oa Editorial [Hot Topic: Upper Airway Disorders in the Neonate (Guest Editor: Oommen P. Mathew)]

Upper airway (UAW) is defined as the extra-thoracic portion of the airway extending from the nose to the intra-thoracic inlet. It is divided into distinct segments such as the nose, pharynx, larynx and trachea. UAW has an exoskeleton of bones and cartilages on which more than 20 pairs of muscles are attached either directly or indirectly. UAW participates in a number of complex motor acts involving both the respiratory and alimentary systems. Although we take airway patency for granted, its significance is highlighted during cardio-pulmonary resuscitation. A patent upper airway is vital for survival. Peter Safar, a CPR pioneer, made the seminal observation which is the basis of UAW maintenance. He recognized the development of oropharyngeal obstruction during general anesthesia [1]. In an elegant study Wilson et al. determined the passive characteristics of the UAW and suggested that the UAW patency is actively maintained in the neonate [2]. Loss of UAW muscle tone with the onset of sleep predisposes the airway to obstruction, especially in obese adults. Research interest in sleep apnea served as further impetus to our understanding of UAW maintenance. Intrapleural negative pressure generated during inspiration acts as an airway collapsing force to the UAW. Nasal resistance, which accounts for nearly one-half the pulmonary resistance, increases markedly in the neonate when a nasogastric tube is inserted. As airway resistance increases, UAW is subjected to even greater airway collapsing force. Although airway obstruction occurs typically during sleep and anesthesia, UAW patency can also be compromised by other factors such as neck flexion or maldevelopment. Congenital airway disorders such as laryngomalacia, choanal atresia and Pierre Robin sequence constitute the major UAW disorders in the newborn. Airway resistance is increased in these disorders, often impairing gas exchange in severe cases and sometimes even threatening survival. Prompt investigations, diagnosis and intervention are required for optimal outcome. Endoscopic evaluation and non invasive imaging such as computerized tomography are very useful tools in this process. In a series of reviews we discuss key issues in these UAW disorders. The passive characteristics of the UAW, neural and chemical regulation of UAW muscles, and effect of sleep and arousal on muscle activity as well as basic pathophysiology of upper airway obstruction are discussed in the first article [3]. Some UAW muscles such as the alae nasi, posterior cricoarytenoid (PCA) influence UAW lumen markedly because of their strategic location. Respiratory activity of these muscles is altered by chemical and mechanical factors. For example, laryngeal mechanoreceptors responding to negative pressure changes promote UAW patency by increasing PCA and genioglosssal activity [4]. Bilateral choanal atresia which occurs as an isolated abnormality or as part of a syndrome (e.g., CHARGE syndrome) manifests clinically with airway obstruction, stridor, and cyanosis in the immediate neonatal period. In the vast majority of patients it is a mixed (bony/membranous) lesion. A temporizing measure such as an oral airway or intubation is often required prior to definitive surgical treatment. Surgical strategies include transnasal puncture, transpalatal resection and endoscopic resection. Typical post-operative management of choanal atresia includes a stenting period. Ramsden reviews in detail the diagnosis, etiology and surgical treatment of choanal atresia [5]. Pierre Robin Sequence is a collection of symptoms and signs including micrognathia, glossoptosis, intermittent upper airway obstruction and typically cleft palate. A majority of the patients responds to prone positioning and careful oral feeding. If airway obstruction persists or growth is inadequate, surgical intervention is indicated: glossopexy, mandibular osteogenesis or tracheostomy. Yu et al. address these critical issues in their review on Pierre Robin Sequence [6]. Stridor in the neonate has multiple causes. A basic physiological approach is needed to establish a diagnosis. This includes a detailed assessment of the characteristics of stridor, its associated features and the levels of respiratory distress. The differential diagnosis includes laryngomalacia, tracheobronchomalacia, subglottic stenosis, cysts, clefts, webs, hemangiomas and masses. Diagnostic laryngoscopy and bronchoscopy are required for most cases. Management ranges from observation and parental education in mild cases to relief of obstruction through surgical means. Masters addresses these and other important issues in his review [7]. Laryngomalacia is the most common cause of stridor in the neonates. It follows a benign, self-limiting course in the vast majority of cases. Surgical intervention is warranted only in a minority of patients. The surgical techniques have evolved over the years to endoscopic supraglottoplasty; tracheotomy can be avoided in most infants. Clinical symptoms, evaluation and surgical approaches are discussed in detail by Bedwell and Zalzal [8]. Endotracheal intubation and mechanical ventilation often help to stabilize the infants with severe upper airway problems. However, subglottic stenosis in the neonate is often acquired and is caused by prolonged mechanical ventilation. The incidence of acquired subglottic stenosis has decreased significantly in recent years. Prior to the introduction of airway reconstruction, tracheotomy was the primary treatment option. Endoscopic airway techniques have expanded the surgical options with laryngotracheal reconstruction as the mainstay for moderate and cricotracheal resection for severe stenosis. Meier and White discuss the management of subglottic stenosis with an emphasis on current surgical techniques [9].....