Parenteral Nutrition

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jannabogie
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47080
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Parenteral Nutrition
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2010-11-17 21:20:55
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Parenteral Nutrition
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Parenteral Nutrition - Therapeutics Week 10
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  1. When might medical malnutrition occur?
    • Insufficient/inadequate intake of nutrients
    • Hypermetabolism
  2. Is medical malnutrition assoc with chronic or acute illness?
    Can be assoc with exacerbations of chronic disease or onset of acute illness
  3. What is Cachexia
    Physical wasting with loss of body weight and muscle mass caused by disease
  4. Conditions/Diseases that increase pt risk for medical malnutrition
    • infants and elderly
    • chronic diseases
    • alcohol abuse
    • critical illness
    • trauma
    • burns
    • cancer
    • surgery
    • severe N/V/D
    • GI malfunction (IBD: ulcerative colitis, Crohn's; Short Bowel Syndrome)
    • advanced AIDS
    • cystic fibrosis
  5. Goals of nutrition support
    • 1. Maintain adequate nutrition status (prevent malnutrition)
    • 2. Correct malnutrition
    • 3. Reduce metabolic response to injury
    • minimize oxidant stress
    • modulate inflammatory-immune response
  6. Steps to formulate a therapeutic plan for nutrition support
    • 1. Nutrition assessment
    • 2. Estimation of calorie needs
    • 3. Determine optimal method of nutrition support
    • 4. Design and implement the nutrition plan
    • 5. Monitor patient for effectiveness and AEs of the nutrition plan
    • 6. Adjust the nutrition plan according to patient response
  7. BMI categories
    • 18.5 or less = underweight
    • 18.5 - 24.9 = normal
    • 25-29.9 = overweight
    • 30+ = obesity
  8. What is the most common route for PN?
    IV
  9. Other names for parenteral nutrition (PN)
    • Total Parenteral Nutrition (TPN)
    • central venous alimentation
    • hyperalimentation
  10. When are nutrition support needs treated as an emergency?
    Never. Though nutrition support should be provided promptly.

    No "stat" TPN or tube feed.
  11. What are the options of things we can give a pt who feels they need their TPN right away?
    • 10% dextrose (D10)
    • IV fluids with 5% dextrose (D5): D5NS, 1/2 D5NS with 20mEq K+
  12. What Macronutrients might be included as usual components of TPN admixtures?
    • Protein (amino acids) 4 kcal/g
    • Carbohydrates (usually dextrose) 3.4 kcal/g
    • Lipids (fat emulsion) 10 kcal/g
  13. What Micronutrients may be included in a typical TPN admixture?
    • Electrolytes (sodium, potassium, phosphorus, magnesium, calcium)
    • Multivitamins (A, D, E (fat soluble); B1, B2, B3, B5, B6, B12, C (water soluble), biotin, folic acid, vitamin K)
    • Minerals/Trace Elements (zinc, copper, manganese, chromium, in special cases: selenium, molybdenum)
  14. True or false: Most drugs are incompatible with TPN admixtures.
    True

    (insulin and some H2 blockers may be compatible)
  15. When do we use TPN?
    • When oral nutrition is absolutely not an option.
    • "benefits outweigh risks"
    • Pts who have failed appropriate EN with appropriate admin route
    • Severe GIT impairment (ileus, bowel obstruction/resection, intractable vomiting, severe diarrhea, GI fistula if EN access cannot be gained below the site, significant oral mucositis or stomatitis as in chemo and radiation, unable to maintain adequate oral intake, pancreatitis but this is not an automatic indication)
    • Surgery patients who cannot eat or tolerate EN
    • Significant aspiration risk
    • Expected NPO status more than 5-7 days
    • In critical care patients: after 7 d in pts in whom EN is not feasible and who were healthy before critical illness with no evidence of malnutrition, ASAP in pts in whom EN is not feasible and who have protein-calorie malnutrition, in pts anticipated to undergo significant upper GI surgery and EN is not feasible - with malnourishment, start PN 5-7 d before surgery and continue post-op, others - do not initiate immediately after surgery, but after 5-7 d and if the duration of the PN will exceed 7 d)
  16. When establishing nutrition goals for a patient, what elements do we look at?
    • energy (calorie) goal - carbs and lipids
    • protein goal
    • fluid goals
    • electrolyte goals
    • multivitamin and trace element goals
  17. Compare Central PN (CPN) to Peripheral PN (PPN) in terms of administration site
    CPN: central venous access catheter (central cath into vena cava, PICC line, subclavian or other central caths) Avoid femoral catheters.

