PEDIATRIC ANESTHESIA
From Challenges for Clinicians in the New Millennium, presented by The University of Chicago Pritzker School of Medicine, December 3-5, 2004
| PITFALLS AND SMOOTH SAILING —Catherine Bachman, MD, Assistant Professor of Anesthesiology, The University of Chicago Pritzker School of Medicine |
| Emergence agitation: defined as crying, restlessness, inconsolability, and disorientation in recovery room; limited in duration; implications include distress to all involved (eg, child, parents, personnel); study on emergence behavior in children found 30% incidence with halothane; more of those who received preoperative midazolam had emergence agitation and more also had prolonged episode |
 | Possible causes: anesthetic agent (eg, sevoflurane); rapid emergence; pain; underlying anxiety |
| Choice of anesthetic agent: study looking at sevoflurane vs halothane in children undergoing hernia repair found halothane had lower incidence of emergence agitation than sevoflurane; younger children (≤2 yr of age) more affected; sedation with midazolam or morphine terminated emergence agitation |
| Sevoflurane: most studies show significant increase in incidence of emergence agitation with use; no difference in long-term behavior changes, compared to halothane; found generalized behaviors (possibly indicating stress) common day after surgery, but gradually decreased with time; study concluded rapid emergence does not explain agitation after sevoflurane anesthesia in children (but emergence agitation higher with sevoflurane, compared to propofol); speaker’s anecdotal study did not find pain to be factor in agitation; another study found incidence with sevoflurane 27% in children with functioning caudal block; multiple studies find agitation even with good postoperative analgesia; Galinkin study of myringotomy and tubes surgery found less postoperative agitation with intranasal fentanyl and no difference in postoperative agitation between halothane and sevoflurane |
| Treatment: self-limited (usually ≤10 min; may last 30 to 45 min in smaller group of patients); effectively treated with midazolam or morphine (but preoperative midazolam may not affect incidence) |
| Summary: may occur with all anesthetic agents, but sevoflurane of particular note; rapid emergence unlikely cause; agitation occurs with or without pain; insufficient data to determine whether certain children at risk for underlying anxiety |
| Propofol toxicity: common clinical features include metabolic acidosis, myoglobinuria (± rhabdomyolysis), lipemic serum, bradyarrhythmias progressing to asystole (usually unresponsive to treatment), and possible renal and/or liver failure; no direct causal relationship established; usually seen in prolonged infusions; possible mechanisms include disruption of fatty acid oxidation; recommendations include avoiding prolonged infusions, avoiding high dose (>4 mg/kg per hour considered high [but only 66 µg/kg per minute]), and avoiding susceptible patient (pediatric intensive care unit [PICU]; upper respiratory tract infection; unsure about metabolic subgroup) |
| Obstructive sleep apnea (OSA): study from 2002 looked at whether OSA predicts postoperative respiratory complications; defined minor postoperative respiratory complication as anyone needing stimulation or O2 , and major complication as anyone needing bag or mask ventilation or intubation; major complications occurred in 7.5% of those with OSA and in 0% of patients without OSA; severity of OSA predicts risk (those with severe OSA at greatest risk of developing postoperative respiratory complications); another study found recurrent hypoxia in young children with OSA associated with reduced opioid requirement for analgesia; pediatric OSA patients have exquisite sensitivity to respiratory depressant effects of opioids (intraoperatively and postoperatively) |
| Characteristics: disorder of chromosome 7; may have facial dysmorphism and developmental delay (similar to high- functioning child with Down’s syndrome); friendly; small stature; cardiac problems; one physician indicates if child has supravalvular aortic stenosis, anesthesia potentially lethal; another had adverse outcome after [cardiac] catheterization (temporally related to dose of protamine) |
