Abstract: SA-PO500
Lactate Gap: A Diagnostic Clue for Diagnosing and Managing Ethylene Glycol Poisoning
Session Information
- Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Simhadri, Prathap, Florida State University, Tallahassee, Florida, United States
- Chandramohan, Deepak, The University of Alabama at Birmingham, Birmingham, Alabama, United States
- Contractor, Renish, Florida State University, Tallahassee, Florida, United States
- Singh, Prabhat, Christus Spohn Health System, Corpus Christi, Texas, United States
- Vaitla, Pradeep, The University of Mississippi Medical Center, Jackson, Mississippi, United States
- Neuman, Michelle, West Virginia University, Morgantown, West Virginia, United States
- Murari, Ujjwala, West Virginia University, Morgantown, West Virginia, United States
Introduction
Ethylene glycol(EG) is a type of toxic alcohol, and its ingestion is associated with the development of an osmolar gap and elevated anion gap metabolic acidosis. Early identification and aggressive management of this condition are critical in improving outcomes. We used lactate gap as a diagnostic tool in two patients with ethylene glycol poisoning.
Case Description
A 59-year-old male with a history of Hepatitis C and hypertension was brought for altered mental status(AMS) and had a GCS of 3. Labs showed serum osmolality of 319 mOsm/Kg with an osmolar gap of 69; Chemistry showed an anion gap(AG) of 28 mmol/l and bicarb of 8 mmol/L, ABG showed pH of 7.02, with blood gas lactate of > 17 mmol/L. Serum lactate was 1.5 mmol/L. EG poisoning was suspected, given the significant lactate cap. He was started on fomepizole and aggressive intermittent hemodialysis. EG level later came back as 1205 mg/dl and was undetectable by 48 hours with aggressive treatment.
A 60-year-old male was admitted for AMS, acute respiratory failure, and shock. He also had an osmolar gap of 135; chemistry showed an AG of 35, bicarb of <5 mmol/L; ABG showed pH of < 7.00, and lactate of > 18 mmol/L and serum lactate of 2.5 mmol/L. EG poisoning was suspected, given the significant lactate cap; the patient was started on fomepizole and aggressive CRRT. EG level later came back as 344 mg/dl, and the CRRT was discontinued once the EG level was < 20 mg/dl.
Discussion
Ethylene glycol metabolizes into glycolic acid and oxalic acid; these metabolites are responsible for elevated anion gap metabolic acidosis. It is also associated with minimal lactic acid production. Lactic acid can be measured using lactate oxidase and lactate dehydrogenase methods. The lactate oxidase method measures the hydrogen peroxide generated from the metabolism of lactic acid to pyruvate via lactic oxidase. Glycolic acid is structurally similar to lactate, and it can also generate hydrogen peroxide, which causes a false elevation of lactic acid. Conversely, the measurement of lactic acid by the dehydrogenase method is not interfered with by glycolic acid. The closure of the lactate gap can hint at the successful removal of ethylene glycol metabolites through dialysis.
Conclusion:
The lactate gap can be a diagnostic tool to diagnose and manage ethylene glycol poisoning.