Acute Stroke in Adults

Quick Reference

Critical Alerts

• "Time is Brain": 1.9 million neurons lost per minute in large vessel occlusion [1]
• FAST recognition: Face-Arm-Speech-Time enables immediate stroke pathway activation
• Thrombolysis window: Alteplase/Tenecteplase within 4.5 hours of symptom onset [2]
• Thrombectomy window: 6-24 hours for large vessel occlusion with imaging selection (DAWN/DEFUSE-3 criteria) [3,4]
• Exclude hemorrhage first: Non-contrast CT mandatory before any reperfusion therapy
• Blood pressure targets: less than 185/110 mmHg pre-thrombolysis; permissive hypertension otherwise
• Door-to-needle target: less than 60 minutes for thrombolysis administration
• Door-to-groin puncture: less than 90 minutes for mechanical thrombectomy

Ischemic vs Hemorrhagic Stroke Differentiation

Emergency Stroke Protocol

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SECTION 1: Clinical Overview

1.1 Definition and Classification

Acute stroke is defined as a clinical syndrome characterized by the sudden onset of focal or global neurological deficits lasting more than 24 hours (or leading to death) with no apparent cause other than vascular origin. The World Health Organization (WHO) definition emphasizes the vascular aetiology and distinguishes stroke from transient ischaemic attack (TIA), which by modern tissue-based definition implies no evidence of acute infarction on neuroimaging. [1]

Classification by Pathophysiology:

1.2 Summary

Acute stroke remains the second leading cause of death worldwide and the leading cause of adult disability in developed countries. The incidence approaches 795,000 new or recurrent strokes annually in the United States, with approximately 15 million strokes occurring globally each year. [5] The concept of "Time is Brain" reflects the urgency of intervention, as approximately 1.9 million neurons are lost every minute during a large vessel occlusion. [1]

The management paradigm has evolved dramatically with the advent of reperfusion therapies. Intravenous thrombolysis with alteplase or tenecteplase remains the standard of care for eligible patients within 4.5 hours of symptom onset. [2] The landmark thrombectomy trials (MR CLEAN, ESCAPE, SWIFT PRIME, EXTEND-IA, REVASCAT) established mechanical thrombectomy as the most effective treatment in acute medicine for large vessel occlusion, with a number needed to treat of 2.6. [6,7]

Extended window thrombectomy, as demonstrated by the DAWN and DEFUSE-3 trials, allows intervention up to 24 hours in selected patients with favorable imaging profiles demonstrating salvageable penumbra. [3,4] Comprehensive stroke unit care with multidisciplinary input further improves outcomes compared to general medical ward management. [8]

1.3 Key Facts

1.4 Clinical Pearls

Diagnostic Pearl - "The Sudden in Stroke": The most critical diagnostic feature is the temporal profile. True strokes reach maximal intensity within seconds to minutes. Gradual onset over hours suggests alternative diagnoses (malignancy, demyelination, metabolic derangement).

Examination Pearl - "Pronator Drift Test": Have the patient hold arms out with palms up and eyes closed. The affected side will slowly pronate and drift downward due to weakness in supinators and extensors — a sensitive indicator of subtle upper motor neuron weakness.

Treatment Pearl - "Permissive Hypertension": Do not aggressively lower blood pressure unless it exceeds 220/120 mmHg (or 185/110 if thrombolysing). Premature lowering collapses collateral flow to the penumbra, potentially extending the infarct. [9]

Pitfall Warning - "The Posterior Circulation Trap": Do not rely solely on FAST criteria. Posterior circulation strokes often present with the "5 Ds": Dizziness, Diplopia, Dysarthria, Dysphagia, Dystaxia. These are frequently missed in emergency settings.

Mnemonic - "BE FAST": Balance (loss), Eyes (vision loss), Face (drooping), Arms (weakness), Speech (difficulty), Time (call emergency services). This expanded mnemonic captures posterior circulation and sensory strokes.

Emergency Pearl - "Hypoglycemia is the Great Mimicker": Always check capillary blood glucose immediately. Hypoglycemia can perfectly mimic focal stroke syndromes, and administering thrombolysis to a hypoglycemic patient would be catastrophic.

Exam Pearl - "NIHSS Limitations": The NIH Stroke Scale is weighted toward anterior circulation (motor/speech). A high NIHSS usually indicates large territory stroke, but a LOW NIHSS does NOT exclude disabling stroke (e.g., isolated distal PCA infarct causing hemianopia).

Wake-up Stroke Pearl: 20-25% of strokes occur during sleep. MRI DWI-FLAIR mismatch or CT perfusion imaging can identify treatment candidates for reperfusion therapy. [10]

1.5 Why This Matters Clinically

Acute stroke represents a true medical emergency where the window for intervention is measured in minutes. Delayed or missed diagnosis results in loss of the opportunity for reperfusion, leading to massive neuronal death and permanent disability. This translates to significant loss of quality-adjusted life years (QALYs) and places an immense burden on patients, families, and healthcare systems.

Healthcare Economics: The cost of acute care, inpatient rehabilitation, and long-term nursing care for a single major stroke can exceed $140,000 in the first year alone. Lifetime costs approach $200,000-$300,000 per patient. The annual economic burden of stroke in the United States exceeds $56.5 billion. [5]

Medico-Legal Considerations: Stroke management is a high-risk area for litigation. Common grounds for claims include:

• Failure to recognize stroke symptoms
• Delay in ordering appropriate imaging
• Failure to administer thrombolysis within the evidence-based window
• Failure to refer for thrombectomy when indicated
• Inadequate documentation of treatment decisions and timing

Training Importance: Stroke is a cornerstone of medical education because it integrates anatomy (Circle of Willis, vascular territories), physiology (cerebral blood flow, autoregulation), pharmacology (thrombolytics, antiplatelets), and clinical reasoning under time pressure.

