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.
(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
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.
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
Refeeding Syndrome Liver steatosis
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
Reassess and redefine nutrition goals - appropriately increase TPN macronutrients
Causes, clinical features, corrective interventions of Hyperglycemia in TPN
Excessive dextrose infusionSepsis
Immune system dysfunction
Increased susceptibility to infx
Impaired wound healing
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
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
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
Causes, clinical features, corrective interventions of GI Intestinal atrophy, Gastroparesis in TPN
lack of stimulation from luminal nutrients
increase intestinal permeability and bacterial translocation
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
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
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?