scholarly journals Anion gap‐opening metabolic acidosis and urinary findings in the early diagnosis of ethylene glycol poisoning: A case report

2022 ◽  
Vol 10 (1) ◽  
Author(s):  
Kentaro Ukita ◽  
Kanako Otomune ◽  
Ryo Fujimoto ◽  
Kanako Hasegawa ◽  
Koichi Izumikawa ◽  
...  
Keyword(s):  
Case Report ◽  
Metabolic Acidosis ◽  
Early Diagnosis ◽  
Ethylene Glycol ◽  
Anion Gap ◽  
Ethylene Glycol Poisoning ◽  
Gap Opening

scholarly journals CORRECTION OF ACID BASE DISORDERS IN RATS WITH ACUTE ETHYLENGLYCOL POISONING

2020 ◽  
Author(s):  
Konstantin Vladimirovich Sivak ◽  
Mikhail Mikhailovich Lyubishin ◽  
Elena Yur’evna Kalinina
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Sodium Bicarbonate ◽  
Creatinine Clearance ◽  
Acute Poisoning ◽  
Anion Gap ◽  
Toxic Encephalopathy ◽  
Experimental Therapy ◽  
Acid Base ◽  
Ethylene Glycol Poisoning

T The aim of the article. The aim of this study was to evaluation of the effectiveness of standard antidote therapy and dimephosphon administration in rats with acute ethylene glycol poisoning. The tasks of the study included modeling acute ethylene glycol poisoning in rats, conducting experimental therapy with ethanol antidote in combination with sodium bicarbonate and dimephosphon therapy, comparing the effectiveness of drugs in relation to indicators of acid-base state impairment and renal function. Materials and methods. Ethylene glycol (EG) was administered per os to Wistar male rats (190-210 g b.w.) at a single dose of 6 mL / kg b.w. through an atraumatic gastric tube. The animals were divided into 4 groups of 6 individuals each: intact (negative control), EG poisoning (positive control), EG + standard antidote therapy, EG + dimephosphon therapy. Experimental therapy was carried out for first 24 hours using standard antidote therapy: ethanol (30% solution 2 mL / kg b.w. i.p. after 1, 4, 6, 12, 18 hours) and sodium bicarbonate (4% solution 6 mL / kg b.w. i.p. 3 times on the first day), as well as administration of dimephosphon (150 mg / kg i.p. 3 times on the first day, 450 mg / kg b.w. per day). Daily urine on day 3 after poisoning was collected in metabolic cages. Creatinine concentration in urine and blood serum samples were measured, and creatinine clearance was calculated. After 24 hours of therapy, the pH, level of sodium, potassium, calcium, magnesium, chlorides, bicarbonates, lactate, d-3-hydroxybutyrate, albumin, urea and creatinine (measured parameters) were determined in venous blood samples. Anion gap, ∆рН, ∆AG, ∆HCO3, ∆AG/∆HCO3 and ∆Gap were calculated. The mechanism of death was determined for the dead animals. Data processing was performed using GraphPad Prism 6.0. Results. Acute poisoning of rats with ethylene glycol leads to the development of toxic encephalopathy and nephropathy, acid-base abnormalities, high anion gap metabolic acidosis due to the presence of metabolites, as well as lactate-ketoacidosis due to depression of the central nervous system and hunger. 100% of the EG-treated (12 mL / kg b.w.) animals died within 3 days. Metabolic acidosis in combination with hypermagnesemia had provided a cardiodepressive effect, which with direct nephrotoxic and neurotoxic effects contributed to the development of a mixed variant of thanatogenesis and death. Death comes from toxic encephalopathy and nephropathy, high anion gap metabolic acidosis caused by direct nephrotoxic and neurotoxic effects of EG and its metabolites. The standard antidote therapy with ethanol in combination with sodium bicarbonate prevented a pH shift, lactic acidosis and ketoacidosis, an increase in urea, but did not affect the level of bicarbonate (p=0.048), creatinine and its clearance (p=0.037) and the anion gap (p=0.033). The dimephosphon therapy prevented a decrease in creatinine clearance and blood bicarbonate level, limited the increase in lactate dehydrogenase activity, had a more pronounced effect on the AG and ∆AG (p=0.042), but did not affect the hypocalcemia (p=0.0076) and hypoalbuminemia (p=0.021). Conclusion. Acute ethylene glycol poisoning leads to the development of a mixed variant of thanatogenesis with damage to the central nervous and urinary systems, as well as the heart. Autopsy and histopathology confirmed the cause of animal death. In the model at a dose of 6 mL / kg of EG the dimephosphon therapy was more conducive to the correction of the main markers of high anion gap metabolic acidosis (HAGMA) than standard antidote therapy (both measured and calculated, p0.05). The dimephosphon therapy prevented a decrease in creatinine clearance. A comparative analysis of two methods for the correction of high anion gap metabolic acidosis in rats in acute poisoning with ethylene glycol showed that dimephosphon therapy vs. standard antidote therapy had a stronger effect on markers of metabolic acidosis and renal impairment.

