Delirium and dementia assessment

Delirium vs Dementia, Perinatal Mood Disorders & Paediatric Psychiatry

Clinical psychiatry encompasses specialized populations that present unique diagnostic and therapeutic challenges across the human lifespan. In Australian healthcare settings, clinicians must adroitly distinguish between acute organic brain syndromes (delirium) and chronic neurodegenerative diseases (dementia) in elderly patients, identify and manage psychiatric emergencies across the perinatal period, and diagnose and treat neurodevelopmental and behavioural disorders in children and adolescents.

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Delirium vs Dementia: Clinical Differentiation & Bedside Assessment

Delirium is an acute neurocognitive syndrome characterized by transient cognitive dysfunction, attentional deficits, and fluctuating consciousness provoked by an underlying medical illness, intoxication, or medication adverse effect. In contrast, dementia (Major Neurocognitive Disorder) represents a gradual, progressive decline in cognitive function that interferes with independent daily activities.

Clinical Subtypes of Delirium

1. Hyperactive Delirium: Characterized by psychomotor agitation, restlessness, combative behaviour, hypervigilance, and prominent visual hallucinations. Readily recognized by ward staff.
2. Hypoactive Delirium: Characterized by lethargy, reduced motor activity, drowsiness, psychomotor slowing, apathy, and poverty of speech. AMC High-Yield Pitfall: Hypoactive delirium is the most common subtype in elderly inpatients but is frequently missed or misdiagnosed as depression, fatigue, or worsening dementia, carrying higher mortality due to delayed investigation.
3. Mixed Delirium: Rapidly oscillates between hyperactive and hypoactive states, often worsening nocturnal confusion ("sundowning").

Validated Bedside Diagnostic Instruments

• Confusion Assessment Method (CAM): Delirium diagnosis requires both Feature 1 and Feature 2, plus either Feature 3 or Feature 4:
  1. Acute Onset and Fluctuating Course (evidence of sudden change from baseline and fluctuating severity).
  2. Inattention (difficulty focusing, easily distracted, unable to keep track of conversation).
  3. Disorganized Thinking (incoherent, rambling, illogical narrative).
  4. Altered Level of Consciousness (hyperalert, lethargic, stuporous).
• 4AT Scale: Rapid, 2-minute clinical tool used across Australian emergency and surgical wards: (1) Alertness, (2) AMT4 (age, date of birth, place, current year), (3) Attention (months of the year backwards), and (4) Acute change or fluctuating course. A score $\ge 4$ suggests delirium.

Etiological Workup: The "PINCHES ME" Mnemonic

Every case of delirium mandates a systematic search for underlying triggers:

• P: Pain (uncontrolled surgical, visceral, or musculoskeletal pain).
• I: Infection (urinary tract infection, pneumonia, cellulitis, sepsis, meningitis).
• N: Nutrition & Dehydration (poor oral intake, severe volume depletion, malnutrition).
• C: Constipation & Faecal Impaction.
• H: Hydration & Electrolytes (hyponatraemia, hypercalcaemia, uremia, hepatic failure).
• E: Endocrine (hypoglycaemia, severe hyperglycaemia, myxoedema coma, thyrotoxicosis).
• S: Stroke & Cardiac (CVA, transient ischemic attack, silent myocardial infarction, heart failure).
• M: Medications (anticholinergics, sedatives, opioids, corticosteroids, polypharmacy) or withdrawal.
• E: Environmental change (ICU admission, sensory deprivation, absent sensory aids).

Management Principles of Delirium

• Non-Pharmacological Measures (First-Line): Frequent reorientation by nursing staff, visible clocks and calendars, re-fitting patient's spectacles and hearing aids, ensuring daytime natural lighting and dark quiet rooms at night, mobilizing early, and involving family members.
• Pharmacological Restraint: Strictly reserved for severe hyperactive delirium where the patient poses imminent danger to self or staff (e.g., attempting to climb over bed rails with fractured hips, pulling out tracheostomies or central lines) and non-pharmacological de-escalation has failed. Low-dose haloperidol ($0.25-0.5\text{ mg}$ oral/IM) or low-dose risperidone ($0.25\text{ mg}$); avoid benzodiazepines unless delirium is caused by alcohol or sedative withdrawal.

