Acute Ischemic Stroke Flashcards

1
Q

what race has higher risk for death from stroke?

A

blacks have nearly twice the risk and much higher death rate from stroke

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2
Q

what is more common, ischemic or hemorrhagic stroke

A

ischemic: 84% hemorrhagic 16%

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3
Q

sub classification of ischemic stroke?

A

thrombotic 53% embolic 31%

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4
Q

sub classification of hemorrhagic stroke?

A

ICH - intra cranial hemorrhage 10% SAH - sub arachnoid hemorrhage 6%

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5
Q

what’s the difference between embolic & thrombotic stroke?

A

embolic: comes from elsewhere besides the brain. thrombotic: place rupture inside the brain

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6
Q

what is the definition of a stroke?

A

-sudden onset of neurologic deficit caused by cerebrovascular etiology -if it lasts longer than 24 hours its ALWAYS a stroke -if it lasts < 24 hours WITH permanent tissue damage its a stroke

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7
Q

what’s the definition of TIA (transient ischemic attack)

A

-sudden onset of focal neurologic deficit caused by cerebrovascular etiology -no permanent tissue damage -lasting < 24 hours without permanent tissue damage -symptoms must be gone within 24 hours -most TIA last < 1 hour (typically <10-20 minutes) -symptoms disappear without interventions

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8
Q

what is the penumbra?

A

-tissue around a stroke core that has decreased blood flow, but remains salvageable -explains much of the early improvement in neurological function after stroke -major principle directing much of our interventions

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9
Q

risk factors for stroke?

A

-sex: F>M -age -race/ethnicity: AA doubles risk than other ethnicities -low birth weight -genetics - hyper coagulable Modifiable -HTN -smoking -diabetes types 1 & 2 (controlled & not controlled) -dyslipidemia -carotid stenosis -cardiac disease -atrial fibrillation -sickle cell disease

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10
Q

less well documented modifiable risk factors for stroke

A

-etoh abuse: intracranial hemorrhage, hyper/hypo tensive -drug abuse -birth control - hyper coagulable -migraines -hyperhomocysteinemia - hypercoagulable -elevated lipoprotein -hypercoagulability -inflammation -infection

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11
Q

what’s the difference between posterior and anterior circulation?

A

Proximal occlusions: 1 & 2, if it’s past M2, A2 then they are distal occlusion, smaller more tortuous vasculature-difficult to access 2 or lower is proximal occlusion generally can’t get to with endoscopic procedure

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12
Q

what is the neurophysiology of occlusion?

A

ischemia: decreased blood flow due to blockage-> neurons are deprived of oxygen and glucose

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13
Q

what is the ischemic cascade?

A

unleashed within seconds to minutes of the loss of perfusion to a portion of the brain resulting in edema and cell death

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14
Q

cause of a thrombotic stroke?

A

Cause: platelet aggregation/vessel occlusion

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15
Q

onset time of thrombotic stroke?

A

during sleep when BP is lowest

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16
Q

risk factors for thrombotic stroke?

A

large vessel disease and atherosclerosis -dissection (trauma) -arteritis - inflammatory process -small vessel disease -chronic HTN

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17
Q

thrombotic stroke mechanisms

A

-most common cause of stroke -atherosclerosis -thrombus occludes the vessel -plaque occludes longitudinally -impedes flow due to stenosis

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18
Q

what are causes of embolic strokes?

A

fragments formed outside the brain break off and travel to a vessel in the brain. -typically from the heart, a-fib/valvular disease (collecting thrombus on valve)

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19
Q

onset of embolic stroke?

A

abrupt, may occur during exercise.

