Deffinition

Sleep Apnea Syndrome is a common sleep-related breathing disorder, which is usually

accompanied by partial or complete respiration cessation during night sleep.
Specifically, there are two main kinds of sleep-related breathing events when sleep apnea
syndrome happens, the Apnea Event and the Hypopnea Event. The Apnea Event is defined as
airflow cessation at mouth and nose, which lasts for at least 10 seconds. The Hypopnea Event is
defined as reduced airflow, which reduces more than 50% of the baseline for at least 10 seconds,
and a fall in blood oxygen saturation (SpO2) at least 4%. The Apnea Hypopnea Index (AHI), which
refers to the average number of apnea and hypopnea per hour during night sleep, is utilized for
medical specialists to diagnose sleep apnea syndrome and its severity. Typically, the OSA
syndrome is defined as an AHI of 5 or greater. An AHI of 5–15 is considered as mild, 15–30 is
moderate and more than 30 events per hour characterizes severe sleep apnea.
Wang Z, Zhou X, Zhao W, Liu F, Ni H, Yu Z. Assessing the severity of sleep apnea syndrome based
on ballistocardiogram. PLoS One. 2017 Apr 26;12(4):e0175351. doi:
10.1371/journal.pone.0175351. PMID: 28445548; PMCID: PMC5405918.

Prevalence
The exact prevalence of OSA is unknown, although estimates range from 2% to 14% in
community-screened populations to a much higher prevalence in certain. OSA is most common
among older males, but it can also affect women and children The incidence rises following
menopause such that rates are similar in postmenopausal women and men.
The estimated prevalence in North America is approximately 15 to 30 percent in males and 10 to
15 percent in females, when OSA is defined broadly as an apnea-hypopnea index (AHI) greater
than five events per hour of sleep. When more stringent definitions are used (eg, AHI ≥5 events
per hour plus symptoms or AHI ≥15 events per hour), the estimated prevalence is approximately
15 percent in males and 5 percent in females. Global estimates using five or more events per
hour suggest rates of 936 million people worldwide with mild to severe OSA, and 425 million
people worldwide with moderate to severe OSA, between the ages of 30 and 69 years of age.
The prevalence of OSA also varies by race. OSA is more prevalent in African Americans who are
younger than 35 years old compared with Caucasians of the same age group, independent of
body weight. The prevalence of OSA in Asia is similar to that in the United States, despite lower
rates of obesity.
The prevalence appears to be increasing and may relate to the increasing rates of obesity or
increased detection rates of OSA.
1. Benjafield AV, Ayas NT, Eastwood PR, et al. Estimation of the global prevalence and
burden of obstructive sleep apnoea: a literature-based analysis. Lancet Respir Med 2019;
7:687.
 1. Peppard PE, Young T, Barnet JH, et al. Increased prevalence of sleep-disordered breathing
in adults. Am J Epidemiol 2013; 177:1006.
2.

Phatophysiology

OSA is caused by repetitive bouts of upper airway obstruction during sleep as a result of the
narrowing of respiratory passages. The most common site of obstruction is the nasopharynx. It is
important to differentiate OSA from the less common central sleep apnea, which is caused by an
imbalance in the brain's respiratory control centers during sleep. While the pathogenesis of OSA is
thought to be multifactorial, anatomic defects are thought to play a major role.
As the patient falls asleep, muscles of the nasopharynx begin to relax and the surrounding tissue
collapses, causing compromise of the airway. As oxygen levels in the body start to drop and
carbon dioxide levels rise, the patient is aroused from sleep; this causes an increase in sympathetic
tone and subsequent contraction of nasopharyngeal tissue, which allows alleviation of the
obstruction. Upon the patient's falling back to sleep, however, the airway is again subjected to
narrowing until the patient is aroused from sleep once again. The cycle continues throughout the
night, causing decreased time spent in rapid eye movement sleep and an overall decrease in quality
of sleep. Most obstructive symptoms happen in the supine position.

