10.3 Harmful and dependent alcohol use

Heavy drinking and alcohol dependence

Harmful use and dependence

• Hazardous drinking is a pattern that raises the risk of harm, while a harmful pattern of use (ICD-11) has already damaged health, without dependence.

• Heavy drinking does not establish dependence, and a modest weekly total does not exclude it.

Epidemiology and risk

• Drinking above 14 units a week is most common in men aged 55 to 64, with men above women at every age and a fall from 65.

• Heavy single-session drinking is concentrated in young drinkers.

• First-degree relatives of people with alcohol problems carry roughly double the population risk.

Cloninger's types

Alcohol dependence syndrome

Edwards and Gross (1976) described seven features, which need not all be present.

Salience is told from compulsion by what it describes: salience is drinking ranked above everything else, compulsion is the struggle to resist it.

Diagnostic criteria

• ICD-11 dependence needs two of three domains: impaired control, increasing priority of alcohol, and physiological adaptation (tolerance, withdrawal or relief drinking).

• Features usually span 12 months, or three months of continuous daily or almost daily use.

• The Alcohol Use Disorders Identification Test screens for problem drinking, and the Severity of Alcohol Dependence Questionnaire measures dependence severity.

Blackouts

• An alcohol-induced blackout is amnesia for a period of conscious intoxication: an anterograde failure of encoding, with immediate and remote memory spared.

• It reflects acute, reversible failure of the hippocampus to consolidate new material, unlike the chronic mammillary body damage of Wernicke-Korsakoff syndrome.

Withdrawal

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• Delirium tremens complicates about 5% (1 in 20) of withdrawal episodes.

• Alcoholic hallucinosis has relatively clear consciousness and mainly auditory hallucinations, whereas delirium tremens has fluctuating attention, disorientation and mainly visual or tactile hallucinations.

• Previous seizures or delirium tremens favour inpatient withdrawal.

Wernicke's encephalopathy

• Wernicke's encephalopathy explains acute confusion with nystagmus and failure of abduction (lateral rectus weakness) in a heavy drinker.

• It comes from thiamine deficiency of any cause, so non-alcoholic states that cut intake or absorption, increase loss or raise demand also predispose to it.

• Lesions are symmetrical and lie in grey matter around the third ventricle and aqueduct: medial thalami, mammillary bodies, periaqueductal grey, tectal plate and floor of the fourth ventricle.

• The mammillary bodies atrophy rather than enlarge.

• Give urgent parenteral thiamine without waiting for the full triad, and do not delay glucose for hypoglycaemia.

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Korsakoff's syndrome

• The characteristic lesion of Korsakoff's syndrome is in the mammillary bodies, part of the Papez memory circuit, from thiamine deficiency.

Other brain and nutritional complications

Assessment and management of alcohol misuse

Drinking levels and units

• The 2016 UK Chief Medical Officers' low-risk guideline, endorsed by the Royal College of Psychiatrists, is no more than 14 units a week for men and women alike. It replaced the earlier male limit of 21 units.

• Units equal the volume in millilitres multiplied by the percentage alcohol by volume (ABV), divided by 1000. Litres multiplied by ABV gives the same answer.

• For a weekly total, multiply the units in one drink by the number of drinks a day, then by seven.

Taking the alcohol history

• Record units, drink types and the pattern across the week, including morning drinking, solitary drinking and emotional triggers.

• Ask about impaired control, failed attempts to cut down and drinking to relieve withdrawal.

• Establish previous withdrawal, seizures or delirium tremens, because these complications favour inpatient withdrawal.

• Assess physical, psychological, relationship, work, financial and legal harms, and ask about previous treatment, mutual aid and reasons for relapse.

• Seek a collateral history with consent. Self-report can underestimate intake, but not every account is inaccurate.

Diagnosis of dependence

Edwards and Gross (1976) described seven elements of the alcohol dependence syndrome: narrowing of repertoire, salience, increased tolerance, repeated withdrawal, relief drinking, subjective compulsion and reinstatement after abstinence.

• Continued use despite harm was not one of the seven original elements; in ICD-11 it contributes to the increasing-priority domain.

• In ICD-11, salience belongs to one of the three dependence domains: drinking takes increasing priority over the rest of life. Craving, reinstatement and narrowed repertoire are supportive features.

• Hazardous alcohol use describes increased risk of harm and is classified outside the mental disorders; it does not by itself establish dependence.

• ICD-11 normally requires dependence features over at least 12 months. This shortens to 3 months when drinking is continuous, meaning daily or almost daily.

Screening and severity instruments

Scores support assessment. They do not settle the diagnosis or the treatment setting on their own.

• An AUDIT score of 8 or more suggests hazardous or harmful drinking. The National Institute for Health and Care Excellence (NICE) recommends AUDIT for staff outside specialist services.

• On receiver operating characteristic (ROC) analysis, the full AUDIT discriminates at-risk drinkers better than older questionnaires and blood markers. This is why NICE builds screening around it.

• NICE advises considering inpatient withdrawal when the SADQ is above 30.

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Examination and bedside tests

• Look for intoxication, tremor, sweating, tachycardia, agitation, injuries, malnutrition, neuropathy and ataxia.

• Look for signs of liver disease: jaundice, spider naevi, palmar erythema, hepatomegaly and ascites.

• A breath alcohol test gives an immediate reading of current alcohol that tracks blood alcohol. Wait at least 20 minutes after a drink to avoid mouth-alcohol error.

• A high breath reading with few signs of intoxication suggests tolerance.

• The Abbreviated Mental Test Score (AMTS) quantifies disorientation in an alert but confused intoxicated patient. The Glasgow Coma Scale rates arousal instead.

• Screen cognition early and reassess after stabilisation and sustained abstinence. Do not hold back support for four weeks while waiting.

• Assess depression, anxiety, psychosis and self-harm, including their timing relative to drinking.

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Blood markers

Heavy drinking causes macrocytosis (a raised mean cell volume, MCV), anaemia, neutropenia, thrombocytopenia and raised liver enzymes.

The recognised markers of sustained heavy drinking are:

• gamma-glutamyl transferase (GGT);

• carbohydrate-deficient transferrin (CDT);

• MCV;

• the transaminases.

Normal results do not exclude dependence.

• An aspartate aminotransferase to alanine aminotransferase ratio (AST to ALT) above 2 supports alcohol-related liver disease but is not diagnostic.

• Ultrasound shows steatosis or structural disease, and elastography assesses fibrosis. Neither diagnoses dependence.

Withdrawal: signs and course

• Withdrawal is central and sympathetic overactivity. Raised blood pressure, tachycardia, sweating, tremor and mild pyrexia are expected; depression is not.

• A fine, fast postural tremor of the hands is the characteristic early sign.

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Uncomplicated withdrawal usually resolves within 3 to 7 days of the last drink.

Delirium tremens and alcoholic hallucinosis

• Delirium tremens is the most severe form of withdrawal. It presents with clouded consciousness, fluctuating confusion, vivid visual hallucinations, agitation, tremor and autonomic overactivity.

• The classic picture is delirium tremens arising two to three days into an admission with enforced abstinence. Signs of central nervous system depression do not belong to it.

• Alcoholic hallucinosis is persistent auditory hallucinations, often third-person and derogatory, in clear consciousness with normal orientation and vital signs. It usually settles within weeks to months of abstinence.

How to tell them apart: delirium tremens clouds consciousness and disturbs vital signs, while hallucinosis does neither.

Choosing the setting for assisted withdrawal

• Any of the following calls for planned medically assisted withdrawal before treating low mood or starting relapse prevention:

  • heavy daily drinking over 15 units a day;

  • an AUDIT score of 20 or more;

  • a history of significant withdrawal.

• Never advise a dependent drinker to stop abruptly without support.

• Community withdrawal needs manageable risk, reliable support, a clear prescribing plan and frequent monitoring.

• Uncomplicated home detoxification is usually finished within about 5 to 9 days.

Consider inpatient or residential withdrawal for:

• previous withdrawal seizures or delirium tremens;

• more than 30 units a day, or a SADQ score above 30;

• 15 to 30 units a day with significant physical or mental illness or cognitive impairment;

• concurrent alcohol and benzodiazepine withdrawal;

• pregnancy, younger age, unstable housing, little support or other vulnerability;

• failed community withdrawal or significant suicide risk.

A single major risk factor can justify admission.

Benzodiazepine regimens

• Benzodiazepines are first-line. They act at gamma-aminobutyric acid type A (GABA-A) receptors, cross-substitute for alcohol, and prevent seizures and delirium tremens.

• Chlordiazepoxide is the usual first choice in a reducing regimen when liver function is normal. It is slow in onset, long-acting through active metabolites, low in potency and low in misuse potential.

• An isolated raised GGT is not liver impairment and does not rule out chlordiazepoxide.

• Check sedation, breathing, alcohol and withdrawal before each dose. A positive breath alcohol reading means withholding the benzodiazepine dose.

• Monitor vital signs, fluids and electrolytes, especially potassium and magnesium.

Liver and lung disease

• In significant liver impairment, use a benzodiazepine cleared by glucuronide conjugation with no active metabolites: oxazepam, lorazepam or temazepam.

• The reason is that phase II conjugation is spared while oxidation fails, so chlordiazepoxide accumulates.

• Lorazepam rather than oxazepam suits decompensated liver disease when the oral route is unavailable, because it can be given parenterally.

• Severe liver disease needs specialist advice.

• Oxazepam is preferred when chronic respiratory disease makes over-sedation dangerous. It is short-acting and has no accumulating active metabolites.

Seizures, delirium tremens and drugs to restrict

• Treat a seizure in acute withdrawal with a quick-acting benzodiazepine such as lorazepam, not an antiepileptic.

• After a previous withdrawal seizure, a long-acting benzodiazepine such as diazepam gives cover through the seizure window. Phenytoin and conventional anticonvulsants do not prevent withdrawal seizures.

• In delirium tremens, benzodiazepines stay first-line. Haloperidol lowers the seizure threshold and prolongs the corrected QT interval (QTc), so it is only an adjunct for persisting agitation or hallucinations.

• Clomethiazole is restricted to inpatients. With alcohol it causes fatal respiratory depression and coma, and it has misuse potential.

• Benzodiazepines and carbamazepine are acceptable for home withdrawal.

Wernicke-Korsakoff syndrome

Features

• Thiamine (vitamin B1) deficiency causes Wernicke's encephalopathy and Korsakoff's syndrome. The deficiency comes from poor intake and poor absorption.

• Wernicke's encephalopathy has a classical triad: acute confusion, ophthalmoplegia (eye signs with nystagmus) and ataxia.

• Few patients show all three features of the triad, so do not wait for the full set before treating.

• The mammillary bodies are the structure most consistently damaged.

• MRI has low sensitivity (about 53%) and high specificity (about 93%), so a normal scan does not exclude the diagnosis.

• Untreated Wernicke's encephalopathy carries a mortality of roughly 10 to 20%.

• Korsakoff's syndrome follows Wernicke's encephalopathy. It is dense anterograde amnesia with confabulation, in clear consciousness, with attention preserved.

Treatment

• Suspected Wernicke's encephalopathy is an emergency. Give high-dose intravenous thiamine at once to prevent permanent damage; oral thiamine or other B vitamins are not enough.

• Thiamine is given parenterally because oral absorption in heavy drinkers is unreliable.

• Do not wait for imaging, and repeat the dose rather than giving it once.

• Current UK guidance uses intravenous thiamine 300 to 500 mg three times daily for 3 to 5 days. Review daily and continue parenteral treatment if symptoms persist.

• Check and correct magnesium.

• Glucose given before thiamine uses up the last thiamine in a depleted drinker and can precipitate or worsen Wernicke's encephalopathy. Glucose must therefore follow thiamine.

• Pabrinex supplies vitamins B1, B2, B3, B6 and C but not folic acid, so folic acid is the vitamin to add.

• With treatment, the ocular palsies recover first, within hours to days. Ataxia, nystagmus, neuropathy and memory recover slowly or incompletely.

• Give parenteral thiamine where staff can manage anaphylaxis. Anaphylaxis is rare and should not delay treatment.

Prophylaxis

• Offer thiamine routinely to every dependent drinker in assisted withdrawal.

  • Inpatients should receive parenteral thiamine as a minimum.

  • Oral thiamine is enough for well-nourished people at low risk who are detoxifying at home.

• High-risk people, such as those with malnutrition or decompensated liver disease, need parenteral thiamine followed by oral thiamine.

• Typical prophylaxis is 200 to 300 mg intramuscularly daily for at least 3 days in the community, or daily for 3 to 5 days in hospital.

Relapse prevention: choosing a drug

• In moderate to severe dependence with an abstinence goal, NICE advises acamprosate or oral naltrexone with psychological support once withdrawal is complete.

• In harmful drinking and mild dependence, NICE advises acamprosate or oral naltrexone with a recommended psychological intervention. This applies when psychological treatment alone has failed or when the person asks for medication.

• Behavioural couples therapy is advised when a regular partner will take part.

• A non-dependent, ambivalent drinker with no chosen goal starts with motivational interviewing. Medication has no place until the ambivalence is resolved.

• NICE commonly advises an initial course of acamprosate or naltrexone for up to 6 months, extended when helpful. Review monthly at first.

• Acamprosate remains usable in two situations where the others are excluded:

  • when opioid treatment rules out naltrexone and nalmefene, which are opioid antagonists;

  • when a vascular or coronary history rules out disulfiram.

Acamprosate

• Acamprosate reduces craving after withdrawal, with some but inconsistent trial evidence.

• It corrects the excitatory and inhibitory imbalance left by chronic drinking. This differs from baclofen, which is a GABA-B agonist.

• It is dosed by body weight using 333 mg tablets, totalling 1332 mg a day below 60 kg.

Naltrexone and nalmefene

• Naltrexone keeps its effect during continued treatment because no pharmacological tolerance develops.

• Naltrexone blocks opioid analgesia and may precipitate opioid withdrawal.

• NICE recommends nalmefene to reduce drinking in dependence at a high risk level, which is over 60 g of alcohol a day for men.

• Nalmefene is for people with no withdrawal and no need for detoxification, whose intake is still high two weeks after assessment.

• It is taken on days the person expects to drink, with psychosocial support.

Disulfiram

• The disulfiram-alcohol reaction causes flushing, nausea and palpitations. Tachycardia and hypotension are why coronary artery disease rules it out.

• Trace alcohol in everyday products, such as over-the-counter medicines and toiletries, can trigger the reaction. This marks an abstinent patient as taking disulfiram rather than acamprosate.

• Start disulfiram at least 24 hours after the last drink. The reaction risk persists for up to 2 weeks after stopping.

• NICE advises that a family member or carer oversee each dose, because the effect depends on the tablet being taken.

• The drug's own side effects are halitosis, drowsiness, fatigue, metallic taste, headache and nausea.

• Metronidazole causes a disulfiram-like reaction by inhibiting aldehyde dehydrogenase, so it is avoided in people who keep drinking.

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Off-label drugs

• Gabapentin has randomised trial evidence of dose-related benefit for abstinence and heavy drinking.

• The early promise of baclofen was not confirmed by a later meta-analysis. It needs caution in renal impairment, sedation and encephalopathy.

• Topiramate is a specialist off-label option.

Psychosocial treatment

• Brief intervention for non-dependent harmful drinking is structured advice over 5 to 10 minutes. Suspected dependence needs fuller assessment instead.

• Brief intervention follows FRAMES: Feedback, Responsibility, Advice, Menu of options, Empathy and Self-efficacy. Its evidence is strongest in primary care.

• Cognitive behavioural relapse prevention builds coping and drink-refusal skills.

• It also tackles the abstinence violation effect: reading a lapse as total failure and then returning to sustained drinking.

• Project MATCH found little difference in drinking outcomes between cognitive behavioural therapy, motivational enhancement therapy and twelve-step facilitation. It also found almost no client-treatment matching effects.

• The UK Alcohol Treatment Trial (UKATT) compared motivational enhancement therapy with social behaviour and network therapy.

• Manualised twelve-step facilitation gives abstinence outcomes comparable to or better than established alternatives.

• Involve family with consent when it is safe to do so.

• Treat coexisting mental illness alongside the drinking.

Risk, harm reduction and recovery

• Ask directly about suicide, especially during intoxication, withdrawal and early recovery.

• Assess falls, concurrent sedatives, violence, domestic abuse and children's welfare.

• Capacity is decision-specific and time-specific. Intoxication or dependence does not automatically remove it.

• Advise affected drivers to stop driving and to notify the Driver and Vehicle Licensing Agency.

• If abstinence is not achievable now, agree safer drinking goals, avoid sedative combinations and continue nutritional support.

• Warn that reduced tolerance makes a return to previous drinking levels dangerous.

• Repeated withdrawals raise seizure risk through kindling.