000074
10.3205/000074
urn:nbn:de:0183-0000748
Review Article
Neonatology/Paediatrics – Guidelines on Parenteral Nutrition, Chapter 13
Neonatologie/Pädiatrie – Leitlinie Parenterale Ernährung, Kapitel 13
Fusch
Fusch
C.
C
Dept. of Pediatrics, McMaster University, Hamilton, Canada
author
Bauer
Bauer
K.
K
Dept. of Paediatrics, Johann-Wolfgang-Goethe University of Frankfurt, Germany
author
Böhles
Böhles
H. J.
HJ
Dept. of Paediatrics, Johann-Wolfgang-Goethe University of Frankfurt, Germany
author
Jochum
Jochum
F.
F
Dept. of Paediatrics, Spandau Hospital, Berlin, Germany
author
Koletzko
Koletzko
B.
B
Dept. Metabolic Diseases & Nutritional Medicine, Dr. von Hauner Children's Hospital, University of Munich, Germany
author
Krawinkel
Krawinkel
M.
M
Institute for Nutritional Science and Centre for Paediatrics, University of Giessen, Germany
author
Krohn
Krohn
K.
K
Dept. Metabolic Diseases & Nutritional Medicine, Dr. von Hauner Children's Hospital, University of Munich, Germany
author
Mühlebach
Mühlebach
S.
S
CSO Vifor Pharma Ltd, Villars-sur-Glâne, Switzerland
University of Basel, Switzerland
author
Working group for developing the guidelines for parenteral nutrition of The German Society for Nutritional Medicine
Working group for developing the guidelines for parenteral nutrition of The German Society for Nutritional Medicine
author
German Medical Science GMS Publishing House
Düsseldorf
610
premature infant
low birth weight infant
newborn infant
monitoring
childhood
Frühgeborenes
Low birth weight infant
Neugeborenes
Monitoring
Kindheit
Special Issue
20090114
20091118
engl
1612-3174
7
GMS German Medical Science
GMS Ger Med Sci
15
Eine besondere Herausforderung bei der Durchführung parenteraler Ernährung (PE) bei pädiatrischen Patienten ergibt sich aus der großen Spannbreite zwischen den Patienten, die von extrem unreifen Frühgeborenen bis hin zu Jugendlichen mit einem Körpergewicht von mehr als 100 kg reicht, und ihrem unterschiedlichen Substratbedarf. Dabei sind alters- und reifeabhängige Veränderungen des Stoffwechsels sowie des Flüssigkeits- und Nährstoffbedarfs zu berücksichtigen sowie auch die klinische Situation, in der eine PE eingesetzt wird. Das Vorgehen unterscheidet sich deshalb ganz erheblich von der PE-Praxis bei erwachsenen Patienten, z.B. ist der Flüssigkeits-, Nährstoff- und Energiebedarf von Früh- und Neugeborenen pro kg Körpergewicht höher als bei älteren pädiatrischen und bei erwachsenen Patienten. In der Regel benötigen alle Frühgeborenen <35. SSW und alle kranken Reifgeborenen während der Phase des allmählichen Aufbaus der enteralen Nahrungszufuhr eine vollständige oder partielle PE. Die Zufuhrmengen der PE bei Neonaten müssen berechnet (nicht geschätzt) werden. Der Anteil der PE sollte zur Minimierung von Nebenwirkungen sobald wie möglich durch Einführung einer enteralen Ernährung vermindert (teilparenterale Ernährung) und schließlich komplett durch enterale Ernährung abgelöst werden. Eine unangemessene Substratzufuhr im frühen Säuglingsalter kann langfristig nachteilige Auswirkungen im Sinne einer metabolischen Programmierung des Krankheitsrisikos im späteren Lebensalter haben. Wenn bei älteren Kindern und Jugendlichen dagegen der Energie- und Nährstoffbedarf eines Patienten im Vorschul- oder Schulalter durch eine enterale Nährstoffzufuhr nicht gedeckt werden kann, ist abhängig von Ernährungszustand und klinischen Umständen spätestens innerhalb von 7 Tagen eine partielle oder totale PE zu erwägen.
There are special challenges in implementing parenteral nutrition (PN) in paediatric patients, which arises from the wide range of patients, ranging from extremely premature infants up to teenagers weighing up to and over 100 kg, and their varying substrate requirements. Age and maturity-related changes of the metabolism and fluid and nutrient requirements must be taken into consideration along with the clinical situation during which PN is applied. The indication, the procedure as well as the intake of fluid and substrates are very different to that known in PN-practice in adult patients, e.g. the fluid, nutrient and energy needs of premature infants and newborns per kg body weight are markedly higher than of older paediatric and adult patients. Premature infants <35 weeks of pregnancy and most sick term infants usually require full or partial PN. In neonates the actual amount of PN administered must be calculated (not estimated). Enteral nutrition should be gradually i<![CDATA[ntr</PlainText></TextGroup>oduced and should replace PN as quickly as possible in order to minimise any side-effects from exposure to PN. Inadequate substrate intake in early infancy can cause long-term detrimental effects in terms of metabolic programming of the risk of illness in later life. If energy and nutrient demands in children and adolescents cannot be met through enteral nutrition, partial or total PN should be considered within 7 days or less depending on the nutritional state and clinical conditions.</Pgraph>
</Abstract>
<TextBlock linked="yes" name="Preliminary remarks">
<MainHeadline>Preliminary remarks</MainHeadline>
<Pgraph>The majority of recommendations on substrate intake (with the exception of the chapters on “Amino acid requirements” and “Information on the selection and production of amino acid solutions” in the attachment, which have been specially drawn up for this set of guidelines) have been drawn up according to the “Guidelines on Paediatric Parenteral Nutrition”, a combined study group from the European Society of Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN, <Hyperlink href="http://www.espghan.org">http://www.espghan.org</Hyperlink>) and the European Society for Clinical Nutrition and Metabolism (ESPEN, <Hyperlink href="http://www.espen.org">http://www.espen.org</Hyperlink>) <TextLink reference="1"></TextLink>. Systematic literature research has already been carried out for the development of the European guidelines, therefore further research for the current guidelines was unnecessary.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Introduction">
<MainHeadline>Introduction</MainHeadline>
<Pgraph>Systematic review in a number of fields produced a series of published studies from which evidence-based recommendations can be drawn up for the neonatal period (1–28 days) and period of infancy (1–12 months). The situation in children and teenagers is, however, different with extremely limited data available from randomised controlled clinical studies on children after the neonatal period. </Pgraph>
<Pgraph>There is a special challenge in implementing parenteral nutrition (PN) in paediatric patients, which arises from the wide range of patients, ranging from extremely premature infants up to teenagers weighing up to and over 100 kg, and their varying substrate requirements. Age and maturity-related changes of the metabolism and fluid and nutrient requirements must be taken into consideration along with the clinical situation during which PN is applied. The indication, the procedure as well as the intake of fluid and substrates are very different to that known in PN-practice in adult patients Therefore, it makes sense to briefly present some of physiological features of paediatric patients that are significant for PN in order to understand the nutritional strategies used for children and teenagers. </Pgraph>
<Pgraph>
<UnorderedList>
<ListItem level="1">The fluid, nutrient and energy intake of premature infants and newborns is higher per kg body weight than that of older paediatric and adult patients (II).</ListItem>
<ListItem level="1">The substrate requirements of paediatric patients cannot be proportionally derived from adult requirements on the basis of body weight, but are determined according to age-specific, physiological conditions (II).</ListItem>
<ListItem level="1">The fluid, nutrient and energy intake during the post-partal adaptation and stabilisation phase is subject to specific conditions, which necessitates a specific approach (II). </ListItem>
<ListItem level="1">In comparison to older paediatric patients or adults, newborns and infants have an extremely low body store of nutrients and in many respects immature regulatory mechanisms, thus requiring an carefully adapted intake to suit their specific requirements in order to prevent imbalances (II).</ListItem>
<ListItem level="1">Inadequate substrate intake in early infancy can cause long-term detrimental effects in terms of metabolic programming of the risk of illness in later life (II).</ListItem>
</UnorderedList>
</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Physiological principles">
<MainHeadline>Physiological principles</MainHeadline>
<Pgraph>The <Mark2>body water content</Mark2> is age-related and diminishes from approx. 90% in a premature infant born after 24 weeks gestation to below 70% in a 12 month old infant <TextLink reference="2"></TextLink>, <TextLink reference="3"></TextLink>. </Pgraph>
<Pgraph>The <Mark2>fluid volume</Mark2> per kg body weight is higher in newborns than in older patients <TextLink reference="4"></TextLink>. Contributing factors for this are <Mark2>renal immaturity</Mark2> (diminished ability to concentrate urine resulting in increased urine volume) <TextLink reference="5"></TextLink>, <Mark2>higher energy expenditure</Mark2>, greater body surface area compared to body volume and epidermis immaturity resulting in<Mark2> high insensible perspiration</Mark2> <TextLink reference="6"></TextLink>. The regulatory mechanisms in the water and electrolyte balance are reduced in comparison to adults due to renal immaturity. Alongside the <Mark2>diminished ability of the kidneys to concentrate urine</Mark2> <TextLink reference="7"></TextLink>, the renal glomerular filtration rate, renal tubular reabsorption and elimination of H<Superscript>+</Superscript>-ions are also lower when compared to those of older children <TextLink reference="8"></TextLink>, <TextLink reference="9"></TextLink>. Based on body weight, the <Mark2>energy and nutrient requirements</Mark2> of newborns are <Mark2>higher</Mark2> than in older patients. This results from the increased (metabolic) activity and growth <TextLink reference="10"></TextLink> resulting in increased nutrient substrate requirements <TextLink reference="11"></TextLink>, <TextLink reference="12"></TextLink>, <TextLink reference="13"></TextLink>, <TextLink reference="14"></TextLink>.</Pgraph>
<Pgraph>Apart from the known nutritional effects of nutrition, there is also increasing evidence of long-term changes in the metabolism triggered by nutrition in early childhood (early metabolic programming of early nutrition on health in later life) <TextLink reference="15"></TextLink>, <TextLink reference="16"></TextLink>. </Pgraph>
<Pgraph>Accordingly, newborns, infants and toddlers require an intake of nutrients that has been carefully adapted to suit their metabolic requirements to a far greater degree than older paediatric patients or adults. It is never appropriate to convert intake recommendations from other patient groups like adults on the basis of body weight and to apply them to infants or toddlers without taking into consideration the different physiological conditions. </Pgraph>
<Pgraph>Apart from age-related changes in nutritional requirements, <Mark2>adaptation processes after birth</Mark2> (to a greater extent in premature infants) pose a special challenge with regard to the individual requirements for fluid and other nutrient substrates. There is a day-to-day increase in fluid and energy requirements due to the adaptation of metabolism and kidney functions as well as initial high perspiration. Daily adjustments to parenteral nutrition are, therefore, required over the first few days of a child’s life <TextLink reference="17"></TextLink>. This <Mark2>adaptation and stabilisation phase</Mark2> (5–7 days after the birth) is followed by the <Mark2>phase of stable growth</Mark2>. After the neonatal period, the hydration percentage in the fat-free body mass changes only slightly and the percentage of body water content is mainly determined by the percentage of fat in the body mass.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Indications for parenteral nutrition">
<MainHeadline>Indications for parenteral nutrition</MainHeadline>
<SubHeadline>Neonatal patients</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">All premature infants <35 weeks of pregnancy and most ill term infants require full or partial PN whilst enteral nutrition is gradually introduced (IV). </ListItem>
<ListItem level="1">The percentage of PN should be reduced as quickly as possible by the introduction of enteral nutrition (partial PN) and finally be replaced completely by enteral nutrition in order to minimise any side-effects from exposure to PN (II).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>There are a variety of reasons why premature infants (<35 weeks gestation) and seriously ill full-term infants may be unable to receive adequate enteral nutrition after birth, such as gastrointestinal tract immaturity with threat of developing necrotising enterocolitis, muscular and neurological immaturity, illnesses etc., and, hence, will require immediate PN in most cases. </Pgraph>
<Pgraph>The choice of nutrition administered (oral, enteral, partial PN or total PN) should be made on an individual basis according to medical indication and based on the principle of such nutrition being “as non-invasive as possible”. This process promotes low complication rates <TextLink reference="18"></TextLink>, <TextLink reference="19"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink> and is the reason why the highest possible percentage of nutrition should be administered orally, or enterally wherever possible. If this is not possible, (partial) parent<TextGroup><PlainText>era</PlainText></TextGroup>l nutrition should be used to supplement the enteral intake to provide adequate nutrition <TextLink reference="22"></TextLink>.</Pgraph>
<Pgraph>Premature infants are born with low food reserves (low subcutaneous fatty tissue, low glycogen reserves in the liver) in comparison to full-term newborns. There is specific risk of hypoglycaemia in connection with their high nutrient requirements. Premature infants <35 full weeks of pregnancy should therefore be prophylactically (<TextGroup><PlainText>re)intr</PlainText></TextGroup>oduced to solid food whilst administering (partial) PN. The “optimum supply” with various different nutritional components in premature and ill newborns is still being discussed. Principally it makes sense to differentiate between the recommendations for the adaptation and stabilisation phase and the recommendations for the phase of stable growth, due to differing nutritional requirements. </Pgraph>
<Pgraph>Published recommendations (e.g. <TextLink reference="11"></TextLink>, <TextLink reference="15"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="24"></TextLink>, <TextLink reference="25"></TextLink>, <TextLink reference="26"></TextLink>) do not always take into consideration the specific conditions of the adaptation and stabilisation phase after birth (5–7 days after birth), which precede the phase of stable growth.</Pgraph>
<Pgraph>This means that the stunted growth occurring during that phase (compared to intrauterine percentiles) is often not regained by the pregnancy due date <TextLink reference="27"></TextLink>. There are discussions about this target stating that the majority of eutrophic premature infants should have once again attained their birth percentile by the pregnancy due date. This target seems necessary, because growth retardation could be a risk factor for long-term neurological development <TextLink reference="27"></TextLink>, <TextLink reference="28"></TextLink>, <TextLink reference="29"></TextLink>. The potential long-term risks of growth retardation and the side-effects of increased substrate intake in the newborn period have to be weighed up as there is no evidence-based data on long-term development when considering the different growth rates of premature infants. The ideal target for premature infants is usually seen as growth corresponding with intrauterine growth percentiles. It is, therefore, necessary to adapt the nutrient supply to the respective needs of the individual premature infant. This is also the case in the phase of continual growth (see below), where the target is not only to attain a positive nitrogen balance, as in the adaptation and stabilisation phase, but also to promote catch-up growth wherever possible right up to the birth percentile. </Pgraph>
<SubHeadline>Older children and teenagers</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">If the energy and nutrient demands of a patient cannot be met through enteral nutrition during pre-school or school age, then partial or total PN is to be considered within 7 days at the latest in dependance on the nutritional state and clinical conditions (C).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>The beginning of (partial) parenteral nutrition in patients above the period of infancy should be specific to the individual circumstances, age and illness of the child or teenager. In contrast to infants, a period of inadequate nutrition and depletion of the body’s store can be tolerated in pre-school and school children with positive nutritional status for up to seven days subject to their clinical conditions.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Energy and nutrient requirements">
<MainHeadline>Energy and nutrient requirements</MainHeadline>
<SubHeadline>Energy requirements</SubHeadline>
<Pgraph>Energy requirements are age-related (see Table 1 <ImgLink imgNo="1" imgType="table"/>) and influenced by illness and therapy. Tables can provide sufficient help in typical clinical situations providing a rough approach to calculating the estimated requirements of individual patients, with the appropriate additions and deductions (e.g. in cases of pyrexia/respiratory therapy). The estimate should account for the fact that all details are based on data taken from healthy patients. Individual circumstances (e.g. reduced physical activity in case of bed rest, infections, inflammatory processes, energy losses from the stomata etc.) result in differences between the actual energy requirements and the calculated (estimated) energy requirements. </Pgraph>
<Pgraph>The actual requirements of the treated patient can be narrowed down further (e.g. weight chart) by means of monitoring measures (cf. chapter “Complications and monitoring” (<Hyperlink href="http://www.egms.de/en/journals/gms/2009-7/000076.shtml">http://www.egms.de/en/journals/gms/2009-7/000076.shtml</Hyperlink>)). </Pgraph>
<Pgraph>If the desired therapy effect (e.g. percentile parallel growth) is not attained with the estimated energy requirements and monitoring offers no solid references regarding an adequate energy intake, then various formulas can be helpful when calculating the evaluation. The equations (WHO 1985, Schofield 1985, and Harris-Benedict 1919 <TextLink reference="30"></TextLink>, <TextLink reference="31"></TextLink>, <TextLink reference="32"></TextLink>) have, however, also been established for healthy children and have to be corrected for individual patients as specified in the figures published in tables. Measuring the energy expenditure is rarely carried out routinely during daily clinical routines and is indicated, if, despite estimation aids and monitoring, there are still doubts regarding an adequate energy intake. </Pgraph>
<Pgraph>We refer to the “Guidelines on Paediatric Parenteral Nutrition” of ESPGHAN and ESPEN for a more detailed overview of aspects regarding the energy requirements of children of various age groups and in case of varying clinical pictures <TextLink reference="1"></TextLink>.</Pgraph>
<SubHeadline>Carbohydrate requirements </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">The endogenous glucose production varies from approx. 2 mg/kg/min (3 g/kg/day) in adults to approx. 8 mg/kg/min (11.5 g/kg/day) glucose in premature infants (II).</ListItem>
<ListItem level="1">The maximum glucose oxidation is approx. 7 mg/kg/min (10 g/kg/day) in premature infants, and approx. 12 mg/kg/min (18 g/kg/day) in full-term infants and infants (II–III).</ListItem>
<ListItem level="1">In full-term infants and children up to two, the glucose intake should usually not exceed approx. 12 mg/kg and min (18 g/kg and day) (C).</ListItem>
<ListItem level="1">The glucose intake should also be adapted to the age and/or clinical situation (e.g. malnutrition, acute illness, drug administration) (C).</ListItem>
<ListItem level="1">An excessively high carbohydrate intake can result in net lipogenesis with hepatic fat deposition and <TextGroup><PlainText>ste</PlainText></TextGroup>atosis of the liver (II–III).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Glucose is the sugar used for PN and usually contributes substantially to osmolarity in the PN solution. The osmolarity of a glucose solution rises significantly with increasing concentration from 255 mosm/l in a 5% glucose solution to 1020 mosm/l in a 20% glucose solution. Based on experience, glucose concentrations of up to 12.5% are well tolerated through a peripheral vein cannula as long as no other osmolarity-increasing agents are added. </Pgraph>
<Pgraph>Glucose can be directly metabolised by the central nervous system. The endogenous glucose production varies from approx. 2 mg/kg/min (3 g/kg/day) in adults to approx. 8 mg/kg/min (11.5 g/kg/day) glucose in premature infants <TextLink reference="33"></TextLink>, <TextLink reference="34"></TextLink>, <TextLink reference="35"></TextLink>, <TextLink reference="36"></TextLink>. The maximum glucose intake should not exceed the glucose oxidation rate in PN. Maximum glucose oxidation is approx. 7 mg/kg/min (10 g/kg/day) <TextLink reference="37"></TextLink>, <TextLink reference="38"></TextLink> in premature infants and approx. 12 mg/kg/min (18 g/kg/day) in full-term newborns and infants under long-term PN <TextLink reference="39"></TextLink>, <TextLink reference="40"></TextLink>, <TextLink reference="41"></TextLink>. In critically ill children with burns, maximum glucose oxidation of 5 mg/kg/min has been described <TextLink reference="41"></TextLink>. </Pgraph>
<Pgraph>Excessive glucose intake results in net lipogenesis and subsequent fat deposition <TextLink reference="42"></TextLink>, <TextLink reference="43"></TextLink>. Excessive intake can lead to hepatic steatosis with an impairment of the liver function <TextLink reference="44"></TextLink>, <TextLink reference="45"></TextLink>.</Pgraph>
<SubHeadline>Special characteristics in neonatal patients (hyper/hypoglycaemia)</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Higher incidence of hyperglycaemia with increasing immaturity (lower gestational age) (II).</ListItem>
<ListItem level="1">An early start of parenteral glucose together with amino acids (2–3 g/kg and day) from the very first day onwards contributes to preventing hyperglycaemia in premature infants. An early insulin therapy is also promising but associated with risks. Further controlled studies should be awaited prior to a general recommendation (B).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>There are often fluctuations in blood sugar levels in premature infants during the adaptation and stabilisation phase which can be influenced by low substrate reserves (hypoglycaemia) or insulin resistance (hyperglycaemia) <TextLink reference="46"></TextLink>, <TextLink reference="47"></TextLink>, <TextLink reference="48"></TextLink>. Common definitions of hypo- or hyperglycaemia, respectively, are a blood glucose level of 50 mg/dl (2.75 mmol/l) or 150 mg/dl (8.3 mmol/l), respectively, although these levels are not based on short and long term outcome studies. The incidence of hyperglycaemia increases with diminishing gestational age <TextLink reference="49"></TextLink>, <TextLink reference="50"></TextLink>. An early supply of intravenous insulin in hyperglycaemia has been proposed in order to more rapidly attain the targeted energy intake and a positive nitrogen balance <TextLink reference="51"></TextLink>, but this advantage should be weighed against potential complications. There are no controlled studies regarding the advantages and disadvantages of an early insulin therapy in premature infants. It has also been suggested that an added amino acid supply of 2–3 g/kg body weight and day should be started from the very first day to reduce hyperglycaemia during the adaptation and stabilisation phase, since it may stimulate endogenous insulin secretion and hence reduce the frequency and extent of neonatal hyperglycaemia <TextLink reference="52"></TextLink>. This approach should be evaluated further in controlled studies.</Pgraph>
<SubHeadline>Amino acid requirements </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">The requirements for essential amino acids are higher per kg body weight in infants, and particularly in premature infants, than in older children or adults (II).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Crystalline amino acid solutions in concentrations of 3.5–15% (osmolarity 450–1450 mosmol/l) are used in PN. Some specifics are to be taken into consideration when using amino acid solutions in children compared to adults due to the special amino acid metabolism and growth-specific requirements.</Pgraph>