| Cardiovascular abnormalities: aortic stenosis (supravalvular); coronary artery leaflets reported; myocardial ischemia; pulmonary artery (PA) stenosis (supravalvular); peripheral PA stenosis (biventricular obstruction) |
| Incidence of sudden death: occurs either in community (at home) or under anesthesia; study from 1996 looked at 10 deaths from Williams syndrome (some from community and others from cardiac catheterization laboratory); coronary artery stenosis evident in some but not all; all had severe biventricular outflow tract obstruction (with biventricular hypertrophy) |
| Conclusion: consult cardiologist before treating patient; if at smaller hospital, patient should be sent to location where more extensive cardiac evaluation available |
| Outpatient tonsillectomy in children with history of OSA: speaker’s practice keeps children with OSA in hospital overnight or ≥12 hr; according to literature, risks vary with severity of OSA (but most children do not have study of severity of OSA); to be safe, every patient should remain in hospital ≥12 hr after tonsillectomy |
| HEART DISEASE— Annette Schure, MD, Resident in Clinical Anesthesiology, The University of Chicago Pritzker School of Medicine |
Repaired Congenital Heart Disease for Noncardiac Surgery | Data: incidence 4 to 9 per 1000 live-born, full-term infants; (32,000 per year in United States, 1.5 million per year worldwide); 35 different congenital cardiac defects; currently ≈1 million patients with heart defects in United States (≈300,000 children <21 yr of age); 38% had ≥1 cardiac surgery; death rates declined by >40% over last 20 yr; at present, >85% of infants expected to reach adulthood |
| Anatomy of congenital heart disease: communicate with cardiologist and other members of surgical team to become familiar with pathophysiology of specific defect |
| Type of repair: definitive repair may be anatomic (simple reconstruction of atrial septal defect [ASD], ventricular septal defect [VSD], or patent ductus arteriosis [PDA]; complex reconstruction with baffle, conduit, and valves; late complications likely) or physiologic (circulation in series; cyanosis corrected; 2-ventricle repair or single-ventricle repair [eg, Fontan]); palliative repair for treatment of severe cyanosis or pulmonary overcirculation (eg, shunts, PA banding) and part of staged repairs (eg, Norwood procedure); interventional cardiac catheterization involves device closure, balloon and stent dilations, and coil embolizations |
| Important factors before repair |
| Age at time of repair: multistaged surgical approach vs one-stage repair in neonate or infant; fewer long-term problems (especially dysrhythmias) with full, definite repair as early as possible |
| Cyanosis and polycythemia: polycythemia is attempt to increase tissue O2 delivery; long-term effects of chronic hyperviscosity lead to poor rheology and risk for thrombus formation; may result in relative coronary insufficiency, asymptomatic subendocardial ischemia, and subsequent fibrosis |
| Congestive heart failure (CHF): neonates and infants can show myocyte hyperplasia and stimulation of angiogenesis; new muscle cells and vascular supply, especially with pressure overload; prevails for first 3 to 4 mo |
| Dysrhythmias: effects of chronic distention or conduction system malfunction; greater risk for long-term reappearance; some may present with palpitations, dizziness, or near syncope (require work-up); other patients may be asymptomatic; exacerbated or triggered by stress of surgery |
| Pulmonary hypertension: degree and duration of preexisting pulmonary hypertension important; if large unrestricted VSD not repaired by 2 yr of age, pulmonary vascular occlusive disease develops; characterized by muscular arterial wall |
| Outcome after surgery: complications include heart block and coronary or ventricular injuries; residual defects may include shunt or outflow tract obstruction; direct consequences of procedure include altered physiology or anatomy (eg, Fontan, Mustard/Senning) |
| Special concerns: risk for endocarditis; associated noncardiac defects; monitoring (difficult intravenous [IV] access or arterial line placement; pelvic/bladder shunt; coarctation repair; risk for thrombosis with central venous line in Fontan patient); psychosocial concerns include multiple hospitalizations |
