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Hyperglycemia in patients receiving PN is primarily the result of excessive dextrose infusion. Factors that exacerbate glucose intolerance include sepsis, surgery, diabetes, pancreatitis, prematurity, and corticosteroid therapy. Elevated blood glucose levels may coincide with PN initiation, but endogenous insulin secretion usually adapts within 48 to 72 hours. Untreated hyperglycemia causes osmotic diuresis that can lead to hyperosmolar, hyperglycemic, nonketotic dehydration with electrolyte disturbances, impaired phagocytosis (42), and liver steatosis (43). The first effort in managing hyperglycemia is to decrease the dextrose load or reduce the infusion rate. However, this may compromise nutritional intake as dextrose is the major source of calories in PN. If reducing dextrose does not improve hyperglycemia, insulin therapy is then indicated. Because infants have variable responses to insulin therapy, adding insulin to the PN solution should be avoided. Instead, a regular insulin drip via alternative IV access should be initiated and titrated based on serial serum glucose checks.

Hypoglycemia with PN is usually the result of a sudden reduction of the PN infusion rate. In patients who receive PN over a portion of the day (“cycled”), hypoglycemia may be avoided by gradually reducing the rate over 1 to 2 hours prior to discontinuation. Premature infants are at higher risk for hypoglycemia due to their underdeveloped metabolic response and often do not tolerate cycling (44). If PN must be unavoidably discontinued, intravenous administration of dextrose 10% in water will prevent symptomatic hypoglycemia (3).

High concentrations of dextrose in the infusate is the primary cause of hypertriglyceridemia in PN patients. Excessive carbohydrate intake enhances hepatic and adipose tissue lipogenesis (45). Other factors that predispose to hypertriglyceridemia in pediatric patients receiving PN include prematurity, lipid overfeeding, critical illness, and sepsis (46).