Faculty Bibliography

BACKGROUND:The Joint Commission requirement is that the US Pharmacopeia Chapter <797> is followed, which recommends that administration of compounded sterile preparations should begin no later than 1 hour after their preparation. We hypothesized that simply spiking the IV fluid in a nonsterile environment does not pose an increased risk of infection to the patient. METHODS:Two 1000-mL bags of IV fluid (normal saline and dextrose 5% in water) were spiked and hung in 5 busy perioperative locations, once a week for a 13-week period. A 10-mL sample was drawn from each bag of IV fluid at time zero and 24 hours resulting in 260 samples in total. All samples were inoculated in 2 separate growth media (sheep's blood agar and thioglycollate broth). The primary outcome was growth versus no growth in any of the specimens. If any growth was noted, the sample was marked as positive and further testing to identify the organism was undertaken. RESULTS:A total of 257 samples (normal saline = 127, dextrose 5% in water = 129) were collected over a period of 13 weeks, yielding 514 specimens. Three samples were excluded from the study secondary to the IV bags being discarded accidentally. No growth was identified in any of the specimens. The 97.5% CIs were as follows: normal saline = 127 (0-0.034) and dextrose 5% in water = 129 (0-0.033), correcting for multiple tests. CONCLUSIONS:No bacterial growth was noted in any of the 257 samples collected. Normal saline and dextrose 5% in water do not support bacterial growth 24 hours after their preparation using standard sterile techniques in the perioperative space.

BACKGROUND:As the number of operative cases increases, there is a greater emphasis on reducing inefficiency while maintaining patient safety. Recently, the issue of prespiking intravenous (IV) bags was raised. No study has assessed whether the risk of infection is related to the length of time a sterile (IV) fluid bag has been spiked. After completion of a pilot study revealed no microbial growth within 24 hours of an IV spike, a larger formal study was undertaken to determine whether there was an increased infection risk within 4 hours of spiking an intravenous fluid bag. METHODS:Five IV administration sets were spiked and hung in busy perioperative areas once a week for a 5-week period. Five samples were drawn from each IV set. Approximately 10 mL was collected per sample. All samples were inoculated in 2 separate growth media. If any growth was noted, the sample was marked as positive. RESULTS:A total of 125 samples were collected over a period of 5 weeks, yielding 250 specimens. No samples were excluded from the study. No growth was identified in any of the specimens. The 95% confidence interval was estimated to be 0, 0.063. DISCUSSION:There was no bacterial growth in prespiked normal saline IV bags in a perioperative environment. Thus, prespiking of normal saline IV bags in advance should pose no risk of infection to a patient if prepared within 4 hours.

BACKGROUND:Propofol is a commonly used intravenous anesthetic agent, which produce rapid induction of and recovery from general anesthesia. Numerous clinical studies reported that propofol can potentially cause amnesia and memory loss in human subjects. The underlying mechanism for this memory loss is unclear but may potentially be related to the induction of memory-associated genes such as c-Fos and Egr-1 by propofol. This study explored the effects of propofol on c-Fos and Egr-1 expression in rat hippocampal slices. FINDINGS/RESULTS:Hippocampal brain slices were exposed to varying concentrations of propofol at multiple time intervals. The transcription of the immediate early genes, c-Fos and Egr-1, was quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). MAPK/ERK inhibitors were used to investigate the mechanism of action. We demonstrate that propofol induced the expression of c-Fos and Egr-1 within 30 and 60 min of exposure time. At 16.8 muM concentration, propofol induced a 110% increase in c-Fos transcription and 90% decrease in the transcription of Egr-1. However, at concentrations above 100 muM, propofol failed to induce expression of c-Fos but did completely inhibit the transcription of Egr-1. Propofol-induced c-Fos and Egr-1 transcription was abolished by inhibitors of RAS, RAF, MEK, ERK and p38-MAPK in the MAPK/ERK cascade. CONCLUSIONS:Our study shows that clinically relevant concentrations of propofol induce c-Fos and down regulated Egr-1 expression via an MAPK/ERK mediated pathway. We demonstrated that propofol induces a time and dose dependant transcription of IEGs c-Fos and Egr-1 in rat hippocampal slices. We further demonstrate for the first time that propofol induced IEG expression was mediated via a MAPK/ERK dependant pathway. These novel findings provide a new avenue to investigate transcription-dependant mechanisms and suggest a parallel pathway of action with an unclear role in the activity of general anesthetics.

This study explored the effects of propofol on c-Fos and Egr-1 in neuroblastoma (N2A) cells. We demonstrate that propofol induced the expression of c-Fos and Egr-1 within 30 and 60 min of exposure time. At 16.8 microM concentration, propofol induced a 6 and 2.5-fold expression of c-Fos and Egr-1, respectively. However, at concentrations above 100 microM, propofol failed to induce expression of c-Fos or Egr-1. Propofol-induced c-Fos and Egr-1 transcription was unaffected by bicuculline, a gamma-aminobutyric acid-A receptor antagonist, but was abolished by PD98059, a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor. Our study shows that clinically relevant concentrations of propofol induce c-Fos and Egr-1 expression through an extracellular signal-regulated kinase mediated and gamma-aminobutyric acid-A independent pathway.