Acute stroke in ICU: ischaemic, haemorrhagic, and neurocritical care

Cinematic ICU scene of an acute stroke patient with a non-contrast CT brain showing a dense middle cerebral artery sign, an alteplase infusion running, a thrombectomy device on the sterile tray, a blood-pressure target on the monitor, clinical-blue lighting, medical educational, no faces, no text — FigureAcute stroke — time is brain, 1.9 million neurons a minute. Ischaemic (80%): alteplase within 4.5h, thrombectomy for large-vessel occlusion within 6–24h (DAWN, DEFUSE-3), permissive hypertension (SBP ≤185 for thrombolysis, ≤220 without). Haemorrhagic (20%): controlled hypotension SBP <140 (INTERACT2), reverse the coagulopathy, evacuate the cerebellar haematoma >3cm. ICU: normoxia, normocapnia, glucose 6–10, normothermia, swallow before any oral intake, DVT prophylaxis.

Ischaemic vs haemorrhagic stroke ICU management

Feature	Ischaemic (80%)	Haemorrhagic (20%)
CT	Hypodense (dark) area or normal early	Hyperdense (bright/white) area
BP target	PERMISSIVE hypertension (SBP ≤220 without lysis, ≤185 with lysis)	CONTROLLED (SBP 130-140 — INTERACT2)
Reversal of anticoagulants	Not needed (unless thrombolysing)	YES — reverse warfarin/DOAC immediately
Thrombolysis	Alteplase if ≤4.5h + no contraindication	CONTRAINDICATED (bleeding)
Thrombectomy	Large vessel occlusion (6-24h — DAWN/DEFUSE-3)	Not indicated
Antiplatelet	Aspirin 300mg within 24h (after lysis: after 24h)	NOT acutely (may worsen bleeding)
Surgery	Decompressive hemicraniectomy (malignant MCA)	Evacuation (cerebellar >3cm, lobar with deterioration)
ICP management	If malignant oedema	Often (haematoma mass effect)
Mortality	10-20% (30-day)	30-40% (30-day)

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Alteplase vs tenecteplase for ischaemic stroke

Feature	Alteplase (rt-PA)	Tenecteplase (TNK)
Mechanism	Native tissue plasminogen activator	Genetically modified rt-PA (higher fibrin specificity, longer half-life)
Dose	0.9 mg/kg (max 90 mg): 10% bolus + 90% over 60 min	0.25 mg/kg (max 25 mg): single 5-second IV bolus
Administration	Bolus + 60-min infusion (pump, dedicated line)	Single bolus — ideal pre-hospital and during inter-hospital transfer
Regulatory status	Licensed for stroke 0-4.5h (NINDS, ECASS-III)	Off-label for stroke (approved for MI) — increasingly used first-line
Evidence	Gold standard (NINDS 1995, ECASS-III 2008)	EXTEND-IA TNK (2018): better reperfusion pre-thrombectomy; non-inferior outcomes
Fibrin specificity	Lower (more systemic fibrinolysis)	~14-fold higher (less systemic bleeding, fewer remote bleeds)
Symptomatic ICH	2-6% (per trial)	Similar or marginally lower
Practical advantage	Licensed, familiar, protocolised	Bolus — bridges seamlessly to thrombectomy ("drip-and-ship")

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Blood pressure targets after acute stroke

Scenario	Systolic target	Diastolic target	Rationale / agent
Before alteplase (eligibility)	<185 mmHg	<110 mmHg	Lower sICH risk; use labetalol 10-20 mg IV or nicardipine 5-15 mg/h
After alteplase (24h)	<180 mmHg	<105 mmHg	Maintain 24h; each 10 mmHg above 180 ~doubles sICH risk
NOT thrombolysed (permissive HTN)	<220 mmHg	<120 mmHg	Preserve penumbral collateral perfusion pressure
Post-thrombectomy (reperfused)	<160-180 mmHg	<105 mmHg	Prevent hyperperfusion syndrome / haemorrhagic transformation
Spontaneous ICH	130-140 mmHg	—	Limit haematoma expansion (INTERACT2); avoid <110 (ATACH-2 harm)
Cerebral venous sinus thrombosis	Normotension	—	Avoid hypotension (worsens venous-outflow ischaemia)

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ICU management of acute stroke

Distinguish ischaemic vs haemorrhagic — CT head (non-contrast) immediately. Ischaemic: may be normal early, hypodense later. Haemorrhagic: bright (blood) immediately. This determines ENTIRE management
ISCHAEMIC — time-critical interventions:
- Thrombolysis: alteplase 0.9 mg/kg (max 90 mg) if ≤4.5h, no contraindication. 10% bolus, 90% over 60 min
- Thrombectomy: large vessel occlusion (ICA, M1, basilar) + salvageable brain (CT perfusion/MRI mismatch) — up to 24h (DAWN, DEFUSE-3)
- Aspirin 300mg (after thrombolysis: wait 24h; without thrombolysis: within 24h)
- BP: permissive hypertension (SBP ≤185 for thrombolysis; ≤220 without)
HAEMORRHAGIC — damage control:
- BP control: SBP 130-140 (INTERACT2 — labetalol/nicardipine IV). Avoid rapid reduction
- Reverse anticoagulants: vitamin K + PCC for warfarin; andexanet for DOAC; protamine for heparin
- Surgery: cerebellar haematoma >3cm or with hydrocephalus/deterioration → evacuation. Lobar with deterioration → consider evacuation
- ICP management: head elevation 30°, osmotherapy (mannitol/hypertonic saline) if raised ICP
BOTH — general ICU care:
- Airway: intubate if GCS <8 or unable to protect airway
- Oxygen: SpO2 ≥94% (normoxia — avoid hyperoxia)
- Normocapnia: PaCO2 35-40 (avoid hypercapnia → vasodilation → raised ICP)
- Normoglycaemia: 6-10 mmol/L (avoid hypo/hyperglycaemia)
- Normothermia: treat fever (paracetamol, cooling — avoid hyperthermia)
- Swallow assessment: BEFORE oral intake (dysphagia → aspiration)
- DVT prophylaxis: LMWH (ischaemic: after 48h; haemorrhagic: after 24-48h stabilisation)
- Nutrition: early enteral (NG/PEG if dysphagic)
Decompressive hemicraniectomy — for malignant MCA syndrome (ischaemic stroke with severe oedema → brain shift → herniation). Within 48h, age <60 (DESTINY, DECIMAL, HAMLET trials)

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Haemorrhagic transformation of ischaemic stroke

Recognise the entity. Haemorrhagic transformation (HT) = bleeding into an ischaemic infarct. Petechial HT occurs in up to 40% of untreated MCA infarcts (often asymptomatic); thrombolysis raises symptomatic ICH (sICH) to 2-6%
Classify radiologically (ECASS definitions). HI-1/HI-2 = haemorrhagic infarct (petechiae along margins, usually asymptomatic, may signal successful reperfusion). PH-1/PH-2 = parenchymal haematoma (space-occupying, >30% infarct + mass effect). Only PH-2 reliably worsens outcome
Identify risk factors. Large infarct volume, high NIHSS, delayed reperfusion, glucose >10 mmol/L, SBP >180 post-lysis, prior antiplatelet/anticoagulant use, cardioembolic aetiology
Strict BP control post-lysis. SBP <180 / DBP <105 for 24h — check every 15 min for 2h, every 30 min for 6h, then hourly. Each 10-mmHg rise above 180 nearly doubles sICH risk
If sICH develops. STOP alteplase infusion immediately; urgent non-contrast CT; give cryoprecipitate (10 units, replenish fibrinogen >1.5 g/L) ± tranexamic acid 1 g IV; reverse any antithrombotic; control BP aggressively; treat raised ICP (osmotherapy, head elevation 30°). Neurosurgical evacuation rarely helpful (deep bleeds) but discuss for large lobar clots
Delay restart of antithrombotics. No antiplatelet/anticoagulant for 24h after lysis; re-image with CT before starting aspirin

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Raised intracranial pressure in acute stroke

Identify the cause. Malignant MCA oedema (ischaemic, peak 24-72h); large ICH with perilesional oedema and mass effect; hydrocephalus from intraventricular extension or posterior-fossa clot obstructing the fourth ventricle; cerebral venous sinus thrombosis
Tier 1 — basics (apply to ALL). Head of bed 30°, neutral neck position (no venous jamming), normoxia (SpO2 ≥94%), normocapnia (PaCO2 35-40), normoglycaemia (6-10 mmol/L), normothermia (<37.5°C), maintain CPP >60 mmHg (avoid hypotension), adequate sedation/analgesia if intubated
Tier 2 — osmotherapy. Mannitol 20% 0.5 g/kg bolus (osmolality target <320, hold if osmolar gap >18) OR hypertonic saline (3% infusion / 5% / 23.4% bolus; Na target 145-155 mmol/L). Sequential or alternating therapy for refractory rises; ensure euvolaemia
Tier 3 — definitive surgical. DECOMPRESSIVE hemicraniectomy (malignant MCA, age <60, within 48h — DESTINY/DECIMAL/HAMLET); external ventricular drain (EVD) for hydrocephalus/intraventricular blood ± intraventricular rt-PA; suboccipital craniectomy + evacuation for cerebellar clot >3 cm with brainstem compression
AVOID. Prophylactic hyperventilation (PaCO2 <30) — use only briefly for impending herniation; corticosteroids (ineffective in cytotoxic stroke oedema, may worsen outcome); aggressive fluid restriction; hypotonic fluids
Monitor. Serial GCS/pupils every 15-30 min; routine CT at 24-72h for large territory strokes; invasive parenchymal ICP monitor if intubated and exam unreliable; continuous EEG if non-convulsive seizures suspected

