Alcohol and Alcohol Abuse
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Alcohol is the most dangerous addictive drug in the world. It kills around 15 Australians every day. Alcohol abuse is widespread in Western Society, and is a common presenting complaint in Emergency Departments, both with and without clinical manifestations.

The recommended weekly intake of alcohol is:

  • 14 Units for all individuals (regardless of gender) – UK Guidelines
  • No more than 2 standard drinks on any given day, and 2 alcohol-free days per week – Australian Guidelines
The recommendations were previously sex-based – with a higher limit (21 units) for men. In 2016 the general based difference was removed.
  • For the same amount of alcohol ingested, women will have a higher blood alcohol level. This level is related to the % of body fat – which of course for women is higher.
Using a units-based method of alcohol intake is not always very easy to convey. There is also some evidence that having ‘alcohol free days’ reduces the risk of long-term complications.
In an attempt to simplify alcohol recommendations, Australia recommends “No more than 2 standard drinks on any day, and 2 alcohol-free days per week”.
The way a ‘standard’ drink is defined is slightly different to a unit, but the two are similar.
  • One unit is 10ml of alcohol
  • One ‘standard drink’ is 10g of alcohol – this actually equivalent to about 12ml of alcohol
To work out the number of units:
Volume Drunk (L)     x       % of alcohol       =      Units
e.g. for a large bottle of vodka:
                                1L   x    40%   = 40 Units
A pint of beer is roughly 0.5L, so in this example you can just ½ the % to get the units – e.g. a pint of 4% is about 2 units.
How much is a unit?
Bottle of wine
9 units
Glass of wine (large – 250ml)
3 units
Bottle of spirits
30 units
Pint of beer
2 units
Strong pint of beer
3 units
Alocpop bottle
2 units
Bottle of cheap cider
10 units
A bottle of spirits has roughly 40% alcohol by volume; which equates to 70% alcoholic proof.
10ml of pure alcohol is ‘one unit’
Susceptibility to alcoholic disease varies widely. 1/3 of serious alcoholics will get cirrhosis. Some may drink 500 units a week for years, and never have any liver problems, but some might drink 100 a week for a year and already start to show serious signs of damage.
It is important to make a distinction between dependence and misuse. Many people misuse alcohol, but not all are dependent. Sign of dependence may include:
  • Withdrawals
  • Cravings – very strong desire to drink
  • Drinking despite negative consequences:
    • On their physical health
    • On their mental health
    • On their social / work life
  • Tolerance – this is said to occur when the individual has to drink larger amount of alcohol to obtain a similar effect.
  • Primacy (put drinking before other activities) – neglecting other activities
  • Loss of control
All of the above factors are true for drugs as well as alcohol. The factors below are specific for alcohol.
  • Rapid re-instatement – people who have stopped drinking, once they start again, they rapidly get up to the level they were previously drinking
  • Narrowing of repertoire – as people become more dependant on alcohol, the range of beverages they drink decline – so that eventually they may only drink 1-2 types of drink. Usually this is the cheapest available. Also, their drinking habits alter, so where as before they may have drunk at the pub, at home, out for a meal, with various people, they tend to often drink just at home, or at the pub, with a very small social circle.
‘Problem drinking’ / misuse of alcohol
We say that this occurs when the consequences of alcohol involve social, physical to psychological harm to an individual.


  • There is a decline in alcohol problems with age
  • Black / Asian / Ethnic minority populations tend to have:
    • Fewer people with ‘an alcohol problem’
    • A similar proportion with ‘alcohol dependency’
  • 20% of psychiatry admissions are due to alcohol
  • Alcohol drinkers are over-represented in hospital – due to the issues alcohol causes:
    • E.g. in A+E – drunken fights etc
    • E.g. on gastro-ward – alcohol related illnesses
    • Some estimates say 30% of hospital admissions are alcohol related

‘An Alcohol Problem’:

  • 38% of men
  • 16% of women
  • (26% overall) – 8.2m people in UK

Bing Drinking

  • 21% men
  • 9% women

Alcohol Dependence

  • 6% men
  • 1.2% women
  • (3.6% overall) – 1.1m People in UK


  • Genetic factors – studies on adopted children have shown that the child is more likely to become an alcoholic if one of their parents is, whether or not they live with the parent. if you have a sibling with an alcohol addiction, you are 2.5x more likely to have one yourself
  • Psychological factors – children who are impulsive, aggressive and hyperactive are more likely to have alcohol problems as adults
  • However!there also is an increased risk for those with anxiety – because having a drink can relax people and take away their anxiety – which can lead to alcoholism. To compound the situation, when withdrawal begins, it can initiate even more anxiety – so there is a vicious cycle.
  • Cultural factors and availability of alcohol

Learning more about addiction and the Stage of Change model might be useful at this point.

