OCR Text |
Show ])ISEASES OF THE IIEART ANI) ITS MEMBRANES. I Siccrtox II. Tutu: VI. I'untxttv S'rxotcs or .\I\'(),\l.\T.A('I.\. I'to. I.-1]'///H'l'fl'()/l//['('[lil/I/‘l/(Il‘f/ noise/rs in HM? left rr-x/h‘t'cfc. A longitudinal section of tlte vetttricle shows its walls to eotttaitt numerous solid infarcts. 'I'owards tlte apex the muscular tissttc had undergone fatty and atherotnatous change: a portiott of the ntyocartliunt looks spotted grav- islt yellow (1'. 71'. If). sottte white fibers binding tlte edges of tlt - altered tissue. ()utside. tlte lteart ltas tlte appearance of a fatty lteart. AVhilst tlte lttetnorrhagic portions look suffused with blood. the balance of tlte heart‘s tisstte looks paler tltatt ttsual. In tltis stage of tlte lesiott the lteart is still capable of cott- traction. The etnbolic condition of tlte corottary artery branches have given rise. itt this case. to stagnation of tlte circulation itt tltc tttttscttlar tisstte. rttptttre of tlte stttall ves- scls attd extravasation intothe wall ofthe ventricle. The apoplectic foci are adjacent to attd within the litttitsof the degenerated tttyocardiac structure. (1". ..f.. apoplcctie fo- ctts: I'. 1).. right ventricle: I'. 51. left ventricle: -I._f.. arclt of the aorta: I'. I'.. pulmonary artery. FIG. 5. Lrlfcrs/HII/c ofJil/rm/II/m-ill. ‘The left ventricle is considerably dilated itt a longitudinal direction. Portions of the wall attd the apex ha\c undergonc connectiw tissue degeneration itt the process of cicatrixatiou: that portion oftlte endoeardium isof a grav- islt white color. perfectly anatmic and ntuchtougher than usual. A large clot islodgcd itt tlt -apcx attd is surrounded by the degeneratedtissttc. It constitutes what is ordinari- ly called a partial attcttristtt. The connective tissue between the tttuscttlar layers oftlte apex isoblitcrated. attd the layers ltave lost their cohesion. so that blood readily infil- tratctlla-twcen them and held them separate. In this ntan- ter the apex becatttc ntot'e dilated attd attenuated. are sometimes so stnall as to escape notice. bttt are readily noticeable by tlte microscope. The cxcresccnees are formed by sttbetttlotlte- together. Within the hyperplastie structures all sorts of degenerative prm-esscs are carried on. Atherontatous and lipontatous de- generations are the tttost frequent. All these cltattges render the valves more or less ittcotnpetettt to perform their work of closure of the ventricles during systole. The sclerotic attd hyperplastie processes lead to constriction or stenosis of the opening. whilst the retraction and deformity of the flaps and the tcndinous cot'tls produce incompetcncy (insufficiency) and inability of eontplete closure. Iial exudation. They may ltave a granular or tiIa-o-granular textare. In tlte granular tnasses many pale lumps are to be seen: they seem to be entlocardial cells undergoing gangrenous coagulation. The inflammation takes place in the tissue. and the exudates cent to enter it and then become coagttlatcd. The surrounding tissttes of the coagula becomecompressed attd mortified.but those sitnply infiltrated with small spherical cells retain their vitality. "This form of inflammation belongs to tlte group of diplttlteritic lesions, and resembles mostly. itt its histological character. superficial diplt- tltet‘ia of mucous membranes and the second stages of variolous dc\‘elopmentF-sfZita/er Pot/info". .lurttom.) More mitigated varieties of endocarditis exist. in which there is no formation of vegetations, attd only consist of cellular infiltration into the connective tissue of the endomrdium. The cause of the inftamtrtatory exttdatiott is. according to Ix'lebs and Eberth (Arc/tic. for crperfm. pat/mfde I'frcfm/e. rhea/tn). alt invasion of the endoeardium by microorganisms. at least in a great number of cases. Ziegler found in acase of highly acute verrucous endocarditis. which led to metastatic inflammation in the muscular tissue of the heart. and in the parenchyma of the, kidneys. a great number of micrococci in the bloodvessels of those organs. Nauwerk, in