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Prevention of anesthesia-induced injection pain of propofol in pediatric anesthesia.

ABSTRACT: Propofol is a new anesthetic agent in clinical practice, but randomized double-blinded prospective studies on its role in pediatric anesthesia remain limited. We aimed to compare the preventive effects of pre-injected lidocaine or ketamine and its pre-mixture on the anesthesia-induced injection pain of propofol using a randomized double-blinded prospective method, and to compare the outcomes with those of medium-/long-chain propofol (M/LCT).A total of 360 pediatric patients (aged 5-12 years old) who received elective surgery were randomly divided into six groups (n= 60) as follows. S group: control group; L group: lidocaine group; L + P group: lidocaine + propofol group; K group: ketamine group; K + P group: ketamine + propofol group; M group: M/LCT group. After the drug fluid completely entered the cubital vein, the venous access was closed. During propofol injection, the injection pain was scored using the VRS 4-point scale. Meanwhile, the heart rates before and during injection were recorded, the adverse reactions during and after injection were observed, and the incidence rate and degree of pain were evaluated.The VRS 4-point scale showed that the incidence rates of injection pain of S group, L group, L + P group, K group, K + P group and M group were 78.3%, 66.67%, 51.66%, 43.33%, 48.33% and 45% respectively. The incidence rates of injection pain of all experimental groups were significantly lower than that of S group (P<0.01). The incidence rates of injection pain of L + P group, K group, K + P group and M group were significantly lower than that of L group (P<0.05). The differences among the other groups were not statistically significant.Intravenous pre-injection of lidocaine, ketamine or those mixed with propofol can all significantly reduce the incidence rate of injection pain of propofol.

SUBMITTER: Cheng D

PROVIDER: S-EPMC5510140 | biostudies-other | 2017 May-Jun

REPOSITORIES: biostudies-other

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Project description:Background: Propofol injection pain, despite various interventions, still occurs during the anesthesia induction and causes intense discomfort and anxiety in patients. This study aimed to explore the effect of intravenous dexmedetomidine on propofol injection pain prior to anesthesia induction with propofol at 4°C. Methods: A total of 251 patients (American Society of Anesthesiologists I-II) who underwent oral and maxillofacial surgery were randomly assigned to a combination group (n = 63), lidocaine group (n = 62), dexmedetomidine group (n = 63), and placebo-control group (n = 63); they received 0.5 ug/kg dexmedetomidine prior to anesthesia induction with propofol at 4°C, 40 mg lidocaine, 0.5 ug/kg dexmedetomidine prior to anesthesia induction, and normal saline, respectively. Incidence of pain, pain intensity, and reaction to the pain stimulus were evaluated by using verbal categorial scoring (VCS), a numerical rating scale (NRS), and the Surgical Pleth Index (SPI), respectively. In addition, hemodynamic parameters such as heart rate (HR) and mean arterial pressure (MAP) were also measured. The VCS and NRS were evaluated at 5 s after propofol injection. In addition, SPI, HR, and MAP were evaluated at three time points (before anesthesia induction and 5 and 30 s after propofol injection). Results: The incidence of pain in the combination group (51%) was significantly lower than that in the lidocaine group (71%), dexmedetomidine group (67%), or placebo-control group (94%) (p < 0.001). VCS and NRS scores in the combination group were also lower compared with the other three groups (p < 0.001), with no statistically significant differences between the lidocaine group and dexmedetomidine group (p > 0.05). The SPI of the combination group decreased significantly in comparison with the other three groups at 5 s after propofol injection (F = 96.23, p < 0.001) and 30 s after propofol injection (F = 4.46, p = 0.005). Further comparisons between HR and MAP revealed no significant differences across the groups (p > 0.05). Conclusion: Because of the sedative nature of dexmedetomidine and analgesic effect of low temperature, this study showed that intravenous dexmedetomidine prior to anesthesia induction with propofol at 4°C is highly effective in attenuating the incidence and severity of pain during injection compared with lidocaine (40 mg), dexmedetomidine 0.5 ug/kg) and placebo. This approach was not associated with any anesthesia complications. Clinical Trial Registration: ClinicalTrials.gov, identifier: ChiCTR-2000034663.

