Intermittent Bolus versus Continuous Infusion of Propofol for Deep Sedation during ABR/Nuclear Medicine Studies.

Objective A comparison of intermittent bolus (IB) versus continuous infusion of propofol for deep sedation. Material and Methods A retrospective review of patients sedated for Auditory Brainstem Response (ABR)/nuclear medicine studies between September 2008 and February 2015. A ketamine bolus (0.5 mg/kg < 20 kg, 0.25 mg/kg > 20 kg) followed by propofol bolus of 1 mg/kg over 2 minutes. In the IB group, maintenance of deep sedation was with incremental bolus of 10 to 20 mg of propofol. In continuous infusion group (CG), maintenance was with a continuous infusion of 83 mcg/kg/min of propofol. Results Of the 326 cases completed, 181 were in CG group and 145 were in IB group. There were no statistical differences in patient's age, weight, and American Society of Anesthesiologist (ASA) classification. The cardiovascular and respiratory parameters in the two groups were not different statistically. Mean total propofol dose was higher in CG group versus IB group (CG 7.6 mg ± 3.6 mg, IB 6.5 mg ± 3.6 mg; p = 0.008). Procedure time in CG group was longer by 8 minutes compared with IB group (CG 49.8 min ± 25.4 min versus 42.3 min ± 19.2 min; p = .003). CG group has both shorter recovery time (CG 8.1 min ± 4.7 min versus IB 10.0 min ± 8.5 min; p = 0.01) and discharge time. Conclusion Satisfactory sedation and completion of the procedure was accomplished with both sedation protocols.

Effect of Hydroxyethyl Starch on Outcomes in High-Risk Vascular Surgery Patients: A Retrospective Analysis.

OBJECTIVE: To assess the effect of using hydroxyethyl starch (HES) for intraoperative fluid therapy on outcomes in high-risk vascular surgery patients. DESIGN: Retrospective case series. SETTING: Single-center academic hospital. PARTICIPANTS: The study included 1,395 adult vascular surgery patients with peripheral vascular disease. INTERVENTIONS: Retrospective review of hospital databases. MEASUREMENTS AND MAIN RESULTS: Outcomes were compared between patients who were intraoperatively administered HES (Voluven [Fresenius Kabi, Bad Homburg, Germany] or Pentaspan [Bristol-Myers Squibb Canada, Montreal, Quebec, Canada]) versus patients who received only crystalloids during their procedure. Logistic regression was used to assess for association between these groups and mortality (in-hospital, 30-day), intensive care unit admission, hemodialysis requirement, vasopressor requirement, and ventilator requirement. Overall, 796 patients had complete fluid records and were included in the analysis. After adjustment for potential confounders, receiving an HES solution was associated with increased likelihood of 30-day mortality (odds ratio [OR] 2.11, 95% confidence interval [CI] 1.05-3.80), postoperative requirement for hemodialysis (OR 6.17, 95% CI 1.09-35.10), intensive care unit admission (OR 3.52, 95% CI 2.15-5.74), and mechanical ventilation (OR 3.16, 95% CI 1.84-5.41). CONCLUSIONS: Intraoperative administration of HES was associated with an increased likelihood of adverse outcomes compared with use of crystalloids alone.

Deep Sedation for Pediatric Dental Procedures: Is this a Safe and Effective Option?

OBJECTIVE: Sedation may be needed for safe, effective completion of pediatric dental procedures. Procedural sedation is performed in a children's hospital based dental office. The three sedation approaches: a propofol-only (P-O) approach (2-3 mg/kg titrated to the needed level of sedation), an approach that includes either i.v. ketamine (K+P) (0.25 or 0.5 mg/kg) or i.v. fentanyl (F+P) (0.5-1 mcg/kg) prior to propofol administration. We sought to determine safety and efficacy of various propofol based sedation protocols. STUDY DESIGN: Retrospective review of 222 patients receiving a propofol-only (P-O), ketamine+propofol (K+P) or fentanyl+propofol (F+P) approach. RESULTS: There were 44 patients in P-O group, 154 in K+P group and 24 in F+P group with mean age (4.8±3.4 y) and mean weight (19.7±6.7 kg). All the patients completed procedures successfully. Mild hypoxemia occurred in 24% of cases and resolved with nasal cannula. Mean total dose of propofol was similar in all groups (P-O 8.2 mg/kg, K+P 9.5 mg/kg, F+P 9.6 mg/kg, p=0.15). Although procedure and recovery times were similar in all groups, discharge times in K+P group were significantly shorter than P-O group and F+P group respectively (K+P 9.35±8.93.min, P-O 13.57±10.42 min, F+P 10.42±4.40 p= 0.002). CONCLUSION: Sedation can be accomplished safely and effectively in a children's hospital based dental office using propofol-based sedation.

