Combined EthyleneGlycolPoisoning with Methemoglobinemia Due to Antifreeze Ingestion. Antifreeze poisoning is potentially life-threatening and often requires multiple antidotal therapies and hemodialysis. Ethylene or propylene glycol toxicity is commonly caused by antifreeze ingestion. However, ingestion of antifreeze is typically not associated with methemoglobinemia. Currently, only one other case of antifreeze ingestion causing combined ethyleneglycolpoisoning and methemoglobinemia has been reported. A 56-year-old man presented after a witnessed, intentional, large-volume antifreeze ingestion. Evaluation revealed dark brown blood and significantly elevated methemoglobin and ethylene glycol levels. He was successfully treated with methylene blue, fomepizole, and hemodialysis. No other
Stiripentol protects against calcium oxalate nephrolithiasis and ethyleneglycolpoisoning. Increased urinary oxalate excretion (hyperoxaluria) promotes the formation of calcium oxalate crystals. Monogenic diseases due to hepatic enzymes deficiency result in chronic hyperoxaluria, promoting end-stage renal disease in children and young adults. Ethyleneglycolpoisoning also results renal function. Patients affected by Dravet syndrome and treated with Stiripentol had a lower urine oxalate excretion than control patients. A young girl affected by severe type I hyperoxaluria received Stiripentol for several weeks: urine oxalate excretion decreased by two-thirds. Stiripentol is a promising potential therapy against genetic hyperoxaluria and ethyleneglycolpoisoning.
Recurrent EthyleneGlycolPoisoning with Elevated Lactate Levels to Obtain Opioid Medications. Malingering is when a patient feigns illness for secondary gain. While most patients with malingering manufacture or exaggerate symptoms, some patients may induce illness. Previous reports of malingering patients inducing illness include sepsis, kidney pain, migraine, and chest pain. However, acute
Rapid Diagnosis of EthyleneGlycolPoisoning by Urine Microscopy BACKGROUND Ethyleneglycolpoisoning remains an important presentation to Emergency Departments. Quick diagnosis and treatment are essential to prevent renal failure and life-threating complications. CASE REPORT In this case report, we present a patient who was admitted unconscious to the hospital. Ethyleneglycolpoisoning was immediately suspected, because the patient had previously been hospitalized with similar symptoms after intake of antifreeze coolant. A urine sample was sent for microscopy and showed multiple calcium oxalate monohydrate (COM) crystals, which supported the clinical suspicion of ethyleneglycolpoisoning. The patient was treated with continuous intravenous ethyl alcohol infusion and hemodialysis. Two days
Simplifying the hemodialysis prescription in patients with ethyleneglycolpoisoning. The management of ethyleneglycolpoisoning is multimodal and usually includes hemodialysis. The usual approach for guiding treatment duration is iterative, based on serial measurements of ethylene glycol concentration and routine biochemistry. In this issue, Iliuta et al. present a simplified approach
Prediction and validation of the duration of hemodialysis sessions for the treatment of acute ethyleneglycolpoisoning. The duration of hemodialysis (HD) sessions for the treatment of acute ethyleneglycolpoisoning is dependent on concentration, the operational parameters used during HD, and the presence and severity of metabolic acidosis. Ethylene glycol assays are not readily available , potentially leading to undue extension or premature termination of HD. We report a prediction model for the duration of high-efficiency HD sessions based retrospectively on a cohort study of 26 cases of acute ethyleneglycolpoisoning in 24 individuals treated by alcohol dehydrogenase competitive inhibitors, cofactors and HD. Two patients required HD for more than 14 days, and two died. In 19 cases
EthyleneGlycolPoisoning Should Not Contraindicate Liver Donation As the number of patients waiting to receive transplants increases, there is a need to explore all possible donation opportunities. In this case report, we describe the transplantation of a liver from a donor who died after ethyleneglycolpoisoning into a woman with alcoholic liver disease with cirrhosis and associated ascites
Serum Calcium Concentration in EthyleneGlycolPoisoning The diagnosis of ethylene glycol intoxication can be challenging. Definitive testing for ethylene glycol is not readily available and clinical decisions are often based on clinical suspicion and the results of more readily available tests. One of these findings is hypocalcemia, presumable through complexation with the ethylene glycol dichotomized by pH ≥ or <7.3. We did observe an inverse relationship between serum calcium and bicarbonate. Hypocalcemia is not commonly observed following ethyleneglycolpoisoning, even in acidotic patients.
