Basic Concepts On Parentheral Nutrition by Irfan

Basic Concepts in Parenteral Nutrition
Objectives
Basic concepts in nutrition support
Basic concepts in parenteral nutrition
Nutrients in parenteral nutrition
- role of amino acids
- role of glucose
-role of fat emulsion
- differentiation of MCT/LCT vs LCT

Multichamber bags
Energy stores of an adult

Store
Quantity
Use
Exhaustion
Net body
protein
10% BW
Glucose precursor
wide, situationdependent
Liver
glycogen
300 g
Glucose precursor
24 h
Fat
20% BW
Fatty acid
40 days
& glucose precursor
Net body protein

glucose
100 g
56 g
Death from protein depletion occurs after loosing 1/3
to 1/2 of net body protein
Caloric value of nutrients

Calories produced by the combustion of 1 gram of
various substrates:
Substrate
Energy (kcal/g)
Amino acids 4
Glucose
4
Fat 9
(10% emulsion: 1.1 kcal/ml)

(20% emulsion: 2 kcal/ml)
Glycerol
4
Alcohol
7
Metabolism, I
Adenosine
triphosphate
(i) Oxidation of food by which energy (ATP) is
produced and
heat is released
Unit of energy used in nutrition is
kilocalorie (kcal) or kilojoules (kJ)
1 kcal = 4.18 kJ
(ii) Biochemical reactions
involving:
Anabolism : Build up of body tissues and
repair of injured
or damaged tissues
Catabolism: Breakdown of body tissues into
simple
molecules for energy
production and recycling
Metabolism, II
Anabolic reactions
In food
In the body
Proteins
Proteins
(Protein synthesis)
Carbohydrates
Glycogen (Glycogenesis)
Carbohydrates
LCT (Liponeogenesis)
LCT
LCT (Fat synthesis)
Main hormone of anabolism: Insulin
Catabolic reactions
Body stores
Breakdown
products
Glycogen
Glucose
(Glycogenolysis)
Proteins
Amino acids
(Proteolysis)
Amino acids
Glucose
(Gluconeogenesis)
Triglycerides (LCT)
Fatty acids
(Lipolysis)
+ Glycerol
LCT = long chain triglyceride
Basic Scheme of Metabolism

In
anaerobic
state,
lactate
Glucose
G6P
LAC
acetylCoA
KB
ketone bodies e.g

cetone, acetoacetate
6-hydroxybutyrate
PYR
Glycogen
Glucose-6phosphate
pyruva
te
AA
NH3
Ac-CoA
LCFA
+
GLY
CIT
OA
Citrat
e
cycle
ATP
glycolys
is
Protein
Urea
cycle Urea
LCT
glycer
ol
Citric acid
cycle = Krebs
cycle=
Tricarboxylic
acid
Metabolic changes during starvation

and stress
Metabolic process
Starvation
Stress
Energy expenditure
Energy source: AA:

Gluc: Fat
~ 5: 5: 90
~ 20: 40: 40
Proteolysis
Gluconeogenesis
unimportant
unimportant
increased
increased
normal
Ketonaemia
variable
Insulinaemia
anabolism
Minimize loss of
lean body mass
Glycogenolysis
Lipolysis
Glycaemia
Effect of feeding
Phases of the stress response after

trauma
Metabolic rate
Increased
duration
depends on
disease and
success of
therapy
Turning
point
Increment
depends on
degree
of
stress
Normal
Decreased
Ebb
Flow (days
(~ 12-24 to weeks)
h)
~1
day
Fat gain
(~ 3
months)
Starvation and stress on energy

expenditure and protein losses
REE Resting
(%
18)
0
16
0
14
0
12
0
10
0
8
0
6
0
0
energy
expenditure
indicator
Nitrogen losses
for protein
(g)
loss
4
0
Major burn
30
Peritonitis
Fracture
Starvation
1
0
0
1
0
2
0
3
0
4 day
0 s
1
0
2
0
3
0
Long (1977) Am. J. Clin. Nutr. 30, 1301-1310
4
0
days
Daily nitrogen losses in adults

Clinical
situation
Nitrogen
loss
(g/day)
Protein
loss
(g/day)
Body
Weight
loss
(g/day)
Normal
11
70
330
Minor
surgery
11-14
75-90
360-420
Major
surgery
14-17
90-110
420-510
Multiple
injury
15-25
95-160
450-750
Head
injuryto great
20-30
125-190
Subject
patient-specific
variations600-900
Sepsis
20-30
125-190
600-900
1 g N 6.25 g protein 30 g muscle

Severe
30-40
190-250
900-1200
mass
burns
Goldstein & Elwyn (1989) Ann Rev Nutr 9, 445-473
(adapted)
Consequences of metabolic changes
Severe wasting of lean body mass

Decrease in critical repair processes
Impairment of immune function
Impairment of vital organ function
Impact of pre-existing malnutrition

n = 709
Well nourished
Malnourished
Complications
16.8%
27.0%
Mortality
4.7%
12.4%
Hospital stay
10.1 11.7
days
16.7 24.5
days
Hospital costs
309%
Correia & Waitzberg (2003) Clin Nutr 22, 235-239
Objective of nutrition therapy

Avoid malnutrition
Maintain body tissue and functioning plasma
protein stores
Prevent macro- and micro-nutrient deficiencies
Normal
muscle mass
visceral protein
organ function
immune
response
wound healing
complications
infections
Multiple organ
failure
(lung, GI, liver,
Possible indications for clinical

nutrition
- malnutrition
- intractable diarrhoea
- anorexia
- pancreatitis
- cancer
- peritonitis
- oropharyngeal trauma - renal failure

- oesophageal strictures - hepatic failure, liver
transplantation
- gastrointestinal
stenosis
- bone marrow
transplantation
- operations of the GI
tract
- multiple trauma
- bowel fistulae
- head injuries, neurosurgery,

strokes
- inflammatory bowel
disease
- severe burns
- radiation enteritis
- sepsis
- short bowel
- AIDS
Nutritional assessment
Medical history, disease severity

Dietary history, recent food intake
Physical examination, physiological function
Anthropometric measurements
- body weight (kg), recent unintentional wt loss
- height (cm)
- body mass index (BMI)

- mid arm circumference (MAC)
- tricep skinfold (TSF),
Laboratory data
Immunocompetence data
Energy requirements during metabolic

stress and its determination
Energy needs should be determined
(i) in relation to expenditure (i.e. requirements)
(ii) ability of a patient to metabolize substrates
(monitor tolerance)
Indirect calorimetry determines energy expenditure
based on O2 intake, CO2 output and minute
ventilation
- has about 95% accuracy
- machine not always available

- require skilled technicians
Harris-Benedict Equation estimates resting energy
requirements based on weight, height, age for each
sex
- equations used based on healthy volunteers
- inclusion of stress, activity and fever factors tends to
overestimate requirements
Basal metabolic rate

Harris-Benedict Equation
BMR (men)= 66 + (13.7 x BW) + (5 x H) - (6.8 x A)
BMR (women) = 655 + (9.6 x BW) + (1.7 x H) - (4.7
x A)
BW = body weight
in kg
H
= height in cm
A = age in years
Actual energy expenditure

AEE = BMR x AF x TF x IF
AF (Activity
Factor)
In bed
1.1
In bed, but mobile
1.2
Mobile
1.3
TF (Thermal
Factor)
38oC
1.1
39oC
1.2
40oC
1.3
41oC
1.4
IF (Injury Factor)
Uncomplicated patient
1.0
Postoperative state 1.1
Fractures
1.2
Sepsis
1.3
Peritonitis
1.4
Multiple trauma
1.5
Multiple trauma
1.6
& sepsis
Burns 30 - 50%
1.7
Energy guidelines
Energy requirements are based on the following
guidelines:
postoperative 25-30 kcal/kg/day
polytrauma 30-35 kcal/kg/day
sepsis
25-40 kcal/kg/day
burns
kcal/kg/day
is30-45
25 - 30 kcal/kg/day
suitable
for most
critically-ill patients
- ASPEN Guidelines, 1993
- Mirtallo et al., 1998
(National Advisory Group of
20 30 kcal/kg/day latest revision, Mirtallo
ASPEN)
et al (2004),
JPEN 28/6, S39-S70
ASPEN Guidelines (1993) JPEN 17/4 Supple, 12SA-26SA
Mirtallo et al. (1998) JPEN 22, 49-66
Concept of nutritional support

Nutritional support should be given:
- when there is loss of weight associated with impairment of
physiological functions, or
- when the patients nutritional status is expected to worsen
Nutritional support can be given either enterally or
parenterally
Key question: Does the patient have a

functional GI tract?
Enteral: If the gut can be used safely, use it

preferentially
Parenteral: When the GIT does not work
When the GIT should be rested
When enteral intake is insufficient
Clinical decision making for nutrition

support
Nutrition Assessment
Decision to initiate specialized nutrition support
Yes
Functional GI
Tract
Enteral Nutrition
Long-term Short-term
Gastrostomy
Jejunostomy
Nasogastric
Nasoduodenal
Nasojejunal
No
Parenteral Nutrition
Short-Term
Peripheral
PN
JPEN 17 (Suppl 4):7SA, 1993
Long-Term or
Fluid Restriction
Central PN
Routes of administration of PN
Central route
can accommodate concentrated, hyperosmolar
solutions
useful when fluid volume is restricted
suitable when feeding patients with a large
nutrient or electrolyte needs, e.g. patients with
significant malnutrition
or severe metabolic stress
can be maintained for prolonged periods (weeks to
years), even at home (HPN)
must be maintained under strict aseptic
techniques to avoid septic complications
Routes of administration of PN
Peripheral route
limited to solutions < 900 mOsm/L
suitable for short term PN (< 2 weeks)
difficult to maintain peripheral access for long
periods
sites may need changing every 72 h, or when
phlebitis occurs
appropriate when parenteral nutrition is used as
a supplement to oral or enteral nutrition
When to start parenteral nutrition

Assuming that there are no incompatibilities to the
nutrients,
PN can commence
- when the patient is in a stable haemodynamic

condition
- when there is no acid-base imbalance
- when there is no electrolyte imbalance
- when there is no overhydration problems
If these problems exist,
they must first be corrected before PN can
commence
Contraindications for specific nutrients

General: - intolerance (e.g. allergy, inherited diseases)
- critically increased levels
Amino acids: - advanced liver disease adapted
hepatic formulation
- infants adapted pediatric formulation
Glucose: - no specific contraindications if handle
correctly
Fat: - severe hypertriglyceridaemia
adults > 450 mg/dL
infants > 250 mg/dL
- severe thrombocytopenia
platelets < 40000/mm3
Types of parenteral nutrition

systems
Bottle system: spike and hang individual bottles of
solutions (e.g. glucose, amino acids, fat emulsion), or
mixtures in bottles or kits (Vitrimix )
Compounding system: Hospital or industrially
(CAPS - centralized admixing pharmacy service)
prepared solutions filled in an ethylene vinyl acetate
and sets) by either gravity
bag (e.g. Nutrimix bags
or by an automated equipment (e.g. Caretronic or
BAXA machine)
Convenience system: ready-to-use 2- chamber
bags (Nutriflex , Aminomix , Clinimix ) or 3-chamber
bags (NuTRIflex Lipid, Kabiven , Clinomel )
Parenteral nutrition - Infusion

regimens
Continuous: Simultaneous infusion of all nutrients in 24 h
- usual procedure in critically-ill patients
- good tolerance due to even blood nutrients
and hormone profiles
Almost continuous: Simultaneous infusion of all
nutrients in 18-20 h
- useful to allow lipid clearance
- tolerance as for 24 h
- glucose 5% infusion during the TPN-free period
Cyclic:
Simultaneous infusion of all nutrients in 8-12
h
- useful in home TPN
- good tolerance after a period of adaptation
Sequential: Not recommended as it does not improve
nitrogen
balance
Infusion regimens
Sequential
AA +
lipids
Glucose
n=
21
AIO bag
n=
21
Continuous
Bolus
8 AM
2 PM
8 PM
2 AM
8 AM
Sandstrom et al. (1995) JPEN 19, 333 - 340
AIO but
5 times
n=
23
Nitrogen balance after continuous, bolus or

sequential TPN
Cumulative Nitrogen Balance
1
Gram N
-4
-9
- 14
- 19
- 24
Continuous
Bolus
Sequential
- 29
- 34
2
Sandstrm et al. (1995) JPEN 19, 333-340
Days
Amounts and concentrations
Calculation of a PN regimen
45 year old man, 60 kg, 172 cm, abdominal surgery, in bed, 38 oC
fever,
Nout = 16 g
Example 1
Calculate energy and protein requirments by Harris-Benedict
equations
Example 2
N intake = 16 g, non-protein calories ~125 kcal/g N

