Geriatric medicine Flashcards
Delirium Dr Deac Pimp
D: Delirium is a neurocognitive disorder characterized by impaired attention, awareness (reduced orientation to the environment), and other disturbed cognitive functions (e.g., memory, language, or perception). Symptoms develop acutely and tend to fluctuate throughout the day. Delirium occurs as a direct physiological consequence of another medical condition. It is most often a complication of polypharmacy, especially in elderly patients, and is also commonly seen in patients admitted to the ICU. Although delirium is a reversible confusional state, it warrants urgent medical attention because it may be the first sign of serious underlying disease. Treatment of delirium focuses on treating the underlying illness and reducing exposure to exacerbating factors. Antipsychotic medications are used for the treatment of agitation in delirious patients.
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D: Dementia. It is important to differentiate the two.
-Delirium:
onset–> sudden, prodromal phase might precede.
course–> rapid and fluctuating. Hours to days.
level of consciousness–> decreased.
attention–> impaired (fluctuating).
memory–> recent memory loss.
thought process–> disorganized.
Hallucinations –>present (often visual or tactike)
psychomotor activity –> increased or decreased.
EEG–> usually abnormal.
Reversibility –> reversible.
Dementia:
Onset–> insidious
course–> slowly progressive deterioration, months to years.
level of consciousness–> intact.
attention–> usually alert, impaired in the advanced phase.
memory–>recent, then remote memory loss
thought process–>impoverished.
hallucinations –>present in 30% of patients in the advanced phase.
psychomotor activity–>usually normal,
eeg–>usually normal.
Reversibility –>usually irreversible.
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A: The exact mechanism responsible for delirium is unknown.
Pediatric, elderly (> 65 years), and hospitalized patients are particularly susceptible.
Typically secondary to:
Metabolic diseases (most common cause; also referred to as metabolic encephalopathy)
Liver or kidney failure
Diabetes mellitus (diabetic ketoacidosis)
Hyperthyroidism or hypothyroidism
Vitamin deficiencies (e.g., vitamin B12, folic acid, or thiamine deficiency)
Electrolyte abnormalities
Infection (e.g., UTIs are a common cause in elderly patients; pneumonia, meningitis)
Trauma (e.g., hip fracture, head injury)
CNS pathology (e.g., stroke, brain tumor)
Hypoxia (e.g., anemia, cardiac failure, COPD, pulmonary embolism)
Acute cardiovascular disease (MI, shock, vasculitis)
Drugs and toxins (also referred to as toxic encephalopathy)
Anticholinergics
Benzodiazepines and barbiturates
Antidepressants and antipsychotics (especially those with anticholinergic activity, e.g., quetiapine)
Antihistamines (particularly in elderly patients)
Opioids
Diuretics (may cause electrolyte abnormalities)
Recreational drugs (intoxication/withdrawal)
Alcohol use disorder and alcohol withdrawal
Heavy metals (e.g., arsenic, lead, mercury)
Sleep deprivation
Major surgery
Hearing or vision loss
Ongoing symptoms, including:
Constipation
Urinary retention
Pain
Dehydration.
For the major causes of delirium, think I WATCH DEATH: Infection, Withdrawal, Acute metabolic disorder, Trauma, CNS pathology, Hypoxia, Deficiencies, Endocrine, Acute vascular, Toxins/drugs, Heavy metals.
C: The main symptom is an acute (hours to days) alteration in the level of awareness and attention.
Other features may include:
Disorganized thinking
Illusions
Hallucinations (mostly visual)
Cognitive deficits (e.g., memory)
Reversal of the sleep-wake cycle
Emotional lability
Agitation, combativeness
The severity of symptoms fluctuates throughout the day and worsens in the evening (termed sundowning).
Symptoms are reversible; their duration and severity depend on the underlying illness.
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I: If the cause of delirium is not obvious based on the patient history and physical findings:
Start with complete blood count, serum glucose, electrolytes, and urinalysis.
If medication or substance use is suspected: urine toxicology or serum drug levels
If a metabolic etiology is suspected: serum creatinine, BUN, liver function tests, arterial blood gas
If pneumonia is suspected: chest x-ray
If a cardiac etiology (e.g., myocardial infarction, arrhythmia) is suspected: ECG
If the patient has focal neurological deficits or the initial workup is negative, further tests may include:
Neuroimaging (CT, MRI)
Lumbar puncture: to rule out meningitis/encephalitis
EEG: usually shows diffuse slowing of background activity in patients with delirium; also useful in patients with a history of head trauma, stroke, or brain lesions
Further diagnostics that may be considered:
Blood culture
HIV, syphilis serology
Thyroid function tests
Vitamin B12, folate, and thiamine levels
Depression screen.
M: Identify and treat the underlying cause (e.g., discontinue causative medications such as anticholinergics)
Supportive medical care
Manage agitation initially with nonpharmacologic strategies (see “Prevention” below).
Administer antipsychotics if the patient is agitated and/or poses harm to themselves or others.
