Delirium & Acute Confusional States

Delirium is a neuropsychiatric syndrome characterised by an acute disturbance in attention, awareness, and cognition that develops over hours to days, represents a change from baseline, and tends to fluctuate in severity over the course of the day. It is a medical emergency reflecting underlying physiological derangement rather than a primary psychiatric disorder.

In Australia, delirium remains significantly under-recognised. Prospective studies in Australian hospitals report detection rates of only 30–50% of cases meeting DSM-5 criteria, with hypoactive and mixed subtypes most frequently missed. The condition carries substantial morbidity and healthcare costs, with an estimated annual burden exceeding $2.7 billion to the Australian healthcare system.

Key Australian Data

The Australian Institute of Health and Welfare (AIHW) reports that older Australians (≥65 years) account for approximately 80% of delirium-related hospitalisations. Aboriginal and Torres Strait Islander Australians, who experience a higher burden of chronic disease at younger ages, may develop delirium at ages 10–15 years younger than the non-Indigenous population. Delirium is associated with a 1.9- to 3.2-fold increase in in-hospital mortality, a 2- to 3-fold increase in rates of new residential aged-care placement, and significantly accelerated long-term cognitive decline.

Early recognition is the single most important step in delirium management. The 2023 ACSQHC Delirium Clinical Care Standard recommends that all patients aged ≥65 years and all patients with known cognitive impairment presenting to any Australian healthcare setting should be screened for delirium using a validated tool.

Core Diagnostic Features (DSM-5-TR)

Confusion Assessment Method (CAM)

The CAM (Inouye et al., 1990) is the most widely validated and recommended bedside tool for delirium screening in Australian clinical practice. The short CAM can be administered in 5 minutes. The CAM-ICU is validated for mechanically ventilated patients. The 4AT (rapid assessment tool) is an alternative that requires no training and has high sensitivity (90%) in ED settings.

Delirium diagnosis by CAM requires Features 1 + 2 + either 3 or 4:

Delirium Subtypes

Differentiating Delirium from Dementia

Practical Screening Protocol for Australian EDs and Wards

• Trigger: All patients aged ≥65 years; all patients with known or suspected cognitive impairment; all post-operative patients (especially hip fracture); all ICU admissions; any acute change in behaviour or consciousness.
• Tool: Short CAM (5 min) or 4AT (2 min, no training required). For ICU: CAM-ICU.
• Frequency: On presentation, then at minimum every shift (q8–12h) for at-risk patients.
• Document: Record CAM result in the medical record and handover to the next clinician.
• If positive: Initiate cause-directed workup immediately (see Investigations and Initial Management).

Delirium is a final common pathway for multiple aetiologies. It is rarely unifactorial — most patients have 2–4 contributing precipitants simultaneously. A systematic approach using the DIMS mnemonic ensures no major category is overlooked.

Drugs — Common Culprits

Medications account for 30–40% of delirium cases in Australian hospitalised patients. Polypharmacy (≥5 medications) is itself an independent risk factor. High-risk drug classes include:

Infection

• Urinary tract infection: Most commonly attributed infectious cause in elderly Australians — but beware of asymptomatic bacteriuria (do not treat in catheterised or non-symptomatic patients simply because delirium is present).
• Pneumonia: Community-acquired and aspiration pneumonia. Consider in any delirious patient with hypoxia or new cough.
• Cellulitis / skin and soft-tissue infection: Particularly in patients with diabetes or peripheral vascular disease.
• COVID-19 and influenza: Delirium may be the presenting feature in older adults, even without prominent respiratory symptoms.
• Meningitis / encephalitis: Consider in patients with fever, neck stiffness, photophobia, focal neurological signs, or immunosuppression.
• Occult bacteraemia: Always obtain blood cultures in the septic, delirious patient.

Metabolic Derangements

Substance Use & Withdrawal

• Alcohol withdrawal delirium (delirium tremens): Typically onset 48–96 hours after last drink. Mortality 5–15% if untreated. Use the CIWA-Ar protocol; manage with benzodiazepines (diazepam or lorazepam) in a monitored setting. PBS-listed diazepam 5–20 mg PO/IV with symptom-triggered dosing.
• Benzodiazepine withdrawal: Can occur after only 2–4 weeks of regular use. Gradual taper recommended; abrupt cessation in ICU patients is a common precipitant.
• Opioid withdrawal: Less commonly causes delirium but contributes to agitation and autonomic instability.
• Anticholinergic toxicity: Flushing, dry skin, mydriasis, tachycardia, urinary retention, agitation. Physostigmine 0.5–2 mg IV (specialist use only) for severe cases.
• Cannabis, methamphetamine, synthetic cannabinoids: Increasingly recognised as delirium precipitants in younger Australian adults, particularly in regional and remote areas.

Structural & Sensory Causes

• Stroke / intracranial haemorrhage: Especially right hemisphere, thalamic, or posterior fossa lesions.
• Post-ictal state: Non-convulsive status epilepticus should be considered in unexplained persistent delirium — EEG monitoring required.
• Pain: Under-treated pain is a major and modifiable cause. Use validated pain scales suitable for non-verbal patients (e.g., Abbey Pain Scale in dementia).
• Urinary retention / constipation: Easily identified and treated; bladder scan and abdominal examination should be routine in delirium assessment.
• Sensory deprivation: Absent hearing aids or glasses, dark single rooms, lack of familiar objects — particularly important for patients with pre-existing dementia.

