Delirium vs. Dementia: Different side on the same coin

Delirium vs. Dementia: Different side on the same coin: A Medical Student Pearl

Khoi Dao, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Todd Way

Copyedited by Dr. Mandy Peach


Mr. D is an 83yo M today presents to Emergency Department through ambulance after a fall. Paramedics report stated that his wife found him pale and heard his complaints of shortness of breath (SoB), chest pain, and feeling weak. She later heard him called for help on the floor and called ambulance. Furthermore, the report also mentioned that he had a fall a week ago. When having a conversation with Mr. D, he stated that everything is fine, that he had no trouble breathing, or chest pain. The only pain that he felt was from his left arm and leg from the fall. He seems to be confused. He stated that he is from Nova Scotia, currently at an airport, and waiting for his friend to pick him up to go to their cabins at New Brunswick.

His initial vitals taken by paramedics was normal except for O2 Sat in 80’s. At the Emergency Department, he received O2 4L in air cannula and his SatO2 quickly brought up to 95%. He was afebrile, blood pressure at normal range, and heart rate was irregularly irregular. There were bruises at his left facial, left upper flank at axillary region, and left arm. There were no signs of basal skull fractures, nor any lacerations on his head. Cranial nerves exam was normal. Upper extremity motor, sensory, and reflex exams were within normal limits. Lower extremity motor found his dorsal flexion and extension on the left side was weaker compared to right side. Patella reflex exam was within normal limits. Respiratory exam was within normal limit. Cardiac exam reveals irregularly irregular pulse, but normal heart sound, no murmur, no extra heartbeat. Abdomen exam was within normal limits.

Past Medical History: hypertension, dyslipidemia, nephrolithiasis, chronic subdural hematoma, infection secondary to left ankle replacement, and Guillain-Barre syndrome (acute inflammatory demyelinating polyneuropathy)

Past Surgical History: bilateral ankle replacements

Initial Investigations:

With his initial presentation, blood work and imaging were ordered. Mr. D’s CBC showed elevated WBC, CRP, with stable Hgb. His ECG showed a new A-Fib.  Chest X-ray found he has consolidation of his left lower lobe, suggestive of pneumonia. Initial CT scan confirmed of left lower lobe consolidation, with multiple new and old rib fractures.

First, establish between Mild Cognitive Impairment (MCI) and Delirium

Dementia, Mild Cognitive Impairment, and delirium are grouped under the umbrella term of neurocognitive disorders, according to DSM-V. However, each of them has their own definitions, underlying pathology, and maybe etiology.

Dementia, or newly named major neurocognitive disorder in DSM-V, is characterized as cognitive decline involving one or more of neurocognitive domains (learning, memory, attention, executive function, perceptual-motor, and social cognition) that is severe enough to interfere with daily function and independence. These daily functioning includes instrumental ADL (iADL) and ADL (Table 1).

To meet the criteria of diagnosing dementia, one must have an evident decline of one or more cognitive domains, either through a collateral history of someone who is close to the patient, or through standardized neuropsychological testing (MMSE, MOCA, …). The decline of cognitive domains should not occur in the context of delirium and are not better explained by another mental disorder.

 Mild cognitive impairment can be considered somewhere between normal cognition and dementia. While it is considered to have deficit of one or more cognitive domains, it does not interfere with daily function activities. Like dementia, the diagnostic criteria require exclusively not in the context of delirium, and that it is not better explained by another mental disorder.

Delirium, on the other hand, is defined of any disturbance of attention and awareness along with cognition (e.g. memory deficit, disorientation, language, visuospatial ability, or perception) over a short period of time (hours to days). It can persist from days to month. Delirium is typically caused by medical conditions, substance intoxications, or medication side effect. Thus, for the diagnostic criteria for delirium to be met, there needs to have evidence from history presentation, physical examination, or laboratory findings of physiological changes that consequently may explain the cognitive disturbances.

Cognition decline as a clinical sign can be challenging for a physician since it is overlapped by neurocognitive disorders. However, there are characteristics that are different between them, which can be shown in Table 2.

Mainly, dementia has a gradual onset, whereas delirium has a more abrupt and acute onset. Attention and orientation are usually impaired in delirium, but generally preserved in dementia in earlier stage.

