S u r g i c a l O p t i o n s fo r t h e

Tre a t m e n t o f O b s t r u c t i v e
Sleep Apnea
a, b
Jon-Erik C. Holty, MD, MS *, Christian Guilleminault, MD, DBiol

KEYWORDS
 Obstructive sleep apnea  Sleep apnea syndromes  Surgery

Obstructive sleep apnea (OSA) is a highly prevalent condition characterized by

increased nocturnal airflow resistance resulting in repetitive episodes of pharyngeal
collapse during sleep.1 Approximately 20% of adults in the United States have OSA
(defined as an apnea-hypopnea index (AHI) R5/h) with up to 10% having moderate
to severe disease (AHI R15/h).2,3 In addition, between 3% and 10% of children
have OSA (AHI R1/h).4–7 Obesity, male gender, advancing age, and mandibular-
maxillary insufficiency are well-characterized risk factors.8 OSA predisposes to
increased cardiovascular and cerebrovascular morbidity and mortality, and is associ-
ated with excessive daytime sleepiness and neurocognitive underperformance.8
Untreated, the 15-year mortality for adults with severe disease is approximately
30% with adjusted mortality hazards ratios of 1.4, 1.7, and 3.8 for mild, moderate,
and severe disease, respectively (P-trend 5 0.004).2
Conventional nonsurgical OSA therapy necessitates indefinite positive airway pres-
sure (eg, continuous positive airway pressure [CPAP] or bilevel therapy) that works by
pneumatically stenting open the upper airway, thus preventing apneas and hypopneas
during sleep.9–11 CPAP is an effective treatment modality for OSA, improving symp-
toms (eg, excessive daytime sleepiness, quality of life) and reducing cardiovascular
mortality.12,13 Unfortunately, more than 50% of patients with OSA are intolerant of
and ultimately reject CPAP therapy.14,15 Common complaints include mask discom-
fort and leak, rhinorrhea, conjunctivitis, dry mouth, nasal congestion, aerophagia,
claustrophobia, and chest wall discomfort.6 Individuals intolerant of CPAP therapy
have a 10% absolute increased mortality risk (compared with adherent subjects) at
5 years.16,17

Contract/Grant Support: None.

Conflict of interest: None.
a
Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, VA Palo
Alto Health Care System, 3801 Miranda Avenue, Palo Alto, CA 94304, USA
b
Division of Sleep Medicine, Stanford University School of Medicine, Stanford Medical Outpa-
tient Center, 450 Broadway Street, Pavillon C, Redwood City, CA 94063-5074, USA
* Corresponding author.
E-mail address: jholty@stanford.edu

Med Clin N Am 94 (2010) 479–515

doi:10.1016/j.mcna.2010.02.001 medical.theclinics.com
0025-7125/10/$ – see front matter. Published by Elsevier Inc.
480 Holty & Guilleminault

Effective surgical therapies for OSA predate the first reported use of CPAP by Sulli-
van and colleagues9 in 1981 and Rapoport and colleagues18 in 1982. Tracheostomy
was employed as early as 196919 and Kuo and colleagues20 in 1979 (and later Bear
and Priest21 in 1980) reported the results of mandibular advancement for the treatment
of OSA. In 1952, Ikematsu22 began removing excessive oropharyngeal tissue to alle-
viate snoring and reported the results of his palatopharynoplasty with partial uvulec-
tomy in 152 habitual snorers in 1962. In the late 1970s, Fujita and colleagues23
adapted Ikematsu’s procedure and introduced the uvulopalatopharyngoplasty as
a new surgical approach to treat OSA.24 Because the anatomic cause of OSA is
heterogeneous with most OSA patients having multiple concurrent pharyngeal abnor-
malities,25–27 surgical procedures have evolved to address specific anatomic airflow
limitations and to augment the effectiveness of existing procedures. This review
describes the pathophysiology of OSA, the rationale for surgery, and the various
surgical techniques used to treat OSA.

PATHOPHYSIOLOGY OF OSA

Patients with OSA have nocturnal airflow restriction resulting from upper-airway
collapse between the naso- and hypopharynx.28 During normal breathing, contraction
of the diaphragm results in an increased thoracic volume that generates negative
intrapleural pressure drawing air down to the alveoli. During a normal negative pres-
sure inspiration, upper-airway reflexes phasically activate pharyngeal muscles (eg,
genioglossus, tensor palatini, geniohyoid, stylohyoid) to dilate and stiffen the upper
airway to maintain patency.29–32 Pharyngeal dilator muscle activity is reduced in
normal and OSA individuals during sleep.30,33 However, patients with OSA have
anatomically smaller upper airways and diminished pharyngeal dilator tone resulting
in clinically significant airflow limitation (eg, apneas and hypopneas) during nocturnal
negative pressure inspiration.28,34,35 Most individuals with OSA have multiple pharyn-
geal abnormalities25 with anatomic airway narrowing primarily in the lateral
dimension.36,37
In addition, patients with OSA are often obligatory mouth breathers during sleep.38
Nasal breathing (compared with mouth breathing) is more efficient because the nasal
cavity has a more constant resistance (compared with the oral cavity) and because
stimulation of nasal receptors is involved in activating the pharyngeal dilators.39 In
normal individuals, a transition from nasal to oral breathing results in a greater risk
of pharyngeal collapse because of greater negative inspiratory pressures needed to
overcome increased airway resistance.39 Experimental nasal obstruction40–42 or inhib-
iting the nasopharyngeal reflex (by applying topical anesthesia)43 causes nocturnal
apneas, hypopneas, and oxygen desaturation in normal individuals.
OSA is in part a neurologic disorder of the upper airway.30,33,44,45 Pharyngeal
collapse is often caused by abnormal activation of pharyngeal dilator muscles from
dysfunctional pharyngeal reflexes.46 In patients with nocturnal upper-airway resis-
tance, repetitive vibratory trauma (eg, snoring) and tremendous swings in pharyngeal
pressures (caused by apneas and hypopneas) during sleep results in pathologic injury
to the pharyngeal dilator muscles and nerves.33,47,48 This irreversible damage predis-
poses the upper airway to inspiratory collapse during sleep.45,49–51

