Obstructive sleep apnea syndrome (OSAS) is one of the common diseases in children, which can cause a series of adverse consequences and has received increasing attention from the society in recent years. OSAS in children refers to a series of pathophysiological changes caused by frequent partial or total upper airway obstruction during sleep, which disrupts normal ventilation and sleep architecture. The literature reports that the prevalence of OSAS in children is about 1% to 3%, and the age of prevalence is 2 to 8 years old, with more males than females.
Etiology
The common causes of OSAS in children include increased upper airway resistance causing compliance changes and affecting neuromodulation, with adenoid hypertrophy and/or tonsillar hypertrophy being the most common causes. Domestic studies have found that among the obstructive causes of snoring and sleep apnea in children.
1. There is a correlation between adenoid hypertrophy and OSAS, and there is a negative correlation between the adenoid A/N ratio and oxygen saturation in the lateral nasopharyngeal slices of children with OSAS, indicating that adenoid hypertrophy obstructs the nasopharyngeal cavity causing upper airway obstruction, which further leads to a decrease in oxygen saturation, the severity of which correlates with the degree of adenoid hypertrophy. Endoscopic examination also reveals that the site of upper airway obstruction in pediatric patients is often at the level of the adenoids.
The tonsillar pharyngeal ratio is also associated with the apnea hypopnea index (AHI).
3. Obesity and overweight are risk factors for OSAS in children.
In addition, any factors that can cause increased upper airway resistance, such as severe allergic rhinitis, chronic sinusitis, craniofacial anomalies and neuromuscular diseases, can also lead to OSAS in children.
Clinical manifestations
The clinical manifestations of OSAS in children are various, mainly snoring, apnea, open-mouth breathing, accompanied by sleep disturbance, nocturia, night terrors, morning headache, dry mouth, as well as abnormal personality and behavior, decreased academic performance, and decreased attention span. Some children may develop adenoidal facies and jaw deformities. In addition, OSAS in children can negatively affect several systems throughout the body and cause related diseases, mainly including the following.
1. effects on growth and development Because children with OSAS hold their breath during sleep and have interrupted sleep, which leads to a reduced sleep state in stages III and IV, it is difficult to achieve normal levels of growth hormone secretion and affects the growth and development of the child [2, 3]. The examination of the physical development of children with OSAS revealed that the weight, height, sitting height and head circumference of the moderate to severe group were lower than those of normal children and correlated with the severity of OSAS. children with OSAS can suffer from mental retardation and memory loss due to long-term chronic hypoxia affecting the development of the central nervous system. However, the long-term effects on children’s growth and development still need to be studied in depth.
2. Effects on the auditory system During sleep apnea, blood flow in the middle cerebral artery slows down significantly, blood rheology changes, whole blood specific viscosity increases, and oxygen saturation decreases. The repeated occurrence of this process can affect the blood and oxygen supply to the hypermetabolic outer hair cells of the cochlea, causing a decrease in inner ear function and delayed excitation transmission in the auditory system, resulting in sensorineural hearing loss. ABR testing in children with severe OSAS revealed prolonged I-wave latency, shortened I-III wave interval, prolonged III-V wave interval, and increased V-wave threshold, reflecting impaired cochlear function [4]. BAEP tests were performed on children with OSAS at different repetition rates of acoustic stimulation of 11.1 Hz and 33.1 Hz, and it was found that low-frequency short acoustic stimulation reflected earlier changes in brainstem function in children with OSAS, and the results of BAEP tests were abnormal in children with severe OSAS, suggesting that OSAS has an effect on both hearing threshold and auditory brainstem conduction function. It has also been reported that otoacoustic emission waveform amplitude and detection rate of aberrant products increase after OSAS, suggesting that long-term OSAS can affect cochlear function. Therefore, early intervention should be performed in children with severe OSAS to avoid impairment of auditory function.
Children with OSAS have a faster fastest heart rate and slower slowest heart rate during sleep and a higher incidence of tachyarrhythmias compared to controls. However, there are some differences in abnormal heart rate and rhythm changes between children with OSAS and adult patients, such as no significant difference in the incidence of slow arrhythmias compared to controls, while adult patients have a significantly higher incidence than controls, suggesting that there may be different pathophysiological mechanisms between children and adults with OSAS. However, there are relatively few studies on this aspect, and more in-depth investigation is needed.
Diagnosis
OSAS in children should be diagnosed based on detailed history taking, careful physical examination, accurate imaging and laboratory tests, and a comprehensive analysis of the results before a correct diagnosis can be made.