Motamedi KK, McClary AC, Amedee RG. Obstructive sleep apnea: a growing problem. Ochsner J. 2009
Fall;9(3):149-53. PMID: 21603432; PMCID: PMC3096276.

Semelka M, Wilson J, Floyd R. Diagnosis and Treatment of Obstructive Sleep Apnea in Adults. Am
Fam Physician. 2016 Sep 1;94(5):355-60. PMID: 27583421.

Risk factors and associated conditions

Several clinical risk factors are associated with OSA and include the following:
Male gender – OSA is approximately two to three times more common in males than females,
although the risk appears to be similar once women are peri- and post-menopausal.
Older age – The prevalence of OSA increases from young adulthood through the sixth to seventh
decade.
Obesity - There is a significant increase in OSA prevalence with increasing body mass index (BMI),
waist-to-hip ratio and neck circumference.
Smoking – Smoking may increase the risk of or worsen OSA. Hypothesized mechanisms for a role
of smoking in OSA include airway inflammation and smoking-related disease, as well as effects of
declining blood nicotine levels on sleep stability.
Craniofacial and upper airway abnormalities – Craniofacial or upper airway abnormalities
increase the likelihood of having OSA . Examples of abnormalities include a wide craniofacial
base, an abnormal maxillary or short mandibular size, and tonsillar and adenoid hypertrophy.
Family history of snoring or OSA – While a family history of snoring or OSA could be due to
shared behavioral or environmental factors, there may also be a genetic predisposition to OSA
through factors such as craniofacial structure.
Nasal congestion at night, whether due to allergic rhinitis, acute upper respiratory tract infection,
or anatomy, has been linked to snoring and OSA.
Others - Alcohol has strong associations with the development and progression of obstructive
symptoms. Alcohol, as well as benzodiazepines and other central nervous system depressants,
preferentially inhibit upper airway muscle activity while also depressing the respiratory centers of
the brain.
Motamedi KK, McClary AC, Amedee RG. Obstructive sleep apnea: a growing problem. Ochsner J.
2009 Fall;9(3):149-53. PMID: 21603432; PMCID: PMC3096276.]
The prevalence of OSA is also increased in patients with a variety of medical conditions, including
the following: Obesity hypoventilation syndrome, Congestive heart failure, Atrial fibrillation,
Pulmonary hypertension, Hypertension (particularly resistant hypertension), cardiovascular
disease, atrial fibrillation, and pulmonary hypertension, End-stage kidney disease, Chronic lung
disease, including asthma, chronic obstructive pulmonary disease (COPD), and idiopathic
pulmonary fibrosis, Stroke and transient ischemic attacks, Pregnancy, Acromegaly,
Hypothyroidism, Polycystic ovary syndrome, Parkinson’s disease, Floppy eyelid syndrome.
Other medical conditions that may have an increased association with OSA include fibromyalgia,
Barrett's esophagus, gastroesophageal reflux disease (GERD), secondary polycythemia, and
Down’s syndrome. ->>>>>>>>> DEZVOLT?

Young, T. (2004). Risk Factors for Obstructive Sleep Apnea in Adults. JAMA, 291(16),
2013. doi:10.1001/jama.291.16.2013

Signs and symptoms

A thorough history and physical examination will often elucidate some of the signs and symptoms
of OSA. Common symptoms include daytime sleepiness, morning headaches, loud snoring,
gasping, choking, snorting, or interruptions in breathing while sleeping.
[Motamedi KK, McClary AC, Amedee RG. Obstructive sleep apnea: a growing problem. Ochsner J.
2009 Fall;9(3):149-53. PMID: 21603432; PMCID: PMC3096276.]
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. Daytime sleepiness may be
underestimated because of its insidious onset and chronicity. The patient may use terms such as
fatigue, low energy, tiredness or poor focus. 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 (do not wake up feeling refreshed) and nocturnal
restlessness in association with their complaint of daytime sleepiness.
Chervin RD. Sleepiness, fatigue, tiredness, and lack of energy in obstructive sleep apnea. Chest
2000; 118:372.

