Embed Size (px)
Citation preview
1 of 35
Number: 0752
Policy *Please see amendment for Pennsylvania Medicaid at the end of this CPB.
I. Diagnosis
A. Aetna considers nocturnal polysomnography (NPSG)
for children and adolescents younger than 18
years of age medically necessary when performed in a
healthcare facility for any of the following indications.
Last Review 08/25/2016
Effective: 04/25/2008
Next Review: 08/24/2017
Review History
Definitions
1. To diagnose obstructive sleep apnea syndrome
(OSAS) and differentiate it from snoring
2. To evaluate hypersomnia
3. Suspected narcolepsy (with MSLT)
4. Suspected parasomnia
5. Suspected restless leg syndrome
6. Suspected periodic limb movement disoder
7. Suspected congenital central alveolar hypoventilation
syndrome
8. Suspected sleep related hypoventilation due to
Clinical Policy Bulletin Notes
2 of 35
neuromuscular disorders or chest wall deformities.
B. Aetna considers NPSG for children medically
necessary when performed in a healthcare facility after
an adenotonsillectomy or other pharyngeal surgery for
OSAS when any of the following is met (study should be
delayed 6 to 8 weeks post‐operatively):
1. Age younger than 3 years; or
2. Cardiac complications of OSAS (e.g., right ventricular
hypertrophy); or
3. Craniofacial anomalies that obstruct the upper airway;
or
4. Failure to thrive; or
5. Neuromuscular disorders (e.g., Down syndrome,
Prader‐Willi syndrome and myelomeningocele); or
6. Obesity; or
7. Prematurity; or
8. Recent respiratory infection; or
9. Severe OSAS was present on pre‐operative PSG (a
respiratory disturbance index of 19 or greater); or
10. Symptoms of OSAS persist after treatment.
C. Aetna considers the use of abbreviated or screening
techniques, such as videotaping, nocturnal pulse
oximetry, unattended home PSG, or facility based,
daytime,
abbreviated cardiorespiratory sleep studies (daytime nap
PSG, Pap Nap testing) experimental and investigational for
diagnosis of OSAS in children because their effectiveness
for this indication has not been established.
D. Aetna considers measurements of circulating adropin
concentrations, plasma pentraxin‐3 or TREM‐1 levels
experimental and investigational for obstructive sleep
apnea in children.
II. Treatment
Aetna considers the following treatments for OSAS in
children with habitual snoring medically necessary when
3 of 35
the apnea index is greater than 1 on a NPSG.
A. Aetna considers adenoidectomy and/or
tonsillectomy medically necessary for treatment of OSAS
in children. Childhood OSAS is usually associated with
adenotonsillar hypertrophy, and the available medical
literature suggests that the majority of cases will benefit
from adenotonsillectomy.
B. Aetna considers continuous positive airway pressure
(CPAP) medically necessary for treatment of OSAS in
children when any of the following is met:
1. Adenoidectomy or tonsillectomy is contraindicated; or
2. Adenoidectomy or tonsillectomy is delayed; or
3. Adenoidectomy or tonsillectomy is unsuccessful in
relieving symptoms of OSAS.
Aetna considers CPAP medically necessary for
treatment of tracheomalacia.
C. Aetna considers oral appliances or functional orthopedic
appliances medically necessary in the treatment of
children with craniofacial anomalies with signs and
symptoms of OSAS.
D. Aetna considers oral appliances or functional orthopedic
appliances experimental and investigational for
treatment of OSAS in otherwise healthy children. There
is insufficient evidence that oral appliances or functional
orthopedic appliances are effective in the treatment of
OSAS in healthy children.
E. Aetna considers uvulopalatopharyngoplasty (UPPP)
medically necessary for the treatment of OSAS in children
with neuromuscular disorders who are deemed to be at
high risk for persistent upper airway obstruction after
adenotonsillectomy alone. Aetna considers UPPP
experimental and investigational for the treatment of
OSAS in otherwise healthy children.
F. Aetna considers the following interventions experimental
and investigational for obstructive sleep apnea in children
because their effectiveness for this indication has not
been established:
4 of 35
1. Cautery‐assisted palatal stiffening procedure (CAPSO);
2. Chiropractic/osteopathic manipulation;
3. Expansion sphincter pharyngoplasty;
4. Flexible positive airway pressure;
5. Hypoglossal nerve stimulation;
6. Injection snoreplasty;
7. Laser‐assisted uvuloplasty (LAUP);
8. Lingual tonsillectomy;
9. Mandibular distraction osteogenesis;
10. Maxillary expander;
11. Midline/partial glossectomy;
12. Nasal surgery;
13. Pillar palatal implant system;
14. Repose system;
15. Somnoplasty or Coblation;
16. Transpalatal advancement pharyngoplasty;
17. Uvulectomy.
See also CPB 0004 ‐ Obstructive Sleep Apnea in Adults (../1_99
/0004.html), CPB 0330 ‐ Multiple Sleep Latency Te st (MSLT)
and Maintenance of Wakefulness Te st (MWT) (../300_399
/0330.html), CPB 0452 ‐ Noninvasive Positive Pressure
5 of 35
Ve ntilation (../400_499/0452.html), and CPB 0549 ‐ Distraction
Osteogenesis for Craniofacial Defects (../500_599/0549.html).
Background
Obstructive sleep apnea syndrome (OSAS) is a disorder of
breathing in which prolonged partial upper airway obstruction
and/or intermittent complete obstruction occurs during sleep
disrupting normal ventilation and normal sleep patterns. The
signs and symptoms of OSAS in children include habitual
snoring (often with intermittent pauses, snorts, or gasps) with
labored breathing, observed apneas, restless sleep, and
daytime neurobehavioral problems. Nocturnal enuresis,
diaphoresis, cyanosis, mouth breathing, nasal obstruction
during wakefulness, adenoidal facies, and hyponasal speech
may also be present. Daytime sleepiness is sometimes
reported but hyperactivity can frequently occur. Case studies
report that OSAS in children can lead to behaviors easily
mistaken for attention‐deficit/hyperactivity disorder as well as
behavioral problems and poor learning; however, most case
studies have relied on histories obtained from parents of
snoring children without objective measurements, control
groups, or sleep studies. Severe complications of untreated
OSAS in children include systemic hypertension, pulmonary
hypertension, failure to thrive, cor pulmonale, and heart
failure.
History and physical examination have been shown to be
sensitive but not specific for diagnosing OSAS in children.
Primary snoring is often the presenting symptom reported by
parents, and should warrant careful screening for OSAS.
Primary snoring is defined as snoring without obstructive
apnea, frequent arousals from sleep or abnormalities in
gaseous exchange. It is estimated that 3 % to 12 % of children
are habitual snorers but only 2 % will be diagnosed with OSAS.
Although surgical treatment has been shown to improve quality
of life, it is not without risks (e.g., bleeding, velopharyngeal
insufficiency, post‐obstructive pulmonary edema). Thus,
clinicians must be able to distinguish between primary snoring
and OSAS. Primary snoring among children without obstructive
6 of 35
sleep apnea is usually considered a benign condition although
this has not been well evaluated.
Nocturnal polysomnography (NPSG) remains the gold standard
diagnostic test to differentiate primary snoring from OSAS in
children. It is the only diagnostic technique that is able to
quantitate the ventilatory and sleep abnormalities associated
with sleep‐disordered breathing and can be performed in
children of any age. A polysomnogram (PSG) is a sleep study
that is performed in a facility/laboratory setting and requires an
overnight stay. PSG is designed to capture multiple sensory
channels including blood pressure, brain waves, breathing
patterns and heartbeat as an individual sleeps. It can also
record eye and leg movements and muscle tension which can
be useful in diagnosing parasomnias. A PSG performed at a
facility will record a minimum of 12 channels which involves at
least 22 wire attachments to the individual. Sensors that send
electrical signals to a computer are placed on the head, face,
chest and legs. This test is attended by a technologist and the
results are evaluated by a qualified physician. A PSG may be
performed in conjunction with a positive airway pressure (PAP)
machine to determine the titration of oxygen flow.
