PHLEBITIS. 



Divisions, traumatic and idiopathic. Causes, punctures, defective blood 

 supply in walls, debile coats, thrombus, infection, overstretching, injury or 

 disease of serosa, irritants in blood, microbic infection. Lesions, exuda- 

 tion, cell growth, breaches in serosa. Adhesive phlebitis, desquaniaiion, 

 granulation, occlusion. Suppurative phlebitis, infection, pyaemia, erysip- 

 elas, metritis, ulceration, neoplasms, phlebolites. Symptoms, local, firm, 

 corded, swollen vein, extends entad, venous congestion, dropsy, gangrene, 

 diagnosis from lymphangitis. Fever, venous congestion in vicinity. 

 Treatment, germicide, rest, cold, antiseptics, blisters. 



Inflammation of veins as seen in the lower animals has usually 

 been a sequel of bleeding and is hence a purely surgical lesion. 

 Animals as well as man however are subject to idiopathic phlebi- 

 tis which as affecting the deeper seated veins may be held to be a 

 medical subject. 



The causes of idiopathic phlebitis are varied. Injury to the 

 walls like the punctures made in bleeding; if they result in the ex- 

 posure of a raw, and above all an inflamed, surface to the blood, 

 tends to the formation of a thrombus, and of local inflammation. 

 Even the inflammation of the outer coat tends in the same way 

 to thrombosis and phlebitis, and the experiment of Nicas.se 

 showed that the dissection of its sheath from a vein, thus robbing 

 it of its vascular and nervous supply promptly induced coagula- 

 tion of the blood in the denuded part. The debilitated or devi- 

 talized walls evidently give off fibrinogen and fibrine ferment in 

 amount that is incompatible with the maintenance of fluidity. All 

 other forms of direct injury to the veins, leading to disturbance 

 of the endothelium or cell enlargement or exudation intheintima, 

 will operate in the same manner. Sometimes as in puerperal 

 phlebitis the inflammatiou extending from the adjacent tissue to 

 the walls of the veins, determines thrombosis, and the invasion by 

 pus microbes determines suppuration. Bruises, over-.stretching, 

 pressure with over-distension, and the circulation in the blood of 

 irritant matters may lead to changes in the wall, thrombus, and 

 inflammation. Such irritants may be septic or other bacterial 

 products, or they may arise from the colonization of bacteria on or 

 in the venous coats with the same final result. 

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