Revised October 2026: thiamine dosing, withdrawal pharmacology and the haloperidol advice have been updated after a fact-check.

Ethanol is a socially sanctioned drug that nevertheless causes great harm. Because of its effects on the central nervous system (CNS), its hepatotoxicity, its effect on almost every body system and its widespread use at hazardous and harmful levels, it is a potent social ill. Counting acute binge drinking, withdrawal and chronic overuse, not to mention the psychological and social consequences, ethanol accounts for as many as 15% of Emergency Department visits.¹ Many of these presentations, including the acute binge, can be life-threatening.

Chronic heavy drinkers often take in few calories other than alcohol, which leads to metabolic derangements and vitamin deficiency syndromes that can also be life-threatening. Both sustained and binge drinking can injure hepatocytes and cause alcoholic hepatitis.

These patients are often unwell and vulnerable. Take a comprehensive approach, so that they come to no harm and receive appropriate care.

Taking the history

Broach the history in a matter-of-fact but kind way, while staying a little guarded: because of the nature of addiction, patients often avoid questions about their drinking, and a kind word goes a long way. Once rapport is established, a non-judgemental CAGE questionnaire screens for ethanol misuse, before you move on to a quantitative account of intake as appropriate:

• C: Have you ever felt that you need to Cut down on your drinking?
• A: Have people Annoyed you by criticising your drinking?
• G: Have you ever felt bad or Guilty about your drinking?
• E: Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (the Eye-opener)?

In the unwell patient who volunteers little, some pointed questions help:

• Have you been vomiting?
• Have you had a fever or chills?
• Have you had any abdominal pain?

Pharmacology in brief

Ethanol is a CNS depressant that enhances GABA-A receptor activity. With chronic use the brain adapts: inhibitory GABA signalling is blunted and excitatory (glutamatergic, NMDA) signalling is enhanced. When ethanol is withdrawn, the loss of this GABA enhancement leaves the CNS over-excited, producing a hyperadrenergic state with anxiety, tremor, diaphoresis, tachycardia and hypertension.¹

Ethanol is metabolised mainly in the liver by alcohol dehydrogenase. At the concentrations seen in intoxication, elimination is saturable and behaves as zero-order, so metabolism is described as non-linear. The usual rate is in the order of 15 to 30 mg/dL per hour (about 3 to 6.5 mmol/L per hour), and chronic drinkers tend to clear ethanol faster.

Alcohol-associated conditions and red flags

• GI bleeding: chronic liver disease, portal hypertension, splanchnic venous congestion (with or without thrombosis), coagulopathy
• Alcoholic pancreatitis
• Alcoholic hepatitis
• Alcoholic ketoacidosis
• Trauma and falls
• Vitamin and nutritional deficiency syndromes: malnutrition, starvation, hypoglycaemia, hyponatraemia
• Withdrawal syndromes: delirium tremens; Wernicke-Korsakoff syndrome
• Alcohol substitution: ethylene glycol, methanol, isopropyl alcohol or Listerine toxicity
• Dyspnoea: aspiration pneumonia, tuberculosis, pulmonary infection
• Weakness: malnutrition, co-ingestion, liver disease, anaemia, muscle atrophy, cachexia
• Tremor and fasciculations: withdrawal seizure, liver disease, hypoglycaemia

Withdrawal syndromes (in order of increasing severity; features are additive)

• Mild withdrawal: tremor, abdominal pain, nausea, vomiting
• Withdrawal seizures and hallucinations: generalised seizures over a short period, which can occur at any time after abstinence
• Delirium tremens (DTs): hyperthermia, altered mental state and adrenergic instability, with:
  • severe tremor
  • tachycardia
  • hypertension
  • tachypnoea
  • diaphoresis
  • fever
  • a profoundly altered mental state

Also consider other drug withdrawal syndromes in the patient who overuses ethanol: benzodiazepine and opiate withdrawal.

Examination and urgent testing

Have a low threshold for diagnostic imaging, because blunt trauma so often accompanies both intoxication and withdrawal. A good first step in either is to completely expose the patient and examine for occult injury.

• Point-of-care BGL
• Serum ethanol: interpret it with the clinical picture to separate intoxication from other conditions. A patient who can communicate appropriately, walk safely, eat and drink, and understand discharge instructions is likely ready for discharge regardless of the blood level. That patient should not drive, should have somewhere to go, and should leave with another adult who has received and understood the discharge instructions.
• FBC: leukocytosis from infection, or leukopenia and thrombocytopenia from chronic bone marrow suppression
• Electrolytes and metabolic panel: apart from the usual K⁺ and Na⁺ disturbances, note the bicarbonate. A low level may indicate an anion gap acidosis, especially alcoholic ketoacidosis. Methanol and ethylene glycol are toxic alcohols that cause profound anion gap acidosis and significant morbidity.
• LFTs: AST is typically much greater than ALT in alcoholic liver disease, and GGT is elevated in heavy drinkers.
• Lipase: may not be raised if the pancreatitis is chronic.
• INR and coagulation studies: chronic liver disease causes both a coagulopathy and thrombophilia.
• Urinalysis: infection, ketones, blood, urobilinogen
• Calcium, magnesium, phosphate: reduced in alcoholism and malnutrition, and essential to metabolism. Serum magnesium falls only in the most severe stages of total-body depletion, so a normal level does not reflect magnesium stores.
• Serum osmolality: a large gap between calculated and measured osmolality (osmolar gap; normal below 10 mOsm/kg) signals osmotically active substances such as methanol, ethylene glycol, isopropanol, acetone or mannitol.

