Nutrition therapy in critical illness

Nutrition therapy in critical illness

Malnutrition in critically ill patients
■ A disorder of body composition results from macronutrient and/or micronutrient deficiency.
■ Consequently followed by reduced organ
function, abnormal results of blood chemistry
studies, reduced body mass and less optimal clinical outcomes.
■ Commonly occur in critically ill
Cerra FB. Chest 1997:111:769-778

Negative impact of hypocaloric feeding and energy balance on clinical outcome in ICU pts
Prospective observational study
N= 48, 669 ICU days
ICU-pts > 5d on ICU
– high risk pts (30-d mortality: 38%)
Time to start feeding 3.1 +_2.2 d
Cummulative energy deficit:
12600 +10520 kcal
Mean energy delivery: 1090 +930 kcal EN, PN, EN+PN
Correlation between caloric deficit
and pts outcome (p=0.001)
– Infections
– Length of hospital stay
3000 า
2000
i 1000
□ Target ■ Delivery < 0 001 ^
-2000■
5000
-5000-
I -10000
I -15000-
g-20000
I -25000
5 -30000
-35000
-40000
B Balance
เา = 43
Weeks after admission
Villet ร, Clin Nutr 2005; 24: 502-509

■ as adjunctive care to provide exogenous fuels to support patient during stress response
■ 3 main objectives:
1. To preserve lean body mass
2. To maintain immune function
3. To avert metabolic complications
Additionally goals: attempting to
■ Attenuate metabolic response to stress
■ Prevent oxidative cellular injury
■ Favorably modulate immune response

Nutrition requirement
■ Energy requirement
■ Protein requirement
■ Fluid requirement
■ Vitamins & minerals requirement

Question 1
• How much energy requirement would be appropriate for critically ill patient?
• A. 20 kcal/kg/d
• B. 25 kca l/kg/d
• c. 30 kca l/kg/d
• อ. 35 kca l/kg/d

Answer 1
• 25 kcal/kg/d

Energy requirement
Direct measurement of energy requirement Indirect calorimetry (metabolic cart)
Calculation ะ
■ Harris-Benedict’s equation
■ Cerra’s estimation
■ Holiday-Segar’s equation
■ Others

Metabolic cart

Harris-Benedict’s equation
Basal energy expenditure
■ Male BEE = 66.5 + 13.7wt(kg) + 5ht(cm)- 6.8age(year)
■ Female BEE = 655 + 9.6wt(kg) + 1.8ht(cm) – 4.7age (year) Activity factors
■ On respirator 0.7 – 0.9
■ Confined to bed 1.2
■ Ambulatory 1.3 Stress factors

Metabolic Response
Injury Stress Factor
Minor surgery 1.00-1.10
Long bone fracture 1.15-1.30
Cancer 1.10-1.30
Peritonitis/sepsis 1.10-1.30
Severe infection/multiple trauma 1.20-1.40
Multi-organ failure syndrome 1.20-1.40
Burns 1.20-2.00
Activity Activity Factor
Confined to bed 1.2
Out of bed 1.3

Example:
Energy
requirements for patient with sepsis เท bed
= BEE X 1.30×1.2
ADA: Manual Of Clinical Dietetics. 5th ed. Chicago: American Dietetic Association; 1996
Lona CL. et al. JPEN 1979:3:452-456

Malnutrition

Ideal Weight
เท malnutrition, energy expenditure must be calculated
based on actual body weight.

Obefity
Actual Weight •*

Ideal Weight
เท obesity, energy expenditure must be calculated on
adjusted ideal weight (AIBW)

Adjusted Ideal body weight (IAIBW)
■ AIBW= IBW+ 25% of the difference between actual weight and IBW
■ IBW Male
■ Height 150 cm, weight 48 kg
■ Every 2.5 cm above 150 cm of height, add 2.7 kg Female
■ Height 150 cm, weight 45 kg
■ Every 2.5 cm above 150 cm of height, add 2.3 kg

Calorie Calculation
“Rule of Thumb”
Calorie requirement = 25 kcal/kg/day

Days in Respiratory Intensive Care Unit
stratified according to mean calorie delivery
Mean calorie delivery of < 50% of recommended significantly
reduced probability of survival
Sinah N. Resoir Care 2009:54:1688 –

Complications of underfeeding
■ Loss of lean body mass (muscle wasting), including cardiac and respiratory muscles
■ Prolonged weaning form mechanical ventilation
■ Delayed wound healing
■ Impaired host defenses
■ Increase nosocomial infections
Robert SR. Crit Care Nurse. 2003:23:49-57

Complications of overfeeding
■ Azotemia
■ Hepatic steatosis
■ Hypercapnia, which may lead to prolonged weaning from mechanical ventilation
■ Hyperglycemia
■ Hyperlipidemia
■ Fluid overload
Robert SR. Crit Care Nurse. 2003:23:49-5

Nutrients
Protein
Carbohydrates
enteral
parenteral
Lipids
Water
Vitamins
– Water soluble
– Fat soluble
Minerals
– Electrolytes
– Trace elements
4 kcal/g
4 kcal/g
3.4 kcal/g
9 kcal/g
ultra trace minerals
and

Macronutrients during Stress
Carbohydrate
■ At least 100 g/day needed to prevent ketosis
■ Carbohydrate intake during stress should be between 30%-40% of total calories
■ Glucose intake should not exceed 5 mg/kg/min
Barton RG. NutrClin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002; 26 Suppl 1:22SA

Macroทนtrientes during Stress
Fat
■ Provide 20%-35% of total calories
■ Maximum recommendation for intravenous lipid infusion: 1.0 -1.5 g/kg/day
■ Monitor triglyceride level to ensure adequate lipid clearance
Barton RG. NutrClin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002,26 Suppl 1:22SA

Macronutrients during Stress
Protein
■ Requirements range from 1.2-2.0 g/kg/day during stress
■ Comprise 20%-30% of total calories during stress
Barton RG. Nutr Clin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002,26 Suppl 1:22SA

Determining Protein Requirements for Hospitalized Patients
Stress Level
Calorie:Nitrogen Ratio
Percent Potein I Total Calories
Protein I kg Body Weight
No
Stress
> 150:1
< 15% protein
0.8
g/kg/day
1.0-1.2
g/kg/day
15-20%
protein
150-100:1
Moderate
Stress
Severe
Stress
< 100:1
> 20% protein
1.5-2.0 g/kg/day