<Pgraph>The composition of amino acid solutions which are suitable for infants and toddlers, have to be adapted to the demands of metabolic immaturity and requirements of physical growth. Apart from the eight classic essential amino acids (Phe, Thr, Val, Leu, Ile, Tyr, Ser, Met), cysteine, tyrosine, histidine, taurine, glutamine and arginine are regarded as essential or conditionally essential especially in premature infants (see “Information on the selection and production of amino acid solutions” in the attachment).</Pgraph>
<SubHeadline>Amino acid requirements for newborns </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Some amino acids regarded as non-essential in older children and adults are regarded as conditionally essential amino acids in newborns (II).</ListItem>
<ListItem level="1">Amino acid imbalances can result in toxic organ damage and may be involved in the development of PN-associated cholestasis (II).</ListItem>
<ListItem level="1">Ursodesoxycholic acid and the reduction of protein intake have a positive effect on the development of PN induced cholestasis in newborns (II).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>The need for essential amino acids is higher in premature infants than in older children or adults <TextLink reference="11"></TextLink>.</Pgraph>
<Pgraph>Various metabolic pathways for metabolising amino acids are immature in newborns (phenylalanine hydroxylase, tyrosine-aminotransferase, cystathionase <TextLink reference="53"></TextLink>, <TextLink reference="54"></TextLink>). As a consequence amino acids regarded as non essential in adults i.e. cysteine, tyrosine, histidine, taurine, glutamine and arginine, become “conditionally” essential amino acids in newborns <TextLink reference="55"></TextLink>, <TextLink reference="56"></TextLink>. Other amino acids like methionine quickly reach high levels because key enzymes are immature. Amino acid imbalances develop quicker in newborns than in adults or older children due to the immaturity of the neonatal metabolism. Such imbalances could have potential negative effects on organ development <TextLink reference="57"></TextLink>.</Pgraph>
<Pgraph>The plasma amino acid levels in infants receiving parent<TextGroup><PlainText>era</PlainText></TextGroup>l nutrition differ to those in breast-fed infants despite extensive endeavours to create optimised amino acid solutions for infants <TextLink reference="58"></TextLink>, <TextLink reference="59"></TextLink>, <TextLink reference="60"></TextLink>. This is partly due to the poor solubility or stability of various amino acids (e.g. glutamine, tyrosine, cysteine) such that not all admixtures can be used. The nitrogen balance is not significantly influenced by the diverse composition of amino acid solutions <TextLink reference="61"></TextLink>, <TextLink reference="62"></TextLink>.</Pgraph>
<Pgraph>The maximum intake is basically influenced by two given facts:</Pgraph>
<Pgraph>
<OrderedList>
<ListItem level="1" levelPosition="1" numString="1.">Physiological rate of protein synthesis subject to age:<LineBreak></LineBreak>According to data by Pohlandt et al. <TextLink reference="63"></TextLink>and Micheli <TextLink reference="64"></TextLink> premature infants, who are physiologically in approx. week 30 of pregnancy, have a maximum rate of protein synthesis with protein requirements of approx. 2.7 g/kg body weight/day, which returns to <2.0 g/kg body weight/day until week 40 of pregnancy. A positive nitrogen balance can usually be attained in premature infants with an amino acid intake of 2.5 g/kg body weight/day and 60–90 kcal/kg body weight/day <TextLink reference="65"></TextLink>. In individual cases an amino acid intake of up to 3.5–4 g/kg body weight/day may be necessary in order to achieve protein synthesis acc<TextGroup><PlainText>ordin</PlainText></TextGroup>g to the intrauterine ratio <TextLink reference="64"></TextLink>.</ListItem>
<ListItem level="1" levelPosition="2" numString="2.">Urea and ammoniac concentrations in plasma:<LineBreak></LineBreak>The urea production rate is a sensitive measurement for amino acid utilisation. Monitoring plasma concentrations of functional proteins like, for example, prealbumin, fibrinogen or retinol binding protein can provide information about the sufficient amino acid supply of the liver. It should be considered that strong insulin secretion due to high glucose intake guides the n-flow to the muscles. </ListItem>
</OrderedList>
</Pgraph>
<Pgraph>Nitrogen balance studies in premature infants receiving parenteral nutrition show that approx. 380 mg (70%) are retained from an intake of 530 mg nitrogen, similar to the ratios found in enteral nutrition <TextLink reference="66"></TextLink>, <TextLink reference="67"></TextLink>. Amino acid imbalances in PN are also discussed as a factor for developing cholestasis in young infants (a frequent side effect of long-term PN; up to 50% of long-term ELBW-premature infants receiving parenteral nutrition develop cholestasis <TextLink reference="68"></TextLink>) <TextLink reference="18"></TextLink>, <TextLink reference="69"></TextLink>, <TextLink reference="70"></TextLink>.</Pgraph>
<SubHeadline>Amino acid requirements in older children and teenagers</SubHeadline>
<Pgraph>References are made to the recommendations for enteral intake of amino acids due to insufficient data regarding the parenteral intake of amino acids in older children <TextLink reference="71"></TextLink> (see Table 2 <ImgLink imgNo="2" imgType="table"/>).</Pgraph>
<SubHeadline>Lipid emulsions</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Lipid emulsions are an integral component of longer-term PN in children (C).</ListItem>
<ListItem level="1">Lipid emulsion should usually amount to approx. 25–40% of the non-protein energy in patients receiving total parenteral nutrition (C).</ListItem>
<ListItem level="1">A glucose intake over 18 g/kg body weight and day induces net lipogenesis in infants and should generally be avoided (B).</ListItem>
<ListItem level="1">To prevent a deficiency of essential fatty acids, a minimum intake of 0.25 g/kg body weight and day of linoleic acid is recommended in premature infants and a minimum intake of 0.1 g/kg body weight and day linoleic acid is recommended in full-term newborns and children (C). </ListItem>
<ListItem level="1">In infants the parenteral lipid intake should usually not exceed 3–4 g/kg body weight and day (0.13–0.17 g/kg body weight and h) (B) generally and in older children it should not exceed 2–3 g/kg body weight and day (0.08–0.13 g/kg body weight and h) (C).</ListItem>
<ListItem level="1">Premature infants, full-term newborns and infants should usually receive lipid emulsions over 24 h (B) or in case of cyclic infusion after the first few months of life along with the residual PN (C).</ListItem>
<ListItem level="1">Triglyceride concentrations in serum or plasma should be specified in patients receiving lipid emulsions especially if there is increased risk of hyperlipidemia (e.g. high lipid intake, catabolism, sepsis, ELBW) (C). </ListItem>
<ListItem level="1">A reduction in lipid intake should be considered if triglyceride concentrations in serum or plasma in continuous infusions exceed 250 mg/dl (2.8 mmol/l) in infants or 400 mg/dl (4.5 mmol/l) in older children (C). </ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Lipid emulsions are used in PN in paediatric patients as they provide an energy source with low osmolarity and high energy content per volume unit. In addition, they also safeguard the essential fatty acid supply. The CO<Subscript>2</Subscript> production is lowered compared to PN with a high proportion of carbohydrates <TextLink reference="72"></TextLink>, <TextLink reference="73"></TextLink>, <TextLink reference="74"></TextLink>. The nitrogen metabolism can be improved by adding lipid emulsions to PN <TextLink reference="75"></TextLink>, <TextLink reference="76"></TextLink>, <TextLink reference="77"></TextLink>. </Pgraph>
<Pgraph>Lipid oxidation depends on the overall energy intake and consumption, intake of carbohydrates and triglycerides and the carbohydrate/lipid ratio <TextLink reference="72"></TextLink>, <TextLink reference="73"></TextLink>. Lipid oxidation decreases as the carbohydrate intake increases and is replaced by lipid storage. Lipogenesis takes place in infants with a carbohydrate intake of 18 g/kg/day and above <TextLink reference="39"></TextLink>, <TextLink reference="72"></TextLink>. In older children the level of carbohydrate intake, above which net lipid deposition takes place, is lower. Lipid oxidation reaches its maximum at a parenteral lipid intake of 40% of non-protein energy intake in neonates <TextLink reference="74"></TextLink> or 50% in infants <TextLink reference="72"></TextLink>. Generally a lipid intake of 25–40 % of non-protein calories is recommended.</Pgraph>
<Pgraph>A deficiency of essential fatty acids can be biochemically shown in parenterally fed premature infants only after a few days with continuous glucose but not lipid infusion <TextLink reference="78"></TextLink>, <TextLink reference="79"></TextLink>, <TextLink reference="80"></TextLink>. At least 0.25 g/kg body weight/day of linoleic acid should be administered to premature infants in order to prevent a deficiency of essential fatty acids <TextLink reference="80"></TextLink>, <TextLink reference="81"></TextLink>. An intake of 0.1g/kg body weight/day is probably sufficient in full-term infants and older children. The different linoleic acid content in varying lipid emulsions has to be taken into consideration in the calculation for lipid intake. It is difficult to define the minimum requirements of alpha linolenic acid. The majority of data on this subject has been gained from animal experiments <TextLink reference="82"></TextLink>. In children there is only one case study on alpha linolenic acid deficiency <TextLink reference="83"></TextLink>. All lipid emulsions used in Germany contain alpha linolenic acid.</Pgraph>
<Pgraph>It is also difficult to define the upper limit for lipid intake. In premature infants an intake of 3 g/kg body weight/day is well tolerated as a continuous infusion according to the concentration of plasma triglycerides and cholesterol and also the ratio of non-esterified fatty acids/albumin <TextLink reference="84"></TextLink>, <TextLink reference="85"></TextLink>, <TextLink reference="86"></TextLink>. In premature infants it may be desirable to achieve a lipid intake surpassing the oxidation capacity in order to attain weight gain and lipid deposition. Caution is, however, recommended in premature infants weighing less than 1000 g as tolerance to intravenous lipid emulsions may be more limited <TextLink reference="87"></TextLink>. </Pgraph>
<Pgraph>Maximum lipid oxidation of 4 g/kg body weight/day is attained in full-term infants with a glucose intake below 18 g/kg per day <TextLink reference="73"></TextLink>, <TextLink reference="75"></TextLink>. </Pgraph>
<Pgraph>It is important to monitor plasma triglycerides because lipid utilisation varies depending on age, the severity of the illness and various other factors. </Pgraph>
<Pgraph>An increase in the concentration of plasma triglycerides is to be expected if the infusion speed of the lipid emulsions exceeds the speed of hydrolosis of the triglycerides. </Pgraph>
<Pgraph>In premature infants the gradual increase in lipid intake compared to immediate administration of the target amount did not result in raised lipid tolerance <TextLink reference="88"></TextLink>. If a gradual increase of 0.5 to 1 g/kg per day is carried out, this can serve the purpose of monitoring with measurements of plasma triglycerides concentrations. </Pgraph>
<Pgraph>In premature infants tolerance of a lipid infusion is raised by continuous versus intermittent administration <TextLink reference="84"></TextLink>, <TextLink reference="86"></TextLink>, <TextLink reference="88"></TextLink>. In stable patients intermittent administration can also be carried out within the framework of cyclic home PN.</Pgraph>
<Pgraph>The speed of triglyceride hydrolysis depends on lipoprotein lipase activity. The activity of the post heparin lipoprotein lipase can be raised by administering heparin but this does not increase lipid utilisation <TextLink reference="89"></TextLink>, <TextLink reference="90"></TextLink>. Raised lipoprotein lipase activity results in increased non-esterified fatty acids, which are not necessarily metabolised at the same speed <TextLink reference="90"></TextLink>, <TextLink reference="91"></TextLink>. </Pgraph>
<Pgraph>Lipid supply may result in enhanced lipid peroxidation and the formation of free radicals <TextLink reference="92"></TextLink>, <TextLink reference="93"></TextLink>, <TextLink reference="94"></TextLink>. An increased lipid utilisation by reducing the carbohydrate/lipid ratio, at a constant lipid intake and therefore reduced energy intake, results in a reduction of lipid peroxidation and free radical formation <TextLink reference="92"></TextLink>. PN should be supplem<TextGroup><PlainText>ente</PlainText></TextGroup>d with multi-vitamin preparations including both vitamin C and vitamin E (alpha-tocopherol) which have anti-oxidative effects <TextLink reference="95"></TextLink>, <TextLink reference="96"></TextLink>, <TextLink reference="97"></TextLink>.</Pgraph>
<Pgraph>PN with 20% lipid emulsions results in more physiological phospholipid and cholesterol levels, due to its low phospholipid content compared with PN containing classic 10% lipid emulsions <TextLink reference="98"></TextLink>. At the same time there is, however, a lower proportion of long-chain polyunsaturated fatty acids (LC-PUFA) contributed by the phospholipid emulsifier. LC-PUFAs are “conditionally” essential for premature infants. Deficiency could result in malformations of the retina and central nervous system <TextLink reference="99"></TextLink>, <TextLink reference="100"></TextLink>.</Pgraph>
<SubHeadline>Vitamin requirements</SubHeadline>
<Pgraph>No age differentiation is indicated in literature due to the limited data situation.</Pgraph>
<SubHeadline>Neonatal patients, older children and teenagers</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Vitamin supplementation should be given during parenteral nutrition (C). </ListItem>
<ListItem level="1">The vitamin requirements of premature infants and newborns (excluding Vitamin D and K) as well as in infants and children have not been extensively e<TextGroup><PlainText>xa</PlainText></TextGroup>mined (IV).</ListItem>
<ListItem level="1">No parenteral vitamin supplement available on the German market meets the current recommendations for premature infants (IV).</ListItem>
<ListItem level="1">Vitamin preparations should, if possible, be administered together with the lipid emulsion (C).</ListItem>
<ListItem level="1">Premature and ill full-term infants should be given their first two doses of Vitamin K subcutaneously/intramuscularly or intravenously (II).</ListItem>
<ListItem level="1">An oral intake of 1000 IU Vitamin D/day is adequate in extremely premature infants (II).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>The optimum time to begin vitamin supplementation in newborns and premature infants is not clear. It should be taken into consideration, that water soluble vitamins, with the exception of Vitamin B12, are inadequately stored. Insufficient thiamine intake can result in severe lactic acidosis within only a few days in children on PN <TextLink reference="101"></TextLink>. It is, therefore, recommended that vitamin substitution is started early with PN. </Pgraph>
<Pgraph>Vitamin intake should be administered daily. All clinical studies have been carried out with commercially available vitamin preparations, therefore existing intake recommendations <TextLink reference="11"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="102"></TextLink> are based on the composition of available preparations. At this time there is no commercially produced vitamin supplement available on the market, which completely meets the current intake recommendations for premature infants as a supplement for long-term PN. </Pgraph>
<Pgraph>In the practical administration of PN it should be considered that vitamins can be degraded by oxygen, light and heat. Degradation reactions can be accelerated by catalytically active trace elements like copper and iron. Fat-soluble vitamins can be adsorbed on specific synthetic materials (infusion needles) in rare cases. Thus, the administered dose is uncontrolled and significantly reduced <TextLink reference="103"></TextLink>. In Europe, combined preparations are available which, by dissolving the vitamins in a lipid emulsion, reduce absorption on plastic. Furthermore, the formation of peroxides in lipid emulsions can be reduced by adding multi-vitamin preparations <TextLink reference="104"></TextLink>. Vitamin preparations should, if possible, be administered together with the lipid emulsion. The clinical impact of free radicals, which can develop in intravenous multi-vitamin emulsions when exposed to light, is being currently discussed. They can result in an increase in peroxide excretion in urine of newborns <TextLink reference="105"></TextLink>. Feed lines with light protection should be used when administering parenteral solutions with vitamins until the clinical significance of these results has been determined <TextLink reference="106"></TextLink>. </Pgraph>
<Pgraph><Mark2>Vitamin D rickets prophylaxis</Mark2>: Oral vitamin D prophylaxis with 1000 IU Vitamin D/day per os from day seven of life is sufficient as a prophylaxis in extremely premature infants <TextLink reference="107"></TextLink>. </Pgraph>
<Pgraph><Mark2>Vitamin K prophylaxis</Mark2>: Premature infants (<week 35 of pregnancy) and ill full-term infants should receive their first two doses of Vitamin K prophylaxis intramuscularly, subcutaneously or intravenously due to the unclear resorption from the gastrointestinal tract <TextLink reference="108"></TextLink>, <TextLink reference="109"></TextLink>. The dose of intravenous Vitamin K prophylaxis is still being discussed at present. Vitamin K levels after one administration of 1 mg Vit K intramuscularly on the first day of life were higher in premature infants than in full-term infants <TextLink reference="110"></TextLink>.</Pgraph>
<Pgraph>Detailed specifications can be found in the “Guidelines on Paediatric Parenteral Nutrition” from ESPGHAN and ESPEN <TextLink reference="1"></TextLink>.</Pgraph>
<SubHeadline>Trace element requirements</SubHeadline>
<Pgraph>No age differentiation is indicated in literature on account of the limited data situation.</Pgraph>
<SubHeadline>Neonatal patients, older children and teenagers</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">The optimum time to begin with trace element supplementation in premature infants <1500 g birth weight is not clear. We recommend beginning supplementation to coincide with an increase in body weight (5<Superscript>th</Superscript> day of life) (C).</ListItem>
<ListItem level="1">The trace element requirements of premature infants and newborns as well as children have not undergone extensive testing (IV).</ListItem>
<ListItem level="1">A parenteral trace element supplement, which meets the current intake recommendations, is not available on the German market (II).</ListItem>
<ListItem level="1">Trace elements should be supplemented in long-term PN (C).</ListItem>
<ListItem level="1">Zinc deficiency has to be excluded in infants and children with unclear, poor development (especially linear growth) and/or skin efflorescences (typically on acra, mechanically burdened parts of the body or in the nappy region) or diarrhoea (II).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Trace element requirements and optimum time to begin supplementation in premature and full-term infants, as well as infants and children, are not completely clear. The enteral absorption of trace elements in partial-parenteral nutrition mainly depends on the existing compound and the composition of the nutrition <TextLink reference="111"></TextLink> such that it is extremely difficult to evaluate the remaining parenteral needs. Requirements for some trace elements have at least been narrowed down by controlled studies <TextLink reference="102"></TextLink>, <TextLink reference="111"></TextLink>, <TextLink reference="112"></TextLink>, <TextLink reference="113"></TextLink>, <TextLink reference="114"></TextLink>. There is no trace element supplement for long-term PN which meets the current recommendations <TextLink reference="102"></TextLink>. In long-term PN (>7 days), where enteral nutrition provides less than 50% of the energy intake, we recommend administering trace element supplements according to manufacturer instructions. </Pgraph>
<Pgraph>Premature and ill full-term infants have an increased risk of developing a trace element deficiency. Premature infants are born with lower trace element stores as the laying down of these stores occurs during the last trimester of the pregnancy. Rapid growth at unidentified requirement levels and variable resorption are further risk factors contributing to the development of a trace element deficiency in premature infants <TextLink reference="115"></TextLink>. In ill full-term infants the requirements and intake vary according to the basic illness. The optimum time to begin supplementation is disputed.</Pgraph>
<Pgraph><Mark2>Zinc</Mark2>: Zinc deficiency should be considered in newborns where the reason for unclear, poor development (especially linear growth) and/or skin efflorescences (acra, mechanically burdened parts of the body) are not clear <TextLink reference="116"></TextLink>, <TextLink reference="117"></TextLink>. A multitude of case studies have been published on zinc deficiency in neonates <TextLink reference="116"></TextLink>. Rare genetically-related trace element metabolic disorders are also to be considered in the case of unclear clinical symptoms <TextLink reference="117"></TextLink>.</Pgraph>
<SubHeadline>Other supplements </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">There is no documentation indicating a benefit from parenteral supplementation of glutamine or arginine in children (C). </ListItem>
<ListItem level="1">Carnitine supplementation should be considered in individual cases in premature and newborn infants on PE (B).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Tests on <Mark2>arginine</Mark2> supplementation <TextLink reference="118"></TextLink> in adult intensive care patients as well as some studies on enteral or parenteral <Mark2>glutamine</Mark2> administration in newborns show potential positive effects <TextLink reference="119"></TextLink>, <TextLink reference="120"></TextLink> (II), although these are controversially discussed. There is no evidence from meta analyses to document the benefit of the parenteral supplementation of glutamine or arginine in premature and newborn infants <TextLink reference="121"></TextLink>. </Pgraph>
<Pgraph><Mark2>Vitamin A</Mark2> is necessary for physiological lung growth (lung epithelial cells). A meta-analysis, which is based on seven randomised, controlled studies, documents the effectiveness of a supranutritive Vitamin A supplementation on reducing oxygen requirements and improving survival at one month of age in premature infants with a birth weight <1000 g. There is a tendency towards lower values regarding the incidence of retinopathy in premature infants <TextLink reference="122"></TextLink>, <TextLink reference="123"></TextLink> (I). The authors of the systematic analysis of the Cochrane database feel there is a need to carry out further studies on the effects of intravenous Vitamin A supplementation.</Pgraph>
<Pgraph><Mark2>Carnitine</Mark2> is necessary for the transportation of long-chain fatty acids via the mitochondrial membrane and its oxidative metabolism. Carnitine is found in breast milk and baby foods, but is not usually added to conventional PN. Low carnitine levels have been measured in body tissues in premature infants on PN <TextLink reference="124"></TextLink>. The clinical significance of this has not been determined. An impairment in fatty acid oxidation is only to be anticipated where a massive drop in serum carnitine concentrations occurs. For the metabolic availability of carnitine its free nonesterified percentage, is essential. The availability of free carnitine is reflected in the concentration and the acyl-carnitine/free carnitine (AC/FC) ratio. This ratio is in dynamic equilibrium with the intramitochondrial acyl-CoA/free CoA ratio. Lower intramitochondrial CoA-availability is assumed with an AC/FC ratio >0.4 (>0.7 when fasting) Carnitine supplementation results in a release of intramitochondrial CoA and should be considered in case of an explicit AC/FC ratio. A meta analysis (based on 14 randomised, controlled studies) showed there to be no effect of carnitine supplementation on the metabolism of lipids, lipogenesis or weight gain <TextLink reference="125"></TextLink>.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Practical procedure">
<MainHeadline>Practical procedure</MainHeadline>
<SubHeadline>Short, medium and long-term (partial) parenteral nutrition</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">The utilisation of an adapted glucose/electrolyte solution (usually 10% glucose) with potassium and sodium supplementation in short-term (<48 h) intravenous intake is recommended in well-nourished toddlers and school children without specific metabolic or nutritional risks (IV).</ListItem>
