On This Page (7 sections)
Check immediately; must be > 60 mg/dL (hypoglycemia mimics focal stroke)
< 20 minutes to non-contrast head CT; interpret < 45 minutes
Within 4.5 hours of Last Known Well (LKW); target door-to-needle < 45 minutes
Lower BP to < 185/110 mmHg prior to lytic infusion; maintain < 180/105 mmHg for 24h
Up to 24 hours for anterior circulation LVO (ICA, MCA-M1) meeting DAWN/DEFUSE-3
Posterior circulation stroke presenting with 'crossed findings' (ipsilateral cranial nerve palsy + contralateral hemiplegia), vertigo, ataxia, locked-in syndrome; endovascular thrombectomy window extended up to 24 hours.
Coma with absence of brainstem reflexes (pupillary, corneal, oculocephalic, oculovestibular, gag, cough) and positive Apnea Test (no respiratory effort with PaCO2 rising >= 20 mmHg above baseline to >= 60 mmHg).
Bottom-Line Clinical Pearl
Time is brain: 1.9 million neurons die every minute of untreated large vessel stroke. Check fingerstick glucose first to exclude hypoglycemia. Non-contrast CT must be completed < 20 minutes to exclude intracranial hemorrhage. IV thrombolysis (Tenecteplase 0.25 mg/kg or Alteplase 0.9 mg/kg) is administered within 4.5 hours of last known well if BP < 185/110 mmHg. Endovascular thrombectomy (EVT) is indicated up to 24 hours for large vessel occlusion (ICA, MCA-M1) with salvageable penumbra.
Acute stroke requires simultaneous resuscitation, neurologic localization, and neuroimaging. Upon Code Stroke activation, triage the patient directly to the CT scanner. Perform an immediate fingerstick blood glucose—hypoglycemia (< 60 mg/dL) produces reversible focal neurologic deficits and is the most common stroke mimic.
| Time Benchmark | Critical ED Action | Standard Goal | Clinical Pitfall |
|---|---|---|---|
| 0 min | Arrival & Triage | Activate Code Stroke, obtain Last Known Well (LKW) | Assuming wake-up stroke is ineligible for EVT without advanced imaging |
| < 10 min | Bedside Evaluation | NIH Stroke Scale (NIHSS) + fingerstick glucose | Failing to check glucose before transporting to CT scanner |
| < 20 min | Non-Contrast Head CT + CTA | Exclude hemorrhage; assess for Large Vessel Occlusion (LVO) | Delaying CTA to wait for serum creatinine (contrast-induced nephropathy risk is negligible compared to stroke disability) |
| < 45 min | Image Interpretation & Decision | Review Alberta Stroke Program Early CT Score (ASPECTS) | Missing early ischemic signs: hyperdense MCA sign, loss of insular ribbon, sulcal effacement |
| < 45 min | Thrombolysis Infusion | Administer IV Tenecteplase or Alteplase | Delaying thrombolysis to obtain peripheral blood labs in patients without known coagulopathy |
| < 60–90 min | Endovascular Puncture | Transport to Interventional Radiology suite for EVT | Failing to notify neurointerventional team while administering IV lytics |
Intravenous thrombolysis is indicated for patients with disabling ischemic stroke symptoms within 4.5 hours of Last Known Well (LKW). Tenecteplase (TNK-tPA) is increasingly preferred over Alteplase due to its single-bolus administration, higher fibrin specificity, and superior recanalization rates in large vessel occlusions.
| Thrombolytic Agent | Dosing Protocol | Administration Route | Key Operational Advantages |
|---|---|---|---|
| Tenecteplase (TNK) | 0.25 mg/kg single bolus (maximum 25 mg) | IV push over 5–10 seconds | Single rapid bolus; no continuous infusion pump needed; enables faster door-to-needle and transfer to angio suite. |
| Alteplase (rt-PA) | 0.9 mg/kg total dose (maximum 90 mg) | 10% given as IV bolus over 1 min; remaining 90% infused over 60 min | Traditional standard. Requires dedicated infusion line and continuous cardiac/blood pressure monitoring. |
Critical Pitfall / Contraindication
Strict Contraindications to IV Thrombolysis: 1) Active internal hemorrhage or acute bleeding diathesis; 2) Significant head trauma or prior stroke within 3 months; 3) Intracranial/intraspinal surgery within 3 months; 4) History of prior intracranial hemorrhage, intra-axial intracranial neoplasm, AVM, or aneurysm; 5) Persistent severe uncontrolled hypertension (BP > 185/110 mmHg refractory to IV antihypertensives); 6) Platelet count < 100,000/uL; 7) Current anticoagulant use with elevated coagulopathy (INR > 1.7, aPTT > 40s, or direct thrombin/factor Xa inhibitor ingestion within 48 hours without reversal).
