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Stroke in the Emergency Room:What do we need to know?
Salah G. Keyrouz, MD, FAHA
March 10, 2012
Stroke in the Emergency Room:What do we need to know?
Disclosure: None
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Outline
• DefinitionI t d ti• Introduction
• Clinical Presentation• Differential diagnosis• Urgent assessment in the ER• Intravenous thrombolysisIntravenous thrombolysis• Post thrombolysis care
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Definition
• A STROKE is an acute, non‐convulsive l i d fi itneurologic deficit
• 3 types: ischemic, Intracerebral hemorrhage, subarachnoid hemorrhage
• Diagnosis is clinicalImaging and laboratory data help differentiate the– Imaging and laboratory data help differentiate the type of stroke, and confirm the diagnosis
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Introduction
• Stroke is an emergency
• The non‐emergent approach to treating stroke is replaced by a rapid and systematic approach (time‐limited treatment)
• Early assessment + intervention start in the pre‐hospital settingpre‐hospital setting
• Therefore, initial minutes‐hour in ED are crucial
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Clinical Presentation
• History is very important (>> examination)– SUDDEN weakness
– SUDDEN numbness/sensory deficits
– SUDDEN loss of ability to understand, produce speech
– SUDDEN dysarthriay
– SUDDEN vision loss (monocular or binocular)
– SUDDEN imbalance, vertigo, dizziness
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Clinical Presentation
• Pain is not a common symptom of stroke– Headache more common with ICH, SAH
• Other pain (Chest, retro‐orbital, cervical) might signal underlying cause of stroke– Aortic dissection, AMI, carotid/vertebral artery dissection
• Memory loss is not a symptom of stroke– Transient Global Amnesia (TGA)
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Clinical PresentationLocalization
• Loss of consciousness occur in stroke when:– Brainstem (ARAS) involved
– Extensive bihemispheric involvement
– Bi‐thalamic involvement
– Large ICH with tissue shifts/midline structures
– IVHIVH
– SAH
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Clinical PresentationLocalization
• Language disturbances (aphasia)– Dominant hemisphere cortical/immediate subcortical area
• Agnosia (neglect, inability to perceive sensory stimulation); Apraxia– Non dominant hemisphere cortical/immediate p /subcortical area
– Anosognosia, asomatognosia
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Clinical PresentationLocalization
• Forced gaze deviation– Away from the weak side: ipsilateral frontal, ipsilateral thalamic
– To the weak side: contralateral pons, contralateral thalamic
• Bilateral ptosis/apraxia of eyelid opening (gives the false impression of sleepiness)– Non dominant hemisphere (large)
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Clinical PresentationLocalization
• Visual fields cut (HH, HQ)– Contralateral occipital, posterior parietal, medial temporal lesion
• Visual loss– Monocular: retina
– Binocular: bilateral occipitalBinocular: bilateral occipital
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Clinical PresentationLocalization
• Diplopia (double vision)– Monocular: retinal, vitreal, corneal, conversion/malingering
– Binocular: thalamus, midbrain, pons, cerebellar
– INO (MLF lesion medial midbrain, pons)
• Skew deviationSkew deviation– Thalamus, cerebellum, pons
• Vertigo, dizziness– Brainstem, cerebellum, inner ear apparatus
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Clinical PresentationLocalization
• Dilated, unreactive pupils– Midbrain (CN III nuclei, fibers)
• Pinpoint pupils– Pons, thalamus
• Midposition pupilsidb i– midbrain
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Differential Diagnosis“Stroke mimics”
• SeizuresNon convulsive– Non‐convulsive
– Complex partial (confusion, aphasia)
– Post‐ictal state, post‐ictal weakness/paralysis
• Migraine (complicated or hemiplegic)
• Hypoglycemia, hyperglycemiaHypoglycemia, hyperglycemia
• Peripheral nerve injuries/palsies (not acute)
• Syncope/cardiac arrhythmias
• Conversion, malingering18
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Urgent assessment in the ER
• ABC, O2 if needed, IV access, CBC, coags, BMP
• History. Particular attention to establishing “last known well time”
• Code stroke: a stroke team member at bedside in 15 min
• CT brain (non contrasted) differentiate ICH• CT brain (non contrasted): differentiate ICH, SAH and others, from IS
• MRI should not delay thrombolysis if indicated
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Urgent assessment in the ER
• Review inclusion & exclusion criteria for th b l ithrombolysis
• Discuss with patient and family members
• EKG, CXRay, CE (should not delay thrombolysis)
• Aggressively treat hyper and hypoglycemia• Aggressively treat hyper and hypoglycemia, hyperthermia
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Urgent assessment in the ER
• Signs of early ischemia on CT:– Loss of Gray‐white differentiationLoss of Gray white differentiation– Loss of differentiation of cortical ribbon (insular cortex)
– Loss of differentiation of caudate head and surrounding white matter (IC)
– Unilateral dense MCA sign• CT also helpful to look for complicationsCT also helpful to look for complications
– Cerebral edema– HCP– Hemorrhagic conversion
