Therapy of fluid and electrolyte disorders should be phased to (1) expand the ECF volume and restore tissue perfusion, (2) replenish fluid and electrolyte deficits while correcting attendant acid-base abnormalities, (3) meet the patient’s nutritional needs, and (4) replace ongoing losses.
The cornerstone of therapy involves a detailed understanding of “maintenance” fluid and electrolyte requirements. “Maintenance” requirements call for provision of enough water, glucose, and electrolytes to prevent deterioration of body stores for a euvolemic patient under normal conditions. During short-term parenteral therapy, sufficient glucose is provided to prevent ketosis and limit protein catabolism, although this usually provides little more than 20% of the patient’s true caloric needs. Prior to the administration of “maintenance” fluids, it is important to consider the patient’s volume status and to determine whether intravenous fluids are truly needed.
Various models have been devised to facilitate calculation of “maintenance” requirements based on body surface area, weight, and caloric expenditure. A system based on caloric expenditure is most helpful, because 1 mL of water is needed for each kilocalorie expended. The system presented in Table 23–1 is based on caloric needs and is applicable to children weighing more than 3 kg.
Table 23–1.Caloric and water needs per unit of body weight. ||Download (.pdf) Table 23–1.Caloric and water needs per unit of body weight.
|Body Weight (kg) ||kcal/kg ||mL of Water/kg |
|3–10 ||100 ||100 |
|11–20 ||1000 kcal + 50 kcal/kg for each kg > 10 kg ||1000 mL + 50 mL/kg for each kg > 10 kg |
|> 20 ||1500 kcal + 20 kcal/kg for each kg > 20 kg ||1500 mL + 20 mL/kg for each kg > 20 kg |
As depicted in Table 23–1, a child weighing 30 kg would need 1700 kcal or 1700 mL of water daily. If the child received parenteral fluids for 2 days, the fluid would usually contain 5% glucose, which would provide 340 kcal/day, or 20% of the maintenance caloric needs. Maintenance fluid requirements take into account normal insensible water losses (Table 23–2) and water lost in sweat, urine, and stool, and assume the patient to be afebrile, at their true dry weight, and relatively inactive. Thus, if excessive losses occur, standard “maintenance fluids” will be inadequate. In contrast, if losses are reduced for any reason, standard “maintenance fluid” administration would be excessive. Maintenance requirements are greater for low-birth-weight and preterm infants. Table 23–3 lists other factors that commonly alter fluid and caloric needs.
Table 23–2.Insensible losses. ||Download (.pdf) Table 23–2.Insensible losses.
|Preterm infant ||40 mL/kg/day |
|Infant ||20–30 mL/kg/day |
|Children, adults and adolescents ||400 mL/m2/day |
Table 23–3.Alterations of fluid requirements. ||Download (.pdf) Table 23–3.Alterations of fluid requirements.