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SECTION 2: Epidemiology

2.1 Incidence and Prevalence

Healthcare Burden: Direct and indirect costs of stroke in the US are estimated at $56.5 billion annually. This includes acute hospitalization, rehabilitation, long-term care, lost productivity, and caregiver burden. [5]

2.2 Demographics and Risk Stratification

2.3 Risk Factors

Non-Modifiable Risk Factors:

Modifiable Risk Factors:

2.4 Protective Factors

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SECTION 3: Pathophysiology

3.1 The Ischemic Cascade

Step 1: Initiating Event - Vascular Occlusion

The pathophysiology begins with abrupt cessation of cerebral blood flow (CBF) due to arterial occlusion. This may occur via:

• Thrombotic occlusion: In-situ thrombus formation over atherosclerotic plaque
• Embolic occlusion: Embolus from cardiac source (atrial fibrillation) or artery-to-artery (carotid stenosis)
• Small vessel occlusion: Lipohyalinosis of penetrating arteries (lacunar stroke)

CBF Thresholds:

Step 2: Energy Failure and Ionic Disruption

When CBF falls below 10-12 mL/100g/min:

1. ATP depletion: Aerobic metabolism fails within seconds
2. Na+/K+ ATPase pump failure: Loss of ionic gradients
3. Anoxic depolarization: Mass influx of Na+, Cl-, and water
4. Cytotoxic edema: Cell swelling occurs within minutes

Step 3: Excitotoxicity and Calcium Overload

Depolarizing neurons release massive amounts of glutamate:

1. NMDA/AMPA receptor activation: Massive Ca²⁺ influx
2. Intracellular calcium levels rise 1000-fold
3. Destructive enzyme activation: Calpains, lipases, endonucleases
4. Mitochondrial damage: mPTP opening, cytochrome C release

Step 4: Oxidative Stress and Inflammation

Secondary injury cascade begins:

1. ROS production: Superoxide, hydroxyl radicals
2. Microglial activation: IL-1β, IL-6, TNF-α release via NF-κB pathway
3. Adhesion molecule upregulation: ICAM-1, VCAM-1
4. Leukocyte infiltration: Neutrophils (6-12 hours), macrophages (days)

Step 5: Blood-Brain Barrier Breakdown

Matrix metalloproteinase (MMP) release:

1. MMP-9 degrades basal lamina: Tight junction proteins (claudin, occludin) disrupted
2. Vasogenic edema: Plasma protein extravasation
3. Hemorrhagic transformation: Red cell extravasation (especially post-thrombolysis)
4. Mass effect: ICP elevation in large infarcts

Step 6: Programmed Cell Death

Penumbral cells may undergo apoptosis over hours to days:

1. Caspase-3 activation: Intrinsic apoptotic pathway
2. BAX/BCL-2 balance shifts: Pro-apoptotic signaling
3. DNA fragmentation: Nuclear condensation
4. Glial scar formation: Astrocyte proliferation at infarct periphery

3.2 The Ischemic Penumbra

The penumbra is the salvageable tissue surrounding the ischemic core:

┌─────────────────────────────────────────┐
│                ISCHEMIC CORE            │
│         CBF less than 10 mL/100g/min             │
│         Irreversible injury             │
│         Infarction within minutes       │
├─────────────────────────────────────────┤
│              PENUMBRA                   │
│         CBF 10-20 mL/100g/min           │
│         Reversible ischemia             │
│         SALVAGEABLE WITH REPERFUSION    │
├─────────────────────────────────────────┤
│         OLIGEMIC ZONE                   │
│         CBF 20-50 mL/100g/min           │
│         Electrical dysfunction          │
│         Usually recovers spontaneously  │
└─────────────────────────────────────────┘

Penumbra Duration: Varies from minutes to hours depending on:

• Collateral circulation adequacy
• Core size and location
• Systemic blood pressure
• Blood glucose levels

3.3 TOAST Classification (Ischemic Stroke Etiology)

3.4 Hemorrhagic Stroke Pathophysiology

Intracerebral Hemorrhage (ICH):

• Hypertensive ICH: Rupture of lipohyalinotic microaneurysms in deep perforators (basal ganglia, thalamus, pons, cerebellum)
• Amyloid angiopathy: Lobar hemorrhages in elderly; high recurrence risk
• Secondary ICH: Tumors, vascular malformations, anticoagulation, hemorrhagic transformation

ICH Expansion: Hematoma expansion occurs in 30% of patients within 24 hours and is associated with worse outcomes. Early blood pressure control and coagulopathy reversal are critical. [11]

Subarachnoid Hemorrhage (SAH):

• 85% due to aneurysm rupture: Circle of Willis, ACOM most common
• 15% non-aneurysmal: Perimesencephalic, traumatic
• Complications: Vasospasm (peak days 4-14), hydrocephalus, rebleeding

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SECTION 4: Clinical Presentation

4.1 Stroke Syndromes by Vascular Territory

Anterior Circulation (Carotid Territory):

Posterior Circulation (Vertebrobasilar Territory):

4.2 Specific Vascular Territory Syndromes

Middle Cerebral Artery (MCA) - Most Common:

Anterior Cerebral Artery (ACA):

• Contralateral leg weakness > arm (motor strip distribution)
• Contralateral leg sensory loss
• Abulia (lack of will), apathy, mutism
• Urinary incontinence
• Alien hand syndrome (if corpus callosum involved)

Posterior Cerebral Artery (PCA):

• Contralateral homonymous hemianopia with macular sparing
• Visual agnosia
• Memory impairment (if hippocampus involved)
• Alexia without agraphia (dominant hemisphere)

Basilar Artery:

• Locked-in syndrome: Quadriplegia, facial paralysis, but preserved consciousness and vertical eye movements
• Coma if bilateral brainstem involvement
• Cranial nerve palsies

4.3 Lacunar Stroke Syndromes

4.4 Symptoms Table

4.5 Signs Table

4.6 The NIH Stroke Scale (NIHSS)

The NIHSS is a standardized, validated 15-item assessment tool used to quantify stroke severity and guide treatment decisions. It has excellent inter-rater reliability (kappa 0.66-0.77) and strong correlation with infarct volume and clinical outcomes. [26]

Detailed Components and Scoring:

Total Score Range: 0-42 points

Score Interpretation and Clinical Implications:

Prognostic Value of NIHSS:

Important NIHSS Pearls and Limitations:

Pearl - "The NIHSS is a Score, Not a Diagnosis": Use NIHSS to quantify severity and track change, but always correlate with clinical context. A patient with isolated severe aphasia (NIHSS 3-4) may be devastatingly disabled despite a "minor" score.

Limitation - Anterior Circulation Bias: The NIHSS is heavily weighted toward cortical (MCA) strokes. Motor and language items account for 23 of 42 points. Posterior circulation strokes (vertigo, ataxia, diplopia, isolated hemianopia) often score less than 5 despite significant disability.

Limitation - Right Hemisphere Underestimation: Left MCA strokes score higher due to aphasia and language testing (items 9-10). Right MCA strokes may have dense hemiplegia and neglect but score lower.

Limitation - Lacunar Strokes: Pure motor or pure sensory strokes may score 1-4 despite complete hemiplegia (if only motor item affected).

Pitfall - Dynamic Scoring: NIHSS can change rapidly with early recanalization (improving) or hemorrhagic transformation (worsening). Always re-score at 2 hours, 24 hours, and 7 days.

