Delirium is a serious neuropsychiatric syndrome characterized by an acute confusional state with global impairments in attention and cognition.[1] Delirium is often associated with a disturbance in the sleep-wake cycle, including daytime sleepiness, nighttime agitation, insomnia, excessive sleepiness, or wakefulness throughout the night. In some cases, complete reversal of the night-day sleep-wake cycle can occur.

  • The community prevalence of delirium is low, between 1 to 2%, but increases with age, rising to 14% in individuals older than 85 years.
  • The prevalence is 10% to 30% in older individuals presenting to emergency departments, where the delirium is a result of a medical illness. Rates are highest in post-surgical (hip surgery), palliative care for advanced cancer (up to 80%), ICU (up to 70%) and dementia populations.[2]
Risk Factors
  • The development delirium can be due to multiple risk factors. Some of these risk factors are modifiable and thus a target in delirium prevention. Up to 40% of cases of delirium are preventable.[3]
  • In elderly patients, dementia is the most common risk factor (in up to two-thirds of all cases of delirium).

Delirium Risk Factors

Modifiable Essentials • Sensory impairment (hearing or vision)
• Immobilization (catheters or restraints)
• Environment (for example, admission to an intensive care unit)
• Emotional distress
• Sustained sleep deprivation
Modifiable Medical • Medications (e.g. - sedative hypnotics, narcotics, anticholinergic drugs, corticosteroids, polypharmacy, alcohol withdrawal or other drugs)
• Acute neurological diseases (e.g. - acute stroke [usually right parietal], intracranial hemorrhage, meningitis, encephalitis)
• Ongoing illness (e.g. - infection (UTI), iatrogenic complications, acute illness, anemia, dehydration (often giving IV fluids will improve things), poor nutrition, trauma, fractures, HIV)
• Metabolic derangement
• Surgery
Non-modifiable Dementia or cognitive impairment
• Advancing age (>65 years)
• History of delirium, stroke, neurological disease, falls or gait disorder
• Multiple comorbidities
• Male sex
• Chronic renal or hepatic disease
Criterion A

A disturbance in attention (i.e. - reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment).

Criterion B

The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day.

Criterion C

An additional disturbance in cognition (e.g. - memory deficit, disorientation, language, visuospatial ability, or perception).

Criterion D

The disturbances in Criteria A and C are not better explained by another preexisting, established, or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of arousal, such as coma.

Criterion E

There is evidence from the history, physical examination, or laboratory findings that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal (i.e. - due to a drug of abuse or to a medication), or exposure to a toxin, or is due to multiple etiologies.


Specify if:

  • Substance intoxication delirium: Criteria A and C predominate in the clinical picture and when they are sufficiently severe to warrant clinical attention
  • Substance withdrawal delirium: Criteria A and C predominate in the clinical picture and when they are sufficiently severe to warrant clinical attention
  • Medication-induced delirium: When criteria A and C arise as a side effect of a medication taken as prescribed.
  • Delirium due to another medical condition: There is evidence from the history, physical examination, or laboratory findings that the disturbance is attributable to the physiological consequences of another medical condition.
  • Delirium due to multiple etiologies: There is evidence from the history, physical examination, or laboratory findings that the delirium has more than one etiology (e.g., more than one etiological medical condition; another medical condition plus substance intoxication or medication side effect).

Severity Specifier

Specify if:

  • Acute: Lasting a few hours or days
  • Persistent: Lasting weeks or months

Hyperactive or Hypoactive Specifier

Specify if:

  • Hyperactive: The individual has a hyperactive level of psychomotor activity that may be accompanied by mood lability, agitation, and/or refusal to cooperate with medical care.
  • Hypoactive: The individual has a hypoactive level of psychomotor activity that may be accompanied by sluggishness and lethargy that approaches stupor.
  • Mixed level of activity: The individual has a normal level of psychomotor activity even though attention and awareness are disturbed. Also includes individuals whose activity level rapidly fluctuates.
  • Patients can present with hypoactive delirium, where they appear lethargic, somnolent, and sluggish. This is often not recognized as they do not cause a “disturbance,” and may be mistakenly identified as depressed.
  • In hyperactive delirium, patients are often agitated, hallucinating, and have inappropriate behaviour. Some patients can have a mixed delirium where they have a combination of both (fluctuations between agitation and lethargy).[4]

Why Is It Important to Identify Delirium?

