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

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.

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

Case Reports in Internal Medicine ◽

10.5430/crim.v1n1p21 ◽

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.

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MON-LB119 Euglycemic Diabetic Ketoacidosis in a Patient on Canagliflozin Presenting With Hypoglycemia

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.2155 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Sindhura Inkollu ◽

Sindhuja Korem ◽

Sudha Ganne

Keyword(s):

Blood Glucose ◽

Diabetic Ketoacidosis ◽

Mental Status ◽

Altered Mental Status ◽

Sglt2 Inhibitors ◽

Anion Gap ◽

Hypoglycemic Agents ◽

Tract Infections ◽

Euglycemic Diabetic Ketoacidosis

Abstract Background: Sodium glucose co-transporter 2 (SGLT-2) inhibitors are newer class of antihyperglycemics that cause reversible inhibition of the sodium-glucose cotransporters in the renal proximal tubules resulting in increased urinary glucose. Common side effects include yeast and urinary tract infections. The US Food and Drug Administration issued a safety warning pertaining to the development of diabetic ketoacidosis (DKA) with the use of SGLT2 inhibitors. The mechanisms by which SGLT2 inhibitors cause euglycemic DKA are unclear. SGLT2 inhibitors may lead to a decrease in either endogenous or exogenous insulin and an increase in glucagon production.1 This insulin deficiency or resistance may be mild in Type 2 diabetics, however, preventing the profound spike in blood glucose seen in traditional DKA. Here, we report a case of euglycemic DKA in a patient on Canagliflozin who presented initially with hypoglycemia. Clinical case: A 70 year old female presented with altered mental status for 1 day duration. Her past medical history is significant for type 2 Diabetes Mellitus, being managed on Canagliflozin, Glimepiride and Janumet. One week prior to admission she had lumbar spinal fusion surgery. Since then she has been feeling weak and tired with poor oral intake, but continued to use her medications. Initial laboratory findings showed blood glucose of 68 (70-100 mg/dl) without any acidosis. Her altered mental status was attributed to higher opioid doses which she received prior. Oral hypoglycemic agents have been held. On 2nd day of hospitalization, patient became more lethargic and complained of nausea. Laboratory testing revealed a serum glucose of 250mg/dL, serum bicarbonate of 13 (21–31mmol/L), and Anion gap of 25 (3.6–11.0mmol/L). With the suspicion of DKA, a beta-hydroxy butyrate level was obtained which was elevated at 90.10 (0 – 4.16 mg/dL). Venous blood gas analysis was significant for pH 7.23 (7.31-7.41) and pCO2 – 28 (41-51 mmHg). Urinalysis showed ketosis and glucosuria. Patient was diagnosed as euglycemic diabetic ketoacidosis from Canagliflozin in presence of precipitating factors - stress and poor intake. Patient was treated with insulin drip and intravenous fluids with reduction in anion gap and correction of acidosis within 24hrs. There was a gradual improvement in her mental status. She was discharged on subcutaneous insulin, and all other diabetic medications were stopped. Conclusion: Our case highlights the importance of being vigilant in a patient on Canagliflozin, euglycemic DKA can occur even if they present initially with hypoglycemia and no acidosis. Reference: 1. Ogawa W, Sakaguchi K. Euglycemic diabetic ketoacidosis induced by SGLT2 inhibitors: possible mechanism and contributing factors. J Diabetes Investig. 2016;7(2):135-138.

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Altered mental status and low anion gap in a patient with sickle cell anemia: a case report

Journal of Medical Case Reports ◽

10.1186/1752-1947-6-72 ◽

2012 ◽

Vol 6 (1) ◽

Cited By ~ 1

Author(s):

Siddharth A Wartak ◽

Reshma A Mehendale ◽

Benjamin Freda ◽

Ashish Verma ◽

David N Rose

Keyword(s):

Case Report ◽

Sickle Cell ◽

Mental Status ◽

Sickle Cell Anemia ◽

Altered Mental Status ◽

Anion Gap

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Severe Ketoacidosis (pH ≤ 6.9) in Type 2 Diabetes: More Frequent and Less Ominous Than Previously Thought

BioMed Research International ◽

10.1155/2015/134780 ◽

2015 ◽

Vol 2015 ◽

pp. 1-5 ◽

Cited By ~ 9

Author(s):

René Rodríguez-Gutiérrez ◽

Carlos R. Cámara-Lemarroy ◽

Dania L. Quintanilla-Flores ◽

Emanuel I. González-Moreno ◽

Juan Manuel González-Chávez ◽

...