Example 3
To give 1.5 g/kg/day AA, 3.5 g/kg/day glucose, 1.0 g/kg/day fat
Example 4
to give 1.5 g/kg/day AA, total calories = 35 kcal/kg/day
Example 1 Calculate energy and protein requirments by Harris-B
PN delivery
Parenteral Nutrition
Nutrients with
calories
Nutrients without
calories
Glucose
Fat
Amino acids
Electrolytes
Parenteral
Nutrition
Water
Vitamins/Minerals
Dosage recommendations for PN
30-40 mL/kg,
Mirtallo et al
(2004)
a)
b)
Dosage per kg and day
ASPEN
dosage guidelines
Recommended dosages, adults
Nutrient
Water
35 - 45 ml
Na+
1 - 3 mmol
K+
1 - 1.5 mmol
Mg2+
0.05 - 0.1 mmol
Ca2+
0.05 - 0.1 mmol
Cl1 - 3 mmol
Cl-/Acetate
1 : 1 ratio
Phosphate
0.2 - 0.5 mmol
Amino acids
1.0 2.0 g
Glucose
3.0 5.0 g
Lipids
0.5 2.0 g
Total energy
25-40 kcal
Vitamins
see appendix
Trace elements see appendix
20 - 40 ml/kg and day

1 - 2 mmol/kg and day + replacem
1 - 2 mmol/kg and day
4 - 10 mmol/day
5 - 7.5 mmol/day
no entry
As needed to maintain acid-base
20 - 40 mmol/day
0.8 2.0 g
< 7.0 g
< 2.5 g
25-30 kcal/kg and day
see appendix
see appendix
a) Diverse sourcesb) JPEN 22 (1998) 49-66
Parenteral nutrition - Electrolytes

Electrolytes: Composition and function of
extracellular and
intracellular spaces,
acid base balance, catalyst
for enzymes, bone mineralisation
- sodium (Na+)
bicarbonate (HCO3-)
- potassium
(K+)
(not
essential, can
- magnesium (Mg2+)
be replaced by
- calcium (2+)
acetate)
- chloride (Cl-)
- phosphates (H2PO4-)
Parenteral nutrition Micronutrients:

Vitamins and trace elements
Important roles in:
- metabolic homeostasis
- enzyme pathways: as co-factors or as
metalloenzymes
- antioxidant activities
- tissue integrity
Requirements are usually
small, but a deficiency
can have major consequences

- overt clinical deficiency: well characterized
- subclinical deficiency: not so well characterized
Insufficient micronutrient intake
impairs ability to utilize macronutrients and
maintain body defense mechanisms
Micronutrients Vitamins
Vitamins: essential organic micronutrients
Lipid soluble vitamins
Water soluble vitamins
A (retinol)
B1 (thiamine)
D (calciferol)
B2 (riboflavin)
E (tocopherol)
K (phylloquinone)
C (ascorbic acid)
Folic acid
Biotin
Pantothenoc acid
B6 (pyridoxine)
B12 (cyanocobalamin)
Niacin (nicotinic acid)
Dosage recommendations for PNVitamins

a)
Children Children
> 11 years
Vitamin
0 - 10 years and adults b)
Retinol (I.U.) c)
230
3330
a) Per kg body weight
Calciferol (I.U.) d)
40
200
and day. For a body
Tocopherol (I. U.) e) 0.7
10
weight > 10 kg dose
as
Phylloquinone (mg) 0.02
f)
for 10 kg
Ascorbic acid (mg)
8
100
b) Per day
Folic acid (g)
14
400
c) 1 I. U. = 0.3 g
Niacin (mg)
1.7
40
retinol
Riboflavin (mg)
0.14
3.6
d) 40 I. U. = 1 g
Thiamine (mg)
0.12
3.0
calciferol
Pyridoxine (mg)
0.1
4.0
e) 1 I. U. = 1 mg D,LCyanocobalamin (g) 0.1
5.0
tocopheryl acetate
Pantothenic acid (mg)0.5
15
or
Biotin (g)
2
60
0.67 mg D--
tocopherol
AMA/NAG, JPEN 3 (1979) 258-265
f) 2 - 4 mg once a
Micronutrients Trace elements

Trace elements: essential inorganic micronutrients
Iron (Fe)
Chromium (Cr)
Zinc (Zn)
Molybdenum (Mo)
Copper (Cu)
Fluoride (F)
Manganese (Mn) Iodine (I)

Selenium (Se)
Cobalt (Cr)

Trace elements
Adults
1) 2)
mg/d
Preterm Term
Children 3) a) Starting 2nd month
infants 3) infants 3) g/kg x d
or after reaching
g/kg x dg/kg x d (max. per d) 2000 g bw
Iron
Zinc
Copper
0.5 - 5.0 200 a)

2.5 - 4.0 400
0.5 - 1.5 20
Chromium 0.01 - 0.02 0.20
Manganese 0.15 - 0.8 1.0
Molybdenum0.01 - 0.03 0.25
0.02 - 0.05 2.0
Selenium
Iodide
Fluoride
0.07 - 0.3
0.5 - 1.0
1.0
e)
100 b)
250 c)/100
20
0.20
1.0
0.25
2.0
1.0
e)
d)
no data b)
20 (300)
c)
0.20 (5.0)
0.20 (5.0)
Not in the
1st three months
For age up to
three months
d) If older than three

months
1.0 (50)
0.25 (5.0)e) Insufficient data
available. Oral
2.0 (30)
1.0 (1.0)
e)
recommendations
are deemed to be
appropriate also
for PN
1) K. N. Jeejeebhoy, New Aspects of Clinical Nutrition (1983) 1 24

2) T. G. Baumgartner, Clinical Guide to Parenteral Micronutrition (1984)
3) H. L. Greene et al., Am. J. Clin Nutr. 48 (1988) 1324-1342
Amino acids in parenteral nutrition
Amino acids (AA)

Essential AA
isoleucineBranche
leucine d chain
AA
valine
(BCAA)
methionine
- Aromatic
phenylalanine
AA
threonine
tryptophan
lysine
Non-essential AA
histidine *
glycine
arginine*
serine*
alanine
proline
asparagine
tyrosine*- Aromatic
(ornithine)
AA
aspartic acid
cysteine*
glutamic acid
glutamine
(* ?)
*Conditionally essential: essential in certain situation e.g.

restricted ability to synthesize or increased requirements that
cannot be met by de novo synthesis
http://www.cryst.bbk.ac.uk/education/AminoAcid/overvi
ew.html
Body proteins: Functions &

consequences of depletion
Every protein in the body has a
function
Loss of protein means loss of
Protein function
Consequences of
function
depletion
Immune response
to infection
Lowered resistance
Tissue regeneration
Impaired wound healing,
wound closure
Colloidosmotic pressure
Development of
interstitial
oedema
Net body
protein
is about 10% of body
weight
Organ
functions
Organ
atrophy and
Weight
loss
associated
with
protein
loss
and
impairment
dysfunction
of
physiological function greatly increases morbidity and
mortality
Daily nitrogen losses in adults

Clinical
situation
Nitrogen
Protein loss
loss (g/day)
(g/day)
Body
Weight loss
(g/day)
Normal
11
70
330
Minor
surgery
11-14
75-90
360-420
Major
surgery
14-17
90-110
420-510
Multiple
injury
15-25
95-160
450-750
Head injury
20-30
125-190
Subject
to great patient-specific
variations 600-900
Sepsis
20-30
125-190
600-900
Nitrogen: Protein = 1 g: 6.25 g
Severe
30-40
190-250
900-1200
burns
Goldstein
& Elwyn (1989) Ann Rev Nutr 9, 445-473
Effects of amino acids and nonprotein

calories
Setting :
N balance
(g/d)
0
- 39 patients with burns or

fractures of more than 2 long bon
-2
- 45-50 kcal/kg and day

(GLC : LIP = 1 : 1)
-4
- N/~ AA intake (g/kg and day):

0/0; 0.1/0.8; 0.2/1.5; 0.25/1.9; 0.3
-6
-8
-10
-12
-14
0 g AA
~ 0.8 g AA
~ 1.5 g AA
~ 1.9 g AA
p < 0.05 vs 0 g AA
Larsson et al (1990) Br J Surg 77, 413-416
~ 2.2 g AA
Recommendation for protein

(nitrogen)
Protein (nitrogen) requirement for adults:
Maintenance: 0.8 - 1.0 (0.12 0.16) (g/kg/day):
Catabolic patients: 1.2 - 2.0 (0.19-0.32) g/kg/day
Complementary source of calorie
Amino
Acids
Proteins:
Structure
Function
Energy: Glucose
Lipids (free fatty
acids)
Non-protein calories = 100 - 200 kcal/g N
grams of nitrogen
Mirtallo et al. (1998) JPEN 22/2, 49-66
Mirtallo et al. (2004), JPEN 28/6, S39-S70
Some other recommendations for

protein (nitrogen)
Source
ASPEN Safe
Practice for PN
revision 2004
Recommendation
Protein for chronic renal failure
with renal replacement therapy 1.2
1.5 g/kg/day
Protein for patients with acute renal
failure and catabolic 1.5 1.8
g/kg/day
ASPEN guidelines
1993 (p34SA)
consensus is that 3 g/kg/day is
appropriate for adequate growth and

nitrogen utilization for low birth
weight infants .
ESPEN guidelines
1997 (p51, Table)
Protein or amino acids

recommendation is 1.0 to 1.2
g/kg/day in liver disease and
transplantation, .
Ziegler & Smith

(1993)
Goal for protein intake in most

diabetic patients should be ~ 1.5
g/kg/day
Types & claimed indications of amino

acid formulation
Formulation
Indication
Standard
Parenteral nutrition for adults
Infant
Parenteral nutrition for neonates
Hepatic
Treatment of hepatic encephalopathy;

parenteral nutrition for patients with
severe liver disease
Renal
Parenteral nutrition for renal failure

patients
High-branched
Parenteral nutrition in sepsis
chain amino acids
Characteristics of standard amino

acid solutions:
Amino acid concentrations of 5 - 15%
With or without electrolytes
With or without carbohydrates (e.g. sorbitol, glucose,
glycerol)
Contains the 8 essential amino acids ~ 35 - 45%
Amounts of each of the 8 essential amino acids generally
based on oral protein intake pattern (Rose, egg protein
potato & egg protein)
Range of non-essential amino acids mostly incomplete,
with relatively high concentrations of a few cheap amino
acids (alanine, glycine) as sources of non-specific nitrogen
Glutamine, tyrosine and cysteine usually missing because
of poor solubility one formulation contains glutamine
dipeptide (Glamin)
Glutamine dipeptide and tyrosine dipeptide overcomes
solubility problems but expensive and under patent
protection
Characteristics of amino acid

solutions for infants

Generally without electrolytes
Generally no carbohydrates content
Contains the 8 essential amino acids ~ 45 - 55%
Amounts of each of the 8 essential amino acids
often based on mothers milk
Contains taurine considered

essential amino
acids in neonates
Special amino acid solutions for

infants
Optimal protein nutrition in this population is
dependent on both the quantity of protein as well as
its quality (composition).
Neonates potentially differ qualitatively from adults
because of their limited capacity to synthesize
certain amino acids
ASPEN Board of Directors Guidelines (2002)
Standard parenteral amino acid formulations are low

in or do not have these amino acids (e.g. taurine,
cysteine).
JPEN 17/4 (Supple), 33SA-36SA; JPEN 26/1

solutions for
severe liver disease (hepa solutions)
Amino acid concentrations of 5, 8 & 10%

No or minimal electrolyte content
No carbohydrates content
Contains essential and non-essential amino acids
Increased amounts of branched-chain (leucine,
isoleucine, valine) and decreased amounts of
aromatic (phenylalanine,
tyrosine) amino acids,
and of methionine compared to standard amino
acid solutions
Nonessential amino acids often incomplete
Special hepatic amino acid solutions

Hepatic
encephalopath
y
Most patients with liver disease who does not have
HE can tolerate a protein source consisting of
standard amino acids. When, in spite of conventional
therapy with lactulose/ and/or neomycin, the
presence of HE makes it impossible to provide
adequate protein to a patient with liver disease, an
enteral or parenteral product containing a liverspecific amino acids mixture
should be used.
JPEN 17/4 (Suppl),14SA-15SA
Special hepatic amino acid solutions

Patients in coma (encephalopathy III-IV) can safely
be given TPN regimens providing 25-30 kcal/kg/day
non-protein
energy
plus
1.0 g/kg/day using BCAA-enriched amino acid
solutions.
Coma solutions containing
only BCAAs ... are
ESPEN Guidelines for nutrition in liver disease and

unbalanced solutions and not recommended as a
transplantation (1997)
nitrogen source for parenteral nutrition.
Clin Nutrition 16, 43-55
Characteristics of HBC amino acids

solutions for high stress (coma
solutions)
Contain only the 3 branched-chain amino acid
(leucine, isoleucine, valine), and hence unsuitable for
nutritional purposes
One radical concept even advocates the use of
valine only
Amino acid solutions for patients with

high stress
Coma solutions: - BCAA only
Coma solutions are unbalanced; not

recommended for parenteral nutrition
- ESPEN consensus guidelines
Plauth et al (1997) Clin Nutrition 16, 43-55

solutions for renal failure

Originally with only the 8 essential amino acids
and histidine (considered to be essential in RF);
sometimes also include arginine no longer
recommended
Later with both the essential and non-essential

amino acids in a ratio of 60: 40 weight percent
Special renal amino acid solutions

On the basis of current evidence, nutritional
support to ARF patients should be accomplished
with an intake containing a balanced mixture of both
essential and non-essential amino acids .
B.Brauns Way
Amino Acid Solutions
Aminoplasmal (B.Braun)
A standard amino acids solution
Versatile range of concentrations (5%E, 10%,
10%E,12.5%E, 15%, 15%E)* in different volumes (250 ,
500 mL) 5% E & 10% E Available in Pakistan
Allows great flexibility in choice to cater for different
nitrogen requirements of patients
Available for central and peripheral route of administration
3 year shelf life
Store at room temperature

Contain no preservatives e.g. sulphite
*See Additional Information from Dr R. Franke for

composition under Standard AA formulations
Aminoplasmal (B.Braun)
Available in
Pakistan
Contains 20 crystalline amino acids*

- breakdown and re-synthesis of additional amino
acids, which
require extra energy expenditure is avoided
Conversion of one non-essential amino acid
into another requires
time, energy and leads
to nitrogen losses
*Get Additional Information from B.Braun Product

Consultant
Aminoplasmal Hepa 10% (B.Braun) Applied for

registration
Product Characteristics
Dosage form
solution for IV infusion
Strength
10%*
Osmolarity
875 mOsm/L
Pack size
500 mL
Container
Glass bottle
Shelf life
3 years
Storage temperature
below 25oC

Consultant
Aminoplasmal Hepa 10% (B.Braun)

Contains
- contains 20 amino acids*
- without carbohydrates
- minimal amount of electrolytes
- no sulphite as preservative (since sulphite may
increase the risk of hepatotoxicity)

Consultant

Indications
Normalization of amino acids imbalance resulting
from liver insufficiency
Prophylaxis and therapy of hepatic encephalopathy
Parenteral nutrition in liver diseases when hepatic
encephalopathy is either imminent or already
manifested

Contraindications:
Disturbed amino acid metabolism of other than
hepatic origin
Renal failure with pathological nitrogen levels
Established cardiac failure
Overhydration
Acidosis
Hypokalemia
Hyponatraemia

Recommendation on route of administration:
central venous
Dosage
Normal dose:
0.7 to 1.0 g/kg/day
(eq. 7 to 10 mL/kg/day)
Maximum dose:
1.5 g/kg/day
(eq. 15mL/kg/day)
e.g. a bottle for a 60 kg weight patient is eq. To

0.8 g/kg/day
~ 8 mL/kg/day

Infusion rates:
Maintenance for PN: up to 1 mL/kg/h
e.g. a 12-h infusion of a bottle to a 60 kg weight
patient is
equivalent to 0.7 mL/kg/h
Treatment of hepatic coma:

e.g. for a 70 kg weight patient, infuse
1st and 2nd h
~ 150 mL/h or 0.2 g/kg/h
3rd and 4th h
~ 75 mL/h or 0.1 g/kg/h
from 5th h ~ 45 mL/h or 0.06 g/kg/h
Aminoplasmal Hepa 10%

(B.Braun)
Clinical studies have shown the following:
- normalization of plasma amino acids profile
- normalization of FQ with concomitant
improvement in HE scores
- reduction of plasma ammonia levels
- improvement in nitrogen
balance and other
parameters of protein
metabolism
- improvement in liver function
Plasma amino acids in cirrhotics
% of normal
400
GLU
ASP
MET
300
PHE
TYR
200
TRY
100
THR
GLY
HIS
SER
LYS TAU
LEU
VAL
ILEU
Essential
PRO ALA
ORN
Non-Essential
Rosen et al. (1977) Gastroenterology 72, 483-487
ARG
Plasma AA imbalances & HE score in

cirrhotics
4
3
2
Fischer quotient (FQ):

ratio
of molar concns of the
BCAA and AAA:
FQ = Val + Leu + Ile
Phe + Tyr
0
0
Alert
2
3
HE score
4
Comatous
Fischer et al (1976) Surgery 80, 77-91
Leweling et al. (1982, 1985)

Prospective, non comparative study on the effects of
a Hepa solution (10%) on HE
n = 21 patients with liver cirrhosis & HE:
- 35 - 40 kcal/kg/day glucose
- 1 g/kg/day BCAA-enriched AA solution
- no neomycin or lactulose
Prospective, non comparative

study on the effects of
a Hepa solution (10%) on parameters of protein
synthesis
n = 11 patients with liver cirrhosis req. TPN because
of gastric bleedings:
- 35 - 40 kcal/kg/day NPC as glucose & lipids
- 1.25 g/kg/day BCAA-enriched AA solution
- daily infusions over 7 - 16 days
Normalization of Fischer Quotient

FQ
4
3
2
21 patients with
HE
(35 infusion
periods)
0
0
p 0.01
8h
Leweling et al. (1982) Aminos & Ammoniakstoffw,
Ammonia levels in blood

g/dL
250
125
10 patients with HE
0
P 0.01
0
8h
Nitrogen balance (example of a patient)

gN
6
4
2
0
-2
-4
1
3 4 5
7 8
Day
9 10 11 12 13 14

193-202
PN with a BCAA-enriched solution in

patients with
liver cirrhosis
%
mg/dL
6
PT
RBP
100
80
3
60
40
0
Start
p < 0.05 End
Start
p < 0.05
Leweling et al. (1985) Klin Ernahr 15, 306-33226
En
d
Visceral protein & serum biochemistry
Leweling et al. (1985) Klin Ernahrung 15, 316 - 322
Glucose in parenteral nutrition
Glucose (Dextrose)
Most important source of energy in diet and in PN
Primary substrate for the generation of energy (ATP)
for cellular metabolism
Each gram of glucose yields 4 kcal of energy
Certain organ systems are dependent solely on
glucose:
- Cells of the brain and CNS
- Cells of the adrenal medulla,

RBC, WBC
Minimum daily requirement for glucose (100 - 150
g/day)
During prolonged starvation, the brain can switch to
using ketone bodies as energy
Proven efficacy in sparing body protein in both
starved and stressed patients
Easy to monitor serum and urine levels
Effect of glucose on protein losses in

healthy subjects
Cumulative protein losses
Glucose
(g)
0
200 g/d
100
200
100 g/d
300
50 g/d
400
0 (fasting)
0
6 day
s
Gamble (1947), Harvey Lectures 42, 247-273
Glucose homeostasis I
Plasma glucose is maintained within a narrow range
Normal fasting level in peripheral venous blood is 4 6 mmol/L or 70 - 110 mg/dL
Mechanisms responsible for glucose homeostasis:

liver & muscle
Glycogenesis: glucose glycogen
Glycogenolysis:
glycogen glucose
Gluconeogenesis:
proteins amino acids
glucose
Liponeogenesis:
glucose fat hepatic glycogen
replenishes plasma glucose;
muscle glycogen only
for local use
liver & kidneys
Glucose homeostasis II
Plasma glucose is influenced by several hormones:
Insulin
Glucagon
Growth
hormone
Corticosteroids
Catecholamines Proinflammatory cytokines
As blood glucose level rises to > 150 mg/dL, insulin
is released and facilitates uptake of glucose
transport into cells, glycogenesis and liponeogenesis
When blood glucose level falls, glucagon is released

and produce the opposite effect of insulin
Both hormones are degraded by the liver
Increased levels of counter-regulatory hormones and
pro-inflammatory
cytokines
results
in
gluconeogenesis
Glucose intake, glucose oxidation and

respiratory quotient (RQ)
Glucose oxidation increases with glucose intake of
up to 6 g/kg/day (4 - 5 mg/kg/min)
Further increase in glucose intake does not cause
increase oxidation, but results in conversion to fat
(liponeogenesis)
Respiratory quotient (RQ) is
carbon dioxide produced
oxygen consumed
Glucose oxidation results in RQ of 1.0
Liponeogenesis results in RQ of 8.7
Effect of glucose intake on glucose

oxidation and liponeogenesis in burn
patients
Direct glucose oxidation
Respiratory quotient
%
5
0
4
1.
2
1.
0
3
0
2
0
1
0
0
oxidation
liponeo
genesis
~ 2.9 ~ 5.8 ~ 8.6 ~

Glucose intake 11.5
(g/kg/day)
oxidation
1
1.
0
0.
9
0.
liponeo
genesis
8
0.
7
0
~
~
~
~
2.9 Glucose
5.8
8.6
11.5
intake
(g/kg/day)
Burke et al. (1979) Ann. Surg. 190, 274-285
Problems with glucose in PN

Problems with glucose in PN are the consequence of
a) too high dosage
b) too high infusion rate
c) poor monitoring of the patient
Clinical problems
Hyperglycaemia
renal overflow
exogenous
Metabolic-clinical problems
Liponeogenesis
fatty
infiltration of the liver
insulin
dehydration
risk of
(risk of
hypoglycaemia
hyperosmolar coma)
increase in
minute
ventilation
Influence of infusion rate on incidence of

hyperglycaemia
Retrospective study in patients not normally
predisposed to hyperglycaemia
Glucose infusion
mg/kg/min
hyperglycaemia cases (%)
19
4.1 5
46
5 (11%)
37
18 (49%)
Rosmarin et al. (1996) Nutr Clin Prac 11, 151-

PRCT 1548 patients
- Conventional gp:
200 mg/dL
blood glucose kept at 180 -
- Insulin therapy gp: blood glucose kept at 80 - 110

mg/dL
Strict glycaemic control at <110 mg/dL with
insulin infusion
Van den Berghe (2004) ESPEN lecture, Lisbon
Strategy for using glucose in PN

Optimize delivery but do not exceed oxidative rate
- infuse glucose slowly, at 2 - 4 mg/kg/min
5 - (6) g/kg/day) maximum
in critically ill patients: 3 - 4 g/kg/day
Ensure normoglycaemia
- in critically ill patients control serum glucose more
aggressively
recommended level 80 - 110 mg/dL (4.4 6.1 mM)
- when discharged from ICU, blood glucose should be
maintained
at 180 200 mg/dL (10.0 11.1 mmol/L)
Minimize liponeogenesis
- use mixed fuel system of glucose + fat
Glucose in pediatric patients

Dosage:
Premature
10 - 20 g/kg/day
Neonates
10 - 20 g/kg/day
Older children
1 - 7 yrs
9 -12 g/kg/day
8 - 12 yrs
7 - 9 g/kg/day
13 18 yrs
4 7 g/kg/day
Start at 6 mg/kg/min to 8 mg/kg/min

Advance by 1 to 2 mg/kg/min to a maximum of 12-14
mg/kg/min/day (17g/kg/day 20 g/kg/day)
Baugh et al (1998) ASPEN Nutrition Support Manual,

Chap 24
PN regimen without lipid

A 50 kg patient requires ~ 30 kcal/kg/day total
energy
Total energy required = 50 x 30 = 1500 kcal/day
If only amino acids and glucose are given,
and amino acids is given at 1 g/kg/day
Total amino acids = 50 x 1 = 50 g (1 bottle 500
mL10% soln)
Protein calories
= 50 x 4 kcal/g
= 200
kcal
Exceedscalories
recommended
Non-protein
= 1500 - 200 = 1300 kcal
= 6.5 g/kg/day
amount of glucose
Amount of glucose = 1300/4
= 325 g
Glucose solutions & their osmolarity

Product
Osmolarity (mOsm/L)
Glucose 5%
278
Glucose 10%
556
Glucose 20%
1110
Glucose 30%
Glucose 40%
Glucose 50%
1660
2220
2770
Glucose 70%
3880
Osmolarity of serum ~ 300 mOsm/L. Solutions with

osmolarity
> 300 mOsm/L are defined as hyperosmotic.
Hyperosmotic and acidic pH of concentrated glucose
solutions warrant their administration via large veins.
Peripheral vein tolerance to hyperosmotic solution is
highly patient-dependent, but tolerance is generally poor
as solution osmolarities approach 800 to 900 mOsm/L.
Glucose alone versus a mixed fuel

system only
Mixed fuel system of glucose and lipids are better
adapted to stress than glucose alone
Provides essential fatty acids
- Adolph et al (1995) Ann Rev Metab 39, 251-260
Produces better nitrogen retention
- Bresson et al (1991) Am J Clin Nutr 54, 370-378
- Nose et al (1987) Pediatr Res 21, 538-541
Less CO2 production with a mixed fuel system
- Askanazi et al (1979) Anaesthesiology 51, 192 Lipids oxidization increased in the critically ill while
glucose oxidation decreased
- Stoner et al (1983) Br J Surg 70, 32-53
- Jeevanandam et al (1990) Crit Care Med 18, 125-135
Serum glucose is better controlled with a mixed fuel
system
- Hempel et al (1981) Infusionstherapie 3, 124-132
Relationship between glucose

oxidation and sepsis scores in
patients on PN
Stoner et al (1983) Br J Surg 70, 32-53
Relationship between fat oxidation

and sepsis scores in patients on PN
Stoner et al (1983) Br J Surg 70, 32-53
Effect of glucose system and mixed

fuel system on ventilation
V
CO2 (mL/min/m2)
300
RQ=1
200
100
RQ=0.7
Gluc (kcal) 2400
1300
Lipids(kcal) 0
.
VE (l/min) 10.8
0
0
100
200
.
VO. (mL/min/m2)
2
300
Askanazi et al. (1979) Anesthesiology 51, 192
1100
6.35
Serum glucose profile during PN

