shazia khan assistant prof. of clinical medicine. usc · lp: erythrocytes and xanthochromia....
Post on 18-May-2019
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Learning objectives
Review the pathophysiology , signs and symptoms of ischemic stroke.
Familiarize our selves with the signs and symptoms.
Use of ABCD , NIHSS .
Primary and Secondary Prevention.
Epidemiology
Incidence of stroke in USA is 795,000/ year in the United States of America
Stroke kills about 140,000 Americans each year –that’s 1 out of every 20 deaths
Stroke: 4th killer in USA (used to be third)
2nd killer in world
Definition
Acute brain injury caused by occlusion or rupture of a blood vessel in the brain .
Ischemic stroke: Reduced blood supply to a region of the brain resulting in brain ischemic and neuronal death (87%)
Hemorrhagic stroke: Primary brain hemorrhage resulting in compression of normal brain tissue (13%)
Anterior and Posterior Cerebral Arterial Circulation
Internal carotid arteries and their branches: supply the anterior circulation
Vertebral arteries and the basilar artery (and their branches): supply the posterior cerebral circulation
Hemorrhagic Stroke
INTRACEREBRAL HEMORRHAGE.
More common in Asian countries.
Two distinct pathologies exist
1. Basal Ganglia – Cerebellum
2. Lobar – likely secondary to Cerebral
myloid angiopathy.
Higher Mortality then Ischemic Stroke.
Sub Arachnoid Hemorrhage.
Likely from rupture of a saccular aneurysm
Rare causes are AVM , Mycotic Aneurysm.
Diagnosis : Ct head , Lumbar puncture.
LP: Erythrocytes and Xanthochromia.
Mechanism of Ischemic Stroke and Transient Ischemic Attacks
Atherosclerotic cerebrovascular disease (20%): 1. Extracranial carotid or vertebral artery disease
2. Intracranial cerbrovascular disease
Penetrating small arterial disease (25%)
Cardiogenic source (20%): 1. Atrial fibrillation & other arrythmias
2. Myocardial infarction
3. Valvular disease
4. Ventricular thrombi
5. Aortic plaque
Unusual causes (<5%): dissection, migraine, illicit drugs, vasculitis, venous strokes, hypercoagulability,…
Cryptogenic source 30 %(no mechanism identified)
Transient Ischemic attack (TIA)
Definition: duration of transient neurologic symptoms lasting less than 1 hour
Transient reduction of blood flow to a region in brain in the absence of evidence of infarction on brain imaging
Mechanisms for TIA similar as for ischemic stroke
Reconstitution of flow to the hypoperfused region hence the resolution of symptoms
Significance of TIAs is increased risk of stroke after a TIA specifically early on after a TIA
Prompt evaluation of mechanism and appropriate treatment
Transient Ischemic Stroke
ABCD2 score
Age ≥ 60 years: score 1
HTN (≥140/90): score 1
Diabetes mellitus: score 1
TIA duration: 10-59 min (score 1); ≥60min (score2)
Clinical: Hemiparesis with or without speech deficit (score 2); speech impairment without hemiparesis (score 1).
Higher ABCD2 scores are associated with greater risk of stroke during the 2, 7, 30, and 90 days
Definite admission for ABCD2 score of ≥4
Caution to work the TIA patients urgently to address underlying source and treat appropriately
Acute Onset of Any of the Below Symptoms
Hemiparesis or quadriparesis ( latter in basilar occlusion)
Facial weakness
Aphasia
Dysarthria
Limb/truncal/gait ataxia +/- nausea & vomiting
Vertigo, tinnitus, hearing deficit (posterior circ.)
Impairment of vision in homonymous visual field defect
Monocular impairment of vision (amaurosis fugax)
Diplopia
Impairment or loss of consciousness or confusion
Hemineglect (visual or sensory)
Headache (non-specific symptom)
New onset seizure (3-4%) or acute new movement abnormality
Adopted from AHA
Differential Diagnosis
Space occupying lesion (tumor, infection/ abscess, Epidural, Subdural Hematomas)
Subarachnoid hemorrhage
Seizures
Hypoglycemia
Migraine
Syncope
Labyrinthine disorders
NIH Stroke Scale
Designed for acute stroke trials.
Quick (5-10 min) & reproducible.
