Chapter 43 Diethylene Glycol
SOURCES
DEG has physical properties similar to those of ethylene and propylene glycol. This solvent is a viscous liquid with a specific gravity of 1.118. It is colorless, nearly odorless, and palatable to children and small animals.1 It is used as an automotive break fluid, an industrial lubricant, a solvent, and in liquid Sterno. DEG is less toxic than ethylene glycol in most species, but more toxic than propylene glycol. It has occasionally been substituted for propylene glycol in pharmaceutical preparations, resulting in the deaths of more than 100 persons in some incidents.2–11 The most recent mass DEG poisoning occurred in India in 1998.12 Almost all (98%) affected children died in a 1996 epidemic in Haiti.13
TOXIC DOSE
The oral median lethal dose (LD50) for DEG in dogs, cats, and most laboratory animals is between 3.6 and 11.6 mL/kg. The lethal dose in children may be less than 1 mL/kg.13
TOXICOKINETICS
Accidental DEG toxicosis has been reported in humans.1–3, 6–8,10,14 Experimental toxicosis has been produced in laboratory animals, cats, dogs, and cattle.1,4,14–19 Toxicosis may result from one oral dose or from cumulative dosing.10,14,20 DEG is absorbed rapidly by the digestive tract. There is a report of DEG toxicosis resulting from topical exposure to damaged skin in burn patients.11 A proportion of a dose of DEG is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase.4,19,21 Most is excreted unchanged in the urine.1,8 Dogs eliminate DEG almost entirely within 36 hours.14 Like ethylene glycol, the kidney is the target organ of DEG, but severe oxalate nephrosis is not seen.3,9,16 The mechanism of DEG toxicosis is not well understood.4,9,16 Like other glycols and alcohols, DEG has a direct narcotic effect.8
CLINICAL SIGNS
Clinical signs of acute DEG poisoning are similar in most species.1,10 Animals may have signs of CNS depression soon after exposure.8,22 Dogs may vomit.10 The initial effects are usually minor unless a large amount has been ingested. When a relatively small amount has been ingested, the initial effects resolve, and the animal usually appears normal for 1 or more days. Anuric renal failure, which may occur several days after ingestion preceded by polyuria or oliguria, is the hallmark of DEG poisoning.13 Lumbar pain has been reported in humans.1,10,13 Vomiting caused by uremia is commonly seen.14 Intoxicated human beings and domestic animals frequently slip into a uremic coma before death.1–4,9,10,14 The author is familiar with one case of DEG poisoning that had an unusual presentation. The dog vomited, collapsed, had bloody diarrhea, and later had seizures. The major postmortem finding was a hemorrhagic syndrome.
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