i schemic stroke
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i schemic stroke. Alison Smock, MD Department of Neurology Medical University of South Carolina. definitions. Transient ischemic attack A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction - PowerPoint PPT PresentationTRANSCRIPT
ALISON SMOCK, MDDEPARTMENT OF NEUROLOGY
MEDICAL UNIVERSITY OF SOUTH CAROLINA
ischemic stroke
definitions
Transient ischemic attack A transient episode of neurological dysfunction caused by
focal brain, spinal cord, or retinal ischemia, without acute infarction
Tissue-based definition rather than time-based definition
Stroke Infarction of the central nervous system May be symptomatic or silent May not be evident by MRI
Stroke. 2009;40:2276-2293
epidemiology
Transient Ischemic Attack Estimated prevalence of self-reported physician-
diagnosis TIA is approximately 2.3% (translates to ~5 million people)
Incidence of TIA increases with age and varies by sex and race/ethnicity Men, blacks, and Mexican Americans have higher rates
of TIA their their female and non-Hispanic white counterparts
Approximately 15% of all strokes are heralded by a TIA 10-15% of patients have a stroke within 3 months, with
half occurring within 48 hoursCirculation. 2013;127:e6-e245
Stroke. 2009;40:2276-2293
epidemiology
TIA ABCD2 score
Clinical score to determine the risk for stroke within the first 2 days following a TIA
Age BP Clinical Features Duration Diabetes1 point ≥ 60 SBP ≥ 140
OR
DBP ≥ 90
Speech disturbance
without unilateral weakness
10-59 min Yes
2 points -- -- Unilateral weakness with or without speech
impairment
≥60 min --
Lancet. 2007;369:283-292.
epidemiology
ABCD2 score 2-day stroke risk Comment
0-3 1.0% Hospital observation may be unnecessary without another indication (ie new onset Afib)
4-5 4.1% Hospital observation justified in most situations
6-7 8.1% Hospital observation worthwhile
Lancet. 207;369:283-292
epidemiology
Stroke prevalence Estimated 6.8 million Americans ≥20 years of age
have had a stroke (2007-2010 data) Overall stroke prevalence during this period is an
estimated 2.8% Older adults, blacks, people with lower levels of
education, and people living in the southeastern United States had higher stroke prevalence
Circulation. 2013;127:e6-e245
epidemiology
Stroke incidence Each year, ~795,000 people experience a new or
recurrent stroke (610,000 are first attacks, 185,000 are recurrent)
Of all strokes, 87% are ischemic, 10% are ICH, 3% are SAH
Each year, ~55,000 more women than men have a stroke Women have a higher lifetime risk of stroke than men Women have a lower age-adjusted stroke incidence than
men White women 45-84 yo have lower stroke risk than white
men, but women >85 yo have elevated risk compared to white men
Analysis of data from FHS and GCNKSS suggests that stroke incidence is declining over time Circulation. 2013;127:e6-e245
epidemiology
Stroke mortality In 2009, stroke accounted for 1 of every 19 deaths in the US When considered separately from other CVDs, stroke ranks
No. 4 among all causes of death From 1999 to 2009, the annual stroke death rate decreased
36.9% and the actual number of stroke deaths declined 22.9%
Circulation. 2013;127:e6-e245
epidemiology
Circulation. 2013;127:e6-e245
http://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_319832.pdf
Circulation. 2013;127:e6-e245
so why does it matter?
