Delirium

• Delirium is an acute, fluctuating disturbance of attention and awareness, with an additional change in cognition, that develops over hours to days.
• It affects up to 50% of older hospitalised patients and carries a high risk of death, longer stay and long-term cognitive decline. ^[1]
• It is usually caused by a combination of a vulnerable brain (dementia, frailty) and one or more acute insults (infection, drugs, surgery, hypoxia, alcohol withdrawal).
• The diagnosis is clinical: the resident team must first notice, then screen with the Confusion Assessment Method or 4AT, then search for the cause.
• Prevention and treatment rest on non-drug measures (reorientation, mobilisation, sleep, hydration, sensory aids, pain control and infection control); drug therapy is only for dangerous agitation, most often short-term low-dose haloperidol.

By the end you should be able to:

1. Define delirium and distinguish hyperactive, hypoactive and mixed subtypes.
2. Estimate who is at risk and explain the predisposing/precipitating (vulnerability + insult) model.
3. Recognise the clinical picture, including the easy-to-miss hypoactive form.
4. Use the CAM or 4AT (and CAM-ICU or ICDSC in critical care) correctly, with their cut-offs.
5. Investigate and work up a delirious patient without over-testing.
6. Treat delirium: treat causes, use non-drug measures first, and use haloperidol safely and only when needed.
7. Describe prevention bundles (NICE CG103 multicomponent interventions, HELP, and the ICU ABCDEF bundle).
8. Manage delirium in special contexts: older adults, the ICU, and alcohol withdrawal. ^[4]

The two essentials are acute onset and fluctuation: delirium is not a person's usual confusion. The rise and fall over a day is part of the illness, not a sign that the patient is "just having a bad moment".

The term "delirium" covers several clinical pictures. ^[2]

• Hyperactive delirium: heightened arousal, restlessness, agitation, sometimes aggression or psychosis. It is the easiest to notice.
• Hypoactive delirium: withdrawal, quietness, sleepiness, slow responses, reduced appetite. It is the most common and the most dangerous, because it is the most often missed. ^[1][4]
• Mixed delirium: a swing between hyperactive and hypoactive phases, often within the same day. ^[4]

Delirium is a syndrome with many causes, not one disease. A delirious patient has "acute brain failure" the way a breathless patient has acute heart failure: it is a common final pathway for many insults. ^[1]

Delirium is common wherever people are acutely ill. ^[1]

• Up to 50% of hospitalised older adults are affected at some point in their stay. ^[1]
• In general medical settings, 18 to 35% already have delirium on admission and another 11 to 14% develop it during the stay. ^[1]
• In intensive care, estimates range from 20 to 80%, with pooled incidence of 26 to 32% in general ICUs and up to 75% in patients receiving mechanical ventilation. ^[4]
• On presentation to an emergency department, 8 to 17% of older adults are delirious (up to 40% of those coming from nursing homes). ^[1]
• After hip fracture or major surgery, rates of 12 to 51% are reported. ^[1]
• Delirium is uncommon in the community (around 1 to 2% prevalence) and usually brings the person into acute care. ^[1]
• Up to 70% of ICU survivors show significant cognitive impairment up to 18 months after delirium; surgical patients also commonly have cognitive dysfunction lasting up to one year postoperatively. ^[4][1]

Delirium in the ICU roughly doubles in-hospital mortality compared with no delirium, and each additional day of delirium lengthens the ICU stay by more than a day. ^{[4] [5]}

Delirium arises from the interaction between a vulnerable brain (predisposing factors) and one or more acute insults (precipitating factors). ^[1][4]

The harder the insult, the more robust the brain has to be to resist it. An older person with dementia may become delirious after one sleeping tablet; a healthy young adult needs several major insults (anaesthesia, surgery, sepsis, sleep deprivation) before delirium develops. ^[1]

Common predisposing factors: ^[1][4]

• Age over 65 (risk rises steeply with age)
• Dementia or other cognitive impairment
• Frailty, functional impairment, bedbound status
• Visual or hearing impairment
• Depression
• History of alcohol abuse
• Previous episode of delirium
• Comorbidity burden (stroke, Parkinson's disease, chronic organ failure, psychiatric illness)
• APOE epsilon-4 carriage, which roughly doubles the risk of ICU delirium ^[4]

