Abstract
IntroductionEthylene glycol poisoning may pose diagnostic difficulties if the history of ingestion is not volunteered, or if the presentation is delayed. This is because the biochemical features of high anion-gap metabolic acidosis and an osmolar gap resolve within 24 to 72 hours as the ethylene glycol is metabolized to toxic metabolites. This case illustrates the less well-known clinical features of delayed ethylene glycol poisoning, including multiple cranial and peripheral neuropathies, and the clinical findings which may point towards this diagnosis in the absence of a history of ingestion.Case presentationA 53-year-old Afro-Caribbean man presented with vomiting, abdominal pain and oliguria, and was found to have acute renal failure requiring emergency hemofiltration, and raised inflammatory markers. Computed tomography imaging of the abdomen revealed the appearance of bilateral pyelonephritis, however he failed to improve with broad-spectrum antibiotics, and subsequently developed multiple cranial neuropathies and increasing obtundation, necessitating intubation and ventilation. Computed tomography of the brain showed no focal lesions, and a lumbar puncture revealed a raised cerebrospinal fluid opening pressure and cyto-albuminological dissociation. Nerve conduction studies revealed a sensorimotor radiculoneuropathy mimicking a Guillain-Barre type lesion with an atypical distribution. It was only about two weeks after presentation that the history of ethylene glycol ingestion one week before presentation was confirmed. He had a slow recovery on the intensive care unit, requiring renal replacement therapy for eight weeks, and complicated by acute respiratory distress syndrome, neuropathic pain and a slow neurological recovery requiring prolonged rehabilitation.ConclusionsAlthough neuropathy as a result of ethylene glycol poisoning has been described in a few case reports, all of these were in the context of a known history of ingestion. As the diagnosis may well be obscured if the history of ingestion is not elucidated, it is important to be aware of this possibility especially if presentation is delayed.
Highlights
Ethylene glycol poisoning may pose diagnostic difficulties if the history of ingestion is not volunteered, or if the presentation is delayed
Conclusions: neuropathy as a result of ethylene glycol poisoning has been described in a few case reports, all of these were in the context of a known history of ingestion
The diagnosis of Ethylene glycol (EG) poisoning is relatively obvious in an individual presenting with a history of ingestion, and a clinical presentation consistent with poisoning, associated with a high anion-gap metabolic acidosis and elevated osmolar gap
Summary
This case illustrates the diagnostic conundrum that a delayed presentation of EG poisoning may pose. In these situations, therapeutic interventions such as alcohol dehydrogenase inhibition therapy are less of an issue as the offending compound would have been metabolized due to its short half-life. Supportive therapy in terms of renal replacement therapy and ventilatory support for severe neurological deficits are the mainstay of treatment. These patients often have a prolonged course and require extensive rehabilitation. Authors' contributions Both authors analyzed and interpreted the patient data and the literature review and co-wrote, read and approved the final manuscript
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