Disability Stroke is the leading cause of serious long-term
disability in the United States In the NHLBI’s FHS, among ischemic stroke survivors
who were ≥65yo, the following disabilities were observed at 6 months after stroke: 50% had some hemiparesis 30% were unable to walk without some assistance 46% had cognitive deficits 35% had depressive symptoms 19% had aphasia 26% were dependent in ADLs 26% were institutionalized in a nursing home
Circulation. 2013;127:e6-e245
etiology
etiology of ischemic stroke
TOAST criteria Thrombosis or embolism due to atherosclerosis of a
large artery Embolism of cardiac origin Occlusion of a small blood vessel Other determined causes
Dissection Aneurysm Vasculitis
Undetermined cause (cryptogenic or incomplete investigation)
traditional other
Hypertension Hyperlipidemia Diabetes mellitus Smoking Coronary artery disease Heart failure Cardiac arrhythmias Chronic kidney disease Physical inactivity Drug use History of prior stroke Family history
Underlying rheumatologic disease
Hypercoagulable states
CNS infectionSepsisSleep apnea
risk factors
Circulation. 2013;127:e6-e245
etiology and presenting symptoms
Large vessel strokes (ICA, MCA, ACA, PCA) Cardio-embolic Atherosclerosis Artery-artery
embolism Dissections Aneurysms
Small vessel strokes Uncontrolled
hypertension Uncontrolled diabetes Uncontrolled
hyperlipidemia Smoking Sympathomimetics
http://www.cixip.com/index.php/page/content/id/1007
Carotids
Internal Carotids and MCAs
http://www.studyblue.com/notes/note/n/airway-77-93/deck/3078597
Circle of Willis
large vessel stroke syndromes – cortical
MCA – dominant hemisphere Contralateral hemiparesis (face/arm > leg) Contralateral hemisensory changes Head and eye deviation toward stroke Contralateral hemianopia Language difficulty Alexia Agraphia Acalculia Apraxia
large vessel stroke syndromes – cortical
MCA – non-dominant hemisphere Contralateral hemiparesis (face/arm > leg) Contralateral hemisensory changes Neglect/extinction Anosognosia Loss of prosody of speech Flat affect
ACA Crural paresis > arm paresis Frontal signs (eg, abulia)
large vessel stroke syndromes – cortical
Posterior Circulation ECVA/ICVA
Dizziness/Vertigo Cranial nerve lesions Cerebellar symptoms
PCA Homonymous hemianopia Hemisensory changes (lateral thalamus) Left PCA – alexia without agraphia, Gerstmann (acalculia,
agraphia, finger agnosia, R/L disorientation) Right PCA – prosopagnosia, visual neglect Bilateral – cortical blindness (Anton’s syndrome)
http://www.neuropenews.org/?attachment_id=2010
large vessel stroke syndromes – cortical
Basilar artery Typically presents as ischemia in the pons Asymmetric but bilateral motor and reflex
abnormalities Bulbar involvement Respiratory involvement “Tip of the Basilar”
Decreased LOC Oculomotor/pupillary abnormalities
small vessel stroke syndromes – subcortical
Pure motor Corona radiata, posterior limb of the internal capsule,
pons, medullaPure sensory
ThalamusSensorimotor
Thalamus, basal gangliaAtaxic hemiparesis
Corona radiata, anterior limb of the internal capsuleDysarthria-clumsy hand syndrome
Upper pons, junction between CR and IC
acute stroke
FDA approved options
(r)tPA (recombinant) tissue plasminogen activator – Gold Standard Approved for use within 3 hours of onset of neurologic
deficits in a defined population of patients
Aspirin 325mg Approved for use in patients who do not receive tPA
who do not have any contraindications (drug allergy) and 24 hours after receiving tPA if there is no hemorrhage on 24h post-tPA CT/MRI scan
tPA mechanism of action
http://www.cvpharmacology.com/thrombolytic/thrombolytic.htm
tPA – evidence based medicine
National Institute of Neurological Disorders and Stroke (NINDS) tPA Trial NEJM.1995;333:1581-1587
European Cooperative Acute Stroke Study (ECASS) I JAMA 1995;274(13):1017-25
ECASS II Lancet. 1998;352(9136):1245-51
ECASS III NEJM. 2008;359:1317-1329
tPA
What do you need to give IV tPA Last known normal Focal neurologic deficits by physical examination Non-contrasted head CT Finger stick blood glucose
thrombectomy
Indications Large vessel strokes (even after receiving IV tPA) Outside of the window for IV tPA Imaging suggestive of penumbra
Contraindications Matched deficit on CTP
stroke = brain attack
Why should you call a BAT Sudden development of focal neurologic findings
Why you should NOT call a BAT Altered mental status (without focal neurologic findings) To get a faster head CT
Who gets paged – it is an emergency after all… Neurology residents on call All vascular neurology attendings All NSICU attendings All neuroradiology attendings On call radiology residents All neurointerventional radiologists NIR techs and nurses CT techs NSICU, 9E and 9W charge nurses
stroke = brain attack
What information is helpful to us? Last known normal Symptoms that prompted the BAT Reason for admission Current medications Current labs – including finger stick Recent vitals DNR/DNI status
MUSC policy for calling a BAT
Altered mental status MET is called first, then the MET resident can
determine if a BAT is warranted
“If an in-patient is experiencing a change in mental status or confusion the Medical Emergency Team (MET) should be paged to the bedside to assess the patient – not the Brain Attack Team!”
