The 3 most common alcohol poisonings result from ethanol, methanol, and isopropanol (isopropyl alcohol). The devastating and potentially life-threatening toxicity that results from ingestions of any of these alcohols makes recognition of alcohol poisoning an essential part of emergency medicine.
History: Humans have a long history of ingesting alcohols. Ethanol is the most common deliberate ingestion of this toxic substance. It is a component of a wide variety of beverages that are consumed nearly worldwide.
Ethanol
Alcoholic beverages are the primary source of ingested ethanol. Other sources include colognes, perfumes, mouthwashes, medications, and aftershave lotions.
Ethanol may be ingested accidentally, as often occurs in children, or deliberately, as by the patient with alcoholism or for recreation.
Ethanol may be associated with other causes of altered mental status (eg, hypoglycemia, head trauma, mixed ingestions, post-ictal state, carbon dioxide narcosis, hypoxia, infection, hepatic encephalopathy). Consider these conditions when evaluating the patient with known alcohol ingestion.
Methanol
Methanol ingestion may result in serious consequences, including blindness and death. A delay in treatment may lead to increased morbidity and mortality. Recognition and timely treatment are essential for a full recovery.
Methanol commonly is found in numerous compounds, including solvents, photocopy inks and diluents, paints, varnishes, antifreeze, gasoline mixtures (eg, gasohol, "dry gas"), canned heat (eg, Sterno), and even wines (as a byproduct of the natural fermentation process). One study of 11 patients seen between 1995 and 1997 identified 8 patients who had ingested windshield wiper fluid, one who drank gas-line antifreeze, and 2 patients with the source unknown.
Toxicity most commonly ensues following accidental or intentional ingestion. Toxicity also may occur following inhalational exposure. Inhalation may be accidental (eg, industrial settings), or it may be deliberate (eg, volatile inhalant abuse, as in "bagging" or "huffing" solvents for their inebriant effects). Transdermal or respiratory tract absorption also may cause toxicity.
Following ingestion, methanol is rapidly absorbed from the GI tract. Peak levels occur within 30-90 minutes of ingestion.
Methanol is predominantly metabolized in the liver by hepatic alcohol dehydrogenase. At low serum concentrations (<20 mg/dL) and during hemodialysis, methanol elimination is quick and first-order, with an elimination half-life of about 3 hours. At higher serum concentrations, methanol elimination is slow and zero-order, at 8.5 mg/dL/h. Thus, following large doses, methanol is metabolized and eliminated very slowly. Duration of the latent period (time from ingestion until clinical toxicity is evident) is highly variable. Latent periods of 40 minutes to 72 hours have been reported; in most cases, onset of toxicity manifests in 12-24 hours. Co-ingestion of ethanol increases both the latent period (40-50 h) and elimination half-life.
Approximately 50% of patients report visual disturbances. These disturbances usually are described as blurry, indistinct, misty, or snowstormlike. Patients also have reported yellow spots, central scotomata, and photophobia.
CNS complaints include headache and vertigo. GI complaints may include nausea, vomiting, and abdominal pain due to direct irritation.
Complaints do not correlate with the amount or severity of the ingestion.
Isopropanol
Isopropanol is the second most commonly ingested alcohol. The most common source is rubbing alcohol (70% isopropyl alcohol). Other sources of isopropanol include window cleaners, antifreeze, detergents, jewelry cleaners, solvents, and disinfectants.
Ingestions typically occur in alcoholic patients, children, and those who attempt suicide. In children, exposure also may occur from inhalation or topical absorption (eg, sponge bath).
CNS complaints include headache, dizziness, poor coordination, and confusion. GI complaints include abdominal pain, nausea, vomiting, and gastritis with hematemesis.
Patients appear intoxicated but do not smell like ethanol; however, they may have the fruity odor of acetone.
Obtaining a history of the substance and quantity ingested is important. The physician may need to acquire the history from emergency medical services (EMS), parents, relatives, or friends accompanying the patient. Consider other differential diagnoses for altered mental status, as more than a single cause may be present.
Physical: Alcohol ingestions may present in somewhat similar manners. An alteration in mental status is seen with all of the alcohols, given the ingestion of a sufficient quantity of the substance. This alteration may be present to varying degrees depending on the patient.
Ethanol
Clinical presentation depends on BAC and tolerance to ethanol.
The patient may have a flushed face or diaphoresis and may be agitated or ebullient and loquacious due to early disinhibition. This condition may progress to ataxia, slurred speech, drowsiness, stupor, or coma. Nystagmus (horizontal) commonly is observed.
Methanol
Ocular physical findings include sluggishly reactive or fixed and dilated pupils. Visual field constriction also may be present. Retinal edema or hyperemia of the optic disc may be seen. Optic atrophy may appear in late stages (permanent blindness). Visual symptomology can occur without visible funduscopic changes. Visual acuity often is abnormal.
CNS signs include lethargy and confusion. Patients also may present in a comatose condition or with seizures. Cases have been reported of putaminal and cortical necrosis observed on MRI of patients surviving methanol ingestion. Neurologic sequelae (eg, parkinsonism, optic atrophy, focal cranial nerve deficits) have been described.
Respiratory signs include dyspnea (rare cases) or even Kussmaul respiration, despite acidosis. Cardiac signs (eg, hypotension, bradycardia) are late signs associated with a poor prognosis.
The patient may have severe abdominal tenderness.
Death usually is due to abrupt cessation of respiration. Until that endpoint, cardiovascular status is generally well maintained.
