3 Altered Mental Status and Toxicology Flashcards

1
Q

What exactly does mental status mean?

A

Assessment of level of patient awareness or consciousness (“behavioral expression of the brain”)

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2
Q

What does “A&Ox3” mean?

A

Alert and oriented to person, place, and time

Sometimes it’s x4, if they are aware of their situation

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3
Q

What should you put instead of A&Ox3 if you don’t actually ask the questions?

A

“Alert and appropriate”

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4
Q

When describing a patient’s level of consciousness, it is more useful to describe _______ and ______ rather than to use terms like stupor or obtunded

A

Patient’s spontaneous behavior and responses to stimuli

That’s because the other terms are vague and have no true quantifiable definition

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5
Q

Examples of the ranges of consciousness

A
Alert 
Lethargic/somnolent
Obtunded
Stuporous/semicomatose
Comatose
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6
Q

What is the level of consciousness:

A patient who is awake and fully aware of surroundings, responds appropriately to normal stimuli

A

Alert

Does not imply capacity to focus attention

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7
Q

What is the level of consciousness:

A patient who is not fully alert and drifts off to sleep when not stimulated

Spontaneous movement decreased

Awareness limited

A

Lethargic or somnolent

Unable to pay close attention, loses train of thought constantly and consistently

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8
Q

What is the level of consciousness:

A patient who is difficult to arouse and when aroused is confused

A

Obtunded

Constant stimulation is required to elicit minimal cooperation

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9
Q

What is the level of consciousness:

A patient who does not rouse spontaneously, requires persistent and vigorous stimulation for very little response

A

Stuporous or semicomatose

When aroused, will moan or mumble

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10
Q

What is the level of consciousness:

A patient who is unarousable and unresponsive

A

Coma

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11
Q

The Glasgow coma scale grades coma severity according to what three categories?

A

Eye opening

Motor function

Verbal responses

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12
Q

Even when you are dead, what score do you get on GCS?

A

3 lol

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13
Q

What are the four levels for eyes on the GCS?

A

Spontaneous = 4

To voice = 3

To pain = 2

None = 1

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14
Q

What are the six levels for motor response on the GCS?

A

Obeys commands = 6

Localized to pain = 5

Withdraws to pain = 4

Flexor posturing (Decorticate) = 3

Extensor posturing (Decerebrate) = 2

None = 1

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15
Q

Flexion with addiction of arms and extension of the legs

A

Decorticate (flexor) posturing

Reflects destructive lesion in CORTICOSPINAL tract from CORTEX TO UPPER MIDBRAIN

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16
Q

Extension, addiction, and internal rotation of the arms and extension of the legs

A

Decerebrate (extensor) posturing

Associated with damage to CORTICOSPINAL tract at the level of BRAINSTEM (pons or upper medulla)

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17
Q

How to remember that Decorticate posturing is flexor

A

COR - hands over heart

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18
Q

______ posturing is worse than ________

A

Decerebrate is worse than Decorticate

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19
Q

What are the five levels for verbal response on the GCS?

A

Conversant and oriented = 5

Conversant and disoriented = 4

Uses inappropriate words = 3

Makes incomprehensive sounds = 2

None = 1

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20
Q

GCS was originally developed for __________

A

Trauma patients, specifically head injury

It is not as useful in conditions other than trauma

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21
Q

A GCS score of ____ or below for longer than 72 indicates a very poor prognosis

A

8

In ED, it is customary to intubate a patient with a GCS ≤8 b/c it is likely that they are unable to protect their own airway

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22
Q

The term “altered mental status” is imprecise and can be referred to as many things, such as…

A
Delirium
Encephalopathy
Acute confusional state
Acute cognitive impairment
Neurocognitive disorder (ie dementia)
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23
Q

What is the new term for dementia?

A

Major neurocognitive disorder

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24
Q

What is the DSM-5 definition for Major Neurocognitive Disorder (formally dementia)?