Protein and calorie requirement
Protein
Maintenance
Catabolic patients
Chronic renal failure
(renal replacement therapy)
Acute renal failure + catabolic
Energy
Total calories
Fluid
0.8-1.0 g/kg
1.2- 2.0 g/kg
1.2- 1.5 g/kg 1.5-1.8g/kg
20-30 kcal/kg 30-40 ml/kg
Task Force for the revision of safe Dractices for Darenteral nutrition. JPEN 2004:28:S39-S7C

Key Vitamins andlMinerals
Vitamin A Vitamin c B Vitamins Pyridoxine Zinc
Vitamin E
Folic Acid, Iron, ธ12
Wound healing and tissue repair
Collagen synthesis, wound healing
Metabolism, carbohydrate utilization
Essential for protein synthesis
Wound healing, immune function, protein synthesis
Antioxidant
Required for synthesis and replacement of red blood cells

Specific substrates
Immunonutrition:
– Omega-3 fatty acids: EPA
– Glutamine
– Arginine
Pre-pro-synbiotic

Omega-3 fatty acids
Metabolized to the 3-series of prostanoids and the 5-series of leukotrienes, which are less inflammatory and less immunosuppessive.
Whereas omega-6 fatty acids are precursors of the 2-and 4-series prostanoids, which are vasoconstrictive and induce platelet aggregation (impair cytotoxic T-lymphocyte function, cytokine secretion, leukocyte migration and reticuloendothelial system function).
Needed for > 1g/day for effectiveness immune enhancing

Role of glutamine in metabolic stress
■ Considered “conditionally essential” for critical patients
■ Depleted after trauma
■ Provides fuel for the cells of the immune system and Gl tract
■ Helps maintain or restore intestinal mucosal integrity
Smith RJ, et al. JPEN 1990; 14(4 Suppl):94S-99S; Pastores SM, et al. Nutrition 1994;10:385-391
Calder PC Clin Nutr 1994;13:2-8; Furst p. EurJ Clin Nutr_ 1994;48:607-616 standen ไ. Bihari D. CurrOnin Clin Nutr Metab Care 2000:3:149-157

Role of arginine in metabolic stress
■ Provides substrates to immune system (immune enhancing agent)
■ Increases nitrogen retention after metabolic stress
■ Improves wound healing in animal models
■ Stimulates secretion of growth hormone and is a precursor for polyamines and nitric oxide
■ Not appropriate for septic or inflammatory patients (immune system is already stimulated).
‘1Giving arginine to a septic patient is like putting gasoline on an already burning fire.
– B. Mizock, Medical Intensive Care Unit, Cook County HospitalChicago, IL
Barbul A. JPEN 1986:10:227-238: Barbul A. et al. J Sura Res 1980:29:228-23!

■ Probiotics:
■ live microorganisms which, when administered in adequate amounts, confer a health benefit on the host
■ Prebiotic:
■ food for probiotic
■ Complex CHOs -not metabolized
■ Energy source for probiotics
■ Syn-biotics:
■ Pairing of pre- and pro-biotics

Route of Nutrition support
Oral
Enteral feeding
– Nasogastric tube & nasoenteric tube
– Gastrostomy/PEG
– Jejunostomy/PEJ/jejunostomy via gastrostomy
Parenteral nutrition
Combination of EN & PN

Question 2
Which route of feeding is prefer for critcally ill pt?
A. enteral
B. parenteral
c. both EN and PN อ. NPO

Answer 2
• Enteral route

Patient admitted to intensive care unit
1
Nursing assessment, including nutritional screening
1
Physician nutritional assessment
1
Registered dietitian nutritional assessment
Functioning
gastrointestinal (Gl) tract
J
\
Choice of therapy
Nonfunctioning Gl tract
i
Parenteral Feeds
-► Enteral Feeds
Therapeutic Oral Diet
t
Taper Therapy
j

Aihara R. J Healthcare Quality 2002:24:22-;

Effects of PN compared with EN: nutrition on Gl functions
■ Gut atrophy*
■ Loss of gut hormone secretion
■ Reduced gut absorption
■ Altered gut microflora
■ Loss of gut barrier
■ Increased bacterial adherence
■ Increased microbe translocation
■ Decreased gut blood flow that is worse with vasopressor administration
Increased apoptosis
Decreased gastric, intestinal, and pancreatic secretions* Increased gut permeability
Slower healing of anastomotic sites
Hepatic dysfunction*
Decreased drug clearance by liver*
Hepatic injury*
Rare hepatic failure* Cholestasis, gallstones*
Zaloaa GP. Lancet 2006:367:1101-11

Effects of PN compared with EN:
nutrition on immune system function Parenteral nutrition is associated with:
■ B and T cell dysfunction
■ Macrophage and neutrophil dysfunction
■ Impaired chemotaxis
■ Impaired phagocytosis
■ Impaired bacterial/fungal killing
■ Loss of gut associated lymphoid tissue
■ Decreased IgA secretion
■ Reticuloendothelial dysfunction
■ Increased infections
■ Increased proinflammatory cytokines
Zaloaa GP. Lancet 2006:367:1101-1

Post-pyloric feeding has no clinical advantages over gastric feeding in most critically ill medical, neurosurgical and trauma patients
Early gastric feeding with an oro-gastric or naso¬gastric tube is favored in most critically ill patients
Promotility agents are recommended in patients with high gastric residuals
Post-pyloric feeding is recommended in patients at high risk of aspiration, in patients undergoing major intra-abdominal surgery and patients who are intolerant of gastric feeding
Marik PE. Critical Care 2003. 7:R46-R5

Algorithms for critical-care nutrition support
At ICU admission:
Should this patient be fed?
^ Yes
Can EN be started within 24 hours?
No
No
Yes
Gastric challenge: Use full-strength concentration Consider prokinetic with challenge Goal: at least 80% of requirements at 72 h Assess q12h
T
Is progression on target to reach at least 80% by 72h?
No

Acceptable conditions: Tolerating adequate oral diet <24 h to oral intake Palliative care
Acceptable conditions:
> Acute pancreatitis*
• Enteric anastomosis*
‘ Ischemic bowel
• Enteric fistula
• Imminent endoscopy
• Bowel obstruction
• High nasogastric losses
• Severe exacerbation of inflammatory bowel disease
‘may still opt for element enteral feeding
T
Use prokinetic Use postpyloric tube
No
เร goal met?
Begin TPN Reassess q12h for EN eligibility
• Continue EN to maximum tolerated
• Supplement with PN
• Continue EN challenges q12h

เร diarrhea present?
“J Yes
Algorithms for critical-care nutrition supporUKp
Is stool clinically significant? No
Yes
1 Yes
Are medications the possible cause?

