Altered Mental Status Flashcards
What constitutes mental status (2)?
- Arousal-awake state, RAS & upper brainstem
2. Content: language & reasoning, communication btwn hemispheres
Delirium may be (4)
ACUTE acute confusional state acute cognitive impairment acute encephalopathy altered mental status
Dementia types
CHRONIC
a. Alzheimer’s
b. AIDS related
Delirium definition and it’s effects on 3 areas
TRUE MEDICAL EMERGENCY
acute onset & often fluctuation of impaired awareness, easy distraction, confusion, disturbance of perception
CONSCIOUSNESS: somnolence or agitation
COGNITION: disorientation & memory deficits
PERCEPTION: hallucinations or delusions
Dementia definition & its effect on 3 areas
CHRONIC w/steady decline in short then long-term memory
CONSCIOUSNESS: varies
COGNITION: often subtle changes in orientation initially then progressively worsening
PERCEPTION: clear
Risk factors for delirium/dementia
age>60 alcohol or drug addiction hx of brain injury dementia >3 medications
Mental status
- involves determining level of consciousness (U) -documented as “alert & oriented x3”
- may be 4th area-sphere or situation (event)
What constitutes an altered mental status?
ANY change in either alertness or orientation
Levels of consciousness (5)
a point on a continuum, 5 levels:
- alertness
- lethargy or somnolence
- obtunded
- stupor or semicoma
- coma
Alertness definition/description (4)
- awake & fully aware of normal external & internal stimuli
- can respond appropriately to any normal stimulus
- able to interact in a meaningful way
- altertness DOES NOT IMPLY the inherent capacity to focus attention
Lethargy or Somnolence definition/description
pt, not fully alert, TENDS TO DRIFT OFF TO SLEEP WHEN NOT ACTIVELY STIMULATED
- ↓spontaneous movements & limited awareness
- when aroused, (U) unable to pay close attention, may lose train of thought & wander from topic to topic
Obtunded: def/description
transitional state btwn lethargy & stupor:
difficult to arouse, when aroused they are CONFUSED
-constant stimulation required to elicit marginal cooperation from patient
-obtunded patient may be acutely confused or in a state of quiet delirium
Stupor or semicoma: def/description
used to describe patients who RESPOND TO ONLY PERSISTENT & VIGOROUS STIMULATION
-doesn’t rouse spontaneously, when aroused can only moan, mumble or move restlessly
Coma def/description
- traditionally applied to patients who remain with their eyes closed & are unable to be aroused
- does not respond to external or internal stimuli
Orientation: in what order do you lose it (3)
lose orientation to TIME, then PLACE, then PERSON
etiologies for a change in orientation (2 broad)
organic vs. psychiatric
Orientation includes which states (5)
confused, delusional, post-ictal, delirium, dementia
Nontraumatic etiologies of altered mental stats
hypoxemia hypo/hyperglycemia medical conditions OD/withdrawal Wericke's encephalopathy sepsis seizure d/o stroke psychiatric d/o
Traumatic etiology of altered mental status
hypoxemia acute brain injury acute spinal cord injury hypovolemia psychogenic
What causes Altered Mental Status
'DEMENTIA' Drugs Electrolytes Metabolic Emotional/psychiatric Neurologic/nutritional Trauma, tumor, temperature (syncope, seizures) Infection, inflammation Alcohol (use, OK, withdrawal)
What are the ABC (D)s
airway
breathing
circulation
dextrose (get finger stick blood sugar)
What do you want to pay attention to over time during the hospital stay?
VITAL SIGNS
What do you do when assessingrespiratory status
rate & effort
supplemental oxygen
How to assess circulatory status
presence of pulses & quality
direct pressure over any obvious bleeding
What must do before the rapid initial assessment?
make sure ABCs are good
Rapid Initial Assesment: what is it
a rapid ‘visual survey’ from head to toe
initial impression of mental status
any obvious signs of airway compromise, breathing difficulty or trauma
Initial impression of mental status
"AVPU" Alert Voice Pain Unresponsive or Unconscious if none & pupillary response
Coma Cocktail Contents
Thiamine 100mg SIVP (slow IV push)
D50 (50% glucose in water) 50 ml (25gm) over 3-4 mins
Naloxone .8-2mg IVP
When to give the coma cocktail?
