Emergence Delirium in children is not related to intraoperative Burst Suppression – prospective, observational Electrography study

doi:10.21203/rs.2.9124/v2

Download PDF

Research article

Emergence Delirium in children is not related to intraoperative Burst Suppression – prospective, observational Electrography study

https://doi.org/10.21203/rs.2.9124/v2

This work is licensed under a CC BY 4.0 License

Journal Publication

published 08 Aug, 2019

Read the published version in BMC Anesthesiology →

You are reading this older preprint version

Read the latest preprint version →

Background: Emergence-delirium is the most frequent brain dysfunction in children recovering from general anaesthesia, though the pathophysiological background remains unclear. The presented study analysed an association between emergence delirium and intraoperative burst suppression activity in the electroencephalogram, a period of very deep hypnosis during general anaesthesia. Methods: In this prospective, observational cohort study at the Charité - university hospital in Berlin / Germany children aged 0.5 to 8 years, undergoing planned surgery, were included between September 2015 and February 2017. Intraoperative bi-frontal electroencephalogram were recorded. Occurrence and duration of burst suppression periods were visually analysed. Emergence delirium was assessed with the Pediatric Assessment of Emergence Delirium Score. Results: From 97 children being analysed within this study, 40 children developed emergence delirium, and 57 children did not. Overall 52% of the children displayed intraoperative burst suppression periods; however, occurrence and duration of burst suppression (Emergence delirium group 55% / 261+462sec vs. Non-emergence delirium group 49% / 318+531sec) did not differ between both groups. Conclusions: Our data reveal no correlation between the occurrence and duration of intraoperative burst suppression activity and the incidence of emergence delirium. Burst suppression occurrence is frequent; however, it does not seem to have an unfavourable impact on cerebral function at emergence from general anaesthesia in children.

Internal Medicine Specialties

Burst suppression

Paediatrics: pre-operative anxiety

EEG: high dose opiates

Postoperative delirium is the most frequent brain dysfunction in patients recovering from general anaesthesia, mainly seen in preschool children as well as in elderly patients (1, 2).

In preschool children, postoperative delirium occurs during emergence from anaesthesia during stay in the post-anaesthesiological care unit (emergence delirium) and presents with acute disorientation, crying, agitation and missing response to the surrounding (3). Emergence delirium (ED) in children is mostly self-limited and has a benign course; however, it increases the risk of self-injury and induces stress to the medical staff as well as to the caregivers. The implications to long-term outcomes in cognitive function in children is still under discussion.

Pediatric anaesthesiologists are concerned, since it has been proposed that anaesthetic agents may be neurotoxic to the developing brain (4, 5).

In children elevated concentrations of the anaesthetic agent Sevoflurane cause an increase of epileptiform discharges during anaesthesia induction (6). In a former EEG analysis - focusing on the period of anaesthesia induction in the same patients group presented here - we had shown that the occurrence of interictal, epileptiform discharges, is positively related to the development of ED (7). In a study from Martin and colleagues, analyzing multichannel EEG characteristics in 12 children, from whom 5 developed ED, ED was associated with arousal from an indeterminate state (low voltage / fast frequency EEG activity) and an increased frontal cortical functional connectivity (8). All these EEG characteristics - interictal, epileptiform discharges; indeterminate state; increased frontal cortical functional connectivity - are related to a cortical state of hyperexcitability.

On the other hand, elevated concentration of anaesthetic agents will induce deeper level of sedation and periods of Burst Suppression in the EEG during general anaesthesia. It has been proved, that periods of Burst Suppression and deep Index level of anaesthesia in elderly patients trigger postoperative delirium (9-12). In contrast in children, two studies analyzing Index level of anaesthesia and its relationship with the occurrence of ED did not find this correlation (13, 14). But a study focusing on intraoperative Burst Suppression periods and the correlation with ED in children is still failing.

The aim of this study is to analyses, if the occurrence and duration of Burst Suppression pattern during general anaesthesia are related to the development of ED in children.

