Abnormally low concentrations of potassium, at times associated with muscular paralysis, have been observed in the serum of diabetic patients while under treatment for acidosis or coma (1)(2)(3)(4). Available data indicate that deficits of cell potassium are also present in at least some of these subjects (5). In an attempt to characterize and quantitate the magnitude of these deficits, exchanges of water, electrolytes, carbohydrate, and protein have been investigated in diabetic acidosis and coma prior to, during, and following the administration of potassium salts. EXPERIMENTAL PROCEDURE AND METHODSEight cases in all have been studied. Of these, two were adults and the remaining six juvenile diabetics 16 years of age or younger. On admission all had Kussmaul breathing, a marked reduction of the serum bicarbonate content, hyperglycemia, glycosuria, and ketonuria.Studies during treatment and recovery were divided into three periods. The first or pre-KCl period extended from admission to the point where the patients had improved sufficiently to be maintained on an oral intake. During this time insulin, 0.9 per cent saline, and, once the blood sugar began to drop, glucose solutions were administered in amounts summarized in Table I. Under this treatment ketosis diminished, overbreathing ceased, hyperglycemia decreased, and mental clarity returned. This interval lasted 12 to 25 hours in the individual subjects. During the second or KC1 period, 22 to 37 hours in length, the patients received insulin, 10.0 to 30.0 grams of KCI per os or intravenously, whole milk containing added carbohydrate, and water as desired. The third or post-KCl period began after the final dose of KC1 and lasted up to 34 hours. During this time the patients received insulin as needed, together with measured amounts of water and milk.In all subjects concentrations of the whole blood nonprotein nitrogen, blood sugar (6-8), and the levels of serum chloride, bicarbonate, sodium, potassium and water were measured at the beginning and end of each period (6,(9)(10)(11)(12). Average values for the electrolyte, carbohydrate, and protein content of fresh milk have been used in calculating the intake (13, 14). Urine excreted during each period was analyzed for nitrogen, sodium, potassium, chloride, and glucose (6, 10, 11, 15, 16). Body weight was determined when possible at the start and end of each period. METHOD OF CALCULATIONAlterations in extracellular fluid volume were calculated from changes in the chloride space, based on the external balance of this anion and corrected for changes in the serum concentrations of chloride as described by Elkinton and co-workers, and by . In view of the dehydration known to develop in the course of diabetic acidosis and coma, the initial extracellular volume was assumed for purposes of this calculation to be 15 per cent of the body weight rather than the usual value of 18.7 to 23 per cent found in non-dehydrated human subjects (20). In two instances a pre-treatment weight could not be obtained. A reasonable assumpt...
Intially corticotropin (ACTH) and cortisone were used only to induce diuresis in children with the nephrotic syndrome, though occasional remissions were produced.1-7 Most of these early trials were of short duration and the amounts of drugs administered were small because of limited supplies and the occurrence of side-effects such as edema, hypertension, and hypokalemia. The demonstration that such changes could be prevented or minimized by means of diets rigidly restricted in sodium and high in potassium 8 enabled us and others 9,10 to undertake more prolonged administration of large amounts of corticotropin and adrenocortical steroids in the hope of influencing the course of the underlying disease. Materials and MethodsDuring the past five years we have treated a total of 106 instances of nephrotic syndrome in children. All had persistent and usually massive proteinuria on admission. Each patient was treated in essentially the same way, and no attempt was made to exclude those with hypertension, formed elements in the urine, or azotemia. Data on 30 of these children have been reported earlier.8 Seventytwo were initial attacks ; the remainder represented exacerbations. From the information in Tables 1A and IB it can be calculated that the mean age at which the initial episode of nephrotic syn¬ drome occurred in the group of 72 children was 4 years 4 months, with \y2 to 2y2 years the com¬ monest age of onset and a range of 4 months to 13 years 7 months in the remainder. There were more boys than girls, 45 versus 27, and the latter were somewhat older at the first manifestation (4 years 9 months versus 4 years 2 months). Symptoms or signs of nephrotic syndrome, or both, had been present for one week to four years prior to hospitalization for the first course of corticotropin, with a mean duration of 27 weeks. This interval was much shorter, averaging four weeks, in patients who developed an exacerbation while under observation in the dispensary. A his¬ tory of an infection prior to or coincident with the first episode of nephrotic syndrome was obtained in 40 of the 72 patients, with upper respiratory in¬ fection in 34, unexplained fever in 3, varicella in 2, and rubeola in 1 (Table 1A). In the 18 patients admitted one to six times with a total of 34 exac¬ erbations, recrudescence followed an upper re¬ spiratory infection in 12 instances, bronchitis in 1 and was unassociated with any recognized infec¬ tion in the remaining 21 (Table IB). Beta-hemo¬ lytic streptococci were isolated from nose and throat cultures in only a minority of the initial and the subsequent attacks, 12% and 6%, respec¬ tively.
