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80 Cards in this Set
- Front
- Back
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Prevalence of stroke subtypes |
Ischemic (85%) > Intracerebral hemorrhage (10%) > Subarachnoid hemorrhage (5%) |
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Epidemiology of stroke |
-800,000 annually in US -Fifth leading cause of death in US -Leading cause of long-term disability -Major racial disparities: blacks more likely to have stroke of all types than whites |
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Ischemic stroke (define) |
Neurologic deficit caused by interruption of cerebral or spinal blood flow -Sx lasting at least 24 hrs OR with radiographic confirmation of infarction |
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Transient ischemic attack (define) |
Transient episode of neurologic dysfunction caused by focal brain, spinal, or retinal ischemia resolving within 24 hours AND without radiographic infarction |
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Risk factors - most important modifiable and non-modifiable |
Modifiable: HTN (for both ischemic + hemorrhagic stroke), diabetes is risk fx for ischemic stroke in middle-aged pts, a-fib in elderly pts Non-modifiable: Age |
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Non-contrast head CT is usually normal in ____ stroke |
acute ischemic |
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Stroke mimics |
-Seizure w/ Todd's paralysis or non-convulsive status epilepticus -Hypo or hyperglycemia -Complicated migraine -Mass lesion -Recrudescence: worsening or emergence of previous deficit due to infection, toxin/metabolic process -Conversion disorder |
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New advances in stroke advanced imaging |
Used to only do non-contrast head CT CT angiography - can show you large vessel stenosis or occlusion (for select pts w/ large blockages, embolectomy is beneficial) Penumbral imaging |
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Large vessel strokes |
>50% stenosis of large artery in the territory of the stroke Extra vs intracranial ~15% of ischemic strokes in US |
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Small vessel strokes |
Small, deep, penetrating vessels <1.5 cm in diameter ~20% of ischemic strokes in US |
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Mechanisms of ischemic stroke |
Large vessel stroke Small vessel stroke Cardioembolic Other defined Unknown |
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Cardioembolic stroke prevalence |
~25% of ischemic strokes in US |
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Two possible mechanisms underlying large vessel stroke |
Artery to artery embolus Hemodynamic failure (atherosclerosis, stenosis) |
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Small vessel stroke pathophysiology |
-Stroke due to occlusion of a small deep perforator (not out in the cortex) -Lipohyalinosis of vessels -Classically associated w/ HTN and DM -Small cortical infarcts are not lacunes! (usually embolic) |
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which image represents a lacune? |
Top image - lacune (deep white matter) Bottom image - not lacune - small cortical infarct - more peripheral |
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Huge risk factor for cardioembolic stroke + most common underlying mechanism? |
Atrial fibrillation and paroxysmal atrial fibrillation |
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Congenital heart condition that is a high risk factor for cardioembolic stroke? |
Patent Foramen Ovale with DVT (not high risk w/out venous clot) |
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High risk factors for cardioembolic stroke |
-A-fib and paroxysmal a-fib -Rheumatic mitral or aortic valve disease -Mechanical heart vales -Atrial or ventricular thrombus -Fibrous nonbacterial endocarditis - pts in lupus, cancer pts -Infective endocarditis -Symptomatic CHF w/ ejection fraction < 30% -Akinetic heart wall -Papillary fibroelastoma -L atrial myxoma -Sick sinus syndrome -Sustained atrial flutter -Recent MI (w/in 1 mo) -PFO w/ DVT |
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Potential risk fx for cardioembolic stroke (not high risk) |
-PFO w/out DVT -Atrial septal aneurysm -Complex atheroma in ascending aorta or proximal arch |
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"Other" possible causes for stroke |
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Management plan for acute ischemic stroke |
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Reperfusion medication |
tPA - FDA approved for acute stroke therapy in 1996; NINDS study - treatment w/in 3 hours |
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Major risk associated w/ tPA? |
Bleeding - symptomatic intracranial hemorrhage is what we worry about the most (~6% risk) |
