While hypernatremia in neonates can result from increased serum sodium levels, most commonly, it is caused by excess water loss or insufficient water intake, or a combination of both. It is important to mention that “hypernatremic dehydration” is not a diagnosis but a sign of underlying illness related to many diverse pathological and physiological processes. This will be discussed in more detail later in this review. Thus, special attention must occur when managing fluids and electrolytes in extremely preterm newborns to prevent hypernatremia. Therefore, sodium loss in preterm infants is directly related to the degree of prematurity. In contrast, preterm infants have immature kidneys with blunted end-organ responsiveness to various hormones. Īfter birth, term newborns can reabsorb the filtered sodium relatively well through their kidneys. This physiological drop must be facilitated in various disease processes, failure of which can lead to long-term morbidities. This physiological transition should still occur for newborns who initially require intravenous (IV) fluids. In the first 4–7 days after birth, term newborns typically have a decrease of up to 10% of their birth weight, while preterm neonates have a decrease of up to 15%, which is regained 10–14 days after birth. By achieving sodium hemostasis, water balance is constantly maintained between the ECF and intracellular fluid (ICF) compartments.ĭuring the transition from fetal to neonatal life, all newborns experience a one-time physiological drop in their ECF and ICF. Most of the sodium filtered from the glomeruli is reabsorbed in proximal tubules, while the remaining amount is absorbed in various locations along the nephrons via a complex interplay between intrarenal hemodynamics, the renin-angiotensin system, vasopressin, antidiuretic hormone (ADH), and aldosterone. The kidneys are the principal organ that controls sodium hemostasis. Sodium is the main driving force for body water to move in and out of the cells and is monitored by multifactorial interactions between the heart, skin, kidney, and various hormones. Potential etiologies of hypernatremia in preterm and term neonates are summarized in Table Table1 1.Ī normal serum sodium level ranges between 135 mEq/L and 145 mEq/L and is the principal cation of the extracellular fluid (ECF) further subdivided into plasma and interstitial fluid. In preterm infants, the reported incidence of hypernatremia is about 40% and is usually due to insufficient fluid intake, excessive fluid loss, or excessive sodium intake. The main risk factors for hypernatremia in term newborns are related to early discharge from the hospital with ineffective lactation support or insufficient milk production leading to lactation failure. However, the reported incidence in term newborns after discharge from the hospital varies from 1% to 1.8% to as high as 5.6%. The precise incidence of hypernatremia in newborns is difficult to ascertain because of variable incidence based on geographical location, limited accessibility to hospital data, and limited post-discharge follow-up data. Mortality and morbidity are related to hypernatremia itself and inappropriate fluid management. Extracerebral complications include acute kidney injury, transaminitis, hyperglycemia or hypoglycemia, metabolic acidosis, and disseminated intravascular coagulation. Late recognition and delayed treatment lead to severe and prolonged hypernatremia with an increased risk of mortality and central nervous system morbidities like seizures, thrombosis, intracranial hemorrhage. Hypernatremia, defined as serum sodium of more than 145 mEq/L, is a common finding in preterm neonates in the neonatal intensive care unit (NICU) and in term infants after discharge from the hospital.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |