The Unconscious Patient

Last updated 1 Jun 2026 · Emergency Medicine / Neurology

📋 Key Information Summary

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The Glasgow Coma Scale (GCS) scores consciousness from 3 (deeply unconscious) to 15 (fully alert) across three domains: Eye Opening (E1–4), Verbal Response (V1–5), and Motor Response (M1–6).
A GCS ≤ 8 defines coma and mandates definitive airway protection — "GCS less than 8, intubate."
The AVPU scale (Alert, Voice, Pain, Unresponsive) is an acceptable rapid bedside alternative when GCS is impractical in the pre-hospital or resource-limited setting.
The most common causes of unconsciousness are grouped into: traumatic (TBI), vascular (stroke, SAH, ICH), metabolic (hypoglycaemia, hypo/hypernatraemia, hepatic encephalopathy), toxicological (opioids, alcohol, benzodiazepines), infectious (meningitis, encephalitis, sepsis), and epileptic (post-ictal state, status epilepticus).
Hypoglycaemia is the single most important reversible cause — check BGL immediately on every unconscious patient before any other investigation.
Follow the structured ABCDE approach: Airway with cervical spine protection, Breathing, Circulation, Disability (GCS, pupils, glucose), Exposure (temperature, rashes, injuries).
Naloxone (200 µg IV, repeat every 2–3 min up to 10 mg) should be given empirically when opioid overdose is suspected; titrate to respiratory effort, not full alertness.
Syncope accounts for up to 3% of ED presentations in Australia; cardiac syncope carries a 1-year mortality of up to 30% and requires urgent investigation and admission.
Transient loss of consciousness (TLOC) must be distinguished from epilepsy, concussive injury, psychogenic pseudosyncope, and vertebrobasilar TIAs — each has a different management pathway.
Aboriginal and Torres Strait Islander Australians have higher rates of unconsciousness from trauma, diabetic emergencies, and rheumatic heart disease-related stroke — low-threshold referral and culturally safe care are essential.
CT brain (non-contrast) is the first-line imaging for acute unconsciousness when intracranial pathology is suspected; availability in rural and remote Australia varies — early retrieval to a major centre is critical.
All unconscious patients must have continuous pulse oximetry, cardiac monitoring, frequent neuro-observations, and venous access established before transfer.

Introduction & Australian Epidemiology

Loss of consciousness (LOC) is a common and potentially life-threatening presentation across emergency departments (EDs), general practices, and pre-hospital settings in Australia. Consciousness is a product of arousal (reticular activating system in the brainstem) and awareness (cerebral cortex and thalamocortical networks); disruption at any point in this circuit produces altered consciousness ranging from drowsiness to deep coma.

In Australia, presentations involving loss or alteration of consciousness account for an estimated 3–5% of all ED attendances annually. Traumatic brain injury (TBI) remains a leading cause, with approximately 19,000 hospitalisations per year according to the Australian Institute of Health and Welfare (AIHW). Hypoglycaemia-related unconsciousness is particularly prevalent among Indigenous Australians and those with insulin-treated diabetes. Alcohol- and drug-related unconsciousness contributes substantially to the burden, particularly in younger demographics.

The clinical challenge of the unconscious patient lies in the broad differential diagnosis and the time-critical nature of several reversible causes — particularly hypoglycaemia, opioid toxicity, and intracranial haemorrhage. A structured, algorithmic approach to assessment and management is essential to reduce morbidity and mortality.

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Time-critical presentation: Every minute of untreated hypoglycaemia or unrecognised intracranial haemorrhage worsens neurological outcomes. Assume reversible causes until proven otherwise and treat empirically when safe to do so.

Five Conscious Levels (Glasgow Coma Scale)

The Glasgow Coma Scale (GCS) was developed by Teasdale and Jennett in 1974 at the University of Glasgow and remains the most widely used tool for objectively grading consciousness in clinical practice worldwide. It assesses three independent behavioural responses — Eye Opening, Verbal Response, and Motor Response — yielding a composite score from 3 (worst) to 15 (best).

Components of the Glasgow Coma Scale

Response	Score	Description
Eye Opening (E)	E4	Spontaneous — eyes open at rest
	E3	To voice — opens eyes in response to verbal command or speech
	E2	To pain — opens eyes only in response to painful stimulus
	E1	None — no eye opening to any stimulus
Verbal Response (V)	V5	Oriented — knows name, place, date
	V4	Confused — converses but disoriented
	V3	Inappropriate words — recognisable single words, no sustained conversation
	V2	Incomprehensible sounds — moaning, groaning, no recognisable words
	V1	None — no verbal response
Motor Response (M)	M6	Obeys commands — performs requested movements
	M5	Localises pain — reaches towards the painful stimulus to remove it
	M4	Withdrawal (flexion) — pulls limb away from painful stimulus
	M3	Abnormal flexion (decorticate) — arm flexion, wrist pronation, leg extension
	M2	Extension (decerebrate) — arm and leg extension, internal rotation
	M1	None — no motor response to pain

Grading Consciousness by GCS

Mild

GCS 13–15

Mild brain impairment. Patient may be confused or disoriented but opens eyes spontaneously and follows commands. Often seen in mild TBI, early metabolic derangement, or medication effect.

