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voLUME 9 — iSSUE 14: TRANScRipT 

Featured Cases: Optimizing Nutritional Support with Protein and 

Energy for Very Low Birth Weight Infants 

Our guest author is David H. Adamkin, Professor of 

Pediatrics, Director of the Division of Neonatal 

Medicine, and Rounsavall Endowed Chair of 

Neonatology at the University of Louisville. 

After participating in this activity, the participant will 

demonstrate the ability to: 

n Describe the importance of starting parenteral 

nutrition in the first hours of life, even in the face 

of critical illness in VLBW infants, 

n Evaluate the role of parenteral amino acids in 

glycemic control, as well as lipids in relation to lung 

dysfunction, in VLBW infants, and 

n Discuss the role of donor-fortified milk in VLBW 

infants. 

This discussion, offered as a downloadable audio file 

and companion transcript, covers the important issues 

related to enhancing nutrition in very low birth weight 

infants in the format of case-study scenarios for the 

clinical practice. This program is a follow up to the 

Volume 9, Issue 13 eNeonatal Review newsletter— 

Optimizing Nutritional Support with Protein and Energy 

for Very Low Birth Weight Infants. 

MEET ThE AUThoR 

David H. Adamkin, MD 

Professor of Pediatrics 

Director, Division of Neonatal 

Medicine 

Rounsavall Endowed Chair of 

Neonatology 

University of Louisville 

Louisville, Kentucky 

Guest Faculty Disclosure 

The author has indicated that he has no financial 

interests or relationships with a commercial entity 

whose products or services are relevant to the 

content of his presentation. 

Unlabeled/Unapproved Uses 

The author has indicated that there will be no 

references to unlabeled/unapproved uses of drugs 

or products. 

Release Date 

October 31, 2013 

Expiration Date 

October 30, 2015 

pRoGRAM DiREcToRS 

Edward E. Lawson, MD 

Professor of Pediatrics 

Johns Hopkins University 

School of Medicine 

Chief, Division of 

Neonatology 

Vice Chair, Department of 

Pediatrics Johns Hopkins 

Children’s Center 

Baltimore, Maryland 

Maureen M. Gilmore, MD 

Assistant Professor of 

Pediatrics 

Director of Neonatology 

Johns Hopkins Bayview 

Medical Center 


Lawrence M. Nogee, MD 

Professor 

Department of Pediatrics 

Division of Neonatology 

The Johns Hopkins 

University School of 

Medicine 


Mary Terhaar, DNSc, RN 

Assistant Professor 

Undergraduate Instruction 


University School of 

Nursing 


Anthony Bilenki, MA, RRT 

Technical Director 

Respiratory Care Services 

Division of Anesthesiology 

and Critical Care Medicine 


Hospital 

Baltimore, Maryland

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STATEMENT oF NEED 

Through discussions with expert physician/educators, a survey of practicing neonatologists, 

and a review of the current literature, including national and regional guidelines and quality-ofcare 

measures, the following core learning gaps have been identified: 

n In addition to cognitive, educational, and behavioral impairments later in life, former 

premature infants with BPD also suffer higher rates of long-term airway obstruction and 

mild exercise intolerance, potentially preventable with better NICU and post-discharge care. 

n Protocols for noninvasive methods of pulmonary support are underused or misused in 

many neonatal care settings, resulting in higher rates of lung injury in preterm infants from 

mechanical ventilation. 

n Neonatologists need a consistent and precise approach to the diagnosis and treatment of 

ventilator-acquired pneumonia (VAP) to minimize ineffective empiric antibiotic treatment. 

n Although major reductions in the burden of CLABSI in NICUs have been achieved, variable 

rates of sepsis in different NICUs indicate that adherence to best practices and vigilant 

preventive interventions are not as uniform as they could and should be. 

n Too few of the ≈90% of premature infants discharged with nutritional deficiencies receive 

calorie- and protein-enriched formulas that prevent near-term developmental deficits and 

long-term damaging health effects, such as metabolic syndrome. 

n Neonatologists are not fully aware of the comparative merits of IV soybean oil-based lipid 

emulsions and parenteral omega-3 lipid emulsions in the PNALD setting. 

iNTENDED AUDiENcE 

This activity has been developed for neonatologists, respiratory therapists, neonatal nurses 

and nurse practitioners, and others involved in the care of patients in the NICU. 

