Alcohol Misuse Flashcards
What is the guidance for alcohol use?
[Volume (mls) x Alcohol by Volume ABV (%)] / 1000 e.g. 250ml of 12% ABV wine will be: [250 x 12 = 3000] / 1000 = 3 units
14units/week for M+F
Generally:
Safe/good to drink a small amount of alcohol, esp red wine, due to BP and HDL ↓- though probably wouldn’t advise this cuz people mix messages
Pregnant women: abstain in 1st trimester and no more than 2units/wk subsequently
Hazardous drinking:
22-50units/M
15-35units/F
Higher risk drinking:
50+units/M
35+units/F
What is some epidemiology for alcohol misuse in he UK?
3.5bn cost to UK society in 2016
1/3rd men + ¼ women exceed recommendation UK
UK 4th in the world for alcohol consumption
Increasing numbers of women that are harmful drinking
Socially acceptable, increased disposable income, advertising, friendlier drinking places
Forensics:
Alcohol involved in ½ violent crime and 1/3rd DA
What are some risk factors that may predispose to alcohol dependence?
Drinking with family from a young age
Childhood problem behaviours relating to impulse control
Early use of alcohol/nicotine/drugs
Poor coping responses to life stress
Depression is a cause not response of problem drinking
Other factors:
Personality, Biology, Family, Culture, Religion, Occupation, Availability, Peer group
How might alcohol misuse present?
Dependence: When the neurons adapt to the repeated drug exposure and only function normally in the presence of the drug Also characterised by - withdrawal symptoms (nausea, sweating, shaking and anxiety), tolerance (need for greater amount of substance for same effects), cravings (cognitive component of desire for drug), loss of control around alcohol
Might present incidentally on investigation or management for alcohol related conditions (pancreatitis, gastritis, HTN, heart attack, neuropathy, stroke, depression etc)
Liver disease:
50% have a fatty liver – though is reversible on stopping
10-20% of heavy persistent drinkers (20+units/day for 10-20 years) develop cirrhosis (People think that this would be higher and so you let patients think that too)
Mortality:
Accidents and violence
Malignancies
CardioV and CerebroV disease
How do you screen for alcohol excess?
CAGE questionnaire:
- ‘have you ever felt you should Cut down’?
- ‘have people Annoyed you by criticising your drinking’?
- ‘ever felt Guilty about the amount you drink’?
- ‘Eye opener - one to get up in the morning’?
2-3 indicates high suspicion, 4 is basically diagnostic
Also AUDIT - assesses quantity + frequency of use, dependence symptoms and problems from alcohol use = ‘gold standard’ assessment; 1-7 low risk; 8-15 hazardous; 16-19 - harmful; 20+ possible dependence
(Also MAST - Michigan Alcohol Screening Test)
Blood tests
What might a typical blood result look like for alcoholism?
Gamma-glutamyl transferase (GGT) - raised
AST>ALT - in alcoholic hepatitis, the ratio of AST to ALT is greater than 1 in 90 percent of patients and is usually greater than 2; the higher the AST:ALT ratio, the greater the likelihood that alcohol is contributing to the abnormal LFTs
Hb - low
MCV - raised
Possible micronutrient deficiencies secondary to insufficient dietary intake and renal loss:
Thiamine/B1 - most important
Mg
Iron
Folate/B12 (possibly responsible for macrocytic anaemia)
Carbohydrate-deficient transferrin (CDT) - can indicate relapse to heavy drinking following abstinence Ethyl glucoronide (EtG) + Ethyl sulfate (EtS) - urine biomarkers for alcohol breakdown
How do you treat alcoholism long term with medication?
Drugs for relapse prevention (not particularly effective):
Disulfiram (Antabuse) – hideous hangovers - irreversibly inhibits aldehyde dehydrogenase
Acamprosate – craving reduction
Naltrexone (specialist use only)
What affects the prognosis of alcoholism?
Most problem drinking is at home, pub drinking tends to be safer
Effects are exacerbated by lower socioeconomic class I.e. bank managers are more able to phone in sick than bank clerks
Any memory impairment from serious thiamine deficiency may be permanent
What is the epidemiology of Wernickes Encephalopathy?
More common in males (naturally due to the higher prevalence of male alcoholics = most common aetiology)
Wernicke’s lesions occurred in 12.5% of alcoholics but evidence to suggest that this is underdiagnosed
Risk factors
i) Alcohol = number one by far
ii) Also malnutrition, various GI diseases, cancer/chemotherapy
What is the pathophysiology of Wernicke’s?
Neurological symptoms due to biochemical lesions of the CNS after exhaustion of B1 (thiamine) reserves
i) Thiamine helps breakdown glucose – co-enzyme in TCA cycle; produce GABA and glutamic acid; lipid metabolism for myelin production
ii) Body has 2-3wks of reserves
Lesions:
Brainstem tegmentum – ocular – pupillary changes, extraocular muscle palsy, gaze palsy and nystagmus
Hypothalamus – vagal dysfunction – temp, cardiocirculatory and respiratory systems
Cerebellum – ataxia
Mamillary bodies – amnestic syndrome for recent memory (see the lost mariner case - Oliver Sacks)
Periaqueductal grey – reduction of consciousness
What is the key triad of symptoms in Wernicke’s present?
