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Symptoms > Delirium > Flashcards

Delirium Flashcards

1
Q

__% of patients arriving to the ED are altered.

__% metabolic or systemic derangements.

__% structural lesions

A

3% of patients arriving to the ED are altered.

85% metabolic or systemic derangements.

15% structural lesions

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2
Q

What are the two components of consciousness?

A

Arousal

Cognition

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3
Q

What is arousal?

How is it controlled?

Where does it act in the CNS?

A
  • Awareness of self & surroundings
  • Ascending reticular activating system
  • Where in the CNS? Dorsal brainstem
    • Controls input of somatic & sensory stimuli, arousal from sleep
    • Vulnerable to small lesions in brainstem
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4
Q

What is cognition?

How is it controlled?

Where does it act in the CNS?

A
  • Combo of orientation (accurate perception of experiences), judgment (process input into meaningful info), & memory (store & retrieve info)
  • Located in cerebral cortex
    • Unilateral lesions rarely cause AMS
    • Possibly bilateral lesions (rare)
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5
Q

What is a coma?

How is it caused?

A
  • Coma = unconsciousness >6 hours
  • Cannot be awakened
  • No response to painful stimuli, light or sound
  • No normal sleep-wake cycle
  • No voluntary actions
  • Causes
    • Damage to brainstem, cortex, both
    • Susceptible to toxins, metabolic derangements, mechanical injury
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6
Q

What are the 3 most common causes of altered mental status?

A
  • Dementia
  • Delirium
  • Psychosis
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7
Q

When you have acute mental status change, what is the difference between fluctuating & non-fluctuating when determining a differential?

A
  • Fluctuating
    • Delirium
  • Non-fluctuating
    • Acute confusional state
    • Differential includes delirium or a long list of CNS insults including toxic metabolic derangement, infection, trauma
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8
Q

What are some common causes of Delirium? (7)

A
  • Metabolic/Endocrine
  • Infectious Disease
  • Cerebrovascular event/Structural CNS
    • Both hemispheres or brainstem
  • Cardiovascular
  • Drugs/Toxic
  • Hypoperfusion
  • Others
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9
Q

What are some examples of drugs that can cause delirium?

A
  • Alcohol withdrawal
  • Diuretics
  • Anti-cholinergics
  • Corticosteroids
  • Digoxin
  • Opioids
  • Anti-depressants
  • Anxiolytics
  • Hallucinogens/Dissociatives
  • Benzodiazepines
  • Sympathomimetics
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10
Q

How do these differ btwn Delirium & Dementia?

  • History
  • Onset
  • Duration
  • Course
  • Level of consciousness
  • Orientation
  • Memory
  • Perception
  • Sleep
  • Reversibility
  • Physiologic changes
  • Attention span
A
  • History
    • Delirium: acute, identifiable date
    • Dementia: chronic, can’t be dated
  • Onset
    • Delirium: rapid
    • Dementia: insidious
  • Duration
    • Delirium: days to weeks
    • Dementia: months to years
  • Course
    • Delirium: fluctuating
    • Dementia: chronically progressive
  • Level of consciousness
    • Delirium: fluctuating
    • Dementia: normal
  • Orientation
    • Delirium: impaired periodically
    • Dementia: disorientation to person
  • Memory
    • Delirium: recent memory markedly impaired
    • Dementia: remote memories seen as recent
  • Perception
    • Delirium: visual hallucinations
    • Dementia: hallucinations less common
  • Sleep
    • Delirium: disrupted sleep-wake cycle
    • Dementia: less sleep disruption
  • Reversibility
    • Delirium: reversible
    • Dementia: mostly irreversible
  • Physiologic changes
    • Delirium: prominent
    • Dementia: minimal
  • Attention span
    • Delirium: very short
    • Dementia: not reduced
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11
Q

What are some common age-related causes of altered mental status or coma?

  • Infant
  • Child
  • Adolescent, Young Adult
  • Elderly
A
  • Infant
    • Infection
    • Trauma, abuse
    • Metabolic
  • Child
    • Toxic ingestion
  • Adolescent, Young Adult
    • Toxic ingestion
    • Recreational drug use
    • Trauma
  • Elderly
    • Medication changes
    • Over-the-counter medications
    • Infection
    • Alterations in living environment
    • Stroke
    • Trauma
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12
Q

What are some diseases that are more likely to cause delirium?

