There accompanying anions, which are mainly chloride

are several causes underlying dysnatremia. Most important are both the
management of dysnatremia and parenteral hydration. In normal status,  the normal range of blood sodium concentrations
are of 135-145 mmol/L. Sodium and its accompanying anions, which are mainly
chloride and bicarbonate, represent for 90% of the extracellular effective
osmolality. The plasma water content is a main determinant of the sodium concentration.
Dysnatremias may have result in central nervous system dysfunction ,whereas
hyponatremia may lead to brain swelling and hypernatremia may lead to brain
shrinkage. According to the extracellular fluid volume status the hyoponatremia
is classified as either hypovolemic or normo-hypervolemic. In children,
vasopressin release is triggered by the low effective arterial blood volume in
case of hypovolemic hyponatremia this is called syndrome of appropriate
anti-diuresis. The primary defect is euvolemic also there is inappropriate
increase in circulating vasopressin levels this is called syndrome of
inappropriate anti-diuresis. To determine presence of hyponatremia may shows
obvious cause such as vomiting or diarrhea. In some status, to discriminate
hypovolemic from normo- hypervolemic hyponatremia may not be obvious. Some
patients have difficult to assess their status volume but there is helpful way
to assess their status by detect urine spot sodium and the fractional sodium
clearance. In state of normovolemic, the major defense against developing
hyponatremia is the ability to dilute urine and excrete free-water. There are
special causes lead to hypotonic hyponatremia which are hospital-acquired
hyponatremia, desmopressin, endurance athlete and diuretics. Hypernatremia is a
net water Loss or a hypertonic sodium gain, with Inevitable hypertonicity
reflects hypernatremia. If sodium concentrations above 160 mmol/ L are usually
sever symptoms evident only with presence of acute and large increases in
concentrations. Almost the cause of hypernatremia is always obvious from the
history. If the cause is not evident, determine of urine osmolality in relation
to the effective blood osmolality and the urine sodium concentration. There are
two mechanisms prevent developing hypernatremia which are: releasing of
vasopressin and a powerful thirst mechanism. Releasing of vasopressin occurs, when
the effective blood osmolality exceeds 275-280 mosmol/ kg H2o and the maxim of
urine concentrate when the effective blood osmolality exceeds 290-295 mosmol/kg
h2o. Breastfeeding and diarrhea or vomiting are causes of hypernatremia in outpatient.
The major problem of breastfeeding is water deficiency. In comparison of the
past, the diarrhea or vomiting is less because of presumably to the advent of
low solute infant formulas and the increased use and availability of oral
rehydration solutions. V2 antidiuretic hormone receptor antagonists or urea
used to manage hyponatremia. To provide water and electrolyte requirements in
fasting patients use intravenous maintenance fluids which is done by Holliday. Intravenous
isotonic crystalloid solutions used in children who resistant to initial oral
rehydration therapy. Traditionally , mange chronic normo-hypervolemic hyponatremia
either by restricting water intake or by giving salt. May be replaced by alternative
way that use nonpeptide vasopressin receptor antagonists. V1a, V1b and V2
receptors are receptors for vasopressin. Vaptans do not administer hyponatremia
in patients who have nephrogenic syndrome of inappropriate childhood
anti-diuresis. In these cases, use oral administration of urea. All in all, pediatricians
must aware of the changing epidemiology of dysnatremia . Also, the hydrated
parenterally with the hypotonic solutions which recommended by Holliday.




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