Cerebrovascular Disease A clinical approach ROBERT CONI, DO.
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Transcript of Cerebrovascular Disease A clinical approach ROBERT CONI, DO.
Cerebrovascular DiseaseA clinical approach ROBERT CONI, DO
Objectives
The participant should be able to:
Learn to take an appropriate stroke history and use that data to define the stroke syndrome.
Apply examination findings to stroke localization.
Be able to choose an appropriate imaging procedure to confirm a diagnostic impression.
Develop and apply an approach to the categorization of cerebrovascular diseases and then be able to apply an appropriate evaluation schema.
Understand the ecology of cerebrovascular diseases and be able to apply that knowledge in initial dx and then to secondary stroke prophylaxis.
What we will cover
The stroke syndrome, a definition
Diagnosis of stroke
Confirmation of a diagnosis
Evaluation of stroke patients
Treatment options
The stroke syndrome
Stroke
Syndrome is defined by a rapid onset of a focal neurological deficit which lasts greater than 24 hours.
TIA
Syndrome defined by a rapid onset of a focal neurological deficit which lasts less then 24 hours and resolves completely.
No imaging abnormality
Amaurosis fugax
Other definitions:
Stroke in evolution (or progressive stroke): a worsening of the focal neurological deficit over time.
Completed stroke: The deficit does not worsen over time and becomes fixed.
Presumptive Dx of Stroke
HISTORY
ECOLOGY
EXAMINATION AND LOCALIZATION
History taking in stroke
Purpose: Determining the mechanism of the stroke
Determining the location of the stroke
Factors helpful at defining mechanism: Activity at onset of symptoms
Temporal course of deficit progression
Accompanying symptoms
Anterior vs posterior circulations
Cortical vs subcortical
Cardiovascular
Prior cerebrovascular symptoms
Examination of heart and vascular system and eyes
Factors in localizing the stroke: Neurological examination
Evaluate signs and symptoms
Evaluate imaging procedures and vascular procedures
Ecology of stroke
Risk factor analysis
Demographics
Ecology of stroke
Non-modifiable risk factors Age
Gender
Ethnicity
Fam Hx
Prior stroke
Modifiable risk factors Hypertension
Cholesterol
Diabetes
Tobacco use
Inactivity
Excessive ETOH use
OSA
Stress
Birth control
Examination and LocalizationQuick review of stroke syndromes
Common Carotid / ICA
Variable presentation; borderzone or watershed infarct
MCA
Contralateral weakness/sensory loss and hemianopia; dominant vs or nondom hemisphere signs; eye deviation
ACA
Weakness (and/or sensory loss) of contralateral foot > leg >> arm
PCA
Contralateral vision loss and possibly cortical blindness; dominant hemisphere language
Vertebral Artery
PICA / Wallenberg syndrome
Basilar Artery
Weakness x 4; CB ataxia; diplopia; dizziness; nystagmus; blindness; coma
Clinical application – Case study one
JV was a 69 yo man, RH, brought to the ED with sudden left sided weakness which developed while shopping at Kroger. He states his left leg gave out on him and he fell. Also he felt he would pass out. He could not get himself off the floor and EMS was called. This occurred about 25 to 30 mins before presentation. He relates a past hx of DM and HTN.Database: Blood glucose was 109; BP 155/85Neurologic examination: Follows commands and gives a clear hx; Lt face droop and VF loss without language or speech loss; Left hemiataxic paresis; Lt sensory absence all modalities and left sided neglect.What else do you want to know?
CT – Negative, NIHSS – 10, No thinners, PT: 10.5 (INR_1.1), PTT: 32.8, Plts: 187Where is this lesion?What is the appropriate treatment at the time of presentation?
NIHSS
A 15-item neurologic examination stroke scale used to evaluate the effect of acute cerebral infarction on:
the level of consciousness and awareness
language
neglect
visual-field loss
extraocular movements and gaze
motor strength
ataxia
dysarthria
sensory loss
A trained observer rates the patent’s ability to answer questions and perform activities. Ratings for each item are scored with 3 to 5 grades with 0 as normal, and there is an allowance for untestable items. The single patient assessment requires less than 10 minutes to complete.
The evaluation of stroke severity depends upon the ability of the observer to accurately and consistently assess the patient.
Case one
The patient went on receive IV rt-PA.
He had a CTA which showed an occlusion of a posterior MCA branch.
Clinical application – case two
KC was a 57 yo RH man working as a custodian cleaning a school when he suddenly collapsed. He had trouble getting up and was noted to have Rt hemiparesis with “confusion”. He was transported to our hospital where he was noted to have nonsensical speech with paraphasic errors and Rt hemiparesis. His EKG showed a sinus rhythm. His BP was 200/115 in the left arm and 185/85 on the right.
Where is the lesion?
What is the likely mechanism?
What would you do?
His CT showed a dense Lt MCA sign. What now?
