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15.4 Epiglottis Collapse asCause ofCPAP Failure andhow
toDiagnose it
It has been previously stated that epiglottic collapse can be a cause of CPAP low
adherence. In fact, according to the European position paper, one of the indications
for DISE are patients who do not tolerate CPAP [33]. Most of the times, DISE will
show the epiglottic collapse and it is assumed that this structure is implicated, especially when the patients report that they feel suffocated during the night. Fig.15.9
(Video 15.2) shows DISE-CPAP titration, with different pressures and jaw thrust
maneuver, in a patient intolerant to CPAP use. Epiglottic collapse occurred despite
high pressure and was even worse with the increase of CPAP level from 13 to 14cm
H2O.Jaw thrust maneuver prevented the hypopharyngeal and epiglottic collapse.
This patient was then indicated to MMA, with success.
The fact that many CPAP intolerant patients undergo DISE might be the cause of
the high rates of epiglottic collapse reported in the literature. In the systematic
review performed by Torre etal. in 2015, the incidence of epiglottic collapse ranged
from 9.6% to 73.5% [34]. This enormous difference in the series published is probably caused by the heterogeneity of the studies (differences in OSA severity, BMI,
anatomy, etc.) but there might also be differences in the terminology used by the
different authors. Some authors may include only primary epiglottic collapse while
others, both primary and secondary epiglottic collapse. Primary collapse is caused
by a oppy epiglottis collapsing in the anteroposterior direction or, even more
rarely, folding laterally, as for example in laryngomalacia. Secondary epiglottic collapse is an anteroposterior collapse due to posterior displacement of the tongue
base, and is more frequent than primary collapse.
In some patients performing DISE and CPAP simultaneously will show the cause
of the intolerance. The case series articles published performing CPAP-DISE
showed that epiglottic collapse was the cause of intolerance in 27–61% of the
patients [10, 27, 35]. The differences in reported numbers is probably caused by the
Fig. 15.9 (Video 15.2) DISE-CPAP titration with different pressures and jaw thrust maneuvers
(► https://doi.org/10.1007/000-bfb)
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Fig. 15.10 DISE-CPAP showing epiglottic collapse in a child 10 years old with persistent OSA
after adenotonsillectomy (left) and in an adult (right)
M. Carrasco-Llatas and J. Vaz de Castro
small sample size in each study and heterogeneity, as in the study by Yui etal.,
where partial epiglottic collapse was also included [35]. Nevertheless, in all these
series there was also persistent collapse in all the UA areas except in the lateral
pharyngeal walls, which caused the CPAP intolerance in other patients. Dieleman
etal. also reported that in 10% of cases in their series, no UA collapse was observed
during CPAP-DISE [27] (Fig.15.10).
When performing CPAP-DISE, it is of the upmost importance to use the same
mask as the patient is using every night, as this may inuence the tolerance. If the
patient usually uses a nasal mask, the berscope can be inserted through the
inferior part of the sealing silicone. In case of an oronasal mask, a exible berscope may be inserted through side holes, under the mask, or with an adapted
mask [27]. Alternatively, a berscope can be passed through a bronchoscopy
swivel adapter with a self-sealing diaphragm between the mask and CPAP circuit
[8] (Fig.15.11).
Some patients with severe OSA and CPAP intolerance might have a high surgical
risk and UA surgery may not be the rst option. Nevertheless, performing CPAPDISE in these patients may be useful. Yui etal. showed that the same pressure of
CPAP applied through an oronasal mask could not open the UA as well as a nasal
mask [36]. As CPAP-DISE is a dynamic exploration where maneuvers can be performed, changing mask type, turning the head, advancing the mandible, or adding a
MAD, ameliorate conditions and lead to reduced pressure and increased adherence.
Videos 15.1 and 15.2 show the image of the pharynx with different maneuvers and
PAP pressures.
As early as 1987, clinical cases reporting epiglottic collapse as a cause for CPAP
failure, using videouoroscopy, emerged in the literature. and at that time the DISE
technique had not even been reported yet [37, 38]. However, DISE offers many
advantages over videouoroscopy; therefore, it should remain the preferred diagnostic tool. During awake beroptic examination, the collapse of a oppy epiglottis
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Fig. 15.11 Insertion of the berscope through the adapted hole of the mask. Adopted from
Dieleman [27]
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observed during inspiration can also raise suspicion for epiglottic collapse associated with CPAP intolerance [39].
The shape of the ow signal during conventional PSG is related to the structure
causing the collapse. It has been reported that the epiglottic collapse causes a specic curve, with features of discontinuity and jaggedness in nasal cannula or pneumotachograph. Meanwhile, non-epiglottic collapse often produces a “at-top” ow
shape [40]. Therefore, exploring the ow curve under CPAP titration might be
another method to discover whether the epiglottis is the cause of intolerance, but as
far as we know, there are no publications on this subject so far. In fact, this noninvasive method could answer the question if some types of epiglottic collapse could be
solved with CPAP. Intuitively, anteroposterior epiglottic collapse due to a oppy
epiglottis may worsen with the increased pressure, but it could happen that lateral
collapse of the epiglottis could be relieved. We could not nd any publications
exploring this idea either.
