Rickets

RHACHISCHISIS, see Spina Bifida. RICKETS. Contents: Historical data..., 357. Geographical distribution and statistics, 358. Socio-hygienic significance, 359. Etiology, 360. Pathogenesis, 366. Pathological anatomy, 370. Biochemical deviations from the norm, 372. Symptoms and course, 372. Diagnosis, 379. Prognosis, 383. Prophylaxis, 384. Treatment, 388. Rickets (from Greek rachis—spine), English disease, is a general disease with a disturbance of metabolism and many body functions, affecting predominantly infants and young children. The very strong prevalence of rickets among the broad masses of the people, its close connection with socio-economic and living conditions, and its influence on the morbidity and mortality of children make it one of the most important social diseases of childhood. Historical data. The first indication of rachitic skeletal deformities was made by Soranus of Ephesus, who observed rickets in children in Rome in the 2nd century AD. In the 15th century, rickets was already a widespread disease in Europe; in the works of Flemish artists of this time, one can often find depictions of children with signs of rickets. Large cities, which grew rapidly in Europe in this historical epoch in connection with the development of international trade, were the main centers of rickets. A classic description of rickets was given in 1650 by the English anatomist and surgeon Glisson in the treatise De rachitide sive morbo puerili, qui vulgo the rickets dicitur. Before that, rachitic deformities had been described by French surgeons Guillemeau (1609) and Ambroise Paré (1633), the Englishman Whistler (1645), and others. After Glisson, nothing essentially new about rickets appeared in medical literature for a long time. Only almost 200 years later did Elsässer (1843) describe the softening of the skull in rickets. The works of Kassowitz (1884–1911), which refined the clinical picture of rickets, emphasized seasonal fluctuations in its frequency—a fact of great importance for understanding the etiology of rickets. An accurate description of pathological-anatomical changes was first made by Pommer (1885). The metabolism of calcium and phosphorus was investigated by Schabad (1909), Orgler, Schloss, and others. The works of Mellanby (1919), McCollum (1922) on the role of vitamin D, and Huldschinsky (1919), A. F. Hess (1921–24) on the significance of ultraviolet rays in rickets have greatly advanced our knowledge about its etiology and pathogenesis. Geographical distribution and statistics. Isolated cases of rickets are found all over the globe, not excluding tropical countries, but as a mass disease in a more severe form, rickets is observed predominantly in countries with a temperate climate, lying approximately in the zone between 60° and 40° north latitude. In this belt are located almost all countries of Europe, significant parts of Siberia, China, the USA, and Canada. The distribution of rickets within this zone is very uneven; both the number of cases and their severity depend on various local climatic features, and on hygienic and living conditions. In countries with a dense population and developed industry, rickets is, for the most part, more widespread than in agricultural countries with a sparse population. The statistics of rickets suffer from very large gaps and shortcomings. There is no mandatory registration of rickets cases anywhere; a significant part of the milder cases does not come under medical observation and thus escapes any registration. The accuracy of statistical data also suffers from the absence of uniform criteria for the diagnosis of mild cases of rickets. Data from different authors are difficult to compare with each other due to the difference in the social composition of the examined children and because the percentage in different works is calculated in relation to different age groups. In pre-revolutionary Russia, data on the prevalence of rickets were first published by N. Voronikhin in 1875; on outpatient material in St. Petersburg, he found 33% rickets, among children under 3 years old—42.7%. Reitz (1882) on the same material found in children under 3 years old—20.2–22.2%, Zhukovsky for 1891–93 up to 1 year—96%, from 1 to 16 years—94%. In other cities, it was found: in Moscow (Kisel, 1897)—children under 3 years old—80%, Kiev (Dukelsky, 1902)—up to 4 years—51.7%, Tula (Strzhelbitsky, 1900)—up to 2 years—83.8%, Vilna (Kovarsky, 1908)—up to 5 years—33%, Irkutsk (Rumyantsev, 1908)—up to 3 years—51.2%. In rural areas: Bystrov (Novgorod province, 1894) in children under 3 years—60%; Gauzner (Ryazan province, 1897)—up to 4 years—39.2%. After the revolution, with the development of a network of children's consultations, it became possible to collect data more accurately reflecting the prevalence of rickets. For example, among Uzbek children living in villages, 38% of rachitics were found (N. K. Kiselev), and among those living in the city—43%. Tajiks in Samarkand show 37% rickets, and in the small town of Ura-Tyube—27%; among nomads (Kazakhs)—34% of rachitics. Granat and Zgorzhelskaya, among the Buryats, who do not take children under a year out of the yurt, found 85% of rachitics. Information regarding other countries is just as incomplete and of the same fragmented nature. In Berlin, Davidsohn found among children under 6 years old (material from an orphanage) before the war 37% of rachitics, after the war—50%. In 1930, according to Nassau, in the eastern (proletarian) part of Berlin, among children under 1 year old—47.7% of rachitics, in the 2nd and 3rd year—74.2%, and between the 4th and 5th years—55.1%. Hilgers, examining children during smallpox vaccination, i.e., under 3 years old, found in Leipzig 49.3% of rachitics, in Königsberg—in 1918—52.5%, in 1921—39.1%; Engel discovered in Dortmund among children from 3 to 10 years old 42.8% of rachitics. In Paris, Marfan estimates the number of rachitics among children under 3 years old visiting outpatient clinics at 40%. In London, J. L. Dick found traces of past rickets in 80% of schoolchildren in the north-eastern (poor) part of the city. In large cities of the USA, according to A. F. Hess and Unger, 3/4 of all children are ill with clinically expressed rickets, and when, in addition to clinical methods, X-ray and biochemical methods were used for diagnosis, almost all children turned out to be affected, especially in the spring. Children of Negroes living in the USA all suffer from rickets, and often in a particularly severe form. The opinion that prevailed among doctors, based on old data, about the almost complete absence of rickets in Scandinavian countries, in the south of Europe, and in Asia, can no longer be considered correct at the present time. Johannessen observed in Oslo (Norway) 40% of rachitics among children aged 6–18 months. Hess reports a significant prevalence of rickets in Italy, Marfan saw many rachitics in Constantinople; reports have been published from Japan, China, and India indicating that rickets is not a rarity there; in most cases, it proceeds in a mild form there, but in some population groups where small children together with women lead a secluded lifestyle, more severe forms are also observed. Despite all the insufficiency of the available statistical data on rickets, they convincingly speak of its enormous and in many cases ever-increasing prevalence. Socio-hygienic significance. Such a long-lasting disease as rickets cannot but harmfully affect the general physical development of the child. Rickets lowers the resistance of the child's organism to other diseases; this is especially clearly seen in diseases of the respiratory organs, where local factors are added to the general causes. A soft rachitic chest, collapsing from the sides with each breath under the influence of atmospheric pressure, or a chest strongly deformed as a result of rickets, prevent sufficient expansion of the lungs and create unfavorable conditions for the course of bronchitis, pleurisy, etc. Although experimental data do not reveal a decrease in immunity in vitamin A deficiency, clinical observations of rachitics suggest the opposite. Measles and whooping cough proceed more severely in rachitics than in normal children. According to Pfaundler, during measles, rachitics get pneumonia three times more often than non-rachitic children, and the possibility of dying from such a complication is twice as high for them as for other children. Deformities of the chest can also create difficulties for the work of the heart. In any disease that places increased demands on the respiratory and circulatory organs, a life-threatening situation can arise due to their functional insufficiency. The deformities of the trunk and limbs remaining after rickets limit the working capacity of the carriers of these deformities, making them less suitable for professions that involve prolonged standing on the feet, carrying heavy loads, and generally significant physical efforts. The consequences of rickets often make young men unfit for military service. An examination of the physical condition of young men of conscription age, carried out in 1918 in England, showed that the largest number of those unfit for military service (up to 63.25%) is found in those areas where a strong prevalence of rickets among children had previously been detected.

In women, there are dangerous consequences. Rickets can manifest as a narrow pelvis, which serves as an obstacle to the normal course of labor. A narrow pelvis is present in 14-20% of all women, and one of the most frequent causes of this deformity is rickets. Thus, rickets, while never being the direct cause of death, can lead in various ways to an increase in morbidity and mortality and to a decrease in the working capacity of the population. Etiology. The set of conditions for the emergence of rickets consists of social factors and biological factors. The various causes are so closely intertwined that it is difficult to consider the effect of any one of them without completely touching upon the others. The discoveries of recent years, which have clarified the etiological role of the insufficient action of ultraviolet rays on the child's organism and the significance of a lack of vitamin D in food, have not only deepened the understanding of the biological side of the rachitic process but have also helped to better understand the way in which socio-economic factors act. The significance of the family's financial situation stands out particularly clearly. It is well known that the most severe forms of rickets are encountered predominantly in the least affluent strata of the population. When breaking down the population into groups according to some indicator characterizing economic status, for example, by the area of the occupied apartment, it becomes clear that the percentage of rachitic individuals in a group is higher the worse its material situation is. Thus, in Dortmund, in apartments consisting of 6 rooms, where there was an average of 1 person per room, rickets was detected in 1/3 of all children, while in one-room apartments, which housed almost 4 people each, 70% of children suffered from rickets (Engel). Antonov, who criticizes these figures of Engel, himself also provides data for Leningrad that speak to the same effect. Since small apartment area or insufficient cubic capacity are not the direct cause of rickets, but serve only as indicators of the family's material situation and at the same time factors acting in a favorable sense may also be present, there is not always a strict correspondence between these data and morbidity. Poverty contributes to the spread of rickets by influencing the nutrition of children and their entire way of life unfavorably. The necessity to buy only cheaper food products leads to children receiving very little butter, eggs, and other animal products and feeding primarily on carbohydrates and vegetable fats, which is significant for the development of rickets. A lack of free time for the mother, the impossibility of having a special person for childcare, and sometimes the absence of warm clothing in winter, lead to children of poorly provided-for population groups going out of the house very little and, thanks to this, being deprived, among other things, of the necessary exposure to ultraviolet rays. A delay in the development of motor functions in infants with poor care in a poor family is also a factor contributing to the development of rickets. F. Engels, back in 1844, while investigating the condition of the working class in England, drew attention to the prevalence of rickets among the children of the industrial proletariat and linked this phenomenon to the terrible hygienic conditions in which significant strata of the proletariat live in capitalist countries, and above all to poor nutrition. Having given a vivid picture of the living conditions of English workers and pointed to the prevalence of tuberculosis among children, he indicates: “The second consequence of this insufficient nourishment of the body during the child's growth is rickets.” The two most important biological factors of rickets—insufficient exposure to ultraviolet rays and insufficient delivery of the antirachitic factor with food—are often economically determined. The fact that in individual cases or in certain population groups, in one locality or another, rickets is also observed in well-off families does not contradict this in the slightest. Such exceptions are usually explained by peculiar domestic, climatic conditions, or nutritional conditions present in these cases. The etiological role of domestic factors and cultural level is revealed particularly clearly in those cases where, due to the customs of the country or religious prejudices, it is customary not to take children out of the house for the first year or longer, or where women lead a secluded lifestyle, and children, spending their first years with their mother, also almost never go out of the house. In such cases, rickets can develop in children despite relatively favorable nutritional or climatic conditions. Such observations were made by Granat and Zgorzhelskaya on Buryat children, Hutchinson in India, and