“Once the Medical Emergency Team (MET) has assessed the patient and determines that a BAT should be called, at that time the BAT will respond.”
VA policy for calling a BAT
Regular hours (730a-530p weekdays) There is always a neurology resident in house, simply
page them After hours
If there is an inpatient that has stroke-like symptoms, the upper level medicine resident is expected to evaluate the patient (ie NIHSS), speak with the neurology resident on call if there is concern for acute stroke and the neurology resident will help direct care while going over to the VA
standard inpatient work up
Neuroimaging 24 hour post tPA scan MRI if indicated Vessel imaging
CTA vs MRA vs carotid dopplersLabs
A1c, lipids, UA, UDS When are TFTs indicated When is B12/folate/RPR indicated
TTE Agitated saline?
PT/OT/SLP consults
primary prevention
non-modifiable risk factors
Age Risk of ischemic stroke and ICH doubles for each successive
decade after age 55Gender
More prevalent in men than in womenLow Birth WeightRace/EthnicityGenetics
A meta-analysis of cohort studies showed that a positive family history of stroke increases risk of stroke by approximately 30% [OR 1.3; 95% CI, 1.2 to 1.5, P < 0.00001]
Cardioembolic stroke is the least heritable type of stroke compared with other ischemic stroke subtypes
modifiable risk factors
HypertensionCigarette smokingDiabetesDyslipidemiaAtrial fibrillationOther cardiac conditionsAsymptomatic carotid stenosisSickle cell diseasePostmenopausal hormone therapyOral contraceptivesDiet and nutritionPhysical inactivityObesity and body fat distribution
secondary prevention
modifiable risk factors
Hypertension <120/80
Diabetes A1c <7%
Lipids LDL-c <70mg/dL Treatment with niacin or gemfibrozil in patients with low HDL-c
Cigarette smoking Advisement to quit Avoid environmental/passive smoking Cessation
Physical activity
interventional approaches to patients with large artery atherosclerosis
Symptomatic extracranial carotid disease CEA recommended if:
Patients with recent TIA or ischemic stroke within the past 6 months and ipsilateral severe (70-99%) stenosis
Patients with recent TIA or ischemic stroke and ipsilateral moderate (50-69%) stenosis, depending on patient-specific risk factors (age, sex, comorbidities)
Indicated for patients with TIA or stroke, surgery within 2 weeks is reasonable rather than delaying surgery
CAS indicated if: Alternative to CEA for symptomatic patients at average
or low risk of complications associated with endovascular intervention with ICA stenosis >70%
interventional approaches to patients with large artery atherosclerosis
Extracranial vertebrobasilar disease Optimal medical therapy Endovascular and surgical treatment of patients with
EVS may be considered if refractory to medical therapy
interventional approaches to patients with large artery atherosclerosis
Intracranial atherosclerosis Stroke or TIA due to 50-99% stenosis of a major
intracranial artery, aspirin preferred over warfarin 90 days ASA 325mg and Plavix 75mg, then ASA
monotherapy thereafter No indication for dual antiplatelet therapy beyond 90 days ASA = Plavix = Aggrenox … except for side effect profile
and cost Aggressive medical management
BP <140/90 mmHg Total cholesterol <200 mg/dL
Angioplasty and/or stent placement is not warranted and considered investigational