This prospective, observational cohort study (NCT02481999) was approved by our local ethics committee on 12 March 2015 (Ethik committee Charité, University Medicine of Berlin / Chairperson Prof. Dr. R. Seeland / EA2/027/15). Written informed consent of either parents or legal proxies was obtained according to the Declaration of Helsinki. We included children aged 0.5 – 8 years, undergoing elective surgery with a planned duration of > 60min at our University hospital – Charité / Berlin. Between September 8, 2015 and February 22, 2017 parents or legal proxies of the child were approached by study staff members during stay in the preoperative evaluation center on the day prior to surgery. Exclusion criteria comprised any history of neurological or psychiatric diseases, any signs of delayed development in the child, isolation required because of multiresistant bacteria, inability of the parents to speak, read or understand the German language, as well as concurrent enrollment in another study.

The a priori primary outcome was ED assessed during stay in the recovery room with the Pediatric Assessment of Emergence Delirium (PAED) Score (15). Values of at least 10 were considered as ED.

Secondary outcomes, related to frontal EEG recordings were depth of anaesthesia and burst suppression duration.

Oral premedication with midazolam was administered in all children. Children were anaesthetised with either Propofol or Sevoflurane as decided by the anaesthesiologist in charge. Standard monitoring included non-invasive blood pressure, electrocardiogram and pulse oximetry. Patients received i.v. Propofol (assessed as mg kg^-1 body weight) or mask induction / maintenance with Sevoflurane (assessed as endtidal concentrations et Vol %). Dosage of Sevoflurane and Propofol was given according to clinical needs and chosen by the anaesthesiologist in charge. Remifentanil was administered as analgesic agent during the induction period in all children, according to clinical needs. If muscle relaxation was needed, Cis-atracurium was administered, adapted to body weight. Before end of surgery, children received Metamizol or Paracetamol and / or Piritramid as analgesia medication. Some children also received regional anaesthesia. The complete anaesthetic procedure and medication were outside of the scope of this study.

ED assessment

ED was assessed according to the PAED Score. From admission to the post-anaesthesiological care unit until discharge, the PAED score was determined 1min after extubation, at arrival in the recovery room, 5min, 10min, 15min, 30min, 45min, and 60min during stay in the recovery room and at discharge from the recovery room by a member of the study staff sitting next to the child. Values > 10 were considered emergence delirium (15). The “Faces Legs Activity Cry Consolability Pain Scale” was used to determine pain events (16). Richmond Agitation Sedation Scale score was used to assess the level of consciousness (17). PAED score was only included in the analysis if the Richmond Agitation Sedation Scale score was above -2 and if it was unlikely that pain was triggering agitated behavior. If inadequate behavior during stay in the recovery room improved after pain-medication, these periods of agitated behavior were not classified as ED. If a member of the study team was unable to take the PAED score in the recovery room, the child were excluded from further evaluation.

EEG recording and analysis

Bi-frontal EEGs were obtained with the Narcotrend Monitor (MT Monitor Technik, Bad Bramstedt, Germany). EEG was recorded continuously from baseline before start of anaesthesia until the end of stay in the recovery room. After skin preparation with alcohol four electrodes (Ambu BlueSensor, Bad Nauheim Germany) were placed on the patients’ forehead at positions Fz, F7 and F8, with a reference at Fp2. The impedances were kept below 8kOhm, differences between electrodes were less than 2kOhm. During the EEG recording, event markers comprising “start of anaesthesia”, “intubation”, “operation” and “extubation” and “recovery room” were placed. “Start of anaesthesia” was defined as the time-point when the anaesthesiologist began to administer the anaesthetic agent, i.e., either Sevoflurane, Propofol or a mixture of both. “Intubation” was defined as the time point, when the anaesthesiologist in charge began to intubate the child. “Operation” indicated a time point within 15 min to 30 min after intubation of stable surgery and anaesthesia, without severe pain events or intraoperative bolus application of Propofol. “Extubation” was defined as the time point, when the anaesthesiologist in charge extubated the child.

