Acute, fluctuating disturbance of attention and awareness from an underlying medical cause.
Also known as: delirium, acute confusional state, encephalopathy, ICU delirium, sundowning
Overview
Acute, fluctuating disturbance of attention, awareness, and cognition that develops over hours to days, caused by an underlying medical condition, substance, or medication, and not better explained by a pre-existing or evolving neurocognitive disorder.
Epidemiology
Affects 15-25% of hospitalized older adults on general wards, up to 50% post-operatively, and 70-87% of ICU patients. Associated with prolonged hospitalization, functional decline, increased mortality, and persistent cognitive impairment.
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Question 1NeurologyMedium
An 82-year-old man with baseline dementia is admitted with community-acquired pneumonia. On hospital day 2 the nursing staff report that he is acutely confused, drifting in and out of attention, agitated at night but drowsy during the day, and having visual hallucinations that fluctuate over hours. His vital signs are stable and a repeat neurologic exam shows no focal deficits. Which of the following best explains the pathophysiologic mechanism underlying his acute change?
AAcute global cerebral dysfunction from illness
BProgressive irreversible cortical degeneration
CFocal cortical ischemia from vessel occlusion
DDemyelination of central white-matter tracts
Reveal answer & full explanation
Correct answer: A — Acute global cerebral dysfunction from illness
AAcute global cerebral dysfunction from illness✓
BProgressive irreversible cortical degeneration
CFocal cortical ischemia from vessel occlusion
DDemyelination of central white-matter tracts
Why Acute global cerebral dysfunction from illness is correct
This is delirium.
Advanced age plus baseline dementia is the single strongest predisposing factor, and an acute infection such as pneumonia is the classic precipitating insult that tips a vulnerable brain into an acute confusional state.
The defining features here are the acute onset, fluctuating course, inattention, altered level of consciousness (hypoactive by day, hyperactive at night), and perceptual disturbances.
The mechanism is acute global cerebral dysfunction produced by a systemic insult (infection, inflammation, and neurotransmitter dysregulation) affecting the brain diffusely rather than any single focal lesion, so that is the correct answer.
Why the others are wrong
Progressive irreversible cortical degeneration — this describes the underlying dementia itself, which develops over months to years and is not the mechanism of the acute, fluctuating, potentially reversible change seen over days.
Focal cortical ischemia from vessel occlusion — a stroke would produce focal neurologic deficits (e.g., hemiparesis, aphasia), which are absent here, and would not fluctuate in the waxing-waning delirium pattern.
Demyelination of central white-matter tracts — demyelinating disease (e.g., multiple sclerosis) causes discrete neurologic deficits over a different time course and does not explain an acute infection-triggered global confusional state.
Diffuse, reversible cerebral dysfunction from a systemic trigger is the hallmark mechanism of delirium.
Question 2NeurologyMedium
An 82-year-old man is admitted for community-acquired pneumonia. On hospital day 2 he becomes acutely confused, pulls at his IV lines, and is inattentive on bedside testing, with symptoms waxing and waning through the night. His daughter notes he has had progressive memory loss and disorientation at home over the past 3 years and was recently told he has Alzheimer disease. Among his baseline characteristics, which of the following is the strongest predisposing risk factor for the delirium he developed?
AMild osteoarthritis
BChronic hypertension
CPrior tobacco smoking
DPreexisting dementia
Reveal answer & full explanation
Correct answer: D — Preexisting dementia
AMild osteoarthritis
BChronic hypertension
CPrior tobacco smoking
DPreexisting dementia✓
Why Preexisting dementia is correct
Baseline dementia or cognitive impairment is the single strongest predisposing risk factor for delirium; a vulnerable, low-reserve brain decompensates with even minor precipitants such as infection.
Here the acute pneumonia is the precipitant, but his underlying Alzheimer disease is the predisposing factor that made delirium so likely. Other potent predisposers include advanced age, sensory impairment, frailty, polypharmacy, and prior delirium.
Why the others are wrong
Chronic hypertension is a common comorbidity but not an independent driver of delirium vulnerability and is not among the established predisposing factors.
Prior tobacco smoking is a weak, nonspecific factor; active nicotine withdrawal during admission can contribute, but a remote smoking history is far less important than dementia.
Mild osteoarthritis does not predispose to delirium; uncontrolled pain can precipitate it, but the chronic joint condition itself is not a predisposing factor.
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Inattention with acute, fluctuating onset is the hallmark; the Confusion Assessment Method (CAM) operationalizes this.
Differential diagnosis
Dementia — Chronic, slow onset, attention relatively preserved early, level of arousal normal; delirium can be superimposed on dementia (and often is)
Depression (pseudodementia) — Persistent low mood, anhedonia, sleep/appetite changes; cognition impaired but attention often intact; subacute
Primary psychiatric illness (psychosis, mania, dissociative) — Usually younger, preserved level of consciousness, sustained psychotic content, history of mental illness
Nonconvulsive status epilepticus — Confusion without obvious convulsion; EEG diagnostic — must consider in any unexplained altered mental status
Wernicke encephalopathy — Triad of confusion, ophthalmoplegia, ataxia; alcohol use, malnutrition, bariatric surgery, hyperemesis; give thiamine BEFORE glucose
Hypoglycemia or hyperglycemic crises — Fingerstick glucose; rapid reversal with treatment
Diagnostic workup
Diagnostic criteria
DSM-5: (A) disturbance of attention and awareness; (B) develops over short period, fluctuates; (C) additional cognitive disturbance; (D) not better explained by another neurocognitive disorder or coma; (E) evidence of underlying physiologic cause. CAM: (1) acute onset and fluctuating course + (2) inattention + either (3) disorganized thinking or (4) altered level of consciousness.