A
Significant cognitive impairment in at least ONE of the following domains:
Learning and memory
Language
Executive function
Complex attention
Perceptual motor function
Social cognition

Impairment must be ACQUIRED and represent SIGNIFICANT DECLINE

Cognitive deficits INTERFERE W/ INDEPENDENCE in ADLs

Cognitive deficits DO NOT OCCUR EXCLUSIVELY in the context of DELIRIUM

Cognitive deficits are NOT BETTER EXPLAINED BY ANOTHER MENTAL DISORDER

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25
Q

DSM-5 for Delirium

A

DISTURBANCE IN ATTENTION and AWARNESS

Disturbance develops OVER A SHORT PERIOD OF TIME (days, hours), tends to FLUCTUATE

Additional disturbance in COGNITION

The disturbances are not better explained by another preexisting, evolving, or established neurocognitive disorder, and not part of a COMA

Hx, PE, or labs suggest disturbance is caused by a MEDICAL CONDITION, SUBSTANCE INTOXICATION/WITHDRAWAL, or MED SIDE EFFECT

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26
Q

A simpler definition of delirium

A

A disturbance of consciousness and altered cognition that develops of a short period of time

Some are drowsy/lethargic, others agitated/confused

Can include VISUAL HALLUCINATIONS, tremulousness, and myoclonus/asterixis

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27
Q

____________ are not characteristic of delirium

A

Focal or lateralized neuro findings

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28
Q

______% of older medical patients experience delirium at some point

A

~30%

Usually during a hospitalization

Incidence higher in those with advanced age and pre-existing brain disease

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29
Q

Mortality is _______ for a patient with a given medical condition PLUS delirium (compared to the patient who has the medical condition alone)

A

Approximately DOUBLE

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30
Q

What are the risk factors for delirium?

A

UNDERLYING BRAIN DISEASE (ie dementia, stroke, Parkinson’s)

Age ≥80

Infection (UTI, PNA)

Polypharmacy

EtOH use

Men>Women

Multiple medical problems

Fractures

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31
Q

Comparing Delirium and Dementia:

Onset

A

Delirium = rapid

Dementia = slow

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32
Q

Comparing Delirium and Dementia:

Course

A

Delirium = Fluctuating

Dementia = Progressive

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33
Q

Comparing Delirium and Dementia:

Vital signs

A

Delirium = often abnormal

Dementia = usually normal

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34
Q

Comparing Delirium and Dementia:

Level of consciousness

A

Delirium = altered

Dementia = normal

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35
Q

Comparing Delirium and Dementia:

Hallucinations

A

Delirium = visual (related to external stimuli)

Dementia = rare

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36
Q

Comparing Delirium and Dementia:

Physical exam

A

Delirium = often abnormal

Dementia = often normal

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37
Q

Comparing Delirium and Dementia:

Prognosis

A

Delirium = Poor if not treated

Dementia = Progressive

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38
Q

Comparing Delirium and Dementia:

Underlying cause

A

Delirium = Organic (myriad)

Dementia = Organic (degenerative)

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39
Q

AEIOU-TIPS

A

Common causes of AMS

Alcohol
Epilepsy, endocrine, exocrine, electrolyte
Infection
Overdose, opioids, oxygen deprivation
Uremia
Trauma, temp, toxins
Insulin
Psychosis
Stroke, shock
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40
Q

MOVE STUPID

A

Common causes of AMS

Metabolic
Oxygen (hypoxia)
Vascular (CVA, bleed, MI, CHF)
Endocrine
Seizure
Trauma, temp, toxins
Uremia
Psychogenic
Infection
Drugs (intoxication or withdrawal)
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41
Q

What do you need to do to evaluate AMS?