I No
Is the patient receiving antibiotics? Yes

Continue same enteral feeding
to tolerance
Check stool for c. difficile toxin, feed to tolerance
1
No
Consider elemental formulation
i
Is the diarrhea resolved? Yes

1 No
Decrease rate until
tolerance achieved

Continue same enteral feeding
Advance to goal rate as tolerance improves
Martin CM. CMAJ. 2004:170:197-20

Algorithms for critical-care nutrition
support
Clinically significant stools:
• Liquid stools > 300 mL/d or
• >4 loose stools per day or
• Risk of contamination of wounds or catheters Medications that commonly cause diarrhea:
• Metoclopramide
• Quinidine
• Xylitol
• Magnesium
• Erythromycin
• Aminophylline
• Sorbitol
• Phosphorus
Martin CM. CMAJ. 2004:170:197-204

Question 3
• We should hold tube feeding when residual volume more than
A. 50 ml
B. 100 ml
C. 150 ml
D. 200 ml

Answer 3
• 200 ml

Algorithms for critical-care nutrition support
Assess gastrointestinal tolerance to tube feeding q 4h Intolerant patients have:
■Clinically significant stools or
■Readily apparent abdominal distension or
■Increased abdominal girth or
■Clinically detected aspiration or
■Gastric residuals >200 mL for nasogastric feeds
Martin CM. CMAJ. 2004:170:197-20

Fig. 3: Cluster-specific mean proportions, and 95% confidence intervals, of patients receiving nutritional support in the appropriately randomized control and interven¬tion hospitals on each study dav. Dav 1 is the dav of ICU admission. The p values

Outcome of the
ROT compared
intervention and control groups
Martin CM. CMAJ. 2004;170:197-204

Prokinetic drugs
Metoclopramide (5HT4 receptor agonist)
■ most widely used in gastric feeding intolerance
■ stimulates gastric and duodenal motility, via an action on efferent myenteric cholinergic neurons releasing acetylcholine
■ some contribution from its properties as dopamine antagonist
■ 10 mg 4 times a day more effective than placebo
■ but the effects rapidly diminish by 3 days
■ feeding success in high gastric residual volumes is <20%
■ not effective in pts with brain injury
■ risk of irreversible tardive dyskinesia with long-term or high-dose use
Fraser RJL. NutrClin Prac 2010:25:26-31

Prokinetic drugs
Erythromycin
* acting as a motilin agonist
* 3 mg/kg stimulates high-amplitude antral contractions, which propagate rapidly across pylorus into duodenum
* highly successful in promoting feeding in pts with high gastric residual volumes
* prolonged administration (>3 or 4 d) reduced efficacy
* by day 7, only 30% of pts continued to receive feedings
* prolonged success of enteral feeding delivery is inversely proportional to erythromycin concentrations
Combination with erythromycin and metoclopramide
* highly effective in promoting prolonged feeding
* rationale for this synergy is unclear

Efficacy of prokinetic therapy over 7
days in feed-intolerant critically ill pts

Days in therapy
Fraser RJL. NutrClin Prac 2010:25:26-3

Studies comparing PN versus EN: Effect on mortality
udy
tH
n/N
PN
nW
Actants พ23 3 /23
ncr70tti 5/28 1 f 21
โ’* 7/31 8/35
Dunhwi J t 1 2 1 /IS
Hadfield 2/\2 e/j.;
Hadley ริ / 21 2/24
Kalis’entzos 1/18 2/20
พ51 1 MS
Moore 1392 8 .110 11 M12
Rapp ; ‘e 3/2C1
Woodcock 9/1? ริ/21
Young 10/28 10/23
*eK95%a) 5′; /378 53 /370
!3t for tatoogeneiy chi-squ.are= i 170 df-1′ 0<เ,2
1st ror a ireTBl affect 7:,0 34 p»0 7
RR
(ma Rindom)
Weight RR
% ima Random) Yesr
35 0.33[0.04,2,97] 1980
3.3 3.75[0 47,29.75] 1994
141 J.99[0 40,2.41 J 199$
2A 1 :^[0.09 17.98] 1994
7jfi จ.20[0.07,1.13] 1995
5.5 1.71 [0.32 9.30] 19S5
3.1 อ.56[0.fJ5.5 62] 1997
23 ปี.88(0.0813.70] 1992
1 a 5 a. 69(0-39.1 ESI 1S92
10.2 33^1-07,10-43] 1933
14.2 2 2?|o ^2.5 4I-| 2001
13J9 0.3^0-42,1 521 1987
1000 1.0310.70.1 J6S]
JN I riwoun £N
5D
1 DO
Favourร P’H
Hevland DK. JPEN. 2003:27:355-37

Studies comparing PN versus EN: Effect Oil infectious?complications
FK โ1แ RR Weight RR
udy ก,พ ftin <B5%CI Rsntfom) % (9ฬฬ:1 tomtom) Vttar
Aclfliftf 1^23 17/23 -» 23.2 omec; 3C} 1966
Kalfarertiot B/lfl 15/20 4 14.5 0 44[0-22,0-90} 1997
’(uciSK 9/5: 18/45 14.3 □.4A[0.22,0 m 1992
Moore 1932 19/118 30/112 —i 22.9 0.46[0.29j0 751 1992
Woodcock B/1B t1 J21 *- 132 0.72[0.34,1£] 2001
Young 5/2S 4/23 I 6.3 1.0310.31 (3.3&1 1987
WCSSftO) 60/254 104 / 244 1CT.0 0J&1|Q.44,1].8+1
atfw heiprogphtitycN”it(USfe=7.94 df=5 เว=0.16
!i1 for overall eri’t๙ ะ=-3 น: P’-O nn}
1 i J ID
fmtnEN firtutsPN
Hevland DK. JPEN. 2003:27:355-37

Studies comparing early versus delayed nutrient intake: Effect on mortality
น [Jy
twiyfcN
n/N
□•layad
RR
(95%CI Random}
WeigW KH
% [95ฬ1 ftjnriom;
Year
c^iflrdli
ChtrtMSlkyl
Ever
(tampan
M-nflrd
Mcote
T
Singh
0/10 I j 21 2/10 0/14 1 112 1 111 1 /3G 4/21
10/159
ist forhefierogene^v dii-square-=4JDS df=6 ::=fj£’ sst for overall effect z=-! .76 p=O.OB
0/10
3/17
2/19
1 m
4/15
2/31
30
4/22
23/156
7i~
0.0
11.1
153 5.4 12.4 ริ.ร 12.7
1UG0
EsttmWe
0 271003,237]
1 00(0,16,639] 0.3310.1)1,7551 0.31(0,04,2^41 0.48(0,OS,ร.07] 0.14(0.02,1 ,09] 1.05(0,30,3.68]
0.52(0.25,-! .OS]
fivourc Er^rlv EN
ID
Favours delayed
ICO
1990
1938
1993
1999
1999 986
2001
1998
Hevland DK. JPEN. 2003:27:355-37