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eNeonatal Review Podcast Transcript, Volume 9: Issue 14

eNEoNATAL REviEw poDcAST TRANScRipT 

MR. BoB BUSKER: Welcome to this eNeonatal 

Review Podcast. 

eNeonatal Review is presented by the Johns Hopkins 

University School of Medicine, and the Institute for 

Johns Hopkins Nursing. This program is supported by 

educational grants from Abbott Nutrition, Cornerstone 

Pharmaceuticals, Ikaria, and Mead Johnson Nutrition. 

Today’s program is a companion piece to our 

eNeonatal Review newsletter issue: Optimizing 

Nutritional Support with Protein and Energy for 

Very Low Birth Weight Infants. 

Our guest today is one of that issue’s authors, Dr. 

David Adamkin, from the University of Louisville. 

This activity has been developed for neonatologists, 

respiratory therapists, nurse practitioners, neonatal 

nurses, and others who work in the NICU. There are 

no fees or prerequisites for this activity. 

The Accreditation and Credit Designation Statements 

can be found at the end of this podcast. For additional 

information about accreditation, Hopkins policies, and 

expiration dates and to take the posttest to receive 

credit online, please go to our website newsletter 

archive, www.eneonatalreview.org, and click the 

Volume 9, Issue 14 podcast link. 

Learning objectives for this audio program are, that 

after completing this activity, the participant will 

demonstrate the ability to: 

n Describe the importance of starting parenteral 

nutrition in the first hours of life, even in the face 

of critical illness in VLBW infants; 

n Evaluate the role of parenteral amino acids in 

glycemic control, as well as lipids in relation to lung 

dysfunction, in VLBW infants; and, 

n Discuss the role of donor-fortified milk in VLBW 

infants. 

I’m Bob Busker, managing editor of eNeonatal 

Review. On the line we have with us Dr. David H. 

Adamkin, Professor of Pediatrics, Director of the 

Division of Neonatal Medicine, and Rounsavall 

Endowed Chair of Neonatology, at the University 

of Louisville. 

Dr. Adamkin has indicated that he has no financial 

interests or relationships with any commercial entity 

whose products or services are relevant to the content 

of this presentation, and his discussion today will not 

reference the unlabeled or unapproved uses of any 

drugs or products. 

Dr. Adamkin, welcome to this eNeonatal Review 

podcast. 

DR. DAviD ADAMKiN: Thank you very much, Bob. 

MR. BUSKER: In your newsletter issue, Doctor, you 

reviewed studies describing the importance of 

enhancing nutrition in very low birth weight infants — 

that would be babies weighing less than 1500gm— to 

decrease morbidities and promote improved 

neurodevelopmental outcomes. What I’d like to do 

today is expand on that information, and discuss how 

it can actually be applied in the NICU. So if you 

would, doctor — start us out with patient scenario. 

DR. ADAMKiN: The case that we’re discussing is 

a 610 gm, small for gestational age, 26-week infant, 

delivered by emergency C-section because of placental 

abruption and fetal distress. Baby’s Apgar scores were 

2, 4, 6, and 8, at 1, 5, 10, and 15 minutes, respectively. 

Infant received positive pressure ventilation in the 

delivery room and was intubated and given surfactant. 

The cord blood pH is 7 with a base excess of -10. The 

infant is started on intravenous fluids of D10W 

through a UVC and D5W in the UAC for total fluids of 

80 cc/kg/daycc/kg/day. 

So this is a tiny baby that’s growth-restricted with a 

difficult initial course, including fetal acidosis, and is 

started on D10 and D5 through the UVC and the UAC. 

At 12 hours of age the morning labs include a plasma 

glucose of 180mg/dLmg/dL after two ACCU-CHEKs 

revealed 140 and 160, and the potassium is 7.3 

mEq/L. The infant’s urine output has been 1.5 

cc/kg/hr, the BUN is 15, and the creatinine is 0.7. 

MR. BUSKER: Why wasn’t this baby started on 

early TPN? 

DR. ADAMKiN: It’s possible, because of the baby’s 

condition at birth, the fetal hypoxia acidosis, that the 

clinicians were concerned about the baby’s ability to 

metabolize TPN and that may have been why the 

clinicians chose not to start TPN. Let’s delve into 

eNeonatal Review Podcast Transcript, Volume 9: Issue 14 

1

that a little bit further and examine exactly what the 

baby is getting with the fluids that were started and 

why it may be problematic that the baby was not 

initiated on early TPN. 