A

Address ABCs first

Assess vitals, mental status (GCS), pupil size, skin temp

Check pulse ox, place on cardiac monitoring

COMPLETE hx and PE to try to determine etiology (review MEDS)

Start interventions (O2, finger-stick glucose, EKG, place IV/draw labs)

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42
Q

Reasonable starting labs for someone with AMS

A

Serum electrolytes, creatinine, glucose, calcium
CBC
UA (esp older patients)
Pregnancy test

EKG if CAD or >50
CXR if resp sx or fever
Head CT if focal neuro findings or trauma
ABG if hypoxic or metabolic acidosis suspected
Lumbar puncture if meningitis/encephalitis suspected

ALL WHILE PROVIDING AGGRESSIVE SUPPORTIVE CARE

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43
Q

What is key to the treatment of AMS?

A

Identifying and treating the UNDERLYING CAUSE

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44
Q

What three interventions should you consider in causes of AMS because they cause little to no harm in using them even if you’re wrong?

A

Thiamine
Dextrose
Naloxone

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45
Q

When should physical restraints be used for people with AMS?

A

Only as a LAST RESORT - really bad for the patient and makes them even less cooperative

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46
Q

What things can you do that can lessen disruptive behaviors in patients with AMS?

A

Frequent reassurance, touch, and verbal orientation

A CAUTIOUS trial of psychotropic meds should be reserved for tx of severe agitation or psychosis with POTENTIAL FOR HARM to patients, providers or family

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47
Q

If you have a patient with AMS who is severely agitated and could potentially harm themselves or others, what drug can you try?

A

Low-dose haloperidol (better than Ativan esp in elderly pt)

48
Q

In undifferentiated AMS, ___________ (drug) should generally be avoided

A

Benzodiazepines

Consider in cases of sedative drug and alcohol withdrawal or sympathomimetic/anticholinergic poisonings

49
Q

What is the exception to the rule about not giving bentos to someone with AMS?

A

Consider in cases of sedative drug and alcohol withdrawal or sympathomimetic/anticholinergic poisonings

50
Q

_____________ are not effective in preventing or treating symptoms of delirium and often create undesirable side effects

A

Cholinesterase inhibitors (ie rivastigmine, donepezil)

51
Q

Delirium may require _______ to fully resolve

A

Weeks or months

52
Q

What is the American Association of Poison Control Centers national hotline phone number?

A

1-800-222-1222

53
Q

What drug should you not forget contains acetaminophen?

A

Percocet!

54
Q

What questions to ask when thinking about toxicology?

A

Which toxin was ingested, inhaled, or absorbed through the skin?

How much was taken?

When was it taken?

What was the patient doing when ill?

55
Q

What poisoning do you think of when someone has been working in a garage?

A

Carbon monoxide

56
Q

What poisoning do you think of when someone has been fumigating a ship?

A

Cyanide

57
Q

What poisoning do you think of when someone has been applying chemical to crops

A

Organophosphates

58
Q

Someone who has had physiologic excitation would present with …

A

CNS stimulation and elevations of HR, BP, RR, Temp

59
Q

Someone who has had physiologic depression would present with …

A

Depressed mental status and reductions in HR, BP, RR, Temp

60
Q

Examples of substances that cause physiologic excitation

A

Anticholinergics (URI meds, atropine, some antidepressents)

Sympathomimetics (cocaine, meth, bath salts and epi/NE)

Central hallucinogen agents (PCP, LSD, MDMA)

Drug withdrawal (EtOH)

61
Q

Examples of substances that cause physiologic depression

A

EtOH, methanol, ethylene glycol

Sedative-hypnotics (benzos, barbiturates)

Opiates (narcotics/pain meds)

Cholinergics (organophosphates)

Sympatholytics (clonidine, beta/alpha blockers)

62
Q

If mixed physiological effects, you should think…

A

Polydrug OD, exposure to metabolic poisons, heavy metals, or agents with multiple MOAs

Ex - metformin, sulfonylureas, ASA, cyanide, iron, TCAs, mixing of street drugs

63
Q

The _______ decontamination is performed, the more effective it is at preventing ___________

A

Sooner —> prevents poison absorption

64
Q

How to decontaminate topical exposures

A

Copious water or saline irrigation (protect yourself during this!!!)

