12.NUTRITION strategy_IN_CRITICAL_CARE.ppt

Nutrition

1. NUTRITION IN CRITICAL CARE
DR. ABHIJIT KHAUND

2. Nutritional requirement of surgical
patients
- Guided by ‘substrate –endocrine’ relation
-Aim – to maintain ‘cellular homeostasis’.
-Cardiac output and microcirculation
determines substrate utilisation by cell.
-Factors affecting perioperative substrate –
endocrine relation- a. starvation, b. trauma, c.
anaesthesia, d. administration of excess
glucose.

3. General principles
•Nutrients are a. structural building blocks of cells
and
b. source of energy.
•Normal individual- a balance of anabolism and
catabolism.
•A. post meal- anabolism prevails-
-↑glycogen synthesis
- ↑triglyceride formation→ ↑adipose
tissue formation
- ↑protein synthesis

4. General principles
•B. between meals and during pathological
conditions catabolism prevails.

5. Body fuels in adult men(70 kg)
Substrate Tissue Gm k.Cal Potential
duration
Triacyl glycerol Adipose 12,000 112,000 46 days
Protein Muscle 6,000 24,000 10 days
Glycogen Muscle 400 1,600 16 h
Glycogen Liver 70 280 3 h
Glucose Blood 20 80 0.8 h

6. Starvation
•↓ intake of glucose→ affects a. RBC
b. renal medula , c. cells of CNS
•Plasma glucose level maintained by two ways
A. ↓ in demand by utilising more fatty
acids mobilised from adipose tissue.
B. adaptation in intracellular glucose
metabolism

7. starvation
•Adaptation in glucose metabolism
a.↑glucose production- by ↑glycogenolysis and by
↑gluconeogenesis in liver and kidney from glycerol,
lactate, pyruvate and amino acids(alanine)
b.Reduction in whole body glucose oxydation by upto
90%. (in TIDM ↓ by 70%, in T II DM by 40%)- d/t ↓ in
activity of PDH complex
c.Amino acids are released from muscle as per
concentration
d.Ketone bodies ↑ in long term stervation (incomplete
oxydation of fatty acid.)

8. starvation
•Adaptations in cellular metabolism-
e. Brain adapts to utilise alternate fuel as ketone bodies
•Endocrinal control of cellular adaptation:
- ↓anabolic gp –a. ↓insulin →↓glycogen, trigl yceride and
protein deposition
b. ↓ growth hormone activity
-↑catabolic gp – a. ↑glucagon- ↑gluconeogenesis and
↑protein catabolism.
b. ↑cortisol - ↑extra hepatic protein
catabolism.
c. ↑catacholamines - ↑lipolysis,
↑glycogenolysis.

9. Stress response to surgery and trauma
•Inter organ substrate fluxes:
liver Amino acids muscles
Adipose
tissue
g
ly
c
e
r
o
l
urea
glucose

10. Stress response
•Metabolic adaptation is d/t neuro humoral response-
↑norepinephrine
↑epinephrine
↑ glucagon
↑cortisol
 clinically-↑HR, ↑contractility, ↑cardiac index.
First few days-↑catabolism, ↑glucose turn over by 2
folds
After few days stress response abates & lean body
mass is restored.

11. Stress response
Effect on respiratory muscles-
Fatigue d/t protein catabolism affecting respiratory
musces.
Spesific deficiencies- -acute areflexic paralysis with
respiratory failure d/t hypophphetemia.
Persistent hyper metabolic states- fatigue- accesory
muscles has to be used
MV and response to co2 ↑ with high protein intake --
high nitrogen load improves respiratory muscle
strength and ventilatoy response.

12. Response to sepsis
•Sepsis is host response to infection
•A continuum of response with increasing
severity.
•It is an additional stress in a patient of trauma
•May lead to multy system organ failure
(MSOF) in 50% cases.
•Marked by initial shock- once resuscitated go
into phase of persistent hypermetabolism
lasting upto weeks.

