Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication

2003 ◽  
Vol 60 (09) ◽  
pp. 205-210 ◽  
Author(s):  
S. Moossavi ◽  
N.K. Wadhwa ◽  
E.P. Nord
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Anion Gap ◽  
Ethylene Glycol Intoxication

Ethylene glycol intoxication presenting with high anion gap metabolic acidosis, acute kidney injury and elevated lactate

2018 ◽  
Vol 60 (2) ◽  
pp. 194-195 ◽  
Author(s):  
Thomas Giner ◽  
Violeta Ojinaga ◽  
Nikolaus Neu ◽  
Miriam Koessler ◽  
Gerard Cortina
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Kidney Injury ◽  
Anion Gap ◽  
Ethylene Glycol Intoxication ◽  
Elevated Lactate

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 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.

Ethylene Glycol Intoxication Presenting as a Metabolic Acidosis Associated with a Motor Vehicle Crash

1998 ◽  
Vol 45 (4) ◽  
pp. 811-813 ◽  
Author(s):  
Joseph F. Buell ◽  
Robert Sterling ◽  
Srinivas Mandava ◽  
Adam C. Berger ◽  
Louis M. Paulilio ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Motor Vehicle ◽  
Motor Vehicle Crash ◽  
Vehicle Crash ◽  
Ethylene Glycol Intoxication

Ethylene glycol induces hyperoxaluria without metabolic acidosis in rats

2005 ◽  
Vol 289 (3) ◽  
pp. F536-F543 ◽  
Author(s):  
Mike L. Green ◽  
Marguerite Hatch ◽  
Robert W. Freel
Keyword(s):  
Drinking Water ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Ammonium Phosphate ◽  
Anion Gap ◽  
Urinary Ph ◽  
Plasma Bicarbonate ◽  
Titratable Acid ◽  
Arterial Ph ◽  
Lower Urinary

Ethylene glycol (EG) consumption is commonly employed as an experimental regimen to induce hyperoxaluria in animal models of calcium oxalate nephrolithiasis. This approach has, however, been criticized because EG overdose induces metabolic acidosis in humans. We tested the hypothesis that EG consumption (0.75% in drinking water for 4 wk) induces metabolic acidosis by comparing arterial blood gases, serum electrolytes, and urinary chemistries in five groups of Sprague-Dawley rats: normal controls (CON), those made hyperoxaluric (HYP) with EG administration, unilaterally nephrectomized controls (UNI), unilaterally nephrectomized rats fed EG (HRF), and a metabolic acidosis (MA) reference group imbibing sweetened drinking water (5% sucrose) containing 0.28 M NH4Cl. Arterial pH, plasma bicarbonate concentrations, anion gap, urinary pH, and the excretion of titratable acid, ammonium, phosphate, citrate, and calcium in HYP rats were not significantly different from CON rats, indicating that metabolic acidosis did not develop in HYP rats with two kidneys. Unilateral nephrectomy alone (UNI group) did not significantly affect arterial pH, plasma bicarbonate, anion gap, or urinary pH compared with CON rats; however, HRF rats exhibited some signs of a nascent acidosis in having an elevated anion gap, higher phosphate excretion, lower urinary pH, and an increase in titratable acid. Frank metabolic acidosis was observed in the MA rats: decreased arterial pH and plasma HCO3−concentration with lower urinary pH and citrate excretion with elevated excretion of ammonium, phosphate and, hence, titratable acid. We conclude that metabolic acidosis does not develop in conventional EG treatments but may ensue with renal insufficiency resulting from an oxalate load.

scholarly journals Ethylene Glycol Toxicity Presenting with Non-Anion Gap Metabolic Acidosis

2009 ◽  
Vol 104 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Sari Soghoian ◽  
Richard Sinert ◽  
Sage W. Wiener ◽  
Robert S. Hoffman
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Anion Gap

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.