Common precipitating factors: ^[1][4]

• Acute infection (pneumonia, urinary infection, sepsis)
• Drugs, especially anticholinergics, opioids, sedative-hypnotics, benzodiazepines and dopamine agonists
• Alcohol or benzodiazepine withdrawal
• Surgery, anaesthesia and postoperative period
• Hypoxia, hypercapnia, or low blood glucose
• Metabolic or electrolyte disturbance (sodium, calcium, magnesium, renal or hepatic failure, acid-base disorder)
• Pain, urinary retention, constipation, dehydration, malnutrition
• Immobility and physical restraint
• Sleep deprivation and a noisy, brightly lit, round-the-clock ward
• Sensory deprivation or sensory overload
• Iatrogenic events and polypharmacy

Delirium tremens is delirium arising during severe alcohol withdrawal. It requires both delirium and severe withdrawal. ^[5]

• Only a small proportion of people with alcohol dependence develop it: under 1% of the general population, around 2% of people with alcohol dependence, and 5 to 12% of those in treatment. ^[5]
• It usually develops 48 to 72 hours after the last drink, after an early sequence of tremor, hallucinations and possibly seizures. ^[5]
• Mortality was historically high but with modern care is roughly 1 to 4%. ^[5]
• Treatment failure and poor outcome usually come from co-morbidities: Wernicke encephalopathy, liver disease, cardiac disease or infection, rather than from the withdrawal itself. ^[5]

Delirium is best thought of as a mismatch between a stressed body and a vulnerable brain: an acute imbalance that disrupts the large-scale neuronal networks for attention, awareness and cognition. ^[1][4]

The exact mechanism of any single episode is rarely found, and several processes usually act together: ^[1][4]

• Cholinergic deficiency / dopamine excess. This is the most widely inferred pathway, which is why anticholinergic drugs and dopaminergic drugs so often precipitate delirium. ^[1]
• Neuroinflammation. In sepsis, peripheral inflammation reaches the brain through vagal afferents, cytokines crossing a leaky blood-brain barrier and activated microglia, leading to inflammation, impaired blood flow and neuronal injury. ^[1]
• Inadequate brain perfusion. Reduced cardiac output and failure of cerebral autoregulation lower total and regional cerebral blood flow, particularly in a damaged brain. ^[1]
• Neurotransmitter disruption from drugs or sedation. Benzodiazepines increase the risk of ICU delirium by roughly a third compared with propofol; anticholinergic load is a strong predictor. ^[4]
• Sleep and circadian disruption. Fragmented sleep, loss of day-night cues and continuous ICU lighting further destabilise cognition. ^[4]
• Brain reserve. Very young brains (underdeveloped networks) and older brains (cumulative neuronal, dendritic and microglial damage, cerebrovascular disease) are the most vulnerable; permanent damage may follow delirium in some patients. ^[1]

In young patients, delirium is usually a marker of severe physiological stress. In older patients, it may itself begin a longer-term cognitive decline. ^[1]

The most useful clue is an observer who knows the patient: "He is not himself." A person living alone may attend with a fall, poor intake or fever, and the confusion be missed unless it is actively sought. ^[1]

Look for changes over hours or days in any of these domains: ^[1][2]

• Cognitive: worsened concentration, slow answers, confusion, disorientation, memory loss, rambling speech, altered language.
• Perceptual: visual or auditory hallucinations, illusions, paranoid ideas.
• Physical: reduced mobility, restlessness, agitation, altered appetite, sleep disturbance, bowel/bladder change.
• Behavioural/social: poor engagement with requests, withdrawal, mood change, changes in communication.

The quiet (hypoactive) form is easy to mistake for depression or fatigue. Always consider delirium in a quiet, sleepy, withdrawn older patient with a new medical problem. ^[1][2]

Delirium is diagnosed at the bedside from the level of consciousness and cognitive testing: ^[1]

• Attention is the core sign: digit spans backwards, serial sevens, or months backwards. An attention task fails early.
• Awareness (orientation, responsiveness) may be reduced, especially in hypoactive forms.
• Acute fluctuation is shown by the history and by repeated examination.
• A third cognitive dimension is present: disorganised thinking, memory impairment, visuospatial or language change.

