Sodium andPotassiumHomeostasisand Management By Maged Zakaria
Sodium Homeostasis Serum Na+ values should be kept between 135-145 mEq/L. In general, as long as the infant’s fluid balance is stable, maintenance Na+ requirements do not exceed 3- 4 mEq/kg/day, and providing this amount usually ensures the positive Na+ balance necessary for adequate growth. Some of the most immature infants may have Na+ requirements of as much as 6-8 mEq/kg/day because of the decreased capacity of their kidneys to retain Na+.
Hyponatremia Hyponatremia (serum Na+ <130 mEq/L) may be caused by either total body Na+ deficit or free water excess. In both situations, total body water may be (hyponatremia with volume contraction), normal, or (hyponatremia with volume expansion).
Hyponatremia To initiate effective treatment, it is important to attempt to determine the primary cause of the hyponatremia and whether there is associated volume expansion or contraction.
Hyponatremia The most common cause of hyponatremia in the sick neonate is excessive administration or retention of free water. In these situations the total body Na+ content is normal, and the appropriate treatment is restriction of free water intake and not administration of Na+.
Hyponatremia In situations of true Na+ deficit, the deficits can be estimated by assuming 70% of total body weight as the distribution space of Na+. The formula for calculating Na+ deficit is: Na+ deficit (or excess) (mEq) = 0.7 × kg × [ (Na+) desired − [ (Na+) actual]
Hyponatremia In most situations of depletional hyponatremia, the Na+ deficit should be replaced on a schedule that provides two thirds replacement in the first 24 hours and the remainder in the next 24 hours. Frequent measurements of serum electrolytes are needed to ensure that the correction is occurring appropriately.
Hyponatremia If the serum Na+ concentration is <120 mEq/L, regardless of whether the hyponatremia is due to free water overload or total body Na+ deficit, then correction of the serum Na+ concentration up to 120 mEq/L is recommended with administration of 3% saline solution. This correction should be done over 4-6 hrs, depending on the severity of hyponatremia and using the previous formula. Rapid IV bolus administration of 4-6 mL/kg of 3% saline
Hyponatremia Additional therapy should be directed at fluid restriction if the hyponatremia is dilutional or Na+ repletion if the hyponatremia is depletional. More stable infants with chronic Na+ losses can also be corrected with enteral NaCl.
Hypernatremia Hypernatremia (serum Na+ >145 mEq/L) reflects a deficiency of water relative to total body Na+ and is most often a disorder of water rather than Na+ homeostasis. Hypernatremia does not reflect the total body Na+ content, which can be high, normal, or low depending on the cause of the condition.
Hypernatremia The hypernatremia-induced hypertonicity causes water to shift from the intracellular to the extracellular compartment, resulting in intracellular dehydration and the relative preservation of the extracellular compartment. This shift is the main reason that neonates with chronic hypernatremic dehydration often do not demonstrate overt clinical signs of intravascular depletion and dehydration until late in the course of the condition.
Hypernatremia The CNS has a unique adaptive capacity to respond to the hypernatremia-induced hypertonicity, leading to a relative preservation of neuronal cell volume. The shrinkage of the brain stimulates the uptake of electrolytes (immediate effect) as well as the synthesis of osmoprotective amino acids and organic solutes (delayed response). These idiogenic osmols aid in maintaining normal brain cell volume during longer periods of hyperosmolar stress.
Hypernatremia As long as hypernatremia develops rapidly (within hours), as in accidental Na+ loading, a relatively rapid correction of the condition improves the prognosis without raising the risk of cerebral edema formation. Intracellular fluid accumulation does not occur because the accumulated electrolytes are rapidly extruded from the brain cells, and cerebral edema is unlikely. In these cases, reducing serum Na+ concentration by 1 mEq/L per hour (24 mEq/L per day) is appropriate.
Hypernatremia However, because of the slow dissipation of idiogenic osmols over a period of several days, in cases of chronic hypernatremia, the hypernatremia should be corrected more slowly, at a maximum rate of 0.5 mEq/L per hour (12 mEq/L per day). If correction is performed more rapidly in these cases, the abrupt fall in the extracellular tonicity results in the movement of water into the brain cells, which have a relatively fixed hypertonicity because of the presence of the osmoprotective molecules. The result is the development of brain edema with deleterious
Hypernatremia In the breastfed term neonate, hypernatremia most commonly develops because of dehydration caused by inadequate breast milk intake, but may also be caused by high Na+ levels in maternal breast milk. Reduction in breastfeeding frequency has been shown to be associated with a marked rise in the Na+ concentration of breast milk.
Hypernatremia The central and nephrogenic forms of diabetes insipidus are much less commonly encountered and result in hypernatremia because of the lack of production of and renal responsiveness to ADH, respectively. Hypernatremia can also develop in response to excessive sodium supplementation, mainly in the sick neonate receiving repeated volume boluses for cardiovascular support. In these cases, clinical signs of edema, increased body weight, and the history of volume boluses help to establish the diagnosis.
Conditions Causing Hypernatremia EUVOLEMIC HYPERNATREMIA 1. Decreased Production of ADH: Central diabetes insipidus, head trauma, CNS tumors (craniopharyngioma), meningitis, or encephalitis 2. Decrease or Absence of Renal Responsiveness: Nephrogenic diabetes insipidus, extreme immaturity, renal insult and medications such as amphotericin, hydantoin, aminoglycosides.
