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(Pediatrics in Review. 1999;20:e56-e62.)
© 1999 American Academy of Pediatrics
OBJECTIVES
After completing this article, readers should be able to:
Introduction
From early in this century, investigators have attempted to determine the optimal nutrient delivery for term infants to promote normal growth and development. In the past 25 years, nutritional investigators have concentrated on the needs of the ideal, healthy preterm infant to try to mimic intrauterine growth and body composition.
Although great progress has been made in characterizing the needs of healthy preterm and term infants, the needs of ill, physiologically unstable infants largely have been neglected. The primary reasons for this lack of investigation are the assumption that the needs of ill infants are similar to those of healthy infants and the difficulty of studying metabolic needs in ill infants. The persistent efforts of several groups of investigators and the development of new techniques to study metabolism now have begun to delineate the specific nutritional needs of this particular patient population.
Drawing on models generated in the adult surgical intensive care literature of the 1980s makes it possible to try to elucidate the effect of common illnesses and conditions (eg, acute pulmonary disease, bronchopulmonary dysplasia[BPD], congenital heart disease[CHD], sepsis, and surgery) on neonatal metabolism and, therefore, nutritional requirements. The assumption is that changes from the norm in metabolism require alterations in substrate delivery (ie, nutrition). As with adults, it is likely that each illness induces characteristic changes in metabolism. The task for the practitioner is to customize nutritional delivery to fit the specific infant's needs.
We will review current knowledge about the metabolic changes induced by common neonatal illnesses by comparing the nutritional needs of ill infants with the well-established standards for healthy newborns. Nutritional needs induced by some diseases have been characterized better than others. For example, there is an extensive literature on the energy (but not the protein) needs of infants who have BPD. The protein and energy needs of infants undergoing surgery have received substantial attention recently. Other aspects of neonatal nutrition, particularly micronutrient requirements, have not been studied specifically in ill compared with healthy infants. Where possible, we have attempted to make specific recommendations for nutrient delivery when such values are available.
Normal Requirements
Understanding the nutritional requirements of healthy term and
preterm infants forms a basis for assessing the effects of disease
processes on nutrient needs. A complete list of normal neonatal
nutritional requirements is beyond the scope of this article; rather,
we focus primarily on nutrients that potentially are affected by
disease states (Table
).
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Acute Pulmonary Disease
Acute pulmonary disease not only is the most common admission diagnosis in the neonatal intensive care unit (NICU), but it is the most common severe illness of the neonate. It encompasses respiratory distress syndrome (hyaline membrane disease), pneumonia, meconium aspiration syndrome, and other disease states, such as congenital diaphragmatic hernia and acute respiratory distress syndrome due to sepsis. Several studies in adults, children, and infants have demonstrated that acute pulmonary disease increases oxygen consumption, thus increasing energy requirements. Infants who have respiratory distress syndrome have a range of estimated resting energy expenditure of 40 to 60 kcal/kg per day, with caloric needs directly proportional to the severity of the illness.
ENERGY NEEDS
The nutritional goal with any ill infant is to attempt to achieve
a positive energy balance. We generally use a two-tiered approach. The
initial objective is to meet resting energy expenditure during acute
illness without superimposing an increased metabolic demand by
providing excess calories. Acutely ill neonates are likely to be
insulin-resistant and have elevated levels of counterregulatory
hormones (eg, cortisol, epinephrine, and norepinephrine) that
promote tissue catabolism to provide amino acids for substrate for
gluconeogenesis. Energy delivered in excess of the amount needed to
fuel the basal metabolic rate is likely to be "wasted" at best and
to increase total energy demand at worst. It is only after the infant
has become more physiologically stable that we attempt to achieve the
second tier of nutrition support—supplying sufficient calories beyond
the resting energy expenditure to achieve optimal growth.
The energy sources available to the neonate are carbohydrates and fat, which provide 4 kcal/g and 9 kcal/g, respectively. Protein, which can provide approximately 4 kcal/g, is not typically used unless total energy expenditure exceeds total energy intake. Because carbohydrates are a ready source of energy, and neonates are particularly dependent on glucose as an energy source, the rate of glucose infusion generally is raised by increasing either the rate of fluid administration or the dextrose concentration in the crystalloid solution. Unfortunately, high rates of carbohydrate delivery (>12.5 mg/kg per minute) increase carbon dioxide production because this nutrient had a high respiratory quotient (RQ) (1.0) when completely oxidized that is even higher (>1.0) when excess glucose is used for fat production. The general risk associated with an increased rate of carbon dioxide production in the infant who has respiratory disease is to raise minute ventilation needs, thereby increasing the work of breathing or exposure to barotrauma in infants who are receiving mechanical ventilation.
