Stroke and TIA Flashcards
What % of stroke/TIA survivors go on to have a further stroke in less than 5 years?
20%
What is the global burden of stroke?
20 million/year
2nd leading cause of death
Describe the “FAST” system for approach to stroke recognition
F: facial weakness
A: arm weakness
S: speech difficulty
T: time to act fast
Associated features of stroke
Weakness, numbness or paralysis of face or limbs
Difficulty speaking or understanding
Dizziness and loss of balance
Loss of vision
Headache (may be severe and abrupt)
Difficulty swallowing
What are the 3 assessments to make in the Cincinnati pre-hospital stroke scale?
Facial droop: smile
Arm drift: close eyes and hold out arms
Speech: say “you can’t teach an old dog new tricks” or similar familiar saying
Define stroke
Brief episodes
Define TIA
Brief neurological episodes (usually less than 24 hours) without damage on imaging
63 year old Mrs Faul with PHx of smoking and untreated HTN experiences sudden onset speech difficulties and R sided weakness with confusion
O/E (90 mins after onset of Sx): alert, BP 170/100, irregular pulse, expressive dysphasia, moderate R hemiparesis, appears frustrated
What should be done next?
Code stroke:
1) Urgent triage and high priority for stroke patient
2) Mobilise stroke team
3) Establish IV access and test glucose, routine biochem, FBE
4) ECG
5) Accurate clinical Dx (exclude mimics)
6) Urgent CT
List 11 recognised stroke mimics
Seizure
Sepsis
Toxic/metabolic
Space-occupying lesion
Syncope/presyncope
Acute confusional state
Vestibular dysfunction
Acute mononeuropathy
Dementia
Migraine
Spinal cord lesion
List 4 clinical features which suggest stroke over some other mimic
Exact time of onset
Patient could recall exactly what they were doing at symptom onset
Well in the last week
Definite focal symptoms or signs, worse NIHSS
List 5 clinical features which suggest stroke mimic over a stroke
What is the NIHSS and what does it assess?
National Institute of Health Stroke Scale
Assesses 11 aspects and provides a score from 0-42 (stratifies as no stroke Sx, minor stroke, moderate, moderate to severe, severe stroke)
Assesses level of consciousness, horizontal eye movement, visual field test, facial palsy, motor (UL, LL), limb ataxia, sensory function, language, speech, extinction and inattention
What is shown on this DWI MRI?
Lightbulb sign
What does this CT show?
Early (4.5 hours) ischaemic changes in a R MCA infarct
What does this scan show?
Deep putamenal ICH
What are the 3 major stroke types?
Ischaemic stroke (cerebral infarction)
Intracerebral haemorrhage (ICH)
Subarachnoid haemorhage (SAH)
What are the 3 main causes of ischaemic stroke?
Large artery thromboembolism
Cardiogenic embolism
Small vessel (lacunar) infarct
What are the most common sites for intracerebral haemorrhage?
Deep HTNive location
Lobar
What are the most common causes of SAH?
Ruptured aneurysm
AVM
What is the most common underlying cardiac cause of a cardiogenic embolism?
AF
What cerebral region is affected in a lacunar infarct?
Subcortical
List 4 rarer causes of ischaemic stroke
Arterial dissection
Drugs
Vasculitis
Rarer arteriopathies (e.g. Moyamoya disease)
What is the most lethal subtype of stroke?
ICH: mortality is 30-40%, patients have worse functional outcomes
How is ICH classified? What sites are affected in each and what is the typical offending pathology?
Deep: affects putamen, thalamus, brainstem, cerebellum, and usually due to HTN and rupture of deep penetrating arteries
Lobar: superficial, often secondary to amyloid angiopathy, tumour, AVM, aneurysm
What is the aim of therapies for ischaemic stroke and ICH?
Limiting stroke growth (rescuing the penumbra)
Mx for ischaemic stroke
Thrombolysis: IV tPA
Admission to stroke unit
Ix for underlying cause (e.g. AF, large artery stenosis)
Why are TIA and ischaemic stroke patients considered high-risk?
5-10% of TIA patients have a stroke at 1/52, 10-20% at 3/12
Even higher recurrence rate if DWI performed
Probably similar for ischaemic stroke
Patients with CVD are at high risk of CHD and vascular death
List 5 non-modifiable RFs for ischaemic stroke
Age
Gender
FHx
Ethnicity
Contraceptive use
List 9 established modifiable RFs for stroke
HTN
DM
Smoking
AF/heart disease
Hyperlipidaemia
EtOH consumption
Prothrombotic factors
Prior TIA
Prior stroke
List 9 possible modifiable RFs for stroke
Physical inactivity
Obesity
Dietary factors
Oral
Lack of HRT
Infection
Stress
Sleep apnoea
SES
What are the main modifiable RFs for stroke and how can these be managed?