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Decompressive hemicraniectomy decision pathway (malignant MCA)

Screen for malignancy risk early. Complete MCA territory infarct (NIHSS >15); >2/3 MCA hypodensity on initial CT; large CT-perfusion or DWI deficit; prior stroke, AF, heart failure, high glucose — these DESTINY/DECIMAL/HAMLET risk factors predict malignant course
Time window. Within 48h of symptom onset (pooled DESTINY/DECIMAL/HAMLET analysis). Earlier surgery = better outcome; do not wait for herniation
Age stratification. Age <60: clear benefit (absolute mortality reduction ~50%, NNT ~2 for survival with mRS ≤3). Age >60 (DESTINY-2): survival benefit but more survivors severely disabled (mRS 4) — decision individualised with goals-of-care discussion
Dominant vs non-dominant hemisphere. Operate on BOTH sides — no evidence to withhold for dominant (left) hemisphere on grounds of aphasia; burden of aphasia is overstated relative to death from herniation
Procedure. Large (>12 cm diameter) fronto-temporo-parietal craniectomy — too small a flap is ineffective and increases outward-bulging complications; durotomy/duroplasty; optional anterior temporal lobectomy
Post-operative ICU care. Brain swells outward through bone defect (lowering ICP); manage swelling, control temperature/glucose/BP, plan cranioplasty at 6-12 weeks once atrophied and stable

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SAQ — Malignant MCA infarction

10 minutes · 10 marks

A 54-year-old man presents 90 minutes after sudden onset of right-sided weakness and global aphasia. NIHSS 22. Non-contrast CT shows a hyperdense left MCA sign and hypodensity involving more than half the left MCA territory. He receives alteplase within the window. Eighteen hours later his GCS drops from 14 to 9 (E1V2M6) with a new right pupillary sluggishness, and repeat CT shows a large left MCA infarct with 7 mm midline shift.

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SAQ — Blood pressure management after thrombolysis

10 minutes · 10 marks

A 68-year-old woman with an acute right MCA ischaemic stroke receives IV alteplase 2 hours after symptom onset after BP was confirmed at 158/86 mmHg. Ninety minutes into the infusion her blood pressure has risen to 195/105 mmHg. She remains asymptomatic with GCS 15 and a normal neurological examination unchanged from baseline.

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SAQ — Acute stroke ICU management after thrombectomy

10 minutes · 10 marks

A 62-year-old man is admitted to ICU intubated and sedated after successful endovascular thrombectomy (TICI 3 reperfusion) for an acute left M1 occlusion. NIHSS was 18 before the procedure and is 8 as sedation weans. Pre-procedure CT perfusion showed a large penumbral mismatch. On arrival his BP is 168/92 mmHg, temperature 37.9°C and glucose 11.4 mmol/L.

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SAQ — Malignant MCA syndrome in an older patient

10 minutes · 10 marks

A 71-year-old woman with known atrial fibrillation presents with sudden left-sided weakness and left hemineglect; NIHSS is 19. She was outside the thrombolysis window. At 36 hours her GCS has fallen from 13 (E3V4M6) to 10 (E2V3M5), her left pupil is 5 mm and sluggish, and CT shows a complete right MCA infarct with 8 mm midline shift at the pineal gland and effacement of the basal cisterns.

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Clinical pearls

Ischaemic vs ICH vs SAH ICU pathway classification and monitoring priorities — FigureClassify stroke type first — BP, anticoagulation, and surgical thresholds diverge completely.

Stroke ICU management board: thrombolysis/thrombectomy windows, ICH BP, decompressive craniectomy criteria — FigureManagement map — door-to-needle/device, ICH BP control, malignant MCA decompression thresholds.

