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Presentación clínica y diagnóstico de la apnea obstructiva

del sueño en adultos
Autor: Dr. Lewis R Kline
Editor de sección: Nancy Collop, MD
Subeditor: Dr. Geraldine Finlay

Todos los temas se actualizan a medida que se dispone de nueva evidencia y se completa nuestro proceso de
revisión por pares.

Revisión de la literatura actualizada a través de: Agosto 2021. | Este tema se actualizó por última vez: 03 de
junio de 2021.

INTRODUCCIÓN

La apnea obstructiva del sueño (AOS) es un trastorno que se caracteriza por apneas obstructivas,
hipopneas y / o excitaciones relacionadas con el esfuerzo respiratorio causadas por el colapso
repetitivo de las vías respiratorias superiores durante el sueño.

La epidemiología, la presentación clínica, el enfoque diagnóstico y las complicaciones de la AOS

se revisan aquí. La patogénesis y el manejo de la AOS se describen por separado. (Ver
"Fisiopatología de la apnea obstructiva del sueño en adultos" y "Manejo de la apnea obstructiva
del sueño en adultos").

EPIDEMIOLOGÍA

La AOS es el trastorno respiratorio más común relacionado con el sueño. La AOS es más común
entre los hombres mayores, pero también puede afectar a mujeres y niños [1]. La incidencia
aumenta después de la menopausia de tal manera que las tasas son similares en mujeres y
hombres posmenopáusicos [2,3].

La prevalencia estimada en América del Norte es de aproximadamente 15 a 30 por ciento en

hombres y de 10 a 15 por ciento en mujeres, cuando la AOS se define ampliamente como un
índice de apnea-hipopnea (IAH) superior a cinco eventos por hora de sueño [4,5]. Cuando se
utilizan definiciones más estrictas (por ejemplo, IAH ≥5 eventos por hora más síntomas o IAH ≥15
eventos por hora), la prevalencia estimada es de aproximadamente el 15 por ciento en hombres y
el 5 por ciento en mujeres [4-6]. Las estimaciones globales que utilizan cinco o más eventos por
hora sugieren tasas de 936 millones de personas en todo el mundo con AOS leve a grave, y 425
millones de personas en todo el mundo con AOS moderada a grave, entre las edades de 30 y 69
años de edad [7].

La prevalencia de la AOS también varía según la raza. La AOS es más frecuente en los
afroamericanos que son menores de 35 años en comparación con los caucásicos del mismo
grupo de edad, independientemente del peso corporal [8,9]. La prevalencia de la AOS en Asia es
similar a la de los Estados Unidos, a pesar de las tasas más bajas de obesidad [10].

La prevalencia parece estar aumentando y puede estar relacionada con el aumento de las tasas
de obesidad o el aumento de las tasas de detección de AOS. En un estudio, la prevalencia
estimada de AOS entre 1990 y 2010 aumentó del 11 al 14 por ciento en hombres adultos y del 4
al 5 por ciento en mujeres adultas [5]. Otro estudio del Reino Unido también demuestra un
aumento significativo en las tasas de AOS y obesidad entre 1994 y 2015 [11].

FACTORES DE RIESGO Y CONDICIONES ASOCIADAS

Varios factores de riesgo clínicos están asociados con la AOS e incluyen los siguientes:

● Edad avanzada: la prevalencia de la AOS aumenta desde la edad adulta joven hasta la
sexta y séptima década, luego parece estabilizarse [4,12,13].

● Género masculino: la AOS es aproximadamente de dos a tres veces más común en los
hombres que en las mujeres, aunque el riesgo parece ser similar una vez que las mujeres
son peri y posmenopáusicas [2,13-16].

● Obesidad – El riesgo de AOS se correlaciona bien con el índice de masa corporal (IMC)
[5,14]. En un estudio, un aumento del 10 por ciento en el peso se asoció con un aumento de
seis veces en el riesgo de AOS [17]. En otro estudio, la AOS de moderada a grave (índice de
apnea-hipopnea [IAH] ≥15) estaba presente en el 11 por ciento de los hombres que tenían un
peso normal, el 21 por ciento que tenían sobrepeso (IMC de 25 a 30 kg / m2), y el 63 por
ciento de los que eran obesos (IMC >30 kg/m2) [13]. De manera similar, en las mujeres, la
AOS estaba presente en el 3 por ciento de los pacientes que tenían un peso normal, el 9 por
ciento de los que tenían sobrepeso y el 22 por ciento de los que eran obesos. La mayoría de
las personas con síndrome de hipoventilación por obesidad (SHO) tienen AOS (90 por
ciento); La SST se discute por separado. (Ver "Manifestaciones clínicas y diagnóstico del
síndrome de hipoventilación de la obesidad".

● Anomalías craneofaciales y de las vías respiratorias superiores: las anomalías

craneofaciales o de las vías respiratorias superiores aumentan la probabilidad de tener AOS
 [14]. Estos factores se reconocen mejor en pacientes asiáticos donde la obesidad no es un
factor de riesgo tan importante en comparación con los Estados Unidos [18]. Los ejemplos de
anomalías incluyen un tamaño maxilar o mandibular corto anormal, una base craneofacial
ancha e hipertrofia amigdalar y adenoide, siendo esta última común en los niños. (Ver
"Evaluación de la sospecha de apnea obstructiva del sueño en niños", sección sobre
'Factores de riesgo'.)

Los factores de riesgo menos bien establecidos incluyen los siguientes:

● Fumar – Fumar puede aumentar el riesgo de o empeorar la AOS. En un estudio, los

fumadores actuales tenían casi tres veces más probabilidades de tener AOS que los
fumadores anteriores o nunca [19].

● Antecedentes familiares de ronquidos o AOS: si bien los antecedentes familiares de

ronquidos o AOS podrían deberse a factores conductuales o ambientales compartidos,
también puede haber una predisposición genética a la AOS a través de factores como la
estructura craneofacial [20]. Se ha sugerido que alrededor del 40 por ciento de la varianza
del IAH tiene una base genética [21]. En otro estudio de brasileños rurales, la heredabilidad
de un IAH >5/hora fue intermedia (25 por ciento) [22]. (Ver "Fisiopatología de la apnea
obstructiva del sueño en adultos").

● Otros – La congestión nasal confiere un aumento de aproximadamente el doble en la

prevalencia de AOS en comparación con los controles, independientemente de la causa [14].
Sin embargo, la AOS puede o no mejorar con la corrección de la congestión nasal. La
exposición a altos niveles de dióxido de nitrógeno ambiental y partículas puede contribuir a
las variaciones en la AOS entre las poblaciones de pacientes [23].

Si bien una variedad de sustancias y medicamentos, incluidos el alcohol, las benzodiazepinas, los
narcóticos y posiblemente los gabapentinoides pueden exacerbar la AOS, no se ha demostrado
un vínculo causal [24,25]. (Ver "Manejo de la apnea obstructiva del sueño en adultos", sección
sobre 'Modificación del comportamiento'.)

La prevalencia de la AOS también aumenta en pacientes con una variedad de afecciones

médicas, incluidas las siguientes ( cuadro 1):

● SHO (ver "Manifestaciones clínicas y diagnóstico del síndrome de hipoventilación por

obesidad")

● Insuficiencia cardíaca congestiva (ver "Insuficiencia cardíaca con trastornos respiratorios del
sueño")

● Fibrilación auricular [26]

● Hipertensión pulmonar [27]

 ● Hipertensión (hipertensión particularmente resistente), enfermedad cardiovascular, fibrilación
auricular e hipertensión pulmonar (ver "Apnea obstructiva del sueño y enfermedad
cardiovascular en adultos")

● Enfermedad renal en etapa terminal (ver "Trastornos del sueño en la enfermedad renal en
etapa terminal", sección sobre 'Apnea del sueño')

● Enfermedad pulmonar crónica, incluyendo asma, enfermedad pulmonar obstructiva crónica

(EPOC) y fibrosis pulmonar idiopática (ver "Evaluación del asma grave en adolescentes y
adultos", sección sobre "Evaluación de afecciones comórbidas" y "Trastornos respiratorios
relacionados con el sueño en la EPOC")

● Accidente cerebrovascular y ataques isquémicos transitorios (ver "Trastornos respiratorios

relacionados con el sueño y accidente cerebrovascular")

● Embarazo (ver "Apnea obstructiva del sueño en el embarazo")

• Diabetes gestacional [28]

• Hipertensión inducida por el embarazo [29]

● Acromegalia (ver "Causas y manifestaciones clínicas de la acromegalia", sección sobre

'Apnea del sueño')

● Hipotiroidismo (ver "Manifestaciones clínicas del hipotiroidismo", sección sobre 'Sistema

respiratorio')

● Síndrome de ovario poliquístico (ver "Manifestaciones clínicas del síndrome de ovario

poliquístico en adultos", sección sobre 'Apnea del sueño')

● Enfermedad de Parkinson [30] (ver "Manifestaciones clínicas de la enfermedad de

Parkinson", sección sobre 'Trastornos del sueño')

● Síndrome del párpado flácido [31-33]

Otras afecciones médicas que pueden tener una mayor asociación con la AOS incluyen
fibromialgia [34,35], esófago de Barrett [36], enfermedad por reflujo gastroesofágico (ERGE)
[33,37], policitemia secundaria [38] y síndrome de Down [39]. No está claro si hay una mayor
prevalencia de AOS en el trastorno de estrés postraumático [40].

CLINICAL FEATURES

Signs and symptoms — Most patients with OSA complain of daytime sleepiness, or their bed
partner reports loud snoring, gasping, choking, snorting, or interruptions in breathing while
sleeping ( table 1). These symptoms are often detected during the evaluation of another
complaint, or during health maintenance or preoperative screening. (See "Surgical risk and the
preoperative evaluation and management of adults with obstructive sleep apnea", section on
'Screening with a questionnaire'.)  

● Daytime sleepiness – Daytime sleepiness is a common feature of OSA. Sleepiness is the

inability to remain fully awake or alert during the wakefulness portion of the sleep-wake cycle
[41]. Daytime sleepiness may be underestimated because of its insidious onset and
chronicity. The patient may use terms such as fatigue, tiredness, low energy, or poor focus
[42]. Targeted questioning of the patient and in particular their loved ones or bed partner,
however, typically reveals a pattern of feeling sleepy or falling asleep in boring, passive, or
monotonous situations. As an example, the patient may admit to consistently falling asleep
while reading, watching television, or even while operating a motor vehicle. In addition,
embarrassing or inappropriate episodes of sleep may be reported (eg, at religious services,
listening to lectures, or driving). Reviewing patient behavior away from the workplace is
essential because daytime sleepiness can be masked by activity. Patients should also always
be asked about behaviors that may mask sleepiness, such as caffeine consumption. Patients
often experience nonrestorative sleep (ie, do not wake up feeling refreshed) and nocturnal
restlessness in association with their complaint of daytime sleepiness.

Sleepiness should be distinguished from fatigue. Fatigue is defined as a subjective lack of

physical or mental energy that is perceived by the individual or caregiver to interfere with
usual and desired activities. To facilitate this distinction, a series of directed questions can be
combined with the Epworth Sleepiness Scale (ESS) to quantitatively document the patient’s
perception of sleepiness, fatigue, or both ( table 2) (calculator 1) [43,44]. An ESS score >9
indicates abnormal sleepiness and should prompt further testing. Since there is often overlap
of both sleepiness and fatigue in patients with OSA, our center administers both the ESS and
the Fatigue Severity Scale (FSS) to help identify and manage these complaints [45,46].

Additional details regarding the approach to a sleepy patient and the differential diagnosis
involved ( table 3) is provided separately. (See "Approach to the patient with excessive
daytime sleepiness", section on 'History'.)

