Lactic acidosis or not? A case of two acidotic siblings

Background: Ethylene glycol is metabolized to glycolic acid which is responsible for anion gap metabolic acidosis (AGMA), and oxalic acid, causing nephrotoxicity. Glycolic acid interferes with some lactate assays resulting in a falsely elevated level. Method: A case of two siblings cared for in a pediatric ICU with toxicology consult. Results: Two siblings presented simultaneously with tachypnea and lethargy requiring intubation. Patient A was an 18-month-old female and patient B was a 2-year-old male. Initial capillary blood gases done on whole blood (WB) using a Radiometer 800 FLEX. Patient A capillaryWB gas: 6.904/21/149/3.9, lactate 22, AG 27. Patient B capillary WB gas: 6.923/19.6/109/3.8, lactate 27, AG 26. Acidosis was refractory to resuscitation. Differential included toxic alcohols/glycols, cyanide, and met formin toxicity. Fomepizole and sodium bicarbonate infusion were initiated within 1 h after arrival. Repeat lactates done on serum using an AU 680 Beckmann: at 6 h post presentation, patient A had a serum lactate of 2 and a simultaneous WB gas lactate of 13.9. Patient B had a serum lactate of 2.5 with a WB gas lactate of 12.5. Predialysis EG levels were 13 mg/dL for patient A and 23 mg/dL for patient B. Low flux, high efficiency HD was performed. Both siblings made a complete recovery without residual renal insufficiency. Source of exposure remains unclear. Discussion: Falsely elevated lactates have been described when using whole blood analyzers to measure lactate in the presence of glycolic acid. To determine the accurate lactic acid, a glycolate insensitive assay should be used. The difference between the lactates, termed \u27lactate gap,\u27 is a clue to the presence of EG. Conclusion: EG poisoning should be considered in patients who present with AGMA, significant lactic acidosis, and a Blactate gap