Positive airway pressure (PAP) titration study is used to set the
right level of PA P which can be administered as continuous
positive airway pressure (CPAP) or bilevel positive airway
pressure (BPAP) once individual tolerance and optimal levels
are determined by a sleep technologist. PA P titration may be
performed in conjunction with a PSG as part of a split night
study if the diagnosis of moderate or severe OSA can be made
within the first two hours of recorded sleep and at least three
hours of PA P titration, including the ability of PA P to eliminate
respiratory events during both rapid eye movement (REM)
sleep and non‐REM sleep, is demonstrated. If this is not
possible, a second night in the sleep center may be necessary
for the CPAP titration study.
It should be noted that interpretation of NPSG values in
children with OSAS is not unanimously agreed upon in the
7 of 35
literature (Sargi and Younis, 2007) and only a limited number of
studies designed to establish normal values for sleep‐related
respiratory variables in children have been reported. However,
based on normative data, an obstructive apnea index of 1 is
frequently chosen as the threshold of normality. Other
normative values reported in the literature for children aged 1
to 15 years include: central apnea index 0.9; oxygen
desaturation, 89 %; baseline saturation, 92 %; and PETCO2
(end‐tidal carbon dioxide pressure) greater than 45 mm Hg for
less than 10 % of total sleep time (Verhulst, 2007; Uliel, 2004;
Schechter, 2002).
Studies have shown that abbreviated or screening techniques,
such as videotaping, nocturnal pulse oximetry, and daytime
nap PSG tend to be helpful if results are positive but have a
poor predictive value if the results are negative. Facility based,
daytime, abbreviated, cardiorespiratory sleep studies (PAP NAP
testing) uses a therapeutic framework that includes mask and
pressure desensitization, emotion focused therapy to overcome
aversive emotional reactions, mental imagery to divert the
individual’s attention from mask or pressure sensations and
physiological exposure to PA P therapy during a 100 minute nap
period which is purported to enhance PA P therapy adherence.
Home/portable monitoring sleep testing is a sleep study
performed in the home utilizing portable monitoring (PM)
devices that are designed to be used by an individual without
supervision of a sleep technologist. PM devices measure fewer
parameters than a laboratory based sleep study and are
therefore not recommended for assessment of sleep disorder in
the pediatric population. Unattended home PSG in children was
evaluated by 1 center (Jacob, 1995) and produced similar
results to laboratory studies; however, the equipment was
relatively sophisticated and included respiratory inductive
plethysmography, oximeter pulse wave form and videotaping.
Unattended home studies in children using commercially
available 4‐ to 6‐channel recording equipment has not been
studied. Portable monitoring based only on oximetry is
inadequate for identifying OSAS in otherwise healthy children
8 of 35
(Kirk, 2003).
Actigraphy is a technique for monitoring body movement
during sleep to detect sleep disorders by using a portable
device known as an actigraph, which is worn on the individual’s
wrist or ankle. An example of an actigraph device is the
Actiwatch.
Prescreening devices or procedures purportedly predict pretest
probability of obstructive sleep apnea (OSA) prior to performing
a sleep study. Examples of prescreening techniques include, but
may not be limited to, acoustic pharyngometry and SleepStrip.
According to the American Academy of Pediatrics guideline on
the diagnosis and management of childhood OSAS (2002),
complex high‐risk patients should be referred to a specialist
with expertise in sleep disorders. These patients include infants
and children with any of the following: craniofacial disorders,
Down syndrome, cerebral palsy, neuromuscular disorder,
chronic lung disease, sickle cell disease, central hypoventilation
syndrome, and genetic/metabolic/storage diseases.
Indications for a repeat NPSG after an adenotonsillectomy or
other pharyngeal surgery for OSAS include (i) high‐risk children,
or (ii) if symptoms of OSAS persist after treatment. High‐risk
children include those of age younger than 3 years, severe
OSAS was present on pre‐operative PSG (a respiratory
disturbance index of 19 or greater), cardiac complications of
OSAS (e.g., right ventricular hypertrophy), failure to thrive,
obesity, prematurity, recent respiratory infection, craniofacial
anomalies, and neuromuscular disorders. Patients with mild to
moderate OSAS who have complete resolution of signs and
symptoms do not require repeat NPSG (AAP, 2002).
The American Academy of Pediatrics’ practice guideline on
“Diagnosis and management of childhood obstructive sleep
apnea syndrome” (Marcus et al, 2012) focused on
uncomplicated childhood OSAS, that is, OSAS associated with
adenotonsillar hypertrophy and/or obesity in an otherwise
9 of 35
healthy child who is being treated in the primary care setting. Of
3,166 articles from 1999 to 2010, 350 provided relevant
data. Most articles were level II to IV. The resulting evidence
report was used to formulate recommendations. The following
recommendations were made: (i) All children/adolescents
should be screened for snoring, (ii) Polysomnography should be
performed in children/adolescents with snoring and
symptoms/signs of OSAS; if polysomnography is not available,
then alternative diagnostic tests or referral to a specialist for
more extensive evaluation may be considered, (iii)
Adenotonsillectomy is recommended as the first‐line treatment
of patients with adenotonsillar hypertrophy, (iv) High‐risk
patients should be monitored as inpatients post‐operatively, (v)
Patients should be re‐evaluated post‐operatively to determine
whether further treatment is required. Objective testing should
be performed in patients who are high‐risk or have persistent
symptoms/signs of OSAS after therapy, (vi) CPAP is
recommended as treatment if adenotonsillectomy is not
performed or if OSAS persists post‐operatively, (vii) Weight loss
is recommended in addition to other therapy in patients who
are over‐weight or obese, and (viii) Intra‐nasal corticosteroids
are an option for children with mild OSAS in whom
adenotonsillectomy is contraindicated or for mild
post‐operative OSAS. The updated guideline did not mention
the use of lingual tonsillectomy as a management tool for OSA
in children and adolescents.
Treatment of OSAS in children depends on the severity of
symptoms and the underlying anatomic and physiologic
abnormalities. Childhood OSAS is usually associated with
adenotonsillar hypertrophy, and the available medical literature
suggests that the majority of cases (75 % to 100 %) will benefit
from adenotonsillectomy (the role of adenoidectomy alone is
unclear). Tonsillectomy and/or adenoidectomy are procedures
that are performed for airway obstruction, especially in
children. Tonsillectomy is the surgical removal of the tonsils,
which are a collection of lymphoid tissue covered by mucous
membranes located on either side of the throat. An
adenoidectomy is the surgical removal of the adenoid glands.
10 of 35
The adenoids are masses of lymphoid tissue located at the back
of the nose in the upper part of the throat.
Other causes of pediatric OSAS include obesity, craniofacial
anomalies, and neuromuscular disorders. Obese children may
have less satisfactory results with adenotonsillectomy, but it is
generally considered the first‐line therapy for these patients as
well. If the patient is not a candidate for adenotonsillectomy,
other treatment options include weight loss (if patient is obese)
and continuous positive airway pressure (CPAP). Nocturnal
masks for CPAP or procedures for mask respiration are effective
in children, but are only used in exceptional cases, such as
when adenotonsillectomy is delayed, contraindicated, or when
symptoms of OSAS remain after surgery.