● Snoring, choking, gasping during sleep – Snoring and associated events (ie, resuscitative
gasping or snorting, witnessed apneic periods, periods of silence followed by loud snoring,
restless or fitful sleep) are common features of OSA. It is usually helpful to have the patient's
bed partner or a family member present during the interview because they often have greater
insight than the patient into the frequency and severity of these symptoms during sleep.

While snoring is associated with a sensitivity of 80 to 90 percent for the diagnosis of OSA, its
specificity is below 50 percent. The actual percentage of snorers who have sleep apnea
varies greatly and solid data are lacking. The complaint of snoring, while common in patients
 with OSA, was found to have no predictive value in one study (likelihood ratio 1.1) [47]. On
the other hand, the absence of snoring (particularly in the absence of risk factors such as
obesity) reduces the likelihood of a diagnosis of OSA. For example, patients with mild snoring
and a body mass index (BMI) lower than 26 are unlikely to have moderate or severe OSA
[47]. A study of 1643 subjects with habitual snoring found a significant positive correlation
between the severity of the OSA and snoring intensity [48]. (See "Snoring in adults".)

Choking or gasping during sleep or wakening with a dry mouth are commonly reported, often
in association with snoring. In a systematic review of six studies that examined the accuracy
of the clinical examination in the diagnosis of OSA, nocturnal choking or gasping had a lower
sensitivity than snoring (52 versus 80 percent) but greater specificity (84 versus 50 percent)
[47].

● Morning headaches – Morning headaches are reported by 10 to 30 percent of patients with

untreated OSA [49,50]. They are usually bifrontal and squeezing in quality, with no associated
nausea, photophobia, or phonophobia. They typically occur daily or most days of the week
and may last for several hours after awakening in the morning. The cause of the headaches is
not well-established and may be multifactorial; proposed mechanisms include hypercapnia,
vasodilation, increased intracranial pressure, and impaired sleep quality. Early morning
headaches may indicate severe disease, although a consistent association with disease
severity has not been found [50-52]. (See "Evaluation of headache in adults".)

● Others – Other less common manifestations of OSA include:

• Sleep maintenance insomnia – Sleep maintenance insomnia with repetitive

awakenings should prompt consideration of OSA. Approximately one-third of patients
with OSA complain of insomnia rather than daytime sleepiness [53]. This phenomenon is
more common in females [53,54].

• Symptoms of associated conditions and complications – Some patients may present

with the symptoms of associated conditions and complications including neuropsychiatric
symptoms, postoperative hypoxemia, or nocturnal cardiovascular events such as chest
pain due to angina pectoris or palpitations due to atrial fibrillation. (See 'Risk factors and
associated conditions' above and 'Complications' below.)

• Nocturia – Nocturia is a common associated symptom of OSA [55]. When patients

repeatedly awaken from apneic events, they experience the urge to urinate, although
other physiological mechanisms may be important [56].

Physical examination — Common physical findings are the following:

● Obesity – While obesity (BMI ≥30 kg/m2) is the most common clinical finding in patients with
OSA, some patients may be overweight (BMI 25 to 29.9 kg/m2) or their weight may be within
 the normal range. (See "Obesity in adults: Prevalence, screening, and evaluation".)

● Crowded oropharyngeal airway – Numerous craniofacial conditions can narrow the upper
airway and contribute to the development of OSA ( table 4). These include retrognathia,
micrognathia, lateral peritonsillar narrowing, macroglossia, tonsillar hypertrophy, an elongated
or enlarged uvula, a high arched or narrow palate, nasal septal deviation, and nasal polyps
[57]. The modified Mallampati classification is commonly used to quantify airway narrowing,
with classes 3 and 4 considered positive for airway narrowing ( figure 1). Both the
Mallampati classification and Friedman tongue position ( figure 2) have been shown to
correlate with OSA severity [58]. (See 'Risk factors and associated conditions' above.)

● Large neck and/or waist circumference – OSA is more strongly correlated with an
increased neck size or waist circumference than general obesity [59,60]. OSA is particularly
prominent among men who have a collar size greater than 17 inches and women who have a
neck size greater than 16 inches [57]. In another study, cutoff values for waist circumference
and for waist-to-height ratio for females with OSA were 95.5 cm and 0.595, respectively,
whereas the values for males were 100.5 cm, and 0.575, respectively [61].

● Signs of associated conditions and complications – Patients with OSA may also have the
signs of associated conditions and complications, most commonly systemic hypertension and
heart failure, and less commonly pulmonary hypertension. (See 'Risk factors and associated
conditions' above and 'Complications' below.)

DIFFERENTIAL DIAGNOSIS

Several conditions may mimic OSA, depending on the presenting symptoms.

● Excessive daytime sleepiness – A variety of conditions similarly present with excessive

daytime sleepiness ( table 3). In general, they can be distinguished from OSA via clinical
history and polysomnography (PSG). However, in many circumstances, home sleep apnea
testing is not useful in evaluating for more complex sleep disorders that present with daytime
sleepiness (eg, periodic limb movement disorder, restless leg syndrome, narcolepsy, central
sleep apnea, and non-OSA related conditions associated with sleep disordered breathing).
The differential diagnosis and approach to daytime sleepiness is discussed in detail
separately. (See "Approach to the patient with excessive daytime sleepiness", section on
'Causes'.).

● Abrupt awakenings or abnormal sounds or sensations during sleep – There are

conditions that should be considered in the differential diagnosis of OSA because they
similarly cause abrupt awakenings or abnormal sounds or sensations during sleep ( table 5
).
 These conditions can also be distinguished from OSA via PSG:

• Primary snoring – Snoring is far more common than OSA. Therefore, even though most
patients who have OSA snore, most patients who snore do not have OSA. Sleep apnea
testing is the only way to distinguish snoring in association with OSA from primary
snoring. (See "Snoring in adults".)

• Gastroesophageal reflux disease – Gastroesophageal reflux disease (GERD) can

mimic OSA by producing a choking sensation and dyspnea at night. In addition, GERD
may improve with positive airway pressure therapy, further mimicking OSA [62]. Patients
may have a history of dyspepsia or symptoms of reflux, although their GERD may be
silent. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".)

• Miscellaneous – Other disorders that can mimic OSA include nocturnal asthma,
swallowing disorders, nocturnal seizures [63], and psychiatric illnesses such as panic
attacks, many of which should be evident clinically and can be distinguished from OSA
by PSG (with the exception of nocturnal seizures, most of these disorders have a
relatively normal PSG).

● Early morning headaches – Early morning headaches may also be associated with space
occupying lesions of the brain and may need to be distinguished from OSA by brain imaging.
Early morning headaches may also be a presenting manifestation of obesity hypoventilation
and may be distinguished from OSA by the presence of hypercapnia/hypercarbia on
laboratory examination. OSA is present in the majority of patients with obesity hypoventilation
syndrome (OHS; >90 percent). (See "Evaluation of headache in adults".)

DIAGNOSTIC EVALUATION

OSA should be suspected whenever a patient presents with excessive daytime sleepiness,
snoring, and choking or gasping during sleep ( table 1), particularly in the presence of risk
factors such as obesity, male gender, and advanced age. Less common manifestations are early
morning headaches, or manifestations of associated disorders (eg, hypertension) or complications
(eg, neuropsychiatric symptoms). (See 'Clinical features' above and 'Risk factors and associated
conditions' above and 'Complications' below.)

Detailed questions that explore the etiologies of daytime sleepiness, snoring, and neuropsychiatric
disease may help to tease out OSA from other conditions ( table 3 and table 2) but sleep
apnea testing is required to make the diagnosis of OSA. Details regarding taking a targeted history
and performing a comprehensive examination in patients with daytime sleepiness is provided
separately. (See "Approach to the patient with excessive daytime sleepiness", section on 'Initial
evaluation'.)
There has been debate in the literature regarding whether non-sleep experts can adequately
evaluate patients with suspected OSA [64-66]. While observational studies have suggested that
evaluation by sleep and non-sleep experts may be similar, many of the non-sleep specialists in
these studies have extensive training or experience in sleep medicine [64]. Accordingly, in support
of the American Academy of Sleep Medicine (AASM) guidelines, a comprehensive evaluation with
follow-up by a clinician who has some level of expertise in sleep medicine is appropriate [65].

Patient selection — OSA is not a clinical diagnosis and objective testing must be performed for
the diagnosis [47,67,68]. Due to the wide differential associated with the symptoms of OSA,
several clinical criteria and data from evaluation tools are used to select those who should be
tested.

Clinical parameters — Diagnostic testing for OSA should be performed on patients with

excessive daytime sleepiness (EDS) on most days and the presence of at least two of the
following clinical features of OSA: habitual loud snoring, witnessed apnea or gasping or choking
during sleep, and diagnosed systemic hypertension [65]. The rationale for these criteria is that
these features predict an increased risk of moderate to severe OSA (ie, a population most likely to
benefit from therapy).

In the absence of these criteria, many experts also perform diagnostic testing in the following:

● EDS alone

● Patients who have other clinical features of OSA (eg, obesity, fatigue, upper airway
abnormalities, snoring) and conditions or complications associated with OSA (eg, refractory
hypertension, atrial fibrillation, nocturnal angina or dysrhythmias, congestive heart failure,
stroke, and transient ischemic attacks).

● Patients in whom OSA needs to be ruled in or out as an underlying cause or potential

contributing factor to their symptoms (eg, unexplained pulmonary hypertension or
polycythemia, or motor vehicle accident due to falling asleep while driving).

Evaluation tool parameters — Most sleep experts do not routinely use evaluation tools to
select those at risk for OSA who need a sleep study since none of these tools have been shown to
be superior to a history and physical examination and their poor accuracy make them imperfect
diagnostic tools [59,65]. However, some non-sleep experts may find them useful in the outpatient
setting. The most common evaluation tools used include the STOP-Bang questionnaire ( table 6
) or variants thereof ( table 7) (calculator 2), and the Epworth Sleepiness Scale (ESS) (
table 2) (calculator 1); for example, the STOP-Bang questionnaire is often used by physicians
during preoperative evaluation to assess the risk of undiagnosed OSA. Other evaluation tools that
are also available include the Berlin score ( table 8 and table 9) and the sleep apnea clinical
score ( table 10). Importantly, none of these diagnostic tools should be used to replace a sleep
apnea testing. (See 'Instruments' below.)

Selecting home or in-laboratory testing — In-laboratory polysomnography (PSG; either full-

night [ie, diagnostic only] or split-night [ie, diagnostic and therapeutic with positive airway
pressure]) is the gold standard diagnostic test. However, for patients in whom uncomplicated OSA
is suspected and the pretest probability is estimated as moderate or severe, unattended home
sleep apnea testing (HSAT) with a Type 3 device is a reasonable alternative to in-laboratory PSG.
(See "Home sleep apnea testing for obstructive sleep apnea in adults", section on 'Type 3 devices
(portable devices)'.)

Several factors influence the choice between home and in-laboratory testing ( algorithm 1 and
table 11). These include the following:

● The patient’s profession (eg, mission-critical worker) (see 'Mission-critical workers with
suspected OSA' below)

● Suspected non-respiratory sleep disorders ( table 12) [69-71] (see 'Suspected non-
respiratory sleep disorders' below)

● Non-OSA-related conditions associated with sleep-disordered breathing ( table 13) (see

'Suspected OSA complicated by other respiratory sleep disorders' below)

● The severity of OSA (See 'Suspected uncomplicated OSA' below.)

