Stroke management Flashcards
Stroke causes
85% ischemic (20% large artery atherosclerosis 25% small vessel lacunar stroke 20% cardioembolism 30% cryptogenic 5% others)
15% hemorrhagic
Ischemic stroke mechanisms
intracranial atherosclerosis small artery disease carotid plaque with emboli carotid stenosis aortic arch plaque a fib valve disease ventricular thrombi cardiogenic emboli
Cardioembolic sources
atrial septal aneurysm patent foramen ovale a fib mitral stenosis mechanical vegetation cardiomyopathy MI
A fib and stroke
1% of population in NA and europe AF
5% of those over 65
2.5 mil Americans
1 of every 6 strokes due to AF
CHADS2
1 point: CHF Hypertension Age > 75 Diabetes
2 points:
stroke, TIA
ACA stroke symptoms
Leg > arm weakness
Leg > arm numbness
Abulia
MCA stroke symptoms
Hemiplegia --> affect motor strip Cortical features: - aphasia - neglect - visual field deficit - gaze deviation
Posterior circulation stroke symptoms
brainstem --> more nucleus/tract defects Visual field defects vertigo Diplopia Ataxia Dysphagia Weakness Numbness
Small vessel disease lacunar stroke syndrome
pure motor pure sensory mixed sensorimotor dysarthria - clumsy ataxia hemiparesis
Hyperacute/acute stroke treatment
iv-tPA endovascular mechanical thrombectomy aspirin stroke unit hemicranectomy
Secondary stroke prevention
antiplatelets (aspirin, clopidogrel, ASA and dipyridimole) anticoagulants (warfarin, NOACs) carotid revascularization (carotid endarterectomy, carotid stent)
Tissue plasminogen activator
serine protease
converts plasminogen –> plasmin
fibrinolytic
only effective FDA approved treatment for acute ischemic stroke
10% bolus then infusion over 1 hour within 3 hours of symptom onset
Antiplatelets for 2ndary stroke prevention (non-cardioembolic)
Aspirin Clopidogrel slightly better than ASA ASA + DP superior to ASA Clopidogrel + ASA NOT indicated ASA + DP NOT superior to clopidogrel Do not combine anticoagulants + antiplatelets!! Start tx as soon as possible long-term treatment
Hypertension control for stroke prevention
absolute target uncertain
benefits associated with overall reduction of 10/5 mmHg
optimal drug regimen uncertain - diuretic + ACEi?
European guidelines for management of hypertension
General:
TIA
episode of neurological deficit where symptoms resolve fully, noe vidence of loss of blood flow
Infarction
injury permanent
Penumbra
dysfunctional but salvageable tissue
Carotid stenosis stroke risk
25% of disabling stroke within one year
Carotid ischemic syndromes
unilateral weakness, numbness (contralateral)
Dysphasia if language dominant hemisphere
Amaurosis fugax: ophthalmic artery branch off carotid artery; transient monocular vision loss due to reduced blood flow to the retina
Endarterectomy indications
symptomatic (strong indication)
asymptomatic - bruit detected (modest indication)
Intra-arterial thrombolysis
direct local delivery of thrombolytic lower dose/decreased systemic effects increased rate of clot lysis expanded time window (6 hours for MCA) requires infrastructure/expertise
Mechanical clot removal
time sensitive -
Intracerebral hemorrhage sources
epidural, subdural: trauma
Subarachnoid: ruptured aneurysm
intraparenchymal - HTN
intraventricular
Amyloid angiopathy
deposition of beta amyloid in vessel wall
lobar hemorrhages
typically in elderly
Common in DOwn’s syndrome
characteristic histology - Congo Red (birefringent rings of amyloid deposition)
Aneurysms
Saccular (berry) fusiform (sausage) arterial weakening typically at branch points: Circle of Willis common cause of subarachnoid hemorrhage
Aneurysm risk factors
thinner intima/media
lack external elastica
medial defects
Location of aneurysms
Ant communicating - 30% Post communicating - 25% MCA - 20% Carotid bifurcation - 8% Basilar bifurcation - 7%
Clinical presentation of subarachnoid hemorrhage
Sudden, severe headache neck pain from increased ICP nausea - chemical irritation photophobia loss/alteration of LOC focal neurological deficits sudden death
Pathological features of SAH
raised ICP, cerebral edema CN injury intracerebral hemorrhage intraventricular hemorrhage hydrocephalus
Epidemiology of SAH
incidence of aneurysm in popn ~2%
10/100,000 per year
most commonly age 40-60
modest female preponderance
Hunt & Hess scale
1: asymptomatic/mild headache
2: severe headache/meningismus
3: drowsy, confused, mild deficit
4: stuporous, severe deficits
5: deep coma, moribund
SAH management
neurosurgical ICU airway, ventilation BP control ICP control - ventriculostomy fluid/electrolyte monitoring early aneurysm repair
SAH complications
recurrent bleeding from aneurysm
- arterial pressure –> tamponade
- clot stops intial bleed, then recurrent bleed can happen
Vasospasm –> narrowing of blood vessels
hydrocephalus
seizures
electrolyte abnormalities (commonly hyponatremia)
Unruptured aneurysm/incidental aneurysms
risk of bleeding 1-3%/year
risk increased with previous history of SAH, large size, HTN, smoking, posterior fossa location
repair if >5 mm
Cerebral A-V malformation
congenital
3 components: feeding arteries, nidus, draining veins
High pressure from artery to vein with no arteriole or capillaries or venule in between
Distended vein –> rupture
Cerebral A-V malformation clinical features
hemorrhage
seizures
headache
focal neurology
Grading of cerebral A-V malformation
size
location
deep venous drainage
Cerebral AV malformation treatment
none microsurgical removal stereotactic radiosurgery embolization combination/multidisciplinary
Stroke mimics
DIIMMSSS Drug intoxication Infection Insanity conversion disorder Metabolic: hypoglycemia, renal failure, hepatic failure Migraines Syncope Seizure Structural: trauma, tumour, subdural hemorrhage
