Abstract
It can be difficult for anesthesiologists to determine the optimal dose of propofol for end-stage kidney disease (ESKD) patients due to changes in drug disposition. The purpose of this study was to evaluate the potency of propofol for inducing loss of consciousness in ESKD patients. Patients with normal kidney function (Control group, n = 15), those with ESKD (ESKD group, n = 15), and those with ESKD undergoing cervical epidural anesthesia (ESKD-CEB group, n = 15) were administered propofol by target-controlled infusion (TCI) using the Schneider model. The effect-site concentration (Ce) of propofol started at 0.5 μg/ml and increased in increments of 0.5 μg/ml until the patient did not respond to verbal commands. The relationship between the probability (P) of loss of consciousness and the Ce of propofol was analyzed in each group using logistic regression. The Ce values of propofol at the time of loss of consciousness were 4.3 ± 0.9, 3.7 ± 0.9, and 3.3 ± 1.0 μg/ml for the Control, ESKD, and ESKD-CEB* groups, respectively (*significant difference vs. control, P < 0.05). The estimated Ce50 values for lost ability to respond to verbal command were 4.56, 3.75, and 3.21 μg/ml for the Control, ESKD, and ESKD-CEB groups, respectively. In conclusion, when inducing anesthesia in ESKD patients, we recommend using an initial dose similar to that of patients with normal kidney function, or rather starting with a lower dose.
Highlights
Propofol is a short-acting, lipophilic intravenous general anesthetic
No signs of central nervous system (CNS) toxicity due to the local anesthetic were detected during the cervical epidural block (CEB) in any patients in the End-stage kidney disease (ESKD)-CEB group
In the ESKD patients who had received a CEB were older with lower BMI and weight
Summary
Propofol is a short-acting, lipophilic intravenous general anesthetic. The hypnotic action of propofol is probably mediated through γ-aminobutyric acid (GABA) receptor (agonist) and N-methyl-D-aspartate (NMDA) receptor (antagonist). Propofol has a protein binding of about 98% and is rapidly metabolized to water-soluble inactive metabolites in the liver and excreted through the kidneys [1, 2]. End-stage kidney disease (ESKD) is defined as irreversible decline in a person’s own kidney function, which is severe enough to be fatal in the absence of dialysis or transplantation [3].
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