Chapter 15 of 27 · 17941 words · ~90 min read

CHAPTER II.

PATHOLOGICAL CONDITIONS.

Section I. OF THE TONGUE.

[=Notice= in examination: size; form; surface coated or clean; furrowed or fissured; marks of bites, stains; color generally; vesicles; ulcers; sloughs; tumors, wounds, etc.]

The diseases of the tongue, the appearance of which we may wish to examine after death, include _cancer_, _syphilitic ulcers or tubercle_, _tumors_, _hypertrophy_, _etc._

=Cancer= is the only disease of this organ likely to result in death. It is said to occur more frequently in females than males. It may assume the various forms of this disease, but is more frequently epithelial or scirrhus, than medullary.

=Syphilitic Ulcers or Tubercle=, may be confounded with cancer, and in some instances, only a previous knowledge of the history of the case, assisted by a microscopic examination, would positively determine the diagnosis.

=Tumors= of various kinds—encysted, fatty, fibrous and erectile—may be found in the substance of the tongue, or underneath it in the floor of the mouth.

=Ranula= is a peculiar form of tumor found under the tongue, often attaining the size of a pigeon’s egg, and filled with a watery or albuminous, or sometimes cretaceous matter. The tumor is usually considered as arising from a dilatation of Wharton’s duct, but of this there is doubt in some cases.

=Hypertrophy= of the tongue is sometimes found, where, from an increase of the connective or areolar tissue, without any change in the muscular fibres, the organ has become greatly enlarged, so as to cause deformity of the mouth, or even of the whole lower part of the face. This condition may involve the whole or a portion only of the tongue.

Section II. OF THE LARYNX AND TRACHEA.

[=Notice= in examination: 1. _Contents_—mucus; lymph; pus or blood; amount; foreign bodies; false membranes, etc. 2. _Larynx_—condition of epiglottis; œdema, ulcers, sloughs, polypi; same of superior opening to cavity. _Ventricles_—condition of mucous membranes, etc. _Vocal Cords_—thickness, color, œdema, ulcers, etc. _Cartilages_—condition of; ossification; caries, etc. 3. _Trachea_—contents; mucous membrane; cartilaginous rings; ossification of; caries; denuded of mucous membrane, etc.]

_Inflammation_, _ulceration_, _œdema_, _necrosis of the cartilages_, _tumors_ and _false membranes_ are the more usual pathological conditions of these parts that may claim the attention in a post-mortem examination.

=Inflammation= of the mucous membrane of the larynx (laryngitis) and trachea, will appear as a diffused redness, with some thickening of the membrane, and within which may be traced many _small, congested blood-vessels_. It may be important to distinguish the redness of inflammation, from that attending the early stage of decomposition, which, it is an interesting fact to know, first appears in these parts. Immediately after death, the mucous membrane is _pale_, except in death from suffocation or laryngitis. In a day or two it becomes of a dusky red, which is distinguished from that of inflammation by _the absence of congested vessels_; the redness of decomposition, also, having a superficial filmy appearance, as if washed with dirty wine.

=Ulceration= of the larynx commences in the mucous membrane, but may extend to the deeper parts. The more usual location is upon the epiglottis, or on the margin of the glottis and vocal cords. Impairment of the voice to a greater or less degree, will have attended either inflammation or ulceration of the vocal cords. It is to be borne in mind, however, that aphonia may arise from some impairment of the nerves of the larynx, in which case, a post-mortem examination will fail to reveal any morbid condition of the mucous membrane or vocal cords.

Pulmonary consumption we sometimes find accompanied with the presence of ulcers upon the posterior walls of the larynx, with evidence of inflammation in the surrounding parts. Whether these arise from tubercles in the mucous membrane, or ulceration of the mucous follicles, is uncertain.

=Œdema= of the larynx, is attended with great swelling of the mucous membrane, from serous effusion into the submucous tissues, and frequently attends chronic inflammation of the parts, with ulceration. It may, however, be of an erysipelatous character, occurring as the result of exposure to infection. The surface appears red, pulpy and swollen, from infiltration of the submucous tissue. Œdema of the larynx, is confined to the parts around the epiglottis, and margins of the glottis, never descending below the true vocal cords, owing to the close adhesion of the mucous membrane to the fibrous structure of the cord, without any intervening areolar tissue.

=Necrosis of the Cartilages= of the larynx, may occur in the advanced stage of laryngitis with ulceration. In this manner the epiglottis, with the arytenoid, the cricoid, and even thyroid cartilages may, to a greater or less extent, be destroyed.

=Abscesses= may also form, where the cartilages are so much involved, these in some cases breaking upon the outside, and establishing fistulous communications through which air may escape during respiration.

=Tumors= of the larynx, may be found _first_, outside of the cavity, imbedded in some portion of its tissues; and may include encysted, fatty or fibrous tumors; or, _second_, they may be found in the interior, springing from the mucous membrane, and resembling polypi in their form and structure. They are sometimes granular or cauliflower-like in appearance, and vary in size from a pea to a hazel-nut.

=False Membranes= may be found in the larynx and trachea in fatal cases of croup or diphtheria. In croup, the membrane adheres but slightly to the mucous structure beneath, which will be found red and congested, but may form a complete tubular lining to both larynx and trachea, extending also into the bronchial tubes.[7] It is usually tougher in the larynx and upper portion of the trachea, becoming softer and more gelatinous in the lower portion of the trachea and bronchial tubes. Much difference of opinion has been entertained as to the nature of this substance. It may, however, be considered as a morbid secretion from the inflamed mucous surfaces, in a semi-fluid form, which, in consequence of the presence of albuminous matter, coagulates upon exposure to air.

The false membrane of croup may generally be distinguished from that of diphtheria by the fact, _First_, That the latter is usually confined to the fauces, sometimes extending to the larynx, rarely to the trachea. _Second_, That diphtheritic membrane occurs more in patches, is tougher, is more directly incorporated with the mucous surface beneath, and is removed with more difficulty. _Third_, A microscopic examination shows the membrane to be composed mainly of fibrine in a fibrillated condition, with granular corpuscles and pus cells.

Section III. OF THE PHARYNX AND ŒSOPHAGUS.

[=Notice= in examination: displacements; their cause, as by tumors, etc.; dilatation; contraction or stricture, seat of; calibre at stricture; above, below; condition of mucous membrane; ulcers, etc. Contents of œsophagus; food, foreign bodies, wounds.]

These parts are liable to _inflammation_, _ulceration_, _stricture_, _dilatation_ and _new growths_.

=Inflammation= of these passages, rarely occurs, except as the result of mechanical injury, as from the lodgment of a foreign body, or from swallowing some caustic or highly irritating substance. Catarrhal or croupous inflammation of the mouth and tonsils, may, however, involve a portion of the walls of the pharynx.

=Ulceration= may result from the same causes, and hence may be confined to a small portion or may involve the greater part of the tube.

=Stricture= of the œsophagus may be either _spasmodic_ or _organic_. The former usually occurs in hysterical women, and may result from the irritation following the removal of some foreign body lodged in the canal. Never proving fatal of itself, we seldom have the opportunity of examining a case of this kind.

_Organic stricture_ is found usually at the commencement of the canal, sometimes at its lower end. It may result from contractions attending the healing of an ulcer, but is more frequently induced by a cancerous affection of the walls, or by the projection of some morbid growth into its interior, as from aneurism of the aorta, or tumors, abscesses, &c., in the lungs or left lobe of the liver.

=Dilatation= of the œsophagus may result from the presence of stricture. When the latter is near the cardiac orifice of the stomach, the entire length of the tube may be involved. The walls in these cases may be either thickened or thinned. From the accumulation of food above the point of stricture, the walls gradually yield to the distending force, until a degree of dilatation is attained that is quite remarkable.

=Tumors= of various kinds are occasionally found within the walls of the pharynx or œsophagus including cystic, fatty and fibrinous tumors of a polypoid form.

_Malignant or cancerous_ growths may appear in any part of the tube, the epithelial form being more common. Beginning in the submucous tissue, the disease will soon involve the whole circumference of the tube, to the extent of from one to three or four inches, producing a hardness of the tissues with more or less contraction. Ulceration ultimately taking place, a dilated cavity may take the place of the original stricture.

Section IV. OF THE PERICARDIUM.

[=Notice=: 1. _External characters_—shape; measurement; amount of fat, etc. 2. _Contents_—serum; quantity; color; how affected by heat; blood; quantity; character; source. 3. _Internal surface_—adhesions; their position, extent and character; as firm, soft, etc.]

The pericardium is subject to the same affections as other serous membranes, including _inflammation_, _adhesions_, _effusions_ or _morbid growths_.

=Inflammation= of the pericardium or _pericarditis_, is characterized by an unusual dryness of the surface, with injection of the vessels in the early stage, while at a later period a layer of plastic lymph will be found adhering to the surfaces. The deposit may be limited to some small portion, or be distributed over the whole inner surface of the membrane and upon the exterior of the heart, giving them the appearance of having been smeared over with some sticky substance. Often the surfaces are rough or villous in appearance, like the mucous membranes of the intestines. Irregular calcareous patches are sometimes found in old chronic cases, developed within the thickened portions of the membrane.

=Adhesions= may also form between the surfaces in contact. The whole cavity may in this manner become obliterated, or bands of adhesion may be found here and there.

=Effusions= may be found in the pericardium, as in other serous cavities. When the result of _pericarditis_, the fluid will often contain floating shreds of lymph. Sometimes the fluid will be found highly albuminous, and again bloody or mixed with pus. This effusion may have taken place so early as to have prevented any adhesion of parts; or it may not have commenced until union had taken place at certain parts, when, from the distension of the sac, these bands may be found greatly elongated, and stretching across the cavity in various directions. When the effusion is but part of a _general dropsy_, it will be clear, while the surfaces of the membrane will be smooth and destitute of evidences of inflammation. In quantity, the fluid found in these cases may vary from a few ounces to a pint or more.

_Blood_ may sometimes be found filling the pericardium, either from a wound of its walls, rupture of the heart, or from the bursting of an aneurism. In scurvy, purpura, etc., small patches of extravasated blood may be found in its walls.

=Morbid Growths.= The more common of these, found in connection with the pericardium, are _cancers_. They are usually secondary in their appearance, and generally will have first developed in the mediastinum.

_Fibrous_ or _cystic_ tumors have been noticed in a few rare cases, while _tubercles_ of the miliary form, are not uncommon within this membrane.

Section V. OF THE HEART.

[=Notice=: 1. _In situ_—exact position and relation to surrounding organs; shape; size; degree of firmness or flabbiness. 2. _After removal_—amount and kind of blood discharged from divided vessels; shape of heart; round or elongated; apex formed by which ventricle; amount of fat on surface; relative size of each cavity. 3. _Right auricle_—character and quantity of blood contained; fibrinous clot. Lining membrane; general condition of; foramen ovale; open or closed; thickness, consistence, etc., of muscular walls. Auriculo-ventricular opening; its shape; estimate of size by introducing fingers; rough or smooth; fibrous or calcareous deposits; circumference. 4. _Right ventricle_—nature and quantity of contents; fluid blood; blood clot; fibrinous clot; size; attachments of same to muscular columns; firm or soft; size of cavity; thickness and condition of muscular walls; color, firmness, etc. 5. _Tricuspid valves_—natural, thickened, thinned or contracted; granulations; patches of calcareous matter; degree of flexibility; can they close the opening? Condition of chordæ tendineæ; length, thickness, flexibility, rupture, etc. 6. _Pulmonary opening_—size and shape; smooth or rough. Semilunar valves; thin and smooth, or thick, rough and inflexible; power of closing the opening; will water pass through when poured in from above? 7. _Left side of heart_—observe same as on right. 8. _Generalities_—weight after removal of blood; wounds; morbid growths; abscesses; malformations; aneurism; rupture, etc.]

