Transcript Cerebrovascular Disease - Home

Cerebrovascular Disease
J. B. Handler, M.D.
University of New England
Physician Assistant Program
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Abbreviations
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BP- blood pressure
MI- myocardial infarction
VHD- valvular heart disease
Sx- symptoms
CV- cardiovascular
CBC- complete blood count
Plts- platelets
PT- prothrombin time
INR- international normalized
ratio
PTT- partial thromboplastin
time
ECG-electrocardiogram
CxR- chest x-ray
PAD- peripheral arterial disease
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MRI-magnetic resonance
imaging
MRA-magnetic resonance
arteriography
CHD- coronary heart disease
Afib-atrial fibrillation
DM- diabetes mellitus
t-PA- tissue specific
plasminogen activator
AVM-arteriovenous
malformation
Dx- diagnosis
Rx-treatment
S/S-signs and symptoms
ESR- erythrocyte sedimentation
rate
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LVH- left ventricular
hypertrophy
Objectives
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Define the stroke syndromes comparing
ischemia/infarct to hemorrhage
Understand the risk factors for strokes and
prevention
Understand the pathology involved in the most
common stroke syndromes
Recognize common presentations
Understand appropriate diagnostic testing
Understand treatment options and planning for
short and long term care
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Case
A 61 y/o man presents to the ED after
developing sudden onset of
weakness/numbness of the right arm
accompanied by difficulty with speech.
Symptoms started 30 minutes ago and have
resolved by the time he reaches the ED.
 Neuro exam: normal
 What is the diagnosis?
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Stroke
 Cerebrovascular accident
 Transient ischemic attack
 Lacunar infarct
 Intracerebral hemorrhage
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Definitions-I
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Stroke (“Brain Attack”): The sudden or rapid
onset of a neurologic deficit in the distribution
of a vascular territory lasting > 24 hours.
TIA: The sudden or rapid onset of a neurologic
deficit in the distribution of a vascular territory
lasting < 24 hours. Most last < 30 minutes.
Reversible ischemic insult to brain cells that
recover but ’s risk of subsequent stroke.
frequency of TIA’s a bad sign.
Brain ischemia vs infarction.
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Definitions II
Stroke-in-evolution (progressive stroke):
worsening signs or symptoms over time.
 Ischemia/Infarct (85%) vs hemorrhage
(15%) as stroke etiologies.
 CVA: Cerebrovascular accident- outdated
term; Do not use.
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Epidemiology
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3rd leading cause of death in the U.S.
– >200,000 deaths per year
– Perception of elderly
Incidence has declined due to prevention. Why?
Men 1.3x > women (MI: men 3x > women).
Blacks 1.3x > whites.
Most common cause of death in patients with
cerebrovascular disease is myocardial infarction.
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Risk Factors
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Hypertension most powerful risk factor,
especially systolic BP (goal<140/90 for most)
Smoking: 2-4x increase risk
Atherosclerosis elsewhere (CHD, PAD)
Diabetes Mellitus: 3x increase risk for stroke
Atrial fibrillation – Cardiac Emboli
Others: male gender, oral contraceptives, ETOH in
excess, hyperlipidemia.
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Etiology & Pathogenesis
 Atherosclerosis: Large vessels often involved
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–Involved in 50% of all ischemic strokes (infarcts)
–Thrombus-in-situ vs artery to artery embolus
–Base of aorta, carotid bifurcation, origin of
internal carotid, external carotid,
vertebral/basilar arteries
Pathological outcomes depend on:
– Adequacy of collateral circulation
– Development of Circle of Willis
– Duration of insult/restoration of blood flow.
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Carotid Disease
Images.google.com
Stable Stenosis vs Unstable
Placque
Stable Stenosis
Unstable Placque
Images.google.com
Etiology & Pathogenesis
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Lacunar infarcts (aka lipohyalinosis): Small
vessel disease- deep penetrating arterioles
thrombose.
 20% of ischemic strokes.
Major risk factor: HTN
– lipids, DM contribute.
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Very small strokes. Defect <1.5 cm (most are
<5mm) on CT or MRI.
May be without symptoms- detected by CT scan
as incidental finding.
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Cerebral Emboli
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Embolism from heart or artery to brain.
