Delayed ethylene glycol poisoning presenting with abdominal pain and multiple cranial and peripheral neuropathies: a case report

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.

Survival and complete recovery after severe acute ethylen glycol poisoning — a case report

“…As the urine test was clearly positive for EG, serial neurological clinical examination excluded any lateralisation, and since progressive neurological improvement was observed, we concluded that the data provided by an early CT or MRI would not drive any further therapeutic action. The complete recovery observed in our patient has been previously observed in other case reports [10].…”

Brake fluid toxicity feigning brain death

“…At the same time, acute renal failure with high anion and high osmolar gap metabolic acidosis sets in. So far published reports on central nervous system toxicity of ethylene glycol focus on the involvement of basal ganglia and brainstem, with concordant brain imaging findings 7. Multiple cranial neuropathy occurring in ethylene glycol poisoning is reported in several case reports 8 9.…”

Prolonged renal failure in the course of atypical ethylene glycol intoxication.

“…Only several case presentations describe similar course of ethylene glycol intoxication, where patients presented late, with established organ damage: renal failure or severe peripheral neuropathy (Kaiser et al, 1993;Baldwin & Sran, 2010). In all cases diagnosis of poisoning and identification of toxin was established only after extensive case analysis and investigations.…”