What is the difference between delirium and dementia?

Delirium comes on suddenly — over hours to days — and fluctuates throughout the day, with the level of consciousness often varying markedly. Dementia develops gradually over months to years, and attention is relatively preserved in the early stages while memory and function decline. A person with dementia can develop delirium on top of their dementia — delirium superimposed on dementia is common and easily missed because behavioural changes are attributed to the dementia. Key signals for delirium are the acuteness of onset (family or carers notice something different) and the fluctuation — periods of appearing almost back to normal interspersed with significant confusion.

Why is delirium dangerous if someone is just confused?

Delirium signals that the brain is under serious stress from an underlying medical problem. It is associated with increased in-hospital mortality (around 25% in some cohorts), prolonged hospital stays, accelerated cognitive decline in people who already have dementia, increased risk of institutionalisation, and a higher likelihood of developing dementia in those who had no prior cognitive impairment. The hypoactive form — quiet, withdrawn, drowsy, not eating — is the most common and the most dangerous precisely because it is often missed or attributed to the patient being tired. Any older person who is acutely more confused than usual needs medical assessment.

What causes delirium?

Delirium is almost always multifactorial — especially in older adults, where three or more contributing factors are common. The DELIRIUM mnemonic covers the main causes: Drugs (anticholinergics, opioids, benzodiazepines, steroids, polypharmacy); Electrolytes (sodium, calcium, magnesium abnormalities); Lack of drugs — withdrawal from alcohol or benzodiazepines; Infection (urinary tract infection, pneumonia, sepsis); Reduced sensory input (missing hearing aids, glasses; ICU environment); Intracranial (stroke, subdural haematoma, seizure); Urinary retention or faecal impaction; Myocardial or metabolic causes (heart attack, low oxygen, thyroid disorders, organ failure). Finding the cause or causes is the priority.

Is medication needed for delirium?

Not usually. The Australian Delirium Clinical Care Standard 2021 recommends non-pharmacological management as the primary approach — treating the underlying cause, restoring familiar people and environments, correcting sensory impairment, mobilising early, maintaining normal sleep and wake cycles. Medications are reserved for situations where the delirium is causing severe distress or significant safety risk to the patient or others, or is preventing essential medical care. When medication is needed, low-dose haloperidol is the most commonly used option. Benzodiazepines are generally avoided in delirium (they can make it worse) except in alcohol or benzodiazepine withdrawal, where they are specifically indicated.

How long does delirium last and does it cause permanent damage?

Recovery time varies. In mild delirium with a straightforward, treatable cause, confusion can clear within days. In severe delirium, particularly in older patients with pre-existing dementia, resolution may take weeks, and in some cases symptoms persist beyond hospital discharge. Long-term, delirium is associated with accelerated cognitive decline — it does not simply return the brain to its pre-delirium baseline. This is why prevention (using multicomponent programmes like the Hospital Elder Life Program) and early treatment of the underlying cause are so important. Family members should be prepared for recovery to take longer than expected and for some residual effects.

Delirium

Delirium: recognising acute confusion in older patients — the AU approach

By Dr HB Lo, FACRRM Reviewed 25 June 2026 13 min read

Delirium is an acute, fluctuating disturbance of attention and consciousness caused by a medical condition, medication, or withdrawal — not a psychiatric illness. It affects 15–25% of older people on general medical wards and up to 80% in intensive care. It is common, dangerous, and frequently missed — especially the quiet, withdrawn form (hypoactive delirium).

The priority is finding and treating the underlying cause, not sedating medications. Non-pharmacological measures — reorientation, sensory restoration, early mobilisation, maintaining sleep–wake rhythms — are the primary approach. Medications are reserved for severe distress or safety risk.

