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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Delirium versus psychosis or dementia

Psychiatry · UK scope · Sources checked 7 Sept 2026 · Clinical review pending

RapidFull
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New confusion needs urgent medical assessment

An acute change in attention, alertness or behaviour may signal hypoxia, hypoglycaemia, sepsis, stroke, poisoning or another time-critical illness.

Action: Assess ABCDE and capillary glucose, obtain observations and collateral history, investigate the likely causes and treat physiological threats immediately while providing a safe, orienting environment.

Overview

Recognise acute disturbed attention as a medical syndrome, distinguish its course from primary psychosis and dementia, and manage uncertainty without delaying reversible-cause treatment.

Delirium is an acute disturbance of brain function expressed through changes in attention, awareness and cognition. The bedside question is whether there has been a recent change from the person's usual state. Symptoms may vary over minutes or hours: someone who gives a coherent morning account can become disoriented and frightened overnight. A single normal conversation therefore does not exclude the syndrome. Document the timeline and seek information from people who observed the change.

Psychotic symptoms describe experiences such as hallucinations, delusions and disorganised thinking, but they do not identify a cause on their own. Visual misinterpretations can occur in delirium, dementia, sensory impairment or intoxication, while auditory hallucinations can occur in several psychiatric and neurological conditions. Attention and level of consciousness, recent medicines and physical findings help discriminate. A previous diagnosis of schizophrenia does not protect a patient from pneumonia-related delirium.

Aetiology

01

Acute systemic stress

Infection, hypoxia, metabolic disturbance, dehydration and organ failure can destabilise cerebral function, often with several contributory processes present during the same admission.

02

Vulnerability and exposure

Older age, cognitive impairment, sensory loss and severe illness lower resilience, while medicines, withdrawal, pain and an unfamiliar environment can precipitate acute confusion.

Pathophysiology

  1. 1
    Attention-network dysfunction

    Acute physiological disturbance disrupts the networks sustaining alertness and selective attention, limiting the patient's ability to interpret and respond consistently to their surroundings.

  2. 2
    Sleep and arousal disturbance

    Fragmented sleep, circadian disruption and sedating treatment can alter wakefulness and perception, reinforcing fluctuation and making bedside cognitive performance inconsistent.

  3. 3
    Reduced cognitive reserve

    Existing neurodegeneration leaves less capacity to compensate for a new insult, so relatively modest illness may produce a conspicuous acute functional decline.

Clinical features and red flags

Acute fluctuating course

A change over hours or days with periods of relative clarity is a strong signal for delirium, especially when corroborated by an informant.

Impaired attention

The patient loses the thread, cannot sustain a simple task or is easily distracted; poor memory alone is less discriminating.

Hypoactive presentation

Drowsiness, slowed responses, reduced movement and withdrawal can be overlooked because the person is not disrupting care.

Longer cognitive trajectory

Months of declining navigation, medication management or finances suggest underlying dementia, but a sudden additional change still needs investigation.

Red flags requiring action

  • A patient with established dementia who becomes newly drowsy, inattentive, agitated or less able to eat has possible delirium superimposed on dementia.
  • Focal neurological signs, meningism, seizure, head trauma, marked fever, severe headache or falling consciousness require urgent targeted medical escalation.

Investigations

  1. 01
    ABCDE, glucose and physiological observationsFirst step
    Why
    Identify immediately reversible threats and determine the urgency of medical intervention.
    Interpretation and limitations
    Hypoxia, low glucose, hypotension, fever or reduced consciousness requires cause-specific treatment while cognitive assessment continues.
  2. 02
    4AT or critical-care delirium instrument
    Why
    Structure detection of altered alertness, cognition, attention and acute change.
    Interpretation and limitations
    Use the setting-appropriate instrument and trained clinical judgement; neither one normal result nor inability to complete a task settles the diagnosis alone.
  3. 03
    Collateral baseline and medication review
    Why
    Establish onset, previous function and potential pharmacological or withdrawal contributors.
    Interpretation and limitations
    Recent opioids, antimuscarinics, benzodiazepines, steroids or abrupt substance cessation may matter; compare administration records with the actual home regimen.
  4. 04
    Targeted laboratory and bedside tests
    Why
    Identify infection, metabolic disturbance, dehydration, retention or other suspected precipitants.
    Interpretation and limitations
    Select renal profile, blood count, calcium, inflammatory testing, cultures, bladder assessment or chest investigations from the history and examination rather than reflexively treating incidental results.

