Definition: Obstructive sleep apnea hypopnea syndromes (OSAHS) refers to a series of pathophysiological changes caused by frequent partial or total obstruction of the upper airway during sleep, which disrupts the normal ventilation and sleep structure of children. Causes: The common causes of OSAHS in children include increased upper airway resistance causing compliance changes and factors affecting neuromodulation. 1. Nose: chronic rhinitis (infectious, allergic), sinusitis, nasal polyps, nasal masses, deviated nasal septum and posterior nasal atresia are the common causes of OSAHS. Nasopharynx and oropharynx: the most common causes are adenoid hypertrophy, tonsillar hypertrophy, and other causes such as hypertrophy of the right lingual body, fat accumulation caused by obesity, pharyngeal and nasopharyngeal masses, and obstruction after cleft palate and palato-pharyngeal flap surgery. Larynx and trachea: congenital laryngeal cartilage softening, laryngeal webbing, laryngeal cyst, laryngotracheal neoplasm and tracheal stenosis. 4. Craniofacial malformations: middle facial developmental defects (Down syndrome, Grouzon syndrome, chondrodysplasia, etc.); mandibular developmental defects, such as Pierre-robin syndrome, mandibular facial hypoplasia, and shy-Drager syndrome. Others, such as mucopolysaccharidosis type II and type IH (Hunter syndrome and Hurler syndrome), and metabolic diseases (e.g., osteosclerosis) are associated with abnormalities of the craniofacial structure. Factors affecting neuromodulation: generalized hypotonia (Down’s syndrome, neuromuscular diseases), application of sedative drugs, and so on. Clinical manifestations and complications of OSAHS in children: snoring, open-mouth breathing, breath-holding, repeated awakenings, enuresis, excessive sweating, hyperactivity, etc. Occasionally, daytime sleepiness may occur. Prolonged open-mouth breathing can lead to obvious maxillofacial developmental deformities, the formation of “adenoidal facies”, cognitive deficits, memory loss, learning difficulties, behavioral abnormalities, growth retardation, hypertension, pulmonary hypertension, right heart failure and other cardiovascular diseases in severe cases. Diagnosis and differential diagnosis 1. Obstructive sleep apnea (OSA) refers to the cessation of oral and nasal airflow during sleep, but thoracic and abdominal respiration still exists. Hypopnea is defined as a 50% reduction in peak oro-nasal airflow signal with a decrease in oxygen saturation of more than 0.03% and/or arousal. The duration of the respiratory event was defined as greater than or equal to 2 respiratory cycles. Polysomnogruphy (PSG) monitoring: Obstructive apnea index (OAI) greater than or equal to 1 time/h or AHI (Apnea Hypopnea Index) greater than 5 during each night of sleep is considered abnormal. Lowest oxygen saturation (LAaO2) below 0, 92 is defined as hypoxemia. OSAHS can be diagnosed by meeting the above two criteria. 2. Diagnostic methods: Nighttime PSG examination is the current standard method for diagnosing sleep apnea, and can be performed on children of any age. Children who do not have the conditions for PSG can refer to medical history, physical examination, lateral nasopharyngeal X-ray, nasopharyngeal endoscopy, snoring sound recording, video recording, pulse oximetry and other means to assist in the diagnosis. Nasopharyngeal X-ray or CT is helpful in determining the site of airway obstruction, and nasopharyngeal endoscopy allows dynamic visualization of upper airway narrowing. The purpose of PSG examination is to: (1) distinguish simple snoring from OSAHS; (2) determine the diagnosis of OSAHS; (3) evaluate the severity of OSAHS; (4) assess the effect of surgery; (5) distinguish central apnea and alveolar hypoventilation; (6) assess the structure of sleep and non-apnea-related sleep disorders (e.g., nocturnal epileptic seizure, etc.). Differential diagnosis should be differentiated from simple snoring, central sleep apnea and hypoventilation syndrome, epileptic sleep disorder, laryngospasm, epilepsy, etc. V. Principles of treatment: early diagnosis and treatment of epilepsy. Treatment principle: early diagnosis, early treatment, relief of upper airway obstruction factors, prevention and treatment of complications. Treatment principles: (i) surgical treatment 1, adenoidectomy and tonsillectomy: tonsils, adenoid hypertrophy caused by OSAHS children can be adenoid, tonsillectomy. When both tonsils and adenoids are enlarged, simple adenoid or simple tonsillectomy has limited efficacy. Most obese children can be effectively treated with adenoid and tonsillectomy. Surgical removal of tonsils and adenoids in infants and young children with severe OSAHS is also indicated when conservative treatment fails. Children younger than 3 years of age with severe OSAHS, pulmonary heart disease, malnutrition, pathologic obesity, neuromuscular tumors, and craniofacial anomalies are at high risk for postoperative complications. In this regard, detailed evaluation should be performed before surgery and close monitoring should be performed after surgery. 2. Other surgical treatments include: craniofacial orthognathic surgery (for children with some craniofacial developmental anomalies), uvulopalatopharyngoplasty, inferior turbinate reduction, tracheotomy, and other treatments that may affect children’s growth and development and their quality of life, so they should be treated with great care. (ii) Non-surgical treatment 1, continuous positive airway pressure (CPAP): For children with contraindications to surgery, large adenoid tonsils, OSAHS after adenoid tonsillectomy, and those who choose non-surgical treatments, CPAP can be chosen. Pressure titration for CPAP must be done in a sleep laboratory and requires periodic adjustment. 2. Oral appliances: For children with mild to moderate OSAHS who are either surgical or cannot tolerate CPAP. Other treatments: ① Treatment of nasal diseases: rhinitis, allergic rhinitis and sinusitis should be treated in a systematic and standardized way; ② Obese children should lose weight.