PROPOFOL 2-PERCENT IN CRITICALLY ILL PATIENTS - EFFECT ON LIPIDS

Objective: To investigate the concentrations of triglyceride, choleste rol, and high-density lipoprotein during a 50-hr infusion of 2% propof ol, starting within 24 hrs of admission to the intensive care unit (IC U). Design: Prospective, clinical study. Setting: ICU, university hosp ital Patients: Thirty adult patients, who were ventilated and expected to be sedated for >2 days, were studied for 50 hrs, begining at 1800 hrs on the first day of ICU admission. Measurements and Main Results: Triglyceride, cholesterol, and high-density lipoprotein were measured at 2000, 0400, and 0800 hrs. Tumor necrosis factor (TNF)-alpha, interl eukin (IL)-6, and C-reactive protein were measured at 2000 hrs. Median cholesterol and high-density lipoprotein concentrations were at the l ow end of the normal range. In seven patients, peak triglyceride conce ntrations were >3 mmol/L up to a maximum of 4.83 mmol/L. Although ther e was no statistical difference in lipid concentrations between days 1 and 2, there was an apparent pattern of increasing triglyceride conce ntrations. There was a correlation between peak triglyceride concentra tion and total propofol consumption, but there was no correlation betw een lipids and age, gender, or Acute Physiology and Chronic Health Eva lutation II scores. There was a direct correlation between triglycerid e and C-reactive protein concentrations, and an inverse correlation be tween cholesterol and C-reactive protein. Twenty-two patients had evid ence of TNF and 11 patients had an IL-6 of > 1000 pg/mL, but there was no relationship between concentrations of cytokines and triglycerides in plasma. Conclusions: Infusion of 2% propofol to critically ill pat ients over a 50-hr period does not result in a significant increase in triglyceride concentrations. Mean cholesterol and high-density lipopr otein concentrations were low throughout the study period. There was a significant direct correlation between triglyceride and C-reactive pr otein and an inverse correlation between cholesterol and C-reactive pr otein, suggesting that the changes in lipids in critically ill patient s may be partly attributable to the acute-phase response.