Early Parenteral Nutrition

of the Preterm Infant

Benefits and risks

Johanes Edy Siswanto

Harapan Kita Women and Children Hospital
Pernatology Working Group

PIT Medan
20- 24 Pebruari 2010

Neonatal Nutrition

The ultimate goal for growth of the infant in

the neonatal intensive care unit (NICU) is
replication of in utero growth.

Due to the immaturity of the prematures gut,

it is often difficult to achieve full enteral feeds in a
timely fashion. In addition, mothers breast
milk is not sufficient to match in utero growth
of the extremely premature infant.

It is however difficult to meet in utero growth

accretion with strictly parenteral nutrition and
complications of parenteral nutrition may
cause severe problems for the premature.

Rate of weight gain in fetus

highest between 26 and 36 weeks

Aim:
Growth standard
Growth of the preterm infant
should be similar to
intrauterine growth of a fetus
at the same gestational age,
approximately 15g/kg/day.
AAP 1998

Body weight in an AGA and SGA 27 week infant

who gains 15g/ kg/ day. (from Cooke R, J Perinatol 2005)

Caloric deficiency in the

NICU
Decreased

caloric reserves at

birth
Increased requirement for
work of breathing
tissue repair
growth

Estimated caloric requirement of

a
growing preterm infant (AAP
Kcal / kg / day
1985)
Resting metabolic rate
Cold stress
Activity
Synthesis / thermic effect of food
Fecal loss
Growth
Total

50
10
15
8
12
25
120

Parenteral Nutrition : Common

Practice
Glucose

infusions started early

Amino acids started in first week of life and
advanced slowly at 0.5 gm. Increments
Lipid infusions started in first week of life and
advanced slowly at 0.5 gm. Increments
Amino acids and lipids frequently delayed or
interrupted
Tradition, Possible Metabolic acidosis, Possible uremia,
Hyperlipidemia, Sepsis, Displacement of bilirubin

Reasons to withhold Parenteral

nutrition
Traditional Approach

Delayed initiation of TPN for 2-3 days:

Electrolyte stability
Metabolic stability
Hemodynamic stability
Practical or technical contraindications

Problems
No medical or scientific reasons for delay
Irrepressible gluconeogenesis and proteolysis
or starvation response
State metabolic shock if no adequate nutrition

We Create Malnutrition
In The NICU ?!!

Early Parenteral Nutrition

Intravenous Nutrition ( IVN ) :

Four General Principles : Bill Hays
Rules
1.
2.

Metabolic and nutritional

requirements do not stop with birth
Intravenous feeding is always
indicated when normal metabolic
and nutritional needs are not met by
normal enteral feeding

Intravenous Nutrition ( IVN

):
Four General Principles

3. Hours, not days, are the longest

periods infants should be allowed to

not receive nutrition, IV or PO
4. The metabolic and nutrient
requirements of the newborn are equal
to or greater than those of the fetus

Indications for TPN

Route
Peripheral

Central

Indication for TPN

Temporary supply of nutrients < 2 wk:
Enteral intake
Functional gut immaturity
Temporary feeding intolerance
Prolonged non-use of the GI tract > 2
wk:
Surgical GI disorders
Necrotizing enterocolitis
Short bowel syndrome
ELBW <1,000 grams

Benefits of Early Parenteral

Nutrition
Using a Strategy Of Early Aggressive
Parenteral Nutrition
Instituted as soon as possible after birth
Providing nutrient delivery at rates that are
safe
and beneficial has potential to :

1.be

cost effective
2.Allow for reasonable nutritional continuity in the
transition from intrauterine to extrauterine life
3.Contributes to reversing the current epidemic of
postnatal growth failure in very preterm neonates
4.Improve developmental outcomes

What we know early parenteral nutrition

Significant protein and caloric deficits occur

in the early neonatal period and are

difficult to recoup in extremely premature
infants.
Embleton, Pediatrics 2001
Protein deficit early in the neonatal period is
an
important contributor to poor growth,
particularly in extremely low birth weight
infants
(ELBW). Replication of intrauterine growth
and
nutrient accretion is difficult for ELBW infants
due

