Lactate gap - A clinical tool for diagnosing and managing ethylene glycol poisoning

Abstract

Ethylene glycol is a toxic alcohol, and its ingestion can cause neurological, cardiovascular, and renal complications, including coma and death. It causes an elevated osmolar gap, and its metabolites, glycolate, and oxalate, are responsible for elevated anion gap metabolic acidosis. Early diagnosis and management of this condition are critical in the emergency department (ED).

The point-of-care (POC) blood gas analyzer, commonly used in the emergency department, measures lactic acid using the lactate oxidase method, which measures the hydrogen peroxide generated from lactate. In contrast, the laboratory analyzer measuring venous lactate uses the lactate dehydrogenase method. Glycolic acid, a metabolite of ethylene glycol, is structurally similar to L-lactic acid, and it cross-reacts with lactate on the POC analyzer. Glycolic acid metabolized by lactate oxidase also leads to increased hydrogen peroxide production similar to L-lactic acid, resulting in spuriously elevated lactate. This discrepancy causes higher lactate levels in POC measurement than the laboratory-measured lactate, a condition called lactate gap.

We present two patients with altered levels of consciousness who had elevated osmolar gap and lactate gap at presentation to the emergency department. Ethylene glycol poisoning was suspected, given the discrepancy between POC lactate and laboratory-measured venous lactate levels. We promptly initiated treatment with fomepizole and hemodialysis while waiting for ethylene glycol levels, prompting early recovery.

We hypothesize that ED physicians should use the lactate gap as an initial diagnostic tool for early diagnosis of ethylene glycol poisoning, and hospitalists and nephrologists can use the closure of the lactate gap to decide on dialysis termination.