Part 13

The accumulation of fat under physiological conditions is obviously brought about, on the one hand, by those causes which permit a free introduction, absorption, and deposition, and, on the other, by those which check its oxidation or elimination with the secretions of the body, as the bile, in which it may be present to a considerable extent. A diet rich in fat, or in albuminates readily converted into fat, offers a favorable element for the absorption of fat by the healthy individual. If the organism demands but little of this fat for oxidation, as in the case of the sedentary person, an accumulation is likely to occur. This may become so considerable that obesity results. Tissues in which normally but little fat is accumulated may become infiltrated to a large extent. The intermuscular fibrous tissue thus becomes loaded, and the activity, as well as the nutrition, of the muscles is impaired. This accumulation may be manifested not only in the voluntary muscles, but in the heart as well, which may present abundant sub-pericardial and sub-endocardial fat, the myocardium also being interlarded with streaks of fat, the so-called fatty infiltration of the heart. The abdominal walls may become thickened to the extent of a couple of inches, and the mesentery, omentum, perinephritic tissue, and liver may become enormously increased in weight from the mass of accumulated fat.

This infiltration of fat may take place under pathological as well as physiological conditions. It is apparent that those causes which check oxidation are likely also to prevent the consumption of fat, and it is well known that the destructive processes in the lung, grouped under the term pulmonary consumption, accomplish this result. Something more, however, is necessary than the obliteration of pulmonary blood-vessels and the destruction of an aërating surface. There may be, as in emphysema of the lung, a diminished respiratory and vascular surface, yet evidences of fatty infiltration, particularly of the liver, are wanting. It seems probable that the constant anæmia, with the loss of the blood-corpuscles, of pulmonary phthisis is an important additional factor in checking oxidation in this disease. This factor, it is needless to say, is not a necessary occurrence in pulmonary emphysema.

Litten has shown that when certain animals are exposed to high temperatures the appearances of fatty infiltration and degeneration are present in various organs of the body. He attributes the fatty degeneration to a direct poisoning of the red blood-corpuscles and a resulting diminution of the oxidizing processes.

It is universally admitted that in chronic alcoholism a fatty liver is frequently met with, even in the absence of those chronic interstitial tissue-changes usually characterized under the name cirrhosis. Alcohol is known to check the reception of oxygen and the elimination of carbonic acid, and, whatever other disturbance of cell-activity it may produce, its effect in favoring the accumulation of fat is directly attributable, in part at least, to this disturbance of oxidation.

In those conditions known as cachexiæ, the constant accompaniment of progressive and wasting diseases, as cancer, leucæmia, chronic dysentery, {78} etc., a fatty infiltration, particularly of the liver, is a frequent accompaniment. A cachexia is dependent upon a complex series of processes, many of which tend to check oxidation, and in this respect is to be grouped with the conditions previously mentioned. That the associated fatty infiltration is intimately connected with the deficient oxidation is not to be doubted, although the agents producing this deficiency may vary in detail.

The causes which favor fatty degeneration are numerous, and the result represents one of the most serious conditions which can affect an organ. As oxidation represents the chief means of normally disposing of fat, so, pathologically, deficient oxidation favors the retention of fat due to degeneration. Were a constant renewal of protoplasm to take place, the degenerated fat might be displaced into the circulation or retained within the cell. If the latter event should occur, the result would be apparent as an infiltration, owing to the increased size of the cell, although the condition giving rise to the presence of the fat is a degenerative process. The importance of impairment of nutrition as the chief cause for fatty degeneration is thus obvious. It may readily be produced, experimentally, by measures which check the flow of blood to a part. The same measures necessarily prevent the presence of abundant oxygen, as fewer red blood-corpuscles are presented.

Fatty degeneration resulting from impaired nutrition is apparent in the heart in consequence of stenosis of its coronary arteries, in the kidneys as a result of interstitial processes obstructing the capillary circulation, in the brain from obliterative processes in the arteries at the base or within the organ, and in blood-vessels from the effect of age.

The cause of fatty degeneration may be general as well as local. In poisoning from phosphorus and arsenic the appearances in most of the organs indicate an actual destruction of protoplasm. Analysis of the secretions confirms this inference, as the production of urea is largely increased. Furthermore, there is less oxygen taken in and less carbonic acid eliminated. As has been previously stated, these conditions may be present in the starving animal. The fatty degeneration is thus easily explained as a metamorphosis of cell-protoplasm, and the deficient oxidation of the fat calls direct attention to its accumulation rather than elimination.

