6.1 Stroke, Transient Ischaemic Attack & Acute Neurological Deficits

Cerebrovascular Accidents: Ischaemic vs. Haemorrhagic Pathophysiology

Acute cerebrovascular accidents (stroke) represent one of the leading causes of adult disability, cognitive decline, and mortality across the Caribbean basin. Rapid clinical triage and hyperacute therapeutic decision-making are paramount because neurological tissue viability decays exponentially with each passing minute ('time is brain').

• Ischaemic Stroke (~85% of cases): Arises from focal cerebral hypoperfusion secondary to arterial occlusion. Etiologies include:
  • Large-artery atherosclerosis: In situ atherothrombosis or artery-to-artery embolism affecting the internal carotid, middle cerebral, or basilar arteries, heavily accelerated by hypertension, diabetes mellitus, dyslipidemia, and cigarette smoking.
  • Cardioembolism: Thrombi originating in the heart, most commonly from non-valvular atrial fibrillation, mural thrombi following acute myocardial infarction, dilated cardiomyopathy, or infective endocarditis.
  • Small-vessel lacunar disease (arteriolosclerosis): Lipohyalinosis and microatheroma affecting deep penetrating lenticulostriate or thalamoperforating arteries, typically associated with chronic hypertension.
  • Other determined etiologies: Carotid or vertebral artery dissection (common in young adults after neck trauma), sickle cell vasculopathy, antiphospholipid syndrome, and systemic vasculitides.
• Haemorrhagic Stroke (~15% of cases):
  • Intracerebral Haemorrhage (ICH, ~10%): Rupture of small penetrating vessels weakened by chronic hypertension (Charcot-Bouchard microaneurysms) in deep brain structures (putamen, thalamus, pons, cerebellum) or cerebral amyloid angiopathy (lobar hemorrhages in elderly patients).
  • Subarachnoid Haemorrhage (SAH, ~5%): Extravasation of blood into the subarachnoid space, primarily caused by the rupture of saccular (berry) intracranial aneurysms or arteriovenous malformations (AVMs).

Clinical differentiation between ischaemic and haemorrhagic stroke based purely on physical examination is unreliable. While severe headache, vomiting, meningism, depressed consciousness, and marked initial blood pressure elevation favor haemorrhage, emergency non-contrast head computed tomography (NCCT) is mandatory before administering any antiplatelet, anticoagulant, or thrombolytic therapy.

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Vascular Territory Syndromes & Localisation

Localizing the neurological deficit to a specific vascular territory guides diagnostic imaging and intervention:

Stroke Vascular Territory Syndromes

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Hyperacute Management of Ischaemic Stroke & Thrombolysis Protocol

When a patient presents with acute focal neurological deficits, the emergency team must rapidly execute the stroke pathway to meet the benchmark door-to-needle time of < 60 minutes (ideally < 45 minutes).

Step 1: Emergency Neuroimaging & Point-of-Care Testing

• Immediate non-contrast head CT to rule out intracranial haemorrhage, subdural hematoma, or intracranial mass lesions.
• Check point-of-care fingerstick blood glucose immediately to exclude hypoglycemia (glucose < 3.3 mmol/L or < 60 mg/dL can mimic acute stroke).
• Obtain baseline complete blood count, coagulation profile (INR, aPTT), serum electrolytes, troponin, and a 12-lead ECG (evaluating for atrial fibrillation or myocardial ischemia).

Step 2: Systemic Intravenous Thrombolysis (Alteplase)

• Indication: Acute ischaemic stroke with measurable, disabling neurological deficit, presenting within 4.5 hours of symptom onset (or last known well time).
• Dosing: Intravenous recombinant tissue plasminogen activator (Alteplase / rtPA) administered at 0.9 mg/kg (maximum total dose 90 mg). The initial 10% of the calculated dose is given as an intravenous bolus over 1 minute, and the remaining 90% is infused intravenously over 60 minutes.
• Thrombolysis Exclusions and High-Risk Circumstances:
  • Do not administer IV thrombolysis for acute intracranial haemorrhage, suspected SAH, active internal bleeding, infective endocarditis or acute aortic dissection.
  • BP must be controlled below 185/110 mmHg before treatment. Platelets <100 x 10^9/L, INR >1.7, PT >15 seconds or aPTT >40 seconds preclude treatment under standard protocols.
  • Recent intracranial/spinal surgery or moderate-to-severe head trauma within 14 days generally precludes IV thrombolysis. Between 14 days and 3 months, consider individual risk with neurosurgical/stroke specialists.
  • Prior ICH, ischaemic stroke within 3 months, and recent GI/GU bleeding within 21 days require individualized stroke-specialist benefit–risk assessment rather than an automatic lifelong/three-month exclusion; assess the cause, severity, timing and whether bleeding risk has been corrected.
  • With DOAC exposure within 48 hours, safety remains uncertain. Assess the drug, last dose, renal clearance and drug-specific testing with the stroke team; neither a normal routine INR/aPTT nor administration of an antidote alone establishes eligibility. Consider thrombectomy eligibility without delaying appropriate reperfusion.