EthyleneGlycolPoisoning: An Unusual Cause of Altered Mental Status and the Lessons Learned from Management of the Disease in the Acute Setting Ethylene glycol is found in many household products and is a common toxic ingestion. Acute ingestions present with altered sensorium and an osmolal gap. The true toxicity of ethylene glycol is mediated by its metabolites, which are responsible
EthyleneGlycolPoisoningEthyleneGlycolPoisoning * Versions * Standard Desktop * Legacy Desktop * Mobile Web * Iphone/Ipad App * * Help Toggle navigation * * Home * Books: A to N * Cardiovascular Medicine * Dentistry * Dermatology * Emergency Medicine * Endocrinology * Gastroenterology * Geriatric Medicine to Palliative Care * * Administration * Patient Satisfaction * Documentation 4 * * advertisement * Home * Emergency Medicine Book * Poisoning and Toxicology Chapter * EthyleneGlycolPoisoningEthyleneGlycolPoisoning Aka: EthyleneGlycolPoisoning, Ingestion of Ethylene Glycol, Ethylene Glycol Antifreeze Ingestion, Ethylene Glycol
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Massive EthyleneGlycolPoisoning Triggers Osmotic Demyelination Syndrome. Ethylene glycol is a toxic organic solvent implicated in thousands of accidental and intentional poisonings each year. Osmotic demyelination syndrome (ODS) is traditionally known as a complication of the rapid correction of hyponatremia. Our aim was to describe how patients with ethylene glycol toxicity may be at risk . The patient was treated for ethyleneglycolpoisoning with fomepizole and hemodialysis. Despite having elevated serum sodium levels, the patient's hospital course was complicated by ODS. Rapid changes in serum osmolality from ethylene glycol toxicity or its subsequent treatment can cause ODS independent of serum sodium levels.
in pregnancy, treatment should be as for the non-pregnant patient and should not be withheld on account of pregnancy. There are very limited data available concerning the use of the antidotes fomepizole and ethanol in pregnancy. However, when indicated, the maternal and fetal benefits of antidote treatment will outweigh the risks associated with untreated ethyleneglycolpoisoning. If treatment
be managed similarly to ethyleneglycolpoisoning with fomepizole and early hemodialysis.Rosen’s In Perspective: Today we’ll discuss the two and one so-so toxic alcohol: focusing on methanol, ethylene glycol (EG), and isopropyl alcohol (isopropanol). For an awesome primer, check out FOAMCAST & CORE-EM. Please see Rosen’s Fig. 141.1 for the metabolism of alcohols in the body.In the end, this chapter is all Rosen’s Box 141.2 for criteria for initiation of ADH blockade for methanol or ethyleneglycolpoisoning[13] List indications for dialysis in toxic alcohol poisoning. * acidosis (pH < 7.3) * renal failure * vision abnormalities with methanol exposure * electrolyte imbalances unresponsive to conventional therapy (ie, hyperkalemia) * hemodynamic instability * methanol or EG concentration more than 50 md
Stiripentol identifies a therapeutic target to reduce oxaluria. Oxalate is a metabolic end-product promoting the formation of calcium oxalate crystals in urine. Massive urine oxalate excretion occurs in genetic diseases, mainly primary hyperoxaluria type I and II, threatening renal function. Ethyleneglycolpoisoning may induce the precipitation of calcium oxalate crystals in renal tubules
volumes.Provoked hyperoxaluria: excessive vitamin C intake, oxalate or ethyleneglycolpoisoning, inhalational anaesthetic reactions, urinary tract glycine irrigation, aspergillus infection, pyridoxine deficiency.EpidemiologyOverall, hyperoxaluria appears to be more of a problem in developed countries. Urolithiasis is undoubtedly common in the UK, although exact figures are hard to come by. Oxalate stones