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Fluid management: NICU Handbook

Provider Education
May 18, 2022

Michael J. Acarregui, MD
Peer Review Status: Internally Peer Reviewed

Fluid and electrolyte management in the newborn

Careful fluid and electrolyte management is essential for the well being of the sick neonate. Inadequate administration of fluids can result in hypovolemia, hypersomolarity, metabolic abnormalities and renal failure. In the near term and term neonate excess fluid administration results in generalized edema and abnormalities of pulmonary function. Excess fluid administration in the very low birth weight infant is associated with patent ductus arteriosis and congestive heart failure, intraventricular hemorrhage, necrotizing enterocolitis and bronchopulmonary dysplasia. A rational approach to the management of fluid and electrolyte therapy in term and preterm neonates requires the understanding of several physiologic principles.

Physiology

  1. Body Composition and Surface Area
    1. The body composition of the fetus changes during gestation with a smaller proportion of body weight composed of water as gestation progresses.
    2. The preterm fetus or neonate is in a state of relative total body water and extracellular fluid excess. After birth this excess water must be mobilized and excreted.
    3. A proportion of the diuresis observed in both term and preterm infants during the first days of life should be regarded as physiologic.
    4. 4. The surface area of the newborn is relatively large and increases with decreasing size. Therefore, insensible water losses will be greatest with small size and decreased gestational age.
     
  2. Hormonal Effects:
    1. The Renin-angiotensin system is very active in the first week of neonatal life resulting in increased vascular tone and elevated levels of aldosterone
    2. Increased aldosterone levels enhance distal tubular reabsorption of sodium resulting in an impaired ability to excrete a large, or acute, sodium load.
    3. Arginine vasopressin (AVP, ADH) levels rise after birth. AVP secretion is increased in response to stress, such as birth, asphyxia, RDS, positive pressure ventilation, pneumothorax and intracranial hemorrhage.
     
  3. Renal Hemodynamics: After birth, renal blood flow increases in response to increased blood pressure (renin-angiotensin) with a secondary increase in glomerular filtration rate. However, the neonatal kidney is less efficient at excreting an acute sodium or water load than the kidney of an infant or child.
  4. Sodium Homeostasis:
    1. Sodium is required for fetal growth with an accretion rate of 1.2 mEq/kg/day between 31-38 weeks.
    2. Sodium retention is aided by increased aldosterone levels in newborns.
    3. In preterm infants <34 weeks sodium reabsorption is decreased, the fractional excretion of Na may exceed 5%. However, the preterm infant is unable to rapidly increase sodium excretion in response to high sodium levels or a large sodium load.
     
  5. Water Handling: Both term and preterm infants are able to excrete dilute urine. Conversely, preterm infants are able to concentrate urine to ~ 600 mOsm/L and the term infant to ~ 700 mOsm/L. (Adults can concentrate to ~ 1300 mOsm/L.) Therefore, both preterm and term neonates generally have the capacity to regulate their intravascular volume within a range of fluid intakes.

Based on the above principles

  1. One should expect a 10-15% weight loss over the first 5-7 days of life (up to 20% in infants <750 g).
  2. Infants which experience significant intrapartum stress will be slow to void and will therefore require less fluid over the first 24-48 hours.
  3. The small or extremely immature infant <1000 g will experience increased insensible water losses (IWL). IWL = (I-O) - (± Δwt).
  4. As the preterm and term infant is able to regulate urine output in response to hypovolemia, urine output will reflect intravascular volume. In other words, the infant will generally not maintain inappropriately high urine output in the face of intravascular volume depletion.

Recommendations

  1. Initiate fluid therapy at 60-80 ml/kg/d with D10W, (80-150 ml/kg/d for infants ≤ 26 weeks).
  2. Infants <1500 g should be covered with a saran blanket and strict I&O should be followed. For infants < 26 weeks the saran blanket should be applied directly upon the infant to minimize IWL.
  3. Infants <1000 g should have electrolytes and weights recorded every 6-8 hours; every 12 hours for infants 1000-1500 grams.
  4. For serum Na+ >145 mEq/L, increase infusate by ~10 mL/kg/d without Na+ in the infusate.
  5. Increase fluids for urine output <0.5 mL/kg/hr by ~10 mL/kg or, in infant ≤ 26 weeks, calculate IWL and change fluids accordingly.
  6. Infuse Na+ free fluids (including flushes) until serum Na+ <145 and good urine output is established (post diuretic phase). Then add 3-5 meq/kg/d Na+.
  7. Add KCl (2-3 meq/kg/d) to IV fluids after urine output is well established and K+ <5 mEq/L (usually 48-72 hours).
  8. Increase fluid administration gradually over the first week of life to 120-130 cc/kg/d by day 7, allowing for expected physiologic weight loss.