Raw EEG data were recorded by a high pass filter of 0.5 Hz and a low pass filter of 45 Hz, sampling rate was 128 / sec. Visual EEG analysis (EEG viewer software: 50µV-100µV and 1s/div) was performed from the time point of “start of anaesthesia” until “extubation”. Raw EEG was analysed by an expert (S. K., neurologist with specialization in clinical neurophysiology and EEG) blinded to the ED outcome, the medication patients received and further clinical data. The presence of Burst Suppression periods was validated by a second expert (C.P. pediatric neurologist with specialization in electroencephalography in children). Short periods (< 5 min within the total anaesthesia procedure) with artifacts (muscle, eyelid, and electricity) were excluded from any further analysis. If persistent artifacts or repeating artifacts were seen, these EEGs were excluded from further analysis.

Burst Suppression periods were assessed by visual inspection of the raw EEG (EEG viewer software: 50µV and 1s/div). Burst Suppression segments were included if duration of isoelectric line exceeded 2 seconds. Duration of intraoperative Burst Suppression was calculated from start of the first isoelectric line segment until the end of the last isoelectric line. Isoelectric line is classified as an EEG activity below 5µV (18). We calculated the duration of the isoelectric line activity by distracting the time duration of the intermittent burst activity. Duration of the isoelectric line is the sum of all periods of isoelectric line presented in the raw EEG. Additionally, we calculated the Burst Suppression strength, by dividing Burst Suppression duration over isoelectric line duration indicating the relationship between the fraction of isoelectric line within the Burst Suppression pattern, were prolonged duration of an isoelectric line will show a Burst Suppression strength value tending towards 1; indicating a deeper stage of coma level.

Statistical Analysis

The present study was designed as a prospective, observational study. Statistical analysis was performed using SPSS, version 25, copyright SPSS, Inc., Chicago, IL 60606, USA. Data are presented as means + SD, in case of unbalanced data distribution as medians (IQR 25/75) or as frequencies (%). For nominal data, statistical analysis was performed by Chi-square test from Pearson. Numerical data were analysed using the Mann-Whitney-U test for non-parametric data. To determine the impact of age, anaesthetic medication, burst suppression and depth of anaesthesia on the incidence of ED, we performed a univariate logistic regression. Odds Ratio with 95% confidence intervals and corresponding p-values were calculated for each risk factor. Spearman Rho correlation test was used to analyse the correlation between age (month) and Burst Suppression duration, isoelectric line duration and Burst Suppression strength. Statistical significance was assumed at p<0.05.

The statistical analysis plan was made prior to data assessment. To calculate the sample size needed, we postulated an ED incidence of 10.5% (from a pilot study in our department 2013 (NCT02358278), resulting in a 10.5% incidence of ED in children aged 0-14 years) and an increased risk to develop ED with an increase in depth of anaesthesia and the occurrence of burst suppression periods. 470 patients were initially planned to be included in this study. An interim analysis was planned (after approximately 1/3 – 1/2 of the total planned sample size) with recalculation of the initial sample size calculation, to adopt the study procedure, when the initial assumptions would differ strongly. At the interim analysis the ED incidence rate were distinctly higher, what is most likely related to the fact that we mainly included younger patients in our actual study compared to the pilot study 2013 in our department. We re-run the sample size calculation taking into account the new incidence rate of 41%. Initially, the study was planned for an odds ratio of 1.6 with an ED incidence rate of 10.5% and a R² of the other covariates of 0.2 resulting into a sample size of 470 children with a power of 80%. Considering the new incidence rate of 41% and without changes of the other parameters, we achieve a power of 80% with 97 children and an odds ratio of 2.1.

A total of 412 children were screened at the preoperative evaluation center. 189 children have been included in this prospective observational study. The study suffers a high dropout rate based on different reasons, however mostly EEG data recording were incomplete because of agitated behaviour in children during anaesthesia induction, were we could not applicate EEG electrodes before anaesthesia induction without increasing the discomfort or reduce the safety for the young children. Finally, intraoperative EEG data analysis could be performed from “start of anaesthesia” until “extubation” in 97 children (Figure s1, Flow chart).

From these 97 children 40 (41%) children developed Emergence delirium (ED group) and 57 (59%) did not (Non-ED group). Patients’ characteristics are presented in Table 1. ED patients were significantly younger of age (P = 0.042).

