Thanks to computers that make it easier and quicker interpretation of sleep recordings, a real boom was given to screening for obstructive sleep apnea (OSA), its treatment and clinical research. OSAS is now considered the most common cause of daytime sleepiness, especially at the wheel of a vehicle, making it a major public health problem.
The decree law issued May 7, 1997 prohibits driving to individuals with sleep pathology.
SLEEP AND MECHANISM OSA:
OSA is currently challenge by repetition of complete obstruction (apnea) or incomplete (hypopnea) of the pharynx.Upon falling asleep, pharynx muscle, the tone is reduced by sleep, literally “sucked” into the airways as a result of the negative intrathoracic pressure and block like a foreign body. Breathing stops, this is an “apnea”, or it is very small, then it is a hypopnea. The brain sends, sooner or later, the order to the muscles of the chest and abdomen to contract to increase thoracic pressure and remove the obstacle.
This causes a muscle contraction “microéveil” (a brief awakening lasting about one second) that awakens the patient not completely, but prevents progression to deep sleep stages. The patient falls asleep, the same phenomenon occurs: aspiration of muscles, blocking breathing and microéveil. This results in a fragmented sleep, disorganized and shallow.
Normal sleep is divided into 4 to 6 cycles of 60 to 90 minutes, with, in order, stages 1 and 2, lighter stages of sleep and stages 3 and 4, deep stages of sleep and sleep dream, called REM sleep.
After REM sleep, a new cycle begins with stages 1 and 2, etc. OSA, which causes microéveils, deconstructs the architecture of sleep, alters its continuity and reduces the abundance of deep stages and REM sleep. In severe cases, there is only a succession of stages 1 and 2 and microéveils, deep and REM sleep stages have entirely disappeared.
This sleep, which is not recuperator, has even become dangerous because at each apnea, hypoxia occurs. To make matters worse, the end of an apnea is associated with stress response (catecholamine secretion), which in turn causes heart rhythm and blood pressure. In OSA, the pharyngeal muscles are subjected to both constant and local efforts to a central control disrupted by hypoxia and drowsiness.
Their dynamics and histological structure are changed. Spontaneously, OSA, non-reversible, can only worsen.
EPIDEMIOLOGY OSA:
The best epidemiological study was conducted in the US among a healthy population of state employees in Wisconsin, aged 30 to 60 years: a mild OSA (apnea index <5 / hour) was present in 1 in 5 adults and a moderately severe OSA (apnea index> 15 / hour) with 1 adult in 15. the study also showed that the diagnosis of OSAS is still very underestimated and that among the sleepy patients, 93% of women and 82% of men had not been recognized.
The existence of a congenital maxillofacial anatomical abnormality or acquired, male gender and age are clearly identified risk factors for the development of snoring and OSA. But in most epidemiological studies, obesity remains the surest predictor.
Certain conditions favor the occurrence of apnea in women: truncal morbid obesity, pregnancy and menopause. The fat distribution plays a role, truncal obesity causing more apneas that obesity gynécoïdes. These women represent approximately 12% of the total population apneic. During pregnancy, snoring sets in, especially during the last three months.
Weight gain, hormonal changes, nasal congestion and pharyngeal edema can explain these respiratory changes.
In pregnant women, snoring appears to be a risk, independent of the weight, age and smoking, of developing hypertension and preeclampsia. After menopause, sleep becomes disorganized, insomnia is very common. Snoring and OSA are also more frequent and favor the appearance of hypertension. Age, hormonal changes, weight gain and the use of anti-anxiety drugs, hypnotics or antidepressants are factors causing respiratory sleep abnormalities in postmenopausal women. In this group, the prevalence of OSA is estimated to be at least 2.5%.
In men as in women, OSA is sometimes secondary to hypothyroidism which causes infiltration of the soft tissues of the oropharynx and macroglossia. When diagnosing OSA, it is advisable to request a TSH. In our patient population, 6% of them suffered from hypothyroidism that had not been recognized. However, studies show that the prevalence of hypothyroidism in the apneic woman is comparable to that of women of the same age non-apneic, that is to say, about 5.9%. Acromegaly is conventionally associated with OSA because it causes, among other things, macroglossia and a change in the oropharyngeal structure. Surgery for pituitary adenoma responsible does not always improve OSA, suggesting that certain structural or biochemical abnormalities due to acromegaly and officials of OSAS are not reversible.
