OBJECTIVE: To determine whether an elevated osmolal gap is specific for toxic alcohol ingestion. DESIGN: Cross-sectional. SETTING: Emergency room and medical and surgical inpatient wards at a university-affiliated hospital. PATIENTS: Twenty-three patients with lactic acidosis, 19 with alcoholic ketoacidosis, and 10 randomly selected controls. MEASUREMENTS AND MAIN RESULTS: Calculated and measured serum osmolality was determined in all study participants. The osmolal gap was increased in patients with lactic acidosis (17.4 +/- 5.4 mmol/kg) and alcoholic ketoacidosis (26.9 +/- 7.6 mmol/kg) when compared with controls (-1.7 +/- 1.7 mmol/kg, P less than 0.05 for both comparisons). When ethanol was included in the calculation, the osmolal gap remained elevated in the lactic acidosis (10.3 +/- 2.0 mmol/kg) and alcoholic ketoacidosis (11.1 +/- 3.2 mmol/kg) groups (P less than 0.05 for both comparisons). CONCLUSIONS: The osmolal gap is often used as a screen for toxic alcohol ingestion. When calculating the osmolal gap, the contribution of ethanol should be considered. An elevated osmolal gap is not specific for toxic alcohol ingestion, as the osmolal gap was elevated in patients with lactic acidosis and alcoholic ketoacidosis. These two conditions should be considered when using the osmolal gap to design therapy (for example, hemodialysis) in the setting of anion gap metabolic acidosis and suspected toxic alcohol ingestion.
OBJECTIVE: To determine whether an elevated osmolal gap is specific for toxic alcohol ingestion. DESIGN: Cross-sectional. SETTING: Emergency room and medical and surgical inpatient wards at a university-affiliated hospital. PATIENTS: Twenty-three patients with lactic acidosis, 19 with alcoholic ketoacidosis, and 10 randomly selected controls. MEASUREMENTS AND MAIN RESULTS: Calculated and measured serum osmolality was determined in all study participants. The osmolal gap was increased in patients with lactic acidosis (17.4 +/- 5.4 mmol/kg) and alcoholic ketoacidosis (26.9 +/- 7.6 mmol/kg) when compared with controls (-1.7 +/- 1.7 mmol/kg, P less than 0.05 for both comparisons). When ethanol was included in the calculation, the osmolal gap remained elevated in the lactic acidosis (10.3 +/- 2.0 mmol/kg) and alcoholic ketoacidosis (11.1 +/- 3.2 mmol/kg) groups (P less than 0.05 for both comparisons). CONCLUSIONS: The osmolal gap is often used as a screen for toxic alcohol ingestion. When calculating the osmolal gap, the contribution of ethanol should be considered. An elevated osmolal gap is not specific for toxic alcohol ingestion, as the osmolal gap was elevated in patients with lactic acidosis and alcoholic ketoacidosis. These two conditions should be considered when using the osmolal gap to design therapy (for example, hemodialysis) in the setting of anion gap metabolic acidosis and suspected toxic alcohol ingestion.