Important role in pathology of strokes and TIA’s
Blood clot breaks off, occludes more distant/distal
vessel.
– Cardiac emboli often lodge in medium sized vessels
(MCA, ACA, etc.).
– Artery to artery emboli also occur. Often cause TIA’s
(lodge, then break up) or small neuro deficits.
» Frequent source: Carotid bifurcation or internal carotid
» Often small emboli: Platelets/fibrin/RBC’s
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Cardioembolism
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Etiology of  20% of ischemic strokes
Atrial Fibrillation-very common, both idiopathic
or combined with other cardiac pathology.
–Importance of prevention with anticoagulation.
MI with mural thrombus: 35% incidence post
large anterior wall MI. 40% will embolize if left
untreated.
Dilated cardiomyopathy
VHD- rheumatic and otherwise; less common
compared to other etiologies.
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Other Etiologies: Interest Only
Vasculitis, Temporal Arteritis, others
 Hematologic abnormalities- Sickle cell
disease, hyperviscosity syndromes
 Drug abuse –cocaine, amphetamines, others
 Sympathomimetic agents- ephedrine,
phenylpropanolamine, etc.
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Stroke: Signs and Symptoms
Abrupt onset of non-convulsive focal
defect in a vascular territory.
 80-90% no warning symptoms.
 10-20% have warning (TIA).
 Variable course: stabilize, improve or
worsen. Essential to make dx early.
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Brain Circulation
Images.google.com
Stroke Syndromes
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Middle cerebral artery (MCA)
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Contralateral hemiparesis or hemisensory loss
Hemianopsia- visual field defect
If dominant hemisphere- Aphasia
If non-dominant- Speech and comprehension
preserved; may develop anosognosia
(denial/neglect of deficit) or a confusional state.
Ref: http://www.ebrsr.com/modules/module2.pdf
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Stroke Syndromes
Anterior cerebral artery (ACA) - less
common- Sx more pronounced in leg,
associated language, gait disturbance.
 Posterior circulation (least common)
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– Vertebral artery (Branch of subclavian artery)
– Crossed contralateral dysfunction
(motor/sensory) plus ipsilateral
bulbar/cerebellar signs: vertigo, dizziness, gait
disturbance, diplopia, facial palsy, dysarthria,
etc.
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Stroke Syndromes
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Lacunar strokes/infarcts
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Hypertension
Deep penetrating arterioles
Small infarcts up to 1.5cm on CT/MRI
Clinical syndrome depending on where infarct is;
may also present as TIA. Examples: contralateral
motor/sensory deficit (infarct of anterior limb of
internal capsule). Prognosis usually good.
Amaurosis fugax (carotid disease present)
– Transient monocular blindness
– Embolism to ophthalmic artery (off of carotid)
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Evaluation
History: Precise onset of Sx, neuro deficit.
 Physical exam – detailed neuro, CV exam.
 Blood pressure- often elevated- caution.
 Lab- CBC, Plts, Glucose, INR, PTT, Lipids,
ESR, Creatinine/BUN.
 ECG- atrial fib/other arrhythmias, MI or
LVH?
 CxR- cardiomegaly or aortic calcification?
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CT Scan
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R/O hemorrhage
– Better than MRI in 1st 48 hrs after intracranial
hemorrhage.
Detection of infarcts limited to size and
timing- only 5% visible in 1st 12 hrs,
>90% visible at one week.
 More readily available than MRI and less
expensive. Does not require contrast.
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CT Ischemic Stroke
Cecil
MRI/MRA
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Magnetic resonance imaging/angiogram.
Changes of infarct may be seen as early as one
hour- usually not available or needed emergently.
– Provides better detail than CT for small lesions and
other pathology.
– Better for imaging posterior fossa.
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MRA- Non invasive with excellent resolution of
large vessels; replaces need for arteriogram in
some patients; may be difficult to differentiate
complete vs near complete occlusions.
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MRI Stroke
Cecil
Ultrasound
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Carotid Doppler Ultrasound (Duplex)Screening tool for evaluating common
carotid and origin of internal carotid artery.
– Combines B mode with doppler ultrasound
May be difficult to differentiate complete vs
near complete occlusions.
 Non-invasive but limited capability.
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Carotid Ultrasound
Images.google.com
Arteriography
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Most accurate- invasive“gold standard” for extra
and intracranial disease.