Severely affected children may require
uvulopalatopharyngoplasty (UPPP) or tracheostomy to relieve
their obstruction; however, neither have been well studied in
children and is rarely indicated. Tracheostomy is a surgical
procedure in which an opening is created through the neck into
the windpipe (trachea) and a tube placed through this opening
to provide an airway. Uvulopalatopharyngoplasty (UPPP) is the
surgical revision of the posterior soft palate and adjacent tissue
to relieve partial obstruction of the nasopharyngeal airway that
causes OSA.
The success of pharmacological treatment of OSAS in children
has not been evaluated in controlled clinical trials (Erler and
Paditz, 2004).
A Cochrane review (2007) on oral appliances and functional
orthopedic appliances for OSA in children 15 years old or
younger reported that there is insufficient evidence to state
that oral appliances or functional orthopedic appliances are
effective in the treatment of OSAS in children. Oral appliances
or functional orthopedic appliances may be helpful in the
treatment of children with craniofacial anomalies that are risk
factors of apnea.
11 of 35
In a meta‐analysis of mandibular distraction osteogenesis, Ow
and Cheung (2008) concluded that mandibular distraction
osteogenesis is effective in treating craniofacial deformities, but
further clinical trials are needed to evaluate the long‐term
stability and to compare the treatment with conventional
treatment methods, especially in cases of OSA or class II
mandibular hypoplasia.
Pang and Woodson (2007) evaluated the effectiveness of a new
method (expansion sphincter pharyngoplasty [ESP]) to treat
OSA. A total of 45 adults with small tonsils, body mass index
(BMI) less than 30 kg/m2, of Friedman stage II or III, of type I
Fujita, and with lateral pharyngeal wall collapse were selected
for the study. The mean BMI was 28.7 kg/m2. The apnea‐
hypopnea index (AHI) improved from 44.2 +/‐ 10.2 to 12.0 +/‐
6.6 (p < 0.005) following ESP and from 38.1 +/‐ 6.46 to 19.6 +/‐
7.9 in the uvulopalato‐pharyngoplasty group (p < 0.005).
Lowest oxygen saturation improved from 78.4 +/‐ 8.52 % to
85.2 +/‐ 5.1 % in the ESP group (p = 0.003) and from 75.1 +/‐ 5.9
% to 86.6 +/‐ 2.2 % in the uvulopalato‐pharyngoplasty group (p
< 0.005). Selecting a threshold of a 50 % reduction in AHI and
AHI less than 20, success was 82.6 % in ESP compared with 68.1
% in uvulopalato‐pharyngoplasty (p < 0.05). The authors
concluded that ESP may offer benefits in a selected group of
OSA patients. These findings need to be validated by studies
with larger sample sizes and long‐term follow‐up.
In a retrospective institutional review board‐approved analysis,
Wootten and Schott (2010) described their experience
of treating retroglossal and base‐of‐tongue collapse in children
and young adults with OSA using combined genioglossus
advancement (Repose THS; MedtronicENT, Jacksonville, FL) and
radiofrequency ablation of the tongue base. A total of
31 patients with a mean age of 11.5 years (range of 3.1 to 23.0)
were included in this analysis. Pre‐operative and post‐operative
polysomnographic data were evaluated for each patient.
Success of surgery was determined using the criteria of a
post‐operative AHI of 5 or fewer events per hour, without
evidence of hypoxemia (oxygen saturation as measured by
12 of 35
pulse oximetry), and without prolonged hypercarbia (end‐tidal
carbon dioxide). Nineteen (61 %) of the 31 subjects had Down
syndrome. The overall success rate was 61 % (19 of 31) (58 %
[12 of 19] success among patients with Down syndrome and 66
% [7 of 12] success among patients without Down syndrome).
Overall, the mean AHI improved from 14.1 to 6.4 events per
hour (p < 0.001); the mean nadir oxygen saturation as
measured by pulse oximetry during apnea improved from 87.4
% to 90.9 % (p = 0.07). The authors concluded that pediatric
OSA refractory to adenotonsillectomy that is due to retroglossal
and base‐of‐tongue collapse remains difficult to treat.
However, most patients in this analysis benefited from
combined genioglossus advancement and radiofrequency
ablation. The findings of this small, retrospective study need to
be validated by well‐designed studies. furthermore, these
finding are confounded by the combinational use of the Repose
system and radiofrequency ablation of the tongue base. It
should be noted that the European Respiratory Society's task
force on non‐CPAP therapies in sleep apneas (Randerath et al,
2011) stated that nasal surgery, radiofrequency tonsil
reduction, tongue base surgery, uvulopalatal flap, laser midline
glossectomy, tongue suspension and genioglossus advancement
can not be recommended as single interventions".
Tracheomalacia is a disorder of the large airways where the
trachea is deformed or malformed during respiration. It is
associated with a wide spectrum of respiratory symptoms from
life‐threatening recurrent apnea to common respiratory
symptoms such as chronic cough and wheeze. Current practice
following diagnosis of tracheomalacia include medical
approaches aimed at reducing associated symptoms of
tracheomalacia, ventilation modalities of CPAP and bilevel
positive airway pressure (BiPAP) as well as surgical interventions
aimed at improving the caliber of the airway.
In a prospective, randomized, controlled study, Essouri et al
(2005) evaluated the efficacy of CPAP ventilation in infants with
severe upper airway obstruction and compared CPAP to BiPAP
ventilation. A total of 10 infants (median age of 9.5 months,
13 of 35
range of 3 to 18) with laryngomalacia (n = 5), tracheomalacia (n
= 3), tracheal hypoplasia (n = 1), and Pierre Robin syndrome (n
= 1) were included in this analysis. Breathing pattern and
respiratory effort were measured by esophageal and trans‐
diaphragmatic pressure monitoring during spontaneous
breathing, with or without CPAP and BiPAP ventilation. Median
respiratory rate decreased from 45 breaths/min (range of 24 to
84) during spontaneous breathing to 29 (range of 18 to 60)
during CPAP ventilation. All indices of respiratory effort
decreased significantly during CPAP ventilation compared to
un‐assisted spontaneous breathing (median, range): esophageal
pressure swing from 28 to 10 cm H(2)O (13 to 76 to 7 to 28),
esophageal pressure time product from 695 to 143 cm H(2)O/s
per minute (264 to 1,417 to 98 to 469), diaphragmatic pressure
time product from 845 to 195 cm H(2)O/s per minute (264 to
1,417 to 159 to 1,183). During BiPAP ventilation a similar
decrease in respiratory effort was observed but with patient‐
ventilator asynchrony in all patients. The authors concluded
that this short‐term study showed that non‐invasive CPAP and
BiPAP ventilation are associated with a significant and
comparable decrease in respiratory effort in infants with upper
airway obstruction. However, BiPAP ventilation was associated
with patient‐ventilator asynchrony.
An UpToDate review on "Tracheomalacia and
tracheobronchomalacia in adults" (Ernst et al, 2012) states that
"[c]ontinuous positive airway pressure (CPAP) can maintain an
open airway and facilitate secretion drainage. This is often
initiated in the hospital during an acute illness. The patient
initially receives continuous CPAP and is gradually transitioned
to intermittent CPAP as tolerated. Patients may use
intermittent CPAP as long‐term therapy. However, CPAP does
not appear to have a long‐term impact on dyspnea or cough.
Positive airway pressure other than CPAP (e.g., bilevel positive
airway pressure) may be used instead if hypercapnic respiratory
failure exists".
An eMedicine article on "Tracheomalacia Treatment &
Management" (Schwartz) stated that "[s]upportive therapy is
14 of 35
provided to most infants. Most respond to conservative
management, consisting of humidified air, chest physical
therapy, slow and careful feedings, and control of infection and
secretions with antibiotics. The use of continuous positive
airway pressure (CPAP) has been recommended in patients
having respiratory distress and may be successful in patients
requiring a short‐term intervention as the disorder
spontaneously resolves".