Haloperidol is used most commonly; however, it should not be used in patients with delirium that is due to alcohol or benzodiazepine withdrawal because it lowers the seizure threshold.
Alternative: atypical antipsychotics (e.g., olanzapine)
Initiate cognitive stimulation therapy to improve cognitive function.
Reduce pain, preferably with nonopioid medications.
Prevent aspiration, incontinence, and skin breakdown.
Benzodiazepines are deliriogenic. Do not treat delirious patients with benzodiazepines unless the delirium is due to alcohol or benzodiazepine withdrawal, in which case haloperidol is contraindicated because it lowers the seizure threshold!
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Delirium prevention
Nonpharmacologic approach
Reduce exposure to modifiable risk factors.
Maintain adequate hydration and nutrition.
Avoid drugs that can worsen delirium (e.g., benzodiazepines, anticholinergics, opioids).
Reorient the patient regularly.
Keep a clock and/or calendar near the patient to help with orientation.
Provide visual and hearing aids for patients with impairments.
Reduce the amount of noise, procedures, and medication administration occurring at night.
Because delirium more frequently occurs and worsens at night, uninterrupted sleep is important for both prevention and management of delirium.
Arrange for regular visits from family and friends.
Arrange for constant observation, preferably by a family member or friend.
Provide physical and occupational therapy to mobilize the patient as soon as possible.
Minimize the use of physical restraints as much as possible.
Pharmacologic
Dexmedetomidine
Cholinesterase inhibitors (e.g., rivastigmine, donepezil)
Second-generation antipsychotics
Melatonin
Dementia dr deac pimp
D: Major neurocognitive disorder (previously called dementia) is an acquired disorder of cognitive function that is commonly characterized by impairments in memory, speech, reasoning, intellectual function, and/or spatial-temporal awareness. The potential causes of dementia are diverse, but the disorder is mainly due to neurodegenerative and/or vascular disease and as such, most forms are associated with increased age. Initial diagnosis should focus on the patient history, followed by cognitive assessments (e.g., the mini‑mental state exam) and physical examination. To confirm or rule out specific etiologies, additional laboratory tests or imaging studies are often necessary. Pharmacotherapy is available but is often met with little success because of the chronic and progressive nature of dementia.
An important differential diagnosis is pseudodementia, which is primarily associated with cognitive deficits in older patients with depression. In contrast to patients with dementia, individuals with pseudodementia can often recall the onset of their cognitive impairments, exaggerate their symptoms, and are remarkably responsive to treatment with antidepressants.
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D: alzeihmer disease, vascular dementia, dementia with lewy bodies, frontotemporal dementia, normal pressure hydrocephalus, wernicke encephalopathy (WE) and Wernicke-korsakoff syndrome (WKS). Late neurosyphilis, psudodementia, normal aging.
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A: Neurodegenerative brain diseases
Alzheimer disease (> 50% of dementia cases)
Parkinson disease
Frontotemporal dementia
Dementia with Lewy bodies
Progressive supranuclear palsy
Huntington disease
Additional causes
Cerebrovascular disease (20% of dementia cases)
Multi-infarct dementia
Diffuse white matter disease (subcortical arteriosclerotic encephalopathy)
Hypoxic brain damage
Normal pressure hydrocephalus
After head trauma, intracranial bleeding or brain tumors
Drug/alcohol‑related (e.g., Wernicke‑Korsakoff syndrome)
Wilson disease
Vitamin deficiencies (thiamine, B6, B12, folate)
Metabolic: exsiccosis, uremia, electrolyte imbalances, hypothyroidism and hyperthyroidism, hypoparathyroidism, and hyperparathyroidism
Environmental toxins
Inflammatory/infectious
Syphilis
Progressive multifocal leukoencephalopathy
HIV
Creutzfeldt-Jakob disease
C: Memory impairment
Additional cognitive impairment
Speech: aphasia, word-finding difficulties, semantic paraphasia
Intellectual capacities, reasoning, planning capabilities, and self-control
Spatial-temporal awareness (however, the awareness of oneself remains stable for a long time)
Apathy
Changes in personality, mood, and behavior
Early stages: depression
Later stages: seemingly unconcerned mood and cognitive impairment is downplayed
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I: General
Personal and collateral history of cognitive and behavioral changes
Drug history
Screening for depression
Physical and neurological examination
Diagnostic criteria for major neurocognitive disorder (previously dementia) in accordance with DSM-5
Significant cognitive decline in at least one of the following domains
Learning and memory
Language
Executive function
Complex attention
Perceptual-motor
Social cognition
Cognitive deficits interfere with everyday life, patient becomes dependent on help with complex activities (e.g., paying bills)
Cognitive deficits do not occur exclusively in the context of a delirium
Cognitive deficits are not better explained by another mental disorder (e.g., major depression)
Cognitive assessment
Mini-Mental State Examination (MMSE)
Definition: a screening tool that assesses the degree of cognitive impairment in individuals with suspected dementia
Diagnostic criteria
A maximum of 30 points is possible
A patient who scores 24 points or less is generally considered to have dementia.