NIHSS and Treatment Thresholds:

• Thrombolysis: No absolute NIHSS cutoff, but typically withheld for NIHSS 0-1 unless disabling deficit
• Thrombectomy: Typically performed for NIHSS ≥6 with LVO (but can consider for lower scores if disabling)
• DAWN criteria: Requires NIHSS ≥10 (or ≥20 depending on age and core volume)
• DEFUSE-3: No strict NIHSS requirement, but enrolled NIHSS ≥6

Validated Modifications:

• Pediatric NIHSS (PedNIHSS): Adapted for children
• Modified NIHSS: Simplified versions exist but not widely used
• NIHSS-8: Excludes items 1a-c, 7, 9, 10, 11 for telemedicine

4.7 Red Flags and Emergencies

[!CAUTION] RED FLAGS — Seek immediate help if:

• Thunderclap headache: "Worst headache of my life" — suggests SAH
• Rapidly declining GCS: Suggests brainstem compression or massive hemorrhage
• Cushing's triad: Bradycardia + Hypertension + Irregular respirations = high ICP
• New onset seizure: Cortical irritation from hemorrhage or CVST
• Neck pain + Horner's syndrome: Carotid or vertebral artery dissection
• Bilateral weakness or bulbar signs: Basilar artery occlusion
• Symptoms progressing while under observation: Consider hemorrhagic transformation or edema

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SECTION 5: Investigations

5.1 Immediate Bedside Tests

5.2 Laboratory Investigations

Note: DO NOT delay thrombolysis for laboratory results other than glucose and platelet count (unless clinical suspicion of coagulopathy).

5.3 Neuroimaging

Non-Contrast CT (NCCT) — The First Essential Test:

CT Angiography (CTA):

• Purpose: Identify large vessel occlusion (LVO)
• Sites: Internal carotid artery, M1/M2 MCA, basilar artery
• Critical for thrombectomy eligibility

CT Perfusion (CTP):

• Purpose: Identify penumbra for extended window treatment
• Core: CBF less than 30% of normal (irreversible)
• Penumbra: Tmax > 6 seconds (salvageable)
• Mismatch ratio: Target ratio > 1.8 and mismatch volume > 15 mL

MRI Brain:

Imaging Protocol for Acute Stroke:

┌─────────────────────────────────────────────────────────────────┐
│              ACUTE STROKE IMAGING ALGORITHM                      │
└─────────────────────────────────────────────────────────────────┘
                              │
                              ▼
              ┌──────────────────────────────┐
              │    NON-CONTRAST CT HEAD      │
              │    (Target less than 20 min from      │
              │          arrival)            │
              └──────────────────────────────┘
                              │
         ┌────────────────────┴────────────────────┐
         ▼                                          ▼
┌─────────────────┐                      ┌─────────────────┐
│   HEMORRHAGE    │                      │   NO HEMORRHAGE │
│   (Hyperdense)  │                      │   (Consider     │
│                 │                      │    ischemia)    │
└────────┬────────┘                      └────────┬────────┘
         │                                         │
         ▼                                         ▼
┌─────────────────┐              ┌────────────────────────────┐
│  ICH Protocol   │              │     CT ANGIOGRAPHY (CTA)   │
│  - BP control   │              │  Identify Large Vessel     │
│  - Reversal     │              │       Occlusion (LVO)      │
│  - Neurosurgery │              └────────────────────────────┘
└─────────────────┘                               │
                                    ┌─────────────┴─────────────┐
                                    ▼                           ▼
                          ┌─────────────────┐        ┌─────────────────┐
                          │  LVO DETECTED   │        │   NO LVO        │
                          │  (ICA, M1, M2,  │        │                 │
                          │   Basilar)      │        │                 │
                          └────────┬────────┘        └────────┬────────┘
                                   │                          │
                                   ▼                          ▼
                    ┌──────────────────────────┐   ┌──────────────────┐
                    │  Consider Thrombectomy   │   │  IV Thrombolysis │
                    │  ± CT Perfusion if       │   │     if less than 4.5h     │
                    │  Extended Window (6-24h) │   │  and eligible    │
                    └──────────────────────────┘   └──────────────────┘

5.4 Cardiac Investigations

5.5 Vascular Imaging

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SECTION 6: Management

6.1 Acute Stroke Algorithm

┌─────────────────────────────────────────────────────────────────┐
│              ACUTE STROKE MANAGEMENT ALGORITHM                   │
└─────────────────────────────────────────────────────────────────┘
                              │
                              ▼
              ┌───────────────────────────────┐
              │     EMERGENCY TRIAGE (T=0)    │
              │  • ABCs, O₂ > 94%, Glucose     │
              │  • STAT Neurology Consult     │
              │  • Last Known Well (LKW) time │
              │  • Activate Stroke Protocol   │
              └───────────────────────────────┘
                              │
                              ▼
              ┌───────────────────────────────┐
              │   IMMEDIATE IMAGING (Tless than 25m)   │
              │  • Non-contrast CT (NCCT)     │
              │  • CT Angiogram (CTA)         │
              │  • ± CT Perfusion (if > 6h)    │
              └───────────────────────────────┘
                              │
         ┌────────────────────┴────────────────────┐
         ▼                                          ▼
┌─────────────────┐                      ┌─────────────────┐
│   HEMORRHAGE    │                      │    ISCHEMIA     │
│   (On NCCT)     │                      │   (No blood)    │
└────────┬────────┘                      └────────┬────────┘
         │                                         │
         ▼                                         ▼
┌─────────────────┐            ┌─────────────────────────────────┐
│   ICH PROTOCOL  │            │     REPERFUSION ELIGIBLE?       │
│ • SBP less than 140 mmHg │            │ • less than 4.5h for IV Thrombolysis     │
│ • Reverse AC    │            │ • less than 24h for Thrombectomy (LVO)   │
│ • NSGY consult  │            │   with imaging selection        │
│ • ICU admission │            └────────────────┬────────────────┘
└─────────────────┘                             │
                               ┌────────────────┴────────────────┐
                               ▼                                  ▼
                     ┌─────────────────┐              ┌─────────────────┐
                     │    ELIGIBLE     │              │   NOT ELIGIBLE  │
                     │                 │              │                 │
                     │ • TNK or tPA    │              │ • Aspirin 300mg │
                     │ • MT if LVO     │              │ • Permissive    │
                     │ • BP less than 185/110   │              │   Hypertension  │
                     └────────┬────────┘              │ • Stroke Unit   │
                              │                       └────────┬────────┘
                              ▼                                 │
                     ┌─────────────────┐                       ▼
                     │  POST-ACUTE     │              ┌─────────────────┐
                     │ • ICU/Stroke U  │              │   WORKUP/REHAB  │
                     │ • NPO/Swallow   │              │ • Echo/Tele     │
                     │ • Serial Neuro  │              │ • Statins       │
                     │ • BP monitoring │              │ • PT/OT/SLP     │
                     └─────────────────┘              └─────────────────┘

6.2 Intravenous Thrombolysis

Intravenous thrombolysis remains the cornerstone of acute ischemic stroke treatment, with a number needed to treat (NNT) of 10 for excellent functional outcome (mRS 0-1) at 3 months when administered within 3 hours, and NNT of 14 when given 3-4.5 hours. [2,13]

Mechanism of Action: Tissue plasminogen activator (tPA) converts plasminogen to plasmin, which enzymatically degrades fibrin in thrombi, thereby recanalization occluded vessels and restoring cerebral perfusion.