The fluids that were provided this baby, D10 in the 

UVC and D5W in the UAC, would provide about 

22 cal/kg/day for this baby. That’s a very modest 

amount of energy and represents a glucose infusion 

rate of about 4 mg/kg/min. That means this baby 

would be catabolic because of the inadequacy of the 

energy provided. And in the absence of protein, as 

we see in both the Senterre article and the Radmacher 

articles that energy without protein will not place the 

baby in positive nitrogen balance. 1,2 

So it is very important additionally to appreciate the 

relationship between early nutrition and severity of 

illness. In other words, because this baby was 

perceived as being so ill, the clinicians decided not to 

initiate the amino acids. This was a perception of 

illness, but as shown in the final paper that we 

reviewed, the paper from Ehrenkranz on how early 

nutrition mediates the influence of severity of illness 

on these babies, we learned that early nutrition, 

despite the baby being more ill, actually improves 

outcome, including prevention of morbidities and 

prevention of mortality. 3 

MR. BUSKER: Doctor, let me ask you to speculate for 

us: is it possible that early TPN might have prevented 

both the nonoliguric hyperkalemia and the 

hyperglycemia in this infant? 

DR. ADAMKiN: It’s quite likely the answer to that 

is yes. We know that early amino acids have 

dramatically reduced the incidence of hyperglycemia 

and nonoliguric hyperkalemia in these extremely low 

birth weight infants. Early amino acids stimulate 

insulin activity and secretion of insulin to promote 

glucose tolerance. The insulin is necessary for 

transport of glucose into the cell and to prevent 

intracellular energy failure, which allows potassium 

to leak out of the cell. That is mediated through an 

enzyme called sodium potassium ATPase. 

This enzyme regulates the maintenance of potassium 

in the cell. When there is intracellular energy failure 

because insulin activity is decreased related to the 

absence of amino acids provided parenterally, then 

potassium will leak out of the cell as this enzyme 

activity decreases. 

MR. BUSKER: Thank you for that clarification, 

Dr. Adamkin. What happened next with this infant? 

DR. ADAMKiN: The next day, at 36 hours of age, 

this baby weighs 595 gm and that represents a 

2.4% postnatal weight loss. The baby is now started 

on TPN, including 3 gm/kg/day of amino acids and 

2 gm/kg/day of lipids. The infant, despite receiving 

two doses of surfactant, remains on 80 % oxygen, a 

rate of 60 on the ventilator, pressures of 20/4, and 

the x-ray demonstrates severe RDS. 

Labs done after being on this TPN for 16 hours 

include a BUN of 40mg/dL, a creatinine of .7mg/dL, 

and a triglyceride level of 220mg/dL. The urine 

output at 52 hours of age has been 4 ml/kg/hr for the 

last 24 hours 

MR. BUSKER: This elevation in the BUN — from 15 

mg/dL to 40 mg/dL— what’s the significance of that? 

DR. ADAMKiN: This is a typical dilemma or 

conundrum for the clinician managing early TPN 

in babies receiving early amino acids. This was also 

addressed in the Radmacher paper reviewed in this 

issue of eNeonatal Review relating to early amino acid 

and the metabolic response of extremely low birth 

weight babies. 2 

An elevated BUN of up to 40 mg/dL has been 

observed in neonates early in life with or without 

TPN. The concern is whether this represents excessive 

amino acid delivery with decreased utilization and 

subsequent oxidation, or more likely it means that the 

BUN is simply reflective of adequate utilization by the 

baby doing what the baby does metabolically in utero 

with amino acids and really is the principle of early 

amino acids asking the immature, extremely 

premature baby to use amino acids not only to make 

lean mass, but to burn as energy. 

In that same paper, the Radmacher paper, it was 

shown that there was no direct relationship between 

BUN and protein dose 2 The reason for that is BUN is 

also dependent on acuity of illness, on renal function 

and on fluid balance. Therefore, we shouldn’t make 

decisions about decreasing the protein in TPN simply 

with just one piece of information, a BUN that may be 

40. Other factors need to be taken into account which 

include the creatinine for renal function, the urine 

output that the baby is having, and the clinical 

condition of the baby. 


