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Introduction

  1. Pharmacology. Glucose is an essential carbohydrate used as a substrate for energy production within the body. Although many organs use fatty acids as an alternative energy source, the brain is totally dependent on glucose as its major energy source; thus, hypoglycemia may rapidly cause serious brain injury. Dextrose administered with insulin shifts potassium intracellularly and maintains euglycemia for the treatment of calcium antagonist and beta-adrenergic blocker poisoning (hyperinsulinemia-euglycemia [HIE] therapy).
  2. Indications
    1. Hypoglycemia.
    2. Empiric therapy for patients with stupor, coma, or seizures who may have unsuspected hypoglycemia.
    3. Use with an insulin infusion for severe calcium antagonist poisoning, beta-blocker poisoning, and hyperkalemia.
  3. Contraindications. No absolute contraindications for empiric treatment of comatose patients with possible hypoglycemia. However, hyperglycemia and (possibly) recent ischemic brain injury may be aggravated by excessive glucose administration.
  4. Adverse effects
    1. Hyperglycemia and serum hyperosmolality.
    2. Local phlebitis and cellulitis after extravasation (with concentrations ≥10%) from the intravenous injection site.
    3. Administration of a large glucose load may precipitate acute Wernicke-Korsakoff syndrome in thiamine-depleted patients. For this reason, thiamine is given routinely along with glucose to alcoholic or malnourished patients.
    4. Administration of large volumes of sodium-free dextrose solutions may contribute to fluid overload, hyponatremia, hypokalemia, and mild hypophosphatemia.
    5. Use in pregnancy. FDA Category C (indeterminate). No currently available studies specifically addressing the risks of use during pregnancy. This does not preclude its acute, short-term use for a seriously symptomatic patient (Introduction).
  5. Drug or laboratory interactions. No known interactions.
  6. Dosage and method of administration
    1. As empiric therapy for coma, give 50-100 mL of 50% dextrose (equivalent to 25-50 g of glucose) slowly (eg, about 3 mL/min) via a secure intravenous line (children: 2-4 mL/kg of 25% dextrose, or 5-10 mL/kg of 10% dextrose; do not use 50% dextrose in children). Dextrose can also be given by intraosseous route in concentrations that range from 10% (neonates) to 25% (children) to 50% (adolescents).
    2. Persistent hypoglycemia (eg, resulting from poisoning by sulfonylurea agent) may require repeated boluses of 25% (for children) or 50% dextrose and infusion of 5-10% dextrose, titrated as needed. Consider the use of octreotide in such situations. Note: Glucose can stimulate endogenous insulin secretion, which may exacerbate a hyperinsulinemia (resulting in wide fluctuations of blood glucose levels during treatment of sulfonylurea poisonings).
    3. Hyperinsulinemia-euglycemia therapy usually requires an initial dextrose bolus of 25 g (50 mL of 50% dextrose) or 0.5 g/kg (children, 0.25 g/kg given in a 10-25% dextrose solution) unless the patient's initial blood glucose is already >200 mg/dL, followed by a dextrose infusion at an initial rate of 0.1-0.5 g/kg/h using a 5-10% dextrose solution to maintain the glucose in a normal range while insulin is infused. Adjust the rate and dextrose concentration (if >10% dextrose solution, administer via a central line) and supplement with dextrose boluses as needed.