Drug levels (lithium, digoxin, anticonvulsants); urine toxicology
Troponin and ECG if cardiac etiology suspected
Lumbar puncture if CNS infection or unexplained encephalopathy
Vitamin B12, thiamine (give empirically if Wernicke suspected)
Imaging
CT head if focal deficits, head trauma, anticoagulation, or no identifiable cause
MRI brain if CT non-diagnostic and concern for stroke or PRES
Chest X-ray for occult pneumonia
EEG if nonconvulsive seizures suspected (also shows generalized slowing in metabolic delirium)
Diagnostic algorithm
Feature
Delirium
Dementia
Depression
Onset
Hours to days
Months to years
Weeks to months
Course
Fluctuating, worse at night
Slowly progressive
Persistent low mood
Attention
Markedly impaired
Preserved early
May be mildly impaired
Level of consciousness
Altered (hyper- or hypoactive)
Normal until late
Normal
Orientation
Impaired
Impaired late
Usually intact
Hallucinations
Common (visual)
Late-stage (or DLB)
Rare (psychotic depression)
Reversibility
Usually reversible
Generally not reversible
Reversible with treatment
Distinguishing delirium, dementia, and depression in older adults.
Treatment
First-line
Identify and treat the underlying cause(s) — usually multifactorial (the 'I WATCH DEATH' or similar mnemonic): Infection, Withdrawal, Acute metabolic, Trauma, CNS pathology, Hypoxia, Deficiencies, Endocrine, Acute vascular, Toxins/drugs, Heavy metals
Nonpharmacologic 'HELP'-style bundle (Hospital Elder Life Program): orient frequently (clock, calendar, familiar faces), restore sensory aids (glasses, hearing aids), early mobilization, sleep hygiene (quiet, dark at night; light during day; minimize nighttime interruptions), hydration and nutrition, avoid restraints and tethers
Review and minimize deliriogenic medications: anticholinergics (diphenhydramine, oxybutynin, TCAs), benzodiazepines, opioids (especially meperidine), corticosteroids, H2 blockers; deprescribe when possible
ABCDEF bundle in ICU: Assess/manage pain, spontaneous Breathing trials, Choice of sedation (avoid benzodiazepines; prefer dexmedetomidine or propofol), Delirium monitoring (CAM-ICU), Early mobility, Family engagement
Second-line / adjunct
Pharmacologic treatment ONLY for severe agitation threatening safety after nonpharmacologic measures fail:
Low-dose haloperidol (e.g., 0.25-0.5 mg PO/IM; QT monitoring); avoid in Parkinson disease and Lewy body dementia
Atypicals: quetiapine, olanzapine, risperidone — useful when EPS or PD considerations apply
Dexmedetomidine (alpha-2 agonist) for ICU delirium — reduces incidence and duration
Benzodiazepines ONLY for alcohol/sedative-hypnotic withdrawal delirium or seizures; otherwise worsen delirium
Treat alcohol withdrawal with symptom-triggered benzodiazepines (CIWA) plus thiamine, folate, multivitamins
AVOID physical restraints when possible — increase agitation and injury
Complications
Prolonged hospitalization and higher mortality (in-hospital and at 1 year)
Functional decline and loss of independence
Persistent cognitive impairment and increased risk of subsequent dementia (especially after ICU delirium)
Falls, fractures, pressure ulcers, aspiration pneumonia
Self-injury or injury to staff during severe agitation
Caregiver and family distress
PTSD-like symptoms after ICU stay
PANCE pearls
Delirium is a medical emergency — find the cause. The default assumption in older adults with acute confusion is delirium until proven otherwise.
Hypoactive delirium is MORE common than hyperactive in elderly and is frequently missed — screen all hospitalized older patients (e.g., CAM, 4AT).
If giving glucose to a patient who may be alcohol-dependent or malnourished, give thiamine FIRST to avoid precipitating Wernicke encephalopathy.
Benzodiazepines worsen non-withdrawal delirium — reserve them for alcohol/sedative withdrawal.
Avoid antipsychotics in Parkinson disease and Lewy body dementia (severe neuroleptic sensitivity); use quetiapine or pimavanserin if absolutely needed.
Postoperative delirium peaks on hospital day 2-3; preventive bundles (HELP) reduce incidence by ~30-40%.
References
DSM-5-TR — American Psychiatric Association Diagnostic and Statistical Manual, 5th ed. Text Revision (2022)
SCCM 2018 — Clinical Practice Guidelines for the Prevention and Management of PAD/Delirium/Immobility/Sleep Disruption in Adult ICU Patients (Devlin et al., Crit Care Med 2018)
AGS 2014 — American Geriatrics Society Clinical Practice Guideline for Postoperative Delirium in Older Adults (Inouye et al., JAGS 2015)
CAM — Confusion Assessment Method (Inouye et al., Ann Intern Med 1990)
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