📋 Key Information Summary
- Stroke is a medical emergency: Call 000 immediately — "Time is Brain." Every minute of untreated large-vessel ischaemic stroke destroys approximately 1.9 million neurons.
- Ischaemic strokes (~85%) result from arterial occlusion; haemorrhagic strokes (~15%) result from intracerebral or subarachnoid haemorrhage. CT brain (± CT angiography) is the first-line investigation to distinguish these.
- Thrombolysis (alteplase 0.9 mg/kg IV, max 90 mg) is indicated for confirmed ischaemic stroke within 4.5 hours of symptom onset. Door-to-needle time target ≤60 minutes.
- Mechanical thrombectomy is the standard of care for anterior circulation large-vessel occlusion within 24 hours (selected patients) at designated comprehensive stroke centres.
- TIA (Transient Ischaemic Attack): transient neurological deficit lasting <24 hours with no acute infarction on imaging. Requires urgent assessment — treat as a stroke warning.
- ABCD² score stratifies TIA stroke risk: ≥4 = high risk (2-day stroke risk ~4%); refer for emergency assessment and commence dual antiplatelet therapy (aspirin + clopidogrel) within 24 hours if non-cardioembolic.
- CHADS₂ and CHA₂DS₂-VASc scores guide anticoagulation decisions in atrial fibrillation (AF). A CHA₂DS₂-VASc ≥2 in men or ≥3 in women warrants oral anticoagulation (DOAC preferred over warfarin).
- Carotid artery stenosis ≥70%: carotid endarterectomy (CEA) or carotid artery stenting (CAS) recommended within 2 weeks of ipsilateral TIA/minor stroke to reduce recurrent stroke risk.
- Cerebral venous thrombosis (CVT) is a rare but important cause of stroke in young adults, especially women on the combined oral contraceptive pill. Diagnosis requires CT/MR venography. Treat with anticoagulation (heparin then warfarin or DOAC).
- Secondary prevention: antiplatelet or anticoagulant therapy, statin (atorvastatin 80 mg), antihypertensive, diabetes management, smoking cessation, and lifestyle modification reduce recurrent stroke risk by up to 80%.
- Aboriginal and Torres Strait Islander Australians experience stroke at 1.7× the rate of non-Indigenous Australians, with higher mortality, younger age of onset, and reduced access to acute stroke services in remote areas.
- FAST recognition (Face, Arms, Speech, Time) remains the cornerstone of pre-hospital stroke identification. Public education campaigns such as the Stroke Foundation's National Stroke Week are critical.
Introduction & Australian Epidemiology
Stroke is the third leading cause of death in Australia and a leading cause of long-term disability. In 2023, approximately 45,000 Australians experienced a new or recurrent stroke — roughly one every 12 minutes. The estimated economic burden exceeds .2 billion annually, including direct healthcare costs, lost productivity, and informal care.
General practitioners play a pivotal role across the entire stroke continuum: identifying at-risk individuals through primary prevention, recognising stroke and TIA presentations in the acute setting, coordinating post-stroke rehabilitation and secondary prevention, and supporting patients and families through long-term recovery. General practice is often the first point of contact for patients with TIA and minor stroke, and timely referral to emergency departments can be life-saving.
The Australian Clinical Guidelines for Stroke Management (Stroke Foundation, 2022 update) provide a nationally consistent, evidence-based framework. These guidelines, along with the National Strategic Framework for Chronic Conditions and state-based stroke clinical networks, underpin stroke care across metropolitan, regional, and remote Australia.
Key epidemiological data for Australia include:
- Incidence: ~50,000 strokes per year (including first-ever and recurrent events)
- Prevalence: ~475,000 stroke survivors living in the community
- Mortality: ~8,400 deaths per year attributable to stroke
- Ischaemic stroke accounts for approximately 85% of all strokes
- Median age at first stroke: 74 years (men) and 78 years (women)
- Stroke incidence in Aboriginal and Torres Strait Islander peoples is 1.7 times that of non-Indigenous Australians, with onset approximately 10 years younger
- Regional and remote Australians have 1.2–1.5 times higher stroke mortality due to reduced access to hyperacute treatments and rehabilitation services
Pathophysiological Groups & Types of Stroke
Understanding stroke pathophysiology is essential for selecting appropriate acute treatment and secondary prevention strategies. Strokes are broadly classified into ischaemic and haemorrhagic subtypes, each with distinct mechanisms and management pathways.
Ischaemic Stroke (~85%)
Ischaemic strokes result from interruption of arterial blood supply to a region of the brain, leading to neuronal ischaemia and infarction. The ischaemic core (irreversibly damaged tissue) is surrounded by the ischaemic penumbra — tissue at risk but potentially salvageable with timely reperfusion.