<ListItem level="1">An adapted glucose/electrolyte solution (usually 10% glucose) with the required supplementation of sodium, potassium, amino acids, lipids and vitamins should be administered in medium-term PN (>2–7 days) (IV).</ListItem>
<ListItem level="1">An additionnal supplementation of magnesium, phosphate, and trace elements (where enteral nutritional provides 50% of the energy intake or less) should be administered in long-term PN (>7 days) (IV).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>If intravenous intake is required in well-nourished toddlers and school children without specific metabolic or nutritional risks, the following situations should be considered when anticipating duration: </Pgraph>
<Pgraph>I: short-term parenteral intake for less than 48 h. <LineBreak></LineBreak>II: medium-term parenteral nutrition for 2 to 7 days.<LineBreak></LineBreak>III: long-term PN for >7 days.</Pgraph>
<Pgraph>
<UnorderedList>
<ListItem level="1">It makes sense to differentiate between short, medium and long-term parenteral intake, because the procedure varies according to the duration of PN </ListItem>
<ListItem level="1">The utilisation of an adapted glucose/electrolyte solution (usually 10% glucose) with potassium and sodium supplementation in short-term (<48 h) intravenous intake is recommended in well-nourished toddlers and school children without specific metabolic or nutritional risks (IV).</ListItem>
<ListItem level="1">An adapted glucose/electrolyte solution (usually 10% glucose) with the required supplementation of sodium, potassium, amino acids, lipids and vitamins should be administered in medium-term PN (>2–7 days) (IV).</ListItem>
<ListItem level="1">An additional supplementation of magnesium, phosphate, and trace elements (where enteral nutritional provides 50% of the energy intake or less) should be administered in long-term PN (>7 days).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Newborns and infants </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">There should be a written concept on the provision of PN in order to minimise errors (C). </ListItem>
<ListItem level="1">Newborns can be divided up into the following groups with regard to their nutrient requirements and PN-support in order to minimise errors: </ListItem>
<UnorderedList>
<ListItem level="2">premature infants <1500 g,</ListItem>
</UnorderedList>
<UnorderedList>
<ListItem level="2">premature infants >1500 g,</ListItem>
</UnorderedList>
<UnorderedList>
<ListItem level="2">ill full-term infants (C).</ListItem>
</UnorderedList>
<ListItem level="1">The actual amount of PN administered must be calculated (not estimated) in neonates (avoid rounding error) (C).</ListItem>
<ListItem level="1">The use of PN standard solutions can reduce the the risk of errors.</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Due to the heterogeneity in pathophysiology and the differing maturity of patients it may be necessary to vary procedures during the neonatal period (e.g. fluid volumes, electrolyte substitution etc.). Classification according to, for example, birth weight is recommended for the calculation of PN in neonates: </Pgraph>
<Pgraph>
<UnorderedList>
<UnorderedList>
<ListItem level="2">premature infants <1500 g, </ListItem>
</UnorderedList>
<UnorderedList>
<ListItem level="2">premature infants >1500 g, and </ListItem>
</UnorderedList>
<UnorderedList>
<ListItem level="2">ill full-term infants.</ListItem>
</UnorderedList>
</UnorderedList>
</Pgraph>
<Pgraph>This differentiation makes sense with regards to variations in the administration of different nutrients. The described protocol can result in the procedures in (partial) parenteral nutrition being structured during the daily clinical routine and errors minimised. </Pgraph>
<Pgraph>A standardised questionnaire or electronic programme, which takes into account partial parenteral nutrition and enteral nutrition (see Table 3 <ImgLink imgNo="3" imgType="table"/> for an example of a procedure questionnaire), should be used for prescribing PN to neonates.</Pgraph>
<Pgraph>The prescription of nutrition for neonates must be calculated and not estimated in order to ensure the nutrient intake in neonates and infants is adapted to their specific needs.</Pgraph>
<SubHeadline>PN in premature infants and newborns</SubHeadline>
<SubHeadline2>PN in the adaptation and stabilisation phase after birth</SubHeadline2>
<Pgraph>
<UnorderedList>
<ListItem level="1">There is no evidence-based data on the scale of postpartal weight loss required during the adaptation and stabilisation phase for long-term development (IV).</ListItem>
<ListItem level="1">Amino acid and lipid supply should begin on the first day of life (B).</ListItem>
<ListItem level="1">The fluid intake in premature infants <1500 g should only replace the estimated losses in the first days of life (mainly perspiratio insensibilis). Electrolyte supplementation is often not necessary (B). </ListItem>
<ListItem level="1">The incidence of hyperkaliaemia can be lowered by supplementing PN with 1 g amino acids from the first day of life in premature infants <1500 g (II).</ListItem>
<ListItem level="1">The maximum parenteral intake of amino acids should be between 2 and max. 4 g/kg body weight per day in premature infants and newborns (B). </ListItem>
<ListItem level="1">Max. lipid intake should not exceed 3–4 g/kg body weight per day in premature infants and newborns (B). </ListItem>
<ListItem level="1">Restricted fluid management with limited supply of sodium chloride results in a reduction in the amount of days with respiratory aids or respiratory therapy (II).</ListItem>
<ListItem level="1">The early enteral (re)establishing of solid foods (within <4 days after the birth) in premature infants lowers the incidence nosocomial infections, the duration of PN and the frequency in the utilisation of central venous catheters (I).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline2>Commentary</SubHeadline2>
<Pgraph>In premature infants and full-term newborns there is a period of adaptation and maturation which occurs in the first seven days after birth (see “Physiological principles” above) which requires daily adjustments in the nutrient intake of ill full-term and premature infants. There is surprisingly little evidence-based data on physiology and nutrient requirements for this stage of life (optimum weight loss, optimum time to begin amino acid and lipid supply). Lipid (0.5–1 g/kg body weight/day) and amino acid intake (0.5–1 g/kg body weight/day) should begin on the first day of life <TextLink reference="126"></TextLink>, and a stepwise increase in amino acid intake to max. 2–3(–4) g/kg body weight/day and lipid intake to 3–4 g/kg body weight/day is widely practised and results in more rapid achievement of a positive nitrogen balance <TextLink reference="52"></TextLink>, <TextLink reference="127"></TextLink>. Questions remain with regard to extremely small premature infants with a birth wieght <800 g with regard to potential adverse effects of early intravenous lipid intake on the first day of life <TextLink reference="128"></TextLink>. A restricted fluid volume improves the outcome of neonates considerably by lowering the “perspiratio insensibilis” <TextLink reference="129"></TextLink>. In premature infants a restrictive “dry” fluid management with sodium chloride restriction seems to have a favourable effect on the duration of respiratory aids / respiratory therapy <TextLink reference="130"></TextLink>, <TextLink reference="131"></TextLink>, <TextLink reference="132"></TextLink>. Only the losses should be replaced in the first days of life in premature infants under 1500 g birth weight <TextLink reference="17"></TextLink>. The incidence of hyperkaliaemia can be lowered by supplementing 1 g amino acids from the first day of life in this patient group. The early (re)establishing of enteral nutrition(<4 days after birth) lowers the incidence of nosocomial infections, the duration of (partial) parenteral nutrition and the utilisation of central venous catheters compared to later (re)establishing <TextLink reference="133"></TextLink>, <TextLink reference="134"></TextLink>. </Pgraph>
<SubHeadline2>PN in premature infants and newborns in the phase of continual growth</SubHeadline2>
<Pgraph>
<UnorderedList>
<ListItem level="1">Parenteral nutrition should be the exception in neonatal patients during the phase of continuous growth. If necessary, treatable reasons for delayed enteral (re)establishing of nutrition should be ascertained (C).</ListItem>
<ListItem level="1">The energy requirement shows great intraindividual and interintervidual variability (II).</ListItem>
<ListItem level="1">The energy intake can be adapted to the weight gain, whereby weight development should aim to be close to the intrauterine growth curve (C). </ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline2>Commentary</SubHeadline2>
<Pgraph>The enteral (re)establishing of nutrition is usually completed in the first week of the continual growth phase (about the 2<Superscript>nd</Superscript> week of life) in premature infants and sick full-term infants. If PN is also required during this phase, treatable reasons for delayed enteral (re)establishing of nutrition should be ascertained. The energy requirements show great variability in this stage of life. They can be estimated according to weight development compared to intrauterine growth curves (if other reasons for growth not following percentiles have been excluded, it should be assumed that a too low energy intake will result in a decline and a too high energy intake will result in gains compared to intrauterine percentiles). The necessary energy to build up 1 g body tissue varies with the lipid content of the newly formed tissue (20–40%) but averages at approx. 5 kcal/g. The proportion of the newly formed fatty tissue is influenced by the nutritional regime. It should be considered with lesser fatty tissue built up, the energy required for growth is lower <TextLink reference="135"></TextLink>.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Methods of access">
<MainHeadline>Methods of access</MainHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Peripheral vein cannulae have a lower complication rate compared to central access points and should be used in infants whenever possible (II). </ListItem>
<ListItem level="1">A routine heparin supply to prevent thrombosis or to proling central venous catheter survival time has no proven benefit in infants and is not recommended (Ib).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Peripheral commercial vein cannulae (PCVC) have a lower complication rate in infants (infection, thrombosis) than central venous catheters (CVC) <TextLink reference="20"></TextLink>. Peripheral commercial vein cannulae (PCVC) can be used in partial or total parenteral nutrition if the osmolarity and state of the veins allow for this (risk of paravasatation/skin necrosis!). </Pgraph>
<Pgraph>Long-term total parenteral nutrition often cannot be applied safely in older children or teenagers without central venous catheters (CVC) due to the osmolarity. An individual decision is required on the choice of access while taking into consideration the underlying illness, therapy, osmolarity of the nutritional solution used or drugs and the expected duration.</Pgraph>
<Pgraph>Two meta-analyses showed no positive effect of heparin supply on central venous catheter lifetime or the formation of thromboses in neonates with percutanous central venous catheters <TextLink reference="136"></TextLink>, <TextLink reference="137"></TextLink>.</Pgraph>
<SubHeadline>Use of standardised or individually tailored PN solutions</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">After requirements have been calculated, standard solutions (e.g. produced by the hospital pharmacy), which are adapted to suit the specific nutrient needs of the respective age group, can be administered in short-term PN (B).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Using ready-made standard solutions requires fewer personnel and allows for less risk regarding dosage errors or microbial contamination. Individually mixed infusions can be adapted to individual characteristics. Standard solutions are suitable for short-term total and partial PN <TextLink reference="138"></TextLink>.</Pgraph>
<SubHeadline>PN provision </SubHeadline>
<Pgraph>A standardised procedure should be followed and the individual steps systematically documented in order to minimise errors. Computer programmes, which enable the fast and exact calculation of enteral and parenteral intake, are recommended (and in part commercially available). The fluid, glucose and electrolyte intakes and additional intakes with drugs can be calculated. </Pgraph>
<Pgraph>The following aspects should be considered: Estimation of the required duration of PN, enteral nutrition, fluid intake, protein and lipid intake, parenteral vs enteral/oral intakes, electrolyte/vitamin and trace element supply, concentration of the glucose solution, infusion speed, monitoring, and validation (see Table 3 <ImgLink imgNo="3" imgType="table"/> “Example of a procedure questionnaire”).</Pgraph>
<SubHeadline>Neonatal patients</SubHeadline>
<Pgraph>A practical example is shown in Table 4 <ImgLink imgNo="4" imgType="table"/>, which illustrates the (re)establishing of enteral food in newborns during the adaptation and stabilisation phase.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Measures to reduce side-effects of PN">
<MainHeadline>Measures to reduce side-effects of PN</MainHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Procedures should be standardised wherever possible in order to minimise errors in the provision or preparation of partial (PPN) or total PN (TPN).</ListItem>
<ListItem level="1">Minimum enteral nutrition minimises the time until (re)establishing of total enteral nutrition and LOS (Length of Hospital Stay) (I).</ListItem>
<ListItem level="1">Non-nutritive sucking during PN reduces LOS (I).</ListItem>
<ListItem level="1">There is a specific risk of developing osteopenia due to the rapid bone growth in premature and full-term infants (III). Osteopenia prophylaxis should be started enterally once the (re)establishing of enteral nutrition has been completed without complications (C).</ListItem>
<ListItem level="1">In order to determine appropriate Ca and P intakes, the Ca and P excretion can be assesed in spot urine samples (B).</ListItem>
<ListItem level="1">The optimum duration of Ca and P supply is unclear (IV), but it appears reasonable to provide a Ca and P supply up to the corrected third month of life in premature infants with a birth weight <1500 g (C). </ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<SubHeadline2>Minimum enteral nutrition</SubHeadline2>
<Pgraph>Total PN reduces the functional and structural integrity of the gastrointestinal mucosa, the secretion of gastrointestinal hormones and the activity of mucosal enzymes like lactase <TextLink reference="139"></TextLink>, resulting in an intolerance to enteral nutrition and an extension of LOS (Length of Hospital Stay). A meta-analysis of eight randomised studies <TextLink reference="134"></TextLink> investigated the effect of minimum enteral nutrition (<25 kcal/kg body weight/day for >5 days) on the development of food intolerance in at-risk premature infants (<1500 g birth weight, <week 33 of gestation) in comparison to total PN. The duration of (re)establishing of nutrition and LOS was significantly reduced. There was no effect on the incidence of necrotising enterocolitis. Side-effects of minimal enteral nutrition cannot be definitely excluded due to the inhomogeneity of the patients included and their low number <TextLink reference="134"></TextLink>.</Pgraph>
<SubHeadline2>Non-nutritive sucking </SubHeadline2>
<Pgraph>A meta-analysis (based on 14 randomised, controlled studies) documented a significant reduction in LOS through non-nutritive sucking in premature infants. No effects have been found on weight gain, energy intake, oxygen saturation, total intestinal transit or heart rate <TextLink reference="140"></TextLink>. </Pgraph>
<SubHeadline2>Osteopenia prophylaxis in premature infants <1500 g</SubHeadline2>
<Pgraph>Due to their high growth rate, premature infants have high calcium and phosphate requirements which cannot be met through breast milk or infant formula. Therefore, premature infants with a very low birth weight (<1500 g) are particularly at risk of developing osteopenia. Osteopenia in premature infants is linked to an increased incidence of fractures, prolonged respiratory therapy or requirement for respiratory aids and the development of a dolichocephalus <TextLink reference="141"></TextLink>, <TextLink reference="142"></TextLink>. Premature infants under 1500 g birth weight should receive Ca/P supplementation depending on their individual requirements. The optimum duration of supplementation is unclear. We recommend supplementation in premature infants with a birth weight <1500 g up to corrected third month of life. The Ca and P excretion from spot urine specimens may be used to adapt the Ca and P supply to requirements, which vary according to growth <TextLink reference="143"></TextLink>, <TextLink reference="144"></TextLink>.</Pgraph>
<SubHeadline>Monitoring</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Due to the low blood volume in infants, staff at facilities in which infants receive medium and long-term parenteral nutrition must have access to a special laboratory with micromethods (IV).</ListItem>
<ListItem level="1">Careful monitoring of the fluid volume must be carried out in premature infants due to their high fluid volume, high body water content in comparison to older patients and immature regulatory mechanisms (IV).</ListItem>
<ListItem level="1">Dehydration in premature infants, with immature kidneys, leads to hyperchloraemia prior to the development of acidosis as one of the first lab signs. </ListItem>
<ListItem level="1">The measurement of the specific weight or osmolarity of urine can only be drawn upon in premature infants and newborns in the first weeks of life when high <TextGroup><PlainText>values</PlainText></TextGroup> are measured. Low (normal) values can be due to low renal concentrating ability in premature infants and newborns as a result of immature kidneys (II).</ListItem>
<ListItem level="1">Daily clinical tests, fluid balances, acid-base status, electrolytes and blood sugar are required during the initial phase of PN, depending on the maturity and illness of neonates, (C). </ListItem>
<ListItem level="1">In medium and long-term PN, routine clinical tests should also be accompanied by the following: documentation of weight, length and head circumference development (in percentile questionnaires), weekly evaluation of acid base status, blood sugar, electrolytes, haematocrit, urea, creatinine, at least one transaminase, Y-GT, urine osmolarity or specific weight (alkaline phosphatase every two weeks) (C). </ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Daily clinical tests, to include the monitoring of the fluid balance, checks of the acid base status, electrolytes and blood sugar, are usually required in the initial phase of PN depending on the age and maturity of the children and their underlying illness. In medium and long-term PN, routine clinical tests should also be accompanied by the following: documentation of weight, length and head circumference development (in percentile questionnaires), weekly evaluation of acid base status, blood sugar, electrolytes, haematocrit, urea, creatinine, at least one transaminase, Y-GT, urine osmolarity or specific weight (alkaline phosphatase every two weeks).</Pgraph>
<SubHeadline>Lipids</SubHeadline>
<Pgraph>The concentration of plasma triglycerides at which undesirable effects occur is not known <TextLink reference="145"></TextLink>. Average triglyceride concentrations of 150 to 200 mg/dl and above are often specified in infants fed with breast milk or infant formula <TextLink reference="86"></TextLink>, <TextLink reference="146"></TextLink>. Values of 250 mg/dl in healthy infants are not unusual. In older children higher concentrations of up to 300 and 400 mg/dl can also be acceptable as the lipoprotein lipase doesn’t become saturated until approx. 400 mg/dl <TextLink reference="147"></TextLink>. When gradually introduced, plasma triglycerides should be initially checked on a weekly basis for every 1 g/kg lipid intake increase and after reaching maximum intake levels.</Pgraph>
<SubHeadline>Newborns </SubHeadline>
<Pgraph>Monitoring the fluid balance in premature infants and sick newborns is extremely important due to their high fluid volume, high body water content in comparison to older patients and immature regulatory mechanisms (see above). Monitoring must take the special physiological features of neonates into consideration to be efficient:</Pgraph>
<Pgraph>
<UnorderedList>
<ListItem level="1">The measurement of the specific weight or osmolarity of urine are only indicative in premature infants and newborns in the first weeks of life when high values are measured. Low (normal) values can be due to low renal concentrating ability in premature infants and newborns because of immature kidneys.</ListItem>
<ListItem level="1">The immaturity of the kidney in premature infants in case of dehydration leads to hyperchloraemia prior to the development of acidosis as one of the first lab-chemical signs.</ListItem>
<ListItem level="1">Due to the low blood volume in neonates, staff at facilities in which neonates can receive medium and long-term parenteral nutrition must have access to a special laboratory with micro methods.</ListItem>
</UnorderedList>
</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Attachment">
<MainHeadline>Attachment</MainHeadline>
<SubHeadline>Information on the selection and production of amino acid solutions </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Several metabolic pathways involved in the synthesis of amino acids are still immature in newborn and premature infants. As a result, some amino acids, which are regarded as non-essential for adults, may become conditionally essential (e.g. cysteine, tyrosine, histidine, taurine, and glutamine). In addition, individual plasma amino acids reach clearly increased levels because significant degradation enzymes are still immature. Amino acid imbalances occur more rapidly in comparison to adults (I).</ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Increased phenylalanine concentrations are toxic for the central nervous system and can result in serious developmental disorders. Both hepatic phenylalanine hydroxylase activity and the enzymatic system of the metabolism of tyrosine are still immature in premature infants. Premature infants (<week 30 of pregnancy) with high amino acid intakes therefore have a tendency to develop hyperphenylalaninaemia and hypertyrosinaemia. </Pgraph>
<Pgraph>The enzyme activities in full-term infants result, however, in a rapid amino acid metabolism, causing low phenylalanine and tyrosine concentrations. Attempts are made to increase the low plasma tyrosine concentrations in infants receiving parenteral nutrition by supplementing with N-acetyl tyrosine, which is more soluble. Newborns and premature infants do still, however, have a reduced deacetylation capacity such that tyrosine may not be sufficiently utilised in this more soluble form <TextLink reference="148"></TextLink>, <TextLink reference="149"></TextLink>, <TextLink reference="150"></TextLink>, <TextLink reference="151"></TextLink>.</Pgraph>
<Pgraph>There is an interaction between the branched-chain and aromatic amino acids: Leucine supports the phenylalanine and tyrosine metabolism <TextLink reference="152"></TextLink>. </Pgraph>
<Pgraph><Mark2>Methionine</Mark2> is a sulphurous, essential amino acid and is regarded as the precursor to cysteine and taurine. Methionine is the major methyl group donator in the hepatic intermediary metabolism. It is converted to homocysteine through demethylation, which remethylates to methionine when tetrahydrofolic acid is introduced or which is finally converted to cysteine via a transsulfuration pathway forming cystathionine. </Pgraph>
<Pgraph><Mark2>Cysteine</Mark2> is a <Mark2>largely essential amino acid</Mark2> in both premature infants and full-term newborns due to its immature cystathionase activity. Plasma cysteine concentration is already a function of methionine intake in premature infants. It is often observed that normal <Mark2>plasma cysteine concentrations</Mark2> only occur if plasma methionine concentrations are raised. As a result cysteine supplementation of amino acid solutions is recommended in young infants <TextLink reference="153"></TextLink>, <TextLink reference="154"></TextLink>. </Pgraph>
<Pgraph>Supplementation with cysteine-HCl is not usually applied because of its low solubility and risk of acidosis. The available N-acetyl cysteine may not be effectively metabolised due to limited deacetylation and immature metabolic rates in premature infants. Procysteine, a preliminary stage of glutathione, has also been tested <TextLink reference="155"></TextLink>. </Pgraph>
<Pgraph><Mark2>Taurine</Mark2> is formed through decarboxylation of cysteine sulfinic acid, an enzyme stage that is still immature in premature infants. The foetus accumulates approx. 50–60 µmol taurine/day during the last trimester of pregnancy <TextLink reference="156"></TextLink>. </Pgraph>
