AIRWAY ISSUES
| SLEEP-DISORDERED BREATHING IN CHILDREN —Carol L. Rosen, MD, Professor, Department of Pediatrics, Division
of Clinical Epidemiology, Case Western Reserve University School of Medicine, and Medical Director, Department of
Sleep Services, Rainbow Babies and Children’s Hospital, Cleveland, OH
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| Epidemiology of sleep-disordered breathing (SDB): 2% of children develop SDB; prevalence about equal in
boys and girls; patients at increased risk—black children; those with family member on continuous positive airway
pressure (CPAP) for sleep apnea; obesity less important factor in children than in adolescents and adults; former preterm
infants at increased risk for obstructive sleep apnea (OSA); prior adenotonsillectomy paradoxic risk factor (need for surgery
suggests presence of other risk factors); patients with family history of SDB; heritable factors—craniofacial structure;
respiratory control; tendency towards obesity
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| Consequences of childhood SDB: in most severe cases, cor pulmonale (right heart failure); failure to thrive (FTT);
excessive daytime sleepiness (however, most common cause poor sleep hygiene, especially in adolescents); persistent
enuresis with snoring; neurocognitive and behavioral problems—attention-deficit/hyperactivity disorder, or other
learning or behavior problems; hypertension and increased risk for cardiovascular morbidities; metabolic syndrome or insulin
resistance
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| Associated findings: if child presents with snoring and enuresis, suspect OSA
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| Pediatric SDB distinguishable from adult SDB: association with obesity less pronounced in children; chief complaint
in children snoring (may be subtle; in adults, sleepiness); airway more resistant to collapse, and patients less arousable
(less sleep fragmentation makes daytime sleepiness less likely); cardiorespiratory features more subtle (may be
difficult to diagnose child in adult sleep laboratory); large tonsils or adenoids common etiology (rare in adults)
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| Pathophysiology of OSA: tension between forces that activate airway and maintain patency and those that narrow airway;
causes of structural narrowing—adenotonsillar hypertrophy (ATH); obesity; edema; mechanical obstruction;
mechanisms of neuromuscular activation—upper airway neuromotor tone; central ventilatory drive; sleep state;
arousal; alcohol and some medications depress activation
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| Contributing factors to SDB: with onset of sleep, small relaxation of upper airway tone may be enough to trigger episode;
neurologic disorders (cerebral palsy, Hunter’s syndrome, infiltrative problems); differences in neuromuscular activation;
environmental issues; inflammation; infection (eg, mononucleosis causing tonsillar hypertrophy); obesity;
craniofacial anomalies
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| Airway findings in OSA: large tonsils; if airway collapses repeatedly, patient may present with edema of soft palate
and uvula
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| What’s different about SDB in children? anatomy earlier risk factor in children than adults; normal ATH of youth
can be “tipover” in smaller less mature airway; stereotypic adult risk factors often missing (eg, obesity, loud snoring); affected
children may have normal examination with slightly enlarged tonsils and adenoids; children better at defending
airway from collapse (obstructive hypoventilation may present without discrete obstructive events); adenotonsillectomy
first-line treatment (paradoxically, prior treatment also risk factor)
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| ATH not sole cause of childhood OSA: children with OSA and ATH do not develop obstruction during wakefulness
(onset may require supine position and loss of tone during sleep); correlation with adenotonsillar size variable; OSA
may persist after removal of adenoids and tonsils, and can recur during adolescence
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| More risk factors for SDB: Prader-Willi syndrome (signs and symptoms include obesity and control-of-breathing issues);
achondroplasia (small airway; relatively large tongue; screening for OSA indicated); Down syndrome (40% of patients
have significant OSA; relatively large tongue, hypotonia, small airway, tendency toward obesity); morbid obesity
(incidence increasing); craniofacial anomalies, eg, Pierre Robin syndrome; neuromuscular conditions (muscular dystrophy,
spinal muscular atrophy, cerebral palsy); congenital central hypoventilation; Treacher Collins syndrome (genetic
craniofacial condition with variable penetrance); spina bifida (respiratory control problems; central apnea; may not sense
O2 or CO2 ; scoliosis and restrictive lung disease); Hunter’s syndrome (liver enlargement, contractures; large tongue; developmental
delay; copious secretions (eg, chronic nasal discharge)
