OBSTRUCTIVE SLEEP APNEA/SINUSITIS
From the 29th Annual Las Vegas Seminars, presented November 15-18, 2007, by the American Academy of Pediatrics,
California District IX, Chapters 1,2,3,4
Michael D. Poole, MD, PhD, Professor of Otolaryngology, Surgery, and Pediatrics, Mercer University School of
Medicine, Macon, GA; Georgia Ear Institute, Savannah, GA
| OBSTRUCTIVE SLEEP APNEA: CURRENT THINKING
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| Sleep-disordered breathing: primary snoring — snoring audible but does not cause significant obstruction, airflow
restriction, or sleep disruption; upper airway resistance syndrome—increased abdominal pressure; paradoxical breathing
(abdomen rises instead of chest); 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
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| 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])
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| Other problems associated with primary snoring: orthognathic features or problems with dentition may result
in chronic mouth breathing, which may predispose patient to URIs (because normal humidification and filtration functions
of nose bypassed); respiratory infections (otitis media [OM] and sinusitis [primarily due to adenoid disease or
obstruction]; pharyngotonsillitis); craniofacial development—animal and human studies show effects of nasal obstruction
and chronic mouth breathing; when mouth closed during sleep, tongue applies constant pressure to palate,
expanding maxilla anteriorly and laterally; chronic mouth breathers have restricted maxillary growth and higher-
arched palate, contributing to nasal obstruction and obstructed breathing; neurobehavioral or neurocognitive problems;
other influences—genetic; behavioral; dietary
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| 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; snoring—continuous in children
(intermittent in adults); adults tend to have complete apnea (children have partial obstruction); 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
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 | Treatment: adults—oropharyngeal surgery sometimes useful in adults, but continuous positive airway pressure (CPAP)
more common (obstruction usually more complex than adenotonsillar disease); base-of-tongue obstruction often
present; chronic mouth-breathing changes dynamics in hypopharynx; hyoid bone drops lower, chin recesses, and hypopharyngeal
airway elongates and becomes more collapsible; children—adenoidectomy and/or tonsillectomy
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| Sequelae of pediatric OSA
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| 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]);
failure to thrive, growth delay (causes)—excessive movement and energy expenditure during sleep;
decreased slow-wave sleep (obstruction worsens with increased relaxation of muscles that occurs during deep sleep;
child briefly arouses to light sleep or awakens); 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; problem
improves after adenotonsillectomy; pediatric OSA increases risk for adult coronary artery disease
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| 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 (as measured
by Connors rating scale) seen in snorers and children with OSA after adenotonsillectomy
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| Role of PSG: gold standard diagnostic tool, but poorly validated; expensive; apnea index of ≥1 events/hr often considered
abnormal in children (7-8 events/hr abnormal in adults); child with negative sleep study still may have significant
sleep problems
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| Role of history and physical: most skilled clinicians can accurately identify obvious and severe cases of OSA; absence
of snoring, characteristic craniofacial features, large tonsils, and 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 [eg, small mandible or midface due to eg, Pierre Robin syndrome or Treacher Collins syndrome);
snoring, especially due to obstructive adenoids, increases risk for OM with effusion; all children with Down
syndrome should have PSG between 3 and 4 yr of age (almost 70% have OSA or abnormal findings on PSG; poor
concordance between parents’ assessment of child’s breathing and sleep patterns and results of PSG)
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| Core challenges: to identify—children with snoring; those who need PSG; those who need treatment because of
sleep-disordered breathing or other problems related to snoring, airway obstruction, tonsils, or adenoids
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| Respiratory events in children (definitions): central apnea—cessation of diaphragmatic effort lasting >2 respiratory
cycles (usually 8-10 seconds, depending on patient age); obstructive apnea—respiratory effort preserved, but
airflow absent >2 respiratory cycles; complete obstruction—<25% of normal tidal volume; hypopnea—25% to 50%
reduction in tidal volume and/or ≈3% decrease in SaO2
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| Abnormal values in pediatric PSG: obstructive apnea index >1 event/hr; apnea-hypopnea index (aka, respiratory
disturbance index [RDI]) >5 events/hr; rising PCO2 or falling SaO2
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| Does adenotonsillectomy cure all? no (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)
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| More treatment options: CPAP; uvulopalatopharyngoplasty; tongue base surgery (occasionally, lymphoid tissue on
