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EMERGENCY

Acute Stroke

High EvidenceUpdated: 2025-12-22

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Red Flags

  • Acute neurological deficit (FAST positive)
  • Altered consciousness
  • Severe headache with neurological signs
  • Signs of raised intracranial pressure
  • Rapid deterioration
Overview

Acute Stroke

1. Topic Overview

Summary

Stroke is a medical emergency caused by interrupted blood supply to the brain, leading to rapid neuronal death and neurological deficit. It is the second leading cause of death globally and a leading cause of disability. Strokes are classified as ischaemic (85%, due to arterial occlusion) or haemorrhagic (15%, due to vessel rupture). "Time is Brain" - every minute of ischaemia destroys 1.9 million neurons. Rapid recognition (FAST), emergency imaging, and timely treatment (thrombolysis, thrombectomy) have revolutionised outcomes. Secondary prevention is critical to reduce recurrence.

Key Facts

  • Mortality: 10-15% at 30 days; 25% at 1 year
  • Disability: 50% of survivors have long-term disability
  • Types: Ischaemic 85%, Haemorrhagic 15%
  • Time Windows: Thrombolysis <4.5h; Thrombectomy up to 24h (select patients)
  • Target: Door-to-needle <60 minutes (ideally <45)
  • Recurrence: 10% at 1 year without secondary prevention
  • Neuronal Loss: 1.9 million neurons/minute during ischaemia

Clinical Pearls

High-Yield Points:

  • FAST: Face drooping, Arm weakness, Speech difficulty, Time to call emergency
  • CT head is mandatory before any treatment decision
  • "Wake-up stroke" may still be eligible for reperfusion (MRI-based selection)
  • Large vessel occlusion (LVO) requires thrombectomy - check for it
  • Avoid rapid BP lowering unless thrombolysis/haemorrhagic
  • Antiplatelet dual therapy (DAPT) for 21 days post-minor stroke/TIA reduces recurrence by 25%

Why This Matters Clinically

Stroke is a leading cause of death and disability affecting all age groups. It is time-critical - delays of even minutes worsen outcomes. Every healthcare professional should recognise stroke immediately and understand the acute management pathway. Secondary prevention reduces recurrence risk from 10% to 2-3% per year.


2. Epidemiology

Prevalence and Incidence

MetricValue
Annual Incidence (UK)100,000 strokes/year
Prevalence1.3 million stroke survivors (UK)
Age: Mean age74 years
SexSlightly more common in males
Global Burden2nd leading cause of death worldwide

Risk Factors

Non-Modifiable:

  • Age (risk doubles each decade over 55)
  • Male sex (until menopause, then equal)
  • Family history
  • Previous stroke or TIA
  • Ethnic minority groups (higher risk)

Modifiable (Target for Prevention):

  • Hypertension (most important)
  • Atrial fibrillation
  • Diabetes mellitus
  • Smoking
  • Dyslipidaemia
  • Obesity
  • Physical inactivity
  • Excessive alcohol
  • Carotid stenosis

3. Pathophysiology

Ischaemic Stroke (85%)

Mechanisms:

  1. Large Vessel Atherosclerosis: Carotid/vertebral stenosis with artery-to-artery embolism
  2. Cardioembolic: Thrombus from AF, mechanical valve, LV thrombus
  3. Small Vessel Disease (Lacunar): Lipohyalinosis of perforating arteries
  4. Other: Dissection, vasculitis, hypercoagulable states

The Ischaemic Penumbra:

  • Core: Irreversibly damaged (CBF <10 mL/100g/min)
  • Penumbra: At-risk but salvageable tissue (CBF 10-20 mL/100g/min)
  • Target of reperfusion therapy

Ischaemic Cascade:

  1. Energy failure (ATP depletion)
  2. Ionic pump failure → Depolarisation
  3. Glutamate release → Excitotoxicity
  4. Calcium influx → Cell death
  5. Inflammation → Secondary damage

Haemorrhagic Stroke (15%)

Intracerebral Haemorrhage (10%):

  • Hypertensive (basal ganglia, thalamus, pons, cerebellum)
  • Cerebral amyloid angiopathy (lobar haemorrhage in elderly)
  • Anticoagulation-related
  • Vascular malformations

Subarachnoid Haemorrhage (5%):

  • Berry aneurysm rupture (85%)
  • AV malformation
  • Trauma

4. Clinical Presentation

Recognition: FAST

LetterSignDescription
FFaceFacial droop (ask to smile)
AArmArm weakness (raise both arms)
SSpeechSlurred or absent speech
TTimeTime to call 999

