Emergence Agitation, Laryngospasm and Anesthesia-Related ...

LESSON 12Volume 44*10/14/2021

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Emergence Agitation, Laryngospasm and Anesthesia-Related Cardiac Arrest:

How to Stay Out of Trouble in Pediatric Anesthesia

Linda Mason, MDProfessor of Anesthesiology and Pediatrics,

Loma Linda UniversityDirector of Pediatric Anesthesiology,

Loma Linda University Medical CenterLoma Linda, California

Elizabeth Ghazal, MDAssociate Professor of Anesthesiology


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151Curr Rev Nurs Anesth 44(12):149-164 2021

Emergence Agitation, Laryngospasm and Anesthesia-Related Cardiac Arrest:

How to Stay Out of Trouble in Pediatric Anesthesia

Linda Mason, MDProfessor of Anesthesiology and Pediatrics, Loma Linda University

Director of Pediatric Anesthesiology,Loma Linda University Medical Center

Loma Linda, California

Elizabeth Ghazal, MDAssociate Professor of Anesthesiology


Upon completion of this lesson the reader should be able to:

LESSON OBJECTIVES

1. Recognize the characteristics of emergence agitation. 2. Identify those anesthetic agents associated with emergence agitation. 3. Develop a treatment strategy for emergence agitation. 4. Understand the etiology of laryngospasm. 5. Review the complications of laryngospasm. 6. Define a treatment plan for laryngospasm. 7. Discuss current etiologies of anesthesia-related cardiac arrest in pediatric patients. 8. List events commonly preceding cardiac arrest in pediatric patients. 9. Name the various registries tracking anesthesia-related cardiac arrest.10. Describe prevention strategies for anesthesia-related cardiac arrest.

IntroductionComplications in pediatric anesthesia still occur despite advances in monitoring, increased medica-tion safety initiatives and highly specialized anes-thesia providers. These complications range from adverse events to those leading to severe sequelae or death. This lesson will focus on emergence agi-tation, laryngospasm and anesthesia-related car-diac arrest in pediatric patients.

Emergence Agitation

Features of EAEmergence agitation (EA) is a well-documented

phenomenon occurring in children and adults in

the immediate postoperative period. EA is de-fined as a dissociated state of consciousness in which the child is inconsolable, irritable, uncompromising or uncooperative. Typically, the child is thrashing, crying, moaning, or incoher-ent with no eye contact and no awareness of sur-roundings. Characteristically, these children fail to recognize familiar and known people or objects. Parents who witness this state claim the behavior is uncustomary for the child. Although generally self-limiting, EA can be severe and may result in physical harm. While EA and emergence delirium (ED) are used synonymously and interchangeably, they differ in that EA denotes physical hyperactiv-ity when compared to ED, which is a psychologic derangement upon awakening.

Current Reviews for Nurse Anesthetists® designates this lesson for 1.5 contact hours in Pharmacology/Therapeutics.


IncidenceEA is not a new phenomenon and is greatest in

children 1 to 5 years of age. It has been reported after the introduction of every new anesthetic, in-cluding most inhalational and intravenous agents. The incidence of EA in all postoperative patients is 5.3% but it occurs more frequently in children (12 - 13%). The reported incidence of EA after halothane, isofl urane, sevofl urane and desfl urane ranges from 2 – 55%. A variable incidence of EA has been reported in the literature because many studies have used non-validated scales.

EtiologyThe cause of EA remains unknown. Some hy-

potheses attribute the etiology to postoperative pain as well as to pharmacokinetics and the phar-macodynamics of anesthetic agents. EA occurs fol-lowing non-painful procedures (e.g. MRI); thus, the involvement of pain in the genesis of EA remains controversial. Likewise, some studies have noted EA in children after sevofl urane despite effective regional anesthesia. It has also been postulated that this phenomenon has become more acutely

noticed with the increased use of agents that have a rapid emergence profi le such as sevofl urane and desfl urane. It was postulated that rapid emergence with lack of adequate pain control was the cause of EA. It must be recognized that in many of the stud-ies, it may be diffi cult to differentiate pain-related agitation from other causes in the early postopera-tive period.

Implications of EAThe long-term psychologic implications of EA

remain unknown. However, agitation on emer-gence from anesthesia can be severe and may result in physical harm to the child, caregiver or site of surgery (including the pulling out of a sur-gical drain or an IV catheter). EA also demands increased nursing care in the post-anesthesia care unit (PACU), may require pharmacologic interven-tion and a prolonged PACU stay while waiting for the effects of the interventional drugs to dissipate.

