Ethylene glycol poisoning occurs when a person ingests ethylene glycol, a toxic chemical commonly found in antifreeze, de-icing solutions, and some industrial products. The poisoning is primarily caused by the body’s metabolism of ethylene glycol into harmful substances that damage organs, especially the kidneys.
When ethylene glycol enters the body, it is initially not very toxic. However, the liver enzyme alcohol dehydrogenase (ADH) begins to metabolize ethylene glycol into several intermediate compounds, including glycolic acid and oxalic acid. These metabolites are much more dangerous than ethylene glycol itself. Glycolic acid contributes to severe metabolic acidosis, a condition where the blood becomes too acidic, disrupting normal cellular functions. Oxalic acid, on the other hand, binds with calcium ions in the blood to form calcium oxalate crystals. These crystals are sharp and insoluble, and they deposit in the kidneys, causing physical damage to the renal tubules and leading to acute kidney failure.
The process can be summarized as follows:
1. **Ingestion of ethylene glycol** — usually accidental or intentional consumption of antifreeze or similar substances.
2. **Metabolism by alcohol dehydrogenase** — ethylene glycol is converted into glycolaldehyde, then further metabolized into glycolic acid.
3. **Further metabolism** — glycolic acid is converted into glyoxylic acid and finally into oxalic acid.
4. **Toxic effects** — oxalic acid binds calcium to form calcium oxalate crystals, which damage the kidneys and cause hypocalcemia (low calcium levels in the blood). Meanwhile, glycolic acid causes metabolic acidosis, which can affect multiple organ systems.
The toxicity mechanism is similar to that of methanol poisoning, where the parent compound is metabolized into toxic acids that cause metabolic disturbances and organ damage. However, the specific metabolites and their effects differ, with ethylene glycol poisoning being particularly associated with kidney damage due to crystal formation.
Symptoms of ethylene glycol poisoning often develop in stages. Initially, a person may experience intoxication-like symptoms such as dizziness, headache, and nausea because ethylene glycol itself acts as a central nervous system depressant. As metabolism progresses, symptoms worsen to include severe metabolic acidosis, rapid breathing, confusion, seizures, and eventually kidney failure if untreated.
Treatment focuses on preventing the metabolism of ethylene glycol into its toxic metabolites. This is achieved by administering antidotes such as fomepizole or ethanol, which competitively inhibit alcohol dehydrogenase. By saturating this enzyme with a safer substrate (ethanol) or blocking it (fomepizole), the conversion of ethylene glycol to glycolic and oxalic acids is slowed or stopped. This allows the unmetabolized ethylene glycol to be excreted by the kidneys without causing damage. Additional treatments may include correcting metabolic acidosis with sodium bicarbonate and removing toxins via hemodialysis.
In summary, ethylene glycol poisoning is caused by ingestion of ethylene glycol followed by its metabolism into toxic acids that cause metabolic acidosis and kidney damage through calcium oxalate crystal deposition. The key to preventing severe outcomes is early recognition and treatment to block the metabolic pathway responsible for toxicity.