    PPN: non-central catheter (superficial veins - upper extremities recommended)
  18. Compare Central PN (CPN) to Peripheral PN (PPN) in terms of nutrient/calorie amount
    CPN: High - can meet daily nutrient and calorie goals

    PPN: Significantly limited - usually not enough to meet metabolic needs (dextrose content NMT 10%)
  19. Compare Central PN (CPN) to Peripheral PN (PPN) in terms of content osmolarity
    CPN: High (can be higher than serum osmolality)

    PPN: Limited (d/t risks of phlebitis and vein collapse) Must be <900 mOsm/L! (cannot be any more concentrated than this)
  20. Compare Central PN (CPN) to Peripheral PN (PPN) in terms of specific complications
    CPN: vascular injury, air embolism, pneumothorax, pleural embolism, cardiac arrhythmia, brachial plexus injury

    PPN: Vein intolerance (collapse), phlebitis, thrombosis, thrombophlebitis (common), extravasation
  21. Compare Central PN (CPN) to Peripheral PN (PPN) in terms of clinical use as TPN
    CPN: very significant and common

    PPN: very limited (transient use)
  22. 4 primary uses of PPN
    • 1. Supplementation of inadequate oral or tube feeding intake
    • 2. Hypocaloric support with low to moderate protein provision
    • 3. Transitional support until central access can be obtained
    • 4. Temporary support until catheter replacement following recurrent catheter-related infection
  23. Different ways of characterizing different types of adult TPN
    • admin routes
    • macronutrients
    • duration of TPN admixture infusion
  24. Characterize TPN according to macronutrients
    "two-in-one": contains only AA and dextrose - lipid infused from a diff container