In acute yellow atrophy of the liver and in cases of severe jaundice fatty degenerations are constantly met with. That the origin and accumulation of fat in these affections is also due to rapid tissue-metamorphosis and checked oxidation is highly probable. Although the elimination of urea diminishes rather than increases, as shown by Schultzen and Riess, there are other links in the chain of retrograde changes, as the appearance of leucin and tyrosin, indicative of the extensive destruction of albuminates.

It is unnecessary in a work of the present character to call attention to all the possible circumstances under which fat is present in the body as the result of degeneration. Mention may be made of the acute parenchymatous (fatty) degeneration of new-born children, of the results of excessive bleeding, and of pernicious anæmia otherwise occasioned. The fatty degeneration of the uterus after parturition, of paralyzed muscles, and of tumors, the atrophic fatty degeneration of the liver in chronic {79} passive congestion (nutmeg liver), are all well-known examples. To these may be added the fatty degenerations associated with amyloid and interstitial processes. It is apparent that in most of these instances the common features of rapid tissue-metamorphosis and deficient oxidation are present, and, being present, offer a ready explanation for the appearance of the fat.

The clinical importance of fatty metamorphosis requires consideration in connection with the description of the diseases in which its occurrence is a constant feature. As the presence of fat in cells is not necessarily pathological, so an interference with the function of the cell is not invariably implied by its presence. When its existence is suggestive of a local destruction of albuminates, a diminution of cell-activity is a necessary consequence. Such diminished activity must produce different results as the cells are those of muscles, of vessels, or of glandular organs.

Even if fat is found in cells under conditions favoring such a suggestion, it does not follow that the destruction of the cell must result. Not only is it possible that the fat may be reserved for eventual oxidation, and its place in the protoplasm be filled by normal constituents, but it is also possible that the fat may be eliminated, as such, from the body. The latter event is made apparent by the experiments of numerous observers referred to by Cohnheim, who have found free fat in the urine after its introduction into the venous current.

Cheesy Metamorphosis, Cheesy Degeneration, Caseation.

Virchow introduced the term cheesy metamorphosis, tyrosis, to designate the process resulting in the incomplete absorption of pus and the production of apparently similar changes in certain other occasional constituents of the body. The characteristic cheesy appearances were regarded as due to the inspissation of the material concerned, in consequence of the absorption of its fluid. With this inspissation there was frequently associated a partial fatty degeneration, and the cheesy matter represented dead material, which might undergo further changes, of which softening and calcification were the more important.

Inflammatory products, as pus and fibrin, were especially prone to become thus transformed, as well as other relatively transitory materials of new formation--viz. tubercle and parts of various tumors. The type of the cheesy metamorphosis was found in the enlarged lymphatic glands, commonly called scrofulous.

The importance of a clear understanding of the cheesy metamorphosis is now a matter of history. It is merely necessary to allude to the fact that these cheesy products were formerly regarded as indicative of the presence of tubercle, and were the tubercles. Tuberculization and the cheesy condition were synonymous terms, and their indiscriminate use led to much confusion with reference to the nature of tubercle.

Quite recently Weigert has called attention to the conditions present in necrosis resulting from the intermediate stoppage of the blood-current in a part. The effect is manifested, under favoring circumstances, by a cheesy appearance of the affected region, to which the terms decolorized hemorrhagic infarction, anæmic or ischæmic necrosis, have been applied. {80} Weigert lays stress upon the existence of a coagulation of the protoplasm of the cells, with an early disappearance of the nuclei, as the essential feature of this form of necrosis, the conditions present being regarded as analogous to those met with in the coagulation of the blood. The term coagulative necrosis has consequently been introduced by Cohnheim to represent the process first fully described in detail by Weigert. The optical and physical properties of the ischæmic or coagulative necroses of tissue are often manifested as cheesy appearances, although the term coagulative necrosis includes conditions which do not present a suggestion of cheese. It is thus apparent that cheesy appearances may result in two ways: 1, by the inspissation of material in a state of partial fatty degeneration; 2, by a coagulation of the constituents of cells whose blood-supply is suddenly and completely cut off. In the more restricted sense these caseous appearances are regarded as indicative of a cheesy metamorphosis which arises by the former of these methods. Cheesy appearances, on the contrary, dependent upon the sudden death of a part, indicate an ischæmic or coagulative necrosis.