Studies have shown that negative nitrogen

balance
in sick premature infants who received
glucose
alone can be reversed with an amino acid
(AA)
intake of 1.1-2.5 g

Denne SC, Poindexter BB. Semin Perinatol 2007; 31:56-60

Numerous studies indicating early parenteral

protein and energy delivery in the first 2
weeks
of life allows for earlier regain of birth weight
that is not due to fluid retention

Longitudinal growth of hospitalized very

low birth weight infants. ( Ehrenkranz RA, et al.
Pediatrics 1999)

Our approach to early

aggressive parenteral
nutrition
The very preterm newborn :
A

NUTRITIONAL EMERGENCY
Glucose stores of only 200 kcal
Catabolic : net protein loss
- with IV glucose alone, loss 1% body
protein/day
-10% loss of protein stores = protein
malnutrition

Our Primary Nutrition Goal :

Protein Accretion- Practical
Aproach
Protein gain is the best indicator of
real
growth
Greatest rate relative protein gain
throughthout life occurs prior to
birth
Minimum parenteral amino acid
intake
- zero balance (i.e. not catabolic)
- can be achieved with 1.0-1.5

Protein Quantity is the

Primary Determinant of Protein
Accretion

Maximum
Parenteral Intake
Yet to be defined, limited by concerns of
toxicity
If goal is to achieve fetal delivery rates
(Ziegler):
- 24-25 weeks 3.75 - 4.0 g/kg/d
- 27-28 weeks 3.5 g/kg/d
- 32 weeks
3.2 g/kg/d
- term infants
2.8 3.0 g/kg/d

Our Parenteral Nutrition Goal :

Early Aggressive Nutritional
Support
Start TPN day of life # 1

Give amino acid to prevent

catabolism and
ideally in amount that produce
growth
Advance glucose and lipids as rapidly
as
tolerated
Early protein loses in ELBW infants
can be
minimized by providing parenteral

Example stockor stater Amino

Acid (AA) solutions
2% AA in D10W at 60ml/kg/d 1.2
g/kg/d/ AA
2% AA in D10W at 80ml/kg/d 1.6
g/kg/d/ AA
5% AA in D10W at 60ml/kg/d 3.0
g/kg/d/ AA
If you start with 5% AA you cant
increase the
fluid rate!
Additional fluids can be co-infused if
glucose

Beneficial Effect of Amino

Acid Intake on
In our 1 vs 3 g/kg/d amino acid intake
Hyperglysemia

study,
insulin concentration correlated with
amino
acid intake
Our incidence of neonatal hyperglycemia
has
dramatically decreased since instituting :
Early parenteral amino acids
Glucose infusion less than the maximal
oxidative glucose capacity

Other benefits of Early Amino

Acids
Several studies have correlated early
and
high protein intake ( enteral and
parenteral )
with improved growth at hospital
discharge

Early and Aggressive nutritional strategy

(parenteral and
enteral) decreases postnatal growth failure in
very low
birth weight infants.
Dinerstein A et al, J Perinatol
2006

Both early and/or late amino acid intake

Potential Benefits of Early Protein

intake on Growth and
Development
Early studies by Lucas and colleagues suggested
that
a higher protein intake early in life in preterm
infants will improve growth and
neurodevelopmental
out comes

They also concluded the first 2 weeks of life in the

preterm infant may represent a critical growth
window during which nutrition (particulary protein
nutrition may have its greatest beneficial and
adverse
effects

Lucas A, Morley R, Cole TJ, Randomized trial of early diet in protein

How Much Protein and How

Quickly ?

