Nefroneural syndrome as a result of poisoning by diethylene glycol

Introduction: Diethylene glycol is a clear, hygroscopic, odorless and toxic liquid for humans. It is widely available in the industry, being widely used in the production of antifreeze, lubricants, cosmetics and plasticizers. Poisoning by ingesting this substance leads patients to an early neurological syndrome consisting of drunkenness, ataxia and, if severe, seizures and coma. Objectives: To review the central aspects of diethylene glycol intoxication, its toxic dynamics and the development of nephroneural syndrome. Methods: A literature review compiled from searches for articles in the PubMed and Medline databases was performed using the descriptors Dietilenoglicol; Ácido 2-hidroxietoxiacético; Toxicidade Renal; Álcoois tóxicos. Results: After ingestion, diethylene glycol is rapidly absorbed and distributed in the body. Metabolism occurs in the liver and the excretion of both the substance and its metabolite 2-hydroxyethoxyacetic acid (HEAA) is renal. HEAA is primarily responsible for kidney and neurological damage, which result in severe nephroneural syndrome, initially characterized by gastrointestinal changes, such as nausea, vomiting and abdominal pain, followed by metabolic acidosis and emerging kidney injury. After 72 hours of intoxication, damage to the optic nerve, functional deficit of cranial nerves, tetraparesis and peripheral neuropathy can occur, which can lead the patient to death or permanent disability. HEAA causes damage to renal and nerve cells to varying degrees depending on the amount of substance ingested or the susceptibility of the intoxicated patient. Conclusion: Early diagnosis and proper patient management, in addition to good industry practices, are essential for the eradication of this intoxication.