Studies comparing early vs delayed nutrient intake:: Effect on infectious! complications
Early EN Del-ayed RR Weight RR
JtJy nffl ฒ mo Random) \ ^95^CI Random) year
Mtnard 6/12 7/15 -1 0- 2V. 1L7[0.492.34] 2GC
Moore 3/32 9/31 H 20.3 0.32(0.10,1.06] 196
Singh 7/21 12/22 42,0 0,61 [0.30,1,25] 199
al[95%Cl) 16/65 28/63 100.0 0.66(0.36,1 22]
St for heterogeneity chi-square=3.00 df=2 p=0.22
5l for overall effect I–1.32 ps0.19
.01 1 fO ■0]
F?vc.Lrs Early =^ Favours delayed
Hevland DK. JPEN. 2003:27:355-37

Comparing small bowel vs. gastrica route of feeding: effect on pneumonia
Study Small Bowel ก;พ Gastric ก)พ RR
(95%CI Random) Weight
% RR
(95%CI Random) Year
Davies 2/31 1 /35 —■ 1.2 2.26(0.22,23.71] 2002
Day 0/14 2/11 i ——— 0.8 0.16(0.01,3.03] 2001
Kearns 4/21 3/23 3.5 1.46(0.37,5.73] 2000
Kortbeek 10/37 13/43 16.3 0.65(0.34,1.22] 1999
Minard 6/12 7/15 10.7 1.07(0.49,2.34! 2000
Montecalvo 4/19 6/19 »■ 5,5 0.67(0.22,1,99] 1992
Montejo 16/50 20/51 -ft 23.5 032(0.43,1.39] 2002
Neumann 1/30 0/30 0.7 3,00(0.13,70.83! 1999
Taylor 18/41 26/41 •* 37.9 0.69(0.46,1.05] 1999
Total(95%CI) 61 / 255 83/268 ♦ 100.0 0.77(0,60,1.00]
Test for heterogeneity chi-square =4,79 df«8 p=0.78
Test for overall effect z=*1.96 p=0.05
.01 .1 I 10 100
Favours Small bowel Favours Gastric
riG. 7. Studies comparing small bowel versus gastric route of feeding: Effect on pneumonia. RR, risk ratio; Cl Random, random effects mode’
Hevland DK. JPEN. 2003:27:355-3′

Comparing combined EN and PN to ENI alone:; effect on” mortality?!1″
Combination EH + PH EH RR Weight RR
study nrtl nJN (95%C1 Random) % (95%CI Random) Year
Bauer 17/60 18/60 – 34.7 0.94(0.54,1.65] 2000
Chiarelli 3/12 4/12 ■ 10.1 075(0.21,2.66] 1996
Dunham 3/10 1/12 0 4.0 3.60(0.44,29.451 1994
Herndon 1987 8/13 8/15 – 3- 29.3 1,15(0.61,2.19] 1SS7
Herndon 1989 10/16 6/23 —II— 22.0 2.40(1.09,526] 1989
‘otal(95%CI) 41/111 37/122 100.0 1,27(0.82,1.94]
‘est for heterogeneity chi-square=5.26 dt*4 p=0.26
esl for overall effect Z=1.08 p-0,3
.01 .1 10 too
Favours comb EN + PN Favours EN
ไ0.8. Studies comparing combined EN and PN to EN alone; Effect on mortality. RR, risk ratio; Cl Random, random effects model.
Hevland DK. JPEN. 2003:27:355-3′

Evaluating PN supplemented with glutamine:: effect on mortality
PH glutamine Control RR Weight RR
Study ก/ม n/N (95%CI Random) % (95%CI Random) Year
Dechelctte 2/53 2/56 3.1 0.97(0.14,6.621 unpub
Griffiths 18/42 25/42 1 61.5 0.72(0.47,1.11] 1997
Powell-Tuck 14/83 20/85 -*■ 30.2 0.7210.39,1.32) 1999
Wlschmeyer 2/15 5/16 i 5.2 0.43(0.10,1.88] 2001
Total(95%CI) 36/198 52/199 ♦ 100.0 0,71(0.50,0,99]
Test for heterogeneity chi-square=0.56 df=3 p=0.91
Test Jor overall effect z=-2.03 p=0.04
.01 .t ID IOC
Favours PN glutamine Fav&urs control
FIG. 9. Studies evaluating PN supplemented with glutamine: Effect on mortality. RR; risk ratio; Cl Random, random effects model.
Hevland DK. JPEN. 2003:27:355-3′

Pre- pro- and synbiotics in adult ICU patients: Systematic review
Study
Control
n/N
Pro/Synbiotics ท/ N
RR (random) 35% Cl
Weight
RR (random)
35% Cl
Jain 26/45 33/45
Kanazawa 12/23 4/21
McNaught 22/51 21/52
Rayes (66) 16/53 1/33
Rayes (90) i/30 3/30
Total (95% Cl) 1S2 181
Total events: 79 (Control), 62 (Synbiotics)
Test for heterogeneity: Chi2 = 18.85, df = 4 (P = 0.0008), I2 Test for overall effect: z = 1.12 (P = 0.26)
: 78.8ๆ
29.8J 0 79 [0.58. 1 07]
J9.9y 2.74 [1.04. 7.19]
2 7.93 1.07 [0.68. 1.69]
9.30 16.00 [2.25, 113.80]
J2.97 1.00 [0.22. 4.56]
100.00 1.50 [0.74.3.06]
0.1 อ. 2 0.5 Favours control
12 5 10 Favours pro/synbiotics
Figure 2 Forest plot showing the effect of pro/synbiotics on proportion of patients with nosocomial infection.
Study Control ๙ผ Pro/Synbiotics
n/N RR (fixed) 95% Cl Weight
% RR (fixed) 95% Cl
Kanazawa 1/23 0/2 J ► 3.48 2.75 [0.12, 64.04]
Knight 17/12? 12/130 ■ 79.82 1.43 [0.7J. 2.871
Rayes (66) 1/33 0/33 ► 3..น 3.00 [0.13.71.07]
Rayes (90) 1/30 2/30 4— J.ใ.36 0.50 [0.05 5.22]
Total (95% Cl) 215 214 100.00 1.40 [0.75, 2.64]
Total events: 20 (Control), 14 (Pro/Synbiotics)
Test for heterogeneity: Chi2= 1.14, df = 3 (P = 0.77), l2= 0% Test for overall effect: z = 1.05 (P = 0.29)
0.1 0.2 0.5 1 2 5 10 Favours control Favours pro/synbiotics
Figure 3 Forest plot showing the effect of pro/synbiotics on proportion of patients with pneumonia.

