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Show DISH ASES ()I‘1 THE ()RGANS ()F RESPIRATIOX. Siit‘TioN 1H,] TABLE V". Fios. 1, 2, 3.-Branchicctrts/s. Curiii'cs_frn'iize(l in. Hm Rig/71f Limo. (Vet/ration (II/(l Circeinscribed Gangrene. (‘.\s1‘:.--.\. man 53 years old. JIisz‘ory-For years he was occasionally seized with fits of epilepsy. The last ten years he was ail'ected with bron- chial catarrh and astlnna. He had rep ‘atedly very prot'use haemorrhages and suffered for years with shortness ofbreath. Com/[tion (UH/ Symptoms S/IOI'H'I/ before (Ic(li.‘/i..-lle lies flat on his back, and is almost unable to occupy any other position. ,1 [is breath is intolerably fetid, and expectorates copiously. large masses of yellowish white, cohesive sputa. of an equally horrible stench. l'ulse almost normal. Per- cussion: dull sound over the posterior portion of the right lung. Ausculfm‘fona moist rale on the same side; the left lung sounds normal. Diagnosml: circawiser/"(ml jut/mo- nmy/ gangrene. Excessive lnemorrhage a day later. The blood is foamy. of a bright red. and without odor. The next day. bronchial respiration and bronchophony at the inferior angle and infraspinous space of the right scapula, extending a few inches inward. beyond that region. Dull sound continues; spitting of blood and diarrh ‘a to a, greater orless extent for several days. A few days before death 7 a support, to the putrid mass. A second, though smaller gangrenous 'avity. situated in the apex ofthe same lung, (1". (£13., Fig. '1) of more recent date, contained a ragged mass adherent to the wall of the cavity. and held together by several small arteries. A third cavity (1". (£13., Fig. 2) is visible in the very center of the same lung, a portion of a large bronchus which communi 'ated with it was gradu- ally corroded and partly obliterated. In the thickest por- tion of the pesterior border of the same lung. :1 large eavity (F.(r'.1t'.. Fig. 3), very sinuous and multilocular, com- municated with seve ‘al bronchi; the lining membrane ofthe tube was very dense, fibrous, and of a reddish brown color. It contained no shreds ot'the tissue. but a quantity of gran- ulating conglomerate extended from the walls. which were. shrunk by cicatrization. This *avity was situated beneath the spinous portion of the scapula where the bronchophony washeard. The destruction extended to the pleura (1'.E.). and had death not arrested it, a communication with the javity (F. (I. (1., Fig 8) would have been formed. (1". G. (7.. Fig. 1) is a cavity in a state ofpartial cicatrization. Around all these cavities not a trace of acute or chronic inflam- mation y'as found. There was no change of color ol‘thc remnants of perivaseular structures in a high state of putrefaction. The vessels escaped destruction and served as impermeable tissue, which was soft, and infiltrated with a brownish serum, which escaped readily 011 the slightest pressure ot'the structures. The older gangrenous portions were surrounded by a. layer of very indurated tissue (in- veterate oedema and dark gray indu 'ation). The balance of the lung tissue was soft, of bluish color, and equally much infiltrated Very voluminous fibrous bands of inter- stitial tissue (Figs. 1, 2, 3) crossed thelung in every (lirec- tion. Theinternal surface of the bronchial mucous incin- brane was intensely red. (13., Fig. 3) shows an opened bronchus. The pulmonary artery and its branches pre- sented a number of plaques on their internal surface (Al. 0., Fig 3). The vessels in the gangrenous portions were filled with thrombi; in the 11¢mgangrenous they were free. The left lung was nearly normal, so were the brain and the abdominal viscera. he becomes exceedingly w ‘ak, is unable to eat, and has a, constant desire for strong drink. during an attack of htemoptysis. Dies from exhaustion Post fifertent P/maomead-'llhe whole of the right thoracic cavity is filled with partly clotted and partly liquid blood of a very recent date. The source of the luemor- rhage is a large rent at the base of the right lung, which is attached to the diaphragm (F 0.1)., Fig. 1), and from which escaped a quantity of clotted blood and portions of decayed lung tissue into the thoracic cavity. (0.5. clots), (E, decayed lung tissue.) By enlarging it, the rent y'as t need to a gangrenous cavity (F. 0.1)., Fig. 2), contain- ing sphacelous debris. These proved on examination to be of inflammation, and differs from the purely cellularinfiltration in lower lobes are emphysematous and enormously enlarged. many of its consequences. It passes invariably into caseous degeneration, especially when inflammation is subacute, and affects a red hepatized parts are now turned into a gray substance, moist and glistening. \Vithin these are scattered prominent dense masses Whole lobe. Catarrhal pneumonia passes certain phases of development. only not so constant as the fibrinous. The phases, according to Fried- which have now lost their grayish-white color (SEC. 111, TAB. VI. lander, are as follows: 1. Hyperzemia and oedema (engoumcnt), which either quickly disappears or passes into, 2. Red hepatization, which might also be re-dissolved and disap- pear, or pass into either of the following phases. 3. Desquamative, transparent, gray hepatization, which consist of a process of exfoliation of the alveolar epithelium, and occa- sional filling up of their spaces. It does not directly pass into the caseous condition. 