Transcript Implication of Parenteral nutrition

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
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.
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’
Disadvantage
aa pattern could not be changes
Advantage
Contained all aa. Required for protein synthesis
Polypeptided contained abundant of Gln
Protein
hydrolysate
Vinnars E. History of parenteral nutrition. JPEN 2003;27: 225-3.
Protien Hydrolysates and Crystalline Amino
Acids
1964
Bansi
Introduced crystalline aa. (base on
Rose’s 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
with puppies with IV feeding using CVC
Dudrick
High dose of glucose without fat, aa, other nutrient
Glucose system
½ of calories as lipid, and the remainder as gulcose
Fat system
Swedish
Rhoads
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
2
Optimum
4
Maximum
7
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
in man
RQ =2.4
•  work of breathing and
time in respirator
Fluid Retention/Electrolyte Disturbance
• Glucose infusion: hyperinsulinemia
• Insulin: antinatriuretic and antidiuresis effect
 fluid retention  cardiopulmonary
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
4
3.5
3
Glucose infusion
Glucose oxidation
There is physiological maximum to the
amount of glucose oxidized in man
2.5
33.1%
2
1.5
32.4%
43.8%
43.7%
1
0.5
0
1m g/kg/m in
2m g/kg/m in
4 m g/kg/m in
Wolfe et al, Metabolism 1979.
4m g/kg/m in+ insulin
Glucose Oxidation in Various Conditions
Glucose oxidation (g/kg/min
Wolfe 1979, Nanni 1984, Nanni 1984 ,
Burke 1980
6
5
5.1
4
4
3
3.75
3.22
2
1
0
Normal
Nonseptic post Septic critically ill
op
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.
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;11:151–156.
Glucose- or Lipid Based PN
Tappy er al, Crit Care Med 1998,26(5):860
VCO 2 ml/min
300
P<0.02
N.S
250
200
150
100
50
0
Basal
TPN-L
Basal
TPN-G
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
1.4
1.35
n.s
1.3
1.25
1.2
1.15
1.1
1.05
TPN-L
Tappy er al, Crit Care Med 1998,26(5):860
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.
Lipid Metabolism
• 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
Exogenous Lipid Administration
• IV lipid emulsion
(IVLE): chylomicron
like particle
• Chylomicron like
particle: hydrolyzed
by LPL
• Liposome: stimulate
cholesterogenesis
and accumulation
of Lp-X
Exogenous Lipid Administration
• Normally admin of LCT or MCT/LCT emulsion
reduced glucose oxidation but not 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
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)
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
1Seider
DL, et al. JPEN 1989;13:614-9,
GL,et al.JPEN 1990;14:467-71,
3Abbott WC, et al, Arch Surg 1984; 119: 1367-71
2Jensen
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
35
*
P<0.05
*
30
Before
During
After
*
25
24.1
*
240
20
184
179
15
149
156
10
5
0
PaO2/FiO2
Qva/Qt (%)
MAP (mmHg)
Venus V et al. Chest 1989;95;1278-1281
PVR (dyne*s/cm3)
LCT Vs. MCT Lipids In Patients With ARDS: Effects On
Pulmonary Haemodynamics And Gas Exchange
Faucher M et al. Chest
2003;124;285-291
40
35
30
25
Before
During
After
*#
*
30
25
250
330
20
260
15
15
10
10
5
5
0
PaO2/FiO2
LCT
Before
During
After
35
*#
20
40
MPAP
Qva/Qt
0
260
PaO2/FiO2
MCT
Intensive Care Med (1998) 24: 1029±1033
270
250
MPAP
Qva/Qt
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;28:289–292.
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
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
can’t 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 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
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
Minerals……………………Electrolytes 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 3-in1
• 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
ASPEN Nutrition Support Practice Manual
2005;precipitates
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
◦ Approximates normal
physiology of intermittent
feeding
◦ Maintains:
• The intermittent
administration of
PN, usually over a
period of 12 – 18
hrs
 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
deline for prevention of intravascular device-related infection.Infectious control and hospital epidemiology 1996;17(7):438-473
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+ 2-4 mmol/kg/day
 PO430.3-0.6 mmol/kg/d
 Mg2+
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
%
p<0.001
18.7
p<0.001
17.6
14.5
15
p<0.001
10
p<0.001
6.8
5.1
5
4.5
3.9
3.1
0.5
0.8
0
Van den Berghe,
2001
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
Target blood glucose
glucose goal range in 140–180 mg/dL (7.8–10
mmol/L).
patients receiving
nutrition support
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
recommendation at this time
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]
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): 596–601