The TOAST (Trial of ORG 10172 in Acute Stroke Treatment) classification divides ischaemic stroke into five aetiological subtypes:
| TOAST Subtype | Mechanism | Proportion | Key Features |
|---|---|---|---|
| Large-artery atherosclerosis | Thrombosis or artery-to-artery embolism from carotid, vertebral, or intracranial atherosclerotic plaque | ~20–25% | Carotid bruit, large-vessel territory infarct on imaging, ≥50% stenosis on CTA/MRA |
| Cardioembolism | Embolism from the heart (most commonly atrial fibrillation, valvular disease, recent MI) | ~20–30% | Large territorial infarct, haemorrhagic transformation, AF on ECG/Holter, elevated NT-proBNP |
| Small-vessel occlusion (lacunar) | Lipohyalinosis/atherosclerosis of small perforating arteries | ~20–25% | Lacunar syndromes (pure motor, pure sensory, ataxic hemiparesis), small (<15 mm) deep infarcts |
| Stroke of other determined aetiology | Dissection, vasculitis, prothrombotic states, CADASIL, moyamoya, sickle cell disease | ~5% | Young patient (<50 years), unusual risk factor profile, specific imaging findings |
| Stroke of undetermined aetiology (cryptogenic) | No cause identified despite comprehensive workup, or ≥2 possible causes | ~25–30% | Consider prolonged cardiac monitoring (30-day Holter, implantable loop recorder) to detect paroxysmal AF |
Haemorrhagic Stroke (~15%)
Type 1
Intracerebral Haemorrhage (ICH)
Bleeding directly into the brain parenchyma. Common causes include chronic hypertension (deep ganglionic bleeds), cerebral amyloid angiopathy (lobar bleeds in the elderly), anticoagulant use, and vascular malformations.
~10–12% of all strokes
Type 2
Subarachnoid Haemorrhage (SAH)
Bleeding into the subarachnoid space, most commonly from a ruptured cerebral aneurysm. Presents with sudden "thunderclap" headache, neck stiffness, photophobia, and reduced consciousness. Requires emergent neurosurgical and endovascular intervention.
~3% of all strokes · High mortality (~40%)
Critical distinction: Ischaemic vs haemorrhagic stroke cannot be reliably differentiated clinically. A non-contrast CT brain is mandatory before initiating thrombolysis. CT has ~95% sensitivity for ICH within the first 6 hours.
Stroke Mimics
Up to 25% of suspected stroke presentations are stroke mimics. Common mimics include hypoglycaemia (check BGL immediately), seizures with postictal paralysis (Todd's paresis), migraine with aura, functional neurological disorder, brain tumour, and metabolic derangements (hyponatraemia, hypocalcaemia).
Transient Ischaemic Attacks (TIA)
A Transient Ischaemic Attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction on imaging. The traditional time-based definition (<24 hours) has been superseded by a tissue-based definition incorporating MRI findings. Most TIAs resolve within 60 minutes.
TIA is a medical emergency. The risk of stroke following TIA is approximately 5% within 48 hours and up to 10–15% within 90 days without treatment. Early investigation and intervention can reduce this risk by up to 80%. All suspected TIA presentations should be assessed within 24 hours — ideally via a dedicated TIA clinic or emergency department referral.
Clinical Features of TIA
Typical TIA symptoms include unilateral weakness or numbness (face, arm, leg), dysphasia or dysarthria, monocular visual loss (amaurosis fugax), homonymous hemianopia, ataxia, vertigo (when accompanied by other brainstem signs), and diplopia. Symptoms are sudden in onset and maximal at onset.
Differential Diagnosis of TIA
| Condition | Distinguishing Features | Investigation |
|---|---|---|
| Hypoglycaemia | BGL <4 mmol/L, diaphoresis, confusion, known diabetes | Point-of-care glucose |
| Migraine with aura | Positive visual phenomena (scintillating scotoma), gradual onset over minutes, headache follows, prior history | Clinical diagnosis; MRI if atypical |
| Seizure (Todd's paresis) | Preceded by convulsive activity or witnessed seizure, postictal confusion, focal weakness improves over hours | EEG, MRI brain |
| Peripheral vestibular disorder | Isolated vertigo without other brainstem signs, positive Dix-Hallpike, nausea | HINTS examination, audiometry |
| Hypertensive encephalopathy | Severe hypertension, headache, visual disturbance, posterior reversible oedema on MRI | BP measurement, MRI brain |
| Functional neurological disorder | Inconsistent examination findings, non-anatomical distribution, positive Hoover's sign | Clinical diagnosis of exclusion |
| Multiple sclerosis | Young patient, relapsing-remitting episodes, optic neuritis history, white matter lesions on MRI | MRI brain/spine, CSF oligoclonal bands |
ABCD² Score for TIA Risk Stratification
The ABCD² score estimates the 2-day and 7-day risk of stroke following a TIA. It is used in Australian emergency departments and TIA clinics to guide urgency of investigation and admission decisions.
| Criteria | Finding | Points |
|---|---|---|
| A — Age | ≥60 years | 1 |
| B — Blood pressure | SBP ≥140 mmHg or DBP ≥90 mmHg | 1 |
| C — Clinical features | Unilateral weakness | 2 |
| Speech disturbance without weakness | 1 | |
| D — Duration | ≥60 minutes | 2 |
| 10–59 minutes | 1 | |
| D — Diabetes | Yes | 1 |
Maximum score: 7
Low Risk
ABCD² 0–3
2-day stroke risk: ~1%. 90-day stroke risk: ~3%.
Urgent outpatient TIA clinic assessment within 7 days. Brain MRI preferred within 24 hours. Commence aspirin 300 mg stat then 100 mg daily.
Moderate Risk
ABCD² 4–5
2-day stroke risk: ~4%. 90-day stroke risk: ~8%.
Emergency department assessment and brain imaging within 24 hours. Consider admission. Dual antiplatelet therapy if non-cardioembolic.
High Risk
ABCD² 6–7
2-day stroke risk: ~8%. 90-day stroke risk: ~12–17%.
Emergency department presentation and urgent imaging (CT ± CTA, MRI/MRA) within hours. Consider admission for monitoring and rapid workup. Dual antiplatelet therapy within 24 hours if non-cardioembolic.
