Nutrition in ICUDr RAHUL VARSHENY

Nutrition in ICUDr RAHUL VARSHENY

▪ It is standard practice to provide nutritional support to critically ill patientsin order to treat existing malnutrition and minimise wasting of lean bodymass. However, despite the universality of this practice, the evidenceunderlying it is often conflicting and of disappointingly poor quality.

▪ The overall efficacy of nutritional support, the need to start nutritionaltherapy (NT) in the first place, and its likelihood to impact patientoutcome are all determined by a number of clinical factors.

▪ When spontaneous oral intake is not possible or insufficient, or feedingpatterns are disrupted, nutritional intervention is valuable. The quantityand quality of nutritional intake varies constantly to adjust to physiologicneeds and thus is highly individualized.

▪ The appropriate route or specific design of therapy for one diseaseprocess cannot necessarily be extrapolated (or expected to be effective)for a different disease process.

Importance of nutrition in critical care

Metabolic changes in

critical illness

Acute phase

response

Catabolism

Insulin resistance

Loss of lean body

mass10% significant

20% critical

≥ 30% lethal

Past And Present

▪ In the past, Goals of nutritional support were to provide adjunctivetherapy to support the stress response, provide exogenous nutrients toreduce the drain on endogenous stores and the depletion of lean bodymass, and prevent the consequences of protein-calorie malnutrition.

▪ Today, providing early enteral feeding to critically ill patients is seen as atherapeutic tool or strategy to attenuate disease severity, modulate theimmune response, restore or maintain gastrointestinal (GI) physiology,and through these effects, favourably impact patient outcome. Basiclaboratory research and extensive clinical trials provide the basis forprovision of NT to those patients who need it.

▪ Less than ideal NT is unfortunately provided to a significant proportionof ICU patients

Assessment in a critically ill patient

▪ All patients need a thorough and careful evaluation of their capacity to eat

and the quantity and quality of their nutritional intake.

▪ Objective assessment of nutritional status is difficult in ICU, because disease

processes confound methods used in the general population.

▪ Anthropometric measures such as triceps skin-fold thickness and mid-arm

circumference may be obscured by oedema. Voluntary handgrip strength is

impractical in unconscious patients.

▪ Laboratory measures, including transferrin, pre-albumin and albumin levels,

lymphocyte counts, and skin-prick test reactivity, are abnormal in critical

illness.

▪ Clinical evaluation – the so-called subjective global assessment – is better

than objective measurement at predicting morbidity.

1. Obtaining an excellent history and physical examination,identifying clinical signs of malnutrition.

2. Evaluate the status of the GI tract.

3. Concept of Ileus - clinical impression that the gut is “not working” canbe misleading because intestinal motility is segmental in nature.

Gastric residual volume, Output from gastric port and passage ofstool and gas are valuable indices.

4. Period of Starvation.

5. Monitor feed tolerance, Blood glucose, TG, Urea, Nitrogen, etc.

Patient selection and Timing of support

▪ Good evidence now supports the early institution of nutritional support,and the trend is both to tolerate much shorter periods without nutritionand to begin feeding more rapidly after initial resuscitation.

▪ This belief is based on the close association between malnutrition,negative nitrogen and calorie balance and poor outcome, and theinevitability of death if starvation continues for long enough.

▪ In 1997, recommendations from a conference sponsored by the USNational Institutes of Health, the American Society for Parenteral andEnteral Nutrition (ASPEN) and the American Society for ClinicalNutrition suggested that nutritional support be started in any critically illpatient unlikely to regain oral intake within 7–10 days.

Nutritional requirements

▪ Two methods are commonly used: indirect calorimetry and predictive equations.

▪ Indirect calorimetry being the gold standard to determine Resting energy expenditure (REE).Clinical studies have shown that REE measurement obtained over 30 mins and extrapolatedto 24 hrs are equivalent to REE measurements performed for the entire day. Although, thereare no clear data to relate measured REE to total energy expenditure in the individual patient.

▪ Presently most ICUs do not use calorimetry as it requires expensive equipments along withtrained personnel.