Requires speech/language cards & safety pin.
Quantifies clinical stroke deficit:
o < 4 = mild stroke
o > 15 = poor prognosis if no treatment
o > 22 = risk for ICH
Initial Evaluation and Management
Urgent transport to the nearest stroke receiving hospital via 911 system
Notification of the destination ED
Alert ED of the need for urgent CT
Initial Evaluation
STAT CT brain
ABC .Pulse ox . IV
c-xray
CBC, Platelet, PT, PTT
Accucheck & blood glucose, serum electrolytes
Cardiac markers, ABG’s
Blood alcohol level, Toxicology screen, Pregnancy test
Initial Evaluation and Rx
IV line: IVF bolus/hydration
2nd IV line in anticipation of IV t-PA
Non contrast CT: rule out hemorrhage
Usually later but may need stat: Ct angiogram ,MRI perfusion MRI and MR-a, CT-a brain and cerebral vessels
Acute Therapy
NINDS Stroke Study group: randomized placebo controlled clinical trial (N Engl J Med 1995)
Intravenous recombinant tissue Plasminogen Activator (IV t-PA) given within 3 hour of symptoms onset in acute ischemic strokes
N=624 patients (IV t-PA or placebo):dose 0.9mg/kg, 10% IV bolus, then the remainder is IV drip over 1 hour
NINDS Stroke Study
Patients in the t-PA arm were at least 30% more likely to have minimal or no disability at 3 months
Symptomatic Intracranial Hemorrhage was 6.4% in the t-PA group versus 0.6% in the placebo arm
Mortality at 3 months was not statistically different between t-PA and placebo
The benefit of IV t-PA was sustained at one year follow up
The earlier the treatment the better the outcome
ECASS III Trial
ECASS 3: N Eng J Med sept 2008 This study showed persistent benefit of IV t-PA up
to 4.5 hours from onset in acute ischemic stroke Excluded patients>80 years of age Excluded patients with severe deficit NIHSS>25 Excluded patients who have combination of
previous stroke and diabetes Excluded patients who were on anticoagulation
regardless of the INR
Intravenous t-PA
Standard FDA approved therapy for acute stroke Rx
Window of treatment has been prolonged after ECASSIII to 4.5 hours
Not all patients are eligible for the 3 to 4.5 hour window
Inclusion Criteria for IV t-PA
Ischemic Stroke clinically
Persistent neurologic deficit beyond an isolated sensory deficit / ataxia
CT brain: No Blood
Initiation of Rx within 3 hours
Exclusion Criteria
Onset to treatment >3 hr (NINDS)
Rapid improvement
Blood on CT
Oral anticoagulant & PT>15 sec, INR>1.7
Heparin (last 48 hr) & increased PTT
Platelet<100,000
SBP >220 or DBP>110
Aggressive treatment of b.p.
Stroke or head trauma (3 months)
Major surgery (2 wks)
Cont’d Exclusion Criteria
Prior ICH
GI tract/ Urinary bleed (14 d)
Seizure at onset
Signs & Sx’s of SAH
Non-compressible site of arterial puncture (7d)
Additional Exclusions for the 3 to 4.5 Hour
Age≥80 years
Any use of anticoagulant regardless of the PT/PTT
NIHSS≥25
Coexistent history of stroke and diabetes mellitus
Management Post Thrombolysis
Admit to ICU
BP monitoring (Q 15 m x2 h, Q 30 m x6 h, Q 1 h x16 h)
Treat SBP for a goal <185 and DBP<110
No anticoagulants, no anti-platelet for 1st 24 hr post t-PA
Cont’d Management of Patients Post-thrombolysis
Worsening of neurologic state---CT brain
ICH---Neurosurgery consult
Possible surgical intervention
Preferably: no foley or NG for 2 hr > t-PA (t1/2-t-PA = 8-12 min)
Endovascular Rx
Mechanical thrombectomy:
Add on-Rx to the standard FDA approved stroke Rx IV t-PA in cerebral infarction with proximal large arterial occlusion within 6 hours from onset.
DAWN and DEFUSE3 Trials
Select patients LVO treated up to 24 hours based on CT perfusion selection.
What do we do given this data ?
