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Hyperlactatemia, increased osmolar gap, and renal dysfunction during continuous lorazepam infusion.
H N Reynolds1, P Teiken, M E Regan
1R Adams Cowley Shock Trauma Center, University of Maryland Medicine, Baltimore, USA.
Critical Care Medicine
|June 2, 2000
Summary
Propylene glycol, the vehicle for lorazepam, can elevate lactate levels and osmolarity. It may also impair renal function, hindering compensation for respiratory acidosis.
Area of Science:
- Pharmacology
- Nephrology
- Critical Care Medicine
Background:
- Lorazepam is frequently used for sedation in intensive care units.
- The intravenous formulation of lorazepam contains propylene glycol, a known potential nephrotoxin.
- Understanding the metabolic effects of lorazepam's vehicle is crucial for patient management.
Observation:
- A case report details a patient experiencing severe respiratory failure requiring high-dose lorazepam.
- The patient exhibited rising lactate and osmolarity levels during lorazepam infusion.
- Renal compensation for hypercapnia was notably absent during lorazepam administration.
Findings:
- Serum lactate and osmolarity levels directly correlated with lorazepam infusion rates.
- The patient's serum bicarbonate levels failed to rise in response to hypercapnia while on lorazepam.
- Discontinuation of lorazepam led to expected decreases in lactate and osmolarity and improved renal compensation.
Implications:
- Propylene glycol in lorazepam can induce hyperlactatemia and increase osmolar gaps.
- Propylene glycol may interfere with renal tubular function, blunting the kidney's ability to correct respiratory acidosis.
- Clinicians should consider the potential nephrotoxic effects of propylene glycol when administering high-dose lorazepam, especially in critically ill patients.