Propofol 2% in critically ill patients

Objective To investigate the concentrations of triglyceride, cholesterol, and high-density lipoprotein during a 50-hr infusion of 2% propofol, starting within 24 hrs of admission to the intensive care unit (ICU). Design Prospective, clinical study. Setting ICU, university hospital. Patients Thirty adult patients, who were ventilated and expected to be sedated for >2 days, were studied for 50 hrs, beginning 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, interleukin (IL)-6, and C-reactive protein were measured at 2000 hrs. Median cholesterol and high-density lipoprotein concentrations were at the low end of the normal range. In seven patients, peak triglyceride concentrations were >3 mmol/L up to a maximum of 4.83 mmol/L. Although there was no statistical difference in lipid concentrations between days 1 and 2, there was an apparent pattern of increasing triglyceride concentrations. There was a correlation between peak triglyceride concentration and total propofol consumption, but there was no correlation between lipids and age, gender, or Acute Physiology and Chronic Health Evaluation II scores. There was a direct correlation between triglyceride and C-reactive protein concentrations, and an inverse correlation between cholesterol and C-reactive protein. Twenty-two patients had evidence 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 patients over a 50-hr period does not result in a significant increase in triglyceride concentrations. Mean cholesterol and high-density lipoprotein concentrations were low throughout the study period. There was a significant direct correlation between triglyceride and C-reactive protein and an inverse correlation between cholesterol and C-reactive protein, suggesting that the changes in lipids in critically ill patients may be partly attributable to the acute-phase response.