Anesthetic Agents and EAVolatile anesthetic agents: All volatile anes-

thetic agents have been recognized as contributing to EA, with the suggestion that sevofl urane has the greatest propensity. In more than one study, chil-dren who received sevofl urane as a maintenance anesthetic had a greater incidence of EA compared with propofol. However, despite EA, sevofl urane still provided a shorter PACU stay than propofol.

ASA American Society of Anesthesiologists

ASAPS American Society of Anesthesiologists physi-cal status

ARCA Anesthesia related car-diac arrest

CA Cardiac arrest

CHD Congenital heart disease

EA Emergence agitation

ED Emergence delirium

ETS Environmental tobacco smoke

IV Intravenous

IM Intramuscular

LMA Laryngeal mask airway

PACU Post-anesthesia care unit

PAED Pediatric Anesthesia Emergence Delirium

POCA Pediatric perioperative cardiac arrest

URI Upper respiratory tract infection

Table of Acronyms

Table 1 The Pediatric Anesthesia

Emergence Delirium (PAED) Scale

1. The child makes eye contact with the caregiver.2. The child’s actions are purposeful.3. The child is aware of his/her surround- ings.4. The child is restless.5. The child is inconsolable.

1, 2, and 3 are reverse scored as 4 = not at all, 3 = just a little, 2 = quite a bit, 1 = very much, 0 = extremely.

4 and 5 are scored as 0 = not at all, 1 = just a little, 2 = quite a bit, 3 = very much, 4 = extremely.

The scores are added to obtain a total PAED scale score. A score of 10 – 12 is diagnostic of EA.

Sikich N, Lerman J. Anesthesiology 2004; 100: 1138-45.


α2 –Agonists: The addition of clonidine given intravenously at 2 μg/kg after induction of anes-thesia decreases EA when compared to the placebo group (in one study). In another study, a single dose of intravenous dexmedetomidine, 0.3 μg/kg after induction, and maintenance of anesthesia with sevofl urane also contributed to decreased EA with no adverse effects. Children in both studies received regional anesthesia. A similar lower inci-dence of EA with dexmedetomidine was duplicated in multiple other studies, with and without surgery.

Benzodiazepines: Preoperative administra-tion of oral midazolam has reduced the incidence of EA as compared with placebo in one study. How-ever, this may be due to slower awakening rather than decreased preoperative anxiety. Other data have contradicted this notion and demonstrated a similar incidence of EA in those who received pre-operative midazolam compared with those who did not. Furthermore, benzodiazepines have been as-sociated with paradoxical reactions and agitation that have been reversed with fl umazenil. Taken together, these data raise doubts about a potential relationship between preoperative anxiety and EA.

Factors Contributing to EA A recent prospective cohort study of EA in the

pediatric PACU gives us more insight into patients at risk for this phenomenon. This study enrolled 521 children (age 3-7 years) who were undergoing general anesthesia for elective outpatient proce-dures. Eighteen percent had EA lasting up to 45 minutes (mean duration, 14 minutes) and 52% re-quired pharmacologic intervention accompanied with a prolonged PACU stay. Factors that were found to be associated with EA are:

• Younger age • No previous surgery• Type of surgery – ophthalmology and oto-

rhinolaryngology procedures• Use of sevofl urane, isofl urane, sevofl urane/ isofl urane, and analgesics • Pre-existing behaviors – low adaptability

(i.e., inability to readily adapt to new situations)• Short time to awakening

This study also identifi ed that otorhinolaryngology procedures, short time to awakening and the use of isofl urane were independent risk factors for EA.

Emergence agitation is greatest in young children, especially after tonsillectomy and strabismus surgery.

EA ScalesThe diagnosis of EA can be made by using the

Pediatric Anesthesia Emergence Delirium Scale

(PAED), as described in Table 1. Five behaviors are scored and a total score value of > 10 – 12 is diagnostic of EA. Several other scales have been developed to measure EA, although only one, the PAED, has been validated.

A risk scale for EA has been developed that includes four predictors: younger age, operative procedures, preoperative behavior score, and anes-thesia time as detailed in Table 2. This scale can be used to predict EA and allow for prophylactic treatment.

Treatment of EAWhen EA does occur, it usually lasts < 15-

20 minutes and resolves spontaneously if the child is left undisturbed. EA may be treated pharmacologically or, alternatively, it will run its natural course. Treatment options in-clude propofol (0.5 mg/kg IV), fentanyl (1 – 2 μg/kg IV), midazolam (0.02 mg/kg IV) or dex-medetomidine (0.3 μg/kg IV). When deciding on therapy, it is important to note that an occasional child may have a paradoxical reaction to midazol-am, characterized by agitation, combativeness or inability to be consoled. If the reaction is suspect-ed, consider the use of fl umazenil (0.01 mg/kg IV, max dose 0.2 mg/dose) at 1 – 2 minute intervals to a maximum of 1 mg. Discharge from the PACU may be delayed while waiting for the delirium to resolve

Table 2 Risk Scale for Emergence Agitation

Values Score

Age 9 minus age

Operative procedure

- Strabismus surgery - Tonsillectomy - Others

770

Preoperative behavior score

- Screaming and shouting - Tearful and/or withdrawn but compliant - Calm and controlled

42

0

Anesthesia Time

- Over 2 hours - 1-2 hours - < 1 hour

420

Total score of 11 – 90% accuracy in predicting EA.

