ETOH WITHDRAWAL & COMPLICATIONS Flashcards
If you newly hospitalized patient is experiencing insomnia, tremulousness, mild anxiety, GI upset, HA, diaphoresis, and palpitations – what might be going on?
ACUTE alcohol withdrawal
What are the 2 major components of alcohol treatment?
Repletion & Psychomotor Agitation
What is involved in repletion treatment?
Banana Bag (IVF, dextrose, Vits/Minerals – especially THIAMINE!!)
Electrolytes (CMP, Mg, and Phos)
What is involved in psychomotor agitation treatment?
BENZOS
Clinical institute Withdrawal Assessment (CIWA)
What are our goals of treating acute alcohol withdrawal?
Symptom management
Observation
Bridging to long-term recovery
When we are observing an acute alcohol withdrawal – what are we looking for?
Delirium tremens
Wernicke’s encephalopathy
Chronic conditions
When does delirium tremens often appear?
48-96 hours after last drink
If a patient is withdrawing from alcohol and now they have delirium, hallucinations, tachycardiac, HTN, and hyperthermia – what is going on?
Delirium tremens
Why is it important that we recognize delirium tremens as its own diagnosis?
There is a mortality risk when delirium tremens sets in (5% nowadays)
How do we treat delirium tremens?
Needs to be in a critical care unit!! IV BENZOS (can be massive doses)
May need aggressive critical care intervention (phenobarbital for seizing)
Get specialists on board (neuro, psych)
What is the triad of Wernicke encephalopathy?
Delirium
Gait Ataxia
Oculomotor Dysfunction
*****
What causes WE? Is WE acute or chronic?
Cause = Thiamine deficiency
ACUTE!!
If we don’t treat Wernicke encephalopathy – what can happen?
Leads to a coma and death
Does a normal Thiamine level exclude WE?
Nope – we don’t even need thiamine levels if they have the triad of sxs!
What can precipitate WE?
Glucose **AKA watch levels when you administer the Banana Bag
How do we treat WE?
Thiamine (500mg x2 days → 250mg x5 days → PO supplementation – but ONLY if they’re still at risk)
What is a consequence of untreated or repeated episodes of WE?
Korsakoff’s Syndrome → chronic, late, neuropsychiatric disorder
What is Korsakoff’s syndrome characterized by?
Cognitive impairment, retrograde amnesia, and brain imaging for atrophy
How do we confirm the diagnosis of Korsakoff’s syndrome?
Specialized neurocognitive testing
If a patient has gait ataxia, poor gross motor coordination, and inability to hand write, dysarthria – what is occurring?
Cerebellar Degeneration
How do we differentiate the gate ataxia with WE and cerebellar degeneration?
Look at the eyes = WE
Cognitive capability remains intact = Cerebellar
If a patient withdrawing from alcohol has JUST hallucinations (no tachy or hyperthermia) – what are we concerned about?
Alcoholic Hallucinations
*Often confused with DT or WE
When do alcoholic hallucinations present?
24 hours AFTER the last drink
If a patient has little twitches or burning pains in the extremities – what is occuring?
Peripheral neuropathy (neuromuscular complication from long term alcohol use)
If a chronic alcoholic and has developed myopathy – what do we need to watch out for?
Rhabdo, Dysphagia, and Heart Failure
Your patient being treated in the hospital for alcohol withdrawal – you notice gait ataxia, nystagmus, and he’s unable to complete a MMSE – what diagnosis? Tx?
WE
Tx = IV Thiamine
The same patient has shown improvement of his WE over the past couple days, but later in the day, he becomes hard to arouse and seems confused. The nurse gets new vitals: HR 120, BP 180/100, and T of 101 – what is going on? Tx?
DT’s
Tx = Diazepam and continue Thiamine