<Pgraph>Taurine has many functions, not all of which are completely understood, although it is of importance to the central nervous system, retina and gastrointestinal tract. The proven relevance of the maturing of acoustically evoked potentials points to the clinical significance of taurine <TextLink reference="157"></TextLink>, <TextLink reference="158"></TextLink>. Young infants on PN are, therefore, dependent on exogenous taurine intake in order to maintain plasma concentrations <TextLink reference="157"></TextLink>, <TextLink reference="159"></TextLink>. </Pgraph>
<Pgraph><Mark2>Threonine:</Mark2> The plasma threonine concentration is directly proportional to the intake as well as inversely proportional to the gestational age in PN for premature infants <TextLink reference="160"></TextLink>. A toxicity of raised plasma threonine concentrations has not yet been proven, although it is kown that concentration levels in the brain increase proportionally to plasma concentrations.</Pgraph>
<Pgraph><Mark2>Lysine:</Mark2> Of all amino acids the materno-foetal gradient is most prominent in lysine. Plasma lysine concentrations in the foetus are approx. four times higher than those of the mother. Both lysine deficiency and surplus have negative effects on growth, brain DNA concentration and the dynamics of urea synthesis <TextLink reference="161"></TextLink>.</Pgraph>
<Pgraph><Mark2>Leucine</Mark2> influences the speed of protein synthesis in the muscles. The demand for <Mark2>branched-chain</Mark2> <Mark2>amino acids</Mark2> is greater in premature infants than in full-term infants, and thus they easily tolerate amino acid solutions with a higher concentration of branched-chain amino acids.</Pgraph>
<Pgraph><Mark2>Histidine:</Mark2> Of all essential amino acids, the plasma concentration of histidine is least influenced by the intake. Histidine is therefore regarded as a conditionally essential amino acid in young infants.</Pgraph>
<Pgraph><Mark2>Arginine:</Mark2> The arginine concentration in an amino acid solution contributes to preventing hyperammonaemia. Premature infants with asymptomatic hyperammonaemia show lower plasma concentrations of urea cycle interm<TextGroup><PlainText>ed</PlainText></TextGroup>iates, which can be normalised by raising the arginine intake. Part of the arginine requirement can also be met by ornithine, which is taken into consideration in some amino acid solutions <TextLink reference="162"></TextLink>. </Pgraph>
<SubHeadline>N-acetyl amino acids</SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">Based on recent data, it is assumed that N-acetyl amino acids are only metabolised to a limited extent in humans and therefore are only of limited significance as alternative amino acid sources in clinical nutrition (IV). </ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>There are no documented benefits of additionally administering N-acetyl cysteine due to limited deacetylation and immature metabolic rates in premature infants. </Pgraph>
<SubHeadline>Notes on differences between lipid emulsions </SubHeadline>
<Pgraph>
<UnorderedList>
<ListItem level="1">PE with a low phospholipid triglyceride ratio (e.g. in 20% lipid emulsions) results in less elevated phospholipid and cholesterol levels (II).</ListItem>
<ListItem level="1">The use of lipid emulsions on the basis of soy bean oil, an olive oil-soy bean oil mixture as well as a coconut oil (MCT)-soy bean oil mixture have been tested in paediatric patients and their use is well established (I). </ListItem>
<ListItem level="1">None of these lipid emulsions have a documented benefit regarding the attained clinical end points (C). </ListItem>
</UnorderedList>
</Pgraph>
<SubHeadline>Commentary</SubHeadline>
<Pgraph>Apart from the long established use of lipid emulsions based on soy bean oil, a new emulsion based on an olive oil and soy bean oil mixture has been available for some time and studies with this new mixture have already shown promising results in children, infants and premature infants <TextLink reference="163"></TextLink>, <TextLink reference="164"></TextLink>. Postulated benefits of the olive oil-based lipid emulsions are reduced lipid peroxidation, lower PUFA intake and higher intake of antioxidative substances. Currently data are insufficient to propose a recommendation for olive oil-based emulsions <TextLink reference="165"></TextLink>.</Pgraph>
<Pgraph>Soy bean and olive oil-based lipid emulsions contain long chain triglycerides. There are also lipid emulsions with the equal proportions of LCT and MCT from coconut oil. They contain less PUFA, and the MCT proportion is oxidised more rapidly <TextLink reference="166"></TextLink>. A further potential benefit is that oxidation of MCT is less dependent on carnitine that of LCT. The energy content of MCT per g fat is, however, approx. 16% lower than that of LCT. Studies in adults and children show a higher lipid oxidation, less influence on the parameters of the liver function, improved leukocyte function and less influence on pulmonary haemodynamics and the gas exchange than with LCT emulsions <TextLink reference="167"></TextLink>, <TextLink reference="168"></TextLink>, <TextLink reference="169"></TextLink>, <TextLink reference="170"></TextLink>, <TextLink reference="171"></TextLink>. There were no significant differences in regard to the plasma lipids and fatty acids <TextLink reference="167"></TextLink>, <TextLink reference="172"></TextLink>, <TextLink reference="173"></TextLink>, <TextLink reference="174"></TextLink>. There is differing data conc<TextGroup><PlainText>ernin</PlainText></TextGroup>g a nitrogen-saving effect when administering a MCT/LCT mixture. One study describes increased nitrogen retention <TextLink reference="175"></TextLink>, <TextLink reference="176"></TextLink>, while another study describes a more unfavourable leucine metabolism than when on LCT intake <TextLink reference="177"></TextLink>. The current studies in children and newborns <TextLink reference="125"></TextLink>, <TextLink reference="167"></TextLink>, <TextLink reference="173"></TextLink>, <TextLink reference="178"></TextLink>, <TextLink reference="179"></TextLink> do not justify any generally favoured utilisation of MCT/LCT emulsions compared to pure LCT emulsions at present <TextLink reference="165"></TextLink>, <TextLink reference="174"></TextLink>. </Pgraph>
<Pgraph>The ratio between phospholipids (PL) and triglycerides (TG) is lower in 20% lipid emulsions than in standard 10% lipid emulsions <TextLink reference="180"></TextLink>. Lipid emulsions with a low PL/TG ratio as in the standard 20% emulsions, should be favoured in PN <TextLink reference="98"></TextLink>, <TextLink reference="125"></TextLink>, <TextLink reference="181"></TextLink>, <TextLink reference="182"></TextLink>. Higher amounts of phospholipids impair the clearance of triglycerides from the plasma, resulting in an increase in the plasma triglyceride concentration and of cholesterol and phospholipids in Low-Density-Lipoproteins <TextLink reference="98"></TextLink>. The emulsion characteristics (dispersity, stability) and various incompatibilities are of great significance in the parenteral intake of lipids.</Pgraph>
</TextBlock>
<TextBlock linked="yes" name="Notes">
<MainHeadline>Notes</MainHeadline>
<Pgraph>This article is part of the publication of the Guidelines on Parenteral Nutrition from the German Society for Nutritional Medicine (overview and corresponding address under <Hyperlink href="http://www.egms.de/en/journals/gms/2009-7/000086.shtml">http://www.egms.de/en/journals/gms/2009-7/000086.shtml</Hyperlink>).</Pgraph>
<Pgraph>English version edited by Sabine Verwied-Jorky, Rashmi Mittal and Berthold Koletzko, Univ. of Munich Medical Centre, Munich, Germany.</Pgraph>
</TextBlock>
<References linked="yes">
<Reference refNo="1">
<RefAuthor>Koletzko B</RefAuthor>
<RefAuthor>Goulet O</RefAuthor>
<RefAuthor>Hunt J</RefAuthor>
<RefAuthor>Krohn K</RefAuthor>
<RefAuthor>Shamir R</RefAuthor>
<RefTitle>1. Guidelines on Paediatric Parenteral Nutrition of the European Society of Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) and the European Society for Clinical Nutrition and Metabolism (ESPEN), Supported by the European Society of Paediatric Research (ESPR)</RefTitle>
<RefYear>2005</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>S1-S4</RefPage>
<RefTotal>Koletzko B, Goulet O, Hunt J, Krohn K, Shamir R. 1. Guidelines on Paediatric Parenteral Nutrition of the European Society of Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) and the European Society for Clinical Nutrition and Metabolism (ESPEN), Supported by the European Society of Paediatric Research (ESPR). J Pediatr Gastroenterol Nutr. 2005;41 Suppl 2: S1-S4. DOI: 10.1097/01.mpg.0000181841.07090.f4</RefTotal>
<RefLink>http://dx.doi.org/10.1097/01.mpg.0000181841.07090.f4</RefLink>
</Reference>
<Reference refNo="2">
<RefAuthor>Friis-Hansen B</RefAuthor>
<RefTitle>Body water compartments in children: changes during growth and related changes in body composition</RefTitle>
<RefYear>1961</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>169-81</RefPage>
<RefTotal>Friis-Hansen B. Body water compartments in children: changes during growth and related changes in body composition. Pediatrics. 1961;28:169-81.</RefTotal>
</Reference>
<Reference refNo="3">
<RefAuthor>Widdowson E</RefAuthor>
<RefTitle>Changes of body composition during growth</RefTitle>
<RefYear>1981</RefYear>
<RefBookTitle>Scientific foundations of paediatrics</RefBookTitle>
<RefPage>330-42</RefPage>
<RefTotal>Widdowson E. Changes of body composition during growth. In: Davis J, Dobbing J, editor. Scientific foundations of paediatrics. London: Heinemann; 1981. p. 330-42.</RefTotal>
</Reference>
<Reference refNo="4">
<RefAuthor>Fusch C</RefAuthor>
<RefAuthor>Hungerland E</RefAuthor>
<RefAuthor>Scharrer B</RefAuthor>
<RefAuthor>Moeller H</RefAuthor>
<RefTitle>Water turnover of healthy children measured by deuterated water elimination</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>Eur J Pediatr</RefJournal>
<RefPage>110-14</RefPage>
<RefTotal>Fusch C, Hungerland E, Scharrer B, Moeller H. Water turnover of healthy children measured by deuterated water elimination. Eur J Pediatr. 1993;152(2):110-14. DOI: 10.1007/BF02072485</RefTotal>
<RefLink>http://dx.doi.org/10.1007/BF02072485</RefLink>
</Reference>
<Reference refNo="5">
<RefAuthor>Spitzer A</RefAuthor>
<RefTitle>Renal physiology and function development</RefTitle>
<RefYear>25-128</RefYear>
<RefBookTitle>The kidney and urinary tract</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Spitzer A. Renal physiology and function development. In: Edelmann CM, editor. The kidney and urinary tract. Boston: Little Brown, 1978: 25-128.</RefTotal>
</Reference>
<Reference refNo="6">
<RefAuthor>Costarino AT</RefAuthor>
<RefAuthor>Baumgart S</RefAuthor>
<RefTitle>Neonatal water and electrolyte metabolism</RefTitle>
<RefYear>1998</RefYear>
<RefBookTitle>Principles of perinatal-neonatal metabolism</RefBookTitle>
<RefPage>1045-75</RefPage>
<RefTotal>Costarino AT, Baumgart S. Neonatal water and electrolyte metabolism. In: Cowett R, editor. Principles of perinatal-neonatal metabolism. New York: Springer; 1998. p. 1045-75.</RefTotal>
</Reference>
<Reference refNo="7">
<RefAuthor>Edelmann CM</RefAuthor>
<RefAuthor>Trompkom V</RefAuthor>
<RefTitle>Renal concentrating ability in newborn infants</RefTitle>
<RefYear>1959</RefYear>
<RefJournal>Fed Proc</RefJournal>
<RefPage>49-54</RefPage>
<RefTotal>Edelmann CM, Trompkom V. Renal concentrating ability in newborn infants. Fed Proc. 1959;18:49-54.</RefTotal>
</Reference>
<Reference refNo="8">
<RefAuthor>Aperia A</RefAuthor>
<RefAuthor>Broberger O</RefAuthor>
<RefAuthor>Elinder G</RefAuthor>
<RefAuthor>Herin P</RefAuthor>
<RefAuthor>Zetterströum R</RefAuthor>
<RefTitle>Postnatal development of renal function in pre-term and full-term infants</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>Acta Paediatr Scand</RefJournal>
<RefPage>183-7</RefPage>
<RefTotal>Aperia A, Broberger O, Elinder G, Herin P, Zetterströum R. Postnatal development of renal function in pre-term and full-term infants. Acta Paediatr Scand. 1981;70:183-7. DOI: 10.1111/j.1651-2227.1981.tb05539.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1981.tb05539.x</RefLink>
</Reference>
<Reference refNo="9">
<RefAuthor>Fawer CL</RefAuthor>
<RefAuthor>Torrado A</RefAuthor>
<RefAuthor>Guignard JP</RefAuthor>
<RefTitle>Maturation of renal function in full-term and premature neonates</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>Helv Paediatr Acta</RefJournal>
<RefPage>11-21</RefPage>
<RefTotal>Fawer CL, Torrado A, Guignard JP. Maturation of renal function in full-term and premature neonates. Helv Paediatr Acta. 1979;34(1):11-21.</RefTotal>
</Reference>
<Reference refNo="10">
<RefAuthor>Bernardi JL</RefAuthor>
<RefAuthor>Goulart AL</RefAuthor>
<RefAuthor>Amancio OM</RefAuthor>
<RefTitle>Growth and energy and protein intake of preterm newborns in the first year of gestation-corrected age</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Sao Paulo Med J</RefJournal>
<RefPage>5-8</RefPage>
<RefTotal>Bernardi JL, Goulart AL, Amancio OM. Growth and energy and protein intake of preterm newborns in the first year of gestation-corrected age. Sao Paulo Med J. 2003;121:5-8. DOI: 10.1590/S1516-31802003000100002</RefTotal>
<RefLink>http://dx.doi.org/10.1590/S1516-31802003000100002</RefLink>
</Reference>
<Reference refNo="11">
<RefAuthor>American Academy of Pediatrics</RefAuthor>
<RefAuthor>Committee on Nutrition</RefAuthor>
<RefTitle>Nutritional needs of preterm Infants</RefTitle>
<RefYear>1998</RefYear>
<RefBookTitle>Pediatric Nutrition Handbook</RefBookTitle>
<RefPage>55-87</RefPage>
<RefTotal>American Academy of Pediatrics, Committee on Nutrition. Nutritional needs of preterm Infants. In: Kleinman RE, editor. Pediatric Nutrition Handbook. Elk Grove Village: American Academy of Pediatrics; 1998. p. 55-87.</RefTotal>
</Reference>
<Reference refNo="12">
<RefAuthor>Butte NF</RefAuthor>
<RefAuthor>Wong WW</RefAuthor>
<RefAuthor>Garza C</RefAuthor>
<RefAuthor>Stuff JE</RefAuthor>
<RefAuthor>Smith EO</RefAuthor>
<RefAuthor>Klein PD</RefAuthor>
<RefAuthor>Nichols BL</RefAuthor>
<RefTitle>Energy requirements of breast-fed infants</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>J Am Coll Nutr</RefJournal>
<RefPage>190-5</RefPage>
<RefTotal>Butte NF, Wong WW, Garza C, Stuff JE, Smith EO, Klein PD, Nichols BL. Energy requirements of breast-fed infants. J Am Coll Nutr. 1991;10(3):190-5.</RefTotal>
</Reference>
<Reference refNo="13">
<RefAuthor>Picaud JC</RefAuthor>
<RefAuthor>Putet G</RefAuthor>
<RefAuthor>Rigo J</RefAuthor>
<RefAuthor>Salle BL</RefAuthor>
<RefAuthor>Senterre J</RefAuthor>
<RefTitle>Metabolic and energy balance in small- and appropriate-for-gestational-age, very low-birth-weight infants</RefTitle>
<RefYear>1994</RefYear>
<RefJournal>Acta Paediatr Suppl</RefJournal>
<RefPage>54-9</RefPage>
<RefTotal>Picaud JC, Putet G, Rigo J, Salle BL, Senterre J. Metabolic and energy balance in small- and appropriate-for-gestational-age, very low-birth-weight infants. Acta Paediatr Suppl. 1994;s405:54-9. DOI: 10.1111/j.1651-2227.1994.tb13399.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1994.tb13399.x</RefLink>
</Reference>
<Reference refNo="14">
<RefAuthor>Putet G</RefAuthor>
<RefAuthor>Senterre J</RefAuthor>
<RefAuthor>Rigo J</RefAuthor>
<RefAuthor>Salle B</RefAuthor>
<RefTitle>Energy balance and composition of body weight</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Biol Neonate</RefJournal>
<RefPage>17-24</RefPage>
<RefTotal>Putet G, Senterre J, Rigo J, Salle B. Energy balance and composition of body weight. Biol Neonate. 1987;52 Suppl 1:17-24. DOI: 10.1159/000242736</RefTotal>
<RefLink>http://dx.doi.org/10.1159/000242736</RefLink>
</Reference>
<Reference refNo="15">
<RefAuthor>Lucas A</RefAuthor>
<RefTitle>Programming by early nutrition in man</RefTitle>
<RefYear>1991</RefYear>
<RefBookTitle>The childhood environment and adult disease (CIBA Foundation Symposia Series 156)</RefBookTitle>
<RefPage>38-55</RefPage>
<RefTotal>Lucas A. Programming by early nutrition in man. In: CIBA Foundation Symposium. The childhood environment and adult disease (CIBA Foundation Symposia Series 156). Chichester: Wiley; 1991. p. 38-55.</RefTotal>
</Reference>
<Reference refNo="16">
<RefAuthor>Koletzko B</RefAuthor>
<RefAuthor>Akerblom H</RefAuthor>
<RefAuthor>Dodds PF</RefAuthor>
<RefAuthor>Ashwell M</RefAuthor>
<RefTitle></RefTitle>
<RefYear>2005</RefYear>
<RefBookTitle>Early nutrition and its later consequences: New opportunities</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Koletzko B, Akerblom H, Dodds PF, Ashwell M. Early nutrition and its later consequences: New opportunities. New York: Springer Publishers; 2005.</RefTotal>
</Reference>
<Reference refNo="17">
<RefAuthor>Fusch C</RefAuthor>
<RefAuthor>Jochum F</RefAuthor>
<RefTitle>Water, Sodium, Potassium, and Chloride</RefTitle>
<RefYear>2004</RefYear>
<RefBookTitle>Nutritional needs of the preterm Infant</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Fusch C, Jochum F. Water, Sodium, Potassium, and Chloride. In: Tsang RC, Lucas A, Uauy R, Zlotkin S, editors. Nutritional needs of the preterm Infant. Baltimore: Williams & Wilkins; 2004.</RefTotal>
</Reference>
<Reference refNo="18">
<RefAuthor>Brown MR</RefAuthor>
<RefAuthor>Thunberg BJ</RefAuthor>
<RefAuthor>Golub L</RefAuthor>
<RefAuthor>Maniscalco WM</RefAuthor>
<RefAuthor>Cox C</RefAuthor>
<RefAuthor>Shapiro DL</RefAuthor>
<RefTitle>Decreased cholestasis with enteral instead of intravenous protein in the very low-birth-weight infant</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>21-7</RefPage>
<RefTotal>Brown MR, Thunberg BJ, Golub L, Maniscalco WM, Cox C, Shapiro DL. Decreased cholestasis with enteral instead of intravenous protein in the very low-birth-weight infant. J Pediatr Gastroenterol Nutr. 1989;9(1):21-7.</RefTotal>
</Reference>
<Reference refNo="19">
<RefAuthor>Center for Disease Control</RefAuthor>
<RefTitle>Nosocomial infection rate for interhospital comparison: limitations and possible solutions</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>Infect Control Hosp Epidemiol</RefJournal>
<RefPage>609-21</RefPage>
<RefTotal>Center for Disease Control. Nosocomial infection rate for interhospital comparison: limitations and possible solutions. Infect Control Hosp Epidemiol. 1991;12:609-21. DOI: 10.1086/646250</RefTotal>
<RefLink>http://dx.doi.org/10.1086/646250</RefLink>
</Reference>
<Reference refNo="20">
<RefAuthor>Sohn AH</RefAuthor>
<RefAuthor>Garrett DO</RefAuthor>
<RefAuthor>Sinkowitz-Cochran RL</RefAuthor>
<RefAuthor>Grohskopf LA</RefAuthor>
<RefAuthor>Levine GL</RefAuthor>
<RefAuthor>Stover BH</RefAuthor>
<RefAuthor>Siegel JD</RefAuthor>
<RefAuthor>Jarvis WR; the Pediatric Prevention Network</RefAuthor>
<RefTitle>Prevalence of nosocomial infections in neonatal intensive care unit patients: Results from the first national point-prevalence survey</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>821-7</RefPage>
<RefTotal>Sohn AH, Garrett DO, Sinkowitz-Cochran RL, Grohskopf LA, Levine GL, Stover BH, Siegel JD, Jarvis WR; the Pediatric Prevention Network. Prevalence of nosocomial infections in neonatal intensive care unit patients: Results from the first national point-prevalence survey. J Pediatr. 2001;139(6):821-7. DOI: 10.1067/mpd.2001.119442</RefTotal>
<RefLink>http://dx.doi.org/10.1067/mpd.2001.119442</RefLink>
</Reference>
<Reference refNo="21">
<RefAuthor>Vaidya UV</RefAuthor>
<RefAuthor>Hegde VM</RefAuthor>
<RefAuthor>Bhave SA</RefAuthor>
<RefAuthor>Pandit AN</RefAuthor>
<RefTitle>Reduction in parenteral nutrition related complications in the newborn</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>Indian Pediatr</RefJournal>
<RefPage>477-84</RefPage>
<RefTotal>Vaidya UV, Hegde VM, Bhave SA, Pandit AN. Reduction in parenteral nutrition related complications in the newborn. Indian Pediatr. 1991;28(5):477-84.</RefTotal>
</Reference>
<Reference refNo="22">
<RefAuthor>Suchner U</RefAuthor>
<RefAuthor>Senftleben U</RefAuthor>
<RefAuthor>Eckart T</RefAuthor>
<RefAuthor>Scholz MR</RefAuthor>
<RefAuthor>Beck K</RefAuthor>
<RefAuthor>Murr R</RefAuthor>
<RefAuthor>Enzenbach R</RefAuthor>
<RefAuthor>Peter K</RefAuthor>
<RefTitle>Enteral versus parenteral nutrition: effects on gastrointestinal function and metabolism</RefTitle>
<RefYear>1996</RefYear>
<RefJournal>Nutrition</RefJournal>
<RefPage>13-22</RefPage>
<RefTotal>Suchner U, Senftleben U, Eckart T, Scholz MR, Beck K, Murr R, Enzenbach R, Peter K. Enteral versus parenteral nutrition: effects on gastrointestinal function and metabolism. Nutrition. 1996;12(1):13-22. DOI: 10.1016/0899-9007(95)00016-X</RefTotal>
<RefLink>http://dx.doi.org/10.1016/0899-9007(95)00016-X</RefLink>
</Reference>
<Reference refNo="23">
<RefAuthor>Deutsche Arbeitsgemeinschaft für künstliche Ernährung (DAKE)</RefAuthor>
<RefAuthor>Österreichische Arbeitsgemeinschaft für künstliche Ernährung (AKE)</RefAuthor>
<RefTitle>Empfehlungen zur parenteralen Infusions- und Ernährungstherapie im Kindesalter</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Klin Pädiatr</RefJournal>
<RefPage>315-7</RefPage>
<RefTotal>Deutsche Arbeitsgemeinschaft für künstliche Ernährung (DAKE), Österreichische Arbeitsgemeinschaft für künstliche Ernährung (AKE). Empfehlungen zur parenteralen Infusions- und Ernährungstherapie im Kindesalter. Klin Pädiatr. 1987;199(4):315-7.</RefTotal>
</Reference>
<Reference refNo="24">
<RefAuthor>Nutrition Committee</RefAuthor>
<RefAuthor>Canadian Paediatric Society</RefAuthor>
<RefTitle>Nutrient needs and feeding of premature infants</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>CMAJ</RefJournal>
<RefPage>1765-85</RefPage>
<RefTotal>Nutrition Committee, Canadian Paediatric Society. Nutrient needs and feeding of premature infants. CMAJ. 1995;152(10):1765-85.</RefTotal>
</Reference>
<Reference refNo="25">
<RefAuthor>Aggett PJ</RefAuthor>
<RefAuthor>Bresson J</RefAuthor>
<RefAuthor>Haschke F</RefAuthor>
<RefAuthor>Hernell O</RefAuthor>
<RefAuthor>Koletzko B</RefAuthor>
<RefAuthor>Lafeber HN</RefAuthor>
<RefAuthor>Michaelsen KF</RefAuthor>
<RefAuthor>Micheli J</RefAuthor>
<RefAuthor>Ormisson A</RefAuthor>
<RefAuthor>Rey J</RefAuthor>
<RefAuthor>de Sousa JS</RefAuthor>
<RefAuthor>Weaver L</RefAuthor>
<RefTitle>Recommended Dietary Allowances (RDAs), Recommended Dietary Intakes (RDIs), Recommended Nutrient Intakes (RNIs), and Population Reference Intakes (PRIs) are not "recommended intakes"</RefTitle>
<RefYear>1997</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>236-41</RefPage>
<RefTotal>Aggett PJ, Bresson J, Haschke F, Hernell O, Koletzko B, Lafeber HN, Michaelsen KF, Micheli J, Ormisson A, Rey J, de Sousa JS, Weaver L. Recommended Dietary Allowances (RDAs), Recommended Dietary Intakes (RDIs), Recommended Nutrient Intakes (RNIs), and Population Reference Intakes (PRIs) are not "recommended intakes". J Pediatr Gastroenterol Nutr. 1997;25(2):236-41. DOI: 10.1097/00005176-199708000-00022</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00005176-199708000-00022</RefLink>
</Reference>
<Reference refNo="26">
<RefAuthor>Tsang R</RefAuthor>
<RefAuthor>Uauy R</RefAuthor>
<RefAuthor>Koledtzko B</RefAuthor>
<RefAuthor>Zlotkin S</RefAuthor>
<RefTitle></RefTitle>
<RefYear>2005</RefYear>
<RefBookTitle>Nutrition of the preterm infant: Scientific basis and practical application</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Tsang R, Uauy R, Koledtzko B, Zlotkin S. Nutrition of the preterm infant: Scientific basis and practical application. 2nd ed. Cincinnati: Digital Education Publication; 2005</RefTotal>
</Reference>
<Reference refNo="27">
<RefAuthor>Embleton NE</RefAuthor>
<RefAuthor>Pang N</RefAuthor>
<RefAuthor>Cooke RJ</RefAuthor>
<RefTitle>Postnatal malnutrition and growth retardation: an inevitable consequence of current recommendations in preterm infants?</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>270-3</RefPage>
<RefTotal>Embleton NE, Pang N, Cooke RJ. Postnatal malnutrition and growth retardation: an inevitable consequence of current recommendations in preterm infants? Pediatrics. 2001;107(2):270-3. DOI: 10.1542/peds.107.2.270</RefTotal>
<RefLink>http://dx.doi.org/10.1542/peds.107.2.270</RefLink>
</Reference>
<Reference refNo="28">
<RefAuthor>Sonntag J</RefAuthor>
<RefAuthor>Grimmer I</RefAuthor>
<RefAuthor>Scholz T</RefAuthor>
<RefAuthor>Metze B</RefAuthor>
<RefAuthor>Wit J</RefAuthor>
<RefAuthor>Obladen M</RefAuthor>
<RefTitle>Growth and neurodevelopmental outcome of very low birthweight infants with necrotizing enterocolitis</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Acta Paediatr</RefJournal>
<RefPage>528-32</RefPage>
<RefTotal>Sonntag J, Grimmer I, Scholz T, Metze B, Wit J, Obladen M. Growth and neurodevelopmental outcome of very low birthweight infants with necrotizing enterocolitis. Acta Paediatr. 2000;89(5):528-32. DOI: 10.1080/080352500750027790</RefTotal>
<RefLink>http://dx.doi.org/10.1080/080352500750027790</RefLink>
</Reference>
<Reference refNo="29">
<RefAuthor>Ziegler EE</RefAuthor>
<RefAuthor>Thureen PJ</RefAuthor>
<RefAuthor>Carlson SJ</RefAuthor>
<RefTitle>Aggressive nutrition of the very low birthweight infant</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Clin Perinatol</RefJournal>
<RefPage>225-44</RefPage>
<RefTotal>Ziegler EE, Thureen PJ, Carlson SJ. Aggressive nutrition of the very low birthweight infant. Clin Perinatol. 2002;29(2):225-44. DOI: 10.1016/S0095-5108(02)00007-6</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0095-5108(02)00007-6</RefLink>