A
  • Severe illness
  • Drug toxicity
  • Fluid & electrolyte disturbances
    • Hyponatremia & azotemia
    • *central pontine myelinolysis*
  • Infections
  • Hypothermia or hyperthermia
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13
Q

What is Central Pontine Myelinolysis?

*stressed in class, info here from First Aid*

A
  • Acute paralysis, dysarthria, dysphagia, diplopia & loss of consciousness
  • Can cause “locked-in syndrome”
  • Massive axonal demyelination in pontine white matter tracts
  • Secondary to osmotic forces & edema
  • Commonly iatrogenic, caused by overly rapid correction of hyponatremia
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14
Q

Delirium is a _____ that has an underlying cause that must be recognized & identified.

The most important clue to delirium is the _________ and _________.

Delirium most commonly occurs in ______ and patients with underlying ____________.

Delirium is very common in _______ patients over the age of ____.

A

symptom

acuity of onset, fluctuation in course

older persons, neurologic disease

sick, hospitalized, 65

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15
Q

What are some predictors of delirium? (7)

A
  • Abnormal sodium level
  • Severe illness
  • Chronic cognitive impairment
  • Hypothermia or hyperthermia
  • Moderate illness
  • Psychoactive drug use
  • Azotemia
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16
Q

What are the first steps in management of a patient presenting with delirium?

A

ABCDEs

  • Airway
    • hypoxia –> CNS dysfunction –> delirium
  • Breathing
    • low minute ventilation
    • respiratory acidosis
  • Circulation
    • hypoperfusion of the brain
    • check pulses
    • Trendelenburg position (picture)
  • Disability
    • Glasgow coma scale
  • Exposures
    • trauma, transdermal meds, dialysis devices, infections, catheter, skin
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17
Q

AMS =

LOC =

A

AMS = altered mental status

LOC = loss/level of consciousness

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18
Q

What type of information gathering is performed with a delirium patient?

A
  • All sources of information
    • EMS (Emergency Medical Services)
    • Family
    • EMR (Electronic Medical Record)
  • GCS for classification
    • Glasgow Coma Scale
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19
Q

What is the Glascow Coma Scale?

A

*Study this table*

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20
Q

What is the next step after ABCs & the GCS?

A
  • Basic neuro exam
  • Differential
  • Work-up
    • “DON’T” coma cocktail
    • Labs
    • Imaging
    • Other tests (EKG, lumbar puncture)
  • Treatment
    • Antidotes, antibiotics, surgery, supportive care, metabolic cofactors (thiamine, folate)
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21
Q

What is the “coma cocktail”?

What is it used for?

A

Alleviates common causes of delirium

  • Dextrose
  • Oxygen
  • Naloxone
  • Thiamine
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22
Q

What causes of delirium could be alleviated by DEXTROSE?

A

Hypoglycemia

  • Insulin (+ don’t eat)
  • Sulfonylureas (+ don’t eat)
  • Anorexia
  • Alcohol (malnourished, children)
    • Drinks, hand sanitizer
  • Beta blockers
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23
Q

What causes of delirium could be alleviated by OXYGEN?

A

Decreased respiratory drive

  • Carbon monoxide exposure
  • Opiates (opioids)
  • Alcohol (drug combos)
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24
Q

What causes of delirium could be alleviated by NALOXONE?

A

Opioids

(morphine, heroin, oxycodone, fentanyl, tramadol, etc.)

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25
Q

What is the Confusion Assessment Method? (CAM)

What is the sensitivity & specificity?

A

Best-validated tool for diagnosing delirium

  • CAM is positive when a patient fulfills both criteria a and b as well as either c or d:
    • A) the mental status change is of acute onset & fluctuating course
    • B) there is inattention
    • C) there is disorganized thinking (or incoherent)
    • D) there is an altered level of consciousness
  • The test characteristics surpass those of an unaided physician assessment
  • Sensitivity: 86%, specificity: 93%
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26
Q

Patient’s who experienced delirium had a higher risk of _______, ____________, & _______ during follow-up.

What are the percentages?