Collateral History:

Initial history taking could be proven to be challenging when patient presents with difficulties with memory or attention. Thus, obtaining a collateral history is pertinent as it is an indicator and a key component to differentiate between dementia and delirium4. Although collateral history is a core clinical skill, it is sometimes overlooked 5. In taking a collateral history, one would need to establish patient’s cognition at their baseline. For instance, questions relate about  a person’s daily activities and whether if they have any difficulties should be explored. Clarification of the onset and progressions of the cognitive changes need to be documented. Furthermore,  other cognitive domains should be also screened, as questions can be seen in Table 2 below 6.

After taking initial history, you thought that Mr. D is confused and could not give a good history of presenting illness, so you decide to call his substitute decision maker (SDM), who happens to be his wife. His wife recalled that he looked pale at lunch, complained of SoB, and when he walked she thought he looked weaker than usual. Then, she heard a called for help and found him on the floor, conscious. He couldn’t get up by himself and so she decided to call an ambulance. His wife mentioned that Mr. D has had some memory loss over half a year, where there were multiple episodes of Mr. D forgetting things. However, a week ago he had a fall walking outside, and she reported that his memory has been progressively worse since the fall. There were several nights when he woke up and asked her what the dates or where he is at. He also appeared to be weak, and, the day before his emergency admission, he complained of chest pain. When asked whether he has any difficulty of performing activity of daily living (ADL), his wife mentioned he had hard time getting dressed. His wife reported he had not seen a specialist for memory decline. She was concerned, however, that his memory was acutely declining over a week compared to the last few months. When asked about EtOH use, he had history of excessively drinking in the past, but currently only one serving per day.

As Mr. D was suspected of delirious that is overlapping of MCI, more investigations were added to investigate the cause of his delirium.

Risk and Precipitating factors of delirium:

Most identified risk factors are involving with underlying brain pathologies (e.g dementia, stroke, or Parkinson)7. With respect to precipitating factors, common examples include, but not limited to, polypharmacy, infection, dehydration, immobility, malnutrition, and the use of bladder catheters (predisposes patient to urinary tract infections)

Differential Diagnoses:

Besides major neurocognitive disorders (e.g. dementia) and mild cognitive impairment that were discussed above, other differential diagnoses should also be considered such as2:

Sundowning – behaviour deterioration seen in evening hours that might be due to impaired circadian regulation or nocturnal factors in the environment

Focal syndromes – includes temporal-parietal, occipital, and frontal dysfunctions

Nonconvulsive status epilepticus – patients often showed non-classical ictal features, but with the following features such as: prominent bilateral facial twitching, unexplained nystagmoid eye movements during obtunded periods, spontaneous hippus, prolonged “postictal state”, automatism, and acute aphasia without structural lesion

Psychiatric illnesses – includes bipolar and depressive disorders with psychotic features

Acute stress disorder – associated with fear, anxiety, and dissociative symptoms, such as depersonalization

Approach to the source of delirium:

As Mr. D was suspected to be delirious, the potential causes can be reflected through laboratory results as well as imaging studies. Sources of cognitive decline can be from systemic illness, isolated organ system dysfunction, drug adverse reactions, intoxications or withdrawal, psychiatric illness, trauma, or neurologic disease2,3. A concise and comprehensive acronym that could be used to establish the source of change in delirium can be used like DIMES8:

Drugs – anticholinergic, anti-emetics, anti-parkinsonian, beta-blockers

Infections – pneumonia, urinary, skin/soft tissue, CNS-related

Metabolics – altered pH, hypo/hyper Na+ or Ca+, acute organ failure, hypoglycemia

Enviromentals – heavy metals,

Structurals – brain injury, CNS pathology, malignancy

Treatment for delirium usually is to manage the underlying cause of the delirium.

Case continues:

                Although Mr. D’s initial imaging investigations found lower lobe consolidation that suggestive of pneumonia, he has a past medical history of chronic subdural hematoma in 2010. A CT head scan was ordered to rule out if there any new bleeding. When the CT head was negative it was most likely his newfound delirium and A-fib were secondary to pneumonia . Blood culture was done, and 2g IV Ceftriaxone was given empirically for his pneumonia. He was transferred to Hospitalist Unit for monitoring for improvement and referred to Geriatric Unit at St. Joseph’s Hospital for further investigation to his MCI.

