Snoring: When is this a Problem in Children?
Evaluation for Pediatric Obstructive Sleep Apnea
“Nina” Melinda DeSell, MS, CRNP
Pediatric Otolaryngology, Head and Neck Surgery
Johns Hopkins Hospital mdesell1@jhmi.edu
Historical Perspective
"The stupid-lazy child who frequently suffers from headaches at school, breaths through his mouth instead of his nose, snores and is restless at night, and wakes up with a dry mouth in the morning, is well worthy of the solicitous attention of the school medical officer."
-- W. Hill, 1889
Historical Perspective
“Chronic enlargement of the tonsillar tissues is an affection of great importance, and may influence in an extraordinary way the mental and bodily development of children”
William Osler, 1892
Sleep disordered breathing
Common cause of morbidity in childhood
Encompasses benign snoring to complete airway obstruction or obstructive sleep apnea (OSA)
Sleep disordered breathing
Primary Snoring
3 to 13% of children snore
No apneas, gas exchange abnormalities, excessive arousals, or daytime symptoms,
Does not appear to progress to OSA
May resolve over time
Specific treatment not recommended
But recent studies suggest possible neurocognitive effects
Primary Snoring- Neurocognitive Effects
13 children with snoring- on PSG had normal AHI, increased arousals & some desats
Compared performance on cognitive tests to non-snorers
Snorers had decrease in mean verbal IQ scores, global IQ scores, selective attention scores, sustained attention scores, memory index
Direct correlation between number of mild desats (3%)/arousals
& severity of neurocognitive deficits
Kennedy JD et al. Pediatric Pulmonol. (2004) 37(4):330-7.
Upper Airway Resistance Syndrome
Snoring and partial airway obstruction during sleep
Sufficient to disrupt/fragment sleep
Daytime symptoms present
PSG does not meet criteria for OSA
No gas exchange abnormalities
Obstructive sleep apnea
OSA 1 to 3% of pediatric population
Continued respiratory effort despite cessation of gas exchange at the level of the mouth and nostrils
Last at least 10 seconds
Occurrence is usually greatest in REM sleep
Pediatric OSA
Two patterns seen in children
• Complete obstructive apneas
• Partial upper airway obstruction with hypoventilation
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Pathophysiology
The Starling resistor model of upper airway. The airway is represented by a tube with a collapsible segment (pharynx) between two rigid segments with fixed diameters, resistances and pressures (nasal and tracheal segments). The airway collapses when the pressure surrounding the airway becomes greater than the pressure within the airway.
Etiology-Multifactorial
Complex interplay between anatomic and neuromuscular factors
Underlying genetic predisposition toward the disease
Major risk factor for OSA
Adenotonsillar hypertrophy
Midface hypoplasia
Small nasopharynx
Micrognathia
Obesity
Hypertonia and hypotonia
Risk Factors
Tonsillar Hypertrophy
Tonsillar Hypertrophy
Tonsils grow up to age 12 years with the greatest size increase during the first few years
Skeletal boundaries of the upper airway gradually grow in size
Tonsils and adenoids are largest between the ages of 3 and 6 years
Tonsil Hypertrophy
Tonsillar obstruction
Risk Factors
Obesity
Pickwickian Syndrome
THE POSTHUMOUS PAPERS OF THE PICKWICK CLUB by Charles
Dickens
“a fat and red-faced boy, (often) in a state of somnolency and constantly snoring”
Obesity
The coexistence of obesity and OSA
Increases morbidity rates
Poorer responses to therapy
Less common risk factors
Allergic rhinitis
Recurrent viral respiratory infections
Deviated nasal septum
Nasal polyps
Enlarged nasal turbinates
Micrognathia
Laryngomalacia
Pharyngeal flap surgery
OSA-Special populations at risk
 Craniofacial anomalies
 Metabolic and genetic disorders
 Down syndrome
 Pierre Robin sequence
 Neuromuscular diseases
 Cerebral palsy
 Muscular dystrophy
 Achondroplasia
 Mucopolysaccharidoses (Hurlers>Hunters)
 Cleft lip/palate repaired

Cleft lip/palate and OSA
Preschool children with cleft lip and/or palate have a risk of obstructive sleep apnea that is as much as five times that of children without cleft.
Craniofacial Syndromes
Trisomy 21
Craniosynostosis
Apert's syndrome
Crouzon's disease
Pfeiffer's syndrome
Treacher Collins syndrome
Pierre Robin syndrome
Goldenhar's syndrome
Saethre-Chotzen syndrome
Medical Complications of OSA
Growth failure
Cardiovascular
Polycythemia
Metabolic
Cardiopulmonary Complications
Severe untreated OSA can lead to pulmonary hypertension & cor pulmonale
Systemic hypertension has also been reported
Children with OSA can develop RVH and LVH
LVH is related to severity of OSA
Rarely seen with early diagnosis & treatment
Metabolic Complications
In a study of adolescents, the presence of OSA had a six-fold increase in the odds of metabolic syndrome (insulin resistance, dyslipidemia, hypertension, and obesity) compared with those without OSA
Similar to adults, when obesity and OSA coincide in children the risk for metabolic disturbances is further increased
Other complications
Daytime somnolence
Behavior problems
Inattention
Hyperactivity
Aggression
Poor performance in school
Attention-deficit disorder
Poor socialization
Developmental delay
SDB and behavior problems
Behavioral problems associated with SDB may not be related to the severity of a child’s sleep disorder
Significant improvement occurred in behavioral scales after adenotonsillectomy, but the degree of improvement is independent of the severity of preoperative SDB.
Mitchell, R. MD; Kelly, J. Behavioral Changes in Children With Mild
Sleep-Disordered Breathing or Obstructive Sleep Apnea After
AdenotonsillectomyLaryngoscope 117: September 2007
Assess sleeping patterns
Bedtime
Awakenings
Daytime naps
Ease of falling asleep and awakening
Distractions in bedroom
Snore Screening
Snoring
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Labored breathing during sleep
Nasal obstruction, mouth breathing
Hyperextension of the neck
Pauses in breathing/Observed apneas
Restless sleep
Diaphoresis
Enuresis
Parasomnias- sleepwalking, sleep-eating, bruxism, night terrors, rhythmic movement
Snoring
Snore Screen-what to ask-Daytime
Difficult to arouse in am
Daytime somnolence
Falls asleep easily in car or watching TV
Morning headache
Dry mouth
Halitosis
Breathing with open mouth posture
Hyponasal speech
Chronic nasal obstruction with or without rhinorrhea
Poor weight gain despite good oral intake
Irritability
Poor academic performance
Unusual daytime behavior
Behavior/learning problems (Including ADHD)
QOL Questionnaires
OSA-18
Physical Exam
General:
Obesity/underweight
Mandible & maxilla position/size
Adenoid facies
Oral Cavity
Nasal structures
Neck: Neck size, circumference, fatty deposition, hyoid position
Neuro: Tone, CN deficits
CV: HTN
Extremities: Edema, clubbing
ENT Exam
Oral Exam
Tongue-size
Palate-long, high, or narrow hard palate
Uvula-length or width
Tonsils-size
Dentition, crowding of oropharynx, overlapping incisors, crossbite, overjet/overbite
Jaw size
Modified mallampati score
Tonsillar grading scale
0 within the tonsillar fossa
1+ <25 percent of the lateral dimension of the oropharynx as measured between the anterior tonsillar pillars.
2+ < 50 percent of the lateral dimension of the oropharynx.
3+ < 75 percent of the lateral dimension of the oropharynx.
4+ 75 percent or more of the lateral dimension of the oropharyx
Mallampatti Score
Describes the tongue size in relation to the oropharynx.
Relaxed tongue and open mouth
Class I: The soft palate, fauces, uvula, anterior and posterior pillars are visualized.
Class II: The soft palate, fauces, and uvula are visualized.

Class III: The soft palate and base of the uvula are visualized.
Class IV: The soft plate is not visualized.
Nasal exam
External deformity
Rhinorrhea
Asymmetry of nares
Nasal valve collapse
Deviated septum
Nasal turbinate enlargement
Diagnostic Testing
Polysomnography
Controversial role in the diagnosis of childhood sleep-disordered breathing.