Delirium has a fluctuating course and can overlap with dementia, which makes it hard to detect. The lack of routine cognitive assessments also makes it hard to monitor changes in a patient's mental status. Delirium is also under appreciated in terms of its importance and consequences. Patients with ongoing delirium have a significantly higher risk of mortality, significant increases in length of stay, increased costs of hospitalization, and increased chance of nursing home placement.[5][6][7][8][9] One final reason includes ageism, the expectation of: “Aren't older people generally confused?”

Delirium is Often Missed!

Doctors and nurses do a poor job of identifying delirium.[10] Even if symptoms are identified, they may be misattributed to depression or dementia. It is particularly under-recognized in patients over age 80, those with hypoactive delirium, impaired vision, and dementia.

Delirium Screening Tools

Name Rater Description Download
Confusion Assessment Method (CAM) Clinician The Confusion Assessment Method (CAM) is a standardized evidence-based tool that allows clinicians to identify and recognize delirium quickly and accurately in both clinical and research settings. It has a sensitivity of 94‐100% and specificity of 90‐95%.[11][12] See the training guide for full instructions. Short Version
Critical Care Version


The mnemonic AIDA can be used to remember the core features of delirium. Remember you need features 1 AND 2, plus 3 OR 4 for an individual to be positive for delirium on the Confusion Assessment Method (CAM).
  1. A - Acute and fluctuating (a change from baseline, AND a change during the day)
    • Is there evidence of an acute change in mental status from the patient’s baseline?
    • Did the (abnormal) behaviour fluctuate during the day, that is, tend to come and go, or increase and decrease in severity?
  2. I - Inattention (difficulty focusing/keeping track, drifting off to sleep, easily distracted)
    • Did the patient have difficulty focusing attention, for example, being easily distractible, or having difficulty keeping track of what was being said?
    • Can use cognitive tests of attention (forward digit span; backward digit span; months of the years backwards; spelling WORLD backwards; serial 7s)
  3. D - Disorganized thinking (incoherent, rambling, irrelevant, illogical, circumstantial, vague)
    • Was the patient’s thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?
  4. A - Altered level of consciousness (lethargic, vigilant, stuporous, drowsy, agitated)
    • Overall, how would you rate the patient’s level of consciousness? (alert [normal], vigilant [hyperalert], lethargic [drowsy, easily aroused], stupor [difficult to arouse], or coma [unarousable])?

Obtaining a good history is key and should be the first step when seeing a patient with delirium. Do not rely on just self-report by the patient. Use as many collateral sources as possible, including family, staff, and the chart.

The following items on history should always be obtained:

  • Medical and Psychiatric History (acute and chronic)
    • Sensory impairments (hearing/vision)
    • Elimination patterns (urinary and bowel frequency)
  • Recent Surgeries
  • Medication History (Prescription, OTC)
  • Substance Use History (especially for alcohol)
  • Previous cognitive functioning, ADLs, and IADLs
  • History of Presenting Illness (HPI)
    • Onset and course of confusion
    • History previous episodes of delirium (and treatment response)
    • Sleep patterns
  • Social History

Before even considering pharmacologically managing delirium, always think about what could be causing delirium in the first place! First consider the non-medical issues that could cause an altered level of consciousness, including: pain, vision deficits, hearing deficits, hunger, constipation (i.e., fecal loading), or urinary retention. Then consider the medical etiologies below. In geriatric populations, also consider the geriatric giants.


The mnemonic DIMS-R can be used to remember the common causes of delirium and provide a structured approach:

  • D - Drugs: Is there a drug intoxication, or conversely, a drug withdrawal? Look for sedating medications, anticholinergic medications, and never forget alcohol withdrawal
  • I - Infections: Is the genitourinary system, chest, skin/soft-issue, or blood infected? If so, consider CXRs or further infectious work up if needed.
  • M - Metabolic: Are there any changes to glucose, electrolytes, extended electrolytes, creatinine, liver enzymes, VBG CO2, TSH, or B12 that would reflect endocrinopathies, renal failure, or liver failure?
  • S - Structural: Think about serious intracranial pathologies like stroke, hemorrhage, seizures, or neoplasms. Neuroimaging (CT, MRI) may be required.
  • R - Retention: Is there fecal impaction or urinary retention? If so, consider abdominal X-rays, palpation, DRE, disimpaction.