Setting: ED assessment; observation; may be suitable for discharge with safety-netting

Moderate

GCS 9–12

Moderate impairment. Patient may be drowsy, confused, or only responding to voice. Requires close monitoring and full investigation. Airway may still be self-maintained but at risk of deterioration.

Setting: ED resuscitation bay; consider HDU admission; continuous monitoring

Severe

GCS ≤ 8

Coma. Patient cannot protect their own airway. Urgent intubation indicated. High risk of aspiration, respiratory failure, and herniation. Requires ICU-level care and emergent cause identification.

Setting: Resuscitation → ICU; immediate airway management; emergency neuroimaging

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Key rule — "GCS less than 8, intubate": A GCS of 8 or below indicates the patient cannot protect their own airway. Endotracheal intubation with rapid sequence induction (RSI) should be performed by a trained clinician as a priority. Document the individual E, V, and M components — not just the total score — as they carry greater clinical and prognostic significance.

The AVPU Scale — A Rapid Alternative

When a full GCS assessment is impractical (e.g. pre-hospital triage, mass casualty), the AVPU mnemonic provides a rapid categorical assessment:

Alert

Eyes open spontaneously, oriented, tracking — roughly equivalent to GCS 15

Voice

Responds to verbal stimulation — roughly GCS 9–14

Pain

Responds only to painful stimulus — roughly GCS 4–8

Unresponsive

No response to any stimulus — GCS 3

Limitations of the GCS

Intubated patients: The verbal component cannot be assessed — record as V1T (tube). Use the GCS Motor component (GCS-M) and Eye Opening (GCS-E) for serial monitoring.
Periorbital swelling / chemosis: Eye opening may be unassessable due to local injury — record as E1C (closed).
Spinal cord injury: Motor responses in paralysed limbs cannot be assessed.
Sedation / paralysis: Pharmacological agents confound assessment — document the drug, dose, and time of last administration.
Pre-verbal children: Use the Paediatric GCS (modified verbal and motor scales) for children under 2 years of age.

Paediatric Glasgow Coma Scale (Modified for Children < 2 Years)

Component	Score	Paediatric Criterion
Verbal (modified)	5	Coos, babbles — age-appropriate vocalisation
	4	Irritable, crying — consolable but persistently irritable
	3	Inconsolable crying — cannot be comforted
Motor (same as adult)	6	Spontaneous movements
	5	Withdraws to touch
	4	Withdraws to pain
	3	Abnormal flexion
	2	Extension
	1	None

Main Causes of Loss of Consciousness

Loss of consciousness arises from either diffuse bilateral cerebral dysfunction or focal brainstem/ascending reticular activating system (ARAS) pathology. A systematic approach to the differential — using the mnemonic "MIDNIGHTS" or a pathophysiological framework — helps avoid premature closure and missed diagnoses.

Pathophysiological Categories

Category	Conditions	Key Clues
Structural / Traumatic	Traumatic brain injury (TBI), intracerebral haemorrhage, subdural haematoma, epidural haematoma, subarachnoid haemorrhage (SAH), cerebral infarction (large vessel occlusion), brain tumour, cerebral abscess, hydrocephalus	Focal neurological signs, unequal pupils, preceding headache (SAH), head injury history, signs of raised ICP (Cushing response: hypertension, bradycardia, irregular respiration)
Metabolic / Biochemical	Hypoglycaemia, hyperglycaemic emergencies (DKA, HHS), hepatic encephalopathy, uraemia, hyponatraemia, hypernatraemia, hypercalcaemia, hypothyroidism (myxoedema coma), adrenal crisis, hypoxia, hypercapnia	Global encephalopathy, flapping tremor (asterixis), history of diabetes, liver disease, renal failure, thyroid disease, or medication use
Toxicological	Opioids, benzodiazepines, alcohol intoxication, tricyclic antidepressants, antipsychotics, anticholinergics, carbon monoxide, methanol, ethylene glycol, serotonin syndrome, neuroleptic malignant syndrome	Pinpoint pupils (opioids), large pupils (anticholinergics, sympathomimetics), needle marks, characteristic odours (alcohol, ketones, cyanide), toxidrome features
Infectious	Meningitis, encephalitis (HSV, arbovirus), cerebral malaria, sepsis with encephalopathy, cerebral abscess, COVID-19 encephalopathy	Fever, neck stiffness, petechial rash (meningococcal), recent travel, immunosuppression, photophobia, positive Kernig's/Brudzinski's signs
Epileptic	Post-ictal state, non-convulsive status epilepticus, convulsive status epilepticus, Todd's paralysis	Witnessed seizure, tonic-clonic movements, tongue biting, incontinence, gradual improvement over minutes to hours, history of epilepsy
Cardiovascular	Cardiac syncope (arrhythmia, aortic stenosis, HOCM, PE), vasovagal syncope, orthostatic hypotension, aortic dissection, cardiac tamponade	Sudden onset, exertional syncope, preceding palpitations, postural symptoms, associated chest pain, mottled peripheries
Psychiatric / Functional	Psychogenic pseudosyncope, dissociative disorder, catatonia	Eyes closed during event (syncope typically has eyes open), normal GCS and vital signs, recurrent episodes without injury, psychiatric history

