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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4538_Библиотеки_им_академика_М_И_Перельмана
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3 Sleep Related Breathing Disorders
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and decreased growth hormone secretion, mood and behavior abnormalities have
been reported. Developmental delay or autism may be present [15].
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3.7.4 Idiopathic Central Alveolar Ventilation
Is dened as the presence of decreased alveolar ventilation, resulting in sleeprelated hypercapnia and hypoxemia, in individuals with presumed normal mechanical properties of the lung, and respiratory pump.
3.7.5 Sleep-Related Hypoventilation DuetoaMedication
or Substance
This disorder is characterized primarily by chronic hypoventilation and hypercapnia
due to prolonged use of medications or substances, known to depress ventilatory
drive and/or impair respiratory muscle mechanics.
These agents include long-acting narcotics, anesthetics, sedative compounds,
and muscle relaxants. In addition, the risk of respiratory insufciency is increased
with the concomitant use of alcohol or with polypharmacy.
3.7.6 Sleep-Related Hypoventilation DueaMedical Disorder
In this disorder, there is a chronic obstructive pulmonary disease (COPD) and
parenchymal lung disease. Polycythemia is accompanied by severe chronic
hypoxemia.
This disease is usually most severe during REM sleep [16].
3.7.7 Sleep-Related Hypoxemia
The disease is related to a signicant hypoxemia during sleep and is secondary to a
medical or neurological disorder. Chronic hypoxemia can develop from airway or
parenchymal pulmonary disease, chest wall disorders, pulmonary hypertension, or
neurologic and neuromuscular disorders.
Hypoxemia due to underlying lower airway obstructive disease, pulmonary
parenchymal disease, vascular pathology, and other causes of hypoventilation is
generally prolonged (several minutes or longer). In contrast, sawtooth uctuations
of oxygen saturation (typically less than 1 min) characterize hypoxemia due to
OSA or CSA.
Prevalence may be higher in patients with more signicant perturbations of pulmonary function or neuromuscular weakness.
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3.8 Isolated Symptoms andNormal Variants
3.8.1 Snoring andOSA
Snoring is a respiratory sound generated in the upper airway during sleep that typically occurs during inspiration but may also occur in expiration.
It occurs without episodes of apnea, hypopnea, RERAs, or hypoventilation. Does
not cause symptoms of daytime sleepiness, insomnia in the patient, or reported by
the partner witnessed breathing pauses.
The snoring intensity may vary and will often disturb the bed partner’s sleep and
even awaken the patient. Occasional snoring is almost universal [17].
So, this type of snoring, has variously been referred to as habitual, primary, or
simple snoring.
But in general, snoring is a cardinal symptom of obstructive sleep apnea.
In addition, those individuals with snoring and comorbid cardiovascular disease
(especially pulmonary or systemic hypertension, coronary artery disease, or atrial
brillation) are at increased risk for the presence of OSA [18].
Therefore, PSG or OCST is required to rule out OSA in such populations effectively. It should also be noted that patients who initially have isolated snoring may
be at risk for developing OSA with aging or weight gain.
Estimates of snoring vary widely, depending on its denition. The incidence of
snoring in children is 10–12%. The Wisconsin cohort study reports habitual snoring
in about 24% of adult women and 40% of adult men.
Prevalence of snoring increases with age in both sexes, except that the most
reported snoring starts to decrease again in men after 70years of age (this may be
due to reduced hearing acuity in older individuals).
Snoring is most common in adult men and is also linked to obesity. Nasal obstruction increases the risk of snoring. Ingestion of alcohol, muscle relaxants, narcotics,
or other substances that decrease upper airway muscle tone predisposes an individual to snore. Smoking, particularly in males, has also been shown to be a risk factor [19].
Snoring increases during pregnancy.
In children, an association has been reported between snoring and adenotonsillar
hypertrophy.
