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: recognition, causes and prevention
Medicine of older adults · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Acute brain failure
New inattention, fluctuating arousal or behavioural change may be the first sign of hypoxia, sepsis, stroke, metabolic failure, drug toxicity, withdrawal or intracranial disease and can rapidly threaten airway, hydration, mobility and safety.
Action: Perform ABCDE, observations and capillary glucose, identify immediate neurological and medical threats, obtain collateral and 4AT, reconcile medicines, investigate several plausible causes in parallel and provide continuous supportive and harm-prevention care.
Overview
Recognise hyperactive, hypoactive and mixed delirium promptly, establish baseline cognition through collateral, identify interacting precipitants without diagnostic closure, and prevent avoidable delirium through a targeted multicomponent bundle.
Ask what changed and when. Direct history may be unreliable, so seek consented collateral from family, carers, records and community professionals about baseline memory, attention, ADLs, sleep and behaviour. Identify last known well, fluctuation through the day, recent illness, falls, surgery, pain, intake and prescription or substance change. A carer's statement that the person is not themselves is important clinical evidence.
Use 4AT when indicators appear at presentation or during admission. Alertness is abnormal when clearly drowsy or agitated; AMT4 tests age, date of birth, place and year; attention uses months backwards; acute change comes from collateral or repeated observation. A score of four or more supports possible delirium, one to three suggests possible cognitive impairment and zero does not exclude a subtle or fluctuating syndrome.
Practice
Two practice questions
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Medicine of older adultsOriginal SBA
Interpreting a low 4AT
A previously independent 81-year-old becomes intermittently drowsy and inattentive after surgery. Her 4AT is 2 during a brighter interval, but her daughter confirms abrupt fluctuation. What is the best interpretation?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Examine from physiology outward: oxygenation, perfusion, temperature, hydration, neurological signs, injury, chest, heart, abdomen, bladder, bowel, skin and pressure areas. Look for pain behaviours when language is limited. Check hearing aids, glasses, dentition and swallowing. Repeat the examination because evolving pneumonia, abdominal disease or focal neurology may be muted initially.
Reconcile all medicines and recent changes from more than one source. Consider anticholinergic load, benzodiazepines, opioids, gabapentinoids, antihistamines, bladder medicines, corticosteroids and dopaminergic therapy. Dehydration and acute kidney injury can make a stable dose toxic. Ask about alcohol and sedative dependence because abrupt withdrawal has a specific treatment pathway.
Select investigations from the clinical hypotheses. Common initial studies include FBC, renal profile, glucose, calcium, liver profile, CRP, urinalysis when urinary symptoms exist and ECG; add cultures, chest imaging, troponin, blood gas, toxicology or endocrine tests when indicated. Do not use urine dipsticks in people aged 65 or over to assign urinary infection without compatible evidence.
Prevention begins at admission for people aged 65 or over, with cognitive impairment, hip fracture or severe illness. Provide a clock, calendar, repeated explanation, family contact and consistent staff; restore glasses and hearing aids; encourage oral fluid, nutrition and mobility; manage pain; protect sleep and avoid unnecessary ward moves. Address constipation, retention, oxygenation and infection promptly.
Review the risk bundle daily and after transfer or procedure. Preserve normal day-night cues, avoid daytime bed rest and cluster unavoidable night care. Remove catheters and lines promptly. Do not use routine antipsychotics for prevention. If delirium occurs despite prevention, continue the bundle because it reduces perpetuating insults while cause treatment proceeds.
Record baseline and current capacity separately. Delirium can impair capacity for a complex decision at one moment without removing all decision-making ability. Support communication, delay non-urgent decisions until a lucid interval where possible and use a documented best-interests process for necessary decisions when capacity is absent.
At discharge, ensure symptoms have resolved or a named team owns persistent delirium. Communicate cause, course, medicine changes, cognitive baseline, functional gap and follow-up. Warn carers that recovery can take weeks and provide triggers for urgent reassessment. Persistent decline warrants dementia assessment only after acute contributors and sensory barriers are addressed.
Key points
Delirium is an acute and fluctuating disturbance of attention, awareness and cognition caused by an underlying physiological or substance-related insult.
First-line recognition uses observation for recent change plus the 4AT; a score of 4 or more suggests possible delirium but clinical concern overrides any score.
4AT assesses alertness, four orientation items, attention by months backwards and acute change or fluctuation; it does not require special training.
Always obtain collateral for baseline cognition, function and exact onset and document whether delirium is hyperactive, hypoactive or mixed.
Use ABCDE and glucose before a lengthy cause list. Serious illness may present through delirium without fever, pain or marked laboratory inflammation.
Search multiple causes using history, full examination, medicines, pain, bowel and bladder, hydration, oxygenation, infection and targeted tests.