1. Energy

▪ The recommendations of the British Association for Parenteral and Enteral Nutrition are:

1. Determine BMR from Schofield’s equations (Table 1).

2. Adjust BMR for stress (Table 2).

3. Add a combined factor for activity- and diet-induced thermogenesis:

▪ Bed-bound, immobile: +10%

▪ Bed-bound, mobile/sitting: +20%

▪ Mobile around ward: +25%.

▪ There are several equations claiming to predict basal metabolic rate (BMR) on the basis ofweight, sex and age. Correction factors exist to convert predictions of BMR into estimatedenergy expenditure.

▪ Despite the popularity of measurements or estimates of energy expenditure it is not

clear that their routine use improves outcome. Many clinicians dispense with both

and simply aim to deliver the ACCP’s recommended target of 25 kcal/kg/day.

REE(Kcal/day)= 25 x Body weight (Kg)

▪ More recently, concerns have been raised that this standard intake may be

excessive. One small study showed no change in ICU or 28-day mortality, but a

reduction in hospital and 180-day mortality, in patients fed with a target of 60–70% of

their calculated requirement compared with those fed at 90–100% of required energy

intake.

▪ Assessment of nitrogen balance by measuring urinary urea nitrogen is too

variable to be useful in estimating protein requirements in ICU. As there is

an upper limit to the amount of dietary protein that can be used for

synthesis, there is no benefit from replacing nitrogen lost in excess of this.

A daily nitrogen provision of 0.15–0.2 g/kg/day is therefore recommended

for the ICU population; this is equivalent to 1–1.25 g protein/kg/day.

Severely hyper-catabolic individuals, such as those with major burns, are

given up to 0.3 g nitrogen/ kg/day, or nearly 2 g protein/kg/day.

2. Protein

▪ Carbohydrates

Standard nutrition regimens use carbohydrates to provide about 70% of the non-protein calories. The human body has limited carbohydrate stores, and daily intakeof carbohydrates is necessary to ensure proper functioning of the central nervoussystem, which relies heavily on glucose as a nutritive fuel. However, excessivecarbohydrate intake promotes hyperglycaemia, which has several deleteriouseffects, including impaired immune responsiveness in leukocytes

▪ Lipids

Standard nutrition regimens use lipids to provide approximately 30% of the dailyenergy needs. Dietary lipids have the highest energy yield of the three nutrient fuels,and lipid stores in adipose tissues represent the major endogenous fuel source inhealthy adults

3. Non – Protein Calories

▪ Critical illness increases the requirements for vitaminsA, E, K, thiamine (B1), B3, B6, vitamin C andpantothenic and folic acids.

▪ Thiamine, folic acid and vitamin K are particularlyvulnerable to deficiency during total parenteralnutrition (TPN).

▪ Deficiencies of selenium, zinc, manganese andcopper have been described in critical illness, inaddition to the more familiar iron-deficient state.

▪ Subclinical deficiencies in critically ill patients arethought to cause immune deficiency and reducedresistance to oxidative stress.

▪ Commercial preparations of both enteral and

▪ parenteral feeding solutions contain standard amountsof micronutrients.

4. Micro- nutrients

Routes of nutrition

Enteral ParenteralSupplemental

Parenteral

Enteral Nutrition

▪ Nasal tubes are preferred to oral, except in patients with a basalskull fracture, in whom there is a risk of cranial penetration.

▪ A large-bore (12–14 Fr) nasogastric tube is usually used at first.Once feeding is established and gastric residual volumes nolonger need to be checked this can be replaced with a morecomfortable fine-bore tube.

▪ Routine use of small-bowel feedings is recommended. If routine use is not feasible,small-bowel feedings should be considered for patients at high risk for intolerance toEN (e.g., patients receiving inotropic or vasoactive drugs, continuous infusion ofsedatives, or paralytic agents; or those with large volumes of nasogastric drainage) orat high risk for regurgitation and aspiration (e.g., patients kept supine). The positionof all tubes must be checked on X-ray before feeding is started, as misplacement is notuncommon and intrapulmonary delivery of feed is potentially fatal.

▪ An alternative method of access in those needing long-term enteral feeding ispercutaneous gastrostomy, which can be performed endoscopically or radiologically.

