How low can you go: recovery after a serum ph of 6.62 due to ethylene glycol poisoning

SESSION TITLE: A Look Into Poisoning and Drug OverdosesSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/18/2022 12:25 pm - 01:25 pmINTRODUCTION: Ethylene glycol (EG) ingestion primarily results in intoxication; however, severe poisoning may result in anion gap metabolic acidosis with acute renal injury. Following a PubMed search, the lowest serum pH reported after presumed EG ingestion was 6.33, though the patient suffered from a cardiac arrest and an EG level was unconfirmed[1]. We report a patient who presented following a confirmed EG ingestion with a serum pH of 6.62 and subsequently made a full neurological recovery without need for long-term renal replacement therapy.CASE PRESENTATION: A 37-year-old female presented after being found unresponsive in her car along with a bottle of antifreeze and doxylamine-dextromethorphan-acetaminophen. On arrival she was obtunded and subsequently intubated. Given the reported ingestion of EG, fomepizole, sodium bicarbonate, thiamine, folate and pyridoxine were administered. Laboratory findings included: potassium 6.1mEq/L, CO2< 5mEq/L, BUN 15mg/dL, creatinine 2.0mg/dL, lactic acid 1.98mmol/L, N-acetyl-p-aminophenol < 3.0mcg/mL, salicylate < 5.0mmol/L, ethanol < 10.0mg/dL, AST 51U/L, ALT of 13U/L, AGAP>30 mmol/L, osmolar gap of 32. An arterial blood gas showed a serum pH of 6.62, pCO2 44mmHg, PaO2 177mmHg, and bicarbonate 4.6mEq/L. Emergent intermittent hemodialysis was initiated for removal of the suspected EG and for the apparent acidosis with renal impairment. Fomepizole was administered. An EG level later resulted at a level of 52mmol/L. Continuous renal replacement therapy (CRRT) was initiated due to a persistent acidemia and hyperkalemia in the setting of acute renal failure. N-acetylcysteine infusions were given due to the possible ingestion of an acetaminophen-containing compound. On day 2, EG levels were undetectable and CRRT was discontinued. On day 3 she had improvement in her mental status and was extubated. Her creatinine peaked at 9.84 mg/dL on day 11 and was 2.4mg/dL prior to discharge. There were no residual neurological or physical deficits by day 23. She was discharged day 28.DISCUSSION: Many clinical findings of EG toxicity are thought to be related to the severe metabolic acidosis and resultant calcium oxalate precipitation. The definitive treatment for EG poisoning remains early initiation of intermittent hemodialysis to remove the parent compound and prevent the formation of toxic metabolites. Interventions such as fomepizole that shift metabolism of EG away from toxic metabolites are useful to assist in delaying significant toxicity. While the patient reported other ingestion of anticholinergic xenobiotics, the largest contribution to her acidosis was EG, proved by her EG concentrations.CONCLUSIONS: We believe this represents the lowest serum pH from EG poisoning with no residual neurological deficits and no need for long-term dialysis. We believe the rapid initiation of hemodialysis in addition to other interventions contributed to the outcome in this case.Reference #1: Almien Smit, Vidya Lalloo, Andreas Engelbrecht, Ethylene glycol poisoning: A diagnostic challenge in a patient with persistent seizures and a severe metabolic acidosis, African Journal of Emergency Medicine, Volume 11, Issue 1, 2021, Pages 37-38, ISSN 2211-419X, https://doi.org/10.1016/j.afjem.2020.10.011 (https://www.sciencedirect.com/science/article/pii/S2211419X20301270)DISCLOSURES: No relevant relationships by Alexander BenyovszkyNo relevant relationships by James BorisNo relevant relationships by Alexis CatesNo relevant relationships by Mariano GiordanoNo relevant relationships by Noelle Provenzano SESSION TITLE: A Look Into Poisoning and Drug Overdoses SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Ethylene glycol (EG) ingestion primarily results in intoxication; however, severe poisoning may result in anion gap metabolic acidosis with acute renal injury. Following a PubMed search, the lowest serum pH reported after presumed EG ingestion was 6.33, though the patient suffered from a cardiac arrest and an EG level was unconfirmed[1]. We report a patient who presented following a confirmed EG ingestion with a serum pH of 6.62 and subsequently made a full neurological recovery without need for long-term renal replacement therapy. CASE PRESENTATION: A 37-year-old female presented after being found unresponsive in her car along with a bottle of antifreeze and doxylamine-dextromethorphan-acetaminophen. On arrival she was obtunded and subsequently intubated. Given the reported ingestion of EG, fomepizole, sodium bicarbonate, thiamine, folate and pyridoxine were administered. Laboratory findings included: potassium 6.1mEq/L, CO2< 5mEq/L, BUN 15mg/dL, creatinine 2.0mg/dL, lactic acid 1.98mmol/L, N-acetyl-p-aminophenol < 3.0mcg/mL, salicylate < 5.0mmol/L, ethanol < 10.0mg/dL, AST 51U/L, ALT of 13U/L, AGAP>30 mmol/L, osmolar gap of 32. An arterial blood gas showed a serum pH of 6.62, pCO2 44mmHg, PaO2 177mmHg, and bicarbonate 4.6mEq/L. Emergent intermittent hemodialysis was initiated for removal of the suspected EG and for the apparent acidosis with renal impairment. Fomepizole was administered. An EG level later resulted at a level of 52mmol/L. Continuous renal replacement therapy (CRRT) was initiated due to a persistent acidemia and hyperkalemia in the setting of acute renal failure. N-acetylcysteine infusions were given due to the possible ingestion of an acetaminophen-containing compound. On day 2, EG levels were undetectable and CRRT was discontinued. On day 3 she had improvement in her mental status and was extubated. Her creatinine peaked at 9.84 mg/dL on day 11 and was 2.4mg/dL prior to discharge. There were no residual neurological or physical deficits by day 23. She was discharged day 28. DISCUSSION: Many clinical findings of EG toxicity are thought to be related to the severe metabolic acidosis and resultant calcium oxalate precipitation. The definitive treatment for EG poisoning remains early initiation of intermittent hemodialysis to remove the parent compound and prevent the formation of toxic metabolites. Interventions such as fomepizole that shift metabolism of EG away from toxic metabolites are useful to assist in delaying significant toxicity. While the patient reported other ingestion of anticholinergic xenobiotics, the largest contribution to her acidosis was EG, proved by her EG concentrations. CONCLUSIONS: We believe this represents the lowest serum pH from EG poisoning with no residual neurological deficits and no need for long-term dialysis. We believe the rapid initiation of hemodialysis in addition to other interventions contributed to the outcome in this case. Reference #1: Almien Smit, Vidya Lalloo, Andreas Engelbrecht, Ethylene glycol poisoning: A diagnostic challenge in a patient with persistent seizures and a severe metabolic acidosis, African Journal of Emergency Medicine, Volume 11, Issue 1, 2021, Pages 37-38, ISSN 2211-419X, https://doi.org/10.1016/j.afjem.2020.10.011 (https://www.sciencedirect.com/science/article/pii/S2211419X20301270) DISCLOSURES: No relevant relationships by Alexander Benyovszky No relevant relationships by James Boris No relevant relationships by Alexis Cates No relevant relationships by Mariano Giordano No relevant relationships by Noelle Provenzano