What Are the Different Sacroiliac Symptoms?

Sleep apnea syndrome (SAS) is the second largest sleep disorder after insomnia. It can cause severe hypoxemia and sleep disturbances, as well as high blood pressure, arrhythmia, cardiovascular and cerebrovascular diseases and breathing. The occurrence of diseases such as failure is closely related, and a small number of patients can die suddenly at night. In addition, due to daytime drowsiness, impaired memory and responsiveness, patients' ability to work decreased, and the incidence of accidents increased. Because of this, SAS has become an important part of a new marginal subject-sleep medicine, and it has received increasing attention from medical circles at home and abroad. In recent years, with the wide application of non-invasive ventilation technology, breakthroughs have been made in the treatment of SAS.

Chinese name: Sleep apnea syndrome in the elderly

Foreign name: Sleep apnea syndrome
Department: ENT

Sleep apnea syndrome symptoms and signs in the elderly

The clinical symptoms of SAS patients are complex and varied, and their severity varies. Many patients have no discomfort during the day. In addition to clinical symptoms including those directly related to SA itself, multiple systemic damage caused by SA can also cause corresponding clinical symptoms (Table 4).

The most important clinical symptoms are sleep snoring, frequent apnea and daytime sleepiness. Snoring is one of the most typical symptoms of SAS. The patient's snoring sound is loud and irregular, intermittent, and the sound is high and low, which is called "resuscitative snoring. Frequent sleep apnea phenomenon is often found by the patient's spouse, and the diagnosis accuracy of this phenomenon is more than 90% for moderate to severe patients. Unconsciously falling asleep regardless of time and place during the day is a manifestation of moderate to severe SAS, and it is also one of the main reasons for patients to see a doctor.

Sleep apnea has a wide range of effects on the cardiovascular system. SAS is a risk factor for hypertension independent of factors such as obesity and age, and is an important cause of secondary hypertension. Arrhythmias are very common in patients with SAS and are the main cause of sudden death in such patients. The most common are sinus arrhythmias (including sinus bradycardia, tachycardia, sinoatrial block, and sinus arrest), followed by pre-atrial and ventricular contractions, and first- to second-degree atrioventricular block and Ventricular tachycardia. The prevalence of ischemic heart disease in patients with SAS increases, and with the worsening of SAS, myocardial ischemia is often exacerbated in patients with known or potential ischemic heart disease, and angina, myocardial infarction, malignant arrhythmias or cardiac function Deterioration and other phenomena. Pulmonary arterial hypertension occurs in 10% to 20% of SAS patients, and is more pronounced in patients with chronic obstructive pulmonary disease, even with right heart failure. SA is also an independent risk factor for cerebrovascular disease.

In patients with long-term sleep apnea, shortness of breath during daytime activities may be a manifestation of alveolar hypoventilation. Loss of libido and impotence are not uncommon in men with severe SAS; SA can cause sleep disturbances and reduced growth hormone secretion. This change is particularly pronounced in children and can seriously affect children's growth and development. Near-memory decline, attention, concentration, comprehension, and personality and behavior abnormalities are not uncommon in patients with severe SAS. These all seriously affect patients' work, study and life. In addition to affecting their own health, it will also cause certain harm to families and society due to traffic accidents and industrial injuries.

The incidence of SA in neonates, especially premature infants, is very high. Pathological SA may be related to sudden infant death syndrome (SIDS). The main reasons for children with SAS patients to go to school are sleepiness in class, poor academic performance, agitation, irritability, and abnormal behavior during the day. Snoring, abnormal sleep movements at night, and enuresis are also common. Growth retardation is very prominent in severe children. Insomnia is the main complaint in elderly patients with SAS. The symptoms of SAS are often atypical due to the combination of other diseases.

CSA also causes repeated hypoxia and sleep disturbances, and the pathophysiological changes are the same as OSAS. However, there are fewer people with CASS obesity, snoring, daytime drowsiness and sexual dysfunction are light, insomnia is easy to wake up, and depression may be present.

