Alcohol Dependence and Withdrawal Flashcards
What is the approach used to tackle harmful drug use or dependence with a patient?
FRAMES
Describe FRAMES
1) Feedback → discuss risks and listen
2) Responsibility → up to them to change
3) Advice → change, harm minimisation
4) Menu → give people options e.g. AA, CBT
5) Empathy → non-judgemental
6) Self-efficacy → project optimism for change
What condition can result from alcohol withdrawal?
Delirium tremens (delirium in the setting of alcohol withdrawal)
What is the typical presentation of someone with delirium tremens?
1) Agitation
2) Sweating
3) Tremor
4) High BP
5) High pulse
6) High temperature
7) Seeing small animals
What are other symptoms sometimes present in someone with alcohol withdrawal?
1) Sensitivity to light and sound
2) Confusion → disorientated to time and place
3) Hallucination (visual)
4) Seizures
When do visual hallucinations usually occur?
In delirium or from medication, not really schizophrenia
What will someone’s BAC be if they are in alcohol withdrawal?
Might be 0 but might be high/over drink drive limit → if drinking excessive alcohol, can go into alcohol withdrawal after an hour of not drinking
How should you assess someone with alcohol withdrawal?
1) Use a structured tool e.g. CIWA → breaks down abnormalities into spectrums and gives score according to how deranged each spectrum is
2) Decide whether to give medication based on score
When is treatment critical in alcohol withdrawal?
First 2 days when there are early symptoms
Describe the time scale of delirium tremens
- Tends to hit on day 3 and peak and day 4
- Most of it calms down by at 7 but if complicated then it can carry on for a couple of weeks
What causes people to die of alcohol overload?
Acute increasing GABA activation and high chloride flow
What happens in chronic alcohol dependence to GABA receptors?
Makes GABA receptors less sensitive to excess alcohol
What is LTP (long term potentiation)?
The process where your brain converts short term to long term memory
Acutely, what does alcohol inhibit?
NMDA-mediated transmission and therefore LTP
What is the chronic alcohol on NMDA receptors?
Leads to receptor up-regulation (adaptation to mitigate against effects on memory)
What happens when you remove alcohol to NMDA and GABA receptors?
- NMDA-mediated transmission is increased
- Glutamate transmission potentiation (bc GABA usually modulates it and there are more receptors)
- Bc GABA modulates NA transmission → sweating tachycardia
- Dopamine → hallucinations
What is the mortality of delirium tremens?
10-25%
How do you treat delirium tremens differently from delirium?
- Need much bigger doses of benzodiazepines (much higher than BNF limits)
- Anti-psychotics don’t work as well + risk of causing arrhythmic arrest
What are risk factors for DT?
- Metabolic disturbances
- Sepsis
What is a cause of sepsis v common in people with alcohol dependence?
Aspiration pneumonia
How is the immune system different in alcohol dependence?
1) Macrophage activation and inflammation in the liver → innate immune system activation
2) Depression in adaptive immune response → so pneumococcal vaccine doesn’t work as well
3) Alveolar macrophages don’t work that well
What is Wernicke’s encephalopathy?
Acute confusional state secondary to thiamine (B1) deficiency
How does alcohol dependence/withdrawal lead to WE?
1) People who are alcohol dependent often struggle to eat bc nausea and vomiting are major side effects of alcohol withdrawal
2) Alcohol is toxic to the gut where thiamine is absorbed
3) Alcohol interferes with thiamine transport and conversion to its active form bc this is done in the liver
How does thiamine deficiency lead to WE?
1) Causes brain to malfunction bc thiamine is important in the Kreb’s cycle and brain needs glucose
2) Thin layered parts of the brain are more sensitive → problems in cerebellum and hippocampus
3) Leads to confusion and internuclear ophthalmoplegia (double vision and paralysis of lateral gaze)
What is the presentation of WE?
- Acting like drunk but not drunk
- Confused
- Can present as DT
- Classically triad of ophthalmoplegia, ataxia and confusion (but normally just look drunk)
How do you treat WE?
Parenteral thiamine → Pabrinex (thiamine + other B vitamins)
- Oral thiamine not effective in patients with alcohol withdrawal and they miss meals
- Window for effect is short
Why is treatment v important in WE?
Bc otherwise can develop Korsakoff’s syndrome (brain damage)
How long do you have thiamine stores?
