7.1 Acute Stroke, TIA & Intracranial Haemorrhage

Acute Stroke, TIA & Intracranial Haemorrhage

Acute cerebrovascular emergencies represent one of the most critical clinical presentations encountered in the acute medical take. Rapid triage, accurate clinical localization, and urgent neuroimaging are essential to differentiate ischaemic stroke from intracranial haemorrhage and to initiate time-critical reperfusion therapies.

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Clinical Recognition & Bedside Stroke Assessment

In the pre-hospital and emergency setting, acute stroke must be distinguished rapidly from stroke mimics (such as hypoglycaemia, seizures with Todd's paresis, hemiplegic migraine, functional neurological disorders, and acute encephalitis).

• FAST Assessment: Face weakness, Arm weakness, Speech disturbance, Time to call 999. In the community, FAST identifies >85% of anterior circulation strokes.
• ROSIER Score (Recognition of Stroke in the Emergency Room): Used in UK emergency departments. It awards points for asymmetric facial weakness (+1), asymmetric arm weakness (+1), asymmetric leg weakness (+1), speech disturbance (+1), and visual field defect (+1); it deducts points for loss of consciousness / syncope (-1) and seizure activity (-1). A score >0 indicates a high probability of acute stroke.
• Mandatory Immediate Bedside Test: Capillary blood glucose must be checked immediately in all suspected stroke patients to exclude and treat hypoglycaemia (<4.0 mmol/L), which can mimic focal neurological deficits perfectly.

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Bamford / Oxford Community Stroke Project (OCSP) Classification

The Bamford classification categorises acute ischaemic stroke purely based on initial clinical neurological deficits. It correlates directly with the underlying anatomical vascular territory, radiological infarct size, risk of complications, and long-term prognosis.

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Hyperacute Ischaemic Stroke Management

Time is brain: approximately 1.9 million neurons are lost each minute an acute ischaemic stroke remains untreated.

1. Emergency Neuroimaging

• All patients with suspected acute stroke must undergo immediate non-contrast CT head within 1 hour of hospital arrival (or immediately if thrombolysis candidates).
• The primary emergency objective of CT head is to rule out intracranial haemorrhage (which appears hyperdense / bright white). In the hyperacute phase (<3–6 hours), ischaemic infarction may appear radiologically normal or show only subtle early signs (e.g. hyperdense MCA sign, effacement of sulcal spaces, loss of insular ribbon, or loss of grey-white matter differentiation).
• CT angiography (CTA) from aortic arch to vertex should be performed simultaneously to identify large vessel occlusions (LVO) eligible for mechanical thrombectomy.

2. Intravenous Thrombolysis (Alteplase or Tenecteplase)

• Drug & Regimen: Intravenous recombinant tissue plasminogen activator (rt-PA / alteplase) at a dose of 0.9 mg/kg (maximum dose 90 mg; 10% administered as an immediate IV bolus over 1 minute, remaining 90% infused over 60 minutes). Since July 2024, NICE (TA990) also recommends tenecteplase 0.25 mg/kg as a single IV bolus (maximum 25 mg) within the same 4.5-hour window; many UK stroke units now use it because no infusion is needed.
• Eligibility Window: Symptoms must have started within 4.5 hours of infusion initiation (or 'last known well' time).
• Strict Blood Pressure Mandate: Blood pressure must be <185/110 mmHg before commencing alteplase, and maintained <180/105 mmHg for the first 24 hours. If BP is elevated, titrate IV labetalol (10–20 mg IV over 1–2 minutes) or IV nicardipine/hydralazine before thrombolysis. Hypertension is a modifiable relative contraindication—treat it actively rather than withholding thrombolysis.
• Absolute Contraindications to Thrombolysis:
  • Evidence of intracranial haemorrhage on neuroimaging
  • Prior history of intracranial haemorrhage at any time
  • Stroke or severe head/spinal trauma within the preceding 3 months
  • Major surgery or severe trauma within the past 14 days
  • Active internal bleeding or gastrointestinal/urinary haemorrhage within past 21 days
  • Therapeutic anticoagulation (INR > 1.7 on warfarin, or direct oral anticoagulant DOAC ingestion within 48 hours unless laboratory tests confirm no anticoagulant effect)
  • Thrombocytopenia (platelets < 100 × 10⁹/L)
  • Uncontrolled severe hypertension (BP persistently ≥185/110 mmHg despite antihypertensive therapy)
  • Severe hypoglycaemia (<2.8 mmol/L) or severe hyperglycaemia (>22.2 mmol/L) that has not been corrected