Who are the heavy drinkers in society?
  • City Workers
  • Barmen (drink 7x greater than average)
  • Chefs (5x)
  • Publicans (10x)
  • Seamen
  • Architects and accountants drink the least
  • Doctors drink just very slightly above the average. Psychiatrists are significantly higher than other specialities.
Which nation are the heaviest drinkers?
  • Russia
  • Scandinavia
  • Eastern Europe
  • France
  • Britain (above average, but not as high as those mentioned above)

Physiology of alcohol and pathological consequences

When we talk about ‘alcohol’ we are actually referring to ethanol.
Alcohol is a CNS depressant. It enhances the effect of the inhibitory neurotransmitter GABA. This has an overall inhibitory effect on neurons. Initially, there is a depression of inhibitory neurons (making you feel ‘relaxed’ and disinhibited), but gradually, there is inhibition of many areas of all CNS functions.
  • The first areas to be affected are those responsible for learned ideas and tasks, whilst mechanical inhibition comes later on.
  • Despite what you may believe at the time – there is no increase in any mental or physical functions – unless these have been previously suppressed by anxiety (e.g. nervousness).
  • All the effects of alcohol are very closely related to the blood alcohol concentration. However, in those with dependence, tolerance can reduce these effects.

Cardiovascular effects

  • Moderate intake – can be cardio-protective – as it reduces the aggregation of platelets, and increases HDL’s. The type of alcohol drunk is probably not important.
    • This effect is probably greatest at 1U/day, and is lost at >3U/day.
  • Higher Intake – increases BP by increasing sensitivity to catecholamines. This increased the risk of IHD, CVA’s and stroke.
  • High intake – can cause arrhythmias – especially AF. This can occur either in acute or chronic alcohol abuse.
    • Alcoholic cardiomyopathy is a dilated cardiomyopathy caused by alcohol. It will only partially recover when alcohol intake is reduced. It can lead to heart failure. 10U/day for 8-10 years will cause this.
    • It is the 3rd most common type of cardiomyopathy. It causes thickening of the heart muscle, which will produce enlarged ECG traces. The most common complication of this is atrial fibrillation, although ventricular fibrillation is not unheard of can be deadly.
  • In the short term, alcohol is generally a vasodilator – that is why people often feel warm when they have had a drink – but in reality you are more likely to lose body heat. In some circumstances (e.g. drunk man falls asleep on park bench), this can result in hypothermia.
Plasma conc.*
Mild pleasant effect, due to suppression of inhibitory pathways in the cortex. Increased risk of accidental injury, more open about emotions and personal details
Legal limit for driving in the UK. For a 75kg (average) man, this is approximately equal to 2 normal strength pints (3-4%) in the first hour of drinking, and 1 further pint every subsequent hour (i.e. you can drink a lot!). The risk of injury in a road accident is doubled
Speech becomes slurred, and other motor abilities are affected
Often produces loss of consciousness
May be fatal – due to respiratory and vasomotor suppression.
*(mg per 100ml, which is the same as BAC%)

Hepatic effects

  • Hypoglycaemia – the metabolism of alcohol produces excess protons – which encourages the conversion of glucose to lactic acid. Alcohol abusers often have a low carbohydrate diet – making the situation worse.
  • Hypoglycaemia tends to occur several hours after heavy alcohol intake (hence having a kebab on the way home!), and is a contributing factor in the seizures seen in withdrawing alcoholics.
  • Lactic acidosis predisposes to the synthesis of saturated fatty acids which lead to fatty liver.
  • Fatty liver – this is the first sign. It can either be steatohepatitis, or steatohepatosis.
  • Alcoholic hepatitisthis leads to fibrosis, then micronodular cirrhosis of the liver.
  • Clotting factors no longer produced – the liver normally produces factors 2, 7, 9 & 10. Without these the patients may easily bruise, and bleeding is not easily stopped.
  • Reduced albumin production – albumin is the thing that holds all the bloods contents in the blood – it provides osmotic pressure. Without it, products normally contained in the blood easily escape into peripheral tissue, causing peripheral oedema.
  • Asterixis – this is a shaking of the hands caused by encephalopathy. Secondary to build up of toxic metabolites in the brain which can no longer be properly metabolised by the liver.
  • Jaundice – the liver is essential for removing bilirubin from the body. It conjugates it so it is soluble and can be excreted in the bile. Some of this is metabolised by bacteria in the gut and re-absorbed, and it is then excreted in the urine. Without proper liver function, this will not happen.
  • You can probably survive with about ¼ of a normal liver. There is a sudden cut off point at which your liver can no longer survive. This varies slightly from person to person, and there is no way to determine where this cut-off point is. When it occurs though, many of these symptoms will start abruptly.
  • Oseophageal Varices – if the liver is damaged, then intra-hepatic pressure increases causing portal hypertension. This then leads to oesophageal and rectal varices, as the blood tries to find another way to bypass the liver back to the systemic circulation. These varices can burst and bleed, and they are a common cause of death. GI bleeding is a common emergency presentation in patients with alcoholic liver damage.
  • Cirrhosis – individual susceptibility varies massively – but in most people drinking 8 U/day for 10 years is enough to cause cirrhosis. In women, it is thought that 4U/day is enough.
  • Induction of drug metabolising enzymes – so some drugs (e.g. warfarin) become less effective.

