A system of practical medicine. By American authors. Vol. 1

by Unknown

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.

Litten³¹ 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.

³¹ Virchow's Archiv, 1877, lxx. 10.

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, 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 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.