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| When is SDB worse? early-stage sleep disturbances include night terrors and parasomnia (sleep walking); periods of
rapid eye movement—later sleep stage (parents may be sleeping and miss it); OSA more likely (individual loses postural
and upper airway tone)
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| Recognition of obstructive SDB: classic symptoms—snoring; difficulty breathing; possible apnea and arousals;
symptoms during sleep difficult to predict from awake examination; parent-reported (may be missed); other signs and
symptoms—mouth breathing sign of nasal obstruction; tonsillar hypertrophy (may be “tipping” factor for patient with
smaller airway or decreased tone or respiratory control; pectus deformity may be variation or marker; sleepiness, hyperactivity,
tiredness or irritability with snoring worth investigating; unusual sleeping position (eg, neck hyperextended, bottom
up in air); sweating during sleep; hypoxia and hypercapnia potent stimuli for diaphoresis; enuresis; growth
impairment or obesity
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| Benign snoring or pathologic SDB? difficult to make diagnosis from awake examination; in some studies, even relatively
low levels of SDB associated with adverse behavioral or cognitive effects; more comorbidities, greater need for
polysomnography (PSG; includes measurement of effort, airflow, and pulse oximetry)
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| American Academy of Pediatrics (AAP) clinical practice guidelines (2002): encourages pediatricians to
screen for snoring; in complex high-risk patients, consider referral to neurologist, pulmonologist or otolaryngologist; patients
with cardiorespiratory failure cannot wait for elective evaluation; diagnostic evaluation (including polysomnography)
useful in discriminating between primary snoring and OSA; tonsillectomy and adenoidectomy (T and A) first-line
treatment for most children; CPAP option if patient not candidate for surgery or not responsive to surgery; not easy to implement
CPAP in children (family involvement key); patients at high risk for sleep apnea may need monitoring as inpatients
after adenotonsillectomy; reevaluate postoperatively to determine whether additional treatment required
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| Management of childhood SDB (overview): surgery has greater role in infants and children (medical therapy, eg,
CPAP, has greater role in adolescents and adults)
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| Treatment of obstructive SDB: surgical—adenotonsillectomy 75% to 100% effective (depends on risk factors and
whether outcome measure improvement or cure); craniofacial surgery may be indicated in patients with underlying abnormalities
(tracheostomy treatment of last resort); CPAP—compliance significant hurdle, especially in adolescents,
even if therapy effective (supportive family helpful); medical—O2 may play palliative role, but delivery blocked if patient
completely obstructed; nasal steroids improve low respiratory disturbance index (RDI) but less effective in severe
cases; other—positioning helpful in some children; weight loss helpful but difficult to achieve; efficacy of oral appliances
not evaluated in children
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| DYNAMIC AIRWAY LESIONS IN CHILDREN: WHEN NOISY BREATHING IS NOT ASTHMA —Shruti M. Paranjape,
MD, Assistant Professor of Pediatrics, Eudowood Division of Pediatric Respiratory Sciences, Johns Hopkins University
School of Medicine, Baltimore, MD
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Evaluation of Noisy Breathing
| Patient history: often chronic in child with noisy breathing secondary to large-airway lesions; elicit—whether noises
occur on inspiration or expiration; age of onset and timing; alleviating or exacerbating factors (eg, position or activity,
occurrence during sleep, response to therapy [first-line therapy bronchodilators, steroids, or antibiotics]); other associated
symptoms (eg, cough, frequency of associated infections)
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| Physical examination of chest
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 | Inspection: note vital signs (respiratory rate, SaO2 ), retractions or increased effort of breathing, and contour of chest
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| Percussion: often overlooked; dullness—rapid attenuation of vibrations over parenchymal consolidation or fluid-filled
portion of pleural cavity; tympanic response—vibrations undampened, eg, over tissue that overlies air-filled cavity;
most helpful in gauging hyperinflation; look for position of domes of diaphragm in, eg, patient with acute exacerbation
of asthma (normally, 1 to 2 cm below inferior tips of scapula); hyperinflation hallmark of small-airway obstruction
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| Palpation: confirms observed findings; look at symmetric excursions of chest; locate trachea and listen to transmissibility