Case two
CTA
Lt ICA Occlusion with Lt M2 posterior branch obstruction and a significant penumbra
The patient received rt-PA and then was sent to MUSC for endovascular intervention
Confirming the Diagnosis
DIFFERENTIAL DIAGNOSIS OF STROKE IMAGING PROCEDURES IN STROKE
Differential diagnosis
Step one is ascertaining if the s/s meet the “stroke syndrome” definition
Next one must differentiate ischemic from hemorrhagic strokes
Finally one must identify the stroke subtype:
Large artery vs small artery
Embolic vs thrombotic
Consider other vascular events:
Arteritis
Cortical venous occlusions
Dissections
Stroke mimics – misdiagnosis has been estimated at about 13%
Stroke mimics
Most common misdiagnosis occurs from unwitnessed or unrecognized seizure with postictal state and/or postictal Todd’s paralysis.
Tumors
Multiple sclerosis
Encephalitis
Vertigo
Hepatic encephalopathy
Radial nerve palsy / Bell’s palsy
Hypoglycemia
Migraine
Metabolic encephalopathy
Functional hemiparesis
Imaging in stroke
Imaging is used to:
Exclude hemorrhage
Determine the vascular insult and identify the stroke subtype
Assess the degree of brain injury
Advanced techniques can be used to determine the volume of injury and of salvageable brain tissue
Initial technique is the CT scan
Imaging in stroke
The early CT scan: Usually does not clearly show stroke within first 24 hours
However, in an analysis of several studies some radiologic signs can be seen early, after 6 hours:
Hypoattenuation in a portion of the MCA distribution
Obscuration of the lentiform nucleus
Cortical sulcal effacement
Hyperdense MCA sign (or other large vessel)
Focal parenchymal hypoattenuation
Loss of the insular ribbon or sylvian fissue
Loss of gray-white differentiation in basal ganglia
Imaging in stroke
CTA – better resolution than MRA
Can obtain perfusion imaging to identify penumbra but there is no clear utility to this technique currently
MRI:
In stroke we include DWI and a sequence for detecting extravasated blood
MRA can overestimate stenosis
Can obtain perfusion / diffusion scans for mismatch to identify penumbra but again no clear advantage as yet identified.
Evaluation of the Patient
VASCULAR DISEASE RISK FACTOR ASSESSMENT
Stroke workup
Labs: PT/PTT; anticardiolipin ab and thrombosis w/u if elevated PTT or young patient
Homocysteine
HgbA1c
Fasting lipid panel
CBC and Platelet count
C-RP and ESR
Chemistries
Consider blood cultures in cardioembolic stroke
MRI: as stated previously, can aid differentiation of TIA from stroke. Review the DWI studies. When MRI is not possible, repeat CT for changes at 24 to 48 hrs
Stroke workup
Carotid artery study: to exclude symptomatic stenosis Duplex ultrasound
CTA or MRA
Seeking degree of stenosis
In patients with severe, symptomatic carotid stenosis, CEA achieves a lower rate of stroke or death than carotid stenting.
Severe stenosis is 70%
In patients with asymptomatic stenosis, medical therapy achieves low death/stroke rates
Cardiac studies: to exclude cardioembolic source ECG
Trans thoracic ECHO
Trans esophageal ECHO
Telemetry and event or holter monitors
Other orders and discharge considerations
Therapy assessments: PT/OT/SLP
If the patient fails the nursing swallow assessment, make pt NPO
Document considerations for rehabilitation
Case management consultation
Consults: Neurology; consider Cardiology and PM&R
Secondary prophylaxis
Antiplatelet agents vs anticoagulants
Statin
Control hypertension
DVT prophylaxis – antithrombotic boots / low dose anticoagulation
Diabetes control; diabetic teaching
Stroke teaching – emphasizing low Na and fat diet, regular exercise
Smoking cessation
Immunizations – influenza and pnemonia
Treatment of the patient
ACUTE THERAPIES
SECONDARY STROKE PROPHYLAXIS
Acute therapies
“Time is brain”
rt-PA
given IV
Given IA
Interventional endovascular approaches
When the patient is out of the t-PA window but within a 6(-8) hr window post stroke
In these cases, perfusion images via CTA or diffusion-perfusion via MRI can give objective evidence of viable penumbra before embarking
In cases of larger vessel occlusions and dense radiographic vessel signs on CT
Secondary stroke prevention
What is at risk?
Often patients are not meeting benchmarks for secondary stroke prevention
There is a 30% risk of stroke recurrence over the first 5 years
800,000 stroke a year of which, 25% or about 185,000 are recurrent events.
20% occur within 30 days and lead to readmissions with increased morbidity and mortality
What percentage of patients who have had a stroke receive all of the appropriate recurrent stroke preventative measures?
1) 10 %
2) 30 %
3) 50 %
4) 70 %
5) 90 %
Secondary stroke prevention
With intensive risk factor and antithrombotic recurrent stroke preventative management, what relative risk reduction for subsequent major vascular events may be achieved?
1) 40 - 50%
2) 51 - 60%
3) 61 - 70%
4) 71 - 80%
5) 81 - 90%
What are these factors?