Management

Acute ethanol intoxication

Cover the ABCs and provide supportive care. Disinhibited or agitated intoxicated patients often need sedation because they may be a danger to themselves and others. Prefer chemical sedation to physical restraint, which is more harmful.

Benzodiazepines (lorazepam, diazepam, midazolam) are the most commonly used agents, though large doses may be needed and can cause significant respiratory depression. Haloperidol causes less respiratory depression, but it lacks GABA effects and is not adequate treatment for withdrawal. It may also lower the seizure threshold, so use it only as an adjunct to adequate benzodiazepine doses and never on its own in a patient who is withdrawing.

Metabolic and nutritional deficiencies

Ethanol is often the predominant, or only, carbohydrate source for these patients, so they miss out on complex carbohydrates and vitamins. Ketoacidosis from glucose lack, and Wernicke encephalopathy from thiamine deficiency, are the two commonly seen.

• Replace vitamins, including thiamine and folate.
• Where appropriate, offer a balanced meal. It tests whether the patient can tolerate food and supplies the calories and carbohydrate needed for metabolism. If the patient cannot eat, give intravenous glucose.
• Fluids and glucose rapidly correct alcoholic ketoacidosis, which can resolve within hours.
• Give thiamine before the glucose where practical, or at the same time, because of the theoretical risk of precipitating Wernicke encephalopathy in a thiamine-deficient patient.
• Replace magnesium and phosphate, which are typically depleted.

Thiamine deficiency and the resulting altered mental state may take several days, and large amounts of vitamin B1, to correct. Severe deficiency generally needs admission.

Thiamine and Wernicke encephalopathy

Thiamine is a cofactor in many enzymatic reactions of energy metabolism. Deficiency leads to lactate accumulation and excess glutamate production, which can cause excessive excitatory neurotransmission and both vasogenic and cytotoxic oedema in the brain.

The daily requirement is about 1 to 2 mg. Thiamine is absorbed inefficiently in the jejunum, and about 30 mg is stored in the liver, less in liver disease. With inadequate intake a previously healthy person can become thiamine-depleted in as little as 2 to 4 weeks, and sooner in acute or chronic illness. Magnesium is a cofactor for thiamine activity and promotes its uptake into cells.²

Recognition

• The classic triad of encephalopathy, ophthalmoplegia and ataxia is present in only a minority of cases (roughly 15%). Delirium is the most consistent feature.
• Horizontal nystagmus is the most common ocular sign and may improve within hours of IV thiamine.
• Ataxia affects the gait more than the arms, and speech is usually spared.
• Other clues are hypothermia (hypothalamic involvement) and hypotension.
• Chronic thiamine deficiency can present as beriberi: dry (peripheral neuropathy) or wet (high-output heart failure, a medical emergency).
• Wernicke encephalopathy typically evolves from nausea and vomiting, to horizontal nystagmus, ocular nerve palsy, fever, ataxia and progressive mental impairment, eventually leading to Korsakoff syndrome.
• A whole-blood thiamine diphosphate level can help where uncertain.

Imaging

• CT does not usually show Wernicke encephalopathy. Its main role is to exclude other causes.
• MRI is about 50% sensitive and 90% specific, and can normalise within days of starting thiamine. The classic pattern is symmetric and paraventricular.

Treatment and prognosis

• With thiamine, eye signs usually begin to improve within about a day, ataxia and confusion within about a week, and confusion generally resolves over a month.
• Recovery is often incomplete. An irreversible Korsakoff psychosis (marked by confabulation) may follow delayed treatment.²

Thiamine doses

• Prophylaxis for all at-risk patients (alcohol misuse or malnutrition): 100 mg IV or IM daily for a few days.² Australian guidelines recommend 300 mg daily IM or IV for 3 to 5 days in people with poor nutritional state, then 300 mg orally daily for several weeks.³
• Suspected or established Wernicke encephalopathy: use a higher dose. Australian guidelines give at least 500 mg IM or IV daily for 3 to 5 days, with 500 mg three times daily recommended initially, followed by at least 300 mg daily for 1 to 2 weeks.³ Avoid the IM route in coagulopathy.
• Magnesium: magnesium sulfate 2 g IV over 30 to 60 minutes acutely. Where renal function permits, continue magnesium oxide 400 mg orally twice daily during hospitalisation.
• Oral step-down: because of poor jejunal absorption, the oral dose must be higher than the IV dose, for example 200 mg twice daily until discharge.²
• After discharge: continue oral thiamine, about 100 mg daily, and for as long as the patient keeps drinking.³

Alcohol withdrawal

Withdrawal causes CNS excitation through loss of GABA enhancement. A GABA agonist reopens chloride channels and reduces that excitation. Mild withdrawal can often be managed as an outpatient after initial stabilisation in the ED, especially with good support.