</Reference>
<Reference refNo="30">
<RefAuthor>Harris JA</RefAuthor>
<RefAuthor>Benedict FG</RefAuthor>
<RefTitle></RefTitle>
<RefYear>1919</RefYear>
<RefBookTitle>A biometric study of basal metabolism in man (Publication no 279)</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Harris JA, Benedict FG. A biometric study of basal metabolism in man (Publication no 279). Washington: Carnegie Institute; 1919.</RefTotal>
</Reference>
<Reference refNo="31">
<RefAuthor>Schofield WN</RefAuthor>
<RefTitle>Predicting basal metabolic rate, new standards and review of previous work</RefTitle>
<RefYear>1985</RefYear>
<RefJournal>Hum Nutr Clin Nutr</RefJournal>
<RefPage>5-41</RefPage>
<RefTotal>Schofield WN. Predicting basal metabolic rate, new standards and review of previous work. Hum Nutr Clin Nutr. 1985;39 Suppl 1:5-41.</RefTotal>
</Reference>
<Reference refNo="32">
<RefAuthor>Food and Agriculture Organization of the United Nations [FAO]; World Health Organization [WHO]; United Nations University [UNU]</RefAuthor>
<RefTitle>Energy and protein requirements; Report of a joint FAO/WHO/UNU expert consultation</RefTitle>
<RefYear>1985</RefYear>
<RefJournal>World Health Organization technical report series</RefJournal>
<RefPage></RefPage>
<RefTotal>Food and Agriculture Organization of the United Nations [FAO]; World Health Organization [WHO]; United Nations University [UNU]. Energy and protein requirements; Report of a joint FAO/WHO/UNU expert consultation. World Health Organization technical report series. 1985;724:1-206. Available from: http://www.popline.org/docs/1444/052220.html</RefTotal>
<RefLink>http://www.popline.org/docs/1444/052220.html</RefLink>
</Reference>
<Reference refNo="33">
<RefAuthor>Kalhan SC</RefAuthor>
<RefAuthor>Kilic I</RefAuthor>
<RefTitle>Carbohydrate as nutrient in the infant and child: range of acceptable intake</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Eur J Clin Nutr</RefJournal>
<RefPage>S94-100</RefPage>
<RefTotal>Kalhan SC, Kilic I. Carbohydrate as nutrient in the infant and child: range of acceptable intake. Eur J Clin Nutr. 1999;53 Suppl 1:S94-100.</RefTotal>
</Reference>
<Reference refNo="34">
<RefAuthor>Denne SC</RefAuthor>
<RefAuthor>Karn CA</RefAuthor>
<RefAuthor>Wang J</RefAuthor>
<RefAuthor>Liechty EA</RefAuthor>
<RefTitle>Effect of intravenous glucose and lipid on proteolysis and glucose production in normal newborns</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>Am J Physiol</RefJournal>
<RefPage>E361-7</RefPage>
<RefTotal>Denne SC, Karn CA, Wang J, Liechty EA. Effect of intravenous glucose and lipid on proteolysis and glucose production in normal newborns. Am J Physiol. 1995;269(2 Pt 1):E361-7.</RefTotal>
</Reference>
<Reference refNo="35">
<RefAuthor>Lafeber HN</RefAuthor>
<RefAuthor>Sulkers EJ</RefAuthor>
<RefAuthor>Chapman TE</RefAuthor>
<RefAuthor>Sauer PJ</RefAuthor>
<RefTitle>Glucose production and oxidation in preterm infants during total parenteral nutrition</RefTitle>
<RefYear>1990</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>153-7</RefPage>
<RefTotal>Lafeber HN, Sulkers EJ, Chapman TE, Sauer PJ. Glucose production and oxidation in preterm infants during total parenteral nutrition. Pediatr Res. 1990;28(2):153-7.</RefTotal>
</Reference>
<Reference refNo="36">
<RefAuthor>Sunehag AL</RefAuthor>
<RefAuthor>Haymond MW</RefAuthor>
<RefAuthor>Schanler RJ</RefAuthor>
<RefAuthor>Reeds PJ</RefAuthor>
<RefAuthor>Bier DM</RefAuthor>
<RefTitle>Gluconeogenesis in very low birth weight infants receiving total parenteral nutrition</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Diabetes</RefJournal>
<RefPage>791-800</RefPage>
<RefTotal>Sunehag AL, Haymond MW, Schanler RJ, Reeds PJ, Bier DM. Gluconeogenesis in very low birth weight infants receiving total parenteral nutrition. Diabetes. 1999;48(4):791-800. DOI: 10.2337/diabetes.48.4.791</RefTotal>
<RefLink>http://dx.doi.org/10.2337/diabetes.48.4.791</RefLink>
</Reference>
<Reference refNo="37">
<RefAuthor>Forsyth JS</RefAuthor>
<RefAuthor>Murdock N</RefAuthor>
<RefAuthor>Crighton A</RefAuthor>
<RefTitle>Low birthweight infants and total parenteral nutrition immediately after birth. III. Randomised study of energy substrate utilisation, nitrogen balance, and carbon dioxide production</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>Arch Dis Child Fetal Neonatal Ed</RefJournal>
<RefPage>F13-6</RefPage>
<RefTotal>Forsyth JS, Murdock N, Crighton A. Low birthweight infants and total parenteral nutrition immediately after birth. III. Randomised study of energy substrate utilisation, nitrogen balance, and carbon dioxide production. Arch Dis Child Fetal Neonatal Ed. 1995;73:F13-6. DOI: 10.1136/fn.73.1.F13</RefTotal>
<RefLink>http://dx.doi.org/10.1136/fn.73.1.F13</RefLink>
</Reference>
<Reference refNo="38">
<RefAuthor>Sauer PJ</RefAuthor>
<RefAuthor>Van Aerde JE</RefAuthor>
<RefAuthor>Pencharz PB</RefAuthor>
<RefAuthor>Smith JM</RefAuthor>
<RefAuthor>Swyer PR</RefAuthor>
<RefTitle>Glucose oxidation rates in newborn infants measured with indirect calorimetry and [U-13C]glucose</RefTitle>
<RefYear>1986</RefYear>
<RefJournal>Clin Sci (Lond)</RefJournal>
<RefPage>587-93</RefPage>
<RefTotal>Sauer PJ, Van Aerde JE, Pencharz PB, Smith JM, Swyer PR. Glucose oxidation rates in newborn infants measured with indirect calorimetry and [U-13C]glucose. Clin Sci (Lond). 1986;70(6):587-93.</RefTotal>
</Reference>
<Reference refNo="39">
<RefAuthor>Jones MO</RefAuthor>
<RefAuthor>Pierro A</RefAuthor>
<RefAuthor>Hammond P</RefAuthor>
<RefAuthor>Nunn A</RefAuthor>
<RefAuthor>Lloyd DA</RefAuthor>
<RefTitle>Glucose utilization in the surgical newborn infant receiving total parenteral nutrition</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>J Pediatr Surg</RefJournal>
<RefPage>1121-5</RefPage>
<RefTotal>Jones MO, Pierro A, Hammond P, Nunn A, Lloyd DA. Glucose utilization in the surgical newborn infant receiving total parenteral nutrition. J Pediatr Surg. 1993;28(9):1121-5. DOI: 10.1016/0022-3468(93)90144-A</RefTotal>
<RefLink>http://dx.doi.org/10.1016/0022-3468(93)90144-A</RefLink>
</Reference>
<Reference refNo="40">
<RefAuthor>Nose O</RefAuthor>
<RefAuthor>Tipton JR</RefAuthor>
<RefAuthor>Ament ME</RefAuthor>
<RefAuthor>Yabuuchi H</RefAuthor>
<RefTitle>Effect of the energy source on changes in energy expenditure, respiratory quotient, and nitrogen balance during total parenteral nutrition in children</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>538-41</RefPage>
<RefTotal>Nose O, Tipton JR, Ament ME, Yabuuchi H. Effect of the energy source on changes in energy expenditure, respiratory quotient, and nitrogen balance during total parenteral nutrition in children. Pediatr Res. 1987;21(6):538-41. DOI: 10.1203/00006450-198706000-00006</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-198706000-00006</RefLink>
</Reference>
<Reference refNo="41">
<RefAuthor>Sheridan RL</RefAuthor>
<RefAuthor>Yu YM</RefAuthor>
<RefAuthor>Prelack K</RefAuthor>
<RefAuthor>Young VR</RefAuthor>
<RefAuthor>Burke JF</RefAuthor>
<RefAuthor>Tompkins RG</RefAuthor>
<RefTitle>Maximal parenteral glucose oxidation in hypermetabolic young children: a stable isotope study</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>JPEN J Parenter Enteral Nutr</RefJournal>
<RefPage>212-6</RefPage>
<RefTotal>Sheridan RL, Yu YM, Prelack K, Young VR, Burke JF, Tompkins RG. Maximal parenteral glucose oxidation in hypermetabolic young children: a stable isotope study. JPEN J Parenter Enteral Nutr. 1998;22(4):212-6. DOI: 10.1177/0148607198022004212</RefTotal>
<RefLink>http://dx.doi.org/10.1177/0148607198022004212</RefLink>
</Reference>
<Reference refNo="42">
<RefAuthor>Robin AP</RefAuthor>
<RefAuthor>Carpentier YA</RefAuthor>
<RefAuthor>Askanazi J</RefAuthor>
<RefAuthor>Nordenstrom J</RefAuthor>
<RefAuthor>Kinney JM</RefAuthor>
<RefTitle>Metabolic consequences of hypercaloric glucose infusions</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>Acta Chir Belg</RefJournal>
<RefPage>133-40</RefPage>
<RefTotal>Robin AP, Carpentier YA, Askanazi J, Nordenstrom J, Kinney JM. Metabolic consequences of hypercaloric glucose infusions. Acta Chir Belg. 1981;80:133-40.</RefTotal>
</Reference>
<Reference refNo="43">
<RefAuthor>Koretz RL</RefAuthor>
<RefAuthor>Lipman TO</RefAuthor>
<RefAuthor>Klein S</RefAuthor>
<RefTitle>AGA technical review on parenteral nutrition</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Gastroenterology</RefJournal>
<RefPage>970-1001</RefPage>
<RefTotal>Koretz RL, Lipman TO, Klein S. AGA technical review on parenteral nutrition. Gastroenterology. 2001;121(4):970-1001. DOI: 10.1016/S0016-5085(01)92000-1</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0016-5085(01)92000-1</RefLink>
</Reference>
<Reference refNo="44">
<RefAuthor>Burke JF</RefAuthor>
<RefAuthor>Wolfe RR</RefAuthor>
<RefAuthor>Mullany CJ</RefAuthor>
<RefAuthor>Mathews DE</RefAuthor>
<RefAuthor>Bier DM</RefAuthor>
<RefTitle>Glucose requirements following burn injury. Parameters of optimal glucose infusion and possible hepatic and respiratory abnormalities following excessive glucose intake</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>Ann Surg</RefJournal>
<RefPage>274-85</RefPage>
<RefTotal>Burke JF, Wolfe RR, Mullany CJ, Mathews DE, Bier DM. Glucose requirements following burn injury. Parameters of optimal glucose infusion and possible hepatic and respiratory abnormalities following excessive glucose intake. Ann Surg. 1979;190(3):274-85.</RefTotal>
</Reference>
<Reference refNo="45">
<RefAuthor>Tulikoura I</RefAuthor>
<RefAuthor>Huikuri K</RefAuthor>
<RefTitle>Morphological fatty changes and function of the liver, serum free fatty acids, and triglycerides during parenteral nutrition</RefTitle>
<RefYear>1982</RefYear>
<RefJournal>Scand J Gastroenterol</RefJournal>
<RefPage>177-85</RefPage>
<RefTotal>Tulikoura I, Huikuri K. Morphological fatty changes and function of the liver, serum free fatty acids, and triglycerides during parenteral nutrition. Scand J Gastroenterol. 1982;17(2):177-85.</RefTotal>
</Reference>
<Reference refNo="46">
<RefAuthor>Cowett RM</RefAuthor>
<RefAuthor>Andersen GE</RefAuthor>
<RefAuthor>Maguire CA</RefAuthor>
<RefAuthor>Oh W</RefAuthor>
<RefTitle>Ontogeny of glucose homeostasis in low birth weight infants</RefTitle>
<RefYear>1988</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>462-5</RefPage>
<RefTotal>Cowett RM, Andersen GE, Maguire CA, Oh W. Ontogeny of glucose homeostasis in low birth weight infants. J Pediatr. 1988;112(3):462-5. DOI: 10.1016/S0022-3476(88)80337-8</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(88)80337-8</RefLink>
</Reference>
<Reference refNo="47">
<RefAuthor>Farrag HM</RefAuthor>
<RefAuthor>Nawrath LM</RefAuthor>
<RefAuthor>Healey JE</RefAuthor>
<RefAuthor>Dorcus EJ</RefAuthor>
<RefAuthor>Rapoza RE</RefAuthor>
<RefAuthor>Oh W</RefAuthor>
<RefAuthor>Cowett RM</RefAuthor>
<RefTitle>Persistent glucose production and greater peripheral sensitivity to insulin in the neonate vs the adult</RefTitle>
<RefYear>1997</RefYear>
<RefJournal>Am J Physiol</RefJournal>
<RefPage>E86-93</RefPage>
<RefTotal>Farrag HM, Nawrath LM, Healey JE, Dorcus EJ, Rapoza RE, Oh W, Cowett RM. Persistent glucose production and greater peripheral sensitivity to insulin in the neonate vs the adult. Am J Physiol. 1997;272(1 Pt 1):E86-93.</RefTotal>
</Reference>
<Reference refNo="48">
<RefAuthor>Pildes RS</RefAuthor>
<RefAuthor>Pyati SP</RefAuthor>
<RefTitle>Hypoglycemia and hyperglycemia in tiny infants</RefTitle>
<RefYear>1986</RefYear>
<RefJournal>Clin Perinatol</RefJournal>
<RefPage>351-75</RefPage>
<RefTotal>Pildes RS, Pyati SP. Hypoglycemia and hyperglycemia in tiny infants. Clin Perinatol. 1986;13(2):351-75.</RefTotal>
</Reference>
<Reference refNo="49">
<RefAuthor>Dweck HS</RefAuthor>
<RefAuthor>Cassady G</RefAuthor>
<RefTitle>Glucose intolerance in infants of very low birth weight; I: Incidence of hyperglycemia in infants of birth weights 1,100 grams or less</RefTitle>
<RefYear>1974</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>189-95</RefPage>
<RefTotal>Dweck HS, Cassady G. Glucose intolerance in infants of very low birth weight; I: Incidence of hyperglycemia in infants of birth weights 1,100 grams or less. Pediatrics. 1974;53(2):189-95.</RefTotal>
</Reference>
<Reference refNo="50">
<RefAuthor>Louik C</RefAuthor>
<RefAuthor>Mitchell AA</RefAuthor>
<RefAuthor>Epstein MF</RefAuthor>
<RefAuthor>Shapiro S</RefAuthor>
<RefTitle>Risk factors for neonatal hyperglycemia associated with 10% dextrose infusion</RefTitle>
<RefYear>1985</RefYear>
<RefJournal>Am J Dis Child</RefJournal>
<RefPage>783-6</RefPage>
<RefTotal>Louik C, Mitchell AA, Epstein MF, Shapiro S. Risk factors for neonatal hyperglycemia associated with 10% dextrose infusion. Am J Dis Child. 1985;139(8):783-6.</RefTotal>
</Reference>
<Reference refNo="51">
<RefAuthor>Binder ND</RefAuthor>
<RefAuthor>Raschko PK</RefAuthor>
<RefAuthor>Benda GI</RefAuthor>
<RefAuthor>Reynolds JW</RefAuthor>
<RefTitle>Insulin infusion with parenteral nutrition in extremely low birth weight infants with hyperglycemia</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>273-80</RefPage>
<RefTotal>Binder ND, Raschko PK, Benda GI, Reynolds JW. Insulin infusion with parenteral nutrition in extremely low birth weight infants with hyperglycemia. J Pediatr. 1989;114(2):273-80. DOI: 10.1016/S0022-3476(89)80797-8</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(89)80797-8</RefLink>
</Reference>
<Reference refNo="52">
<RefAuthor>Thureen PJ</RefAuthor>
<RefAuthor>Melara D</RefAuthor>
<RefAuthor>Fennessey PV</RefAuthor>
<RefAuthor>Hay WW Jr</RefAuthor>
<RefTitle>Effect of low versus high intravenous amino acid intake on very low birth weight infants in the early neonatal period</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>24-32</RefPage>
<RefTotal>Thureen PJ, Melara D, Fennessey PV, Hay WW Jr. Effect of low versus high intravenous amino acid intake on very low birth weight infants in the early neonatal period. Pediatr Res. 2003;53(1):24-32.</RefTotal>
</Reference>
<Reference refNo="53">
<RefAuthor>Gaull G</RefAuthor>
<RefAuthor>Sturman JA</RefAuthor>
<RefAuthor>Räihä NC</RefAuthor>
<RefTitle>Development of mammalian sulfur metabolism: absence of cystathionase in human fetal tissues</RefTitle>
<RefYear>1972</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>538-47</RefPage>
<RefTotal>Gaull G, Sturman JA, Räihä NC. Development of mammalian sulfur metabolism: absence of cystathionase in human fetal tissues. Pediatr Res. 1972;6(6):538-47.</RefTotal>
</Reference>
<Reference refNo="54">
<RefAuthor>Räihä NC</RefAuthor>
<RefTitle>Biochemical basis for nutritional management of preterm infants</RefTitle>
<RefYear>1974</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>147-56</RefPage>
<RefTotal>Räihä NC. Biochemical basis for nutritional management of preterm infants. Pediatrics. 1974;53(2):147-56.</RefTotal>
</Reference>
<Reference refNo="55">
<RefAuthor>Holt LE Jr</RefAuthor>
<RefTitle>Amino acid requirements of infants</RefTitle>
<RefYear>1967</RefYear>
<RefJournal>Curr Ther Res Clin Exp</RefJournal>
<RefPage>149-56</RefPage>
<RefTotal>Holt LE Jr. Amino acid requirements of infants. Curr Ther Res Clin Exp. 1967;9(3 Suppl):149-56.</RefTotal>
</Reference>
<Reference refNo="56">
<RefAuthor>Rigo J</RefAuthor>
<RefAuthor>Senterre J</RefAuthor>
<RefTitle>Is taurine essential for the neonates?</RefTitle>
<RefYear>1977</RefYear>
<RefJournal>Biol Neonate</RefJournal>
<RefPage>73-6</RefPage>
<RefTotal>Rigo J, Senterre J. Is taurine essential for the neonates? Biol Neonate. 1977;32(1-2):73-6. DOI: 10.1159/000240997</RefTotal>
<RefLink>http://dx.doi.org/10.1159/000240997</RefLink>
</Reference>
<Reference refNo="57">
<RefAuthor>Olney JW</RefAuthor>
<RefAuthor>Ho OL</RefAuthor>
<RefAuthor>Rhee V</RefAuthor>
<RefTitle>Brain-damaging potential of protein hydrolysates</RefTitle>
<RefYear>1973</RefYear>
<RefJournal>N Engl J Med</RefJournal>
<RefPage>391-5</RefPage>
<RefTotal>Olney JW, Ho OL, Rhee V. Brain-damaging potential of protein hydrolysates. N Engl J Med. 1973;289(8):391-5.</RefTotal>
</Reference>
<Reference refNo="58">
<RefAuthor>Brunton JA</RefAuthor>
<RefAuthor>Ball RO</RefAuthor>
<RefAuthor>Pencharz PB</RefAuthor>
<RefTitle>Current total parenteral nutrition solutions for the neonate are inadequate</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Curr Opin Clin Nutr Metab Care</RefJournal>
<RefPage>299-304</RefPage>
<RefTotal>Brunton JA, Ball RO, Pencharz PB. Current total parenteral nutrition solutions for the neonate are inadequate. Curr Opin Clin Nutr Metab Care. 2000;3(4):299-304. DOI: 10.1097/00075197-200007000-00010</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00075197-200007000-00010</RefLink>
</Reference>
<Reference refNo="59">
<RefAuthor>Poindexter BB</RefAuthor>
<RefAuthor>Ehrenkranz RA</RefAuthor>
<RefAuthor>Stoll BJ</RefAuthor>
<RefAuthor>Koch MA</RefAuthor>
<RefAuthor>Wright LL</RefAuthor>
<RefAuthor>Oh W</RefAuthor>
<RefAuthor>Papile LA</RefAuthor>
<RefAuthor>Bauer CR</RefAuthor>
<RefAuthor>Carlo WA</RefAuthor>
<RefAuthor>Donovan EF</RefAuthor>
<RefAuthor>Fanaroff AA</RefAuthor>
<RefAuthor>Korones SB</RefAuthor>
<RefAuthor>Laptook AR</RefAuthor>
<RefAuthor>Shankaran S</RefAuthor>
<RefAuthor>Stevenson DK</RefAuthor>
<RefAuthor>Tyson JE</RefAuthor>
<RefAuthor>Lemons JA; National Institute of Child Health and Human Development Neonatal Research Network</RefAuthor>
<RefTitle>Effect of parenteral glutamine supplementation on plasma amino acid concentrations in extremely low-birth-weight infants</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>737-43</RefPage>
<RefTotal>Poindexter BB, Ehrenkranz RA, Stoll BJ, Koch MA, Wright LL, Oh W, Papile LA, Bauer CR, Carlo WA, Donovan EF, Fanaroff AA, Korones SB, Laptook AR, Shankaran S, Stevenson DK, Tyson JE, Lemons JA; National Institute of Child Health and Human Development Neonatal Research Network. Effect of parenteral glutamine supplementation on plasma amino acid concentrations in extremely low-birth-weight infants. Am J Clin Nutr. 2003;77(3):737-43.</RefTotal>
</Reference>
<Reference refNo="60">
<RefAuthor>Van Goudoever JB</RefAuthor>
<RefAuthor>Sulkers EJ</RefAuthor>
<RefAuthor>Timmerman M</RefAuthor>
<RefAuthor>Huijmans JG</RefAuthor>
<RefAuthor>Langer K</RefAuthor>
<RefAuthor>Carnielli VP</RefAuthor>
<RefAuthor>Sauer PJ</RefAuthor>
<RefTitle>Amino acid solutions for premature neonates during the first week of life: the role of N-acetyl-L-cysteine and N-acetyl-L-tyrosine</RefTitle>
<RefYear>1994</RefYear>
<RefJournal>JPEN J Parenter Enteral Nutr</RefJournal>
<RefPage>404-8</RefPage>
<RefTotal>Van Goudoever JB, Sulkers EJ, Timmerman M, Huijmans JG, Langer K, Carnielli VP, Sauer PJ. Amino acid solutions for premature neonates during the first week of life: the role of N-acetyl-L-cysteine and N-acetyl-L-tyrosine. JPEN J Parenter Enteral Nutr. 1994;18(5):404-8. DOI: 10.1177/0148607194018005404</RefTotal>
<RefLink>http://dx.doi.org/10.1177/0148607194018005404</RefLink>
</Reference>
<Reference refNo="61">
<RefAuthor>Duffy B</RefAuthor>
<RefAuthor>Gunn T</RefAuthor>
<RefAuthor>Collinge J</RefAuthor>
<RefAuthor>Pencharz P</RefAuthor>
<RefTitle>The effect of varying protein quality and energy intake on the nitrogen metabolism of parenterally fed very low birthweight (<1600 g) infants</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>1040-4</RefPage>
<RefTotal>Duffy B, Gunn T, Collinge J, Pencharz P. The effect of varying protein quality and energy intake on the nitrogen metabolism of parenterally fed very low birthweight (<1600 g) infants. Pediatr Res. 1981;15:1040-4. DOI: 10.1203/00006450-198107000-00013</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-198107000-00013</RefLink>
</Reference>
<Reference refNo="62">
<RefAuthor>Rigo J</RefAuthor>
<RefAuthor>Senterre J</RefAuthor>
<RefTitle>Significance of plasma amino acid pattern in preterm infants</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Biol Neonate</RefJournal>
<RefPage>41-9</RefPage>
<RefTotal>Rigo J, Senterre J. Significance of plasma amino acid pattern in preterm infants. Biol Neonate. 1987;52(Suppl 1):41-9. DOI: 10.1159/000242738</RefTotal>
<RefLink>http://dx.doi.org/10.1159/000242738</RefLink>
</Reference>
<Reference refNo="63">
<RefAuthor>Pohlandt F</RefAuthor>
<RefAuthor>Michatsch WA</RefAuthor>
<RefTitle>Wichtige Aspekte der enteralen Ernährung von sehr kleinen Frühgeborenen</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Monatsschr Kinderheilkd</RefJournal>
<RefPage>S38-45</RefPage>
<RefTotal>Pohlandt F, Michatsch WA. Wichtige Aspekte der enteralen Ernährung von sehr kleinen Frühgeborenen. Monatsschr Kinderheilkd. 2001;149(13 Suppl 1):S38-45. DOI: 10.1007/s001120170007</RefTotal>
<RefLink>http://dx.doi.org/10.1007/s001120170007</RefLink>
</Reference>
<Reference refNo="64">
<RefAuthor>Micheli JL</RefAuthor>
<RefAuthor>Schutz Y</RefAuthor>
<RefTitle>Protein</RefTitle>
<RefYear>1993</RefYear>
<RefBookTitle>Nutritional Needs of the Preterm Infant</RefBookTitle>
<RefPage>29-46</RefPage>
<RefTotal>Micheli JL, Schutz Y. Protein. In: Tsang RC, Lucas A, Uauy R, Zlotkin S, editors. Nutritional Needs of the Preterm Infant. Williams & Wilkins; 1993. p. 29-46.</RefTotal>
</Reference>
<Reference refNo="65">
<RefAuthor>Ghisolfi J</RefAuthor>
<RefTitle>Taurine and the premature</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Biol Neonate</RefJournal>
<RefPage>78-86</RefPage>
<RefTotal>Ghisolfi J. Taurine and the premature. Biol Neonate. 1987;52(Suppl 1):78-86. DOI: 10.1159/000242741</RefTotal>
<RefLink>http://dx.doi.org/10.1159/000242741</RefLink>
</Reference>
<Reference refNo="66">
<RefAuthor>Chessex P</RefAuthor>
<RefAuthor>Zebiche H</RefAuthor>
<RefAuthor>Pineault M</RefAuthor>
<RefAuthor>Lepage D</RefAuthor>
<RefAuthor>Dallaire L</RefAuthor>
<RefTitle>Effect of amino acid composition of parenteral solutions on nitrogen retention and metabolic response in very-low-birth weight infants</RefTitle>
<RefYear>1985</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>111-7</RefPage>
<RefTotal>Chessex P, Zebiche H, Pineault M, Lepage D, Dallaire L. Effect of amino acid composition of parenteral solutions on nitrogen retention and metabolic response in very-low-birth weight infants. J Pediatr. 1985;106(1):111-7. DOI: 10.1016/S0022-3476(85)80478-9</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(85)80478-9</RefLink>
</Reference>
<Reference refNo="67">
<RefAuthor>Kovar IZ</RefAuthor>
<RefAuthor>Saini J</RefAuthor>
<RefAuthor>Morgan JB</RefAuthor>
<RefTitle>The sick very low birthweight infant fed by parenteral nutrition: studies of nitrogen and energy</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Eur J Clin Nutr</RefJournal>
<RefPage>339-46</RefPage>
<RefTotal>Kovar IZ, Saini J, Morgan JB. The sick very low birthweight infant fed by parenteral nutrition: studies of nitrogen and energy. Eur J Clin Nutr. 1989;43(5):339-46.</RefTotal>
</Reference>
<Reference refNo="68">
<RefAuthor>Beale EF</RefAuthor>
<RefAuthor>Nelson RM</RefAuthor>
<RefAuthor>Bucciarelli RL</RefAuthor>
<RefAuthor>Donnelly WH</RefAuthor>
<RefAuthor>Eitzman DV</RefAuthor>
<RefTitle>Intrahepatic cholestasis associated with parenteral nutrition in premature infants</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>342-7</RefPage>
<RefTotal>Beale EF, Nelson RM, Bucciarelli RL, Donnelly WH, Eitzman DV. Intrahepatic cholestasis associated with parenteral nutrition in premature infants. Pediatrics. 1979;64(3):342-7.</RefTotal>
</Reference>
<Reference refNo="69">
<RefAuthor>Beath SV</RefAuthor>
<RefAuthor>Davies P</RefAuthor>
<RefAuthor>Papadopoulou A</RefAuthor>
<RefAuthor>Khan AR</RefAuthor>
<RefAuthor>Buick RG</RefAuthor>
<RefAuthor>Corkery JJ</RefAuthor>
<RefAuthor>Gornall P</RefAuthor>
<RefAuthor>Booth IW</RefAuthor>
<RefTitle>Parenteral nutrition-related cholestasis in postsurgical neonates: multivariate analysis of risk factors</RefTitle>
<RefYear>1996</RefYear>
<RefJournal>J Pediatr Surg</RefJournal>
<RefPage>604-6</RefPage>
<RefTotal>Beath SV, Davies P, Papadopoulou A, Khan AR, Buick RG, Corkery JJ, Gornall P, Booth IW. Parenteral nutrition-related cholestasis in postsurgical neonates: multivariate analysis of risk factors. J Pediatr Surg. 1996;31(4):604-6. DOI: 10.1016/S0022-3468(96)90507-2</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3468(96)90507-2</RefLink>
</Reference>
<Reference refNo="70">
<RefAuthor>Heird WC</RefAuthor>
<RefAuthor>Dell RB</RefAuthor>
<RefAuthor>Helms RA</RefAuthor>
<RefAuthor>Greene HL</RefAuthor>
<RefAuthor>Ament ME</RefAuthor>
<RefAuthor>Karna P</RefAuthor>
<RefAuthor>Storm MC</RefAuthor>
<RefTitle>Amino acid mixture designed to maintain normal plasma amino acid patterns in infants and children requiring parenteral nutrition</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>401-8</RefPage>
<RefTotal>Heird WC, Dell RB, Helms RA, Greene HL, Ament ME, Karna P, Storm MC. Amino acid mixture designed to maintain normal plasma amino acid patterns in infants and children requiring parenteral nutrition. Pediatrics. 1987;80(3):401-8.</RefTotal>
</Reference>
<Reference refNo="71">
<RefAuthor>Deutsche Gesellschaft für Ernährung e.V. (DGE); Österreichische Gesellschaft für Ernährung (ÖGE); Schweizerische Gesellschaft für Ernährungsforschung (SGE); Schweizerische Vereinigung für Ernährung (SVE)</RefAuthor>
<RefTitle></RefTitle>
<RefYear>2000</RefYear>
<RefBookTitle>Referenzwerte für die Nährstoffzufuhr</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Deutsche Gesellschaft für Ernährung e.V. (DGE); Österreichische Gesellschaft für Ernährung (ÖGE); Schweizerische Gesellschaft für Ernährungsforschung (SGE); Schweizerische Vereinigung für Ernährung (SVE). Referenzwerte für die Nährstoffzufuhr. Frankfurt am Main: Umschau Braus Verlag; 2000.</RefTotal>