Hino M, Mihara T, Miyazaki S, et al. Anesth Analg 2017;125:550-5.


spontaneously or for the effect of the pharmacologic intervention to dissipate.

Prevention of EAStrategies to improve outcomes and decrease

EA include non-pharmacologic techniques to de-crease preoperative anxiety, choice of anesthetic technique and medications and the provision of adequate analgesia. Pharmacologic prophylactic measures are listed in Table 3.

Diff erential DiagnosisIt is important to remember that several life-

threatening considerations (e.g., hypoxia, severe hypercarbia, hypotension, hypoglycemia, increased intracranial pressure) may also result in disorien-tation and altered mental status. These entities must be diagnosed and treated promptly.

EA remains a signifi cant post-anesthetic prob-lem that may present a diagnostic challenge in the PACU and interfere with the child’s recovery. An understanding of the potential risk factors that contribute to EA and implementation of preventive

measures will aid in decreasing the incidence and severity of EA and overall increase parental satis-faction.

LaryngospasmLaryngospasm is a relatively frequent an-esthetic complication, which may result in signifi cant morbidity. This condition occurs as a result of an exaggerated and prolonged laryngeal closure refl ex triggered by me-chanical (manipulation of pharynx/larynx) or chemical stimuli (secretions, gastric fl uids). The diagnosis is based on clinical suspicion and manifests as partial or complete airway obstruction. When complete laryngospasm oc-curs, breath sounds and air movement are absent. Late clinical signs are oxygen desaturation, brady-cardia and cyanosis.

Incidence and ComplicationsThe overall incidence of laryngospasm in chil-

dren has been reported as 1-2% with the highest

Prophylactic Measure

Dose, timing and effect

Propofol (IV) • TIVA, a brief infusion of 3 mg/kg over 3 minutes after sevofl urane.• A single dose at the end of anesthesia (1 mg/kg).

Opioids • Do not defi nitely decrease EA.• Adequate analgesia warrants use, as pain behavior can be misrep- resented as EA.

Midazolam • May not decrease EA. • Decreased preoperative anxiety and maladaptive behavior postopera- tively warrants use.

Dexmedetomidine • Decreased incidence and degree of EA (pre- or intra-operatively).• 1-2 μg/kg intranasally preoperatively.• 0.3 μg/kg - 1 μg/kg at emergence.

Gabapentin • Decreased severity of EA in healthy children; not commonly used.• 15 mg/kg po premedication.

Ketamine • Premedication decreases EA ; 1mg/kg IV or 6 mg/kg orally.• 1 mg/kg IV followed by 1 mg/kg/hr (equally effective as dexmedetomidine).

Magnesium • May decrease incidence of EA after adenotonsillectomy.• 30 mg/kg IV followed by 10 mg/kg/hr.

Melatonin • Decreased incidence of EA.• No effect on preoperative anxiety.• 0.25 – 0.5 mg/kg premedication.

Regional Anesthesia

• No defi nitive evidence to suggest that, in combination with sevofl urane, decreases EA.

Table 3 Prophylactic Measures to Prevent Emergence Agitation


incidence (2.8%) in infants 1-3 months of age. The incidence of laryngospasm is increased in children with an upper respiratory tract infection (URI), in airway surgery and in those being cared for by an inexperienced anesthesia provider.

Although treatable, occasionally laryngospasm may result in severe hypoxemia and cardiac arrest (CA). Other complications include bronchospasm, gastric aspiration, arrhythmias, delayed recovery and negative pressure pulmonary edema.

Etiology and Risk FactorsLaryngospasm occurs as a response to glottic or

subglottic mucosal stimulation and continues long after the stimulus is gone. Risk factors include younger age, oral airway or naso-gastric tube place-ment, oral secretions, endoscopy or esophagoscopy, upper respiratory infections or volatile anesthetics.

