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Paediatric clinical pharmacology
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
The harm caused by poisons, which must undergo metabolic processing to exert any toxic effect, can be modulated by preventing their metabolism. Treatment of ethylene glycol poisoning is based on inhibition of the enzyme alcohol dehydrogenase. Historically, treatment involved administering ethanol-utilising competitive inhibition of alcohol dehydrogenase to prevent significant metabolism of the ethylene glycol. Although elegant from a pharmacological perspective (Figure 3), ethanol can produce profound hypoglycaemia in young children and this antidote strategy was not without its risks. Fomepizole, a specific inhibitor of alcohol dehydrogenase, is now the treatment of choice (Figure 3).
Medical Child Abuse and Homicide
Published in David J. George, Poisons, 2017
Misdiagnosis of MCA could happen in circumstances in which there is a legitimate basis for considering this possibility. Errors can be made in good faith and concern for a child’s welfare stemming from limited information, incomplete investigation, unrecognized illness, or misunderstandings about caretaker motivation. Guidelines for minimizing the risk of misdiagnoses of MCA can be found in a number of authoritative medical reviews of factitious disorders. An often cited case of misdiagnosis of MCA involved the death of a child suffering from an unrecognized rare medical condition. A mother was accused of killing her child by poisoning with ethylene glycol. This mother was convicted and sent to prison. It was shown later that the child had died because of a rare genetic disorder known as methylmalonic acidemia. This condition produces symptoms similar to those seen with ethylene glycol poisoning.
Cardiology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Simultaneous heart and renal failure:1 HTN.2 DM.3 Generalised (coronary and renovascular) atherosclerosis.4 Vasculitides (PAN, etc).5 Thrombosis (antiphospholipid syndrome).6 Emboli (infective endocarditis).7 Fibrosis (systemic sclerosis; amyloidosis).8 Ethylene glycol poisoning.
Treating ethylene glycol poisoning with alcohol dehydrogenase inhibition, but without extracorporeal treatments: a systematic review
Published in Clinical Toxicology, 2022
Jessie Beaulieu, Darren M. Roberts, Sophie Gosselin, Robert S. Hoffman, Valery Lavergne, Knut Erik Hovda, Bruno Megarbane, Derrick Lung, Ruben Thanacoody, Marc Ghannoum
Subjects of all ages and comorbidities with a diagnosis of ethylene glycol poisoning, confirmed from history or detectable ethylene glycol in blood, treated with ethanol and/or fomepizole without extracorporeal treatment initially were included. All types of exposures (acute, staggered, chronic) and all routes of exposure (ingestion, injection, inhalation) were eligible for inclusion. Multiple temporally separate cases in the same patient were considered as distinct cases due to variation in the amount taken, time to presentation, and treatment given. Cases were also evaluated by type of ADH inhibitor (i.e., ethanol or fomepizole) received.
The serum glycolate concentration: its prognostic value and its correlation to surrogate markers in ethylene glycol exposures
Published in Clinical Toxicology, 2022
Darren M. Roberts, Robert S. Hoffman, Jeffrey Brent, Valéry Lavergne, Knut Erik Hovda, William H. Porter, Kenneth E. McMartin, Marc Ghannoum
Subjects of all ages and comorbidities with a diagnosis of ethylene glycol poisoning, confirmed from history or detectable ethylene glycol in blood, were included. All types of exposures (acute, staggered, chronic) and all routes of exposure (ingestion, injection, inhalation) were eligible for inclusion. Multiple temporally separate cases in the same patient were counted as distinct cases given that each varied with the amount taken, time to presentation, coingestion of alcohol, and treatment given.