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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
214
A. Dunn and N. Kaplish
14
14.1 Introduction
Continuous positive airway pressure (CPAP) therapy
is considered to be initial and gold standard therapy
for obstructive sleep apnea (OSA). It is a safe and costeffective therapy [1], though compliance with CPAP can
be challenging in many patients with OSA. It has been
reported that as high as 10% of patients may refuse CPAP
therapy [2]. Discussions about treatment other than CPAP
therapy are common in both academic and non-academic
sleep medicine clinics as patients often seek alternatives
options. The scope of this chapter is to discuss other nonPAP treatment options and emerging therapies for the
treatment of OSA. Patients with OSA can be counseled
on these options as clinically appropriate.
14.2 Positional Therapy
OSA is often found to be prominent in supine or REM
sleep. Positional obstructive sleep apnea is often dened
when the AHI is twice as high in the supine sleep compared to non-supine sleep. Stricter denitions of positional therapy include normalization of AHI (<5/hr) in
the lateral position.
The prevalence of positional OSA is estimated to be
as high as 55–60% [3] but much higher in Asian population, reaching nearly 70% [4]. On average patients with
positional OSA are younger, thinner, and have less severe
OSA than their counterparts [3, 4]. When using stricter
criteria for positional OSA, with normalization of AHI
(<5) in the lateral position, the prevalence of positional
OSA was found to be about 27%. When severity of OSA
is considered, in patients with mild OSA, the prevalence
was about 50%. The prevalence dropped dramatically to
only about 19% of moderate severity OSA and 6.5% in
cases with severe OSA [5].
There is a strong inverse correlation with BMI and
position-dependent OSA; changes in body weight have
been shown to affect positional dependence [3]. Patients
with positional OSA who over time converted to nonpositional OSA had gained weight and had overall worsening of OSA.The converse was also shown in patients
with non-positional OSA converting to less severe, positional OSA with weight loss [6].
The supine position is associated with increased
apnea severity in terms of apnea duration, desaturation, arousal length, and frequency. [7] Few studies have
examined the anatomical changes in the airway during
lateral position and the exact mechanisms responsible
for the improvement in breathing in the lateral position
is not entirely known but the effect of gravity likely plays
a role. Anatomical optical coherence tomography of the
upper airway in awake OSA patients and controls in the
supine and lateral positions has shown airway changes
from a more transversely oriented elliptical shape when
supine to a rounder shape in the lateral recumbent position, but it does not show changes in the overall crosssectional area [8]. The increased circularity of the airway
in the lateral position may render it less likely to collapse.
Drug-induced sleep endoscopy performed on OSA
patients investigated the effect of body posture on the
site of airway obstruction. When changing from supine
to lateral position, obstruction at the tongue base and
larynx was signicantly improved; however, the prevalence of lateral wall obstruction was not affected suggesting that those with non-positional OSA have
persistent lateral wall obstruction [9].
There are numerous strategies developed to maintain
the lateral position during sleep. One of the simplest has
been called the “tennis ball technique.” This therapy
consists of a tennis ball fastened to the back by straps
or in a pocket or similar construction. Commercially
made waist-bands with foam pillows worn on the back
to prevent supine sleep are also available. More recently,
a vibrating device worn on the neck to alert the user of
being in the supine position has been developed.
While the tennis ball technique has been shown to
signicantly reduce AHI and time spent in the supine
position, studies on long-term compliance have been
poor with 38% reporting compliance at 6months and
less than 10% reporting continued use over 30months
[10, 11]. The main reasons for discontinuing therapy
were discomfort, ineffectiveness due to the ball moving
too much or no improvement in sleep quality or daytime
sleepiness [10].
Self-made and commercially made waistbands
for positional therapy have been shown to be successful in reducing AHI (by ≥50% and below 20) in 68%
and reducing AHI < 5 in 40% of patients with positional OSA, with no statistically signicant differences
between ESS and time spent supine [12]. Despite reduction in AHI, 60% of those treated with these positional
devices had stopped therapy after 13months.