Delirium is one of the most common and most dangerous conditions in hospital medicine, yet it remains frequently undetected — particularly its quiet, withdrawn form. In the general medicine ward, it affects 15–25% of older patients. In the intensive care unit, up to 80%. After hip fracture surgery, up to 50%. Despite this prevalence, it is often attributed to the patient “just being confused” from age or dementia, and the reversible underlying cause goes untreated. The Australian Delirium Clinical Care Standard 2021 exists precisely because under-recognition is the norm, not the exception. The general practice role is to maintain a high index of suspicion, lead the collateral history, and understand when referral or escalation is needed for the delirious patient encountered in the community, residential aged care, or at the point of hospital discharge.

A. Core clinical — the AU general practice framework

Definition and diagnostic criteria

Delirium is defined in DSM-5 by five criteria: (A) a disturbance in attention and awareness; (B) acute onset over hours to days, representing a change from baseline, and fluctuating during the day; (C) an additional cognitive disturbance (memory, disorientation, language, visuospatial, or perception); (D) features not better explained by a pre-existing or evolving neurocognitive disorder or coma; and (E) evidence that the disturbance is caused by a medical condition, substance, toxin exposure, or multiple factors. The fluctuating course — periods of relative clarity punctuating marked confusion — is characteristic.

Subtypes

The ANZSGM and RACGP recognise three clinical subtypes:

Hyperactive delirium (15–25% of cases) — restless, agitated, hyperalert, vocal, often experiencing hallucinations or paranoid beliefs. Easily recognised; sometimes mistaken for a primary psychiatric illness.
Hypoactive delirium (>50% of cases) — withdrawn, drowsy, slowed responses, reduced oral intake, decreased spontaneous movement. The most common and the most dangerous — frequently missed, attributed to fatigue or depression, associated with worse prognosis.
Mixed delirium (~30% of cases) — alternates between hyperactive and hypoactive features within the same day.

Differential diagnosis

Key conditions to distinguish from delirium:

Dementia — chronic, progressive decline over months to years; attention relatively preserved early; memory is the primary deficit; may co-exist with delirium (delirium superimposed on dementia is the most common scenario in older hospitalised patients).
Depression and pseudodementia — mood is prominent; orientation usually preserved; onset over weeks not hours.
Primary psychosis — typically younger; prior psychiatric history; attention less affected; less fluctuating.
Non-convulsive status epilepticus (NCSE) — persistent unexplained confusion without clear cause warrants EEG.
Wernicke’s encephalopathy — confusion, ataxia, and ophthalmoplegia in the setting of alcohol use or malnutrition; requires urgent thiamine (IV thiamine is standard in at-risk patients presenting to hospital).
Stroke or TIA — focal neurological signs; acute onset; CT or MRI brain required.
Post-ictal state — following a witnessed or suspected seizure.

Finding the cause — the DELIRIUM mnemonic

Most delirium is multifactorial. eTG and the Delirium Clinical Care Standard recommend systematic review using a structured approach. The DELIRIUM mnemonic covers the major categories:

D — Drugs and drug withdrawal. The most modifiable cause. Anticholinergics (first-generation antihistamines, TCAs, oxybutynin, hyoscine patches, many antipsychotics); opioids (pethidine is particularly deliriogenic — best avoided; morphine in renal impairment accumulates); benzodiazepines; corticosteroids; polypharmacy (≥5 medications) even with individually low-risk agents. Withdrawal from alcohol (delirium tremens 48–96 hours post-cessation) or benzodiazepines is a distinct, serious cause requiring specific management.
E — Electrolytes and endocrine. Sodium (hypo- or hypernatraemia), calcium (hypercalcaemia particularly), magnesium, phosphate, hypo- or hyperglycaemia, thyroid dysfunction (hypo- or hyperthyroidism), adrenal insufficiency.
L — Lack of drugs. Alcohol withdrawal; benzodiazepine withdrawal; opioid withdrawal (less commonly produces frank delirium but causes significant distress).
I — Infection. Urinary tract infection is the most commonly cited cause in older patients — but asymptomatic bacteriuria is very common and should not be reflexively treated as the explanation for delirium without corroborating clinical evidence. Pneumonia, sepsis from any source, skin and soft-tissue infection, and CNS infection (rare but high-stakes) are all possibilities.
R — Reduced sensory input, Restraints, sleep deprivation. Missing hearing aids or glasses dramatically increases delirium risk; the ICU environment — continuous noise, bright lights, frequent interruptions, immobility — is inherently deliriogenic. Physical restraints are associated with prolonged delirium, not reduced delirium.
I — Intracranial. Stroke or haemorrhage; subdural haematoma (especially in elderly patients on anticoagulants who have fallen); raised intracranial pressure; seizure or post-ictal state; autoimmune or viral encephalitis.
U — Urinary retention and faecal impaction. Both are extremely common precipitants in older patients and easily treatable. Urinary retention is particularly common post-surgery and with anticholinergic medications or BPH. Always check for a palpable bladder or perform a bladder scan.
M — Myocardial and metabolic. Acute myocardial infarction (which may be painless in older patients); cardiac arrhythmia; heart failure; pulmonary embolism and hypoxia; hepatic encephalopathy; uraemic encephalopathy; severe anaemia.

