Dose-Response Effect of Propofol Upon Serum Triglyceride Concentrations in Critically Ill Patients

Sunday, March 22, 2026

2:30 PM - 3:30 PM Central Time

Location: Connections Central - RST 04

JW

Jonathon Kameron Walker, Pharm.D.

Tennessee

Disclosure(s): No relevant financial relationship(s) to disclose.
Emma Lemke, Pharm.D.

TriStar Horizon Medical Center

Disclosure(s): No relevant financial relationship(s) to disclose.
JF

Julie Farrar, PharmD, BCCCP

Assistant Professor of Clinical Pharmacy and Translational Science
University of Tennessee College of Pharmacy

Disclosure information not submitted.
SB

Saskya Byerly, MD, MS

Assistant Professor of Surgery
University of Tennessee Health Science Center

Disclosure information not submitted.
DF

Dina Filiberto, MD, MS

Associate Professor of Surgery
University of Tennessee Health Science Center

Disclosure information not submitted.
RD

Roland Dickerson, PharmD, BCNSP, FCCP, FASHP, FCCM, FASPEN

Professor of Clinical Pharmacy and Translational Science
University of Tennessee College of Pharmacy

Disclosure information not submitted.

Introduction: Introduction/Hypothesis: This study aimed to evaluate the dose-response effect of continuous intravenous lipid-emulsion containing propofol infusion upon serum triglyceride concentrations (TG) in critically ill trauma patients.

Methods:

Methods: Adult patients, >17 yrs old, who received a continuous intravenous propofol infusion for at least 24 hours and had a TG determination, and had accurate fluid intake and output documentation were retrospectively included for evaluation. The amount of lipid emulsion from propofol given 24 hours prior to TG determination was used to evaluate the dose-TG response relationship. Patients were classified as hypertriglyceridemic (hyperTG) if TG was > 400 mg/dl. The dose-TG response relationship was examined for the hyperTG and non-hyperTG groups. Linear and nonlinear correlative relationships were interpolated for the best fit using curve-fitting software. Continuous data are given as median [25th,75th percentile]. A p value < 0.05 was established as significant.

Results:

Results: One hundred and ninety-five TG determinations were performed in 100 patients. Fifty-nine patients had one TG determination and 41 had multiple TG determinations. Twenty-five patients developed hyperTG while receiving propofol of which 4 exhibited a TG > 1000 mg/dl. Lipid intake from propofol was greater in those with hyperTG (0.22 [0.15, 0.45] g/kg/d vs 0.13 [0.1, 0.25] g/kg/d, p=0.002). The best fit, defined by the highest correlation (r), was non-linear and linear for the hyperTG and non-hyperTG groups, respectively. The hyperTG group (n=57 TG determinations) exhibited a significant concave non-linear relationship (TG=29+292*elipid dose(g/kg/d); r=0.731, p=0.001) between lipid dose and TG as the lipid dose increased. The non-hyperTG group (n=138 TG determinations) had a flattened dose-TG response with a poor linear relationship (TG=160+61*lipid dose(g/kg/d); r=0.263, p=0.002).

Conclusions:

Conclusions: The hyperTG group exhibited a non-linear concave dose-TG response with evidence of triglyceride accumulation whereas the non-hyperTG group’s dose-TG response was flattened with increases in propofol dosage. Due to unpredictability in dose-TG response, frequent TG monitoring is warranted for patients who receive prolonged or high doses of propofol.