Step 3: Endovascular Mechanical Thrombectomy (EVT)

• Obtain urgent vascular imaging to identify a treatable large-vessel occlusion (LVO).
• For eligible anterior circulation internal carotid or proximal MCA (M1) occlusion, perform thrombectomy urgently within 6 hours; selected patients benefit up to 24 hours. Selection uses clinical status and brain/vascular imaging and now includes selected large-core infarctions; eligibility is not limited to the original DAWN/DEFUSE-3 small-core mismatch criteria.
• Selected basilar artery occlusion also benefits from EVT within 24 hours, with strong evidence in patients with NIHSS >=10 and favorable posterior-circulation imaging.
• If eligible for IV thrombolysis within 4.5 hours, administer it promptly without waiting for a clinical response or delaying thrombectomy/transfer.

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Blood Pressure Management Across Stroke Subtypes

Arterial blood pressure targets differ markedly depending on whether the stroke is ischaemic, whether thrombolysis is administered, or whether intracranial haemorrhage is present.

1. Ischaemic Stroke Planned for Reperfusion

• Blood pressure must be reduced to Systolic BP < 185 mmHg and Diastolic BP < 110 mmHg BEFORE alteplase infusion can begin. Before thrombectomy without IV thrombolysis, maintaining BP <= 185/110 mmHg is reasonable; use the stroke-team protocol during and after the procedure.
• During and for 24 hours following alteplase infusion, blood pressure must be maintained strictly < 180/105 mmHg to prevent fatal hemorrhagic transformation.
• Preferred first-line agents: Intravenous Labetalol 10 mg to 20 mg IV push over 1 to 2 minutes (may repeat once), or intravenous Nicardipine infusion 5 mg/h, titrated by 2.5 mg/h every 5-15 minutes (maximum 15 mg/h).

2. Ischaemic Stroke Without IV Thrombolysis or Thrombectomy (Permissive Hypertension)

• Without IV thrombolysis or thrombectomy, and without another urgent indication for BP treatment, elevated blood pressure may support collateral perfusion to the ischaemic penumbra.
• Antihypertensive therapy is withheld unless blood pressure exceeds Systolic BP > 220 mmHg or Diastolic BP > 120 mmHg.
• If BP exceeds 220/120 mmHg, lower blood pressure cautiously by 15% over the first 24 hours using oral or gentle IV medications. Lowering blood pressure precipitously extends the infarcted core into the hypoperfused penumbra.
• Immediate BP reduction is indicated only if comorbid life-threatening hypertensive emergencies coexist: acute myocardial infarction, acute pulmonary edema, aortic dissection, or hypertensive encephalopathy.

3. Acute Intracerebral Haemorrhage (ICH)

• In spontaneous ICH, elevated blood pressure promotes ongoing hematoma expansion, secondary brain edema, and herniation.
• For patients presenting with SBP between 150 and 220 mmHg without contraindications, acutely lower blood pressure to a target Systolic BP of 130 to 140 mmHg within 1 hour (as validated in the INTERACT-2 and ATACH-2 trials).
• Utilize continuous IV infusions (nicardipine or labetalol) to ensure smooth, controlled titration while avoiding precipitous drops below 130 mmHg, which can induce cerebral hypoperfusion.
• Immediately reverse therapeutic anticoagulation (e.g. 4-factor Prothrombin Complex Concentrate [PCC] and IV Vitamin K for warfarin; Idarucizumab for dabigatran; Andexanet alfa for factor Xa inhibitors).

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Subarachnoid Haemorrhage (SAH)

Aneurysmal subarachnoid haemorrhage usually results from rupture of a saccular (berry) aneurysm near the brain base. Common sites include the anterior communicating artery, the internal carotid–posterior communicating junction and middle cerebral artery bifurcations.

