Nutrition and Selected Disorders of the Gastrointestinal Tract




Part One


Nutrition for the High-Risk Infant


David H. Adamkin, Paula G. Radmacher, Salisa Lewis


The goal of nutritional support for the high-risk infant is to provide sufficient nutrients postnatally to ensure continuation of growth at rates similar to those observed in utero. The preterm infant presents a particular challenge in that the nutritional intake must be sufficient to replenish tissue losses and permit tissue accretion. However, during the early days after birth, acute illnesses such as respiratory distress, patent ductus arteriosus, and hyperbilirubinemia preclude maximal nutritional support. Functional immaturity of the renal, gastrointestinal, and metabolic systems limits optimal nutrient delivery. Substrate intolerances are common, limiting the nutrients available for tissue maintenance and growth.


During the last trimester of pregnancy, nutrient stores are established in preparation for birth at 40 weeks’ gestation. Fat and glycogen are stored to provide ready energy during times of caloric deficit. Iron reserves accumulate to prevent iron-deficiency anemia during the first 4 to 6 months of life. Calcium and phosphorus are deposited in the soft bones to begin mineralization, which continues through early adult life. However, the infant who is delivered before term has minimal nutrient stores and higher nutrient requirements per kilogram than the full-term infant.


Infants weighing less than 1.5 kg have a body composition of approximately 85% to 95% water, 9% to 10% protein, and 0.1% to 5% fat. The fat is primarily structural with only negligible amounts of subcutaneous fat; hepatic glycogen stores are virtually nonexistent. The growth of these infants lags considerably after birth. Such infants, especially those less than 1000 g birth weight (extremely low birth weight [ELBW]), typically do not regain birth weight until 2 to 3 weeks of age. The growth of most less than 1500 g (very low-birth-weight [VLBW]) infants proceeds at a slower rate than in utero, often by a large margin. Although many of the smallest VLBW infants are also born small for gestational age (SGA), both appropriate for gestational age (AGA), VLBW, and SGA infants develop “extrauterine growth restriction” (EUGR). Figure 7-1 from the National Institute of Child Health and Human Development (NICHD) Neonatal Research Network demonstrates the differences between normal intrauterine growth and the observed rates of postnatal growth in the NICHD study. These postnatal growth curves are shifted to the right of the reference curve in each gestational age category. This “growth faltering” is common in ELBW infants.




Figure 7-1


Mean body weight versus gestational age in weeks for infants with gestational ages at birth of 24 to 29 weeks.


Nutrient intakes received by VLBW infants are much lower than what the fetus receives in utero—an intake deficit that persists throughout much of the infants’ stay in the hospital and even after discharge. Although nonnutritional factors (comorbidities) contribute to the slower growth of VLBW infants, suboptimal nutrient intakes are critical in explaining their poor growth outcomes. Considerable evidence exists that early growth deficits, which reflect inadequate nutrition, have long-lasting effects, including short stature and poor neurodevelopmental outcomes. The most convincing data concerning the neurodevelopmental consequences of inadequate early nutrition are those reported by Lucas et al. They demonstrated that premature infants fed a preterm formula containing a higher content of protein and other nutrients over the first postnatal month of life had higher neurodevelopmental indices at both 18 months and 7 to 8 years of age compared with infants fed a term formula.


Nutritional management of VLBW infants is marked by a lack of uniformity from one neonatal intensive care unit (NICU) to the next as well as within individual practices. This heterogeneity of practice persists from the first hours after birth to hospital discharge and beyond. Diversity of practice thrives where there is uncertainty. Because under-nutrition is, by definition, nonphysiologic and undesirable, any measure that diminishes it is inherently good, providing safety is not compromised. Avoiding inadequate nutrition is a priority in neonatal nutrition today.


This chapter addresses the nutrient needs of the sick and LBW infant, methods for provision of nutrients both parenterally and enterally, and methods for assessing nutritional status. Figure 7-2 provides an overview of the important aggressive nutrition strategies that will be reviewed in a timeline configuration based on a “typical” ELBW infant growth curve.




Figure 7-2


Aggressive nutrition and prevention of extrauterine growth restriction (EUGR).

AA, Amino acid; D/C, discharge; E/N, enteral nutrition; HC, head circumference; ICF, intracellular fluid; IWL, insensible water loss; MEN, minimal enteral nutrition; PTF, preterm formula; PWL, postnatal weight loss; RTBW, [return to birth weight]; TPN, total parenteral nutrition.

(Adapted from Adamkin DH: Feeding the preterm infant. In Bhatia J, editor: Perinatal nutrition: optimizing infant health and development, New York, 2005, Marcel Dekker, pp 165-190.)




Fluid


In the fetus at 24 weeks’ gestation, the total body water (TBW) represents more than 90% of the total body weight, with approximately 65% in the extracellular compartment, 25% in the intracellular compartment, and 1% in fat stores. The TBW and extracellular fluid volumes decrease as gestational age increases; by term, the infant’s TBW represents 75% of total body weight with extracellular and intracellular compartments comprising 40% and 35%, respectively.


Compared with the full-term infant, the preterm infant is in a state of relative extracellular fluid volume expansion with an excess of TBW. The dilute urine and negative sodium balance observed during the first few days after birth in the preterm infant may constitute an appropriate adaptive response to extrauterine life. Therefore, the initial diuresis should be regarded as physiologic, reflecting changes in interstitial fluid volume. This should be included in the calculation of daily fluid needs. As a result, a gradual weight loss of 10% to 15% in a VLBW infant and 5% to 10% in a larger baby during the first week of life is expected without adversely affecting urine output, urine osmolality, or clinical status. Provision of large volumes of fluid (160 to 180 mL/kg/d) to prevent this weight loss appears to increase the risk of the development of patent ductus arteriosus, cerebral intraventricular hemorrhage, bronchopulmonary dysplasia (BPD), and necrotizing enterocolitis (NEC). Therefore, a careful approach to fluid management is currently appropriate. It appears that the preterm infant can adjust water excretion within a relatively broad range of fluid intake (65-70 mL/kg/d to 140 mL/kg/d) without disturbing renal concentrating abilities or electrolyte balance.