|Increased Requirements |
|Factor ||Altered Requirement |
|Fever ||12% per degree >38°Ca |
|Hyperventilation ||10–60 mL/100 kcal |
|Sweating ||10–25 mL/100 kcal |
|Hyperthyroidism ||Variable: 25%–50% |
|Hyperosmolar states (ex. diabetic ketoacidosis) ||Variable, assess volume status (see Chapter 35) |
|Gastrointestinal loss (vomiting, diarrhea, NG output) ||Monitor and analyze output. Adjust therapy accordingly. |
|Decreased Requirements |
|Factor ||Altered Requirement |
|Hypothermia ||Variable |
|Increased environmental humidity ||Variable |
|Hypometabolic states ||Variable |
|Renal failure ||Restrict to insensible losses plus urine output |
Electrolyte losses occur primarily through the urinary tract and to a lesser degree via the skin and stool. Although maintenance sodium and potassium electrolyte needs have historically been approximated to be in the 3 mEq Na/100 kcal and 2 mEq K/100 kcal range, leading to the common use of hypotonic intravenous fluids with 38 or 77 mEq/L of sodium (¼ and ½ normal saline) and 20 mEq/L of potassium. Over the past 10 years many authors have drawn attention to the serious problem of hospital-acquired hyponatremia in children with the use of hypotonic IV solutions; notably, hyponatremia is the most common electrolyte abnormality in children and affects approximately 25% of hospitalized pediatric patients. Furthermore, the astute clinician will bear in mind the dynamic nature of clinical context in treating patients and that the choice of IV solution (Table 23–4) and rate of infusion must be made on an individual basis and must be reassessed often. A child with profound water loss stools and hypernatremia who is placed on hypotonic IV fluids and whose diarrhea ceases, but is continued on hypotonic solution without close monitoring of serum electrolytes is at grave risk for the devastating clinical consequences related to sequelae of rapid changes in sodium balance. In recent years, there also has been a trend for total parenteral nutrition solution sodium, and other electrolytes to be calculated and ordered on a milliequivalents-per-kilogram basis rather than the more classic milliequivalents-per-liter basis (eg, 0.2 or 0.45 normal). If the administered fluid volume is decreased in this setting, as the child is weaned from supplemental IV fluids to enteral intake, the sodium and other electrolytes will need to be reduced accordingly to avoid progressively increasing IV fluid tonicity that can result in hypernatremia or other electrolyte derangements.
Table 23–4.Composition of common intravenous fluid solutions. ||Download (.pdf) Table 23–4.Composition of common intravenous fluid solutions.
|Fluid ||Dextrose g/L ||Na+ mEq/L ||Cl– mEq/L ||K+ mEq/L ||Lactate mEq/L |
|Lactated ringers (LR) ||0 ||130 ||109 ||4 ||28 |
|D5W ||50 ||0 ||0 ||0 ||0 |
|D5 0.2 NS ||50 ||38 ||38 ||0 ||0 |
|D5 0.45 NS ||50 ||77 ||77 ||0 ||0 |
|D5 0.9 NS ||50 ||154 ||154 ||0 ||0 |
|Normal saline (NS) ||0 ||154 ||154 ||0 ||0 |
|Hypertonic saline (3% NaCl) ||0 ||513 ||513 ||0 ||0 |
Patient weight, urinary output, fluid input, and urine-specific gravity should be monitored daily. Of note, if stress-induced non-osmotic release of ADH is operative in a given patient, serial monitoring of the urine-specific gravity may give the false impression of intravascular volume contraction, despite being fluid replete, but still generating a concentrated urine. If fluid or electrolyte balance is abnormal, serial determination of serum electrolyte concentrations, blood urea nitrogen, and creatinine are necessary; for example, inpatients with significant burns, anuria, oliguria, or persistent abnormal stool or urine losses.
Depletion of body fluids is one of the most commonly encountered problems in clinical pediatrics. The clinical evaluation of a child with dehydration, or volume contraction, should focus on the composition and volume of fluid intake and losses (vomiting, diarrhea, urine, “insensible losses”). An updated weight is central to calculating the magnitude of volume depletion. Important clinical features in estimating the degree of dehydration include the capillary refill time, postural blood pressure, and heart rate changes; dryness of the lips and mucous membranes; lack of tears; lack of external jugular venous filling when supine; a sunken fontanelle in an infant; oliguria; and altered mental status (Table 23–5). Children generally respond to a decrease in circulating volume with a compensatory increase in pulse rate and may maintain their blood pressure in the face of severe dehydration. A low or falling blood pressure is, therefore, a late sign of shock in children, and when present should prompt emergent treatment. Salient laboratory parameters include a high urine-specific gravity (in the absence of an underlying renal concentrating defect as seen in diabetes insipidus or chronic obstructive or reflux nephropathy), a relatively greater elevation in blood urea nitrogen than in serum creatinine, a low urinary [Na+] excretion (< 20 mEq/L) or fractional excretion of sodium less than 0.1%, and an elevated hematocrit or serum albumin level secondary to hemoconcentration.
Table 23–5.Clinical manifestations of dehydration.