TIA Initial Management — Acute
Aspirin
Aspro-Protect® · Astrix® · Cartia® · Antiplatelet
Loading dose
300 mg PO stat (chewed or dissolved for faster absorption)
Maintenance dose
100 mg PO daily
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Clopidogrel
Plavix® · Iscover® · Clopidogrel Sandoz® · Antiplatelet
Loading dose
300 mg PO stat (or 600 mg in selected cases)
Maintenance dose
75 mg PO daily
Duration
21 days of dual therapy (aspirin + clopidogrel) for minor stroke/high-risk TIA, then clopidogrel monotherapy
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
CHANCE / POINT trial evidence: Short-term dual antiplatelet therapy (DAPT) with aspirin + clopidogrel for 21 days, started within 24 hours of minor stroke or high-risk TIA, reduces recurrent stroke by ~25% compared with aspirin alone. This is now recommended in the Australian Clinical Guidelines for Stroke Management 2022. After 21 days, revert to single antiplatelet therapy.
Clinical Presentation & Diagnostic Criteria
FAST Assessment (Pre-Hospital)
F
Face
Ask the person to smile. Does one side of the face droop?
A
Arms
Ask the person to raise both arms. Does one arm drift downward?
S
Speech
Ask the person to repeat a simple phrase. Is their speech slurred or strange?
T
Time
If you observe any of these signs, call 000 immediately. Note the time of symptom onset.
Time of onset is critical. Eligibility for thrombolysis (alteplase) is determined by the time the patient was "last known well" — not the time symptoms were discovered. If the patient wakes with symptoms, the time of onset is when they went to sleep or were last observed to be normal.
Lateralising Signs by Vascular Territory
| Territory | Artery | Typical Presentation |
|---|---|---|
| Anterior circulation — MCA | Middle cerebral artery | Contralateral hemiparesis (face and arm > leg), contralateral hemisensory loss, contralateral homonymous hemianopia, gaze deviation towards the lesion. Dominant hemisphere: global/expressive/receptive aphasia. Non-dominant: neglect, visuospatial dysfunction. |
| Anterior circulation — ACA | Anterior cerebral artery | Contralateral hemiparesis (leg > arm), abulia, grasp reflex, urinary incontinence |
| Posterior circulation — PCA | Posterior cerebral artery | Contralateral homonymous hemianopia (with macular sparing), visual agnosia, thalamic sensory loss |
| Posterior circulation — Vertebrobasilar | Vertebral / basilar artery | Diplopia, vertigo, nystagmus, dysarthria, dysphagia, crossed signs (ipsilateral cranial nerve + contralateral limb weakness), ataxia, "locked-in" syndrome (basilar occlusion) |
| Lacunar syndromes | Small perforating arteries | Pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome. No cortical signs (no aphasia, no neglect). |
NIH Stroke Scale (NIHSS)
The NIHSS is a 15-item neurological assessment tool used to quantify stroke severity. Scores range from 0 (no deficit) to 42 (most severe). It is routinely performed in Australian emergency departments and stroke units at presentation, 24 hours post-thrombolysis, and at discharge. A score ≥6 generally indicates moderate-to-severe stroke.
Investigations
Acute Investigations (Emergency Department)
Essential
Non-contrast CT brain
First-line imaging. Differentiates ischaemic from haemorrhagic stroke. Should be performed within 20 minutes of ED arrival (door-to-CT target). Sensitivity for acute ischaemic stroke ~60% in the first 6 hours (improves with CT perfusion).
Essential
CT angiography (CTA) — arch to vertex
Identifies large-vessel occlusion (LVO) amenable to thrombectomy, carotid stenosis, dissection, and aneurysm. Performed immediately after non-contrast CT.
Available
CT perfusion (CTP)
Maps ischaemic core vs penumbra. Identifies salvageable tissue for extended-window thrombectomy (up to 24 hours). Available at comprehensive stroke centres in Australian capital cities.
Available
MRI brain (DWI/FLAIR/MRA)
Superior sensitivity for acute ischaemic stroke within minutes of onset (DWI). Recommended for TIA workup within 24 hours. DWI-FLAIR mismatch helps determine onset time. Not always available acutely in regional centres.
Essential
Blood tests
FBC, EUC (including glucose), coagulation studies (INR, APTT), lipids, HbA1c, troponin. Do not delay thrombolysis for results unless coagulopathy suspected.
Essential
12-lead ECG
Detects atrial fibrillation (present in ~25% of ischaemic strokes), acute myocardial infarction, and other arrhythmias. Perform in all suspected stroke presentations.
Available
Carotid duplex ultrasound
Non-invasive assessment of extracranial carotid stenosis. First-line vascular screening in the workup of anterior circulation TIA/stroke. Accessible in most Australian hospitals and vascular labs (MBS item 11600 series).
Extended Workup (Inpatient / TIA Clinic)
Available
Echocardiography (transthoracic ± transoesophageal)
Identifies cardiac sources of embolism: valvular disease, intracardiac thrombus, PFO, akinetic ventricular segments. TEE is more sensitive for PFO and aortic arch atheroma.
Available
Continuous cardiac monitoring / Holter / implantable loop recorder
Detects paroxysmal atrial fibrillation. 24-hour Holter detects AF in ~5% of cryptogenic stroke. Extended monitoring (30-day event monitor or implantable loop recorder) detects AF in ~15–30%. Medicare rebate available for Holter (MBS item 11704).
Specialist
Thrombophilia screen
Consider in young stroke patients (<50 years) with no vascular risk factors. Includes protein C, protein S, antithrombin III, factor V Leiden, prothrombin gene mutation, antiphospholipid antibodies. Refer to haematology.