of voice through chest wall
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| Auscultation: may be most important component
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| Description of breath sounds: not well standardized
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| Normal: bronchial (tubular) breath sounds (loudness equal on expiration and inspiration); vesicular sounds slightly
louder on inspiration, with soft expiratory phase
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| Abnormal
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| Respiratory phase: stridor—results from oscillations of narrowed extrathoracic airways and heard primarily on inspiration;
crackles—short nonmusical discontinuous sounds that result from passage of air through secretions or
across air-liquid interfaces; heard at end of inspiration in patient with advanced-stage cystic fibrosis (CF);
wheezes—long, musical, and continuous; result from oscillations in narrow airways; typically heard on expiration
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| Location and quality: small-airway obstruction—wheezes peripheral and polyphonic; large-airway obstruction—
wheezes more centrally located, low-pitched, and monophonic
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| Origins of lung sounds: turbulent flow loud (laminar quiet); most sounds come from trachea and medium-sized bronchi
as result of turbulent flow at branch points or carinae; peripheral airways conduct by laminar flow and contribute little
to total respiratory resistance (nearly silent under normal conditions)
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Dynamic Airway Lesions in Newborns and Infants
| Wheezing since birth: noisy breathing on first day of life worrisome (suggests congenital lesions); consider possibility
of vascular ring, tracheal webs, absence of pulmonary valves, or congenital lobar emphysema; all result in tracheal compression
and noisy breathing
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| Vascular rings: 1% of congenital cardiovascular anomalies; anatomic variants of aortic arch system result in encirclement
of trachea and esophagus and extrinsic obstruction of both structures; diagnosis—consider 3-dimensional computed
tomography (CT) to view airway and mediastinal anatomy; right-sided arch on chest x-ray sensitive but not
specific finding (coupling with tracheal narrowing or interruption of tracheal air column on lateral view suggests vascular
ring)
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| Congenital lobar emphysema: rare; 50% of cases present in neonatal period or infancy; deficiency of bronchial cartilage
to upper lobe results in overinflation and airway compression; case—overinflated left upper lobe compressing trachea,
with atelectasis of subjacent lobes; surgery often indicated in patients with marked respiratory compromise; early
lobectomy results in long-term normal pulmonary function and compensatory growth
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| Tracheomalacia and bronchomalacia: softening of large airway; many patients do not present until 6 to 12 mo of
age (symptoms more pronounced as infant becomes more mobile); parents describe fremitus (palpable chest vibrations);
on physical examination, lung volumes may be normal; typically, lack of retractions and peripheral wheezes; parents report
poor response to bronchodilators (eg, albuterol); tracheobronchomalacia can result from any congenital airway lesion
(eg, tracheoesophageal fistula, tight vascular rings); physical findings—usually unilateral; uniform fremitus or
monophonic wheeze; louder on expiration; 85% to 90% of cases resolve by 1 yr of age
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| Laryngomalacia: floppiness of larynx (most common cause of chronic inspiratory noise in infants); noise on inspiration
due to narrowing of extrathoracic portion of airway; may affect epiglottis, arytenoid cartilages, or both; course similar to
that of tracheobronchomalacia, with onset by 2 mo of age and resolution at 18 to 24 mo of age; acquired laryngomalacia
seen in central nervous system (CNS) disease and gastroesophageal reflux disease (GERD); endoscopic view (case)—
omega-shaped epiglottis; short aryepiglottic (AE) folds, and redundant arytenoid tissue; with inspiration, prolapse of
arytenoid tissue and supporting structures into airway, with reduction of airway almost to pinpoint (sometimes epiglottis
flops closed); airway reopens with passive expiration
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Dynamic Airway Lesions in Toddlers
| Foreign-body aspiration: potential source of noisy breathing; can occur at any age, but most common in toddlers and
preschoolers; choking history often negative; physical findings might reveal unilateral and monophonic wheezes; using
differential stethoscope, might hear phase delay on affected side; most foreign bodies radiolucent; inspiratory and expiratory
films may be difficult to obtain in younger patients; left and right bilateral decubitus films might show persistence of