Key "Can't-Miss" Diagnoses

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Life-threatening causes to exclude immediately:

Hypoglycaemia — check BGL within the first 30 seconds of assessment
Opioid toxicity — administer naloxone if pinpoint pupils and respiratory depression
Intracranial haemorrhage — urgent CT brain; neurosurgical consultation if surgical lesion
Subarachnoid haemorrhage — thunderclap headache, CT then LP if CT negative
Meningitis / encephalitis — empiric antibiotics (ceftriaxone + dexamethasone) + aciclovir should not be delayed for imaging or LP
Status epilepticus — benzodiazepines IV/IM/PR within 5 minutes
Carbon monoxide poisoning — consider in any unexplained unconsciousness, especially in enclosed spaces with multiple affected individuals
Adrenal crisis — hypotension, hyponatraemia, hyperkalaemia — give IV hydrocortisone 100 mg immediately

The "MIDNIGHTS" Mnemonic

M — Metabolic (hypoglycaemia, DKA, HHS, hepatic encephalopathy, uraemia, electrolyte derangement)
I — Infection (meningitis, encephalitis, sepsis, cerebral abscess, malaria)
D — Drugs / toxins (opioids, benzodiazepines, alcohol, TCA, anticholinergics, CO poisoning)
N — Neurological (epilepsy/post-ictal, stroke, SAH, raised ICP, tumour)
I — Insulin (hypo- and hyperglycaemia — diabetic emergencies)
G — General / trauma (TBI, hypothermia, hyperthermia)
H — Hypoxia / hypercapnia (respiratory failure, PE, pneumothorax, CO poisoning)
T — Temperature (heat stroke, hypothermia, thyroid storm, myxoedema coma)
S — Space-occupying / structural (tumour, abscess, hydrocephalus, haematoma)

Immediate Management Approach

The management of the unconscious patient follows a structured, time-critical ABCDE approach. Every team member should understand their role, and the senior clinician should lead the primary survey without distraction. The goal of the initial assessment is to identify and treat life-threatening conditions simultaneously, not sequentially.

Step 1: Scene Safety & Handover

Scene Safety

Ensure safety for staff and patient. Don PPE (gloves, face shield). In pre-hospital settings, check for environmental hazards (traffic, gas, needles, violence).

Structured Handover

Use ISBAR (Introduction, Situation, Background, Assessment, Recommendation) for clinical handover. Obtain collateral history from bystanders, paramedics, family — medications, medical history, events preceding collapse.

Step 2: Primary Survey — ABCDE

A — Airway (with Cervical Spine Protection)

Assess airway patency: listen for snoring (partial obstruction), gurgling (secretions/vomit), or silence (complete obstruction).
Open airway with head-tilt/chin-lift (or jaw thrust if cervical spine injury suspected).
Suction oropharynx if secretions or vomitus present.
Insert oropharyngeal airway (OPA) if GCS ≤ 8 and no gag reflex. Nasopharyngeal airway (NPA) is an alternative if jaw clenching is present (avoid if basal skull fracture suspected).
Maintain cervical spine immobilisation if trauma mechanism (manual in-line stabilisation until cleared or collar applied).
Definitive airway (endotracheal intubation) if GCS ≤ 8, unable to maintain patency, or ongoing aspiration risk.

B — Breathing

Assess respiratory rate, depth, pattern, and effort. Look for asymmetry of chest expansion.
Apply high-flow oxygen (15 L/min via non-rebreather mask) to maintain SpO₂ ≥ 94%. Target 88–92% if COPD/chronic hypercapnia suspected.
Note abnormal breathing patterns: Cheyne-Stokes (bilateral cortical/brainstem disease), ataxic/Biot's (medullary lesion), cluster breathing (posterior fossa pathology).
If ventilatory support needed: bag-valve-mask (BVM) ventilation at 10–12 breaths/min, then proceed to intubation.

C — Circulation

Assess heart rate, blood pressure (both arms if aortic dissection considered), capillary refill time (central and peripheral), skin colour and temperature.
Establish IV access: two large-bore (16–18 G) cannulae. Intraosseous (IO) access if IV fails within 2 attempts or time-critical.
Take bloods at time of IV access: FBC, UEC, LFTs, glucose, lactate, coagulation, troponin, blood gas (ABG/VBG), blood cultures if febrile.
Fluid resuscitation: 500 mL 0.9% sodium chloride (normal saline) bolus if hypotensive; reassess after each bolus. Avoid aggressive fluids if raised ICP suspected (use isotonic fluids judiciously).
If cardiac arrhythmia suspected: continuous cardiac monitoring and 12-lead ECG.