Feeding Formulas

▪ Feeding formulas are available with caloric densities of 1 kcal/mL, 1.5 kcal/ml, and 2 kcal/ml.

Most tube feeding regimens use formulas with 1 kcal/ml. The high-calorie formulas (2 kcal/ml)

are intended for patients with severe physiological stress (e.g., multisystem trauma and

burns), but they are frequently used when volume restriction is a priority.

▪ In standard feeding formulas, non-protein calories account for about 85% of the total calories.

Daily caloric requirements should be provided by non-protein calories.

▪ Most enteral formulas contain intact proteins that are broken down into amino acids in the

upper GI tract. These are called polymeric formulas.

Feeding formulas are also available that contain

small peptides, called semi-elemental formulas

and individual amino acids called elemental formulas

that are absorbed more readily than intact protein.

▪ Carbohydrates (usually polysaccharides) are the major source of calories in feedingformulas, and provide 40–70% of the total calories.

▪ Fiber is added to some feeding formulas to promote the viability of the mucosa in thelarge bowel. The fiber in most feeding formulas is a mixture of fermentable andnonfermentable varieties

▪ Standard feeding formulas contain polyunsaturated fatty acids from vegetable oils.The lipid content is adjusted to provide about 30% of the caloric density of theformula

Creating a Feeding Regimen

Regimen

▪ Start delivering around 30 mL/h and build up to the target intake depending on tolerance,as judged by gastric residual volumes. These are assessed by aspiration of the tube every4 hours.

▪ Head-injured patients fed with target intake from the outset have fewer infectivecomplications, and the practice has subsequently been shown to be safe in unselected ICUpatients.

▪ Gastric residual volumes over 150 mL on two successive occasions have been associatedwith an increased incidence of ventilator-associated pneumonia in one study; but incontrast others have found no link between high residual volumes and the risk ofaspiration.

▪ In refractory cases a nasojejunal tube often permitssuccessful enteral feeding, because small bowelfunction is resumed quicker than gastric emptying.

▪ Absence of bowel sounds is common in ventilated patients and should not be taken to indicate ileus.

Complication

▪ Regurgitation

▪ Diarrhoea

Common causes include antibiotic therapy, Clostridium difficile infection, faecalimpaction, malabsorption, Lactose intolerance, sorbitol composition and non-specificeffect of critical illness. Slowing the rate of feeding sometimes helps; diluting theformula does not.

▪ Tube Occlusion

Standard preventive measures include flushing the feeding tubes with 30 mL of waterevery 4 hours, and using a 10-mL water flush after medications are instilled.

▪ Independent risk factor for ventilator-associated pneumonia

▪ Fine-bore tubes are vulnerable to misplacement in the trachea or to perforation of thepharynx, oesophagus, stomach or bowel.

▪ Metabolic complications include electrolyte abnormalities and hyperglycaemia.

▪ Severely malnourished patients are at risk of refeeding syndrome.

Parenteral nutrition

▪ Definition:

Pharmacological therapies where nutrients, vitamins,electrolytes and medications are delivered via venous routeto those patients whose GIT is not functioning and areunable to tolerate enteral nutrition.

Parenteral nutritional support is indicated when adequate enteral intake

cannot be established within an acceptable time. In some cases absolute

gastrointestinal failure is obvious, whereas in others it becomes apparent only

after considerable efforts to feed enterally have failed. As discussed above, there

is increasing evidence that if enteral feeding cannot be established early then

the parenteral route should be used until it can. Nevertheless, the aim in all

patients fed intravenously should be to revert to enteral feeding as this becomes

possible.

▪ Parenteral feeding solutions maybe prepared from their componentparts under sterile conditions.

▪ Readymade solutions also exist,but any necessary additions mustbe made in the same way.

▪ In ICU patients the dailyrequirements are infusedcontinuously over 24 hours. Carefulbiochemical and clinical monitoringis important, particularly at theoutset

Selection of PN

▪ In almost all critical care patient populations involving a wide range of disease processes(from surgery and pancreatitis to trauma, burns, and critically ill patients on mechanicalventilation), EN is first-line therapy and should be chosen before PN.