2

So in this particular case, a BUN of 40 with a normal 

creatinine, normal urine output, normal postnatal 

weight loss, would not appear to represent any 

problem with the early initiation of amino acids. 

The second issue that needs to be addressed is that 

when amino acids are used for energy, per our 

discussion just a moment ago, the amino acids are 

converted to carbon dioxide and ammonia. The 

ammonia is converted to urea. That’s why there is an 

elevated BUN and it does not represent toxicity, it 

simply represents adequate utilization of the amino 

acid solution. 

MR. BUSKER: As you described, this baby’s 

triglyceride level is 220mg/dL. What’s the reason for 

that elevated level? 

DR. ADAMKiN: The elevated triglyceride levels in 

this patient probably represent low enzyme activity 

for lipoprotein lipase, which is the enzyme that breaks 

down or hydrolyzes the intravenous fat solution. We 

know that the extremely low birth weight infant and, 

in particular, small for gestational age infants, have 

the lowest levels of this particular enzyme and are at 

the greatest risk to develop hypertriglyceridemia. This 

baby is both an ELBW baby and is also an SGA infant. 

The triglyceride levels probably should be kept below 

200 or perhaps even less than 150 mg/dL in these 

patients. We know that when babies have significant 

elevations of triglyceride, then some of the fat can end 

up in cells lining the intestine and also theoretically 

in the lung. 

There is a simple way to prevent hypertriglyceridemia 

in the majority of babies. It has to do with what I call 

the lipid infusion rate. We know that if we don’t 

exceed a rate of 0.12 gm/kg/hr of lipids, then the 

majority of babies that we treat with intravenous 

lipids will not develop hypertriglyceridemia. However, 

in this particular case, the baby was receiving 2 grams 

per kilogram per day of lipid infused over 24 hours, 

and that comes out to .08 grams per kilogram per 

hour, which is certainly below the .12 grams per 

kilogram per hour that we recommended. However, 

again, what’s unique about this baby is the fact that 

the baby was born growth restricted or SGA. For the 

majority of babies, again, if we don’t exceed the .12 

grams per kilogram per hour, these babies will not 

develop hypertriglyceridemia. Therefore, the 

maximum dose of lipid recommended by the 

Committee of Nutrition of the Academy of Pediatrics 

is 3 gm/kg/day of lipids. When we infuse that dose 

over 24 hours, it comes out to 0.12 gm/kg/hr which 

is the rate of infusion that we recommend. Therefore, 

the simplest strategy is to infuse babies over 24 hours 

with whatever their lipid dose is so that we know at 

the maximum dose we won’t exceed the .12 gm/kg/hr. 

MR. BUSKER: You also noted that this baby has 

severe RDS and requires a high concentration of 

oxygen. Is it safe to administer lipids to an infant 

with these problems? And overall, what can you tell 

us about the implications of hypertriglyceridemia 

on lung disease? 

DR. ADAMKiN: This is also a controversial area in 

the management of the extremely low birth weight 

baby. A potential hazard of hyperlipidemia resulting 

from the failure to clear the infused lipid in the system 

is an adverse effect on gas exchange in the lungs. In 

particular, significant concerns have been raised 

about the high polyunsaturated fatty acid content of 

the lipid emulsions that we use in the United States 

that have a very high content of an omega-6 fatty acid 

called linoleic acid. 

The solutions in the United States contain over 50% 

of the fatty acids come from linoleic acid. Why is that 

important? Linoleic acid is an 18-carbon-2-doublebond 

omega-6 fatty acid and it is the essential fatty 

acid. It is converted to a 20-carbon-4-double-bond 

omega-6 compound, which is called arachidonic acid. 

Here’s where things become important. Arachidonic 

acid is converted into vasoactive mediators that may 

cause pulmonary vasoconstriction or decrease the 

ability of the baby to oxygenate. These compounds 

include eicosanoids, prostaglandins, thromboxanes, 

and leukotrienes, and all of these increase vasomotor 

tone. Therefore, we recommend that for late preterm 

babies or term babies who have persistent pulmonary 

hypertension, the clinician be very judicious with the 

use of lipids in those babies, restricting them to even 

no lipids during the height of their illness or a very 

modest dose, and the extension to the babies that 

we’re talking about today, the extremely low birth 

weight baby like this one with surfactant deficiency 

that one may want to be conservative with dosing 

lipids 1 gm/kg/day to 2 gm/kg/day in babies who 

have severe lung disease, and once they’re recovering 

we can increase the dose to the maximum of 

3 gm/kg/day. 


