1. Explain the difficulties in validating the use of home sleep monitoring devices and consider methods for increasing their utility.

2. Describe the continuum and associated sequelae of sleep-disordered breathing in children.

3. Choose appropriate therapy for managing sleep disordered breathing and OSA in children .

4. Identify factors associated with an increased risk for perioperative complications in patients undergoing surgery for OSA.

5. Describe recommended steps in preoperative assessment and planning, and postoperative care of patients undergoing surgery for OSA

Indications for Ambulatory Sleep Studies
Samuel T. Kuna, MD, Associate Professor of Medicine, University of Pennsylvania School of Medicine, and Chief Pulmonary, Critical Care, and Sleep Medicine, Veterans Affairs Medical Center, Philadelphia

Types of sleep studies: type I—attended in-laboratory PSG; type II—comprehensive portable PSG (relegated to research studies; not practical for widespread use in clinical care); type III—modified portable sleep apnea testing (records respiratory signals but does not include sleep staging); type IV—continuous single or dual bioparameter (eg, pulse oximetry)

Examples of portable monitors (PMs): type III—Embletta; Stardust II; apnea risk evaluation system (ARES); type IV— WatchPAT uses peripheral arterial tone to measure arousals and changes in sympathetic activity, heart rate, pulse oximetry and actigraphy; comment—monitors lack standardization, even within categories of monitors; new subcategories now account for new sensor types

Validation of portable diagnostic monitors: almost all validation studies to date have been direct head-to-head comparisons of in-laboratory PSG (gold standard) and unattended home sleep studies (HSS) done with PMs; studies have tended to fail because of differences in equipment and environment, and failure to address night-to-night variability in the apnea/ hypopnea (AHI) index on in-laboratory PSG (most important factor accounting for differences in comparison studies)

Reasons for difficulty in validating home type III PM studies: lack of association of single AHI threshold on in-laboratory PSG with clinical symptoms (so upper limit for starting treatment unknown); many published studies use different AHI thresholds for analysis; lack of uniform scoring criteria for hypopneas makes it difficult to compare studies; night-to-night variability of AHI index on in-laboratory PSG not addressed in most validation studies; type III and IV monitors underestimate AHI; significant differences among PMs within same class; currently available validation studies underpowered, and majority used monitors with older technology

Keys to increasing utility of PM testing: minimize number of negative studies; minimize number of failed studies (through careful in-laboratory instruction on use of monitors before sending patients home to do HSS)

Alternative clinical pathway for managing patient with suspected OSA: after initial evaluation, patient gets either standard in-laboratory PSG or sent home to do HSS with type III PM; patient who tests negative on PM (AHI<15) brought back for in-laboratory PSG to rule out false-negative finding; patient diagnosed with OSA (AHI>15) started on home automatic (auto)-CPAP titration

Auto-CPAP titration at home: current generation of auto-CPAP machines adjust pressure throughout night in response to snoring, apneas/hypopneas, and inspiratory flow limitation; many capable of simultaneous pulse oximetry; no established guidelines or protocols on how to perform in-laboratory manual CPAP titration (gold standard); across-night comparisons of in-laboratory CPAP titration with auto-CPAP do not produce same results; auto-CPAP titration has not been tested in patients with congestive heart failure (CHF) and chronic obstructive pulmonary disease (COPD); several studies have favorably compared outcomes with home auto-CPAP titration and in-laboratory CPAP PSG

Pediatric Obstructive Sleep Apnea
Michael D. Poole, MD, PhD, Professor of Otolaryngology, Surgery, and Pediatrics, Mercer University School of Medicine, Macon, GA; Georgia Ear Institute, Savannah, GA

Sleep-disordered breathing: primary snoring—does not cause significant obstruction, airflow restriction, or sleep disruption; upper airway resistance syndrome—increased abdominal pressure; paradoxical breathing; obstructive sleep apnea (OSA)—complete or nearly complete obstructive events associated with lack of airflow during breathing; intermittent symptoms—nasal obstruction caused by upper respiratory infections (URIs) or exacerbations of allergic rhinitis

Epidemiology: incidence of OSA peaks in children 4 to 6 yr of age; chronic snoring occurs in 5% to 12% of children (>2% have overt OSA on polysomnography [PSG])

