18sleep Apnea and Sleep Disorders

18 Sleep Apnea and
Sleep Disorders
Tamekia L. Wakefield | Derek J. Lam | Stacey L. Ishman
Key Points
■ Snoring affects at least 40% of men and 20% of women and often accompanies sleep-disordered
breathing. However, only 2% of women and 4% of men older than 50 years of age have
symptomatic obstructive sleep apnea (OSA).
■ OSA is defined by five or more respiratory events—apneas, hypopneas, or respiratory effort–

related arousals—in association with excessive daytime somnolence; waking with gasping, choking,
or breath holding; or witnessed reports of apneas, loud snoring, or both.
■ Negative health effects have been attributed to untreated OSA; these include increased mortality,

an increase in cardiovascular disease, and neurocognitive difficulties. In addition, untreated OSA
has been demonstrated to be an independent risk factor for insulin resistance, gastroesophageal
reflux disease, motor vehicle accidents, and decreased attention, working memory, and executive
function.
■ The most common symptoms of OSA include loud snoring, restless sleep, and daytime

hypersomnolence. However, polysomnography is required and is considered the gold standard for
diagnosis of OSA.
■ Fiberoptic laryngoscopy is an important tool to identify whether the level of obstruction is nasal,

retropalatal, or retrolingual. Most people have multilevel obstruction.
■ Uvulopalatopharyngoplasty is the most commonly performed surgical procedure for OSA
and is often misused as the first-line surgical therapy regardless of coexistent patient factors
such as obesity, retrognathia, and the existence of other sites of obstruction. As a result,
uvulopalatopharyngoplasty is often unsuccessful in treating OSA in unselected patients.
■ Partial midline glossectomy, lingualplasty, and radiofrequency tongue base ablation are procedures

that have been developed in an attempt to address the retrolingual collapse or narrowing that
occurs in OSA.
■ Surgical treatment of the hypopharyngeal area comprises procedures designed to prevent tongue

collapse into the airway during sleep. These include genioglossal advancement and hyoid myotomy,
which are both used to create an enlarged retrolingual airway.
■ Of patients whose OSA was diagnosed in a sleep disorder center, 31% were found to have

coexistent sleep disorders, with the most common being inadequate sleep hygiene (15%) and
periodic limb movement disorder (8%).
■ Insomnia is defined as difficulty with sleep initiation, maintenance, consolidation, or quality; it is

recurrent despite adequate occasion and opportunity for sleep and causes daytime dysfunction.
■ Circadian rhythm sleep disorders occur when personal sleep-wake patterns are misaligned with the
societal clock on a persistent or recurrent basis, leading to excessive daytime sleepiness or
insomnia and resulting in impaired function.
■ Parasomnias are undesirable movements or subjective phenomena that occur during sleep and
while falling asleep or waking up.
O ver the past decade, interest in sleep and sleep disorders surgical treatments. The recognition that sleep disorders
has increased substantially. Most of this renewed interest within require a multidisciplinary approach has led to the creation of
the otolaryngology community has been focused on obstructive a new medical discipline—sleep medicine—with teams made
sleep apnea (OSA), a sleep-related breathing disorder. As the up of internists, pulmonologists, otolaryngologists, neurolo-
waistline of the average American has grown, so too has the gists, pediatricians, psychiatrists, oral/maxillofacial surgeons,
incidence of OSA. Population-based studies suggest that 2% of dentists, behavioral psychologists, and nutritionists who work
women and 4% of men over age 50 have symptomatic OSA.1 together to take care of patients with sleep disorders. Consider-
Advances have also been made in the understanding of the able advances have been made in the diagnosis and manage-
pathophysiology of OSA, diagnostic methods, and medical and ment of sleep disorders, and otolaryngologists are at the
252
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18 | SLEEP APNEA AND SLEEP DISORDERS 253
forefront of this new field, providing a host of both traditional

TABLE 18-1. Respiratory Event Definitions and Types
and novel operative techniques to facilitate treatment.
Respiratory Event Definition
HISTORIC PERSPECTIVES Apnea A cessation of airflow for at least 10 seconds

Hypopnea A reduction in airflow (≥30%) at least 10
The idea of obesity being intimately associated with daytime seconds with ≥4% oxyhemoglobin
somnolence seems to have been first written about by Charles desaturation
Dickens in The Posthumous Papers of the Pickwick Club, originally OR a reduction in airflow (≥50%) at least 10
published in 1837. Dickens gives a vibrantly descriptive picture seconds with ≥3% oxyhemoglobin
of Joe, a boy so obese that he has difficulty breathing, sounds desaturation or an electroencephalogram
as if he is snoring even when awake, and frequently falls asleep (EEG) arousal
while standing. In addition, there is evidence to suggest that Respiratory Sequence of breaths for at least 10 seconds
some of our most noted leaders and dictators suffered from this effort–related with increasing respiratory effort or
problem. The twentieth president of the United States, William arousal (RERA) flattening of the nasal pressure waveform,
Howard Taft, had a body mass index (BMI) of 42 kg/m2 while leading to an arousal from sleep when the
in office and was reported to snore, to fall asleep during the sequence of breaths does not meet the
criteria for an apnea or a hypopnea
day frequently, and to have hypertension.2 Chouard and col-
leagues3 describe several reasons to suspect Napoleon I Obstructive Continued thoracoabdominal effort in the
(1769–1821) had OSA in the last decade of his life: he was setting of partial or complete airflow
obese and retrognathic, his neck was short and thick, he had cessation
nasal obstruction, he frequently slept during the day, he com- Central The lack of thoracoabdominal effort in the
plained of declining energy and intellect, and he was quite tired setting of partial or complete airflow
looking and somewhat disheveled. In 1956, Bicklemann and cessation
colleagues4 drew on Dickens’ description in their case report Mixed A respiratory event with both obstructive
titled “Extreme Obesity Associated with Alveolar Hypoventila- and central features, with mixed events
tion: a pickwickian Syndrome.” This frequently cited paper generally beginning as central events and
served as the first description of the pickwickian syndrome in ending with thoracoabdominal effort
an academic journal. Sleep apnea was first described as a clini- without airflow
cal entity in 1965, but it was not until the 1970s that Elio Luga- From Kushida CA, Littner MR, Morgenthaler T, et al. Practice param-
resi’s group5 provided a complete description of the OSA eters for the indications for polysomnography and related proce-
syndrome with its potential adverse cardiovascular effects. dures: an update for 2005. Sleep 2005;28:499-521.
In the infancy of this new diagnosis, treatment options were
limited to tracheostomy or weight loss. This changed in the
early 1980s with the introduction of the uvulopalatopharyngo- habitual audible snoring occurs with an apnea hypopnea index
plasty (UPPP) as described by Fujita and colleagues6 and (AHI) of less than five events per hour without daytime symp-
Simmons and colleagues.7 Not long after the introduction of toms. Polysomnography (PSG) is not required for diagnosis,
UPPP, it was recognized that although this new surgical inter- but when performed it reveals an audible microphone signal
vention was helpful in many cases, it left half of the patients not associated with arousals, desaturations, airflow limitation,
with persistent sleep apnea and could be a painful procedure. or arrhythmias.9
It was during this same time that Colin Sullivan, a young Aus-
tralian medical researcher, developed nasal continuous positive
airway pressure (CPAP), which today remains the first-line treat-
UPPER AIRWAY RESISTANCE SYNDROME
ment for adult OSA. The term upper airway resistance syndrome (UARS) was first used
As treatment for OSA has evolved so too has therapy aimed to describe patients who do not meet the criteria for OSA syn-
at treating snoring. The development of office-based surgical drome but who experience excessive daytime somnolence and
treatments, over-the-counter devices, and pharmacologic inter- other debilitating somatic complaints.10 UARS is characterized
ventions has increased considerably in recent years. by respiratory effort–related arousals (RERAs), defined as a
sequence of breaths over at least 10 seconds with increasing
CLASSIFICATION OF OBSTRUCTIVE
SLEEP-RELATED BREATHING TABLE 18-2. Indexes of Sleep-Disordered Breathing
DISORDERS Index Definition
Apnea index Number of apneas per hour of total
Sleep-related breathing disorders range from partial airway col- sleep time
lapse and increased upper airway resistance to episodes of
hypopnea or complete airway collapse with sleep apnea (Table Hypopnea index Number of hypopneas per hour of
total sleep time
18-1). In addition, a number of indices are used to describe
sleep-disordered breathing (Table 18-2). Apnea-hypopnea index Number of apneas and hypopneas
per hour of total sleep time
Respiratory effort–related Number of RERAs per hour of total
SNORING arousal (RERA) index sleep time
Snoring is sound generated by the vibration of the pharyngeal Respiratory disturbance Number of apneas, hypopneas, and
soft tissues. It is often louder during inspiration than expira- index RERAs per hour of total sleep time
tion. It affects at least 40% of men and 20% of women Central apnea index Number of central apneas per hour
and often accompanies sleep-disordered breathing.8 However, of total sleep time
snoring can occur in isolation and by definition is not associ-
ated with symptoms of excessive daytime sleepiness (EDS) or Mixed apnea index Number of mixed apneas per hour
of total sleep time
insomnia. In the absence of OSA, snoring is documented when
254 PART II | GENERAL OTOLARYNGOLOGY
OSA associated with laryngeal obstruction from bilateral laryn-