others. It has already been mentioned above that rickets is more widespread in industrial countries than in agricultural ones; this happens not only because there is a more numerous stratum of poorly provided-for proletariat here, but also because in industrial countries a more significant part of the population lives in large cities, where there are a number of additional harmful conditions favoring the development of rickets. Over a large city, especially over its factory part, where the working part of the population usually lives, there is always a cloud of smoke, soot, and vapors, which retains the greater part of the ultraviolet rays of the solar spectrum, so that light reaching the surface of the earth there is only very poor in ultraviolet rays. Even more important is that the extreme cost of land in cities and speculation in apartments have led to a method of construction that has reduced the unbuilt area to a minimum, especially in working-class neighborhoods. The complete absence of parks, narrow streets, and cramped courtyards, with the ever-increasing number of floors in new buildings, deprives children of the sun not only in apartments but also outside them. The rural population is in more favorable conditions in this respect, and if peasant children among us still suffer from rickets in a large percentage, this is explained by the presence of other unfavorable conditions, such as complete ignorance of the elementary requirements of hygiene, as a result of which children are not taken out of the house at all for many months in a row, etc. The role of ultraviolet rays. It has long been noted that the constant stay of children in closed rooms contributes to the development of rickets, whereas staying outdoors prevents the disease and contributes to the recovery of those who are ill. Kassowitz, back in 1884, drew attention to the fact that during the winter months rickets intensifies annually, while in the spring and summer, rachitic individuals recover. However, the quantity of sunlight falling on one locality or another alone does not yet fully determine the degree of the prevalence of rickets there. In a locality with a large number of sunny days in a year, there can still be quite a lot of rachitic individuals. The quality of the light, the composition of its spectrum, is what matters. The discovery by Huldschinsky (1919) that the light of a mercury-quartz lamp, rich in ultraviolet rays, surely and quickly cures rickets, contributed much to the clarification of this side of the issue. Soon after this, Hess and his colleagues, using filters that transmit only rays with a wavelength of a certain length, showed that the favorable effect of sunlight on rickets is also due to the presence of ultraviolet rays in its spectrum; it was precisely the rays having a wavelength from 290 to 313 mμ that proved effective against rickets. These rays do not pass through ordinary glass and are easily absorbed by the earth's atmosphere, especially if it contains many water vapors. The more humid the climate of the locality and the longer the path traveled by the sunbeam through the atmosphere (and this path depends on the geographical latitude of the locality), the poorer the light will be in ultraviolet rays upon reaching the earth's surface. Seasonal fluctuations in the incidence of rickets in children also depend on the varying intensity of the action of ultraviolet rays at different times of the year, which in turn is connected with the changing position of the earth's axis in relation to the sun (see also Heliotherapy). The content of ultraviolet rays in sunlight that has reached the earth is weakest in the winter months, begins to increase in March and April, reaches a maximum in June and July, and then rapidly weakens again. Besides direct sunlight, scattered light reflected from the sky and clouds also produces an antirachitic effect. Ultraviolet rays possess only a very weak ability to penetrate deep into body tissue. According to Hasselbach's data, they penetrate the skin to a depth of no more than 0.1 mm. Under such conditions, it was difficult to explain the general effect of ultraviolet rays on the organism. Hess and his colleagues showed that skin taken from a corpse, subjected to ultraviolet irradiation, and fed to an animal protects it from rickets; non-irradiated skin does not exhibit such an effect. From these experiments, it could be concluded that the action of ultraviolet rays boils down to some process in the skin itself, and moreover, to such a process that is possible even in dead tissue. Subsequently, however, Anderson and Macht proved that shorter ultraviolet rays penetrate much deeper into living skin than was previously thought, specifically to 1.2 mm.

Therefore, they can cause changes not only in the superficial layers of the skin but also in deeper tissues and in the blood. Further clarification of the role of ultraviolet rays is connected with the discovery of vitamin D and the study of the antirachitic action of food products (see below). Nutrition. Gleason already linked the occurrence of rickets with overfeeding; this is confirmed at the present time by many physicians, including Czerny and Jundell. Indeed, among rachitic children with initial forms of the disease, there are many who are abundantly fed and gaining weight rapidly. Accelerated growth, accompanied by increased expenditure of the vitamin reserves present in the body, is a circumstance favoring the development of rickets, while a slowing of growth hinders its occurrence. Mellanby, on the basis of experiments on animals, came to the conclusion that a diet rich in carbohydrates contributes to the development of rickets; he observed an especially harmful effect from oatmeal. The latter circumstance was confirmed by Holst. Breastfeeding is a circumstance that protects a child from more severe forms of rickets, which are observed almost exclusively in children fed artificially. But breastfeeding does not exclude the occurrence of rickets. A fully developed case of rickets (with sweating, craniotabes, rosary, and other symptoms) is often observed in children fed exclusively on breast milk. Hess and Weinstock, investigating the antirachitic action of human milk in experiments on animals, found that it contains almost no antirachitic vitamin. The same result was obtained by other authors. The favorable effect of human milk on children in terms of protecting them from severe forms of rickets depends, therefore, not on the antirachitic vitamin, but on some other causes, perhaps on a favorable ratio of ions in it, which facilitates the absorption and retention of calcium and phosphorus. The influence of the nutrition of a pregnant woman and a nursing mother on the child's predisposition to rickets is also significant, but this side of the question has not yet been sufficiently clarified. Under the influence of irradiation of a nursing mother with ultraviolet rays, the antirachitic properties of her milk increase (Gerstenberger). Cow's milk and butter have a weak antirachitic effect. The antirachitic effect discovered in coconut oil depends on the action of ultraviolet rays on the raw material from which the oil is obtained, on the so-called copra, which is usually dried in the sun; if the drying of copra is carried out in an oven, the oil obtained from it does not have antirachitic properties. Vegetables and fruits, with rare exceptions, contain almost no antirachitic factor; their favorable effect on children suffering from rickets, just like the effect of human milk, is connected with their other properties: the content of vitamins A, B, and C, necessary salts, etc. The number of food products with a pronounced antirachitic effect is very small. This includes, first of all, cod liver oil. Analogous to cod liver oil, although somewhat weaker, the fats of some other fish and marine animals act in rickets: herring, salmon, sea bass, dolphin, seal, and others. The time of harvesting, the nature of processing, and the method and duration of storage of the fat strongly influence its quality. The absence of rickets in children in Arctic countries, despite the negligible amount of ultraviolet radiation and unhygienic living conditions, is explained mainly by the fact that in the far north, a great deal of fish products rich in the antirachitic factor are included in the diet. Egg yolk also shows a clear antirachitic effect, and the content and nutrition of the hens affect its effectiveness (see also Vitamins). Thus, the food received by children at the age when rickets usually develops is comparatively poor in the antirachitic factor, and under ordinary conditions, the child's organism must cover its need for it from other sources. Vitamin D (see Vitamins and Avitaminoses, D-avitaminosis). In cod liver oil, which is especially rich in the antirachitic vitamin, it is found in its unsaponifiable part and can be isolated from there in a concentrated form. The clarification of the nature of the antirachitic vitamin was greatly assisted by the discovery that products not possessing antirachitic properties acquire them after irradiation (see Irradiated preparations). Before this discovery, two points of view stood in opposition regarding the etiology of rickets. One of them, represented by Mellanby, saw the basic cause of rickets in nutritional deficiencies; from this point of view, it was difficult to explain why rickets does not develop in southern countries or among many primitive peoples despite poor nutrition. The other point of view, expressed mainly by Findlay, attributed the cause of rickets to hygienic deficiencies, especially living in poor, dark premises; this point of view could not satisfactorily explain the absence of rickets in the far north with insufficient lighting and despite unhygienic housing conditions. With the discovery of the fact that under the influence of ultraviolet irradiation an antirachitic factor can be formed in the organism, it became possible to synthesize these two points of view in the sense that in some cases the lack of antirachitic vitamin in food is compensated by the action of ultraviolet rays on children, and in other cases, the insufficient action of light is compensated by large quantities of vitamin D in food. The classification of rickets as an avitaminosis is not accepted by everyone without reservation, since the vitamin does not play such a role in its etiology as in other avitaminoses, for example, in scurvy (Marfan, Pfaundler). Infections and intoxications were previously attributed great importance in the etiology of rickets. Most physicians long held the view, first expressed by Petit (J. L. Petit, 1741), according to which rickets is the result of chronic intoxication from artificial feeding and premature weaning. Boerhaave, Parrot, and Fournier considered syphilis to be the cause of rickets. Marfan still believes that rickets is caused by chronic infections and intoxications of all kinds. At the present time, these views cannot be supported. Rachitic children do not react to tuberculin more often than other children of the same age and do not give a positive Wassermann reaction. Attempts (Morpurgo, J. Koch) to prove the etiological significance of infection in rickets experimentally have also proven unconvincing. It cannot be denied, however, that infections, intoxications, and other diseases, by disrupting the delivery of the vitamin with food and normal metabolism and by increasing the expenditure of the vitamin reserves existing in the child's body, contribute to the development of rickets. Heredity and constitution. The role of hereditary and constitutional predisposition in the etiology of rickets is assessed differently by various authors: while some (Czerny, Pfaundler) consider this factor decisive, others (Holt, Dick, Degkwitz) do not attach great importance to it. The fact of the predominance of boys among children suffering from rickets, which is revealed in large statistics, speaks in favor of the significance of the endogenous factor. Thus, among 11,535 rachitic children observed by Voronikhin, there were 6,545 (56.7%) boys and 4,990 (43.3%) girls. Late rickets is observed in young men many times more often than in young women (Fromme). Stockard observed a predominance of one sex in the spontaneous development of rickets in dogs. Predisposition, especially sharply manifested in Negroes living in the USA, is linked by Hess to skin pigmentation; the predisposing influence of pigmentation has also been discovered in experiments on animals. Premature infants fall ill with rickets especially easily; the assumption that they have a smaller reserve of vitamin D in their bodies than full-term infants has been refuted by the experimental studies of Hess and Weinstock; the predisposing moment in such cases is faster growth and a lack of salts in the body. Summarizing what has been said about the etiological role of various factors, it can be said that in rickets, as in any other disease, heredity, constitutional predisposition, and other endogenous factors, such as the speed of growth, etc., certainly play a role, but exogenous factors have the predominant significance, among which the nature of nutrition and lighting conditions are most important, which ultimately boil down to one basic factor—vitamin D; at the same time, socio-economic factors play a decisive role in the sense that they create conditions under which the favorable or, conversely, unfavorable action of biological factors comes into effect. Pathogenesis. Depending on the views prevailing in one era or another, various theories were put forward in pathology to explain the pathogenesis of rickets: dyscrasia—in the era of humoral pathology, inflammatory process—with the development of cellular pathology, bacterial theory—during the heyday of the bacteriological era, etc. The pathogenesis of rickets remains unexplained even now, despite a huge number of studies. The social pathogenesis of rickets was partially considered together with socio-economic etiological factors. Life in a modern capitalist big city with its overcrowding and factory smoke already carries with it a number of rachitogenic factors.

