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  1. Pharmacology

    1. Insulin, a hormone secreted by the beta cells of the pancreas, promotes cellular uptake of glucose into skeletal and cardiac muscles and adipose tissue. Insulin shifts potassium intracellularly.

    2. The mechanism by which insulin-dextrose (hyperinsulinemia-euglycemia [HIE]) therapy improves inotropy and increases peripheral vascular resistance is not known. Calcium antagonists inhibit insulin secretion by blocking the L-type calcium channels of pancreatic islet cells and induce insulin resistance. Insulin may reverse the hyperglycemia, hypoinsulinemia, and acidosis commonly observed in calcium antagonist poisoning. In calcium antagonist and beta-adrenergic blocker overdose, myocardial metabolism shifts from free fatty acid to carbohydrate metabolism. Insulin stimulates myocardial metabolism and inhibits free fatty acid metabolism. Insulin may also improve glucose uptake by cardiac myocytes.

    3. Human regular insulin is biosynthetically prepared with recombinant DNA technology. The onset of action to decrease blood glucose for regular insulin is 30 minutes–1 hour, and the duration of action is 5–8 hours. The serum half-life of regular insulin is 4–5 minutes after IV administration.

  2. Indications

    1. Hyperglycemia and diabetic ketoacidosis.

    2. Severe hyperkalemia (See Diagnosis of Poisoning).

    3. Administration with dextrose for hypotension induced by calcium antagonists (See Beta-Adrenergic Blockers) and beta-adrenergic blockers (See Arsine). Improved hemodynamics have been reported in case reports of patients with calcium antagonist toxicity and beta-adrenergic blocker overdose.

  3. Contraindications. Known hypersensitivity to the drug (less frequent with human insulin than with animal-derived insulin).

  4. Adverse effects

    1. Hypoglycemia.

    2. Hypokalemia.

    3. Lipohypertrophy or lipoatrophy at injection site (more common with repeated use).

    4. Fluid overload and hyponatremia with high-dose insulin infusion.

    5. Use in pregnancy. FDA Category B (See Warfare Agents–Chemical). Human insulin does not cross the placental barrier.

  5. Drug or laboratory interactions

    1. Hypoglycemia may be potentiated by ethanol, sulfonylureas, and salicylates.

    2. Corticosteroids (by decreasing peripheral insulin resistance and promoting gluconeogenesis), glucagon (by enhanced glycogenolysis), and epinephrine (via beta-adrenergic effects) may antagonize the effects of insulin.

  6. Dosage and method of administration

    1. Hyperglycemia. Administer regular insulin 5–10 U IV initially, followed by infusion of 5–10 U/h, while monitoring the effect on serum glucose levels (children: 0.1 U/kg initially, then 0.1 U/kg/h).

    2. Hyperkalemia. Administer regular insulin 0.1 U/kg IV with 50 mL of 50% dextrose (children: 0.1 U/kg insulin with 2 mL/kg of 25% dextrose).

    3. Hypotension from calcium antagonists and beta-adrenergic blockers unresponsive to conventional therapy (hyperinsulinemia-euglycemia therapy):

      1. Bolus of regular human insulin 1 U/kg IV. If blood glucose is below 200 mg/dL, give 50 mL (25 g) of 50% dextrose IV (children: 0.25 g/kg of 25% dextrose).

      2. Continuous infusion. Wide variations in insulin dose and duration have been reported. Doses as high as 10 U/kg/h have been administered. Dose may be titrated upward as quickly as every 10 minutes. Dilute 500 U of regular human insulin in 500 mL of 0.9% saline (insulin concentration, 1 U/mL). Follow bolus with insulin infusion of 0.5–1 U/kg/h titrated to systolic blood pressure of 100 mm Hg or higher and mean arterial pressure above 60 mm Hg. Begin 10% dextrose infusion at 100 ml/h and administer dextrose boluses (50% dextrose for adults) as ...

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