GJ WILSON1,2, J ROWLAND1, MR DOWLING1, L FRANCIS3, GT JOHN1,2,AL KARK1,2
1Department of Renal Medicine, Royal Brisbane and Women’s Hospital, Herston, Queensland; 2School of Clinical Medicine, University of Queensland, Herston, Queensland; 3Department of Pathology, Royal Brisbane and Women’s Hospital, Herston, Queensland
Background: Ethylene glycol toxicity is a well-known cause of acute kidney injury (AKI) and high anion gap metabolic acidosis. However, it is a rare presentation in Australia with only 22 cases reported in 2014. The diagnosis of ethylene glycol toxicity is challenging in the absence of a history of ingestion and can be misdiagnosed as lactic acidosis which, due to structural similarities with glycolate, causes falsely elevated lactate levels on some instruments.
Case Report: A 36 year-old female presented to the emergency department with an altered level of consciousness and tachypnoea requiring urgent intubation. She was anuric and had an AKI (creatinine 182 umol/L). An iSTAT venous blood gas demonstrated a high anion gap metabolic acidosis (pH 7.08, HCO3 6, CO2 19, anion gap 34) and an elevated serum lactate (9.4 mmol/L). She was provisionally diagnosed with type B lactic acidosis and transferred to ICU for ventilation and continuous veno-venous haemodiafiltration. Upon extubation, the patient denied any toxic ingestions and renal biopsy was performed demonstrating crystalloid material birefringent under polarised light consistent with oxalate nephropathy. Urinary organic acids were requested and urinary glycolate and oxalate levels were elevated (2200 mmol/mol Cr and 520 mmol/mol Cr). Ethylene glycol levels were requested from admission bloods and demonstrated a toxic level of 8.8 mmol/L confirming a diagnosis of ethylene glycol toxicity. The patient continued to deny any ethylene glycol ingestion even after psychiatric consultation.
Conclusions: Ethylene glycol toxicity is a well-known but rare cause of AKI and high anion gap metabolic acidosis. It should be considered in all patients with AKI and high anion metabolic acidosis even in the absence of a history of ingestion.