The American Academy of Pediatrics’ practice guideline on
“Diagnosis and management of childhood obstructive sleep
apnea syndrome” (Marcus et al, 2012) focused on
uncomplicated childhood OSAS, that is, OSAS associated with
adenotonsillar hypertrophy and/or obesity in an otherwise
healthy child who is being treated in the primary care
setting. The updated guideline did not mention the use of
lingual tonsillectomy as a management tool for OSA in children
and adolescents.
Kim and colleagues (2013) noted that OSA is a common health
problem in children and increases the risk of cardiovascular
disease (CVD). Triggering receptor expressed on myeloid cells‐1
(TREM‐1) plays an important role in innate immunity and
amplifies inflammatory responses. Pentraxin‐3 is
predominantly released from macrophages and vascular
endothelial cells, plays an important role in atherogenesis, and
has emerged as a biomarker of CVD risk. Thus, these
researchers hypothesized that plasma TREM‐1 and pentraxin‐3
levels would be elevated in children with OSA. A total of 106
children (mean age of: 8.3 ± 1.6 yrs) were included after they
underwent over‐night polysomnographic evaluation and a
fasting blood sample was drawn the morning after the sleep
study. Endothelial function was assessed with a modified
hyperemic test after cuff‐induced occlusion of the brachial
artery. Plasma TREM‐1 and pentraxin‐3 levels were assayed
using commercial enzyme‐linked immunosorbent assay kits.
Circulating microparticles (MPs) were assessed using flow
cytometry after staining with cell‐specific antibodies. Children
with OSA had significantly higher TREM‐1 and pentraxin‐3 levels
15 of 35
(versus controls: p < 0.01, p < 0.05, respectively). Plasma
TREM‐1 was significantly correlated with both BMI‐z score and
the obstructive AHI in uni‐variate models. Pentraxin‐3 levels
were inversely correlated with BMI‐z score (r = ‐0.245, p < 0.01),
and positively associated with endothelial MPs and platelet
MPs (r = 0.230, p < 0.01 and r = 0.302, p < 0.01). Both plasma
TREM‐1 and pentraxin‐3 levels were independently associated
with AHI in multi‐variate models after controlling for age, sex,
race, and BMI‐z score (p < 0.001 for TREM‐1 and p < 0.001 for
pentraxin‐3). However, no significant associations emerged
between TREM‐1, pentraxin‐3, and endothelial function. The
authors concluded that plasma TREM‐1 and pentraxin‐3 levels
were elevated in pediatric OSA, and may play a role in
modulating the degree of systemic inflammation. Moreover,
they stated that the short‐term and long‐term significance of
elevated TREM‐1 and pentraxin‐3 in OSA‐induced end‐organ
morbidity remains to be defined.
Gozal and associates (2013) tested the hypothesis that
concentrations of adropin, a recently discovered peptide that
displays important metabolic and cardiovascular functions, are
lower in OSA, especially when associated with endothelial
dysfunction. Age‐, sex‐, and ethnicity‐matched children (mean
age of 7.2 ± 1.4 years) were included into 1 of 3 groups based
on the presence of OSA in an over‐night sleep study, and on the
time to post‐occlusive maximal re‐perfusion (Tmax greater than
45 seconds) with a modified hyperemic test. Plasma adropin
concentrations were assayed using a commercial enzyme‐linked
immunosorbent assay kit. Among controls, the mean morning
adropin concentration was 7.4 ng/ml (95 % CI: 5.2 to 16.3
ng/ml). Children with OSA and abnormal endothelial function
(EF) (OSA+/EF+ group) had significantly lower adropin
concentrations (2.7 ± 1.1 ng/ml; n = 35) compared with
matched controls (7.6 ± 1.4 ng/ml; n = 35; p < 0.001) and
children with OSA and normal EF (OSA+/EF‐ group; 5.8 ± 1.5
ng/ml; n = 47; p < 0.001). A plasma adropin concentration less
than 4.2 ng/ml reliably predicted EF status, but individual
adropin concentrations were not significantly correlated with
age, BMI z‐score, obstructive AHI, or nadir oxygen saturation.
16 of 35
Mean adropin concentration measured after
adenotonsillectomy in a subset of children with OSA (n = 22)
showed an increase in the OSA+/EF+ group (from 2.5 ± 1.4 to
6.4 ± 1.9 ng/ml; n = 14; p < 0.01), but essentially no change in
the OSA+EF‐ group (from 5.7 ± 1.3 to 6.4 ± 1.1 ng/ml; n = 8; p >
0.05). The authors concluded that plasma adropin
concentrations were reduced in pediatric OSA when endothelial
dysfunction is present, and returned to within normal values
after adenotonsillectomy. They stated that assessment of
circulating adropin concentrations may provide a reliable
indicator of vascular injury in the context of OSA in children.
These preliminary findings need to be validated by
well‐designed studies.
Posadzki and colleagues (2013) critically evaluated the
effectiveness of osteopathic manipulative treatment (OMT) as a
treatment of pediatric conditions. A total of 11 databases were
searched from their respective inceptions to November 2012.
Only randomized clinical trials (RCTs) were included, if they
tested OMT against any type of control in pediatric patients.
Study quality was critically appraised by using the Cochrane
criteria. A total of 17 trials met the inclusion criteria; 5 RCTs
were of high methodological quality. Of those, 1 favored OMT,
whereas 4 revealed no effect compared with various control
interventions. Replications by independent researchers were
available for 2 conditions only, and both failed to confirm the
findings of the previous studies. Seven RCTs suggested that
OMT leads to a significantly greater reduction in the symptoms
of asthma, congenital nasolacrimal duct obstruction (post‐
treatment), daily weight gain and length of hospital stay,
dysfunctional voiding, infantile colic, otitis media, or postural
asymmetry compared with various control interventions. Seven
RCTs indicated that OMT had no effect on the symptoms of
asthma, cerebral palsy, idiopathic scoliosis, obstructive apnea,
otitis media, or temporo‐mandibular disorders compared with
various control interventions. Three RCTs did not perform
between‐group comparisons. The majority of the included
RCTs did not report the incidence rates of adverse effects. The
authors concluded that the evidence of the effectiveness of
17 of 35
OMT for pediatric conditions remains unproven due to the
paucity and low methodological quality of the primary studies.
There is also a lack of evidence regarding the clinical
effectiveness of chiropractic manipulation for the treatment of
sleep apnea.
The evidence on the use of midline/partial glossectomy for the
treatment of OSA is not RCT‐based; the data are mostly from
case‐series studies.
The Adult Obstructive Sleep Apnea Task Force of the American
Academy of Sleep Medicine's clinical guideline on "The
evaluation, management and long‐term care of obstructive
sleep apnea in adults" (Epstein et al, 2009) stated that "
Tracheostomy can eliminate OSA but does not appropriately
treat central hypoventilation syndromes (Consensus). Maxillary
and mandibular advancement can improve PSG parameters
comparable to CPAP in the majority of patients (Consensus).
Most other sleep apnea surgeries are rarely curative for OSA
but may improve clinical outcomes (e.g., mortality,
cardiovascular risk, motor vehicle accidents, function, quality of
life, and symptoms) (Consensus). Laser‐assisted
uvulopalatoplasty is not recommended for the treatment of
obstructive sleep apnea (Guideline)". This guideline does not
mention the use of midline glossectomy.
The American Sleep Disorders Association's practice parameters
on "The surgical modifications of the upper airway for
obstructive sleep apnea in adults" (Aurora et al, 2010) did not
mention midline/partial glossectomy as a therapeutic option.
The European Respiratory Society task force on non‐CPAP
therapies in sleep apnea (Randerath et al, 2011) noted that
"Nasal surgery, radiofrequency tonsil reduction, tongue base
surgery, uvulopalatal flap, laser midline glossectomy, tongue
suspension and genioglossus advancement cannot be
recommended as single interventions".
