stroke management Flashcards
initial evaluation of sstroke presentation
ABCDE
clinical assessment: risk factors, last known normal, time of onset of symptoms
imaging
non contrast CT to evaluate for acute haemorrhage
diffusion weighted MRi to detect acute ischaemia
consider further neurovascular imaging depending on the type of stroke: Can be noninvasive (e.g., duplex sonography of the carotid arteries, magnetic resonance angiography) or invasive (e.g., conventional angiography).
non-contrast head CT
first line
CT allows for the detection of ischemic changes within 6–24 hours after stroke onset. Remember to compare to previous CT results when possible.
allows for detection of acute haemorrhage
non-contrast head CT cannot be used to identify
ischaemic changes prior to 6 hours after onset
non contrast head CT is indicated for
Indicated in all patients suspected of having an acute stroke to rule out intracranial hemorrhage before administering thrombolytic therapy
diffusion weighted MRI
Allows identification of ischemia earlier than a CT (within 3–30 minutes after onset) [29]
Allows detection of hyperacute hemorrhage
Evaluates reversibility of ischemic injury
how does diffucion weighted MRI evaluate reversibility of ischaemic injury
Perfusion-weighted imaging (PWI): visualizes areas of decreased perfusion and allows quantification of perfusion parameters, e.g., mean transit time (MTT), cerebral blood flow (CBF) and cerebral blood volume (CBV)
Perfusion-diffusion mismatch MRI: allows identification of the penumbra (or “tissue-at-risk”)
laboritory investigations
should not delay imaging for acute stroke
serum glucose
FBC, electrolytes, coagulation parameters, urine drug screen for recreational substances eg. cocaine
blood alcohol level
serum troponin
why do serum glucose
For most patients with acute ischemic stroke, only serum glucose is required prior to administration of tPA. Symptoms of hyper- and hypoglycemia can resemble a stroke.
postictal paralysis
The development of focal weakness after a seizure, which typically resolves within 48 hours. Thought to result from exhaustion of the primary motor cortex.
vestibular neuritis
An idiopathic inflammation of the vestibular nerve. Typically manifests with acute-onset vertigo, nausea, vomiting, and gait instability with increased risk of falling to the affected side. Prognosis is good with vestibular rehabilitation therapy.
stabilization and monitoring
maintain euvolaemia with fluid replacement as needed: Avoid free water, which may exacerbate cerebral edema in patients with acute stroke.
maintain oxygen and consider intubation if the patient shows signs of increase ICP
maintain euglycaemia
maintain normothermia
cardiac monitoring
maintain normal acid base status
electrolyte repletion as needed
analgesia as needed
monitor for sign of elevated intracranial pressure
seizures should be treated pharamcologically
evaluate for dysphagia
blood pressure managemnt
always treat hypotension: with fluid replacement, vasopressors
ischaemic stroke: permissive hypertension
only treat if >220 systolic or 120 diastolic
hemorrhagic: reduce systolic to 140-160
permissive hypertension
Hypertension is treated less aggressively in ischemic stroke than in hemorrhagic stroke; in ischemic stroke, the perfusion of the penumbra depends on the mean arterial pressure.
nitrates
should be avoided because they increase ICP
cushing reflex
A hypothalamic response to maintain cerebral perfusion in patients with elevated ICP. Results in the Cushing triad, which consists of increased systolic blood pressure, bradycardia, and irregular breathing
neurological complications of all strokes
elevated ICP and brain herniation (cushing triad)
seizures
syndrome of innappropriate secretion of antidiuretic hormone
persistant neurological deficits
central post stroke pain
neuropathic pain
central post stroke pain
Affects < 10% of all stroke patients
Can occur with thalamic lesions
Unilateral facial pain and/or extremity pain associated with previous stroke
Contralateral or ipsilateral initial paresthesia followed by neuropathic pain (e.g., allodynia, dysesthesia)
ischaemic stroke neurological complications
haemorrhagic transformation
vascular dementia
risk factors for haemorrhagic transformation
onset: usually 1–2 days after the inciting ischemic event
Risk factors: thrombolytic medications (e.g., alteplase), antiplatelet therapy (e.g., aspirin, clopidogrel), and/or thrombosis prophylaxis (e.g., heparin, enoxaparin) within 24 hours of ischemic injury
Management: discontinuation of anticoagulation and/or antiplatelet therapy, admission to a neurointensive care unit, and neuroprotective measures
neuroprotective measures
tight blood pressure and glycemic control, targeted temperature management, electrolyte repletion
haemorrhagic stroke neurological complications
Vasospasm (typically occurs 5–7 days after SAH) → ischemic stroke
Recurrent hemorrhage
Intraventricular hemorrhage
Hydrocephalus
carotid artery stenosis management
ultrasonography of the neck
symptomatic CAS may include TIA, ameurosis fugax or ischameic stroke
in patients with CAS, US shows a focally increased velocity of blood flow
it can quantify the degree of stenosis
antiplatelet therapy is used for prevention of stroke
bell palsy
unilateral facial paralysis
recovery over weeks
sensation not affected
anterior cerebral artery stroke
upper motor neuron weakness resulting in contralateral positive babinski sign, incontinence, and sensory deficits in the contralateral lower limb
pure motor stroke of the posterior limb of the internal capsule presents with
contralateral hemiparesis without sensory loss or cortical signs (e.g., aphasia).
usually caused by occlusion of the lanticulostriate artery
MCA stroke manifestations
contralateral facial droop
contralateral muscle weakness
contralateral pronator drift downward
do ischeamic strokes typically cause headaches?
nah
thalamus stroke manifestations
hemiparesis, hemisensory deficits, miotic and nonreactive pupils, gaze deviation downward and toward the affected side of the body (ie. away from the side of the brain lesion)
wrong way eyes
characteristic of thalamic haemorrhage
eyes deviate downward and away from affected brain side
ballismus
A condition of uncontrolled, large amplitude movements of the arms (and sometimes legs) that can have a flailing quality. Unilateral ballismus (hemiballismus) occurs following contralateral subthalamic nucleus damage, usually from ischemia.
broca aphasia
preserved comprehension
nonfluent telegraphic speech
A form of aphasia caused by lesions in the inferior frontal gyrus of the dominant hemisphere.
how does alteplase work
it converts plasminogen to plasmin which degrades fibrin and lyses formed clots
effective when administered within 4.5 hours of onset
wernecke’s aphasia
Wernicke aphasia is caused by lesions in the superior temporal gyrus of the dominant (usually left) hemisphere, usually along the left middle cerebral artery (MCA) distribution. Patients with Wernicke aphasia typically present with impaired repetition and language comprehension; although they can speak fluently, they produce nonsensical phrases. Furthermore, these patients lack awareness of their impairment
gaze deviation in MCA stroke is
towards the side of the deviation
reactive gliosis
Following CNS damage (e.g., stroke, traumatic brain injury), astrocytes at the margin of the damaged region proliferate and enlarge (reactive gliosis) to form a permanent glial scar. The process of reactive gliosis usually begins 1–2 weeks after the injury.
horner syndrome
symptom triad of miosis (an abnormally small pupil)
partial ptosis (drooping of the upper eyelid)
facial anhydrosis (absense of sweating)
lesions that interupt the ipsilateral symapthetic nervous supply to the head, eye and neck
