328 HISTOLOGY OF THE MORBID PROCESSES. 



walls as to give rise to an excessive transudation of serum and 

 occasion oedema and ascites. 



Similar chronic passive hyperaemias may follow those inflam- 

 matory lesions in the valves of the heart which cause either 

 agglutination and permanent adhesions of the valvular curtains, 

 stenosis ; or a contraction of one or more of those curtains, so that 

 their proper closure is prevented, incompetency. In either case the 

 circulation is impeded and the flow of blood from the organs behind 

 the lesion interfered with (Fig. 289). 



Haemorrhage is another of the frequent results of damage. It 

 may be recognized by the presence of blood outside of the vessels. 

 This blood at first contains the red and white corpuscles in their 

 normal proportions, but after a lapse of time the clot which forms 

 becomes infiltrated with leucocytes as the expression of an inflam- 

 matory reaction induced by the extravasated blood. Subsequently 

 the blood disintegrates, productive inflammation is induced, and the 

 lesion heals, with the production of a scar. This is often colored 

 brown or gray, from the presence of pigment derived from the 

 hemoglobin of the red blood-corpuscles. This pigment may be 

 in the form of reddish-brown rhombic crystals, or granules, of 

 haematoidin ; or it may take the form of small granules of haemo- 

 siderin. The latter substance contains iron, from which the former 

 is free, and under the action of sulphuretted hydrogen produced 

 by decomposition may give rise to sulphide of iron, changing its 

 brown color to black, and the color of the pigmentation from a 

 brown to some shade of gray. 



Haemorrhage may be among the direct results of damage to the 

 tissues, or it may follow necrotic changes in the vascular wall. 

 This is a not infrequent occurrence in virulent forms of infection, 

 and results in the formation of small, punctiform haemorrhages ; 

 for the vessels necrosed are usually of small calibre and surrounded 

 by tissues sufficiently firm to check the flow of blood under the 

 slight pressure within those vessels (Fig. 290). But more copious 

 haemorrhages may occur in the course of slowly progressing infec- 

 tions, notably in pulmonary tuberculosis. It will be remembered 

 that the walls of the larger vessels are composed of a dense 

 fibrous tissue rich in elastic fibres (Fig. 97). Such a tissue resists 

 the necrosing action of tuberculosis for a longer time than the 

 more succulent tissues of the lung. It therefore occasionally hap- 

 pens that a cavity may be formed by the destruction of the pul- 



