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Total parenteral nutrition (TPN) as used today in the neonatal intensive care unit (NICU) became a part of modern medicine in the late 1960s. Dudrick et al, in groundbreaking work, first demonstrated in beagle puppies the technique for parenterally administering nutrients.1 Shortly thereafter, Wilmore and Dudrick2 reported the use of this technique in an infant who had virtually no remaining small intestine and was totally dependent on these parenterally delivered nutrients of glucose, fibrin hydrolysate, minerals, and vitamins. There were no intravenous fat emulsions available, so plasma was given in small aliquots to provide some essential fatty acids (EFAs) and trace elements.2 Although this historic patient did not survive, normal growth and development was maintained for several months solely on this primitive solution. By the early 1970s, the technique was being used extensively in infants and children with congenital or acquired surgically correctable lesions of the gastrointestinal tract3,4 and in infants with intractable diarrhea.4,5 Use in the low birth weight infant soon followed.4,6,7


Today, TPN is a firmly established strategy in modern neonatal intensive care. The extremely low birth weight (ELBW) infant (<1000 g birth weight) with limited endogenous stores of nutrients and an increased rate of resting energy expenditure is at risk for rapid development of malnutrition or even actual starvation.8 The pioneering work of Dudrick and Wilmore has led to the current practice of early amino acids as the first infusate within hours of life in a 500-g infant. This chapter focuses on the use of TPN in very low birth weight (VLBW) infants (<1500 g birth weight).


The ELBW infants have unique nutritional requirements characterized by high metabolic rate, high protein turnover, and high glucose utilization. The ELBW infant has endogenous energy reserves of about 200 kcal, only enough energy to last days without exogenous sources. The 23-week infant has reserves that will be exhausted within hours. These infants are extremely vulnerable to inadequate nutrition.


Nutrient intakes provided to ELBW infants parenterally are much lower than what the fetus receives in utero. This intake deficit may persist throughout the infants’ stay in the NICU and even after discharge.9 These suboptimal nutrient intakes are critical in explaining the poor growth these infants often experience. The early growth deficit has long-lasting effects, including short stature and poor neurodevelopmental outcomes.10,11 Therefore, the observation of postnatal growth failure is a “surrogate” for inadequate nutrition and the likelihood of adverse neurodevelopmental outcome. Early aggressive TPN theoretically allows the transition from fetal to extrauterine life to occur with minimal interruption of growth and development and has been a successful strategy to improve growth and prevent inadequate nutrition.12,13




Immaturity of the gastrointestinal tract and critical illness in ELBW infants precludes substantive nutritional support from enteral nutrition the first days or even weeks of life; thus, nearly all of these infants are supported parenterally. Large amounts of amino acids are available to the fetus ...

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