13. sepsis
•Hypermetabolic state:
Heamodynamically stable
↑co2 (upto 10 to 12 litres/min)
TPR ↓
O2 consumption ↑ by 2 fold
Resp. gas quotient ↓to .8 -.85 (greater reliance on fat.
Very high metabolic demand
Plasma lactate ↑by 2 to 3mg/dl , not accompanied by
metabolic acidosis.
Lactate/ pyruvate ratio is within normal limit
Energy utilisation is consistent with O2 supply

14. sepsis
•Advanced sepsis
Haemodynamic and metabolic dysfunctions set in
O2 delivery begins to fall
Hyperlactatemia associated with acidosis
O2 consumption falls with organ system failure
Respiratory dysfunction CO2 retention
Profound myocardial insufficiency – hypodynamic
state -- hypoperfused organs
In stable hyperdynamic state patient needs
maximal nutritional suppiort.

15. sepsis
Gross metabolic changes;
Skeletal muscle protein metabolism:
-protein wasting
-earliest changes- ↑ urea excretion.
- negative nitrogen balance- ↓synthesis and ↑degradation.
-fast twitch muscles are mostly affected
-glutamine represents 65% of free amino acid of muscles–
gets reduces by 50%. (not an essential aa but supplemented in
TPN as dipeptides to improve nitrogen balance.)
-addition of ornithine-α- keto gluterate improves nitrogen
balance.

16. sepsis
•Fatty acid meatabolism-
 it is the preffered fuel
 ↑ hepatic triglyceride is characteristic
feature
↑ ketone bodies
 lipogenolysis is also augmented.

17. Metabolic substrates
•three types of carbon based fuels are used-
a. carbohydrate, b. fat and c. protein
•Energy production is measured as heat
production in kilo calories per gram of
substrate (k. cal )
•Example-
1 gm glucose + 0.74 L of O2 → 0.74 l of CO2
+3.75 k.cal

18. Metabolic substrates
FUEL VO2 (L/g) VCO2 (L/g) RQ ENERGY YIELD
k.cal.
LIPID 2.00 1.40 0.70 9.1
PROTEIN 0.96 0.78 0.80 4.0
GLUCOSE 0.74 0.74 1.00 3.75
Respiratory quotient: RQ = VCO2/VO2

19. DAILY ENERGY EXPENDITURE
Harris Benedict equations-
• based on actual measurement of energy
expenditure on a group of healthy men and women.
•Basal energy expenditure (BEE) : heat production of
basal metabolism in resting and fasting state.
•BEE -- MEN :
BEE (k. cal./ 24 hrs)= 66 + (13.7 x wt ) + (5 x ht ) –
(6.7 x age )
WOMEN: BEE = 655 + ( 9.6 x wt ) + (1.8 + ht. )- ( 4.7 x
age)
Wt in kg, height in inches , ideal body weight to be
taken for calculation.

20. Energy expenditure
•REE : resting energy expenditure (Burszein & Sephar)- BEE+
thermal effect of food
 REE = [(3.9 xVO2) + (1.1 x VCO2) – 61 ] x 1440
or REE = BEE x 1.2
VO2 & VCO2 measured in ml/min
•Handy assesment-
BEE ( k.cal/ day) = 25 x wt ( in kg)
Predictive equations overestimate by 20 to 60%
Direct measurement is more accurate.

21. Energy expenditure
•Indirect calorymetry – measures whole body
VO2 & VCO2 – REE is calculated out.
•Method – metabolic carts are used to measure
exchange of O2 & CO2.
•Can be done bedside.
•Data of 15 to 20 min. is extrapolated to 24 hr REE
.
•Limitations : expensive equipments, trained
persons required, O2 sensors not reliable above
fiO2 0f .5, available at few centres.

22. Source of energy
•Ideally daily reqirement of energy to be provided by
carbohydrates and fats , protein intake be spared for
maintainance of essential protein stores.
•Carbohydrates provide 70% of non protein calories-
excessive consumption may lead to
1. ↑insulin production, inhibition of mobilisation of fatty
acid, 2. ↑CO2 production
• Lipids – highest energy yield, should be supplied
exogenously to provide 30 % of daily energy rquirement
•Linoleic acid (18 carbon polyunsaturated FA) is considered
only essential FA. Deficiency- scaly dermopathy, cardiac
dysfunction and↑ susceptibility to infection.

