Stroke & TIA Flashcards
1
Q
CVA
A
- cerebovascular accident
- evolving
- complete
- > 24 hr irreversible
2
Q
TIAs
A
-transient ischmic attack
-< 24 hr reversible
> 24 hr <7d may be partially reversible
3
Q
Stroke causes
A
- Ischemic: thrombotic vs. embolic
- hemorrhagic: intracerebral vs subarachnoid
- all strokes are ischemic it is whether they are thrombotic or embolic
- atherosclerosis
- A-fib (big risk factor)
- arteritis
- hematologic disorder
- complications of angiography
- dissecting aortic aneurysm
- trauma to the carotid artery
- hypotension
- migraine
- hypoxia
- radiation
- closed head injury
4
Q
Ischemic
A
- thrombotic vs. embolic
- virtually the same with respect to etiology
- thrombotic is local
- embolic is distant (clot is elsewhere and then go to the brain)
- atherothromotic is an appropriate term
5
Q
Ischemic (atherothrombotic) stroke
A
- majority are embolic, w/o local cerebral causes
- vulnerable plaque ruptures and forms thrombus, which enters cerebral vasculature
- minority are due to intracerebral atherosclerotic disease
6
Q
Intracerebral hemorrhagic stroke
A
- hypertensive intracerebral hemorrhage (big one)
- trauma
- hematologic disorders & anticoagulant therapy (big one)
- hemorrhage into tumors
- septic embolism or mycotic aneurysms
- amyloid angiopathy
- vasculitis
- vasopressor drugs
- encephalitis and postinfectious encephalopathy
7
Q
Subarachnoid hemorrhage
A
- rupture of aneurysm at Circle of Willis
- severe thunderclap HA
- “worst HA of my life”
- LOC common
- seizures
- meningeal signs, +/- funduscopic bleeding, monocular blindness
- increase sympathetic tone (BP and glucose, EKG changes)
- CT scan to search for bleeding
- very high risk for rebleeding
- control HTN aggressively
- trauma
- anticoagulant therapy
8
Q
Vascular supply
A
- Carotid arteries: internal and external (internal for stroke)
- vertebral arteries
9
Q
Vascular occlusion
A
- anterior cerebral: lower > upper
- middle cerebral: upper> lower, aphasia (dominant hemisphere)
- vertebral (posterior): cerebellum issues like vision and labyrinthine
- labyrinthine: balance and coordination problems
10
Q
TIA clinical presentation
A
- amaurosis fugax: opthalmic nerve occlusion (transient- minutes to hours)
- “mini-strokes”: weakness/paresthesias/hemiplegias, dysphagia, visual disturbances, dipopia, amnestic episodes, ataxia, imbalance, staggering, “drop attacks”
- TIA defined as resolved by 24 hr otherwise a “complete stroke”
11
Q
TIA differential diagnosis
A
- migraine
- seizures
- acute hyperventilation syndromes
- cerebral tumor or subdural hematoma
- multiple sclerosis
- hypoglycemia
- labyrinthine vertigo including Meniere
- cataplexy
- leaking intracranial aneurysm or arterovenous malformation
- ingested drugs or toxic agents
12
Q
TIA/Stroke considerations
A
- explore modifiable risk factors
- evaluate comorbid conditions and coagulation status
- carotid bruits may be present (on US if < 70% stenosis just need to stabilized plaque not scrape it out)
- A-fib: treat and anticoagulate (high risk)
- antiplatelet therapy for non cardioembolic stroke/TIA
- statin drugs for plaque stabilization of lipid control
13
Q
TIA / Stroke modifiable risk factors
A
- HTN
- smoking
- DM
- carotid artery disease
- A-fib
- cardio vascular disease
- sickle cell
- hyperlipidema
- alcohol/drugs
- obesity
14
Q
Ischemic stroke
A
- sudden onset
- usually progressive
- often at night and wake up with sx
- loss of consiousness in some cases, drowsiness, stupor, confusion more common
- often preceded by TIAs
- pt with atherothrombotic risk factors
- focal neurological deficits, depending on site of occlusion
15
Q
MCA vs ACA territory ischemic stroke
A
- MCA: middle cerebral artery,
- most common thrombotic stroke
- face and upper extremity affected > lower extremity
- dysphasia if in dominant hemisphere
- nondominant parietal sx complex and emotional
- ACA: anterior cerebral artery
- lower extremity affected > upper extremity/face
16
Q
tPA indications
A
- clotbuster
- over 17
- clinical dx of disabling ischemic stroke firmly established
- time of sx onset well established to be less than 180 min (3hr) before tx would beging
- previously independent functional status
- recommended “door to tPA time” = 60 min
- don’t give to a pt with a hemorrhagic stroke
17
Q
tPA risk-benefits
A
- benefits out way risk under 3 hours (now maybe 4)
- over 3 hour window increased risk for intracranial hemorrhage
- associated w/ increase in good neurologic outcomes
- associated with lower death rate
18
Q
Ischemic stroke initial management / tx
A
- hospital/ER
- consider other differential dx
- TPA if less than 3 hr into stroke
- if unconscious, ABCs, IV, intermittent cathererization
- Do not aggressively reduce BP (providers perfusion)
- assess and document extent of neurologic deficits
- EKG, head CT, cbc, bmp
19
Q
Ischemic stroke management / tx
A
- admit to hospital for supportive care
- physical therapy ASAP when pt is stable
- acute anticoagulation in some cases
- platelet inhibition in most cases after complete stroke
- aggressively control risk factors (HTN, DM)
- depression is present in a very high percentage of poster - CVA pt
20
Q
Vertebrobasilar (PCA) sx
A
- homolateral cerebellar ataxia
- vertigo, hiccups, sympathetic invovlement (Horner’s, ptosis, miosis/anisocoria, anhydrosis)
- other brainstem syndromes (BP, pulse, respiration visual cortex)
- vertebrobasilar insufficiency: TIA like sx in posterior distribution
21
Q
Hemorrhagic stroke
A
- HTN almost always a factor
- lacunar, parenchymal, subarachnoid hemorrhage
- lacunar infarcts small, w/ lesser neurological effects, often transient
- parenchymal hemorrhage often sudden, severe and fatal
- presentation: more in daytime, severe HA, n/v, LOC, seizures, hemiparesis, local neurologic signs
- increased ICP: no LP
- treated like ischemic stroke
22
Q
Subarachnoid hemorrhage acute care
A
- moderate control of BP to lessen bleeding, but maintain perfusion
- surgical clipping or endovascular coli insertion of aneurysms that have bled
- Ca channel blocker to prevent vasospam
