stroke Flashcards
can do what in 5 secs of walking in room
ABCs (pt speaking) when did this start? -if woke up with stroke not eligible for tPA -vitals: BP! -oriented/confused -family present
if on coumadin
not candidate for tPA
family can…
sign for tPA consent
verify onset
stroke vs. bells
stroke spares the forehead, can wrinkle
stroke brkdwn
80% ischemic, 20% hemorrhagic
global: low CO (MI, a fib)
focal: occlusion (thrombotic, emolic)
*3rd leading cause of death
strokes can be caused by
emobolism, thrombus,
hypoxic etiologys: hypoperf, or hypoxemia
happens during cerebrovasc. sx: affects watershed areas
risk factors for ischemic stroke
DM HTN smoking fam hx high cholesterol afib drugs (cocaine) hx of TIA or recent MI hx of CHF OCPs
ant. vs posterior circulation
will affect what type stroke
watershed zones: area covered by 2 arteries
ant and mid cerebral aa
post and mid cerebral aa
usually from hypotension
upper leg and upper arm weakness
defects in higher order visual processing
autoregulation
maintains constant level of CBF despite changing perfusion pressure
CPP normally driven by
pCO2, ICP dec. as CO2 dec. via vasoconstriction
- hypervent theory in trauma, CVA*
- can actually cause more damage
hypoxemia will
inc. CPP IF PO2
CPP=
MAP (BP)-ICP
if CPP=0–>brain dead
via blood flow study
a dec. in BP or inc. in ICP results in lowering of CPP
know charts
pg 463
chronic HTN
lower/upper levels of autoreg are raised–>tolerance of higher blood pressures, but more intolerance to lower BP
*used to give clonidine to reduce high BP-won’t stroke out–>but they do from low BP!
now we do NOT abruptly lower BP in asymptomatic chronic HTN pts it’s relative
put on antiHTN, not rapid
cerebral ischemia will lead to
liquefactive necrosis
emo/throm: focal OR
dim. syst: global OR
hypoxia
prolonged ischemia–>infaction
young or old
penumbra
transition zone between normal tissue and infarcted tissue
need to save!
ischemic histo timeline
12-48 hr—red neurons 24-72 hr—necrosis w neutrophils 3-5 days—macrophages (microglia) 1-2 wks—reactive gliosis w vascular proliferation >2ks—glial scar
irrev. damage
after 5 min hypoxia
most vulnerable areas
*hippocampus, neocortex, cerebellum, watershed areas
cerebral edema accumulates..
over 3-5 days after stroke–>death
2/3 ischemic strokes
cerebral atherosclerosis
1/3 ischemic strokes
cardiogenic emboli
afib
patent foramen ovale-DVT
etiology in younger pts: things that make you clot
arterial dissections DRUGS: *cocaine, OCPs(pro-coag), heroin(hypoximic) endocardidtis protein C or S deficiency antithrombin III deficiency anti-PL AB SCD SLE PFO: patent foramen ovale
stroke prevention
control risk factors/reverse them diet smoking HTN-don't take of BP meds DM high cholesterol afib
a fib inc. CVA risk
17x
coum/warf therapy: INR 2-3x basement
Chad’s score/Chad 2 score/Chad vasc score know
-who with a fib need anticoags?
carotid stenosis
> 70% carotid endarterectomy(cleaned out) if high risk–>stunting
60–70% early carotid endarectomy best rather then deferring
TIA
transient neuro deficit
NO infection, neg MRI*
Lasting usually
lacunar stroke
Small lesions
anterior strokes
MCA, ACA, lateral striate, ophthalmic
Ophthalmic artery stroke
amaurosis fugax: sudden vis loss 1 eye, usually transient
ant cerebral art
(Motor and sensory cortex of lower limb)
Weakness + sensory loss contralateral leg
Urinary incontinence possible
Abulia: state of akinetic mutism (inability to make a decision) via B/L frontal lobe dysfunction.
