P R A N I T H I H O N G S P R A B H A S M D .

Year
1628
1662
William Harvey
Lower
Discovery of circulation
Blood transfusion of sheep to young man
1665
1712
1818
1831-32
1873
1869
1904
Christopher Wren
William Courten
Blundell
Latta
Edward Hodder
Infusion of wine, ale, opiates in dogs
(same inebriating effect as oral form)
Infused olive oil in dogs:
(Severe respiratory distress from fat emboli)
Suggest possibility of blood transfusion in pt with bleeding in ICU
Saline infusion in cholera patients
(Rapid improvement)
Infuse fat in form of milk in 3 cholera pts
(2 recovered completely, 1 died)
Menzel and Perco Give fat subcutaneously to dogs
(feasible)
Paul Friedrich Subcutaneous administration of nutrients
(Painful)
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

1859 Claude Bernard Le milieu interior/ importance of glucose for metabolism
1896
1915
Beidl and Krauts
Woodatt
Matas
Zimmerman
First infuse glucose in human (200-300 ml of 10% glucose solution)
Febrile reaction: glucose fever
Constant infusion of glucose by pump, varied infusion rate to establish dose response relationship of urinary glucose excretion
Continuous glucose drip 1924
1945 Infuse IV solution through IV catheter placed in SVC
1944-52 Danis and Kalson Infuse 20% glucose along with vitamins, electrolytes and plasma in IBD patients
1968 Dudrick and
Wilmore
Long term PN in dog
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

1930 Whipple, Holman,
Madden
Albright
Yuilie
Allen
Protein requirement of dog could be provided by infusing plasma protein by vein during free protein diet
Metabolic fate of infused plasma protein in humans and demonstrate + N balanced
Infused labeled plasma protein in dogs and found gradual  tissue radioactivity and fall of 14 CO
2
Growth of puppies achieved by provision of IV plasma protein
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

Protien Hydrolysates and Crystalline Amino
Acids
1913
1930
1937
1944
Protein hydrolysate
Henriques and Anderson Infused beef hydrolysate into goat and achieved +N balance
Vanslyke and Meyer
Rose
Metabolism of aa obtaind from hydrolysis of casein or beef protein infused into dogs
Determine EAA in humans and proposed ideal mixture of aa that could be support protein syntlesis in healthy adults
Elman
Father of IV nutrition
Wretlind
Vitrum Co.
Sweden
Aboot Co.
IL
Infuse aa in form of fibrinogen hydrolysate in man
Protein hydrolysate marketed ‘ AMINOSOL ’ cacein hydrolysed enzymatically and dialysed)
Hydrolysate of cacein ‘AMINOSOL’
Disadvantage aa pattern could not be changes
Advantage Contained all aa. Required for protein synthesis
Polypeptided contained abundant of Gln
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

Protien Hydrolysates and Crystalline Amino
Acids
1964
Late
1969
1970
Bansi
Writlind
Introduced crystalline aa. (base on
Rose’s work: AA requrrement of man)
More complete crystalline aa solution
‘Vamin”
More effective in postop N balance
Protein hydrolysate disappear
It was difficult to include Tyr, Cys, cystine, Gln in aa. Solution (technical reason)
1980 Furst Glutamin dipeptide (Gln-Tyr)
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

Positive N Balance In Cancer Patients Receiving
Addition Of Cacein Hydrolysate To An Infusion
Of Glucose

1920-1960
1961
1962
1968
USA and Japan
Upjohn Co USA
Wretlind and Schuberth
Vitrum Co
Sweden
Dudrick
Dudrick
Swedish
Rhoads
Developed and tested fat emulsion
Lipomul eas poduced
Adverse effects: (chill, fever, hypoxia and hypotension)  withdrawn
Fat emulsion prepared from soybean oil and eff yolk phospholipid: safely infused
Commercialization ‘Intralipid’
First symposium of parenteral nutrition
Arvid Wretlind: ‘father of complete parenteral nutrition’
First report of long term growth and survival in puppies with puppies with IV feeding using CVC
High dose of glucose without fat, aa, other nutrient
Glucose system
½ of calories as lipid, and the remainder as gulcose
Fat system
Depleted or hypermetabolic pts should receive more than requirements ‘ hyperalimentation’
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