Lipids are an excellent source of energy because they are calorically dense. They have a lower RQ (0.7) and, therefore, create less carbon dioxide when metabolized. This may confer an advantage to a neonate who is receiving mechanical ventilation. However, lipid emulsions have been shown to have a direct effect on pulmonary function by impairing gas exchange. This has been attributed to the production of vasoactive metabolites, which uncouples hypoxic vasoconstriction and increases ventilation/perfusion mismatching. Infusing the lipid solution over at least 16 hours during a 24-hour period may decrease this effect. Despite being associated with problems such as hypoxia and pulmonary hypertension (which generally occur at substantially higher rates of infusion than currently recommended), early initiation of lipids seems prudent because significant growth failure is associated with severe lung disease.
The initial objectives in beginning lipid infusions is to prevent essential fatty acid deficiency, resume growth, and facilitate the transition to enteral feedings. In general, lipid emulsion can be started at 1 g/kg per day and advanced in increments of 0.5 to 1 g/kg per day, depending on serum triglyceride clearance. The addition of carnitine to parenteral nutrition in the preterm infant has been shown to promote fatty acid oxidation and prevent the rare occurrence of carnitine deficiency. Although further investigation is needed, medium-chain triglycerides may be an alternative fat source because they are calorically more efficient and reduce fat storage rates.
Energy expenditure increases with worsening acute pulmonary disease. A balanced delivery of energy from carbohydrates and lipids (rather than exclusively one or the other) is indicated. The initial goal is to meet resting energy expenditure (60 kcal/kg per day) to reduce catabolism and is followed by advancing energy intake to a level that supports weight gain.
PROTEIN
Negative nitrogen balance occurs in both adults and older children
who have severe respiratory distress. Respiratory muscle strength and
function in adults can be compromised significantly by undernutrition,
but improvement in both follows improvement in nutritional status. Poor
or undernutrition not only alters the lung's response to barotrauma,
hyperoxia, and infection, but it exacerbates pulmonary structure and
biochemical immaturity and can lead to reduced alveolar formation.
Finally, poor protein status leads to low oncotic pressure, which can
result in or exacerbate pulmonary edema.
In healthy very low-birthweight infants, both stable isotope and nitrogen balance studies have shown that most plasma amino acid concentrations decline significantly after birth if the infant has no protein intake. The degree of protein loss is approximately 1.2 to 1.4 g/kg per day and can be ameliorated by providing that amount of protein. However, because the daily in utero protein accretion is 2.1 g/kg per day, a total of at least 3.5 (1.4+2.1) g/kg per day is needed to keep the preterm infant on track with expected in utero accretion rates.
Preterm infants who have varying degrees of respiratory distress syndrome and are receiving 1 g/kg per day of amino acids are in negative nitrogen balance. Recent studies from Thureen et al (see Suggested Reading) demonstrate no evidence of protein intolerance in ventilated neonates during the first week of life who are receiving amino acid intakes of up to 2.9 g/kg per day. Thus, sufficient protein delivery to achieve positive nitrogen balance can be attained by providing at least 1.5 g/kg per day and increasing the intake by 0.5 to 1.0 g/kg per day to a total of 3.0 to 4.0 g/kg per day of amino acids parenterally. In addition, studies suggest that it may not be necessary to increase protein administration incrementally; infants can be started at or close to the maximal protein dose. There appears to be no need to increase protein delivery simply on the basis of degree of respiratory illness because the degree of nitrogen loss is not related to the severity of respiratory distress.
MINERALS
Disorders of calcium, phosphorus, and magnesium metabolism are
common in acute pulmonary disease. Maintaining homeostasis and normal
serum concentrations of these minerals is important because
hypocalcemia, hypophosphatemia, and hypomagnesemia each can affect
optimal respiratory and cardiac function. Transient neonatal
hypocalcemia often is exacerbated by acute respiratory disease and,
when severe, can cause tetany and cardiac arrhythmias. Typically, we
add 600 mg of calcium gluconate per 100 mL of intravenous fluids
on day 1 in infants who have acute pulmonary disease to provide
prophylaxis against hypocalcemia. Similarly, hypophosphatemia and
hypomagnesemia can cause muscle weakness, lethargy, and poor
respiratory effort. Hypermagnesemia can lead to apnea, which is seen
commonly among infants whose mothers have been treated with magnesium
sulfate for preterm labor or pregnancy-induced hypertension. Monitoring
calcium, phosphorus, magnesium, and alkaline phosphatase levels is
important in assessing nutrient delivery, remembering that calcium
levels always will be maintained at the expense of bone.