Low vs High Amino Acid Intake Study

Hypothesis :
In ELBW infants in the first 48 hours of life
receiving Low ( 1 g/kg/d ) versus High ( 3
g/kg/d ) IV amino acid intake, the High
intake would be :
1) More efficacious (improved protein
accretion)
2) Safe : no significant acidosis,
elevated
BUN, abnormal amino acid
concentrations

Study Conclusions
Efficacy

: ELBW neonates on 3 g/kg/d

parenteral amino acids immediately
after birth have significantly greater
rates of protein accretion compared to
those on 1 g/kg/d
Safety : Based on BUN and plasma
amino acid measurements, 3 g/kg/d
amino acid IV amino acid intake
appears to be tolerated immediately
after birth in ELBW neonates

Poindexter, in a study for the NICHD (National

Institute of Child Health and Development)
Research Network, demonstrated that 3 g/kg
of amino acids in the first five days of life in
premature infants was associated with
significantly better outcomes at 36 weeks
postmenstrual age (gestational age plus
chronological age) and less suboptimal head
growth at 18 months chronologic age.
Poindexter BB, Langer JC. Early provision of parenteral amino acids in extremely
low birth weight infants: relation to growth and neurodevelopmental outcome. J
Pediatr 2006; 148: 300-5

The efficiency of protein retention during

parenteral nutrition is approximately 70%.
Based on this assumption and the proven
benefits of early AA intake in limiting protein
catabolism, it is reasonable to recommend 2.5
3.0 g/kg/day of AA intake directly after birth
in premature infants.
Parenteral protein of 3.5-4 g/kg/day may be
required in ELBW infants to maintain
endogenous stores, taking into account
accretion goals and the rate of protein loss in
the neonatal period.

Safety and Benefits of Early Amino

Acids Administration For VLBW
Infants
STUDY
Anderson (1979)
Saini (1989)

AA Solution
Aminosyn
Vamin-9

Van Lingen (1992)

Aminovenous

Rivera (1993)

Aminosyn-PF

Kashyap (1994)

Trophamine

Van Goudover (1995)

Primene

Thureen (1998)

Trophamine

Thureen (2003)

Trophamine

te Braake (2005)

Primene

None of the above specificaly designed for the

ELBW infants

Early Parenteral Nutrition :

Risks and Unresolved
Issues
Effect of Quality of Parenteral Amino Acid Intake
on Maximizing Protein growth
Maximal protein accretion depends on providing
the
perfect balance of amino acids
The optimal ratio of amino acids in parenteral
nutrition of the preterm infant is unknown
In theory, deficiency of one essential amino acid
will
~ limit overall protein synthesis, and
~ all other amino acids will be in relative
excess
and will be preferentially oxidized (used for

How Much Protein and How Quickly

Are Early High Amino Acids Safe ?
Current

markers used to determine

parenteral amino acid intolerance :
Metabolic acidosis : All LBW infants receiving up to
3
g/kg/d amino acids develop metabolic acidosis
between 2-5 days after birth irrespective of dose and
duration of
parenteral amino acid administration,
and this is exaggerated by associated co-morbidities
such as PDA.
-

High ammonia concentration

Elevated blood urea nitrogen ( BUN )

Abnormal plasma amino acid levels

Reliable

and sensitive markers of amino

acid intolerance still need to be defined

Carbohydrate
In utero the foetus glucose utilisation matches
the umbilical glucose uptake; hence, there is no
need for either glycogenolysis or gluconeogenesis. This
changes upon birth. In the term infant, glucose
utilisation is 3-5 mg/kg/min, however utilisation in
the premature may be as high as 8 mg/kg/min.
The exact definition of both hypoglycaemia and
hyperglycaemia has remained problematic. However, it
seems prudent to maintain a premature infants
blood glucose between 40-50 mg% and 150 mg%
Ehrenkranz RA. Early Semin Perinatol 2007; 31:
48-55.

This necessitates the initiation of an intravenous

glucose infusion at a rate of roughly 6 mg/kg/min in
the premature immediately following birth.

