Emergence Delirium (ED) in Children

Review Article

INTRODUCTION

The introduction of a new generation of inhaledanesthetics like sevoflurane and desflurane into pediatricclinical practice has been associated with a greater incidenceof ED, a short-lived, but troublesome clinical phenomenonof uncertain etiology [1]. A variety of anesthesia-, surgery-,patient-, and adjunct medication-related factors have beensuggested to play a potential role in the development of suchan event. Restless behavior upon emergence causes not onlydiscomfort to the child, but also makes the caregivers andparents feel unhappy with the quality of recovery fromanesthesia. Although the severity of agitation varies, it oftenrequires additional nursing care, as well as treatment withanalgesics or sedatives, which may delay discharge fromhospital. To reduce the incidence of this adverse event, it isadvisable to identify children at risk and take preventivemeasures, such as reducing preoperative anxiety, removingpostoperative pain, and providing a quiet, stress-freeenvironment for post anesthesia recovery.

Emergence delirium (ED) also referred to as emergenceagitation (EA) is a well documented phenomenon occurringin children and adults in the immediate postoperative period.With the recent popularity of the newer inhalation agent’sdesflurane and sevoflurane, numerous clinical studies havebeen published questioning the association of theseanesthetics with an increased incidence of emergencedelirium.

Emergence delirium is defined as a dissociated state of

EMERGENCE DELIRIUM (ED) IN CHILDREN

K RaghavendranSenior Consultant & Coordinator, Apollo Children’s Hospitals, 21, Greams Lane, Off Greams Road,

Chennai 600 006, India.

Emergence delirium in children is a state of mental dissociation that occurs while recovering from anestheticagents and manifests as disorientation, restlessness, irritability, screaming and involuntary activity. It usuallyevolves in the first half hour after awakening from anesthesia, often lasts up to 20 minutes and usually resolveson its own. Many factors have been suggested to play a potential role in the development of such an event.Post anesthesia agitation has been noted more often with the newer, less soluble, inhaled anesthetics, suchas desflurane and sevoflurane, than with other volatile ones; however administration of other anestheticagents can also cause this disturbing recovery phenomenon. Emergence delirium occurs more often inpreschool children and seen frequently after head and neck surgeries like tonsillectomy, adenoidectomy,tongue tie release, strabismus surgery, nasal operations etc. Treatment is with pharmacological andenvironmental. Prevention may be the best treatment but no one medication is entirely effective.

Key words: Post anesthetic, Emergence delirium, Sevoflurane, Desflurane.

consciousness in which the child is inconsolable, irritable,uncompromising or uncooperative, typically thrashing,crying, moaning, or incoherent [2]. Additionally paranoidideation has been observed in combination with theseemergence behaviors. Characteristically these children donot recognize or identify familiar and known objects orpeople. Parents who witness this state claim the behavior isunusual and uncustomary for the child. Although generallyself limiting (5-15 min) ED can be severe and may result inphysical harm to the child and particularly the site ofsurgery.

Emergence delirium has been reported after theintroduction of every new anesthetic including mostinhalational agents and intravenous agents includingmidazolam, remifentanil and propofol. Other drugs knownto be associated with ED include (i) atropine or scopo-lamine, (ii) ketamine, (iii) droperidol, (iv) barbiturates andpossibly, (v) benzodiazepines [3]. The incidence ofemergence delirium in all postoperative patients is 5.3%with a more frequent incidence in children (12-13%). Theincidence of emergence delirium after halothane,isoflurane, sevoflurane and desflurane ranges from 2-55%.It has been postulated that this phenomenon has becomemore acutely noticed with the increased use of agents suchas sevoflurane and desflurane that have a rapid emergenceprofile due to their low blood gas solubility profile. It wasthought that rapid emergence with lack of adequate paincontrol before emergence contributed or was the cause ofthis problem. This has been supported by the finding that

99 Apollo Medicine, Vol. 8, No. 2, June 2011

Apollo Medicine, Vol. 8, No. 2, June 2011 100

Review Article

ketorolac administration decreased the incidence ofemergence delirium three to fourfold after myringotomywith either halothane or sevoflurane anesthesia. Severalstudies have documented a reduction in ED with theadministration of fentanyl 2.5 μg/kg intraoperatively or 2.0μg/kg fentanyl administered intranasal, 1 μg/kg in eachnostril after the induction of anesthesia. However, otherstudies have noted emergence delirium in children aftersevoflurane anesthesia despite effective regional blocks toprevent postoperative pain. These studies demonstrated thatdelirium occurred more frequently in preschool agechildren, 1 to 5 years of age, lasted 5-15 minutes in therecovery room and often resolved spontaneously. Studiesthat have also called into question whether adequate painmanagement is the cause of ED include sevoflurane vs.halothane administration in patients undergoing MRI (nosurgery) where the incidence of ED was 33% in sevofluranetreated patients versus 0% in halothane treated children.

