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Ethylene glycol poisoning and the lactate gap

Ethylene glycol poisoning and the lactate gap Ethylene glycol is often ingested either by accident or deliberately, and accumulation of toxic metabolites glycolic and oxalic acids can lead to severe acidosis with neurological, cardiovascular and renal complications, and death [1]. The biochemical assay for ethylene glycol is not always readily available, but many point-of-care blood gas analysers give an erroneously high lactate level in the presence of glycolate [2]. Recent attention has been given in the literature to the value of the ‘lactate gap’ between laboratory and point of care testing in aiding diagnosis [3]. We would like to report a case where elevated lactate alone enabled a diagnosis to be considered and appropriate treatment started. A 38-year-old woman presented to the emergency department with severe vomiting, and exhibiting signs of severe dehydration. She admitted consuming nothing but vodka and energy drinks for the previous five days. Initial blood gas analysis showed a severe metabolic acidosis, with a pH of 7.02, a base excess of )24.4 mmol.l and a lactate of 22 mmol.l. After initial fluid resuscitation she was transferred to the intensive care unit for further management. The laboratory biochemistry results are displayed in Table 1. The seemingly disproportionately high lactate prompted concerns over the ingestion of glycol, so we sent blood to the regional poisons unit for analysis and commenced haemofiltration. Ethylene glycol levels were later reported as 280 mg.l. After twelve hours of treatment with alcohol infusion, glycol was undetectable in the serum, and the patient made a full recovery. Glycol is metabolised in the liver by alcohol dehydrogenase and aldehyde dehydrogenase into glycolic acid, the compound that is largely responsible for the metabolic acidosis seen in patients with glycol poisoning. Most point-of-care analysers work by the use of a lactate oxidase based system, where lactate is converted to pyruvate and hydrogen peroxide, which is then detected by the machine. Glycolate is structurally similar and equally serves as a substrate in this reaction, leading to a falsely raised lactate result. Laboratory analysers generally use a different assay (using lactate dehydrogenase) that is not subject to the same error. A disparity in pointof-care and laboratory results gives the so-called ‘lactate gap’ which is strongly suggestive of the presence of glycolate and can be useful in guiding treatment. However in our hospital, the laboratory and point-of-care analysers both rely on the lactate oxidase method, which led to the raised lactate being shown on both results. Results from automated analysers are very useful in aiding decision-making about the care of our patients; however, without an understanding of the physiology and cellular processes underlying them, they cannot properly be interpreted in a clinical context. Clinicians need to be aware of the limitations of assays to avoid acting on erroneous information.