • Warfarin – INR > 3
  • New oral anticoagulants – CrCl < 30 mL/min
22
Q

Other secondary prevention of stroke

A
  • *BP lowering most important for long term prevention of ischemic and hemorrhagic
    • Restart BP medications 24-72 h after acute phase w/ target of < 140/90
    • Selection of agent not as important about actual BP control
  • Statin therapy – recommended for most px who have had ischemic stroke or TIA
  • Diabetes management
  • Lifestyle changes – smoking cessation, avoid alcohol consumption, increase physical activity, weight loss, diet less in saturated fats
  • Depression screening