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20
Q

embolic stroke mechanisms

A

-atrial fibrillation -mitral stenosis -PFO (thrombus can collect in the shunt between R& L atrium) -prosthetic cardiac valve (not appropriately anti-coagulated) -left atrial of ventricular thrombus -endocarditis (septic emboli, infective and non-infective) -atrial myxoma (atrial mass that comes out of the atrial septum causing blood to pool in the LV/LA)

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21
Q

physical exam findings of issues with anterior circulation, anterior cerebral artery

A

-it’s the front of the head -medial aspects of motor and sensory strips (contralateral weakness) -altered mental status (frontal lobe) -impaired judgement (frontal lobe) -contralateral lower extremity weakness and hypoesthesia -gait apraxis (difficulty with motor planning)

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22
Q

physical exam findings with anterior circulation, middle cerebral artery?

A

-generally language deficit -lateral cortex of each hemisphere (language, motor, sensory) -contralateral hemiparesis (arm and face is usually worse than that of the lower limb) -contralateral hypoestheisa -contralateral homonymous hemianopsia -gaze preference toward the side of the lesion -agnosia is common (inability to recognize objects or people) -receptive or expressive aphasia

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23
Q

physical exam findings with posterior circulation, posterior cerebral artery

A

-impaired short term > long term memory -cortex (undersurface of temporal, parietooccipital, brainstem, cerebellum, thalamus) -visual deficits: homonymous hemianopsia, cortical blindness, visual agnosia -altered mental status -impaired memory -dizziness -limb weakness -nausea (since N/V centers are in the cerebellum) -language dysfunction

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24
Q

physical exam findings with posterior circulation, vertebrobasilar system

A

-medulla, cerebellum, pons, midbrain, thalamus and occipital cortex -wide variety of cranial nerve, cerebellar and brainstem deficits -vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, syncope and ataxia -variety of neurologic syndromes (locked in - basilar artery occlusion) -in contrast to hemispheric lesions, cortical deficits such as aphasia and cognitive impairments are absent.

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25
Q

what are the goals of management of ischemic stroke?

A

-rapid diagnosis (save the penumbra) -rapid management of acute complications (hemorrhagic transformation, airway management, hemodynamic monitoring) -initiate acute therapy if indicated (IV vs IA therapy) -observe for acute neurological and medical changes -facilitate medical and surgical interventions (hemicraniectomy) -plan for long term secondary prevention (ASA, coumadin, etc) -initiate rehabilitation since brain will regenerate neural networks around areas of ischemia

26
Q

when do you initiate long term secondary prevention for stroke?

A

start 24 hours after interventions to start secondary prevention, as long as no hemorrhagic transformation -would only start dual anti platelet therapy if they have failed on just ASA previously,

27
Q

emergent benchmarks

A

<10 minutes initiate MD evaluation and lab work <15 minutes notify stroke team <25 minutes initiate imaging scan, review patient history and establish time of last known well/symptom onset. Assess using NIHSS < 45 minutes: interpret imaging scan and labs. review patient eligibility for tPA < 60 minutes give tPA bolus and initiate infusion in eligible patients

28
Q

what is code stroke?

A

an organized protocol for emergency evaluation and treatment plan to begin tPA within 60 minutes -acute stroke team include MD/RN/Lab/Radiology -use of stroke rating scale (preferably NIHSS) -lab tests (CBC, BMP, coats, tox screen, ETOH, pregnancy) -baseline ECG - thought does not delay tPA -baseline troponin - dose not delay tPA -CXR only if indicated

29
Q

imaging suggestions for stroke?

A

imaging is recommended prior to therapy -CT provides the info you need, could get MRI but slower -IV tPA is recommended in setting of early ischemic changes on imaging (no frank hypo density) -non-invasive intracranial vascular study (CTA/MRA) is recommended if considering intra-arterial tPA or mechanical thrombectomy (do not delay tPA) -must be interpreted within 45 minutes of ED arrival by MD w/ expertise in racing imaging

30
Q

what does MRI help with?