Adult vs pediatric OSA: body habitus—obesity-associated OSA common among adults; in children, OSA may be associated with failure to thrive; abnormal sleeping position (eg, opisthotonus) in children may signal upper airway obstruction; some children have normal body habitus but large tonsils and adenoids; behavioral sequelae—sleep disruption often leads to daytime fatigue and hypersomnolence in adults; children more likely to display hyperactivity and difficulty focusing; sex differences—OSA occurs more often in men than women (ratio 2:1); no sex differences in children

Treatment: adults—oropharyngeal surgery sometimes useful; CPAP more common; children—adenoidectomy and/or tonsillectomy

Sequelae of pediatric OSA

Classic: cor pulmonale; respiratory failure; association with hypertension unclear; excessive daytime sleepiness; enuresis due to disruption of normal sleep cycle; abnormal sleep position (ie, opisthotonos [neck and back hyperextend]); causes of failure to thrive and growth delay—excessive movement and energy expenditure during sleep; decreased slow-wave sleep; growth hormone preferentially secreted during slow-wave sleep; reduced appetite may be related to decreased growth hormone; posterior nasal obstruction may reduce sense of smell and taste; difficulty coordinating mouth breathing with swallowing; chronic inflammatory disease—viral or bacterial infections may trigger enlargement of adenoids and tonsils; inflammation of regional lymph nodes typical with viral infections; increases in inflammatory cytokines and decreases in anti-inflammatory cytokines involved; improves after adenotonsillectomy; pediatric OSA increases risk for adult coronary artery disease

Neurobehavioral problems: poor attention span; poor learning; inability to focus; IQ scores (decreased, relative to children without OSA) improve after adenotonsillectomy; excessive daytime fatigue; snoring 3 times more common among children with behavioral problems or attention-deficit/hyperactivity disorder; improved behavior seen in snorers and children with OSA after adenotonsillectomy

Role of PSG: gold standard but poorly validated; expensive; apnea index (AI) of ≥1 event/hr often considered abnormal in children; child with negative sleep study still may have significant sleep problems

History and physical examination: most skilled clinicians can identify obvious and severe cases of OSA; absence of snoring, characteristic craniofacial features, large tonsils, or difficulty breathing through nose helps identify patients at low risk for OSA; in equivocal cases, further evaluation indicated; physical examination pearls—not all large tonsils obstructive, and not all obstructive tonsils large (what matters is size of tonsils relative to airway); not all snoring and OSA caused by large tonsils or adenoids (other causes include allergic rhinitis, nasal polyps, abnormal craniofacial structure; snoring, especially due to obstructive adenoids, increases risk for otitis media (OM) with effusion; all children with Down syndrome should have PSG between 3 and 4 yr of age

Respiratory events in children: central apnea—cessation of diaphragmatic effort lasting >2 respiratory cycles (usually 8- 10 sec, depending on patient age); obstructive apnea—respiratory effort preserved, but airflow absent for >2 respiratory cycles; complete obstruction—<25% of normal tidal volume; hypopnea—25% to 50% reduction in tidal volume, and/or >3% decrease in SaO2

Abnormal values in pediatric PSG: AI >1 event/hr; apnea-hypopnea index (AHI; also called respiratory disturbance index [RDI]) >5 events/hr; rising PCO2 or falling SaO2

Adenotonsillectomy: cure rate >85%; obesity increases failure rate; unclear whether preoperative severity of OSA affects postoperative prognosis; patients with significant postoperative snoring may benefit from sleep study (to guide further management)

American Academy of Pediatrics (AAP) clinical practice guidelines for OSA syndrome, 2002: screening—screen all children for snoring; refer high-risk patients for clinical evaluation; treatment—tonsillectomy and adenoidectomy first- line therapy; high-risk patients should be kept as inpatients postoperatively; careful postoperative evaluation indicated; controversies in pediatric OSA—diagnostic criteria; candidates for testing; indications for treatment; short- and long-term sequelae of withholding treatment; postoperative monitoring; AAP guidelines in practice—raise awareness about problem; stimulate research; understate role of diagnostic data other than PSG; note—large regional variations in diagnosis and treatment