RFs: smoking, HTN, DM, obesity
Mx: smoking cessation, weight loss, increased physical activity, healthy diet, anti-HTN, in high risk of CVD consider aspirin (but no clear indication for antiplatelet treatment in low risk or intermediate risk - i.e. uncomplicated DM, HTN, hyperlipidaemia - of stroke)
By what % do anti-HTN drugs reduce risk of primary stroke?
Up to 40%
Give 3 examples of NOACs and their mechanisms of action
Direct thrombin inhibitors: dabigatran
Factor Xa inhibitors: rivaroxaban, apixaban
When are NOACs indicated in stroke prevention?
Prevention of stroke (or systemic embolism) in non-valvular AF in a patient with one or more RFs for developing stroke
What is the risk of haemorrhage with oral anticoagulation?
1-1.5% per annum (greater if over 80 years old)
CHADS2
Cardiac failure
HTN
Age >75
DM
Previous Stroke or TIA (2 points)
If 1 or more, recommend oral anticoagulant
If 0, undertake a more comprehensive risk assessment (e.g. VASc)
By what % do oral antiocoagulants reduce the risk of stroke in people with AF?
Risk of stroke reduced by 60%
What is the recurrent stroke risk after a first stroke?
4% per annum
ABCD^2 score
AGE: 60 or above - 1
BP: SBP 140 or above, DBP 90 or above - 1
CLINICAL: focal weakness - 2, speech impairment without focal weakness - 1
DURATION: 60 min or more - 2, 10-59 min - 1
DM - 1
Low risk = 0-3, moderate risk = 4-5, high risk = 6-7
What are the principles of secondary prevention in stroke?
BP lowering
Cholesterol lowering and statins
Antiplatelet therapy
AF and anticoagulation
Carotid revascularisation (endarterectomy and stenting)
At what level should BP and cholesterol lowering medications be initiated post-stroke?
ANY level; any reduction is beneficial
What is the polypill and what is its expected impact on CVD rates?
Statin, 3 BP drugs (e.g. thiazide, B blocker, ACEI), aspirin, folic acid
What is the effect of aspirin on risk of subsequent stroke and all vascular events?
Reduces risk of subsequent stroke by ~13%
Reduces risk of all vascular events by 20%
When is dipyridamole + aspirin indicated over aspirin alone?
If patient at moderate to severe absolute risk, or in cases of recurrent stroke
SE of headache common
When is clopidogrel recommended post-stroke over aspirin?
Modestly more effective than aspirin in prevention of serious high risk vascular events so prescribed in these contexts
When might there be a role for aspirin + clopidogrel post-stroke?
In first 90 days after stroke or TIA
List 4 complications of CEA
Death or stroke
Cranial nerve palsy
Wound complications
CVS complications
What are some of the limitations of CEA?
Only marginal benefits on annual rates of ipsilateral stroke for patients with asymptomatic or moderate lesions; dramatic benefit is only seen for high-grade (above 70%) symptomatic stenoses
Benefits are time-linked to last symptomatic event (best within 30 days)
Risk of complications
What is more effective at reducing risk of ipsilateral stroke and perioperative death in patients with advanced symptomatic carotid artery disease: CEA or medical therapy?
CEA
Mrs Faul has had an ischaemic stroke secondary to carotid artery thromboembolism, managed with thrombolysis (to which she had a good response)
Post-stroke Mx for Mrs Faul?
Lifestyle issues: smoking cessation, regular exercise, weight reduction and maintenance
BP: reduce to 120/80
Statin
CEA or stenting
Long-term anticoagulation with dabigatran or other NOAC
Summarise important principles of secondary prevention for stroke
High-risk patients benefit from BP and cholesterol reduction regardless of baseline
Antiplatelet therapy is routine if patient not anticoagulated
Warfarin for AF may be replaced by NOAC
CEA proven therapy for carotid artery stenosis, but carotid stenting may be equivalent for patients less than 70 years old
Dipyridamole
Inhibits PDE which normally breaks down cAMP (increasing cellular cAMP levels and blocking the platelet aggregation response to ADP), and/or cGMP (resulting in added benefit when given together with nitric oxide or statins)
Inhibits cellular reuptake of adenosine into platelets, RBCs and endothelial cells leading to increased extracellular concentrations of adenosine