Blood pressure management differs radically between thrombolysis candidates, non-thrombolysis patients, and acute intracerebral hemorrhage. Permissive hypertension is mandatory in non-thrombolysis ischemic stroke to preserve perfusion across the collateral vascular beds supplying the ischemic penumbra.
| Clinical Scenario | Target Blood Pressure | First-Line Antihypertensive Agents | Key Management Principles |
|---|---|---|---|
| Candidate for Thrombolysis (Pre-lytic) | BP must be < 185/110 mmHg | Labetalol 10–20 mg IV push over 2 min (may repeat x 1) OR Nicardipine 5 mg/h IV titrated by 2.5 mg/h q5–15min (max 15 mg/h) | If BP cannot be maintained < 185/110 mmHg, thrombolysis is strictly contraindicated. |
| Post-Thrombolysis (First 24 Hours) | Maintain BP < 180/105 mmHg | Nicardipine infusion 5–15 mg/h OR Clevidipine 1–2 mg/h titrated; Labetalol 10–20 mg IV boluses | Check BP q15min for 2h, then q30min for 6h, then q1h for 16h. Rapidly treat spikes to prevent hemorrhagic conversion. |
| Ischemic Stroke (NOT receiving lytics) | Permissive hypertension up to 220/120 mmHg | Do NOT treat unless SBP > 220 mmHg or DBP > 120 mmHg (or concurrent aortic dissection, ACS, acute heart failure) | If treating, lower MAP by only 15% over the first 24 hours to prevent acute penumbral hypoperfusion. |
| Spontaneous Intracranial Hemorrhage (ICH) | Target SBP 140 mmHg (maintain 130–150 mmHg) | Nicardipine 5–15 mg/h IV infusion OR Labetalol 20 mg IV push | INTERACT-2/ATACH-2 trials: Rapid BP reduction reduces hematoma expansion; avoid extreme drops (SBP < 130 mmHg). |
Endovascular Thrombectomy (EVT) with stent retrievers and direct aspiration catheters has revolutionized stroke care for anterior circulation Large Vessel Occlusions (Internal Carotid Artery or Middle Cerebral Artery M1 segment). EVT achieves 80–90% recanalization rates compared to under 30% with IV thrombolysis alone.
| EVT Window | Trial Evidence | Inclusion Criteria | Imaging Modality |
|---|---|---|---|
| 0–6 Hours | HERMES Meta-analysis | Pre-stroke mRS 0–1; NIHSS >= 6; ASPECTS >= 6; confirmed occlusion of ICA or MCA-M1 | Non-contrast CT + CTA head and neck |
| 6–16 Hours | DEFUSE-3 Trial | Initial infarct core < 70 mL, mismatch ratio >= 1.8, absolute mismatch volume >= 15 mL | CT Perfusion (CTP) or MRI DWI showing salvageable ischemic penumbra |
| 6–24 Hours | DAWN Trial | Clinical-core mismatch: High NIHSS (>= 10 or >= 20) with disproportionately small core infarct (< 21 mL or < 51 mL) | CT Perfusion or MRI DWI |
Spontaneous ICH accounts for 15–20% of strokes but causes more than 50% of stroke-related mortality. In patients taking oral anticoagulants, hematoma expansion occurs in up to 40% within the first 6 hours. Emergency reversal of coagulopathy must be initiated immediately upon CT confirmation of blood.
| Anticoagulant Class | Specific Agent | First-Line Reversal Regimen | Secondary/Adjuvant Therapy |
|---|---|---|---|
| Vitamin K Antagonist | Warfarin (Coumadin) | 4-Factor Prothrombin Complex Concentrate (4F-PCC: Kcentra) 25–50 units/kg IV based on INR | Vitamin K 10 mg slow IV in 100 mL saline over 30 min (maintains hepatic synthesis of factors after PCC clears). |
| Direct Thrombin Inhibitor | Dabigatran (Pradaxa) | Idarucizumab (Praxbind) 5g IV (administered as two consecutive 2.5g IV boluses) | If unavailable: 4F-PCC 50 units/kg IV OR emergency hemodialysis. |
| Factor Xa Inhibitor | Apixaban (Eliquis)/Rivaroxaban (Xarelto) | Andexanet alfa (Andexxa) IV bolus + 2h infusion (Low or High dose depending on drug timing) | If unavailable: 4-Factor PCC (Kcentra) 50 units/kg IV bolus. |
| Heparin (UFH/LMWH) | Unfractionated Heparin/Enoxaparin | Protamine Sulfate: 1 mg per 100 units of UFH (max 50 mg); 1 mg per 1 mg Enoxaparin (if given < 8h) | Administer slowly over 10 min to avoid severe hypotension and anaphylactoid shock. |
Rupture of an intracranial saccular (berry) aneurysm causes 85% of non-traumatic subarachnoid hemorrhages. Patients describe a 'thunderclap' headache peaking within seconds. Non-contrast head CT within 6 hours of headache onset has > 99.9% sensitivity on modern 3rd-generation scanners. If CT is performed > 6 hours after onset or is equivocal, a lumbar puncture (LP) is mandatory to assess for xanthochromia and persistent red blood cells.
