Exicosis

EXICOSIS (from the Latin siccus-dry), drying, dehydration, a pathological state that arises as a result of the acute loss by the organism of significant quantities of water and salts, depletion of the body's water depots, and in cases of impaired ability of cells and tissues to bind water (see Dehydration). The term "exicosis" is especially widely used in pediatric literature in connection with the significance of E. in the origin of the symptoms of the toxic symptom complex in infants. Czerny, Finkelstein, Heim, and John already in 1900 and 1910 emphasized the significance of rapid water loss in the pathogenesis of toxicoses, without yet using the term E. In 1921, Bessau in Germany, applying the term "exication," and simultaneously Marriott in America placed the significance of E. first in the origin of intoxication in infants. The clinical picture of E. (dehydration according to the terminology of French authors, anhydremia according to the terminology of Americans) is expressed in a rapid fall of the weight curve (by 300-400 g in 2-3 days), dryness of the mucous membranes, especially of the mouth and lips, dryness of the skin, a sharp loss of turgor, expressed in the inability to smooth out skin folds; at the same time, a doughy consistency of the skin may be observed, edema of it on the extremities and even sclerema. Dryness is also detected on the serous membranes, e.g., the peritoneum, pleurae, in the cavities of which often no free fluid is found at all (acute gastroenteritis, cholera, uremia, etc.). The expression of the face changes sharply: sunken eyes, a pointed nose, recession of the large fontanelle; thirst, dysuria, often anuria; in small children of the first months of life, the bones of the skull are observed to lie one on another. The loss of weight in this state is not connected with the breakdown of the subcutaneous fat layer, in contrast to the processes observed in hypotrophies and atrophies, where a gradual, not rapid, fall of weight is noted. One clinical picture does not give a complete idea of E., of its degree. Studies of the blood supplement the symptomatology of E. An increase in the percentage of Hb, the number of erythrocytes, an increase in the dry residue, viscosity of the blood, an increase in the amount of protein, serum, resp. plasma, indicate thickening, therefore depletion of the aqueous part of the blood. According to some authors, this thickening of the blood is the basic pathognomonic sign of E. (Schiff). However, the gradual, slow loss of blood, which is observed in hypotrophies, can in a number of cases also lead to thickening of the blood (Rosenbaum, Berkovich). On the other hand, in a number of cases of clinically sharply expressed dehydration, thickening of the blood, determined refractometrically, is not noted. The absence of a parallelism between clinically expressed E. and the presence of thickening of the blood can be explained to a certain extent by the simultaneous loss by the organism of both water and salts and proteins. Furthermore, the questions of regulation of the water economy (see Metabolism, Water Exchange) are so complex, depend on such a quantity of diverse factors, that it is hardly possible to expect in all cases a complete parallelism of water exchange both in the blood and in the tissues. In the origin of E., great significance is attached to both age and constitutional peculiarities. The phenomena of E. arise more easily and proceed more violently, the younger the child; besides, there exist children distinguished by an unstable water exchange, with a reduced capacity of water regulation, who are more prone to the phenomena of E. E. can be caused by various causes: both enteric infection, for example toxic dysentery, typhoid infection, etc., and parenteral and alimentary factors, overheating can lead to a rapid sudden loss of water by the organism, to the exhaustion of its water depots. In this case, the loss of water goes mainly not at the expense of diarrhea and vomiting, which to a certain degree can be compensated by oliguria, but at the expense of loss of water by another extrarenal pathway. E. with the thickening of the blood observed in it has great significance in slowing the current of blood, which together with other factors determines the hemodynamic picture of collapse (Zeckel). In order to elucidate the significance of E. in the origin of toxicoses, a very large number of experimental works have been performed. Schiff caused a whole series of symptoms of E., as well as of toxicosis, in healthy children by suddenly reducing the amount of water given to them, approximately by 1/5 together with giving food rich in protein. The cardinal difference between experimental E. and E. during intoxication lies in the following: in experimental E., the introduction of water compensating for the lost water restores the water exchange and eliminates the symptoms of E. In the already occurring toxicosis, giving water often does not succeed in eliminating either the already occurring E. or the toxicosis: the colloidal state of the protoplasm of cells is so disturbed that it becomes irreversible, they lose the ability to swell, retain water, water entering the composition of tissue and cellular colloids is lost (constitutional water, see Metabolism, Water). But clinically it is impossible to establish that limit beyond which the irreversibility of the colloids of the blood, cells, and tissues, their inability to retain water, occurs. Studies of the ability to swell of muscle tissue in children who died of toxicosis, in whom a sharp E. was noted during life, indeed indicate in them a reduced ability of muscle tissue to swell, to bind water (Stransky). Rosenbaum reproduced experimentally on dogs the entire toxic symptom complex by dehydration of dogs by giving laxatives, overheating, feeding concentrated food and simultaneously introducing parenterally colien-dotoxins or a mixture of amines. In general, all theories about the significance of E. in the pathogenesis of intoxications reduce themselves to two directions: 1) the basis lies in the dehydration of the organism-E., which causes disturbances of intermediate metabolism, and after it the entire toxic symptom complex (see Infant Intoxication); 2) damage to the function of cells, first of all hepatic, and their colloids by bacterial toxins or products of protein breakdown leads to disturbances of water exchange and to E., which in turn sharply disturbs the entire intermediate metabolism. Great significance is attached to E. as a factor promoting the disturbance of the protective barriers of the organism; thus, Rosenbaum explains the nervous phenomena observed in toxicoses by increased permeability of the hemato-encephalic barrier with respect to toxins, which occurs as a result of the occurring E. The permeability of the intestinal wall with respect to toxins, in the opinion of Bessau, is also to a certain extent a consequence of the E. present. But whatever the views on the significance of E. in the pathogenesis of intoxications, all pediatricians unanimously recognize the severe consequences of acute loss of water by the child's organism, and the measures of all schools are directed toward restoring the disturbed water exchange. Therapeutic measures in E. are the same as in infant intoxication (see Infant Intoxication).