Cerebrovascular Dz Flashcards
anterior circulation
anterior and middle cerebral arteries
arise from internal carotid
posterior circulation
vertebral a. –> basilar a. –> posterior cerebral a.
posterior circulation supplies
thalamus, brainstem, cerebellum
stroke
acute loss of brain function due to disturbance in blood supply to brain/brain region
potential causes of strokes (6)
arterial thrombus arterial dissection embolism systemic hypoperfusion hemorrhage
stroke due to embolism/thrombus
type
CVA
stroke due to hemorrhage type of stroke
intercerebral hemorrhage (ICH) subarachnoid hemorrhage (SAH)
ischemic stroke etiologies
include embolism, thrombus, systemic hypo perfusion (shocK)
80% of strokes
hemorrhagic stroke
bleeding of brain causing decreased perfusion downstream from bleed + mass effect of blood and irritation of tissue
TIA
focal, ischemic neurological event without infection visible on imaging (typically lasts 1 hr)
reversible ischemia, <24hrs
TIA is a risk…
pts with TIA have an increased risk of CVA
esp. in first 48 hrs**
can be a sign to adjust some risk factors, or come in ASAP next time
important to ID TIA bc
can mimic an evolving CVA
CVA and TIA both have relapsing/remitting presentations
differential ddx of TIA
focal seizure Todd's paralysis cerebral tumor complex migraine hypoglycemia syncope
Todd’s paralysis
transient neurological defect that follows a seizure
typically weakness of hand, arm, leg
TIA management (as a PCP)
most TIA patients should go to the hospital
To determine management: ABCD2 algorithm to predict CVA in 48hrs following TIA
ABCD2 score recommendation
hospital eval if >3
Outpatient eval 0-2 (if can be done in 48hrs)
hospitalize if thought other dz causing
TIA workup
- EKG/Echo (looking for AFib)
- Lab evaluation (CBC, PT/INR, PTT, Chem Panel, glucose)
- Neuroimaging
- Neurovascular studies
cardiac rhythm evaluation TIA
12 lead EKG and possible 2D echo
looks for L atrial thrombus
neuroimaging TIA
MRI NON CONTRAST ***
CT w/IV contrast can be done
TIA management (following work up)
ER admission for 1 day (outpatient management 48hrs)
no etiology determined = secondary prevention
CVA epidemiology
highest risk in BLACKS, OLDER, MEN
2nd MC cause of death worldwide, 3rd MC cause of disability
non modifiable risk factors for Ischemic TIA
older age
race (black) sex male
Fibromuscular dysplasia, Sickle Cell, Migraine
modifiable risk factors for Ischemic TIA
HTN, DM, cardiac DZ, dyslipidemia, elevated homocysteine levels, OCs
neurovascular studies TIA
anterior: carotid ultrasound, CTA
posterior: MRA
this is a SCREENING procedure
risk factors for thrombosis ischemic stroke
cardiovascular risk factors (I.e. HTN, DM, age, smoking)
rupture clot and get in situ thrombosis of cerebral arteries
common etiologies of embolic TIA/CVA + source/cause (4)
cardiac emboli (AF, mural thrombus, endocarditis)
peripheral emboli (DVT + atrial septal defect)
arterial emboli (carotid a. stenosis)
fat emboli (break long bone)
uncommon TIA/CVA causes
blood vessel disorders (inflammation, vasospasm, compression, dissection)
hematologic causes (sickle cell, hyper coagulable, polycythemia vera)
CVA patho
interruption of blood flow - decreased supply of oxygen and glucose to the neurons
- Swelling of neuron (ion channels fail causing edema) causes release of free radicals that degrade neighboring cells
- Extracellular edema (decreased fluid removal from space) = vasogenic edema
- liquefaction necrosis and breakdown of affected tissue = parenchymal brain tissue loss
s/s of ANTERIOR loss (carotid)
weakness/numbness/paresthesia of contralateral extremities or face
aphasia
dysphagia
vision loss ipsilateral
flaccid weakness, hyperreflexia
vertebrobasilar CVA s/s
POSTERIOR
vertigo
diplopia
perioral numbness/paresthesia
dysarthria
ataxia
drop attacks
Broca’s aphasia
expressive aphasia
inability to communicate in full sentences/FORM fluent speech
wernicke’s aphasia
receptive aphasia
inability to comprehend speech
speech will have no relationship to consent of conversation
ataxia
loss of voluntary coordination of muscle movements
cerebellar strokes
apraxia
inability to execute learned purposeful movements
not due to sensory loss, incoordination, or weakness
dysmetria
type of ataxia characterized by lack of coordinated movement (I.e. overshoot/undershoot)
homonymous hemianopsia
unilateral field of vision loss
same field on same side in both eyes
