The resolved deficit — transient ischaemic attack in the emergency department

(a) Definition, tissue-based implication, and ABCD2 (5 marks).

• TIA is a transient episode of focal neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction — the modern tissue-based definition (AHA/ASA 2009, PMID 19423857). It replaces the old 24-hour clock with the scan: a lesion on diffusion-weighted MRI is an infarct, and the event is then a stroke, not a TIA.^[1]
• Implication: a diffusion-weighted MRI should be obtained — if it shows infarction the diagnosis is a stroke with a higher recurrence risk and a stroke-grade workup; if negative it is a true TIA. The deficit has resolved, but the underlying lesion is unstable.
• ABCD2 (Johnston 2007, PMID 17258668):
  • Age 68 (≥60) = 1
  • Blood pressure 156/92 (≥140 systolic and ≥90 diastolic) = 1
  • Clinical feature — right arm weakness = unilateral weakness = 2 (the maximum; speech does not add)
  • Duration 45 minutes (10 to 59) = 1
  • Diabetes (on metformin) = 1
  • Total = 6 (high risk) — two-day stroke risk about 8.1 per cent, 90-day about 18 per cent.^[2]
• Because the score is high and the ECG shows atrial fibrillation, she is high-risk by both ABCD2 and mechanism and warrants same-day specialist assessment.

(b) ED workup and disposition (4 marks).

• Confirm resolved: any deficit still present is a stroke and goes on the thrombolysis pathway — here the deficit has resolved, so manage as suspected TIA.
• Workup aimed at the mechanism: 12-lead ECG (atrial fibrillation already seen), bloods (full blood count, coagulation, urea and electrolytes, fasting lipids), and crucially carotid imaging within 24 hours (duplex ultrasound, with CT or MR angiography to grade stenosis) in case she is a candidate for endarterectomy. Diffusion-weighted MRI defines the tissue-based diagnosis. Echocardiography and prolonged cardiac monitoring consolidate the cardioembolic workup.
• Disposition: she is high-risk (ABCD2 6, atrial fibrillation, suspected carotid disease) → admit or fast-track to the stroke team for same-day specialist assessment and carotid imaging, not routine outpatient review. The evidence is EXPRESS (PMID 17928046): same-day assessment plus treatment cut the 90-day recurrent-stroke risk from 10.3 per cent (32 of 310) to 2.1 per cent (6 of 281).
• Give aspirin 300 mg immediately after haemorrhage is excluded; start the secondary-prevention bundle in parallel.

(c) Secondary prevention and the time-critical intervention (4 marks).

• Antiplatelet (this is a non-cardioembolic working diagnosis pending imaging): aspirin 300 mg immediately, then aspirin plus clopidogrel 300 mg load and 75 mg daily for 21 days, then clopidogrel 75 mg monotherapy — supported by CHANCE (PMID 23803136) and POINT (PMID 29766750), the 21-day limit because POINT's bleeding signal accrued beyond 21 days.
• High-intensity statin — atorvastatin 80 mg daily (SPARCL).
• Blood-pressure control to secondary-prevention targets once the acute event has settled; diabetes optimisation; smoking cessation if applicable.
• The time-critical intervention: if carotid imaging shows symptomatic severe stenosis (70 per cent or greater NASCET, without near-occlusion), refer for carotid endarterectomy within two weeks — the pooled endarterectomy trials (PMID 12531577) show a large durable benefit for severe stenosis (16.0 per cent absolute risk reduction at five years, NNT about 6) that falls steeply with delay.
• Caveat — atrial fibrillation: if the event is confirmed cardioembolic, the prevention is anticoagulation (a direct oral anticoagulant) rather than an antiplatelet, and because there is no infarct it can be started early after haemorrhage is excluded. The fast-track stroke team reconciles this with the carotid result.