Key points:

  1. Delirium is characterized as disturbance in attention and in cognition domain over a short period of time that could not be explained by other neurocognitive disorder.
  2. Delirium shared many cognitive declines feature with dementia and MCI. However, features such as acute onset, inattention, and evidence of physiological changes can be used to differentiate
  3. Collateral history is an important clinical tool to identify between delirium and other neurocognitive disorders.
  4. Mnemonics in approaching for delirium can be remembered as DIMES


  1. American Psychiatric Association. (2013). Neurocognitive Disorders. In American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders.
  2. Francis J., Young, G.B. (2021). Diagnosis of delirium and confusional states. Retrieved from
  3. Larson, E.B. (2021). Evaluation of cognitive impairment and dementia. UpToDate. Retrieved from
  4. Dyer, A. H., Foley, T., O’Shea, B., & Kennelly, S. P. (2018). Cognitive assessment of older adults in general practice: the collateral history. Irish Journal of Medical Science (1971-), 187(3), 683-687
  5. Fitzpatrick, D., Doyle, K., Finn, G., & Gallagher, P. (2020). The collateral history: an overlooked core clinical skill. European Geriatric Medicine, 11(6), 1003-1007.
  6. Mahdy, R., Amer, M. S., Adly, N. N., & Rasheedy, D. (2021). The Value of Collateral History in Screening for Mild Cognitive Impairment in Elderly with Diabetes Mellitus in Outpatient Clinics. The Egyptian Journal of Geriatrics and Gerontology, 8(1), 21-28.
  7. Fick, D. M., Agostini, J. V., & Inouye, S. K. (2002). Delirium superimposed on dementia: a systematic review. Journal of the American Geriatrics Society, 50(10), 1723-1732.
  8. Melady, D. (2013). Cause of delirium. In Geri-EM. Retrieved from
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ED Rounds – Delirium in the ED

Delirium in the ED: How can we help?

Presented by: Dr Cherie-Lee Adams


Incidence of Delirium

  • 40% admitted patients >65yo
  • 10-20% on admission
  • 5-10% more during admission

Increased Risk of Delirium:

  • Male
  • >60yo, more prevalent >80yo
  • Hearing/visual impairment
  • Dementia
  • Depression
  • Functional dependence
  • Polypharmacy
  • Major medical/surgical illness

DSM-V Criteria

  • A) Disturbance in attention and awareness
  • B) Disturbance is ACUTE
  • C) Concurrent cognitive impairment
  • D) Not evolving dementia, nor coma
  • E) Can be explained by Hx/Px/Ix



Non – Pharmacological Approach

  • Nutritional support
  • Optimize hearing/sight
  • Maximize day/night/date/time cues
  • Minimize pain
  • Rehabilitate- ambulate, encourage self-care
  • Avoid restraints

Pharmacological Options

  • Treat only if distress/agitated/safety concern
      • don’t treat hypoactive delirium, wandering, or prophylactically
  • monotherapy
  • low dose
  • short course
  • Benzos- reserve for withdrawal
  • APs
        • Haldol 0.25-0.5mg
        • risperidone 0.25mg od-bid
        • olanzapine 1.25-2.5mg/d
        • quetiapine 12.5-50mg/d


Take Home Points

  • Delirium is common, esp in elderly
  • Significant morbidity/mortality associated
  • Brief screening with DTS/bCAM works
  • Intervention focus on limiting pathology, normalizing activities, minimizing drugs
  • Low dose APs for short period for agitation



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ED Rounds – April 2015

We were treated to 4 great presentations today, including some original research from Dr Robin Clouston. This months presenters included Dr Paul Vanhoutte, Dr Joanna Middleton, Dr Robin Clouston PGY2 and Dr Reid Sadoway PGY1.

Delirium in the Emergency Department

Dr Paul Vanhoutte

Acute Confusional State

  • Delirium
  • Dementia
  • Amnesia
Common Neuro pathway – structure, neurotransmission


Its believed that acetylcholine levels are involved (low levels were noted in some studies)
Anticholinergic drugs therefore may make it worse
Environmental stressors are important
4 Key Features
  • Disturbance of consciousness
  • Change in cognition –  (dementia has a more insidious onset)
  • Short period of time
  • Clinical evidence
also psycho motor, sleep disturbance, emotional


Insidious, Progressive, non fluctuating, months to years, normal attention
BUT – both can be confused with Psychiatric disorder
Long list of etiologies – see attached pdf of presentation


Extended lytes – e.g Ca
Cultures – if febrile

Risk Factors

Previous brain injury
Senosry impairment

Some Stats

64% of pts sent to ED from NH had some delirium
10-15% of all hospital admissions
5-10% of ED visits for altered mental status
70% mortality rate in elderly
70% miss rate

