Ethylene glycol intoxication
General description
Ethylene glycol poisoning is a serious medical condition that typically occurs through the ingestion of automotive antifreeze, which contains this colorless, odorless, and deceptively sweet-tasting substance. Cases arise either through accidental consumption or deliberate ingestion in suicide attempts.
The toxicity develops through a complex metabolic process in which the liver breaks down ethylene glycol using alcohol dehydrogenase, producing harmful byproducts such as glycolic acid and oxalic acid. These metabolites are responsible for causing severe metabolic acidosis and kidney damage in affected individuals.
The condition manifests in distinct phases, beginning with symptoms that resemble alcohol intoxication, accompanied by vomiting and abdominal pain. As the poisoning progresses, patients may experience more severe symptoms including decreased consciousness, headache, and seizures.
Pathological examination reveals significant tissue changes, including diffuse edema, inflammatory cell infiltration, varying degrees of vacuolar degeneration, and neuronal loss.
Without proper treatment, ethylene glycol poisoning can lead to severe long-term complications, most notably kidney failure and brain damage. This combination of metabolic disruption and organ damage makes ethylene glycol poisoning a particularly dangerous form of intoxication requiring prompt medical intervention.
Radiographic features
MRI shows bilateral symmetric T2WI and FLAIR hyperintensity in the basal ganglia, thalamus, amygdala, hippocampus, insular cortex, and brainstem. Abnormal signals may also be seen in the cortical and white matter regions of the temporal lobe.
T2WI and FLAIR hyperintensity
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Caudate nucleus
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Putamen
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Globus pallidus
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Thalamus
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CerebrumTemporal lobeAmygdala
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CerebrumTemporal lobeHippocampus
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CerebrumInsula
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CerebrumTemporal lobeCerebral cortex
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CerebrumTemporal lobeCerebral white matter
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Brainstem
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