TOTAL PARENTERAL NUTRITION

2. IMPACT OF CRITICAL ILLNESS
• Increased energy expenditure
– Pain
– Anxiety
– Fever
– Muscular effort, shivering

3. METABOLIC RESPONSE TO CRITICAL
ILLNESS:

5. NEED FOR NUTRITION IN CRITICALLY
ILL CHILD
• Physiologic stress response: Catabolic phase
• increased caloric needs, urinary nitrogen losses
• inadequate intake wasting of endogenous protein
stores, gluconeogenesis
• mass reduction of muscle-protein breakdown

6. NUTRIENT METABOLISM AND THE METABOLIC
CONSEQUENCES OF THE STRESS RESPONSE

7. Protein Metabolism
• Amino acids are the key building blocks required
for growth and tissue repair. The vast majority
(98%) is found in existing proteins, with the
remainder residing in the free amino acid pool.
Proteins themselves are not static as they are
continually degraded and synthesis.Clinically
significant negative protein balance is
characterized by skeletal muscle wasting, weight
loss, and immune dysfunction. Apart from the
need for acute-phase protein production in the
inflammatory response, another driving force for
increased protein catabolism is the obligate
production of glucose from amino acids through
the process of gluconeogenesis in the process of
protein turnover

8. ENERGY METABOLISM
• During critical illness, increases in the metabolic
turnover of protein, carbohydrate, and lipid result
in an increased basal energy requirement for the
pediatric patient. Conversely, the dietary
provision of excess calories from glucose results
in an increased production of carbon dioxide
(CO2), with no change in loss of lean body mass.
• Administration of high-caloric (glucose load) diets
in the early phase of critical illness may
exacerbate hyperglycemia, increase carbon
dioxide generation with increased load on the
respiratory system, promote hyperlipidemia
resulting from increased lipogenesis, and result in
a hyperos-molar state.

9. CARBOHYDRATE METABOLISM
• Analogous to protein and carbohydrate metabolism, lipid turnover is
generally accelerated by critical illness, surgery, and trauma.
• Because of the increased demand for lipid use in critical illness coupled
with the limited lipid stores in the pediatric patient, critically ill children
are susceptible to the evolution of biochemically detected essential
fatty acid deficiency if administered a fat-free diet.66,67 In infants,
linoleic and linolenic acid are considered essential, whereas arachidonic
acid and docosahexaenoic acid are thought to be conditionally
essential.
• The provision of commercially available lipid solutions to parenterally
fed critically ill children reduces the risk of essential fatty acid
deficiency, results in improved protein use, and does not sig-nifi cantly
increase CO2 production or metabolic rate.
• There are disadvantages, however, with lipid administration, including
hypertriglyceridemia, increased rates, of infection, and decreased
alveolar oxygen diffusion capacity.

10. ELECTROLYTE METABOLISM
• Requirements for the basic electrolytes—Na, K, Cl, HCO3,
and Ca2—must be evaluated frequently in the critically ill
patient. In addition to routine electrolyte monitoring, careful
attention to phosphate and magnesium levels is recom-
mended.
• Hypophosphatemia may lead to hemolytic anemia and
respiratory muscle dysfunction and may also be seen with
refeeding syndrome in the ill child. Renal failure can result in
the reten-tion of phosphate, and nutritional allotments must
be reduced accordingly.
• Defi ciency of magne-sium can cause fatal cardiac
arrhythmia. Abnormalities of acid–base physiology in the
critically ill child can also influence the nutritional regi-men.
• Alkalemia tends to inhibit the respiratory drive, shift
potassium intracellularly, and decrease ionized calcium
concentrations by increasing the affinity of albumin for
calcium.

11. VITAMIN AND TRACE MINERAL
METABOLISM
• Vitamin and trace mineral metabolism in critically ill and
postoperative patients has not been extensively studied. For
the neonate and the child required vitamins include fat-
soluble vitamins (A, D, E, and K) and water-soluble vitamins
(ascorbic acid, thiamin, ribofl avin, pyridoxine, niacin,
pantothenate, biotin, folate, and vitamin B12), and these are
routinely administered.
• Required vitamins include fat-soluble vitamins (A, D, E, and
K) and water-soluble vitamins (ascorbic acid, thiamin,
riboflavin, pyridoxine, niacin, pantothenate, biotin, folate,
and vitamin B12), and these are routinely administered.
• In children with severe hepatic failure, copper and
manganese accumulation can occur; thus, parenteral trace
mineral supplementation should be reduced.
•

12. ASSESMENT OF NUTRITIONAL STATUS
• Nutritional assessment of the critically ill child
is challenging and clinicians use a combination
of anthropometric and laboratory data to
diagnose undernourishment.

