Obstructive Sleep Apnea (OSA) was first diagnosed in children in 1976 and subsequent studies have found it to be a highly prevalent condition. Obstructive sleep apnea hypopnea syndrome (OSAHS) is a sleep breathing disorder characterized by intermittent partial or complete obstruction of the upper airway during sleep. Chronic sleep apnea and hypoventilation may result in stunted growth, altered cardiac function, conductive deafness, facial deformities, memory loss, decreased intelligence and personality changes in children. Domestic definition of OSAHS in children: Obstructive sleep apnea hypoventilation syndrome in children refers to a series of pathophysiological changes caused by frequent partial or total upper airway obstruction during sleep, which disrupts the normal ventilation and sleep structure of children. I. Pathophysiology Due to the combined effects of soft tissue hypertrophy, maxillofacial deformities, neuromuscular hypofunction and obesity, children with OSAHS have increased upper airway resistance during sleep. However, most children with OSAHS can obtain prolonged stable breathing during sleep, which indicates that there are other factors controlling airway patency, such as: neuromuscular regulation, control of ventilation volume, and alteration of arousal threshold. The sequelae of OSAHS in children: 1. Metabolic sequelae According to early case reports, 27-62% of children with OSAHS fail to thrive. The possible reason for this is the reduced secretion of insulin-like growth factor (IGF) and growth hormone. children with OSAHS have reduced IGF binding protein 3 (IGFBP-3), which is associated with the secretion of growth hormone. Levels of IGF-1 and IGFBP-3 are increased after adenoide and tonsillectomy, along with catch-up weight and height gains in children. Abroad, in recent years, with better understanding of the sequelae of OSAHS, cases of children failing to thrive due to OSAHS are rare, but half of the patients present with obesity. leptin is a peptide secreted by adipocytes, Leptin regulates metabolism, hunger and inflammation, and stimulates ventilation. leptin levels are increased in children with OSAHS, and decreased after CPAP treatment. and decreased after CPAP treatment. Obesity in children is accompanied by metabolic syndrome, i.e., insulin resistance, dyslipidemia, and hypertension. The metabolic syndrome is associated with cardiovascular accidents in adults. Other factors that may influence the expression of the metabolic syndrome include genes, diet, physical activity, and OSAHS. the role of OSAHS in the development of the metabolic syndrome is complex, and in obese children, OSAHS has been independently associated with insulin resistance, dyslipidemia, and dysregulated blood pressure. In contrast, OSAHS does not increase the risk of insulin resistance in lean or morbidly obese children. The combination of obesity and OSAHS may amplify the pro-inflammatory complications in both conditions. 2. Cardiovascular sequelae: Children with OSAHS can develop a range of cardiac diseases from vegetative dysfunction to structural heart disease, and have higher morbidity and mortality than adults. The pathophysiological changes are multifaceted and include autonomic homeostasis, oxidative stress, inflammatory cytokines, vascular remodeling, and vascular endothelial cell dysfunction. children with OSAHS have elevated urinary levels of catecholamines [and increased sympathetic impulses. Importantly, these abnormalities are present in patients with OSAHS regardless of sleep or wakefulness, suggesting that phytodysfunction is widespread. the cardiovascular pathogenesis of OSAHS is influenced by a combination of obesity, genetic susceptibility, and environment. 3. Neuropsychological sequelae Children with OSAHS can have a wide range of neuropsychological dysfunction, including cognition, hyperactivity, sleepiness, memory, executive ability, attention, school performance, and behavior. Even mild OSAHS can produce detrimental neurodevelopmental outcomes.