There is a vibration of the uvula and soft palate during snoring, although it may
also involve the faucial pillars, pharyngeal walls, and larynx.
If PSG is performed, snoring tends to be loudest during stage N3 or REM sleep.
Some studies have suggested that adult snorers may have a higher prevalence of
cardiovascular disease, including hypertension, stroke, and ischemic heart disease.
Snoring tends to increase during pregnancy.
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3.8.2 Catathrenia
Catathrenia, also known as sleep-related groaning, is included in the Sleep-Related
Breathing Disorders (SRBD) section because it appears to be associated with prolonged expiration, usually during REM sleep.
Typically, a deep inspiration is followed by prolonged expiration and a monotonous vocalization resembling groaning. The pattern is sometimes called bradypnea.
The affected individual is usually unaware of the problem, but the clinical evaluation is sought, due to complaints of the bed partner or family members.
It is thought to be rare and more common in men.
Several episodes may occur nightly and often in clusters.
The long-term consequences of catathrenia are unknown, but the disorder is primarily a social problem for the affected individual.
3.9 Clinical Presentation ofOSA
Sleep and wake symptoms of OSA
Nocturnal symptoms Daytime symptoms
Snoring Excessive daytime sleepiness
Fatigue
Witnessed apneas Morning headaches
Dyspnea (choking/gasping)
Night sweats
Bedwetting
Drooling Diminished quality of life
Dry mouth Mood and personality changes:
Bruxism Sexual dysfunction:
Restless sleep/multiple arousals
Fragmented sleep
Gastroesophageal reux
Nocturia
Neurocognitive impairment:
Vigilance
Executive functioning
Motor coordination
Memory or concentration issues
Depression
Anxiety
Irritability
Decreased libido
Impotence
Abnormal menses
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The golden standard for the diagnosis of OSA, is polysomnography.
However, the process is time consuming, labor intensive, and costly.
Moreover, the interpretation sometimes is difcult. Different sleep problems
often coexist, potentially complicating the diagnosis and management.
The screening for OSA includes the sleep history, review of symptoms, and
physical examination.
So, symptoms and signs and clinical history are essential, and necessary for evaluation of the clinical picture of SRD, and knowledge of other associated
comorbidities.
Whenever possible, the patient should come with the bed partner. However, the
clinical history is still necessary to elaborate on a questionnaire of suspicion and
severity of OSA, such as the Epworth Sleepiness scale or STOP-BANG.No symptoms or signs by themselves are predictive of OSA or its severity. Therefore, they
are important for the evaluation of the clinical picture of SRD and to knowledge of
other associated comorbidities.
However, no symptoms or signs by itself are predictive of OSA or its severity.
Some authors propose that age, sex, BMI, and medical history are superior to the
symptoms variables for predicting OSA [20].
Many patients with OSA remain undiagnosed (0.3–5%).
Many studies prove that adverse health outcomes are associated with OSA,
regardless of daytime sleepiness.
We must refer that some comorbidities, can carry important information, such as
resistant hypertension (the risk of OSA is 80%), diabetes, headache, and so on.
With this information, we can identify patients for OSA study.
Then a polysomnography can be done.
A study in Switzerland in 2015, reported 50% of men, and 25% of women had
moderate OSA.
In 2002, Sleep Heart Health study revealed that 24% of men and 9% of women
aged 30–49 had mild OSA.
In the United States, it is estimated that 82% of men and 93% of women have
undiagnosed OSA.
Unmodiable and modiable factors inuence the risk of OSA [21].
The rst group includes male sex, age, race, genetic predisposition or family history, and cranial facial anatomy.
The second includes obesity, medications such as muscle relaxants or drugs (opiates, benzodiazepines, alcohol), endocrine disorders (hypothyroidism, hypothalamic disease, polycystic ovarian syndrome, smoking, and nasal obstruction.