Treatment of sleep apnea syndrome in the elderly

1. Etiological treatment Hypothyroidism is one of the affirmative causes of SA. SA can often be reduced or disappeared after thyroid hormone replacement therapy. SA is present in half of patients with heart failure, and CSA is the predominant one. CSA can be improved after improved cardiac function with medication.

2. Oxygen therapy for the vast majority of SAS patients. Oxygen therapy is not necessary; those who are indicated by aerobic therapy should also be combined with continuous positive airway pressure to avoid CO2 retention and aggravation of sleep disturbances by simply inhaling oxygen and prolonging the duration of SA.

3. General treatment guides patients to develop good sleeping habits, get enough sleep time and the best sleep quality. Weight loss, smoking cessation, alcohol cessation, cautious use of sedative and sleeping drugs, sleep in the lateral position, and application of nasal mucosal contraction agents to keep the nasal passages open, may be effective for patients with mild or simple snoring.

4. Drug treatment of medroxyprogesterone (anhydroprogesterone) and acetazolamide have respiratory excitement. All have been tried for the treatment of CASS, but due to the poor efficacy and large side effects, they are now rarely used.

5. The application of continuous positive airway pressure (CPAP) for continuous positive airway pressure (CPAP) in the treatment of OSA is to increase the positive pressure in the pharyngeal cavity to counteract negative suction pressure and prevent airway collapse. It was first applied in 1981 and is effective for both OSAS and CASS, and has become the preferred method for treating SAS. Bi-level positive airway pressure ventilator (BiPAP) and intelligent CPAP ventilator, which are more in line with physiological characteristics, have been applied in the clinic. The main problem is to strengthen follow-up and improve patient compliance with long-term use.

6. Mouthpiece treatment mainly includes mandible movement device and tongue fixation device, which is a treatment method for laryngo-pharyngeal stenosis. The former enlarges the upper airway by moving the mandible forward to advance the tongue, and the latter directly pulls the tongue to prevent the root of the tongue from falling back. Can be used for patients with mild to moderate SAS or intolerant to CPAP.

7. Surgical treatment Surgical treatment is mainly based on two purposes: bypass the pharyngeal airway which is prone to obstruction during sleep and establish a second respiratory passage. For different obstruction sites, remove the anatomical stenosis and enlarge the airway. Because of its invasiveness and limited efficacy, except for some patients with surgical indications, young mild patients or those who have failed CPAP treatment, surgical treatment is not the first choice for most patients with OSAS; it is not effective for patients with CASS. The main surgical methods include tracheostomy, uvulopalatopharyngoplasty (UPPP), tonsillitis, adenoidectomy, nasal septum deviation correction, nasal polyp removal, turbinate resection and other nasal surgery and laryngeal surgery. Spharyngeal anatomy such as jaw forward surgery, hyoid suspension, tongue angioplasty.

In short, the surgery for OSA is complex and diverse. Preoperative examinations must be carefully performed, surgical indications must be strictly selected, and multiple surgical staging procedures must be combined if necessary.

Sleep apnea syndrome diet care for the elderly

Diet should be light-based, pay attention to a reasonable diet, balanced nutrition. Change sleep and eating habits: take a sleep in the lateral position, avoid oversuppering at dinner, quit smoking, alcohol, lose weight, and avoid taking sedatives.

Preventive care of sleep apnea syndrome in the elderly

Change sleep and eating habits: take a sleep in the lateral position, avoid oversuppering at dinner, quit smoking, alcohol, lose weight, and avoid taking sedatives.

Pathogenesis of sleep apnea syndrome in the elderly

1. The main cause of obstructive sleep apnea syndrome is upper airway stenosis during sleep. Sullivan et al. Believe that the mechanisms that cause upper airway stenosis are as follows: Due to the anatomical stenosis of the upper airway, muscles relax during sleep, the negative pressure in the chest increases during inhalation, and the base of the tongue is closely attached to the pharynx wall. Airway occlusion; has nothing to do with pleural cavity pressure during inhalation, airway occlusion due to decreased excitability during sleep of upper airway diastolic muscle group; airway occlusion caused by incoordination of upper airway diastolic muscle group; Active upper airway contraction stenosis caused by abnormal reflex. Obese people often have narrow upper airways. In addition, upper airway lesions related to obstructive sleep apnea include abnormalities in the nasal structure, pharyngeal wall hypertrophy, tonsil hypertrophy, acromegaly, giant tongue, congenital malformation of the jaw, and structural abnormalities of the pharynx and throat.

