A PPt presentation on nutrition in the ICU care setup

1. Presented by:
Dr. Md. Zareer Tafadar
Post Graduate Resident
Deptt. Of Anaesthesiology &Critical Care
Silchar Medical College & Hospital.

2. • Nutritional management poses a vital
challenge to the intensivist in the ICU.
• The extent of muscle wasting and weight loss
in the ICU is inversely correlated with long-term
survival of the patients.
• The use of conventional nutritional support
and the role of newer adjunctive techniques
used in the critical care setting will be
discussed.

3. • Numerous studies on hospital malnutrition have
been published.
• Prevalence of malnutrition in U.S. Hospitals
today ranges from 30% to 50%.
• Patient’s nutritional status declines with
extended hospital stay.
• Appropiate institution of nutrition in the ICU -
enteral or parenteral is associated with lesser
morbidity, lesser complications and reduction in
the duration of hospital stay with increased
survival rates.

4. 69%
Adequate
Nutritional
State
10%
Severely Malnourished
21%
Moderately
Malnourished
Detsky et al. JPEN 1987

5.  Patients who are stressed from injury, infection,
or chronic inflammatory illness are in a
hypermetabolic state.
 The hypermetabolic patient undergoes rapid
breakdown of body mass and is at high risk for
developing PCM/kwashiorkor if nutritional
needs are not met.
 Consequences
– Host defenses are compromised.
– Delayed healing or even failure to heal.
– Gastroparesis and diarrhea with enteral feeding.
– Risk of GI bleeding from stress ulcers.
– Overwhelming infection despite antibiotic therapy.
– Ultimately death may occur.

6. Physiologic
Characteristics
Hypometabolic/No
nstressed Patient
(Marasmic)
Hypermetabolic,
Stressed Patient
(Kwashiorkor Risk*)
Cytokines, Catecholamines,
Gucagon, Cortisol, Insulin
↓ ↑
Metabolic rate, O2
consumption
↓ ↑
Proteolysis, Gluconeogenesis ↓ ↑
Urea Synthesis & excretion ↓ ↑
Fat catabolism, Fatty acid
Utilization
Relative ↑ Absolute ↑
Adaptation to starvation Normal Abnormal

7.  Goal : To detect nutritional problems and to prevent
concluding that isolated findings indicate nutritional
problems when they do not.
 Identifying The High-Risk Patient
 Underweight (body mass index <18.5) and/or recent loss of 10%
of usual body mass.
 Poor intake: Anorexia, or NPO status > 5 days
 Protracted nutrient losses: Malabsorption, enteric fistulas,
draining abscesses or wounds, renal dialysis.
 Hypermetabolic states: Sepsis, protracted fever, extensive trauma
or burns.
 Drug history: Alcohol abuse, steroids, antimetabolites (e.g.,
methotrexate), immunosuppressants, antitumor agents.
 Impoverishment, isolation, advanced age.

8. Physical Findings of Nutritional
Deficiencies
 Hair, Nails: Corkscrew hairs and unemerged
coiled hairs,Easily pluckable hair, Flag sign
(transverse depigmentation of hair), Sparse
hair,Transverse ridging of nails.
 Skin: Cellophane appearance, Cracking (flaky
paint or crazy pavement dermatosis), follicular
hyperkeratosis, petechiae (especially
perifollicular), purpura, pigmentation andscaling
of sun-exposed areas, poor wound healing and
decubitus ulcers.
 Perioral: Angular stomatitis, Cheilosis (dry,
cracking, ulcerated lips), Glossitis.
 Neurologic: Confabulation, disorientation,
Dementia, Peripheral neuropathy
 Others: Oedema, night blindness, heart failure
hepatomegaly.

9. Anthropometry:
– Body weight, height, triceps skinfold (TSF), and
midarm- muscle circumference (MAMC).
– The reference standard for normal body
weight, body mass index (BMI: weight in kg
divided by height in m, squared),.
• <18.5 : Underweight
• 18.5–24.9: Normal
• 25–29.9: Overweight
• >30: Obese.
 Laboratory Studies
 Serum albumin, pre-albumin
 Serum Fe, ferritin, TIBC
 Serum creatinine, BUN,
 24 hr urinary creatinine, 24 hr urine urea nitrogen
 PT, INR.