If snoring and poor sleep are accompanied by growth retardation, excessive daytime sleepiness or irritability, inattention and poor memory, OSAS is highly suspected.
2. Physical examination Careful physical examination is an important part of the diagnosis of OSAS in children, including comprehensive examination of successive parts, such as asymmetry of nostrils, deviation of nasal septum, hypertrophy of inferior turbinates, nasal collapse during breathing, tonsillar hypertrophy, abnormal craniofacial development, and obesity. Multiple sites of anatomical stenosis have a cumulative effect, and the most important risk factors are tonsillar and adenoid hypertrophy, but all stenoses present in the upper airway are factors that should be considered and must be judged comprehensively.
3. Imaging and laboratory tests Lateral nasopharyngeal plain film A/N ratio determination provides a simple, convenient, economical and practical method of measuring the size and morphology of adenoids in children by X-ray. The vertical distance from the most prominent point of the adenoids to the bony surface of the skull base is the thickness of the adenoids (A), and the distance between the posterior end of the hard palate and the intersection of the pterygoid plate and the skull base is the width of the nasopharynx (N), which is pathologically enlarged if the A/N ratio is ≥0.71. In contrast, fiberoptic nasopharyngoscopy allows observation of the degree of adenoidal blockage of the posterior nasopharynx: blockage of 25% is 1+, 26% to 50% is 2+, 51% to 75% is 3+, and >75% is 4+. As a rule, 3+ with clinical symptoms is diagnosed as adenoid hypertrophy. Polysomnography (PSG) is currently considered the “gold standard” for the diagnosis of sleep disordered breathing disorders and can be performed in children of any age. According to the latest domestic OSAS diagnostic criteria (draft), an obstructive apnea index (OAI) greater than 1 or AHI greater than 5 times/h during the whole night is considered abnormal, and a minimum arterial oxygen saturation of less than 92% is defined as hypoxemia. 10 is mild, 10-20 is moderate and >20 is severe. Pulse transit time (PTT) monitoring is a new non-invasive method of detecting respiratory effort, which refers to the time interval of pulse pressure conduction from the aortic valve to the periphery and is negatively correlated with blood pressure. PTT monitoring of respiration in children has the advantage of helping to determine the type of respiratory event and to infer the magnitude of respiratory effort. Recent studies have shown that the test can be used to infer fluctuations in negative thoracic pressure in children and to determine changes in inspiratory effort.
Treatment
The clinical management of OSAS in children is based on the principles of early diagnosis, early treatment, release of upper airway obstruction, and prevention and treatment of complications.
Since the main cause of OSAS in children is adenoid hypertrophy and/or tonsillar hypertrophy, surgical removal of adenoids and tonsils is the main method of surgical treatment. After surgery, most children can achieve a satisfactory outcome without the need to adhere to age restrictions, thus reducing the occurrence of secondary symptoms [5,6]. Other surgical treatments include craniofacial orthognathic surgery (for children with partial craniofacial anomalies), uvulopalatopharyngoplasty (UPPP), and inferior turbinate reduction, but they may affect the growth and quality of life of children and should be performed with great caution. If accompanied by allergic rhinitis, chronic sinusitis and other diseases, systematic and standardized drug treatment should be continued after surgery.
2.Non-surgical treatment includes continuous positive airway pressure (CPAP) and oral orthoses.
(1) CPAP can be considered for children with OSAS who have contraindications to surgery, sleep apnea even after adenoid tonsillectomy, and those who choose non-surgical treatment. Preoperative application of CPAP in children with severe OSAS can enable them to safely survive the perioperative period. It is worth emphasizing that appropriate CPAP pressure is essential to ensure successful treatment, that pressure titration must be done under PSG guidance, and that regular follow-up and adjustment are required. Due to the rapid craniofacial growth in young children, periodic evaluations should be made especially, and annual examinations by a craniofacial specialist should be performed to confirm that the CPAP mask is not causing abnormal maxillary development.
(2) Oral orthoses are generally indicated for children with mild to moderate OSAS who are inoperable or cannot tolerate CPAP treatment.
(3) Intranasal glucocorticoids have been used for the treatment of children with mild to moderate OSAS and children with sleep apnea even after adenoid tonsillectomy, with short-term effects in most patients, but their long-term effects need to be further observed. At the same time, children with severe OSAS should not rely on hormone therapy, and surgery is still the mainstay. The overuse of glucocorticoids in the treatment of children with OSAS still affects the growth and development of children, and the abuse or unregulated use of hormones is a common phenomenon in non-professional treatment at present.