Two areas have come into focus as relative to the risk of development of laryngospasm. First, in a study of children in a day surgery unit who had general anesthesia, those who developed laryngo-spasm were 2.05 times more likely to have an ac-tive URI. They were also more likely to be younger and undergoing airway surgery. Furthermore, anesthetizing a child with a URI may have a higher incidence of complications if the patient requires intubation. In children with a URI, laryngeal mask airway (LMA) use, instead of intubation, results in a laryngospasm rate equal in both groups, but the incidence of mild bronchospasm is higher in the in-tubated group. Therefore, LMA use may be a suit-able alternative if the decision is made to proceed with anesthesia in a child with a URI. However, with LMA use, children with the presence of any 2 risk factors (cold < 2 weeks, wheezing < 12 months, wheezing with exercise, nocturnal dry cough, ec-zema, passive smoking, family history of hay fever/asthma/eczema) benefi ted from an IV induction with propofol rather than an inhalation induction with sevofl urane (in decreasing respiratory ad-verse events).

Second, children exposed to environmental to-bacco smoke (ETS), were studied. Of those exposed to ETS, 9.4% developed laryngospasm while in those without domestic ETS exposure, only 0.9% developed laryngospasm. All occurred on emer-gence from general anesthesia. The risk for laryn-gospasm is greater if the source of passive smoke is from the caretaker.

ManagementLaryngospasm may present as complete or in-

complete airway obstruction. If incomplete airway obstruction occurs, sounds should be present (e.g., grunts, expiratory “squeaks”). The initial treatment for airway obstruction is jaw thrust and chin lift. The middle fi nger of each hand should be placed in the “laryngospasm notch”, behind the lobule of the

Table 4 POCA Data 1994-1997

Mechanism of Cardiac Arrest

Mechanism Arrests, %

Medication-related • Cardiovascular depression from halothane alone or in combination; 2/3 of all medication- related arrests • Intravascular injection of local anesthetic with caudal (4 cases/150), 0.25% bupivacaine with epi 1/200,000 (3 needle, 1 catheter)

37

Cardiovascular • Hemorrhage • Inadequate/inappropriate fl uid therapy • Arrhythmia • Hyperkalemia • Air embolism • Pacemaker-related • Vagal response • Pulmonary hypertension • Tetralogy hypercyanotic spell

32

Respiratory • Laryngospasm • Airway obstruction • Diffi cult intubation • Inadequate oxygenation • Inadvertent extubation • Presumed respiratory, unclear etiology • Inadequate ventilation • Bronchospasm

20

Equipment-related • Central line • Breathing circuit • Peripheral intravenous catheter

7

Multiple events 3

Hypothermia <1

Unclear etiology <1

Morray et al Anesthesiology 2000; 93:6-14.


pinna of each ear. It is bounded anteriorly by the ascending ramus of the mandible, posteriorly by the mastoid process of the temporal bone and ceph-alad by the base of the skull. Firm inward pressure toward the base of the skull while simultaneously lifting and displacing the mandible forward may be effective in converting laryngospasm to laryngeal stridor and unobstructed respirations within 1 or 2 breaths. This maneuver should include the admin-istration of 100% oxygen with gentle positive pres-sure while keeping in mind that incomplete airway obstruction may rapidly become complete.

Complete airway obstruction shares many of the signs of incomplete airway obstruction – tra-cheal tugging, chest wall retractions with marked abdominal respiration – but there is no sound present. Positive pressure will not “break” laryn-gospasm in the presence of complete airway ob-struction. It may worsen it by forcing supraglottic tissues downward into the glottic opening. High pressure generated by the fl ush valve may dilute anesthetic gases, and lead to a lighter level of an-esthesia. It may also force gas down the esophagus into the stomach making ventilation more diffi cult.

Positive pressure will not “break” laryngo-spasm in the presence of complete airway obstruction.

If IV access is present, succinylcholine 0.5 – 1 mg/kg with atropine 0.02 mg/kg can be given. If no IV access is present IM succinylcholine 4 mg/kg is recommended to be given in the deltoid muscle. If laryngospasm is sustained and the child is ex-tremely hypoxic it may be necessary to intubate the trachea. If these measures have not proved suc-

cessful in securing the airway, cricothyrotomy or emergency tracheostomy may be required.

PreventionAvoiding extubation, mucosal stimulation and

tracheal suctioning during a light plane of anesthe-sia helps prevent laryngospasm. The effect of lido-caine on laryngospasm prevention is controversial. Intravenous lidocaine 2 mg/kg given one minute before extubation may attenuate or prevent laryn-gospasm. However, one study suggested that lido-caine does not prevent laryngospasm if extubation after swallowing occurs.

Anesthesia-Related Cardiac Arrest (ARCA)

Historical PerspectivePerioperative cardiac arrest (CA) in children is

a rare but catastrophic event. The increased risk of CA in children compared to adults was fi rst report-ed in the 1950s. The etiology of CA in the pediatric patient has changed as practice has evolved over the last half-century. With respect to morbidity and mortality, available data comes from 3 sources: closed claims analysis, large-scale studies of ARCA and institutional audits. These reports will be re-viewed in chronological order.