Although it may be important to maintain normal hemoglobin concentrations in infants who have acute pulmonary disease to optimize oxygen delivery, iron rarely is the limiting factor. Most infants are born with sufficient iron stores to maintain them through the period of acute disease, and rapid decreases in hemoglobin (due to blood drawing) are treated best by transfusion, not by infusion of parenteral iron.
VITAMINS
It is unclear whether acute pulmonary disease has any specific
effects on vitamin metabolism. Recent studies suggest that infants who
are at high risk for BPD and have low vitamin A levels may benefit
from vitamin supplementation during the time of acute pulmonary
disease. The current recommended dose is at least 2,000 U
intramuscularly (IM) every other day. The goal is to achieve a serum
retinol level of greater than 20 mcg/dL.
Bronchopulmonary Dysplasia
ENERGY NEEDS
Infants who have BPD have 25% higher resting energy expenditures,
which results in a 10% to 15% increase in total caloric need compared
with infants who do not have BPD. Much of this is related to their
pulmonary status and increased work of breathing, with a correlation
between degree of respiratory compromise and oxygen consumption. Energy
requirements for growth generally are in the range of 130 to
150 kcal/kg per day. Options to meet this increased metabolic
demand are aimed at decreasing the work of breathing, increasing the
caloric intake, or both. Fat is a good nutritional adjuvant for infants
who have compromised lung function, such as those who have BPD, because
of both its high caloric density and its low RQ. Fat should not provide
more than 60% of the total calories.
PROTEIN
There are few specific studies of protein status among infants who
have established BPD except to note that they typically have lower
somatic muscle stores. This finding, combined with their high fat mass,
suggests that these infants are chronically receiving less-than-optimal
amounts of protein for the amount of energy intake. Stable isotope
studies of protein needs in infants who have BPD have been performed
primarily within the context of studying the effect of
glucocorticosteroids on protein status. Using stable isotopic
techniques, van Goudoever et al (see Suggested Reading)
demonstrated that high-dose dexamethasone (0.5 mg/kg per day)
reduced linear growth and weight gain by markedly increasing protein
breakdown, albeit without affecting rates of protein synthesis. Whether
this effect can be tempered by administering higher amounts of protein
during treatment with steroids currently is under investigation.
Because these infants already frequently are receiving high-solute, high-nitrogen diets, we do not routinely increase protein delivery during steroid treatment. Rather, we try to limit the duration and magnitude of exposure of young preterm infants to this drug. Overall, enterally fed infants who have BPD and are receiving more than 120 kcal/kg per day require protein intakes of at least 3.5 g/kg per day. Any increase in the caloric intake through supplementation of fat or carbohydrate should be accompanied by increased protein delivery.
MINERALS
Infants who have BPD often are receiving diuretic therapy.
Unfortunately, the diuretics commonly used (eg, furosemide and
bumetanide) cause increased urinary sodium, potassium, chloride, and
calcium losses. Whereas the baseline sodium requirement for a healthy
preterm infant is 3 to 4 mEq/kg per day, diuretic usage may
increase this need to as high as 12 mEq/kg per day. Similarly, the
potassium requirement, which normally averages 2 to 4 mEq/kg
per day in the healthy infant, will rise to 7 to 10 mEq/kg
per day under diuretic pressure. Because the primary deficit is of
chloride, sodium and potassium must be repleted as sodium chloride and
potassium chloride. Infants who have persistent hyponatremia exhibit
poor growth, and severe hypochloremia has been associated with sudden
infant death in those who have BPD. The infant receiving diuretics and
electrolyte supplements may demonstrate wide swings in serum potassium
levels.
Urinary calcium loss with diuretics exacerbates an already tenuous balance and increases the risk of osteopenia of prematurity and nephrocalcinosis. Whereas the in utero rate of calcium accretion in the third trimester is 150 to 180 mg/kg per day, the calcium requirements of the preterm infant who has BPD and is receiving furosemide is nearly 200 to 225 mg/kg per day. The addition of glucocorticosteroids will increase bone remodeling and calcium needs further.