1937
1953
1961
1968
1974
1976
1984
Eman
Seldinger
Schuberth &
&Wretlind
Dudrick
Solassol
Many authers
Rhoads
Many authers
Successful IV protein hydrolysate in man
Describe catheter over wire technique
Development of a safe IV fat emulsion
First report of long term growth and survival in puppies with puppies with IV feeding using CVC
Demonstrates that fat emulsions can be safely mixed with crystalline aa and dextrose solutions confirm that fat emulsions have equivalent N sparing effect as glucose
Depleted or hypermetabolic pts should receive more than requirements ‘hyperalimentation’
Confirm that few surgical patients will require more than 2000 kcal/d

• Energy
• glucose
• + intravenous lipid emulsion
• Nitrogen: aa, of peptides
• Water
• Mineral
• Vitamins
• Trace elements

Concepts and Considerations: CHO
Metabolism
Nitrogen sparing effect
• suppress endogenous glucose production: first few hrs
• direct infused glucose oxidation: several hrs, need insulin
• effect of insulin (minimal)
When load: RQ >1 = lipogenesis from CHO
• fatty liver
• increased metabolic rate: increased VO2, VCO2, water production
In catabolic stress
• insulin resistance:  glucose oxidation in insulin dependent tissue and prefer
FA for oxidative process
• GH resistance: attenuate protein synthesis
Glucose is major CHO used in PN
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

CHO Metabolism:
Glucose Infusion Rate
Glucose infusion
Basal
Optimum
Maximum mg/kg/min
2
4
7
Driscoll DF, et al in Rombeau JL, Rolandelli RH Clinical Nutrition: Parenteral Nutrition 2001

Infusion glucose
• Oxidative pathway
• Non oxidative pathway
• glycogen storage
• de novo lipogenesis
• other complications
Adverse Effect of Non
Oxidative Disposal of Glucose
• Hyperglycemia
• De novo lipogenesis
• Respiratory decompensation
• Fluid retention
• Electrolyte disorder

Adverse Effect of Non Oxidative Disposal of Glucose
De Novo Lipogenesis
• Fatty liver
• impaired liver function
• increased VCO
2
Respiratory Decompensation
• VCO
2
/VO
2
= respiratory
• glucose oxidation:
• RQ=1
• Lipid oxidation:
• RQ=0.7
• de novo lipogenesis RQ =8
RQ =2.4 in man
•  work of breathing and time in respirator

• Glucose infusion: hyperinsulinemia
• Insulin: antinatriuretic and antidiuresis effect
 fluid retention  cardiopulmonary dysfunction
• Insulin: anabolic effect
• K, Mg, P shift intracellularly

• Counter-regulatory hormones: cortisol, glucagon, E, NE
• Hepatic gluconeogenesis
• Peripheral insulin resistance
• Hyperglycemia
• Decrease glucose uptake (post receptor defect)
• Decreased glucose oxidation
• Decreased non oxidative glucose disposal:  glycogen synthetase activity

Glucose Is Not Metabolized Proportionally to the
Quantity Infused
4
3.5
3
2.5
2
Glucose infusion
There is physiological maximum to the amount of glucose oxidized in man
33.1%
32.4%
43.8%
43.7%
1.5
1
0.5
0
1m g/k g/m in 2m g/k g/m in 4 m g/k g/m in 4m g/k g/m in+ ins ulin
Wolfe et al, Metabolism 1979.