The greater general morbidity of children from economically weaker population groups compared to children of the wealthy classes is also a factor favoring the spread of rickets, specifically among the proletariat and the rural poor, because any disease, by disrupting the stability of metabolism and increasing the expenditure of the body's existing vitamin reserves, facilitates and accelerates the development of rickets. The lack of consideration for social factors hindered a correct understanding of both the etiology of rickets and its pathogenesis; a number of phenomena in the pathology of rickets, for example, certain peculiarities in its distribution across the globe and among different social groups, remained misunderstood for a long time for this very reason. The frequency of rickets in children of certain population groups in countries rich in sunlight seemed to stand in contradiction to the position regarding the protective role of light; but the study of living conditions made it possible to clarify this apparent contradiction. The presence of rickets in affluent families seemed to argue against the social conditioning of this disease. Only a proper assessment of both biological and social conditions simultaneously allowed for untangling and correctly explaining such facts, which seemed paradoxical. Facts discovered during the study of metabolism in rachitic patients are of great importance for clarifying the pathogenesis of rickets. Shabad was the first to systematically investigate the lime balance in rachitic patients and established that during the development of rickets, the lime balance decreases due to its increased excretion through the intestines and can even become negative. He also drew attention to the importance of studying phosphorus metabolism in rickets and pointed out that phosphorus in rickets is also excreted from the body in an amount increased above the norm. The site of phosphorus excretion in rickets is mainly the intestines, and its amount in the urine decreases compared to the norm, so that there is relative hypophosphaturia. These data were generally confirmed by other researchers (Orgler, Schloss, and others). Corresponding to the changes in the lime balance, Shabad distinguished three periods of rickets: with a negative or very low positive balance at the beginning of the disease; with a sharply positive balance (2-3 times higher than the norm) during the recovery period; and with a normal or slightly below-normal balance in the interval between these two periods. When comparing the amounts of lime and phosphorus excreted in rickets, it turns out that they are not excreted in the same ratio as they are found in the bones: significantly more phosphorus is excreted than the equivalent amount of lime. Shabad concluded from this that the disorder in phosphorus metabolism in rickets cannot be a consequence of lime metabolism in the bones; he expressed the opinion that the disorder of phosphorus metabolism is the primary factor here. Rominger and his colleagues, using an improved methodology that allows for studying metabolism in children over a very long time, confirmed Shabad's data on the leading significance of the disturbance in phosphorus metabolism in rickets and proposed distinguishing the following 4 phases of balance disorder in rickets. 1st phase: a significant deterioration in the phosphorus balance, while the lime balance still remains normal; clinically, this phase corresponds to the initial symptoms of the disease. 2nd phase: a worsening lime balance is added to the poor phosphorus balance; clinically, at this time, there is a full development of the disease. 3rd phase: the phosphorus balance improves, but the lime balance still remains unsatisfactory; clinically, an improvement in the general condition is observed at this time. 4th phase: a normal balance of both phosphorus and lime; clinically, recovery. In mild cases, the patient can go directly from the first phase, bypassing the second, into the third and then into the fourth. It was natural to see the cause of the deterioration of the lime and phosphorus balance in rickets in the unfavorable conditions of absorption of these substances from the intestines. This point of view is currently supported by Howland, Findlay, and others. Howland believed that rachitic patients are unable to normally utilize the inorganic components of food, in particular phosphates, which is why the amount of inorganic phosphorus in the blood serum decreases. Cartilage, bathed in plasma containing a reduced amount of phosphorus compared to the norm, does not capture tricalcium phosphate. Telfer explains the poor phosphorus balance in rickets not by the fact that it is excreted from the blood into the intestinal cavity in an increased amount, but by the fact that food phosphorus forms a poorly soluble compound with lime in the intestines (which is especially favored by the alkaline reaction of the chyme) and is excreted together with feces. When conditions in the intestines change, phosphorus absorption improves. Thus, when a large amount of fatty acids appears in the intestines, they bind the lime, which is why the phosphorus remains free and is absorbed. In rickets, both in children and in experiments on animals, there is indeed, for the most part, an alkaline reaction of the feces. Confirmation of Telfer's views can also be seen in the fact that breastfed children, whose feces usually have an acidic reaction, suffer less from rickets than those fed artificially, whose feces more often have an alkaline reaction. But other facts do not agree with the views of Telfer and his supporters. Thus, long-term feeding of children with acidic food mixtures does not prevent rickets (Hess); increased excretion of lime and phosphorus with feces can also result from the subcutaneous administration of these salts (Grosser); improvement in absorption is observed under the influence of such factors as irradiation with ultraviolet rays, administration of irradiated ergosterol, etc., which do not directly affect the processes in the intestinal cavity. According to data from Klinke, Hesse, and others, the absorption of salts from the intestines depends relatively little on their solubility. Much suggests, therefore, that the conditions of absorption from the intestines probably do not play a dominant role in the pathogenesis of rickets, but this entire question has not yet been sufficiently clarified. Not a little effort has been put into clarifying the question of why rachitic bone remains uncalcified, but so far no satisfactory answer has been obtained. Studies by Marriott, Kramer, Shipley, and others have proven that rachitic cartilage placed in normal serum is well impregnated with salts. The same happens even in an aqueous solution of salts if they have the same concentration as in normal serum; if the concentration of lime or inorganic phosphate salts is below the norm or if the reaction of the solution is too acidic (pH less than 7.25), then no deposition of salts in the cartilage occurs. However, even in a normal environment, cartilage that has been pre-heated or poisoned by something is not impregnated with salts. Robison emphasizes the role of the enzyme phosphatase, which cleaves PO₄ ions from their compound with hexose and thus facilitates the impregnation of cartilage with salt. The delay in the ossification of rachitic bone could be explained by insufficient phosphatase activity; but, as Demuth, May, and others have shown, the cartilage of rachitic bone is richer in phosphatase than normal cartilage. A detailed theory of the pathogenesis of rickets was provided by Gyorgy as a result of a series of works carried out jointly with Freudenberg, Brehme, and others. Based on the decrease in reserve alkalinity found in rickets, the increased excretion of acidic metabolic products with urine, and some other facts, Gyorgy and Freudenberg classify rickets as a process occurring with an "acidotic direction of metabolism." Gyorgy considers the cause of this acidosis to be a slowed metabolism, which can be caused by insufficient lighting and a lack of vitamin D in food, which are specific to rickets, or by various other non-specific factors, such as domestication, restriction of movement, post-infectious states, a monotonous, too fatty diet, a lack of vitamins in food (other than vitamin D), etc. The increased excretion of acidic phosphates with urine observed in rickets, as in any acidosis, leads to a depletion of phosphorus in the body, which in turn results in a further slowing of metabolism. A peculiar "vicious circle" is created. Freudenberg and Gyorgy are inclined to view the delay in bone calcification partly as a consequence of slowed metabolism and the accumulation of intermediate metabolic products in the body; they showed that amino acids, peptides, guanidine, creatine, urea, and other metabolic products prevent the deposition of lime in tissues. For normal bone calcification, the elimination of this obstacle at the site of lime deposition is required; in rickets, this does not happen, which is why the calcification process is disrupted. Gyorgy's theory leaves unanswered the legitimate question of why other conditions accompanied by slowed metabolism, such as hypothyroidism or various dystrophies in children, do not lead to rickets. The very existence of acidosis in rickets has also been questioned. Bosanyi, investigating the reaction of tissues, found that rachitic cartilage has a more alkaline reaction than normal: its pH=7.6, while the pH of normal cartilage is 7.2-7.0.

Marfan, who sees the cause of rickets in chronic infections, explains their effect through their influence on the bone marrow and lymphatic organs, as a result of which disorders of bone growth, anemia, muscular hypotonia, and other symptoms of rickets develop. Some confirmation of this view can be seen in the experiments of Bozzani, who found that normal bone marrow and an aqueous extract from it protect animals from rickets, whereas the bone marrow of a rachitic individual does not have such an effect. In a disease such as rickets, which is based on a general metabolic disorder accompanied by significant changes in blood chemistry, the endocrine glands and the autonomic nervous system associated with them cannot help but play a role. Therefore, one can tentatively speak of a "hormonal-autonomic shift" in rickets (Medovikov), but there are still no strictly verified and fully clarified data in favor of the participation of any endocrine gland in the pathogenesis of the changes characteristic of rickets. Most likely, one can expect to discover a connection between rickets and the activity of the parathyroid glands. Their removal causes, as is well known, tetany, which is closely related to rickets. Erdheim, Pappenheimer, and others have described the enlargement of the parathyroid glands in rickets in children and animals. Hyperplasia and tumors of these glands are accompanied by an increase in the amount of calcium in the blood, and we observe the same change in the blood as a result of the prolonged administration of large doses of vitamin D. On the other hand, after the removal of the parathyroid glands, animals do not show an increase in the level of calcium in the blood even under the influence of very large doses of vitamin D (Hess, Weinstock, Rivkin). And conversely: in animals fed a diet devoid of vitamin D, the injection of parathyroid hormone does not cause the usual reaction in the form of hypercalcemia. All these data suggest that there is some connection between rickets and the function of the parathyroid glands; but what it consists of has not yet been clarified. An increase in the amount of diastase in the urine of rachitic individuals and some deviations in sugar metabolism have given grounds to put forward a hypothesis about the participation of the pancreas in the pathogenesis of rickets, but this assumption has not yet been proven. The absence of a specific influence of the endocrine glands on the rachitic process does not, however, exclude the possibility of a favorable effect on it of preparations of such glands; the favorable effect of endocrine preparations can be explained by the acceleration of metabolism which they cause. Experimental rickets. The first attempts to reproduce rickets in animal experiments date back to 1839 and belong to Guerin; by depriving puppies of mother's milk and prematurely switching them to a meat diet, he observed in them a disease which he considered to be rickets. The poverty of rachitic bone in lime led researchers to the idea that the cause of rickets must be a lack of this substance in the diet. Therefore, most previous experimenters kept animals on a diet poor in lime; in Russia, such experiments were published by Korsakov in 1883; in this case, osteoporosis developed in the animals, but the lack of clarity regarding the pathological histology of rickets did not allow for a correct assessment of the results obtained at that time. Rickets can be induced in many young animals (in puppies, piglets, rabbits, chickens, monkeys, etc.), but recently rats have been used predominantly, as they present a number of technical advantages for such experiments. Thanks to the work of Pappenheimer and Sherman and McCollum and his colleagues, the conditions under which rickets invariably develops in these animals have been precisely clarified. For the experiments, rat pups about a month old, weighing 40-60 g, are taken and placed individually or in small groups in cages, which are placed in a room protected from bright sunlight. As food, the animals receive a mixture of food substances and salts, selected in such a way that there is no vitamin D, less than the norm of phosphorus, and more than the norm of calcium. Under such conditions, rickets develops in rats in approximately 3 weeks. The pathogenesis of this disease is not identical to the pathogenesis of childhood rickets, since in children rickets develops even with the correct ratio of phosphorus and calcium in the diet, but the pathological-anatomical changes in the bones in experimental rickets, the reaction to ultraviolet rays, to the addition of vitamin D to the feed, and to some other preventive and therapeutic measures in experimental rickets are