Related Experiment Video
Updated: Jul 2, 2026
07:45
Estimation of Urinary Nanocrystals in Humans using Calcium Fluorophore Labeling and Nanoparticle Tracking Analysis
Published on: February 9, 2021
Hyperoxaluria after ethylene glycol poisoning.
Ludwig Stapenhorst1, Albrecht Hesse, Bernd Hoppe
1Department of Pediatrics, University Children's Hospital, 50924, Cologne, Germany. Ludwig.stapenhorst@web.de
Pediatric Nephrology (Berlin, Germany)
|August 13, 2008
Summary
Ethylene glycol poisoning requires rapid treatment with alcohol dehydrogenase inhibitors and hemodialysis. Despite treatment, elevated oxalate levels persisted, risking crystal deposition, highlighting the complexity of managing severe poisoning.
Area of Science:
- Toxicology
- Nephrology
- Emergency Medicine
Background:
- Ethylene glycol poisoning is a life-threatening condition requiring prompt medical intervention.
- Effective treatment involves alcohol dehydrogenase inhibitors and hemodialysis to clear the toxin and its metabolites.
- Preventing calcium-oxalate deposition is crucial for mitigating organ damage.
Observation:
- A 12-year-old girl ingested a massive dose of ethylene glycol, presenting with a high serum concentration.
- Treatment with ethanol and hemodialysis successfully reduced ethylene glycol levels.
- Despite treatment, plasma and urinary oxalate levels significantly increased, indicating ongoing metabolite formation and risk of crystal deposition.
Findings:
- The patient developed severe hyperoxaluria and elevated plasma oxalate levels post-treatment.
- Alkaline citrate administration, intended to increase oxalate solubility, did not prevent nephrocalcinosis.
- Nephrocalcinosis developed despite the absence of metabolic acidosis, hypocalcemia, or neurological symptoms.
Implications:
- This case underscores the persistent risk of calcium-oxalate crystal deposition even after successful ethylene glycol clearance.
- Management strategies for severe ethylene glycol poisoning may need to address prolonged hyperoxaluria.
- Further research into optimizing preventive measures against oxalate nephropathy in poisoning cases is warranted.
Related Concept Videos
01:26Anticholinesterase Agents: Poisoning and Treatment
Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...
01:14Prevention of Further Absorption of Poison
In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
01:26Enhanced Elimination of Poison
Poison can be effectively removed from the gastrointestinal (GI) tract through various decontamination procedures.
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
01:30Toxidromes: Clinical Features
Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...
01:26Pharmaceutical Poisoning: Treatment Strategies
Treatment strategies for poisoning are a critical aspect of emergency medicine, focusing on preventing the absorption of toxins and enhancing their elimination. When a poisoning incident occurs, the first response is to halt exposure and decontaminate the patient, particularly through gastrointestinal (GI) methods if the poison was ingested.Gastrointestinal Decontamination Techniques:Activated charcoal is the cornerstone of GI decontamination. It works through adsorption, binding the toxin to...