Carbohydrate
Hyperglycaemia is quite common in the
extremely premature infant and has been
associated with a number of significant
morbidities including sepsis, intraventricular
haemorrhage, retinopathy of prematurity and
ultimately death.
It is most commonly caused by low insulin
levels due to defective proinsulin processing,
and relative insulin resistance due to the
stress response
Mitanchez-Mokhtari D, Lahlou N, Magny JF et al. Pediatrics 2004; 113:
537-41

Carbohydrate
A glucose infusion of 6 mg/kg/min should be
started on all premature infants upon
admission to the nursery. This should be
gradually increased to 10 mg/kg/min over the
first week of life. The infants blood glucose
level should be maintained between 50-120
mg%.
Should the infant become
hyperglycaemic early on, an insulin
infusion (0.01-0.1 units/kg/hr) should be
started rather than decreasing the
dextrose concentration to less than 5%.

Lipid
Starting IV lipid in very low birth weight VLBW
infants at an early age has the advantage of
providing a source of essential fatty acids, as
well as supplying non-carbohydrate
calories.
Essential fatty acid deficiency can develop
in as few as three days in extremely
premature infants.
Lipid infusion may be safely started on day 1
of life at 0.5-1.0 g/kg/day and may be
increased by up to 1 g/kg/day to a maximum
of 3-4 g/kg/day
Triglyceride levels should be followed and lipid

Lipid
There have been alternative lipid infusions proposed
that differ in composition from current solutions. A
recent review paper summarised several in vitro and in
vivo studies comparing olive oil to soybean oil-based
intralipid preparations.
Olive oil solutions contain decreased
concentrations of n-6 poly unsaturated fatty acid
(PUFA) which has been noted to adversely affect
leukocyte recruitment, and also contain tocopherol, a naturally occurring antioxidant.
Olive oil-based infusions are well tolerated, and
may offer advantages for immune function and
decreased oxidative stress in the very-low birth
weight infant.
Vila A, Barbosa VM, Calder PC. Olive oil in parenteral nutrition. Curr Opin Clin
Nutr Metab Care 2007; 10: 165-174

Rationale for Providing Lipids

Early
Endogenous

lipid stores are about 20 g in a

1000 g ELBW. How long will this last ?
Essential Fatty Acid (EFA) status in early
infancy is low and is rapidly exacerbated
with lipid free nutrition
Long Chain Polyunstaturated Fatty Acid
(LCPUFA) derivatives from EFAs are
important in brain and retinal development
Prevention of catabolism and protein
sparing

ENERGY REQUIREMENTS
Optimal

early nutrition is critical for growth, long-term

outcome and decreased morbidities in the low birth
weight preterm (LBW).
The goal is to achieve a growth rate similar to in utero
foetal growth: 15-20 g/kg/d, which requires 120 cal/kg/d
enterally.
Yu VYH, Simmer K, Digital Education Publishing, Inc. 2005: 311-332

If

on TPN, positive nitrogen balance can be attained with

60 cal/kg/d with about 2.5 g/kg/d of protein
Minimal caloric intake for weight gain is about 80
cal/kg/d
if on TPN

When to start lipids

ASAP

at least enough to prevent EFA

deficiency (0,5 gr/kg/d)

Usssually

not more than 3,0 gm/kg/d should

be provided
Hyperlipidemia tough to monitor
Prolonged infusions usually safe (<0,2
gm/kd/d)

IV Lipids in Premature
Essential
Infantsfatty acid (EFA) deficiency
- IV lipid emulsion (intralipid) is 50% EFA
- Prevented and/or treated with 0.5 g/kg/d
~ 4 % energy intake

Energy source (calorie distribution~40%)

- Administer continuosly over 24 h
- Use 20 % IL not 10 % IL
- Increase dose daily by 1.0 g/kg/d Max dose 3.0 g/kg/d
- Long-term TPN 3.5-4.0 g/kg/d

Monitor serum triglycerides (arbitrary value< 150

mg/dL)

- After each change in dose

- Weekly
- During any stress (infection,respiratory)

Essential Fatty Acid

Deficiency in Premature
infants

Clinical manifestation
Dermatitis
Hepatic steatosis
Hematologic disturbances
Diminished immune system status

 Intravenous
Lipids Are Poison ?