</Reference>
<Reference refNo="72">
<RefAuthor>Bresson JL</RefAuthor>
<RefAuthor>Narcy P</RefAuthor>
<RefAuthor>Putet G</RefAuthor>
<RefAuthor>Ricour C</RefAuthor>
<RefAuthor>Sachs C</RefAuthor>
<RefAuthor>Rey J</RefAuthor>
<RefTitle>Energy substrate utilization in infants receiving total parenteral nutrition with different glucose to fat ratios</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>645-8</RefPage>
<RefTotal>Bresson JL, Narcy P, Putet G, Ricour C, Sachs C, Rey J. Energy substrate utilization in infants receiving total parenteral nutrition with different glucose to fat ratios. Pediatr Res. 1989;25(6):645-8. DOI: 10.1203/00006450-198906000-00018</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-198906000-00018</RefLink>
</Reference>
<Reference refNo="73">
<RefAuthor>Pierro A</RefAuthor>
<RefAuthor>Carnielli V</RefAuthor>
<RefAuthor>Filler RM</RefAuthor>
<RefAuthor>Smith J</RefAuthor>
<RefAuthor>Heim T</RefAuthor>
<RefTitle>Metabolism of intravenous fat emulsion in the surgical newborn</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>J Pediatr Surg</RefJournal>
<RefPage>95-102</RefPage>
<RefTotal>Pierro A, Carnielli V, Filler RM, Smith J, Heim T. Metabolism of intravenous fat emulsion in the surgical newborn. J Pediatr Surg. 1989;24(1):95-102. DOI: 10.1016/S0022-3468(89)80310-0</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3468(89)80310-0</RefLink>
</Reference>
<Reference refNo="74">
<RefAuthor>Salas-Salvado J</RefAuthor>
<RefAuthor>Molina J</RefAuthor>
<RefAuthor>Figueras J</RefAuthor>
<RefAuthor>Masso J</RefAuthor>
<RefAuthor>Marti-Henneberg C</RefAuthor>
<RefAuthor>Jimenez R</RefAuthor>
<RefTitle>Effect of the quality of infused energy on substrate utilization in the newborn receiving total parenteral nutrition</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>112-7</RefPage>
<RefTotal>Salas-Salvado J, Molina J, Figueras J, Masso J, Marti-Henneberg C, Jimenez R. Effect of the quality of infused energy on substrate utilization in the newborn receiving total parenteral nutrition. Pediatr Res. 1993;33(2):112-7. DOI: 10.1203/00006450-199302000-00004</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199302000-00004</RefLink>
</Reference>
<Reference refNo="75">
<RefAuthor>Bresson JL</RefAuthor>
<RefAuthor>Bader B</RefAuthor>
<RefAuthor>Rocchiccioli F</RefAuthor>
<RefAuthor>Mariotti A</RefAuthor>
<RefAuthor>Ricour C</RefAuthor>
<RefAuthor>Sachs C</RefAuthor>
<RefAuthor>Rey J</RefAuthor>
<RefTitle>Protein-metabolism kinetics and energy-substrate utilization in infants fed parenteral solutions with different glucose-fat ratios</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>370-6</RefPage>
<RefTotal>Bresson JL, Bader B, Rocchiccioli F, Mariotti A, Ricour C, Sachs C, Rey J. Protein-metabolism kinetics and energy-substrate utilization in infants fed parenteral solutions with different glucose-fat ratios. Am J Clin Nutr. 1991;54(2):370-6.</RefTotal>
</Reference>
<Reference refNo="76">
<RefAuthor>Macfie J</RefAuthor>
<RefAuthor>Smith RC</RefAuthor>
<RefAuthor>Hill GL</RefAuthor>
<RefTitle>Glucose or fat as a nonprotein energy source? A controlled clinical trial in gastroenterological patients requiring intravenous nutrition</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>Gastroenterology</RefJournal>
<RefPage>103-7</RefPage>
<RefTotal>Macfie J, Smith RC, Hill GL. Glucose or fat as a nonprotein energy source? A controlled clinical trial in gastroenterological patients requiring intravenous nutrition. Gastroenterology. 1981;80(1):103-7.</RefTotal>
</Reference>
<Reference refNo="77">
<RefAuthor>Sunehag AL</RefAuthor>
<RefTitle>The role of parenteral lipids in supporting gluconeogenesis in very premature infants</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>480-6</RefPage>
<RefTotal>Sunehag AL. The role of parenteral lipids in supporting gluconeogenesis in very premature infants. Pediatr Res. 2003;54(4):480-6. DOI: 10.1203/01.PDR.0000081298.06751.76</RefTotal>
<RefLink>http://dx.doi.org/10.1203/01.PDR.0000081298.06751.76</RefLink>
</Reference>
<Reference refNo="78">
<RefAuthor>Cooke RJ</RefAuthor>
<RefAuthor>Zee P</RefAuthor>
<RefAuthor>Yeh YY</RefAuthor>
<RefTitle>Essential fatty acid status of the premature infant during short-term fat-free parenteral nutrition</RefTitle>
<RefYear>1984</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>446-9</RefPage>
<RefTotal>Cooke RJ, Zee P, Yeh YY. Essential fatty acid status of the premature infant during short-term fat-free parenteral nutrition. J Pediatr Gastroenterol Nutr. 1984;3(3):446-9. DOI: 10.1097/00005176-198406000-00024</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00005176-198406000-00024</RefLink>
</Reference>
<Reference refNo="79">
<RefAuthor>Friedman Z</RefAuthor>
<RefAuthor>Danon A</RefAuthor>
<RefAuthor>Stahlman MT</RefAuthor>
<RefAuthor>Oates JA</RefAuthor>
<RefTitle>Rapid onset of essential fatty acid deficiency in the newborn</RefTitle>
<RefYear>1976</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>640-9</RefPage>
<RefTotal>Friedman Z, Danon A, Stahlman MT, Oates JA. Rapid onset of essential fatty acid deficiency in the newborn. Pediatrics. 1976;58(5):640-9.</RefTotal>
</Reference>
<Reference refNo="80">
<RefAuthor>Lee EJ</RefAuthor>
<RefAuthor>Simmer K</RefAuthor>
<RefAuthor>Gibson RA</RefAuthor>
<RefTitle>Essential fatty acid deficiency in parenterally fed preterm infants</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>J Paediatr Child Health</RefJournal>
<RefPage>51-5</RefPage>
<RefTotal>Lee EJ, Simmer K, Gibson RA. Essential fatty acid deficiency in parenterally fed preterm infants. J Paediatr Child Health. 1993;29(1):51-5. DOI: 10.1111/j.1440-1754.1993.tb00440.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1440-1754.1993.tb00440.x</RefLink>
</Reference>
<Reference refNo="81">
<RefAuthor>Cooke RJ</RefAuthor>
<RefAuthor>Yeh YY</RefAuthor>
<RefAuthor>Gibson D</RefAuthor>
<RefAuthor>Debo D</RefAuthor>
<RefAuthor>Bell GL</RefAuthor>
<RefTitle>Soybean oil emulsion administration during parenteral nutrition in the preterm infant: effect on essential fatty acid, lipid, and glucose metabolism</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>767-73</RefPage>
<RefTotal>Cooke RJ, Yeh YY, Gibson D, Debo D, Bell GL. Soybean oil emulsion administration during parenteral nutrition in the preterm infant: effect on essential fatty acid, lipid, and glucose metabolism. J Pediatr. 1987;111(5):767-73. DOI: 10.1016/S0022-3476(87)80265-2</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(87)80265-2</RefLink>
</Reference>
<Reference refNo="82">
<RefAuthor>Anderson GJ</RefAuthor>
<RefAuthor>Connor WE</RefAuthor>
<RefTitle>On the demonstration of omega-3 essential-fatty-acid deficiency in humans</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>585-7</RefPage>
<RefTotal>Anderson GJ, Connor WE. On the demonstration of omega-3 essential-fatty-acid deficiency in humans. Am J Clin Nutr. 1989;49(4):585-7.</RefTotal>
</Reference>
<Reference refNo="83">
<RefAuthor>Holman RT</RefAuthor>
<RefAuthor>Johnson SB</RefAuthor>
<RefTitle>Linolenic acid deficiency in man</RefTitle>
<RefYear>1982</RefYear>
<RefJournal>Nutr Rev</RefJournal>
<RefPage>144-7</RefPage>
<RefTotal>Holman RT, Johnson SB. Linolenic acid deficiency in man. Nutr Rev. 1982;40(5):144-7.</RefTotal>
</Reference>
<Reference refNo="84">
<RefAuthor>Brans YW</RefAuthor>
<RefAuthor>Andrew DS</RefAuthor>
<RefAuthor>Carrillo DW</RefAuthor>
<RefAuthor>Dutton EP</RefAuthor>
<RefAuthor>Menchaca EM</RefAuthor>
<RefAuthor>Puleo-Scheppke BA</RefAuthor>
<RefTitle>Tolerance of fat emulsions in very-low-birth-weight neonates</RefTitle>
<RefYear>1988</RefYear>
<RefJournal>Am J Dis Child</RefJournal>
<RefPage>145-52</RefPage>
<RefTotal>Brans YW, Andrew DS, Carrillo DW, Dutton EP, Menchaca EM, Puleo-Scheppke BA. Tolerance of fat emulsions in very-low-birth-weight neonates. Am J Dis Child. 1988;142(2):145-52.</RefTotal>
</Reference>
<Reference refNo="85">
<RefAuthor>Hilliard JL</RefAuthor>
<RefAuthor>Shannon DL</RefAuthor>
<RefAuthor>Hunter MA</RefAuthor>
<RefAuthor>Brans YW</RefAuthor>
<RefTitle>Plasma lipid levels in preterm neonates receiving parenteral fat emulsions</RefTitle>
<RefYear>1983</RefYear>
<RefJournal>Arch Dis Child</RefJournal>
<RefPage>29-33</RefPage>
<RefTotal>Hilliard JL, Shannon DL, Hunter MA, Brans YW. Plasma lipid levels in preterm neonates receiving parenteral fat emulsions. Arch Dis Child. 1983;58:29-33. DOI: 10.1136/adc.58.1.29</RefTotal>
<RefLink>http://dx.doi.org/10.1136/adc.58.1.29</RefLink>
</Reference>
<Reference refNo="86">
<RefAuthor>Kao LC</RefAuthor>
<RefAuthor>Cheng MH</RefAuthor>
<RefAuthor>Warburton D</RefAuthor>
<RefTitle>Triglycerides, free fatty acids, free fatty acids/albumin molar ratio, and cholesterol levels in serum of neonates receiving long-term lipid infusions: controlled trial of continuous and intermittent regimens</RefTitle>
<RefYear>1984</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>429-35</RefPage>
<RefTotal>Kao LC, Cheng MH, Warburton D. Triglycerides, free fatty acids, free fatty acids/albumin molar ratio, and cholesterol levels in serum of neonates receiving long-term lipid infusions: controlled trial of continuous and intermittent regimens. J Pediatr. 1984;104(3):429-35. DOI: 10.1016/S0022-3476(84)81111-7</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(84)81111-7</RefLink>
</Reference>
<Reference refNo="87">
<RefAuthor>Brans YW</RefAuthor>
<RefAuthor>Andrew DS</RefAuthor>
<RefAuthor>Carrillo DW</RefAuthor>
<RefAuthor>Dutton EB</RefAuthor>
<RefAuthor>Menchaca EM</RefAuthor>
<RefAuthor>Puelo-Scheppke BA</RefAuthor>
<RefTitle>Tolerance of fat emulsions in very low birthweight neonates: effect of birthweight on plasma lipid concentrations</RefTitle>
<RefYear>1990</RefYear>
<RefJournal>Am J Perinatol</RefJournal>
<RefPage>114-7</RefPage>
<RefTotal>Brans YW, Andrew DS, Carrillo DW, Dutton EB, Menchaca EM, Puelo-Scheppke BA. Tolerance of fat emulsions in very low birthweight neonates: effect of birthweight on plasma lipid concentrations. Am J Perinatol. 1990;7:114-7. DOI: 10.1055/s-2007-999459</RefTotal>
<RefLink>http://dx.doi.org/10.1055/s-2007-999459</RefLink>
</Reference>
<Reference refNo="88">
<RefAuthor>Brans YW</RefAuthor>
<RefAuthor>Dutton EB</RefAuthor>
<RefAuthor>Andrew DS</RefAuthor>
<RefAuthor>Menchaca EM</RefAuthor>
<RefAuthor>West DL</RefAuthor>
<RefTitle>Fat emulsion tolerance in very low birth weight neonates: effect on diffusion of oxygen in the lungs and on blood pH</RefTitle>
<RefYear>1986</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>79-84</RefPage>
<RefTotal>Brans YW, Dutton EB, Andrew DS, Menchaca EM, West DL. Fat emulsion tolerance in very low birth weight neonates: effect on diffusion of oxygen in the lungs and on blood pH. Pediatrics. 1986;78(1):79-84.</RefTotal>
</Reference>
<Reference refNo="89">
<RefAuthor>Dhanireddy R</RefAuthor>
<RefAuthor>Hamosh M</RefAuthor>
<RefAuthor>Sivasubramanian KN</RefAuthor>
<RefAuthor>Chowdhry P</RefAuthor>
<RefAuthor>Scanlon JW</RefAuthor>
<RefAuthor>Hamosh P</RefAuthor>
<RefTitle>Postheparin lipolytic activity and Intralipid clearance in very low-birth-weight infants</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>617-22</RefPage>
<RefTotal>Dhanireddy R, Hamosh M, Sivasubramanian KN, Chowdhry P, Scanlon JW, Hamosh P. Postheparin lipolytic activity and Intralipid clearance in very low-birth-weight infants. J Pediatr. 1981;98(4):617-22. DOI: 10.1016/S0022-3476(81)80777-9</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(81)80777-9</RefLink>
</Reference>
<Reference refNo="90">
<RefAuthor>Spear ML</RefAuthor>
<RefAuthor>Stahl GE</RefAuthor>
<RefAuthor>Hamosh M</RefAuthor>
<RefAuthor>McNelis WG</RefAuthor>
<RefAuthor>Richardson LL</RefAuthor>
<RefAuthor>Spence V</RefAuthor>
<RefAuthor>Polin RA</RefAuthor>
<RefAuthor>Pereira GR</RefAuthor>
<RefAuthor>Hamosh P</RefAuthor>
<RefTitle>Effect of heparin dose and infusion rate on lipid clearance and bilirubin binding in premature infants receiving intravenous fat emulsions</RefTitle>
<RefYear>1988</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>94-8</RefPage>
<RefTotal>Spear ML, Stahl GE, Hamosh M, McNelis WG, Richardson LL, Spence V, Polin RA, Pereira GR, Hamosh P. Effect of heparin dose and infusion rate on lipid clearance and bilirubin binding in premature infants receiving intravenous fat emulsions. J Pediatr. 1988;112(1):94-8. DOI: 10.1016/S0022-3476(88)80129-X</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(88)80129-X</RefLink>
</Reference>
<Reference refNo="91">
<RefAuthor>Berkow SE</RefAuthor>
<RefAuthor>Spear ML</RefAuthor>
<RefAuthor>Stahl GE</RefAuthor>
<RefAuthor>Gutman A</RefAuthor>
<RefAuthor>Polin RA</RefAuthor>
<RefAuthor>Pereira GR</RefAuthor>
<RefAuthor>Olivecrona T</RefAuthor>
<RefAuthor>Hamosh P</RefAuthor>
<RefAuthor>Hamosh M</RefAuthor>
<RefTitle>Total parenteral nutrition with intralipid in premature infants receiving TPN with heparin: effect on plasma lipolytic enzymes, lipids, and glucose</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>581-8</RefPage>
<RefTotal>Berkow SE, Spear ML, Stahl GE, Gutman A, Polin RA, Pereira GR, Olivecrona T, Hamosh P, Hamosh M. Total parenteral nutrition with intralipid in premature infants receiving TPN with heparin: effect on plasma lipolytic enzymes, lipids, and glucose. J Pediatr Gastroenterol Nutr. 1987;6(4):581-8.</RefTotal>
</Reference>
<Reference refNo="92">
<RefAuthor>Basu R</RefAuthor>
<RefAuthor>Muller DP</RefAuthor>
<RefAuthor>Papp E</RefAuthor>
<RefAuthor>Merryweather I</RefAuthor>
<RefAuthor>Eaton S</RefAuthor>
<RefAuthor>Klein N</RefAuthor>
<RefAuthor>Pierro A</RefAuthor>
<RefTitle>Free radical formation in infants: the effect of critical illness, parenteral nutrition, and enteral feeding</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>J Pediatr Surg</RefJournal>
<RefPage>1091-5</RefPage>
<RefTotal>Basu R, Muller DP, Papp E, Merryweather I, Eaton S, Klein N, Pierro A. Free radical formation in infants: the effect of critical illness, parenteral nutrition, and enteral feeding. J Pediatr Surg. 1999;34(7):1091-5. DOI: 10.1016/S0022-3468(99)90573-0</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3468(99)90573-0</RefLink>
</Reference>
<Reference refNo="93">
<RefAuthor>Pironi L</RefAuthor>
<RefAuthor>Guidetti M</RefAuthor>
<RefAuthor>Zolezzi C</RefAuthor>
<RefAuthor>Fasano MC</RefAuthor>
<RefAuthor>Paganelli F</RefAuthor>
<RefAuthor>Merli C</RefAuthor>
<RefAuthor>Bersani G</RefAuthor>
<RefAuthor>Pizzoferrato A</RefAuthor>
<RefAuthor>Miglioli M</RefAuthor>
<RefTitle>Peroxidation potential of lipid emulsions after compounding in all-in-one solutions</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Nutrition</RefJournal>
<RefPage>784-8</RefPage>
<RefTotal>Pironi L, Guidetti M, Zolezzi C, Fasano MC, Paganelli F, Merli C, Bersani G, Pizzoferrato A, Miglioli M. Peroxidation potential of lipid emulsions after compounding in all-in-one solutions. Nutrition. 2003;19(9):784-8. DOI: 10.1016/S0899-9007(03)00099-6</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0899-9007(03)00099-6</RefLink>
</Reference>
<Reference refNo="94">
<RefAuthor>Pitkänen O</RefAuthor>
<RefAuthor>Hallman M</RefAuthor>
<RefAuthor>Andersson S</RefAuthor>
<RefTitle>Generation of free radicals in lipid emulsion used in parenteral nutrition</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>56-9</RefPage>
<RefTotal>Pitkänen O, Hallman M, Andersson S. Generation of free radicals in lipid emulsion used in parenteral nutrition. Pediatr Res. 1991;29(1):56-9. DOI: 10.1203/00006450-199101000-00011</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199101000-00011</RefLink>
</Reference>
<Reference refNo="95">
<RefAuthor>Greene HL</RefAuthor>
<RefAuthor>Moore ME</RefAuthor>
<RefAuthor>Phillips B</RefAuthor>
<RefAuthor>Franck L</RefAuthor>
<RefAuthor>Shulman RJ</RefAuthor>
<RefAuthor>Ament ME</RefAuthor>
<RefAuthor>Murrell JE</RefAuthor>
<RefAuthor>Chan MM</RefAuthor>
<RefAuthor>Said HM</RefAuthor>
<RefTitle>Evaluation of a pediatric multiple vitamin preparation for total parenteral nutrition. II. Blood levels of vitamins A, D, and E</RefTitle>
<RefYear>1986</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>539-47</RefPage>
<RefTotal>Greene HL, Moore ME, Phillips B, Franck L, Shulman RJ, Ament ME, Murrell JE, Chan MM, Said HM. Evaluation of a pediatric multiple vitamin preparation for total parenteral nutrition. II. Blood levels of vitamins A, D, and E. Pediatrics. 1986;77(4):539-47.</RefTotal>
</Reference>
<Reference refNo="96">
<RefAuthor>Keenoy B</RefAuthor>
<RefAuthor>Nonneman L</RefAuthor>
<RefAuthor>De Bosscher H</RefAuthor>
<RefAuthor>Vertommen J</RefAuthor>
<RefAuthor>Schrans S</RefAuthor>
<RefAuthor>Klütsch K</RefAuthor>
<RefAuthor>De Leeuw I</RefAuthor>
<RefTitle>Effects of intravenous supplementation with alpha-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Eur J Clin Nutr</RefJournal>
<RefPage>121-8</RefPage>
<RefTotal>Keenoy B, Nonneman L, De Bosscher H, Vertommen J, Schrans S, Klütsch K, De Leeuw I. Effects of intravenous supplementation with alpha-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides. Eur J Clin Nutr. 2002;56(2):121-8. DOI: 10.1038/sj.ejcn.1601294</RefTotal>
<RefLink>http://dx.doi.org/10.1038/sj.ejcn.1601294</RefLink>
</Reference>
<Reference refNo="97">
<RefAuthor>Wu GH</RefAuthor>
<RefAuthor>Jarstrand C</RefAuthor>
<RefAuthor>Nordenström J</RefAuthor>
<RefTitle>Phagocyte-induced lipid peroxidation of different intravenous fat emulsions and counteractive effect of vitamin E</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Nutrition</RefJournal>
<RefPage>359-64</RefPage>
<RefTotal>Wu GH, Jarstrand C, Nordenström J. Phagocyte-induced lipid peroxidation of different intravenous fat emulsions and counteractive effect of vitamin E. Nutrition. 1999;15(5):359-64. DOI: 10.1016/S0899-9007(99)00052-0</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0899-9007(99)00052-0</RefLink>
</Reference>
<Reference refNo="98">
<RefAuthor>Haumont D</RefAuthor>
<RefAuthor>Deckelbaum RJ</RefAuthor>
<RefAuthor>Richelle M</RefAuthor>
<RefAuthor>Dahlan W</RefAuthor>
<RefAuthor>Coussaert E</RefAuthor>
<RefAuthor>Bihain BE</RefAuthor>
<RefAuthor>Carpentier YA</RefAuthor>
<RefTitle>Plasma lipid and plasma lipoprotein concentrations in low birth weight infants given parenteral nutrition with twenty or ten percent lipid emulsion</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>787-93</RefPage>
<RefTotal>Haumont D, Deckelbaum RJ, Richelle M, Dahlan W, Coussaert E, Bihain BE, Carpentier YA. Plasma lipid and plasma lipoprotein concentrations in low birth weight infants given parenteral nutrition with twenty or ten percent lipid emulsion. J Pediatr. 1989;115(5 Pt 1):787-93. DOI: 10.1016/S0022-3476(89)80663-8</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(89)80663-8</RefLink>
</Reference>
<Reference refNo="99">
<RefAuthor>Koletzko B</RefAuthor>
<RefAuthor>Agostoni C</RefAuthor>
<RefAuthor>Carlson SE</RefAuthor>
<RefAuthor>Clandinin T</RefAuthor>
<RefAuthor>Hornstra G</RefAuthor>
<RefAuthor>Neuringer M</RefAuthor>
<RefAuthor>Uauy R</RefAuthor>
<RefAuthor>Yamashiro Y</RefAuthor>
<RefAuthor>Willatts P</RefAuthor>
<RefTitle>Long chain polyunsaturated fatty acids (LC-PUFA) and perinatal development</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Acta Paediatr</RefJournal>
<RefPage>460-4</RefPage>
<RefTotal>Koletzko B, Agostoni C, Carlson SE, Clandinin T, Hornstra G, Neuringer M, Uauy R, Yamashiro Y, Willatts P. Long chain polyunsaturated fatty acids (LC-PUFA) and perinatal development. Acta Paediatr. 2001;90(4):460-4.</RefTotal>
</Reference>
<Reference refNo="100">
<RefAuthor>Uauy R</RefAuthor>
<RefAuthor>Hoffman DR</RefAuthor>
<RefAuthor>Peirano P</RefAuthor>
<RefAuthor>Birch DG</RefAuthor>
<RefAuthor>Birch EE</RefAuthor>
<RefTitle>Essential fatty acids in visual and brain development</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Lipids</RefJournal>
<RefPage>885-95</RefPage>
<RefTotal>Uauy R, Hoffman DR, Peirano P, Birch DG, Birch EE. Essential fatty acids in visual and brain development. Lipids. 2001;36(9):885-95. DOI: 10.1007/s11745-001-0798-1</RefTotal>
<RefLink>http://dx.doi.org/10.1007/s11745-001-0798-1</RefLink>
</Reference>
<Reference refNo="101">
<RefAuthor>Lange R</RefAuthor>
<RefAuthor>Erhard J</RefAuthor>
<RefAuthor>Eigler FW</RefAuthor>
<RefAuthor>Roll C</RefAuthor>
<RefTitle>Lactic acidosis from thiamine deficiency during parenteral nutrition in a two-year-old boy</RefTitle>
<RefYear>1992</RefYear>
<RefJournal>Eur J Pediatr Surg</RefJournal>
<RefPage>241-4</RefPage>
<RefTotal>Lange R, Erhard J, Eigler FW, Roll C. Lactic acidosis from thiamine deficiency during parenteral nutrition in a two-year-old boy. Eur J Pediatr Surg. 1992;2:241-4. DOI: 10.1055/s-2008-1063451</RefTotal>
<RefLink>http://dx.doi.org/10.1055/s-2008-1063451</RefLink>
</Reference>
<Reference refNo="102">
<RefAuthor>Greene HL</RefAuthor>
<RefAuthor>Hambidge KM</RefAuthor>
<RefAuthor>Schanler R</RefAuthor>
<RefAuthor>Tsang RC</RefAuthor>
<RefTitle>Guidelines for the use of vitamins, trace elements, calcium, magnesium, and phosphorus in infants and children receiving total parenteral nutrition: report of the Subcommittee on Pediatric Parenteral Nutrient Requirements from the Committee on Clinical Practice Issues of the American Society for Clinical Nutrition</RefTitle>
<RefYear>1988</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>1324-42</RefPage>
<RefTotal>Greene HL, Hambidge KM, Schanler R, Tsang RC. Guidelines for the use of vitamins, trace elements, calcium, magnesium, and phosphorus in infants and children receiving total parenteral nutrition: report of the Subcommittee on Pediatric Parenteral Nutrient Requirements from the Committee on Clinical Practice Issues of the American Society for Clinical Nutrition. Am J Clin Nutr. 1988;48(5):1324-42.</RefTotal>
</Reference>
<Reference refNo="103">
<RefAuthor>Gillis J</RefAuthor>
<RefAuthor>Jones G</RefAuthor>
<RefAuthor>Pencharz P</RefAuthor>
<RefTitle>Delivery of vitamins A, D, and E in total parenteral nutrition solutions</RefTitle>
<RefYear>1983</RefYear>
<RefJournal>JPEN J Parenter Enteral Nutr</RefJournal>
<RefPage>11-4</RefPage>
<RefTotal>Gillis J, Jones G, Pencharz P. Delivery of vitamins A, D, and E in total parenteral nutrition solutions. JPEN J Parenter Enteral Nutr. 1983;7(1):11-4. DOI: 10.1177/014860718300700111</RefTotal>
<RefLink>http://dx.doi.org/10.1177/014860718300700111</RefLink>
</Reference>
<Reference refNo="104">
<RefAuthor>Silvers KM</RefAuthor>
<RefAuthor>Sluis KB</RefAuthor>
<RefAuthor>Darlow BA</RefAuthor>
<RefAuthor>McGill F</RefAuthor>
<RefAuthor>Stocker R</RefAuthor>
<RefAuthor>Winterbourn CC</RefAuthor>
<RefTitle>Limiting light-induced lipid peroxidation and vitamin loss in infant parenteral nutrition by adding multivitamin preparations to Intralipid</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Acta Paediatr</RefJournal>
<RefPage>242-9</RefPage>
<RefTotal>Silvers KM, Sluis KB, Darlow BA, McGill F, Stocker R, Winterbourn CC. Limiting light-induced lipid peroxidation and vitamin loss in infant parenteral nutrition by adding multivitamin preparations to Intralipid. Acta Paediatr. 2001;90(3):242-9.</RefTotal>
</Reference>
<Reference refNo="105">
<RefAuthor>Laborie S</RefAuthor>
<RefAuthor>Lavoie JC</RefAuthor>
<RefAuthor>Chessex P</RefAuthor>
<RefTitle>Increased urinary peroxides in newborn infants receiving parenteral nutrition exposed to light</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>628-32</RefPage>
<RefTotal>Laborie S, Lavoie JC, Chessex P. Increased urinary peroxides in newborn infants receiving parenteral nutrition exposed to light. J Pediatr. 2000;136(5):628-32. DOI: 10.1067/mpd.2000.105131</RefTotal>
<RefLink>http://dx.doi.org/10.1067/mpd.2000.105131</RefLink>
</Reference>
<Reference refNo="106">
<RefAuthor>Chessex P</RefAuthor>
<RefAuthor>Laborie S</RefAuthor>
<RefAuthor>Lavoie JC</RefAuthor>
<RefAuthor>Rouleau T</RefAuthor>
<RefTitle>Photoprotection of solutions of parenteral nutrition decreases the infused load as well as the urinary excretion of peroxides in premature infants</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Semin Perinatol</RefJournal>
<RefPage>55-9</RefPage>
<RefTotal>Chessex P, Laborie S, Lavoie JC, Rouleau T. Photoprotection of solutions of parenteral nutrition decreases the infused load as well as the urinary excretion of peroxides in premature infants. Semin Perinatol. 2001;25(2):55-9.</RefTotal>
</Reference>
<Reference refNo="107">
<RefAuthor>Agostoni C</RefAuthor>
<RefAuthor>Buonocore G</RefAuthor>
<RefAuthor>Carnielli VP</RefAuthor>
<RefAuthor>De Curtis M</RefAuthor>
<RefAuthor>Darmaun D</RefAuthor>
<RefAuthor>Decsi T</RefAuthor>
<RefAuthor>Domellöf M</RefAuthor>
<RefAuthor>Embleton ND</RefAuthor>
<RefAuthor>Fusch C</RefAuthor>
<RefAuthor>Genzel-Boroviczeny O</RefAuthor>
<RefAuthor>Goulet O</RefAuthor>
<RefAuthor>Kalhan SC</RefAuthor>
<RefAuthor>Kolacek S</RefAuthor>
<RefAuthor>Koletzko B</RefAuthor>
<RefAuthor>Lapillonne A</RefAuthor>
<RefAuthor>Mihatsch W</RefAuthor>
<RefAuthor>Moreno L</RefAuthor>
<RefAuthor>Neu J</RefAuthor>
<RefAuthor>Poindexter B</RefAuthor>
<RefAuthor>Puntis J</RefAuthor>
<RefAuthor>Putet G</RefAuthor>
<RefAuthor>Rigo J</RefAuthor>
<RefAuthor>Riskin A</RefAuthor>
<RefAuthor>Salle B</RefAuthor>
<RefAuthor>Sauer P</RefAuthor>
<RefAuthor>Shamir R</RefAuthor>
<RefAuthor>Szajewska H</RefAuthor>
<RefAuthor>Thureen P</RefAuthor>