High-yield acute stroke ICU points for CICM/FFICM exam

Time is brain. Ischaemic stroke: 1.9 million neurons lost per minute without reperfusion. THROMBOLYSIS within 4.5h (alteplase). THROMBECTOMY up to 24h (if large vessel + salvageable brain — DAWN, DEFUSE-3). Each minute of delay → worse outcome. Door-to-needle (thrombolysis) target: <45 min. Door-to-groin puncture (thrombectomy): <90 min.[1] }
Thrombectomy extended window: DAWN and DEFUSE-3. DAWN (2018): thrombectomy 6-24h after symptom onset (with CT perfusion/MRI mismatch — salvageable penumbra). Reduced disability (functional independence 49% vs 13%). DEFUSE-3 (2018): 6-16h window, similar benefit. REQUIREMENTS: large vessel occlusion (ICA, M1, basilar) + salvageable brain (perfusion mismatch). These trials DOUBLED the thrombectomy window (from 6h to 24h).[2] }
Alteplase (thrombolysis) — within 4.5h, with contraindications. DOSE: 0.9 mg/kg (max 90 mg) — 10% bolus over 1 min, 90% infusion over 60 min. CONTRAINDICATIONS: prior ICH, recent surgery/trauma, active bleeding, INR >1.7, platelets <100, SBP >185 (or >185 after labetalol), recent MI. MAJOR BLEEDING (symptomatic ICH): 2-6% (acceptable for benefit). NINDS trial (1995): alteplase within 3h improved outcomes. ECASS III (2008): extended to 4.5h.[1] }
Permissive hypertension for ischaemic stroke. WITHOUT thrombolysis: SBP ≤220 mmHg (allow high BP to perfuse penumbra — collateral flow depends on pressure). WITH thrombolysis: SBP ≤185 mmHg (before lysis) and ≤180 for 24h after (reduce haemorrhagic transformation risk). AVOID: rapid BP reduction (may worsen ischaemia by reducing collateral perfusion). If treating: labetalol (IV — careful titration), nicardipine (IV infusion — smooth).[1] }
Controlled hypotension for haemorrhagic stroke (ICH). INTERACT2 (2013): intensive BP lowering (SBP <140) vs standard (<180). Result: trend to better functional outcome (OR 0.87, p=0.06 — borderline significant) and LESS haematoma expansion. ATACH-2 (2016): even more intensive (<110-140) → NO additional benefit, MORE renal adverse events. CURRENT: target SBP 130-140 (not <110). Reduce SLOWLY (avoid sudden drop → ischaemia).[4] }
Reverse anticoagulants immediately in ICH. WARFARIN: vitamin K 10 mg IV + PCC (prothrombin complex concentrate — 25-50 IU/kg, faster than FFP). DOAC: andexanet alfa (for apixaban, rivaroxaban) OR PCC (if andexanet unavailable). HEPARIN: protamine sulphate. ANTIPLATELETS: platelet transfusion controversial (PATCH trial — may worsen) — generally NOT transfused unless surgical. TIME IS CRITICAL — ongoing anticoagulation → haematoma expansion → worse outcome.[5] }
Decompressive hemicraniectomy for malignant MCA syndrome. DESTINY, DECIMAL, HAMLET trials (2007-2014): decompressive hemicraniectomy (within 48h of stroke onset) for malignant MCA infarction (large MCA stroke → severe oedema → midline shift → herniation) in patients <60. Result: REDUCED mortality (from 80% to 20%) and improved functional outcomes (many survivors independent or mildly dependent). AGE <60: clear benefit. Age >60: less clear benefit (DESTINY-2 — some survive but more severely disabled).[1] }
Cerebellar haemorrhage — surgery can be life-saving. INDICATIONS for evacuation: (1) Haematoma >3 cm diameter. (2) Brainstem compression. (3) Hydrocephalus (fourth ventricle obstruction). (4) Deteriorating consciousness. SUBOCCIPITAL craniectomy + haematoma evacuation → relieves brainstem compression → can prevent death. LOBAR haemorrhage: surgery more controversial (STICH I/II — no overall benefit; selected cases with superficial haematoma + deterioration).[5] }
Swallow assessment BEFORE oral intake. Dysphagia after stroke: 50-80% (neurological impairment of swallow). Aspiration risk: HIGH (silent aspiration common). PRACTICE: nil by mouth until swallow assessment. Screen: bedside (water swallow — 3 oz water, no coughing/choking). If fail: formal assessment (SLP — speech language pathology). If dysphagia: NG tube (short-term) or PEG (long-term). Aspiration pneumonia: major cause of death post-stroke.[1] }
Normoglycaemia — avoid hypo/hyperglycaemia. HYPOGLYCAEMIA: mimics stroke (focal deficits), worsens ischaemic brain injury. Treat (<3.5: 50 mL 50% dextrose IV). HYPERGLYCAEMIA: worsens outcome (glucose >10 → worse outcomes in ischaemic and haemorrhagic stroke). Treat: insulin (sliding scale or infusion — target 6-10 mmol/L). Avoid: hypoglycaemia from over-treatment (insulin). GIST (Glucose Insulin in Stroke Trial): insulin infusion in hyperglycaemic stroke — no clear benefit, but glycaemic control still recommended.[1] }
Normothermia — treat fever. FEVER after stroke: worsens outcome (increased metabolic demand, excitotoxicity, blood-brain barrier disruption). CAUSES: infection (pneumonia, UTI), central (hypothalamic injury), DVT. TREAT: paracetamol (1g QDS), physical cooling (cooling blankets — if refractory). AVOID: therapeutic hypothermia for stroke (COOL-AID, ICTuS — no clear benefit in ischaemic stroke; used for cardiac arrest, not routine stroke). Target: temperature <37.5°C.[1] }
Normocapnia — avoid hypercapnia. Hypercapnia (PaCO2 >45): cerebral vasodilation → increased cerebral blood volume → raised ICP. Hypocapnia (PaCO2 <35): cerebral vasoconstriction → reduced CBF → ischaemia (especially penumbra). TARGET: PaCO2 35-40 mmHg (normocapnia). If ventilated: monitor EtCO2 and PaCO2. Avoid: prophylactic hyperventilation (only for acute ICP crisis — temporary).[1] }
DVT prophylaxis — balance bleeding vs thrombosis. Stroke patients: HIGH VTE risk (immobility, paresis). ISCHAEMIC: LMWH (enoxaparin 40 mg) — start after 48h (PREVAIL trial — started day 2, reduced VTE, low symptomatic ICH risk). HAEMORRHAGIC: LMWH after 24-48h stabilisation (no haematoma expansion). If high bleeding risk: mechanical (TEDS, IPC) first, then LMWH when safe. Duration: throughout hospitalisation + post-discharge (if immobile).[1] }
Malignant MCA — recognise early. Large MCA stroke (NIHSS >15, >2/3 MCA territory on CT) → high risk of malignant oedema (24-72h). Signs: deteriorating GCS, pupillary changes (uncal herniation), CT: midline shift >5mm. Treatment: decompressive hemicraniectomy (within 48h — if <60). Medical: osmotherapy (mannitol 0.5 g/kg, hypertonic saline — temporary). Hemicraniectomy: removes skull → brain swells outward (not inward → no herniation) → life-saving.[1] }
Haemorrhagic transformation — radiological spectrum matters. ECASS divides HT into HI-1/HI-2 (petechiae within infarct, often asymptomatic and a marker of successful reperfusion) and PH-1/PH-2 (parenchymal haematoma, >30% of infarct with mass effect). Only PH-2 reliably worsens outcome. The feared complication is SYMPTOMATIC ICH (sICH, NIHSS worsening ≥4 with blood on CT) — drives the strict BP limits after thrombolysis.[1] }
The 185/110 then 180/105 rule post-lysis. Before alteplase: lower SBP to <185 / DBP <110 with labetalol 10-20 mg IV push (repeat ×2) or nicardipine infusion 5-15 mg/h. If unachievable: do NOT thrombolyse. After the bolus+infusion: maintain SBP <180 / DBP <105 for 24h — BP every 15 min for 2h, every 30 min for 6h, then hourly. EACH 10-mmHg increment above 180 nearly doubles sICH risk. Small relaxations of protocol have outsized bleeding costs.[1] }
WAKE-UP and EXTEND — from clock to tissue physiology. WAKE-UP (2018): MRI-guided (DWI-FLAIR mismatch) thrombolysis for wake-up stroke. EXTEND (2019): perfusion-imaging-selected thrombolysis up to 9h. Both shift selection from time-of-onset to tissue-salvageability. EXTEND-IA TNK (2018): tenecteplase 0.25 mg/kg non-inferior to alteplase with better pre-thrombectomy reperfusion — increasingly preferred first-line thrombolytic.[14][15][22] }
INTERACT3 — outcome is a bundle, not a single target. INTERACT3 (2023) tested a combined acute-ICH bundle: intensive SBP <140 within 1h, glucose 6-10 mmol/L, temperature <37.5°C, anticoagulation reversal within 1h. Result: improved functional outcome (common OR 0.82) and lower mortality. Reinforces that ICU targets (glucose, temperature, BP) act together — and the targets mirror ischaemic stroke except BP direction reverses.[21] }
Glucose 6-10 — the sweet spot, not tighter. Hypoglycaemia (<3.5 mmol/L) mimics stroke with focal deficits and directly injures neurones. Hyperglycaemia (>10) worsens outcome in both ischaemic and haemorrhagic stroke (lactic acidosis, BBB disruption, increased sICH). GIST (Glucose Insulin in Stroke Trial) showed no outcome benefit from insulin infusion — but pragmatic control to 6-10 mmol/L via sliding-scale remains standard. AVOID aggressive insulin infusions that risk inadvertent hypoglycaemia.[1] }
Temperature <37.5°C — every degree counts. Fever >37.5°C within 72h of stroke roughly doubles mortality and worsens functional outcome (raised metabolic demand, excitotoxicity, BBB leak). Treat the source (pneumonia is #1) AND give paracetamol 1g QDS ± surface cooling blankets. Therapeutic hypothermia is NOT routine for ischaemic stroke (COOL-AID, ICTuS neutral) — reserved for post-cardiac-arrest anoxic brain injury.[1] }
Posterior circulation stroke — basilar occlusion is life-or-death. BASICS (2021): endovascular therapy for basilar-artery occlusion showed no clear overall benefit, but the severe-deficit subgroup (decreased consciousness, NIHSS >10) suggested benefit. BAOCHE extended the window to 24h with positive results. Clues: vertigo, diplopia, dysarthria, ataxia, crossed motor/sensory signs, locked-in syndrome. CTA is mandatory for any suspected brainstem stroke — do NOT rely on non-contrast CT alone.[24] }
Cerebral venous sinus thrombosis — the haemorrhagic stroke you must anticoagulate. Young patient, headache, seizures, parasagittal haemorrhagic infarct; risk factors OCP, pregnancy/puerperium, otitis, thrombophilia. PARADOX of treatment: ANTICOAGULATE even when the venous infarct is haemorrhagic (prevents clot propagation, restores venous outflow). Severe cases with coma/impending herniation: endovascular mechanical thrombectomy ± intrasinus thrombolysis. Often mislabelled as arterial ICH on non-contrast CT — CTV/MRV resolves it.[1] }
Anosognosia and neglect — do not under-triage right-MCA strokes. Non-dominant (right) MCA stroke: left-sided hemineglect, anosognosia (denial of deficit), extinction, poor safety awareness — these patients may appear cheerful and minimise deficits yet have major infarcts; higher fall and aspiration risk. Dominant (left) MCA stroke: aphasia (receptive/Wernicke vs expressive/Broca) with right hemiparesis. A smiling, talking patient with right-MCA stroke can still need thrombolysis/hemicraniectomy — let NIHSS and CT, not affect, drive decisions.[1] }
Seizures post-stroke — early vs late, and cEEG for the unexplained. Early seizures (within 7 days) occur in 5-10% — higher with haemorrhagic, cortical, and large strokes. Treat individual seizures; prophylactic antiseizure medication is NOT recommended. Late seizures (>7 days) define post-stroke epilepsy — treat per epilepsy protocol. In any stroke with unexplained depressed consciousness, consider non-convulsive status — continuous EEG (cEEG) is diagnostic and may reveal sub-clinical seizures mimicking/worsening deficits.[1] }
Mobilisation — early but not aggressive (AVERT). AVERT (2015): very early (within 24h), frequent, high-dose mobilisation after stroke was HARMFUL — worse mRS at 3 months vs usual care. Take-home: do NOT over-mobilise in the first 24h; the recovering brain has vulnerable autoregulation. Balance immobility risks (DVT, pneumonia, deconditioning) by beginning gentle mobilisation from day 2. Applies mainly to ischaemic strokes; haemorrhagic strokes mobilise once stable.[23] }
Start secondary prevention in the ICU — it is time-sensitive. Antiplatelet: aspirin 24h after lysis (or immediately if not lysed). Statin: high-intensity atorvastatin 80 mg (SPARCL — reduced recurrent stroke). Newly detected AF: oral anticoagulation — timing individualised (small stroke/TIA → after 24h re-CT; large stroke → defer ~2 weeks to limit haemorrhagic conversion). Symptomatic carotid stenosis 70-99%: endarterectomy within 2 weeks. Long-term BP lowering benefits both ischaemic and haemorrhagic stroke.[25] }
Dysphagia is the leading driver of post-stroke pneumonia. Aspiration pneumonia kills more stroke survivors than the infarct itself in the subacute phase. Screen every patient BEFORE any oral intake (water-swallow test, 3 oz / 90 mL sipped — coughing/choking or wet voice = fail). Failed screen → formal SLP assessment; nil by mouth with NG feeding in the interim; PEG if prolonged. Head-turn to the weak side, chin-tuck, thickened fluids all reduce aspiration. The single highest-yield ICU nursing intervention after acute stroke is the bedside swallow check.[1] }
Reperfusion injury and hyperperfusion syndrome. After successful thrombolysis/thrombectomy, the reperfused territory can develop BBB disruption, oedema, and haemorrhage (the substrate of haemorrhagic transformation). After carotid endarterectomy/stenting for tight stenosis, HYPERPERFUSION syndrome may follow over days: ipsilateral headache, seizures, focal deficits, cerebral oedema — driven by lost autoregulation in chronically hypoperfused vasculature. Treat with gradual BP lowering (SBP <140) and seizure control. Anticipate it; do not dismiss new headache/seizure post-revascularisation as anxiety.[1] }
Dual antiplatelet therapy (DAPT) — for minor stroke/TIA only, not major stroke. CHANCE and POINT trials: aspirin + clopidogrel for 21-90 days reduces recurrent stroke after minor ischaemic stroke (NIHSS ≤3) or high-risk TIA. KEY constraints: short course (21 days in CHANCE, then aspirin alone — POINT stopped early for haemorrhage with longer use), NOT for moderate-severe stroke (bleeding risk outweighs benefit), and NOT after thrombolysis until the 24h CT excludes haemorrhage. Antiplatelet choice and timing are exam favourites.[1] }

