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  1. Pharmacology. Glucose is an essential carbohydrate that is 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 cause serious brain injury rapidly. Dextrose administered with insulin shifts potassium intracellularly and maintains euglycemia for 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 (See Calcium Channel Antagonists), beta blocker poisoning (See Beta-Adrenergic Blockers), and hyperkalemia (See Diagnosis of Poisoning).

  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 (occurs 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 (See Thiamine (Thiamin, Vitamin B1) 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). This does not preclude its acute, short-term use for a seriously symptomatic patient (See Introduction in Section III).

  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 10% can also be given by intraosseous route.

    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 (See 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 (unless the patient's initial blood glucose is >250 mg/dL), followed by a dextrose infusion at a rate of 0.5 g/kg/h with a 5–50% dextrose solution (if >25% dextrose solution, administer via a central line) as needed to maintain euglycemia while insulin is infused (See Insulin).

  7. Formulations

    1. Parenteral. Dextrose (d-glucose) Injection 50%, 50-mL ampules, vials, and prefilled injector; 25% dextrose, 10-mL syringes; various solutions of 2.5–70% dextrose, some in combination with saline or other crystalloids.

    2. Suggested minimum stocking levels to treat a 100-kg adult for the first 8 hours and 24 hours: dextrose, first 8 hours: 450 g or six prefilled injectors (50%) and three bottles or bags (10%, 1 L each); ...

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