More recently, vibrating neckband has been developed, which senses when the user has rolled in to the
supine position and alert the user to turn to the lateral
position. One such commercially available device, Night
Shift, is worn around the neck. This device has been
shown to signicantly reduce sleep in the supine position and reduce AHI by 69% in patients with positional
OSA (dened as overall AHI ≥ to 1.5 times greater
than the non-supine AHI) [13]. The device was shown
to improve sleep architecture, decrease cortical arousals,
increase N2 sleep, and decrease N1 sleep and improve
Epworth Sleepiness Scale scores. Over the 4-week study
7.4–13.4% of participants reported perceived worsening sleep quality due to the device. No long-term studies
Other Therapies andEmerging Options forManagement ofOSA
215
14
have been done to assess compliance, but at 4weeks, the
median compliance was 96%.
A chest-worn device, commercially available as
NightBalance device, vibrates to alert the user when in
the supine positon. After 1 month of usage in patients
with mild-to-moderate positional OSA dened as AHI
at least twice as high in the supine position compared
to non-supine, AHI was signicantly decreased from
a mean of 16.4–5.2. About 48% of the study patients
demonstrated resolution of OSA with an overall
AHI<5 [14]. This device has been also shown to effectively decrease time spent in the supine position, from a
median of 49% to 0%, and improved subjective sleepiness and sleep quality. At 6months, compliance dened
as 4 hours of nightly use was 64.4% and median ESS
decreased from 11 at baseline to 8 [15].
In patients with mild positional OSA, with AHI
<5 in the lateral position, positional therapy using a
commercially available foam pillow secured to the back
(ZZoma Positional Sleeper) has been found to be as
effective as CPAP in treated OSA, with the same proportion of patients achieving AHI < 5 with the positioning device as CPAP with no differences in sleep quality
or oxygen saturation [16]. This study was limited to one
night of therapy and therefore efcacy over long term
remains unclear.
CPAP has been compared with positional therapy in
patients with positional OSA. A study comparing treatment of positional OSA, dened as 50% reduction of OSA
in the lateral position, with 2weeks of CPAP and 2weeks
of positional therapy, found CPAP to be more effective
reducing AHI and improving oxygen saturation than
positional therapy [17]. Despite this nding, there were no
signicant differences in sleep architecture, ESS, MWT,
mood, or quality of life measures between therapies.
A similar study using a thoracic anti-supine band
(TASB) mimicking the tennis ball technique compared
the efcacy of positional therapy in mild–moderate
positional OSA patients to nasal CPAP. This study
found that with CPAP, there was a statistically signicant greater reduction in AHI and higher percentage
of patients achieving treatment success (AHI <10) than
with positional therapy [18]. TASB signicantly reduced
the time spent in the supine position to a mean of 6.3%
versus 35.4% with CPAP.
In summary, positional therapy has been shown
to reduce AHI and time spent in the supine position.
Positional therapy may be benecial and potentially as
effective as CPAP in a select population whose OSA
normalizes to AHI< 5 in the lateral position. Limited
studies have shown long-term compliance with positional therapy is poor demonstrating the need for close
clinical follow-up and also need for more comfortable
positional therapy options.
14.2.1 Weight Loss
It is estimated that in the United States, 5.7% adults
aged 30–69years have moderate or severe sleep disordered breathing (SDB) and 58% of those adults have
sleep disordered breathing attributable to excess weight
[19]. If this is expanded to include adults with mild
SDB, the percentage with sleep disordered breathing
increases to 17%, with 41% attributable to excess weight
[19]. In people with SDB, there is a dose–response relationship between weight gain and severity of SDB,
with each percentage change in weight was associated
with a 3% change in AHI or for each 1kg/m2 increase
in baseline BMI, an increase in AHI of about 1% [20].
A 10% weight gain was found to be associated with a
32% increase in AHI, relative to maintaining a stable
weight and a sixfold increase in the odds of developing moderate- to-severe obstructive sleep apnea [20].
This strong relationship between SDB and the obesity
epidemic suggests the weight loss strategies should be
an integral part of management of SDB.The current
American Academy of Sleep Medicine quality measures recommend at least yearly discussion of weight
management for adult patients with moderate-to-severe
obstructive sleep apnea [21].