Emergent intravenous therapy is indicated when there is evidence of compromised perfusion (inadequate capillary refill, tachycardia, poor color, oliguria, or hypotension). The initial goal is to rapidly expand the plasma volume and to prevent circulatory collapse. A 20-mL/kg bolus of isotonic fluid should be given intravenously as rapidly as possible. Either colloid (5% albumin) or crystalloid (normal saline or Ringer lactate) may be used. Colloid is particularly useful in hypernatremic patients in shock, in malnourished infants, and in neonates. If no intravenous site is available, fluid may be administered intra-osseously through the marrow space of the tibia. If there is no response to the first fluid bolus, a second bolus may be given. When adequate tissue perfusion is demonstrated by improved capillary refill, decreased pulse rate and improved and mental status, deficit replacement may be instituted. If adequate perfusion is not restored after 40 mL/kg of isotonic fluids, other pathologic processes must be considered such as sepsis, occult hemorrhage, or cardiogenic shock. Isotonic dehydration may be treated by providing half of the remaining fluid deficit over 8 hours and the second half over the ensuing 16 hours in the form of 5% dextrose with 0.45% saline containing 20 mEq/L of KCl. In the presence of metabolic acidosis, potassium acetate may be considered. Maintenance fluids and replacement of ongoing losses should also be provided. Typical electrolyte compositions of various body fluids are depicted in Table 23–6, although it may be necessary to measure the specific constituents of a patient’s fluid losses to guide therapy. If the patient is unable to eat for a prolonged period, nutritional needs must be met through hyperalimentation or enteral tube feedings.
Table 23–6.Typical electrolyte compositions of various body fluids. ||Download (.pdf) Table 23–6.Typical electrolyte compositions of various body fluids.
| ||Na+ (mEq/L) ||K+ (mEq/L) ||HCO3– (mEq/L) |
|Diarrhea ||10–90 ||10–80 ||40 |
|Gastric ||20–80 ||5–20 ||0 |
|Small intestine ||100–140 ||5–15 ||40 |
|Ileostomy ||45–135 ||3–15 ||40 |
Oral rehydration may be provided to children with mild to moderate dehydration and commercially available solutions provide 45–75 mEq/L of Na+, 20–25 mEq/L of K+, 30–34 mEq/L of citrate or bicarbonate, and 2%–2.5% of glucose (Table 23–7). Clear liquid beverages found in the home, such as broth, soda, juice, and tea are inappropriate for the treatment of dehydration. Frequent small aliquots (5–15 mL) should be given to provide approximately 50 mL/kg over 4 hours for mild dehydration and up to 100 mL/kg over 6 hours for moderate dehydration. Oral rehydration is contraindicated in children with altered levels of consciousness or respiratory distress who cannot drink freely; in children suspected of having an acute surgical abdomen; in infants with greater than 10% volume depletion; in children with hemodynamic instability; and in the setting of severe hyponatremia ([Na+] < 120 mEq/L) or hypernatremia ([Na+] > 160 mEq/L). Failure of oral rehydration due to persistent vomiting or inability to keep up with losses mandates intravenous therapy. Successful oral rehydration requires explicit instructions to caregivers and close clinical follow-up of the child.
Table 23–7.Composition of oral rehydration solutions. ||Download (.pdf) Table 23–7.Composition of oral rehydration solutions.
|Fluid ||Carbohydrate g/L ||Na+ mEq/L ||HCO3− mEq/L ||K+ mEq/L |
|Pedialyte ||25 ||45 ||30 ||20 |
|Enfalyte ||30 ||50 ||30 ||25 |
|WHO (2002) ||13.5 ||75 ||30 ||20 |
The type of dehydration is often characterized by the serum [Na+]. If relatively more solute is lost than water, the [Na+] falls, and hyponatremic dehydration ([Na+] < 130 mEq/L) ensues. This is important clinically because hypotonicity of the plasma contributes to further volume loss from the ECF into the intracellular space. Thus, tissue perfusion is more significantly impaired for a given degree of hyponatremic dehydration than for a comparable degree of isotonic or hypertonic dehydration. It is important to note, however, that significant solute losses also occur in hypernatremic dehydration. Furthermore, because plasma volume is somewhat protected in hypernatremic dehydration, it poses the risk of the clinician underestimating the severity of dehydration. Typical fluid and electrolyte losses associated with each form of dehydration are shown in Table 23–8.