Drug Options and Evidence:

Current Trend: Tenecteplase is increasingly preferred due to ease of administration and non-inferior efficacy. Some centers have completely transitioned to TNK as first-line agent.

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6.2.1 Inclusion Criteria for Thrombolysis

Core Criteria (All Must Be Met):

1. Clinical diagnosis of acute ischemic stroke causing measurable neurological deficit
2. Onset time ≤4.5 hours from last known well (or wake-up stroke with DWI-FLAIR mismatch)
3. Age: No upper age limit (benefit extends to > 80 years per IST-3)
4. Imaging: Non-contrast CT or MRI excluding hemorrhage and mimics
5. No absolute contraindications (see below)

Extended Window Indications (4.5-9 hours):

• Wake-up stroke with MRI showing DWI-positive, FLAIR-negative mismatch (WAKE-UP trial) [10]
• Unknown onset time with perfusion imaging showing salvageable penumbra
• Clinical improvement: If patient improving rapidly, may still benefit from lysis to prevent re-occlusion

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6.2.2 Absolute Contraindications

Strict Contraindications (DO NOT LYSE):

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6.2.3 Relative Contraindications (Individualize Risk-Benefit)

Carefully Consider - May Still Lyse:

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6.2.4 Pre-Thrombolysis Blood Pressure Management

Strict BP Control Required Before Lysis:

If BP Cannot Be Controlled: DO NOT GIVE THROMBOLYSIS. Elevated BP during/after lysis increases symptomatic ICH risk from ~6% to > 15%.

Agents to AVOID: Sublingual nifedipine (unpredictable precipitous drop), hydralazine (unpredictable response).

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6.2.5 Administration Protocol

Step-by-Step Checklist:

1. ☑️ Confirm no contraindications: Review checklist
2. ☑️ Confirm weight: Actual body weight in kg (use scale if possible)
3. ☑️ Calculate dose: 0.9 mg/kg for alteplase (max 90 mg); 0.25 mg/kg for tenecteplase (max 25 mg)
4. ☑️ BP control: Achieve SBP less than 185/110 mmHg
5. ☑️ Consent: Discuss risks (6-7% symptomatic ICH) and benefits
6. ☑️ Stop all antiplatelets/anticoagulants: Hold for 24 hours
7. ☑️ Prepare ICU bed: For post-lysis monitoring

Alteplase Administration:

• Draw up 10% of total dose → give as IV bolus over 1 minute
• Draw up remaining 90% → infuse over 60 minutes via pump
• No other medications in same IV line during infusion

Tenecteplase Administration:

• Draw up total dose → give as IV bolus over 5-10 seconds
• Faster, simpler, fewer errors

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6.2.6 Post-Thrombolysis Monitoring and Complications

Intensive Monitoring Protocol:

Signs of Hemorrhagic Transformation:

• Sudden worsening of neurological deficit
• New severe headache
• Nausea/vomiting
• Decline in level of consciousness
• Seizure

Management of sICH (Symptomatic Intracranial Hemorrhage):

1. STOP thrombolytic immediately
2. Stat CT head (within 5 minutes)
3. Type and cross for blood products
4. Labs: PT, APTT, INR, fibrinogen, CBC
5. Reverse fibrinolysis:
   • Cryoprecipitate: 10 units IV (replaces fibrinogen; aim fibrinogen > 150 mg/dL)
   • Tranexamic acid: 1000 mg IV over 10 min (antifibrinolytic; controversial)
   • Platelets: 1-2 units if platelet count low or dysfunction
6. Neurosurgery consult: For possible hematoma evacuation
7. BP control: Target SBP less than 140-160 mmHg

Symptomatic ICH Rate: 6-7% with tPA (NINDS trial); slightly lower with TNK in some studies.

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6.2.7 Outcomes of Thrombolysis

Efficacy (Pooled Meta-Analysis Data):

Time-Dependency of Benefit:

Every 15 minutes of delay = 4% lower odds of excellent outcome and 1 month of disability-free life lost. [28]

6.3 Mechanical Thrombectomy

Mechanical thrombectomy represents the most effective intervention in acute medicine, with a number needed to treat of 2.6 for one-grade improvement in mRS and NNT of 7 for functional independence (mRS 0-2). [6] The HERMES meta-analysis of 5 randomized trials demonstrated thrombectomy's superiority over medical therapy alone, establishing it as standard of care for large vessel occlusion.

Mechanism: Endovascular retrieval of thrombus using stent retrievers (Solitaire, Trevo) or direct aspiration catheters (Penumbra), achieving TICI 2b/3 reperfusion (≥50% or complete reperfusion) in 70-90% of cases.

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6.3.1 Indications for Mechanical Thrombectomy

Core Inclusion Criteria (0-6 Hour Window):

1. Large Vessel Occlusion (LVO) on CTA/MRA:

   • Internal carotid artery (ICA) — terminus or proximal
   • M1 segment of middle cerebral artery (MCA)
   • Proximal M2 MCA (select cases)
   • Basilar artery (posterior circulation)
   • Vertebral artery (select cases)

2. NIHSS ≥6 (evidence threshold from trials)

   • Lower NIHSS may qualify if disabling deficit (e.g., dominant hand weakness, aphasia, hemianopia affecting driving)

3. Pre-stroke mRS 0-1 (functionally independent)

   • Trials excluded patients with severe baseline disability
   • Some flexibility for mRS 2 if patient/family preference

4. ASPECTS ≥6 on non-contrast CT

   • Alberta Stroke Program Early CT Score
   • Assesses extent of early ischemic change in MCA territory
   • 10 regions scored; 1 point deducted for each region with hypodensity
   • ASPECTS 6-10: Good collaterals, small core, favorable for thrombectomy
   • ASPECTS 0-5: Large established infarct, high complication risk

5. Age: No strict upper limit, but trials enrolled mostly less than 85 years

6. Time from onset less than 6 hours from last known well

Basilar Artery Occlusion:

