Alcohol-related disorders

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.

See breakdown of ethanol for 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%, 10–300 mg/dL)	Severe intoxication (BAC > 0.3%; > 300 mg/dL)
Increased agitation, euphoria, disinhibition, urge to speak, impaired judgment Unsteady gait and difficulties standing upright Skin flushing Mild tachycardia and hypotension	Pronounced disinhibition Significant reduction of attention, responsiveness, alertness, and reaction time Impaired vision and sound localization Increasing unsteadiness of gait and slurred speech Dizziness Psychomotor agitation Nausea and vomiting Amnestic gaps (blackouts)	Delusions and hallucinations Severe dysarthria Nausea and vomiting Ataxia Nystagmus Alcoholic coma (usually occurs at BAC levels 0.40–0.50%) including: Severely impaired consciousness Lack of response to external stimuli Absent airway defense reflexes and respiratory depression

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.

• Treatment
  • Agitation and/or aggression management
    • Sedation with benzodiazepines or typical antipsychotics (e.g., haloperidol)
    • Mechanical restraints may be used for individuals who pose a danger to themselves and/or others if de-escalation and medication strategies have been unsuccessful.
  • Aggressive fluid therapy
  • Thiamine: for Wernicke encephalopathy prophylaxis or treatment
  • Correction of electrolyte disbalance, hypoglycemia, and hypothermia
  • Thorough assessment for occult trauma (e.g., imaging), if suspected

Haloperidol may worsen respiratory depression secondary to alcohol intoxication!

References:^{[1][2][3][4][5][6][7][8]}

• 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.

Minor withdrawal

• Onset: 6–36 hours after last drink
• Clinical features
  • Tremor
  • Insomnia
  • Anxiety, palpitations, and sweating
  • Gastrointestinal upset
  • Headache
• Duration: 24–48 hours

Withdrawal seizures

• Onset: 6–48 hours after last drink
• Clinical features: : brief, generalized tonic-clonic seizure (usually a single episode)

Alcoholic hallucinosis

• Onset: 12–48 hours after last drink
• Clinical features
  • Consciousness is usually intact.
  • Normal vital signs
  • Auditory and/or visual hallucinations are common; (tactile hallucinations are also possible).
  • Delusions
• Duration: 24–48 hours after onset

Delirium tremens

• Definition: persistent alteration of consciousness and sympathetic hyperactivity due to alcohol withdrawal
• Onset: most commonly occurs 48–96 hours after last drink
• Clinical features
  • Symptoms of altered mental status
    • Impaired consciousness and disorientation
    • Visual and tactile hallucinations (usually small moving objects, e.g., mice, crawling insects)
    • Increased suggestibility
  • Symptoms of autonomic instability
    • Tachycardia
    • Hypertension
    • Sweating
    • Nausea
  • Symptoms of neurological impairment
    • Generalized tonic-clonic seizures
    • Rest and intention tremor (first high-frequency, then low-frequency)
    • Hyperreflexia
• Duration: 1–5 days

In contrast to patients with alcoholic hallucinosis, patients with delirium tremens have impaired consciousness and abnormal vital signs.

Treatment

• IV fluid therapy and electrolyte disbalance correction
• Thiamine: for Wernicke encephalopathy prophylaxis or treatment (administer prior to glucose)
• Dextrose
• Folate and multivitamins
• IV benzodiazepines for control of psychomotor agitation and seizures
  • Long-acting (e.g., diazepam, chlordiazepoxide) OR
  • Short-acting (e.g., lorazepam; , oxazepam): especially for patients with liver disease
• 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

Lorazepam, Oxazepam, and Temazepam are preferred in those who drink a LOT because they are not metabolized by the liver and therefore safe in alcoholic liver disease.

In the case of alcohol withdrawal seizures, benzodiazepines are preferred over other anticonvulsants to prevent further seizures.

References:^{[1][2][3][4][5][6][7][8]}

• 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
• Etiology
  • Most commonly occurs in malnourished individuals with AUD
  • Associated with recent episodes of binge drinking complicated by poor food intake, dehydration, and vomiting
• Onset: typically occurs 1–2 days after cessation of drinking
• Pathophysiology: accumulation of ketone bodies (see ketogenesis) as a result of:
  • Depleted glycogen stores in the liver (malnutrition/decreased carbohydrate intake)
  • Increased lipolysis and free fatty acid release
    • Decreased energy intake (e.g., starvation) → decreased insulin secretion and excess secretion of glucagon, catecholamines, and cortisol
    • Increased NADH:NAD⁺ ratio: chronic alcohol intake → impaired hepatic gluconeogenesis → hypoglycemia → decreased insulin secretion
  • Volume depletion (e.g., vomiting, poor oral fluid intake) → impaired renal perfusion → decreased ability to excrete ketone bodies
• Clinical features
  • Nausea, vomiting, and abdominal pain
  • Tachypnea
  • Features of dehydration and electrolyte imbalance (e.g., hyponatremia, hypokalemia, hypophosphatemia), including hypotension and altered mental status
  • Features of alcohol withdrawal: e.g., tremors, seizures, tachycardia
• Diagnostics
  • Arterial blood gas analysis: elevated anion gap metabolic acidosis
  • Ketonemia (acetoacetate, β-hydroxybutyrate, acetone in blood) and ketonuria
  • Blood glucose: low, normal, or only moderately increased
  • Blood ethanol: not detectable or low
• Treatment
  • Initially: parenteral administration of thiamine to prevent Wernicke encephalopathy
  • Followed by: IV fluid therapy with 5% dextrose in 0.9% saline
  • Correction of electrolyte imbalances
  • Treatment of alcohol withdrawal and complications of chronic alcohol abuse (see alcohol withdrawal management in “Treatment” above)
• Prognosis: The condition is reversible with appropriate treatment.

In contrast to diabetic ketoacidosis, blood glucose levels are normal or low in alcoholic ketoacidosis.

References:^{[1][2][3][4][5][6][7][8]}