A non-exhaustive list of potential causes for delirium include:

Common Potential Causes of Delirium

Gage L. and Hogan D.B. (2014). 2014 CCSMH Guideline Update: The Assessment and Treatment of Delirium. Toronto: Canadian Coalition for Seniors’ Mental Health
Course of Delirium Examples Consider if:
Drug-induced Sedative-hypnotics, anticholinergics, opioids, anticonvulsants, anti-parkinsonian agents The drug in question has central nervous system effects; a toxic level is documented or there is improvement with dose reduction or discontinuation; and, the time course coincides with the use of the drug.
Alcohol and drug withdrawal Alcohol, benzodiazepines Recent and long-term use of alcohol or sedative drug; evidence of withdrawal (e.g., autonomic hyperactivity, seizure) or improvement when the same or similar agent given; and, delirium occurs within week of cessation.
Post-operative delirium - Delirium occurs shortly after surgical procedure.
Infectious Lower respiratory tract infection, urinary tract infection Signs of infection present; infection is confirmed by cultures or other indicators; and, the temporal course coincides with the infection.
Fluid-electrolyte disturbance Dehydration/hypovolemia (hyponatremia) Clinical evidence of changes in hydration status present (e.g., history of GI losses, signs of hypovolemia/dehydration, signs of volume overload); abnormal laboratory studies (e.g., abnormal electrolytes, high urea/ creatinine ratio); and, temporal course coincides with the abnormality
Metabolic/endocrine Uremia, hepatic encephalopathy, hypo/hyperglycemia, hypo/hyperthyroidism, adrenal insufficiency, hypercalcemia The metabolic abnormality is known to induce a change in mental status; clinical and laboratory confirmation of the disturbance; and, the temporal course coincides with the disturbance.
Cardiopulmonary (hypoperfusion and/or hypoxia) Congestive heart failure/pulmonary edema, shock, respiratory failure Clinical evidence of a low cardiac output/hypotension or pulmonary compromise; laboratory or radiographic evidence of suspected abnormality (e.g., arterial blood gases); and, the time course coincides with cardiopulmonary disturbance.
Intracranial Stroke, traumatic brain injury, cerebral edema, subdural hematoma, meningitis, seizures Clinical evidence of an intracranial process has occurred; laboratory or radiological evidence of the suspected abnormality; and, time course coincides with the disturbance.
Sensory/Environmental Visual/hearing impairment, physical restraint use, bladder catheter use, settings (acute care, especially ICU) There is evidence of a pre-existing dementia and/or significant auditory/visual disturbance; mental status improves with orienting stimuli; and, mental status worsens with recent environmental changes or occurs predominantly at night.
  • In the geriatric population, it is important to differentiate between delirium, dementia, and depression, which can be difficult to distinguish.[13][14][15] The prevalence of delirium superimposed on dementia ranges anywhere from 22% to 89% of hospitalized and community populations aged 65 and older with dementia.
  • The negative outcomes of these co-occurring conditions include accelerated and long-term cognitive, functional decline, institutionalization, re-hospitalization, and increased mortality.[16]