• More permissive criteria due to high mortality without intervention
• Consider up to 24 hours even without perfusion imaging
• NIHSS may be misleading (locked-in syndrome has variable NIHSS)

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6.3.2 Extended Window Thrombectomy (6-24 Hours)

DAWN Trial Criteria (6-24 Hours): [3]

Enrollment based on clinical-core mismatch (DWI or CTP core volume):

Additional DAWN Criteria:

• LVO: ICA or M1 MCA occlusion
• Pre-stroke mRS 0-1
• Last known well 6-24 hours prior

DAWN Results:

• 49% achieved mRS 0-2 (thrombectomy) vs 13% (control) — NNT = 2.8
• 90-day mortality: 19% vs 38%

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DEFUSE-3 Trial Criteria (6-16 Hours): [4]

Enrollment based on perfusion mismatch (penumbra vs core ratio):

Additional DEFUSE-3 Criteria:

• LVO: ICA or M1/M2 MCA occlusion
• Pre-stroke mRS 0-2
• NIHSS ≥6
• Age 18-90 years
• Last known well 6-16 hours prior

DEFUSE-3 Results:

• 45% achieved mRS 0-2 (thrombectomy) vs 17% (control) — NNT = 3.6
• Earlier reperfusion = better outcomes (each hour delay = 10% lower odds of good outcome)

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6.3.3 Imaging Selection for Thrombectomy

CT Perfusion (CTP) Parameters:

ASPECTS (Alberta Stroke Program Early CT Score):

10-point scale assessing MCA territory on non-contrast CT:

Supraganglionic Level (4 regions):

• M1: Anterior MCA cortex
• M2: MCA cortex lateral to insular ribbon
• M3: Posterior MCA cortex
• Insula

Ganglionic Level (6 regions):

• C: Caudate
• L: Lentiform nucleus (putamen)
• IC: Internal capsule
• M4: Anterior MCA immediately superior to M1
• M5: Lateral MCA territory superior to M2
• M6: Posterior MCA territory superior to M3

Scoring: Start at 10; subtract 1 for each region with hypodensity, loss of gray-white differentiation, or swelling.

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6.3.4 Thrombectomy Technique

Procedural Steps:

1. Vascular Access: Femoral artery (most common) or radial artery
2. Guide Catheter: Advanced to cervical ICA or vertebral artery
3. Microcatheter Navigation: Across thrombus under fluoroscopy
4. Reperfusion Technique:
   • Stent Retriever: Deploy stent across clot, wait 3-5 min for integration, retrieve with aspiration
   • Direct Aspiration (ADAPT): Large-bore catheter advanced to clot, direct suction applied
   • Combined Technique: Stent retriever + proximal balloon guide catheter aspiration (SAVE technique)
5. Assess Reperfusion: Angiography to determine TICI score

TICI (Thrombolysis in Cerebral Infarction) Score:

Target: TICI 2b or 3 (achieved in 70-90% of modern cases)

Number of Passes: Minimize to reduce endothelial injury; most experts aim for ≤3 passes

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6.3.5 Anesthesia for Thrombectomy

General Anesthesia (GA) vs Conscious Sedation (CS):

Current Evidence: Multiple RCTs (SIESTA, ANSTROKE, GOLIATH) show no difference in outcomes. Recent meta-analyses suggest possible benefit with CS due to faster times. [29]

Recommendation: Use conscious sedation unless:

• Patient agitated or uncooperative
• GCS less than 8 or loss of airway reflexes
• Posterior circulation stroke with risk of herniation
• Conversion to GA if aspiration occurs

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6.3.6 Complications of Thrombectomy

Overall Safety: Serious adverse events in less than 10% of cases; benefit far outweighs risk.

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6.3.7 Thrombectomy + Thrombolysis (Bridging Therapy)

Should We Give tPA Before Thrombectomy?

Yes (Bridging) - Standard practice in most stroke systems:

• May recanalize small vessel occlusions before thrombectomy
• No delay if systems run in parallel (tPA bolus → immediate transfer to angio)
• HERMES trials used bridging in majority

No (Direct Thrombectomy) - Some emerging evidence:

• DIRECT-MT, DEVT, SKIP trials: Direct thrombectomy non-inferior to bridging
• Avoids tPA-related sICH risk
• May be preferred if tPA contraindications (e.g., recent surgery)

Current Recommendation: Bridging therapy remains standard unless contraindications to tPA exist. Some centers practicing direct thrombectomy for select patients.

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6.3.8 Posterior Circulation Thrombectomy

Basilar Artery Occlusion (BAO):

• High mortality without treatment (70-90%)
• More permissive time windows (up to 24h) due to devastating natural history
• Lower quality evidence (BEST, BASICS trials ongoing)
• Consider even with ASPECTS not applicable (use pc-ASPECTS for posterior circulation)

Indications:

• Basilar artery occlusion on CTA/MRA
• NIHSS variable (locked-in may have low NIHSS)
• Symptoms less than 24 hours (some centers extend further)
• No massive infarction on imaging

Outcomes: TICI 2b/3 reperfusion associated with 40-50% mRS 0-3 vs less than 10% without reperfusion.

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6.3.9 Thrombectomy Outcomes

Efficacy Data (HERMES Meta-Analysis): [6]

Factors Associated with Better Outcome:

• TICI 2b/3 reperfusion achieved
• Shorter time to reperfusion (less than 6 hours best)
• Smaller baseline core volume
• Good collateral circulation
• Younger age
• Lower NIHSS at presentation

6.4 Intracerebral Hemorrhage Management

Blood Pressure Control:

Reversal of Anticoagulation:

Surgical Intervention:

• Cerebellar hemorrhage > 3 cm with hydrocephalus or brainstem compression → Surgical evacuation
• Lobar hemorrhage with deterioration → Consider evacuation (STICH trials showed limited benefit for supratentorial ICH)
• IVH with hydrocephalus → External ventricular drain (EVD)

6.5 Blood Pressure Management in Acute Stroke

Blood pressure management in acute stroke is complex and context-dependent. Elevated BP is common (70-80% of patients) due to physiologic stress response, loss of cerebral autoregulation, and pre-existing hypertension. Premature or excessive lowering can extend infarct by collapsing penumbral perfusion; however, severe hypertension increases hemorrhagic transformation and cerebral edema risk.

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6.5.1 Permissive Hypertension in Acute Ischemic Stroke (No Reperfusion Therapy)

Rationale: Elevated BP maintains collateral flow to ischemic penumbra. Cerebral autoregulation is disrupted in acute stroke, making perfusion pressure-dependent. [9]

Guidelines (AHA/ASA 2019): [2]

Agents for Cautious Lowering (if SBP > 220 or DBP > 120):

Avoid: Sublingual nifedipine (precipitous, uncontrolled drop → ischemia extension)

Pearl: Lower BP gradually. Aggressive lowering can precipitate stroke extension or new infarction in watershed zones.

