STRUCTURAL CHANGES DUE TO DAMAGE. 



315 



In this way a fibrous thickening of the pleura is formed, which 

 remains as an enduring evidence of the inflammation that caused it 

 (Fig. 272). Again, it may happen that the inflammatory process is 

 communicated to the costal pleura where it is in contact with the 

 visceral layer. In this case fibrin is formed on both pleural surfaces, 

 which become agglutinated in case they are in contact. When, in 

 such cases, the interposed fibrin is replaced by cicatricial tissue, per- 

 manent fibrous adhesions between the lung and thoracic wall result. 

 When the exudate contains sufficient serum to prevent the agglutina- 

 tion of the two pleural surfaces such adhesions do not take place, but 

 each pleural surface receives a permanent layer of fibrous thickening. 

 Fibrinous inflammation may affect other tissues than those of the 

 serous membranes (Figs. 278 and 279). 



FIG. 278. 





Fibrinous leptomeningitis : a, cerebral cortex ; b, torn bloodvessel entering the brain from 

 the pia mater; c, fibrous tissue of the pia mater; d, the same tissue infiltrated with emi- 

 grated leucocytes ; e, fibrinous exudate in the wide-meshed areolar tissue of the pia 

 mater. 



4. Serous Inflammations. Like the fibrinous, these inflammations 

 are common affections of the serous membranes. Pleurisy is often 

 an inflammation of this sort. The exudation is chiefly serous, of a 

 light-straw color, and either quite clear or containing flakes of 