Current gold standard
Not required for diagnosis
Excess cost/availability
The technology used in the majority of sleep labs may be inadequate to diagnose
Lack of consensus on interpretation of polysomnograms
Polysomnogram
EEG
EKG
Submental EMG
Anterior tibialis EMG
EOG
Nasal/oral airflow
Pulse oximetry
Respiratory effort
Sleeping position
+/-Esophageal manometry
Polysomnography
Events that can be evaluated include:
Obstructive sleep apnea syndrome (OSA)
Periodic leg movements (PLM)
Nocturnal seizures
Parasomnias
Issues related to nocturnal gas exchange
Periodic leg movements (PLM)
Nocturnal movements of the legs (and occasionally arms) that last between 0.5 and 5 seconds
PLM disorder may be due to diabetes mellitus, spinal cord tumor, sleep apnea syndrome, narcolepsy, uremia, or anemia
Parasomnias
Sleepwalking, confusional arousals, and night terrors
Thought to result from incomplete arousal from sleep
Value of the Sleep Study
Definitive diagnosis
Assess severity
Guide the pace of treatment
Predict risk of perioperative/post op complications
Predict outcome after T&A
Baseline data
Objective assessment of severity to assess all other parameters
Quality of life data
Developmental/Cognitive Issues
Other clinical signs and symptoms
Components of sleep study
Sleep architecture - percentage of total sleep time (TST) spent in stage I/II, stage III/IV, stage REM, and wakefulness.
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Sleep latency -the time after lights out until sleep is achieved
Sleep efficiency -amount of the total time in bed that the patient spends asleep
Types of apnea evaluated
Obstructive apnea -pause of airflow with respiratory effort
Central apnea -pause of airflow without respiratory effort
Mixed apnea -characteristics of both
Hypopnea -Hypoventilation secondary to partial obstruction
Respiratory event related arousals (RERAs) - partial blockage in airflow with an associated arousal.
Hypopnea
Obstructive apnea
Absence or reduction in airflow in the upper airway despite ongoing respiratory effort, frequently in combination with paradoxical breathing efforts and/or snoring
For at least 10 seconds OR
For 2 breath cycles in older children OR
For 6 seconds or 1.5 to 2 breaths in infants
2011 Clinical Practice Guideline: Polysomnography for Sleep-
Disordered Breathing Prior to Tonsillectomy in Children
1. PSG should be obtained before tonsillectomy in children with sleep-disordered breathing who have conditions that increase their risk of complications from surgery or anesthesia, including obesity, Down syndrome, craniofacial abnormalities (e.g., cleft palate), neuromuscular disorders (e.g., muscular dystrophy), sickle cell disease, or mucopolysaccharidoses (metabolic problems in digesting sugars).
2. Doctors should encourage otherwise healthy children (without any of the conditions in #1) to have PSG when either the need for tonsillectomy is uncertain (e.g., differing opinions or observations among parents, family members, primary care doctors, and specialists) or when size of the tonsils is smaller than what would be expected from the severity of snoring or sleep disturbance.
3. When a child does get PSG before tonsillectomy, the surgeon should communicate the test results to the anesthesiologist before surgery begins in case the anesthesia approach needs to be modified.
4. Children should be admitted to the hospital for overnight monitoring after tonsillectomy if they are under 3 years of age, because they may require oxygen or breathing assistance after surgery.
5. Children should be admitted to the hospital for overnight monitoring after tonsillectomy if PSG indicates they have severe obstructive sleep apnea, which is a type of sleep-disordered breathing in which the child’s oxygen levels drop below 80%, there are 10 or more breathing obstructions (weak breaths or apneas lasting 10 seconds or longer) every hour, or both.
6. When PSG is indicated to assess sleep-disordered breathing prior to tonsillectomy, doctors should obtain laboratory-based
PSG (an overnight study attended by a technician in a sleep laboratory), not home-based PSG (with a portable, unattended monitoring device), because more is known about the accuracy and interpretation of laboratory-based testing.
Pediatric OSA
Obstructive Apnea
Sleep Study Results
AHI Apnea/Hypopnea Index = apneas + hypopneas/hour of sleep for non-REM (NREM) and REM sleep. Index=’#of events divided by the number of hours of sleep.