23. proteins
•Protein requirement:
-Normal metabolism- 0.8 to 1.0 gm /kg/day
-Hypercatabolism : 1.2 to1.6 g /kg/day
-Measurement of protein catabolism – by measurement of
urinary nitrogen excretion.
-Nitrogen balance :( 2/3
rd
of nitrogen derived from protein
breakdown is excreted in urine– protein is 16% nitrogen—
each gm of urinary nitrogen (UN) represents 6.25 gm of
degraded protein.)
Nitrogen balance (g) = (protein intake in gm /6.25)- UUN + 4)
UUN = urinary urea nitrogen excretion in gm in 24 hrs.
4 = daily nitrogen loss other than UUN

24. proteins
•The goal is to maintain positive nitrogen balance of 4
to 6 gm
•Total vs. urea nitrogen:
oNormally 85% of nitrogen is contained in urea.
oPost trauma/surgery it is < 50% --- so UUN may
underestimate protein loss. So urinary ammonia has to be
estimated.
•To keep positive nitrogen balance provide enough non
protein calories to meet daily energy requirement.
•If non protein calory intake is inadedquate catabolism
sets in.

25. micronutrients:vitamins
Vitamins Daily enteral dose Daily parenteral dose
Vit A 1000 μg 3300 IU
B12 3 μg 5 μg
C 60 mg 100 mg
D 5 μg 200 IU
E 10 mg 10 IU
K 100 μg 10 mg
B1 2mg 3mg
B2 2mg 4mg
B6 2mg 4mg
Folate 400 μg 400 μg
Biotin 150 μg 400 μg`
Pantothenic acid 6 mg 15 mg

26. Essential trace elements

27. Essential trace elements
•Selenium – an endogenous anti oxydent-
deficiency occurs within 1 week of onset of
acute illness. Usually not included in tpn
formulae
•Supplementation should be done @ 200 μg
Per day.

28. The importance of enteral
nutrition
•Differential response to feeding and
starvation:
–The functional and structural integrity of the GI
tract is greatly influenced by state of starvation
(non use) and its utility (use of enteral feeding).
Effects of gut disuse (local and systemic):
Gut disuse with or without PN lead to
deterioration of functional and structural
integrity .

29. Effects of gut disuse
•Villus atrophy (↓in villus height)
•10 to 15% ↓ in mucosal mass
•Injury followed by starvation ↑mucosal
permeability
•↓peristalsis – bacterial overgrowth
•↓ secretion of bile salt and sIgA – promotes
bacterial adherence to gut mucosa.
•Aerobic bacterial growth in gut – translocation to
portal circulation of bacteria and endotoxins (may
reach systemic circulation via lymphatics also)

30. Effect of gut disuse
•↑ in gut permeability leads to sepsis and organ
disfunction.
•↓mucosal lymphoid tissue mass -- ↓ sIgA --↑
susceptibility to respiratory viral infection.
•Loss of immune modification role of Th2 leading
to overwhelming response to bacterial invasion
mediated by Th1 (Th1→↑proinflamatory
response →↑IL-2,IFNγ &TNF →self injury ; Th2
modifies this response through IL-4,IL-6 & IL-10.
•In starvation Th1 response may be overwhelming.

31. Effect of gut disuse
•Gut disuse →↓ homing of B cells in peyers
patch → atrophy of peyer’s patches in the
mucosa.
•Accumulation of polymrph. neutrophils is
promoted in all mucosa particularly in lungs→
further inflamatory injuries to the organ.

32. Benefits of enteral nutrition
•Maintains mucosal mass.
•Stimulates cellular proliferation and production of brush
border enzymes.
•Maintains villus height
•Maintains integrity of tight junctions between intestinal
epithelial cells.
•↑ gut blood flow.
•Promotes release of endogenous agents –
a.cholysystokinin.
b. gastrin

33. Benefits of EN
c. bombesin (can reverse all histologic & functional
deficits caused by PN)
d. bile salt (coats bacteria within the gut preventing
adherence.)
e. ↑ antimicrobial secretion→ pancreatic engymes/
proteases/ lactoferrin.
7 . Normal anaerobic flora of the gut is
maintained→colonisation resistance.
8. Immune response modification through Th2 CD4 cells.
9.↑Ig A → stimulates cytokine production(IL4,5,6,10 & 13)
10. Reverses all effect ↓of B cell population &peyer’s patch
atrophy.