18 of 35
Furthermore, an UpToDate review on “Management of
obstructive sleep apnea in children” (Paruthi, 2014) states that
“Tongue reduction surgery has been proposed for the
management of OSA related to macroglossia (e.g., Beckwith‐
Wiedemann syndrome, Down syndrome). Additional studies
are needed to determine the efficacy of this procedure in such
patients, especially since a case series of 13 patients with
Beckwith‐Wiedemann syndrome found that
adenotonsillectomy was more effective than tongue reduction
in relieving upper airway obstruction”.
Kerschner et al (2002) noted that children with neurologic
impairment often present with airway obstruction that may
require intervention. No single method of airway intervention
is universally appropriate and effective in this patient
population. These researchers examined the effectiveness of
using adenotonsillectomy and UPPP in resolving obstructive
apnea (OA) in patients with neurologic impairment. These
investigators performed a retrospective chart review of 15
patients with neurologic impairment and OA treated with
adenotonsillectomy and UPPP between 1986 and 1998 at
Children's Hospital of Wisconsin (CHW). All patients in the
series had their primary area of obstruction in the posterior
oropharynx involving the soft palate, pharyngeal walls and base
of tongue. Post‐operative improvement following
adenotonsillectomy and UPPP was examined. Measures of
improvement were based primarily on recorded lowest oxygen
saturations, but clinical parameters, flexible upper airway
endoscopy and PSG were used as well. Patient improvement
was documented in 87 % of patients treated with this modality.
For the group, the mean lowest recorded oxygen saturation
demonstrated a statistically significant improvement from 65 %
pre‐operatively to 85 % post‐operatively (p = 0.005). In
long‐term follow‐up of these patients, 77 % (10 of 13) of those
showing initial improvement have done well and have required
no further airway intervention. However, 23 % of these
patients demonstrated the need for further airway intervention
during follow‐up. The authors concluded that
adenotonsillectomy with UPPP is worthy of consideration in
19 of 35
certain neurologically impaired patients with moderate‐
to‐severe OA, limited primarily to the posterior pharyngeal
area. Moreover, they stated that initial improvement may not
be permanent and close long‐term follow‐up of patients is
imperative.
Randerath and colleagues (2011) stated that in view of the high
prevalence and the relevant impairment of patients with OSAS,
lots of methods are offered that promise definitive cures for or
relevant improvement of OSAS. These investigators
summarized the effectiveness of alternative treatment options
in OSAS. An inter‐disciplinary European Respiratory Society
task force evaluated the scientific literature according to the
standards of evidence‐based medicine. Evidence supports the
use of mandibular advancement devices in mild‐to‐moderate
OSAS. Maxillo‐mandibular osteotomy seems to be as efficient
as CPAP in patients who refuse conservative treatment.
Distraction osteogenesis is usefully applied in congenital
micrognathia or mid‐face hypoplasia. There is a trend towards
improvement after weight reduction. Positional therapy is
clearly inferior to CPAP and long‐term compliance is poor.
Drugs, nasal dilators and apnea‐triggered muscle stimulation
cannot be recommended as effective treatments of OSAS at the
moment. Nasal surgery, radiofrequency tonsil reduction,
tongue base surgery, uvulopalatal flap, laser mid‐line
glossectomy, tongue suspension and genioglossus advancement
cannot be recommended as single interventions.
Uvulopalatopharyngoplasty, pillar implants and hyoid
suspension should only be considered in selected patients and
potential benefits should be weighed against the risk of
long‐term side‐effects. Multi‐level surgery is only a salvage
procedure for OSA patients.
The American Academy of Pediatrics’ clinical practice guideline
on “Diagnosis and management of childhood obstructive sleep
apnea syndrome” (Marcus et al, 2012) did not mention UPPP as
a management tool.
Furthermore, an UpToDate review on “Management of
20 of 35
obstructive sleep apnea in children” (Paruthi, 2015) states that
“Uvulopalatopharyngoplasty (UPPP) is not widely used for the
management of OSA in children because it is associated with
significant complications, such as nasopharyngeal stenosis,
palatal incompetence, and speech difficulties. It has been
successfully combined with adenotonsillectomy in children with
neuromuscular disorders who are deemed to be at high risk for
persistent upper airway obstruction after adenotonsillectomy
alone”.
Hypoglossal Nerve Stimulation:
Hypoglossal nerve stimulation technology (eg, Inspire UAS
system) utilizes an implantable, programmable device that
electrically stimulates the hypoglossal nerve which leads to the
contraction of the genioglossus muscle. This purportedly
prevents airway collapse and the development of upper airway
obstruction during sleep.
Certal et al (2015) systematically reviewed the evidence
regarding the safety and effectiveness of hypoglossal nerve
stimulation (HNS) as an alternative therapy in the treatment of
OSA. Scopus, PubMed, and Cochrane Library databases were
searched (updated through September 5, 2014). Studies were
included that evaluated the effectiveness of HNS to treat OSA in
adults with outcomes for AHI, oxygen desaturation index (ODI),
and effect on daytime sleepiness (Epworth Sleepiness Scale
[ESS]). Te sts for heterogeneity and subgroup analysis were
performed. A total of 6 prospective studies with 200 patients
were included in this review. At 12 months, the pooled fixed
effects analysis demonstrated statistically significant reductions
in AHI, ODI, and ESS mean difference of ‐17.51 (95 % CI: ‐20.69
to ‐14.34); ‐13.73 (95 % CI: ‐16.87 to ‐10.58), and ‐4.42 (95 % CI:
‐5.39 to ‐3.44), respectively. Similar significant reductions were
observed at 3 and 6 months. Overall, the AHI was reduced
between 50 % and 57 %, and the ODI was reduced between 48
% and 52 %. Despite using different hypoglossal nerve
stimulators in each subgroup analysis, no significant
heterogeneity was found in any of the comparisons, suggesting
21 of 35
equivalent effectiveness regardless of the system in use. The
authors concluded that the findings of this review showed that
HNS therapy may be considered in selected patients with OSA
who fail medical treatment. They stated that further studies
comparing HNS with conventional therapies are needed to
definitively evaluate outcomes.
Diercks et al (2016) noted that OSA is more common in children
with Down syndrome, affecting up to 60 % of patients, and may
persist in up to 50 % of patients after adenotonsillectomy.
These children with persistent moderate to severe OSA require
CPAP, which is often poorly tolerated, or even tracheotomy for
severe cases. Hypoglossal nerve stimulation produces an
electrical impulse to the anterior branches of the hypoglossal
nerve, resulting in tongue protrusion in response to respiratory
variation. It supposedly allows for alleviation of tongue base
collapse and improving airway obstruction. These researchers
described the first pediatric HNS; it was performed in an
adolescent with Down syndrome and refractory severe OSA
(AHI: 48.5 events/hour). The patient would not tolerate CPAP
and required a long‐standing tracheotomy. Hypoglossal nerve
stimulation was well‐tolerated and effective, resulting in
significant improvement in the patient's OSA (overall AHI: 3.4
events/hour; AHI: 2.5 to 9.7 events/hour at optimal voltage
settings depending on sleep stage and body position). Five
months after implantation, the patient's tracheotomy was
successfully removed and he continues to do well with nightly
therapy. This was a single‐case study; its findings need to be
validated in well‐designed studies.
Uvulopharyngopalatoplasty:
An UpToDate review on “Adenotonsillectomy for obstructive
sleep apnea in children” (Garetz, 2016) states that
“Uvulopalatopharyngoplasty (UPPP) is not widely used for the
management of OSA in children, but has been successfully
combined with adenotonsillectomy in small studies of children
with neuromuscular disorders who are thought to be at high
risk for persistent upper airway obstruction after
22 of 35
adenotonsillectomy alone, including children with Down
syndrome or other developmental delays. Only one of these
studies employed objective evaluation of improvement in OSA.
