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Abstract: SA-PO1012

Amantadine Toxicity: An Unexpected Case of Metabolic Acidosis

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Sharma, Divya, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Sinnakirouchenan, Ramapriya, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
Background

Propylene glycol is a solvent used to dissolve a variety of medications and can become toxic when administered in large doses. We present a case of severe metabolic acidosis in a patient taking toxic doses of amantadine, which in some formulations contain the carrier propylene glycol.

Methods

A 66-year-old woman with a history of multiple sclerosis (MS) and end stage renal disease (ESRD) was admitted from Neurology clinic with concerns for MS flare. Her last dialysis was the day prior to admission. Labs revealed BUN 36 mg/dL, Cr 5.81 mg/dL, and bicarbonate 16 mmol/L. That evening she developed severe respiratory distress requiring transfer to the intensive care unit where she was urgently intubated. Arterial blood gas showed pH 6.98, pCO2 <20 mmHg, pO2 104 mmHg, and bicarbonate 3 mmol/L. Basic metabolic panel revealed BUN 59 mg/dL, Cr 7.32 mg/dL, and bicarbonate 4 mmol/L. Other significant labs included lactic acid 20 mmol/L and serum osmolality 322 mOsm/kg. She had an elevated anion gap of 44 mmol/L and an osmolar gap of 18 mOsm/kg. A toxicology screen, including aspirin, acetaminophen, acetone, ethanol, isopropanol, and methanol was negative. The patient underwent emergent hemodialysis for severe acidosis and was extubated the next day.

Conclusion

It was subsequently found that our patient was started on amantadine 3 weeks prior for MS related fatigue. She was prescribed 100 mg oral twice daily, instead of the recommended dose for ESRD of 200 mg oral weekly. Upon further investigation, we noted that some dosage forms of amantadine contain propylene glycol, which in large amounts can be potentially toxic and be associated with hyperosmolality, lactic acidosis, increased anion gap metabolic acidosis, and respiratory depression. As no other etiology for her acidosis was identified, propylene glycol toxicity was presumed to be the etiology as she was essentially receiving 7 times the dose recommended for her level of renal function. Amantadine was discontinued immediately, and she had no further recurrences of acidosis. This case illustrates the importance of obtaining a thorough history from our patients, including all medications. Not only must we be especially vigilant to dose medications for level of renal function, but to recognize solvents such as propylene glycol that are carriers for a variety of medications and the widespread and potentially harmful effects they may have.