A CT head is not routine for every delirium; use it for trauma, focal neurology, seizure, anticoagulation with concern or unexplained persistent reduction.
Prevention is multicomponent: orientation, familiar contact, hydration, nutrition, pain control, mobility, sleep, oxygen, medication review and sensory aids.
Avoid unnecessary catheters, bed moves, restraints and night disturbance; identify a consistent team member and communicate baseline and preferences.
Document the syndrome and probable contributors explicitly so later teams do not misread delirium as new dementia or behavioural choice.
Aetiology
01
Predisposing vulnerability
Dementia, frailty, severe illness, sensory loss, dehydration, malnutrition, polypharmacy and prior delirium reduce cognitive reserve, so several modest insults may combine.
02
Acute medical precipitants
Infection, hypoxia, vascular events, organ failure, pain, fracture, retention, constipation, metabolic disturbance and surgery are common causes that frequently coexist.
03
Medicine and substance effects
Anticholinergics, sedatives, opioids, corticosteroids, dopaminergic drugs, intoxication, withdrawal and renal or hepatic drug accumulation can initiate or sustain delirium.
04
Environmental disruption
Sleep interruption, immobility, restraints, catheters, unfamiliar staff, isolation and absent hearing or visual aids amplify disorientation and stress during illness.
Pathophysiology
1
Network-level brain dysfunction
Delirium reflects acute failure of attention and arousal networks rather than one anatomical lesion, producing rapid fluctuation across hours.
2
Neurotransmitter imbalance
Reduced cholinergic signalling with altered dopamine, serotonin, GABA and noradrenergic activity helps explain vulnerability to anticholinergic and psychoactive medicines.
3
Inflammatory and endothelial signalling
Systemic cytokines, microglial activation and blood-brain-barrier dysfunction disturb synaptic function, especially in neurodegenerative and frail brains.
4
Metabolic energy failure
Hypoxia, hypoglycaemia, electrolyte disturbance, dehydration and impaired perfusion limit cerebral energy delivery and destabilise cognition before focal signs emerge.
5
Perpetuating hospital cascade
Poor intake, sleep loss, immobility, pain and iatrogenic devices sustain stress after the original trigger begins to improve.
Clinical features and red flags
Acute fluctuating inattentionRed flag
Hours-to-days onset, distractibility and variable performance across a conversation or shift is the defining bedside pattern.
Hypoactive deliriumRed flag
Drowsiness, reduced movement, sparse speech and poor intake can look cooperative or depressed and requires active screening.
Hyperactive delirium
Agitation, hallucinations, sleep reversal and attempts to leave are visible but still require physiological diagnosis rather than a behavioural label.
Mixed motor pattern
The person alternates between agitation and withdrawal, making snapshot assessment particularly unreliable.
Superimposed on dementia
A clear acute change in arousal or attention occurs over a chronic cognitive and functional baseline.
Subsyndromal concern
A 4AT below four with convincing fluctuation, carer concern or evolving physiology still warrants repeated clinical assessment.
Red flags requiring action
Reduced consciousness, airway compromise, hypoxia, shock, hypoglycaemia, seizure or focal neurology requires immediate resuscitation and cause-specific escalation.
Sudden headache, head injury, anticoagulation, focal deficit or persistent unexplained reduced arousal lowers the threshold for urgent brain imaging.
Rigidity, fever, autonomic instability or clonus after medicine change raises neuroleptic malignant syndrome, serotonin toxicity or severe withdrawal.
Hypoactive delirium presents as quiet withdrawal, slow response or reduced intake and is easily mistaken for sleep, depression or advanced dementia.
Known dementia does not explain an abrupt fluctuation; delirium and dementia commonly coexist and both baseline and acute change must be documented.
A positive urine dipstick or bacteriuria without compatible symptoms or systemic evidence must not end the search for another cause.
Investigations
01ABCDE and capillary glucoseFirst step
Why
Identify immediate physiological threats. within a safe older-adult assessment.
Interpretation and limitations
Correct hypoxia, shock, hypoglycaemia, seizure and other instability before extended screening and continue repeated observations.
024AT
Why
Screen rapidly for delirium and cognitive concern.
Interpretation and limitations
Four or more supports possible delirium; one to three suggests cognitive impairment; any result requires interpretation with collateral and fluctuation.
03Collateral baseline history
Why
Prove acute change and avoid mislabelling dementia.
Interpretation and limitations
Record baseline cognition, ADLs, IADLs, communication, usual behaviour, onset and within-day variation from reliable sources.
04Full examination and medicine review
Why
Find interacting precipitants. within a safe older-adult assessment.
Interpretation and limitations
Assess neurological, cardiopulmonary, abdominal, bladder, bowel, skin, pain, injury, hydration and sensory status and reconcile recent medicines.
05Targeted laboratory and microbiology
Why
Test the leading medical hypotheses.
