Potential causes of upper airway obstruction are shown in Tibie 1.4.-1. Basic management of the obstructed airway is discussed in Chap.8. Most of these entities cause soft tissue swelling or themselves are soft tissue masses that compromise the upper airway, but a few need mentioning. Certain medical diseases like respiratory syncytial virus (RSV) and cystic fibrosis produce copious secretions in the upper airway that can lead to partial or complete occlusion. Angioedema may present with soft tissue swelling sufficient to preclude an oral airway, requiring a nasal pharyngeal airway, nasotracheal intubation, or surgical intervention to reestablish patency. Laryngospasm, the feared complication of any invasive airway technique, needs to be considered in any patient with a compromised airway, especially in children. It is defined as closure of the glottis by the constriction of intrinsic/extrinsic laryngeal muscles, which can completely restrict ventilation. This pathophysiologic state often persists long after the stimulus has ceased. Laryngospasm may occur secondary to contact with the upper airway receptors on the tongue, palate, and oropharynx. Light touch to the upper airway, anal stretch, traction on the pelvic/abdominal viscera, chemical irritation, secretions, blood, water, and vomitus may all cause laryngospasm. Hypoxia and hypercapnea depress the activity of laryngeal adductor neurons, so laryngospasm is somewhat self-limited. Laryngospasm and bronchospasm occur more frequently in children and particularly following a recent respiratory tract infection.
TABLE 14-1 Causes of Upper Airway Obstruction
Altered mental status, somnolence, or even sleep can depress the intrinsic and extrinsic muscle tone of the airway and produce obstruction. Some authors question the long-standing belief that the tongue falling back and occluding the lower pharynx is the major cause of airway obstruction in the somnolent or comatose patient. In a supine individual, the degree of extension of the head required to open the airway depends on elevation of the occiput above the horizontal plane. Relative to the neck, the more the occiput is elevated, the less extension is required to open the airway, which explains why patients with airway compromise need to have their heads in the "sniffing" position. One can place a folded towel or foam rubber device behind the patient's occiput (not neck) to create this position. Flexion of the neck has a marked effect of closing the airway, specifically the oropharynx. Recently, it has been shown that during anesthesia in the supine patient, the tongue does in fact displace posteriorly, but it does not appear to occlude the pharynx. Upper airway obstruction in the unconscious patient occurs primarily because the epiglottis occludes the laryngeal inlet due to intrinsic muscle relaxation, which can be relieved simply by extending the neck. Extension of the neck and anterior displacement of the mandible moves the hyoid bone anteriorly and, in turn, lifts the epiglottis away from the laryngeal inlet. Recent magnetic resonance imaging (MRI) studies show that the soft palate also relaxes significantly during sedation, partially occluding the nasopharynx and causing complete obstruction when the patient is fully anesthetized. Moreover, retraction of the anterior tongue does not appear to relieve this obstruction. 1
Esophageal foreign bodies can also obstruct the airway. They can impinge upon the larynx or trachea, causing either acute or subacute obstruction. Some foreign bodies, such as large fruit pits, may have been present for some time; thus there may not be a history of swallowing an object.
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