Graham W. Chance

Late hyponatremia in very low birthweight infants. (less than 1.3 kilograms).

Extract: Late hyponatremia (plasma Na+ <130 mEq/liter) occurred frequently (on 54 of 159 occasions) in 46 very low birthweight (VLBW) infants (<1.3 kg at birth) between 2 and 6 weeks of age while receiving a sodium intake of ≤2 mEq/kg/24 hr. To elucidate possible pathogenetic mechanisms five groups of such infants were studied while receiving a commercially available formula reconstituted to give two different volumes and two different Na+ concentrations. Sodium intake in the nonsupplemented (NS) infants (n = 23) was less than 2 mEq/kg/24 hr. Supplemented (S) infants (n = 16) received approximately 3 mEq Na+/kg/24 hr. A further group of seven infants given a high volume (200 ml/kg/24 hr), high caloric (100 cal/dl) formula and Na+ supplementation (to 3 mEq/kg/24 hr) was also included. Infants were studied from age 14 days until they weighed 1.80 ± 0.05 kg at a mean age of 47 days.At the time of start of the study, 6 of 20 NS and 6 of 19 S infants were hyponatremic. After supplementation only two episodes of hyponatremia occurred in S infants, both during the first study week, whereas the high incidence of hyponatremia in NS infants remained unchanged throughout the first 3 weeks of the study period.During baseline urine collections all infants excreted between 80 and 100 ml/kg/24 hr urine, but those receiving 150 ml/kg/24 hr formula decreased their urinary output rapidly to 50 ml/kg/24 hr, whereas infants receiving high volume feeds (200 ml/kg/24 hr) did not decrease their urinary output until the third balance at an average age of 45 days. All infants excreted between 1.0 and 1.2 mEq/kg/24 hr of sodium in their urine during the initial collection. Nonsupplemented infants reduced their urinary Na+ excretion more rapidly than supplemented babies (NS: from 1.03 to 0.55 mEq/kg/24 hr, first vs second balance; S: from 1.00 to 0.80 mEq/kg/24 hr, first vs third balance). Mean potassium excretion remained unchanged in NS and S infants during the study period and was not affected by the volume or caloric content of the formula.Extracellular volume (ECV) and total body water (TBW) were measured serially, and there were no differences between S and NS infants in the distribution of body water. The percentage of TBW and ECV decreased in all groups with increasing postnatal age.Speculation: VLBW infants are prone to hyponatremia in the first 6 weeks of life because of the combined influence of renal immaturity, which permits relatively high urinary sodium loss in the presence of low plasma [Na+], and low intake of sodium (≤2 mEq/kg/24 hr), the amount provided by some current formulas based on breast milk. Dilutional factors are not involved, but the role of aldosterone remains unresolved. Supplementation of the formula to provide a daily total sodium intake of 3 mEq/kg/24 hr until a weight of 1.5 kg is reached is corrective.

Neonatal transport: A controlled study of skilledassistance

To attempt to demonstrate the need for skilled care of sick neonates in transport, a modified randomized controlled study of infants being transported to this institution was carried out. Although special equipment was used, ambulances were not modified. Results of the first phase reported here show that infants weighing P

Impaired assimilation of nasojejunal feeds in healthy low-birth-weight newborn infants

We compared nasojejunal with nasogastric tube feeding in 18 healthy low-birth-weight infants from eight to 15 days of age. NJ-fed infants had significantly more stools and excreted significantly more fat and potassium in their stools. Growth and weight gain did not differ between the groups during the study period. Future use of NJ feeding in LBW infants should take into account the possibility of malabsorption associated with this technique.

Postnatal growth of infants of <1.3 kg birth weight: Effects of metabolic acidosis, of caloric intake, and of calcium, sodium, and phosphate supplementation

Weekly increments of length, weight, head circumference, and skinfold thickness in response to a series of dietary changes were measured in 108 healthy infants who weighed

Supplemental intravenous alimentation in low-birth-weight infants

Comparative effects of intravenously administered 10 per cent dextrose solution with and without the addition of 3.5 per cent fibrin hydrolysate were evaluated in the supplemental alimentation of gastric-fed, low-birth-weight infants (

A NEW SYNDROME OF FAMILIAL PANCREATIC AGENESIS: THE ROLE OF INSULIN AND GLUCAGON IN SOMATIC AND CELL GROWTH

Two sibs of a consanguineous union were born with severe intrauterine growth retardation and agenesis of the pancreas confirmed at autopsy. We report the association between the growth failure and absence of fetal insulin and glucagon, and some of the changes in somatic and cell growth occurring in one of the infants at age 6 weeks. Birth weight 1280 gm at term; length 37 cm; head circ. 29 cm; (all <3rd centile). The brain weighed 214 gm (<3rd centile), and the liver weighed 95.7 gm (<25th centile). All other visceral organs were extremely small, particularly the adrenals whose combined weight of 1 gm was less than that of a 24-week old fetus. The total DNA in the cerebrum was 172 mg (N=258), in the cerebellum 95.6 mg (N=120), and in the liver 200 mg (N=320), respectively, indicating a reduction in the cell number in each of these organs. Protein/DNA ratio was normal or increased in brain and liver indicating a relatively greater reduction in DNA content than in protein. In muscle, the total DNA was reduced as calculated from muscle mass and the protein/DNA ratio of 58 was extremely low (N=100). The results in brain and muscle were similar to those seen in infants with severe postnatal marasmus, and suggest that insulin and glucagon are key hormones for normal fetal growth.