● Others – Additional factors that influence the choice between performing a home or in-
laboratory study include the following:

• The values and preferences of the patient (eg, access to a sleep laboratory,
homelessness, space constraints, cost, wait time, concern for operator error for home
monitoring)

• The practices of the institution and preferences of the clinician

• The preference of the payer (eg, many insurers in the United States require that patients
receive home testing first)

Mission-critical workers with suspected OSA — Mission-critical workers should be tested

using attended in-laboratory PSG. The rationale for this approach is that the risk to the patient and
to others of missing a diagnosis of OSA is sufficiently high to justify laboratory testing. There is no
definition of what “mission-critical” means but it should be self-evident to the clinician that if a
patient has a job where falling asleep has a major negative impact (eg, airline pilots, bus drivers,
taxi drivers, ride-sharing drivers, truck drivers, train operators, police, security, military posts,
astronauts), then an in-laboratory sleep study is recommended. (See 'Polysomnography' below.)
 Suspected non-respiratory sleep disorders — When clinicians suspect that symptoms are
due to a non-respiratory sleep disorder or that a non-respiratory sleep disorder coexists with or
contributes to OSA, PSG should be performed. Examples of non-respiratory sleep disorders
include narcolepsy or other hypersomnia disorders, severe insomnia, parasomnias, movement
disorders (eg, periodic limb movement disorder) ( table 12). (See 'Polysomnography' below and
"Clinical features and diagnosis of narcolepsy in adults" and "Approach to abnormal movements
and behaviors during sleep" and "Polysomnography in the evaluation of parasomnias and
epilepsy" and "Clinical features and diagnosis of restless legs syndrome and periodic limb
movement disorder in adults" and "Classification of sleep disorders".)

Suspected OSA complicated by other respiratory sleep disorders — Complicated OSA

refers to the presence of medical conditions that could potentially affect respiration during sleep
and create additional respiratory abnormalities over and above those associated with OSA (
table 13). This population should have PSG testing since the detection of nonobstructive
events is underestimated and less accurate on most devices used for home testing. (See
'Polysomnography' below and "Home sleep apnea testing for obstructive sleep apnea in adults".)

Determining whether or not suspected OSA is “complicated” is practically achieved by clinically

identifying conditions that increase the risk of nonobstructive sleep disordered breathing.
Examples of conditions associated with complex sleep-disordered breathing include chronic
obstructive pulmonary disease (Global Obstructive Lung Disease [GOLD] stage 1, 2, 3) (
table 14), heart failure (New York Heart Association [NYHA] class III or IV ( table 15)),
hypoventilation syndromes (eg, obesity hypoventilation syndrome), neuromuscular weakness,
chronic opioid use, and stroke ( table 13). (See "Clinical manifestations and diagnosis of obesity
hypoventilation syndrome".)

Suspected uncomplicated OSA — Uncomplicated OSA is that which is not complicated by

other conditions that could potentially affect respiration during sleep (see 'Suspected OSA
complicated by other respiratory sleep disorders' above). Testing in this population depends upon
the suspected degree of severity of OSA.  

Pretest probability of moderate to severe OSA — We agree with the AASM, which states
that patients at high pretest probability of moderate to severe OSA include those with daytime
hypersomnolence and at least two of the following three criteria: habitual loud snoring, witnessed
apnea or gasping/choking, or diagnosed hypertension [65]. Based on an apnea-hypopnea index
(AHI) >15, the prevalence is estimated to be 64 percent in a high-risk population [59,65]. We
consider this population suitable for HSAT, provided it is performed with an adequate device (eg,
Type 3 device) and under adequate supervision with interpretation by a clinician knowledgeable in
sleep medicine ( algorithm 1 and table 11). The rationale for this approach is that HSAT has
been shown in this setting to similarly detect obstructive events compared with PSG. (See 'Home
sleep apnea testing' below and "Home sleep apnea testing for obstructive sleep apnea in adults".)
However, for those in whom a reliable assessment for the risk of OSA cannot be made using the
above criteria, such as those who do not have hypersomnolence, in-laboratory PSG is preferred.
(See 'Polysomnography' below.)

Importantly, for those in whom suspicion for OSA remains and HSAT is negative, inconclusive, or
technically inadequate, PSG should be performed; this approach is based upon the observation
that many home devices may miss nonobstructive events including arousals or limb movement
that are seen in other complex sleep disorders, which could explain the patient's symptoms.  

Pretest probability of mild OSA — For patients with suspected OSA who do not fit the
definition of a high pretest probability of moderate to severe OSA per the AASM criteria,
polysomnography is the preferred test. However, many insurers request that providers perform
HSAT first, and if negative and the suspicion for OSA remains, then proceed to in- laboratory
testing. (See 'Polysomnography' below.)

DIAGNOSTIC TESTS

Polysomnography — Attended, in-laboratory polysomnography (PSG) is considered the gold-

standard diagnostic test for OSA. Diagnostic in-laboratory PSG (full-night or split-night) rather
than home testing, is preferred in patients with the following ( algorithm 1):

● Suspected complicated OSA (eg, conditions associated with nonobstructive sleep disordered
breathing such as chronic obstructive pulmonary disease ( table 13)) (see 'Suspected OSA
complicated by other respiratory sleep disorders' above)

● Suspected nonrespiratory sleep disorders other than OSA (eg, narcolepsy ( table 12)) (see
'Suspected non-respiratory sleep disorders' above)

● Uncomplicated OSA that does not fit the definition of suspected moderate or severe OSA by
the American Academy of Sleep Medicine (AASM) criteria (see 'Pretest probability of mild
OSA' above)

● Patients with suspected OSA who are mission-critical workers (eg, airline pilots) (see
'Mission-critical workers with suspected OSA' above)

● Patients with negative, inconclusive, or technically inadequate home testing in whom the
suspicion for OSA remains high (see 'Home sleep apnea testing' below and "Home sleep
apnea testing for obstructive sleep apnea in adults")

● Patients in whom home testing is not feasible (eg, physical impairment precluding HSAT)  

Full-night study — Full-night PSG involves monitoring the patient during the patient's typical
sleep period, which is generally nighttime. For patients who are diagnosed with OSA during a full-
night study and who choose positive airway pressure (PAP) therapy, a return visit to the sleep
laboratory is sometimes required for another study, during which PAP therapy is titrated. (See
"Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)

Split-night study — Split-night PSG is similar to full-night testing, except the diagnostic portion
of the study is performed during the first part of the night only. Those patients who are diagnosed
with OSA during the first part of the night and choose PAP therapy can have PAP therapy titrated
during the second part of the night.

Many experts consider the full-night test as the gold-standard but split-night studies are commonly
used in practice.

● According to the AASM practice parameters for PSG and related procedures, a split-night
study is a valid alternative to full-night diagnostic PSG (followed by a second full night of PAP
titration) if the following criteria are met [65]: moderate to severe degree of OSA is observed
during a minimum of two hours of recording time on the diagnostic polysomnogram, and at
least three hours remain available for continuous positive airway pressure (CPAP) titration.

● Additional criteria set out by the Centers for Medicare and Medicaid Services (CMS) state that
the apnea-hypopnea index (AHI) be >15 per hour for ≥2 hours of testing and ≥3 hours of
sleep time is remaining for CPAP titration [72]. Per CMS, CPAP titration can be achieved in
the majority of cases in one night and is considered the current standard approach. Despite
CMS guidelines, insurance requirements for split-night studies are variable and need to be
checked if such testing is contemplated. Moreover, many insurance companies will not issue
a CPAP billing code for the first night of a diagnostic study, limiting coverage for a split-night
protocol.

● Some experts also specify PSG-documentation of the elimination or near-elimination of

obstructive events with PAP during rapid eye movement (REM) and non-REM (NREM) sleep.
This should include REM sleep in the supine position, when apneas are most likely to occur
[73]. (See "Titration of positive airway pressure therapy for adults with obstructive sleep
apnea".)

Further details on the therapeutic implications of split-night studies are provided separately. (See
"Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on
'Initial settings and titration during polysomnography' and "Titration of positive airway pressure
therapy for adults with obstructive sleep apnea".)

Choosing between full- and split-night studies — Although full-night studies are the gold-
standard, split-night studies are commonly chosen since, in most instances, they can provide an
accurate appraisal of disease severity and establish the correct level of PAP in a single night in the
majority of patients [71]. In general, the majority of patients, when educated to the options of
testing, prefer a split-night protocol due to the convenience and an opportunity to start therapy
after the test. Split-night PSG also decreases health care costs, minimizes scheduling delays, and
does not appear to adversely affect compliance, despite decreased available time to educate the
patient during the night [74]. Clinical practice guidelines also suggest that, if clinically appropriate,
a split-night diagnostic protocol, rather than a full-night diagnostic protocol for PSG be used for the
diagnosis of OSA [65].  

However, while a split-night study is typically the default, the decision may be changed by the
sleep technician supervising the study, depending upon his or her observations of sleep-related
events as the study progresses. Alternatively, the sleep technician may proceed with full-night
testing in a patient who does not meet the AASM criteria for a split-night study or in whom a
complex sleep disturbance is noted during the initial phase of the study. The decision may also be
affected by the clinician's suspicion that a full-night study is required. For example, based on the
guidelines, patients who are suspected to be mild are not appropriate for split-night testing.
Patients with associated complaints of insomnia also do not do well with a split-night protocol.
Also, full-night studies may be preferred in patients in whom a more complex sleep disturbance is
suspected (eg, central sleep apnea) or those in whom a split-night study has failed to elicit a clear
diagnosis of OSA. Alternatively, some of the patients who are appropriate for split-night testing
include severely symptomatic patients, older adults, those who are mentally and physically
handicapped, shift-workers needing special time arrangements, and patients with difficult
schedules due to family and work. Further details regarding CPAP titration are discussed
separately. (See "Titration of positive airway pressure therapy for adults with obstructive sleep
apnea" and "Mode selection for titration of positive airway pressure in adults with obstructive sleep
apnea".)

Despite its reputation as the gold-standard test, negative in-laboratory polysomnography should
be repeated if the clinical suspicion for OSA is high. This is supported by several studies that have
demonstrated significant night-to-night variability in PSG results [75-77] and is supported by the
AASM [65].

Polysomnography (including technique, measured variables, and derived information) is discussed

in detail separately. (See "Overview of polysomnography in adults" and "Polysomnography in the
evaluation of sleep-disordered breathing in adults".)

Home sleep apnea testing — In patients with a high pretest probability of moderate to severe
uncomplicated OSA (ie, absence of another condition known to increase the risk of sleep-
disordered breathing ( table 13)), home sleep apnea testing (HSAT) with an adequate device is
an appropriate alternative to PSG provided there is no suspicion for nonrespiratory sleep disorders
(eg, narcolepsy ( table 12)), the patient is not a mission-critical worker, and a sleep expert is
available to interpret it ( algorithm 1 and table 11) [65,78]. Importantly, should a single HSAT
be negative, inconclusive, or technically inadequate, and the suspicion remains for OSA, HSAT
should not be repeated (although some insurers prefer a second negative HSAT before
proceeding with PSG). Rather, it is strongly recommended that an in-laboratory study be
performed, due to the higher likelihood that a second test will also be negative, inconclusive, or
technically inadequate. (See 'Pretest probability of moderate to severe OSA' above.)