Carbohydrate only
Carbohydrate + fat
5th day
9th day
5th day
Hempel et al (1981) Infusionstherapie 3, 124132
9th day
Lipids in parenteral nutrition
Lipids
Naturally occurring organic compounds from plant
and animals that are water insoluble
Some types of lipids to know
- triglycerides (or triacylglycerols) ester of glycerol
+ 3 fatty acids
- phospholipids ester of glycerol + 2 fatty acid + X,
with X =
phosphate group tog with N-cpds (e.g.
choline, ethanolamine),
hydrophilic
has a polar head and 2 non-polar tails
water loving
- cholesterol (most common steroid and precursor of

all other
steroids in animals)
- others e.g. glycolipids related to brain and other
hydrophobic
nervous tissues
- water repeling
Roles of lipids
Serve several functions in the body:
- main source of stored energy (in adipose tissues,
LCT)
9 kcal/g
- metabolic fuel
- essential component of cell membranes
- insulate against injury and heat loss
- pad critical organs
- act as precursors of important regulatory
compounds such as
prostaglandins and eicosanoids
- serve as carriers of various lipid soluble
substances e.g. fat
soluble vitamins (A, D, E, K) in plasma
Characteristics of lipid emulsions for

PN
Oil-in-water emulsions with 10%, 20% or 30%
triglycerides
Different types of triglycerides
Different ratios of 3, 6, 9
Egg yolk phospholipid as emulsifier
Glycerol to adjust for osmolality (~ 300 mOsm/kg)
pH ~ 8, unbuffered
Mean lipid droplet size ~ 0.3 m
High caloric density (10% ~ 1 kcal/mL, 20% ~ 2
kcal/mL)
Content of essential fatty acids mostly in the soya
oil
Representation of an oil-in-water lipid

emulsion
Water
- -
Triglyceride
Phospholipid
- -
(+ glycerol)
- -
Triglycerides
- esters of glycerol and 3 fatty acids, also called
triacylglycerols
- classified depending on chain lengths of free fatty
acids attached to glycerol
backbone e.g. SCT,
SCFA
SCFA
Short chain triglyceride
MCT, LCT
(SCT)
SCFA
MCFA
MCFA
Medium chain triglyceride
(MCT)
MCFA
Long chain triglycerideLCFA
(LCT)
LCFA
LCFA
Classification of triglycerides
Structured triglyceride (SL)
MCFA
MCFA
Defined
Random
LCFA
MCFA/LCFA
MCFA/LCFA
MCFA/LCFA
+ MCT + LCT
Free fatty acids

hydrocarbon chains
carboxyl gp
Free fatty acids (FFA) - empirical formula R-COOH

Has linear chain of even number of carbon atoms,
that can be
- saturated (no double bonds)
- monounsaturated (1 C C) or
- polyunsaturated ( 2 C C)
FFA are named

- SCFA with R = 2 and 4
- MCFA with R = 6, 8, 10 and 12
- LCFA
with R = (14), 16, 18, 20, 22 and 24
Essential FFA are
- linoleic acid (omega 6, 6; 18: 2n6)
- -linolenic acid (omega 3, 3; 18:3n3)
Names of the saturated fatty acids

C2 :
C4 :
C6 :
C8 :
C10:
C12:
Acetic acid
(ethanoic acid)
Butyric acid
(butanoic acid)
Caproic acid
(hexanoic acid)
Caprylic acid
(octanoic acid)
Capric acid
(decanoic acid)
Lauric acid
(dodecanoic acid)
C14:
Myristic acid
(tetradecanoic acid)
C16: Palmitic acid
(hexadecanoic acid)
C18: Stearic acid
(octadecanoic acid)
C20 : Araquidic acid
(eicosanoic acid)
C22 : Behenic acid
(docosanoic acid)
C24: Lignocerotic acid
(Tetracosanoic acid)
Names of some of the unsaturated

fatty acids
Name
Abbreviation
C16:1, 7
Palmitoleic acid
Oleic acid
C18:1, 9
Linoleic acid
C18:2, 6
-Linolenic acid
C18:3, 6
Dihomo--linolenic Cacid
20:3, 6
, 6
Arachidonic acid C20:4
-Linolenic acid
C18:3, 3
Eicosapentaenoic acid
C20:5, 3
Docosahexaenoic acid
C22:6, 3
Structure
COOH
COOH
COOH
COOH
COOH
COOH
COOH
COOH
COOH
no of carbon atoms from

and the closest double bond
= methyl terminus,
total no of double bonds
non carboxyl carbon
otal no. of carbon atoms
Other components of lipid emulsions:

Phospholipids (egg yolk lecithin)
- have both a hydrophobic (water repelling) and hydrophilic (water
attracting) part, which enable interaction at both water and fatsoluble interfaces, making them ideal emulsifying agents
Glycerol
- to adjust the osmolarity of the emulsion to that of blood
Sodium Oleate
- to maintain stability of fat emulsions, especially when stored at
room temperature
to
- its stabilising effect is due
its acting as a co-emulsifier and
its causing a pH shift to higher values and neutralization of
free fatty acids formed by hydrolysis of lipids during storage
Alpha tocopherol (only in BBraun lipid emulsion)
- to protect against in vitro peoxidation and maintains vitamin E
status
Storage temperature of lipid

emulsions
Note well
Types of lipid emulsions

e.g.
Intralipid
LipofundinStructolipidNonNonLipofundin
existen
existen
N
MCT/LCT
t
t
Clinoleic,
SLr
SLd
L
M/L
M
Omegaven
SLr
SLd
L
L
M/L
L
M/L
M/L
SLr
SLd
SLr
SLd
LPL/HL
LCFA + Glycerol MCFA + LCFA + Glycerol
Types of lipid emulsions

100% LCT emulsions: Intralipid , Ivelip , Lipovenos ,
Lipofundin N
Mixed LCT emulsions: Liposyn II (Abbott) safflower
oil: soya oil of 1:1), Clinoleic (Baxter- olive oil: soya oil
of 4:1)
Special LCT emulsion: Omegaven (only fish oil)
Physical mixed MCT/LCT:
Lipofundin MCT/LCT (BBraun
- MCT oil: soya oil of 1:1 (by weight)), Lipovenos MCT

Fresenius Kabi same as Lipofundin MCT/LCT)
Structured lipids: Structolipid (Fresenius Kabi randomized SL of MCT: LCT of 36:64 (by weight))
Evolution in parenteral lipid emulsions
LCT: long chain triglyceride; MCT: medium chain triglyceride;

PUFA: polyunsaturated fatty acids; FA: fatty acid; FO: fish oil
Driscoll et al. (2001) Chapter 3, Rombeau &

Rolandelli 3rd Ed.
Use of lipids I
Indication
- as a source of essential fatty acids
- as a source of energy
Contraindication
- in patients with disturbances in normal fat
metabolism e.g. pathological
hyperlipaemia, lipoid
nephrosis or acute pancreatitis accompanied by

lipaemia, or that which is aggravated by
hyperlipaemia
- in conditions of shock and/or acid base imbalance,
these conditions should be corrected before
parenteral nutrition should be considered
Use of lipids II
Adverse reactions
Immediate reactions:
nausea, vomiting, fever, sweating, chills, sleepiness,
chest and back pains, dyspnoea, cyanosis, allergic
reactions, hyperlipaemia, coagulability
Delayed reactions:
enlarged liver, jaundice, enlargement of spleen,
thrombocytopenia, leucopenia, transient
disturbances in liver function test, overloading
syndrome
AVOID COLD INFUSION OF FAT EMULSION
Use of lipids III

Precautions
Infusion rate should not exceed 0.11 g/kg/h as too
rapid an infusion of fat emulsion can cause fat
overloading; in critically ill patients, infusion should be
as slow as possible (over 24 h)
When Lipofundin MCT/LCT is given too rapidly,
hyperketonaemia (with metabolic acidosis) may result,
especially if glucose is not given simultaneously
Monitoring of plasma triglyceride is essential
Monitoring of haemogram, blood coagulation, liver
function and platelet counts are important esp. if fat
emulsion is given for extended period
Ensure patient is not intolerant to any component of
the lipid emulsion e.g. egg yolk phospholipid) or is
getting lipids from another source (in ICU when
propofol is used for sedation)
Stop if platelet counts < 40000/cm3
Practical aspects of fat infusion I

Recommended daily
dose
adult: 1.0 - 2.0 g/kg

infant: 1.0 - 3.0 g/kg
Infusion rate
<0.11 g/kg/day; preferably over 24 h in

critically ill patients
Amount of fat
15 to 40% of total calories. In selected

hypermetabolic patients, with resistance to
glucose utilization or impaired ventilatory
capacity, the proportion of lipid calories could
be increased
up to 50 or 55% of total calorie
intake
Type of lipid emulsions 20% better than 10%;

MCT/LCT better than LCT emulsion
Practical aspects of fat infusion II

Mode of
delivery
As a separate bottle or as part of an

all-in-one admixture
Use of in-line filter

Additions to
lipid emulsions
Use a 1.2 m, and not a 0.22 mfilter

Other than fat soluble vitamins, it is not
recommended to add drugs or additives
to the lipid emulsion, unless its
compatibility and stability in the fat
emulsion has been verified
Once opened, the bottle must be used

within 24 h
Hang time of
lipid emulsion
Special
monitoring
Check for hypertriglyceridaemia
Hypertriglyceridaemia with infusion of

lipid emulsions
Severe hypertriglyceridaemia is defined as:
> 450 mg/dl in adults
> 250 mg/dL for infants
Hypertriglyceridaemia develops mostly because of:

- high dosage
- fast infusion rate
Some clinical conditions are known to be

accompanied by hypertriglyceridaemia or reduced
capacity to clear lipids, e.g.
- acute pancreatitis
- acute and chronic renal failure
- diabetes mellitus
- sepsis
Differences between MCT and LCT
Energy
MCT
LCT
- saturated
- monounsaturated
- polyunsaturated
linoleic (6)
-linolenic (3)
+++
Structure Function
0
++
++
++
++
(+)
(+)
+
+
+++
+++
+++
+++
Driscoll et al. (2001) Chapter 3, Rombeau &

Rolandelli 3rd Ed.
Characteristics of MCT vs LCT
Metabolism of lipid emulsion

FA
FA
Lipid emulsion
FA
Triglyceride
Glycerol
glucose
precursor
Phospholipid
s
Hydrolysis
re
esterification
of
triglycerides
CO2 +
Free fatty acid Oxidation
H 2O
Ketone
bodies
-oxidation
reesterification of
triglycerides
Hydrolysis of LCT in blood
LCFA
LCFA
LCFA
Lipoprotein lipase
Apolipoprotein
C-II
Albumin
LCFA
LCFA
LCFA
Transport bound to albumin
Hydrolysis of MCT in blood
MCFA
MCFA
MCFA
Lipoprotein lipase
No
need for apolipoprotein C-II
No need for albumin
MCFA
MCFA
MCFA
Transport not bound to albumin
Hydrolysis of MCT & LCT by

lipoprotein lipase and hepatic lipase
in vitro
Free fatty acid release

Lipoprotein lipase
(nmol/l
)
400
200
0
Hepatic lipase
(nmol/l
)
800
400
0
20
40 (min)
LCT
20
40 (min)
MCT
Deckelbaum et al., Biochemistry 29 (1990) 1136-1142
Intracellular metabolism of medium

(MCFA) and long-chain fatty acids
(LCFA)
LCFA
LCFA-CoA
Cytos
LCFAol
Carnitine
LCFA
MCFACoA
LCT
MCT
AcCoA
MCFA
KB
Mitochondri
on
ATP
MCF
A
Oxidation rates of MCT/LCT & LCT in

severely injured patients
p < 0.0002
Oxidation rates
(%)
40
30
20
10
0
MCT/LCT
(13C8)
LCT
(13C18)
Adolph et al (1988) Clin Nutrition 7 (Supple), 78
Clinically relevant issues when using

lipid emulsions in PN
Clearance of lipids
Protein sparing
Impact on liver function
Disturbances of immune functions
Impact on pulmonary gas exchange and
haemodynamic parameters
Peroxidative damage
Stability of all-in-one mixtures
Clearance of lipids: MCT/LCT vs LCT

Clearance of MCT/LCT is faster than LCT
Wicklmayr et al (1988)
Diabetic type II
patients
JPEN 12, 68-71
Jiang et al (1993)
Surgical patients
Annals Surgery 217, 175-184
Neonates and pediatrics

Menci et al (2004) Neonates
Clin Nutr 23/4, 906
Elimination from blood: MCT/LCT vs

LCT
%
100
Diabetic type IIb patients

after overnight fast
MCT/LCT
(half-life 39.8 min)
LCT
(half-life 64.2 min)
n=7
50
0
20
40
60
80min
Wicklmayr et al (1988) JPEN 12, 68-71
Metabolic tolerance in neonates