13. Laboratory Tests
• Serum albumin is frequently used as a tool for nutritional assessment
in the ICU. Levels <2.2 g/dL refl ect malnutrition.
• However, the long half-life of albumin (14 to 20 days) makes it less
responsive to acute changes in nutritional status. Serum albumin
concentrations may be affected by albumin infusion, dehydration,
sepsis, trauma, and liver disease, independent of nutritional status.
• Chemistry profile should be monitored on admission and repeated
periodically. Other proteins used for nutritional assessment include,
RBP, transferrin, fi bronectin, and insulin-like growth factor 1 (IGF-1)
• Other laboratory tests that help in overall nutritional assessment
include serum electrolytes, blood urea nitrogen, glucose, coagulation
profi le, iron, magnesium, calcium, and phosphate. The adequacy of
cellular immunity can be estimated through the measurement of total
lymphocyte count (TLC) and by delayed-type hypersensitivity testing
with a series of common antigens (eg, Candida, trichophyton,
tuberculin).

14. NEED FOR NUTRITION IN CRITICALLY
ILL CHILD
increased caloric needs, urinary
nitrogen losses
inadequate intake wasting of
endogenous protein stores,
gluconeogenesis
mass reduction of muscle-protein
breakdown

15. INDICATIONS
• Prolonged ventilator dependency
• Prolonged ICU stay
• Heightened susceptibility to nosocomial
infections
• Increased mortality with mild/moderate or
severe malnutrition

16. • Prevent/treat macro/micronutrient
deficiencies
• Dose nutrients compatible with existing
metabolism
• Avoid complications
• Improve patient outcomes

17. ENTERAL NUTRITION

18. • WHEN TO INITIATE ENTERAL NUTRITION
• usually within 24 hours in severe trauma,
burns and catabolic states
• Contraindications to enteral nutrition:
– Nonfunctional gut, anatomic disruption, gut
ischemia
– Severe peritonitis
– Severe shock states

19. ROUTE OF FEEDING
• Transpyloric
– Effective in gastric atony/ colonic ileus
– Silicone/polyurethane tubing
• Nasogastric
– Requires gastric motility/emptying
– uoroscopic/ pH/ endoscopic guidance
• Percutaneous/surgical placement
– PEG if > 4 weeks nutritional support anticipated
– Jejunostomy if GE reflux, gastroparesis, pancreatitis

20. POTENTIAL DRAWBACKS OF ENTERAL
FEEDS
• Gastric emptying impairments
• Aspiration of gastric contents
• Diarrhea
• Sinusitis
• Esophagitis /erosions
• Displacement of feeding tube

21. PARENTERAL NUTRITION
The PN formulation is based on:
• Fluid Requirements
• Energy Requirements
• Vitamins
• Trace elements
• Other additives-Heparin, H2 blocker etc

22. Alternative Names
IV fluids - infants; TPN - infants; Intravenous
fluids - infants; Hyperalimentation - infants

23. Purposes of TPN
• preventing unwanted weight loss and skin
breakdown, promoting positive nitrogen
balance, and maintaining visceral and somatic
protein stores.
• To promote adequate nutrition.
• TPN reduces morbidity and mortality,
• promotes tissue repair, and
• enhances the immune response

24. Indications
• Paralytic ileus
• Intestinal obstruction
• Acute pancreatitis
• Malabsorption
• Persistent vomiting
• Severe diarrhea
• Congenital anomalies
• Major abdominal surgery

25. • Cancer patients undergoing chemotherapy or
radiation therapy
• Alcoholic hepatitis
• Mild acute pancreatitis
• Acute colitis
• Crohn's disease (steroid therapy is indicated as
being more effective)
• Acquired immunodeficiency syndrome (AIDS)
• Pulmonary disease

26. Types
Central total parentral nutrition
• Total nutrient admixture (TNA) is a highly
concentrated form of parenteral nutrition that is
given through a central vein. It contains a
dextrose solution of 20% or higher. Higher
glucose concentration should be administered
through a central venous line because the high
venous flow rate rapidly dissipates the high
osmolarity. TNA is indicated for parenteral
nutrition needed for more than 7 days.