2. Central sleep apnea syndrome is mainly caused by abnormalities in respiratory regulation. The following diseases can occur in respiratory regulation: cerebrovascular accident, neurological disease, anterior amputation of spinal cord, vascular embolism or degenerative disease Causes bilateral spinal cord disease, familial autonomic nerve abnormalities, insulin-related diabetes, and encephalitis. Others include muscle disorders, malformations of the occipital foramen, polio, and congestive heart failure.

Diagnosis of sleep apnea syndrome in the elderly

SAS can affect various systems throughout the body. The clinical manifestations during the day are complex and diverse, lacking specificity, and are easily misdiagnosed as diseases of other systems, such as neurosis and heart disease. The key to avoiding misdiagnosis and missed diagnosis is to strengthen the understanding of sleep disorders. Daytime drowsiness is one of the most prominent symptoms of SAS, and it is also the main cause of patient visits, and it should be identified (Table 5).

Test methods for sleep apnea syndrome in the elderly

Laboratory inspection:

Those who are suspected of inadequate daytime ventilation or dyspnea may perform tests such as blood routine and blood gas analysis.

Other auxiliary checks:

1. Skull X-ray examination can quantitatively understand the degree of abnormalities of the maxillofacial region. Nasopharyngoscopy can help evaluate the degree of abnormalities of the upper airway anatomy. It is helpful to consider surgical treatment. Suspected hypothyroidism can measure thyroid hormone levels. Patients suspected of inadequate daytime ventilation or respiratory failure may perform blood routine, blood gas analysis, and pulmonary function tests. Dynamic electrocardiogram examination found sleep arrhythmia or large fluctuations in heart rate during sleep, often suggesting the possibility of SAS.

2. Sleep breathing monitoring With the help of spouses and family members, by carefully asking about the medical history and systemic examination, we can basically understand the patient's sleep and breathing situation, provide diagnostic clues about SAS, suggest possible causes and complications, and initially determine its severity degree. However, to finally establish or exclude the diagnosis, a polysomnograph (PSG) must be applied to the sleep center for sleep respiration monitoring. The monitoring signals include the following three aspects: Sleep conditions: EEG, eye movement, and genioglossus muscle electromyogram. Respiratory conditions: Oral and nasal airflow, chest and abdominal breathing movements, and dynamic SpO2 monitoring. ECG. If necessary, simultaneous monitoring of ambulatory blood pressure, esophageal pressure, snoring, leg movements and body position changes can be performed simultaneously. In recent years, traditional paper-based records have gradually been replaced by computerized data collection, storage, and analysis systems. Home-based, simple bedside screening devices at the bedside have even been used for remote monitoring via remote central work systems. Because PSG is expensive, and some patients have difficulty falling asleep in different places. SaO2 dynamic monitoring at night can be used as screening.

Sleep apnea syndrome complications in the elderly

Complications such as hypertension, right heart dilatation sign, bradycardia, arrhythmia, erythrocytosis, and sexual dysfunction.

Prognosis of sleep apnea syndrome in the elderly

Due to the severity of the disease and individual differences, there is insufficient data to indicate the untreated progression of SAS. However, reports of cardiac and cerebrovascular complications caused by SAS are increasing, and they are significantly related to the degree of the disease. Kryger has reported 142 patients with SAS. The mortality rate was significantly higher in patients with RDI> 20 than in patients with RDI <20. Effective treatment can improve patients' symptoms and may reduce comorbidities and mortality, but there are insufficient data from prospective studies.

