IMPLICATION OF

PARENTERAL NUTRITION
PRANITHI HONGSPRABHAS MD.

History of Parenteral Nutrition

Year
1628

William Harvey

Discovery of circulation

1662

Lower

Blood transfusion of sheep to young man

1665

Christopher Wren

Infusion of wine, ale, opiates in dogs

(same inebriating effect as oral form)

1712

William Courten

Infused olive oil in dogs:

(Severe respiratory distress from fat emboli)

1818

Blundell

Suggest possibility of blood transfusion in pt with

bleeding in ICU

1831-32 Latta

Saline infusion in cholera patients

(Rapid improvement)

1873

Edward Hodder

Infuse fat in form of milk in 3 cholera pts

(2 recovered completely, 1 died)

1869

Menzel and Perco

Give fat subcutaneously to dogs

(feasible)

1904

Paul Friedrich

Subcutaneous administration of nutrients

(Painful)

Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.

Studies with Glucose

1859

Claude Bernard

Le milieu interior/ importance of glucose for

metabolism

1896

Beidl and Krauts

First infuse glucose in human (200-300 ml of 10%

glucose solution)
Febrile reaction: glucose fever

1915

Woodatt

Constant infusion of glucose by pump, varied infusion

rate to establish dose response relationship of urinary
glucose excretion

1924

Matas

Continuous glucose drip

1945

Zimmerman

Infuse IV solution through IV catheter placed in SVC

194452

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.

Use Of Plasma As Protein Sources

1930

Whipple, Holman,
Madden

Protein requirement of dog could be

provided by infusing plasma protein by
vein during free protein diet

Albright

Metabolic fate of infused plasma

protein in humans and demonstrate +
N balanced

Yuilie

Infused labeled plasma protein in

dogs and found gradual tissue
radioactivity and fall of 14CO2

Allen

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

Henriques and
Anderson

Infused beef hydrolysate into goat and

achieved +N balance

Vanslyke and Meyer

Metabolism of aa obtaind from hydrolysis of

casein or beef protein infused into dogs

1930

Rose

Determine EAA in humans and proposed ideal

mixture of aa that could be support protein
syntlesis in healthy adults

1937

Elman
Father of IV nutrition

Infuse aa in form of fibrinogen hydrolysate in

man

1944

Wretlind
Vitrum Co.
Sweden

Protein hydrolysate marketed AMINOSOL

cacein hydrolysed enzymatically and
dialysed)

Aboot Co.
IL

Hydrolysate of cacein AMINOSOL

Protein
Disadvantage
hydrolysate Advantage

aa pattern could not be changes

Contained all aa. Required for protein

synthesis
Vinnars E. History of parenteral
nutrition. JPEN
2003;27: 225-3.
Polypeptided
contained
abundant of Gln

Protien Hydrolysates and Crystalline

Amino Acids
1964

Bansi

Introduced crystalline aa. (base on

Roses work: AA requrrement of man)

Late
1969

Writlind

More complete crystalline aa solution

Vamin
More effective in postop N balance

1970

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

Development Of Safe Fat Emulsions

1920-1960

1961

USA and Japan

Developed and tested fat emulsion

Upjohn Co USA

Lipomul eas poduced

Adverse effects: (chill, fever, hypoxia and
hypotension)withdrawn

Wretlind and Schuberth

Fat emulsion prepared from soybean oil and eff yolk

phospholipid: safely infused
Commercialization Intralipid

Vitrum Co
1962

Sweden

First symposium of parenteral nutrition

Arvid Wretlind: father of complete parenteral nutrition

1968

Dudrick

First report of long term growth and survival in puppies

Dudrick
Swedish
Rhoads

with puppies with IV feeding using CVC

High dose of glucose without fat, aa, other nutrient
Glucose system
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.

