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An EM Approach to Syncope in Adults

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Medical Student Pearl

Samarth Fageria

Med 3

Memorial University of Newfoundland Class of 2024

Reviewed by Dr. J Gross

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ An EM Approach to Syncope by SFargeria

 

Case

A 60-year-old male presented to the ED after experiencing recurrent episodes of syncope. The first episode occurred at a convenience store in an upright position. He denied prodrome and exertional activity at the time of syncope. After a transient loss of consciousness, he woke up confused with urinary incontinence. He felt nauseous and had emesis in the ambulance on the way to ED. He had two more episodes of syncope over the span of two hours. On assessment in the ED, he endorsed a past history of light-headedness preceded by laughing and holding his breath. He denied dyspnea and chest pain. He had no significant past medical history. There was no family history of cardiovascular disease and syncope, and social history was unremarkable.

 

On examination, he was alert and oriented. He had a minor laceration on his forehead from the fall. His respiratory and cardiovascular exams were unremarkable, neurological exam was normal. In the ED, his blood work was unremarkable. He was placed on telemetry when he had two more episodes of syncope. The monitor showed 20-second-long sinus pauses corresponding with the syncopal episodes. Cardiology was consulted and he was temporarily placed on intermittent transcutaneous pacing.

 

 

Differential Diagnosis of Syncope2

True Syncope

1. Reflex (autonomic hypersensitivity)

  • Vasovagal, carotid sinus hypersensitivity, situational

2. Orthostatic hypotension

  • Volume depletion, autonomic failure

3. Cardiac

  • Valvular (aortic stenosis, mitral stenosis), dysrhythmias (bradyarrhythmia, ventricular tachyarrhythmia, supraventricular tachyarrhythmia), mechanical (pacemaker dysfunction), cardiomyopathy, infiltrative (eg. hemochromatosis, sarcoidosis, amyloidosis), acute MI, ARVC, cardiac tamponade, acute aortic dissection

Other Causes

1. Medication/ Drug-induced

  • Anti-hypertensives, QT prolonging meds, insulin, alcohol, anti-depressants, anti-glycemic agents, diuretics, anti-anginal agents, etc

2. Transient Loss of Consciousness (TLOC)

    • Traumatic brain injury, seizure disorders, intoxications, hindbrain TIA, conversion disorders and metabolic abnormalities

 

Background

Syncope is defined as a brief, sudden, transient loss of consciousness due to cerebral hypoperfusion1. The three broad categories of syncope are reflex, orthostatic and cardiac syncope. The most common cause of cardiac syncope includes dysrhythmias1. A good past medical history of cardiovascular disease is important as it is 85-94% sensitive and 64-83% specific in predicting a cardiac etiology of syncope1.

Diagnostic Workup

Diagnostic workup for syncope requires a thorough history, physical exam, and a 12-lead ECG. Cardiac monitoring is necessary in patients that present to ER with an acute presentation of syncope, and a strong suspicion for cardiac etiology2. History should consist of identifying high-risk features that warrant a prompt cardiology consult2. A detailed HPI should consist of asking about an absence of a prodrome, exertional or supine syncope, concomitant trauma, past medical history of cardiovascular disease and family history of sudden cardiac death (<50 years)2. Low-risk features include presence of a prodrome, specific triggers (eg. dehydration, stress, laughter), syncope while upright and the absence of cardiovascular disease2. Vital signs and a cardiac exam should be completed2. If cardiac causes of syncope cannot be ruled out on first assessment, a 12-lead ECG should be placed to assess for dysrhythmias or conduction disease, and serial troponin values should be collected2.

 

Though there are multiple clinical decision rules for syncope, the following have been externally validated: Evaluation of Guidelines in Syncope Study (EGSYS), San Francisco Syncope Rule and Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL)1. Patients that are stratified as high risk require admission for further evaluation. EGSYS predicts the probability of cardiac syncope at two years based on abnormal ECG findings (eg. BBB, sinus bradycardia), heart disease (eg. ischemic, structural), palpitations before syncope, as well exertional and positional syncope, symptoms of prodrome (nausea/vomiting) and predisposing/precipitating factors1. An admission is warranted if the patient scores a three or higher as there is a 21% mortality risk at two years1. The OESIL risk score estimates a 1-year all-cause mortality in patients presenting with syncope1. The factors include age (>65), history of cardiovascular disease, lack of prodrome and abnormal ECG characteristics (eg. BBB, AV conduction disorders and hypertrophy)1. Admission is warranted for one or more variables1. The Canadian Syncope Risk Score can be used in patients presenting to ER with syncope to predict a 30-day serious adverse events2.  It consists of factors such as abnormal QRS axis, corrected QT interval >480 ms, elevated troponin (>99th percentile of normal population) and ED diagnosis based on evaluation to stratify patients into risk categories: very low (-3 to -2), low (-1 to 0), medium (1 to 3), high (4 to 5) and very high (6 to 11)2.

The Canadian Journal of Cardiology recommends a disposition algorithm for patients presenting to ER with syncope that is based on history of a serious medical condition and high-risk features3. Figure 1 illustrates an approach to disposition from the ER. Patients that have an unclear etiology and intermediate risk should be considered for an urgent cardiology assessment.

 

Figure 1: A disposition plan for patients presenting to the ER with syncope (Canadian Cardiovascular Society 2020).

Best Practice for Treatment

Given the benign course, treatment for vasovagal syncope is based on lifestyle modification, education and reassurance2. Lifestyle modification consists of educating patients on identifying and managing prodromes early and managing triggers (eg. dehydration, defecation, micturition, laughing, coughing and crowded environments)2.

Treatment for orthostatic syncope also relies on lifestyle modification, education and reassurance2. Lifestyle modification consists of re-adjusting diuretics, ACE-inhibitors, angiotensin receptor blockers, calcium channel and beta blockers to ensure optimal blood pressure and hydration control2.

Managing cardiac syncope requires addressing the underlying etiology through antiarrhythmic medications (eg. tachyarrhythmias), cardiac pacing (eg. bradyarrhythmias), catheter-directed ablation and ICD insertion1. Cardiac pacemaker therapy is indicated for patients that have intermittent sinus node disease if correlation is identified between sinus pauses on ECG and syncope3. Selected patients that are diagnosed with the bradycardia-tachycardia form of sick sinus syndrome, can benefit from a percutaneous cardiac ablative technique3.  Dual-chamber pacing is recommended for patients with sinus node dysfunction provided there is an increased risk of AV block4.

Case continued

The patient was admitted and had no further asystole after receiving atropine and intermittent transcutaneous pacing. He was accepted for a dual-chamber pacemaker insertion and was discharged with the diagnosis of syncope with sinus arrest and vagal overtones.

Take Home Points

  1. Patients presenting to the ER with new-onset syncope require a thorough history and physical exam to rule out cardiogenic causes.
  2. Validated clinical decision-making tools can be helpful to supplement clinical judgement for assessing the risk of a future cardiac event, identifying the need for a cardiology consult and creating a disposition plan.

References

  1. Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017;95(5):303-312. https://www.aafp.org/pubs/afp/issues/2017/0301/p303.html#:~:text=A%20standardized%20approach%20to%20syncope,%2C%20physical%20examination%2C%20and%20electrocardiography
  2. UpToDate. www.uptodate.com. https://www.uptodate.com/contents/syncope-in-adults-clinical-manifestations-and-initial-diagnostic-evaluation
  3. Sandhu RK, Raj SR, et al. Canadian Cardiovascular Society Clinical Practice Update on the Assessment and Management of Syncope. Can J Cardiol. 2020;36(8):1167-1177. doi:10.1016/j.cjca.2019.12.023 https://www.onlinecjc.ca/article/S0828-282X(19)31549-1/fulltext
  4. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39(21):1883-1948. doi:10.1093/eurheartj/ehy037https://academic.oup.com/eurheartj/article/39/21/1883/4939241?login=false
  5. Dakkak W, Doukky R. Sick Sinus Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 18, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470599/

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Headaches and Herpes Zoster

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Headache and Herpes Zoster

Medical Student Pearl

 

James Tang

Dalhousie University Class of 2023

Reviewed by: Dr. Erin Slaunwhite

Copyedited by: Dr. Janeske Vonkeman

Case

Mr. H is a 57 yo gentleman who presents to the ED complaining of a 3-day history of headache. He describes a progressive worsening of a constant dull ache unilaterally above his left eye. It’s currently a 4-5/10 in severity and does not radiate. He has not had any nausea or vomiting, and no phonophobia but asks you to dim the lights in the room if that’s possible. He has no previous history of the same. He has not noticed any shooting pains associated with eating or drinking cold foods/liquids. He denies any associated autonomic symptoms on that side. Mr. H tells you he’s tried Tylenol and Advil at home and although it seemed to help a bit initially, the pain has continued to worsen over the last couple of days. He hasn’t noted any changes in the severity of his headache with physical activity.