The several morbid conditions of the heart may be classified as follows:

1. Inflammation │of muscular walls. │Carditis. „ │of serous membranes. │Pericarditis. „ │ „ │Endocarditis. │ │ 2. Diseases of valves. │Thickening. „ │ „ │Ossification. „ │ „ │Atrophy. │ │ 3. Changes in the walls of the heart, │Hypertrophy. influencing the size of the cavities. │ „ │ „ │Dilation. „ │ „ │Atrophy. │ │ 4. Morbid conditions of the walls alone. │Fatty degeneration. „ │ „ │Morbid growths. „ │ „ │Ossification of │ │ coronary arteries. „ │ „ │Malformations. „ │ „ │Abscess. „ │ „ │Aneurism. „ │ „ │Rupture. │ │ 5. Displacements. │Congenital. │Ectopia cordis. „ │Pathological. │Transposition. │ │ 6. Contents of cavities. │Heart clots.

1. Inflammatory Affections.

=Carditis.= Inflammation of the muscular substance of the heart is by no means a common disease, and when present, is probably always associated either with endocarditis, or more frequently pericarditis. We may recognize this condition after death, by the light yellow color of the heart; with a relaxed, flabby, and in some instances a softened condition of the walls. Upon cutting into the muscular walls, there will be found exuding a semi-purulent fluid and often small cavities, varying in size from a pin’s head to a small pea, will be found filled with pus. This condition may involve the whole heart, or may be confined to one or more portions. Inflammation of the muscular substance of the heart, may, undoubtedly, be one of the primary causes leading to aneurism or even to rupture. The symptoms of this disease are not readily recognized during life, being always combined with inflammation of the peri- or endocardium.

=Pericarditis.= Affections of the pericardium have been noticed in the previous section.

=Endocarditis.= Inflammation of the lining membrane of the heart (_endocardium_) most frequently occurs in connection with an attack of articular rheumatism. It may, however, result from blows or injuries of the chest, and has been induced by violent muscular efforts. It is said also, to be often connected with some vitiated condition of the blood, as in pyæmia or Bright’s disease of the kidneys, and has been noticed also in cases of measles, typhus and puerperal fever.

Endocarditis more frequently attacks the left, than the right side of the heart. The anatomical appearances, are a loss of smoothness and transparency of the membrane, with an injected condition of its vessels. Deposits of lymph may be found adhering to the free surface at various points, or to the tendinous cords or valves, giving a roughened, or even warty appearance to all those parts. These may become detached, and swept on with the blood, and finally lodging in some of the arteries of the head or extremities, where they are known as _emboli_, they may become a source of serious trouble. The inflammation may extend to the muscular structure, resulting in softening or the formation of purulent cysts.

It is, however, upon those folds of the lining membrane constituting the valves, and particularly upon the left side of the heart, that the effects of endocardial inflammations are especially manifested. In this way originates most of the so-called

2. Valvular Affections of the Heart.

One of the most common of the results of inflammation extending to the valves, is

=Thickening.= This may depend either upon a deposit of lymph beneath or between the layers of membrane constituting the valves, thus rendering them thick and inflexible while the surface is left smooth, or, at the same time, a deposit upon the exterior may be found, rendering them rough and even warty in appearance, and so stiffened and irregular upon their borders as to greatly interfere with the performance of their functions, and thus permitting _regurgitation_ to take place at the imperfectly closed opening.[8] The tendinous cords, at the same time, may be found thickened, hardened, and contracted, or even ruptured, while the auriculo-ventricular openings may also be found greatly contracted from the thickening of the base of the valves and the fibrous tissues forming the borders of the openings. In one case the contraction on the left side of the heart was so great as scarcely to admit the little finger, while the thumb should readily pass that opening.

The semilunar valves of the aorta are liable to the same changes, their thickened condition preventing their folding back completely into the sinuses of the artery during the systolic action of the heart, or of completely closing the vessel upon pressure from above.

=Calcification.= This condition of the valves may result from a progressive change from simple thickening with fibrinous deposits, to a cartilaginous state, accompanied with so-called bony, or more properly _calcareous_ patches, which may involve large portions of the valves. Ossification of the valves upon the right side of the heart, is but rarely found; upon the left, both the mitral and aortic valves are liable to this affection.

=Atrophy.= The aortic, pulmonary, and sometimes mitral valves, are occasionally found greatly thinned; and this condition may result either in a gradual stretching of the central portion of the valve from pressure of the blood, giving rise to _aneurism_ of the valves, or, it may become _perforated_ with small irregular openings, or, from its weakened condition, _rupture_ may take place, producing sudden death. This condition appears to consist in a gradual wearing away of the substance of the valves, from unusual brittleness of their structure, the result probably of chronic inflammation.

Again, the valves may be found greatly contracted, (_stenosis_) hard and rigid, which will be attended with imperfect closure and consequent regurgitation. Dilatation of the orifices without any change in the valves, may also be found, resulting in the same imperfect closure.

Disease of the valves of the heart, by obstructing the orifices, is likely to result in

3. Changes Affecting the Size of the Cavities.

=Hypertrophy.= Hypertrophy of the heart, is a condition in which there is an increased thickness of its walls, and generally also enlargement of its cavities. Yet there may be thickening—very rarely however—with a diminution in the size of the cavities. It may affect both sides of the heart, but is frequently confined to the left ventricle.

The main cause of hypertrophy of the heart, is the existence of some obstruction to the circulation, either in the heart, or some portion of the arterial system, as by aneurism, pressure of tumors, etc., or by disease of the kidneys. It is most frequently, however, associated with disease of the valves or large arteries. It may sometimes result from continued functional excitement, and generally accompanies cases of partial adhesion of the surfaces of the pericardium, while complete adhesion is more likely to be followed by dilatation or atrophy. On the right side of the heart, hypertrophy is usually the result of some obstruction to the circulation through the lungs, as in an emphysematous condition of that organ.

The following measurements, &c., of the normal heart, will serve as a guide in judging of cases of enlargement:

_Size._ Lænnec has stated, that the heart in its normal condition, is about the size of the closed fist of the individual. This comparison, however, is not very satisfactory. It will be usually found to measure about 5 inches in length, 3½ in its greatest width, and 2½ in its extreme thickness, from its anterior to its posterior surface.

_Weight._ From an examination of four hundred cases, the average weight was found to be 9½ ounces in the male, and 8¼ ounces in the female. In a robust, muscular male, the heart may, however, be found to weigh as much as 12 ounces, and still be normal in all its parts.

_Thickness of Walls._ Right auricle, 1 line; left, 1½ lines. Right ventricle, 1½ lines, and left, a little over 5 lines, or half an inch, at its middle, being a little thinner both at the base and apex.

_Size of Orifices._ Circumference of auriculo-ventricular opening of the right side, nearly 4 inches; of left side, 3½ inches; of the pulmonary artery, 2⅝ inches; of aorta, 2⅜ inches.

When enlarged, the heart may be found measuring 6 to 7 inches in length, as much in breadth, and 12 to 16 inches in circumference. The weight may also be increased to 15, 20 or 25 ounces, and the walls may increase in thickness to nearly a-half inch, and upon the left to over an inch.

Hypertrophy of the heart, has been divided into three forms:—1st, _simple_ hypertrophy; 2d, _eccentric_; and 3d, _concentric_ hypertrophy.

In the first form, the walls are thickened, while the cavities remain unchanged. (Simple hypertrophy.)

In the second form, the thickening of the walls is attended with an _enlargement_ or _dilatation_ of the cavities. (Eccentric hypertrophy.[9])

In the third form, the thickening is attended with a _diminution_ in the capacity of the cavities. (Concentric hypertrophy.)

It has been observed in cases where an examination has been made very soon after a sudden, violent death, attended with loss of blood, as in decapitation, etc., that the cavities have been nearly obliterated, while the walls were greatly thickened. By maceration for a few days, the ventricles have become relaxed to their natural size and capacity. This state of the heart has been observed in persons in whom, during life, none of the symptoms of disease of the heart had been manifested, and hence the condition is to be considered as the immediate effect of the peculiar character of the cause of death.

=Dilatation.= Dilatation of the cavities of the heart, is a condition which may also result from the presence of obstacles or impediments to the circulation, as from ossification of the valves; narrowing of the pulmonary or aortic orifices; employments requiring powerful muscular efforts; and in consolidation, tubercular induration, emphysematous condition of the lungs, or fatty degeneration.

The muscular substance is usually soft and flaccid, sometimes of a violet color, again pale and yellowish. The thinning may be so great, as to reduce the thickest part of the left ventricle to two lines or even less, when the walls will appear to be composed of but little more than a thin layer of fat covered with the pericardium.

Three forms of dilatation are recognized: _active_, _simple_ and _passive_.

Active dilatation is associated with _hypertrophy_ of walls, constituting eccentric hypertrophy.

In simple hypertrophy, the walls retain their _normal thickness_, while the shape may be changed according to the cavity affected.

Passive dilatation, on the other hand, is accompanied with _thinning_ of the walls, and usually results from fatty degeneration, atrophy, or some other change in the muscular fibre.

=Atrophy.= In this condition there is a uniform decrease in the size of the heart. Its cavities becomes small, and its walls thin. It usually attends diseases accompanied with great impoverishment of the blood, as in cancer, diabetes, etc., or may result from obstruction of the coronary arteries from calcification, atheroma or thrombi.

Paget mentions a case where the heart of a cancerous man, fifty years old, weighed only five ounces, four drachms; and that of a diabetic woman, which weighed only five ounces, one drachm. It is usually accompanied with a general wasting of the tissues and organs of the body, and frequently will be found associated with fatty degeneration, which will now be noticed.

4. Morbid Condition of the Walls Alone.

=Fatty Degeneration.= Two forms of fatty diseases of the heart have been recognized. In the first, which should be known as “_fatty growth_,” to distinguish from “_fatty degeneration_,” there is an unusual quantity of adipose matter in those parts of the heart where more or less is usually found, viz.:—Along the furrows through which the vessels run, and particularly about the base of the heart. The fatty masses may dip more or less into the substance of the walls, displacing the muscular fibres, although the latter are generally normal in color and density, even when imbedded in masses of fat. This condition may be found in persons who are otherwise thin, as well as in the obese.

But the more frequent form of fatty disease, is that known as _fatty degeneration_. In this, we find upon opening the heart, that it has lost the reddish-brown color characteristic of the muscular fibre in its normal condition, and is pale, soft and flabby. The whole organ feels soft, doughy and inelastic, much like a heart beginning to decompose. If the wall of the left ventricle be partly cut through, the remainder is easily torn, and the surfaces have a granulated appearance.