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

untreated OSA. They are usually bifrontal and squeezing in quality, with no associated nausea,
photophobia, or phonophobia. 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. They typically occur daily or most days of the week and may
last for several hours after awakening in the morning.
Snoring, gasoing, choking during sleep – Snoring and associated events such as resuscitative
gasping or snorting, witnessed apneic periods, periods of silence followed by loud snoring,
restless or fitful sleep are common features of OSA. 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. Choking or
gasping during sleep or wakening with a dry mouth are commonly reported, often in association
with snoring.
Myers KA, Mrkobrada M, Simel DL. Does this patient have obstructive sleep apnea?: The Rational
Clinical Examination systematic review. JAMA 2013; 310:731.

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, being more common in females.
Nocturia – Nocturia is a common associated symptom of OSA. When patients repeatedly awaken
from apneic events, they experience the urge to urinate.
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.
Physical examination

Features on physical examination that are associated with OSA include signs of central obesity
(e.g., increased waist circumference, increased neck circumference), nasal septal deviation or
turbinate hypertrophy, crowding of the posterior oropharynx as estimated by the Mallampati or
Friedman score, or retrognathia. Oropharyngeal crowding may be caused by tonsillar
enlargement, soft palate elongation, macroglossia or changes in dental occlusion. 18 The
pathophysiologic mechanisms predisposing to OSA are complex and overlapping; 19 thus, neither
history nor physical examination is sufficiently accurate to exclude the diagnosis of OSA
Laratta CR, Ayas NT, Povitz M, Pendharkar SR. Diagnosis and treatment of obstructive sleep apnea
in adults. CMAJ. 2017 Dec 4;189(48):E1481-E1488. doi: 10.1503/cmaj.170296. PMID: 29203617;
PMCID: PMC5714700

Diagnosis

OSA should be suspected whenever a patient presents with excessive

daytime sleepiness, snoring, and choking or gasping during sleep,
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).

Detailed questions that explore the etiologies of daytime sleepiness,

snoring, and neuropsychiatric disease may help to tease out OSA from
other conditions, but sleep apnea testing is required to make the
diagnosis of OSA.

Polysomnography, also known as a “sleep study,” is the current “gold-standard” of OSA

diagnostic testing. In polysomnography, the patient is kept overnight and is monitored for several
physiologic variables in a sleep laboratory. Variables monitored include body position, oxygen
saturation, limb movement, cardiac rhythm and rate, respiratory effort, brain activity, eye
movements, and stages of sleep. While a positive polysomnography study result reinforces a
previous clinical diagnosis of OSA, current literature dictates that a negative polysomnography
result, with strong clinical suspicion of OSA, does not rule out the disease because of the high
levels of variability, technician error, and lack of standardization involved in testing. Additional
diagnostic modalities for OSA include portable sleep monitors, radiographic studies for anatomic
analysis, and empiric treatment.
Motamedi KK, McClary AC, Amedee RG. Obstructive sleep apnea: a growing problem. Ochsner J.
2009 Fall;9(3):149-53. PMID: 21603432; PMCID: PMC3096276.
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])
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)

The diagnosis of OSA is confirmed if either of the two criteria below is present:
 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.
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.

Screening

Questionnaires are available to screen and assess OSA risk in the primary care setting for the
advantages of simple operation and low labor cost. Commonly used assessment questionnaires
for sleep disorders include:
1. Berlin questionnaire, which is an assessment tool based on 10 questions about snoring
behavior, daytime sleepiness or fatigue, and presence of obesity or hypertension to identify the
sleep apnea risk in the primary healthcare settings;
2. STOP-Bang questionnaire (SBQ) a screening for preoperative assessment, eight dichotomous
items (yes/no): snoring, tiredness, observed apnea, high blood pressure, body mass index, age,
neck circumference, and male gender);
3. NoSAS is used to assess by medical records reviews which include neck circumference, body
mass index, snoring, age and gender), and
4. Epworth sleepiness scale (ESS, the most widely used questionnaire to assess daytime
sleepiness, and low sensitivity for OSA.
To discriminate the severity of OSA, NoSAS showed better performance than SBQ .
Amra B, Rahmati B, Soltaninejad F, Feizi A. Screening Questionnaires for Obstructive Sleep Apnea:
An Updated Systematic Review. Oman Med J. 2018 May;33(3):184-192. doi:
10.5001/omj.2018.36. PMID: 29896325; PMCID: PMC5971053.