1.All patients eligible for IV t-PA should receive it ..Quickly ! 2.Patients with in 6 hours should recieve a CTA to look for a large vessel occlusion (LVO) 3.If LVO is present , endovascular therapy should occur ,even following IV-tPA regardless of perfusion data.
4. If the patient has a LVO and presents between 6-24 hours ,CT perfusion required and selects patients who should receive endovascular therapy
Poor Outcome Predictors in Ischemic Stroke
Age
Elevated blood sugar
Initial NIHSS score which is a measure of the patient’s initial deficit
Cerebral infarction changes on CT brain
Anti platelet therapy
Aspirin after 24 hours of Iv t-PA .
160mg – 300mg .
In patients with minor stroke ,treatment for 21 days with dual therapy (aspirin and plavix ) can be beneficial for secondary stroke prevention for a period of 90 days.(CHANCE)
Oxygen : >94 % Blood pressure :< 180 /105 Temp <38 Glucose 140-180mg/dl DYSPHAGIA SCREEN Nutrition :Enteral diet should be initiated within 7
days DVT Prophylaxis Depression Screen REHAB!!
Primary Prevention
Primary prevention starts at the level of the physician playing the role of the primary care and occasionally at the level of the cardiologist and the stroke neurologist
Key is identification of underlying risk factors and modification and treatment of modifiable risk factors
Primary Prevention Elements
Establishing good medical history and family history
Identifying the patient’s vascular risks including medical illnesses, habits such as smoking and substance use and genetic predisposition through review of significant family history for cardiovascular risk factors and stroke
Exam elements which are key: pulse (rate and establishing how regular), blood pressure, carotid auscultation (bruits), cardiac auscultation (murmurs and abnormal rhythm), symmetry and detection of pulses, diabetic peripheral changes
Non-modifiable Risk Factors
Age: the risk of stroke doubles with every decade after the age of 55 years
Sex: lifetime risk in Male>Female but risk in F>M after age of 80 years
Race and ethnicity: Stroke incidence and subtypes: higher in African
Americans and Hispanics >Caucasians Stroke related mortality is higher in African
American population Asian population has an increased risk of
hemorrhagic stroke subtype compared to Caucasians
Non-modifiable Risk Factors Genetic Factors
Family history: inherited susceptibility, inherited predisposition to risk factors, similar culture and lifestyle
Hyperhomocysteinemia:)
Inherited coagulopathies: FV Leiden mutations, prothrombin gene mutation PC, PS deficiencies Anticardiolipin antibodies/LA are genetic in 10% cases Others
CADASIL: Cerebral autosomal dominant arterof iopathy with subcortical infarcts and leukoencephalopathy: NOTCH 3 gene mutation on chromosome 19
Others: Marfan and NF I and II, Fibromuscular dysplasia (FMD), Ehlers-Danlos syndrome IV, polycystic kidney disease
Novel genes identified which may have specific associations with large artery stroke
Well Documented Modifiable Risk Factors
Hypertension Smoking Diabetes Mellitus Carotid disease Cardiac disease: Atrial Fibrillation, Myocardial
infarction secondary to coronary artery disease Dyslipidemia or hyperlipidemia (high cholesterol,
high LDL, low HDL) Migraine with aura in women Obstructive sleep apnea
Less-Documented Potentially Modifiable Risk Factors
Obesity Lack of exercise Poor diet Alcohol abuse Hyperhomocystei-
nemia
Illicit drug abuse
Hypercoagul-opathy
Sickle cell disease
Estrogen/HR hormonal therapy
Inflammation
Infection
Hypertension (HTN)
Prevalence in USA is 29%- Improved control of HTN over the years 50%
More than 2/3 of patients ≥ 65 yrs of age have hypertension
Major risk factor for ischemic and hemorrhagic strokes
the higher the blood pressure the greater the risk of stroke
HTN is undertreated
It ‘s prevalence is increasing partly due to increased prevalence of patients who are overweight and obese
One of the most important modifiable risk factors for stroke
Hypertension Evaluation and Treatment Current Guidelines
Regular blood pressure screening
Behavioral life style modifications :
management of obesity/ weight loss,
diet: low salt, encourage vegetables. Reduce red meat (AHA, DASH, Mediterranean diets)
Encouragement of exercise
Treatment with antihypertensive agents to achieve BP< 140/90 mm Hg
Cigarette Smoking
Cigarette smoking doubles the risk of ischemic stroke
It also increases subarachnoid hemorrhage by 2-4 folds
Inconsistent data for parenchymal intracerebral hemorrhage
Inconsistent data with second hand smoking Contributes to increased risk of stroke by:
Increased thrombus generation in atherosclerotic arteries
Increased atherosclerosis
Diabetes Mellitus
Close to 11% of US population are estimated to have diabetes mellitus
Studies have shown that diabetes mellitus increases the risk of stroke 1.8 - 6 fold
This increase in stroke risk is related to increased risk of atherosclerosis & increased pro-atherogenic risk factors in diabetic patients
Diabetes Mellitus: Glycemic control?
