WORKUP	Section 5 of 10
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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

	TREATMENT	Section 6 of 10
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Prehospital Care: Follow established protocols.

• Obtaining a detailed history of the ingestion or exposure from all available sources is important.

• Inspect bottles of ingested substances to help identify possible alcohols.

• Follow standard protocols for treating patients with airway obstruction, unconsciousness, or altered mental status.

Emergency Department Care: Provide airway, breathing, and circulation evaluation and support as necessary. Orogastric lavage with a large-bore (eg, Ewald) tube is not recommended. Standard-size nasogastric (NG) tube insertion, aspiration, and rapid lavage may be beneficial soon after ingestion and may be attempted up to 4 hours following ingestion (ie, food in the stomach may significantly delay alcohol absorption). Activated charcoal does not bind alcohols well but should be administered if a mixed ingestion is suspected. Administer naloxone if opiates are suspected. Administer thiamine (100 mg) and dextrose D50W (25-50 g) IV for the obtunded patient.

• Ethanol

• Treatment of acute intoxication involves providing supportive measures (eg, fluid monitoring, oxygen, airway protection).

• Remember that intoxicated patients are at an increased risk for other traumatic and medical pathologies, which must be ruled out or appropriately treated.

• Methanol

• Supportive measures are indicated for patients with methanol ingestion. Monitor fluids and oxygen, and provide airway protection. Forced diuresis is recommended, since methanol is excreted renally; however, dialysis works better and has less danger of pulmonary edema, cerebral edema, or acute respiratory distress syndrome (ARDS).

• Attempted correction of acidosis using sodium bicarbonate is indicated if pH is less than 7.20; note that patients may require large quantities. An alkalemic pH makes it more likely that formic acid will exist as its anion (formate), which cannot access the CNS and optic nerve as readily.

• Administer folic acid (leucovorin) 50 mg IV every 4 hours for several days to potentiate the folate-dependent metabolism of formic acid to carbon dioxide and water.

• Ethanol infusion is recommended for patients with suspected methanol ingestion and/or levels greater than 20 mg/dL. Consider ethanol infusion in any patient with an unexplained osmolar gap and/or elevated anion-gap metabolic acidosis that is unaccounted for by ethanol, until a definitive diagnosis negating its administration is made.
  • Ethanol is a competitive inhibitor of alcohol dehydrogenase and, thereby, impairs the metabolism of methanol and ethylene glycol. Ethanol has 10-20 times greater affinity for alcohol dehydrogenase than methanol does. This measure increases the half-life to approximately 40 hours.

  • Maintain blood ethanol concentrations between 100-150 mg/dL. This level is intoxicating for nonalcoholics; the dosage may need to be increased for chronic drinkers. Ethanol levels must be followed frequently.

  • Ethanol may be given PO or IV. PO administration requires an alert patient and may have variable rates of absorption and wide fluctuations in blood levels. Administration of ethanol also causes gastritis. IV administration provides more constant blood levels, but it may cause thrombophlebitis. Parenteral alcohol is indicated if the patient has evidence of pancreatitis.

  • Begin treatment with a loading dose of 0.6-0.8 g/kg IV or PO. Maintenance levels typically range from 0.8-1.4 g/kg/h. For infusion with 10% ethanol in D5W, loading dose is 10 mL/kg, and maintenance is 1.6 mL/kg/h. Administration of an oral loading dose is possible using commercially available beverages. Dosage may be calculated using the following equation: Ethanol in grams = (mL beverage) X 0.8 X (proof/2).

  • The goal of ethanol administration is to maintain a serum ethanol concentration more than or equal to 100 mg/dL. Maintain this ethanol level until the methanol level is less than 20 mg/dL. Some physicians advocate continuing ethanol infusion until the methanol level reaches zero.

• Dialysis may be needed to remove methanol and its principal toxic metabolite, formate. Dialysis is 40-50 times faster than renal clearance. Hemodialysis is recommended for intractable/severe acidosis (ie, pH <7.20), renal failure, visual symptoms, or methanol serum concentrations more than 50 mg/dL.

• Studies have shown that prognosis is not dependent on the blood concentration of methanol but on the degree of metabolic acidosis present. This observation is logical when considering toxins as the cause of the acidosis; worsening acidosis means more toxic metabolites are present. Prognosis probably correlates closely with the plasma formate concentration on presentation (a test not readily available).

• Isopropanol

• Treat hypotension with fluids and pressors, if needed. NG suctioning is ineffective, since minimal resecretion to the stomach occurs.

• Initiate emergent hemodialysis for patients with refractory hypotension or blood levels more than 400 mg/dL.

Consultations:

• Consultations depend on the substance and severity of the ingestion and as well as the patient's age.

• Ethanol
  • For acute ethanol intoxication, patients may not need admission. Patients may require monitoring if a concurrent injury or other problem exists.

• For chronic ethanol abuse, the patient may need admission for ongoing medical problems (eg, liver, GI, hematologic, metabolic, CNS effects). Consider and offer referral for substance abuse treatment.

• Methanol
  • For acute methanol ingestion, the patient may need admission for dialysis, ethanol or fomepizole therapy.

  • The patient may need monitoring in an ICU setting.

• Isopropanol
  • For acute isopropanol ingestion, the patient may need admission for treatment of GI bleeding in a monitored setting.

  • The patient also may need treatment for CNS depression in a monitored setting.

	MEDICATION	Section 7 of 10
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Methanol poisoning only: Alcohol dehydrogenase has greater affinity for ethanol than methanol; therefore, ethanol infusions are used to inhibit methanol breakdown to toxic metabolites (eg, formaldehyde, formic acid).
Fomepizole (eg, 4-methylpyrizole, 4-MP, Antizol) has greater affinity for alcohol dehydrogenase than ethanol or methanol and has a considerably better safety profile than ethanol. Fomepizole recently was approved by the US Food and Drug Administration (FDA) for ethylene glycol poisoning, but it is useful for managing methanol poisoning as well.

	MISCELLANEOUS	Section 9 of 10
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Medical/Legal Pitfalls:

• Assuming that ingestion of an alcohol accounts for altered mental status rather than conducting a thorough search for head injuries and other etiologies (eg, trauma, infection, psychogenic causes, seizure/syncope, alcohol, encephalopathy/endocrinopathy/electrolytes, insulin, opiates, uremia [TIPS AEIOU]), especially in patients with profound or prolonged depression in mental status or whose history of present illness is unreliable or unobtainable

• Treatment of the patient based solely on ethanol concentration rather than including the patient's physical examination

• Failure to follow serial levels of alcohols (especially methanol)

• Failure to realize that extremely small amounts of methanol can lead to life-threatening toxicity

• Failure to institute or delay in instituting ethanol or fomepizole therapy for significant methanol ingestion

• Failure to consider methanol as a potential toxin because both anion and osmolal gaps are normal (late presentations)

• Failure to consider ingestion of alcohols as a possible cause of altered mental status, especially in children