Propylene Glycol–Induced Lactic Acidosis in a Patient with Normal Renal Function: A Proposed Mechanism and Monitoring Recommendations

Abstract

Our case highlights the development of propylene glycol-induced lactic acidosis secondary to high-dose lorazepam infusion not associated with renal dysfunction.

Are Excipients Really Inert Ingredients? A Review of Adverse Reactions to Excipients in Oral Dermatologic Medications in Canada

“…107 As lactic acid is a metabolic product of PG, lactic acidosis can also occur when PG is used in parenteral medications. 108,109 This is most commonly observed with lorazepam. 108,109 There is 0.83 mg of PG per milliliter of lorazepam, and infusions ranging from 5 to 12 mg per hour are predictive of PG accumulation.…”

“…108,109 This is most commonly observed with lorazepam. 108,109 There is 0.83 mg of PG per milliliter of lorazepam, and infusions ranging from 5 to 12 mg per hour are predictive of PG accumulation. 110,111 Hemolysis, hyperosmolality, and central nervous system depression have also been reported after IV administration of medication.…”

Medication-Related Complications in the Trauma Patient

“…54 Published recommendations for the monitoring of PG toxicity include measuring biweekly serum osmolality for patients administered ≥5 mg/h of propofol for >5 days; for values >320 mOsm/kg, authors suggest administering alternative agents. 52 Dexmedetomidine is an additional agent that may be considered for sedation in the trauma patient, particularly during the weaning phase of mechanical ventilation or in difficult-to-control polysubstance abuse patients. It is an α 2 agonist with sedative, analgesic, and anxiolytic properties, with minimal amnestic effects.…”

Acute kidney injury, hyperosmolality and metabolic acidosis associated with lorazepam

“…13 Although these observations show proximal tubular injury to be at the center of propylene glycol toxicity, propylene-glycol-induced lactic acidosis associated with clinical deterioration has also been observed in patients with no laboratory evidence of AKI. 14 In adults with normal hepatic and renal function, the terminal half-life of propylene glycol is within the range 1.4-3.3 hours. 13 Commercial propylene glycol is a 50:50 mixture of d and l isomers of propylene glycol.…”