Ziegler's pathological laboratory, similarly found nticrococci in the intlamed endo‘ardium; they existed not only in the hypertrophied valves, but also in tlteunaltcred portions of the endoeardium and myocardium. In rheumatic polyar‘hritis it forms the most frctptent cotnplications. In typhus and typhoid fevers of the graver sorts. itt general sttppurativc ulcerations of the tissues. itt carcinontatous attd kindred diseases. it exists as a part affection. Ley- den fotutd it in chronic sttppurative glcet. Taken altogether. its causes are many. bttt they seem to be more connected with microparasites than with anything else. Itosenbaclt (in .Irc/t. fur/trim rim. put/ml.) in his article on valvttlar lesions artificially produced. cor- rectly observes: "IIow uncomplicated endocarditis in man is pro- duccd I do not vettture to say: anyway it must be clearly distinguished frotn Imctcric ctafocurtlt'ffs. There is indeed no tttore reason forthe non~existence of such unconqtlicated lesion than for non-existence of simple pleuritis, which nobody would ever tltink of attributing to infection. ()11 an inflamed valve, vegetations fortn very readily." The subsequent results of cndocarditis vary according to the nature of the individttal cases. The upper layers oftlte vegetations are never organizable. Small portions ntay become absorbed: now and then they undergo acaleareous change. )Iost frequently they decay and fornt detritus, parts of which are carried away by the blood t‘alcitied masses may also pass ittto the blood cttrrent. But botlt lead to formation of entboli. Loss of tissue is produced by removal of dead substance resulting from ulceration, which may be slight or very extensive. In the so~alled ulcerative entlocarditis the destruction penetrates deep ittto the cardiac substance, attd an extensive portion of the valve will be deeply ulcerated. The cttfeebled and inflamed structure of the. valve will be dilated and acttte valvular aneurism will result. Should the destructive,process contitttte still farther. perforation of the valve with loss of considerable portions of its tissue will be the result. The sattte ulcerative destruction may happen iii the chordte tendinea-, and they may be tortt from the flaps. The ttlccrative form of endocartlitis is especially found in inflatmnation. Itavittg its origin itt py:emia or septic infection. \'errucous attd uleerative endocarditis differ only in the eausesof their prodttctiott. bttt ttot an» atomically. The pernicious or ulcerative fortn seems due to pytentia. whilst the vcrrucous is due to rheumatic arthritis. When the acttte stage ofinflammation does ttot lead to death. then the prodttctive ittflattttnatory process. which leads to formation of ttcw eottttective tissue and cicatrixation. follows the exttdative attd gangrenous disintegration. The tissue which ltas ttot been gravely involved is the one from which the reparative work proceeds. weeks attd montlts the ltyperplastic tissue may be found iii a " ~ of quasi granulation. Migratory leukocytes. from the vessels. attd cells produced by proliferation of the fixed tissue. very likely cottstitute the elements of newly-formed structures. Large numbers of new vessels supply it with nutrition. 13y this plastic process the endocardiunt becomesconsiderably ltypertropltic. The neoplasmata appear on the walls of the auricles and ventricles as fibrous. white. transparent spots. sometimes disseminated and somet itncs cottfitted to certaitt localities. The valve flaps are thickened. sclerotic. retracted attd grown together. and deformed Ill various ways. The (‘IItJI'tILL‘ tendinetc are likewise shortened. thickened and also grown Stenosis and ineompetene ' tre very often associated. The nums ber of grades. possible to exist itt this class ot'deformities. is too great to be described itt detail. The consequences ofsttclt valvular diseases ltave been described above. 