Metabolic Complications of Parenteral Nutrition
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Metabolic Complications of Parenteral Nutrition:

Condition Suspected Cause Suggested Treatment
Hyperglycemia Glucose load exceeds endogamous insulin secretion Advance rate slowly, do not increase until hyperglycemia is controlled
Steroid therapy Add insluin to parenteral solution or give subcutaneously
Underlying disease state, eg, sepsis, diabetes mellitus, trauma, major surgery Provide fewer kcals as dextrose and increase fat provision
Hyperosmolar / glycemic, nonketotic dehydration, and coma (HHND) Uncontrolled hyperglycemia and persistant glycosuria producing osmotic direseis accompanied by deteriorated mental status and coma Stop parenteral solution immediately. Provide hydration with hypotonic solution. Provide insulin and correct electrolyte imbalances
Hypoglycemia Abrupt discontinuation of hypertonic dextrose solution due to medical emergency or mechanical problem Treat hypoglycemia with IV bolus infusion of 50% dextrose
Decreased insulin rate or requirement Monitor glucose levels and adjust inulin in bottle accordingly
Hyperkalemia Decreased renal function Discontinue present solution. Administer replacement fluid as 10% dextrose at same rate until new solution available
Excessive Potassium administration Reduce or hold amount of potassium given in next bottle
Low cardiac output, tissue necrosis, and systemic sepsis Monitor serum level closely and adjust potassium in TPN solution accordingly
Hypokalemia Synthesis of protein during anabolism increases requirement Increase amount given in solution. Additional IV supplementation may be needed via "piggy back" or peripherally
Potassium loss as in diuresis, gastointestinal losses, steroid therapy, and with potassium wasting drugs  
Hypernatremia Dehydration resulting from fever, inadequate amount of fluids, hyperventilation, diuresis, antidiuretic hormone (ADH) deficiency, and head trauma Continue parenteral solution. Provide additional hydration with 5% dextrose
Hyponatremia True sodium depletion
Sodium losses resulting from sodium wasting diuretics, sodium losing nephropathy, GI losses, and adrenal insufficiency
Increase amount of sodium in parenteral solution. Additional isotonic or hypertonic saline IV may be indicated
Dilutional hyonatremia
Extracellular fluid overload as in congestive heart failure (CHF), renal failure, liver disease/cirrhosis, and edema, or due to excessive administration of fluids
Increase concentration of dextrose, amino acids, and lipids. Discontinue any additional large-volume IV solutions
Hypo- phosphatemia Inadequate administration Decrease amount given in solution
Increaed needs during anabolism and protein synthesis Increase amount of phosphorus in solution until serum level normalizes. Peripheral replacement may be needed.
Hyper- phosphatemia Excessive administration Decrease amount given in solution
Renal insufficiency Consider amount of phosphorus being provided by fat emulsion (phospholipids) 20% lipid emulsions contain less phosphorus per kcal than 10% emulsions
Hypo/hyper - vitaminosis Inadequate or excessive administration Adjust amount given in solution
Hypo- magnesemia Increased needs during anabolism and protein synthesis Provide additional MgSO, in solution until serum level normalizes. Peripheral replacement may be needed
Hyper- magnesemia Excessive administration Decrease amount given in solution
Renal failure Start with decreased amount
Hypocalciuria Excessive administration Decrease amount given in solution and adjust accordingly based on serum levels
Renal Failure  
Excessive vitamin D administration  
Tumor Lysis  
Hypocalciuria Increased requirement due to underlying medical condition, eg, pregnancy Increase amounts given in solution within limitations of solubility
Hypoalbuminemia There is approximately 0.8 mg/dL decrease in serum calcium for every 1.0 g/dL drop in albumin concentration*
Hyper- triglyceridemia Intolerance due to underlying disease state Obtain baseline tryglyceride level and evalutate tolerance to test dose
Inability to clear lipids Reduce amount given to only amount needed for prevention of essential fatty acid deficiency (EFAD)
Essential Fatty Acid Deficiency (EFAD) Inadequate provision of lipids Provide approximately 4 - 10% of daily kcals as lipids for treatment of existing dificiency and 500 mL of 10% lipids 1-2 tiomes per week for maintenance
Prerenal axotemia Excessive provision of protein kcals Decrease protein content of solution and provide adequate NPC:N
Insufficient provision of nonportein kcals from carbohydrate and fat  
Inadequate hydration Icneased hydration with non-amino acid-containing solution  
Hyper- ammoniemia Hepatic dysfunction Decrease protein content of solution
Use of protein hydrolysate instead of cystalline amino acids Standard amino acid solutions are now crystalline amin acids
Hyperchloremic metabolic acidosis Excessive administration of chloride Replace chloride salts with acetate salts
Metabolic alkalosis GI losses Replace acetate salts with chloride salts
Hypokalemia Correct with increased potassium. Peripheral replacement may be needed
Zinc deficiency Failure to provide supplemental dosage Provide minimum recommended dosage
Increased needs due to GI losses or wound healing Incease amount in infusion
Copper dificiency Failure to provide supplmeental dosage Provide minimum recommended dosage
Hepatic / biliary complications Elevated liver fucntion tests including SGPT, SGOT, alkaline phosphatase, total bilirubin Avoid excess provision of kcals
Fatty liver Provide adequate amount of amino acids
Cholestasis  
Respiratory complications Increased CO2 production and difficulty weaning from mechanical ventilation Provide less kcals as dextrose and increase fat provision. Avoid overfeeding

*Determin ionized calcium level corrected for hypoalbuminemia: Ionized CA = (meausred serum CA) + (40 - actual albumin (g/dL)) x 0.8

From ADA Diet Manual Chicago: ADA 199