There are a variety of devices that are used for in-home, unattended monitoring of
cardiorespiratory parameters during sleep, few of which typically include electroencephalography.
Many HSAT devices have been validated against standard PSG, typically by testing the same
patient with both modalities in the sleep laboratory. In general, the sensitivity and specificity seem
to be high in populations at high risk of moderate to severe OSA on the basis of clinical symptoms,
assuming there are no significant comorbid medical disorders that affect sleep or non-respiratory
sleep disorders. Data that support HSAT as a viable alternative to in-laboratory PSG in this
population include the following:

● One unblinded trial randomly assigned 373 patients with suspected moderate to severe OSA
to either in-laboratory PSG with conventional CPAP titration or to HSAT with autotitrating
CPAP and subsequent transition to fixed CPAP [70]. Among patients who had moderate to
severe OSA (ie, AHI >15 events per hour), there were no differences in the number of
effective titrations, titration pressures, time to treatment, or indices of daytime sleepiness.
Patients who underwent HSAT with autotitrating CPAP were more likely to use CPAP for ≥4
hours at night.

● A randomized controlled trial compared HSAT for diagnosis followed by one night of auto-
CPAP (APAP) titration against a traditional in-laboratory approach in managing 172 clinic
patients with suspected OSA [79]. Modified intention-to-treat analysis of those with AHI
≥15/hour on CPAP reported that HSAT resulted in a similar Epworth sleepiness score and
greater improvement in Sleep-Apnea-Quality-of-Life-Index at three months. In addition, the
waiting time for all steps from diagnosis through treatment was significantly shorter than in the
group with in-laboratory testing.

● A multicenter randomized noninferiority study compared limited data obtained from PSG with
full polysomnographic data [80]. Data from PSG studies were given to sleep physicians at
varying levels: level 1 (L1; full PSG data), level 3 (L3; information on airflow,
thoracoabdominal bands, body position, electrocardiography, oxygen saturation which
simulates data included from in-home studies), and level 4 (L4; oxygen saturation and heart
rate). Diagnoses and treatment recommendations were made based upon the information
provided and outcomes including the functional outcomes of sleep questionnaire score
(FOSQ) were measured. There was no difference in the FOSQ score or in the distribution of
initial diagnoses with L1, L3, or L4 testing. However, L4 testing was associated with less
improvement in sleepiness, less CPAP use, and lower physician diagnostic confidence. While
 this study supports in-home-style testing, none of the studies were done at home, which was
a major limitation. Further validation with in-home testing is needed.

There are several commercially available devices that can be used for home testing, not all of
which compare adequately with PSG such that only devices that are considered adequate should
be used (eg, Type 3 devices). Further details regarding devices are provided separately. (See
"Home sleep apnea testing for obstructive sleep apnea in adults", section on 'Sleep monitoring
devices'.)

In-hospital testing — In response to increased requests for sleep medicine consultation, many
hospital-based centers and respiratory departments now provide bedside monitoring for inpatients
with a high pretest suspicion for sleep apnea (see 'Pretest probability of moderate to severe OSA'
above). However, most experts question the accuracy of data obtained in the hospital, given the
higher rates of co-morbidities that can affect sleep and paucity of data to support its use.
Diagnosis and management of OSA in the inpatient setting is reviewed in more detail separately.
(See "Sleep disorders in hospitalized adults: Evaluation and management", section on 'Obstructive
sleep apnea'.)

DIAGNOSIS

The diagnosis of OSA is based upon the presence or absence of related symptoms, as well as the
frequency of respiratory events during sleep (ie, apneas, hypopneas, and respiratory effort-related
arousals [RERAs])

Criteria — The diagnostic criteria and indices used on official sleep study reports vary according
to whether the data are polysomnography (PSG)- or home sleep apnea testing (HSAT)-derived (
table 16):

● PSG – The diagnosis of OSA is confirmed if either of the two criteria below is present [69]:

• There are five or more predominantly obstructive respiratory events (obstructive and
mixed apneas, hypopneas, or RERAs) per hour of sleep in a patient with one or more of
the following:

- Sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms

- Waking up with breath holding, gasping, or choking
- Habitual snoring, breathing interruptions, or both noted by a bed partner or other
observer
- Hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke,
congestive heart failure, atrial fibrillation, or type 2 diabetes mellitus
 • There are 15 or more predominantly obstructive respiratory events (apneas, hypopneas,
or RERAs) per hour of sleep regardless of the presence of associated symptoms or
comorbidities.

PSG data can generate two indices as quantitative measures of sleep-related obstructive
events per hour of sleep:

• The apnea-hypopnea index (AHI = [apneas + hypopneas] / total sleep time in hours)
• The respiratory disturbance index (RDI = [apneas + hypopneas + RERAs)] / total sleep
time in hours)

Because of the inclusion of RERAs, the RDI classifies more patients as having OSA than
does the AHI, using the same threshold values. However, there is no consensus on whether
the AHI or RDI should be the gold-standard index for diagnosis and their use varies across
insurance carriers. In our laboratory, we report both the AHI and RDI. There is conjecture that
the AHI may correlate better with cardiovascular outcomes, while the RDI may yield more
information about daytime sleepiness and symptoms. We prefer the RDI since this index
imparts more information about sleep fragmentation (RERAs) in addition to apneas and
hypopneas and adds greater sensitivity to the diagnosis of OSA. Outcome studies are needed
to determine which index is preferred. Interpretation of polysomnography-identified apneas,
hypopneas, and RERAs are provided separately. (See "Polysomnography in the evaluation of
sleep-disordered breathing in adults".)

● HSAT – Most HSAT devices do not include electroencephalogram (EEG) monitoring, and
therefore RERAs and hypopneas characterized by arousals cannot be reliably identified.
Accordingly, the number of respiratory events per hour of recording time rather than total
sleep time is used to generate the respiratory event index (REI) ( table 16). In validated
HSAT devices, the REI correlates well with AHI and RDI, but is typically lower since the
denominator (ie, total recording time) is larger than total sleep time used to calculate AHI and
RDI. Moreover, outcomes in properly selected high risk patients tested by HSAT are similar to
patients undergoing in-laboratory studies. Evidence does show that the length of the
recording time used to generate the REI with HSAT should be at least four hours [65,81]. With
these caveats in mind, cutoff values that are used for REI to diagnose OSA are similar to
those in whom in laboratory sleep testing is performed. Thus, patients with a REI ≥15 events
per hour and REI 5 to 14 and symptoms is supportive of a diagnosis of sleep apnea. Patients
with a negative study, inconclusive results or a technically inadequate study should be
evaluated in a laboratory setting. Differences among portable devices are discussed
separately. (See "Home sleep apnea testing for obstructive sleep apnea in adults".)

Classification of severity — Patients who meet criteria for a diagnosis of OSA are traditionally
classified as having mild, moderate, or severe disease on the basis of the AHI and symptoms [82].
This classification is based on consensus, and depending on definitions of "hypopnea," there can
be great variance in the AHI [83]. With increasing use of HSAT, similar stratification is being used
for REI. This is, however, also arbitrary. Moreover, the literature is confusing, often interchanging
AHI for RDI.

Although the AHI alone is not entirely predictive of the presence and severity of symptoms and
complications, the following is a general description of patients in each category.

● Mild – Patients traditionally classified as having mild OSA are those with an AHI/RDI/REI
between 5 and 14 respiratory events per hour of sleep. Such patients may be relatively
asymptomatic or report sedentary (ie, passive) daytime sleepiness, becoming noticeable once
the patient is unstimulated. The daytime sleepiness often does not impair daily life, although it
may be recognized by family members. Alternatively, daytime sleepiness may become
apparent to the patient only after it improves due to weight loss, alcohol abstinence, or
treatment of OSA. The sleep stages and slow wave sleep are generally preserved in mild
OSA. Even when asymptomatic, mild OSA is associated with increased risk of hypertension,
and this becomes a stronger association at younger ages [84]. However, using the latest
AASM definition of hypopnea, symptomatic patients with mild OSA are without increased
cardiovascular risk [85].

● Moderate – Patients traditionally classified as having moderate OSA are those with an
AHI/RDI/REI between 15 and 30 respiratory events per hour of sleep. Such patients are
typically aware of daytime sleepiness and take steps to avoid falling asleep at inappropriate
times (eg, taking a nap or avoiding driving long distances). They are able to continue their
daily activities, but at reduced levels, and they may have an increased incidence of motor
vehicle violations or accidents. Systemic hypertension may coexist. Sleep fragmentation is
observed in moderate OSA, but sleep architecture (ie, the timing and percentage of sleep
stages) is better conserved than with severe disease.

● Severe – Patients classified as having severe OSA are those with an AHI/RDI/REI greater
than 30 respiratory events per hour of sleep. Such patients more often have daytime
sleepiness that interferes with normal daily activities. They tend to fall asleep often during the
day (in a sitting posture) and are at risk for accidental injury from sleepiness. Patients with
severe OSA are at increased risk for all-cause mortality and a variety of cardiovascular
comorbidities, including hypertension, coronary artery disease, and arrhythmias. (See
'Complications' below.)

Upper airway resistance syndrome — Upper airway resistance syndrome (UARS) occurs when
airflow limitation due to increased upper airway resistance (ie, RERAs) induces arousals from
sleep, leading to excessive daytime sleepiness [86]. More commonly, the presence of prolonged
partial upper airway obstruction is a common phenotype of sleep-disordered breathing, and is
underreported [87]. In one study of patients referred for polysomnography, 29.9 percent presented
with OSA, whereas 10.8 percent had prolonged partial obstruction with a normal AHI [88]. During
recordings of nasal airflow, periods of flow limitation longer than a hypopnea (minimum one to
three minutes) are often used as indicative of sustained upper airway resistance [87]. However,
there is no consensus about the optimal detection, proper measurement, or degree of clinical
impact. A PSG rather than HSAT is recommended for the detection of UARS, since it is better at
identifying prolonged flow limitation via the nasal cannula.

While UARS was previously classified as an independent disorder, it is now considered a type of
OSA. It presents similarly to classic OSA but it is common in thin women with certain craniofacial
abnormalities [89,90], and may be more common in females referred for OSA than has been
appreciated [87]. Unlike patients with classic OSA, patients with UARS have few discrete apneas
or hypopneas or episodes of desaturation, but do have prolonged flow limitation and evidence of
arousals on PSG, albeit with less overall sleep fragmentation than OSA. Thus, the study may be
interpreted as absent or mild OSA, requiring no treatment. Partial upper airway obstruction is
treatable with nasal continuous positive airway pressure (CPAP) and patients have good
adherence to therapy [87]. We have also used dental appliances with good success.  

COMPLICATIONS

Patients with OSA are at increased risk for several adverse clinical outcomes.

● Drowsy driving and motor vehicle crashes – Motor vehicle accidents are two to three
times more common among patients with OSA than without OSA [91]. (See "Drowsy driving:
Risks, evaluation, and management".)

● Neuropsychiatric dysfunction – OSA can induce or worsen inattention, memory, and

cognitive deficits which, together, can result in impaired executive function and increase the
likelihood of errors and accidents [4,91-100]. Additional neuropsychiatric manifestations
include moodiness and irritability as well as depression, psychosis, and sexual dysfunction
[95,101-104]. (See "Insufficient sleep: Definition, epidemiology, and adverse outcomes" and
"Risk factors for cognitive decline and dementia", section on 'Obstructive sleep apnea'.)

● Cardiovascular and cerebrovascular morbidity – Patients with OSA, particularly when it is

moderate or severe and untreated, are at increased risk for systemic hypertension, coronary
artery disease, cardiac arrhythmias, heart failure, and stroke. (See "Obstructive sleep apnea
and cardiovascular disease in adults" and "Sleep-related breathing disorders and stroke".)

● Pulmonary hypertension or right heart failure – OSA is classically associated with group 3
pulmonary hypertension, particularly when OSA coexists with either obesity hypoventilation
syndrome or an alternative cause of daytime hypoxemia (eg, chronic lung disease). Severe
hypoxemia may also cause secondary polycythemia. (See "Pulmonary hypertension due to
 lung disease and/or hypoxemia (group 3 pulmonary hypertension): Epidemiology,
pathogenesis, and diagnostic evaluation in adults".)

