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All alcohols are potentially toxic and cause clinical inebriation and an anion gap metabolic acidosis. Ethanol and isopropanol are the most commonly ingested alcohols and cause direct toxicity, while methanol and ethylene glycol cause toxicity as a result of conversion to toxic metabolites.
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Although acute ethanol intoxication may cause death directly from respiratory depression, morbidity and mortality are usually related to trauma from impaired cognitive function. On an average, nondrinkers eliminate ethanol from the bloodstream at a rate of 15 to 20 milligrams/dL/h and chronic drinkers at about 30 milligrams/dL/h.
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Signs and symptoms of ethanol intoxication include slurred speech, disinhibited behavior, central nervous system (CNS) depression, and altered coordination. Manifestations of serious head injury or hypoglycemia may be identical to, or clouded by, ethanol intoxication. Nystagmus and a characteristic odor of ethanol may be observed.
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Diagnosis and Differential
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Check a bedside glucose in all patients with altered mental status. Serum ethanol levels will confirm ethanol intoxication but are not required for mild to moderate intoxication. Consider comorbid disease or injury in the inebriated patient and obtain additional labs as indicated: electrolytes may demonstrate an anion gap acidosis; liver enzymes may reveal hepatic damage; a urine toxicology screen may reveal coingestion of other drugs of abuse. Obtain imaging as indicated by external signs of trauma in the inebriated patient.
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Emergency Department Care and Disposition
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The mainstay of treatment is observation. A careful physical examination should be performed to evaluate for complicating injury or illness.
Treat hypoglycemia with IV dextrose. Thiamine 100 milligrams IV or IM may be given concurrently if Wernicke encephalopathy is suspected.
Consider secondary causes of deterioration or lack of improvement during observation and manage accordingly.
Discharge the patient once sober enough to pose no threat to self or others.
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Isopropanol is commonly found in rubbing alcohol, solvents, skin and hair products, paint thinners, and antifreeze. Acetone is the principle toxic metabolite.
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Clinically, isopropanol intoxication is similar to that of ethanol but lasts longer with deeper CNS depression. The smell of rubbing alcohol or the fruity odor of ketones may be noted on the patient's breath. Severe poisoning presents as coma, respiratory depression, and hypotension. Hemorrhagic gastritis is common and causes nausea, vomiting, abdominal pain, and upper gastrointestinal bleeding.
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Diagnosis and Differential
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Check a bedside glucose in all patients with altered mental status. Classic isopropanol toxicity is associated with an elevated osmolal gap, ketonemia and ketonuria, without acidosis. In the setting of upper GI bleeding, coagulation studies, a CBC, and a type and screen should be obtained. When available, a serum isopropanol and acetone level confirm the diagnosis.
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Emergency Department Care and Disposition
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Treat hypotension with aggressive infusion of IV crystalloids though persistent hypotension ...