Box 18-1. SYMPTOMS OF SLEEP-DISORDERED
geal paralysis, laryngomalacia, and obstructing laryngeal lesions
BREATHING
has also been reported.
Restless sleep Fujita13 classified the patterns of obstruction by anatomic
Loud snoring location: type I is collapse in the retropalatal region only; type
Observed apnea, choking, or gasping episodes II is collapse in both retropalatal and retrolingual regions; and
Excessive daytime sleepiness type III is collapse in the retrolingual region only. Subsequent
Morning fatigue or irritability studies have evaluated the prevalence of retropalatal versus
Memory loss
Decreased cognitive function
retrolingual obstruction in patients with OSA and snoring and
Depression found that both retrolingual (77% vs. 40%) and retropalatal
Personality or mood changes (100% vs. 70%) obstruction are increased in OSA patients,
Decreased libido and impotence confirmed by PSG, compared with snorers.14
Morning and nocturnal headaches Nasal obstruction contributes to increased airway resistance
Nocturnal sweating and may worsen OSA, but it is rarely the sole cause. Nasal
Nocturnal enuresis obstruction may contribute to open-mouth breathing during
sleep, which increases upper airway collapsibility and may
decrease the efficacy of dilator muscles.15 Snoring is often a
respiratory effort that terminates with an arousal.11 A RERA is presenting symptom of OSA and can be caused by nasal obstruc-
detected using esophageal pressure manometry, which reveals tion. Surgical procedures aimed at improving nasal breathing
a pattern of progressively increasing negative esophageal pres- have demonstrated subjective improvement in snoring follow-
sure followed by an arousal.11,12 PSG reveals frequent arousals ing correction of nasal obstruction.16 Even though isolated
associated with snoring, abnormally negative intrathoracic pres- treatment of the nasal airway rarely leads to cure of OSA, it may
sure, or increased diaphragmatic electromyogram activity.10 allow for decreased CPAP levels to be used for subsequent treat-
The current International Classification of Sleep Disorders ment.17 Nasal obstruction can be caused by bony and cartilagi-
does not consider UARS to be a separate sleep disorder, but nous deformation or from soft tissue changes. Because many
recommends that it be included under the definition of OSA, causes of nasal obstruction are possible, they all warrant inves-
because the pathophysiology is similar.9 tigation when evaluating a patient with OSA.
Obesity is a major risk factor for OSA. The increased fat
deposition around the neck and parapharyngeal spaces is pos-
OBSTRUCTIVE SLEEP APNEA SYNDROME tulated to narrow and compress the upper airway and may offset
OSA syndrome is defined by five or more respiratory events— the effects of dilator muscles that maintain airway patency.18
apneas, hypopneas, or RERAs—in association with excessive Obesity is also thought to contribute to OSA through its
daytime somnolence; waking with gasping, choking, or breath deleterious effects on metabolism, ventilation, and lung volume,
holding; or witnessed reports of apneas, loud snoring, or both. resulting in a mismatch between alveolar ventilation and pul-
Each episode of apnea or hypopnea must last a minimum of monary perfusion. Obesity can significantly reduce lung
10 seconds, is commonly accompanied by reductions in blood volume, which results in a reduction of functional residual
oxygen saturation of at least 3% to 4%, and is usually termi- capacity. It has been observed that changes in lung volume
nated by brief, unconscious arousals from sleep. Snoring significantly reduce pharyngeal upper airway size through the
between apneas is a frequent complaint of bed partners and is mechanical effect of tracheal and thoracic traction, referred to
often the symptom that prompts these patients to seek medical as tracheal tug, increasing the risk for airway collapse.19
attention, although excessive daytime somnolence is a common Adenotonsillar hypertrophy is the major cause of OSA in
initial complaint. Automobile accidents and increased cardio- children. In adults, multiple structural characteristics are asso-
vascular morbidity and mortality are frequent complications if ciated with OSA. Craniofacial variations that have been associ-
OSA is left untreated. Many OSA sufferers complain of awaken- ated with OSA include increased distance of the hyoid bone
ing from sleep with morning headache, sore throat, and fatigue from the mandibular plane, decreased mandibular and maxil-
or a feeling of being unrefreshed regardless of the duration of lary projection, a downward and posterior rotation of mandibu-
sleep (Box 18-1). OSA is exacerbated by ingestion of alcohol, lar and maxillary growth, increased vertical facial length,
sedative use, and weight gain. The American Academy of Sleep increased vertical length of the posterior airway, and increased
Medicine classifies mild OSA as 5 to 15 events per hour, moder- cervical angulation.20
ate as 15 to 30 events, and severe as 30 events or more. Neuromuscular tone contributes to the patency of the upper
airway. During sleep this tone decreases, and the airway tends
toward collapse. The genioglossus muscle is considered to be
PATHOPHYSIOLOGY the most important muscle in maintaining airway patency in
The obstruction that occurs in OSA results from collapse of the OSA. Elevated genioglossal and tensor palatini muscle activity
pharyngeal airway during sleep. The etiology and mechanism has been observed in awake OSA patients compared with
of collapse is multifactorial but is largely due to the interaction normal awake subjects who have lower levels of activity. This
of an easily collapsible upper airway with relaxation of the suggests that even while the patient is awake, airway dilator
pharyngeal dilator muscles. Obesity, soft tissue hypertrophy, muscle activity compensates for a more anatomically compro-
and craniofacial characteristics such as retrognathia add to this mised upper airway in the OSA patient.18 Studies are ongoing
propensity for collapse by increasing the extraluminal tissue to determine the extent and importance of neuromuscular
pressures surrounding the upper airway. However, structural tone in maintaining airway patency during sleep.
compromise of the airway alone is not always sufficient to
produce OSA. Notably, patients without anatomic abnormali-
ties may also have OSA. This may occur because the complex CONSEQUENCES OF UNTREATED
reflex pathways from the central nervous system to the pharynx,
which control the action of pharyngeal dilator muscles, may fail
OBSTRUCTIVE SLEEP APNEA
to maintain pharyngeal patency. The three major areas of A number of negative health effects have been attributed to
obstruction are the nose, palate, and hypopharynx, although untreated OSA including increased mortality, an increase in
cardiovascular disease, and neurocognitive difficulties. In a ret-

rospective study, He and colleagues21 found that untreated OSA EPWORTH SLEEPINESS SCALE
patients with an apnea index (AI) greater than 20 had a statisti-
cally significant increase in mortality compared with patients Please answer the following questions based on this scale:
with an AI less than 20, and they also found that untreated
0. Would never fall asleep
patients with an AI greater than 20 had a 63% probability of
1. Slight chance of dozing
surviving 8 years, compared with 96% in those with an AI less 2. Moderate chance of dozing
than 20. Additionally, untreated OSA is reported to increase 3. High chance of dozing
the risk of fatal and nonfatal motor vehicle accidents by 2.5-
fold.22 A significant proportion of the mortality and morbidity
Situation Chance of Dozing
related to OSA occurs through its effects on the cardiovascular
system, which can result in hypertension, coronary heart Reading
disease, congestive heart failure, arrhythmias, pulmonary
hypertension, stroke, and sudden death. Untreated moderate Watching TV
and severe OSA has been reported to result in a threefold
Sitting in a public place (e.g., theater or meeting place)
increase in fatal and nonfatal cardiovascular events, compared
with both healthy men without OSA and men with CPAP- Driving a car, stopped at a traffic light
treated OSA.23 Treatment of OSA with CPAP has also been
reported to lower blood pressure by 10 mm Hg.24 As a passenger in a car for an hour without a break
Untreated OSA has been demonstrated to be an indepen-
During quiet time after lunch without alcohol
dent risk factor for insulin resistance.25 Recently, it has been
suggested that OSA may contribute to the development of Lying down to rest when circumstances permit
diabetes and metabolic syndrome, the term used to describe the
commonly occurring conditions of obesity, insulin resistance, Total Score:
hypertension, and dyslipidemia. However, further research is
needed to determine whether there is an independent link Epworth Score <10 = Normal
between OSA and metabolic abnormalities.
The prevalence of gastroesophageal reflux disease in OSA
FIGURE 18-1. Epworth Sleepiness Scale.
patients is significantly higher than in the general population.26-28
Even though these disorders commonly occur together, no
temporal or causal relationship has ever been demonstrated suspicion among physicians or underreporting of the classic
between the two. This may reflect the fact that they share symptoms by female patients. Women with OSA are more likely
similar risk factors. Treatment of OSA with CPAP has been to report symptoms of insomnia, heart palpitations, and ankle
demonstrated to decrease the occurrence of gastroesophageal edema.35
reflux disease.29 Although the presence of daytime somnolence and loud
Aside from the obvious physical effects of OSA, such as EDS snoring are frequently the signs that prompt OSA sufferers
and impaired mood, neurocognitive deficits have also been to seek medical attention, the physical examination findings
associated with OSA. Untreated OSA has been documented to strengthen the likelihood of the diagnosis. The BMI calcula-
cause problems with attention, working memory, and executive tion, blood pressure measurement, and neck circumference
function, all of which are improved with CPAP treatment.30 Bed are important general assessment parameters. In addition,
partner dissatisfaction is also a common complaint among OSA body habitus, mandible and maxilla position and size, and
patients, and treatment has been shown to improve the quality facial characteristics should be noted. Assessment of the nose
of life in both the treated individuals and their bed partners.31 should include evaluation of any external deformity, adequacy
Thus the benefits of treating OSA are substantial and well of the nasal valve, septal position, turbinate size, nasal mucosa
documented. swelling, and the presence or absence of polyps, purulence, and
rhinorrhea. In the oral cavity, appraisals of the tongue size and
position, elongation of the palate and uvula, tonsil size, modi-
DIAGNOSIS fied Mallampati score, dentition, and crowding of oropharynx
The most common symptoms of OSA include loud snoring, should follow. In the neck, its size, hyoid position, and jaw posi-
restless sleep, and daytime hypersomnolence. However, a broad tion, including retrognathia, should be evaluated (Box 18-3).
range of signs and symptoms have been reported to occur in
OSA (see Box 18-1). Obesity is a common finding in patients
with OSA, and 70% of adult patients with OSA are reportedly Box 18-2. MEDICAL CONDITIONS THAT PRODUCE
obese.32 Screening that includes a detailed sleep history and FATIGUE
physical examination is recommended for all obese patients.
The Epworth Sleepiness Scale is a widely used tool that assesses Severe anemia
Endocrine dysfunction, including hypothyroidism and Addison disease
daytime sleepiness (Fig. 18-1). OSA may be suspected in patients Chronic fatigue syndrome
with an Epworth Sleepiness Scale score greater than 10.33 Sleep- Pulmonary disease, including asthma, emphysema, and pickwickian
iness or fatigue may also be precipitated by a number of other syndrome
medical conditions that should be considered when evaluating Cardiovascular disease, including congestive and left heart failure
patients for possible OSA (Box 18-2). In addition, the presence Neoplasms, including disseminated and central nervous system lesions
of additional sleep disorders should be considered. Anticancer chemotherapy
Because of the increased prevalence of OSA in patients with Collagen vascular diseases
hypertension, coronary artery disease, congestive heart failure, Chronic infections, including mononucleosis, hepatitis, and influenza
cerebrovascular accident, and diabetes mellitus, these popula- Depression and other psychiatric disorders
Malnutrition
tions must be carefully screened for the signs and symptoms Neurologic disorders, including Parkinson disease and multiple sclerosis
of OSA.34 It has also recently been recognized that OSA may Medication side effects
be underdiagnosed in women because of a lower index of
Box 18-3. PHYSICAL EXAMINATION FINDINGS