Infants who have BPD are faced with the classic dilemma of the risks and benefits of iron. Iron is necessary for normal organ function, but it is potentially toxic because it can create strong oxidant stress. The infant who has BPD may well benefit from a higher circulating hemoglobin concentration, which can be induced with consistent enteral iron therapy. However, iron delivered in excess of serum iron binding capacity may place the infant at greater oxidant risk. It appears that current recommendations for healthy preterm infants also are appropriate for those who have chronic lung disease.
VITAMINS
Vitamin A is a biologic antioxidant. Antioxidants are
important in protecting cell membranes from oxygen free radical damage.
Vitamin A influences epithelial growth, differentiation, and repair.
Vitamin A deficiency and its possible association with the development
of BPD has been the subject of several investigations. The overall
consensus seems to be that persistent low serum retinol concentrations
(<20 mcg/dL) are associated with a higher risk of BPD. Vitamin
A deficiency also affects T-cell proliferation and phagocytic
immunomodulatory activity of polymorphonuclear leukocytes. Prevention
of vitamin A deficiency or treatment of infants at risk for BPD
who have vitamin levels less than 20 mcg/dL with at least 2,000 IU
administered IM every other day appears to be an effective strategy for
reducing BPD risk.
Vitamin E is a biologic antioxidant that protects the polyunsaturated fatty acids of cell membranes from peroxidation. Deficiency of this vitamin compromises cellular and humoral immunity and antimicrobial phagocytic action. It can cause a severe hemolytic anemia, which will be made worse with iron therapy. On the other hand, it has been difficult to link vitamin E status with other diseases due to oxidant stress, such as BPD, retinopathy of prematurity, and intra-ventricular hemorrhage. Results of studies examining the role of vitamin E supplementation in preventing or treating these conditions have not been convincing. As with most other nutrients, it appears prudent to maintain sufficient vitamin E status without running the risks of oversupplementation. We currently supplement preterm infants who have low vitamin E levels with 50 to 75 IU/d, and levels are monitored weekly.
Congenital Heart Disease
ENERGY NEEDS
Infants who have CHD, particularly with an element of congestive
heart failure, have higher resting and total energy expenditures.
Infants who have heart disease and are undernourished or malnourished
tend to have a body composition that is higher in lean body mass and
lower in fat content. Lean body mass is more metabolically active. The
administration of optimal energy to these infants is a challenge
because of the high metabolic demands of the myocardium, the muscles of
respiration, and the hematopoietic system. High-energy feedings have
been shown to improve both energy balance and growth.
The effects of cardiac surgery have been studied extensively in adults, less in children, and even less in neonates. In the immediate postoperative period, meeting the nutritional/energy needs of the neonate always is a challenge based on their delicate fluid balance, type of repair (curative versus palliative), respiratory compromise, and degree of renal failure. Additionally, catecholamine medications that increase oxygen consumption (eg, epinephrine, dopamine, and dobutamine) typically are required for cardiac support until the myocardium has recovered. As with the management of acute respiratory disease, the initial goal is to reduce catabolism by trying to meet the infant's resting energy requirements (60 kcal/kg per day). As the infant recovers, the energy delivery is increased to promote adequate growth (130 to 150 kcal/kg per day).
Common problems seen in these infants include delayed gastric emptying, fatigability with feeds, vomiting, and malabsorption. Infants who have congenital heart disease, particularly when it is complicated by congestive heart failure, cyanosis, or both, generally require a diet that is not only high in calories but also calorically dense. They may need as much as 150 kcal/kg per day to achieve optimal growth, which can be difficult to achieve in infants who have poor oral intake. Studies have shown that continuous enteral feedings are more beneficial than intermittent bolus feedings.
PROTEIN
The effect of CHD on protein needs, either in the immediate
postoperative period or chronically, has not been studied extensively.
Because investigators have demonstrated substantial protein needs
following noncardiac surgery, it seems reasonable to assume that
infants are similarly catabolic immediately after cardiac surgery and
have increased protein requirements. Based on these data, it seems
prudent to provide at least 2.5 g/kg per day of protein in the
immediate postoperative period with the intent to increase the delivery
ultimately to 3.5 g/kg per day as tolerated.
The protein requirement of the infant who has chronic congestive heart failure frequently is underestimated. Because these infants have high energy needs, a common strategy is to supplement standard formulas with carbohydrates (glucose polymers) or lipids (oils, fats). Providing increased energy without concurrently increasing protein intake results in relative protein insufficiency and suboptimal growth. Because total protein should constitute 8% to 10% of the infant's diet, it is important to supplement formulas with protein as well. However, delivery of too much protein adds to the renal solute load in infants who already receive limited free water, which could lead to decreased nitrogen utilization. Maintaining a nonprotein energy-to-gram nitrogen ratio of 150 to 200:1 appears to be optimal.