65
Q

Should you use activated charcoal for decontaminating a patient who has ingested a toxic substance?

A

Less popular in recent years

Ask poison control!

Don’t do it unless it will HELP the patient and they can tolerate it

66
Q

What are some other examples of GI decontamination besides activated charcoal?

A
Gastric lavage
Whole bowel irrigation
Endoscopy
Surgery
Dilution
Cathartics

Consult a toxicologist to find out what to do!

67
Q

What are some procedures that enhance elimination of a poison?

A

Forced diuresis
Urine ion trapping
Hemodialysis
Exchange transfusion

68
Q

What is the cornerstone of treatment for poisoning?

A

SUPPORTIVE CARE

“Treat the patient, NOT the poison”

In some instances though there are known antidotes that are potentially lifesaving

69
Q

______ dramatically reduce morbidity and mortality in certain intoxications but they are unavailable for most toxic agents and therefore are used in only a small fraction of cases

A

Antidotes

70
Q

What are some ways in which antidotes work?

A

Prevent absorption
Bind and neutralize poisons directly
Antagonize end-organ effects
Inhibit conversion to more toxic metabolites

71
Q

Toxicity may recur if the antidote…

A

Is eliminated more rapidly than the ingested substance

Naloxone is a good example - reverses opioid effects but symptoms recur in approx. 1/3 of cases b/c the elimination half-life of naloxone is only 60-90 min and opioid half-life is longer

Some antidotes may require repeated administration or continuous infusion

72
Q

Just because you have an antidote, doesn’t mean you should always use it.

Take flumazenil for example…

A

It’s an antidote for benzodiazepines but can precipitate seizures in patients who use benzos chronically

73
Q

Antidote for acetaminophen

A

N-Acetylcysteine

74
Q

Antidote for Amitriptyline

A

Sodium Bicarbonate

75
Q

Antidote for anticholinergics

A

Physostigmine

76
Q

Antidote for beta-blockers

A

Glucagon

77
Q

Antidote for benzos

A

Flumazenil

UNLESS they use benzos chronically (seizures)

78
Q

Antidote for CCBs

A

Calcium!

79
Q

Antidote for Coumadin

A

Vitamin K, FFP

80
Q

Antidote for cyanide

A

Hydroxocobalamin/Nitrates

81
Q

Antidote for Digoxin

A

Digoxin antibodies (Digibind)

82
Q

Antidote for heparin

A

Protamine

83
Q

Antidote for hydrofluoric acid

A

Calcium

84
Q

Antidote for iron

A

Desferrioxamine

85
Q

Antidote for methanol/ethylene glycol

A

Ethanol

86
Q

Antidote for methemoglobin

A

Methylene blue

87
Q

Antidote for opiates

A

Naloxone

88
Q

Antidote for Organophosphates/anti cholinesterase SS

A

Atropine, 2-PAM

89
Q

Antidote for salicylates

A

Urine alkalization, dialysis

90
Q

Antidote for sulfonylureas

A

Octreotide

91
Q

What toxic substances do you test for with urine drug screens?

A
Opioids
Benzos
Cocaine
THC
Barbiturates
Amphetamines/methamphetamines
TCAs
Buprenorphine
92
Q

What toxic substances do you test for with serum screening?

A
Acetaminophen
Salicylate
Carboxyhemoglobin
Digoxin
Lithium
Iron, lead, mercury
Ethylene glycol
Antiepileptic drugs
93
Q

How long are amphetamines detectable in urine?

A

2-3 days

94
Q

How long is cocaine detectable in the urine?

A

2-3 days

95
Q

How long is marijuana detectable in the urine?

A

1-7 days (light use)

1 month with chronic moderate to heavy use

96
Q

How long are opiates detectable in the urine?

A

1-3 days

97
Q

How long is Phencyclidine detectable in the urine?