mid cerebral art
embolic typically
contralat wkness loss of sense: face, arm, leg (arm>leg) via motor/sensory cortex lesion
gaze pref AWAY from side of weakness
temporal lobe lesion: Wernicke
frontal lobe lesion: Broca
aphasia if in dominant (typ. left) and hemineglet in nondominant side
mid cerebral artery dominant hem
global aphasia (expr and receptive)
mid cerebral artery nondominant hem
anosognosia-unawareness of weakness
-hemineglect
lateral striate art
lesion in striatum, int capsul
contralat wkness
common location of lacunar infarcts bc of uncontrl HTN
comm artery strokes
lesions typ. aneurysms impinging on CNS, not strokes
acomm-visual field def, aneurysm most common, can lead to stroke
Pcomm: down and out: CNIII palsy ptosis and mydriasis, saccular aneurysm
posterior strokes
ASA, PICA, AICA, PCA, basilary artery
vertebrobasilar ischemia
dissiness , fluctuating drowsiness, diplopia, ataxia, bilat sens/motor symptoms
may be mistaken as vertigo
basilar art stroke
occlusion of bl vertebral arteries
massive BS damage
coma, pinpoint pups, flaccid quadrip/sens loss
often fatal
spares medulla–>dysarthr,
locked in syndrome, somnolence, amnesia
pons, med, lower mdbran, CST and corticobulbar tracts, ocular cranial nerve nuc, paramedian pontine retic. formation
blinking and consciousness unaffected
post cerebral art
lesion at occipital and visual cortex
thalamic synd: contralat hemisens distr–>pain, hyperpathia
contralat wkness
contralat homonymous heminopsia
macular vision may be spared-central
ant spinal art strke
contralat hemiparesis of arm and leg, (LCST)
dec. contralat proprioception (ML)
ipsilat hypoglossal dysfuntion–>tongue deviates ipsilat* (hypoglos. nerv)
lesion of lat corticospinal tract; medial lemniscus; caudal medulla-hypoglossal nerve
PICA
vomiting, vertigo, nystagmus, ataxia
dec. pain temp
ipsilat face, contralt body:
*crossed findings**
hoarse, dysphagia, dec. gag
ipsilate Horner's lateral medullary (wallenberg) syndrome
lesion at inf cerebellar peduncle, lateral medullat, sp Trigem nuc, nuc ambiguussp. to PICA, sympathetic fibers
Horner’s
ptosis
miosis
dec. sweating ipsilat face
*with PICA stroke
Wallenberg’s
loss of pain/temp
contralto body, ipsilat face
*crossed finding dx for this syndrome
*PICA
AICA stroke
-ant inf cerebellar
vomit, vert, nystag, ataxia
paralysis of face, dec pain/temp ipsilat
contralat dec. pain/temp of body
- dec. lacrimation, salivation*
- dec. tast ant 2/3 tongue*
dec. corneal reflex
ipsilat Horner’s
dec. hearing ipsilat
lesion at middle and inferior cerebellar peduncles, lateral pons—cranial nerve nuclei, vestibular nuclei, facial nucleus (specific for AICA), spinal trigeminal nucleus, cochlear nuclei, sympthetic fibers
cerebral venous thrombosis
- occlusion of saggital sinus*
usually: difficult to dx, hyperviscosis, hypercoag, preg, maxillofacial inf. SCD
symp: ha**, seizure, papilledema, focal neurolog def
dx: CT w. IV contrast or MRA
tx: steroid to lower ICP, anticoag
typ. present as ha not going away typically pregnant
if do CT w.OUT contrast, will not see unless v. large
aphasia
higher order inab. to speak
dysarthria
motor inab to speak
Broca
nonfluent aphasia, broken up, comprehension intact-understanding, can’t speak effectively, impaired repetition
inferior frontal gyrus of frontal lobe
most commonly seen
Wernike
fluent aphasia, impaired comprehension and repetition; very wordy, w.out making sense
*superior temporal gyrus of temporal lobe
Broca’s aphasia
“expressive” cannot get words out, know what to say, start crying, intact comprehension
Wernicke’s aphasia
“receptive”
fluent speech, meaningless
impaired comprehension, don’t know something is wrong
conduction aphasia
Poor repetition
Fluent speech
Intact comprehension
Lesion: arcuate fasciculus
Can’t repeat phrases such as “no ifs ands or buts”
global aphasia
Both wernicke and broca
Nonfluent aphasia
Impaired comprehension
what kind of stroke? ischemic or hemorrhagic?? can tell from
CT
thom or emolic?
H/P, cardiac echo, EKG
where in brain?
