SOFT 2004 Meeting Abstracts - Society of Forensic Toxicologists

C25
PROPYLENE GLYCOL IN EXTREMELY HIGH ION GAP LACTIC ACIDOSIS
Robert L. Fitzgerald* and David A. Herold
V A Healthcare System San Diego and University of California-San Diego, San Diego, CA.
A 31-year-old male presented to the ED disoriented in acute distress. His admission laboratory data were
remarkable for the degree of acidosis present. An arterial blood gas measurement showed his pH to be 6.85
(reference range 7.35 to 7.45) with a pC02 of 14 mm Hg (reference 35 to 45) and a lactic acid of 30
mmollL (reference range 0.7 to 2.1). Additional labs included an ethanol of217 mg/dL, and a measured
osmolality of 376 mOsmikg (270 - 310). Taking the effect of ethanol into account, the patient had an
unexplained osmol gap of 65 mOsmikg. In addition to the unexplained osmol gap the patient had an anion
gap of 50 mEq/L (reference range 10 to 20), the L-Iactate of 30 explained this gap. Based on the
unexplained osmol gap, the acidosis, and a high anion gap, stat methanol and ethylene glycol were ordered.
Negative finding for methanol and ethylene glycol prompted a search for other causes of hyperosmolality.
Discussion of the case with the toxicology laboratory revealed the presence of a large peak on the gas
chromatographic tracing from a volatiles screen that was not reported initially. This peak represented 40
mgldL of propylene glycol. Either ethanol or propylene glycol can result in a high anion gap lactate
acidosis. The profound acidosis and extremely high L-Iactate was a result of the patient drinking for 5 days.
While the osmol gap could not be completely explained, the high anion gap could be explained by L-Iactate
and the implied D-Iactate resulting from the propylene glycol metabolism.
Based on the laboratory data, the patient was treated with intravenous bicarbonate and IV fluid replacement
in an attempt to correct the acidosis. Despite 4 ampules of bicarbonate, the patients arterial blood gas pH
did not increase significantly nor was there a significant increase in urinary output. Due to the impending
renal failure and acidosis, the patient was hemodialyzed. Four hours of hemodialysis corrected his
acidlbase imbalance. Unfortunately, after hemodialysis, the patient developed acute respiratory distress
syndrome and required ventilation assistance. The patient also became septic and was treated with
antibiotics. After a twelve day hospital stay which included intermittent hemodialysis for renal failure, the
patient recovered and was discharged in apparent good health.
This presentation will review the common causes of hyperosmolality in clinical toxicology and the
diagnostic pathway for identifying various intoxicants that cause high anion gap metabolic acidosis. The
importance of communicating directly with the laboratory to help identity unusual causes of combined
osmol/anion gap metabolic acidosis will be emphasized.
Key words: propylene glycol, metabolic acidosis, ethanol
Page 243