27. Peripheral Parenteral nutrition
• Peripheral Parenteral nutrition (PPN) is given through a
peripheral vein and has a lower concentration of
glucose that should not exceed 12.5%. Higher
concentrations of glucose have a high osmolarity that
can cause damage to the peripheral venous
endothelium, resulting in venous thrombosis and
sclerosis. PPN has fewer calories and usually a larger
percentage of calories are provided by lipids rather
than carbohydrates. PPN is indicated for parenteral
nutrition needed for less than 7 days. PPN is not used
in some facilities because the risk of infection
outweighs the short term nutritional benefits

28. Administration
• Remove TPN and lipids from the refrigerator at least an
hour before hanging. TPN solution should be clear, not
cloudy. Lipids will be white. Do not use the fluid if
cracking or creaming of the fluid is present because it
may indicate fluid separation.
• TPN must be administered using an IV pump and
infused via a dedicated line or lumen of the central
venous catheter (CVC). TPN should be filtered with a
0.2 micron filter. Lipids may not be filtered. If so a 1.2
micron filter is needed to avoid clogging up the fluid.
Line integrity should not to be compromised except for
changing the bag or line. No bolus injections may be
given into a TPN line.

29. • TPN should be infused at a constant rate over 24 hours
unless otherwise ordered . Once a patient is stabilized,
cyclic TPN can be provided in a shorter time if appropriate.
• The facilities procedure for site care and line changes
should be followed. When flushing a central line, use a 10
cc syringe or larger. Smaller syringes exert excessive
pressure that might break the line.
• The power flushing technique creates turbulence in the
line for more effective clearing of the line. To do this you
briskly inject 2 ml of saline, stop very briefly, and then
inject another 2 ml. Continue this process until you have
completed the flush. As you inject the last 2 ml, clamp the
catheter.

30. • Saline flush prior to using the line to administer any
medication. Heparin is not compatible with other
medications. If you inject medication into the line without
clearing the heparin flush, the medication may precipitate.
• A-Administer the medication.
• S-Saline flush to clear the medication from the line before
administering the heparin flush.
• H-Heparinize the catheter when not in use.

31. Duration
• Short-term PN may be used if a person's digestive
system has shut down (for instance by
peritonitis), and they are at a low enough weight
to cause concerns about nutrition during an
extended hospital stay.
• Long-term PN is occasionally used to treat people
suffering the extended consequences of an
accident, surgery, or digestive disorder. PN has
extended the life of children born with
nonexistent or severely deformed organs.

32. Complications
Infection Blood clots
Fatty liver
and liver
failure

33. Other complications
• Total parenteral nutrition increases the risk of acute
cholecystitis due to complete disuse of gastrointestinal
tract, which may result in bile stasis in the gallbladder.
• Other potential hepatobiliary dysfunctions include
steatosis, steatohepatitis, cholestasis, and cholelithiasis
• In newborn infants with short bowel syndrome with
less than 10% of expected intestinal length, thereby
being dependent upon total parenteral nutrition, 5
year survival is approximately 20%.
• Complications are either related to catheter insertion,
or metabolic, including refeeding syndrome.

34. • Catheter complications include pneumothorax, accidental
arterial puncture, and catheter-related sepsis..
• Metabolic complications include the refeeding syndrome
characterised by hypokalemia, hypophosphatemia and
hypomagnesemia.
• Hyperglycemia. Hypoglycaemia is likely to occur with
abrupt cessation of TPN.
• Liver dysfunction can be limited to a reversible cholestatic
jaundice and to fatty infiltration (demonstrated by elevated
transaminases). Severe hepatic dysfunction is a rare
complication. Overall, patients receiving TPN have a higher
rate of infectious complications.

35. IMMUNONUTRITION
• The use of enteral formulae supplemented
with immunonutrients such as glutamine,
arginine, fatty acids, nucleotides, taurine,
cysteine, certaic complex carbohydrates and
probiotic bacteria has been demonstrated to
modulate gut function, inflammatory and
immune responses.

36. • This help in reinforcement of mucosal barrier
and cellular defence and some down-
regulation of local or sy temic inflammatory
response, thus reducing morbidity and the risk
of infectious complication in critically ill
patients)

37. IMMUNE MODULATION
• Reduction of duration and magnitude of
inflammatory response
• This disrupt the balance between pro and
anti-inflammatory processes
• Of the multiple ingredients in these special
formulas: which is “the” one
• Beneficial effects seen in patients achieving
early EN