Table 23–8.Estimated water and electrolyte deficits in dehydration (moderate to severe). ||Download (.pdf) Table 23–8.Estimated water and electrolyte deficits in dehydration (moderate to severe).
|Type of Dehydration ||H2O (mL/kg) ||Na+(mEq/kg) ||K+(mEq/kg) ||Cl− and (mEq/kg) |
|Isotonic ||100–150 ||8–10 ||8–10 ||16–20 |
|Hypotonic ||50–100 ||10–14 ||10–14 ||20–28 |
|Hypertonic ||120–180 ||2–5 ||2–5 ||4–10 |
Hyponatremia may be factitious in the presence of high plasma lipids or proteins, which decrease the percentage of plasma volume that is water. Hyponatremia in the absence of hypotonicity also occurs when an osmotically active solute, such as glucose or mannitol, is added to the ECF. Water drawn from the ICF dilutes the serum [Na+] despite isotonicity or hypertonicity.
Patients with hyponatremic dehydration generally demonstrate typical signs and symptoms of dehydration (see Table 23–5), as the vascular space is compromised as water leaves the ECF to maintain osmotic neutrality. The treatment of hyponatremic dehydration is fairly straightforward. The magnitude of the sodium deficit may be calculated by the following formula:
Half of the deficit is replenished in the first 8 hours of therapy, and the remainder is given over the following 16 hours. Maintenance and replacement fluids should also be provided. The deficit plus maintenance calculations often approximate 5% dextrose with 0.45% or higher saline. The rise in serum [Na+] should not exceed 0.5 mEq/L/h or 6–8 mEq/L/24 h unless the patient demonstrates central nervous system (CNS) symptoms that warrant more rapid initial correction. The dangers of too rapid correction of hyponatremia include cerebral dehydration and injury due to fluid shifts from the ICF compartment, a condition known as osmotic demyelination syndrome.
Hypovolemic hyponatremia also occurs in cerebral salt-wasting (CSW) associated with CNS insults, a condition characterized by high urine output and elevated urinary [Na+] (> 40 mEq/L) due to an increase in ANP. CWS is a diagnosis of exclusion represented by an inappropriate natriuresis in a patient with a contracted effective circulatory blood volume in the absence of other causes for Na+ excretion. This must be distinguished from the syndrome of inappropriate secretion of ADH (SIADH), which may also manifest in CNS conditions and pulmonary disorders (Table 23–9). In contrast to CSW, SIADH is characterized by euvolemia or mild volume expansion and relatively low urine output due to ADH-induced water retention. Urinary [Na+] is high in both conditions, though generally not as high as in SIADH. It is important to distinguish between these two conditions, because the treatment of cerebral salt wasting involves replacement of urinary salt and water losses, whereas the treatment of SIADH involves water restriction. It is also important to remember that in SIADH patients are not necessarily oliguric, and that their urine does not need to be maximally concentrated but merely inappropriately concentrated for their degree of serum tonicity.