Post operative agitation can indicate any number ofsources, including pain, physiological compromise, oranxiety. Delirium may be confused with agitation, but it mayalso be a cause of agitation. As most of the literature on thissubject cannot differentiate between these two terms, werefer to the problem as EA/ED for the purpose of this article.

Possible etiological factors of pediatricemergence delirium

• Rapid emergence

• Intrinsic characteristics of an anesthetic

• Postoperative pain

• Surgery type

• Age

• Preoperative anxiety

• Child temperament

• Adjunct medication

ANESTHESIA-RELATED FACTORS

Rapid emergence

Post anesthesia agitation has been noted more often withthe newer, less soluble, inhaled anesthetics, such asdesflurane and sevoflurane, than with other volatile ones. Ithas been postulated that rapid awakening after the use of theinsoluble anesthetics may initiate EA/ED by worsening achild’s underlying sense of apprehension when finding himin an unfamiliar environment. Some parents claim thepatient’s behavior upon emergence was the same as when hewas suddenly awakened from deep sleep. Older childrenand adults usually become oriented rapidly, whereas

preschool aged children, who are less able to cope up withenvironmental stresses, tend to become agitated anddelirious. However, recovery from propofol anesthesiawhich is also rapid is smooth and pleasant. Several studieshave shown that sevoflurane anesthesia is associated with ahigher incidence of EA/ED compared with propofol.Similar results were obtained when desflurane/nitrousoxide anesthesia was compared with protocol/remifentanilanesthesia. Delaying emergence by a slow, stepwisedecrease in the concentration of inspired sevoflurane at theend of surgery did not reduce the incidence of EA, and thusquestions the role of abrupt awakening in the developmentof EA. Studies have shown a similar incidence of EA amongchildren who entered the post anesthesia care unit (PACU)still asleep and those who entered awake.

Intrinsic characteristics of an anesthetic

Most authors have documented that EA/ED occursmore often after sevoflurane than after halothane anesthesiawhich has been confirmed by the manufacturer itself .Someauthors have speculated that two unique, intrinsiccharacteristics of sevoflurane might account for thedevelopment of EA/ED. First, this anesthetic exerts anirritating side effect on the central nervous system (CNS).Second, although sevoflurane degradation products appearto cause no organ damage themselves, data are lacking ontheir possible interactions with other types of medications.Epileptiform activity has been reported during the use ofsevoflurane anesthesia in both patients and volunteers withno medical history of seizures [4]. However, such caseshave been sporadic and have had an uneventful recovery.Furthermore, desflurane,which has no proconvulsantproperties, has been associated with a similar, if not a greaterincidence of EA when compared with sevoflurane. Thesefacts suggest that the causality between theCNS effects ofsevoflurane and EA/ED is unlikely. As for the eventualneurotoxic influence of sevoflurane degradation products,there is no supporting scientific evidence. Postanesthesiaagitation has been described not only with sevoflurane anddesflurane, but also with isoflurane and, to a much lesserextent, with halothane. In a prospective trial that included521 children aged 3-7 year who were scheduled for electiveoutpatient surgery, isoflurane was identified as anindependent risk factor for EA.Children who receivedsevoflurane/isoflurane for the induction/maintenance ofanesthesia were twice as likely to develop EA whencompared with children who had any other anestheticregimen. Considering that sevoflurane-induced electro-encephalogram changes are similar to those observedduring the administration of either desflurane or isoflurane,but different from changes recorded with halothane, EA/EDmay be related to the similar CNS effects of theseanesthetics, which may affect brain activity by interfering

Review Article


with the balance between neuronal synaptic inhibition andexcitation in the CNS .