Also examine for the underlying causes: focal neurological signs (stroke), meningeal signs, occult infection (warm skin, new murmur, lung crackles), deep venous thrombosis, dehydration, abdominal pain, pain, retention of urine or stool, and sensory impairment. ^[1]

Every patient with suspected delirium needs a documented cognitive screen. Tools include the Mini-Cog, Short Portable Mental Status Questionnaire, Montreal Cognitive Assessment, or simply orientation plus an attention task (days of the week or months of the year backwards, serial sevens, or digits backwards). ^[1]

A range of bedside attention tests are used. An EEG records diffuse slowing with increased theta and delta activity in delirium, and is mainly useful when non-convulsive seizures, a functional disorder or a dementia-with-superimposed problem is suspected. ^[1]

Most ICU patients with delirium are intubated or non-verbal. The CAM-ICU is therefore used: a two-step test of altered/altered/fluctuating mental status with inattention, plus either disorganised thinking or an altered level of consciousness. It takes one to two minutes. ^[5][4]

The main distinction is between delirium, dementia, depression and primary psychiatric disorder. Delirium can also sit on top of dementia (delirium superimposed on dementia), which is common and often missed; when in doubt, treat delirium first. ^[2]

Also consider stroke, non-convulsive seizures, hypoglycaemia, drug intoxication, Wernicke encephalopathy, hepatic encephalopathy, and normal pressure hydrocephalus when the picture does not fit a routine medical cause. ^[5]

There is no single test for delirium. Computed tomography (CT) and magnetic resonance imaging (MRI) are low-yield in unselected cases and are reserved for focal neurological findings, head trauma, suspected encephalitis, or unexplained altered consciousness. ^[1]

Delirium is a clinical diagnosis. The reference standard criteria are DSM-5-TR and ICD-11 (paraphrased, not quoted; the full criteria are copyrighted). ^[1] In short: disturbed attention and awareness with an acute, fluctuating course; an additional cognitive disturbance; not better explained by a pre-existing neurocognitive disorder; and with evidence of a medical cause, substance or withdrawal. ^[4]

At the bedside we use a structured screening test. Two are common in general wards; two are used in the ICU.

CAM is the most widely used tool, validated in high-quality studies covering over 1000 patients, with sensitivity of 94%, specificity of 89% and high inter-rater reliability when used with a brief cognitive test. It is available in over 12 languages and adapted for the ICU, the emergency department and long-term care. ^[1]

Four features; CAM is positive when features 1 and 2 and either 3 or 4 are present:

1. Acute onset and fluctuating course.
2. Inattention (difficulty focusing or sustaining or shifting attention).
3. Disorganised thinking (rambling, irrelevant or illogical speech).
4. Altered level of consciousness (anything other than alert).

NICE (CG103, recommendation 1.6.1) recommends the 4AT in most hospital settings. The 4AT takes about two minutes, needs no special training, and includes a brief cognitive test and attention test, so it picks up cognitive impairment as well as delirium. ^[2][3]

Scoring (0 to 12): ^[3]

• Alertness: normal = 0; mild sleepiness under 10 seconds then normal = 0; clearly abnormal = 4.
• AMT4 (age, date of birth, hospital or building, current year): no mistakes = 0; one mistake = 1; two or more or untestable = 2.
• Attention (months of the year backwards from December): seven or more correct = 0; fewer than seven or refusal = 1; untestable = 2. ^[3]
• Acute change or fluctuating course over the last two weeks, still evident in the last 24 hours: no = 0; yes = 4.

Interpretation: ^[3]

• 4 or more: delirium likely (guide further assessment and clinical judgement).
• 1 to 3: cognitive impairment but not delirium.
• 0: no delirium and no moderate-severe cognitive impairment, but does not fully exclude either. ^[3]

The 4AT can always be scored, even when the patient cannot speak (for example a drowsy patient scores 2 on each of the two cognitive items, giving 4 and supporting suspicion of delirium). ^[3]

Postoperatively, the 4AT is often repeated daily for 3 to 7 days. ^[3]

In critical care, or in the recovery room after surgery, use CAM-ICU or ICDSC instead of the 4AT. ^[2][4]