RATIONAL FOR OSA SURGERY

The aim of OSA surgery is to eliminate airway collapse and reduce airway resistance
during sleep without causing impairment to the normal functions of the upper airway
and associated structures. Indications for surgery depend on: (1) the severity of OSA
 OSA Surgical Treatment 481

and comorbid medical conditions; (2) the severity of symptoms (eg, excessive daytime
sleepiness); and (3) the anatomic location(s) causing obstruction. General indications
for surgery include moderate-severe OSA, severe excessive daytime sleepiness (even
when the AHI is %20/h), OSA with comorbid conditions (eg, arrhythmias, hyperten-
sion), OSA with anatomic airway abnormalities, and failure of medical OSA manage-
ment.52 Upper-airway abnormalities amenable to surgery include those within the
nasal cavity (eg, deviated septum, polyps, hypertrophic turbinates, collapsible nasal
valves), nasopharynx (eg, stenosis, adenoids), oropharynx (eg, palatine tonsils, elon-
gated uvula, redundant mucosal folds, low hanging palate, webbing), and hypo-
pharynx (eg, lingual tonsils, large tongue base, redundant aryepiglottic folds)
(Table 1). Relative contraindications to surgery include morbid obesity (except for
bariatric surgery and tracheostomy), severe or unstable cardiopulmonary disease,
active alcohol/illicit drug abuse, older age, unstable psychological problems, or unre-
alistic expectations from surgical therapy.
All adult OSA patients should be offered a nonsurgical treatment option (eg, CPAP)
before proceeding to surgery. Even in patients electing to proceed directly to surgery,
a trial of CPAP therapy may be helpful as this is a noninvasive means to determine the
expected extent of symptom abatement after surgery. Preoperative CPAP is indicated
in patients with severe OSA (AHI >40/h with severe nocturnal oxygen desaturation
<80%) and should be continued postoperatively until 2 weeks before the postopera-
tive polysomnogram.53
In children, early recognition of OSA and prompt correction of anatomic upper-
airway abnormalities is paramount. By the age of 4 years, 60% of the adult craniofacial
skeleton is attained, with 90% by age 12 years.54–56 Children with pharyngeal obstruc-
tion (eg, tonsillar hypertrophy, turbinate enlargement) protect the patency of the
airway by sleeping in the prone or side position with an extended, flexed head, and
an anteriorally displaced tongue.57 Anterior displacement of the tongue is associated
with narrower upper and shorter lower dental arches,57–61 posterior displacement of
the mandible,60,62 with resultant development of mandibular retrusion, increased over-
jet, and facial height63–68 (all known risk factors for OSA).58,69 Thus, early recognition

Table 1
Anatomic location of pharyngeal obstruction in relationship to surgical procedure

Anatomic Treatment Effect Anatomic Obstruction Surgical Procedure

1. Bypass upper airway Collapsed airway Tracheostomy
2. Soft tissue removal Nasal cavity Polypectomy, radiofrequency
ablation of the turbinates
Nasopharynx Adenoidectomy
Oropharynx Tonsillectomy
Uvulopalatopharyngoplasty
Laser-assisted
uvulopalatoplasty
Hypopharynx Midline glossectomy
Tongue base reduction
3. Skeletal/soft tissue modification Nasal cavity Septoplasty
Oropharynx Rapid maxillary expansion
Hypopharynx Mandibular advancement
Genioglossal advancement
Hyoid myotomy suspension
Oro- and hypopharynx Maxillomandibular
advancement
482 Holty & Guilleminault

and surgical correction of significant airway obstruction in children is necessary to

prevent abnormal craniofacial development and the irreversible damage to the
pharyngeal dilator reflexes that potentially can lead to the lifelong consequences of
OSA.
In adults and children, preoperative upper airway assessment is necessary to deter-
mine the level of obstruction (anywhere between the nose and epiglottis) and plan the
optimal surgical approach. Preoperative fiberoptic endoscopy (performed with
a Müller maneuver) and cephalometric analysis are helpful to classify the type of
airway obstruction and identify obstructions of the hypopharynx.26,70 Computed
tomography may have added benefit.71 The anatomy of the upper airway is classified
into 3 general obstructive types (Fujita classification): (1) type 1: narrow oropharynx
(eg, large tonsils, enlarged uvula, pillar webbing) with normal palatal arch position;
(2) type 2: low arched palate with relatively large tongue; further subdivide into 2a
(predominantly oropharyngeal abnormality) and 2b (abnormality involves oro- and
hypopharynx); (3) type 3: hypopharyngeal obstruction (eg, retrognathia, floppy
epiglottis, enlarged linguinal tonsils) with normal oropharynx.72,73 The type of obstruc-
tion is often modified whether nasal obstruction concurrently exits. Surgical proce-
dures address specific upper-airway abnormalities (eg, uvulopalatopharyngoplasty
for type 1, genioglossus advancement for type 3, maxillomandibular advancement
for combined type 1, 2 and 3). Preoperative pharyngeal anatomy, OSA severity, and
patient preference (eg, recovery time, prolonged facial paresthesias, and malocclu-
sion) are all contributing factors influencing the surgical decision.

SURGICAL SUCCESS

Various surgical procedures are now available to increase the posterior airspace and
treat OSA in CPAP intolerant patients. However, no surgical treatment is 100% effec-
tive. Similar to previous reviews of OSA surgery,74,75 we defined surgical success as
an AHI less than 20 and a reduction in AHI of 50% or more after surgery.76 Where
possible, we provide surgical cure rates (defined as an AHI <5/h in adults and <1/h
in children).77

PHARYNGEAL SURGICAL PROCEDURES

Individual surgical procedures are described in the following sections for the treatment
of OSA organized by the treatment effect on the anatomic airway obstruction (eg,
bypassing the upper airway obstruction, removal of soft tissue structures, or skeletal
(or soft tissue) modification) (see Table 1).
Procedures that Bypass the Upper Airway Obstruction
Tracheostomy
In 1965, Valero and Alroy78 reported improvement in nocturnal oxygenation in a patient
with progressive respiratory failure secondary to traumatic micrognathia. Kuhlo and
colleagues in 196919 followed by Lugaresi and colleagues in 197079,80 were the first
to effectively treat OSA (or Pickwickian syndrome) by means of a tracheostomy. By
bypassing the upper airway, tracheostomy is purported to be curative for OSA.81
Although many studies purport resolution of airway obstruction after tracheos-
tomy,82–85 relatively few studies report pre- and posttracheostomy polysomnography
parameters (eg, AHI) (Table 2).81,86–91
The largest case series (n 5 50) reported complete resolution of obstructive
apneas after tracheostomy.81 Of 9 studies evaluating 61 patients, tracheostomy
was highly effective at eliminating obstructive apneas (apnea index went from
 Table 2
Efficacy of tracheostomy for OSAa