SURGERY-RELATED FACTORS

Pain

Postoperative pain has been the most confoundingvariable when assessing a child’s behavior upon emergencebecause of the overlapping clinical picture with EA/ED.Inadequate pain relief may be the cause of agitation,particularly after short surgical procedures for which peakeffects of analgesics may be delayed until the child iscompletely awake. In several studies, the preemptiveanalgesic approach successfully reduced EA/ED,suggesting that pain may be its major source.Intraoperativeadministration of IV ketorolac 1 mg/kg for minorotorhinolaryngological procedures decreased the incidenceof EA three to four times after both halothane (42% vs. 12%)and sevoflurane anesthesia (38% vs. 14%). Fentanyl, giveneither IV 2.5μg/kg or intranasal 2μg/kg during moderatelypainful surgery, also decreased EA.Alpha2 receptoragonists may offer advantages in preventing EA becausethey have both analgesic and sedative properties. On theother hand, post anesthesia agitation has been observedwhen pain was efficiently treated or even when absent.

Surgery type

Surgical procedures that involve the tonsils, thyroid,middle ear, and eye have been reported to have higherincidences of postoperative agitation and restlessness [5]. Ithas been speculated that a sense of suffocation duringemergence from anesthesia may contribute to EA in patientsundergoing head and neck surgery. However, there are nosupporting scientific data to date.

PATIENT-RELATED FACTORS

Age

Aono, et al. found that ED appeared more often withsevoflurane than with halothane in pre schoolboys aged 3-5year (40% vs 10%) [6]. The difference was not observed inthe school-aged population. All children received oraldiazepam for premedication and a caudal block forpreoperative pain control. The authors speculated that thepsychological immaturity of pre-school children, coupledwith the rapid awakening in a strange environment, mayhave been the main cause of ED.Generally, youngerchildren are more likely to show altered behavior uponrecovery from anesthesia. The sub population of those aged2-5 year seems to be the most vulnerable as they are easilyconfused and frightened by unexpected and unpredictableexperiences [7]. In a recent commentary on the diagnosis ofdelirium in pediatric patients, Martini addressed the role of

brain maturation in the genesis of this phenomenon [8]. Hepointed out that the pediatric brain is almost a mirror imageof a normal age-related regressive process with aconsequent decline in nor epinephrine, acetylcholine,dopamine, and gamma amino butyric acid (GABA). Thus,the development of cholinergic function and thehippocampus may suggest clues about the relativesusceptibility of younger children to delirium.

Preoperative anxiety

Intense preoperative anxiety, both in children and theirparents, has been associated with an increased likelihood ofrestless recovery from anesthesia. Kain, et al.retrospectively searched their database to determine therelationship between preoperative anxiety, ED, andpostoperative maladaptive behaviors [9]. They recruited791 children who were not premedicated and underwentsurgery and genera anesthesia using sevoflurane. The oddsof having marked symptoms of ED were increased by 10%for each increment of 10 points in the child’s state anxietyscore. However, a cause effect relationship between the twophenomena could not be demonstrated. Other authors failedto show a correlation between preanesthetic distress andED, possibly because of the small total number of patientsstudied and the use of a self-developed, no standardizedobservational scale for evaluating children’s distress.

Temperament

Children who are more emotional, more impulsive, lesssocial, and less adaptable to environmental changes wereidentified to be at risk for developing post anesthesiaagitation [10]. It is likely that there is some substrate innateto each child that will elicit, to a larger or lesser extent, afearful response to outside stimuli, depending on theinteraction between the child and the environment. Thisreactivity, which describes the excitability, responsivity, orarousability of the child , might be the underlying substratefrom which both preoperative anxiety and ED arise. Patient-related factors are an important source of variability amongstudies in the incidence of EA/ED as they are most difficultto control when investigating this phenomenon. In generalchildren who are calm and quiet upon arrival to thepreoperative area and do not show any signs of distress forprocedures like venepuncture or inhalational induction withface mask hardly show any signs of ED/EA in the postoperative period. This is a consistent finding in our hospital.

ADJUNCT MEDICATION

Numerous drugs, including anticholinergics,droperidol, barbiturates, opioids, benzodiazepines, andmetoclopramide, may contribute to behavioral disturbancesafter anesthesia.


Review Article

In summary, none of the above-discussed factors hasbeen proven to be the sole underlying cause of EA/ED.However, each factor, especially when combined with theothers, may influence the behavior of a child emerging fromanesthesia. The greatest barrier to a better understanding ofthe EA/ED etiology arises from the difficulty in comparingstudies that used different definitions, age spans, surgicalprocedures, and measuring tools, as well different sedative,analgesic, and other adjunct medication.

