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Hypernatremia in Children - Uptodate 15/08/18 19�54 Hypernatremia in children - UpToDate 15/08/18 1954 Official reprint from UpToDate® www.uptodate.com ©2018 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Hypernatremia in children Authors: Michael J Somers, MD, Avram Z Traum, MD Section Editor: Tej K Mattoo, MD, DCH, FRCP Deputy Editor: Melanie S Kim, MD All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jul 2018. | This topic last updated: Mar 10, 2017. INTRODUCTION — Hypernatremia is typically defined as a serum or plasma sodium greater than 150 mEq/L. Although pediatric hypernatremia is an uncommon electrolyte abnormality, there can be significant neurologic injury in patients with severe hypernatremia, especially those with acute and rapid changes in serum sodium. The etiology, clinical findings, diagnosis, and evaluation of pediatric hypernatremia are reviewed here. EPIDEMIOLOGY — The true incidence of pediatric hypernatremia is unknown, as published data are based on hospitalized children. As an example, a Scottish study reported an overall incidence of hypernatremia (defined as a plasma sodium >150 mEq/L) of 0.04 percent for all pediatric hospitalizations in pediatric patients over two weeks of age over a study period from 1996 to 2006 [1]. However, the risk of hypernatremia was 10 times greater in neonates less than two weeks of age, with an incidence of 0.4 percent. Neonatal hypernatremia was almost exclusively seen in breastfed infants with excessive weight (water loss). Of note, the incidence of neonatal hypernatremia in breastfed infants was higher than reported in previous studies (0.03 to 0.07 percent) (see "Initiation of breastfeeding", section on 'Excessive weight loss'). In older patients between two weeks and 17 years of age, the most common cause of hypernatremia on admission was excess water loss due to gastroenteritis or systemic infection. However, in this cohort, it was more common for hypernatremia to develop during hospitalization, particularly in patients with systemic infection or those who underwent cardiac surgery. In addition, approximately one-third of the patients had an underlying neurologic condition. In an earlier study from a tertiary children's hospital in Texas from 1992 to 1994, hypernatremia (defined as a serum sodium greater than 150 mEq/L) was detected in 1.4 percent of sodium values in a laboratory database, but only 0.2 percent of patients were discharged with a diagnosis of hyperosmolality due to hypernatremia [2]. Of the 68 children with a final discharge diagnosis of hyperosmolality/hypernatremia, two- thirds of the children developed hypernatremia during hospitalization, and the most common cause of hypernatremia was inadequate fluid intake. PATHOPHYSIOLOGY — Hypernatremia is caused by an imbalance in the body's handling of water, resulting in a relative excess of effective plasma osmolality (tonicity) to total body water. The plasma tonicity is defined as the concentration of solutes that do not easily cross the cell membrane, which is primarily due to sodium https://www.uptodate.com/contents/hypernatremia-in-children/print?source=history_widget Página 1 de 18 Hypernatremia in children - UpToDate 15/08/18 1954 salts in the extracellular space. As a result, serum or plasma sodium is used as a surrogate for assessing tonicity. (See "General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)", section on 'Plasma tonicity'.) The formulas used to estimate plasma tonicity are similar to those for the plasma osmolality, with the one exception that the contribution of urea (an ineffective osmole) is not included. The multiplier factor of "2" accounts for the osmotic contributions of the anions that accompany sodium, the primary extracellular cation: ● Plasma tonicity = 2 x [Na] + [glucose]/18 (if glucose is measured in mg/dL) ● Plasma tonicity = 2 x [Na] + [glucose] (if glucose is measured in mmol/L) Plasma tonicity is tightly regulated by the release of antidiuretic hormone (ADH) from the posterior pituitary promoting water retention, and by thirst-prompting water ingestion (figure 1). These homeostatic mechanisms that mediate plasma tonicity and water balance are similar in adults and children, resulting in a normal range of plasma sodium between 135 and 145 mEq/L that does not vary by age. (See "General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)", section on 'Regulation of plasma tonicity'.) Hypernatremia is most often caused by the failure to replace water losses, which, in children, are most commonly due to gastrointestinal fluid loss. In these patients, the sodium plus potassium concentration in the fluid that is lost is less than the plasma sodium concentration. As