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Lippincott Nursing Pocket Card
Parenteral nutrition (PN) is a form of nutritional supplementation containing dextrose, amino acids, electrolytes, vitamins, minerals, trace elements, and fluids delivered intravenously. Lipid emulsion may be infused separately or added to the solution, called total nutrient admixture (TNA) or 3-in-1 parenteral nutrition. PN should be prescribed only in patients who cannot utilize the enteral (intestinal) route for nourishment. The goals of PN therapy include improving nutritional status, preserving muscle mass, promoting weight gain, and supporting healing (Seres, 2017; Malone, 2014).
Unmanageable diarrhea, impaired absorption
Short bowel syndrome with weight loss
High-output enterocutaneous fistula
Severe infectious colitis, such as Clostridium difficile
Small bowel obstruction
Severe inflammatory bowel disease Ischemic bowel
Motility disorders
Prolonged ileus
Pseudo-obstruction
Scleroderma
Inability to achieve or maintain enteral access
Hemodynamic instability
Massive gastrointestinal bleeding
Water: Adults require about 30 to 40 mL/kg of fluid daily.
Carbohydrate: dextrose, available in 40, 50, and 70% concentrations.
Fat: intravenous lipid emulsion (IVLE).
Protein: crystalline amino acids (essential and nonessential); concentrations of 5.5% to 15%.
Electrolytes: sodium, potassium, magnesium, calcium, phosphorus, chloride and acetate.
Vitamins: based on patient requirements to prevent deficiency without causing toxicity. High intake of fat-soluble vitamins A, D, E, and K can lead to toxicity.
Trace elements: include chromium, copper, manganese, and zinc (iron and iodine not typically added). Act as cofactors for enzymes and transport of substances across cell membranes.
Insulin: may be added to control hyperglycemia; monitor glucose levels per unit protocol.
Initiating PN
Monitoring
Complications
Refeeding Syndrome: In patients with significant weight loss or long-term malnutrition, starting PN can induce “refeeding syndrome” manifested by electrolyte disturbances and fluid shifts or overload. Hypophosphatemia (may be lethal), hypokalemia, low magnesium and any electrolyte imbalance should be corrected before PN is started. In patients at risk, begin PN at 25% of estimated daily needs and slowly increase to goal. Provide supplemental thiamine for the first 3 days.
Central Line Associated Bloodstream Infection (CLABSI): high risk due to malnourishment, immunocompromised state, and long-term IV therapy.
Adhere to your institution’s central line bundle protocol
Dedicated single-lumen subclavian catheter for PN administration may decrease CLABSI.
PN-associated liver disease (PNALD): symptoms range from transient elevations in liver function tests (LFTs) to fibrosis, cirrhosis, and irreversible hepatic failure.
Metabolic bone disease (MB): abnormal bone metabolism resulting in decreased bone density and increased fracture risk; monitor serum calcium, phosphorus, and magnesium.
Destabilization of formula which may lead to emboli: monitor PN solution for faint cream layer, separation of oil and water.
Hyperglycemia: compounded by metabolic stress, steroid therapy, diabetes, obesity, sepsis and excessive glucose formulations.
Hypercapnea: results from oxidation of glucose to carbon dioxide.
Transitioning to enteral nutrition (EN) (Malone, 2014): In patients stabilized on PN, periodically repeated efforts should be made to initiate EN.
As tolerance improves and the volume of EN calories delivered increases, the amount of PN calories supplied should be reduced.
PN should be discontinued when ≥ 60% of target energy requirements are being delivered by the enteral route.
References:
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