Differential diagnosis

01

Primary psychotic illness

Delusions or hallucinations may occur with relatively preserved alertness and a different time course, but medical and substance-related causes must still be considered.

02

Progressive dementia

A sustained decline over months or years points towards chronic cognitive disease, whereas a sudden deterioration in attention raises concern for an additional acute process.

03

Depression or catatonia

Reduced movement and speech can resemble hypoactive delirium, requiring examination of attention, motor signs, mood history and possible concurrent physiological illness.

Management

01Suspected deliriumTreat the acute syndromeFirst stepRecent altered attention or awareness is reported or observed, with or without pre-existing cognitive impairment.+
  1. 1Establish the change from baseline and assess immediate physiological threats, using the appropriate delirium instrument to support detection.
  2. 2Search actively for several simultaneous contributors and treat infection, pain, hypoxia, dehydration, retention or medication problems according to the findings.
  3. 3Provide repeated simple orientation, daylight cues, sleep protection, familiar support and hearing or visual aids, with mobilisation and nutrition as tolerated.
02Uncertain diagnosisKeep medical causes activePsychotic symptoms or established dementia obscure whether an acute medical process is present.+
  1. 1Use collateral history to separate longstanding beliefs or memory deficits from newly altered behaviour and attention.

Complications

01

Loss of function

Immobility, reduced oral intake and disrupted rehabilitation may lead to deconditioning and increased support requirements beyond resolution of the initial precipitating illness.

02

Iatrogenic injury

Falls, restraint, excess sedation and unnecessary devices can compound the original brain dysfunction and expose the patient to further preventable complications.

03

Persistent cognitive difficulty

Some patients recover slowly or reveal previously unrecognised cognitive impairment, making reassessment and communication with primary care important after acute treatment.

Monitoring and follow-up

  • Record delirium features and fluctuations at least daily and reassess when staff or relatives notice a new change, using the same baseline comparison.
  • Track hydration, intake, mobility, sleep, pain, bowel and bladder function alongside physiological observations and treatment of the precipitating illness.
  • Review newly prescribed sedatives or antipsychotics daily, documenting benefit, adverse effects and a stop plan to avoid unintended continuation after discharge.
  • Explain the diagnosis and recovery expectations to the patient when able and include delirium and medication changes in handover and discharge communication.
  • When delirium persists, reconsider missed contributors and arrange follow-up for possible underlying dementia once acute illness and confounding medicines have been addressed.

Special situations

A normal interval misleads

Fluctuation is part of delirium, so a coherent answer during one ward round does not invalidate a reliable account of severe overnight confusion.

Quiet patients need attention

Hypoactive delirium may be associated with poor intake and immobility, yet receive less urgent review because it does not demand staff attention.

Symptoms do not assign specialty

Hallucinations in an acutely ill patient can reflect brain dysfunction requiring medical treatment, with liaison psychiatry contributing to rather than replacing that care.

Recovery can be uneven

Orientation, attention and practical function may improve at different speeds, and discharge planning should address actual support needs rather than one cognitive score.

Common pitfalls

  1. 01

    Explaining a sudden decline as the patient's usual dementia without asking someone who knows their daily function.

  2. 02

    Using the presence of hallucinations as evidence that a presentation is psychiatric and omitting glucose or physiological observations.

  3. 03

    Giving antipsychotics to every delirious patient or continuing a hospital-started prescription indefinitely after the distress has settled.

  4. 04

    Prescribing haloperidol in Parkinson's disease or Lewy-body dementia without recognising the specific contraindication.

  5. 05

    Treating an incidental positive test as the complete explanation while pain, retention, dehydration or drug effects remain unaddressed.

Practice

Two practice questions

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Question 1 of 2
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PsychiatryOriginal SBA

Acute change on dementia

An 82-year-old has had gradually worsening memory for two years. Over two days they become newly drowsy, inattentive and unable to follow familiar conversations. Relatives confirm this is a marked change. Which working formulation best guides the initial assessment?

Choose one answer, then submit
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Sources and review status4 sources · checked 7 Sept 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 7 Sept 2026; clinical approval remains outstanding.

