The expansion of the lung is maintained by the pressure difference between
the alveoli, which are normally in free communication with the atmosphere, and the subatmospheric pressure of the pleural space.
The causes of collapse (atelectasis)
of the lung are pleural filling, bronchial obstruction with absorption of
the intra-alveolar gas, and changes in surfactant function.
Atelectasis is the incomplete expansion or collapse of parts of or a whole
The lung collapses when compressed by
pleural effusions, tumours, other space-occupying intrathoracic lesions,
or elevation of the diaphragm.
Lung collapsed because of entrapment by
thick pleural fibrosis can have a tumour-like roentgenographic image
called rounded atelectasis.
In pneumothorax lung collapses because air
gains access to the pleural space, permitting the negative pleural
pressure to rise.
This can occur as the result of thoracic
trauma, perforation of the esophagus, extension of lung abscess or other
infections through the pleura with formation of a bronchopleural fistula,
or rupture of air-containing cysts or bullae associated with emphysema or
other forms of diffuse or localized lung disease.
In young adults without generalized
underlying pulmonary disease, pneumothorax develops most often in tall
slender persons who have a few localized bullae, usually in the upper lung
The histologic changes in the walls
of the bullae are nonspecific, consisting of fibrosis, chronic
inflammation, focal alveolar epithelial hyperplasia, and a few hemosiderin-laden
Neither the underlying cause of the bullae nor the reason for their rupture is known, but it seems doubtful
that they can be explained by the greater vertical gradient in
transpulmonary pressure that exists in taller persons because of gravity.
A few such persons have abnormalities of connective tissue such as Marfan’s syndrome or Ehlers-Danlos syndrome.
Both the parietal and visceral pleura
respond to pneumothorax by the exudation of fibrin associated with a
proliferation of macrophages, giant cells, mesothelial cells, and
eosinophils known as reactive eosinophilic pleuritis.
It is important not to confuse this
nonspecific reaction to pneumothorax with the lesions of eosinophilic
granuloma, which is one underlying cause of pneumothorax.
Behind a totally occluded bronchus,the
absorption of alveolar gas can produce collapse of the lung.
This happens rapidly in patients breathing
100% oxygen when, for example, mucus plugs an airway. In persons breathing
room air, however, relatively minor volume loss follows bronchial
obstruction because the nitrogen in the air spaces is absorbed only slowly
and is replaced by edema fluid.
Gradual occlusion of a bronchus leads to
lipid pneumonia , chronic organizing pneumonia, and
, rather than simple collapse.
Shallow respiration also leads to alveolar
collapse as a result of rising surface tension in the alveolar lining.
The process is incompletely understood, but
deep ventilation acts as a stimulus to surfactant secretion by type II
epithelial cells and is required for the formation of a stable surface
Collapse because of
shallow ventilation is particularly likely to occur in postoperative
patients whose respiration is depressed because of anesthetics and who
have a shallow pattern of ventilation because of incisional pain.
The administration of oxygen only increases
If a small volume of lung is collapsed, the pleura is dark and sunken below the level of the pink, well-expanded
When an entire lobe or lung is affected,
the pleura is wrinkled.
The involved parenchyma is dark, firm, and
Microscopically the alveolar walls are
compressed, giving the tissue a solid appearance.
The vascularity of the alveolar walls helps
distinguish normal airless lung from fibrosis.
After collapse there is a progressive rise
in pulmonary vascular resistance in the involved better-ventilated tissue.
Several mechanisms are probably involved,
including hypoxia, tortuosity and distortion of the vascular bed, and