Neonates (1750 g 3930 g, aged 8-21
days, n = 22)
Menci et al (2004) Clin Nutrition 23/4,

Clearance of lipids
Protein sparing
Impact on pulmonay gas exchange and
Peroxidative damage
Protein sparing: MCT/LCT vs LCT

Protein sparing: MCT/LCT is superior to LCT
Adults
Dennison et al. (1988)
Malnourished after GI
surgery
Ball (1993) ICU (mixed surgical/trauma)
Czarnetzki et al.(1988)
Acute pancreatitis
Jiang et al. (1993) GI surgery
Garnacho-Montero et al (2002)
Septic patients
Neonates & Paediatrics
Bresson et al. (1986)
Infants
Lima et al., 1989
preterm neonates
Lai & Chen, 2000 pediatrics after surgery
Gentili et al., 2001 preterm & term neonates (mixed
surgical/medical)
Protein sparing: MCT/LCT vs LCT

Adult
Dennison et al. (1988) JPEN 12, 15-19
Lohlein et al (1989) Beitr. Inf. Klin Ern. 20, 156-164
Ball (1993) Intensive Care Med 19, 89-95
Czarnetzki et al.(1988) Proc 10th Cong ESPEN Aug
1988, pp 83-99
Jiang et al (1993) Annals
Surg 217, 175-184
Garnacho-Montero et al (2002), Nutrition 18, 134-138
Pediatric
Bresson et al. (1986) Clin Nutr 5 (Suppl), 54
Lima (1989)
Lai & Chen (2000) Nutrition 16, 401-406
Gentili et al (2000) RINPE 18, 134-142 [MCT/LCT only]
Garnacho-Montero et al (2002):
MCT/LCT vs LCT
Prospective, randomized controlled trial in septic
patients with peritonitis (26 /group)
Regimen:
30 kcal/kg day (glucose: fat ratio = 60:40)
1.4 0.2 g AA/kg/day
lipids as 10% MCT/LCT or 10% LCT
TPN for 10 days postoperative
Nutrition 18, 134-138
Protein metabolism: MCT/LCT vs LCT

Nitrogen balance
g/24 h
Retinol binding protein

mg/dL
p < 0.01
p < 0.001
16
n = 26/gp
1.5
12
0.5
MCT/LCT
LCT
MCT/LCT
LCT
Garnacho-Montero et al (2002) Nutrition 18, 134-138
Lai & Chen (2000): MCT/LCT vs LCT

Prospective randomized double blind study
Paediatric surgical patients (2 - 6 years old), n =
20/group
Regimen: total energy: ~71 kcal/kg/day
over 24 h
amino acid: 2 g/kg/day
12 g/kg/day
glucose:
lipids: 1.5 g/kg/day over 12 h as MCT/LCT or
LCT
TPN started 2 days postop, for 14 days
Nutrition 16, 401-406
Protein metabolism: MCT/LCT vs LCT

N balance in surgical paediatric patients
*#
mg/kg/day
80
60
*#
*
#
19/group
*#
*#
MCT/LCT
LCT
40
20
0
1
2
3
4
* vs day1 p < 0.05
14 day
6
7
# vs LCT p < 0.05

Clearance of lipids
Protein sparing
Peroxidative damage
Liver function: MCT/LCT vs LCT

Liver function: MCT/LCT superior to LCT
Adults
Balderman et al.(1989)
Dennison et al.(1988)
surgery patients
Carpentier et al.(1988)
bowel syndrome
Stroke patients
Malnourished GI
Patients with short

Lai & Chen, 2000 pediatrics
Gentili et al., 2001 preterm & term neonates
Liver function: MCT/LCT vs LCT

Adult
Dennison et al (1988) JPEN 12, 15-19
Carpentier et al (1989) Clin Nutr 8 (Supple), 31
Baldermann et al (1991) JPEN 15, 601-603
Paediatric
Goulet et al (1992) Nutrition 8, 333-337 [HPN]

Gentili et al (2000) RINPE 18, 134-142 [MCT/LCT
only]
Liver function tests: MCT/LCT vs LCT

3 patients with SB on HPN. 50% of NPC as
U/LMCT/LCT
p < 0.01 week 1 vs weeks
250
4-9
MCT/LCT
LCT
200
-GT
150
SGPT
100
50
SGOT
0
1
9 10 11 12 weeks
Carpentier et al. (1989) Clin Nutrition 8, (Supple) 31
Liver function test: MCT/LCT Conversion

vs LCT product from
haem of RBCs
mg/d
L serum bilirubin
3
*
Setting:
TPN after
abdominal
surgery (n = 15)
each lipid was
infused over 5
days
*
2
MCT/LCT
LCT
*p < 0.05 MCT/LCT
vs LCT
0
1
5 days
Dennison et al. (1988) JPEN 12, 15-19
Gentili et al. (2000) MCT/LCT in

neonates
Prospective non-comparative study
Critically-ill neonates - 26 term and 26 preterm,
mixed medical and surgical cases (include 13
LBW, 7 VLBW and 2 ELBW infants)
Regimen:
80-90 kcal/kg/day
7-18 g/kg/day glucose
2 g/kg/day
Lipofundin MCT/LCT20%
3 g/kg/day amino acids

fluid intake ~ 90 - 140 mL/kg/day
TPN duration: 21.3 11.2 days (range 10-49)
Gentili et al. (2000) RINPE (2000) 18, 134-142
Liver function tests: MCT/LCT

Plasma transaminase
IU
100
AST
80
n= 52
ALT
60
40
20
0
BFN
D1
D3
D7
D14 D28 D49
AfPN
Gentili et al. (2000) RINPE 18, 134-142 (adapted)

Clearance of lipids
Protein sparing
Peroxidative damage
Immune function: MCT/LCT vs LCT

Immune function: MCT/LCT superior to LCT
Adults
Gogos et al (1990) Malnourished, cancer patients
Marsili et al (1992) COPD patients
Waitzberg et al (1997)
Malnourished cancer
patients
Kuse et al (2002) Liver transplant patients
Sedman et al (1991)
Malnourished cancer
patients
Jouanneau et al (1996)
premature neonates
Lai & Chen, 2000 pediatrics
Immune function: MCT/LCT vs LCT

Adult
Gogos et al (1990) Am J Clin Nutr 51, 119-122
Sedman et al (1991) Br J Surg 78, 1396-1399
Marsili et al (1992) Clin Nutr 11 (Supple), 45
Waitzberg et al (1997) 13, 128-132
Kuse et al (2002) Transpl Int 15, 272-277
Grau et al (2003) Nutr Hosp18, 259-266

Jouanneau et al (1996) Arch Pediatr 4, 912
Immune function (Thelper / Tsuppressor cell

ratio): MCT/LCT vs LCT
B: TPN in COPD patients
A: TPN in int. med. patients
2.15
2.11
2.10
1.931.89
1.90
2.0
1.70
1.65
1.0
E = 1316
0 10
0 E
0 E
0 10 days
ns
p < 0.05
ns
p < 0.05
A: Gogos et al. (1990) Am J Clin Nutrition 51, days
119-122
B: Marsili et al. (1992) Clin Nutrition 11(suppl), 45
Phagocyte function: MCT/LCT vs LCT

100
Setting:
preoperative TPN of
malnourished GI
cancer patients
n = 10
% killed bacteria
90
80
70
60
Fig shows
differences
of values before
and after lipid
infusion
50
40
30
MCT/LCT
LCT
Waitzberg et al. (1997) Nutrition 13, 128-132
Intra-abdominal abscesses after major

GI surgery
% patients
MCT/LCT (n =
26)
LCT (n =
31)
All
pts
Noncancer
Canc
er
Grau et al (2003) Nutr Hosp 18, 259-266

Clearance of lipids
Protein sparing
Peroxidative damage
Haemodynamics and gas exchange:

MCT/LCT vs LCT
Haemodynamics and pulmonary gas
exchange: MCT/LCT superior to LCT
Adults
Fiaccadori et al (1997)
Heart valve replacement
Smyrniotis et al (2001)
Acute pancreatitis/ARDS
Faucher et al (2003)
Patients with ARDS
Radermacher et al (1992) Septic patients

[MCT/LCT only)
Neonates & Paediatric
lacking comparative studies
Lung function: MCT/LCT vs LCT

Adult
Radermacher et al (1992) Intensive Care Med 18,
231-234 [non-comparaive study]
Fiaccadori et al (1997) RINPE 15, 6-14
Smyrniotis et al (2001) Clin Nutr 20, 139-143
Faucher et al (2003) Chest 124, 285-291
Neonates & Paediatric

Lacking comparative studies [adverse findings
with LCT]
Haemodynamic parameters: MCT/LCT

vs LCT
Systemic vascular resistance
Cardiac index
Setting:
Heart valve
replacement
patients
(13/group)
20% MCT/LCT or
LCT, infused at 1
mL/kg/h
for 2 h (0.2
g/kg/h),
via CVC,
24 h after
operation
Pulmonary gas exchange: MCT/LCT vs

LCT
Systemic O2 consumption
O2 delivery
Setting:
Heart valve
replacement
patients
(13/group)
20% MCT/LCT or
LCT, infused at 1
mL/kg/h
for 2 h (0.2
g/kg/h),
via CVC,
24 h after
operation
Effects on haemodynamics and gas

exchange
Patients
Lipid
MPAP
emulsion
No
change
(p<0.05)
Cardiac
surgery1
MCT/LCT
LCT
Sepsis,
ARDS2
No
MCT/LCT change
LCT
(p<0.05)
No
change
QVA/QT
-
PaO2/FiO2
-
No
change
No
change
(p<0.05)
(p<0.05)
No
change
No
change
Pancreati
MCT/LCT
tis
LCT
RINPE 15,
3
(1)
Fiaccadori
et al (1997)
6-14, (2) Smirniotis
et al.
ARDS
(p<0.05) (3)
(p<0.05)
(p<0.05)
(1998) Int Care Med 24, 1029-1033,
Smyrniotis
et al.
(2001) Clin Nutrition 20, 139-143 (4) Faucher et al.
(2003)
Chest 124, 285-291

lipid emulsions in TPN
Clearance of lipids
Protein sparing
Peroxidative damage
Lipid emulsion & Peroxidation

Lipid emulsions made up of LCT contain high amounts of
LC-PUFA but relatively little amounts -tocopherol
LC-PUFA are particularly vulnerable to free radical attack,
with an increased production of peroxidative catabolites
Lipid hydroperoxides decompose to form highly toxic
products such as aldehydes, which can cause severe
damage to cell membranes
- inactivating receptors
- inactivating membrane-bound
enzymes
- affecting the fluidity of the cell membranes

Complications arising from peroxidation:
- increased haemolysis
- pulmonary complications
- impairment of immune response
- tissue damage (e.g.retinopathy in premature infants,
pulmonary
dysplasia
Peroxidation: MCT/LCT vs LCT

Peroxidation: MCT/LCT is less susceptible
than LCT
Zimmermann et al (1993) J Pharm Clin 12, 300301
Siderova et al (1995) Clin Nutr 14, 47-48
Arborati et al (1998) JPEN 22, S5
Clin Nutr 16 Supple 2, 31
De Leeuw et al (1998)
Manuel-y-Keenoy et al (2002) Eur J Clin Nutr 56,
121-128
Peroxidation (TBARS production):

MCT/LCT vs LCT
mol per L emulsion
2000
1000
LCT
MCT/LC
T
10
20
30
45 min
TBARS = Thiobarbituric acid reactant
substances
Zimmerman
et al. (1993) J Pharm Clin 12, 300-301
Fatty acid composition of LCT and

MCT/LCT emulsions
FA (g/100g total)
8:0
10:0
12:0
14:0
16:0
16:1n-7
18:0
18:1n-9
18:2n-6
18:3n-3
20:0
20:4n-6
22:6n-3
LCT 20%
0.01
10.07
4.25
1.74
MCT/LCT 20%
31.4
17.5
0.29
0.01
5.10
0.09
0.05
2.24
23.80
12.08
53.91
27.46
5.78
2.90
0.75
0.36
0.19
0.
0.0
Dahlan et al (1992) Clin Nutr 11, 262-268
Lipids,
B.Braun,s Way
Lipofundin N and MCT/LCT
*See Additional Information from Dr R. Franke under Product

Compositions: Lipids
-tocopherol (g/mL)
Plasma Vitamin E in HPN patients

supplemented with 200 mg tocopherol/day
30
n=8
20
10
6 months
-1
Siderova et al. (1995) Clin Nutrition 14, 47-48

lipid emulsions in TPN
Clearance of lipids
Protein sparing
Peroxidative damage
Oil-in-water emulsion
Lipid emulsion particles kept apart by net negative
charges
described as Zeta potentials
Oil-in-water emulsion
Normal size ~ 0.3 M
high cation concentrations
pH changes
Oversize fat globules > 5 M
Advantage of MCT/LCT: Stability