A month
What is Korsakoff’s syndrome?
Inability to develop new memories → stuck at point that developed KS, can’t function
What questions do you want to ask to determine if someone is at risk of WE/KS?
1) Do you miss meals?
2) Do you suffer from pins and needles in hands or feet?
What are the imaging characteristics of WE (only present in 50% of cases)?
1) L sign → hyperintensity around third ventricle
2) Hyper intensities on T2 or FLAIR MRI
3) Contrast enhancement
4) Midbrain CN nuclei, PAG, maxillary bodies and medial thalamus
5) In established WE, maxillary atrophy
What is central pontine myelinolysis and what can it be caused by?
- Demyelination of pons
- Often people with alcohol withdrawal can become hyponatraemic and CPM can occur if try to reverse this too rapidly
What is another condition that can look the same as DT?
Hepatic encepholopathy
How do you exclude hepatic encephalopathy and why is it important to do this?
- Check bilirubin, albumin, NIR and whether they have a diagnosis of cirrhosis
- If give benzodiazepines, it can tip them into a coma
What are the symptoms of CPM?
Confusion, nausea, gait changes, hyperrreflexia
How can you determine if someone with alcohol withdrawal will suffer from DT?
1) Number of previous detoxifications → more likely if > 2 detoxifications
2) History of DT
3) History of seizures
4) Acute medical illness e.g. sepsis
5) Metabolic derangements e.g. low Cl, Na and K
6) High ALT and GGT → liver leaky and inflamed
How can you determine if someone with alcohol withdrawal will suffer from seizures?
1) History of seizures
2) GGT → indicates oxidative stress in the liver
What is the main treatment for someone in uncomplicated alcohol withdrawal and what does it do?
- Benzodiazepines → potentiate action of GABA, replacing alcohol with e.g. diazepam which has much longer half life (3oh)
- They break down into active metabolites which stay in system for 3-4 weeks
- Slows down process and reduces mortality of alcohol withdrawal, reduces severity, v effective
Which benzodiazepines do you give in people without cirrhosis and in people with cirrhosis?
- Without cirrhosis → diazepam/chlordiazepoxide (librium)
- With cirrhosis → lorazepam/oxazepam bc worried about accumulation and these break down into inactive compounds which are excreted
How do you give benzodiazepines?
Reduce dose over 5 days, cutting down about 20% each day
What are the two approaches to uncomplicated alcohol withdrawal treatment?
1) Symptom triggered
2) Fixed dose
Describe the symptom triggered approach to uncomplicated alcohol withdrawal treatment
- Measure alcohol withdrawal according to a scale 2-4 hourly for 24h then reduce dose according to that
- Requires adequate levels of staffing by nurses trained in assessment of alcohol withdrawal
Describe the fixed dose approach to uncomplicated alcohol withdrawal treatment
- Prescribe a fixed dose schedule estimating what you think the pt will need based on how much they drink
- Best idea for people at high risk of complications
- However risks excess sedation, longer stay than necessary (bc BZDs can make people delirious)
What are characteristics of interventions universal to people with delirium?
- Nurse 1:1
- Side room in order to reduce stimulation
- Family present to reassure if/when possible
How do you manage delirium tremens (more aggressive that uncomplicated alcohol withdrawal)?
1) Hourly high dose (1-2mg) lorazepam until symptoms controlled (or 20mg once 2 hourly, max 100mg/day) → after 4 hours decide whether need ITU or if situation is more controlled
2) Monitor for respiratory depression bc of high amount of BZDs and have flumazenil (BZD antagonist) PRN → need to worry about undiagnosed COPD bc smoking
3) Let ICU know bc risk of cardiac arrhythmic arrest
4) Let psychiatry know bc risks of behavioural disturbance and aggression
What else do you want to look out for and treat in DT?
Other contributions to the delirium e.g. sepsis, dehydration and catabolic derangements
What do you always have to treat additionally with DT?
As if WE is present (treatment dose of Pabrinex or at least preventative dose)
What is the preventative dose of Pabrinex?
1 pair of ampules x 3 lots IM or IV (IM v painful so preferably IV esp. for confused patient)
What is the treatment dose of Pabrinex?
2 pairs of ampoules 3 x day for 5 days
What treatment is often effective to treat depression in alcohol dependence?
Detoxification
What is alcohol a major modifiable risk factor in?
Suicide