Are there contraindications to

parenteral lipids ?
Concerns

have been raised about potential

adverse effects including :
- Increased risk for chronic lung disease (CLD)
- Increase in pulmonary vascular resistance
- Impaired pulmonary gas diffusion
- Bilirubin toxicity
- Interference with immune function and/or
platelet
function
- Sepsis
- Free radical stress

May need to decrease lipid 0,5 1.0

g/kg/d
for a short period of time in infants with :
PPHN
Severe lung disease
Severe infection
Steroid use
Elevated level bilirubin concentrations
Hyperglycemia
Hypertriglyceridemia

Electrolytes and Trace

Element Deficiencies
Most

deficiencies of electrolytes and

trace elements are secondary to improper
supplementation and monitoring.
Excess fluid loss, from vomiting, diarrhea,
wounds or other secretions, may result in
additional electrolyte losses and loss of
some trace elements, such as zinc.
Careful monitoring of electrolytes and
fluid losses is necessary to avoid
deficiencies. Adequate calcium intake is
essential for bone growth.

Electrolyte Body Fluid

Composition in Neonates (in
mmol/L)13

.Fanaroff A, Martin R, editors. Neonatal-Perinatal Medicine. 5th edition. St. Louis: Mosby
Year Book. Chapter 31.

Na+

K+

C1-

120-140

5-15

90-120

20-80

5-20

100-150

Small intestine

100-140

5-15

90-120

Ileostomy Fluid

45-135

3-15

20-120

Diarrhea

10-90

10-80

10-110

Bile
Gastric
Secretions

Contoh FORMULA TPN :

Total cairan yang diberikan untuk bayi = 80 mL/kg
bb/hari
Kebutuhan asam amino
bila dibutuhkan asam amino 3 g/kg/hari dan digunakan
sediaan Aminosteril infant 6% (6gr/100mL) maka
diperlukan 50 mL/kg bb/hari
Kebutuhan karbohidrat
GIR (mg / kg / menit) = Volume (mL / kg / hari) x
Konsentrasi Glukosa 144
bila dibutuhkan karbohidrat 4 g/kg/hari dan digunakan
D40% maka diperlukan 10 mL/kg bb/hari. GIR : (10 x
40 )/144 = 2,8 mg / kg /menit
6 g/kg/hari D40% diperlukan 15 mL/kg bb/hari.
GIR :15 x 40 )/144 = 4,2 mg / kg /menit sedangkan AA
6% 2,7 gr/kg/hari

Kebutuhan calsium pada infant 1 3 mEq /kg.

Misal dibutuhkan calsium 1,5 mEq maka dibutuhkan
calsium sebanyak 0,75 mmol. Sediaan yang ada :
calsium glukonat 100mg/mL (10mL) dimana 1 gram
Calsium glukonat setara dengan 2,2 mmol Calsium.
Jadi , 0,75 mmol Calsium setara dengan 340 mg Ca,
dibutuhkan 3,4 mL
Sediaan TPN :
AA 6%
D40%
Ca glukonat
Ad Aqua

: 50 mL/kg bb/ hari

: 10 mL/kg bb/ hari
: 3,4 mL
: 16,2 mL
80 mL /kg bb /hari

OSMOLALITAS
Perhitungan Osmolalitas Sediaan TPN yang biasa
digunakan :
Asam amino 6 %