▪ The presence of protein-calorie malnutrition (PCM) reverses the choice between standardtherapy and PN. In general, PN has greater efficacy in patients with PCM, and the chance of afavourable impact on patient outcome is more likely with PN than with standard therapy.Those patients with severe PCM, the ones most likely to benefit from PN, usually represent avery small minority of patients. The prevalence of severe PCM in some studies of ICU patientsranged from 8.3% to 12.6%.

▪ Critically ill patients with sepsis and multiple organ dysfunction respond poorly to PN.

▪ When EN is not feasible, aggressive nutritional support may have to be held for 7 to 10 daysfollowing an injury or an acute event. These patients, despite critical illness, sepsis, andmultiple organ dysfunction, are better managed by standard therapy with no PN support overthis initial period. Only if there is evidence of PCM (and EN is not feasible) should PN be givenpreferentially over standard therapy in the first week.

Access

▪ Insertion site: subclavian lines have lower infection

rates than internal jugular or femoral lines.

▪ Tunnelling may reduce infection rates in internal

jugular lines but apparently not in short-term

subclavian lines. It is not recommended for routine

use.

▪ Expertise of operator and adequacy of ICU nurse

staffing levels affect infection rate.

▪ Skin preparation: 2% chlorhexidine in alcohol is the

most effective.

The major concern with central venous access for TPN is prevention of infection. The

following considerations apply:

▪ Sterile technique: maximal sterile barrier procedures (mask, cap, gown, gloves, andlarge drape) are known to reduce catheter-related bacteraemia rates six-fold. Thereis a bewildering resistance to use of these precautions outside ICUs.

▪ Dressings: permeable polyurethane transparent dressings are superior toimpermeable.

▪ Antimicrobial catheters: catheters coated with either chlorhexidine and silversulfadiazine or rifampicin and minocycline are several times less likely to causebacteraemia than standard polyurethane catheters.

▪ Scheduled exchange has not been proven to reduce catheter-related sepsis.

▪ If a multi-lumen catheter is used, one lumen should be dedicated to administration ofTPN and not used for any other purpose. Three-way taps should be avoided andinfusion set changes carried out daily under sterile conditions.

Composition▪ Energy is provided by a combination of carbohydrate and lipid. The optimal balance

between the two is unknown; often 30–40% of non-protein energy is given as lipid.Alternatively, glucose may be relied upon for almost all the energy, with lipid beinginfused once or twice a week to provide essential fatty acids.

▪ Glucose is the preferred carbohydrate and is infused as a concentrated solution.Exceeding the body’s capacity to metabolise glucose (4 mg/kg/min in the septic patient)can lead to hyperglycaemia, lipogenesis and excess CO2 production. Endogenousinsulin secretion increases to control blood sugar levels. However, many patientsrequire additional insulin. This may be infused separately, but when requirements arestable it is more safely added to the TPN solution. Persistent hyperglycaemia is betteraddressed by reducing the glucose infusion rate than by large doses of insulin.

▪ Lipid provides essential fatty acids (linoleic and linolenic acids) and is a moreconcentrated energy source than glucose. It may thus avoid the complications ofexcess glucose administration. However, there are concerns of immunosuppressionfrom lipid infusion. Current lipid preparations consist of soybean oil emulsified withglycerol and egg phosphatides.

▪ Nitrogen is supplied as crystalline solutions of L-amino acids. Commercially availablepreparations vary in their provision of conditionally essential amino acids. Standardamino acid solutions are balanced mixtures of 50% essential amino acids and 50%nonessential and semi-essential amino acids. Available concentrations range from 3.5% up to 10%, but 7% solutions (70 g/L) are used most often. Glutamine, tyrosine andcysteine are absent from many because of instability.

▪ Vitamin and trace element preparations are added to TPN solutions in appropriateamounts. Thiamine, folic acid and vitamin K are particularly vulnerable to depletionand additional doses may be necessary.

▪ Amino acid preparations contain

varying quantities of electrolytes;

additional amounts may need to

be added to the solution.