A

helps determine the penumbra, but don’t need it before you treat w/ tPA

31
Q

what is hypo density of CT and what does it look like

A

approximately 48 hours out, the tissue is all dead, tPA would cause the area to hemorrhage

32
Q

facts on IV tPA

A

-gold standard, you can use this and endovascular -quick to administer and access -easy screening tool for eligibility -many contraindications for administration (< 1/3 of the hemisphere can’t have hypodensity, if >1/3 then there is already too much ischemia, the patient is too far gone)

33
Q

contraindications to IV tPA

A

-BP > 180 that is uncontrolled -last known normal > 3 to 4.5 hours ago -recent surgery -ICH

34
Q

facts on IA therapy

A

can help extend therapies, basilar artery occlusion - this is the patients last option, so we generally go outside of the normal 8 hour window -IA mechanical thrombectomy -beneficial to those who do not meet eligibility requirements for IV treatment -longer window of opportunity -takes time to get patient to table -blood clot will turn into rock if you want too long to take it out

35
Q

what are the indications for IV TPA?

A

-acute neurologic deficit expected to result in significant long term disability -non-contrast CT showing no hemorrhage or well established acute infarct -acute ischemic stroke symptoms with onset, or time last know well, clearly defined less than 3 hours before tPA will be given -2009 expanded timeframe to 3-4.5 hours after LKN

36
Q

what are exclusion criteria for the 3-4.5 hour time frame for IV tPA

A

> 80 years old -NIHSS baseline > 25 -taking anticoagulation -PMH stroke & DM

37
Q

bleeding complications of thrombolytic therapy

A

-should not be used unless the treatment facility is staffed and equipped to handle bleeding complications if bleeding happens: -discontinue the infusion -stat head CT scan if hemorrhage: draw PT/INR/aPTT, platelet count, fibrinogen -give platelets, FFP, or cryoprecipitate -consult neurosurgery

38
Q

acute blood pressure management

A

Eligible for tPA? Pre rx: SBP < 185, DBP, < 110 Post rx: SBP < 180, DBP, <105 not eligible for tPA SBP <220, DBP <120 rapidly lowering BP dose cause harm

39
Q

intra arterial therapy information

A

-patient is eligible for IV tPA should receive IV, even if being considered for IA tPA -< 6 hours for selected patients who are not eligible for IV tPA -not FDA approved -no agreed upon dosing - typical is 20 mg -must be at an experienced stroke center with immediate access to angio and interventionist (generally comprehensive stroke centers)

40
Q

IV tPA inclusion criteria

A

-onset of symptoms lest than 3-4.5 hours before beginning treatment -no head trauma or prior stroke in past 3 months -no MI in prior 3 months -no GI/GU hemorrhage in previous 21 days -no arterial puncture in noncompressisble site during prior 7 days -no major surgery in prior 14 days -no history of prior intracranial bleed -systolic BP < 185, DBP < 110 -no evidence of acute trauma or bleeding -not taking an oral anticoagulant, or if yes, INR < 1.7 -if taking heparin w/in 48 hours, a normal aPTT -platelet count of more than 100K -blood glucose > 50 -no seizure with residual poetical impairments -CT scan dose not show evidence of multi-lobar infarction (hypo density over 1/3 hemisphere)

41
Q

criteria for intra-arterial therapy

A

-longer windows of opportunity depending on vessel occluded (6-12 hours) -proximal large vessel occlusion benefits usually outweigh risks if they don’t meet IV tPA criteria

42
Q

two options for intra-arterial treatments for acute CVA

A
  1. mechanical thrombectomry: stent retrievers, aspiration, combo procedures “Solumbra” 2. intra arterial tPA: injected directly into clot within cerebral artery IV tPA is still first & quickest intervention
43
Q

what is a penumbra device?

A

aspiration device, removes clot intact w/ suction -quick removal of large occlusions, as no need to deploy/position stent

44
Q

solumbra technique?

A

penumbra + stent retriever -use of stent retriever along with aspiration benefits: prevents distal thrombus break-off

45
Q

what is the modified rankin score & when is it used?

