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• W2013185475 abstract "Ethylene glycol (EG) poisoning may lead to brain death and acute renal failure caused by metabolic acidosis and shock. We report on a 44-year-old female patient who died from EG overdose 8 days after intentional ingestion. Her liver, heart, and lungs were successfully transplanted. This case demonstrates that EG intoxication does not preclude liver transplantation if acceptable liver function and histology are preserved. EG can be ingested voluntarily by adults as a substitute for drinking ethanol or to commit suicide. Unintentional ingestion may occur in children. EG is a sweet-tasting nonvolatile liquid that is commonly used as an antifreeze, a coolant, or an industrial solvent. Following oral ingestion, EG is rapidly absorbed and metabolized in the liver to glycolaldehyde by alcohol dehydrogenase (ADH). The poisoned patient may progress through 3 stages.1 The first 12 hours after ingestion are characterized by central nervous depression (lethargy to coma). Secondly, after 12 to 24 hours, severe metabolic acidosis occurs with ensuing osmolal and anion gaps. After 24 to 72 hours, acute renal failure develops due to oxalic acid excretion and calcium oxalate nephrosis along with acidosis. Death results from cerebral edema and brain stem lesions or multiorgan failure, eventually.1 EG, ethylene glycol; ADH, alcohol dehydrogenase; GA, glycolic acid. A 44-year-old female was found comatose after drinking an undetermined amount of antifreeze agent containing ethylene glycol but not methanol. She was known to be addicted to alcoholism. She was intubated and transferred to a community hospital. Her stomach contents were removed by a nasogastric tube and irrigation. The same day she was admitted to the intensive care unit of this hospital. On arrival at the intensive care unit, arterial blood gas showed a pH of 6.8, base excess of −23, and a bicarbonate of 5.7 mmol/L. Serum sodium was 155 mmol/L, and calcium was 1.4 mmol/L. Plasma osmolality was 362 mOsm/Kg The anion gap and the calculated osmolality gap were increased to 49 mmol/L and 27 mOsm/Kg water, respectively. Blood tests showed a creatinine of 2.4 mg/dL and a serum lactate of 1.7 mmol/L. Ethanol content of blood was only 16 mg/dL on admission. Toxicologic investigation of blood and gastric contents taken the day after admission did not show EG. Massive excretion of calcium oxalate crystals was observed in the urine sediment, and the patient developed anuria. Fomepizole (4-methylpyrazole), a competitive inhibitor of ADH, was administered, starting with a loading dose of 15 mg/Kg and followed by doses of 10 mg/Kg every 12 hours. Sodium bicarbonate was given, and hemodialysis was immediately initiated to correct acidosis and to remove EG metabolites. Despite treatment, brain death was documented on day 8 after ingestion, and the relatives agreed to organ donation. The liver tests prior to procurement were aspartate aminotransferase of 59 U/L (peak, 59 U/L), alanine aminotransferase of 35 U/L (peak, 66 U/L), gamma-glutamyltransferase of 49 U/L, bilirubin of 0.13 mg/dL, and international normalized ratio of 0.9. Just before organ retrieval, mean arterial blood pressure was 115 mmHg without inotropic support. A liver biopsy of the donor liver taken during organ retrieval showed mild perivenous microvesicular steatosis (10% of hepatocytes) and scarce round cell infiltrates of periportal spaces. There were no crystal deposits. The liver was offered by Eurotransplant to several centers but rejected for medical reasons. Eventually, the liver was transplanted to a 32-year-old patient from the own center's waiting list who suffered from hemophilia A, hepatitis C–induced liver cirrhosis (model for end-stage liver disease score, 18) and human immunodeficiency virus (HIV) infection known for 18 years (pretransplant Centers for Disease Control stage A3). Cold ischemia time was 8.5 hours. The transplantation using Factor VIII concentrates was carried out without venovenous bypass with caval cross-clamping and vena cava replacement. Postoperative recovery was uneventful. Transaminases peaked on day 1 with an alanine aminotransferase of 375 U/L. On postoperative day 8, bilirubin was 0.8 mg/dL and the international normalized ratio was 1.0. Initial immunosuppression included cyclosporine A and prednisolone at standard dosages. Antiretroviral therapy was initiated at day 8, including abacavir, tenofovir, and zidovudine. The patient could be discharged with unremarkable liver function and in a good general condition on day 15. At 12 months' follow-up, the patient