Table 23–9.SIADH and cerebral salt wasting. ||Download (.pdf) Table 23–9.SIADH and cerebral salt wasting.
| ||Serum Na+ ||Serum Osmolality ||Urine Na+ ||Urine Output ||Urine Osmolality ||Volume status ||Treatment |
|SIADH ||< 135 mEq/L ||< 280 mOsm/kg ||> 40 mEq/L ||Low ||> 100 mOsm/kga ||Euvolemia or mild volume expansion ||Water restriction |
|Cerebral Salt Wasting ||< 135 mEq/L ||< 280 mOsm/kg ||> 40 mEq/L ||High ||Variableb ||Hypovolemia ||Sodium and water replacement |
In cases of severe hyponatremia (serum [Na+] < 120 mEq/L) with CNS symptoms, intravenous 3% NaCl may be given over 1 hour to raise the [Na+] to 120 mEq/L to alleviate CNS manifestations and sequelae. In general, 1 mL/kg of 3% NaCl will raise the serum [Na+] by about 1 mEq/L. If 3% NaCl is administered, estimated Na+ and fluid deficits should be adjusted accordingly. Further correction should proceed slowly, as outlined earlier.
Hypervolemic hyponatremia may occur in edematous disorders such as nephrotic syndrome, congestive heart failure, and cirrhosis, wherein water is retained in excess of salt. Treatment involves restriction of Na+ and water and correction of the underlying disorder. Hypervolemic hyponatremia due to water intoxication is characterized by a maximally dilute urine (specific gravity < 1.003) and is also treated with water restriction.
Although diarrhea is commonly associated with hyponatremic or isonatremic dehydration, hypernatremia may develop in the presence of persistent fever or decreased fluid intake or in response to improperly mixed rehydration solutions. Extreme care is required to treat hypernatremic dehydration appropriately. If the serum [Na+] falls precipitously, the osmolality of the ECF drops more rapidly than that of the CNS. Water shifts from the ECF compartment into the CNS to maintain osmotic neutrality. If hypertonicity is corrected too rapidly (a drop in [Na+] of > 0.5 mEq/L/h), cerebral edema, seizures, and CNS injury may occur. Thus, following the initial restoration of adequate tissue perfusion using isotonic fluids, a gradual decrease in serum [Na+] is desired (6–8 mEq/L/day). This is commonly achieved using 5% dextrose with 0.2% saline to replace the calculated fluid deficit over 48 hours. Maintenance and replacement fluids should also be provided. If the serum [Na+] is not correcting appropriately, the free water deficit may be estimated as 4 mL/kg of free water for each milliequivalent of serum [Na+] above 145 mEq/L and provided as 5% dextrose over 48 hours. If metabolic acidosis is also present, it must be corrected slowly to avoid CNS irritability. Potassium is provided as indicated—as the acetate salt if necessary. Electrolyte concentrations should be assessed every 2 hours in order to control the decline in serum [Na+]. Elevations of blood glucose and blood urea nitrogen may worsen the hyperosmolar state in hypernatremic dehydration and should also be monitored closely. Hyperglycemia is often associated with hypernatremic dehydration and may necessitate lower intravenous glucose concentrations (eg, 2.5%).
Patients with diabetes insipidus, whether nephrogenic or central in origin, are prone to develop profound hypernatremic dehydration as a result of unremitting urinary-free water losses (urine-specific gravity < 1.010), particularly during superimposed gastrointestinal illnesses associated with vomiting or diarrhea. Treatment involves restoration of fluid and electrolyte deficits as described earlier as well as replacement of excessive water losses. Formal water deprivation testing to distinguish responsiveness to ADH should only be done during daylight hours after restoration of normal fluid volume status.
However, if a child presents with marked dehydration and a serum Na+ greater than 150 mEq/L, it may prove helpful and timely to obtain a plasma vasopressin level at the time of their initial presentation. The evaluation and treatment of nephrogenic and central diabetes insipidus are discussed in detail in Chapters 24 and 34, respectively.
Hypervolemic hypernatremia (salt poisoning), associated with excess total body salt and water, may occur as a consequence of providing improperly mixed formula, excessive NaCl or NaHCO3 administration, or as a feature of primary hyperaldosteronism. Treatment includes the use of diuretics, and potentially, concomitant water replacement or even dialysis.