the same as in childhood rickets. The possibility of experimentally inducing rickets in animals not only contributed greatly to the successes achieved in recent times in clarifying the etiology, prevention, and therapy of rickets in children, but also helped to clarify a whole series of more general, theoretically important questions. A more detailed study of ultraviolet rays acting against rickets, the clarification of the difference between the anti-xerophthalmic and antirachitic factors, the discovery of the activating effect of ultraviolet irradiation on food products, the clarification of the chemical nature of vitamin D and its factory production, the testing of various preventive and therapeutic methods against rickets—all this would have been impossible to accomplish with such success and in such a short time if it had not been possible to use the method of experimental reproduction of rickets. Pathological anatomy. Changes in the bones come to the fore in the pathological-anatomical changes in rickets; they have been studied better than changes in other organs. In far-advanced cases of rickets, the bone is softer than normal and is relatively easily cut with a knife. On a longitudinal section of a long bone, cartilaginous layers expanded beyond the norm are visible between the epiphyses and the diaphysis; the boundaries of the epiphyseal cartilages facing the diaphysis have irregular zigzag outlines [see separate table (pp. 247-248), fig. 6]. The cortical layer of the bone is thinned. The bone marrow is redder than normal. The most characteristic histological changes for rickets are visible at the border between the epiphysis and the diaphysis, in the region of endochondral ossification (see Bone). The histological picture of rachitic bone presents the following main differences from normal bone at the height of the process: the transition from resting cartilage to proliferating cartilage is sharp; due to the delay in the process of transforming cartilage into bone, the thickness of the proliferating layer exceeds the norm several times [see separate table (pp. 247-248), fig. 6]. Vessels penetrating from the periosteum into the cartilage sometimes form 2-3 levels. The zone of preliminary calcification is absent, only in places are there sections of cartilage whose ground substance is impregnated with salts. From the cartilaginous layer, more or less long columns of cartilage cells extend, protruding into the bone marrow cavity. On the other hand, the vessels of the bone marrow adjacent to the cartilage in places extend far into the cartilaginous layer. The boundary between the cartilage and the bone marrow therefore does not form a straight line, as in the normal state, but is completely disorganized. The bone trabeculae are arranged chaotically and are surrounded by a wide layer of osteoid substance [see separate table (pp. 247-248), fig. 5] due to the fact that the newly forming bone tissue is not impregnated with salts in a timely manner. In the area of subperiosteal bone development, the bone trabeculae are also surrounded by an abnormally wide osteoid border. In flat bones, which develop, for example, like the bones of the cranial vault, not from a cartilaginous but from a connective tissue base, the edges are thinned and soft in rickets; conversely, in the centers of ossification of flat bones, thickenings arise, forming tubercles (e.g., the frontal and parietal tubercles of the rachitic skull). The histological difference of rachitic bone in the form of a wide osteoid border surrounding the bone trabeculae is also present in flat bones. Upon recovery, salt deposits reappear in the zone of preliminary calcification; in place of the excessively accumulated cartilage, bone tissue develops, and the osteoid substance, with the exception of a narrow border, is also impregnated with salts, so that the new spongy bone tissue consists of abnormally thick bone trabeculae; as a result, the bones of a rachitic individual may turn out to be denser and heavier than normal upon the conclusion of the rachitic process. The described changes are found throughout the skeleton, but they are expressed to varying degrees in different bones; they are strongest where there is the most intensive growth at the time of the development of rickets. Regarding the significance of changes in the bone marrow in rickets, there is no consensus of opinion yet. Pommer, Schmorl, and Oehme do not find significant changes in the bone marrow in the initial stages of rickets. Marfan and his colleagues see the primary factor in the increased activity of the bone marrow, leading to the changes in cartilage and bone characteristic of rickets. Lymphatic organs (tonsils, lymph nodes, spleen, sometimes the thymus gland) are usually hyperplastic or sclerosed. Most researchers see these changes as the result of infections that often accompany rickets and do not attribute them to the primary process. Marfan considers the changes in the lymphatic apparatus to be an essential part of the rachitic process and proposes replacing the very name rickets with the name "osteolymphatism."

Erdheim, Ritter, Pappenheimer, and Minor found enlarged parathyroid glands in infantile rickets. In the striated musculature of rachitic patients, Bing and Banu described changes in the form of loss of cross-striation, proliferation of nuclei, etc. The brain of rachitic patients is in some cases larger than normal, which most authors explain by the presence of some hydrocephalus; Czerny believes that there is an increase in the brain substance itself. Biochemical deviations from the norm. Rachitic bones contain relatively much water and little ash. In a normal dried bone, the weight ratio of ash to organic components is 3:2, while in a rachitic one it is 1:4. While normal bone in infants contains about 60% ash, in rickets the amount of ash decreases, according to Shabad, to 31% and even to 21%. The decrease occurs mainly at the expense of lime and phosphorus, which form the bulk of the ash. Some authors have found an increase in the magnesia content. In the blood plasma and serum of a rachitic patient, the amount of calcium lies within the normal range (9-11 mg per 100 cm³), unless the rickets is complicated by tetany, which is accompanied by a decrease in the calcium level. An important feature of the blood of a rachitic patient is its hypophosphatemia, a reduced amount of inorganic phosphorus in the serum, specifically 2-3 mg per 100 cm³ instead of the 5 mg normal for children. Small fluctuations in the amount of inorganic phosphorus in the blood are also observed in normal conditions; they have a seasonal character and run parallel to the amount of ultraviolet rays in sunlight, i.e., the amount of phosphorus decreases in winter and increases in summer; but in rickets, the decrease is especially pronounced; it occurs at the very beginning of rickets and passes as soon as improvement begins. In tetany, which often accompanies rickets, the amount of inorganic phosphorus in the blood can be normal or even above normal. The formation of acidic products of intermediate metabolism is increased; in connection with this, the amount of reserve alkali in the blood is reduced, and the excretion of acids and the ammonia neutralizing them in the urine is increased; all this together gives reason to speak of an acidotic direction of metabolism. The excretion of diastase in the urine is also increased. The breakdown of sugar in the blood is slowed down, as a result of which the amount of lactic acid found in the blood is reduced compared to healthy children of the same age. Symptoms and course. Initial manifestations of rickets are often observed in children who are gaining weight well. In a child developing rickets, unusual restlessness and timidity appear; he starts at unexpected noises, sleep becomes less deep, and sweating appears, most noticeable on the head, especially during nursing and sleep. If the child turns his head a lot, as is usually the case with rachitic children, the hair on the back of the head wears off. On the skin of the forehead, neck, and trunk, prickly heat or folliculitis is often found. Upon careful palpation of the skull at this time, it is already possible in most cases to detect abnormal pliability of the edges of the large fontanelle or even soft areas in the parietal bones near the lambdoid suture. X-ray examination does not yet give a picture typical of rickets, but the amount of inorganic phosphorus in the blood may already be reduced. In fully developed rickets, symptoms from the skeleton come to the fore, with more noticeable changes being found in those parts of the skeleton that, at the time of the development of rickets, are precisely in a state of accelerated growth. Therefore, in children of different ages, the most pronounced rachitic bone symptoms are localized differently. For the occurrence of rachitic changes in the skeleton, in addition to growth disorders, various mechanical factors are important, such as the action of body weight, muscle pull, etc. If rickets develops in the first half of the first year, when the head is increasing especially rapidly, rachitic changes are discovered primarily on the skull; a little later, changes on the chest become more prominent; in the second year, when children begin to stand and walk for long periods and the pressure of body weight on the legs acquires more significance, curvatures of the lower extremities intensify, etc. On the bones of the skull, craniotabes develops first of all; softening of the flat bones of the cranial vault occupies more or less extensive areas in the posterior parts of the parietal bones; abnormal pliability can also be detected along the cranial sutures; the edges of the large fontanelle thin and soften, so that in many cases it increases in size or closes later than in a healthy child, i.e., not at the end of the first year or the beginning of the second, but significantly later. Due to the thickening of the periosteum on the flat cranial bones and the subsequent formation of osteophytes, the frontal and parietal eminences protrude on the skull more than normal; with excessive development of the parietal eminences, the outlines of the back of the skull acquire a resemblance to buttocks, hence the name caput natiforme; with strong development of the frontal eminences, a so-called "Olympic forehead" is obtained; in the case of sharp development of both pairs of eminences, the skull has a saddle shape with a flat cross-shaped depression in the middle; with flattening of the occiput, a brachycephalic or, as it is inaccurately called, a "square" skull (caput quadratum); the pliable base of the skull, under the pressure of the spine, protrudes into the cranial cavity more than normal (Recklinghausen). This circumstance, together with the delay in the development of certain cranial bones, can be the cause of the deep position of the bridge of the nose and changes in the shape of the orbit; the latter, in turn, contributes to the appearance of a certain exophthalmos observed in rachitic patients. The upper jaw is flattened from the sides, which causes its anterior part to protrude forward; in connection with this, the arch of the hard palate is often narrow and high in rachitic patients, which can lead to deformation of the nasal septum. The lower jaw is flattened in front, so that its shape approaches a trapezoid. As a result of these jaw deformations, an incorrect bite of the teeth occurs (see also Teeth). The chest undergoes diverse deformations (see Chest - chest deformations). Kyphosis develops in the region of the lower thoracic vertebrae, as the weak back musculature cannot hold the torso straight. Initially, this curvature is easily correctable if the child is placed on his stomach, but subsequently, it becomes more fixed. Sometimes there is also scoliosis with corresponding asymmetric rib deformations. In the shoulder girdle, curvatures of the clavicle appear, the normal S-shaped curvature of which is pathologically increased; fractures are also not uncommon on it. On the upper limb, the thickening of the distal epiphyses of the forearm bones stands out the most. The humerus is slightly curved, its convex side facing outward and forward. The bones of the forearm are curved in the lower third; the radius sometimes forms a spiral bend around the ulna. The habit of rachitic children to sit while propping themselves up with their hands intensifies these limb curvatures. Due to the thickening of the phalanges, the jointed structure of the fingers is especially emphasized, which gave German authors reason to compare the fingers of a rachitic patient to a string of pearls. The pelvis of rachitic patients is smaller than normal; due to the insufficient development of that part of the pelvis which is formed by the ilium, and due to the forward tilt of the upper part of the sacrum under the action of body weight, the true conjugate (conjugata vera) is especially strongly shortened. Under the influence of lateral pressure from the femoral heads, the outlines of the pelvic inlet can approach the shape of a triangle. In more severe cases, the lateral parts of the pelvis even protrude inward, the symphysis region is pulled forward, and a number of other changes appear, bringing the shape of the pelvis closer to the shape observed in osteomalacia (see Pelvis). The significance of these deformations for the mechanism of labor is obvious. On the lower extremities, there is most often a curvature of the bones in the lower third of the shin, with the convex side facing outward; less frequent are curvatures in the knee area inward, outward, or backward: genu valgum, genu varum, genu recurvatum (see Knee joint). In the femur, a curvature with the convexity outward is often observed; with the simultaneous presence of genu varum, both legs form the outline of the letter O; with bilateral genu valgum, a resemblance to the letter X is obtained; genu valgum, in connection with the weakness of the musculature and ligaments characteristic of rickets, contributes to the development of flat feet. Czerny believes that in the occurrence of rachitic curvatures of the limbs, in addition to mechanical factors, the uneven tension of antagonistic muscle groups is also of importance.