GI problems

  • Gastritis – probably caused by increased gastric secretions that are induced by alcohol intake. Peptic ulcers are also 3x more common in heavy drinkers.
  • Pancreatitis – may be precipitated by high triglycerides, or due to proteinous secretions induced by alcohol intake.
    • 50% of all cases of chronic pancreatitis are due to heavy drinking
  • Mouth – alcoholics often have poor dental care. They will have bad teeth, and often will have scurvy due to lack of vitamin C. Scurvy causes inflammation and recession of the gums.
  • Oesophagus
    • Varices
    • Reflux oesophagitis due to alcohol’s relaxation effect – the lower oesophageal sphincter becomes dilated, as does the stomach
    • Mallory-Weiss tear
  • Stomach
    • Gastritis
    • Increased risk of ulcers
  • Diarrhoea
  • Malnourishment; due to:
    • Not much food eaten
    • Low nutritional quality of food eaten
    • Pancreatitis means food might not be properly digested
    • Liver damage means food is not metabolised properly

Blood disorders

There rarely can be Iron deficiency anaemia, or a macrocytic anaemia (form folate deficiency), or a megaloblastic anaemia from B12 deficiency. Or there can be a mixed picture of all of these! Usually the MCV is raised.
Bone marrow damage can also occur – this can lead to reduced platelet production, which along with the liver damage can severely hamper clotting ability

Sexual function

  • Sexual desire is increased in the short term, but the ability to maintain erection is reduced (due to vasodilation)
  • In the long term, there can be damage to the Leydig cells resulting in less testosterone production, which can cause:
  • There may also be alteration of steroid production which can cause gynaecomastia in men as a result of increased oestrogen production.

Neuropsychiatric effects

  • Alcoholics are likely to have vitamin deficiency due to poor diet, as a result of neglecting their need for food in favour of their addiction. A combination of high alcohol intake, low vitamin B6 and low thiamine (B1) can predispose peripheral neuropathy and dementia. In the acute withdrawal setting this can be particularly problematic (discussed later). The peripheral neuropathy can be both sensory and motor, and is most prominent in the lower limbs. It will rarely improve with treatment.
  • Alcohol is an anticonvulsant. Thus in withdrawal, it can cause convulsions – even in those with no history of epilepsy.
  • Effects on sleep – alcohol tends to allow you to get to sleep more easily, but the quality of sleep it induces is poorer; there is decreased REM sleep but increased stage 4 sleep. Withdrawal induces periods of REM sleep – which is associated with nightmares.
  • Impaired memory
  • Depression / anxiety
  • Subdural haematomarare – but more common after head injury than in non-drinkers.
  • Korsakoff’s syndrome – this is caused by a lack of thiamine (vitamin B1) in the brain. In this condition, consolidation of new memories is not possible, but usually, old memories are not forgotten. These patients may hold a conversation with you in which they totally make up what they are talking about; e.g. ‘Oh I saw you down in the café getting a snack’ – ‘oh yes – I had a jacket potato too’ – when in actual fact they have been in bed all day! Often alcoholics present just before their deficiencies are low enough for this syndrome to occur, so every alcoholic coming into hospital is put on a thiamine drip within an hour of admission!
  • General thiamine deficiency – It causes irreversible cerebellar nerve damage and thus will affect gait and eye movement.
  • Peripheral neuropathy – like that seen in diabetes – it affects the extremities of the body – hands, feet and toes. However, unlike diabetes, it is very painful.

Carcinogenesis and teratogenesis

  • ↑Risk of mouth, oesophagus and liver with heavy alcohol use
  • Foetal alcohol syndrome – this can occur even if the mother just drinks on one occasion only during the whole pregnancy term! Obviously the risks are greater, the more the mother drinks. The risk is also greatest if alcohol is drunk during the early part of pregnancy. it is most common in children who had a heavy drinking mother. It causes impaired learning and memory in the child.
  • Genetic susceptibility of the foetus plays a part.
Many of the condition relating to alcohol are caused by, or made worse by the dietary deficiencies that often accompany alcoholism.