Pediatric Closed Claims Study, 1993 Since 1985, the Committee on Professional Li-

ability of the American Society of Anesthesiologists (ASA) has evaluated closed anesthesia malpractice claims. The database fi ndings were fi rst published in 1993 and revealed that respiratory events were the most common cause of CA, accounting for 43% of the claims. These events resulted in a severe de-gree of injury and signifi cant liability with larger payments awarded for permanent injury (as op-posed to death). In the opinion of the reviewers, the majority of the claims were related to inadequate ventilation and could have been prevented with better monitoring with pulse oximetry and capnog-raphy.

Pediatric Perioperative Cardiac Arrest (POCA) Registry, 1994-1997

The POCA Registry was formed in 1994 with 63 institutions voluntarily enrolling. Over the initial study period, more than a million anesthetics were administered in these institutions. Of the reported cases, 150 were determined to be ARCAs with an overall incidence of 1.4 per 10,000. The profi le of the 150 cases of ARCA is detailed in Table 4.

An increased incidence of cardiovascu-lar causes (32%) compared to the Pediatric Closed Claims Study (13%) was observed in


Most Common Events (One or More) Preceding Cardiac Arrest

Event %

Bradycardia 54

Hypotension 49

SpO2 abnormality 46

Inability to measure BP 25

ETCO2 abnormality 21

Cyanosis 21

Arrhythmia 16

No recognized warning 11

Morray et al Anesthesiology 2000; 93:6-14.


the POCA Registry. This may be due to the fact that providing chest compressions was a necessary entry criterion to the Registry. Another factor may be that better monitoring occurred during this time period. The majority of arrests occurred during in-duction or maintenance, usually following one or more of the antecedent events listed in Table 5. An additional 21% occurred during emergency surgery.

Another fi nding was that infants younger than 1 year of age accounted for 55% of the ARCAs. Sev-eral other studies confi rmed that infants < 1-year have the highest anesthetic risk and that mortal-ity is inversely proportional to age with the high-est risk in the < 1-month age group. This may be notably related to a higher ASA Physical Status (ASAPS) Classifi cation with underlying disease, particularly congenital heart disease (CHD), and also to cardiovascular depression by inhalational agents. During this same time frame, other studies


Cause of Cardiac Arrest (n=193)

Cause % of 193

Cardiovascular • Hypovolemia associated with blood loss, 12% • Electrolyte imbalance, 5% • Hypovolemia (non-hemorrhage), 3% • Air embolism, 2%

41

Respiratory • Airway obstruction, Laryngospasm, 6% • Airway obstruction, other, 3% • Inadequate ventilation/ oxygenation, 5% • Diffi cult intubation, 1% • Esophageal intubation, 2% • Bronchospasm, 2% • Pneumothorax, 1% • Aspiration, 1%

27

Medication 18

Equipment 5

Multiple events 2

Miscellaneous 1

Unknown 6

Bhananker SM et al. Anesth Anlag 2007;105:344-50

showed that sevofl urane was less of a myocardial depressant and had less potential for producing bradycardia than halothane in infants.

One third of all cardiac arrests occurred in pre-viously healthy ASAPS 1-2 patients. Medication-related arrests were more common and cardiovas-cular etiologies less common in ASAPS 1-2 patients than in ASAPS 3-5 patients.

Severe underlying disease and emergency surgery are strongly associated with poor outcomes following cardiac arrest.

The outcome in 26% of cases resulted in death while 6% suffered permanent injury. CHD was present in 38% of the patients who did not survive. After multivariate analysis, the database fi ndings showed that ASAPS 3-5 was the strongest predictor of death. The mortality rate in this group was 37% compared with 4% in ASAPS I – II pa-tients.

In summary, patients younger than 1 year of age accounted for > 50% of all arrests, and medi-cation-related and cardiovascular causes of arrest were most common (together accounting for 69% of all arrests). Severe underlying patient disease and emergency surgery were the factors most strongly associated with poor outcomes following cardiac ar-rest in anesthetized children.

POCA Registry Update, 1998-2004In a subsequent report, an additional 397 cases

from 80 institutions were reported to the POCA Registry, and 49% of these were ARCAs. The profi le of cardiac arrest in anesthetized children changed as halothane use declined in favor of sevofl urane. Medication-related causes decreased with the near disappearance of cardiovascular depression from inhaled agents. However, cardiovascular causes increased as detailed in Table 6. Hypovolemia, often from hemorrhage in spine fusion or craniectomy/craniotomy, and the metabolic consequences of massive transfusion (usually hyperkalemia) were the most frequent identi-fi able causes of arrest in this category. The ex-act cause of arrest could not be determined in some cases in the cardiovascular category, but frequently these were children with CHD and an ASAPS 3-5.

