Saturday, February 29, 2020

Body fluid and salt metamoblism

Body fluid and salt metamoblism There are several causes underlying dysnatremia. Most significantly 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 in dilutional hyponatremia 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: release vasopressin and a powerful thirst mechanism. When the effective blood osmolality exceeds 275-280 mosmol/ kg H2o, release of vasopressin occurs and when the effective blood osmolality exceeds 290-295 mosmol/kg H2o that results in maximally concentrated urine. There are two causes of hypernatremia in outpatient which are breastfeeding and diarrhea or vomiting . In breastfeeding the major problem is water deficiency that cause sodium concentration raises as a result of low volume intake and a loss of water. Diarrhea or vomiting comparison to the past is less because of presumably to the advent of low solute infant formulas and the increased use and availability of oral rehydration solutions. In management of hyponatremia, used either V2 antidiuretic hormone receptor antagonists or urea. In fasting patients, Intravenous maintenance fluids done by Holliday are used to provide water and electrolyte requirements. used administer intravenous isotonic (or near isotonic) crystalloid solutions in children who resistant to initial oral rehydration therapy. Traditionally, mange chronic normovolemic (or hypervolemic) hyponatremia either by restricting water intake or by giving salt. May be the use of nonpeptide vasopressin receptor antagonists as alternative. There are several receptors for vasopressin which are v1a, V1b and v2receptors. In patients who have nephrogenic syndrome of inappropriate childhood anti-diuresis the vaptans do not correct hyponatremia. 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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