Idiopathic OSA is considered a complex genetic disease. The study of families in several countries has shown familial aggregation index of apnea hypopnea and clinical symptoms in adults and children.
Genetic factors are associated some phenotypic markers already mentioned such as abnormalities of the upper airway, ventilatory control disorders and obesity. The genetics of OSA appears influenced by ethnicity. In Caucasian families have been identified genetic linkage map of common human genome OSA and obesity.
A pathophysiological continuum between snoring and OSA increasing severity is an attractive hypothesis: after 10 years of snoring, the structure of oropharyngeal muscles is altered, making them both larger and easier to be collapsed.
DIAGNOSTIC:
Clinic:
The diagnosis is suggested by two major symptoms, snoring and sleepiness.
Nocturia and nocturnal breathing pauses described by the spouse are both signs of serious call. The other most common symptoms are obesity android, morning headaches and nocturnal hypertension. The diagnosis must also be considered in a depressive snorer, in a chronic Headache, in an uncontrollable hypertension, in a nycturique, and in a patient of a unknown origin polycythemia. No clinical examination allows for the diagnosis of OSA. Only polygraphy and polysomnography may evaluate the breathing of a sleeper.
Ventilatory polygraphy:
This exam is offered as first line to any patient suspected of suffering from OSAS.
It includes the recording of snoring and respiratory parameters (airflow, oxygen saturation, chest and abdominal movements, position and heart rate).
It allows to decide between simple snorers (snoring without oxygen desaturation less than 10 apneas or hypopneas per hour) severe sleep apnea (more than 30 apneas per hour that result in significant desaturation cyclical oxyhemoglobin). In 80% of cases, this examination is sufficient to initiate therapy.
Polysomnography:
This review, more complete, which usually requires hospitalization, is performed when the number of apneas recorded on the polygraph is intermediate between 10 and 30 apneas per hour. Polysomnography includes the parameters of ventilatory polygraphy and sleep parameters (electroencephalography, electrooculography, electromyography).
Since it shows the quality of sleep, it helps to answer the following questions: Does the patient sleep? He was sleeping normally organized and there were repeated awakenings? Fragmentation by microéveils? A nocturnal restlessness?The index of apnea, desaturation of hemoglobin oxygen and sleep architecture disruption are the three factors that will allow choosing a treatment.
COMPLICATIONS OF OSA:
Neurological complications:
Drowsiness:
Drowsiness, that is to say, the occurrence of unintended and inappropriate sleepiness is the first symptom of OSAS in a snorer. He is neither tired nor lack of energy, these complaints occur independently. The sleepiness during the day or have no recovery irrepressible character. Drowsiness is assessed by questioning the patient or, more formally but always subjectively, making him complete analog scales (Karolinska, Stanford, etc.) or more circumstantial in which the soporific power of each situation is directly involved, such as Epworth scale, for example. This has the merit of allowing a form of “weighting” of sleepiness, more acceptable if sleep occurs in passive and monotonous circumstances (long travel in public transport, for example) that during a more challenging situation like a discussion with a friend.
Even the Epworth scale is not infallible and its usefulness depends much on the honesty and the patient’s motivation.There are other more objective tests, such as multiple sleep latency and wake keeping, well codified and valid results, but they are heavier and expensive. Pupillometry based on the observation that an intact vigilance comes with a dilated pupil and stable, while a decrease of vigilance leads to a small and unstable pupil. It was tested in aerospace and driving, but its value is uncertain for screening drowsiness, since many drug and medical terms also alter the pupil diameter.
Neuropsychological disorders:
Poor memory, psychomotor retardation, decreased attention unrelated drowsiness occur in all untreated patients. This deterioration, type subcortical, is characterized by an executive cognitive dysfunction of frontal-type (psychomotor retardation for spots requiring programming in time and space, adaptation to change and set a constructive skill). The psychometric tests show a wide dispersion of data and in particular the absence of linear correlation with the index of apnea, desaturations oxyhémoglobinées night and sleep fragmentation.
Personality also changes and the scores of the patients are very high for the items “obsessive compulsive” and “depression-paranoia”.
The depressive trait is extremely common in most apneic patients. This is not a true depression but a “depression” characterized by a lack of motivation, taste for novelty and an overall disinterest. The libido is often diminished.