inflation, which raises suspicion of foreign body; lack of response to previous medical therapy
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Dynamic Airway Lesions in School-Aged and Older Children
| Chronic congestion: chronic wet cough in older child red flag; differential diagnosis—asthma; postnasal drainage;
GERD; CF; ciliary dyskinesia; passive smoke exposure; humoral immunodeficiencies (IgA deficiency and deficiencies
of IgG subclasses 2 and 4); retained foreign bodies can cause persistence of wheezing; other causes—exercise hyperventilation;
vocal cord dysfunction
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| Gastroesophageal reflux disease: can affect upper and large airways; recurrent croup frequent sign; other symptoms
hoarseness, laryngomalacia, or poorly controlled asthma
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| Diagnostic approach: careful history and physical examination; consider—spirometry (shape of inspiratory and expiratory
flow loops can give indication of whether large or small airways obstructed); chest radiography useful; airway and
chest wall fluoroscopy to diagnose tracheobronchomalacia (not necessary in straightforward cases); chest wall fluoroscopy
helpful in detecting foreign body; barium swallow may be helpful as initial study for assessing GERD and aspiration,
or indentations of trachea and esophagus associated with vascular rings; flexible fiberoptic bronchoscopy good for
assessing lesions of large airway; extraction of foreign body difficult to perform with flexible scope (rigid bronchoscopy
safer)
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| Treatment: most conditions resolve spontaneously (especially tracheomalacia and bronchomalacia); consider possibility
of comorbid conditions (eg, GERD, asthma); GERD may require acid suppression; tracheobronchomalacia often responds
to nebulized ipratropium (weak bronchodilator, but can dry secretions and make breathing less noisy); might be
helpful to avoid β-agonist in severe tracheomalacia, but consider it in patient with evidence of large- and small-airway
obstruction; for tracheomalacia and most large-airway lesions, surgery rarely indicated unless underlying vascular ring or
tracheoesophageal fistula (TEF) present
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Suggested Reading
Emancipator JL et al: Variation of cognition and achievement with sleep-disordered breathing in full-term and preterm
children. Arch Pediatr Adolesc Med 160:203, 2006; Farber JM: Clinical practice guideline: diagnosis and management
of childhood obstructive sleep apnea syndrome. Pediatrics 110:1255, 2002; Finder JD: Understanding
airway disease in infants. Curr Prob Pediatr 29:65, 1999; Hart CN et al: Health-related quality of life among children
presenting to a pediatric sleep disorders clinic. Behav Sleep Med 3:4, 2005; Rosen CL et al: Health-related quality
of life and sleep-disordered breathing in children. Sleep 25:657, 2003; Rosen CL et al: Prevalence and risk factors
for sleep-disordered breathing in 8- to 11-yr-old children: association with race and prematurity. J Pediatr 142:383,
2003; Rosen CL: Obstructive sleep apnea syndrome in children: controversies in diagnosis and treatment. Pediatr
Clin North Am 51:153, 2004; Schecter MS, Section on Pediatric Pulmonology, Subcommittee on Obstructive
Sleep Apnea Syndrome: Technical report: diagnosis and management of childhood obstructive sleep apnea
syndrome. Pediatrics 109:704, 2002; Sulit LG et al: Associations of obesity, sleep-disordered breathing, and
wheezing in children. Am J Respir Crit Care Med 171:659, 2005.
Educational Objectives
| The goal of this program is to improve diagnosis and management of sleep-disordered breathing (SBD) and airway
lesions in children. After hearing and assimilating this program, the clinician will be better able to:
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| 1. Identify signs, symptoms, and consequences of SBD.
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| 2. Develop a treatment plan for managing SBD.
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| 3. Recognize relevant physical findings in a child with noisy breathing that suggest a diagnosis other than
asthma.
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| 4. Describe typical airway lesions seen in children.
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| 5. Develop an approach to managing airway lesions in children.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty 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 following has been disclosed: Dr. Rosen has received support from Advanced
Brain Monitoring and Cephalon.
Acknowledgments
Dr. Rosen was recorded at Pediatrics Today, Common Pediatric Problems, presented April 17, 2007, in Cleveland, OH,
by the Department of Pediatrics, Case Western Reserve University School of Medicine, and University Hospitals, Cleveland;
Dr. Paranjape was recorded at the 35th Annual Pediatric Trends, presented April 16-20, 2007, in Baltimore, MD, by
Johns Hopkins Children’s Center, Baltimore.
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