Alcohol toxicity or poisoning is caused by drinking large quantities of alcohol in a short period of time. According to Centers for Disease Control (CDC) data released January 2015, an average of 6 people died of alcohol poisoning each day in the US from 2010-2012. Seventy-six percent of alcohol poisoning deaths are among adults ages 35-64 years old, the majority of whom are men and non-Hispanic whites. While alcohol dependence was identified as a factor in 30% of alcohol poisoning deaths, binge drinking (defined as more than 5 drinks on an occasion for men or 4 or more drinks on an occasion for women) can also lead to death from alcohol poisoning. A “standard drink” in the US is considered either 12 ounces (oz) of beer (5% alcohol), 8 oz of malt liquor (7% alcohol), 5 oz of wine (12% alcohol), or 1.5 oz of distilled spirits (40% alcohol; 80 proof). The current Dietary Guidelines for Americans recommend not to exceed 1 drink a day for women or 2 drinks a day for men.

Any alcohol can be toxic if ingested in large enough quantities. While alcohol toxicity most commonly results from the abuse of ethanol (“drinking alcohol”) found in alcoholic beverages, it can also result from the ingestion of isopropanol (rubbing alcohol) and the “toxic alcohols” which include methanol (found in commercially available products such as solvents, windshield washing fluids and paint removers) and ethylene glycol (the primary ingredient in ‘anti-freeze’). Toxic alcohols share the characteristic of the parent compounds causing inebriation with little toxicity while their active metabolites have the potential to cause metabolic acidosis and significant end organ damage.

Toxic alcohol poisoning is far less prevalent than ethanol abuse, with most exposures in the US resulting from unintentional ingestion of methanol. In 2008, 2008 exposures to methanol were reported to the American Association of Poison Control Centers with 10 associated deaths. In the same year 5532 exposures (also mostly by ingestion) were reported for ethylene glycol, with 21 associated deaths. Toxic alcohol ingestions are also more likely to occur in those with a known history of severe ethanol abuse in which toxic alcohols are ingested as an ethanol substitute with or without ethanol for the purpose of intoxication, or in those with concomitant depression and suicidality, with or without ethanol or other co-ingestions, with the intent of self harm.

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Acute intoxication with any of the alcohols can result in respiratory depression, aspiration, hypotension and cardiovascular collapse. The inebriating effects of all alcohols are directly proportional to their molecular weight.

Isopropanol is a heavier molecule than ethanol and can result in a sedative hypnotic effect approximately twice that of ethanol with a significantly longer duration of action. Isopropanol abuse results in intoxication and central nervous system (CNS) depression but is also associated with gastric irritation. Abdominal pain, hemorrhagic gastritis and vomiting can be observed. Ketosis and an osmolar gap without acidosis often characterizes isopropanol toxicity, as isopropanol is metabolized to a ketone (acetone) and not a ketoacid.

Glycolic acid is a directly cytotoxic metabolite of ethylene glycol and responsible for the metabolic acidosis in ethylene gycol poisoning. Glycolic acid is further metabolized to oxalic acid which can complex with calcium, resulting in hypocalcemia and the precipitation of calcium oxalate crystals in tissues and urine. The combined effects of glycolic acid cytotoxicity, calcium oxalate crystal deposition in tissues and hypocalcemia can result in cardiac dysrhythmia and central nervous system toxicity manifesting as seizures, cerebral edema, meningismus and noninfectious meningoencephalitis. Progressive toxicity may result in multiorgan system failure. Renal failure is the most common major complication of serious ethylene glycol poisoning and may require renal replacement therapy (hemodialysis).

Formic acid is the metabolite responsible for acidosis and end organ injury following methanol ingestion. End organ injury typically involves the retina and optic nerves (manifesting as photophobia and blurred vision in initial stages), although putamen necrosis, subcortical white matter damage, intracranial hemorrhage and other patterns of brain injury including a parkinsonian syndrome have been reported.

