A is the correct answer

“Wait a second,” you might say. “I have (or get) to do some math?!” Let’s take it away!

 

It is not uncommon for patients to present to the emergency department with altered mental status, and all too often, the mental status changes are due to some type of toxic ingestion. While some clinicians grow excited about determining the toxidrome that best fits with the clinical picture, others may cringe and sigh that they have to institute their less-often-used math skills. To make this educational discussion less complex, we are simply going to focus on the toxic alcohols:

 

1. Methanol: toxicity from ingesting windshield wiper fluid or making distilling or fermenting errors
2. Ethanol: toxicity from drinking alcohol
3. Isopropyl alcohol: toxicity from ingesting rubbing alcohol
4. Ethylene glycol: toxicity from ingesting antifreeze
5. Propylene glycol: toxicity that may occur from the use of medications mixed with the substance (ICU usually)

 

Early diagnosis of a specific toxic alcohol ingestion is essential since certain antidotes need to be administered. Unfortunately, toxic alcohol ingestions can present similarly, often with an altered and depressed mental status. However, an awake patient might report blurry vision or blindness in the setting of methanol toxicity. Other clues might help you narrow the diagnosis, such as the use of a Wood lamp to detect ethylene glycol toxicity in the urine and lactic acidosis that might suggest isopropyl alcohol toxicity. But ultimately, the best way to determine whether you have an isolated or mixed toxic alcohol ingestion is to analyze the anion gap acidosis and determine the serum osmolality. 

 

The traditional equation calculates serum osmolality: 2 sodium + (blood urea nitrogen / 2.8) + (glucose / 18) + (ethanol / 4.6). (There are options for osmolality equations, including the traditional and the Purssell equations, with toxicologists and critical care physicians preferring the traditional equation.) 

 

Toxic alcohols are osmotically active substances that increase measured serum osmolality but are not accounted for in the osmolality equation. We already know this patient ingested ethanol since his level is 332 mg/dL. The presence of a toxic alcohol in addition to ethanol in the serum results in a wide osmolar gap, a difference between the measured serum osmolality and the calculated serum osmolality. An osmolar gap > 10 mOsm/kg should raise concern for the ingestion of another toxic alcohol. Using the equation above, the patient’s calculated osmolality is 334 mOsm/kg. The osmolar gap is thus 16 mOsm/kg. The presence of a wide osmolar gap means this patient ingested something else in addition to ethanol.

 

Further analysis of the patient’s acid-base status can help narrow the differential further. In this case, the patient has no associated anion gap acidosis (the anion gap is 11 mEq/L). Methanol is metabolized into formic acid, which contributes to tissue injury and is associated with anion gap acidosis. Ethylene glycol is metabolized into oxalic acid, which contributes to renal tubular necrosis through the formation of calcium oxalate crystals and is also associated with anion gap acidosis. Intoxication with methanol or ethylene glycol, with or without concomitant ethanol, would be associated with the presence of both an osmolar gap and an anion gap acidosis. Therefore, this patient did not ingest either substance.

 

Instead, this patient has ketosis (urinary ketones) without an associated anion gap acidosis. This suggests intoxication with isopropyl alcohol, which is metabolized to acetone, a ketone (not a ketoacid). Therefore, this patient’s overall presentation is most likely a combined ingestion of ethanol and isopropyl alcohol.

 

See, not too challenging!

 

Treatment for this combined ingestion is supportive care. There is no indication to give fomepizole. In fact, the ethanol he has on board would have been protective in a methanol or ethylene glycol combined ingestion since the ethanol would have competed for use of alcohol dehydrogenase for further metabolism, which would limit the formation of other toxic metabolites.

References:

1. Kraut JA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378(3):270–280.
2. Lima R. Toxic alcohols. NUEM blog website. Accessed March 27, 2023.