A Comparison of Delirium, Dementia, and Depression

Adapted from: Fong, T., et al. Delirium in elderly adults: diagnosis, prevention and treatment. Nature Reviews Neurology 5.4 (2009): 210.
Delirium Dementia Depression
Cardinal feature Confusion and Inattention Memory loss Sadness, anhedonia
Onset Acute or subacute Insidious Slow
Course Fluctuating, often worse at night Chronic, progressive (but stable over the course of a day) Single or recurrent episodes; can be chronic
Duration Hours to months Months to years Weeks to years
Level of Conciousness (LOC) Impaired, fluctuates Normal in early stages Normal
Attention (i.e. - able to focus on tasks) Poor Normal (except in
late stages)
May be impaired
Orientation (i.e. - date, location) Fluctuates Poor Normal
Memory (i.e. - short-term memory) Poor Poor May be impaired
Hallucinations Common (visual) Rare, except in
late stages (and depends on type of dementia)
Not usually (only if psychotic depression)
Delusions Fleeting, non-systematized Often absent Not usually (only if psychotic depression)
Psychomotor Increased (hyperactive) or reduced (hypoactive) No Yes
Reversibility Yes Rarely Yes
EEG Findings Moderate to severe background slowing Normal or mild diffuse slowing Normal (usually)
Delirium should be thought of as a symptom, not a diagnosis. That is, you must recognize it and treat the underlying condition causing the delirium! Also don't forget that delirium is often multifactorial in etiology and therefore requires a multifactorial approach.
  • One of the prevailing theories of the pathogenesis of delirium is acetylcholine deficiency.[17]
  • Acetylcholine plays an extensive role in attention and consciousness, and deficiencies are thought to result in the core symptoms of both hypoactive and hyperactive delirium. These symptoms include inattention, disorganized thinking, and hallucinations.[18][19] Dopaminergic excess, inflammation (via interleukin-1, interleukin-2, interleukin-6, TNF-α, interferon), chronic stress (resulting in hypercortisolism), and diurnal changes are also thought to be factors that lead to the development of delirium.[20]
  • Routine investigations include:
    • Bloodwork
      • CBC, electrolytes, BUN/Cr, electrolytes (Na, Cl), extended electrolytes (Ca, Mg, phosphate), CK
      • LFTs, lipase, albumin, troponin
      • Random glucose, B12
      • TSH, free T3, free T4 (Hashimoto's)
      • Oxygen saturation or ABGs
    • Imaging
      • Chest X-Ray (CXR) (pneumonia)
      • Abdominal X-Ray (fecal loading or constipation, especially in patients with dementia or confusion who cannot report this accurately)
      • CT Head (acute stroke or intracranial abnormality)
      • ECG
    • Infectious etiology work up includes HIV, syphilis (EIA), lactate
    • Inflammatory work up, including CRP, lupus (ANA
    • Urinalysis (cultures), urine drug screen, urine/serum toxicology screen
  • Neuroimaging generally has low yield in detecting delirium. Only consider this if there are new focal neurologic signs, a history of head trauma (suggesting a subdural hemorrhage), infections (encephalitis), or if there is no identifiable cause or improvement.
  • EEGs may also be useful in identifying occult seizures and differentiate delirium from psychiatric disorders.
  • Certain features on EEG have close to 80% accuracy in differentiating delirious from non‐delirious patients, including:[21][22][23][24]
    • Slowing or dropout of the posterior dominant rhythm
    • Reduced alpha wave frequency[25]
    • Generalized theta or delta slow-wave activity
    • Poor organization of the background rhythm and and diffuse slowing
    • Loss of reactivity of the EEG to eye opening and closing
“An exclusively reductionist, biomedical approach to this condition will not likely work”
– National Guidelines for Seniors’ Mental Health: The Assessment and Treatment of Delirium (2006)[26]

In non-ICU setting patients, always start with non-pharmacological interventions first, both in the prevention and management of delirium.[27][28][29] Multiple risk factors should be mitigated as suggested by the table below:

Non-pharmacological Delirium Prevention

Adapted from: Inouye, Sharon K., et al. A multicomponent intervention to prevent delirium in hospitalized older patients. New England journal of medicine 340.9 (1999): 669-676.
Risk Factor Intervention
Cognitive impairment Orient the patient by having a clock, watch, or calendar. Have a board with team member names, a schedule, ongoing communication to reorient them (e.g. - remind the patient where they are, get a sitter, asking family members to stay, asking family to bring items that can keep patient occupied). Do therapeutic activities including: cognitively stimulating activities TID (e.g. - current events, word games, structured reminiscence [get them to recall events in the past]).
Sleep deprivation Warm drinks, relaxation tapes, back massages at night. Enhance sleep by implementing unit‐wide noise reduction and schedule adjustments to allow sleep. Coordinate schedules (drugs, vitals, procedures) to allow uninterrupted sleep at night (low noise and lighting). Encourage normal sleep–wake cycles (open blinds, encourage wakefulness and mobility during daytime)
Immobility Implement early mobilization including ambulation or active range of motion exercises TID. Minimize use of catheters, IVs, and restraints.
Visual impairment Make sure they have visual aids such as glasses, and other adaptive equipment. Reinforce use of aids daily.
Hearing impairment Make sure they have hearing aids, portable amplifying devices, earwax disimpaction if needed, and special communication techniques. Reinforce use of aids daily.
Volume depletion Early recognition and repletion with fluids
Enivronment Avoid putting delirious patients in the same room together, and minimize room changes
  • Medications that might be contributing delirium should be withdrawn whenever possible. Psychoactive medications, including those with anticholinergic effects, and/or drugs recently initiated or with a dosage change are more likely to be precipitants of delirium.
  • If the medication cannot be withdrawn, the lowest possible dose should be used, or substituted with a similar but lower risk medication.[30]

