scholarly journals Ethylene Glycol Poisoning: An Unusual Cause of Altered Mental Status and the Lessons Learned from Management of the Disease in the Acute Setting

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
R. Singh ◽  
E. Arain ◽  
A. Buth ◽  
J. Kado ◽  
A. Soubani ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Mental Status ◽  
Kidney Injury ◽  
Altered Mental Status ◽  
Lessons Learned ◽  
Anion Gap ◽  
Tubular Damage ◽  
Elderly Male ◽  
Laboratory Findings

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 for the increased anion gap metabolic acidosis, renal tubular damage, and crystalluria seen later in ingestions. Early intervention is key; however, diagnosis is often delayed, especially in elderly patients presenting with altered mental status. There are several laboratory tests which can be exploited for the diagnosis, quantification of ingestion, and monitoring of treatment, including the lactate and osmolal gaps. As methods of direct measurement of ethylene glycol are often not readily available, it is important to have a high degree of suspicion based on these indirect laboratory findings. Mainstay of treatment is bicarbonate, fomepizole or ethanol, and, often, hemodialysis. A validated equation can be used to estimate necessary duration of hemodialysis, and even if direct measurements of ethylene glycol are not available, monitoring for the closure of the anion, lactate, and osmolal gaps can guide treatment. We present the case of an elderly male with altered mental status, acute kidney injury, elevated anion gap metabolic acidosis, and profound lactate and osmolal gaps.

scholarly journals Hemodynamically significant atrial fibrillation in a previously healthy man with ethylene glycol toxicity

2014 ◽  
Vol 1 (1) ◽  
pp. 21
Author(s):  
Ryan Thompson ◽  
Allan R. Mottram
Keyword(s):  
Atrial Fibrillation ◽  
Renal Failure ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Mental Status ◽  
Altered Mental Status ◽  
Late Presentation ◽  
Electrical Cardioversion ◽  
Anion Gap ◽  
Healthy Man

Ethylene glycol ingestion is a well-described phenomenon that results in altered mental status, anion gap metabolic acidosis, and renal failure. Cardiac sequelae of ethylene glycol ingestion have not been well described in the literature. We report a case of a young, previously healthy man who developed atrial fibrillation successfully treated with electrical cardioversion in the setting of a large ethylene glycol ingestion with a late presentation.

Adolescent Presents With Altered Mental Status and Elevated Anion Gap After Suicide Attempt by Ethylene Glycol Ingestion

2016 ◽  
Vol 32 (10) ◽  
pp. 688-690 ◽  
Author(s):  
Jessica C. Schoen ◽  
Meghan R. Cain ◽  
Jeffrey A. Robinson ◽  
Brenda M. Schiltz ◽  
Mark S. Mannenbach
Keyword(s):  
Suicide Attempt ◽  
Ethylene Glycol ◽  
Mental Status ◽  
Altered Mental Status ◽  
Anion Gap

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.

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 Recurrent noncirrhotic hyperammonemia causing acute metabolic encephalopathy in a patient with a continent ileocecal pouch: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
T. M. Skipina ◽  
S. Macbeth ◽  
E. L. Cummer ◽  
O. L. Wells ◽  
S. Kalathoor
Keyword(s):  
Emergency Department ◽  
Metabolic Acidosis ◽  
Mental Status ◽  
Rare Case ◽  
Liver Function Tests ◽  
Altered Mental Status ◽  
Potassium Citrate ◽  
Metabolic Encephalopathy ◽  
History Of ◽  
Normal Urine

Abstract Introduction Acute encephalopathy, while a common presentation in the emergency department, is typically caused by a variety of metabolic, vascular, infectious, structural, or psychiatric etiologies. Among metabolic causes, hyperammonemia is relatively common and typically occurs in the setting of cirrhosis or liver dysfunction. However, noncirrhotic hyperammonemia is a rare occurrence and poses unique challenges for clinicians. Case presentation Here we report a rare case of a 50-year-old Caucasian female with history of bladder cancer status post chemotherapy, radical cystectomy, and ileocecal diversion who presented to the emergency department with severe altered mental status, combativeness, and a 3-day history of decreased urine output. Her laboratory tests were notable for hyperammonemia up to 289 μmol/L, hypokalemia, and hyperchloremic nonanion gap metabolic acidosis; her liver function tests were normal. Urine cultures were positive for Enterococcus faecium. Computed tomography imaging showed an intact ileoceal urinary diversion with chronic ileolithiasis. Upon administration of appropriate antibiotics, lactulose, and potassium citrate, she experienced rapid resolution of her encephalopathy and a significant reduction in hyperammonemia. Her hyperchloremic metabolic acidosis persisted, but her hypokalemia had resolved. Conclusion This case is an example of one of the unique consequences of urinary diversions. Urothelial tissue is typically impermeable to urinary solutes. However, when bowel segments are used, abnormal absorption of solutes occurs, including exchange of urinary chloride for serum bicarbonate, leading to a persistent hyperchloremic nonanion gap metabolic acidosis. In addition, overproduction of ammonia from urea-producing organisms can lead to abnormal absorption into the blood and subsequent oversaturation of hepatic metabolic capacity with consequent hyperammonemic encephalopathy. Although this is a rare case, prompt identification and treatment of these metabolic abnormalities is critical to prevent severe central nervous system complications such as altered mental status, coma, and even death in patients with urinary diversions.

