Diethylene Glycol Poisoning: Report on Two Cases

Wordley, E.

doi:10.1136/jcp.1.1.44

Cited by 18 publications

(3 citation statements)

References 3 publications

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“…The neurological manifestation was first reported by Wordley 16 in 1947 when he described 2 cases. One patient drank half a bottle of pure DEG and went into deep coma.…”

Section: Discussionmentioning

confidence: 94%

Neurological Manifestation of Recreational Fatal and Near-Fatal Diethylene Glycol Poisonings

Imam¹,

Kamran²,

Karim³

et al. 2014

Medicine

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Diethylene glycol is a common industrial solvent which is responsible for accidental and epidemic poisoning as early as the 1930s. Due to the unavailability and unaffordability of ethanol, people in Qatar among the low income group are consuming household chemicals, some of which contain diethylene glycol, for recreational purposes.The history of ingestion is usually not volunteered and the initial clinical presentation is usually nonspecific, making it difficult to diagnose from the clinical presentation. Moreover, the biochemical profile varies with time, making the diagnosis more difficult. The neurological course and toxicity is less well characterized than its renal counterpart. Moreover, reports in the literature of such recreational poisoning is lacking particularly in the region.Three cases of recreational diethylene glycol poisoning seen in Hamad General Hospital, Doha, Qatar from 2009 to 2012 are detailed here.These illustrate the clinical course with emphasis on the neurological sequelae that include encephalopathy and multiple cranial and peripheral neuropathies with fatal and near-fatal outcomes. Neuroimaging in 2 were initially normal, but follow-up imaging showed brain atrophy. The third patient’s neuroimaging showed diffuse brain edema with evidence of transtentorial herniation. Nerve conduction studies were performed in 2 of the 3 cases and showed evidence of mixed sensorimotor neuropathy. The outcomes were death in 1 and severe neurological morbidity and disability in 2 cases.Diethylene glycol is a dangerous substance when ingested and can result in mortality and severe morbidity, particularly from the renal and neurological manifestations. Whereas the mechanism of damage is less well known, the damage is likely dose related. The typical clinical pattern of evolution of the poisoning in the absence of cost-effective ways to detect it in the serum can help clinicians in making the diagnosis.Neurological manifestations may include encephalopathy and multiple cranial and peripheral neuropathies with subsequent brain atrophy. Public awareness of the danger of such recreational use should be raised.

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“…The neurological manifestation was first reported by Wordley 16 in 1947 when he described 2 cases. One patient drank half a bottle of pure DEG and went into deep coma.…”

Section: Discussionmentioning

confidence: 94%

Neurological Manifestation of Recreational Fatal and Near-Fatal Diethylene Glycol Poisonings

Imam¹,

Kamran²,

Karim³

et al. 2014

Medicine

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“…Nephrotoxicity is measurable 4 to 8 days following the intraperitoneal administration of DEG in rats after a single dose of 5 mL (5.59 g) DEG/kg body weight (Kraul et al, 1991). A slight-to-moderate and reversible renal impairment is produced following a single oral dose of 8 g DEG/kg body weight (Freundt and Weis, 1989), and a lethal dose is approximately 20 g/kg body weight (Wordley, 1947). In this study, 4 mL (4.46 g) DEG/kg body weight produced typical signs of DEG-associated renal damage and killed less than 1/5 of the test rat.…”

Section: Discussionmentioning

confidence: 99%

Pre-existing liver cirrhosis reduced the toxic effect of diethylene glycol in a rat model due to the impaired hepatic alcohol dehydrogenase

Huang

Peng

et al. 2011

Toxicol Ind Health

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Hepatic metabolizing enzymes of diethylene glycol (DEG) are impaired in liver diseases. Thus, the purpose of this study was to increase our understandings in metabolism and toxicology of DEG by clarifying the influences of pre-existing liver disease. Forty Sprague-Dawley rats with carbon tetrachloride-induced liver cirrhosis and 20 control rats were intraperitoneally administered a single dose of DEG, and randomly killed 1, 2, 5 or 8 days following exposure. Compared with control rats, the model rats had significantly higher blood CO(2)-combining power, lower blood urine nitrogen, serum creatinine and alanine aminotransferase levels on the second day and a lower mortality rate on the eighth day following DEG exposure. Enlargements of liver and kidneys and degeneration and necrosis of hepatocytes and renal tubules in the model rats was also less serious than in the control rats. Urine DEG levels were significantly higher on the first day in the model rats than the control rats (46.65 ± 8.79 mg vs 18.88 ± 6.18 mg, p < 0.01), but DEG concentrations in the blood, liver and kidneys were lower. Hepatic alcohol dehydrogenase (ADH) activity in the model rats was significantly lower than that in the control rats, which was positively related to renal damage. The toxic effects of DEG in rats with pre-existing liver cirrhosis are significantly reduced, which may be due to the decreased hepatic ADH activity. It suggests that the metabolite of ADH is responsible for DEG poisoning, and this toxic metabolite may mainly originate in the liver.

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“…There is an accentuated clear (negative image) dilatation of the cytoplasm like ballooned or fatty degeneration in tubular cells. 27,31 Tubular lesions mainly occur in the proximal convoluted tubules and are restricted to the cortical regions of the kidney. 24 Toxic lesions of proximal tubules also manifest as cortical infarctions and/or necrosis, with vascular congestion, diffuse interstitial hemorrhage, and edema.…”

Section: Morphological Aspects Of Diethylene Glycol Kidney Toxicitymentioning

confidence: 99%

Renal toxicity caused by diethylene glycol: an overview

et al. 2023

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Diethylene glycol (DEG) is nephrotoxic, potentially resulting in high morbidity and mortality. Its main nephrotoxic by-product is diglycolic acid (DGA). This narrative overview summarizes selected literature with a focus on clinical ndings, pathophysiology, diagnosis including morphological features of renal biopsies, and management. The kidney injury in DEG poisoning is secondary to proximal tubular necrosis caused by DGA. Marked vacuolization and edema of epithelial cells obstruct the lumen, reducing urine ow and, consequently, resulting in anuria and uremia. The clinical alterations due to DEG poisoning are dose-dependent. Patients may present with gastrointestinal symptoms and anion gap metabolic acidosis, followed by renal failure, and, later, encephalopathy and neuropathy. Although this three-phase pattern has been described, signs and symptoms may be overlapping. Data about DEG intoxication is scarce. Sometimes the diagnosis is challenging. The management includes supportive care, gastric decontamination, correction of acid-base disorders, and hemodialysis. The understanding of the metabolic processes related to DEG poisoning may contribute to its management, preventing death, serious sequels, or irreversible lesions.

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Diethylene Glycol Poisoning: Report on Two Cases

Cited by 18 publications

References 3 publications

Neurological Manifestation of Recreational Fatal and Near-Fatal Diethylene Glycol Poisonings

Neurological Manifestation of Recreational Fatal and Near-Fatal Diethylene Glycol Poisonings

Pre-existing liver cirrhosis reduced the toxic effect of diethylene glycol in a rat model due to the impaired hepatic alcohol dehydrogenase

Renal toxicity caused by diethylene glycol: an overview

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