Mr. H has no relevant past medical history and does not take any regular medications. He enjoys drinking 1-2 beers on the weekends, does not use cannabis, and has never used any other recreational drugs.

On physical exam, Mr. H appears his stated age and appears quite tanned from his job in construction. His vital signs are within normal limits. On close inspection, you make note of an area of erythematous macules and papules forming on his left forehead and extending 1-2 cm above and below his scalp line. The area is mildly tender to touch. His cranial nerve exam was otherwise normal. His remaining neuro exam, as well as head and neck, cardiac, respiratory, and abdominal exams were all normal.

A general approach to primary headache – Tension TIC TAC TOE

The International Headache Society (IHS) outlines specific diagnostic criteria for headache disorders within their International Classification of Headache Disorders (ICHD 3rd edition).1 Below is an abbreviated summary of the select common diagnoses that the ICHD discusses in much greater detail2-5:

Danger signs – features suggestive of secondary headache (e.g. space-occupying lesion, sub-arachnoid hemorrhage, cervical artery dissection, giant cell arteritis, infection, trauma, etc)2,4,5:

  • Systemic symptoms including fever, weight loss, progressive N/V
  • Neoplasm history
  • Neurologic deficit (including confusion, weakness, vision loss, numbness, impaired alertness, side locked headache)
  • Onset is sudden or abrupt (thunderclap)
  • Older age (> 50 yo)
  • Pattern change from previous headaches
  • Positional headache
  • Precipitated by Valsalva or exertion
  • Papilledema
  • Progressive headache and atypical presentations
  • Pregnancy or puerperium
  • Post-traumatic onset of headache
  • Pathology of the immune system such as HIV

Patients with danger signs suggestive of secondary headache should be considered for imaging. If a primary headache is suspected but imaging is performed for no other reason than reassurance, it can be detrimental to the patient if the results return incidental findings (e.g. vascular lesion) likely unrelated to the headache.

But our patient’s presentation doesn’t really seem to fit into any of these categories…

Herpes Zoster

In immunocompetent individuals, the diagnosis of herpes zoster is based solely on the clinical presentation: unilateral, usually painful vesicular eruption with a well-defined dermatomal distribution (see Figure 1). Prodromal symptoms include malaise, headache, photophobia, abnormal skin sensations, and occasionally fever. These symptoms may occur one to five days before the appearance of the rash. Age is the most important risk factor for the development of herpes zoster. A dramatic increase in the age-specific incidence of herpes zoster begins at approximately 50 years of age with 40% occur in people at least 60 years of age.6 It is estimated that approximately 50% of persons who live to 85 years of age will have had an episode of herpes zoster.6

Figure 1. Vesicular eruption in keeping with herpes zoster ophthalmicus with a crusted skin rash following the V1 dermatomal distribution and does not cross midline.7

Antiviral therapy is the first-line treatment and should be initiated within 72 hours of rash onset to increase the rate of healing, decrease the duration of acute herpes zoster, and decrease severity and pain. Ideally, initiation of antiviral therapy should be started during the pre-eruptive phase of herpes zoster, but often the diagnosis can only be confidently made once the distinctive rash presents.

See Table below for antiviral doses9:

Pain management

For acute herpes zoster, mild to moderate pain may be controlled with acetaminophen and/or nonsteroidal anti-inflammatory drugs. For those with moderate pain not responding to acetaminophen and nonsteroidal anti-inflammatory drugs, a short course of a short acting opioid such as hydromorphone or morphine could be considered or a course of corticosteroids. If the pain does not rapidly respond to opioid analgesics or if opioids are not tolerated, the addition of an adjunctive therapy should be considered including nortriptyline, gabapentin, or pregabalin. Despite these adjunctive therapies not having been extensively studied in patients with acute herpes zoster pain, they have evidence for other forms of nerve-type pain.8 The addition of corticosteroids to acyclovir decreases the pain of acute herpes zoster and speeds lesion healing and return to daily activities. Combination therapy with corticosteroids and antivirals should be considered in older patients with no contraindications.8