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6.5.2 BP Management for Thrombolysis Candidates

Strict Targets (MANDATORY):

Critical Rule: If BP cannot be controlled to less than 185/110 mmHg, DO NOT give thrombolysis. Risk of symptomatic ICH increases from 6% to > 15% with uncontrolled hypertension.

Management Algorithm:

Pre-Thrombolysis BP > 185/110 mmHg
           ↓
  Labetalol 10-20 mg IV push
           ↓
  Recheck BP in 10 minutes
           ↓
    ┌──────────────────┐
    ↓                  ↓
Still > 185/110     less than 185/110
    ↓                  ↓
Repeat labetalol   Proceed with lysis
or start           Monitor q15min
nicardipine 
infusion
    ↓
If still uncontrolled
after 300 mg labetalol
→ DEFER thrombolysis

Post-Thrombolysis BP Elevation:

• If SBP > 180 or DBP > 105 mmHg: Start IV nicardipine or labetalol
• If severe elevation (SBP > 230): Emergent CT to rule out hemorrhage, then aggressive IV therapy

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6.5.3 BP Management in Intracerebral Hemorrhage (ICH)

Aggressive BP Lowering in ICH: Unlike ischemic stroke, ICH benefits from early intensive BP reduction to prevent hematoma expansion.

Evidence:

• INTERACT-2 (2013): SBP less than 140 mmHg safe but no significant functional benefit (primary outcome neutral) [9]
• ATACH-2 (2016): SBP 110-139 mmHg vs 140-179 mmHg → No benefit, possible harm in renal function [14]

AHA/ASA Guidelines for ICH (2015, updated 2022): [11]

Contraindication to Aggressive Lowering:

• Large ICH with significant mass effect (CPP = MAP - ICP; lowering MAP may worsen CPP)
• Suspicion of elevated ICP (consider ICP monitoring)

Agents for ICH BP Control:

Monitoring: Continuous arterial line recommended for ICH with severe hypertension (SBP > 200) to allow real-time titration.

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6.5.4 BP Management Post-Acute Phase (Days 2-7)

Ischemic Stroke: After the hyperacute phase (first 24-48h), begin gradual transition to long-term BP control.

Targets:

• Days 2-7: Aim SBP less than 140-160 mmHg (avoid rapid drops)
• After 7 days: Initiate guideline-directed long-term therapy (target less than 130/80)

Transition from IV to PO:

• If patient able to swallow and neurologically stable, transition to oral agents
• Common regimens: Amlodipine 5-10 mg daily, Lisinopril 10-20 mg daily, Losartan 50 mg daily

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6.5.5 Special Considerations

Wake-Up Stroke: Permissive hypertension unless receiving thrombolysis/thrombectomy

Posterior Circulation Stroke: May tolerate lower BP better (brainstem has better autoregulation)

Lacunar Stroke: Often associated with chronic hypertension; permissive hypertension acutely, then aggressive long-term control

Stroke with Concurrent MI: Balanced approach; avoid extremes; cardiology co-management

Dissection: BP control to SBP less than 140 to prevent propagation (similar to aortic dissection principles)

6.6 General Acute Stroke Care

Beyond reperfusion therapy, meticulous supportive care in the first 24-72 hours significantly impacts outcomes. Stroke unit care reduces mortality and disability by 20-30% compared to general ward care, driven by protocol-based management, specialized nursing, and early rehabilitation. [8]

Fever Management:

• Source control: Urinalysis, CXR, blood cultures
• Acetaminophen 650-1000 mg q6h PRN
• Cooling blankets if persistent fever > 38.5°C
• Avoid NSAIDs acutely (may interfere with antiplatelet effects)

Glucose Management:

• Insulin sliding scale if glucose > 180 mg/dL
• Avoid hypoglycemia (less than 70 mg/dL) — associated with worse outcomes
• Target HbA1c less than 7% long-term

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6.7 Medical Management (First-Line Medications)

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SECTION 7: Secondary Prevention

Secondary prevention is critical to reduce the 5-year recurrent stroke risk from 25-30% to 10-15%. The EXPRESS study demonstrated that immediate risk factor modification and treatment initiation within 24 hours reduces recurrent stroke by 80% in the first 90 days. [23] A comprehensive secondary prevention strategy addresses antiplatelet therapy, anticoagulation, statins, blood pressure control, diabetes management, lifestyle modification, and revascularization.

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7.1 Antiplatelet Therapy

Antiplatelet therapy is the cornerstone of secondary prevention for non-cardioembolic ischemic stroke and TIA, reducing recurrent stroke risk by 20-25%.

Single Antiplatelet Therapy (Long-Term Maintenance):

Recommendation: Clopidogrel 75 mg daily is preferred for most patients due to superior efficacy and tolerability compared to aspirin alone.

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7.1.1 Dual Antiplatelet Therapy (DAPT) for Minor Stroke and High-Risk TIA

Indication: Minor stroke (NIHSS ≤3) or high-risk TIA presenting within 24 hours of symptom onset.

Definition of High-Risk TIA:

• ABCD² score ≥4, OR
• Symptomatic intracranial or extracranial stenosis ≥50%, OR
• Multiple ischemic lesions on DWI MRI

Evidence from Major Trials:

Interpretation:

• DAPT is most beneficial in the first 21-30 days post-event
• Longer duration (90 days) increases bleeding risk without additional benefit
• Loading dose of clopidogrel (300-600 mg) on day 1 is standard

Current Guideline Recommendation (AHA/ASA 2021): [2]

• Aspirin 75-100 mg + Clopidogrel 75 mg × 21 days, then single antiplatelet
• Start within 24 hours of minor stroke or high-risk TIA
• Avoid if plan for thrombolysis (wait 24h post-lysis)
• Avoid if plan for anticoagulation

DAPT Protocol:

Day 0 (Presentation):
  - Aspirin 300 mg PO
  - Clopidogrel 300 mg PO loading dose

Days 1-21:
  - Aspirin 75-100 mg daily
  - Clopidogrel 75 mg daily

After Day 21:
  - STOP aspirin
  - CONTINUE clopidogrel 75 mg daily long-term

Contraindications to DAPT:

• Recent ICH
• Active bleeding
• Severe thrombocytopenia (less than 50,000)
• Planned anticoagulation for AF
• High bleeding risk (HAS-BLED ≥3)

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7.2 Anticoagulation for Atrial Fibrillation

Atrial fibrillation (AF) is present in 15-20% of ischemic strokes and confers a 5-fold increased risk of recurrent stroke. Anticoagulation reduces stroke risk by 60-70% compared to no treatment. [30]

CHA₂DS₂-VASc Score (Stroke Risk Stratification):

Maximum Score: 9 points

Annual Stroke Risk by CHA₂DS₂-VASc:

Note: A history of stroke/TIA automatically qualifies for anticoagulation (score ≥2).