    "three-in-one": contains AA, dextrose, and lipid

    (neither is medically or scientifically better than the other)
  25. Characterize TPN by duration of TPN admixture infusion
    • Continuous - infused continuously over 24 hours
    • Cyclic - infused less than 24 hours daily with interruptions (e.g. 12 h). Usually for pts requiring long-term and/or home TPN therapy
  26. How are most TPN admixtures compounded?
    using automatic compounders - in a sterile environment that meets USP797 guidelines
  27. What percent solutions do macronutrients come in for TPN compounding?
    • Protein/AA: 5-20% concentrated sol'n
    • Dextrose: 70% concentrated sol'n
    • Lipids: 10%, 20%, 30% emulsion (10-20 for 2-in-1, 20-30 for 3-in-1)
  28. What might be a problem with TPN in a patient on severe fluid intake restriction?
    They may not meet calorie goals because if the goal is large, a large volume of TPN admixture would need to be made. The restriction may not allow for that volume of fluid to be given.
  29. What is the equation for TPN osmolarity?
    (grams dextrose/liter x 5) + (grams AA/liter x 10) + mEq cations/liter
  30. What is normal serum osmolarity?
    280-295 mOsm/L
  31. What osmolarity is acceptable for central TPN?
    >1000
  32. What is the acceptable osmolarity for Peripheral TPN?
    < 900 mOsm/L
  33. Which nutrients contribute much to TPN osmolarity?
    dextrose and AA
  34. What is the limit for sodium in TPN? Why?
    < 150 mEq/L Because if you put more, your TPN will be hypertonic. Serum sodium is 154.
  35. What can happen if Calcium and phosphorus are mixed in a TPN?
    precipitation
  36. What influences whether calcium and phosphorus will precipitate or not?
    • Concentration of Ca or PO4. (limit both. calcium < 5 mEq/L with PO4. Can calculate to predict)
    • Concentration of AAs (> 2.5% final conc. Avoid Ca/PO4 in PPN)
    • Calcium salt used (use gluconate instead of chloride)
    • Other electrolyte concentrations
    • pH and temp of the admixture
    • Sequence of additives (add PO4 to AA and dextrose before adding Ca and add lipids last for 3-in-1)
  37. Which drugs are commonly added to TPN admixtures?
    Insulin and H2 blockers. Most drugs are incompatible.
  38. What issues are there with TPN stability?
    • Loss of TPN components over time
    • More problematic with 3-in-1 (lipid falling out)
    • Multivitamin stability over time
  39. What type of catheter should be used for patients who require long-term intermittent vascular access such as long-term cyclic TPN
    Special port - totally implantable access device
  40. In adults, why use upper extremity site for catheter insertion rather than lower?
    risk of blood clots
  41. Why inspect TPN for visible particles before infusion?
    Risk of embolus
  42. TPN should always be infused using a dependable mechanical pump through a sterile filter. What size filter should be used and how often should it be changed?
    • 0.6 micron for 2-in-1
    • 1.2 micron for 3-in-1
    • Change daily.
  43. How long are TPN admixtures good for?
    • 24 hours hanging - toss it after that! Can make prior, but never good for longer than 48 h. Still 24 hanging.
    • With lipid emulsions (with 2-in-1 admixtures) this is only good for 12 hours.
  44. How often do the tubes need to be changed when they are used to admin lipids? Why?
    q24h. Because lipid infusion is assoc with infx, especially fungal infx.
  45. How often do the tubes need to be changed when they are used to admin dextrose/amino acid sol'n?
    q72h (no longer)
  46. Are transnasal or systemic antimicrobial prophylaxis recommended before insertion or during use of an IV catheter to prevent colonization of the catheter of infx of the bloodstream?
    no
  47. Are low dose anticoagulants recommended to prevent thrombosis for central TPN?
    no
  48. How and when might anaphylaxis be a complication of TPN therapy?
    Allergic rxns to TPN (IV lipid and egg allergy). Occurs early in therapy.
  49. How and when might vascular access be a complication of TPN therapy?
    • Malpositioning of catheter tips - early therapy
    • injury to surrounding tissue - early therapy
    • dislodgement of catheter tips - anytime
  50. How and when might infection (bacterial and fungal) be a complication of TPN therapy?
    • (more common in critical care and long-term TPN patients)
    • -catheter-related infx; significant microorganisms - anytime
    • -coagulase-negative staphylococci - anytime
    • -Staph aureus - anytime
    • -Klebsiella pneumonia (sometimes) - anytime
    • -Fungal infection (IV lipid emulsion); Candida spp - anytime
  51. How and when might mechanical complications (inability to infuse admixture or draw blood) be a complication of TPN therapy?
    • Catheter dislodgement/fracture - anytime
    • Catheter occlusion (e.g. blood clot, precipitated admixture) - anytime
  52. How and when might phlebitis be a complication of TPN therapy?
    TPN osmolarity - may be preventable with saline flushes - anytime
  53. How and when might metabolic complications be a complication of TPN therapy?
    • Refeeding Syndrome - early therapy
    • Overhydration/dehydration - anytime
    • Overfeeding/underfeeding - anytime
    • Hyper/hypoglycemia - anytime
    • Hyperlipidemia/essential fatty acid deficiency - anytimeHypercapnia - anytime
    • Acid-base disturbance - anytime
    • Electrolyte abnormalities - anytime
    • Hepatobiliary complications - anytime
    • GI complications - anytime
    • Renal complications - long term
    • Minerals and trace elements toxicity/deficiency - long term
  54. Causes, clinical features, corrective interventions of overhydration in TPN
    Excessive TPN volume

    • Hyponatremia
    • Fluid overload (edema, pleural effusion, etc.)

    • Reduce TPN volume
    • Supportive care (e.g. loop diuretics)
  55. Causes, clinical features, corrective interventions of dehydration in TPN
    Insufficient TPN volume

    • Hypernatremia
    • Hypotension
    • Acute renal insufficiency (azotemia, increased SrCr)

    • Increase TPN volume
    • Supportive care (e.g. short-term, additional IV fluid for hypotension)
  56. Causes, clinical features, corrective interventions of Overfeeding in TPN
    Overestimated calorie and/or protein goals or intake

    • Hypercapnia
    • Refeeding Syndrome
    • Liver steatosis
    • Obesity

    Reassess and redefine nutrition goals - appropriately reduce TPN macronutrients
  57. Causes, clinical features, corrective interventions of Underfeeding in TPN
    Underestimated calorie and/or protein goals or intake

    Medical malnutrition

    Reassess and redefine nutrition goals - appropriately increase TPN macronutrients
  58. Causes, clinical features, corrective interventions of Hyperglycemia in TPN
    • Excessive dextrose infusion
    • Sepsis
    • Diabetes
    • Acute pancreatitis
    • Corticosteroids use

    • Immune system dysfunction
    • Increased susceptibility to infx
    • Impaired wound healing
    • Hypertriglyceridemia
    • Hepatic steatosis

    • Initiate TPN dextrose to goal slowly (over several days)
    • Limit dextrose infusion rate at 5 mg/kg/min
    • Insulin therapy (IV insulin infusion or insulin added to TPN)
  59. Causes, clinical features, corrective interventions of Hypoglycemia in TPN
    • Sudden interruption of TPN with dextrose
    • Excessive insulin

    • Symptomatic sympathetic nervous system stimulation
    • CNS dysfunction (e.g. acute mental status change, etc.)