Landmarks of The Development of

TPN
1937

Eman

Successful IV protein hydrolysate in man

1953

Seldinger

Describe catheter over wire technique

1961

Schuberth &
&Wretlind

Development of a safe IV fat emulsion

1968

Dudrick

First report of long term growth and survival in

puppies with puppies with IV feeding using CVC

1974

Solassol

Demonstrates that fat emulsions can be safely

mixed with crystalline aa and dextrose solutions

1976

Many authers

confirm that fat emulsions have equivalent N

sparing effect as glucose

Rhoads

Depleted or hypermetabolic pts should receive

more than requirements hyperalimentation

Many authers

Confirm that few surgical patients will require

more than 2000 kcal/d

1984

Parenteral Nutrition Components

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

mg/kg/min

Basal

Optimum

Maximum

Driscoll DF, et al in Rombeau JL, Rolandelli RH Clinical Nutrition: Parenteral Nutrition 2001

Glucose Infusion Issues

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 VCO2

Respiratory Decompensation

VCO2/VO2 = respiratory
quatient (RQ)
glucose oxidation:
RQ=1

Lipid oxidation:
RQ=0.7
de novo lipogenesis RQ =8

=2.4

in man

RQ

work of breathing and

time in respirator

Fluid Retention/Electrolyte
Disturbance
Glucose infusion: hyperinsulinemia
Insulin: antinatriuretic and antidiuresis
effect fluid retention cardiopulmonar
y dysfunction
Insulin: anabolic effect
K, Mg, P shift intracellularly

Glucose Metabolism In Critical

Illness
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

There is physiological maximum

to the amount of glucose oxidiz
ed in man
33.1%

43.8%

43.7%

Wolfe et al, Metabolism 1979.

32.4%

Glucose oxidation (g/kg/min

Glucose Oxidation in Various

Conditions
Wolfe 1979, Nanni 1984, Nanni 1984 ,

Burke 1980

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;190:274285.

Recommendation
CHO should not exceed 7 g/kg/d1
Glucose infusion rate should be kept at 4
mg/kg/min2
In adult critically ill patients and should not
exceed 60% of total daily energy2

1.ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA

2. Rosmarin DK, et al. Nutr Clin Pract. 1996;11:151156.

Glucose- or Lipid Based PN

Tappy er al, Crit Care Med 1998,26(5):860

VCO 2 ml/min
N.S

P<0.02

O2 Consumption and CO2 Production

P<0.02

Tappy er al, Crit Care Med 1998,26(5):860

Glucose- or Lipid Based PN

Tappy er al, Crit Care Med 1998,26(5):860

Energy expenditure kcal/min

P<0.03
n.s

Tappy er al, Crit Care Med 1998,26(5):860

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.

Lipid Metabolism
Peripheral lipolysis: FFA + glycerol

Hormones: catecholamines, glucagon

Cytokines: TNF-, IL-1, IFN-, IFN-
Lean > obese
Visceral fat > subcutaneous fat

FFA -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

Exogenous Lipid Administration

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

Exogenous Lipid Administration

Normally admin of LCT or MCT/LCT
emulsion reduced glucose oxidation but no
t uptake
Critically ill IVLE failed to suppress glucose
oxidation1
Fat emulsions : well oxidized when admin
to septic and trauma2
Pt with sepsis and MOFS efficiently
metabolize IVLE3
Tissot S et al. Am J Physiol 1995;269:E753-8.
Nordenstrom et al. Ann Surg 1982;196:221-31.
3
DrumlW et al. JPEN 1998.22:217-23
1
2

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)

Resolution Of Inflammation
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)

Lipid Emulsion: RE System

Dysfunction
Dose response
RES suppression when infusion > 0.13g/
kg/hr1,2
No evidence of RES suppression when
receiving lipid < 0.054 g/kg/hr3

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
1

Lipid Emulsion:
Hypertriglyceridemia
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
PGE2, PC2: increased shunt
TxA2: pulmonary hypertension

Hemodynamic And Gas Exchange Of

IVLE In ARDS
*

P<0.05

Venus V et al. Chest 1989;95;1278-1281

LCT Vs. MCT Lipids In Patients With ARDS: Effects

On Pulmonary Haemodynamics And Gas Exchange
Faucher M et al. Chest
2003;124;285-291
*

*#

*#

LCT

MCT

Intensive Care Med (1998) 24: 10291033

Lipid emulsion in ICU

Recommendation
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 Hypertg3
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;28:289292.

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

Negative

ALB
PAB
TFN
RBP

A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed. 3-37.