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Urgent assessment in the ERblood pressure treatment in IS
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Urgent assessment in the ERblood pressure treatment in IS
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IV thrombolysis
• Remains the only approved acute therapy for i h i t kischemic stroke
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Tissue plasminogen activator
plasminplasminTissue plasminogen
plasminogenplasminogen
plasminplasmin
plasminplasminplasminogen activator
Fibrin
Fibrinogen
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IV thrombolysis
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IV thrombolysis up to 4.5h
• Exclusion (different than 0 to 3 hours):– Age > 80y
– Severe stroke (NIHSS score>25 or >1/3 of MCA territory on CT or MRI)
– Patients on oral anticoagulants regardless of INR
– Previous stroke AND Diabetes
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Implications of ECASS III
• AHA guidelines: IV t‐PA should be considered f li ibl ti tfor eligible patients
• Not FDA approved yet (approved in Europe)
• Widely adopted in most stroke centers
• Benefit < than that seen between 0‐3h
/• Consent; adherence to inclusion/exclusion criteria
• Time is brain
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IV thrombolysis
• IV t‐PA dose 0.9mg/Kg (max 90mg)–10% of dose given as bolus over 1 min
–90% infusion over one hour•Pharmacokinetics
–Half‐life 10 to 15 min
•Adverse events:•Adverse events:–Bleeding–Angioedema (1 to 2% of patients on ACE‐)
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Who is eligible to receive IV t‐PA
• Clinically
– Clinical diagnosis of ischemic stroke causing measurable– Clinical diagnosis of ischemic stroke causing measurable deficit
– Onset of symptoms < 4.5 hours prior to starting IV t‐PA
– No symptoms suggestive of subarachnoid hemorrhage (thunderclap headache, LOC)
– Symptoms not rapidly improving
– no head trauma, prior stroke in previous 3 months
– no history of intracerebral hemorrhage
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Who is eligible to receive IV t‐PA
• Clinically
– No major surgery in previous 14 days– No major surgery in previous 14 days
– No GI or UT hemorrhage in previous 21 days
– No arterial puncture at non‐compressible site in previous 7 days
– No evidence of active bleeding of major trauma on exam
– No seizure with post‐ictal neurologic deficits
– BPs < 185 mmHg and BPd < 110 mmHg (not requiring more than 3 doses of IV anti‐hypertensive to lower)
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Who is eligible to receive IV t‐PA
• Laboratory and Imaging
– Head CT showing no blood (ICH SDH SAH EDH)– Head CT showing no blood (ICH, SDH, SAH, EDH)
– Platelets > 100,000
– INR < 1.5
– PTT within normal range
– Glucose > 50 mg/dL
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Who is eligible to receive IV t‐PA
• WarningsHi h NIHSS ( > 22)– High NIHSS score ( > 22)
– Older patients ( > 77 years)
– Patients with early ischemic changes on head CT
…however, to increase # of patients treated with t‐PA, and given lack of evidence for most exclusionand given lack of evidence for most exclusion criteria, many are relaxing criteria to t‐PA administration (with no increase in rate of complications)
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IV t‐PA in the era of new anticoagulants
• Direct thrombin inhibitors (Dabigatran)
F t X i hibit (A i b Ri b )• Factor Xa inhibitors (Apixaban, Rivaroxaban)
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IV t‐PA in the era of new anticoagulants
• Direct thrombin inhibitors (Dabigatran)Ch k th bi ti (TT) 10 i– Check thrombin time (TT). 10 min
– If normal (laboratory/coagulation analyzer specific; 16 –22 sec) proceed with IV t‐PA regardless of time of last dose
• Factor Xa inhibitors (Apixaban, Rivaroxaban)– Check a prothrombin timep
– If < upper limit of normal (laboratory/coagulation analyzer specific; 15.7 sec) proceed with IV t‐PA regardless of time of last dose
• Written consent43
Beyond IV thrombolysis
• if onset > 4.5h OR• patient ineligible for IV t‐PA OR• fails to improve following IV t‐PA OR
• on new oral AC, consider other interventions–IA t‐PA–Mechanical embolectomy and thrombectomy
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Post thrombolysis care• Following t‐PA administration:
– BP check and control (ok in arm with IV)– Frequent neurologic evaluation (beware new HA or one with changing characteristics)
– NIHSS at 24 hours– No invasive procedure unless necessary– No ASA, Plavix, or Aggrenox. No Lovenox or Heparin x 24 hoursHeparin x 24 hours
– NPO until swallowing evaluated– ± CT head at 24 hours
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Complications following t‐PA• Beware angioedema
– Treat with steroids H1 and H2 blockers for 24h (orTreat with steroids, H1 and H2 blockers for 24h (or longer if needed)
• Bruising common. If severe in one place, consider Fx
• Mucosal bleeding is usually self‐limited and does t i ifi thnot require any specific therapy
• Deterioration and/or new HA warrants brain CT, stopping infusion (if ongoing), type and screen
• If bleeding: PLTS, cryoprecipitate, FFP47
Stroke mimics and IV t‐PA
• Risk of complications is low to non‐existent
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Stroke mimics and IV t‐PA
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Thank You