High anion gap metabolic acidosis and an increased serum osmolal gap in patients with a history of alcoholism can be due to methanol or ethylene glycol intoxication, lactic acidosis, and alcoholic or diabetic ketoacidosis. Isopropyl alcohol intoxication occurring in this context is also associated with an osmolal gap, but acidosis is uncommon in the absence of sufficient hypoperfusion to produce lactic acidosis. It is important to be able to correctly identify the cause and to initiate appropriate treatment. Unfortunately, a history of exposure to these substances is not always obtained, and such clinical clues as blindness in methanol intoxication or urinary crystals in ethylene glycol intoxication are not always present.
The metabolic acidosis and increased serum osmolal gap are also not always present together. For example, with methanol and ethylene glycol intoxication, an increased serum osmolality is present early after exposure, but metabolic acidosis is absent. As the parent alcohol is metabolized, the serum osmolality decreases, and a high anion gap metabolic acidosis becomes evident. When all of the parent alcohol has been metabolized, the high anion gap metabolic acidosis will be present alone (1). Moreover, in alcoholic or diabetic ketoacidosis, the serum osmolal gap can be normal or increased, depending not only on the ethanol concentration in the blood (in alcoholic ketoacidosis) but also on the concentration of other osmotically active metabolites arising in the course of these disorders, such as acetone (or isopropyl alcohol, as in this case) (2).
Given the potentially serious consequences of methanol and ethylene glycol intoxication, or lactic acidosis and alcoholic ketoacidosis, these disorders need to be recognized very early in their course. There is a need for simple and rapid tests to exclude these disorders, and various laboratories are working toward that goal (3). The case presented underscores the challenges faced by the clinician investigating patients with serious acid–base disorders and the value of understanding their pathophysiology in making an appropriate diagnosis.
Author Contributions: All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article.
Authors' Disclosures or Potential Conflicts of Interest: No authors declared any potential conflicts of interest.
- Received for publication February 16, 2011.
- Accepted for publication February 24, 2011.
- © 2011 The American Association for Clinical Chemistry