Reports describing trials of exchange resins in removing cations from the gastrointestinal tract of experimental animals have been limited to toxicity studies and to measurements of the relative magnitudes of the oral intake and the stool output (1-3). In the experiments presented in this paper changes in serum, urine, and stool components, as well as the external and internal balances of certain electrolytes and of nitrogen have been determined in dogs receiving a carboxylic cation exchange resin in one of two forms. The chemical and physical characteristics of these agents have been described in detail in the introductory paper (4). MATERIALS AND METHODSMongrel female dogs, maintained on a commercial feed ("Friskies") 1 and allowed free access to water, received a carboxylic cation exchange resin in the hydrogen or the sodium form for periods of seven to 11 days. In some instances beef extract or milk and sugar were used to enhance palatability, but many animals nonetheless lost weight partly or entirely as a consequence of anorexia induced by the regimens employed. Since this occurred to an equal degree when control and recovery periods of comparable length were alternated with resin periods it represented a common denominator in our experiments. The beginning and the end in each interval of the study were marked by catheterization of the urinary bladder, measurement of body weight and withdrawal of venous blood for analysis of blood nonprotein nitrogen (NPN) and sugar, and of serum carbon dioxide content, chloride, sodium, potassium, calcium, phosphorus and water, using previously described methods (5-7). The pH of anaerobic samples of serum was determined by means of the glass electrode. Food and resin intake, stool and urine output as well as any vomitus or rejected food were collected, measured, and analyzed separately for nitrogen, sodium, potassium and chloride content (8-10). Stools were removed from the cage and weighed immrediately. Procedures for partitioning the external balances into extracellular and cellular components have been described only in part in previous publications (11)(12)(13)(14)(15)(16)(17) and are therefore appended in detailed form.1 Content per 100 g.: Na, 17.6 meq.; K, 10.2 meq.; Cl, 162 meq.; and N, 3.42 g.With but minor exceptions all findings have been subjected to conventional statistical analyses (18). In the case of the body weight and the serum constituents values observed at the end of each control, experimental, or recovery interval were subtracted from those present at the start of the particular period under scrutiny and expressed as increments or decrements (±t A). After the means of these changes had been calculated (values greater than 2 S. D. were discarded) the resin and post resin values were compared with those of the control periods. Changes were considered significantly different statistically when "p" for the "t" test was 0.05 or less. Urinary and stool output and the balance data were analyzed in terms of per diem values.
It is known that hypopotassemia may appear during therapy of diabetic acidosis or coma, at times associated with muscular paralysis (1-9). This is not, however, an invariable occurrence, nor have the origins of such decreases in the serum and interstitial fluid potassium concentrations been clearly defined. It seems probable that one or more mechanisms are responsible. These include the possibilities that hypokaliemia 1 develops as a result of a continued loss of potassium in urine, that it is a manifestation of dilution of body fluids by potassium-free solutions administered during therapy, and, finally, that it results from movements of potassium into body cells. The studies herein reported evaluate the role of each of these factors in a limited number of patients, chiefly pre-adult, in whom intensive study using the balance method was possible. MATERIALS AND METHODSNine patients have been studied during a total of 11 admissions for the treatment of diabetic acidosis. Two of the subjects were young adults; the remainder were children seven to 16 years of age. Over-breathing was definitely present in each case; the serum carbon dioxide content ranged from 2.6 to 10.4 m.eq. per liter on admission. All patients were conscious, though difficult to arouse. Definite vascular collapse was present in only one patient, R. J., requiring three transfusions. Anuria did not develop in any of the subjects. Insulin was administered subcutaneously to all patients, although J. K. and T. W. also received large intravenous injections initially. Data on the retention of potassium salts administered in large amounts during convalescence to eight of the cases have been presented in a previous communication (9). The studies herein reported are based on observations from the time of admission and continued until convalescence was well established. During these inter-1 This term has been taken to refer solely to diminished concentrations of potassium in blood serum or plasma and the contiguous interstitial fluid, and does not necessarily indicate any decrease in the total amount of potassium in these fluids. vals the patients received insulin, glucose, saline, and only little, if any, potassium.The experimental procedure employed and the methods of calculation have been previously described in detail (9-12). Briefly they may be summarized as follows: the chloride space, corrected for the external balance of this ion and for changes in the chloride concentration in serum, has been used as an index of alterations in the volume of extracellular fluid. The intake and the urinary excretion of sodium, potassium, chloride, glucose, and nitrogen were measured during intervals marked at the start and finish by determinations of the values of these various components in serum. The retention or loss of these cations and of nitrogen has been apportioned between the extracellular fluid and the cells. In the case of nitrogen, suitable corrections for changes in the concentration of the whole blood nonprotein nitrogen were made. The values for the c...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.