Complications: contrast
reaction, kidney failure,
placque rupture, stroke.
Use of non-ionic contrast
has reduced complication
rate.
Images.google.com
Prevention
CHD (and stroke) prevention
 Risk factor modification; aggressive
control of blood pressure, lipids, diabetes;
smoking cessation, exercise, diet, etc.
 Atrial Fibrillation and embolization
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– Full anticoagulation for most patients
– Warfarin (Coumadin) therapy long term
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TIA’s
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Abrubt onset of symptoms with transient focal
neuro deficit dependent on involved anatomy
(anterior, posterior circulation). Sx may vary
during episodes. Exam between episodes is
normal. Warning for subsequent stroke.
Etiology likely:
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Embolic from carotid stenosis/placque* or
Embolic from cardiac source
Severe carotid stenosis with transient hypotension
Small vessel occlusion: Lacunar infarcts may mimic
*Important to listen with stethoscope for bruit
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Carotid TIA/Incomplete Stroke:
Surgical Rx
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Carotid Endarterectomy: Remove plaque
– Best results if symptomatic blockage and
>70% stenosis. Significantly reduces risk of
subsequent ipsilateral stroke.
– Selected patients with symptoms and 50-70 %
stenosis
– Risks: Stroke and complications of surgery
Carotid angioplasty/stenting a promising
alternative, but long term data is lacking; option in
poor surgical candidates.
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Carotid TIA’s-Medical Rx
Patients: Poor operative risk, <70% stenosis
or asymptomatic carotid disease.
 Risk factor modification: HTN, smoking,
lipids, DM.
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– Aggressive BP control.
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Carotid TIA’s-Medical Rx
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Anti-platelet agents indicated for all
patients with < 70% stenosis and TIA
symptoms, diffuse cerebrovascular disease,
patients who are poor operative candidates,
and patients with asymptomatic carotid
disease. These agents prevent platelet
aggregation and release of vasoactive
substances like thromboxane A2.
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Aspirin
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Inhibits cyclooxygenase.
Inhibits synthesis of thromboxane A2, decreasing
both platelet aggregation and vasoconstriction.
Permanent, life of platelet (about 8 days).
325 mg/daily*; GI side effects and bleeding.
Decreases frequency of TIA’s and risk of
subsequent stroke. Also applies to patient with
prior stroke- incidence of recurrence.
*ASA 25 mg + dipyridamole ER 200mg- orally 2x/D- alternative
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to ASA alone with likely improved protection at a cost
Clopidogrel (Plavix)
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75mg/day
Inhibits platelet aggregation and prevents
activation of glycoprotein IIb/IIIa (a fibrinogen
binder).
Decreases atherosclerotic events
Slightly better outcomes compared to ASA alone
but expensive- alternative to ASA in patients with
recurrent TIA’s or ASA intolerance/allergy.
Diarrhea, rash
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Lacunar Infarcts: Treatment
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Small lesion – infarct in distribution of penetrating
arterioles. Small infarcts with discreet symptoms
(TIA or stroke) related to distribution; may be
incidental finding in asymptomatic patient.
Usually good prognosis for recovery over 4-6
weeks.
Treatment – supportive measures plus ASA or
Clopidogrel. Aggressive long term Rx of BP and
lipids.
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Stroke: Treatment
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Hospitalize all stroke patients; most TIA (1st
episode) patients.
HTN-Avoid rapid BP reduction-decreases
perfusion- brain will auto regulate perfusion.
– BP often elevated during strokes- leave as is unless BP
markedly elevated (>200/100); wait 2 wks for oral
meds if possible.
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Supportive (IV fluids, etc.)
Consider thrombolytic therapy- see below
When to anticoagulate?
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Cerebral Infarct
Thrombotic or embolic occlusion of major
vessel. Treatment dependent on timing.
 1st: Obtain head CT to r/o hemorrhage.
 If onset of symptoms <3 hours,
thrombolytic therapy with t-PA
(bolus/infusion up to 90 mgs) over 1 hr.
 No benefit for thrombolytics after 3 hours
from onset of symptoms.
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Thrombolytic Therapy
Thrombolytic therapy requires team
approach- best done in large treatment
centers.