Dietary weight loss has been shown to improve
OSA.In OSA patients with diabetes, an intensive lifestyle interventions consisting of a behavioral weight
loss program, portion-controlled diet with a prescribed
calorie intake, and 175minutes of physical activity per
week has shown to be more effective than diabetes education and support [22]. The participants in the lifestyle
intervention lost signicantly more weight than those
in the diabetes support and education group, 10.8 kg
versus 0.6 kg with signicantly greater reductions in
waist and neck circumferences. AHI in the intensive
lifestyle intervention group decreased from 22.9 to
18.3, with an adjusted mean decrease of 9.7 events per
hour, versus increased from 23.5 to 28.3in the diabetes
education group. The difference in the two groups was
due to changes in the obstructive apnea episodes and
not hypopneas. In patients in the lifestyle intervention
group, there were also signicant changes in the severity
of OSA as well with remission of OSA (AHI <5) being
three times more common compared to the diabetes
education group. The greatest benet was found to be
in men and participants with higher baseline AHI values. At 4years, the benecial effects of intensive lifestyle
intervention persisted despite weight gain of almost
50%.
Very low-calorie diets have been shown to improve
OSA in obese patients (with BMI between 30 and 40)
with moderate-to-severe OSA, with the greatest effect
on those patients with severe disease [23]. The diet for
216
A. Dunn and N. Kaplish
14
one such study consisted of a very low-calorie liquid diet
for 7weeks followed by 2weeks of gradual introduction
of normal, followed by a weight loss maintenance program. Signicant weight loss was achieved by 9weeks,
and 73% of patients following the diet were no longer
classied as obese, losing an average of 18 kg. Weight
loss following this diet was associated with a reduction
in AHI by 21 events per hour. Weight gain was noted at
the 1-year mark, with 56% of participants being categorized as obese. However, despite weight gain, at 1-year
follow-up, the average reduction in AHI was largely
maintained at 47% of baseline (reduced by a mean of 17
events/hr) with 10% having total remission of OSA at 1
year. Patients with severe OSA showed greater reduction
in the AHI amounting to 25 events per hour. In patients
with moderate OSA, AHI was reduced by seven events
per hour.
In overweight and obese patients (with BMI between
28 and 40) with mild OSA, following a very low-calorie diet (VLCD), that is, 600–800 calories per day) for
12 weeks, was more effective in terms of weight loss
and improvement in OSA compared to lifestyle intervention (diet and exercise counseling) [24]. Weight was
reduced by 10.6% in the VLCD group compared to
2.6% in the lifestyle intervention group. After 12weeks,
AHI of those in the VLCD group was reduced by 40%,
from 10 to 5.6, with 61% having complete resolution of
OSA.With lifestyle intervention, there was a 14% reduction in AHI from 9 to 8.3, with 32% demonstrating resolution of OSA.At 1 year, the odds ratio for having mild
OSA was 0.24in the VLCD group compared to the lifestyle intervention group. In this study, a weight reduction of 5kg corresponded to a reduction in AHI by two
events per hour.
Meta-analysis of nine studies investigating the
effects of dietary weight loss on OSA, including lowcalorie diets (800–8000kcal/day), very low-calorie diets
(600–800 kcal/day), and weight loss programs, found
a reduction in AHI from 52.5 to 28.3 events/hr with
higher weight loss associated with greater reduction in
OSA.OSA cure rates ranged from 61% at 3months to
<10% at 1 year [25].
Weight loss surgery has been shown to improve or in
some cases resolve OSA.A meta-analysis of investigating the effects of various bariatric procedures on OSA,
including gastric banding, Roux-en-Y, biliopancreatic
bypass, and gastroplasty, found a mean reduction in
BMI from 55.3 to 37.7 kg/m
2
. There were signicant
reductions in mean AHI from 54.7 to 15.8 events per
hour (71% from baseline) after bariatric surgery [26].
This is a signicant reduction in AHI; however, the
mean AHI after surgery was still consistent with moderate OSA.Notably, in 6 of the 12 studies for which individual patient data were available, 25% effectively cured
OSA with surgery, attaining AHI<5. Those “cured” of
OSA were overall younger (38.9years vs 46.5years) and
lighter at baseline (102.7 vs 173.3kg) than those with
residual OSA after surgery [26].
When comparing the specic types of weight loss
surgeries, the results of a 2014 meta-analysis of 69 studies including 13,900 patients found 75% patients of all
procedure types had improvement in obstructive sleep
apnea [27]. Biliopancreatic diversion was the most successful with 99% of patients experiencing improvement in OSA and 82.3% experiencing resolution of
OSA. Laparoscopic gastric banding was the least successful with 32% with resolution of OSA, though 70.5%
had improvement in OSA.