Selection of High Risk Medications That May Contribute to Delirium

Gage L. and Hogan D.B. (2014). 2014 CCSMH Guideline Update: The Assessment and Treatment of Delirium. Toronto: Canadian Coalition for Seniors’ Mental Health
Sedative-hypnotics Benzodiazepines
• Barbituates
• Antihistamines (e.g. - diphenhydramine)
Narcotics • Meperidine appears to be particularly likely to precipitate delirium
Drugs with anticholinergic effects • Oyybutynin
• Tolteridine
• Anti-nauseants (antihistamines, antipsychotics)
• Promotility agents
• Tricyclic antidepressants (especially tertiary amine tricyclic agents such as amitriptyline, imipramine and doxepin)
Antipsychotics (e.g. - low potency neuroleptics such as chlorpramazine)
• Cumulative effect of multiple medications with anticholinergic effects
Histamine-2 Blocking agents • Cimetidine
Antiparkinsonian medications Dopamine agonists
Anticonvulsants • Mysoline
• Phenobarbitone

ABC! Always Be Conservative

Pharmacologic management should only be used if the symptoms of delirium threaten the patient's own safety, the safety of others, or would result in the interruption of essential therapy. Always start low and go slow, even if other healthcare providers might insist on higher doses earlier. (Remember that no drug is currently approved by any regulatory agency for the treatment of hospital-associated delirium).
Don't forget to order a baseline ECG for a QTc, especially if you are starting out with haloperidol.
  • Antipsychotic medications should not be used as standard treatment for delirium, and should only be considered for patients with delirium experiencing severe agitation or distress.[31]
  • Most studies have shown that haloperidol (at doses < 3.5 mg daily), risperidone, and olanzapine are all equally effective in managing delirium.
  • There is no evidence that prophylactic or preventative pharmacologic treatment works.[32][33]
  • Antipsychotics if prescribed, should be at the lowest effective dose for the shortest possible duration and be reevaluated at or shortly after discharge.[36]
  • There is some emerging evidence that melatonin and melatonin agonists may be effective in the prevention and management of delirium.[37][38]

Pharmacological Management of Delirium

Medication Use Recommended Dosing Side Effects Clinical Pearls
Haloperidol First-line 0.5‐1 mg PO/IM bid and q4h PRN Extrapyramidal Symptoms (EPS) at higher doses (> 3mg), QTc prolongation, and neuroleptic malignant syndrome, somnolence, falls. Both typical and atypical antipsychotics increase the risk of death and cerebrovascular events, compared with placebo in elderly patients (> 65 years) with dementia.[39] In the elderly with Parkinson's disease or Lewy Body Dementia, atypical antipsychotics are preferred.
Risperidone First-line 0.5 mg BID Extrapyramidal Symptoms (EPS) (less likely than typicals like haloperidol, but still a risk, especially at higher doses), QTc prolongation, neuroleptic malignant syndrome, somnolence, falls. Both typical and atypical antipsychotics increase the risk of death and cerebrovascular events, compared with placebo in elderly patients (> 65 years) with dementia.[40] In the elderly with Parkinson's disease or Lewy Body Dementia, atypical antipsychotics are preferred.
Olanzapine First-line 2.5‐5 mg PO daily Same as risperidone Both typical and atypical antipsychotics increase the risk of death and cerebrovascular events, compared with placebo in elderly patients (> 65 years) with dementia.[41] In the elderly with Parkinson's disease or Lewy Body Dementia, atypical antipsychotics are preferred.
Quetiapine First-line 25 mg BID Same as risperidone Both typical and atypical antipsychotics increase the risk of death and cerebrovascular events, compared with placebo in elderly patients (> 65 years) with dementia.[42] In the elderly with Parkinson's disease or Lewy Body Dementia, atypical antipsychotics are preferred.
Lorazepam Second-line 0.5‐1 mg PO q4h PRN Paradoxical reactions, respiratory depression, sedation/somnolence, falls. Lorazepam may worsen or prolong delirium! Although a recent network meta-analysis suggested the use lorazepam in delirium, this result cannot be generalized to routine clinical practice because the result was derived from only one study.[43][44]
Lorazepam should only be used for patients with alcohol withdrawal, or patients with antipsychotic sensitivity (i.e. - Parkinson's or Lewy Body)

