Alcohol Use Disorders
NICE Clinical guideline [CG115] Alcohol-use disorders: diagnosis, assessment and management of harmful drinking (high-risk drinking) and alcohol dependence. Last updated: Oct 2014.
NICE Clinical guideline [CG100] Alcohol-use disorders: diagnosis and management of physical complications. Last updated: Apr 2017.
NICE CKS Alcohol – problem drinking. Last revised May 2025.
Background information has been added accordingly.
Date: 09/11/25
Note that alcohol-related liver disease is covered in a separate article.
Definition and Terminology
Low-Risk Drinking Guidelines
The following advice should be given to ALL patients who drink alcohol:
- Drink maximum of 14 units of alcohol per week + spread it over 3 days or more
- i.e. if someone drinks 10 units a day once a week, that is NOT considered low-risk drinking
- Avoiding drinking completely during pregnancy
Calculating units of alcohol:
- Definition: 1 unit of alcohol = 10 mL (8 grams) of pure ethanol
- To calculate the number of units of alcohol in a drink: total volume of the drink (mL) x alcohol % / 1000
- Example: how many units of alcohol in a small glass (125 mL) or red wine (12% alcohol)
- Working: 125 x 12 / 1000 = 1.5 units of alcohol
One unit of alcohol is roughly equivalent to:
- Half a pint of lower-strength beer, lager, or cider (around 3.6% alcohol)
- A small pub measure (25 mL) of spirits (40% alcohol)
- A standard pub measure (50 mL) of fortified wine, for example, sherry or port (20% alcohol)
Alcohol Use Disorder Terminology
Problem alcohol use: non-specific term defined as exceeding low-risk drinking guidelines
Alcohol use disorder is an umbrella term, including:
- Hazardous (increasing risk) drinking: pattern of alcohol consumption increases the risk of harm, defined by amount of alcohol consumption (male: 14-50 units a week; female: 14-35 units a week)
- Harmful (higher-risk) drinking: pattern of alcohol consumption that causes health problems directly related to alcohol (e.g. alcoholic liver disease, acute pancreatitis, depression)
- Alcohol dependence: characterised by craving, tolerance, a preoccupation with alcohol, and continued drinking in spite of harmful consequences (e.g. alcoholic liver disease, depression)
Alcohol withdrawal is a complication of alcohol dependence, referring to symptoms that occur after stopping or reduced alcohol consumption.
Alcohol Use Disorder
Long-Term Complications
Key long-term complications: [Ref]
| Organ system | Examples |
|---|---|
| GI and liver |
|
| Nervous system |
|
| Cardiovascular system |
|
| Musculoskeletal system |
|
| Cancer |
|
| Mental health |
|
Identification and Assessment
NICE recommends the following assessment tools:
| Assessment tool | Purpose |
|---|---|
| AUDIT | Identification of alcohol misuse and routine outcome measure
AUDIT PC and AUDIT-C questionnaires are shorter and can be used in primary care or where time is limited |
| SADQ / LDQ | Assess severity of alcohol dependence |
Management – Promoting Abstinence and Preventing Relapse
Offer motivational intervention at initial assessment
- Consider residential rehabilitation (maximum 3 months) in those who are homeless
For harmful drinkers with mild alcohol dependence
- 1st line: psychological intervention (e.g. cognitive behavioural therapies, behavioural therapies or social network and environment-based therapies)
- 2nd line: psychological intervention + drug (acamprosate / naltrexone)
- NICE noted that evidence for acamprosate is less robust than naltrexone
- Nalmefene is an option if there is no need for immediate detoxification + alcohol consumption >60g per day (men) >40g per day (women) + without withdrawal symptoms
Patients with mild-alcohol dependence do NOT typically require assisted alcohol withdrawal (i.e. there is no need to give the benzodiazepine regimen).
However, patients with moderate / severe alcohol dependence may require assisted alcohol withdrawal due to the risk of withdrawal upon cessation / cutting down. See the alcohol withdrawal section below.
Alcohol Withdrawal
Definition
Alcohol withdrawal is a clinical syndrome that occurs after abrupt reduction or cessation of alcohol consumption, in the context of previous heavy and prolonged alcohol use.
Pathophysiology
Ethanol acts as a CNS depressant, by enhancing GABA (inhibitory) neurotransmission and inhibiting glutamatergic (excitatory) neurotransmission
- After prolonged exposure to alcohol (in alcohol use disorder), the brain compensates by downregulating GABA neurotransmission and upregulating glutamatergic neurotransmission
- When alcohol intake is abruptly reduced / stopped → this causes decrease in inhibitory GABA neurotransmission and increase in excitatory glutamatergic neurotransmission
- Net effect: CNS hyperexcitability
Clinical Features
Key features of mild / moderate alcohol withdrawal:
- Nausea or vomiting
- Tremor
- Abnormal sweating
- Anxiety
- Agitation
- Headache
- Tactile disturbances (e.g. pins and needles, itching, feeling of bugs crawling under the skin)
Features of delirium tremens (the most severe manifestation of alcohol withdrawal)
- Altered mental status (fluctuating level of consciousness / impaired consciousness / severe confusion / disorientation / prominent psychomotor agitation)
- Visual hallucinations (tactile and auditory hallucinations may also occur)
- Autonomic instability (tachycardia, hypertension)
- Alcohol withdrawal seizures (usually generalised tonic-clonic) can occur
Timing: [Ref]
- Alcohol withdrawal syndrome typically begin within 4-12 hours after the last drink
- Peak risk of alcohol withdrawal seizures is 24 hours after the last drink
- Peak risk of delirium tremens is 72 hours after the last drink
Assisted Alcohol Withdrawal (Prevention of Alcohol Withdrawal)
Assisted alcohol withdrawal is for those who are NOT actively withdrawing. Assisted alcohol withdrawal is purely a preventive measure to prevent the patient from developing alcohol withdrawal upon cutting down alcohol consumption.
