Report on the Patliolo(jical Anatomy of Pleuro-pnenmonia. 199 
And there does not seem the least reason for supposing that 
the disease of the vessel wall precedes that of the surrounding 
tissue. On the contrary, such an idea is rendered most im- 
probable by the fact that the neighbouring parts are always 
more extensively diseased than the vascular wall, the inner coat 
being the least affected, and often escaping altogether. These 
points will appear more obvious when the course of the bronchial 
lesion is discussed. 
Both the other forms of consolidation obviously depend upon 
causes quite distinct from that which induces infarction ; and, 
moreover, a little consideration shows that the mode of com- 
mencement of one of these is very unlike that of the other. 
Fig. 5. — Semi-diagraphic Sketch to illustrate the mode of extension 
of the Disease. (A portion of three neighhoiiring lobes is shown J) 
The darkest p^rt of the central lobe (A) is the starting-point {opaijue cotisulidation) : the lighter 
part of satne (B) shows extension of the clear exudation via bronchial lymphatics (C) by means 
of the pleura (P). (E) Pleural exudation. Reduced to one-fourth. 
The clear exudation is always more wide-spread and super- 
ficial, less solid and less defined, than the opaque induration. 
The tissue elements remain normal even after the exudation 
has become intense. The vessels and air-passages are pervious 
and little altered. It might be described as intense inflam- 
matory oedema, while the other may be termed croupous con- 
solidation. From the distribution and relations of this clear 
exudation, it appears certain, as just stated, that it is the result 