Estimation of daily fluid requirements includes insensible water losses (IWLs) from the respiratory tract and skin, gastrointestinal losses (emesis, ostomy output, and diarrhea), urinary losses, and losses from drainage catheters (chest tubes). IWL is a passive process and is not regulated by the infant. However, the environmental conditions in which the infant is nursed should be controlled to minimize losses ( Box 7-1 ). The transepithelial losses are dependent on gestational age, the thickness of the skin and stratum corneum, and blood flow to the skin. The preterm infant has a high body surface area-to-body weight ratio with thinner, more permeable skin that is highly vascularized. These factors increase heat and fluid losses. In addition, the use of open bed platforms with radiant warmers as well as phototherapy lights may increase the IWL by more than 50%. This excessive IWL may be reduced with the use of humidified isolettes to care for the infant. The measurement of urine specific gravity is commonly used to predict urine osmolality. Although this is a reliable means of predicting hyperosmolality (urine osmolality of greater than 290 mOsm/kg water with a urine specific gravity 1.012 or greater), its reliability in predicting hypo-osmolality (urine osmolality of <270 mOsm/kg water with a urine specific gravity 1.008 or less) is variable, ranging from 71% to 95% accuracy, and in predicting iso-osmolality (urine osmolality of 270 to 290 mOsm/kg water with a urine specific gravity of 1.008 to 1.012), the accuracy is even less. In addition, glucose and protein in the urine may increase the urine specific gravity, giving a falsely high estimate of urine osmolality. Therefore, urine specific gravity should be checked only to rule out hyperosmolar urine; a test for sugars and proteins in the urine should be conducted at the same time. The maximal concentrating capabilities in the neonate are limited compared with those in adults; thus, an infant with a urine osmolality of approximately 700 mOsm/kg water (urine specific gravity of 1.019) may be dehydrated. One can estimate the urine osmolality by determining the potential renal solute load of the infant’s feeding and the fluid intake ( Box 7-2 ). Infants at risk for high urine osmolality are those who are receiving a concentrated formula and those whose fluid intake is restricted.



Box 7-1

Factors Affecting Insensible Water Loss in Preterm Neonates


Severe prematurity


Open warmer bed


Forced convection


Phototherapy


Hyperthermia


Tachypnea



Box 7-2

Renal Solute Load Calculation


Potential renal solute load (PRSL): 4 (g protein/L) + mEq sodium/L + mEq potassium/L + mEq chloride/L = PRSL (mOsm/L)


Example:


Preterm formula 24 (PT 24 ) contains:


22 g protein/L × 4 = 88


15.2 mEq sodium/L × 1 = 15.2


26.9 mEq potassium/L × 1 = 26.9


18.6 mEq chloride/L × 1 = 18.6


PRSL = 148.7 mOsm/L


Baby A is a 2-week-old former 32-week AGA infant weighing 1400 g now receiving 150 mL/kg/d of PT 24 .


Estimated fluid losses are:


Stool10 mL/kg/d


Insensible water loss70 mL/kg/d


Total water loss80 mL/kg/d


150 mL/kg/d intake – 80 mL/kg/d output = 70 mL/kg/d available for urine output


The PRSL of PT 24 is 148.7 mOsm/L:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='148.7mOsm1000mL×XmOsm150mL’>148.7mOsm1000mL×XmOsm150mL148.7mOsm1000mL×XmOsm150mL
148.7 mOsm 1000 mL × X mOsm 150 mL


22.3 mOsm = X


This infant has 70 mL/kg/d to excrete 22.3 mOsm of potential renal solute.


<SPAN role=presentation tabIndex=0 id=MathJax-Element-2-Frame class=MathJax style="POSITION: relative" data-mathml='22.3mOsm70mL×1000=XmOsm/L’>22.3mOsm70mL×1000=XmOsm/L22.3mOsm70mL×1000=XmOsm/L
22.3 mOsm 70 mL × 1000 = X mOsm / L


318.6 mOsm = X


Therefore, the estimated osmolality of the urine is 319 mOsm/L.


AGA, Appropriate for gestational age .



Water balance may be maintained with careful attention to input and output. Infants should be weighed nude and at approximately the same time of day. During the first week of life, VLBW infants should be weighed daily; ELBW infants should be weighed twice daily. Meticulous records of fluid intake (with the use of accurate infusion pumps and careful measurement of enteral feedings) and output (by weighing diapers and collecting urine, ostomy output, and drainage from any indwelling catheters) are necessary to compute fluid requirements. Serum glucose, electrolytes, blood urea nitrogen (BUN), and creatinine may be monitored two to three times per day during the first 2 days in critically ill ELBW infants and then daily or as needed thereafter. Urine glucose is routinely tested and urine specific gravity is measured as necessary.


Pauls et al. published data on 136 medically stable ELBW infants receiving early and aggressive parenteral and enteral nutrition. From their data, they developed a series of weight-stratified growth curves of this population over the first months of life. The fluid and nutrient administration was uniform in these patients and included (1) initiation of fluid intake at 60 to 70 mL/kg/day on day 1 with 15 mL/kg daily increases up to a maximum of 160 to 180 mL/kg/day; (2) targeted postnatal weight loss of 10% below birth weight; (3) 1 g/kg/day intravenous (IV) amino acid intake started on day 1 and increased by 0.5 g/kg/day up to 3 g/kg/day; (4) IV lipid started 1 g/kg/day at day 2 and increased 0.5 g/kg/day up to 3 g/kg/day as long as triglyceride concentrations remained normal; and (5) initial total energy intakes of 27 kcal/kg/day, increasing by 10 kcal/kg/day to 100 kcal/kg/day. In addition, minimal enteral feedings were initiated on day 1 in the form of 24 calorie per ounce fortified human milk or preterm formula and were advanced as tolerated. In all groups, maximal weight loss averaged 10.1% ± 4.6% (SD), and occurred on day of life 5.4 ± 1.7. The age at which birth weight was regained was 11 ± 3.7 days. Small-for-gestational age infants had lower maximal weight loss and regained birth weight at a significantly earlier age. Mean weight gain after day 10 was 15.7 ± 7.2 g/kg/day, which is within the recommended in utero growth rates of 14 to 20 g/kg/day. Although this was a small study, it shows that aggressive nutritional strategies with higher earlier amino acid intakes are affecting the growth curves of these ELBW infants. However , the maximal fluid volumes may be excessive in this population. If possible, the maximal fluid volume should be limited to 140 mL/kg/day.




Electrolytes


Often the electrolyte management of the infant is difficult due to the various sources of electrolyte input. For example, in a 600-g infant, the isotonic saline solution infused to maintain the patency of the umbilical arterial catheter may result in administration of sodium and chloride in excess of estimated daily requirements. Although VLBW infants are capable of regulating sodium balance by altering renal sodium excretion, this may not be sufficient to prevent changes in serum sodium and serum chloride concentrations. Because administration of high amounts of sodium may increase the risk of hypernatremia in the VLBW infant, careful calculation of total intake of sodium, potassium, chloride, glucose, and water from all sources (i.e., maintenance IV fluids, flushes, medications, and bolus injections) is necessary. As fluid requirements are adjusted, recalculation should be done frequently to ensure that appropriate quantities of nutrients are given ( Table 7-1 ).



