In 1942, Jackson first described a group of clinicopathophysiological phenomena of inward collapse of supraglottic tissue during inspiration, and proposed the name laryngomalacia. More than half a century of research has gradually revealed the clinical features of this group of diseases and their possible pathophysiological mechanisms and etiologies. It is a common disease in infants and children, occasionally in older children or in late-onset laryngomalacia, due to dysfunction of the laryngeal muscle tissue, which accounts for about 50%-75% of congenital malformations of the larynx. The pathogenesis is probably due to immaturity and softening of the laryngeal cartilage leading to airway obstruction caused by collapse of the soft tissues in the upper part of the voice box into the larynx during inspiration. Pathophysiology In recent years, there have been many new developments in pathology and physiology, and literature reports have shown that anatomic morphology, innervation and function, and inflammatory factors are all closely related to the formation of laryngeal tenderness. Anatomical factors The following anatomical abnormalities are important factors: inward collapse of the arytenoid fold and enlargement of the cuneiform cartilage; softened or overgrown tubular adductor structures; forward and inward collapse of the arytenoid cartilage; posterior contact of the adductor with the posterior pharyngeal wall or inward collapse of the adductor with the vocal cords during inspiration; short arytenoid folds and forward collapse of the cuneiform and microangular cartilage. Neuromuscular factors Neuromuscular insufficiency or deficiency is another possible core pathophysiological mechanism. Coordinated movement of the caudate-pharyngeal, palatopharyngeal, hyoid-lingual, and bicuspid muscles serves to dilate the supraglottic structures. Hypotonia secondary to neuromuscular dysfunction leads to laryngeal stridor and varying degrees of airway obstruction and dyspnea. Inflammatory factors The literature mentions that gastroesophageal reflux is closely related to laryngeal flaccidity. Increased negative thoracic pressure during inspiration due to inward collapse of the supraglottic structures increases the reflux of gastric contents into the esophagus, while increasing the edema of the posterior wall of the supraglottic structures and secondary to laryngeal tenderness. This phenomenon may be an explanation for why newborns are born without symptoms of laryngeal tenderness. These edematous mucous membranes collapse into the vocal fold during the reaspiratory phase, but the causality is difficult to determine. The conventional view is that laryngeal cartilage immaturity causes the tendency of softening to collapse inward during inspiration; however, this hypothesis cannot explain the absence of an increased incidence of laryngeal tenderness in preterm infants. Also, evidence of critical histological abnormalities is lacking. Symptoms Laryngeal tenderness is the most common cause of laryngeal stridor in infants and children. It presents as an intermittent, low-pitched, inspiratory laryngeal wheeze that worsens with forceful inspiration. It is secondary to vibration of the tissues surrounding the epiglottic folds of the vocal cords. It is the most common congenital malformation of the larynx. The incidence is 2:1 in males and females, with onset a few days to a few weeks after birth, most commonly at 2 weeks after birth, with the most severe symptoms at 6 months of age, followed by stabilization and gradual remission, and disappearance of symptoms at 18 to 24 months of age. The laryngeal stridor is aggravated by crying, eating and supine position. Moderate to severe cases may be associated with feeding difficulties, gastroesophageal reflux, growth arrest, cyanosis, intermittent complete obstruction or heart failure, and in very severe cases, death by asphyxiation. Treatment: The prognosis of the disease is good in most cases, and most cases recover spontaneously without any treatment. Postural adjustments in the pediatric population are of great value for recovery from the disease; supination and agitation can worsen symptoms. Also, avoid or reduce the occurrence of gastroesophageal reflux and treat primary or secondary GERD with medications if necessary. Surgical treatment Surgical treatment techniques have seen tremendous advances in recent years, with traditional tracheotomy being the only effective means until the 1980s until spontaneous healing. It is now used only in very severe cases and only in the presence of severe life-threatening symptoms of airway obstruction. Newer surgical techniques and approaches are more numerous, with Lane et al. first describing the treatment of the disease by removing excess obstructive tissue from the posterior part of the supraglottis, using a cupped microscope and scissors. Epiglottoplasty (epiglottoplasty) was later described by Zalzal et al. The problem of inspiratory invagination of the supraglottic tissue was solved by trimming the excess mucosa of the epiglottic rim, aryepiglottic fold, aryepiglottic cartilage and cuneiform cartilage and called epiglottoplasty. roger et al. reported the results of a retrospective study of 115 cases of aryepiglottoplasty with a success rate of 98%, only 2 cases of surgical failure were remedied by tracheotomy and 7 cases were reoperated. the results of a clinical study by Olney et al. suggest that direct laryngoscopy and tracheoscopy should not be performed as part of the routine examination for laryngeal tenderness, but only when clinical and physical examination reveals the presence of a compound lesion of the airway. The mean time to resolution of laryngeal stridor in simple laryngeal tenderness is 36 weeks, and by 72 weeks 75% of infants and children have resolution of laryngeal stridor. The results of unilateral versus bilateral supraglottoplasty were evaluated by Reddy et al. In a retrospective study of 106 cases, 59 bilateral supraglottoplasties and 47 unilateral supraglottoplasties were performed. 96% had significant clinical relief, 15% of unilateral supraglottoplasties required contralateral surgery, 3% had supraglottic stenosis with bilateral supraglottoplasties, and unilateral supraglottoplasties did not have supraglottic stenosis. The supraglottic stenosis did not occur with unilateral supraglottoplasty. There is no unified name for supraglottoplasty technique for laryngeal tenderness, and common names such as supraglottoplasty, epiglottoplasty, aryepiglottoplasty, aryepiglotticfold division, and epiglottic fusion (epiglottopexy) are used. epiglottopexy), etc. For the nomenclature of this disease, a combination of recent scholarly opinions suggests that suprasellar plication should be the most appropriate nomenclature. This nomenclature is appropriate for any form of surgical technique to remove the softened supraglottopexy obstructive tissue, and the location and extent of removal depends on the specific obstruction mechanism of each child. In addition, the presence of compound malformations is highly valued when surgical intervention is performed, and direct laryngoscopy and tracheoscopy are performed prior to surgery. The results of related studies suggest that rigid tube laryngoscopy and endotracheal endoscopy are crucial in the management of laryngeal softening and associated airway compound lesions, and the presence of airway compound lesions is an important factor in the outcome of supraglottoplasty. Therefore, simultaneous surgical intervention for composite lesions is critical. Complications Surgical failure rates reported in the literature range from 2% to 8.8%, or only partial improvement occurs in those with concomitant other congenital malformations. Severe complications such as granulomatous hyperplasia, edema or purulent structure formation; supraglottic stenosis is the most serious complication, which follows extremely rarely but requires high attention, and the strategy of prevention is to avoid excessive resection and to allow re-surgical resection if the resected tissue proves to be insufficient after surgery.