Propofol-Based Procedural Sedation with or without Low-Dose Ketamine in Children.

Objective Examine comparative dosing, efficacy, and safety of propofol alone or with an initial, subdissociative dose of ketamine approach for deep sedation. Background Propofol is a sedative-hypnotic agent used increasingly in children for deep sedation. As a nonanalgesic agent, use in procedures (e.g., bone marrow biopsies/aspirations, renal biopsies) is debated. Our intensivist procedural sedation team sedates using one of two protocols: propofol-only (P-O) approach or age-adjusted dose of 0.25 or 0.5 mg/kg intravenous ketamine (K + P) prior to propofol. With either approach, an initial induction dose of 1 mg/kg propofol is recommended and then intermittent dosing throughout the procedure to achieve adequate sedation to safely and effectively perform the procedure. Approach: Retrospective evaluation of 754 patients receiving either the P-O or K + P approach to sedation. Results A total of 372 P-O group patients and 382 K + P group. Mean age (7.3 ± 5.5 years for P-O; 7.3 ± 5.4 years for K + P) and weight (30.09 ± 23.18 kg for P-O; 30.14 ± 24.45 kg for K + P) were similar in both groups (p = NS). All patients successfully completed procedures with a 16% combined incidence of hypoxia (SPO2 < 90%). Procedure time was 3 minutes longer for K + P group than P-O group (18.68 ± 15.13 minutes for K + P; 15.11 ± 12.77 minutes for P-O; p < 0.01), yet recovery times were 5 minutes shorter (17.04 ± 9.36 minutes for K + P; 22.17 ± 12.84 minutes for P-O; p < 0.01). Mean total dose of propofol was significantly greater in P-O than in K + P group (0.28 ± 0.20 mg/kg/min for K + P; 0.40 ± 0.26 mg/kg/min for P-O; p < 0.0001), and might explain the shorter recovery time. Conclusion Both sedation approaches proved to be well tolerated and equally effective. Addition of ketamine was associated with reduction in the recovery time, probably explained by the statistically significant decrease in the propofol dose.

Comparison of cold crystalloid and colloid infusions for induction of therapeutic hypothermia in a porcine model of cardiac arrest.

INTRODUCTION: Large-volume cold intravenous infusion of crystalloids has been used for induction of therapeutic hypothermia after cardiac arrest. However, the effectiveness of cold colloids has not been evaluated. Therefore, we performed an experimental study to investigate the cooling effect of cold normal saline compared to colloid solution in a porcine model of ventricular fibrillation. METHODS: Ventricular fibrillation was induced for 15 minutes in 22 anesthetized domestic pigs. After spontaneous circulation was restored, the animals were randomized to receive either 45 ml/kg of 1°C cold normal saline (Group A, 9 animals); or 45 ml/kg of 1°C cold colloid solution (Voluven, 6% hydroxyethyl starch 130/0.4 in 0.9% NaCl) during 20 minutes (Group B, 9 animals); or to undergo no cooling intervention (Group C, 4 animals). Then, the animals were observed for 90 minutes. Cerebral, rectal, intramuscular, pulmonary artery, and subcutaneous fat body temperatures (BT) were recorded. In the mechanical ex-vivo sub study we added a same amount of cold normal saline or colloid into the bath of normal saline and calculated the area under the curve (AUC) for induced temperature changes. RESULTS: Animals treated with cold fluids achieved a significant decrease of BT at all measurement sites, whereas there was a consistent significant spontaneous increase in group C. At the time of completion of infusion, greater decrease in pulmonary artery BT and cerebral BT in group A compared to group B was detected (-2.1 ± 0.3 vs. -1.6 ± 0.2°C, and -1.7 ± 0.4 vs. -1.1 ± 0.3°C, p < 0.05, respectively). AUC analysis of the decrease of cerebral BT revealed a more vigorous cooling effect in group A compared to group B (-91 ± 22 vs. -68 ± 23°C/min, p = 0.046). In the mechanical sub study, AUC analysis of the induced temperature decrease of cooled solution revealed that addition of normal saline led to more intense cooling than colloid solution (-7155 ± 647 vs. -5733 ± 636°C/min, p = 0.008). CONCLUSIONS: Intravenous infusion of cold normal saline resulted in more intense decrease of cerebral and pulmonary artery BT than colloid infusion in this porcine model of cardiac arrest. This difference is at least partially related to the various specific heat capacities of the coolants.