    • Avoid sudden disruption of TPN infusion; infusion of 10% dextrose (D10) immediately after discontinuation of TPN, or gradual tapering of TPN over 2+ hours before complete discontinuation
    • Discontinue the TPN with excessive insulin
  60. Causes, clinical features, corrective interventions of Hypercapnia (mechanically ventilated patients) in TPN
    Excessive CO2 production d/t excessive calories and dextrose, esp in severely malnourished pts

    Increased respiratory work load, resulting in difficulty weaning off from mechanical ventilation

    Reduced calorie and dextrose in TPN
  61. Causes, clinical features, corrective interventions of Hyperlipidemia in TPN
    • Excess of lipids or dextrose in the TPN
    • Propofol use (a lipid-based (lipid emulsion) sedative drug that provides 1.1 kcal/mL of infusion)
    • Impaired lipid clearance - obesity, diabetes, sepsis, pancreatitis, liver disease

    Acute pancreatitis (esp. when serum TG levels are above 500 mg/dL)

    • No IV lipids when TG > 400
    • Reduce dextrose and then lipid in TPN
    • Reduce lipid in TPN in pts receiving concurrent propofol
  62. Causes, clinical features, corrective interventions of Essential fatty acid deficiency (EFAD, linoleic acid and linolenic acid) in TPN
    Chronic deficiency of lipid intakes; lack of lipids in TPN over long time periods

    Rare; alopecia, scaly dermatitis, thrombocytopenia, growth retardation in children

    Lipid replacement, at least once weekly (e.g. 20 g/week)
  63. Causes, clinical features, corrective interventions of Hepatobiliary Transiently elevated LFTs and bilirubin, Hepatic steatosis, Cholestatis in TPN
    • High doses of lipid emulsions and rarely EFAD
    • Excessive calorie, lipid and dextrose

    Often asymptomatic

    • Resolve with d/c of TPN therapy
    • Reduce calorie (lipid and dextrose); role of protein reduction unclear
  64. Causes, clinical features, corrective interventions of Significantly elevated BUN (> 50 mg/dL) in TPN
    (pay careful attention in renal patients)

    Excessive amino acid in TPN; renal dysfunction

    Often asymptomatic

    Reduce AA goal and in TPN
  65. Causes, clinical features, corrective interventions of Electrolyte abnormalities in TPN
    • Excessive/Insufficient amount in TPN
    • Drug intx (e.g. K+ and loop diuretics, insulin dose changes, etc)

    Electrolyte specific

    Adjust accordingly (e.g. hyponatremia - check fluids)
  66. Causes, clinical features, corrective interventions of Acid-base disturbance in TPN
    • Excessive chloride (acidosis) or acetate (alkalosis)
    • Underlying physiological conditions

    Condition specific

    • Acidosis - reduce chloride and increase acetate
    • Alkalosis - increase chloride and decrease acetate
  67. Causes, clinical features, corrective interventions of Multivitamin Toxicity and Deficiency in TPN
    Excessive/Insufficient amount in TPN (e.g. Vitamin K deficiency)

    Vitamin specific; often asymptomatic

    MV usually standardized; adjust accordingly in special cases
  68. Causes, clinical features, corrective interventions of Minerals/Trace element toxicity and Deficiency in TPN
    Excessive/Insufficient amount in TPN; aluminum contamination

    Mineral/element specific

    Adjust accordingly
  69. Causes, clinical features, corrective interventions of GI Intestinal atrophy, Gastroparesis in TPN
    lack of stimulation from luminal nutrients

    increase intestinal permeability and bacterial translocation

    • Enteral nutrition
    • Glutamine and arginine supplementation?
  70. Causes, clinical features, corrective interventions of Renal: Hyperoxaluria and hypercalciuria, Tubular renal defects in TPN
    Hyperoxaluria and hypercalciuria are assoc with excessive Vitamin C and amino acid load

    Rare; usually in chronic TPN patients. Progression to chronic renal failure not expected.