● Metabolic syndrome and type 2 diabetes – Patients with OSA have an increased
prevalence of insulin resistance as well as type 2 diabetes and diabetes complications [105-
108]. While this association can be manifested through shared risk factors such as obesity
[109,110], an independent association between OSA severity, insulin resistance, and type 2
diabetes has been reported in several studies [107,111-115]. In one study, about 12 percent of
patients with OSA developed diabetes over a 67-month period; patients with severe OSA
(apnea-hypopnea index [AHI] ≥30 events per hour) had an approximately 30 percent higher
risk of incident diabetes compared with patients without OSA [107]. In patients with the
metabolic syndrome, OSA has been independently associated with increased glucose and
triglyceride levels as well as markers of inflammation, arterial stiffness, and atherosclerosis,
suggesting that OSA may exacerbate the cardiometabolic risk attributed to obesity and the
metabolic syndrome [116]. (See "Metabolic syndrome (insulin resistance syndrome or
syndrome X)".)

● Nonalcoholic fatty liver disease (NAFLD) – Patients with OSA, particularly those with
severe OSA, have a two- to threefold increased prevalence of NAFLD that is independent of
shared risk factors such as obesity [117-120]. (See "Epidemiology, clinical features, and
diagnosis of nonalcoholic fatty liver disease in adults" and "Pathogenesis of nonalcoholic fatty
liver disease".)

● Miscellaneous – Patients with OSA may have an increased risk of developing gout
compared with patients who do not have OSA (4.9 versus 2.5 percent) [121]. One large
retrospective study from a French cohort suggested a possible association between cancer
and nocturnal hypoxemia in patients being investigated for OSA [122].

SCREENING QUESTIONNAIRES

We agree with the American Academy of Sleep Medicine (AASM) that screening tools, including
questionnaires should not be routinely used in asymptomatic patients in the community to screen
for OSA [65]. However, these tools, in particular, the STOP-Bang questionnaire, are being
increasingly used as preoperative evaluation tools to evaluate those without a known diagnosis of
OSA who may be at risk of perioperative complications. Further details in this population are
provided separately. (See "Surgical risk and the preoperative evaluation and management of
adults with obstructive sleep apnea", section on 'Screening with a questionnaire'.)

In general, these diagnostic tools display poor accuracy in the sleep clinic for any level of selected
apnea-hypopnea index (AHI) stratification and are rarely if ever used in clinical practice by sleep
experts. However, while nonsleep experts may use these tools in practice, their validity in that
setting still remains weak [59,65].

Efficacy — Several clinical prediction rules, questionnaires, and scores have been evaluated as
screening tools using common signs and symptoms of OSA that are easily obtained and
interpreted in the primary care setting. While these tools may have some value in detecting OSA
in highly symptomatic patients in a high-risk setting (eg, preoperative evaluation), they cannot be
used as true screening tools in asymptomatic patients based upon the following:

● Most tools have been derived from sleep center or preoperative referral-based populations
(ie, symptomatic patients), which likely have a higher prevalence of OSA. Thus, the sensitivity
and specificity of most instruments are likely overestimated in relation to their value in an
unselected asymptomatic community-based population.

● There is marked heterogeneity in OSA definitions in studies testing the validity of screening
questionnaires [47,123].

● The high false positive rate of questionnaires diminishes their diagnostic value such that when
the score is high, patients do not always have OSA; in contrast, when the score is low,
patients are unlikely to have OSA [124]. Thus, questionnaires are sensitive but not specific
and are generally only helpful when they are negative (ie, low score).

Highlighting their limited use as a screening tool in asymptomatic patients, the United States
Preventive Services Task Force (USPSTF) reviewed 110 studies evaluating the accuracy of OSA-
related screening questionnaires or prediction tools. The USPSTF found that although some tools
could predict the presence of severe OSA, these studies were performed in high risk individuals,
rendering them less useful as true screening tools [125,126]. In addition, there were no
randomized trials comparing screening with no screening in asymptomatic individuals and no
studies that reported improved outcomes in association with their use. The USPSTF concluded
that there was insufficient evidence to make a recommendation on the use of these tools for the
screening of OSA in asymptomatic individuals in the community [126]. For similar reasons, the
AASM also supports not using these tools to screen asymptomatic patients for OSA [65].

Instruments — Examples of such questionnaires include the following:

● STOP-Bang – The STOP-Bang questionnaire is an eight-item survey that incorporates

information on snoring, tiredness, observed apneas, blood pressure, Body mass index (BMI),
age, neck circumference, and gender ( table 6). A score of three or higher has a sensitivity
and specificity of 84 and 56 percent for the diagnosis of OSA using an AHI threshold of 5 to
14 events per hour, and a sensitivity and specificity of 93 and 43 percent for an AHI of 15 to
29 (ie, moderate to severe OSA) [124,127]. Among the questionnaires, the STOP-Bang
questionnaire has the highest sensitivity (88 percent for mild OSA, 90 percent for moderate
 OSA, and 93 percent for severe OSA) but the specificity is poor (42 percent for mild OSA, 36
percent for moderate OSA, 35 percent for severe OSA) [124,128]. One meta-analysis of 47
studies from several geographic regions reported that a STOP-Bang score of at least 3 had
sensitivity >90 percent and had the discriminative power to exclude moderate to severe and
severe OSA, with negative predictive values of 77 and 91 percent, respectively [129]. The
diagnostic accuracy of a STOP-Bang score of at least 3 to detect moderate to severe OSA
was maintained in all regions except East Asia. A modified version is used by some experts
as a preoperative evaluation tool (calculator 2) ( table 7). (See "Surgical risk and the
preoperative evaluation and management of adults with obstructive sleep apnea", section on
'Screening with a questionnaire'.)

● Sleep apnea clinical score (SACS) – The SACS is a four-item questionnaire that
incorporates information on neck circumference, hypertension, habitual snoring, and
nocturnal gasping or choking to generate a score ranging from 0 to 100 ( table 10)
[130,131]. Scores greater than 15 result in a probability of OSA (defined as an AHI >10
events per hour) of 25 to 50 percent.

● Berlin questionnaire – The Berlin questionnaire consists of 10 items relating to snoring,

nonrestorative sleep, sleepiness while driving, apneas during sleep, hypertension, and BMI
[132]. The results stratify patients as having a high or low risk for OSA. A high risk score on
the Berlin questionnaire is associated with a sensitivity and specificity of 80 and 46 percent
when OSA is defined as an AHI of 5 to 14 events per hour, and 91 and 37 percent when OSA
is defined as an AHI ≥15 events per hour ( table 9 and table 8) [124,132].

● The NoSAS score – The NoSAS score assigns points based upon five parameters (neck
circumference, body mass index, snoring, age, and gender). In a derivation and validation
analysis, a score ≥8 identified individuals at risk of clinically significant sleep-disordered
breathing with an area under the curve (AUC) of 0.74, higher than that associated with the
STOP-Bang (AUC 0.67) and Berlin questionnaires (AUC 0.64) [133]. While encouraging, this
score requires further validation before it can be used in a clinical setting.

● Multivariable Apnea Prediction (MVAP) instrument – The MVAP instrument is based on a

formula consisting of three questions about the frequency of symptoms of sleep apnea, along
with BMI, age, and gender. MVAP values ranged from 0 to 1, with 1 representing the highest
likelihood of sleep apnea. Two studies were performed using this instrument in primary care
and community populations (elderly patients complaining of sleepiness, and hypertensive
patients visiting an internist, respectively) [134,135]. In the Medicare patients with daytime
sleepiness, this tool had a sensitivity of 91 percent and a specificity of 64 percent to predict
severe OSA (AHI ≥30 and Epworth Sleepiness Scale [ESS] score >10) [134]. The MVAP tool
had a sensitivity of 92 percent and a specificity of 44 percent to predict severe OSA in
 hypertensive patients [135]. However, both study populations likely carry a higher prevalence
of OSA, creating a bias in these study results.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Sleep-related breathing
disorders in adults".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Sleep apnea in adults (The Basics)")

● Beyond the Basics topics (see "Patient education: Sleep apnea in adults (Beyond the
Basics)")

SUMMARY AND RECOMMENDATIONS

● Obstructive sleep apnea (OSA) is a disorder that is characterized by obstructive apneas,

hypopneas, and/or respiratory effort related arousals caused by repetitive complete or partial
collapse of the upper airway during sleep. The prevalence of OSA in the general adult
population varies depending on the definition but is approximately 15 to 30 percent in males
and 5 to 15 percent in females (when OSA is defined as an apnea-hypopnea index [AHI]
greater than five events per hour of sleep). (See 'Introduction' above and 'Epidemiology'
above.)

● Well-defined risk factors for OSA include older age, male gender, obesity, and craniofacial
and upper airway abnormalities. Potential risk factors include smoking, family history of
 snoring or OSA, and nasal congestion. Rates of OSA are also increased in association with
certain medical conditions, most commonly obesity hypoventilation syndrome, pregnancy,
end-stage kidney disease, congestive heart failure, chronic lung disease, type 2 diabetes
mellitus, and stroke; others include acromegaly, hypothyroidism, polycystic ovary syndrome,
and floppy eyelid syndrome. (See 'Risk factors and associated conditions' above.)

● Most patients with OSA complain of daytime sleepiness, or their bed partner reports loud
snoring, gasping, choking, snorting, or interruptions in breathing while sleeping ( table 1).
Less common symptoms include nonrestorative sleep, nocturnal restlessness, morning
headaches, sleep maintenance insomnia, and nocturia. Key clinical questions ( table 2)
and the Epworth Sleepiness Scale (ESS) may facilitate the distinction between sleepiness
and fatigue (calculator 1); an ESS score >9 indicates abnormal sleepiness and should prompt
further testing. Examination findings include obesity, a crowded oropharynx, craniofacial
abnormalities, and a large neck, and/or waist circumference. Patients may also present with
the manifestations of associated conditions and complications (eg, cognitive deficits, mood
changes, sexual dysfunction, signs of pulmonary hypertension, motor vehicle crashes). (See
'Clinical features' above.)

● The differential diagnosis of the manifestations of OSA is wide ( table 5) and includes
several conditions that present with daytime sleepiness (eg, periodic limb movement disorder,
restless leg syndrome, narcolepsy, central sleep apnea, non-OSA related conditions
associated with sleep disordered breathing, and sedative drugs ( table 3)), many of which
can be distinguished from OSA via clinical history and polysomnography (PSG). Other
conditions that similarly cause abrupt awakenings or abnormal sounds or sensations during
sleep are in the differential and include primary snoring, gastroesophageal reflux disorder,
swallowing disorders, nocturnal seizures, nocturnal asthma, insomnia, and panic attacks.

● Guidelines for diagnostic testing include the following (see 'Diagnostic evaluation' above):

• We recommend diagnostic testing in patients who have excessive daytime sleepiness

and two out of three of the following: habitual snoring, witnessed apnea, gasping, or
choking during sleep, or diagnosed hypertension. We also frequently perform testing in
patients who have excessive daytime sleepiness alone, patients who have other clinical
features of OSA ( table 1) and associated conditions or complications (eg, refractory
hypertension), and patients in whom OSA needs to be ruled in or out as an underlying
cause or potential contributing factor to their symptoms (eg, unexplained pulmonary
hypertension or motor vehicle accident due to falling asleep). Evaluation tools or
questionnaires (eg, ESS, Berlin, STOP-Bang questionnaires) are not typically used to
select patients for diagnostic testing since they are inaccurate and have not been shown
to be superior to a good history and physical examination. (See 'Patient selection'
above.)
 • For patients with suspected mild OSA, suspected complicated OSA (eg, chronic
obstructive pulmonary disease) ( table 13), suspected non-respiratory sleep disorders
(eg, narcolepsy ( table 12)), or patients with suspected OSA who have mission-critical
jobs, we recommend full-night or split-night, attended, in-laboratory PSG rather than
home sleep apnea testing (HSAT). This approach is based upon the inadequacy of most
HSAT devices to detect complex or mild sleep-related events and the lack of evidence to
support its use. (See 'Selecting home or in-laboratory testing' above and 'Mission-critical
workers with suspected OSA' above and 'Suspected non-respiratory sleep disorders'
above and 'Pretest probability of mild OSA' above and 'Polysomnography' above.)  

