Ondansetron does not modify emergence agitation in children.
In this prospective, placebo-controlled study, we evaluated the
effect of prophylactic ondansetron therapy on emergence agitation of
children who underwent minor surgery below the umbilicus. Seventy
children aged one to six years and American Society of Anesthesiologists
physical status I were studied. Children were premedicated with
midazolam rectally and were randomly assigned to receive either
ondansetron (Group O) or placebo (Group P) in combination with caudal
anaesthesia. Children in Group O received intravenous ondansetron (0.1
mg/kg for children weighing <40 kg, 4 mg for children weighing >40
kg) and Group P (n=35) received normal saline 2 ml following anaesthesia
induction with sevoflurane. Airway management was provided with
LMA-Proseal without muscle relaxation and anaesthesia maintenance was
provided with a 60:40 [N.sub.2]O:[O.sub.2] mixture and sevoflurane.
Emergence agitation was evaluated with a ten point scale and pain level
was assessed every 10 minutes for the first 30 minutes after admission
to the recovery room.
There were no significant differences between the placebo and ondansetron groups with respect to demographic, anaesthetic and surgical details. Incidences of emergence agitation in ondansetron and placebo groups were similar (32.4% and 30.3% at 10 minutes respectively). Mean modified Children's Hospital of Eastern Ontario pain scale scores and mean ten-point scale scores and emergence agitation incidences decreased similarly after 10 minutes in both groups. Ready time for discharge was similar between the groups. Agitated patients had significantly increased ready time for discharge compared to non-agitated patients (P=0.001).
Prophylactic intravenous ondansetron administration does not reduce emergence agitation comparing to placebo after sevoflurane anaesthesia.
Key Words: seratonin receptor antagonist, ondansetron, emergence agitation, children
|Article Type:||Clinical report|
(Dosage and administration)
Child psychopathology (Prevention)
Child psychopathology (Research)
Sevoflurane (Complications and side effects)
Pediatric anesthesia (Research)
|Publication:||Name: Anaesthesia and Intensive Care Publisher: Australian Society of Anaesthetists Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 Australian Society of Anaesthetists ISSN: 0310-057X|
|Issue:||Date: July, 2011 Source Volume: 39 Source Issue: 4|
|Topic:||Event Code: 310 Science & research|
|Geographic:||Geographic Scope: United States Geographic Code: 1USA United States|
Emergence agitation (EA) is defined as "a disturbance in a
child's awareness and attention to the environment with
disorientation and perceptual alterations including hypersensitivity to
stimuli and hyperactive motor behavior in the immediate postanesthesia
Many factors such as age, stressful induction, rapid awakening in an unfamiliar environment, presence of pain, duration of the anaesthesia, anaesthetic technique and medication (scopolamine, droperidol, barbiturates, ketamine, opioids, benzodiazepines, metoclopramide and atropine) and type of surgery may contribute to EA (2-5). On the other hand, primary metabolic disturbances, hypoxaemia or bladder distension may be the cause of agitation which should be distinguished from EA (6).
It has been suggested that alterations in plasma serotonin (5-hydroxytryptamine, 5-HT) levels might promote EA. It has been concluded that serotonin metabolism is significantly suppressed in EA which may be attributed to an uncertain mechanism in sevoflurane anaesthesia (7). Bayindir et al (8) achieved successful results in postcardiotomy delirium with ondansetron, which is a 5H[T.sub.3] receptor antagonist. Similarly, Lankinen et al (9) found that the usage of tropisetron, another 5H[T.sub.3] receptor antagonist, was of use in preventing EA in children. On the contrary, in some other studies, serotonin levels were found to be decreased in patients with postoperative delirium (10,11).
Medications which have been used to prevent and treat EA in children include midazolam, clonidine, dexmedetomidine, fentanyl, ketorolac and physostigmine (12). Ondansetron is a drug commonly used in anaesthesia-related nausea and vomiting. It is also used in other central nervous system related disorders (13,14). The aim of this randomised, placebo-controlled study was to assess the efficacy of prophylactic ondansetron therapy in children who experienced EA following sevoflurane anaesthesia.