Respiratory-related causes increased and ac-counted for 27% of arrests and the most frequent cause was laryngospasm. None of the laryngo-spasm arrests resulted in death, although 3 of 11 patients developed negative pressure pulmonary edema. Respiratory-related arrests often occurred in patients with an unprotected airway during emergence or recovery.

Equipment problems, mainly complications from central venous catheter placement, have


stayed fairly constant as a cause of arrest in pedi-atric patients, around 5 – 7%.

The demographic profi le since 1998 also changed and the characteristics are displayed in Table 7. Three quarters of the arrests occurred in patients of ASA PS 3 –5 and there were proportionately few-er patients < 1-yr. A comparison of the changing causes of ARCA in children in the two time periods of the POCA Registry is provided in Figure 1.

Cardiovascular events were the most identifi -able cause of anesthesia related cardiac ar-rests in the latest POCA Registry.

Finally, in the current study, hypovolemia was the most common cause of cardiovascular arrest. Therefore, the anesthesia provider involved in these high-risk cases must pay close attention to anticipating, estimating, and replacing blood loss. Other strategies to reduce blood loss should be uti-lized including autologous transfusions, blood sal-vage, antifi brinolytics and control of arterial blood pressure.

As far as outcome of ARCA, mortality was simi-lar to the initial report. The only factors predictive of mortality after CA were ASAPS and emergency surgery.

Other StudiesSeveral single-institution (including tertiary

care referral centers) studies show similar fi ndings where ASA PS ≥ 3, age < 1-year, the presence of CHD and/or cardiac surgery were identifi ed as the main risk factors for CA. In addition, both CA inci-dence and mortality were highest among neonates undergoing cardiac procedures. Most patients who experienced POCA had underlying CHD.

Advances in monitoring and the declining use of halothane have led to a change in the types of complications in pediatric anesthesia over recent decades. Despite safety improvements in anesthe-sia from the 1950s until the present, 2 risk factors

in ARCA remain constant: young age and ASAPS ≥ 3, especially in those with CHD.

High Risk Settings and Preventive Strategies

The historical perspective from various registries and single institutions has allowed the recognition of trends and high-risk situ-ations. This information provides useful in-sight and places the entire care delivery team on alert. These high-risk situations may be sum-marized as:

1) Age: An increased rate of ARCA in chil-dren < 1-year of age compared to older chil-dren. Children < 1- month of age accountedfor 24% of all cardiac arrests and had a mortality of 72%, the highest for any age group

2) ASAPS and emergency surgery: Death fol-lowing ARCA was predicted most strongly by these two factors.

3) Heart Disease: Children with congenital or acquired heart disease have an increased risk of anesthesia related morbidity and mortality with the risk directly related to the severity of disease. High-risk conditions include: unrepaired complex cardiac lesions, systemic arterial to pulmonary ar-terial shunts, Williams syndrome, pulmonary hy-pertension with pulmonary artery pressures equal to or higher than systemic, valvular heart disease with signifi cant valvular gradients, hypertrophic obstructive cardiomyopathy or ventricular assist devices.

Anesthesia related cardiac arrest risk factors are young age, ASA physical status ≥ 3, espe-cially with congenital heart disease.

The greatest value of risk profi ling is identifi -cation of high-risk patients and the ability to for-mulate the best possible management plan. A summary of high-risk patients and complication prevention strategies is provided in Table 8.

Table 7: POCA Registry Demographic Comparison

1994-1997 1998-2004

ASA I – II 33 25

Age < 1 year 56 38

Emergency 21 21

Mortality 26 28

Bhananker SM et al. Anesth Analg 2007;105:344-50


Condition Potential Complication Prevention Strategy

Former premature infant Increased risk for postopera-tive apnea until > 55 weeks of postconceptual age.

Monitoring until at least 12 apnea-free hours have elapsed.

Irritable airway, recent URI Laryngospasm Avoid airway instrumentation during light plane of anesthesia; consider early placement of an IV catheter.

Spine fusion or craniotomy procedures

Hypovolemia from blood loss. Reliable vascular access; blood available in OR.

Massive transfusion Hyperkalemia Use of fresh PRBCs and saline washing of irradiated cells.

Congenital or acquired heart disease with high-risk lesions

Perioperative cardiac arrest. Consider assignment of anesthesia providers experienced in the man-agement of such patients.

Placement of central venous pressure catheters

Pneumothorax, hemothorax or hemopericardium.