D — Disability (Neurological Assessment)

GCS — record E, V, M separately (see GCS section above).
Pupils: Size, symmetry, and reactivity to light. Unilateral fixed dilated pupil suggests ipsilateral herniation (III nerve compression). Bilateral fixed dilated pupils indicate severe brainstem injury or prolonged anoxia. Pinpoint pupils suggest opioid toxicity or pontine lesion.
Blood glucose — measure immediately using point-of-care glucometer. Treat hypoglycaemia before any other diagnostic step.
Temperature — hypothermia (< 35°C) or hyperthermia (> 40°C) both require urgent correction.
Limb tone, reflexes, and posturing — document asymmetry (focal signs suggest structural cause).

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Empiric treatments to give early: IV glucose (50 mL of 50% glucose or 200 mL of 10% glucose — preferred in paediatrics) for BGL < 4.0 mmol/L. IV naloxone (200 µg, repeat every 2–3 min) for suspected opioid toxicity. IV thiamine 300 mg (before glucose if Wernicke's encephalopathy suspected in alcohol-dependent patients). Benzodiazepines for active seizure. Empiric IV antibiotics + aciclovir if meningitis/encephalitis suspected.

E — Exposure & Environment

Fully expose the patient to identify injuries, rashes (petechiae in meningococcaemia), injection sites (drug use), skin changes (chronic liver disease, jaundice, uraemic frost).
Check axillary temperature or use oesophageal/rectal probe if hypothermia or hyperthermia suspected.
Prevent hypothermia — warm blankets, warmed IV fluids. Unconscious patients are prone to heat loss.
Log-roll to assess spine and examine the back for injuries.

Immediate Reversal Agents

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Glucose (IV)

Glucocil® / Generic · Carbohydrate

Adult dose 50 mL of 50% glucose (25 g) IV slow push, or 200 mL of 10% glucose (20 g) IV over 15 min (preferred peripheral vein option)

Paediatric dose 2–5 mL/kg of 10% glucose (0.2–0.5 g/kg) IV bolus

Indication BGL < 4.0 mmol/L in unconscious or symptomatic patient

Renal adjustment None required

PBS status ✔ PBS General Benefit

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Naloxone

Narcan® · Opioid antagonist

Adult dose 200 µg IV (titrated), repeat every 2–3 min up to 10 mg total; IM 400–800 µg if no IV access; IN 1.8 mg each nostril (pre-hospital)

Paediatric dose 10 µg/kg IV/IO, repeat every 2–3 min; IM/IN if no IV access

Indication Suspected opioid toxicity — respiratory depression, pinpoint pupils, reduced GCS

Duration Onset 1–2 min IV; shorter half-life than most opioids — observe for re-sedation for ≥ 1 hour

PBS status ✔ PBS General Benefit

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Thiamine (Vitamin B1)

Generic · Vitamin supplement

Adult dose 300 mg IV in 100 mL 0.9% NaCl over 30 min (administer BEFORE glucose if Wernicke's suspected)

Paediatric dose 50–100 mg IV for older children; seek specialist advice

Indication Alcohol-dependent patients, malnourished, suspected Wernicke's encephalopathy

Renal adjustment None required

PBS status ✔ PBS General Benefit

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Flumazenil

Anexate® · Benzodiazepine antagonist

Adult dose 200 µg IV, repeat every 60 sec up to 1 mg total (max 3 mg if recurrent sedation)

Paediatric dose 10 µg/kg IV (max 200 µg per dose); repeat every 1 min up to 40 µg/kg or 1 mg

Indication Benzodiazepine-induced sedation in benzodiazepine-naive patients only

Contraindications Chronic benzodiazepine use (seizure risk), co-ingestion of pro-convulsant drugs (TCA, bupropion), suspected raised ICP

PBS status ✔ PBS General Benefit

Immediate Investigations

ESSENTIAL Point-of-care blood glucose Perform within first 30 seconds. BGL < 4.0 mmol/L = treat immediately.

ESSENTIAL 12-lead ECG Detect arrhythmia (VT, VF, complete heart block, Brugada, long QT), ischaemia, or drug effect (TCA widening of QRS).

ESSENTIAL Arterial / venous blood gas pH, pCO₂, pO₂, lactate, glucose, sodium, potassium, ionised calcium, methaemoglobin, carboxyhaemoglobin (CO poisoning).

AVAILABLE CT brain (non-contrast) First-line imaging for suspected intracranial pathology. Should be performed within 1 hour of presentation for suspected stroke. Access varies in rural/remote Australia — consider early retrieval to a major centre.

AVAILABLE Blood tests (FBC, UEC, LFTs, coagulation, lactate, ethanol, ammonia) Drawn at time of IV access. Results guide ongoing management. Blood cultures if febrile.

SPECIALIST CT angiography / MRI brain If stroke or SAH suspected. CTA for large vessel occlusion (mechanical thrombectomy eligibility). MRI for posterior fossa pathology and non-convulsive status.

SPECIALIST Lumbar puncture After CT if SAH suspected (CT sensitivity declines after 6 hours). Contraindicated if raised ICP, coagulopathy, or local infection. Send CSF for cell count, protein, glucose, Gram stain, culture, xanthochromia.