Diet and BG control; exercise; ASA; statin tx; BP control
Risk factor control
Hypertension
Hypertension is the single most important modifiable risk factor for both hemorrhagic and ischemic strokes
Affects 1/3 of adults in the USA: 140/90 or greater
Another 30% have “prehypertension”: Systolic between 120-139 and 80-89 diastolic
Every 10 mm Hg reduction in BP gives a 33% risk reduction in primary prevention
In secondary prevention there is a 25% relative risk reduction with or without preexisting HTN
Elevated BP in the postacute phase is associated with recurrent stroke; the goal s/be 120-140/80-90
With DM or renal disease goal s/be < 130/80
In all cases, seek a 10 mm hg reduction in systolic pressure and 5 mm hg in diastolic
Risk factor modification
Dyslipidemia
25% of adults have elevated cholesterol
LDL is most associated with risk of CV disease, not HDL or triglyceride levels
LDL lowering is the primary goal of therapy
For each 39 mg/dl reduction in LDL, a 21% relative risk reduction in stroke risk was obtained.
Goal level has been < 100 mg/dl but recent changes for secondary stroke prevention made the goal less than 70 mg/dl
Studies have shown the most efficacy with atorvastatin and rosuvastatin
For low HDL levels, tx with Niacin may be considered despite lack of efficacy in cardiovascular risk
Risk factor modification
Diabetes Mellitus Defined as HgbA1c > 6.5%; affects 19 million in US but 90 million have prediabetes
Trials of aggressive tx for secondary prevention have not shown efficacy when targets are HgbA1c < 6.5
Targets thus are set at <7.0 using diet, exercise, and medications AND BP goals (less than 130/80) as well as statin LDL goals (less than 70)
During acute stroke, hyperglycemia > 140mg/dl during the first 24 hours post stroke is a poor prognostic indicator
We recommend treatment in acute stroke to keep glucose at a level < 180 mg/dl
Obstructive Sleep Apnea Associated with several physiologic changes: BP, cardiac hypertrophy, a fib
While data on RRR with CPAP are lacking, evaluation post stroke for OSA and treatment when found are recommended
Risk factor modification
Smoking Cessation
Relative risk of stroke in smokers was 2.3 in men and 3.1 in women in the Framingham study. Also there is a dose response relationship
Consider secondhand smoke a risk
After 5 years of not smoking risks return to nonsmoker levels
Physician counseling has some benefit (7.5% quit rate)but support groups and group counseling do better (20% quit rates)
Spontaneous quit rates are 3-5%
Consider nicotine replacement and bupropion or varenicline or even combinations which do best
Risk factor modification
Diet Fat
Cochrane Meta-analysis showed: Reduced dietary fat yielded a 14% reduction in CV events and the major contribution was reduced saturated fat
Sodium
Studies show a decrease below 1800 mg/day are associated with:
2 mm Hg systolic and 1 mm Hg diastolic bp drop in non hypertensive pts
5 mm Hg systolic and 2.7 mm Hg diastolic bp drop in hypertensive pts
Thus the AHA recommends less than 1500 mg/day of dietary Sodium
Other possibilities: High fiber, low dairy and animal protein and the Mediterranean diet
Physical activity AHA recommends 30 min of moderate activity 5 days a week or 25 mins of
vigorous activity 3 days a week
Risk factor modification
Antithrombotic therapy
ASA should be initiated in all patients within 48 hours and if no reperfusion therapy is administered, it should start in the ED
In cases of reperfusion tx, it is initiated after 24 hours and only after a negative CT
Early tx leads to a 1% absolute recurrent stroke risk reduction in the next 2 weeks
Under study in the early post acute phase is a combination of ASA and clopidogrel, shown in China to add benefit
It has been well established that anticoagulation with heparin does not improve outcome in unselected patients
Risk factor modification
Atrial fibrillation 5% annual risk of stroke in general but other risks stratified better under CHADS2 scores
Despite score, a history of stroke or TIA is typically enough to justify anticoagulation
Higher risk of death, stroke recurrence and severity of stroke with institutionalization in strokes associated with atrial fibrillation
A fib is likely to be underdiagnosed in cryptic stroke
Warfarin with INR at 2.0 to 3.0 effectively reduces risk 68%; corresponding to an absolute risk reduction in the annual stroke rate to 1.5%
ASA in contrast only reduces risk 21%
For patients unsuitable for anticoagulation, adding clopidogrel to ASA increases stroke risk reduction but at a cost of added risk of major bleeding
Can use the HASBLED score to determine risk
Newer agents approved: Direct Thrombin inhibitors or Factor 10a antagonists
Risk factor modification
Non Vit K antagonist drugs
Less risk of cerebral hemorrhage
Digatraban and rivaroxiban have a higher incidence of GI bleeding than warfarin
Disadvantages:
Liver and kidney disease limit use
No specific antidote
Lack of a reliable test for compliance
Expense
Increased stroke risk if stopped
What about anticoagulation in acute stroke?
Risk of hemorrhagic transformation can be influenced by
size of the infarct
Blood pressure
Evidence of bleeding on special MRI sequences, SWAN
Thank you for your attention