Abstract:DEG ingestion can lead to serious complications that may prove fatal. Prognosis may be improved, however, with prompt supportive care and timely use of fomepizole or ethanol.
“…Historical data on median or average doses associated with toxicity or lethality from past medication-associated, DEG mass poisonings are limited. Following are the available data: USA (1937), 1.0 ml DEG/ kg or approximately 1,118 mg/kg [1,11]; Argentina (1992), 14-174 mg DEG/kg [1,[12][13][14]; Haiti (1995), 1.34 ml DEG/kg or approximately 1,500 mg/kg [3]; Panama (2006), 310 mg/kg (Nestor Sosa, MD, unpublished data, 2009). In comparison, the more conservative toxic minimum value (14 mg/kg) of these four mass poisoning events (Argentina, 1992) was more than 150 times higher than the highest daily dose estimated in our study (0.09 mg/kg).…”
Section: Estimated Deg Doses Compared With Toxic Doses Reported In Thmentioning
confidence: 99%
“…Supplement Background Diethylene glycol (DEG) is used in antifreeze, brake fluids, cosmetics, lubricants, and other commercially available products. It causes renal insufficiency and failure, peripheral neuropathy, encephalopathy, coma, and death [1]. At least ten DEG mass poisonings have occurred over the past 70 years.…”
Diethylene glycol (DEG), a chemical that has been implicated in multiple medication-associated mass poisonings, can result in renal and neurological toxicity if ingested. Three previous such mass poisonings implicated Chinese manufacturers as the origin of contaminated ingredients. No literature exists on potential DEG or triethylene glycol (TEG), a related compound, contamination of health products imported from Asian countries to the USA. Our primary objective was to quantitatively assess the amount of DEG present in a convenience sampling of these health products. The study's secondary objectives were to: (1) evaluate for, and quantify TEG levels in these samples; (2) compare DEG and TEG levels in these products directly to levels in medications implicated in previous similar mass poisonings; and (3) to estimate DEG dose (in mg/kg) based on the manufacturer's instructions and compare these values to toxic doses from past mass poisonings and the literature. A quantitative assessment of DEG and TEG was performed in a convenience sampling of over-the-counter health products imported from Asian countries. Results were converted to volume to volume (v/v) % and compared with DEG levels in medications implicated in previous mass poisonings. Estimated doses (based on the manufacturer's instructions) of each product with detectable levels of DEG for a 70 kg adult were compared to toxic doses of DEG reported in the literature. Seventeen of 85 (20%) samples were not able to be analyzed for DEG or TEG due to technical reasons. Fifteen of 68 (22%) samples successfully tested had detectable levels of DEG (mean, 18.8 μg/ml; range, 0.791-110.1 μg/ml; and volume to volume (v/v) range, 0.00007-0.01%). Two of 68 (3%) samples had TEG levels of 12.8 and 20.2 μg/ml or 0.0012% and 0.0018% TEG v/v. The product with the highest DEG% by v/v was 810 times less than the product involved in the Panama DEG mass poisoning (8.1%). The lowest reported toxic dose from a past DEG mass poisoning (14 mg/kg) was more than 150 times higher than the highest daily dose estimated in our study (0.09 mg/kg). Sixty-eight of 85 (80%) samples were able to be successfully analyzed for DEG and TEG. DEG and TEG were detectable in 15/68 (22%) and 2/68 (3%) samples, respectively. Based on current standards, these levels probably do not represent an acute public health threat. Additional research focusing on why DEG is found in these products and on the minimum amount of DEG needed to result in toxicity is needed.