| Type of surgery: noninvasive diagnostic procedure much different from 8-hr scoliosis surgery (with patient in prone position and substantial blood loss) or emergency laparotomy in septic child |
| Atrial septal defect: common; various types; spontaneous closure (especially during first 4 yr of life); closure with device may occur in catheterization laboratory (avoiding surgery and long-term consequences); most benign heart defect known; pulmonary hypertension occurs with late repair in adult >40 yr of age or with von Willebrand disease or trisomy 21; high altitude another factor that can exacerbate pulmonary hypertension; increased risk if prerepair dysrhythmias present; dependent on shunt size and age at repair; persistent right ventricular (RV) dilation can be seen for up to 2 yr on chest x-ray and up to 5 yr on echocardiography |
| Ventricular septal defect: common; considered benign; several types; evidence of spontaneous closure; surgical options include palliative PA banding, direct patch closure (atrial approach; ventriculotomy), and device closure; pulmonary hypertension (only if repair done later in life or in trisomy 21); dysrhythmias and conduction defects (complete heart block rare; right bundle branch block, ventricular arrhythmia, and sudden death occur after ventriculotomy); ventricular dysfunction (late repair) |
| Transposition of great arteries: parallel circulation; mixing via ASD, VSD, and PDA; surgical options include switches on atrial level, ventricular level, or level of great arteries; atrial baffle procedures involve redirection of blood flow (BF) to appropriate ventricle via intra-atrial baffle; Rastelli procedure involves intraventricular baffle and extracardiac conduit; arterial switch involves switching great vessels at origin of ventricles |
| Atrial baffle procedures: systemic venous return (SVR) flows past mitral valve to left ventricle (LV), pulmonary artery, and lungs; pulmonary venous return (PVR) flows past tricuspid valve, right ventricle (RV), aorta, and out to body; this type of repair has fallen out of favor due to many long-term problems; many patients have severe dysrhythmias, baffle obstructions (systemic venous obstruction and pulmonary venous obstruction), and ventricular failure |
| Arterial switch: involves switching great vessels at origin of ventricles; potential problems include supravalvular pulmonary stenosis and coronary abnormalities; arrhythmias rare; cardiac function usually excellent |
| Tetralogy of Fallot: one of most common cyanotic diseases; 30% of patients have associated anomalies (eg, DiGeorge syndrome; velocardiofacial syndrome); various surgical options (eg, 2-stage vs 1-stage; transannular patch; ventricular vs atrial plus transpulmonary approach; anomalous coronary); after repair, some patients may have residual VSD, residual right ventricular outflow tract (RVOT) obstruction, pulmonary valve regurgitation, right ventriculotomy (scarring and fibrosis predisposes to dysrhythmias and dysfunction), LV dysfunction (anomalous coronaries and ischemic injury), and aortopulmonary collaterals; long-term consequences include dysrhythmias (10% have ventricular arrhythmia at rest, 30% with exercise; conduction abnormalities; risk for sudden death) and RV dysfunction (volume overload from residual VSD or pulmonary regurgitation; pressure overload from residual RVOT obstruction; often asymptomatic, but exercise tolerance decreased) |
| Hypoplastic left heart syndrome: parallel circulation; single ventricle provides systemic and pulmonary BF; divided into 3 groups, 1) balanced flow (pulmonary BF same as systemic BF), 2) pulmonary system overcirculated, systemic hypoperfusion, and 3) severe hypoxemia with adequate systemic perfusion |
| Norwood procedure: involves creation of “neoaorta,” atrial septectomy, and right modified Blalock-Taussig shunt; goals are to provide pulmonary BF, to provide systemic perfusion, to preserve function of single ventricle, and allow normal maturation of pulmonary vasculature |
