General characteristics

Atelectasis is defined as diminished volume affecting all or part of a lung, which may or may not include loss of normal lucency in the affected part of lung (this finding is not to be confused with diminished volume produced by resection of pulmonary tissue)(1).

The term collapse is used when a whole lobe or lung is involved.

Types of Atelectasis

Pulmonary atelectasis can be divided into six types, based on mechanism:

  • resorptive,
  • adhesive,
  • compressive,
  • passive,
  • cicatrization,
  • gravity-dependent.

Resorptive atelectasis

Resorptive atelectasis, the most common type, results from resorption of gas from the alveoli when communications between the alveoli and the trachea are obstructed. Resorptive atelectasis is therefore also referred to as obstructive atelectasis. The obstruction can occur at the bronchial or bronchiolar level. The most important condition producing intrinsic bronchial obstruction is bronchogenic carcinoma.

Other causes of bronchial obstruction include:

  • other primary lung and metastatic neoplasms,
  • inflammatory etiologies (especially tuberculous or fungal infection),
  • aspirated foreign bodies,
  • mucous plugging,
  • malpositioned endotracheal tube,
  • extrinsic compression of an airway (by neoplasm, lymphadenopathy, aortic aneurysm, or cardiac enlargement).

Resorptive atelectasis is most commonly caused by obstruction of the small peripheral bronchioles, from impairment of mucociliary transport and pooling of retained secretions in the smaller airways. The larger airways are often patent and filled with air, resulting in air bronchograms within the atelectatic lung (Fig. 11-2). The presence of air bronchograms within the atelectatic lung usually, but not always, indicates the absence of a central obstructing neoplasm.

Adhesive atelectasis

Atelectasis resulting from surfactant deficiency is termed adhesive atelectasis. Insufficient surfactant leads to alveolar collapse; once collapsed, the alveolar walls tend to adhere, making re-expansion difficult. Diffuse surfactant deficiency can result from hyaline membrane disease, acute respiratory distress syndrome, smoke inhalation, cardiac bypass surgery, uremia, and prolonged shallow breathing (5).

Compressive atelectasis

Compressive atelectasis is caused by any space-occupying lesion of the thorax compressing the lung and forcing air out of the alveoli. Such space-occupying lesions include pleural effusion (including empyema), pneumothorax, pleural tumors, large pulmonary parenchymal masses, large emphysematous bullae, and lobar emphysema (6). Diaphragmatic hernias and abdominal distension from a variety of causes can also compress the lung.

Cicatrization atelectasis

Volume loss resulting from decreased pulmonary compliance as the result of pulmonary fibrosis is termed cicatrization atelectasis. This type of atelectasis is often associated with bronchiectasis in the affected lung. A number of conditions can result in pulmonary fibrosis and cicatrization atelectasis—for example, idiopathic pulmonary fibrosis, sarcoidosis, pneumoconioses, collagen vascular diseases, chronic tuberculous and fungal infections, and radiation fibrosis.

Gravity-dependent atelectasis

Normally, the most gravity-dependent portions of lung receive greater perfusion and have less alveolar expansion than non-gravity-dependent portions of lung. These gravity-dependent alterations in alveolar volume are normal but can exacerbate atelectasis in the dependent portions of the lungs, particularly in bedridden hospitalized patients with prolonged shallow breathing. Atelectasis occurring from these forces is termed gravity-dependent atelectasis.

Lobar atelectasis

In an adult with lobar atelectasis, a central obstructing neoplasm should always be considered as the underlying cause. Bronchogenic carcinoma is relatively uncommon in adults under the age of 40, when bronchial carcinoid tumor is more likely. In children with lobar collapse, an aspirated foreign body or asthma is the usual cause. In postoperative patients, the most common cause is a mucous plug.

With right upper lobe atelectasis, the major and minor fissures move upward; with severe atelectasis, the lung can approximate the mediastinum and lung apex. With complete atelectasis, or collapse of the right upper lobe, the minor fissure parallels the mediastinum and resembles pleural thickening or mediastinal widening. Compensatory hyperexpansion of the middle and right lower lobes leads to outward and upward displacement of the right lower lobe pulmonary artery

Nonlobar Atelectasis

Round atelectasis

For descriptive purposes, atelectasis can be divided into several types other than lobar atelectasis, depending on the anatomic location of the atelectatic lung. Round atelectasis is a form of chronic atelectasis associated with pleural disease, often benign asbestos-related pleural disease.

Discoid atelectasis

Discoid atelectasis, also referred to as platelike or linear atelectasis, is a form of peripheral pulmonary volume loss that is not secondary to bronchial obstruction.

Subsegmental atelectasis

The radiographic identification of subsegmental atelectasis can be difficult. When atelectasis is present at the subsegmental level, many secondary pulmonary lobules within the affected segment or lobe may remain aerated, whereas others collapse. In such cases, and when multifocal, the degree of volume loss can be minimal, and the radiograph may show only patchy opacities resembling bronchopneumonia. As more secondary pulmonary lobules collapse within the affected segment or lobe, crowded vessels and bronchi, hilar displacement, or fissural displacement will become apparent.

Generalized atelectasis

Generalized or diffuse atelectasis is a term used to describe widespread volume loss in the lungs in the absence of specific signs of linear, segmental, or lobar atelectasis (5). There can be marked arteriovenous shunting, but the opacification of the lungs may be mild or unapparent; high positioning of the diaphragm may be the only radiographic clue to the presence of volume loss.