34. Impact of EN on outcome
•Meta-analysis comparing EN with PN has not
shown significant diffrence in mortality.
•However, compared with PN , EN was
associated with significant reduction in
infectious complication.
•Early EN has shown benefits of reduced
mortality and fewer infectious complication as
compared to delayed nutrition and PN.

35. Impact of EN on outcome
•As per route of administration:
a. Delivering food to small bowel, beyond
pylorus ↓frequency of regurgitation and
aspiration - ↓VAP
b. Small bowel feed is associated with ↑protein
and calory delivery and shorter time to attain
target dose of nutrition.

36. Strategy to minimise risk of EN
•Prefered modality is small bowel feeding particularly in
patient with –
a.high risk for intolerence to EN (on ionotrop, vasoactive
drug support,on sedative infusion, patint with large vol. of
gastric drainage. Or
b. patient with high risk of regergitation- nursing in
supine position.
•Head of the bed elevation to 30 to 45⁰.
•Use of GI promotility drugs.
•Reducing dose of opiods.
•Using nurse directed feeding protocol (including frequent
checking of gastric residual volume.)

37. Assesment nutritonal needof critically
ill
•Need for additional nutritional rquirement
than estimated.(i.e. APACHE II score > 10)
•Assesment of PCM: PCM suspected when
1. patient significantly underweight
2. sustained recent weight loss.
3. fasting significantly prior to assault.

38. Assesment of critcally ill
•Evaluate status of GI tract
Intravascular volume status, presence of shock
/hypotension or use of vasopressors.
GI motility-(it is segmental)
- gastric emtying- a. presence or absence of
nausia /vomiting.
b. high residual volume
c.high output from NG tube.
-colonic motility- whether passing stool or gas
-small bowel motility- abdominal distension and
presence or absence of bowel sounds.

39. Assesment cntd.
•GI status
Absorption of nutrient from small bowel does need
motility.
 when there is malassimilation / diorrhoea formulae
cotaining oligopeptides have shown enhenced absorption.
When EN started tolerence must be monitored-
- gastric stasis,
-diorrhea -
- circulating levels of glucose/ triglycerides/urea nitrogen
and creatinin ratio.

40. PN or EN ?
•Only in patient with very severe illness PN may be
considered– severe trauma, burn, ac. pancreatitis, ac
respiuratory failure requiring ventilation.
•Patient with ATI score > 25 has shown more septic
complications with PN.
• At least 60 to 65% of estimated caloric goal has to be
delivered enterally- to get benefits
maintaining normal intestinal permeability,
↓ duration of mechanical ventilation,
faster return of cognitive function in head injury,
↓ICU stay length.

41. immunonutrition
•These are specific nutrients thought to modify immune
system : L-glutamine
L- arginine
Omega-3 fatty acid
selenium
Vit E/A/C
L -arginine:- plays fundemental role in protein metabolism &
a critical substrate for nitric oxide synthesis(NO)
it stimulates release of growth hormone,insulin
growth factor and helps in wound healing.

42. Imuno nutrition
•-NO formed by nitric oxide synthase (NOS) has benificial
effect on tissue oxygenation and immune functions
•But no data so far has supported use of L Arginine and
improvement in outcome.
•Large dose ssupplimentation with PN has caused
increased mortality.
Omega 3 fatty acid:-
•Incorporated into phospholipids and influence the structure and
function of cellular membranes.
•Substrate for enzymes cycloxygenase/ lypooxygenase→ formation of
prostaglandins/ thromboxanes/ leukottrienes.

43. Immuno nutrition
•Omega 3 fatty acid:-
-presrnt in fish oil.
- no supportive study show benefit as supplemet.
L- glutamine:
-not an essntial aa under normal conditions.
- aa used as a major fuel by rapidly deviding cells
(lymphocytes, gut epithelial cells.)
-substrate for important endogenous antioxydent-
glutathione.

44. immunonutrition
•Metaanalysis of studies show↓mortality,with L-
glutamine supplementaion, ↓in infection & no effect
on length of icu stay.
•Benefits shown only in pt on PN or EN with severe
trauma or burn.