An anion gap metabolic acidosis that is not otherwise explained (e.g., by lactic acidosis or diabetic ketoacidosis) is often associated with ingestion of a toxic alcohol (methanol or ethylene glycol). However, it is important to be mindful that the acidosis and toxicity will not present immediately after exposure since the parent alcohols must first be converted to their toxic metabolites. This can take 4-12 hours to occur in the case of ethylene glycol and 12-24 hours following methanol ingestion. The metabolism of both of these alcohols to their toxic metabolites may be further delayed if ethanol is present and competing for hepatic metabolism.

Given the high potential for morbidity, isolated or co-ingestion of the toxic alcohols is critical to consider and recognize early since appropriate management is critical to minimize morbidity and mortality. See the chapters entitled: Overdose of Ethylene Glycol and Overdoses and Poisoning for further information.

The diagnosis of acute ethanol intoxication is usually straightforward and suggested by a history of recent ethanol abuse (within hours) provided either by the patient or bystanders in association with the typical clinical syndrome of ethanol intoxication.

Ethanol is a sedative-hypnotic and acute intoxication (inebriation) typically manifests with a spectrum of CNS effects. In mild to moderate intoxication, mild incoordination, euphoria, ataxia, nystagmus, disinhibition and impaired judgment may result. With more severe intoxication, miosis, hypothermia, hypotension, bradycardia and respiratory suppression, stupor and coma may occur. Death can occur from severe intoxication (poisoning) as a result of marked CNS depression and respiratory arrest. The spectrum of observed CNS effects ranges in severity based on whether the patient has developed ethanol tolerance after years of ongoing abuse.

It is crucial to consider and exclude other disorders that may accompany or mimic clinical intoxication or altered mental status, including narcotic intoxication or poisoning by other sedative-hypnotics (see “Overdoses and poisoning”), toxic alcohol intoxication and poisoning (methanol, ethylene glycol, isopropanol), hypoxemia, hypoglycemia, intracerebral hemorrhage or stroke, hepatic encephalopathy, sepsis, hypothermia, profound acidosis, hypoactive delirium or encephalopathy from infectious etiologies including viral and bacterial meningoencephalitis.

Co-ingestion or isolated ingestion of one of the alcohols other than ethanol may be reported or suggested by the clinical history, or by the clinical presentation. As reviewed earlier, isopropanol abuse is associated with gastric irritation which can be severe and occurs early following ingestion. The fruity odor of acetone or the smell of rubbing alcohol may be present on the breath. An unexplained anion gap metabolic acidosis should raise suspicion for ingestion of methanol or ethylene glycol. Acute visual changes such as photophobia or blurred vision may suggest methanol toxicity. Acute kidney injury, symptomatic hypocalcemia may suggest ethylene glycol toxicity.

Unfortunately, methanol and ethylene glycol assays are often not available at all or in a timely enough manner to assist in rapid and appropriate clinical decision making in cases of suspected toxic alcohol poisoning. If the ingestion of a toxic alcohol is suspected but cannot be reliably confirmed by history (i.e., a witnessed ingestion), measurement or calculation of the osmolar gap may serve as a surrogate marker for the presence of toxic alcohols. See the chapters entitled: Overdose of Ethylene Glycol and Overdoses and Poisoning for further information.

Findings on physical examination include:

Head, Eyes, Ears, Nose, Throat:

  • Facial flushing and conjunctival injection. Approximately 36% of East Asians (Japanese, Koreans, Chinese) have an inherited deficiency of aldehyde dehydrogenase 2, an enzyme involved in the metabolism of ethanol. Without this enzyme, ingestion of ethanol results in facial flushing, occasionally with nausea and tachycardia, in a syndrome colloquially known as the “Asian flush.”

  • Nystagmus.

  • Miosis.

  • Complaints of photophobia, blurry vision, findings of papilledema and nonreactive mydriasis may suggest advanced and severe methanol toxicity.

  • Fruity odor of breath (suggests marked ketosis possibly associated with isopropanol intoxication).

  • Odor of ethanol or other alcohol (particularly isopropanol or ‘rubbing alcohol’).


  • Respiratory depression.


  • Hypotension (especially orthostatic) from ethanol induced venodilation, tachycardia, volume depletion, new onset atrial and ventricular tachyarrhythmias (e.g., “holiday heart”).


  • Complaints of nausea and or vomiting. Marked gastric irritation may suggest any alcohol exposure, however, isopropanol is particularly irritative to the gastric mucosa.