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Essence of time in treatment |
Everyminute you delay reperfusion = more cells that are dying Oddsratio of good outcome decreases quicklyNotsome magic cut-off Earlieryou treat the better Willtreat up to 4.5 hrsbut benefit is less; not FDA approved |
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Limitations of tPA |
Reperfusion is dependent upon available substrate and time to lyse clot Stimulates platelet activation May not be as effective w/ larger or older clots Hemorrhagic transformation Endovascular therapy may be alternative for some of these limitations |
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Early endovascular trials |
-All negative trials w/ result to primary endpoint (no benefit for embolectomy) -Limitations: all had minimal use of stent-retrievers (first gen devices), did not mandate that pts had proven large vessel occlusion, long delay from onset and imaging to endovascular therapy |
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AHA updates guidelines - standard of care now embolectomy + tPA for which patient population? |
-Prestroke mRS score 0-1 -Acute ischemic stroke receiving IV t-PA within 4.5 hrs of onset according to guidelines -Causative occlusion of the internal carotid artery or proximal MCA (M1) -Age >/= 18 yrs -NIHSS score of >/= 6 -ASPECTS >/= 6 -Treatment can be initiated (groin puncture) w/in 6 hrs of onset |
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Mechanisms to limit cellular injury |
-Maintain cerebral perfusion (monitor BP - don't lower precipitously) -Maintain cerebral oxygenation (pulse ox - oxygen only if sats low) -Maintain normothermia (vitals - temp - acetominophen prn to lower fever) -Maintain euglycemia - check serum glucose (we don't really know if there is benefit to tight glycemic control in stroke care) -No proven neuro-protective drugs |
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Neurologic complications of ischemic stroke |
-Stroke extension or recurrence -Mass effect/herniation: edema increases over 3-5 days, hemicraniectomy (younger pts w/ large strokes), hypertonic saline? -Seizures: ~5% in acute setting, no role for prophylactic AEDs |
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Systemic complications of acute ischemic stroke |
-Aspiration (NPO, early dysphagia screen) -DVT (especially if bedridden - can lead to PE), prevent w/ subQ heparin, compression devices -Infection (UTIs common - take out Foley catheter when possible), Early mobilization -Skin breakdown (nursing care, mobilization) -Depression (treat if found) |
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Workup for ischemic stroke |
-Brain imaging (CT to start, but also MRI) -Vascular imaging -EKG -Telemetry (pts not necessarily in afib when they show up in the ER, but good to monitor in case it is paroxysmal) -Echocardiography -Basic labs: CBC, glucose/basic chemistry/electrolytes, INR/PTT, cardiac enzymes, fasting lipids -PT/OT/speech eval Help to ID ischemic stroke mechanism |
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Primary stroke center metrics |
-tPA for eligible pts -VTE prophylaxis -Antithrombotic therapy by day 2 -Discharge on antithrombotic therapy -Anticoagulant therapy for afib -Discharge on statin unless contraindicated -Stroke edu provided -Screen for rehab |
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Ischemic stroke subtypes - subsequent stroke risk |
-Highest early risk of recurrent stroke is in patients w/ large vessel stenosis (highest probability even w/in next week) -Cardioembolic has a very high rate of recurrence if not treated/managed appropriately -Lacunar strokes have lowest rate of recurrence |
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Medical mgmt for symptomatic carotid stenosis > 70% (REWATCH) |
-Carotid endarterectomy is generally unsatisfactory for pts who are reasonable surgical candidates: high risk for recurrence in this population -Possible role for heparin until surgery? (not standard of care) |
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Symptomatic carotid stenosis 50-69% (moderate) (REWATCH) |
ANSWER |
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Score used to determine risk for stroke based on presence of Afib |
CHADS score 0-6 score: Recent CHF (1), HTN (1), Age >/= 75 (1), diabetes (1), ischemic stroke or TIA in past (2) Higher score = more likely to have a stroke |
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Medical treatment based on CHAD scores |
CHADS score of 0 - aspirin only CHADS score of 1 - aspiring and/or anticoags (use other deciding factor stratification) CHADS score of 2+ - should be treated w/ anticoag unless contraindicated |
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Warfarin vs aspirin |
Warfarin is more effective than aspirin(+ placebo) for preventing ischemic stroke (however benefit depends on your risk factors [ex - previous stroke] - less benefit if you are low risk/no stroke hx) |