Indications and Choice of Setting
Offer community-based assisted withdrawal or specialist alcohol service (if there are safety concerns) if
- Patient drinks >15 units per day, and/or
- AUDIT ≥20 (possible dependence)
Inpatient or residential assisted withdrawal is indicated if any of the following:
- >30 units per day
- ≥30 on SADQ
- History of epilepsy
- Previous withdrawal-related seizures / delirium tremens during previous assisted withdrawal programmes
- Need concurrent withdrawal from alcohol and benzodiazepines
- Regularly drink between 15-30 units per day and significant psychiatric or physical comorbidities or significant learning disability or cognitive impairment
If none of the above criteria is met, the patient can be managed with active observation without medication.
Choice of Regimen
Choice of regimen:
- Community settings: fixed dose regimen
- Inpatient / residential settings: fixed dose regimen or symptom-triggered regimen
Choice of Drug
Benzodiazepine is the drug class of choice for medically assisted withdrawal:
- 1st line: chlordiazepoxide / diazepam
- If patient has liver impairment: lorazepam preferred
- Family member or carer should preferably oversee the administration of medication
- Monitor the patient every other day during assisted withdrawal
After Successful Withdrawal
Offer psychological intervention + pharmacological intervention to prevent relapse and promote abstinence
- 1st line: acamprosate / naltrexone
- 2nd line: disulfiram
Management – Acute Alcohol Withdrawal
Mild / Moderate Alcohol Withdrawal
CIWA-Ar is used to assess the severity of alcohol withdrawal and to decide where medication is needed or not:
- CIWA-Ar ≥10 is a threshold to consider medications to treat withdrawal symptoms
- 0-9: mild withdrawal symptoms
- 10-15: moderate withdrawal symptoms
- >15: severe withdrawal symptoms
Offer a symptom-triggered regimen
- 1st line: benzodiazepine (chlordiazepoxide / diazepam, use lorazepam in liver impairment) or carbamazepine
- 2nd line: clomethiazole
Disclaimer: NICE does not explicitly recommend a CIWA-Ar score cutoff to guide when medically assisted withdrawal is indicated., NICE recommends using clinical judgment combined with CIWA-Ar.
However, many clinical protocols and other guidelines use approximately CIWA-Ar score of 10 as a cut-off to consider medically assisted withdrawal to prevent progression.
Delirium Tremens
Delirium tremens is a medical emergency, patients would require immediate pharmacological management (benzodiazepine and supportive care) and CIWA-Ar scoring is not required to determine need for therapy.
- 1st line: oral lorazepam
- 2nd line: parenteral lorazepam or haloperidol
Alcohol Withdrawal Seizures
- 1st line: IV lorazepam
Do not offer phenytoin to treat alcohol withdrawal seizures
Acute Alcohol Use Complications
Key non-withdrawal-related complications include:
- Acute alcohol intoxication
- Alcoholic ketoacidosis
- Thiamine-related complications (Wernicke’s encephalopathy and Korsakoff syndrome)
Acute Alcohol Intoxication
Clinical Features
Alcohol intoxication presents with clinical features that vary by severity: [Ref]
| Mild intoxication |
|
| Moderate intoxication | Characterised by more pronounced neurological impairment
Other
|
| Severe intoxication | Characterised by profound CNS depression |
The manifestation, severity, and duration of symptoms depend on various factors:
- Genetics (e.g. acetaldehyde dehydrogenase activity)
- Alcohol absorption and metabolism
- Any concurrent use of recreational drugs
Complications
Complications mainly arise from severe intoxication, key ones include:
- Head injury
- Aspiration
- Respiratory depression
- Hypoglycemia
- Hypothermia
Management
Management is supportive:
- Maintain a clear airway + measures to reduce risk of aspiration
- Oral / IV hydration
- Correction of hypoglycemia or electrolyte disturbances
- Cardiorespiratory monitoring and support if necessary
2 most important thing to watch-out for in acute alcohol intoxication are:
- Any possible head injury
- Any possible aspiration
Alcoholic Ketoacidosis (AKA)
AKA is defined as a high anion gap metabolic acidosis with ketosis occurring in the context of recent or chronic alcohol use, typically following a period of binge drinking and subsequent starvation or poor oral intake
Pathophysiology:
- Ethanol metabolism increases the NADH/NAD⁺ ratio, inhibiting gluconeogenesis and promoting conversion of fatty acids to ketone bodies
- Starvation and vomiting lead to glycogen depletion, decreased insulin, and increased glucagon, further driving ketogenesis
Management:
- Thiamine supplementation
- Aggressive IV fluid resuscitation with dextrose-containing solution
Note that alcohol binge-drinking is a well-recognised trigger for DKA, therefore it’s important to distinguish between AKA and DKA
- Both AKA and DKA causes a high anion-gap metabolic acidosis with ketosis
- Glucose is very high in DKA; while glucose is often low / normal in AKA
Thiamine-Related Complications
See the Wernicke’s Encephalopathy and Korsakoff Syndrome article.
References