| Ottawa SAH Rule Criteria (Apply to alert patients >= 15 yr with new acute non-traumatic headache peaking in < 1h) | Risk Status | Clinical Significance |
|---|---|---|
| 1. Age >= 40 years | Present (Any 1 of 6) | 100% Sensitivity for SAH; mandates immediate non-contrast head CT. |
| 2. Neck pain or stiffness on examination | Present (Any 1 of 6) | Meningeal irritation from subarachnoid erythrocyte breakdown. |
| 3. Witnessed loss of consciousness at onset | Present (Any 1 of 6) | Transient spike in intracranial pressure exceeding cerebral perfusion pressure. |
| 4. Onset during physical exertion | Present (Any 1 of 6) | Valsalva-induced aneurysm transmural pressure rupture. |
| 5. Thunderclap headache (instantly peaking) | Present (Any 1 of 6) | Classic hallmark; distinguished from gradual-onset tension/migraine headaches. |
| 6. Limited neck flexion on examination | Present (Any 1 of 6) | Nuchal rigidity; inability to touch chin to chest. |
- SAH Medical Management: Blood pressure target SBP < 140–160 mmHg using IV Nicardipine or Labetalol to prevent rebleeding.
- Nimodipine: 60 mg PO q4h started immediately. Nimodipine is a neuroprotective calcium channel blocker that reduces delayed cerebral ischemia (DCI) and vasospasm. DO NOT give intravenously (causes lethal hypotension).
- Seizure Prophylaxis: Levetiracetam (Keppra) 1000–1500 mg IV in aneurysmal SAH to prevent seizure-induced rebleeding spikes.
- Emergent Neurosurgical Consultation: For external ventricular drain (EVD) placement in acute hydrocephalus and definitive aneurysm coiling or surgical clipping.
Vertebrobasilar (posterior circulation) strokes present with vertigo, ataxia, vomiting, and visual disturbances, often misdiagnosed as benign peripheral vertigo. Look for the '5 D's': Dizziness, Dysarthria, Dysphagia, Diplopia, and Dysmetria. The three-step HINTS exam (Head Impulse, Nystagmus, Test of Skew) is more sensitive than early MRI (99% vs 80%) in the first 24–48 hours for distinguishing central cerebellar/brainstem stroke from benign acute vestibular syndrome (vestibular neuritis).
| HINTS Component | Benign Peripheral Vertigo (Vestibular Neuritis) | Central Stroke (Cerebellar/Brainstem Infarct) |
|---|---|---|
| Head Impulse Test (HIT) | Abnormal (Refixation saccade present when head rapidly rotated toward affected side) | NORMAL (Vestibulo-ocular reflex intact; eyes stay fixed on examiner's nose without catch-up saccade) |
| Nystagmus | Unidirectional, horizontal, beats only in one direction regardless of gaze; suppresses with fixation | Bidirectional/Direction-changing on eccentric gaze OR pure vertical/torsional nystagmus |
| Test of Skew | No vertical ocular misalignment | Vertical misalignment on alternating cover test (skew deviation; one eye shifts up/down when uncovered) |
Clinical Caution
HINTS Mnemonic for Stroke ('INFARCT'): Impulse Normal, Fast-phase Alternating, Refixation on Cover Test. Any ONE central finding indicates acute stroke and mandates emergency neurology consultation and vascular neuroimaging.
Test Your Acute Ischemic & Hemorrhagic Stroke Clinical Acumen
Directly launch an active-recall practice block from our validated question bank with comprehensive explanations and distractor analyses.
Distinguish primary life-threats from mimics. On board exams (COMLEX Level 1, 2-CE, 3 & USMLE), initial stabilizing interventions (airway, IV access, non-invasive ventilation, empiric reversal) always take precedence over diagnostic imaging.
Evaluate autonomic tone: Sympathetic viscerosomatics (T1–L2) cause acute paraspinal tissue texture changes (erythema, bogginess, hypertonicity). Suboccipital release (CN X Vagus) and rib raising normalize autonomic outflow and thoracic cage mechanics.