  • NICE CG103 delirium recommendationsUpdated detection instruments, differential assessment and management.
  • MHRA haloperidol risks in elderly deliriumContraindications, ECG, electrolyte and adverse-effect precautions.
  • Haloperidol 1mg per ml oral solution UK SmPCLicensed adult and older-patient dose limits and review.
  • NICE NG97 dementia assessment and managementDementia diagnosis and assessment of distressing symptoms.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Dementia is characterised by acquired cognitive decline that interferes with everyday function, typically evolving over a much longer period. The boundary is less tidy in Lewy-body disease, which may include fluctuation and hallucinations, and in advanced dementia, where baseline testing is difficult. Delirium frequently adds a sudden deterioration to an existing deficit. Ask about usual conversation, mobility, continence, eating, sleep and recognition of familiar people, not merely whether memory problems were already present.

Clinical diagnosis follows assessment; a screening score supports rather than replaces reasoning. NICE recommends the 4AT in most hospital and care-home settings when delirium indicators are identified, and CAM-ICU or ICDSC in critical care or the postoperative recovery room. An untestable or aphasic person still needs examination and collateral evidence. Repeat assessment if suspicion persists, as severity, communication and sedating medicines can affect performance.

Management combines correction of contributors with consistent supportive care. Several factors often coexist: infection, dehydration, constipation, urinary retention, pain, reduced mobility, sleep disruption and drug effects. Review the need for catheters, unfamiliar room changes and sedating medication. Explain to relatives that recovery may lag behind correction of the trigger and arrange reassessment if cognition or function does not return towards baseline.

Key points

  • Delirium usually develops over hours or days and fluctuates; impaired attention and altered awareness are central clues.
  • Dementia generally causes a longer progressive decline, while primary psychosis often preserves basic alertness and orientation.
  • Hypoactive delirium can look like depression, fatigue or cooperation; reduced interaction does not mean the patient is well.
  • Establish the patient's usual cognition and function through family, carers, records and staff who know them.
  • Use the 4AT when delirium indicators are present; in critical care or recovery after surgery use CAM-ICU or ICDSC.
  • If delirium and dementia cannot be distinguished, manage delirium first and reassess cognition after recovery.
  • Treat causes, support sleep and orientation, optimise hearing and vision, and reserve antipsychotics for specific distress or risk after other measures fail.
  • 05
    Neurological escalation and imaging
    Why
    Investigate features suggesting stroke, haemorrhage, seizure activity, encephalitis or structural disease.
    Interpretation and limitations
    New focal signs, head injury, seizure or otherwise unexplained reduced consciousness justify urgent specialist assessment; routine imaging is not a substitute for examining the patient.
    • 2
    Manage likely delirium while pursuing the differential; avoid making a new dementia diagnosis solely during an acute confusional illness.
  • 3Seek liaison psychiatry, geriatric or neurological support when uncertainty persists, ensuring that responsibility for medical treatment remains clear.
    • 03Severe distressUse medication selectivelyEscalationDelirium causes serious distress or risk and de-escalation and supportive measures have been ineffective or inappropriate.+
    1. 1Correct the immediate trigger where possible and check whether pain, retention, fear or an unfamiliar procedure is sustaining the distress.
    2. 2Consider short-term haloperidol only when suitable, starting at the lowest clinically appropriate dose and reviewing contraindications, ECG and electrolytes.
    3. 3Review benefit and adverse effects promptly and stop as soon as possible; arrange specialist alternatives for Parkinson's disease or dementia with Lewy bodies.
    Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
    Symptom control when delirium-related distress or risk remains after de-escalation, rather than routine treatment for every delirious patient.

    Haloperidol for distressing delirium

    When haloperidol is appropriate, use it briefly, usually one week or less, starting at the lowest suitable dose. The cited oral-solution SmPC gives adults 1–10 mg orally per day in one to three doses, with increments no more often than every two to four hours if agitation persists. The corresponding older-patient initial dose is 0.5 mg orally; titrate cautiously, with a usual maximum 5 mg daily. Exceeding that requires prior higher-dose tolerance and individual benefit-risk reassessment.

    Avoid in Parkinson's disease or dementia with Lewy bodies and check QT-related contraindications. Obtain baseline ECG and correct electrolytes; monitor swallowing, extrapyramidal effects, orthostatic hypotension and cardiac symptoms. Individual frailty often warrants doses near the bottom of the range. Halve the initial dose in hepatic impairment; severe renal impairment may require smaller doses and slower adjustments.