Table 7-1

Characteristics of Intravenous Fluids

Adapted from Wolf BM, Yamahata WI: In Zeman FJ, editor: Clinical nutrition and dietetics, Lexington, Mass, 1983, DC Heath.



















































































































































Cations Anions
Type of Fluid Na (mEq/L) K (mEq/L) Ca (mEq/L) Cl (mEq/L) HCO 3 (mEq/L) Osmolarity (mOsm/L)
DEXTROSE IN WATER SOLUTIONS
D 5 W 252
D 10 W 505
D 20 W 1010
D 50 W 2525
DEXTROSE IN SALINE SOLUTIONS
D 5 W and 0.2% NaCl 34 34 320
D 5 W and 0.45% NaCl 77 77 406
D 5 W and 0.9% NaCl 154 154 559
D 10 W and 0.9% NaCl 154 154 812
SALINE SOLUTIONS
½ NS (0.45% NaCl) 77 77 154
NS (0.9% NaCl) 154 154 308
NS (3% NaCl) 513 513 1026
MULTIPLE ELECTROLYTE SOLUTIONS
Ringer’s solution 147 4 5 155 309
Lactated Ringer’s 130 4 3 109 28 273
D 5 W in Lactated Ringer’s 130 4 3 109 28 524
LIPID EMULSIONS
Lipid emulsions (20%) 258-315
























An easy way to approximate the osmolarity of an IV fluid is to consider that for each 1% dextrose, there are 55 mOsm/L; for each 1% amino acids there are 100 mOsm/L; and for each 1% NaCl there are 340 mOsm/L. Therefore:
D 10 W and 0.45% NaCl (½ NS)
D 10 W = (10 × 55) =
550 mOsm/L
0.45% NaCl = (0.45 × 340) = 153 mOsm/L
Total 703 mOsm/L
12.5% dextrose and 17 g amino acids/L (or 1.7% amino acids)
D 12.5 W = 12.5 × 55 =
687 mOsm/L
1.7% AA = 1.7 ×100 = 170 mOsm/L
Total
Parenteral nutrition solutions with an osmolarity >900 mOsm/L should be infused through a central line.
857 mOsm/L

Or its equivalent in lactate, acetate, or citrate.


Osmolarity of the blood is 285-295 mOsm/L.



Sodium is required in quantities sufficient to maintain normal extracellular fluid volume expansion, which accompanies tissue growth. In animal studies, if insufficient amounts are provided, the extracellular fluid volume expansion is suppressed and there are subsequent alterations in quantitative and qualitative somatic growth.


Catheter flushes (using isotonic saline solution) may contribute significant quantities of electrolytes, including chloride, to the infant’s total intake. Hyperchloremic metabolic acidosis in LBW infants has been associated with chloride loads greater than 6 mEq/kg/day. The intake can easily be decreased by substituting acetate or phosphate for chloride in the IV solution.


Hypochloremia has also been associated with poor growth. Supplementation with chloride to normalize serum chloride concentrations in infants with BPD resulted in improved growth. Hypochloremia has been noted in infants with BPD who did not survive; however, whether this is a predictor of poor outcome or a symptom of severe illness remains to be resolved.


Potassium chloride (2 mEq/kg/day) is added to the IV fluid within the first days of life as soon as urinary output is established and hyperkalemia is not present. The potassium dose may be adjusted dependent on urine output and use of diuretics. However, it is often difficult to obtain accurate determinations of serum potassium, especially when the blood samples are from heel-sticks, which may lead to excessive red blood cell hemolysis and spuriously high serum potassium levels. If an elevated potassium concentration is obtained, a second blood sample from venipuncture should be obtained for confirmation of the level. If infused via a peripheral vein, concentrations of potassium chloride up to 40 mEq/L are usually tolerated and do not cause localized pain. However, if higher concentrations are needed because of fluid restriction, a central vein should be used.




Total Parenteral Nutrition


Immaturity of the gastrointestinal tract in VLBW infants precludes substantive enteral nutritional support. Thus, nearly all of these infants are supported with total parenteral nutrition (TPN), which has been a huge success , particularly in the management of the ELBW infant.


Historically, the initiation of TPN has been delayed during the first week of life. Reasons for this delay have not been clear but probably have been related to metabolic derangements seen when solutions designed for adults were infused in the neonatal population. There were also concerns about VLBW infants’ ability to catabolize amino acids. Data and clinical experience have defined the requirements for parenteral nutrients and led to the development of new products and new methods of delivery designed specifically for use in the neonate. Guidelines for certain minerals and vitamins were published in 1988 and then updated ( Table 7-2 ). Tables 7-3 and 7-4 contain recommended vitamin and mineral intakes for parenteral and enteral nutritional support.



Table 7-2

Parenteral Multivitamin Dosing Guidelines

From Groh-Wargo S, Thompson M, Cox JH, editors: Nutritional care for high-risk newborns, rev ed 3, Chicago, 2000, Precept Press, p 15.















































































































































ASCN Recommended Dose Product Guidelines
30% Dose for Infants <1 kg 65% Dose for Infants 1-3 kg
Weight ≤2500 g 500 g 950 g 1000 g 2000 g 3000 g
Lipid-Soluble
A (µg) 280 420 221 455 228 152
A (IU) 933 1380 726 1495 748 498
E (mg) 2.8 4.2 2.2 4.5 2.2 1.5
K (µg) 80 120 63 130 65 43
D (µg) 4 6 3.2 6.5 3.2 2.2
D (IU) 160 240 126 260 130 87
Water-Soluble
Ascorbic acid (mg) 32 48 25 52 26 17
Thiamin (mg) 0.48 0.72 0.34 0.78 0.39 0.26
Riboflavin (mg) 0.56 0.84 0.44 0.91 0.46 0.30
Pyridoxine (mg) 0.4 0.6 0.32 0.65 0.33 0.22
Niacin (mg) 6.8 10.2 5.4 11.1 5.6 3.7
Pantothenate (mg) 2.0 3.0 1.4 3.3 1.6 1.1
Biotin (µg) 8.0 12.0 6.3 13.0 6.5 4.3
Folate (µg) 56 84 44 91 46 30
Vitamin B 12 (µg) 0.4 0.6 0.32 0.65 0.33 0.22

40% dose/kg body weight, maximum not to exceed term infant dose. The 1988 ASCN Subcommittee report suggested that until a preterm parenteral multivitamin is available, pediatric formulations meeting the 1975 AMA-NAG pediatric guidelines should be used at 40% of the standard dose per kg. The maximum dose should not exceed 100% of the term infant dose. Infants weighing >2500 g receive 100% of the standard dose.