F. Fernandes
3.10 Comorbidities
OSA is associated with several comorbidities, including stroke, myocardial infarction, hypertension, arrhythmias including atrial brillation, pulmonary hypertension, congestive heart failure, hyperlipidemia, glucose intolerance, type 2 diabetes,
and depression.
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Patients with cardiovascular disease have a great prevalence of OSA, moderate
or severe OSA hypertension (30–83%), heart failure (55–20%), arrhythmias
(50–20%), stroke (75–57%) and coronary heart disease (38–65%) [19, 20].
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3.10.1 Sleep History
The sleep history starts with patients, total sleep time based on bedtime, time to fall
asleep and wake up, difculty falling asleep, staying asleep, or daytime naps.
In some patients, their insufcient sleep determinates attention decit and memory.
There are some indirect data, as sometimes of caffeine abuse, which means, that
the patient uses it to combat daytime sleepiness.
Sleep deprived or OSA patients suffer from drowsy diving that make them prone
to accidents mainly in long distance trips [20].
3.11 Risk Factors
The morbidity rate of OSA in population is between 9 and 38% and is higher in
male, obese, and older patients.
Recent studies have also shown OSA patients to have a higher prevalence of
psoriasis compared to general population [22].
3.11.1 Sex
Men are at higher risk than women (two- or threefold risk in men). It is less severe
in women than men, with the same BMI.
The exception is during pregnancy, which is of particular risk in women.
Snoring and witnessed apneas are more common in men. On the other hand,
daytime excessive sleepiness, insomnia, and fatigue are more common in women.
OSA is prevalent in 60–70% of women with polycystic ovary [23].
3.11.2 Excessive Body Weight
Excessive body weight is a common clinical nding, in more than 60% of patients
referred for a diagnosis for sleep evaluation.
A strong correlation between increased obesity and OSA. It correlates with
abdominal and neck circumference.
An increase of 10% in BMI, increases by sixfold moderate OSA to severe and
rises the Apnea/Hypopnea Index (AHI) index by 32%. A 10% decrease in BMI lowers AHI in 26%.
Excessive body weight affects breathing in numerous ways.
Weight loss is very effective to reduces the severity of OSA.
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3.11.3 Age
Epidemiologic surveys reveal that more than 50% of adults over the age of 65years
have had some form of chronic sleep-related complaints.
The risk of OSA increases with age.
Prevalence in men older than 65–72years is 23%, and 30% in older than 80.
On the other hand, despite the high prevalence of OSA with age, the partner’s
witnessed snoring decrease, may be due to deafness [21].
3.11.4 Race
The sleep heart study reveals the risk of severe OSA in blacks is 20% and whites 17%.
Another study shows the prevalence of OSA is 30% in whites, 32% in blacks,
38% in Hispanics, and 39% in Chinese.
While Asians are generally, less obese than whites, disease prevalence is similar
to in the west. Moreover, for a given age, sex, and BMI, Asians have more signicant disease severity than whites.
Snoring, a cardinal sign of obstructive sleep apnea, has been reported in 27.8%
of Hispanic men and 15.3% of women [24].
3.11.5 Familial andGenetic Predisposition
Family susceptibility to OSAS increases directly with the number of affected
relatives.
Craniofacial and cephalometric abnormalities, volume of lateral parapharyngeal,
tongue, and genetic determinants of obesity and fat distribution are predisposing
factors [25].
3.11.6 Alcohol
Alcohol intake can induce apneic activity and apnea duration and worsen the severity of hypoxemia.
Long-term alcohol abuse on OSA is not well known.
3.11.7 Smoking
Sleep instability occurs due to the reduction of night nicotine and the inammatory
process of the airway.
Smokers are three times more likely to have OSA than no smokers.
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3.11.8 Other Causes
OSA is related to menopause, not due to hormonal changes, fat deposition, and
weight gain, and can be controlled by Hormone Replacement Therapy.
Also, patients with hypothyroidism have increased susceptibility to OSA [5].
