The following signs and symptoms are particularly suggestive of UAO (Table 25-3).

During asphyxia and severe choking episodes, very forceful inspiratory efforts markedly lower the intrathoracic pressure, increase the cardiac output, and stimulate the release of catecholamines and other stress hormones. The increased loading conditions of the heart, in conjunction with augmented transcapillary filtration pressures, encourage the formation of pulmonary edema.

The diagnostic workup of UAO may include routine films, computed tomography (CT) or magnetic resonance imaging (MRI) scans of the neck and trachea, and direct visualization by bronchoscopy or laryngoscopy (mirror, direct, or fiberoptic). Reconstructed or 3-dimensional (3D) CT images are often highly informative. Main bronchial obstruction caused by foreign body, tumor, or mediastinal fibrosis may give rise to strikingly asymmetric ventilation and perfusion scans. Similar information may be available through a comparison of full inspiratory with full expiratory chest radiographs. In stable, cooperative patients, pulmonary function tests should include inspiratory/expiratory flow-volume loops, maximal voluntary ventilation, and diffusing capacity as well as routine unforced and forced expiratory spirometry (Table 25-4). Typically, UAO impairs inspiratory flow more than expiratory flow, impairs peak flow and airway resistance disproportionately to FEV₁, and responds extraordinarily well to a low-density gas (helium-oxygen) but not well to bronchodilators (unless there is simultaneous bronchospasm). Maximum voluntary ventilation typically is much less than the value predicted from spirometry, whereas vital capacity may be comparatively normal, relative to FEV₁.

Diffuse airway diseases such as asthma and COPD tend to produce a different pulmonary function test profile. However, asthma can have a significant upper airway component, and occasionally, stridor will be a prominent presenting sign. Often, these patients benefit from anxiolytics or psychotropic drugs as well as bronchodilators and steroids. Unlike the diffuse obstructive diseases, which alter lung volume, distribution of air-flow, and diffusing capacity, UAO tends to leave the parenchyma unaffected. Diffusing capacity is relatively well preserved.

The flow-volume loop contour depends on (a) the fixed or variable nature of the obstruction and (b) the intrathoracic or extrathoracic location (Fig. 25-1). A fixed lesion inside or outside the thorax blunts the maximal inspiration and maximal expiration to a similar degree,
giving a “squared off” loop contour. A variable extrathoracic lesion, surrounded by atmospheric pressure, retracts inward when subjected to negative inspiratory airway pressure but dilates when exposed to positive airway pressure. Conversely, a variable intrathoracic lesion, surrounded by a pleural pressure more negative than airway pressure, dilates on inhalation. On exhalation, the lesion is pushed inward to critically narrow the airway. Unilateral obstruction of a main bronchus may not generate such characteristic curves.

The basic principles of managing UAO can be summarized as follows: Patients with symptoms at rest should be kept under continual surveillance and well monitored until the acute crisis resolves. Although certainly indicated, pulse oximetry may give a false sense of security, as O₂ saturation may remain within broad normal limits until the brink of total airway obstruction, physical exhaustion, or full respiratory arrest is reached. Postextubation glottic edema and laryngeal swelling resulting from injury usually peak within 12 to 24 h and then recede over the following 48 to 96 h. Racemic epinephrine aerosols may help reduce glottic edema as they cause topical vasoconstriction and bronchodilate the lower airway to reduce the vigor of breathing efforts. For spontaneously breathing patients not already receiving ventilatory support, continous positive airway pressure (CPAP) or BiPAP delivered by mask is often helpful. Upright positioning is favored. For unusually labile or otherwise precarious patients, intubation and tracheostomy kits, as well as a 14-gauge needle (for cricothyroid puncture), should be at the bedside for emergent use. In an emergency, oxygen can be insufflated via the needle until an airway is secured (see Chapter 6). Relief of bronchospasm is particularly important in the setting of a UAO. Relief of lower (small) airway obstruction reduces the intrapleural pressure swings and the severity of upper airway (particularly extrathoracic) obstruction. If there is inflammatory obstruction, tactile stimulation of the involved region must be avoided, and steroids may be helpful. Heliox may also be a reasonable option, especially for those who cannot tolerate or do not respond well to pressurized masks and whose oxygen exchange is well preserved. The patient should be kept calm but alert in a head-up posture. Endotracheal intubation or tracheostomy may be needed if ventilatory failure ensues or secretions cannot be cleared. These procedures should be attempted only by experienced personnel. For otherwise stable patients in whom the airway is “high risk” or known to be difficult to intubate, consideration should be given to conducting intubation and/or extubation in an operating environment where the full range of instruments and supporting measures is available.