Glucose homeostasis in preterm rhesus monkey neonates.

Summary: Response to a primed glucose infusion (0.5 g/kg injected over 3 min and 8 mg/kg/min infused for 3 hr) was studied in 5 term and 11 preterm rhesus monkey neonates 2–3 hr after delivery by cesarian section. The glucose challenge perturbed a steady state glucose specific activity achieved in the previous 100 min by a primed trace infusion of 2-[3H]glucose (6 μCi and 0.2 μCi/min). This allowed the determination of changes in endogenous glucose turnover in response to exogenous glucose in the immediate newborn period.With glucose challenge, the 5 term animals and 6 of the 11 preterm animals developed a new steady state glucose concentration (80–100 ml/dl). Coincident with this was a marked reduction in endogenous hepatic glucose output and a moderate increase in peripheral glucose utilization as measured by the tracer methodology. In contrast, the other five preterm monkeys developed hyperglycemia upon glucose challenge (190–210 mg/ dl). All groups had similar glucose-stimulated insulin release which peaked after 60 min of glucose infusion. However, in comparison to the other groups, the group that was to develop hyperglycemia exhibited: (1) lower basal insulin and higher basal glucose values; (2) no suppression of endogenous hepatic glucose output or lipolysis despite glucose-stimulated insulin release; (3) lower birth weight and gestational age, and increased eventual mortality. Hypoxia was not evident in any group as evidenced by clinical signs and decreasing lactate/ pyruvate ratios during the glucose infusions.Speculation: The inability of certain preterm rhesus monkeys to maintain normoglycaemia, but rather to develop hyperglycemia in the face of a glucose infusion might be related to inappropriate adrenergic activity unrelated to cither hypoxia or hypothermic stress. This represents an animal model for the further study of hyperglycemia seen in certain human preterm neonates.

944 TRANSPORT OF SICK NEONATES <1.5kg BIRTHWEIGHT: PERSONNEL REQUIREMENTS

The effect of transport of sick neonates by skilled personnel with necessary equipment on physiological parameters on admission to a neonatal intensive care unit and on outcome, was evaluated in a controlled study. In phase I routine care by staff from the hospital of birth was compared with that provided by a trained nurse/physician team. In phase II care in transport was provided for each infant by only one of the trained nurses of phase I. Results(mean±SD)for infants <1.5kg birthweight are presented:We conclude that two trained individuals, one being preferably a physician, are necessary for safe transport of infants <1.5kg birthweight.

GROWTH OF VERY LOW BIRTHWEIGHT |[lpar]|VLBW|[rpar]| INFANTS: EFFECTS OF ACIDOSIS, CALORIC INTAKE AND HYPONATREMIA

Our aim is to achieve a growth rate comparable to that in utero in the VLBW (<1.3 kg). Sixty-seven infants were grouped according to gestational age (GA) and birthweight, and studied from age 14 days to weight 1.8 kg. Weight, length, head circumference and skinfold thickness were measured serially. Prevention of metabolic acidosis led to a 21% greater length growth (p<0.02). Increased caloric intake from 130 to 150 cal/kg/day led to greater gains in length (to 1.08 cm/wk), body weight, and skinfold thickness (p<0.05). Plotting postnatal weight against length, curves of individuals, initially >97th centile, approached the 75th centile at 1.8 kg. Episodic hyponatremia (Na <130 mEq/1) in some infants fed “Improved” SMA S-26, 150 cal/day, was associated with decreased length growth (p <0.05 in appropriate GA infants). Increasing Na intake from 2 to 3 mEq/kg/day prevented hyponatremia without expansion of ECF space. Increased caloric intake to 180 cal/kg/day led to weekly length increments of 1.2 cm (= 50th intrauterine centile), weight increments of 200 g/week (= 45th centile, p <0.05), and a slight increase in head circumference compared to infants fed 150 cal/kg/day. Thus, by carefully controlling metabolic acidosis, hyponatremia and caloric intake intrauterine growth rates could be maintained after age 14 days in the VLBW.

A controlled study of intravenous fibrin hydrolysate supplement in prematures < 1.3 kg

We have compared the effect of early supplemental intravenous 3.5% fibrin hydrolysate plus 10% dextrose to 10% dextrose alone on the mortality, morbidity, weight gain and biochemical changes in 2 equal groups of 15 low birth weight infants of appropriate gestation. The initial alimentation was intravenous with gradual repalcement by oral formula over the first 2 weeks of life. Total fluid intake of 200 ml/kg/day was maintained. Total caloric intake and urinary output did not differ between groups. The amino acid infants received twice the amount of protein (g/kg/day) as the controls. Mortality did not differ between groups when infants were assessed by body weight. In the survivors apnoca was significantly less frequent in those receiving amino acid and regain of birth weight more rapid. Total protein and BUN were higher in those on amino acid reflecting increased N2 intake, and serum PO4 lower. Serum electrolytes, sugar, osmolality, HCO3 did not differ. Fatal cases in the amino acid group, many <1.0 kg, exhibited an excessive rise in BUN, and high plasma osmolality within 3 days of infusion.