Glucose Oxidation in Various Conditions
4
3
6
5
2
1
0
Wolfe 1979, Nanni 1984, Nanni 1984 , Burke 1980
4
3.22
3.75
Normal
5.1
Nonseptic post op
Septic critically ill Burn injury

Exogenous Glucose And CHO
Administration
Normally
• CHO inhibit fat oxidation,  glucose oxidation and
 fat storage
In stress
• CHO: not effectively inhibit fat oxidation
• Not or minimally diminish rate of gluconeogenesis
•  feeding starved pt
• In hypermetabolic burn patients, glucose oxidation reaches a plateau of 5 mg/kg/min glucose infusion
Glucose tolerance : depends rate of infusion and underlying conditions
•  in stressed patients, DM, acute pancreatitis, and medications
Burke JF, Wolfe RR, Mullany CJ, et al. Ann Surg. 1979;190:274–285.

• CHO should not exceed 7 g/kg/d 1
• Glucose infusion rate should be kept at ≤4 mg/kg/min 2
• In adult critically ill patients and should not exceed 60 % of total daily energy 2
1.ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA
2. Rosmarin DK, et al. Nutr Clin Pract. 1996;11:151–156.

Tappy er al, Crit Care Med 1998,26(5):860
150
100
50
0
300
VCO
2 ml/min
N.S
250
200
Basal TPN-L
P<0.02
Basal TPN-G

2
2
P<0.02
Tappy er al, Crit Care Med 1998,26(5):860

Tappy er al, Crit Care Med 1998,26(5):860
Energy expenditure kcal/min
1.4
1.35
1.3
1.25
1.2
n.s
1.15
1.1
1.05
TPN-L
Tappy er al, Crit Care Med 1998,26(5):860
P<0.03
TPN-G

Concepts and Considerations: Lipid
Metabolism
In catabolic stress
• increased fatty acid oxidation
• Eicosanoid and prostanoid production
 6: PG 2-series, TA 2-series, LTB 4-series
• thrombogenic
 3: PG 3-series, LTB 5-series
• bleeding diathesis
• What is  -3/  -6 optimal ratio???
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

• Peripheral lipolysis: FFA + glycerol
• Hormones: catecholamines, glucagon
• Cytokines: TNF , IL-1, IFN , IFN
• Lean > obese
• Visceral fat > subcutaneous fat
• FFA  β-oxidation:  Relative contribution of fat oxidation in EE
•  re-esterification of unoxidized FFA to TG
(liver)   VLDL production
•  LPL activity in sepsis: decreased clearance
 hypertriglyceridemia
Calder PC. Lipid and the critically ill patient. In: Cynober L, Moore FA (eds) Nutrition and critical care. Nestle
Nutriition workshop series clinical&performance program, vol 8: 75-98

• IV lipid emulsion
(IVLE): chylomicron like particle
• Chylomicron like particle: hydrolyzed by LPL
• Liposome: stimulate cholesterogenesis and accumulation of Lp-X

• Normally admin of LCT or MCT/LCT emulsion reduced glucose oxidation but not uptake
• Critically ill IVLE failed to suppress glucose oxidation 1
• Fat emulsions : well oxidized when admin to septic and trauma 2
• Pt with sepsis and MOFS efficiently metabolize IVLE 3
1 Tissot S et al. Am J Physiol 1995;269:E753-8.
2 Nordenstrom et al. Ann Surg 1982;196:221-31.
3 DrumlW et al. JPEN 1998.22:217-23

Omega-3 And Omega-6 Fatty Acids Pathways
In Humans

Glaser C, et al. Role of FADS1 and FADS2 polymorphisms in polyunsaturated fatty acid metabolism. Metabolism 2010;59 (7): 993- 99

Acute Inflammation : Physiologically Necessary To
Protection Host Against Infection/Injuries
• Activation of inflammatory cells: PMN
• Altered vascular permeability
• Activation of pro-inflammatory mediators
• Cytokines
• Chemokines
• Lipid mediators
• Steroid
• Growth factors
Lee HN, et al. Article in Press. Biochemical Pharmacology (2012)

• Down regulate of pro-inflammatory signaling and release of endogenous anti-inflammatory mediators
• After degrade pathogens by phagocytosis, PMNs, undergo apoptosis
• Macrophages engulf apoptotic PMNs (efferocytosis)
• Macrophages exit inflamed site by lymphatic drainage
Lee HN, et al. Article in Press. Biochemical Pharmacology (2012)