Treatment of Hypernatremia Thorough analysis of the medical history and the changes in clinical signs, laboratory findings, and body weight usually aid in determining the major etiologic factor in hypernatremia and thus the appropriate treatment. Although some cases of hypernatremia are a result of sodium excess with normal or high TBW, most cases in neonates are due to hypernatremic dehydration.
Treatment of Hypernatremia Treatment of this condition is generally divided into two phases: the emergent phase where the intravascular volume is restored, usually by administration of 10-20 mL/kg of isotonic saline, and the rehydration phase, where the sum of the remaining free water deficit and usual maintenance needs are administered evenly over at least 48
Treatment of Hypernatremia The free water deficit can be calculated as: H2O deficit (or excess) (L) = [ 0.7 × kg ] × It is important to note that the amount of free water required to decrease the serum Na+ by 1 mEq/L is 4 mL/kg with moderate hypernatremia, but only 3 mL/kg when the hypernatremia is as high as 195 mEq/L.
Treatment of Hypernatremia Therefore the amount of free water required to decrease serum Na+ by 12 mEq/L over a 24-hour period when hypernatremia is moderate is calculated as: Free water required = Current weight × 4mL/kg × 12mEq/L or Current weight × 48 mL/kg/day And the amount of free water required to decrease Na+ sodium by 12 mEq/L over a 24-hour period when hypernatremia is severe is calculated as: Free water required = Current weight × 36 mL / kg / day
Potassium Homeostasis Serum potassium should be kept between 3.5-5 mEq/L. In the early postnatal period, neonates, especially immature preterm infants, have higher Na+ and K+ concentrations than older persons. In general, K+ supplementation should be started only after urine output has been well
Potassium Homeostasis Supplementation should be started at 1-2 mEq/kg/day and increased over 1-2 days to the usual maintenance requirement of 2-3 mEq/kg/day. Some preterm infants may need more K+ supplementation after the completion of their postnatal volume contraction, because of their increased plasma aldosterone concentrations, prostaglandin excretion, and disproportionately high urine flow rates. Most term and preterm neonates will require K+ supplementation if they are receiving diuretics.
Hypokalemia Hypokalemia in the neonate is usually defined as a serum K+ level of < 3.5 mEq/L. Hypokalemia can occur from K+ loss due to diuretics, diarrhea, renal dysfunction, or nasogastric drainage from inadequate K+ intake or from intracellular movement of K+ in the presence of alkalosis.
Hypokalemia Except in patients receiving digoxin, hypokalemia is rarely symptomatic until the serum K+ concentration is less than 2.5 mEq/L. ECG manifestations of hypokalemia include flattened T waves, prolongation of the QT interval, or the appearance of U waves. Severe hypokalemia can result in cardiac arrhythmias, ileus, and lethargy.
Treatment of Hypokalemia Hypokalemia is treated by slowly replacing K+ either IV or orally, usually in the daily fluids. Rapid administration of KCl is not recommended, because it is associated with life- threatening cardiac dysfunction. In extreme emergencies, K+ can be given as an infusion over 30 to 60 minutes of not more than 0.3 mEq/kg KCl. If hypokalemia is secondary to alkalosis, the alkalosis should be corrected before considering increasing the K+ intake.
Hyperkalemia Hyperkalemia in the neonate is defined as a serum K+ level > 6 mEq/L in a nonhemolyzed specimen. It is important to understand that most of the body’s K+ is contained within cells; therefore serum K+ levels do not accurately reflect total body stores. However, a serum K+ > 6.5-7 mEq/L can be life threatening, even if stores are normal or low, because of its effect on cardiac rhythm.
Hyperkalemia ECG manifestations of hyperkalemia include peaked T waves (the earliest sign), a widened QRS configuration, bradycardia, tachycardia, SVT, ventricular tachycardia and ventricular fibrillation. Because pH affects the distribution of K+ between the intracellular and the extracellular space, serum K+ levels rise during acidosis, which may occur acutely. The clinician should be aware of the potential for life-threatening arrhythmias to occur in infants with chronic lung disease on diuretics and K+ supplements who develop a sudden respiratory deterioration with acidosis.
Hyperkalemia Another common cause of hyperkalemia is renal dysfunction, of particular concern in very preterm and asphyxiated infants. In addition, infants who have suffered IVH or tissue trauma and those with intravascular hemolysis often have hyperkalemia caused by the release of K+ during breakdown of RBCs. Finally, hyperkalemia may be one of the earliest manifestations of congenital adrenal hyperplasia.
Treatment of Hyperkalemia1. Eliminate all sources of K+ from the diet or IVF .2. Administer a cation exchange resin such as Kayexalate® (sodium polystyrene sulfonate) or Sorbisterit® (calcium polystyrene sulfonate).3. Administer IV NaHCO3 1 mEq/kg IV over 10 to 30 min (causes a rapid shift of K+ into cells) (used with caution; can precipitate hypocalcemia and Na+ overload).4. Infusion of glucose and insulin (Glucose 0.5 g/kg; insulin 0.1 U/kg IV over 30 min)5. Beta-agonists (Salbutamol 0.4 mg (0.08 mL)/kg/dose Q2h via nebulizer; can cause tachycardia).
Treatment of Hyperkalemia6. Exchange transfusion with washed packed cells.7. Calcium gluconate 0.5 to 1.0 mL/kg IV over 5 to 10 min should be administrated in presence of ECG changes (with continuous ECG monitoring for bradycardia and arrhythmias) to counteract the effects of hyperkalemia on the myocardium.8. The definitive therapy for significant