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Show Sizcrtox IV] DISEASES OF THIS BLOOD V'ESEELS. TABLE V. J'm'ofmxt‘ millet/It‘lez‘fi'f/s of" {/10 r/(q/Mfcmm‘r/f art/21W. mu/ Us (lie/shuns below} l/te prof'mu/u. [er/aiutlt‘fuf/ in gout/reap of HM; wit/dc [fl/III. ('.\si-:.--.\ woman of fifty-eight years. Ilf.s/n/'I//.--\\ias atl'ected for many years with core/mono rec/f. producing extensive siippiiratingsinuses iiitotlie vag- inal cavity. atid extending to the cervix uteri. ,R'f/mploms.-She was exceedingly anaemic and very much emaciated. Three days before death she was taken with excruciating pain in the toes of the right foot; it was at first thought that the pain was ofneuralgic character. and treated accordingly. but without allitrding any relief. The next day the pain extended along the course of the arteries of the foot and leg. and gangrene at the toes appeared. which spread with great rapidity upward. Amputation in her condition was out of the question. All ineansto pre- vent the spread oftlie gangrene and afford relief. were used. but without avail. She died the third night after the beginning of appearance of gaiigi‘eiit'-. J'osf morime-It‘ was found that the recto-vaginal sep111111 was completely gangrent'tus. The vessels in that region were obstructed, The uterus was but slightly affected. The gangrenous foot and leg were black. and the inortil'ieatioii had Cliietly affected the anterior and external sur- faces. showing posteriorly distinct lines of demarcation. Se/rt'ow's oar] Alt/"urom/I, of N «ls, Sclerosis of arteries is called -tli:ttstatein which there are local centers ot thickening or conden- sation of the inner coat, There may be formed larger or smaller projections upon its surface. ofditi‘erent forms: they inay he traiiss parent, gelatinous. yery dense like cartilage. or libi'inous. Such condensations may take place from the origin of the aorta. and its valves at the heart. down to the farthest arteriole. The number of such condensed spots may be very small. or'e 'ceedingly great. The iiitiina of the aorta is. occasionally. tliortitugltly sch"i'otie, and without a single spot of normal tissue, In such a widespread changethcrcare found gray transparent plates by the side of cartilaginous knots. and yellowish white or clear white plaques. They may have rough or smooth surfaces. ()t'ten themortitied pors tioii ot' the tissues forms ulcers.and contains wltiiedet rittis ofthe t'ornier cellular structure. Sometimes the rough .surtaces are covered by abee. .' and decaying thrombi. The yellowish white spots are designated as: v/I/oremnfo, I/o deer/s as: .r/t/w'rw/tatons tiff/V's. The whole process is the result of the sclerotic alteration. Very frequently lime is: deposited upon the altered and mortitietl spots. which become hard and white. and have the appearance of bone. Formerly such a Condition was described as arterial (issitieation, front which it differs greatly. The veins are not nearly as often affected by sclerosis and atlieroma as the arteries. Condensation and thickening of the inner vascular.membrane not only interfere with its physiologieal function of keeping the blood in a litpiid state. btit al ‘0 product- antemia 01' its own tissue and that of tlte internal lay . ot'tlic middle coat, for both receive their nutrition from the blood in the vessel directly. The antenna causes fatty degeneration anddecay of both. Although a constant reparativc proce s: is goiiigoii, side by side with the decay. by means of cell-prttliteratioit iii the vascular wall, the destruction is going on so much quicker than the repair. that the muscular tissue of the middle coat swiftly disappears. and its place is tilled by the atheronr atotis: detritus. which consists of fatty molecules if Various sizes. calcareous granules and cholesterin crystals. The inner coat. although primarily affected. resists the destruction inueh longer. and remains intaet.nntil the pressure of the middle coat. growii o tronger. tinally breaks: it through. and the tttllCl't'tllttthdh detritu einptied into theeavity of fllt‘i\ l. .