    Reduce Vitamin C contents in pts with renal insufficiency receiving chronic TPN
  71. What is Refeeding Syndrome?
    Characterized by simultaneous hypophosphatemia, hypokalemia, and hypomagnesemia. And sometimes thiamine deficiency and hypernatremia. In the absence of excessive fluid change when malnourished individuals receive food, oral nutrition, or parenteral nutrition.
  72. Presentation of refeeding syndrome
    Pt may present with weakness, convulsions, respiratory failure, cardiac decompensation. Could die from complications.
  73. Pathophysiology of refeeding syndrome
    • During starvation carb intake and insulin secretion are reduced
    • Fat metabolism (and some protein) becomes main energy source
    • Intracellular electrolytes are lost (phosphate, potassium)

    • When feeding begins,
    • Sudden shift from fat to carb metabolism occurs and insulin secretion increases, leading to:
    • - high demand for production of the phosphorylated intermediates of glycolysis (ATP & DPG)
    • - sudden cellular uptake of phosphate leading to profound hypophosphatemia

    Severe hypophosphatemia can lead to severe neurologic, cardiac, respiratory, and hematologic abnormalities, and even death.
  74. Prevention of refeeding syndrome
    Identify at-risk patients (classical marasmus/kwashiorkor, significant recent weight loss, hospitalized pts admitted from nursing homes, pts unfed from 5-10 days with evidence of stress or nutritional depletion, chronic disease with undernutrition, anorexia nervosa, alcoholics/excessive alcohol intake, critical illness, severe trauma, burns)

    Avoid overfeeding with food or nutrition support

    Initiate nutrition support conservatively - Start low and go slow in reaching calorie and carb goals

    Thiamine supplementation - 50-100 mg PO/IV daily for 5-7 days
  75. Treatment of refeeding syndrome
    • Symptomatic pts: stop nutrition support immediately; initiate 10% dextrose sol'n
    • Slow down the approach to calorie goal; reduce calorie goals?
    • Replace electrolytes as needed
    • Supportive care (e.g. O2 for resp distress, diuresis for edema)
  76. Baseline evaluation for TPN
    • Nutrition Assessment: Body weight, Lab studies (basic metabolic panel, Ca, Mg, P, CBC with differential, Serum albumen, prealbumin, AST/ALT, PT/INR, serum TGs), 24-hour UUN
    • Ability to use GIT
    • Functional status
  77. What is prealbumin?
    • A nutritional marker (normal is 20-40).
    • If it's low, the protein synthesis is low and the patient needs more carbs and AAs.
  78. Monitoring parameters while on TPN
    • Ability to use GIT
    • Functional status
    • Blood glucose, Fluid I/O, Fluid Status, Body Weight, BMP, Mg Ca P, Albumin, Serum TGs, CBC with differential, Prealbumin, PT/PTT, AST, ALT, Trace Elements levels.
  79. Where is Albumin made? What is it half life? What are the levels for depletion?
    • Made in the liver.
    • Half-life of 20 days.
    • Depletion: Mild 2.8 - 3.5 g/dL
    • Moderate 2.1 - 2.7 g/dL
    • Severe < 2.1 g/dL
  80. What is prealbumin, its half life, and the normal range and the ranges for depletion?
    • It is a plasma protein.
    • Also a specific nutrition marker.
    • Half life is 2-3 days.
    • Normal range is 20-40 mg/dL
    • Helps us know how pt is progressing
    • Depletion: Mild 10-15 mg/dL, Moderate 7-10 mg/dL, Severe < 7 mg/dL
  81. What is transferrin?
    A blood plasma protein for iron delivery (occasionally used)
  82. What is usually improved with TPN (after weeks of therapy)?
    • nutrition status
    • increased serum total protein and serum albumin
    • nitrogen balance (prealbumin in normal range)
    • functional status
    • transition to oral nutrition if feasible
  83. Pharmacist's role in TPN therapy
    • ID appropriate use & duration
    • Select appropriate types of TPN
    • ID admin route and related issues
    • Determine nutrient goals (macro and micro)
    • Design, optimize, and adjust TPN admixture to meet nutrient goals accdg to pt's condition
    • ID compounding issues - osmolarity, compatibility, stability, sterility
    • Prepare and dispense the nutritional formulations
    • Monitor pts for effectiveness and adverse outcomes of TPN
    • Transition pts into other forms of nutrition support when appropriate
    • Participate in quality improvement for pt care and operational processes
    • Develop policy and procedures for nutrition support therapy
    • Engage in multidisciplinary team for nutrition support

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