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). In general, they can be distinguished from OSA via clinical history
and polysomnography (PSG). Complex sleep disorders that present with daytime
sleepiness are periodic limb movement disorder, restless leg syndrome, narcolepsy,
central sleep apnea, and non-OSA related conditions associated with sleep disordered
breathing.
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
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.
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. Patients may
have a history of dyspepsia or symptoms of reflux, although their GERD may be silent.
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).
Miscellaneous – Other disorders that can mimic OSA include nocturnal asthma,
swallowing disorders, nocturnal seizures 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).

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.

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 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.
However, using the latest AASM definition of hypopnea, symptomatic patients with mild OSA are
without increased cardiovascular risk.
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 (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 (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.
Hudgel DW. Sleep Apnea Severity Classification - Revisited. Sleep. 2016 May 1;39(5):1165-6. doi:
10.5665/sleep.5776. PMID: 27070135; PMCID: PMC4835315.

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].
●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. Additional neuropsychiatric manifestations include
moodiness and irritability as well as depression, psychosis, and sexual dysfunction.
●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
●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 (chronic lung disease). Severe
hypoxemia may also cause secondary polycythemia.
 ●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.
●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].
●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)

Harding, S. M. (2000). Complications and consequences of obstructive sleep apnea. Current

Opinion in Pulmonary Medicine, 6(6), 485–489. doi:10.1097/00063198-200011000-00004

Treatment

The goals of OSA therapy are to resolve signs and symptoms of OSA, improve sleep quality, and
normalize the apnea-hypopnea index (AHI) and oxyhemoglobin saturation levels. OSA should be
approached as a chronic disease that requires long-term, multidisciplinary management. The
potential benefits of successfully treating OSA include clinical improvement (eg, less daytime
sleepiness), reduced health care utilization and costs, and, possibly, decreased cardiovascular
morbidity and mortality.
Common to all guidelines is the recommendation that, in addition to reviewing the behavioral
modifications reviewed in the next section, all patients diagnosed with OSA should be offered
positive airway pressure as initial therapy.
In patients with mild to moderate OSA who prefer not to use positive airway pressure or who fail
to respond to it, oral appliances are an alternative therapy that have been shown to improve signs
and symptoms of OSA and may be better tolerated in some patients than positive airway
pressure. Upper airway surgery may supersede oral appliances as alternative therapy in patients
with severe, surgically correctable, obstructing lesions of the upper airway.

Education and behaviour

Once the diagnosis of OSA is confirmed and its severity determined, the results of all testing
should be reviewed with the patient. The patient should be educated about the risk factors, natural
history, and consequences of OSA. Importantly, all patients should be warned about the
increased risk of motor vehicle accidents associated with untreated OSA and the potential
consequences of driving or operating other dangerous equipment while sleepy. Patients should
also be counseled to avoid activities that require vigilance and alertness if sleepy.
Patients should be counselled that they should always inform their medical providers that they
have sleep apnea, especially if they are to have surgery or start opiate medications.
Weight loss and exercise — Weight loss and exercise should be recommended to all patients
with OSA who are overweight or obese. While rarely leading to complete remission of OSA,
weight loss, including that from bariatric surgery, has been shown to improve overall health and
metabolic parameters, decrease the apnea-hypopnea index (AHI, the number of apneas and
hypopneas per hour of sleep), reduce blood pressure, improve quality of life, and probably
decrease daytime sleepiness.
Epstein LJ, Kristo D, Strollo PJ Jr, et al. Clinical guideline for the evaluation, management and
long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009; 5:263.

