Case Presentation:
A 58 year‐old man with a history of hypertension, stroke, seizures and chronic kidney disease was admitted as a stroke alert with left sided weakness and left visual field defect. There was also a history of depression and a previous suicide attempt. Examination was significant for a confused male with an acetone odor, tachycardia and tachypnea. An arterial blood gas showed a pH of 7.18, pCO2 of 18 and pO2 of 43. His blood glucose was 104 mg/dL. These findings heightened a concern about some type of alcohol ingestion and further labs revealed an anion gap of 31, serum osmolar gap of 34 and a creatinine of 3.6 mg/dL. CT scan of the head showed old infarcts with the possibility of new infarcts. The patient deteriorated rapidly and soon thereafter it was reported that a bottle of antifreeze was found near him at home. Fomepizole was started along with a bicarbonate drip and dialysis was initiated. The patient then developed status epilepticus which was eventually controlled. An MRI revealed acute infarctions scattered throughout the brain along with generalized edema and midline shift. He remained dialysis dependent. After many days off of sedation, the patient was not following commands and showed no neurological improvement. Due to the severity of presentation and his hospital course, the family decided to withdraw life support and he expired later that day.
Discussion:
The severe neurological damage in ethylene glycol poisoning is a rare manifestation that can be fatal. As little as 30 mL (2 tablespoons) can cause severe toxicity and death. Ethylene glycol is relatively nontoxic before it is metabolized to glycolate, glyoxylate, and oxalate. The pathogenesis is metabolism of substantial portions of parent alcohol to its toxic byproducts and obstruction of blood vessels due to precipitation of oxalate crystals. Recognizing ethylene glycol toxicity early can abort or reduce neurological severity and patient morbidity. Early treatment with bicarbonate, fomepizole and hemodialysis are the cornerstone of the management. It can be distinguished from isopropyl alcohol ingestion which does not cause a high anion gap metabolic acidosis and is usually less severe. Methanol toxicity is treated similarly although eye complaints are a common feature.
Conclusions:
High index of suspicion for ethylene glycol poisoning is essential in patients with profound anion gap metabolic acidosis and a high osmolar gap. Unusual presentations such as stroke due to neurological damage from ethylene glycol toxicity can be life threatening if not recognized and managed in a timely fashion. Although our case resulted in an unfortunate outcome, rapid recognition and early treatment by hospitalists can potentially improve morbidity and mortality in patients with ethylene glycol poisoning.