10. • The three organic (carbon-based) fuels
used by the human body are
carbohydrates, proteins, and lipids.
• The summed metabolism of all three
organic substrates determines the total-body
O2 consumption (VO2), CO2
production (VCO2), and energy
expenditure (EE) for any given period.
• The 24-hour EE then determines the daily
calorie requirements that must be
provided by nutrition support.

11. • Carbohydrates supply approximately 70% of the
non-protein calories in the average diet.
• Daily intake of carbohydrates is necessary to
ensure proper functioning of the CNS, which
relies heavily on glucose as its principal fuel
source.
• Excessive intake of carbohydrates can prove
detrimental
• Release of insulin inhibits the mobilization of free fatty
acids from adipose tissue
• Produces an abundance of CO2 relative to the oxygen
consumed.

12. • Dietary lipids have the highest energy yield
of the three organic fuels
• Lipid stores in adipose tissues represent
the major endogenous fuel source in
healthy adults
• Exogenous lipids provide approximately
30% of the daily energy needs.
• The only dietary fatty acid that is
considered essential is linoleic acid. Goal
must be to provide 0.5% of the dietary
fatty acids as linoleic acid.

13.  The goal of protein intake is to match the rate of
protein catabolism in the individual patient.
 Condition Daily Protein Intake
• Normal metabolism: 0.8 to 1.0 g/kg
• Hypercatabolism: 1.2 to 1.6 g/kg
 Nitrogen Balance
• Provides accurate assessment of protein
catabolism and consequently the daily protein
requirements.
• N balance (g) = [Pr. Intake (g) / 6.25 – (UUN +4)]
• The goal of the nitrogen balance is to maintain a
positive balance of 4 to 6 gms.

14. • Nitrogen Balance and Caloric Intake
– The first step in achieving a positive nitrogen
balance is to provide enough non-protein
calories to spare proteins from being
degraded to provide energy.
– When the daily intake of non-protein calories
is insufficient, increasing the protein intake
becomes an inefficient method of achieving a
positive nitrogen balance.

15. • 12 vitamins are considered an essential part of
the daily diet.
• Daily vitamin requirements may be much higher
in seriously ill, hypermetabolic patients.
• Antioxidant Vitamins
– Two vitamins serve as important endogenous
antioxidants: Vitamin C and Vitamin E.
– Oxidant-induced cell injury may play an
important role in multiorgan failure. Hence it
is recommended to maintain adequate body
stores of the antioxidant vitamins.

16. • Thiamine (vitamin B1)
– Thiamine is a component of TPP, an essential
cofactor in carbohydrate metabolism.
– Thiamine deficiency is likely to be common in
patients in the ICU for the following reasons.
• Lack of thiamine intake could result in depletion
of endogenous thiamine stores after just 10 days.
• Use of thiamine is increased beyond expected
levels in hypercatabolic conditions and in patients
receiving nutritional support with glucose-rich
formulas.
• Urinary thiamine excretion is increased by
furosemide.
• Mg depletion causes a “functional” form of
thiamine deficiency.

17. Vitamin Enteral Dose Parenteral Dose
Vitamin A 1000 μg 3300 IU
Vitamin B12 3 μg 5μg
Vitamin C 60 mg 100mg
Vitamin D 5 μg 200 IU
Vitamin E 10 mg 10 IU
Vitamin K 100 μg 10 mg
Thiamine (B1) 2 mg 3 mg
Riboflavin 2 mg 4 mg
Pyridoxine (B6) 2 mg 4 mg
Pantothenic acid 6 mg 15 mg
Biotin* 150 μg 60 μg
Folate 400 μg 400 μg