Calculation of daily requirement

▪ Sample calculation for 60 kg, stable, euvolemic patient with good urine output and moderate stress

▪ Fluid requirement: 35ml/kg = 2100 ml/day

▪ Calories: 25kcal/kg = 1500 kcal/day

▪ Proteins: 1g/kg = 60 g/day = 240 kcal/day (4kcal/g)

▪ Fats: 30% of total calories = 450 kcal/day = 50g fat(9kcal/g)

▪ Carbohydrates: 1500 – (240+450) = 810kcal = 202.5g of dextrose(4kcal/g)

Convert requirements into prescription

▪ Determine volume of lipid emulsion: 10% lipid emulsion

Fluid volume reqd. = Amt. of substance(gm) X 100Conc. Of substance(%)

Volume of lipid emulsion = 50/10 x 100 = 500 ml

▪ Determine volume of amino acid infusion: 10 % solution

Volume of amino acids = 60/10 X 100 = 600 ml

▪ Selection of dextrose infusion: in remaining 1000 ml volume, 202.5g dextrose needs to be infused.

1000 = 202.5 X 100

Conc. of subst.

▪ Concentration of substance = 202.5/1000 X 100 = 20.25%

= 20% approx.

▪ Prescription: Pt. needs

500ml of 10% lipid emulsion

600ml of 10% amino acid and

1000 ml of 20% dextrose

Termination of parenteral nutrition

▪ 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.

Lipid Content

▪ Intralipid with PN is controversial because past studies have shown that long-chain

fats can cause immune suppression. It can promote dysfunction of the

reticuloendothelial system, enhance formation of prostanoids and leukotrienes,

increase generation of ROS, and adversely affect the composition of cell

membranes.

▪ Among trauma patients, the use of PN without lipids versus with lipids was

associated with a significant reduction in pneumonia (48% versus 73%; P=0.05),

catheter-related sepsis (19% versus 43%; P=0.04), length of ICU stay (18 versus

29 days; P=0.02), and length of hospital stay (27 versus 39 days; P=0.03).

▪ However, some fat—at least 5% of total calories—has to be provided as lipid

emulsion to prevent essential fatty acid deficiency, although this issue is usually not

important until after the first 10 days of hospitalization.

Hyperglycemia

▪ Hyperglycemia might be a key factor in the reduced efficacy and increased rate ofcomplications associated with PN. Hyperglycemia impairs neutrophil chemotaxis andphagocytosis, leads to glycosylation of immunoglobulins, impairs wound healing,alters function of the complement cascade, and exacerbates inflammation.

▪ In an early meta-analysis, routes of feeding in trauma patients, mean blood glucoseconcentration was greater than 200 mg/dL in the PN group on postoperative days 7to 9, whereas it was only 132 mg/dL during the same period in patients receiving EN(P<0.05). Incidence of infection was 44% in the PN group and 17% in the EN group(P<0.05).

▪ Therefore, one can infer that hyperglycemia (defined as a circulating glucoseconcentration > 200 mg/dL) is associated with poor outcome in different critically illpatient populations including trauma, strokes, and acute coronary syndromes. Usingconventional glucose monitoring systems, glucose levels below 180 mg/dL shouldbe maintained in critically ill patients.

Complications

Other Parenteral nutrition has the potential for severe complications.

▪ Catheter-related sepsis and misdirected catheter.

▪ Electrolyte abnormalities include hypophosphataemia, hypokalaemia and

hypomagnesaemia, especially in the first 24–48 hours.

▪ Hyperchloraemic metabolic acidosis may result from amino acid solutions with a high

chloride content. Replacing some chloride with acetate in the TPN solution will

resolve this where necessary.

▪ Rebound hypoglycaemia may occur when TPN is discontinued suddenly. TPN should

be weaned over a minimum of 12 hours. If it cannot be continued, an infusion of 10%

dextrose should be started and blood sugars closely monitored.