 Neurologic outcome improved at 3 mos and
1 yr with decrease in expected deficit and
reduction of initial deficit.
 Increases the chances of a favorable
outcome by ~50%.
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Thrombolytic Therapy
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Ideal scenario is large referral hospital with
consultants available.
– ? Management in small community hospitals.
Risks of t-PA: Cerebral hemorrhage- 6 to
7% incidence, half will die.
 Contraindications: recent bleeding, prior
stroke, BP>185/110, recent major surgery.
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Full Anticoagulation
Indications include:
–Embolus from heart (stroke or TIA)
–Atrial fibrillation > 72 hours
 Risk is cerebral hemorrhage.
 Must do CT to r/o hemorrhage before use.
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Anticoagulants-Heparin
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Unfractionated Heparin: Bolus and continuous
infusion per hour based on weight and PTT.
– 2-10% bleed risk
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Low molecular weight heparin
– Enoxaparin (and other LMW heparins) given
subcutaneous every 12-24 hours
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Heparin preparations are used for immediate
and short term anticoagulation (days). They
work (simplistically) by inhibiting the action of
clotting factors – to be covered in detail during
pharmacology course.
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Anticoagulants - Warfarin
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Long term oral anticoagulation (aka Coumadin):
Inhibits production of clotting factors in liver.
Stroke or TIA from cardiac embolism- proven
by 2 large randomized studies- subsequent
stroke risk.
Chronic Atrial Fibrillation: ’s stroke risk.
Monitored by INR (2-3x control) and requires
frequent follow-up for dosing.
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Post Stroke Management
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Prevention of complications
– Avoid prolonged bed rest (UTI’s, skin
infection/ulcers, PE)
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Physical therapy, occupation therapy,
speech therapy very important.
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Hemorrhagic Stroke
Intracerebral (HTN, AVM, and Trauma)
 Subarachnoid space (Aneurysm, AVM)
 CT scan is usually diagnostic
 Spinal tap if CT is negative to R/O SAH.
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Intracerebral Hemorrhage
Rupture of small arteries or
microaneurysms of the perforating vessels.
 Hypertension: major risk factor.
 Hematologic and bleeding disorders
(leukemia, thrombocytopenia, hemophilia).
 Trauma
 Anticoagulant therapy, liver disease
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Intracerebral Hemorrhage
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Rapid evolution of neuro deficit often
progressing to hemiparesis, hemiplegia or
hemisensory loss; 50% mortality.
– Focal signs and symptoms dependent on
location of the hemorrhage.
Loss of or impaired consciousness
develops in 50%.
 Vomiting and headache are common.
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Intracerebral Hemorrhage
Cecil
Hemorrhagic Stroke: Treatment
Cautious BP reduction where applicable.
 Treatment: conservative and supportive;
some patients will benefit from surgical
evacuation of the hematoma.
 Surgery: Decompression- limited usefulness
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– Best in cerebellar bleeds- improves outcomes
– Bleeding AVM
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Subarachnoid Bleeds
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Most due to bleeding from saccular aneurysms
– Present in 3-4% population, usually without symptoms
– 2-3% risk bleed per year
– Highest risk if >6mm
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Sudden onset of severe headache followed by N
& V, impaired or loss of consciousness +/- neuro
deficit. Meningeal signs often present:
– Kernigs and Brudzinski signs
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Subarachnoid Hemorrhage
Images.google.com
Subarachnoid Dx and Rx
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CT: identifies blood in subarachnoid space.
If suspected and CT negative do CSF tap and look
for blood or xanthochromia.
Treatment: If patient is conscious- bed rest,
symptomatic and supportive care with cautious
reduction of B.P.
Angiography once patient stable- aneurysym
Surgery or coil placement to prevent re-bleeding
where applicable.
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Aneurysm
Images.google.com
Arterial Venous Malformations
(AVM’s)
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Most common vascular malformation of CNS often
involving MCA and branches.
Tangled web of arteries connected directly to veinscongenital; up to 70% bleed, often by age 40.
Males>Females, some familial trends
2-3% risk bleed per year
S/S: hemorrhage (30-60%), headache (5-25%), recurrent
seizure (20-40%), focal deficits.
CT may confirm hemorrhage; angiography necessary for
diagnosis.
Treatment: surgery if lesion is accessible.
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AVM
Images.google.com