18. • 7 trace elements are considered essential in humans
Trace Element Enteral
Dose
Parenteral
Dose
Chromium 200 μg 15 μg
Copper 3 mg 1.5 mg
Iodine 150 μg 150 μg
Iron 10 mg 2.5 mg
Manganese 5 mg 100 μg
Selenium 200 μg 70 μg
Zinc 15 mg 4 mg

19. • Iron and Oxidation Injury
– Iron in the reduced state (Fe-II) promotes the
formation of OH- which are considered to be
the most reactive oxidants causing cell injury.
– Reduced serum Fe level in a critically ill patient
should not prompt replacement therapy unless
there is evidence of total-body iron deficiency.
• Selenium
– Co-factor for glutathione peroxidase, one of
the important endogenous antioxidant
enzymes
– Increased selenium use and lack of daily
supplementation may make deficiency
common in patients in the ICU.

20.  The daily energy expenditure is expressed as the basal energy
expenditure (BEE)
 Basal Energy Expenditure (BEE): Heat production of basal
metabolism in the resting and fasted state .
 Harris–Benedict Equations
• Men:
BEE (kcal/24hr) = 66 + (13.7 × wt) + (5.0 × ht) - (6.7 × age)
• Women:
BEE (kcal/24hr) = 655 + (9.6 × wt) + (1.8 × ht) - (4.7 × age)
 Resting Energy Expenditure (REE): Energy expenditure of
basal metabolism in the resting but not fasted state.
• REE (kcal/24hr) = BEE × 1.2
Calorie requirement = BEE x Activity factor x Stress factor

21. AF = Activity factor DF = Disease factor TF = Thermal factor
1.2 Bed rest 1.25 General surgery 1.1 38ᵒC
1.3 Out of bed 1.3 Sepsis 1.2 39ᵒC
1.6 Multiorgan failure 1.3 40ᵒC
1.7 30-50% burns 1.4 41ᵒC
1.8 50-70% burns
2.0 70-90% burns

22.  Indirect Calorimetry
• Most accurate method for determining the daily
energy requirements of individual patients.
• The metabolic energy expenditure is measured
indirectly by measuring the whole-body VO2 and
VCO2.
REE (kcal/24hr) = [(3.9 × VO2) + (1.1 × VCO2) - 61] ×
1440
• Limitation : Expensive and time consuming.
Unreliable at higher FiO₂ (> 60%)

23. • Nutrients May Not Correct Malnutrition in
the ICU
– Malnutrition that accompanies serious illnesses is due to
abnormal nutrient processing. As such, the intake of nutrients
may not correct the malnutrition in the ICU unless primary
disease process is controlled.
 Nutrients as Toxins in the ICU
 In the setting of abnormal nutrient processing, nutrient intake
can be used to generate metabolic toxins.
 In a study conducted on patients undergoing abdominal
aneurysm surgery, administration of 5% dextrose solution
resulted in increase of blood lactate by 3 mmol/L as compared
to 1 mmol/L in the patients who received glucose-free (Ringer's)
solution.

24. • Primary indication : Preventing or treating
malnutrition among patients unable or unwilling to
sustain sufficient oral intake.
• Acute phase of stressful illness.
• Preoperative malnutrition : Benefit demonstrated
only in severely malnourished, who had fewer
noninfectious postoperative complications.
• Postoperative nutritional support: Patients not
anticipated to resume adequate oral intake within 7 to
8 days after surgery.
• Mechanically ventilated ICU patients : Enteral
nutrition started 24 to 48 hours of ICU admission,
shown to reduce infectious complications and
duration of hospitalization.

26. Enteral Parenteral
Advantages
• Simpler
• Cheaper
• No CVC required
• Less monitoring
• Less complication
Advantages
• Independent of GIT functions
Disadvantages
• Dependent on GIT functions
•-Diarrhea
•-Feed intolerance
• NG tube malposition
• Pulmonary aspiration
Disadvantages
• Non physiological
• Requires venous access
• Higher risk of systemic
infection
• Expensive
• More complication

28. • Trophic Effect of Enteral Nutrients
– The bowel mucosa relies on nutrients in the bowel
lumen to provide its nutritional needs.
– Complete bowel rest is accompanied by progressive
atrophy and disruption of the intestinal mucosa.
– The amino acid glutamine is considered the principal
metabolic fuel for intestinal epithelial cells.
• Translocation
– During periods of bowel rest in critically ill patients
mucosal disruption from lack of luminal nutrients occurs.
Enteric pathogens move across the bowel mucosa and
into the systemic circulation.
– Enteral nutrition could help prevent translocation and
subsequent sepsis by maintaining the functional
integrity of the bowel mucosa.

29. Photomicrographs showing the normal appearance
of the small bowel mucosa (upper), and the mucosal
disruption after 1 week of a protein-deficient diet
(lower)

30. • Absolute Contraindications
– Circulatory shock,
– Intestinal ischaemia
– Complete mechanical bowel obstruction
– Ileus.
• Partial (low volume) Enteral Support May Be Possible
In
 Mechanical bowel obstruction
 Severe or unrelenting diarrhea
 Pancreatitis
 High-volume (>500 mL daily) enterocutaneous fistulas.

31. Nasogastric tube
Naso-duodenostomy tube
Nasojejunal tube
Jejunostomy tube
Percutaneous feeding gastrostomy

32. Delivery method Common indications Precautions
Nasogastric/
orogastric
-Unable to consume oral nutrition ( eg.
Intubated, sedated, neurologically
impaired)
- Hypermetabolism in the presence of
functional GIT ( e.g. burns)
-Tube must be secured
- Verify placement of tube
by blue litmus method or
by x-ray
Nasoduodenal/
Nasojejunal
-Inadequate gastric motility
(e.g.gastroparesis)
-Partial gastric outlet obstruction
- Severe aspiration risk
- Oesophageal reflux
- After upper GI surgery
-Tube must be secured
-Verify placement of tube
by X-ray or endoscopically
-Potential dumping
syndrome
Gastrostomy
-Percutaneous
endoscopic (PEG)
-Surgical
-Anyone who requires medium to long
term NG tube feeding ( > 1 mnth)
-Head and neck injury/surgery
-Caution in patients with
severe GE reflux or
gastroparesis
- Contraindicated in
patients with ascites and
coagulopathies.
Jejunostomy
-PEJ
-Surgical
- Injury, obstruction or fistula proximal to
jejunum
- Potential dumping
syndrome

33. Initiating Water Trial
 A volume of water that is equivalent to the
desired hourly feeding volume should be infused
over 1 hour.
 After the infusion, the feeding tube should be
clamped for 30 minutes.
 The tube should then be unclamped and residual
volume should be aspirated. If the 4 hour gastric
residual volume is less than 200 mL, gastric
feeding can proceed.
 If the residual volume is excessively high,
duodenal or jejunal feedings may be more
appropriate.

34. • Starter Regimens
– Starter regimens(dilute formulas with slow infusion
rate) are unnecessary for gastric feedings.
– Because of the limited reservoir function of the small
bowel, starter regimens are usually required for
duodenal and jejunal feedings.
• Tube feedings are usually infused for 12 to 16 hours in
each 24-hour period.
• A period of bowel rest in between feeds is necessary to
prevent malabsorption and diarrhoea.

35. • Tube Occlusion
– Preventive measures include flushing the feeding
tubes with 30 mL of water every 4 hours, and
using a 10 mL water flush after medications are
instilled.
– Relieving the Obstruction: If there is still some
flow through the tube, warm water should be
injected into the tube and agitated with a syringe.
If this is ineffective, pancreatic enzyme + sodium
carbonate solution can be used. A flexible wire or
a drum cartridge may be used to clear a complete
obstruction.

36. • Aspiration
– Risk of reflux in gastric feedings is the same as that in
duodenal feedings . Elevating the head of the bed to
30 to 45 degrees can reduce the risk
– Glucose Reagent Strips: A glucose concentration
greater than 20 mg/dL in tracheal aspirates is
evidence of aspiration.
• Diarrhoea
– Causes: Osmotic diarrhea, sorbitol-containing drug
preparations, Clostridium difficile enterocolitis.
– A Stool Osmolal Gap greater than 160 mOsm/kg
suggests an osmotic diarrhoea secondary to
hypertonic tube feedings or medicinal elixirs, whereas
a smaller osmolal gap suggests a secretory diarrhea
caused by C. difficile enterocolitis.