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 MON-LB65 Lithium: The Culprit of Multiple Endocrinopathies

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Alice Yau ◽  
Gul Bahtiyar ◽  
Giovanna Rodriguez ◽  
Jose R Martinez Escudero
Keyword(s):  
Bipolar Disorder ◽  
Diabetes Insipidus ◽  
Mental Status ◽  
Nephrogenic Diabetes Insipidus ◽  
Kidney Injury ◽  
Urine Osmolality ◽  
Altered Mental Status ◽  
Clinical Findings ◽  
Volume Depletion ◽  
Collecting Tubules

Abstract Background: Lithium, commonly used to treat various psychiatric disorders such as bipolar disorder, can cause acute toxicity that presents with nausea, vomiting and diarrhea. Lithium can also cause life-threatening endocrine abnormalities, including hypercalcemia, hypernatremia, and both hypo- and hyperthyroidism. Clinical Case: A 61-year old female with hypothyroidism, bipolar disorder, hyperparathyroidism with two-gland parathyroidectomy on lithium for over 30 years presented with altered mental status. Initial labs revealed elevated creatinine 1.92 mg/dL (0.8-2.00mg/dL) compared to baseline 0.82 mg/dL, sodium 154 mg/dL (135-147 mg/dL), Corrected calcium 11.7 mg/dL (8.5-10.5 mg/dL), PTH 96 pg/mL (15-65 pg/mL), and high lithium levels 1.45 mmol/L (0.60-1.20 mmol/L). Further studies showed hypotonic polyuria with no increase in urine osmolality after desmopressin, consistent with nephrogenic diabetes insipidus. Lithium was held and she was treated with aggressive intravenous hydration with dextrose 5% water. Hypercalcemia is thought to result from increased secretion of PTH due to an increased set point at which calcium suppresses PTH release; this often resolves once lithium is stopped. Lithium can also unmask previously unrecognized mild hyperparathyroidism, and/or raise serum PTH concentrations independent of calcium levels.1 The drug interferes with the kidneys’ ability to concentrate urine in the collecting tubules by desensitizing response to antidiuretic hormone, causing diabetes insipidus. The resulting volume depletion from excessive urinary water loss in turn lead to acute kidney injury and hypernatremia.2 Hypothyroidism results from lithium-inhibited synthesis and release of thyroid hormones and decreases iodine trapping. Conclusion: Although these are infrequent complications of lithium use, they remain pertinent clinical findings to consider due to their morbidity. In this case, our patient may have avoided multiple chronic electrolyte abnormalities leading to altered mental status if lithium toxicity had been recognized earlier. References:1. García-Maldonado, Gerardo, and Rubén de Jesús Castro-García. “Endocrinological Disorders Related To The Medical Use Of Lithium. A Narrative Review”. Revista Colombiana De Psiquiatría (English Ed.), vol 48, no. 1, 2019, pp. 35-43. Elsevier BV, doi:10.1016/j.rcpeng.2018.12.005. 2. Tasci, E. “Lithium-Induced Nephrogenic Diabetes Insipidus Responsive To Desmopressin”. Acta Endocrinologica (Bucharest), vol 15, no. 2, 2019, pp. 270-271. ACTA Endocrinologica Foundation, doi:10.4183/aeb.2019.270.

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.

Altered Mental Status in an Elderly Male

2018 ◽  
Vol 54 (2) ◽  
pp. 232-237
Author(s):  
Paul S. Jansson ◽  
Christopher Kabrhel ◽  
Emily S. Miller
Keyword(s):  
Mental Status ◽  
Altered Mental Status ◽  
Elderly Male

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.

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