It is impossible to say with certainty whether the intellectual disorders and personality changes are due to sleep fragmentation or nocturnal hypoxemia. It seems however that sleepiness is responsible for a deficit of attention and memory while the nocturnal hypoxemia would account for the slowdown of the executive processes.
These disorders do not always disappear with treatment of OSAS.
Headache and pain:
Headache sleep apnea syndrome are common, but are characteristics or by their intensity or their location or duration.Morning headaches are generally holocrâniennes and constrictive. They disappear around 11 hours. They are due to changes in blood pressure associated with apnea, to cerebral vasodilation induced by hypoxia, the direct effect of hypoxia on brain parenchyma. They are sometimes charged to major neck movements that accompany respiratory recovery at the end of apnea.
Nocturnal headache, migraine, cluster headache, non-specific thoracic pain, are more marked than sleep architecture is disturbed.
In almost 100% of cases of significant OSA, there are headaches upon waking or night, and in 55% of cases of nocturnal headaches a sleep disorder can be illustrated by polysomnography.
The sleep disturbance is manifested by an increase in the amount of light sleep, which promotes the sensation of pain.
Pain is itself a source of disintegration of sleep. There would therefore reciprocal relationship between sleep quality and pain.
Epilepsy:
Epilepsy and OSA are rarely associated. However, in a well-controlled epilepsy, recurrence of seizures, weight gain and the notion of snoring suggest the possible occurrence of OSAS. Sleep, fragmented, induces chronic sleep deprivation promotes crises.
Hemodynamic disorders and stroke:
Several studies in apneic subjects retrospectively selected in prospective cohorts strongly suggests that OSA is associated with excess mortality, mainly cardiovascular. He et al, after analyzing the survival of the population of patients followed Henry Ford Hospital (Detroit, USA) between 1978 and 1986, reported a higher mortality in the most severe patients. The average probability of survival at 8 years was 96% when the initial apnea index was less than 20 per hour and 63% when the index exceeded 20, mortality is mainly due to acute cardiovascular accidents.
None of the patients effectively treated by tracheotomy or positive airway pressure (CPAP) has died during this period.
High blood pressure (hypertension):
Over 50% of apneic patients are hypertensive.
Epidemiological studies have established a “dose-response” between the severity of OSA and risk of developing hypertension four years later. This has been demonstrated in the general population by controlling all other known risk factors. The factors involved in the genesis of the HTA are transient hypoxia and microéveil accompanying each apnea.
However, treatment with CPAP does not systematically cause frank decrease in blood pressure and does not even allow, in most cases, reduce the number of antihypertensive drugs.
Arrhythmia:
The arrhythmia occurs in 18% of cases of OSA and it is only nocturnal rule. Stimulation of the sympathetic and parasympathetic systems causes atrial and ventricular premature beats. The QT interval is growing significantly during the apneas to shorten abruptly when ventilatory recovery.
These repolarization abnormalities may favor the occurrence of arrhythmia. Sudden death from arrhythmia, however, is exceptional. Atrial fibrillation is often associated with OSAS: 49% of patients with atrial fibrillation also suffer from OSA.
CPAP suppresses nocturnal arrhythmias in most patients.
Left heart failure:
The prevalence of OSA in patients who suffer from severe heart failure is 31%. In congestive heart failure, sleep apnea syndrome can be obstructive or central. OSA in heart failure does not offer clinical and polysomnographic features. The central apnea is from 30 to 50% of apnea syndromes and heart failure often takes up very particular aspect of periodic ventilation Cheyne-Stokes. Exacerbated sympathetic stimulation causes an increase in the afterload of the left ventricle and the acceleration of the heart rate, which causes an increase in the myocardial oxygen consumption. This increased oxygen need arises when it is less available due to hypoxemia induced apnea.
Treatment with CPAP improves left ventricular function by removing apnea and nocturnal hypoxia for both syndromes Obstructive sleep apnea that plants at the cost of a decrease in venous return and cardiac output.
This result, however, an overall improvement in exercise tolerance.
CHD:
A significant association between OSAS and myocardial ischemia has been demonstrated in particular by studying twins. There is also a significant association between OSA and angina.
Stroke:
The Stroke is a rare complication that previous and the frequency of which is difficult to estimate (about 7% of apneic patients may make a stroke). That studies are prospective or retrospective, the share of the OSA in the occurrence of stroke is always biased and questionable. Indeed, patients with OSA already have many risk factors to stroke (hypertension, diabetes, obesity, smoking, hyperlipidemia).
Some studies estimate it as an independent risk factor around 2.3. Conversely, 70% of patients with cerebral infarction suffer from OSA, and 30% have an apnea index of more than 40 per hour. Some cases of transient ischemic cured by ventilation CPAP make it even more likely the relationship between cerebral infarction and OSA. Brain MRI and cervical doppler does not show more lesions in a population of the same age not apneic.
Hemodynamic disturbances seem kind of an altered endothelium and are mainly localized in subcortical.
Finally at night, especially during REM sleep, so that cerebral metabolism is increased, hypoxemia is maximum, apneas are very long, the vasodilation is maximum, the brain therefore receives a desaturated blood under low pressure. Thrombosis and / or a low rate cause cerebral infarction. The patient wakes hemiplegic.
Disturbances of the genitourinary system:
The nocturia is a highly suggestive symptom of OSA in patients who do not suffer from prostate disorders.Inappropriate secretion of atrial natriuretic peptide, linked to an identified mechanical phenomenon, right atrial dilatation during apneas, appears to be responsible for everything as it is edema of the face and frequent lower limbs in patients with severe sleep apnea. Treatment with CPAP immediately remove these symptoms. Bedwetting is a very rare symptom of OSAS in.
In contrast, 20% of patients with OSA complain of impotence and 50% of men presenting with organic impotence suffer from OSA. This means that the association between the two diseases is greater. When sleep is very disturbed, pituitary hormones do not follow the usual patterns of production. There is a selective decrease in testosterone and bound protein sex hormone binding globulin (SHBG).
Three months after treatment with positive airway pressure, there occurs an increase of testosterone and SHBG. In sleep apnea syndrome, hormonal production of pituitary origin is probably affected by nocturnal hypoxia.
Another factor that could explain the decline of certain hormones extreme obesity is affecting some patients and which also leads to lower levels of testosterone and SHBG. The bond that united the two diseases is more complex than just hormonal imbalance: the apneic patient is hypertensive, high cholesterol, diabetes, heart. Arteritis of the dorsal artery of the penis or diabetic neuropathy can cause impotence.
Finally, fatigue, drowsiness and chronic depression contribute to maintaining impotence that does not always disappears after treatment with CPAP.
Endocrine:
Lack of sleep alters many hormonal cycles related to the sleep-wake rhythm.
Prolactin, responsible for libido and fertility, TSH, the renin angiotensin aldosterone system, growth hormone, sex hormones, and many others, have weathered to a varying degree, by OSA, resulting in inappropriate responses.
chronic fatigue, hot flashes, urinary frequency and nocturia are common.
Changes in growth hormone levels are likely responsible, at least in part, to the difficulty diet of these patients. In patients with diabetes non-insulin dependent, SOAS prevalence is about 18% and hyperinsulinemia is exacerbated regardless of body mass.
Leptin produced by adipocytes controls appetite, energy expenditure and acts as a regulatory signal in fat mass by acting on receptors in hypothalamic nuclei.
Leptin acts on endothelial cells and smooth muscle cells of the vessels and causes an alteration of the arterial distensibility. In OSA, there is a close correlation between plasma leptin and apnea hypopnea index.
The hyperleptinemia decreases during the start of CPAP.
Digestive system:
Patients complain of nocturnal acid regurgitation. The thoracoabdominal efforts exerted to keep the airway open cause functional hiatal hernia.
The stomach is drawn into the thoracic cavity.
On the other hand, nocturnal hypoxemia impairs the gastric mucosa which causes hypersecretion of hydrochloric acid.
Acid regurgitation disappear from the first night of treatment with CPAP.
Ocular complications:
An ischemic optic neuropathy, manifested by a defi cit of the nasal visual field and in some cases the paracentral visual field was observed in some apneic patients. The ratio between the Druze and OSAS remains mysterious.
Some patients with drusen of the optic nerve (hyaline body of the Bruch membrane of the retina) and with severe OSA had their visual field significantly improved by CPAP.