Lipid emulsion combined with epinephrine and vasopressin does not improve survival in a swine model of bupivacaine-induced cardiac arrest.

BACKGROUND: This study sought to evaluate the efficacy of lipid emulsion in reversing bupivacaine-induced cardiovascular collapse when added to a resuscitation protocol that included the use of epinephrine and vasopressin. METHODS: After induction of general anesthesia and instrumentation, 19 mixed-breed domestic swine had cardiovascular collapse induced by an intravenous bolus of 10 mg/kg bupivacaine. After 5 min of resuscitation including chest compressions, epinephrine (100 microg/kg) and vasopressin (1.5 U/kg), animals were randomized to receive either a bolus of 20% lipid emulsion (4 ml/kg) followed by a continuous infusion (0.5 ml x kg(-1) x min(-1)) or an equal volume of saline. Investigators were blinded to the treatment assignment. The primary endpoint was return of spontaneous circulation (mean arterial pressure of at least 60 mmHg for at least 1 min). RESULTS: Treatment groups were similar with respect to baseline measurements of weight, sex, and hemodynamic and metabolic variables. The rates of return of spontaneous circulation were similar between groups: (3 of 10) in the lipid group and 4 of 9 in the saline group (P = 0.65). Total serum bupivacaine concentrations were higher in the lipid group at the 10-min timepoint (mean +/- SEM: 23.13 +/- 5.37 ng/ml vs. 15.33 +/- 4.04 ng/ml, P = 0.004). More norepinephrine was required in the lipid group compared to the saline group to maintain a mean arterial pressure above 60 mmHg during the 60-min survival period (mean +/- SEM: 738.6 +/- 94.4 vs.. 487.3 +/- 171.0 microg). CONCLUSIONS: In this swine model, lipid emulsion did not improve rates of return of spontaneous circulation after bupivacaine-induced cardiovascular collapse.

Regional changes in glial cell line-derived neurotrophic factor after cardiac arrest and hypothermia in rats.

Hypothermia after resuscitation from cardiac arrest reduces functional and histological brain injury. Stimulation of neurotrophic factors may contribute to the beneficial effects of hypothermia. This study examined the effects of cardiac arrest and induced hypothermia on regional levels of glial cell line-derived neurotrophic factor (GDNF) over the first 24 h after rat cardiac arrest. Hypothermia increased GDNF in hippocampus at 6 h, but did not prevent a subsequent decline in hippocampal GDNF. In contrast, hypothermia prevented early increases in cortical levels of GDNF at 3 and 6 h. Cerebellar GDNF increased slightly over 24 h in hypothermia-treated rats, but brainstem levels of GDNF did not change in response to cardiac arrest or hypothermia. These results suggest that temperature after resuscitation produces regionally specific changes of GNDF levels in brain.

Hypothermic reperfusion after cardiac arrest augments brain-derived neurotrophic factor activation.

Induction of mild hypothermia improves neurologic outcome after global cerebral ischemia. This study measured levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal tissue of rats after resuscitation from 8 minutes of normothermic, asphyxial cardiac arrest. After resuscitation, rats were maintained either at normal temperature (37 degrees C) or cooled to mild hypothermia (33 degrees C, beginning 60 minutes after resuscitation). After 12 or 24 hours, neurotrophin levels in hippocampus were measured by immunoblotting. Ischemia and reperfusion increased hippocampal levels of BDNF. Induction of hypothermia during reperfusion potentiated the increase in BDNF after 24 hours, but not after 12 hours. Levels of NGF were not increased by postresuscitation hypothermia. Hypothermia also increased tissue levels and tyrosine phosphorylation of TrkB, the receptor for BDNF. Increased BDNF levels were correlated with activation of the extracellularly regulated kinase (ERK), a downstream element in the signal transduction cascade induced by BDNF. In contrast to the many deleterious processes during ischemia and reperfusion that are inhibited by induced hypothermia, increasing BDNF levels is a potentially restorative process that is augmented. Increased activation of BDNF signaling is a possible mechanism by which mild hypothermia is able to reduce the neuronal damage typically occurring after cardiac arrest.