  • Drowsiness, stupor, coma, disinhibition, confusion, memory difficulty, anterograde amnesia, slurred speech, incoordination, dysmetria, ataxia, diminished reflexes, unsteady gait.

There is no single physical examination finding or laboratory test that confirms the diagnosis of acute alcohol toxicity.

  • Peripheral oximetry. Rapidly evaluates oxygenation status and can exclude hypoxemia as a contributing cause to encephalopathy.

  • Blood glucose. Hypoglycemia is common in ethanol intoxication/toxicity due to ethanol induced suppression of gluconeogenesis and marked hypoglycemia can be causative or contributive to an altered mental status.

  • Temperature. Fever suggests infection or other toxidrome. Hypothermia can result from environmental exposure or severe metabolic effects of alcohol poisoning.

  • Serum toxicology, including ethanol concentration and tests for the presence of benzodiazepines, barbiturates and for common co-ingestants in poisoning such as salicylates and acetaminophen – especially in suspected intentional ingestion or “overdose” with the intent of self-harm. Measurement of an ethanol level is not necessarily required in cases of mild to moderate clinical intoxication when the history of ethanol intake is clear and no other abnormality is suspected. Serum ethanol levels often correlate poorly with the degree of clinical intoxication especially in chronic abuse, where tolerance has developed. For example, in a non-habituated individual, respiratory failure and death may result at blood concentrations of 400 mg/dL (milligrams/deciliter), while at a similar blood alcohol concentration a longstanding heavy user with tolerance may exhibit only mild clinical inebriation.

  • Urinalysis and urine toxicology for the presence of opiates and cocaine metabolites, ketonuria or evidence of infection.

  • Urine human chorionic gonadotropin (HCG) in females of reproductive age to determine if the patient is pregnant so that fetal health can evaluated in cases of severe alcohol intoxication.

  • Chemistry 20. To evaluate for evidence of acidosis, renal injury, hepatotoxicity, pancreatitis, coagulopathy, underlying chronic liver disease, electrolyte imbalances (e.g., hypomagnesemia, hypophosphatemia, hypocalcemia and hypokalemia) and malnutrition. Transaminase elevations with an aspartate transaminase (AST): alanine transaminase (ALT) ratio over 2 and an absolute AST elevation less than 8 times the upper limit of normal, along with a gamma-glutamyl transpeptidase (GGT) elevation over twice the upper limit suggests hepatocellular injury from ethanol abuse and alcoholic liver disease.

  • Creatine phosphokinase. To evaluate for evidence of prolonged immobilization, rhabdomyolysis and risk of renal injury.

  • Complete blood count. To evaluate for cytopenias, leukocytosis suggesting occult infection, occult hemorrhage.

  • Serum Osmole. Measured and calculated for determination of the osmolal gap when toxic alcohol ingestion is suspected.

  • Arterial blood gas analysis to assess oxygenation, ventilation and pH in patients in whom respiratory failure is present or suspected due to alcohol poisoning.

  • Blood cultures if concomitant sepsis is suspected.

  • Head computed tomography (CT) scan – in patients with an altered mental status from suspected ethanol intoxication if occult intracerebral injury is suspected, especially in the presence of evidence of trauma by history or exam, and/or if the patient is comatose or has focal neurologic findings.

  • Chest x-ray – if there is hypoxemia, tachypnea, respiratory distress, suspicion of aspiration with alcohol induced emesis, or evidence of trauma by history or exam.

  • Other trauma series as indicated by history or physical examination if occult traumatic injury is suspected or if focal neurologic findings are referable to the spinal cord (e.g. cervical spine computed tomography [CT] or plain radiographs, spine, hip, or pelvic plain radiographs).

  • Electrocardiogram (EKG) – for evaluation for arrhythmias, abnormal cardiac conduction associated with associated electrolyte abnormalities (especially hypokalemia, hypomagnesemia from malnutrition in chronic alcoholism, marked acidosis or co-ingestions (i.e. QRS widening in tricyclic antidepressant overdose).