• CAM-ICU: two-step. Altered or fluctuating mental status with inattention, plus either disorganised thinking or an altered level of consciousness (RASS not "alert and calm"). Takes one to two minutes. ^[5][4]
• ICDSC: an eight-item checklist covering a period of time rather than a single moment. It accounts for fluctuation but is generally less sensitive and specific and places a heavier burden on staff. ^[4]
• 4AT gives sensitivities and specificities around 85% in large, multicentre studies overall, but two items require verbal interaction, so it is often impractical in ventilated patients. ^[4]

If needed, severity can be tracked with the Delirium Rating Scale-Revised-98 or Memorial Delirium Assessment Scale, or by the CAM-ICU-7 in ICU. ^[1][4]

The management of delirium follows three simultaneous priorities: protect the patient, search for the causes, and manage distressing symptoms. ^[1]

1. Identify and treat underlying causes (infection, hypoxia, drug effects, withdrawal, retention, constipation, pain, metabolic disturbance). ^[1][2]
2. Use non-drug measures first to reorient, calm and support. ^[1][2]
3. Keep the patient safe without restraints, tethers or bed alarms, which increase delirium, injury and persistence. ^[1]
4. Avoid or remove psychoactive and anticholinergic drugs, substituting less toxic alternatives and avoiding "as needed" dosing. ^[1][2]
5. Use drug therapy only for the agitated, distressed or psychotic patient whose agitation risks getting them hurt or interrupting life-supporting treatment, and keep it short and low-dose. ^[1][2]

These are the first-line strategy and should be started as soon as delirium is suspected: ^[1][2]

• Communication and reorientation: explain repeatedly where the person is, who they are and what your role is; involve family and friends.
• Environment: clear signage, appropriate lighting, a visible clock and calendar, noise reduced at night, procedures avoided during sleep, medication rounds timed to protect sleep.
• Sensory: correct hearing and visual impairment (glasses and hearing aids in good working order, impacted wax removed).
• Mobility: get up soon after surgery, walk with aids accessible, active range-of-motion exercises even if bedbound.
• Nutrition and fluids: good intake, treat constipation, subcutaneous or intravenous fluids if needed (with care in heart or kidney disease).
• Hygiene: avoid unnecessary catheterisation; infection control; look for and treat infection.
• Pain: assess, including non-verbal signs in people who cannot speak, and treat promptly.
• Sleep: daytime light, discourage napping, nighttime quiet with low light.
• Company: familiar staff, family visits, avoid unnecessary moves between wards or rooms.
• Medication review: for people on many drugs, weighing up both type and number.

These measures also prevent delirium: NICE CG103 packages them as a tailored multicomponent intervention delivered within 24 hours of admission and by a trained multidisciplinary team. ^[2]

Drug treatment is reserved for patients with severe agitation, which interrupts essential medical therapy, or for extremely distressing psychotic symptoms. ^[1][2]

• Haloperidol (short-term only): usually 1 week or less; lowest clinically appropriate dose, titrated cautiously to symptoms. NICE recommends starting at the lowest effective dose. ^[2]
• Typical dose in older adults: haloperidol 0.25 to 0.5 mg by mouth or intramuscularly, twice daily, used short term. ^[1]
• Safety cautions: haloperidol carries cardiac (QT prolongation) and neurological risks, especially in older adults, in Parkinson's disease and in dementia with Lewy bodies; follow the Medicines and Healthcare products Regulatory Agency advice. ^[2]
• Haloperidol lowers the seizure threshold; if it must be used in alcohol withdrawal, check the ECG and electrolytes first and look for hypokalaemia and hypomagnesaemia. ^[5]
• Atypical antipsychotics appear close in effectiveness; quetiapine is not more effective than haloperidol in the ICU, and haloperidol carries the higher risk of extrapyramidal side effects. ^[4]
• Pharmacologic prevention is not supported: no drug (haloperidol, risperidone, olanzapine, rivastigmine, melatonin, ketamine, dexmedetomidine) has convincing, reproducible evidence of clear efficacy for prevention or treatment, and some (rivastigmine, olanzapine in some studies) produced worse outcomes. ^[1][4]

ICU delirium is common (pooled prevalence about 32%), usually hypoactive, and associated with worse outcomes and long-term cognitive impairment in up to 70% at 18 months. ^[4]