51.5% (n=50) of all children developed Burst Suppression periods during anaesthesia procedure, while the remaining 48.5% (n=47) did not. Burst Suppression started within ~ 4min after “start of anaesthesia” (223 sec (IQR 123 to 412), and ended ~ 11min after “start of anaesthesia” (676 sec (IQR 417 to 1413)). Burst Suppression duration was 294 + 502 sec and isoelectric line duration was median 179 + 375 sec.

Occurrence and duration of Burst Suppression, duration of isoelectric line as well as Burst Suppression strength is not significantly different between ED patients and Non ED patients (Table 2).

Calculation of univariate logistic regression for confounders considered as risk factors triggering ED [age (months), anaesthetic agent given at induction / maintenance (Sevoflurane vs. Propofol), anaesthesia duration (min), and EEG suppression (occurrence, duration (sec)] only age (P = 0.046) and anaesthesia duration (P = 0.025) showed a significant association (Table 3).

To rule out the risk, that younger age would have biased our results, we recalculated the impact of Burst Suppression duration (sec), isoelectric line duration (sec) and Burst Suppression strength on ED in a pair – wise age matched group (matching rules: age should not differ more than 2 month in children younger than 60 month and not more than 6 month in children being older than 60 month). But again we did not find an impact of Burst Suppression duration, isoelectric line duration and Burst Suppression strength on the risk to develop ED (Supplement material Table s1).

However, Burst Suppression strength showed a high correlation with age (month), a tendency to display a longer fraction of isoelectric line within the Burst Suppression pattern in younger children (Spearman-Rho Correlation coefficient 0.528, p < 0.0001; Supplement material Figure s4; Table s1), whereas Burst Suppression duration (sec) and isoelectric line duration (sec) did not show a correlation with age (month) (Supplement material Table s2).

We show that occurrence and duration of Burst Suppression in children aged 0.5 – 8 years is not associated with the incidence of ED. Overall, Burst Suppression occurred in about 52% of all children aged 0.5 – 8 years, appearing mainly within the first ~ 4 min after application of the anaesthetic agents at start of anaesthesia.

Delirium is the most frequent brain dysfunction seen after anaesthesia procedures, mainly occurring in elderly patients and preschool children (19). In elderly patients it has been shown, that periods of Burst Suppression and deep Index level of anaesthesia are related to postoperative Delirium (9-12), however, in two studies analyzing Index level of anaesthesia in children a relationship with the occurrence of ED was not found (13, 14).

Faulk and colleagues examined 400 children aged 1 – 12 years, scheduled for dental procedures. Deep hypnosis was defined as a level of BIS Index reading of less than “45”. They did not find a correlation between deep hypnosis and the occurrence of ED (13).

Frederick and colleagues, undertook a randomized controlled trial including 40 children aged 2-8 years, randomized in a low-normal group (BIS Index values 40-45) versus high-normal group (BIS-Index values 55-60). They found no significant effect of deep versus light anaesthesia on the incidence of ED (14).

The underlying hypothesis that deep Index levels of anaesthesia in children might be related to ED, were not confirmed. This is in line with our data, where we found that the occurrence and duration of Burst Suppression activity was not related to ED in children. Burst suppression segments in the EEG are characterized by an isoelectric line interrupted by high-voltage EEG bursts, indicating a very deep state of unconsciousness with a marked reduction in brain metabolism (20). The occurrence of Burst Suppression during general anaesthesia in elderly patients is positively correlated to the incidence of postoperative delirium, hence one might propose, that elderly patients struggle to restore preoperative brain metabolism level. In contrast, in children neuronal hyperexcitability – as seen by occurrence of interictal, epileptiform discharges during anaesthesia induction or increased frontal connectivity during emergence of general anaesthesia – has been related to ED (7, 8). These striking differences in EEG activity related to delirium in children compared with elderly patients extends into its clinical presentation, where delirious children present with crying, agitation, disorientation and altered response to their surroundings, whereas elderly patients present primarily with a hypoactive form of delirium.

