Delirium Flashcards

1
Q

Frequency of cognitive impairment and delirium in patients on admission to PCU

A
  • around 40% for each
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2
Q

Incidence of terminal delirium

A

80%

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3
Q

Criteria for diagnosis of delirium

A

DSM-5:

  • Disturbance in attention (distractibility)
  • Develops over a short period of time, is a change from baseline, and fluctuates through the day
  • An additional disturbance in cognition (memory deficit, disorientation, language, visuospatial ability, perception)
  • Not better explained by a neurocognitive disorder
  • Disturbance is likely caused by medical condition, intoxication, withdrawal, or med side effect.

MMSE should not be used to screen for delirium, as it has the least useful LR of all studied instruments. As per JAMA, LR+s for delirium:

  • Global attentiveness rating (LR + 65)
  • CAM positive (LR 7.3 by nurses, 19 by physicians)
  • MMSE <24, LR+ 1.6
CAM:
- Acute onset and fluctuating course
- Inattention
And one of:
- Disorganized thinking
- Altered LOC
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4
Q

Clinical subtypes of delirium

A
  • Hyperactive
  • Hypoactive
  • Mixed form

Hypoactive and mixed are most common in palliative care

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5
Q

Reasons for misdiagnosis or failure to recognise delirium

A
  • Ambiguous terms used to define
  • Failure to regularly screen for delirium
  • Fluctuation in symptoms
  • Hypoactive subtype may be less recognisable
  • Dementia may cloud the picture
  • Misdiagnosis of depression (hypoactive or emotionally labile)
  • Misdiagnosis of mania, psychosis, anxiety, or akathisia (hyperactive subtype)
  • Misdiagnosis of dementia
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6
Q

Risks of missing a delirium diagnosis

A
  • Increase in morbidity or mortality (especially if reversible, underlying cause)
  • Treatment with a benzo or antidepressants could worsen delirium
  • Treatment with opioids if misinterpreted as pain could also worsen delirium
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7
Q

History and physical assessment in delirium

A
  • Collateral history to establish baseline, temporal onset, and whether fluctuation is present
  • Formal cognitive assessment if appropriate
  • Physical examination/observation for signs of opioid induced neurotoxicity (hallucinations, sedation, myoclonus, hyperalgesia or allodynia)
  • Comprehensive PE for underlying causes (dehydration, infection, neuro signs suggestive of leptomeningeal disease, asterixis, myoclonus, primitive reflexes that may be present in diffuse encephalopathies)
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8
Q

Use for assessment of cognitive status

A

Dementia

  • MMSE
  • FAB (for frontotemporal dementia)
  • MOCA (for frontotemporal dementia as it includes a clock drawing)
  • Clock drawing (executive function)
Delirium
- Confusion Assessment Method
CAM:
- Acute onset and fluctuating course
- Inattention
And one of:
- Disorganized thinking
- Altered LOC
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9
Q

Causes associated with delirium in advanced cancer patients

A
  1. Intracranial disease
    - Brain tumour (primary or secondary)
    - Leptomeningeal disease
    - Post-ictal state
  2. Medications
    - Psychoactive (benzos, opioids, TCAs, anticholinergices, SSRIs, antipsychotics, antihistamines)
    - Steroids
    - Cipro
  3. Organ failure
    - Cardiac, hepatic, renal, respiratory
  4. Infection (especially pulmonary or urinary)
  5. Heme
    - Anemia
    - DIC
  6. Metabolic
    - Dehydration
    - Hypercalcemia
    - Hyponatremia
    - Hypoglycemia/hyperglycemia
  7. Paraneoplastic
    - Encephalitis
  8. Withdrawal
    - Benzos, opioids, EtOH
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10
Q

Risk factors associated with delirium in advanced cancer patients

A
  • Cachexia
  • Hypoalbuminemia
  • Advanced age
  • Pre-existing cognitive impairment
  • Reduced sensory input (vision, deafness)
  • Urinary retention
  • Constipation
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11
Q

Pathogenesis of delirium

A
  • Global disorder of brain dysfunction reflecting imbalance in neurotransmission and reduced cerebral oxidative metabolism
  • Likely relatively decrease in cholinergic to dopaminergic transmission, but other neutrotransmitters and cytokines also implicated
  • Decreased cholinergic transmission would explain the role of anticholinergics in increasing risk of delirium
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12
Q

How do opioids increase risk for delirium

A
  • Morphine metabolite (M-3-G) may be neuroexcitatory, as is Hydromorphone metabolite (H-3-G)
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13
Q