• Avoid benzodiazepines where possible: compared with propofol, midazolam-class drugs increase delirium risk by about a third. Propofol is an intermediate risk. ^[4]
• Dexmedetomidine reduces delirium incidence by about a third and mean mechanical ventilation and stay by about a day in tightly controlled trials, but with mixed findings in pragmatic trials; the 2025 Society of Critical Care Medicine guidance gives a conditional recommendation for dexmedetomidine over propofol when light sedation and reducing delirium are the priority. ^[4]
• Sedation targets and breaks: titrate to light sedation and consider daily sedation interruption; this is part of standard care even though the certainty of delirium benefit is low. ^[4]
• The ABCDEF bundle: Assess and manage pain; spontaneous awakening and breathing trials; choice of analgesia and sedation; Delirium monitoring and management; Early exercise and mobility (mobilisation within 72 hours of admission is readily achievable in many); Family engagement and re-orientation. ^[4]
• The ICU Liberation Campaign wraps these measures with implementation support; in large studies, implementation reduced coma, delirium, restraint use, ventilator days, and increased survival and home discharge. ^[4]
• Non-drug care: family voice re-orientation, early mobilisation, sleep hygiene (daylight, eye masks, earplugs), structured multidisciplinary care and ICU diaries to support recovery. ^[4]
• Follow-up matters: cognitive impairment, depression (about a third), anxiety (just under half) and post-traumatic stress (about a quarter) are common in ICU survivors; ICU follow-up at 2 to 3 months and an ICU diary can help people make sense of what happened. ^[4]

Delirium tremens is a medical emergency. ^[5]

• Where it is managed: inpatient, ideally in the ICU in severe or refractory cases. ^[5]
• Benzodiazepines are the mainstay, with long-acting agents (diazepam or chlordiazepoxide) preferred for self-tapering, and lorazepam if liver dysfunction or poor intramuscular absorption. ^[5]
• Regimens: ^[5]
  • Front-loading with diazepam: 5 to 20 mg intravenously repeated until light, arousable sedation or CIWA-Ar under 8 (stated as "bring CIWA-Ar below 8"). Diazepam 5 mg IV then 5 mg IV (repeat after 10 min), or 10 mg IV repeated, 20 mg IV after 10 min, then 5 to 20 mg per hour; aim CIWA-Ar under 8. Requires ventilator availability and is avoided with suspected head injury or liver dysfunction.
  • Symptom-triggered with diazepam: 10 to 20 mg intravenously every 1 to 4 hours until CIWA-Ar under 8.
  • Symptom-triggered with lorazepam: 4 mg intravenously, repeated every 10 minutes until CIWA-Ar under 8 or sedation; if severe delirium persists after 16 mg total, give an 8 mg intravenous bolus. ^[5]
  • Fixed-dose regimens are reserved for outpatient management, not delirium tremens.
• CIWA-Ar thresholds: under 8 mild; 8 to 15 moderate; over 15 severe and predictive of seizures and delirium tremens. ^[5]
• Other measures: thiamine 500 mg intravenously over 30 minutes once or twice daily for 3 days (and three times daily for 5 days if Wernicke's encephalopathy is suspected) before any intravenous dextrose, plus multivitamins; magnesium only if documented deficiency; avoid intravenous dextrose before thiamine; adequate fluids and electrolytes; screen for infection, liver and cardiac disease, WE. ^[5]
• Refractory delirium tremens (persistent CIWA-Ar over 25 despite treatment, or large benzodiazepine requirements as in the thresholds "200 mg diazepam in 3 h or 400 mg in 8 h, or 30 mg lorazepam in 3 h or 60 mg in 8 h"): treat in ICU. Add phenobarbital first (60 mg IV bolus every 15 minutes, halve the benzodiazepine if not intubated, intubate on signs of respiratory depression), then propofol infusion (0.3 to 1.25 micrograms/kg/h, maximum 4 micrograms/kg/h, maximum 48 hours) if needed, then dexmedetomidine up to 0.7 micrograms/kg/h as an adjunct. Haloperidol (0.5 to 5 mg IV or IM every 30 to 60 minutes, up to 20 mg per dose; or 0.5 to 5 mg orally every 4 hours up to 30 mg) only for uncontrolled agitation or hallucinations. ^[5]
• Wernicke encephalopathy is common (autopsy evidence in 1.4% of heavy-drinking hospitalised patients, up to 58% with severe alcohol problems) but the classic triad is present in only 8%. Use Caine's criteria (two of: dietary deficiency, eye signs, cerebellar dysfunction, altered mental state or memory), which have sensitivity 85%; brain MRI shows symmetrical changes with 53% sensitivity and 93% specificity; untreated cases progress to Korsakoff syndrome in roughly 60%. ^[5]