3. Mechanical Thrombectomy

• Indicated within 6 hours of symptom onset for patients with acute ischaemic stroke and confirmed large vessel occlusion (LVO) in the anterior circulation (proximal MCA M1 or internal carotid artery), regardless of whether they received IV alteplase.
• Can be performed between 6 and 24 hours after symptom onset if CT perfusion or diffusion-weighted MRI demonstrates salvageable penumbral brain tissue ('clinical-infarct mismatch').

4. Acute Antiplatelet Initiation

• Aspirin 300 mg daily is the cornerstone of acute antiplatelet therapy.
• Timing Post-Thrombolysis: In patients who receive IV alteplase, aspirin 300 mg must be delayed for 24 hours. A repeat non-contrast CT head at 24 hours must confirm the absence of haemorrhagic transformation before initiating aspirin.
• Non-Thrombolysed Patients: In patients not eligible for thrombolysis, aspirin 300 mg is commenced immediately (orally, enterally, or rectally).

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Secondary Prevention & Carotid Interventions

Following the hyperacute phase, comprehensive secondary prevention must be established:

1. Antiplatelet Monotherapy: After completing 2 weeks of acute aspirin 300 mg, switch to Clopidogrel 75 mg once daily monotherapy indefinitely as the first-line long-term antiplatelet agent (NICE guidelines). If clopidogrel is contraindicated or poorly tolerated, aspirin 75 mg combined with modified-release dipyridamole 200 mg twice daily is an alternative.
2. Lipid Optimization: High-intensity statin therapy with Atorvastatin 80 mg once daily is initiated. In acute ischaemic stroke, statin initiation is typically delayed until 48 hours post-stroke onset.
3. Blood Pressure Control: In the hyperacute phase (<48 hours) of ischaemic stroke, permissive hypertension is maintained to preserve cerebral collateral perfusion. NICE NG128 recommends lowering BP only for thrombolysis candidates (to 185/110 mmHg or lower) or when there is a hypertensive emergency with a serious concomitant condition (hypertensive encephalopathy, nephropathy or cardiac failure, myocardial infarction, aortic dissection, or pre-eclampsia/eclampsia); the US threshold of 220/120 mmHg is not a NICE criterion. Long-term, BP is optimized to a target of <130/80 mmHg using ACE inhibitors or calcium channel blockers.
4. Carotid Endarterectomy (CEA): Indicated for people with non-disabling stroke or TIA and symptomatic ipsilateral internal carotid stenosis of 50–99% (NASCET criteria; 70–99% by ECST criteria). NICE NG128 requires assessment and referral within 1 week of symptom onset and surgery as soon as possible, within 2 weeks. Endarterectomy is not indicated for complete occlusion (100%) or for symptomatic stenosis below 50% (NASCET).
5. Anticoagulation in Atrial Fibrillation: For stroke caused by cardioembolic AF, anticoagulation with a DOAC (apixaban, edoxaban, rivaroxaban, dabigatran) is started once haemorrhage is excluded on imaging. NICE NG128 traditionally advises waiting until 14 days after a disabling ischaemic stroke (aspirin 300 mg in the meantime), whereas the 2023 National Clinical Guideline for Stroke (UK and Ireland), informed by the ELAN and TIMING trials, supports earlier DOAC initiation decided by the stroke team according to infarct size (for example within days for minor or moderate strokes).

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Transient Ischaemic Attack (TIA)

A Transient Ischaemic Attack (TIA) is defined as transient focal neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction on neuroimaging.