  • Serial measurement of the serum ethanol concentration is not indicated unless the syndrome of acute intoxication is not resolving and surreptitious ongoing ethanol or other alcohol ingestion is suspected. There are published case reports of inpatients ingesting alcohol-based hand cleansers commonly available institutionally. Additionally, serum clearance of ethanol does not correlate reliably with resolution of clinical intoxication, and cannot therefore be used as support for a safe disposition or discharge.

  • Assessment of airway and ensuring adequate oxygenation and ventilation. Alcohol intoxication causes CNS depression with diminished respiratory drive along with diminished protection of the airway. Nausea and vomiting may also occur due to alcohol toxicity with resultant aspiration events and the patient should be positioned in side lying accordingly. Endotracheal intubation may be required.

  • Protection from self-injury and staff injury if agitation and or aggressive behavior are evident through frequent reorientation, continual supervision, physical restraint or chemical (benzodiazepine or antipsychotic) restraint as needed.

  • Immediate assessment of oximetry, blood glucose and temperature with correction as indicated. Parenteral thiamine, 100 mg intravenous (IV) or intramuscular (IM) should be administered prior to the administration of any dextrose or glucose to all patients with altered mental status in whom acute alcohol intoxication and/or chronic alcohol abuse is suspected in order to avoid precipitating the acute syndrome of Wernicke’s encephalopathy (confusion, oculomotor dysfunction and gait ataxia – alone or in combination).

  • As alcohols are rapidly absorbed through the gastric mucosa, there is no role for gastric decontamination or activated charcoal following significant alcohol exposure or poisoning.

  • Immediate correction of clinical volume depletion and hypotension with isotonic crystalloid infusion (saline). Chronic alcohol abuse can result in an alcoholic cardiomyopathy and in those patients whose history/examination and EKG are suggestive, caution should be applied with fluid resuscitation in order to avoid precipitating acute pulmonary edema. Similar caution is advised when hydrating those patients with concurrent ischemic heart disease and known systolic or diastolic dysfunction.

  • Reviewing the history of alcohol ingestion, co-ingestions, and trauma if available (identification of the source of a toxic alcohol ingestion with obtainment of the original container if possible).

  • Laboratory and neurologic examination as outlined above and imaging as clinically indicated by the history and physical examination.

  • Correction of electrolyte derangements. The electrolyte derangements commonly associated with acute intoxication and chronic alcoholism and malnutrition (hypokalemia, hypomagnesemia, and hypophosphatemia) require monitoring and repletion to avoid significant alterations to cardiac conduction and predisposition to arrhythmias. An EKG should be part of the initial evaluation in the setting of acute alcohol toxicity, and continuous cardiac telemetry should be considered.

  • Consultation with a toxicologist if toxic alcohol ingestion or other poisoning suspected.

As clearance of serum ethanol by laboratory testing cannot reliably indicate resolution of a clinical intoxication, repeat physical and neurologic examination for the resolution or worsening of intoxication is paramount. Monitoring for and management of secondary complications of alcohol intoxication is also indicated during this time. Follow up management includes:

Continued re-assessment of airway protection, monitoring for potentially self-injurious behavior.

Monitoring for the development of clinical alcohol withdrawal, which is more likely in those with a history of chronic alcohol abuse or history of alcohol withdrawal syndrome. If there is a history of withdrawal seizures or the patient has a known seizure disorder, seizure precautions should be considered.

Evaluation for the development of right upper quadrant tenderness, icterus, jaundice, ascites, or encephalopathy with or without asterixis, indicating the progression to alcoholic hepatitis (this condition typically occurs after decades of heavy alcohol abuse, and can develop following weeks of total abstinence).

Evaluation for epigastric pain which may suggest secondary complications including pancreatitis or significant gastritis. Careful monitoring for occult or overt GI bleeding should be considered including testing of the stool for occult blood on initial evaluation, especially if initially hematocrit is lower than baseline suggesting recent or ongoing bleeding.

Continued monitoring of electrolyte balance and repletion as indicated to avoid significant alterations to cardiac conduction and pre-disposition to arrhythmias. Potassium, magnesium, and phosphorus may fall markedly after reintroduction of sugars into the diet with subsequent insulin release, which drives these electrolytes intracellularly. Those with chronic alcohol abuse and alcoholic cardiomyopathy may have an additional risk for arrhythmias in the setting of alcohol withdrawal. An EKG should be repeated in the setting of persistent electrolyte derangements and continuous cardiac telemetry should be considered.