REFERRAL Continuous EEG monitoring For suspected non-convulsive status epilepticus (persistent unexplained altered consciousness despite normal CT and metabolic correction). Contact neurology / arrange EEG within 24 hours.

Management Timeline

0 min

Assess responsiveness. Call for help. Ensure scene safety.

0–2 min

Open airway (head-tilt/chin-lift or jaw thrust). Assess breathing. Apply high-flow O₂. Check BGL immediately.

2–5 min

IV access × 2 (or IO). Bloods drawn. Treat hypoglycaemia if BGL < 4.0. Administer naloxone if opioid toxidrome. Apply cardiac monitoring.

5–15 min

Complete primary survey (ABCDE). GCS, pupils, vital signs documented. 12-lead ECG. Blood gas. Consider intubation if GCS ≤ 8. Cervical spine protection if trauma.

15–30 min

CT brain (non-contrast) if structural cause suspected. Empiric antibiotics (ceftriaxone 2 g IV) + aciclovir (10 mg/kg IV) if meningitis/encephalitis possible. Arrange ICU admission if required.

30–60 min

Review CT results. Neurosurgical / neurology consultation if indicated. Specialist retrieval coordination for rural/remote patients. Secondary survey and ongoing monitoring.

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Antibiotics must not be delayed: If bacterial meningitis or encephalitis is suspected, administer IV ceftriaxone (adult: 2 g; child: 50–100 mg/kg, max 2 g) + dexamethasone (adult: 0.15 mg/kg IV) + IV aciclovir (10 mg/kg) BEFORE lumbar puncture and BEFORE CT if imaging will cause a significant delay. Time-to-antibiotics is the single most important modifiable factor in meningitis outcomes.

Episodic Causes — Blackouts, Syncope & Transient Loss of Consciousness

Transient loss of consciousness (TLOC) is defined as a spontaneous, transient loss of consciousness with complete recovery. It accounts for up to 3% of all ED presentations in Australia. The key diagnostic challenge is distinguishing between syncope (global cerebral hypoperfusion), epileptic seizure, and rare causes such as psychogenic pseudosyncope or vertebrobasilar TIA.

Classification of Transient Loss of Consciousness

Type	Mechanism	Key Features	Risk Level
Vasovagal syncope (reflex)	Vasodilation ± bradycardia triggered by pain, emotion, micturition, prolonged standing	Prodrome (nausea, pallor, diaphoresis, tunnel vision), postural trigger, rapid recovery, may have brief clonic jerks (convulsive syncope)	Low risk — usually benign
Orthostatic hypotension	Failure of compensatory vasoconstriction on standing (volume depletion, autonomic neuropathy, medications)	Onset within 3 min of standing; improves with sitting/lying; medications (antihypertensives, diuretics, alpha-blockers, antidepressants); dehydration; Parkinson's disease; diabetes	Low–moderate risk
Cardiac syncope — arrhythmic	Bradyarrhythmia (complete heart block, sick sinus syndrome) or tachyarrhythmia (VT, SVT, AF with rapid ventricular response, long QT, Brugada)	Sudden onset without prodrome, exertional, palpitations, may occur while sitting/lying, family history of sudden cardiac death	HIGH RISK — 1-year mortality up to 30%
Cardiac syncope — structural	Aortic stenosis, hypertrophic cardiomyopathy (HOCM), pulmonary hypertension, cardiac tamponade, aortic dissection, massive PE	Exertional syncope, chest pain, new murmur, signs of right heart failure, risk factors for VTE	HIGH RISK
Epileptic seizure	Abnormal excessive cortical neuronal activity	Tonic-clonic movements, tongue biting (lateral), incontinence, prolonged post-ictal confusion (> 5 min), cyanosis during event, headache, known epilepsy	Variable — depends on aetiology
Psychogenic pseudosyncope / pseudoseizure	Non-epileptic / functional neurological disorder	Eyes closed during event (eyes are typically open in true syncope), prolonged duration, asynchronous movements, pelvic thrusting, no post-ictal confusion, psychiatric history	Low immediate risk — requires specialist follow-up
Vertebrobasilar TIA	Transient posterior circulation ischaemia	Associated vertigo, diplopia, dysarthria, ataxia, bilateral visual field loss; usually older patients with vascular risk factors	High risk — stroke precursor

Differentiating Syncope from Seizure

Feature	Syncope	Epileptic Seizure
Trigger	Posture, pain, emotion, Valsalva	Sleep deprivation, alcohol withdrawal, missed medications
Prodrome	Nausea, pallor, diaphoresis, tunnel vision	Aura (déjà vu, epigastric rising, flashing lights)
Eyes during event	Open (upward gaze common)	Open, deviated
Movements	Brief myoclonic jerks (< 15 sec), generalised	Rhythmic tonic-clonic, > 15 sec
Tongue biting	Tip of tongue	Lateral tongue (highly specific)
Incontinence	Rare	Common (urinary)
Recovery	Seconds to 1–2 minutes	Minutes to hours (post-ictal confusion, drowsiness, headache)
Cyanosis	Brief or absent	Often present during tonic phase