Perioperative Care in OSA Surgery
Andrew N. Goldberg, MD, Professor, Department of Otolaryngology-Head and Neck Surgery, University of California, San Francisco, School of Medicine

Estimate of perioperative complications: survey of complications of uvulopalatopharyngoplasty (UP3)—complications reported included 46 cases of nasopharyngeal stenosis, 42 of palatal incompetence, 16 fatalities and 7 near fatalities

Risk for perioperative complications (Esclamado 1990): majority (14) had airway problems; other 4 had postoperative hemorrhage

Risk factors: medical—patients with complications had significant difference in minimum O2 saturation and apnea index (AI); comorbidities not significant factor; surgical—risk not related to primary operation or concurrent nasal procedure; anesthetic complications—rate and total dose of intraoperative narcotic significantly higher in patients with extubation complications; percentage of ideal body weight (IBW) greater in patients with intubation complications; use of narcotics not influenced by IBW; study by Kezirian et al (2006)—comorbidities cause twofold greater risk for each increase in American Society of Anesthesiologists (ASA) grade; fivefold greater risk with UP3 plus nonnasal OSA procedure, eg, base of tongue procedure; subset analysis of 43 patients showed tongue procedures independently associated with complications

Preoperative: assessment—previous anesthetics; routine review of systems (eg, history of chest pain; palpitations; shortness of breath; gastroesophageal reflux disease [GERD]); due diligence (use of aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], gingko biloba, vitamin E); planning—optimize medical condition and arrange for consultants; secure monitored bed; arrange for postoperative CPAP (most patients have had previous CPAP)

Anesthesia and airway: plan method of securing airway with anesthesiologist; have contingency plan; carefully titrate sedative agents during case; recheck oral cavity for edema before extubation; have physician present at intubation and extubation who is able to secure surgical airway if necessary; securing airway—many patients can be intubated orally (particularly those with Fujita type I or IIa obstruction; establish ventilation prior to paralysis if possible); if difficulties with patient’s airway, do awake fiberoptic nasal or oral intubation; adequate topical anesthesia critical (apply all at once and begin procedure minimum of 10 min later); laryngeal mask airway (LMA) sometimes helpful when ventilation difficult; tracheotomy (awake or postintubation)

Awakening: must have full reversal of muscle relaxants; extubate when patient awake and reflexes restored (avoid “deep extubation”); may need to delay extubation 24 to 48 hr in rare cases; steroids can be given to decrease edema; make sure patient does not go back to sleep after tube removed; have nasal trumpet and oral airway available; tracheotomy tray should be available

Postoperative management: acute effects of UP3 (Sanders 1988)—comparison of PSG performed on postoperative day 2 with preoperative studies found patients’ respiratory disturbance index (RDI) remained relatively stable; recommendations (monitor O2 postoperatively; routine prophylactic tracheotomy not warranted; CPAP if RDI persistently high); Terris et al (1998)—study looked at 125 procedures; majority multilevel surgery; conclusions (no need for routine postoperative monitoring; blood pressure control most common issue; patients at high risk cannot be identified preoperatively); Ulnick et al (2000)—study looked at 38 patients (31 had UP3 alone); recommendations (stepdown unit monitoring with O2 monitoring); Spiegel et al (2005)—looked at 117 patients who had UP3 with or without other procedures; virtually all complications occurred within 3 hr of surgery; conclusions (same-day surgery possible as long as patient kept in hospital for adequate period of observation)

Postoperative resources required: study by Bruno et al (2005) looked at 42 patients who underwent UP3; authors analyzed hospital resource utilization and concluded hospitalization justified for patient comfort and pain control

Complications of surgical treatment: airway problems majority of serious complications after OSA surgery; mortality rare but most commonly caused by perioperative airway loss; tracheotomy or intubation necessary for airway compromise from edema in awake patient; if OSA exacerbated after surgery, nasal CPAP recommended; cardiac monitoring appropriate for patients with O2 saturations <60%

Anesthesia in patients with OSA undergoing non-OSA surgery: pose same risks for intubation as in OSA surgery; extubation risk higher than in patient without OSA but not as high as in upper airway surgery