Early Chloride Intake Does Not Parallel That of Sodium in Extremely‐Low‐Birth‐Weight Infants and May Impair Neonatal Outcomes

Abstract

Cumulative Cl intake >10 mmol/kg during the first 3 days (ie, 3.3 mmol · kg (-1) · day(-1) on average) and >45 mmol/kg during the first 10 days (ie, 4.5 mmol · kg (-1) · day(-1) on average) may have unwanted metabolic consequences and should be avoided. Imbalance between electrolytes provided by the parenteral nutrition solution need to be detected and corrected.

Electrolyte and Mineral Homeostasis After Optimizing Early Macronutrient Intakes in VLBW Infants on Parenteral Nutrition

“…Providing balanced electrolyte and mineral intakes from birth allows for improving biochemical homeostasis in VLBW infants in regards to publications (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). This study also supports the provision of early electrolyte and mineral intakes from birth onward.…”

Parenteral Nutrition in Premature Infants

“…Additionally, excessive urine output above 5 mL/kg/h needs to be rapidly compensated volume for volume with 0.45 % sodium chloride infusion to balance water and sodium losses. Excessive sodium intakes from medications should be controlled to avoid any sodium overload and hypernatremia [54,[76][77][78]. In VLBW infants, urine sodium fractional excretion is high due to immature kidney functions.…”

“…Despite any evidence, several concerns persist about potential toxicities of such high AA intakes. The association that has been described between PN and metabolic acidosis is not related to early high AA intakes but is mainly due to imbalance in the electrolyte content in PN solutions [49,[52][53][54]. Uremia, or blood urea nitrogen (BUN), is frequently used to evaluate the adequacy of protein intakes in infants considering that BUN reflects protein degradation and AA oxidation.…”

“…Therefore, as a result of the poor ability of the premature kidney to eliminate acid load, an excessive chloride intake frequently induces metabolic acidosis. Thus, limiting chloride intakes and providing sodium and potassium intakes as organic phosphate or as sodium or potassium acetate/citrate in PN preparation might prevent hyperchloridemic metabolic acidosis [49,47,54,72,[90][91][92][93][94].…”

“…Due to their renal immaturity, urine output and fractional sodium excretion might also be deregulated. Therefore, fluid and electrolytes disturbances are frequently observed and are associated with increased morbidity, mortality, and adverse developmental outcomes, especially in VLBW infants [54,[73][74][75]. In particular, dehydration (weight loss above 10 %) combined with or without inadvertent increase sodium intake frequently induces severe hypernatremia above 150 mmol/L and brain injuries [54,74,[76][77][78].…”