GRAND ROUNDS JUNE 2024 NUTRITION powerpoint

▪ It is standard practice to provide nutritional support to critically ill patients
in order to treat existing malnutrition and minimise wasting of lean body
mass. However, despite the universality of this practice, the evidence
underlying it is often conflicting and of disappointingly poor quality.
▪ The overall efficacy of nutritional support, the need to start nutritional
therapy (NT) in the first place, and its likelihood to impact patient
outcome are all determined by a number of clinical factors.
▪ When spontaneous oral intake is not possible or insufficient, or feeding
patterns are disrupted, nutritional intervention is valuable. The quantity
and quality of nutritional intake varies constantly to adjust to physiologic
needs and thus is highly individualized.
▪ The appropriate route or specific design of therapy for one disease
process 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
mass
10% significant
20% critical
≥ 30% lethal

Past And Present
▪ In the past, Goals of nutritional support were to provide adjunctive
therapy to support the stress response, provide exogenous nutrients to
reduce the drain on endogenous stores and the depletion of lean body
mass, and prevent the consequences of protein-calorie malnutrition.
▪ Today, providing early enteral feeding to critically ill patients is seen as a
therapeutic tool or strategy to attenuate disease severity, modulate the
immune response, restore or maintain gastrointestinal (GI) physiology,
and through these effects, favourably impact patient outcome. Basic
laboratory research and extensive clinical trials provide the basis for
provision of NT to those patients who need it.
▪ Less than ideal NT is unfortunately provided to a significant proportion
of 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” can
be misleading because intestinal motility is segmental in nature.
Gastric residual volume, Output from gastric port and passage of
stool 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 nutrition
and 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 the
inevitability of death if starvation continues for long enough.
▪ In 1997, recommendations from a conference sponsored by the US
National Institutes of Health, the American Society for Parenteral and
Enteral Nutrition (ASPEN) and the American Society for Clinical
Nutrition suggested that nutritional support be started in any critically ill
patient 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
extrapolated to 24 hrs are equivalent to REE measurements performed for the entire day.
Although, there are 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 with
trained 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 of
weight, sex and age. Correction factors exist to convert predictions of BMR into estimated
energy 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 intake
of carbohydrates is necessary to ensure proper functioning of the central nervous
system, which relies heavily on glucose as a nutritive fuel. However, excessive
carbohydrate intake promotes hyperglycaemia, which has several deleterious
effects, including impaired immune responsiveness in leukocytes
▪ Lipids
Standard nutrition regimens use lipids to provide approximately 30% of the daily
energy 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 in
healthy adults
3. Non – Protein Calories

▪ Critical illness increases the requirements for vitamins
A, E, K, thiamine (B1), B3, B6, vitamin C and
pantothenic and folic acids.
▪ Thiamine, folic acid and vitamin K are particularly
vulnerable to deficiency during total parenteral
nutrition (TPN).
▪ Deficiencies of selenium, zinc, manganese and
copper have been described in critical illness, in
addition to the more familiar iron-deficient state.
▪ Subclinical deficiencies in critically ill patients are
thought to cause immune deficiency and reduced
resistance to oxidative stress.
▪ Commercial preparations of both enteral and
▪ parenteral feeding solutions contain standard
amounts of micronutrients.
4. Micro- nutrients

Routes of nutrition
Enteral Parenteral
Supplemental
Parenteral

Enteral Nutrition
▪ Nasal tubes are preferred to oral, except in patients with a basal
skull 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 no
longer need to be checked this can be replaced with a more
comfortable 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 to
EN (e.g., patients receiving inotropic or vasoactive drugs, continuous infusion of
sedatives, or paralytic agents; or those with large volumes of nasogastric drainage) or
at high risk for regurgitation and aspiration (e.g., patients kept supine). The position
of all tubes must be checked on X-ray before feeding is started, as misplacement is not
uncommon and intrapulmonary delivery of feed is potentially fatal.
▪ An alternative method of access in those needing long-term enteral feeding is
percutaneous 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 feeding
formulas, and provide 40–70% of the total calories.
▪ Fiber is added to some feeding formulas to promote the viability of the mucosa in the
large bowel. The fiber in most feeding formulas is a mixture of fermentable and
nonfermentable 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 the
formula

