Thrombophlebitis
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
Thrombophlebitis is the formation of a thrombus in a vein due to inflammation of its wall. It can occur from periphlebitis or endophlebitis and is often caused by bacterial infection.
Encyclopedia article (1928–1936)
THROMBOPHLEBITIS (from Greek thrombos - clot, blood clot and phleps - vein), formation of a thrombus in a vein during inflammation of its wall. T. arises due to violation of the integrity of the inner lining of the vein, which is observed in inflammatory processes localized in its vicinity, as well as in the fixation of bacteria contained in the blood on the intima. In the first case, the cause of T. is periphlebitis, in the second - endophlebitis. In periphlebitis, the infection spreads to the venous wall from surrounding tissues, in endophlebitis the process begins with the inner lining. In far-advanced cases, due to involvement of all layers of the venous wall in the process, the histological difference between peri- and endophlebitis becomes blurred. At the inflammatory focus that has developed around a vein in connection with slowing of blood flow and the action of bacterial toxins, inflammatory thrombosis of the smallest venous branches usually develops. The vein wall under the influence of the surrounding inflammatory process becomes more permeable to bacteria and their toxins, which can penetrate to the inner lining. In a purulent process surrounding large veins from all sides, the vasa vasorum of the veins become involved in the process. Thrombosis of the vasa vasorum themselves leads to worsening of nutrition of the venous walls, which is a factor contributing to the formation of thrombi. In endophlebitis, the process begins with the fixation of circulating bacteria in the blood on the intima, its necrosis and subsequent formation of thrombi. The formed thrombi, upon death of the causative agents and subsidence of the process, in some cases may undergo organization, in others their purulent melting occurs, sometimes with generalization of the process. T. is usually caused by pyogenic infection - staphylo- and streptococcus. In T. of otogenic origin, pneumococci were often found. In the literature, about 20 cases of T. of the small and great saphenous veins have been described, the cause of which was gonorrheal infection. Thrombophlebitis often develops in the veins of the extremities, pelvic and other organs (vv. spermaticae, hypogastricae et femorales); in the sigmoid and transverse sinuses of the dura mater in otitis, in complicated furuncles and carbuncles of the face, in the umbilical veins in infection of the umbilical cord of newborns; in the portal vein in acute appendicitis, dysentery, typhoid fever, etc. Among the general causes contributing to the occurrence of thrombophlebitis are changes in the composition of blood that occur in infectious processes, changes in blood in the postoperative period, weakening of cardiac activity, general weakening of the body, etc. Thrombophlebitis can occur with suppuration and without it. In purulent thrombophlebitis, infiltration of the venous wall and surrounding tissues is observed, and the formed thrombus may undergo purulent melting. Sometimes pus, after destruction of the venous wall, penetrates into the surrounding tissues, causing limited suppuration of the abscess type, or the process takes on the character of phlegmon. True, the latter type of suppuration occurs much less frequently. Non-purulent T. manifests as edema of the extremity, painful swelling along the course of the corresponding vein and subfebrile temperature. With superficial location of the thrombosed veins, the latter are palpable as a dense, painful cord. T. of deep veins is recognized on the basis of indirect signs. Purulent T. proceeds with an increase in temperature to 39-40°, with more significant pain and edema. Thrombophlebitis of the lower extremities is most often localized on the left side (according to Trinkler in 82%). Hampton and Wharton in T. of gynecological origin noted involvement of the veins of the left leg in 66% and of the right in 9%. Trinkler explains such a significant predominance of lesions of the left lower extremity by embryonic features. Genetically, v. iliaca sin. does not develop independently, but is a descendant of a weaker anastomosis between the embryological vv. cardinales caudales, which creates greater weakness and underdevelopment of the entire venous network of the left leg. Riedel sees the cause in anatomical differences. He believes that the left iliac vein is under greater pressure (three times) than the right, as it is crossed by the middle epigastric, sacral and hypogastric arteries almost at a right angle. Hochenegg believes that the higher frequency of left-sided T. depends on infection penetrating from the sigmoid colon, especially with its chronic overflow with fecal masses. Postoperative T. also more often occur on the left side. Some authors explain their origin by aseptic thrombosis, in favor of which they cite their later appearance 2-3 weeks after the operation, but most authors still consider infection as the main etiological factor, since in a completely afebrile course, the action of bacteria can manifest itself later in distant parts of the body. The cause of postpartum T. are postpartum parametritis. The diagnosis of superficial T. presents no difficulties. In some cases, T. may resemble various types of lymphangitis. Thrombosed veins are usually palpable as painful cords, the skin over which appears reddened and slightly edematous. In T. of deep venous trunks, pain and feverish state are usually observed. Due to impaired blood outflow, the leg or the thrombosed area swells and takes a more or less cyanotic color. Sometimes it is possible to palpate dense, painful cords corresponding to the anatomical location of the veins. Treatment of acute T. of large veins should consist of complete rest and the application of heat in the form of compresses and hot water bottles and the elevated position of the corresponding extremity. Often, for complete subsidence of inflammatory phenomena and organization of the thrombus, a period of 4 to 6 weeks is required, and sometimes more. Mild forms of T. pass much more quickly, and sometimes after organization of the thrombus, the lumen of the vein may partially or completely be restored. In other cases, T. ends with persistent closure of the vein lumen. When T. turns into suppuration, it is necessary to make incisions with opening of the suppuration area of the vein. Cases of T. proceeding with chills, remittent temperature, severe general condition and signs of embolism suggest purulent melting of thrombi. In these cases, ligation of the thrombosed vein above the occlusion and subsequent opening of the infected vein is indicated. In the clinic of W. Muller (Rostock), ligation of veins due to ascending T. that developed with their varicose dilation was performed 500 times. In the clinic of E. R. Hesse, ligation of the iliac vein was performed several times. Most often, ligation of v. jugularis internae was performed in purulent T. of the transverse sinus, accompanying carbuncle or furuncle of the face, purulent processes of the middle ear, etc. In chronic T., good results are obtained by mud therapy. Recently, many authors have successfully applied leeches locally. Prevention of postoperative T. should be considered as careful observance of asepsis, refusal to operate after recently suffered infections. Recently, many surgeons to combat T. introduce early rising after surgery. According to statistical data, this measure reduces the percentage of T.
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“Thrombophlebitis.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/thrombophlebitis/