Red flags

Subtle and easily-missed stroke ICU red flags

Wake-up / unknown-onset stroke — use MRI DWI-FLAIR mismatch or CT perfusion to find candidates for thrombolysis (WAKE-UP, EXTEND).[14][15] }
Posterior circulation / basilar occlusion — CTA every brainstem presentation; "vertigo + any motor sign" = basilar until proven otherwise.[24] }
Cerebral venous sinus thrombosis — young patient, parasagittal haemorrhagic infarct → ANTICOAGULATE (do not withhold for blood).[1] }
Haemorrhagic transformation post-lysis — any NIHSS worsening within 24h: STOP infusion, urgent CT, cryoprecipitate ± TXA.[1] }
Malignant MCA trajectory — NIHSS >15 with >2/3 MCA hypodense on early CT: prepare for hemicraniectomy within 48h.[16][17] }
Posterior-fossa clot — sudden deterioration at 24-48h = hydrocephalus/brainstem compression → EVD ± suboccipital evacuation.[5] }
Hyperglycaemia >10 mmol/L — doubles sICH risk and mortality; start sliding-scale insulin.[1] }
Fever >37.5°C — roughly doubles mortality; treat source + paracetamol + active cooling.[1] }
Newly detected AF — anticoagulation timing matters (large stroke → defer ~2 weeks; small/TIA → earlier).[1] }

Prognosis

DAWN trial (Nogueira 2018, NEJM) — thrombectomy 6-24h

RCT: 206 patients with anterior circulation large vessel occlusion, 6-24h from symptom onset, with CT perfusion mismatch (salvageable penumbra). Thrombectomy vs standard medical therapy.

Primary outcome (functional independence at 90 days, mRS 0-2): thrombectomy 49% vs medical 13% (p<0.001)
Mortality: thrombectomy 19% vs medical 18% (similar)
CONCLUSION: Thrombectomy up to 24h (with perfusion imaging to identify salvageable brain) dramatically improves functional outcomes. EXTENDED the thrombectomy window from 6h to 24h. [1]

DEFUSE-3 (Albers 2018, NEJM): similar — thrombectomy 6-16h, functional independence 45% vs 17%. INTERACT2 (2013, NEJM): intensive BP lowering (SBP <140) in ICH — trend to better outcomes (OR 0.87, p=0.06). ATACH-2 (2016, NEJM): even more intensive (<110-140) — no additional benefit, more renal adverse events. Ischaemic stroke mortality: 10-20% (30-day). ICH mortality: 30-40% (30-day).

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NINDS rt-PA Stroke Study (1995, NEJM) — the foundation of thrombolysis

RCT: 624 patients with ischaemic stroke. Alteplase within 3h vs placebo.

Outcome: alteplase — minimal/no disability at 3 months significantly more common (OR 1.7)
Symptomatic ICH: 6.4% alteplase vs 0.6% placebo
CONCLUSION: first RCT proving thrombolysis benefit in acute ischaemic stroke. Established the 3h window and founded modern stroke reperfusion therapy.[7]

ECASS-III (Hacke 2008, NEJM) — extending the window to 4.5h

RCT: 821 patients; alteplase 3-4.5h after symptom onset vs placebo.

Outcome: mRS 0-2 at 90 days — alteplase 52% vs placebo 45% (OR 1.34)
Symptomatic ICH: 2.5% alteplase vs 0.3% placebo
CONCLUSION: extended the thrombolysis window from 3h to 4.5h. The 4.5h ceiling remains the time-based threshold (imaging-based extension per WAKE-UP and EXTEND).[8]

EXTEND-IA TNK (Campbell 2018, NEJM) — tenecteplase before thrombectomy

RCT: 202 patients; tenecteplase 0.25 mg/kg bolus vs alteplase 0.9 mg/kg infusion, both before endovascular thrombectomy.

Outcome: substantially better reperfusion before thrombectomy (22% vs 10%)
Functional independence (mRS 0-2): similar between groups; non-inferiority met
CONCLUSION: tenecteplase non-inferior to alteplase, with the bolus advantage favouring pre-hospital and "drip-and-ship" bridging therapy. Increasingly adopted as first-line thrombolytic.[22]

Pooled DESTINY/DECIMAL/HAMLET (Vahedi 2007, Lancet Neurol) — decompressive hemicraniectomy

Individual-patient meta-analysis of 93 patients, age <60, malignant MCA infarction, hemicraniectomy within 48h vs conservative.

Mortality: hemicraniectomy 24% vs conservative 71% (NNT ~2 for survival)
Favourable outcome (mRS ≤3): hemicraniectomy 43% vs conservative 21%
CONCLUSION: decompressive hemicraniectomy within 48h in patients <60 halves mortality and triples the chance of favourable outcome. DESTINY-2 (Jüttler 2014) extended the evidence to patients >60: a survival benefit persists, but more survivors are left with mRS 4 — prompting goals-of-care discussion.[16][17]

WAKE-UP (Thomalla 2018, NEJM) — thrombolysis for unknown-onset stroke

RCT: 503 patients with wake-up stroke; MRI DWI-FLAIR mismatch used to estimate stroke onset <4.5h. Alteplase vs placebo.

Outcome: mRS 0-1 — alteplase 53% vs placebo 42% (OR 1.61)
Symptomatic ICH: 2.0% alteplase vs 0.4% placebo
CONCLUSION: MRI-based tissue selection enables thrombolysis for wake-up / unknown-onset stroke — shifting the paradigm from the wall-clock to brain physiology.[14]

INTERACT3 (Ma 2023, Lancet) — combined care bundle in acute ICH

RCT: 7,036 patients with acute ICH. Combined early bundle (SBP <140 within 1h, glucose 6-10 mmol/L, temperature <37.5°C, anticoagulation reversal within 1h) vs usual care.

Outcome: improved functional outcome (common OR 0.82); reduced death or dependency
CONCLUSION: ICH outcome is a BUNDLE, not a single intervention. Neurocritical targets mirror ischaemic-stroke ICU targets (glucose, temperature) with reversed BP direction. Standardised early bundles save lives.[21]

References

[1]Powers WJ, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke, 2019.PMID 31662037
[2]Nogueira RG, et al. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct N Engl J Med, 2018.PMID 29129157
[3]Albers GW, et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging N Engl J Med, 2018.PMID 29364767
[4]Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage N Engl J Med, 2013.PMID 23713578
[5]Hemphill JC, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke, 2015.PMID 26022637
[6]Qureshi AI, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage N Engl J Med, 2016.PMID 27276234
[7]NINDS rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke N Engl J Med, 1995.PMID 7477192
[8]Hacke W, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke N Engl J Med, 2008.PMID 18815396
[9]Berkhemer OA, et al. A randomized trial of intraarterial treatment for acute ischemic stroke N Engl J Med, 2015.PMID 25517348
[10]Campbell BCV, et al. Endovascular therapy for ischemic stroke with perfusion-imaging selection N Engl J Med, 2015.PMID 25671797
[11]Saver JL, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke N Engl J Med, 2015.PMID 25882376
[12]Goyal M, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke N Engl J Med, 2015.PMID 25671798
[13]Jovin TG, et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke N Engl J Med, 2015.PMID 25882510
[14]Thomalla G, et al. MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset N Engl J Med, 2018.PMID 29766770
[15]Ma H, et al. Thrombolysis Guided by Perfusion Imaging up to 9 Hours after Onset of Stroke N Engl J Med, 2019.PMID 31067369
[16]Vahedi K, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials Lancet Neurol, 2007.PMID 17303527
[17]Jüttler E, et al. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke N Engl J Med, 2014.PMID 24645942
[18]Mendelow AD, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial Lancet, 2013.PMID 23726393
[19]Baharoglu MI, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial Lancet, 2016.PMID 27178479
[20]Sherman DG, et al. Prevention of venous thromboembolism, recurrent stroke, and other vascular events after acute ischemic stroke: the role of low-molecular-weight heparin and antiplatelet therapy J Stroke Cerebrovasc Dis, 2006.PMID 17904084
[21]Ma L, et al. The third Intensive Care Bundle with Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT3): an international, stepped wedge cluster randomised controlled trial Lancet, 2023.PMID 37245517
[22]Campbell BCV, et al. Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke N Engl J Med, 2018.PMID 29694815
[23]AVERT Trial Collaboration. Efficacy and safety of very early mobilisation within 24 h of stroke onset (AVERT): a randomised controlled trial Lancet, 2015.PMID 25892679
[24]Langezaal LCM, et al. Endovascular Therapy for Stroke Due to Basilar-Artery Occlusion N Engl J Med, 2021.PMID 34010530
[25]Amarenco P, et al. High-dose atorvastatin after stroke or transient ischemic attack N Engl J Med, 2006.PMID 16899775
[26]EFFECTS Trial Collaboration. Safety and efficacy of fluoxetine on functional recovery after acute stroke (EFFECTS): a randomised, double-blind, placebo-controlled trial Lancet Neurol, 2020.PMID 32702335