Lee HN, et al. Article in Press. Biochemical Pharmacology (2012)

• Dose response
• RES suppression when infusion >
0.13g/kg/hr 1,2
• No evidence of RES suppression when receiving lipid < 0.054 g/kg/hr 3
1 Seider DL, et al. JPEN 1989;13:614-9,
2 Jensen GL,et al.JPEN 1990;14:467-71,
3 Abbott WC, et al, Arch Surg 1984; 119: 1367-71

• Factors determining hyperTG
• amount
• rate of infusion
• Type of lipid: MCT vs. LCT
• amount of phospholipids/TG
• Consequence
• acute pancreatitis
• immunosuppression

Lipid Emulsion: Pulmonary Gas Exchange
Abnormality
• IVLE: linoleic : precursor of arachidonic acid
• Prostanoid 2-series: vasoactive
• PGE
2
, PC
2
: increased shunt
• TxA
2
: pulmonary hypertension

Hemodynamic And Gas Exchange Of IVLE
In ARDS
35
30
25
20
15
10
5
0
24.1
*
240
184
PaO2/FiO2
*
P<0.05
Qva/Qt (%)
* Before
During
After
*
149
179
156
MAP (mmHg) PVR (dyne*s/cm3)
Venus V et al. Chest 1989;95;1278-1281

LCT Vs. MCT Lipids In Patients With ARDS: Effects On
Pulmonary Haemodynamics And Gas Exchange
40
35
30
25
20
15
10
5
0
Before
During
After
*#
PaO2/FiO2
LCT
*
250
330
260
MPAP
*#
Faucher M et al. Chest
2003;124;285-291
Qva/Qt
40
35
30
25
20
15
10
5
0
PaO2/FiO2
260
270
250
MPAP
MCT
Intensive Care Med (1998) 24: 1029 ± 1033
Before
During
After
Qva/Qt

Lipid emulsion in ICU

• Ivle 0.8-1.5 G/Kg/D (Critical Care Should Not Exceed
1 G/Kg/D)
• 30-40% Of Total Calorie (≤30% 2 )
• Rate ≤ 0.12 G/Kg/Hr To Avoid Hypertg 3
• Prevent EFADS:
• 10%IVLE 500 Ml, 2-3/Wk
• 0.1g/Kg/D (Children)
• Monitor Triglyceride Level To Ensure Adequate Lipid
Clearance
1. ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA
2.Chan S, et al. Chest 1999;115:145S-148S.
3.Iriyama K, et al. Surg Today 1998;28:289–292.

Concepts and Considerations: Protein
Metabolism
Normal
• protein synthesis ~300 g/d
• very sensitive and highly regulated balance between synthesis and breakdown
In severe stress
•  muscle protein synthesis
•  protein breakdown
To minimized protein breakdown
• by analgesia, sedatives, temp control,  -blockade
To stimulate protein synthesis
• traditional PN not enough
• specialized aa: Gln
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

Protein Metabolism:  Liver Protein
Synthesis
Positive
• CRP
• Fibrinogen
• Prothrombin
• Antihemophilic
• Plasminogen
• Complement
• Haptoglobulin
• Ceruloplasmin
• ALB
• PAB
• TFN
• RBP
Negative
A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 3-37.

• Aim to attenuate breakdown of endogenous protein
• N- balance remains –ve into the convalescent stage
• Recommended 1.2-2.0 g/kg/d
• Higher amount do not promote further N retention
• Increase intake in external loss of protein: burn, CVVHD
Weissman C. Nutrition in the intensive care unit. Critical Care 1999;3:R67-R75
Barton RG. Nutr Clin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA

Definition: Total Parenteral Nutrition (TPN)
The administration of complete and balanced nutrition by IV infusion in order to support anabolism, body weight maintenance or gain, and nitrogen balance, when oral or enteral nutrition are not feasible or are inadequate

Nomenclature
• TPN: Total Parenteral Nutrition
• IVH: Intravenous Hyperalimentation
• TNA: Total Nutrient Admixture
• TPN: Total Parenteral Nutrition
• 3-In-1 Admixture
• All-In-One Admixture
• PPN: Peripheral Parneteral Nutrition or Partial
Parenteral Nutrition