Injuries potentially preventable with the use of ultrasound or pressure waveform monitoring.

Regional anesthesia Intravascular local anesthetic injection despite negative aspi-ration or negative test dose.

Use of agents with less myocardial toxicity, e.g., ropivacaine and incre-mental rather than bolus dosing.

Table 8: High RIsk Situations and Prevention Strategies

Figure 1: Causes of Anesthesia-Related Cardiac Arrest in Children: POCA Registry, Two Time Periods


SummaryComplications in pediatric anesthesia are a true challenge for healthcare professionals. However, with a careful preoperative evaluation, anticipa-tion and training, it is possible to significantly re-duce the number of these events and ensure excel-lent outcomes.

ReferencesEmergence AgitationHino M, Mihara T, Miyazaki S, et al. Develop-ment and validation of a risk scale for emergence agitation after general anesthesia in children: A prospective observational study. Anesth Analg 2017;125:550-5.

Hauber JA, Davis PJ, Bendel LP, et a. Dexmedeto-midine as a rapid bolus for treatment and prophy-lactic prevention of emergence agitation in anes-thetized children. Anesth Analg 2015; 121: 1308-15

Mason KP. Paediatric emergence delirium: a com-prehensive review and interpretation of the litera-ture. BJA 2017; 118 (3): 335-43.

Sikich N, Lerman J. Development and Psychomet-ric Evaluation of the Pediatric Anesthesia Emer-gence Delirium Scale. Anesthesiology 2004; 100 (5): 1138-45.

LaryngospasmOlsson G, Hallen B. Laryngospasm during anesthe-sia. A computer-aided study in 136,929 patients. Acta Anaesthesiol Scand 1984; 28: 567-570.

Perioperative Cardiac ArrestBhananker SM, Ramamoorthy C, Geiduschek JM, et al. Aensthesia-related Cardiac Arrest in Chil-dren: Update from the Pediatric Perioperative Car-diac Arrest Registry. Anesth Analg 2007; 105: 344-50.

Flick RP, Sprung J, Harrison TE, et al. Periopera-tive Cardiac Arrests in Children between 1988 and 2005 at a Tertiary Referral Center. Anesthesiology 2007; 106: 226-37.

Morray JP, Geiduschek JM, Caplan RA, et al. A comparison of Pediatric and Adult Anesthesia Closed Malpractice Claims. Anesthesiology 1993; 78:461-7.

Morray JP, Geiduschek JM, Ramamoorthy C, et al. Anesthesia-related Cardiac Arrest in Children. Anesthesiology 2000; 93:6-14.

Odegard KC, DiNardo JA, Kussman BD, et al. The frequency of Anesthesia-Related Cardiac Arrests in Patients with Congenital Heart Disease Undergo-ing Cardiac Surgery. Anesth Analg 2007; 105: 335-43.


Generic Name Common Brand Name(s)

Atropine AtroPen®, Aterza®, Sal-Tropine®

Clonidine Catapres®, Duraclon®, Kapvay®

Dexmedetomidine Precedex®

Fentanyl Actiq®, Duragesic®, Fentora®, Haldid®, Onsolis®, Lazanda®

Flumazenil Romazicon®

Halothane Fluothane®

Isofl urane Forane®, Terrell®

Lidocaine Xylocaine®

Midazolam Versed®, Dormicum®, Hypnovel®, Nayzilam®, Seizalam®

Propofol Diprivan®, Propoven®

Sevofl urane Ultane®, Sojourn®

Succinylcholine Anectine®, Quelicin®

Medications Cited


Linda J. Mason, M.D.

Dr. Mason is Professor of Anesthesiology and Pediatrics at Loma Linda University and Director of Pediatric Anesthesiology at Loma Linda University Medical Center.

She received her medical degree from Loma Linda University. She was an intern in internal medi-cine and completed her anesthesiology training at Loma Linda University Medical Center. This was followed by a pediatric anesthesiology and critical care fellowship at the Children’s Hospital of Philadelphia, University of Pennsylvania. She is board certified in Anesthesiology with subspe-cialty boards in Critical Care Medicine and Pediatric Anesthesiology.

Dr. Mason has been particularly recognized by both national anesthesiology societies: the Ameri-can Society of Anesthesiologists and the International Anesthesia Research Society as a refresher course lecturer which defines the body of knowledge in the subspecialty of pediatric anesthesiology.

She is Past President, Association of Anesthesiology Subspecialty Program Directors (AASPD) (2008-2010) and is a Member, Accreditation Council for Graduate Medical Education (ACGME) Review Committee for Anesthesiology (2010-2016). Dr. Mason is also the immediate Past President for the American Society of Anesthesiologists.

