Edematous Disease (is a disease characterized by significant)

Edematous Disease is a disease characterized by significant disturbances in the metabolism of urine, blood, and excretions in patients with E.D. These metabolic disturbances affect proteins, fats, and carbohydrates, as well as mineral salts and water. Patients with E.D. have a sharply negative nitrogen balance and lose significant amounts of nitrogen, up to 5.2 grams per day (Jansen), accordingly, there is increased excretion of uric acid, ammonia, amino acids, sulfur compounds, and especially creatinine in urine; residual nitrogen in blood is increased with normal kidney excretory capacity. The deep disturbances in intermediate metabolism characteristic of starvation should be considered as the cause of ketonemia and ketonuria, as well as the significant decrease in blood phosphorus-containing lipids 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 edemas under normal nutritional conditions, patients are able to retain enormous amounts of food nitrogen - up to 16 grams (Schittenhelm, Schlecht). This circumstance supports the view that although patients with E.D. are in a severe state of negative nitrogen balance, the dynamics of their metabolism are not disturbed, as is the case with constitutional and endocrine metabolic disorders. Among mineral substances, significant losses of calcium and phosphorus salts are noted. The metabolism of chlorides itself is not disturbed, and the excretion of table salt is even increased in patients with E.D., so that edemas cannot be associated with the retention of chlorides in tissues. There are also no disturbances in water retention, and patients excrete large amounts of urine. But with the simultaneous introduction of table salt and water, a quite peculiar disturbance of metabolism with retention of water and chlorides in the body is observed (Schittenhelm and Schlecht). Thus, E.D. is a true disease of starvation with the breakdown of fat 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 of nutritional conditions for the starving organism. Patients with proper food supply quickly lose edemas, but the restoration of metabolic equilibrium and especially of muscle tissue and fat requires a long time, and recovery therefore occurs very slowly. Mortality in E.D. is not precisely established; on average it is about 13%. In one study of 22,842 patients, there were 1,028 deaths; Dmitriev observed high mortality among prisoners of war in Germany. Mortality from E.D. is particularly high among children. Persistent diarrhea should be considered an extremely unfavorable symptom, expressing deep metabolic disturbances; they significantly increase mortality. Besides the sharply expressed forms of E.D., there are also milder rudimentary forms - 'edematous disease without edema' in the form of periodic polyuria and pollakiuria; the disease lasts from six months to 1½ years and presents metabolic disturbances resembling E.D. Patho-anatomical changes amount to the complete disappearance of fat tissue, atrophy of muscles, loss of weight of the liver, heart and other organs, and complete loss of fat and glycogen in the liver. Changes in striated muscle with sharp atrophy of individual fibers, separated from each other by edematous connective tissue, as well as deep changes in endocrine glands, especially the thyroid gland (Luria), deserve special attention. These changes also shed some light on the pathogenesis of E.D. If the etiology of E.D. 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 E.D. sharply differs from the picture of exhaustion in complete absence of food. The avitaminotic origin of E.D. is rejected by most researchers, and precisely during epidemics of E.D., for example, the appearance of scurvy is not observed. It is very possible that the matter concerns a nutritional disorder when the general, completely insufficient caloric content of food is combined with the introduction of low-value carbohydrates and large amounts of fluid in the absence of necessary mineral salts, especially calcium salts. The pathogenesis and mechanism of the edemas themselves are even less clear. The enormous atrophy of striated muscle deprives the body of a reserve for fluid, which the starving person introduces in particularly large quantities (Luria). The change in the active role of capillaries in the exchange of fluids of subcutaneous tissue (Eppinger), disturbed due to lipid starvation in E.D., is no less important. Finally, the patho-anatomical changes in the endocrine apparatus, especially the thyroid gland, play a considerable role in the appearance of edemas. In any case, the mechanism of edemas in E.D. comes down to several pathological factors united by a single basic process - deep metabolic disturbance due to a peculiar starvation of the body. Prevention of E.D. coincides with social and political measures guaranteeing the working class and laboring peasantry from such shocks as war, lack of food supply during famines, etc. The very existence of E.D. is the best proof of the class nature of this disease in capitalist society. Treatment consists of rest, i.e., keeping the patient in bed for a more or less prolonged period, and proper nutrition. It is very important to prescribe sufficient amounts of fat in the form of butter, lard, and especially fish oil; the introduction of fatty food is not contraindicated despite diarrhea. One should not forget to temporarily prescribe hydrochloric acid, pepsin, pancreatin. Cardiac and diuretic agents are contraindicated. There are grounds for prescribing calcium salts (Calcium chloratum, Calcium glycerophosphoricum) and thyroid gland preparations (thyroiodin 0.1). In the recovery period - physiotherapeutic treatment, quartz irradiation, heliotherapy.

P. Luria.