A

used to assess physical disabilities after stroke 0: no symptoms 1: no significant disability, despite symptoms, able to perform all usual duties & activities 2: slight disability; unable to perform all previous activities but able to look after own affairs without assistance 3: moderate disability; requires some help, but able to walk without assistance 4: moderately severe disability: unable to walk without assistance and unable to attend to own bodily needs with assistance 5: severe disability; bedridden, incontinent, and requires constant nursing care and attention 6: death

46
Q

what is TICI scoring?

A

thrombosis in cerebral infarction 0: no perfusion 1: perfusion past the initial obstruction but limited distal branch filling with little or slow distal perfusion 2a: perfusion of less than half of the vascular distribution of the occluded artery 2b: perfusion of half or greater of the vascular distribution of the occluded artery 3: full perfusion with filling of all distal branches

47
Q

what does TICI scoring do?

A

helps to quantify revascularization after ischemic event

48
Q

what is goal for TICI scoring?

A

2b/3

49
Q

what do all of the studies (ESCAPE, EXTEND-IA, MR CLEAN) show?

A

intra-arterial therapy for acute ischemic stroke in proximal anterior circulation is now proven to improve -mRs -mortality -NIHSS -reperfusion after 24 hours -QOL *there are no trials for posterior circulation, but we use it b/c they can be left with severe deficit.

50
Q

what is important to note for intra arterial therapy?

A

focus on TIMING is still key to saving tissue, however endovascular treatments allow us to extend windows and include more complex patients.

51
Q

what are general admission management guidelines?

A

-use of comprehensive, specialized stroke care -use of standardized stroke order sets -early mobilization (crate networks around the areas that were occluded/ischemic) -swallow eval before eat/drinking (if fail get SLP) -if cannot swallow, provide NG/OG/PEG nutrition -DVT prophylaxis with SQ AC (if TPA first down 24 hours treatment, use SCDs) -treatment of concomitant medical disease (HTN, HLD, DM, AFIB, smoking cessation)

52
Q

what is good post stroke management?

A

-cardiac monitor x 24 hours -airway / ventilatory support if decreased LOC or lower cranial nerve dysfunction (9-11 - not good cough/gag) -goal temperature, normothermic -correct symptomatic cardia arrhythmia -glycemic control (treat BG<60, goal <180)

53
Q

anti-platelet post stroke managment

A

-aspirin: initial dose 325 mg in ED (if can’t get tPA) -given within 24-48 hours of stroke onset (after IV/IA tx)

54
Q

blood pressure management in stroke patients

A

-in exceptional cases, hypotensive patient with neurological decline, may receive vasopressors to improve cerebral blood flow -need close CV and neuro monitoring -put them on pressers to provide distal perfusion, let the patient’s neuro exam guid the treatment with pressors

55
Q

BP management with known HTN

A

restart home anti-HTN meds is reasonable after 24 hours from acute ischemic stroke, provided neurologically and hemodynamically stable if BP is below 120 & clinically correlated then might push up BP a bit

56
Q

what can you do for neuroprotection?

A

statin & lipid panel induced hypothermia - not well established, more clinical trials are needed

57
Q

how to treat acute complications

A

treat increased ICP: -mannitol -hypertonic saline -hyperventialtion (temporary; goal CO2 normal - CO2 dilates vessels) -CSF diversion - EVD -HOB 30 degrees to allow normal venous return -for risk of malignant cerebral edema, transfer to medical center with neurosurgical expertise (hemicraniectomy) -avoid hypotonic solutions (D5W)

58
Q

do you need to treat recurrent seizures?

A

no - don’t need to prophylaxis them, no keppra

59
Q

should you give steroids after stroke?

A

no steroids - cytotoxic cell death. vasogenic edema responds to steroids. This apoptosis/cell death from stroke doesn’t respond to steroids.

60
Q

what additional workup would you do?

A

Lab: TSH, RPR, homocysteine, cholesterol, LDL, HDL, triglycerides A1C TTE w/ bible study (looking for: PFO, valvular abnormalities) carotid dopplers