There are several causes of dysnatremia.
Mostsignificantly are both the management of dysnatremia and parenteral hydration.In normal status, the normal range ofblood sodium concentrations are of 135-145 mmol/L. Sodium and its accompanyinganions, which are mainly chloride and bicarbonate, represent for 90% of theextracellular effective osmolality. The plasma water content is a maindeterminant of the sodium concentration.
Dysnatremias may have result incentral nervous system dysfunction whereas hyponatremia may lead to brainswelling and hypernatremia may lead to brain shrinkage. According to theextracellular fluid volume status the hyoponatremia is classified as eitherhypovolemic or normo-hypervolemic. In children, vasopressin release is triggeredby the low effective arterial blood volume in case of hypovolemic hyponatremiathis is called syndrome of appropriate anti-diuresis. The primary defect iseuvolemic also there is inappropriate increase in circulating vasopressinlevels this is called syndrome of inappropriate anti-diuresis. To determinepresence of hyponatremia may shows obvious cause such as vomiting or diarrhea.In some status, to discriminate hypovolemic from normo- hypervolemichyponatremia may not be obvious.
Some patients have difficult to assess theirstatus volume but there is helpful way to assess their status by detect urinespot sodium and the fractional sodium clearance. In state of normovolemic, diluteurine and excrete free-water is a major defense againstdeveloping hyponatremia. There are special causes lead to hypotonichyponatremia which are hospital-acquired hyponatremia, desmopressin, enduranceathlete and diuretics. Hypernatremia is loss of water or gain of hypertonicsodium. If sodium concentrations above 160 Mmol/ L are usually sever symptomsevident only with presence of acute and large increases in concentrations. Almostthe history cover the causes of hypernatremia but if the cause is not obvious,determine of urine osmolality in relation to the effective blood osmolality andthe urine sodium concentration. There are two mechanisms prevent developinghypernatremia which are: releasevasopressin and a powerful thirst mechanism.
Releasing of vasopressin occurs, whenthe result blood osmolality above 275-280 mosmol/ kg H2o and the maxim of urineconcentrate when the result of blood osmolality above 290-295 mosmol/kg H2o. Breastfeedingand diarrhea or vomiting are causes of hypernatremia outpatient. The majorproblem of breastfeeding is water deficiency that cause sodium concentrationelevated due low volume intake and a loss of water.
In comparison of the past,the diarrhea or vomiting is less because of presumably to the advent of lowsolute infant formulas and the increased use and availability of oralrehydration solutions. V2 antidiuretichormone receptor antagonists or urea used to manage hyponatremia. To providewater and electrolyte requirements in fasting patients use intravenousmaintenance fluids which is done by Holliday. Intravenous isotonic crystalloidsolutions used in children who resistant to initial oral rehydration therapy. Traditionally, mange chronic normo-hypervolemic hyponatremia either by restricting waterintake or by giving salt. May be replaced by alternative waythat use nonpeptide vasopressin receptor antagonists. V1a, V1b and V2 receptorsare receptors for vasopressin.
In patients who have nephrogenic syndrome ofinappropriate childhood anti-diuresis the vaptans do not correct hyponatremia.In these cases, use oral administration of urea. All in all, pediatricians mustaware of the changing epidemiology of dysnatremia .
Also, the hydratedparenterally with the hypotonic solutions which recommended by Holliday.