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# Alcohol use disorder

Alcohol use disorder is a pattern of drinking that a person cannot control despite harm. It damages the brain, liver and many organs and is treatable.

Updated 2026-11-01

## Structures involved

Tap one to see what it is and open it in 3D.

- [Frontal lobe](https://durgical.com/en/anatomy/superior-frontal-gyrus/)
- [Cerebellum](https://durgical.com/en/anatomy/anterior-quadrangular-lobule/)
- [Liver](https://durgical.com/en/anatomy/liver/)
- [Thalamus](https://durgical.com/en/anatomy/thalamus/)
- [Hippocampus](https://durgical.com/en/anatomy/hippocampus/)
- [Pancreas](https://durgical.com/en/anatomy/pancreas/)
- [Stomach](https://durgical.com/en/anatomy/stomach/)
- [Esophagus](https://durgical.com/en/anatomy/esophagus-abdominal-part/)

## In embryology

- [Alcohol: fetal alcohol spectrum disorder](https://durgical.com/en/embryology/alcohol-fetal-alcohol-spectrum-disorder/)

## In the clinical exam

- [Medicines, allergies and habits: tobacco, alcohol and other substances](https://durgical.com/en/clinical-exam/medicines-allergies-and-habits-tobacco-alcohol-and-other-substances/)
- [Cerebellar tests: finger–nose, heel–shin and rapid alternating movements](https://durgical.com/en/clinical-exam/cerebellar-tests-finger-nose-heel-shin-and-rapid-alternating-movements/)
- [Cerebellar syndrome](https://durgical.com/en/clinical-exam/cerebellar-syndrome/)

## Why it happens

- [Alcohol: how it injures the liver, brain, heart and fetus](https://durgical.com/en/general-pathology/alcohol-how-it-injures-the-liver-brain-heart-and-fetus/)
- [Cancer epidemiology: age, environment, predisposing conditions (and Colombia)](https://durgical.com/en/general-pathology/cancer-epidemiology-age-environment-predisposing-conditions/)
- [The main neurotransmitters](https://durgical.com/en/physiology/the-main-neurotransmitters/)
- [Ethanol metabolism](https://durgical.com/en/biochemistry/pathways/ethanol-metabolism/)

## What it is

A problematic pattern of alcohol use causing clinically significant impairment or distress, with loss of control, craving, continued use despite harm, tolerance and withdrawal. Severity is mild, moderate or severe according to the number of criteria met.

## Who gets it

Worldwide, alcohol causes millions of deaths a year and hundreds of millions of people have an alcohol use disorder. In the Americas, consumption is above the global average and heavy episodic drinking is common, with men most affected but women's drinking rising. In Colombia, alcohol is the most used psychoactive substance and is linked to traffic injuries, violence and liver disease, while treatment coverage stays low.

## Causes

- Genetic vulnerability (about half of the risk)
- Repeated exposure that remodels the brain's reward and stress systems
- Social and cultural factors that encourage heavy drinking

## Risk factors

- Family history of alcohol use disorder
- Early start of drinking in adolescence
- Heavy episodic (binge) drinking
- Depression, anxiety, trauma and other mental disorders
- Easy access, low price and social norms that accept heavy drinking
- Male sex

## Pathophysiology

Alcohol enhances GABA-A and inhibits NMDA glutamate receptors and releases dopamine in the reward pathway. Chronic use downregulates GABA and upregulates glutamate receptors, so stopping causes a hyperexcitable state (withdrawal). The prefrontal cortex loses control over craving, thiamine deficiency damages the brain (Wernicke encephalopathy, Korsakoff syndrome) and the cerebellar [vermis](https://durgical.com/en/anatomy/central-lobule/) degenerates; in the liver, alcohol metabolism leads to steatosis, hepatitis and cirrhosis.

## Classification

- Mild: 2 to 3 criteria
- Moderate: 4 to 5 criteria
- Severe: 6 or more criteria
- Related states: intoxication, withdrawal, withdrawal delirium (delirium tremens)

## Symptoms and signs

- Drinking more or for longer than intended and failed attempts to cut down
- Craving and much time spent obtaining, drinking and recovering
- Neglect of work, study or family; continued drinking despite problems
- Tolerance
- Withdrawal: tremor, sweating, anxiety, insomnia, tachycardia, nausea
- Signs of chronic use: macrocytosis, raised liver enzymes, spider angiomas, unsteady gait

## Red flags

- Withdrawal seizures or delirium tremens (confusion, hallucinations, fever, autonomic instability), usually 48 to 96 hours after the last drink
- Confusion, ataxia and eye-movement abnormalities (Wernicke encephalopathy)
- Vomiting blood or black stools (variceal bleeding)
- Severe abdominal pain (pancreatitis)
- Suicidal thoughts, often during intoxication or depression

## Diagnosis

**Clinical**
Screening with AUDIT or AUDIT-C, or the CAGE questions (Cut down, Annoyed, Guilty, Eye-opener). Diagnosis by DSM-5 criteria (at least 2 of 11 in 12 months). Withdrawal severity is scored with the CIWA-Ar scale.