The degree of weight lost and reduction in AHI has
been shown to be greater in those patients undergoing weight loss surgery than with medical weight loss.
Laparoscopic gastric banding in obese adults (BMI >35
and<55) with moderate-to-severe OSA has been shown
to be a more effective weight loss method than medical weight loss. Those who underwent gastric banging
lost 27.8kg on average compared to 5.1kg with medical
weight loss [28]. AHIs in both groups showed reduction
from baseline; however, the mean reduction in AHI in
the laparoscopic gastric banding group was 25.5 events
per hour compared to 14.0 events in the medical weight
loss group; however, the difference in AHI reduction
between groups was not statistically signicant. Only
one participant in the study, in the medical weight loss
group, had remission of OSA (AHI < 5); however,
reduction to mild OSA (AHI <15) was achieved by 27%
of the surgical group compared to 7% of the medical
weight loss group.
A study comparing effects of weight loss from Rouxen- Y gastric bypass (RYGB) to intensive lifestyle intervention (ILI) on patients with all severities of OSA found
signicantly greater weight loss and reduction in AHI in
the RYGB group [29]. Participants undergoing RYGB
had a mean weight loss of 42kg (reduction if BMI by
14 kg/m
2
) compared to 12.1 kg, reduction in BMI of
5.4kg/m2 in the ILI group. The mean reduction in AHI
of 21.6 events per hour in the RYGB group, compared
to mean reduction in ILI group of AHI of 8.8 events per
hour. In this study, a signicantly larger proportion of
participants undergoing RYGB had remission of OSA
(AHI <5, 66%), compared to 40% of participants in the
intensive lifestyle intervention.
A meta-analysis of surgical versus nonsurgical
weight loss methods demonstrated that both methods
were associated with statistically signicant overall
reductions in AHI and BMI; however, the reductions in
AHI and BMI were greater with surgical intervention
[30]. Weight loss surgery was associated with a 15 kg/
2
reduction in BMI compared to 3.1kg/m2 with non-
m
surgical interventions. Surgical weight loss was associated with a decrease in AHI by 29 events/hr compared to
Other Therapies andEmerging Options forManagement ofOSA
217
14
11 events/hr with nonsurgical weight loss. In this metaanalysis, nonsurgical weight loss included lifestyle modication through exercise, dietary invention, or both, and
in some cases, behavioral counseling and pharmacotherapy were used.
Patients considering weight loss surgery should be
counseled regarding the expected weight loss but also
about improvement or resolution of their sleep apnea
as measured by AHI.Follow-up with the treating physician is necessary and repeat sleep apnea testing should
be performed following signicant weight to assess for
residual OSA.
14.2.2 Nasal EPAP Therapy
The nasal EPAP device is a bidirectional valve, which is
applied externally to each nostril and kept in place by an
adhesive that forms seal between the valve and the nare.
Each device is one size ts all, disposable, and designed
for a single night of use. The valve has a xed expiratory
resistance of 80cm H
sec [31]. There is minimal inspiratory resistance, thus
making exhalation through the nose more difcult creating expiratory positive airway pressure. Unlike CPAP,
no inspiratory positive pressure is provided in the nasal
EPAP device.
The exact mechanism by which nasal EPAP treats
OSA is not known. Several mechanisms have been
proposed including positive pressure at end expiration
leading to dilation of the airway carrying over into
inspiration and preventing collapse and increased lung
volume creating traction on the upper airway making it
less collapsible. [32, 33].
The device is FDA cleared for treatment of obstructive sleep apnea and requires a prescription [34]. Nasal
EPAP is contraindicated in patients with severe respiratory disorders, hypercapnic respiratory failure, respiratory muscle weakness, bullous lung disease, bypassed
upper airway (tracheostomy), pneumothorax, pneumomediastinum, severe heart disease including congestive heart failure, hypotension (pathologically low
blood pressure), acute upper respiratory inammation
or infection (including sinus, nasal, and inner ear), or
perforation of the ear drum. [35].