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New anticoagulants (compared to Warfarin) |
•Dabigatran,direct thrombin inhibitor•Apixaban,factor Xainhibitor •Rivaroxaban,factor Xainhibitor •Edoxaban,factor Xainhibitor •Allcomparable or better than warfarin for ischemic stroke prevention with lessintracranial bleeding •Downside to these drugs: Noantidote (w/ exception of dabigatran), more costly |
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Antithrombotic drugs w/ no indication for anticoagulant? |
Antiplatelet drugs -Aspirin -Clopidogrel (probably slightly better than Aspirin) -ASA + extended release dipyridamole (probably slightly better than aspirin, HA in 30%) (this is very rarely prescribed anymore) -ASA + clopidogrel not useful long-term (any reduction in ischemic stroke risk if offset by inc risk of bleeding); use monotherapy longterm |
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Location of bleeding in SAH vs ICH |
ICH= rupture of small blood vessels w/inthe brain parenchyma SAH = damage to vessel insubarachnoid space; typically from ruptured aneurysm |
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Spontaneous intracerebral hemorrhage |
Abrupt onset of HA, altered LOC, or focal deficit associated with a collection of blood within the brain parenchyma which is not due to trauma or hemorrhagic conversion of cerebral infarction |
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ICH locations |
-Lobar: gray matter, subcortical white matter -Deep hemispheric: basal ganglia, periventricular white matter, internal capsule, thalamus, pure IVH -Cerebellar -Brainstem: midbrain, pons, medulla (cerebellar and brainstem often lumped in w/ deep hemispheric ICH) |
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Odds ratio for non-lobar ICH |
Risk for any given patient when compared to an equivalent pt without non-lobar ICH -Prior ischemic stroke -Untreated HTN -1st degree relative -< high school ed (marker of other SES variables) -Warfarin -Normal cholesterol -Diabetes (interestingly enough, high cholesterol is actually protective) |
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Attributable risk |
whenyou have a population, if you get rid of a risk factor, how many cases of thatdisease will go away – depends on potency AND prevalence of risk factor false |
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Attributable risk for non-lobar ICH |
-Normal cholesterol -Untreated HTN -< HS edu -Prior ischemic stroke -Warfarin -Diabetes -1st degree relative |
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odds ratio for lobar ICH |
-Warfarin use -Prior stroke -Untreated HTN (controversial for lobar ICH) -< HS edu -Current smoking -Apo E2/4 (marker for amyloid angiopathy) |
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Attributable risk for lobar ICH |
•ApoE 2/4 (26) •UntreatedHTN (21) {controversial for lobar ICH}•Currentsmoking (17) • •Warfarinuse (13) •Priorischemic stroke (4) |
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Cerebral amyloid angiopathy |
-Pathology: destruction of normal cortical vasculature due to deposition of abnormal amyloid protein - vessels are fragile and tend to rupture -Mostly elderly patients except for genetic risk -Microbleeds on MRI (asymptomatic or minor transient sx) -Lobar ICH association -Association w/ Apo E2/E4 |
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What determines outcome after ICH? (more likely to lead to poor outcome) |
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Large ICH volume = |
worse outcome |
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Intracranial hemorrhage - hemorrhage growth |
Increased volume = worse outcome May explain gradual worsening in pts w/ ICH |
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Treatment for ICH |
-Supportive care -BP control (aggressive BP control early on may improve outcomes, however benefit was marginal) -Surgery for select pts (~10%) -If coagulopathy - correct immediately (Vitamin K, PCC + Fresh Frozen Plasma warfarin), protamine for heparin -Control ICP/prevent herniation: edema from cell death (cytotoxic edema) and through taken blood vessels (vasogenic edema) |
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Cerebral perfusion pressure |
-CPP = MAP - ICP -Goal is > 60 mm Hg -50 mm Hg = cerebral dysfunction -20 mm Hg = cerebral ischemia |
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Vascular malformations - most common underlying ICH? |
ateriovenous malformation (AVM) |
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Vascular malformations that can underlie ICH |
Arteriovenous malformation Cavernous agniomas Venous malformations (venous angiomas) Telangiectasis |
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Arterovenous malformation (define) |
•Arteriesand connecting to veins without intervening capillary bed and usually abnormalbrain tissue |
