Alcohol-related disorders, including alcohol intoxication, alcohol use disorder (AUD), and alcohol withdrawal, are a group of conditions associated with disruptive patterns of alcohol use. Alcohol intoxication is the acute onset of behavioral and psychomotor impairment shortly after an episode of drinking. Alcohol use disorder (AUD) is characterized by clinically significant psychosocial and behavioral problems associated with alcohol use. Alcohol withdrawal develops after a sudden cessation or reduction of alcohol use in patients with a history of excessive drinking. The diagnosis of an alcohol-related disorder can be established using the DSM-5 criteria. The most important aspect of management for all alcohol-related disorders is the cessation of alcohol use. Therapeutic management is guided by the severity of the disorder.
Seefor a review of alcohol metabolism pathways.
- Definition: : a temporary condition in which excessive consumption of alcohol alters a person's consciousness, cognition, perception, judgment, affect, and/or behavior
- Pathophysiology: The majority of alcohol consumed is absorbed by the proximal small intestine. Only a small amount of alcohol gets absorbed by the oral, esophageal, and/or gastric mucosa.
- Clinical features
|Mild intoxication (BAC 0.01–0.1%, < 100 mg/dL)||Moderate intoxication (BAC 0.1–0.3%, 100–300 mg/dL||Severe intoxication (BAC > 0.3%; > 300 mg/dL)|
In the US, the maximum legal limit for driving under the influence of alcohol is a BAC of 0.08%.
Because alcohol has a long absorption time (approx. 40 min), patients with alcohol intoxication may deteriorate over time.
- Laboratory tests: See “ ” below.
- Agitation and/or aggression management
- Thiamine: for Wernicke encephalopathy prophylaxis or treatment
- Correction of electrolyte disbalance, hypoglycemia, and hypothermia
- Thorough assessment for occult trauma (e.g., imaging), if suspected
AUD is a chronic condition in which an uncontrolled pattern of alcohol use leads to significant physical, psychological, and social impairment or distress. Symptoms of withdrawal emerge when drinking is discontinued. Not all individuals who drink heavily develop AUD, and not all individuals with AUD have a history of heavy alcohol use.
- Alcohol consumption results in > 3 million deaths worldwide per year.
- US lifetime prevalence is ∼ 29%
- More common in Native Americans and Alaska Natives
- Peak incidence: 21–34 years
- Sex: ♂ > ♀ (2.5:1) 
- Associated comorbidities
- Genetic factors
- Neurobiological factors
- Psychosocial factors
- Family history of AUD 
- Environmental influence: e.g., social pressure to consume alcohol, economic disadvantage (e.g., unemployment), stressful life events
Diagnosis of AUD begins with a screening test, which is followed by a confirmatory test based on patient history. Commonly used screening tests include AUDIT-C and CAGE tests. Diagnosis is confirmed if the patient history meets the DSM-V criteria for AUD.
- Three questions based on the Alcohol Use Disorders Identification Test (AUDIT)
- Every response is given a score from 0 to 4 points.
- The total score can range from 0 to 12.
- A positive test suggests the presence of an alcohol use disorder.
- ≥ 4 in men
- ≥ 3 in women
|How often did you have a drink containing alcohol in the past year?||Never||0|
|2–4 times a month||2|
|2–3 times a week||3|
|≥ 4 times a week||4|
|How many drinks did you have on a typical day when you were drinking in the past year?||1–2||0|
|How often did you have ≥ 6 drinks on one occasion in the past year?||Never||0|
|< Once per month||1|
|Daily or almost daily||4|
A series of four questions (CAGE) is used to screen for AUD
- Cut down drinking: Have you ever felt you should cut down on your drinking?
- Annoyed: Have people annoyed you by criticizing your drinking?
- Guilty: Have you ever felt guilty about drinking?
- Eye-opener: Have you ever felt you needed a drink first thing in the morning (eye-opener) to steady your nerves or to overcome a hangover?
- Every “yes” response counts as one point.
- The CAGE test is considered positive for AUD if ≥ 2 questions are answered in the affirmative.
- A series of four questions (CAGE) is used to screen for AUD
Diagnostic criteria (according to DSM-5)
- 11 criteria based on the patient's history within the past 12 months
A diagnosis of AUD is established once ≥ 2 criteria are met.