Additionally, we found that preschool children display Burst Suppression periods to a lower extent during general anaesthesia procedures (52%) compared with older patients (aged 62 + 14 years; 89%), however younger adults seem to have the lowest risk (below ~ 25%) to show Burst Suppression activity during general anaesthesia (12; 21).

Limitations

In our study, children receiving a mask induction with Sevoflurane were significantly younger compared with children receiving an i.v. induction with Propofol, due to standard operating procedure in our clinic, trying to avoid children’s discomfort during anaesthesia induction. Since younger age as well as Sevoflurane anaesthesia has been described to cause ED, this may have biased our results. However, Non-ED versus ED-group did not show a significant difference between anaesthetic agent used for induction or maintenance and in an age-matched sub-group analysis did also not reveal a correlation between Burst Suppression duration and ED.

Conclusion

Intraoperative Burst Suppression activity in the EEG is not associated to ED in young children. Burst Suppression activity is a characteristic EEG feature of a pathological, profoundly inactivated brain, but despite its pathological character, this does not render to the occurrence of ED in children.

ED Emergence delirium

EEG Electroencephalography / Electroencephalogramm

Ethics approval and consent to participate: This prospective, observational cohort study (NCT02481999) was approved by our local ethics committee on 12 March 2015 (Ethik committee Charité, University Medicine of Berlin / Chairperson Prof. Dr. R. Seeland / EA2/027/15).

Consent for publication: Written informed consent of either parents or legal proxies was obtained according to the Declaration of Helsinki.

Availability of data and material: The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Competing interests: Claudia Spies received material support by Narcotrend-Gruppe, MT Monitortechnik GmbH, Maienbaß 27, 24576 Bad Bramstedt. The authors declare no further competing interests.

Funding: This work was supported by the Charité-Humboldt University Berlin. Susanne Koch was supported by the Lydia-Rabinowitsch Grant from the Charité-Humboldt University Berlin 2013/2014. Further support was provided from institutional and departmental sources.

Authors’ contributions: SK, SyK and CS conceived and designed the experiments. SK, AMS and LR performed the experiments. SK, AMS, LR, JR, CP, SyK and AF analysed the data. SK and CS contributed to the materials/analysis tools. SK and JR wrote the paper. All authors read and approved the final manuscript.

Acknowledgements: Martin Krebs M.D. and Evjenia Toubekis M.D., Consultant in the department of Anaesthesiology and operative Intensive Care Medicine, Charité - Universitätsmedizin Berlin, Campus Charité Mitte and Virchow-Klinikum, Berlin, Germany. The authors thank Martin Krebs and Evjenia Toubekis, who provided intraoperative care for the study patients.

1. Dahmani S, Delivet H, Hilly J. Emergence delirium in children: an update. Current Opinion in Anaesthesiology 2014; 27: 309-15.

2. Inouye SK, Westendorp RG, Saczynski JS. Delirium in elderly people. Lancet 2014; 383: 911-22.

3. Somaini M, Engelhardt T, Fumagalli R, Ingelmo PM. Emergence delirium or pain after anaesthesia--how to distinguish between the two in young children: a retrospective analysis of observational studies. British Journal of Anaesthesia 2016; 116: 377-83.

4. Jevtovic-Todorovic V. Functional implications of an early exposure to general anesthesia: are we changing the behavior of our children? Molecular Neurobiology 2013; 48: 288-93.

5. Berndt N, Rosner J, Haq RU, et al. Possible neurotoxicity of the anesthetic propofol: evidence for the inhibition of complex II of the respiratory chain in area CA3 of rat hippocampal slices. Archives of Toxicology 2018; 92: 3191-205.

6. Kreuzer I, Osthaus WA, Schultz A, Schultz B. Influence of the sevoflurane concentration on the occurrence of epileptiform EEG patterns. PLoS One 2014; 9: e89191.

7. Koch S, Rupp L, Prager C, Wernecke KD, Kramer S, Fahlenkamp A, Spies C. Emergence delirium in children is related to epileptiform discharges during anaesthesia induction: An observational study. European Journal of Anaesthesiology 2018; 35: 929 - 936.