Initial treatment for weight loss should be aimed at decreasing food intake and, when possible
increasing energy expenditure. Available strategies for weight loss include behavioral
modification, dietary therapy, exercise, drug therapy, and surgery.
Sleep position — During the diagnostic sleep study, some patients will be observed to have OSA
that develops or worsens during sleep in the supine position. Such patients tend to have less
severe OSA, to be less obese, and to be younger than non-positional patients. Sleeping in a non-
supine position (eg, lateral recumbent) may correct or improve OSA in such patients and should
be encouraged but not generally relied upon as the sole therapy.
Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice parameters for the medical therapy of
obstructive sleep apnea. Sleep 2006; 29:1031.

Jokic R, Klimaszewski A, Crossley M, et al. Positional treatment vs continuous positive airway

pressure in patients with positional obstructive sleep apnea syndrome. Chest 1999; 115:771.

Alcohol avoidance — All patients with untreated OSA should avoid alcohol, even during
the daytime, because it can depress the central nervous system, exacerbate OSA,
worsen sleepiness, and promote weight gain. Acute alcohol consumption often worsens
the duration and frequency of obstructive respiratory events during sleep as well as the
degree of oxyhemoglobin desaturation and snoring. In patients who snore but do not
have OSA at baseline, alcohol consumption can prompt frank OSA.

Concomitant medications — Any clinician who prescribes medication for the patient
should be informed that the patient has OSA, since certain medications with inhibitory
effects on the central nervous system should be avoided if reasonable alternatives exist.
In particular, benzodiazepines should be avoided in untreated patients.
Other medications that may exacerbate OSA and theoretically worsen daytime sleepiness
include benzodiazepine receptor agonists, barbiturates, other antiepileptic drugs,
sedating antidepressants, antihistamines, and opiates. Antidepressants that cause weight
gain might be particularly problematic in these patients. Some antidepressants may
worsen sleep by causing restless legs syndrome or periodic limb movements.

POSITIVE AIRWAY PRESSURE THERAPY

Positive airway pressure therapy is the mainstay of therapy for adults with OSA. The
mechanism of continuous positive airway pressure (CPAP) involves maintenance of a
positive pharyngeal transmural pressure so that the intraluminal pressure exceeds the
surrounding pressure. CPAP also stabilizes the upper airway through increased end-
expiratory lung volume. As a result, respiratory events due to upper airway collapse (eg,
apneas, hypopneas) are prevented.
Jordan AS, McSharry DG, Malhotra A. Adult obstructive sleep apnoea. Lancet 2014; 383:736.

Direct comparisons of positive airway pressure to mandibular advancement devices (MAD) have
used CPAP as the mode of positive airway pressure. Trials indicate that CPAP is more effective
than MADs at reducing the frequency and severity of both respiratory events and oxyhemoglobin
desaturation episodes during sleep, but symptomatic improvement is similar.
Some studies have indicated that patients prefer oral appliances over CPAP therapy, at least with
short-term follow-up.

Modes of administration — The most common modes of positive airway pressure administration
include continuous positive airway pressure (CPAP), bilevel positive airway pressure (BPAP), and
autotitrating positive airway pressure (APAP) …………..dezvoltam?????

Adherence — Decreased adherence can lessen the potential benefits of CPAP therapy. It is
estimated that 20 to 40 percent of patients do not use their positive airway pressure device and
many others do not use it all night, every night.

Follow-up — Patients who elect to be treated with positive airway pressure should be evaluated
frequently, especially during the first few weeks of therapy . This may include frequent telephone
calls and as-needed opportunities to meet face to face with a clinician. Adherence and efficacy
can be monitored remotely with PAP devices that include modems. Communication with the
devices can be bidirectional so that pressures can be adjusted remotely. The purpose of frequent
evaluations is to quickly identify and manage any side effects that develop, since this may affect
long-term adherence with the therapy.