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7.2.1 Choice of Anticoagulant

Direct Oral Anticoagulants (DOACs) — Preferred Over Warfarin:

Warfarin:

• Dose: Individualized to achieve INR 2.0-3.0
• Requires frequent monitoring
• Multiple drug/food interactions
• Reserve for: Severe CKD (CrCl less than 15), mechanical valves, rheumatic mitral stenosis

Evidence: RE-LY, ROCKET-AF, ARISTOTLE, ENGAGE AF-TIMI 48 trials all showed DOACs non-inferior or superior to warfarin with lower ICH risk. [30]

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7.2.2 Timing of Anticoagulation After Stroke

The "1-3-6-12 Day Rule" (based on stroke size and hemorrhagic transformation risk):

Rationale: Early anticoagulation (within 24-48h) in large infarcts increases hemorrhagic transformation risk. Delayed initiation balances recurrent stroke risk vs bleeding risk.

Factors Favoring Early Anticoagulation (consider 1-3 days):

• High thromboembolic risk (prior stroke, LV thrombus, recent MI)
• Mechanical heart valve
• Small infarct size on imaging
• No hemorrhagic transformation on 24h CT

Factors Favoring Delayed Anticoagulation (7-14 days):

• Large infarct (> 50% MCA territory or ASPECTS less than 6)
• Hemorrhagic transformation on imaging
• Uncontrolled hypertension (SBP > 180)
• High fall risk

Bridging Therapy: NOT recommended. Start DOAC directly without heparin bridge (BRIDGE trial showed no benefit and increased bleeding).

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7.3 Statin Therapy

High-intensity statin therapy reduces recurrent stroke by 15-20% and all cardiovascular events by 20-30%, regardless of baseline LDL cholesterol. [18]

Recommendation: ALL ischemic stroke patients should receive high-intensity statin unless contraindicated.

High-Intensity Statins:

LDL Target: less than 70 mg/dL (1.8 mmol/L), or ≥50% reduction from baseline.

2023 Update: AHA/ASA now recommends LDL less than 55 mg/dL for very high-risk patients (recurrent stroke, polyvascular disease).

Monitoring:

• Baseline: Lipid panel, ALT, CK
• Repeat lipid panel at 4-12 weeks to assess response
• ALT if symptoms of hepatotoxicity; discontinue if ALT > 3× ULN
• CK if symptoms of myopathy; discontinue if CK > 10× ULN or rhabdomyolysis

Statin Intolerance (5-10% of patients):

• Symptoms: Myalgias, weakness, elevated CK
• Management:
  • Try alternative statin (rosuvastatin better tolerated)
  • Lower dose with ezetimibe 10 mg to reach LDL goal
  • PCSK9 inhibitors (evolocumab, alirocumab) if severe intolerance

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7.4 Blood Pressure Management

Long-term blood pressure control is critical for secondary prevention. Hypertension is the most important modifiable risk factor for recurrent stroke (40% RRR with optimal control). [19]

Target: less than 130/80 mmHg (AHA/ASA 2021 guidelines) [2]

Exception: Bilateral carotid stenosis or vertebral stenosis — consider higher target (SBP 140-150) to maintain perfusion.

Timing: Initiate or resume antihypertensive therapy after the acute phase (48-72 hours), once patient neurologically stable. Avoid abrupt lowering in first 24 hours (risk of extending infarct).

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7.4.1 Preferred Agents

First-Line Agents (Evidence-Based):

Avoid: Beta-blockers as first-line (less effective for stroke prevention compared to ACE-I/ARB).

Typical Regimen:

• Start: Lisinopril 10 mg + Amlodipine 5 mg
• Titrate: Lisinopril to 20-40 mg, Amlodipine to 10 mg
• Add: Chlorthalidone 12.5-25 mg if still above target
• Goal: SBP less than 130 mmHg, DBP less than 80 mmHg

Monitoring: Home BP monitoring preferred; target average less than 130/80.

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7.5 Diabetes Management

Diabetes increases stroke risk 2-fold and worsens post-stroke outcomes. However, intensive glycemic control has NOT been proven to reduce recurrent stroke risk (ACCORD trial showed no stroke benefit with HbA1c less than 6% vs less than 7%).

Target HbA1c: 6.5-7.0% (individualized based on age, comorbidities, hypoglycemia risk)

Avoid: Hypoglycemia (less than 70 mg/dL) — associated with increased stroke risk and worse outcomes.

Preferred Agents (Cardiovascular Benefit):

Avoid Pioglitazone in stroke patients with heart failure (fluid retention).

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7.6 Carotid Revascularization

Symptomatic carotid stenosis (stroke/TIA in the territory of a stenotic carotid artery) warrants urgent revascularization.

Indications for Carotid Endarterectomy (CEA) or Carotid Stenting (CAS):

Evidence:

• NASCET (North American Symptomatic Carotid Endarterectomy Trial): 70-99% stenosis → CEA reduced 2-year stroke risk from 26% to 9% (NNT=6)
• ECST (European Carotid Surgery Trial): Confirmed benefit for 70-99% stenosis
• EXPRESS Study: Early surgery (less than 14 days) reduced 90-day stroke risk by 80% vs delayed surgery [23]

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7.6.1 CEA vs CAS

Carotid Endarterectomy (CEA):

• Gold standard surgical technique
• Lower periprocedural stroke risk
• Preferred in most patients

Carotid Artery Stenting (CAS):

• Percutaneous endovascular approach
• Higher periprocedural stroke risk (especially in elderly)
• Indications: High surgical risk, radiation-induced stenosis, restenosis post-CEA, anatomically inaccessible lesion

CREST Trial: CEA and CAS had similar long-term outcomes, but CEA had lower periprocedural stroke risk, while CAS had lower MI risk.

Recommendation: CEA preferred for most patients; CAS for selected high surgical risk cases.

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7.7 Lifestyle Modifications

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7.8 Patent Foramen Ovale (PFO) Closure

Indication: Cryptogenic stroke in patients age less than 60 with PFO and atrial septal aneurysm or large right-to-left shunt.

Evidence: CLOSE, RESPECT, REDUCE trials showed PFO closure superior to medical therapy alone in select patients (NNT=10-20). [30]

Procedure: Percutaneous transcatheter PFO closure device (Amplatzer, Gore Cardioform).

