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Show DISEASES OF THE BLOOD VESSELS. TABLE VI. l Tiinoiiiiosis or THE INFERIOR Vich C.\v.\. Patriarc'l‘ASIS AND VAuicns. I'tinULing EXDo-riimani'ris. (Asia-An old woman. 111'sloi7/.-Ati'ected with uterine cancer. lowerextremities. (Edema of Complained of much pain in the right thigh and along the femoral vein. After death the following alte 'ations oftlie vessels were found: Fig. l. The inferior vena cava ( l'. 0.1.) up to the renal veins ('l'.]t'., VB.) was filled with clots, adherent to the wall. A iitiniber of sacs or varices. filled with pus and other saiiguinous detrittis,separatc from each other by thick membranes. The. intiina of the vessel is in many places covered with very red spots. F. I). is an emptied sac. showing the vascular wall. F. P. was not emptied. and shows its heterogeneous Contents. . 1)., a smaller sac, with formation of the clots. Now and then front the injured walls masses ot'connective tissue protrude into the aneurisin,'but none of these collected masses ever organize, nor do they ever form a safeguard against, the strong blood pressure; for very frequently the blood passes between the formed strata, softens them and causes them to be carried away into the circulation as very dangerous thrombi. In very rare cascs,calcarcous masses,produced by intercurreut endoartcriitisavill close tip narrow caviticsof smallaneurismalarteries. According to (J/tctrrot (Leena), cranial lizcinorrliages prodticed in old age are always due to ruptured aneurisms of the cerebral arte« i‘ies. Etc/dcr, chkcr and Jt'ot/t hold the saute opinion. Capillary chtasz's. A state of capillary dilatation is always produced in chronic deraiigenientof the circulation, when there is either stagnation or continuous turgidity of the vessels, as met with in stctiosisof the initral valves. The pulmonary and ltepatic capillaries are thtis found dilated. In congenital na ras, in muscular atrophy, in caveriiotis ttunors, iii tuberculosis, and according to Rot/1, [Ire/1r], and l't‘re/totti, in congenital cerebral gliomata such capillary cdasts is found. l'artr and P/t/t'twtasia. Any cause producing long standing venous stagnation superinduces dilatation of a whole or a part of a vein. In the lower portions of the bodv, and especially in that portion of the skin where the venous circulation meets with the greatest resistance, varices and phlebectasis are most frequent. The dilatations may be cylindrical, fttsiforin, or like sacs. They usually become tortuous and very wide at the point of their division. When two such veins meet, they unite to form a wide sac; both cavities communicat i, and form a cavernous structure. Such condition is found in anal tumors (haunorrhoids, piles). The 'arices often produce ruptttre oftlie vessel, with more or le severe litemorrhages or phlegmonous ulceration, followed by inctasr ‘ When putridsubstancesare there formed, or when microorganisms invade theulcerated tissues, they become a source of dangerous and often fatal infection. Very often phleboliths, or calcareous precipitates, are formed in varicose veins. They generally close up smaller veins; larger veins they cause to ulcerate, by endophlebitis. Such ulcerations often form very infectious thrombi. At other times such thrombi organ» ize and stop the vessels up altogether. Solid/mt of (.‘ott/z'ttilttj/ of littstrafttr ll'ttlfs. Ruptures ofaneurisms and varices are the most frequent causes of spontaneousliaiinorrhages. Degenerative and decaying processes going on in the vascular walls cause them to break, even without being dilated. A healthy vessel always resists the wliolc blood pressure, however great it may become. When an artery breaks into a tissue, the hannorrhage from the vessel will continue until the clot formed is capable of resisting the blood pressure. Such clots are called 12a t)7(lfU/tt(lf't. The rent in the blood vessel is closed tip by colorless corpuscles and blood discs, which gradually form a colorless inass extending into the vessel, and protruding outside. (Sc/tufts.) The internal portion of the mass becomes absorbed, whilst the external remains continuous with the external wall. Adhesive intlainmation always following such ruptures, gradually forms a sac around the external clots. Such a sac is called a false aneurisni. This kind of aneurisni often breaks through and causes great liteinorrhage, or is filled tip by newly-forintal connective tissue within the sac-(Schultz) Vessels derived front the repaired vascular wall, often start cicatricial tissue and extend it over the sac, and eventually obliterate it by eicatricial constriction. Venous wounds are often healed in this manner. Such sacs are called false varices.-(t\'r/ttilts.) (Run-shot wounds of blood vessels, [SECTION IV. very thick walls and stratified contents, Jf. Hf. The two common iliac veins (_ l‘. I. I'.) contain solid, cylindrical colorless clots. In the left liypogast‘ric veiif (l. 11.). and a little above, to the right, newly-formed thrombi were found ($17., 51. The blood in the left external iliac vein had a peculiar yellowish. creamy color. ()n the riglit.the clot was formed at the origin of the saphena "28.), and extended into the deep and superlicial femoral veins. 0n the left. thephlebitis extended along the whole course of the sapliena vein. In the deep femoral veins colorless thrombi \\ ere found In the collateral circulation which supplied the tissues of the lower extremities. no clots were found. The phlelntic process stopped at thrnewly-(leveloped venous valves. Figs. 2,3 show the varices and their thrombotic contents. Also the newly developed valves where the collateral circulation begun. ually destroyed, and the aneurism breaks into the vein. It forms an aneurisinal varix. When a vein and an artery are together perforated, for instance, by a stab. a false aneurisinal varix will ensue. When an opened artery breaks into a vein and dilates it, then an an~ eurisinal varix is formed. The vein becomes dilated and thickened. Thrombosis. Inlraraxctdnr Coagulation. Death of the blood is generally followed by coagulation, that is, solid masses are separated from the liqtiitl portion of the blood, as so eallctljiln'f/z. (.