A

death, institutionalization, dementia

  • mortality rate = 38%
  • institutionalization = 33.4%
  • dementia = 62.5%
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27
Q

Many acutely ill, older patients who have an acute deterioration in mental status are suffering from ______.

Delirium can occasionally “unmask” an underlying ______.

A

delirium

dementia

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28
Q

1 day old male born at term, still in hospital, & you are called bedside because he is lethargic. He had a C-section due to large gestational size. Poor suck. Mother IDDM.

  • A - intact
  • B - slow respirations
  • C - femoral pulses intact, cap refill 5 seconds

What bedside test do you do? What is most likely?

What should be considered?

A
  • Blood glucose, could give dextrose
  • Hypoglycemia, Sulfonylureas
  • Consider:
    • Opioid withdrawal (irritable, poor suck, shrill cry)
    • Infection (low immune system, group B strep, birth trauma)
    • Hypoventilation (hypoxia, low cap refil, full lungs)
    • Trauma (head bleed, intentional trauma)
    • Inborn errors of metabolism
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29
Q

What would your differential diagnosis be if the child was 6 wks old, had no prenatal care, and was febrile to 38 degrees C & came in lethargic?

A
  • Meningitis (bacteria)
    • Herpetic lesions on head = HSV
  • Dehydration
  • Alcohol (whiskey)
  • Nitrites in well water
    • Methemoglobinemia
  • Abuse (shaking)
  • Honey - botulism
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30
Q

What would your differential diagnosis be if this child were 1 year old, hypoglycemic, lethargic, just at grandma’s house, who has a PMH of DM & HTN?

A
  • Drug cabinet & pill containers
    • Boys > girls (65% of poisoned 1 year olds)
  • TCAs = seizure, hypoglycemia, altered state
  • “1 pill can kill” for toddler
    • Sulfonylureas
    • Beta blockers
  • High risk for child with manual dexterity
31
Q

What are some examples of “1 pill can kill” for a toddler?

A
  • Beta blockers
  • Sulfonylureas
  • Ca2+ channel blockers
  • Clonidine
  • Buprenorphine
  • Oxycotin
  • Methadone
  • Fentanyl
  • Anti-psychotics
32
Q

What kinds of symptoms predominate with hypoglycemia?

A

CNS symptoms predominate

  • Brain relies almost entirely on glucose
  • During prolonged starvation, the brain can use ketones
  • Other major organs (heart, liver, skeletal muscle) function during hypoglycemia (use various fuel sources
33
Q

How does insulin receptor density vary in diabetes?

What is the mean glucose in hypoglycemia?

A
  • In diabetes, density of neuronal insulin receptors varies w/ glycemic control
  • Poor glycemic control –> fewer neuronal glucose receptors
  • Hypoglycemic symptoms at higher concentrations of glucose
  • Mean [glucose] for symptomatic hypoglycemia 78 + 5 mg/dL vs. 53 + mg/dL
34
Q

What is the interaction btwn sulfonylureas & insulin?

A
  • Normally, insulin released w/ elevation of intracellular ATP
  • Sulfonylureas potentiate the effects of ATP at its “sensor”
    • Increased intracellular K –> increased intracellular potential opens voltage-gated Ca2+ channels –> increases intracellular Ca2+ concentration
    • Increased calcium –> release of insulin
    • Binding of sulfonylureas to receptor sites –> insulin release
35
Q

What is the interaction btwn Meglitinides & insulin?

A
  • Bind to K channels on pancreatic cells –> increased insulin secretion
  • Hypoglycemic effects shorter duration
36
Q

What is the mechanism of Metformin?

Does this cause hypoglycemia?

A

does NOT cause hypoglycemia

  • Glucose stabilizing by several mechanisms
    • Inhibits gluconeogenesis –> decreased hepatic glucose output
    • Enhanced peripheral glucose uptake
    • Decreased fatty acid oxidation
    • Increased intestinal use of glucose
    • In skeletal muscle & adipose cells, enhanced activity & translocation of glucose transporters
37
Q

Previously healthy 17 year old male presenting with AMS. He was found on doorstep by parents, acting paranoid & inappropriate. Has a history of drug & alcohol abuse. Had been at a party with friends, possibly used drugs.