45. PN
Patient selection:
When gut is intact EN to be preffered over PN
In presence of PCM (>10% to 15% body weight loss )
and low BMI PN has to be considered .
In cases with svere PCN PN has shown
a.↓infectious complecations.
b. ↓major complications
c. ↓ mortality in comparison to standard therapy.
:: Prvelence of severe PCM in ICU patient ranges 8.3 to
12.6%

46. TPN
When gut is not in use for prolonged period
PCM sets in.
PN to be considered only after 7to 10 days
folowing an injury/assault.

47. TPN
 Composition:
•Lipid content of PN:
Use of emulsified lipid (intralipid) with PN is
controversial- as studies have confirmed long chain fatty
acid can cause immune suppression—
 promote disfunction of RE system.
↑ generation of ROS (reactive oxygen species).
Adversely affects composition of cell membranes
So only some fat, at best 5% of total calory need to be
provided as lipid emulsion to prevent essential FA
deficiency.
But on patient needing more than 10 days of TPN effect of
lipid free formulation has not been studied.

48. TPN
Dextrose
•Standard nutritional support regimen uses
carbohydrates to supply 70% of non protein
calories.
•Provide as dextrose solutions
•So these are hyperosmoler . Should be infused
through a large central vein

49. TPN- compositions
Amino acid solutions;
•Usually mixed together with dextrose solution.
•Contains – a. essential amino acids 50%
b. non & semi essential 50%
•Essential aa are converted pertially to non essential aa
→corresponding urea nitrogen production is less.
•aa preparation for renal failure is rich in essential aa
•Hypercatabolic state and hepatic failure cases can be
supplemented with more branched chain aa.
Electrlytes : most solutions contain sodium,chloride,
potassium, magnesium,calcium and phosphorus as
supplement.

50. Complications of PN
1.Catheter related problems:
a. infectius complications- catheter colonisation and sepsis.
b. venous thrombosis.
2.Hyperglycemia: ↑rate of complications associated with fatty
acids
a. impares neutrophil chemotaxis.
b glycosylation of immunoglobulins
c. impares wound healing.
d. exacerbates inflammation.
-Hyperglycemia ( > 220mg/dl) has been shown to occur in > 50%
nondiabetic patients receiving PN>35kcal/kg/day.
-Insulin resistant patiens shows hyperglycemia at lower rate of
supplementation.

51. PN- complications
3.Hypophosphatemia:d/t enhenced uptake of
phosphate into cells associated with glucose
entry to cell.
4. Fatty liver – excess glucose calories lead to
lipogenesis in the liver.
5. hypercapnia: carbohydrate combustion is
associated with ↑CO2 production.
6. Lipid infusion lead to immune suppression and
oxydation induced cell injury.
7. Structural and functional alteration of unused
gut.

52. TPN – complications (metabolic)
Early complications Late complications
Volume overload Essential fatty acid deficiency
Hyperglycemia Trace mineral deficiency
Refeeding syndrome Vitamin deficiency
Hypokalemia Metabolic bone disease
Hypophosphatemia Hepatic staetosis
Hypomagnesemia Hepatic cholestasis
Hyperchloremic metabolic
acidocis

53. PN –metabolic complications
Refeeding syndrome:
• Refeeding of severely malnourished patients may result in
"refeeding syndrome
• characterised by acute decreases in circulating levels of potassium,
magnesium, and phosphate.
•The sequelae of refeeding syndrome adversely affect nearly every
organ system and include cardiac dysrhythmias, heart failure, acute
respiratory failure, coma, paralysis, nephropathy, and liver
dysfunction.
•The primary cause of the metabolic response to refeeding is the
shift from stored body fat to carbohydrate as the primary fuel
source. Serum insulin levels rise, causing intracellular movement of
electrolytes for use in metabolism.