The predominantly intracellular distribution of potassium is maintained by the actions of Na+-K+-ATPase in the cell membranes. Potassium is shifted into the ECF and plasma by acidemia and into the ICF in the setting of alkalosis, hypochloremia, or in conjunction with insulin-induced cellular glucose uptake. The ratio of intracellular to extracellular K+ is the major determinant of the cellular resting membrane potential and contributes to the action potential in neural and muscular tissue. Abnormalities of K+ balance are potentially life threatening. In the kidney, K+ is filtered at the glomerulus, reabsorbed in the proximal tubule, and excreted in the distal tubule. Distal tubular K+ excretion is regulated primarily by the mineralocorticoid aldosterone. Renal K+ excretion is primarily dependent on the urinary flow rate, and continues for significant periods even after the intake of K+ is decreased. Thus, by the time urinary [K+] decreases, the systemic K+ pool has been depleted significantly. In general, the greater the urine flow the greater the urinary K+ excretion.
The causes of net K+ loss are primarily renal in origin. Gastrointestinal losses through nasogastric suction or vomiting reduce total body K+ to some degree. However, the resultant volume depletion results in an increase in plasma aldosterone, promoting renal excretion of K+ in exchange for Na+ reclamation to preserve circulatory volume. Diuretics (especially thiazides and loop diuretics), mineralocorticoids, and intrinsic renal tubular diseases (eg, Bartter syndrome) enhance the renal excretion of K+. Systemic K+ depletion in hypokalemic metabolic acidosis may lead to “paradoxic aciduria” and low urine pH wherein H+ is preferentially exchanged for Na+ in response to aldosterone. Clinically, hypokalemia is associated with neuromuscular excitability, decreased peristalsis or ileus, hyporeflexia, paralysis, rhabdomyolysis, and arrhythmias. Electrocardiographic changes include flattened T waves, a shortened PR interval, and the appearance of U waves. Arrhythmias associated with hypokalemia include premature ventricular contractions; atrial, nodal, or ventricular tachycardia; and ventricular fibrillation. Hypokalemia increases responsiveness to digitalis and may precipitate overt digitalis toxicity. In the presence of arrhythmias, extreme muscle weakness, or respiratory compromise, intravenous K+ should be given. If the patient is hypophosphatemic ([PO43–] < 2 mg/dL), a phosphate salt may be used. The first priority in the treatment of hypokalemia is the restoration of an adequate serum [K+]. Providing maintenance amounts of K+ is usually sufficient; however, when the serum [K+] is dangerously low and K+ must be administered intravenously, it is imperative that the patient have a cardiac monitor. Intravenous K+ should generally not be given faster than at a rate of 0.3 mEq/kg/h. Oral K+ supplements may be needed for weeks to replenish depleted body stores.
Hyperkalemia—due to decreased renal K+ excretion, mineralocorticoid deficiency or unresponsiveness, or K+ release from the ICF compartment—is characterized by muscle weakness, paresthesias, and tetany; ascending paralysis; and arrhythmias. Electrocardiographic changes associated with hyperkalemia include peaked T waves, widening of the QRS complex, and arrhythmias such as sinus bradycardia or sinus arrest, atrioventricular block, nodal or idioventricular rhythms, and ventricular tachycardia or fibrillation. The severity of hyperkalemia depends on the electrocardiographic changes, the status of the other electrolytes, and the stability of the underlying disorder. A rhythm strip should be obtained when significant hyperkalemia is suspected. If the serum [K+] is less than 6.5 mEq/L, discontinuing K+ supplementation may be sufficient if there is no ongoing K+ source, such as cell lysis, and if urine output continues. If the serum [K+] is greater than 7 mEq/L or if potentiating factors such as hyponatremia, digitalis toxicity, and renal failure are present, more aggressive therapy is needed (Table 23–10). If electrocardiographic changes or arrhythmias are present, treatment must be initiated promptly. Intravenous calcium gluconate will rapidly ameliorate depolarization and may be repeated after 5 minutes if electrocardiographic changes persist. Calcium should be given only with a cardiac monitor in place and should be discontinued if bradycardia develops. The intravenous administration of a diuretic that acts in the loop of Henle, such as furosemide, will augment renal K+ excretion and can be very helpful in lowering serum and total body [K+]. Administering Na+ and increasing systemic pH with bicarbonate therapy will shift K+ from the ECF to the ICF compartment, as will therapy with a β-agonist such as albuterol. In nondiabetic patients, 0.5 g/kg of glucose over 1–2 hours will enhance endogenous insulin secretion, lowering serum [K+] 1–2 mEq/L. Administration of intravenous glucose and insulin may be needed as a simultaneous drip given over 2 hours with monitoring of the serum glucose level every 15 minutes.