Specialist
CT venography (CTV) / MR venography (MRV)
Diagnosis of cerebral venous thrombosis (CVT). Indicated in young patients, headache with focal deficits, haemorrhagic infarction in non-arterial territory, or papilloedema.
CHA₂DS₂-VASc Criteria & Atrial Fibrillation Management
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and a major cause of cardioembolic stroke. Approximately 2–4% of the Australian adult population has AF, with prevalence increasing with age (≥10% in those aged ≥80 years). AF increases stroke risk five-fold, and AF-related strokes tend to be larger, more disabling, and have higher mortality than non-AF strokes.
CHA₂DS₂-VASc Score
The CHA₂DS₂-VASc score stratifies stroke risk in non-valvular AF and guides anticoagulation decisions. It supersedes the original CHADS₂ score in Australian and international guidelines.
| Risk Factor | Points |
|---|---|
| C — Congestive heart failure (or LVEF ≤40%) | 1 |
| H — Hypertension | 1 |
| A₂ — Age ≥75 years | 2 |
| D — Diabetes mellitus | 1 |
| S₂ — Prior stroke, TIA, or thromboembolism | 2 |
| V — Vascular disease (prior MI, PAD, aortic plaque) | 1 |
| A — Age 65–74 years | 1 |
| Sc — Sex category (female) | 1 |
Maximum score: 9
Anticoagulation Recommendations Based on CHA₂DS₂-VASc
Low Risk
Score 0 (men) / 1 (women)
Annual stroke risk <1%. No anticoagulation recommended.
Reassess annually
Intermediate
Score 1 (men) / 2 (women)
Annual stroke risk 1–2%. Consider anticoagulation based on patient preference and bleeding risk (HAS-BLED score).
Shared decision-making; consider DOAC
High Risk
Score ≥2 (men) / ≥3 (women)
Annual stroke risk ≥2–15%. Oral anticoagulation recommended. DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin.
Anticoagulate with DOAC; reassess bleeding risk
Direct Oral Anticoagulants (DOACs) for AF-Related Stroke Prevention
Apixaban
Eliquis® · DOAC (Factor Xa inhibitor)
Adult dose
5 mg PO BD
Dose reduction
2.5 mg PO BD if ≥2 of: age ≥80, weight ≤60 kg, Cr ≥133 µmol/L
Renal adjustment
CrCl 15–29 mL/min: use with caution. CrCl <15: not recommended
PBS status
✔ PBS Authority Required
Rivaroxaban
Xarelto® · DOAC (Factor Xa inhibitor)
Adult dose
20 mg PO daily with food
Dose reduction
15 mg PO daily if CrCl 15–49 mL/min
Renal adjustment
CrCl 15–49: 15 mg daily. CrCl <15: avoid
PBS status
✔ PBS Authority Required
Dabigatran
Pradaxa® · DOAC (Direct thrombin inhibitor)
Adult dose
150 mg PO BD
Dose reduction
110 mg PO BD if age ≥80, on verapamil, or high bleeding risk
Renal adjustment
CrCl 30–49: 110 mg BD (or 150 mg BD with caution). CrCl <30: avoid
Reversal agent
Idarucizumab (Praxbind®) — specific reversal agent, available in Australian hospitals
PBS status
✔ PBS Authority Required
Warfarin
Marevan® · Coumadin® · Vitamin K antagonist
Adult dose
Individualised; typically 2–5 mg PO daily initially, adjusted to target INR 2.0–3.0
Indications for use over DOAC
Mechanical heart valve, moderate-to-severe mitral stenosis (valvular AF), antiphospholipid syndrome
Monitoring
INR every 1–4 weeks once stable; more frequent during initiation or dose changes
Reversal agent
Vitamin K (phytomenadione) IV/oral + prothrombin complex concentrate (PCC) for urgent reversal
PBS status
✔ PBS General Benefit
DOACs vs Warfarin: DOACs are recommended over warfarin for non-valvular AF in Australian guidelines (NHFA/CSANZ AF guidelines 2018; PBS Authority Required). DOACs have comparable or superior efficacy, lower intracranial haemorrhage risk, no routine INR monitoring, and fewer drug–food interactions. Warfarin remains indicated for valvular AF (mechanical valves, moderate–severe mitral stenosis).
Rate and Rhythm Control
In addition to anticoagulation, AF management includes rate control (target resting HR <110 bpm with lenient control, or <80 bpm with strict control) using beta-blockers (metoprolol, bisoprolol) or rate-limiting calcium channel blockers (diltiazem, verapamil). Rhythm control (cardioversion, antiarrhythmic drugs such as flecainide, amiodarone, or catheter ablation) may be considered in symptomatic patients. Refer to cardiology for consideration of catheter ablation in recurrent symptomatic AF despite pharmacotherapy.
Carotid Artery Stenosis & Cerebral Venous Thrombosis
Carotid Artery Stenosis
Carotid artery stenosis accounts for approximately 10–15% of ischaemic strokes. Atherosclerotic narrowing of the internal carotid artery (ICA) at the bifurcation can cause stroke via artery-to-artery embolism, haemodynamic compromise, or in-situ thrombosis. Carotid revascularisation — carotid endarterectomy (CEA) or carotid artery stenting (CAS) — is one of the most evidence-based surgical interventions for secondary stroke prevention.
Key trials (NASCET, ECST, CREST): CEA reduces the 5-year risk of ipsilateral stroke by approximately 50% in patients with 70–99% symptomatic carotid stenosis. Benefit is greatest when surgery is performed within 2 weeks of the index event. Patients with 50–69% stenosis gain moderate benefit; those with <50% stenosis do not benefit from surgery.
| Degree of Stenosis | Symptomatic | Asymptomatic |
|---|---|---|
| <50% | Medical management (antiplatelet + statin + risk factor modification). No surgery. | Medical management. No surgery. |
| 50–69% | Consider CEA if perioperative stroke/death risk <6%. Benefit is moderate (absolute risk reduction ~5% over 5 years). Refer to vascular surgery within 2 weeks. | Medical management preferred. CEA/CAS may be considered in selected high-risk patients with good life expectancy. |
| 70–99% | CEA recommended within 2 weeks. Greatest benefit from revascularisation. Absolute risk reduction ~16% over 5 years. Refer urgently to vascular surgery. | CEA may be considered in selected patients with good surgical risk and life expectancy >5 years. Shared decision-making. |
| Near-occlusion / occlusion | No proven benefit from surgery. Optimal medical management. | Medical management. |
Carotid Endarterectomy (CEA) vs Carotid Artery Stenting (CAS)
- CEA remains the gold standard for symptomatic carotid stenosis in most patients, supported by the NASCET and ECST trials. Perioperative stroke/death rate should be <6% for symptomatic and <3% for asymptomatic patients.
- CAS is a reasonable alternative in patients at high surgical risk (hostile neck from prior surgery/radiation, contralateral carotid occlusion, severe cardiac/pulmonary comorbidity). The CREST trial showed comparable long-term outcomes between CEA and CAS, though CAS had a slightly higher periprocedural stroke rate and CEA had a slightly higher myocardial infarction rate.
- Age >70 years: CTA tends to favour CEA over CAS due to increased peri-procedural stroke risk with CAS in older patients.
All patients with carotid stenosis should receive optimal medical therapy regardless of whether revascularisation is performed:
- Antiplatelet therapy (aspirin 100 mg daily or clopidogrel 75 mg daily)
- High-intensity statin (atorvastatin 40–80 mg daily)
- Blood pressure management (target <130/80 mmHg)
- Smoking cessation
- Diabetes optimisation (HbA1c target <53 mmol/mol / <7%)
Cerebral Venous Thrombosis (CVT)
Cerebral venous thrombosis (CVT) accounts for approximately 0.5–1% of all strokes but is an important diagnosis to consider, particularly in young adults and women. CVT involves thrombosis of the cerebral venous sinuses (superior sagittal sinus most commonly), cortical veins, or deep cerebral veins, leading to venous congestion, raised intracranial pressure, and potential parenchymal infarction or haemorrhage.
Risk Factors for CVT
| Category | Risk Factors |
|---|---|
| Prothrombotic | Inherited thrombophilia (factor V Leiden, prothrombin G20210A, protein C/S deficiency), antiphospholipid syndrome, pregnancy and puerperium |
| Exogenous hormones | Combined oral contraceptive pill (most common modifiable risk factor in young women), HRT |
| Infectious | Mastoiditis, sinusitis, meningitis, otitis media (more common in children) |
| Other | Head trauma, neurosurgery, malignancy, inflammatory bowel disease, Behçet's disease, severe dehydration, COVID-19 |
Clinical Presentation of CVT
CVT has a highly variable presentation. The most common symptoms include:
- Headache (present in ~90%): often subacute and progressive; may mimic migraine or idiopathic intracranial hypertension. Sudden onset ("thunderclap") occurs in ~10–15%.
- Seizures (~40%): focal or generalised; may be the presenting feature
- Focal neurological deficits (~40%): hemiparesis, aphasia, visual field defects — often due to venous infarction
- Papilloedema (~30%): due to raised intracranial pressure
- Altered consciousness: in severe cases, with risk of cerebral herniation
Diagnosis of CVT
CT venography (CTV) or MR venography (MRV) is the gold standard for diagnosis. Non-contrast CT may show the "empty delta sign" (filling defect in the sagittal sinus with contrast) or haemorrhagic infarction in a non-arterial territory. D-dimer has moderate sensitivity (~90%) but limited specificity — a normal D-dimer does not exclude CVT. If clinical suspicion is high, proceed directly to CTV/MRV regardless of D-dimer result.
Management of CVT
Anticoagulation is the mainstay of treatment for CVT, even in the presence of haemorrhagic venous infarction. Unfractionated heparin (UFH) or LMWH is used acutely, transitioning to oral anticoagulation (warfarin target INR 2–3, or a DOAC) for 3–6 months if provoked CVT, or 6–12 months or longer if unprovoked or with confirmed thrombophilia.
Enoxaparin (LMWH)
Clexane® · Anticoagulant
Adult dose
1 mg/kg SC BD (or 1.5 mg/kg SC OD)
Monitoring
Anti-Xa levels if renal impairment or extremes of weight
Renal adjustment
CrCl <30 mL/min: reduce dose to 1 mg/kg SC OD; consider UFH
PBS status
✔ PBS Authority Required
Additional measures include seizure management (levetiracetam or phenytoin), management of raised intracranial pressure (head elevation, osmotherapy, consider CSF drainage), and identification and treatment of underlying causes (e.g., discontinue OCP, treat mastoiditis/sinusitis).
Acute Stroke Management
Hyperacute Treatment — Ischaemic Stroke
Thrombolysis window: 0–4.5 hours from symptom onset. Every 15-minute reduction in door-to-needle time reduces in-hospital mortality by approximately 5%. Australian targets: door-to-CT ≤20 minutes, door-to-needle ≤60 minutes. Administer aspirin 300 mg immediately after thrombolysis (wait 24 hours before the dose if no thrombolysis).