54. PN Metabolic complications
Recommendations to reduce the risk of refeeding syndrome include:
•Recognize patients at risk
-Anorexia nervosa
-Classic kwashiorkor or marasmus
-Chronic malnutrition
-Chronic alcoholism
-Prolonged fasting
-Prolonged IV hydration
-Significant stress and depletion
•Correct electrolyte abnormalities before starting nutritional support
•Administer volume and energy slowly
•Monitor pulse, I/O, electrolytes closely
•Provide appropriate vitamin supplementation
•Avoid overfeeding

55. Guidelines for nutrition support
therapy in adult critically ill patients.
•.jointly formulated (2009) by of Society of
critical Care Medicine and American Society
for Parenteral and Enteral Nutrition.
Traditionally nutritional support was regarded
as adjunctive care with the objectives:-
a. to preserve lean body mass.
b. to maintain immune function
c. to avert metabolic complications.

56. Guidelines for nutrition support
therapy in adult critically ill patients.
•Recently these goals have become more focused
on nutrition therapy attempting to-
- attenuate the metabolic response to stress
- prevent oxydative cellular injury
- favorably modulate the immune response.
Focus is on- 1.early EN. 2. appropriate macro
and micro nutrient delivery and 3. meticulous
glycemic control.

57. Guidelines cntd.
•Initiate enteral feeding
1.Traditional tools of assesment (albumin,
prealbumin,anthropometrty) are not validated.
Assesment includes – weight loss,nutrient intake
before admission,disease severity, comorbid condition
& function of GI tract.
2.Initiated in patints who is unable to maintain volitional
intake of food.
3.EN is preffered over PN.
4.Early EN (24 to 48 hours of admission)to be initiated
and should be advanced towards energy goal over next
48 to 72 hrs.

58. Guidelines cntd.
•Intiating enteral feeding-
5. In the setting of haemo-dynamic compromise EN
to be withheld until fully resuscitated.(E)
6. In ICU setting neither presence nor absence of
B/S and evidence of passage of flatus and stool is
requred for initiation of EN.(B)
7. Either gastric or small bowel feed is acceptable.
Switch to small bowel feed in patient with high
risk of regurgitation and aspiration and
intolerance to gastric feed. (C)

59. Guidelines cntd.
•When to use PN ?
1.When EN could not be initiated or feasible within first
7 days of admission & PCM is detected .(E)
2.PCM present at admission and EN not feasible-
appropriate to initiate PN as soon as possible.(C)
3.Pt planned for upper GI surgery and EN not feasible-
a.if patiend is malnourished initiate PN 5-7 day
preoperatively (B)
b. otherwise PN can be delayed 5-7 days
postoperatively.(B)
c. should be initiated only duration is anticipated to
be more than 7 days.(B)

60. Gudelines cntd.
•Dosing of Enteral Feeding
1.Target goal of EN should be set using predictive
equations or by indirect calorimetry (preferable).
2.Effort to be made to provide atleast 50 to 65% of goal
calories to achieve clinical benefit of EN.
3.If unable to meet energy requirement (100% of target)
after 7 to 10 days of EN alone consider supplemental
PN.
4.Ongoing assesment of adequecy of protein provision.
Additional modular protein supplementation for pts
with BMI < 30 ( requires 1.2 to 2 g/kg actual BW).

61. Guidelines cntd.
•Dosing of EN
5. In critically ill obese patien permissive
underfeeding is recmmended ( goal should not
exceed 60 to70 % of target energy, or 11 to 14.5
kcl/kg actual BW)
Monitoring tolerence and adequecy of EN:-
1.Evidence of bowel motility not required in ICU to
initiate EN.
2.Monitor for tolerence – c/o pain, distension on
physical examination,passage of flatus / stool
and abdominal radiograph.

62. Guidelines cntd.
2. – inappropriate cessasion should be avoided-
-- for gastric residual volume < 500 ml in absence of
other sign of intolerene EN should be cntnd.
3. Enteral feeding protocols to be adopted.
4. To asses for risk of aspiration and steps to reduce risk.
5.Blue food coloring and glucose oxydase strips as
markers for aspiration are not recommended.
6.Development of diarrhoea further warrants for
evaluation of etiology.

63. Guidelines cntd.
•Measures to reduce risk of aspiration.
- the head of the bed to be elevated by 30 to 45⁰)( C ).
-for high risk pt showing intolerence to gastric
feedinng EN to be switched over to continuous
infusion.(D)
-agents to promote motility such as -
prokinetics(metoclopramide,erythromycin)or narcotic
antagonists( naloxone ,alvimopan ) should be initiated
whenever feasible
- diverting the level of feeding by post pyloric tube
placement should be considered.