Risk Stratification of Syncope — San Francisco Syncope Rule / Canadian Syncope Risk Score

Several validated tools assist in risk-stratifying patients presenting with syncope in the ED:

High-Risk Features Requiring Admission / Urgent Investigation

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Admit and investigate urgently if ANY of the following are present:

Abnormal ECG (new arrhythmia, ischaemic changes, long QT > 450 ms, Brugada pattern, bifascicular block, pre-excitation)
Syncope during exertion
Syncope while supine
Family history of sudden cardiac death at age < 40 years
Severe structural heart disease or known cardiomyopathy
Heart failure (known or suspected)
Haemodynamic instability at presentation (SBP < 90 mmHg, HR < 40 or > 150 bpm)
Signs/symptoms suggesting acute coronary syndrome
Signs suggesting PE (pleuritic chest pain, DVT risk factors, hypoxia)
Severe anaemia (Hb < 70 g/L) or active gastrointestinal bleeding
Persistent neurological signs after event (suggesting stroke)

Investigations for TLOC

ESSENTIAL 12-lead ECG Mandatory for every TLOC presentation. Look for arrhythmia, ischaemia, QTc prolongation, Brugada pattern, WPW, hypertrophy.

ESSENTIAL Orthostatic blood pressure Measure lying and standing BP. A sustained drop in SBP ≥ 20 mmHg or DBP ≥ 10 mmHg within 3 min of standing is diagnostic of orthostatic hypotension.

ESSENTIAL Blood glucose + FBC + UEC Rule out hypoglycaemia, anaemia, electrolyte derangement, renal impairment.

AVAILABLE Continuous cardiac monitoring (telemetry) Minimum 24 hours for patients with suspected cardiac syncope. Consider prolonged monitoring (Holter 7–14 days, implantable loop recorder) for recurrent unexplained syncope.

AVAILABLE Echocardiography If structural heart disease suspected (murmur, abnormal ECG, heart failure). Assess for aortic stenosis, HOCM, LV function, pulmonary hypertension.

AVAILABLE Troponin If ACS or PE suspected. High-sensitivity troponin at 0 and 2 hours.

SPECIALIST Tilt-table test For recurrent unexplained syncope with suspected vasovagal mechanism. Performed in cardiology / autonomic laboratory.

SPECIALIST Electrophysiology study (EPS) For suspected arrhythmic syncope when non-invasive testing is inconclusive. Requires MBS item 18260 or equivalent.

SPECIALIST EEG If epileptic seizure suspected but diagnosis uncertain. Not routinely recommended after a single TLOC with clear syncope features.

Convulsive Syncope — Benign Myoclonic Jerks

It is important to recognise that brief generalised myoclonic jerks (typically < 15 seconds) are common during true syncope and do not indicate epilepsy. This "convulsive syncope" is caused by transient cortical hypoxia and can mimic tonic-clonic seizure. Distinguishing features include: very brief duration of jerking, absence of tonic-clonic progression, rapid full recovery (within seconds), and a clear syncopal prodrome. These patients do not require anti-epileptic medications.

Disposition Guidelines for TLOC

Presentation	Disposition	Follow-up
Classic vasovagal syncope, normal ECG, no red flags	Discharge from ED with advice	GP review in 1–2 weeks; education on prodrome recognition and physical counter-pressure manoeuvres
Orthostatic hypotension — medication-related	Discharge with medication review	GP to review and adjust antihypertensives/diuretics within 1 week
Possible cardiac syncope or any red flag	Admit for telemetry + investigation	Cardiology consultation; echocardiography; prolonged monitoring if initial workup negative
Suspected epileptic seizure	Observe until post-ictal recovery; admit if first seizure or status	Urgent neurology referral; first seizure clinic if available; EEG within 2 weeks
Recurrent unexplained TLOC	Admit or arrange rapid-access TLOC clinic	Cardiology + neurology assessment; consider implantable loop recorder; driving restrictions per Austroads guidelines

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Austroads driving guidelines: After a TLOC episode, patients must be advised about driving restrictions as per the Austroads Assessing Fitness to Drive guidelines (2022). Vasovagal syncope: no driving restriction unless recurrent and unexplained. Cardiac syncope: private vehicle licence cessation for ≥ 6 months; commercial licence cessation for ≥ 12 months. Epileptic seizure: private vehicle ≥ 6 months seizure-free; commercial vehicle ≥ 10 years seizure-free and off AEDs. State and territory requirements may vary.

Special Populations

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Paediatrics

Use the Paediatric GCS for children < 2 years (modified verbal component).

The most common causes of paediatric unconsciousness are febrile seizure (post-ictal), head trauma (including non-accidental injury — always consider NAI), hypoglycaemia, meningitis, ingestion/poisoning, and epilepsy.

Glucose: use 10% glucose 2–5 mL/kg IV (0.2–0.5 g/kg). Avoid 50% glucose in paediatric patients — causes severe phlebitis and osmolar injury.

Empiric antibiotics for suspected meningitis: Ceftriaxone 50–100 mg/kg IV (max 2 g) + dexamethasone 0.15 mg/kg (for children > 6 weeks with suspected bacterial meningitis).