1 din uptodate

Once any side effects of the positive airway pressure are successfully managed and the patient is
adhering to the therapy, the patient should be asked whether the symptoms of OSA have
resolved.

Xia F, Sawan M. Clinical and Research Solutions to Manage Obstructive Sleep Apnea: A Review. Sensors
(Basel). 2021 Mar 4;21(5):1784. doi: 10.3390/s21051784. PMID: 33806496; PMCID: PMC7961570.

Alternative therapies

Oral appliances (mandibular advancement devices, tongue retaining devices) are an alternative
therapeutic strategy in OSA that may be offered to patients with mild to moderate OSA who
decline or fail to adhere to positive airway pressure therapy and who have a preference for such
treatment.
Oral appliances — For patients with mild or moderate OSA who decline or fail to adhere to
positive airway pressure therapy, an oral appliance is a reasonable alternative to positive airway
pressure. This is based upon the recognition that while positive airway pressure is generally more
effective than an oral appliance at normalizing respiratory events and oxyhemoglobin desaturation
episodes during sleep], most patients prefer an oral appliance, adherence is an essential aspect
of successful treatment, both modalities are effective compared to no treatment or a sham
treatment, and both modalities have a similar effect on symptoms and quality of life.
Xia F, Sawan M. Clinical and Research Solutions to Manage Obstructive Sleep Apnea: A Review. Sensors
(Basel). 2021 Mar 4;21(5):1784. doi: 10.3390/s21051784. PMID: 33806496; PMCID: PMC7961570.

Oral appliances have variable efficacy in patients with severe OSA and/or significant sleep-related
hypoxemia; such patients are not good candidates for an oral appliance as first-line therapy and
should be encouraged to use positive airway pressure therapy.
There are an increasing number of oral appliances that are designed to either protrude the
mandible forward (ie, mandibular advancement/repositioning splints, devices, or appliances) or
hold the tongue in a more anterior position (ie, tongue retaining devices). Either design holds the
soft tissues of the oropharynx away from the posterior pharyngeal wall, thereby maintaining upper
airway patency.
Oral appliances decrease the frequency of respiratory events, arousals, and episodes of
oxyhemoglobin desaturation, compared to no treatment or a sham intervention. They may also
improve daytime sleepiness, quality of life, and neurocognitive function. Their impact on mortality
is unknown.
Upper airway surgery — There is no consensus regarding the role of surgery in patients with
OSA of varying degrees of severity, nor have optimal screening or imaging procedures been
established that accurately predict which patients are most likely to benefit from surgery. We
generally consider surgical therapy when positive airway pressure or an oral appliance is declined
or ineffective (after at least a three-month trial of therapy). Surgical treatment appears to be most
effective in patients who have OSA due to a severe, surgically correctable, obstructing lesion of
the upper airway. Examples of surgically correctable lesions that may obstruct the upper airway
include tonsillar hypertrophy, adenoid hypertrophy, or craniofacial abnormalities.
Strollo PJ Jr, Soose RJ, Maurer JT, et al. Upper-airway stimulation for obstructive sleep apnea. N
Engl J Med 2014; 370:139.

Pharmacologic — A variety of pharmacologic agents have been investigated in randomized trials

as primary therapeutic agents for the management of sleep-disordered breathing on OSA, with
the goal of replacing the more burdensome therapies described above. This includes drugs that
might act to stimulate respiratory drive directly (theophylline) or indirectly (acetazolamide), drugs
that reduce upper airway collapsibility (desipramine), antimuscarinics (oxybutynin), or
noradrenergic agents (eg, atomoxetine). However, no pharmacologic agent has proven to be
sufficiently effective to warrant replacement of such therapies.
Mason M, Welsh EJ, Smith I. Drug therapy for obstructive sleep apnoea in adults. Cochrane
Database Syst Rev 2013; :CD003002.