ICU vs. Non-ICU Patients

The management of delirium in ICU patients may be different compared to a general medical ward. Recent trials have shown that antipsychotics may have limited efficacy in ICU patients with hypoactive delirium.[45][46]
  • Proactive involvement with a specialist geriatrics consultation team may also play a role in reducing delirium in acute hospital settings.[47]

Delirium Myths

Adapted from: Oldham, Mark A., et al. Responding to ten common delirium misconceptions with best evidence: an educational review for clinicians. The Journal of neuropsychiatry and clinical neurosciences 30.1 (2018): 51-57.
Misconception/Myth Best Evidence
This patient is oriented to person, place, and time. They’re not delirious. Delirium evaluation minimally requires assessing attention, orientation, memory, and the thought process, ideally at least once per nursing shift, to capture daily fluctuations in mental status.[48]
Delirium always resolves. Especially in cognitively vulnerable patients, delirium may persist for days or even months after the proximal “causes” have been addressed.
We should expect frail, older patients to get confused at times, especially after receiving pain medication. Confusion in frail, older patients always requires further assessment.
The goal of a delirium work-up is to find the main cause of delirium. Delirium etiology is typically multifactorial.
New-onset psychotic symptoms in late life likely represents primary mental illness. New delusions or hallucinations, particularly nonauditory, in middle age or later deserve evaluation for delirium or another medical cause.
Delirium in patients with dementia is less important because these patients are already confused at baseline. Patients with dementia deserve even closer monitoring for delirium because of their elevated delirium risk and because delirium superimposed on dementia indicates marked vulnerability.
Delirium treatment should include psychotropic medication. The role of psychotropic medications in delirium remains unclear. They are best used judiciously, if at all, for specific behaviors or symptoms rather than delirium itself.
The patient is delirious due to a psychiatric cause. Delirium always has a physiological cause.
It’s often best to let quiet patients rest. Hypoactive delirium is common and often under-recognized.
Patients become delirious just from being in the intensive care unit. Delirium in the intensive care unit, as with delirium occurring in any setting, is caused by physiological and pharmacological insults.
  • Delirium may serve as a marker for future cognitive decline and risk for future development of dementia.[49] Incomplete recovery from delirium (even after discharge from hospital) can be common, and patients may need weeks or months to gradually recover.[50] Some patients may have vivid recollections of their hospitaliation after an episode of delirium, and in some cases may develop posttraumatic stress disorder.[51] Thus close post-discharge follow up and monitoring should be done for high-risk patients.

Delirium Guidelines

Guideline Location Year PDF Website
Canadian Coalition for Seniors' Mental Health (CCSMH) Canada 2006, 2014 2014 Update
2006 Guideline
Pocket Card
CCSMH Delirium
National Institute for Health and Care Excellence (NICE) UK 2010, 2019 - Link
American Geriatrics Society (AGS) USA 2015 - Link
Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the ICU USA 2018 - Link
Journal of the American Medical Association (JAMA) USA 2017 - Link
American Psychiatric Association (APA) USA 1999, 2004 - Guideline (1999)
Guideline Watch (2004)
Quick Reference
Clinical Practice Guidelines for the Management of Delirium in Older People Australia 2008 - Link