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PEDIATRIC ANESTHESIOLOGY

Somatosensory Evoked Potentials by Median Nerve Stimulation in Children During Thiopental/Sevoflurane Anesthesia and the Additive Effects of Ketoprofen and Fentanyl

Susanna Westerén-Punnonen, MD^*, Heidi Yppärilä-Wolters, PhD^*, Juhani Partanen, MD, PhD^*, Kari Nieminen, MD, Antti Hyvärinen, MD^||, and Hannu Kokki, MD, PhD^¶

From the *Department of Clinical Neurophysiology, Kuopio University Hospital, Finland; VTT Information Technology, Tampere, Finland; Department of Clinical Neurophysiology, Helsinki University Hospital, Jorvi Hospital, Espoo, Finland; Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Finland; ||Department of Otorhinolaryngology, Kuopio University Hospital, Finland; ¶Department of Pharmacology and Toxicology, University of Kuopio.

Address correspondence and reprint requests to Susanna Westerén-Punnonen, Department of Clinical Neurophysiology, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland. Address e-mail to susanna.westeren-punnonen{at}kuh.fi.

Abstract

BACKGROUND: Somatosensory evoked potentials (SEPs) are used to determine the spinal cord and brain function during surgical procedures. In general, SEPs are sensitive to volatile anesthetics, but little is known about the effects of anesthesia maintenance with sevoflurane on SEPs in children. Analgesics are often provided during anesthesia, and supplementary drugs may also affect the SEPs. In this prospective clinical trial of 27 healthy, 3- to 8-yr-old children, we evaluated the effects of sevoflurane anesthesia after IV induction with benzodiazepine and barbiturate on median nerve SEP. In addition, the effects of two analgesics (ketoprofen and fentanyl) on SEPs were evaluated.

METHODS: Median nerve SEPs were recorded before premedication with midazolam 0.1 mg/kg IV, and at three separate times during anesthesia maintenance with sevoflurane 2% end-tidal concentration in air/oxygen (after 15 min of sevoflurane inhalation), supplemented with/without ketoprofen 1 mg/kg (after 25 min) and fentanyl 1 µg/kg (after 35 min).

RESULTS: Compared with baseline measurements, an increase both in N20 latency (P = 0.015) and in central conduction time (P = 0.001) was noted during anesthesia maintenance with sevoflurane. The administration of analgesics did not have an influence on the N20 latency or central conduction time. In children 5 to 8 yr of age, the mean cortical N20-P25 amplitude was decreased (P = 0.008). In addition, in older children, the N20-P25 amplitude decreased after the co-administration of ketoprofen and fentanyl compared with the values measured before the analgesics (P = 0.03). These decreases were not seen in the younger children.

DISCUSSION: In children, anesthesia maintenance with 2% sevoflurane prolongs median SEP latencies in a manner that is similar to those reported for other volatile anesthetics. However, SEP monitoring can be done with sevoflurane inhalation, but the dosage should be adjusted due to interindividual variabilty. Co-administration of ketoprofen, and fentanyl did not affect the SEP latencies, but post hoc analysis suggested that older children had a decrease in cortical amplitudes.

Somatosensory evoked potentials (SEPs) are used in anesthetized children to monitor the somatosensory pathways during neurosurgical and orthopedic spinal procedures. When performing SEPs intraoperatively, median nerves or posterior tibial nerves are most often used. Cortically generated SEP components are sensitive to anesthetics, and the effects of various anesthetics have been extensively investigated in adults.1–4 It has been shown that subcortical and peripheral responses were more resistant to the effects of anesthesia than cortical waves.5

Sevoflurane, a potent halogenated volatile anesthetic, is often used to induce and maintain anesthesia in pediatric patients.6 In 2004, half of the general anesthetics sold in Finland were halogenated inhalation drugs, and most of the administered inhaled anesthetics (>80%) were sevoflurane.7 Halogenated inhaled anesthetics usually produce a dose-related increase in latency and reduction in amplitude of the cortically recorded SEPs in adults.8 In children, cortical responses are more variable, and the inherent instability seems to be greatly increased by anesthetics.9 The variability is dependent upon the anesthetic regimen used. Anesthesia induction with IV anesthetics (e.g., with midazolam and thiopental) and maintenance of anesthesia with sevoflurane is a common technique.10 Reported experience concerning the effects of sevoflurane maintenance on median nerve SEPs in children has been limited.