In this study, 15 children with neurologic impairments and OSA
were treated with UPPP in conjunction with
adenotonsillectomy. There was a statistically significant
improvement in mean oxygen saturation nadir from 65 to 85 %
(p = 0.005). In long‐term follow‐up, 77 % (10 of 13) of the
patients did not require additional airway intervention. Small
sample size, absence of control groups, and paucity of validated
outcome measures preclude analysis of the utility of this
procedure in the broader pediatric population. Potential
complications include nasopharyngeal stenosis, palatal
incompetence, and speech difficulties”.
CPT Codes / HCPCS Codes / ICD‐10 Codes
Information in the [brackets] below has been added for
clarification purposes. Codes requiring a 7th character are
represented by "+":
ICD‐10 codes will become effective as of October 1, 2015:
Diagnosis:
CPT codes covered if selection criteria are met:
95808 Polysomnography; any age, sleep staging with 1‐3
additional parameters of sleep, attended by a
technologist
95810 age 6 years or older, sleep staging with 4 or more
additional parameters of sleep, attended by a
technologist [nocturnal]
95811 age 6 years or older, sleep staging with 4 or more
additional parameters of sleep, with initiation of
continuous positive airway pressure therapy or
bilevel ventilation, attended by a technologist
[nocturnal]
95782 younger than 6 years, sleep staging with 4 or more
additional parameters of sleep, attended by a
technologist
23 of 35
95783 younger than 6 years, sleep staging with 4 or more
additional parameters of sleep, with initiation of
continuous positive airway pressure therapy or
bi‐level ventilation, attended by a technologist
CPT codes not covered for indications listed in the CPB:
76120 ‐
76125
Cineradiography/videoradiography, except where
specifically included
95800 Sleep study, unattended, simultaneous recording;
heart rate, oxygen saturation, respiratory analysis
(eg, by airflow or peripheral arterial tone) and sleep
time
95801 minimum of heart rate, oxygen saturation, and
respiratory analysis (eg, by airflow or peripheral
arterial tone)
95806 Sleep study, simultaneous recording of ventilation,
respiratory effort, ECG or heart rate, and oxygen
saturation, unattended by a technologist
95807 Sleep study, simultaneous recording of ventilation,
respiratory effort, ECG or heart rate, and oxygen
saturation, attended by a technologist
94762 Noninvasive ear or pulse oximetry for oxygen
saturation; by continuous overnight monitoring
(separate procedure)
Other CPT codes related to the CPB:
42700 ‐
42999
Surgery of pharynx, adenoids, and tonsils
HCPCS codes not covered for indications listed in the CPB:
E0445 Oximeter device for measuring blood oxygen levels
non‐invasively [nocturnal]
G0398 Home sleep study test (HST) with type II portable
monitor, unattended; minimum of 7 channels: EEG,
EOG, EMG, ECG/heart rate, airflow, respiratory effort
and oxygen saturation
24 of 35
G0399 Home sleep test (HST) with type III portable monitor,
unattended; minimum of 4 channels: 2 respiratory
movement/airflow, 1 ECG/heart rate and 1 oxygen
saturation
G0400 Home sleep test (HST) with type IV portable monitor,
unattended; minimum of 3 channels
ICD‐10 codes covered if selection criteria are met:
E64.3 Sequelae of rickets [chest wall deformities]
F11.182,
F11.282,
F11.982,
F13.182,
F13.282,
F13.982
Drug induced sleep disorders [hypersomnia]
F51.11 Primary hypersomnia [Hypersomnia associated with
depression (major) (minor)]
F51.19 Other hypersomnia not due to a substance or known
physiological condition [Hypersomnia associated
with acute or intermittent emotional reactions or
conflicts]
F51.8 Other sleep disorders not due to a substance or
known physiological condition
G25.81 Restless legs syndrome
G47.10 ‐
G47.19
Hypersomnia
G47.33 Obstructive sleep apnea (adult) (pediatric) [OSAS]
G47.35 Congenital central alveolar hypoventilation
syndrome
G47.36 Sleep related hypoventilation in conditions classified
elsewhere
G47.41 ‐
G47.429
Cataplexy and narcoplexy
G47.50 ‐
G47.59
Parasomnia
25 of 35
G47.61 Periodic limb movement disorder
G70.00 ‐
G70.9
Myasthenia gravis and other myoneural disorders
G71.0 Muscular dystrophy
M95.4 Acquired deformity of chest and rib
Q67.8 Other congenital deformities of chest [wall]
R06.83 Snoring [habitual, during sleep]
Treatment: tonsils & adenoids:
CPT codes covered if selection criteria are met:
42820 ‐
42821
Tonsillectomy and adenoidectomy
42825 ‐
42826
Tonsillectomy, primary or secondary
42830 ‐
42831
Adenoidectomy, primary
42835 ‐
42836
Adenoidectomy, secondary
ICD‐10 codes covered if selection criteria are met:
J35.03 Chronic tonsillitis and adenoiditis
J35.3 Hypertrophy of tonsils with hypertrophy of adenoids
Treatment: CPAP:
CPT codes covered if selection criteria are met:
94660 Continuous positive airway pressure ventilation
(CPAP), initiation and management
HCPCS codes covered if selection criteria are met:
A7027 Combination oral/nasal mask, used with continuous
positive airway pressure device, each
A7028 Oral cushion for combination oral/nasal mask,
replacement only, each
A7029 Nasal pillows for combination oral/nasal mask,
replacement only, pair
A7030 Full face mask used with positive airway pressure
device, each
26 of 35
A7031 Face mask interface, replacement for full face mask,
each
A7032 Cushion for use on nasal mask interface,
replacement only, each
A7033 Pillow for use on nasal cannula type interface,
replacement only, pair
A7034 Nasal interface (mask or cannula type) used with
positive airway pressure device, with or without
head strap
A7035 Headgear used with positive airway pressure device
A7036 Chinstrap used with positive airway pressure device
A7037 Tubing used with positive airway pressure device
A7038 Filter, disposable, used with positive airway pressure
device
A7039 Filter, non‐disposable, used with positive airway
pressure device
A7044 Oral interface used with positive airway pressure
device, each
A7045 Exhalation port with or without swivel used with
accessories for positive airway devices, replacement
only
A7046 Water chamber for humidifier, used with positive
airway pressure device, replacement, each
E0470 Respiratory assist device, bi‐level pressure capability,
without back‐up rate feature, used with noninvasive
interface, e.g., nasal or facial mask (intermittent
assist device with continuous positive airway
pressure device)
E0472 Respiratory assist device, bi‐level pressure capability,
with back‐up rate feature, used with invasive
interface, e.g., tracheostomy tube (intermittent assist
device with continuous positive airway pressure
device)
27 of 35
E0485 Oral device/appliance used to reduce upper airway
collapsibility, adjustable or non‐adjustable,
prefabricated, includes fitting and adjustment
[covered for children with craniofacial anomalies
only]
E0486 Oral device/appliance used to reduce upper airway
collapsibility, adjustable or non‐adjustable, custom
fabricated, includes fitting and adjustment [covered
for children with craniofacial anomalies only]
E0561 Humidifier, non‐heated, used with positive airway
pressure device
E0562 Humidifier, heated, used with positive airway
pressure device
E0601 Continuous positive airway pressure (CPAP) device
ICD‐10 codes covered if selection criteria are met:
G47.33 Obstructive sleep apnea (adult) (pediatric) [OSAS]
J39.8 Other specified disease of upper respiratory tract
[tracheomalacia]
P28.3 Primary sleep apnea of newborn
Other Treatments:
CPT codes covered if selection criteria are met:
42145 Palatopharyngoplasty (e.g.,
uvulopalatopharyngoplasty, uvulopharyngoplasty)
[for transpalatal advancement pharyngoplasty]
[covered for obstructive sleep apnea syndrome in
children with neuromuscular disorders who are
deemed to be at high risk for persistent upper airway
obstruction after adenotonsillectomy alone]
CPT codes not covered for indications listed in the CPB:
20692 ‐
20697
Multiplane external fixation system [mandibular
distraction osteogenesis]
30000 ‐
30999
Surgery/Respiratory System, nose/nasal
28 of 35
30801 Cautery and/or ablation, mucosa of inferior
turbinates, unilateral or bilateral, any method;
superficial [for somnoplasty or coblation]
30802 intramural [for somnoplasty or coblation]
41512 Tongue base suspension, permanent suture
technique [Repose System]
41530 Submucosal ablation of the tongue base,
radiofrequency, one or more sites, per session [for
somnoplasty or coblation]
42140 Uvulectomy, excision of uvula
42160 Destruction of lesion, palate or uvula (thermal, cryo
or chemical) [for laser assisted uvuloplasty]
42870 Excision or destruction lingual tonsil, any method
(separate procedure)
42890 Limited pharyngectomy
42950 Pharyngoplasty (plastic or reconstructive operation
on pharynx) [for CAPSO] [expansion sphincter
pharyngoplasty]
HCPCS codes covered if selection criteria are met:
E0485 Oral device/appliance used to reduce upper airway
collapsibility, adjustable or non‐adjustable,
prefabricated, includes fitting and adjustment
[covered for children with craniofacial anomalies
only]
E0486 Oral device/appliance used to reduce upper airway
collapsibility, adjustable or non‐adjustable, custom
fabricated, includes fitting and adjustment [covered
for children with craniofacial anomalies only]
HCPCS codes not covered for indications listed in the CPB:
C9727 Insertion of implants into the soft palate; minimum
of three implants
S2080 Laser‐assisted uvulopalatoplasty (LAUP)
ICD‐10 codes covered if selection criteria are met:
29 of 35
G12.0 ‐
G12.9
Spinal muscular atrophy and related syndromes
G47.33 Obstructive sleep apnea (adult) (pediatric) [OSAS]
G70.00 ‐
G70.9
Myasthenia gravis and other myoneural disorders
G71.0 ‐
G71.9
Primary disorders of muscles
The above policy is based on the following references:
1. American Academy of Pediatrics (AAP). Clinical practice
guideline: Diagnosis and management of childhood
obstructive sleep apnea syndrome. Pediatrics.
2002;109(4):704‐712. .
2. Schechter MS. American Academy of Pediatrics. Technical
report: Diagnosis and management of childhood
obstructive sleep apnea syndrome. Pediatrics.
2002;109(4):e69.
3. D'Andrea LA. Diagnostic studies in the assessment of
pediatric sleep‐disordered breathing: Techniques and
indications. Pediatr Clin North Am. 2004;51(1):169‐186.
4. Sherman M, Kaley D. California Thoracic Society Position
Paper: Guidelines for the use of home pulse oximetry in
infants and children. Medical Section of the American
Lung Association of California. Tustin, CA: 2006. Available
at: http://www.thoracic.org/sections/chapters/thoracic‐
society‐chapters/ca/publications/. Accessed February 26,
2008.
5. Leong A. California Thoracic Society Position Paper:
Assessing sleep‐disordered breathing in children. Medical
Section of the American Lung Association of California.
Tustin, CA: 2006. Available at: http://www.thoracic.org
/sections/chapters/thoracic‐society‐chapters
/ca/publications/. Accessed February 26, 2008.
6. Lim J, McKean M. Adenotonsillectomy for obstructive
sleep apnoea in children. Cochrane Database Syst Rev.
30 of 35
2001;(3): CD003136.
7. Carvalho FR, Lentini‐Oliveira DA, Machado MA, et al. Oral
appliances and functional orthopaedic appliances for
obstructive sleep apnoea in children. Cochrane
Database Syst Rev. 2007;(2): CD005520.
8. Sundaram S, Lim J, Lasserson TJ . Surgery for obstructive
sleep apnoea. Cochrane Database Syst
Rev. 2005:(4): CD001004.
9. Brietzke SE, Gallagher D. The effectiveness of
tonsillectomy and adenoidectomy in the treatment of
pediatric obstructive sleep apnea/hypopnea syndrome: A
meta‐analysis. Otolaryngol Head Neck Surg.
2006;134(6):979‐984.
10. Erler T, Paditz E. Obstructive sleep apnea syndrome in
children: A state‐of‐the‐art review. Treat Respir Med.
2004;3(2):107‐122.
11. Sargi Z, Younis RT. Pediatric obstructive sleep apnea:
Current management. ORL J Otorhinolaryngol Relat Spec.
2007;69(6):340‐344.
12. Smith SL, Pereira KD. Tonsillectomy in children:
Indications, diagnosis and complications. ORL J
Otorhinolaryngol Relat Spec. 2007;69(6):336‐339.
13. Uong EC, Epperson M, Bathon SA, et al. Adherence to
nasal positive airway pressure therapy among
school‐aged children and adolescents with obstructive
sleep apnea syndrome. Pediatrics.
2007;120(5):e1203‐1211.
14. Jacob SV, Morielli A, Mograss MA, et al. Home testing for
pediatric obstructive sleep apnea syndrome secondary to
adenotonsillar hypertrophy. Pediatr Pulmonol.
1995;20(4):241‐252.
15. Kirk VG, Bohn SG, Flemons WW, et al. Comparison of
home oximetry monitoring with laboratory
polysomnography in children. Chest.
2003;124(5):1702‐1708.
16. Uong EC, Epperson M, Bathon SA, et al. Adherence to
nasal positive airway pressure therapy among
school‐aged children and adolescents with obstructive
sleep apnea syndrome. Pediatrics. 2007;120(5):e1203‐
31 of 35
e1211.
17. Verhulst SL, Schrauwen N, Haentjens D, et al. Reference
values for sleep‐related respiratory variables in
asymptomatic European children and adolescents.
Pediatr Pulmonol. 2007;42(2):159‐167.
18. Uliel S, Tauman R, Greenfeld M, et al. Normal
polysomnographic respiratory values in children and
adolescents. Chest. 2004;125(3):872‐878.
19. Marcus CL, Omlin KJ, Basinki DJ, et al. Normal
polysomnographic values for children and adolescents.
Am Rev Respir Dis. 1992;146(5 Pt 1):1235‐1239.
20. Mitchell RB. Adenotonsillectomy for obstructive sleep
apnea in children: Outcome evaluated by pre‐ and
postoperative polysomnography. Laryngoscope.
2007;117(10):1844‐1854.
21. Mitchell RB, Kelly J. Outcome of adenotonsillectomy for
obstructive sleep apnea in obese and normal‐weight
children. Otolaryngol Head Neck Surg. 2007;137(1):43‐48.
22. Matsumoto E, Tanaka E, Tabe H, et al. Sleep architecture
and the apnoea‐hypopnoea index in children with
obstructive‐sleep apnoea syndrome. J Oral Rehabil.
2007;34(2):112‐120.
23. Leiberman A, Stiller‐Timor L, Tarasiuk A, et al. The effect
of adenotonsillectomy on children suffering from
obstructive sleep apnea syndrome (OSAS): The Negev
perspective. Int J Pediatr Otorhinolaryngol.
2006;70(10):1675‐1682.
24. Brietzke SE, Gallagher D. The effectiveness of
tonsillectomy and adenoidectomy in the treatment of
pediatric obstructive sleep apnea/hypopnea syndrome: A
meta‐analysis. Otolaryngol Head Neck Surg.