lacunar infarction + areas commonly affected
infection of small arteries that come off the MCA (penetrate deep into brain)
most commonly affects basal ganglia, subcortical white matter, pons
lacunar infarction associated with + where affected
poorly controlled HTN + DMN
MC affects basal ganglia, subcortical white matter, pons
MC types of Lacunar infarctions
- pure motor hemiparesis
- pure sensory
- sensorimotor
- ataxic hemiparesis
- dysarthria-clumsy hand syndrome
ataxic hemiparesis
ipsilateral weakness and gait ataxia out of proportion to motor deficit
type of lacunar infarction
dysarthria-clumsy hand syndrome
type of lacunar infarction
facial weakness, dysarthria/dysphagia and weakness/clumsiness of the hand
signs of cerebral stroke
cranial nerve deficit
aphasia
dysarthria
unilateral weakness/paresthiesia/snesory loss
signs cerebellar stroke
dysdiadochokinesia
imbalance
tremor
coordination difficulties
infarct of corticospinal tract
from cerebral hemisphere
deficit will be on contralateral side
anterior cerebral artery
frontal lobes
disinhibition
AMS
impaired judgement
urinary incontinence
weaknesss and sensory loss in CONTRALATERAL leg»_space; arm>face
middle cerebral artery infarct
dominant source of blood supply for cerebral hemisphere
Contralateral arm/face>>>> leg Homonymus hemianopsia Aphasia Neglect Gaze preference to side of lesion
posterior cerebral artery infarct
Diplopia
Dizziness
Dysphagia
Dysarthria
+thalamic syndrome
thalamic syndrome
contralateral hemisensory disturbance and development of spontaneous pain and hyperpathia
cerebellar signs
infarct of vertebral/baslar a. and cerebellar a.
dizziness, diplopia, ataxia vertigo, nystagmus
hallmark finding of cerebellar stroke
crossed findings
IPSILATERAL cranial n. deficits and CONTRALATERAL motor deficit
TIA/CVA standardization assessment
NIHSS
allows you to quantify neuroimpariment/localization of stroke
lower number = less severe
does NOT measure posterior infarct
neuroimaging of TIA/CVA
CT Non Contrast in ER
diagnostic: MRI non contrast
+ carotid US, CTA, 2 D echo
why do we CT first? TIA/CVA
rules out hemorrhage, tumor, and really large stroke
DOES NOT show changes in early stroke
first decision to make with a stroke pt
thrombolytic therapy?
goal of TIA/CVA management
rapidly restore blood flow to ischemic areas not yet infarcted
best thing we can do is move quickly
IV thrombolytics TIA/CVA + risk
approved to restore blood flow BUT
risk of hemorrhagic transformation = more morality and worsen outcomes
IV thrombolytic used in stroke + risk/reward
tPA/Alteplase
6% risk of conversion, but 50% no disability 3 months post stroke
time line for IV thrombolytic therapy
must be within 3-4.5 hrs of stroke ONSET (after realization, trip to ER, diagnosis)
inclusion criteria for IV thrombolytic tx
- clinical stroke diagnosis
- age > 18
- time < 4.5 hrs
exclusion criteria for IV thrombolytic tx (8)
- stroke/head trauma <3 months
- any hx of hemorrhage
- intracranial neoplasm, AVM, aneurysm
- recent intracranial/intraspinal sx
- hypoglycemia, HTN >185/110
- active internal diathesis
- recent heparin use
- Coumadin use (INR >1.7)
mechanical thrombectomy
surgical intervention
grasp and aspirate clot or deliver clot lysis and restore blood flow
anti platelet options TIA/CVA
ASA
Clopidigrel (Plavix)
Dipyridamole/ASA (Aggrenox)
ASA TIA/CVA
decrease mortality, repeat stroke risk, and death
325 mg po or 300 mg rectal ASAP
Clopidigrel (Plavix)
just as effective as ASA in secondary prevention
pro-drug (must be metabolized)
75mg/day
Anticoagulant options TIA/CVA
given if cardioembolic source
Warfarin (INR 2-3, AVR 2.5-3.5)
Dabigitran (pradaxa)
Apixiban (eliquis)
Rivaroxaban (Xarelto)
anti platelet options TIA/CVA
ASA
Clopidigrel (Plavix)
Dipyridamole/ASA (Aggrenox)
ASA TIA/CVA
decrease mortality, repeat stroke risk, and death
325 mg po or 300 mg rectal ASAP
Clopidigrel (Plavix)
just as effective as ASA in secondary prevention
pro-drug (must be metabolized)
75mg/day
Anticoagulant options TIA/CVA
given if cardioembolic source
Warfarin (INR 2-3, AVR 2.5-3.5)
Dabigitran (pradaxa)
Apixiban (eliquis)
Rivaroxaban (Xarelto)
HTN management TIA/CVA
not using tPA
keep BP where it is
carotid auto regulation has adjusted to this BP
sudden correction will cause worsening of stroke due to hypo perfusion
HTN goal no tPA TIA/CVA
170-220/100-120
tPA BP goal
<185/105
how is HTN urgency managed
sodium nitroprusside drip
when do we correct the HTN?