• Immediate Community / ED Management: Administer Aspirin 300 mg daily immediately unless contraindicated or the patient is already taking therapeutic anticoagulation.
• Specialist TIA Referral: Current NICE guidance has replaced risk-stratification scores (such as ABCD2). All patients with suspected TIA must undergo urgent specialist assessment by a stroke specialist within 24 hours of symptom onset (within 7 days if they present more than a week after symptoms).
• Short-Term Dual Antiplatelet Therapy: For confirmed TIA or minor ischaemic stroke (NIHSS 3 or less) in people not needing anticoagulation, the 2023 National Clinical Guideline for Stroke recommends clopidogrel (300 mg loading, then 75 mg daily) plus aspirin (300 mg loading, then 75 mg daily) started within 24 hours and continued for 21 days, followed by clopidogrel 75 mg alone.
• DVLA Driving Restrictions: Following a TIA or acute stroke, patients must not drive for at least 1 month. If there are no residual neurological deficits after 1 month, driving may resume without informing the DVLA (for ordinary car Group 1 licences). If residual deficits remain at 1 month, the DVLA must be notified.

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Spontaneous Intracranial Haemorrhage

Intracranial haemorrhage accounts for 15–20% of all acute strokes but carries substantially higher early mortality and morbidity.

1. Subarachnoid Haemorrhage (SAH)

• Etiology: 85% caused by rupture of an intracranial saccular ('berry') aneurysm, most commonly at the anterior communicating artery, posterior communicating artery, or middle cerebral artery bifurcation. Strongly associated with smoking, hypertension, autosomal dominant polycystic kidney disease (ADPKD), and Ehlers-Danlos syndrome.
• Clinical Presentation: Sudden, instantaneous 'thunderclap' headache, classically described as the 'worst headache of my life', peaking in intensity within seconds (often occipital, feeling like being struck with a blunt object). Associated with neck stiffness, photophobia, vomiting, transient loss of consciousness, and subhyaloid retinal haemorrhages on fundoscopy.
• Diagnostic Algorithm:
  1. Immediate Non-contrast CT Head: Sensitivity exceeds 98% within the first 6 hours of headache onset. Shows hyperdense blood in the basal cisterns, sylvian fissures, or sulcal spaces.
  2. Lumbar Puncture (LP): If non-contrast CT head performed >6 hours after onset is negative or equivocal, an LP must be performed. Crucially, the LP must be delayed until ≥12 hours after symptom onset to allow in vivo lysis of red blood cells and enzymatic conversion of oxyhaemoglobin to bilirubin. Bilirubin is detected objectively using CSF spectrophotometry (xanthochromia), definitively distinguishing true SAH from a traumatic procedural tap.
• Acute Medical & Surgical Management:
  • Nimodipine: Administer 60 mg orally or via nasogastric tube every 4 hours for 21 days. Nimodipine is a dihydropyridine calcium channel blocker that prevents secondary cerebral ischaemia from delayed vasospasm.
  • Definitive Revascularisation: Urgent catheter CT cerebral angiography followed by endovascular coiling (preferred over surgical clipping due to superior clinical outcomes in the ISAT trial) within 24–48 hours to prevent catastrophic aneurysmal re-bleeding.

2. Spontaneous Intracerebral Haemorrhage (ICH)

• Etiology: Chronic hypertension (leading to Charcot-Bouchard microaneurysms in deep perforating arteries supplying the basal ganglia, internal capsule, thalamus, pons, and cerebellum) and Cerebral Amyloid Angiopathy (CAA; beta-amyloid deposition in cortical vessels causing lobar haemorrhages in elderly patients).
• Emergency Blood Pressure Lowering: In patients presenting within 6 hours of symptom onset with SBP between 150 and 220 mmHg, urgently lower systolic blood pressure to a target of 130–140 mmHg within 1 hour (using IV labetalol, nicardipine, or hydralazine infusions) to restrict haematoma expansion.
• Emergency Anticoagulation Reversal:
  • For Warfarin: Immediate IV Vitamin K 10 mg PLUS 4-Factor Prothrombin Complex Concentrate (PCC) (Beriplex / Octaplex; dose 25–50 units/kg). PCC rapidly normalises INR within 10–15 minutes, whereas fresh frozen plasma (FFP) is slow and risks volume overload.
  • For Dabigatran: Administer the specific humanised monoclonal antibody fragment Idarucizumab (Praxbind) 5 g IV.
  • For Factor Xa Inhibitors (Apixaban, Rivaroxaban): Administer Andexanet alfa or 4-factor PCC.