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Define cavernous angioma |
•Clustersof dilated capillaries without any intervening brain= |
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Define venous malformation (venous angiomas) |
•Enlargedbut functional draining veins |
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Define telangiectasis |
•Enlarged,ectaticcapillaries |
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Symptoms, risk of bleeding, potential treatments for AVMs |
•Maybe symptomatic or asymptomatic: Hemorrhage,seizures, headaches •Riskof bleeding much higher after the first hemorrhage •Potentialtreatments include surgery, radiotherapy, and/or embolization |
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Cavernous angioma - presentation, hemorrhage, imaging appearance, treatment |
•Canpresent with hemorrhage or seizures. •Typicallyhave varying ages of hemorrhage: Popcorn-likelesion on MRI •Symptomaticlesions may be treated surgically3 |
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Most commonly found venous malformation? Venous malformation most likely to cause ICH? |
Venous angioma most common Arteriovenous malformation most likely to cause ICH |
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SAH most often caused by ______. |
•Most often caused by a ruptured saccular (berry) aneurysm |
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Prevalence of unruptured aneurysm, likelihood of rupturing, what happens if rupture |
•2% of the general population havean unruptured aneurysm •If ruptures, 25% mortality rate. •Rupture risk depends upon size,location, and environmental factors (e.g. blood pressure, cocaine use) |
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Prevalence of aneurysm characteristics |
Saccular >> Fusiform >> dissecting, mycotic |
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Where do berry aneurysms most commonly occur? |
Vessel branch points -- most common is at anterior communicating artery |
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Genetics of aneurysms |
Genetic evidence: ~10% of pts have a first-degree relative w/ hx of SAH Reports of aneurysms located in same location among identical twins Associated w/ genetic disease (polycystic kidney disease) |
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Environmental risk factors for aneurysms |
•Smoking: Most important modifiablerisk factor for SAH -- 70-75%of persons with SAH have a prior history of smoking •Hypertension •Heavy alcohol use •Black race (in USA) •Female gender |
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Clinical presentation of SAH |
-Worst HA of my life - "Thunderclap HA" -LOC, vomiting, vertigo, nausea, meningeal signs -CT scan will detect 95% of SAH -If strong suspicion but negative CT -- LP -Xanthrochromia develops 6-12 hrs and lasts a few weeks (LP) |
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Treatment for SAH |
•Initially, bed rest, quiet •Prevention of recurrent hemorrhage •70%mortality rate if a second hemorrhage occurs. •Blood pressure control untilaneurysm secured •Nimodipine •Clipping vs. coiling |
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Surgical procedures for SAH |
Clipping: definitive treatment but much higher risk, can be done for aneurysms w/ no neck Coiling: less invasive, but maybe less durable (if coils compact, some residual aneurysm); coils inserted via catheter |
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Rebleeding after SAH |
-Unsecured aneurysm -4-15% on day 1, 20-30% in first month than 3% per year -80% of pts with rebleed have poor outcome |
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Cardiac dysfxn after SAH |
-Clinically significant in ~10-20% of pts -Troponin bumps common -Subendocardial band necrosis w/ "stunned myocardium" and PE -Arrythmias in 4% |
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Acute hydrocephalus following SAH |
20-30% of pts |
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Seziures after SAH |
10-20% of pts Common at onsetC |
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Hyponatremia after SAH |
20-30% of patients Often volume depleted - hypertonic fluids treatment |
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Vasospasm of SAH |
•Radiographic evidence of vasospasm in 70% •Delayed cerebral ischemia occurs in 20-30% of patients with SAH •Day 3-16; peak day 8 |
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Complications after SAH |
Rebleeding (unsecured aneurysm) Cardiac dysfunction Acute hydrocephalus Seizures Hyponatremia Vasospasm (delayed cerebral ischemia) |
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Treatment options for vasospasm |
•‘Triple H’ – hypertension, hypervolemia and hemodilution. •Nimodipine: Calcium channel blocker •Intra-arterial verapamil •Transluminal angioplasty (not done very often anymore) •Monitoring patients: Transcranial doppler ultrasound |
