Introduction

As the field of neonatal intensive care began to emerge in the mid-1960s, efforts were made to save prematurely born babies that were previously thought to be nonviable. Many of these infants were considered to be “too unstable” to feed. They were provided neither enteral feedings nor intravenous glucose, essentially being starved for several days after birth. Some investigators recognized that this caused catabolism with subsequent endogenous tissue breakdown and introduced the practice of providing intravenous glucose to sick premature infants, which unsurprisingly reduced catabolism and improved survival. Although we have made progress in the past 40 years, the practice of withholding enteral support to sick infants remains prevalent. The provision of parenteral support with lipids, amino acids, vitamins, minerals, and trace elements likewise, is frequently delayed and/or interrupted for poorly substantiated reasons. As a result, most of these infants experience a significant delay in the growth they would have attained in utero (Figure 24.1). Although many of these individuals catch up in somatic growth to their nonpremature peers over a period of years, it should be recognized that optimum nutrition for the rapidly developing neonate should be aimed at goals beyond simply improved weight gain. The short- and long-term effects of undernutrition during a critical window of susceptibility to several illnesses, as well as the potential for poor neurodevelopment, should not be underestimated.