Post-Procedure: DAPT × 6 months, then aspirin indefinitely.

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7.9 Comprehensive Secondary Prevention Checklist

Every ischemic stroke patient should have:

☑️ Antiplatelet therapy (aspirin, clopidogrel, or DAPT if minor stroke) ☑️ Anticoagulation if AF (DOAC preferred) ☑️ High-intensity statin (atorvastatin 40-80 mg) ☑️ Blood pressure control (less than 130/80 mmHg with ACE-I or ARB) ☑️ Diabetes management (HbA1c less than 7%, GLP-1 RA or SGLT2i if applicable) ☑️ Carotid imaging and revascularization if 50-99% symptomatic stenosis ☑️ Lifestyle counseling: smoking cessation, diet, exercise, weight ☑️ Swallow assessment and speech therapy if dysphagic/aphasic ☑️ PT/OT for rehabilitation ☑️ Depression screening and treatment (affects 30-50%) ☑️ Driving assessment (most countries require MD clearance post-stroke)

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SECTION 8: Complications

8.1 Immediate Complications (0-72 hours)

8.2 Malignant Middle Cerebral Artery Syndrome

Definition: Life-threatening edema following large MCA infarct, causing herniation.

Risk Factors:

• Age less than 60 years
• NIHSS > 15

• 50% MCA territory infarct

• Decreased LOC within 24 hours

Management:

• Decompressive hemicraniectomy: Within 48 hours
• DESTINY, DECIMAL, HAMLET trials: Reduces mortality from 78% to 29% [20]
• Age consideration: Greatest benefit in patients less than 60 years

8.3 Late Complications

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SECTION 9: Prognosis and Outcomes

9.1 Prognostic Factors

9.2 Outcome Measures

Modified Rankin Scale (mRS):

9.3 Natural History and Treatment Outcomes

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SECTION 10: Evidence and Guidelines

10.1 Key Guidelines

AHA/ASA Guidelines for the Early Management of Acute Ischemic Stroke (2019, 2021 Update) [2]

• IV thrombolysis with alteplase or tenecteplase for eligible patients within 4.5 hours (Class I)
• Mechanical thrombectomy for LVO within 6 hours (Class I)
• Thrombectomy up to 24 hours with perfusion imaging selection (Class I)
• Dual antiplatelet therapy for minor stroke/high-risk TIA (Class I)
• Stroke unit care for all stroke patients (Class I)

European Stroke Organisation (ESO) Guidelines (2021)

• Recommendations align with AHA/ASA
• Emphasis on regional stroke networks and telestroke

10.2 Landmark Trials

Thrombolysis Trials:

Thrombectomy Trials:

Secondary Prevention Trials:

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SECTION 11: Patient and Layperson Explanation

11.1 What is a Stroke?

A stroke happens when blood flow to part of the brain is blocked (like a clogged pipe) or when a blood vessel in the brain bursts (like a burst pipe). When brain cells don't get blood, they start to die within minutes. This is why doctors call it a "brain attack" — just like a heart attack, but in the brain.

Two main types:

1. Ischemic stroke (85%): A blood clot blocks an artery. This is like a traffic jam stopping all the cars.
2. Hemorrhagic stroke (15%): A blood vessel bursts and bleeds into the brain. This is more dangerous and harder to treat.

11.2 How Do I Recognize a Stroke? (BE FAST)

Remember: Every minute matters! Treatments work best when given within hours. "Time is brain."

11.3 Why Does It Matter?

Every minute of a major stroke, nearly 2 million brain cells die. The sooner treatment is given:

• The more brain is saved
• The better the recovery
• The more likely you are to walk, talk, and live independently

11.4 What Happens at the Hospital?

1. Immediate CT scan — to see if it's a clot or a bleed
2. Blood tests — to check your blood sugar and clotting
3. Clot-busting medicine — if it's a clot and you arrived in time
4. Clot removal procedure — if there's a large clot, doctors can pull it out with a special wire
5. Monitoring — in a specialized stroke unit

11.5 After a Stroke

• Rehabilitation: Physical therapy, occupational therapy, speech therapy
• Medications: Blood thinners, cholesterol medications, blood pressure medications
• Lifestyle changes: Stop smoking, healthy diet, exercise, control blood pressure and diabetes
• Follow-up: Regular appointments with your stroke team

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SECTION 12: Examination Focus

12.1 Common Exam Questions (MRCP, USMLE, FRCS)

Question 1 (MRCP): A 72-year-old man presents 2 hours after sudden onset of right-sided weakness and speech difficulty. BP is 195/110 mmHg. CT head shows no hemorrhage. What is the most appropriate next step?

• Answer: Lower BP to less than 185/110 with IV labetalol or nicardipine, then administer IV tenecteplase or alteplase.

Question 2 (USMLE): A patient with acute ischemic stroke is found to have an M1 MCA occlusion on CTA. Symptom onset was 8 hours ago. What additional imaging is required to determine thrombectomy eligibility?

• Answer: CT perfusion (or MRI DWI/perfusion) to assess core infarct volume and penumbra (DAWN/DEFUSE-3 criteria).

Question 3 (FRCS): What is the most common cause of death within 1 week of a large MCA infarct?

• Answer: Cerebral edema and transtentorial herniation.

Question 4 (MRCP): A patient with atrial fibrillation presents 5 days after a minor ischemic stroke (NIHSS 2). When should anticoagulation be started?

• Answer: 1-3 days after minor stroke. Given NIHSS 2, consider starting at day 3-5 after repeat imaging excludes hemorrhagic transformation.

Question 5 (USMLE): What is the NIHSS component that is most commonly affected in a right MCA stroke but often underscores severity?

• Answer: Extinction/inattention (hemispatial neglect). The NIHSS underestimates right hemisphere strokes.

12.2 Viva Opening Statement

"Stroke is a medical emergency caused by the sudden interruption of cerebral blood flow, either due to arterial occlusion (ischemic, 85%) or vessel rupture (hemorrhagic, 15%). It is characterized by sudden-onset focal neurological deficits corresponding to a vascular territory. Recognition using FAST or BE-FAST criteria enables immediate activation of hyperacute stroke pathways. The cornerstone of ischemic stroke treatment is rapid reperfusion through intravenous thrombolysis within 4.5 hours and mechanical thrombectomy for large vessel occlusion up to 24 hours in selected patients. 'Time is brain' — every minute of delay results in loss of 1.9 million neurons. Secondary prevention with antiplatelets, statins, and blood pressure control reduces recurrence. Hemorrhagic stroke requires blood pressure control, reversal of anticoagulation, and consideration of surgical intervention."

12.3 High-Yield Facts for Exams

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Last Reviewed: 2026-01-09 | MedVellum Editorial Team