I20 Disturbances of Circulation. 



bleeding, haemorrhage {al^a, blood: ^^705, rupture) or extravasation 

 { extra, without ; 'vas, vessel). 



The most common causes of haemorrhage are wounds and 

 lacerations of the vessel walls. Anything which severs the con- 

 tinuity of the vascular wall by puncture, incision, tearing, con- 

 cussion or contusion affords opportunity for the effusion of blood 

 (traumatic liccniorrJiage). In the same way all conditions which 

 impair the resistive strength of the vessel walls to the pressure 

 of the blood favor haemorrhage, as the lesions caused by the 

 action of corrosive fluids, fatty degeneration of the walls of the 

 vessels, vascular inflammations leading to brittleness and fragility 

 of their tissues (corrosion hcruiorrJiage, spontaneous hcemorrhage). 

 Exaggeration of blood pressure (increase of pressure from sud- 

 den and powerful cardiac contraction and from hyperVemia) per- 

 mits the rupture of these weakened vessels, or perhaps even nor- 

 mal pressure may be sufficient. Rupture of the liver is not infre- 

 quently met with from such a cause after fatty degeneration of its 

 vessels and tissues. Or when the muscle of an artery (after 

 chronic inflammation) is in a degenerate state its walls may be 

 distended to form permanent dilatations [aneurisms] ; here the wall 

 comes to consist of but little more than connective tissue, which 

 tears when the distension becomes great. 



Haemorrhages of the types mentioned are spoken of as haem- 

 orrhages per rhexin ( prj^is, rupture; prjyvwai, to burst through), or, 

 ])articularly where the wall has been weakened by pathological 

 changes, as haemorrhages per diabrosin ( bia-^i^pdocrKiLv , to eat 

 through ) . 



The blood maw however, leak out of the smaller vessels, 

 capillaries and veins, without the apparent existence of any lesion 

 in the continuity of structure, because of some abnormal pemie- 

 ability of their walls. Such haemorrhage is known under the 

 names diapedesi::, or luemorrhage per diapedesin ( from Sia-v-ndav, 

 to burst through). The increased permeability of the vessel wall 

 is explained by the fact that under the influence of toxic, infec- 

 tious, thermic or other injurious agencies, as well as from marked 

 engorgement and distension of the capillaries (passive hyperaemia, 

 stasis), the cement substance between the endothelial cells becomes 

 porous ; for example, the endothelial cells may shrink into globular 

 form and separate from each other, or openings may result 

 from destruction of the cells. The red corpuscles then slip 

 through between the cells or are forced out along with the plas- 