8. Martin JC, Liley DT, Harvey AS, Kuhlmann L, Sleigh JW, Davidson AJ. Alterations in the functional connectivity of frontal lobe networks preceding emergence delirium in children. Anesthesiology 2014; 121: 740-52.

9. Radtke FM, Franck M, Lendner J, Kruger S, Wernecke KD, Spies CD. Monitoring depth of anaesthesia in a randomized trial decreases the rate of postoperative delirium but not postoperative cognitive dysfunction. British Journal of Anaesthesia 2013; 110 : i98-105.

10. Chan MT, Cheng BC, Lee TM, Gin T, Group CT. BIS-guided anesthesia decreases postoperative delirium and cognitive decline. Journal of Neurosurgical Anesthesiology 2013; 25: 33-42.

11. Whitlock EL, Torres BA, Lin N, et al. Postoperative delirium in a substudy of cardiothoracic surgical patients in the BAG-RECALL clinical trial. Anesthesia & Analgesia 2014; 118: 809-17.

12. Fritz BA, Kalarickal PL, Maybrier HR, et al. Intraoperative Electroencephalogram Suppression Predicts Postoperative Delirium. Anesthesia & Analgesia 2016; 122: 234-42.

13. Faulk DJ, Twite MD, Zuk J, Pan Z, Wallen B, Friesen RH. Hypnotic depth and the incidence of emergence agitation and negative postoperative behavioral changes. Paediatric Anaesthsia 2010; 20: 72-81.

14. Frederick HJ, Wofford K, de Lisle Dear G, Schulman SR. A Randomized Controlled Trial to Determine the Effect of Depth of Anesthesia on Emergence Agitation in Children. Anesthesia & Analgesia 2016; 122: 1141-6.

15. Sikich N, Lerman J. Development and psychometric evaluation of the pediatric anesthesia emergence delirium scale. Anesthesiology 2004; 100: 1138-45.

16. Merkel SI, Voepel-Lewis T, Shayevitz JR, Malviya S. The FLACC: a behavioral scale for scoring postoperative pain in young children. Pediatric Nursing 1997; 23: 293-7.

17. Kerson AG, DeMaria R, Mauer E, Joyce C, Gerber LM, Greenwald BM, et al. Validity of the Richmond Agitation-Sedation Scale (RASS) in critically ill children. Journal of Intensive Care 2016; 4: 65.

18. Zschocke S. EEG bei diffusen Erkrankungen des Gehirns. In: Hansen H-C. Klinische Elektroenzephalographie. Berlin, Heidelberg, New York: Springer-Verlag; 2011: 314 - 48.

19. Costi D, Cyna AM, Ahmed S, et al. Effects of sevoflurane versus other general anaesthesia on emergence agitation in children. Cochrane Database of Systematic Reviews 2014; DOI: 10.1002/14651858.CD007084.

20. Brown EN, Lydic R, Schiff ND. General anesthesia, sleep, and coma. The New England Journal of Medicine 2010; 363: 2638-50.

21. Purdon PL, Pavone KJ, Akeju O, Smith AC, Sampson AL, Lee J, et al. The Ageing Brain: Age-dependent changes in the electroencephalogram during propofol and sevoflurane general anaesthesia. British Journal of Anaesthesia 2015; 115: i46-i57.

Table 1 Patient characteristics for children without emergence delirium (Non ED group) and children with ED (ED group).