Elizabeth A. Ghazal, M.D.

Dr. Ghazal is an Associate Professor of Anesthesiology at Loma Linda University where she is the Associate Director of the Pediatric Anesthesiology Fellowship.

She is a graduate of Loma Linda University School of Medicine and completed her anesthesiology training and pediatric anesthesiology fellowship at Loma Linda University Medical Center. Dr. Ghazal is board certified in Anesthesiology with subspecialty certification in Pediatric Anesthesiol-ogy. Her clinical interests include perioperative care of neonates, pediatric craniofacial surgery and medical education.


Tips for Your Clinical Practice: Key Points

Monte Lichtiger, MDEditor, Current Reviews®

● Pediatricemergence agitation (EA) typicallypresentswiththrashing,crying,incoherenceanda lackofeyecontactandawarenessofone’ssurroundings.Althoughitscauseisunknown,somehy- pothesesattributeitsetiologytothepharmacokineticsandphamacodynamicsofanestheticagents.

● Toprevent EA (or improve its outcomes),someadvocatedecreasingpreoperativeanxiety,pro- vidingadequateanalgesiaandchoosinganesthetictechniquesandmedicationsthatareassociated withsmootherrecoveries.

● Laryngospasm,causingpartialorcompleteobstructionoftheairway,canbetriggeredbymechani- calorchemicallaryngealstimulation.Itisimportanttorealizethatcompleteairwayobstructionby laryngospasmshouldnotbetreatedwithpositivepressure.

● Ifpositivepressureisutilizedtotreatcomplete airway obstruction secondary to laryngospasm, itmayworsen the obstruction (bypushingsupraglottictissuesdownward)andforcegasintothe stomach,makingventilationmoredifficult.

● The risk factors for pediatric operative cardiac arrest (POCA)includeage(childrenlessthan1 yearoldaccountedfor24%),ASAphysicalstatus,emergencysurgeryandcongenitaloracquired heartdisease.

● Inthemostcurrentstudy(1998-2004),hypovolemiawasthemostcommoncauseofPOCA.Ef- fectivelyanticipating,estimatingandreplacingblood lossisoftheutmostimportanceinpreventing thiscatastrophicproblem.

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MARK THIS PAGE AND KEEP FOR YOUR RECORDS.

POST-STUDY QUESTIONS

LESSON

MARK ALL ANSWERS ON BOTH THIS PAGE AND YOUR ANSWER CARD 12

1. Which of the following characterize emergence delirium?□A. Failuretorecognizeoridentifyfamiliarandknown peopleorobjects.□B. Cryingandthrashingyetmaintainingeyecontact andawarenessofsurroundings.□C. Irritablebutconsolable.□D. Lowerincidenceinchildren1to5yearsofage.

2. Factors that are associated with emergence agitation in children include:□A. Previoussurgery.□B. Youngerage.□C. Orthopedicprocedures.□D. Useoftotalintravenousanesthesia(TIVA).

3. When emergence agitation occurs: □A. Itrarelyrequirespharmacologictreatment.□B. Itcanbeexpectedtolast>45minutesifthe childisleftundisturbed.□C. Treatmentoptionsdonotincludepropofoland midazolam.□D. DischargefromthePACUmaybedelayedwhile waitingforthedeliriumtoresolveorfortheeffect ofthepharmacologicinterventiontodissipate.

4. Which age group has the highest reported incidence of laryngospasm?□A. 1-3months□B. 6-12months□C. 1-2years□D. 2-5years

5. Which of the following statements accurately describe the treatment of incomplete laryngospasm?□A. Theinitialtreatmentistheadministrationofintra- venousorintramuscularsuccinylcholine.□B. Positivepressuremaybreaklaryngospasminthepresenceofcompleteairwayobstruction.□C. Negativepressurepulmonaryedemaneveroccurs inpediatricpatients.□D. Pressureinthelaryngospasmnotchwithsimulta- neousapplicationofgentlepositivepressureand 100%oxygenbymaskisofteneffective.

6. The Pediatric Closed Claims Study database findings in the early 1990s revealed the that the most common cause of cardiac arrest was:□A. Medication-related.□B. Respiratoryevents.□C. Cardiovascularinnature.□D. Equipment-related.

7. Events that most frequently preceded cardiac arrest in the 1994-1997 Perioperative Cardiac Arrest Registry database were:□A. Norecognizedwarning.□B. Arrhythmiasandcyanosis.□C. ETCO2abnormality.□D. Bradycardiaandhypotension.

8. According to the 1994-1997 Perioperative Cardiac Arrest Registry database, congenital heart disease was present in what percentage of patients who did not survive?□A. 20%□B. 38%□C. 50%□D. 65%

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