Efcacy of the device was evaluated by Rosenthal
et al. in a multicenter study of 34 adult subjects with
OSA with mean age 49.8, mean BMI 30.1, 21.4% female
[36]. Subjects were excluded if they had previously
tried CPAP, had uncontrolled or serious illness, or had
comorbid sleep conditions. Subjects were also excluded
if nasal patency was poor due to blockage of one or both
nostrils, difculty breathing through the nose, sinusitis,
frequent, and/or poorly treated nasal allergies. The participants completed four polysomnograms (PSGs) in
O/L/sec at a ow rate of 100mL/
2
random order. PSGs included one control night and
three nights using the device with varying expiratory
resistances. Subjects then used the device with the resistance most effective at reducing AHI at home for 30days.
On the control night, average AHI was 24.5. The AHI
was signicantly reduced to an average of 13.5 on the
rst treatment night and 15.5 after 30days of use. At
the 30-day follow-up, 41% had an AHI reduction greater
than or equal to 50% compared to control. Statistically
signicant improvement in mean oxygen saturation was
noted between the control night and nal therapy; however, the mean improvement was 0.4%, which is usually
not the goal in clinical practice. ESS scores improved
signicantly from 8.7 at baseline to 6.9 after 30 days of
treatment, and PSQI scores improved signicantly from
7.4 at baseline to 6.5 at 30-day follow- up. Despite these
ndings, there was no improvement in sleep architecture
after the initial night of treatment or after 30days of
use [36]. There were no signicant differences in ODI,
minimum oxygen saturation between the control night
and any of the treatment nights. Participants reported
using the device all night for 94.4% of nights.
Patel etal. investigated factors predictive of response
to treatment. Patients with position-dependent OSA,
dened as lateral AHI lower than supine AHI, were
more likely to respond to treatment, dened as a>50%
reduction in RDI from baseline and an absolute
RDI < 20/hr, but this was not statistically signicant
[32]. Demographic factors and severity of baseline OSA
were also not predictive of therapeutic success.
The long-term efcacy of nasal EPAP was investigated by [37] during a 12-month study of the device
involving 41 participants with mean age of 50.1 years,
mean BMI of 32.5 kg/m
the duration of the study, there was a statistically signicant reduction in AHI, from 15.7 to 4.7 at month
12 of treatment. ODI was decreased from 12.62 to 7.6
at 12months. Additionally, there were statistically signicant reductions in median arousal index from 23.9
to 19.0 [31]. After 12months, the median proportion of
sleep time spent snoring was reduced by 74.4%. After
12 months of treatment, signicant improvement was
noted in sleepiness measured by the Epworth Sleepiness
Scale with scores decreasing from 11.1 to 6.0. Median
device usage during the 12months was 89.3% of nights
for the entire night. Participants with a positive clinical
response at month 3 were found to have excellent adherence for the remainder of the 12months. Forty-two percent of the participants reported adverse events with the
device; difculty exhaling, nasal discomfort, dry mouth,
headache, and insomnia were reported most frequently.
The effects of nasal EPAP after withdrawal of CPAP
were investigated by Rossi etal. This study aimed to test
the effectiveness of nasal EPAP to prevent recurrence
of obstructive sleep apnea following CPAP withdrawal.
2
, and 63.4% were male. Over
218
A. Dunn and N. Kaplish
14
Sixty-seven participants, previously diagnosed with moderate-to-severe OSA and using CPAP, were randomized
to continuing CPAP, nasal EPAP, or placebo nasal EPAP
for 2 weeks. The baseline characteristics of all three
groups were reported to be similar. After 2weeks, there
was recurrence of obstructive sleep apnea in the nasal
EPAP and placebo nasal EPAP groups. There was no
signicant difference in AHI or ODI between the groups
treated with nasal EPAP versus the placebo. Mean AHI
in the nasal EPAP group was signicantly higher than
the group continuing treatment with CPAP with AHIs of
27.6 and 2.4, respectively. Additionally, ODI was 4.3in
the group using CPAP versus 35.8 with nasal EPAP [38].
The ndings of this study suggest that the device may not
be a suitable alternative for use in patients with moderate-to-severe OSA currently using CPAP.
14.2.3 Oral Pressure Therapy
A proprietary oral pressure therapy device, Winx Sleep
Therapy System (ApniCure Inc., Redwood City CA),
was introduced as an alternative to CPAP for patients
who are unable to tolerate PAP therapy or are unwilling to use CPAP.The device consists of a pump console
connected to a polymer mouthpiece via tubing. Oral
pressure therapy is delivered as a light negative pressure
(as a vacuum) in the oral cavity. This negative pressure
allows for stabilization of the tongue and pulls the soft
palate forward with an expectation of the dilatation of
the retropalatal area.