• For patients in whom there is a high likelihood of moderate or severe uncomplicated OSA
(ie, without non-OSA-related sleep-related breathing disorders ( table 13)) and who
have no other suspected non-respiratory sleep disorders (eg narcolepsy ( table 12)),
we suggest unattended, in-home portable monitoring with a technically adequate Type 3
device, the results of which are interpreted by providers who have experience in clinical
sleep medicine ( algorithm 1 and table 11). (See 'Pretest probability of moderate to
severe OSA' above and 'Home sleep apnea testing' above.)

• Several additional factors that influence the choice between performing a home or in-
laboratory study include the values and preferences of the patient (eg, access to a sleep
laboratory, homelessness, cost, space constraints, wait time, concern for operator error
for home monitoring), the practices of the institution and preferences of the clinician, and
the preference of the payer (eg, many insurers in the United States require that patients
receive home testing first). (See 'Selecting home or in-laboratory testing' above.)

• Importantly, if either PSG or HSAT is negative and the suspicion for OSA remains, PSG
should be repeated or performed, respectively. (See 'Diagnostic tests' above.)

● The diagnosis of OSA is based upon the presence or absence of related symptoms, as well
as the frequency of respiratory events during sleep (ie, apneas, hypopneas, and respiratory
effort-related arousals [RERAs])

• In patients who undergo PSG, the diagnosis of OSA is confirmed if either of the two
criteria below are met ( table 16) (see 'Diagnosis' above):

- There are 15 or more apneas, hypopneas, or RERAs per hour of sleep (ie, an AHI or
respiratory disturbance index [RDI] ≥15 events per hour) in an asymptomatic patient.

- There are five or more obstructive apneas, obstructive hypopneas, or RERAs per
hour of sleep (ie, an AHI or RDI ≥5 events per hour) in a patient with the following:
sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms; waking up with
breath holding, gasping, or choking; habitual snoring, breathing interruptions, or both
 noted by a bed partner or other observer; and/or hypertension, mood disorder,
cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial
fibrillation, or type 2 diabetes mellitus

• In patients who undergo HSAT, actual sleep time is not recorded such that the respiratory
event index (REI) is calculated based on recording time from the HSAT device; REI
appears to correlate well with in-laboratory measured AHI and RDI. With a moderate or
high suspicion of OSA, an REI ≥15 events per hour is supportive of a diagnosis of OSA
while those with an REI <15 events per hour or those with inconclusive results or a
technically inadequate study should be evaluated with PSG.

● Adverse outcomes associated with OSA include drowsy driving and motor vehicle crashes,
neuropsychiatric dysfunction, cardiovascular and cerebrovascular morbidities, pulmonary
hypertension, metabolic syndrome and type 2 diabetes, and nonalcoholic fatty liver disease.
(See 'Complications' above.)

● Screening tools such as questionnaires should not be routinely used in asymptomatic

patients in the community to screen for OSA. However, these tools (in particular, the STOP-
Bang questionnaire ( table 6)) are being increasingly used as preoperative evaluation tools
to evaluate those who may be at risk of perioperative complications due to undiagnosed OSA.
(See 'Screening questionnaires' above and "Surgical risk and the preoperative evaluation and
management of adults with obstructive sleep apnea", section on 'Screening with a
questionnaire'.)

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131. Grover M, Mookadam M, Chang YH, Parish J. Validating the Diagnostic Accuracy of the
Sleep Apnea Clinical Score for Use in Primary Care Populations. Mayo Clin Proc 2016;
91:469.
132. Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identify patients at
risk for the sleep apnea syndrome. Ann Intern Med 1999; 131:485.
133. Marti-Soler H, Hirotsu C, Marques-Vidal P, et al. The NoSAS score for screening of sleep-
disordered breathing: a derivation and validation study. Lancet Respir Med 2016; 4:742.
134. Morales CR, Hurley S, Wick LC, et al. In-home, self-assembled sleep studies are useful in
diagnosing sleep apnea in the elderly. Sleep 2012; 35:1491.
135. Gurubhagavatula I, Fields BG, Morales CR, et al. Screening for severe obstructive sleep
apnea syndrome in hypertensive outpatients. J Clin Hypertens (Greenwich) 2013; 15:279.
Topic 7706 Version 56.0
GRAPHICS

Clinical features of obstructive sleep apnea (OSA)

Examination findings

Narrow or "crowded" airway

Obesity

Large neck circumference

Craniofacial abnormalities (eg, retrognathia)

Symptoms

Daytime sleepiness

Nonrestorative sleep

Loud snoring

Witnessed apneas by bed partner

Awakening with choking or gasping

Nocturnal restlessness

Insomnia with frequent awakenings

Lack of concentration

Cognitive deficits

Changes in mood

Morning headaches

Vivid, strange, or threatening dreams

Nocturia

Associated conditions

Obesity hypoventilation syndrome

Systemic hypertension

Cardiovascular disease (eg, heart failure)

Cerebrovascular disease (eg, stroke, transient ischemic attacks)

Cardiac dysrhythmias (eg, atrial fibrillation)

Pulmonary hypertension

Cor pulmonale

End-stage kidney disease

Type 2 diabetes mellitus

Chronic lung disease

Pregnancy

Acromegaly

Hypothyroidism

Gastroesophageal reflux

Secondary polycythemia

Floppy eyelid syndrome

 Polycystic ovary syndrome

Parkinson disease

Other medical conditions that may have an association with OSA include fibromyalgia, gastroesophageal reflux
disease, and secondary polycythemia. For further information refer to UpToDate content on clinical evaluation of
obstructive sleep apnea.

Graphic 55633 Version 15.0

Key questions in evaluating the tired patient

Key questions in the evaluation of a patient who complains of sleepiness, tiredness,

fatigue, or low energy
Questions about sleepiness

Do you feel sleepy during the day?

Is daytime sleepiness a problem for you?
Is it difficult to keep your eyes open at times during the day?
Do you struggle to stay awake during the day?
Do you take naps?
How often and how long do you nap during the day?
Do you fall asleep at times you do not want to (ie, watching a movie, reading a book, or on long drives)?

Questions about tiredness, fatigue, and low energy

Do you lack the energy to go about your daily activities?

Do you tire easily, or sooner than others, when you are active?
Do you feel physically or mentally exhausted?

Questions to differentiate sleepiness from related complaints

Does your problem bother you more if you sit to read for an hour, or if you go out shopping for an hour?
Which of the following is the single most important problem for you: sleepiness, tiredness, fatigue, or lack of
energy?
Which of the following most interferes with your ability to accomplish what you would like to: sleepiness,
tiredness, fatigue, or lack of energy?
Which of the following is the one problem you would most like to address effectively: sleepiness, tiredness,
fatigue, or lack of energy?

Adapted from:

1. Bodkin CL, Manchanda S. Office evaluation of the "tired" or "sleepy" patient. Semin Neurol 2011; 31:42.
2. Chervin RD. Sleepiness, fatigue, tiredness, and lack of energy in obstructive sleep apnea. Chest 2000; 118:372.

Graphic 86812 Version 2.0

Differential diagnosis of excessive daytime sleepiness

Insufficient sleep
Sleep deprivation

Environmental intrusions

Sleep disorders
Obstructive sleep apnea

Central sleep apnea

Sleep-related hypoventilation or hypoxemia

Central disorders of hypersomnolence 

Narcolepsy type 1 or 2
Kleine-Levin syndrome
Idiopathic hypersomnia

Circadian rhythm sleep-wake disorders

Delayed sleep-wake phase disorder
Advanced sleep-wake phase disorder
Irregular sleep-wake rhythm disorder 
Non-24-hour sleep-wake rhythm disorder 
Jet lag
Shift work

Restless legs syndrome

Periodic limb movement disorder

Other neurologic disorders

Neurodegenerative disease
Parkinson disease
Dementia with Lewy bodies
Alzheimer disease
Multiple system atrophy

Myotonic dystrophy

Multiple sclerosis

Amyotrophic lateral sclerosis (via sleep-related breathing disorders)

Structural lesions affecting thalamus, hypothalamus, or brainstem

Traumatic brain injury

Encephalitis lethargica

Cerebral trypanosomiasis

Medical and genetic disorders

Hypothyroidism

Obesity

End-stage renal disease

Adrenal insufficiency

Hepatic encephalopathy

Niemann-Pick type C

Prader-Willi syndrome

Psychiatric disorders
Depression

Anxiety
 Substance abuse
Alcohol
Narcotics
Prescription opioid abuse
Stimulant withdrawal

Psychogenic sleepiness

Medications
Benzodiazepines

Nonbenzodiazepine sedatives

Antipsychotics

Opioid analgesics

Beta-blockers (lipophilic)

Barbiturates

Antihistamines

Anticonvulsants

Sedative antidepressants

Graphic 86811 Version 11.0

Conditions leading to increased upper airway resistance

Obesity (increased fat deposition)

Nasal obstruction

Micrognathia and retrognathia

Tonsillar hypertrophy

Uvular hypertrophy

Hypothyroidism

Acromegaly

Macroglossia

Tissue edema or fibrosis

Other craniofacial abnormalities (eg, high arched palate)

Graphic 55220 Version 1.0

The modified Mallampati classification for difficult laryngoscopy and
intubation

The modified Mallampati classification [1] is a simple scoring system that relates the amount of
mouth opening to the size of the tongue and provides an estimate of space available for oral
intubation by direct laryngoscopy. According to the Mallampati scale, class I is present when the soft
palate, uvula, and pillars are visible; class II when the soft palate and the uvula are visible; class III
when only the soft palate and base of the uvula are visible; and class IV when only the hard palate
is visible.

Reference:
1. Samsoon GL, Young JR. Difficult tracheal intubation: a retrospective study. Anaesthesia 1987;
42:487.

Graphic 75229 Version 10.0

Friedman tongue position

(A) FTP I allows visualization of the entire uvula and tonsils/pillars.

(B) FTP IIa allows visualization of most of the uvula, but the tonsils/pillars are absent.

(C) FTP IIb allows visualization of the entire soft plate to the base of the uvula.

(D) In FTP III some of the soft palate is visualized but the distal structures are absent.

(E) FTP IV allows visualization of the hard palate only.

Note that tongue should be relaxed within the mouth, not protruded.

Reproduced from: Friedman M. Friedman tongue position and the staging of obstructive sleep apnea/hypopnea syndrome. In:
Apnea and Snoring: Surgical and Nonsurgical Therapy, Scheidt S, Clansey N (Eds), Philadelphia, Elsevier 2009. Illustration us
permission of Elsevier Inc. All rights reserved.

Graphic 91839 Version 2.0

Disorders that mimic obstructive sleep apnea

Primary snoring

Underlying pulmonary disease (eg, nocturnal desaturations, mucus impaction)

Sleep-related laryngospasm

Abnormal swallowing disorder

Panic attacks

Nocturnal asthma

Gastroesophageal reflux disease

Sleep-choking disorder

Nocturnal seizures

Insomnia (repetitive awakenings)

Graphic 50784 Version 5.0

STOP-Bang questionnaire

Yes No Snoring?
Do you snore loudly (loud enough to be heard through closed doors, or your bed partner
elbows you for snoring at night)?