• Intestinal obstruction
• Severe malabsorption syndromes: SBS(<100 cm small bowel remains)
• Proximal intestinal fistula
• Inflammatory bowel disease
• Severe paralytic ileus
• Severe pancreatitis with inadequate EN
• Practically all patients requiring nutrition support but can’t tolerate enteral feeds, or C/I to enteral feeding

• Conditions requiring complete bowel rest for prolonged periods
• Pre and post-operative support in patients with preexisting malnutrition, in whom GI function is impaired
• Malignancy undergoing treatment, surgery, radiation, chemo who are unable to obtain adequate nutrition by an enteral route

Unable To Meet Energy Requirements (Target Goal
Calories)
• ASPEN: not achieve target after 7-10 days by EN alone, consider initiating supplemental PN (E)
• Initiating PN prior 7-10 d: not improve outcome and may be detrimental to the patient
• In PCM: Initiate PN as soon as possible following admission and adequate resuscitation (C)
• ESPEN: not achieve target after 2 days, considered supplemental PN
Not expected to be on normal nutrition in 3days, consider PN within24-48 hr (EN C/I or not tolerate) (c)
(ESPEN)
ASPEN Guideline. JPEN 2009; 33; 277. ESPEN Guideline. Clin Nutr 2009;28:387-40.

• PPN vs. TPN
Veins
Osmolarity
Period
Central
Subclavian, jugular
>850 mosm/L
Long time (>2 weeks)
Peripheral
Basilic/cephallic
<850 mosm/L
Short term (<2 weeks)

Normal Diet TPN
• Carbohydrates………..........Dextrose
• Protein………………...........Amino Acids
• Fat………………………………….Lipid Emulsion
• Vitamins……………….........Multivitamin Infusion
• Minerals……………………Electrolytes and Trace elements

• Dextrose: 5-50%, provide 3.4 kcal/g
• Can be the only source of energy
• Closely related to solution osmolality
• Dextrose infusion rate should not exceed 5 mg/kg/min
Hill GL, et al. Br J Surg 1984;71:1

• Prevent EFADs: (4-10% of calrorie)
• Non-protein source of energy
• Recommended dose: 0.8-1.5 g/kg/day (~1g/kg/d)
• Available in 10%, 20% and 30% concentrations
• Included as LCT or a mix of MCT/LCT at 10% and 20%
• Added to basic PN solutions or administered individually
• Less hyperglycemia, lower concentrations of serum insulin
• Less risk of hepatic damage
• High doses can interfere with immune functions
• High infusion rates can affect respiratory functions
• Should be used with care in:
• Hyperlipidemia
• thrombocytopenia
• Critical illness
Trimbo SL, et al. Nutr Supp Serv 1986;6:18

• Zero gen: cotton seed oil: lipomul
• First gen:
• Soy base: intralipid, lipovenos
• Second gen:
• Mixed MCT/LCT, structure lipid (mixed MCT/LCT)
• Third generation
• Fish oil: omegaven
• Mixed: SMOF, lipidem (soy, MCT, fish oil)
• Concentration: 10%  1.1kcal/ml
20%  2 kcal/ml

Intravenous Lipid Emulsion In Critically Ill
Patients
• IVLE: provide energy and ensure essential fatty acid
• ESPEN: IVLE (LCT, MCT or mixed): 0.7-1.5 g/kg/d over
12-24 hr (B)
• Mixed MCT/LCT: well tolerate
• Olive oil base: well tolerate (B)
• Fish oil enriched lipid emulsion: effects on cell membrane and inflammation (B)
• ASPEN:
• In the first week ,PN without soy based lipids (D)
ASPEN Guideline. JPEN 2009; 33; 277. ESPEN Guideline. Clin Nutr 2009;28:387-40