“…Historical data on median or average doses associated with toxicity or lethality from past medication-associated, DEG mass poisonings are limited. Following are the available data: USA (1937), 1.0 ml DEG/ kg or approximately 1,118 mg/kg [1,11]; Argentina (1992), 14-174 mg DEG/kg [1,[12][13][14]; Haiti (1995), 1.34 ml DEG/kg or approximately 1,500 mg/kg [3]; Panama (2006), 310 mg/kg (Nestor Sosa, MD, unpublished data, 2009). In comparison, the more conservative toxic minimum value (14 mg/kg) of these four mass poisoning events (Argentina, 1992) was more than 150 times higher than the highest daily dose estimated in our study (0.09 mg/kg).…”
Section: Estimated Deg Doses Compared With Toxic Doses Reported In Thmentioning
confidence: 99%
“…Supplement Background Diethylene glycol (DEG) is used in antifreeze, brake fluids, cosmetics, lubricants, and other commercially available products. It causes renal insufficiency and failure, peripheral neuropathy, encephalopathy, coma, and death [1]. At least ten DEG mass poisonings have occurred over the past 70 years.…”
Diethylene glycol (DEG), a chemical that has been implicated in multiple medication-associated mass poisonings, can result in renal and neurological toxicity if ingested. Three previous such mass poisonings implicated Chinese manufacturers as the origin of contaminated ingredients. No literature exists on potential DEG or triethylene glycol (TEG), a related compound, contamination of health products imported from Asian countries to the USA. Our primary objective was to quantitatively assess the amount of DEG present in a convenience sampling of these health products. The study's secondary objectives were to: (1) evaluate for, and quantify TEG levels in these samples; (2) compare DEG and TEG levels in these products directly to levels in medications implicated in previous similar mass poisonings; and (3) to estimate DEG dose (in mg/kg) based on the manufacturer's instructions and compare these values to toxic doses from past mass poisonings and the literature. A quantitative assessment of DEG and TEG was performed in a convenience sampling of over-the-counter health products imported from Asian countries. Results were converted to volume to volume (v/v) % and compared with DEG levels in medications implicated in previous mass poisonings. Estimated doses (based on the manufacturer's instructions) of each product with detectable levels of DEG for a 70 kg adult were compared to toxic doses of DEG reported in the literature. Seventeen of 85 (20%) samples were not able to be analyzed for DEG or TEG due to technical reasons. Fifteen of 68 (22%) samples successfully tested had detectable levels of DEG (mean, 18.8 μg/ml; range, 0.791-110.1 μg/ml; and volume to volume (v/v) range, 0.00007-0.01%). Two of 68 (3%) samples had TEG levels of 12.8 and 20.2 μg/ml or 0.0012% and 0.0018% TEG v/v. The product with the highest DEG% by v/v was 810 times less than the product involved in the Panama DEG mass poisoning (8.1%). The lowest reported toxic dose from a past DEG mass poisoning (14 mg/kg) was more than 150 times higher than the highest daily dose estimated in our study (0.09 mg/kg). Sixty-eight of 85 (80%) samples were able to be successfully analyzed for DEG and TEG. DEG and TEG were detectable in 15/68 (22%) and 2/68 (3%) samples, respectively. Based on current standards, these levels probably do not represent an acute public health threat. Additional research focusing on why DEG is found in these products and on the minimum amount of DEG needed to result in toxicity is needed.
“…Diethylene glycol (DEG) is found in several products including brake fluid, fog machine fluid, and cooking fuel and has been implicated in several mass poisonings throughout history [21,22]. Ingestion of DEG results in the characteristic development of intoxication with an associated AGMA and gastrointestinal irritation, followed by a worsening metabolic acidosis with renal and hepatotoxicity [21].…”
Section: Case Continuedmentioning
confidence: 99%
“…Ingestion of DEG results in the characteristic development of intoxication with an associated AGMA and gastrointestinal irritation, followed by a worsening metabolic acidosis with renal and hepatotoxicity [21]. Patients who survive initial toxicity may develop peripheral neuropathies, particularly of cranial nerve VII [21]. The exact cause of the metabolic acidosis and end-organ toxicity associated with DEG is unclear, but may be the result of accumulation of the DEG metabolites 2-hydroxyethoxyacetic acid and diglycolic acid [21][22][23].…”
Section: Case Continuedmentioning
confidence: 99%
“…Patients who survive initial toxicity may develop peripheral neuropathies, particularly of cranial nerve VII [21]. The exact cause of the metabolic acidosis and end-organ toxicity associated with DEG is unclear, but may be the result of accumulation of the DEG metabolites 2-hydroxyethoxyacetic acid and diglycolic acid [21][22][23]. Triethylene glycol (TEG) may also be found in brake fluid, though ingestions are rare.…”
A 17-year-old female was brought into the emergency department (ED) by ambulance after being found unresponsive by her parents at home. She was last seen normal 4 hours previously, and a text message sent to her boyfriend indicated her intention to overdose on ondansetron and loratadine. Upon arrival of emergency medical services, she was administered naloxone without effect, and supportive measures including bag valve mask ventilation were initiated. En route to the ED, she had a witnessed generalized tonic-clonic seizure, and she was treated with midazolam.In the ED, the patient's vital signs were BP 125/53 mmHg, HR 130/min, RR 18/min, and temperature 33.9°C (rectal). Her physical exam was notable only for a Glasgow Coma Scale (GCS) of 3 without a gag reflex. Her pupil size was not commented upon, and she was immediately intubated for airway protection.
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