Winx Sleep Therapy System consists of a mouthpiece, tubing, and a console. The mouthpiece has a
built- in-lip seal with a connector to the tubing. While
the mouthpiece is not customizable, it is available in ten
sizes, sized using a bite wax impression to determine
the width and arc measurements. The console has the
pump that generates the oral pressure that is transferred
via the tubing and delivered to oral cavity. Console also
holds the reservoir that collects any saliva that is drained
via the mouthpiece and tubing. The proprietary technology oral pressure therapy (OPT) has been shown to treat
obstructive sleep apnea [39]. Efcacy of the therapy is
contingent upon patient’s ability to breathe through
their nose while using the oral pressure therapy for it
to be effective. The negative pressure delivered is nontitratable; however, feedback control maintains a continuous negative pressure. Once the console has reached
the target vacuum level of 51cm of water, the indicator
light on the console is turned on.
A study of utilizing magnetic resonance imaging in
wakefulness has shown that the negative pressure generated by the device moves the soft palate anteriorly
and superiorly and the anterior–superior segment of
the tongue forward increasing the retropalatal airway
caliber in the lateral and anterior-posterior dimensions
[40]. Patients with a clinical response to the device have
been shown to have a signicantly greater superior displacement of the soft palate and anterior displacement
of the tongue than nonresponders and greater increases
in cross-sectional areas of the retropalatal region
Interestingly, in the same study, responders to treatment
were shown to have signicant decreases in retroglossal
cross- sectional area [40].
The efcacy of the Winx device has been investigated in adults with OSA in a multicenter prospective,
randomized, crossover trial. [39] The study population
included 63 subjects with mild (apnea–hypopnea index
[AHI]≥5 and < 15) to severe (AHI≥ 30) obstructive
sleep apnea, with and without prior treatment with
CPAP. The study population primarily consisted of
men (69.8%) with mean age 53.6 and mean BMI 32.3.
Study excluded patients with poor nasal patency, poor
mouthpiece t, severe medical or dental conditions, or
were unable to tolerate the device. The subjects underwent initial PSG without the device, with the device, and
again with the device after 28days of use at home. The
sequence of the initial PSG (control or with the device)
was randomized.
Overall success rate was low in this study, though success was seen in patients with moderate (50%) and severe
(23%) obstructive sleep apnea. The median AHI was
27.5 events per hour on the control night. With the device,
there was clinically signicant response, dened by the
study team as treatment AHI ≤ 10/hr and≤50% of control values, in 20 of 63 (31.7%) subjects. Average nightly
use of the device during the 28-day period of home use
was 6 hours, and 84% of subjects used the device for
>4 hours per night. Over the 28-day treatment period,
the mean Epworth sleepiness scale score was signicantly
reduced from 12.1 to 8.6 among subjects who were naïve
to treatment for OSA and remained unchanged in subjects using CPAP up until the trial period.
The device was generally well tolerated with three
subjects discontinuing the study due to discomfort and
76% indicating that they would use the device to treat
their OSA.Adverse events were reported on average of
50% of nights of use, were generally mild, and included
oral or dental discomfort or irritation and dry mouth.
No signicant occlusal or tooth movement was demonstrated over the 28-day period of use.
Subsequent studies done have shown the success
rate, achieving AHI ≤ 10 events/hr with OPT have
remained below 50% [41, 42]. In general, the success
rates were higher in patients with moderate obstructive
sleep apnea, which may be due to denition of success
in the study group.
The device is available without a prescription
though many insurances are not covering the cost of
therapy. OPT may be a signicant out-of-pocket cost
.
Other Therapies andEmerging Options forManagement ofOSA
219
14
for most patients, ascertaining the effectiveness of
OPT may be more desirable. Winx can be connected
to polysomnogram (PSG) system using the Winx PSG
adapter. Sleep study using OPT would allow to ascertain frequency of apneas/hypopneas, hypoxemia, and
improvement in the sleep architecture. In addition to
ascertaining efcacy, PSG with OPT would also assess
for tolerance and assess for maintenance of target oral
pressure of 50–51cm of water. Sleep center providing
this test must have a wide array of mouthpiece sizes
available, as well as staff trained for appropriate tting.
This may be resource intensive for some centers limiting its clinical use.