[1] [1]

Ischaemic vs haemorrhagic stroke ICU management

Feature	Ischaemic (80%)	Haemorrhagic (20%)
CT	Hypodense (dark) area or normal early	Hyperdense (bright/white) area
BP target	PERMISSIVE hypertension (SBP ≤220 without lysis, ≤185 with lysis)	CONTROLLED (SBP 130-140 — INTERACT2)
Reversal of anticoagulants	Not needed (unless thrombolysing)	YES — reverse warfarin/DOAC immediately
Thrombolysis	Alteplase if ≤4.5h + no contraindication	CONTRAINDICATED (bleeding)
Thrombectomy	Large vessel occlusion (6-24h — DAWN/DEFUSE-3)	Not indicated
Antiplatelet	Aspirin 300mg within 24h (after lysis: after 24h)	NOT acutely (may worsen bleeding)
Surgery	Decompressive hemicraniectomy (malignant MCA)	Evacuation (cerebellar >3cm, lobar with deterioration)
ICP management	If malignant oedema	Often (haematoma mass effect)
Mortality	10-20% (30-day)	30-40% (30-day)

[1]

Alteplase vs tenecteplase for ischaemic stroke

Feature	Alteplase (rt-PA)	Tenecteplase (TNK)
Mechanism	Native tissue plasminogen activator	Genetically modified rt-PA (higher fibrin specificity, longer half-life)
Dose	0.9 mg/kg (max 90 mg): 10% bolus + 90% over 60 min	0.25 mg/kg (max 25 mg): single 5-second IV bolus
Administration	Bolus + 60-min infusion (pump, dedicated line)	Single bolus — ideal pre-hospital and during inter-hospital transfer
Regulatory status	Licensed for stroke 0-4.5h (NINDS, ECASS-III)	Off-label for stroke (approved for MI) — increasingly used first-line
Evidence	Gold standard (NINDS 1995, ECASS-III 2008)	EXTEND-IA TNK (2018): better reperfusion pre-thrombectomy; non-inferior outcomes
Fibrin specificity	Lower (more systemic fibrinolysis)	~14-fold higher (less systemic bleeding, fewer remote bleeds)
Symptomatic ICH	2-6% (per trial)	Similar or marginally lower
Practical advantage	Licensed, familiar, protocolised	Bolus — bridges seamlessly to thrombectomy ("drip-and-ship")

[1]

Blood pressure targets after acute stroke

Scenario	Systolic target	Diastolic target	Rationale / agent
Before alteplase (eligibility)	<185 mmHg	<110 mmHg	Lower sICH risk; use labetalol 10-20 mg IV or nicardipine 5-15 mg/h
After alteplase (24h)	<180 mmHg	<105 mmHg	Maintain 24h; each 10 mmHg above 180 ~doubles sICH risk
NOT thrombolysed (permissive HTN)	<220 mmHg	<120 mmHg	Preserve penumbral collateral perfusion pressure
Post-thrombectomy (reperfused)	<160-180 mmHg	<105 mmHg	Prevent hyperperfusion syndrome / haemorrhagic transformation
Spontaneous ICH	130-140 mmHg	—	Limit haematoma expansion (INTERACT2); avoid <110 (ATACH-2 harm)
Cerebral venous sinus thrombosis	Normotension	—	Avoid hypotension (worsens venous-outflow ischaemia)

[1]

ICU management of acute stroke

Distinguish ischaemic vs haemorrhagic — CT head (non-contrast) immediately. Ischaemic: may be normal early, hypodense later. Haemorrhagic: bright (blood) immediately. This determines ENTIRE management
ISCHAEMIC — time-critical interventions:
- Thrombolysis: alteplase 0.9 mg/kg (max 90 mg) if ≤4.5h, no contraindication. 10% bolus, 90% over 60 min
- Thrombectomy: large vessel occlusion (ICA, M1, basilar) + salvageable brain (CT perfusion/MRI mismatch) — up to 24h (DAWN, DEFUSE-3)
- Aspirin 300mg (after thrombolysis: wait 24h; without thrombolysis: within 24h)
- BP: permissive hypertension (SBP ≤185 for thrombolysis; ≤220 without)
HAEMORRHAGIC — damage control:
- BP control: SBP 130-140 (INTERACT2 — labetalol/nicardipine IV). Avoid rapid reduction
- Reverse anticoagulants: vitamin K + PCC for warfarin; andexanet for DOAC; protamine for heparin
- Surgery: cerebellar haematoma >3cm or with hydrocephalus/deterioration → evacuation. Lobar with deterioration → consider evacuation
- ICP management: head elevation 30°, osmotherapy (mannitol/hypertonic saline) if raised ICP
BOTH — general ICU care:
- Airway: intubate if GCS <8 or unable to protect airway
- Oxygen: SpO2 ≥94% (normoxia — avoid hyperoxia)
- Normocapnia: PaCO2 35-40 (avoid hypercapnia → vasodilation → raised ICP)
- Normoglycaemia: 6-10 mmol/L (avoid hypo/hyperglycaemia)
- Normothermia: treat fever (paracetamol, cooling — avoid hyperthermia)
- Swallow assessment: BEFORE oral intake (dysphagia → aspiration)
- DVT prophylaxis: LMWH (ischaemic: after 48h; haemorrhagic: after 24-48h stabilisation)
- Nutrition: early enteral (NG/PEG if dysphagic)
Decompressive hemicraniectomy — for malignant MCA syndrome (ischaemic stroke with severe oedema → brain shift → herniation). Within 48h, age <60 (DESTINY, DECIMAL, HAMLET trials)

[1]

Haemorrhagic transformation of ischaemic stroke

Recognise the entity. Haemorrhagic transformation (HT) = bleeding into an ischaemic infarct. Petechial HT occurs in up to 40% of untreated MCA infarcts (often asymptomatic); thrombolysis raises symptomatic ICH (sICH) to 2-6%
Classify radiologically (ECASS definitions). HI-1/HI-2 = haemorrhagic infarct (petechiae along margins, usually asymptomatic, may signal successful reperfusion). PH-1/PH-2 = parenchymal haematoma (space-occupying, >30% infarct + mass effect). Only PH-2 reliably worsens outcome
Identify risk factors. Large infarct volume, high NIHSS, delayed reperfusion, glucose >10 mmol/L, SBP >180 post-lysis, prior antiplatelet/anticoagulant use, cardioembolic aetiology
Strict BP control post-lysis. SBP <180 / DBP <105 for 24h — check every 15 min for 2h, every 30 min for 6h, then hourly. Each 10-mmHg rise above 180 nearly doubles sICH risk
If sICH develops. STOP alteplase infusion immediately; urgent non-contrast CT; give cryoprecipitate (10 units, replenish fibrinogen >1.5 g/L) ± tranexamic acid 1 g IV; reverse any antithrombotic; control BP aggressively; treat raised ICP (osmotherapy, head elevation 30°). Neurosurgical evacuation rarely helpful (deep bleeds) but discuss for large lobar clots
Delay restart of antithrombotics. No antiplatelet/anticoagulant for 24h after lysis; re-image with CT before starting aspirin

[1]

Raised intracranial pressure in acute stroke

Identify the cause. Malignant MCA oedema (ischaemic, peak 24-72h); large ICH with perilesional oedema and mass effect; hydrocephalus from intraventricular extension or posterior-fossa clot obstructing the fourth ventricle; cerebral venous sinus thrombosis
Tier 1 — basics (apply to ALL). Head of bed 30°, neutral neck position (no venous jamming), normoxia (SpO2 ≥94%), normocapnia (PaCO2 35-40), normoglycaemia (6-10 mmol/L), normothermia (<37.5°C), maintain CPP >60 mmHg (avoid hypotension), adequate sedation/analgesia if intubated
Tier 2 — osmotherapy. Mannitol 20% 0.5 g/kg bolus (osmolality target <320, hold if osmolar gap >18) OR hypertonic saline (3% infusion / 5% / 23.4% bolus; Na target 145-155 mmol/L). Sequential or alternating therapy for refractory rises; ensure euvolaemia
Tier 3 — definitive surgical. DECOMPRESSIVE hemicraniectomy (malignant MCA, age <60, within 48h — DESTINY/DECIMAL/HAMLET); external ventricular drain (EVD) for hydrocephalus/intraventricular blood ± intraventricular rt-PA; suboccipital craniectomy + evacuation for cerebellar clot >3 cm with brainstem compression
AVOID. Prophylactic hyperventilation (PaCO2 <30) — use only briefly for impending herniation; corticosteroids (ineffective in cytotoxic stroke oedema, may worsen outcome); aggressive fluid restriction; hypotonic fluids
Monitor. Serial GCS/pupils every 15-30 min; routine CT at 24-72h for large territory strokes; invasive parenchymal ICP monitor if intubated and exam unreliable; continuous EEG if non-convulsive seizures suspected