Delirium pathophysiology is multifactorial and incompletely understood. Current evidence supports a model of widespread neuroinflammation, neurotransmitter imbalance, and impaired connectivity in brain networks subserving attention and executive function.

Key Neurobiological Mechanisms

• Neuroinflammation: Systemic inflammatory mediators (IL-1β, IL-6, TNF-α) cross a disrupted blood–brain barrier, activate microglia, and cause widespread neuronal dysfunction. This "sickness behaviour" model explains why systemic infection causes cerebral dysfunction.
• Cholinergic deficiency: The most consistent neurotransmitter finding. Acetylcholine is essential for attention, arousal, and memory encoding. Anticholinergic medications and acetylcholinesterase depletion in ageing brains directly impair these functions.
• Dopaminergic excess: Excess dopamine contributes to hyperactive delirium and psychotic features. This underpins the use of dopamine-blocking antipsychotics in symptomatic management.
• GABA/glutamate imbalance: Impaired GABAergic inhibition and excessive glutamatergic excitation (NMDA receptor dysfunction) contribute to neuronal excitotoxicity. Hepatic encephalopathy represents a GABA-ergic excess model.
• Impaired network connectivity: Functional MRI studies demonstrate reduced connectivity between the thalamus, prefrontal cortex, and posterior parietal cortex — regions critical for attention and consciousness.
• Chronic vulnerability (brain reserve): Patients with pre-existing neurodegeneration (Alzheimer's, Lewy body, vascular dementia) have reduced brain reserve and are more susceptible to delirium from any given physiological insult.

The delirium workup should be directed by clinical assessment, but a minimum set of baseline investigations is recommended for all patients with new-onset delirium. Additional tests are guided by the DIMS screen and clinical findings.

Essential Investigations

Directed Investigations (Based on Clinical Suspicion)

Identifying High-Risk Patients

Prevention begins with identifying those at greatest risk. The following factors are independently associated with delirium in Australian hospital cohorts:

Severity Assessment

There is no single validated "severity score" for delirium used universally in Australian practice. However, the following clinical framework guides escalation:

Richmond Agitation–Sedation Scale (RASS)

Management of delirium follows three parallel tracks: (1) identify and treat the underlying cause(s), (2) implement non-pharmacologic supportive measures, and (3) consider cautious pharmacologic management for severe distress or safety concerns. Prevention in high-risk patients is the fourth pillar.

Track 1 — Identify and Treat the Cause

The single most effective intervention for delirium is treating the underlying precipitant. Every delirious patient should undergo a systematic cause-directed workup using the DIMS mnemonic (see Common Precipitants section). Key actions include:

• Medication review: Cease or reduce dose of all anticholinergic, sedative, and psychoactive medications where clinically safe. Involve a pharmacist for anticholinergic burden scoring.
• Infection management: Commence empirical antibiotics per local hospital antibiogram if infection suspected. For community presentations, refer to eTG Antibiotic guidelines — amoxicillin + clavulanate for UTI, ceftriaxone + azithromycin for pneumonia (adjust for local resistance patterns and patient allergies).
• Metabolic correction: Replace electrolytes, correct glucose, manage renal/hepatic failure. Administer IV thiamine 300–500 mg before glucose in any malnourished or alcohol-dependent patient.
• Pain management: Treat unrecognised pain with regular simple analgesia (paracetamol 1 g QID PO/IV) and judicious opioid titration. Paradoxically, both untreated pain and excessive opioids can cause delirium — use the lowest effective dose.
• Hydration and nutrition: Assess fluid status; commence IV normal saline if dehydrated. Ensure adequate oral intake with assistance at mealtimes.
• Manage constipation and urinary retention: Bladder scan (retention if >400 mL post-void). Laxatives (macrogol or lactulose) for constipation.

Track 2 — Non-Pharmacologic Multicomponent Interventions

Non-pharmacologic measures are first-line for all patients with delirium and form the cornerstone of prevention for high-risk patients. The Hospital Elder Life Program (HELP) model, adapted for Australian hospitals, has a strong evidence base.

Track 3 — Cautious Antipsychotic Use

Track 4 — Prevention in High-Risk Patients

Prevention is more effective than treatment. Multicomponent non-pharmacologic interventions can reduce new-onset delirium by 30–40% in high-risk populations. The Hospital Elder Life Program (HELP) and equivalent Australian models (e.g., Melbourne Ageing Research Collaboration guidelines) provide the framework.

In-Hospital Monitoring

Monitoring Antipsychotic Therapy

• ECG: Baseline and at 24–48 hours for haloperidol. Discontinue if QTc >500 ms or increases by >60 ms from baseline.
• Neurological status: Assess for extrapyramidal symptoms (EPS), akathisia, neuroleptic malignant syndrome (NMS) — fever, rigidity, autonomic instability, elevated CK. Stop antipsychotic immediately if NMS suspected.
• Sedation level: RASS target 0 to −1 for patients on antipsychotics. Over-sedation masks delirium and impedes assessment.
• Falls risk: Antipsychotics increase fall risk by 1.5–2× in elderly patients. Implement falls precautions.
• Cessation plan: Taper and cease antipsychotics within 48–72 hours of delirium resolution. If continuing beyond 1 week, formal specialist review is required with documented rationale.

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