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 every
4 hours.
▪ Head-injured patients fed with target intake from the outset have fewer infective
complications, and the practice has subsequently been shown to be safe in unselected
ICU patients.
▪ Gastric residual volumes over 150 mL on two successive occasions have been associated
with an increased incidence of ventilator-associated pneumonia in one study; but in
contrast others have found no link between high residual volumes and the risk of
aspiration.
▪ In refractory cases a nasojejunal tube often permits
successful enteral feeding, because small bowel
function 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, faecal impaction,
malabsorption, Lactose intolerance, sorbitol composition and non-specific effect of critical
illness. Slowing the rate of feeding sometimes helps; diluting the formula does not.
▪ Tube Occlusion
Standard 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.
▪ Independent risk factor for ventilator-associated pneumonia
▪ Fine-bore tubes are vulnerable to misplacement in the trachea or to perforation of the
pharynx, 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 route
to those patients whose GIT is not functioning and are
unable 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 may
be prepared from their component
parts under sterile conditions.
▪ Readymade solutions also exist,
but any necessary additions must
be made in the same way.
▪ In ICU patients the daily
requirements are infused
continuously over 24 hours. Careful
biochemical and clinical monitoring
is important, particularly at the
outset

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 mechanical
ventilation), EN is first-line therapy and should be chosen before PN.
▪ The presence of protein-calorie malnutrition (PCM) reverses the choice between standard
therapy and PN. In general, PN has greater efficacy in patients with PCM, and the chance of a
favourable 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 a
very small minority of patients. The prevalence of severe PCM in some studies of ICU
patients ranged 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 days
following an injury or an acute event. These patients, despite critical illness, sepsis, and
multiple organ dysfunction, are better managed by standard therapy with no PN support over
this initial period. Only if there is evidence of PCM (and EN is not feasible) should PN be
given preferentially 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, and
large drape) are known to reduce catheter-related bacteraemia rates six-fold. There
is a bewildering resistance to use of these precautions outside ICUs.
▪ Dressings: permeable polyurethane transparent dressings are superior to
impermeable.
▪ Antimicrobial catheters: catheters coated with either chlorhexidine and silver
sulfadiazine or rifampicin and minocycline are several times less likely to cause
bacteraemia 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 of
TPN and not used for any other purpose. Three-way taps should be avoided and
infusion 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 being
infused 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. Endogenous
insulin secretion increases to control blood sugar levels. However, many patients
require additional insulin. This may be infused separately, but when requirements are
stable it is more safely added to the TPN solution. Persistent hyperglycaemia is better
addressed by reducing the glucose infusion rate than by large doses of insulin.
▪ Lipid provides essential fatty acids (linoleic and linolenic acids) and is a more
concentrated energy source than glucose. It may thus avoid the complications of
excess glucose administration. However, there are concerns of immunosuppression
from lipid infusion. Current lipid preparations consist of soybean oil emulsified with
glycerol and egg phosphatides.

▪ Nitrogen is supplied as crystalline solutions of L-amino acids. Commercially available
preparations vary in their provision of conditionally essential amino acids. Standard
amino 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 and
cysteine are absent from many because of instability.
▪ Vitamin and trace element preparations are added to TPN solutions in appropriate
amounts. Thiamine, folic acid and vitamin K are particularly vulnerable to depletion
and 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 100
Conc. 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 of
complications associated with PN. Hyperglycemia impairs neutrophil chemotaxis and
phagocytosis, 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 glucose
concentration was greater than 200 mg/dL in the PN group on postoperative days 7
to 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 glucose
concentration > 200 mg/dL) is associated with poor outcome in different critically ill
patient populations including trauma, strokes, and acute coronary syndromes. Using
conventional glucose monitoring systems, glucose levels below 180 mg/dL should
be maintained in critically ill patients.