Pathogenesis of sleep apnea syndrome in the elderly

1. Predisposing factors and mechanism of obstructive sleep apnea Sleep apnea is not an independent disease, but a common pathological manifestation of multiple lesions, and its occurrence is the result of a combination of multiple factors (Table 1). A comprehensive understanding of these susceptible factors can help guide further treatment. For example, for some patients with anatomical upper airway stenosis (Table 2), surgical treatment may be effective.

The key to OSA is the collapse of the pharyngeal airway during sleep. The airway obstruction can be in the nasopharynx, oropharynx, or laryngo-pharynx. More than 80% of patients have a combined occlusion of the oropharynx and laryngo-pharynx. The causes of upper airway obstruction include both anatomical abnormalities and functional defects. They all work by increasing the collapsibility of the pharyngeal airway and affecting the contrast of its opening and closing forces (Figure 1).

The pharyngeal airway lacks the support of bony or cartilage structures. It is a soft duct composed of muscles and is collapsible. Due to anatomical and functional defects of the pharyngeal airway in patients with OSA, coupled with the effects of obesity and edema, their collapsibility is further increased. The main force that causes the pharyngeal airway to close is the negative pressure in the pharyngeal airway, which is generated by the contraction movement of the diaphragm and other respiratory muscles during inhalation; the activity of the pharyngeal dilator, mainly the genioglossus, is to counteract the negative pressure in the pharyngeal cavity, The main force to keep the upper airway open. After falling asleep. Respiratory central drive is reduced, pharyngeal dilatation muscle activity is weakened, and upper airway resistance is increased. When the respiratory drive is reduced to a certain level, the negative pressure of the pharyngeal cavity produced by the inspiratory muscles such as the diaphragm muscles prevails. "Critical pressure" (critical pressure), the balance of power to maintain airway opening and closing was broken, the airway collapsed, and OSA appeared. During the occurrence of OSA, blood oxygen gradually decreases, CO2 gradually increases, and the negative pressure in the pharyngeal cavity increases. They all stimulate the corresponding chemical and baroreceptors and excite the brainstem reticulum activation system to cause short-term awakening, airflow recovery, and OSA. End. For example, decreased sensitivity of chemoreceptors, suppression of baroreceptive reflexes, respiratory muscle dysfunction, and drinking, anesthesia, and sedative sleeping pills can cause reduced arousal ability and prolong OSA duration.

2. Causes and mechanisms of central sleep apnea When central sleep apnea occurs, central respiratory drive is temporarily lost, airflow and breathing movements in the thorax and abdomen disappear, and the intrathoracic pressure is zero. The relationship between CSA and respiratory control dysfunction is relatively clear (Table 3).

Cheyne-Stokes respiration and periodic respiration are common types of CSA. They occur in the NREM sleep stage and , and are found in those with cardiac insufficiency and those who first enter the plateau. After falling asleep, the high CO2 reactivity of the respiratory center decreased, that is, the response threshold increased, PaCO2 was not enough to excite breathing, and CSA appeared; with the increase of SA time, PaCO2 gradually increased, and after the reaction threshold was reached again, the patient experienced a short wakefulness Respiration resumes, and the central high CO2 response threshold decreases. Higher PaCO2 levels cause hyperventilation, and PaCO2 drops to lower levels. After falling asleep again, CSA occurred again and again and again and again (Figure 2). It can be seen that the lower the sensitivity of the respiratory center to high CO2 and low oxygen during sleep, that is, the higher the response threshold. The more prone to CSA; the more awakening after falling asleep, the more unstable the respiratory control function is, and the more prone to CSA; during NREM sleep stage and . CSA is prone to occur due to light sleep and prone to awakening; with the deepening of sleep, NREM III and IV sleep periods are entered. The number of awakenings decreased, respiratory regulation stabilized, and the number of CSAs decreased. In the REM sleep period, the random adjustment function still plays a certain role, the dependence of breathing on chemical regulation is reduced, and CSA is also decreasing.

3. Frequent pathophysiology of SA can cause severe blood gas abnormalities and sleep disturbances, which affects various systems throughout the body. In recent years, the autonomic nervous system dysfunction caused by SA has also caused widespread damage to the cardiovascular system (Figure 3).