Table 7-3

Recommended Intakes of Parenteral and Enteral Vitamins

Adapted from Tsang RC, Uauy R, Koletzko B, et al, editors: Nutrition of the preterm infant, ed 2, Cincinnati, 2005, Digital Educational Publishing, pp 415-416.


































































































































































































ELBW and VLBW
Day 0per kg/day Transitionper kg/day Growingper kg/day
Vitamin A (IU) Parenteral 700-1500 700-1500 700-1500
Enteral 700-1500 700-1500 700-1500
Vitamin D (IU) Parenteral 40-160 40-160 40-160
Enteral 150-400 150-400 150-400
Vitamin E (IU) Parenteral 2.8-3.5 2.8-3.5 2.8-3.5
Enteral 6-12 6-12 6-12
Vitamin K (µg) Parenteral 500 IM per child 10 10
Enteral 500 IM per child 8-10 8-10
Thiamin (µg) Parenteral 200-350 200-350 200-350
Enteral 180-240 180-240 180-240
Riboflavin (µg) Parenteral 150-200 150-200 150-200
Enteral 250-360 250-360 250-360
Niacin (mg) Parenteral 4-6.8 4-6.8 4-6.8
Enteral 3.6-4.8 3.6-4.8 3.6-4.8
Vitamin B 6 (µg) Parenteral 150-200 150-200 150-200
Enteral 150-210 150-210 150-210
Folate (µg) Parenteral 56 56 56
Enteral 25-50 25-50 25-50
Vitamin B 12 (µg) Parenteral 0.3 0.3 0.3
Enteral 0.3 0.3 0.3
Pantothenic acid (mg) Parenteral 1-2 1-2 1-2
Enteral 1.2-1.7 1.2-1.7 1.2-1.7
Biotin (µg) Parenteral 5-8 5-8 5-8
Enteral 3.6-6 3.6-6 3.6-6
Vitamin C (mg) Parenteral 15-25 15-25 15-25
Enteral 18-24 18-24 18-24
Taurine (mg) Parenteral 0-3.75 1.88-3.75 1.88-3.75
Enteral 0-9 4.5-9 4.5-9
Carnitine (mg) Parenteral 0-2.9 0-2.9 0-2.9
Enteral 0-2.9 0-2.9 0-2.9

Day 0 = Day of birth.

Transition: The period of physiologic and metabolic instability following birth, which may last as long as 7 days.


Table 7-4

Recommended Mineral Intakes for Very Low Birth Weight Infants

Adapted from Tsang RC, Uauy R, Koletzko B, et al, editors: Nutrition of the preterm infant, ed 2, Cincinnati, 2005, Digital Educational Publishing, pp 415-416.






































































































































ELBW and VLBW
Day 0per kg/day Transitionper kg/day Growingper kg/day
Sodium (mg) Parenteral 0-23 46-115 69-115 (161 )
Enteral 0-23 46-115 69-115 (161 )
Potassium (mg) Parenteral 0 0-78 78-117
Enteral 0 0-78 78-117
Chloride (mg) Parenteral 0-35.5 71-178 107-249
Enteral 0-35.5 71-178 107-249
Calcium (mg) Parenteral 20-60 60 60-80
Enteral 33-100 100 100-220
Phosphorus (mg) Parenteral 0 45-60 45-60
Enteral 20-60 60-140 60-140
Magnesium (mg) Parenteral 0 4.3-7.2 4.3-7.2
Enteral 2.5-8 7.9-15 7.9-15
Iron (mg) Parenteral 0 0 0.1-0.2
Enteral 0 0 2-4
Zinc (µg) Parenteral 0-150 150 400
Enteral 0-1000 400-1200 1000-3000
Copper (µg) Parenteral 0 ≤20 20
Enteral 0 ≤150 120-150
Selenium (µg) Parenteral 0 ≤1.3 1.5-4.5
Enteral 0 ≤1.3 1.3-4.5

Day 0 = day of birth.

Transition: The period of physiologic and metabolic instability following birth, which may last as long as 7 days.

May need up to 160 mg/kg/day for late hyponatremia.



Supporting an infant on TPN is not without risk. This method of nutrient delivery should not be undertaken without knowledge of the potential metabolic and mechanical (or catheter-related) complications. Most complications can be avoided with careful monitoring and prompt intervention. Complication rates are minimized when parenteral nutrition is administered with strict adherence to established protocols.


Energy


Energy needs are dependent on age, weight, rate of growth, thermal environment, activity, hormonal activity, nature of feedings, and organ size and maturation ( Table 7-5 ). Measurement of a true basal metabolic rate requires a prolonged fast and cannot ethically be determined in VLBW infants; therefore, resting metabolic rate (RMR) is used to estimate energy needs, dietary-induced thermogenesis, minimum energy expended in activity, and the metabolic cost of growth. The metabolic rate increases during the first weeks of life from an RMR of 40 to 41 kcal/kg/day during the first week to 62 to 64 kcal/kg/day by the third week of life. The extra energy expenditure is primarily due to the energy cost of growth related to various synthetic processes. The metabolic rate of the nongrowing infant is approximately 51 kcal/kg/day, which includes 47 kcal/kg/day for basal metabolism and 4 kcal/kg/day for activity.



Table 7-5

Estimation of the Energy Requirement of the Infant with Low Birth Weight.

Adapted from the Committee on Nutrition of the Preterm Infant, European Society of Paediatric Gastroenterology and Nutrition, Bremer HJ, Wharton BA: Nutrition and feeding of preterm infants , Oxford, 1987, Blackwell Scientific and American Academy of Pediatrics: Pediatric nutrition handbook , ed 6, Elk Grove Village, Ill, 2009, p 83.































Average Estimation, kcal/kg/day
Energy expended 40-60
Resting metabolic rate 40-50
Activity 0-5
Thermoregulation 0-5
Synthesis 15
Energy stored 20-30
Energy excreted 15
Energy intake 90-120

Energy for maintenance.


Energy cost of growth.



The contribution of activity to overall energy expenditure is speculative but seems to be small, between 3 and 5 kcal/kg/day to the total energy expenditure. Because of the large amount of time spent in the sleep state, energy expenditure in muscular activity in immature infants is relatively small in comparison to their resting metabolism. As infants mature, they become more active; therefore, energy expenditure from activity increases.


The exposure of infants to a cold environment affects energy expenditure with small alterations in the thermal environment making a significant contribution to energy expenditure. Infants nursed in an environment just below thermal neutrality increase energy expenditure by 7 to 8 kcal/kg/day; any handling adds to this energy loss. A daily increase of 10 kcal/kg/day should be allowed to cover incidental cold stress in the preterm infant. Infants who are intrauterine growth restricted, particularly the asymmetrical type, have a higher RMR on a per kilogram body weight basis because of their relatively high proportion of metabolically active mass. Other factors that may increase metabolic rate are speculative; the effects of fever, sepsis, and surgery on the infant’s energy requirements are uncertain.


