Literature Reviews: Pediatric Endocrinology: Effect of Rehydration Fluid With 75 mmol/L of Sodium on Serum Sodium Concentration and Serum Osmolality in Young Patients With Diabetic Ketoacidosis Rother KI, Schwenk WF. Mayo Clin Proc. 1994; 69:1149-1153

1995 ◽  
Vol 34 (9) ◽  
pp. 511-512
1980 ◽  
Vol 2 (6) ◽  
pp. 187-190
Author(s):  
Robert C. Kelsch ◽  
William J. Oliver

Hyponatremia is usually recognized following an electrolyte screen since it is not symptomatic, except in its severest degrees. The pathophysiologic implications of hyponatremia and its therapy are quite varied. The purpose of this review is to present a diagnostic plan which in most instances will resolve the therapeutic dilemma. This approach is a minor modification of that developed by Schrier and Berl1 for evaluating hyposmolar states. GENERAL PRINCIPLES The occurrence of hyponatremia indicates a failure of those receptor and effector mechanisms designed to assure that the quantity of water in the body will closely relate to the amount of solute in the major bodywater spaces. The principal sensors are designed to recognize osmolar changes, not changes in sodium concentration. Nevertheless, measurement of serum sodium concentration is the most readily available tool for estimation of disturbances in osmolality. Fanestil2 has recorded 14 formulae designed to estimate osmolality from serum sodium concentration or sodium, glucose, and urea concentrations. The simplest of these formulae, osmolality = 2 x Na+ + 10, is satisfactory in the vast majority of clinical circumstances occurring in pediatrics. Diabetes mellitus is the only relatively common state that requires the use of alternate formulations to correct for hyperglycemia. The contribution to serum osmolality by glucose can be approximated by adding to the above formula 1 mOsm for each 18 mg/100 ml of blood glucose above the level of 100 mg/100 ml.


1994 ◽  
Vol 86 (3) ◽  
pp. 285-290 ◽  
Author(s):  
Ann-Charlotte Ekman ◽  
Olli Vakkuri ◽  
Olli Vuolteenaho ◽  
Juhani Leppäluoto

1. The aim of this study was to elucidate the role of atrial natriuretic peptides in the regulation of water and electrolyte balance after alcohol intake. To this end we measured the plasma concentrations of ethanol, atrial natriuretic peptide 99–126 and the N-terminal fragment of pro-atrial natriuretic peptide (atrial natriuretic peptide 1–98), serum osmolality and serum sodium concentration, and urine output, urine osmolality and urinary sodium excretion for 12 h after administration of ethanol (0, 0.5 and 1.0 g body weight/kg) and placebo drinks to nine healthy subjects according to a double-blind cross-over design. 2. Intake of ethanol (at 19.00–19.45 hours) inhibited the nocturnal increase in the plasma atrial natriuretic peptide 99–126 level dose-dependently (P < 0.05), but had no effect on the plasma atrial natriuretic peptide 1–98 level. Serum osmolality and serum sodium concentration were elevated dose-dependently for 2–5 h after the ethanol intake. Urine volume increased after the higher ethanol dose (net loss of 0.6 litre of water). 3. Since the plasma atrial natriuretic peptide 1–98 level was not changed after ethanol intake, we propose that the alcohol-induced inhibition of the nocturnal rise in the plasma atrial natriuretic peptide 99–126 level is not caused by an inhibition of release, but may rather reflect an increased peripheral elimination of atrial natriuretic peptide 99–126.


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