In favor of such a hypothesis speak the pathological changes discovered by Krasnogorsky in the muscle contraction curve in rickets (shortening of the latent period, a slower and higher rise of the curve). The neck of the femur may be bent such that it forms not an obtuse, but a right or even acute angle with the shaft of the bone (coxa vara); with this deformity, children walk with a characteristic waddling "duck" gait. The curvature of the long bones of the limbs results in a relative shortening of the limbs. The articular ligaments are more pliable than normal, which favors the appearance of curvatures in the spine and in the joints of the limbs. Thanks to muscular hypotonia and the flaccidity of the ligaments, more extensive excursions are possible in rachitic joints than in healthy ones; thus, a rachitic child easily bends in two, "like a pocketknife," takes their toes into their mouth, or even places their leg on the back of their head. The flaccidity of the musculature is also the main cause of the large size of the "frog" belly of the rachitic child. Upon the conclusion of the period of active rickets, the normal tone of the musculature is gradually restored. The question of the time of appearance and the condition of the milk teeth in rickets was the subject of a long discussion. At the present time, it can be considered established that, on average, the time of appearance of the first teeth in a rachitic child is delayed compared to healthy children. However, individual variations in the time of tooth eruption are very great even in normal conditions; on the other hand, besides rickets, there exists a number of other causes leading to the delayed appearance of the first teeth, such as, for example, myxedema, mongolism, and certain other diseases, therefore this symptom has relatively little significance. Of greater importance are irregularities in the order of tooth eruption and abnormally large pauses between the appearance of two members of the same pair of teeth, which are observed not infrequently in rachitic children. Anomalies in the development of milk teeth, enamel defects, etc., can be caused, just like delayed eruption, by the most diverse metabolic disorders that coincide in time with the period of tooth development. Deformations and small sizes of the jaws sometimes lead to an incorrect position of the permanent teeth as well in children who suffered from rickets in early childhood. Regarding the histological structure of teeth in rickets, see Dentin. The organs of respiration and circulation also suffer in severe degrees of rickets. As a result of a number of bony and muscular rachitic defects of the chest, the lung expands quite insufficiently during inhalation, and atelectatic areas form in it, especially in the posterior and lower parts. A child with severe rickets of the chest always experiences some shortness of breath. With increased demands on tissue respiration, for example, during a febrile illness, the insufficiency of respiratory function reaches an extreme degree in rachitic children and can even, as Engel showed, lead to death without there being pneumonic foci in the lungs. The high percentage of mortality from pneumonia among rachitic children is the result, mainly, of the unfavorable conditions indicated here, in which the function of respiration proceeds. The above-described deformations of the chest, insufficient function of the diaphragm, and changes in the lungs create difficulties for the work of the heart as well, especially its right half. The disorder of cardiac activity, in turn, worsens the prognosis of pulmonary diseases in rachitic children even more. Rachitic children often suffer from acute or chronic intestinal disorders, the etiological connection of which with rickets is difficult to establish precisely. In many, constipation with fatty-soapy stools is observed. Meteorism with atony of the musculature of the abdominal and intestinal walls leads to an increase in the size of the abdomen. The liver is rarely significantly enlarged in rickets, but due to congestion, its edge is often palpable somewhat below the costal arch; furthermore, the narrowed and deformed chest also causes a downward displacement of the liver. Whether lymphatic organs are enlarged in rachitic children is a subject of discussion. Thus, Marfan notes among rachitic children 80% with enlarged lymph nodes, 78% with adenoids, and 65% with enlarged tonsils. Corresponding to his views on the etiology of rickets, Marfan sees in the enlargement of the lymphatic apparatus the result of the action of etiological factors specific to rickets. Other authors, for example, Gyorgy, see here only a coincidence, quite natural in countries where both rickets and hyperplasia of the lymphatic organs are very common. Hess reports that in Kingston, Jamaica, where rickets is almost never encountered, adenoids are a very common phenomenon. Specific antirachitic agents, such as cod liver oil and ultraviolet rays, often have no effect on these changes in the lymphatic apparatus, which also speaks against a connection between these changes and rickets. In any case, a noticeable enlargement of the peripheral glands in rickets usually cannot be noted, and if it is present, one must look for other causes for it: exudative diathesis, tuberculosis. The situation is analogous with the question regarding the relationship of an enlarged spleen to rickets. While Marfan classifies chronic megalosplenia as a symptom of rickets, the majority of other authors do not agree with this. Kuskow draws attention to the lack of parallelism between the severity of rickets and the degree of enlargement and induration of the spleen, as well as between the number of rachitic children and children with an enlarged spleen among different groups of children. Hess found the spleen enlarged in rachitic children only slightly more often than in non-rachitic children (in 25% against 20%) and does not classify enlargement of the spleen as a symptom of rickets. In many cases of rickets, there is anemia, expressed by a decrease in the amount of hemoglobin and erythrocytes; often, anisocytosis, poikilocytosis, and also erythroblasts are found in this condition, especially in patients with significant enlargement of the liver and spleen, representing a transition to von Jaksch's anemia (Hochsinger). On the part of the white blood cells, there is usually relative lymphocytosis, sometimes leukocytosis. Some authors (Marfan, Ashenheim, Hutinel, Benjamin, Barberi) link this anemia etiologically with rickets, while others (Czerny, Kuskow, Findlay, Wieland, Hess) deny such a connection, pointing to the lack of parallelism between rickets and anemia and to the fact that specific antirachitic agents do not have an influence on the anemia accompanying rickets, and vice versa: iron preparations and other agents against anemia do not influence rickets. Gyorgy, while considering alimentary and infectious harmful factors to be the main cause of the anemia observed in rachitic children, still attaches importance to the acidosis accompanying rickets in its emergence. The systolic murmur, which is sometimes heard in rachitic children in the area of the large fontanelle (Fischer's sign) and was previously considered a sign of rickets, is an anemic murmur and represents nothing characteristic of rickets. On the part of the nervous system, pathological phenomena are discovered very early; already the first symptoms—timidity, irritability, sweating—indicate its involvement. At the beginning of the disease, the rachitic child often protests with crying against any touch, but this is apparently the result of a negativistic mood, and not an increase in pain sensitivity. The aforementioned muscular hypotonia also speaks for the involvement of the nervous system. The development of static functions is slowed: rachitic children do not learn to hold their head, sit, stand, or walk for a long time; when taken under the arms and lifted, a rachitic child who does not yet know how to stand keeps their legs pulled up to their abdomen, as if not knowing their use. In some, cataleptic phenomena, noted for the first time by Epstein, are observed: the prolonged maintenance of an artificially imposed posture. The tonic convulsions in the form of laryngospasm and general clonic convulsions often observed in rachitic children do not, strictly speaking, belong to the clinical picture of rickets, but depend on the tetany that often accompanies it. In rachitic children, there is, in the opinion of Czerny, an increase in the brain substance itself ("hypertrophia cerebri"). Based on the calculation of a special "cranial index" (the ratio between the area of the base and the area of the largest horizontal section of the skull), Goldchinsky confirms this indication of Czerny. Sometimes a small degree of hydrocephalus is observed in rachitic children (see Hydrocephalus). The psyche of the rachitic child presents a number of peculiarities. The tearfulness, irritability, and negativism observed at the beginning can in severe cases be replaced by apathy: children lie motionless for long periods, looking indifferently at their surroundings. Czerny also notes a blunting of taste sensations: rachitic children can indifferently drink cod liver oil or a quinine solution. The presence of cerebral symptoms ("cerebral component" according to Czerny) gave grounds to assume mental retardation in rachitic children. Goldchinsky even finds it possible to speak of "rachitic dementia" (dementia rachitica). The delayed acquisition of the ability to move limits the life experience of rachitic children compared to the experience of their healthy peers; furthermore, among rachitic children, there are more children neglected in pedagogical terms than among non-rachitic children, for reasons of a socio-economic order. In severe and long-lasting cases of rickets, there is usually a significant decline in nutrition, which can also contribute to a delay in development. By all this, the retardation in mental development sometimes observed in rachitic children can be fully explained.

That rickets does not leave long-term traces on the mental development of children is also acknowledged by Gulchinsky. The complex of symptoms of rickets creates in most cases a characteristic general appearance of the child, sometimes allowing a diagnosis to be made from a distance. The plumpness of rachitic children is often excessive ("fat rickets"); in children of this type, rachitic changes are often expressed particularly strongly. Upon general examination, the large head draws attention; it is enlarged mainly at the expense of the cranial vault. The facial skeleton, on the contrary, is weakly developed, which causes small facial features, against the background of which the aforementioned exophthalmos stands out particularly. Furthermore, edema and drooping of the upper eyelid ("ocular symptom") are noted in 20% of all rachitic children. The "Olympic" forehead overhanging the small face gives it a characteristic appearance. Compared to the large head, the stunted and laterally flattened chest produces a particularly pitiful impression. Together with the "frog" abdomen, they form a pear-shaped torso. If this figure also stands on bowed legs, a significant shortening of the total body length results. However, as Dombrovskaya showed, the sitting height is also reduced in rachitic children, which depends not only on kyphosis but also on the retardation in the development of the cartilaginous skeleton. The course of rickets reveals a peculiar cyclicity, which is conditioned, on one hand, by age, and on the other, by climatic influences associated with the change of seasons. The question of at what age rickets can arise is closely connected with another question: is rickets congenital? In newborns, softness of the cranial bones is sometimes observed, which Kassowitz considered a symptom of congenital rickets. The dispute that flared up around this question can now be considered resolved by the works of F. Chistovich, A. Razumovsky, Kuskov, Wieland, Schmorl, Pommer, Abels, Hottinger, Hess, and others (Wieland, Abels, Hottinger). Clinical, anatomical, and biochemical studies show that the soft areas on the cranial bones of a newborn represent not rachitic changes but developmental defects, and that congenital rickets, if observed at all, is very rare. However, it seems that children with congenital ossification defects are more predisposed than others to the development of rickets. Manifestations of the rachitic process are observed in most cases no earlier than the 3rd month of life. The metabolic disorder associated with rickets may begin earlier, but it usually takes several weeks for the changes it causes to reach such a degree that they can be detected by clinical research methods. After the second year of life, when the intensity of growth significantly weakens, fresh cases of the disease are encountered very rarely. Thus, rickets is observed predominantly between the ages of 2 months and 2 years. In children under 8-9 months of age or in premature infants, who grow particularly rapidly, the disease can develop quite quickly, almost like an acute illness. When there is a full development of symptoms of fresh rickets while the child's good general condition is preserved, one speaks of "florid" rickets (rachitis florida). When a child around a year old or older falls ill, or when the sick child is not entirely deprived of the action of ultraviolet rays and vitamin D in food, then the disease proceeds more chronically and does not reach very severe degrees. Within the indicated age limits, the number of fresh cases fluctuates strongly depending on the time of year. As Kassowitz first noted, in winter and especially closer to the beginning of spring, the greatest number of new cases is observed; Hansemann confirmed this observation on pathological-anatomical material; he pointed out that on the corpses of children born in the spring and who died in the autumn, signs of rickets are almost never seen, while the corpses of children born in the autumn and who died in the spring show such signs very often. Periodic exacerbations and improvements associated with the change of seasons can repeat several times, as clinical observations and pathological-anatomical studies show. If children are rarely taken out into the sun even in summer, or if climatic conditions hinder the action of ultraviolet rays, for example, due to a high content of water vapor in the air, summer remissions may not occur.

