Resident The Children's Hospital at Montefiore New york, New York, United States
Background: Fatty acids are an integral component of perinatal nutrition. Essential fatty acids are not produced by the body, and require dietary provisions. The majority of placental transfer of essential fatty acids, linoleic acid (LA), alpha-linoleic acid (ALA), arachidonic acid (ARA) and docosahexaenoic acid (DHA), occurs in the third trimester of gestation. Preterm infants are therefore at increased risk of essential fatty acid deficiency (EFAD), and supplementation recommendations for term infants may not meet the requirements of a preterm infant. Objective: The goal of this study was to compare variations in fatty acid profiles of premature infants and to investigate EFAD among premature infants receiving either parenteral or enteral fat sources. Design/Methods: This is an ongoing prospective observational pilot study of preterm infants aged 23 to 36 gestational age in the Neonatal Intensive Care Units of two tertiary care centers. Neonates who received >80% of their daily source of nutrition as either SMOFlipid (soybean oil, MCT oil, olive oil, fish oil) or enteral sources (maternal breast milk, donor breast milk, formula) were included in the study. High stool output, parenteral fat source other than SMOFlipid, sepsis, and acute liver failure were exclusion criteria. A serum fatty acid panel was obtained once between 2 and 4 weeks of age. EFAD was defined by the Holman index of triene:tetraene (mead:arachidonic acid) ratio >0.2. Results: Of the 33 participants enrolled to date, 29 (88%) demonstrated essential fatty acid sufficiency, regardless of fat source. 4 participants (12%) demonstrated EFAD, with Holman indices of 0.22, 0.53, 0.54, and 0.96. 1 received 3g/kg SMOF, 2 received 2g/kg SMOF, and 1 received fortified donor breast milk of 24 kcal. These 4 patients were between 24 and 30 weeks gestational age and had cholestasis with direct bilirubin levels between 5 and 5.3 mg/dL. Additionally, these 4 fatty acid profiles showed low levels of ARA and elevated levels of mead acid. Low LA levels were present in 3 of the 4 with EFAD. All 33 patients in the study had normal DHA levels.
Conclusion(s): Preterm infants are at higher risk of EFAD due to lower fat stores and impaired fatty acid utilization. In this observational pilot study, infants with cholestasis had EFAD despite receiving fortified donor breast milk and SMOFlipid, which were expected to provide adequate fatty acid provisions. Further investigation is needed to assess whether patients with cholestasis, or patients receiving donor breast milk or SMOFlipid require closer screening for fatty acid deficiency.