A

7-14 days

98
Q

Signs/symptoms that occur consistently as a result of a particular toxin, clinically notable and distinguishable by changes in vital signs and end organ manifestations

A

Toxidrome

99
Q

What labs should you do for ALL poisonings, toxidromes, and patients with AMS?

A

Serum pregnancy test in all women of childbearing age

Fingerstick glucose to quickly rule out hypoglycemia

Acetaminophen and salicylate testing to rule out common co-ingestion that can be fatal but have effective treatment strategies

100
Q

Examples of cholinergics

A
Organophosphates and carbamate insecticides***
Nerve agents (sarin)***
Nicotine***
Pilocarpine
Physostigmine
Edrophonium
Bethanechol
Urecholine
101
Q

What is the cholinergic toxidrome?

A

SLUDGE and the Killer Bs

Salivation
Lacrimation
Urination
Defecation
GI pain
Emesis

Bradycardia, Bronchorrhea, Bronchospams

Also, MIOSIS***

102
Q

How do you treat cholinergic toxidrome?

A

Aggressive decontamination (get the agent OFF)

Moderate to severe toxicity will usually require intubation

ATROPINE, ATROPINE, ATROPINE - to help dry them up
—> As much atropine as it takes (watch for pupils to dilate)

Pralidoxime (2-PAM) for organophosphates

103
Q

How does 2-PAM work?

A

Reactivates cholinesterase that had been inactivated by phosphorylation

104
Q

Anticholinergic Toxidrome

A

Blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone

The bowel and bladder lose their town and the heart runs alone

Causes: antihistamines, atropine, belladonna, jimson weed

105
Q

Earliest and most reliable sign of anticholinergic toxidrome

A

Tachycardia (“the heart runs alone”) - but not very specific

106
Q

How to treat anticholinergic poisoning

A

Control agitation with benzos

Consider activated charcoal if ingestion was relatively recent (must have relatively normal mental status and good airway)

PHYSOSTIGMINE - controversial but should be considered with poison control guidance

107
Q

Sympathomimetic toxidrome

A
Hyperthermia
Tachycardia/dysrhythmia
HTN
Diaphoresis
Agitation, hallucinations, paranoia
Dilated pupils
Seizures (more common than with anticholinergics)

Examples: cocaine, amphetamines, bath salts, caffeine

108
Q

What appears similar to a sympathomimetic toxidrome?

A

Alcohol withdrawal

109
Q

First line treatment for sympathomimetic toxidrome

A

Benzos

110
Q

Anticholinergics and sympathomimetics have very similar toxidromes EXCEPT…

A

Cutaneous:
Sympathomimetic = diaphoresis, moist mucous membranes
Anticholinergics = dry skin and mucous membranes

GI:
Sympathomimetic = hyperactive bowel sounds
Anticholinergics = decreased or absent bowel sounds

111
Q

Opioid toxidrome

A

“Cold depression”

Hypothermia
Bradycardia and hypotension
Bradypnea/apnea
Flash pulmonary edema***(esp in younger patient)
CNS depression, coma
MIOSIS
112
Q

Mainstay of treatment for opioid toxidrome

A

Supportive care and NALOXONE

113
Q

For chronic narcotic users that are breathing, how should you administer naloxone?

A

Start with lower doses (0.4mg) to avoid precipitating withdrawal

114
Q

Sedative-hypnotic toxidrome

A
Hypothermia
Vitals usually relatively normal (maybe Brady/hypotension)
Bradypnea/apnea
CNS depression, coma
Hyporeflexia***
VARIABLE pupils***

Examples: Benzos, barbiturates, alcolol

115
Q

What are roofies?

A

Flunitrazepam - 10x as potent as diazepam

Can cause sedative-hypnotic toxidrome

116
Q

How to treat sedative-hypnotic toxidrome

A

Supportive care - TINCTURE OF TIME

Rarely - flumazenil (but can induce seizures in chronic benzo users)