<RefAuthor>Turck D</RefAuthor>
<RefAuthor>van Goudoever JB</RefAuthor>
<RefAuthor>Ziegler E; for the ESPGHAN Committee on Nutrition</RefAuthor>
<RefTitle>Enteral nutrient supply for preterm infants: Commentary from the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition</RefTitle>
<RefYear>2009</RefYear>
<RefJournal>J Pediatr Gastro Nutr</RefJournal>
<RefPage></RefPage>
<RefTotal>Agostoni C, Buonocore G, Carnielli VP, De Curtis M, Darmaun D, Decsi T, Domellöf M, Embleton ND, Fusch C, Genzel-Boroviczeny O, Goulet O, Kalhan SC, Kolacek S, Koletzko B, Lapillonne A, Mihatsch W, Moreno L, Neu J, Poindexter B,Puntis J, Putet G, Rigo J, Riskin A, Salle B, Sauer P, Shamir R, Szajewska H, Thureen P, Turck D, van Goudoever JB, Ziegler E; for the ESPGHAN Committee on Nutrition. Enteral nutrient supply for preterm infants: Commentary from the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition. J Pediatr Gastro Nutr. 2009 Oct 29. [Epub ahead of print].</RefTotal>
</Reference>
<Reference refNo="108">
<RefAuthor>Greer FR</RefAuthor>
<RefTitle>Vitamin K deficiency and hemorrhage in infancy</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>Clin Perinatol</RefJournal>
<RefPage>759-77</RefPage>
<RefTotal>Greer FR. Vitamin K deficiency and hemorrhage in infancy. Clin Perinatol. 1995;22(3):759-77.</RefTotal>
</Reference>
<Reference refNo="109">
<RefAuthor>Greer FR</RefAuthor>
<RefTitle>Vitamin metabolism and requirements in the micropremie</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Clin Perinatol</RefJournal>
<RefPage>95-118, vi</RefPage>
<RefTotal>Greer FR. Vitamin metabolism and requirements in the micropremie. Clin Perinatol. 2000;27(1):95-118, vi.</RefTotal>
</Reference>
<Reference refNo="110">
<RefAuthor>Kumar D</RefAuthor>
<RefAuthor>Greer FR</RefAuthor>
<RefAuthor>Super DM</RefAuthor>
<RefAuthor>Suttie JW</RefAuthor>
<RefAuthor>Moore JJ</RefAuthor>
<RefTitle>Vitamin K status of premature infants: implications for current recommendations</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>1117-22</RefPage>
<RefTotal>Kumar D, Greer FR, Super DM, Suttie JW, Moore JJ. Vitamin K status of premature infants: implications for current recommendations. Pediatrics. 2001;108(5):1117-22.</RefTotal>
</Reference>
<Reference refNo="111">
<RefAuthor>Jochum F</RefAuthor>
<RefAuthor>Fuchs A</RefAuthor>
<RefAuthor>Cser A</RefAuthor>
<RefAuthor>Menzel H</RefAuthor>
<RefAuthor>Lombeck I</RefAuthor>
<RefTitle>Trace mineral status of full-term infants fed human milk, milk-based formula or partially hydrolysed whey protein formula</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>Analyst</RefJournal>
<RefPage>905-9</RefPage>
<RefTotal>Jochum F, Fuchs A, Cser A, Menzel H, Lombeck I. Trace mineral status of full-term infants fed human milk, milk-based formula or partially hydrolysed whey protein formula. Analyst. 1995;120:905-9. DOI: 10.1039/an9952000905</RefTotal>
<RefLink>http://dx.doi.org/10.1039/an9952000905</RefLink>
</Reference>
<Reference refNo="112">
<RefAuthor>Aggett PJ</RefAuthor>
<RefAuthor>Fairweather-Tait S</RefAuthor>
<RefTitle>Adaptation to high and low copper intakes: its relevance to estimated safe and adequate daily dietary intakes</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>1061S-3S</RefPage>
<RefTotal>Aggett PJ, Fairweather-Tait S. Adaptation to high and low copper intakes: its relevance to estimated safe and adequate daily dietary intakes. Am J Clin Nutr. 1998;67(5 Suppl):1061S-3S.</RefTotal>
</Reference>
<Reference refNo="113">
<RefAuthor>Ehrenkranz RA</RefAuthor>
<RefAuthor>Gettner PA</RefAuthor>
<RefAuthor>Nelli CM</RefAuthor>
<RefAuthor>Sherwont EA</RefAuthor>
<RefAuthor>Williams JE</RefAuthor>
<RefAuthor>Ting BT</RefAuthor>
<RefAuthor>Janghorbani M</RefAuthor>
<RefTitle>Zinc and copper nutritional studies in very low birth weight infants: comparison of stable isotopic extrinsic tag and chemical balance methods</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>298-307</RefPage>
<RefTotal>Ehrenkranz RA, Gettner PA, Nelli CM, Sherwont EA, Williams JE, Ting BT, Janghorbani M. Zinc and copper nutritional studies in very low birth weight infants: comparison of stable isotopic extrinsic tag and chemical balance methods. Pediatr Res. 1989;26(4):298-307. DOI: 10.1203/00006450-198910000-00004</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-198910000-00004</RefLink>
</Reference>
<Reference refNo="114">
<RefAuthor>Vuori E</RefAuthor>
<RefTitle>Intake of copper, iron, manganese and zinc by healthy, exclusively-breast-fed infants during the first 3 months of life</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>Br J Nutr</RefJournal>
<RefPage>407-11</RefPage>
<RefTotal>Vuori E. Intake of copper, iron, manganese and zinc by healthy, exclusively-breast-fed infants during the first 3 months of life. Br J Nutr. 1979;42:407-11. DOI: 10.1079/BJN19790131</RefTotal>
<RefLink>http://dx.doi.org/10.1079/BJN19790131</RefLink>
</Reference>
<Reference refNo="115">
<RefAuthor>Aggett PJ</RefAuthor>
<RefTitle>Trace elements of the micropremie</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Clin Perinatol</RefJournal>
<RefPage>119-29</RefPage>
<RefTotal>Aggett PJ. Trace elements of the micropremie. Clin Perinatol. 2000;27(1):119-29. DOI: 10.1016/S0095-5108(05)70009-9</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0095-5108(05)70009-9</RefLink>
</Reference>
<Reference refNo="116">
<RefAuthor>Bausen C</RefAuthor>
<RefAuthor>Jochum F</RefAuthor>
<RefAuthor>Fusch C</RefAuthor>
<RefTitle>Perinatale Dermatitis durch Zinkmangel bei einem ehemaligen Frühgeborenen (25+1 SSW)</RefTitle>
<RefYear>2002</RefYear>
<RefBookTitle>Mengen und Spurenelemente</RefBookTitle>
<RefPage>1018-22</RefPage>
<RefTotal>Bausen C, Jochum F, Fusch C. Perinatale Dermatitis durch Zinkmangel bei einem ehemaligen Frühgeborenen (25+1 SSW). In: Anke M, Müller R, Schäfer U, Stoeppler M, editors. Mengen und Spurenelemente. Leipzig: Verlag Harald Schubert; 2002. p. 1018-22.</RefTotal>
</Reference>
<Reference refNo="117">
<RefAuthor>Jochum F</RefAuthor>
<RefAuthor>Lombeck I</RefAuthor>
<RefTitle>Genetic Defects Related to Metals Other Than Copper</RefTitle>
<RefYear>2000</RefYear>
<RefBookTitle>Inborn Metabolic Diseases – Diagnosis and Treatment</RefBookTitle>
<RefPage></RefPage>
<RefTotal>Jochum F, Lombeck I. Genetic Defects Related to Metals Other Than Copper. In: Fernandes J, Saudubray JM, editors. Inborn Metabolic Diseases – Diagnosis and Treatment. Berlin: Springer Verlag; 2000.</RefTotal>
</Reference>
<Reference refNo="118">
<RefAuthor>Suchner U</RefAuthor>
<RefAuthor>Heyland DK</RefAuthor>
<RefAuthor>Peter K</RefAuthor>
<RefTitle>Immune-modulatory actions of arginine in the critically ill</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Br J Nutr</RefJournal>
<RefPage>S121-32</RefPage>
<RefTotal>Suchner U, Heyland DK, Peter K. Immune-modulatory actions of arginine in the critically ill. Br J Nutr. 2002;87 Suppl 1:S121-32. DOI: 10.1079/BJN2001465</RefTotal>
<RefLink>http://dx.doi.org/10.1079/BJN2001465</RefLink>
</Reference>
<Reference refNo="119">
<RefAuthor>Neu J</RefAuthor>
<RefAuthor>Roig JC</RefAuthor>
<RefAuthor>Meetze WH</RefAuthor>
<RefAuthor>Veerman M</RefAuthor>
<RefAuthor>Carter C</RefAuthor>
<RefAuthor>Millsaps M</RefAuthor>
<RefAuthor>Bowling D</RefAuthor>
<RefAuthor>Dallas MJ</RefAuthor>
<RefAuthor>Sleasman J</RefAuthor>
<RefAuthor>Knight T</RefAuthor>
<RefAuthor>Auestad N</RefAuthor>
<RefTitle>Enteral glutamine supplementation for very low birth weight infants decreases morbidity</RefTitle>
<RefYear>1997</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>691-9</RefPage>
<RefTotal>Neu J, Roig JC, Meetze WH, Veerman M, Carter C, Millsaps M, Bowling D, Dallas MJ, Sleasman J, Knight T, Auestad N. Enteral glutamine supplementation for very low birth weight infants decreases morbidity. J Pediatr. 1997;131(5):691-9. DOI: 10.1016/S0022-3476(97)70095-7</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(97)70095-7</RefLink>
</Reference>
<Reference refNo="120">
<RefAuthor>Poindexter BB</RefAuthor>
<RefAuthor>Ehrenkranz RA</RefAuthor>
<RefAuthor>Stoll BJ</RefAuthor>
<RefAuthor>Wright LL</RefAuthor>
<RefAuthor>Poole WK</RefAuthor>
<RefAuthor>Oh W</RefAuthor>
<RefAuthor>Bauer CR</RefAuthor>
<RefAuthor>Papile LA</RefAuthor>
<RefAuthor>Tyson JE</RefAuthor>
<RefAuthor>Carlo WA</RefAuthor>
<RefAuthor>Laptook AR</RefAuthor>
<RefAuthor>Narendran V</RefAuthor>
<RefAuthor>Stevenson DK</RefAuthor>
<RefAuthor>Fanaroff AA</RefAuthor>
<RefAuthor>Korones SB</RefAuthor>
<RefAuthor>Shankaran S</RefAuthor>
<RefAuthor>Finer NN</RefAuthor>
<RefAuthor>Lemons JA; National Institute of Child Health and Human Development Neonatal Research Network</RefAuthor>
<RefTitle>Parenteral glutamine supplementation does not reduce the risk of mortality or late-onset sepsis in extremely low birth weight infants</RefTitle>
<RefYear>2004</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>1209-15</RefPage>
<RefTotal>Poindexter BB, Ehrenkranz RA, Stoll BJ, Wright LL, Poole WK, Oh W, Bauer CR, Papile LA, Tyson JE, Carlo WA, Laptook AR, Narendran V, Stevenson DK, Fanaroff AA, Korones SB, Shankaran S, Finer NN, Lemons JA; National Institute of Child Health and Human Development Neonatal Research Network. Parenteral glutamine supplementation does not reduce the risk of mortality or late-onset sepsis in extremely low birth weight infants. Pediatrics. 2004;113(5):1209-15. DOI: 10.1542/peds.113.5.1209</RefTotal>
<RefLink>http://dx.doi.org/10.1542/peds.113.5.1209</RefLink>
</Reference>
<Reference refNo="121">
<RefAuthor>Tubman TR</RefAuthor>
<RefAuthor>Thompson SW</RefAuthor>
<RefAuthor>McGuire W</RefAuthor>
<RefTitle>Glutamine supplementation for prevention of morbidity in preterm infants</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefArticleNo>CD001457</RefArticleNo>
<RefTotal>Tubman TR, Thompson SW, McGuire W. Glutamine supplementation for prevention of morbidity in preterm infants. Cochrane Database Syst Rev. 2001;4:CD001457.</RefTotal>
</Reference>
<Reference refNo="122">
<RefAuthor>Darlow BA</RefAuthor>
<RefAuthor>Graham PJ</RefAuthor>
<RefTitle>Vitamin A supplementation for preventing morbidity in very low birthweight infants</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage></RefPage>
<RefTotal>Darlow BA, Graham PJ. Vitamin A supplementation for preventing morbidity in very low birthweight infants. Cochrane Database Syst Rev. 2000;CD000501.</RefTotal>
</Reference>
<Reference refNo="123">
<RefAuthor>Darlow BA</RefAuthor>
<RefAuthor>Graham PJ</RefAuthor>
<RefTitle>Vitamin A supplementation for preventing morbidity in very low birthweight infants</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage></RefPage>
<RefTotal>Darlow BA, Graham PJ. Vitamin A supplementation for preventing morbidity in very low birthweight infants. Cochrane Database Syst Rev. 2002;CD000501.</RefTotal>
</Reference>
<Reference refNo="124">
<RefAuthor>Magnusson G</RefAuthor>
<RefAuthor>Boberg M</RefAuthor>
<RefAuthor>Cederblad G</RefAuthor>
<RefAuthor>Meurling S</RefAuthor>
<RefTitle>Plasma and tissue levels of lipids, fatty acids and plasma carnitine in neonates receiving a new fat emulsion</RefTitle>
<RefYear>1997</RefYear>
<RefJournal>Acta Paediatr</RefJournal>
<RefPage>638-44</RefPage>
<RefTotal>Magnusson G, Boberg M, Cederblad G, Meurling S. Plasma and tissue levels of lipids, fatty acids and plasma carnitine in neonates receiving a new fat emulsion. Acta Paediatr. 1997;86(6):638-44. DOI: 10.1111/j.1651-2227.1997.tb08948.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1997.tb08948.x</RefLink>
</Reference>
<Reference refNo="125">
<RefAuthor>Cairns PA</RefAuthor>
<RefAuthor>Stalker DJ</RefAuthor>
<RefTitle>Carnitine supplementation of parenterally fed neonates</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage>CD000950</RefPage>
<RefTotal>Cairns PA, Stalker DJ. Carnitine supplementation of parenterally fed neonates. Cochrane Database Syst Rev. 2000;4:CD000950. DOI: 10.1002/14651858.CD000950</RefTotal>
<RefLink>http://dx.doi.org/10.1002/14651858.CD000950</RefLink>
</Reference>
<Reference refNo="126">
<RefAuthor>Wilson DC</RefAuthor>
<RefAuthor>Cairns P</RefAuthor>
<RefAuthor>Halliday HL</RefAuthor>
<RefAuthor>Reid M</RefAuthor>
<RefAuthor>McClure G</RefAuthor>
<RefAuthor>Dodge JA</RefAuthor>
<RefTitle>Randomised controlled trial of an aggressive nutritional regimen in sick very low birthweight infants</RefTitle>
<RefYear>1997</RefYear>
<RefJournal>Arch Dis Child Fetal Neonatal Ed</RefJournal>
<RefPage>F4-11</RefPage>
<RefTotal>Wilson DC, Cairns P, Halliday HL, Reid M, McClure G, Dodge JA. Randomised controlled trial of an aggressive nutritional regimen in sick very low birthweight infants. Arch Dis Child Fetal Neonatal Ed. 1997;77:F4-11. DOI: 10.1136/fn.77.1.F4</RefTotal>
<RefLink>http://dx.doi.org/10.1136/fn.77.1.F4</RefLink>
</Reference>
<Reference refNo="127">
<RefAuthor>Wilson DC</RefAuthor>
<RefAuthor>Fox GF</RefAuthor>
<RefAuthor>Ohlsson A</RefAuthor>
<RefTitle>Meta-analyses of effects of early or late introduction of intravenous lipids to preterm infants on mortality and chronic lung disease</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>599</RefPage>
<RefTotal>Wilson DC, Fox GF, Ohlsson A. Meta-analyses of effects of early or late introduction of intravenous lipids to preterm infants on mortality and chronic lung disease. J Pediatr Gastroenterol Nutr. 1998;26(5):599. DOI: 10.1097/00005176-199805000-00263</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00005176-199805000-00263</RefLink>
</Reference>
<Reference refNo="128">
<RefAuthor>Sosenko IR</RefAuthor>
<RefAuthor>Rodriguez-Pierce M</RefAuthor>
<RefAuthor>Bancalari E</RefAuthor>
<RefTitle>Effect of early initiation of intravenous lipid administration on the incidence and severity of chronic lung disease in premature infants</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>975-82</RefPage>
<RefTotal>Sosenko IR, Rodriguez-Pierce M, Bancalari E. Effect of early initiation of intravenous lipid administration on the incidence and severity of chronic lung disease in premature infants. J Pediatr. 1993;123(6):975-82. DOI: 10.1016/S0022-3476(05)80397-X</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(05)80397-X</RefLink>
</Reference>
<Reference refNo="129">
<RefAuthor>Bell EF</RefAuthor>
<RefAuthor>Warburton D</RefAuthor>
<RefAuthor>Stonestreet BS</RefAuthor>
<RefAuthor>Oh W</RefAuthor>
<RefTitle>High-volume fluid intake predisposes premature infants to necrotising enterocolitis</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>Lancet</RefJournal>
<RefPage>90</RefPage>
<RefTotal>Bell EF, Warburton D, Stonestreet BS, Oh W. High-volume fluid intake predisposes premature infants to necrotising enterocolitis. Lancet. 1979;314(8133):90. DOI: 10.1016/S0140-6736(79)90135-1</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0140-6736(79)90135-1</RefLink>
</Reference>
<Reference refNo="130">
<RefAuthor>Bell EF</RefAuthor>
<RefAuthor>Oh W</RefAuthor>
<RefTitle>Water requirement of premature newborn infants</RefTitle>
<RefYear>1983</RefYear>
<RefJournal>Acta Paediatr Scand Suppl</RefJournal>
<RefPage>21-6</RefPage>
<RefTotal>Bell EF, Oh W. Water requirement of premature newborn infants. Acta Paediatr Scand Suppl. 1983;72(s305):21-6. DOI: 10.1111/j.1651-2227.1983.tb09854.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1983.tb09854.x</RefLink>
</Reference>
<Reference refNo="131">
<RefAuthor>Bell EF</RefAuthor>
<RefAuthor>Acarregui MJ</RefAuthor>
<RefTitle>Restricted versus liberal water intake for preventing morbidity and mortality in preterm infants</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage></RefPage>
<RefTotal>Bell EF, Acarregui MJ. Restricted versus liberal water intake for preventing morbidity and mortality in preterm infants. Cochrane Database Syst Rev. 2000;CD000503. DOI: 10.1002/14651858.CD000503.pub2</RefTotal>
<RefLink>http://dx.doi.org/10.1002/14651858.CD000503.pub2</RefLink>
</Reference>
<Reference refNo="132">
<RefAuthor>Hartnoll G</RefAuthor>
<RefAuthor>Betremieux P</RefAuthor>
<RefAuthor>Modi N</RefAuthor>
<RefTitle>Randomised controlled trial of postnatal sodium supplementation on body composition in 25 to 30 week gestational age infants</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Arch Dis Child Fetal Neonatal Ed</RefJournal>
<RefPage>F24-8</RefPage>
<RefTotal>Hartnoll G, Betremieux P, Modi N. Randomised controlled trial of postnatal sodium supplementation on body composition in 25 to 30 week gestational age infants. Arch Dis Child Fetal Neonatal Ed. 2000;82:F24-8. DOI: 10.1136/fn.82.1.F24</RefTotal>
<RefLink>http://dx.doi.org/10.1136/fn.82.1.F24</RefLink>
</Reference>
<Reference refNo="133">
<RefAuthor>Kennedy KA</RefAuthor>
<RefAuthor>Tyson JE</RefAuthor>
<RefAuthor>Chamnanvanikij S</RefAuthor>
<RefTitle>Early versus delayed initiation of progressive enteral feedings for parenterally fed low birth weight or preterm infants</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefArticleNo>CD001970</RefArticleNo>
<RefTotal>Kennedy KA, Tyson JE, Chamnanvanikij S. Early versus delayed initiation of progressive enteral feedings for parenterally fed low birth weight or preterm infants. Cochrane Database Syst Rev. 2000;CD001970.</RefTotal>
</Reference>
<Reference refNo="134">
<RefAuthor>Tyson JE</RefAuthor>
<RefAuthor>Kennedy KA</RefAuthor>
<RefTitle>Minimal enteral nutrition for promoting feeding tolerance and preventing morbidity in parenterally fed infants</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefArticleNo>CD000504</RefArticleNo>
<RefTotal>Tyson JE, Kennedy KA. Minimal enteral nutrition for promoting feeding tolerance and preventing morbidity in parenterally fed infants. Cochrane Database Syst Rev. 2000;CD000504.</RefTotal>
</Reference>
<Reference refNo="135">
<RefAuthor>Putet G</RefAuthor>
<RefAuthor>Senterre J</RefAuthor>
<RefAuthor>Rigo J</RefAuthor>
<RefAuthor>Salle B</RefAuthor>
<RefTitle>Nutrient balance, energy utilization, and composition of weight gain in very-low-birth-weight infants fed pooled human milk or a preterm formula</RefTitle>
<RefYear>1984</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>79-85</RefPage>
<RefTotal>Putet G, Senterre J, Rigo J, Salle B. Nutrient balance, energy utilization, and composition of weight gain in very-low-birth-weight infants fed pooled human milk or a preterm formula. J Pediatr. 1984;105(1):79-85. DOI: 10.1016/S0022-3476(84)80368-6</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(84)80368-6</RefLink>
</Reference>
<Reference refNo="136">
<RefAuthor>Shah PS</RefAuthor>
<RefAuthor>Ng E</RefAuthor>
<RefAuthor>Sinha AK</RefAuthor>
<RefTitle>Heparin for prolonging peripheral intravenous catheter use in neonates</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefArticleNo>CD002774</RefArticleNo>
<RefTotal>Shah PS, Ng E, Sinha AK. Heparin for prolonging peripheral intravenous catheter use in neonates. Cochrane Database Syst Rev. 2002;CD002774. DOI: 10.1002/14651858.CD002774.pub2</RefTotal>
<RefLink>http://dx.doi.org/10.1002/14651858.CD002774.pub2</RefLink>
</Reference>
<Reference refNo="137">
<RefAuthor>Shah P</RefAuthor>
<RefAuthor>Shah V</RefAuthor>
<RefTitle>Continuous heparin infusion to prevent thrombosis and catheter occlusion in neonates with peripherally placed percutaneous central venous catheters</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefArticleNo>CD002772</RefArticleNo>
<RefTotal>Shah P, Shah V. Continuous heparin infusion to prevent thrombosis and catheter occlusion in neonates with peripherally placed percutaneous central venous catheters. Cochrane Database Syst Rev. 2001;CD002772.</RefTotal>
</Reference>
<Reference refNo="138">
<RefAuthor>Krohn K</RefAuthor>
<RefAuthor>Babl J</RefAuthor>
<RefAuthor>Reiter K</RefAuthor>
<RefAuthor>Koletzko B</RefAuthor>
<RefTitle>Parenteral nutrition with standard solutions in paediatric intensive care patients</RefTitle>
<RefYear>2005</RefYear>
<RefJournal>Clin Nutr</RefJournal>
<RefPage>274-80</RefPage>
<RefTotal>Krohn K, Babl J, Reiter K, Koletzko B. Parenteral nutrition with standard solutions in paediatric intensive care patients. Clin Nutr. 2005;24(2):274-80. DOI: 10.1016/j.clnu.2004.11.004</RefTotal>
<RefLink>http://dx.doi.org/10.1016/j.clnu.2004.11.004</RefLink>
</Reference>
<Reference refNo="139">
<RefAuthor>Suchner U</RefAuthor>
<RefAuthor>Senftleben U</RefAuthor>
<RefAuthor>Askanazi J</RefAuthor>
<RefAuthor>Peter K</RefAuthor>
<RefTitle>Nichtenergetische Bedeutung der enteralen Ernährung bei kritisch kranken Patienten [The non-energetic importance of enteral nutrition of critically ill patients]</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>Infusionsther Transfusionsmed</RefJournal>
<RefPage>38-46</RefPage>
<RefTotal>Suchner U, Senftleben U, Askanazi J, Peter K. Nichtenergetische Bedeutung der enteralen Ernährung bei kritisch kranken Patienten [The non-energetic importance of enteral nutrition of critically ill patients]. Infusionsther Transfusionsmed. 1993;20(1-2):38-46.</RefTotal>
</Reference>
<Reference refNo="140">
<RefAuthor>Pinelli J</RefAuthor>
<RefAuthor>Symington A</RefAuthor>
<RefTitle>Non-nutritive sucking for promoting physiologic stability and nutrition in preterm infants</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefArticleNo>CD001071</RefArticleNo>
<RefTotal>Pinelli J, Symington A. Non-nutritive sucking for promoting physiologic stability and nutrition in preterm infants. Cochrane Database Syst Rev. 2001;CD001071. DOI: 10.1002/14651858.CD001071.pub2</RefTotal>
<RefLink>http://dx.doi.org/10.1002/14651858.CD001071.pub2</RefLink>
</Reference>
<Reference refNo="141">
<RefAuthor>Pohlandt F</RefAuthor>
<RefTitle>Bone mineral deficiency as the main factor of dolichocephalic head flattening in very-low-birth-weight infants</RefTitle>
<RefYear>1994</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>701-3</RefPage>
<RefTotal>Pohlandt F. Bone mineral deficiency as the main factor of dolichocephalic head flattening in very-low-birth-weight infants. Pediatr Res. 1994;35(6):701-3. DOI: 10.1203/00006450-199406000-00016</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199406000-00016</RefLink>
</Reference>
<Reference refNo="142">
<RefAuthor>Pohlandt F</RefAuthor>
<RefTitle>Hypothesis: myopia of prematurity is caused by postnatal bone mineral deficiency</RefTitle>
<RefYear>1994</RefYear>
<RefJournal>Eur J Pediatr</RefJournal>
<RefPage>234-6</RefPage>
<RefTotal>Pohlandt F. Hypothesis: myopia of prematurity is caused by postnatal bone mineral deficiency. Eur J Pediatr. 1994;153(4):234-6. DOI: 10.1007/BF01954508</RefTotal>
<RefLink>http://dx.doi.org/10.1007/BF01954508</RefLink>
</Reference>
<Reference refNo="143">
<RefAuthor>Karlén J</RefAuthor>
<RefAuthor>Aperia A</RefAuthor>
<RefAuthor>Zetterström R</RefAuthor>
<RefTitle>Renal excretion of calcium and phosphate in preterm and term infants</RefTitle>
<RefYear>1985</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>814-9</RefPage>
<RefTotal>Karlén J, Aperia A, Zetterström R. Renal excretion of calcium and phosphate in preterm and term infants. J Pediatr. 1985;106(5):814-9. DOI: 10.1016/S0022-3476(85)80364-4</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(85)80364-4</RefLink>
</Reference>
<Reference refNo="144">
<RefAuthor>Pohlandt F</RefAuthor>
<RefTitle>Prevention of postnatal bone demineralization in very low-birth-weight infants by individually monitored supplementation with calcium and phosphorus</RefTitle>
<RefYear>1994</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>125-9</RefPage>
<RefTotal>Pohlandt F. Prevention of postnatal bone demineralization in very low-birth-weight infants by individually monitored supplementation with calcium and phosphorus. Pediatr Res. 1994;35(1):125-9. DOI: 10.1203/00006450-199401000-00027</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199401000-00027</RefLink>
</Reference>
<Reference refNo="145">
<RefAuthor>Shulman RJ</RefAuthor>
<RefAuthor>Phillips S</RefAuthor>
<RefTitle>Parenteral nutrition in infants and children</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>587-607</RefPage>
<RefTotal>Shulman RJ, Phillips S. Parenteral nutrition in infants and children. J Pediatr Gastroenterol Nutr. 2003;36(5):587-607. DOI: 10.1097/00005176-200305000-00002</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00005176-200305000-00002</RefLink>
</Reference>
<Reference refNo="146">
<RefAuthor>Desci T</RefAuthor>
<RefAuthor>Molnár D</RefAuthor>
<RefAuthor>Klujber L</RefAuthor>
<RefTitle>Lipid levels in very low birthweight preterm infants</RefTitle>
<RefYear>1990</RefYear>
<RefJournal>Acta Paediatr Scand</RefJournal>
<RefPage>577-80</RefPage>
<RefTotal>Desci T, Molnár D, Klujber L. Lipid levels in very low birthweight preterm infants. Acta Paediatr Scand. 1990;79(6-7):577-80. DOI: 10.1111/j.1651-2227.1990.tb11519.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1990.tb11519.x</RefLink>
</Reference>
<Reference refNo="147">
<RefAuthor>Connelly PW</RefAuthor>
<RefAuthor>Maguire GF</RefAuthor>
<RefAuthor>Vezina C</RefAuthor>
<RefAuthor>Hegele RA</RefAuthor>
<RefAuthor>Kuksis A</RefAuthor>
<RefTitle>Kinetics of lipolysis of very low density lipoproteins by lipoprotein lipase. Importance of particle number and noncompetitive inhibition by particles with low triglyceride content</RefTitle>
<RefYear>1994</RefYear>
<RefJournal>J Biol Chem</RefJournal>
<RefPage>20554-60</RefPage>
<RefTotal>Connelly PW, Maguire GF, Vezina C, Hegele RA, Kuksis A. Kinetics of lipolysis of very low density lipoproteins by lipoprotein lipase. Importance of particle number and noncompetitive inhibition by particles with low triglyceride content. J Biol Chem. 1994;269(32):20554-60.</RefTotal>