As of yet, there are no predictors of success with
the Winx device, and thus successful treatment with
the device should be conrmed. The device is not recommended for use in patients under 18 years of age,
patients with central sleep apnea, or with severe pulmonary disease, pneumothorax, loose teeth, or advanced
periodontal disease. OPT may not be appropriate in
patients with BMI ≥ 40 and nasal obstruction. OPT
leads to reduction in the AHI in select group of patients
with obstructive sleep apnea, though majority may still
have residual sleep apnea. Oral pressure therapy may be
an option in patients with claustrophobia or less than
optimal dentition [43].
14.2.4 Hypoglossal Nerve Stimulation
At this time, the only commercially available hypoglossal
nerve stimulator is the Inspire device (Inspire Medical
Systems, Inc.), which is an implantable programmable
neurostimulator, FDA approved for the treatment of
obstructive sleep apnea. The device consists of three
implanted components: the neurostimulator, the sensing
lead, and the stimulation lead. The neurostimulator is
implanted in the right infraclavicular region and is connected to the sensing lead, placed between the internal
and external intercostal muscles, and the stimulation
lead placed on the medial division of the right hypoglossal nerve. The neurostimulator delivers electrical pulses
to the hypoglossal nerve via the stimulation lead, which
is synchronized with respiration by the sensing lead. The
device can be turned on and off by the patient using a
hand-held remote control. [44].
A study of 15 patients being treated with upper airway stimulation (UAS) examined hypoglossal stimulation effects on retropalatal and retrolingual dimensions.
Comparisons of the airway during awake laryngoscopy
and drug-induced sleep endoscopy (DISE) found that
unilateral stimulation of the hypoglossal nerve, timed
with ventilation, leads to multilevel increases in airway area [45]. The study demonstrated increases in the
anterior- posterior area of the retropalatal airway area
by 180% and retrolingual area by 130% with stimulation at a therapeutic amplitude during DISE compared
to wakefulness with progressive increases in area with
higher amplitudes of stimulation. During awake endoscopy, both responders (dened as a 50% reduction from
baseline AHI and treatment AHI < 20) and nonresponders had signicant changes in retrolingual area;
however, on DISE “responders” to treatment were also
found to have larger, statistically signicant retropalatal
enlargement than nonresponders [45].
A small retrospective study of 14 patients treated
with UAS sought to examine the tongue motions associated with stimulation. Three motions were identied
in the cohort: right protrusion, bilateral protrusion,
and mixed activation (all other tongue motions). After
6months, patients with bilateral protrusion were found
to have a greater reduction in AHI than patients with
mixed activation [46].
As per the device manufacturer, the Inspire device is
indicated in patients of ages 22 or greater, in those with
moderate-to-severe OSA with AHI of 15–65 with less
than 25% central apneas, and in those without complete
concentric collapse of airway at the level of the palate. The device is indicated in patients who have failed
PAP, dened as AHI> 15 despite PAP use, or in those
with PAP intolerance dened as unable to use CPAP for
>4hours per night for at least ve nights per week or
unwillingness to use PAP. Treatment with hypoglossal
nerve stimulation in patients with BMI> 32 is not recommended due to unknown effectiveness in this population as these patients were excluded in trials of the
device.
In the original trials of the device, subjects with
moderate-to-severe OSA with difculty accepting or
adhering to CPAP treatment were eligible for enrollment. Subjects were excluded for BMI > 32, with signicant neurological, active psychiatric disease or
cardiopulmonary disease. After initial screening with
polysomnogram, subjects were excluded if AHI was
less than 20 or more than 50 events per hour, if sleep
disordered breathing comprised >25% mixed or central
events, or if the AHI in a non-supine position was <10
per hour. Subjects were also excluded on the basis of
airway anatomy for anatomical abnormalities preventing the effective assessment of stimulation or if complete concentric collapse of the retropalatal airway was
observed on DISE [44].
