The severe metabolic acidosis combined with suspected automotive fluid exposure suggests toxic alcohol ingestion.

Toxic alcohols found in common household products include: methanol (classically associated with windshield wiper fluid), ethylene glycol (classically associated with antifreeze), diethylene glycol, propylene glycol, and isopropyl alcohol.

Mild ingestions produce inebriation similar to ethanol intoxication. Severe anion-gap acidosis is the hallmark of toxic alcohol poisoning and results from toxic metabolites formed by the breakdown of ethylene glycol (oxalic acid) and methanol (formic acid).

Oxalic acid forms a complex with calcium and precipitates as calcium oxalate monohydrate crystals in the renal tubules, causing nephrotoxicity. Formic acid has a high affinity for the CNS, and in particular, the eye, resulting in visual disturbances.

Fomepizole or an alcohol drip (titrated to a serum ethanol level of 100 mg/dL) should be initiated as early as possible. Fomepizole and ethanol both work by inhibiting alcohol dehydrogenase, as shown below.

However, the cornerstone of therapy is hemodialysis, which removes both the parent compound and toxic metabolite, and corrects any acid-base disturbance. Indications for hemodialysis include refractory acidosis, cardiopulmonary collapse, end-organ manifestations, or a concentration > 50mg/dL.

Other adjunctive therapy includes sodium bicarbonate, thiamine (for ethylene glycol poisoning), pyridoxine (for ethylene glycol poisoning), and folic acid (for methanol poisoning).

Testing includes BMP, ethanol/methanol/ethylene glycol levels, blood osmolality, urinalysis, ABG, and an ECG. Don’t forget to calculate the anion and osmolar gap (see below)!

Anion Gap Calculation: Na – (Cl + HCO3)

Osmolar Gap Calculation: Measured Osmolality – Calculated Osmolality

Calculated Osmolality: 2 x Na + (Glucose/18) + (BUN/2.8) + (Ethanol/4.6)

Measurement of methanol and ethylene glycol concentrations will confirm the diagnosis, but are often not immediately available. Measurement of ethanol concentration is important to note the presence of any ADH inhibition at outset. An ethanol concentration > 100 mg/dL makes toxic alcohol unlikely as the cause of an unknown anion gap metabolic acidosis. A high osmolar gap may suggest toxic alcohol ingestion, but has many limitations and is neither sensitive nor specific. A normal or negative osmolar gap does not exclude toxic alcohol poisoning. Patients with intentional ingestions should also have serum salicylate and acetaminophen concentrations determined.

The length of observation before discharge should be 6 hours in suspected ethylene glycol accidental ingestions and 12 hours in suspected methanol accidental ingestions. Any patient with mild symptoms or biochemical abnormalities should be admitted for further monitoring. Patients with severe signs and symptoms should be admitted to an intensive care setting. Patients without any sign or symptom of toxic alcohol ingestion during the period of observation can be discharged.