Project description:ObjectivePrevious studies suggested that slow injection of propofol may increase the hypnotic effect during induction of anesthesia. The aim of the present study was therefore to investigate whether injection rate of propofol has an influence on its maximum effect.DesignRandomized, single-blind trial.SettingThis study has been carried out in the operating rooms of a university hospital. An anesthesiologist and a resident performed the study with the aid of changing nursing staff.ParticipantsWe investigated 99 unpremedicated patients aged 18 to 60 years with American Society of Anesthesiologists (ASA) physical status 1-3.InterventionsAnesthesia was induced by intravenous injection of propofol (2 mg/kg). Propofol was manually injected in group 1 over a period of 5 s; in group 2 (120-s injection interval), and in group 3 (240-s injection interval), propofol was administered by an injection pump. After loss of consciousness, mask ventilation was performed with 100% oxygen. Bispectral index (BIS) was used to measure the hypnotic effect of propofol. After the decrease of BIS to the minimum value (i.e., maximum hypnotic effect) and the following increase of BIS to 60, the study period was finished and anesthesia was performed according to clinical criteria.Outcome measuresWe analyzed whether injection speed has an influence on the maximum hypnotic effect of a given dose of propofol (2 mg/kg).ResultsBIS(min) marks the maximum electroencephalogram (EEG) effect of the propofol bolus as measured by the BIS. The lowest mean BIS(min) was measured in group 1 (28.7 +/- 10.3). In group 2, BIS(min) was 33.0 (+/-13.9), and in group 3, BIS(min) was 36.4 (+/-11.0). There were no significant differences between group 2 and groups 1 or 3, but there were significant differences between groups 1 and 3. In group 1, BIS(min) was reached after 102.91 s (+/-44.20), in group 2 after 172.33 s (+/-29.76), and in group 3 after 274.21 s (+/-45.40). These differences were statistically significant for all comparisons. In summary, the lowest value for BIS(min) was achieved in the group with the fastest rate of propofol injection (group1, 5 s). The highest BIS(min) was obtained in the group with the slowest rate of injection (group 3, 240 s). The hemodynamic parameters were not significantly different among groups.ConclusionsThe hypnotic peak effect of propofol is lower with extremely slow injection (240 s versus 5 s). For clinically usual injection rates (5 s and 120 s), there was no significant difference in propofol peak effect.

Project description:General anesthesia has revolutionized healthcare over the past 200 years and continues to show advancements. However, many phenomena induced by general anesthetics including paradoxical excitation are still poorly understood. Voltage-gated sodium channels (Na V ) were believed to be one of the proteins targeted during general anesthesia. Based on electrophysiological measurements before and after propofol treatments of different concentrations, we mathematically modified the Hodgkin-Huxley sodium channel formulations and constructed a thalamocortical model to investigate the potential roles of Na V . The ion channels of individual neurons were modeled using the Hodgkin-Huxley type equations. The enhancement of propofol-induced GABAa current was simulated by increasing the maximal conductance and the time-constant of decay. Electroencephalogram (EEG) was evaluated as the post-synaptic potential from pyramidal (PY) cells. We found that a left shift in activation of Na V was induced primarily by a low concentration of propofol (0.3-10 μM), while a left shift in inactivation of Na V was induced by an increasing concentration (0.3-30 μM). Mathematical simulation indicated that a left shift of Na V activation produced a Hopf bifurcation, leading to cell oscillations. Left shift of Na V activation around a value of 5.5 mV in the thalamocortical models suppressed normal bursting of thalamocortical (TC) cells by triggering its chaotic oscillations. This led to irregular spiking of PY cells and an increased frequency in EEG readings. This observation suggests a mechanism leading to paradoxical excitation during general anesthesia. While a left shift in inactivation led to light hyperpolarization in individual cells, it inhibited the activity of the thalamocortical model after a certain depth of anesthesia. This finding implies that high doses of propofol inhibit the network partly by accelerating Na V toward inactivation. Additionally, this result explains why the application of sodium channel blockers decreases the requirement for general anesthetics. Our study provides an insight into the roles that Na V plays in the mechanism of general anesthesia. Since the activation and inactivation of Na V are structurally independent, it should be possible to avoid side effects by state-dependent binding to the Na V to achieve precision medicine in the future.

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Prevention of anesthesia-induced injection pain of propofol in pediatric anesthesia.

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