Whatever may be the origin of the cheesy condition, the material presenting this appearance is liable to further changes, known as softening and calcification. The former event results from the soaking of the dead part with liquid, in consequence of which a detritus results. The softening usually begins at the oldest part of the cheesy mass, and advances toward the periphery. The sanatory evacuation of the emulsive detritus is permitted when a surface continuous with that of the external surface of the body is reached, as instanced by the escape of softened cheesy material from the lungs through a bronchus. The possibility of the complete removal of the dead mass is thus at hand, and an eventual obliteration of the resulting cavity may take place by an adhesive inflammation of its walls.

The complete absorption of the cheesy material of an ischæmic necrosis may occur by the extension into the latter of a granulation-tissue from the periphery. Whenever cheesy appearances are found on surfaces, as the degenerated tubercles of mucous membranes or the circumscribed necroses in diphtheritic inflammation or in typhoid fever, healing may be accomplished by their detachment as sloughs, a clean ulcer being left. Cheesy material is frequently encapsulated--i.e. imbedded in a layer of dense connective tissue, a condition which indicates a local cessation of the process through which the cheesy appearances arose. The same may be said of the infiltration of the cheesy mass with earthy salts--calcification--an event which will again be referred to in connection with the consideration of the general subject.

Hyaline Degeneration, Fibrinous Degeneration, Croupous Metamorphosis.

Certain of the conditions now regarded as indicative of a coagulative necrosis or a hyaline degeneration were previously described by Wagner as the result of a croupous or fibrinous metamorphosis. According to this observer, the cell-contents were transformed, under certain circumstances, into a substance resembling externally clotted fibrin. The formation of croupous and diphtheritic membranes, especially of the larynx, pharynx, and trachea, was thus explained, also the hyaline casts of the kidney.

{81} The results of this metamorphosis presented a hyaline appearance under the microscope, and the term hyaline degeneration is now applied more especially to indicate the production of microscopic changes, while the hyaline appearances visible to the eye are rather included under mucous, colloid, or amyloid metamorphoses.

The limitations in the use of the term hyaline degeneration are but ill defined. On the one hand, there is included the transformation of muscular tissue, first discovered by Zenker; on the other, the various changes described by Recklinghausen and others, among which are embraced the results of Wagner's croupous metamorphosis. As the hyaline appearances are a frequent result of coagulative necrosis, these terms are frequently used to indicate the same condition, according as the optical or etiological features are uppermost in the mind of the observer.

The hyaline or waxy degeneration of muscular fibre described by Zenker represents a metamorphosis of the protoplasm of striated muscle in particular, although the fusiform cells of the muscular coat of the stomach and intestine may present a similar transformation.

The microscopic appearances are more characteristic than those visible to the naked eye. To the latter the muscle appears paler, more translucent, and homogeneous, and proves to be more brittle than normal. The muscular fibres are found with the microscope to be swollen, irregular in outline, the myosin transformed into flaky, glistening masses, without evidence of the normal transverse striation. These appearances have given rise to the term waxy degeneration, which suggests a possibility of confusion with the earlier recognized waxy degeneration of organs, due to the presence of amyloid material. The waxy transformation of muscular fibre, however, does not present the reaction with iodine characteristic of amyloid substance. The degeneration of the muscle is usually regarded as the result of a coagulation of the myosin, and it is claimed by Cohnheim that the latter takes place only in dead muscle, either during the life of the individual or as a post-mortem appearance.

The hyaline degeneration of muscular fibre is found in certain febrile diseases, as typhoid and typhus fevers, scarlatina, variola, and cerebro-spinal meningitis. It may also be met with when a muscle has been exposed to violence, as in the insane who have been placed under mechanical restraint. It has further been found in the vicinity of tumors, especially where muscles have been invaded by their growth. Cohnheim and Weil describe a similar condition in the tongue of frogs after ligature of the lingual artery.

The pathological importance of the above-mentioned degeneration of muscle is most prominent in cases of typhoid fever. The occurrence in this disease of the hæmatoma or blood-tumor of the rectus abdominis is thus explained, the degenerated muscle and its contained blood-vessels being ruptured. The muscles of the thigh and the diaphragm frequently undergo this degeneration; the change is more rarely met with in other muscles of the body.

Recklinghausen regards a hyaline substance, hyalin, as a normal constituent of cell-protoplasm which escapes in drops when the cell dies. Its presence indicates a diminution in the vitality of the cell from various causes. Under the microscope it appears as a sharply defined, highly refractive meshwork, enclosing spaces of irregular shape and size, in {82} which are frequently found nuclei, more rarely cells or granules. Langhans has described this appearance as channelled fibrin. It has been met with in the placenta, diphtheritic membranes, blood-vessels, tubercles, and gummata.