Intravenous Alteplase (Thrombolysis)
Alteplase (tPA)
Actilyse® · Thrombolytic
Adult dose
0.9 mg/kg IV (max 90 mg). 10% as IV bolus over 1 minute, remainder infused over 60 minutes.
Window
Within 4.5 hours of symptom onset
Key exclusions
Haemorrhage on CT, BP >185/110 mmHg uncontrolled, INR >1.7, platelets <100 × 10⁹/L, major surgery within 14 days, recent stroke within 3 months
Post-thrombolysis
Admit to stroke unit. BP target <180/105 mmHg for 24 hours. Repeat CT at 24 hours. No anticoagulants or antiplatelets for 24 hours post-alteplase.
PBS status
⚠ PBS Authority Required — Hospital only
Mechanical Thrombectomy
Endovascular thrombectomy is the standard of care for acute ischaemic stroke caused by large-vessel occlusion (LVO) of the anterior circulation (ICA terminus, M1 or M2 MCA segments). It can be performed up to 24 hours from symptom onset in selected patients with salvageable penumbra demonstrated on CT perfusion or DWI-FLAIR mismatch (DAWN and DEFUSE 3 trials).
- Performed at designated comprehensive stroke centres — in Australia these are primarily major metropolitan hospitals in each state/territory capital
- Thrombectomy-capable centres include Royal Melbourne, Westmead, Royal Adelaide, Royal Brisbane, Sir Charles Gairdner, Royal Hobart, Canberra Hospital, and Royal Darwin (with retrieval networks)
- Can be performed in addition to IV alteplase ("bridging therapy") — standard of care
- Requires interventional neuroradiology services
- Patients in regional and remote areas require emergency aeromedical retrieval (RFDS, state retrieval services) — time-critical
Haemorrhagic Stroke — Initial Management
1
Blood Pressure
Target SBP <140 mmHg (INTERACT2 trial). IV labetalol or nicardipine infusion. Avoid precipitous drops.
2
Reverse Anticoagulation
Warfarin: Vitamin K IV + PCC. DOACs: idarucizumab for dabigatran; andexanet alfa (limited availability) or PCC for factor Xa inhibitors.
3
Neurosurgical Referral
Consider evacuation for cerebellar haemorrhage >3 cm, or supratentorial haemorrhage with deterioration. External ventricular drain for hydrocephalus.
4
ICP Management
Head elevation 30°, osmotherapy (mannitol or hypertonic saline), sedation, short-term hyperventilation as a bridge.
Secondary Prevention
Secondary prevention is a critical role for general practice. Approximately 10–15% of stroke survivors will have a recurrent stroke within 5 years without optimal secondary prevention. A comprehensive approach targeting modifiable risk factors can reduce this risk by up to 80%.
Antiplatelet Therapy (Non-Cardioembolic Stroke)
First-line long-term
Clopidogrel 75 mg PO daily
Ongoing
Preferred monotherapy (professor trial evidence)
Alternative first-line
Aspirin 100–300 mg PO daily
Ongoing
If clopidogrel intolerant
Combination alternative
Aspirin 25 mg + dipyridamole 200 mg PO BD
Ongoing
Aggrenox®. Slightly more effective than aspirin alone. GI side effects common.
Acute TIA/minor stroke
Aspirin 300 mg stat + clopidogrel 300 mg load, then aspirin 100 mg + clopidogrel 75 mg daily
21 days, then monotherapy
CHANCE/POINT evidence; non-cardioembolic only
Statin Therapy
Atorvastatin
Lipitor® · Statin (HMG-CoA reductase inhibitor)
Dose
40–80 mg PO daily (high-intensity)
Target
LDL-C <1.8 mmol/L (or ≥50% reduction from baseline)
Monitoring
LFTs at baseline, lipid profile at 6–8 weeks, CK if myalgia
PBS status
✔ PBS General Benefit
Blood Pressure Management
Target BP: <130/80 mmHg for most stroke/TIA patients (Australian Clinical Guidelines 2022). Commence or optimise antihypertensives once the patient is neurologically stable (usually ≥48 hours post-stroke). ACE inhibitors (perindopril, ramipril), ARBs (telmisartan, candesartan), and calcium channel blockers (amlodipine) are first-line agents.
Diabetes Management
Target HbA1c ≤53 mmol/mol (7%). SGLT2 inhibitors (empagliflozin, dapagliflozin) and GLP-1 receptor agonists (liraglutide, semaglutide) offer cardiovascular and renal benefits beyond glucose lowering. Refer to endocrinology or GP shared-care protocols.
Lifestyle Modifications
- Smoking cessation: highest-yield lifestyle intervention. Offer NRT, varenicline (Champix® — PBS listed), or bupropion. Referral to Quitline (13 7848).
- Alcohol: reduce to ≤10 standard drinks/week (NHMRC guidelines 2020)
- Physical activity: ≥150 minutes moderate-intensity aerobic exercise per week
- Diet: Mediterranean or DASH-style diet, reduce sodium to <5 g/day, increase fruit, vegetables, whole grains
- Weight management: target BMI 18.5–24.9 kg/m²; waist circumference <94 cm (men) / <80 cm (women)
- OSA screening: obstructive sleep apnoea is highly prevalent post-stroke. Consider sleep study and CPAP if indicated.
Monitoring & Follow-Up
Post-stroke care requires a structured, multidisciplinary approach. The general practitioner is the central coordinator of long-term care, ensuring secondary prevention is optimised and complications are identified early.