Upon the inner surface, beneath the endocardium, numerous small thickly set spots, or sometimes wavy lines, of a pale buff, or light yellow color, may be noticed. This appearance does not depend upon a deposit of fat among the muscular fibres, but rather upon a change in that tissue; and an examination with the microscope, will show fatty degeneration of the fibre.

This condition of the heart, may involve the whole organ, or may be confined to one or more portions. It is much less common in the auricles, than in the ventricles, and more frequent in the left ventricle than in the right. It will be generally found more advanced in the upper portion of the septum of the ventricles, and in the large, fleshy columns of the left side; or it may be found in these columns alone, which accounts for the occasional rupture of the latter.

_Fatty Degeneration_ may be associated with _fatty growth_, or with hypertrophy, or thinning and dilatation, and may be the cause of rupture. The general character of softness, paleness, and mottled color, should lead to _suspicion_ of the existence of this disease, when a microscopic examination being resorted to, the conclusion would be decisive. A small portion of fibre, examined with a power of 300 or 400 diameters, will present, in fatty degeneration, instead of the striated appearance of the normal fibre, a granular appearance, with numerous minute oil globules scattered through the fibre. In the palest part of the heart, the disease will be generally most advanced; but even here, the microscope will show some fibres in a healthy condition, while others around them are rendered completely granular.

Exhausting diseases of various kinds, typhus and other severe fevers, phosphorus poisoning, etc., may result in this peculiar condition of the heart.

5. Morbid Growths.

Under this head may be placed _tumors_, _cancers_, _melanosis_, and _hydatids_.

=Tumors= of various kinds are occasionally found in connection with the heart. _Fibrous_ tumors of a small size may develop within the muscular walls, while _syphilitic_ growths, _cysts_, and _tubercular_ deposits may also, in rare cases, be discovered.

=Cancer.= Cancer of the heart has been noticed in two forms—_epithelial_ and _medullary_. A man, fifty-eight years old, had an epithelial cancer of the eye, which was removed. Two years after, the man died with a large cancerous tumor over the parotid gland. A post-mortem examination revealed a cancerous mass, about an inch and a-half in diameter, imbedded in the apex of the right ventricle and septum of the heart. A microscopic examination revealed its epithelial character.[10]

_Medullary_ cancer of the heart has been usually found associated with the same disease in the lungs and liver, and forms an investing mass which may involve the whole organ.

=Melanosis= of the heart presents the same character as in other parts of the body, and is considered but a variety of the medullary cancer, pigmentary matter being added. It may be developed upon the surface, or may infiltrate the substance of the whole organ.

=Hydatids= have been occasionally found in the heart, the most of which have probably been animal in their character, (_acephalocysts_.) A female, forty years old, who had been suffering pain in the region of the heart for some months, suddenly died, after running rapidly up stairs. One ounce of fluid was found in the pericardium. A considerable tumor was found at the apex of the heart, which slightly fluctuated. This tumor was about three inches in diameter, globular in form, and encroached considerably upon the cavity of the right ventricle. When laid open, it was found to contain a large number of small cysts or hydatids, varying in size from that of a small pea to that of a pigeon’s egg, the space between which was filled with a soft curdlike substance, of a yellow color.[11]

=Ossification of Coronary Arteries.= That condition of the arteries of the heart usually termed _ossification_ is more properly one of _calcification_, consisting of a deposit of hard, gritty, calcareous matter, in which there is none of the true character of real bone, no trace of bone-corpuscle or vascular canals ever being discovered in them. Chemical analysis has shown the deposits to be composed of 50 parts of animal matter, with 47½ of the phosphate and 2 of the carbonate of lime in every 100. This matter being deposited in circular layers, the artery becomes gradually converted into a hard, bony-like tube, which may be traced with the finger along the grooves of the heart through which the coronary artery runs. This is peculiarly a disease of old people, and may accompany a similar condition of the arch of the aorta or of the semilunar valves, and by interfering with the proper nutrition of the heart may result in other forms of disease, as fatty degeneration, dilatation, &c.

=Abscess.= Abscess of the heart, may unquestionably follow an attack of carditis, or inflammation of the muscular substance. The cut surface of the heart in these cases, not unfrequently shows small cavities containing a purulent fluid, and in some instances a distinct abscess is found.

A man, sixty years old, was suddenly attacked, while at work, with coma and great feebleness, followed by death on the third day. The left ventricle being opened, an abscess was discovered near the apex, irregular in form, and containing a bloody, purulent-looking fluid. The coronary arteries were much ossified.

=Malformations= of the heart, are extremely rare in adults, or even in children that have passed the early days of infancy. They consist frequently in arrest of development of the auricular septum, or, in other words, of a patulous foramen ovale, which, by permitting of a mixture of arterial and venous blood upon the left side of the heart, results in early death. I have in several instances found this foramen imperfectly closed in the adult heart, but the opening has been so small—barely sufficient to permit the passage of a probe—as to offer little or no obstacle to the proper performance to the heart’s function. Malformation of the heart is undoubtedly one of the many causes of death in utero, which might be demonstrated by a post-mortem examination.

=Aneurism.= Partial aneurism, or false aneurism of the heart, consists in the formation of a sac or pouch, in some portion of the walls of the organ, communicating with the cavity of the chamber, in the walls of which it has been formed. They may form in any part of the muscular walls of the heart, but are more frequent in the left ventricle. They would seem to result from a separation of some of the muscular fibres, when, by their retraction, a cavity or pouch, of a rounded or oval form results, which, in some instances, has its walls composed of the pericardium alone, there being a complete destruction of the muscular fibres.

The interior of these pouches, may be found filled with layers of coagulated fibrinous deposits, as in the case of aneurism of arteries; or, if they communicate with the ventricular cavity by a large opening, they may be filled with a simple soft clot of blood.

The size of these aneurismal pouches, vary from that of a cherry, to a pigeon’s egg, or larger, when they change much the usual figure of the heart, by their projection upon the external surface.

The following conditions have been supposed to favor the formation of these aneurismal sacs:—1st, softening of the muscular tissue of the heart; 2d, ulceration of the lining membrane; and 3d, rupture of the muscular fibres.

=Rupture= of the walls of the heart sometimes happens, producing sudden death. It may result from severe contusions of the chest, in which case, the auricles are more likely to give way. More frequently, rupture will result from softening of the walls in fatty degeneration or ulceration, or from the bursting of an aneurism of the heart, or from stenosis of the aorta. In the latter cases, the left ventricle will be usually the seat of the rupture.

6. Displacements.

_Changes of Position_ of the heart, are by no means unfrequent. They may be congenital in their origin, or the result of disease in the surrounding organs. Of congenital displacement, we may mention first:

_Ectopia Cordis_, where, from some arrest of development, in the inclosing parts, the heart may be found in some position other than its normal one. From deficiency of the sternum and ribs, the heart has been found protruding from the chest, (_ectopia pectoralis_,) or from absence or deficiency of the diaphragm, it may be found in the abdomen with the abdominal viscera. Such cases live but a short time after birth.

_Transposition_ of the heart is found in those cases where all the viscera, abdominal and thoracic, are exactly reversed in position. A case of this kind was discovered in the dissecting-room a few years ago, by Dr. R. B. Weaver, demonstrator of anatomy, in the Hahnemann Medical College. The heart was here upon the right side, the aorta curving to the left; the liver upon the left; the stomach with its pylorus to the left; the colon commencing in the left iliac fossa; in short, everything completely reversed in position. The subject was a female of about thirty years, and undoubtedly suffered no inconvenience from the abnormal positions.

The more frequent displacements of the heart, however, are those resulting from disease in the surrounding structures. It may be crowded from its normal position, by pleuritic effusions, accumulations of air (pneumothorax), or even by a highly emphysematous lung. Displacements may also result from the presence of aneurismal or other tumors in the chest; curvatures of the spine; or from a hernial protrusion of some of the abdominal viscera through an opening in the diaphragm; or the presence of tumors, enlarged viscera, dropsies, etc., within the abdomen.

7. Contents of the Cavities.

=Heart Clots.= This subject is one that has until recently, been but imperfectly understood; and now even, our knowledge relating to it, is by no means complete. Enough is known, however, to convince us that _heart clots_, are a more frequent cause of sudden death, than has been heretofore supposed.

Having in a recent paper, read before the Philadelphia County Homœopathic Medical Society, quite fully treated of this subject, I shall here merely transcribe the leading points of the same.[12]

_Fibrinous heart clots_, _polypus of the heart_, _or fatty deposits_, as they are sometimes called, differ from ordinary clots of blood, in the absence of the blood corpuscles, and hence, presenting the buff color characteristic of the coagulated fibrin of the blood. Ordinary blood clots, with the corpuscles entangled with the fibrin—and hence presenting the red color of blood—are usually found in the cavities of the heart and large blood-vessels after death, but in greater quantity upon the right side.

_Color._ The shade of color presented by the fibrinous clot varies in different cases. While _buff_ is the prevailing color, the shade varies from a light drab to a decided yellow.

_Consistency._ In this respect a good deal of variation is also found; the difference depending, probably, in part upon the character of the disease, and in part upon the rapidity or slowness of the formation; those of a rapid or very recent formation, having a soft, fatty, or jelly-like character;[13] while, on the other hand, those of a more gradual formation, and with more sthenic forms of disease, acquire a considerable degree of density, the surface presenting a smooth appearance, as if acted upon by a current of blood, and in all respects resembling the dense fibrinous masses, found blocking up the cavities of aneurismal tumors.

_Position._ In every case reported below, the clot has been on the _right_ side of the heart, although in some, a small, soft clot has been found on the _left_. I am not sure that I have ever found one of these clots on the left side of the heart of such a size and consistency, or under such circumstances, as to have led me to suppose that it might have been a cause of death.

The body of the clot is usually found in the ventricle, extending from this, either up into the pulmonary artery, or through the opening into the auricle. In all cases, the clot has been more or less entangled with the tendinous cords of the valves and muscular columns of the heart, requiring, in some instances, considerable force to tear it away from its attachments.

_Time of formation._ An important question to be decided in regard to these heart clots, is the time of their formation. Are they _ante_ or _post_-mortem in their origin? And upon the solution of this query depends the conclusion as to whether they are the _cause_ or the _result_ of death in the cases where found. That a fibrinous clot may sometimes be formed in the coagulation of the blood _outside_ of the body, is a fact well known; as in the blood drawn from patients suffering from acute inflammatory affections, where, from the retarding of the coagulation, the blood corpuscles, from their greater specific gravity, have time to fall towards the bottom of the vessel, thus giving the “buffy coat” to the upper portion of the clot. The same cause—retarded coagulation—unquestionably may give rise to a clot _in the heart_ after death, presenting the same character, viz., with the upper portion, of the buff, fibrinous character, while the lower portion, from the presence of corpuscles, will present the appearance of an ordinary blood clot. Such clots are not unfrequently found after death.

But have we any evidence that the fibrin of the blood may be deposited, forming clots within the vessels during life? In proof of this, we have only to refer to the result of the application of a ligature to an artery; where the interval between the point of application and the first vessel coming off above, will be filled with a fibrinous clot, which performs an important part in the closing up of the vessel; or, to the well-known deposits of fibrinous layers within aneurismal tumors, sufficient, in many cases, to so fill up the sac as to result in a cure; therefore, the favoring conditions being present, it is not unreasonable to claim that fibrinous clots _may_ form within the heart, of such size and in such positions as to be an immediate cause of death.