Demographics Apnea Indexb AHI (REM)c Apnea-Hypopnea Index (NREM)c

Follow-up
Study N Age (y) (mo) Pre-Trach Post-Trach P-valued Pre-Trach Post-Trach P-valued Pre-Trach Post-Trach P-valued
Haapaniemi et al, 7 53.4  9.8 60.9  30.7 – – – – – –
200186
Kim et al, 199887 23 47.0  12.4 – – – 58.5  34.1 26.0  31.2 92.5  39.1 19.8  26.3
Fletcher, 198995 1 – 51.0 114.0 0.0 – – – –
Fletcher et al, 8 55.4  6.8 9.0  3.2 84.6  38.7 0.0  0.0 – – – –
198788
Guilleminault 4 – 30.0  6.9 94.5  19.8 0.4  0.5 – – – –
et al, 198181
Sugita et al, 1 40.0 3.0 77.0 0.0 – – – –
198090
Weitzman et al, 10 47.5  2.4 0.3  0.4 96.1  21.9 1.1  3.3 79.0  18.6 26.5  25.2 113.7  23.0 25.8  25.4
198096
Motta et al, 6 47.0  4.0 7.5  6.3 73.0  12.2 0.0  0.0 – – – –
1978101
Weitzman et al, 1 67.0 0.5 96.7 4.1 – – – –
1978100
Summary 61 49.3  9.9 19.0  26.3 88.4  25.7 0.5  1.9 <0.001 63.8  31.9 26.2  29.2 <0.001 98.9  36.0 21.6  25.8 <0.001

Abbreviations: N, number; NREM, nonrapid eye movement sleep; REM, rapid eye movement sleep; Trach, tracheostomy.
a
Mean (or percent)  standard deviation. – denotes not reported.
b
The apnea index is the average number of obstructive apneas per hour during sleep.
c
The AHI is the average number of obstructive apneas and hypopneas per hour during sleep.
d
P-value calculated via an extended t-test and evaluates pre- and posttracheostomy measures.

483
484 Holty & Guilleminault

88/h before to 0.5/h after tracheostomy; P<.001) (see Table 2). However, patients
may have persistent hypopneas with a surgical success rate of approximately
73% (see Tables 2 and 3). Rodman and Martin92 reported persistent (although
generally improved) obstructive apneas and oxygen desaturations in 3 morbidly
obese patients after tracheostomy caused by kinking of the tracheostomy tube
during sleep or external obstruction by the patient’s own soft tissues. Haapaniemi
and colleagues86 reported that although obstructive apneas improved after trache-
ostomy (mean follow-up 5.1 years), most patients had persistent oxygen desatura-
tions with many having oxygen dip indexes (R4%) of R15/h. Fletcher and
Brown93 reported persistent REM-associated desaturations after tracheostomy in
patients with OSA with concomitant chronic obstructive pulmonary disease.
Despite improvements in obstructive apneas after tracheostomy, emergence or
worsening of central apneas is frequently observed, although generally resolves
within 3 to 6 months.80,81,89,94–98
Tracheostomy is effective at preventing OSA-related arrhythmias,98–100 reducing
pulmonary artery pressures,80,81,101 and improving hypertension81,88,100–103 and
diabetes102 in patients with OSA. Many (but not all)86 studies have reported near complete
resolution of nocturnal symptoms and daytime sleepiness.80,81,84,90,91,96,100,101,103–106 A
retrospective analysis by He and colleagues107 suggested a mortality benefit of tracheos-
tomy (0% vs 38% mortality at 8 years) compared with no OSA therapy. Partinen and
colleagues108,109 found similar mortality benefits (0% vs 11% at 5 years) after
tracheostomy.
Unfortunately, tracheostomy has several problems including patient dissatisfaction
(eg, psychosocial aspects), perioperative complications (eg, wound infection, tissue
necrosis, bleeding), recurrent bronchitis, granulation tissue, trachea-innominate fistula
formation, and stoma stenosis (often requiring surgical revision).105,110–115 Periopera-
tive mortality is higher in obese individuals than in nonobese individuals.116 Permanent
tracheostomy (either tube111 or tube-free117) is currently used in highly select cases
with severe OSA who are intolerant of CPAP (and poor candidates for other surgical
procedures). A temporary tracheostomy is occasionally used before other OSA proce-
dures (eg, uvulopalatopharyngoplasty, bariatric surgery) to protect the airway, partic-
ularly in morbidly obese subjects.118
Closure of a permanent tracheostomy (after resolution of OSA by other surgeries or
weight loss119) may be associated with a relatively high complication rate (w30%),
especially when done with a 3-layer as opposed to a de-epithelialization tech-
nique.120,121 In addition, long-term tracheostomy may cause pharyngeal tissue
obstruction (eg, granulation tissue, tracheomalacia) that may predispose to OSA after
closure.122,123

Procedures that Remove Soft Tissue

Laser-assisted uvulopalatoplasty (LAUP)
This office-based procedure (similar to uvulopalatopharyngoplasty, but omitting
tonsillectomy) uses a CO2 laser to shape the soft palate and is an effective surgical
technique for snoring (w90% success), but has limited OSA efficacy (see Table 3).124
Two randomized trials of LAUP found no significant change in the AHI after surgery
compared with those randomized to no surgery.125,126 A meta-analysis of these 2
studies found no statistically significant difference in daytime sleepiness (measured
by the Epworth sleepiness scale) between surgery and control groups (mean differ-
ence 1.4; 95% confidence interval [CI] 5.0–2.2).127 More worrisome is that LAUP
may worsen OSA in up to 21% of patients.128 LAUP is not approved by the American
Academy of Sleep Medicine to treat OSA.129 In addition, complications are common
 Table 3
Comparison of surgical efficacy for OSAa