Anterior Circulation (Carotid Territory)

SyndromeVesselFeatures
Total Anterior Circulation (TACS)MCA ± ACAAll 3: Hemiparesis, hemisensory, higher cortical dysfunction
Partial Anterior Circulation (PACS)MCA branch2 of 3 above
Lacunar (LACS)Perforating arteriesPure motor, pure sensory, ataxic hemiparesis

Higher Cortical Features:

Posterior Circulation (Vertebrobasilar)

FeatureFrequency
VertigoCommon
DiplopiaCommon
AtaxiaCommon
DysarthriaCommon
Visual field defectOccipital involvement
Decreased consciousnessBrainstem involvement

Red Flag: Posterior circulation stroke is easily missed - have high suspicion with "dizziness + any other neuro sign"


Dominant (L)
Aphasia, apraxia
Non-dominant (R)
Neglect, anosognosia
5. Clinical Examination

Neurological Assessment

Conscious Level: GCS

Cranial Nerves:

  • Facial weakness (upper vs lower motor)
  • Eye movements (gaze deviation toward lesion)
  • Visual fields

Motor:

  • Power in all 4 limbs
  • Pronator drift
  • Tone (may be flaccid acutely)

Sensation:

  • Light touch, pain, proprioception

Cerebellar:

  • Ataxia, dysmetria, dysdiadochokinesia

Speech:

  • Dysarthria vs dysphasia

NIHSS (National Institutes of Health Stroke Scale)

  • Standardised assessment of stroke severity
  • Score 0-42
  • Used to guide treatment decisions
  • NIHSS ≥6 suggests large vessel occlusion

6. Investigations

Immediate (Hyperacute)

InvestigationPurposeTiming
CT Head (Non-contrast)Exclude haemorrhageImmediately (<25 mins)
CT AngiographyIdentify LVO, carotid stenosisWith plain CT
Blood GlucoseExclude hypoglycaemiaImmediately
ECGAF detectionImmediately

Acute Phase

InvestigationPurpose
CT PerfusionPenumbra assessment for extended window
MRI BrainDiffusion-weighted for acute infarct; wake-up stroke
EchocardiogramCardiac source of embolism
Carotid DopplerStenosis (if anterior circulation)
24-72h cardiac monitoringParoxysmal AF
FBC, U&Es, coagulation, lipids, HbA1cBaseline and risk factors

7. Classification

By Mechanism (TOAST)

  1. Large artery atherosclerosis
  2. Cardioembolic
  3. Small vessel occlusion (lacunar)
  4. Stroke of other determined aetiology
  5. Stroke of undetermined aetiology (cryptogenic)

By Timing

TermDefinition
TIASymptoms <24h, no infarct on imaging
Minor StrokeNIHSS ≤3
Major StrokeNIHSS >

Bamford Classification (Clinical)

  • TACS, PACS, LACS, POCS (Posterior Circulation Syndrome)

8. Management

Hyperacute Phase (Golden Hour)

1. Recognition and Transport:

  • Pre-alert stroke team
  • FAST positive → Emergency department

2. Immediate Assessment:

  • ABC, glucose, NIHSS
  • CT head within 25 minutes

3. Reperfusion Therapy (Ischaemic Only):

IV Thrombolysis (Alteplase 0.9 mg/kg):

  • Eligibility: <4.5 hours from onset
  • Contraindications: Active bleeding, recent surgery, haemorrhage on CT
  • NNT: 10 for improved outcome

Mechanical Thrombectomy:

  • Large vessel occlusion (ICA, M1, M2, basilar)
  • Up to 6 hours (standard); up to 24 hours (selected with perfusion imaging)
  • NNT: 2-3 for improved outcome
  • Transformative for LVO stroke

4. Haemorrhagic Stroke:

  • Reverse anticoagulation (if applicable)
  • BP control (target SBP <140 mmHg)
  • Neurosurgical referral if indicated

Acute Phase (24-72 hours)

If Thrombolysed:

  • BP control (SBP <180/105)
  • No aspirin for 24 hours
  • Repeat imaging if deteriorates

All Ischaemic Stroke:

  • Aspirin 300 mg once daily for 14 days
  • Consider clopidogrel loading if high-risk TIA/minor stroke
  • DVT prophylaxis (pneumatic compression)
  • Swallow screen before oral intake
  • Early mobilisation (AVERT trial - avoid bed rest)
  • Stroke unit care (reduces mortality)

