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Fluid and electrolyte therapy in newborns

Jochen Profit, MD, MPH
Section Editors
Steven A Abrams, MD
Kathleen J Motil, MD, PhD
Deputy Editor
Melanie S Kim, MD


Water and electrolyte homeostasis in newborn infants is influenced by physiologic adaptations following birth, and developmental effects on the distribution of total body water and water loss. Fluid and electrolyte therapy must account for these factors in determining maintenance requirements and correction of any abnormalities.


Total body water is composed of extracellular fluid (ECF), which includes intravascular and interstitial fluid, and intracellular fluid. The distribution between these compartments changes with increasing gestational age [1]. Compared with an infant born at 27 weeks, a newborn term infant has a total body water that comprises a smaller fraction of body weight (75 versus 80 percent) and an ECF volume that is a smaller fraction of total body water (45 versus 70 percent) [2].

Infants normally lose weight during the first week after birth. This weight loss is greater in preterm than term infants (approximately 10 to 15 versus 5 percent) and is associated with a diuresis. The postnatal diuresis is approximately 1 to 3 mL/kg per hour in term infants and is greater in preterm infants. Physiologic weight loss results primarily from an isotonic reduction in extracellular water, although the mechanism for this process is uncertain [1].


Water loss can occur through the kidneys, skin, and lungs. The absolute and relative amounts of water loss through these routes change with development. Excessive loss of other fluids, such as stool, gastric drainage, or thoracostomy output, can lead to water and electrolyte disturbances.

Renal — A urine volume of approximately 45 mL/kg per day, or 2 mL/kg per hour, allows excretion of a normal solute load, typically in a dilute urine. Changes in urinary water and electrolytes occur with changes in blood flow and maturation of renal function. The proportion of cardiac output directed to the kidneys increases during gestation and after birth. This proportion is 2 percent during the first week after birth at term, 8.8 percent at five weeks of age, and 9.6 percent at one year [3]. In contrast, approximately 16 percent of cardiac output in adults goes to the kidneys [4].