\ portion of the debris is swept 5 The skin was dry and shrivelcd.aiid the tissues. althou gh dead. were not putrid. They emitted an extremely nati- seous odor. The muscular structures were still coherent and perfectly distinct. The anteriortibial artery andtli c anterior tibial nerve were not at all altered exteriorly. Fig. 1 represents the gangrenous foot and lower portion of the leg. The skin has been dissected off, to Show the subcutaneous structures. Figs. 2. 3. show the femoral artery from a little below the groin. downward. The femoral and popliteal arteries and their branches are filled with cal ‘arcotis masses. and remain perfectly cylindrical after being cut. The solid masses formed rings within the cavity. and when passed between the fingers. feel like larger branches of bronchi. The femoral artery (A. 1".),Fig. 2, from below, the pro- funda femoris (Al'JBf) is filled with many colored clots. The same is the ease with the popliteal (41.1%). Fig. 2. anterior t‘ibeal (.1. TA. ). Fig 3. and the trunk of the tibio pero- neal artery (‘1. T. Pf). Fig. 3. The posteriortibial artery (A.T.P.) is exceedingly small. The clots extendcdto all branches of those Vessels. The yeiitc comitcs were like- wise filled with clots and calcareous masses. Figs. 4. 3. 7. 8 show the ditt‘erent stages of atheroma- tons development tipon the inner and middle coats of the largest arteries. Fig ti shows an obturated and altered artery. 0. 7). hyper- trophy ot' the external coat. low grade ot vitality. But when such an atheromatous change he- falls a terminal branch of an artery, as in the brain. the liver, etc, then no rest/tune rel «Vita/rum ever takes: place. The tissues supplied by such a vessel are hopeless y lost. for very soon antcmia. and gangrene will overtake them. .\ slower but no l dangerous form of vascular lesion, caused by atheroma and sclerosis. is the formation of thrombi in the cavity of vessels: for. when a portion of the thrombus is swept front it into the general circulation emboli will till up the vessels which they enter. especially if the vessels be small. Larger ve_scls may be closed up by enormous hypertrophy of the inner wall, caused by plastic endot'u'teriitis which the thrombi call forth. Ill/Ides ("If/t. f'afou JIM/fr. No. 86‘, 101, 1.71, 1'71. 1909.) (l'oisz'n, (Johnston, [Juli/fit Jot/i1. ‘YLIlV, 18/77,) (Hr obit/"r. .li‘t'fhf. [10.1%, 3,}[. 1870,) lL/t/i't'lftl/HN. lv/i/‘I'ft. rli'l‘fi/It‘. J6.) (Kit. I t'. TY/‘I't‘fl. Jfl/il‘C-S'btfl‘ffi'hf, 1875.) t The ijl/r/o' zlffffo' (hr I'm/Ito]. Hesiof. "I 1851)According to all observations and clinical experience, rlieumas tism. gout. chronic alcoholism, syphilis and tuberculosis are the ehiet‘ causes ot‘the sclerotic process ot'the intima. (G't'oranni',Arch. Ital. «fr. B/o/ut/t'w.) (Israel, Fire/t, Arrlt rol. Mi.) (Trot/be, Berlin [\V/tlo. "DC/Hustle, 1871.) Ancilrz‘sia, T'arz'r, S/ettosz‘s. When all coats of an artery are ccccntrically dilated, aneurism is said to exist in the vessel. As a rule, one or more of these are atrophied. the inner coat the mo: .although the inner tunic as well as the middle may be almost obliteratedr andthe vascular contents held by a thickened external coat only. The ancurismal (lilatations may be cylindrical in form, spindle-shaped, oras a wide irregularlyshaped sac; or one part of the wideningr may have one form, and another part another form. The whole length of an arteryor only a small section maybe thus atfectcd. The dilatations maycommunicate with each other when there are several. or may remain separate. .