Keyword(s):

Type 2 Diabetes ◽

Mental Status ◽

Insulin Infusion ◽

Case Series ◽

Altered Mental Status ◽

Anion Gap ◽

University Hospital ◽

Acid Decarboxylase ◽

Metabolic Complication

Diabetic ketoacidosis is a life-threatening acute metabolic complication of uncontrolled diabetes. Severe cases of DKA (pH ≤ 7.00, bicarbonate level ≤ 10.0, anion gap > 12, positive ketones, and altered mental status) are commonly encountered in patients with type 1 diabetes and are thought to carry an ominous prognosis. There is not enough information on the clinical course of severely acidotic type 2 diabetes (pH ≤ 6.9) patients with DKA, possibly because this condition is rarely seen in developed countries. In this series, we present 18 patients with type 2 diabetes, DKA, and a pH ≤ 6.9 that presented to a tertiary university hospital over the past 11 years. The objective was to describe their clinical characteristics, the triggering cause, and emphasis on treatment, evolution, and outcomes. The majority of the patients were female (61%). Mean age was 40.66 years (23–59). The patients had been first diagnosed with type 2 diabetes on average 5.27 ± 3.12 years before admission. Glutamic acid decarboxylase (GAD65) antibodies were negative in all patients. The origin of DKA could be attributed to two main causes: treatment omission in 8 (44.4%) patients and infections in 7 (38.8%) patients. The most common symptoms described were general malaise, dyspnea, altered mental status, and abdominal pain. Mean serum glucose on admission was 613.8 ± 114.5 mg/dL. Mean venous pH was 6.84 ± 0.03 with an anion gap of 30.3 ± 2.9 and a venous HCO3level of 3.62 ± 1.35 mmol/L. All patients had acute renal failure on admission, with a mean serum creatinine of 1.57 ± 0.35 mg/dL compared to 0.55 ± 0.21 mg/dL at discharge. All patients received regular insulin infusion, aggressive fluid repletion, and 12 patients (66%) received bicarbonate infusion. Mean total insulin infusion dose was 181.7 ± 90.4 U (on average 0.14 ± 0.05 U/Kg/h). Mean time on infusion was 24.4 ± 12.6 hours. We recorded no mortality in this case series. Mean in-hospital stay was 5.0 ± 4.1 days. In conclusion, very severe DKA in type 2 diabetes is not uncommon in our population, shares many features with non-very-severe cases of DKA (bicarbonate therapy did not make a difference in mortality), and can be managed following standard published or institutional guidelines.

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Acidosis and coma after hemodialysis.

Journal of the American Society of Nephrology ◽

10.1681/asn.v85853 ◽

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.

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Spurious point-of-care lactate elevation in ethylene glycol intoxication: rediscovering a clinical pearl

BMJ Case Reports ◽

10.1136/bcr-2020-239936 ◽

2021 ◽

Vol 14 (2) ◽

pp. e239936

Author(s):

Laurence Poirier-Blanchette ◽

Camille Simard ◽

Blair Carl Schwartz

Keyword(s):

Lactic Acidosis ◽

Ethylene Glycol ◽

Mental Status ◽

Point Of Care ◽

Clinical Signs ◽

Altered Mental Status ◽

Blood Gas ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Renal Replacement Therapy Initiation

A 76-year-old man was found unresponsive and brought to the emergency department. Initial workup showed profound lactic acidosis on a point-of-care arterial blood gas, without clinical signs of hypoperfusion. Investigations for types A and B lactic acidosis revealed no unifying diagnosis to explain both his altered mental status and profound lactic acidosis. A toxicology workup revealed an increased osmolar gap and an elevated ethylene glycol level. The lactic acidosis and his mental status completely normalised within 8 hours of renal replacement therapy initiation and fomepizole administration. Ethylene glycol metabolites have similar molecular structure with L-lactate. Some blood gas analysers are unable to differentiate them, resulting in an artefactual lactate elevation. Our case highlights the importance of recognising a falsely elevated lactate, which should raise clinical suspicion of ethylene glycol poisoning, as the treatment is time-sensitive to prevent complications and mortality.

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