ASSESSMENT TOOLS FOR MEASURING EA/ED

Applying more than 15 different rating scales tomeasure EA/ED in clinical investigations suggests thatnone are sufficiently specific and sensitive to assesschildren’s behavior upon emergence In addition, it isdifficult to interpret behavior in small children who are notable to verbalize pain,anxiety, hunger, or thirst. Finally,opinions diverge on the point at which emergence extendsbeyond “normal”. Agitation, which is simple to assess, is themost frequently used descriptor for emergence behavior inchildren Most authors developed 3-5 point rating scales thatused either crying or thrashing requiring restraint as theirthreshold for agitation, which had a significant influence onthe calculated incidence of the event. Thus, Cravero, et al.recorded EA in 80% of sevoflurane patients when cryingwas used as a threshold, but in 33% of patients only whenthrashing was applied as the threshold for agitation [5].Several studies have tried to distinguish pain-relatedagitation from other sources by incorporating both pain andagitation scales into the methodology. Postoperativeagitation alone, however, does not always indicatesignificant behavioral changes associated with delirium. Anaccurate differen-tiation of delirium from other sources ofagitation requires the identification of more complexsymptoms of an acute mental disturbance. Thisdifferentiation may be difficult in young children who areoften oppositional and unable or unwilling to answer.Przybylo, et al. described an assessment tool that is based onthe items listed in the Diagnostic and Statistical Manual ofMental Disorders-IV for the diagnosis of delirium, buteliminated signs and symptoms that required verbalizationor skill demonstration [11]. Their scoring system studiedperceptual disturbances, hallucinations, and psychomotoragitation in 25 children aged 2-9 years who werepremedicated with midazolam and randomized to receiveeither isoflurane or remifentanil for strabismus surgery.Rectal acetaminophen was given for postoperative painrelief. The authors concluded that while 44% of childrenshowed altered behavior upon emergence, only 20% hadcomplex symptoms that were consistent with delirium.Furthermore, none of these children either verbalized painor received pain medication during the assessment period,reflecting the measurement of the phenomenon that was

independent of pain induced agitation.Sikich and Lermandeveloped the pediatric anesthesia emergence delirium(PAED) rating scale that consists of five psychometric itemsfor the measurement of ED in children [12]. According tothe Diagnostic and Statistical Manual of Mental Disorders -IV, three of these items are an important part of delirium andmay be crucial to its differentiation from pain .A decreasedability of the child to make eye contact with the caregiverand a declined awareness of his surroundings reflectdisturbances in consciousness with a reduced ability tofocus, sustain, or shift attention. Less purposeful actionssuggest cognitive changes that include perception andmemory impairment as well as disorganized thinkingpatterns. Two other items, restlessness and inconsolablecrying, reflect a disturbance in psychomotor behavior andemotion, although they may also suggest pain orapprehension. The PAED scale score correlated negativelywith the child’s age and time to awakening and wassignificantly greater in children who received sevofluranethan in those who received halothane. These results andthose of another study support the reliability and validity ofthe PAED scale. Unfortunately, the authors did not definethe ED threshold, which makes the calculation of itsincidence impossible and the development of therapeuticapproaches rather difficult.

PREVENTION AND TREATMENT

Given that the EA/ED etiology is still unknown, a clearcut strategy for its prevention has not been developed. Dataon the possible role of premedication in reducing EA/EDhave been conflicting. Preoperative administration ofmidazolam decreased postoperative agitation after bothsevoflurane and desfluraneanesthesia, with no delay indischarge from hospital. When analyzing those rare trialsthat failed to reveal the difference between sevoflurane andhalothane in the incidence of EA/ED, it was striking to notethat midazolam was used consistently, although at differentdosages and via different routes of administration.Sevoflurane at high concentrations has been shown toenhance, and at low concentrations to block, GABA Areceptor-mediated inhibition of neurotransmission in theCNS. Olsen, et al. Suggested that midazolam may improverecovery after sevoflurane administration by enhancing theinhibitory effects of GABA A receptors [13]. Thisproposition is supported by findings of a calmer recoveryfrom sevoflurane-maintained anesthesia when induced withpropofol but not with sevoflurane. Another possibleexplanation is that stressful induction and/or a rapid returnto consciousness in non-premedicated children may resultin more behavioral disturbances upon emergence .On theother hand, there are studies in which midazolampremedication did not show any benefit on the quality ofrecovery from anesthesia.This finding may possibly be the