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Literature review current through: Sep 2016. | This topic last updated: Jun 4, 2014.
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  1. Dell KR. Fluid, electrolytes, and acid-base homeostasis. In: Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant, 9th, Martin RJ, Fanaroff AA, Walsh MC (Eds), Elsevier Mosby, St. Louis 2011. Vol 1, p.669.
  2. FRIIS-HANSEN B. Body water compartments in children: changes during growth and related changes in body composition. Pediatrics 1961; 28:169.
  4. Seikaly MG, Arant BS Jr. Development of renal hemodynamics: glomerular filtration and renal blood flow. Clin Perinatol 1992; 19:1.
  5. Beck JC, Lipkowitz MS, Abramson RG. Characterization of the fetal glucose transporter in rabbit kidney. Comparison with the adult brush border electrogenic Na+-glucose symporter. J Clin Invest 1988; 82:379.
  6. Constantinescu AR, Lane JC, Mak J, et al. Na(+)-K(+)-ATPase-mediated basolateral rubidium uptake in the maturing rabbit cortical collecting duct. Am J Physiol Renal Physiol 2000; 279:F1161.
  7. Devuyst O, Burrow CR, Smith BL, et al. Expression of aquaporins-1 and -2 during nephrogenesis and in autosomal dominant polycystic kidney disease. Am J Physiol 1996; 271:F169.
  8. Horster M. Embryonic epithelial membrane transporters. Am J Physiol Renal Physiol 2000; 279:F982.
  9. Williams PR, Oh W. Effects of radiant warmer on insensible water loss in newborn infants. Am J Dis Child 1974; 128:511.
  10. Baumgart S. Reduction of oxygen consumption, insensible water loss, and radiant heat demand with use of a plastic blanket for low-birth-weight infants under radiant warmers. Pediatrics 1984; 74:1022.
  11. Engle WD, Baumgart S, Schwartz JG, et al. Insensible water loss in the critically III neonate. Combined effect of radiant-warmer power and phototherapy. Am J Dis Child 1981; 135:516.
  12. Oh W, Karecki H. Phototherapy and insensible water loss in the newborn infant. Am J Dis Child 1972; 124:230.
  13. Bertini G, Perugi S, Elia S, et al. Transepidermal water loss and cerebral hemodynamics in preterm infants: conventional versus LED phototherapy. Eur J Pediatr 2008; 167:37.
  14. Riesenfeld T, Hammarlund K, Sedin G. Respiratory water loss in fullterm infants on their first day after birth. Acta Paediatr Scand 1987; 76:647.
  15. Riesenfeld T, Hammarlund K, Sedin G. Respiratory water loss in relation to gestational age in infants on their first day after birth. Acta Paediatr 1995; 84:1056.
  16. Omar SA, DeCristofaro JD, Agarwal BI, La Gamma EF. Effects of prenatal steroids on water and sodium homeostasis in extremely low birth weight neonates. Pediatrics 1999; 104:482.
  17. Ali R, Amlal H, Burnham CE, Soleimani M. Glucocorticoids enhance the expression of the basolateral Na+:HCO3- cotransporter in renal proximal tubules. Kidney Int 2000; 57:1063.
  18. Baum M, Amemiya M, Dwarakanath V, et al. Glucocorticoids regulate NHE-3 transcription in OKP cells. Am J Physiol 1996; 270:F164.
  19. Omar SA, DeCristofaro JD, Agarwal BI, LaGamma EF. Effect of prenatal steroids on potassium balance in extremely low birth weight neonates. Pediatrics 2000; 106:561.
  20. Roberts KB. Fluid and electrolytes: parenteral fluid therapy. Pediatr Rev 2001; 22:380.
  21. Baumgart S, Costarino AT. Water and electrolyte metabolism of the micropremie. Clin Perinatol 2000; 27:131.
  22. Adrogué HJ, Madias NE. Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med 1981; 71:456.
  23. Fulop M. Serum potassium in lactic acidosis and ketoacidosis. N Engl J Med 1979; 300:1087.
  24. Rees L, Brook CG, Shaw JC, Forsling ML. Hyponatraemia in the first week of life in preterm infants. Part I. Arginine vasopressin secretion. Arch Dis Child 1984; 59:414.
  25. Ford DM. Fluid, electrolyte, and acid-base disorders and therapy. In: Current pediatric diagnosis and treatment, 14th ed, Hay WW, Hayward AR, Levin MJ, Sondheimer JM (Eds), Appleton and Lange, Stamford, CT 1999. p.1109.
  26. Siegel SR, Oh W. Renal function as a marker of human fetal maturation. Acta Paediatr Scand 1976; 65:481.
  27. Moritz ML, Manole MD, Bogen DL, Ayus JC. Breastfeeding-associated hypernatremia: are we missing the diagnosis? Pediatrics 2005; 116:e343.
  28. Escobar GJ, Liljestrand P, Hudes ES, et al. Five-year neurodevelopmental outcome of neonatal dehydration. J Pediatr 2007; 151:127.
  29. Koklu E, Gunes T, Ozturk MA, et al. A review of 116 cases of breastfeeding-associated hypernatremia in rural area of central Turkey. J Trop Pediatr 2007; 53:347.
  30. Blum D, Brasseur D, Kahn A, Brachet E. Safe oral rehydration of hypertonic dehydration. J Pediatr Gastroenterol Nutr 1986; 5:232.
  31. Lorenz JM, Kleinman LI, Markarian K. Potassium metabolism in extremely low birth weight infants in the first week of life. J Pediatr 1997; 131:81.
  32. Mildenberger E, Versmold HT. Pathogenesis and therapy of non-oliguric hyperkalaemia of the premature infant. Eur J Pediatr 2002; 161:415.
  33. Shaffer SG, Kilbride HW, Hayen LK, et al. Hyperkalemia in very low birth weight infants. J Pediatr 1992; 121:275.