  • A - intact
  • B - normal breath sounds bilaterally
  • C - bounding peripheral pulses, tachycardic

What is the most likely diagnosis? What else is on the differential?

A

Sympathomimetics

  • Stimulant use
    • Amphetamines (adderall, cocaine)
    • Methamphetamines
    • PCP
    • Robutussin
    • Salvia divinorum (dysphoria)
    • MDMA (SIADH)
  • Bath salts, anticholinergic toxicity (diphenhydramine), thyrotoxicosis, psychiatric break, hypoglycemia, head trauma, meningitis, withdrawal (alcohol, barbiturates)
38
Q

What would be your differential if he was a known alcoholic?

If he lived in New Mexico?

A

Withdrawal

Methamphetamine

39
Q

All of the following sympathomimetic drugs inhibit the uptake of NE except:

  • Cocaine
  • Amphetamine
  • Venlafaxine
  • Buproprion
  • Dobutamine
A

Dobutamine

ß1 > ß2, alpha

40
Q

What is the action of sympathomimetics?

What are the two types?

A
  • Stimulate sympathetic nervous system
  • Direct-acting
    • Bind post-synaptic receptors
    • Direct stimulation
  • Indirect-acting
    • Increase synaptic concentration of NTs
41
Q

Describe the components of the monoamininergic synapse

A
  • VMAT
  • MAO
  • Presynaptic receptor
  • Post-synaptic receptor
  • DAT, NET, SERT
  • COMT
42
Q

What are the post-synaptic receptors in the NE synapse and what are their effects?

A
  • Galpha(i)​
    • CNS: inhibition
    • Peripheral: vasoconstriction
  • Galpha(s)
    • CNS: excitation
    • Peripheral: bronchodilation, increased HR, vasodilation
43
Q

What are the cellular responses at the dopamine synapse?

A
  • Brain
    • Addiction
    • Drug craving
    • Choreoathetosis
    • Tourette syndrome
    • Psychoses
  • Peripheral
    • Vasodilation
44
Q

What are the mechanisms of these indirect acting sympathomimetics?

  • Cocaine
  • Amphetamines
  • Molly/Ecstasy (MDMA)
  • Bath salts/cathinones
A
  • Cocaine
    • Transport blocker
    • DAT, NET, SERT
  • Amphetamines
    • False substrate
    • DAT, NET, VMAT
  • Molly/Ecstasy (MDMA)
    • False substrate
    • DAT, NET, SERT, VMAT
  • Bath salts/cathinones
    • False substrates/transport blocker
    • DAT, NET, SERT, VMAT
45
Q

What are the mechanisms of these indirect acting sympathomimetics?

  • Clorgyline, Pargyline, Selegiline
  • Tolcapone
A
  • Clorgyline, Pargyline, Selegiline: MAO
  • Tolcapone: COMT
    • Note: 5-HT is indolamine, not catecholamine
46
Q

Describe the False Substrate Mechanism of sympathomimetics

A
  • Amphetamine fills up vesicles
  • High amphetamine transport into the presynaptic cell
  • Transporters can reverse, amphetamine takes DA with it when it leaves
    • High concentration of presynaptic DA in the cytoplasm
    • DA purged from presynaptic terminal via reverse transport through transporters
    • Activity independent purging of DA & NE from the presynaptic terminals
  • High concentrations can have profound pharmacologic effects
    • Catecholamines (DA, NE) are very oxidizable
    • Brain only has a limited capacity to inhibit oxidation of these compounds
    • DA will form oxidized products –> mitochondrial damage in presynaptic terminals (distressed terminals)
  • Summary: false substrates can be dangerous!
47
Q

What is a toxidrome?

A
  • Describes groups of signs & symptoms consistently attributed to particular toxins
  • Usually a combination of vital signs & end organ damage (clinically apparent)
48
Q

What are the components of the sympathomimetic toxidrome?

A
  • Hypertension
  • Hyperthermia
  • Tachycardia
  • Mydriasis
  • Diaphoresis
49
Q

What are the components of the Anticholinergic toxidrome?

A

Low potency antipsychotics, oxybutinin, ipratropium, ACh receptor antagonists

  • Increased HR & BP
  • Increased temp
  • Mydriasis
  • Decreased bowel sounds
  • Decreased diaphoresis
50
Q

What are the components of the Cholinergic toxidrome?

