If the adenoids or tonsils are large and thought to be significantly contributing to UAO, then the most effective treatment is removal. Because the adenoids are not a discrete organ but rather consist of lymphoid tissue, regrowth is possible, especially in preschool children. If the tonsils are large and the obstruction is severe, then removing the tonsils in addition to the adenoids may be necessary.
Choanal stenosis/atresia is a congenital problem presenting inthe neonatal period. It may be bilateral or unilateral and is relatively rare. Neonates are generally obligate nose breathers, soobstruction of nasal passages can cause significant respiratorydistress, especially when feeding. Crying bypasses the obstruction because crying infants breathe though their mouths. Inability to easily pass a small catheter through the nostrils shouldraise the suspicion of choanal atresia. The diagnosis is confirmed by CT scan and by inspecting the area directly with aflexible nasopharyngoscope. An oral airway may be useful inthe short term, but the definitive treatment is surgery.
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SEE CHAPTER 107.
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SEE CHAPTER 107.
SEE CHAPTER 107.
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Laryngomalacia is due to exaggerated collapse of the glottic structures, especially the epiglottis and arytenoid cartilages, during inspiration. It may be due to decreased muscular tone of the larynx and surrounding structures or to immature cartilaginous structures. Inspiratory stridor beginning at or shortly after birth should raise the suspicion of laryngomalacia (see Table 135-1). This is the most common cause of stridor in infants. It usually does not result in significant respiratory distress, but occasionally it is severe enough to cause hypoventilation, with hypercarbia, hypoxemia, and difficulty with feeding.
The primary sign of laryngomalacia is inspiratory stridorwith little or no expiratory component. The stridor is typically loudest when the infant is feeding or active and decreases when the infant is relaxed or placed prone, or when the neck is flexed. Any condition that increases upper airway inflammation will exacerbate laryngomalacia, including viral respiratory infections, dysphagia (swallowing dysfunction), and gastroesophageal reflux. Laryngomalacia normally peaks by 3 to 5 months of age and resolves between 6 and 12 months of age. However, occasionally it can persist in otherwise normal children up until 24 months of age and even longer in children with underlying conditions, especially those with neurologic diseases affecting control of upper airway muscles (such as cerebral palsy).
In many infants with presumed laryngomalacia, the diagnosis can be tentatively established by history and physical examination. If the patient follows the typical course for laryngomalacia, then no further workup is necessary. However, to firmly establish the diagnosis, which is important in more severe or atypical cases, the patient should undergo flexible nasopharyngoscopy to assess the patency and dynamic movement (collapse) of the larynx and surrounding structures. This procedure can also identify vocal cord abnormalities and airway lesions above the vocal cords.
In most cases, no therapy is required for laryngomalacia. The infant should be observed closely during times of respiratory infection for evidence of respiratory compromise. Infants with severe laryngomalacia resulting in hypoventilation, hypoxia, or growth failure may benefit from a surgical procedure (aryepiglottoplasty) or, in extreme cases, a tracheostomy to bypass the upper airway.
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Subglottic stenosis is the narrowing of the portion of the trachea immediately below the vocal cords. It may be congenital but more often is acquired. Endotracheal intubation, especially prolonged or repeated intubation required in some premature infants, can lead to inflammation and scarring of the subglottic space.