Review Article


result of applying a nonspecific measuring tool or aprovision of inadequate pain control. The combination ofmidazolam and a small dose of diazepam may extend thebeneficial effects of premedication until the recovery phase,which decreases the incidence of EA/ED. Paradoxically,Cole, et al. reported an almost nine fold higher risk of thedevelopment of EA in children who were premeditated withmidazolam over those who were not premedicated beforeoutpatient surgery under either isoflurane or halothaneanesthesia [7]. Benzodiazepines themselves are associatedwith paradoxical reactions and agitation that are reversedwith flumazenil. Furthermore, theantianalgesic effects ofmidazolam might worsen pain and increase the incidence ofnonspecific agitation that resembles ED. Premedicationwith melatonin has proven to be a good alternative tomidazolam in reducing postoperative excitementOxycodone has been shown to decrease the frequency ofagitation in children undergoing halothane, but notsevoflurane, anesthesia for myringotomy procedures. Bothoral ketamine and oral transmucosal fentanyl citrate werealso helpful, although the latter increased the incidence ofside effects. Some authors have advocated switchinganesthetics after induction, despite a lack of scientificevidence supporting this practice.Various preemptiveanalgesic approaches, including caudal block, fentanyl,ketorolac, clonidine, and dexmedetomidine, have beenrecommended to eliminate pain as a potential source ofdiscomfort and agitation. One trial suggests that IV fentanyl1μg/kg before the conclusion of sevoflurane anesthesiadecreases EA even after no painful procedures, whileleaving the time of discharge unchanged [14]. On the otherhand, parental presence in the operating theater appeared tohave no influence on the incidence and/or severity ofdistress behavior upon emergence. As for managing EA/ED, certain steps should be taken to protect the child fromself-injury. Holding, as a means of providing physicalrestraint, and engaging more than one caregiver are oftennecessary. As the child may be upset by environmentalstimuli, it is important to provide a quiet, darkened recoveryroom. The decision of whether to treat EA/ED withadditional medication depends upon the severity andduration of symptoms. Many studies have shown that EA/ED is self-limited, resolving without pharmacologicalintervention over time. Rescue medication includesanalgesics, benzodiazepines, and hypnotics. Fentanyl IV 1-2μg/kg, propofol IV 0.5-1.0 mg/kg, and midazolam IV0.02–0.10 mg/kg have all been used for the treatment of ED[15]. A single bolus dose of dexmedetomidine 0.5μg/kg wasalso shown to be efficient in the PACU forED. Voepel-Lewis, et al. found that PACU nurses caring for agitatedchildren most often administered analgesics/sedatives asthe first intervention, irrespective of the primary cause ofagitation [16]. However, the most effective intervention was

reuniting with a parent. The authors also developed thepostoperative agitation algorithm, which may serve as aguide for the assessment and treatment of ED in the PACU.

LONG-TERM CONSEQUENCES

There is no evidence that EA/ED has any impact onlong-term outcome [17]. Akin, et al. suggested that ED andnew-onset postoperative maladaptive behavior changes areclosely associated. The authors found that the odds ratio ofhaving one or more new onset postoperative maladaptivebehavior changes is 1.43 for children with markedemergence status when compared with children with nosymptoms of ED, but did not suggest a cause effectrelationship between these two phenomena.

SUMMARY

It appears that almost half a century after the first casesof emergence agitation/emergence delirium(EA/ED) werereported [18], we do not know much more about its etiology,nor do we have a reliable assessment tool or clear-cutpreventive strategy for this short lived but troublesomeclinical event. Both sevoflurane and desflurane (andpossibly isoflurane) are indisputably associated with ahigher incidence of altered behavior upon emergence thanare either halothane or propofol. It is doubtless that youngerage, preoperative anxiety, and pain are all importantcontributory factors. However, there are still manyquestions that deserve answers. What links the above-mentioned inhaled anesthetics to EA/ED? Are we able toidentify a child who is at risk for the development of EDwithout engaging psychologists to interpret extensivequestionnaires about their temperaments? Will the use ofcomplicated psychometric tests for the evaluation of achild’s mental status upon emergence change ourtherapeutic approach when either agitation or deliriumoccurs? Finally, shall we wait for this behavior to resolvespontaneously and risk a child’s self injury and parentaldistress, or treat it routinely and face potential adverseeffects of the given medication? Obviously, further trials arenecessary to discover the underlying causes of EA/ED andto determine which factors might help predict andpotentially prevent it. For consistency, it seems reasonablefor studies to target the most vulnerable population ofpreschool aged children scheduled for similarly painfulsurgical procedures and to stratify patients with regard totheir temperament. In addition, pain must be tightlycontrolled and standardized measuring tools used toevaluate post anesthesia behavior.