37. • Motility of the small bowel is often unimpaired after abdominal
surgery. Jejunal feedings allows immediate postoperative nutrition
in abdominal surgeries and for nutritional support of patients with
pancreatitis.
• Feeding Method
• Starter regimens are recommended for jejunal feedings.
• Feedings are usually initiated at a rate of 15 to 25
mL/hour, and gradually increased over the next few
days until full nutritional support is achieved .
• Needle Catheter Jejunostomy:
– A feeding jejunostomy can be performed as a complementary
procedure during laparotomy. only for temporary nutritional
support (approximately 1 week).
– If more prolonged jejunal feedings are desired, a needle
catheter jejunostomy can be converted to a standard
jejunostomy.

38. • The term “Immunonutrition” has been used to
describe enteral feeding formulas that have been
supplemented with components that have beneficial
or potentially beneficial effects on immune function.
Components
• Arginine
– Studies have demonstrated that supplemental
arginine can improve nitrogen balance,
potentiate T-cell immune function and increase
collagen deposition in wound grafts.
– Also functions as a secretagogue increasing GH,
IGF-1 and prolactin levels .

39. • Glutamine
– Amino acid that serves as an oxidative fuel for rapidly
dividing cells like enterocytes.
– Also serves as a nitrogen shuttle and primary
component of the anti-oxidant glutathione
– Not present in PN formulas because it is unstable in
solution
• Omega-3 Fatty Acids
– ώ- 3 fatty acids like eicosapentanoic acid and
docosahexanoic acid compete with arachidonic acid
and influence production of Prostagalandins,
leucotrienes, thromboxanes and prostacyclines.
– Addition of EPA and DHA to enteral nutriion products
results in reduction of pro-inflammatory mediators in
stressed patients.

40. • Nucleotides
 Animal studies have shown that diets supplemented
with nucleotides improves the immune response and
increases the survival rate in response to an
infectious challenge.
• Antioxidants
– This includes Vitamin E, Vitamin C, selenium and Zinc.

41. • Probiotics
 Critical illness causes virulence of gut bacteria;
treatment worsens gut function .
 Probiotics inhibit growth of pathogenic enteric
bacteria .
 Block epithelial invasion by pathogens and eliminate
pathogenic toxins .
 Improve mucosal barrier function .
 Enhance T-cell and macrophage function.
 Reduce production of pro-inflammatory cytokines.

42.  Indication:All patients who are not expected to be on a full
oral diet within 3 days should receive EN.
 Indication of Early Enteral Nutrition: Critically ill patients,
who are haemodynamically stable and have a functioning
GI tract should be fed early (<24 h).
 Amount:
• Acute phase: 20–25 kcal/kg BW/day
• Recovery (anabolic flow phase): 25–30 total kcal/kg
• Severe undernutrition: 25–30 total kcal/kg BW/day
 Route: No significant difference in the efficacy of jejunal
versus gastric feeding in critically ill.
 In patients who cannot be fed sufficient enterally, the
deficit should be supplemented parenterally.

43.  Indications of immune-modulating formula
• In elective upper GI surgical patients.
• Patients with a mild sepsis (APACHE II<15)
• Trauma patients.
• ARDS
 Contraindications of immune-modulating formula
• ICU patients with very severe illness and who do not
tolerate more than 700 ml EN/day
• Severe sepsis (APACHE II>15)
 Glutamine supplementation
• Glutamine should be added to a standard enteral
formula in burn patients and trauma patients.
• Sufficient data not available to support enteral
glutamine supplementation in surgical or
heterogenous critically ill patients.

44. • Definition: Delivery of all the
necessary, required substrates
(combination of concentrated
glucose + amino acids + lipids)
via a central vein thus bypassing
the GI tract.

45. • Dextrose Solutions
 The standard nutritional support regimen uses
carbohydrates to supply approximately 70% of the
daily (non-protein) calorie requirements.
 The dextrose solutions must be concentrated to
provide enough calories to satisfy daily requirements.
 The dextrose solutions used for TPN are hyperosmolar
and should be infused through large central veins.

47.  The standard amino acid solutions contain
approximately 50% essential amino acids (n = 9)
and 50% nonessential (n = 10) and semiessential
(n= 4) amino acids.
 Nutritional formulas for hypercatabolic conditions
(e.g.,trauma) and hepatic failure can be
supplemented with branched chain amino acids
(isoleucine, leucine, and valine).
 Glutamine
– Glutamine-supplemented TPN may play an important
role in maintaining the functional integrity of the bowel
mucosa and preventing bacterial translocation.
– Glutamine levels in blood and tissues drop precipitously
in acute, hypercatabolic conditions (e.g. trauma), so
glutamine may be a “conditionally essential” amino acid.

49. • IV lipid emulsions consist of submicron droplets
(=0.45 mm) of cholesterol and phospholipids
surrounding a core of long-chain triglycerides.
• Lipid emulsions are available in 10% and 20%
strengths providing approximately 1 kcal/mL, 2
kcal/mL respectively.
• Lipid emulsions are roughly isotonic to plasma
and can be infused through peripheral veins.
• Lipids can promote oxidant-induced cell injury,
restricting the use of lipids in critically ill patient
is recommended.
• Maximum recommended rate of infusion is 50
mL/hour

51. • Commercially available mixtures of
electrolytes, vitamins, and trace elements are
added directly to the dextrose–amino acid
mixtures.
• These mixtures are designed to provide the
normal daily requirements of each of these
elements.
• Trace element mixtures do not contain iron
and iodine. It is prudent to select a trace
element additive that contains selenium.

52. • Initiate PN slowly with volumetric infusion
pump; 50% on day 1, 75% on day 2 and
100% on day 3-4.
• Within 3-5 days, most pts. tolerate 3 L of
solution per day.

53. • History: Fever, h/o fluid overload or glucose and electrolyte
imbalance.
• Vital signs: Temp., HR, BP, RR
• Fluid balance: Input/Output chart. Weight
• Local care: Inspection and dressing of site of vascular
access.
• Delivery system: Inspection of solution for contamination
and functioning of infusion pump.

54. Test Frequency
Fingerstick glucose test 3 times daily until pt. stable
Blood Glucose, Na+, K+, Cl-,
HCO₃ , BUN
Daily until glucose infusion load
and pt. stable, then twice
weekly
LFT, S.Creatinine, S. Albumin,
PO₄, Ca, Mg, Hb/Hct, WBC
Baseline, then twice weekly
Coagulation Profile Baseline, then weekly
Micronutrient test As indicated

55. Goal: restart oral/enteral food intake as soon as GI
function improves.
 Gradual transition from PN to oral/enteral nutrition.
 Reduce infusion rate to 50% for 1-2 hrs before
stopping PN (minimizes risk of rebound
hypoglycemia).
 When 60% of total energy and protein requirements
are taken orally/enterally, PN may be stopped.
 Oral or IV electrolytes supplementation may be
needed.

56. Step 1
• Estimate the daily protein and calorie requirements.
Step 2
• Take a standard mixture of 10% amino acids (500 mL) and
50%dextrose (500 mL) [A10–D50] and determine the volume of
this mixture that is needed to deliver the estimated daily protein
requirement.
Step 3
• The next step is to determine the total calories that will
be provided by the dextrose in the mixture.
Step 4
• The deficit remaining can be provided by an
intravenous lipid emulsion.