How might you determine what caused this
if the pt is unconscious & unresponsive w/no history
-if they wake w/in 2-3 mins, then the dx is likely either hypoglycemia or opiate OD
if not, keep looking
Laboratory workup in altered mental status
Blood: CMC, CMP (glucose, electrolyties, Ca/Mg, hepatic/renal fxn, thyroid panel), BAL, drug levels, blood cultures, ABG
Urine: UA, culture, UDS
Others: CSF
EKG, CXR, other x-rays as indicated, CT scan
Important components of history in altered mental status
- try to determine baseline mental status
- onset & duration of current episode
- any specific complaints
Physical Exam in altered mental status
[exam might not be done iin the (U) head-to-toe manner]
Vitals: repeat often
Skin: color, moist/dry, temp, flushing, needle tracks/sores
Neck: check for meningeal irritation, JVD
Chest: breath sounds, heart sounds, chest wall integrity
Abdomen: soft, rigid, bowel sounds, organomegaly
Neurologic: stability of pelvis, movement
Psych: agitation, tremulousness, hallucinations
fruity breath odors a/w (3)
DKA, nitrites, isopropyl alcohol
bitter almonds breath odor a/w
cyanide
rotten eggs breath odor a/w
hydrogen sulfide
oil or gasoline breath odor a/w
hydrocarbons
odorless but fluorescent green breath a/w
ethylene glycol (antifreeze)
pharmacokinetics refers to
body’s processing
pharmacodynamics refers to
effect of drugs & their MOA
In elderly, how often can altered mental status be attributed to medications
22-39%
If someone was fumigating a ship when they exp. altered mental status, they may be intoxicated by and you would note
cyanide
bitter almond breath smell
In altered mental status a/w drug intoxication, what questions should try you answer?
which toxin was ingested, inhaled or absorbed through the skin
how much was taken?
when was it taken?
Causes of CHOLINERGIC poisoning (3)
- organophosphates
- nerve gas
- mushrooms
CHOLINERGIC POISONING treatment
2-PAM (pralidoxime)
or
Atropine
Cholinergic poisoning: symptoms onset when
may lead to (4)
most are symptomatic within 8 hours
may lead to seizures, coma, respiratory & circulatory failure
Cholinergic intoxication symptom mnemonics
SLUDGE+Killer Bs Salivation Lacrimation Urination Defecation GI pain Emesis Bradicardia, bronchorrhea, bronchospasms -also muscle weakness
ANTICHOLINERGIC intoxication sxs
hot as a hare (FEVER), blind as a bat (MYDRIASIS), dry as a bone (decreased BS, urinary retention, dry MM), red as a beet (flushing), mad as a hatter (toxic psychosis)
Causes of anticholinergic intoxication (4)
- cyclic antidepressants
- antipsychotics
- antihistamines
- Jimson weed
Anticholinergic intoxication tx
observation, monitoring (including temperature) & good supportive care
IE-you REALLY CAN’T REVERSE THESE
Cardiovascular effects of TCA intoxication
pulmonary edema, anticholinergic effects, AV blocks (Na/K blockade), hypotension
CNS effects of TCA intoxication
confusion, agitation, hallucinations, seizures or coma
TCA intoxication tx
EKG monitoring, activated charcoal, Sodium Bicarbonate, benzodiazepines
Opioid intoxication sxs& tx of intoxication
CNS depression, miosis, respiratory depression
-ventilation & naloxone
Sympathomimetics (Coke & meth) intoxication sxs & tx
psychomotor agitation, hydriasis, diaphoresis, tachycardia, hypertension
if sever or prolonged: rhabdomyolysis, MI
tx-cooling, sedation, hydration
Acetaminophen antidote
Acetylcysteine
Anticholinergics specific antidote
Physostigmine
Benzodiazepines specific antidote
Flumazenil
Narcotics specific antidote
Naloxone
Digoxin specific antidone
Digibind
3 most common drug withdrawal types
- Delerium tremens (alcohol W/D)
- Sedative-hypnotic withdrawal
- Withdrawal seizures