A

ACh receptor agonists, AChEIs (Donepezil)

  • Miosis
  • Increased bowel sounds
  • Increased diaphoresis
51
Q

What are the components of the Opioid toxidrome?

A

morphine, heroin, hydromorphone

  • Decreased HR & BP
  • Decreased RR
  • Decreased temp
  • Miosis
  • Decreased bowel sounds
  • Decreased diaphoresis
52
Q

What are the components of the Sympathomimetic toxidrome?

A

epinephrine, cocaine, amphetamine, methylphenidate

  • Increased HR & BP
  • Increased RR
  • Increased temp
  • Mydriasis
  • Increased bowel sounds
  • Increased diaphoresis
53
Q

What are the components of the Sedative-Hypnotic toxidrome?

A

benzos, barbs, Z-drugs, anti-histamines

  • Decreased HR & BP
  • Decreased RR
  • Decreased temp
  • Decreased bowel sounds
  • Decreased diaphoresis
54
Q

What medications would you give to a patient with a sympathomimetic toxidrome?

What if they became too sedated?

What caution should you take with this?

A
  • Give benzodiazepines
  • If too sedated, give flumazenil
  • Be concerned about withdrawal
55
Q

What is the mechanism of Flumazenil?

Why is it’s use limited?

Who is the ideal recipient of it?

A
  • Competitive benzodiazepine receptor antagonist
  • Role in patients w/ unknown overdose is limited because seizures & dysrhythmias may develop
  • Can induce benzo withdrawal symptoms, including seizures in those who are benzo dependent
  • Ideal antidote for the few patients who:
    • Are both naive to benzos & who overdose soley on a benzo OR
    • benzo-naive patients whose benzo component must be reverse after procedural sedation
56
Q

50 year old male found down by family in bathroom. History of chronic back pain. Has multiple ED visits for pain in the last month.

  • A - intact
  • B - RR 4
  • C - weak pulses, cyanotic

What is the most likely diagnosis? What do you give?

A
  • Could be hypnotic, but classic presentation for opioid toxidrome
    • Altered mental status
    • Decreased respiration
    • Pinpoint pupils (left out of history)
  • Administer Naloxone
57
Q

What are the 3 components of the opioid toxidrome?

A
  • Altered mental status (stupor, coma)
  • Miosis
  • Respiratory depression
58
Q

What is the mechanism by which opioids such as morphine produce respiratory depression?

A
  • They decrease chemoreceptor sensitivity to carbon dioxide
  • Don’t have the “drive to breathe”
59
Q

What are some examples of amino acid sequence similarities among endogenous opiates?

A
  • ß-endorphin
    • Tyr-Gly-Gly-Phe-_Met_
  • Methionine enkephalin
    • Tyr-Gly-Gly-Phe-_Met_
  • Leucine enkephalin
    • Tyr-Gly-Gly-Phe-_Leu_
  • Dynorphin A
    • Tyr-Gly-Gly-Phe-_Leu_
  • alpha-neoendorphin
    • Tyr-Gly-Gly-Phe-_Leu_
60
Q

Which endogenous peptides are selective for µ and δ receptors? What about κ receptors?

A
  • µ and δ
    • Met-enkephalin
    • Leu-enkephalin
    • ß-Endorphin
  • κ
    • Dynorphin A
    • Dynorphin B
    • α-Neoendorphin
61
Q

What is the structure of the opioid receptor?

A
  • Gα1 coupled
  • Reduction in AC –> decreased cAMP
  • Open K+ channels –> hyperpolarization
62
Q

What are the opioid clinical effects on each of these systems?

  • Cardiovascular
  • Dermatologic
  • Endocrinologic
  • Gastrointestinal
  • Neurologic
  • Ophthalmologic
  • Pulmonary
A
  • Cardiovascular
    • Orthostatic hypotension, bradycardia, peripheral vasodilation
  • Dermatologic
    • Itching, Flushing (histamine)
  • Endocrinologic
    • Prolactin release, reduced ADH & gonadotropin release
  • Gastrointestinal
    • Increased anal sphincter tone, increased biliary tract pressure, reduced gastric acid secretion, reduced motility
  • Neurologic
    • Analgesia, anti-tussive, euphoria, sedation, coma, seizures (meperidine, propoxyphene)
  • Ophthalmologic
    • Miosis
  • Pulmonary
    • Acute lung injury, bronchospasm (histamine), respiratory depression
63
Q

What is the classic triad of Wernicke’s Encephalopathy?