In conclusion, the studies performed with CPAP-DISE show that the epiglottis is
the structure responsible for CPAP intolerance in an important number of patients.
The easiest way to diagnose epiglottic collapse is DISE and it is performed in a high
proportion of patients with CPAP intolerance and less frequently on those with optimal CPAP adaptation. To elucidate which epiglottic characteristics could predict
CPAP (in)tolerance, it would be interesting to perform DISE-CPAP on all patients
before CPAP therapy initialization.
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M. Carrasco-Llatas and J. Vaz de Castro
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Orofacial Myofunctional Therapy
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CarlosO’Connor-Reina andMarinaCarrasco-Llatas
16.1 Introduction toOrofacial Myofunctional Therapy:
AnOverview
The pathophysiological mechanisms of obstructive sleep apnea (OSA) are not fully
known, and a multifactorial origin has been suggested [1]. In OSA, the interaction
between anatomical and functional factors seems to determine whether the upper
airway (UA) collapses as a result of an imbalance between the forces that tend to
close and those that keep the UA open [2]. Since the studies of Remmers etal., it is
believed that the forces that prevent pharyngeal obstruction are produced by the
dilator muscles, the main dilator of the UA being the genioglossus muscle, and that
these are involved in the pathogenesis of OSA [3–6]. Studies have found a≈15%
increase in the percentage of type IIA muscle bers (fast-twitch bers that use aerobic and anaerobic metabolism, but have a low fatigue threshold) in airway muscles
such as the uvula in patients with OSA [7].
Guilleminault considered hypotony of the muscles of UA as the main pathophysiological reason for OSA, and this is the main therapeutic objective of the therapist. Orofacial myofunctional therapy (OMT) is one of the newest treatments for
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-34992-8_16. The videos can be accessed individually by click-
ing the DOI link in the accompanying gure caption or by scanning this link with the SN More
Media App.
C. O’Connor-Reina (*)
Head of Otorhinolaryngology Department in Hospital Quironsalud Marbella, Marbella, Spain
e-mail: carlos.oconnor@quironsalud.es
M. Carrasco-Llatas
Department of Otorhinolaryngology, Hospital Universitario Dr. Peset, Valencia, Spain
Department of Otorhinolaryngology, IMED Hospital, Valencia, Spain
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
M. Delakorda, N. de Vries (eds.), The Role of Epiglottis in Obstructive Sleep
Apnea, https://doi.org/10.1007/978-3-031-34992-8_16
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C. O’Connor-Reina and M. Carrasco-Llatas
sleep-disordered breathing (SDB) [8]. OMT is based on daily exercises with the aim
of strengthening the oropharyngeal muscles and facilitating UA opening [9]. OSA
originates from suboptimal function of the dilator muscles of the airway. OMT is a
therapy designed, theoretically, to deal with the anatomical mechanism underlying
this disease [10]. The patient is instructed to perform OMT exercises regularly for
20–40min daily for at least 3months under the supervision of a speech therapist.
The exercises can be guided with the use of diagrams, apps, or videos. The idea of
this therapy is to improve the tone of the UA muscles by reducing their volume and
collapsibility. However, there is no evidence regarding who is the most suitable
candidate for OMT.
16.1.1 Exercises
Suitable patients for this therapy should have no anatomical limitations and should
be able to breathe through the nose. Therefore, short lingual frenulum, temporomandibular joint dysfunction, and the presence of anatomical nose obstruction can
affect the results obtained from this therapy.
Classically, OMT exercises are based on isometric and isotonic contractions performed rhythmically, preferably before going to sleep (Fig.16.1). The genioglossus
is the main muscle activated. These exercises should be performed over the long
term and adherence is important [11].
Different protocols for these exercises have been reported, and there is no consensus on which is most suitable. Most of these exercises are based on the randomized
clinical trial (RCT) of Guimarães etal., in which the oropharyngeal exercises were
based on those used to treat speech–language pathologies and included soft palate,
tongue, and facial muscle exercises as well as stomatognathic function exercises [12].
Fig. 16.1 (Video 16.1) An example of conventional orofacial myofunctional speech therapy for
SDB (► https://doi.org/10.1007/000-bfg)
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Fig. 16.2 (Video 16.2) Telemedicine orofacial myofunctional speech therapy based on sensory
motor rehabilitation (► https://doi.org/10.1007/000-bfe)
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Adherence to the OMT exercises is the main difculty for patients. Some studies
have reported adherence rates as low as 10% [11]. Newer concepts about the type of
exercises have been reported recently, including the concept of sensory motor rehabilitation, which is based on the proprioceptive concept (Fig. 16.2) [13]. These
authors consider this kind of exercise to be most suitable for patients with OSA with
sensorial and motor decits.