_Causes._ In looking for the causes, or conditions promoting the formation of these fibrinous deposits, we have to consider, first, variations in the character of the blood itself; and secondly, peculiarities in its circulation and in the circulatory apparatus. Fibrin, one of the normal constituents of the blood, is estimated by physiologists as forming from 2 to 3 parts in 1000, while it may fall as low as 1, or rise to 7½ parts. We find it reduced to the minimum quantity in all diseases which present a hæmorrhagic tendency, as in true typhus, yellow fever, certain malignant forms of disease, and as the effect of many poisons, both animal and vegetable. In these cases, the loss of fibrin results in the effusion of blood into the tissues, producing petechial spots, or upon the mucous surfaces, giving rise to epistaxis, black vomit, hæmaturia, etc., while very feeble, if any, coagulation of the blood will be found after death.

In scurvy, however, where we have a condition of the blood not unlike that above referred to, there appears to be a marked tendency to the formation of clots, as has been noticed by many observers, and as has been verified by Dr. J. C. Morgan, in several cases which came under his notice while in the army.

But it is in cases where there is at least a _relative increase_ of fibrin, that heart clots are more liable to form. Such a condition we find in cases where, while the fibrin remains normal in quantity, the water of the blood, the menstruum in which the fibrin is held in solution, is below the normal standard, this reduction favoring the tendency to deposit. Thus, in all cases where there has been an exhausting and rapid flux from the bowels, as in cholera, or excessive purging from drastic cathartics, or from the colliquative sweating of phthisis, we have the favoring condition, and death may be the immediate result of a fibrinous clot in the heart.

The _most_ favorable condition, however, for the formation of heart clots, is undoubtedly that in which there is an _absolute_ increase of fibrin, and this we find in a large number of diseases marked by acute inflammatory symptoms; as in pleurisy, pneumonia, diphtheria, croup, acute rheumatism, erysipelas, puerperal fever, etc. In a large number of deaths from these diseases, a post-mortem examination would undoubtedly bring to light a heart clot, which has at least served to hasten, if it has not been the immediate cause of the fatal termination.

Again, the formation of heart clots is evidently promoted by any circumstances or conditions, resulting in great feebleness or languor of the circulation, independent of variations in the amount of fibrin. A complete stasis of the blood is certain to be followed by coagulation; as in employment of pressure in the treatment of aneurism; so in cases of great prostration of the powers of life, attended with extreme feebleness of the circulation, as 1st. In cases of shock, where life is not immediately destroyed; 2d. In certain cases of poisoning, as by opium, where the action of the heart is greatly depressed; and 3d. In syncope, either with or without loss of blood. In all of these cases the danger of the formation of the heart clot is very great, and probably in a large number this is the immediate cause of death.

It is a fact well established, that loss of blood, either by hæmorrhages or venesection, is followed by an increased coagulability of that fluid; hence, the fearful hæmorrhages which sometimes attend parturition, if accompanied with syncope, are in great danger of being followed by the formation of the heart clot, and thus ending in death.[14]

Another circumstance tending to promote the formation of fibrinous clots in the heart, is evidently to be found in the peculiar formation of the valves guarding the auriculo-ventricular openings. It is well known how fibrin may be collected from fresh blood, by beating the same with a bundle of twigs, the latter soon becoming coated with shreds of fibrin; so the _chordæ tendineæ_ and fleshy columns of the heart, between which the blood is continually being driven, affords convenient points for collecting the same from the feebly circulating or overcharged blood; and from the close intermingling of the tendinous cords, with the substance of the clot, it is probably upon these that the deposit first begins to form.

In explanation of the fact that fibrinous clots are almost universally found on the _right_ or _venous_ side of the heart, notwithstanding that arterial blood is richer in fibrin than venous, the following has been suggested to my mind: _First._ While venous blood contains a smaller proportion of fibrin, may not its deoxydized condition favor the more ready deposit of this substance, than by the more highly vitalized arterial blood? _Second._ The feebler muscular power of the right side of the heart would necessarily be attended with a slower circulation through its cavities, the partial stasis of the blood giving another condition favorable for the formation of a clot; and _Third._ The valves of the right side of the heart, present three flaps or folds, instead of two as on the left, and hence, with their numerous tendinous cords, offer an increased number of obstructing points, around which the deposit may be made. These several circumstances would seem sufficient to account for the admitted fact.

_Symptoms._ The symptoms attending the formation of fibrinous clots in the heart, are usually sudden in their accession, frequently attended with a chill, and marked by great oppression in breathing, coldness of surface, and _pallor of face and lips_, the latter symptom distinguishing from the dyspnœa attending croup, asthma, pneumonia, etc., where the face is _livid_ from venous congestion. The pulse is usually rapid and feeble; the action of the heart labored, palpitating, and sometimes intermitting, while auscultation will reveal a tumultuous churning-like action, the normal sounds being quite undistinguishable.

Pulsation of the jugulars will be present in most cases, and where the clot greatly obstructs the play of the tricuspid valves, a double pulsation will be likely to be noticed. In the last stage, a copious cold perspiration appears upon the whole surface of the body.

As might be anticipated, fibrinous formations, while of small size, are sometimes washed away from their attachments and swept on with the current of blood into the arteries and carried to distant parts of the body, as is sometimes the case also in aneurism, thus producing the embolic masses often found blocking up arteries in different parts of the body. When upon the right side, the embolus would be carried into the pulmonary artery, obstructing the circulation through the lungs, and producing symptoms more or less grave, according to the size of the clot. Upon the left side of the heart, from the greater force of the circulation, these bodies are probably more frequently swept away from their attachments and carried into the aorta, and thus on, perhaps, through the carotids to the head, or into the subclavian, or down the aorta, finally lodging in some of the branches of the lower extremities. Convulsions, paralysis, etc., are not unfrequently produced by the lodgment of emboli in some of the arteries of the brain, while, when carried into the arteries of the extremities, pain, falling of temperature, impairment of sensation, contraction of muscles, atrophy, and even gangrene may result.

The following examples will serve to illustrate the class of cases to which I refer:

CASE I.—_Death from Heart Clot in Anæmia._

A lad, 11 years old, and very anæmic, went to school in the morning in his usual health; while there was taken with a chill. On his way home vomited freely. The chill lasted for a long time, and was accompanied with an oppression in breathing, which gradually increased through the day and night, and until the time of my first visit at 11 o’clock A. M. the next day. I then found him extremely pallid, lips bloodless, perspiring freely, suffering from great restlessness and distress, with extreme dyspnœa; mind wandering, pulse irregular and feeble; action of the heart very tumultuous, the normal sounds being unrecognizable. In the neck noticed a rapid rolling pulsation of the jugulars, which presented two beats to one of the artery at the wrist.

At my second visit, made at 4 o’clock P. M., the patient had just expired.

The autopsy, made twenty hours after death, gave the following results: Upon opening the abdomen found the liver presenting a dark mottled appearance, and highly congested; other abdominal organs natural; pericardium contained about one ounce of serum. Upon opening the right auricle of the heart, found a firm fibrinous mass, extending downwards through the ventricular opening, and which, upon the latter cavity being opened, was found firmly attached to the tricuspid valves, and entangled with the fleshy columns and tendinous cords.

The presence of such a body in this position, and with such attachments, it was evident, must have so interfered with the passage of the blood from the auricle to the ventricle, as, upon the contraction of the former cavity, to have caused a backward pressure into the veins, and thus have produced the _first_ of the double pulsations of the jugulars.

Again, the position of this clot, preventing the closure of the valves upon the contraction of the ventricle, there would have been a regurgitation into the auricle, and the same backward flow into the veins, thus producing the _second_ pulsation of the jugulars seen during life.

CASE II.—_Death from Heart Clot in Pregnancy._

A lady, 28 or 30 years old, also very anæmic, and three months pregnant, had been suffering occasional fainting spells. For some days before her decease she had suffered from dyspnœa, and on that day, after ascending a flight of stairs, fell upon the floor, and before a physician could be obtained breathed her last. A post-mortem showed all the thoracic and abdominal viscera in a healthy condition, while the right side of the heart contained a large fibrinous clot, with attachments similar to those found in Case I.

CASE III.—_Death from Heart Clot in Diphtheria._

A boy, 3 years old, had an attack of diphtheria. The case presented no unfavorable symptoms until about the fourth day, when he was taken with great restlessness and oppression in breathing, and while sitting on the chamber at stool, suddenly died. The autopsy here again revealed the heart clot, as in the other cases.

CASE IV.—_Death from Heart Clot in Consumption._

A man, 30 years of age, a furrier by trade, was suffering from tubercular disease of the lungs. He had never given up his work, though he was much reduced in flesh, had a bad cough, diarrhœa, and night sweats. While at his employment, he was one day taken with great oppression, increased cough, etc., and in twenty-four hours expired.

The post-mortem showed that, while the upper portion of both lungs contained large deposits of tubercles, there were no abscesses, and the lower portions presented sufficient sound lung tissue to have maintained life. Upon opening the heart the usual fibrinous clot was found in the right ventricle, extending upwards into the auricle.

CASE V.—_Death from Heart Clot in Rheumatism._

A strong colored man, of 25 years, had an attack of inflammatory rheumatism. The disease presented the usual characters, the inflammation wandering from joint to joint. During the second week he was suddenly attacked with great difficulty in breathing, violent and irregular action of the heart, and great distress, followed by rapid prostration and death. The post-mortem examination revealed thickened tricuspid valves, with a firm clot of large size adhering to the same.

CASE VI.—_Death from Heart Clot in Debility._

A gentleman, 55 years old, who had been for some time in feeble health, was taken, upon rising in the morning, with oppression and distress in the region of the heart, dying in twelve hours. The heart clot was found here, as in the other cases, upon the right side of the heart.

CASE VII.—_Heart Clot in Death from Over-dose of Morphia._

A gentleman, of about 50 years, a physician, was found one morning dead in his bed. His health had been previously good, excepting that he was troubled with neuralgia which gave him sleepless nights, and for which he sometimes took morphia. On the night previous to his death he came home and retired at a late hour. An open bottle of morphia and small spatula were found on his desk next morning, the spatula showing evidence of having been thrust deeply into the morphia, and probably a large and over-dose carelessly removed and taken. The autopsy here again revealed a large and firm fibrinous heart clot.

CASE VIII.—_Death from Heart Clot in Acute Gastritis._

A lady of about 60 years, had an attack of acute gastritis, but was considered convalescing, and her physician (Dr. Martin) made his last visit in the evening. The next morning she was found dead in her bed. The post-mortem showed the spleen somewhat enlarged, and its capsule greatly thickened.[15] Other organs healthy, while the heart contained an unusually large fibrinous clot, which has been preserved in the College Museum.[16]

The above include the more marked cases of death that have come under my notice, where that result could, in my mind, be fairly attributed to the formation of fibrinous clots in the heart.

The following inferences may, we think, be fairly deduced from the several cases reported:

_First._ In some instances the fibrinous clots are apparently the _sole cause_ of death. (Cases 1, 2, and 3.)