back of tongue causes obstruction); for adults, moving maxillary and mandibular teeth forward creates more room in
airway (most effective surgery); tracheostomy
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| 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
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| Key messages: management decisions in OSA should be based on global assessment of patient and downsides of therapy;
large variation in tonsillectomy outcomes, partly dependent on surgeon’s experience and methods
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| PEDIATRIC SINUSITIS: DIAGNOSIS AND MANAGEMENT
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| Diagnosis: physicians cannot consistently differentiate viral from bacterial disease, even with x-rays, computed tomography
(CT) and magnetic resonance imaging (MRI); although negative findings have good negative-predictive
value, positive findings not much help; treatment—reserve antibiotics until likelihood of simple viral infection has diminished
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| Duration of symptoms in URIs (rhinovirus study): fever and sore throat improve in first week, but cough and
nasal drainage often persist up to 2 wk; cough and drainage associated with other viruses (eg, respiratory syncytial virus
or influenza viruses) may persist even longer
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| Pathophysiology of sinusitis: often misstated; inciting event (usually viral infection) damages respiratory tract mucosa;
overgrowth of common pathogens (eg, Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella) may occur
without presence of abscess cavity or obstruction; viral vaccines probably reduce load of bacterial infections;
management—allow time for recovery; administer corticosteroids or antimicrobials, as needed; generally, avoid surgical
drainage of incidentally obstructive infection (rarely indicated)
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| Purulent rhinosinusitis in infancy: infants born with ethmoid and maxillary sinuses (sphenoid and frontal sinuses
aerate variably between 6 and 12 yr of age); newborns immunologically and physically susceptible to infection (but
generally have less exposure to pathogens, compared to toddlers); every year speaker sees children <4 mo of age with
failure to thrive due to nasal obstruction caused by infection
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| Comment: if periorbital disease with abscess present, first inclination often to consult ophthalmologist or oculoplastic
surgeon (but underlying problem sinus disease); often easier and more complete to drain abscess intranasally, and patients
recover more quickly than when external incision not performed
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| Viral or bacterial etiology: usually both present; viral infection damages mucosa of respiratory tract; overgrowth of
local bacteria often follows
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| Problems associated with CT: abnormalities on CT or MRI lag behind radiographic and microbiologic clearance;
mucosal edema starts to improve, but patient gets sick again (ie, new infection); CT continues to show abnormal findings,
failing to reflect episodic nature of disease; ≈70% of children who attend daycare have abnormal findings on CT
during winter months; if nasal symptoms present, CT will have abnormal findings (but nasal symptoms detectable
clinically, so CT not needed); sinus CT useful in patients with respiratory tract infection without sinonasal symptoms
(eg, bronchospastic disease or persistent problematic cough; look for occult problems in sinuses)
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| Recurrent URIs: common masqueraders of so-called “chronic sinusitis”; preschool children have ≈8 infections/yr;
typical duration of symptoms ≈3 wk (even for common cold)
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| Role of cultures: cultures typially recover “usual suspects” (S pneumoniae, Moraxella, and/or H influenzae), often
identified by laboratory as normal nasal flora; high colony count and presence of mucosal disease indicates infection;
if disease not improving and purulence believed part of disease process, culture reasonable; in general, blind cultures
not useful (label sample appropriately)
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| Adenoids: large adenoids may contribute to rhinosinusitis by obstructing posterior nasal cavity and eustachian tubes
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| Antibiotics: essentially same efficacy against sinusitis as against OM; quinolones not recommended for routine use, but
somewhat more effective than ceftriaxone and amoxicillin-clavulanate; generally, amoxicillin more active than oral cephalosporins,
but not effective against β-lactamase producers
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| Pediatric vs adult sinusitis: pathogens—children typically have high bacterial counts and multiple types of organisms
(interferes with efficacy of amoxicillin; β-lactamase producers often mixed with S pneumoniae); for patients
with purulent sinusitis with bacterial etiology, empiric treatment with broader spectrum antibiotics probably
more effective than amoxicillin; involvement of adenoids—in children, adenoids often involved (do not need to be
especially enlarged); colony count from adenoids (not size of adenoids) best predicts recurrence of OM and sinusitis;
frequency—on average, adults have 3 infections/yr; children have 7 or 8