Nasal Obstruction
Septal deviation
Turbinate hypertrophy
Nasal valve collapse
Adenoid hypertrophy
Nasal tumors or polyps
Oropharyngeal Obstruction
Large soft palate
Palatine tonsillar hypertrophy
Posterior pharyngeal wall banding
Macroglossia
Large mandibular tori
Narrow skeletal arch
Hypopharyngeal Obstruction
Lateral pharyngeal wall collapse FIGURE 18-3. Fiberoptic view of base of tongue obstruction. (From Troell
Omega-shaped epiglottis RJ, Riley RW, Powell NB, Li K. Surgical management of the hypopharyngeal airway
Hypopharyngeal tumor in sleep disordered breathing. Otolaryngol Clin North Am 1998;13:983.)
Lingual tonsillar hypertrophy
Retrognathia and micrognathia
collapse (Figs. 18-4 and 18-5). Sher and associates37 performed
Laryngeal Obstruction
both seated and supine examinations using the Müller maneu-
True vocal cord paralysis ver in OSA patients, selected those patients who experienced
Laryngeal tumor
palatal collapse, and found that 73% had at least a 50% reduc-
General Neck Obstruction tion in the respiratory disturbance index (RDI) after UPPP.
Increased neck circumference Aboussouan36 found that using the Müller maneuver to guide
Redundant cervical adipose tissue the decision on UPPP resulted in an AHI reduction of 50% in
General Body Habitus 78% of patients who had velopalatal collapse, compared with
Obesity 36% for multilevel obstruction. Thus even though the Müller
Achondroplasia maneuver can help guide surgical decision making when the
Chest wall deformity area of collapse is purely retropalatal, it appears to be less useful
Marfan syndrome in patients who have multilevel obstruction, which is the major-
Cardiovascular Signs ity of patients.
Arterial hypertension, especially morning hypertension To better identify the site or sites of obstruction in patients
Peripheral edema with OSA, drug-induced sleep endoscopy (DISE) has been used
to guide more effective surgical intervention. DISE involves the
use of fiberoptic nasopharyngoscopy to evaluate the site of
Fiberoptic nasopharyngoscopy and laryngoscopy are airway collapse during pharmacologically induced sleep.38,39
important for evaluation of the airway. This examination can Although this evaluation is most commonly performed using
be performed in multiple positions—nasal, retropalatal, or some combination of midazolam and propofol for sedation,
retrolingual—in awake and asleep patients and is an important some authors who perform DISE primarily in children have
tool to identify level of obstruction (Figs. 18-2 and 18-3). suggested using dexmedetomidine as the primary agent for
Numerous studies have described the benefits and limitations sedation.40-42 This is because it causes less respiratory depression
of the addition of the Müller maneuver to this examination for and cardiovascular instability and thus better mimics natural
preoperative prediction of the effectiveness of surgical inter- sleep.43,44 This technique has been demonstrated to be a useful
ventions.36,37 The Müller maneuver is performed in an awake tool for assessing the location, severity, and pattern of
patient, who generates negative pressure by inhaling against a airway obstruction during sleep.45-47 A proposed method of
closed glottis with the nose and mouth closed to trigger airway
FIGURE 18-4. Fiberoptic view of the hypopharyngeal airway before the

FIGURE 18-2. Fiberoptic view of the normal hypopharyngeal airway. (From Müller maneuver. (From Troell RJ, Riley RW, Powell NB, Li K. Surgical manage-
Troell RJ, Riley RW, Powell NB, Li K. Surgical management of the hypopharyngeal ment of the hypopharyngeal airway in sleep disordered breathing. Otolaryngol
airway in sleep disordered breathing. Otolaryngol Clin North Am 1998;13:983.) Clin North Am 1998;13:983.)
S
N
SNA 82
SNB 80 PNS
PAS 11 ANS
PNS-P 35 P A
MP-H 15
Go
PAS
FIGURE 18-5. Fiberoptic view of hypopharyngeal collapse during the MP B
Müller maneuver. (From Troell RJ, Riley RW, Powell NB, Li K. Surgical manage- H
ment of the hypopharyngeal airway in sleep disordered breathing. Otolaryngol
Gn
Clin North Am 1998;13:983.)
FIGURE 18-6. Standard cephalometric tracing. A, subnasale; ANS, anterior

standardizing the DISE findings called the velum, oropharynx, nasal spine; B, supramentale; Gn, gnathion; Go, gonion; H, hyoid; MP, man-
tongue base, epiglottis (VOTE) classification has demonstrated dibular plane; MP-H, mandibular plane to hyoid ; N, nasion; P, tip of uvula;
good intrarater and interrater reliability.47,48 Recent studies PAS, posterior airway space; PNS, posterior nasal spine; PNS-P, length of the
have used this system to prognosticate outcomes of surgical soft palate; S, sella; SNA, maxilla to cranial base; SNB, mandible to cranial
intervention.49,50 Most investigators have demonstrated that base. (From Riley R, Powell N, Guilleminault C. Obstructive sleep apnea syn-
multilevel collapse and complete collapse at the velum or drome: a review of 306 consecutively treated surgical patients. Otolaryngol Head
tongue base predispose to worse outcomes of surgical interven- Neck Surg 1993;108:117.)
tion. Others have attempted to use image processing software
to objectively measure the percent change in airway cross-
sectional area during waking and sleep.51 Nocturnal PSG is the gold standard for diagnosis of OSA. A
A number of radiologic techniques have been used to aid full-night diagnostic study is considered to be the most accurate
in the identification of the site and severity of upper airway instrument for measuring the presence and severity of OSA.
obstruction or collapse in OSA. Because most of the radiologic The parameters monitored during PSG include electroenceph-
techniques for evaluation of OSA are performed in awake alogram, electrooculogram, submental electromyogram, elec-
patients, they provide limited information about obstruction trocardiogram, airflow, thoracoabdominal effort, and oximetry
during sleep. The most frequently used imaging modality has (Box 18-4). The information obtained from the study is
been the cephalometric radiograph. The cephalogram is a two- analyzed by a trained PSG technologist and interpreted by a
dimensional representation of the airway, a standardized evalu- sleep physician. Classification of disordered breathing events
ation system with broad availability and relatively low cost (Fig. recorded during PSG have been standardized to guide practice
18-6).52 These films provide information on both the bony (Figs. 18-8 through 18-10).34
skeleton and the overlying soft tissues. Multiple studies using
cephalometry have confirmed that OSA patients have inferior
displacement of the hyoid, a smaller posterior airway space, and
longer soft palates than do non-OSA patients (Fig. 18-7).53-56
26
Even so, the differences between OSA and non-OSA patients
noted on cephalometry have not been significant enough to 24
allow for the use of lateral cephalograms as a sole diagnostic 22
tool.57 20
Volume CT scan (mL)
Awake computed tomography (CT) provides good anatomic 18

detail of the bone and soft tissue. Like the cephalogram, CT
has poor sensitivity for diagnosing OSA; however, multiple 16
studies have demonstrated that it is a better modality to 14
illustrate postoperative anatomic changes that correlate with 12
improved PSG parameters.57 10
Magnetic resonance imaging (MRI) provides excellent soft r .93
tissue differentiation and does not require radiation exposure. 8
However, it can be hard to tolerate, is expensive, has limited 6
availability, and is noisy, which may preclude asleep evaluations. 4
Like CT and cephalometry, MRI has not been useful in distin- 2
guishing OSA from non-OSA patients.58
Lastly, fluoroscopy has been used as a dynamic airway exami-
nation to directly evaluate the sites of obstruction. Somnofluo- 1 2 3 4 5 6 7 8 9 10 11 12
roscopy, a study done while the patient is asleep, has been PAS (mm)
shown to improve UPPP success rates, when the site of initial FIGURE 18-7. Comparison of the hypopharyngeal airway volume by com-
obstruction is identified (67% vs. 42%); however, these studies puted tomography (CT) scan to posterior airway space (PAS), measured on
are time intensive and expose patients to increased radiation, cephalometric radiographs. (From Riley R, Powell N. Maxillofacial surgery and
which limits their utility.59 obstructive sleep apnea syndrome. Otolaryngol Clin North Am 1990;23;809.)
Box 18-4. POLYSOMNOGRAPHY MONITORS TABLE 18-3. European Respiratory Society Task Force
2011 Recommendations for Obstructive Sleep Apnea
Electroencephalogram (C3 or C4, O1 or O2, F1)
Electrooculogram Recommended Not Recommended
Nasal and oral airflow monitors: thermistors, nasal pressure Weight reduction Positional therapy (except in
transducers, or inductance plethysmography carefully selected patients)
Submental electromyogram
Anterior tibial electromyogram Oral appliances (mild to Apnea-triggered muscle stimulation
Body-position monitors moderate OSA)
Chest respiratory effort monitor Intranasal coricosteroids Tongue-retaining devices
Abdominal respiratory effort monitor
Electrocardiogram Adenotonsillectomy Drug therapy
Pulse oximetry (pediatric OSA)
Tracheal microphone Tonsillectomy (adults with Nasal dilators
Optional: tonsillary hypertrophy)
End-tidal carbon dioxide monitor
Uvulopalatal flap with Nasal surgery as single intervention
Esophageal pressure monitor
tonsillectomy
Nasal continuous positive airway pressure and bilevel positive airway
pressure Maxillomandibular Uvulopalatopharyngoplasty (except
advancement in carefully selected patients)
Distraction osteogenesis Laser-assisted UPP
TREATMENT Radiofrequency surgery of the soft
palate
To provide effective treatment for OSA, careful consideration Uvulopalatal flap as single
of the individual patient, available medical and surgical thera- intervention
pies, and inherent risks and complications of those interven- Pillar implants (except in carefully
tions must be taken into account. The deleterious effects of selected patients)
untreated OSA on cardiovascular and neurocognitive health Radiofrequency surgery of the
are well documented; however, the treating physician should tongue base
Hyoid suspension as a single
have knowledge of all available interventions, including their intervention
success rates and risks of complications, and the need for Laser midline glossectomy/tongue
further surgery must be carefully assessed when outlining a suspension
treatment plan. Genioglossus advancement as a
single procedure
Multilevel surgery as first-line
MEDICAL TREATMENT therapy
Because OSA is a multilevel, multifactorial problem that can From Randerath WJ, Verbraecken J, Andreas S, et al. Non-CPAP thera-
occur in people with severe underlying morbidity, many treat- pies in obstructive sleep apnoea. Eur Respir J 2001:37((May)5):
ment options exist to address it. Generally, it is recommended 1000-1028.
that treatment be approached in a stepwise manner and that it OSA, obstructive sleep apnea; UPP, uvulopharyngoplasty.
begin with conservative medical measures. In 2011, an interdis-
ciplinary European Respiratory Society (ERS) task force evalu- gathered by the ERS support this observation, and weight
ated the scientific literature for non-CPAP treatment options reduction is now recommended to decrease the underlying
and made recommendations regarding therapies in OSA accord- risk factor of obesity.60
ing to the standards of evidence-based medicine (Table 18-3).60 CPAP is considered the gold standard of treatment for mod-
Weight loss should be recommended for all overweight erate to severe OSA. Studies have demonstrated its effectiveness
patients with OSA. However, sustained weight reduction is dif- in reducing the AHI and in subjectively improving sleep quality;
ficult, and patients often regain the lost weight; therefore however, patient adherence remains a significant obstacle.12,63,64
other interventions are often also recommended. Consulta- CPAP acts as a pneumatic splint that prevents upper airway
tion with a bariatric surgeon can be considered when treating collapse by providing constant positive intraluminal pressure
morbidly obese patients. Recent evidence reveals that surgi- during inspiration and expiration. Numerous effects of CPAP
cally induced weight loss significantly improves obesity-related treatment have been described, chief among these being the
OSA and parameters of sleep quality,61 and this improve- reduction in AHI, improvement in objective and subjective
ment can occur as early as 1 month after surgery.62 The data sleepiness, improvement in overall quality of life, reduction in
Airflow
Apnea obstructive (16.16 s)
Airflow
Chest effort
Abd effort
90
90
90
90
89
88
88
87
87
86
86
85
85
85
85
84
84
84
84
84
83
82
82
82
82
82
82
SaO2
FIGURE 18-8. Polysomnographic tracing of an obstructive apnea. Abd, abdominal.
Hypopnea (21.15 s)
Airflow
Airflow
Chest effort
Abd effort
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
97
96
96
96
96
96
96
96
96
96
96
96
96
96
96
95
95
95
95
95
95
94
94
94
94
94
92
92
91
91
90
SaO2 Desaturation (27.00 s) [7.0%]
FIGURE 18-9. Polysomnographic tracing of a hypopnea. Abd, abdominal.
risk of cardiovascular events, and reduction in the risk of motor from oral appliance therapy are tooth and jaw muscle pain,
vehicle accidents.21,65,66 Recently, interest has also surrounded difficulty chewing in the morning, and excessive salivation.
the beneficial effects of CPAP on cardiovascular health as a Although oral appliance therapy is cost-effective and has higher
result of decreased inflammation, as measured by a decrease in rates of patient adherence, CPAP has proven to be more effec-
the inflammatory markers C-reactive protein and interleukin-6; tive in reducing AHI.76 According to the ERS, oral appliances
improved endothelial function; and reduced diurnal sympa- are recommended for treatment of patients with mild to mod-
thetic activity.67-69 Bilevel positive airway pressure (BiPAP) and erate OSA and for patients who do not tolerate CPAP.60 There-
autoadjusting positive airway pressure (APAP) were developed fore this intervention can be recommended as second-line
to improve pressure titration and to treat patients with neuro- therapy for mild to moderate OSA; however, reevaluation with
muscular disorders and ventilatory disease. BiPAP delivers a a sleep study with the device in place is recommended to
separately adjustable, lower expiratory positive airway pressure confirm effective treatment.
and higher inspiratory positive airway pressure. Although Pharmacologic therapy has been proposed as a treatment
BiPAP has not been shown to improve adherence in an alternative in patients intolerant of CPAP; however, current
unselected patient population, a change in the method of deliv- evidence is insufficient to recommend the use of drug therapy
ery of positive airway pressure may significantly improve adher- as primary therapy for the treatment of OSA.77 The many pro-
ence in individual patients.70 APAP devices autotitrate positive posed mechanisms by which drugs may reduce the severity of
airway pressure to select an effective level of CPAP, which pre- OSA include increasing upper airway dilator muscle tone, ven-
vents upper airway collapse. The pressure changes in response tilatory drive, and cholinergic tone during sleep versus reduc-
to variations in snoring and airflow magnitude, limitation, or ing the proportion of REM sleep, airway resistance, and surface
impedance.71-73 tension in the upper airway.77 Modafinil is a central stimulant
Oral appliances have been used with success in patients with of postsynaptic α1-adrenergic receptors, which acts by promot-
mild, moderate, and some severe OSA (Fig. 18-11), increasing ing alertness. It is currently used for treatment of narcolepsy
the posterior oropharyngeal airway. Ferguson and colleagues74 and idiopathic hypersomnia. Modafinil is also approved by the
conducted a crossover study to compare oral appliance therapy Food and Drug Administration to alleviate residual sleepiness
and nasal-CPAP therapy and concluded that oral appliances are in patients with OSA who were regular users of CPAP but still
effective in some patients with mild to moderate OSA (AHI 14 experienced EDS.78 However, modafinil should not be used in
to 50) and are associated with greater satisfaction than CPAP. the absence of definitive treatment of underlying OSA. At this
Adherence rates of oral appliance therapy have been reported time, drug therapy is not recommended as primary treatment
to be as high as 77%.75 The most often reported complications for OSA.60
Airflow
Central apnea (24.2 s)
Chest
effort
Abd effort
98
97
97
97
97
97
97
97
97
97
97
97
97
97
96
96
96
96
96
96
96
96
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95
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94
94
94
93
93
93
93
91
92
92
92
92
92
92
91
90
90
90
90
90
90
90
90
89
89
89
SaO2 Desaturation (21.3 s) [9%]
FIGURE 18-10. Polysomnographic tracing of a central apnea. Abd, abdominal. Abd, abdominal.
Box 18-5. SURGICAL INDICATIONS FOR TREATMENT

