Stroke/TIA Flashcards
Stroke/TIA - PRICMCP?
P: weakness, numbness, speech, vision, duration (stroke if >24h). Bleeding (N+V+headache) or Ischaemic. Duration of symptoms. Residual symptoms. Ask - was this a convincing dx of TIA? Neck pain (dissection)
R: HTN**, lipids, DM, FH, smoking, AF. Thrombophilia (e.g. APS), vasculitis.
I: MRI/CTA/CTB demonstrated stroke or patient does not know
C: injury (fall), residual deficits/disability, increased level of care, recurrence.
M: thrombolysis (clot buster via drip?), thrombectomy, anticoagulation, rehab.
C: ongoing disability vs. asymptomatic.
P: understanding of risk factors and chance of recurrence, adherence.
Stroke/TIA examination (5)
Full CNS/PN exam, including speech (+higher function if time).
- Residual deficit
- Carotid bruit
- Cardiac murmur
- BP
- Mobility
How would you investigate this patient with suspected TIA?
T: NIHSS score, CTB (rule out ICH), CTA (?ECR - anterior circulation infarct, vasculitis, intracranial stenosis), CT perfusion study (to estimate size of the infarct, size of tissue that is critically hypoperfused/salvageable - for thrombolysis)
Exclude alternative diagnosis + causative conditions - FBC (anaemia), ESR (GCA), Glucose (hypoglycaemia), Lipids (RF for stroke), ECG + Holter (IHD, arrhythmia, HB, AF…etc), TFT (if in AF), urine for glucose/protein. Also brain imaging to rule out SOL. If young patient: thrombophilia, APS abs, ANA
Source: Carotid dopplers (in ACA + MCA territory), TTE (LV size - a predictor of embolic risk)/TOE (bubble study ?PFO)
Treatment baseline: PLT (DAPT), Hb, renal function (NOAC), INR (warfarin)
Screen complications:
Features of TACI (total anterior circulation infarcts)? (4)
= large cortical stroke affecting both MCA and ACA. Typically proximal MCA or ICA (much worse clinically)
All 3 of below must be present
- Homonymous hemianopia
- Contralateral hemiplegia (upper>lower limbs) +/- Hemisensory loss
- Higher center involvement (Global dysphagia, visuospatial disorder)
Clinical features of PACI (partial anterior circulation stroke)?
Is a less severe form of TACI, where only part of anterior circulation (i.e. ICA - MCA/ACA) has been affected.
2/3 of below must be fulfilled.
- Homonymous hemianopia
- Contralateral hemiplegia (upper>lower limbs) +/- Hemisensory loss
- Higher center involvement (Global dysphagia, visuospatial disorder)
Can be further classified to superior MCA, inferior MCA, proximal ACA infarct.
What are 3 sub-types of PACI and what are their clinical features?
- Superior MCA: contralateral hemiplegia + hemisensory + conjugate gaze paresis with forced gaze towards the lesion + broca’s (if left sided stroke)
- Inferior MCA: contralateral hemianopia +visuo-spatial intention, receptive dysphasia
- Proximal ACA: contralateral lower limb > upper limb + primitive reflexes + frontal signs
Clinical features of POCI (posterior circulation infarct) - 5
One of the following need to be present.
Involves cerebellum/brainstem/visual cortex.
- CN palsy + Contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate gaze paresis (e.g. horizontal)
- Cerebellar dysfunction
- Isolated homonymous hemianopia
Clinical features of LACI (lacunar syndrome)?
= subcortical stroke that occurs from small vessel disease. There is no loss of higher centre (e.g. dysphasia)
One of the
- Pure motor
- Pure sensory
- Pure sensory/motor
- Hemiparesis
- Ataxia
- Dysarthria
Management of TIA? (5)
TIAs go home In C-A-B.
Treat as medical emergency - high-risk of stroke (10%)
Investigate for the cause: carotid USS, TTE, ECG, CTB (exclude bleeding)
- If symptomatic 70-99% need revascularization with CEA (some evidence for stent if younger). If asymptomatic, medical Mx (aspirin, statin, BP meds)
Cholesterol: smoking cessation, the Mediterranean diet (mixed-nuts) → biggest benefit in stroke reduction, Statin
Antithrombotic: if NIHSS > 5 → Aspirin, if ≤5 → DAPT (aspirin + clopidogrel) for 3 weeks (reduces risk of recurrent stroke + small inc in mod-sev bleeding risk). Loading dose for both.
BP-lowering: salt restriction, exercise, weight loss, anti-hypertensives
Driving (i.e. they go home in a CAB): NO driving for 2 weeks
If patient is already on aspirin (or plavix) and they have a TIA (no AF). How would you treat?
DAPT for 1st 3 weeks (i.e. treat as high-risk TIA).
Patient with AF and they have a TIA. How would you manage?
- NOAC
- Warfarin
- Continue NOAC. Check compliance. Investigate for the mechanism of TIA → may be reasonable to add single antiplatelet, if the mechanism is due to atherosclerosis than to cardioembolism.
- Warfarin - check level. If therapeutic + still had TIA → as above. If subtherapeutic, consider bridging Heparin.
What is ABCD2 score?
Age (≥60 = 1, <60 = 0)
BP (1 point for systolic ≥140 or diastolic ≥90)
Clinical features (unilateral weakness = 2; speech only = 1, other = 0)
Duration (≥60min = 2, 10-59 min = 1; <10min = 0)
Diabetes (1 for yes)
High-risk of stroke if ≥4 points.
Contraindications to thrombolysis for acute ischaemic stroke presenting <4.5h? (5)
ICH/GI/GU bleeding last 3 months
Active bleeding
BP > 185 or diastolic 110 (persistent)
INR > 1.7 (with current anticoagulation use) or deranged APTT/PT/TT/Xa assay in the context of current anticoagulation (last dose <48h)
PLT <100
What is your approach to anti-thrombotic therapy in acute, ischaemic stroke (non-thrombolysis/ECR eligible)?. Patient is currently not on antiplatelet or anticoagulation.
- Assess the severity of stroke - it is a severe stroke if NIHSS ≥4.
- For minor stroke (NIHSS <4) → DAPT for 3 weeks (with loading doses). Only continue further for a total of 90 days if stroke was caused by intracranial large artery atherosclerosis.
- For major stroke (NIHSS ≥4) → Aspirin only (given haemorrhagic risk?)
What is your approach to anti-thrombotic therapy in acute, ischaemic stroke (non-thrombolysis/ECR eligible)?. Patient is currently on a single antiplatelet.
- Assess the severity of stroke - it is a severe stroke if NIHSS ≥4.
- For minor stroke (NIHSS <4) → Switch to DAPT for 3 weeks (with loading doses). Only continue further for a total of 90 days if stroke was caused by intracranial large artery atherosclerosis.
- For major stroke (NIHSS ≥4) → continue existing antiplatelet therapy only.