Monitoring for alcoholic ketoacidosis, which is commonly seen in the setting of chronic alcohol abuse, but also described in unhabituated binge drinking. It usually develops 24-48 hours after abstinence, when patients are unable to consume calories due to abdominal pain, nausea, a withdrawal syndrome, or other acute medical illness relating to their ethanol toxicity. The depletion of enzymes required for ethanol metabolism (Nicotinamide adenine dinucleotide or NAD) along with this relative starvation and stress response to volume depletion from nausea and vomiting inhibit aerobic metabolism and lead to the release of counter-regulatory hormones favoring anaerobic metabolism and the stimulation of lipolysis. This ultimately results in the metabolism of acetyl coenzyme A to the ketoacids betahydroxybutyrate and acetoacetate, resulting in an anion gap metabolic acidosis. Nausea, vomiting, and abdominal pain may result from this metabolic acidosis and ventilatory compensation may manifest as Kussmaul’s respirations. It is still important to consider alternative etiologies of metabolic acidosis such as lactic acidosis from profound volume depletion, sepsis, or bowel ischemia, and in diabetic patients, diabetic ketoacidosis (DKA). A serum glucose less than 250 mg/dL usually indicates alcoholic as opposed to diabetic ketoacidosis. Toxic alcohol ingestions or coingestions may also lead to metabolic acidosis (typically profound). The presence of a large osmolar gap after correction for any ethanol still present in the serum may help to identify the presence of a toxic alcohol. Treatment involves the administration of intravenous dextrose in saline (after thiamine administration as outlined above). The administration of carbohydrates stimulates insulin release which suppresses further lipolysis and resultant ketoacid formation. Insulin administration is generally not required, unless concomitant diabetes is present warranting insulin therapy.

Deep vein thrombosis (DVT) prophylaxis should be given to patients at risk or those who are not ambulatory. Careful consideration should be given to the use of heparin and other anticoagulants in the setting of methanol toxicity with evidence of intracranial hemorrhage, in cirrhotics with a concern for acute or recent variceal bleed or in severe alcoholic gastritis with recent, likely, or ongoing gastrointestinal bleeding.

Nutritional services consultation should be considered.

Physical Therapy evaluation should be considered for gait instability.

  • Social work and Addiction Medicine consultation is indicated to assist in counselling regarding cessation of alcohol abuse and for referrals to community-based resources to assist in the management of alcohol abuse and addiction, most notably Alcoholics Anonymous meetings and sponsors.

  • Psychiatry consultation may be indicated to assist in the management of comorbid depression, which frequently accompanies alcohol abuse; and especially following ethanol and/or toxic alcohol ingestion with the intent of self harm (suicidality).

  • Evaluate and re-evaluate airway, oxygenation, ventilation; when able, position intoxicated patient in side-lying to minimize the risk of aspiration in the event of emesis.

  • Consider competing diagnoses that may mimic clinical alcohol intoxication: narcotic intoxication or poisoning by other sedative-hypnotics (see “Overdoses and poisoning”), toxic alcohol intoxication and poisoning (methanol, ethylene glycol, isopropanol), hypoxemia, hypoglycemia, intracerebral hemorrhage or stroke, hepatic encephalopathy, sepsis, hypothermia, profound acidosis and hypoactive delirium or encephalopathy from a variety of toxic, metabolic, and infectious etiologies including viral and bacterial menigoencephalitis.

  • Give parenteral thiamine (100 mg IV or IM) prior to the administration of any glucose or dextrose.

  • Consider possible coingestion of other toxins, including toxic alcohols (methanol, ethylene glycol, and isopropanol), acetaminophen, and salicylates. See Overdose of Ethylene Glycol and Overdoses and Poisoning for further information.

  • Assess for chronic alcohol abuse and/or dependence and monitor for potential secondary complications including as alcohol withdrawal syndrome, alcohol hepatitis, malnutrition.