Pre- pro- and synbiotics in adult ICU patients: Systematic review
The use of pre- pro- or synbiotics in adult critically ill patients confers no statistically significant benefit in the outcome criteria studied.
Study Control
rv N Pro/Synbiotics
๗ INI RR (fixed) 95% Cll Weight RR (fixed) 95% Cll
Gomersall 40/168 50/162 39.94 0.77 [0,54, 1.10]
Jain 20/45 22/45 17.26 0.91 [0.58 1.42]
Kanazawa 0/23 0/21 Not estimable
Klarin 2/7 2/8 1.46 1.14 [0.21.6.11]
Knight 42/129 35/130 27.35 1.21 [0.83. 1.76]
McN aught 18/51 1&/52 13.98 1.02 [0.60 1.73]
Rayes (66) 0/30 0/30 Not estimable
Rayes (90) 0/30 0/30 Not estimable
Total (95% Cl) 483 478 100,00 0.96 [0.78, 1.17]
Total events: 122 (Control), I

Test for heterogeneity: Chi2 = 3.05. df = 4 (P = 0.55), I2 = 0%
Test for overall effect: z = 0.44 (P = 0.66)
0.1 0.2 0.5 1 2 5 10
Favours control Favours pro/synbiotics
Figure 4 Forest plot showing the effect of pro/synbiotics on hospital mortality.
Study N Control Mean (SD) N Pro/Synbiotics
Mean (SD) WMD (fixed) 95% Cl Weight WMD (fixed)
95% Cll
Kanazawa 23 1.30 (0.70 ) 21 1.30 CO.90) 1 1 97.64 0.00 [-0.48, 0.48]
Klarin 16.43 (15.73) 8 14.25 (10.67) 4 * 0.12 2.18 [-1L62, 15.98]
Rayes (66) 33 10.20 (7.71) 33 8,80 (5.17) 224 1.40 [-1,77, 4,57]
Total (95% Cl) 63 62 100.00 0.03 [-0.44,0.51]
Test for heterogeneity: Chi2 = 0.83. df = 2 (P = 0.66). I2 = 0%
Test for overall effect: z = 0.14 (P = 0,89)
-10 -5 0 5 10
Favours control Favours pro/synbiotics
Figure 5 Forest plot showing the effect of pro/synbiotics on length of ICU stay in days.

Effect of immunomodulating diets
on mortality with treatment effect
Trealmerrt Control Odds Ratio Odds Ratio
Study M Subgroup Events Total Events Total WjjgM M-H, Random. 85% Cl Year M-แ, Random, 95% ct
U1 leu
0๓3 1990 1 11 1 9 OJQ* o.eo [O.M. 14.89} 1990
Sower 1996 33 147 10 ใ:!2 m 2.26 [t.03r 4.95] 1996 1
Rodrigo 1997 2 โ& 1 14 1.2% 18610.16,2300) 19&7
Atkinson 1998 55 197 05 193 11.2% 1.10 [0.79,1.76] 1990
GAM 1999 11 70 IS 7S 0.56 [0.24,1.28] 1999
Jotพ 12 26 ID 24 4.5% 1.20 [0.39,3.68] 1999
Galhai2000 1? 89 2& 87 7,7% 0.50 [0.25.1.00] 2000 –
Caparo&2001 25 122 29 Sfl 8.5% 0,61 [0.33 1,14] 2001
Cmejeffl 20เพ 14 47 9 37 m 1 32(0.50 351] 2002 “
Hall 2003 26 m 2b 184 0.8% 1.0S [0.60,1.95] 2003
Kieft 2005 a4 m 78 295 11.0% ใ,07 [0.75 ไ.54] 2005
Pontes-Aflwda20Q& 18 55 25 48 0.7% 0 45(0 20.0.99] 2006 —
Snger2006 Subtotal {mcij 13 # 1307 2B 49
m m
&5.2% 0.30 [013.0.701 0,85 [0.62,1,15) 2006
4
Total everts 341 346 1 1 1
Heterogeneity: พ=0-14; Qtf– Test for overall effect t-108 (P 1 ฐ- = 11 IP=0.01); p=5 5% 1 1
0.01 0,1 Favours trealmervt 1 10 10๐ Favours cBrtroi
Marik PE. Intensive Care Med 2008:34:1980-1990

Odds ratio of the treatment effect of immunomodulating diets on mortality
Burns A-FO – ICU A-FO- ICUGI- ICUAFG- 1CU FO – Trauma Arg- Trauma A-FO-
\
£>■

Arg: arginine,
A-FO: arginine + fish oil FO: fish oil
AFG:arginine + fish oil + glutamine Gl: glutamine
IIIIfill
TIIVIrTT
\
Favors Treatmeni
Favors Control
Marik PE. Intensive Care Med 2008:34:1980-199C

Use of EN with fish oil
The use of products with fish oils, borage oils, and antioxidant should be considered in patients with ARDS.
It was associated with a reduction in days
receiving supplemental oxygen, fewer days of
ventilator support, fewer days in ICU and fewer new organ failure.
Hevland DK. JPEN. 2003:27:355-3′

Effect of immunomodulating diets
on acquisition of new infections
Treatment Control Odds Ratio
Study Of Sufcgfflip Ewjjj Total fcrcnte Total Wetato M-H, Random, 95% Cl Year
2.1.1 ICU
Bower 1995 86 147 90 132 9.7% 066 [0,40,1.0ft]
RtxtigoW 5 10 3 14 2,7% 1.67 [0.32,8.74]
Jones 1999 0 26 5 24 1J0% 0.D7 [0.0D, 1.28]
Gadeh 1999 30 70 47 76 8.1% 0,46 [0.24,0,90]
Galban200C 39 &9 44 67 a;7% 0,76 [0.42,1.38]
Coftqeffl20G2 ก 47 17 37 m 0.36 jo. H 0,02]
mm 35 1» 44 184 m 0.77(0.47,1,28]
mm 130 302 123 295 11.3% 1,06 [0.76,1.46]
Porrtes-Arruda 2006 6 55 11 48 5,0% 0.41 mi m
Subtotal (96% Cl) W1 m 62.0% 0,$9[Q.51| 0,92
Total events 342 384
Heterogeneity: Tau1=OL0/; QW = 1to& df – 8 (P ะ 0.09); Test tor overadl fitted: I = 2,48 (P” 0.01)
m
1997
1999 +
m
2000 2002 2003 2006 2m
h
Odds Ratio M-H, Random, jflt Cl
■f
0,01 0,1 1 10 100 Favcxjrs trealment Favours confmJ
Marik PE. Intensive Care Med 2008:34:1980-1990.