Assessment tools

CAM (Confusion Assessment Method) is the most validated and widely used tool. It requires four features:

Acute onset and fluctuating course (from informant or nursing observation).
Inattention — ask the patient to name the months of the year backwards, or to squeeze the hand on the letter ‘A’ in a sequence read aloud.
Disorganised thinking — simple questions about context and a simple command.
Altered level of consciousness — anything other than fully alert.

Delirium is diagnosed if features 1 and 2 are present, plus either feature 3 or 4.

4AT is a rapid four-item tool (Alertness, Abbreviated Mental Test 4, Attention, Acute change) taking approximately two minutes, well-suited to emergency department and ward settings. A score of ≥4 indicates possible delirium.

Collateral history from a family member, regular carer, or aged care facility staff is essential — the patient themselves cannot reliably describe their own fluctuating state. GP records providing a cognitive baseline are invaluable.

Investigations

Investigations are targeted to find the cause or causes; not every patient needs every test:

Bloods — FBC; U&E (sodium, creatinine); calcium and magnesium; blood glucose; LFTs; TFTs; CRP; B12 and folate; ammonia (if hepatic encephalopathy suspected); troponin (if cardiac cause possible).
Urine — dipstick and midstream urine culture where UTI is clinically suspected (not as a reflex investigation for all delirium).
ECG — arrhythmia, myocardial infarction, QTc baseline before initiating antipsychotics.
Chest X-ray — pneumonia, pulmonary oedema, cardiac enlargement.
CT brain — selective, not universal. Indicated for focal neurological signs, head trauma, anticoagulated patients, persistent unexplained delirium, or suspected stroke, haemorrhage, or subdural haematoma. CT is not required as a routine screen in every confused older patient.
EEG — reserved for suspected NCSE or atypical/refractory delirium without a clear cause.
Lumbar puncture — where CNS infection or autoimmune encephalitis is clinically suspected after CT brain.

B. Prevention and non-pharmacological management

The strongest evidence in delirium management is for multicomponent non-pharmacological interventions — and the evidence is for prevention, not just treatment.

Cochrane reviews (Siddiqi 2016, 2024) demonstrate that multicomponent programmes reduce delirium incidence by approximately 30% in hospitalised older patients. The Hospital Elder Life Program (HELP) is the most studied model, and many Australian hospitals have adapted versions. The components:

Orientation — visible clock and dated calendar, regular named introductions by staff, reorientation to place and time; minimise bed moves and ward transfers.
Sensory restoration — hearing aids in and working, glasses on, dentures in place; well-lit during the day, dim at night; reduce unnecessary noise.
Family presence — familiar voices and faces are therapeutic; flexible visiting; structured approaches such as the ‘TOP 5’ personalised carer information card.
Mobility — early and regular mobilisation; OT and physiotherapy involvement; avoid prolonged bed rest.
Hydration and nutrition — proactive oral hydration; assistance with meals; preferred foods; dentures fitting.
Sleep — minimise nocturnal observations unless clinically essential; no caffeine in the afternoon; daytime activity to promote night-time sleep; avoid sedatives where possible (they frequently worsen delirium).
Reduce iatrogenic risk — remove unnecessary intravenous lines, catheters, and nasogastric tubes as early as clinically feasible; minimise anticholinergic prescribing; limit polypharmacy.
Pain management — both under-treated and over-treated pain contributes to delirium. Proactive non-opioid analgesia and regular pain review is preferable to relying on PRN opioids.
Bowel and bladder care — regular toileting schedule; bladder scan to rule out retention; bowel management to prevent impaction.