MINERALS
As in the infant who has BPD, the use of diuretics to treat CHD
can compromise sodium, potassium, chloride, calcium, and phosphorus
balances significantly. Potassium balance bears particular attention in
the infant who has cardiac disease in whom hypokalemia, but more
particularly hyperkalemia, can result in fatal arrhythmias. Close
attention to calcium and phosphorus delivery and serum levels of these
nutrients is warranted. Infants who undergo cardiac surgery also are at
risk for transient but significant hypocalcemia in the immediate
pre- and postoperative period because of the generous use of citrated
blood products. Adequate phosphorous must be delivered to support
generation of adenosine triphosphate for optimal myocardial
function.
Infants who have cyanotic congenital heart disease have high iron requirements because of their expanded red cell mass. Persistent cyanosis increases production of endogenous erythropoietin, resulting in secondary polycythemia, to improve tissue oxygen delivery. The synthesis of each additional gram of hemoglobin requires an additional 3.4 mg of elemental iron. It is important to screen infants who have cyanotic CHD for iron deficiency using ferritin, red cell indices, and total iron-binding capacity saturation because the hemoglobin may be within the normal range for noncyanotic infants even though the infant is deficient in iron. It appears that a minimum dose of 2 mg/kg day of iron is prudent in these infants.
VITAMINS
Although no specific studies have addressed the effect of CHD on
vitamin levels and requirements, it is likely that congestive heart
failure decreases intestinal absorption of fats in general and
fat-soluble vitamins in particular. In addition, if cardiac surgery is
complicated by traumatic chylothorax, fat-soluble vitamin status can be
reduced significantly. Water-soluble forms of vitamin A and
vitamin E are available and can be used as alternative forms of
supplementation when there is a question of fat malabsorption.
Sepsis
ENERGY NEEDS
The energy requirements during sepsis are well-characterized in
adults. In this "hypermetabolic" state, there is a marked catabolic
response, with profound changes in energy and protein metabolism. The
state is driven by increased levels of cytokines (particularly tumor
necrosis factor[TNF] alpha, interleukin 6[IL6], and IL1b) and
increased activity of the sympathetic nervous system, with increased
catecholamine levels, increased oxygen consumption, and negative
nitrogen balance.
The metabolic response to and nutritional requirements of sepsis in the neonate are not well-defined. Several clinical studies in neonates who had sepsis and necrotizing enterocolitis have demonstrated increased levels of both TNF alpha and IL6, cytokines known to be involved in the septic response and multisystem organ failure syndrome seen in adults. Energy requirements in these neonates were elevated in proportion to the degree of septic illness. The septic neonates required higher energy delivery during the acute phase of their illness than similarly ill nonseptic infants. A goal of at least 60 kcal/kg per day seems prudent to meet the energy requirements during the acute phase of illness.
PROTEIN
Sepsis alters protein requirements more acutely by its effect on
cytokine-mediated muscle catabolism. In adults this condition causes a
dramatic increase in muscle catabolism, most likely to provide a ready
source of amino acids to the liver for acute-phase reactant synthesis.
Sepsis causes the most profound changes in negative nitrogen balance
among all adult illnesses. A recent study suggests that the same
catabolic effect occurs in septic neonates in which the degree of
negative nitrogen balance is related directly to the severity of
physiologic instability. There are concomitant increases in cytokine
and acute-phase reactant protein concentrations. The mean nitrogen
balance in these septic patients was -141±316 mg/kg per day, but
it was as great as -800 mg/kg in certain patients. The same study
demonstrated that some infants remained in negative nitrogen balance
for as long as 10 days after the sepsis began. The concern is that
this duration of negative nitrogen balance would lead to long-term
morbidity (predisposition to further episodes of sepsis) and growth
delay. No study has assessed whether provision of extra protein will
reduce this catabolic response, but at this point it seems prudent to
provide at least 2.5 g/kg per day of protein to the septic
infant.
MINERALS
Sepsis has no known specific effect on mineral homeostasis, but it
is important to recognize that significant fluid shifts requiring the
use of colloid for blood pressure and volume support can occur with
sepsis syndrome, which will alter fluid and electrolyte balance.
Therefore, close attention to serum electrolyte and mineral levels is
necessary.