_Second._ In other, and a larger number of diseases, as in acute rheumatism, pneumonia, croup, etc., which otherwise would recover, a fatal termination results from the formation of heart clots. (Cases 3 and 5.)

_Third._ In still other diseases, which are of themselves necessarily fatal, as in phthisis, cholera, etc., death is often hastened by these formations. (Case 4.)

Section VI. THE AORTA AND ARTERIES GENERALLY.

[=Notice=: 1. _Before Opening Vessel_—size; course; condition of external coat and surrounding tissues. 2. _After Opening Vessel_—character of blood within; coagulated or not; size, color, consistence, etc., of clot; size of canal; thickness of walls; rigid or flexible. _Lining Membrane_—smoothness; transparency, etc.; readiness of detachment; thickness, etc.; if rough, the apparent cause; fibrinous, atheromatous or calcareous deposits. _Middle Coat_—its thickness; color; deposits within, and their character. _External Coat_—general condition.

ANEURISMS:—1. _External Characters_—size; shape; is the dilatation lateral or general in its relation to the vessel? Openings as seen externally; size, position, etc.; blood effused; quantity, etc. _After opening, notice_—contents; blood fluid or coagulated; fibrinous contents; laminations; their thickness; number; density; dryness; difference between outer and inner layers. Channel for blood: size; character of inner surface; how formed? Walls of aneurism: how formed; by all, or one coat of artery. Size of artery above and below aneurism.]

The diseases of the aorta, and of arteries generally, which may claim attention in a post-mortem examination, are _inflammation_, _fatty degeneration_, _calcification_, _aneurism_, and _rupture_.

=Inflammation.= This process may be found involving either the outer or inner coats of arteries. In the former case the walls appear thickened and infiltrated with a soft, jelly-like substance, which appears, at a more advanced stage in some cases, to degenerate into a purulent condition, while in others, great thickening of the coats, or even obliteration results. Inflammation of the inner coat generally precedes atheromatous or calcareous deposits, and is mostly confined to old persons. The roughened inner surface thus produced, may serve to collect fibrinous shreds from the blood, and thus be the occasion of the formation of emboli.

Inflammation of arteries may result from injuries, from the presence of emboli, or may be spontaneous in its origin. While the more frequent seat of the disease is in the aorta, it may occur in any other artery.

=Fatty Degeneration=, or atheromatous disease of arteries, is an important affection of those vessels, and is usually associated with aneurism. It is seen more frequently in the arch of the aorta, and consists in the presence of fine white streaks, situated in the substance of the lining membrane. The disease may be found in children as young as from three to seven years of age, but is more common with adults. As the disease advances, the middle coat becomes involved. The streaks gradually change into large, white, opaque patches. The middle coat becomes thinned, loses its elasticity, assumes a gray, semi-transparent appearance, and, at a later stage, becomes soft and cheesy, and sometimes even undergoes a form of liquification into a creamy fluid resembling pus, but dependent upon the abundant formation of fat globules, with scales of cholesterine and granular matter.

While these destructive changes are going on in the inner and middle coats, and tending to their rupture, by a conservative process, the outer coat, upon which the strength of the vessel mainly depends, becomes thickened and strengthened by the accumulation of plastic matter.

=Ossification.= Ossification of the aorta, like that of the coronary and other arteries, consists rather in a process of _calcification_. The deposits are largely confined to the arch, and consist mainly of patches of calcareous matter of various sizes. We seldom find the whole circumference of the vessel involved, as in the case of smaller arteries. The aortic valves will generally be found more or less loaded with the same deposits.[17]

=Aneurism.= This disease is said to occur more frequently in the aorta, than in any other artery. It may be developed in any portion of this vessel or its principal branches, but is more commonly found in the arch. The walls of the vessel being weakened by fatty degeneration, they become less and less able to resist the pressure of the contained blood, and gradually yielding to the systolic force of the heart, become more and more distended, until the complete aneurismal sac is formed.

Aneurism may be either _true_, in which there is a dilatation of all the coats of the vessel, or _false_, where there is rupture of the inner, and perhaps also of the middle, and dilatation of the outer coat alone. The latter form, when developed upon the aorta, may become very large, and by pressure, cause absorption of the sternum, costal cartilages and ribs, and even of the clavicle.

In some cases, the inner and middle coat having ruptured, the blood instead of being confined in a sac formed by the outer coat, becomes diffused between the middle and outer, or between the layers of the middle coat, thus constituting what is known as _dissecting_ aneurism. In these cases, the blood may extend the whole length of the aorta, and even upwards upon the carotids to their bifurcation.

In an examination of an aneurismal sac, the _true_ aneurism will be recognized by the walls presenting all the coats of the artery, and generally by the indication of the presence of atheromatous and calcareous deposits, which are confined to the inner and middle coats. In these cases also, the communication between the sac and the aorta is large and free. If the aneurism be _false_, however, there will be an absence of those deposits, the opening into the artery will be comparatively small, and the inner and middle coats will terminate abruptly at its margin.

The interior of aneurismal sacs will usually be found containing a quantity of fibrine deposited from the blood, and arranged in concentric layers. In color, these fibrinous layers are of a light buff, the outer layers being dry and firm, while the inner ones are softer and more moist, and the central portion, at the same time, filled with a dark mass of coagulated blood. A spontaneous cure will sometimes be effected by a complete blocking up of the sac with fibrinous deposits, thus preventing further dilatation or danger of rupture.

The following case, which has been before reported,[18] shows a combination of both true and false aneurism, with spontaneous cure of the latter:

CASE.—_Spontaneous cure of aneurism of ascending portion of arch of aorta, with death from bursting of aneurism of descending portion into the œsophagus._

Mr. H——, of this city, aged sixty years, while walking in his yard one day after a hearty dinner, was taken with a sudden sensation of faintness and nausea, which was soon followed by vomiting the contents of his stomach, with a considerable quantity of blood. After entering his house, the vomiting was frequently repeated, and at each effort large quantities of pale blood ejected. Sinking rapidly, in an hour he was dead.

Twenty-four hours after, I made a post-mortem examination. Upon exposing the chest, found at the right border of the sternum, just below the clavicle, a hard, inelastic tumor beneath the skin, of the size of a small orange. While not adherent to the integument, it appeared firmly attached to the walls of the chest beneath. Upon turning aside the integument and pectoral muscles, the tumor was found connected by a long pedicle to parts within the chest; absorption of considerable portions of the sternal ends of the first and second ribs, with the side of the sternum, having resulted from pressure of the tumor upon those parts, and finally permitting its appearance beneath the skin.

The removal of the sternum at once demonstrated the aneurismal character of the tumor by showing its connection with the ascending portion of the arch of the aorta, while a section of the same, exhibited the interior filled with dense concentric layers of fibrinous matter, separable from one another, the outer layers being dry and hard, while the inner portion was less firm and moist. This aneurism was plainly of the _false_ variety. The neck of the tumor was not much larger than the thumb, and of sufficient length to reach from the arch of the aorta to the dilated sac beneath the skin, outside the chest.

A further examination of the aorta brought to light a second and _true_ aneurism of the descending portion of the arch, the dilatation involving all the coats of the vessels, and which, having _burst into the œsophagus_, explained at once the cause of the hæmorrhage and sudden death.

Upon inquiring of the family, I learned that the tumor upon the chest had been known to have existed for fifteen or twenty years; that for some years the pulsations of the tumor were strong, but that for many years all beating had ceased; that he had never discontinued his work, that of a carpenter, and in fact, it had given him so little trouble that he had never consulted a physician in regard to it. For a year or so previous to death, he had been troubled with a cough, particularly upon exercising, but otherwise had been in good health.

A remarkable and interesting feature of this case was, the little inconvenience experienced by the patient from so grave a malady, and one usually attended with great suffering.

=Rupture.= Spontaneous rupture of the aorta is a very rare occurrence, and probably never happens except the coats have first been weakened by disease. Hence, in all of these cases, there will be found atheromatous softening, and generally thinning of the walls by dilatation. In this condition, some violent muscular effort may result in rupture at the most weakened point, and this will be generally at that portion of the aorta within the pericardium, the external coat being weaker here than at any other point.

Where the dilatation of the diseased and weakened vessel has resulted in the formation of an aneurism, rupture of this will be the more frequent termination. This may take place into the œsophagus, as in the case reported, or into the trachea, the pericardium, either pleural cavity, or upon the surface of the body.

Rupture of the coronary arteries, of the arteries of the brain, various branches of the abdominal aorta, and arteries of the extremities, have occasionally been found, when softened by fatty degeneration or atheromatous disease.

Section VII. THE PLEURA.

[=Notice=: _Condition of membrane_—inflamed; extent and position of; thickened; transparent or opaque; rough or smooth. _Contents_—blood, gas, serum, pus, amount and probable source of. _Adhesions_—general or local; firmness of, etc.]

Like other serous membranes, the pleura is liable to _inflammation_, both acute and chronic, with their results—_plastic_, _serous_, or _purulent effusions_, _adhesions_, etc.

=Inflammation.= The first change which is observed in inflammation of the pleura (pleurisy) is a loss of the shining, transparent appearance of that membrane, it becoming dull and opaque. Red injected vessels, in minute ramifications, sometimes radiating from single points, in others more uniformly diffused, will be noticed. Often the surface will present a red mottled appearance, with here and there small points of extravasation. This condition having existed for from six to twenty-four hours, certain results follow—at least in the acute form—which give rise to what is known as

=Plastic Effusion.= Soon after the inflammatory process is fully established, there will appear upon the surface a small quantity of clear fluid, which, as it increases in quantity, undergoes coagulation, and thus gradually covers the surface with a jelly-like layer of variable thickness and honey-comb surface. A thin fluid of a straw color, will be found oozing from the surface, which is increased as the coagulated membrane is cut or torn. This condition may be extended over the whole surface of both the costal and pulmonary pleura, or may be confined to a limited portion.

=Adhesions.= The two layers of the pleura being in immediate contact, the consequence of this effusion of coagulated lymph will be an early adhesion of the applied surfaces. This is accomplished by a blending of the layers of coagulated matter in contact, and a gradual organization of the same by an extension of blood-vessels from the pleura into the new formation. At the same time that these changes are progressing, the watery part of the exudation trickles down to the most dependent portion of the cavity, and there forms a serous or sero-purulent accumulation. Adhesions are more frequent at the upper portion of the lungs, but may be found at any point, as between the inner surface and the mediastinum, or the lower surface and diaphragm; or, from repeated attacks of pleuritis, involving different portions of the serous membrane, the whole of the exterior of the lung may become united to the adjoining surfaces.

The strength of the adhesions will be somewhat in proportion to their age, those of long standing requiring considerable force to break them up, and in many instances the lung tissues becoming lacerated before the attachments can be torn away.

Unusual thickness of the pleura is often found at points where no adhesions exist, this being unquestionably the result of the effusion of plastic matter into the subserous tissue during an attack of inflammation.