Impact of delirium on patients

A
  • Thought to be highly distressing for patients and likely contributes to caregiver stress
  • Increased risk of falls and injuries
  • Loss of capacity for decision making (both medical and financial)
  • Loss of meaningful communication with family prior to death
  • Difficulty for healthcare providers in assessing pain and managing symptoms appropriately (delirious patients tend to receive more breakthrough opioids - either due to agitation causing more pain, or agitation being misinterpreted as pain)
  • Frustration from family members towards healthcare team, particularly if they feel agitation is driven by pain, but HCPs are trying to minimize medication given risk of worsened delirium
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14
Q

General approach to dementia

A

Identify, Consider, Meet, Treat, Support (ICMTS)

  • Identify potential underlying cause and appropriateness of investigating/treating
  • Consider burden of correcting underlying causes of delirium and impact on QOL (e.g. IV line for IVF)
  • Meet with the patient and family to facilitate informed decision making and consensus on goals of care, with patient input as appropriate
  • Treat symptoms of delirium (neuroleptics, non-pharm measures, communicate and explain to family and caregivers particularly around poor prognosis when delirium occurs near EOL)
  • Emotional support for the family
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15
Q

Prognosis of delirium

A
  • Potential for reversal in up to 50% of cases, depending upon underlying cause
  • Terminal delirium has a poor prognosis
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16
Q

Investigations for Delirium

A
  • CBC
  • Lytes
  • Urea/Cr
  • Calcium/albumin
  • Mg
  • Glucose
  • Bili and liver
  • Urinalysis/urine culture
  • Infectious workup (CXR, blood cultures)
  • CT head if focal neuro findings
  • History for constipation (AXR if desperate)
17
Q

Treatment of delirium

A
  1. Antipsychotics
    - Most commonly used as they are dopamine antagonists and may help to restore cholinergic/dopaminergic balance in the brain
    - Atypicals (Haldol) associated with increased risk of extrapyramidal side effects
    - Haldol often first line
    - Olanzapine or nozinan may be useful for patients with more hyperactivity
  2. Benzos
    - Avoid - deliriogenic
    - Drugs of choice if delirium is related to EtOH/benzo withdrawal
  3. Non-pharm management
    - Frequent orientation of patient
    - Encourage family with reorientation
    - Hearing aids and glasses
    - Strategically place clock and calendar
    - Optimal natural light (window)
    - Noise reduction
    - Limited staff changes as possible
    - Avoid physical restraints
  4. Reduce polypharmacy
  5. Reduce lines if possible
  6. Appropriate pain control
18
Q

Extrapyramidal symptoms

A
  • Dystonia (continuous spasms, muscle contractions)
  • Akathisia
  • Parkinsonism (rigidity, bradykinesia, tremor)
  • Tardive dyskinesia (irregular, jerky movements)
19
Q

Medications most associated with EPS

A
  1. Typical antipsychotics (most likely)
    - Haldol at higher doses
    - Chlorpromazine
    - Prochlorpromazine
  2. Methotrimeprazine (somewhere in the middle)
  3. Atypical antipsyhotics
    - Risperidone (worst offender, risk with doses > 6mg/day)
    - Quetiapine (most sedating, low risk)
    - Olanzapine (low risk)
  4. Other drugs
    - Maxeran
    - SSRIs
    - SNRIs
    - NDRIs
20
Q

How to treat delirium in lewy body dementia

A

If antipsychotics are needed for behavior, avoid 1st generation (e.g. Haldol) as this may result in irreversible parkinsonism, impaired consciousness. If required, use atypicals (olanzapine, quetiapine, risperidone)

21
Q

How to treat delirium in patient with Parkinsonism vs Lewy Body

A

Quetiapine if PD (preferred for psychosis)

Risperidone (preferred for LBD)

Benzos and first gen antipsychotics (e.g. Haldol) should generally be avoided.

22
Q

Lewy Body Dementia

A

Lewy Body Dementia:

  • Impaired STM, poor judgment, confusion, with hallucinations, dysautonomia, sleep disorders.
  • May have co-occuring PD within a year of onset.
  • On MMSE, early appearance of impaired visuospatial (overlapping pentagons), clock drawing, serial sevens or WORLD backwards.

Diagnosis = Two of:
Visual hallucinations, fluctuating cognition, Parkinsonism (onset within a year)

Treatment: Cholinesterase inhibitors are first line, with mixed data for memantine.

Avoid Benzos and antipsychotics. If antipsychotics are needed for behavior, avoid 1st generation (e.g. Haldol) as this may result in irreversible parkinsonism, impaired consciousness. If required, use atypicals (olanzapine, quetiapine, risperidone, clozapine)