20–24 points: mild dementia
13–20 points: moderate dementia
< 13 points: advanced dementia
Montreal Cognitive Assessment (MoCA)
Definition: a screening tool that assesses cognitive impairment
Includes testing of memory, visuospatial ability (e.g., by drawing a clock and copying a drawing of a cube), executive function, attention, language, abstraction (e.g., identifying similarity between a train and a bicycle), recall, and orientation to time and place.
Diagnostic criteria
A maximum of 30 points is possible
18–25 points: mild cognitive impairment
10–17 points: moderate cognitive impairment
< 10 points: severe cognitive impairment
Saint Louis University Mental Status Examination (SLUMS)
Definition: a screening tool to assess the degree of cognitive impairment in individuals with suspected dementia
Diagnostic criteria
A maximum of 30 points is possible
A patient who scores 19 points or less suffers from neurocognitive impairment
Clock-drawing test
Procedure: The patient is given a sheet of paper with an empty circle on which they are asked to draw a clock indicating the current time (including numbers and hands).
Purpose: If an individual is unable to correctly draw the numbers and hands on the clock, a deficit in spatial or abstract thinking may be present. These deficits are commonly already present during the early stages of dementia.
Neuropsychologic testing
Lab tests
In all patients: screening for vitamin B12 deficiency (cobalamin) and hypothyroidism
More specialized tests should be ordered in patients with a rapid progressive course of dementia, young patients (< 60 years), or patients with symptoms giving reason to suspect the presence of a certain disease
Serum electrolytes, renal and liver function tests, folate, homocysteine
Ceruloplasmin: decreased in Wilson disease (may be associated with symptoms of dementia)
ApoE genotyping
Lumbar puncture and CSF analysis (only in selected patients with suggestive clinical features or other abnormal tests)
To reveal CNS infection/inflammation (e.g., in meningitis or encephalitis)
Imaging
In all patients: noncontrast head CT or MRI
To detect reversible causes of dementia (e.g., brain tumor, subdural hematoma, NPH, past cerebral ischemia)
Multiple lacunar infarcts in vascular dementia
Reduced hippocampal volume in Alzheimer disease
PET, SPECT: in selected patients with suggestive clinical features/abnormal other tests to distinguish between different neurodegenerative disorders (e.g., Alzheimer disease, atypical parkinsonian disorders, and frontotemporal dementia)
EEG: when structural abnormality is suspectedNeuropsychologic testing
Lab tests
In all patients: screening for vitamin B12 deficiency (cobalamin) and hypothyroidism
More specialized tests should be ordered in patients with a rapid progressive course of dementia, young patients (< 60 years), or patients with symptoms giving reason to suspect the presence of a certain disease
Serum electrolytes, renal and liver function tests, folate, homocysteine
Ceruloplasmin: decreased in Wilson disease (may be associated with symptoms of dementia)
ApoE genotyping
Lumbar puncture and CSF analysis (only in selected patients with suggestive clinical features or other abnormal tests)
To reveal CNS infection/inflammation (e.g., in meningitis or encephalitis)
Imaging
In all patients: noncontrast head CT or MRI
To detect reversible causes of dementia (e.g., brain tumor, subdural hematoma, NPH, past cerebral ischemia)
Multiple lacunar infarcts in vascular dementia
Reduced hippocampal volume in Alzheimer disease
PET, SPECT: in selected patients with suggestive clinical features/abnormal other tests to distinguish between different neurodegenerative disorders (e.g., Alzheimer disease, atypical parkinsonian disorders, and frontotemporal dementia)
EEG: when structural abnormality is suspected.
M: Memory training
Cognitive capabilities can be improved through targeted stimulation (e.g., practicing image recognition, completing arithmetic or combinatorial problems).
Recalling past memories
Antidementia drugs
Cholinesterase inhibitors
Recommendation
First-line treatment for Alzheimer dementia (particularly mild to moderate stages) and vascular dementia
May be beneficial in cases of dementia with Lewy bodies, frontotemporal dementia, and Parkinson disease
Drugs: donepezil, rivastigmine, galantamine
Effect: Reversible cholinesterase inhibition leads to increased acetylcholine (ACh) concentration and can thus improve symptoms of some types of dementia.
Adverse side effects
Nausea
Dizziness
Insomnia
See also symptoms of cholinergic crisis.
To remember Donepezil, rivastigmine, and galantamine, think of “Dona Riva dances at the nursing home gala.”
Memantine
Recommendation
Particularly used in moderate to advanced cases of Alzheimer disease or vascular dementia
Memantine may be used in combination with cholinesterase inhibitors.
Effect: NMDA-receptor antagonism, resulting in decreased glutamate-induced calcium-mediated excitotoxicity
Adverse side effects: mostly affect the central nervous system
Headaches and dizziness
Confusion, hallucinations
Seizures
In general, anticholinergic substances (e.g., tricyclic antidepressants) should be avoided, as they may lead to further deterioration in cognitive functioning!
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