3

MR. BUSKER: And we’ll continue with Dr. Adamkin 

from the University of Louisville in just a moment. 

DR. MAUREEN GiLMoRE: Hello. I’m Maureen 

Gilmore, assistant professor of pediatrics and director 

of neonatology at Johns Hopkins Bayview Medical 

Center. I’m one of the program directors of 

eNeonatal Review. 

eNeonatal Review is a combination newsletter and 

podcast program delivered via email to subscribers. 

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neonatal nurses and nurse practitioners, and other 

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Bimonthly podcasts are also available as 

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Subscription to eNeonatal Review is provided without 

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Continuing education credit for each issue and each 

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eNeonatal Review without charge, and access 

back-issues, please go to our website: 

www.eneonatalreview.org. Thank you. 

MR. BUSKER: Welcome back to this eNeonatal 

Review podcast. I’m Bob Busker, managing editor of 

the program. Our guest is Dr. David Adamkin, 

Director of the Division of Neonatal Medicine at the 

University of Louisville. And our topic is Optimizing 

Nutritional Support with Protein and Energy for Very 

Low Birth Weight Infants. 

We’ve been following Dr. Adamkin’s presentation of 

a 26 week SGA infant who did not receive TPN until 

36 hours of life. As we’ve discussed, the baby shows 

severe RDS, hypertriglyceridemia, and elevated BUN. 

Let me ask you to continue the case for us now, if you 

would, doctor, with the infant at 30 days old. 

DR. ADAMKiN: This infant remains oxygen and flow 

dependent and has significant chronic changes on 

chest x-ray consistent with evolving BPD. Since the 

mother did not provide her milk to feed this baby, the 

baby was started on donor milk feedings. At this time, 

the infant has finally come off of TPN and remains on 

the donor human milk at 120 cc/kg/day, and the PICC 

line has been removed. 

The infant is on caffeine and diuretics for chronic lung 

disease, but still has recurring episodes of apnea, 

bradycardia and desaturations. Feeding progress has 

been slowed by a couple of episodes of feeding 

intolerance with residuals and abdominal distention. 

This is a very typical course for such an extremely low 

birth weight baby and particularly one that is growth 

restricted at birth. The infant’s weight at 30 days is 

800 grams and the postmenstrual age now at a month 

of age is 30 weeks. So this baby remains well below 

the third percentile and this baby has postnatal 

growth failure. 

MR. BUSKER: Now there’s an extremely strong 

evidence base that shows that human milk is the 

preferred diet for extremely low birth weight infants 

to prevent infection and NEC, and it’s also been 

shown to lead to better neurocognitive development. 

The donor milk that’s being given to this infant: how 

much nutrition is that providing at this time, and 

what considerations should be made for fortification? 

DR. ADAMKiN: The donor milk or even the mother’s 

own milk does not provide all of the nutrients that the 

very low birth weight babies, and in particular, the 

extremely low birth weight babies require. That’s the 

reason why many of the tinier babies do not grow very 

well on donor human milk and must be fortified, 

receive human milk fortification. 

The human milk fortification will supplement the 

baby with nutrients, most importantly protein, 

energy, calcium and phosphorus, will allow the baby 

to grow better with the protein and more energy, and 

mineralize the bones for length growth with calcium 

and phosphorus. 

Let’s spend a moment on donor human milk. Donor 

human milk is typically provided by mothers who 

have had term infants who are contributing their milk 

at around two to three months of lactation to a milk 

bank. It turns out that donor human milk has less 


4

protein than the milk from the baby’s own mother, 

so it has the lowest protein, around 1 gm/dL of 

protein or even a little bit less, whereas the mother’s 

own milk, at least early on in lactation, has about 

1.5 grams per deciliter. 

We do know, however, that even the mother’s own 

milk, which starts out with more protein than donor 

milk has, actually decreases as lactation continues. 

So that the mother’s own milk delivering a premature 

baby, the protein in that milk declines, and over time 

may look more similar to donor or term milk. 

Therefore, human milk provided to extremely low 

birth weight infants, babies less than a kilogram, 

is likely to have inadequate protein content. 