	Non-ED Group (n=57)	ED Group (n=40)	P value
Age [months]	58 (15.75 / 78	22 (13 / 60)	0.042
Weight (kg)	17 (9.7 / 22)	11 (9.3 / 22)	n.s.
Height (cm)	107.5 (80 / 131)	86 (81.5 / 119.5)	n.s.
ASA Score (I / II / III) (%)*	46 / 11 / 0 (81 / 19 / 0)	32 / 7 / 1 (80 / 17,5 / 2,5)	n.s.
Gender male / female (%)	35 / 22 (61 / 39)	25 / 15 (62,5 / 37,5)	n.s.
Procedures (%) Cleft-lip-palate; Oral / neck surgery	6 (11)	13 (33)	n.s.
Inguinal hernia / Circumcision / Orchidopexy / Cystoscopy	15 (26)	8 (20)	n.s.
Otorhinolaryngology surgery	7 (12)	4 (10)	n.s.
Intraabdominal surgery / long procedures (>60min)	14 (25)	9 (23)	n.s.
Limb surgery / short procedures (< 60min)	15 (26)	6 (15)	n.s.
Midazolam premedication (mg/kg body weight)	0.64 + 0.17	0.67 + 0.18	n.s.
Induction Agent Sevoflurane / Propofol / mixed (%)	12 / 23 / 22 (21 / 41 / 39)	9 / 13 / 18 (22,5 / 32,5 / 45)	n.s.
Maintance Agent Sevoflurane / Propofol / mixed (%)	38 / 18 / 1 (67 / 32 / 2)	27 / 13 / 0 (67,5 / 32,5 / 0)	n.s.
Anaesthesia duration (min)	102 + 71	146 + 113	n.s.

Values are median (IQR range), number (propotion) or mean + SD. Age (p=0.042) differed significantly between NonED group vs. ED group (Mann-Whitney-U Test). *ASA: American Society of Anesthesiologists.

Table 2 Comparing EEG suppression during anaesthesia for children with Emergence delirium (ED group) and children without Emergence delirium (Non ED group). (Mann-Whitney-U Test).

	Non-ED Group (n=57)	ED Group (n=40)	P value
Burst Suppression yes / no (%)	28 / 29 (49 / 51)	22 / 18 (55 / 45)	n.s.
Burst Suppression duration (sec)	318 + 531	261 + 462	n.s.
Isoelectric line duration (sec)	192 + 407	159 + 328	n.s.
Burst Suppression strength	3.3 + 3.6	2.5 + 1.9	n.s.

Values are number (propotion) or mean + SD. Burst Suppression strength is calculated by dividing Burst Suppression duration over isoelectric line duration. *ED: Emergence delirium.

Table 3 Univariate logistic regression accounting for confounders considered risk factors triggering emergence delirium after general anaesthesia in children.

Confounders	Odds ratio	95% CI lower limit	95% CI upper limit	p Value
Age (months)	0.986	0.973	1.000	0.046
Anaesthesia Induction (Sevoflurane / Propofol / mix of both)	0.691	0.275	1.737	0.432
Anaesthesia Maintenance (Sevoflurane / Propofol)	0.699	0.427	2.420	0.971
Concentration of Midazolam (mg/kg body weight)	2.886	0.253	32.867	0.393
Concentration of Remifentanil (µg/kg body weight / min)	0.465	0	798.215	0.840
Anaesthesia duration (min)	1.005	1.001	1.010	0.025
Burst suppression occurrence (yes / no)	1.266	0.563	2.848	0.569
Burst suppression duration (sec)	1	0.999	1.001	0.583

Only age (months) and anaesthesia duration (min) showed a significant association.

Download PDF

Journal Publication

published 08 Aug, 2019

Read the published version in BMC Anesthesiology →

Editorial decision: Minor revision
16 Jul, 2019
Review #2 received at journal
10 Jul, 2019
Reviewers invited by journal
26 Jun, 2019
Reviewer #1 agreed at journal
26 Jun, 2019
Reviewer #2 agreed at journal
26 Jun, 2019
Review #1 received at journal
26 Jun, 2019
Submission checks completed at journal
24 Jun, 2019
Editor invited by journal
24 Jun, 2019
Editor assigned by journal
24 Jun, 2019

You are reading this older preprint version

Read the latest preprint version →

Emergence Delirium in children is not related to intraoperative Burst Suppression – prospective, observational Electrography study

Status:

Journal Publication

Version 2

Abstract

Figures

Background

Methods

ED assessment

EEG recording and analysis

Statistical Analysis

Results

Discussion

Limitations

Conclusion

Abbreviations

ED Emergence delirium

EEG Electroencephalography / Electroencephalogramm

Declarations

References

Tables

Supplementary Files

Status:

Journal Publication

Version 2