showed stable liver tests having been on immunosuppression with cyclosporine A (trough level, 75 ng/mL), including bilirubin of 1.2 mg/dL, international normalized ratio of 1.0 mg/dL, and mildly elevated transaminases of alanine aminotransferase at 60 U/L and aspartate aminotransferase at 72 U/L. His CD4 cell count was 220/μL and HIV RNA was <50 copies/mL under antiviral therapy with tenofovir, abacavir and zidovudine. There was a negative hepatitis C RNA polymerase chain reaction under therapy with interferon and ribavirin. The heart and both lungs were equally transplanted successfully with good primary function. Lethal EG poisoning occurs infrequently. However, exposure and major complications are quite common. In the 2003 annual report of the Toxic Exposure Surveillance System, 5,816 exposures to EG, mostly with antifreeze agents, were reported in the United States, resulting in 23 deaths and 257 near fatalities.2 In the 2002 annual report there were 6,077 exposures to EG, resulting in 40 deaths and 254 near fatalities. EG is rapidly absorbed from the gastrointestinal tract. Peak blood concentrations are 1 to 4 hours after ingestion. Eighty percent of EG is metabolized in the liver, and 20% is excreted unchanged by the kidneys. The elimination half-life of EG is approximately 3 hours.1, 3 The speed of metabolization in this alcoholic with induced ADH activity may explain why EG blood levels were already negative the day after ingestion. Following metabolization of EG to glycoaldehyde by ADH, further oxidization results in the formation of toxic acidic metabolites, in particular glycolic acid (GA). The accumulation of GA causes severe metabolic acidosis. While GA is transformed to various metabolites, the conversion to oxalate by the enzyme GA oxidase is most important. In humans, low plasma oxalate levels are observed after EG poisoning, since oxalate rapidly precipitates as calcium oxalate in the brain and kidneys.1, 5 The lethal dose of EG (density, 1.11g/L) is estimated to be 100 mL (1.4 mL/Kg or 1.6 g/Kg body weight) in adults. Toxic symptoms are not correlated to EG blood levels but rather to GA levels and acidosis, since EG is rapidly metabolized.4, 5 Therefore, a possible spreading of toxic amounts of EG or GA from the transplanted liver is unlikely when acidosis and osmolar and anion gaps have been corrected to a normal range. Donors with an interval of less than 2 days between ingestion and brain death showing persistent metabolic acidosis may carry a risk of transmitting toxic metabolites such as GA. Interestingly, the liver whole-organ EG content and tissue concentration in patients who died from EG poisoning were higher compared to the concentrations in the brain and kidneys. However, deposits of calcium oxalate crystals have not been observed in the human liver.3 It remains unclear why the liver is spared from calcium oxalate deposits and damage in contrast to the brain and kidneys even though the tissue concentrations of EG may be high. There is evidence of liver injury by EG from rat experiments.6 However, metabolic clearance and, therefore, toxicity is different in humans compared to rodents.7 Specific therapy aims to block EG metabolism by antidotes that inhibit ADH activity, such as high-dose ethanol or the more recently described fomepizole.1, 8 Symptomatic treatment consists of correction of acidosis and electrolyte imbalances and hemodialysis in renal failure.1, 3 To the best of our knowledge, this is the first report of a case transplanted with a liver from a donor who deceased from EG intoxication more than a week after ingestion. There is only 1 recent case report of successful liver transplantation from a donor who died from EG overdose 48 hours after intake.9 This report clearly indicates that a liver from a donor who died from ethylene glycol ingestion can be transplanted successfully if liver function tests and liver biopsy show acceptable results. Thus, in times of cadaveric donor shortage, a liver of an EG-poisoned brain-dead donor should not be rejected on principle. The authors thank Dr. H.P. Fischer (Institute of Pathology, Bonn University) and Dr. S. Eidt (Cologne) for help in discussing the liver biopsies, the Deutsche Stiftung Organtransplantation for providing data regarding the heart and lung recipients, and the Institute of Forensic Medicine of the University of Bonn for the EG determinations." @default.
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• W2013185475 title "Successful transplantation of a liver from a donor with fatal ethylene glycol poisoning" @default.
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