Endocrine effects

  • Problems with metabolism of oestrogen to testosterone – this causes feminisation of many patients – they will lose their body hair, their testicles will atrophy etc.
  • Diabetes due to liver cirrhosis

Psychological effects

Depression and anxiety are very common amongst alcohol abusers. There are three possible routes by which depression can be linked to alcohol:
  • Alcohol is a depressive – it naturally inhibits brain activity
  • Alcohol abuse can cause social problems – e.g. relationship problems, employment issues, debts, problems with friends
  • The depression starts first and the individual turns to alcohol for relief – in the short term, alcohol use can provide an escape from depression, and many people use it as a coping mechanism.
More info about alcohol and depression:
  • ½ of all men who attempt suicide are alcohol dependant
  • Anxiety is particularly marked during alcohol withdrawal
Hallucinations related to alcohol are very rare, and should be distinguished from hallucinations that result from withdrawal. In alcohol induced hallucinations, the individual may here second person voices that are usually derogatory. Usually these symptoms will subside within a few days. In cases where the voices do not subside, it is likely there is underlying schizophrenia

Memory disorders

  • Alcoholic amnesia – not being able to remember what happened during a period of heavy drinking (e.g. not remember what happened the night before when you wake up in the morning)
  • Korsakov’s Syndrome
  • Alcoholic dementia – may resolve on cessation of alcohol intake

Social Problems

  • At work
  • At home – don’t forget impotence!
  • Crime

Pharmacokinetics of alcohol

  • Some absorbed in stomach, most from small intestine
  • High conc. Of alcohol (>20%), presence of food (particularly fat and carbohydrate) all inhibit gastric emptying – and thus alter the peak blood alcohol concentration – with long periods of gastric emptying the peak concentration is likely to be reduced.
  • Has large first pass metabolism. This metabolism has a fixed capacity – so if you absorb a lot of alcohol slowly (e.g. when drinking with food), more alcohol will be removed by first pass than if you drink on an empty stomach.
  • Continued alcohol metabolism is at a constant rate (about 8-10ml/hour)
  • The effects on the brain are most pronounced as the concentration of alcohol rises – this shows that the brain exhibits a short-term tolerance of alcohol.
  • 90% is removed by the liver – mostly by the enzyme alcohol dehydrogenase – producing acetaldehyde. This is then further metabolised by aldehyde dehydrogenase to acetic acid. The other 10% is expired from the lungs,or excreted in the urine unchanged – this occurs at a rate proportional to the blood concentration of alcohol – and thus forms the basis of the breath test, and the urine test.

Drug interactions

METRONIDAZOLE and CHLORPORPAMIDE inhibit the action of acetaldehyde dehydrogenase and thus there is acetaldehyde accumulation if you drink whilst taking these drugs. This leads to symptoms of:
Even after very small amounts of alcohol

Taking an alcohol history

Basis screening for alcohol in a ‘normal’ hospital patient
  • CAGE questions may be useful (but NOT in a psychiatric / full alcohol history)
  • ↑ MCV
  • ↑γGT
  • Take a good alcohol history!
Current drinking behaviour
  • Ask specifically about alcohol intake in the last 24 hours, and the last 7 days. You may also want to ask about a typical day.
    • Try to elicit if there is a binge pattern – days of very large intake, with days of no drinking at all, or if they drink constantly.
  • Is the first drink of the day taken to stop any withdrawal symptoms
  • Do they drink throughout the day, or do they have sessions at specific times.
  • Do they drink to get drunk? Do they get drunk? Do they have blackouts/falls?
  • Where do they drink? Who do they drink with?
  • CAGE questions
    • C – have people ever told you that you should cut down your alcohol intake?
    • A – have you ever been annoyed by people criticising your drinking?
    • G – Have you ever felt guilty about your drinking?
    • E – Do you ever need to have an eye-opener in the mornings?
Development of drinking behaviour
  • When did they start drinking?
  • When did they start drinking heavily? Were there any precipitating life events? Job (e.g. joined the army, or got sacked), relationships etc
  • Have they ever tried to come off alcohol before? Did they have support? If they have, how long did it last, and why did they start again?
  • Forensic history – have they ever been in trouble with the police? Particularly related to drinking

Physical exam

Abdominal Exam:

  • Hepatomegaly
  • Capa medusa
  • Ascites
  • Jaundice
  • Pancreatitis
    • Location of pain
    • Grey-Turner’s sign?
  • Flapping tremor


  • Peripheral neuropathy
  • Ataxia
  • Co-ordination (cerebellar dysfunction)


  • BP
  • Pulse

Context of drug and alcohol abuse
Smoking – 120 000 deaths/year in the UK
Alcohol – 20 000 deaths/year in the UK
All other drugs combined – probably <10 000
E.g. there are about 50 deaths ever reported in the UK for ecstasy use only (more when combined with other things – most commonly alcohol)
Changing drinking behaviour on a national level
Several things are known to have an influence of public alcohol consumption
  • Price of alcohol – a high price reduces consumption
  • Advertising – has little effect on overall consumption, but can influence children’s attitudes and behaviour.
  • Portrayal in the media – it is thought that the portrayal of alcohol in the media is generally positive (or when negative it is melodramatic), and this makes alcohol look ‘cool’. There is scope to alter this portrayal to alter people’s views of alcohol.