observed by Zhukovsky in old St. Petersburg, or they are weakly expressed and are discovered only towards autumn, as described under the name of "summer" rickets by Schonen in Greifswald. Under these conditions, the most severe forms of the disease can develop. At the III All-Union Congress of Pediatricians (1925), a temporary working classification of rickets was adopted, in which 3 degrees of it are distinguished: 1st degree is characterized by a small number of weakly expressed signs without disturbance of the general condition; 2nd degree—with moderately expressed symptoms, an enlarged spleen (not necessarily) with a good general condition; 3rd degree—with severe changes in the bones, muscles, and nervous system, with sharp anemia, a large spleen, general decline in nutrition, and retardation in development. Rare forms of rickets. Late rickets (rachitis tarda). This primarily includes prolonged and recurrent cases in which symptoms develop after the age of four. Schmorl called such cases "rachitis inveterata" (chronic rickets). Less frequently, late diseases are observed in individuals who did not suffer from rickets at all in early childhood or in whom rickets of early age had long since passed. In these cases, the disease usually occurs between 12 and 18 years of age and coincides with the period of puberty (rachitis adolescentium). Boys fall ill significantly more often than girls, and those who suffer are predominantly individuals employed in such professions where one has to stand on one's feet for a long time, walk a lot, or carry heavy loads (messengers, delivery men, etc.). In countries that were subjected to a hunger blockade during the war of 1914–18 (in Austria and Germany), mass diseases were observed in 1918–20, the so-called "wartime juvenile osteopathies," which apparently represented a variety of late rickets. Some authors (Schmorl, Mikulicz) also classify isolated curvatures, such as scoliosis or deformities of the lower extremities, etc., often observed in older childhood and adolescence, as late rickets. Others (Czerny, György) do not link these forms to rickets, considering them merely the result of mechanical factors. Under the name of renal rickets, a very rare disease was described (predominantly by English authors), characterized by retardation of children in growth, bone symptoms of rickets, and sclerotic changes in the kidneys; this condition was also designated as "renal infantilism" or "renal dwarfism." The disease is usually discovered at preschool or school age. Histological examination of the kidneys reveals a picture of a shrunken kidney. Specific antirachitic agents (ultraviolet rays, irradiated ergosterol) prove ineffective in this disease. Most patients die at a young age with symptoms of uremia. The pathogenesis of this condition has not yet been clarified. Some authors, e.g., Hess, distinguish as a special intestinal form of rickets (coeliac rickets) those cases that are observed in children with so-called "intestinal infantilism" (Coeliakie, Herter-Heubner disease) (see Infantilism). Diagnosis. Despite the fact that pronounced cases of the common form of rickets do not present difficulties for recognition, diagnostic errors are made not infrequently. According to the "temporary working classification of rickets" adopted at the III All-Union Congress of Pediatricians (see above), the diagnosis of rickets must be based on the presence of at least 2 symptoms, one of which must necessarily be skeletal; only in the presence of craniotabes is it permissible to diagnose rickets on the basis of a single symptom. However, not every softening of the skull is a symptom of rickets. Softenings observed in newborns or in children younger than 2–3 months, in the vast majority of cases, represent congenital defects of ossification. Besides the time of appearance, they differ from rachitic craniotabes by their localization (predominantly along the course of the sagittal suture, and not in the posterior parts of the parietal bones) and more sharply defined boundaries. In newborns, small curvatures of the shins are often observed, which, like the softenings of the skull, are not connected with the rachitic process, but depend on the position of the fetus in the uterus. Insignificant thickenings at the border between the ribs and the costal cartilages in the form of a narrow ridge should also not be considered as a sign of rickets. Such thickenings are often palpable even in newborns free from rickets. Only more significantly pronounced swellings of the costal cartilages in the presence of other signs of rickets can be recognized as rachitic "rosary." A certain pliability of the chest and its flattening in the lower parts during inhalation due to insufficient hardness of the ribs is sometimes encountered in atrophic children even without rickets. That the delay in the appearance of milk teeth can be caused not only by rickets has already been mentioned. The same should be said regarding the delayed development of static functions. All these data must be kept in mind so as not to diagnose rickets more often than it actually occurs. In the differential diagnosis of rickets, one must keep in mind a number of diseases with which it was often confused in the past. A child suffering from congenital syphilis may present a number of symptoms similar to the symptoms of rickets. Old French clinicians—Parrot, Fournier, and others—saw in the rachitic symptom complex the result of syphilitic infection. Marfan even at the present time classifies as "syphilitic rickets" cases observed in children up to 3 months of age and characterized by large cranial bosses, enlargement of the spleen, and significant anemia. But syphilitic deformities of the skull are usually much more sharply expressed than rachitic ones; periosteal thickenings on the long bones are often painful; the "saber shin" protrudes for the most part anteriorly, and not laterally as in rickets, and its peculiar shape is caused not so much by curvature as by abnormal deposits on the anterior surface. On the other hand, a rachitic child never has that peculiar general appearance which is observed in syphilitics and depends on a special skin color (the color of old wax or the color of smokers' fingers), the absence of eyebrows, the presence of radiating scars around the mouth, etc. Besides the characteristic general appearance, the following can serve to distinguish congenital syphilis from rickets: an anamnesis typical for a syphilitic family (illness of parents, miscarriages, premature children, illness of other children), the time of appearance of symptoms (rachitic changes do not usually manifest before the third month), the presence of chronic rhinitis, specific rash, Parrot's pseudoparalysis, osteochondritis, enlargement of lymph glands, especially above the condyles at the elbow joint, positive Wassermann reaction. Syphilitic osteochondritis (see) differs from rachitic changes in the bones and on an X-ray image. It is understandable that in a syphilitic child, under appropriate conditions, rickets can also develop. Like any prolonged disease, syphilis favors the development of rickets; then a combination of symptoms of both diseases is observed. Infantile scurvy (see Barlow's disease) can be mistaken for rickets due to the appearance of thickenings near the epiphyses on the limbs and a "rosary" on the ribs and due to the disorder of static functions and movements. The differences are: nutritional deficiencies in the past characteristic of Barlow's disease (feeding the child excessively long with boiled or melted milk, absence or sharp deficiency of vegetables and vegetable juices in the diet over a long period, etc.); sharp pain in the bones upon pressure due to the presence of subperiosteal hematomas or fractures; hemorrhage in the skin or on the gums (if teeth are already present), hematuria; Rumpel-Leede sign. Mild degrees of hypothyroidism are sometimes mistaken for rickets, but in this disease, there is never softening of the cranial bones as in rickets, the edges of the fontanelle are hard and unyielding; there is no "rosary" and thickenings of the epiphyses on the limbs. The skin is dry and rough, in contrast to the smooth, often moist skin of a rachitic child. The growth retardation present in hypothyroidism is an obstacle to the development of rickets, which is why these two diseases are not encountered together. Chondrodystrophy, or achondroplasia (see), unlike rickets, is a congenital disease, developing already in the period of intrauterine life, hence the old name "fetal rickets." Clinically, one can distinguish chondrodystrophy from rickets most likely by the disproportionately short limbs with coarse outlines of the bones. This congenital deformity does not yield to antirachitic treatment. Congenital fragility of bones, or osteopsathyrosis (see Osteogenesis imperfecta, Osteopsathyrosis), in which there are sharp deformities of the skeleton, and sometimes a soft skull, presents a similarity to severe rickets, but while rachitic deformities are caused by bending of the bones, sometimes accompanied by fractures (fissures), but almost never show complete fractures, in osteopsathyrosis there are multiple complete fractures, often with displacement of fragments. In many cases of osteopsathyrosis, blue (due to the translucency of the underlying tissues) sclerae are noted as a manifestation of hypoplasia of all mesenchymal formations in the body.