= 50 cc/kg BB/hari

= 0.573 x 50 = 28.65 mOsm

D40%

= 10 cc/kg BB/hari

= 2.018 x 10 = 20.18 mOsm

Ca. Gluconas

= 3.2 cc

= 0.308 x 3.2=

0.98 mOsm

49.81

Aqua inj
= 16.8 cc
________________________________
80 cc/kgBB/hari
mOsm

Jika dikonversi ke dalam satuan mOsm/Liter maka

diperoleh osmolalitas 622,63 mOsm/L. larutan
bersifat hipertonis.
Disarankan
infus Central
Nutrition
Asam amino 6 % metode
= 45 cc/kg BB/hari
= 0.573 x 45Parenteral
= 25.79
mOsm
D40%
= 15 terjadinya
cc/kg BB/hari
= 2.018 x 15
= 30.27mOsm
untuk
mencegah
tromboplebitis
dan
Ca. Gluconas
= 3.2 cc
= 0.308 x 3.2
= 0.98 mOsm
ekstravasasi
oleh
adanya
calsium.
Aqua inj
= 16.8 cc
________________________________
80 cc/kgBB/hari

738 mOsm/L

= 57,04 mOsm

Osmolaritas
Osmolaritas adalah konsentrasi dari zat terlarut (solute) dalam suatu
larutan per unit dari pelarut (solven), biasanya mmol solute per liter
Tonicity is the effective osmolality and is equal to the sum of
the concentrations of the solutes which have the capacity to
exert an osmotic force across the membrane.

Complications of
TPN

Dextrose-Related
Complications
Hypo- and hyperglycemia are common
problems found with the administration
of parenteral nutrition.11,13,15 Neonates
are more prone to hypo- or
hyperglycemia than older infants and
children. Neonates have inadequate
stores of glycogen and a limited ability
for glycogenolysis, due to poor enzyme
activity.
Hypoglycemia frequently occurs when
parenteral nutrition solutions are
stopped. For this reason, infusion rates
should be tapered down prior to

Dextrose-Related
Complications
Hyperglycemia is a more common problem in the
neonate. Immature alpha-cell and beta-cell
function, slow release of insulin and a diminished
tissue response all contribute to the
development of hyperglycemia. In addition,
hepatic glucose output is not reduced in
response to external glucose. For this reason,
parenteral nutrition solutions should be started
with low dextrose concentrations or at slow
infusion rates.
High blood glucose concentrations result in an
increase in serum osmolarity and the
development of osmotic diuresis and
dehydration, and increase the risk of intracranial
hemorrhage. Blood glucose should be monitored

Lipid-Related Complication
Use of lipid emulsions has been
associated with certain complications in
the neonate, including hyperlipidemia,
hyperbilirubinemia and changes in
pulmonary function when the rate of
administration is too fast.
Too rapid infusion of lipid emulsions may
result in hyperlipidemia in the neonate.
The ability of the neonate to effectively
clear and utilize intravenous lipids is
dependent on enzyme systems that vary
with both weight and gestational age.

Lipid-Related Complication
Hyperbilirubinemia and jaundice occur frequently
because the liver enzymes needed to conjugate
bilirubin are reduced in the immature liver. When
lipids are infused more quickly than they can be
cleared from the blood, free fatty acid
concentrations are increased. Bilirubin and free
fatty acids both compete for binding to albumin.
This displacement of bilirubin by free fatty acids
results in higher serum concentrations of bilirubin
and an increased risk of kernicterus.
Lipid may also cause changes in pulmonary
function in the neonates. PO2 levels may be
lowered due to changes in pulmonary
microcirculation in neonates with RDS. Reducing
the fat-to-carbohydrate ratio may minimize the
adverse effects of lipids.

Complications of TPN
Although TPN is necessary to provide nutrition to
the LBW/VLBW neonate, there are several
complications associated with its administration.
Prolonged TPN therapy frequently
necessitates placing a central IV catheter
whose use carries with it several risks,
including nosocomial infections, vascular
thrombosis and cardiac tamponade.
TPN associated cholestasis (TPNAC) has long
been recognised as a metabolic complication of
chronic TPN administration. It is characterised by
intracanalicular and intracellular cholestasis. It has
been reported that 8-50% of ELBW infants show
signs of biochemical cholestasis after two weeks of
TPN therapy.

