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Obstructive Sleep Apnea in Children Page 1 of 18 http://qawww.aetna.com/cpb/medical/data/700_799/0752_draft.html 11/19/2014 Aetna Better Health® 2000 Market Street, Suite 850 Philadelphia, PA 19103 AETNA BETTER HEALTH® Clinical Policy Bulletin: Obstructive Sleep Apnea in Children Revised April 2014 Number: 0752 Policy I. Diagnosis A. Aetna considers nocturnal polysomnography (NPSG) for children and adolescents younger than 18 years of age with habitual snoring during sleep medically necessary when performed in a healthcare facility to differentiate primary snoring versus obstructive sleep apnea syndrome (OSAS). Note: In addition to obstructive sleep apnea, other medically necessary indications for NPSG in children include hypersomnia, suspected narcolepsy, suspected parasomnia, suspected restless leg syndrome, suspected periodic limb movement disorder, suspected congenital central alveolar hypoventilation syndrome, and suspected sleep related hypoventilation due to 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; or 4. Failure to thrive; or 5. Neuromuscular disorders; or 6. Obesity; or 7. Prematurity; or 8. Recent respiratory infection; or 9. Severe OSAS was present on pre-operative PSG (a

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Obstructive Sleep Apnea in Children Page 1 of 18

http://qawww.aetna.com/cpb/medical/data/700_799/0752_draft.html 11/19/2014

Aetna Better Health® 2000 Market Street, Suite 850 Philadelphia, PA 19103

AETNA BETTER HEALTH®

Clinical Policy Bulletin: Obstructive Sleep Apnea in Children

Revised April 2014

Number: 0752 Policy

I. Diagnosis

A. Aetna considers nocturnal polysomnography (NPSG) for children

and adolescents younger than 18 years of age with habitual snoring

during sleep medically necessary when performed in a healthcare

facility to differentiate primary snoring versus obstructive sleep

apnea syndrome (OSAS). Note: In addition to obstructive sleep

apnea, other medically necessary indications for NPSG in children

include hypersomnia, suspected narcolepsy, suspected parasomnia,

suspected restless leg syndrome, suspected periodic limb

movement disorder, suspected congenital central alveolar

hypoventilation syndrome, and suspected sleep related

hypoventilation due to 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; or

4. Failure to thrive; or

5. Neuromuscular disorders; or

6. Obesity; or

7. Prematurity; or

8. Recent respiratory infection; or

9. Severe OSAS was present on pre-operative PSG (a

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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, daytime nap PSG,

measurements of circulating adropin concentrations, plasma

pentraxin-3 and TREM-1 levels, or unattended home PSG,

experimental and investigational for diagnosis of OSAS in

children because their effectiveness for this indication has not been

established.

II. Treatment

Aetna considers the following treatments for OSAS in children with habitual

snoring medically necessary when 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 the following interventions experimental and

investigational for obstructive sleep apnea in children because their

effectiveness for this indication has not been established:

1. Cautery-assisted palatal stiffening procedure (CAPSO);

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2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

Chiropractic/osteopathic manipulation;

Expansion sphincter pharyngoplasty;

Flexible positive airway pressure;

Injection snoreplasty;

Laser-assisted uvuloplasty (LAUP);

Lingual tonsillectomy;

Mandibular distraction osteogenesis;

Maxillary expander;

Midline/partial glossectomy;

Nasal surgery;

Pillar palatal implant system;

Repose system;

Somnoplasty or Coblation;

Transpalatal advancement pharyngoplasty;

Uvulectomy.

See also CPB 0004 - Obstructive Sleep Apnea in Adults, CPB 0330 - Multiple

Sleep Latency Test (MSLT), CPB 0452 - Noninvasive Positive Pressure

Ventilation, and CPB 0549 - Distraction Osteogenesis for Craniofacial Defects.

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.

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Primary snoring among children without obstructive 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. It should be noted that interpretation of NPSG values in children with

OSAS is not unanimously agreed upon in the 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.

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 (Kirk, 2003).

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). 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. 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

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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.

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).

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

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measured by 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, 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.

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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 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". http://emedicine.medscape.com/article/426003-treatment.

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. 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.

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

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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 (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. 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.

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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 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".

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

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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”.