AHI >5 and <14 with excessive daytime sleepiness
AHI >15
Oxyhemoglobin desaturation <90%
Upper airway resistance syndrome, preferably with objective
improvement of neurocognitive dysfunction and medical therapy
Significant cardiac arrhythmias associated with obstructions
Unsuccessful or refused medical therapy and desire for surgery
Medically stable enough to undergo recommended procedures
regarding plans for airway management. A stepwise algorithm

frequently used includes using an oropharyngeal airway to
prevent airway obstruction by the tongue, refraining from using
paralyzing agents until the patient can be easily ventilated with
a mask, and preparing alternative methods of ventilation in
case intubation is unsuccessful. The surgeon should also have
a frank discussion with the patient about the possibility of tra-
cheotomy. A preoperative evaluation by the primary doctor or
the anesthesia team is critical and includes evaluation for latent
cardiovascular disease.
FIGURE 18-11. Mandibular advancement appliance for mild to moderate
sleep apnea.
Patients with OSA are usually managed using a staged, step-
wise surgical protocol. The site of obstruction must be deter-
mined in each patient to determine the type and extent of
Intranasal steroids have been investigated as treatment for surgical intervention. Generally, patients with isolated palatal
OSA, and fluticasone has shown some success in treating OSA obstruction undergo palatal surgery, and those with obstruction
patients with coexistent rhinitis. Kiely and colleagues79 reported at the base of the tongue undergo procedures aimed at treating
that the AHI was lower in 24 patients given intranasal flutica- this area. Endoscopic examination is performed to determine
sone compared with those given placebo (23.3 vs. 30.3). the site of obstruction. Most patients are symptomatic because
Brouillette and coworkers80 gave children with OSA and both the palatal and base of tongue areas are obstructed.
adenotonsillar hypertrophy a 6-week course of intranasal flu Before therapy is initiated, patients should be counseled
ticasone and reported a decreased frequency of mixed and regarding the possible need for multiple surgical procedures
obstructive apneas and hypopneas. Given these demonstrated to achieve a symptomatic cure. Sleep endoscopy may be the
benefits, treatment with intranasal fluticasone warrants further optimal method of airway evaluation in these cases (Box 18-6).
investigation. As a single intervention, intranasal steroids are Patients with laryngeal obstruction should be treated appropri-
not recommended for treatment of adult OSA; however, ately to alleviate the obstruction and should be considered
they are recommended for pediatric OSA in the prescence of for tracheostomy if improvement is not achieved surgically or
coexisting rhinitis and/or upper airway obstruction as a result with CPAP.
of adenotonsillar hypertrophy.60 The leukotriene receptor Critical to this decision process is the identification of any
antagonist montelukast has also shown promise by reducing sites of obstruction. Several endoscopic studies have evaluated
the adenoid size and respiratory-related sleep disturbances in the prevalence of retropalatal and retroglossal obstruction in
children with mild OSA.81 patients with OSA. In 2000, Steinhart and colleagues14 evalu-
The use of nasal dilator strips and topical decongestants has ated 117 OSA patients and found that 100% had retropalatal
been advocated in patients who have OSA and severe nasal
obstruction. McLean and colleagues82 found that treating nasal
obstruction with 0.4 mL oxymetazoline 0.05% and nasal dilator
strips reduced mouth breathing during sleep and reduced OSA Box 18-6. SURGICAL TREATMENT OPTIONS
severity, but it did not effectively alleviate OSA. The ERS further Nasal Surgery
elaborates that the published data do not support the use of Nasal septoplasty
nasal dilators for reduction of snoring and improvement of Inferior turbinate reduction
sleep-disordered breathing or sleep architecture in OSA. Adenoidectomy
However, nasal dilator strips have been shown to significantly Nasal tumor or polyp resection
reduce snoring, mouth breathing, and sleepiness in patients Nasal valve reconstruction
who do not have OSA.84 Palatal Surgery
Palatal radiofrequency ablation
Pillar implants
SURGICAL TREATMENT Injection snoreplasty
Factors important in making the decision to treat OSA with a Tonsillectomy
surgical procedure include the patient’s wishes, CPAP toler- Uvulopalatopharyngoplasty/Z-palatoplasty
ance, severity of symptoms, severity of disease, patient comor- Transpalatal advancement pharyngoplasty
bidities, and site and severity of upper airway collapse (Box Hypopharyngeal Surgery
18-5). As mentioned previously, OSA patients are frequently Lingual tonsillectomy
overweight, hypertensive, and have other cardiac risk factors. Partial midline glossectomy
These patients must be cautiously screened with a comprehen- Tongue base radiofrequency ablation
sive medical examination before considering surgery for treat- Mandibular osteotomy and genioglossal advancement
Hyoid myotomy and suspension
ment of OSA. Tongue-suspension suture
The surgical planning for patients with OSA should include Maxillomandibular osteotomy and advancement
a discussion between the anesthesia team and the surgeon
obstruction and 77% had retroglossal obstruction, thus illus- I II

