Introduction: Ammonia detoxification is processed in the liver’s mitochondrial urea cycle. This biochemical pathway is subject to disruption by ingested oxidative agents. Sparse data exists on acute ethylene glycol poisoning's association with hyperammonemia (HA) especially at supra-physiologic neurotoxic levels. Ethylene glycol remains a common substance in attempted suicides
Description: A 60-year-old man with a history of depression, alcoholism and self-harm is found at home by his spouse, unresponsive and agonally breathing. On EMS arrival he has a 5min seizure and proceeds into cardiac arrest for 3min. He is intubated in the ED. Initial lab tests show a pH 6.67, lactic 12.9, potassium 7.4, an anion gap of 30, creatinine of 1.6, HCO3 < 2mmol/L, serum osmolarity 374, and an Osmolar gap of 64. The patient has no transaminasemia, or valproic acid level elevation. In the ICU he decompensates into refractory circulatory shock. He is treated empirically for acute alcoholic toxidrome with 15mg/kg of fomepizole and emergent hemodialysis. His encephalopathy work-up reveals an incidental serum HA of 873umol/L confirmed on repeat testing. MRI shows incomplete CSF signal suppression within the sulci of the cerebral hemispheres, and punctate acute infarcts of the cerebellum. His lumbar puncture shows elevated protein and neutrophil predominance without viral or bacterial PCR positivity. Laboratory reports his ethylene glycol level of 87mg/dl. Over 3 days of hemodialysis his serum ammonia and metabolic acidosis slowly normalizes. On admission day 4 he is extubated without any overt neurological deficits and recounts the events leading towards his suicide attempt
Discussion: The metabolite N-acetyl-L-Glutamic acid (NAG) is the first precursor in liver ureagenesis. Toxic alcohols like ethylene glycol and methanol cause secondary HA by NAG inhibition. NAG supply also decreases during severe organic acidemias. Finally, Glutamine is a paradoxical detoxicant upregulated in the liver during acute HA. It has the unfortunate side effect of releasing intracellular astrocyte ammonia and worsening neurotoxicity. Emergent dialysis and early antitoxin delivery terminate the ethylene glycol toxin cascade. An early obtained serum Ammonia level may be of diagnostic and prognostic value in hyperacute toxic alcohol poisonings