Interpretation and limitations
Use blood count, renal, glucose, calcium, liver, inflammation and source-led cultures or other tests; interpret all against baseline and treatment.
06Imaging or EEG
Why
Investigate specific intracranial, traumatic or seizure concern.
Interpretation and limitations
CT follows trauma, focal signs, seizure, anticoagulation concern or unexplained persistence; EEG supports suspected non-convulsive seizure rather than routine delirium.
Differential diagnosis
01
Dementia progression
Dementia is usually chronic and progressive; abrupt onset, altered alertness and fluctuation favour superimposed delirium, although collateral may uncover both.
02
Depression or severe distress
Withdrawal, slow responses and poor concentration overlap with hypoactive delirium, but day-to-day mood chronology and preserved arousal help separation.
03
Primary psychosis or mania
Late first presentation is uncommon; clouded attention, visual misperception, medical instability and medication change require organic assessment first.
04
Aphasia or sensory impairment
Stroke, hearing loss, visual loss and language barriers can mimic confusion; focal examination and accessible communication reveal the mechanism.
05
Non-convulsive seizure
Fluctuating unresponsiveness, automatisms or unexplained persistent altered awareness may require EEG and neurological input. Distinguish it through chronology, examination and targeted testing.
Management
01First-line recognitionStabilise, screen and establish acute changeFirst stepFirst lineNew confusion, drowsiness, agitation, fall or functional decline occurs.+
1Perform ABCDE, glucose and urgent treatment and obtain last-known-well and baseline collateral.
2Use 4AT and full examination, reconcile medicines and investigate several plausible causes in parallel.
3Record delirium type, contributors, capacity and prevention plan and repeat assessment with fluctuation.
02Prevention bundleReduce modifiable risk every dayA person has age, cognition, hip fracture or severe-illness risk factors.+
1Orient with people and environment, optimise hearing and vision and reduce unnecessary moves and night disruption.
2Maintain hydration, nutrition, oxygenation, pain relief, bowel and bladder function and early mobility.
3Review medicines and devices daily and involve family and familiar routines where the person wishes.
03Persistent or unexplained courseReopen high-consequence causesAttention, arousal or function fails to improve as expected.+
1Repeat examination, observations, medicine and withdrawal history and verify delivery of cause treatment and prevention.
3Seek senior geriatric, neurological or specialist review and plan ongoing capacity, function and cognitive follow-up.
Complications
01
Falls and traumatic injury
Inattention, urgency, postural instability and attempts to leave an unfamiliar setting cause fracture, head injury and fear-driven restraint.
02
Aspiration and malnutrition
Reduced alertness, dysphagia and inability to sustain intake lead to dehydration, aspiration pneumonia and impaired recovery.
03
Functional and cognitive decline
Delirium accelerates deconditioning and is associated with persistent cognitive loss, institutionalisation and greater future dementia risk.
04
Iatrogenic harm
Sedation, restraint, catheterisation and indiscriminate antibiotics can prolong delirium, cause pressure injury, infection and medicine toxicity.
05
Death and carer distress
Delirium marks severe physiological vulnerability and is associated with mortality while frightening hallucinations and personality change burden families.
Monitoring and follow-up
Repeat 4AT and clinical assessment after a material behavioural or arousal change; trajectory matters more than a single score.
Trend oxygenation, hydration, renal function, infection and other identified causes alongside attention, sleep, intake and mobility.
Review pain, constipation, retention, sensory aids, devices, medicines and night disruption every day.
Track decision-specific capacity and use lucid periods for important discussion without assuming global incapacity.
Before discharge compare cognition and ADLs with baseline and assign follow-up for persistent symptoms or new dependency.
Special situations
Attention is central
Memory can be poor in dementia, but inability to sustain attention with fluctuation strongly supports delirium.
Quiet delirium is dangerous
Hypoactive cases are missed more often because they do not disrupt staff despite severe illness and poor intake.
Several causes are usual
Finding bacteriuria, constipation or one medicine does not prove it is the sole precipitant.
Prevention is clinical care
Orientation, hydration, mobility, sleep and sensory support are active interventions rather than optional comforts.
Recovery can outlast physiology
Delirium may persist after infection or biochemistry improves and needs ownership, rehabilitation and follow-up.
Scores support, not veto
A low 4AT cannot overrule convincing acute fluctuation or deteriorating physiology.
Common pitfalls
01
Diagnosing dementia from a low cognitive score during acute illness.
02
Missing hypoactive delirium because the patient is quiet and does not wander.
03
Ending the cause search after a positive urine dipstick without compatible urinary evidence.
04
Ordering routine CT while delaying ABCDE, glucose, examination and collateral.
05
Using antipsychotic medication as delirium prevention or to make ward care easier.
06
Discharging persistent delirium without communicating baseline, function, medication changes and named review.