Infants who have sepsis do not need treatment with iron and, in theory, such treatment may exacerbate the syndrome. Iron is an essential nutrient for bacterial proliferation, and the body appears to "hide" iron during infection by decreasing serum concentrations.
VITAMINS
The roles of fat-soluble vitamins such as A and E have not
been well defined in neonatal sepsis. Vitamin E supplementation has not
proven to be beneficial in decreasing infection or improving response
to infection. Excess vitamin E may impair the bactericidal capacity of
white blood cells and increase the infant's risk of sepsis.
Antibiotics used in the treatment of sepsis syndrome significantly reduce bacterial colonization of the gastrointestinal tract, which decreases the inherent production of vitamin K by gastrointestinal flora. We recommend administering vitamin K 1 mg at least two times per week to infants who are receiving antibiotic therapy.
Surgery
ENERGY NEEDS
Although surgery increases energy requirements in the adult, its
effect on neonatal energy metabolism is less clear. Surgery increases
endogenous catecholamine and cytokine levels in neonates, but this
response is of a shorter duration than in adults. Although this
probably has a significant effect on protein metabolism, infants
undergoing an uncomplicated operation who are receiving adequate
anesthesia postoperatively have no apparent increase in energy
requirements. In contrast, infants undergoing surgery who are
physiologically unstable due to an acute underlying illness have the
expected rise in energy requirements seen with nonsurgical acute
illnesses. Lipid peroxidation is increased in direct proportion to the
degree of physiologic stress. Lipids are well-used and are an important
source of energy in acutely stressed infants who are having surgery.
Because excess carbohydrate delivery will shift the RQ cellular
metabolism toward greater production of carbon dioxide, a balanced
mixed-fuel (carbohydrate and lipid) approach should be used to
provide nutritional support to these infants.
PROTEIN
Elective surgery in adults causes a small but significant
reduction in nitrogen balance, but there is little evidence for
induction of a full hypercatabolic response. Similarly, stable neonates
undergoing elective, uncomplicated surgery do not have markedly
increased protein requirements. Anderson et al (see Suggested Reading)
have studied infants operated on within the first 24 hours of life
for gastroschisis or congenital diaphragmatic hernia. The infants were
started on parenteral nutrition with a fentanyl infusion (which appears
to suppress the catabolic response to surgery in adults). Infants
receiving 2.5 g/kg per day of amino acids remained in positive
nitrogen balance immediately postoperatively, had higher amino acid
values, and had no evidence of toxicity. Thus, it appears that infants
can receive 2.5 g/kg per day of protein on postoperative day 1
with minimal risk and with positive effects on nitrogen balance.
MINERALS
Surgery has no known specific effect on electrolytes, trace
elements, and vitamins. Nevertheless, surgery and therapies associated
with surgery and postoperative management (eg, diuretics, citrated
blood products) can affect fluid balance and mineral homeostasis.
Therefore, it is important to monitor calcium and phosphorus levels
closely in infants receiving colloid and/or blood products and
electrolytes in infants receiving postsurgical diuretics. We typically
add 600 to 1,200 mg of calcium gluconate per 100
mL of intravenous fluid. Similarly, sodium and potassium dosages may
approach 10 and 8 mEq/kg per day, respectively.
Summary
It is important for the clinician to appreciate the specific nutrient requirements associated with various disease states and their therapies in the ill newborn. Neonatal illnesses significantly alter energy, protein, and mineral metabolism in disease-specific manners. Alterations in metabolism during illness translate directly into changes in nutrient requirements from the healthy state. Failure to provide appropriate nutritional support during illness may delay recovery from or even exacerbate common neonatal diseases.
Suggested Reading
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Anderson MS, Thureen PJ, Bacon KA, Bass KD, Melara DL, Hay WW Jr. Achieving positive protein balance in the immediate postoperative period in neonates with amino acid administration plus narcotic analgesia. Pediatric Research. 1999;45:276A
Barton J, Hindmarsh P, Scrimgeour C, Rennie M, Preece M. Energy expenditure in congenital heart disease. Arch Dis Child. 1994;70:5-9[Abstract]
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Tsang RC, Zlotkin SH, Nichols B, Hanson JW. Nutrition During Infancy: Principles and Practice. 1997 Cincinnati, OH.: Digital Educational Publishing, Inc
Tsang RC, Uauy R, Zlotkin S. Nutritional Needs of the Preterm Infant: Scientific Basis and Practical Guidlines. 1993 Philadelphia, Penn.: Williams and Wilkins
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