The ACSQHC Delirium Clinical Care Standard 2021 contains eight quality statements, of which statements 6 and 7 focus on non-pharmacological intervention as the primary treatment and minimisation of pharmacological treatment. This reflects the current evidence consensus.

Pharmacological prevention — melatonin 2–5 mg nocte has modest evidence from small randomised controlled trials for reducing delirium incidence and may be considered in high-risk patients. Routine antipsychotic prophylaxis is not recommended — randomised trials have not demonstrated benefit, and risks (extrapyramidal side effects, QTc prolongation, falls) are real.

C. Pharmacological treatment — judicious and restrictive

Medications are indicated for delirium only when non-pharmacological measures have been tried and have not adequately addressed:

Severe distress from paranoid hallucinations or profound agitation.
Immediate safety risk to the patient or others.
Delirium that is preventing essential investigation or treatment.

Hypoactive delirium should not be treated pharmacologically as a routine — there is no evidence that medications benefit quiet, withdrawn delirium, and the risks of over-sedation are significant.

Antipsychotics — low dose, short course, reassessed daily:

Haloperidol 0.5–1 mg oral/IM/subcutaneous every 4–6 hours as needed (maximum 5 mg/day) is first-line per eTG and AMH. Check QTc on ECG before initiating. Avoid in Parkinson’s disease and Lewy body dementia — D2 blockade can cause acute parkinsonism and neuroleptic malignant syndrome.
Risperidone 0.25–0.5 mg twice daily — alternative; fewer extrapyramidal side effects than haloperidol.
Quetiapine 12.5–25 mg twice daily — preferred when Parkinson’s disease or Lewy body dementia is present or suspected; lower D2 affinity; sedating; use cautiously.
Duration — reassess daily; discontinue as soon as clinically feasible; short courses of three to seven days are the standard expectation. These are off-label uses of antipsychotics for delirium.

Benzodiazepines are not recommended for routine delirium management — they frequently cause paradoxical agitation, prolonged sedation, and worsen rather than resolve delirium. They are specifically indicated in:

Alcohol withdrawal delirium (delirium tremens) — diazepam loading or symptom-triggered dosing per CIWA-Ar protocol; high mortality if undertreated.
Benzodiazepine withdrawal — a reducing taper using an appropriate agent.
Refractory agitation in palliative/end-of-life delirium — midazolam subcutaneous under specialist palliative care guidance.

Thiamine — high-dose IV thiamine (Pabrinex or equivalent; PBS-listed) is essential in any patient with alcohol use disorder or significant malnutrition presenting with confusion, to prevent or treat Wernicke’s encephalopathy. Do not delay for serum thiamine results.

Physical restraints should be used only as a last resort, with documented rationale, the least restrictive option chosen, and regular review — physical restraint is associated with prolonged delirium and injury, not improved outcomes.