=Serous Effusion.= While in the majority of cases of pleuritic inflammation, we shall find _plastic effusions_ followed by adhesions of the inflamed with the adjoining surface, in some instances a serous or watery fluid is rapidly poured out, and, accumulating in the pleural sac, constitutes _hydrothorax_ or dropsy of the chest. The fluid in these cases may present a variety of shades of color, from a pinkish or light straw color, to a dark brownish shade. It may be transparent or opaque, and generally will be more or less albuminous. The quantity may vary from a few ounces to three, four, or five pints, or more. When in large quantity, the lung will be found more or less collapsed, shrunken, and pressed against the posterior walls of the chest and spinal column.

In the general dropsy attending diseases of the heart, kidneys or liver, effusions may take place into the pleural cavities, to such an extent as to give rise to great dyspnœa from compression of the lungs.

=Sero-Purulent or Puriform Effusions=, consist in the presence of a quantity of granular particles with albuminous matter, which subside to the bottom of the vessel when drawn off, and always contains floating flakes of lymph. It may be found in cases of both acute and chronic pleurisy, and, like serous effusions, may be found in large quantity.

=Purulent Fluid=, as found in the cavity of the chest, consists of a white or cream-colored, opaque, and homogeneous fluid, combined with more or less albuminous matter, in the form of shreds and flakes, yet destitute of the granular matter of the sero-purulent fluids, and not separating into a fluid and solid portion when at rest, as is the case with the latter.

It is a fact well established, that genuine purulent matter may be formed in the pleural cavity, as well as in other serous cavities, without ulceration of any portion of the surface, or discharge of an abscess into the same, it being the result of a more advanced stage of the process which gives rise to the serous or plastic effusions. It may be secreted directly from the capillaries of the inflamed surface, or, in some instances, it would appear to be derived from the organized false membranes, which have taken on a suppurative action.

=Pneumothorax.= Air may enter the pleural cavity, by perforation of the walls of the chest from external injury, or, as is more common, by the destruction of the pulmonary portion of the membrane, from the bursting of a distended air-cell, or from softening of tubercular deposits, or bursting of an abscess. If there are but few or no adhesions, the accumulation of air in the cavity may be accompanied by a more or less complete collapse of the lung, as in hydrothorax. This condition, during life, is not readily distinguished from emphysema, both being accompanied with similar oppression in breathing, distension of the chest, and displacements of the heart, and with increased clearness on percussion. Serous or sero-purulent effusions will frequently accompany the presence of air in the cavity, and thus give rise to many of the peculiar physical signs which may have been noticed during life, as metallic tinkling, a splashing sound on shaking the chest, etc.

Section VIII. THE LUNGS AND BRONCHIAL TUBES.

[=Notice=: 1. While _in situ_—degree of collapse; adhesions; position and character of; wounds, etc. 2. _After removal_—external character; color; peculiarity of shape; adhesion of lobes; puckerings at apex; solid or compressible; crepitation; where most noticeable; effect of inflation on color and size. _Tubercular deposits_—size; location. 3. _Substance of lung_—solid or porous when cut; extent of solidified portions; fluids escaping; character and quantity of. _Abscesses_—position; number; size; character of contents; color; odor, etc.; condition of lung around cavities; character of walls; thick or thin; smooth or rough; crossed by bands; communication with bronchial tubes. _Gangrene_—location and extent of. _Bronchial tubes_—contents; contraction or dilatation; measurements at, above and below these points; condition of mucous membrane; congested or ulcerated; walls of tubes; thicker or thinner than natural. _Extravasation of blood_—(apoplexy of lung;) portion and extent of lung involved; condition of surrounding tissue; blood infiltrated or encysted. _Adventitious deposits—cretaceous bodies_; situation; size; density; condition of surrounding tissues. _Tubercles_—seat; size; number; color; density, etc.; condition of surrounding tissue. _Cancerous masses_—size; location, etc. _Carbonaceous deposits_—around bronchial tubes; beneath pleura. _Result of placing entire lungs in water_—do they sink or float? If they sink, is it rapidly or slowly? If they float, is it above, below, or at the surface of the water? Results with portions of each lung.]

The pathological conditions of the lungs, may be arranged as follows:—_Inflammation_ and its results, _hepatization_, _suppuration_, _abscess_, _gangrene_, _hæmorrhage_, _pulmonary apoplexy_, _emphysema_, _tubercular disease_, _morbid growths_, and _parasitical animals_.

When in a healthy condition, the lungs will present the following appearance:—Upon opening the chest, there will be a more or less complete collapse of both organs, partly from atmospheric pressure, and partly from the elasticity of the lung tissue. They will then have a shrunken, shrivelled appearance, crepitating under pressure, and have an ashen gray color. If inflated, the surface becomes smooth and shining, showing an indistinct outline of the lobules, which, with the dark pigmentary matter seen here and there, gives the surface more or less of a mottled appearance.

Where pleurisy had previously existed, there may be adhesions preventing the collapse of the lungs, until these have been broken up. When cut into, healthy lung tissue has a soft, spongy character, the upper portions will be quite destitute of blood, while the posterior portions may be more or less filled with that fluid from gravitation, giving them a dark congested appearance.

Inflammation and its Results.

=Pneumonia=, or inflammation of the lungs, may affect both the air cells, when the latter become filled with fibrinous exudations, and the connective areolar tissue, which then become increased in quantity.

The following characters present themselves, corresponding to the three recognized stages of the disease:—First, _congestion_; second, _red hepatization_; third, _gray hepatization or softening_.

=Congestion.= From the peculiar structure of the lungs, in connection with the free circulation through the same, these organs are peculiarly liable to the several forms of congestion. In many cases of death, without any original disease of the lungs, there will be a tendency for these organs to become loaded with blood, giving rise to post-mortem appearances, often with difficulty distinguished from those of a pathological origin. In this post-mortem, or, as it has been called _hypostatic_ congestion, the posterior and inferior portions of the lungs are chiefly affected, as the blood after death, obeying the law of gravitation, sinks to the lowest point. The congested portion presents a dark red color, and though firmer than other portions, crepitates under the finger and floats in water, the latter circumstance serving to distinguish this form of congestion from that of an inflammatory origin. If the congestion be confined to one lung, or to the anterior parts of either, we may safely attribute it to a pathological cause.

In all cases of congestion, upon opening the chest, although there may be no adhesions, the lung does not collapse, or does so feebly. When cut, it is found to be loaded with blood, and upon pressure, much bloody serum escapes, while the divided bronchial tubes will be found filled with frothy mucus.

=Red Hepatization.= This condition of the lungs soon follows that of congestion. The change is a gradual one, and is first marked by an effusion of serum and coagulable lymph into the connective tissue and air cells, thus rendering the lungs more solid, while as the change becomes complete, the blood itself, which had during the congestive stage been confined to the vessels, is now found extravasated into the interstices of the tissues. The portion of the lung thus affected is not only of a dark red or violet color, but solid, firm, does not crepitate, sinks when thrown into water, and when cut and washed, the section shows patches of a rough, granular aspect, totally different from that of healthy lung tissue. The pleura in this condition may be wholly unchanged, even though the solidification may have been of long standing.

=Gray Hepatization=, which characterizes the third stage of pneumonia, is known by the lung presenting a firm, semi-solid, inelastic, and more or less incompressible character. Failing to collapse, the lung is found more or less completely filling the chest. The pleura will generally present evidences of inflammation in the presence of patches of lymph and more or less points of adhesions. The upper lobe may be soft and compressible, while the lower is solid from hepatization. When divided with the knife, the substance is found of a gray, red, or dirty yellow color; compact, but friable and easily broken down with the fingers, while the smaller bronchial tubes are filled with fibrinous plugs. Bloody purulent matter, with much turbid serous fluid, will ooze from the cut surfaces. Pus globules will be detected in the escaping fluids by a microscopic examination.

_Resolution_ of a hepatized lung, consists in the gradual softening of the effused substances within the smaller bronchial tubes and air cells, and the discharge of the same by cough and expectoration.

Inflammation of the lung usually commences in the lower lobe, and while the disease here may extend to complete hepatization, the middle lobe may be found merely congested, while the upper is quite healthy. Inflammation may attack one or both lungs. In the former case it is known as single, and in the latter as double pneumonia. From an examination of a large number of cases, it has been ascertained that inflammation of the right lung is more frequent than that of the left in the proportion of about three to one, and that single pneumonia is more common than double pneumonia in the ratio of six to one.

Pneumonia is sometimes divided into _Catarrhal_ and _Croupous_. In the former, the exudation contains little or no fibrinous matter, while the bronchial mucous membranes are also involved, the disease at the same time being confined mostly to the lobules of the lungs. In the _croupous_ form, the exudation contains a large proportion of fibrine, and the disease usually involves the greater part of a lobe, or may extend to the whole of one or both lungs.

Both forms of the disease may run through the three stages of congestion, red and gray hepatization.

A peculiar form of inflammation of the lungs, found mostly in children and young persons, and usually chronic in character, has been described as

_Lobular Pneumonia._ The inflammation here being confined to the lobules, these, after the disease is perfectly developed, present the appearance of a multitude of rounded nodules, of the size of small nuts, scattered through the substance of the lungs. The exterior of these is reddish, firm, and vascular, while the interior is of a grayish color, containing effused lymph, with more or less purulent matter.

This form of pneumonia being frequently associated with diseases of the joints and bones, as well as with inflammation and ulceration of the glands of the intestines, it has been considered as depending upon a strumous diathesis, and as, in fact, but the early stage of tubercular consumption. Seldom proving fatal in the early stage, or before the disease has extended to the whole substance of the lung, and perhaps resulted in the formation of cavities, we much less frequently meet with this form of pneumonia in post-mortem examinations.

=Suppuration and Abscess.= Gray hepatization must be looked upon as a form of _suppuration_ of the lungs; as the purulent-looking fluid found infiltrating the tissues, filling the air cells and smaller bronchial tubes, upon a microscopic examination, is found containing undoubted pus globules. This, however, is not an abscess, the matter not being confined within a cavity, but diffused through the tissues of the part. That a distinct abscess of the lungs may form, as a result of pneumonia, is generally admitted, though they are usually small and confined to the lower lobes. From softening of tubercular masses, abscesses not unfrequently form in any portion of the lungs. That they do not occur more frequently in pneumonia, may result from the fact that the disease often proves fatal by suffocation, before there has been time for it to have reached the suppurative stage.

The pleura over the seat of the abscess will generally be found much thickened, and frequently adherent to the opposite walls of the chest. Pulmonary abscess may be wholly discharged by expectoration—the cavity communicating with the bronchial tubes—or it may discharge into the pleural cavity, or when adhesions have first formed, it may work its way between the ribs, and the matter escape upon the surface of the body.

=Metastatic or Secondary Abscess.= This form of abscess in the lungs, is well understood to be the result of suppuration in some distant part or organ, which, being attended with phlebitis of the part, purulent matter is introduced into the circulation, and thus conveyed to the lungs or perhaps the liver. This original suppuration may be at the uterus after delivery, or from a fistulo in ano, psoas abscess, or any other similar affection.

From the fact, probably, that the whole volume of the blood flows through the lungs, at each round of the circulation, these organs are more frequently affected with this form of abscess than any other, it occurring next in frequency in the liver. These abscesses may be recognized as spots of yellow pus, varying in size from a pin’s head to a walnut, generally situated near the surface of the organ and surrounded by a dark, well defined layer of congested tissue, while beyond this, the structure is in a healthy condition. Several of such abscesses may be found in various parts of the lungs.