16.1.2 Scientific Evidence
In 2009, Guimarães etal. reported the rst RCT to use OMT in the treatment of
patients with OSA [12]. They used their exercise protocol to increase the strength
and tone of the UA muscles and increase its patency. The patients were recently
diagnosed with mild to moderate OSA and were aged 25–65years. In the experimental group, 16 patients completed the study, giving an adherence rate of 84.25%;
in the control group given sham therapy, only 15 patients completed the study,
yielding an adherence rate of 75%. The parameters studied were sleep efciency,
apnea–hypopnea index (AHI) in the rapid eye movement (REM) and non-REM
stages, and subjective values assessed using the Berlin and Epworth questionnaires.
Guimarães et al. reported a signicant reduction in the AHI from 22 ± 4.8 to
13.7±8.5 events/h in the intervention group, but no signicant change in the control
group (22.4±5.4 to 25.9±8.5 events/h) [12].
The meta-analysis by Hsu etal. was based on nine studies with 394 adults and
children diagnosed with mild to severe OSA.Eight of the nine studies measured the
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AHI and reported an average 39% improvement from the baseline value after
OMT. There was no statistically signicant improvement in ESS from baseline
(P = 0.062). Nevertheless, the Pittsburgh questionnaire score improved by −1.3
from 21 (95% CI=−2.4 to −0.2; P = 0.026). Snoring intensity also improved in the
intervention group and differed signicantly from the control group (P= 0.044).
Hsu et al. concluded that OMT could be considered an alternative therapy for
OSA.However, given the small number of studies included and the heterogeneity of
the records, the conclusions may have been affected by bias [14].
Meghpara etal. published a meta-analysis of 15 studies with 237 patients who
reported OSA outcomes before and after OMT. The mean AHI decreased from
28.0± 16.2 events/h to 18.6± 13.1 events/h. The AHI standard mean difference
(SMD) was −1.34, which indicated a large effect (95% CI = −0.84 to −1.85;
P < 0.00001). The lowest O2 saturation (LSAT) in 197 patients improved from
83.18%±6.10% to 85.13%±7.01%. The LSAT SMD was 0.44 (95% CI=0.75 to
0.12; P<0.007). Sleepiness measured with the ESS in 156 patients decreased from
12.71±5.73 to 8.78±5.80 points. The ESS score SMD was −1.0 (95% CI=−0.50
to −1.50; P<0.0001). The authors concluded that OMT in adults reduced the AHI
by 34% and ESS score by 4 points and improved LSAT by 2%, and that OMT is a
possible adjunct treatment for OSA [15].
Ieto etal. published the rst RCT on the use of OMT to treat snoring in 39
patients randomly assigned to an intervention group that performed exercises or a
control group. The intervention group performed exercises for 8min three times/
day, and the sham therapy involved breathing exercises. Both groups performed
exercises for 3months. The intensity and number of snores were analyzed. In the
intervention group, snore index (snores >36dB/h) decreased by ≈ 50% from 99.5
[49.6–221.3] to 48.2 [25.5–219.2] (P = 0.017) and the total snore index (total
power of snore/h) decreased from 60.4 [21.8–220.6] to 31.0 [10.1–146.5]
(P=0.033) [16]. The results of some studies on OMT are summarized in Table16.1
[12, 16, 18, 19].
Carrasco et al. reported that the available evidence demonstrates a positive
effect of OMT in reducing OSA in adults as assessed using polysomnography
(PSG) and clinical variables. The available evidence is solid for snoring reduction
in adults. There is no evidence to support the use of OMT to treat UA resistance
syndrome, including how long the effects last or which OMT protocol is better in
children or adults. Despite these knowledge gaps, the available evidence indicates
that OMT is safe. The available evidence for the use and safety of OMT suggests
that OMT should be initially offered as a noninvasive therapy to patients with
SDB [20].
Although there are other possible treatment options for some patients with OSA,
such as oral appliances or surgery, Rueda etal. consider OMT to be noninvasive,
inexpensive, and with no major risks. It may be a safe and acceptable option for
many patients with OSA and would be economically accessible for lower-income
people and countries [21].
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After treatment
events/h AHI change (%)
Basal AHI,
event/h
27.8±20.3 30.6±21.8 10.1
−50.4
After
treatment
events/h AHI change (%)
22.4±5.4 25.9±8.5 15.6
−38.8
−11.3
25.7±5.7 22.8±7.33
14.6±5.2 15.18±3.15 4.0
−24.4%
−50.0
−9.9
4.56±3.22 4.11±2.73
−62.2
4.87±2.96 1.84±1.36
OSA Intervention group Control group
Table 16.1 The results of some studies on OMT
Mild OSA
(AHI, 5–15 events/h);
moderate OSA (AHI, 15–30
events/h); severe OSA
(AHI>30 events/h) AHI basal
26% mild 28.0±22.7 13.9±18.5
32% moderate
Diaferia etal., 2013
[17]
42% severe
Moderate OSA 22.4±4.8 13.7±8.5
Guimarães etal., 2009
[12]
n=14 mild
Ieto etal., 2015 [16] Mild to moderate OSA 22.4±4.89 19.2±6.44
Kuo etal., 2017 [18] Mild to moderate 16.5±7.93 9.9±3.56
n=11 moderate
AHI>5 events/h for those
with moderate to severe
OSA
Villa etal., 2015 [19] Paediatric participants:
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