</Reference>
<Reference refNo="148">
<RefAuthor>House JD</RefAuthor>
<RefAuthor>Thorpe JM</RefAuthor>
<RefAuthor>Wykes LJ</RefAuthor>
<RefAuthor>Pencharz PB</RefAuthor>
<RefAuthor>Ball RO</RefAuthor>
<RefTitle>Evidence that phenylalanine hydroxylation rates are overestimated in neonatal subjects receiving total parenteral nutrition with a high phenylalanine content</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>461-6</RefPage>
<RefTotal>House JD, Thorpe JM, Wykes LJ, Pencharz PB, Ball RO. Evidence that phenylalanine hydroxylation rates are overestimated in neonatal subjects receiving total parenteral nutrition with a high phenylalanine content. Pediatr Res. 1998;43(4):461-6. DOI: 10.1203/00006450-199804000-00004</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199804000-00004</RefLink>
</Reference>
<Reference refNo="149">
<RefAuthor>Lucas A</RefAuthor>
<RefAuthor>Baker BA</RefAuthor>
<RefAuthor>Morley RM</RefAuthor>
<RefTitle>Hyperphenylalaninaemia and outcome in intravenously fed preterm neonates</RefTitle>
<RefYear>1993</RefYear>
<RefJournal>Arch Dis Child</RefJournal>
<RefPage>579-83</RefPage>
<RefTotal>Lucas A, Baker BA, Morley RM. Hyperphenylalaninaemia and outcome in intravenously fed preterm neonates. Arch Dis Child. 1993;68:579-83. DOI: 10.1136/adc.68.5_Spec_No.579</RefTotal>
<RefLink>http://dx.doi.org/10.1136/adc.68.5_Spec_No.579</RefLink>
</Reference>
<Reference refNo="150">
<RefAuthor>Moss RL</RefAuthor>
<RefAuthor>Haynes AL</RefAuthor>
<RefAuthor>Pastuszyn A</RefAuthor>
<RefAuthor>Glew RH</RefAuthor>
<RefTitle>Methionine infusion reproduces liver injury of parenteral nutrition cholestasis</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>664-8</RefPage>
<RefTotal>Moss RL, Haynes AL, Pastuszyn A, Glew RH. Methionine infusion reproduces liver injury of parenteral nutrition cholestasis. Pediatr Res. 1999;45(5 Pt 1):664-8. DOI: 10.1203/00006450-199905010-00009</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199905010-00009</RefLink>
</Reference>
<Reference refNo="151">
<RefAuthor>Puntis JW</RefAuthor>
<RefAuthor>Edwards MA</RefAuthor>
<RefAuthor>Green A</RefAuthor>
<RefAuthor>Morgan I</RefAuthor>
<RefAuthor>Booth IW</RefAuthor>
<RefAuthor>Ball PA</RefAuthor>
<RefTitle>Hyperphenylalaninaemia in parenterally fed newborn babies</RefTitle>
<RefYear>1986</RefYear>
<RefJournal>Lancet</RefJournal>
<RefPage>1105-6</RefPage>
<RefTotal>Puntis JW, Edwards MA, Green A, Morgan I, Booth IW, Ball PA. Hyperphenylalaninaemia in parenterally fed newborn babies. Lancet. 1986;328(8515):1105-6. DOI: 10.1016/S0140-6736(86)90513-1</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0140-6736(86)90513-1</RefLink>
</Reference>
<Reference refNo="152">
<RefAuthor>Toledo-Eppinga L</RefAuthor>
<RefAuthor>Kalhan SC</RefAuthor>
<RefAuthor>Kulik W</RefAuthor>
<RefAuthor>Jakobs C</RefAuthor>
<RefAuthor>Lafeber HN</RefAuthor>
<RefTitle>Relative kinetics of phenylalanine and leucine in low birth weight infants during nutrient administration</RefTitle>
<RefYear>1996</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>41-6</RefPage>
<RefTotal>Toledo-Eppinga L, Kalhan SC, Kulik W, Jakobs C, Lafeber HN. Relative kinetics of phenylalanine and leucine in low birth weight infants during nutrient administration. Pediatr Res. 1996;40(1):41-6. DOI: 10.1203/00006450-199607000-00008</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199607000-00008</RefLink>
</Reference>
<Reference refNo="153">
<RefAuthor>Heird WC</RefAuthor>
<RefAuthor>Gomez MR</RefAuthor>
<RefTitle>Parenteral nutrition in low-birth-weight infants</RefTitle>
<RefYear>1996</RefYear>
<RefJournal>Annu Rev Nutr</RefJournal>
<RefPage>471-99</RefPage>
<RefTotal>Heird WC, Gomez MR. Parenteral nutrition in low-birth-weight infants. Annu Rev Nutr. 1996;16:471-99. DOI: 10.1146/annurev.nu.16.070196.002351</RefTotal>
<RefLink>http://dx.doi.org/10.1146/annurev.nu.16.070196.002351</RefLink>
</Reference>
<Reference refNo="154">
<RefAuthor>Zlotkin SH</RefAuthor>
<RefAuthor>Bryan MH</RefAuthor>
<RefAuthor>Anderson GH</RefAuthor>
<RefTitle>Cysteine supplementation to cysteine-free intravenous feeding regimens in newborn infants</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>914-23</RefPage>
<RefTotal>Zlotkin SH, Bryan MH, Anderson GH. Cysteine supplementation to cysteine-free intravenous feeding regimens in newborn infants. Am J Clin Nutr. 1981;34(5):914-23.</RefTotal>
</Reference>
<Reference refNo="155">
<RefAuthor>Bjelton L</RefAuthor>
<RefAuthor>Fransson GB</RefAuthor>
<RefTitle>Availability of cysteine and of L-2-oxo-thiazolidine-4-carboxylic acid as a source of cysteine in intravenous nutrition</RefTitle>
<RefYear>1990</RefYear>
<RefJournal>JPEN J Parenter Enteral Nutr</RefJournal>
<RefPage>177-82</RefPage>
<RefTotal>Bjelton L, Fransson GB. Availability of cysteine and of L-2-oxo-thiazolidine-4-carboxylic acid as a source of cysteine in intravenous nutrition. JPEN J Parenter Enteral Nutr. 1990;14(2):177-82. DOI: 10.1177/0148607190014002177</RefTotal>
<RefLink>http://dx.doi.org/10.1177/0148607190014002177</RefLink>
</Reference>
<Reference refNo="156">
<RefAuthor>Gaull GE</RefAuthor>
<RefAuthor>Rassin DK</RefAuthor>
<RefTitle>Taurine in development and nutrition</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>Ciba Found Symp</RefJournal>
<RefPage>271-88</RefPage>
<RefTotal>Gaull GE, Rassin DK. Taurine in development and nutrition. Ciba Found Symp. 1979;72:271-88. DOI: 10.1002/9780470720554.ch17</RefTotal>
<RefLink>http://dx.doi.org/10.1002/9780470720554.ch17</RefLink>
</Reference>
<Reference refNo="157">
<RefAuthor>Ghisolfi J</RefAuthor>
<RefTitle>Taurine and the premature</RefTitle>
<RefYear>1987</RefYear>
<RefJournal>Biol Neonate</RefJournal>
<RefPage>78-86</RefPage>
<RefTotal>Ghisolfi J. Taurine and the premature. Biol Neonate. 1987;52 Suppl 1:78-86. DOI: 10.1159/000242741</RefTotal>
<RefLink>http://dx.doi.org/10.1159/000242741</RefLink>
</Reference>
<Reference refNo="158">
<RefAuthor>Lourenco R</RefAuthor>
<RefAuthor>Camilo ME</RefAuthor>
<RefTitle>Taurine: a conditionally essential amino acid in humans? An overview in health and disease</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Nutr Hosp</RefJournal>
<RefPage>262-70</RefPage>
<RefTotal>Lourenco R, Camilo ME. Taurine: a conditionally essential amino acid in humans? An overview in health and disease. Nutr Hosp. 2002;17(6):262-70.</RefTotal>
</Reference>
<Reference refNo="159">
<RefAuthor>Tyson JE</RefAuthor>
<RefAuthor>Lasky R</RefAuthor>
<RefAuthor>Flood D</RefAuthor>
<RefAuthor>Mize C</RefAuthor>
<RefAuthor>Picone T</RefAuthor>
<RefAuthor>Paule CL</RefAuthor>
<RefTitle>Randomized trial of taurine supplementation for infants less than or equal to 1,300-gram birth weight: effect on auditory brainstem-evoked responses</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Pediatrics</RefJournal>
<RefPage>406-15</RefPage>
<RefTotal>Tyson JE, Lasky R, Flood D, Mize C, Picone T, Paule CL. Randomized trial of taurine supplementation for infants less than or equal to 1,300-gram birth weight: effect on auditory brainstem-evoked responses. Pediatrics. 1989;83(3):406-15.</RefTotal>
</Reference>
<Reference refNo="160">
<RefAuthor>Anderson TL</RefAuthor>
<RefAuthor>Muttart CR</RefAuthor>
<RefAuthor>Bieber MA</RefAuthor>
<RefAuthor>Nicholson JF</RefAuthor>
<RefAuthor>Heird WC</RefAuthor>
<RefTitle>A controlled trial of glucose versus glucose and amino acids in premature infants</RefTitle>
<RefYear>1979</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>947-51</RefPage>
<RefTotal>Anderson TL, Muttart CR, Bieber MA, Nicholson JF, Heird WC. A controlled trial of glucose versus glucose and amino acids in premature infants. J Pediatr. 1979;94(6):947-51. DOI: 10.1016/S0022-3476(79)80230-9</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(79)80230-9</RefLink>
</Reference>
<Reference refNo="161">
<RefAuthor>Tews JK</RefAuthor>
<RefAuthor>Bradford AM</RefAuthor>
<RefAuthor>Harper AE</RefAuthor>
<RefTitle>Induction of lysine imbalance in rats: relationships between tissue amino acids and diet</RefTitle>
<RefYear>1981</RefYear>
<RefJournal>J Nutr</RefJournal>
<RefPage>968-78</RefPage>
<RefTotal>Tews JK, Bradford AM, Harper AE. Induction of lysine imbalance in rats: relationships between tissue amino acids and diet. J Nutr. 1981;111(6):968-78.</RefTotal>
</Reference>
<Reference refNo="162">
<RefAuthor>Batshaw ML</RefAuthor>
<RefAuthor>Wachtel RC</RefAuthor>
<RefAuthor>Thomas GH</RefAuthor>
<RefAuthor>Starrett A</RefAuthor>
<RefAuthor>Brusilow SW</RefAuthor>
<RefTitle>Arginine-responsive asymptomatic hyperammonemia in the premature infant</RefTitle>
<RefYear>1984</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>86-91</RefPage>
<RefTotal>Batshaw ML, Wachtel RC, Thomas GH, Starrett A, Brusilow SW. Arginine-responsive asymptomatic hyperammonemia in the premature infant. J Pediatr. 1984;105(1):86-91. DOI: 10.1016/S0022-3476(84)80369-8</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(84)80369-8</RefLink>
</Reference>
<Reference refNo="163">
<RefAuthor>Göbel Y</RefAuthor>
<RefAuthor>Koletzko B</RefAuthor>
<RefAuthor>Böhles HJ</RefAuthor>
<RefAuthor>Engelsberger I</RefAuthor>
<RefAuthor>Forget D</RefAuthor>
<RefAuthor>Le Brun A</RefAuthor>
<RefAuthor>Peters J</RefAuthor>
<RefAuthor>Zimmermann A</RefAuthor>
<RefTitle>Parenteral fat emulsions based on olive and soybean oils: a randomized clinical trial in preterm infants</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>161-7</RefPage>
<RefTotal>Göbel Y, Koletzko B, Böhles HJ, Engelsberger I, Forget D, Le Brun A, Peters J, Zimmermann A. Parenteral fat emulsions based on olive and soybean oils: a randomized clinical trial in preterm infants. J Pediatr Gastroenterol Nutr. 2003;37(2):161-7. DOI: 10.1097/00005176-200308000-00015</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00005176-200308000-00015</RefLink>
</Reference>
<Reference refNo="164">
<RefAuthor>Goulet O</RefAuthor>
<RefAuthor>de Potter S</RefAuthor>
<RefAuthor>Antébi H</RefAuthor>
<RefAuthor>Driss F</RefAuthor>
<RefAuthor>Colomb V</RefAuthor>
<RefAuthor>Béréziat G</RefAuthor>
<RefAuthor>Alcindor LG</RefAuthor>
<RefAuthor>Corriol O</RefAuthor>
<RefAuthor>Le Brun A</RefAuthor>
<RefAuthor>Dutot G</RefAuthor>
<RefAuthor>Forget D</RefAuthor>
<RefAuthor>Perennec V</RefAuthor>
<RefAuthor>Ricour C</RefAuthor>
<RefTitle>Long-term efficacy and safety of a new olive oil-based intravenous fat emulsion in pediatric patients: a double-blind randomized study</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>338-45</RefPage>
<RefTotal>Goulet O, de Potter S, Antébi H, Driss F, Colomb V, Béréziat G, Alcindor LG, Corriol O, Le Brun A, Dutot G, Forget D, Perennec V, Ricour C. Long-term efficacy and safety of a new olive oil-based intravenous fat emulsion in pediatric patients: a double-blind randomized study. Am J Clin Nutr. 1999;70(3):338-45.</RefTotal>
</Reference>
<Reference refNo="165">
<RefAuthor>Deckelbaum RJ</RefAuthor>
<RefTitle>Intravenous lipid emulsions in pediatrics: time for a change?</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>J Pediatr Gastroenterol Nutr</RefJournal>
<RefPage>112-4</RefPage>
<RefTotal>Deckelbaum RJ. Intravenous lipid emulsions in pediatrics: time for a change? J Pediatr Gastroenterol Nutr. 2003;37(2):112-4. DOI: 10.1097/00005176-200308000-00004</RefTotal>
<RefLink>http://dx.doi.org/10.1097/00005176-200308000-00004</RefLink>
</Reference>
<Reference refNo="166">
<RefAuthor>Deckelbaum RJ</RefAuthor>
<RefAuthor>Hamilton JA</RefAuthor>
<RefAuthor>Moser A</RefAuthor>
<RefAuthor>Bengtsson-Olivecrona G</RefAuthor>
<RefAuthor>Butbul E</RefAuthor>
<RefAuthor>Carpentier YA</RefAuthor>
<RefAuthor>Gutman A</RefAuthor>
<RefAuthor>Olivecrona T</RefAuthor>
<RefTitle>Medium-chain versus long-chain triacylglycerol emulsion hydrolysis by lipoprotein lipase and hepatic lipase: implications for the mechanisms of lipase action</RefTitle>
<RefYear>1990</RefYear>
<RefJournal>Biochemistry</RefJournal>
<RefPage>1136-42</RefPage>
<RefTotal>Deckelbaum RJ, Hamilton JA, Moser A, Bengtsson-Olivecrona G, Butbul E, Carpentier YA, Gutman A, Olivecrona T. Medium-chain versus long-chain triacylglycerol emulsion hydrolysis by lipoprotein lipase and hepatic lipase: implications for the mechanisms of lipase action. Biochemistry. 1990;29(5):1136-42. DOI: 10.1021/bi00457a006</RefTotal>
<RefLink>http://dx.doi.org/10.1021/bi00457a006</RefLink>
</Reference>
<Reference refNo="167">
<RefAuthor>Donnell SC</RefAuthor>
<RefAuthor>Lloyd DA</RefAuthor>
<RefAuthor>Eaton S</RefAuthor>
<RefAuthor>Pierro A</RefAuthor>
<RefTitle>The metabolic response to intravenous medium-chain triglycerides in infants after surgery</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>689-94</RefPage>
<RefTotal>Donnell SC, Lloyd DA, Eaton S, Pierro A. The metabolic response to intravenous medium-chain triglycerides in infants after surgery. J Pediatr. 2002;141(5):689-94. DOI: 10.1067/mpd.2002.128889</RefTotal>
<RefLink>http://dx.doi.org/10.1067/mpd.2002.128889</RefLink>
</Reference>
<Reference refNo="168">
<RefAuthor>Radermacher P</RefAuthor>
<RefAuthor>Santak B</RefAuthor>
<RefAuthor>Strobach H</RefAuthor>
<RefAuthor>Schror K</RefAuthor>
<RefAuthor>Tarnow J</RefAuthor>
<RefTitle>Fat emulsions containing medium chain triglycerides in patients with sepsis syndrome: effects on pulmonary hemodynamics and gas exchange</RefTitle>
<RefYear>1992</RefYear>
<RefJournal>Intensive Care Med</RefJournal>
<RefPage>231-4</RefPage>
<RefTotal>Radermacher P, Santak B, Strobach H, Schror K, Tarnow J. Fat emulsions containing medium chain triglycerides in patients with sepsis syndrome: effects on pulmonary hemodynamics and gas exchange. Intensive Care Med. 1992;18(4):231-4. DOI: 10.1007/BF01709838</RefTotal>
<RefLink>http://dx.doi.org/10.1007/BF01709838</RefLink>
</Reference>
<Reference refNo="169">
<RefAuthor>Roth B</RefAuthor>
<RefAuthor>Ekelund M</RefAuthor>
<RefAuthor>Fan BG</RefAuthor>
<RefAuthor>Hägerstrand L</RefAuthor>
<RefAuthor>Salehi A</RefAuthor>
<RefAuthor>Lundquist I</RefAuthor>
<RefAuthor>Nilsson-Ehle P</RefAuthor>
<RefTitle>Biochemical and ultra-structural reactions to parenteral nutrition with two different fat emulsions in rats</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Intensive Care Med</RefJournal>
<RefPage>716-24</RefPage>
<RefTotal>Roth B, Ekelund M, Fan BG, Hägerstrand L, Salehi A, Lundquist I, Nilsson-Ehle P. Biochemical and ultra-structural reactions to parenteral nutrition with two different fat emulsions in rats. Intensive Care Med. 1998;24(7):716-24. DOI: 10.1007/s001340050650</RefTotal>
<RefLink>http://dx.doi.org/10.1007/s001340050650</RefLink>
</Reference>
<Reference refNo="170">
<RefAuthor>Smirniotis V</RefAuthor>
<RefAuthor>Kostopanagiotou G</RefAuthor>
<RefAuthor>Vassiliou J</RefAuthor>
<RefAuthor>Arkadopoulos N</RefAuthor>
<RefAuthor>Vassiliou P</RefAuthor>
<RefAuthor>Datsis A</RefAuthor>
<RefAuthor>Kourias E</RefAuthor>
<RefTitle>Long chain versus medium chain lipids in patients with ARDS: effects on pulmonary haemodynamics and gas exchange</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Intensive Care Med</RefJournal>
<RefPage>1029-33</RefPage>
<RefTotal>Smirniotis V, Kostopanagiotou G, Vassiliou J, Arkadopoulos N, Vassiliou P, Datsis A, Kourias E. Long chain versus medium chain lipids in patients with ARDS: effects on pulmonary haemodynamics and gas exchange. Intensive Care Med. 1998;24(10):1029-33. DOI: 10.1007/s001340050711</RefTotal>
<RefLink>http://dx.doi.org/10.1007/s001340050711</RefLink>
</Reference>
<Reference refNo="171">
<RefAuthor>Yeh SL</RefAuthor>
<RefAuthor>Lin MT</RefAuthor>
<RefAuthor>Chen WJ</RefAuthor>
<RefTitle>MCT/LCT emulsion ameliorate liver fat deposition in insulin-treated diabetic rats receiving total parenteral nutrition</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Clin Nutr</RefJournal>
<RefPage>273-7</RefPage>
<RefTotal>Yeh SL, Lin MT, Chen WJ. MCT/LCT emulsion ameliorate liver fat deposition in insulin-treated diabetic rats receiving total parenteral nutrition. Clin Nutr. 1998;17(6):273-7. DOI: 10.1016/S0261-5614(98)80319-1</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0261-5614(98)80319-1</RefLink>
</Reference>
<Reference refNo="172">
<RefAuthor>Angsten G</RefAuthor>
<RefAuthor>Boberg M</RefAuthor>
<RefAuthor>Cederblad G</RefAuthor>
<RefAuthor>Meurling S</RefAuthor>
<RefAuthor>Stiernström H</RefAuthor>
<RefTitle>Metabolic effects in neonates receiving intravenous medium-chain triglycerides</RefTitle>
<RefYear>2002</RefYear>
<RefJournal>Acta Paediatr</RefJournal>
<RefPage>188-97</RefPage>
<RefTotal>Angsten G, Boberg M, Cederblad G, Meurling S, Stiernström H. Metabolic effects in neonates receiving intravenous medium-chain triglycerides. Acta Paediatr. 2002;91(2):188-97. DOI: 10.1080/080352502317285207</RefTotal>
<RefLink>http://dx.doi.org/10.1080/080352502317285207</RefLink>
</Reference>
<Reference refNo="173">
<RefAuthor>Rubin M</RefAuthor>
<RefAuthor>Harell D</RefAuthor>
<RefAuthor>Naor N</RefAuthor>
<RefAuthor>Moser A</RefAuthor>
<RefAuthor>Wielunsky E</RefAuthor>
<RefAuthor>Merlob P</RefAuthor>
<RefAuthor>Lichtenberg D</RefAuthor>
<RefTitle>Lipid infusion with different triglyceride cores (long-chain vs medium-chain/long-chain triglycerides): effect on plasma lipids and bilirubin binding in premature infants</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>JPEN J Parenter Enteral Nutr</RefJournal>
<RefPage>642-6</RefPage>
<RefTotal>Rubin M, Harell D, Naor N, Moser A, Wielunsky E, Merlob P, Lichtenberg D. Lipid infusion with different triglyceride cores (long-chain vs medium-chain/long-chain triglycerides): effect on plasma lipids and bilirubin binding in premature infants. JPEN J Parenter Enteral Nutr. 1991;15(6):642-6. DOI: 10.1177/0148607191015006642</RefTotal>
<RefLink>http://dx.doi.org/10.1177/0148607191015006642</RefLink>
</Reference>
<Reference refNo="174">
<RefAuthor>Ulrich H</RefAuthor>
<RefAuthor>Pastores SM</RefAuthor>
<RefAuthor>Katz DP</RefAuthor>
<RefAuthor>Kvetan V</RefAuthor>
<RefTitle>Parenteral use of medium-chain triglycerides: a reappraisal</RefTitle>
<RefYear>1996</RefYear>
<RefJournal>Nutrition</RefJournal>
<RefPage>231-8</RefPage>
<RefTotal>Ulrich H, Pastores SM, Katz DP, Kvetan V. Parenteral use of medium-chain triglycerides: a reappraisal. Nutrition. 1996;12(4):231-8. DOI: 10.1016/S0899-9007(96)00089-6</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0899-9007(96)00089-6</RefLink>
</Reference>
<Reference refNo="175">
<RefAuthor>Lai H</RefAuthor>
<RefAuthor>Chen W</RefAuthor>
<RefTitle>Effects of medium-chain and long-chain triacylglycerols in pediatric surgical patients</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>Nutrition</RefJournal>
<RefPage>401-6</RefPage>
<RefTotal>Lai H, Chen W. Effects of medium-chain and long-chain triacylglycerols in pediatric surgical patients. Nutrition. 2000;16(6):401-6. DOI: 10.1016/S0899-9007(00)00268-9</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0899-9007(00)00268-9</RefLink>
</Reference>
<Reference refNo="176">
<RefAuthor>Uhlemann MPC</RefAuthor>
<RefAuthor>Heine KD</RefAuthor>
<RefAuthor>Wutzke M</RefAuthor>
<RefAuthor>Müller M</RefAuthor>
<RefAuthor>Kracht M</RefAuthor>
<RefTitle>MCT-fat emulsions enhance efficacy of whole body protein metabolism in very small preterm neonates</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Clin Nutr</RefJournal>
<RefPage>53</RefPage>
<RefTotal>Uhlemann MPC, Heine KD, Wutzke M, Müller M, Kracht M. MCT-fat emulsions enhance efficacy of whole body protein metabolism in very small preterm neonates. Clin Nutr. 1989;8:53.</RefTotal>
</Reference>
<Reference refNo="177">
<RefAuthor>Liet JM</RefAuthor>
<RefAuthor>Piloquet H</RefAuthor>
<RefAuthor>Marchini JS</RefAuthor>
<RefAuthor>Maugère P</RefAuthor>
<RefAuthor>Bobin C</RefAuthor>
<RefAuthor>Rozé JC</RefAuthor>
<RefAuthor>Darmaun D</RefAuthor>
<RefTitle>Leucine metabolism in preterm infants receiving parenteral nutrition with medium-chain compared with long-chain triacylglycerol emulsions</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Am J Clin Nutr</RefJournal>
<RefPage>539-43</RefPage>
<RefTotal>Liet JM, Piloquet H, Marchini JS, Maugère P, Bobin C, Rozé JC, Darmaun D. Leucine metabolism in preterm infants receiving parenteral nutrition with medium-chain compared with long-chain triacylglycerol emulsions. Am J Clin Nutr. 1999;69(3):539-43.</RefTotal>
</Reference>
<Reference refNo="178">
<RefAuthor>Baldermann H</RefAuthor>
<RefAuthor>Wicklmayr M</RefAuthor>
<RefAuthor>Rett K</RefAuthor>
<RefAuthor>Banholzer P</RefAuthor>
<RefAuthor>Dietze G</RefAuthor>
<RefAuthor>Mehnert H</RefAuthor>
<RefTitle>Changes of hepatic morphology during parenteral nutrition with lipid emulsions containing LCT or MCT/LCT quantified by ultrasound</RefTitle>
<RefYear>1991</RefYear>
<RefJournal>JPEN J Parenter Enteral Nutr</RefJournal>
<RefPage>601-3</RefPage>
<RefTotal>Baldermann H, Wicklmayr M, Rett K, Banholzer P, Dietze G, Mehnert H. Changes of hepatic morphology during parenteral nutrition with lipid emulsions containing LCT or MCT/LCT quantified by ultrasound. JPEN J Parenter Enteral Nutr. 1991;15(6):601-3. DOI: 10.1177/0148607191015006601</RefTotal>
<RefLink>http://dx.doi.org/10.1177/0148607191015006601</RefLink>
</Reference>
<Reference refNo="179">
<RefAuthor>Lima LA</RefAuthor>
<RefAuthor>Murphy JF</RefAuthor>
<RefAuthor>Stansbie D</RefAuthor>
<RefAuthor>Rowlandson P</RefAuthor>
<RefAuthor>Gray OP</RefAuthor>
<RefTitle>Neonatal parenteral nutrition with a fat emulsion containing medium chain triglycerides</RefTitle>
<RefYear>1988</RefYear>
<RefJournal>Acta Paediatr Scand</RefJournal>
<RefPage>332-9</RefPage>
<RefTotal>Lima LA, Murphy JF, Stansbie D, Rowlandson P, Gray OP. Neonatal parenteral nutrition with a fat emulsion containing medium chain triglycerides. Acta Paediatr Scand. 1988;77(3):332-9. DOI: 10.1111/j.1651-2227.1988.tb10657.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1988.tb10657.x</RefLink>
</Reference>
<Reference refNo="180">
<RefAuthor>Haumont D</RefAuthor>
<RefAuthor>Richelle M</RefAuthor>
<RefAuthor>Deckelbaum RJ</RefAuthor>
<RefAuthor>Coussaert E</RefAuthor>
<RefAuthor>Carpentier YA</RefAuthor>
<RefTitle>Effect of liposomal content of lipid emulsions on plasma lipid concentrations in low birth weight infants receiving parenteral nutrition</RefTitle>
<RefYear>1992</RefYear>
<RefJournal>J Pediatr</RefJournal>
<RefPage>759-63</RefPage>
<RefTotal>Haumont D, Richelle M, Deckelbaum RJ, Coussaert E, Carpentier YA. Effect of liposomal content of lipid emulsions on plasma lipid concentrations in low birth weight infants receiving parenteral nutrition. J Pediatr. 1992;121(5 Pt 1):759-63. DOI: 10.1016/S0022-3476(05)81912-2</RefTotal>
<RefLink>http://dx.doi.org/10.1016/S0022-3476(05)81912-2</RefLink>
</Reference>
<Reference refNo="181">
<RefAuthor>Goel R</RefAuthor>
<RefAuthor>Hamosh M</RefAuthor>
<RefAuthor>Stahl GE</RefAuthor>
<RefAuthor>Henderson TR</RefAuthor>
<RefAuthor>Spear ML</RefAuthor>
<RefAuthor>Hamosh P</RefAuthor>
<RefTitle>Plasma lecithin: cholesterol acyltransferase and plasma lipolytic activity in preterm infants given total parenteral nutrition with 10% or 20% Intralipid</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>Acta Paediatr</RefJournal>
<RefPage>1060-4</RefPage>
<RefTotal>Goel R, Hamosh M, Stahl GE, Henderson TR, Spear ML, Hamosh P. Plasma lecithin: cholesterol acyltransferase and plasma lipolytic activity in preterm infants given total parenteral nutrition with 10% or 20% Intralipid. Acta Paediatr. 1995;84(9):1060-4. DOI: 10.1111/j.1651-2227.1995.tb13825.x</RefTotal>
<RefLink>http://dx.doi.org/10.1111/j.1651-2227.1995.tb13825.x</RefLink>
</Reference>
<Reference refNo="182">
<RefAuthor>Morris S</RefAuthor>
<RefAuthor>Simmer K</RefAuthor>
<RefAuthor>Gibson R</RefAuthor>
<RefTitle>Characterization of fatty acid clearance in premature neonates during intralipid infusion</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Pediatr Res</RefJournal>
<RefPage>245-9</RefPage>
<RefTotal>Morris S, Simmer K, Gibson R. Characterization of fatty acid clearance in premature neonates during intralipid infusion. Pediatr Res. 1998;43(2):245-9. DOI: 10.1203/00006450-199802000-00015</RefTotal>
<RefLink>http://dx.doi.org/10.1203/00006450-199802000-00015</RefLink>
</Reference>
</References>
<Media>
<Tables>
<Table format="png">
<MediaNo>4</MediaNo>
<MediaID>4</MediaID>
<Caption>
<Pgraph>
<Mark1>Table 4: Example of the (re)establishing of nutrition in premature and ill full-term infants</Mark1>
<Mark1>
<Superscript>1</Superscript>
</Mark1>
</Pgraph>
</Caption>
</Table>
<Table format="png">
<MediaNo>3</MediaNo>
<MediaID>3</MediaID>
<Caption>
<Pgraph>
<Mark1>Table 3: Example of a procedure questionnaire in premature and ill full-term infants</Mark1>
</Pgraph>
</Caption>
</Table>
<Table format="png">
<MediaNo>1</MediaNo>
<MediaID>1</MediaID>
<Caption>
<Pgraph>
<Mark1>Table 1: Benchmark for overall parenteral energy intake (incl. amino acids) in stable patients [1]</Mark1>
</Pgraph>
</Caption>
</Table>
<Table format="png">
<MediaNo>2</MediaNo>
<MediaID>2</MediaID>
<Caption>
<Pgraph>
<Mark1>Table 2: Reference values for enteral protein intake according to new reference values for nutrient intake in Germany, Austria and Switzerland (DACH reference values) [71]</Mark1>
</Pgraph>
</Caption>
</Table>
<NoOfTables>4</NoOfTables>
</Tables>
<Figures>
<NoOfPictures>0</NoOfPictures>
</Figures>
<InlineFigures>
<NoOfPictures>0</NoOfPictures>
</InlineFigures>
<Attachments>
<NoOfAttachments>0</NoOfAttachments>
</Attachments>
</Media>
</OrigData>
</GmsArticle>
]]></plaintext></textgroup></pgraph></abstract></origdata></gmsarticle>