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)
True or false: Most drugs are incompatible with TPN admixtures.
True
(insulin and some H2 blockers may be compatible)
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)
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
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.
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)
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
Different ways of characterizing different types of adult TPN
admin routes
macronutrients
duration of TPN admixture infusion
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)
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
How are most TPN admixtures compounded?
using automatic compounders - in a sterile environment that meets USP797 guidelines
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)
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.
What is the equation for TPN osmolarity?
(grams dextrose/liter x 5) + (grams AA/liter x 10) + mEq cations/liter
What is normal serum osmolarity?
280-295 mOsm/L
What osmolarity is acceptable for central TPN?
>1000
What is the acceptable osmolarity for Peripheral TPN?
< 900 mOsm/L
Which nutrients contribute much to TPN osmolarity?
dextrose and AA
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.
What can happen if Calcium and phosphorus are mixed in a TPN?
precipitation
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)
Which drugs are commonly added to TPN admixtures?
Insulin and H2 blockers. Most drugs are incompatible.
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
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
In adults, why use upper extremity site for catheter insertion rather than lower?
risk of blood clots
Why inspect TPN for visible particles before infusion?
Risk of embolus
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.
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.
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.
How often do the tubes need to be changed when they are used to admin dextrose/amino acid sol'n?
q72h (no longer)
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
Are low dose anticoagulants recommended to prevent thrombosis for central TPN?
no
How and when might anaphylaxis be a complication of TPN therapy?
Allergic rxns to TPN (IV lipid and egg allergy). Occurs early in therapy.
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
How and when might infection (bacterial and fungal) be a complication of TPN therapy?
(more common in critical care and long-term TPN patients)
Supportive care (e.g. short-term, additional IV fluid for hypotension)
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
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
Causes, clinical features, corrective interventions of Hyperglycemia in TPN
Excessive dextrose infusionSepsis
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/minInsulin therapy (IV insulin infusion or insulin added to TPN)
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 discontinuationDiscontinue the TPN with excessive insulin
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
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)
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
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
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
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?
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
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.
Presentation of refeeding syndrome
Pt may present with weakness, convulsions, respiratory failure, cardiac decompensation. Could die from complications.
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.
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
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)
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
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.
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.
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
What is prealbumin, its half life, and the normal range and the ranges for depletion?
