Phlebitis

PHLEBITIS, phlebitis (from the Greek phleps—vein), inflammation of a vein. Morphologically, inflammatory processes in veins are subdivided in the same way as in any inflammation of a vessel in general (see Vasculitis). If the main changes are concentrated predominantly in the area of the inner lining, then such phlebitis is designated as endophlebitis; if the middle lining is predominantly affected, one can speak of mesophlebitis. In cases where the inflammatory process plays out predominantly in the area of the outer lining, it is designated as periphlebitis. However, due to the great thinness of the vein wall and its high permeability, it is extremely rare to strictly carry out the above-mentioned subdivision into endo-, meso-, and periphlebitis. Usually, panphlebitis is observed with predominant involvement of one layer or another. The very character of the inflammatory process varies. Phlebitis with a predominance of the alterative element is encountered, such as, for example, necrotic destructive phlebitis in typhus, or in allergic inflammation. Phlebitis can be purulent (usually with thrombus formation, see Thrombophlebitis), i.e., of the exudative type. Finally, phlebitis with a sharp predominance of the proliferative element is often encountered, for example, obliterating endophlebitis in syphilis. The cause of the onset of phlebitis is usually the introduction of one microorganism or another. Most often, the pyogenic group figures in this. However, phlebitis is encountered where microorganisms as such play no role; this is a group of phlebitis caused by increased sensitivity of the venous wall (allergic experimental inflammations, rheumatism?). In cases where the type of microorganism is established, an etiological classification of phlebitis is also permissible. Thus, one speaks of tuberculous phlebitis, syphilitic, actinomycotic, gonorrheal, etc. (see Veins). The mechanism of the development of phlebitis is varied. Microorganisms can penetrate into a vein without leaving any traces at the site of entry, and then, circulating through the venous bed, become fixed in any section. Usually, local prerequisites in the form of varicose veins, venous stasis, etc., contribute to the fixation of microorganisms and the development of phlebitis. True thrombophlebitis, for example in the region of the extremities, sometimes arises without any open trauma to the vein and even without an inflammatory focus in the immediate vicinity. But it is often possible to trace the path of infection from the site of entry with the development of an inflammatory focus to the venous wall, to which the process, as it were, spreads from the surrounding soft tissues. Such spread of inflammation from the surrounding tissues specifically to the veins, and not to the arteries, depends on the fact that the connection of the vein with the surrounding tissues is more intimate; moreover, there is a large number of lymphatic ducts in the walls of the vein. When analyzing each individual case with phenomena of phlebitis in the center of an inflammatory focus, it is necessary to remember that primary damage to soft tissues with involvement of the vein is not at all necessary; often it is the other way around—first phlebitis, then periphlebitis, paraphlebitis, and finally the development of an extensive inflammatory focus around it. An example of this can be liver abscesses as a result of pylephlebitis, i.e., phlebitis of the branches of the portal vein. An argument in favor of secondary damage to the veins is the spread of phlebitis away from the inflammatory focus. In general, the venous bed is one of the favorite pathways of infection. In particular, purulent thrombophlebitis is the most frequent prerequisite for the development of pyemia. The mechanism of development of non-infectious phlebitis is apparently always the same: absorption of the corresponding products, their circulation in the blood, and their fixation in areas of greatest sensitivity. The significance of the latter is, however, also great in infectious phlebitis. Migratory phlebitis—see Thrombophlebitis migrans.