| Bidirectional Glenn: pulmonary BF via superior vena cava (SVC) provides passive BF through lungs; inferior vena cava (IVC) blood mixes with fully saturated blood in single ventricle; O2 saturation 80% to 85%, but volume load decreased and ventricular remodeling can be provided |
| Modified fenestrated Fontan: SVC and IVC connected directly to PA to create serial circulation; passive pulmonary BF dependent on transpulmonary gradient; recent modifications include lateral tunnel and fenestration; improved morbidity and mortality; baffle pressure 10 to 15 mm Hg, dependent on unobstructed venous return, adequate preload, and low intrathoracic pressure; low atrial pressure on other side of equation dependent on sinus rhythm, competent atrioventricular (AV) valve, and normal ventricular function |
| Management: look for baffle pressure; maintain or increase preload; low intrathoracic pressure; avoid increases in PVR; early resumption of spontaneous ventilation; maintain left atrial pressure as low as possible |
| Special anesthetic considerations: include arrhythmias, thromboembolism, protein-losing enteropathy, decreased exercise tolerance, monitoring, and open fenestration |
Educational Objectives
| The goal of this program is to educate the listener about issues in pediatric anesthesia. After hearing and assimilating this program, the participant will be better able to: |
| 1. Discuss the diagnosis and treatment of emergence agitation in children. |
| 2. Summarize the issue of propofol toxicity in the pediatric patient. |
| 3. Explain obstructive sleep apnea. |
| 4. Review the presentation and management of Williams syndrome. |
| 5. Describe the proper management of the pediatric patient with repaired congenital heart disease who presents for noncardiac surgery. |
Discussed on This Program
Acetaminophen (N -acetyl-P -aminophenol; APAP) [Tylenol, many others] Desflurane [Suprane] Fentanyl [Sublimaze] Halothane [Fluothane] Isoflurane [Forane] Midazolam HCl [Versed] Morphine sulfate (several trade names) Naloxone HCl [Narcan] Propofol [Diprivan] Protamine sulfate Sevoflurane [Ultane]
Suggested Reading
Bird LM et al: Sudden death in Williams syndrome: report of ten cases. J Pediatr 129:926, 1996; Brown KA et al: Recurrent hypoxemia in young children with obstructive sleep apnea is associated with reduced opioid requirement for analgesia. Anesthesiology 100:806, 2004; Cohen IT et al: Rapid emergence does not explain agitation following sevoflurane anaesthesia in infants and children: a comparison with propofol. Paediatr Anaesth 13:63, 2003; Cole JW et al: Emergence behaviour in children: defining the incidence of excitement and agitation following anaesthesia. Paediatr Anaesth 12:442, 2002; Galinkin JL et al: Use of intranasal fentanyl in children undergoing myringotomy and tube placement during halothane and sevoflurane anesthesia. Anesthesiology 93:1378, 2000; Holzki J et al: Death after re- exposure to propofol in a 3-year-old child: a case report. Paediatr Anaesth 14:265, 2004; Keaney A et al: Postoperative behavioral changes following anesthesia with sevoflurane. Paediatr Anaesth 14:866, 2004; Odegard KC et al: Anesthetic considerations during caval inflow occlusion in children with congenital heart disease. J Cardiothorac Vasc Anesth 18:144, 2004; Waters KA et al: Effects of OSA, inhalational anesthesia, and fentanyl on the airway and ventilation of children. J Appl Physiol 92:1987, 2002; Weldon BC et al: The effect of caudal analgesia on emergence agitation in children after sevoflurane versus halothane anesthesia. Anesth Analg 98:321, 2004; Wilson K et al: Can assessment for obstructive sleep apnea help predict postadenotonsillectomy respiratory complications? Anesthesiology 96:313, 2002; Withington DE et al: A case of propofol toxicity: further evidence for a causal mechanism. Paediatr Anaesth 14:505, 2004.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported nothing to disclose.
Drs. Bachman and Schure spoke in Chicago at Challenges for Clinicians in the New Millennium, held December 3-5, 2004, and sponsored by The University of Chicago Pritzker School of Medicine. The Audio-Digest Foundation thanks the speakers and the sponsor for their cooperation in the production of this program.
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