Treatment depends on severity. Consider the Clinical Institute Withdrawal Assessment for Alcohol, revised (CIWA-Ar): a score below 10 usually needs no additional medication. It scores ten items:

• Nausea and vomiting: 0 (nil) to 7 (constant)
• Tremor (arms extended, fingers spread): 0 to 7 (severe, even without arms extended)
• Paroxysmal sweats: 0 to 7 (drenching)
• Anxiety: 0 to 7 (acute panic state)
• Agitation: 0 (normal activity) to 7 (paces back and forth during most of the interview)
• Tactile disturbances: 0 (nil) to 1 to 3 (itching) to 7 (continuous hallucinations)
• Auditory disturbances: 0 to 7 (continuous)
• Visual disturbances: 0 to 7 (continuous)
• Headache, fullness in the head: 0 to 7 (extremely severe)
• Orientation and clouding of sensorium: 0 (oriented, performs serial additions) to 4 (disoriented to person or place)

Benzodiazepines are the agents most often used, especially diazepam and lorazepam. Withdrawal peaks at 2 to 3 days and can last 5 to 7, so longer-acting agents are generally preferred: they avoid frequent re-dosing, wear off slowly, and let patients take the next dose before significant symptoms return.

• Diazepam has a long half-life (often quoted as 20 to 50 hours, with active metabolites lasting longer), which makes it a much better outpatient oral choice than lorazepam (half-life about 10 to 20 hours). Oxazepam (half-life about 4 to 15 hours) is also commonly used.
• Short-acting agents are preferred where prolonged sedation is a concern, for example in the elderly, after head injury or in liver failure.³
• Parenteral benzodiazepines are generally used for moderate to severe withdrawal in the ED, especially if the patient is vomiting or unwilling to take oral medication. IM diazepam is poorly absorbed and not recommended.³
• Lorazepam is the preferred parenteral agent to stop an actively seizing patient. Apart from treating the seizure, therapy for severe withdrawal is otherwise similar to mild withdrawal.

Delirium tremens

DTs are uncommon but life-threatening, with severe alteration of mental state and abnormal vital signs. Death is usually due to decompensation from adrenergic instability.

• Aggressive GABAergic therapy
  • Benzodiazepines: large doses, often continuous infusions, watching for respiratory depression and prolonged sedation. Australian guidelines note doses often exceed 100 mg diazepam or equivalent, titrated to light sedation.³
  • Phenobarbital (phenobarbitone): a single IV dose in the ED, typically 130 to 260 mg, then repeat doses of 65 to 130 mg as needed to control tremulousness and withdrawal symptoms. Its long half-life (80 to 120 hours) means it stays on board for as long as the patient is at risk.
  • Propofol: in severe cases needing intubation, a strong GABA agonist that may be more effective than benzodiazepines or barbiturates.
• Volume replacement
• Correction of electrolyte abnormalities¹

Other agents that may help include gabapentin and clonidine. Antipsychotics are only adjuncts to adequate benzodiazepine doses. Mortality from DTs is substantially lower with modern intensive care than historically, but it remains significant, and it is worth treating every case as potentially fatal.

The acute abdomen

Alcoholic patients not infrequently present with an acute abdomen. Consider the life-threatening causes first, including alcoholic ketoacidosis:

• Occult infection
• Gastrointestinal tract bleeding
• Pancreatitis
• Hepatitis
• Perforated ulcer
• Trauma

These are managed by standard protocol.

Kindness is good medicine

Some patients consume alcohol at the cost of consuming something far more nutritious. They invariably suffer some metabolic, neuropsychiatric and hepato-synthetic deficiency. Bringing them in, keeping them warm and offering a plate of food are simple acts of human kindness that go a long way towards resolving not only the acute medical crisis, but the long-term situational one.

By all means, know that propofol has a place in severe, refractory withdrawal, and know the dose of intravenous lorazepam. But do not underestimate the value of warmly offering a plate of food and a glass of water. It is the decent thing to do, and it is also good medicine.

---

References

1. Rose JS, Laurin EG. “Alcohol-related emergencies.” In: Mahadevan SV, Garmel GM, eds. An Introduction to Clinical Emergency Medicine. 2nd ed. Cambridge: Cambridge University Press; 2012:163-175.
2. Farkas J. “Wernicke encephalopathy.” The Internet Book of Critical Care. 14 Oct 2020. https://emcrit.org/ibcc/wernicke/
3. Guidelines for the Treatment of Alcohol Problems (Australia). Thiamine and other supplements; Preventing and treating Wernicke’s encephalopathy; Alcohol withdrawal delirium: medication. https://alcoholtreatmentguidelines.com.au/

Further reading

• University of Michigan Alcohol Withdrawal Guidelines. https://www.med.umich.edu/clinical/images/ETOHCompleteTeachingPacket_FINAL082509.pdf