The modified Yale Preoperative Anxiety Scale (mYPAS) score was used for preoperative anxiety assessment (23 to 100) (15). This was performed by the preoperative anaesthesia technician who noted the child's vital signs before rectal midazolam premedication (0.5 mg/kg). Thirty minutes after premedication, the patients were separated from their parents and transported to the operating room. Heart rate, non-invasive mean arterial pressure and peripheral haemoglobin oxygen saturation (SpO2) were monitored. After pre-oxygenation, general anaesthesia was induced by facemask with 8% sevoflurane and 50% nitrous oxide in oxygen. After insertion of an intravenous line and laryngeal mask airway without the use of a neuromuscular blocking agent, patients were assigned to two groups. Group O (n=35) received ondansetron (Zofer 4 mg/2 ml amp, ADEKA, Turkey) (0.1 mg/kg for children weighing <40 kg, 4 mg for children weighing >40 kg) and Group P (n=35) received 0.9% NaCl 2 ml. Ondansetron was diluted in 2 ml saline as needed. Then a single-dose caudal blockwas performed in all patients with 0.8 ml/kg 0.25% levobupivacaine by the same anaesthetist (TH). Anaesthesia was maintained with 1.0 to 2.0% sevoflurane (corrected for stable intraoperative haemodynamic measurements). All patients were ventilated mechanically with a 60 to 40% nitrous oxide-oxygen mixture with a laryngeal mask airway in situ. Fifteen minutes after the caudal block, surgery commenced. The caudal block was judged as inadequate if the child's heart rate and/or blood pressure increased by more than 10% of pre-incision values at the beginning of the skin incision. The insufficient analgesia was treated with a rescue opioid analgesic (fentanyl 1 [micro]g/kg) and the patient was excluded from the study. After skin closure, anaesthetic gases were discontinued and replaced with 100% oxygen 5 l/minute. The laryngeal mask airway was removed when patients were fully conscious and they were then transferred to the recovery room. No other antiemetic drugs were given during anaesthesia. Intraoperatively, heart rate, mean arterial pressure and Etsevoflurane concentration were recorded every 10 minutes. Intraoperative fluid therapy was standardised and all children received lactated Ringer solution according to body weight (16). Assessments of the EA and pain levels were performed every 10 minutes for the first 30 minutes after admission to the recovery room. Assessment of EA was performed by a 10-point scale (TPS), ranging from 1 (calm or asleep) to 10 (worst possible and inconsolable agitation) and EA was defined as TPS >5 (17). The patients' pain scores were evaluated using a modified Children's Hospital of Eastern Ontario pain scale (mCHEOPS) (18) (Table 1). A postoperative pain score of >4 was regarded as inadequate analgesia and the patient was given 40 mg/kg rectal paracetamol and excluded from the study. The incidence of EA was defined as at least one event during any given assessment observation period when compared to the agitated and non-agitated groups. If the scores in the TPS continued between 8 to 10 points for longer than five minutes, intravenous propofol (0.5 mg/kg) was given as rescue therapy and the child was excluded from the study. The patients were considered as 'ready for discharge' from the recovery room when they had no pain, a calm status and a modified Aldrete score of >10. Intraoperative and postoperative data were collected by an independent observer (MO) blinded to the group assignment. Major complications such as oxygen desaturation (Sp[O.sub.2] <95), laryngospasm, arrhythmia and allergic reaction were recorded.
The sample size required to reduce EA incidence, which was 37% with placebo according to the results of a previous study, to 10% with ondansetron was calculated as 34 for each group taking alpha 0.05 and beta 0.80 (19). We included 35 patients in each group to increase the power of the study and also to secure patient dropouts for any reason. The SPSS 13.0 statistical software system (SPSS Inc., Chicago, IL, USA) was used for statistical analyses. Results are presented as mean [+ or -] standard deviation or frequences (n) and percentages (%). Statistical comparison of the groups was performed with independent t-test for parametric analyses and Mann-Whitney U test for non-parametric analyses. Levene's Test was run for the parametric values to assess whether the parameters' variances were equal. The changes occurring within groups were analysed by Bonferroni and Wilcoxon signed-rank test.
Seventy children were initially randomised for the study. Three children were excluded from further evaluation; one in each group received fentanyl following skin incision and one patient had a mCHEOPS score >4 in Group P. Finally, 33 children met the criteria for the placebo group and 34 children for the ondansetron group. EA incidence at 10 minutes was 31.3% which differed significantly from the 30 minute results (19.4%, P=0.03) (Table 2). The patients neither required rescue propofol in the postoperative period nor had high mYPAS scores. There were no significant differences between the placebo and ondansetron groups with respect to demographic, anaesthetic and surgical details. Preoperative mYPAS scores were similar. Ten children (30.3%) in the placebo group and seven children (20.6%) in the ondansetron group vomited. Times to 'ready for discharge' were similar in both groups (Table 3). Intraoperative heart rate and mean arterial pressure decreases were comparable in both groups (Figures 1 and 2).