[1]

Decompressive hemicraniectomy decision pathway (malignant MCA)

Screen for malignancy risk early. Complete MCA territory infarct (NIHSS >15); >2/3 MCA hypodensity on initial CT; large CT-perfusion or DWI deficit; prior stroke, AF, heart failure, high glucose — these DESTINY/DECIMAL/HAMLET risk factors predict malignant course
Time window. Within 48h of symptom onset (pooled DESTINY/DECIMAL/HAMLET analysis). Earlier surgery = better outcome; do not wait for herniation
Age stratification. Age <60: clear benefit (absolute mortality reduction ~50%, NNT ~2 for survival with mRS ≤3). Age >60 (DESTINY-2): survival benefit but more survivors severely disabled (mRS 4) — decision individualised with goals-of-care discussion
Dominant vs non-dominant hemisphere. Operate on BOTH sides — no evidence to withhold for dominant (left) hemisphere on grounds of aphasia; burden of aphasia is overstated relative to death from herniation
Procedure. Large (>12 cm diameter) fronto-temporo-parietal craniectomy — too small a flap is ineffective and increases outward-bulging complications; durotomy/duroplasty; optional anterior temporal lobectomy
Post-operative ICU care. Brain swells outward through bone defect (lowering ICP); manage swelling, control temperature/glucose/BP, plan cranioplasty at 6-12 weeks once atrophied and stable

[1]

SAQ — Malignant MCA infarction

10 minutes · 10 marks

[1]

SAQ — Blood pressure management after thrombolysis

10 minutes · 10 marks

[1]

SAQ — Acute stroke ICU management after thrombectomy

10 minutes · 10 marks

[1]

SAQ — Malignant MCA syndrome in an older patient

10 minutes · 10 marks

[1]