Delirium itself is associated with: ^[1][4]

• Increased mortality: roughly 2 to 4-fold in the ICU both in and out of hospital; 1.5-fold on general medical or geriatric wards over the following year; around 70% increased risk at six months after an emergency department visit. ^[1][4]
• Longer ICU and hospital stays, increased ventilation and healthcare cost.
• Falls, pressure injuries, aspiration, infections from catheters, functional decline.
• Long-term cognitive decline, institutionalisation, dementia, depression, anxiety and post-traumatic stress, particularly after ICU delirium.
• Readmission and loss of independence.

Most episodes resolve over days once the cause is treated, but many leave a mark. ^[1][4]

• Mortality is high when delirium occurs in the context of severe illness, especially in the ICU and in fractured hips in older patients.
• Cognitive improvement in surgical patients can continue for months; some never return to their baseline.
• If delirium does not resolve, re-evaluate for missed causes and later assess for possible dementia. ^[1][2]
• Delirium tremens usually lasts 3 to 4 days (up to 8) and classically ends with a prolonged sleep; refractory cases are more dangerous. ^[5]

Delirium is preventable in 30 to 40% of cases, so prevention is the main evidence-based strategy. ^[1][4]

NICE CG103 (last updated January 2023) recommends identifying risk at admission: age 65 or older; cognitive impairment (past or present) or dementia; current hip fracture; or severe illness. ^[2] Then look again at every opportunity, because risk changes. ^[2]

At presentation (within hours or days) look for changes in: cognition (worsened concentration, slow responses, confusion), perception (hallucinations), physical function (reduced mobility, restlessness, agitation, appetite and sleep change), behaviour (difficulty following requests, withdrawal, communication or mood change). Hypoactive changes are often missed and should be sought deliberately. ^[2]

Every at-risk patient should receive a tailored multicomponent intervention, started within 24 hours of admission, by a trained multidisciplinary team: ^[2]

• Reorientation, appropriate lighting and clear signage, a visible clock and calendar, stimulating activity, family visits.
• Hydration (encourage drinking, fluids if needed, with care in heart failure or renal disease) and bowel regularity.
• Hypoxia assessment and oxygen if needed, mindful of oximeter errors.
• Infection control and treatment, avoiding unnecessary catheterisation.
• Early mobilisation, walking aids accessible, range-of-motion exercises.
• Pain assessment, especially non-verbal pain, with prompt analgesia.
• Medication review considering type and number of drugs.
• Good nutrition and well-fitting dentures.
• Sensory aids (glasses, hearing aids in good order) and reversible sensory problems fixed.
• Sleep hygiene: no unnecessary nocturnal procedures or medication rounds, minimum noise.

The best-evidenced ward-based programme is the Hospital Elder Life Program (HELP): a multicomponent intervention targeting cognition, immobility, hydration, sleep, hearing and vision, delivered by a trained interdisciplinary team, with proven effectiveness and cost-effectiveness and savings of roughly 9,000 US dollars per patient per year. It has been implemented in over 200 hospitals worldwide, though adaptation is needed with limited resources. ^[1]

In the ICU, prevention is the ABCDEF bundle described above, supported by the Society of Critical Care Medicine ICU Liberation Campaign. ^[4]

The older adult is the most common patient. Delirium here is often the first sign of serious illness (pneumonia, myocardial infarction, medication toxicity), and missing hypoactive delirium is a common cause of harm. Risk rises with age, dementia, frailty, comorbidity, sensory impairment and medications. ^[1][4]

The American Geriatrics Society 2015 best-practice statement on postoperative delirium in older adults underpins assessment, prevention and care in the perioperative period; together with the European Society of Anaesthesiology 2017 guideline on postoperative delirium (updated in 2024) and the UK Intensive Care Society guidance, it forms the peri-operative standard alongside the SCCM Pain, Agitation, Delirium, Immobility and Sleep guidance. ^[6][7][4][2]

Delirium occurs in paediatric intensive care and is diagnosed with paediatric-adapted criteria and tools (for example the p-CAM-ICU or CAPD), which are not covered here in depth; the principles are the same (identify and treat triggers, protect sleep, mobilise, avoid unnecessary sedation).