Effect of immunomodulating diets
on length of hospital stay (LOS)
Traiment control Mean Difference
Study or Subgroup Mean SD Total Mean SD ฒ Weight IV, Random, M Cl Year
3,1,1 ICU
Cm 1990
Bower TO
Attorn 1993
GaMira
36.7 8,5 11 547 10,5 9 m -ฒเ-26.50,-9.50] 1999
■3.30 [-9,11,2,5111995
■2.50 [-8,28,3,23! 1993
-3. 20 [-9,44,304! 1999
27.6 23 147 30.9 26.2 132 9,2%
20.6 26,3 197 23.1 31.6 193 9,2%
PonteW๒d)2006 19,3 ท 55 257 64 43 113% -7.4ofฒM7qj 2006
Subtotal im cr) 480 458 38.6% ■ร,14[m, -2,44]
Heterogefieity: Tan1 ร 1,99; Chi1 ะ 3.97, df: 3 (P=0.26); I1 ะ 24%
Test tor wall effect-1 ะ 3 73 (p: 0.0002)
fan Difference
IV, Random, 95% Cl
’20 -10 0 10 20 favours treatment Favours control
I
Marik PE. Intensive Care Med 2008:34:1980-1990.

Immune nutrients: summary of clinical
practice recommendations
Nutrients lilective surgery General Peptic Trauma Burns Au/ARDS
Arginine’
CCPG No f’L’f No (Jt’fh’ftt /farm No benefit No benefit No benefit
ESPLN Benefit (li; No rec Benefit (miid)(B) Ham fsera?/(iij Benefit (it) No rec No rec
SCCM/ASPLN Benefit (A) ;JD55 Ih’f ใ รfit (A) Poss benefit (mild/mod) (B)
lJDSS /iGPTTI (serePT^fiiJ Benefit (A) Benefit (A) No rec
Glutamine*
CCPG No f’L’f No vec No rec benefit benefit No rec
BSPBN No If c No nee No p ec Benefit (A) Benefit [A] No vec
SCCM/ASPLN No rec iJD55 benefit ffl) No rec benefit (B) benefit (B) No rec
Q-2 fatty acids3
CCPG’ No rec No vec No rec No PTFC No rec Benefit
US PUN No rec No vec No rec No vec No rec Benefit(B)
SCCM/ASPLN No rec No vec No rec No rec No rec Benefit(A)
Anti oxidants^
CCPG No rec Foss benefit No rec No vec No vec No rec
LSPLN No rec No vec No rec No rec Benefit (A) No rec
SCCM/ASPLN No rec Benefit (B) Benefit (B) Benefit (B) Benefit (B) Benefit (B)
* Arginine administered in context of immune-enhancing diet that also contains fish oil, antioxidants, ± nucleotides.
1 Bnteral glutamine added to enteral nutrition regimen.
: Fish-oil-derived fl-3 fatty acids (BPA and DHA) administered in context of immune-enhancing diet that also contains borage oil and antioxidants.
* Antioxidant vitamins (including selenium) and trace elements.
recommended, should be considered, should not be used, no recommendation due to inadequate data

Dietary formulas
1. Polymeric diet: nutren, ensure, panenteral, isocal, blenderized diet (BD)
2. Semi-elemental or elemental diet: peptamen
3. Disease specific formula: glucerna SR, Nutren balance, Aminoleban-EN, Nepro, immunonutrition
4. Modular formula: protein powder

Enteral delivery
Intermittently
■ More physiologic
■ Free the patient from feeding equipment
■ 400 cc q 4 hr is well tolerated
■ May cause aspiration and abdominal discomfort
■ May not appropriate for critically ill patients

Enteral delivery
Continuous feeding
■ Via infusion pump over 24 hr
■ Less nursing supervision
■ Small residual volume
■ Lower risk of aspiration
■ Use when feeding into duodenum or jejunum
■ More appropriate for critically ill patients

Table 3. Suggested Parenteral-Nutrition Requirements for Critically III Adult Patients;”
Variable
Energy
Dextrose Lipid emulsion
Essential and nonessential amino acids (g/kg/day) Normal renal and hepatic function Hepatic failure (cholestasis)
Encephalopathy
Acute renal failure เท patients not on renal-replacement therapy
Renal failure in patients on renal-replacement therapy
Dose’i
Resting energy expenditure in kcal/dayxl.o to 1.2, or 20 to 25 kcal/kg/dayj:
Initial parenteral nutrition order with 60 to 70% of non¬amino acid calories as dextrose’)
Initial parenteral nutrition order with 30 to 40?^ of non¬amino acid calories as lipid?,
1.2-1.51
0.6-1.2 (based on estimated function)
0.6 (may be temporarily discontinued)
G.6-1.G (based on renal function)
1.2-1.5
ZiealerTR. N Enal J Med 2009:361:1088-9

Hypocaloric parenteral nutrition
Hypocaloric feeding of PN (reduced both CHO and fat or
withhold lipids) was associated with a trend toward a
reduction in infectious complications, no difference in mortality or length of stay between groups.
เท critically ill patients who are not malnourished, are
tolerating some EN, or when PN is indicated for short-term use (<10 days), hypocaloric PN should be considered.
There are insufficient data about the use of hypocaloric PN
in ะ those requiring PN for long term (>10 days), obese and malnourished critically ill patients.
Hevland DK. JPEN. 2003:27:355-3;

Lipids in parenteral nutrition
No effect of withholding lipids on mortality.
A meta-analysis showed a significant reduction in infections in the group that received no lipids.
เท critically ill patients who are not malnourished and are tolerating some EN, or when PN is indicated for short term use (<10 days), withholding lipids should be considered.
There are insufficient data about withholding lipids in critically ill patients who are malnourished or those requiring PN for long term (>10 days).
Hevland DK. JPEN. 2003:27:355-3′