=Gangrene.= Gangrene of the lungs, rarely results from an attack of ordinary pneumonia, but appears more frequently to take place either as a concomitant of pestilential fevers in general, or as an accompaniment of certain cases of tubercular vomicæ of the lungs, or as a primary and peculiar species of inflammatory affection of those organs.

In the first instance, a patient suffering a severe form of typhoid fever, presents symptoms of pulmonary disorder, as hurried respiration, livid face, cough, first dry and soon moist, with thick orange-colored and finally dark or bloody and extremely offensive expectoration, and fetid breath. With these symptoms are generally associated great feebleness, delirium, with tendency to gangrene of the extremities and prominent points of the hips, sacrum, etc.; and finally, with increased difficulty in respiration and fetor of breath, death ensues.

In the second case, a patient suffering from clearly recognized tubercular disease of the lungs, which has passed on to softening of tubercular masses, and the formation of vomicæ, has an aggravation of all his symptoms, accompanied with the expectoration of a highly offensive dark matter, plainly resulting from a gangrenous condition of the interior of a tubercular cavity.

In the third case, the disease comes on at first as an affection of the lungs. The attack commences either as pulmonary inflammation, or bronchial disease, or with spitting of blood with more or less pain in the chest. The patient becomes rapidly worse, the cough increasing, with reddish-brown or bloody sputa, and offensive breath. The countenance is anxious and livid, the eye heavy, sometimes wild and glaring. The fetid breath is not always an early symptom, but when it does appear, the disease in general tends rapidly to a fatal termination, although recovery sometimes takes place.[19]

The appearances after death, in cases of gangrene of the lungs, are of two kinds, according as the disease is _diffuse_ or _circumscribed_.

“In the _first_ case, a mass of lung, two and a-half or three inches wide, but irregular in figure and outline, is converted into a soft, pulpy, dark, ash-colored substance, which, when it is handled or pressed by the fingers, falls down into a loose, moist mass, emitting a fetid, offensive odor, without trace of the usual structure of the lungs, except a few bronchial tubes, and blood-vessels, and shreds of filamentous tissue. This mass is generally bounded by, but it does not terminate abruptly in, healthy lung. It is soft, dingy, and infiltrated with a dark, ash-colored, dirty, serous liquor. Occasionally the surrounding portion of the lung is hepatized or infiltrated with blood or bloody serum; the bronchial tubes always contain much bloody, viscid mucus; and sometimes the pleura is reddened, covered with lymph or adhesions, and contains fluid in its cavity.”

The portion of the lung thus affected is usually within the lower or middle lobe, the upper portion being rarely involved.

In the _second_, or _circumscribed_ form, a portion of the lung, generally near the surface, presents a dark-colored, hard patch, varying in size from a quarter, to a half-dollar piece or more, often quite circular, and bounded all round by healthy lung. This circular hard patch, which resembles closely an eschar produced by caustic potash, may adhere or be easily detached. In the latter case, it generally leaves a cup-like cavity, the surface of which is firm, granular, with the blood-vessels and bronchial tubes closed, and with the surrounding lung more softened, but generally presenting marks of pleurisy, pneumonia, and bronchitis all combined, which may be looked upon as an effort of nature to isolate and detach the diseased mass.

=Pulmonary Hæmorrhage=—_Hæmoptysis_. Discharge of blood from the lungs by coughing, may result from a variety of causes, among which may be mentioned: 1, mechanical shock or injury, as in falls or blows upon the chest; 2, inflammatory action within the lungs; 3, disease of the heart; 4, disease of the arteries; 5, tubercular deposition; 6, tubercular destruction, with ulceration of vessels.

In the first instance the expectorated blood may be copious or slight, according to the severity of the injury. If death soon results, an examination of the lungs will disclose one or more of the bronchial tubes filled with blood, which has plainly arisen from a rupture of some of the capillaries of the bronchial mucous membrane. The blood discharged in many cases of the early stage of consumption, and in young females after the suppression or retention of the menstrual flow, is from the same source.

Hæmorrhage from the lungs may also take place as a result of tubercular deposits. The presence of tubercular masses must necessarily produce more or less pressure on the adjoining vessels, interfering with the flow of the blood through the same, and thus inducing congestion, and even rupture of some of the capillary branches. Again, where tubercular masses have progressed to softening, and a cavity has been formed, the ulcerative process may open a large vessel, and death result in a few minutes from excessive hæmorrhage. A post-mortem will here show the cavity, as well as the bronchial tubes and trachea, filled with coagulated blood.

The blood expectorated during the early stage of an attack of pneumonia, is never copious, consisting mainly of streaks of blood through the saliva, while at a later stage, from being more uniformly diffused, it gives the peculiar _rusty sputa_ characteristic of this disease. The post-mortem appearances have already been given under the head of _pneumonia_.

Certain forms of disease of the heart, as ossification of the mitral valves, with contraction of the orifice, or in hypertrophy of the left ventricle, with disease of the aortic valves, are frequently attended with hæmoptysis. In either case, the obstruction to the free circulation through the left side of the heart, must induce an over distension of the pulmonary veins, which, upon some unusual exertion, may readily result in extravasation through the bronchial mucous membrane, causing the bloody expectoration which takes place during life, or into the pulmonary connective tissue, giving origin thus to what is known as

=Pulmonary Apoplexy=. The post-mortem appearances in these cases, are as follows:—The portion of the lung involved, fails to collapse on opening the chest. It is firm, and of a dark red color; and when cut into, thick blood issues from the cut surfaces. The portion involved may include from one to four cubic inches. It will be found circumscribed with healthy lung tissue, and looks not unlike a clot of venous blood; these circumstances serving to distinguish it from hepatization, which terminates more or less gradually in sound lung.

While these hæmorrhagic effusions may, in many cases, cause early death by their size and number, in others, the clot may soften, the lung around become inflamed, or even gangrenous, resulting in the formation of an irregular cavity filled with dark, offensive, semi-fluid contents. In still other cases, where the clot is small, and in part within the air cells, it may soften and become absorbed or coughed up, and the air again enter the cells, or these may contract into a fibrous indurated mass.

=Emphysema.= Emphysema of the lungs, is usually described as of two forms—_vesicular_ and _interlobular_.

_Vesicular emphysema_, consists essentially in a dilatation or over-distension of a greater or less number of air cells, resulting in giving the portion involved greater buoyancy in water, from diminished specific gravity, lessening the crepitation on pressure, preventing collapse on the opening of the chest, and rendering the affected portion more or less dry and bloodless. From the loss of elasticity, there will be during life, a difficulty in the lungs emptying themselves of air as they should, hence the patient will be subject to severe attacks of oppression upon the slightest aggravating cause. If one lung only is affected, the corresponding side becomes enlarged and less movable than the other; the adjoining viscera, as the heart or abdominal organs, are more or less displaced, the intercostal spaces swell out, and the ribs becoming more horizontal, give a barrel-shape to the chest, which is quite characteristic of emphysema.

This distension of the air cells, is more marked along the edges of the lungs, the vesicles at these parts being probably the least supported. Patches of dilated cells may be found, however, at other parts, which, if superficial, will project beyond the surface of the surrounding healthy portions, and appear like large bladders, from the coalescing of several vesicles.

This form of emphysema may be induced by any cause interfering with the ready escape of the air from any portion of the lungs, especially if accompanied with severe cough, as in many forms of bronchial disease, enlargement of the bronchial glands, etc.

_Interlobular Emphysema_, consists in an effusion of air into the connective or areolar tissue of the lungs, from a rupture of air cells or smaller bronchial tubes, or from the laceration of the lungs from a broken rib, when the air may accumulate in the pleural cavity, constituting pneumothorax, and may also be accompanied with emphysema of the chest, neck and head, from an escape of the air at the point of injury into the tissues of those parts. This form of emphysema may involve a large part or the whole of the lung, while the vesicular form is generally limited to definite portions. By disturbing the circulation through the lungs, emphysema is liable to induce dilatation of the right side of the heart.

From an evolution of gases within the lungs after death, we may have similar appearances to that above described, requiring some care to distinguish between the two. In the latter case, the general indications of decomposition, with the ease with which these distended vesicles may be emptied by pressure, will aid in determining the character of the case.

Tubercular Disease of the Lungs.

I shall not attempt to present here the various theories that have been promulgated as to the nature and origin of tubercle, contenting myself by giving a description of their anatomical characters, as presented in the several stages of tubercular disease.

_Tubercle_, or tubercular matter, may be described as consisting of a yellowish-white substance, opaque, friable and unorganized. It may be deposited in most of the tissues or organs of the body, but its more common seat is the free surfaces of mucous membranes, though often found in connection with the serous.

Tubercular deposits in the lungs, are not uniformly distributed through all parts of those organs, being in the large majority of cases confined to the upper and back part of the upper lobes, and in those cases where they are more or less distributed through the whole lung, they will be found more numerous and larger in those parts.

Tubercles may exist as fine points, not larger than a pin’s head, (_miliary tubercle_,) or the matter may accumulate in masses of the size of a kernel of corn, of a cherry, or of a robin’s egg. In other cases, the pulmonic exudation in some portion of the lung attending an attack of pneumonia, may become transformed into tubercular matter, having an irregular outline and no distinct boundary, (_infiltrated tubercle_.)

Tubercular matter is undoubtedly, in most instances, deposited within the air cells, so filling these, as to more or less interfere with the admission of the air, and giving greater density to the portion of lung involved. While the secreted matter is at first soft, or semi-fluid and partially translucent, it gradually acquires greater density, becomes opaque and cheesy in its character, and in all respects acting as a foreign body within the lungs. Sooner or later, the presence of tubercles will excite inflammation in the surrounding tissues. In this manner these bodies may become softened and their substance expectorated. If large numbers be aggregated together, the ulcerative process may completely destroy the tissues between, an abscess or vomica resulting.

In the early stage of the disease, before the inflammatory and ulcerative processes have been set up, the presence of tubercular matter, by interfering with the capillary circulation, may give rise to a hæmorrhage into the bronchial tubes, constituting the hæmoptysis so frequently present in this disease; while at a later period, from a destruction of some of the larger vessels from ulceration, a profuse and even fatal hæmorrhage may result.

Post-mortem Appearances.

In examining the lungs of those who have died after suffering the usual symptoms of pulmonary consumption, we shall find the upper portion of one or both lungs, more or less indurated, and occupied by one or more irregular shaped cavities, containing either air, or air and a quantity of viscid, puriform, dirty-looking fluid. Generally the apex of the affected lung, will be found firmly attached to the inner surface of the chest, by means of a thick, firm, false membrane, which unites the two layers of the pleura. In some instances, nearly or quite the whole surface of the lung will be found thus adhered, while the lobes will also be united by an interlobular false membrane. When the adhesions are confined to the upper portions of the lungs, the pleura covering the lower portion will frequently be found more or less rough from albuminous exudation, while a quantity of sero-purulent fluid will be found in the posterior part of the thoracic cavity.