The incidences of EA in ondansetron and placebo groups were 32.4% and 30.3% at 10 minutes; 23.5% and 18.2% at 20 minutes; and 20.6% and 18.2% at 30 minutes. EA incidence decreased after 10 minutes in both groups with comparable values. Mean mCHEOPS scores and mean TPS scores also decreased after 10 minutes in both groups. All changes were similar between groups (Table 4).
[FIGURE 1 OMITTED]
Comparison of agitated and non-agitated patients showed that distributions of age, gender, mYPAS scores, anaesthetic and surgical features, fluid therapy, Etsevoflurane concentrations at the end of the surgery, mCHEOPS scores and vomiting ratios were similar in agitated and non-agitated groups. Agitated patients had significantly increased 'ready time for discharge' compared to non-agitated patients (P=0.001) (Table 5).
[FIGURE 2 OMITTED]
The clinical findings in acute delirium and EA are similar in many aspects, with a dissociative state and altered cognitive perception (20). Greater incidence of agitation after sevoflurane anaesthesia is observed in preschool-age children compared with school-age children (1,2). Previous investigators found the incidence of EA with preschool-age range between 6.3% and 74.1% (21).
Although there are many studies regarding the role of the serotonergic system and 5-H[T.sub.3] receptors in acute delirium, there is no consensus on their effects (7-9). Ogasawara et al (7) observed significant increases in plasma serotonin levels during sevoflurane anaesthesia. Bayindir et al8 had successful results with ondansetron in treatment of post-cardiotomy delirium, which was assumed to be because of increased serotonin levels due to cardiopulmonary bypass. A 5H[T.sub.3] receptor antagonist tropisetron was used successfully after sevoflurane anaesthesia to prevent EA in small children (9). Despite the probable anxiolytic effect of ondansetron (22), the exact mechanism of tropisetron in preventing EA could not be clarified (9). On the other hand, in other studies serum serotonin levels were found to be decreased in patients with delirium (10,11). In addition, it was reported that anaesthetic agents may cause consumption of serotonin at a steady rate, while they increase the plasma level of melatonin in rats (23). Thus, the medical literature lacks a consensus about the serotonin levels and both increased and decreased serotonergic activity have been found to be associated with delirium (24).
The only study using 5H[T.sub.3] antagonists in EA was that by Lankinen et al which compared the effects of prophylactic tropisetron with placebo in children undergoing adenoidectomy (9). The EA incidence in the placebo group was found to be 62%, which is twice that of our placebo group results. The difference may be due to the type of surgery, as otorhinolaryngological procedures may contribute to increased incidence of EA (25). On the other hand, the difference may be also because of the lack of premedication in their study (9). It is obvious that the use of midazolam in our study reduced the preoperative anxiety in our patients (25,26). The differences may also be attributable to individualised conditions.
Otorhinolaryngological procedures have high incidences of postoperative nausea and vomiting, and 5-H[T.sub.3] receptor antagonists have well-established roles in the prophylaxis and treatment of postoperative nausea and vomiting (27). Thus, it is possible that the reduction in the EA incidence observed by Lankinen et al (9) was due to the antiemetic property of tropisetron. However, this hypothesis could not be verified and the exact mechanism remains unclear. We were not able to find a reduction in the incidence of EA in the ondansetron group. We believe that the difference between that study (9) and ours is probably due to the difference of the study population. Although recent studies and current antiemetic guidelines showed that tropisetron, ondansetron and granisetron are equivalent in efficacy (28), there are some differences in metabolism and receptor specificities. For example, cytochrome p450 enzyme systems are slow metabolisers in some individuals secondary to a mutation, the frequency of which is reported as 6% in caucasians (29).
Primary metabolic disturbances and pain should be excluded in agitated children in order to make a differential diagnosis with EA. In our study, mCHEOPS scores in the recovery room were similar in agitated and non-agitated groups. We did not observe any episode of oxygen desaturation and fluid therapy was similar. Therefore, we excluded metabolic change as a cause of agitation.
Although the occurrence of EA in children after sevoflurane anaesthesia due to high blood sevoflurane concentrations was commonly reported (30), in our study Etsevoflurane concentration at the end of the surgery was similar between agitated and non-agitated groups.
In conclusion, our study demonstrated that prophylactic administration of intravenous ondansetron did not reduce EA compared to placebo after sevoflurane anaesthesia in preschool children who underwent minor surgery below the umbilicus.