57. • Example:
• For a person weighing 70 kg.
 Total Caloric Requirement:70 X 25 =1750 kcal/day
 Total Protein requirement: 70X 1.4 = 98 g/day
 Amount of A10–D50 needed: 98/50 = 1.9 l (approx)
 Energy provided by A10–D50: 1.9 X 250X 3.14 kcal
= 1615 kcal
 Deficit: 1750- 1615 = 135 kcal
 Amount of 10% lipid emulsion needed = 135 ml
• Daily TPN orders
 1. Provide standard TPN with A10–D50 to run at 80
mL/hour.
 2. Add standard electrolytes, multivitamins, and
trace elements.
 3. Give 10% Intralipid: 135 mL to infuse over 6
hours

58.  Hyperglycemia: Persistent hyperglycemia usually
requires the addition of insulin to the TPN solutions.
 Hypophosphatemia: Movement of glucose into cells is
accompanied by intracellular PO4 shift. May lead to the
“refeeding syndrome” in malnourished patients.
Characterized by Rhabdomyolysis, and leucocyte
dysfunction. In extreme cases it may lead to respiratory
and cardiac failure, Seizures, coma and even sudden
death.
 Fatty Liver: When glucose calories exceed the daily
calorie requirements, there is lipogenesis in the liver
which can progress to fatty infiltration of the liver.

59. • Hypercapnia: Excess carbohydrates promote CO2
retention in patients with respiratory insufficiency
• Lipid Infusions: Increased risk of oxidation-induced cell
injury. Lipid infusions in TPN formulations are associated
with impaired oxygenation and prolonged respiratory
failure.
• Mucosal atrophy: Can predispose to bacterial
translocation and sepsis of bowel origin. Glutamine-supplemented
TPN may help reduce the risk.
• Acalculous Cholecystitis

60.  Parenteral nutrition can occasionally be delivered via
peripheral veins for short periods
 Goal: To provide just enough non-protein calories to
spare the breakdown of proteins to provide energy.
 Not intended for patients who are protein depleted who
are hypercatabolic and at risk of becoming protein
depleted.
 The osmolality should be kept below 900 mOsm/L and
the pH within 7.2–7.4 to slow the rate of osmotic
damage to vessels.
 Therefore, PPN must be delivered with dilute amino acid
and dextrose solutions.

61. Solution Volume
(ml)
Calories
(kcal)
Osmolarity
(mosm/L)
Route Dextrose
(grams)
Amino
acids
(grams)
Lipids
(grams)
Celemix 1000 800 670 PPN 37.5 37.5 50
Nutriflex 1000 480 900 PPN 80 40 -
Intralipid
10%
500 550 272 PPN - - 50
Intralipid
20% 500 1000 273 PPN - - 100

62. • Indications: All patients who are not expected to be on
normal nutrition within 3 days should receive PN within
24 to 48 h if EN is contraindicated or if they cannot
tolerate EN.
• Amount: ICU patients should receive a complete
formulation. The aim should be to provide energy as
close as possible to the measured energy expenditure in
order to decrease negative energy balance. In the
absence of indirect calorimetry, ICU patients should
receive 25 kcal/kg/day increasing to target over the next
2–3 days.
• Supplementary PN with EN: All patients receiving less
than their targeted enteral feeding after 2 days should
be considered for supplementary PN.

63. • Carbohydrates: The minimum amount of
carbohydrate required is about 2 g/kg of glucose
per day. Blood glucose should be maintained
between 4.5 and 6.1 mmol/L. Hyperglycemia
(glucose >10 mmol/L) should also be avoided.
• Lipids: Essential fatty acid provision in long-term
ICU patients is mandatory. Intravenous lipid
emulsions (LCT, MCT or mixed emulsions) can be
administered safely at a rate of 0.7 g/kg to 1.5
g/kg over 12 to 24 hrs. Addition of EPA and DHA
to lipid emulsions has demonstrable effects on cell
membranes and inflammatory processes.

64. • Amino Acids: When PN is indicated, a balanced
amino acid mixture should be infused at
approximately 1.3–1.5 g/kg ideal body weight/day
in conjunction with an adequate energy
supply.The amino acid solution should contain
0.2–0.4 g/kg/day of L-glutamine
• Micronutrients: All PN prescriptions should
include a daily dose of multivitamins and of trace
elements.
• Route: Peripheral venous access devices may be
considered for low osmolarity (<850 mOsmol/L)
mixtures. If peripherally administered PN does not
allow full provision of the patient’s needs then PN
should be centrally administered.