Opioid analgesics are often provided during anesthesia, and inhaled anesthesia may be supplemented with a short-acting opioid agonist, e.g., fentanyl.11 Effective preventive pain management in children undergoing surgery has increased the use of perioperative nonopioid analgesics, e.g., a nonsteroidal antiinflammatory drugs.12 However, little is known about the SEP effects of analgesics during anesthesia maintenance.1,13

We planned this prospective clinical trial of anesthesia induction with IV midazolam and thiopental followed by a maintenance with sevoflurane in combination with IV opioid with or without ketoprofen, (a traditional nonsteroidal antiinflammatory drug). We recorded the median nerve SEP before premedication and three times during anesthesia maintenance. The aim of our pediatric study was to 1) evaluate the SEP effects of sevoflurane maintenance after induction with IV midazolam and thiopental, and 2) to determine the effect of two analgesic adjuvants (ketoprofen and fentanyl) on the latencies and amplitudes of the median nerve SEP. Our hypothesis was that analgesic adjuvants may be used safely during sevoflurane inhalation without adversely affecting the SEP monitoring.

METHODS

The present trial is a part of our SEVO-SEP-study in which we evaluated, in addition to SEPs, different cardiovascular and electroencephalogram variables of young children anesthetized with sevoflurane. The electroencephalogram data of these children has already been published.10 The study protocol was approved by the Research Ethics Committee of the Hospital District of Northern Savo, Kuopio, Finland and was conducted in accordance with the Declaration of Helsinki.14 Both parents and children received information, and all parents of children asked to participate gave a written consent.

Patients
We studied 30 generally healthy children (aged, 3–8 yr) who underwent adenoidectomy in our day-case surgery unit. Patients having a history of neurological disorders, medication affecting the nervous system, asthma, kidney, liver dysfunction, or bleeding diathesis were excluded.

Study Protocol
A standardized anesthetic technique was used for all children (Fig. 1). All children had an IV cannula placed in the right arm. After midazolam 0.1 mg/kg IV premedication, anesthesia was induced with thiopental 5 mg/kg IV. Tracheal intubation was facilitated by cisatracurium 0.1 mg/kg IV and the lungs were ventilated with 40% oxygen in air. Sevoflurane was started 4 min after the induction, the end-tidal concentration was set at 2% and the children were kept normothermic, body temperature >36.5°C (monitored continuously by Cardiocap/5, Datex-Ohmeda, Helsinki, Finland).

View larger version (12K): [in this window] [in a new window]   Figure 1. Flowchart of the study.

This was a double-blind study and the patients were randomized using a computer-generated randomization sequence into two study groups. Children randomized into the ketoprofen group received ketoprofen (Ketorin, Orion, Espoo, Finland) 1 mg/kg mixed with normal saline to 10 mL injected IV over 2 min. Children in the placebo group received normal saline. Drug syringes with a similar appearance were prepared by a nurse not otherwise involved in the study, thus ensuring blinding. All children were given fentanyl 1 µg/kg IV 10 min after test drug injection.

The SEPs were recorded four times from each patient:

• At baseline before premedication (Baseline).
  
• Four minutes after the sevoflurane 2% end-tidal concentration was reached (Sevoflurane).
  
• Four minutes after the test drug injection (Ketoprofen/Placebo).
  
• Four minutes after the fentanyl injection (Fentanyl).
  

Recording of SEPs
SEPs to median nerve stimulation were recorded with a four channel evoked potential analyzer (Neuropack Four Mini®, Nihon Kohden, Tokyo, Japan). The left median nerve was stimulated at the wrist using surface electrodes. Constant current square wave pulses of 0.2 ms duration were delivered at a frequency of 5 Hz, and the stimulus amplitude was adjusted to produce a visible thumb twitch. During anesthesia, the stimulus intensity was doubled and it ranged from 2.4 to 5.6 mA.

