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A preterm infant, whose course was complicated by sepsis, necrotizing enterocolitis with jejunal perforation, intraventricular hemorrhage and cerebellar hemorrhage, suffered permanent and total paralysis below the neck from extravasation of parenteral nutrition fluids through a femoral venous catheter. MRI imaging revealed extravasation of fluid into the paraspinus musculature with extension into the spinal canal. This fluid was identified as hyperalimentation and intralipid. Postmortem examination found evidence of necrosis of the spinal cord as well as perforation of the right iliac vein.

I developed a single equation that simulated previously published growth charts for very low-birth-weight infants, using birth weight as the only variable. The intent of this study was to validate the equation using infants admitted to our neonatal intensive care unit (NICU) and to determine if this equation could be used as a research tool to compare weight gain among populations. All 171 surviving infants with birth weight < or = 1500 g who received care in our NICU were studied retrospectively. The individual daily weights were compared with the predicted daily weights for each infant using the relative error of the prediction. The relative error of the prediction on all days for all infants was 0.45 +/- 0.13% (mean +/- SEM), and the maximum mean daily relative error of 2.73 +/- 0.90% occurred on Day 9. Black infants had a more positive relative error than white infants (p = 0.0001), due to faster weight gain. Twins gained faster than singletons (p = 0.023). Infants with patent ductus arteriosus (PDA) gained more slowly than normal infants (p = 0.001) after an initial rapid weight gain. Infants with lung disease had initial rapid weight gain similar to infants with PDA, but subsequently were similar to infants without lung disease. This equation accurately predicts weight gain in our population of very low-birth-weight infants. The relative error of the prediction is a useful research tool for determining the effect of clinical conditions or interventions on weight gain.

The cause of hyperglycemia in extremely-low-birth-weight (ELBW) infants is not well understood. We studied infants weighing <1,000 g to investigate the relationship of hyperglycemia to blood levels of insulin-like growth factor (IGF)-I and IGF-II. We also compared two methods of treatment for hyperglycemia: continuous insulin infusion and reduction of glucose intake. Fifty-six ELBW infants were enrolled on day 2 of life. Intravenous glucose intake was increased incrementally to a maximum of 12 mg/kg/min on day 6. Infants who developed hyperglycemia were randomly assigned to receive reduced glucose intake (n = 11) or insulin infusion (n = 12). Infants whose blood sugar remained normal served as controls (n = 33). Blood was drawn on days 3, 8 and 15 in all infants, and again when they developed hyperglycemia. Nutritional intake and laboratory results for the treatment groups were compared with controls. Hyperglycemic infants had lower birth weights than controls. Hyperglycemic infants treated with glucose reduction remained <60 kcal/kg/day longer than control or insulin infusion groups (8.6 +/- 1.3 days vs. 4.1 +/- 0.2 and 5.5 +/- 0.6 days). No infants became hypoglycemic during insulin infusion. There was no difference in baseline blood levels of IGF-I or IGF-II among the groups, and these growth factors did not change in response to hyperglycemia. Hyperglycemic infants had baseline levels of insulin which were similar to normal controls, and endogenous insulin increased in response to hyperglycemia in 15 of the 23 infants who developed hyperglycemia. IGF-I and IGF-II are not related to hyperglycemia. In our population, hyperglycemic infants did not have baseline insulin deficiency and most had a normal insulin response to hyperglycemia. Insulin infusion appears safe in these infants and helped to maintain normal caloric intake, whereas glucose reduction was associated with a prolonged caloric deprivation.

Glutamine, described as a "conditionally essential" amino acid for critically ill patients, has not been routinely added to parenteral amino acid formulations for critically ill neonates and is provided in only small quantities by the enteral route when enteral intake is low. We conducted a blinded, randomized study of enteral glutamine supplementation in 68 very low birth weight neonates randomly assigned to receive glutamine-supplemented premature formula versus premature formula alone between days 3 and 30 of life. Primary end points consisted of hospital-acquired sepsis, tolerance to subsequent enteral feedings (days with no oral intake), and duration of hospital stay. Hospital acquired sepsis was 30% (control group) and 11% (glutamine group). Logistic regression with birth weight as a covariate showed that: (1) feeding group was significant (p = 0.048) in determining the probability of developing proven sepsis over the course of hospitalization and (2) the estimated odds of developing sepsis were 3.8 times higher for infants in the control group than for those treated with glutamine. Glutamine-supplemented infants had better tolerance to enteral feedings as measured by percent of days on which feedings needed to be withheld (mean percentage of 8.8 vs 23.8, p = 0.007). Analysis of T cells demonstrated a blunting of the rise in HLA-DR+ and CD16 subsets in glutamine-supplemented infants. There were no differences in growth; in serum ammonia, urea, liver transaminase, or prealbumin concentrations; or in mean hospital stay. This study provides evidence for decreased morbidity in very-low-birth-weight neonates who receive enteral glutamine supplementation.

The ontogeny of small intestinal glutaminase (GA) and glutamine synthetase (GS) was studied with relation to the maternal administration of dexamethasone (DEX). Pregnant Sprague-Dawley rats were administered 0.2 mg/kg of DEX or saline twice daily on days 19 and 20 of gestation. Activity of GA did not increase from the fetus to the 10-day-old rat; however, GS activity increased 7-fold. DEX induced doubling of GA activity and mRNA, but only a slight increase is GS activity and mRNA was observed in the fetus. GA and GS activities appear to be regulated by different mechanisms.