trating that a majority of patients have a combination of the
two. In 2005, den Herder and colleagues84 evaluated 127
patients who underwent a similar evaluation and found that
88% had retropalatal obstruction and 49% had retroglossal
obstruction. In this study, 51% exclusively had palatal obstruc-
tion, whereas only 12% solely had obstruction at the base of
the tongue. In 2011, Ravesloot and de Vries50 evaluated 100
patients undergoing evaluation for OSA. They demonstrated
palatal obstruction in 83%, tongue-base obstruction in 56%,
epiglottis obstruction in 38%, and oropharyngeal obstruction
in 7%. Multilevel obstruction was observed in 76%. These find-
ings were correlated with PSG findings such that patients with
multilevel obstruction were found to have a significantly worse
AHI than those with a single level of obstruction (24 vs. 12.6; III IV
P = .007). Two other studies reported the results of surgery that
was tailored based on the results of DISE. In 2012, Gillespie and
colleagues47 reported on 38 patients who underwent DISE prior
to planned surgery. They altered the surgical plan based on the
DISE findings in 62% of patients, and 73% had multilevel
obstruction, whereas far fewer patients had only palatal (16%)
or tongue-base (11%) collapse. Also in 2012, Koutsourelakis
and associates49 reported a study of 49 patients who underwent
DISE followed by a combination of palate surgery, radiofre-
quency tongue ablation, and hyoid suspension. Even with a
surgical plan tailored to DISE findings, 53% were nonre-
sponders. Compared with responders, these patients were FIGURE 18-12. Modified Mallampati palate position. I, The entire uvula can
observed to have a higher occurrence of complete circumfer- be seen with the tongue at rest. II, A partial view of the uvula is seen. III,
ential velar collapse (42% vs. 4%) and complete anterior- Only the soft and hard palate can be seen. IV, Only the hard palate can be
posterior collapse at the tongue base (77% vs. 30%). seen.
Nasal Surgery III patients have only an 8% success rate (Table 18-4). These
Nasal obstruction has been associated with poor sleep quality, results demonstrate that clinical staging clearly improves the
snoring, and OSA.85-87 Septoplasty, turbinate reduction, nasal overall success rate and is critical to identify which patients are
valve surgery, and sinus surgery are procedures that have been unlikely to benefit from UPPP. Complications associated with
used to treat nasal obstruction associated with OSA, and the UPPP include temporary nasal reflux in 12% to 15% of patients,
selection of a nasal procedure is based on pathology. However, postoperative bleeding in 1% to 5%, infection in 2%, and rare
even though nasal procedures are unlikely to significantly altered speech.91 Therefore UPPP should only be considered
improve OSA when used alone,17 improving nasal patency may in carefully selected patients with obstruction limited to the
help restore physiologic breathing and may allow for the use oropharyngeal area.
of nasal CPAP in patients previously unable to tolerate it. Con- To improve on the traditional UPPP procedure, other tech-
sideration should be made to address nasal obstruction as an niques have been suggested to address retropalatal obstruction.
initial step in OSA management so as to facilitate better CPAP Woodson and colleagues92 introduced the transpalatal advance-
adherence. ment pharyngoplasty, which aims to decrease retropalatal
obstruction by altering the bony hard palate and the soft tissue
Palatal Surgery attachments of the posterior maxilla. With this procedure, a
In 1981, Fujita and colleagues6 described the UPPP, the first 1-cm portion of the hard palate is removed, and the soft palate
palatal procedure for OSA treatment. UPPP with tonsillectomy is then advanced and secured medially and laterally in the
was developed to eliminate palatal obstruction by resection of tensor aponeurosis, which enlarges the retropalatal region.
redundant palatal and pharyngeal tissue. It is the most com- Woodson and colleagues92 reported success with this procedure
monly performed surgical procedure for OSA and is often when used in patients who have persistent retropalatal obstruc-
misused as the first-line surgical therapy for OSA regardless of tion after UPPP and in those with OSA who have small tonsils
coexistent patient factors such as obesity, retrognathia, and the without the characteristic long, thick, soft palate (Fig. 18-13).
existence of other sites of obstruction.88 As a result, it is often Another procedure, the Z-palatoplasty, was introduced by
unsuccessful in treating OSA in unselected patients. The site of Friedman and associates93,94 for use as a primary or revision
pharyngeal collapse has a marked effect on the probability of palatal procedure in selected patients (Fig. 18-14).
the success of UPPP. In a meta-analysis of 37 published reports To reduce the resultant pain, cost, and morbidity of UPPP,
of results from UPPP, success rates were at best 50% and were less invasive office techniques have been developed. The palatal
related to severity of OSA.89 Success in this case was defined as implant was designed to reduce soft palate airway collapse and
a respiratory disturbance index (RDI) of less than 20 or an AHI obstruction through placement of three woven implants, which
of 10 or less, along with at least a 50% improvement in the stiffen the palate. The porosity of the implants also encourages
RDI.89 Using a staging system based on palate position, tonsil the formation of a fibrotic capsule, which connects the three
size, and BMI, Friedman and colleagues90 demonstrated the implants and further stiffens the palate. Nordgard and col-
value of staging OSA patients for the prediction of success for leagues95 reported a significant reduction in AHI, daytime som-
UPPP. In this staging system, tonsil size, BMI, and palate posi- nolence, and snoring using palatal implants in patients with
tion based on the modified Mallampati staging are used to mild to moderate OSA, as long as BMI was maintained. The
stratify patients (Fig. 18-12). Stage I patients have an 80% most common complication of this procedure is partial implant
success rate, stage II patients have a 40% success rate, and stage extrusion. Potential advantages include the fact that it can be
TABLE 18-4. Preoperative Versus Postoperative Data Obtained During Polysomnography in UPPP Only and in UPPP
with Radiofrequency Ablation of the Tongue Base
Stage I Stage II Stage III
Apnea Index
UPPP only Preoperative 5.4 ± 14.2 16.0 ± 26.9 8.7 ± 14.5
Postoperative 0.3 ± 1.3* 2.7 ± 5.4* 12.4 ± 24.8
UPPP + TBRF Preoperative — 11.5 ± 15.5 9.3 ± 18.2
Postoperative — 2.7 ± 7.8* 3.2 ± 7.4*†
Apnea-Hypopnea Index
Postoperative 6.7 ± 4.7* 34.2 ± 29.9* 39.1 ± 22.7
UPPP + TBRF Preoperative — 47.9 ± 26.6 41.7 ± 21.8
Postoperative — 19.5 ± 16.4*† 28.5 ± 21.9*†
Minimum SpO2 (mm Hg)
Postoperative 93.1 ± 1.9* 85.3 ± 8.2* 82.8 ± 12.9
UPPP + TBRF Preoperative — 82.1 ± 9.7 79.9 ± 14.3†
Postoperative — 87.5 ± 6.7* 83.8 ± 14.8*
Data from Friedman M, Ibrahim H, Joseph NJ. Staging of obstructive sleep apnea/hypopnea syndrome: a guide to appropriate treatment. Laryn-
goscope 2004;114:454.
*Significantly different from preoperative value.
†Significantly different from UPPP only.
SpO2, arterial oxygen saturation; TBRF, tongue base radiofrequency ablation; UPPP, uvulopalatopharyngoplasty.
done in a single office visit, has minimal morbidity, and has colleagues98 reported the results of a randomized trial that
been noted to significantly reduce snoring. Because of its low compared UPPP to lateral pharyngoplasty among 27 patients
morbidity, the palatal implant procedure is commonly used to with at least moderate OSA and retropalatal collapse on endos-
treat snoring and may be useful in patients with mild OSA. copy. They found significant improvements in mean AHI (41.6
decreasing to 15.5, P = .002) and percentage of time spent in
Oropharyngeal Surgery deep sleep stages (9.8 increasing to 16.3, P = .03) with lateral
Tonsillectomy has been used to address the upper airway com- pharyngoplasty, whereas UPPP did not show any statistically
promise caused by tonsillar hypertrophy. Recently, new tech- significant PSG changes.
niques of tonsillectomy and tonsil volume reduction have been Another variation of the lateral pharyngoplasty was de
utilized to decrease resultant operative and postoperative com- scribed by Pang and Woodson99 in 2006. This involves bilateral
plications associated with the traditional procedure. Radiofre- tonsillectomy, transection of the inferior aspect of the palato-
quency tonsil reduction by intracapsular tonsillectomy has pharyngeus, and superolateral rotation and figure-eight sutur-
gained popularity and is being used in the treatment of OSA ing of the mobilized muscle to the arch of the anterior soft
in children. Although this procedure appears to be minimally palate (Fig. 18-15). In 2007, Pang and Woodson100 reported the
invasive and has limited morbidity, the ERS concluded that results of a randomized trial that compared UPPP to lateral
evidence is insufficient to recommend it as a single procedure pharyngoplasty among nonobese patients with small tonsils and
for the treatment of OSA. More research with these newer lateral wall collapse on flexible nasendoscopy. In this study,
techniques is required to determine their efficacy in the treat- lateral pharyngoplasty demonstrated a higher success rate,
ment of OSA. defined as a 50% reduction in AHI and postoperative AHI
Lateral pharyngoplasty was first described by Cahali96 in below 15, than UPPP (78.2% vs. 45.5%), and a larger improve-
2003 as an alternative to UPPP. The technique involves bilateral ment was noted in AHI (32.2 ± 8.4 vs. 18.5 ± 7.6).
tonsillectomy, longitudinal incision of the superior pharyngeal
constrictor, diagonal incision through the superior palatopha- Hypoglossal Nerve Stimulation
ryngeus, Z-plasty closure of the superior aspect of the tonsillar Because OSA is primarily associated with relaxation of the pha-
fossa, and suturing of the anterior and posterior pillars together ryngeal musculature during sleep, electrical stimulation of the
at the inferior aspect of the tonsillar fossa. In a series of 10 hypoglossal nerve has been proposed as a method to improve
patients with at least moderate OSA and lateral pharyngeal wall the neuromuscular tone of the pharynx during sleep, particu-
collapse on endoscopy, Cahali noted a significant decrease in larly the genioglossus. Early reports demonstrated that it was
mean AHI (45.8 preoperatively decreasing to 15.2 postopera- possible to stimulate the hypoglossal nerve and thereby increase
tively, P = .009) as well as subjective improvements in sleep the muscular tone of the pharynx and improve inspiratory
quality and daytime alertness. All 10 patients experienced some airflow without awakening the patient.101,102 Subsequently, an
degree of dysphagia that eventually resolved, but the median implantable hypoglossal nerve-stimulating device was devel-
time to normal swallowing was 14.5 days, and one patient expe- oped that could reliably detect the onset of the inspiratory
rienced dysphagia for 70 days. In a more recent report by Mesti phase of respiration through chest wall pressure sensors, allow-
and Cahali97 based on 20 patients, the authors were able to ing the electrical stimulation of the hypoglossal nerve to be
achieve a more consistent return to normal swallowing with a timed with inspiration. In 2001, Schwartz and colleagues103
range of 14 to 33 days (mean 21.6 days). This was attributed to implanted this device into 8 patients and demonstrated a
a careful preservation of the stylopharyngeus during dissec- significant improvement in mean AHI during both non–rapid-
tion of the superior constrictor muscle. In 2004, Cahali and eye-movement sleep (NREMS; 52 vs. 23 events/hour when
Ant. bundle levator

Palatine aponeurosis Auditory
Osteotomy tube
Levator veli
* palatini
Salpingo-
pharyngeus
Palato-
pharyngeus
A
FIGURE 18-14. Z-palatoplasty. Note the anterolateral direction of pull

(arrows) on the soft palate, which widens the retropharyngeal space. (From
Friedman M, Schalch P. Z-palatoplasty. Oper Techn Otolaryngol 2007;18:2.)
B
A
B
FIGURE 18-13. Midsagittal depiction of palate showing palatal advance-

