Wake-up stroke with M1 occlusion, warfarin and a perfusion mismatch
A 71-year-old man is brought at 07:30 with dense left hemiparesis, hemianopia and neglect; he was last seen well at 23:00 the previous night when his wife checked on him. NIHSS is 14. He takes warfarin for atrial fibrillation; INR is 1.6, platelets 130 × 10⁹/L, glucose 6.8 mmol/L, blood pressure 178/96 mmHg. Non-contrast CT shows no haemorrhage, a hyperdense right M1 segment and an ASPECTS of 8. CT angiography confirms a right M1 occlusion. CT perfusion shows a core of 12 mL with a Tmax >6 s lesion of 95 mL. He weighs 92 kg and has no prior disability (mRS 0). It is now 08:10 and the angiography suite can accept him by 09:00. His wife confirms he has taken warfarin regularly and there has been no recent dose change, fall or head injury, and he is on no other anticoagulant or antiplatelet.
1. Is he eligible for intravenous thrombolysis? Justify your answer using the unknown onset time, the INR and the perfusion imaging.
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Yes - but only via imaging-based selection, not via the clock.
Onset time: last known well 23:00, found at 07:30. He is outside the standard 4.5-hour window from last known well, so time-based lysis is not permissible. He is, however, a wake-up stroke with a target perfusion mismatch: core 12 mL, penumbra 95 mL, mismatch ratio ~7.9 and penumbra volume >10 mL. This satisfies the EXTEND-type criteria (lysis up to 9 hours from midpoint of sleep/last known well with core <70 mL, mismatch ratio >1.2 and penumbra >10 mL), and the DEFUSE-3/DAWN framework supports reperfusion in this profile.
INR 1.6 on warfarin: intravenous alteplase is permitted in warfarin-treated patients with INR ≤1.7, provided there is no other coagulopathy (platelets 130 × 10⁹/L is acceptable). Had he been on a direct oral anticoagulant within 48 hours, lysis would be contraindicated. Confirm there was no recent dose escalation and no occult overdose.
Other checks: blood pressure 178/96 mmHg is below the 185/110 mmHg threshold, so lysis can proceed, but pressure must be kept below 180/105 mmHg during and after infusion; glucose is acceptable; no seizure, no recent surgery or GI bleed.
Decision: proceed with alteplase (0.9 mg/kg, 10% bolus, remainder over 60 minutes, total dose capped at 90 mg) while simultaneously activating the thrombectomy pathway. Consent should acknowledge the higher haemorrhage risk of lysis on warfarin plus the large penumbra at stake.
2. He receives lysis and proceeds to thrombectomy. Specify the periprocedural blood pressure and sedation strategy, and the post-procedure monitoring that most determines outcome.
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Blood pressure: maintain <180/105 mmHg during and for 24 hours after lysis, avoiding both hypertensive surges (haemorrhage) and hypotension (penumbral hypoperfusion). Use titratable agents - labetalol boluses or nicardipine infusion - and avoid rapid, large reductions. Once reperfused, a MAP of at least 70–80 mmHg is desirable; a systolic target of <140–160 mmHg after successful recanalisation is reasonable but intensive lowering below 130 mmHg has not been shown to help and may harm.
Sedation: conscious sedation is preferred where the airway is protected and the patient cooperative, because general anaesthesia with hypotension is associated with worse outcomes in observational data and delays reperfusion; convert to general anaesthesia if there is airway compromise, agitation preventing safe puncture, or vomiting. Whichever route, dedicate one person to blood pressure and airway.
Post-procedure monitoring that determines outcome:
- Hourly NIHSS and GCS for 24 hours - any deterioration triggers immediate non-contrast CT to look for haemorrhagic transformation, malignant oedema or re-occlusion.
- Neurovascular observations and groin/access-site checks.
- No antiplatelet or anticoagulant for 24 hours after lysis; follow-up imaging before starting any antithrombotic.
- Swallow screen before oral intake, glucose and temperature control, and early dysphagia/mobilisation pathways.
- Blood pressure variability matters more than the absolute number; avoid both hypotension and labile hypertension.
3. On day 2 imaging shows a 60 mL right MCA infarct with no haemorrhagic transformation. When and how would you start anticoagulation, and what findings would change your timing?
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He has AF-related stroke; anticoagulation is indicated, but not immediately and not bridged.
Timing: the infarct is moderate-to-large (60 mL). For moderate infarcts, a direct oral anticoagulant is typically started around day 4–7 after stroke onset, and later (day 7–14) for large infarcts or those with any haemorrhagic transformation. Before starting, repeat CT or MRI to exclude petechial or parenchymal haemorrhage and re-examine the NIHSS; his imaging is clear on day 2, so plan a further scan before the first dose.
How: start a DOAC at full therapeutic dose according to age, weight and creatinine clearance (apixaban 5 mg twice daily unless two of: age ≥80, weight ≤60 kg, creatinine ≥1.5 mg/dL). Do not bridge with low molecular weight heparin - bridging after cardioembolic stroke increases bleeding without reducing recurrence. Continue secondary prevention (statin, blood pressure control, lifestyle, and carotid/echocardiographic evaluation as indicated).
What would change the timing: any haemorrhagic transformation on the pre-treatment scan, uncontrolled hypertension, a large territory infarct with mass effect or planned decompressive surgery, a fall with head injury, or a recurrent embolic event while awaiting anticoagulation (which would push toward earlier initiation and consideration of alternative causes such as endocarditis). If he had a mechanical valve rather than AF, warfarin - not a DOAC - would be the agent, and the timing discussion would change accordingly.