Accepted for publication on March 17, 2011.
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(6.) Moos DD. Sevoflurane and emergence behavioral changes in pediatrics. J Perianesth Nurs 2005; 20:13-18.
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(8.) Bayindir O, Akpinar B, Can E, Guden M, Sonmez B, Demiroglu C. The use of the 5-HT3-receptor antagonist ondansetron for the treatment of postcardiotomy delirium. J Cardiothorac Vasc Anesth 2000; 14:288-292.
(9.) Lankinen U, Avela R, Tarkkila P. The prevention of emergence agitation with tropisetron or clonidine after sevoflurane anesthesia in small children undergoing adenoidectomy. Anesth Analg 2006; 102:1383-1386.
(10.) Van der Mast R C, Fekkes D, Moleman P, Pepplinkhuizen L. Is postoperative delirium related to reduced plasma tryptophan? Lancet 1991; 338:851-852.
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(13.) Akhondzadeh S, Mohammadi N, Noroozian M, Karamghadiri N, Ghoreishi A, Jamshidi AH et al. Added ondansetron for stable schizophrenia: a double blind, placebo controlled trial. Schizophr Res 2009; 107:206-212.
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(20.) Dahmani S, Stany I, Brasher C, Lejeune C, Bruneau B, Wood C et al. Pharmacological prevention of sevoflurane- and desflurane-related emergence agitation in children: a meta-analysis of published studies. Br J Anaesth 2010; 104:216-223.
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T. Hosten *, M. Solak ([dagger]), L. Element, M. Ozgun [section], K. TOKER ([dagger]) Department of Anesthesiology and Reanimation, Kocaeli University Medical School, Kocaeli, Turkey
* M.D., Assistant Professor.
([dagger]) M.D., Professor and Consultant.
([double dagger]) M.D., Assistant Professor and Consultant, Department of Pediatric Surgery, Kocaeli University Medical School.
([section]) M.D., Resident.
Address for correspondence: Dr T. Hosten, email: firstname.lastname@example.org
Table 1 Modified CHEOPS scoring Item structure Parameter Points Crying None 0 Crying, moaning 1 Screaming 2 Facial expression Smiling 0 Neutral 1 Grimacing 2 Verbal expression Positive 0 None or another complaint 1 Complaining of pain 2 Torso Neutral 0 Squirming, tense, upright 1 Restrained 2 Legs Neutral 0 Kicking, restless foetal position 1 Restrained 2 CHEOPS=Children's Hospital of Eastern Ontario pain scale. Table 2 Statistical analyses of emergence agitation incidences Time after emergence n (%) P Agitation 10 min 21 (31.3) incidence 20 min 14 (20.9) 0.05 30 min 13 (19.4) 0.03 * * Comparison of emergence agitation incidence according to 10 minute values with Wilcoxon signed-rank test. Table 3 Statistical analyses of demographic, anaesthetic and surgical details in the placebo and ondansetron groups (mean [+ or -] SD or numbers) Group P, n=33 Age, y 3.1 [+ or -] 1.4 Weight, kg 14.5 [+ or -] 5.1 Gender, female/male 25/8 mYPAS score 29.3 [+ or -] 6.4 Anaesthesia duration, min 49.3 [+ or -] 0.7 Surgery duration, min 63.5 [+ or -] 10.1 Fluid therapy, ml 156.7 [+ or -] 44.4 Time to eye-opening, min 8.6 [+ or -] 4.4 [Et.sub.Sevo] concentration end 1.26 [+ or -] 0.07 of the surgery, % Ready time for discharge, min 29.1 [+ or -] 6.0 Vomiting, yes/no 10/23 Group O, n=34 Age, y 3.1 [+ or -] 1.6 Weight, kg 15.3 [+ or -] 4.8 Gender, female/male 25/9 mYPAS score 28.8 [+ or -] 5.0 Anaesthesia duration, min 49.3 [+ or -] 8.2 Surgery duration, min 63.6 [+ or -] 7.2 Fluid therapy, ml 154.6 [+ or -] 62.3 Time to eye-opening, min 9.9 [+ or -] 4.0 [Et.sub.Sevo] concentration end 1.25 [+ or -] 0.07 of the surgery, % Ready time for discharge, min 27.6 [+ or -] 4.9 Vomiting, yes/no 7/27 P Age, y 0.80 Weight, kg 0.53 Gender, female/male 0.83 mYPAS score 0.71 Anaesthesia duration, min 0.98 Surgery duration, min 0.97 Fluid therapy, ml 0.87 Time to eye-opening, min 0.23 [Et.sub.Sevo] concentration end 0.32 of the surgery, % Ready time for discharge, min 0.26 Vomiting, yes/no 0.36 mYPAS=modified Yale Preoperative Anxiety Scale. Table 4 Statistical analyses of agitation scores, pain scores and agitation incidences between the placebo and ondansetron groups, (mean [+ or -] SD or numbers (%)) Group P, n=33 P * Emergence agitation 10 min 10 (30.3) 20 min 6 (18.2) 0.10 30 min 6 (18.2) 0.10 TPS score 10 min 3.18 [+ or -] 2.99 20 min 2.58 [+ or -] 2.63 0.40 30 min 2.42 [+ or -] 2.33 0.10 mCHEOPS score 10 min 2.76 [+ or -] 0.44 20 min 2.64 [+ or -] 0.49 0.76 30 min 2.58 [+ or -] 0.50 0.24 Group O, n=34 P * Emergence agitation 10 min 11 (32.4) 20 min 8 (23.5) 0.25 30 min 7 (20.6) 0.15 TPS score 10 min 3.50 [+ or -] 3.03 20 min 2.62 [+ or -] 2.69 0.07 30 min 2.44 [+ or -] 2.23 0.13 mCHEOPS score 10 min 2.68 [+ or -] 0.47 20 min 2.56 [+ or -] 0.50 0.31 30 min 2.50 [+ or -] 0.51 0.09 Group O, n=34 P ** Emergence agitation 10 min 11 (32.4) 0.85 20 min 8 (23.5) 0.59 30 min 7 (20.6) 0.80 TPS score 10 min 3.50 [+ or -] 3.03 0.66 20 min 2.62 [+ or -] 2.69 0.94 30 min 2.44 [+ or -] 2.23 0.97 mCHEOPS score 10 min 2.68 [+ or -] 0.47 0.46 20 min 2.56 [+ or -] 0.50 0.52 30 min 2.50 [+ or -] 0.51 0.54 TPS=10-point scale, mCHEOPS=modified Children's Hospital of Eastern Ontario pain scale. * In-group comparison of 10-minute values with Wilcoxon signed-rank and Bonferroni tests. ** Inter-group comparison at the same measurement time values with Mann-Whitney U test and t-tests. Table 5 Statistical analyses of demographic, anaesthetic and surgical details between the agitated and non-agitated patients (mean [+ or -] SD or numbers) Agitated, n=21 Age, y 3.01 [+ or -] 1.3 Weight, kg 15.3 [+ or -] 8.1 Gender, female/male 18/3 mYPAS score 29.95 [+ or -] 5.7 Anaesthesia duration, min 52.6 [+ or -] 11.7 Surgery duration, min 66.2 [+ or -] 9.9 Fluid therapy, ml 141.43 [+ or -] 60.3 Time to eyes opening, min 10.0 [+ or -] 4.4 EtSevo concentration end of the surgery, % 1.24 [+ or -] 0.08 mCHEOPS score 2.57 [+ or -] 0.5 Vomiting, yes/no 8/13 Ready time for discharge, min 31.5 [+ or -] 4.7 Non-agitated, n=46 Age, y 3.1 [+ or -] 1.5 Weight, kg 14.7 [+ or -] 5.1 Gender, female/male 32/14 mYPAS score 28.6 [+ or -] 5.8 Anaesthesia duration, min 47.8 [+ or -] 7.9 Surgery duration, min 62.4 [+ or -] 8.0 Fluid therapy, ml 162.1 [+ or -] 50.0 Time to eyes opening, min 8.9 [+ or -] 4.1 EtSevo concentration end of the surgery, % 1.26 [+ or -] 0.07 mCHEOPS score 2.8 [+ or -] 0.4 Vomiting, yes/no 9/37 Ready time for discharge, min 26.9 [+ or -] 5.3 P Age, y 0.77 Weight, kg 0.57 Gender, female/male 0.16 mYPAS score 0.36 Anaesthesia duration, min 0.10 Surgery duration, min 0.13 Fluid therapy, ml 0.14 Time to eyes opening, min 0.32 EtSevo concentration end of the surgery, % 0.37 mCHEOPS score 0.10 Vomiting, yes/no 0.10 Ready time for discharge, min 0.001 * mYPAS=modified Yale Preoperative Anxiety Scale, mCHEOPS=modified Children's Hospital of Eastern Ontario pain scale. * t-test.
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