114 patients evaluated for OSA, 3 had primary open-angle glaucoma and 2 a normal-tension glaucoma. This percentage of glaucoma patients (7.2%) is significantly higher than the general population (2%), which could make OSAS a major risk factor for developing glaucoma.
The authors OSAS alters the vascularization of the papilla by altering its self or reducing oxygenation. The floppyeyelid syndrom e should suggest OSA. It usually occurs in middle-aged men and associated chronic papillary conjunctivitis with unilateral or bilateral laxity of the upper eyelid, which is easily everted. During sleep, eversion of the upper eyelid is constant.
ENT complications:
Several studies concern audiogram and auditory evoked potentials (AEP) apneic patients. The results are disparate.
Some note of “hearing holes” on the audiogram to the frequency of ronfl ement. Other highlight abuses endocochléaires.
Some of the signs pointing to a breach of the upper brainstem.
Blood changes:
The increased sympathetic tone that causes platelet activation. There is also an increase in circulating fibrinogen levels, hematocrit, blood viscosity and reduced fibrinolysis.
All these changes are reversible under CPAP.
In apneic, there is a disturbance of the immune system, secondary to sleep fragmentation, lack of deep sleep, hyperactivity of the autonomic nervous system and nocturnal hypoxia. The rate of C-reactive protein, interleukin 6, CD4 + lymphocytes and CD4 + / CD8 + cells are increased.
One night of CPAP therapy normalizes all these parameters.
Miscellaneous:
In the elderly, the OSA can manifest as insomnia. Apnea are obstructive and / or plants, they fragment sleep and cause prolonged awakenings.
The diagnosis of OSA was not necessary immediately, because there is no daytime sleepiness in this population group, but a significant fatigue and depression. The alarm clock in the morning of vertigo are another relatively common symptom. These are dizziness attributed to many neck movements qu’effectuent apneic when they catch their breath. Cervicobrachialgies of rarer probably have the same origin.
Many patients complain of tinnitus.
In some cases, these tinnitus disappeared under CPAP, suggesting that they are dependent on the OSA or associated vascular disturbances.
Some patients without heart or respiratory disease, told us to breathe much better during the day, since they were under CPAP. OSA provoked in them a kind of “trouble breathing deeply” during the day.
TREATMENT:
Lifestyle changes:
Removal of the alcohol and hypnotics at least two hours before bedtime must be routinely recommended. Excess weight is supported, if possible. In most cases, these measures are insufficient and must be associated with a more targeted treatment.
Positional treatment:
When polysomnography showed a net positional factor, usually a predominance of apneas and hypopneas supine, positional treatment can be offered (tennis balls inserted in several pockets sewn into the pajama top, for example).The effectiveness of this treatment must be confirmed by a new polysomnography.
Positive pressure ventilation continues nasally (CPAP):
Introduced in 1981 by C. Sullivan, CPAP is now the standard treatment for OSA.
His constant efficacy, safety, simplicity of its manual explains its success. The level of continuous positive airway pressure must be determined during polysomnography because CPAP to be effective in all stages of sleep, including REM sleep and in all positions, including supine. A threshold of 30 apneas and hypopneas per hour was adopted for the management of treatment by health insurance is accepted. This arbitrary limit gives rise to discussion, some patients being objectively sleepy with an index of less apnea. The inclusion in the index of microéveils (the number of microéveils per hour) therefore also involved in the assessment of disease severity. Today, more than 20 000 patients are treated in France and the pace of limitations is about 5000 per year.
Despite its binding, the extreme effectiveness of this treatment promotes a remarkable compliance (more than 5 hours per night to more than 70% of patients). Excessive daytime sleepiness is fine in a fortnight. The number of traffic accidents and domestic life is significantly reduced.
If significant complications are rare, reported in the literature in each case (pneumoencéphalie, intracranial hypertension, etc.), side effects, however, are not rare. Furthermore claustrophobia felt by some patients and skin irritations due to pressure by the mask, dry mucous membranes, epistaxis, rhinitis occur in almost one in two patients.They are related to the dry air from the flow and the mouth leaks associated generator.
The addition of a heated humidifier to the circuit allows in most cases to compensate for these discomforts.
Approximately 8% of patients remain under CPAP drowsy and must look for other causes drowsiness. Yet it remains about 2% of cases where no explanation is found: this is a residual sleepiness in CPAP that can be treated by stimulating alertness.