Yes No Tired?
Do you often feel tired, fatigued, or sleepy during the daytime (such as falling asleep
during driving)?

Yes No Observed?
Has anyone observed you stop breathing or choking/gasping during your sleep?

Yes No Pressure?
Do you have or are being treated for high blood pressure?

Yes No Body mass index more than 35 kg/m 2?

Yes No Age older than 50 years old?

Yes No Neck size large? (measured around Adam's apple)

Is your shirt collar 16 inches or larger?

Yes No Gender (biologic sex) = Male?

Scoring criteria:

Low risk of OSA: Yes to 0 to 2 questions

Intermediate risk of OSA: Yes to 3 to 4 questions

High risk of OSA: Yes to 5 to 8 questions

OSA: obstructive sleep apnea

References:

1. Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: a tool to screen patients for obstructive sleep apnea.
Anesthesiology 2008; 108:812.
2. Chung F, Subramanyam R, Liao P, et al. High STOP-Bang score indicates a high probability of obstructive sleep
apnoea. Br J Anaesth 2012; 108:768.

Graphic 87572 Version 10.0

Enhanced STOP-Bang questionnaire [1-3]

Yes No Snoring?
Do you snore loudly (loud enough to be heard through closed doors, or your bed partner
elbows you for snoring at night)?

Yes No Tired?
Do you often feel tired, fatigued, or sleepy during the daytime (such as falling asleep
during driving or talking to someone)?

Yes No Observed?
Has anyone observed you stop breathing or choking/gasping during your sleep?

Yes No Pressure?
Do you have or are being treated for high blood pressure?

Yes No Body mass index more than 35 kg/m 2?

Yes No Age older than 50 years old?

Yes No Neck size large? (measured around Adam's apple)

Is your shirt collar 16 inches or larger?

Yes No Gender (biologic sex) = Male?

Scoring criteria:

Low risk of OSA: Yes to 0 to 2 questions

Intermediate risk of OSA: Yes to 3 to 4 questions

High risk of OSA: Yes to 5 to 8 questions

or Yes to 2 or more of 4 STOP questions + male gender (biologic sex)

or Yes to 2 or more of 4 STOP questions + BMI >35 kg/m 2

or Yes to 2 or more of 4 STOP questions + neck circumference ≥ 16 inches/ 40 cm

This is an enhanced version of the STOP-Bang questionnaire. Patients who initially score at intermediate risk of
OSA can be further stratified based on the specific STOP-Bang questions that are positive. Simpler STOP-Bang
scoring is shown in the UpToDate graphic STOP-Bang questionnaire.

OSA: obstructive sleep apnea.

References:
1. Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: a tool to screen patients for obstructive sleep apnea.
Anesthesiology 2008; 108:812.
2. Chung F, Subramanyam R, Liao P, et al. High STOP-Bang score indicates a high probability of obstructive sleep
apnoea. Br J Anaesth 2012; 108:768.
3. Chung F, Abdullah HR, Liao P. STOP-Bang Questionnaire: A Practical Approach to Screen for Obstructive Sleep
Apnea. Chest 2016; 149:631.

Graphic 117089 Version 4.0

Berlin questionnaire scoring

Patients can be classified into high risk or low risk based on their responses to the individual items and their overall
scores in the symptom categories:

High risk: if there are two or more categories where the score is positive

Low risk: if there is only one or no categories where the score is positive

Additional question: item 9 should be noted separately

Categories and scoring:

Category 1: items 1, 2, 3, 4, 5
Item 1: if 'Yes', assign 1 point
Item 2: if 'c' or 'd' is the response, assign 1 point
Item 3: if 'a' or 'b' is the response, assign 1 point
Item 4: if 'a' is the response, assign 1 point
Item 5: if 'a' or 'b' is the response, assign 2 points
Add points. Category 1 is positive if the total score is 2 or more points.
 
Category 2: items 6, 7, 8 (item 9 should be noted separately)
Item 6: if 'a' or 'b' is the response, assign 1 point
Item 7: if 'a' or 'b' is the response, assign 1 point
Item 8: if 'a' is the response, assign 1 point
Add points. Category 2 is positive if the total score is 2 or more points.
 
Category 3 is positive if the answer to item 10 is 'Yes' OR if the BMI of the patient is greater than
30 kg/m 2.

(BMI must be calculated. BMI is defined as weight (kg) divided by height (m) squared, ie, kg/m 2).

BMI: body mass index.

From Annals of Internal Medicine, Netzer NC, Stoohs RA, Netzer CM, et al, Using the Berlin Questionnaire to identify
patients at risk for the sleep apnea syndrome, vol. 131, p. 485. Copyright © 1999 American College of Physicians, Inc.

Graphic 96753 Version 7.0

Berlin questionnaire

Height (m) Weight (kg) Age Male/Female __________ __________ __________

Please choose the correct response to each question.

Category 1 1. Do you snore?

_ a. Yes
_ b. No
_ c. Don't know
If you snore:
2. Your snoring is:
_ a. Slightly louder than breathing
_ b. As loud as talking
_ c. Louder than talking
_ d. Very loud – can be heard in adjacent rooms
3. How often do you snore
_ a. Nearly every day
_ b. Three to four times a week
_ c. One to two times a week
_ d. One to two times a month
_ e. Never or nearly never
4. Has your snoring ever bothered other people?
_ a. Yes
_ b. No
_ c. Don't know
5. Has anyone noticed that you quit breathing during your sleep?
_ a. Nearly every day
_ b. Three to four times a week
_ c. One to two times a week
_ d. One to two times a month
_ e. Never or nearly never

Category 2 6. How often do you feel tired or fatigued after your sleep?
_ a. Nearly every day
_ b. Three to four times a week
_ c. One to two times a week
_ d. One to two times a month
_ e. Never or nearly never
7. During your waking time, do you feel tired, fatigued or not up to par?
_ a. Nearly every day
_ b. Three to four times a week
_ c. One to two times a week
_ d. One to two times a month
_ e. Never or nearly never
8. Have you ever nodded off or fallen asleep while driving a vehicle?
_ a. Yes
_ b. No
If yes:
9. How often does this occur?
_ a. Nearly every day
_ b. Three to four times a week
 _ c. One to two times a week
_ d. One to two times a month
_ e. Never or nearly never

Category 3 10. Do you have high blood pressure?

_ Yes
_ No
_ Don't know

From Annals of Internal Medicine, Netzer NC, Stoohs RA, Netzer CM, et al, Using the Berlin Questionnaire to identify
patients at risk for the sleep apnea syndrome, Vol 131, Pg 485. Copyright © 1999 American College of Physicians. All
Rights Reserved. Reprinted with the permission of American College of Physicians, Inc.

Graphic 91571 Version 6.0

Sleep apnea clinical score

Neck Not hypertensive historical

Hypertensive historical features
circumference features*
(cm) None One Both None One Both

28 0 0 1 0 1 2

30 0 0 1 1 2 4

32 0 1 2 1 3 5

34 1 2 3 2 4 8

36 1 3 5 4 6 11

38 2 4 7 5 9 16

40 3 6 10 8 13 22

42 5 8 14 11 18 30

44 7 12 20 15 25 42

46 10 16 28 21 35 58

48 14 23 38 29 48 80

50 19 32 53 40 66 110

Sleep apnea clinical score to predict the apnea-hypopnea index using the linear model of neck circumference,
hypertension, and historical features of habitual snoring and partner's observation of nocturnal choking or
gasping. Begin on the line of the patient's neck circumference and then choose the appropriate value based upon
the presence or absence of hypertension and whether the patient has none, one, or both of the above historical
features.

A clinical score of 15 or greater indicates a high risk of obstructive sleep apnea.

* Historical features are habitual snoring and partner reports of nocturnal choking or gasping.

Redrawn from: Flemons WW, Whitelaw WA, Brant R, Remmers JE. Am J Respir Crit Care Med 1994; 150:1279.

Graphic 52357 Version 5.0

HSAT versus PSG

HSAT: home sleep apnea testing; PSG: polysomnography; GOLD: global initiative for obstructive lung disease; COPD: chronic
disease; NYHA: New York Heart Association; CSA: central sleep apnea; OSA: obstructive sleep apnea; AASM: American Acade
CPAP: continuous positive airway pressure; CMS: Centers for Medicare and Medicaid Services; AHI: apnea hypopnea index; R
index; PAT: peripheral arterial tonometry.

* While PSG is ideal, many insurers require a negative HSAT before proceeding with PSG.

¶ We agree with the AASM that a split-night rather than full-night in-laboratory PSG may be appropriate in most patients in w
OSA is observed during a minimum of two hours during PSG testing AND in whom at least three hours are available for CPAP
will accept an AHI or RDI that is calculated based upon less than two hours of recorded sleep, if the total number of recorded
or RDI during sleep testing is at least the number of events that would have been required in a two hour period.

Δ In-laboratory PSG remains the gold standard for diagnostic testing for OSA; HSAT is an alternative in a select group of pati
with suspected mild OSA, in-laboratory PSG is preferred since HSAT may lead to the underdetection of sleep-related events in
patients with suspected moderate to severe OSA, HSAT is adequate only in a select group of patients.

◊ We favor the AASM definition when clinically assessing patient risk for OSA. The AASM states that patients at high risk of m
include those with daytime hypersomnolence and at least two of the following three criteria: habitual loud snoring, witnessed
or diagnosed hypertension. However, for those in whom reliable assessment for the risk of OSA cannot be made, such as thos
hypersomnolence, in-laboratory polysomnography is preferred. Refer to UpToDate text on clinical presentation and diagnosis
in adults.

§ Patients may have reasons that prohibit home or laboratory sleep testing such as inability to get to a laboratory, cost, hom
constraints.

¥ In the rare circumstance that a patient has reasons that prohibit both HSAT and in-laboratory PSG, additional testing (eg, o
tools, questionnaires, predictive algorithms) is insensitive. Recurrent attempts should be taken to resolve the issues and get s
or to empirically treat those who are assessed as having OSA.

‡ HSAT should be performed with a technically adequate device that incorporates a minimum of nasal pressure, chest and ab
plethysmography, and oximetry, OR PAT with oximetry and actigraphy. In addition, it should only be administered by an accre
the supervision of a board-certified sleep physician. If one HSAT is negative, inconclusive, or technically inadequate AND the s
in-laboratory PSG should be performed, if feasible. In patients with conditions that increase the risk of non-obstructive breath
less accurate and may underdiagnose OSA and/or not detect other sleep-related events.

Graphic 113434 Version 5.0

Indications for HSAT or polysomnography

Indications for in-laboratory

Indications for HSAT
polysomnography

Diagnostic testing in an adult patient who is at high
risk of moderate to severe uncomplicated OSA*
Diagnostic testing in an adult patient in whom in-
laboratory testing is not feasible for unresolvable
issues ¶
Followup of therapies when symptoms suggest
persistent moderate to severe OSA or when in-
laboratory polysomnography is not feasible
Diagnostic testing in an adult patient suspected to
have mild OSA
Diagnostic testing in an adult patient suspected to
have OSA complicated by:
Conditions that place the patients at risk of non
obstructive sleep disordered breathing. For
example:
Patients with significant cardiorespiratory
disease Δ
Respiratory muscle weakness due to
neuromuscular condition
Awake or possible sleep related
hypoventilation (eg, central sleep apnea,
obesity hypoventilation)
Chronic opioid medication use
History of stroke
Suspected non-OSA sleep disorders (eg,
narcolepsy, severe insomnia, ◊ parasomnias,
movement disorders)
Diagnostic testing for OSA in a mission-critical
employee §
Diagnostic testing in a patient with suspected OSA in
whom:
Initial HSAT is negative, inconclusive or technically
inadequate
Environmental/personal factors preclude adequate
HSAT data (eg, space constraints)
Assessment of initial response to the following
therapies: ¥
Oral appliance therapy
Surgery for OSA
Weight loss

HSAT: home sleep apnea testing; OSA: obstructive sleep apnea; GOLD: global initiative for chronic obstructive lung
disease; NYHA: New York Heart Association.