The mean age of participants was 54.5 years with
83% male with mean BMI 28.4. Seventeen percent of
participants had undergone prior uvulopalatalpharyngoplasty. At 12months, 66% of subjects responded to
therapy, as median AHI scores decreased 68% from
25.4events per hour to 7.4 events per hour. The median
ODI decreased 70% from 25.4 events per hour to
7.4 events per hour. Score on the Function Outcomes
220
A. Dunn and N. Kaplish
14
of Sleep Questionnaire increased from 14.3 to 17.3, and
Epworth sleepiness scale scores decreased from a mean
of 11.6 to 7.0 at 12months and were stable at 36-month
follow-up. At 3 years, decreases in AHI remained stable
with the average AHI of 14.2 at 36 months and with
a median AHI of 7.3. Sixty-ve percent of the cohort
were deemed responders at 36months dened as a least
50% reduction in AHI from baseline and treatment AHI
of less than 20 [47].
Analysis of baseline characteristics of long-term
responders versus non-responders over the 36-month
period demonstrated statistically signicant differences in baseline AHI with responders’ baseline AHI
28.8 versus 35.0in nonresponders. Eighty-one percent
of the subjects reported the use of nightly therapy at
36 months. Eighty-four percent reported use at least
4days per week.
During clinical trials, 40% of the participants
reported discomfort related to stimulation. By 3 years,
reports of discomfort decreased to 24 from 80 in year
1. Throughout the rst year, 21% reported tongue soreness. In most cases, this resolved after acclimatizing to
therapy or after the device was reprogrammed. In some
instances, a tooth guard was necessary. Temporary
tongue weakness was experienced by 18% of participants, but no permanent tongue weakness was reported.
At two instances, there were device-related serious
adverse effects causing discomfort, necessitating repositioning of the neurostimulator. Most nonserious adverse
effects were related to the surgical procedure and were
expected postsurgical events.
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223
Surgical Management
ofOSA
Contents
Chapter 15 Surgical Management of OSA: Adenotonsillectomy–225
Allison G. Ordemann and Ron B. Mitchell
Chapter 16 Nasal Obstruction and Sleep-Disordered
Breathing–243
William C. Scott and David T. Kent
Chapter 17 Palatal Surgery for OSA Patients–259
Chandra M. Cherukuri, Neeraj Kaplish,
and Jeffrey J. Stanley
IV
Chapter 18 Hypopharyngeal Surgery for OSA Patients–269
Pratyusha Yalamanchi and Paul T. Hoff
Chapter 19 Management of Obstructive Sleep Apnea (OSA)
inCraniofacial Patients–281
Mikhail Daya and Jason E. Portnof
Chapter 20 Miniscrew-Assisted Maxillary Expansion Techniques
for Treatment of Obstructive Sleep Apnea–293
Audrey Jung-Sun Yoon, Stanley Yung-Chuan Liu,
and Christian Guilleminault
Chapter 21 Orthognathic Surgical Considerations for Obstructive
Sleep Apnea–305
Yong-Il Kim, Ki Beom Kim, and Reza Movahed
Chapter 22 Individualized
Patients with Obstructive Sleep Apnea Syndrome to
Obtain Improvement of Respiratory Function and Facial
Esthetics: Conventional Maxillomandibular
Advancement (MMA) Versus Modied MMA with
Segmental Osteotomy–323
Sung Ok Hong, Seung-Hak Baek, and Jin-Young Choi
Treatment Planning for Asian Adult
225
Surgical Management ofOSA:
Adenotonsillectomy
AllisonG.Ordemann andRonB.Mitchell
Contents
15.1 Introduction: Background Information – 227
15.2 Tonsil andAdenoid Anatomy, Physiology, Immunology,
Purpose – 227
15.3 OSA asanIndication forAdenotonsillectomy:
Guidelines–227
15.4 Preoperative Assessment – 227
15.4.1 Physical Examination – 227
15.4.2 Polysomnography – 229
15.4.3 Clinical History – 229
15
15.5 Preoperative Consent – 230
15.6 Preoperative Assessment – 230
15.6.1 Surgical Setting – 230
15.6.2 Special Laboratory Evaluation or Imaging – 231
15.6.3 Screening Tools forIdentifying At-Risk Children
inthePerioperative Period – 231
15.7 Tonsillectomy Technique: Extracapsular Versus
Intracapsular–231
15.8 Instrumentation – 232
15.8.1 Tonsillectomy – 232
15.8.2 Adenoidectomy – 233
15.9 Postoperative Management – 233
15.9.1 Pain – 233
15.9.2 Diet – 234
15.9.3 Follow-Up – 235
© Springer Nature Switzerland AG 2021
K. B. Kim et al. (eds.), Management of Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-030-54146-0_15