65. • Burns
 A number of trials indicate that enteral nutrition started within a
few hours of admission reduces the magnitude of the stress
response to burns.
 Caloric intake must be closely monitored in burn patients. If
inadequate calories are being ingested supplementation can be
provided with parenteral nutrition.
 Sepsis
 Oral/ enteral feed should be administered, amount as tolerated.
 Mandatory full caloric feeds, should be avoided at first. Low
caloric feeds should be started, advancing only as tolerated.
 Combine IV glucose/ enteral nutrition/ par-enteral nutrition as
required during 1st week of diagnosis.
 No immunomodulating supplementation required in severe
sepsis.

66. Hepatic Dysfunction
 Patients with cirrhosis are frequently nutritionally depleted
secondary to anorexia, large losses of protein into ascites,
and hypermetabolism. They have hyperinsulinemia, insulin
resistance, accelerated gluconeogenesis, increased lipid
oxidation, and, possibly, reduced glycogenesis.
 They need increased protein/amino acid intakes (1.2-
1.5 g/kg/day) to replace the losses due to ascites
formation and high caloric intake to account for
hypermetabolism (25-40 kcal/day)
 If patients develop encephalopathy protein intake must be
limited to 0.8 g/day. Branched-chain amino acid–enriched
solutions and feedings should be considered and aromatic
amino acids should be avoided.

67. • Renal Dysfunction
• Such patients are insulin resistant, catabolic, and hypermetabolic, like
other stressed patients.
• Uraemia exacerbates catabolism because it exacerbates insulin
resistance, metabolic acidosis, and circulating proteases.
• There area also major abnormalities in protein/amino acid handling.
• The protein/amino acid intake may need to be increased because of
dialysis-related loss of amino acids.
• Current recommendations are to provide a combination of essential and
nonessential amino acids.
• Glucose-containing solutions used as replacement solutions during
haemofiltration can be a source of calories.This glucose load must be
considered when designing nutritional regimens.
• Insulin therapy may be needed to reduce hyperglycemia.
• Nutritional regimens for renal failure patients should not contain PO4,
K+, or Mg2+ because conc. of these electrolytes are already elevated.
Ca2+ intake may need to be increased, whereas Na+ content should be
nearly isotonic because of an inability to regulate serum Na+.
concentrations.

68.  Pancreatitis
• The current recommendation is to begin enteral
nutrition early (within 48-72 hours).
• Current evidence suggests that compared with TPN,
enteral nutrition is associated with less infectious
morbidity, shorter hospital lengths of stay, and less
organ failure, with no effect on mortality.
• In addition, enteral nutrition may be associated with
less hyperglycemia and reduced insulin requirements.
• Therefore, enteral nutrition is the preferred route of
nutritional support in patients with acute pancreatitis
and TPN should be used only when enteral nutrition
is not tolerated.

69. Congestive Heart Failure
– A low-sodium intake is essential
– Ischemic cardiac muscle derives all its energy from
anaerobic metabolism, so TPN with adequate glucose,
potassium, phosphate, and insulin may optimize
substrate delivery to areas limited to anaerobic
glycolysis.
– Patients treated with diuretics(eg, furosemide) are at
an increased risk for thiamine deficiency and
supplementation of thiamine is necessary to
counteract the risk for high-output congestive heart
failure associated with thiamine deficiency.

70. • Recognition and management of malnutrition is
essential to improve clinical outcome in the critical
care setup.
• Since conventional nutritional therapy of
malnourished critically ill patients has not been
demonstrated to produce anabolism, blunting of the
catabolic state may be the more effective strategy.
• Whenever possible, early enteral feeding should be
started and provision of adequate calories, proteins
and micronutrients must be ensured.
• Parenteral nutrition must be considered if adequate
enteral nutrition is not possible.
• Finally aggressive nutritional therapy leading to
overfeeding must also be avoided.