It is important to remember that several life threateningconsiderations (e.g., hypoxia, severe hypercarbia, hypo-tension, hypoglycemia, increased intracranial pressure)may also result in disorientation and altered mental status.


Review Article

These entities must be diagnosed and treated promptly.Bladder distention may also yield a similar clinical picture.

REFERENCES

1. Holzki J, Kretz FJ (editorial). Changing aspects ofsevoflurane in pediatric anesthesia: 1975-1999. PaediatrAnaesth 1999; 9:283-286.

2. Jerome EH. Recovery of the pediatric patient fromanesthesia. In Gregory GA, ed. Pediatric anesthesia. 2ndEd. New York: Churchill Livingstone, 1989, 629.

3. Gordano P. Vlajkovic, Radomir P. Sindjelic. EmergenceDelirium in Children: Many Questions, Few Answers.Anesth Analg 2007; 104: 84-91.

4. Bosenberg AT. Convulsions and sevoflurane. PediatricAnaesth 1997; 7: 477-478.

5. Davis PJ, Greenberg JA, Gendelman M, Fertal K.Recovery characteristics of sevoflurane and halothane inpreschool-aged children undergoing bilateralmyringotomy and pressure equalization tube insertion.Anesth Analg 1999; 88:34-38.

6. Aono J, Mamiya K, Manabe M. Preoperative anxiety isassociated with a high incidence of problematic behavioron emergence after halothane anesthesia in boys. ActaAnaesthesiol Scand 1999; 43: 542-544.

7. Cole JW, Murray DJ, McAllister JD, Hirschberg GE.Emergence behavior in children: defining the incidence ofexcitement and agitation following anesthesia. PediatricAnaesth 2002; 12: 442-447.

8. Martini DR. Commentary: the diagnosis of delirium inpediatric patients. J Am Acad Child Adolescent Psychiatry2005; 44: 395-398.

9. Kain ZN, Mayes LC, Wang SM, et al. Parenteral presenceduring induction of anesthesia versus sedative

premedication: which intervention is more effective?Anesthesiology 1998; 89:1147-1156.

10. Cravero JP, Beach M, Dodge CP, Whalen K. Emergencecharacteristics of sevoflurane compared to halothane inpediatric patients undergoing bilateral pressureequalization tube insertion. J Clin Anesth 2000; 12: 397-401.

11. Przybylo HJ, Martini DR, Mazurek AJ, et al. Assessingbehavior in children emerging from anesthesia: can weapply psychiatric diagnostic techniques? PediatricAnaesth 2003; 13:609-616.

12. Sikich N, Lerman J. Development and psychometricevaluation of the pediatric anesthesia emergence deliriumscale. Anesthesiology 2004; 100: 1138-1145.

13. Olsen RW, Yang J, King RG, et al. Barbiturate andbenzodiazepine modulation of GABA receptor binding andfunction. Life Sci 1986; 39:1969-1976.

14. Cravero JP, Beach M, Thyr B, Whalen K. The effect of smalldose fentanyl on the emergence characteristics ofpediatric patients after sevoflurane anesthesia withoutsurgery. Anesth Analg 2003; 97:364-367.

15. Cohen IT, Finkel JC, Hannallah RS, et al. The effect offentanyl on the emergence characteristics after desfluraneor sevoflurane anesthesia in children. Anesth Analg 2002;94:1178-1181.

16. Voepel-Lewis T, Burke C. Differentiating pain and deliriumis only part of assessing the agitated child. J PerianesthNurse 2004; 19: 298-299.

17. Kain Z. Postoperative maladaptive behavioral changes:incidence, risks factors, and interventions. ActaAnesthesia Scand 2000; 51:217-226.

18. Eckenhoff JE, Kneale DH, Dripps RD. The incidence andetiology of post anesthetic excitement. Anesthesiology1961; 22:667-673.

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Emergence Delirium (ED) in Children

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