ment. A, Drill holes are placed from the oral cavity to the nose and are
anterior to bone removal (orange). A strong rim of bone supports the sutures.
The anterior extent of the middle flap is placed in the thinner palatal mucosa.
Mucosa is thicker posteriorly (asterisk). B, After osteotomy, sutures are
placed through the drill holes, and the bone fragment with attached tendon
and ligaments is advanced. Ant., anterior. (From Woodson BT. Transpalatal
advancement pharyngoplasty. Oper Tech Otolaryngol 2007;18;11.)
C D
stimulated, P < .001) and rapid-eye-movement sleep (REMS; 48
vs. 17 events/hour when stimulated, P < .001). In a series of 21
patients who had a similar device implanted and used it for an
average of 5.8 hours per night, Eastwood and colleagues104
found a similar improvement after 6 months (mean AHI was
43 at baseline vs. 20 stimulated). Using a standard definition of
surgical success (AHI <20 and >50% reduction in AHI postop-
eratively), they noted a 67% (12/18) success rate. A follow-up
study of 30 patients reported by Schwartz and associates105 dem-
onstrated a dose-response relationship between the amplitude
of current used to stimulate the hypoglossal nerve and the E
maximal inspiratory airflow. Goding and colleagues102 studied
26 patients who had a hypoglossal nerve stimulator implanted FIGURE 18-15. Expansion sphincter pharyngoplasty technique. A, Preop-
erative view of the oropharynx. B, Exposure of the palatopharyngeus (verti-
with cross-table fluoroscopy and found improvement in the cal fibers). C, Elevation of the palatopharyngeus. D, Rotation and tunneling
width of both the retrolingual (100% of patients) and retro- of the palatopharyngeus toward the hamulus. E, Suture suspension and
palatal (65%) airways. Van de Heyning and colleagues106 carried approximation. (From Woodson BT, Sitton M, Jacobowitz J. Expansion sphincter
out a two-part prospective intervention study to investigate the pharyngoplasty and palatal advancement pharyngoplasty: airway evaluation and
predictors of success with hypoglossal nerve stimulation. In part surgical techniques. Oper Techn Otolaryngol 2012;23:6.)
A B
FIGURE 18-16. The genioglossal advancement procedure: rectangular geniotubercle osteotomy modification. A, Anterior view. The rectangular geniotubercle
osteotomy modification offers excellent tension on the genioglossus muscle with a minimal fracture risk, and it is technically reliable. The geniotubercle frag-
ment is rotated enough to allow bony overlap. A single inferiorly placed miniscrew is used to fix the fragment. B, Lateral view. (From Troell RJ, Riley RW, Powell
NB, Li K. Surgical management of the hypopharyngeal airway in sleep disordered breathing. Otolaryngol Clin North Am 1998;13:983.)
one, 22 patients with a BMI below 35 kg/m2 and an AHI of 25 treatment method, especially in light of the fact that most
or greater had a hypoglossal nerve stimulator implanted and patients require multiple sessions.111
were evaluated for predictors of response to treatment (AHI
reduced ≥50% from baseline and an AHI <20 at 6 months). Hypopharyngeal Procedures
The combination of AHI of 50 or below and BMI of 32 kg/m2 Surgical treatment of the hypopharyngeal area comprises pro-
or less were significantly associated with therapy success. In cedures designed to prevent tongue collapse into the airway
patients who met these criteria, the success rate was 55% (6 of during sleep. Genioglossal advancement (GA) and hyoid
11) compared with 0% of patients who did not meet these myotomy (HM) both create an enlarged retrolingual airway. In
criteria. In part two, patients were specifically selected for GA, the genial tubercle of the mandible, which is the anterior
device implantation based on these criteria, and in these 8 attachment of the genioglossus muscle, is mobilized by means
patients, mean AHI improved from a baseline of 39 to 10 of limited osteotomy (Fig. 18-16). The segment is then advanced
(P < .01) at 6 months after implantation. Taken as a whole, the and fixed into place at the inferior aspect of the osteotomy. In
results of these investigations suggest that hypoglossal nerve four case series, GA performed as a solo procedure has been
stimulation is promising, but it likely can only produce a partial shown to have success rates from 39% to 78% in patients with
response, and not all patients will benefit equally. Further severe OSA (mean preoperative RDI 53 to 59).111 HM requires
studies are required to refine the synchronization algorithms that the hyoid be mobilized via inferior myotomy and fixed
used to time the electrical pulses and to better determine which anteriorly and inferiorly by attachment to the thyroid cartilage
patients would be the best candidates for this device. As of early (Fig. 18-17). Success rates for HM performed with UPPP range
2013, these devices were not yet approved for patient use from 52% to 78% in three series that included patients
outside of clinical trials. with mean BMIs below 30.111 However, in one series with a
patient mean BMI of 34.1, the success rate was only 17%
Tongue-Base Procedures (5/29).112 These procedures result in an enlarged retrolingual
Partial midline glossectomy (PMG), lingualplasty, and radiofre- airway by fixing the major dilators of the pharyngeal airway
quency ablation (RFA) of the tongue base have been developed forward without changing dental occlusion. Complications
to address the retrolingual collapse or narrowing that occurs in associated with GA and HM include permanent numbness in
OSA. Lingual tonsillectomy may also be helpful in patients with 6%, infection in 2% to 5%, need for a root canal in 4%, and
lingual tonsillar hypertrophy. PMG creates a larger retrolingual seroma in 2%. In addition, the risk of mandibular fracture,
airway by removal of a midline rectangular strip of the posterior aspiration, and death is less than 1%.113 The ERS recommends
half of the tongue. In selected patients, lingual tonsillectomy, that both GA and HM be reserved for multilevel surgery in
reduction of the aryepiglottic folds, and partial epiglottectomy carefully selected candidates with retrolingual/hypopharyngeal
are also performed.107 With lingualplasty, additional tongue obstruction.60
tissue is removed posteriorly and laterally to that portion The Repose tongue suspension procedure fixes the tongue
excised in PMG. Woodson and Fujita108 reported that lingual- forward, thereby preventing collapse into the airway. Via an
plasty resulted in a 79% response rate in patients who had previ- intraoral incision made in the frenulum, a titanium screw is
ously failed UPPP. Because of the significant degree of tongue placed at the lingual cortex of the geniotubercle of the man-
swelling that often occurs after these procedures, they are often dible, and a permanent suture is passed through the parame-
performed in combination with a tracheotomy for airway dian tongue musculature along the length of the tongue,
protection. through the tongue base, and then back through the length of
RFA of the tongue base decreases upper airway collapse by the tongue musculature. It is then anchored to the screw to
producing a volumetric reduction in tongue-base tissue via the pull the tongue base anteriorly.114 When performed with UPPP,
generation of scar tissue. An insulated probe that delivers RF reported success rates range from 20% to 57%,111 although one
energy at 465 KHz109 is introduced into several areas of the study demonstrated a 3-year surgical success rate of up to 78%
tongue base and produces coagulation necrosis and healing by for patients with severe OSA who refused nasal CPAP.115 Pres-
scar. The procedure is often performed in an outpatient setting ently, tongue suspension is not recommended as a single treat-
under local anesthesia and may require multiple treatments to ment option for obese patients with moderate to severe OSA.
achieve the desired results.110 A review of 11 series showed Maxillomandibular advancement increases the retropalatal
success rates from 20% to 83% with multiple RFA applications and retrolingual airway (Fig. 18-18). The maxilla and mandible
and concluded that this procedure is not adequate as a sole are advanced by means of Le Fort I maxillary and sagittal-split
which resulted in death); 3 patients had hemorrhage; and 1

patient had arrhythmia. Patients with intubation problems
were more likely to be heavier, whereas the patients with extu-
bation complications had been given significantly more nar-
cotic pain medications during the procedure. Risk of a
perioperative complication was unrelated to age, preoperative
symptoms, concurrent medical problems, or the performance
of simultaneous septoplasty or tonsillectomy. In 1990,
Fairbanks91 did a national survey of 72 sites carrying out UPPP
and found that over 9 years, there were 16 deaths, with 46 cases
of nasopharyngeal stenosis and 42 cases of palatal incompe-
tence. Additional complications reported include hemorrhage
and wound dehiscence.
Because of the recognized temporary increased risk of
airway compromise after surgery, patient care algorithms have
been developed to minimize patient morbidity and mortal-
ity.118,119 Hospitalization is recommended for most patients who
undergo airway surgery, and admission to the intensive care
unit should be considered in multilevel surgery.120 A prospec-
tive evaluation of patients with severe OSA showed that nasal
CPAP used for the first postoperative night was effective in
keeping oxygen saturations above 90%, even though the mean
preoperative oxygen saturation level was 51.5%.121 Based on
these findings, it is recommended that patients with severe OSA
use CPAP for the first 2 weeks after surgery. In addition, it is
recommended that postoperative PSG be carried out in 3 to 4
months to evaluate the response to surgery.
SLEEP DISORDERS
FIGURE 18-17. The modified hyoid myotomy and suspension procedure.
(From Riley R, Powell N, Guilleminault C. Obstructive sleep apnea and the hyoid: Otolaryngologists generally focus their attention on the diag-
a revised surgical procedure. Otolaryngol Head Neck Surg 1994;111:717.) nosis and treatment of OSA, and little consideration is given to
the presence of additional sleep disorders in patients suspected
to have OSA. A 2005 study retrospectively reviewed 643 con-
mandibular osteotomies. This procedure is usually performed secutive patients diagnosed with OSA in a sleep disorder center
after other surgical intervention has been unsuccessful, and and found that 31% had coexistent sleep disorders.122 In this
potential complications include malocclusion, relapse, nerve population, 19 different sleep disorders were concomitantly
paresthesia, nonunion or malunion, temporomandibular joint
problems, infection, bleeding, and the need for subsequent
dental work. The success rate of this procedure approaches
90%.116
Tracheotomy
Tracheotomy represents the traditional gold standard of surgi-
cal management of OSA. It relieves OSA by completely bypass-
ing the portion of the airway that most commonly collapses
during sleep. However, the associated psychosocial problems,
perceived inconvenience, and morbidity rarely make trache-
otomy a desirable surgical option. However, it should be con-
sidered in patients who have failed all other OSA treatments,
in those who have life-threatening OSA and are unable to toler-
ate CPAP, or in patients who are neurodevelopmentally
impaired.117 Tracheotomy may also be the best option for the
morbidly obese or as an interim measure for patients undergo-
ing base of tongue surgery.
POSTOPERATIVE MANAGEMENT
With the trend toward multisite surgical treatment of OSA,
there may be an increased chance of postoperative airway
obstruction because of resultant edema in multiple sites in the
upper airway. In addition, postanesthesia sedation along with FIGURE 18-18. The maxillomandibular advancement procedure, lateral
altered respiration secondary to narcotic pain medications can view. Le Fort I maxillary osteotomy with rigid plate fixation and a bilateral
sagittal split mandibular osteotomy with bicortical screw fixation. The
be additive in patients with an already compromised airway. advancement is at least 10 mm. A previous genioglossal advancement is
In a retrospective review of 135 patients who underwent shown. (From Powell NB, Riley RW, Guilleminault C. The hypopharynx: upper
surgery for OSA, Esclamado and colleagues118 identified com- airway reconstruction in obstructive sleep apnea syndrome. In Fairbanks DNF,
plications in 13% of patients: 14 were airway issues, such as Fujita A, eds: Snoring and obstructive sleep apnea, ed 2. New York: Raven Press;
failed intubation and airway obstruction after extubation (1 of 1994:205.)
TABLE 18-5. Prevalence of Concomitant Sleep Disorders in Patients with Obstructive Sleep Apnea
Prevalence Among Prevalence Among
Disorder Number Other Disorders (%) Total Cohort (%)
Inadequate sleep hygiene 93 41.7 14.5
Periodic limb movement disorder 52 23.3 8.1
Narcolepsy 16 7.2 2.5
Primary (idiopathic) insomnia 14 6.3 2.2
Central alveolar hypoventilation 9 4.0 1.4
Shift-work disorder 5 2.2 0.8
Psychophysiologic insomnia 5 2.2 0.8
Bruxism 5 2.2 0.8
Idiopathic hypersomnia 4 1.8 0.6
Sleepwalking 3 1.3 0.5
Sleep talking 3 1.3 0.5
Environmental sleep disorder 3 1.3 0.5
Hypnotic-dependent sleep disorder 3 1.3 0.5
Delayed sleep phase syndrome 3 1.3 0.5
Toxin-dependent sleep disorder 1 0.1 0.2
Sleep terrors 1 0.4 0.2
Nightmares 1 0.4 0.2
Enuresis 1 0.4 0.2
Confusional arousals 1 0.4 0.2
Data from Scharf SM, Tubman A, Smale P. Prevalence of concomitant sleep disorders in patients with obstructive sleep apnea. Sleep Breath 2005;9:50.
diagnosed in patients with OSA, with the most common being characterized by specific electroencephalographic patterns.
inadequate sleep hygiene (15%) and periodic limb movement Stage N1, previously stage 1, is a transition stage between sleep
disorder (8%; Table 18-5). Therefore screening for the pres- and wake in which a mixed voltage pattern emerges with waves
ence of concurrent sleep disorders is important both at the of 3 to 7 cycles/sec. People may feel that they are awake in this
time of OSA diagnosis and in patients with persistent disease stage. Stage N2, previously stage 2, is identified by the presence
after medical or surgical treatment. of spindles and K complexes and may be the first true sleep
stage. Stage N3, previously stages 3 and 4, is also referred to as
slow-wave sleep and is distinguished by delta waves, which are
CLASSIFICATION OF SLEEP DISORDERS high-amplitude waves (up to 2 cycles/sec) that make up at least
The second edition of the International Classification of Sleep 20% of a 30-second scoring period, known as an epoch. Stage R,
Disorders (ICSD-2) changed the classification of sleep disorders REM sleep, is characterized by rapid eye movements and low-
from a dichotomized system of intrinsic and extrinsic sleep frequency mixed-amplitude waves. REM periods usually alter-
disorders to a categoric system with six main disease groupings nates with NREM periods in 90-minute cycles, with REM periods
and two sections of miscellaneous conditions (Box 18-7).9 increasing in length as the night goes on.
These disease categories include insomnia, sleep-related
breathing disorders, hypersomnias of central origin, circadian Insomnia
rhythm sleep disorders, parasomnias, sleep-related movement Insomnia is defined as recurrent difficulty with sleep initiation,
disorders, isolated symptoms/apparently normal variants/ maintenance, consolidation, or quality; insomnia causes
unresolved issues, and other sleep disorders. OSA, the sleep daytime dysfunction that exists despite adequate occasion and
disorder most commonly treated by otolaryngologists, is opportunity for sleep.123 This may include sleep that is non-
covered in the sleep-related breathing disorders category. restorative or of poor quality. Using this definition, the National
Sleep is divided into rapid-eye-movement (REM) and non– Institutes of Health State-of-the-Science Conference estimated
rapid-eye-movement (NREM) stages. About 80% of the night that insomnia occurs in 10% of adults.124 Children also suffer
is spent in NREM, which is divided into three stages from insomnia, which has been reported to occur in 20% to
30% of infants, toddlers, and preschoolers125 and in 12% to
30% of adolescents.126 In children, caregivers may report that
Box 18-7. CLASSIFICATION OF SLEEP DISORDERS a child has difficulty with sleep initiation, reluctance to go to
Insomnia bed, or an inability to sleep independently. Daytime symptoms
Sleep-related breathing disorders must include at least one of the following: fatigue or malaise,
Hypersomnias of central origin cognitive impairment (attention, concentration, or memory),
Circadian rhythm sleep disorders social/vocational difficulty or poor school performance, mood
Parasomnias impairment or irritability, daytime sleepiness, reduced motiva-
Sleep-related movement disorders tion or energy, and tendency to be accident prone in addition
Isolated symptoms, apparently normal
Variants and unresolved issues
to physical symptoms such as headache, muscle tension, GI
Other sleep disorders symptoms, or concerns about sleep itself. A number of different
subtypes of insomnia have been described (Box 18-8).9
sleep apnea syndromes along with disorders related to hypoven-