Delirium in pregnancy usually signals a severe physical illness (infection, thrombosis, eclampsia, drug effect or withdrawal) and the diagnosis is the same as in any other adult, with attention to fetal and maternal drug safety; short-term low-dose haloperidol and benzodiazepine decisions should follow national formularies and specialist advice.

Relatives should be told that delirium is common and usually temporary, that it reflects an underlying illness, and that early telling of staff about sudden behaviour change hastens both diagnosis and recovery. ^[2]

Delirium is still often missed in low-resource settings, but the diagnosis needs no expensive test: it is made from a careful history from someone who knows the patient, plus a brief attention task and a search for triggers. ^[1]

• Use a single bedside attention test (digit span backwards, serial sevens, or months backwards) and recheck.
• Correct glasses and hearing aids work, remove impacted wax, provide adequate light and dark, and give families the role of reorienting the patient.
• Avoid urinary catheters, restraints and unnecessary sedatives.
• Run a simple prevent bundle: mobilise three times a day, offer fluids by mouth, sleep protected at night, pain assessed, infection actively sought.
• Send every patient home with an explanation and plan (delirium can persist for weeks), and document the diagnosis for follow-up, because delirium may be the first sign of dementia.
• Where benzodiazepines for alcohol withdrawal are scarce, a symptom-triggered oral or intramuscular regimen may be the safer fallback; arrange ICU or ventilator support locally before front-loading dosing. ^[5]

• Delirium is an acute, fluctuating disturbance of attention and awareness (plus a cognitive change) that develops over hours to days. ^[1]
• It affects up to half of hospitalised older adults and carries a high mortality and long-term cognitive cost. ^[1][4]
• It arises from a mix of predisposing brain vulnerability (dementia, frailty, sensory loss, age) and precipitating insults (infection, drugs, surgery, hypoxia, withdrawal, pain, retention). ^[1][4]
• Hypoactive (quiet) delirium is the most common and most missed form; always think of it in a withdrawn, sleepy, poorly engaging patient. ^[1][2]
• Delirium is a clinical diagnosis built on an acute fluctuating course plus inattention plus an additional cognitive disturbance. ^[1][4]
• CAM (sensitivity 94%, specificity 89%) and 4AT (0 to 12; 4 or more suggests delirium) are the common bedside tools; use CAM-ICU or ICDSC in critical care. ^[1][3][4]
• There is no single diagnostic test; investigations are chosen from the history and examination. ^[1]
• Treatment starts with finding and treating causes, plus non-drug care (reorientation, environment, mobilisation, sleep, hydration, nutrition, sensory aids, pain control). ^[1][2]
• Antipsychotics are reserved for severe agitation or distressing psychosis; low-dose short-term haloperidol (typically 0.25 to 0.5 mg by mouth or intramuscularly twice daily) is the usual choice, with careful attention to cardiac and neurological risks, and usually one week or less. ^[1][2]
• No drug reliably prevents or treats delirium; benzodiazepines and anticholinergics should be minimised. ^[1][4]
• Prevention works in 30 to 40% of cases: the NICE CG103 multicomponent bundle, HELP in wards, and the ABCDEF bundle in the ICU. ^[1][2][4]
• Delirium tremens is a medical emergency arising 48 to 72 hours after cessation; benzodiazepines (front-loading or symptom-triggered) are the mainstay, with thiamine before glucose and ICU care for refractory cases. ^[5]
• In the ICU avoid benzodiazepines where possible; sedate lightly with breaks; mobilise early and engage families. ^[4]
• Screen all at-risk adults (age 65 or older, cognitive impairment or dementia, hip fracture, severe illness) and re-screen as risk evolves. ^[2]
• Document and communicate the diagnosis; if it does not resolve, re-evaluate causes and later assess for dementia. ^[2]

Mood and anxiety problems, dementia and cognitive impairment, substance-use disorders including alcohol-use disorders, Wernicke encephalopathy, sepsis and fever, stroke and intracranial haemorrhage, hypoglycaemia, and critical-care sedation. Delirium also sits among the topics of safe geriatric prescribing and non-pharmacological nursing care.