MCT/LCT is more stable than LCT in AIO
emulsions
Mller & Heinemann (1994) Int J Pharm 107, 121132
Driscoll et al (2000) JPEN 24, 15-22
Driscoll et al (2001) Clin Nutr 20, 151-157
Driscoll et al (2003)Clin Nutr 22, 489-496
Protocol of Driscoll et al. (2000)

Particle size distribution of lipid emulsion
TNA admixtures with:
total calories: 25 kcal/kg/day
total volume: 25 mL/kg/day
AA: 1.5 g/kg/day
glucose 2.8 g/kg/day
fat: ~ 20% of total calories

as LCT or MCT/LCT 20%
plus electrolyte, micronutrients
JPEN 24, 15-22
Particle size distribution of lipid

emulsion
TNA admixtures at different sampling time
Samples
Time of sampling
T1
T2
T3
T4
T5
immediately after preparation of TNA

after 4 days storage at 4oC
after 6 h at 25oC
h at 25oC
after 24
after 30 h at 25oC
Particle size was quantified using a single particleoptical sensing device that uses laser light
extinction. Mean particle size of the lipid droplets
was determined by dynamic light scatter using a
submicron particle sizer
Driscoll et al. (2000) JPEN 24, 15-22
Mean particle sizes (MPS) between

TNA formulations
400
* p<0.05
p<0.005
MCT/LCT
LC
T
**
MPS (mm)
380
360
**
340
320
300
T1
T2
T3
T4
T5
Lipid droplet counts (%fat) of TNA

formulations
0.7
MCT/LCT
LC
T
* p<0.01
PFAT > 1.75 m
0.6
0.5
0.4
0.3
0.2
0.1
0.0
T1
T2
T3
T4
T5
Lipid droplet counts (%fat) of TNA

formulations
MCT/LCT
LC
T
0.35
0.30
*
*
p<0.01
0.25
PFAT > 5
m
0.20
0.15
0.10
0.05
0.00
T1
T2
T3
Driscoll et al (2000) JPEN 24,
T4
T5
Advantages of MCT/LCT vs LCT

Compared to LCT, MCT/LCT emulsion
Gives more rapid clearance of lipids
Gives better nitrogen balance
Diminishes TPN-related incidences of liver
dysfunction
Maintains immune function
Has no adverse influence

on haemodynamic
status
Has no adverse influence of pulmonary function
Is less susceptible to peroxidative damage
Is more stability in all-in-one mixtures
Other issues: ketogenesis
Ketonaemia in different situations

Ketonaemia
(mmol/l
)1
2
1
0
8
11.5
6.25
4
2
0
A : 12 h fast or LCT infusion

(1,2)
B : 18 h fast or MCT/LCT infusion
(1,2)
C : 3 d fast (1)
D : 7 d fast (1)
E : ketoacidosis in type I diabetics
(3)
0.3 0.6
A
3.
0
C
1) Sapir et al.(1975) Metabolism 24, 23-33

46
2) Dawes et al.(1986) World J. Surg. 10, 38-
Acid-base balance with MCT/LCT

Setting : Infusion of 50 g lipids (MCT/LCT) into type I
diabetics after an overnight fast and without
administration of insulin
(mmol/l)
7.45
26
pH
7.40
24
7.35
22
7.30
20
Infusion
0 1 2 3 4
(mm
Hg)
48
HCO3-
44
40
36
Infusion
24 h
pCO2
0 1 2 3 4
Infusion
24 h
0 1 2 3 4
24 h
Sailer (1988), Beitr. Infusionsther. klin. Ernhr. 20, 88-98
Ketogenesis: Lipid alone and in the

presence of glucose
MCT/LCT only
MCT/LCT +
gluc
Kolb & Sailer (1984) JPEN 8, 285-289
Ketogenesis in paediatric patients
Lima et al (1988) Acta Scand Paediatr 77,
Ketones as fuel
Organ
Fuel
Skeletal, Cardiac muscle
Fatty acids
glucose
Ketones
Nervous system, Blood

cells
Glucose
Ketones
Liver
Fatty acids (medium > long)

Glucose
Intestinal mucosa
Glutamine
Aspartic acids
Ketones
Colonic mucosa
Fatty acids
Glutamine
Ketones
Lymphocytes
Fatty acids
Glucose
Ketones
Glutamine
Lipofundin MCT/LCT: Summary

wide clinical experience with Lipofundin MCT/LCT
Extensive clinical data cf Structolipid or Clinoleic;
papers quoted for Lipovenos MCT mainly those
using Lipofundin MCT/LCT
Lipofundin MCT/LCT has been on market for since
1984 in Europe
Use in HPN patients > 6 months
Safe and efficacious in preterm and term neonates
Safe and efficacious in patients with sepsis,
diabetes, renal failure, liver failure, pancreatitis,
and also in pregnancy
Stability in compounding mixtures and
convenience systems established
Multichamber PN bags
Challenges facing nutrition support

Patients differ
After illness or trauma, their metabolic conditions
and requirements differ
The challenges are:
- to provide nutrition support adapted to their
individual
requirement
- with appropriate amount of nutrients

- in a timely manner
- by the most suitable route
Types of parenteral nutrition

systems
Bottle system: spike and hang individual bottles of
solutions (e.g. glucose, amino acids, fat emulsion), or
mixtures in bottles or kits (Vitrimix )
Compounding system: Hospital or industrially
(CAPS - centralized admixing pharmacy service)
prepared solutions filled in an ethylene vinyl acetate
and sets) by either gravity
bag (e.g. Nutrimix bags
or by an automated equipment (e.g. Caretronic or
BAXA machine)
Convenience system: ready-to-use 2- chamber
bags (Nutriflex , Aminomix , Clinimix ) or 3-chamber
bags (NuTRIflex Lipid, Kabiven , Clinomel )
Parenteral nutrition system: Single

bottle system
Glucos
e
AA
Lipids
Glucos AA
e
Lipids
Parenteral nutrition system: Kit system

- Vitrimix
250
Intralipid 20%
ml
lipi
ds
Transfer
set
Vamin
Glucos
e
Do
not
cover
basal
need
s
Under
partial
vacuu
m
750
ml
Osmolarity not suitable for PPN
Comments on Vitrimix
Still quite popular in many countries, though it has
considerable disadvantages as compared to more modern
and convenient concepts
Among the disadvantages are:
- need to combine two separate bottles every 12 h
- electrolyte contents do not even cover basal daily
requirements
- need for further additions of electrolytes or for their
separate
administration
- osmolality of 1130 mOsm/kg does not allow
administration of
Vitrimix through peripheral veins, without a high risk of
producing thrombophlebitis
Parenteral nutrition system:

Compounding
Can be without or with lipids in the bag
All-in-one (AIO) or Total Nutrient Admixture (TNA) infers inclusion of lipids
Meguid (1989) Nutrition 5, 343344
Error rates of manual vs partially

automated AIO
(%)
40
37
30
22
20
10
AIO - manual preparation
AIO - partially automated

preparation
Flynn et al. (1997), Am. J. Health-Syst. Pharm. 54, 904-912
Advantages of multichamber bags

Storage at room temperature
Storage at the ward is possible
Fast mixing of chamber content
Uniform preparation
Higher level of safety resulting from lower rate of
errors
resulting from reduced
Higher level of safety
danger of contamination
Simplified logistical organisation
Savings of costs and time
Convenience vs. Compounding
Metabolic benefits of AIO

administration
Better nitrogen balance and fat utilization when
given in a continuous infusion over 24 h
Less effect on immune function (e.g. from
disturbance of fat clearance by RES)
Less electrolyte fluctuations
Cumulative Nitrogen Balance
1
Gram N
-4
-9
- 14
- 19
- 24
Continuous
Bolus
Sequential
- 29
- 34
2
Days
Two-chamber bags: Nutriflex

(B.Braun)
Peri
Basal
Plus
Special
Amino acids (g/L)
40
32
48
70
Glucose (g/L)
80
125
150
240
Total energy (kcal/L)
480
630
790
1240
Non-protein calories
(kcal/L)
320
500
600
960
Osmolarity (mOsm/L)
900
1150
1400
2100
Pack Size (L)
1, 2
1, 2
1, 1.5, 2
1, 1.5
Shelf life (yr)
1.5
<25
<25
<25
<25
Storage temp (oC)
Shelf lives after allowed additions of

electrolytes, vitamins, and trace
elements
Shelf life after mixing + additions (lipids,
Original shelf life electrolytes, vitamins, trace elements)
Nutriflex peri 24 months at < 25C
6 days at 2-8C + 48 h at room temp.
a) b)
Nutriflex basal24 months at < 25C

b)
Nutriflex plus 24 months at < 25C

c)
Nutriflex special
18 months at < 25C
c)
a) With Lipofundin MCT/LCT 10% and no further electrolyte additions only 48 h at room temperatu
b) Only with Lipofundin MCT/LCT 10% and 20%. With Lipofundin N 20% and Intralipid 20% onl
temperature.
c) Only with Lipofundin MCT/LCT 10% and 20%. With Lipofundin N 10%/20% and
Intralipid 20% limitation to 48 hours at room temperature.
Allowed additions of vitamins and

trace elements
to Nutriflex regimens with lipids
Tracutil or Vitalipid SoluvitCernevit
Unit (ml) Additrace N Adult
Nutriflex peri 2000 + 500a)
Nutriflex basal2000 + 500a)
Nutriflex plus 2000 + 500b)
Nutriflex special
1500 + 500b)
a) Lipofundin MCT/LCT 10% and 20%, Lipofundin N 20%, Intralipid 20%.

b) Lipofundin MCT/LCT 10% and 20%, Lipofundin N 10% and 20%, Intralipid 2
Allowed electrolyte additions to

Nutriflex regimens with lipids
Maximal final content (mmol)
Unit (ml)
Na+ + K+Mg2+
Ca2+ Phosphate (i + o)
Nutriflex peri 2000 + 500a)
200c)
15
15
11.4 + 4.8d)/7.3e)
Nutriflex basal 2000 + 500a)
400
20
20
25.6 + 4.8d)/7.3e)
Nutriflex plus 2000 + 500b)
400
20
20
40
Nutriflex special
1500 + 500b)
300
15
16
22.1 + 4.8d)/7.3e)
+ 4.8d)/7.3e)
a) Lipofundin MCT/LCT 10% and 20%, Lipofundin N 20%, Intralipid 10% and 20%.
b) Lipofundin MCT/LCT 10% and 20%, Lipofundin N 10% and 20%, Intralipid 20%.
c) Limitation in order to maintain possibility of peripheral administration, not due to instability.
d) Organic phosphate from 10% lipid emulsions.
e) Organic phosphate from 20% lipid emulsions.
Nutriflex Lipid
Handling NuTRIflex Lipid
1. Always start by
pressing the upper left
chamber (glucose) to mix
with the lower chamber
(amino acids).
2. Add electrolytes and

trace elements via the
additive port (red cap).
3. Finally, press the upper

right chamber containing
MCT/LCT lipid emulsion to
mix with the lower
chamber. Add vitamins.
Mix thoroughly before inserting the giving

set.
5. To save space, fold the bag

and hang it on the drip stand
using the loop.
Port system
Low risk for needle stick
injury
Easy to grip and firm
fitting
No leakage after removal
Stable ports
made of hard
plastic
Self-sealing
Other products
Small overly pliable ports with

increase risk of needlestick
injuries
Features of bag materials and

handling
Feature
NuTRIflex
Lipid
Clinomel / Kabiven /St

OliClinomel ructoKabiv
en
Co-extruded bag
foil
Yes
Not known
Not known
Free of latex
Yes
Yes
Yes
Additions to the
lipid-free
mixture
Possible
&
easy
Possible
but difficult
Impossible
Shelf life at 20oC
24 months
24 months
24 months
Functionality of
peel seals
Tight, easy
to open
(Too) easy
to open
Tight, easy
to open
Easy, by
hand
Easy, by
hand
Easy, by
hand
Opening of
protective
overwrap
NuTRIflex Lipid - the material (V90)

PVC free
Three-layer film (co-extruded):
Exterior:
Polyamide
Medial:
Polypropylene extrusion binder
Interior:
Polypropylene
No adhesive between the film layers
Polypropylene is inert to solution components - in
particular to lipids
Can be heat sterilised in autoclaves
Fulfils ecological criteria
Harder than PVC. This together with the overwrap
(V97d) provides optimal protection against the
infiltration of atmospheric oxygen and easy
opening of the peel seam
No aluminium foil packaging is necessary
Properties of the multilayer foil

The lower the water and oxygen permeability the
better
NuTRIflex
Kabiven Oliclinome
Lipid
l
H 20
permeability
(g/m2/d)
0.25
O2
permeability
(mL/m2/d)
150
0.66
1.79
1570
1380
Dupertuis et al., 2005, JPEN 29/2, 125130Data from
NuTRIflex Lipid
Prospective comparative study on administration
time of TPN
2000
Time in
sec
1600
1200
800
1524
312
1221
48
675
95
400
0
Single Bottle Hospital