Is an acute confusional state (unlike Korsakoff’s) and an emergency
Ophthalmoplegia or generally eye movement disorders
(L-R lateral nystagmus most common)
Ataxia or other cerebellar signs (e.g. tremor)
Altered mental status e.g. confusion, delirium
Though don’t frequently all co-occur
Occurs after 2-3wks if no thiamine is consumed at all, as all stores are exhausted by then
What are some other features of Wernicke’s?
Pupillary changes, retinal haemorrhage, vision loss etc
Hearing loss
Fatiguability, irritability, apathy
Dysphagia
Seizures
Memory impairments, depression, psychosis
Polyneuropathy
Hypothermia = significant infection risk = significant cause of death
What is Korsakoff’s syndrome/psychosis? What are its 7 key features?
A chronic memory disorder caused by severe deficiency of thiamine
- Anterograde amnesia – post onset of syndrome memory loss
- Retrograde amnesia – may extend back some time – years in fact
- Fixation amnesia – loss of immediate memory, of past few minutes
- Confabulation – invented memories taken by patient as true gaps in memory
- Minimal content in conversation
- Apathy
- Lack of insight
When Wernicke’s and Korsakoff’s occur together = Wernicke-Korsakoff syndrome – most commonly co-diagnosed as such
80% of patients Dxed with Wernicke’s who abuse alcohol develop Korsakoff’s
What are delerium tremens?
Post acute alcohol withdrawal state
Usually begins 48-72hrs after withdrawal
Presentation: Anxiety attacks, severe depression Increased confusion Poor sleep + frightening dreams Low grade pyrexia Sweating Tachycardia (100-120bpm) Hallucinations provoking fear e.g. spiders, formication, Disorientation to time and place Hand tremor - coarse Ataxia
What is the mechanism for alcohol withdrawal?
Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
Alcohol withdrawal is thought to be lead to the opposite = decreased inhibitory GABA and increased NMDA glutamate transmission
What is the timeline for alcohol withdrawal?
Symptoms - 6-12hrs - shaking, sweating, tachycardia, anxiety, craving
Peak withdrawal +/-seizures - 36hrs
Delerium tremens - 48-72hrs
How do you manage alcohol withdrawal?
Patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised
Establish IV access
4hrly baseline observations
Benzodiazepines:
- Chlordiazepoxide is the benzodiazepine of choice to aid in acute withdrawals
- Often given as part of an individualised treatment plan based on a scoring system e.g. Glasgow Modified Alcohol Withdrawal Score (GMAWS) OR on a standardised reducing regimen
Pabrinex:
- As will be deficient in B vitamins
- SLOW IV usually 2-3x daily for 5/7 or until max clinical improvement gained; slow as if given fast there is an increased rate of anaphylaxis
- Also treat any other nutritional deficiencies (usually correctable)
Correct likely hypoglycaemia
- 5% glucose infusion
- Ensure thiamine given concurrently (or glucose before) otherwise Krebs cycle will consume remaining thiamine reserves and exacerbate condition/precipitate Wernicke’s
DTs:
Lorazepam PO or parentral if cannot tolerate oral; failing this haloperidol
If DTs occur during treatment regimen - review regimen
Seizures:
Short acting benzodiazepine e.g. Lorazepam - prevents recurrence of seizures
DO NOT use phenytoin for seizures
Arrange a gastro R/V
What options are there for detox?
Outpatient:
Saliva/urine sample - discussion of plan - pointing to local peer-support groups - keyworker assigned - may receive: CBT, drug wind-down program/substitute (chlordiazepoxide), meds to help you stop drinking (disulfuram, acamprosate)
Inpatient:
Similar support but in a more condensed time-frame, often for those at higher risk e.g. previous DTs/seizures
SPECIFIC CRITERIA?
What does Pabrinex contain?
Thiamine (B1) - the deficiency of which is the most concerning
Riboflavin (B2)
Nicotinamide/niacinamide (B3) - prevents pellagra (niacin deficiency)
Pyridoxine (B6)
Vitamin C
What non-pharmacological management is important in a patient admitted for alcohol withdrawal?
Factors to reduce delirium - private rooms, well lit but not at night, big clocks, continuity of staff, family presence
Arranging social care + outpatient alcohol service referrals
What is alcoholic hallucinosis?
Effectively an alcohol induced psychosis
Hallucinations +/- paranoia +/- delusions +/- mood disturbance) during or shortly following (24-36hrs) a period of heavy alcohol consumption
Often 3rd person auditory hallucinations, often derogatory or command; visual hallucinations not typical
Clears within 30 days (but can last another month)
Different from DTs:
Hallucinosis is rarer with a better prognosis and hallucinations are as above (whereas visual and tactile are more typical of DTs)
Absence of autonomic instability + are not disoriented
Hallucinosis may progress to DTs within the same episode however
Hospitalisation + treatment with an antipsychotic may be required
Once one episode has occurred, recurrence is likely with a subsequent increase in drinking; 5-20% go on to develop schizophrenia