Complications of TPN
The pathophysiology of PNAC is still incompletely
understood,
but felt to be multifactorial in aetiology.
Recent studies have focused on soybean oilbased lipid
solution as possibly being causative of TPNAC.
Phytosterols in soybean oil can damage the
biliary tract
and disrupt bile flow.
A clinical study was performed on infants with PNAC
while
receiving soybean oil-based lipid emulsions. They were
given
fish oil-based lipid emulsions, and compared to an
historical

Complications of Parenteral Nutrition : PNAC

Parenteral Nutrition Associated Cholestasis
Etiology

of PNAC is unknown and likely to be

multifactorial ; long list of associations with
PNAC but minimal data on prevention
Risk Factors Include :
- Younger gestational age
* Significantly increased if infants <1000 g at birth

Duration of TPN (especially if > 3 weeks)

Absence of enteral feeding
Sepsis, cholangitis, bacterial translocation
Number of operative procedures
Male sex in surgical neonates (2002)
Length of hospital stay

Parenteral Nutrition Associated

Cholestasis
PNAC defined as direct serum bilirubin above
5 mg/100 ml at any time in the first 28 days of life
Being

SGA is an independent risk factor for PNAC

Pediatrics, 2008, Robinson and Ehrenkranz

Risk

factors include for those who developed PNAC

vs those who did not :
- Longer duration of TPN exposure
- Higher cummulative dose of amino acids
- More often had PDA, severe IVH
- More often treated with steroids by 28 days of age

Clark RH and the amino Acid study Group; J Perinat 2008

Toxicity of TPN
components

Animal studies :

Decreased bile flow with glucose infusions

Cholestatic effect of amino acid infusions (esp.

methionine,sulfur containing amino acids)

Choline deficiency causes steatosis in rats

Human studies :

Hepatic dysfunction with infusion of excessive calories

Cholestatic effect of amino acid infusions ( trytophan,

methionine, excess homocystine )

Impaired bilirubin excretion in adults receiving high dose

intravenous lipids

Free radical production is increased by administration of TPN

in infants

PNAC

Potential Therapeutic
Strategies
Avoid glucose overload
Provide

a mix of calories (dextrose, protein, and

lipids) in appropriate ratios.
Early detection and treatment of infection
Focused on making the transition to enteral
feeds
***Oral refeeding as soon as possible
Ursodeoxycholic Acid ( UDCA ), a bile acid used
in adult cholestatic liver disease.
Prevent free radical production (cover lipid and
TPN to avoid photo-oxidation )
Increase anti-oxidant capacities of TPN solutions

PNAC
Potential Therapies
There

is increasing evidence that fish oil

based products may :
Decrease the incidence of cholestasis and
Ameliorate or even reverse existing
cholestatic disease

Its efficacy in treating and preventing

TPNAC is controversial, as studies
have not consistently shown benefit.

remember

TPN

TPN is important Its not everything

But without TPN especially in ELBW is nothing

Conclusions
The

goal of neonatal nutrition is to try to

replicate in utero growth patterns. This is often
not possible, particularly in the smallest
infants.
The development of intravenous solutions for
nutrition of preterm infants has been a lifesaving development allowing for provision of
protein and energy in the immediate neonatal
period
Nevertheless, parenteral nutrition is still far
from being the optimal method for promoting
long-term growth in very preterm infants

Conclusions
Several management strategies to try to reach
this goal :
1.Amino acids of as much as 3 g/kg/day should be
started parenterally as part of the infants initial IV
solution.
2.Glucose at a rate of 6 mg/kg/min should be started
immediately after birth.
3.Severe hyperglycaemia should be managed with an
insulin infusion if the infant remains hyperglycaemic on
a 5% dextrose infusion.
4.An IV lipid solution of 1 g/kg/day should be started as
early as day one or two of life.
5.The major complication of parenteral nutrition, namely
TPN associated cholestasis, is ultimately treated by
advancing enteral feeds.
6.Newer lipid preparations, however, show some

Terimakasih