The SEPs were recorded with Ag/AgCl surface disk electrodes for elbow joint (the active electrode over the fossa cubitalis, and the reference on the medial epicondyle), cervical C II (active electrode over the second cervical spinous process, and reference electrode over the frontal scalp), and cortical (active electrode over the right somatosensory cortex, 2 cm posterior to vertex and 7 cm towards the auricular helix, reference electrode at Fz) SEP components. Electrode-skin impedances were kept less than 5 k Ohm throughout the study.

The sampling frequency was set at 10 kHz, the bandpass filter at 20 Hz to 3 kHz, and the analysis time for each channel at 50 ms. Automatic artifact rejection was used for rejecting epochs including noise. Two-hundred responses, repeated two times for each patient, were averaged at each recording condition. The reproducibility was assessed by superimposing the traces on the screen.

Analysis of SEPs
Analysis of the median nerve SEPs was conducted off-line. The peaks were labeled according to their polarity and peak latency in adults. We simultaneously recorded the potential N6 from the left elbow joint, the potential N13 from the upper neck (CII-Fz), and the potential N20 from the postcentral scalp overlying the somatosensory cortex (C4'-Fz). The latencies were determined at the negative peak of the wave for the N6 and N20 potentials. The recordings from the upper neck revealed a sequence of 1–3 negative potentials, and the N13 peak latency was measured at the maximum amplitude of the broad N13 complex. The N13 amplitude was measured from baseline to peak, whereas the amplitude of the N20–P25 complex was measured from the maximum negative deflection (N20) to the maximum of the following positive deflection (P25). Interpeak latencies N6–N13 (peripheral conduction time) and N13–N20 (central conduction time) were calculated as well.

Statistical Analysis
We did not perform formal sample size calculation, but a sample size of 12 children in both study groups was considered to be sufficient while evaluating the effect of two analgesic regimens. For post hoc analysis, while investigating the influence of patient age on the anesthesia-induced changes in SEP amplitude and latency values, patients (n = 27) were divided into two groups based on their age (3–4 yr [n = 17] and 5–8 yr [n = 10]).

The influence of patient age and height on the SEP amplitude and latency was investigated with univariate general linear model analysis. To analyze the effects of sevoflurane, ketoprofen, and fentanyl on the peripheral conduction time and SEP latency, analysis of variance for repeated measurements was applied. The Wilcoxon’s signed ranks test was used to investigate the effect of anesthesia on SEP amplitude and central conduction time, whereas the Mann-Whitney test was applied for post hoc analysis to investigate the differences between the groups divided based on patient age. In all tests, the level of significance was set to be P < 0.05. All statistical analysis comparisons were conducted with the Statistical Package for Social Sciences (SPSS for Windows 11.5, SPSS, Chicago).

RESULTS

There were three major protocol deviations; two children received midazolam and one child received thiopental before the baseline measurements because they were too agitated for recordings. They were excluded from the analysis. There were also some minor protocol deviations: the cervical N13 was not recordable in four children at baseline and in one child during sevoflurane anesthesia, and N20 was not recordable in one child at baseline. Thus, the total number of children analyzed was 27, and a complete data set was recorded for 22 children. Patient characteristics are shown in Table 1.

Cervical (N13) and cortical (N20) potential latencies, interpeak latencies (N6–N13 and N13–N20), and cortical N20–P25 amplitude at the various stages of the study are shown in Table 2. When adjusted for height, the SEP latencies and peripheral conduction times did not correlate to age.

Sevoflurane inhalation of 20–30 min duration at end-tidal concentration of 2% prolonged the cortical N20 latency compared with the latency at baseline [at baseline 15.9 (sd 0.7) ms vs after sevoflurane 19.7 (sd 2.0) ms; mean difference 3.9 ms; 95% confidence interval of the difference: 3.1 to 4.6 ms; P = 0.015]. Sevoflurane did not affect the N6 and N13 latencies. During sevoflurane anesthesia, the somatosensory central conduction time increased (interpeak latency N13–N20; P = 0.001) (Fig. 2), while the peripheral conduction time (interpeak latency N6–N13) did not change.