In eNeonatal Review, the article reviewed from Sauer 

and Kim talks about analyzing human milk with a 

spectrophotometer. 4 We also do that here at the 

University of Louisville. It allows us to examine in real 

time the content of the mother’s milk each day before 

it’s provided to the baby. This technology takes about 

20 seconds after a human milk sample is provided to 

the device and prints out the macronutrient content 

of that milk that’s being fed to the baby that day 

including the amount of energy. That allows us to 

individualize and customize the human milk that that 

baby is receiving. 

For this particular baby, the 120 ml/kg/day of donor 

milk could be providing as little as 1 gm/kg/day to 

1.2 gm/kg/day in an infant whose protein 

requirement is 4 gm/kg/day. So it is not hard to 

understand that this baby is not going to grow very 

well. And I believe that we’ll talk more about 

fortification in a moment. 

MR. BUSKER: Actually, Doctor, let’s take that 

moment right now. Tell us more about adjustable 

fortification and human milk macronutrient analysis. 

DR. ADAMKiN: Sure, thank you. There are two ways to 

go about fortifying human milk with a fortifier. One is 

an adjustable method. The adjustable method tries to 

make up for the changing protein that is decreasing by 

analyzing the baby’s BUN as a surrogate for protein 

adequacy. So if the BUN is below a certain level — 9 

was used in the study that analyzed this strategy — 

if the BUN is less than 9, they added more fortifier; 

if the BUN was greater than 14, they took away some 

fortifier or protein powder. 

The method that I alluded to would be called targeted, 

or individualized, fortification, where we measure 

the protein in the milk, the energy in the milk, and 

then we can adjust the nutrient intake based on the 

results of the analysis. And again, the paper from 

Sauer and Kim in eNeonatal Review showed how to 

go about using the point of care spectrophotometry 

in the nursery. 4 

MR. BUSKER: Thank you for that explanation, 

Doctor, and for presenting today’s case discussion. 

I want to switch gears now and ask you to look into 

the future for us. What upcoming advances do you 

see regarding nutritional support for these very low 

birth weight infants? 

DR. ADAMKiN: I think there is going to be a lot of 

excitement about the relationship between nutrition 

provided to these very low birth weight babies and 

their cognitive outcomes and their risk of adult 

diseases later on in life. The so-called programming 

of disease that may occur early in life and express 

itself later. 

The things that I’m referring to for our tiny babies is 

methodologies to look at body composition of these 

babies. To look at whether or not our feedings are 

making them fat or lean. We know that body 

composition of these babies may be associated with 

the risk later on in life of cardiometabolic diseases. 

Another technology that may become available to 

use at the bedside in a standard fashion would be 

measuring energy expenditure: how are the babies 

using the nutrients that we’re giving them, how many 

calories are they burning, can we tailor their nutrition 

more for the individual baby than simply feeding all of 

these babies the same amount of fuel and seeing how 

they do. I think measuring body composition and 

learning more about their energy expenditure will be 

part of the future in optimizing management and 

outcomes of these babies. 

MR. BUSKER: Thank you for sharing those thoughts, 

doctor. To wrap things up, let’s review the key points 

of today’s discussion in light of our learning 

objectives. So to begin: the importance of starting 

parenteral nutrition in the first hours of life in very 

low birth weight infants, even in the face of critical 

illness. 


5

DR. ADAMKiN: The early initiation of amino acids is 

very important in preventing specific metabolic 

abnormalities. We have learned from a number of 

papers, including in this issue’s eNeonatal Review 

from Richard Ehrenkranz, the importance of energy 

the first week of life.3 That study showed less 

morbidity and mortality related to more energy the 

first week of life in these babies. Another study 

correlated energy in the first week of life in babies 

of this size having higher cognitive scores out to 

30 months of life. So the first week of life is a critical 

window for optimizing early nutritional support based 

on recent recommendations in very low birth weight 

babies from Senterre and Rigo. 1 

MR. BUSKER: And second: the role of parenteral 

amino acids in glycemic control and of lipids with 

lung disease in very low birth weight infants. 

DR. ADAMKiN: We know that the amino acids turn 

on insulin. Insulin will allow the baby to be more 

glucose tolerant, and the baby who is more glucose 

tolerant will be able to receive more energy and more 

energy in the first week of life equals better outcome. 

The insulin also keeps potassium in the cell and 

prevents nonoliguric hyperkalemia, which can be 

life threatening. 

