AMS/Delirium/Coma/etc, Flashcards
elements of mental status (7)
- Level of consciousness
- attention/concentration/memory
- speech and language
- visual spatial perceptions, executive function
- mood and affect
- thought content
- praxis
levels of consciousness
ALOC
alert and oriented
lethargic
obtunded
coma
praxis
performance of action in absence of primary deficits in motor and spatial ability
apraxia
inability to perform purposeful action
Altered mental status
alteration in consciousness characterized by:
disordered attention + diminished speed, clarity, coherence
AMS history
determine what is considered AMS for the individual patient
determine if problem is due to medical, psychiatric, neuro illness
what indicates neuro cause of AMS
memory problems
problems with thought = psychiatric
important signs on PE of AMS
abnormal vitals
depressed levels of consciousness
signs of toxidrome
focal neurological impairment
tools used to asses mental states (4)
Six Item Screener
CAMs
Glascow coma scale
brain death exam
six item screener
easier than MMSE in ED
broad, allows you to ID AMS
score below 5 indicates cognitive impairment
foremost concern when dealing with altered patient?
patient and staff safety!
steps in AMS management
- Quiet room and clam conversation
- Sedative (Lorazepam/Ativan)
- Chemical sedation (B-52 - Benadryl + Haldol + Ativan)
Delirium
special AMS characterized by increased vigilance with psychomotor and autonomic over activity
ACUTELY ILL **
epidemiology of delirium
30% of older medical pts during hospitalization
highest in elderly, cardiac surgery pts
more severe the illness, more likely to have presentation of delirium (ICU MC)
delirium pathology
multifactoral
disruption of reticular activating system
cytokine inflammation (I.e. sepsis) provokes microglia
Acetylcholine disregulation (I.e. 2/2 anticholinergic drugs) `
challenges in delirium history
first challenge: avoid bias
next: determine baseline
test done used to identify delirium
CAMS
CAM algorithm
- acute onset and fluctuating course
- inattention/distractibility
- disorganized thinking, illogical, unclear ideas
- alteration in consciousness
must have 1 and 2, either 3 or 4
delirium clinical presentation
ACUTE onset (over hours to days, persists for days to months)
disorientation, auditory/visual hallucinations
common in elderly and may be only finding of a more severe illness
etiologies of delirium (8)
MEDICATION LIST *****
alcohol withdrawal
CNS infection
sepsis due to systemic infection
electrolyte derangement
encephalopathy
CNS conditions
Systemic organ failure
hepatic encephalopahty
medications causing delirium
- sedating medications
- over the counters
- drug withdrawal/alcohol withdrawal
- poisons
- polypharmacy
- side effects from medications
delirium tremens
most severe form of alcohol withdrawal
severe hallucinations, disorientation, tachycardia, HTN, fever, agitation, diaphoresis
can persist for 1 week, be fatal (cardio)
delirium tremens diagnosis
clinical features (hx of alcoholism withdrawal symptoms
delirium tremens prevention
Benzo bolus if suspected or history of withdrawal seizures
management of delirium tremens
supportive care
benzos IV/PO
severe: phenobarbital/propofol/dexmedetomidine
CNS infections and delirium
meningitis and encephalitis can cause
if unsure source of delirium, consider a LP
systemic infection delirium
UTI, PNA, cellulitis, intra abdominal infection
wernicke’s encephalopathy
uncommon cause of delirium
due to thiamine (B1) deficiency
typically in alcoholics, hemodialysis pts
clinical triad of wernicke’s encephalopathy
encephalopathy (delirium)
oculomotor dysfunctoin
gait ataxia
Korsakoff syndrome
untreated wernicke’s encephalopathy
form of dementia/psychosis, memory loss, lack of insight, apathy, and confabulate
can cause coma, death
tx of korsakoff/wernicke’s
500 mg thiamine IV
daily thiamine
glucose and thiamine
administration of glucose can cause the encephalopathy bc glucose causes thiamine reserves to be used up
Hepatic encephalopathy
caused by cirrhosis, due to impaired clearance of ammonia and other toxins
clinical présentation of Hepatic encephalopathy
cognitive defects with impaired neuromuscular function
bradykinesia, asterixis
Hepatic encephalopathy management
supportive, restrict protein intake
lower ammonia levels via: lactulose, rifaximin
hypercarbia induced delirium
found in pts with COPD
given too much oxygen, slowing down drive the breathe therefore causing levels of CO2 to increase
check ABG in pts with delirium
mimics of delirium
dementia (insidious, chronic)
non convulsive epilepsy
primary psychiatric disorders (depression, mania)
diagnostic tests for delirium
common labs (chem panel + tox)
EKG, CXR
CT Scan
LP ( + CT)
tx of delirium
treatment of underlying condition
close monitoring
pharm is risky bc can worsen delirium (haldol for agitation)
when are physical restraints used in delirium
immediate threat to themselves or others
only for a short period of time
coma
un-arousable, unaware of surroundings
unresponsive to external stimulation
within 2 weeks, will either go to one of two categories
two categories of coma pts
persistent vegetative state
brain death
persistent vegetative state
wakefulness without awareness or surroundings
no movements, no interaction with others
brain death
irreversible cessation of cerebral brainstem function
acute coma
acute alteration in arousal
life threatening, prompt intervention required
historical information for coma pts
DRUG USE history (illegal, prescription)
recent illness
focal neuro losses
recent trauma?
general exam of pt with coma
vital signs + ABCs skin pupillary response, eye movements reflexes Glasgow coma scale
which way do the eyes go in caloric testing?
movement towards stimulus
coma neuro exam
coma postures
decorticate
decerebrate
flaccid
pts in persistent vegetative state are which coma posture
flaccid
decorticate posture
damage to cerebral hemispheres, internal capsule and thalamus
NOT brain death
decerebrate
damage to brain stem
NOT brain death
progression from decorticate indicates herniation
brain death
hypoxic-ischemic brain injury
via cardiopulmonary arrest, vascular catastrophe, poisoning, head trauma
absence of cerebral and brainstem function
req. to diagnose brain death
- imaging of acute CNS catastrophe
- exclusion of other conditions that may have confounded assessment
- no drug intoxication
- core temp >97
- SBP > 100
brain death exam
imaging
neurologic exam to determine absence of function
apnea test
response that indicated brain stem dysfunction? Brain death?
oculocephalic and caloric response
asymmetric = brain stem
non response = coma
apnea test
done in brain death patients to determine if spontaneous respirations occur
can’t be don for those with spinal cord injury, nmj paralysis, high CO2 retainer history
spinal reflexes and brain death
some reflexes come from the spine therefore present despite brain death
facial nerve movement, finger movements, Lazarus (neck displacements)
liver mortis
lividity that occurs to the corpse after death due to pooling of blood from gravity
20 min - 3 hrs after death
causes of dizziness
peripheral vertigo (in ear) central vertigo pre-syncope disequilibrium nonspecific dizziness
key historical aspect of vertigo
indicators of peripheral vertigo
exacerbate via head movement
transient nystagmus
Dix Hallpike maneuver provokes it
indicators of Meniere’s Dz
peripheral vertigo
hearing loss or tinnitus
tx of vertigo
medications that suppress vestibular system
antihistamines, phenothiazine, benzos
suggestions of central vertigo
ataxic gait, HA, doubled or loss of vision, slurred speech, numbness, weakness, clumsiness, incoordination
non contrast CT
