Cerebrovascular Disease Flashcards
3 different stroke etiologies
1) Embolic - thrombus somewhere else, flicks off and happens to go to brain - consider AFib or valve disease, arterial dissection elsewhere or carotid artery stenosis
2) Thrombotic - cerebrovascular disease in artery to brain - plaque ruptures - distal tissue poorly perfused. AS, HTN, DM, CAD, PVD
3) Hemorrhagic - blood is an irritant to brain. If you have brain bleed you can lose brain parenchyma
- Sub-arachnoid or IPH
Various patient presentations in stroke
FND!!! plus
1) HTN diabetic smoker with bad cholesterol and is old (for CAD old is 45F, 55M)
2) AFib, prosthetic valve off anticoagulation
3) Young woman with neck pain
4) Thunderclap HA (prob proceeded by sentinel HA 1-2w before)
Various infarct locations and body areas involved
ACA - Feet, legs
MCA - arms, hands, face, speech - broca’s is in superior division, wernicke in inferior
PCA - vision changes, homonymous hemianopsia
Basilar and vert - locked in, syncope
Cerebellum - ataxia, disdiatokinesia, coordination
Basic treatment for hemorrhagic stroke
Lower BP
Neurosurg - clip, coil, craniotomy
FFP (reverses risk of bleeding)
Basic treatment of ischemic stroke
tPA
Then next day get EKG, Echo, Carotid US*, maybe MRI, MRA
If EKG shows AFib - anticoagulation
If Echo shows thrombus - anticoagulation - hep-warf bridge
If patient is ASx and Carotid US shows more than 80% stenosis OR if patient is Sx and shows 70% then consider CEA or stent. CEA is better. Wait 2w for the surgery.
If patient is Asx OR less than 70% stenosis then medical management
TIA is when symptoms resolve on own and improve within 24h. MRI without evidence of stroke.
Management of acute stroke
1) tPA? Yes if less than 4.5 hrs from LKN. Avoid if previous ICH, risk of current bleeding like GI bleed or recent surgery
2) Heparin? No
3) Warfarin? No
4) Anti-platelets? ASA 325
5) BP? Permissive HTN less than 220/120. This is to preserve the penumbra
6) DM? Gluc less than 140
7) Statins? Start high-potency statin since they will go home on it anyway. Atorva 80
Management of stroke chronically
1) tPA? no
2) Heparin? No
3) Warfarin? Afib or CHADS2 at or higher than 2 (must be anticoagulated). CHF, HTN, Age over 75, DM, stroke, stroke
4) Anti-platelets? ASA 81, stroke on ASA then ASA + dipyridamole. If can’t tolerate ASA then clopidogrel
5) BP? ACEi, diuretics, BP less than 140/90
6) DM? A1C less than 7
7) Statins? High dose statin like atorva 40/80 or rituvastatin 20/40
What are the 5 lacunar syndromes?
1) Pure motor - internal capsule
2) Pure sensory - thalamus
3) sensorimotor - both
4) Ataxic hemiparesis
5) Dysarthria clumsy hand - subcortical white matter
L MCA vs R MCA
Left - aphasia (brocas and wernickes are on the left if you are R dominant)
Right - neglect, apraxia
Contraindications to tPA
1) not a candidate - greater than 4.5 hrs, rapidly resolving symptoms, GI bleed, low platelets
2) Large hypodensity on CT (too late! it’s stroked out and we don’t want to bleed into it)
3) BG less than 50 or higher than 400
4) Stroke within 3 months (high risk of hemorrhagic conversion)
5) Prior ICH
6) Recent major surgery last 2w
7) Catheter in non-compressible site
8) Oral anticoagulation (ASA is ok). INR less than 1.7 is ok or if they haven’t taken in a few days is ok.
9) recent GI bleed
10) SBP higher than 185 or DBP higher than 110
11) High PT or PTT
How long can you do an INR procedure?
less than 6hrs
Management after tPA
Before: BP less than 185/110
After: BP less than 185/105
Labetalol 10-20IV, Nicardipine drip
BP monitoring q15m for 2h. q30 for 4h. q1h for 16h
Neuro exams at same intervals
Stability CT at 24h (r/o hemorrhage from tpa)
No ASA, heparin, lovenox until that stability CT
Management of inpatient stroke - couldn’t get TPA
Permissive HTN less than 220/120
Dysphagia screen or NPO
ASA/Statin
Resume home B blockers, hold anti-hypertensives
DVT ppx
Avoid sedating meds
Fall risk
Aspiration risk
Inpatient workup for stroke
Tele Echo (w/bubble) Vessel imaging (carotid doppler/TCD) Speech and swallow eval Hypercoag workup (PFO, SLE, anticardiolipin) PT/OT/Rehab eval TEE (L atrial dilatation, it sees the aortic arch better) Fasting lipids, A1C, hypercoag
Anterior circulation syndromes
From carotids
Can include deficits related to damage to cortex of frontal, parietal, or temporal lobes, basal ganglia, internal capsule
Aphasia and heminopsia can only be cortical
Agraphesthesia, extinction to dual simultaneous stimulation and neglect are all cortical as well
Lesion with dense hemiparesis is likely internal capsule from lacunae
Posterior circulation syndromes
Vertebro-basilar
usually diplopia (cranial nerve nucleii), vertigo (vestibular nucleii), ataxia (cerebellum or its connections), n/v, crossed deficits (hemisensory loss on ipsilateral face and contralateral body), dysarthria/dysphagia (nucleus ambiguus)
Wallenberg syndrome AKA Dorsolateral medullary syndrome: dysarthria, n/v, vertigo, crossed sensory defecit, horners
Weber syndrome: ipsilateral oculomotor paresis with contralateral hemiparesis
Medial medullary syndrome: contralateral hemiparesis and ipsilateral tongue paresis
Ataxia-hemiparesis syndrome: from pontine lacunae
Dysarthria-clumsy hand syndrome: also in pons
Hyperacute onset with full deficit present from the beginning
Embolic etiology likely, esp is patient has AFib
Stuttering onset
Usually thrombotic
Stuttering onset with sudden deterioration
may suggest hemorrhagic conversion
Carotid bruit on exam on the suspected side of lesion
Suspicious for large vessel atherosclerotic disease
Irregular pulse
May suggest underlying AFib and cardioembolic stroke
Methods for evaluating the carotid arteries
MRA, CTA, duplex US and catheter based carotid angiogram
Most common is Doppler US
MRA can be done with or without contrast
CTA MUST have contrast. CTA without contrast may demonstrate calcification in the wall of the carotid artery but will not evaluate the patency or degree of stenosis
Amaurosis fugax
Transient monocular blindness
Most commonly caused by atheroembolus to ophthalmic artery from internal carotid.
If a patient with retinal or cerebral ischemia in the anterior circulation has ipsilateral carotid stenosis that is high grade, then carotid revasculatization is indicated.
CEA is better than stenting.
Confirm high grade stenosis by concordance on 2 different noninvasive tests (doppler, CTA, MRA) OR with catheter angio
Risk of stroke in untreated vs treated Carotid artery stenosis
In patients with high grade stenosis who are symptomatic in the distribution of the stenotic ICA, the 2yr stroke risk is 24% with medical treatment and 9% with addition of CEA