4. Small-celled or whitish gray hepatization, which beginsin the earliest stages of the inflammation, and speedily spreads to the ad- jacent portions of the lung tissue. This may' also pass into resolu- tion when the inflammation is originally not intense; otherwise it invariably leads to castration. The infiltrated portion isatlirst sur- rounded by red hepatization, and eventually passes into the desquamative state (Size. Ill, TABLE Ill, Figs. 1, 2). In'the hyperzemic stage the tracheal and bronchial mucous membranes are intensely red, and covered with much mucous and pus. A considerable portion of the lung tissue contains no air, the upper lobe or lobes are usually perfectly infiltrated. The lowerlobes are only infiltrated in spots. In the air cells there is some serum, some bloated epithelial cells. a few colored and coloilcss eorpuscles and some fibrin. ted hepatization occasionally involves a whole upper lobe; the tissue is not so dense as in the filn'inous form, and is usually intermingled with gray, giving it a marbled appearance. Here and there white dense masses of difi'erent sizes project above the red portion, and are perfectly bloodless, opaque and dry. The larger bronchi are usually filled with tough, purulent mucous. A cut- surt'ace of a hepatized part will show small yellow spots; they are transverse sections ofsmall bronchiol.‘ (Sec. 111. 'll.\n.\'l,l*‘ig. 7). Great quantities of fibrinousdeposits are found uponthe pleural surfaces. The red portions contain red corpuscles, variable quan- tities of fibrin and small-celled elements and quantities of exfoliated epithelium. In the grayish-\i'hite infiltrated portions the air cells are. turgid, with densely-crowded small, colorless corpuscles, and compress the interalveolar septa. The capillaries are obstructed. The larger vessels are either partly empty, or filled with a dispro- portionately large quantity of colorless blood col'puscles. Thein- terstitial tissue accompanying the vessels and bronchi are of double or triple the volume of the normal and filled with the same smallcelled elements. The irritation caused by the infiltrate causes the inner coats of the artericsto proliferate, and the space betweenthe endothelium and the elastic laminzr becomes filled with cellular elements. When the disease process is primarily not intense, in the early stages of liel'iatization, there may still be a prospect for recovery by softening and absorption. 3111 when from the begin- ning there has been very extensive serous and sanguinous extra- Fig. (3, 13.13.), and become ycllow caseous. The They differ in size (Fig. chi-141.). The bronchi of the infiltrated portion are dilated and filled with a yellow thick pus. The colored blood corpuscles of the red hepatization have now disappeared and are replaced in the air cells by colorless corpuscles and large swollen epithelial cells, easily rec- ognizable by their vesicular nuclei; only a few lymphoid cells are to be found (desquamative stage). As the air cells are notnow turgid, the capillaries are filled with blood. The septa are now infiltrated with lymphoid cells, and the air cells contain some serum. In the grayish yellow infiltrated portion(Si£c. Ill, TAD. 1V, Fig.1.) a condition of far advanced stage of fatty degeneration of the cells exists. The whole structure has lost its contours, and is converted into a uniform caseous mass, involving bronchi, vessels and lung tissue. Close to the pleura such a condition suImrinduces purir lent pleuritis (Slit). lll, TAB. 1V, Figs. 1, ‘2 . In the desquamative form we find at this stage ancnormous pro- liferation of the interstitial tissue. It has a distinctly gelatinous, transparent, grayish appearance, especially in the perivascnlar and peribronchial portions. leer the microscope they present a fine, granulating tissue, and in all stages of development, from the spher"lithin the septa a number of wide oid to the spindle-shaped. lymphatics, filled with lymphoid b0dies,surround the arteries. Cell- proliferation in the coats of the artery commences later than in the perivascular structure, but then it goes on with great vigor. lt involves segments of the vessel, and the cellular elements consist of spheroid and large connective tissue cells. A little later large cells make their appearance in the alveoli. near the exfoliated cells. They are sometimes of a size to fill up a whole air cell,and contain as many as fifty nuclei. They usually occupy the pcriphcrry of the cell (giant cells). The nuclei rt seinblc those of the inononuclear epithelial cells, and probably are of vasation, the upper lobes especially. are completely infiltrated and the same origin as these. At this stage the progressive processes of the disease have reached their maximum height. Under favor- able circumstances softening of the histological elements and their absorption may take place, and the debris be expectoratcd. (in the other hand, where the bronchi are obstructed by too great quanti- ties of dcbris, and these are lodged within their cavities for any length of time, dilatationot‘the cavity ensues. ln thecascons portions no change takes place. The tissue becomes more and more atrophic from lack of nutrition: the affected portions approach each other by shrinking of the atrophic tissue, and the bronchi become more and more dilated and filled with turbid liquid pus. Although desquamativc pneumonia invariably passes into ('it>(‘ous. it does not necessarily follow thatthe latteris always pl'otlilced bv the former. The transition of the desquamative into caseous is brought about when from any cause (such as obstruction ot‘ihc vessels. or in the bronchi) the exfoliated epithelial cells cannot be removed from the centerot'the air cellszthey undergo necrotic change, and though they may liquil'y. the same obstructions will prevent their elimination or absorption. This will cause a further exfolia- contain no air: the lower are in the same condition at the hilus. affected parts have increased in volume. are tough and heavy. of thc newly-ext'oliatcd epithelium, which will accumulate as an The The tion from the walls of the air cell, and a still further degeneration |