Exogenous Protein Administration

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

Total Parenteral Nutrition

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

Indications For TPN

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 cant tolerate enteral feeds, or C/I to enteral
feeding

Indications for TPN

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

Critically Ill Patients: When To Use PN

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.

Parenteral Nutrition (PN)

PPN vs. TPN
Central

Peripheral

Veins

Subclavian,
jugular

Basilic/cephallic

Osmolarity

>850 mosm/L

<850 mosm/L

Period

Long time (>2

weeks)

Short term (<2

weeks)

TPN formulation

Normal Diet
TPN
Carbohydrates..........Dextrose
Protein...........Amino Acids
Fat.Lipid Emulsion
Vitamins.........Multivitamin Infusion
MineralsElectrolytes and Trace
elements

Carbohydrate

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

Lipids

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

Intravenous Lipid Emulsion

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

Amino Acid
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

Glutamine (Gln)
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)

Other Requirements
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

TPN: Compounding Methods

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 3in-1

Dextrose, amino acids, lipid, additives
are mixed together in one container
Lipid is provided as part of the dailyPN
mixture Important energy substrate

TNA
Advantage
nursing time
risk of touch
contamination
pharmacy prep time
Cost savings
Easier administration in
HPN
Better fat utilization
Physiological balance of
macronutrients

Disadvantage
stability and

compatibility
IVFE (IV fat emulsions)
limits the amount of
nutrients that can be
compounded
Limited visual inspection
of TNA; reduced ability
to detect precipitates

ASPEN Nutrition Support Practice Manual 2005; p. 98-99

Type of Infusion: Continuous PN

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

Type of Infusion: Continuous PN

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

Type of Infusion: Cyclic PN

Advantages

The intermittent
administration of
PN, usually over
a period of 12
18 hrs

Approximates
normal physiology
of intermittent
feeding
Maintains:
Nitrogen balance
Visceral proteins

Ideal for ambulatory

patients
Allows normal activity
Improves quality of
life

Complication of PN

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

e for prevention of intravascular device-related infection.Infectious control and hospital epidemiology 1996;17(7):438-47

Refeeding Syndrome (Nutrition Recovery Syndrome)

Metabolic complication occurs when
nutritional support given to severely
malnourished
Electrolyte abnormalities
Hypo K+, Mg2+, PO43- from intracellular shift
Weakness
Respiratory failure
arrhythmia

Na/fluid retention from Insulin/Glucagon

ratio (antinatriuresis)
Refeeding edema, Fluid overload

Metabolic
thiamin demand
Substrate shift: from FA to glu VCO2/O2
and work of breathing

Risk For Refeeding Syndrome

1
BMI
<16
Unintentional weight loss >15% in 3-6 months
10 days with little or no nutritional intake
Low Mg2+, K+, or PO43- before feeding

2
BMI
<18.5
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 1st 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, PO43- and Mg intake.
K+
PO43 Mg2+

2-4 mmol/kg/day
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

Glycemic Control In Critically Ill

Van den Berge

2001 Surgical ICU

Van den Berge 2006

Medical ICU
More hypoglycemia

Brunkhorst 2008
More
hypoglycemia

Intensive Insulin Therapy

Rate of Hypoglycemia (<40 mg/dl) 30

Conventional
Intensive

25

p<0.001

20
%

18.7

p<0.001
p<0.001

17.6

14.5

15
p<0.001

10

p<0.001

6.8

5.1

3.1

4.5
0.5

0.8

Van den Berghe,

2001

3.9

Van den Berghe

2006

VISEP, 2008

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

Grade

Desired blood
glucose goal range
in patients receiving
nutrition support

Target blood glucose

140180 mg/dL (7.810
mmol/L).

Strong

Hypoglycemia
defined in patients
receiving nutrition
support?

Hypoglycemia: blood
glucose <70 mg/dL (<3.9
mmol/L).

Strong

DM specific EN
formulas
be used for patients
with hyperglycemia

Cannot make
Further
recommendation at this time research

Adapted from A.S.P.E.N. Clinical Guidelines: Nutrition Support of Adult Patients With Hyperglycemia. JPEN2012
June 29[Epub ahead of print]

Monitoring
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

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

Management
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): 596601