Nutrition: Parenteral & Enteral Flashcards

1
Q

How should nutrition be initiated in the neonate?

A

early & consistently to maintain the rate of intrauterine growth for term and preterm babies

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2
Q

What is adequate nutrition linked with?

A

brain growth, health status and repair; ex: repair of damaged tissues with chronic lung dz

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3
Q

How do you know when nutrition status is optimal?

A

allows for maximum growth without adverse effects

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4
Q

What infants have the best neurocognitive outcomes?

A

infants who grow at the highest quartile ; IUGR and related comorbidites have inadequate nutrition and can lead to poor outcomes

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5
Q

What is the goal of neonatal nutritional care?

A

to facilitate a rate of growth that approximates the rate of intrauterine growth of a normal fetus at the same post conceptual age (approximately 15-30g/kg/d)

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6
Q

What is the typical kcal requirement for a preterm infant?

A

120kcal/kg/d for LBW, could be more for an infant with high metabolic needs or catch up growth needs

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7
Q

What population of infants has higher caloric intake requirements?

A

chronic lung dz, NEC, sepsis, cardiac anomalies- have been shown to have higher metabolic needs and to gain wt more slowly than their peers (may need 140kcal/kg/d); 25-45% more energy

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8
Q

What are the benefits of TPN?

A

promote overall nutritional health of the infant, decreases the magnitude of the nadir of postnatal weight loss- supporting an earlier return to BW, decreases our dependence on the baby’s tolerance of enteral feeding (especially important in babes c h/o GI surgery or EPTL

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9
Q

What is the recommended caloric intake for TPN?

A

80-100kcal/kg/d; parenteral needs are less r/t negligible fetal loss and increase absorption with parenteral nutrition

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10
Q

What is the composition of calories in TPN?

A

CHO should not exceed 50%, protein should not exceed 12% and IL should not exceed 40%

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11
Q

As it r/t enteral nutrition, to approximate the equivalent of 3rd trimester intrauterine weight gain, what should caloric intake be?

A

a minimum of 120kcal

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12
Q

What is the goal of protein administration?

A

to prevent negative energy balance, negative nitrogen balance and catabolism

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13
Q

What is the clinician hoping to achieve by beginning AA early in neonatal life?

A

by beginning AA administration in the first neonatal hours, we are avoiding a period of early malnutrition; first strategy to prevent critical growth failure and promote and enhance neurodevelopment outcome and glucose tolerance

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14
Q

What are the benefits of early AA infusion?

A

stimulates the endogenous release of insulin and prevents nonoliguric hyperK; prevent metabolic shock

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15
Q

How does early AA infusion promote glucose tolerance?

A

may stimulate endogenous insulin secretion consistent with the concept that forestalling the starvation response improves glucose tolerance

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16
Q

How does early AA infusion prevent nonoliguric hyperK?

A

when the plasma levels of argentine and luciene decrease, secretions of insulin also decreases. this contributes to the leakage of intracellular K

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17
Q

Where should AA infusion begin?

A

with 1g/kg/d and increase by 1g/kg/d until the goal is reached (3-4g/kg/d); 1.5-2g/kg/d is sufficient to avoid catabolism in all groups

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18
Q

What is catabolism?

A

the break down of muscle

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19
Q

What is anabolism?

A

the gain of muscle

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20
Q

In what conditions are most neonates anabolic?

A

at 2/g/kg/d of AA and 50kcal/kg/d

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21
Q

Protein deposits or the gain of muscle is directly correlated to what?

A

with protein intake if superimposed catabolic conditions are not present

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22
Q

What occurs when an infant only receives supplemental glucose?

A

loose 1% of protein stores each day, a negative nitrogen balance and catabolic state

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23
Q

In VLBW infants, what is the progression of metabolic shock?

A

some key AA can decline from the time the cord is cut, this shock may trigger a starvation response for which endogenous glucose production is a prominent feature.

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24
Q

What is the etiology of glucose intolerance in the VLBW baby?

A

Irrepresible glucose production may be the cause of this so called glucose intolerance that often limits the amount of energy that can be given; glucose tolerance improves substantially by the introduction of early AA

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25
Q

How many calories are in each gram of protein?

A

4

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26
Q

How much nitrogen is in each gram of protein?

A

1g protein= 1g AA= 0.16g nitrogen

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27
Q

What is the effect of increasing glucose concentration?

