Persistent bilateral sensorineural hearing loss after ingestion of an analytically confirmed diethylene glycol-containing beverage: a case report

Diethylene glycol (DEG) poisoning is a rare but potentially fatal intoxication characterized by severe metabolic acidosis, acute kidney injury (AKI), and delayed neurological complications. Persistent bilateral sensorineural hearing loss associated with magnetic resonance imaging (MRI) findings suggestive of toxic leukoencephalopathy has rarely been reported. A previously healthy 45-year-old Vietnamese man ingested approximately 140 mL of homemade alcohol later found to contain 47% diethylene glycol, 1.5% ethylene glycol, and 1.1% propylene glycol. Six hours after ingestion, he developed profuse vomiting, dyspnea, and progressive weakness. At presentation to a local hospital, he had severe metabolic acidosis (pH 7.0, bicarbonate 2.4 mmol/L), circulatory shock, and acute kidney injury. Emergency intermittent hemodialysis (IHD) was initiated 11 hours after ingestion. Despite correction of acidosis, he remained anuric and was transferred to our Poison Control Center 75 hours after ingestion. Laboratory investigations demonstrated severe acute kidney injury, marked elevation of cardiac biomarkers, rhabdomyolysis, and marked transaminase elevation, likely reflecting combined skeletal muscle and hepatic injury. Brain MRI performed during the delayed neurological phase demonstrated bilateral symmetrical periventricular white matter abnormalities suggestive of toxic leukoencephalopathy. Cerebrospinal fluid examination performed during neurological evaluation demonstrated markedly elevated protein concentration (3.86 g/L) with minimal pleocytosis. Pure-tone audiometry performed after the onset of hearing impairment demonstrated severe bilateral sensorineural hearing loss, and stapedius reflexes were absent bilaterally. After two months of hospitalization and repeated IHD sessions, hepatic and cardiac abnormalities resolved; however, the patient remained dialysis-dependent and had profound persistent hearing loss. This case illustrates the classic progression of severe DEG poisoning from metabolic acidosis and AKI to delayed neurotoxicity. Persistent bilateral sensorineural hearing loss associated with MRI findings suggestive of toxic leukoencephalopathy and marked cerebrospinal fluid protein elevation may represent a severe manifestation of delayed DEG-associated neurotoxicity, although contributions from critical illness cannot be completely excluded.

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Journal
BMC Neurology
Published
2026-09-14
DOI
https://doi.org/10.1186/s12883-026-05335-0
Primary Topic
Poisoning and overdose treatments
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article
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article

Persistent bilateral sensorineural hearing loss after ingestion of an analytically confirmed diethylene glycol-containing beverage: a case report

Nguyen Dang Duc, Lam Nguyen Hong Khanh, Vu Thi Diem Quynh, Nguyen Trung Nguyen
BMC Neurology
Poisoning and overdose treatments
article

Persistent bilateral sensorineural hearing loss after ingestion of an analytically confirmed diethylene glycol-containing beverage: a case report

Nguyen Dang Duc, Lam Nguyen Hong Khanh, Vu Thi Diem Quynh, Nguyen Trung Nguyen
article en

Abstract

Diethylene glycol (DEG) poisoning is a rare but potentially fatal intoxication characterized by severe metabolic acidosis, acute kidney injury (AKI), and delayed neurological complications. Persistent bilateral sensorineural hearing loss associated with magnetic resonance imaging (MRI) findings suggestive of toxic leukoencephalopathy has rarely been reported. A previously healthy 45-year-old Vietnamese man ingested approximately 140 mL of homemade alcohol later found to contain 47% diethylene glycol, 1.5% ethylene glycol, and 1.1% propylene glycol. Six hours after ingestion, he developed profuse vomiting, dyspnea, and progressive weakness. At presentation to a local hospital, he had severe metabolic acidosis (pH 7.0, bicarbonate 2.4 mmol/L), circulatory shock, and acute kidney injury. Emergency intermittent hemodialysis (IHD) was initiated 11 hours after ingestion. Despite correction of acidosis, he remained anuric and was transferred to our Poison Control Center 75 hours after ingestion. Laboratory investigations demonstrated severe acute kidney injury, marked elevation of cardiac biomarkers, rhabdomyolysis, and marked transaminase elevation, likely reflecting combined skeletal muscle and hepatic injury. Brain MRI performed during the delayed neurological phase demonstrated bilateral symmetrical periventricular white matter abnormalities suggestive of toxic leukoencephalopathy. Cerebrospinal fluid examination performed during neurological evaluation demonstrated markedly elevated protein concentration (3.86 g/L) with minimal pleocytosis. Pure-tone audiometry performed after the onset of hearing impairment demonstrated severe bilateral sensorineural hearing loss, and stapedius reflexes were absent bilaterally. After two months of hospitalization and repeated IHD sessions, hepatic and cardiac abnormalities resolved; however, the patient remained dialysis-dependent and had profound persistent hearing loss. This case illustrates the classic progression of severe DEG poisoning from metabolic acidosis and AKI to delayed neurotoxicity. Persistent bilateral sensorineural hearing loss associated with MRI findings suggestive of toxic leukoencephalopathy and marked cerebrospinal fluid protein elevation may represent a severe manifestation of delayed DEG-associated neurotoxicity, although contributions from critical illness cannot be completely excluded.

BMC Neurology
Vinh University (VN), Bạch Mai Hospital (VN)
Good health and well-being
Openalex Percentile: Top 9%
Poisoning and overdose treatments
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