Clinical pearls

High-yield acute stroke ICU points for CICM/FFICM exam

Time is brain. Ischaemic stroke: 1.9 million neurons lost per minute without reperfusion. THROMBOLYSIS within 4.5h (alteplase). THROMBECTOMY up to 24h (if large vessel + salvageable brain — DAWN, DEFUSE-3). Each minute of delay → worse outcome. Door-to-needle (thrombolysis) target: <45 min. Door-to-groin puncture (thrombectomy): <90 min.[1] }
Thrombectomy extended window: DAWN and DEFUSE-3. DAWN (2018): thrombectomy 6-24h after symptom onset (with CT perfusion/MRI mismatch — salvageable penumbra). Reduced disability (functional independence 49% vs 13%). DEFUSE-3 (2018): 6-16h window, similar benefit. REQUIREMENTS: large vessel occlusion (ICA, M1, basilar) + salvageable brain (perfusion mismatch). These trials DOUBLED the thrombectomy window (from 6h to 24h).[2] }
Alteplase (thrombolysis) — within 4.5h, with contraindications. DOSE: 0.9 mg/kg (max 90 mg) — 10% bolus over 1 min, 90% infusion over 60 min. CONTRAINDICATIONS: prior ICH, recent surgery/trauma, active bleeding, INR >1.7, platelets <100, SBP >185 (or >185 after labetalol), recent MI. MAJOR BLEEDING (symptomatic ICH): 2-6% (acceptable for benefit). NINDS trial (1995): alteplase within 3h improved outcomes. ECASS III (2008): extended to 4.5h.[1] }
Permissive hypertension for ischaemic stroke. WITHOUT thrombolysis: SBP ≤220 mmHg (allow high BP to perfuse penumbra — collateral flow depends on pressure). WITH thrombolysis: SBP ≤185 mmHg (before lysis) and ≤180 for 24h after (reduce haemorrhagic transformation risk). AVOID: rapid BP reduction (may worsen ischaemia by reducing collateral perfusion). If treating: labetalol (IV — careful titration), nicardipine (IV infusion — smooth).[1] }
Controlled hypotension for haemorrhagic stroke (ICH). INTERACT2 (2013): intensive BP lowering (SBP <140) vs standard (<180). Result: trend to better functional outcome (OR 0.87, p=0.06 — borderline significant) and LESS haematoma expansion. ATACH-2 (2016): even more intensive (<110-140) → NO additional benefit, MORE renal adverse events. CURRENT: target SBP 130-140 (not <110). Reduce SLOWLY (avoid sudden drop → ischaemia).[4] }
Reverse anticoagulants immediately in ICH. WARFARIN: vitamin K 10 mg IV + PCC (prothrombin complex concentrate — 25-50 IU/kg, faster than FFP). DOAC: andexanet alfa (for apixaban, rivaroxaban) OR PCC (if andexanet unavailable). HEPARIN: protamine sulphate. ANTIPLATELETS: platelet transfusion controversial (PATCH trial — may worsen) — generally NOT transfused unless surgical. TIME IS CRITICAL — ongoing anticoagulation → haematoma expansion → worse outcome.[5] }
Decompressive hemicraniectomy for malignant MCA syndrome. DESTINY, DECIMAL, HAMLET trials (2007-2014): decompressive hemicraniectomy (within 48h of stroke onset) for malignant MCA infarction (large MCA stroke → severe oedema → midline shift → herniation) in patients <60. Result: REDUCED mortality (from 80% to 20%) and improved functional outcomes (many survivors independent or mildly dependent). AGE <60: clear benefit. Age >60: less clear benefit (DESTINY-2 — some survive but more severely disabled).[1] }
Cerebellar haemorrhage — surgery can be life-saving. INDICATIONS for evacuation: (1) Haematoma >3 cm diameter. (2) Brainstem compression. (3) Hydrocephalus (fourth ventricle obstruction). (4) Deteriorating consciousness. SUBOCCIPITAL craniectomy + haematoma evacuation → relieves brainstem compression → can prevent death. LOBAR haemorrhage: surgery more controversial (STICH I/II — no overall benefit; selected cases with superficial haematoma + deterioration).[5] }
Swallow assessment BEFORE oral intake. Dysphagia after stroke: 50-80% (neurological impairment of swallow). Aspiration risk: HIGH (silent aspiration common). PRACTICE: nil by mouth until swallow assessment. Screen: bedside (water swallow — 3 oz water, no coughing/choking). If fail: formal assessment (SLP — speech language pathology). If dysphagia: NG tube (short-term) or PEG (long-term). Aspiration pneumonia: major cause of death post-stroke.[1] }
Normoglycaemia — avoid hypo/hyperglycaemia. HYPOGLYCAEMIA: mimics stroke (focal deficits), worsens ischaemic brain injury. Treat (<3.5: 50 mL 50% dextrose IV). HYPERGLYCAEMIA: worsens outcome (glucose >10 → worse outcomes in ischaemic and haemorrhagic stroke). Treat: insulin (sliding scale or infusion — target 6-10 mmol/L). Avoid: hypoglycaemia from over-treatment (insulin). GIST (Glucose Insulin in Stroke Trial): insulin infusion in hyperglycaemic stroke — no clear benefit, but glycaemic control still recommended.[1] }
Normothermia — treat fever. FEVER after stroke: worsens outcome (increased metabolic demand, excitotoxicity, blood-brain barrier disruption). CAUSES: infection (pneumonia, UTI), central (hypothalamic injury), DVT. TREAT: paracetamol (1g QDS), physical cooling (cooling blankets — if refractory). AVOID: therapeutic hypothermia for stroke (COOL-AID, ICTuS — no clear benefit in ischaemic stroke; used for cardiac arrest, not routine stroke). Target: temperature <37.5°C.[1] }
Normocapnia — avoid hypercapnia. Hypercapnia (PaCO2 >45): cerebral vasodilation → increased cerebral blood volume → raised ICP. Hypocapnia (PaCO2 <35): cerebral vasoconstriction → reduced CBF → ischaemia (especially penumbra). TARGET: PaCO2 35-40 mmHg (normocapnia). If ventilated: monitor EtCO2 and PaCO2. Avoid: prophylactic hyperventilation (only for acute ICP crisis — temporary).[1] }
DVT prophylaxis — balance bleeding vs thrombosis. Stroke patients: HIGH VTE risk (immobility, paresis). ISCHAEMIC: LMWH (enoxaparin 40 mg) — start after 48h (PREVAIL trial — started day 2, reduced VTE, low symptomatic ICH risk). HAEMORRHAGIC: LMWH after 24-48h stabilisation (no haematoma expansion). If high bleeding risk: mechanical (TEDS, IPC) first, then LMWH when safe. Duration: throughout hospitalisation + post-discharge (if immobile).[1] }
Malignant MCA — recognise early. Large MCA stroke (NIHSS >15, >2/3 MCA territory on CT) → high risk of malignant oedema (24-72h). Signs: deteriorating GCS, pupillary changes (uncal herniation), CT: midline shift >5mm. Treatment: decompressive hemicraniectomy (within 48h — if <60). Medical: osmotherapy (mannitol 0.5 g/kg, hypertonic saline — temporary). Hemicraniectomy: removes skull → brain swells outward (not inward → no herniation) → life-saving.[1] }
Haemorrhagic transformation — radiological spectrum matters. ECASS divides HT into HI-1/HI-2 (petechiae within infarct, often asymptomatic and a marker of successful reperfusion) and PH-1/PH-2 (parenchymal haematoma, >30% of infarct with mass effect). Only PH-2 reliably worsens outcome. The feared complication is SYMPTOMATIC ICH (sICH, NIHSS worsening ≥4 with blood on CT) — drives the strict BP limits after thrombolysis.[1] }
The 185/110 then 180/105 rule post-lysis. Before alteplase: lower SBP to <185 / DBP <110 with labetalol 10-20 mg IV push (repeat ×2) or nicardipine infusion 5-15 mg/h. If unachievable: do NOT thrombolyse. After the bolus+infusion: maintain SBP <180 / DBP <105 for 24h — BP every 15 min for 2h, every 30 min for 6h, then hourly. EACH 10-mmHg increment above 180 nearly doubles sICH risk. Small relaxations of protocol have outsized bleeding costs.[1] }
WAKE-UP and EXTEND — from clock to tissue physiology. WAKE-UP (2018): MRI-guided (DWI-FLAIR mismatch) thrombolysis for wake-up stroke. EXTEND (2019): perfusion-imaging-selected thrombolysis up to 9h. Both shift selection from time-of-onset to tissue-salvageability. EXTEND-IA TNK (2018): tenecteplase 0.25 mg/kg non-inferior to alteplase with better pre-thrombectomy reperfusion — increasingly preferred first-line thrombolytic.[14][15][22] }
INTERACT3 — outcome is a bundle, not a single target. INTERACT3 (2023) tested a combined acute-ICH bundle: intensive SBP <140 within 1h, glucose 6-10 mmol/L, temperature <37.5°C, anticoagulation reversal within 1h. Result: improved functional outcome (common OR 0.82) and lower mortality. Reinforces that ICU targets (glucose, temperature, BP) act together — and the targets mirror ischaemic stroke except BP direction reverses.[21] }
Glucose 6-10 — the sweet spot, not tighter. Hypoglycaemia (<3.5 mmol/L) mimics stroke with focal deficits and directly injures neurones. Hyperglycaemia (>10) worsens outcome in both ischaemic and haemorrhagic stroke (lactic acidosis, BBB disruption, increased sICH). GIST (Glucose Insulin in Stroke Trial) showed no outcome benefit from insulin infusion — but pragmatic control to 6-10 mmol/L via sliding-scale remains standard. AVOID aggressive insulin infusions that risk inadvertent hypoglycaemia.[1] }
Temperature <37.5°C — every degree counts. Fever >37.5°C within 72h of stroke roughly doubles mortality and worsens functional outcome (raised metabolic demand, excitotoxicity, BBB leak). Treat the source (pneumonia is #1) AND give paracetamol 1g QDS ± surface cooling blankets. Therapeutic hypothermia is NOT routine for ischaemic stroke (COOL-AID, ICTuS neutral) — reserved for post-cardiac-arrest anoxic brain injury.[1] }
Posterior circulation stroke — basilar occlusion is life-or-death. BASICS (2021): endovascular therapy for basilar-artery occlusion showed no clear overall benefit, but the severe-deficit subgroup (decreased consciousness, NIHSS >10) suggested benefit. BAOCHE extended the window to 24h with positive results. Clues: vertigo, diplopia, dysarthria, ataxia, crossed motor/sensory signs, locked-in syndrome. CTA is mandatory for any suspected brainstem stroke — do NOT rely on non-contrast CT alone.[24] }
Cerebral venous sinus thrombosis — the haemorrhagic stroke you must anticoagulate. Young patient, headache, seizures, parasagittal haemorrhagic infarct; risk factors OCP, pregnancy/puerperium, otitis, thrombophilia. PARADOX of treatment: ANTICOAGULATE even when the venous infarct is haemorrhagic (prevents clot propagation, restores venous outflow). Severe cases with coma/impending herniation: endovascular mechanical thrombectomy ± intrasinus thrombolysis. Often mislabelled as arterial ICH on non-contrast CT — CTV/MRV resolves it.[1] }
Anosognosia and neglect — do not under-triage right-MCA strokes. Non-dominant (right) MCA stroke: left-sided hemineglect, anosognosia (denial of deficit), extinction, poor safety awareness — these patients may appear cheerful and minimise deficits yet have major infarcts; higher fall and aspiration risk. Dominant (left) MCA stroke: aphasia (receptive/Wernicke vs expressive/Broca) with right hemiparesis. A smiling, talking patient with right-MCA stroke can still need thrombolysis/hemicraniectomy — let NIHSS and CT, not affect, drive decisions.[1] }
Seizures post-stroke — early vs late, and cEEG for the unexplained. Early seizures (within 7 days) occur in 5-10% — higher with haemorrhagic, cortical, and large strokes. Treat individual seizures; prophylactic antiseizure medication is NOT recommended. Late seizures (>7 days) define post-stroke epilepsy — treat per epilepsy protocol. In any stroke with unexplained depressed consciousness, consider non-convulsive status — continuous EEG (cEEG) is diagnostic and may reveal sub-clinical seizures mimicking/worsening deficits.[1] }
Mobilisation — early but not aggressive (AVERT). AVERT (2015): very early (within 24h), frequent, high-dose mobilisation after stroke was HARMFUL — worse mRS at 3 months vs usual care. Take-home: do NOT over-mobilise in the first 24h; the recovering brain has vulnerable autoregulation. Balance immobility risks (DVT, pneumonia, deconditioning) by beginning gentle mobilisation from day 2. Applies mainly to ischaemic strokes; haemorrhagic strokes mobilise once stable.[23] }
Start secondary prevention in the ICU — it is time-sensitive. Antiplatelet: aspirin 24h after lysis (or immediately if not lysed). Statin: high-intensity atorvastatin 80 mg (SPARCL — reduced recurrent stroke). Newly detected AF: oral anticoagulation — timing individualised (small stroke/TIA → after 24h re-CT; large stroke → defer ~2 weeks to limit haemorrhagic conversion). Symptomatic carotid stenosis 70-99%: endarterectomy within 2 weeks. Long-term BP lowering benefits both ischaemic and haemorrhagic stroke.[25] }
Dysphagia is the leading driver of post-stroke pneumonia. Aspiration pneumonia kills more stroke survivors than the infarct itself in the subacute phase. Screen every patient BEFORE any oral intake (water-swallow test, 3 oz / 90 mL sipped — coughing/choking or wet voice = fail). Failed screen → formal SLP assessment; nil by mouth with NG feeding in the interim; PEG if prolonged. Head-turn to the weak side, chin-tuck, thickened fluids all reduce aspiration. The single highest-yield ICU nursing intervention after acute stroke is the bedside swallow check.[1] }
Reperfusion injury and hyperperfusion syndrome. After successful thrombolysis/thrombectomy, the reperfused territory can develop BBB disruption, oedema, and haemorrhage (the substrate of haemorrhagic transformation). After carotid endarterectomy/stenting for tight stenosis, HYPERPERFUSION syndrome may follow over days: ipsilateral headache, seizures, focal deficits, cerebral oedema — driven by lost autoregulation in chronically hypoperfused vasculature. Treat with gradual BP lowering (SBP <140) and seizure control. Anticipate it; do not dismiss new headache/seizure post-revascularisation as anxiety.[1] }
Dual antiplatelet therapy (DAPT) — for minor stroke/TIA only, not major stroke. CHANCE and POINT trials: aspirin + clopidogrel for 21-90 days reduces recurrent stroke after minor ischaemic stroke (NIHSS ≤3) or high-risk TIA. KEY constraints: short course (21 days in CHANCE, then aspirin alone — POINT stopped early for haemorrhage with longer use), NOT for moderate-severe stroke (bleeding risk outweighs benefit), and NOT after thrombolysis until the 24h CT excludes haemorrhage. Antiplatelet choice and timing are exam favourites.[1] }

Red flags

Subtle and easily-missed stroke ICU red flags

Wake-up / unknown-onset stroke — use MRI DWI-FLAIR mismatch or CT perfusion to find candidates for thrombolysis (WAKE-UP, EXTEND).[14][15] }
Posterior circulation / basilar occlusion — CTA every brainstem presentation; "vertigo + any motor sign" = basilar until proven otherwise.[24] }
Cerebral venous sinus thrombosis — young patient, parasagittal haemorrhagic infarct → ANTICOAGULATE (do not withhold for blood).[1] }
Haemorrhagic transformation post-lysis — any NIHSS worsening within 24h: STOP infusion, urgent CT, cryoprecipitate ± TXA.[1] }
Malignant MCA trajectory — NIHSS >15 with >2/3 MCA hypodense on early CT: prepare for hemicraniectomy within 48h.[16][17] }
Posterior-fossa clot — sudden deterioration at 24-48h = hydrocephalus/brainstem compression → EVD ± suboccipital evacuation.[5] }
Hyperglycaemia >10 mmol/L — doubles sICH risk and mortality; start sliding-scale insulin.[1] }
Fever >37.5°C — roughly doubles mortality; treat source + paracetamol + active cooling.[1] }
Newly detected AF — anticoagulation timing matters (large stroke → defer ~2 weeks; small/TIA → earlier).[1] }

Prognosis

DAWN trial (Nogueira 2018, NEJM) — thrombectomy 6-24h

RCT: 206 patients with anterior circulation large vessel occlusion, 6-24h from symptom onset, with CT perfusion mismatch (salvageable penumbra). Thrombectomy vs standard medical therapy.

