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Ethylene glycol poisoning of incidental or suicidal intention can cause life-threatening metabolic acidosis, diverse secondary damage, and even lead to death. Beside hemodialysis effective therapy consists of the administration of fomepizole and ethanol. We describe a patient after repeated ethylene glycol poisoning with high anion gap metabolic acidosis and acute renal failure. Using hemodialysis, with dialysate containing a specific amount of ethanol, and intravenous ethanol administration we were able to prevent severe secondary organ damage.

A Sweet Drink with Consequences Abstract. Intoxications with ethylene glycol are rare, however, small quantities from the substance can be life-threatening. Regarding the treatment it is important to recognize the intoxication quickly and to immediately start the appropriate treatment. Intoxications with ethylene glycol or with methanol should always be considered as differential diagnosis in patients with severe metabolic acidosis. It is also very important to calculate the osmolal gap.

CME: Ethylene Glycol Intoxication Abstract. Ethylene glycol is a sweet-tasting alcohol used in common antifreeze and other industrial solutions. Without appropriate therapy, intoxication with ethylene glycol can result in severe metabolic acidosis, acute renal failure, and in death. After gastrointestinal resorption, hepatic metabolism starts with oxidation by alcohol dehydrogenase and results in severe anion gap metabolic acidosis. Other metabolic products are calcium oxalate crystals, which can deposit in several tissues like the kidneys and lead to acute tubular necrosis with reversible renal failure. The crucial therapeutic step is rapid inhibition of alcohol dehydrogenase with fomepizole or ethanol to avoid the formation of toxic metabolites. Additionally, haemodialysis is the most effective way to eliminate ethylene glycol as well as its toxic metabolites. If therapy is initiated rapidly, prognosis is favorable.

A 42-year-old man evidently had died from an intoxication. On the basis of the findings at scene it was primarily assumed that the man had ingested a larger quantity of an ethylene glycol-containing antifreeze for suicidal purposes. The man was said to have had an alcohol problem and did not only consume drinking alcohol, but also other alcoholic liquids. At autopsy, a bluish liquid with an aromatic smell was found in the oesophagus and stomach. However, toxicological analyses did not furnish evidence of ethylene glycol--as expected--but a potentially fatal concentration of ethanol (blood alcohol concentration 4.01 per mille). The blue colour (patent blue C.I.42051) came from a liquid used in the wind-screen washer system in winter, which now contains ethanol (denatured with 2-butanone) instead of ethylene glycol. The results of the toxicological findings including the analysis of congener alcohols and the differential diagnostics of blue-coloured stomach contents are discussed.

Ethylene glycol is an alcohol, which is mainly used as antifreeze. Intoxication with ethylene glycol can cause neurological and cardiopulmonary symptoms, metabolic acidosis and acute renal failure. Therapeutic options include reversal of metabolic acidosis, inhibition of alcohol dehydrogenase and early hemodialysis. In survivors of the acute phase, lasting damage is rare. The case of a 49-year-old patient with ethylene glycol intoxication is reported which was characterized by progressive impairment of consciousness, tetraparesis, hyperventilation and metabolic acidosis.

We report on a patient after brain injury additionally showing signs of ethylene glycol intoxication. CT-scan showed a subdural hematoma, which in spite of increasing neurological deficit didn't show any enlargement. Metabolic acidosis with an increased anion gap and osmolar gap led to the diagnosis of ethylene glycol intoxication. Then intensive hemodialysis and i.v. ethanol were administered and the intoxication could be treated successfully.

A 36-year-old man known as chronic alcohol abuser presently suffered from arthralgia and showed bilateral petriefied kidneys by sonography and computed tomography. Because of an unclear renal failure a kidney biopsy was performed and presented typical chronic renal oxalosis with massive oxalate crystal deposits, tubular atrophy and interstitital fibrosis. Since the man had never shown signs of hyperoxaluria in his life before, a secondary oxalosis was supposed. The subsequently prompted exploration established a three to four times abuse of rocket fuel with cola lemonade 12 years before during the patient's army time as a marine soldier. Such fuels contain ethylene glycol (glysantin) as antifreeze commonly known to cause in toxic doses acute renal tubular necrosis with hyperoxaluria. The presented case, however, suggests a rare sublethal ethylene glycol poisoning with initial renal tubular damage, oxalate crystal deposition and subsequent chronic interstitial oxalate nephritis with tubular atrophy, interstitial fibrosis and chronic renal failure. Undergoing chronic hemodialysis, the patient died 5 months after the kidney biopsy diagnosis by acute heart failure. At autopsy, progressed chronic renal oxalosis could be confirmed. Decompensated oxalate cardiomyopathy with disseminated myocardial oxalate crystal deposits caused acute heart failure promoted by myocardial hypertrophy in renal hypertension.