The patient is ready for discharge when acute intoxication has resolved in the absence of complications outlined above (ongoing significant withdrawal, end organ injury from toxic alcohol ingestion and toxicity requiring ongoing inpatient management).

  • General medicine/primary care: within 2 weeks of discharge.

  • Psychiatry (where appropriate): within 2 weeks of discharge.

  • Specialist clinics e.g., Nephrology, Neurology: as indicated depending on toxic alcohol exposure and organ-specific injury.

  • Referral to inpatient or outpatient rehabs (e.g., Alcoholics Anonymous local meeting) as soon as possible in patients with recognized alcoholism and an interest in trying to quit/abstain from further ethanol use.

With the assistance of social work, patients and their families (where appropriate) should be counselled on the deleterious long term effects of ongoing alcohol abuse, including the potential for irreversible harm to multiple organ systems including: predisposition to oral, esophageal, gastric, pancreatic, and breast cancers; cirrhosis of the liver possibly requiring transplantation; CNS injury (brain atrophy and peripheral neuropathy with effects on memory, cognition, walking, and global functioning); and the cardiovascular system (acceleration of coronary artery disease, risk of alcoholic cardiomyopathy, and predisposition to abnormal heart rhythms).

The increased risk of accidental and traumatic injury associated with alcohol abuse should be discussed including increased risk of motor vehicle accidents and resultant fatality. Rates of depression and suicide are also higher among abusers of alcohol.

In addition to the physical impacts and medical risks that chronic alcohol abuse may engender, the patient should also be counselled on the negative effects of sustained alcohol abuse on multiple other domains of optimal health and function including: social relationships, marriages, family dynamics including associations with domestic violence, vocational and professional success and performance, and legal risks surrounding motor vehicle operation and domestic violence.

There are no current Joint Commission core performance measures that apply specifically to the management of acute alcohol toxicity by a hospitalist in a general inpatient medical setting.

Anderson, IB, Olson, KR. “Ethylene Glycol and Other Glycols”. Poisoning & Drug Overdose. 2007.

Anderson, IB, Olson, KR. “Methanol”. Poisoning & Drug Overdose. 2007.

Brooks, PJ, Enoch, MA, Goldman, D, Li, TK, Yokoyama, A. “The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption”. . vol. 6. 2009. pp. 0258-0263.

Huecker, MR, Danzl, DF, Tintinalli, JE, Stapczynski, JS, Cline, DM, Ma, OJ, Cydulka, RK, Meckler, GD. “Metabolic and Endocrine Emergencies”. . 2010.

Kearney, TE, Olson, KR. “Thiamine (Thiamin, Vitamin B1)”. Poisoning & Drug Overdose. 2007.

Lucey, MR, Mathurin, P, Morgan, TR. “Alcoholic Hepatitis”. . vol. 360. 2009. pp. 2758-2769.

Matteucci, MJ, Olson, KR. “Isopropyl Alcohol”. Poisoning & Drug Overdose. 2007.

Olsen, KR, Olson, KR. “Emergency Evaluation and Treatment”. Poisoning & Drug Overdose. 2007.

Schuckit Marc, A, Fauci, AS, Braunwald, E, Kasper, DL, Hauser, SL, Longo, DL, Jameson, JL, Loscalzo, J. “Alcohol and Alcoholism”. . 2008.

Smith, JC, Quan, D, Tintinalli, JE, Stapczynski, JS, Cline, DM, Ma, OJ, Cydulka, RK, Meckler, GD. “Alcohols”. . 2010.

Vonghia, L, Leggio, L, Ferrulli, A. “Acute Alcohol Intoxication”. Eur J Intern Med. vol. 19. 2008. pp. 561

Williams, SR, Olson, KR. “Ethanol”. Poisoning & Drug Overdose. 2007.

Williams, SR, Sztajnkrycer, MD, Thurman, JR, Knoop, Kevin J., Stack, Lawrence B., Storrow, Alan B., Thurman, R. Jason. “Toxicological Conditions”. . 2010.

Woods, WA, Perina, DG, Tintinalli, JE, Stapczynski, JS, Cline, DM, Ma, OJ, Cydulka, RK, Meckler, GD. “Alcoholic Ketoacidosis”. . 2010.