Consequences of hyperglycemia in
hospitalized patients
■ Insulin resistance (‘glucose toxicity’)
■ Increased proteolysis in the skeletal muscle
■ Immune dysregulation in macrophages, neutrophils, immunoglobulins and complement
■ Increased oxidative stress
■ Impaired wound healing (glycosylation of collagen)
■ Hyperosmolality
■ Glycosuria, osmotic diuresis, and dehydration
Inclusion of lipids in PN regimens allows for a lower supply of glucose and helps to avoid hyperglycemia and its deleterious consequences

dy NT Control Risk ratio (95% Cl)
xed ICU
et al.39 4/28 4/27 0.96(0.27-3.47)
nderson et al.31 5/32 7/35 0.78 (0.28-2.22)
tchell et al.35 9/35 3/35 3.00(0.89-10.16)
sng et al.33 7/58 26/58 0.27 (0.13-0.57)
evedo et al.22 38/168 42/169 0.91 (0.62-1.34)
Mullin et al.M 6/11 4/9 1.23(0.49-3.04)
VOS et al.13 107/550 89/551 1.20 (0.93-1.55)
jnkhorst et al.11 98/247 102/288 1.12(0.90-1.39)
lichino et al.33 15/45 12/45 1.25 (0.66-2.36)
et al.30 16/58 29/64 0.61 (0.37-1.00)
ang et al.® 4/168 6/170 0.67 (0.19-2.35)
La Rosa Gdel et al.12 102/254 96/250 1.05(0.84-1.30)
abi et al.10 72/266 83/257 0.84(0.64-1.09)
ickenzie et al.33 39/121 47/119 0.82(0.58-1.15)
:E-SUGAR’S 829/3010 751/3012 1.10(1.01-1.20)
mixed ICU patients 1351/5051 1301/5089 0.99(0.87-1.12)
‘dical ICU
ind et al.25 1/5 2/5 0.50(0.06-3.91)
ท den Berghe et al.9 214/595 228/605 0.95(0.82-1.11)
alters et al.37 1/13 0/12 2.79(0.12-62.48)
■ah et al.27 22/41 22/48 1.17 (0.77-1.78)
sanen etal.36 13/39 18/51 0.94(0.53-1.68)
jno et al.26 2/31 0/15 2.50(0.13-49.05)
medical ICU patients 253/724 270/736 1.00(0.78-1.28)
rgical ICU
ท den Berghe et al.8 55/765 85/783 0.66 (0.48-0.92)
;y et al.33 4/34 6/27 0.53 (0.17-1.69)
otta et al.24 6/40 7/38 0.81 (0.30-2.20)
et al.29 7/150 6/38 0.30(0.11-0.83)
otta et al.23 5/48 6/49 0.85 (0.28-2.60)
surgical ICU patients 77/1037 110/935 0.63(0.44-0.91)
I ICU patients 1681/6812 1681/6760 0.93 (0.83-1.04)
0

Risk ratios of mortality comparing intensive insulin therapy (NT) to conventional glycemic control
10 Griesdale DEG. CMAJ 2009:180(8):821

No. events / total no. patients Favours IIT
Study IIT Control Risk ratio (95% Cl)
Van den Berghe et al.8 39/765 6/783 6.65 (2.83-15.62)
Henderson et al.31 7/32 1/35 7.66(1.00-58.86)
Bland et al.25 1/5 1/5 1.00 (0.08-11.93)
Van den Berghe et al9 111/595 19/605 5.94 (3.70-9.54)
Mitchell et al.35 5/35 0/35 11.00(0.63-191.69)
Azevedo et a I.22 27/16S 6/169 4.53 (1.92-10.68)
De La Rosa Gdel et al.12 21/254 2/250 10.33 (2.45-43.61)
Devos et al.13 54/550 15/551 3.61 (2.06-6.31)
Oksanen et al.35 7/39 1/51 9.15 (1.17-71.35)
Brunkhorst et al.” 42/247 12/290 4.11 (2.21-7.63)
lapichino et al.32 8/45 3/45 2.67 (0.76-9.41)
Arabi et al.10 76/266 8/257 9.18 (4.52-18.63)
Mackenzie et al.33 50/121 9/119 5.46 (2.82-10.60)
NICE-SUGAR’S 206/3016 15/3014 13.72 (8.15-23.12)
Overall 654/6138 98/6209 5.99 (4.47-8.03)

Intensive insulin therapy and mortality among critically ill patients: a meta-analysis
■ 26 trials,13567 patients
■ Pt in surgical ICUs appear to benefit from NT (RR 0.63, 95% Cl 0~44-0.91)
– Pt in other ICU did not (medical ICU: RR 1.0, 95% Cl 0.78-1.28; mixed ICU: RR0.99, 95% Cl 0.86-1.12)
■ The different targets of IIT (BS <110 mg/dL V. < 150 mg/dL) did not influence either mortality or risk of hypoglycemia
■ Interpretation: IIT significantly t risk of hypoglycemia and conferred no overall mortality benefit among critically ill patients. However, it may be beneficial to pt admitted to a surgical ICU.
Griesdale DEG. CMAJ 2009:180(8):821
แผ่นแปะเท้าดีท็อกซ์
Goal for blood glucose levels
Insulin therapy should be initiated for treatment of persistent hyperglycemia starting at a threshold of 180 mg/dL
Once insulin is started, a glucose range of 140- ISO mg/dL is recommended for the majority of critically ill patients
Intravenous insulin protocol has demonstrated efficacy and safety in achieving the desired glucose range without increasing risk for severe hypoglycemia
Diabetes Care 2010:33(‘SUDDI1’):S4-1

Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient:
Society of Critical Care Medicine and American Society for Parenteral and Enteral
Nutrition 2009

Traditional nutrition assessment tools are not validated in critical care (albumin, prealbumin, and anthropometry).
Nutritional assessment: evaluation of weight loss and previous nutrient intake before admission, level of disease severity, comorbid conditions, and function of Gl tract
Enteral nutrition (EN) should be initiated in critically ill pt who is unable to maintain adequate energy intake
EN is the preferred route over parenteral nutrition (PN) for critically ill pt who requires nutrition support therapy
Enteral feeding should be started early within 24-48 hours following admission
Advance feedings toward goal over the next 48-72 hours