View larger version (22K): [in this window] [in a new window]   Figure 2. The somatosensory central conduction time (interpeak latency N13–N20). Somatosensory evoked potentials (SEP) recordings were performed at baseline before premedication (Baseline), after the sevoflurane 2% end-tidal concentration was reached (Sevo), after the test drug injection (Tested drug), and after the fentanyl injection (Fentanyl). The results are shown as mean + sd. *P < 0.001.

At baseline, the amplitude of the cortical N20–P25 complex ranged between 1 and 9 µV. The mean cortical N20–P25 amplitude was decreased (P = 0.002) during sevoflurane inhalation compared with baseline (Fig. 3). The post hoc analysis revealed that the N20–P25 amplitude was decreased in older children (aged, 5–8 yr) (P = 0.008), but this was not seen in the younger children (aged, 3–4 yr). However, the variation of anesthesia-induced SEP amplitude change was significantly higher in patients younger than 5 yr of age (Fig. 4).

View larger version (19K): [in this window] [in a new window]   Figure 3. The mean cortical N20–P25 amplitude. SEP recordings were performed at baseline before premedication (Baseline), after the sevoflurane 2% end-tidal concentration was reached (Sevo), after the test drug injection (Tested drug), and after the fentanyl injection (Fentanyl). The results are shown as mean + sd. *P = 0.002.

View larger version (14K): [in this window] [in a new window]   Figure 4. Anesthesia-induced SEP N20–P25 amplitude change as a function of patient age.

After the co-administration of ketoprofen and fentanyl, both the N13 and N20 latencies, central conduction time, and the N20–P25 amplitude remained stable compared with the values measured after the sevoflurane 2% end-tidal concentration was reached. However, the post hoc analysis revealed that the N20–P25 amplitude was decreased (P = 0.03) in older children (aged, 5–8 yr) after the co-administration of the two analgesics as compared with the values measured during the sevoflurane inhalation (data not shown).

DISCUSSION

Intraoperative monitoring of SEPs is used in spinal and intracranial surgery to assess the functional integrity of the sensory pathways. However, cortical SEPs are sensitive to anesthetics.5 Evoked potentials have been extensively evaluated during anesthesia in adults,15 but less is known about the anesthetic effects on SEPs in children. SEPs are also increasingly used as monitoring tools in pediatric surgery; therefore, it is important to gather background information in the target population.

In clinical trials, volatile anesthetics are commonly administered as single drugs to avoid interaction with other drugs. However, this is not often the clinical routine, and therefore we designed the present study to determine the effects of anesthesia maintenance with sevoflurane after IV induction with midazolam and thiopental.

This study showed that sevoflurane increased the latency of the cortically recorded median nerve N20 component by 25% following induction with midazolam and thiopental in children. The latency delay of the cortical components resulted from the increased somatosensory central conduction time, while no or only minor changes were recorded in the peripheral and cervical SEP latencies after median nerve stimulation. In addition to the increase in N20 latency, some changes were also recorded in the amplitudes. The mean cortical N20–P25 amplitude decreased by 32% during sevoflurane anesthesia compared with baseline, but there was a large interindividual amplitude variation in the responses to sevoflurane anesthesia (–77% to + 118%). Moreover, it should be noted that the 4 min of constant end-tidal sevoflurane may not have been enough time for a maxium SEP effect to be seen.

The post hoc analysis revealed that the variation of anesthesia-induced SEP amplitude changes was significantly higher in children less than 5 yr of age, than in children of ages 5 to 8 yr. This phenomenon could be explained by the higher sensitivity and increased variability of the cortical response in young children. This may be related to maturational changes that take place in the somatosensory system in the first decade of life, and these changes are thought to be a combination of asynchronous myelination and synaptogenesis.9,16 In young children, this inherent instability of the cortical response seems to be greatly increased by anesthetics.9

Studies in adults have shown that, in adults, volatile anesthetics produce a dose-dependent increase in the SEP latency, an increase in the central conduction time, and a decrease in the amplitude.15 Sevoflurane causes a dose-related increase in the latency of early cortical SEP components17 and a decrease in the N20–P25 amplitude.18 Increases in the latency and decreases in amplitude occur at doses of 1.5 minimum alveolar concentration (MAC) sevoflurane or less, with minimal effects on subcortical SEP components.15 Jäntti et al.19 reported that a high-amplitude early cortical SEP waveform is found with the absence of all later potentials during 1.5–2.5 MAC sevoflurane administration at low stimulation rates. In the present study, we used sevoflurane at the end-tidal concentration of 2% which corresponds to 1 MAC in this age group.20 Similar effects on early cortical SEP components were found as have been earlier reported in adults.15,17,18 Unfortunately, we did not record the late cortical potential components which are the most sensitive to volatile anesthetics. Thus, we cannot comment on the effects of sevoflurane inhalation on these components in young children.