Special cases

While the above guidelines are more directed toward the LBW infant, especially <1000 g, they are generally applicable to most neonates; however, there are instances where these guidelines should be modified. Some of the more common modifications are noted below:

  1. Postoperative abdominal surgery: Fluid requirements may be twice or three times that noted above. The more extensive the procedure the greater the needs! These infants may require 125-150 ml/kg/day immediately postoperative with subsequent increases as determined by blood pressure measurements and urine output. Isotonic saline also may be required because of third spacing of fluid into tissues and other spaces, e.g., the bowel lumen. Strict I&O is mandated. Gastric drainage is replaced q8-12h, depending on volume, with isotonic saline. Colloid also may be needed because of rapid fluid shifts, decreases in arterial pressure, and increases in capillary filling time (i.e., > 3 sec.).
  2. Asphyxiated infants: These infants may have increased secretion of arginine vasopressin (which is likened to SIADH) and are thought to be at increased risk for cerebral edema. Their fluid intake should be kept on the low side for 48-72 h, i.e., ≤ 60 ml/kg/day, or until seizures are no longer considered a problem. These infants require close monitoring of serum sodium and weight. Treatment of SIADH is by restriction of fluids, not increased sodium intake.
  3. Infants of diabetic mothers: These infants receive i.v. glucose because of increased danger of hypoglycemia; however, they frequently do not receive sodium and have been found to develop rather substantial hyponatremia at 24 h if this is not added at or before this time. This danger is greater the greater rate of glucose needed to maintain blood glucose. Addition of sodium should be considered at 16-18 h.

Fluid therapy in the neonate

Fluid therapy for the neonate can be rationally planned if several physiologic concepts are kept in mind. Firstly, the neonate has an excess of total body water at birth, particularly extracellular water, which must be redistributed and excreted. The renin-angiotensin system is in high gear during the first week after birth; thus not only is plasma angiotensin II likely to be elevated, but also aldosterone, which is a mineralocorticoid and has the potential to modulate sodium excretion/reabsorption. The surface of the newborn is large and increases with decreasing size; therefore there is a greater likelihood of excess insensible water loss (IWL), which may be exaggerated as birth weight and gestational age decrease and open radiant warmers rather than incubators are used. Finally, in most instances the neonatal kidney has the capacity to not only dilute urine, but also to concentrate it, reaching values of 600-700 m0sm/L (specific gravity ≤ 1.015). It should be noted, however, that this is less than that seen in adults or term infants. These observations are contrary to previous "beliefs," and each of these aspects of the neonate are reviewed elsewhere (J Pediatr 101:387, 1982).

Our goal in the low-birth-weight (LBW) infant ≤1599 g is to allow a gradual weight loss over the first week, i.e., 5-6% over the first 24 h and 12-15% by the end of the first week. We also attempt to maintain urine output ≥ 0.5 ml/kg hr. If IWL plus urine output significantly exceeds intake, weight loss may be greater than desired and occur more rapidly in the preterm LBW infant. This in turn may result in development of hypernatremia since fluid losses through the skin are essentially free water. To take each of these into account, the first approach to fluid therapy is adequate monitoring and appropriate supportive care. Thus, all infants ≤1000 g birth weigh should be maintained on a bed scale, kept on "strict" input and output measurements, and covered with a "saran blanket" to minimize IWL, especially if cared for in an open radiant warmer.

It is estimated that the nongrowing neonate requires 60-75 kcal/kg/day and that fluid losses are closely related to caloric expenditure. Thus, in the first 1-3 days after birth fluid requirements are likely to be in the range of 65-75 ml/kg/day in a neutral thermal environment. To accomplish this we use 10% dextrose in water (D10W). Therefore, at 24 h the fluid should be changed to D10 with 1/4 isotonic saline. The addition of KCl to the infusate should be considered by day 3 if there are no contraindications, e.g., poor renal function or hemolytic disease, at 2-3 mEq/kg/day. Although negative potassium balance occurs with this approach it is quickly corrected.

Our approach to fluid therapy has been to gradually increase the volume to approximately 75-80 ml/kg/day on day 2, 90-95 ml/kg/day on day 3, and -125 ml/kg/day by day 7. At 14 days most infants are receiving about 135 ml/kg/day.

References:

  1. J Pediatr 101:387, 1982.
  2. J Pediatr 101:423, 1982.
  3. The Body Fluids in Pediatrics, Winters RW (ed), Boston, Little Brown & Co., 1973.
  4. Clinics in Perinatology 9:483, 1982.
  5. The Micropremie: The Next Frontier, 99th Ross Conference on Pediatric Research, Columbus, OH, 1990.