**Tests**
Supportive markers: GGT, AST and ALT (AST:ALT ratio often above 2), mean corpuscular volume, carbohydrate-deficient transferrin, and blood alcohol level. Also glucose, electrolytes, magnesium, phosphate, lipase and coagulation when complications are suspected.

**Imaging**
[Liver](https://durgical.com/en/anatomy/liver/) ultrasound for steatosis or cirrhosis; brain CT after head trauma or with focal signs; MRI may show changes in Wernicke encephalopathy.

## Differential diagnosis

- Other sedative or substance use disorders
- Primary depression or anxiety
- Delirium from other causes (infection, hepatic encephalopathy, hypoglycaemia) in withdrawal
- Other causes of raised liver enzymes (viral hepatitis, metabolic dysfunction-associated fatty liver disease)

## Goal of treatment

Safe management of withdrawal, abstinence or a large reduction in drinking, treatment of medical and mental health complications and lasting recovery.

## Treatment

**Acute**
Withdrawal: benzodiazepines (symptom-triggered by CIWA-Ar) are first-line; thiamine is given before glucose to prevent Wernicke encephalopathy; fluids, electrolytes and magnesium are corrected.

**Medical**
Relapse prevention: naltrexone and acamprosate are first-line; disulfiram (aversive) in motivated, supervised people; other options include topiramate and baclofen. Naltrexone is avoided in liver failure and with opioid use.

**Conservative**
Brief interventions in primary care, motivational interviewing, cognitive behavioural therapy and mutual-help groups.

**Follow-up**
Nursing in withdrawal: vital signs, CIWA-Ar scores, seizure and fall precautions, orientation, hydration and nutrition; then follow-up of liver function and relapse.

## Drugs for this condition

- [Acamprosate](https://durgical.com/en/pharmacology/acamprosate/)
- [Disulfiram](https://durgical.com/en/pharmacology/disulfiram/)

## Complications

- Alcohol-related liver disease: steatosis, alcoholic hepatitis and cirrhosis
- Acute and chronic pancreatitis
- Wernicke encephalopathy and Korsakoff syndrome (thiamine deficiency); cerebellar degeneration
- Peripheral neuropathy and alcoholic cardiomyopathy
- Gastritis, upper gastrointestinal bleeding and Mallory-Weiss tears
- Cancers of the mouth, throat, oesophagus, liver, colon and breast
- Injuries, violence, traffic accidents and suicide
- Fetal alcohol spectrum disorder when drinking in pregnancy

## Prognosis

Relapse is common, but many people achieve long remission with treatment; outcomes are better with social support and treatment of coexisting disorders. Continued heavy drinking shortens life through liver disease, cancer, injuries and suicide.

## Prevention

- Screening and brief intervention in primary care
- Population policies on price, availability and marketing of alcohol
- Delaying first use in adolescents
- No alcohol in pregnancy

## Test yourself

Think of the answer, then tap the question to see it.

## What are the four CAGE questions about?

Cutting down, being Annoyed by criticism, feeling Guilty and needing an Eye-opener in the morning.

## Which drug class is first-line for alcohol withdrawal?

Benzodiazepines, usually symptom-triggered with the CIWA-Ar scale.

## Why is thiamine given before glucose in heavy drinkers?

Glucose can precipitate or worsen Wernicke encephalopathy in thiamine deficiency.

## When does delirium tremens typically appear?

About 48 to 96 hours after the last drink.

## Which two drugs are first-line to prevent relapse?

Naltrexone and acamprosate.

[Add to my cards (5)](https://durgical.app/estudiar/?add=/en/conditions/alcohol-use-disorder/)

## Related conditions

- [Alcoholic liver disease (biochemistry)](https://durgical.com/en/conditions/alcoholic-liver-disease/)
- [Wernicke encephalopathy (thiamine deficiency)](https://durgical.com/en/conditions/wernicke-encephalopathy/)
- [Cirrhosis](https://durgical.com/en/conditions/cirrhosis/)
- [Acute pancreatitis](https://durgical.com/en/conditions/acute-pancreatitis/)
- [Chronic pancreatitis](https://durgical.com/en/conditions/chronic-pancreatitis/)
- [Upper gastrointestinal bleeding](https://durgical.com/en/conditions/upper-gastrointestinal-bleeding/)
- [Portal hypertension](https://durgical.com/en/conditions/portal-hypertension/)
- [Major depressive disorder](https://durgical.com/en/conditions/major-depressive-disorder/)
- [Suicidal behaviour and suicide risk](https://durgical.com/en/conditions/suicidal-behaviour-and-suicide-risk/)

Educational information, not medical advice. For any symptom, see a health professional.

Sources: [Alcohol](https://www.who.int/news-room/fact-sheets/detail/alcohol) (World Health Organization, 2024); [Alcohol](https://www.paho.org/es/temas/alcohol) (Organización Panamericana de la Salud (OPS/OMS), 2025); [Alcohol Use Disorder (AUD)](https://medlineplus.gov/alcoholusedisorderaud.html) (MedlinePlus (National Library of Medicine), 2025).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/conditions/alcohol-use-disorder/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/conditions/alcohol-use-disorder/