Few studies have been performed on the associated effects of inhaled anesthesia on SEPs in children. Mason et al.21 have demonstrated dose-related changes in the N20 and P22 components of the median nerve SEP with increasing end-tidal concentrations of isoflurane. da Costa et al.22 have shown a dose-dependent amplitude reduction and increase in latency in the SEP potentials when sevoflurane is used alone. An additional suppression was seen when nitrous oxide was added to sevoflurane. Contrary to the present study, where the baseline measurements were made on unmedicated children, in da Costa et al. ’s study all children received a relatively large dose of midazolam 0.7 mg/kg orally 30 min before induction of anesthesia.

Midazolam is frequently used for premedication in pediatric anesthesia.23 In the absence of other drugs, midazolam 0.2 mg/kg IV followed by an infusion of 5 mg/h produced a depression of cortical SEP amplitude and a slight prolongation of median SEP latency.24 In our study, the children only received a midazolam bolus 0.1 mg/kg 5 min before anesthesia induction and, therefore, the influence of midazolam was assumed to be minor.

A single dose of thiopental 4 mg/kg causes only a minor increase in the latency of the early cortical median SEP.25,26 The response of cortical amplitude to thiopental is variable. In some previous studies, thiopental had no significant effect on the cortical amplitude.1,25 In contrast, Sloan et al.26 reported that the most marked change is a reduction in cortical amplitude, an effect that lasts for at least 12 min after the IV injection of thiopental; however, the individual response of the amplitude was variable. Therefore, the effect of thiopental on the SEPs in our study cannot be completely excluded.

In the present study, we also evaluated the effect of analgesic adjuvants (ketoprofen and fentanyl) on the latencies and amplitudes of the median nerve SEP in children. The present study demonstrated that no significant changes in SEP latencies or amplitudes are observed after a single dose of fentanyl or ketoprofen administered during sevoflurane anesthesia.

However, the co-administration of ketoprofen and fentanyl may have an additional depressant effect on cortical amplitude. In a post hoc analysis, that was more significant in the older children (5–8 yr of age). Large variability in amplitudes seen in the younger children may have precluded finding any difference. Further studies with a larger sample size are needed to define this phenomenon more precisely.

In children, inhaled anesthesia is commonly supplemented with intraoperative fentanyl.11 In earlier studies in adults, high-dose fentanyl was reported to produce a modest increase in the cortical median nerve SEP latency25,27 and a variable decrease in the cortical response amplitude.27 However, no modification in SEPs was observed after an analgesic dose of fentanyl 1 µg/kg28 or after low-dose fentanyl 200 µg used alone.29 Although, the addition of fentanyl 10 µg/kg to midazolam has no significant effect on evoked potentials, when administered in conjunction with thiopental, fentanyl has an additional depressant effect on cortical amplitude.1 To our knowledge, there are no previous studies on the effect of ketoprofen on median nerve SEPs.

In conclusion, this study shows that in children maintenance of anesthesia with 2% sevoflurane increases the median nerve SEP latencies. Addition of ketoprofen or fentanyl to sevoflurane has no significant effect on median nerve SEPs, but co-administration of these two analgesics may decrease cortical SEP amplitudes in older children.

Footnotes

Accepted for publication April 25, 2008.

Supported by funds from the Kuopio University Hospital but not from external sources.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Westerén-Punnonen, S. Articles by Kokki, H. Search for Related Content PubMed PubMed Citation Articles by Westerén-Punnonen, S. Articles by Kokki, H. Related Collections Neuroanesthesia Monitoring (Non-cardiac) Clinical Pharmacology Pediatrics Pharmacology