Theoretical models suggest that reducing pain during the acute phase of herpes zoster may stop the initiation of the mechanisms that cause chronic pain, thus reducing the risk of postherpetic neuralgia.8

 

Postherpetic neuralgia

Postherpetic neuralgia is the most common complication of herpes zoster.9 It occurs in ~30% of patients older than 80 years and ~20% of patients 60 to 65 years; it is rare in patients younger than 50 years.6 Postherpetic neuralgia may persist from 30 days to more than 6 months after the lesions have healed, and most cases resolve spontaneously.9 Although antiviral medications slow the production of the virus and decrease the viral load in the dorsal root ganglia, evidence showing that these medications alter the incidence and course of postherpetic neuralgia is inconsistent.8 The major risk factors for postherpetic neuralgia are older age, greater acute pain, and greater rash severity.8

Case conclusion

Mr. H’s headache did not fit into any specific category of headache as is often the case. Although he did meet the criteria for certain danger signs (e.g. age >50), imaging was forgone due to the finding of an erythematous maculopapular rash over his forehead. Mr. H’s rash followed the dermatomal distribution of the ophthalmic branch of the trigeminal nerve and was highly suspicious of an early herpes zoster outbreak.

The patient was given a prescription for valacyclovir to take for 7 days with instructions to seek care if lesions break out close to his eye or his pain becomes unmanageable with over-the-counter analgesia. Herpes zoster opthalmicus can be a sight-threatening condition that requires close ophthalmology follow up if there is any concern of lesions near or in the eye or the patient has clinical signs or symptoms. Mr H inquired about getting the shingles vaccine and was advised to follow up with his family doctor to arrange this following resolution of his rash.

Key Takeaways

  • Have a structured approach to understanding the different classes of primary headaches
  • Know the danger signs that could be suggestive of a secondary headache
  • Clinical judgement should be prioritized in determining who to image
  • Herpes zoster is a clinical diagnosis in immunocompetent individuals
  • Appropriate pain management of acute herpes zoster and vaccination can help prevent chronic pain syndromes

 

References

  1. The International Classification of Headache Disorders – ICHD-3. Accessed June 24, 2022. https://ichd-3.org/
  2. Evaluation of Acute Headaches in Adults. Accessed June 24, 2022. https://www.aafp.org/pubs/afp/issues/2001/0215/p685.html
  3. Primary care management of headache in adults Clinical Practice Guideline | September 2016 2 nd Edition. Published online 2016.
  4. Ponka D, Kirlew M. Top 10 differential diagnoses in family medicine: Headache. Can Fam Physician. 2007;53(10):1733. Accessed June 24, 2022. /pmc/articles/PMC2231438/
  5. Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697
  6. Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate. Accessed June 24, 2022. https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster
  7. Darren Shu JT, Ghosh N, Ghosh S. Herpes zoster ophthalmicus. BMJ : British Medical Journal (Online). 2019;364. doi: https://doi.org/10.1136/bmj.k5234.
  8. Herpes Zoster and Postherpetic Neuralgia: Prevention and Management. Accessed June 24, 2022. https://www.aafp.org/pubs/afp/issues/2011/0615/p1432.html
  9. Clinical Overview of Herpes Zoster (Shingles) | CDC. Accessed June 24, 2022. https://www.cdc.gov/shingles/hcp/clinical-overview.html
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Delirium vs. Dementia: Different side on the same coin

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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

Case:

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

References:

  1. American Psychiatric Association. (2013). Neurocognitive Disorders. In American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders. https://doi-org.ezproxy.library.dal.ca/10.1176/appi.books.9780890425596.dsm17
  2. Francis J., Young, G.B. (2021). Diagnosis of delirium and confusional states. Retrieved from https://www.uptodate.com/contents/diagnosis-of-delirium-and-confusional-states?search=delirium&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  3. Larson, E.B. (2021). Evaluation of cognitive impairment and dementia. UpToDate. Retrieved from https://www.uptodate.com/contents/evaluation-of-cognitive-impairment-and-dementia?search=delirium%20and%20dementia&source=search_result&selectedTitle=4~150&usage_type=default&display_rank=4
  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 https://geri-em.com/cognitive-impairment/causes-of-delirium/
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