• Standard
• Gen I: aminosol
• Gen II: amiparen, aminosteril, aminoplasma-l
• Disease specific
• Nephro formula
• Hepatic formula
• Glutamine –dipeptide
• Concentration
• 3, 3.5, 5, 7, 8.5,10, 15% concentration
• Provide 4kcal/g
6.25g/g N

• Conditionally indispensible amino acid
• Mechanism
• Systemic antioxidant effect
• Maintenance of gut integrity
• Induce heat shock proteins
• Fuel source for rapid replicating cell
• ESPEN CPG 2006:
• Gln should be added in
STD EN in Trauma and
Burn (A)
• Insufficient data for surgical or heterogeneously critically ill
• ASPEN CPG 2009
• Should be considered in burn, trauma, and mixed ICU patients (B)

• Fluid: 30 to 40 ml/kg
• Electrolytes
• Calcium, magnesium, phosphorus, chloride, potassium, sodium, and acetate
• Forms and amounts are titrated based on metabolic status and fluid/electrolyte balance
• Must consider calcium-phosphate solubility
• Use acetate or chloride forms to manage acidosis or alkalosis
• Vitamins
• Trace elements

• 2-in-1 solution of dextrose, amino acids, additives
• Typically compounded in 1-liter bags
• Lipid is delivered as piggyback daily or intermittently
• Total nutrient admixture (TNA) or 3-in-
1
• Dextrose, amino acids, lipid, additives are mixed together in one container
• Lipid is provided as part of the dailyPN mixture  Important energy substrate

Advantage Disadvantage
•  nursing time
•  risk of touch contamination
•  pharmacy prep time
• Cost savings
• Easier administration in
HPN
•  stability and compatibility
• IVFE (IV fat emulsions) limits the amount of nutrients that can be compounded
• Better fat utilization
• Physiological balance of macronutrients
• Limited visual inspection of TNA; reduced ability to detect precipitates

Advantages
• Well tolerated
• Requires less manipulation
•  nursing time
•  potential for
“touch” contamination
Disadvantages


Persistent anabolic state
◦ altered insulin: glucagon ratios
◦  lipid storage by the liver
 mobility in ambulatory patients

Advantages
• Well tolerated
• Requires less manipulation
•  nursing time
•  potential for
“touch” contamination
Disadvantages
• Persistent anabolic state
• altered insulin: glucagon ratios
•  lipid storage by the liver
•  mobility in ambulatory patients

• The intermittent administration of
PN, usually over a period of 12 – 18 hrs
 Advantages
◦ Approximates normal physiology of intermittent feeding
◦ Maintains:
 Nitrogen balance
 Visceral proteins
◦ Ideal for ambulatory patients
 Allows normal activity
 Improves quality of life

• Line sepsis: CRI
• Metabolic derangement/ re-feeding syndrome
• Fluid/ electrolyte/ acid-base imbalance
• Overfeeding syndrome
• Liver complication

Infectious Complication
‘Catheter related infection’ (CRI)
• Tunnel site infection
• Hub contamination
• Infusate contamination
• Seeding of other site of infection
Guideline for prevention of intravascular device-related infection.Infectious control and hospital epidemiology 1996;17(7):438-4 73

Refeeding Syndrome (Nutrition Recovery Syndrome)
Metabolic complication occurs when nutritional support given to severely malnourished
 Electrolyte abnormalities
 Hypo K + , Mg 2+ , PO
4
3-
 Weakness
 Respiratory failure
 arrhythmia from intracellular shift
 Na/fluid retention from  Insulin/Glucagon ratio
(antinatriuresis)
 Refeeding edema, Fluid overload
 Metabolic
  thiamin demand
 Substrate shift: from FA to glu   VCO
2 and work of breathing
/O
2

 ≥ 1
 BMI <16
 Unintentional weight loss >15% in 3-6 months
 ≥ 10 days with little or no nutritional intake
 Low Mg
 ≥ 2
 BMI
2+ , K + , or PO
<18.5
4
3before feeding
 Unintentional weight loss <15% in 3-6 months
 ≥ 5 days with little or no nutritional intake
 Alcohol misuse, chronic diuretic, antacid, insulin use, or chemotherapy