Primary outcome (functional independence at 90 days, mRS 0-2): thrombectomy 49% vs medical 13% (p<0.001)
Mortality: thrombectomy 19% vs medical 18% (similar)
CONCLUSION: Thrombectomy up to 24h (with perfusion imaging to identify salvageable brain) dramatically improves functional outcomes. EXTENDED the thrombectomy window from 6h to 24h. [1]

[1]

NINDS rt-PA Stroke Study (1995, NEJM) — the foundation of thrombolysis

RCT: 624 patients with ischaemic stroke. Alteplase within 3h vs placebo.

Outcome: alteplase — minimal/no disability at 3 months significantly more common (OR 1.7)
Symptomatic ICH: 6.4% alteplase vs 0.6% placebo
CONCLUSION: first RCT proving thrombolysis benefit in acute ischaemic stroke. Established the 3h window and founded modern stroke reperfusion therapy.[7]

ECASS-III (Hacke 2008, NEJM) — extending the window to 4.5h

RCT: 821 patients; alteplase 3-4.5h after symptom onset vs placebo.

Outcome: mRS 0-2 at 90 days — alteplase 52% vs placebo 45% (OR 1.34)
Symptomatic ICH: 2.5% alteplase vs 0.3% placebo
CONCLUSION: extended the thrombolysis window from 3h to 4.5h. The 4.5h ceiling remains the time-based threshold (imaging-based extension per WAKE-UP and EXTEND).[8]

EXTEND-IA TNK (Campbell 2018, NEJM) — tenecteplase before thrombectomy

RCT: 202 patients; tenecteplase 0.25 mg/kg bolus vs alteplase 0.9 mg/kg infusion, both before endovascular thrombectomy.

Outcome: substantially better reperfusion before thrombectomy (22% vs 10%)
Functional independence (mRS 0-2): similar between groups; non-inferiority met
CONCLUSION: tenecteplase non-inferior to alteplase, with the bolus advantage favouring pre-hospital and "drip-and-ship" bridging therapy. Increasingly adopted as first-line thrombolytic.[22]

Pooled DESTINY/DECIMAL/HAMLET (Vahedi 2007, Lancet Neurol) — decompressive hemicraniectomy

Individual-patient meta-analysis of 93 patients, age <60, malignant MCA infarction, hemicraniectomy within 48h vs conservative.

Mortality: hemicraniectomy 24% vs conservative 71% (NNT ~2 for survival)
Favourable outcome (mRS ≤3): hemicraniectomy 43% vs conservative 21%
CONCLUSION: decompressive hemicraniectomy within 48h in patients <60 halves mortality and triples the chance of favourable outcome. DESTINY-2 (Jüttler 2014) extended the evidence to patients >60: a survival benefit persists, but more survivors are left with mRS 4 — prompting goals-of-care discussion.[16][17]

WAKE-UP (Thomalla 2018, NEJM) — thrombolysis for unknown-onset stroke

RCT: 503 patients with wake-up stroke; MRI DWI-FLAIR mismatch used to estimate stroke onset <4.5h. Alteplase vs placebo.

Outcome: mRS 0-1 — alteplase 53% vs placebo 42% (OR 1.61)
Symptomatic ICH: 2.0% alteplase vs 0.4% placebo
CONCLUSION: MRI-based tissue selection enables thrombolysis for wake-up / unknown-onset stroke — shifting the paradigm from the wall-clock to brain physiology.[14]

INTERACT3 (Ma 2023, Lancet) — combined care bundle in acute ICH

RCT: 7,036 patients with acute ICH. Combined early bundle (SBP <140 within 1h, glucose 6-10 mmol/L, temperature <37.5°C, anticoagulation reversal within 1h) vs usual care.

Outcome: improved functional outcome (common OR 0.82); reduced death or dependency
CONCLUSION: ICH outcome is a BUNDLE, not a single intervention. Neurocritical targets mirror ischaemic-stroke ICU targets (glucose, temperature) with reversed BP direction. Standardised early bundles save lives.[21]

References

[1]Powers WJ, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke, 2019.PMID 31662037
[2]Nogueira RG, et al. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct N Engl J Med, 2018.PMID 29129157
[3]Albers GW, et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging N Engl J Med, 2018.PMID 29364767
[4]Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage N Engl J Med, 2013.PMID 23713578
[5]Hemphill JC, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke, 2015.PMID 26022637
[6]Qureshi AI, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage N Engl J Med, 2016.PMID 27276234
[7]NINDS rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke N Engl J Med, 1995.PMID 7477192
[8]Hacke W, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke N Engl J Med, 2008.PMID 18815396
[9]Berkhemer OA, et al. A randomized trial of intraarterial treatment for acute ischemic stroke N Engl J Med, 2015.PMID 25517348
[10]Campbell BCV, et al. Endovascular therapy for ischemic stroke with perfusion-imaging selection N Engl J Med, 2015.PMID 25671797
[11]Saver JL, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke N Engl J Med, 2015.PMID 25882376
[12]Goyal M, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke N Engl J Med, 2015.PMID 25671798
[13]Jovin TG, et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke N Engl J Med, 2015.PMID 25882510
[14]Thomalla G, et al. MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset N Engl J Med, 2018.PMID 29766770
[15]Ma H, et al. Thrombolysis Guided by Perfusion Imaging up to 9 Hours after Onset of Stroke N Engl J Med, 2019.PMID 31067369
[16]Vahedi K, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials Lancet Neurol, 2007.PMID 17303527
[17]Jüttler E, et al. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke N Engl J Med, 2014.PMID 24645942
[18]Mendelow AD, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial Lancet, 2013.PMID 23726393
[19]Baharoglu MI, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial Lancet, 2016.PMID 27178479
[20]Sherman DG, et al. Prevention of venous thromboembolism, recurrent stroke, and other vascular events after acute ischemic stroke: the role of low-molecular-weight heparin and antiplatelet therapy J Stroke Cerebrovasc Dis, 2006.PMID 17904084
[21]Ma L, et al. The third Intensive Care Bundle with Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT3): an international, stepped wedge cluster randomised controlled trial Lancet, 2023.PMID 37245517
[22]Campbell BCV, et al. Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke N Engl J Med, 2018.PMID 29694815
[23]AVERT Trial Collaboration. Efficacy and safety of very early mobilisation within 24 h of stroke onset (AVERT): a randomised controlled trial Lancet, 2015.PMID 25892679
[24]Langezaal LCM, et al. Endovascular Therapy for Stroke Due to Basilar-Artery Occlusion N Engl J Med, 2021.PMID 34010530
[25]Amarenco P, et al. High-dose atorvastatin after stroke or transient ischemic attack N Engl J Med, 2006.PMID 16899775
[26]EFFECTS Trial Collaboration. Safety and efficacy of fluoxetine on functional recovery after acute stroke (EFFECTS): a randomised, double-blind, placebo-controlled trial Lancet Neurol, 2020.PMID 32702335

Your progress

SAQ — Malignant MCA infarction

SAQ — Blood pressure management after thrombolysis

SAQ — Acute stroke ICU management after thrombectomy

SAQ — Malignant MCA syndrome in an older patient

Clinical pearls

Red flags

Prognosis

DAWN trial (Nogueira 2018, NEJM) — thrombectomy 6-24h

NINDS rt-PA Stroke Study (1995, NEJM) — the foundation of thrombolysis

ECASS-III (Hacke 2008, NEJM) — extending the window to 4.5h

EXTEND-IA TNK (Campbell 2018, NEJM) — tenecteplase before thrombectomy

Pooled DESTINY/DECIMAL/HAMLET (Vahedi 2007, Lancet Neurol) — decompressive hemicraniectomy

WAKE-UP (Thomalla 2018, NEJM) — thrombolysis for unknown-onset stroke

INTERACT3 (Ma 2023, Lancet) — combined care bundle in acute ICH

References

Acute stroke in ICU: ischaemic, haemorrhagic, and neurocritical care

Your progress

SAQ — Malignant MCA infarction

SAQ — Blood pressure management after thrombolysis

SAQ — Acute stroke ICU management after thrombectomy

SAQ — Malignant MCA syndrome in an older patient

Clinical pearls

Red flags

Prognosis

DAWN trial (Nogueira 2018, NEJM) — thrombectomy 6-24h

NINDS rt-PA Stroke Study (1995, NEJM) — the foundation of thrombolysis

ECASS-III (Hacke 2008, NEJM) — extending the window to 4.5h

EXTEND-IA TNK (Campbell 2018, NEJM) — tenecteplase before thrombectomy

Pooled DESTINY/DECIMAL/HAMLET (Vahedi 2007, Lancet Neurol) — decompressive hemicraniectomy

WAKE-UP (Thomalla 2018, NEJM) — thrombolysis for unknown-onset stroke

INTERACT3 (Ma 2023, Lancet) — combined care bundle in acute ICH

References