Caloric intake above maintenance is used for growth. On average, for each 1-g increment in weight, approximately 4.5 kcal above maintenance energy need are required. Therefore, to attain the equivalent of the third trimester intrauterine weight gain (10 to 15 g/kg/day), a metabolizable energy intake of approximately 45 to 70 kcal/kg/day above the 51 kcal/kg/day required for maintenance must be provided, or approximately 100 to 120 kcal/kg/day. Increasing metabolizable energy intakes beyond 120 kcal/kg/day with energy supplementation alone does not result in proportionate increases in weight gain. However, when energy, protein, vitamins, and minerals are all increased, weight gain with increases in rates of protein and fat accretion can be realized. The higher the caloric intake, the more energy that is expended through excretion, dietary-induced thermogenesis, and tissue synthesis. The energy cost of weight gain at 130 kcal/kg/day was reported to be 3.0 kcal/g of weight gain. However, at an intake of 149 kcal/kg/day and 181 kcal/kg/day, the energy cost of weight gain has been estimated to be 4.9 and 5.7 kcal/g of weight gain, respectively. In summary, to increase lean body mass accretion and limit fat mass deposition, an increase in protein-to-energy ratio in enteral diets is necessary.


The energy needs of the parenterally nourished infant differ from the enterally fed infant in that there is no fecal loss of nutrients. Preterm infants who are appropriately grown for gestational age are able to maintain positive nitrogen balance when receiving 50 nonprotein calories (NPCs)/kg/day and 2.5 g protein/kg/day. At an NPC intake of greater than 70 NPC/kg/day and a protein intake of 2.7 to 3.5 g/kg/day, preterm infants exhibit nitrogen accretion and growth rates similar to in utero levels.


The sources of energy for parenteral nutrition in infants are either as glucose or lipid, or a combination of the two. Although both glucose and fat provide equivalent nitrogen-sparing effects in the neonate, studies have demonstrated that a nutrient mixture using IV glucose and lipid as the nonprotein energy source is more physiologic than supplying glucose as the only nonprotein energy source. The amount of glucose required to meet the total energy needs approximates 7 mg/kg/min (10 g/kg/day). The excess glucose administered is converted to fat or triglycerides. A nutrient mixture with glucose and lipids providing NPCs as well as essential fatty acids is suggested.


When 60% to 63% of the NPCs given to LBW infants are derived from lipids, nitrogen retention is decreased and temperature control is adversely effected. A moderate IV fat intake comprising approximately 35% of the NPCs is preferred.


There is a paucity of studies available to examine energy expenditure in VLBW infants on assisted ventilation. Technical difficulties and methodologic limitations affect interpretation of data. Leitch and Denne reviewed 12 studies, with 29 of 75 patients studied in the first 2 to 3 days of life. Early studies suggest a mean energy expenditure of approximately 54 kcal/kg/day.


Carbohydrates


Carbohydrates are the main energy substrate for the preterm infant receiving parenteral nutrition. At least at the outset, lipids play a minor role in supplying energy, although they play an important role at all times in providing essential fatty acids. Clearly, the infant must eventually transition to enteral feedings, which provide about half the energy from fat. However, while receiving TPN, carbohydrate remains the dominant energy substrate.


Glucose intolerance, defined as inability to maintain euglycemia at glucose administration rates of less than 6 mg/kg/min, is a frequent problem in VLBW infants, especially those weighing less than 1000 g. Hyperglycemia in VLBW infants may also occur with nonoliguric hyperkalemia. These two comorbid conditions were frequently observed in ELBW infants before the practice of early initiation of amino acids. Endogenous glucose production is elevated in VLBW infants compared with term infants and adults. Also, high glucose production rates are found in VLBW infants who received only glucose compared to those receiving glucose plus amino acids and/or lipids. Clinical experience with glucose intolerance suggests that glucose alone does not always suppress glucose production in VLBW infants. It is not clear what circumstances or metabolic conditions lead to glucose intolerance. It appears likely, however, that persistent glucose production is the main cause, fueled by ongoing proteolysis that is not suppressed by physiologic concentrations of insulin. There is uncertainty whether abnormally low peripheral glucose utilization is also involved.


The glucose infusion rate should maintain euglycemia. Depending on the degree of immaturity (<26 weeks), 5% glucose or 10% glucose may be used. Another objective becomes the achievement of higher energy intakes. Glucose intolerance can limit delivery of energy to the infant to a fraction of the resting energy expenditure, leaving the infant in negative energy balance. Several strategies are used to manage this early hyperglycemia in ELBW infants: (1) decreasing glucose administration until hyperglycemia resolves (unless the hyperglycemia is so severe that this strategy would require infusion of a hypotonic solution); (2) administering IV amino acids, which decrease glucose concentrations in ELBW infants, presumably by enhancing endogenous insulin secretion; (3) initiation of exogenous insulin therapy at rates to control hyperglycemia ; and (4) using insulin to control hyperglycemia and to increase nutrient uptake. The first and third strategies prevent adequate early nutrition and the safety of the last has been questioned in this population because of the possible development of lactic acidemia. Several studies have shown that insulin, used as a nutritional adjuvant, successfully lowers glucose concentrations and increases weight gain in preterm infants without significant risk of hypoglycemia. However, excessive energy is associated with increased fat accretion, not accompanied by lean mass or increase in head circumference, and little is known about its effects on counterregulatory hormone concentrations. A study examined the effect of insulin using a hyperinsulinemic-euglycemic clamp in ELBW infants receiving only glucose. These infants were normoglycemic before the initiation of insulin. They demonstrated a significant elevation in plasma lactate concentrations and the development of significant metabolic acidosis.


The administration of amino acids early after birth appears to prevent the need for IV insulin, perhaps through stimulation of insulin by amino acids (e.g., arginine and leucine). Improved glucose tolerance enables appropriate energy intake for growth. Therefore, amino acids are administered aggressively from the first hours of life to avoid the period of early neonatal malnutrition.


The human placenta actively transports amino acids to the fetus, and animal studies indicate that fetal amino acid uptake greatly exceeds protein accretion requirements. Approximately 50% of the amino acids taken up by the fetus are oxidized and serve as a significant energy source. Urea production is a by-product of amino acid oxidation. Relatively high rates of fetal urea production are seen in human and animal fetuses compared with the term neonate and adult, suggesting high protein turnover and oxidation rates in the fetus. Therefore, a rise in blood urea nitrogen, which is often observed after the start of TPN, is not an adverse effect or sign of toxicity in the absence of other signs of renal compromise or severe dehydration. Several controlled studies have demonstrated the efficacy and safety of amino acids initiated within the first 24 hours of life. There were no recognizable metabolic derangements, including hyperammonemia, metabolic acidosis, or abnormal aminograms.


A strong argument for the early aggressive use of amino acids is the prevention of “metabolic shock.” Concentrations of some key amino acids begin to decline in the VLBW infant from the time the cord is cut. This metabolic shock may trigger the starvation response, of which endogenous glucose production is a prominent feature. Irrepressible glucose production may be the cause of the so-called “glucose intolerance” that often limits the amount of energy that can be administered to the VLBW infant. It makes sense to smooth the metabolic transition from fetal to extrauterine life. Withholding TPN for days or even hours means unnecessarily sending the infant into a metabolic emergency. Thus, the need for parenteral nutrition may never be more acute than right after birth. It is noteworthy that Rivera et al. made the unexpected observation that glucose tolerance was substantially improved in the group receiving early amino acids. Early amino acids may stimulate insulin secretion, consistent with the notion that forestalling the starvation response improves glucose tolerance. Recent data show that ELBW infants receiving earlier and higher dosages of amino acids (3 g/kg/day) had lower glucose levels than those receiving early amino acids but at lower dosages the first 5 days of life.


Dose of Amino Acids


Figure 7-3 shows protein loss that occurs in mechanically ventilated, 26-week gestation 900-g–birth weight infants at 2 days of age who were receiving glucose alone. Clinically stable 32-week gestation premature infants and normal term infants are also shown for comparison. It is clear that there is a significant effect of gestation on protein metabolism because the rate of protein loss in ELBW infants is twofold higher than in normal term infants.




Figure 7-3


Protein losses measured in three groups of infants receiving glucose alone at 2 to 3 days of age. Protein losses are calculated from measured rates of phenylalanine catabolism.

(Adapted from Denne SC: Protein and energy requirements in preterm infants, Semin Neonatal 6:377, 2001.)


The impact of this rate of protein loss is shown in Figure 7-4 . At 26 weeks’ gestation, a 1000-g–birth weight infant begins with body protein stores of ~88 g. Without any protein intake, the infant loses more than 1.5% of body protein per day. Compare this with the normal fetus who would accumulate body protein in excess of 2% per day. It is obvious that significant body protein deficits can accumulate rapidly in ELBW infants if early aggressive amino acid administration is not offered.




Figure 7-4


Change in body protein stores in a theoretical 26-week gestation, 1000-g premature infant receiving glucose alone with a fetus in utero.

(Adapted from Denne SC: Protein and energy requirements in preterm infants, Semin Neonatal 6:377, 2001.)


The first studies of early TPN used doses between 1 and 1.5 g/kg/day, an amount that will replace ongoing losses. Dosages have recently been increased toward 3 g/kg/day with initiation within hours of birth. Ultimate amino acid intake should be 3 g/kg/day; however, one can consider intakes of 3.5 to 4 g/kg/day for infants weighing less than 1200 g in situations where enteral feeds are extremely delayed or withheld for prolonged periods. A desirable protein to energy ratio is 25 kcal/kg for every gram of protein/kg or 2 to 3 mg/kg/min of glucose per gram of protein intake.


Protein quality, or amino acid composition, in parenteral nutrition can influence nitrogen utilization as well as the metabolic responses. Histidine is known to be necessary for protein synthesis and growth in the neonate but exact requirements are not known. Certain other amino acids are considered semi-essential or conditionally essential in that the capacity to synthesize them is limited in the preterm infant. Therefore, if these conditionally essential amino acids are not exogenously available or available only in limited amounts, the infant’s requirements may not be met. Three of these semi-essential amino acids are cysteine, tyrosine, and taurine.


Cysteine is synthesized in vivo from methionine by the enzyme cystathionase. Because the hepatic activity of cystathionase has been found to be low or absent during fetal development and in the preterm and term neonate, it has been considered an essential amino acid for the infant. Zlotkin and Anderson observed reduced hepatic cystathionase activity in preterm infants compared with full-term infants at the time of birth with the activity increasing in the preterm infant over the first month of life ; however, mature levels were not attained until approximately 8 months. When total cystathionase activity was estimated, which included the enzyme activity in the liver, kidneys, pancreas, and adrenal glands, they concluded that even the preterm infant has the capacity to endogenously produce adequate cysteine if adequate methionine is provided. In fact, increased parenteral methionine has been shown to increase urinary cysteine excretion. Supplementation of parenteral amino acid solutions with cysteine hydrochloride has not been shown to affect either nitrogen balance or growth in LBW infants. However, the two pediatric amino acid solutions, Trophamine (McGaw, Inc., Irvine, Calif) and Aminosyn-PF (Abbott Laboratories, Abbott Park, Ill), are low in methionine content, 81 and 45 mg/2.5 g of amino acids, respectively, and do not contain cysteine. Therefore, supplementation with cysteine hydrochloride is recommended.


Tyrosine, which is endogenously synthesized from phenylalanine through the activity of phenylalanine hydroxylase, has also been considered an essential amino acid; however, the enzyme activity is not low during development. The low plasma tyrosine concentrations seen in infants on tyrosine-free parenteral nutrition infusates appear to be independent of the plasma phenylalanine levels and not all infants on tyrosine-free parenteral nutrition solutions have low plasma tyrosine levels. In addition, extremely preterm infants have been shown to convert substantial quantities of phenylalanine to tyrosine. Therefore, the requirement for an exogenous source of this amino acid remains uncertain.


Taurine, which is synthesized endogenously from cysteine, is a sulfur amino acid, which is not part of structural proteins but is present in most tissues of the body; it is particularly high in the retina, brain, heart, and muscle. The biological function of taurine in mammals includes neuromodulation, cell membrane stabilization, antioxidation, detoxification, osmoregulation, and bile acid conjugation; however, its conjugation with bile acids is the only adequately documented metabolic reaction in humans. Depletion of taurine during long-term parenteral nutrition has resulted in abnormal electroretinograms in children and auditory brainstem-evoked responses in preterm infants. Taurine supplementation of preterm infant formula has been shown to improve fat absorption, especially saturated fats, in LBW infants. Human milk is rich in taurine; infants fed human milk have higher plasma and urine concentrations of taurine than infants fed unsupplemented infant formula. Infant formulas and pediatric parenteral amino acid solutions are supplemented with taurine.


Currently, there are two kinds of crystalline amino acid solutions available for use in the neonate. The standard solutions originally designed for adults are often used for infants but are not ideal. The adult products contain little or no tyrosine, cysteine, or taurine, and contain relatively high concentrations of glycine, methionine, and phenylalanine. Because the plasma amino acid patterns reflect the amino acid composition of the amino acid solution infused, the resulting abnormal plasma amino acid levels could be potentially harmful. Hyperglycinemia, for example, may have adverse effects on the central nervous system because glycine is a potent neurotransmitter inhibitor. The pediatric amino acid solutions have a greater distribution of nonessential amino acids (particularly less glycine), greater amounts of branched-chain amino acids, less methionine and phenylalanine, and more tyrosine, cysteine, and taurine.


Studies of these products have demonstrated improved nitrogen retention and plasma aminograms resembling those of full-term breast-fed infants at 30 days of life. However, studies of protein turnover and urea production (protein oxidation) have not shown any difference between Trophamine and other amino acid mixtures. Because of the lower pH of the pediatric crystalline amino acid solutions, greater concentrations of calcium and phosphorous may be added without precipitation, which is an advantage particularly for the preterm neonate because the requirements for both minerals are quite high.


