TABLE 6.15. Possible Etiologies and Treatment of Common Complications of Central Parenteral Nutrition.

Problem	Possible etiology	Treatment
Glucose
Hyperglycemia, glycosuria, hyperosmolar nonketotic dehydration or coma	Excessive dose or rate of infusion; inadequate insulin production; steroid administration; infection	Decrease the amount of glucose given; increase insulin; administer a portion of calories as fat
Diabetic ketoacidosis	Inadequate endogenous insulin production and/or inadequate insulin therapy	Give insulin; decrease glucose intake
Rebound hypoglycemia	Persistent endogenous insulin production by islet cells after long-term high carbohydrate infusion	Give 5%-10% glucose before total parenteral infusion is discontinued
Hypercarbia	Carbohydrate load exceeds the ability to increase minute ventilation and excrete excess CO2	Limit glucose dose to 5mg/kg/min. Give greater percentage of total caloric needs as fat (up to 30%-40%)
Fat
Hypertriglyceridemia	Rapid infusion; decreased clearance	Decrease rate of infusion; allow clearance (approximately 12h) before testing blood
Essential fatty acid	Inadequate essential fatty acid administration efficiency	Administer essential fatty acids in doses of 4%-7% of total calories
Amino acids
Hyperchloremia metabolic acidosis	Excessive chloride content of amino acid solutions	Administer Na+ and K+ as acetate salts
Prerenal azotemia	Excessive amino acids with inadequate caloric supplementation calories	Reduce amino acids; increase the amount of glucose
Miscellaneous
Hypophosphatemia	Inadequate phosphorus administration with redistribution into tissues	Give 15mm phosphate/1000 i.v. evaluate antacid and Ca2+; administration
Hypomagnesemia	Inadequate administration relative to increased losses (diarrhea, diuresis, medications)	Administer Mg2+ (15-20mEq/1000kcal)
Hypermagnesemia	Excessive administration; renal failure	Decrease Mg2+ supplementation
Hypokalemia	Inadequate intake relative to increased needs for anabolism; diuresis	Increase K+ supplementation
Hyperkalemia	Excessive administration, especially in metabolic acidosis; renal decompensation	Reduce or stop exogenous K1; if EKG changes are present, treat with Ca gluconate, insulin, diuretics
Hypocalcemia	Inadequate administration; reciprocal response to phosphorus repletion without simultaneous calcium infusion	Increase Ca2+ dose
Hypercalcemia	Excessive administration; excess vitamin D administration	Decrease Ca2+ and/or vitamin D administration
Elevated liver transaminases or serum alkaline phosphatase and bilirubin	Enzyme induction secondary to amino acid imbalances or overfeeding	Reevaluate nutritional prescription