‘oagulation taking place in a vessel during life, is called thrombosis. the eoagula, thrombi. When the blood is st- gnaiit in the vessel, the thrombus is of a dark red color, and con. ts of granular albuminous masc s, a. few colorless, and a great quantity of colored corpuscles. Vessels closed by permanent stasis contain red thrombi, which are at first soft and spongy, containing blood serum. They grow more solid, contract. and become reddish-ltrawn. in still flowing blood only portionsof it are precipitated as, coagula. which are tnade tip chiefly of colorless corpuscles and blood discs (Zn/oi,Blzzozero), they are grayish or reddish yellow, or mixed in lighter and darker colored layers. \\'liite thrombi often collect along the vascular wall, and contain great quantities of fibrin. As the endotheliuin of the vessel is capablcof kccpingthe blood in a liquid condition, whenever this tissue becomes diseased, or is unable to perform its function. the blood will coagulate, the same as when it dies from poison or becomes stagnant from mechanical causes. Endocarditis as well as endoarteriitis are the most frequent causes of thrombosis. Thrombi may be formed along the vascular wall, along the venous or cardiac valves. They may close the vessel tip either by primary or secondary formations, or may at first occlude it and then by contraction of the thrombus free a portion of the cavity and render circulation possible through it. Thrombi are always formed in such localities and under such eircunistances, where and when the blood is deprived ofits contact with the eiidothelium and is stagnant. They are therefore more frequent in veins, at the valves than any where else, and spread from the smaller into larger veins. Pareiichyinatous intlammations resulting in gangrene are the most frequent causes of thrombosis of small vessels. The most favorable results are. those in which the perfectly formed thrombus becomes contracted and hardened,by absorption of its liquid portions. They are then as a rttle converted into calcareous masses, and either close up the vascular cavity by causing their walls to shrink. or leave a portion of the cavity open to re-establisbed circulation, l'/t/c/io/t!/ts are calcareous masses formed in the centers of thrombi. As a rule, new endotheliuni covers such creta- ceous masses and prevents the formation of new thrombi. Softening of the thrombotic ccntra are far less favorable to the vessels and the tissues enclosing them. The softened portions cithcr forin red or grayish-red masses of corpuscular and granular'debris and blood cry stals, which. when carried into the general cir- ctilation, forin dai rous cinboli. I'urulent and gangrenous, or yellow and greenish softened masses formed in the centers of the thrombi, cons st of decomposed and decayed fibrin. blood corpuscles and other detritus of the blood. They act not only as inflammatory foci upon the adjacent vascular walls, which they corrode and cause to undergo purulent inflammation, but also the gangrenous particles. usually found to contain highly putrid substances and large quantities of inicrococci. C(ilii‘ plctely destroy the inner and middle coat, and both become the most dangerous sources of ptitrid infection to the whole circulation. I'urulent thrombitphlebitis is called the purulent softening of a venous thrombus with infiltratitni of its walls. are, very often, spontaneously repaired in this manner.-(o'c/tult: Org/om'mtfoa oft/1c Thrombi/s. and chbs.) Aaron's/nodissect/us. Anew/"stun! l'art'r. \Vhen it happens that onlytlie inner and middle arterial tunies are broken. btit not the external, the blood does not enter the tis- The new tissue is formed from infiltrated colorless corpusclcs The endotht-linin of the vessel has gcuerally but little to do with the tissue reparation. whilst the thrombus itscli acts more as a slight irritant upon the newly developed connective tissue. Newlv formed vessels gradtially penetrate the organizing mass of spindle shaped cells. and form a incinbrane very intich like a newly forming serous liit‘li:lil‘2tllt*. The intervascular spaces gradually till tip by infiltration of round cells. which develop into connective tissue cells. The l issue formation in such organization differs in young sue, btit passes between the coats. The external coat becomes tuniiitied, and the greatest portion of itis severed from the other coats. Stun a condition, which is frequent iiithe ascendingaorta, is called (Ititll/‘I'h‘fiitl (tissue/ts. The clots -are Sometimes so extensive as to 1015911 the whole extent ofthcexternal vascular coat front the othcrs, and the separation only ceases at the entrance of the vessels into the parcnchyinatous organs. The quantity ofthe blood between the tunics is occasionally very great. (in See. I\', Table IV the and vigorousindividuals and old or antcioic pcrsons. Emigration (th'ottliil cells into the organizingthrombus takes place from the vasa aorta is thus dis. ‘ctt‘tl to a great extent.) vasortini of the thrombotic vessel itself and the nearest capillaries. When an aiiettrisnial sac ot'aii artery is united with a vein by adhe- The healing of ligated \csst-ls is thus brought about' A tl‘l'fi‘ltl- sive iiitianiniation, the latter becomes, coinpresscdahe \\ alls are grad- bus is formed above the ligature, consisting chiefly of coicrlcss |