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| Duration of treatment: traditional recommendation to continue to treat until child well for 7 days; if minimum inhibitory
concentration exceeded at site of infection, pathogens eradicated in 3 to 5 days; longer treatment may have
prophylactic function; speaker prescribes antibiotics for ≤10 days (5-14 days reasonable); optimal duration of treatment
not well studied
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| Adjunctive therapy: no evidence that any adjunctive medications reduce duration or magnitude of symptoms of bacterial
sinusitis; all studies of nasal steroids show that treatment improves symptom scores but increases period of viral
shedding; speaker’s choice—saline; allergic etiology rare in young children
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| Surgical intervention: overwhelming opinion among otolaryngologists that there is little, if any, role for sinus surgery
for managing sinusitis in young children; sinusitis mucosal disease; opening of sinuses has no proven role in preventing
new infections and may predispose patient to unusual infections (eg, fungal or methicillin resistant
Staphylococcus aureus infection)
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| Patients deserve better diagnosis than “chronic sinusitis”: diagnosis too broad (etiology may be viral, bacterial,
allergic, or fungal); important to determine whether problem caused by intercurrent illness, unspecified respiratory
disease, bacterial infection that resolved, or bacterial infection that persisted; all individual cases of bacterial
sinusitis in children treatable (may require culture); diagnosis of chronic sinusitis inappropriate in children (however,
acute sinusitis may be persistent or recurrent)
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| Areas of disinformation: “child has same infection again”—explain to parent that child has new infection caused
by different virus (patient may have same symptom complex); “sinuses blocked up”—simplistic prosurgical explanation;
contradicted by presence of abundant drainage; “nothing works for patient”—treatment works; child just sick
again; “CT abnormalities prove seriousness of infection”—no correlation between CT findings and disease severity;
“all sinus symptoms due to allergy”—usually not true
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Suggested Reading
Anon JB et al: Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg
130:46, 2004; Anon JB et al: Sinusitis. N Engl J Med 352:203, 2005; Fauroux B: What’s new in pediatric sleep?
Pediatr Resp Rev 8:85,2007; Huang YS et al: Attention-deficit/hyperactivity disorder with obstructive sleep apnea:
a treatment outcome study. Sleep Med 8:18, 2007; Mitchell RB: Adenotonsillectomy for obstructive sleep apnea in
children: outcome evaluated by pre- and postoperative polysomnography. Laryngoscope 117:1844, 2007; Montgomery-Downs
HE et al: Cognition, sleep and respiration in at-risk children treated for obstructive sleep apnea.
Eur Resp J 25:336, 2005; O’Brien LM et al: Neurobehavioral correlates of sleep-disordered breathing in children.
J Sleep Res 13:165, 2004; Poole MD: A mathematical therapeutic outcomes model for sinusitis. Otolaryngol Head
Neck Surg 130:46, 2004; Poole MD: Acute bacterial rhinosinusitis: clinical impact of resistance and susceptibility.
Am J Med 117:29S, 2004; Poole MD, Portugal LG: Treatment of rhinosinusitis in the outpatient setting. Am J Med
118:45S, 2005; Schecter MS, Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep
Apnea Syndrome: Technical report: diagnosis and management of childhood obstructive sleep apnea syndrome.
Pediatrics 109:e69, 2002; Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea
Syndrome, American Academy of Pediatrics: Clinical practice guideline: diagnosis and management of childhood
obstructive sleep apnea syndrome. Pediatrics 109:704, 2002; Tarasiuk A et al: Elevated morbidity and health
care use in children with obstructive sleep apnea syndrome. Am J Respir Crit Care Med 175:55, 2007.
Educational Objectives
| The goal of this program is to improve the care of children with obstructive sleep apnea (OSA) and sinusitis.
After hearing and assimilating this program, the clinician will be better able to:
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| 1. Recognize clinical and polysomnographic findings suggestive of pediatric OSA.
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| 2. Describe the continuum of sleep-disordered breathing in children and associated sequelae.
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| 3. Choose appropriate therapy for managing OSA.
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| 4. Identify signs and symptoms of sinusitis in children.
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| 5. Evaluate treatment options for managing sinusitis.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and planning
committee members to disclose relevant financial relationships within the past 12 months that might create any
personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes
quality in health care and not a proprietary business or commercial interest. For this program, the faculty
and planning committee reported nothing to disclose.
Acknowledgments
Dr. Poole was recorded at the 29th Annual Las Vegas Seminars, presented November 15-18, in Las Vegas, NV, by
the American Academy of Pediatrics, California District IX, Chapters 1,2,3,4. The Audio-Digest Foundation
thanks Dr. Poole and the sponsor for their cooperation in the production of this program.
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