Obstructive Atelectasis.

The most common form of atelectasis is obstructive or resorptive atelectasis. It is caused by intrinsic or extrinsic obstruction of an airway by conditions as neoplasm, infection, foreign body, or heavy secretions.2,6 Over time, air distal to the airway obstruction is resorbed and not replaced, leading to an airless, radiolucent, collapsed portion of lung tissue (Figs. 22-1 to 22-5). Often, the lung distal to bronchial obstruction exhibits increased radiopacity correlating to replacement of the alveolar air with inflammatory transudate, exudate, or other substance. Less commonly, a check valve or obstruction develops, creating a hyperlucent, overinflated portion of lung tissue.

A check-valve mechanism involves accumulation of air distal to an airway obstruction. Airways dilate during inhalation, permitting air to pass by a partial bronchial obstruction. Airways constrict tightly around an obstruction during exhalation, effectively limiting the expiration of air distal to the obstruction. With each breathing cycle, more air is “pumped” into the overinflated lung tissue distal to the obstruction. Check-valve obstructions in a small airway are of limited clinical significance; however, they may result in respiratory distress when occurring in a large airway.

Passive Atelectasis.

Passive (relaxation) atelectasis is the second form of atelectasis. It results from the presence of a space-occupying lesion external to the lung. Pleural fluid (blood, exudate, transudate, and chyle) or air may accumulate to such an extent that the adjacent lung is “pushed” aside, resulting in partial or complete pulmonary collapse. Diaphragmatic elevation or herniation of abdominal viscera also may compress the lung. The amount of collapse is proportional to the size of the space-taking lesion.

Compressive Atelectasis.

Compressive atelectasis is a form of passive atelectasis in which the space-occupying lesion is located within the involved lung. Large bullae, neoplasms, abscesses, or other large lesions may result in compressive atelectasis of adjacent lung tissue.

Adhesive Atelectasis.

Adhesive atelectasis is nonobstructive, noncompressive pulmonary collapse secondary to decreased surfactant production by the type II pneumonocytes.³¹ Pneumonocyte damage results from genetic defects, general anesthesia, ischemia, or radiation damage. Adhesive atelectasis is seen in neonates with hyaline membrane disease.

Cicatrization Atelectasis.

Finally, cicatrization atelectasis represents scarring and contracture of pulmonary tissue after infection, pneumoconioses, scleroderma, radiation, idiopathic pulmonary fibrosis, and so on. This may appear localized (tuberculosis in the lung apices) or generalized (interstitial pulmonary fibrosis).

Imaging Findings

The presence of atelectasis is suggested by direct and indirect radiographic signs (Box 22-1). Displacements of intralobar fissures are the most reliable findings. The radiographic appearance differs based on the degree of lung involvement, location, and type of atelectasis (Table 22-1). Combined lobar collapse may complicate the radiographic appearance.¹⁶ Rounded atelectasis is a form of peripheral pulmonary collapse that must be differentiated from neoplastic masses with similar radiographic appearance.^20,32

Clinical Comments

Whenever atelectasis is found, it should prompt a vigorous search for a cause. Although several mechanisms of collapse have been identified, obstruction of the airway resulting from neoplasm is another common cause of lobar or segmental atelectasis that should direct patient management.