Presented by:Dr. Md. Zareer Tafadar

Post Graduate Resident

Deptt. Of Anaesthesiology &Critical Care

Silchar Medical College & Hospital.

• 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.

• 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.

69% Adequate Nutritional State

21% ModeratelyMalnourished

10% Severely Malnourished

Detsky et al. JPEN 1987

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.

Physiologic Characteristics

Hypometabolic/Nonstressed 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

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.

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 andscalingof 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.

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.

• 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.

• 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.

• 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.

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.

• 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.

• 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.

• 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.

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

• 7 trace elements are considered essential in humans

Trace Element EnteralDose

ParenteralDose

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

• 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.

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

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

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%)

• 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.

• 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 : Enteralnutrition started 24 to 48 hours of ICU admission, shown to reduce infectious complications and duration of hospitalization.

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

• 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.

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

• 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.

Nasogastric tube

Naso-duodenostomy tube

Nasojejunal tube

Jejunostomy tube

Percutaneous feeding gastrostomy

Delivery method Common indications Precautions

Nasogastric/orogastric

-Unable to consume oral nutrition ( eg. Intubated, sedated, neurologicallyimpaired)- 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-Percutaneousendoscopic (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

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.

• 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.

• 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.

• 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.

• 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.

• 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 .

• 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.

• 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.

• 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.

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 jejunalversus gastric feeding in critically ill.

In patients who cannot be fed sufficient enterally, the deficit should be supplemented parenterally.

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 enteralformula in burn patients and trauma patients.

• Sufficient data not available to support enteralglutamine supplementation in surgical or heterogenous critically ill patients.

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

• 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 hyperosmolarand should be infused through large central veins.

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.

• 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

• 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.

• 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.

• 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.

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

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.

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.

• 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

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 leucocytedysfunction. 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.

• 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

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.

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 -

Intralipid10%

500 550 272 PPN - - 50

Intralipid20% 500 1000 273 PPN

- - 100

• 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.

• 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.

• 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.

• 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.

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 ascitesformation 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.

• 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.

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.

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.

• 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.