Consider non-accidental injury (NAI) in any infant or young child with unexplained unconsciousness, inconsistent history, or retinal haemorrhages. Mandated reporting obligations apply in all Australian states and territories.

Corticosteroids: use with caution in paediatric meningitis — evidence less robust than in adults; discuss with paediatric infectious disease specialist.

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Pregnancy

In pregnant patients, assume left lateral tilt (15–30°) to avoid aortocaval compression (supine hypotension syndrome).

Unique causes of LOC in pregnancy: eclampsia (seizures + hypertension + proteinuria), amniotic fluid embolism, placental abruption, pulmonary embolism (hypercoagulable state), peripartum cardiomyopathy, and venous sinus thrombosis.

Eclampsia: treat with IV magnesium sulfate 4 g over 15 min (loading), then 1 g/hour maintenance. Urgent obstetric review for delivery.

CT brain: use without hesitation when clinically indicated — radiation risk to the fetus is minimal (< 0.05 mGy) and the benefit of diagnosing intracranial pathology outweighs theoretical risk.

Lumbar puncture: safe in pregnancy; no modification to technique required.

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Elderly

Falls in the elderly may be misattributed to "tripping" when the true cause is syncope or TIA — always assess for underlying cardiac or neurological aetiology.

Polypharmacy is a major contributor to LOC — review all medications, particularly antihypertensives, diuretics, opioids, benzodiazepines, anticholinergics, and antipsychotics.

Orthostatic hypotension is common due to autonomic impairment, dehydration, and medications. Measure lying-standing BP in all elderly patients presenting with collapse.

Subdural haematoma may present insidiously — consider in elderly patients on anticoagulants with fluctuating consciousness and no clear precipitant.

UTI and pneumonia are common triggers for delirium/unconsciousness in the elderly — but avoid attributing LOC solely to infection without excluding life-threatening causes first.

Aged care facilities: consider medication errors, dehydration, and missed doses as precipitants. Obtain full medication chart and recent changes.

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Renal Impairment

Uraemic encephalopathy is a cause of progressive unconsciousness in end-stage kidney disease (eCKD Stage 5 / eGFR < 15). Requires urgent dialysis.

Hyponatraemia-related LOC is common in CKD — correct slowly (max 8–10 mmol/L per 24 hours) to avoid osmotic demyelination syndrome.

Many drugs accumulate in renal impairment — adjust doses of gabapentin, pregabalin, opioids, benzodiazepines, and antibiotics accordingly. Avoid meperidine (pethidine) in CKD (normeperidine neurotoxicity).

Dialysis patients: assess fistula/graft patency and consider dialysis-related complications (disequilibrium syndrome, air embolism, hypoglycaemia).

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Hepatic Impairment

Hepatic encephalopathy (HE) is graded I–IV; Grade III–IV presents with stupor or coma. The West Haven criteria classify severity.

First-line treatment: lactulose 20–30 mL PO/NG every 2–6 hours until 2–3 soft stools/day, then titrate. Rifaximin 550 mg PO BD is added for secondary prophylaxis (PBS Authority Required).

Avoid all sedatives (benzodiazepines, opioids) in hepatic encephalopathy — reduced hepatic clearance and increased cerebral sensitivity lead to profound and prolonged sedation.

Exclude spontaneous bacterial peritonitis (SBP) as a precipitant — diagnostic paracentesis with ascitic fluid cell count (> 250 polymorphs/mm³ = SBP). Empiric ceftriaxone 2 g IV.

Coagulopathy: check INR before LP or procedures. FFP or prothrombin complex concentrate may be required. Thrombocytopenia is common — consider platelet transfusion if < 50 × 10⁹/L and procedural bleeding risk.

🛡️

Immunocompromised

Immunocompromised patients (HIV, chemotherapy, transplant recipients, biologics, long-term corticosteroids) have an expanded differential: opportunistic CNS infections (cryptococcal meningitis, toxoplasmosis, CMV, PML, TB meningitis, listeria), CNS lymphoma, and drug-related encephalopathy.

Empiric therapy should cover Listeria monocytogenes (add ampicillin 2 g IV every 4 h to standard meningitis regimen) and consider Cryptococcus (amphotericin B + flucytosine — requires specialist input).

HIV-positive patients with GCS reduction: consider cerebral toxoplasmosis (ring-enhancing lesion on CT), primary CNS lymphoma, cryptococcal meningitis (India ink, CrAg), and HIV-associated neurocognitive disorder.

Transplant patients on calcineurin inhibitors (tacrolimus, cyclosporine): check drug levels — neurotoxicity is common at supratherapeutic levels. Posterior reversible encephalopathy syndrome (PRES) presents with seizures, headache, visual disturbances, and altered consciousness.

Blood cultures, CT, and LP are lower threshold in immunocompromised patients. Discuss with infectious disease specialist early.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Higher burden of disease

Aboriginal and Torres Strait Islander Australians experience significantly higher rates of traumatic brain injury (2–3 times the non-Indigenous rate), diabetic emergencies (hypoglycaemia and hyperglycaemic crises), and rheumatic heart disease-related stroke and cardiac syncope compared to the general Australian population (AIHW, 2023).