D. Australian operations

MBS items

MBS Online items relevant to delirium:

Item	Context
23, 36, 44 — GP attendance	Standard consultation
92 — GP home or RACF visit	GP attendance in residential aged care; key item for delirium assessment without hospital transfer
701/703/705 — CMA	Comprehensive Medical Assessment for new RACF resident; includes cognitive baseline
707 — 75+ Health Assessment	Annual comprehensive assessment including cognitive screen
900/903 — HMR/RMMR	Pharmacist-led Home Medicines Review or Residential Medication Management Review — high value post-delirium to identify and deprescribe deliriogenic medications

PBS medications

PBS-listed items relevant to delirium management:

Haloperidol (Serenace) — tablets, oral liquid, injection — General Schedule.
Risperidone (Risperdal) — General Schedule; Authority Required (Streamlined) for behavioural disturbances in dementia.
Quetiapine (Seroquel) — PBS for schizophrenia/bipolar; off-label for delirium in PD/DLB; accessible.
Diazepam, lorazepam — General Schedule; critical for alcohol withdrawal management.
Thiamine — PBS-listed for thiamine deficiency and Wernicke’s; IM/IV preferred in at-risk patients.

Australian Delirium Clinical Care Standard 2021

The ACSQHC Delirium Clinical Care Standard contains eight quality statements applicable to any healthcare setting, including general practice and aged care:

Risk screening on admission.
Cognitive screening for at-risk or suspected patients.
Comprehensive assessment for diagnosis.
Patient-centred care plan.
Treatment of underlying cause.
Non-pharmacological multicomponent intervention.
Minimising pharmacological treatment.
Documented transitions of care.

Residential aged care

The GP has a particularly important role in managing delirium in residential aged care. A timely GP visit (item 92) to assess an acutely confused RACF resident can prevent unnecessary emergency department presentations. The Caring for Cognitive Impairment national campaign supports both facility staff training and GP engagement. The Aged Care Quality Standard 5 (Personal and Clinical Care) includes assessment of acute cognitive change; and the National Aged Care Mandatory Quality Indicator Program captures antipsychotic use, providing accountability for chemical restraint practices.

Discharge summaries after delirium should document the episode, likely causes, response to treatment, and any newly ceased medications — with clear communication to the receiving GP or RACF to support the post-discharge cognitive follow-up.

E. Special populations

Dementia. Delirium superimposed on dementia is the most common delirium presentation in aged care and hospital settings. The baseline cognitive impairment is the single biggest predictor of delirium. Family carers are essential informants — they can identify the acute change from the chronic baseline that defines delirium. Recovery may be incomplete or protracted. Post-delirium cognitive follow-up at four to eight weeks helps distinguish residual delirium from progression of the underlying dementia.

Alcohol use disorder. Alcohol withdrawal delirium (delirium tremens) typically occurs 48–96 hours after last drink and carries significant mortality if not treated. Diazepam (loading dose or symptom-triggered CIWA-Ar protocol) per eTG is the standard AU approach. High-dose IV thiamine must be given before or with any glucose to prevent precipitation of Wernicke’s encephalopathy. Refer to the alcohol use disorder article for detailed management.

Palliative and end-of-life care. Delirium occurs in up to 80% of patients in the last 48 hours of life. When the cause is irreversible, the goal shifts entirely to comfort and dignity. Distressing agitation may be managed with haloperidol or subcutaneous midazolam in consultation with specialist palliative care. Family education about the meaning of delirium near the end of life, and the fact that it often reflects disease progression rather than inadequate care, is a priority.

ICU and post-surgical patients. ICU delirium — assessed with CAM-ICU or ICDSC — is independently associated with increased mortality, prolonged ventilation, and long-term cognitive impairment. The ABCDEF bundle (Assess, Both SAT and SBT, Choice of sedation, Delirium assess and manage, Early mobility, Family engagement) is the international evidence-based framework. Dexmedetomidine as an alternative to benzodiazepine sedation reduces delirium incidence in mechanically ventilated patients.

When to escalate

Refer to hospital or geriatric medicine when:

Delirium is of unknown cause after initial assessment in the community or RACF — investigate and treat in the appropriate inpatient setting.
Alcohol or benzodiazepine withdrawal delirium is suspected — requires close monitoring and specific protocol management.
Suspected intracranial cause (focal neurology, head injury, anticoagulated patient, persistent unexplained delirium) — CT brain is required.
Suspected CNS infection (fever, neck stiffness, headache, immunocompromised) — urgent referral.
Patient is unsafe to remain at home or in a facility without inpatient-level monitoring.