Lipids


There are two roles for lipids as part of a TPN regimen. The first function is to serve as a source of linoleic acid. When used in small amounts, it can prevent or treat essential fatty acid deficiency. The second function is its use as an energy source. Larger quantities serve as a partial replacement for glucose as a major source of calories ( Table 7-6 ).



Table 7-6

Composition of Intravenous Lipid Emulsions

Other sources: Drug facts and comparisons , St. Louis, 1990, JB Lippincott.







































Product Oil Base Linoleic Acid (%) Linolenic Acid (%) Glycerin (%) Osmolarity (mOsm/L)
Intralipid 100% Soybean 44-62 4-11 2.25 260
Nutrilipid 100% Soybean 49–60 6-9 2.21 315
Soyacal 100% Soybean 49-60 6-9 2.21 315
Liposyn III § 100% Soybean 54.5 8.3 2.5 284

KabiVitrum, Alameda, Calif. Data from product insert.


McGaw, Inc., Irvine, Calif.


Alpha Therapeutic, Los Angeles, Calif.


§ Abbott Laboratories, Abbott Park, Ill. Data from product insert.



The preterm neonate is especially susceptible to the development of essential fatty acid deficiency because tissue stores of linoleic acid are small and requirements for essential fatty acids are large because of rapid growth. The human fetus depends entirely on placental transfer of essential fatty acids. A VLBW infant with limited nonprotein calorie reserve must mobilize fatty acids for energy when receiving IV nutrition devoid of lipid. Studies in these infants confirm other studies that show essential fatty acid deficiency can develop in the VLBW infant during the first week of life on lipid-free regimens.


The importance of long-chain polyunsaturated fatty acids (LC-PUFAs) for the development of the brain and the retina has been recognized. Infants are not capable of forming sufficient quantities of LC-PUFAs from the respective precursor fatty acids (linoleic and α-linolenic acids), and thus depend on an exogenous source of LC-PUFAs. Intravenous lipid emulsions contain small amounts of these fatty acids as part of the egg phospholipid used as a stabilizer.


The “routine” use of IV lipid emulsions has not been universally accepted in critically ill, ventilated VLBW infants because of potential complications. Hazards most pertinent to the ventilated VLBW infant include adverse effect s on gas exchange and displacement of bilirubin from albumin. Both Brans and Adamkin found no difference in oxygenation between infants randomly assigned to various lipid doses (including controls without lipids) when using lower rates and longer infusion times of IV lipids. The displacement of bilirubin from binding sites on serum albumin may occur even with adequate metabolism of infused lipid. In vitro, displacement of albumin-bound bilirubin by free fatty acids (FFAs) depends on the relative concentrations of all three compounds. An in vivo study has shown no free bilirubin generated if the molar FFA to albumin ratio is less than 6. Data with lipid initiation at 0.5 g/kg/day of lipids in VLBW infants on assisted ventilation with respiratory distress syndrome showed a mean FFA to albumin ratio of less than 1. No individual patient value exceeded a ratio of 3 when daily doses were increased to 2.5 g/kg/day (in increments of 0.5 g/kg/day) over an 18-hour infusion time. Other investigators found no adverse effect on bilirubin binding when lipid emulsion was infused at a dose of 2 g/kg/day over either 15 or 24 hours. Proper use includes slow infusion rates (≤0.15 g/kg/hr), slow increases in dosage, and avoidance of unduly high doses (e.g., >3 g/kg/day).


Concerns have been raised regarding the possible adverse effects of IV lipids on pulmonary function, but these have generally proved to be unfounded. For the late preterm infant with increased pulmonary vascular resistance (PVR) and respiratory disease, however, it appears that a more prudent approach with IV lipids should be taken. Significant concerns have been raised because of the high polyunsaturated fatty acid (PUFA) content of lipid emulsions as excessive omega 6 (linoleic acid, 18:2ω6) acids are required substrates for arachidonic acid pathways which lead to synthesizing prostaglandins and leukotrienes ( Fig. 7-5 ). It is speculated the IV lipid infusion may enhance thromboxane synthesis activity, which increases thromboxane production. The prostaglandins may cause changes in vasomotor tone with resultant hypoxemia. In addition, the production of hydroperoxides in the lipid emulsion also might contribute to untoward effects by increasing prostaglandin levels.




Figure 7-5


Metabolic derivatives of linoleic acid and ARA, PPHN , Persistant palmonary hypertension.

(Adapted from Adamkin DH: Nutrition in very very low birth weight infants, Clin Perinatol 13[2]:419, 1986.)


Although there is no firm evidence of the effects of lipid emulsions in infants with severe acute respiratory failure with or without pulmonary hypertension, it appears prudent to avoid high dosages in these patients. For those with respiratory diseases without increased pulmonary vascular resistance, provide IV lipids at a dosage to prevent essential fatty acid deficiency. For those with elements of persistent pulmonary hypertension (PPHN), avoidance of lipids during the greatest labile and critical stages of their illness should be considered. When the infant is more stable, IV lipids at a modest dosage can be initiated.


Common practice is to begin IV lipids on the second day of life following initiation of amino acids shortly after delivery. Starting dose is 0.5 g/kg/day or 1.0 g/kg/day. Plasma triglycerides are monitored after each increase in dose and levels are maintained less than 200 mg/dL. A 20% lipid emulsion is used exclusively with an infusion rate less than or equal to 0.15 g/kg/hr. Therefore, a dose of 3 g/kg/day would be infused over 24 hours.


Lipid emulsions are supplied as either 10% or 20% solutions, providing 10 or 20 g of triglyceride/dL, respectively. Both contain the same amount of egg yolk phospholipid emulsifier (approximately 1.2 g/dL) and glycerol (approximately 2.25 g/dL). However, each contains more phospholipid than is required to emulsify the triglyceride. The excess is formed into triglyceride-poor particles with phospholipid bilayers called liposomes. For any given dose of triglyceride, twice the volume of 10% emulsion must be infused compared with the 20% emulsion. Therefore, for a fixed amount of triglyceride, the 10% emulsion provides at least twice and perhaps up to four times the amount of liposomes as the 20% emulsion. The 10% emulsion has been shown to be associated with higher plasma triglyceride concentrations and an accumulation of cholesterol and phospholipid in the blood of the preterm infant, probably because of the higher phospholipid content. LBW infants infused with lipids at 2 g/kg/day of 10% emulsion had significantly higher plasma triglycerides, cholesterol, and phospholipids than infants infused with 4 g lipid/kg/day as 20% emulsion. It is speculated that the excessive phospholipid liposomes in the 10% emulsion compete with the triglyceride-rich particles for binding to lipase sites, resulting in slow triglyceride hydrolysis. It is, therefore, recommended that 20% lipid emulsions be used for the LBW and VLBW infants.


