Ethylene glycol toxicity
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At the time the article was created Frank Gaillard had no recorded disclosures.View Frank Gaillard's current disclosures
At the time the article was last revised Daniel J Bell had no recorded disclosures.View Daniel J Bell's current disclosures
Ethylene glycol toxicity is a type of toxic leukoencephalopathy. Ethylene glycol, best known as a component of antifreeze, has been ingested both deliberately and accidentally, resulting in neurotoxicity and renal failure.
Ethylene glycol is found in many compounds including antifreeze. It is injected either accidentally or deliberately as a suicide attempt or for its intoxicating effect 1. As such, the demographics of affected individuals is varied.
A delay is present between ingestion and development of symptoms. Initial symptoms of ethylene glycol toxicity is typically a severe encephalopathy (similar clinically to acute basilar artery occlusion) 1. In some instances, patients also develop Parkinsonian-like syndrome 1.
Ingestion of ethylene glycol indirectly results in central nervous system compromise, cardiopulmonary depression, and renal failure 1. Once absorbed from the gastrointestinal tract, which occurs rapidly, ethylene glycol is converted to glyoxylic acid and oxalic acid which are the compounds responsible for toxicity, and metabolic acidosis 1. Furthermore, autopsy studies have demonstrated deposition of calcium oxalate crystal in the walls of intracranial blood vessels with associated inflammatory cellular infiltration 1.
Imaging features are variable but tend to involve basal ganglia, thalami and brainstem as well as white matter. MRI is the investigation of choice to assess these features.
CT abnormalities will depend on the elapsed time from ingestion.
In the first 1-2 days, CT will generally demonstrate cerebral edema. Over the next few days, hypodensity in the deep grey matter (thalami and basal ganglia) and brainstem develop 1.
MRI is more sensitive to the aforementioned changes, with bilateral symmetric regions of high T2 signal and restricted diffusion in the brainstem, basal ganglia and thalami, as well as amygdala and hippocampi 1. Occasionally hemorrhagic change in the lentiform nuclei is also encountered 1.
Treatment and prognosis
With prompt and appropriate therapy, ethylene glycol toxicity can be minimized. Treatment is primarily with haemodialysis, administration of bicarbonate (to counteract metabolic acidosis), and fomepizole 1.
The differential diagnosis is relatively broad, with imaging features and clinical presentation similar to a number of other conditions including: