Beyond the Usual Suspects: Ethylene Glycol Poisoning Complicated by Rare Neurological Sequelae

Ethylene glycol poisoning is a known clinical entity with established diagnostic and management protocols. However, instances presenting with rare neurological complications pose diagnostic challenges and necessitate prompt recognition and intervention. This report details the case of ethylene glycol poisoning in a 38-year-old male patient who initially presented with a history of brake oil consumption at his residence, followed by a delayed presentation with vomiting, abdominal pain, and reduced urine output, and subsequently developed unusual neurological sequelae, including unsteadiness, hearing difficulties, and an inability to close his eyes. Diagnostic assessment revealed cerebellar ataxia with bilateral sensory-neural hearing loss and facial nerve palsy. The patient was subsequently managed primarily for ethylene glycol poisoning, with conservative management for the neurological sequelae, and improved with no residual deficits. This case underscores the importance of promptly managing ethylene poisoning to prevent complications and sequelae as well as reduce morbidity for patients.


Introduction
Despite its innocuous appearance and taste, ethylene glycol is a highly toxic compound.Found in everyday items like antifreeze, air conditioning systems, and windscreen de-icing fluid [1], its rapid absorption into the bloodstream leads to toxicity primarily from its by-products rather than the compound itself [2].Poisoning with ethylene glycol can occur intentionally for intoxication, suicidal ideation, or accidentally.
Additionally, severe cases may exhibit a fourth phase characterized by neurological sequelae, including delayed cranial neuropathies, cerebral edema, seizures, increased intracranial pressure, stroke-like symptoms, diaphragmatic paralysis, sensory radiculopathies, and autonomic nervous system dysfunction [3].
These neurological complications highlight the multifaceted nature of ethylene glycol toxicity, necessitating thorough evaluation and management.We report a unique combination of cerebellar ataxia, bilateral sensory-neural hearing loss, and bilateral lower motor neuron facial nerve palsy as delayed sequelae of ethylene glycol.

Case Presentation
A 38-year-old male of Indian ethnicity reportedly consumed 250 ml of brake oil, containing ethylene glycol, in a suicidal attempt at his residence.Three days later, the patient developed complaints of abdominal pain, vomiting, and reduced urine output.It was not until the fifth day that the patient disclosed his ingestion to family members, prompting his admission to the emergency room.
During the initial evaluation, the patient appeared conscious and cooperative, albeit with signs of physiological distress: tachycardia (106/min), tachypnea (26/min), normal oxygen saturation (99% in room air), blood pressure of 144/84 mmHg, and capillary blood glucose level of 106 mg/dl.A comprehensive systemic examination revealed no overt abnormalities.
Laboratory investigations unveiled significant findings, including a high anion gap, metabolic acidosis, acute kidney injury, mild hyponatremia, transaminitis, and a normal serum osmolal gap (Table 1).

Blood work Value Reference range
Hemoglobin (Hb)  The patient received immediate treatment with an intravenous bolus dose of fomepizole (1 g), thiamine (200 mg), and pyridoxine (50 mg).The subsequent monitoring revealed no improvement in urine output over the following three hours, prompting the initiation of urgent hemodialysis.Continuous treatment involved maintenance doses of fomepizole (650 mg every six hours), oral vitamin supplements, and daily hemodialysis for the first two cycles, transitioning to alternate-day hemodialysis thereafter.The patient remained anuric until day five of hospitalization, with a peak creatinine level of 12.3 mg/dl, before gradually showing signs of improvement in both renal function and urine output.
On day 10 of hospitalization, the patient complained of difficulty closing both his eyes.On examination, the patient had weakness in eye closure, loss of nasolabial folds, and an inability to smile.The remainder of the neurological examination was within normal limits.A diagnosis of bilateral lower motor neuron-type facial nerve palsy was made, and appropriate investigations were scheduled.On day 13 of hospitalization, the patient complained of dizziness, difficulty hearing, and difficulty maintaining balance.Subsequent physical examination showed signs suggestive of cerebellar impairment, including dysdiadochokinesia, impaired finger-nose test, impaired heel-shin, and tandem walking, but no dysarthria (Videos 1, 2).The examination also showed signs of vestibulocochlear nerve impairment.

VIDEO 2: Demonstrating impaired heel-shin test
View video here: https://vimeo.com/919017541?share=copyMRI with gadolinium contrast was normal (Figures 1, 2).A nerve conduction study (NCS) of the face showed findings consistent with demyelinating neuropathy.Pure tone audiometry revealed mixed hearing loss with sensi-neural components at higher frequencies.The patient was managed conservatively for his neurological symptoms with physiotherapy and programmed exercise.

Discussion
Our patient presented with a unique combination of neurological sequelae; its temporal association with ethylene glycol (EG) consumption as well as consistent neurological investigation provide compelling evidence of EG as the etiology.While ataxia has been documented in previous studies [4,5], the occurrence of cerebellar ataxia specifically has not been reported.Additionally, our patient exhibited cranial nerve palsies, including bilateral facial and vestibulocochlear nerve involvement, consistent with common neurological sequelae [6,7].
As a consequence of delayed presentation, on the fifth day post-EG consumption, our patient was already in phase 3 of intoxication.This accounts for the normal serum osmolal gap [8] and relatively low serum EG levels.Although fomepizole was administered as a precautionary measure, its efficacy in this scenario is debatable due to the delayed presentation [9].
The onset of neurological sequelae aligns with timelines observed in previous studies [6,7].While the exact mechanism remains incompletely understood, it is believed to involve the deposition of oxalate crystals within CNS blood vessels, leading to endothelial injury [10,11].Notably, the cerebellar ataxia observed in our case presents a distinct feature.With the absence of dysarthria, normal neuroimaging findings, and intact sensory and motor extremities, the likely site of involvement appears to be the cerebellum's connection to the brainstem and higher centers.This conclusion is supported by research demonstrating EG-induced brainstem involvement and white matter tract damage on MRI [12].
Another noteworthy aspect is the presence of demyelinating neuropathy in nerve conduction studies, contrary to the anticipated axonal pattern [13].Possible explanations for this discrepancy include a recovering lesion [14] or procedural errors during the study.

TABLE 1 : Laboratory workup on admission Urine
screens for common toxins, including paracetamol, salicylates, and paraquat, were negative, while serum ethylene glycol levels were measured at 7 mg/dl.Additional diagnostic tests, such as the electrocardiogram (ECG), chest radiograph, and abdominal ultrasonogram, returned unremarkable results.