- Drinking more or over a longer period than intended
- Tried to cut down or stop more than once, but couldn't
- Spends a lot of time drinking or recovering from aftereffects
- Strong desire to drink alcohol
- Drinking has a negative impact on everyday function (social, work etc)
- Continued drinking despite social or interpersonal problems
- Given up interests and activities that were important because of drinking
- Drinking in physically hazardous situations more than once
- Continued drinking despite physical or psychological problems
- Increasing amount of drinks to maintain same effects as before
- Features of withdrawal when the effects of alcohol wear off (see alcohol withdrawal below)
- Mild: presence of 2–3 criteria
- Moderate: presence of 4–5 criteria
- Severe: presence of ≥ 6 criteria
- AUD is a clinical diagnosis, and laboratory tests are not usually required, although they may provide evidence of problematic alcohol use in patients who cannot provide a conclusive history.
- Acute alcohol intoxication: high BAC
Chronic alcohol intoxication
- Liver damage
- Carbohydrate-deficient transferrin (CDT)
- Malnutrition and bone marrow damage
- Psychosocial support (e.g., Alcoholics Anonymous): helps the patient maintain abstinence for longer periods and provides support to the patient's close family and friends.
- Pharmacotherapy (to promote alcohol cessation)
- first-line agent): (reduces cravings for alcohol
- Disulfiram: exacerbates intoxication symptoms and induces negative conditioning (only recommended in patients who show strong motivation and commitment for abstinence)
- Acamprosate: blocks central glutamate receptors and reduces cravings for alcohol
- Topiramate or gabapentin: for patients who do not tolerate or respond to other medications
- Vitamin supplementation
- steatosis, hepatitis, fibrosis) (e.g.,
- Testicular atrophy
- Alcoholic cerebellar degeneration
- Marchiafava–Bignami disease
- Mood disturbance: anxiety, depression, irritability, aggression
- Vitamin deficiency
- Cytochrome P-450 induction
- In pregnancy:
- Caused by a sudden reduction or cessation of alcohol intake after a prolonged period of heavy drinking
- Onset and duration vary among different syndromes.
- May be assessed using the CIWA-Ar score
- Delirium tremens is the most severe form of alcohol withdrawal.
Individuals with chronic alcohol use often develop withdrawal symptoms 48–72 hours after hospitalization because they do not have access to alcohol in the hospital.
- Onset: 6–36 hours after last drink
- Clinical features
- Duration: 24–48 hours
- Onset: 6–48 hours after last drink
- Clinical features: : brief, generalized tonic-clonic seizure (usually a single episode)
- Onset: 12–48 hours after last drink
- Clinical features
- Duration: 24–48 hours after onset
- Definition: persistent alteration of consciousness and sympathetic hyperactivity due to alcohol withdrawal
- Most commonly occurs 48–96 hours after last consumption of alcohol
- Symptoms commonly manifest during hospitalization, when the patient is no longer able to drink alcohol.
- Symptoms of altered mental status
- Symptoms of autonomic instability
- Symptoms of neurological impairment
- Duration: 1–5 days
- IV fluid therapy and electrolyte disbalance correction
- Thiamine: for Wernicke encephalopathy prophylaxis or treatment (administer prior to glucose)
- Folate and multivitamins
- IV benzodiazepines for control of psychomotor agitation and seizures
- Anticonvulsants (e.g. carbamazepine): if seizures persist despite benzodiazepines administration
Antipsychotics (e.g., haloperidol, risperidone)
- May be used for management of psychotic symptoms (never as independent medication)
- Should be avoided, if possible, or administered in low doses
- Definition: elevated anion gap metabolic acidosis due to increased production of ketone bodies with normal or low glucose levels resulting from the combined effects of alcohol and starvation on glucose metabolism
- Onset: typically occurs 1–2 days after cessation of drinking
Pathophysiology: accumulation of ketogenesis) as a result of: (see
- Depleted glycogen stores in the liver (malnutrition/decreased carbohydrate intake)
- Increased lipolysis and free fatty acid release
- Volume depletion (e.g., vomiting, poor oral fluid intake) → impaired renal perfusion → decreased ability to excrete ketone bodies
- Clinical features
- Prognosis: The condition is reversible with appropriate treatment.