Adverse side effects of IV lipid emulsions have been reported, including displacement of indirect bilirubin from albumin-binding sites, increasing the risk of kernicterus, suppression of the immune system, coagulase-negative staphylococcal and fungal infection, thrombocytopenia, and accumulation of lipids in the alveolar macrophages and capillaries, subsequently altering pulmonary gas exchange. As noted earlier, because FFAs compete with bilirubin for binding to albumin, the use of IV lipid emulsions in jaundiced newborns has been questioned. However, it is more a theoretical concern, in that FFA concentrations do not reach high enough levels to cause displacement of bilirubin and increase free bilirubin to a very high range. Careful monitoring of plasma triglycerides has been suggested when lipids are administered to babies with hyperbilirubinemia .


There may be a beneficial effect of infusing lipids. Infusion of lipid emulsion exerts a beneficial effect on the vascular endothelium of peripheral veins leading to longer venous patency time. Malhotra et al. noted that hyperbilirubinemic infants given a lipid infusion of 1 to 2 g/kg/day had a significant increase in lumirubin, a water-soluble structural isomer of bilirubin that can be excreted in the bile without hepatic conjugation. Therefore, IV lipid infusions may enhance the effect of, and may be a useful adjunct to, phototherapy.


Suppression of immune function and increased risk of sepsis have been associated with the use of IV lipid emulsions. Diminished motility and metabolic activity of polymorphonuclear (PMN) leukocytes exposed to fat emulsion in vitro have been reported. However, this could not be demonstrated in vivo in full-term and preterm infants given lipid 0.5 to 3 g/kg/day over 16 hours. On the contrary, some aspects of PMN migratory properties and their oxidative metabolism improved during the study period, most likely the result of chronologic and functional maturity. There have been reports of fungal infections with Malassezia furfur and coagulase-negative staphylococci associated with lipid administration. Freeman and colleagues have reported that 56.6% of all cases of nosocomial bacteremia in two neonatal intensive care units in Boston were highly correlated with lipid administration. However, they stress that the benefits derived from the lipids outweigh the apparent risk of infection.


Carnitine


Carnitine is an essential cofactor required for the transport of long-chain fatty acids (LCFAs) across the mitochondrial membrane for β-oxidation. Because the preterm infant is born with limited carnitine reserves and low plasma carnitine levels develop when parenteral nutrition is not supplemented with carnitine, several investigators have suggested adding carnitine to parenteral nutrition with lipids for preterm infants. Addition of supplemental carnitine does increase oxidation of fat and circulating ketone body levels and results in increased tolerance to IV lipids. However, data on increase in weight gain and nitrogen retention are not as convincing. Therefore, carnitine is recommended only for LBW infants who require prolonged (over 2 to 3 weeks) parenteral nutrition. IV carnitine dosage has been used at 8 to 10 mg/kg/ without any observable side effects.


Parenteral Vitamins


The parenteral multivitamin guidelines proposed by the American Medical Association have been accepted for the pediatric formulation. A special committee of the American Society for Clinical Nutrition made recommendations for a new multivitamin preparation specifically for the preterm infant. Although no preparation meets these guidelines, the committee recommends that MVI-Pediatric (Armour Pharmaceutical, Kankakee, Ill) should be used for preterm infants at 40% of a vial (or 2 mL) per kilogram body weight per day, not to exceed a total daily dose of one vial (5 mL); infants and children should receive one vial (5 mL) daily (see Table 7-2 ).


Intravenous vitamins, especially vitamin A, riboflavin, ascorbic acid, and pyridoxine, may be lost through adherence to the plastic tubing or through photodegradation caused by light exposure. There is often high light intensity in a special care nursery and the TPN fluid in the tubing moves slowly; therefore, it is exposed to light for prolonged periods. For these reasons, vitamins are added to the TPN shortly before infusing and some nurseries have the TPN bags and infusion tubings covered with foil or opaque material to minimize light exposure.


Trace Minerals


Because the infant has minimal endogenous stores, trace minerals are added to the TPN solution (see Table 7-4 ). The need for iron supplementation should be evaluated. Intravenous iron should be used with caution because excess iron can easily be given and may result in iron overload, increased risk of gram-negative septicemia, and an increase in the requirement for antioxidants, especially vitamin E.


Calcium, Phosphorus, Magnesium, and Vitamin D


Preterm infants require increased intakes of calcium and phosphorus for optimal bone mineralization. The intrauterine accretion rates for calcium in the last trimester range from 104 to 125 mg/kg/day at 26 weeks’ gestation to 119 to 151 mg/kg/day at 36 weeks’ gestation; phosphorus accretion rate is 63 to 86 mg/kg/day. These levels of calcium and phosphorus intake cannot be attained with conventional TPN solutions because they would be insoluble. The pediatric crystalline amino acids solutions, however, have a lower pH, especially when cysteine hydrochloride is added; therefore, greater concentrations of calcium and phosphorus can remain in solution.


VLBW infants should receive 60 to 80 mg/kg/day of calcium, 45 to 60 mg/kg/day of phosphorus, 4 to 7 mg/kg/day of magnesium, and 25 IU of vitamin D. A calcium-to-phosphorus ratio of 1.3 to 1 is suggested, although others have noted improved mineral retention with a 1.7 to 1 ratio. These high calcium and phosphorus infusions should be given through a central venous line and not through a peripheral line.


Practical Hints for Fluid and TPN Management





  • During the first few days of life, provide sufficient fluid to result in urine output of 1 to 3 mL/kg/hour, a urinespecific gravity of 1.008 to 1.012, checking urine for sugar and protein at the same time, and a weight loss of approximately 5% or less in full-term and approximately 15% or less in VLBW infants.



  • Weigh infants twice a day the first 2 days of life, then daily thereafter to accurately monitor input and output.



  • Use birth weight to calculate intake until birth weight is regained.



  • Record fluid intake, output, and weight.



  • If the infant is hyperbilirubinemic, provide lipids 0.5 to 1 g/kg/day, maintaining a serum triglyceride no greater than 150 mg/dL. Serum triglyceride should be checked before the start of the first lipid infusion, as lipids are being advanced, and weekly thereafter.



  • Aim for a parenteral nutrition goal of 90 to 100 kcal/kg/day and 2.7 to 3 g protein/kg/day with a nonprotein caloric-to-nitrogen ratio (NPC:N) of 150 to 250. The NPC:N ratio can be calculated as follows:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-3-Frame class=MathJax style="POSITION: relative" data-mathml='lipid calories+dextrose calories(grams of protein)(0.16)=NPC1g N’>lipid calories+dextrose calories(grams of protein)(0.16)=NPC1g Nlipid calories+dextrose calories(grams of protein)(0.16)=NPC1g N
lipid calories + dextrose calories ( grams of protein ) ( 0.16 ) = NPC 1 g N

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Sep 29, 2019 | Posted by in PEDIATRICS | Comments Off on Nutrition and Selected Disorders of the Gastrointestinal Tract

Full access? Get Clinical Tree

Get Clinical Tree app for offline access