The greater part of the upper lobe, may be found converted into one irregular cavity; more frequently, the upper lobe presents two or three, either isolated or communicating. The largest, when several are present, is most commonly in the upper portion of the lobe. When entirely or partially filled with matter, such cavities are usually termed _vomicæ_ or abscesses, while when empty, they are generally called _tubercular cavities_ or excavations.

In the lower part of the upper lobes, the cavities are few and small. The middle lobe of the right lung, rarely presents cavities, while the lower lobes of both lungs are entirely free. The whole of these parts, however, may be more or less indurated by the presence of hard, irregular shaped masses, the result, probably, of inflammatory action.

_Tubercular cavities_ present a considerable variety, both in size and shape. They may not be larger than a pea, or bean, or may reach the size of an egg, or even of an orange. Always of an irregular shape, they often consist of one large cavity, communicating with two or three smaller ones. The interior will be found traversed by bands, or cords, passing in various directions, but generally taking a longitudinal course, and probably the remnants of blood-vessels and bronchial tubes.

The tissues immediately around a cavity, and forming its walls, will be found firm, inelastic, almost cartilaginous in character, and of a dark red, or brown color. The density of the structures is caused partly by tubercular deposits in the lung, and partly by inflammatory induration.

While tubercular disease of the lungs is almost universally fatal, there is reason to believe that, in a very small proportion of cases recovery has taken place, and the post-mortem appearances of the lungs have accorded with this view. These appearances may be described as follows:

We sometimes observe in examining the lungs of individuals who may have died from diseases of other organs, that the pleura covering the upper lobe of the lung, presents, at a certain point, a puckered, shrivelled appearance, with a leather-like feel, and with a rounded, firm mass beneath. Upon dividing the latter with the knife, the interior is found composed either of a soft substance like putty, or more frequently of a chalky nature. This is looked upon as a cicatrized or contracted vomica, the putty or chalk-like contents being the residuary matter of the softened tubercle, the thinner portion having been expectorated or removed by absorption. In some instances, these bodies are of almost a stony hardness, grating against the knife.

In other cases, cavities lined with a smooth, semi-cartilaginous false membrane are found, containing air only, and with dilated bronchial tubes opening into the same, no appearance of ulceration being visible, everything indicating that a tubercular mass had once occupied the cavity, its softening and expectoration having been followed by a healing of the inner surface.

Morbid Growths.

=Cancer.= Malignant disease of the lungs is by no means frequent, yet we have abundant evidence that cancer in its several forms may be developed in these organs. Colloid cancer, has been usually found more or less infiltrated through the substance of the lungs, while other forms appear in nodules or isolated tumors.

It is seldom, perhaps, that cancer exhibits itself as a primary affection of the lungs, the disease first appearing in some other part, and more frequently, it is said, in the bones or testicles; operation for the removal of cancer in these parts being very liable to be followed by an early development of the disease in the lungs or other internal organs. On the other hand, where the cancer is connected with any organ whose veins form a part of the portal system, as the stomach, spleen, pancreas, intestines, etc., the disease does not so frequently extend to the lungs, while in those cases the liver is more liable to become affected.

The _encephaloid_ form of cancer, is that more frequently met. It may be connected either with the bronchial glands, when the diseased mass will be mainly confined to the mediastinum, and may consist of bodies varying in size from that of a cherry to that of a large apple, or, the disease may commence directly in the substance of the lungs, the tumor rapidly increasing in size, and crowding the lungs from their normal position. After death, the encephaloid mass may be found compressing the lungs into a very small space. The tumor presents the usual character of this disease, some of the lobules being soft and pulpy, or brain-like, others of a more firm, cheese-like consistence.

=Melanosis.= Two forms of melanotic deposits are observed in the lungs: one, _true melanosis_, and frequently associated with encephaloid disease; the other a deposit of carbonaceous matter from coal dust, smoke, etc., which has been inhaled during life, and distinguished as _spurious melanosis_.

_True melanosis_ consists in a deposit of a dark pigmentary matter in the substance of the bronchial glands, found at the bifurcation of the trachea, and along the main bronchi. The glands are at the same time enlarged. The coloring matter may be solid, or slightly fluid, or pasty. At the same time the melanotic matter may be infiltrated to some extent into the substance of the lungs, or deposited in cysts within the same.

In _spurious melanosis_, the dark carbonaceous matter is diffused more or less through the whole lung, and may be seen distinctly through the pleura. The bronchial mucous membrane is more or less tinged with the same substance, and generally a quantity of black-colored fluid may be expressed from the cut surfaces.

=Hydatids.= Acephalocysts or animal hydatids, have not unfrequently been found in the lungs, and in several instances they have been discharged by expectoration.

These cysts vary in size from a cherry to an egg, and consist of a double membrane containing a limpid fluid within which other hydatids may be found, of the same character as the parent cyst. They may excite inflammation and suppuration in the tissues around, and thus become discharged into the bronchial tubes, the pleural cavity, or through the diaphragm into the abdominal cavity.

_Cystic_, _Fibrous_, _Cartilaginous_, and other forms of tumors, are occasionally found in the lungs, and, while they are generally small, they may acquire such size as to become a source of trouble during life.

The Bronchial Tubes.

The examination of the trachea and bronchial tubes in post-mortem examinations, is too frequently omitted. The lungs having been removed from the chest, they may be readily opened along their posterior aspect, and the bronchial tubes traced into the substance of the lungs. The pathological conditions of the bronchial tubes which may claim our attention, are _inflammation_ in its various forms, _obliteration_, and _dilatation_.

=Bronchitis.= Bronchial inflammation has been divided into two varieties, according to the portion of the tubes affected. In one case the disease may be confined to the large and medium sized tubes; it is then known as _tubular bronchitis_. In the other, it is seated principally in the terminal ends, where the lining membrane is more delicate, and the tubes much smaller, and from this, extending to the air cells, forms what has been called _vesicular bronchitis_. The latter form is closely allied to pneumonia; in fact the two diseases pass into each other, and in most cases probably coexist.

Ordinary, or _tubular bronchitis_, is not often a fatal disease, hence we cannot speak accurately of its anatomical characters; yet, being frequently associated with other forms of fatal disease, we have opportunities of examining it under those circumstances. The lining membrane is then found thickened, rough, of a dark red or brown color, with more or less contraction of the calibre of the tube, and covered with a viscid, jelly-like mucus, often streaked with blood, and in some cases of a puriform character. This form of bronchitis may occur as a primary disease, or it may accompany tubercular consumption; is frequent in cases of heart disease, and may arise in the course of typhoid fever, measles, scarlet fever, and small-pox.

_Vesicular bronchitis_, from its involving the smaller tubes and air cells, is much more frequently fatal than the tubular form of the disease, although in fatal cases the two forms will usually coexist. In a post-mortem examination of these cases, we find the bronchial membrane red and injected, pulpy and thickened. In a more advanced stage, the air cells and smaller tubes are filled with a viscid, puriform mucus, which prevents the air from reaching the vesicles during life, and the lungs from collapsing upon opening the chest after death. Minute ulcers are not uncommon upon the mucous membrane, the effect of these, being that of changing the character of the secretion from a transparent mucoid, to an opaque purulent form.

Bronchial inflammation, as has been stated in another place, may result in emphysema of the lungs. In these cases, a valvular-like obstruction is produced in some of the bronchial tubes, which, offering little impediment to the entrance of the air, interferes with its escape, and thus by producing increased pressure upon the air cells supplied by the obstructed tube, a gradual dilatation or rupture ensues, resulting in the former case in vesicular, and in the latter, in interlobular emphysema.

Disease of the heart may also result from chronic bronchial inflammation. Not only respiration, but the circulation may be so impeded as to exert a direct influence upon the heart. From the difficulty which the blood encounters in flowing through the branches of the pulmonary artery, the main trunk of that vessel becomes permanently dilated, while the right ventricle, from the increased force required to overcome the obstruction in the lungs, becomes gradually dilated, and at the same time, perhaps, hypertrophied. From the union of the two ventricles, the excessive action of the right may induce a similar action in the left, and thus in time result in that hypertrophy of both ventricles, which is sometimes found in persons who have suffered from chronic bronchitis.

=Narrowing or Obliteration of Bronchial Tubes.= In some cases, in carefully tracing the bronchial tubes, we may find either a remarkable narrowness of the vessel, or a complete closure of the same. In the former cases, there is a distinct thickening of the walls of the tube, by an effusion of lymph, or blood and lymph, into the submucous tissues; or, from induration of the lung tissue around the smaller bronchial tubes, from tubercular or other deposits, a similar narrowing may result from external pressure.

Complete closure may be found in any portion of the tubes, in the large trunks, arising from the main branches, as well as in the smaller branches. They may be detected by passing a blunt probe into the tubes. The branches will frequently be found continuing from the points of closure, as a fibrous cord. The most common seat of these closures is in the upper lobe of the lung, yet they have been found in the lower lobes.

The causes of obliteration of the bronchial tubes is not well understood, yet, they are more frequently observed in persons who have suffered repeated attacks of bronchitis, or of chronic pneumonia.

=Dilatation of the Bronchial Tubes.= This condition of the bronchial tubes is more frequent in its occurrence than obliteration. It takes place in two forms, either several tubes are uniformly dilated, like the fingers of a glove, or a single tube may form a cavity, by undergoing a sacular enlargement. Some mechanical obstruction, by interfering with the free passage of air through the tubes, will usually have caused the difficulty, as an enlarged bronchial gland, pressing one of the bronchi. Here the free exit of the respired atmosphere being prevented, an accumulation of air takes place behind the narrowed point. Any impediment to the entrance or exit of the air into the lungs will produce irregular and forcible breathing, and throw a greater strain upon those parts especially which are in the vicinity of the obstacle. If, at the same time, the patient suffers an attack of asthma, bronchial catarrh, or whooping-cough, the violence of the cough materially aids in developing the dilatation.

The degree of dilatation is greatly variable. Tubes which, in their natural state, are not larger than a crow-quill, may, especially in the lower and middle lobes, reach the size of the finger, while at various points, sacular dilatations may occur, which at first sight may appear as vomicæ, but which upon more careful inspection, prove to be dilated portions of the bronchial tubes. The tubes in this state are usually filled with a puriform fluid, upon the removal of which the lining membrane is seen to be reddened and softened, or perhaps ulcerated.

This condition of the bronchial tubes may frequently be detected during life. The voice is hoarse, like a person in croup. The cough is also hoarse and brazen, while the breathing is difficult, and mucus rattling is heard in the middle or lower portion of the lung.

The post-mortem appearances in cases of _foreign bodies_ in the bronchial tubes, may be readily anticipated and easily recognized.

The Mediastinum.

_Inflammation_ may arise in the anterior mediastinum, from fracture or caries of the sternum; and in the posterior, from injury, inflammation, caries, or necrosis of the vertebræ. This inflammation may also result in the formation of an

_Abscess_; or, ulceration and perforation of the œsophagus, or inflammation of the lymphatic glands may lead to the same results. These abscesses may reach large size, resulting in displacement of the heart, and may rupture into the pleural cavity, the trachea or œsophagus.

_Tumors_ of various kinds, may also develop within this space, including the several forms of _cancerous growths_. The latter will frequently have their origin in the bronchial or lymphatic glands, or, perhaps, in the remnant of the thymus gland.

PART III. THE ABDOMEN AND PELVIS.