Demographics AHIb
Study N Studies Age (y) Before Surgery After Surgery % Change Cure (%)c Success (%)c Ref.
f 338,339
Bariatric surgery 437 16 38.8  14.9 53.3  38.2 15.3  18.7 72.6  60.6 44 –
134
GA 91 4 – 53.9 17.3 67.8 – 62
134
HS 101 4 – 38.7 25.0 33.0 – 50
134
HS and GA (or mortised genioplasty) 328 7 – 33.5 15.2 58.0 – 55
77
LAUP 72 3 – – – – 7 49
266
MMA 627 22 44.4  9.4 63.9  26.7 9.5  10.7 85.0  18.2 43 86
134
Midline glossectomy 74 5 – 53.0 24.2 54.4 – 50
134
Radiofrequency ablation (tongue) 394 11 – 37.0 23.4 35.7 – 36
RME
320
Children 88 3 7.1  0.7 10.9  4.7 0.8  1.3 91.0  20.2 – –
d 321
Adults 10 1 27.0  0.6 19.0  1.3 7.0  1.3 63.2  7.1 70 90
177,178
Tonsillectomy 1,079 23 6.5 18.6 4.9 73.7 60 –
134
Tongue base suspension 77 6 29.0 16.3 32.9 – 35
e 87,96
Tracheostomy 33 2 47.2  10.4 98.9  36.0 26.2  29.2 79.2  25.8 – 73
75,77
UPPP 992 37 48.1 60.0 – 38.2 16 52
Multimodality surgeryg 1,978 58 46.2 48.0 – 60.3 – 66 74

OSA Surgical Treatment

Abbreviations: BMI, body mass index; GA, genioglossus advancement; HS, hyoid suspension; LAUP, laser-assisted uvulopalatoplasty; MMA, maxillomandibular
advancement; N, number; RME, rapid maxillary expansion; UPPP, uvulopalatopharyngoplasty.
a
Plus-minus values are mean (or percent)  standard deviation. – denotes not reported.
b
The AHI is the average number of apneas and hypopneas per hour during sleep.
c
Surgical success defined as the percent of subjects with an AHI <20/h and a R50% reduction in the AHI after surgery. Surgical cure defined as an AHI <5/h after
surgery. For tonsillectomy, surgical cure was defined as an AHI <1/h after surgery.
d
Surgically assisted RME involved horizontal osteotomies.
e
The AHI for tracheostomy reported during non-REM sleep only and included only obstructive apneas and hypopneas.
f
A statistical significant reduction in BMI was noted at 18 months after bariatric surgery (pre-BMI 53.9  15.7 vs post-BMI 37.8  14.8 kg/m2; P<.001).
g
Multimodality surgery refers to simultaneous nasal, palate, and/or base of tongue surgery for OSA.

485
486 Holty & Guilleminault

including early postoperative pharyngeal edema,130,131 with up to 59% complaining of

persistent side effects (27% difficulty swallowing; 27% globus sensation in throat)
after LAUP.127

Midline glossectomy
Surgical removal of the center portion of the tongue base (usually via laser) was
proposed by Fujita and colleagues132 and Woodson and Fujita133 in 1991 for the treat-
ment of OSA in patients with hyopharyngeal obstruction. A review of 5 case series (n 5
74) showed a surgical success rate of approximately 50% (see Table 3).134 Postoper-
ative bleeding and pharyngeal edema requiring protective tracheostomy is not
uncommon after surgery.132,133
Radiofrequency ablation of the tongue
Radiofrequency ablation uses a probe to precisely direct temperature-controlled
radiofrequency energy to heat (between 60 and 90 C) and ablate target tissues
without causing collateral damage to adjoining structures.135 Radiofrequency treat-
ment of the tongue base does not require general anesthesia, but usually requires
multiple treatment sessions over several weeks, and is successful at eliminating
snoring.135–137 Eleven case series describing 394 patients with OSA (mean AHI 37/h)
undergoing radiofrequency ablation of the tongue reported a surgical success rate
of only 36% (see Table 3).134 Statistically significant improvements in subjective
daytime sleepiness and health-related quality of life were observed in most, but not
all studies.135,138–145 Radiofrequency ablation of the tongue is generally considered
adjunctive (not primary) OSA treatment in select patients.134

Radiofrequency ablation of the turbinates (and other nasal procedures)

A relationship between nasal obstruction, mouth breathing and symptoms of OSA was
first described in the 1800s.146–150 Increased nasal resistance may result from septal
deviation, turbinate hypertrophy, chronic nasal congestion, polyps, or collapsible
valves. Various procedures include polypectomy, radiofrequency ablation of the turbi-
nates, alar valve or rim reconstruction, and septoplasty (eg, straightening of the
septum). Nasal surgery is generally not curative,151,152 but can improve the AHI, and
is often used in a multimodality surgical approach or to decrease CPAP pressure
requirements.153–155 In addition, surgical correction of nasal obstruction improves
health-related quality of life in patients with OSA.156
Inferior turbinate enlargement is a frequent cause of nasal obstruction. Radiofre-
quency ablation is a highly successful surgical procedure producing volumetric inferior
turbinate reduction. Radiofrequency ablation heats the hypertrophied turbinates
causing scar tissue with resulting shrinkage over 1 to 3 weeks.157 This procedure is
generally performed in the outpatient setting with minimal discomfort beyond nasal
stuffiness lasting 3 to 5 days.158
Radiofrequency volumetric soft palate tissue reduction (somnoplasty)
Somnoplasty involves directed radiofrequency energy to ablate and reduce soft
tissues of the palate.157,159–161 Decreased snoring occurs via scar-induced stabiliza-
tion of the soft palate. Although symptom (eg, snoring) improvement after surgery is
reported,136,162 evidence for improvement of OSA is lacking.163–165 A recent random-
ized placebo-controlled trial in patients with mild OSA found no statistically significant
improvement in the AHI or symptoms after somnoplasty.166
Tonsillectomy
Tonsillectomy is one of the most common surgical procedures in children.167,168 OSA
is a frequent indication for tonsillectomy and is considered first-line therapy for
 OSA Surgical Treatment 487