* Risk of moderate to severe OSA is indicated by the presence of daytime hypersomnolence, and at least two of the
following three criteria: habitual loud snoring, witnessed apnea or gasping/choking, or diagnosed hypertension. Examples
of conditions that can "complicate" OSA and in whom HSAT should NOT be performed include significant cardiorespiratory
disease (eg, heart failure, chronic obstructive pulmonary disease), disorders that contribute to hypoventilation
(neuromuscular disorders, obesity hypoventilation, opioids, stroke), and other non-respiratory sleep disorders (eg,
narcolepsy, severe insomnia).

¶ Clinicians should be aware that HSAT is suboptimal diagnostically in patients with mild OSA and may be less sensitive
for the detection of central respiratory events.

Δ Significant cardiorespiratory disease includes but is not limited to: GOLD stage 2, 3, 4 chronic obstructive pulmonary
disease, NYHA class III or IV heart failure.

◊ Severe insomnia can interfere with the accuracy of HSAT.

§ Examples of a mission critical worker is an airline pilot.

¥ Most experts prefer in laboratory polysomnography when following the response to therapy in patients with OSA. This is
based upon the rationale that patients who undergo successful treatment with an oral appliance or surgery, or experience
weight loss (ie, symptomatic improvement) are reasonably expected to have mild or no OSA which is suboptimally
detected on HSAT. HSAT may be an option in those in whom moderate to severe OSA is suspected or those in whom in-
laboratory polysomnography is not feasible.

Graphic 119877 Version 3.0

Non-respiratory sleep disorders [1]

Disorders of chronic insomnia

Central disorders of hypersomnolence

Narcolepsy type I

Narcolepsy type II

Idiopathic hypersomnia

Kleine-Levin syndrome

Hypersomnia due to a medical disorder

Hypersomnia due to a medication or substance

Hypersomnia associated with a psychiatric disorder

Insufficient sleep syndrome

Parasomnias
Non-rapid eye movement (NREM)-related parasomnias

Disorders of arousal from NREM sleep

Confusional arousals

Sleepwalking

Sleep terrors

Sleep-related eating disorders

Rapid eye movement (REM)-related parasomnias

REM sleep behavior disorder

Recurrent isolated sleep paralysis

Nightmare disorder

Other parasomnias

Circadian rhythm sleep-wake disorders

Delayed sleep-wake phase disorder

Advanced sleep-wake phase disorder

Irregular sleep-wake rhythm

Non-24-hour sleep-wake rhythm disorder

Shift work disorder

Jet lag disorder

Circadian rhythm sleep-wake disorder not otherwise specified

Sleep-related movement disorders

Restless leg syndrome

Periodic limb movement disorder

Sleep-related leg cramps

Sleep-related bruxism

Sleep-related rhythmic movement disorder

Propriospinal myoclonus at sleep onset

 Sleep-related movement disorder due to medical disorder

Sleep-related movement disorder due to medication or substance

Sleep-related movement disorder, unspecified

Reference:
1. International Classification of Sleep Disorders, 3rd ed, American Academy of Sleep Medicine, Darien, IL 2014.

Graphic 121157 Version 1.0

Non OSA-related conditions associated with sleep-disordered breathing
Category
Pulmonary diseases
Cardiac diseases
Neuromuscular-diseases and
hypoventilation syndromes
Effects of drugs including
substance use/abuse
OSA: obstructive sleep apnea.
Graphic 121158 Version 2.0
Examples
Chronic asthma, chronic obstructive pulmonary disease (eg, global obstructive
lung disease stage 2, 3, 4), interstitial lung diseases (eg, idiopathic pulmonary
fibrosis), occupational lung diseases, restrictive lung disease (eg, kyphoscoliosis,
scleroderma, congenital chest wall abnormalities, flail chest), and other (eg,
lymphangioleiomyomatosis).
Intracardiac shunts and disorders with elevated pulmonary capillary wedge
pressure (eg, class III or IV congestive heart failure with reduced or preserved
left ventricle ejection fraction, hypertrophic cardiomyopathy), mitral valve
disease.
Central sleep apnea, obesity hypoventilation, stroke, transient ischemic attacks,
diaphragmatic paralysis, multiple sclerosis, muscular dystrophy, paralytic
disorders, myasthenia gravis, encephalopathies (eg, hepatic, viral, vasculitis,
endocrine, brain injury).
Benzodiazepines, anti-seizure drugs, opiates, barbiturates, alcohol.
Multidimensional assessment of COPD

GOLD "ABCD" groups: Assessment of symptoms and risk of exacerbations for initiation
of COPD therapy

Assess exacerbation risk: Assess symptoms

Exacerbations/Hospitalizations mMRC* 0 to 1; CAT <10 ¶ mMRC ≥2; CAT ≥10

0 or 1 exacerbations without A B
hospitalization

≥2 exacerbations or ≥1 C D
hospitalization
 

GOLD: Severity of airflow limitation (based on postbronchodilator FEV 1 )

Stage Severity FEV 1 (percent predicted)

In patients with FEV 1 /FVC <0.7: Δ

GOLD 1 Mild ≥80

GOLD 2 Moderate 50 to 79

GOLD 3 Severe 30 to 49

GOLD 4 Very severe <30

COPD: chronic obstructive pulmonary disease; GOLD: Global Initiative for Chronic Obstructive Lung Disease; mMRC:
modified Medical Research Council dyspnea scale; CAT: COPD Assessment Test; FEV 1 : forced expiratory volume in one
second; FVC: forced vital capacity.

* mMRC dyspnea scale: Refer to UpToDate graphic.

¶ http://www.catestonline.org.

Δ The GOLD guidelines (www.goldcopd.org) prefer the threshold of <0.7 to the alternative of the fifth percentile lower
limit of normal (LLN) for FEV 1 /FVC.

From the Global Strategy for the Diagnosis, Management and Prevention of COPD 2017, © Global Initiative for Chronic
Obstructive Lung Disease (GOLD), www.goldcopd.org. Adapted with permission. The content within this table is still
current as of the 2019 GOLD report.

Graphic 82690 Version 11.0

NYHA and other classifications of cardiovascular disability
NYHA functional
Class
classification [1]
I Patients with cardiac
disease but without
resulting limitations of
physical activity. Ordinary
physical activity does not
cause undue fatigue,
palpitation, dyspnea, or
anginal pain.
II Patients with cardiac
disease resulting in slight
limitation of physical
activity. They are
comfortable at rest.
Ordinary physical activity
results in fatigue,
palpitation, dyspnea, or
anginal pain.
III Patients with cardiac
disease resulting in
marked limitation of
physical activity. They are
comfortable at rest. Less-
than-ordinary physical
activity causes fatigue,
palpitation, dyspnea, or
anginal pain.
IV Patients with cardiac
disease resulting in
inability to carry on any
physical activity without
discomfort. Symptoms of
cardiac insufficiency or of
the anginal syndrome may
be present even at rest. If
any physical activity is
undertaken, discomfort is
increased.
NYHA: New York Heart Association.
References:
1. The Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of
the Heart and Great Vessels, 9 th ed, Little, Brown & Co, Boston 1994. p.253.
2. Campeau L. Grading of angina pectoris. Circulation 1976; 54:522.
Canadian
Cardiovascular
Society functional
classification [2]
Ordinary physical activity,
such as walking and
climbing stairs, does not
cause angina. Angina with
strenuous or rapid
prolonged exertion at work
or recreation.
Slight limitation of
ordinary activity. Walking
or climbing stairs rapidly,
walking uphill, walking or
stair-climbing after meals,
in cold, in wind, or when
under emotional stress, or
only during the few hours
after awakening. Walking
more than 2 blocks on the
level and climbing more
than 1 flight of ordinary
stairs at a normal pace
and in normal conditions.
Marked limitation of
ordinary physical activity.
Walking 1 to 2 blocks on
the level and climbing 1
flight in normal conditions.
Inability to carry on any
physical activity without
discomfort. Anginal
syndrome may be present
at rest.
Specific activity
scale [3]
Patients can perform to
completion any activity
requiring ≥7 metabolic
equivalents (ie, can carry
24 lb up 8 steps; do
outdoor work [shovel
snow, spade soil]; do
recreational activities
[skiing, basketball,
squash, handball, jog/walk
5 mph]).
Patients can perform to
completion any activity
requiring ≥5 metabolic
equivalents (eg, have
sexual intercourse without
stopping, garden, rake,
weed, roller skate, dance
foxtrot, walk at 4 mph on
level ground) but cannot
and do not perform to
completion activities
requiring ≥7 metabolic
equivalents.
Patients can perform to
completion any activity
requiring ≥2 metabolic
equivalents (eg, shower
without stopping, strip and
make bed, clean windows,
walk 2.5 mph, bowl, play
golf, dress without
stopping) but cannot and
do not perform to
completion any activities
requiring >5 metabolic
equivalents.
Patients cannot or do not
perform to completion
activities requiring >2
metabolic equivalents.
Cannot carry out activities
listed above (specific
activity scale III).
 3. Goldman L, Hashimoto B, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing
cardiovascular functional class: Advantages of a new specific activity scale. Circulation 1981; 64:1227.

Graphic 52683 Version 19.0

Diagnosis obstructive sleep apnea

Sleep testing
Index Diagnostic criteria for OSA
device

Polysomnography* AHI AHI 5 to 14/hour sleep PLUS one or more sleep-associated conditions ¶
OR
AHI 15 ≥15/hour sleep

RDI RDI 5 to 14/hour sleep PLUS one or more sleep associated conditions ¶
OR
RDI 15 ≥15/hour sleep

Home sleep apnea REI REI ≥15/hour total recording time

device Δ

For the diagnosis of obstructive sleep apnea (OSA), respiratory events should be identified as primarily obstructive
(ie, apneas, hypopneas, arousals that are associated with respiratory effort). These events are used to generate
the following indices:
AHI: apnea-hypopnea index (apneas + hypopneas / total sleep time in hours)
RDI: respiratory disturbance index (apneas + hypopneas + respiratory effort-related arousals [RERAs] /
total sleep time in hours)
REI: respiratory event index (apneas + hypopneas/total recording time)

* Most polysomnography studies will report AHI, RDI, or both values. The clinician should recognize that the RDI may
overestimate or the AHI underestimate the number of respiratory events during sleep. However, no consensus has been
reached regarding which value is more accurate.

¶ Sleep-associated conditions include the following:

Sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms
Waking up with breath holding, gasping, or choking
Habitual snoring, breathing interruptions, or both noted by a bed partner or other observer
Hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial
fibrillation, or type 2 diabetes mellitus

Δ Home devices vary significantly in what data they collect. For example, type 3 and 4 devices do not typically detect
arousals from sleep because they do not include electroencephalography (EEG) data. The clinician should be aware of the
limitations of the device used.

Graphic 121160 Version 1.0

Contributor Disclosures
Lewis R Kline, MD Nothing to disclose Nancy Collop, MD Nothing to disclose Geraldine Finlay,
MD Nothing to disclose

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