A

increasing osmolality

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28
Q

What is the glucose utilization rate of a preterm baby compared with term?

A

preterm>term; the increased brain to body weight ration , decrease fat stores and increased energy expenditures

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29
Q

What is the glucose utilization rate for a preterm infant?

A

5-8mg/kg/min

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30
Q

What is the glucose utilization rate for a term infant?

A

3-5mg/kg/min

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31
Q

What is the maximal oxidative capacity of glucose?

A

the max amount of glucose that is no longer needed to supply the energy needs of the body. the conversion of glucose into fat is an energy inefficient process that results in increased energy expenditure, increased O2 consumption and increased CO2 production

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32
Q

What should be done if there is unexplained CO2 retention?

A

decrease GIR, may have found maximum oxidative capacity; probably around 12-13; there are no good lab means for determining when this threshold has been exceeded

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33
Q

How can maximum oxidative capacity exacerbate respiratory course?

A

increased CO2 production

34
Q

What are the advantages of IL administration?

A

prevention of essential fatty acid deficiency, normal growth and development, concentrated energy sources and a vehicle of the transport of the fat soluble vitamins

35
Q

Why is 20% concentration preferred over 10% in all GA and wt classes?

A

decrease in risk of hypertriglyceridemia, hypercholesterolemia and hyperphospholipidemia; the phospohlipid content of 10% impedes plasma triglyceride clearance resulting in a increased tri and cholesterol serum concentration

36
Q

How are IL prepared?

A

from soy and/or saffol oils, fatty acids, egg yolk. phospholipids and glycerin

37
Q

What can happen if exogenous fats are not given?

A

fatty acid deficiency disorder can develop within 72h; can be prevented c as little as 0.5-1g/kg/d

38
Q

The prevention of fatty acid deficiency can prevent what complications in the newborn?

A

decrease the incidence of complications a/w free radical formation such as BPD and ROP; manifests with dry, flaky skin

39
Q

What are the fat soluble vitamins?

A

ADEK

40
Q

How does IL fair in the peripheral vein?

A

relatively low osmolality and well tolerated; evidence to support that IL helps to maintain vessel latency

41
Q

Where should your tri level be?

A

<150mg/dL

42
Q

What is critical for brain development?

A

milk fat; specific fatty acids are required for myelin formation and neuronal growth, retinal development and as key complements for cell membranes

43
Q

Why is the very preterm infant vulnerable to fatty acid supply insufficiency?

A

bc the major period for in utero fat secretion does not occur until the last trimester

44
Q

What other additives can be found in TPN?

A

electrolytes, minerals, vitamins, trace elements and heparin

45
Q

What are the special considerations for Na and K infusion?

A

we have daily needs for Na and K; do not add K until UOP has been est; other daily needs include acetate and Cl

46
Q

What are the special considerations for mineral infusion?

A

Ca Gluconate, when considering how much to add, consider the route of administration- very caustic to the peripheral vein- limit Ca if giving PIV

47
Q

What are the special considerations for vitamin infusion?

A

based on GA and current weight

48
Q

What are the special considerations for trace element infusion?

A

neotrace: if pt has cholestasis, need to remove the copper and manganese (or decrease), if renal dysfx, then the chromium needs to be removed

49
Q

Why is heparin added to the solution?

A

incudes lipoprotein lipase activity that enhances the clearance of triglycerides when administering IL, also decrease risk of thrombosis, decrease risk of catheter related sepsis and decrease phlebitis in peripheral lines and for PIV

50
Q

How do you dose IL administration?

A

start at 0.5-1g/kg/d in a stable infant and increase by 0.5-1g/kg/d to 3g/kg/d

51
Q

When does osmotic diuresis occur?

A

when spill a lot of glucose into the urine, and water follows

52
Q

What are complications a/w protein administration?

A

metabolic acidosis with no other explanation (protein tolerance) and excessive elevation of BUN

53
Q

What are complications a/w glucose administration?

A

osmotic diuresis, hyperosmolality, noter upper limits of glucose oxidative capacity, note lower limits of GIR in infants with hyperglycemia, if continued hyperglycemia, ensure that AA is being given, consider dc IL and consider insulin gtt

54
Q

What are complications a/w IL administration?

