A 17-year-old boy is brought to the emergency department due to confusion. He also has abdominal pain, vomiting, and blurred vision. Temperature is 36.8 C (98.2 F), blood pressure is 110/60 mm Hg, pulse is 110/min, and respirations are 22/min. Physical examination is notable for dry mucous membranes. Lungs are clear to auscultation. Abdominal examination shows mild epigastric tenderness without rebound or guarding. Ophthalmoscopy reveals optic disc hyperemia. No other abnormalities are noted. Laboratory results are as follows:
| Sodium | 136 mEq/L |
| Chloride | 100 mEq/L |
| Bicarbonate | 7 mEq/L |
| Blood urea nitrogen | 30 mg/dL |
| Creatinine | 0.8 mg/dL |
| Blood glucose | 80 mg/dL |
| Serum ketones | negative |
| Plasma lactate | 2 mEq/L (normal: <2) |
Which of the following is the most likely cause of this patient's symptoms?
Features of commonly ingested alcohols | |||||
Substance typically ingested | Major metabolite | ↑ Osmolal gap | ↑ | Other clinical features | |
Ethanol | Beer, wine, liquor | Acetaldehyde (minor toxicity) | Yes | Yes (if ketosis) | Confusion |
Methanol | Windshield washer fluid, homemade liquor | Formic acid (major toxicity)* | Yes | Yes | Confusion, vision deficits |
Ethylene glycol | Antifreeze | Glycolic & oxalic acids (major toxicity)* | Yes | Yes | Confusion, calcium oxalate crystals (AKI, flank pain) |
Isopropyl alcohol | Rubbing alcohol, hand sanitizer | Acetone (minor toxicity) | Yes | No** | Confusion |
*Treatment of choice is fomepizole to inhibit production of toxic metabolites. **No acidosis (anion gap or non–anion gap) is present with isopropyl alcohol ingestion. AKI = acute kidney injury. | |||||
This adolescent patient with encephalopathy (eg, confusion), abdominal pain, vomiting, and blurred vision has a markedly low serum HCO3− indicating metabolic acidosis (with tachypnea due to respiratory compensation). A significantly elevated anion gap of 29 mEq/L denotes an anion gap metabolic acidosis (AGMA). The most common cause of AGMA in adolescents is new-onset type 1 diabetes mellitus complicated by diabetic ketoacidosis, which could explain this patient's symptoms; however, a normal serum glucose and negative ketones exclude this diagnosis (Choice B).
Another potential cause of AGMA is ingestion of a toxic alcohol (eg, ethylene glycol, methanol), which is common in patients who are suicidal or seeking inebriation but lack access to ethanol (eg, financially unable, underage). Methanol ingestion is highly likely in this patient given the ophthalmoscopic finding of optic disc hyperemia, which signifies optic neuritis caused by formic acid (the major toxic metabolite of methanol). Fomepizole can be used to inhibit methanol metabolism into formic acid, and hemodialysis can be considered in severe cases. Although early treatment can partially reverse vision damage, full recovery is rare.
(Choice A) Aspirin overdose can also cause encephalopathy, abdominal pain, vomiting, and AGMA, but findings of optic neuritis (eg, optic disc hyperemia) would not be expected.
(Choice C) Ethylene glycol and methanol toxicity both cause AGMA and encephalopathy. However, ethylene glycol ingestion does not cause optic neuritis; kidney dysfunction (tubular injury) due to calcium oxalate stone formation would more likely be present. This patient's elevated BUN is due to dehydration (volume depletion) from vomiting.
(Choice E) Toluene (a hydrocarbon found in many commercial products) is sometimes inhaled recreationally (eg, glue sniffing), particularly among adolescents because of ease of access. Although encephalopathy and abdominal symptoms can occur, optic neuritis would be rare. In addition, nonanion gap metabolic acidosis (not AGMA) would be typical, caused by toluene-induced type 1 renal tubular acidosis. AGMA can occasionally be seen in severe toxicity associated with kidney failure or lactic acidosis (both of which are absent in this patient).
Educational objective:
Methanol toxicity is characterized by encephalopathy, abdominal pain/vomiting, and high anion gap metabolic acidosis. Optic neuritis is a common complication that distinguishes methanol ingestion from other toxic alcohol ingestions (eg, ethylene glycol).