Here, the hypophosphatemia characteristic of rickets is absent, nor are there the X-ray features typical of rickets in the form of a curved and serrated border between the epiphysis and diaphysis; however, there is a strongly pronounced osteoporosis with a very thin cortical layer and sparse, delicate trabeculae in the spongy bone. Combinations of osteopsathyrosis with rickets are encountered. In pure cases of osteopsathyrosis, specific anti-rachitic agents are ineffective. The large head of rachitic children often suggests the presence of hydrocephalus. Above (see symptoms) it was indicated that in rickets there is sometimes indeed a slight hydrocephalus. The further course and the effect of anti-rachitic therapy or, if necessary, a lumbar puncture can clarify the cause of the increase in skull circumference. Muscle weakness and lethargy can be so sharply pronounced in rickets that they arouse suspicion of the presence of paralysis. A detailed examination of the nervous system clarifies the matter. Tuberculous spondylitis, which presents an external resemblance to rachitic kyphosis, involves only a small number of vertebrae, forms a sharper angle rather than a gentle arc, is accompanied by pain during movement, and does not disappear when the child is placed on their stomach (see above). Congenital dislocation of the hip joint, which bears a resemblance to coxa vara rachitica due to the "duck" gait and the high position of the trochanter, can be recognized by clinical signs (see Dislocations) and with the help of X-ray examination. X-ray diagnostics of rickets utilizes the pathologico-anatomical changes described above; in the bones, this appears as an abnormally wide layer that has arisen between the epiphysis and diaphysis, consisting of cartilage, osteoid tissue, blood vessels, and bone marrow cavities, which absorbs X-rays poorly due to a deficiency of salts. These changes are best seen in the long bones, but since their development requires time, measured in weeks and sometimes 1-2 months, other symptoms (from the nervous system or softening of the flat bones of the skull) can often be detected earlier. X-ray radiography is therefore not a method for the early diagnosis of rickets. The great merit of this method, however, lies in the fact that it leaves us with an objective document that allows us (if images are taken repeatedly) to follow the course of the process and thus precisely check, for example, the influence of therapeutic measures. Due to technical convenience, images for diagnostic purposes are produced primarily from the distal ends of the bones of the forearm. At the beginning of the disease, on the X-ray image, the border between the diaphysis and the epiphyseal cartilage is seen less clearly than in the norm, as a result of the absence of a zone of preliminary calcification in the cartilage. In later stages, this border becomes serrated, as if fringed; even later, the general contour of the border acquires in some bones, for example in the ulna, the shape of an arc with its convexity facing the epiphysis, so that the diaphysis ends as if in a flat bowl. At the same time, the outlines of the cortical layer also become less clear, and the entire bone gives a less intense shadow due to the poverty of salts. During recovery, a narrow strip of shadow first appears in the light area, at some distance from the diaphysis, as a result of the restoration of the zone of preliminary calcification in the cartilage. In cases where rickets has relapsed and the recovery process has begun twice, one can detect two such strips running parallel. As improvement continues, the abnormally wide layer between the diaphysis and the epiphysis also begins to cast a shadow due to increasing salt deposition. The shadow of the entire bone becomes more intense again; a shadow from newly formed osteophytes under the periosteum also appears. Hypophosphatemia, observed in rickets (see above), occurs very early, is a very constant sign, and therefore has great diagnostic significance, but the methods for its detection proposed so far are quite complex and cannot be widely applied under any conditions. Since in rickets the amount of calcium in the blood is usually not reduced and amounts (according to Hess) to about 10 mg per 100 cm³ of serum, and the amount of inorganic phosphorus is less than 4 mg, Howland and Kramer established a diagnostic rule according to which rickets can be considered excluded if the product of the numbers representing the amount of calcium and phosphorus in milligrams is greater than 40. This rule, suitable for the majority of cases, can be violated in rickets complicated by tetany. Besides tetany and rickets, other diseases can influence the amount of phosphorus in the blood, such as chronic nephritis, in which it increases, or pneumonia and other febrile diseases, in which it can be lowered. It must also be kept in mind that there is not always a strict correspondence between hypophosphatemia and the clinical symptoms of rickets. When recovery begins, the amount of phosphorus in the blood approaches normal again very soon, whereas clinical manifestations may persist significantly longer. Therefore, the diagnostic use of the amount of phosphorus in the blood should be performed with caution, taking into account all circumstances that may influence this symptom. Prognosis. Mild cases of rickets proceed favorably and leave no consequences. More severe cases are almost always accompanied by various complications, which mainly determine the outcome. Whether rickets in a given child will proceed as a mild or severe disease depends on many circumstances. Besides familial or racial characteristics, other congenital factors may have significance here; thus, premature infants almost always suffer from a more severe form of rickets than full-term ones. But conditions surrounding the child after birth have greater significance than congenital factors. Children born in the spring and who had the opportunity to be in the sun during the first 6-8 months of their lives usually suffer from a milder form of rickets. Conversely, children born in the autumn usually all suffer (in our latitudes) from a relatively more severe form of rickets. Socio-economic and living conditions also have a great influence on the course of rickets. Among the complications that have great significance for the outcome of rickets, diseases of the respiratory organs, and above all bronchopneumonia, occupy the first place. It was already indicated above that rachitic children fall ill with pneumonia more often than others and that among those who fall ill with it, the mortality rate is much higher than among children free from rickets. The reason for this lies not only in the unfavorable mechanical conditions of breathing arising from the softening of the chest cage but also in the reduced immunity of the rachitic child. Infectious diseases proceeding with phenomena from the respiratory organs, such as measles or whooping cough, present a particularly great danger for the rachitic child, as in combination with rickets they give many complications and a high mortality rate. The prognosis of each individual case of rickets depends further on whether it is accompanied by phenomena of tetany or not. György considers rickets and tetany as two phases of one and the same metabolic disorder. In children, tetany almost always develops on the basis of rickets. The addition of tetany sometimes means a mortal danger for the rachitic child from general convulsions, laryngospasm, cardiac arrest, etc. When making a prognosis for rickets, one must keep in mind not only those diseases that accompany it during the active period but also more distant consequences. How often rickets leaves traces for many years is evident from the data of Pye (Rune), who examined 30,000 school-age children in this regard in Magdeburg (Germany) and found among them only 20% to 30% without any traces of rickets. If a significant part of the rachitic changes on the skeleton does not have great practical significance and if many of them gradually pass with the years, for example, not very severe curvatures of the lower extremities, there are still not a few such cases where the consequences remain for life, influence the function of the lungs, heart, and other systems unfavorably, and are reflected in morbidity and working capacity. Prophylaxis. Public measures for combating rickets. Since the economic and cultural level of the main masses of the population plays an important role among the etiological factors of rickets, all measures that raise this level are favorably reflected in the incidence of rickets, although they are not aimed directly against it. The correct planning of buildings in cities, compliance with hygienic norms in the ratios between built-up and non-built-up areas, between the height of houses and the width of streets, etc., has great significance for the fight against rickets. The layout and character of buildings must be such that sunlight is not blocked from courtyards and apartments and that enough space remains for green spaces, playgrounds, etc. Naturally, under the conditions of the capitalist system, there could be no talk of real, broad measures that could change this situation.

Changes in the daily life of the broad working masses, associated with the housing policy of the Soviet government, along with the growing strengthening of the population's well-being, the broad development of public catering, and the deployment of preventive institutions, have caused a huge shift in the problem of rickets, but intense work is still required for the further improvement of working-class life and the maximum introduction of hygiene rules into it. The observance of hygiene requirements during construction, which is extremely important in new construction and at new building sites, must be one of the most important measures of public prevention of rickets. Sanitary education is of no less importance for the fight against rickets than housing construction. In cities where a significant portion of women are covered by the sanitary-educational work of maternity and infancy protection institutions, where it has been possible to weaken the exaggerated fear of colds and ensure that infants are taken out into the fresh air sufficiently and at all times of the year, severe forms of rickets are already encountered less frequently. The greater spread of sanitary education and especially its strengthening in the countryside should lead to a further reduction in the incidence of rickets. The main measures of preventive struggle against rickets are the promotion and organization of taking children out into the fresh air from the earliest age, proper nutrition and care, the expansion of the bases of public forms of upbringing (crèches at enterprises, institutions, housing cooperatives, summer rural crèches, public catering), etc. Among the measures of a public nature aimed directly at the fight against rickets, one should first of all name the organization of special registration of children particularly at risk for rickets. Consultations must keep separate lists of children living in particularly poor conditions, those born in the autumn, premature infants, twins, etc., who, as experience shows, almost inevitably contract rickets. Subsequently, the consultation ensures that these groups of children receive proper prevention and, if necessary, treatment in the first instance. At consultations for children, at crèches, kindergartens, housing cooperatives, etc., playgrounds are set up where children can receive air, sun, or sand baths and other physiotherapeutic procedures. In large cities, it is desirable to move some of these playgrounds outside the city limits, where the climate, factors important for the fight against rickets, act much more strongly than in the city itself. Settling children for 2-3 months in colonies or sanatoriums in the mountains, where ultraviolet radiation is very intense, or on the seashore, where, in addition to ultraviolet radiation, there are other factors essential in the prevention and therapy of rickets (sea and sand baths, air movement and its character, etc.), represent a very powerful means of influencing rickets, but they cannot yet have great significance; there is not yet a sufficient number of well-appointed mountain climatic stations where young children could be settled; among seaside resorts, the southern ones (on the Caucasian and Crimean coasts of the Black Sea) present a danger of overheating for young children in the summer; the climate of the Murmansk coast is unsuitable for young children; there remains the coast of the Gulf of Finland, which has only local significance. It must be clearly understood that the prevention of rickets is the prevention of huge masses, and it must be carried out on the spot. For the prevention and treatment of rickets in the cold season and in cloudy weather, physiotherapeutic offices at children's institutions, equipped with a source of ultraviolet rays, such as the mercury-quartz lamp of Jesionek, Bach, an arc lamp, etc., can serve as auxiliary methods. Ultraviolet irradiation of pregnant women and nursing mothers can also be performed here. To increase the throughput of physiotherapeutic offices, chambers with such lighting installations are sometimes set up at them, which allow for the irradiation of a significant group of children at once. Goldberg designed a pavilion in which strong quartz lamps are installed on the sides, and a moving walkway passes through the middle, on which the children being irradiated are placed. The power of the lamps is such that during the child's movement from the entrance to the exit, he receives a sufficient dose of ultraviolet rays. The speed of the walkway can be adjusted as desired. This device allows up to 250 children to be processed per hour. After Hess and Steenbock discovered the activating effect of ultraviolet irradiation on certain food products, in a number of cities in the USA and Western Europe, centralized supply of the child population with irradiated milk was organized for the purpose of mass prevention and therapy of rickets. Irradiated butter, egg yolks, and other products were also tested. When factory-made preparations of irradiated ergosterol (see Irradiated preparations) appeared, it became possible, instead of irradiating milk, to mix ergosterol into it before distribution, which significantly simplified and cheapened the process. Degkwitz proposed mixing irradiated ergosterol into flour, and Vollmer successfully used cookies with ergosterol. Hess, Lewis, MacLeod, and colleagues, instead of irradiated milk, used milk from cows to which irradiated ergosterol or irradiated yeast had been added to their feed as a rich source of ergosterol. All these experiments have not yet received wide application, but all have yielded a positive result. Public prevention and therapy of rickets with the help of irradiated food products or those enriched with irradiated ergosterol has a number of advantages over direct irradiation of children with a mercury-quartz lamp: there is no need to transport them to the place where the lamp is installed; the danger of mutual infection of children with various infections when they gather there is eliminated; it is easier to carry out treatment over a long period of time, since the therapeutic effect on children occurs imperceptibly and automatically; finally, this method could be cheaper than direct irradiation of children if the price of equipment and the exorbitantly high profits of manufacturers of activated preparations were lowered. However, when it became known about the adverse side effects of (mainly German) preparations of irradiated ergosterol (see below), voices began to be raised (Jundell, Czerny, etc.) about the inadmissibility of widespread and uncontrolled consumption of irradiated or ergosterol-enriched products and about the necessity of dispensing them only by doctors' prescriptions. The modern silicate industry manufactures glass that transmits ultraviolet rays at a price only slightly higher than ordinary glass. Glazing children's institutions and children's rooms in apartments with such glass could be of great importance for the prevention of rickets if the light penetrating into the premises contained a sufficient amount of ultraviolet rays, which at the present time occurs only to a small degree. When the replanning of old cities and the construction of new ones make the penetration of direct sunlight into houses sufficiently possible, and especially when the electrification of factories, plants, and railway junctions frees large cities from the cloud of soot and vapors hanging over them, which block ultraviolet rays, then the glazing of buildings with ultraviolet-transmitting glass will be able to acquire very important significance among the measures for the fight against rickets. At the present time, for the public prevention and therapy of rickets, the use of such electric lamps for artificial lighting of buildings, which send not only visible light rays but also the necessary amount of ultraviolet rays with a wavelength of the appropriate length and which can serve simultaneously for two purposes: for lighting and for treatment, is of great importance. By selecting a suitable recipe for the glass mass, it is possible to manufacture such glass that transmits in sufficient quantity the ultraviolet rays important for the fight against rickets with a wavelength of about 290-310 mµ and at the same time does not transmit rays with a wavelength shorter than 270-280 mµ, which have an irritating effect on the skin and eyes and require great caution and constant medical supervision during their use. From such glass, which is hard enough to withstand strong heating, bulbs for lamps are manufactured, inside which there is a tungsten incandescent filament or tungsten electrodes. Goldchinsky and Gerstenberger, who studied the results of using such lamps and obtained a clear antirachitic effect, note the similarity of their action in some respects (in terms of the nature of the tan, gradualness, etc.) to the natural action of the sun. Uncontrolled use of such lamps, like the free sale of irradiated food products, can lead to an overdose with its harmful consequences. Public measures for the fight against rickets also include state control and standardization of medicines, devices, and other appliances used for the prevention and treatment of rickets.