Sedative-Hypnotic withdrawal occurs when, often involves which drugs
occurs when pt has been taking large doses or drug over a period of 1 month or more & has abrupt discontinuation
-frequently involves barbiturates & benzodiazepines
Clinical findings a/w sedative-hypnotic withdrawal (6)
- agitation
- tremor
- nausea/vomiting
- tachycardia
- hallucinations
- flushing
for benzos sxs may not be present for several days after d/c
Sedative-hypnotic withdrawal tx
give short acting barbiturate then switch to equivalent dose of long-acting
INITIALLY give PENTOBARBITAL 300mg PO or 200mg IM q 2 hrs; repeat until patient becomes aroused
switch to PHENOBARBITAL PO then taper the dose over a max of 10 days
may need to reintroduce a benzo
Withdrawal seizures occur with which substances & occur when
often earliest manifestion of abrupt decrease or abstinence from alcohol
-may be seen w/some sedative/hypnotics also
~90% of seizures occur between 6-48 hours after abstinence
What happens if withdrawal seizures are left untreated
about 30% will go to develop DTs
Withdrawal seizures: associated clinical findings
(U) focal seizure activity rather than tonic-clonic activity
- pt may still be able to respond to verbal stimuli
- rarely will lose bowel/bladder control
- (U) NO post-ictal state
Tx of withdrawal seizures
(U) self-limited & do not require anticonvulsant therapy
- close observation for first 24 hours for reoccurrence of seizure activity
- repetitive seizures may need single dose of Phenobarbital or Valium
…Dilantin is INEFFECTIVE
What is the most common electrolyte abnormality
hyponatremia
When do neurological sxs occur in hyponatremia?
when serum sodium levels fall below 120 mEq/L
Elecrtrolyte abnormalities present with:
delirium, drowsiness & lethargy
-can progress to seizures & coma
Treatment of electrolyte abnormalities?
aimed at underlying cause
Common etiologies of metabolic disturbances in AMS?
endocrine, renal & hepatic d/os
- can also see with thyroid storm
- look for hx of pre-existing systemic dz
systemic metabolic dz AMS presentation
market fluctuation in patient’s mental status w/intermittent periods of lucidity
& no focal abnormalities is characteristic of metabolic encephalopathy
What should you think about first in metabolic dz a/w metabolic disturbances?
think endocrine first: hypo- or hyperglycemia (DM?), thyroid storm
hx (U) most helpful
physical exam rarely reveals etiology
How to distinguish metabolic etiology vs. acute psychiatric etiology in AMS?
may be difficult
in acute psychiatric dz, orientation to person may be as altered as to time & place (rare in organic dz)
Psychotic pts (U) retain recent memory & are able to perform single calculations (rarely preserved in organic states)
Hallucinations
Psychosis= (U) auditory
Metabolic= (U) visual
in a large & or psych d/o there is coexisting etoh/drug use/abuse
Acute stroke presentation
can vary widely
AMS, dyspasic or slurred speech, loss of movement and/or strength of one or both sides of body, asymmetrical facial features
if resolved w/in 24hrs, may be TIA
Post-ictal states AMS
period after seizure when pt gradually has clearing of mental status
- known hx of seizure d/o, witnessed seizure activity
- may have loss of bowel/bladder control or fxn
- should return to pre-ictal state within abt 1 hour
Thrombotic Thrombocytopenia Purpura: description, affects who, rltd to/cause, tx
acute onset of fever, bleeding/rash, renal failure, neurologic changes
(U) affects women 20-40yo
-may be related to drugs, pregnancy, lupus infection
Cause: rltd to von Willebrand Factor where form small blood clots
Tx: plasma exchange & steroids
In acute head trauma, there is a good chance of what?