Box 18-8. INSOMNIA DISORDERS
tilation and hypoxemia (Box 18-9).
Adjustment insomnia (acute insomnia) Central sleep apnea (CSA) is characterized by an absence in
Psychophysiologic insomnia respiratory effort that results in an absence of airflow. Central
Paradoxic insomnia hypopneas, which are categorized with central apneas, are char-
Idiopathic insomnia acterized by a reduction in respiratory effort that results
Insomnia as a result of a mental disorder
in a reduction of airflow because of nervous system or cardio-
Inadequate sleep hygiene
Behavioral insomnia of childhood pulmonary dysfunction, such as chronic obstructive pulmonary
Insomnia as a result of a drug or substance disease or congestive heart failure.130 Patients with CSA often
Insomnia as a result of a medical condition come to medical attention with symptoms similar to OSA, such
Insomnia not as a result of a substance or known physiologic condition, as EDS, snoring, witnessed apneas, and waking up with short-
unspecified (nonorganic insomnia) ness of breath. Similar to OSA, CSA in adults is defined by
Physiologic (organic) insomnia, unspecified greater than five apneas per hour, although they are differenti-
ated by being central in nature.9 Infants often outgrow central
sleep apnea as they age.131
Sleep-related hypoventilation/hypoxemic syndromes are
Psychophysiologic insomnia is associated with anxiety about subcategorized as congenital, idiopathic, or the result of
sleep and difficulty falling asleep in planned situations. Often, medical conditions such as parenchymal pulmonary disease,
learned behaviors prevent the onset of sleep in these patients. vascular disease, and neuromuscular or chest wall disorders.
Psychophysiologic insomnia may occur in up to 2% of the Hypoventilation is a physiologic condition characterized by
general population.9 Paradoxic insomnia, although less common, hypercapnea with arterial carbon dioxide tension greater than
is also associated with daytime dysfunction, but it may be far 45 mm Hg in an arterial blood gas measurement.9 This eleva-
less than would be expected given the patient’s complaints. tion is precipitated by an imbalance between the elimination
Patients with paradoxic insomnia may report little or no sleep, and production of carbon dioxide and is chronic in nature
but there is often a mismatch between perceived sleep time and (i.e., not precipitated by an acute event within the past month).
time recorded by sleep study or actigraphy. Idiopathic insomnia Ventilation is usually adequate while patients are awake, but
often begins during infancy or childhood, is lifelong, and has hypoventilation occurs with the shallow breathing and decreased
no other identifiable cause. Behavioral insomnia of childhood, tidal volumes of sleep.132
on the other hand, is related to specific, identifiable limit-
setting issues or sleep-onset behavioral patterns that prevent Hypersomnias of Central Origin
children from falling asleep. These are often associated with Central hypersomnias are disorders that are not due to circa-
caregiver behaviors or patterns and may manifest as require- dian rhythm disorders, sleep-related breathing disorders, or
ments for special rituals or extended processes to fall asleep.127 other causes of disturbed nocturnal sleep. They are primarily
Inadequate sleep hygiene is diagnosed when insomnia per- characterized by EDS, but they are diagnosed only after the
sists for at least 1 month and includes at least one of the fol- previously mentioned sleep disorders have been ruled out.
lowing: improper sleep scheduling that includes frequent Central hypersomnias include narcolepsy, recurrent hypersom-
daytime naps; variable bedtime or wake time or excessive nia, and idiopathic hypersomnia (Box 18-10).
amount of time in bed; the routine use of narcotics, caffeine, Daytime sleepiness is characterized by difficulty staying
or alcohol, especially before bed; participation in mentally or awake or alert, resulting in inadvertent sleep during the day.
physically stimulating activities close to bedtime; frequent use Sleepiness is most commonly measured by the multiple sleep
of the bed for other activities, such as television watching or
reading; or failure to maintain a comfortable sleep setting that
includes appropriate temperature, lighting, and bedding.9 Box 18-9. SLEEP-RELATED BREATHING DISORDERS
Although sleep hygiene is not often the primary cause of insom-
nia, it may complicate adequate treatment unless addressed.128 Central Sleep Apnea Syndromes
In addition, inadequate sleep hygiene is often present in con- Primary central sleep apnea
junction with other sleep disorders and may be diagnosed as a Central sleep apnea as a result of Cheyne-Stokes breathing pattern
secondary sleep disorder. Central sleep apnea as a result of high-altitude periodic breathing
Insomnia in very young children is often related to a mis- Central sleep apnea as a result of a medical condition other than
match between caregiver expectations and childhood develop- Cheyne-Stokes breathing
Central sleep apnea as a result of a drug or substance
ment.127 Behavioral insomnia of childhood should be considered Primary sleep apnea of infancy
in younger children. Often insomnia in the pediatric popula-
tion is treated with appropriate sleep hygiene, strict limit Obstructive Sleep Apnea Syndromes
setting, and/or behavioral therapy. In addition, common-sense Obstructive sleep apnea, adult
methods such as decreasing fluids before bed and timing stimu- Obstructive sleep apnea, pediatric
lant medications, such as those used for attention deficit– Sleep-Related Hypoventilation/Hypoxemic Syndromes
hyperactivity disorder, should be instituted before considering Sleep-related nonobstructive alveolar hypoventilation, idiopathic
pharmacologic intervention. The occurrence of the delayed Congenital central alveolar hypoventilation syndrome
sleep phase circadian rhythm disorder (defined later) should Sleep-related hypoventilation/hypoxemia as a result of a medical
also be evaluated in older children and adolescents. In addi- condition
Sleep-related hypoventilation/hypoxemia as a result of a pulmonary
tion, special populations such as those with autism or Asperger parenchymal or vascular pathology
syndrome have been shown to have an increased incidence of Sleep-related hypoventilation/hypoxemia as a result of lower airway
insomnia.129 obstruction
Sleep-related hypoventilation/hypoxemia as a result of neuromuscular
Sleep-Related Breathing Disorders and chest wall disorders
Conditions included in this section are distinguished by disor- Other Sleep-Related Breathing Disorders
dered breathing during sleep, whether of an obstructive or Sleep apnea/sleep-related breathing disorder, unspecified
central nature. This section includes central and obstructive
adults.139 In this disorder, sleep onset is delayed, usually more