Discharge
Stroke team handover to GP. Medication reconciliation. Discharge summary with stroke subtype, imaging findings, NIHSS at discharge, rehabilitation goals, and follow-up plan. Carer education provided.
2 weeks
GP review. Assess neurological recovery, medication adherence, blood pressure, mood (PHQ-2/PHQ-9 screening for post-stroke depression — affects ~33%). Ensure carotid imaging and cardiac workup results are reviewed if not yet completed.
6 weeks
Follow-up with stroke specialist or neurologist. Repeat brain imaging if indicated. Review rehabilitation progress. Occupational therapy driving assessment (varies by state — in Victoria, notify VicRoads; in NSW, notify RMS). Discuss return to work and ADLs.
3 months
GP review. Lipid panel, HbA1c, renal function. Assess BP control. Review AF management if applicable. Screen for cognitive impairment (MoCA or MMSE). Continue rehabilitation as needed.
6–12 months
Annual comprehensive review. Repeat vascular risk factor assessment. Carotid duplex ultrasound follow-up if revascularisation was performed. Ongoing mood, cognition, and functional independence assessment. Consider re-referral to rehabilitation if new deficits emerge.
Key Monitoring Parameters
| Parameter | Target | Frequency |
|---|---|---|
| Blood pressure | <130/80 mmHg | Every visit (home BP monitoring encouraged) |
| LDL cholesterol | <1.8 mmol/L (or ≥50% reduction) | 6–8 weeks after statin initiation, then annually |
| HbA1c (if diabetic) | ≤53 mmol/mol (7%) | Every 3–6 months |
| INR (if on warfarin) | 2.0–3.0 (TTR >70%) | Every 1–4 weeks when stable |
| Renal function (on DOAC) | CrCl >30 mL/min (or dose-adjusted) | Every 6–12 months (more often if elderly or CKD) |
| Mood (PHQ-9) | <10 (no/mild depression) | 2 weeks, 3 months, 6 months, then annually |
| Cognition (MoCA/MMSE) | MoCA ≥26/30 | 3 months, then annually |
Post-Stroke Complications to Screen For
- Post-stroke depression: affects ~33% of survivors. Screen with PHQ-9. Treat with SSRIs (sertraline, citalopram — preferred due to low drug interaction profile). Refer for psychology/counselling (Mental Health Treatment Plan — MBS items 80110–80125).
- Post-stroke cognitive impairment: affects up to 30%. Screen with MoCA. Refer to memory clinics if progressive.
- Spasticity: physiotherapy, botulinum toxin injection (MBS item 18360), intrathecal baclofen for severe cases.
- Shoulder pain / subluxation: hemiplegic shoulder. Physiotherapy, taping, positioning.
- Dysphagia: speech pathology assessment before oral intake. Modified diet and fluids as needed.
- DVT/PE: thromboprophylaxis in immobile patients. LMWH followed by antiplatelet therapy when safe.
- Falls risk: multifactorial falls risk assessment. Physiotherapy, home safety assessment (MBS item 10950 for GP chronic disease management plans).
Special Populations
Pregnancy
Stroke risk
Stroke risk is increased 2–3-fold during pregnancy and the puerperium, particularly in the third trimester and first 6 weeks postpartum. Causes include eclampsia/HELLP syndrome, CVT, paradoxical embolism (PFO), and dissection.
Diagnosis
MRI without gadolinium is preferred (avoid gadolinium in pregnancy). CT brain is acceptable if MRI unavailable and diagnosis is time-critical. Lead shielding for CT if performed.
Thrombolysis
Alteplase is pregnancy category B3 (TGA). It does not cross the placenta. May be considered in life-threatening ischaemic stroke after multidisciplinary discussion (neurology, obstetrics, haematology).
Anticoagulation
Warfarin is teratogenic (Category D) — avoid in first trimester. LMWH (enoxaparin) is the preferred anticoagulant in pregnancy. DOACs are contraindicated in pregnancy and breastfeeding.
Antiplatelets
Low-dose aspirin (100–150 mg daily) is considered safe in pregnancy and is widely used for pre-eclampsia prevention. Clopidogrel — limited data; discuss with haematology.
Paediatrics
Incidence
Paediatric stroke (including neonatal stroke) occurs in approximately 2–3 per 100,000 children per year. Neonatal arterial ischaemic stroke (AIS) presents with seizures in the first 72 hours of life. Childhood AIS presents with hemiparesis, speech disturbance, or seizures.
Aetiology
Congenital heart disease, sickle cell disease, moyamoya disease, prothrombotic disorders, varicella infection (within 12 months), arterial dissection, and FVL/PTG20210A mutations.
Acute treatment
Thrombolysis is NOT routinely recommended in paediatric stroke in Australia (off-label, insufficient evidence). Mechanical thrombectomy is increasingly performed in adolescents with LVO. Acute management is primarily supportive: aspirin 1–5 mg/kg/day, hydration, seizure control. Consult paediatric neurology urgently.
Secondary prevention
Aspirin 1–5 mg/kg/day is the mainstay of secondary prevention. Warfarin for cardioembolic stroke. Long-term rehabilitation is essential — children have significant neuroplasticity and may show remarkable recovery.
Referral
Refer to a tertiary paediatric neurology service (e.g., RCH Melbourne, Westmead Children's, QCH Brisbane). Australian Paediatric Stroke Alliance provides family resources and support.
Elderly (≥80 years)
Thrombolysis
Alteplase is safe and effective in patients aged ≥80 years within 3 hours. The EXTEND trial showed benefit up to 4.5 hours in selected patients ≥80 years using perfusion imaging. Do not withhold thrombolysis based on age alone.