CT: might not rev CVA for 6-24 hrs***
MRI/MRA: not available acutely? 3-30 min after CVA (takes about 45 min!)
doppler: ant only: carotids
cardiac echo
carotid duplex
US of carotids, shows how much blockage: %
hyperdense MCA sign
Indicative of acute thrombus within the middle cerebral artery
Seen on CT brain usually by 90 minutes
99% sensitivity, 30% specificity
see white arch in MCA
-determine density
stroke dx
cardiac workup
CBC, PT/INR, PTT, lipids, BMP, cardiac enzymes, ekg, CT head without contrast, CXR
hypercoag studies? not in ER, but if young will do
UDS ??: not unless young–>cocaine, etc
ddx stroke
Todd’s paralysis: unilat paralysis after seizure, typ. benign, determine seizure etiology
complicated migraine: involves neuro symps: unilat paralysis, numb, tingling, visual defects
stroke tx : general
ABCs DVT prophylaxis (inpatient) Early OT, PT, Speech tx, and Swallowing Evaluation Blood pressure and glucose control Temperature control Management of depression
stroke tx: anticaog: Heparin?
Heparin: used to be used, no evidence to support routine use for acute stroke, MIGHT reduce risk of recurrent stroke, offset by risk of ICH
*select pts
stroke tx: antiplatelet tx?
tx of choice to prevent recurrent thromboembolism
-everyone gets ASA or plavix
stroke tx: thrombolysis (tPA)
+1 signature, from family*
death
Benefits…stroke and symptoms resolve
antidote to tPA?
aminocaprioic acid
exclusions to tPA
Cva or head trauma
BP >185/110, reduce 1st if want to give, sacrifice perfusion
sx 15 seconds
glucose 400 could be having non-thrombotic stroke (hypo/hyperglycemic stroke)
cerebral edema management
Worry about brain shift and herniation; only with large hemispheric infarctions
airway control-intubate
hypervent?? not really
mannitol: diuretic for brain
craniotomy
HTN management in acute CVA
If SBP 220 or DBP>120-too high!
Titratable short acting IV drugs
Labetalol, nitroprusside, nicardipine
BP goal?: 180-200/100
180/110 for tPA
-protect the penumbra!, do not lower BP dramatically
if give nitro
BP improves, stroke may get worse, edema, penumbra enlargers, involves consciousness
ICH: “bleeding stroke”
Diffuse (SAH)
Focal (intraparenchymal)
20% of all strokes
causes of ICH
HTN—undiagnosed, noncompliant AVM drugs aneurysm bleeding disorders trauma/tumor
intraparenchymal hemorrhage
“paintball to brain”
HTN causes it
goal: reduce mass effect:
mannitol or sx (last-ditch, hydrocephalus, high risk herniation)
putamen most common site: 40% dec. LOC: mass effect, rise in ICP, or direct BS involvement high BP, AMS may extend into ventricles-->hydrocephalus
SAH
usually berry aneurysm rupture strenuous activity: sex, exercise thundeclap, HA, post. neck pain LOC, N/V CT/LP: blood or xanthochromia 2-3 days later: vasospasm -->rebleeding
SAH: sentinel hemorrhages
baby SAHs: sm. aneurysmal leak, resolve after 1-2 days
like a TIA-precursor
Charcot-Bouchard
chronic HTN
small vessels: basal gang, thalamus
microaneurysm
saccular berry aneurysm
bifurcation in circle of Willis:
-bifurcation of anterior comm. and anterior cerebral aa
rupture most common comp: SAH, hem. stroke
bitemp hemianopia via optic chiasm compression
risk: older, HTN, tobacco, african amer
marfan’s, Ehlers danlos, polycystic kidney disease (ADPKD)
AVM
tangles of arteries connected dir. to vv w.out intervening capillaries**–>bleeding
cause: congenital
HA, seizures, tinnitus, blurry vision, or hemorrhage
younger pts: sx excision, embolization, irradiation
>55: conservative
right MCA sign
left arm>left leg weakness, slurred speech
subarachnoid hemorrhage, diffuse on both sides
complications: vasospasm/rebleed
slide 95 pics
blood in ventricles, hydrocephalus
poor px
intraparenchymal hemorrhage, typ. from uncontrolled HTN
first aid
pg 466
Chads2Vas score
65-74: 1
>75: 2
female: 1 CHF hx: 1 HTN hx: 1 stroke/TIA/thromboembolism hx: 2 vasc. disease hx: 1 DM: 1