<1 normal
1-4 mild

5-10 moderate
>10 severe
Oxygen saturation >92% normal
CO2 <51 mmHg normal
Respiratory Distress Index (RDI) = Disordered breathing index
(DBI) = apneas + hypopneas + RERAs. Reported in # of events per hour.
Other evaluation
Assessment of right ventricular dysfunction:
Electrocardiogram
Echocardiogram
Assessment of pharyngeal airway:
Lateral neck radiograph
Dynamic fluoroscopy
MRI upper airway
Flexible nasopharyngoscopy
Assessment of consequences:
Hypoxemia - Hematocrit
Hypercapnia - Serum bicarbonate
X-ray
Cine MRI
Treatment of OSA
Approach to treatment
Identify underlying abnormalities and the site of obstruction
Determine the presence or absence of contributing neurologic or functional abnormalities
Medical management
Weight loss in obese children
Antibiotics for recurrent tonsillitis or adenoiditis
Allergy testing and treatment
Nasal steroids
Leukotriene Modifiers
Leukotriene Modifiers
Increased # leukotriene receptors in tonsils of sleep apnea patient
Montelukast daily use x 16 wks in 24 patients with mild OSA –
Improvement in hypercarbia and AHI
Decrease in adenoid size
Medical Treatment-CPAP
CPAP provides a continuous level of pressure
Approved by the US FDA for use in children 7 years of age.
Indicted in children that are not surgical candidates or did not respond to surgery
Approximately 20% of children can tolerate
Complications: skin breakdown, conjunctivitis and rhinitis, midfacial bony deformation or hypoplasia
Surgical Treatment
Adenotonsillectomy
Treatment of choice with SDB or OSA
Curative in 80% of OSA
Improvements in PSG parameters have been demonstrated in 75–
100% of children
May improved hyperactivity, inattention, and sleepiness, and even in the diagnosis of attention deficit-hyperactivity disorder.
Preoperative Teaching
Complications of T & A
Dehydration (1-3 %)
Hemorrhage (1-2%) immediate and delayed
Velopharyngeal insufficiency (< 1%)
Anesthesia-related complications including death
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Airway obstruction, hypoxemia, apnea
Nasopharyngeal stenosis
Pulmonary edema
Nausea and Emesis
Pain (local, odynophagia, otalgia)
Infection
Post-op tonsillectomy bleed
Adenotonsillectomy for OSAS
Inpatient vs. Outpatient Surgery
Surgical options
Nasal Surgery
Turbinate reduction
Septoplasty
Nasal valve reconstruction
Retropalatal Surgery
T&A
UPPP
UPPP/Palatoplasty
Addresses retropalatal obstruction
Indications
Long or thick soft or uvula
Redundant lateral pharyngeal wall
Modest adenotonsillar hypertrophy but severe OSA
Consider in kids with Downs, CP, neurological impairment, or teens
Retroglossal/hypopharyngeal Surgical options
Tongue reduction for macroglossia
Genioglossal advancement
Hyoid myotomy and suspension
Mandibular Osteotomy for mandibular deficiency/microgenia
Mandibular Distraction/Expansion
Distraction
Tracheotomy -Reserved for use in children with severe OSA who have failed to improve with other medical and surgical treatments
AAP Clinical Practice Guideline on Childhood OSAS (2002)
All children should be screened for snoring
Complex high-risk patients should be referred to a specialist
Patients with cardiorespiratory failure cannot await elective evaluation
Gold standard for evaluation is polysomnography
Adenotonsillectomy is 1 st
line treatment
AAP Clinical Practice Guideline on Childhood OSAS (2002)
CPAP is an option for those who are not surgical candidates and those who do not respond to surgery
High-risk patients should be monitored as inpatients after surgery
Patients should be reevaluated after surgery to determine whether additional treatment is required
Summary of AAP Guidelines http://aappolicy.aappublications.org/cgi/content/full/pediatrics;1
09/4/704
Sleep-disordered breathing in children is a spectrum of disease
OSA is seen in 1-3% of children
Polysomnography remains the gold standard for diagnosis and severity assessment, but it is not widely used
T&A is the first-line therapy for pediatric OSA