Refer to geriatric medicine or psychogeriatrics for:

Complex delirium in frail older patients where comprehensive geriatric assessment would guide management.
Diagnostic uncertainty between delirium, dementia, and depression.
Refractory delirium not responding to standard management.

What this article is and is not

This is general health information drawn from Australian and international delirium guidelines — ACSQHC Delirium Clinical Care Standard 2021, ANZSGM position statements, eTG, RACGP, NICE CG103, AMH, Cochrane reviews — and is intended to support informed conversations between patients, families, and their treating clinicians. It is not personal medical advice and does not create a doctor–patient relationship. Clinical decisions about investigation, pharmacological management, and care setting are made individually with a treating GP and specialist.

For patient and carer information: HealthDirect — Delirium, Caring for Cognitive Impairment, Better Health Channel.

For acute mental health crisis: Lifeline 13 11 14, Beyond Blue 1300 22 4636.

Sources cited

Frequently asked questions

What is the difference between delirium and dementia?

Delirium comes on suddenly — over hours to days — and fluctuates throughout the day, with the level of consciousness often varying markedly. Dementia develops gradually over months to years, and attention is relatively preserved in the early stages while memory and function decline. A person with dementia can develop delirium on top of their dementia — delirium superimposed on dementia is common and easily missed because behavioural changes are attributed to the dementia. Key signals for delirium are the acuteness of onset (family or carers notice something different) and the fluctuation — periods of appearing almost back to normal interspersed with significant confusion.
Why is delirium dangerous if someone is just confused?

Delirium signals that the brain is under serious stress from an underlying medical problem. It is associated with increased in-hospital mortality (around 25% in some cohorts), prolonged hospital stays, accelerated cognitive decline in people who already have dementia, increased risk of institutionalisation, and a higher likelihood of developing dementia in those who had no prior cognitive impairment. The hypoactive form — quiet, withdrawn, drowsy, not eating — is the most common and the most dangerous precisely because it is often missed or attributed to the patient being tired. Any older person who is acutely more confused than usual needs medical assessment.
What causes delirium?

Delirium is almost always multifactorial — especially in older adults, where three or more contributing factors are common. The DELIRIUM mnemonic covers the main causes: Drugs (anticholinergics, opioids, benzodiazepines, steroids, polypharmacy); Electrolytes (sodium, calcium, magnesium abnormalities); Lack of drugs — withdrawal from alcohol or benzodiazepines; Infection (urinary tract infection, pneumonia, sepsis); Reduced sensory input (missing hearing aids, glasses; ICU environment); Intracranial (stroke, subdural haematoma, seizure); Urinary retention or faecal impaction; Myocardial or metabolic causes (heart attack, low oxygen, thyroid disorders, organ failure). Finding the cause or causes is the priority.
Is medication needed for delirium?

Not usually. The Australian Delirium Clinical Care Standard 2021 recommends non-pharmacological management as the primary approach — treating the underlying cause, restoring familiar people and environments, correcting sensory impairment, mobilising early, maintaining normal sleep and wake cycles. Medications are reserved for situations where the delirium is causing severe distress or significant safety risk to the patient or others, or is preventing essential medical care. When medication is needed, low-dose haloperidol is the most commonly used option. Benzodiazepines are generally avoided in delirium (they can make it worse) except in alcohol or benzodiazepine withdrawal, where they are specifically indicated.
How long does delirium last and does it cause permanent damage?

Recovery time varies. In mild delirium with a straightforward, treatable cause, confusion can clear within days. In severe delirium, particularly in older patients with pre-existing dementia, resolution may take weeks, and in some cases symptoms persist beyond hospital discharge. Long-term, delirium is associated with accelerated cognitive decline — it does not simply return the brain to its pre-delirium baseline. This is why prevention (using multicomponent programmes like the Hospital Elder Life Program) and early treatment of the underlying cause are so important. Family members should be prepared for recovery to take longer than expected and for some residual effects.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.