This measure is necessary because the quality of individual batches of cod liver oil, factory-made pharmaceutical preparations, various batches of ultraviolet glass, burners for mercury-quartz lamps, etc., is highly inconsistent and often very low. Despite the brilliant successes achieved by technology in the field of "activation" of food products and in artificial lighting, the public fight against rickets should be based mainly not on these measures, but on the creation of such housing, living, and general hygienic conditions for children that allow them to use the sun as much as possible as the main natural defense against rickets. Artificial measures, which are still an inferior substitute for sunlight, should be used only where, for one reason or another, it is not possible to use natural ones sufficiently. Individual prophylaxis. Since every child can develop rickets under appropriate conditions, all children need prophylaxis for it. Individual characteristics of the child (prematurity, growth rate, past illnesses, method of feeding, etc.), family or racial differences, climatic and living conditions can make this need more or less acute and require more or less energetic measures. It has been proven experimentally many times that it is possible to increase the resistance of offspring to rachitogenic harmful factors by influencing the pregnant mother (Korenchevsky, McCollum). Similar experiments on humans have not yet yielded a clear result. Breastfeeding, although it does not guarantee children against rickets, protects them from its more severe forms; therefore, natural feeding is one of the most important preventive measures against rickets. By irradiating the nursing mother with ultraviolet rays or by giving her preparations of irradiated ergosterol, it is possible to increase the antirachitic effect of milk, but even then, a full guarantee against rickets is not obtained. It is not possible to create such a reserve of the antirachitic factor in the child's body that would protect him from rickets for a long time. Even such a strongly acting agent against rickets as illumination with a mercury-quartz lamp does not always protect against rickets when used prophylactically (Guldchinsky, Göttinger). If the action of rachitic factors continues, rickets may still develop some time after the cessation of illumination. Therefore, Guldchinsky recommends repeating the course 3 months after the first prophylactic course of illumination, which lasts 1 month, if the time falls in winter. Preventive measures have to be repeated in the second or even third year of the child's life, especially in areas where a long and harsh winter prevents keeping children in the open air for a sufficiently long time every year for a number of months. General hygienic conditions of the child's care have great preventive significance: sufficient opportunity to move the limbs freely (do not swaddle) and crawl, a long stay in the open air, where not only direct sunlight but also scattered light has an antirachitic effect; if possible, sleeping in the open air or with an open window, light clothing that allows aeration and leaves (in warm weather) the arms and legs open, etc. Taking the child to the countryside in the summer makes light therapy and other measures more effective. Jundell recommends for the prevention of rickets giving children complementary foods of vegetables, fruits, fish, and meat as early as possible, but limiting the total amount of food to 60-70 calories per 1 kg of weight per day. Of the specific antirachitic agents, cod liver oil is used most of all prophylactically, which can be started as early as the second half of the first month, 5 drops 2-3 times a day, in the second month 10 drops 2-3 times, in the third month 1/2 teaspoon, in the fourth 1 teaspoon 2-3 times a day. Egg yolk, which can be given raw at 1/2-1 piece per day, has a less constant effect. The effect of chicken liver and bone marrow is also inconsistent. Individual prophylaxis of rickets with medications and other special means (e.g., physiotherapeutic) largely coincides with its treatment. Treatment. Since rickets almost always develops very slowly, those around the child often do not suspect the onset of the disease for a long time and seek medical help only when some serious changes have already occurred. Very often, rickets is discovered in outpatient clinics by chance in children who have come for an appointment for another reason. Therefore, for the timely start of treatment, it is necessary to catch the corresponding cases, and not wait for them to come. This can best be done by a children's consultation center if its staff pays attention to the detection of early symptoms of rickets. Where the population, as in villages, is not sufficiently covered by a consultation center, an examination of children of the appropriate age (i.e., approximately from 6 to 18 months) is carried out 1-2 times in the winter by the outpatient clinic or the nearest consultation center. The organization of assistance to children in collective farms and state farms is of great importance in this regard. Physical methods of treatment. The use of natural sunlight in the form of sunbaths is of the greatest practical importance. They are not applicable only to very small and weak children due to the easily occurring skin irritation, overheating, and subsequent agitation; they should be replaced in such children with local baths, exposing only the legs, arms, and face to light and covering the torso and head with white fabric. The air temperature during sunbaths should be at least 20°. Start with 3-5 minutes, depending on the intensity of the light, and, increasing the exposure daily by 3-5 minutes, reach 30 minutes. The most favorable time is the morning hours or the late afternoon; one should not take sunbaths near noon at the highest intensity of light (see also Heliotherapy). With air baths (see Aerotherapy), not only thermal irritation of the skin but also ultraviolet rays reflected from the sky and clouds and scattered, the strength of which is no weaker than the action of direct sunlight, have a favorable effect on the rachitic process. The possibility of using air baths even in cloudy weather makes them an extremely important means against rickets in those areas where there are few clear sunny days. In order for an air bath to produce the proper light-therapeutic effect, it must be carried out in an open place, e.g., on a balcony, veranda, platform, etc., where there is sufficient diffuse radiation. Previously, the child must be accustomed to lying naked in the room. The air temperature should be at least 25°; if there is wind, screens, etc., are installed on the sides or a more protected place is chosen. The duration of the bath is gradually increased from 10-15 minutes to 1-2 hours or more, depending on the air temperature. It is desirable that the child moves and crawls during the bath; it is advisable to rub him from time to time; if he begins to feel cold (appearance of goosebumps, shivering, etc.), the bath is stopped. Of the artificial light sources, the use of the Bach mercury-quartz lamp (see Bach mercury-quartz lamp) has become most widespread in the treatment of rickets. Illuminations are usually performed every other day; it is possible, using small doses, to illuminate daily, or, conversely, bringing it to an erythema dose, to illuminate less often, e.g., once a week. At the beginning of treatment, the burner is set at a distance of 80 cm from the patient; it is gradually brought closer to 70-60 cm. The duration of irradiation is initially 2-3 minutes from the front and back; gradually increasing the exposure by 1-2 minutes, the duration of the session is brought to 30 minutes. Fair-haired and atrophic children require very careful dosage. After only a few illuminations, the general condition (sleep, sweating, motor skills) improves. In the presence of craniotabes, one can detect a decrease in its size after 1-2 weeks and judge the speed of improvement objectively by it. Recovery occurs after 10-15-20 sessions, depending on the case and the dosage used. Like prophylactic irradiations, the course of light therapy should be repeated after three months if it was carried out at the beginning of winter. Satisfactory results can also be obtained with significantly lower doses (Vollmer). Instead of a mercury-quartz lamp, an arc lamp of sufficient power (about 15 amperes) can be used; its advantages are that maintenance is simpler and it does not cause burns as easily, but it consumes significantly more electrical energy and its therapeutic effect is weaker, which is why the duration of exposure should be twice as long. Salt baths are used to accelerate metabolism. For the technique of application, see Baths, baths for a child. Sand baths made of sand heated in the sun are used for small children only locally: for the legs and the lower part of the torso. In view of the possibility of contamination of the sand with urine and excrement and infection with worm eggs, the use of sand baths in a home setting is permissible only if it is possible to thoroughly wash and calcine the sand. On the seashore, where sand is used for baths, which has previously been washed for a long time by tides and surf, aired, and heated in the sun, the danger of contamination is less.

The temperature of the sand can be brought up to 40-45°, and the duration to 1/2-1 hour. Exposed parts of the body, and especially the head, must be protected from direct sunlight during this. For the purpose of increasing muscle tone and improving motor functions, gymnastics and massage (see) are used. Diet therapy for Rickets. It is known from experience that abundant nutrition contributes to the development of Rickets, therefore, rachitic children should receive only the strictly necessary amount of food; Yundel suggests 60-70 calories per day per 1 kg of weight. Since the relative richness of food in carbohydrates has an unfavorable effect in Rickets, one should refrain from giving a rachitic child significant amounts of sugar, white bread, cookies, potatoes, oatmeal, etc. Adding egg yolk to the basic diet and introducing complementary foods containing butter and fish as early as possible can somewhat increase the amount of vitamin D in the diet. To a much greater extent, this goal can be achieved by introducing irradiated milk into the diet, which is given in an amount of about 500 cm³ per day. Medicinal treatment. Cod liver oil (1/2-1 teaspoon 2-3 times a day) remains one of the best medicines against rickets, despite the appearance of highly active preparations of irradiated ergosterol: its merit lies mainly in the fact that, in addition to the antirachitic factor, it also contains vitamin A. In view of the great unevenness in the potency of different batches of oil, preparations of cod liver oil are currently being manufactured in which the content of the antirachitic factor is brought to a certain level by adding irradiated ergosterol. Fats from other fish and some marine animals (dolphin, seal, etc.) also contain the antirachitic factor, but usually in a somewhat smaller amount than cod liver oil. The question of the therapeutic value of phosphorus in Rickets still remains controversial. Kassowitz, who introduced phosphorus into the therapy of Rickets in 1884, proceeded from Wegner's observations on the sclerosing effect of minimal doses of phosphorus, but Kisel could not confirm Wegner's experiments. Hess and Weinstock managed to induce the formation of a sclerosed band in the bones of rats as a result of adding phosphorus to their feed, but this band was located in the diaphysis; in the epiphyseal cartilage, where the rachitic disorder of bone tissue growth is localized, no changes were observed, and phosphorus did not protect the animals from experimental Rickets. The named authors therefore believe that phosphorus could be useful only in cases of rickets accompanied by osteoporosis. Stoltzner finds that phosphorus added to cod liver oil can increase its activity, and Marfan, like Kassowitz, uses phosphorus not only in a mixture with cod liver oil but also with other oils, for example, almond oil. It should not be forgotten that phosphorus is a highly poisonous substance. Cases of poisoning from the use of its ordinary doses have been described. Therefore, it must be used with the greatest caution. As Shabad and Schloss showed in metabolic experiments, calcium preparations (calcium phosphate, calcium acetate, calcium lactate, etc.) in combination with other antirachitic agents are useful for those rachitic infants who are breastfed; due to the relative poverty of human milk in calcium, there may not be enough of it in the infant's diet for the calcification of the skeleton during the recovery period. The most rapid therapeutic effect is given by preparations of irradiated ergosterol (vigantol, acterol, preformin, etc.). The activity of different preparations varies: the maximum daily dose of vigantol for infants is 1-2 mg. Marfan recommends using ergosterol with breaks: after 20 days of treatment, a break of 15 days; this advice is especially appropriate in view of the observed toxic effect. First in experiments on animals (Pfannenstiel, Kreitmair, Moll, and others), and then in observations on children (Degkwitz, Pfaundler, Gyorgy, and others), anorexia, weight loss, and kidney damage were discovered. In experimental animals, calcium deposits were also found in the vessels, kidneys, gastric mucosa, lungs, and other tissues. Hess and Lewis found a sharp increase in the amount of calcium in the blood. Subsequently, similar changes were discovered in children as a result of excessive use of irradiated ergosterol. Orthopedic and surgical methods of treating rachitic deformities are used after the process has ended and it can be expected that it will not resume. Curvatures of mild and moderate degree very often pass during the process of further growth of the skeleton without special treatment. For deformities of the chest, a plaster bed, special corsets, corrective gymnastics, etc., are prescribed. For curvatures of the lower limb, splint apparatuses are used or, in more severe cases, surgical intervention (osteoclasis, osteotomy, etc.). See the corresponding deformities.