Edematous Disease (DISEASE)

EDEMATOUS DISEASE

of urine, blood, and also feces in patients with edematous disease. Metabolic disorders involve proteins, fats, and carbohydrates, as well as mineral salts and water. Patients with edematous disease have a sharply negative nitrogen balance and lose a significant amount of nitrogen, up to 5.2 g per day (Jansen); correspondingly, the excretion of uric acid, ammonia, amino acids, sulfur compounds, and especially urinary creatine is increased; residual nitrogen in the blood is increased with normal excretory capacity of the kidneys. The reflection of profound disorders of intermediary metabolism, characteristic of starvation, must be considered ketonemia and ketonuria, as well as a significant decrease in phosphorus-containing lipoids in the blood with an increase in soluble phosphorus compounds. It is characteristic that this nitrogen loss is the result of purely functional disorders, since after the disappearance of edema under normal nutritional conditions, patients are able to retain huge amounts of dietary nitrogen—up to 16 g (Schittenhelm, Schlecht). This circumstance speaks in favor of the fact that although patients with edematous disease are in a severe state of negative nitrogen balance, the dynamics of their metabolism is not disturbed as it happens in constitutional and endocrine disorders thereof. Among mineral substances, significant losses of calcium and phosphorus salts are noted. Chloride metabolism in itself is not disturbed, and the excretion of sodium chloride is even increased in patients with edematous disease, so there is no reason to associate edema with the retention of chlorides in tissues. Also, there are no disturbances in water retention, and patients excrete large amounts of urine. But with the simultaneous intake of sodium chloride and water, a completely peculiar metabolic disorder is observed with the retention of water and chlorides in the body (Schittenhelm and Schlecht). Thus, edematous disease is a true disease of starvation with the breakdown of fatty and protein compounds of the body and a peculiar disturbance of water and chloride metabolism. The course of the disease depends on the timely change in the nutritional conditions of the starving organism. Patients with proper food intake quickly lose edema, but the restoration of metabolic equilibrium and especially muscle tissue and fat requires a lot of time, and recovery therefore occurs very slowly. Mortality in edematous disease has not been precisely established; on average, it is about 13%. Yakim for 22,842 patients had 1,028 deaths; Dmitriev observed a higher mortality among prisoners of war in Germany. Mortality from edematous disease is especially high among children. Persistent diarrhea, which is an expression of profound metabolic disorders, must be considered an extremely unfavorable symptom; it significantly increases mortality. In addition to pronounced forms of edematous disease, there are also milder rudimentary forms—"edematous disease without edema" in the form of periodic polyuria and pollakiuria; the disease lasts from half a year to 1 1/2 years and represents metabolic disorders resembling edematous disease. Pathological and anatomical changes boil down to the complete disappearance of adipose tissue, atrophy of the musculature, loss of weight of the liver, heart, and other organs, and the complete loss of fat and glycogen in the liver. Of particular note are changes in striated musculature with sharp atrophy of individual fibers separated from each other by edematous connective tissue, as well as profound changes in the endocrine glands, especially the thyroid (Luria). These changes shed some light on the pathogenesis of edematous disease as well. If the etiology of edematous disease leaves no doubt that its cause is starvation, the question of the type of starvation in this disease cannot be considered clarified. In any case, the clinical picture of edematous disease differs sharply from the picture of exhaustion in the complete absence of food. The vitamin-deficiency origin of edematous disease is rejected by most researchers, and precisely during epidemics of edematous disease, for example, the appearance of scurvy is not observed. It is very likely that this is a nutritional disorder where general, completely insufficient caloric content of food is combined with the introduction of low-value carbohydrates and a large amount of fluid in the absence of necessary mineral salts, especially calcium salts. The pathogenesis and mechanism of the edema itself are even less clear. The enormous atrophy of the striated musculature deprives the organism of a reserve for fluid, which the starving person introduces in particularly significant quantities (Luria). Of no less importance is the change in the active role of capillaries in the exchange of subcutaneous tissue fluids (Eppinger), disturbed as a result of lipoid starvation in edematous disease. Finally, pathological and anatomical changes in the endocrine apparatus, especially the thyroid gland, play a significant role in the appearance of edema. In any case, the mechanism of edema in edematous disease comes down to several pathological factors united by a basic single process—profound metabolic disorder due to a peculiar starvation of the organism. The prophylaxis of edematous disease coincides with social and political measures guaranteeing the working class and working peasantry from such shocks as war, lack of food supplies during crop failures, etc. The very existence of edematous disease is the best proof of the class character of this disease in capitalist society. Treatment boils down to rest, i.e., bed rest for the patient for a more or less prolonged period, and proper nutrition. It is very important to prescribe a sufficient amount of fat in the form of butter, lard, and especially fish oil; the supply of fatty food is not contraindicated despite diarrhea. One must not forget to simultaneously prescribe hydrochloric acid, pepsin, pancreatin. Cardiac and diuretic agents are contraindicated. There are grounds for prescribing calcium salts (Calcium chloratum, Calcium glycerophosphoricum) and thyroid preparations (thyroidin 0.1). In the recovery period—physiotherapeutic treatment, quartz irradiation, helioatherapy.

R. Luria.