A
  • Confusion
  • Ophthalmoplegia
  • Ataxia
64
Q

What are the 2 types of Thiamine deficiency?

What is the difference between them?

A
  • Wet beriberi: CV disease
    • High output cardiac failure
    • Peripheral vasodilation & formation of arteriovenous fistulae
  • Dry beriber: Wernicke-Korsakoff Syndrome
    • Classic Wernicke triad
      • Confusion
      • Ophthalmoplegia
      • Ataxia
    • Korsakoff Syndrome
      • Confabulation, memory loss, personality change
      • Chronic
    • 10-20% mortality
    • Peripheral neuropathy common
65
Q

What are the 2 major molecular targets of ethanol?

What are their functions?

A
  • GABA receptors
    • Suppress neuronal transmission
    • Help maintain resting membrane potential in some neurons
  • NMDA receptors
    • Learning & memory
66
Q

What is the structure of the GABA-A receptor?

What is the mechanism of action?

A
  • Pentameric receptor complex
    • 2 alpha
    • 2 beta
    • 1 gamma
  • Activation promotes hyperpolarization via chloride flux
67
Q

What is the interaction btwn alcohol & GABA-A?

What other drugs interact with this receptor?

A
  • Alcohol potentiates GABA & sedative hypnotics
  • Chronic alcohol use results in cross tolereance to sedative hypnotics
  • Other interactions
    • Benzodiazepines (Flumazenil)
    • Diprivan (propofol)
    • Neurosteroids
    • Barbiturates
    • Volatile anesthetics (isoflurane)
68
Q

What are the 2 major pathways and 2 minor pathway of alcohol metabolism?

A
  • Alcohol dehydrogenase (ADH)
    • lower stomach ADH in women
  • Microsomal Ethanol-Oxidizing System (MEOS)
    • Primarilty CYP450 2E1 (induced in alcoholics), 1A2, 3A4
    • Induction by chronic alcohol intake
    • Increases in clearance of other drugs
  • Catalase is a minor metabolic pathway of alcohol
69
Q

How does alcohol react with NMDA receptors?

What about Ketamine & PCP?

What is a common side effect?

A
  • Alcohol is an antagonist of NMDA receptors
  • Ketamine & PCP are also antagonists
  • Depolarization to remove Mg2+ block
  • Side effect: Nystagmus
70
Q

What are the symptoms & chronology of alcohol withdrawal?

A
71
Q

What are the symptoms of Delirium Tremens?

A
  • Hallucinations (visual & tactile)
  • Disorientation
  • Hypertension
  • Tachycardia
  • Fever
72
Q

What are the high risks of Delirium Tremens?

When does this usually occur?

Mortality?

A
  • High risk for seizures & dangerous ventricluar arrhythmias
  • Seen in 5% of patients w/ alcohol withdrawal
  • 2-4 days after the last drink
  • Untreated mortality = 30%
    • <5% with treatment
73
Q

Elderly man with mild COPD. Had surgery complicated by transient hypotension & excessive blood loss. After extubation, wife noted him to be confused on post-op day 3.

  • A - intact
  • B - RR 12
  • C - good distal pulses

What is the diagnosis? differential?

A

Delirium

  • Hyponatremia, electrolyte imbalance
  • Infection
  • Stroke
  • Alcohol withdrawal
  • Opioids
  • Hypoxic, hypercardic, elevated CO2
  • Acute MI
  • Seizure
74
Q

What are 6 things we can do to treat & minimize delirium?

A
  • Treat the underlying cause
  • Administer fluids to treat & prevent dehydration
  • Avoid sleep deprivation
  • Provide a quiet environment
  • Keep nightime awakenings to a minimum
  • Protect from falls or self-inflicted injury
    • Sitters
    • Low-dose neuroleptics

Symptoms (17 decks)

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