NuTRIflex
System Compounding
Lipid
Pichard et al. (2000), Clin Nutrition 19, 245-251
NuTRIflex Lipid
Prospective comparative study on application
costs of TPN
costs in %
200
150
100
150 %
120
%
100 %
50
0
Single Bottle
Hospital
NuTRIflex
System
Compounding
Lipid
Pichard et al. (2000), Clin Nutrition 19, 245-251
NuTRIflex Lipid Regimens
Additional additives
Shelf lives of NuTRIflex Lipid after

additions of electrolytes, vitamins ,
and trace elements
NuTRIflex Lipid
peri
NuTRIflex Lipid
plus
NuTRIflex Lipid
plus
without electrolytes
NuTRIflex Lipid
special
NuTRIflex Lipid
special without
electrolytes
Original shelf life Shelf life after mixing + additions

(electrolytes, vitamins, trace
elements)
24 months at
4 days at 2-8C + 48 h at room
<25C
temp
24 months at
<25C
temp
24 months at
<25C
temp
24 months at
<25C
24 months at
<25C

temp
temp
Multichamber bags target

Possible with ~ 80 % of adult patients who are
stable
Target areas of Nutriflex and NuTRIflex Lipid
- intensive care wards
- surgical wards
- medical wards
- pharmacy
- out patient markets - Home TPN
Not possible neonates and infants less than
2 years old
Advantages of the NuTRIflex Lipid

system
Chamber configuration assures safe mixing the
only multichamber bag system that allows
admixture according to compounding guidelines
Special port system provides easy grip, prevents
needle injuries and no leakage after removal
Range of products provides well balanced
compositions of protein and energy for patients in
ICU and general wards

Electrolytes content covers basic requirements,
reducing the need for further additions, although
compatibility and stability data offer safe limits for
additions
Only system that comes with Lipofundin MCT/LCT
(3-chamber bag)
Additional Information from B.Braun

Product Consultant

Recommended dosages, adults
Nutrient
a)
Dosage per kg and day
ASPEN
dosage guidelines
Water
35 - 45 ml
Na+
1 - 3 mmol
K+
1 - 1.5 mmol
Mg2+
0.05 - 0.1 mmol
Ca2+
0.05 - 0.1 mmol
Cl1 - 3 mmol
Cl-/Acetate
1 : 1 ratio
Phosphate
0.2 - 0.5 mmol
Amino acids
1.0 2.0 g
Glucose
3.0 5.0 g
Lipids
0.5 2.0 g
Total energy
25-40 kcal
Vitamins
see appendix
Trace elements see appendix
b)
20 - 40 ml/kg and day

1 - 2 mmol/kg and day + replacem
1 - 2 mmol/kg and day
4 - 10 mmol/day
5 - 7.5 mmol/day
no entry
As needed to maintain acid-base
20 - 40 mmol/day
0.8 2.0 g
< 7.0 g
< 2.5 g
25-30 kcal/kg and day
see appendix
see appendix
a) Diverse sourcesb) JPEN 22 (1998) 49-66

Water and electrolytes, children
For body weight:
< 1500 g
1500 - 2000 g
2.5 - 10 kg
> 10 - 20 kg
> 20 kg
Daily water:
120 - 150 ml/kg
110 - 130 ml/kg
100 ml/kg
1000 ml for 10 kg + 50 ml/ kg for each kg > 10
1500 ml for 20 kg + 20 ml/ kg for each kg > 20
Electrolytes:
Neonates
Infants/childrenAdolescents
Na+ (mmol)
2 - 5 /kg x day
2 - 6 /kg x day Individualised
K+ (mmol)
1 - 4 /kg x day
Mg2+ (mmol) 0.15 - 0.25 /kg x day
0.15 - 0.25 /kg x day5 - 15/day
Ca2+ (mmol)
1.5 - 2.0 /kg x day
0.5 - 1.25 /kg x day 5 - 10/day
Cl- (mmol)
1 - 5 /kg x day
Phosphate (mmol) 1 - 2 /kg x day 0.5 - 1 /kg x day 10 - 40/day
JPEN 22 (1998) 49-66

Calorific nutrients, children
Calorific nutrient
Dosage
a) b)
Protein
Neonates
Infants
Children
Adolescents
2.5 - 3.0 g/kg x day

2.0 - 2.5 g/kg x day
1.5 - 2.0 g/kg x day
0.8 - 2.0 g/kg x day
NP calories
< 6 months 120
6 - 12 months
90
1 - 7 years
80
7 - 12 years
60
> 12 - 18 years 30
Lipids
< 4 g/kg x day for neonates
140 kcal/kg x day

120 kcal/kg x day
100 kcal/kg x day
75 kcal/kg x day
60 kcal/kg x day
< 3 g/kg and day for SGA neonates and

preterm neonates less than 32 weeks GA
a) JPEN 22 (1998) 49-66

Calorific nutrients, children
Calorific nutrient
Dosage
a) b)
Total calories
Preterm neonate
85 - 150
Term neonate
100 - 120
Infants
80 - 100
Children 1 3 years 75 - 90
Children 4 - 6 years 65 - 75
Children 7-10 years 55 - 75
Children 10
40 - 60
- 18 years
kcal/kg x day
kcal/kg x day
kcal/kg x day
kcal/kg x day
kcal/kg x day
kcal/kg x day
kcal/kg x day
Protein
Infant/child (< 11 years)

2.0 3.0
Adolescent (> 11 years)
1.5 2.5
g/kg x day
g/kg x day
Glucose

~ 14.4 20.2g/kg x day
max. ~ 8.6 g/kg x day
Lipids

3.0 (max. 4.0)
g/kg x day
2.5 3.0
g/kg x day
S. ACRA; Pediatric Annals 28 (1999) 113-120

Vitamins
a)
Children Children
> 11 years
Vitamin
0 - 10 years and adults b)
Retinol (I.U.) c)
230
3330
a) Per kg body weight
Calciferol (I.U.) d)
40
200
and day. For a body
Tocopherol (I. U.) e) 0.7
10
weight > 10 kg dose
as
Phylloquinone (mg) 0.02
f)
for 10 kg
Ascorbic acid (mg)
8
100
b) Per day
Folic acid (g)
14
400
c) 1 I. U. = 0.3 g
Niacin (mg)
1.7
40
retinol
Riboflavin (mg)
0.14
3.6
d) 40 I. U. = 1 g
Thiamine (mg)
0.12
3.0
calciferol
Pyridoxine (mg)
0.1
4.0
e) 1 I. U. = 1 mg D,LCyanocobalamin (g) 0.1
5.0
tocopheryl acetate
Pantothenic acid (mg)0.5
15
or
Biotin (g)
2
60
0.67 mg D--
tocopherol
AMA/NAG, JPEN 3 (1979) 258-265
f) 2 - 4 mg once a

Trace elements
Adults
1) 2)
mg/d
Preterm Term
Children 3)
infants 3) infants 3) g/kg x d
g/kg x dg/kg x d (max. per d)
Iron
Zinc
Copper
0.5 - 5.0 200 a)

2.5 - 4.0 400
0.5 - 1.5 20
Chromium 0.01 - 0.02 0.20
Manganese 0.15 - 0.8 1.0
Molybdenum0.01 - 0.03 0.25
0.02 - 0.05 2.0
Selenium
Iodide
Fluoride
0.07 - 0.3
0.5 - 1.0
1.0
e)
100 b)
250 c)/100
20
0.20
1.0
0.25
2.0
1.0
e)
d)
no data
20 (300)
0.20 (5.0)
0.20 (5.0)
1.0 (50)
0.25 (5.0)
2.0 (30)
1.0 (1.0)
e)
a) Starting 2nd month

or after reaching
2000 g bw
b) Not in the
1st three months
c) For age up to
three months
d) If older than three

months
e) Insufficient data
available. Oral
recommendations
are deemed to be
appropriate also
for PN
1) K. N. Jeejeebhoy, New Aspects of Clinical Nutrition (1983) 1 24

2) T. G. Baumgartner, Clinical Guide to Parenteral Micronutrition (1984)
3) H. L. Greene et al., Am. J. Clin Nutr. 48 (1988) 1324-1342
Product composition: Standard AA

formulations
B. Braun
Aminoplasmal-
FreAmine
5% E 10% 10% E12.5% E15% 15% E III
14
Number of amino acids
20
20
20
20
18
18
97
Amino acids
(g/l)
50
100 100
125
150
150
15.3
Nitrogen
(g/l)
8
16
16
20
24
24
0
Carbohydrate
(g/l)
0
0
0
0
0
0
388
Total calories
(kcal/l) 200 400 400
500
600
600
10
Sodium
(mmol/l) 43 0
43
43
0
50
0
Potassium
(mmol/l) 25
0
25
25
0
30
0
Magnesium
(mmol/l) 2.6
0
2.6
2.6
0
2.6
0
Calcium
(mmol/l) 0
0
0
0
0
0
20
Inorganic phosphate
(mmol/l) 9
0
9
9
0
9
<3
Chloride
(mmol/l) 29
57
57
72
0
36
0
Anionic acetate (mmol/l) 59
0
59
59
0
35
950
Osmolarity
(mOsm/l)590 885 1035 1250 1290 1480
Product composition: Lipids

Lipofundin N and Lipofundin
MCT/LCT
N
10%
Soya oil (g/l)
Medium-chain
triglycerides (g/l)
Egg yolk
phospholipids (g/l)
Glycerol (g/l)
-Tocopherol (mg/l)
Osmolarity (mOsm/kg)
Calories (kcal/l)
100
200
50
100
50
100
12
12
25
25
25
25
90 + 20 180+ 4085 + 20170+ 40
350-380290-320 345 a) 380 a)
1072
2008
1022
1908
Phosphate equivalents (mmol/l)

9.7
a) mOsm/l.
Lipofundin
N
MCT/LCT
MCT/LCT
20%
10%
20%
14.5
9.7
14.5
Product composition: 2-chamber bags

(B. Braun)
Nutriflex, 1000 ml
Nutriflex/... without el.

Total volume (ml)
Amino acids (g)
Nitrogen
(g)
Glucose
(g)
Glucose calories
(kcal)
Total calories (kcal)
Sodium
(mmol)
Potassium
(mmol)
Magnesium (mmol)
Calcium
(mmol)
Zinc
(mmol)
Chloride
(mmol)
Phosphate
(mmol)
Acetate (anionic)
(mmol)
Osmolarity
(mOsm/l)
peri
1000
40
5.7
80
320
480
27
15
4.0
2.5
0
31.6
5.7
19.5
900
basal
1000
32
4.6
125
500
630
49.9
30
5.7
3.6
0
50
12.8
35
1140
plus
1000
48.1
6.8
150
600
790
37.2/0
25/0
5.7/0
3.6/0
0
35.5/0
20/0
22.9/0
1400/1250
special
1000
70
10.0
240
960
1240
40.5/0
25.7/0
5.0/0
4.1/0
0
49.5/0
14.7/0
22/0
2100/1940

(B. Braun)
Nutriflex, 1500 ml and 2000 ml
Nutriflex/...without el.
peri
Total volume (ml)
2000
Amino acids (g)
80
Nitrogen
(g)
11.4
Glucose
(g)
160
Glucose calories
(kcal)
640
960
Sodium
(mmol)
54
Potassium
(mmol)
30
Magnesium (mmol)
8.0
Calcium
(mmol)
5.0
Zinc
(mmol)
0
Chloride
(mmol) 63.2
Phosphate
(mmol) 11.4
Acetate (anionic)
(mmol)
39
Osmolarity
(mOsm/l) 900
basal
plus
plus
special
1500
2000
2000
1500
64
72.2
96.2
105
15.0
9.2
10.2
13.6
360
250
225
300
1440
1000
900
1200
1260
1185
1580
1860
99.8
55.8/0
74.4/0
60.8/0
60
37.5/0
38.6/0
50/0
11.4
8.55/0
7.5/0
11.4/0
7.2
5.4/0
7.2/0
6.15/0
0
0
0
0
100
53.3/0
71/0
74.3/0
25.6
30/0
40/0
22.1/0
70
34.4/0
45.8/0
33/0
1140 1400/1250 1400/1250 2100/19
40

(B. Braun)
NuTRIflex Lipid peri
NuTRIflex Lipid peri
1250 ml 1875 ml 2500 ml

Total volume (ml)
2500
1250
1875
Amino acids (g)
60
80
40
Nitrogen
(g)
5.7
8.6
11.4
Glucose
(g)
80
120
160
50
Lipids
(g)
75
100
Glucose calories
(kcal)
320
480
640
Lipid calories (kcal)
475
715
950

955
1435
1910
Sodium
(mmol)
50
75
100
Potassium
(mmol)
30
45
60
Magnesium (mmol)
3.0
4.5
6.0
Calcium
(mmol)
3.0
4.5
6.0
Zinc
(mmol)
0.03
0.045
0.06
Chloride
(mmol)
48
72
96
Phosphate (i +(mmol)
o)
7.5 + 3.6 11.3 + 5.4 15 + 7.3
Acetate (anionic)
(mmol)
40
60
80
Osmolality
(mOsm/kg) 920
920
920
No electrolyte-free version available.
Lipids:
Lipofundin
MCT/LCT 20%

(B. Braun)
NuTRIflex Lipid plus
NuTRIflex Lipid plus/...without el.
1250 ml
1875 ml
Total volume (ml)
1250
1875
Amino acids (g)
48
72
Nitrogen
(g)
6.8
10.2
Glucose
(g)
150
225
Lipids
(g)
50
75
Glucose calories
(kcal)
600
900
475
715

1265
1900
Sodium
(mmol)
50/0
75/0
Potassium
(mmol)
35/0
52.5/0
Magnesium (mmol)
4.0/0
6.0/0
Calcium
(mmol)
4.0/0
6.0/0
Zinc
(mmol)
0.03/0
0.045/0
Chloride
(mmol)
45/0
67.5/0
o)
18.6/3.6
27.9/5.4
Acetate (anionic)
(mmol)
45/0
67.5/0
Osmolality
(mOsm/kg)
1540/1350 1540/1350
2500 ml
2500
96
13.6
300
100
1200
950
2530
100/0
70/0
8.0/0
8.0/0
0.06/0
90/0
Lipids:
37.3/7.3
Lipofundin
90/0
1540/1350 MCT/LCT 20%
Value after the slash for the electrolyte-free version.