Diabetes and hypoglycaemia

Type 2 diabetes prevalence in Indigenous Australians is 3–4 times higher than in non-Indigenous Australians. Insulin-treated patients in remote communities may be at increased risk of hypoglycaemia due to food insecurity, limited health literacy, and reduced access to monitoring. Glucometers and glucose supplies must be available in all community health centres.

Rheumatic heart disease (RHD)

RHD is largely a disease of Aboriginal and Torres Strait Islander Australians, particularly in the Northern Territory, Queensland, and Western Australia. RHD-related cardiac arrhythmia (atrial fibrillation, complete heart block) and embolic stroke are important causes of unconsciousness. Echocardiography access in remote communities is limited — arrange for screening and specialist outreach clinics through RHDAustralia and END RHD programs.

Trauma and interpersonal violence

Head trauma from interpersonal violence, motor vehicle accidents, and falls is a leading cause of unconsciousness in Indigenous communities, particularly among young adults and in remote areas. Culturally safe triage, clear communication, and early retrieval are critical. Trauma-informed care must address the psychosocial context.

Remote and rural access

Many Aboriginal and Torres Strait Islander Australians live in remote communities with limited access to emergency medical services, CT scanning, laboratory facilities, and specialist physicians. Health workers and nurses in remote clinics must be trained in the primary survey (ABCDE) and early retrieval protocols. The Royal Flying Doctor Service (RFDS) and state retrieval services must be contacted early for any unconscious patient in a remote setting. Telehealth consultation with emergency physicians is recommended while awaiting retrieval.

Alcohol and substance use

Alcohol-related unconsciousness and Korsakoff's/Wernicke's encephalopathy are more prevalent in some Indigenous communities. Ensure IV thiamine (300 mg) is administered before glucose in alcohol-dependent patients. Culturally appropriate drug and alcohol services should be integrated into the management pathway. Community-based dry zones and alcohol management plans may reduce harm.

Cultural safety

Gender considerations: some patients may prefer a health practitioner of the same gender, particularly for examination and procedures. Wherever possible, accommodate this preference. Use Aboriginal Health Practitioners (AHPs) and Aboriginal Liaison Officers (ALOs) to facilitate communication and ensure culturally safe care. "Sorry Business" (bereavement obligations) may affect family availability for consent and decision-making — be respectful of cultural practices. Recognise the role of traditional healers and incorporate cultural beliefs into care planning where appropriate.

Language and communication

English may be a second or third language for many Indigenous Australians, particularly in remote communities. Use interpreter services (Aboriginal Interpreter Service [AIS] in the NT; state equivalents) for clinical communication. Avoid medical jargon. Written discharge and safety-netting information should be in plain language and, where available, in the patient's first language. Visual communication tools may be helpful.

📚 References

1. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974;304(7872):81–84.
2. Teasdale G, Maas A, Lecky F, et al. The Glasgow Coma Scale at 40 years: standing the test of time. Lancet Neurol. 2014;13(8):844–854.
3. Australian Institute of Health and Welfare (AIHW). Head injury hospitalisations in Australia 2019–20. AIHW; 2023. Available at: www.aihw.gov.au.
4. Shen WK, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope. J Am Coll Cardiol. 2017;70(5):e39–e110.
5. Australasian College for Emergency Medicine (ACEM). Guideline on the management of transient loss of consciousness in adults. Melbourne: ACEM; 2019.
6. Stecker EC, Vickers C, Waltz J, et al. Population-based analysis of sudden cardiac death with and without left ventricular systolic dysfunction. J Am Coll Cardiol. 2006;47(6):1161–1166.
7. Royal Australian College of General Practitioners (RACGP). Red Book: Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2016.
8. Australasian Society of Clinical Immunology and Allergy (ASCIA); Australian and New Zealand Society of Critical Care. Anaphylaxis guidelines. Sydney: ASCIA; 2023.
9. National Health and Medical Research Council (NHMRC). Australian guidelines for the prevention and control of infection in healthcare. Canberra: NHMRC; 2019.
10. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework 2023. Canberra: AIHW; 2023.
11. RHDAustralia (RHD Australia). The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 3rd edn. Darwin: Menzies School of Health Research; 2020.
12. Austroads. Assessing Fitness to Drive: Medical standards for licensing and clinical management guidelines. Sydney: Austroads; 2022.
13. van Dijk JG, Thijs RD, van Zwet E, et al. The semiology of tilt-induced reflex syncope in relation to electroencephalographic changes. Brain. 2014;137(2):576–585.
14. Lewis M, Handelman B, Dallan G, et al. Evidence-based emergency medicine/systematic review abstract: use of the Glasgow Coma Scale in the prehospital setting. Ann Emerg Med. 2019;73(1):68–71.
15. van de Beek D, Cabellos C, Dzupova O, et al. ESCMID guideline: diagnosis and treatment of acute bacterial meningitis. Clin Microbiol Infect. 2016;22(Suppl 3):S37–S62.

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.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).