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Delirium

SNOMED: 49481000Updated 03/03/2026
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Exam Tips

  • In OSCEs, diagnose delirium by proving acute onset + fluctuation + inattention, then present likely precipitants systematically (infection, drugs, metabolic, retention/constipation, pain).
  • Always seek collateral history to establish baseline cognition and function; this is often the discriminating step versus dementia.
  • Hypoactive delirium is common and easily missed; a quiet withdrawn patient with new drowsiness is delirium until proven otherwise.
  • State safety priorities explicitly: 1:1 supervision if needed, falls prevention, avoid restraints where possible, and rapid treatment of reversible causes.
  • Before haloperidol, mention contraindications (Parkinson's/Lewy body dementia, prolonged QTc) and need for ECG/electrolyte review.
  • Image memory aid: see a standard geriatrics textbook figure of the vulnerability-precipitant model (predisposition on one axis, insult severity on the other) to explain why minor insults can trigger delirium in frail patients.

Definition

Delirium is an acute, fluctuating neuropsychiatric syndrome caused by global cerebral dysfunction (acute encephalopathy), with prominent disturbance of attention and awareness plus cognitive or perceptual change. It develops over hours to days, usually on a background of vulnerability (for example frailty or dementia) with one or more acute precipitants such as infection, drugs, metabolic disturbance, or pain.

Pathophysiology

Delirium is multifactorial and best explained by the interaction of baseline vulnerability and acute physiological stressors. Proposed mechanisms include reduced cholinergic transmission, relative dopaminergic excess, neuroinflammation (peripheral cytokines disrupting blood-brain signalling), impaired cerebral oxidative metabolism, circadian dysregulation, and network disconnectivity in attention/executive systems. These processes produce fluctuating inattention, altered arousal, and disorganised thinking, with hypoactive, hyperactive, or mixed motor phenotypes.

Risk Factors

  • Age over 65 years
  • Pre-existing cognitive impairment or dementia
  • Frailty and multiple comorbidities (for example stroke, heart failure, COPD)
  • Recent surgery or hip fracture
  • Polypharmacy and high-risk medicines (opioids, benzodiazepines, anticholinergics, corticosteroids, some antihypertensives/antiarrhythmics)
  • Alcohol excess or withdrawal history
  • Visual or hearing impairment
  • Functional dependence, immobility, or physical restraint
  • Malnutrition or dehydration
  • Terminal illness/palliative phase

Clinical Features

Symptoms

  • Acute onset confusion with fluctuating severity (often worse at night)
  • Reduced attention (cannot sustain or shift focus)
  • Memory and language problems (poor recall, word-finding difficulty)
  • Disorganised thinking (rambling, illogical flow)
  • Perceptual disturbance (visual hallucinations, misperceptions, paranoid ideas)
  • Sleep-wake disturbance (daytime drowsiness, night-time insomnia, reversal)
  • Emotional lability (anxiety, fear, irritability, apathy, low mood)

Signs

  • Altered level of consciousness from hypervigilance to drowsiness
  • Inattention on bedside tests (for example months backwards/digit span errors)
  • Disorientation to time/place and fluctuating cognition during assessment
  • Hyperactive signs: agitation, wandering, restlessness
  • Hypoactive signs: reduced movement, withdrawn behaviour, reduced speech
  • Falls, poor oral intake, and new functional decline as early warning signs
  • Clinical clues to precipitant (fever, urinary retention, constipation, hypoxia, dehydration)

Investigations

Collateral history + baseline cognition comparison (for example previous GPCOG/AMTS if available):Acute change from baseline with fluctuating course supports delirium over chronic dementia progression
4AT bedside delirium screen:Score 4 or more suggests possible delirium and prompts urgent cause-finding
Observations and bedside assessment (NEWS2, capillary glucose, pain, urine retention, bowel status):May reveal hypoxia, sepsis physiology, hypo/hyperglycaemia, uncontrolled pain, retention, or faecal impaction
Blood tests (FBC, U&E, CRP, LFT, calcium, TFT when indicated, venous/arterial gas if unwell):Infection markers, electrolyte disturbance, renal/hepatic dysfunction, hypercalcaemia, thyroid disease, or acid-base disorder
Urinalysis and urine culture (if symptomatic):Supports UTI only when clinical features are consistent; asymptomatic bacteriuria alone should not be overcalled
ECG:Identifies arrhythmia/ischaemia and baseline QTc prolongation before antipsychotic use
Chest X-ray:May show pneumonia, pulmonary oedema, or other thoracic precipitant
CT head (selected patients):Useful if focal neurology, head injury/fall, anticoagulation, reduced consciousness, or suspicion of stroke/subdural haematoma

Management

Lifestyle Modifications

  • Treat the underlying cause(s) urgently (infection, hypoxia, metabolic disturbance, retention, constipation, pain, withdrawal states)
  • Deliver a multicomponent non-pharmacological bundle: orientation cues (clock/calendar), regular reorientation, family/carer presence, calm lighting/noise control
  • Optimise hydration and nutrition with assisted oral intake where needed
  • Correct sensory deficits (ensure glasses/hearing aids are available and functioning)
  • Promote sleep hygiene (reduce nighttime interruptions, daytime mobilisation, avoid unnecessary sedatives)
  • Early mobilisation, pressure-area care, falls prevention, and minimisation of lines/catheters/restraints
  • Medication review: stop or reduce non-essential deliriogenic drugs and simplify regimens

Pharmacological Treatment

Antipsychotic (short-term, only if severe distress or immediate risk after non-drug measures fail)

  • Haloperidol 0.5 mg oral initially (or 0.5 mg IM if oral not possible), then 0.5 mg every 2-4 hours if required; use the lowest effective dose for the shortest duration

Avoid in Parkinson's disease and Lewy body dementia; check ECG/QTc and correct K+/Mg2+ before use; caution in cardiovascular disease and with other QT-prolonging drugs; monitor for extrapyramidal effects, oversedation, and aspiration risk.

Benzodiazepine (specific indications)

  • Lorazepam 0.5-1 mg oral/IM, repeated cautiously according to response

Reserve for alcohol-withdrawal delirium or when antipsychotics are contraindicated; may worsen non-withdrawal delirium, cause respiratory depression, falls, and paradoxical agitation (especially older adults).

Cause-directed pharmacotherapy

  • Paracetamol 1 g oral/IV every 4-6 hours (max 4 g/day; lower max in low body weight/frailty/liver disease)
  • Empirical antimicrobials according to local sepsis/source guidelines (for example amoxicillin 500 mg to 1 g three times daily for susceptible chest sources, adjusted for renal function and allergy status)

Do not use antipsychotics as routine treatment for delirium itself; prescribe only for clear indication and review daily for de-escalation.

Complications

  • Increased short- and medium-term mortality
  • Longer hospital stay and higher risk of hospital-acquired infection
  • Falls, pressure ulcers, incontinence, and malnutrition
  • Functional decline and loss of independence
  • Increased risk of care-home admission and hospital readmission
  • Persistent delirium after discharge
  • Accelerated cognitive decline and higher long-term dementia risk
  • Significant psychological distress for patients and carers

Prognosis

Course is fluctuating: some patients recover within days, but recovery may take weeks to months, especially in older or frail inpatients. Poorer outcomes are linked to pre-existing dementia, hypoactive subtype, greater severity/duration, hypoxic illness, visual impairment, and frailty. Mortality risk remains elevated for months after discharge, and cognitive/functional decline may persist.

Sources & References

💊BNF Drug References(1)

✅NICE Guidelines(1)

📖Textbook References(4)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 284)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1055, 1056)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1056, 1057)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 283, 284)[context]

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