Confusion Assessment Method  (CAMS)

  1. Acute onset and fluctuating course
  2. Inattention/distractibility
  3. Disorganised thinking
  4. Alteration

Delirium if 1 and 2 with either 3 or 4


O2 in all (careful if COPD)
Check blood sugar

A discussion on the use restraint followed
Maybe necessary in some circumstances
But should be closely observed
Enables diagnosis of cause and initial treatment

ACEP Guidelines on pharmacoligic treatment

  • Undifferentiated agitation: monotherapy with lorazepam/midazolam, droperidol or haliperidol
  • Agitation and psychosis: atypical or typical antipsychotic
  • Agitated and violent: combo therapy
  • Coma cocktail: Thiamine, dextrose, naloxone
  • Glucagon IM if no IV access for hypoglycemia
  • Treat underlying cause

Take Home Message

  • Need to differentiate ACS into Delirium vs Dementia vs Psychiatry
  • Big list of triggering differential diagnosis
  • High mortality
  • Majority will require early stabilisation and admission
  • Some maybe appropriately discharged e.g those from NH or with good family

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Diagnostic Utility of CRP in the ED

Dr Joanna Middleton

Should we be using it?
How should we use it?

Discussion Point 1

Nurses have noticed that its use has increased in last 2 years

?Change in practice, ?Switch from ESR to CRP

Is CRP the new D-DIMER?


An interesting historical outline – see attached pdf of presentation

Discovered in 1930

Used in the 50’s and 60’s extensively
Then lost favour
Resurgence in the 1990’s

Will it loose favour again?


Injury/illness stimulus (Tissue Injury)
IL-6 produced and stimulates liver production of CRP
Takes 4-6 hrs to appear in blood

Exponential rise

Peaks at 48-73hrs
Short hallf life
Levels drop quickly
Therefore good for following disease

What is Normal

Median – 0.8
90th – 3
99th – 10

Horizon: < 4.9


Most published literature has a CRP cut off of 10


Numerous causes of CRP elevation

Cannot differentiate viral from bacterial

Obseity elevate CRP
Class 1 obesity – 11% > 10


Take Home Points

Point #1 for EM CRP levels are not reliable in the first 12 hours after a stimulus…

Point #2: Serial measurements are much more useful than an isolated result

Point # 3 Healthy patients should have a CRP <2-3

Point #4: Much of the published literature used a CRP cut-off of 10…

POINT #5: LOTS OF THINGS ELEVATE CRP – Anything that causes tissue/cell damage

Point #6: CRP cannot differentiate between viral and bacterial unless…

Point # 7: CRP >100 is probably a bacterial infection


Point #9: STEROIDS SCREW UP CRP LEVELS – So do some Auto-immune disease

Point #10 – Joanna’s Rule: If your patient in the ED has a CRP <0.3*…. Then there is probably nothing wrong with them – provided they have had symptoms for > 24hrs (excluding point 9)


See the pdf attached to this post for an analysis of CRP performance in specific conditions


Bottom Line

Maybe helpful in differentiating neonates with serious infection, but requires serial testing.

Maybe helpful in combination with WBC and PMN ratio for ruling out adult appendicitis if they present with pain > 24hrs


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Safety in the Emergency Department

Local research: Comparison of ED Crowding Scores

Dr Robin Clouston iFMEM PGY2

Dr Robin Clouston presented her research on ED Safety and Crowding.

The primary goal is to determine which of the six ED Crowding tools and five single variables studied is the best tool to measure the intensity of ED crowding, as compared to the outcome variable of physician rating, measured by Visual Analogue Scale (VAS). i.e. Which ED crowding tool produces a score most closely correlated with the physician VAS?

A secondary goal will be to determine which tool is the best correlated with early emergency department crowding, defined in this study as detection of crowding up to four hours before recognized by clinicians via the Visual Analogue Scale.

Key Results

Of the six formal crowding tools, the DEC ED Saturation Score had the best predictive value with sensitivity of 76.2% and specificity of 64.3%.

For predictions of current safety: the NEDOCS score had the best combined sensitivity and specificity at 80% each,

Single variable with the highest predictive value of safety at time 0 was the “# patients in beds/waiting

For prediction of safety in 2 hours: again the NEDOCS score most predictive, with sensitivity = 92.7% and specificity=89.5%.

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Burns – ED Assessment and Management – Literature Review

Dr Reid Sadoway PGY1

Download (PDF, 1.65MB)



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