Box 18-10. HYPERSOMNIAS OF CENTRAL ORIGIN
than 2 hours, and often it is later than desired. Sleep duration
NOT A RESULT OF CIRCADIAN RHYTHM SLEEP
and quality are usually normal, but the natural wake-up time is
DISORDER, SLEEP-RELATED BREATHING DISORDER, OR
OTHER CAUSES OF DISTURBED NOCTURNAL SLEEP delayed; if people affected with this disorder are allowed to
sleep according to their desired sleep schedule, they will have
Narcolepsy with cataplexy difficulty falling asleep at a conventional sleep time and will
Narcolepsy without cataplexy wake up late after an appropriate sleep duration.
Narcolepsy as a result of a medical condition The advanced sleep phase type is also common but is more
Narcolepsy, unspecified frequently seen in older adults.140 These patients have difficulty
Recurrent hypersomnia
staying awake as late as they would like and commonly wake up
Klein-Levin syndrome
Menstrual-related hypersomnia earlier than desired. They may be less likely to seek medical
Idiopathic hypersomnia with long sleep time attention, because fewer social problems result from early
Idiopathic hypersomnia without long sleep time morning awakening. These patients also have normal sleep
Behaviorally included insufficient sleep syndrome duration and quality for their age, but their natural sleep-onset
Hypersomnia as a result of a medical condition time is shifted earlier in time than desired.
Hypersomnia as a result of a drug or substance The shift-work type of CRSD may affect up to 32% of night-
Hypersomnia not as a result of a substance or known physiologic time shift workers and 26% of rotating shift workers.141 It has
condition (nonorganic hypersomnia) been estimated that 18% of the U.S. population may be engaged
Physiologic (organic) hypersomnia, unspecified
in shift work that falls at least partially outside the daytime
hours of 6 am to 6 pm.142 It is characterized by insomnia or EDS
associated with a work schedule that overlaps the normal sleep
time and persists for at least 1 month.9 This tends to remit if
latency test (MSLT) after a documented night without signifi- sleep onset returns to a more traditional sleep time.
cant sleep-disordered breathing. The ESS may also be used to Lastly, the jet lag type of CRSD is a temporary condition
screen for sleepiness in this population.133 The MSLT is a test associated with travel across at least two time zones, causing
of the tendency to fall asleep in darkened, quiet situations insomnia or EDS. Its onset is usually 1 to 2 days after travel, and
during the day. It is the primary test for daytime sleepiness and resolution depends on the number of time zones crossed and
is only considered valid if at least 6 hours of polysomnographi- the direction of travel; eastward travel, or phase advancement,
cally characterized sleep occurs before initiation and at least is harder to adjust to than westward travel.143
2 hours passes between the nap opportunities. The time to
sleep onset and the occurrence of sleep-onset REM periods Parasomnias
(SOREMPs) is recorded for four or five naps during the day.134 Parasomnias are undesirable movements or subjective phenom-
Narcolepsy is strongly suspected with two or more SOREMPs ena that occur either while falling asleep, while waking up, or
and an average nap sleep onset of less than 8 minutes. Charac- during sleep itself. These phenomena include autonomic
teristic features include sleep paralysis, the inability to move nervous system activation and abnormal movements, dreams,
upon awakening in 25%, hypnagogic hallucinations, the sensa- emotions, or behaviors.9 As a group, parasomnias tend to
tion of dreaming while awake in 30%, and cataplexy, a sudden appear early in childhood and often have a steady and gradual
and transient loss of muscle tone in response to strong emo- transformation with resolution of symptoms that suggests that
tions in 70%.135 Narcolepsy is subdivided into two categories, the etiology may be maturational. Spontaneous remission with
one with cataplexy and one without. In addition, a cerebrospi- age is common, and no obvious clinical abnormalities are
nal fluid hypocretin-1 level below 110 pg/mL is highly specific usually apparent while the affected individual is awake. Few
for narcolepsy with cataplexy.136 Narcolepsy rarely occurs before pathophysiologic abnormalities have been identified to explain
4 years of age, and only 6% of patients who come to medical parasomnias. They are categorized as disorders of arousal
attention do so at an age younger than 10 years.137 The onset (during NREM) or as REM sleep–related parasomnias and
primarily occurs from 15 to 30 years of age and has equal other parasomnias (Box 18-12).
prevalence among men and women. Sleep terrors, sleepwalking, and confusional arousals are
Idiopathic hypersomnia is characterized by severe EDS with disorders of arousal that usually occur in the first third of the
either normal sleep time (6 to 10 hours) or prolonged sleep night, predominate in childhood, and commonly decrease in
time (>10 hours) and great difficulty awakening either from frequency with age.144 Most of these can be treated with reas-
nocturnal sleep or naps. It also results in an average nap sleep surance or improved sleep hygiene. Pharmacologic interven-
onset of less than 8 minutes on MSLT but with fewer than two tion is rarely necessary.
SOREMPs (often none), and the REM-intrusion features of REM sleep–related parasomnias include REM sleep behav-
narcolepsy are absent. This disorder usually has an onset earlier ior disorder (RBD), isolated recurrent sleep paralysis, and
than 25 years of age and is insidious in nature.138
Circadian Rhythm Sleep Disorders
The body’s internal clock is located in the suprachiasmatic Box 18-11. CIRCADIAN RHYTHM SLEEP DISORDERS
nucleus. This endogenous system, along with external light and Circadian rhythm sleep disorder, delayed sleep phase type
social cues, keeps people regulated on a 24-hour clock. Circa- Circadian rhythm sleep disorder, advanced sleep phase type
dian rhythm sleep disorders (CRSDs) occur when personal Circadian rhythm sleep disorder, irregular sleep-wake type
sleep-wake patterns are misaligned with the societal clock on a Circadian rhythm sleep disorder, free-running type
persistent or recurrent basis, thus leading to EDS or insomnia Circadian rhythm sleep disorder, jet lag type
and resulting in impaired function. A number of disorders fall Circadian rhythm sleep disorder, shift-work type
within this category, but the underlying dysfunction in all of Circadian rhythm sleep disorder as a result of a medical condition
them is that people are unable to sleep when they need to Other circadian rhythm sleep disorder (circadian rhythm disorder not
otherwise specified)
(Box 18-11). Other circadian rhythm sleep disorder as a result of a drug or
The most common of the CRSDs is the delayed sleep phase substance
type. It is especially common among adolescents and young
Box 18-12. PARASOMNIAS Box 18-14. SLEEP-RELATED MOVEMENT DISORDERS

Disorders of Arousal (from NREM Sleep) Restless leg syndrome
Confusional arousals Periodic limb movement disorder
Sleepwalking Sleep-related leg cramps
Sleep terrors Sleep-related bruxism
Sleep-related rhythmic movement disorder
Parasomnias Usually Associated with REM Sleep Sleep-related movement disorder, unspecified
REM sleep behavior disorder (including parasomnia overlap disorder Sleep-related movement disorder as a result of a drug or substance
and status dissociatus) Sleep-related movement disorder as a result of a medical condition
Recurrent isolated sleep paralysis
Nightmare disorder
Other Parasomnias
Sleep-related dissociative disorders comorbid sleep apnea is suspected. However, in patients who
Sleep enuresis experience sleep-related violent behaviors or EDS, or when
Sleep-related groaning (catathrenia) events are frequent, age of onset is unusual, or clinical features
Exploding head syndrome are unusual, PSG may be indicated.144
Sleep-related hallucinations
Sleep-related eating disorder Sleep-Related Movement Disorders
Parasomnia, unspecified
Sleep-related movement disorders are characterized by repeti-
Parasomnia as a result of a drug or substance
Parasomnia as a result of a medical condition tive movements that occur during sleep and lead to sleep dis-
ruption (Box 18-14). The most common of these are restless
REM, rapid eye movement; NREM, non–rapid eye movement. leg syndrome (RLS) and periodic limb movement disorder
(PLMD).148,149 RLS is defined as an uncomfortable sensation in
nightmare disorder. RBD results from a persistence of muscle the legs causing an urge to move them. This discomfort is
tone during REM, and injurious movements may occur while worsened by inactivity, occurs more commonly in the evening
acting out dreams. RBD is often associated with, and may or night, and usually is relieved by movement. In children,
precede the onset of, neurologic disorders such as Parkinson diagnosis may be aided by a family history of RLS or documen-
disease and Lewy body dementia.145 PSG is indicated because tation by PSG of more than five periodic limb movements per
patients with OSA may have arousals during REM that mimic hour.150 Current research investigating the pathophysiology of
RBD.146 Nightmare disorder is characterized by recurrent epi- RLS has implicated low iron levels and disruption in the nigro
sodes of awakenings from sleep with recall of intensely disturb- striatal dopaminergic system. For this reason, evaluation should
ing dreams, usually accompanied by dysphoric emotions such include ferritin and transferrin saturation levels. Iron defi-
as fear, anxiety, or anger and with full alertness on awakening ciency should be treated for ferritin levels below 18 g/L or for
and immediate and clear recall.9 It is common in both child- a transferrin saturation below 16%.151
hood and adulthood and may be especially associated with PLMD is characterized by repetitive stereotypical leg move-
acute stress events or posttraumatic stress disorder. Treatment ments that occur while sleeping and result in sleep disturbance
may include reassurance, cognitive behavioral therapy, or phar- or daytime fatigue.152 Unlike RLS, in which daytime symptoms
macologic intervention.147 occur, these patients are usually unaware of the leg movements
Several parasomnias have been specifically associated with or the sleep disturbance. The prevalence of PLMD is estimated
OSA or OSA treatment (Box 18-13). These include OSA- to be between 4% and 11% of people aged 15 to 100 years, and
induced arousals from REM sleep that mimic RBD, with the it has been shown to increase with age.149 Because these disor-
occurrence of complex or violent behaviors upon arousal that ders have also been related to changes in the nigrostriatal
are dream related, and a second type that occurs after an dopaminergic system, it is hypothesized that the onset of PLMD
arousal in NREM sleep, with similar complex or violent behav- may signal a decline in dopaminergic function.149 A limited
iors that can easily be confused with disorders of arousal or a number of studies have shown some reduction in PLMD with
seizure. OSA-induced arousals in NREM can also lead to sleep- clonazepam (mechanism unknown) and dopamine agonist
related eating disorder, which itself can lead to worsening clini- therapy.153-156
cal OSA. Another associated parasomnia is the OSA-induced
cerebral anoxic attack, or nocturnal seizure, which can also
manifest with parasomnia-type complex or violent behavior.
Isolated Symptoms, Apparently Normal
Lastly, the use of nasal CPAP for OSA may result in a significant Variants, and Unresolved Issues
increase in REM, or REM rebound, leading to confusional Conditions highlighted in this group are generally thought to
arousals, sleepwalking, or sleep terrors.9 Except when RBD is occur on a continuum between normal and abnormal sleep
suspected, PSG is rarely necessary in these patients, unless (Box 18-15).9 This includes long sleepers, who generally sleep
Box 18-15. ISOLATED SYMPTOMS, APPARENTLY

Box 18-13. PARASOMNIAS ASSOCIATED WITH NORMAL VARIANTS, AND UNRESOLVED ISSUES
OBSTRUCTIVE SLEEP APNEA
Long sleeper
OSA-induced arousals from REM sleep Short sleeper
OSA-induced arousals in NREM sleep Snoring
OSA-induced cerebral anoxic attacks or nocturnal seizures Sleep talking
REM rebound from CPAP use leading to: Sleep starts (hypnic jerks)
Confusional arousals Benign sleep myoclonus of infancy
Sleepwalking Hypnagogic foot tremor and alternating leg muscle activation during
Sleep terrors sleep
Propriospinal myoclonus at sleep onset
CPAP, continuous positive airway pressure; NREM, non–rapid eye movement; Excessive fragmentary myoclonus
OSA, obstructive sleep apnea; REM, rapid eye movement.
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18sleep Apnea and Sleep Disorders

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18 Sleep Apnea and

forefront of this new field, providing a host of both traditional

HISTORIC PERSPECTIVES Apnea A cessation of airflow for at least 10 seconds

OSA associated with laryngeal obstruction from bilateral laryn-

cardiovascular disease, and neurocognitive difficulties. In a ret-

Box 18-3. PHYSICAL EXAMINATION FINDINGS

FIGURE 18-4. Fiberoptic view of the hypopharyngeal airway before the

FIGURE 18-6. Standard cephalometric tracing. A, subnasale; ANS, anterior

Awake computed tomography (CT) provides good anatomic 18

FIGURE 18-8. Polysomnographic tracing of an obstructive apnea. Abd, abdominal.

FIGURE 18-9. Polysomnographic tracing of a hypopnea. Abd, abdominal.

SaO2 Desaturation (21.3 s) [9%]

Box 18-5. SURGICAL INDICATIONS FOR TREATMENT

regarding plans for airway management. A stepwise algorithm

obstruction and 77% had retroglossal obstruction, thus illus- I II

Ant. bundle levator

FIGURE 18-14. Z-palatoplasty. Note the anterolateral direction of pull

FIGURE 18-13. Midsagittal depiction of palate showing palatal advance-

which resulted in death); 3 patients had hemorrhage; and 1

sleep apnea syndromes along with disorders related to hypoven-

adults.139 In this disorder, sleep onset is delayed, usually more

Box 18-12. PARASOMNIAS Box 18-14. SLEEP-RELATED MOVEMENT DISORDERS

Box 18-15. ISOLATED SYMPTOMS, APPARENTLY

26. Heinemann S, Graf KI, Karaus M, et al: Occurrence of obstructive

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