children with OSA.167,169 Surgical tonsillectomy techniques vary, but generally

complete resection of the tonsils with adenoidectomy (if necessary) is preferred
(Fig. 1).170 Partial intracapsular tonsillectomy (eg, tonsillotomy) has been found to
reduce postoperative morbidity (eg, pain),171–175 but postoperative objective
measures of efficacy (eg, AHI reduction) are lacking.176
Tonsillectomy is curative (AHI <1/h) in 60% of pediatric cases of OSA (see
Table 3).177,178 Higher presurgery AHI and body mass index (BMI, calculated as
weight in kilograms divided by the square of height in meters) are risk factors for
residual disease after tonsillectomy.179,180 In complicated cases of pediatric OSA
(eg, morbid obesity, severe OSA), tonsillectomy is curative in 39% of children
compared with 74% in uncomplicated cases.178 Children with residual OSA after
tonsillectomy may benefit from rapid maxillary expansion.181 Tonsillectomy improves
quality of life parameters (short- and long-term) in children with OSA,182,183 with
improvements in behavior scores184 and sleep disturbances.185,186
Self-limited pain and swelling of the throat is common after tonsillectomy. Risks for
postoperative complications include younger age (<24 months), increased severity of
OSA, craniofacial abnormalities, obesity, poor functional status (eg, hypotonia, failure
to thrive) and cor pulmonale.182,187 Life-threatening complications are rare,188 but
postoperative respiratory failure requiring mechanical ventilation (usually transiently
during postsurgery recovery) occurs in approximately 30% of children.187,189
However, children left intubated electively after tonsillectomy have higher complica-
tion rates.190 Hemorrhage, dehydration, and pulmonary edema occur in approximately
9% of cases.191

Uvulopalatopharyngoplasty
Fujita and colleagues23 and Conway and colleagues24 adapted Ikematsu’s surgical
snoring procedure22 and reported his uvulopalatopharyngoplasty (UPPP) results for
treating OSA in 1980. This operation enlarges the oropharyngeal airway lumen by

Fig. 1. Tonsillectomy. The primary treatment of OSA in children with tonsillar enlargement is
tonsillectomy usually with concurrent adenoidectomy. To prevent collapse and improve OSA
success, it is preferable that the lateral pharyngeal walls are sutured.
488 Holty & Guilleminault

excising redundant tissues from the soft palate, tonsillar pillars, and uvula (Fig. 2).
UPPP is currently the most widely performed OSA pharyngeal surgical technique in
adults.77 Several variations of the UPPP have been proposed including the methods
of Fujita and colleagues,23,192,193 Simmons and colleagues,194 Fairbanks,195 Dickson
and Blokmanis,196 Friedman and colleagues,197 and Powell and colleagues198 (uvulo-
palatal flap surgery). Uvulopalatal flap surgery (Fig. 3) reduces the risk of nasopharyn-
geal incompetence and is associated with less postoperative pain, but is
contraindicated in patients with excessively long or bulky soft palates (or
uvulas).199–201 Woodson and Toohill202 developed transpalatal advancement phar-
yngoplasty, which combines a UPPP with removal of the posterior hard palate (via
a curvilinear palatal incision), with subsequent advancement of the mucoperiosteal
flap and suturing to the alveolar mucoperiosteum (Fig. 4). This technique is associated
with a decrease in retropalatal collapsibility and an increase in the retropalatal
airspace compared with traditional UPPP, and may provide higher surgical success
and cure rates.201,203
There are no known randomized controlled trials of UPPP that assess pre- and post-
surgery AHI,74,204,205 and many studies do not report objective postsurgery sleep
data.206 One randomized trial found no statistically significant difference in the oxygen
desaturation index between the surgery and conservative management groups.204,207
UPPP is highly effective for eliminating snoring, with success rates between 70% and
90%.193 However, several meta-analysis have reported surgical success rates for
OSA between 40% and 60%, and a surgical cure rate (an AHI <5/h) of only 16%

Fig. 2. Uvulopalatopharyngoplasty. This operation enlarges the oropharyngeal airway

lumen by excising redundant tissues from the soft palate, tonsillar pillars, and uvula. Shown
is Friedman’s submucosal uvulopalatopharyngoplasty technique (A–F). (Reproduced from
Friedman M, Schalch P. Surgery of the palate and oropharynx. Otolaryngol Clin N Am
2007;40:835; with permission from Elsevier.)
 OSA Surgical Treatment 489

Fig. 3. Uvulopalatal flap. A modification of Fujita’s uvulopalatopharyngoplasty involves

retracting and advancing the uvula superiorly under the soft palate without removal.

(see Table 3).74,75,134 A recent retrospective analysis of the Mayo Clinic experience
found a similar UPPP cure rate of 24%.208 Predictors of surgical cure in this analysis
included younger age, lower preoperative BMI and AHI. Unfortunately, most patients
with initial improvement in AHI after UPPP have recurrence within 5 years of
therapy.209 Fortunately, UPPP likely confers a mortality benefit in CPAP intolerant

Fig. 4. Transpalatal advancement pharyngoplasty. Woodson’s transpalatal advancement

pharyngoplasty combines a uvulopalatopharyngoplasty with soft palate advancement. (Re-
produced from Friedman M, Schalch P. Surgery of the palate and oropharynx. Otolaryngol
Clin N Am 2007;40:840; with permission from Elsevier.)
490 Holty & Guilleminault

patients (compared with no treatment), even when most patients do not obtain
surgical cure.210–212 However, because UPPP is likely to eliminate snoring but will
often leave residual OSA causing silent apnea, all patients must have postoperative
sleep studies to rule out persistent disease.
UPPP is generally more effective at reducing apneas than hypopneas,75,193 and is
most effective in patients with primarily oropharyngeal obstruction (as opposed to
hypopharyngeal abnormalities).70,193 However, using fiberoptic endoscopy to select
patients with predominantly soft palate pharyngeal collapse during a Müller maneuver
has shown variable improvement in surgical success (45%–85%).213–216 Although the
efficacy to cure OSA is suboptimal, UPPP may be useful in lowering positive airway
pressure requirements, thus improving CPAP compliance in select patients.217
However, UPPP may promote air leak during future CPAP therapy,218,219 although
a recent study disputes this finding.220 Approximately 70% of patients are satisfied
after UPPP.221,222
Early postoperative complications include wound dehiscence, hemorrhage, infec-
tion, and transient velopharyngeal incompetence (eg, nasal regurgitation and hyper-
nasal speech).195 Late postoperative complications include pharyngeal discomfort
(eg, dryness, tightness), postnasal secretions, dysphagia, inability to initiate swallow-
ing, odynophagia, nasopharyngeal stenosis, taste and speech disturbances, tongue
numbness, and rarely permanent velopharyngeal incompetence. Up to 30% of
patients complain of persistent although generally mild dysphagia.223–226 A systematic
review reported a serious complication rate of 2.5% with 30 deaths (w0.2% mortality)
and persistent side effects in 58% (31% nasal regurgitation, 13% voice changes, 5%
taste disturbances) of patients after UPPP.127 Voice changes are generally mild.227 A
recent study noted that health-related quality of life measurements were better in
patients with post-UPPP side effects compared with CPAP users (independent of
compliance) with side effects.228
Procedures that Modify or Advance the Skeletal or Soft Tissue Structures
Genioglossus advancement
In the mid-1980s, Riley and colleagues229,230 first described genioglossus muscle
advancement (GA) to improve the posterior airspace (eg, base of tongue). Their initial
technique (a modified horizontal mandibular osteotomy) was later improved in 1986 to
include a limited inferior parasagittal mandibular osteotomy (Fig. 5).230,231 Advancing
the geniotubercle forward of the mandible positions the genioglossus and geniohyoid
muscles anteriorly, thus enlarging the retrolinguinal space.232 Variations of this proce-
dure include mortised genioplasty, circle genioplasty, and standard genioplasty.233,234
Four case series describing 91 patients with severe OSA (mean AHI 54/h) undergoing
GA as sole treatment report a surgical success rate of 67% (range 39%–79%) (see
Table 3).134 GA is generally used within a multimodality approach to treat base of
tongue obstructions.

Hyoid myotomy and suspension

In the mid-1980s, Riley and collagues229,230,235 developed a hyoid suspension proce-
dure to improve the posterior (retrolinguinal) airspace (Fig. 6). The hyoid bone is
located in the anterior neck below the mandible and is involved in maintaining upper
airway patency.236,237 Several protocols have been described including hyoid to
mandibular suspension (hypomandibular), hyoid to thyroid cartilage suspension (thy-
rohyoid), and hyoid expansion.238 Hyoid suspension is generally used within a multi-
modality approach238–240 with a surgical success rate (performed with previous or
concurrent palate surgery) of approximately 50% (see Table 3).134 However, there
 OSA Surgical Treatment 491

Fig. 5. Mandibular osteotomy with genioglossus advancement. Limited inferior parasagittal

mandibular osteotomy (eg, a rectangular window in the symphyseal bone with advance-
ment, rotation, and immobilization of the geniotubercle) with advancement of the genio-
glossus and geniohyoid muscles. (Reproduced from Li KL. Hypopharyngeal airway surgery.
Otolaryngol Clin N Am 2007;40:848; with permission from Elsevier.)

are no reliable preoperative predictors for success with hyoid suspension following
UPPP.241 Furthermore, combining genioglossus advancement with hyoid suspension
marginally improves surgical success (w55%) (see Table 3),134 and 1 study of hyoid
suspension with radiofrequency of the tongue reported a surgical success rate of only
49%.242 Excessive daytime sleepiness generally improves after hyoid suspension,
albeit inconsistently.239,243–246

Mandibular (or maxillary) distraction osteogenesis

Distraction osteogenesis (DO) of the mandible (and/or maxilla) involves bilateral
segmental osteomies followed by gradual distraction (via an expandable intra- or
extraoral device) with subsequent ossification and bone lengthening.247 DO of the
mandible effectively improves OSA in children with genetic craniofacial abnormali-
ties.248–251 One study of 5 otherwise normal adults with OSA reported a decrease in
AHI from 49/h to 7/h after mandibular (or maxillary) DO.247 However, this study

Fig. 6. Hyoid myotomy suspension. Hyoid to thyroid cartilage suspension (thyrohyoid)

involves isolation of the hyoid bone that is advanced, sutured, and immobilized to the
thyroid cartilage. (Reproduced from Li KL. Hypopharyngeal airway surgery. Otolaryngol
Clin N Am 2007;40:848; with permission from Elsevier.)
492 Holty & Guilleminault

reported several problems with DO including the technical difficulty of the procedure,
a high risk of malocclusion, subsequent need for orthodontics because of limited
control of the distractor vector, and poor patient satisfaction (eg, treatment required
4 months of stabilization via intraoral arch bars that inhibited mastication and speech).

Maxillomandibular advancement
In 1979, Kuo and colleagues20 reported improvements in polysomnographic parame-
ters and subjective sleepiness in 3 patients with OSA with retrognathia after mandib-
ular osteotomy with advancement. Similar improvements in OSA parameters after
mandibular advancement were noted by others.21,252,253 However, by the mid-
1980s, mandibular advancement alone was largely supplanted by combined maxillary
and mandibular advancement to preserve the maxilla-mandibular relationship and
from the recognition that the physiologic cause for OSA is often from concomitant
mandibular and maxillary deficiency.235,254 Mandibular osteotomy with advancement
is currently relegated to the treatment of mandibular hypolasia in syndromic children
with OSA.255
Maxillomandibular advancement (MMA) involves Le Fort I maxillary and bilateral
sagittal ramus split mandibular osteomies with advancement of the maxilla and
mandible followed by rigid fixation (Fig. 7).256 Generally, the maxilla is advanced first,
with the mandible advanced into occlusion. Combined MMA alleviates pharyngeal
obstruction by expanding the skeletal framework that the tongue and other soft tissue

Fig. 7. Maxillomandibular advancement. Before (A) and after (B) maxillomandibular

advancement surgery via a Le Fort I osteotomy (with rigid plate fixation) and bilateral
sagittal split mandibular osteotomy (with bicortical screw fixation). (Reproduced and modi-
fied from Li KL. Hypopharyngeal airway surgery. Otolaryngol Clin N Am 2007;40:849; with
permission from Elsevier.)
 OSA Surgical Treatment 493

structures attach to resulting in reduced upper-airway restriction and collapsibility