CPT Codes / HCPCS Codes / ICD-9 Codes

Diagnosis:

CPT codes covered if selection criteria are met:

95782

95783

95808

95810

95811

CPT codes not covered for indications listed in the CPB:

76120 -

76125

95800

95801

95806

95807

94762

Other CPT codes related to the CPB:

42700 -

42999

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

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

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G0400 Home sleep test (HST) with type IV portable monitor,

unattended; minimum of 3 channels

ICD-9 codes covered if selection criteria are met:

327.23 Obstructive sleep apnea (adult) (pediatric) [OSAS]

786.09 Other dyspnea and respiratory abnormality [habitual snoring

during sleep]

Other ICD-9 codes related to the CPB:

034.0 Streptococcal sore throat

079.6 Respiratory syncytial virus (RSV)

278.00 -

278.02

Overweight and obesity

358.00 -

358.9

Myoneural disorders

429.3 Cardiomegaly

460 - 466.19 Acute respiratory infections

487.0 - 488 Influenza

756.0 Anomalies of skull and face bones

765.00 -

765.19

Extreme immaturity and other preterm infants

780.50 -

780.59

Sleep disturbances

783.41 Failure to thrive

Treatment: tonsils & adenoids:

CPT codes covered if selection criteria are met:

42820 -

42821

ICD-9 codes covered if selection criteria are met:

474.02 Chronic tonsillitis and adenoiditis

474.10 Hypertrophy of tonsils and adenoids

Treatment: CPAP:

CPT codes covered if selection criteria are met:

94660

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CPT codes not covered for indications listed in the CPB:

20692 -

20697

30000 -

30999

30801

30802

41512

41530

42140

42145

42160

42870

42890

42950

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

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

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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)

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

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-9 codes covered if selection criteria are met:

327.23 Obstructive sleep apnea (adult) (pediatric) [OSAS]

519.19 Other diseases of trachea and bronchus [tracheomalacia]

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770.81 Primary apnea of newborn

Other ICD-9 codes related to the CPB:

748.3 Other anomalies of larynx, trachea, and bronchus [congenital

tracheomalacia]

756.0 Anomalies of skull and face bones

780.50 -

780.59

Sleep disturbances

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. Available at:

http://www.pediatrics.org/cgi/content/full/109/4/704. Accessed February 28,

2008.

2. Schechter MS. American Academy of Pediatrics. Technical report:

Diagnosis and management of childhood obstructive sleep apnea

syndrome. Pediatrics. 2002;109(4):e69. Available at:

http://pediatrics.aappublications.org/cgi/content/full/109/4/e69. Accessed

February 28, 2008.

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. 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.

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management. ORL J Otorhinolaryngol Relat Spec. 2007;69(6):340-344.

Smith SL, Pereira KD. Tonsillectomy in children: Indications, diagnosis and

complications. ORL J Otorhinolaryngol Relat Spec. 2007;69(6):336-339.

Uong EC, Epperson M, Bathon SA, et al. Adherence to nasal positive

airway pressure therapy among school-aged children and adolescents with

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apnea in obese and normal-weight children. Otolaryngol Head Neck Surg.

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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.

Leiberman A, Stiller-Timor L, Tarasiuk A, et al. The effect of

adenotonsillectomy on children suffering from obstructive sleep apnea

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Brietzke SE, Gallagher D. The effectiveness of tonsillectomy and

adenoidectomy in the treatment of pediatric obstructive sleep

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Robb PJ. Adenoidectomy: does it work? J Laryngol Otol. 2007;121(3):209-

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positive airway pressure therapy in children with obstructive sleep apnea.

Pediatrics. 2006;117(3):e442-451.

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sleep apnea in neurologically impaired pediatric patients. Int J Ped

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Ow AT, Cheung LK. Meta-analysis of mandibular distraction osteogenesis:

Clinical applications and functional outcomes. Plast Reconstr Surg.

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Kuhle S, Urschitz MS, Eitner S, Poets CF. Interventions for obstructive

sleep apnea in children: A systematic review. Sleep Med Rev. 2009;13

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Friedman M, Wilson M, Lin HC, Chang HW. Updated systematic review of

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Pang KP, Woodson BT. Expansion sphincter pharyngoplasty: A new

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ventilation in infants with upper airway obstruction: Comparison of

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tongue obstruction in pediatric obstructive sleep apnea. Arch Otolaryngol

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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.

CPT only copyright 2008 American Medical Association. All Rights Reserved.

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