Consequences due to drunkenness

  • Trauma
    • Fights
    • Falls
  • Vomiting – this can lead to aspiration, which if light, is likely to cause pneumonia, but if serious could lead to death as the patient is unable to breathe.
  • Radial nerve palsy – if you fall asleep with your arm in an unusual position (e.g. over the back of a chair) then your radial nerve can get stuck in the radial groove and compressed. This can lead to nerve damage. The typical sign of this damage is a drooping wrist. Sometimes it is permanent, but in some cases it may only last a couple of weeks.
  • Risk taking behaviours – e.g. climbing trees, swimming across rivers etc.
  • Vasodilatation – this is not necessarily very dangerous, unless you combine it with being in a cold place for a long time – e.g. sleeping in the park after a drunken night out. In this case it may lead to hypothermia.
  • Hyperglycaemia
  • 50% of weekend hospital admissions in some cities (Manchester included) are due to alcohol.


Early symptoms – these occur within a few hours of not drinking:
  • Tremor
  • Nausea
  • Sweating
  • Agitation
  • Tachycardia / palpitations
  • Raised BP
These symptoms are often experienced in the morning by people dependent on alcohol. Having a drink will relieve these symptoms. They are the result of autonomic overactivity due to the withdrawal of the inhibiting effect provided by alcohol.
Late symptoms – these peak at 24-48 hours after withdrawal
  • Delusions
  • Confusion
  • Diarrhoea
  • Epileptic seizures (convulsions)
  • Auditory hallucinations
  • After 48 hours – delirium tremens
  • Alcohol is a GABA agonist; GABA neurones are inhibitory. Therefore, alcohol suppresses brain activity.
  • Withdrawal therefore is related to overactivity of the nervous system.
    • Hallucinations – these are almost always persecutory; e.g. imagining spiders and snakes crawling all over them.
    • “Tremens” – this is due to overactivity of the peripheral nervous system. The patient will be very sweaty (possibly sweating up to 10L of fluid a day!) and will shake.
    • Epilepsythis is usually unilateral and will often result in a tonic-clonic seizure.
    • Cardiac problems – arrhythmias
    • Hypertension
    • Tachycardia
    • Vomiting
    • Diarrhoea
    • Loss of appetite
  • The drugs used to treat the withdrawal symptoms are benzodiazepines. The one most commonly used to treat alcohol withdrawal is librium (chlordiazepoxide). Patients will generally be on one of these for several, with a gradually reducing dose. The doses are often very large in comparison to doses of these drugs for other indications. Check you hospital policy for more details.
  • Other examples of benzodiazapines include diazepam (aka valium) which is often used to treat anxiety, and lorazepam. These drugs nearly always end in –epam.
  • If you consciously decide to stop drinking alcohol and pro-actively seek help to do it then you have a 10% chance of success. If, on the other hand you stop ‘opportunistically’ i.e. you come into hospital for something else, and see that you can get help to stop, then you only have a 5% chance of success.
  • Complications of withdrawal are treated in their own right.
  • Frequent ‘detoxing’ increases the risk of epilepsy. For this reason, and its lower success rate, opportunistic cessation of drinking is not normally encouraged by practitioners.

Delirium Tremens (DT)

This typically occurs in middle-aged men with a history of many years of drinking, although it can occur after only a few months of drinking. It only occurs in about 5% of acute alcohol withdrawal cases.
It presents about 3-4 days after withdrawal, and is similar to other acute brain syndromes.
  • Restlessness
  • Fear
  • Paranoia
  • Confusion / clouded consciousness
  • Terror-stricken face
  • Ataxia / tremor
  • Sweaty / tachycardia / pyrexia / flushing / pallor
  • Visual Hallucinations – these tend to occur even later in the progression. Usually they are terrifying for the patient and may involve insects, pink elephants and other animals. These visual hallucinations may be accompanied by tactile hallucinations – classically insects crawling on the skin. this phenomenon is known as formication.
  • Auditory hallucinations – often persecutory.
Delirium Tremens is a medical emergency! Death occurs in around 10-15% of cases (up to 35% if untreated).It results from epileptic seizure, heart failure, self-injury and infection. Treatment is similar to that of a controlled alcohol withdrawal:
  • Benzodiazepine – for sedation and anti-convulsant effects. Even if the acute symptoms have subsided, you should still continue with these for up to 10 days at night to help avoid nightmares.
  • B vitamins – remember – the early you give these, the greater the chance of reducing encephalopathy
  • Fluid replacement
  • Dextrose – to avoid hypoglycaemia
  • Be aware of infection and (head) injury – as these commonly accompany DT
  • On recovery – check for signs of alcohol brain damage. Asses the patient motivation to permanently change.
DT usually resolves after 3-4 days, but continuing anxiety may go on for months.
The effects of DT are due to the long term changes of alcohol on the brain. During long term alcohol use there is a decrease in GABA receptors as tolerance develops. so when alcohol is withdrawn, the patient is left with a very low number of inhibitory receptors – and nothing acting on them! so they can an overactivity in the CNS.

Wernicke’s encephalopathy and Korsakov’s Syndrome

  • Wernicke’s encephalopathy – this is an acute syndrome caused by thiamine deficiency
  • Korsakov’s Syndrome – this is a chronic condition also caused by thiamine deficiency. It is sometimes called Korsakov’s psychosisalthough it is an organic brain disease and not a true psychosis.
  • It is possible in some cases that what may initially present as Wernicke’s will continue chronically, thus becoming Korsakov’s.
Clinical Features
  • Ocular palsies, particularly of the abducens nerve.
  • Ataxic gait
  • Nausea
  • Memory Problems
  • It can occur in any type of thiamine deficiency, not just alcohol, e.g. dietary, gastric carcinoma, pernicious anaemia
The Wernicke’s Triad:
  • Eye signs
    • Nystagmus
    • Ophthalmoplegia (paralysis of eye muscles)
  • Ataxic gait
  • Confsuion
This is basically a state of impaired memory function that is present after the signs of Wernicke’s encephalopathy have subsided. It is an anterograde memory disorder – meaning that old memories can be accessed, but that new memories cannot be consolidated. Patients still have the ability to immediately recall facts (e.g. within a few minutes), but have no ability to get this information into long term memory.
  • Patients often have little / distorted sense of time
  • They often make up events, e.g. ‘I went to MacDonald’s for dinner’ – when infact they have been sat at home all day. This is not a conscious attempt to mislead, but a feature of Korsakov’s Syndrome. The answers to these questions are often very plausible. This phenomenon is called confabulation.
    • Patients often also answer these questions in a very laid-back manner, apparently unconcerned that their answers are incorrect.
  • Memory recall for events before the Syndrome is usually fine
  • There is no clouding of consciousness
  • There is often peripheral neuropathy.
  • Acute brain syndrome of miscellaneous cause. in these other syndromes there will be:
    • Clouding of consciousness
    • Check alcohol history
    • No neurological sings (e.g. ataxia, ocular palsy)
  • Delirium Tremens – 4x as common as Wernicke’s. there are no neurological signs.
  • Chronic brain syndromes – have a different patter of memory loss – long term memory recall is also likely to be affected.
    • Chronic alcohol intake can actually lead to chronic brain syndrome due to atrophy of the cerebrum.
  • Give lots of thiamine! Usually give in conjunction with other B vitamins. IV or IM if necessary
  • Sedation (similar to DT if necessary)
  • Fluid / electrolytes
This is a life-long chronic illness, for which there isn’t really any treatment. thiamine supplements may be useful for some, but after the acute phase, they are unlikely to provide any benefit. Eventually, many patients will require care.
  • Palsies – usually clear with appropriate treatment
  • Ataxia – ataxia will usually resolve on its own over several months
  • Neuropathy – may resolve slowly, unlikely to resolve fully
  • Amnesia – ½ of all patients will not recover from this

Treatment of alcohol addiction

High alcohol intake – but not dependant – these people may benefit from methods to help them moderate their drinking without total abstinence (controlled drinking). Such interventions usually involve self-help materials (e.g. a diary of drinking) in conjunction with counselling sessions.
Alcohol dependence – total abstinence is advised. It is highly unlikely that someone in this position will be able to control their alcohol intake to a ‘reasonable’ level. Becoming totally abstinent will require the individual to undergo a period of ‘detoxification’. This is most likely to be successful if done in a controlled environment. This can be at home or in a medical ward or rehabilitation ward at hospital (not a psychiatric ward!). Methods:

  • At home – this may be suitable for those with:
    • No history of DT or other withdrawal syndromes
    • Good family / social support
    • No psychological complications (e.g. depression)
    • No physical complications )e.g. liver disease)
    • It will involve a community alcohol team.
    • Drugs (see below)
    • In recent years there has been more emphasis on helping patients to detox at home. Studies have shown that it is safe, with high completion rates. Some studies have suggested it is more effective than detox in an inpatient unit, and is between 10-20x time cheaper!
    • Contraindications include:
      • Previous withdrawal seizures
      • Suicidal ideation
      • Co-existing drug addiction
      • History of DT
      • No access to safe housing or appropriate social support
  • At hospital – if the patient does not meet the above criteria, they can be treated in hospital

Example of when home detox may be appropriate

Daily standard drinks / units10-1415-2530-4050+
Detox settingHomeHomeInpatientInpatient

Principles of managing alcohol dependence

Knowing ‘when to give up’ is a difficult question. Many patients know they ‘should’ give up, but struggle with the motivation to:

  • Plan a serious detox attempt
  • Stick to the detox regimen
  • Maintain abstinence

Using the 5As approach to assess and treat may be appropriate (see Addiction and drug abuse).

Benzodiazepines – these are given both for sedation, and also for their anticonvulsant effects. Thus you should chose a drug which has both these effects. The dose is gradually reduced over 7-10 days. Usually you start off reducing the dose by 20%, but if the patient is still experiencing severe symptoms, reduce the dose at a lower rate.

  • Chlordiazepoxide is often the drug of choice (in the UK), but diazepam may also be used (1st line in Australia).
  • Clomethiazole used to be used but it has a high risk of dependence. Clonidine is particularly useful at reducing the sympathetic effects seen in withdrawal.
  • These can be given every 4 hours (orally), or IV if necessary. You should not give them for more than 14 days due to risk of benzodiazepine addiction
    • Dosing of benzodiazepines is often based on withdrawal symptoms – e.g. in hospital – guided by the patient alcohol withdrawal scale score
  • Lorazepam, haloperidol – these drugs may be used to control aggression in alcoholics in the acute situation.

Thiamine and other vitamin supplements – these are essential! They help to prevent Wernicke’s encephalopathy. They often have to be given IV – and may need to be given for up to 1 month after.
Fluid replacement – dehydration can be particularly severe. There is also a very real risk of Hypocalcaemia and hypomagnesia.
Disulfiram – is a drug that inhibits acetaldehyde dehydrogenase and thus causes nasty side effect when taken with alcohol. It can help to maintain abstinence – although it usually needs to be given with psychotherapy to be effective
Acamprosate – inhibits glutamate – which is an excitory amino acid implicated in cravings. Acamprosate can help reduce cravings.

The most important predictor in determining if total abstinence is achievable is motivation. The patient has to have strong motivation to want to stop, whatever their reasons may be.
There are also ‘social’ rehab centres – e.g. run by religious groups – which encourage detox, but they have no medical input.

Managing alcohol detox at home

  • Consider a contract with the patient (example at NPS medicine wise – box 1)
  • Consider urine drug screen (co-existing drug abuse is a contraindication to home detox)
  • Take a set of baseline observations (HR, BP, temperature)
  • Take some baseline blood tests – including LFTs, U+Es, FBC, iron studies, random glucose, CMP
  • Prescribe thiamine. This redcues the risk of Wernicke’s encephalopathy
    • 300mg PO or IV for 3-5 days in acute withdrawal, then 100mg for 1 week
    • In those with a planned detox give 200mg OD for 2 weeks
    • The dose for continuing drinkers is lower – 100mg OD
  • Prescribe a weaning regimen of benzodiapines
    • Chlordiazepoxide or diazepam recommended in UK
    • Diazepam recommended in Australia. Oxazepam may be considered in patients with significant hepatic impairment
    • Typically the dose is weaned over 7 days
  • Review daily – either by GP or specialist nurse
  • Consider other supportive treatemnts
    • Melatonin may help with sleep disturbance
    • Advise to eat frequent, small meals, high in protein. This can help to prevent hypoglycaemia as well as supplementing thiamine intake
    • Encourage patient to enrol in a alcohol support programme – such as Alcoholic’s Anonymous (AA)

Possible weaning regimens with diazepam

15mg QID10mg QID
25mg TDS5mg QID
35mg BD5mg TDS
45mg nocte5mg BD
55mg nocte5mg nocte
6n/a5mg nocte

Mild and moderate based on criteria listed above. From the Author – Dr Tom Leach – I must admit that in my practice (I work in Emergency as well as in primary care) I typically use higher doses in primary care that are listed here – based on clinical experience  from the doses I have seen given, and been advised to give by the drug and alcohol team in hospital!

  • eTherapeutic Guidelines recommends 20mg diazepam every 2 hours PRN – maximum daily dose of 60mg

Managing Alcohol Addiction in the acute admission

Patients known or suspected to have a high alcohol intake on presentation to hospital should be placed on an Alcohol Withdrawal Scale (AWS) and doses of benzodiazepines should be titrated to their score on this. Patients are commonly underused with benzodiazepines. 
  1. Give IV vitamin B12 + thiamine (pabrinex : vitamin B1) + other B vitamins –  Patients are likely to be deficient as a result of diet, due to the fact they are drinking so much – they are unlikely to eat properly for various reasons (Alcohol is appetite suppressant, maybe not able to afford food, etc.). There is often coexistent macrocytic anaemia. these also protect against Wernicke encephelopathy and the longer term Korskoff’s Syndrome
    1. Thiamine 300mg IV or oral for 3-5 days recommended in acute withdrawal
  2. Drain any ascites and test the fluid (infection, blood, transudate / exudate)
  3. Give diazepam or librium (chlordiazepoxide). Typical dose (librium) of 10-50mg/Kg every 6 hours for the first 3 days. Then wean over the following 7-14 days. Reduces hallucinations.
    1. Doses used in the inpatient setting are generally higher than outpatients
  4. Provide Adequate nutrition – 35Kcal/Kg/day in non-protein energy, PLUS 1.5g/Kg/day of protein. This has been shown to reduce sepsis, mortality and encephalopathy.
  5. Consider the use of Steroids – calculate the Maddrey Discriminant Factor. a score of >32 indicates severe disease, and should be treated with 40mg/day for 5 days, with a tapering dose of the subsequent 3 weeks. Mortality correlated with the Maddrey Discriminant Factor Score.
    1. Severe disease mortality – 50% in the first 30 days
    2. Mild disease mortality – 5% in the first 30 days
    3. 1 year mortality regardless of severity40%
  6. Give tramadol and laxatives. Tramadol is an opiod used commonly to relieve neuralgia. You should give the laxatives to avoid constipation. Constipation can be dangerous as it can allow excess production of bacterial toxins, which the liver is unable to remove..
  7. Give potassium sparing diuretics (e.g. spironolactone). Loop diuretics are more effective at diuresis in normal patients, but are contraindicated in alcoholics:
    1. Alcoholic patients have a low blood volume due to hypoalbuminaemia. The synthetic function of the liver is damaged, and so alcoholic patients have a low blood albumin level. Their renin-angiotensin system is already activated to a much larger extent than usual due to their low blood volume. This system causes retention of sodium to retain fluid in the body. However in patients with liver failure, the sodium doesn’t stay in the blood, and instead dissipates to the peripheral tissues causing oedema and ascites. So, you must block this system, to allow proper fluid excretion..
    2. Patients should be weighed every day to see if they are losing fluid. Ideally they should lose 0.5-1kg a day (i.e. 0.5-1L of fluid) for the first few days, until the noticeable oedema is gone. After this, they should lose no more than 0.5L per day. To ensure this is achieved, you have to restrict the patient’s fluid intake. Losing more weight per day than this can cause dangerous fluid shifts.
    3. Huge doses are often required! (e.g. 200-300mg spironolactone)
    4. Many patients will also be on furosemide

Long-term management of patients with alcohol dependence

  • Alcohol dependence should be viewed as a a chronic relapsing and remitting condition
  • It is associated with a change in the motivation and control systems in the brain
  • Long-term management of alcohol dependence aims to target these regulation systems
  • These management strategies should include psychological and rehabilitation therapies, in conjunction with a pharmacological approach (where indicated)
    • Pharmacological strategies are generally reserved for those with more severe disease
  • Typical treatment plans will last 3-6 months

Three main medications are available to assist with long-term management of alcohol dependence – Acamprosate, disulfiram and naltrexone. However, they have different indications:

  • Acamprosate and disulfiram are recommended for those who have achieved abstinence and with to maintain it
  • Naltrexone is recommended for patients who wish to reduce their alcohol intake

There are several other medications that may also be used, but are typically prescribed only by specialist in particular situations. These can include baclofen, topiramate and disulfiram.


  • Useful in patient still drinking to reduce the positive effects
  • Can also be used in those who have stopped drinking as a deterrent to restarting
  • A mu opioid receptor antagonist
    • Contraindicated in those on opioids
    • Related to the opiod overdose reversal agent – naloxone
    • If opiates are prescribed, naltrexone should be ceased
  • It reduces the euphoric reward feeling associated with alcohol
  • It can be given in combination with acamprosaate but evidence in this setting is lacking
  • Side effects:
    • Headache
    • Nausea
    • Lethargy
    • Dysphoria
    • There are no specific negative effects if patients drink whilst taking naltrexone
  • Contraindications
    • Taking opioids
    • Liver failure – an important consideration in this context
      • Do NOT prescribe if ALT >3x normal limit
  • Typical dose
    • 50mg PO OD
    • Half dose may be recommended in those who are still drinking


  • First line in those seeking to maintain abstinence
    • Much more effective than alternative medications for this purpose
  • A structural analogue of GABA (neurotransmitter)
  • Thought to work by altering the action of calcium channels and affecting neurotransmission on GABA and glutamine pathways in the brain
  • It does not interact with other medications commonly prescribed around the time of alcohol withdrawal – such as benzodiazepines, antidepressants or naltrexone
  • It can be given safety in liver failure
  • It does not have any potential for abuse
  • Dose: 333mg tabs x2 TDS (if weight >60Kg)
    • If <60kg – 333mg x2 tabs mane, 1 tab lunch and 1 tab dinner
    • Compliance may be difficult due to the large number of tablets to be taken


Disulfiram – Antibuse

  • Disulifram interferes with the metabolism of alcohol
  • If patients drink after taking it – they generally feel quite unwell!
  • As a result of the altered alcohol metabolism, it causes an increase in the levels of acetaldehyde dehydrogenase – which results in:
    • Hot flushes
    • Sweating
    • Palpitations
    • Tachycardia
    • Headaches
    • Dyspnoea
    • Hyperventilation
    • Chest pain
    • “Feeling of impending doom”
    • Can result in seizures and cardiorespiratory failure – deaths have been reported
    • Contraindications include ischaemic heart disease, psychosis
  • Patients should be highly motivated not to drink – and should be warned of these effects if alcohol is consumed
  • Dose – 100mg PO OD, increasing to 300mg OD. Increase dose slowly over a period of weeks


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

This Post Has 2 Comments

  1. Florence Sumner

    Thiamine is not B12 it’s B1

    1. tom

      Thanks for that – fixed it up – Tom

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