Ethylene Glycol Intoxication

1992 ◽  
Vol 7 (5) ◽  
pp. 234-243 ◽  
Author(s):  
James A. Kruse
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Specific Treatment ◽  
Severe Metabolic Acidosis ◽  
Presumptive Diagnosis ◽  
Cardiorespiratory Failure ◽  
Toxic Metabolites ◽  
Ethylene Glycol Intoxication

Commonly available as automotive antifreeze, ethylene glycol can cause toxicity and death if ingested. It is metabolized to several aldehyde and acid intermediates that can cause severe metabolic acidosis, central nervous system derangements, cardiorespiratory failure, and acute renal failure. A presumptive diagnosis can often be made by assessment of the anion gap and the osmol gap and the finding of metabolic acidosis. Corroborating findings include oxalate crystalluria and urine that fluoresces on exposure to ultraviolet light. Recognition is important because there are specific treatment methods available. Therapy consists of administering sodium bicarbonate to counter the acidosis, ethanol to slow the generation of toxic metabolites, and vitamin cofactors, which may speed detoxification of these intermediates. Hemodialysis is employed to remove both ethylene glycol and its metabolites, to correct the acidbase disturbances, and as treatment for acute renal failure.

scholarly journals Diagnostic Challenge in a Patient with Severe Anion Gap Metabolic Acidosis

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Eugene M. Tan ◽  
Ejaaz Kalimullah ◽  
M. Rizwan Sohail ◽  
Kannan Ramar
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Anion Gap ◽  
Diagnostic Challenge ◽  
Nursing Facility ◽  
Random Blood Sugar ◽  
Beta Hydroxybutyrate ◽  
Osmolal Gap ◽  
Urine Levels

The approach to the patient with acute renal failure and elevated anion and osmolal gap is difficult. Differential diagnoses include toxic alcohol ingestion, diabetic or starvation ketoacidosis, or 5-oxoproline acidosis. We present a 76-year-old female with type 2 diabetes mellitus, who was found at home in a confused state. Laboratory analysis revealed serum pH 6.84, bicarbonate 5.8 mmol/L, pCO2 29 mmHg, anion gap 22.2 mmol/L, osmolal gap 17.4 mOsm/kg, elevated beta-hydroxybutyrate (4.2 mmol/L), random blood sugar 213 mg/dL, creatinine 2.1 mg/dL, and potassium 7.5 mmol/L with no electrocardiogram (EKG) changes. Fomepizole and hemodialysis were initiated for presumed ethylene glycol or methanol ingestion. Drug screens returned negative for ethylene glycol, alcohols, and acetaminophen, but there were elevated urine levels of acetone (11 mg/dL). The acetaminophen level was negative, and 5-oxoproline was not analyzed. After 5 days in the intensive care unit (ICU), her mental status improved with supportive care. She was discharged to a nursing facility. Though a diagnosis was not established, our patient’s presentation was likely due to starvation ketosis combined with chronic acetaminophen ingestion. Acetone ingestion is less likely. Overall, our case illustrates the importance of systematically approaching an elevated osmolal and anion gap metabolic acidosis.

scholarly journals Ethylene Glycol Intoxication Requiring ECMO Support

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Raphael Rosen ◽  
Shelief Robbins-Juarez ◽  
Jacob Stevens
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Extracorporeal Membrane Oxygenation ◽  
Kidney Injury ◽  
Neurological Injury ◽  
Severe Metabolic Acidosis ◽  
Toxic Metabolites ◽  
Ethylene Glycol Intoxication

Ethylene glycol is commonly used in antifreeze, and ingestion of even a small amount can result in acute kidney injury, severe metabolic acidosis, and neurological injury. When cases are recognized early, treatment involves administration of alcohol dehydrogenase inhibitors to prevent conversion to toxic metabolites of glycolate, glyoxolate, and oxalate. In later presentations with more severe renal injury, hemodialysis may be required for clearance of toxic metabolites and supportive care for renal failure. We present the first reported case of severe ethylene glycol intoxication requiring support of extracorporeal membrane oxygenation (ECMO) due to refractory cardiopulmonary collapse.

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