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Pathology of Lung Collapse (Atelectasis) and Pneumothorax

Dr Sampurna Roy MD




Pulmonary Pathology Online

http://www. histopathology-india.net/Pulmonary Pathology.htm 

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 lung.  

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 fields.

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 macrophages.

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 bronchiectasis , 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 film.

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 the problem.

If a small volume of lung is collapsed, the pleura is dark and sunken below the level of the pink, well-expanded lung.

When an entire lobe or lung is affected, the pleura is wrinkled.

The involved parenchyma is dark, firm, and without crepitance.

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 reflex vasoconstriction.

                                                 

There are three basic types, all of which are reversible :

1. Resorption atelectasis : Follows complete obstruction of an airway ( Example: Excessive bronchial secretion, as in bronchial asthma or chronic bronchitis, foreign body aspiration or bronchial tumours.

2. Compressive atelectasis : Pleural space is expanded by fluid (Example: effusion from cardiac failure or tumors, blood from rupture of a thoracic aneurysm) or by air (pneumothorax ).

3. Patchy atelectasis :  Develops when there is loss of pulmonary surfactant, as in neonatal respiratory distress syndrome.

March 2015

 

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

 

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