Neurocognitive DO - Collins Flashcards
What is Delirium
transient, reversible cognitive impairment
- acute onset; attention, awareness, cognitive and memory impacted
often fluctuating - 24 hour period
who is at higher risk of delirium
anyone adding “insult to injury”
- polypharmacy
-multiple medical co-morbidities
- sensory impairment (vision, hearing)
substance or alcohol use
What are the three likely causes of delirium
Drugs
Dehydration
Infection
what are mental status exam findings in Delirium
Attention impairment
altered LOC
disorientation
delusions/hallucinations/paranoia
confusion
disordered thinking and/or speech
erratic or irregular behaviors
irritability/agitation
lethargy/withdrawn
poor insight and or judgement
irregular sleeping/eating
What are the diagnostic criteria for Delirium
Disrupted attention/awareness
develops over a short period and fluctuates
acute change in cognition - memory, language, perception, thinking
What is CAM
confusion assessment method
sensitivity: 94-100%
Specificity: 90-100%
what is the difference between Delirium and dementia
delirium: acute, fluctuating, impaired awareness, disturbed attention, poor working memory, short lived or changing, fragmented sleep
Dementia: insidious onset, gradual deterioration, often clear awareness, often good attention, poor short-term memory, more fixed delusions, sleep-wake reversal
what is the treatment of Delirium
treat the underling cause - prevention is the best medicine
remove/treat any exacerbating factors
agitation: Haloperidol IM/IV
high mortality rates
higher risk for long-term cognitive and functional decline
What is Wernicke’s encephalopathy (WE)
first step on the continuum of Wernick-Korsakoff syndrome
acute neuropsychiatric disorder
reversible with appropriate treatment
what are the cerebllar tests
1 rapid alternating movement
2 finger to nose
3 gait and balance
4 heel to shin
5 pronator drift
If WE is left untreated what can happen
it can progress to Korsakoff’s syndrome - more often irreversible
what is the pathophysiology of WE
inadequate thaimine (B1)
ETOH use leads to - GI inflammation -reduced absorption
Poor nutritional intake
what is the classic presentation of WE
delirium
AMS
hypotension
+/- peripheral neuropathy
ataxia - broad based gait - inability to ambulate
Ocular: nystagmus, CN plasies, Sluggish pupils, ptosis, anisocoria
what is the classic Triad of Symptoms for WE:
AMS
Gait ataxia
Ophthalmoplegia (weakness/paralysis)
How is WE trated
Cessation of ETOH use
Thiamine replacement
MUST have thaimine prior to any glucose treatment in AUD patients