A

lipid intolerance, altered glucose metabolism, increased free bilirubin concentrations, acute impaired pulmonary function and interference with immune function and plt fx

55
Q

What are common complications of TPN?

A

nosocomial infx, hyperglycemia, metabolic bone dz and cholestatic jaundice

56
Q

What are the most common nosocomial infx r/t TPN administration?

A

staph epi, staph aureus, candida albican and malessezia furfur

57
Q

What is the pathoetiology of metabolic bone dz secondary to TPN?

A

caused by an imbalance of vitamin D, minerals and trace elements primarily due to inadequate Ca and Phosphorus and inadequate ratios of each

58
Q

What is the pathoetiology of cholestatic jaundice secondary to TPN?

A

portal inflammation and bile duct proliferation, occurs in 7-10% of babies on prolonged TPN. enteral feeds stimulate bile flow and stimulate hormones that prevent cholestasis

59
Q

Why can’t glucose and calcium be maximized with peripheral vascular access?

A

bc of local irritation and the risk of infiltration

60
Q

How should an infant be transitioned to enteral feds?

A

as soon as the baby’s condition allows, enteral feeds are safer, more physiologic and cost effective, avoids s/e of parenteral nutrition and stimulates the development of the GI tract

61
Q

What can the deprivation of enteral feeds lead to?

A

atrophic ∆ in the gut and may render the gut vulnerable to pathologic organisms and NEC

62
Q

What is the estimated caloric expenditure a/w resting metabolic rate?

A

50kcl/kg/d

63
Q

What is the estimated caloric expenditure a/w activity?

A

15kcl/kg/d

64
Q

What is the estimated caloric expenditure a/w cold stress?

A

10kcl/kg/d

65
Q

What is the estimated caloric expenditure a/w nutritional processing?

A

45kcl/kg/d

66
Q

What is included in the recommended administration of 120-150kcal/kg/d of enteral nutrition?

A

resting metabolic rate, activity, cold stress and nutritional processing

67
Q

What conditions necessitate a delay to the introduction of enteral feeds?

A

any situation a/w GI hypoxia or decreased intestinal blood flow, including: mechanical ventilation (high settings, acute stage of illness), asphyxia, hypoxemia, hypotension, indomethacin and blood product transfusion

68
Q

Some evidence suggests that feeds are better tolerated and better absorbed if given via which route?

A

transpyloric

69
Q

What are the benefits of gut stimulating feeds?

A

stimulates normal postnatal gut hormone surges even at low rates, insulin is released helping glucose tolerance, significant increase in plasma concentrations of enteroglucagon, gastrin and gastro inhibiting polypeptide in preterm infants after feeding

70
Q

What can be expected with the residuals of an infant receiving gtt feeds?

A

not necessary to check residuals, not unusual to have 30-50% residuals

71
Q

What is the gastrocolic reflex?

A

5x baby’s wt in kg= volume necessary to stimulate this emptying reflex

72
Q

What protein is found in EBM?

A

whey; more easily digestible and is a/w more rapid emptying time, better absorption of nutrition, lower renal solute load and higher quality protein

73
Q

What are contraindications for breast feeding?

A

illicit drugs- heroine, cocaine, meth, HIV, HSV lesion on breast, symptomatic with pos PPD or pos CXR, active breast abcesses, galactosemia, lithium, cyclosproine, methotrexate, radioactive agents and some chemo agents

74
Q

When is portagen the formula of choice?

A

fat is derived from MCT oil and used in patient with bile obstruction, severe cholestasis or fat malabsoprtion

75
Q

What is galactosemia?

A

a condition of primary lactase deficiency; temporary lactase deficiency often occurs with gastroenteritis

76
Q

What formula should be prescribed to a patient with a documented cow’s milk allergy?

A

protein hydrazaline formula, not soy

77
Q

When is the use of soy based formula indicated?

A

glactosemia, lactase deficiency and parents wanting a vegetarian diet

78
Q

For what populations is the use of soy base formula not recommended?

A

babes with BW <1800g, known osteopenia; may over time have decreased wt gain and poor phosphorus absorption

79
Q

What clinical finding indicates that protein intake is inadequate?

A

BUN <4

80
Q

In what values is EBM inadequate?

A

zinc, calcium, phosphorus, protein and sodium

81
Q

What are signs of HMF intolerance?

A

guiac positive stools, loose and frequent stools, abnormal and exam and increased and girth