Acute Ischemic Stroke Flashcards
what race has higher risk for death from stroke?
blacks have nearly twice the risk and much higher death rate from stroke
what is more common, ischemic or hemorrhagic stroke
ischemic: 84% hemorrhagic 16%
sub classification of ischemic stroke?
thrombotic 53% embolic 31%
sub classification of hemorrhagic stroke?
ICH - intra cranial hemorrhage 10% SAH - sub arachnoid hemorrhage 6%
what’s the difference between embolic & thrombotic stroke?
embolic: comes from elsewhere besides the brain. thrombotic: place rupture inside the brain
what is the definition of a stroke?
-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
what’s the definition of TIA (transient ischemic attack)
-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
what is the penumbra?
-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
risk factors for stroke?
-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
less well documented modifiable risk factors for stroke
-etoh abuse: intracranial hemorrhage, hyper/hypo tensive -drug abuse -birth control - hyper coagulable -migraines -hyperhomocysteinemia - hypercoagulable -elevated lipoprotein -hypercoagulability -inflammation -infection
what’s the difference between posterior and anterior circulation?
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
what is the neurophysiology of occlusion?
ischemia: decreased blood flow due to blockage-> neurons are deprived of oxygen and glucose
what is the ischemic cascade?
unleashed within seconds to minutes of the loss of perfusion to a portion of the brain resulting in edema and cell death
cause of a thrombotic stroke?
Cause: platelet aggregation/vessel occlusion
onset time of thrombotic stroke?
during sleep when BP is lowest
risk factors for thrombotic stroke?
large vessel disease and atherosclerosis -dissection (trauma) -arteritis - inflammatory process -small vessel disease -chronic HTN
thrombotic stroke mechanisms
-most common cause of stroke -atherosclerosis -thrombus occludes the vessel -plaque occludes longitudinally -impedes flow due to stenosis
what are causes of embolic strokes?
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)
onset of embolic stroke?
abrupt, may occur during exercise.
embolic stroke mechanisms
-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)
physical exam findings of issues with anterior circulation, anterior cerebral artery
-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)
physical exam findings with anterior circulation, middle cerebral artery?
-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
physical exam findings with posterior circulation, posterior cerebral artery
-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
physical exam findings with posterior circulation, vertebrobasilar system
-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.
what are the goals of management of ischemic stroke?
-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
when do you initiate long term secondary prevention for stroke?
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,
emergent benchmarks
<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
what is code stroke?
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
imaging suggestions for stroke?
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
what does MRI help with?
helps determine the penumbra, but don’t need it before you treat w/ tPA
what is hypo density of CT and what does it look like
approximately 48 hours out, the tissue is all dead, tPA would cause the area to hemorrhage
facts on IV tPA
-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)
contraindications to IV tPA
-BP > 180 that is uncontrolled -last known normal > 3 to 4.5 hours ago -recent surgery -ICH
facts on IA therapy
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
what are the indications for IV TPA?
-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
what are exclusion criteria for the 3-4.5 hour time frame for IV tPA
> 80 years old -NIHSS baseline > 25 -taking anticoagulation -PMH stroke & DM
bleeding complications of thrombolytic therapy
-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
acute blood pressure management
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
intra arterial therapy information
-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)
IV tPA inclusion criteria
-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)
criteria for intra-arterial therapy
-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
two options for intra-arterial treatments for acute CVA
- 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
what is a penumbra device?
aspiration device, removes clot intact w/ suction -quick removal of large occlusions, as no need to deploy/position stent
solumbra technique?
penumbra + stent retriever -use of stent retriever along with aspiration benefits: prevents distal thrombus break-off
what is the modified rankin score & when is it used?
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
what is TICI scoring?
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
what does TICI scoring do?
helps to quantify revascularization after ischemic event
what is goal for TICI scoring?
2b/3
what do all of the studies (ESCAPE, EXTEND-IA, MR CLEAN) show?
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.
what is important to note for intra arterial therapy?
focus on TIMING is still key to saving tissue, however endovascular treatments allow us to extend windows and include more complex patients.
what are general admission management guidelines?
-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)
what is good post stroke management?
-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)
anti-platelet post stroke managment
-aspirin: initial dose 325 mg in ED (if can’t get tPA) -given within 24-48 hours of stroke onset (after IV/IA tx)
blood pressure management in stroke patients
-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
BP management with known HTN
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
what can you do for neuroprotection?
statin & lipid panel induced hypothermia - not well established, more clinical trials are needed
how to treat acute complications
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)
do you need to treat recurrent seizures?
no - don’t need to prophylaxis them, no keppra
should you give steroids after stroke?
no steroids - cytotoxic cell death. vasogenic edema responds to steroids. This apoptosis/cell death from stroke doesn’t respond to steroids.
what additional workup would you do?
Lab: TSH, RPR, homocysteine, cholesterol, LDL, HDL, triglycerides A1C TTE w/ bible study (looking for: PFO, valvular abnormalities) carotid dopplers