Thrombectomy
Mechanical thrombectomy has demonstrated benefit in patients ≥80 years with LVO (HERMES collaboration). Selection based on pre-stroke functional status and infarct burden rather than age.
Anticoagulation in AF
DOACs are preferred over warfarin in the elderly (lower ICH risk). Apixaban 2.5 mg BD (dose reduction criteria). Monitor renal function more frequently (every 3–6 months). Falls risk — the risk of stroke from AF outweighs the risk of ICH from anticoagulation even in fallers.
Polypharmacy
Review medications for interactions (e.g., DOAC + antiplatelet = increased bleeding risk). Consider deprescribing. Home Medicines Review (HMR) — MBS item 900.
Renal Impairment
DOAC dosing
All DOACs require dose adjustment or avoidance in CKD. Apixaban is the safest in severe CKD (CrCl 15–29). Dabigatran is predominantly renally cleared — avoid if CrCl <30. Rivaroxaban: 15 mg daily if CrCl 15–49. Check CrCl at least every 6 months.
Dialysis
Warfarin is the traditional choice for patients on haemodialysis with AF, as DOACs lack evidence in this population. Consult nephrology and haematology.
Statins
Atorvastatin does not require dose adjustment in renal impairment. Avoid high-dose simvastatin if on ciclosporin or certain antivirals.
Hepatic Impairment
DOACs
DOACs are contraindicated in severe hepatic impairment (Child-Pugh C). Use with caution in moderate impairment (Child-Pugh B). Rivaroxaban and apixaban are hepatically metabolised. Warfarin requires careful INR monitoring in liver disease.
Statins
Avoid statins in active liver disease or unexplained persistent transaminase elevation (ALT >3× ULN). Atorvastatin and rosuvastatin are metabolised hepatically — use with caution in moderate impairment.
Immunocompromised
HIV
HIV infection is associated with increased stroke risk (accelerated atherosclerosis, vasculopathy, prothrombotic state, opportunistic infections). Manage in conjunction with infectious disease specialist. Antiretroviral drug interactions with DOACs and statins must be reviewed (e.g., protease inhibitors increase DOAC levels — avoid dabigatran; use caution with rivaroxaban/apixaban).
Transplant recipients
Calcineurin inhibitors (ciclosporin, tacrolimus) and mTOR inhibitors (sirolimus, everolimus) interact with statins (increased myopathy risk). Immunosuppression-related vasculopathy may cause stroke. Multidisciplinary management with transplant team essential.
Cancer-associated stroke
Malignancy (particularly mucin-secreting adenocarcinomas) increases VTE and stroke risk via hypercoagulability. Consider malignancy screening in cryptogenic stroke patients with unexplained D-dimer elevation. Chemotherapy and radiation to the neck may accelerate carotid atherosclerosis.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Stroke is a significant contributor to the health gap experienced by Aboriginal and Torres Strait Islander Australians. Indigenous Australians experience stroke at approximately 1.7 times the rate of non-Indigenous Australians, with onset occurring approximately 10 years younger. Cardiovascular disease (including stroke) is the second leading cause of the Indigenous health gap, accounting for approximately 21% of the total gap in health outcomes (AIHW 2022).
Key disparities: Aboriginal and Torres Strait Islander peoples are more likely to have a stroke before age 55, have higher rates of haemorrhagic stroke, have higher in-hospital mortality, are less likely to receive thrombolysis or thrombectomy, and have lower rates of rehabilitation completion and secondary prevention follow-up.
Strategies to Improve Stroke Outcomes
- Fund and expand Aboriginal Health Worker/Practitioner roles within acute stroke teams and rehabilitation services
- Support ACCHOs to deliver chronic disease management programs targeting stroke risk factors (MBS item 721 — GP Management Plan; MBS item 723 — Team Care Arrangement)
- Increase access to telestroke services in regional and remote hospitals to enable rapid specialist assessment and thrombolysis decision-making
- Provide culturally adapted stroke education resources (co-designed with communities) emphasising FAST recognition and the importance of calling 000
- Strengthen partnerships between stroke services and ACCHOs for seamless hospital-to-community transitions of care
- Address social determinants of health — housing, education, employment, food security — that contribute to the disproportionate burden of stroke risk factors
- Support research into Indigenous stroke epidemiology, culturally safe interventions, and community-led stroke prevention programs
📚 References
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- 2. National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (NHFA/CSANZ). Australian Clinical Guidelines for the Diagnosis and Management of Atrial Fibrillation 2018. Heart Lung Circ. 2018;27(10):1209–1266.
- 3. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines. Stroke. 2019;50(12):e344–e418.
- 4. Pan Y, Elm JJ, Li H, et al. (CHANCE-2 Trial). Ticagrelor versus clopidogrel in CYP2C19 loss-of-function carriers with stroke or TIA. N Engl J Med. 2021;385(27):2520–2530.
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- 7. Nogueira RG, Jadhav AP, Haussen DC, et al. (DAWN Trial). Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med. 2018;378(1):11–21.
- 8. Australian Institute of Health and Welfare (AIHW). Stroke and its management in Australia: an update. Cat. no. CDK 17. Canberra: AIHW; 2023.
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- 11. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325(7):445–453. (NASCET)
- 12. Brott TG, Hobson RW, Howard G, et al. (CREST Investigators). Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010;363(1):11–23.
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- 14. RHDAustralia (ARF/RHD writing group). National Aboriginal and Torres Strait Islander Rheumatic Fever and Rheumatic Heart Disease Guidelines. 3rd ed. Darwin: Menzies School of Health Research; 2020.
- for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.