So early amino acids have very important roles. The 

use of lipids is somewhat more controversial with lung 

disease, but we ought to at least be aware that the 

possibility exists that the lipid dosage may have to be 

modified in babies with lung disease because of the 

possibility of lipid adminstration being associated 

with pulmonary vasoconstriction and decreasing 

oxygenation. 

MR. BUSKER: And finally: the use of donor human 

milk and the need for fortification in very low birth 

weight infants. 

DR. ADAMKiN: It’s clear that these extremely low 

birth weight babies need human milk — own mother’s 

milk first choice, donor human milk second choice — 

because it improves outcomes, decreases morbidities, 

and prevents necrotizing enterocolitis and infection. 

However, from a growth standpoint, the levels of 

protein, calcium, and phosphorus are inadequate in 

human milk and therefore the human milk must be 

fortified to provide the benefits of growth along with 

all the other important things that human milk does 

to improve the outcome for these babies. 

MR. BUSKER: Dr. David Adamkin from the 

University of Louisville, thank you for participating in 

this eNeonatal Review podcast. 

DR. ADAMKiN: Thank you very much, and I hope our 

audience can benefit from the information provided. 

Thank you. 

MR. BUSKER: This podcast is presented in 

conjunction with the eNeonatal Review Newsletter, 

a peer-reviewed literature review certified for 

CME/CE credit, emailed monthly to clinicians 

treating patients in the NICU. 

This activity has been planned and implemented 

in accordance with the Essential Areas and Policies 

of the Accreditation Council for Continuing Medical 

Education, through the joint sponsorship of the 

Johns Hopkins University School of Medicine and 

The Institute for Johns Hopkins Nursing. The Johns 

Hopkins University School of Medicine is accredited 

by the ACCME to provide continuing medical 

education for physicians. 

For physicians, the Johns Hopkins University School 

of Medicine designates this enduring material for a 

maximum of 0.5 AMA PRA Category 1 Credit(s). 

Physicians should claim only the credit commensurate 

with the extent of their participation in this activity. 

The Institute for Johns Hopkins Nursing is accredited 

as a provider of continuing nursing education by the 

American Nurses Credentialing Center’s Commission 

on Accreditation. 

The Institute for Johns Hopkins Nursing and the 

American Nurses Credentialing Center do not 

endorse the use of any commercial products 

discussed or displayed in conjunction with this 

educational activity. 

For nurses, this 0.5 contact hour Educational Activity 

is provided by The Institute for Johns Hopkins 

Nursing. Each podcast carries a maximum of 

0.5 contact hour. 

This educational resource is provided without charge, 

but registration is required. To register to receive 

eNeonatal Review via e-mail, please go to our website, 

www.eneonatalreview.org. 


6

The opinions and recommendations expressed by 

faculty and other experts whose input is included in 

this program are their own. This enduring material is 

produced for educational purposes only. 

Use of names of the Johns Hopkins University School 

of Medicine and The Institute for Johns Hopkins 

Nursing implies review of educational format, design, 

and approach. Please review the complete prescribing 

information for specific drugs, combinations of drugs, 

or use of medical equipment, including indication, 

contraindications, warnings, and adverse effects, 

before administering therapy to patients. 

eNeonatal Review is supported by educational grants 

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Thank you for listening. 

This program is copyright 2013, with all rights 

reserved, by the Johns Hopkins University School of 

Medicine and The Institute for Johns Hopkins 

Nursing. 


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REFERENcES 

1. Senterre T, Rigo J. Optimizing Early Nutritional Support Based on Recent Recommendations in VLBW 

Infants and Postnatal Growth Restriction. J Pediatr Gastroenterol Nutr. 2011 Nov;53(5):536-542. 

2. Radmacher PG, Lewis SL, Adamkin DH. Early amino acids and the metabolic response of ELBW infants 

(≤ 1000 g) in three time periods. J Perinatol. 2009 Jun;29(6):433-437. 

3. Ehrenkranz RA, Das A, Wrage LA, et al. Early nutrition mediates the influence of severity of illness on 

extremely LBW infants. Pediatr Res. June;69(6):522-529. 

4. Sauer CW, Kim JH. Human milk macronutrient analysis using point-of-care near-infrared spectrophotometry. 

J Perinatol. 2011 May;31(5):339-343. 


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