▪ Oleic acid, is one of the lipids in TPN, is a standard method for producing the acuterespiratory distress syndrome (ARDS), and this might explain why lipid infusions areassociated with impaired oxygenation

▪ Refeeding syndrome may occur when normal intake is resumed after a period ofstarvation. It is associated with profound hypo-phosphataemia, and possiblyhypokalaemia and hypomagnesaemia. With the restoration of glucose as a substrate,insulin levels rise and cause cellular uptake of these ions. Depletion of adenosinetriphosphate (ATP) and 2,3-diphosphoglyceric acid (2,3-DPG) results in tissuehypoxia and failure of cellular energy metabolism. This may manifest as cardiac andrespiratory failure, with paraesthesia and seizures also reported. Thiamine deficiencymay also play a part.

▪ Liver dysfunction is common during TPN. Causes include hepatic steatosis,intrahepatic cholestasis and biliary sludging from gallbladder inactivity. The problemsnecessitating TPN in the first place may also cause liver dysfunction.

▪ Deficiencies of trace elements and vitamins (especially thiamine, folic acid andvitamin K) may occur.

Adjunctive nutrition

Certain substances have been used as adjuncts to feeding solutions, in attempts to modulate the metabolic and immune responses to critical illness.

▪ Glutamine

▪ Arginine

▪ Selenium

▪ Antioxidants Vitamins

Glutamine

▪ The amino acid, Glutamine, plays a central role in nitrogen transport within thebody. It is used as a fuel by rapidly dividing cells, particularly lymphocytes and gutepithelial cells and is also a substrate for synthesis of the important endogenousantioxidant, glutathione.

▪ Although l-glutamine is not an essential amino acid under normal conditions,plasma l-glutamine concentration decreases during critical illness, and lowcirculating levels of l-glutamine have been associated with immune dysfunctionand increased mortality. Thus, glutamine may be regarded as a “conditionallyessential” amino acid.

▪ glutamine supplementation is associated with a significant reduction in mortality,reduction in infectious complications and no overall effect on length of stay.

▪ Therefore, glutamine has been recommended as a daily nutritional supplement inICU patients (0.2– 0.4 g/kg/day).

ARGININE AND IMMUNONUTRITION

▪ In the absence of illness, l-arginine supplementation fails to demonstrate any significant effects onimmune function. Upon immune activation, l-arginine transport is significantly increased in bothmyeloid and lymphoid cells.

▪ Guidelines for arginine supplementation can be summarized as follows:

1. Higher than normal arginine supplementation is necessary. Normal is 3 to 5 g/d.

2. Combination of arginine, omega-3 fatty acids, and nucleotides have been extensively tested andproven to provide a clear clinical benefit. Arginine alone should not be used.

3. Patients undergoing major elective surgery benefit from the use of immuno-nutrition formulascontaining arginine. The risk of infections is reduced approximately 40%. This has been endorsedas a grade A recommendation by all major nutrition societies and the Society of Critical CareMedicine (SCCM).

4. Ideally it should be started preoperatively as an oral dietary supplement and continued in thepostoperative period as early as possible. In general, these diets should be started 5 days prior tosurgery and continued 5 to 10 days postoperatively.

5. A clear benefit of l-arginine-containing immuno-nutrition has not been observed in medicalpatients, particularly those with sepsis.

SELENIUM

▪ Selenium is necessary in the regulation of glutathione peroxidase, the major scavengingsystem for oxygen free radicals. Low plasma selenium levels are common in ICU patients,and a number of small studies have shown potential benefits, but these could not bereproduced in two recent larger trials.

ANTIOXIDANT VITAMINS

▪ In critical illness, oxidative stress arises as the result of an imbalance between protectiveantioxidant mechanisms and generation of ROS.

▪ This imbalance may be due to excess generation of ROS, low antioxidant capacity, or both.Plasma and intracellular concentrations of the various antioxidants are abnormally low insubpopulations of critically ill patients.

▪ Thus for critically ill patients, selenium supplementation in combination with other antioxidants(vitamin E or alpha tocopherol, vitamin C, N-acetylcysteine, zinc) may be beneficial.

Elective

Surgery

Critically Ill

General Septic Trauma Burns Acute Lung Injury

Arginine Benefit No benefit Harm(?) (Possible

benefit)No benefit No benefit

Glutamine Possible

BenefitPN Beneficial

(Recommend)

… EN Possibly

Beneficial:

Consider

EN Possibly

Beneficial:

Consider

…

Omega 3 FFA … … … … … Recommend

Anti-oxidants … Consider … … … …

Canadian Clinical Practice Guidelines JPEN 2003;27:355

Which Nutrient for which population!!!