good chance of spinal trauma so PROTECT THE SPINE
-need thorough assessment to determine if there is a spinal cord injury
NEXUS criteria
CANNOT clear C-spine if: Intoxication Distracting injuries Midline posterior point tenderness Any alteration in mental stats Focal neurologic deficits
Diagnostic exams/studies used in acute head trauma
CT (U) most helpful dx study
C-spine films
Rectal exam:
sphincter tone intact=injury is LIKELY intracranial
little or no tone=coexisting spinal cord injury
repeat neurological examinations
Hypothermia: temp, physiological responses
skin temp near 91 F
peripheral vasoconstriction, shivering, altered mental status, cardiovascular changes, respiratory changes
Moderate hypothermia
92-86 F
apathy, lethargy, ataxia
Hyperthermia: types (2), temps & signs a/w each
Heat exhaustion: core temp may be normal 106F
signs: may be all above except CNS dysfxn
In very young or very old ppl. with AMS, what should you think abt?
infection
elderly: urosepsis, pneumonia
infants: meningitis, sepsis
How might infection/inflammatory AMS present?
may not be febrile
lab studies will most often reveal cause
-inflammatory cause rarely seen in ED (may be seen in lupus, giant cell arteritis, sarcoidosis)
Acute intoxication effects/sxs
produces metabolic encephalopathy similar to that produced by sedative-hypnotic drugs
peripheral vasodilation, tachycardia, hypotension, hypothermia
When does stupor occur?
in non-chronic alcoholics, stupor occurs when BAL reaches 250-300 mg/dL
chronic alcoholics: ALL BETS ARE OFF!!!
Wernicke’s Encephalopathy:
what is it, what causes it, what is it characterized by, a/w, progression
medical emergency caused by ACUTE THIAMINE DEFICIENCY coupled with CONTINUED CARBOHYDRATE INGESTION
characterized by ophthalmoplegia, ataxia & confusion
most cases a/w alcoholism, malnutrition or both
failure to recognize & tx may result in death or permanent neurologic impairment
More findings a/w Wernicke’s encephalopathy
ophthalmoplegia, ataxia & confusion
- Nystagmus: horizontal, vertical or both
- Sixth CN palsy
- Truncal ataxia: wide-based, unsteady gait
- May have extremity ataxia only, but less (C) than truncal
- Confusion: frank delirium in 20% of cases
- Apathy, decreased spontaneous speech
- Tachycardia
- Exertional dyspnea
- Minor EKG abnormalities
- Orthostatic hypotension
- Peripheral neuropathy in ~80% of cases
Sixth CN palsy: which mm. effected
lateral rectus
(fyi:LR6
SO4
AO3)
Treatment of Wernicke’s encephalopathy
Thiamine 100mg IV immediately
continued IV infusion of 50mg per day along w/multivitamins->aka. “banana bag”
-Magnesium deficiency common, give IV replacement
-Bed rest b/c of fragile cardiovascular status
Delirium Tremens (DTs): prevalence, when & how long does it occur
uncommon but life-threatening illness seen in practicing alcoholics after abstinence
(U) appears after 3-4 days of abstinence from alcohol
duration of DT is less than 24 hours in 15% and less the 3 days in 80% of cases
clinical findings a/w delirium tremens
- profoundly delirious state a/w tremulousness & agitation
- excessive motor activity & purposeless activity such as picking at the bed sheets
- hallucinations, typically visual
- tachycardia, dilated pupils, fever, excessive sweating
- no sense of situation or sphere
Tx of delirium tremens
monitor for hypertension & hyperprexia
pt (U) dehydrated-needs fluid replacement therapy
Thiamine 100mg per day (IV/IM)
Multivitamin, esp. B complex & vit C
LIBRIUM (a benzo) for more tapered withdrawal & to prevent seizures
7 most common causes of AMS
- Neurological-28% (stroke, seizure, etc)
- Toxicologic-21%
- Trauma-14%
- Psychiatric-14%
- Infectious-10%
- Endocrine/Metabolic-5%
- Pulmonary-3%
Major Medicolegal Pitfalls
- failing to exclude organic causes for mental status changes
- vital signs are overlooked
- beware of occult changes in mental status