North Manhattan Study: subjects who had diabetes and fasting blood glucose (FBG)> 126 mg/dl had 2.7 fold increase in stroke risk versus no increase in risk if FBG<126 mg/dl
3 clinical trials: ACCORD, ADVANCE, and a trial which enrolled US veterans
Failure to demonstrate reduction in stroke in the group of intensive glycemic control
ACCORD: halted earlier due to increased all-cause mortality in the intensive-glycemic control group
Diabetes mellitus: Glycemic Control
Use standard guidelines for glycemic control
Avoid lowering of HbA1c<6.5 in patients with cardiovascular disease or the presence of vascular risk factors
Diabetes Mellitus and Lipid Altering Rx
Clinical evidence of the benefit of statins in stroke risk reduction in diabetic patients
No supportive evidence for fibrates in stroke prevention in diabetic patients
Use of Aspirin in Primary Prevention of Stroke in Diabetes Mellitus
No statistically significant benefit from aspirin in prevention of stroke in diabetes mellitus has been found
Use in patients with established carotid disease or coronary artery disease
Lipids
Modest association of elevated total cholesterol or LDL with increased risk of ischemic stroke
Association between low HDL and increased risk of ischemic stroke
Relationship between low total cholesterol as well as LDL-C and a higher risk of hemorrhagic stroke
ACC/AHA Guidelines for the Treatment of Blood Cholesterol in Primary Prevention
Recommendations based on the 10 year risk for cardiovascular disease
Shifts away from specific cholesterol goals
Estimated risk dictates intensity of statin Rx: high risk mandates high intensity statin Rx
Atorvastatin 10 mg is moderate intensity statin Rx and 40 t0 80 mg is high intensity
10 year Risk calculator
Statins in Secondary Prevention of Stroke
Statin therapy with intense lipid lowering effect is recommended to reduce stroke risk in the population of ischemic stroke and TIA patients (SPARCL)
Target LDL-C<70 mg/dl or 50% lowering of baseline LDL
May use other agents if patient can not take statins (Niacin, Gemfibrozil)
No established benefit in stroke reduction
Carotid Endarterectomy
Indicated with proven benefit in severe symptomatic extracranial carotid artery disease
Symptomatic = clinical or radiologic evidence of stroke in the distribution of that carotid artery
Stenting is an alternative in patients who are not eligible for CEA
Asymptomatic Carotid Artery Disease
Increased risk of stroke with carotid artery stenosis Asymptomatic Carotid Artery Study (ACAS) Asymptomatic Carotid Surgery Trial (ACST) Number needed to treat to prevent 1 stroke patient
was 40 The low benefit may not justify the risks of carotid
revascularization: individualize patients and assess risk factors
The annual rate of stroke associated with asymptomatic carotid stenosis has significantly declined with intensive medical management ≤1% (Statins and antiplatelet Rx)
May consider carotid revascularization in severe asymptomatic carotid artery stenosis but with
perioperative and surgical risk <3 %
Cardioembolic sources of Stroke
Cardiac arrhythmias with increased risk of cardiac clots and cardioembolism: atrial fibrillation
Coronary artery disease, myocardial infarction/ ischemic cardiomyopathy
Valvular heart disease (septic embolism or thromboembolism)
Aortic arch atheroma
Paradoxical embolism: presence of right to left shunt such as a PFO in the presence of a venous thrombus
Atrial Fibrillation
Both persistent and paroxysmal atrial fibrillation are potent predictors of first as well as recurrent stroke
Atrial fib >2 million Americans
Increases with age
Atrial fibrillation patients with prior strokes and TIAs have the highest risk of recurrent stroke
Other risk factors: age, HTN, CHF, diabetes mellitus
CHADS2
Age ≥ 75 years (1)
HTN (1)
DM (1)
CHF (1)
Ischemic stroke or TIA (2)
--------------------------------------------------------
Total score: ------ (maximum is 6)
Antithrombotic Rx in Atrial Fibrillation
Anticoagulation: CHADS2 >1
Antiplatelet Rx for CHADS=0
CHADS2=1 either anticoagulation or antiplatelet
ASA plus clopidogrel maybe used in patients who have contraindication to anticoagulation
If there is Stroke/TIA with atrial fibrillation then anticoagulation is the recommendation
Patient has to be cleared for the absence of fall risk
Oral Anticoagulants
Warfarin (valvular and non-valvular A.Fib.)
Apixaban((approved for non-valvular A.Fib.)
Rivaroxaban(approved for non-valvular A.Fib.)
Dabigatran (approved for non-valvular A.Fib.)
Migraine with Aura
An independent risk factor for stroke in women
It is still unknown if migraine preventive therapy will reduce the risk of stroke
A woman who has migraines with aura, who smokes tobacco and who is on oral contraceptive pills has a 7-9 fold increase in the risk of stroke
Cessation of smoking and consideration of avoiding OCPs in patients with migraines with aura
Obstructive Sleep Apnea (OSA)
Increases risk of stroke and cardiovascular disease
Screening for symptoms of OSA and appropriate referrral to sleep center for evaluation and treatment when appropriate
Hormonal Replacement Therapy and Oral Contraceptive Pills
Some increased risk of ischemic stroke
May avoid or stop using if additional risk factors for stroke
Stop/avoid use if patient is a smoker and esp. if it is a woman who has migraines with aura
Substance Use
Alcohol beyond 2 drinks/day for men and beyond
1 drink /day for women increases the risk of stroke
Illicit drug use increases the risk of intracerebral hemorrhage (ICH) and ischemic strokes esp. with Cocaine and Amphetamines/ derivatives
Substance use increases the risk of development of poorly controlled BP and its complications
Cessation should be recommended however with the help of detox and rehab programs
Antiplatelet Therapy in Primary Stroke Prevention: No Benefit
No benefit in primary prevention
Consider in diabetic patient with high risk factors and carotid artery disease
Recent FDA warning about use of aspirin in primary prevention due to increased hemorrhagic risks which are not offset by any significant benefit.
Summary
Goal should be primary prevention in stroke
Role of the primary care and sometimes the neurologist and cardiologist in assessing risk factors for stroke
Intervention with education about life style modification and treatment of risk factors for stroke
Summary
Family history: identify people who have higher risk and counseling those patients
Genetic counseling for rare genetic disorders
Non-invasive imaging/ screening for patients with specific disorders: screen for cerebral artery aneurysms in patients with ≥ 2 first degree members with SAH/cerebral aneurysms, EDS IV, polycystic kidney disease
Summary:
Physical activity is recommended:
Moderate to vigorous intensity aerobic
Suggested ≥ 40 min/ time, 3-4 days /wk 2013 AHA/ACC guidelines
Weight reduction for BMI≥ 25
Dietary restriction of salt and increased potassium in diet (HTN conrtol)
DASH, AHA, Mediterranean diets
Summary: Primary Prevention
Cessation of smoking esp. in women who have migraines with aura and who are on OCPs
Cessation of illicit drugs
Cessation of alcohol or limitation to ≤1 drink/day for women and ≤2 drinks/day for men
Summary: Primary Prevention
Control of BP<140/90 mm Hg
Control of blood sugar but avoid intensive glycemic control
Use of statins in diabetic patients maybe protective and particularly if high risk factors
Maximize medical management with statins and antiplatelets in carotid artery disease
Anticoagulation is reserved for atrial fibrillation and cardiac thrombi or potent hypercoagulable states (latter in secondary prevention)
Summary: Primary Prevention
Use of ACE Inhibitors and or an angiotensin II receptor blocker (ARB) in diabetes mellitus
No documented benefit for aspirin in primary prevention of stroke (may consider patients with high risk factors) with the exception of some possible benefit for women>65 years old
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