Isopropanol
Nystagmus or miosis may be observed.
The patient usually appears intoxicated but smells of acetone instead of ethanol.
Sinus tachycardia may be present, but examination usually reveals no other cardiac dysrhythmias.
Isopropanol is a GI irritant that causes abdominal pain, nausea, vomiting, and gastritis with hematemesis.
Severe ingestions may result in coma, respiratory depression, and hypotension secondary to vasodilatation and negative cardiac inotropy. Loss of deep tendon reflexes (DTRs) also may be observed.
In rare cases, myoglobinuria, acute tubular necrosis, hepatic dysfunction, and hemolytic anemia may occur.
Lab Studies:
Finger stick for blood glucose level
With ethanol and methanol toxicity, the patient may be hypoglycemic.
With isopropanol toxicity, the patient is not hyperglycemic. This distinction helps differentiate alcohol toxicity from diabetic ketoacidosis (DKA).
Serum electrolytes, blood urea nitrogen, creatinine, and glucose levels
For ethanol and methanol toxicity, look for increased serum osmolal gap accompanied by an increased serum anion gap and hypoglycemia.
Isopropanol toxicity also produces an elevated osmolal gap, but generally no abnormal anion gap, although this may be seen as a result of hypotension and lactic acidosis. A spurious increase in serum creatinine as a result of acetone may be seen.
Serum formic acid levels are a better indication of toxicity than are methanol levels. Formate concentrations are rarely available and are not accessible in time to guide therapy.
Serum amylase or lipase level for detecting any associated pancreatitis
Complete blood count
Ethanol: Leukocytosis, anemia, or thrombocytopenia may be present. Such findings are more common in the individual with chronic alcoholism.
Methanol: Anemia may be present.
Isopropanol: Hemolytic anemia may appear in rare instances.
Serum osmolality
The osmolal gap is calculated by subtracting calculated serum osmolality from the measured serum osmolality (see Procedures for calculation).
Ethanol increases osmolal gap by 22 mOsm/L for each 100 mg/dL. Methanol increases the osmolal gap by 32 mOsm/L for every 100 mg/dL. Isopropanol increases the osmolal gap 17 mOsm/L for each 100 mg/dL of isopropanol and by 18 mOsm/L for each 100 mg/dL of blood acetone.
While usually helpful in guiding management, the osmolal gap is neither sensitive nor specific for the presence of a toxic alcohol or glycol. The absence of an osmolal gap does not rule out significant toxic alcohol ingestion.
Arterial blood gas
Methanol: A severe anion gap metabolic acidosis is the hallmark. Severity of acidosis is the best predictor of prognosis when clinical status also is considered.
Isopropanol: The patient is not acidotic.
Urinalysis
Urine may possess an odor of formaldehyde.
Ethanol serum concentration: Used for confirmation of ethanol intoxication.
Ethanol concentration also is important for methanol ingestions, since it predicts prolongation of toxic levels and of the latent period before onset of symptoms.
Ethanol effects at various BAC levels for nonhabituated drinkers are as follows:
20-50 mg/dL – Decreased fine motor function
50-100 mg/dL – Impaired judgment and coordination
100-150 mg/dL – Difficulty with walking and balance
150-250 mg/dL – Lethargy
300 mg/dL – Coma
400 mg/dL – Respiratory depression
500 mg/dL – Potential death
Methanol concentration: This study confirms ingestion and helps guide treatment. Remember that low serum concentrations (ie, < 20 mg/dL) do not rule out significant toxicity; late presenters may have low methanol concentrations but elevated formic acid levels and severe clinical toxicity (eg, severe metabolic acidosis, blindness, coma). Methanol concentrations at various BAC levels are as follows:
0-20 mg/dL – Usually asymptomatic
20-50 mg/dL – Treatment required
150+ mg/dL – Potentially fatal if untreated
Levels more than 20 mg/dL are considered toxic and are the action level (ie, when treatment should be initiated based on level alone.)
Isopropanol concentration: This laboratory study confirms and quantitates alcohol concentration. Clinical presentation is a better indicator of prognosis.
Serum ketones may be increased within 30 minutes of ingestion of isopropanol because of acetone production.
Acetone is detected in urine 3 hours after ingestion.
Procedures:
Osmolal gap
To find the osmolal gap, subtract calculated serum osmolality from the measured serum osmolality.
The osmolal gap equals (measured serum osmolality) - [2(Na+) + (Glucose/18) + (BUN/2.8) + (serum ethanol/4.6)].
Serum osmolality is normally 285-300 mOsm/kg. Normal osmolal gap is 10-12 mOsm/kg. Elevation of the gap is due to presence of additional, unmeasured, low-molecular weight molecules that are osmotically active. The differential for an elevated osmolal gap may be recalled using the mnemonic "ME DIE" (Methanol; Ethylene glycol; Diuretics, such as glycerol, mannitol, and sorbitol; Isopropanol; Ethanol).
Anion gap
The anion gap is an indirect measure of phosphates, sulfates, and organic acids.
The anion gap equals [Na+] - ([HCO3-] + [Cl-]).
Normal anion gap is 12-16 mEq/L.
Increases in the anion gap are seen with excessive acid production or with addition of exogenous acids. The differential for an increased anion gap acidosis can be readily recalled using the mnemonic "CAT MUD PILES" (Carbon monoxide, Cyanide, Alcoholic ketoacidosis, Toluene, Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Phenformin, Iron, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates).