64. Guidelines cntd.
•Selecting appropriate enteral formulation;
1.Immune modulating formulations to be resereved for
appropriate sub population :- major elective surgery, major
trauma, burns, head and neck cancer . To be cautious in
patients with severe sepsis.
2.Patient with ARDS and severe ALI should be placed on an
enteral formulation with anti inflammatory lipid profile
(omega- 3 fish oil, borage oil) and anti oxydents.(A)
3.To get benefit of immune modulating supplements atleast
50 to 60% of target calory to be given enterally.
4.In case of diarrhoea – soluble fibre containing or small
peptide formulations to be considered.

65. Guidelines cntd.
•Adjunct therapy
1.Probiotics has shown improved outcome in specific groups
(involving transplantation, major abdominal surgery, severe
trauma. Not recommended for general ICU use.
2.Combination of antioxydant vitamins and trace minerals
(specifically selenium) should be provided to patients
receiving specialised nutrion therapy.
3.Addition of enteral glutamine to patients of burn and
trauma.(B)
4. soluble fibres for patients with diarrhoea is recommended.
Both soluble and insoluble fibres to be avoided in patients
at high risk of bowel ischemia or severe dysmotility. ( C ).

66. Guidelines cntd.
•When indicated ,maximize efficacy of PN
1.If the patient is deemed to be candidate for PN steps to maximise
efficacy (dose, content ,monitoring, choice of additive etc.) should
be taken.
2.Initial mild permissive underfeeding (80% of estimated energy). For
obese patient recommendation is same as in EN.
3.If PN has to be given in the 1
st
week of hospitalisation formulation
without soy-based lipid to be used.(D)
4.Protocol to control moderately strict control of serum glucose (110
to 150 mg/dl) to be adopted.
5.Consideration for parenteral glutamine.
6.Once stabilised on PN , effort to be made periodically to start EN.

67. Guidelines cntd.
Pulmonary failure :-
1.High-lipid ,low carbohydrate formulations
designed to manipulate resp. quotient and
reduce CO2 production are not recommended
in ICU pt. with ac. Respiratorty failure.
2.Fluid restricted calorically dense formulation to
be considered.
3.Serum phosphate level to be monitored closely
and replaced appropriately.

68. Guidelines cntd.
•Renal failure
1.ICU patients with ARF or AKI should be placed on
standard enteral formulation. If significant
electrolyte abnomalities occur – specialised
formulation to be considered.(E)
2.Patient on haemodialysis or CRRT should receive
increased protein upto 2.5 gm/kg/day . Protein
should not be restricted in patients with renal
insufficiency as a measure to delay initiation of
dialysis.( C )

69. Guidelines – cntd.
•Hepatic failure:
1.Traditional assesment tools are less effective d/t
presence of ascites, intravascular volume
depletion,edema, portal hypertension and
hypoalbuminemia.(E)
2.EN is preffered route. Regimes should not be protein
restricted.(E)
3.Standard enteral formulation for ac. and chronic liver
disease. Branched chain aa formulations to be
reserved for rare encephalopathic patients refractory
to standard therapy with luminally active antibiotics
and lactulose.

70. Gudelines cntd.
•Acute pancreatitis
1.At admission: to be evaluated for disease
severity. For severe ac. pancreatitis naso-gastric
tube EN should be initiated as soon as fluid
volume resuscitation is complete.(c)
2.Patient with mild to moderate ac pancreatitis
does not require nutrition support therapy,
unless there is failure to advance to oral diet
within 7 days.( c)
3.Ac severe pancreatitis pts may be fed enterally by
gastric and jejunal route.

71. Guidelines cntd.
•Ac.pancreatitis:-
4. Tolerance to EN may be enhanced by :
-minimising the period of ileus by early initiation of EN.
(D)
-displacing the level of infusion more distally in the GI T.
- changing the content of EN from intact protein to small
peptides, and long chain fatty acid to medium chain
triglycerides or fat free elemental formulation. (E)
- switching from bolus to continuous infusion.
5. When EN is not feasible in severe disease PN to be
initiated but not before first 5 days of hospitalisation.

72. Thanks