Table 23–10.Drugs for the Treatment of Hyperkalemia in Children. ||Download (.pdf) Table 23–10.Drugs for the Treatment of Hyperkalemia in Children.
|Drug ||Dose ||Actions ||Notes |
|Calcium gluconate (10% solution) ||0.2–0.5 mL/kg IV given over 2–10 min (maximum dose 20 mL). ||Cardiac membrane stabilization. Does not alter the serum K+ level. ||Cardiac monitoring needed. May repeat dose if EKG changes persist. Discontinue if bradycardia develops. |
|Sodium polystyrene sulfonate ||1 g/kg oral every 6 h or rectal every 2–6 h. ||Ion exchange resin that exchanges K+ for Na+. Will decrease total body K+. ||Do not use in neonates and patients with bowel hypomotility or bowel obstruction due to risk of intestinal necrosis. May cause hypernatremia, hypocalcemia, and hypomagnesemia. |
|Sodium bicarbonate ||1 mEq/kg (maximum dose 50 mEq). ||Transient shift of K+ from the ECF to the ICF compartment. ||Avoid use if alkalosis or hypocalcemia is present. May cause hypernatremia, hypocalcemia. |
|Furosemide ||1–2 mg/kg IV. ||Diuretic that increases renal K+ excretion. Will decrease total body K+. ||May need higher doses in patients with chronic kidney disease to achieve desired effect. |
|Albuterol (nebulized) || |
Infants and children < 5 years of age: 2.5 mg in 2 mL of saline.
Children > 5 years of age: 5 mg in 2 mL of saline
Adolescents: 10 mg in 2 mL of saline.
|Transient shift of K+ from the ECF to the ICF compartment. ||May repeat for 1 additional dose. Tachycardia may limit repeat dosing. |
|Insulin (regular) ||Glucose 0.5–1 g/kg with 0.3 units of insulin per gram of glucose given over 2 h. ||Transient shift of K+ from the ECF to the ICF compartment. ||Must be given with a glucose infusion to prevent severe hypoglycemia. Diabetic patients may not require glucose infusion. Requires close monitoring of serum glucose. |
The therapies outlined above provide transient benefits. Ultimately, K+ must be reduced to normal levels by reestablishing adequate renal excretion using diuretics or optimizing urinary flow, using ion exchange resins such as sodium polystyrene sulfonate orally or as a retention enema, or by dialysis.
et al: Renal salt-wasting syndrome in children with intracranial disorders. Pediatr Nephrol 2012;27:733–739
et al: Association between maintenance fluid tonicity and hospital acquired hyponatremia. J Pediatr 2013;163:1646–1651
et al: Hypotonic versus isotonic maintenance fluids after surgery for children: a randomized controlled trial. Pediatrics 2011;128:980–983
T: Clinical practice. The syndrome of inappropriate antidiuresis. N Engl J Med 2007;356:2064
A: Fluid therapy for children: facts, fashions and questions. Arch Dis Child 2007;92:546–550
JC: Prevention of hospital-acquired hyponatremia: do we have the answers? Pediatrics 2011;128:980–983
et al: High antidiuretic hormone levels and hyponatremia in children with gastroenteritis. Pediatrics 2005;116:1401–1407
KB: Fluid and electrolytes: parenteral fluid therapy. Pediatr Rev 2001;22:380
RH: Disorders of plasma sodium—causes, consequences, and correction. N Engl J Med 2015;372:55–65