permissive HTN for 2-3 days, lower BP to goal (130/80)
ACE I/TZD
additional CVA care
increased risk of DVT = LMWH/UFH
DM care (A1c 7% - >9%= insulin)
evaluate swallowing
early mobilization Pt/OT
disposition discussion
statin
sleep apnea
how to ID cerebral edema in TIA/CVA
mass effect in initial imaging
increased ICP = neuron checks q 2hrs
will show postural change, chyene stokes respiration
how is cerebral edema treated?
IV steroid (decahedron), mannitol, hyperventilation, neurosurgical decompression
additional CVA care
increased risk of DVT = LMWH/UFH
lipid lowering therapy
high intensity statin REGARDLESS of cholesterol level (anti-inflammatory)
what drugs are given for HTN management
Cardiac Dz
DM
CKD
CHF
cardiac dz: BB
dm: ACE/ARB
CKD: ACE/ARB
CHF: ACE/ARB + BB
long term stroke management
majority of stroke related deaths occur from complications (PNA, MI, sepsis)
counsel about risk factors (smoking cessation)
secondary CVA prevention
small vessel dz/cryptogenic
ASA 81 mg OR 75 mg Plavix/Clopidogrel daily lifelong
secondary CVA prevention
large vessel arteriosclerotic dz
DAPT with ASA and clopidigrel x 90 days
then single anti-platelet therapy
secondary CVA prevention
cardioembolic source
large or hemorrhage transformation: ASA mg daily 7-14 days, then anticoagulation
NO: anticoagulation
secondary CVA prevention
carotid dz
CEA or CAS
secondary CVA prevention CEA
DAPT before then ASA 81 mg after
secondary CVA prevention CAS
DAPT with ASA 81 mg and clopidigrel 75 mg daily prior to and 90+ days after stent
long term single agent
anticoagulation, who gets what agent?
CKD: warfarin/apixaban
AF due to Mitral dz: warfarin
AF mural thrombusL warfarin only
OR watchman define
use CHADS2VAS to determine
paroxysmal AF tx?
anti-platelet therapy until AFib is able to be diagnosed
then start anticoagulation
these patients have SAME risk as regular AF
statin dosages
given to every
LDL < 100 (<70 if at risk)
Atorvastatin (Lipitor) 40-80 mg
Rosuvastatin (crestor) 20-40 mg
primary stroke prevention
counsel how to recognize a stroke
FAST (face, arm, speech = time to go!)
stop smoking, control HTN/DM/lipid
daily ASA if only at stroke risk
CHADS2VAS criteria
CHF HTN Age > 75 DM Stroke/TIA + 2 Vascular dz Age >65 Sex- female
CHADS2VAS interpretation
0-1: ASA only
2: anti-coagulant OR ASA (AC preferred)
>3: anti-coagulate
carotid stenosis and CVA
> 75% occlusion is at a high risk of stroke, typically have other CV risk factors
evaluated with carotid US or CTA
carotid stenosis CVA values
> 70%
refer to vascular surgeon for CEA or CAS
life expectancy > 5 yrs
IF 100% = do nothing :)
carotid stenosis CVA values
60-70%
consider referral
anti-platelet therapy and pts will need monitoring
carotid stenosis CVA values
<60%
anti platelet therapy and semi annual repeat study
amaurosis fugax
infarction of renal artery (unilateral)
transient, typically present to eye doc
“shade pulled over eye”
same work up
