The general nutrition of the cachectic is bad, even though the bloated face, the edema of the legs over the emaciated muscles, conceals more or less the disappearance of the fat. Gaylor characteristically describes the general impression of the cachectic in the words, "Tumidi ventres, lienosi, inflatis cruribus, flavo viridive colore exsangues."
Cachectics always look much older than they are. Even cachectic children have somewhat of an aged appearance; still more so, cachectics in middle life.
The organism of the child succumbs to cachexia even more readily than that of the adult. It is not rare to see children manifest a general dropsy after a few paroxysms. On frequent recurrence of the attacks the general picture of cachexia develops as in adults. In relation to this Bohn says: "Inmalarial cachexia the subcutaneous fat eventually disappears, the muscles become thin, flabby, and powerless, the skin whitish yellow, grayish green, or grayish brown, and, as a special characteristic, an immense splenic tumor develops. Spleens from 22 to 24 cm. long and 6 to 11 cm. broad, reaching obliquely to the umbilicus or perpendicularly into the iliac fossa and to the pubic bone, are not uncommon. Sometimes the hypertrophic organ grows more upward or in breadth and interferes with respiration. In contrast to the general emaciation the abdomen is irregularly enlarged, either throughout or in its left half. These chronic splenic tumors are always tender on pressure and sometimes spontaneously painful. They occasionally interfere with the movement of the left leg, and in a six year old boy produced eccentric pains in it. Chronic intestinal catarrh is scarcely ever absent. The petechiae and purpura that sometimes cover the whole body are likewise to be attributed to the cachexia.
The course and duration manifest striking differences. Acute cachexia ordinarily runs a more rapid course, especially when accompanied by gangrene, hemorrhages, etc. Chronic cachexia extends over months and years, yet a pernicious attack or one of the previously named severe complications may at any time prove fatal.
Mild cases of cachexia usually end in recovery. This is complete only when the parenchymatous organs have suffered no structural changes, making compensation impossible. Cases with advanced disease, especially of the liver, spleen, and kidneys, offer a bad prognosis. Such people may escape their fate for years, become even capable of doing light work, yet the danger continually hangs over them of falling a victim to a relatively mild intercurrent affection. To them is applicable Doni's description of the home coming reapers: "Horum plerosque videas morbosos, pallidosque aspectu, ac vix fir matis vestigiis catervatim moestos ingredi, quippe seorum magna pars in urbanis nosocomiis vel vitam relinquunt, vel longo tempore cum morte luctantur."
The end may occur under the most different intercurrent affections, among which certain secondary affections of the liver, like hypertrophic cirrhosis, cholangitis, atrophic cirrhosis, simple atrophy, play a prominent role. These produce death under feverish and cholemic symptoms, with or without icterus. Trousseau and Duclos (de Tours) state that, at a certain stage,, a progressive continued fever, with marked increase in the pulse rate, ordinarily breaks out, which leads to a fatal termination in days or weeks. Death in these cases usually occurs under coma.
The general syndromes presented by cachectics show many similarities, yet there are certain differences which are sufficiently pronounced to make a division of cachexia in several forms justifiable.
In the introduction we distinguished an acute and a chronic cachexia. This differentiation is not limited to the greater or less rapidity with which the cachexia develops, but is evident, too, in certain characteristic symptoms.
Acute cachexia is characterized by the predominance of hydremic, hemorrhagic, and nutritive disturbances, to which mixed infections that show a striking tendency to gangrene are frequently added. The picture is dominated by a rapidly occurring general dropsy, hemorrhages from different regions, phlegmons, abscesses, gangrenous processes, and decubitus.
We mentioned before that this form of cachexia affects especially badly nourished, worn out individuals. Kelsch and Kiener describe it under the name "cachexie hydroemique, et gangrene," and I consider it an error when French writers identify Haspel's "fievre putride scorbutique epidemique" with acute malarial cachexia. In my opinion, Haspel's observations were applied to epidemics of scorbutus which carried off advanced cachectics, as well as individuals whose nutrition and resisting power had been lessened by some other preceding disease. After every effort to attribute the scorbutic affection to a similar etiology as malaria , Haspel himself writes *: " Cette maladie ne passait pas toujours par les phases de la fievre intermit tente, ou la vit se declarer dans les salles, chex les convalescents de diverses maladies." Moreover, we find, among his three anamneses, no case with dropsy and only one with a moderately sized splenic tumor.
Chronic cachexia is much more frequent. Its course is monotonous in comparison with that of acute cachexia. Edema, enlargement of the liver and spleen, different disturbances due to anemia, feverish or latent relapses, constitute the principal symptoms, while hemorrhagic, septicemic, and other complications occur only occasionally.
Kelsch and Kiener, to whom we owe the most thorough investigation of this question, have endeavored to divide chronic cachexia into subclasses. They differentiate: 1. Chronic cachexia the result of the overloading of the parenchymatous organs, especially the liver, with pigment (siderosis, "Surcharge ferrugineuse du foie"). 2. Chronic cachexia with general atrophy of the organs, especially the liver. 3. Amyloid degeneration.
While recognizing all that we owe to the splendid work of these two French investigators, we cannot regard this classification as final and objectionless. Without entering into a deep discussion, we may remark that this classification lacks a common factor. In form 1 the overloading of the parenchymatous organs with pigment is made the point of differentiation, and we would, therefore, logically conclude that in form 2 no siderosis was present. Yet this is not the case. Quantitative distinctions that may be slight can scarcely be taken as criteria on which to base a classification.