However, even if the treatment is effective, once rid of their sleepiness, 50% of patients prefer to stop it. It must then offer them another treatment.
Mandibular advancement device:
This treatment is indicated in case of failure or refusal of CPAP. Its principle is to enlarge the oropharyngeal airway and retro basilinguale propelling the mandible, soft palate and tongue. This is a denture, night port. Only individually prostheses made by dentists or chirurgiensdentistes are effective.
Broadly, there are two types of dentures: mandibular protrusion bi block orthotics and orthotic piece may be associated with a language scavenger.
Titration of the prosthesis to judge its effectiveness is performed initially on the disappearance of clinical symptoms especially snoring, then a second time with a ventilatory polygraphy testing.
Several settings of the prosthesis are often necessary before observing maximum efficiency. Indications are reserved mainly to moderate OSA and means. Orthotics can however be effective for severe OSA except in cases of major obesity.
The against-indications related to local problems such as a significant loss of teeth or periodontal problems, and poor Oral Hygiene. The choice of the prosthesis is performed in accordance cephalometric analyzes to clearly identify the position of the jaws relative to the base of the skull. The effectiveness of this treatment is of the order of 80% but its compliance to more than a year is less than 50%.
Surgical treatment:
Young patients who have failed CPAP and dental orthotics are the best candidates for surgery. The principle of surgical treatment is to correct anatomical abnormalities found in the OSA, so as to restore a better permeability of the upper airway.
The site of the obstruction can be single or multiple, whether a bike tonsillar hypertrophy, a macroglossia or digging position mandibular and / or maxillary.
Determining Site obstructive employs many methods, but none is completely reliable. Endoscopy and imaging lateral cephalometric radiograph for cephalometric analysis are most frequently performed.
Several surgical techniques are possible: uvulo palato pharyngoplasty with tonsillectomy is reserved for the patient with major tonsillar hypertrophy bike.
ANAES recommended in 1999 not book this intervention than patients with moderate sleep apnea syndrome (Apnea Hypopnea Index / Time: IAH / H <30) without retrusion maxillomandibular majeure on cephalometric analysis .
The surgery of the soft palate can be performed as an outpatient laser or radio frequency but is still reserved for the moderate sleep apnea syndrome.
Interventions to antérioriser inserts language by transposing the mastoid genius, hyoid suspension, give inconsistent results. The Advanced maxillomandibular surgery is a heavy gesture but crowned with a rate of very important and lasting success in time.
Finally, the tongue reduction surgery may also be helpful for some patients with macroglossia without maxillomandibular retrusion.
The bimaxillary or lingual surgeries are reserved for severe sleep apnea syndrome in check CPAP or dental brace.The cons-indications are related to the age and general condition.
Beside these surgeries, other procedures can be associated:
– Nasal surgery aims to reperméabiliser airway nasorhinopharyngée by septoplasty or turbinate associated. It is often associated with other surgeries but can be practiced in isolation before putting the CPAP or dental brace;
– The obesity surgery (gastric banding or bypass) may be an effective treatment of OSA through the treatment of obesity.
Being evaluated treatments:
Many surgical research is envisaged for the treatment of sleep apnea syndrome:
– Lingual stimulation transcutaneous stimulation or simulator located on the hypoglossal nerve, seeks a lingual protraction at the time of apnea;
– Mandibular distraction. After making simple sections, cortical bone of the maxilla or mandible, a device is set up, allowing a gradual Advanced jaw until correction of obstructive respiratory abnormalities;
– Radiofrequency is a minimally invasive, instrumental and non-surgical treatment, resulting in a volume reduction effect. The radio frequency may be performed at nasal level, tonsillar bicycle, basilingual, in single site or multi-site processing. The results are still being evaluated, especially for severe sleep apnea syndrome.
CONCLUSION:
OSA is a common disease, which concerns 4-6% of adults between 30 and 60 years. The two main clinical signs are the night snoring and daytime sleepiness or an equivalent such as non-restorative sleep sensation or morning asthenia.
This syndrome is responsible for hypertension and is an independent risk factor for cardiovascular disease.Spontaneously, OSA is only getting worse.
All facets of OSAS, highly multidisciplinary disease, are subject to dramatic developments and generate an important research activity persists because a considerable proportion of clinical and epidemiological unknown in this disease.