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Dementia Subtypes & Management Principles

Major Neurocognitive Disorder involves substantial cognitive decline across one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) that impairs functional independence.

1. Alzheimer's Disease (AD)

• Most prevalent dementia subtype. Neurodegeneration begins in the entorhinal cortex and hippocampus, driven by amyloid plaques and neurofibrillary tangles, leading to severe cholinergic deficits.
• Clinical Presentation: Insidious short-term episodic memory impairment (forgetting recent conversations, repeating questions, misplacing items), followed by dysphasia, dyspraxia, visuospatial disorientation, and executive impairment. Long-term semantic memories are preserved until late stages.
• Pharmacotherapy:
  • Cholinesterase Inhibitors (AChEIs): Donepezil, rivastigmine, and galantamine for mild-to-moderate AD. Common side effects: nausea, vomiting, diarrhoea, anorexia, vivid dreams, bradycardia, and syncope (contraindicated in severe sick sinus syndrome or high-grade AV block).
  • NMDA Receptor Antagonist: Memantine blocks pathologically elevated tonic levels of glutamate, preventing excitotoxic neuronal damage; used in moderate-to-severe AD either as monotherapy or combined with an AChEI.

2. Vascular Dementia (VaD)

• Stepwise or abrupt deterioration associated with cerebrovascular insults. Patients exhibit early and prominent executive dysfunction (impaired abstract reasoning, poor planning, psychomotor slowing) out of proportion to episodic memory loss.
• Physical examination demonstrates focal neurological signs (asymmetrical hyperreflexia, extensor plantars, pseudobulbar affect, gait disturbance).
• Vascular cognitive impairment: Treat vascular risks. Antiplatelets or anticoagulants require a suitable vascular indication; the dementia label alone is not an indication. Assess cognition, function, mood, medicines and reversible contributors.

3. Dementia with Lewy Bodies (DLB)

• Characterized by intracellular alpha-synuclein inclusions (Lewy bodies) in subcortical and neocortical neurons. Clinically defined by a core triad/tetrad:
  1. Fluctuating Cognition: Pronounced variations in attention, alertness, and functional capacity occurring over hours to days.
  2. Recurrent Vivid Visual Hallucinations: Typically well-formed, detailed figures of people, animals, or children, often non-distressing.
  3. Spontaneous Parkinsonism: Rigidity, bradykinesia, and postural instability emerging concurrently with or within 12 months of cognitive decline (unlike Parkinson's Disease Dementia where motor symptoms precede cognitive decline by years).
  4. REM Sleep Behaviour Disorder (RBD): Loss of normal muscle atonia during REM sleep, leading to violent dream enactment.
• CRITICAL AMC BLACK BOX PRECAUTION: Patients with DLB possess extreme, potentially fatal neuroleptic hypersensitivity. Exposure to first-generation antipsychotics (haloperidol) or standard-dose atypical antipsychotics can precipitate catastrophic irreversible parkinsonism, acute severe rigidity, profound sedation, autonomic collapse, or fatal Neuroleptic Malignant Syndrome. If psychosis requires treatment, cholinesterase inhibitors are first-line; if severe distress persists, very low-dose quetiapine or clozapine is used with extreme caution.

4. Frontotemporal Dementia (FTD)

• Characterized by localized degeneration of the frontal and anterior temporal lobes, presenting at a younger age ($50-65\text{ years}$). Subtypes include Behavioural Variant FTD (bvFTD) and Primary Progressive Aphasia (PPA).
• Behavioural Variant FTD (bvFTD): Early and profound personality change, social disinhibition (tactless remarks, inappropriate sexual behaviour, shoplifting), loss of empathy and emotional warmth, apathy, hyperorality (marked dietary changes, binging on sweets, smoking), and repetitive stereotypic motor behaviours. Remarkably, episodic memory and visuospatial orientation remain intact in early disease.

Primary references (checked 7 October 2026): RCH ADHD guidance.