a result, water is lost in excess of sodium plus potassium, which will tend to increase the plasma sodium concentration. In individuals with intact thirst mechanisms, the intake of free water promptly corrects any increase in plasma sodium. However, when water losses cannot be replaced because of a lack of free access to water, excessive loss in acute illnesses, or impaired thirst mechanism, sodium concentration increases and may result in hypernatremia. Infants and children who are significantly neurodevelopmentally impaired are at particular risk for hypernatremia, as they may be unable to communicate their thirst and are dependent on others for fluid repletion. Pediatric hypernatremia also may result from urinary or skin loss of free water without adequate water replacement. Less commonly, pediatric hypernatremia may be caused by intake of sodium in excess of water (eg, administration of a hypertonic salt solution). In this setting, patients also are unable to access free water to correct the plasma tonicity. ETIOLOGY — The causes of pediatric hypernatremia can be separated into the two previously discussed mechanisms that result in pediatric hypernatremia (see 'Pathophysiology' above): ● Water loss that is not replaced ● Excessive salt intake relative to water ingestion Excess water losses — Loss of body fluids with a sodium plus potassium concentration that is less than serum or plasma sodium (hypotonic fluids) will result in an increase in sodium concentration if the water losses are not replaced. Sources of hypotonic body fluid losses include gastrointestinal fluids, dilute urine, and skin loss due to sweat or burns. In addition, inadequate water intake that fails to replace ongoing normal fluid losses will result in excess water loss and increases in serum or plasma sodium. Gastrointestinal loss — In children, the most common cause of hypernatremia is hypotonic gastrointestinal losses without replacement, which result in effective water loss. In particular, gastroenteritis https://www.uptodate.com/contents/hypernatremia-in-children/print?source=history_widget Página 2 de 18 Hypernatremia in children - UpToDate 15/08/18 1954 due to rotavirus can present with profuse watery diarrhea and hypernatremia [3]. In addition, losses due to vomiting or nasogastric drainage can lead to excess free water loss and hypernatremia. Urinary water loss — Excessive urinary free water loss may be caused by disorders with impaired urinary concentration (eg, diabetes insipidus [DI]) or osmotic diuresis. Without adequate water replacement, sodium concentration will rise and may result in hypernatremia (table 1). Urinary concentration defects — Impaired urinary concentration is typically due to antidiuretic hormone (ADH) deficiency or resistance, which leads to excretion of a dilute urine (urine osmolality less than plasma osmolality) and excessive urinary free water loss. ● Central DI – Central DI is caused by inadequate production or release of ADH. Central DI has multiple etiologies, including congenital central nervous system (CNS) malformations and genetic syndromes with associated CNS anomalies, and acquired causes due to CNS tumors, infiltrative processes of the hypothalamic-pituitary stalk, and sequelae from neurosurgery and trauma. (See "Clinical manifestations and causes of central diabetes insipidus", section on 'Causes'.) ● Nephrogenic DI – Nephrogenic DI is caused by an inadequate renal tubular response to circulating ADH. The multiple causes of pediatric nephrogenic DI can be further divided into the following categories (see "Clinical manifestations and causes of nephrogenic diabetes insipidus", section on 'Causes'): • Congenital nephrogenic DI – Congenital nephrogenic DI is most often the result of mutations in the vasopressin type 2 receptor (AVPR2), found at the locus Xp28. In this X-linked disorder, male infants typically present in the first weeks of life with fussiness, low-grade fever, and polyuria with hypernatremia. In addition, hereditary nephrogenic DI may be caused by a mutation in the aquaporin-2 gene (AQP2) at 12q13, which encodes the ADH-sensitive water channels. Congenital nephrogenic DI is also observed in other inherited disorders, including Bardet-Biedl and Bartter syndromes, nephronophthisis, cystinosis, and familial hypomagnesemia with hypercalciuria and nephrocalcinosis. • Acquired nephrogenic DI – Drug toxicity is the most common cause of acquired DI. Lithium toxicity is the most frequent cause of drug-induced nephrogenic DI, and its use has increased in children and adolescents with mood disorders. Lithium also can cause interstitial nephritis and fibrosis, further exacerbating urinary concentrating capacity.
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