scholarly journals Acidosis and coma after hemodialysis.

1997 ◽  
Vol 8 (5) ◽  
pp. 853-856
Author(s):  
R Taylor ◽  
J Bower ◽  
M M Salem
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Suicide Attempts ◽  
Altered Mental Status ◽  
Anion Gap ◽  
Toxic Metabolites ◽  
Ethylene Glycol Poisoning ◽  
Rapid Clearance ◽  
Dialysate Solution ◽  
Osmolal Gap

Ethylene glycol poisoning is a rare yet potentially fatal illness seen most commonly in association with ingestion by alcoholics or in suicide attempts. It is characterized by an elevated anion gap metabolic acidosis, osmolal gap, calcium oxalate crystals in the urine, and a well-defined clinical picture. Prompt treatment is crucial because effective intervention can prevent the neurologic, cardiac, pulmonary, and renal sequelae associated with ethylene glycol poisoning. Hemodialysis offers rapid clearance of ethylene glycol and its toxic metabolites. In this article, the case of a hemodialysis patient who suffered contamination of the dialysate solution with ethylene glycol, leading to altered mental status, coma, and severe anion gap metabolic acidosis, is reported. Despite prolonged dialysis and correction of the acidosis, the patient remained comatose and subsequently died.

Value of glycolic acid analysis in ethylene glycol poisoning: A clinical case report and systematic review of the literature

2018 ◽  
Vol 290 ◽  
pp. e9-e14 ◽  
Author(s):  
Gaspar Tuero ◽  
Jesús González ◽  
Laura Sahuquillo ◽  
Anna Freixa ◽  
Isabel Gomila ◽  
...  
Keyword(s):  
Systematic Review ◽  
Case Report ◽  
Ethylene Glycol ◽  
Glycolic Acid ◽  
Clinical Case ◽  
Review Of The Literature ◽  
Ethylene Glycol Poisoning

scholarly journals Profound metabolic acidosis from pyroglutamic acidemia: an underappreciated cause of high anion gap metabolic acidosis

CJEM ◽  
2010 ◽  
Vol 12 (05) ◽  
pp. 449-452 ◽  
Author(s):  
Thomas J. Green ◽  
Jan Jaap Bijlsma ◽  
David D. Sweet
Keyword(s):  
Emergency Department ◽  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Inborn Errors Of Metabolism ◽  
Pyroglutamic Acid ◽  
Anion Gap ◽  
Emergency Patient ◽  
Inborn Errors ◽  
Chronic Ingestion

ABSTRACTThe workup of the emergency patient with a raised anion gap metabolic acidosis includes assessment of the components of “MUDPILES” (methanol; uremia; diabetic ketoacidosis; paraldehyde; isoniazid, iron or inborn errors of metabolism; lactic acid; ethylene glycol; salicylates). This approach is usually sufficient for the majority of cases in the emergency department; however, there are many other etiologies not addressed in this mnemonic. Organic acids including 5-oxoproline (pyroglutamic acid) are rare but important causes of anion gap metabolic acidosis. We present the case of a patient with profound metabolic acidosis with raised anion gap, due to pyroglutamic acid in the setting of malnutrition and chronic ingestion of acetaminophen.

A Case of Uremic Pericarditis and Cardiac Tamponade That Developed after Ethylene Glycol Poisoning - A Case Report -

2010 ◽  
Vol 25 (3) ◽  
pp. 176 ◽  
Author(s):  
Ki Ju Kim ◽  
Jung Gil Park ◽  
Han Jun Ryu ◽  
Yeoun Su Jung ◽  
Sung-Ho Kim ◽  
...  
Keyword(s):  
Case Report ◽  
Ethylene Glycol ◽  
Cardiac Tamponade ◽  
Ethylene Glycol Poisoning
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