01' cottrse when theblood cannot readily pass the orifices arid the ventricles emptied. it will regurgitatc and be dammed up iii the portionsof tltecirculation back of the valve. and dilatation ofthese parts will ensue. For the purpose of cotnpettsating for this disturbance, the portion of the ntttscttlar tissue of the heart which ltas to propel the stagnant blood will be~ cotnehypertropltic. I‘lrequently the inflammation will extend from the endocardittm to the tissues situated beneath. or it will begin beneath attd extend to the endoeardium; either way there will be. complications. The histological character of this form of intlantntation is distinguished by infiltration of stttall cells into the tissues. 7 The anatomical alterations taking place in this form of myocarditis are either indttrattott or formation of abscesses. In the first case hyperplastie connective tissue will form what is called a cardiac callosity. It consists of white. glistening fibrous strings or cords. The endoeardium will contain spots ofsimilar appcarattce and consistence. The tttttscttlarbundles are frequently thus altered. Such small callus will 11c\cl‘ show any derangt‘tment of function. provided there are not too many. Larger ones will prevent the complete contraction of the heart. Should they be large and yielding, they will gradually fornt a diverticttlttttt itt the cavity. and a so-called anettrism of the heart will be produced. l'urulent myocarditis results. from pya-mic infection. and is brought about by bacteria carried by the corottary arteries into the. tttyocardittttt. There are formed yellowish white orgrayish abscesses. When these break open, ulceration of the heart will be the re- sult: should they break through externally, purulent pericarditis will follow. Extensive myocarditis often causes rttptttre of the heart. (I't't/c Sect, ll. Tabs. »l, :1.) The cattses of myocarditis are generally the same as those of endocartlitis. Ia-ytlen found myocarditis frequently to follow diph< theritis. Itosenbaclt found itt cases of diphtheria granular concrements of the heart iii a state of waxy degeneration. Small pox. epidemic meningitis and recurrent typhus are. according to la-ydeu. often complicated with myocarditis. The Inost frequent cardiac infectious granttlomata are those of a tuberculous. seldom of a sypltilitic nature. The first are generally complications of general tuberculosis, and are mostly found iii the endta-ardiunt of the right ventricle. Large caseous tttasses are tnore seldom than tniliary tubercles. They are generally scquella‘ ot'pericardial result/tat. Itare gunnnatous nodes are found intbedded Ill hyperplastie connective tissue in the cardiac walls, in tlteshape of gray or grayish red foci. either as soft, or dry and friable masses. .\Iore frequently than these sclerotic inflatntnattons of the myocartliunt are to be found in hereditary syphilis. I'rimary fibrous, lipomatous. ntyxomatousor sarcomatous tumors proper are of very rare occurettcc in the heart. The most frequent are the carcinomatous secondary deposits. produced by infections front other parts: ofthebotly. They may occupy any place 111 the heart. 'l‘lteresultsof tumors (outside of the malignitv of their nature) always vary according to their size attd the position they occupy in the heart. attd may range frottt the very mildcst to the most per» nicious grades ofinjury to the organ and to the body. fiI'IXI-IIIAI. I'.\'I'IIH|.(HEY HI" 'l'IIIi I‘Iil‘tlf‘AItltll'M. Inflatnntation oftlte pericardium, the most important of its discases. is connected with exudation. which like those of any other serous membrane, may assume a great variety of forms: and these ntav undergo ntanifoldchanges. some of which may lead to the dcstruction of the person affected. or may not itt tltc least endanger the life or even the health of the person. (‘onheim in his classic researches into the process of inflammation has graphically set forth the successive phases of inflammation of this serous membrane. which are. shortly. as follows: The first stage consists iii the formation ofatt t'Xll‘ltllt' of serum. containing cells. which collect within the tissue Itself and on its surfaces. and is followed by partial disquamation attd destruction of the epithe- |