during inspiration.257 Mandibular advancement advances the tongue and suprahyoid
muscles.258 Maxillary advancement pulls forward the velum and velopharyngeal
muscles,259 increases the nasopharyngeal and hypopharyngeal spaces,260,261 and
increases alar width with a concomitant decrease in nasal airway resistance.262,263
Improvements in pharyngeal obstruction after MMA occur along the entire upper
airway in the lateral and anterioposterior dimensions.27,264
MMA is the most effective craniofacial surgery (in adults) for the treatment of
OSA.76,265 A recent meta-analysis of 22 studies (627 subjects with OSA) determined
that MMA is highly effective with a mean decrease in AHI from 64/h to 11/h (P<.001)
with pooled surgical success and cure (AHI <5/h) rates of 86% and 43%, respectively
(see Table 3).266 Predictors of increased surgical success include younger age, lower
preoperative AHI and BMI, and greater degree of maxillary advancement.266 Further-
more, MMA maintains its efficacy at long-term follow-up.267,268 Following MMA, most
patients report improvements in health-related quality of life, depression, excessive
daytime sleepiness, memory impairment, and hypertension.267,269–279 Candidates
for MMA include adults and adolescents (after the cranial sutures have completely
ossified) with maxillomandibular insufficiency or those who have failed previous ther-
apeutic interventions for OSA.256,265 In addition, MMA is successful in patients with
obesity or with severe OSA.265
MMA is generally safe with no reported deaths and a major complication rate of only
1.0% (mostly cardiac causes).266 Between 0% and 15% of MMA patients experience
mild surgical relapse without apparent symptoms or worsening of the AHI.267,280–282
However, relapse is not associated with the degree of mandibular advance-
ment.281,283,284 Mild malocclusion occurs in up to 44% of patients and is generally
treatable with prosthetics or minor occlusional equilibration.267,285 Transient facial
paresthesia (ie, inferior alveolar nerve neurosensory deficits) after MMA is common
(w100%), although most cases (86%) resolve within 1 year.266 Velopharyngeal insuf-
ficiency or mild speech and swallowing deficits are rarely reported after
MMA.272,280,286,287 Patients completing sequential phase I (UPPP) and phase II
(MMA) surgery generally report less pain after MMA compared with phase I
surgery.287,288 The average hospitalization time is less than 1 week with most patients
returning to work within 4 to 10 weeks after surgery.275,288
After MMA, most patients report a positive perception of facial aesthetics.289 Li and
colleagues289,290 noted 6 months after surgery that 50% of patients report a younger
facial appearance, 36% report a more attractive appearance, and only 9% report
a less attractive facial appearance. In this same study, all patients (100%) reported
satisfaction with the surgical outcome. Three other studies reported no patients
(0%) were bothered by postoperative facial aesthetics.272,274,286 Modified MMA tech-
niques, particularly using counterclockwise rotation and pre- or postsurgical ortho-
dontics, have been developed to prevent maxillary protrusion and improve
aesthetics.291

Maxillomandibular expansion
Surgically assisted maxillomandibular expansion (MME; limited osteotomy at Le Fort I
level and midline maxilla followed by expansion) may be an effective therapy for OSA
in adults (Fig. 8).292,293 One study (n 5 6) reported improvements in excessive daytime
sleepiness and OSA (AHI from 13/h to 5/h) at a mean follow-up of 18 months after an
average mandibular and maxillary expansion of 9.5 and 10.3 mm, respectively.293 The
investigators concluded that nonobese adolescents or young adults with mild OSA
and who require orthodontic treatment are ideal candidates for MME.
494 Holty & Guilleminault

Fig. 8. Maxillomandibular expansion. Before (A) and after (B) surgically assisted maxillo-
mandibular expansion with Le Fort I osteotomy and pterygomaxillary (midline) dysjunction
followed by expansion using a orthodontic screwlike device.

Pillar palatal implants

This minimally invasive procedure involves inserting matchstick size rigid polyester
implants via a hollow needle delivery tool into the soft palate.294 Pillar implants
improve snoring by stiffening the soft palate, but their effect on OSA is less clear
and the long-term benefits on OSA are unknown.295–298 In a prospective nonrandom-
ized trial of 25 patients with mild-moderate OSA (mean AHI 16.2/h), the surgical
success and cure rates were 40% and 28%, respectively.296 Friedman and
colleagues295 in a randomized trial of 62 nonobese patients with mild-moderate
OSA (mean AHI 23.5/h), found a statistically significant improvement in AHI after pillar
implants (compared with placebo procedure), although the mean AHI after surgery
was still within the moderate range (mean AHI 15.9/h) with a surgical success rate
of 45%. Complications are rare, but include infrequent postinsertion extrusion.

Rapid maxillary expansion

In 1860, Angell299 reported the first use of rapid maxillary expansion (RME) to correct
a transverse maxillary deficiency. RME is currently a common orthodontic procedure
to correct dental crowding and to ensure a normal mandibular-maxillary relation-
ship.300 RME expands the mid-palatal suture via a screw-type orthodontic appliance
resulting in an increase in the upper transverse width.300 RME induces normal tongue
positioning via palatal widening and flattening, downward and forward displacement
of the maxilla, widening of the nasal vault (with subsequent decreased resistance
and improvement in nasal breathing) and transforms a class III to a class I prognathoid
position.301–312 After 2 to 4 weeks of expansion, a 2- to 6-month retention period is
necessary while ossification between the expanded mid-palatal suture line is
completed.304 The suture line in prepubertal children is cartilaginous and easily
 OSA Surgical Treatment 495

separated, but horizontal osteotomy is often required in adults (whose suture line is
generally ossified) before RME.313
Children without known OSA often report quieter nighttime breathing, reduced
snoring, and improved sleep quality after RME.303,314,315 In 1996, Palmisano and
colleagues316 reported the first use of RME to successfully treat OSA (AHI went
from 22/h to 4/h) in a 22-year-old with maxillary constriction and a class I malocclu-
sion. Subsequently, 3 studies evaluating RME in children with OSA (n 5 88; mean
expansion 6.2  2.1 mm)181,317–319 reported a mean decrease in AHI from 11/h to
0.8/h after RME (P<.001) with subjective improvements in snoring, excessive daytime
sleepiness, and behavioral problems (see Table 3).320 One study of 10 adults with
OSA who received surgically assisted RME (mean expansion 12.1 mm) reported
statistically significant improvements in AHI (19/h to 4/h; P<.05) with a 70% cure
rate (AHI <5/h).321

SINGLE-STAGE MULTIMODALITY APPROACH

Pharyngeal surgeries are often combined to address airway obstruction(s) at multiple

levels (eg, nose, palate, tonsils, hypopharynx). Multilevel surgery may improve surgical
success compared with single-site therapy.322–324 The most common single-stage
multimodality procedure combines UPPP with a second procedure designed to
improve the hypopharyngeal airway (eg, genioglossal advancement, hyoid suspen-
sion, base of tongue resection [uvulopalatopharyngoglossoplasty]). Lin and
colleagues74 in a meta-analysis of 58 studies emphasized the benefits of a multimodal-
ity approach reporting a surgical success rate of 66% (see Table 3).
Unfortunately, multimodality surgery does not always guarantee increased efficacy.
A meta-analysis of hypopharyngeal surgery by Kezirian and Goldberg134 concluded
combination procedures such as genioglossus advancement with hyoid suspension
or tongue radiofrequency treatment with tongue stabilization have lower surgical
success rates and poorer AHI improvement compared with the same procedures
performed alone.

