Appropriate evaluation to determine the cause of hyponatremia begins with a thorough physical examination in order to estimate volume status History may reveal obvious sources of sodium loss or raise the concern for water intoxication Laboratory tests should include serum electrolytes, osmolality, and assessment of renal function Concomitant urine studies should include osmolality, urine sodium, and urinalysis In children with hyponatremia and concentrated urine, the urine sodium may distinguish between states of decreased effective circulating volume (urine sodium 40 mEq/L) Clinical manifestations The symptoms of hyponatremia are primarily neurologic and due to the development of cerebral edema The symptoms mirror the severity of cerebral edema, which in turn is related to the degree of hyponatremia and the acuity of the process The mechanisms of cellular adaptation include movement of intracellular electrolytes to the extracellular space, which can occur within minutes Over hours to days, organic solutes move to the extracellular space Given the ability for cerebral adaptation, the degree of cerebral edema and neurologic symptoms are less severe in chronic hyponatremia Early neurologic symptoms include nausea and malaise, and may be seen when the serum sodium concentration falls below 125 mEq/L With progressive derangement of cerebral cell volume, symptoms of headache, altered mental status, lethargy, ataxia, and psychosis may ensue Signs of severe cerebral edema include seizures, coma, and respiratory depression TABLE 100.5 CAUSES OF HYPONATREMIA BASED UPON TOTAL BODY SODIUM CONTENT Low total body sodium Normal total body sodium High total body sodium Diarrhea Vomiting Ostomy losses Bleeding Diuretic use Mineralocorticoid deficiency Salt-wasting renal disease Cystic fibrosis Marathon running SIADH Adrenal insufficiency Hypothyroidism Acute renal failure Water intoxication Pseudohyponatremia Congestive heart failure Nephrotic syndrome Liver failure (cirrhosis) Multiorgan dysfunction Management For children with hyponatremia associated with hypovolemia, isotonic solutions should be provided to restore intravascular volume Children with symptomatic hyponatremia require urgent treatment to avoid progressive neurologic complications Symptoms are more likely to develop if hyponatremia evolves rapidly, as water will move along an osmotic gradient from the extracellular space to the intracellular space Given the effect of cell volume regulatory mechanisms, an important goal is to control the rate of rise in serum sodium to prevent rapid fluid shifts into the extracellular space and avoid the development of osmotic demyelination The general recommendation for a child with severe hyponatremia is to increase the serum sodium no more rapidly than 12 mEq/L in the first 24 hours or an average of 0.5 mEq/L/hr An exception to this recommendation would be symptomatic hyponatremia and evolving cerebral edema and seizures Symptomatic hyponatremia calls for a more aggressive initial correction of the serum sodium of approximately mEq/L/hr for to hours, which should result in clinical improvement This can be achieved with the administration of hypertonic 3% saline (513 mEq/L of sodium) In general, mL/kg of 3% saline would be expected to raise serum sodium by approximately mEq/L A practical approach is to administer doses of mL/kg (maximum dose 100 mL) until seizures stop After the initial correction is achieved, the goal for the daily correction remains approximately 12 mEq/L in the first 24 hours (including the initial emergent correction) Frequent assessment of serum sodium is necessary to avoid rapid correction, which may lead to the osmotic demyelination syndrome Patients who have asymptomatic hyponatremia and euvolemia not require urgent intervention The care of these patients should be planned carefully and based upon the underlying diagnosis with the aim of gradual correction If hyponatremia is associated with an edema-forming state, providing supplemental sodium will worsen the state volume excess The goal of therapy would be to achieve negative water balance in excess of negative sodium balance To achieve this effectively, the underlying pathophysiology must be considered, although initial water restriction is generally indicated Sodium restriction and diuretic therapy may also be warranted The treatment of SIADH begins with water restriction, though this may be insufficient Some cases of SIADH require the administration of salt supplements and loop diuretics to achieve the desired negative water balance, as guided by consultation with a pediatric nephrologist Hypernatremia Hypernatremia can result from an increase in the total body solutes, a decrease in body water, or a reduction of body water relatively greater than a concurrent reduction in total body solutes Protective mechanisms to prevent the development of hypernatremia include the stimulation of thirst and the ability to excrete concentrated urine, thereby minimizing free water loss For these mechanisms to be effective, there must be adequate access to and the ability to retain free water Given the potential for limited access to water, infants and children with significant developmental delay are predisposed to hypernatremic dehydration The causes of hypernatremia based on total body sodium are outlined in Table 100.6 Hypernatremia due to isolated water deficit is termed dehydration If both salt and water deficits are present, this condition is termed hypovolemia Diarrhea is a common cause of hypernatremia in the acute care setting Although the degree of sodium deficit may vary, generally children who present for care have true hypovolemia Breastfed infants may be at increased risk of hypernatremia due to inadequate intake Hypernatremia due to salt excess is rare but it can occur with the improper mixing of infant formulas or iatrogenic administration of a salt load The latter can result after sodium bicarbonate infusion during cardiopulmonary resuscitation or during therapy of refractory metabolic acidosis Hypernatremia secondary to nearly pure water loss may develop if replacement of insensible water loss from the skin and respiratory tract is inadequate Central diabetes insipidus is due to insufficient release of ADH from the hypothalamus, and nephrogenic diabetes insipidus is due to a renal resistance to the effect of ADH Most children affected with these disorders have normal thirst and free access to water and are able to maintain acceptable water balance However, infants who not have free access to water and children with intercurrent illness precluding adequate intake of free water are at risk for the development of hypernatremic dehydration The cause of hypernatremia is usually evident from the presenting history Feeding history in breastfed infants may reveal inadequate intake In formula-fed infants, an accurate account of formula preparation should be pursued to evaluate for inappropriate mixing, which would result in increased renal osmotic load Inquiries of urine volume should also be made, as the production of significant urine in a child who presents with apparent hypernatremic dehydration suggests diabetes insipidus The physical examination should assess weight, perfusion, and mental status During hypernatremic hypovolemia, water moves from the intracellular to the extracellular space Given the relative preservation of the extracellular volume, the objective signs of volume depletion may develop later in the patient’s course of illness than with other types of dehydration Laboratory studies should include serum electrolytes, serum osmolality, BUN, and renal serum creatinine If the underlying diagnosis remains in question, urine studies may be informative Urine osmolality should be compared to serum osmolality and would be elevated if renal concentrating mechanisms are intact If the urine osmolality is inappropriately low when compared to ... loop diuretics to achieve the desired negative water balance, as guided by consultation with a pediatric nephrologist Hypernatremia Hypernatremia can result from an increase in the total body