(B. Braun)
NuTRIflex Lipid
special
NuTRIflex Lipid special/...without el.
1250 ml
1875 ml
Total volume (ml)
1250
1875
Amino acids (g)
71.8
108
Nitrogen
(g)
10.0
15.0
Glucose
(g)
180
270
Lipids
(g)
50
75
Glucose calories
(kcal)
720
1080
475
715

1475
2215
Sodium
(mmol)
67/0
100.5/0
Potassium
(mmol)
70.5/0
47/0
Magnesium (mmol)
7.95/0
5.3/0
Calcium
(mmol)
7.95/0
5.3/0
Zinc
(mmol)
0.06/0
0.04/0
Chloride
(mmol)
90/0
60/0
o)
23.6/ 3.6
35.4/5.4
Acetate (anionic)
(mmol)
60/0
90/0
Osmolality
(mOsm/kg)2090/1840 2090/1840
2500 ml
2500
144
20.0
360
100
1440
950
2950
134/0
94/0
10.6/0
10.6/0
0.08/0
120/0
Lipids:
47.3/7.3
Lipofundin
120/0
2090/1840 MCT/LCT 20%
Value after the slash for the electrolyte-free version.
List of abbreviations
a = Age
AA
= Amino acids
AAA
= Aromatic amino acids
Ac
= Acetate
Ac-CoA
= Acetyl coenzyme A
AEE
= Actual energy expenditure
AEEestim.. = Measured actual energy
expenditure
AIDS
= Acquired immunodeficiency
syndrome
Ala
= Alanine
Ala-Gln = Alanyl-glutamine
ALAT
= Alanine amino transferase
ALB-FA
= Albumin-Fatty acids-Complex
Apo-CII = Apolipoprotein CII
approx. = Approximately
ARF
= Acute renal failure
Arg
= Arginine
ASAT
= Aspartate amino transferase
Asp
= Aspartic acid
ATP
= Adenosine triphosphate
= Alpha
BCAA
=
BMR
=
BSA
=
BUN
=
BUNE
=
hours
BUNS
=
bw
=
C = Carbon
C
=
2+
Ca/Ca
=
C. albicans
C-C
=
CFU
=
CIT
=
Cl/Cl=
cm
=
CMR
=
CNS
=
CO2
=
COOH
=
3+
Cr/Cr
=
Cu/Cu2+ =
CVC
=
Branched-chain amino acids

Basal metabolic rate
Body surface area
Blood urea nitrogen
Blood urea nitrogen after 24
Blood urea nitrogen at 0 hours
Body weight
Degrees Celsius
Calcium
= Candida albicans
Carbon-Carbon bond
Colony-forming unit
Citrate
Chloride
Centimetres
Chylomicron remnants
Central nervous system
Carbon dioxide
Carboxylic group
Chromium
Copper
Central venous catheter
d = Day
dl = Decilitre
= Delta (difference)
+ e.
= with electrolytes
EAA
= Essential amino acids
EAA + His= Essential amino acids plus
histidine
E. coli
= Escherichia coli
EEAA
= Energy expenditure from amino
acids
e.-fr.
= Electrolyte-free
e.g.
= For example (exempli gratia)
EN
= Enteral nutrition
etc.
= And so on (et cetera)
EVA
= Ethyl vinyl acetate
F/F
= Fluoride
FA
= Fatty acid
3+
Fe/Fe
= Iron
FQ
= Fischer quotient
Ftbw
= Factor for total body water
g = Gramme
gN
= Grammes of nitrogen
GA
= Gestational age
GAP
= Glyceryl aldehyde phosphate
GI
= Gastrointestinal
GLC
= Glucose
GLC : LIP = Glucose : Lipid calorie ratio
g/d
= Grammes per day
g/kg
= Grammes per kilogramme body
weight
g/kg bw = Grammes per kilogramme body
weight
g/kg bw x d
= Grammes per kg body
weight and day
g/kg bw x h
= Grammes per kg body
weight and hour
g/kg x d = Grammes per kg body weight and
day
g/l
= Grammes per litre
Gln
= Glutamine
Glu
= Glutamic acid
Gly
= Glycine
GLY
= Glycerol
Gly-Gln = Glycyl-glutamine
GLY-P
= Glyceryl phosphate
Gly-Tyr
= Glycyl tyrosine
2
g/m BSA = Grammes per square meter body
surface area
-GT
= Gamma-glutamyl transpeptidase
h = hour
H = Hydrogen
HBC
= High branched-chain
HCO3= Hydrogen carbonate
(bicarbonate)
HE
= Hepatic encephalopathy
H2PO4
= Dihydrogen phosphate
(inorganic phosphate)
H2SO4
= Sulphuric acid
His
= Histidine
HL
= Hepatic lipase
H2 O
= Water
ht= height
I = Iodine
ICU
= Intensive care unit
i.e.
= that is (id est)
Ile
= Isoleucine
i. + o.
= Inorganic and organic
I. U.
= International units
i. v.
= Intravenous
JPEN
= Journal of Parenteral and
Enteral
Nutrition
K/K+
= Potassium
KB
= Ketone bodies
kcal
= Kilocalories
kcal/d
= Kilocalories per day
kcal/g
= Kilocalories per gramme
kcal/kg
= Kilocalories per kg body
weight
kcal/kg bw
= Kilocalories per
kg body weight
and
day
kcal/kg bw x d = Kilocalories per kg
body
weight and day
kcal/l
= Kilocalories per litre
kcal/ml
= Kilocalories per millilitre
kcal%
= Percent of total
kilocalories
kg
= Kilogramme
kJ
= Kilojoules
kJ/l
= Kilojoules per litre
l
= Litre
mg/d
= Milligrammes per day
LAC
= Lactate
mg/dl
= Milligrammes per decilitre
LAK
= Lymphokine-activated killer
mg/kg bw x d
= Milligrammes per kg body
LCFA
= Long-chain fatty acids
weight
and day
LCFA-CoA = Long-chain fatty acids coenzyme A
Mg/Mg2+ = Magnesium
LCFA-Carn...
= Carnitine ester of LCFA
MG
= Monoglyceride
LCT= Long-chain triglycerides
min
= Minutes
Lctl.
= Lactulose
ml
= Millilitres
Leu = Leucine
ml/kg
= Millilitres per kg body weight
LIP = Lipids
ml/kg bw x min = Millitres per kg body
log = logarithmic
weight per
minute
LPL = Lipoprotein lipase
mm3
= Cubic millimetres
LPS = LIpopolysaccharide
mmol
= Millimoles
Lys = Lysine
mmol/l
= Millimoles per litre
m2 = Square metres
2+
Mn/Mn
= Manganese
max.
= maximally
Mo
= Molybdenum
MCFA
= Medium-chain fatty acids
= Milliosmoles
MCFA-CoA= Medium-chain fatty acids coenzyme A mOsm
mOsm/kg = Milliosmoles per kg solvent
MCT
= Medium-chain triglycerides
Met= Methionine
mOsm/l = Milliosmoles per litre of solution
mg = Milligrammes
MR
= Metabolic rate
g = Microgrammes
g/kg x d = Microgrammes per kg body weight
and
day
m = Micrometres
mol
= Micromoles
mol/l
= Micromols per litre
N = Nitrogen
Na/Na+
= Sodium
Nbal = Nitrogen balance
NBT
= Nitroblue tetrazolium
NEAA
= Nonessential amino acids
Neom.
= Neomycin
NH3 = Ammonia
Nin = Nitrogen intake
NK = Natural killer cells
N/kg bw = Nitrogen per kg body weight
Nout = Nitrogen loss
no. = Number
NP = Nonprotein kilocalories
NP-kcal/g N
= Nonprotein kilocalories per
gramme N
n. s.
= not significant
O/O2
= Oxygen
OA
= Oxaloacetate
OP
= Oligopeptides
Orn
= Ornithine
orig. + add.
= Originally contained
plus additions
p<
= Probability of error lees than
p>
= Probability of error more than
P = Phosphate
P. aeruginosa = Pseudomonas aeruginosa
pH
= Potentia hydrogenii
Phe
= Phenylalanine
Pi = Inorganic phosphate
PICC
= Peripherally inserted central
catheter
PL
= Phospholipids
PN
= Parenteral nutrition
p. o. day = Postoperative day
Pro
= Proline
PT
= Prothombin time
PYR
= Pyruvate
RBC
= Red blood cells
RBP
= Retinol-binding protein
REE
= Resting energy expenditure
Ren. med.= Renal medulla
RQ
= Respiratory quotient
S
= Sulphur
S. aureus = Staphylococcus aureus
SCFA
= Short-chain fatty acids
SCT
= Short-chain triglycerides
Se
= Selenium
Ser
= Serine
SGA
= Small for gestational age
SIRS
= Systemic inflammatory
response
syndrome
SLd
= Defined structured lipids
SLr
= Randomised structured
lipids
SPC
= Summary of product
characteristics
suppl.
= Supplement
Tau
TBARS
= Taurine
= Thiobarbituric acid reactive
substances
temp.
= Temperature
TF
= Thermal factor
TG
= Triglycerides
TH
= T-helper cell
TH/TS
= T-helper to T-suppressor cell ratio
Thr
= Threonine
TPN
= Total parenteral nutrition
tot. en.
= Total energy
Try
= Tryptophan
TS = T-suppressor cells
Tyr
= Tyrosine
U = Units
U/l
= Units per litre
UUN
= Urinary urea nitrogen
Val
= Valine
VCO2
= Volume of expired carbon dioxide
VLDL
= Very low density lipoproteins
VO2
= Volume of consumed oxygen
vs.
= versus
= Omega
Zn/Zn2+ = Zinc

Basic Concepts On Parentheral Nutrition by Irfan

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Basic Concepts On Parentheral Nutrition by Irfan

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Basic Concepts in Parenteral Nutrition

- differentiation of MCT/LCT vs LCT

Energy stores of an adult

Net body protein

Caloric value of nutrients

(10% emulsion: 1.1 kcal/ml)

Basic Scheme of Metabolism

ketone bodies e.g

Metabolic changes during starvation

Energy source: AA:

Phases of the stress response after

Starvation and stress on energy

Long (1977) Am. J. Clin. Nutr. 30, 1301-1310

Daily nitrogen losses in adults

1 g N 6.25 g protein 30 g muscle

Consequences of metabolic changes

Severe wasting of lean body mass

Impact of pre-existing malnutrition

Correia & Waitzberg (2003) Clin Nutr 22, 235-239

Objective of nutrition therapy

Possible indications for clinical

- oropharyngeal trauma - renal failure

- head injuries, neurosurgery,

Medical history, disease severity

- body mass index (BMI)

Energy requirements during metabolic

- has about 95% accuracy

- machine not always available

Basal metabolic rate

Actual energy expenditure

Concept of nutritional support

Nutritional support can be given either enterally or

Key question: Does the patient have a

Enteral: If the gut can be used safely, use it

Clinical decision making for nutrition

JPEN 17 (Suppl 4):7SA, 1993

When to start parenteral nutrition

- when the patient is in a stable haemodynamic

Contraindications for specific nutrients

Types of parenteral nutrition

Parenteral nutrition - Infusion

Sandstrom et al. (1995) JPEN 19, 333 - 340

Nitrogen balance after continuous, bolus or

Sandstrm et al. (1995) JPEN 19, 333-340

Amounts and concentrations

N intake = 16 g, non-protein calories ~125 kcal/g N

Example 1 Calculate energy and protein requirments by Harris-B

Dosage recommendations for PN

Recommended dosages, adults

20 - 40 ml/kg and day

a) Diverse sourcesb) JPEN 22 (1998) 49-66

Parenteral nutrition - Electrolytes

Parenteral nutrition Micronutrients:

can have major consequences

Water soluble vitamins

Dosage recommendations for PNVitamins

AMA/NAG, JPEN 3 (1979) 258-265

Micronutrients Trace elements

Manganese (Mn) Iodine (I)

Dosage recommendations for PN

0.5 - 5.0 200 a)

d) If older than three

1) K. N. Jeejeebhoy, New Aspects of Clinical Nutrition (1983) 1 24