• Clinical Presentation: Classically described as a sudden-onset, explosive 'thunderclap' headache reaching peak intensity within seconds ('the worst headache of my life'). Accompanied by nausea, vomiting, meningism (neck stiffness, photophobia), transient loss of consciousness, and preretinal or subhyaloid hemorrhages (Terson syndrome).
• Diagnostic Workup:
  • Non-Contrast Head CT: Obtain urgently. In a patient without a new neurological deficit, a high-quality scan within 6 hours, interpreted by an appropriately experienced radiologist, can exclude SAH. Sensitivity declines with time; a negative later scan does not end the investigation when suspicion remains.
  • Lumbar Puncture (LP): After a negative CT obtained >6 hours from onset, or when otherwise indicated by the specialist assessment, investigate CSF for SAH. The NICE bilirubin pathway samples at least 12 hours after onset and uses spectrophotometry for elevated bilirubin (xanthochromia). Interpret red-cell counts with the other findings: clearing between tubes alone cannot safely exclude SAH, and a traumatic tap may coexist with haemorrhage.
• Emergency Medical & Surgical Management:
  • Strict bed rest, analgesia, antiemetics, and avoidance of straining.
  • Blood pressure control: Maintain SBP < 160 mmHg (or MAP < 110 mmHg) to balance rebleeding risk against cerebral perfusion before aneurysm securement.
  • Delayed Cerebral Ischemia (Vasospasm) Prevention: Vasospasm occurs typically between days 4 and 14 post-hemorrhage. Administer oral Nimodipine 60 mg every 4 hours for 21 days. Nimodipine improves neurological outcomes and reduces delayed cerebral ischemia. Systemic hypotension can occur; monitor BP and manage it while maintaining treatment when tolerated. Euvolemia is maintained with isotonic crystalloids (prophylactic hypervolemic 'triple-H' therapy is no longer recommended).
  • Aneurysm Repair: Endovascular coiling or neurosurgical clipping as early as feasible, preferably within 24 hours, to reduce catastrophic early rebleeding risk.

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Acute Status Epilepticus: Stepwise Emergency Protocol

Status epilepticus is a medical emergency with substantial morbidity and mortality. Neuronal injury and pharmacoresistance increase progressively with seizure duration.

• Operational Definitions (ILAE Guidelines):
  • Time Point 1 (t1 = 5 minutes): The time when a generalized convulsive seizure is abnormally prolonged and unlikely to terminate spontaneously; emergency pharmacotherapy must be initiated immediately.
  • Time Point 2 (t2 = 30 minutes): The time beyond which continuous seizure activity results in permanent neuronal damage, hippocampal sclerosis, systemic metabolic exhaustion, and refractory status.

Stepwise Management Algorithm

1. Stabilization Phase (0 to 5 Minutes):

   • Airway, Breathing, Circulation (ABCs); deliver high-flow oxygen via non-rebreather mask; obtain pulse oximetry and continuous ECG monitoring.
   • Obtain IV access; draw blood for electrolytes, glucose, renal/liver panels, calcium, magnesium, anticonvulsant levels, and toxicology.
   • Immediate Bedside Blood Glucose: If blood glucose is < 3.3 mmol/L (< 60 mg/dL), administer 50 mL of 50% dextrose IV. In adults with alcohol dependency or malnutrition, give 100 mg IV thiamine promptly, concurrently when available. Do not delay glucose for hypoglycaemia while waiting for thiamine; suspected Wernicke encephalopathy requires higher-dose parenteral treatment.

2. Phase 1: Initial Emergent Therapy (5 to 10 Minutes):

   • First-Line Benzodiazepine:
     • If IV access established: Intravenous Lorazepam 4 mg (0.1 mg/kg) slow IV push over 2 minutes (may repeat once at 5-10 minutes if seizures persist).
     • If IV access NOT established: Intramuscular Midazolam 10 mg (for body weight > 40 kg; 5 mg for 13-40 kg) injected into the vastus lateralis or deltoid.
     • Alternative: IV Diazepam 10 mg (less preferred due to rapid redistribution into peripheral adipose tissue leading to brief anticonvulsant brain levels).

3. Phase 2: Urgent Control Therapy (10 to 30 Minutes):

   • If seizures persist despite adequate first-line benzodiazepine dosing, immediately initiate a second-line, non-sedating intravenous anti-seizure medication (established by the landmark ESETT trial):
     • Intravenous Levetiracetam: 60 mg/kg (maximum 4500 mg) infused over 10 minutes; OR
     • Intravenous Fosphenytoin: 20 mg PE/kg (maximum 1500 mg PE) infused at up to 150 mg PE/min with continuous cardiac rhythm and blood pressure monitoring; OR
     • Intravenous Sodium Valproate: 40 mg/kg (maximum 3000 mg) infused over 10 minutes.
   • All three agents demonstrate equivalent efficacy (~50% seizure termination). Levetiracetam is often preferred due to absence of hepatic metabolism and minimal cardiac side effects.

4. Phase 3: Refractory Status Epilepticus (30 to 60 Minutes):

   • If seizures continue past 30 minutes despite second-line therapy, this constitutes refractory status epilepticus.
   • Immediate endotracheal intubation, continuous intensive care hemodynamic monitoring, and initiation of general anesthetic infusions titrated to electroencephalographic (EEG) burst-suppression:
     • Propofol: Bolus 1-2 mg/kg, then infusion 2-10 mg/kg/h (monitor for Propofol Infusion Syndrome);
     • Midazolam: Bolus 0.2 mg/kg, then infusion 0.05-2 mg/kg/h; OR
     • Pentobarbital: Load 5–15 mg/kg IV at no more than 50 mg/min, then 0.5–5 mg/kg/h, titrated under continuous ICU/EEG monitoring.