\ny of the above named alterations of the vascular wall maybe the direct or indirect cause ot an aneurism. yet, as a rule, diseases of the inner and middle coats. which render them inelastic and iiicapable of resisting the blood pressure. are liable to produce such abnormal dilatations of the vessel. I'm/(tick, l'x'rc/mit'. .1 i'e/i..Jo', describes a special form which he calls intothecirculateinaningling with the blood and prmlucingthrombi in smaller vessels. which eventually are closed tip lvy emboli: a portion adheres: to the mlgt ., of the tissure. and causes: a roughness of the inner vascular surface upon which ltlrt‘ltt is pi ecipitated by the «wool/crow tom/2. and says that it is: produced by destruction of the fit/{am by calcareous ma _ " formed upon the endocardium and carried into the circulation. obstaclth created by the ('ttletti'eotts itlltl elttdt sterin inns "s. to the in the brain are mostly due tolesions ot'tlte external coat and t0 periarteriitis. The most t‘reotttnt place ot'aneurism is in the HUIIYl/‘fl' aorta (Sec. free movement of the blood. Finally. the lild'itt and other t'ithei‘om- aiotts‘ material till tip the vasetilar cavity more and more. and call forth. by stagnation ofthe blood they product-newinorltid proee ses. such as eiidoarteriiiis. t'attymiid granular degeneration. etc. The cavity left by the discharge of the atheromatotis substances. in the vascular wall. is tilled with pits. atid its walls uinlei‘go ttlt'et'ttllolt (atheroinatous ulcers), tiaugrene and other necrotic destructions soon take place in the uh-er. especially whtn iiiicroorganisms are brought into it from the circulation (which happens very often), and new dangers: to the vaseular tissue are created. Very often infections thrtinibi are then pt'lalttt'ed, which. when cai ricd into the circulation. become a source of multiple itietastatie abscesses in the body, It; small vessels; atlieromatotis pi'oet sses. thrombi. and tibi'iiioii: de- posits cattsc a complett closingot' the cavity. and they are converted into solid cylinders. lti larger vessels. the tavities are not perfectly obliterated. somecirculation may still be carried on. but tinally the blood pressure upon the partly diseastd walls: causes them to give way iii places: pocketsand ._ "‘tl'g‘etttt'ltt~ or dilatations of one or all of its ttttties \\'ill ctistte. A. a rule. all the coats ldetitl by adhesive lltllillllltttttitllt into one liistologieally moditied membrane. The rate of tissues in which such a process is going on is variable. When collateral circulation is estttllltsltr d ltL‘tWLL'll the .still sotllid part of the vessel and any anastomotie braneli ot a near vessel. l't pair and partial recovery take place, tit-iterally the newly-tiurinedvsti'ueture is "Cally: and lid: the character of cicatt'ieial L'eitttteettVe tl::tte of a ("/torrot. in item.»- .oo' [ts infill/dim. etc.. holds that aneurisms formed l\'. Tab. lll) and in theam tit/fay portion of the are/1 of that vessel (Ste. l\'. Tab ll t. They often attain enormous sizes. compress the adjacent tissues and cause enormous destruction of viscera by the fatal aiiteinia they bring about. I\ xt to the aorta is the pttplitealartery, which is most frequently zitiettt'isiittttlc. Dilatations ot' the I'tttlt]10ttttl‘}' arteries are occasionally found, bitt tlteyettititot be called aneurismatie.t'or the inner and middle coats are almost intact. (It is 1105:"th that the lesser volume and force of the right ventricular walls have not force sufficient to producetrue aiietirisiir The frequency of anetirisms in the brain is very likely due to the great thinness of the arterial walls. and the very tortuous course of most of the smaller ones. In ptilntonary tuberculosis, great numbers ot niiliai 'aneurisins ot' the liner branchlets ofthc pulmonary artery are very frequent. ‘ An artery atl'eeted bv aneurisnt never reeoy ers, nor is its dilatation ever repaired: contrary. the vessel beeomes wider and wider. until its walls are desti'ovt d, lla morrhages following such destruction are more orl dangerous, according to the size and position of the \‘t .ssel. ‘lee. . . ,riiallv small arteries are closed up by elots iii the sac, and form solid evlindtts ltv connective tissue. The cavities: of largeraiieiirisins zireotten tilledto a coiisidt rable extent. with many colored clots, arranged in strata; usually indicating the age of the |