How To Prevent and Management of Refeeding
Syndrome
In high risk patients
 Start 10 kcal/kg/d, gradually  within a week
 Before/during of 1 st 10 d of feeding
 oral thiamin 200-300 mg/day
 +1-2 vitamin B co strong tablets 3 times/d or IV vitamin B
 +balanced multivitamin and mineral supplement each day
 monitor and supplement oral, enteral, or intravenous
K, PO
4
3and Mg intake.
 K + 2-4 mmol/kg/day
 PO
4
3-
 Mg 2+
0.3-0.6 mmol/kg/d
0.2 mmol/kg/d IV or 0.4 mmol/kg/d oral

Metabolic Complication to Overfeeding
• Hyperglycemia
• Hypertriglyceridemia
• Hypercapnia
• Fatty liver
• Hypophosphatemia, hypomagnesemia, hypokalemia
Barton RG. Nutr Clin Pract 1994;9:127-139

Van den Berge 2001
Surgical ICU
Van den Berge 2006
Medical ICU
More hypoglycemia
Brunkhorst 2008
More hypoglycemia

Rate of Hypoglycemia (<40 mg/dl) -
30
25
Conventional
Intensive
20
%
15
10 p<0.001
5.1
5
0
0.8
Van den Berghe,
2001 p<0.001
18.7
3.1
Van den Berghe
2006 p<0.001
17.6
4.5
VISEP, 2008 p<0.001
14.5
p<0.001
6.8
3.9
0.5
NICE-SUGAR,
2009
GluControl,
2006

The NICE SUGAR Study Investigators 2009
NICE-SUGAR study NEJM 2009 Volume 360:1283-1297

ASPEN Guideline Recommendations in Adult Hospitalized
Patients With Hyperglycemia
Recommendation
Desired blood glucose goal range in patients receiving nutrition support
Hypoglycemia defined in patients receiving nutrition support?
DM specific EN formulas be used for patients with hyperglycemia
Target blood glucose
140–180 mg/dL (7.8–10 mmol/L).
Hypoglycemia: blood glucose <70 mg/dL (<3.9 mmol/L).
Cannot make recommendation at this time
Grade
Strong
Strong
Further research
Adapted from A.S.P.E.N. Clinical Guidelines: Nutrition Support of Adult Patients With Hyperglycemia. JPEN 2012 June
29[Epub ahead of print]

• PN tolerance
• Vital sign as needed-daily
• BW daily- weekly
• Fluid: I/O daily
• Electrolyte: daily in first 3-5 d then 2/wk
• CBC, LFT 1-2/weeks

Monitoring Patient on Parenteral Nutrition
Metabolic
• Glucose
• Fluid and electrolyte balance
• Renal and hepatic function
• Triglycerides and cholesterol
Assessment
• Body weight
• Nitrogen balance
• Plasma protein
• Creatinine/height index
Campbell SM, Bowers DF. Parenteral Nutrition. In: Handbook of Clinical Dietetics. Yale University Press, 1992

Adults
 Steatosis
 Steatohepatitis
 Cholestasis
 Biliary sludge
 Cholelithiasis
 Acalculous cholecystitis
 Fibrosis
 Micronodular cirrhosis

• Advancement to full EN and discontinue PN is the best treatment for PNALD
• PN cycling
• Drug Rx with ursodeoxycholic acid, cholecystokinin, oral antibiotics
• Nutrient restriction: soybean-based IVFE and providing conservative protein and dextrose calories to prevent overfeeding
• Glucose infusion rate (GIR)  5mg/kg/min
• Lipid infusion : <1 g/kg/d of conventional  6 LCT
• Other lipid
• Combined mixture of MCT/LCT, or MUFA containing lipid emultion as opposed to the traditional LCTs
• Omega-3fatty acids
• anti-inflammatory properties
•  Associated with fewer hepatic complications

Effects Of Nutrition On Intestinal Mucosa
A: TPN
B: EN
C: IMN
D: Control
Ulusoy H, et al. Journal of Clinical Neuroscience 2003;10(5): 596–601