Secondary Prevention

Antiplatelets:

  • Clopidogrel 75 mg long-term (first-line, NICE)
  • OR Aspirin + Dipyridamole (if clopidogrel contraindicated)
  • DAPT (Aspirin + Clopidogrel) for 21 days post-minor stroke/TIA

Anticoagulation (if AF):

  • DOAC (Apixaban, Rivaroxaban, Edoxaban)
  • Start 2-14 days post-stroke depending on size

Blood Pressure:

  • Target <130/80 after acute phase
  • ACE-I + CCB/diuretic often used

Lipids:

  • High-intensity statin (Atorvastatin 80 mg)
  • LDL target <1.8 mmol/L

Carotid Revascularisation:

  • Symptomatic stenosis ≥50%: Endarterectomy within 2 weeks

Lifestyle:

  • Smoking cessation, exercise, diet, alcohol reduction

9. Complications

Acute

ComplicationManagement
Haemorrhagic transformationReverse anticoagulation, BP control
Cerebral oedemaOsmotherapy, decompressive craniectomy
Aspiration pneumoniaNBM if swallow unsafe, antibiotics
SeizuresUsually not prophylaxis; treat if occur
DVT/PEPneumatic compression, LMWH when safe

Chronic

  • Spasticity
  • Post-stroke depression (30-50%)
  • Cognitive impairment/dementia
  • Epilepsy (2-5%)
  • Chronic pain
  • Fatigue

10. Prognosis

Mortality

TimeframeMortality
30 days10-15% (ischaemic), 30-50% (haemorrhagic)
1 year25%
5 years50%

Functional Outcome

  • 50% of survivors have permanent disability
  • 25% require nursing home care
  • Better outcomes with: younger age, lower NIHSS, early reperfusion, stroke unit care

11. Evidence and Guidelines

Key Guidelines

GuidelineOrganisationYear
Stroke and TIANICE NG1282019 (Updated 2022)
Acute Ischaemic StrokeAHA/ASA2019
Mechanical ThrombectomyRCP2021

Key Trials

  • NINDS (1995): Thrombolysis works
  • MR CLEAN, EXTEND-IA, ESCAPE (2015): Thrombectomy for LVO
  • DAWN, DEFUSE-3 (2018): Extended time window thrombectomy
  • CHANCE, POINT: Dual antiplatelet for minor stroke/TIA

12. Patient/Layperson Explanation

What is a Stroke?

A stroke happens when blood flow to part of your brain is interrupted, either by a blockage (clot) or a bleed. Without blood, brain cells start to die within minutes, which is why stroke is a medical emergency.

How do I recognise a stroke? (FAST)

  • Face: Has their face dropped on one side?
  • Arms: Can they raise both arms?
  • Speech: Is their speech slurred or strange?
  • Time: Time to call 999 immediately

What happens in hospital?

  • A brain scan is done immediately to check for bleeding or clot
  • If it's a clot, you may receive clot-busting medication or have the clot removed
  • If it's a bleed, different treatment is needed
  • After the emergency phase, rehabilitation helps recovery

How can I prevent another stroke?

  • Take all medications as prescribed (blood thinners, cholesterol tablets, BP tablets)
  • Stop smoking
  • Eat a heart-healthy diet, exercise regularly
  • Manage diabetes and high blood pressure

14. References
  1. Powers WJ, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke. 2019;50(12):e344-e418. PMID: 30662432

  2. NICE. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management (NG128). 2019. nice.org.uk

  3. Goyal M, et al. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis. Lancet. 2016;387(10029):1723-1731. PMID: 26898852

  4. Johnston SC, et al. Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA (POINT). N Engl J Med. 2018;379(3):215-225. PMID: 29766750


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. It does not replace professional medical judgement.

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22
Emergency Protocol

Red Flags

  • Acute neurological deficit (FAST positive)
  • Altered consciousness
  • Severe headache with neurological signs
  • Signs of raised intracranial pressure
  • Rapid deterioration

Clinical Pearls

  • **High-Yield Points:**
  • - FAST: Face drooping, Arm weakness, Speech difficulty, Time to call emergency
  • - CT head is mandatory before any treatment decision
  • - "Wake-up stroke" may still be eligible for reperfusion (MRI-based selection)
  • - Large vessel occlusion (LVO) requires thrombectomy - check for it

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines