Mental Health

Alcohol dependence

A chronic alcohol-use disorder in which neuroadaptation, impaired control and continued drinking despite harm create a potentially dangerous withdrawal syndrome when alcohol is reduced or stopped.

In a nutshell

Alcohol dependence is characterised by impaired control, craving, tolerance and withdrawal. Sudden reduction can cause tremor, autonomic symptoms, seizures or delirium tremens, so withdrawal requires clinically assessed setting and monitoring. Give risk-based thiamine, use a monitored benzodiazepine regimen when indicated, and arrange psychosocial relapse prevention with medication considered after withdrawal.

Classic presentation

A person drinking heavily and regularly develops morning anxiety, sweating, tremor, nausea or palpitations that improve after alcohol; symptoms worsen after stopping and may progress to hallucinations, seizures or delirium.

Key points

AUDIT or AUDIT-C supports screening, but diagnosis and withdrawal planning require a confidential history, examination, comorbidity assessment and collateral information where appropriate.
Do not advise a dependent person to stop suddenly or self-detoxify; agree a medically supervised plan and choose community, residential or inpatient care according to risk.
Previous withdrawal seizure or delirium tremens, severe dependence, pregnancy, significant physical or mental illness, high Wernicke risk, concurrent sedative dependence or an unsafe home lowers the threshold for inpatient care.
Benzodiazepine reducing regimens are standard withdrawal treatment; use a fixed-dose community regimen or a trained symptom-triggered hospital pathway with close monitoring for oversedation.
Give prophylactic thiamine according to risk and setting. Suspected Wernicke’s encephalopathy is an emergency requiring prompt parenteral thiamine; do not wait for the complete triad.
Seizure, delirium tremens, severe worsening tremor or suspected Wernicke’s encephalopathy requires urgent acute-hospital assessment.
After successful withdrawal, offer psychological and social support and consider acamprosate or naltrexone after checking relevant renal, liver and opioid-related risks.
Assess suicidality, safeguarding, pregnancy, liver disease, nutrition, housing, driving and concurrent drug use throughout the pathway.

First-line investigation

Structured alcohol-use assessment with AUDIT or AUDIT-C, detailed last-drink and withdrawal history, examination and vital signs, mental-health and safeguarding assessment, and baseline FBC, liver function, renal function, electrolytes, glucose, albumin and INR when assisted withdrawal or complications are being assessed.

Management

Recognise withdrawal risk and prevent unsafe cessation

Take a detailed drinking and withdrawal history, assess immediate medical and psychiatric risk, and arrange clinician-supervised withdrawal rather than sudden cessation or self-detoxification.^1,3,9,4

Choose the safest setting

Use community withdrawal only after individual assessment with trained monitoring, emergency access and suitable support; previous severe withdrawal, major comorbidity, pregnancy, high Wernicke risk or an unsafe home favours inpatient care.^3,2,5

Treat withdrawal and prevent neurological complications

Give risk-based thiamine and use a locally approved, monitored benzodiazepine reducing regimen; escalate immediately for seizure, delirium tremens or suspected Wernicke’s encephalopathy.^3,2,6,7

Address comorbidity, safeguarding and recovery goals

Assess mental health, suicidality, nutrition, liver disease, pregnancy, other substances, domestic abuse, housing and capacity, and involve specialist alcohol and safeguarding services where needed.^1,8,5

Use relapse-prevention medication appropriately

After successful withdrawal, combine psychosocial support with a medically assessed choice of acamprosate or naltrexone; consider disulfiram only when its risks and monitoring are understood and the goal is abstinence.^1,2,7

Monitor closely and safety-net

Provide frequent early review, monitor withdrawal and medication effects, give written ambulance triggers, and maintain longer-term relapse-prevention and social support after detoxification.^5,2,10

Exam traps

A high AUDIT score is not the same as a safe detoxification plan; previous seizures, delirium tremens, comorbidity and social support determine risk.
CIWA-Ar is an adjunct to trained clinical assessment and does not replace examination, vital signs, mental-state assessment or a safe setting.
Delirium tremens is a medical emergency; haloperidol is not monotherapy and must not replace adequate benzodiazepine treatment.
Do not use phenytoin for alcohol-withdrawal seizures.
Thiamine prophylaxis and urgent treatment of suspected Wernicke’s encephalopathy are separate from the benzodiazepine withdrawal regimen; a complete classical triad is not required.
Acamprosate and naltrexone are relapse-prevention options after withdrawal, not treatments for acute withdrawal; naltrexone requires explicit opioid-interaction counselling.

Illustrations

GABA/glutamate rebound mechanism in withdrawalSchematic of chronic alcohol-induced inhibitory-excitatory neuroadaptation and the resulting hyperexcitability when alcohol is withdrawn.PassFinals · original

Wernicke’s encephalopathy risk pathwayDiagram showing how poor nutrition and thiamine deficiency create risk of Wernicke’s encephalopathy, and the need for prompt thiamine treatment when it is suspected.PassFinals · original

Withdrawal assessment and escalationLayout showing structured withdrawal assessment, monitoring for oversedation and escalation for seizure, delirium tremens or suspected Wernicke’s encephalopathy.PassFinals · original

Key sources

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.