2006;134(6):979‐984.
25. Robb PJ. Adenoidectomy: does it work? J Laryngol Otol.
2007;121(3):209‐214.
26. Marcus CL, Rosen G, Ward SL, et al. Adherence to and
effectiveness of positive airway pressure therapy in
children with obstructive sleep apnea. Pediatrics.
2006;117(3):e442‐451.
27. Kosko Jr, Derkay GS. Uvulopalatopharyngoplasty:
32 of 35
Treatment of obstructive sleep apnea in neurologically
impaired pediatric patients. Int J Ped Otorhinolaryngol
1995;32:241‐246.
28. Ow AT, Cheung LK. Meta‐analysis of mandibular
distraction osteogenesis: Clinical applications and
functional outcomes. Plast Reconstr Surg.
2008;121(3):54e‐69e.
29. Kuhle S, Urschitz MS, Eitner S, Poets CF. Interventions for
obstructive sleep apnea in children: A systematic review.
Sleep Med Rev. 2009;13(2):123‐131.
30. Friedman M, Wilson M, Lin HC, Chang HW. Updated
systematic review of tonsillectomy and adenoidectomy
for treatment of pediatric obstructive sleep
apnea/hypopnea syndrome. Otolaryngol Head Neck Surg.
2009;140(6):800‐808.
31. Pang KP, Woodson BT. Expansion sphincter
pharyngoplasty: A new technique for the treatment of
obstructive sleep apnea. Otolaryngol Head Neck Surg.
2007;137(1):110‐114.
32. Xu H, Yu Z, Mu X. The assessment of midface distraction
osteogenesis in treatment of upper airway obstruction. J
Craniofac Surg. 2009;20 Suppl 2:1876‐1881.
33. Aurora RN, Zak RS, Karippot A, et al; American Academy
of Sleep Medicine. Practice parameters for the
respiratory indications for polysomnography in children.
Sleep. 2011;34(3):379‐388.
34. Roland PS, Rosenfeld RM, Brooks LJ, et al; American
Academy of Otolaryngology‐Head and Neck Surgery
Foundation. Clinical practice guideline: Polysomnography
for sleep‐disordered breathing prior to tonsillectomy in
children. Otolaryngol Head Neck Surg. 2011;145(1
Suppl):S1‐S15.
35. Essouri S, Nicot F, Clément A, et al. Noninvasive positive
pressure ventilation in infants with upper airway
obstruction: Comparison of continuous and bilevel
positive pressure. Intensive Care Med.
2005;31(4):574‐580.
36. Wootten CT, Shott SR. Evolving therapies to treat
retroglossal and base‐of‐tongue obstruction in pediatric
33 of 35
obstructive sleep apnea. Arch Otolaryngol Head Neck
Surg. 2010;136(10):983‐987.
37. Kuhle S, Urschitz MS. Anti‐inflammatory medications for
obstructive sleep apnea in children. Cochrane Database
Syst Rev. 2011;(1):CD007074.
38. Randerath WJ, Verbraecken J, Andreas S, et al; European
Respiratory Society task force on non‐CPAP therapies in
sleep apnoea. Non‐CPAP therapies in obstructive sleep
apnoea. Eur Respir J. 2011;37(5):1000‐1028. Available
at: http://www.ers‐education.org/media/2011/pdf
/156487.pdf. Accessed January 3, 2012.
39. Ernst A, Carden K, Gangadharan SP. Tracheomalacia and
tracheobronchomalacia in adults. Last reviewed July
2012. UpToDate Inc., Waltham, MA.
40. Walton J, Ebner Y, Stewart MG, April MM. Systematic
review of randomized controlled trials comparing
intracapsular tonsillectomy with total tonsillectomy in a
pediatric population. Arch Otolaryngol Head Neck Surg.
2012;138(3):243‐249.
41. Marcus CL, Brooks LJ, Draper KA, et al; American
Academy of Pediatrics. Diagnosis and management of
childhood obstructive sleep apnea syndrome. Pediatrics.
2012;130(3):576‐584.
42. Marcus CL, Moore RH, Rosen CL, et al; Childhood
Adenotonsillectomy Trial (CHAT). A randomized trial of
adenotonsillectomy for childhood sleep apnea. N Engl J
Med. 2013;368(25):2366‐2376.
43. Kim J, Gozal D, Bhattacharjee R, Kheirandish‐Gozal L.
TREM‐1 and pentraxin‐3 plasma levels and their
association with obstructive sleep apnea, obesity, and
endothelial function in children. Sleep.
2013;36(6):923‐931.
44. Gozal D, Kheirandish‐Gozal L, Bhattacharjee R, et al.
Circulating adropin concentrations in pediatric
obstructive sleep apnea: Potential relevance to
endothelial function. J Pediatr. 2013;163(4):1122‐1126.
45. Epstein LJ, Kristo D, Strollo PJ Jr, et al; Adult Obstructive
Sleep Apnea Task Force of the American Academy of
Sleep Medicine. Clinical guideline for the evaluation,
34 of 35
management and long‐term care of obstructive sleep apnea in
adults. J Clin Sleep Med 2009;5(3):263‐276.
46. Aurora RN, Casey KR, Kristo D, et al. Practice parameters for the
surgical modifications of the upper airway for obstructive sleep
apnea in adults. Sleep 2010;33(10):1408‐1413.
47. Posadzki P, Lee MS, Ernst E. Osteopathic manipulative
treatment for pediatric conditions: A systematic review.
Pediatrics. 2013;132(1):140‐152.
48. Paruthi S. Management of obstructive sleep apnea in children.
UpToDate [serial online]. Waltham, MA: UpToDate; reviewed
June 2014.
49. Aurora RN, Lamm CI, Zak RS, et al. Practice parameters for the
non‐respiratory indications for polysomnography and multiple
sleep latency testing for children. Sleep.
2012;35(11):1467‐1473.
50. Kerschner JE, Lynch JB, Kleiner H, et al.
Uvulopalatopharyngoplasty with tonsillectomy and
adenoidectomy as a treatment for obstructive sleep apnea in
neurologically impaired children. Int J Pediatr Otorhinolaryngol.
2002;62(3):229‐235.
51. Randerath WJ, Verbraecken J, Andreas S, et al. Non‐CPAP
therapies in obstructive sleep apnoea. Eur Respir J.
2011;37(5):1000‐1028.
52. Marcus CL, Brooks LJ, Draper KA, et al; American Academy of
Pediatrics. Diagnosis and management of childhood obstructive
sleep apnea syndrome. Pediatrics. 2012;130(3):576‐584.
53. Paruthi S. Management of obstructive sleep apnea in children.
UptoDate inc., Waltham, MA. Last reviewed June 2015.
54. Certal VF, Zaghi S, Riaz M, et al. Hypoglossal nerve stimulation
in the treatment of obstructive sleep apnea: A systematic
review and meta‐analysis. Laryngoscope.
2015;125(5):1254‐1264.
55. Diercks GR, Keamy D, Kinane TB, et al. Hypoglossal nerve
stimulator implantation in an adolescent with Down syndrome
and sleep apnea. Pediatrics. 2016;137(5).
56. Garetz SL. Adenotonsillectomy for obstructive sleep
apnea in children. UpToDate Inc., Waltham, MA. Last
reviewed June 216.
35 of 35
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering
plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains
only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not
provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are
independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates.
Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy
Bulletin may be updated and therefore is subject to change.
Copyright © 2001‐2016 Aetna Inc.
AETNA BETTER HEALTH® OF PENNSYLVANIA
Amendment to Aetna Clinical Policy Bulletin Number: 0752
Obstructive Sleep Apnea in Children
There are no amendments for Medicaid.
www.aetnabetterhealth.com/pennsylvania
Updated 03/2017