3.12 OSA Sleep-Related Nocturnal Symptoms
The most frequent night symptom is snoring.
It can be simple, habitual without apnea, or associated with apnea, a cardinal
symptom. It is exacerbated by alcohol intake, weight gain, sedatives or opioids,
sleep deprivation, or supine position. It is aggravated by nasal obstruction.
It leads to difculty with bed partner.
Snoring is very common in the general population (35–45% in men and 15–28%
in women). However, only 6% of patients with OSA do not snore. The description
by the partner is essential for the medical history. The patient doesn’t recognize that
they snore (about 75%).
Those who snore and have cardiovascular changes, are at risk of having OSA.The
prevalence of snoring increases with age till 70years.
In patients without OSA, and with a BMI less than 30, increasing snoring correlates with a signicant increase in cause mortality.
Non palatal snoring is associated with increased in observed all-cause mortality
controlling for age, sex, BMI, and AHI.
There is a relation between snoring and carotid artery atherosclerosis, especially
in sound frequencies of snoring.
The odds of high-risk features are four to eight times higher in snorers than nonsnorers in the same conditions.
The snoring increases during pregnancy [18, 19, 26].
3.12.1 Witnessed Apneas
They are the second most important symptom in OSA, observed by bed partners (up
75%). It is associated with loud effort for breathing, gasps, moans, body movements, and brief wakening. Patients have no conscious of the situation.
Nocturnal dyspnea is sometimes described by patients, as a choking sensation or
suffocation. These episodes occur with arousals and may be associated with feelings of panic, and anxiety.
It must be distinguished from causes of paroxysmal nocturnal dyspnea, such as
Cheyne–Stokes breathing, left heart failure, nocturnal asthma, and laryngeal stridor.
Other common symptoms are drooling (30%) and dry mouth (75%) caused by
mouth breathing due to nasal obstruction.
In OSA, about 40–54% suffer from it.
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3.12.2 Bruxism
Bruxism may be caused by micro-arousals, occurring during sleep, and are considered the primary causal factor of night jaw closing muscle activation.
It is characterized by clenching and grinding the teeth, or by breathing and thrusting the mandible. The causes are multifactorial and mostly of central origin.
Sleep bruxism occurs mainly in non-REM sleep, N1, and N2, when there is a
uctuation of sympathetic/parasympathetic activity. It can be a defense mechanism
against obstruction of the upper airway [27, 28].
3.12.3 Restless Sleep
When this occurs, patients wake up tired in the morning, maybe accompanied by
nocturnal sweat (>65%), due to respiratory effort and autonomic instability during
sleep. However, diaphoresis may appear in many other diseases [29].
3.12.4 Gastroesophageal Reflux
It occurs in 64–73% of patients. Some authors say that in OSA upper airway
obstruction leads to increased intra-abdominal pressure, combined with more negative intrathoracic pressure, which results in increased intradiaphragmatic pressure
gradient, which leads gastric contents to the esophagus.
Some studies shows that when the patient is treated with CPAP, the reux
decreases around 48% [30].
3.12.5 Nocturia
It is present in 28% of patients and is related to the severity of OSA.The pathophysiological mechanism includes the increased secretion of natriuretic peptide
with an increase in intra-abdominal pressure [31].
3.13 Sleep-Related Daytime Symptoms
3.13.1 Excessive Daytime Sleepiness
It is a cardinal feature of OSA syndrome and results from abnormal sleep.
The most common is daytime sleepiness. The reason is sleep fragmentation with
arousals, and insufcient sleep [32].
During the day, the patient has a tendency to fall asleep during diverse situations
as after lunch, driving, working, etc.
It can be registered through questionnaires like the Epworth Sleep Scale [33, 34].
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If severe, it can cause vehicle and machinery accidents, poor school and job performance, and relationship problems.
Several studies have shown that patients with OSA tend to high motor vehicle
crash rates [35].
