Carlos R. Salvarezza

Some authors consider that atelectasis and collapse are synonymous. Collapse is the decrease in the volume of a segment, a lobe or a lung, while atelectasis is a volume reduction, plus alveolar air reabsorption subsequent to an obstruction or a loss of surfactant. In both pathologies, circulation is preserved.

The trachea is divided into two snoring that separate and go towards the corresponding pulmonary hilum where they penetrate the lung and cross it to the base, giving numerous ramifications. The main bronchi are divided into lobar bronchi and these into segmental ones, which in turn continue to divide until giving the respiratory bronchioles, the alveolar ducts and the alveolar sacs; the alveoli are born from the walls of the latter.

The alveolar surface is covered by a thin lipoprotein film called surfactant, which is synthesized in the lung from glycerol. The surfactant reduces the surface tension of two alveoli, favoring their stability and preventing them from collapsing, and also contributes to keeping the alveoli dry by preventing liquid transudation.


The mechanisms by which atelectasis occurs are various.

Obstruction. Complete and rapid obstruction of a bronchus of a certain size can be caused by endobronchial involvement or extrinsic compression.

Endobronchial causes are: mucous plugs, blood clots, foreign bodies, benign and malignant bronchogenic tumors, endobronchial metastases, scarring of the bronchial mucosa.

Extrinsic compression most often caused by lymphadenopathy of various origins, extrabronchial tumors, and aneurysms.

When bronchial obstruction occurs, the total pressure of the trapped air approaches 760 mm Hg, and the sum of the partial pressures of the venous blood is less than the atmospheric one. Then the air diffuses into the blood slowly (hours or days) and there is adhesion of the alveolar walls. After a few hours, the absorbed air is replaced by edema.

Loss of surfactant. In the newborn, the air inhaled in the first breath usually distends the alveolar ducts and subsequent breaths do the same with the alveoli. This process is aided by the surfactant film, which reduces the surface tension of the alveoli and allows them to expand with less effort.

The pressure in the pulmonary circuit of the child until birth is equal to the systemic: at that time it drops sharply about ten times. Occasionally, and for reasons not exactly known, there is severe constriction of the small pulmonary arteries and aretrioles, which causes ischemia and damage to the alveolar epithelium with loss of surfactant and atelectasis. This syndrome is called acute respiratory distress of the newborn, and they have a high mortality.

Other diseases that can cause atlectasis due to loss of surfactant is pulmonary embolism.

Collapse . External compression of the lung generates lung collapse. The absence of bronchial obstruction allows secretions to drain freely and prevent infection. Pleural effusions, pneumothorax, thoracoplasties can collapse the lung.

The collateral ventilation that occurs through the Kohn (interalveolar communication), Lambert (alveolar bronchioles) and Martin (interbronchial) pores, prevents the reabsorption of small collapsed areas.

Symptoms and signs

Small atelectasis are generally asymptomatic, so much so that large atelectasis can present with a cough, usually dry, spontaneous or exertional dyspnea, and pain referred to the affected area. When they become infected, expectoration and hyperthermia are added. The symptoms also depend on the functionality of the pulmonary parenchyma and the pathology that gave rise to it.

For the physical examination to be positive, the atelectasis must be of a certain size.

On inspection, only large atelectasis present with respiratory immobility and intercostal pulling. Vocal vibrations are diminished or abolished on palpation, while on percussion dullness or submatidity is detected. On auscultation the respiratory sound is diminished or abolished.

Study methodology

Anemnesis and physical examination are of little value in diagnosing atelectasis, and only allow a presumptive diagnosis.

Chest radiograph . From the front and in profile, it allows the diagnosis of pulmonary, lobar and segmental atelectasis.

Atelectasis . The affected lung deviates into the posterior chest wall and the heart as well, while the healthy lung herniates through the midline.

The radiographic image is that of a homogeneous opacity of the entire affected hemithorax, with the mediastinum and trachea deviating towards atelectasis, the hemidiaphragm raised, and the healthy lung inflated bulging behind the sternum in the diseased hemithorax (pneumonocele). In the lateral projection, atelectasis is difficult to visualize because its anterior border does not produce a clear image and its density balances the radiolucency of the hyperinflated lung.

Lobular atelectasis . The signs are as follows: there is radiopacity with displacement of the fissures, the vessels of the adjacent lobes separate and curve toward telectasia, the trachea deviates toward the affected hemithorax in the upper lobes, and the hilum moves upward. On rare occasions, the hilum descends into lower lobe atelectasis.

Segmental atelectasis . The radiographic signs are similar to those of lobar atelectasis, but many of them are difficult to recognize because the atelectasis volume is small. Profile radiography is very useful to delimit the diseased segment.

Linear tomography. Computed axial tomography . These methods are more easily recognizable for atelectasis, but are rarely indicated as frontal and profile chest radiographs are sufficient to establish the diagnosis.

Bronchography . He detects bronchial interruption, but is exceptionally indicated for the reasons already stated.

Laboratory . The data depend on the etiology of atelectasis.

Fibrochoscopy . It allows to study the bronchial tree up to the subsegmental orifices. Endobronchial lesions and narrowing of the bronchial lumen can be seen due to extrinsic compression. It is the most important method to study the etiology of atelectasis.