Why Use the Gut??

The Role of enteral tube feeding in protecting against infections is summerized as follows:

▪ Enteral nutrients maintain the integrity of tight junctions between intestinal epithelial cells,stimulate blood flow to the gut, and promote release of a variety of endogenous agents such ascholecystokinin, gastrin, bombesin, and bile salts - substances with trophic effects on intestinalepithelium.

▪ Gut disuse, with or without PN, can lead to deterioration of the functional and structural integrity ofthe gut. Intestinal changes caused by starvation in humans are less pronounced than in rodents,but whereas gut disuse may result in a 40% decrease of mucosal mass in rats, the decrease inhumans still appears to be about 10% to 15%.

▪ Starvation alone may be insufficient to increase gut permeability, but injury followed by starvationincreases mucosal permeability proportional to the severity of disease. Increased permeability isprevented through early feeding.

▪ Bacterial translocation, a process whereby bacteria transgress the mucosal barrier, is associated with aerobic bacterial overgrowth and decreased intestinal sIgA levels. The significance of acterialtranslocation in humans as a cause of systemic illness is still unclear.

Impact of Enteral nutrition on outcome

▪ A recently published systematic analysis reviewed data from 13 randomized controlled studiescomparing EN and PN in heterogeneous populations of ICU patients, including those with headtrauma, sepsis, and severe acute pancreatitis, among other conditions. When a meta-analysis wascarried out, there was no apparent difference in mortality rate between patients treated with ENand those treated with PN (relative risk [RR] 1.08; 95% confidence interval [CI], 0.70-1.65).However, compared with PN, EN was associated with a significant reduction in infectiouscomplications.

▪ Eight randomized controlled trials that compared early EN with more delayed forms of nutritionwere recently reviewed and analysed. When these studies were aggregated, early EN wasassociated reduced mortality (RR 0.52; 95% CI, 0.25-1.08) and fewer infectious complications(RR 0.66; 95% CI, 0.36-1.22) compared with delayed nutrient intake. However, there were nodifferences in complications between the groups.

▪ In a recent meta-analysis, there were seven randomized trials that evaluated the effect of route offeeding on rates of ventilator-associated pneumonia. When these results were aggregated,there was a significant reduction in ventilator associated pneumonia with feeding distal tothe pylorus (RR 0.76; 95% CI, 0.59-0.99). These studies also demonstrated that small-bowelfeeding is associated with an increase in protein and calories delivered and a shorter time to attainthe target dose of nutrition.

Supplemental Total Parenteral Nutrition

▪ Few studies have looked at the impact of supplemental PN in patients receiving an

insufficient volume of enteral feeding.

▪ Meta-analysis evaluated five randomized trials that addressed the clinical benefits

of supplemental PN in critically ill patients.125 The aggregated results

demonstrated a trend toward increased mortality associated with the use of

combination EN and PN (RR 1.27; 95% CI, 0.82-1.94; P=0.3). Supplemental PN

was not associated with a difference in the incidence of infection (RR 1.14; 95% CI,

0.66-1.96; P=0.6). Supplemental PN had no effect on hospital stay (standardized

mean difference −0.12 days; 95% CI, −0.45 to 0.2 days; P=0.5) or ventilator days.

Thus, there appears to be no clinical evidence to support the practice of

supplementing EN with PN when EN is initiated. Supplemental PN adds nothing

and may actually worsen the outcome for patients already on EN.

DURATION AND TIMING OF PARENTERAL NUTRITION

▪ The timing of PN initiation is based on the underlying nutritional status of the

patient.

1. critically ill patient who has not resumed oral intake, it is reasonable to wait 7

to 10 days before initiating PN.

2. After 14 days, increased mortality is seen in most patients who are not yet

eating and remain on standard therapy with no nutritional support.

3. PN is indicated over standard therapy for the first 7 to 10 days when the

enteral route is not available in malnourished patients.

Thank You