เท hemodynamic compromise, EN should be withheld until pt is fully resuscitated and/or stable
เท ICU patient, neither the presence nor absence of bowel sounds and evidence of passage of flatus and stool is required for initiation of enteral feeding
Either gastric or small bowel feeding is acceptable in the ICU setting.
Critically ill patients should be fed via an enteral access tube placed in small bowel if at high risk for aspiration or after showing intolerance to gastric feeding
Withholding of enteral feeding for repeated high gastric residual volumes alone may be a sufficient reason to switch to small bowel feeding

When to use PN
เท healthy pt before critical illness, PN should be reserved and initiated only after 7 days of hospitalization (when EN is not available)
If PCM at admission and EN is not feasible, initiate PN as soon as possible following admission and adequate resuscitation
PN 5-7 days: no outcome effect and may increased risk to pt
Initiate PN only anticipated to be used > 7 days

Detemine target goal of EN
Energy requirements: calculated by predictive equations or measured by indirect calorimetry
Efforts to provide >50% to 65% of goal calories to achieve clinical benefit of EN over 1st week of hospitalization
If unable to meet 100% energy requirements after 7¬10 days by EN alone, consider supplemental PN
Assessment of adequacy of protein provision

Use of additional modular protein supplements is a common practice (standard enteral formulations tend to have a high nonprotein calorie: nitrogen ratio)
เท pt with BMI < 30, protein requirements 1.2-2.0 g/kg actual BW/d, and may higher in burn or multiple trauma
เท the critically ill obese patient, permissive underfeeding or hypocaloric feeding with EN is recommended
For BMI is >30, the goal of EN regimen <60-70% of target energy requirements or 11-14 kcal/kg actual BW/d (or 22-25 kcal/kg IBW/d). Protein >2.0 g/kg IBW/d for obesity, 2.5 g/kg IBW/d for morbid obesity

—. …51 tolerance and adequacy of EN
Evidence of bowel motility is not required to initiate EN
Monitored for tolerance of EN (pain, distention, passage of flatus and stool, abdominal radiographs)
Inappropriate cessation of EN should be avoided
Avoid holding EN for gastric residual volumes <500 mL in the absence of other signs of intolerance
NPO pt surrounding diagnostic tests or procedures should be minimize! to prevent inadequate delivery of nutrients and prolonged periods of ileus
Implement enteral feeding protocols to increases overall percentage of goal calories provided
Assessed for risk of aspiration for EN

tolerance and
adequacy of EN
Steps to reduce risk of aspiration should be used
■ เท intubated pt, elevate head of bed 30°- 45°
■ Continuous infusion of EN
■ Agents to promote motility: prokinetic drugs (metoclopramide and erythromycin) or narcotic antagonists (naloxone and alvimopan)
■ Postpyloric tube placement
■ Use of chlorhexidine mouthwash twice a day to reduce risk of ventilator-associated pneumonia
Development of diarrhea associated with EN warrants further evaluation for etiology

Immune-modulating formulations (supplemented with arginine, glutamine” nucleic acid,omega-3 fatty acids, and antioxidants)
■ Use in major elective surgery, trauma, burns, head and neck cancer, and critically ill patients on mechanical ventilation
■ Deliver > 50-65% of goal energy requirements to get benefit
■ Being cautious in patients with severe sepsis
Other ICU patients: standard formulations
Patients with ARDS and severe acute lung injury: formulation with omega-3 fish oils, borage oil and antioxidants
If diarrhea, use soluble fiber-containing or small peptide formulations

■ Probiotic agents: decreasing infection in transplantation, major abdominal surgery, and severe trauma
■ No recommendation in general ICU population because of lack of consistent outcome effect
■ Provide antioxidant vitamins and trace minerals to all critically ill pt receiving specialized nutrition therapy
■ Consider add glutamine to an EN regimen in burn, trauma and mixed ICU pt
■ Soluble fiber may be beneficial for hemodynamically stable critically ill pt receiving EN who develops diarrhea
■ Avoid insoluble fiber in all critically ill pt
■ Avoid both soluble and insoluble fiber in pt at high risk for bowel ischemia or severe dysmotility

When indicated, maximize efficacy of PN
If pt is a candidate for PN, maximize efficacy regarding dose, content, monitoring, and choice of additives
Use mild permissive underfeeding at least initially (80% of requirements as the ultimate goal of PN)
As pt stabilizes, t PN to meet energy requirements
Develop protocol to promote moderately strict control of serum glucose (110-150 mg/dL)
Supplementation with parenteral glutamine
Periodically repeat efforts to initiate EN
As tolerance improves and the volume of EN calories delivered increases, reduce PN calories supplied
Terminate PN when > 60% of target energy requirements by EN

Specialty high-lipid low-CHO formulations are not recommended for routine use in ICU pt with acute respiratory failure
Consider fluid-restricted calorically dense formulations for pt with acute respiratory failure
Monitor serum phosphate levels closely, and replaced appropriately when needed

Use standard enteral formulations in ICU patients with ARF or AKI
Follow standard ICU recommendations for protein and calorie provision
If significant electrolyte abnormalities, a specialty formulation designed for renal failure may be considered
Pt receiving HD or CRRT, increased protein, up to max of 2.5 g/kg/day.
Protein should not be restricted in pt with renal insufficiency as a means to avoid or delay initiation of dialysis therapy

EN is the preferred route in ICU patients with acute and/or chronic liver disease
Nutrition regimens should avoid restricting protein in patients with liver failure
Use standard enteral formulations in ICU pt with acute and chronic liver disease.
Reserve BCAA for the rare encephalopathic pt who is refractory to standard therapy with luminal-acting antibiotics and lactulose
Martindale RG. Crit Care Med 2009:37:1757-6

■ Place NG tube in Pt with severe acute pancreatitis and start EN as soon as complete fluid volume resuscitation
■ Pt with mild to moderate acute pancreatitis do not require NST
■ Pt with severe acute pancreatitis may be fed enterally by gastric or jejunal route
■ Tolerance to EN may be enhanced by
■ Minimizing period of ileus by early initiation of EN
■ Displacing level of infusion of EN more distally in Gl tract
■ Changing content of EN from intact protein to small peptides and long-chain fatty acids to MCT or a nearly fat-free elemental formulation
■ Switching from bolus to continuous infusion
■ If EN is not feasible, consider PN
■ PN should not be initiated until after 5 days of hospitalization
Martindale RG. Crit Care Med 2009:37:1757-61

■ Specialized nutrition therapy is not obligatory in cases of end-of-life situations
■ The decision to provide nutrition therapy should be based on effective patient/family communication, realistic goals, and respect for patient autonomy
Martindale RG. Crit Care Med 2009;37:1757-61

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