Complications
Other Parenteral nutrition has the potential for severe complications.
▪ Catheter-related sepsis and misdirected catheter.
▪ Electrolyte abnormalities include hypophosphatemia, hypokalaemia and
hypomagnesaemia, especially in the first 24–48 hours.
▪ Hyperchloremic 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 acute
respiratory distress syndrome (ARDS), and this might explain why lipid infusions are
associated with impaired oxygenation
▪ Refeeding syndrome may occur when normal intake is resumed after a period of
starvation. It is associated with profound hypo-phosphatemia, and possibly
hypokalaemia and hypomagnesaemia. With the restoration of glucose as a substrate,
insulin levels rise and cause cellular uptake of these ions. Depletion of adenosine
triphosphate (ATP) and 2,3-diphosphoglyceric acid (2,3-DPG) results in tissue
hypoxia and failure of cellular energy metabolism. This may manifest as cardiac and
respiratory failure, with paraesthesia and seizures also reported. Thiamine deficiency
may also play a part.
▪ Liver dysfunction is common during TPN. Causes include hepatic steatosis,
intrahepatic cholestasis and biliary sludging from gallbladder inactivity. The problems
necessitating TPN in the first place may also cause liver dysfunction.
▪ Deficiencies of trace elements and vitamins (especially thiamine, folic acid and
vitamin 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 the
body. It is used as a fuel by rapidly dividing cells, particularly lymphocytes and
gut epithelial cells and is also a substrate for synthesis of the important
endogenous antioxidant, glutathione.
▪ Although l-glutamine is not an essential amino acid under normal conditions,
plasma l-glutamine concentration decreases during critical illness, and low
circulating levels of l-glutamine have been associated with immune dysfunction
and increased mortality. Thus, glutamine may be regarded as a “conditionally
essential” 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 in
ICU 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 on immune
function. Upon immune activation, l-arginine transport is significantly increased in both myeloid 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 and proven
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 formulas containing
arginine. The risk of infections is reduced approximately 40%. This has been endorsed as a grade A
recommendation by all major nutrition societies and the Society of Critical Care Medicine (SCCM).
4. Ideally it should be started preoperatively as an oral dietary supplement and continued in the
postoperative period as early as possible. In general, these diets should be started 5 days prior to
surgery and continued 5 to 10 days postoperatively.
5. A clear benefit of l-arginine-containing immuno-nutrition has not been observed in medical patients,
particularly those with sepsis.

SELENIUM
▪ Selenium is necessary in the regulation of glutathione peroxidase, the major scavenging
system 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 be
reproduced in two recent larger trials.
ANTIOXIDANT VITAMINS
▪ In critical illness, oxidative stress arises as the result of an imbalance between protective
antioxidant 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 in
subpopulations 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
Benefit
PN 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 summarized 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 as
cholecystokinin, gastrin, bombesin, and bile salts - substances with trophic effects on intestinal
epithelium.
▪ Gut disuse, with or without PN, can lead to deterioration of the functional and structural integrity
of the 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 in humans still appears to be about 10% to 15%.
▪ Starvation alone may be insufficient to increase gut permeability, but injury followed by
starvation increases mucosal permeability proportional to the severity of disease. Increased
permeability is prevented 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 bacterial translocation 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 studies
comparing EN and PN in heterogeneous populations of ICU patients, including those with head
trauma, sepsis, and severe acute pancreatitis, among other conditions. When a meta-analysis was
carried out, there was no apparent difference in mortality rate between patients treated with EN
and 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 infectious
complications.
▪ Eight randomized controlled trials that compared early EN with more delayed forms of nutrition
were recently reviewed and analysed. When these studies were aggregated, early EN was
associated 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 no
differences in complications between the groups.
▪ In a recent meta-analysis, there were seven randomized trials that evaluated the effect of route of
feeding on rates of ventilator-associated pneumonia. When these results were aggregated,
there was a significant reduction in ventilator associated pneumonia with feeding distal to
the pylorus (RR 0.76; 95% CI, 0.59-0.99). These studies also demonstrated that small-bowel
feeding is associated with an increase in protein and calories delivered and a shorter time to attain
the 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.

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