STAGED SURGICAL PROTOCOL

The Riley-Powell-Stanford surgical protocol was developed to address the multilevel

airway abnormalities that often contribute to OSA (Fig. 9).325 Phase 1 consists of inter-
ventions directed at the site(s) of obstruction in the nasal, pharyngeal, or hyopharyng-
eal regions (eg, UPPP for oropharyngeal obstruction, genioglossus advancement for
hypopharyngeal obstruction).326 Approximately 6 months after surgery, repeat poly-
somnography is performed and patients who do not obtain surgical success (or
cure), proceed to phase 2 surgery consisting of MMA.327 The Stanford group reports
a staged protocol surgical success rate of 95%.325
However, the appropriateness of the staged protocol has been questioned. Wagner
and colleagues274 noted that two-thirds of their MMA failures had previous phase 1
surgery (eg, UPPP). Others have proposed that MMA should be performed first with
UPPP (or other palatal and hypopharyngeal surgeries) performed in those patients
with residual OSA.268 A review by the American Sleep Disorders Association found
insufficient evidence to assess the efficacy of a staged verses primary MMA surgical
approach.75 A recent meta-analysis of MMA found that patients with previous UPPP
before MMA were less likely to obtain surgical cure (25% vs 45%; P 5 .002) compared
with those without previous surgery following MMA.266 However, this finding was likely
confounded by greater obesity and more severe OSA in patients with previous palatal
surgery. The investigators concluded that, ‘‘further research is needed to identify
496 Holty & Guilleminault

Fig. 9. Riley-Powell-Stanford surgical staged protocol. (Reproduced from Riley RW, Powell
ND, Li KK, et al. Surgery and obstructive sleep apnea: long-term clinical outcomes. Otolar-
yngol Head Neck Surg 2000;122:416; with permission from Mosby-Year Book, Inc.)

preoperative patient and clinical characteristics to select those patients who would
benefit most from a staged versus primary MMA surgical approach.’’266

BARIATRIC SURGERY

Approximately 65% of adults in the United States are overweight (BMI >25 kg/m2) and
more than 30% are obese (BMI >30 kg/m2).328 Surgically induced weight loss was first
performed in 1967329 and is now a preferred weight reduction modality for morbidly
obese individuals (BMI R40 kg/m2) with more than 100,000 procedures performed
annually in the United States.330 Bariatric surgery is generally safe, results in marked
and sustained weight loss, and is associated with improved mortality compared with
conventional weight-loss strategies.331–333 Procedures are classified as predomi-
nantly malabsorptive (eg, biliopancreatic diversion, duodenal switch, jejunoileal
bypass), predominantly restrictive (eg, vertical banded gastroplasty, adjustable
gastric banding, sleeve gastrectomy, intragastric balloon), or combined malabsorptive
and restrictive (eg, Roux-en-Y gastric bypass, sleeve gastrectomy with duodenal
switch).333 Candidates for bariatric surgery should fulfill the 1991 National Institutes
of Health guideline criteria that includes a BMI R40 kg/m2, or a BMI R35 kg/m2
with associated comorbidity (eg, OSA).334,335
Obesity is a leading cause of OSA with an estimated 40% prevalence in obese
persons (BMI R30 kg/m2).336 A 10% increase in BMI results in a 32% increase in
the AHI.336 Mild to moderate weight reduction can improve sleep apnea and daytime
sleepiness.336,337 Two recent meta-analyses have evaluated the effectiveness of bari-
atric surgery to treat OSA.338,339 Holty and colleagues339 found OSA to be highly prev-
alent (79%) among bariatric candidates (of these 76% had moderate to severe
disease), but exceedingly underdiagnosed (only 30% preoperatively). There were no
identifiable presurgical symptoms or clinical findings predictive of polysomnographi-
cally confirmed OSA.339 Greenberg and colleagues338 noted that after surgically
 OSA Surgical Treatment 497

induced weight loss (BMI went from 55 to 38 kg/m2), the AHI improved from 55 to 16/h
(see Table 3). However, more than 50% of bariatric recipients with preoperative OSA
have residual disease despite weight loss.339 Predictors of greater AHI reduction (or
OSA cure) included younger age, but not symptom improvement (eg, excessive
daytime sleepiness) or the degree of BMI change.338,339 In addition, initial improve-
ments in AHI appeared to wane at follow-up despite maintained weight loss.339

SUMMARY

OSA is a prevalent condition associated with increased morbidity and mortality.

Although CPAP is the preferred treatment, poor compliance is common. Fortunately,
several surgical treatments exist to address a variety of pharyngeal abnormalities.
Case series suggest that MMA has the highest surgical efficacy (86%) and cure rate
(43%). Morbidly obese individuals may benefit from bariatric surgery, although less
than 50% are cured after surgically induced weight loss. Soft palate surgical tech-
niques are less successful, with UPPP having an OSA surgical success and cure
rate of 50% and 16%, respectively. Patients may benefit from a multimodality surgical
approach. In conclusion, individuals intolerant of CPAP may benefit from surgical ther-
apies that address their particular airway obstruction(s). However, further research is
needed to more thoroughly assess clinical outcomes (eg, quality of life, morbidity),
better identify key preoperative patient and clinical characteristics that predict
success, and confirm long-term effectiveness of surgical modalities to treat OSA.

ACKNOWLEDGMENTS

We thank Kasey K. Li, MD, DDS, for graciously providing the figures illustrating
tonsillectomy, uvulopalatal flap, and maxillomandibular expansion procedures.

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