In a study in Swedish patients, the authors found that baseline snoring and sleepiness were signicantly related to occupational injuries. Patients with OSA, or heavy
snoring, were two or threefold as likely to have occupational injury, in the past
10years.
In patients with OSA without treatment, 41% manifested sleepiness at the wheel.
The Epworth Sleep Scale (ESS), depressive symptoms, and the risk of exposure
(annual mileage) are predictors of sleepiness.
Other behavioral factors are sleep deprivation, shift work, and nonrestorative sleep.
In a recent survey, 17% of European drivers reported episodes of sleepiness at
the wheel in the previous 2 years [36].
In a study, around 3% of Australian adults reported a diagnosed OSA with elevated ESS, having a signicant tendency to doze off, during the daytime, including
while driving.
Car crashes accident rate has been estimated to be fatal in 11% of sleepy drivers,
in contrast to a 5% of the general population [37].
Near miss accidents in sleepy drivers is 10%.
We must distinguish between fatigue or lethargy, or depression. Also, other reasons for chronic insomnia, are depression, bromyalgia, medication or substance
abuse, or other organic diseases such as cardiac disease.
A direct relationship between snoring and daytime sleepiness is independent of
AHI [36, 37].
ESS questionnaire may measure this situation especially when accompanied by
the STOP-BANG questionnaire.
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3.13.2 Morning Headaches
These are frequent in half of OSA patients. When the patient wakes up, it is dull,
scattered, and lasts 1 or 2 h. However, it is not specic and can be associated with
other situations, like hypertension, sinusitis, depression, and other medical
conditions.
It is related to hypoxemia and hypercapnia during sleep, with vasodilation.
Treating OSA solves the problem [38].
3.13.3 Neurocognitive Impairment
It is due to sleep fragmentation. The resulting hypoxemia can lead to anoxic brain
damage, and affects the executive, vigilance and motor coordination, and short and
long-term memory.
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Some recent studies mention the relationship between OSA and Alzheimer’s disease, in relation to the β amyloid and tau in CSF.OSA can accelerate the process of
Alzheimer’s disease [39, 40].
F. Fernandes
3.13.4 Mood Alterations
These are frequent and lead to a decreased quality of life the most common symptom is depression.
Other behavioral manifestations are irritability, anxiety, aggression, and emotional liability.
Treatment with CPAP alleviates the symptoms of depression and improves the
quality of life [41].
3.13.5 Sexual Dysfunction
Sexual dysfunction, erectile dysfunction (ED), and decreased libido are associated
with OSA.The sleep-related erection is a natural involuntary phenomenon in REM
in healthy males, regulated by the hypothalamus. In a Korean study, ED is associated with OSA accompanied by low-oxygen saturation, vascular endothelial dysfunction, and a pudendal neuropathy [42].
CPAP or surgical sleep treatment improves sexual quality of life [37].
Severe OSA may cause vertigo due to hypoxia of the posterior labyrinth and can
damage the brainstem [43].
3.14 Clinical Signs
3.14.1 OSA Common Physical Findings
During physical examination, it is important to observe the body mass of the patient
as obesity is frequently associated with OSA.Obesity (BMI >30kg/m2) has high
sensitivity (93%) and specicity (73%) for OSA.
In the ENT examination, we must check the neck circumference in men >43cm,
and women ≥39cm. It is a high predictor of OSA, with a sensitivity 61% and a
specicity 93% [21].
In OSA, airway obstruction occurs between the nares and the trachea.
We must begin our observation in the nose, the rst structure on superior airway
anatomy.
It is an important in OSA and should not be forgotten.
The nares should be observed, asking the patient to breath, paying attention to
the movement of lateral cartilage during inspiration, and the function of the internal
valve. There is a need to watch the septum if it is deviated and obstructive. Inferior
turbinate hypertrophy may block the nasal cavity and produce difculty breathing.
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